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Institute of Neurolog

ROCKEFELLER
MEDICAL
LIBRARY

National Hospital
Queen Squate
LONDON

I —

NATIONAL HOSPITAL LIBRM-.Y
Not to be taken away.

A TREATISE ON THE DISEASES OF THE
NERVOUS SYSTEM.

A TREATISE

THE DISEASES

OF THE

NERVOUS SYSTEM,

JAMES ROSS, M.D.

MEMBER OF THE ROYAL COLLEGE OF PHYSICIANS, LONDON ;
ASSISTANT PHYSICIAN TO THE MANCHESTER ROYAL INFIRMARY ;
CONSULTING PHYSICIAN TO THE MANCHESTER
SOUTHERN HOSPITAL.

ILLUSTRATED WITH LITHOGRAPHS, PHOTOGRAPHS, AND
TWO HUNDRED AND EIGHTY WOODCUTS.

Volume II.

LON DON :

J. & A. CHURCHILL, NEW BURLINGTON STREET.

1881.

MANCHESTER :
PRINTED BY ALEXANDER IRELAND AND CO.,
PALL MALL.

CONTENTS OF VOLUME II.

BOOK II.

SPECIAL PATHOLOGY OF THE NERVOUS SYSTEM (Continued).

Part III.

DISEASES OF THE SPINAL CORD AND MEDULLA

OBLONGATA.

PAGE.

Chapter I. Anatomical and Physiological Introduction ... 3

Chapter II. Morbid Anatomy and Classification of the
Diseases of the Spinal Cord and Medulla
Oblongata.

(i.) Morbid Anatomy ... ... 84

(il.) Classification 100

Chapter III. System Diseases of the Spinal Cord and
Medulla Oblongata.

(i.) Poliomyelopathies.

1. Poliomyelitis Anterior Acuta 105

2. Poliomyelitis Anterior Chronica ... 136

3. Progress! Ve" Muscular AtropJkj., » ... ... 145

4. Prirnary fAbio-glos'so-Laryngeal Paralysis 173

5. Pseido^-.Hypertropmc Paralysis' ' ... 185

Chapter IV. System dIseas-es of the Spinal' Cord and
Medulla Oblongata {continued)'. . j
(n.) Leucomyelopaiines. J. •. \

1. Progressive Locomotor Ataxy, "„'. • 211

2. Sclerosis of the Columns of GoH ... 249

3. Sclerosis of the Direct Cerebellar Tracts ... 250

4. Lateral Sclerosis 251

TABLE OF CONTENTS.

PAGE.

Chapter V. Mixed Diseases op the Spinal Cord and
Medulla Oblongata.

(i.) Paralysis Ascendens Acuta ... ... 264

(n.) Acute Diffused Myelitis 272

(in.) Chronic Diffused Myelitis " 292

(iv.) Myelomalacia 308

Chapter VI. Vascular Diseases op the Spinal Cord and
Medulla Oblongata.

(i.) Anaemia, Thrombosis, and Embolism of the Spinal Cord
and Medulla Oblongata.

1. Anaemia of the Spinal Cord ... 310

2. Anaemia of the Medulla Oblongata — Throm-

bosis and Embolism — -Necrotic Softening. 313

(n.) Hypereemia and Haemorrhage of the Spinal Cord and
Medulla Oblongata.

1. Hyperaemia of the Spinal Cord and its Mem-

branes ... ... 317

2. Haemorrhage into the substance of the

Spinal Cord ... ... ... ... ... 321

3. Hyperaemia and Haemorrhage of the Medulla

Oblongata ... ... ... ... ... 327

Chapter VII. Functional and Secondary Diseases op the
Spinal Cord and Medulla Oblongata.

(i.) Spinal Irritation 332

(n.) Neurasthenia Spinalis ... ... ... ... ... 335

(in.) Keflex and Secondary Paralogia 339

(rv.) Saltatory Spasm 341

(v.) Tonic Spasms in Muscles capable of Voluntary Movement 342

(vi.) Intermittent Spinal Paralysis 343

(vn.) Toxic Spinal Paralysis 344

(vm.) Hysterical Paraplegia ... ... ... ... ... 344

Chapter VIII. Traumatic Diseases, Tumours, and Abnor-
malities op the Spinal Cord and Medulla
Oblongata.

(i.) Wounds of the Spinal Cord and Medulla Oblongata ... 346
(n.) Slow Compression of the Spinal Cord and Medulla

Oblongata ... ... ... ... 351

(in.) Hemiplegia et Hemiparaplegia Spinalis ... ... 361

(iv.) Concussion of the Spinal Cord ... ... ... ... 368

(v.) Tumours of the Spinal Cord and Medulla Oblongata 372

TABLE OF CONTENTS. Vll

PAGE.

Chapter IX. Diseases of the Membranes of the Spinal Cord
and Medulla Oblongata,
(i.) Vascular Diseases of the Membranes.

1. Hyperaeniia of the Spinal Membranes ... 381

2. Meningeal Apoplexy (Hsematorrhachis)... 381

(n.) Pachymeningitis Spinalis.

1. Pachymeningitis Spinalis Externa ... ... 384

2. Pachymeningitis Spinalis Interna (Hyper-

trophica et Haeniorrhagica) ... ... 386

(in.) Leptomeningitis Spinalis.

1. Leptomeningitis Spinalis Acuta 391

2. Leptomeningitis Spinalis Chronica ... ... 396

(iv.) Tumours of the Spinal Membrane ... ... ... 400

(v.) Deformities of the Spinal Membranes ... ... ... 404

Part IV.

DISEASES OF THE ENCEPHALON.
Chapter I. Anatomical and Physiological Introduction ... 409

Chapter II. Morbid Anatomy and Classification of the
Diseases of the Encephalon.

(i.) Morbid Anatomy of the Encephalon ... 501

(il.) Classification of the Diseases of the Encephalon 508

Chapter III. General Consideration of Focal Diseases,
According to the Nature of the Lesion.

1. Occlusion of the Intracranial Vessels 511

(a) Occlusion of the Cerebral Arteries ... ... 511

(b) Thrombosis of the Cerebral Sinuses ... 518

Chapter IV. General Consideration of Focal Diseases,
According to the Nature of the Lesion {con-
tinued).

2. Intracranial Haemorrhage 525

(a) Cerebral Haemorrhage ... ... ... 525

(b) Meningeal Haemorrhage ... 543

Chapter V. General Consideration of Focal Diseases,
According to the Nature of the Lesion (con-
tinued).

3. Intracranial Tumours 547

Vlll TABLE OF CONTENTS.

PAGE.

Chapter VI. Special Consideration op Focal Diseases,
According to the Localisation of the Lesion.

1. Affections of the Peduncular Fibres and Internal Capsule.

a. Affections of the Pyramidal Tract.

(i.) Hemiplegia ... 568

(ii.) Hemispasm ... 569

b. Affections of the Sensory Peduncular Tract.

Hemiansesthesia 582

Chapter VII. Special Consideration of Focal Diseases,
According to the Localisation of the Lesion
(continued).

2. Cortical Lesions.

a. Lesions in the Area of the Middle Cerebral

Artery.

(i.) Monospasms and Unilateral Convul-
sions ... ... ... 594

(ii.) Cortical Paralyses and Monoplegiae . . . 599
(iii.) Affections of Speech from Cortical

Disease ... 612

b. Lesions in the Area of the Posterior Cere-

bral Artery 633

c. Lesions in the Area of the Anterior Cere-

bral Artery ... ... 640

Chapter VIII. Special Consideration of Focal Diseases,
According to the Localisation of the Lesion
(continued).

3. Lesions of the Basal Ganglia, External Capsule, and

Claustrum.

(a) Lesions of the Lenticular Nucleus ... ... 643

(b) Lesions of the Caudate Nucleus . . . 645

(d) Lesions of the Corpora Quadrigemina . . . 649

(e) Lesions of the Claustrum and External

Capsule ... ... ... 650

(/) Lesions of the Base of the Skull.

(i.) Lesions of the Anterior Fossae of the

Skull 651

(ii.) Lesions of the Middle Fossae of the

Skull ... ' ... 651

(iii.) Haemorrhage into the Lateral Ven-
tricles ... ... ... ... ... 655

(iv.) Tumours in the neighbourhood of the

Pituitary Body • ... 655

TABLE OF CONTENTS. IX

I'AGK.

Chapter IX. Special Consideration op Focal Diseases,
According to the Localisation of the Lesion

(continued).

4. Lesions localised in the Structures situated below the
Tentorium.

a. Lesions in the Pons and Peduncles of the

Cerebrum ••• 661

b. Lesions in the Peduncles of the Cerebellum 670

c. Lesions in the Cerebellum ... 671

Chapter X. Diffused Diseases of the Encephalon.
(i.) Ansemia and Hypersemia of the Brain.

(i.) Anemia of the Brain • • • 685

(ii.) Hyperemia of the Brain 693

Chapter XL Diffused Diseases of the Encephalon (con-
tinued).

(n.) Atrophy and Hypertrophy of the Brain.

(i.) Atrophy of the Brain ... ... 703

(ii.) Hypertrophy of the Brain ... ... ... 706

Chapter XII. Diffdsed Diseases of the Encephalon (con-
tinued).

(in.) Shock and Concussion.

(i.) Shock 710

(ii.) Concussion 716

Chapter XIII. Diffused Diseases of the Encephalon (con-
tinued).

(iv.) Encephalitis.

1. Diffused or General Encephalitis 724

2. Partial or Local Encephalitis 724

a. Acute Encephalitis complicating affections

of the Bones of the Skull 727

b. Acute Pysemic Encephalitis 728

c. Encephalitis around pre-existing Lesions in

the Brain 728

d. Chronic Abscess of the Brain 731

TABLE OF CONTENTS.

PAGE.

Chapter XIV. Diseases op the Membranes op the Brain.

(i.) Diseases of the Dura Mater.

(i.) External Pachymeningitis ... ... ... 743

(ii.) Internal Hemorrhagic Pachymeningitis ... ... 745

Chapter XV. Diseases op the Membranes op the Brain (con-
tinued).

(n.) Diseases of the Pia Mater.

1. Leptomeningitis Infantium 751

2. Tubercular Meningitis 754

Chronic Hydrocephalus ... ... 770

3. Basilar Meningitis 774

4. Meningitis of the Convexity of the Brain ... ... 778

5. Metastatic Meningitis ... ... 784

6. Traumatic Meningitis 786

Part V.

DISEASES OF THE ENCEPHALO-SPINAL SYSTEM.

Chapter I. Paralysis Agitans, and Multiple Sclerosis.

(i.) Paralysis Agitans ... ... ... ... 791

(n.) Multiple Sclerosis 801

Chapter II. Chorea, and Meniere's Disease.

(i.) Chorea 814

(n.) M6nie*re's Disease 830

Chapter III. Epidemic Cerebro-spinal Meningitis, Tetanus,
and Hydrophobia.

(i.) Epidemic Cerebro-spinal Meningitis 834

(n.) Tetanus 842

(ill.) Hydrophobia 855

Chapter IV. Hysteria 865

Chapter V. Catalepsy, Trance, Ecstasy, and other Allied
Conditions.

(i.) Catalepsy 904

(n.) Trance .... 907

I . (in.) Ecstasy 907

(iv.) Somnambulism and Hypnotism 908

TABLE OF CONTENTS. xi

PAGE.

Chapter VI. Epilepsy and Eclampsia.

(i.) Epilepsy 913

(n.) Eclampsia 945

Chapter VII. Toxic, and Febrile and Post-febrile Nervous
Disorders.

(i.) Alcoholic Nervous Diseases 953

(n.) Saturnine Nervous Diseases ... ... ... ... 955

(in.) Mercurial Nervous Diseases 961

(iv.) Syphilitic Nervous Diseases 962

(v.) Febrile and Post-Febrile Nervous Diseases 975

BOOK II.

SPECIAL PATHOLOGY OF THE NERVOUS SYSTEM.

6*—

SPECIAL PATHOLOGY OF THE NERVOUS

SYSTEM.

Part III. — DISEASES OF THE SPINAL CORD AND
MEDULLA OBLONGATA.

CHAPTER I.
ANATOMICAL AND PHYSIOLOGICAL INTRODUCTION.

(I.) —STRUCTURE OF THE SPINAL MEMBRANES.

The spinal cord is surrounded by a compound connective-tissue
sheath, consisting of (1) the dura mater, (2) the arachnoid,
and (3) the pi a mater.

§ 349. (1) Tlie dura mater is composed of lamellae, each of
which consists of a layer of parallel bundles of fine connective-
tissue fibres. Flattened, more or less branched connective-tissue
cells lie between the lamellae; they lie in spaces which com-
municate with one another, the latter constituting the lymph-
canalicular system. The inner surface of the dura mater is
lined by a thin hyaline elastic membrane, which is covered by
a continuous layer of nucleated endothelial plates. The outer
surface is also covered with a continuous layer of endothelium.
The dura mater is richly supplied with blood-vessels and nerves.

(2) The arachnoid sheath is a delicate membrane, composed
of parallel bundles of connective-tissue fibres, longitudinally
disposed, with connective-tissue corpuscles lying between them.
The outer surface is covered by one or two layers of endothelial
plates, constituting an endothelial membrane. On the inner
surface is a fenestrated membrane, composed of anastomosing,
transversely disposed trabeculae of connective-tissue fibres, the

ANATOMICAL AND PHYSIOLOGICAL INTRODUCTION.

inner surface of which is covered by a single layer of endo-
thelial plates.

(S) The pia mater consists of an external and internal
portion. The former is composed of longitudinal bundles of
connective-tissue fibres, and its external surface is covered by
an endothelial layer (Klein). The internal portion, or intima pise,

Fig. 100.

Fig 100 (After Key and Retzius). Transverse Section of the Spinal Cord in the
upper dorsal region, with its membrane*.- Close on the inner surface of the dura
STlies the arachnoid (B), which is thrown into longitudinal folds at interval.
In the posterior subarachnoidal space (the part behind the hgamenta denticu-
lata, G), the septum posticum (C) may be observed in the middle, with its .
numerous partitions, along with the subarachnoidal spaces which they enclose .
The septum becomes partly attached to the arachnoid externaUy, and partly
spreadsPlaterally o ver the inner surface of that membrane (D) The septum spreads
internally over the pial sheath as the epipial subarachnoidal tissue (E), forming:
numerous small spaces. Two vessels may be observed m this epipial space. .
]Tthe posterior nerve roots, surrounded by the subarachnoidal membranes
The space (I) between the latter membranes and the septum posticum is of,
variable depth. K is the space between the posterior nerve roots, with their
membranes, and the ligamentum denticulatum ; this space bemg free ] from
Sbrane throughout the entire length of the cord the subarachnoidal flmdj
finds a freer paslage through it than through any other part of the posterior
subarachnoidal space. Anterior to the ligamenta denticulata (G), the antenori)
subarachnoidal space may be observed free from membrane. H, the anteno
.. nerve roots.

Fig. 101.

Fig. 101 (From Key and Retzius). Diagram of a Transverse ^fj^Si^^flff,
Cord and its mLbranes, showing tlie natural size and relative positions of U
cord, membranes, and spaces.

ANATOMICAL AND PHYSIOLOGICAL INTRODUCTION. 5

J is a meshwork of bundles of connective-tissue fibres, its inner
J- surface being lined by a layer of endothelial cells. The pia
I. mater contains numerous blood-vessels, which lie between the
J external and internal layers, whence they penetrate into the
I substance of the cord being surrounded by a prolongation of the
1 pial sheath.

The subarachnoidal tissue consists of a plexus of trabecular
of fibrous connective tissue ensheathed in endothelium and con-
taining a few elastic fibres. It forms a spongy tissue between
the arachnoidal and pial sheaths, and subdivides the subarach-
noidal space into numerous minute lacunar. It is a prolongation
of the inner portion of the arachnoid, and its trabecular contain
larger and smaller blood-vessels.

Ligamentum denticulatum stretches like a diaphragm
between the arachnoid and pial sheaths on each side of the
cord, from the foramen ovale magnum down to the filium ter-
minale, between the anterior and posterior nerve roots. The
subarachnoidal space is consequently divided into an anterior
and posterior chamber. The ligamentum denticulatum consists
of trabecular of connective-tissue bundles, the trabecular being
covered with endothelium. The tissue passes into the external
layer of the pia mater (Klein).

Isolated connective-tissue trabecular also extend between the
dura mater and arachnoid; they are ensheathed in endothelium,
while blood-vessels and nerves pass from the one membrane to
the other. These trabecular are most numerous in the posterior
parts of the cord.

Between the dura mater and arachnoid is the subdural, and
between the arachnoid and pia mater is the subarachnoidal
lymph space. Neither of these spaces form one open and free
cavity, inasmuch as numerous connective-tissue trabecular pass
between the dura mater and arachnoid, and between the latter
and pia mater. The two spaces do not, however, communicate
with one another.

The nerve roots receive a prolongation from both the
arachnoidal and dural sheaths, and consequently the lymph
spaces of the peripheral nerves and their ganglia have been
injected from the subarachnoidal and subdural spaces re-
spectively (Key and Retzius).

6 ANATOMICAL AND PHYSIOLOGICAL INTRODUCTION.

(II.)- STRUCTURE OF THE SPINAL CORD AND MEDULLA

OBLONGATA.

The spinal cord consists of a framework, with grey and white
matter embedded in it.

§ 350. The framework consists of the following parts : —

(1) Connective-tissue Processes. — Processes of fibrous con-
nective tissue pass from the intima pise into the anterior
fissure, and at different points of the circumference of the
cord, where they form septa, which divide the white columns of
the cord into segments. These prolongations of the intima
pise carry blood-vessels into the cord.

(2) Neuroglia. — The chief part of the framework consists of
a semi-fluid substance named the neuroglia-matrix. This
substance presents a granular aspect under certain reagents,
but is homogeneous in the fresh condition. Numerous minute
fibrils, which anastomose with one another in a network, are

Fig. 102.

150
I

Fig. 102 (Fi om Henle's Anatomie). Diagram of the Spinal Cord and its Membranes.
1, the dura mater ; 2, the arachnoid, and (3) the pia mater ; 4, the cortical .
layer of the neuroglia.

ANATOMICAL AND PHYSIOLOGICAL INTRODUCTION. 7

embedded in this substance. These fibrils have a longitudinal
direction, except in the septa, where they form transverse net-
works, and in the grey substance, where they extend uniformly
in all directions (Klein). Flat, branched, nucleated connective-
tissue corpuscles are found in connection with the network of
the neuroglia fibrils. The neuroglia, therefore, is composed of
neuroglia-matrix, neuroglia fibrils, and branched cells, the latter
being named Beitevs cells (Fig. 103).

Fig. 103.

Fig. 103 (From Henle's Anatomie). Deiter's Cells.

Distribution of tlw Neuroglia. — The neuroglia is abundant in the fol-
lowing parts : —

(a) On the external surface of the cord, where it forms a peripheral
crust beneath the intima pise, the latter being easily separated from the
former.

(6) In the septa which pass between different sections of the white
matter ; the posterior fissure being, indeed, only a septum of this kind
(Klein).

(d) A layer of neuroglia of considerable thickness surrounds the epi-
thelial lining of the central canal, named the central grey nucleus of
Kolliker.

(e) A peculiar form of neuroglia is found in the posterior portion of the
posterior grey horns forming the substantia gelatinosa of Rolando.

The neuroglia is always more abundant near the grey matter and in
the peripheral crust than in the parts between them.

ANATOMICAL AND PHYSIOLOGICAL INTRODUCTION.

§ 351. The grey matter occupies the central parts of the cord
in the well-known shape of an H. The median part contains the
central canal, and the "central grey nucleus" of Kolliker the
anterior grey and white commissures lying in front and the pos-
terior commissure behind it. The lateral parts or columns con-
sist of an anterior, middle, and posterior part ; the first of these
representing the anterior, and the last the 'posterior grey
horn ; while the middle portion on each side of the central
canal consists of the vesicular column of Clarke, and what may
be called the central column. The central grey nucleus of
Kolliker may indeed be regarded as a portion of the central
column.

The grey matter consists of a (1) matrix of neuroglia, (2)
ganglion cells, and (3) nerve fibres.

(1) The neuroglia of the grey matter is similar to that of
the white. It is looser in texture and more spongy in the
central grey column than in either the anterior or posterior
horns, and in this situation it also contains a relatively larger
number of Deiter's cells.

(2) The ganglion cells of the anterior horns are relatively
large, branched cells, containing in some animals masses of
yellow pigment ( § 13 ). These cells are surrounded by a
lymph space, through which the processes of the cell pass.
The ganglion cells of the posterior horns are much smaller and
less branched than those of the anterior horns. Some of the
latter appear spindle-shaped, but each extremity is branched
into several processes.

(3) The nerve fibres of the grey matter are of different kinds.
The great bulk of the grey matter is composed of a minute and
dense network of fine fibrils, named Gerlach's nerve network.
The nerve network surrounding the central grey nucleus of
Kolliker is less dense than in other parts. The branched pro-
cesses of the ganglion cell attach themselves to Gerlach's nerve
network; while the unbranched processes pass into a rnedul--
lated nerve fibre of the anterior root. The cells of the pos-
terior horns are not directly connected with any nerve fibres,
but anastomose with them indirectly through Gerlach's nerve.1
network (Klein).

ANATOMICAL AND PHYSIOLOGICAL INTRODUCTION. 9

§ 352. The white matter is composed of medullated nerve
fibres, by far the greater number being arranged in a longitudinal
direction. A vertical section of the spinal cord is represented in
Fig. 104, showing the longitudinal disposition of the fibres in
the anterior and lateral columns. Each nerve fibre possesses
an axis cylinder, and a medullary sheath, but there is no definite
evidence of the presence of a sheath of Schwann, or of nerve
corpuscles, as in the medullated fibres of the cerebro-spinal
nerves. The nerve fibres are embedded in neuroglia as pre-
viously described ; they vary much in size, some being broad,
some of medium size, while others are very fine.

Fig. 104.

Cga

Willi

Fig. 104 (From Henle's Anatomie). — Fl, Anterior column; Cga, Anterior grey
horn ; Fa, Lateral column ; Ca, Posterior grey horn.

The white matter also contains nerve fibres that have
an oblique or hoiizontal direction. The following may be
distinguished : —

(1) The fibres of the posterior roots pass into the grey matter of the
posterior horns as horizontal fibres. These fibres on entering the cord
spread out laterally in the form of a fan, so that an external fasciculus, an
internal fasciculus, and a median portion may be distinguished. The
fibres of the external fasciculus wind forwards round the external margin
of the posterior horn, and at least some of them pass forwards through
the anterior commissure, a few even passing between the longitudinal
fibres of the anterior column, so as to reach the internal and anterior
groups of ganglion cells of the anterior grey horn of the opposite side

10 ANATOMICAL AND PHYSIOLOGICAL INTRODUCTION.

(Fig. 134, p"). The fibres of the internal fasciculus pass between the
longitudinal fibres of the posterior root-zone to gain the posterior horn
(Fig. 334, pr'). Some of them then wind round the vesicular column of
Clarke, but it is not known whether they are connected with the cells of
that column. A few of these fibres appear to pass behind the vesicular
column of Clarke and to decussate with the corresponding fibres of the
opposite side in the posterior commissure. The median portion of the
posterior root enters the white matter of the posterior column, and its
fibres pass for a longer or shorter distance in a longitudinal direction,
either upwards or downwards, before joining the posterior grey horns.

(2) The medullated nerve fibres of the anterior nerve roots pass in an
oblique direction from the grey matter of the anterior horns through the
white matter.

(3) The anterior commissure is said by Gerlach to be composed of
medullated nerve fibres that pass from the grey matter of the anterior
horn of one side into the white matter of the anterior tract of the oppo-
site side. Some of the fibres, however, pass from the anterior horn of one
side to the pyramidal tract of the opposite side, while others, as already
described, pass from the internal fasciculus of the posterior roots of one
side to the anterior grey horn of the opposite side.

(4) Medullated nerve fibres emerge from the sides of the grey matter
of the anterior horns, and after a short course enter the white matter of
the lateral tracts (Klein).

(5) Nerve fibres emerge from the posterior grey horns, and after a
longer or shorter horizontal course enter the white matter of the posterior
column (Gerlach). It is probable that they leave the posterior tracts again
as the nerve fibres of the posterior roots (Klein).

(6) Fibres emerge from the cells of the vesicular column of Clarke, which
pass obliquely outwards and upwards to enter the direct cerebellar tract
(Flechsig). These fibres form round bundles at the junction of the grey
substance and the lateral column, and are cut transversely in hori-
zontal sections. These bundles are represented in Figs. 134 to 140 as
dark round spots near the formatio reticularis (fr).

§ 353. Distribution of the Vessels of the Spinal Cord,
Medulla Oblongata, and Pons.

The vertebral artery is the first and largest branch of the subclavian
artery. It arises from the posterior aspect of the trunk, and ascends
through the foramina in the transverse processes of all the cervical verte-
brae, except the last. It winds backwards around the articulating process
of the atlas, pierces the dura mater, enters the skull through the foramen
magnum, and terminates at the lower border of the pons Varolii by uniting
with the corresponding vessel of the opposite side to form the basilar artery.

The basilar artery runs forward in the groove on the anterior surface of
the pons Varolii, and divides at the anterior border of the pons into two
terminal branches, one to either side.

ANATOMICAL AND PHYSIOLOGICAL INTRODUCTION. . 11

Fig. 105.

Fig. 105 (After Duret). Arteries of the Medulla Oblongata, Pons, and Inferior

Surface of the Cerebellum.

1, Root arteries of the spinal accessory nerve.

2, Anterior spinal arteries.

3, Arteries of the pneumogastric and glosso-pharyngeal nerves.

4, Inferior arteries of the auditory and facial nerves (vertebral branches).

5, Hoot arteries of the sixth nerve.

6 and 7, Arteries of the sub-olivary fossa.

8, Superior arteries of the auditory and facial nerves (branches of the middle

cerebellar artery).

9, Arteries of the trigeminal nerve.

10, Arteries of the hypoglossal nerve (branches of the vertebral and anterior

spinal arteries).

A, Inferior cerebellar artery.

B, Middle cerebellar artery.

C, Superior cerebellar artery.

D, Posterior cerebral artery.

Branches.— The branches of
following : —

Vertebral.
Lateral spinal,
Muscular branches,
Posterior meningeal,
Anterior spinal,
Posterior spinal,
Inferior cerebellar.

the vertebral and basilar artery are the

Basilar.

Transverse,
Middle cerebellar,
Superior cerebellar,
Posterior cerebral.

12 ANATOMICAL AND PHYSIOLOGICAL INTRODUCTION.

The lateral spinal branches enter the intervertebral foramina, and
taking the course of the roots of the spinal nerves, are distributed to
the spinal cord and vertebras. Where the vertebral artery curves round
the articular process of the atlas, it gives off several muscular branches.

Tlie posterior meningeal arteries are small branches which enter the
cranium through the foramen magnum, to be distributed to the dura
mater of the cerebellar fossae, and to the falx cerebelli. '

Fig. 106.

Fig. 106 (After Duret). Arteries of the Pons and Medulla.

1 V, Anterior spinal artery, the bulbar

branches.

2 2' 2", Inferior arteries of the pons.

3 3", Median arteries of the pons.

4, Superior arteries of the pons.

5, Posterior spinal arteries, median

branches.

A, Left vertebral artery.

B, Basilar artery.

C, Middle cerebellar artery.

D, Superior cerebellar artery.

E, Posterior cerebral artery.

ANATOMICAL AND PHYSIOLOGICAL INTRODUCTION. 13

The anterior spinal artery is a small branch which unites with its
fellow of the opposite side, on the front of the medulla oblongata. The
artery formed by the union of these two vessels descends along the
anterior aspect of the spinal cord, to which it distributes branches, and
forms the commencement of the anterior median artery.

The posterior spinal artery winds around the medulla oblongata to
reach the posterior aspect of the cord, and descends on either side to
the cauda equina. It communicates very freely with the spinal branches
of the intercostal and lumbar arteries, and near its origin sends a branch
upwards to the fourth ventricle.

The inferior cerebellar arteries wind around the upper part of the
medulla oblongata to reach the under surface of the cerebellum, to which
they are distributed. They pass between the filaments of origin of the
hypoglossal nerve in their course, and anastomose with the superior
cerebellar arteries. Small branches derived from these trunks pass to
the choroid plexus of the fourth ventricle.

Fig. 107.

Flo 107 (After Duret). Distribution of the Arteries on the Floor of the Fourth

Ventricle.

A A', Posterior spinal artery.
B B', Its pyramidal branches.
T\ Tv^riu' Emergence of the median arteries.

D > Choroid plexus drawn to one side. (Two or three arteries may be seen
to emerge from it.)

E E" E'", Arteries of the restiform bodies coming from the inferior
cerebellar artery.

14 ANATOMICAL AND PHYSIOLOGICAL INTRODUCTION.

The transverse branches of the basilar artery supply the pons Varolii,
and adjacent parts of the brain.

The middle cerebellar artery arises from the trunk of the basilar, about
its middle. It runs parallel to the transverse branches, and passes along
the middle peduncle to be distributed to the anterior part of the under
surface of the cerebellum. It gives off a small branch, auditiva interna,
which accompanies the auditory nerve into the meatus auditorius internus,
and to the labyrinth of the ear. The auditory branch is frequently de-
rived directly from the basilar.

The superior cerebellar arteries wind around the crus cerebri on each
side, lying in relation with the fourth nerve, and are distributed to the

Fig. 108.

Fig. 108 (After Duret). Arteries of the Posterior Part of the Medulla and the

Cerebellum.

A, Choroid plexus. B, Choroid velum. C, Posterior opening,

forming a communication between the fourth ventricle and the
posterior subarachnoid space. D, Posterior pyramid.

1, Inferior cerebellar artery.

2 2", Artery of the choroid plexus.

3 3 3 3, Arteries of the choroid velum._ Some proceed to the floor of the

fourth ventricle; they are capillary.

5, Posterior spinal artery.

6, Its ascending or pyramidal branch.

7, Its descending branch.

8, Its median branch.

ANATOMICAL AND PHYSIOLOGICAL INTRODUCTION. 15

upper surface of the cerebellum anastomosing with the inferior cerebellar.
Branches of the superior cerebellar arteries run inwards to supply the
valve of Vieussens aud the posterior part of the velum.

The ascending cervical branch of the inferior thyroid artery gives oft
one or two branches (spinal branches) which enter the intervertebral
foramina along with the cervical nerves, and assist in supplying the bodies
of the vertebra and the spinal cord and its membranes.

The spinal branches of the aortic intercostal arteries enter the inter-
vertebral foramina of the dorsal region, and supply the vertebra?, spinal
cord, and membranes.

The spinal branches of the lumbar, ilio-lambar, and lateral sacral arteries
enter the spinal canal through the intervertebral foramina ; they are dis-
tributed like the other spinal arteries, and anastomose with them.

§ 35-k The following arteries are distributed to the medulla
oblongata and pons : —

1. Thk Root Arteries. — These arteries are directed laterally towards
the roots of the nerves, which they penetrate near their point of emergence.
They subdivide into an ascending branch, which is directed towards the
nuclei of origin of the nerves, and a descending branch which descends
towards the periphery.

(a) Anterior Root Arteries (Fig. 109, ar).

(1) The arteries of the hypoglossal nerve are derived from both

the anterior spinal and vertebral arteries.

(2) The arteries of the sixth nerve are derived from the basilar.

(3) The arteries of the third nerve are derived from the trunk

of the basilar near its termination.

(6) Lateral Root Arteries (Fig. 109, Ir).

(1) The arteries of the spinal accessory nerve are derived from
the inferior cerebellar and vertebral arteries.

Q2) The arteries of the pneumogastric and glosso-pharyngeal
nerves arise from the vertebral artery.

(3) The arteries of the auditory, facial, and portio intermedia

(nerve of Wrisberg) are derived from the vertebral a little
before its termination, and from a branch of the basilar.
Branches may also descend perpendicularly from the middle
cerebellar artery.

(4) The artery of the trigeminus is comparatively large and

constant, and is derived directly from the basilar about its
middle. Another branch is derived from the middle
cerebellar artery.

(5) The fourth nerve, as well as the optic and olfactory nerves,

receives its arterial supply from the branches of the circle
of Willis.

16 ANATOMICAL AND PHYSIOLOGICAL INTRODUCTION.

Fig. 109. Section of the Medulla Oblongata, showing the Distribution of the Vessels.

R, Artery of the Median Raphe".

Ill, Branches to the formatio reticularis.
1'. Branch to the olivary body.

1", Branches to the hypoglossal nucleus. .
X'" „ „ floor of the fourth ventricle, and to the internal,
inferior nuclei of the facial (if),
p, Pyramidal arteries.
ar, Anterior root artery (hypoglossal) .

2', Branch to olivary body. ,
2", Branches to the formatio reticularis. It terminates in branches to the?
hypoglossal nucleus.
lr. Lateral root artery (vagus). . , . V . - •

5, Branch to the restiform body and the inner division of the interior

cerebellar peduncle. , ,

5', Branches to the nucleus of the vagus. Also gives branches to the
ascending root of the fifth and the formatio reticulai-i*.

ANATOMICAL AND PHYSIOLOGICAL INTRODUCTION. 17

2. Arteries of the Median Raphe (Fig. 109, R).

(a) Bulbar arteries derived from the anterior spinal artery (Fig. 106, 1).

(b) Inferior arteries of the pons derived from the lower end of the

basilar (Fig. 106, 2 2' 2").

basilar (Fig. 106, 3 3").

(d) Superior arteries of the pons, derived from the superior end of

the basilar (Fig. 106, 4).
The annexed diagram (Fig. 110) shows that a double row of vessels
enter the Raphe", the vessels on each side of the middle line entering at
different levels. A vertical section of the olivary body shows that the
vessels enter the hilus in a similar manner ; so that the branches from
the anterior root artery and the artery of the Raphe are never seen in the
same horizontal section as represented in Fig. 109.

3. The Lateral Arteries op the Medulla Oblongata.

(a) Anterior lateral artery (Fig. 109, ala) passes into the substance of
the medulla behind the olivary body. It gives branches to the

ala, The anterior lateral artery of the medulla oblongata. It supplies
branches to the formatio reticularis, olivary body, anterior nucleus
of the lateral column (ale), and terminates in branches to the hypo-
glossal nucleus.

rala, The middle lateral artery of the medulla oblongata. It supplies
branches to the formatio reticularis, the posterior nucleus of the
lateral column (pic), and terminates in branches which are dis-
tributed to the external accessory nucleus of the facial (ef).

pla, The posterior lateral arteries of the medulla oblongata. They supply
the restiform bodies.
C, Central artery.

3 3' 3", Branches to the hypoglossal and external accessory facial nuclei.
mp, Median posterior artery.

4 4' 4", Branches to the external accessory facial and pneumogastric

nuclei.

ep, External posterior artery. It supplies branches to the internal division

of the inferior peduncle of the cerebellum and restiform body.
i, Internal group of ceUs of the hypoglossal nucleus.
al, Anterolateral ,, „
pi, Postero-lateral „ „
a, Anterior

ale, Anterior nucleus of the lateral column.

pic, Posterior ,,
vni, Inferior portion of the posterior median acoustic nucleus.

if, Internal accessory facial nuclei.

«/, External accessory facial nucleus.

/, Fasciculus rotundus.
XII, Hypoglossal nerve,
x, Pneumogastric nerve.

Column of GolL

pr, Posterior root-zone. The direct cerebellar tract forms a thin band lying ex-
ternal to the column of Goll and posterior root-zone.
cn, Clavate nucleus.
tn, Triangular nucleus.
o, Olivary body.

po, Parolivary body.
np, Nucleus of the pyramid.
pn, Nucleus of the arciform fibres.
Anterior pyramid.

18 ANATOMICAL AND PHYSIOLOGICAL INTRODUCTION.

olivary body, the anterior lateral nucleus, and terminates between
the groups of ganglion cells of the hypoglossal nerve.

(b) Middle lateral artery {Fig. 109, mla) passes into the substance of

the medulla in front of the restiform body. It gives branches
to the posterior lateral nucleus, and terminates between the group
of cells, which give origin to the lateral mixed system of nerves.

the restiform body behind the roots of origin of the mixed lateral
system of nerves.

4. The Central Artery (Fig. 109, c) of the medulla oblongata is a
continuation of the central artery of the spinal cord. It subdivides inf o
internal, middle, and external branches (Fig. 109, 3 3' 3"), which are
distributed between the groups of cells of the hypoglossal nucleus.

5. The Median Posterior Artery (Fig. 109, mp) enters the sub-
stance of the medulla oblongata on the floor of the fourth ventricle. It is
probably derived from the choroid plexus. It is mainly distributed to
the groups of cells which give origin to the nerves of the lateral mixed
system.

.6. The External Posterior Artery (Fig. 109, ep) enters the sub-
stance of the medulla at the junction of the grey substance with the
restiform body.

Fig. 110.

EiG. 110 (From Henle's Anatomie). Vertical Section of RapU of the Medulla
Oblongata, showing the entrance of the vessels.

ANATOMICAL AND PHYSIOLOGICAL INTRODUCTION. 1.9

§ 355. Arteries of the Spinal Cord.

The anterior median artery gives off a series of small branches, which pass
backwards in the anterior median fissure, and reach the anterior commis-
sure, hence these vessels may be called the arteries of the anterior median
fissure (Fig. Ill, of). Each of these vessels on reaching the anterior com-
missure divides into two main trunks, which enter the grey substance of
the anterior horns ; these may be called the arteries of the anterior com-
missure (Fig. Ill, ac).

Fig. 111.

ea a \ m

Fig. 111. Diagram, of the Distribution
Anterior median artery.
af, Arteries of the anterior median
fissure.

ac, Artery of the anterior commis-
sure.

1, Anterior branch,
l'j Median branch.
1", Posterior branch.
Central artery.

2, Anterior branch.
%, Median branch.
2", Posterior branch.

, Posterior root arteries.
» 0 b , Arteries of posterior horns.
ia, Internal anterior root artery.
ea, External anterior root artery.
3 3', Internal and external branch.

ca.

pa,

mr,

pr,

ip,

of the Blood-vessels in the Spinal Cord,
ar, Antero-lateral branch.
4, Anterior branch.
4', Median branch.
4", Posterior branch.
Median lateral artery.
5 5', Anterior and posterior branches.
Posterior lateral arteries.
Internal posterior artery.
mp, External posterior artery.

g, Arteries of the column of Goll.
pc, Artery of the posterior commissure.
VC, Vesicular column of Clarke,
t, Internal group of cells.
a, Anterior group.
al, Antero-lateral group.
pi, Postero-lateral group,
c, Central group.
m, Median area.

20 ANATOMICAL AND PHYSIOLOGICAL INTRODUCTION.

The artery of the anterior commissure subdivides into three branches,
■which, from their position, may respectively be named the anterior
{Fig. Ill, 1), median {Fig. Ill, 1'), and posterior {Fig. Ill, 1") branches.
The anterior branch curves forwards, and is distributed to the anterior
and internal portion of the grey substance ; the median is distributed to
the lateral portion of the anterior horn, while the posterior is directed
backwards to the posterior horn.

The central artery also gives off an anterior {Fig. Ill, 2), median
{Fig. Ill, 2'), and posterior {Fig. Ill, 2") branch, which are distributed
respectively to the anterior, lateral, and posterior portions of the grey
substance. The median branches of the two main vessels, besides sup-
plying the grey substance, are also distributed to the pyramidal tract of
the lateral column.

Tlxe posterior spinal artery {Fig. Ill, pa) gives off branches, which
pass by the side of the posterior roots to enter the grey substance of the
posterior horns, where they subdivide into a variable number of small
branches {Fig. Ill, 6 6' 6"), which may be called arteries of the posterior
horns. In addition to the vessels just described, a large number pass from
the pia mater into the substance of the cord, and some of these are so
large and so constant as to deserve special mention ; two run by the side
of the bundles of fibres which constitute the anterior roots of the nerves,
hence they may be called the anterior root arteries. The branch nearest
the median fissure may be called the internal anterior root {Fig. Ill, ia),
and the other the external anterior root {Fig. Ill, ea) artery.

The internal anterior root artery {Fig. Ill, ia), on entering the grey
substance, joins the anterior branches of the first subdivision of the artery
of the anterior median fissure and of the central artery.

The external anterior root artery {Fig. Ill, ea), on entering the grey
substance, subdivides into two branches, the inner {Fig. Ill, 3) of which
is distributed along with the vessels just mentioned ; while the outer
branch {Fig. Ill, ?>') passes between what we may call the antero-lateral
{Fig. Ill, al) and central groups {Fig. Ill, c) of cells.

A very constant vessel passes to the grey substance from the pia mater, .
at the point of junction of the anterior and lateral columns of the cord,,
and it may therefore be called the antero-lateral artery {Fig. Ill, ar). Oni
reaching the grey substance it frequently divides into three brauches, one?
of which passes in front {Fig. Ill, ar, 4 4' 4"), another behind, and another:
into the substance of the antero-lateral group of cells. Another constant-
vessel {Fig. Ill, mr) passes from the lateral aspect of the cord, and om
reaching the grey substance it subdivides into two branches, the one oii
which passes in front and the other behind the postero-lateral group oil
cells {Fig. Ill, pi), and this vessel may from its position be called the;
median-lateral artery. Small branches (Fig. Ill, jw) pass at short inter-r;
vals through the posterior part of the lateral column, and, together witli
the median branches of the first subdivision of the artery of the auterio:
median fissure, and of the central arteries, supply the posterior part oofe.

ANATOMICAL AND PHYSIOLOGICAL INTRODUCTION. 21

the lateral columns ; hence these vessels may be called posterior lateral
arteries.

Two vessels pass from the pia mater into the substance of the posterior
column ; the one nearest the posterior median fissure, and which may
therefore be called the internal posterior artery (Fig. Ill, ip), passes
between the column of Goll and the posterior root-zone ; and after passing
through about two-thirds of the depth of the posterior column, it curves
outwards to reach the posterior grey horn. The other vessel may be
named the external or median posterior artery {Fig. Ill, mp) ; it passes
into the substance of the posterior column at the middle of the posterior
root-zone, and on reaching about one-third the depth of the posterior
column, it curves outwards to reach the posterior grey horn, where
it terminates. Small vessels (Fig. Ill, g) pass from the pia mater of
the posterior median fissure into the substance of the column of GolL
Another vessel, which may be called the artery of the posterior commissure
(Fig. Ill, pc), passes from the pia mater along the posterior margin of the
posterior commissure, and winds backwards along the internal edge of the
posterior horn.

§ 356. Grouving of the Ganglion Cells. — The ganglion cells
of the anterior horns are arranged in groups which are pretty
constant for the same portions of the cord, although the
arrangement varies considerably when sections at different
elevations are compared. A diagram of the topographical
distribution of these groups is given in Fig. 111. Beginning
at the posterior and lateral aspect of the anterior horn,
a group is observed which from its position is called the
postero-lateral group (pi). It is bounded behind by the pos-
terior and in front by the anterior twig of the median branch
of the central artery ; while on its external aspect it receives
branches from the median lateral artery, one of which passes
behi nd and another in front of it. Anterior to this group is
another, which from its position is called the antero-lateral
group (al). On its external aspect the group receives branches
from the anterior lateral artery, one of these passing behind
and another in front of it, while a median branch of the artery
may often be seen to pass into" its substance. A branch from
the external anterior root artery winds round its inner border
to gain the posterior aspect ; while the anterior branch of the
central artery passes along its internal and anterior aspects.

It has already been mentioned that the internal and external
anterior root arteries, on reaching the grey substance, divide

22 ANATOMICAL AND PHYSIOLOGICAL INTRODUCTION.

into two branches; and the external branch of the former and
internal of the latter converge so as to meet at a point like the
limbs of the letter V. In the small area of grey matter which
lies between these vessels several distinct cells are so constantly-
observed as to deserve a special name. These cells may from
their position be called the anterior group (a). Another group
of large cells, which may be called the internal group (i), is
bounded anteriorly and internally by white substance, and od
the external aspect by the anterior branch of the first subdivision
of the artery of the anterior median fissure. Another group of
cells may be observed towards the centre of the anterior horns,
and it may therefore be termed the central group (c). It is
bounded in front and on its internal and external borders by
the external and internal branches of the external anterior
root artery ; and behind* and also on its internal border by the
median and anterior branches of the central artery. A very
important area lies between the internal group on the one
hand and the antero-lateral and central groups on the other,
while the anterior group passes into its anterior border, like
a small wedge, so as to divide it into the form of the letter Y.
The cells of this median area (m) are much smaller than those
of the other groups, and the area itself is exceedingly vascular, .
being supplied by the two anterior root arteries, the anterior ;
branch of the first division of the artery of the anterior median i
fissure, and the anterior branch of the central artery. A final!
group of cells lies near the internal, border of the posteriori
grey horn near the posterior commissure called the vesicularr
column of Clarke (vc). • We must again direct attention to th
fact that Fig. Ill is only a diagram ; and although it is more like,
the upper part of the lumbar and lower portion of the cervical
enlargements than any other part of the cord, yet it is not ai
strictly accurate representation of any one section. The dis-
tribution of these groups at various elevations of the cord wil';
be better understood after the history of the development o?
the grey substance has been sketched. *

§ 357. Development of the Central Grey Tube.

The parts which subsequently correspond to the anterior grey horn ,
are the first portions of the cord to be developed. These are soon sue

ANATOMICAL AND PHYSIOLOGICAL INTRODUCTION. 23

ceeded by lateral masses, and somewhat later by the posterior horns. The
anterior grey commissure is then formed, and this is soon followed by the
development of the posterior commissure, and it is only at a considerably
later period that the white commissure appears. When the tube which
forms the rudiment of the cord has closed, it is seen to be somewhat oval
on section, and at this period it consists almost entirely of grey substance.

The grey substance is at first composed of small round cells, not
much larger than lymphoid corpuscles, with a distinct nucleus, and no
difference can be detected between one portion and another ; the whole
is simple and indefinite in its structure. A section of the cord at the
third month of embryonic life {Fig. 112) shows that the central canal has
contracted to a small oval opening, covered by columnar epithelium, while
the grey substance has assumed the general outline characteristic of the
grey substance of the adult cord. The grey substance is also surrounded
by a mantle of white substance, but we shall entirely neglect the history
of the development of the latter in the meantime.

Fig. 112.

§ 358. Development of the Anterior Grey Horns.
The most noticeable feature about the grey substance at the third
month is that the anterior grey horns are distinctly differentiated from
the posterior horns, not simply in their general outline, but in their
intimate structure. The groups of gan-
glion cells are now beginning to be
distinctly recognisable. Of these, the
antero-lateral group is the most advanced
in its development. Large, mostly round,
cells, with a distinct nucleus, are observed
embedded in the embryonic tissue ; but
the cells have not yet assumed distinct
processes. The small internal group is
also well represented by several distinct
large cells, but the cells are more elon-
gated, and not quite so large or so distinct
as in the antero-lateral group. A few cells
may be observed in the anterior group.
The postero-lateral group is represented
by four or five large round cells, but the
central group is not yet represented. The
areas in which the median and central
groups are subsequently developed, and
the area which separates the antero-lateral
and postero-lateral groups, are composed entirely of embryonic tissue,
with small round cells. The vehicular column of Clarke can also be
distinguished at this period, by a slight increase in the size of the cells in
comparison with those of the surrounding tissue, but the group does not
appear in the portion of the cord from which this section was taken.

Fig. 112. Section from the middle
of the Cervical Enlargement of
the Spinal Cord at the third month
of Embryonic Life. — C, Central
canal. The other letters indicate
the same as the corresponding
letters in Fig. 111.

24 ANATOMICAL AND PHYSIOLOGICAL INTRODUCTION.

A still further advance in development is recognisable at the end of the
fifth month of embryonic life (Figs. 113 and 1 14). The cells of the antero-
lateral group have not only increased still further in size, but their pro-
cesses are now well developed {Fig. 114, 1), and each may be seen to lie in a
distinct cavity. Those of the anterior and internal groups are also well
developed, and the same may be- said with respect to the cells of the centre
of the postero-lateral group ; and even those of the central group are
fairly well developed, although only two or three of them have as yet
developed processes. The area in which the median group is subsequently
developed, and the margins of the postero-lateral and central groups still
consist of embryonic tissue. The larger eells of these areas are represented
in Fig. 114, 2. The section represented in Fig. 113 was taken from the
middle of the cervical enlargement, and the vesicular column of Clarke is
not represented ; but the cells of this column are fairly well developed at
the fifth month in the lower end of the cervical enlargement and in the
dorsal region and upper end of the lumbar enlargement. The section repre-
sented in Fig. 114 was taken from the middle of the lumbar enlargement,
and no trace of the postero-lateral group could be discovered ; but in the
upper portion of the lumbar enlargement it occupies a similar position to

Fig, 113. • Fig. 114.

Figs. 113 and 114 (Young). Sections of Spinal Cord of a Fire Months Huma
Embryo, from the middle of the cervical and lumbar enlargements respe
tively. — i, internal; a, anterior; al, antero-lateral ; pi, postero-laten?
c, central, m, median, and groups of ganglion cells : 1, ganglion cell of tl
centre of the antero-lateral group ; 2, ganglion cell of median group

ANATOMICAL AND PHYSIOLOGICAL INTRODUCTION. 25

hat which it occupies in the cervical enlargement, as represented in
Tig. 113. The vesicular column of Clarke does not appear in the lumbar
•nlargement.

The ganglion cells of the various groups have become still further deve-
oped at the ninth mouth (Figs. 115 and 116) ; while by the development

Fic. 115. Fig. 116.

Figs. 115 and 116 (Young). Sections of Spinal Cord of a Nine Months Human
Embryo, from the middle of the lumbar and cervical enlargements respec-
tively.—A, anterior, and P, posterior horns. The small letters indicate the
same as in Figs. 113 and 114. The normal size of the section from which
the drawing was made is shown above each figure.

of caudate cells in the central and postero-lateral groups the various
groups have became so approximated as not to be so distinctly recog-
nisable from each other as they were at the fifth month of embryonic
life. The section represented in Fig. 115 was taken from the middle of the
lumbar enlargement, and the postero-lateral group is not so well repre-
sented as it is in the upper part of the lumbar region. The median area
now contains distinct ganglion cells instead of consisting entirely of em-
bryonic tissue. These cells are, however, not much larger than those of
the antero-lateral group at the third month ; while they are by no means
so well developed as those of the latter at the fifth month. The cells of
the median group are small, angular masses with a distinct nucleus, but
only a relatively small number of these have developed processes. It is
not necessary to say much at present with respect to the adult cord. The
most noticeable feature in which the cervical and lumbar enlargements of
the adult cord differ from the corresponding parts of the cord of a nine

26 ANATOMICAL AND PHYSIOLOGICAL INTRODUCTION.

months embryo is in the fact that the ganglion cells of the median group ^
have developed processes like those of the other groups. The cells of the
median group, however, especially in the cervical enlargement, are not
only much smaller than those of the other groups, but they are much
thinner and more transparent. These cells are so transparent that they
may be very readily overlooked altogether in sections cleared by oil of
cloves, and mounted in Canada balsam ; while the cells of the antero-
lateral group not only intercept the light, but require considerable change
of focus, in order to bring their anterior and posterior surfaces clearly
into view.

The relationship which the developing cells bear to the distribution of a
the blood-vessels is exceedingly interesting. The earlier-developed cells s
appear to be thrust further and further away from the vessels as develop--!
ment advances. The postero-lateral group, for instance, first shows itself f
by the development of four or five large cells, which appear about thee
centre of the spot in which the completed group is subsequently situated ; ;
and, as ganglion cell after ganglion cell becomes developed around this*
centre, the area becomes increased in size by the growth of additionaLl
embryonic tissue around the circumference of the group in the parka
which is in relation with the arterioles (Fig. 111). The ganglion cells ofel
the centre of the group are the first to be developed, and the group
increases in size by the gradual development of new cells around thee!
central ones. The marginal cells of the group are consequently the lasts!
to be developed. Similar remarks apply to the ganglion cells of the
central group, as well as to the antero-lateral, anterior, and internal;
groups, except that the last three groups, instead of being surrounded on:
all sides by grey substance, are on one of their sides in contact with:
white substance.

§ 359. Tlxe Accessory Nerve Nuclei of the Spinal Cord.
(1) Median Area. — The comparatively late period in the development o
the cord at which the ganglion cells of the median area of the anterior horn:.;
assume processes shows that this area must be regarded as an accessor^
structure (§ 33). The relatively large size of this area in the cervical, ad
compared with the lumbar enlargement, shows that it is a much more imd
portant structure in the former than the latter region. In the fifth montl j
of embryonic life the mediau area is not larger in the cervical than in tho
lumbar region, as shown in Figs. 113 and 114, where it will be seen that therri
is scarcely any difference in the general outline of the anterior horns in tbil
sections from the middle of the cervical and lumbar enlargements respec-
tively. In the embryo of the ninth month, however, the mediau area
the cervical is decidedly larger than in the lumbar enlargement (Figs. Ill
and 116), and consequently the anterior grey horn in the former region,
is extended laterally to make room for this area. The relative increase ii<
the size of the median area in the cervical enlargement of the humad
adult cord, as compared with that of the lumbar enlargement, is still mon

ANATOMICAL AND PHYSIOLOGICAL INTRODUCTION. 27

larked than in the cord of a nine months embryo, as may be seen in
figs. 117 and 118, where the median area occupies a large space, and the
iteral outgrowth of the anterior grey horn of the cervical region is very
i ecided.

On observing the large relative size of the median area in the cervical
nlargement of the adult human cord, as compared with that of the lumbar
nlargement, and even as compared with that of the cervical enlargement
f the cord of the embryo, it occurred to me that this area might not

Fig. 117.

Fig. 118.

Figs. 117 and 118 (Young\ Sections of the Adult Spinal Cord from the middle of
the Lumbar and Cervical Enlargements respectively.— The letters indicate the
same as those in Figs. 113 and 114.

possess any relative importance in the cervical enlargement of the spinal
cord in animals. In order to test this conclusion I applied to Mr. Larmutb,
of the Owens College, whose beautiful sections of the spinal cord are well
known in Manchester, and asked him if he would be kind enough to let
me have sections of the lumbar and cervical enlargements, as well as
from the middle of the dorsal region and the upper portion of the cer-
vical region of the spinal cord of the ox. Mr. Larmutb, in kindly con-
senting to let me have what I wanted, volunteered the statement that
it was quite unnecessary to have a section of both the cervical and lumbar
regions, as the two were so alike as to be indistinguishable, and both were
like the lumbar enlargement of the human cord. This was, to a large
extent, the very fact I was in search of. I have had an opportunity
since that time of examining these sections more minutely A section
from the cervical enlargement of a calf is represented in Fig. 119, and it

28 ANATOMICAL AND PHYSIOLOGICAL INTRODUCTION.

will be at once seen that the general outline of the grey substance is a
very like that of the grey substance of the lumbar enlargement in mai
and the median area occupies a still smaller area in the former than ia
the latter. The median area, indeed, can scarcely be said to exist ia
the spinal cord of the calf, and this is also true with respect to the cord
of the ox.

(2) The medio-lateral area lies between the antero-lateral and postero-
lateral groups of ganglion cells, and it will be hereafter seen that it is a
very important structure in the dorsal and upper cervical regions of the
cord {Figs. 120 and 121, ml). The cells of this area are not well!
developed at the ninth month of embryonic life in these regions of the.--
oord, and it is entirely unrepresented in the spinal cords of the ox and dog.;

Fig. 119.

Fig. 119 (Young). Section of Cervical Enlargement of Calf.— The letters indicatr

the same as Fig. 113.

We have just noticed that the cells of the median and medio-laterc
areas are not only developed at a comparatively late period of embryoni.
life, but that they are also much smaller in size than those of the othe<
groups of the anterior horns. It might, therefore, be concluded that tbi I
size of a ganglion cell may be accepted as a true test of the time at whiciB
it began to develop. This test can, however, be relied upon only withi I
certain very narrow limits. The cells at the margins of the posters j

ANATOMICAL AND PHYSIOLOGICAL INTRODUCTION. 29

tceral group in the lumbar and cervical enlargements are nearly if
»t quite as large as those of the centre of the group, although the
tter began to develop at a much earlier period than the former ; while
e cells of the nuclei of origin of the third and fourth nerves are small,
though they have begun to develop at a comparatively early period,
►he size of the cell may be accepted as a rough test of its age during the
iriod of development, and no longer, just as the size of a growing
ijnian being may be accepted as a rough test of age until the adult
Imdition is attained, when it ceases to be a test any longer. The
ze of the ganglion cells of the anterior horns of the cord of the
iult appears to depend mainly if not entirely upon the size of the
mscle over whose function it presides ; hence the cells of the nuclei of
ae third and fourth nerves are small, while the greater number of the
ells of the cervical enlargement are large, and those of the lumbar
nlargement are still larger. It frequently happens that the later-
eveloped cells of the cord are small in the adult condition, but this is
ecause the most special muscular adjustments are effected by the con-
ractions of small muscles.

§ 360. Development of the Neuroglia.

So far we have spoken only of the development of the ganglion
ells, but we must now briefly refer to that of the neuroglia. In the
arly weeks of foetal life the neuroglia consists of small round nucleated
ells, or rather of a nucleus surrounded by a layer of soft protoplasm, and
?ith scarcely a trace of basis substance. As development advances,
he protoplasm contracts round the nuclei, and the latter become
:mbedded in a fibrillated, some say granular basis substance. The
leuroglia becomes denser and more compact in proportion as it acquires
nore and more of the basis substance and loses its cellular character.
This change does not occur in every part of the grey substance at the
jame time. Speaking broadly, the neuroglia assumes a fibrillated texture
n the very portions of which the ganglion cells are earliest developed ;
;vhile it maintains its embryonic condition in the margins of the
jroups of ganglion cells of the anterior horns and along the line of the
olood-vessels. And when a section of the adult cord is held up to the
tight the groups of large ganglion cells may be seen as dark spots inter-
cepting the light, and strongly contrasting with the transparency of the
median area and of the margins of the antero-lateral and postero-lateral
groups along the lines of the vessels. The transparent portion also em-
braces the anterior and posterior grey commissures and the central column
of the grey substance as far back as the substantia gelatinosa, with the
exception of the area occupied by the vesicular column of Clarke. The
transparency of the area just described is no doubt due in some measure
to the fact that the small ganglion cells themselves are more transparent
than the large ganglion cells, but it is also in great measure due to the
loose and spongy character of the neuroglia in the former areas as com-

32 ANATOMICAL AND PHYSIOLOGICAL INTRODUCTION.

On passing now to the upper cervical region of the cord, it
will be observed that a transposition of the ganglion groups
takes place somewhat similar to that which occurs in the dorsal
region. Above the level of the fifth cervical vertebra the area
of the median group of small cells rapidly diminishes in size,
so. that the antero-lateral approximates the internal group,
and the small anterior, and probably also the central groups dis-
appear. An area of small cells is, however, interposed between:,
the antero-lateral and postero-lateral groups, which begins too
show itself as low down as the sixth cervical nerve, and gradually;.-
increases in size to the upper end of the cord. There the.,
median group disappears entirely, so that the internal and
antero-lateral groups are only separated by a small vesselr
while a considerable area of small cells lies between thei
antero-lateral and postero-lateral groups (Fig. 120 ml). The,

Fig. 120.

Fig. 121.

Figs. 120 and 121 (Young). Sections of the Adult Human Spinal Cord, frcv
the upper cervical and dorsal regions respectively. —A, anterior, and !
posterior horns ; aa, anterior roots ; cc, central canal ; ml, the medio-later-:
area. The other letters indicate the same as the corresponding ones i
Figs. 113 and 114. The size of the sections from which the drawing w«
taken is indicated above each. .In Fig. 121, rc represents the vesicul:
column of Clarke.

ANATOMICAL AND PHYSIOLOGICAL INTRODUCTION. 33

istribution of the different groups in the upper cervical region
3, indeed, very similar to that which occurs in the dorsal region,
it will, however, be seen, on comparing Figs. 120 and 121, that
he ceutral group is unrepresented in the upper cervical, while it
s represented in the dorsal region, but this difference is unim-
)ortant since I am not sure that the group is always absent in
he upper cervical, or always present in the dorsal region.
)ne important difference, however, exists between the dorsal
md upper cervical regions of the cord, and that is the presence
»f the vesicular column of Clarke in the former and its absence
n the latter. The vesicular column of Clarke begins at the
lpper end of the lumbar enlargement, where it consists of a
jroup of large bipolar cells ; it is continued upwards throughout
he whole of the dorsal region, although its cells are consider-
ibly smaller here than in the upper lumbar region, and it ter-
ninates in the lower part of the cervical enlargement.

$ 364. The Grey Substance of the Medulla Oblongata, Pons,

and Crura Cerebri.
In the upper segment of the spinal cord both the grey and
.vhite substances undergo extensive rearrangement. One im-
oortant alteration of the white substance is that the column
jf Goll increases in size by the addition of grey matter — the
:lavate nucleus — in its interior (Fig. 122, G, cn), and at a little
higher level the posterior root-zone also increases in size by the
formation of the triangular nucleus in its substance (Fig. 122,
pr, tn). The increased size of the posterior columns displaces the
gelatinous substance of the posterior grey horns (Fig. 122, s/y),
so that they extend in a lateral direction instead of posteriorly
as in the cord. Another rearrangement of the white substance
(is produced by the crossing of the lateral columns, so as to form
Ithe anterior pyramids of the medulla (Fig. 122, x, P). These
(fibres by their crossing cut off the anterior grey horns from the
rest of the grey substance, while they thrust the commissures,
the central grey column, and the central canal further towards
[the posterior surface of the medulla. The principal alterations
| of the grey substance, therefore, consist in the lateral displace-
I ment of the posterior horns, the slight posterior displacement of
I the central canal, central grey column, and commissures, and the

34 ANATOMICAL AND PHYSIOLOGICAL INTRODUCTION.

detachment of the anterior horns from the central greycolumrj.
A careful examination, however, shows that one or two other'
minor but exceedingly important alterations have taken place
The triangular nucleus and, at a little higher level, the clavate
nucleus (Fig. 122, tn, en) give off arcuate fibres, which are

Fig. 122.

Fig. 122 (Young). Section of the Lower End of the Medulla Oblongata on a lei
with the crossing of the fibres of the lateral column.

A, Anterior grey horns, showing that the grey matter has become mixed up wi
the white substance of the anterior root-zone, and with arcuate fibres.

i x al, Internal group and a portion of the antero-lateral group.

ale, Anterior nucleus of the lateral column, being a portion detached from til
antero-lateral group.

pic, Posterior nucleus of the lateral column, being a portion detached from t':\
postero-lateral group.
sg, Substantia gelatinosa displaced laterally.

at, Ascending root of the trigeminus.

/, Fasciculus rotundus.

vc, Vesicular column of Clarke ?
P, Pyramidal tract.

x, Crossing of the fibres.
ar, Internal portion of the anterior root-zone.
ar', External portion of the anterior root-zone.

xii, Hypoglossal nerve.

XI, Spinal accessory nerve.
G, The column of Goll — the slender fasciculus.

cn, The clavate nucleus.
pr, The posterior root-zone — the cuneate fasciculus.

tn, The triangular nucleus. cc, The central canal.

ANATOMICAL AND PHYSIOLOGICAL INTRODUCTION.

rected forwards and upwards in a semicircular manner to
ach the olivary body of the same side. These fibres pass
rough the posterior horns and thrust them still further in a
teral direction, and, indeed, almost entirely separate the
eater portion of each horn with its substantia gelatinosa from
e grey substance which surrounds the central canal. The
cuate fibres interlace with the fibres of the lateral columns
the latter bend forwards to cross, and also detach a portion
the antero-lateral and postero-lateral groups of cells, so that
portion of these groups now extends into the white substance
the anterior root-zones {Fig. 122, ale, pic).
The continuation of the anterior root-zones {Fig. 122, ar
id ar') of the cord through the medulla oblongata is broken
) into a reticulated formation — the formatio reticularis — first

Fig. 123.

enle's Anatomie) Formatio Reticularis of the Medulla Oblongata,
showing the ganglion cells distributed Uirough it.

36 ANATOMICAL AND PHYSIOLOGICAL INTRODUCTION.

Fie. 124.

Flo. 124 (Young). Section of the Medulla Oblongata on a level with the Gl<

pharyngeal Nerve.

P, Pyramid.

p, Accessory portion of the pyramid.
XII, Hypoglossal nerve.

H, Nucleus of hypoglossal. The internal, anterolateral, and postero-lat
groups.

a, Anterior group of cells(
IX, Glossopharyngeal nerve.

ngp, Nucleus of glossopharyngeal.

Vni, Lower part of the posterior median acoustic nucleus.
if, Internal accessory facial nuclei.
ef, External accessory facial nuclei.
ale, Anterior nucleus of the lateral column.
pic, Posterior nucleus of the lateral column.
/, Fasciculus rotundus.

ip, Internal division of the inferior peduncle of the cerebellum.
G, Column of Goll.

cn, Clavate nucleus.

ANATOMICAL AND PHYSIOLOGICAL INTRODUCTION. 37

the arcuate fibres of the triangular and clavate nuclei, and
en by the arcuate fibres of the inferior peduncles of the cere-
llum, and the whole of this tissue is thickly studded with
udate ganglion cells, as represented in Fig. 123. Whether
I these cells are the representatives of those detached by the
cuate fibres from the antero-lateral and postero-lateral groups

the cord is not known. The cells detached from these
oups, however, aggregate into two more or less distinct groups

the lateral part of the formatio reticularis of the medulla.
iese groups may from their position be called the anterior and
)sterior nuclei of the lateral column of the medulla (Figs. 122,
24, and 125, ale, pic); while the terms antero-lateral and
istero-lateral may still be retained to designate what I
Jieve to be the upward continuations of the portions of the
itero-lateral and postero-lateral (Fig. 109, at, pi) groups of
e cord which have retained their connection with the grey
atter that may be considered as representing the anterior
•rnua.

§ 365. Continuation of the Anterior Grey Horns of the
oinal Cord through the Medulla Oblongata, Pons, and Crura
srebri. — This slight digression into the examination of the
arrangement of the white substance, which takes place in
issing from the spinal cord to the medulla oblongata, appeared
pessary iu order fully to understand the redistribution of
ie groups of ganglion cells occurring in the medulla. At
ie lower end of the medulla portions of the antero-lateral
id postero-lateral groups may be seen to extend laterally
ito the substance of the anterior root-zone, or into the lateral
)lumn of the medulla oblongata as it may now be called.

•, Posterior root-zone.

tn, Triangular nucleus.
, The direct cerebellar tract lying on the surface of the posterior root-zone, and

the ascending root of the tiigeminus.
, Ascending root of the trigeminus.

sg, Substantia gelatinosa.
, Posterior longitudinal fasciculus.

•, The portion of the formatio reticularis, which represents the internal division
. of the anterior root-zone of the spinal cord.

, The portion of the formatio reticularis, which represents the external division

of the anterior root-zone of the spinal cord.
Olivary body.

np, Nucleus of the pyramid.

po, Parolivary body.

38 ANATOMICAL AND PHYSIOLOGICAL INTRODUCTION.

From the anterior nucleus of the lateral column (Fig. 122, ale'
fibres maybe observed proceeding inwards and passing between
the antero-lateral and postero-lateral groups. Some of thes
fibres cross over and appear to be connected with the spim
accessory nerve of the opposite side. Others wind round th!
postero-lateral group to get to the spinal accessory nerve (
the same side. From the posterior nucleus of the lateral colum
{Fig. 122, pic), fibres proceed inwards to reach the grey sul
stance, and wind backwards along the boundary line between thi
white and grey substance to reach the spinal accessory nerve
the same side. The nuclei of the lateral column, therefo
appear to give origin to some at least of the fibres of tt
spinal accessory nerve ; and we have only to suppose that tli
same arrangement is carried out as we ascend the medulla am
pons in order to understand the origin of the motor fibres
the pneumogastric and glosso-pharyngeal nerves, those of
large part of the facial nerve, and of the motor root of the fift:
The arrangement of the fibres from the nuclei of the laterr
column which pass out along with the glosso-pharyngeal nerve < I
represented in Fig. 124. The fibres from the anterior nucle i!
(Fig. 124, ale) proceed backwards and inwards, and pass betwet
what will be afterwards described as the antero-lateral an
postero-lateral. groups. I have not been able to assure rnys&
that any of these fibres cross over to the opposite side, althou<
this is probable ; but some of them may be distinctly observe
to wind round the postero-lateral nucleus to proceed in ti
direction of the glosso-pharyngeal nerve. The fibres from t:
posterior nucleus (Fig. 124, pic) proceed backwards and inwarr
and on reaching the grey substance bend abruptly outwan
along the edge of the white substance to reach the nerve,
similar arrangement may be observed, at a lower level, wil
respect to the pneumogastric and spinal accessory nerves,
a higher elevation the fibres from the nuclei of the late
column proceed backwards and inwards, the majority of tka'
(genu nervi facialis) wind round the nucleus of the sixth ner
and proceed outwards to join the facial nerve. The fibres fix
the posterior nucleus of the lateral column (Fig. 126, p
appear to me to pass backwards and to the outside of the nucld<
of the sixth nerve to join the facial. The anterior nucleus-

ANATOMICAL AND PHYSIOLOGICAL INTRODUCTION. 3<)

ie lateral column appears to terminate on a level with the
'igin of the facial nerve. Fibres, however, seem to pass upwards
ad backwards from this nucleus to join the motor root of the
fth nerve. In Fig. 127 the anterior nucleus of the lateral
[damn of the medulla is not represented, but the fibres trans -
ersely cut at (?•) shows that these have joined the others from

Fig. 125.

Fio. 125 (Modified from Flechsig). Section of the Medulla Oblongata on a level

with the superficial origin of the Acoustic Nerve.
R vin, Root of the acoustic nerve.

VXn, Posterior median acoustic nucleus.
yiu'\. Posterior lateral acoustic nucleus.
U., Nucleus of the hypoglossal nerve.
>P, Internal division of the inferior peduncle of the cerebellum
f,\ ^xterna! division of the inferior peduncle of the cerebellum.
J> s, Jj ormatio-reticularis.

a, Axciform fibres. The remaining letters indicate the same as the corresponding
letters in Fig. 124.

40 ANATOMICAL AND PHYSIOLOGICAL INTRODUCTION.

a different level, and I believe that these fibres bave ascended .
from the anterior nucleus of the lateral column. The motor -
nucleus of the fifth {Fig. 127, v) appears to be the continuation i
upwards of the posterior nucleus of the lateral column. The -
nucleus now lies close to the sensory fibres of the nerve, and itsr
fibres, instead of winding backwards at first, as they do at a*
lower level, appear to pass outwards at once by the side of ther
sensory fibres.

The groups of cells of the anterior horns may be traced
upwards more or less distinctly to the nucleus of origin oftt
the hypoglossal nerve. The hypoglossal nerve begins on a
level with the upper limit of the crossing of the fibres of the j
pyramidal tract. The crossing of the fibres had detached the|

Fig. 126.

Fig. 126 (Modified from Erb). Transverse Section of the Pons on a level with j
Abducens and Facial Roots, from a nine months embryo.— The right half repp'i
Bents a section made a little lower than the left. P, Pyramidal tract ;
accessory portion of the pyramidal tract ; Tr and Tr', transverse fibres of Itf
pons ; so, superior olivary body ; ale and p/c, anterior and posterior nuclei of 1 -
lateral column respectively, representing the nucleus of the facial nerve ; BT\
root of the facial nerve ; vr, nucleus of the sixth nerve ; RVi, root of the sir-
nerve ; at, ascending root of the trigeminus. B, The internal division of !
peduncle of the cerebellum as it passes from the cerebellum ; L, posterior lor;
tudinal fasciculus; ar and ar', the upward continuation of the internal i-.
external divisions of the anterior root-zone of the spinal cord ; t, fasciculus ten I

ANATOMICAL AND PHYSIOLOGICAL INTRODUCTION. 41

.nterior horns from the grey substance surrounding the central
nal ; but when the crossing is completed, these two portions
igain become united. The olivary body is, however, inter-
:alated, the whole of the grey matter is thrust further and
farther back until the posterior commissure disappears, and the
;entral canal opens at the calamus scriptorius on the floor of
;he fourth ventricle. The nucleus of the hypoglossal nerve is
Dften described as if its cells constituted one group. These
cells are, however, distinctly arranged into several groups which
correspond so closely with the arrangement of the groups in the
anterior horns of the cord that I have no hesitation in regard-
ing those of the former as continuations of the latter. An

Fig. 127.

Fro. 127 (Modified from Erb\ Transverse Section of the Pons on a level with the origin
of the Trigeminus, from a nine months human embryo.— P, pyramidal tract ■ p
accessory portion of the pyramidal tract ; Tr, Tr1, transverse fibres of the pons •
at, ascending root of the trigeminus and gelatinous substance ; dt, descending root
ot the trigeminus ; r, root-fibres of the trigeminus cut transversely • v motor
nucleus of the trigeminus ; v', middle sensory trigeminal nucleus : rv, root of
trigeminus ; C, roots of the fifth proceeding from the cerebellum ; I, Poste-
rior longitudinal fasciculus ; ar and ar1, upward continuation of the internal
ana external portions respectively of the anterior root-zone of the spinal cord.

42 ANATOMICAL AND PHYSIOLOGICAL INTRODUCTION.

internal, anterolateral, and postero-lateral (Fig. 109, i, al, pi)
group may be distinguished, and these appear to correspond to
the groups of the same name in the cord ; while a large number
of cells may be observed at the roots of the hypoglossal nerve
(Fig. 109, a), which may be called the anterior group, and
which corresponds to the anterior group in the cord. All that
has been previously said with regard to the development of
the groups of cells in the anterior horns of the cord applies
equally to those of the hypoglossal nucleus. The central cells
of the latter groups develop first; while the marginal cells
develop last and close to the blood-vessels which ramify between
the groups as they do in the cord.

Fig. 128.

1 cc

'Fid. 128 (Modified from Meynert). Transverse Section of the Pons on a level with tin
upper end of the Fourth Ventricle, from a nine months human embryo— P, pyra-
midal tract ; p, accessory portion of the pyramidal tract ; Tr, Tr', transverse!
fibres of the pons; B, superior brachium of the pons ; L, posterior longitudinal.!
fasciculus ; ar and ar1, upward continuation of the internal and external portions/,
respectively of the anterior root-zone of the spinal cord; v', middle sensory^
trigeminal nucleus ; dt, descending root of the trigeminus ; iv, nucleus of thtt
fourth nerve ; cc, aqueduct of Sylvius.

ANATOMICAL AND PHYSIOLOGICAL INTRODUCTION. 43

It is not easy to trace the continuation of the groups of cells
of the anterior horns of the cord beyond the nucleus of the hypo-
glossal nerve, inasmuch as the groups become separated longitu-
dinally by tbe transverse fibres of the pons. It is, however, pro-
bable that the nucleus of the sixth nerve (Fig. 126, vi') represents
the posterolateral group, and the bending of the fibres of the
facial nerve round the nucleus corresponds to the similar bend-
in°- of the fibres which issue from the anterior nucleus of the
lateral column in the lower part of the medulla round the

Fig. 129.

Fig. 129 (Modified from Krause). Transverse Section of the Cms Cerebri on a level
with the anterior pair of Corpora Quadrigemina, from a nine months embryo. —
cc, crusta ; P, pyramidal tract ; p, accessory portion of the pyramidal tract ;
LN, locus niger ; RN, red nucleus of the tegmentum ; L, posterior longitudinal
fasciculus; ar and ar1, upward continuation of the internal and external portions
respectively of the anterior root-zone of the spinal cord ; III, third nerve ;
m', nucleus of the third nerve; iv, fourth nerve; iv', nuclexis of the fourth
nerve ; iv", crossing of the fibres of the fourth nerves to opposite sides ; dt,
descending root of the trigeminus ; cc, aqueduct of Sylvius ; x, crossing of the
fibres of the superior peduncles of the cerebellum ; pf, fasciculus of medullated
fibres proceeding to the anterior pair of corpora quadrigemina.

44 ANATOMICAL AND PHYSIOLOGICAL INTRODUCTION.

postero -lateral group to join the spinal accessory nerve. The
postero-lateral group cannot be traced beyond the nucleus of
the sixth nerve, and probably ceases there. The internal, an-
terior, and antero-lateral groups are dislocated upwards, as aa
result probably of the longitudinal extension of the central grey
tube, which is rendered necessary in order to provide accommo-
dation for the large mass of the transverse fibres of the pons-
These groups reappear in front of the aqueduct of Sylvius, anc
form the nuclei of the third and fourth nerves (Fig. 129, in', iv')
The fourth nerve is in my opinion merely a portion detach ec
from the third by the decussating fibres of the superion
peduncles of the cerebellum, and' thus compelled to seek it:
destination by an independent route. The fourth nerve, there
fore, appears to belong to the system of anterior motor nerves !
represented by the hypoglossal, sixth, and third nerves, anc.
not to the " mixed lateral system" represented by the spinaJ
accessory, vagus, glosso-pharyngeal, and fifth nerves. Althouglj
the facial is a purely motor nerve, it appears to belong sa
least in part to that lateral system. That the nucleus Cij
the sixth on the one hand and that of the third and fourttt
on the other really belong to the same nucleus, and aril
only separated from one another by some structure beiml
intercalated in the course of evolution, is rendered probable b
the fact that the nucleus of the sixth is connected with a portio: I
of the nucleus of the third of the opposite side by a distinct 1
bundle of fibres (Duval). The fact that these nerves are ssi
closely related in their functions affords further corroborative
evidence in favour of this opinion.

§ 366. Continuation of the Posterior Grey Horns of ti
Spinal Cord through the Medulla Oblongata, Pons, and Crur v\
Cerebri. — We have already seen that the substantia gelatinor . i
of the posterior horns was not only thrust out laterally, but alia
almost detached from the rest of the grey substance by tli
arcuate fibres, and we must now observe that it maintains th 1
lateral and superficial position as high as the level of the poii i
of emergence of the fifth nerve (Figs. 124 to 127, at).
may, indeed, be said that this structure is continued upwarrj
to the level of the opening of the aqueduct of Sylvius into tt '■<

ANATOMICAL AND PHYSIOLOGICAL INTRODUCTION. 45

! third ventricle, since the descending root of the fifth nerve
' appears to be a somewhat similar structure to the ascending
' root and gelatinous substance (Figs. 127 to 129, dt). The
1 white substance of the ascending root appears to be the analogue
f of the posterior root-zones of the cord — a mere continuation
" upwards of these zones, after what belongs to the spinal portion
of the central grey tube has terminated in the clavate nucleus.

;. § 367. Continuation of the Central Column and the Vesicular
Column of Clarke through the Medulla Oblongata.

In the lower end of the medulla the central column becomes
■' separated from the anterior horn by the decussating pyramidal
:' fibres, and almost separated from the posterior grey horns by
the lateral displacement of the latter. A bundle of transverse
fibres still connect the central column and the posterior horns,
and these separate so as to leave an interspace in which longi-
tudinal fibres may be observed to ascend towards the medulla.
These form a round bundle (Figs. 1 22 and 124, /), which reaches
as far as the upper end of the glosso-pharyngeal nucleus, and has
been called the " ascending root of the lateral mixed system "
by Meynert, and the " respiratory fascicle" by Krause. In the
dorsal region of the spinal cord the middle portion of the grey
substance is represented by two columns on each side of the
central canal — the vesicular column of Clarke, and the central
column — but the column of Clarke is unrepresented in the lum-
bar and cervical regions of the cord. It appears to me, however,
that the vesicular column of Clarke again becomes represented
in the lower end of the medulla. A group of cells may be
observed near the posterior and internal margin of the central
column in the lower end of the medulla (Fig. 122, vc), corre-
sponding to the position occupied by the vesicular column of
Clarke in the dorsal region ; and the cells of both groups mani-
fest a tendency to be bipolar instead of multipolar, like those of
the anterior horns. Assuming, therefore, that the group of cells
in the middle portion of the grey matter in the lower end of the
medulla is the upward continuation of the vesicular column of
Clarke, and that the remaining portion represents the central
column in the cord, we shall have no difficulty in tracing the
disposition of these portions of grey substance in the medulla.

46 ANATOMICAL AND PHYSIOLOGICAL INTRODUCTION.

Immediately above the crossing of the pyramidal fibres, where
the anterior horns are pressed backwards towards the central;
canal, the central' column lies posterior to the groups of cells-
representing the anterior horns, and close to the central canal,
while the representative of the vesicular column of Clarke lies-
external to the central column, and posterior to the groups-
representing the anterior grey horns (Fig. 130, XI). The
nucleus which represents the vesicular column of Clarke con-
tains pigmented bipolar cells, and constitutes the posteriorr
nucleus of the spinal accessory nerve (Fig. 130, Xl'). And';
when the central canal has opened into the floor of the fourth.

Fig. 130.

Fiu. 130 (Young). Section of the Medulla Oblongata, a little beloio the point of t.

Calamus Scriptorius, showing the gro^s of cells of the grey substance.
Rxi, Fibres of origin of the eleventh or spinal accessory nerve.

XI, Posterior nucleus of the eleventh nerve.

xi', Accessory nucleus of the eleventh nerve.
Rxn, Fibres of origin of the twelfth or hypoglossal nerve.

a, i, al, pi, Anterior, internal, antero-lateral, and postero-late.ral groups c
cells respectively.

ah, Accessory hypoglossal nucleus.

i f, Internal accessory facial nuclei.

ef External accessory facial nucleus.
C, Central canal.
/, Fasciculus rotundus.

ANATOMICAL AND PHYSIOLOGICAL INTRODUCTION. 47

•entricle, the representative of the vesicular column of Clarke
3 thrust backwards, and laterally so as to form the principal
>art of the nuclei of origin of the spinal accessory, vagus, and
;losso-pharyngeal nerves, while the central column winds round
he groups representing the anterior horns {Fig. 124, H), so as
o lie internal, posterior, and external to them. The posterior
>ortion of the central column is elevated into a ridge (funiculus
eres) close to the median fissure in the inferior part of the floor
>f the fourth ventricle (Fig. 124, if). The central column is
:ontinuecl upwards, as a thin film of grey substance, on the
loor of the fourth ventricle, and lying behind the fibres of
>rigin of the facial {Fig. 126, t) and the fifth (Fig. 127, r);
vhile in the upper end of the pons and crura it is represented
>y the grey matter which immediately surrounds the aqueduct
►f Sylvius (Figs. 128 and 129, cc).

The characteristics of the central column are, as we have
lready seen, that its texture is spongy, rendering it transparent
n section, and that its cells are comparatively late in their
evelopment. We saw reason, indeed, to regard the central
olumn as being the embryonic part of the central grey tube,
.nd that the portions of it which are first developed are thrust
utwards as new layers grow about the central canal. If this
)e true, we may expect to find that any additional nuclei which
nay form in the medulla oblongata in the course of development
vill grow in the representative of the central column. This

xpectation is realised. Whether the spongy portion of grey
ubstance, which lies internal, posterior, and external to the
ivpoglossal nucleus, be or be not the continuation upwards
'f the central column, several groups of cells may be observed
n it which do not become developed until subsequently to the
linth month of embryonic life, and which do not appear to be

epresented in the spinal cord ; they may, therefore, be called
he accessory nuclei of the medulla oblongata. These nuclei
nust be carefully distinguished from the nuclei of origin of the

pinal accessory nerve.

§ 3G8. Accessory Nuclei of the Medulla Oblongata.
(1) Accessory Nuclei of the Facial Nerve. — The first of these
vhich I shall mention is what has been described by Dr. Lock-

48 ANATOMICAL AND PHYSIOLOGICAL INTRODUCTION.

hart Clarke as the inferior facial nucleus. This nucleus consistf
really of several small nuclei. Two of these, which may bo
called the internal accessory facial nuclei {Fig. 1 30, if), appear
as two small round nuclei close to the inner side of the hypo
glossal nucleus and the central canal ; and when the canal open
on to the floor of the fourth ventricle, they are situated imme
diately beneath the ependyma of the ventricle, and close to th
middle line (Fig. 124, if). Fibres from these nuclei ascend i
the funiculus teres and enter the fasciculus, teres (Fig. 126. t
through which they join the other fibres of the facial nerve.

Another somewhat larger group of small cells is situate
at first posterior (Fig. 126, ef) and then external (Fig. 12
ef) to the nucleus of the hypoglossal. The fibres whic
issue from it also join, I believe, the fasciculus teres, and tl
group may, therefore, be called the external accessory facii
nucleus (Fig. 109, ef). The cells of these nuclei are small, an
destitute of processes in a nine months embryo.

(2) Accessory Nuclei of the Eleventh Nerve. — Two groups
small cells, which develop at a comparatively late period, m,|
be observed lying behind the posterior nucleus of the eleven]
nerve (Fig. 130, xi"). Meynert thinks that the cells of the*
groups are connected with commissural fibres which run behii
the central canal, before it opens into the fourth ventricle.

(3) Accessory Nucleus of the Hypoglossal Nerve. — The nec
most important nucleus of this category is one which I hasj
constantly observed in the hypoglossal nucleus of one side on
(Fig. 130, ah). As I have not marked my sections, I ami!
present unable to say whether it is found on the right or II
side. This nucleus is of a round form, and appears as if:
were surrounded by a layer of white fibres, arranged lonii
tudinally, which separates it from the surrounding tissue,
contains a large number of very small caudate cells, ea
being not one-fifth the diameter of the cells of the hyi:
glossal nucleus. The nucleus in some sections lies betw>
the internal and external convolute of the nucleus of
hypoglossal; while at other times it is embedded in the ?M
stance of the internal convolute, being then situated near 1
margin of the group (Fig. 130). This nucleus is almost entiil
limited to one side, although faint traces of it may occasion. ' |

ANATOMICAL AND PHYSIOLOGICAL INTRODUCTION.

3 observed in the opposite side; it is scarcely recognisable on
ther side of the medulla at the ninth month of embryonic
re. The most reasonable supposition with regard to it is that
regulates the movements of articulation, and that it is con-
acted with the third left frontal convolution of the brain.

$ 3G9. Special Nuclei of the Medulla Oblongata and Pons.
(1) The acoustic nuclei can scarcely be said to be repre-
mted by any portion of the grey substance of the cord. These
uclei are four in number : —

(a) The posterior median nucleus of the acousticus
fig, 125, vni) comes in contact with the nucleus of the
igus, but is more superficially situated than that of the
.tter, and somewhat to the outer side of the glosso-
laryngeal nucleus. It occupies the whole space between
te ala cinerea and inferior peduncle of the cerebellum up
I the anterior border of the striae medullares. The posterior
»ot of the acoustic nerve takes its origin chiefly from this
acleus, and passes out partly in superficial fasciculi (stria;
;ousticse) and partly through the body of the medulla.
I (b) The posterior lateral acoustic nucleus {Fig. 125, vm")
a grey nodule lying in the peduncle of the cerebellum,
jitween the deep and superficial fibres of origin of the acoustic
srve.

(c) The anterior median acoustic nucleus belongs to the
iterior roots of the acoustic nerve, and is situated anterior
) the stria? medullares. It occupies the external angle of the
>urth ventricle, about the middle of the cerebellar peduncle.

(d) The anterior lateral acoustic nucleus appears like a
rolongation of the posterior lateral acoustic nucleus, and is
edged in between the middle peduncle and the flocculus,
i gives origin to the portio intermedia Wrisbergii. Some
latomists believe that the fibres which pass in the chorda
rmpani, and which confer taste on the anterior two-thirds of
ie tongue, are derived from the nerve of Wrisberg (Bigelow).

- is also probable that one of the other nuclei — perhaps the
Dsterior lateral acoustic nucleus — gives origin to the fibres
ipplied to the labyrinth, and is not connected with the purely
rustic fibres.

50 ANATOMICAL AND PHYSIOLOGICAL INTRODUCTION.

(2) The corpora quadrigemina and geniculate bodies are the !
nuclei of origin of the second or optie nerve ; but we are unable
to say, in the present state of our knowledge, what structures i
constitute the nuclei of origin of the first or olfactory nerve.

§ 370. Superadded Grey Matter of the Medulla, Oblongata

and Pons.

(1) The Clavate Nucleus. — The columns of Goll contain in i
the lower part of the medulla a nucleus of grey matter, which is ;
from its form called the clavate nucleus (Figs. 122 and 124, cn).
It is a longitudinal pillar of grey substance, and produces the \
enlargement in the fasciculus gracilis, known as the clava.

(2) The triangular nucleus (Figs. 122" and 124, tn) is a,
grey nucleus enclosed in the cuneate fasciculus, the latter oft
which is the continuation upwards of the posterior root-zones >
of the cord. It is a longish grey body on the inner border of;
the cuneiform column, and enlarging as it ascends. The clavate
and triangular nuclei extend to the posterior end of the postero-
lateral acoustic nucleus. [

(3) The olivary body (Fig. 124, 6) is situated in the lateral;
columns of the medulla, close to the anterior pyramid. In form i
it is like a bean or an almond, with the hilus directed inwards.
It contains a number of small ganglion cells, and is in substance;
very similar to the corpus dentatum of the cerebellum.

(4) The parolivary body (Fig. 124, po) is a band of grey,
matter which bounds the internal half of the posterior border:
of the olivary body.

(5) The nucleus of the pyramid (Fig. 124, np) (internal
parolivary body) lies opposite the pyramid, in front and to
the inside of the olivary body.

(6) The superior olivary body (Fig. 126, so) is a longish,
grey column, situated in the pons in front of the facial nucleus. ;

(7) The red nucleus of the tegmentum (Fig. 129, RN) of I
Stilling, or superior olive of Luys, is situated in the crus cerebri,
between the crus and tegmentum, and is similar in structure e
to the olivary body.

(8) The middle sensory nucleus of the trigeminus (Figs. 127
and 128, v') is also a superadded structure. This nucleus is -
situated in the substance of the afferent fibres of the trigeminus, -

ANATOMICAL AND PHYSIOLOGICAL INTRODUCTION. 51

ot far from their entrance into the pons. In structure it
5 somewhat similar to that of the ganglia of the posterior
oots, and it may represent the ganglion of the descending
oots, while the Gasserian ganglion represents that of the
scendinsr roots of the nerve.

§ 371. Development of the White Substance of the Cord.

The white substance is formed on the surface of the deeper grey
•abstauce. Soon after the tube which forms the rudiment of the cord
as closed, it is seen to be somewhat oval on section, with a central canal,
.t this period the cord consists almost entirely of grey matter ; and by
le appearance of lateral slits each lateral half becomes imperfectly
ivided into two parts, the anterior and posterior. In the human embryo
zone of white substance appears towards the end of the first month on
ie exterior of each of these parts ; and these may respectively be called
le anterior and posterior root-zones {Fig. 131, a, p). The anterior portions

Fig. 131.

131 (From Kolliker). Transverse Section of the Cervical Part of the Sjmial
Cord of a Human Embryo of six weeks.— c, Central canal; e, e', Its epithelial
lining ; g, Grey substance ; ar, Anterior roots ; pr, Posterior roots ; a, Anterior
root-sones ; p, Posterior root-zones.

what are afterwards the lateral columns of the cord develop as parts of
ie anterior root-zones, but the posterior portions do not begin to develop
itil about two weeks later. The portions last developed appear to belong
■ the posterior root zones, and join them in the medulla to form the
stiform bodies; and Flechsig thinks that they pass directly to the cortex

the cerebellum, hence they may be called the direct cerebellar fibres of
ie lateral columns.

At the end of the eighth week, then, the grey substance of the cord in
ie human embryo is covered anteriorly, posteriorly, and laterally by a

52 ANATOMICAL AND PHYSIOLOGICAL INTRODUCTION.

layer of white substance ; but at tbis period very remarkable changes take
place. Two bundles of longitudinal fibres, one for each side, are inter-
calated between the direct cerebellar fibres of the lateral columns and the-.-
posterior horns of grey matter. These bundles on being traced upwards>
are found to pass forwards at the lower end of the medulla, and after
decussating with one another they push aside the anterior columns, and I
form the inner and larger portion of the anterior pyramids of the medulla;,
hence the fibres may be called the pyramidal fibres of the lateral columns-
{Fig. 132, P, P'). About the same time analogous formations appeau
in the anterior columns, one on each side of the median fissure which::
separates the anterior root-zones. These bundles are very variable in size
and form, but are generally wedge-shaped or elliptical ; they form the
outer and lesser portion of the anterior pyramids of the medulla, but dc
not decussate with one another. They are called the columns of Turek<
or of Lockhart Clarke ; and they may also be called the pyramidal
fibres of the anterior columns {Fig. 132, T). At the same period al
which these bundles begin to develop, somewhat similar formation.'
appear between the posterior root-zones, one on each side of the posteriori
median fissure, and these are called the columns of Goll {Fig. 132, G)
The anterior white commissure {Figs. 134 to 140, ac) also appears at the
same time, that is, about the eighth week. A most important point to notice
in connection with the development of the white substance is that the fibre
when first developed are destitute of a medullary sheath, and only becom

Fig. 132.

rlc

Fig. 132. Cord of Human Embryo at five months. — ah, ah', anterior horns of gr
substance ; ph. ph', posterior horns of grey substance ; ar, ar', anterior roc
zones ; pr, pr', posterior root-zones ; P, P\ pyramidal fibres of lateral column:
T, columns of Tiirck; (?, columns of Goll; dc, dc', direct cerebellar fibn
c, anterior commissure.

ANATOMICAL AND rHYSIOLOGICAL INTRODUCTION. 53

ledullated at a later period of development. The law of development already
tated might, indeed, have led us to anticipate that such would be the case.
l. correlated fact is that the fibres of the bundles which are first formed
evelop a medullary sheath at a time when the fibres of the later-formed
undies are non-medullated. "When the cord of a human embryo is
xamiued at the end of the fifth month it will be found that the pyramidal
bres of the lateral columns, the fibres of the columns of Tiirck and of the
olumns of Goll, are non-medullated ; while the fibres of the anterior and
osterior root-zones, and those of the cerebellar fibres of the lateral
olumns, are medullated. "When a transverse section of the cord is
xamined iu glycerine after hardening in chromic acid, the bundles com-
osed of the non-medullated fibres will be found to transmit the light
lore readily than those composed of the medullated fibres, so that the
ction exhibits the appearances represented {Fig. 132,) in the cervical
gion of the cord of a human embryo at the fifth month. Even when
samined by the naked eye after hardening in chromic acid the bundles
imposed of non-medullated fibres are seen to be of a much darker colour
lan the bundles constituted of medullated fibres ; and the former also
come much more deeply stained with carmine than the latter. The
undies composed of the non-medullated fibres are, indeed, to the naked
re and in their reactions to staining fluids, more like the grey than the
hite substance of the adult cord.

The Accessory Portion of the White Fig. 133.

ubstance. — Inasmuch as the greater
art of the fibres of the anterior and
isterior root-zones, as well as those
the direct cerebellar tract, are me-
ullated as early as the fifth month of
nbryonic life, it may be presumed
lat all of them are fully developed
birth. The case, however, is dif-
ferent with regard to the fibres of the
pramidal tract, some of them being
tedullated and fully developed at
ie ninth month of embryonic life,
hile others are not. The fibres of
ie columns of Goll are probably also
ot all fully developed at birth. The
bres of the pyramidal tract in the
>rd are separated by the septal of
ijuroglia and the branching vessels into

nail lozenge-shaped spaces (Fin. 133). rm „, „
hp latAr f™™„ l flu x • JjIG- 133, T^nsverse Section of a

ne iater-tormed fibres appear to in- portion of the Pyramidal Tract

nuate themselves from above down- magnified.— 1, Fibres of large
ards air,™ tV,a ■ * al. diameter ; 2, fibres of small dia-

aras along the margins of these meter; 3, Deiter's cells ; 4, twig

)aces, so that the earlier-formed fibres of ^e median branch of the cen-
tral artery of the spinal cord.

54 ANATOMICAL AND PHYSIOLOGICAL INTRODUCTION.

occupy their centres ; the older being therefore further removed from thee t
blood-vessels than the younger fibres. It may be assumed that the earlier- •
formed fibres connect the cortex of the brain with the earlier- formed orrp
fundamental ganglion cells of the anterior horns, while the later-formed ij[
fibres connect the cortex with the accessory cells. What has already beennjj
said with regard to the size of the ganglion cells as a test of the stage cf 3

Fig. 134.

Fig. 134. Middle of Lumbar Enlargement. Section of Spinal Cord from the middle 6
the Lumbar Enlargement.— A P, anterior and posterior grey cornua respe* I ..
tively ; SG, substantia gelatinosa ; cc, central canal ; ac, .pc, anterior an- I
posterior commissure respectively ; G, column of Goll ; pr, posterior root-zom
p, posterior root ; p\ external radicular fasciculus ; p'r, internal radicul i
fasciculus ; a, a, a, anterior roots ; ar, ar1, anterior root-zone ; fr, formats I
reticularis ; pt, pyramidal tract ; T, column of Tiirck.

ANATOMICAL AND PHYSIOLOGICAL INTRODUCTION. 55

tevelopment of the cell is equally true with respect to the diameter of the
aedullated fibres. The diameter of these fibres may be accepted as a
ough test of the age of the fibres during the period of development, but
10 longer. It is very probable that the small medullated fibres of the
pyramidal tract connect together the small cells of the anterior horns and
elatively small cells in the cortex of the brain ; while on the contrary the
hick fibres connect the large ganglion cells of the anterior horns and large
;ells of the cortex. The largest cells of the spinal cord, for instance, are
bund in the lumbar region, and the largest in the cortex of the brain in the
paracentral lobule — the centre of the movements of the leg — and it is pro-
vable that these cells are connected with each other by thick fibres. We

Fig. 135.

a r

1 10. 135. Upper end of Lumbar Enlargement. — The letters indicate the same as the

corresponding ones in Fog. 134.

nave already seen that, as a rule, the accessory are smaller than the funda-
mental ganglion cells of the anterior horns, and it may therefore be in-
erred that the accessory fibres of the pyramidal tract are as a rule smaller
;han the fundamental ones. The smaller fibres are found in greater
numbers in the internal and posterior part of the lateral column, the
portion of the white column which adjoins the grey substance. At this
*pot the septa of connective tissue are larger, the neuroglia is more

56 ANATOMICAL AND PHYSIOLOGICAL INTRODUCTION.

spongy, and the lozenge-shaped spaces already described {Fig. 133) am
more distinctly marked than in the more external layers of the whita
substance. The formatio reticularis of the spinal cord appears indeed
to owe its structural peculiarities mainly to the fact that it consists
in great part of longitudinal fibres of small diameter separated intc
bundles by comparatively large septa of loose neuroglia. This portioE I
of the cord also transmits fibres which issue from the grey substance tc
ascend in the pyramidal tract, and from the vesicular column of Clarke tc
pass out to the direct cerebellar tract. But the longitudinal fibres of srnal I
diameter, which are so abundant in this portion of the cord, would appeal I
to belong to the accessory portion of the pyramidal tract. Indeed, tht

Fig. 136. Lower end of Dorsal Region. — T, column of Tiirck ; dc, direct cerebellar
tract. The other letters indicate the same as the corresponding ones in Fig. 134 I

spongy character of the neuroglia and the vascularity of this area rende
it peculiarly adapted for the growth of new fibres. The fibres of tha
columns of Goll are also separated by the distribution of the blood -vessehj
and septa of connective tissue into lozenge-shaped spaces. The fibres as
the margins of these spaces are not medullated at nine months of embryoui
life, and they are as a rule less in diameter in the adult cord than th
fibres which occupy the centres of the spaces. These small fibres mus i
therefore be regarded as belonging to the accessory system. The fibres c
the posterior root-zones are smaller than those of the anterior and latera >

Fig. 136.

ar T

ANATOMICAL AND PHYSIOLOGICAL INTRODUCTION. 57

lumns with the exception of some of the accessory fibres of the pyramidal
act The reason of this appears to be that the fibres of the posterior
ot-zones connect the cells of the posterior horns with each other, and
.e latter being themselves small the intercommunicating fibres are also
nail.

§ 372. Longitudinal Distribution of the White Substance.
These, then, are the component parts of the spinal cord,
msidered with reference to its transverse section; the longi-
idinal distribution of these parts must now be described.

Fig. 137.

Fig. 137. Middle of Dorsal Region.

he grey matter extends the whole length of the cord, and its
ize maintains a constant relation to the number and variety
f the movements to be co-ordinated ; hence it is larger in the
lumbar and cervical regions, where the movements of the
imbs are co-ordinated. The anterior and posterior root-zones
Aso extend the whole length of the cord, and, speaking
roadly, their size maintains a pretty constant relation to the

ANATOMICAL AND PHYSIOLOGICAL INTRODUCTION.

size of the grey matter, although there is probably a slight!
increase of size from below upwards. The most noticeable J
feature with regard to the remaining bundles of fibres is, that tj
they increase steadily in size from below upwards. The fibres \
of Goll (Figs. 134 to 140, G) extend the whole length of the]
cord, but they gradually diminish in size from the medulla, sod
that mere traces of them are to be found in the lumbar region..
The pyramidal fibres of the lateral columns (Figs. 134 to 140, pt\
also extend the whole length of the cord, but steadily diminish:.

Fig. 138.

Fig. 138. Upper end of Dorsal Region.

in size from above downwards, so that they are reduced
comparatively small bundles in the lumbar region. The direc
cerebellar fibres of the lateral columns (Figs. 136 to. 140, dc)
appear in the cervical region as thin lamellte of fibres, one on
each side, external to the pyramidal fibres. They diminish
in size from above downwards, and disappear somewhat below-
the middle of the dorsal region, so that in the lower dorsal and

ANATOMICAL AND PHYSIOLOGICAL INTRODUCTION.

mbar regions the pyramidal fibres come to the surface of the
rd. The fibres of Turck (Figs. 136 to 140, T) also diminish

size from above downwards, and disappear about the middle

the dorsal region.

The relative size and position of the different segments of
white substance may be seen in Figs, 134 to 140, which

Fig. 139.

Fig. 139. Middle of Cervical Enlargement.

^present sections of the spinal cord of a nine months human
mbryo at different elevations. The fibres of the pyramidal
^acts (pt) of the lateral columns, and of the columns of Goll
->) and of Turck (T), have assumed a medulla at the ninth
lonth, and are not, therefore, so distinctly marked off from
he remaining portions of the white substance as they are

ANATOMICAL AND PHYSIOLOGICAL INTRODUCTION.

represented in the figures, the latter being in this respect mor:
like the appearances presented by the cord between the fiftl l5
and sixth months of embryonic life, at a time when the fibres o<
the anterior and posterior root-zones and the direct cerebellar
tract are alone medullated.

Fig. 140. Section on a level with the Second Cervical Nerve, —sa, Spinal accessory
nerve. The other letters indicate the same as the corresponding ones in
Figs. 134 and 136.

§ 373. Continuation upward of the various Segments of th
White Substance of the Cord through the Medullc
Pons, and Crus Cerebri.
(1) Columns of Goll and Posterior Root-zones. — A tranai
verse section of the lower half of the medulla shows tba
the columns of Goll are continued upwards into the mednll

ANATOMICAL AND PHYSIOLOGICAL INTRODUCTION. Gl

I the form of two bundles of fibres, one on each side of the
sterior median fissure. Each bundle contains a nucleus of
jy matter, which from its form is called the clavate nucleus,
d the bundle itself is called the pyramidal column, or
iciculus gracilis {Fig. 122, G, cri). External to this fasciculus
placed a wedge-shaped bundle, called the fasciculus cuneatus,
lding in its interior a grey nucleus, called from its form the
angular nucleus (Fig. 122, pr, tn). The greater portion of
3 fibres of the posterior root-zone of the cord terminates in
e cuneate fasciculus and its enclosed grey nucleus. The
;nder and cuneate fasciculi of the medulla are much larger in
:e than the column of Goll and posterior root-zone of the
rd, owing to the interposition of the grey nuclei ; hence the
sterior horn of grey matter is displaced outwards and forwards
: the medulla, so that the continuation of the gelatinous sub-
mce forms a mass of grey matter on the lateral aspect of the
sdulla, known as the grey tubercle of Rolando (Fig. 122, sg).
lis mass of grey matter is continued upwards in the medulla
d pons to the level of the point of emergence of the fifth
rve, and gives origin to the ascending root of the latter.

close relationship with the external surface of this grey
ass is a bundle, the fibres of which are medullated in a
ne months embryo. This bundle is the homologue in the
sdulla of the posterior root-zone of the cord, and is frequently
und diseased in locomotor ataxy (Figs. 122 to 127, at).
One of the most remarkable rearrangements of fibres in the
edulla arises from the fact that the cuneate fasciculus, through
e intermediation of its nucleus, resolves itself into arcuate
)res, which pass forwards and upwards to be connected with
e nucleus of the olivary body on the same side ; and it is
so probable that the slender fasciculus through its nucleus has
similar termination.

A transverse section of the upper part of the medulla shows
at the fibres have undergone a still further rearrangement,
id that they are greatly reinforced in number ; but the course
the additional fibres will be more readily traced if we follow
tern from the cerebellum to the medulla, instead of from below
p wards.

(2) Connections of the Peduncles of the Cerebellum ivith

ANATOMICAL AND PHYSIOLOGICAL INTRODUCTION.

the Medulla Oblongata, Pons, and Crura Cerebri. — The
f trior peduncle of the cerebellum, according to Stilling, brer
up, on entering the medulla, into an internal (Fig. 125, ep) a
an external (Fig. 125, ip) division, the latter of which he cal
the "restiform body." The fibres of the internal divis.-
spring from the roof-nuclei of Stilling, and on reaching 11
medulla resolve themselves into arcuate fibres, which p
downwards and inwards, interlacing with the ascending fibj
of the anterior root-zone behind the olivary body of the sai
side ; and some anatomists believe that they cross the med:
raphe to reach the olivary body of the opposite side. H
fibres of the restiform body are derived from the cortex of 1i
cerebellum, and from a layer of fibres surrounding the dent;
nucleus ; and this division, on descending to the medulla, sv
divides into two bundles, which are separated from one anotl
by the direct cerebellar fibres of the lateral columns of v
cord in their ascent towards the cerebellum (Fig. 125, dc).
a nine months human embryo the fibres of the restiform be;
are non-medullated (Fig. 125, ep) ; while those ascending fr[
the lateral columns are medullated (Fig. 125, dc), so that the ttj
sets can be readily distinguished from one another. The fib
of the restiform body, like those of the internal division of 1
peduncle, resolve themselves into arcuate fibres ; the exterj
bundle forming the zonular layer which passes in front of 1
olivary body, and the fibres of which reach the median raphe' !
passing both in front and behind the anterior pyramid. Tho
which pass in front of the anterior pyramid are called arcifo
fibres (Fig. 125, a); they wind backwards to reach the mednj
raphe' (Fig. 141), where, after ducussating with the correspon
ing fibres of the opposite side, they bend outwards to rea
the olivary body of the opposite side where they terminate,
great part of the arcuate fibres of the internal bundle se2
to pass through the olivary body of the same side without beij
connected with its grey substance ; and after gaining the raj.]]
they also cross over to pass into the interior of the olivary btf
of the opposite side, in the grey substance of which all 1;
arcuate fibres of the restiform body terminate. The oliv:
body, therefore, is the medium of communication between i|
cuneate fasciculus and probabl3r also the slender fasciculus?

ANATOMICAL AND PHYSIOLOGICAL INTRODUCTION.

same side on the one hand, and the restiform body and
bably the internal division of the cerebellar peduncle of the
Dosite side on the other hand.

The fibres of the middle peduncle of the cerebellum are
ived from the cortex ; they pass in front of and through the

t >stance of the pons {Figs. 126 to 128, Tr and Tr'), where
jy separate the ascending fibres of the anterior pyramids
o bundles (Figs. 126 to 128, P, p), and interlace in the
idle line with the fibres of the middle peduncle of the

^osite side. On reaching the opposite side they are supposed
terminate in the cells of interposed grey matter, by means
which they are connected with fibres descending from the
sta. The close relationship of the middle peduncles with
lateral lobes of the cerebellum is well illustrated by the

I b that in those animals in which the latter are deficient or
ent the transverse fibres of the pons are few or entirely
ating.

Fig 141.

"'anLZ'Tr^J^3 U,Anal01™ "]• , Vtyrm of a horizontal section of the

SJsrd^ Ffb^f^ *■ Medulla 0il9»»a*- Ant--

64 ANATOMICAL AND PHYSIOLOGICAL INTRODUCTION.

The fibres of the superior peduncles are derived from the
dentate nuclei ; they decussate with one another in tg
tegmentum, the fibres of one side passing over to be connected ii
with the red nucleus of the opposite side (Fig. 129, x). The ip
fibres of the superior peduncles are medullated in a nine H
months embyro ; they may be seen surrounding, and even wjm
the substance of the red nucleus (Fig. 129, RJST), and a con-
siderable proportion of them pass upwards uninterruptedly &
into the tegmental portion of the internal capsule, and either e
end in the inferior or external surface of the thalamus, or, a&sl
I am inclined to believe, pass uninterruptedly along its external i
border upwards to be connected with the central convolutions |
of the cortex of the cerebrum.

Some anatomists think that part of the fibres of the anterioi
root-zones pass through the crusta to join the lenticular nuclei: ff
but a very important fact has been ascertained by Flechsig. I
which renders this doubtful. Flechsig found that in a nine j
months human embryo the pyramidal fibres in the crusta are the f
only ones which have acquired a medullary sheath ; and my owd i>.
sections confirm this (Fig. 129, P). But the fibres of the anterioiOT
root-zones in the cord are medullated at a very early period oi I
development, and long before the pyramidal fibres have acquired |
a medullary sheath ; hence it may be inferred that none of tht •■
fibres of the anterior root-zones pass up into the crusta oi
motor tract of the crura, although it is very probable that ne^ I
fibres become developed, which connect the corpora striata anc
the cord, and that these pass through the crusta and becornf I
mixed with the fibres of the anterior root-zones. The clcst •
connection which is maintained between the anterior root-zone: j
and that portion of the central grey tube which is in immediati I
relation with the efferent nerves, seems to indicate that thi
former consist of fibres which co-ordinate the various segment \>.
of the cord longitudinally ; and there are other grounds fo k
believing them to consist of a series of looped fibres whicl k
originate and terminate in the anterior part of the central gre;
tube.

(3) The direct cerebellar fibres are represented by a thii1
lamella of longitudinal fibres lying on the surface of the cuneat
fasciculus and of the grey tubercle of Rolando (Figs. 124 am

ANATOMICAL AND PHYSIOLOGICAL INTRODUCTION. 65

' , dc). They pass upwards to the cortex, and thus form an
nterrupted connection between its grey matter and the cord,
ire the fibres are supposed to pass inwards between the
idles of the pyramidal fibres of the lateral columns, to
ninate in the cells of the group known as Clarke's column.
}ir function, however, is not yet ascertained.
4) Tlie Pyramidal Tract. — The pyramidal fibres of the
;ral columns at the upper end of the cervical region of the
i pass forwards and inwards towards the anterior median
ire. These fibres decussate with one another in the
lulla, so that those of the right side pass to the left, and
se of the left to the right. The decussation frequently begins
the upper portion of the cord ; while the homologues of
pyramidal fibres, which arise from the nerve-nuclei of the
>oglossal and facial nerves, cross separately in the pons
ve the decussation of the pyramids. The pyramidal fibres
,he lateral columns during and subsequent to their decus-
on come forwards into the anterior median fissure, and
h. aside the columns of Tiirck {Fig. 140, T), so that the latter
a a prismatic bundle of fibres external to the former, and
ind without decussating with one another. These two sets
ibres constitute the anterior p}Tamids of the medulla {Figs.
to 125, P) ; they can be traced through the pons {Figs. 126
28, P), where they receive a large accession to their size,
' the peduncles of the cerebrum. According to the researches
?lechsig, which my own sections confirm, the pyramidal
3s, after being separated into distinct bundles in the
s, come together so as to form one compaet bundle in
i peduncle {Fig. 129, P). This bundle occupies about the
die third of the crust of the cerebral peduncle, and,
,rary to what has hitherto been believed, it passes into
posterior segment of the internal capsule, lying between
lenticular nucleus and optic thalamus opposite the middle
id of the latter. The pyramidal bundle is separated from
' caudate nucleus by a layer of fibres, which ascend from the
BiTnal surface of the optic thalamus to reach the corona
n ata, while it rests on the three successive segments of the
" icular nucleus, and reaches the corona radiata opposite the
ki d quarter of the caudate nucleus (reckoning from before

ANATOMICAL AND PHYSIOLOGICAL INTRODUCTION.

backwards). Having emerged from between the basal gangl;|
without anywhere communicating with them, the fibres of it
pyramidal bundle radiate in all' directions towards the surfas
of the cerebrum, and are mainly distributed to the centu
convolutions about the sulcus of Rolando, the so-called " mo\\
area" of the cortex (Fig. 142, P").

Fig. 142 'After Flechsig). Diagram of the Grey Sfasses of the Spinal Coro I
Brain, showing the course of the Conducting Paths.

B, Fissure of Rolando.

P" P, T and Pt, Course of the fibres of the pyramidal tract from i I
origin in the central convolutions to their termination in the anterior |
horns (a, a').

ANATOMICAL AND PHYSIOLOGICAL INTRODUCTION. 67

Che cardinal facts which concern us at present are, that
res issue from the central convolutions of the cerebrum,
lich pass through the internal capsules without communicating
:h the basal ganglia ; that the same fibres pass through the
ebral peduncles to enter the pons, where they at once begin
diminish in number. The fibres of this kind, which pass
•ough the pons, collect together to form the anterior pyramids
the medulla, which also diminish in size from above down-
rds, showing that some of these fibres are lost in the medulla
elf. The internal and by far the larger portion of the
ramids decussate with one another, and these portions pass
okwards so as to form in the cord the bundles of pyramidal
res in the lateral columns — bundles which extend the whole
igth of the cord, but gradually diminish from above down-
rds. The external and lesser portion of the pyramids pass
ectly downwards to form the columns of Tiirck — columns
ich dwindle gradually until they disappear, usually about the
ddle of the dorsal region. It is not yet proved anatomically
w these fibres end in the cord ; but other considerations
ider it probable that they end in the grey matter of the
terior horns and its continuation through the medulla, pons,
d around the aqueduct of Sylvius. The pyramidal fibres, in
3 word, form an uninterrupted connection between the central
1 volutions of the brain and the central grey tube of the
:d.

/, //, III, First, second, and third portions of the lenticular nucleus [JVL\
JVC, Caudate nucleus. Th, Optic thalamus.

D, C, B, A, Points from which fibres issue connecting the cortex of the brain
and basal ganglion, and also the grey substance of the pons (PO). Bd,
Fibres connecting the cerebellum and optic thalamus ; and Gap, those
connecting the cerebellum and the grey substance of the pons.

aq, and pq, Anterior and posterior pair of corpora quadrigemina respectively.

x, Upper, and oc', lower fibres connecting the olivary body and the corpora
quadrigemina.

FR, Formatio reticularis of the medulla oblongata, formed by fibres from the
optic thalamus [Th), the internal division of the inferior peduncle of the
cerebellum (icp), from the spinal cord {/>; ar, and aiJ), and probably also
from the clavate nucleus (Nc).

o, Olivary body ; ecp, Fibres of the restiform bodies connecting the olivary
bodies and cerebellum ; other fibres connect it with the triangular (Npr)
and clavate (JVC) nuclei.

dP, Decussation of the pyramids.

pr>. Fibres of the posterior roots which pass upwards and downwards into the

grey substance, and pursue only a short course.
a, a , a", a'", a"", Anterior roots.
P, pr, pr', pr», G, Fibres of the posterior roots.

68 ANATOMICAL AND PHYSIOLOGICAL INTRODUCTION.

The Accessory Portion of the Pyramidal Tract. — We have
seen that the accessory fibres of the pyramidal tract occupy
the margins of the lozenge-shaped spaces into which the lateral
column and column of Tiirck are divided {Fig. 133), and that they
are very abundant in the portion of the lateral column which
adjoins the grey substance, and especially in the formoiw
reticularis. But on ascending to the anterior pyramid of the
medulla the accessory fibres become much more abundant, and

Fig, 143.

a ■

Fig. 143 (After Flechsig). Diagram of Transverse Section of the Spinal Cord «

upper half of the Dorsal Region.
G, Anterior commissure.

dc', Fibres which pass from the vesicular column of Clarke \vc) to the

cerebellar tract.
P, Posterior horn.

Figs. 142 and 143 (After Flechsig).— Letters common to Figs. 141 and 142.

Pt, Pyramidal tract of the lateral column.
T, Columns of Tiirck.
dc, Direct cerebellar tract.
ar. Internal portion of the anterior root-zone.
ar, External portion of the anterior root-zone.
pr, Posterior root-zone.
G, (roll's columns.

fr, Reticular formation of the spinal cord.
a, Anterior grey horns of the spinal cord.

ANATOMICAL AND PHYSIOLOGICAL INTRODUCTION. G9

lough some of them may still mix with the other fibres,
v awre^ate in the internal and anterior margin of the
amid, so as to occupy a circumscribed area of the pyramid
hout admixture with other fibres. This area is shown in
is. 124j and 125, p, which represent sections of the medulla of
ine months embryo. On passing through the pons the non-
dullated fibres occupy the inner portion of the longitudinal
nculi {Figs. 126 to 128, p), pass to the inner side of the
dullated fibres in the crust of the crus cerebri (Fig. 129, p),
1 reach the cortex mainly by passing through the anterior
f of the internal capsule.

5) The Anterior Root-zones. — The continuation of the
erior root-zones through the medulla, pons, and crus,
erves special attention. The course of the fibres of these
es in the medulla is obscured by the fact that they do
form a defined mass, as in the cord. They are separated
> bundles by the arcuate fibres of the medulla, so as to
n what is called from its reticular appearance the formatio
eularis (Fig. 125, frs). The zones consist of two portions,
internal, which lies between the anterior median fissure
I the anterior roots (Figs. 134? to 140, ar), and an external,
sisting of the remaining portion (Figs. 134 to 140, ar').
3 internal portions of the anterior root-zones are pushed
le in the lower part of the medulla by the decussating fibres
the pyramidal tract, but above the level of the decussation,
3re the olivary body is intercalated, the internal portion
:hrust backwards behind the pyramids and close to the
dian raphe, while the fibres of the hypoglossal nerve separate
internal from the external portion of the anterior root-zone,
the spinal cord the internal portion of the anterior root-zone
intains a close relation to the internal group of ganglion
s, and this relation is apparently maintained throughout its
rse in the medulla, pons, and crus. The portion which is
I led the posterior longitudinal fasciculus in the medulla
igs. 124 to 128, L), pons, and crus, appears to be the con-
uation upwards of the part of the internal portion of the
terior root-zone which adjoins the grey matter, and this
•ciculus always lies to the inner side of the roots of the
terior motor nerves, at their origin in the motor ganglion

70 ANATOMICAL AND PHYSIOLOGICAL INTRODUCTION.

cells. The upward continuation of the part of the internal!
portion of the anterior root-zone which is remote from the grey
matter is represented by ar in Figs. 124 to 129.

In the crus the posterior longitudinal fasciculus is situated in .
front of the aqueduct of Sylvius, in close relationship with the
nucleus of origin of the third nerve (Fig. 129, L). A portion of this •
bundle is continued forwards in the thalamus in the walls of j
the lateral ventricle, while the remaining fibres bend backward-
to join the posterior commissure of the third ventricle. The z
fibres of the latter portion are the first to become medullated s
in the cerebrum of the human embryo.

The external portion of the anterior root-zone of the cord is
continued upwards into the formatio reticularis of the medulk
(Figs. 124 to 128, ar1). The continuation of the external
portion of the anterior root-zone lies behind the olivary body, x
and comes to the surface of the medulla in its lateral column.
It is bounded internally by the root fibres of the anterior motor ■-"
nerves, and externally by the root fibres of the nerves of the
lateral mixed system, and posteriorly by grey matter. The
interlacing fibres of the pons (Figs. 126 to 128, Tr) pass in from
of this portion (ar1), while in the crus the latter comes agai
further forwards, the locus niger lying between it and the c:
(Fig. 129, ar').

(III).-FUNCTIONS OF THE SPINAL CORD AND MEDULLA

OBLONGATA.

It would occupy too much space to describe fully the func-
tions of the spinal cord and medulla oblongata, and the reader 1
is referred to physiological manuals for the usual information
on the subject. My main object at present is to elicit a few
points which will be of subsequent use to us in interpreting
the phenomena of disease, and in connecting symptoms with
morbid alterations of structure.

§ 374. Voluntary Action. — The special functions of the cord .
are those by which the spinal centres are subordinated to the
motor centres of the cortex of the brain. It is probable that
all the spinal centres are connected with the motor centres ot
the cortex of the brain, or are, in other words, under voluntary

ANATOMICAL AND PHYSIOLOGICAL INTRODUCTION. 71

trol; but the later-acquired movements of man are more
iroughly under voluntary guidance than the earlier-acquired
undaraental actions. Inasmuch as the observation of the
elopment of the cord has enabled us to draw a broad dis-
ition between the fundamental and accessory portions of the
icture of the spinal cord, it will be well to endeavour first to
nect the later-acquired or accessory functions with the later-
uired or accessory structure. The earlier-acquired or funda-
ntal functions will then be left as a residuum to be con-
ted with the fundamental structure of the cord.

1) The Accessory Functions of the Spinal Cord and Medulla Oblongata.
) movements of the haud afford the best example of the accessory
stions of the spinal cord. These movements are peculiar to man,
by far the greater number of them are acquired after birth. It
-, therefore, be expected that the development of the structure, which
•esents these movements in the spinal cord, must also take place after
h.

The movements which are most characteristic of the upper ex-
nity in man are those of pronation and supination of the forearm
the complicated movements of the hand and fingers, and it is exceed-
y probable that the structural representatives of some if not all of
*e movements are to be found in the median group of cells. These
4 appear at a late period of the development of the cord, hence they
n a speciality of structure which corresponds to some speciality of
ction ; again they maintain a small size even in the adult cord, and
sequently may be expected to preside over the action of small muscles,
b. of these conditions being realised in the hand.

The smaller median area in the lumbar enlargement of the cord
sides probably over the movements of the lower limbs, which dis-
,ruish the adult man from the lower animals and also from the human
-nt. These movements are mainly executed by the extensors of the
on the thigh and probably also by the adductors, and by the flexors of
foot on the leg. Indeed, the slight elevation of the ball of the toe, so
■o allow the passive leg to swing forwards by its own weight in walking,
■he last movement acquired by the child ; and we shall subsequently
that it is the first movement to be affected in disease. If, then, the
iian area of small cells be the structural correlative of the later-acquired
I more special movements of the limbs, it must be absent in those por-
is of the cord which do not supply nerves to limbs, and we have already
n that this area is absent in the dorsal and upper cervical regions of
i cord.

It must be remembered that the muscles of the hand are connected
■h the earlier-formed or fundamental cells of the anterior horns, and

72 ANATOMICAL AND PHYSIOLOGICAL INTRODUCTION.

that the small cells of the median area do not of themselves suffice
the regulation of their movements. The increased development
the median area in the cervical enlargement represents merely a coj
plication on the previous structure of the cord corresponding to |
complication of muscular adjustments which distinguishes the hand
man from the anterior extremity of animals.

The hypoglossal accessory nucleus, and the internal and extern
accessory facial nuclei, appear to be the homologues in the medujl-
oblongata of the median area in the cervical and lumbar enlargements o:
the spinal cord. The hypoglossal accessory nucleus seems to be the ■
additional structural complication rendered necessary by the compli-.:
cated movements executed in the production of articulatory speech ; while j
the facial accessory nuclei are the structural counterparts in the medulla.!
of the movements of facial expression.

The next accessory function which I shall mention is the muscular^
adjustments necessary for maintaining the erect posture in man. Theses
adjustments are also acquired a considerable time after birth, hence if
may be inferred that their structural counterparb in the cord is not welli
developed at birth. The medio-lateral area corresponds in my opinion to-.!
these adjustments in the dorsal region of the cord. The cells of this area-
are not well developed at birth, and the area is entirely absent in thffll
lower animals. These cells are also of small size, even in the adult cord,<i
and if, as we have already stated, the size of the ganglion cell is related tcfe
the size of the muscle with which it is connected, the erectores spinse arerl
the muscles of the trunk which best correspond to this description. The !
medio-lateral area appears also in the upper cervical region, and it may I
be presumed that the small muscles which extend the vertebral column imj
the neck, and draw back and rotate the head, are supplied from these 9
cells. We have already seen that some of the fibres of the eleventh-
nerve (spinal accessory) are derived from the postero-lateral group in the
cord, and it is very probable that the accessory nucleus of this nerve in
the medulla is the homologue of the medio-lateral area in the upper cer-"
vical and dorsal regions of the cord. The accessory nucleus of the
eleventh nerve is the additional organisation rendered necessary by the 1
complicated movements of the human larynx.

The marginal cells of the postero-lateral, antero-lateral, and central;1
groups appear late in the development of the cord, and these therefore
must be regarded as belonging to the accessory system, even although:
the ganglion cells are of comparatively large size. The fact that these
cells are of large size shows that they must be engaged in the
regulation of the movements of large muscles. It is probable that
these marginal cells in the lumbar region regulate the contractions
of the large muscles of the lower extremity which are engaged m
maintaining the erect posture. The great relative size of the gluteus
maximus in man, as compared with the lower animals, would appear tc
render necessary a corresponding increase in the number of ganglion cells

ANATOMICAL AND PHYSIOLOGICAL INTRODUCTION. 73

;he spinal nucleus which regulates its movements in the former, as com-
•ed with that in the latter. And inasmuch as the gluteus maximus is not
ich called into action until a considerable time after birth, these super-
led cells must belong to the accessory system. These additional
Is may probably be represented by the marginal cells of the postero-
eral group in the lumbar region. The alternate upward rotation of the
.vis which takes place in walking, and which is mainly effected by
ltraction of the gluteus medius and minimus, is likewise a very special
>vement ; and it also may be regulated by the later-developed cells of
3 or other of these groups of ganglion cells in the anterior horns.
! We have seen that the postero-lateral group in the upper cervical region
'es ofFthe spinal portion of the spinal accessory nerve, and that this portion
'ms the external branch of the nerve, which is distributed to the sterno-
ido mastoid muscle and the upper portion of the trapezius. But in man
3 sterno-cleido mastoid is in close relation with the clavicular portion of
3 peetoralis major, being only separated from it by the clavicle, and in
)se animals in which the clavicle is deficient it runs with the anterior
rt of the trapezius muscle into the deltoid, forming a mastoido-humeral
iscle. All of these muscles are closely associated in their actions, and
is, therefore, probable that all are innervated from the postero-
eral group, while the latissimus dorsi, rhomboidei, and several other
iscles may perhaps be added to this list. It is very probable indeed
it the muscles which may be compendiously summed up with reference
their functions as the accessory muscles of inspiration are innervated
■m this group in the cervical and dorsal regions. These muscles are
efly the sterno-mastoids and scaleni, the peetoralis major and minor,
3 serrati postici et superiores, the subclavius, and the elevators of the
ad and spinal column.

The postero-lateral and medio-lateral groups of ganglion cells consist
a series of superimposed ganglionic centres, constituting a column of
la which extends from the lumbar region, through the dorsal and cer-
;al regions of the cord to the medulla and pons. Speaking broadly,
is column regulates the muscular contractions necessary for the main-
lance of the erect posture, the contraction of the extraneous muscles of
jpiration, in part at least that of the muscles supplied by the spinal
:essory, vagus, glosso -pharyngeal, seventh, and by the motor branch
the fifth nerves. The portion of the facial nerve supplied by the
itinuation of the postero-lateral group in the medulla probably pre-
les over the function of the facial muscles in their relation with
istication and respiration. The series of superimposed ganglionic
atres of which the postero-lateral group consists cannot act inde-
ndently of each other; and in order to secure harmony of action,
me of these centres must become subordinate to other centres, either of
ie same column or of some other part of the nervous system. All of
em are doubtless co-ordinated in the cortex of the brain, but it is not
iprobable that the inferior centres of the column are also subordinated

74 ANATOMICAL AND PHYSIOLOGICAL INTRODUCTION.

to one of the superior centres in the medulla oblongata. If such sho
be the case, there is no occasion for assuming the existence of a distin
respiratory centre in the medulla oblongata apart from the upward con
tinuation of the postero-lateral column of cells. It is much more pro«
bable that the respiratory centre is merely an enlargement in the medulla ;
of the postero-lateral column of cells. It is also quite likely that this en-
largement is closely connected with the other groups of cells which have
been continued upwards from the cord into the medulla.

(2) Fundamental Voluntary Functions. — With respect to the functions*
of the antero-lateral group, I must content myself by saying very little.
The cells of this group always maintain the lead in the course of develop-
ment. It is not only that they begin to develop and assume processes?
at an earlier period than the cells of the other groups, but the greater
portion if not all of them appear almost simultaneously, and maintain
an equal rate of growth during development. The antero-lateral differs in.:
this respect from the postero-lateral and central groups, which increase*!
in size by the gradual addition of new ganglion cells at their margins. 10
may be expected, therefore, that this group will regulate the fundamental I
actions, or the actions which are carried on in a reflex manner, and which, i
are in great measure independent of the cephalic ganglia. In this cona
nection the intercostal muscles, the diaphragm, abdominal muscles, and
the muscles constituting the floor of the pelvis will immediately suggest
themselves. In the lower extremity the most general movements m&jk
be expected to be regulated by the antero-lateral group. These move
ments are flexion of the thigh on the body, of the leg on the thigh, anc I
elevation of the heel. It may be said that elevation of the heel is (
movement almost peculiar to man, but this is rendered necessary durint
locomotion, owing to the depression of the heel which has been effecte(
in the course of evolution, by the progressive increase in the strength o
the flexors of the foot on the leg.

On watching the first movements of the human infant it will be seere
that the power to elevate the heel is acquired early, while the elevation o •
the toe so as to allow the foot to swing forwards by its own weight is th<
last movement acquired ; hence it is the most special movement, and it wil
be represented in the cord by the superaddition of new ganglion cells t<
those already existing. What the movements are which are regulated b;
means of the antero-lateral group in the cervical region I can only niak
a rough conjecture. They are no doubt the simplest movements, au<
those which man possesses in common with the lower animals. The mos i
probable of these movements are flexion at the wrist, simple flexion ani
extension at the elbow, and the backwards and forwards movements a
the shoulder, and flexion of the neck and head. Some of the muscle
engaged in these actions we have already found reason to believe wer
innervated by the postero-lateral group ; but this does not exclude th
possibility of their being innervated also by the antero-lateral grou[
There is so much uncertainty, however, with regard to the function of th

ANATOMICAL AND PHYSIOLOGICAL INTRODUCTION. 75

iro-lateral group in the cervical region that it would be hazardous
nake auy assertion with regard to it. There is also quite as much
srtainty with respect to the functions of the central, internal, and
jrior groups.

j 375. Reflex Action. — The production of reflex action is one
the earliest and most fundamental functions of the spinal
d. As we have already seen, every reflex act requires for its
•formance an afferent and an efferent fibre, and a centre-
e earlier-formed ganglion cells of the anterior grey horns con-
;ute the centres of reflex action; and it is probable that the
lex afferent fibres pass to them directly, without the inter-
ltion of the grey substance of the posterior horns. Inasmuch
the reflex afferent fibres are formed at an early period in the
velopment of the cord, they must be thrust out laterally
ring the development of the posterior grey horn, so that
;y will occupy an external position in the fan formed by
; spreading out of the fibres of the posterior roots. We
;e already seen that there are grounds for believing that the
;.3rent fibres of the tendinous reflexes pass in the inner radi-
ar fasciculus, and it is not improbable that the afferent
res of the cutaneous reflexes pass in the outer radicular
ciculus. The efferent reflex fibres pass out in the anterior
its, and the same fibres probably convey both reflex and
untary impulses.

§ 376. Trophic Function of the Cord. — It is well known that
3 ganglion cells of the anterior horns of the cord exercise a
•phic influence^on the muscles ; but whether there are trophic
Is endowed with special functions, or whether all the cells
3 endowed with both motor and trophic functions, I am unable
say. With some degree of qualification, I feel inclined to
opt the latter view.

It is well known that within certain limits, increased func-
>nal activity of a muscle is followed by an increase in its
lk, and, conversely, that a diminution of its activity is followed
diminution of its bulk. When, therefore, the mechanism in
e cord, which regulates the movements of the muscle, is in a
ite of activity, this is followed by an increase in the function of
e muscle, and consequently by an increase in its bulk. If, in

76 ANATOMICAL AND PHYSIOLOGICAL INTRODUCTION.

addition to an increase in its bulk, the muscle be called upon
to make a new adjustment in response to altered circumstances,
the new adjustment can only become permanent in the race
when it is organised in the cord by the growth of new cells and
fibres in addition to the original mechanism by which its move-
ments were guided.* But if the new cells and fibres become
incapacitated from any cause, the muscle will soon lose the
structural modification which corresponded to its recently-
acquired functional adjustment, but no other change will take
place in it. As long as the original mechanism is maintained
in the cord, so long will the nutrition of the great bulk of the
muscle go on as before. ■ But the case is very different when
the function of the original mechanism is destroyed ; then the
nutrition of the muscle is injured at its very foundation, and
profound trophic changes occur. It is very probable, therefore,
that the influence exerted by the later-developed ganglion cells
of the anterior horns on the nutrition of the muscles is small,
while that of the earlier-developed cells is very great.

§ 377. Automatic Action. — ■The spinal cord contains a con-
siderable number of what are regarded as automatic centres,
but it is probable that many of these act in a reflex manner.
The lumbar portion of the cord contains centres for the
regulation of the acts connected with micturition, defecation,
erection and ejaculation, and parturition. The oculo-pupillary
centres in the upper dorsal and cervical regions of the cord have
already been described.

Yaso-motor centres exist in the eord by meg»ns of which the
tonus of the muscular coat of the vessels is maintained. It
has been thought that the spinal cord also exercises a tonic
action over the skeletal muscles, but this opinion is doubtful.
The tone of the sphincters of the bladder and rectum, however,
is undoubtedly maintained by the lumbar part of the cord,
and is probably reflex in character. The peristaltic movements
of the oesophagus, stomach, and intestines are regulated by the
central grey tube. Little is known beyond conjecture of the
localisation of the centres of visceral innervation in the cord.
That they are not situated in the anterior grey horns is ren-
dered certain by the fact that the visceral movements, and

ANATOMICAL AND PHYSIOLOGICAL INTRODUCTION. 77

ie automatic actions of defecation, micturition, erection, and
arturition remain unaffected in disease limited to the anterior
rey horns.

Several considerations may be adduced tending to show that
ie vesicular column of Clarke contains the spinal centres of
isceral innervation. The cells of this column are bipolar, like
lose of the sympathetic, and not multipolar, like those of the
aterior horns which regulate the complicated actions of the
ieletal muscles. This column is absent in the lumbar and
arvical enlargements, the portions of the cord which supply
erves to the limbs, and in the upper half of the cervical
3gion which supplies nerves to the muscles of the neck. It
, on the other hand, present in the upper lumbar and the
Drsal regions of the cord — the portions from which the trunk

innervated, and is again represented in the medulla oblongata
» the principal nucleus of origin of the vagus — the most im-
)rtant visceral nerve of the body. It may be assumed that all
ie actions regulated through the vesicular column of Clarke
•*e subordinated to the highest expanded portion of it which
onstitutes the nucleus of the vagus; hence there is no reason
) assume that the medulla oblongata contains a circumscribed
iso-motor centre distinctly separated from the nucleus of the
igus.

! 378. Functions of the Posterior Grey Hoims and Posterior

Boots.

Afferent impulses are conducted to the spinal cord by the
Dstenor roots. As already remarked, it is probable that the
ferent impulses, which have undergone the highest organi-
ition in the cord, are conducted by the fibres which occupy the
sriphery of the fan, formed by the spreading out of the fibres
7 the posterior roots as they enter the substance of the cord,
i the anterior horns the most specialised actions are repre-
mted, partly by the development of new processes to the
dsting ganglion cells, and partly by the growth of additional
slls; but in the posterior horns the fibres, which conduct the
lost specialised impulses, have become adapted to their
inctions by the gradual development in connection with them
f special peripheral terminal organs on the one hand, and

78 ANATOMICAL AND PHYSIOLOGICAL INTRODUCTION.

central terminal organs on the other. The stimulation of
certain fibres in an early stage of development may give rise
only to diffused and irregular contractions, while at a higher
stage of development complicated and apparently purposive
reflex movements are produced by a similar stimulation; again,
a stimulation which at an early stage of development gives
rise only to a diffused sensation of pain, may at a higher stage
of development evoke intellectual sensations of touch and tem-
perature. It may, therefore, be expected that the fibres which
conduct reflex impulses, and those that conduct the impulses
which on reaching the cortex of the brain give rise to the
intellectual sensations, will occupy the periphery of the fan of
the posterior roots; while those which conduct the impulses
which on reaching the cortex give origin to the common or
emotional sensations will occupy its centre. We have already
seen reason for believing that the afferent fibres of the tendinous
reflexes pass through the internal radicular fasciculus to reach
the posterior horn, and it is probable that the afferent fibres of
the sense of touch and locality also pass through the same fasci-
culus. We have also supposed that the cutaneous reflex fibres
pass through the external radicular fasciculus, and it is probable
that the afferent fibres of the sense of temperature likewise pass
through this bundle. The afferent fibres of the common sensa-
tion of pain pass through the centre of the posterior roots
directly into the grey matter of the posterior horns.

Section of the white posterior column destroys the sensation
of touch permanently in the regions situated below the
section, but leaves the sensation of pain unaffected ; and, con-
versely, section of the entire grey substance, leaving the posterior
columns intact, destroys the sense of pain and leaves that of
touch (Schiff).

A retardation of the conduction of sensation occurs when the
posterior grey horns are cut, and the more the grey substance is
diminished the more marked is the retardation. The conduction
of sensory impressions decussates in the cord soon after the root
fibres enter it, but considerable difference of opimon exists as to
the mode and extent of this decussation with regard to the con-
ducting paths of the different kinds of sensation. The further
course of the afferent fibres through the cord is not well known.

ANATOMICAL AND PHYSIOLOGICAL INTRODUCTION. 79

It is supposed that the sensory paths of the lower extremities
lie at first in the lateral columns, and do not enter the posterior
columns till they reach a higher level. The posterior column
of the lumbar region is said to contain only the nerves of touch
for the pelvic region, sexual organs, perinseum, and anal region
(Erb).

§ 379. Functions of tlie Central Grey Column. — The central
grey column is not supposed to be endowed with any active func-
tions, yet, pathologically regarded, it is, as will hereafter
appear, one of the most important portions of the grey sub-
stance of the spinal cord. The continuation of this column in
the medulla oblongata contains, as we have seen, the accessory
nuclei ; and the median areas of the anterior horn in the cervical
and lumbar enlargements, as well as the medio-lateral areas
in the dorsal and upper cervical regions, may be regarded
respectively as anterior and lateral outgrowths of the central
column, instead of being regarded as portions of the anterior
horns. These areas, indeed, constitute the border-land between
the central column and anterior horn, and they are involved
in the diseases of both structures.

§ 380. Functions of the Special Nuclei of the Medulla
Oblongata, Pons, and Crura. — The functions of the special
nuclei do not require extended consideration at present. All
of them serve to transmit impulses received through the nerves
of special sense, not only to the cortex of the brain, but probably
also to the cortex of the cerebellum, while likewise ministering
to complex reflex actions. The corpora quadrigemina, for instance,
are anatomically connected, not only with the cerebrum, but
also with the superior peduncles of the cerebellum ; while they
have been proved, both anatomically and experimentally, to
form an important reflex centre between the retina and the
internal and external muscles of the eye. It is, indeed, likely
that still more extensive and complex reflex actions are regu-
lated by the corpora quadrigemina, since they are known to be
anatomically connected with the upward continuation of the
anterior root -zones of the spinal cord. Two of the four nuclei
of origin of the auditory nerve are intimately connected with

80 ANATOMICAL AND PHYSIOLOGICAL INTRODUCTION.

the inferior and middle peduncles of the cerebellum, and it is
probable that one of them at least conducts labyrinthine im-
pressions to the cerebellum.

The corpora quadrigemina are homologous with the optic lobes in fishes
and the lower vertebrata — organs which are developed in connection with
the sense of sight. These ganglia appear to be the centres for the reflex
co-ordination of all the muscular actions concerned in the movements of
the eyeballs and of the reflex contraction of the pupils caused by light
falling on the retinae. It is through these bodies, and not directly, that
the optic tracts come into relation with the cerebellum ; hence it may be
expected that they will be associated with the latter in its functions. We
have already seeu that the corpora quadrigemina are connected with the
anterior root-zones, or the system of fibres which co-ordinate the actions
of the cord longitudinally on the side of the outgoing currents ; hence the
inferior segments of the body are to a considerable extent brought under
the regulative influence of these ganglia. The corpora quadrigemina are,
however, simple co-ordinating centres, and their regulative action on the
inferior segments of the body is of a purely reflex character. The
following may be taken as an illustration of the manner in which I
believe them to act : — While a fish is swimming through the water
a sudden impression is made on the right eye by the shadow of a
large approaching object, and immediately the muscles of the tail on
the left side contract, and the head is turned away from the object.
Such a movement would tend to secure the safety of the fish from
capture by a more powerful antagonist. If, on the other hand, the
impression is made by a relatively small object, the muscles of the tail
on the same side might contract, so as to turn the head towards
the object — a movement which would tend to secure prey. In these
movements the main regulative centres are the optic lobes, and there is
no occasion to believe that the actions are in any way of a different
character from the ordinary reflex movements of the spinal cord. It may,
however, be remarked, in passing, that since a large approaching object
would produce a greater impression than a small object, a rudimentary
eye would be more useful to its possessor for avoiding capture than in
securing prey ; and, consequently, the primary and fundamental connection
between the eye and the inferior segments of the body would be a crossed
one. The most ready communication, therefore, would be between the
right eye and the muscles of the left side of the body. And this helps to
explain the crossing of the optic nerves, not only in the lower animals with
rudimentary eyes, but in the higher organisms ; since, during the develop-
ment of the latter from the former, the primary and fundamental crossing,
however much it may be modified, is still retained. It is, indeed, very
probable that the crossed connection which may be supposed to exist in
the lower vertebrata between the rudimentary eyes and the muscles of the

ANATOMICAL AND PHYSIOLOGICAL INTRODUCTION. 81

body was the main factor in determining daring the course of development
the crossed connection which exists between the cerebral hemispheres and
the spinal cord in the higher vertebrata.

§ 381. Functions of the Superadded Grey Substance of the
Medulla Oblongata, Pons, and Crura— We have already seen
that there are no grounds for believing that the centres of
respiration, deglutition, mastication, and the regulation of the
heart's action, the vaso-motor diabetic, and so-called con-
vulsive centre of Nothnagel, are represented by grey matter
in the medulla, apart from that which is the upward con-
tinuation of the grey substance of the spinal cord, and conse-
quently the masses of grey matter which are superadded in the
medulla, pons, and crura, must preside over other important
functions. Little, however, is known with respect to these. The
most reasonable supposition I can form is that all of them are
connected with the cerebellospinal system, and are, therefore,
engaged in regulating- the tonic muscular contractions rendered
necessary to maintain the various attitudes of the body.

§ 382. Functions of the White Substance. — According to the
fundamental law of development already mentioned, we may
expect that the parts of the cord which begin to develop at an
early period are engaged in the most general actions ; while
those which develop at a late period are engaged in the most
• special actions. The most general actions of the cord are those
which it performs as a group of simple co-ordinating centres;
and the most special are those which it performs in subordina-
tion to the compound and doubly compound co-ordinating
centres. We may, therefore, expect to find that the anterior
and posterior root-zones, which appear at a comparatively early
period in the development of the cord, belong to the spinal
system of simple co-ordinating centres, while the direct cere-
bellar fibres, the column of Goll, and the pyramidal tract, which
appear at a comparatively late period of development, bring the
simple co-ordinating centres of the cord under the control and
guidance of the compound and doubly compound co-ordinating
encephalic centres. So far as can be ascertained, this expectation
is realised.

82 ANATOMICAL AND PHYSIOLOGICAL INTRODUCTION.

§ 383. Functions of the Anterior and Posterior Root-zones.
These consist, as already stated, of looped fibres, which connect
ganglion cells at different elevations in the cord. The anterior
root-zone maintains a close relationship with the anterior grey
horns, and its fibres probably assist in co-ordinating efferent
impulses from above downwards. But although the anterior
root- zone belongs primarily to the spinal system, it is not im-
probable that it may have become at a subsequent stage of
development connected indirectly, if not directly, with some
of the cephalic centres. The close relationship of the olivary
body with the anterior root-zone in the medulla would seem
to imply that the latter may be the medium of conveying
efferent impulses from the cerebellum. The anterior root-zone
is also probably connected with the corpus striatum, and may
therefore be the channel through which the efferent impulses
from the latter are conveyed downwards to the cord. It is also
connected with the corpora quadrigemina, and may serve to
convey reflex impulses originating in the retina down the cord.
The posterior root-zone, on the other hand, maintains an equally
close relationship with the posterior grey horns, and its fibres
probably assist in co-ordinating afferent impulses from below
upwards. We have seen that, with the exception of the part
which belongs to the sensory roots of the fifth nerve and the
fasciculus rotundus, the posterior root-zone terminates in the
triangular nucleus, and that the latter is connected by arcuate
fibres with the olivary body, which in its turn is connected
with the opposite half of the cerebellum. This indirect con-
nection with the cerebellum would appear to indicate that
some at least of the fibres of the anterior root-zone belong to
the cerebellospinal system.

§ 384. Functions of the Direct Cerebellar Tract. — This tract
belongs to the cerebellospinal system, its fibres connecting the
vesicular column of Clarke and the cortex of the cerebellum
(Flechsig). Little is known with regard to the functions of
these fibres, except that they appear to convey afferent im-
pulses. This is presumed to be the case, because when the
fibres of the tract are injured in any part of their course, the
portions above the seat of injury undergo rapid degeneration.

ANATOMICAL AND PHYSIOLOGICAL INTRODUCTION. 83

§ 385. Functions of the Column of GolL — This column must
be regarded as a special structure from the comparatively late
period at which it is developed. Its fibres also undergo rapid
degeneration above the seat of injury; hence it may be inferred
that they convey afferent impulses, but nothing further is known
with regard to their functions.

§ 386. Functions of the Pyramidal Tract. — This tract is now
well known to be the means of communication between the
motor area of the brain and the anterior grey horns of the cord.

The fibres which pass into the lateral column connect the
anterior grey horn of one side with the cortex of the opposite
side ; while those which constitute the column of Tiirck connect
the anterior horns and cortex on the same side. When the
fibres of the tract-are injured in any part of their course the
portions below the seat of injury undergo rapid degeneration,
and this fact alone is sufficient to indicate that these fibres
convey efferent impulses. This tract is, indeed, the channel by
means of which voluntary impulses are conveyed from the cortex
of the brain to the spinal cord. The crossed and direct connec-
tion which this tract forms between the cortex of the brain and
the grey anterior horns, is rendered necessary by the fact that
every movement of one side of the body alters the centre of
gravity, and necessitates a new adjustment of the opposite side.
I obtained this idea in a conversation with Dr. Hughlings
Jackson, and he illustrated his meaning by showing that when
a man stands on the ball of the right foot, and stretches his
right arm upwards and forwards to reach an object, the body
being also inclined forwards, the left leg is instinctively thrust
backwards, and the left arm downwards and backwards, in order
to keep the centre of gravity as far back as possible and so to
prevent the line of gravity from passing in front of the ball of
the right foot. The muscular contractions of the right side of the
body may be supposed to be regulated in this action from the left
cortex of the brain through the fibres of the pyramidal tract of
the lateral column of the right side, while the movements of
the left arm and leg are also regulated from the left cortex, but
the impulses are conveyed to the same side of the cord and of
the body by the fibres of the column of Tiirck.

CHAPTER II.

MORBID ANATOMY AND CLASSIFICATION OF THE
DISEASES OF THE SPINAL CORD AND MEDULLA
OBLONGATA.

(I.)— MORBID ANATOMY OF THE SPINAL CORD AND
MEDULLA OBLONGATA.

In the preceding chapter we have traced the operation of the
law of evolution in the development of the spinal cord and
medulla oblongata ; we must now trace the operation of the
law of dissolution in the breaking down of the structure of
these organs by disease.

§ 387. Histological Changes. — The histological changes
which occur in the various elements of the structure of the cord
must first be briefly described.

1. Morbid Changes of the Ganglion Cells.

(a) Hypertrophy. — In acute inflammation of the cord the ganglion cells
become swollen, their contents cloudy and granular, the processes also
taking part in the changes {Fig. 144, 2). These cells often contain a
large amount of yellow pigment, a condition which has been described
by Dr. Allbutt as " yellow degeneration " {Fig. 144, 3).

(b) Shrinking.— In the acute diseases of the grey substance of the
cordj the ganglion cells, especially the small cells of the median areas,
become shrivelled, their fluid contents appear to have escaped, and the
cell wall to have shrunk around the nucleus and a small quantity of
yellow pigment {Fig. 144, 4). At a subsequent "period the cells lose their
processes and become converted into small angular masses, in which
even a nucleus cannot be detected.

(c) Multiplication of the Nucleus and Nucleolus. — The nucleus and
nucleolus may at times be observed either to have divided into two, or
to exhibit an hour-glass contraction indicating that the process of division
has commenced.

{d) Vacuolation. — Two or three large spherical air spaces, named

MORBID ANATOMY OF THE SPINAL CORD.

vacuoles, may sometimes be observed in ganglion cells wbich have under-
gone a granular degeneration (Fig. 144, 7).

(e) Colloid Degeneration. — The hypertrophied cells of the early stage
of inflammation may subsequently undergo colloid degeneration. Their
processes become transparent, glistening, brittle, and a large number of
them are broken off so that the cells assume a rounded form. The cell
wall has a glassy appearance, and assumes brilliant tints when stained by
various aniline dyes. The colloid appearances may probably be the result
of post-mortem changes, and consequently considerable caution must be
exercised in accepting them as evidences of disease.

(J) Pigmentary Degeneration. — The best examples of pigmentary de-
generation are seen in the chronic diseases of the cord. The cell wall

Fig. 144.

V u (Y?un&)- Ganglion Cells of the Anterior Grey Horns of the Spinal Cord. -
A, Healthy caudate cell ; 2, Hypertrophied cell ; 3, Yellow degeneration (the
yellow colour cannot be represented here) ; 4, Shrivelled cell ; 5, Chronic
atrophy, a group of cells from a case of pseudo-hypertrophic paralysis ; 6, Pig-
mentary atrophy ; 7, Vacuolation, from a case of canine chorea (Growers) •
at h"C atr°P fr°m * 03,86 0i progresaive muscular atrophy- -" yellow

MORBID ANATOMY OF THE

becomes contracted around a mass of dark granular" pigment, the nucleus
and nucleolus are indistinct or obliterated, the processes are atrophied,
and many of them have disappeared {Fig. 144, 6).

(g) Atrophy. — In chronic diseases the cell wall becomes dense and
contracted, the processes broken off, and the remnant of the cell converted
into a small angular mass, without recognisable nucleus or nucleolus, and
finally all traces of the cell may be lost {Fig. 144, 5 and 8).

(Ji) Calcareous degeneration of the ganglion cells of the cord is rarely
observed (Forster).

2. Morbid Changes of the Nerve Fibres.

The medullated nerve fibres of the spinal cord undergo alterations
more or less similar to those which have already been described in the
case of the fibres of the peripheral nerves, and consequently these changes
need not be described here in detail.

{a) Hypertrophy of the Axis Cylinder. — In myelitis it is not rare to
observe on transverse section that the axis cylinders of many of the fibres
have increased to two or three times their normal dimension. In longitu-
dinal sections it is seen that the swelling does not extend the whole length
of the axis cylinder ; the latter presents a varicose appearance, so that
its diameter is much diminished in size at some points.

(6) Atrophy of the nerve fibres, similar to that which occurs in the peri-
pheral nerves when the fibres are severed from their trophic centres, may
be observed in the medullated fibres of the spinal cord. This atrophy
begins by coagulation of the myeline, which becomes granular and broken
up into globular masses that are finally absorbed. The axis cylinder per-
sists for a long time after the medullary sheath has disappeared, but by-
and-by it also diminishes in size, and ultimately disappears.

3. Morbid Changes of the Neuroglia and Connective Tissue.

(a) Qluge's corpuscles consist of large globular cells filled with granular
contents. These cells may be observed in the spinal cord of the embryo,
but are never met with in considerable numbers in the cord of the adult,
except in cases of disease. They are supposed to derive their origin from
fatty degeneration of the cells of the connective tissue and neuroglia, the
white corpuscles of the blood, and the endothelial cells of the vessels and
of the capsules of the ganglion cells.

(b) Amyloid Corpuscles and Colloid Bodies. — Amyloid corpuscles (cor-
pora amylacea) are small, round, concentrically laminated bodies. Most of
them are turned blue, or bluish grey, when acted on by iodine alone, and
assume a beautiful bright blue tint on the addition of sulphuric acid.
Colloid bodies are irregular masses, consisting apparently of changed
myeline ; they assume beautiful tints on being stained with logwood, or
some of the aniline dyes. It is probable that these bodies may be the

SPINAL CORD AND MEDULLA OBLONGATA.

result of post-mortem decomposition, and neither they nor the amyloid
corpuscles afford trustworthy evidences of disease.

(d) Hypertrophy and Hyperplasia of the Connective Tissue. — The septa
of connective tissue become swollen, and the nuclei of the neuroglia
largely increased in number. It is also probable that leucocytes, which
have migrated from the vessels during inflammatory processes, may sub-
sequently become organised, and thus increase the normal volume of the
connective tissue of the cord.

(c) Sclerosis and Retraction.— When hyperplasia of the connective
tissues has once taken place, the newly-formed tissue may subsequently
undergo cicatricial contraction, and thus lead to the destruction of the
nervous elements. The process which leads to sclerosis often begins in
the nerve cells and fibres, and may be called parenchymatous sclerosis. At
other times the morbid changes appear to begin in the connective tissue
or neuroglia, the nerve cells and fibres being secondarily invaded ; this
form may be called interstitial sclerosis.

4. Morbid Alterations of the Vessels.

(a) Intravascular Changes. — The vessels are at times greatly distended
with blood, but this is not a trustworthy evidence of disease, inasmuch as
the distension may have occurred from the mode of dying, or from hypo-
static congestion after death. The capillary arteries may at times be
distended with emboli.

(b) Changes in. the walls of the spinal vessels are observed in chronic
Bright's disease, identical with those which occur in the vessels of the.
body generally in that disease.

(c) Perivascular Changes.— The most important perivascular changes
Dbserved in disease of the spinal cord are caused by migration of the white
corpuscles of the blood into the perivascular lymph-spaces and surround -
.ng tissues. The number of leucocytes surrounding a vessel may some-
simes be so great as to constitute what has been called a miliary abscess
Tlate V., Fig. 2). Rupture of a vessel may occur, giving rise to
haemorrhage into the tissues. Red blood corpuscles are at times localised
in a perivascular space, but it is difficult to determine in these cases
whether the red corpuscles have escaped by rupture, or have, like the white
corpuscles, migrated through the wall of the vessel.

§ 388. Let us now pass from the details of the morbid changes
)f the cord to the general principles which underlie them. In
accordance with the law of dissolution (§ 35) we may expect
that the accessory portions of the cord will form parts of least
resistance to the inroads of disease.

In the grey substance the least resistance to disease will be

MORBID ANATOMY OF THE

offered by the central column, which is, as we have already
seen, the embryonic area of the cord, and by the median area
of the anterior grey horn in the lumbar and cervical enlarge-
ments and the medio-lateral area in the dorsal and upper
cervical regions — areas which, as already remarked, may be
regarded as outgrowths of the central column. These areas
contain the accessory nuclei of the spinal cord, and since these
ganglion cells not only are developed at a comparatively late
period, but also frequently maintain a relatively small size in
the adult, the resistance offered to the invasion of disease
becomes still less. This law must necessarily be true whether
the disease begin in the ganglion cells themselves, in the
neuroglia, or in the vessels, or whether it be caused by a poison
circulating in the blood, provided that the poison possess no
special affinity for any one set of the ganglion cells more than
for others.

The cell walls of the small and recently-developed cells are
much thinner than those of the larger and earlier-developed
cells, hence the exchange of materials, which is the necessary
accompaniment of nutrition, takes place more readily in the
former than in the latter. But this is not all. A large cell
presents, in proportion to its bulk, a smaller surface to its
environment for the absorption of nourishment than a small
cell, and consequently the relative amount of nourishment
absorbed by the large will be less than that absorbed by the
small cell (§ 9). But high nutritive activity is associated with
great instability, which declares itself in increased readiness to
give out energy or to multiply, the latter process, of course,
involving the disorganisation of a highly-organised tissue.

When, therefore, the ganglion cells of the anterior horns
become diseased, it may be expected that the later-developed
and small cells will be the first to suffer, and when a poison
like strychnine circulates in the blood, the same cells will also
be the first to be affected, supposing the drug not to possess a
special affinity for one ganglion cell more than for another.
The reason of this is, that the quantity of the poison which
will enter the substance of the small cell will be much larger
in proportion to its bulk than that which will enter into the
substance of the large cell. If the disease begin in the neu-

SPINAL CORD AND MEDULLA OBLONGATA.

roglia, it may be expected that the spongy and loose neuroglia
of the later-developed portions of the grey substance will resist
its inroads less effectually than the dense neuroglia surrounding
the earlier-developed groups of ganglion cells. The central
grey column possesses a loose and spongy neuroglia, and we
have seen that it may be regarded as the embryonic area of
the spinal cord, so that it may be expected to offer little
resistance to the invasion of disease. We shall hereafter see
that some of the most rapidly fatal diseases of the cord appear
to ascend in the central grey column. It has been pointed out
that the later-formed cells of the anterior horns grow close to
the arteries, while the earlier-developed cells are pushed, in the
course of development, away from them. When, therefore,
rapid exudation takes place from the vessels, whether it consist
of a fluid and granular exudation
or of migration of white blood Fig. 145.

corpuscles, the cells in the neigh-
bourhood of these vessels will
suffer sooner and in greater de-
gree than those more remote.

That the lines of least resis-
tance to disease in the lumbar
region are in the direction of the
vessels is well illustrated by Fig.
145, which is taken from a section
of the middle of the lumbar en-
largement in a case of infantile
paralysis, under the care of Dr.
Humphreys, at the Pendlebury
Hospital for Sick Children. This
case is described in the " Transac-
tions of the Pathological Society
of London" for 1879, and will
be subsequently mentioned. My
present object is to show that
even in an acute disease like
infantile paralysis the cells near
the vessels have become de-
stroyed in preference to the

Fig. 145 (Young). Section of the Lum-
bar Region of the Spinal Cord from
a case of infantile spinal paralysis,
pi, postero- lateral group; ai,
antero-lateral group ; c, central
group. The internal and anterior
groups have disappeared, and the
marginal cells of the remaining
groups are also destroyed.

MORBID ANATOMY OF TUE

others. If Fig. 145 be compared with Fig. Ill, it will be seen
at once that the disease is most marked in the vascular
areas of the cord, and that the cells which have been
last developed are, on the whole, those which have suffered
most will be apparent by referring to the previous description
and illustrations of the development of the cord. It is true
that the earlier-developed cells of the internal and anterior
groups have disappeared; but the cells of the anterolateral,
and those of the central portions of the postero-lateral and of
the central group are well preserved ; while the marginal cells
of the two latter groups and all the cells of the median area
are completely destroyed. It is not likely that this law will
always be observed in a disease having such an acute and
sudden onset as infantile paralysis ; but an examination of the
diagrams given by Clarke, Charcot, and Joffroy, shows so many
indications of the fulfilment of this law that its occurrence
cannot be regarded as accidental. The same law is observed,
at least very frequently, in cases of acute and subacute ascend-
ing central myelitis, as well as in tetanus and hydrophobia. It
was while examining cases of this kind that my attention was
first directed to this subject. In all the acute diseases affecting
the grey substance of. the spinal cord I observed that, unless
the destruction was so great as to involve the anterior horns
in their entire extent, the small cells and those in the line of
the distribution of the arteries manifested evidences of disease
to a much greater extent than the large cells and those removed
from the vessels.

The distribution of the disease in the cervical enlargement
is similar to that in the lumbar region, except that the median
area being much larger in the former than in the latter, injury
to this area forms a more conspicuous feature of disease in the
former than the latter. When the dorsal region of the cord
is affected by acute disease of the grey substance, the most
marked morbid changes are observed in the postero-lateral
or rather the medio-lateral group; and the same is the case in
the upper cervical region. A section of the middle of the cer-
vical enlargement is represented in Fig. 146, taken from a case
of subacute ascending spinal paralysis. The disease began after
exposure to severe cold with sudden paralysis of the lower

SPINAL CORD AND MEDULLA OBLONGATA.

extremities, without much disturbance of sensibility. This was
followed by rapid wasting of the muscles, and loss of faradic
contractility. The paralysis in the course of a few weeks
gradually invaded the muscles of the trunk, the muscles of the
upper extremity, and ultimately the muscles of respiration.
Death took place five weeks from the commencement of the
paralysis. In the lumbar region the white as well as the grey
substance was implicated, and there was ascending sclerosis of
both the columns of Goll and of the direct cerebellar tracts
throughout the entire length of the cord ; the remaining por-
tions of the white substance were healthy in the dorsal and
cervical regions. The central grey column was diseased
throughout the whole length of the cord, the cells of the
postero -lateral group and medio -lateral area having entirely
disappeared in the dorsal region, and again in the upper
cervical regions; while the anterior groups of cells appeared

Fro 1-16 (Young\ Section of the Middle of the Cervical Enlargement of the Spinal
inT •fl'on\a case °f central myelitis.— i, The internal group j the remaining letters
Unm i t t,he,8an?e aa the corresponding ones in Fig. 145. The median area was
completely destitute of cells, and a large number of the marginal cells of the
uuierent groups of the anterior horn were destroyed or diseased.

MORBID ANATOMY OF THE

to be quite normal. In the cervical enlargement (Fig. 146)
the cells of the median area had entirely disappeared, and the
marginal cells of the central and postero-lateral groups were
notably altered, while the fundamental cells of the groups
presented beautiful long processes, and appeared in every
respect normal.

§ 389. In the white substance the last developed fibres will
also, other things being equal, offer less resistance to the inroads
of disease than the earlier-developed fibres. In proceeding to
verify this statement, we must compare the later with the earlier-
formed fibres of the same segment, or, in other words, the same
functional system of the white substance, otherwise the whole
result will be vitiated. The posterior and anterior root-zones,
for instance, are developed about the same time, yet the
former is more liable to become diseased than the latter.
The posterior is probably more exposed to the exciting causes
of disease, such as peripheral injuries and ascending neuritis,
than the anterior root-zone, and the small fibres of the former
are more apt to be injured in inflammatory affections of the
cord than the larger fibres of the latter. But if the accessory
be compared with the fundamental fibres of the pyramidal
tract, it will be seen that the former are much more exposed to
injurious influences than the latter. The small diameter of
the greater number of the accessory fibres permits a relatively
larger amount of nourishment to gain access to their interior
than can take place in fibres of larger diameber ; hence both
reparative and destructive changes are more rapidly effected in
the former than in the latter.

The accessory fibres are, as we have seen, more closely related
to the connective tissue septa of the cord than the fundamental
fibres, hence the former are more liable to be injured in the
course of the diseases which begin in the connective tissue and
neuroglia than the latter. An appearance which is presented by
the spinal cord in various diseases, and which for a long time
puzzled me very much, is that which has been described as miliary
sclerosis (Rutherford, Kesteven). This condition appears to
consist of a swelling or thickening of the septa in which the
blood-vessels run. In the lozenge-shaped spaces (Fig. 133) of

SPINAL CORD AND MEDULLA OBLONGATA.

uhe pyramidal tract a considerable number of the small
□bres which lie close to the vessels are destroyed, while the
larger central fibres remain more or less healthy. When a
transverse section of the cord is examined under these circum-
stances the part presents a spotted appearance, but instead of
the miliary spots being in a state of sclerosis, they really are
the most healthy portions of the section. The proximity of
the fibres of the accessory system to the blood-vessels renders
them also more liable than the fundamental fibres to be injured
by inflammatory and other effusions.

§ 390. Secondary Degenerations.

The medullated fibres of the spinal cord undergo degene-
ration -whenever their continuity is interrupted. The short
ooped fibres of the anterior and posterior root-zones, however,
>nly degenerate in the neighbourhood of the lesion, probably
)ecause they soon terminate in grey matter. But the fibres
vhich pass from one end of the cord to another are sometimes
bund degenerated throughout their whole length. As a rule,
,iowever, a focal lesion interrupts the continuity of the long
fibres in some part of their course, and the fibres either above
ir below the seat of disease undergo degeneration. Some
)athologists think that an irritative change spreads from the
>rimary lesion as a centre along these fibres, but the most
easonable supposition is that the degeneration is analogous to
vhat occurs in the fibres of peripheral nerves after they have
Deen severed from their trophic centres. The trophic centres
>f the fibres of the columns of Goll and of the direct cere-
)ellar tract are situated at their inferior extremities — the
iosterior horn containing the trophic centres of the former,
ind the vesicular column of Clarke possibly that of the
atter. When, therefore, the continuity of these fibres is inter-
'upted at any point, the portions above the seat of the lesion
mdergo degeneration, consequently degeneration of these fibres
s called ascending sclerosis. But the trophic centres of the
ibres of the pyramidal tract are situated at their superior
jxtremities, these centres being probably formed by the large
janglion cells of the fourth layer of the cortex of the brain.
When the continuity of these fibres is interrupted at any

9fc

MORBID ANATOMY OF THE

point of their course, the portions below the seat of the lesion
undergo degeneration, consequently this form is called descend-
ing sclerosis. The time occupied by the degeneration appears
to be from four to eight weeks. Schiefferdecker found in
experiments on dogs that it began at the end of fourteen days,
was well marked at the end of four to five weeks, but changes
in the connective tissue were not observed until the eighth
week. Degeneration of the fibres of the spinal cord appears
always to take place in the line of their conduction. When a
transverse section of the spinal cord is examined by the naked
eye the degenerated portion usually presents a grey or greyish
discolouration, but in recent cases the cord presents no abnormal
appearances until it is hardened in chromic acid or bichromate
of ammonia. In cases of long standing the degenerated
columns may be atrophied to such an extent that the syni-
metry of the cord becomes altered.

Microscopic examination shows that in the earlier stages the
nerve fibres are exclusively affected. The medullary sheaths
undergo fatty degeneration and ultimately disappear, while
there is a considerable development of granule cells ; the axis-
cylinders, however, persist for some time afterwards.

In the later stages of degeneration the nerve fibres disappear
entirely, the neuroglia is increased in quantity, and changes
into a dense finely fibrillated tissue, which contains numerous
nuclei and spindle cells.

1. History. — Secondary atrophy, extending to the pons and pyramids
of the medulla, was observed in disease of the brain by Cruveilhier and
Rokitansky, but they did not follow it to the spinal cord. Tiirck made a
thorough examination of the secondary degenerations of the spinal cord
in 1851 and 1853, and their histological characters were investigated in
1863 by Leyden. Various French authors, as Charcot, Cornil, and others,
published cases in which these degenerations were observed, but the most
exhaustive work on the pathology of the affection was published by
Bouchard in 1866. Soon afterwards Westphal showed that secondary
degenerations could be produced experimentally in dogs, and this was
afterwards confirmed by Vulpian.

2. Distribution of the Degeneration. — The observations of Charcot and
Pierret, and subsequently of Flechsig, tend to show that these secondary
degenerations of the spinal cord are determined by the order of its deve-
lopment. The development of the fuuctioual systems of the white sub-

SPINAL CORD AND MEDULLA OBLONGATA.

.'stance of the cord affords a good illustration of the law of evolution,
while the secondary degenerations afford an almost equally good illustra-
tion of the law of dissolution. The distribution of these degenerations,
therefore, may be readily understood by reference to Figs. 134 to 140,
which illustrate the development of the cord.

(a) Ascending degeneration takes place above the seat of the lesion in
the columns of Goll, aud terminates in the upper end of the medulla
oblongata, where the fibres end in the cuneate nucleus. The direct
cerebellar fibres also undergo ascending degeneration. It may begin as a
thin lamella of degenerated tissue on the external surface of the lateral
column in the lower dorsal region, the area of the degeneration gradually
increasing in size upwards along the cord and the external surface of the
restiform bodies. In lesions of the cauda equina, and sometimes after
severe traumatic injuries of the sciatic nerve, the posterior root-zones, as
well as the columns of Goll, undergo ascending degeneration in the lumbar
\nd greater portion of the dorsal regions, but the degeneration becomes
itnited to the columns of Goll in the upper dorsal and cervical regions.

Fig. 147.

Fig. 148.

Fig. 149.

SPlGS. 147, 148, and 149. Transverse Sections of the Spinal Cord, from the middle of
the cervical enlargement, middle of the dorsal region, and middle of the lumbar
region respectively, showing ascending degeneration of the column of Goll (g),
and of the direct cerebellar tract (dc).

(b) Descending degeneration occurs in all destructive lesions of the brain
>r spinal cord which injure the fibres of the pyramidal tract in their
>assage through the corona radiata, internal capsule, crus cerebri, pons,

Fig. 151.

A A

igs. loO, ^lol, and 152 (After Charcot). Transverse Sections of the Spinal cord, from
tne middle of the cervical enlargement, middle of the dorsal region, and middle of
We lumbar region respectively, showing primary lateral sclerosis of the cord or
secondary to a lesion high up in the cord or medulla oblongata —A A A Dp.
generated pyramidal tracts. , , a, ue

MORBID ANATOMY OF THE

Fig. 153.

medulla, or cord. In the diseases of the cord, the degeneration is generally
bilateral and symmetrical, and the position occupied by the diseased por-
tions of the cord in the lateral columns is represented in Figs. 150, 151,

and 152 ; the degeneration of the
columns of Tiirck is, however, not
shown. The position occupied by the
diseased portion in the medulla ob-
longata is represented in the annexed
woodcut {Fig. 153, A). In cerebral
lesions the degenerative tract is gene-
rally limited to one side — the side of the
cord opposite the lesion in the brain —
as represented in Figs. 154 to 156.
The columns of Tiirck on the same
side as the lesion of the brain are also
usually simultaneously degenerated,
but this is not represented in the
figure.

Fig. 153 (After Charcot). Transverse
section of the medulla oblongata,
on a level with the middle of the
olivary body. — A, A, Sclerosis of
the anterior pyramids.

Fig. 154.

Fig. 155.

Figs. 154, 155, and 156 (After Charcot]. Transverse Sections of the Spinal Cord, from
the middle of the cervical enlargement, middle of the dorsal region, and middle o_
the lumbar region respectively, showing descending sclerosis of the pyramidal
tract in the lateral column secondary to a cerebral lesion. — A, A, A, De-
generated pyramidal tract.

3. Degeneration of the Spinal Cord Secondary to Amputation. — 1
changes which occur in the spinal cord after amputation have been studie
by Be"rard, Cruveilhier, Tiirck, Dickinson, Lockhart Clarke, Vulpian, and
others; and, in a recent number of the Journal of Anatomy and Physio
logy, Dr. Dreschfeld has given a good resume' of the previous observations
of others, while adding new observations of his own. The general result
appears to be that the peripheric nerves and the white substance of the
cord are unaffected, the posterior roots are often slightly diminished in
size, and changes in the ganglion cells of the anterior horns are of constant
occurrence. Some of the ganglion cells of the anterior horns have com-
pletely disappeared, whilst those that remain are atrophied and shorn of
their processes. Judging from the various drawings, the ganglion cells of
the margins of the various groups disappear first, and those of their centres
remain to the last. The cells of the postero-lateral group are particularly
liable to be affected. No mention is made of the disappearance of any of
the ganglion cells from the anterior horn on the side opposite to that of

SPINAL CORD AND MEDULLA OBLONGATA.

the amputated limb ; but judging from the diagrams which illustrate Dr.
Dreschfeld's paper, I should think that the number of cells in the internal
group of the opposite side is much diminished. The fibres of the external
fasciculus of the posterior root pass through the anterior commissure to
join the cells of the internal group, and in future cases it would be worth
while to observe whether a streak of degeneration might not be detected
along the course of these fibres to reach the internal group of the opposite
side. Hayeni tore out the sciatic nerve of one side in rabbits, and found
in the lumbar region of the cord on the same side sclerosis of the posterior
root and posterior grey matter, along with degenerative atrophy of the
ganglion cells of the intermedio-lateral tract.

§ 391. Deformities and Malformations of the Spinal Cord.
The deformities and malformations of the spinal cord may
be subdivided into — (1) the congenital deformities which are
incompatible with the maintenance of extra-uterine life ; (2)
the congeDital deformities which are compatible with life,
tud do not betray themselves by any symptom during life ; (3)
the congenital deformities which may be recognised during life ;
{4) acquired deformities resulting from pathological processes
Syringomyelia, Hydromyelus acquisitus) (Leyden).

The following are the more frequent conditions observed
(Leyden} : —

1 . Congenital Deformities of Still-bom Children.

(a) Amyelia, or absence of the spinal cord. It is only met with when
;he brain is also absent.

(6) Atelomyelia, or imperfect development of the spinal cord. The
lpper end of the cord is lacking or imperfectly developed, the brain being
tlso absent (anencephalia ), or the head defective (acephalia ). The me-
iulla oblongata is absent or exists only in a rudimentary form.

(c) Diastematomyelia is a condition in which the two lateral halves of
;he cord either do not unite, or unite only throughout a portion of their
jxtent. This malformation occurs with anencephalia.

(d) Diplomyelia, or duplication of the spinal cord, appears in the various
brms of double monsters.

2. Congenital Deformities which cannot be recognised during Life.
(a) Anomalies in the Length and Thickness of the Cord. — The cord is
round at times thick and voluminous, and at other times thin and small.
Lt descends at times to the third lumbar vertebra, and ends at other times
>pposite the eleventh or twelfth dorsal.

(6) Abnormal smallness of the entire spinal cord and medulla oblon-
gata, with corresponding smallness of the nerve fibres and axis cylinders,
H

98 MORBID ANATOMY OF THE

has recently been described by F. Schultze, in one of Friedreich's cases of
" hereditary ataxy."

(d) Abnormalities of the Pyramidal Tracts. — Flechsig has recently
shown that the fibres of the pyramidal tracts are very variable in their
distribution. Each pyramid may send its mass of fibres into the spinal
cord, either entirely crossed or only partly crossed, or down the anterior
columns almost entirely uncrossed. These tracts are absent in anence-
phalbus monsters (Flechsig).

In cases of congenital absence or intra-uterine arrest of development
of certain extremities atrophy of definite portions of the spinal cord may
be observed producing asymmetry, which is limited to the cervical or
lumbar enlargement according to the extremity affected.

In a case of congenital talipes equino-varus of both legs, I found the
conus medullaris remarkably thin and tapering. On transverse section
the anterior grey horns were seen to be deformed, the internal border
which in health runs parallel with the anterior fissure being drawn out-
wards and backwards, so as to be almost in a line with the anterior border of

Fig. 157.

Fig. 157. Transverse Section of the upper end of the Conus Medullaris of the Spinj
Cord, from a case of congenital talipes equino-varus.— A, P, Anterior and postenn
horns respectively ; i, internal group showing healthy cells ; a, anterior, <j
anterolateral, pi, postero-lateral, and c, central groups of cells, each bem
represented only by a few small round cells without processes.

SPINAL CORD AND MEDULLA OBLONGATA. 99

:he anterior commissure. The ganglion cells of the internal group were well
ieveloped, although it was displaced from its usual position {Fig. 157., i).
A. few cells were observed in the postero-lateral area; but the cells
)f the anterior, central, and antero-lateral groups were entirely absent
n many sections, while in others a few imperfectly-developed cells were
observed in these areas {Fig. 157, a, c, al). The fine fibrillated texture of
3erlach's network and the small glistening nuclei of the neuroglia appeared
to have been replaced by a loose connective tissue, thickly studded with
connective tissue corpuscles. Mr. Hardie long ago maintained that con-
genital talipes is due to an arrest of development, and that the feet occupy
oostures similar to those of the embryo.

Unusual outgrowths or absence of portions of the grey matter, such as
}f the tractus mtermedio-lateralis, are occasionally met with. Duplica-
sions of one of the grey horns for a longer or shorter distance have also
been observed.

3. Congenital Deformities which may be recognised during Life.

{a) Congenital Enlargement of the Central Canal, a condition which has
)een variously called hydrorrhachis interna, hydromyelus, or hydromyelus
. 'ongenitus. In the lighter grades of the congenital affections the central
:anal in the foetus is converted into a cavity varying in width from that
>f an ordinary knitting needle to that of a crow's quilL The canal may
xtend the entire length of the cord, but is at other times restricted to
Lertain portions, generally the cervical or lumbar enlargement, while the
ililatation may occasionally be moniliform, or the anterior and posterior
Ivalls may have grown together across the middle giving rise to the
i.ppearance of a double canaL The cord does not appear to undergo any
bnormal changes apart from the displacement of its various segments
occasioned by the great dilatation of the canal.

In the higher grade of congenital hydromyelus either the spinal cord
isappears entirely, or becomes split into two halves for a greater or lesser
•istance, while the cavity of the central canal freely communicates with
he cavity of the spinal arachnoid ; the hydrorrachis interna is then merged
ato hydrorrachis externa, as not unfrequently happens in spina bifida.

(b) Spina bifida consists of an abnormal accumulation of fluid within
lie cavity of the spinal arachnoid, associated with a greater or lesser
eformity of the vertebral column. As it gives rise to serious symptoms
uring life it will be subsequently described in detail along with the
iseases of the membranes of the spinal cord.

4. Acquired Deformities resulting from Pathological Processes.

{a) Syringomyelia, or the pathological formation of cavities, may be
nused in various ways.

(i.) Cavities are formed by the softening of the central portions of new
)rmations, such as gliomata, gliomyxomata, and gliosarcomata. The
imour is sometimes so completely disintegrated that only a capsule of
hnnective tissue or mere traces of the tumour remain. This softening

100

MORBID ANATOMY OF THE

is sometimes initiated by hemorrhage into the interior of the tumour.
This accident is particularly apt to occur in the telangiectatic varieties.

(ii ) Breaking down and softening of apoplectic foci.

(iii.) Central softening in areas of grey degeneration and chronic j

^(^Obstruction of lymph channels produced by the pressure of a
tumour and other causes (Westphal). Cavities have been formed in the
spinal cords of animals subsequent to various injuries, and these have
been supposed to have been caused by obstruction of lymph channels
(Naunyn and Eichhorst).

(b) Hydromyelus aoquisitus, or acquired dilatation of the central canal,

may result from the following causes :—

(i ) Peri-ependymal myelitis, which consists of a proliferation of the
connective tissue surrounding the central canal, may cause secondary
dilatation by the shrinking of the newly-formed tissue (Hallopeau).

(ii) Chronic msningitis, by producing adhesions of the pia mater to ,
the dura mater at definite points, may also cause dilatation of the central I
canal, probably by shrinking of the newly-formed tissue (Simon).

(iii.) Obliteration of the canal a£ one point may lead to dilatation ot the
neighbouring portions.

The cavities vary greatly in size. They may indeed be only a few
millimetres in length, or extend the entire length of the cord. Their j
number also varies ; in many cases one only is found, but at other times
a large number of them may be present. They are almost always
situated near the centre of the cord, and their relations to the central
canal can only be determined by careful examination. The transverse
diameter of these cavities may vary from that of a needle to the tip
of a man's little finger. On transverse section their form is roundish
oval, or angular, and their contents consist of light and clear or turbid and

yellowish fluid. . [

The walls of the cavities may be smooth and firm, and are often
lined with a layer of cylindrical epithelium, or they may be rough, ragged, .
and uneven. Their walls may also be dense, and formed of cirrhotic tissue
' or of tissue which has undergone grey degeneration, or of the various new l
formations which have already been described.

The symptoms caused by the formation of cavities in the cord depend
entirely upon their situation, and no definite disease which can bee
recognised during life can be ascribed to the presence of these cavities.

(II ^CLASSIFICATION OF THE DISEASES OF THE SPINAL
CORD AND MEDULLA OBLONGATA.

§ 392. The rule which has hitherto been followed in this work,
is to describe first the simplest and most elementary diseases-
and to reserve consideration of the most complicated affection

SPINAL CORD AND MEDULLA OBLONGATA. 101

0 the last. In no diseases is it more advisable to follow this
ule than in those affecting the spinal cord and medulla oblon-
gata, with their membranes. The annexed table, in which
hese diseases are classified, carries with it in the main its own
ixplanation, but it may not be out of place to make a few
•emarks with regard to the principle adopted in arranging the
tructural diseases of the nervous organs themselves as dis-
inguished from those of their membranes and vessels, their
'unctional affections, injuries, malformations, and neoplasms.

It has already been remarked that the spinal cord may be
livided into longitudinal segments, each of which possesses

1 functional unity, and may be separately diseased. Diseases
)f one of the functional segments of the cord are called
•ystem-diseases or fasciculated diseases, while those involving
everal of these segments may be called mixed diseases. In
he simple system-diseases one functional segment of the cord
.nd medulla oblongata alone is affected ; but it sometimes
lappens that two or more of them become simultaneously or
onsecutively attacked, and these affections may be called com-
pound system-diseases.

The system-diseases may be divided into those affecting the
jrey matter or the poliomyelopathies, and those affecting the
vhite matter or the leucomyelopathies. The poliomyelopathies
nay be subdivided into the diseases affecting the anterior grey
lorns, the central grey column, and the posterior grey horns;
>ut the latter is never a true system-disease, being always com-
)licated by lesions of other structures, such as the posterior
oots and posterior columns. Disease of the central column is
--lso probably never observed as an isolated affection, the promi-
ient symptoms being caused by extension of the lesion into the
-nterior horns; but we shall nevertheless classify some at least of
he diseases of the central column amongst the system-diseases.

The leucomyelopathies consist theoretically of diseases of the
)osterior root-zone (locomotor ataxy) ; of the anterior root-zone,
iisease of which is probably not capable of being separated
rom disease of the anterior roots and anterior grey horns ; of
he column of Goll and the direct cerebellar tract, to both of
vhich, however, no definite symptoms have been observed to
attach, and of the pyramidal tract (primary lateral sclerosis).

102

MORBID ANATOMY OF THE

The compound system-diseases are probably numerous, but
only one of them — amyotrophic lateral sclerosis — is recognised
as a distinct type of disease. The annexed diagram (Fig. 158),
copied from Charcot, represents the localisation of the lesion on
transverse section of the cord in the various system-diseases.

In the mixed diseases of the spinal cord and medulla oblon-
gata Landry's paralysis is first mentioned, not because it has
been proved to be connected with anatomical changes in the
cord, but because it is closely allied clinically with the acute
forms of central myelitis. The classification adopted of the
different forms of acute and chronic myelitis does not require
any explanation.

Fig. 158.

Pig. 158 (After Charcot). Diagram of the Morbid Anatomy of the System-Diseases •
of the Sjrinal Cord. —A, A, Pyramidal tract of the lateral column ; A', Columns •
of Tiirck ; B, B, Posterior root-zones ; C, C. Posterior grey horns ; D, D.
Anterior horn ; P, P, Anterior root-zone ; E, Columns of Goll.

A. Diseases of the Spinal Cord and Medulla Oblongata.

I. System diseases.

(i.) Poliomyelopathies.

1. Poliomyelitis anterior acuta.

(a) Infantile spinal paralysis.

(b) Atrophic spinal paralysis of adults.

SPINAL CORD AND MEDULLA OBLONGATA.

103

2. Poliomyelitis anterior chronica.

3. Progressive muscular atrophy.

4. Labio-glosso-laryngeal paralysis.

5. Pseudo-hypertrophic paralysis.

(n.) Leucomyelopathies.

1. Posterior sclerosis (Locomotor ataxy).

2. Sclerosis of the columns of Goll.

(a) Primary.

(b) Secondary and Ascending.

3. Sclerosis of the direct cerebellar tract. Secondary and

Ascending sclerosis.

4. Lateral sclerosis.

(a) Primary — Tabes dorsalis spasmodica.

(b) Compound — (i.) Amyotrophic lateral sclerosis.

(ii.) Combined posterior and lateral
sclerosis.

II. Mixed diseases of the spinal cord and medulla oblongata.

(i.) Paralysis ascendens acuta (Landry's paralysis),
(ii.) Acute myelitis.

1. Acute central myelitis.

2. Hyperacute central myelitis (hoematomyelitis).

3. Acute bulbar myelitis.

4. Acute transverse myelitis.

5. Acute hemilateral myelitis.

6. Acute myelomeningitis.

7. Acute disseminated myelitis.

(ill.) Chronic myelitis.

1. Chronic central myelitis.

2. Chronic transverse myelitis.

3. Universal progressive myelitis.

4. Chronic bulbar myelitis.

5. Chronic myelomeningitis.

6. Chronic disseminated myelitis or multiple sclerosis,
(iv.) Myelomalacia.

III. Vascular diseases of the spinal cord and medulla
)blongata.

(i.) Ansemia, Thrombosis, and Embolism,
(ii.) Hyperemia and Haemorrhage.

104 MOEBID ANATOMY OF THE SPINAL CORD.

IV. Functional and secondary diseases of the spinal cord
and medulla oblongata.

(i.) Spinal irritation,

(il.) Neurasthenia spinalis,

(in.) Reflex and secondary paraplegiae.

(IV.) Saltatory spasms,

(v.) Reflex muscular spasms,

(vi.) Intermittent spinal paralysis,

(vn.) Toxic spinal paralysis,

(vin.) Hysterical paraplegia.

V. Traumatic diseases, tumours, and abnormalities of the
spinal cord and medulla oblongata.

(i.) Wounds of the cord and of the medulla oblongata,
(n.) Slow compression of the cord and of the medulla

oblongata,
(in.) Hemiparaplegia spinalis,
(iv.) Concussion.

(v.) Tumours, and abnormalities of the spinal cord and
medulla oblongata.

B. Diseases of the Membranes of the Spinal Cord and

Medulla Oblongata.

I. Vascular diseases.

(i.) Hypersemia of the membranes,
(il.) Meningeal haemorrhage.

II. Inflammation of the spinal dura mater.

(i.J External pachymeningitis.
(11.) Internal pachymeningitis.

III. Inflammation of the spinal pia mater and arachnoid,
(i.) Acute spinal leptomeningitis.

(il.) Chronic spinal leptomeningitis.

IV. Tumours and abnormalities of the membranes.

105

CHAPTER III.

L— SYSTEM DISEASES OF THE SPINAL CORD AND
MEDULLA OBLONGATA.

(I.) POLIO MYELOPATHIES.

1. Poliomyelitis Anterior Acuta (Kussmaul).

Icute Inflammation of the Grey Anterior Horns. — Acute Atrophic Spinal Paralysis.

§ 393. Definition. — Acute atrophic spinal paralysis begins
uddenly with fever, general convulsions, or other cerebral
ymptoms, and paralysis which reaches its maximum intensity
,t once. The paralysis is variable in its distribution, the
iffected muscles are flaccid, reflex action is diminished or
ibolished, some of the muscles implicated undergo rapid
itrophy, and there is entire absence of sensory disturbances
md of disorders of the functions of the bladder and rectum.

§ 394. History. —This disease was first described by Underwood in
.784, but he did not separate it distinctly from other forms of paralysis to
vhich children are liable. The affection, indeed, does not appear to have
ittracted much notice until Heine, in 1840, directed particular attention
•o it. A good description of it was given by Barthez and Rilliet, in
851 ; but it was much more thoroughly investigated about the same
ime by Duchenne, who named it parali/sie atrophique graisseuse de
renfance. In 1864, two monographs appeared — the thesis of Duchenne
he younger, and that of Laborde — both of which are very important on
iccount of the wealth of clinical facts contained in them. Dr. Muller
las recently collected and analysed all the published cases of atrophic
ipinal paralysis in the adult from the time of Duchenne to the present day.

§ 395. Etiology.— The most remarkable feature with respect
'O the etiology of this paralysis is the strong predisposition to
;he affection manifested by the age of childhood. In thirty-two
)ut of forty-four cases observed by Dr. West, the disease came

106

SYSTEM DISEASES OF THE

on between the age of six months and three years ; while, if we
analyse the cases collected by Heine, Duchenne the younger,
and those observed by Barlow, more than three-fourths (154 out
of 205) of all the cases occurred between the age of six months
and two years. But Duchenne reports a case in a child twelve
days old, and another in a child a month old, while essentially
the same disease occurs in the adult.

Sex does not appear to exercise any influence in its pro-
duction, nor has any direct or indirect hereditary tendency to the
affection been traced. Heine, indeed, asserts that the disease
attacks by preference the healthiest and most robust children.

The disease appears to be most common during the summer
months; thus, out of fifty-three cases in which the date of
attack could be fixed with accuracy by Dr. Barlow, twenty-seven
occurred in the months of J uly and August.

The exciting causes of the affection are equally obscure, and
it occurs frequently in the midst of robust health. Of all the
alleged causes, difficult or even normal dentition is the one most
frequently assigned ; and it is probable that too much rather
than too little importance has been attributed to this process in
the production of the affection. Injuries of various kinds are
often assigned as causes of the disease; while nurses are fre-
quently blamed unjustly by parents, who, unable to believe that
such a striking phenomenon as paralysis can occur suddenly
without appreciable cause, imagine that the child has been lamed
by a fall through the carelessness of its attendant.

Exposure to cold, more especially when the body is over-
heated, appears to have immediately preceded the paralysis in
a considerable number of cases ; and the affection often occurs
in children during the progress or soon after an attack of measles,
scarlatina, smallpox, typhus, and other acute affections.

§ 396. Symptoms. — Although this disease is essentially the
same in children and in adults, yet the symptoms in each differ
so much as to demand separate description. The disease as it
occurs in children will be first described.

{a) Infantile Spinal Paralysis.
It will conduce to clearness of description if, like Laborde, we

SPINAL CORD AND MEDULLA OBLONGATA. 107

divide the clinical history of this affection into four periods :
Tl) Invasion ; (2) Remission ; (3) Regression of paralytic pheno-
mena ; (4) Atrophy and deformities. It must, however, be
remembered that these periods overlap, instead of being dis-
tinctly separated from each other, and that this subdivision

merely adopted for the sake of convenience.

(1) Period of Invasion. — The disease is commonly ushered
m by a more or less intense fever, which is often preceded by
general malaise, pain in the head, mental irritability, fretfulness,
ind startings. The fever is as a rule of short duration, lasting
only from one to two days. In some cases it passes off in a few
hours, while in other cases it may continue from six to fourteen
Jays, or even longer. As the fever becomes established the cere-
bral symptoms become more pronounced, confusion of ideas and
slight somnolency are observed, the child may become uncon-
scious, or delirium of varying degrees of intensity may supervene.

The disease is not unfrequently ushered in by convulsions.
Sometimes the paralysis occurs after a single convulsion of
short duration, while at other times they are repeated many
;imes at variable intervals before the paralysis is definitely
declared (Laborde). The convulsions, according to Laborde,
often assume the tonic form, the spasms, as a rule, being re-
stricted to the extremities, and only extending on rare occasions
to the face ; and he believes that even in these latter cases the
attacks are unaccompanied by any other cerebral symptoms.
But in one of the cases quoted by Laborde in support of this
opinion the convulsion was accompanied by unconsciousness,
so that there are not sufficient grounds for believing that
these attacks differ in any way from ordinary eclamptic attacks
so common in children. In the cases ushered in by convul-
sions fever is often not mentioned as having been present,
but, as Laborde suggests, it is probable that the convulsions
assume such paramount proportions in the minds of the atten-
dants that minor symptoms are not observed. In some few cases
all general symptoms are absent, the child is put to bed
apparently in good health and is found in the morning paralysed.
In most of these cases the paralysis is limited to a portion of a
limb, indicating that the primary lesion is circumscribed. It
is, however, probable that in many of these cases transitory

108

SYSTEM DISEASES OF THE

fever and other general symptoms may have been present, and
overlooked owing to the defective observation of parents.

(2) Period of Remission— The initial symptoms subside in a
few days and the general health improves, but when the child
is taken out of bed to be bathed, or for some other purpose, it
is observed for the first time that one or all the limbs bang
down relaxed and powerless. The paralysis is as a rule developed
with great rapidity; probably never with the instantaneousness
of that caused by cerebral hemorrhage ; but it creeps on some-
what gradually during several hours, half a day or a night
before attaining its acme. In some few cases the paralysis
may spread more slowly, and not reach its maximum for several
days. In other cases two or more attacks of paralysis succeed
one another; at the first one limb is affected, and this is
followed by improvement, but the child relapses in a few days
into a feverish state, when another limb is found paralysed
(Althaus). Still more remarkable cases are recorded by
Laborde, in which the paralysis did not become permanently
established until the third attack.

But notwithstanding slight variations, one of the most
characteristic features of this affection is that the paralysis
reaches its maximum of extent and intensity within a com-
paratively brief space of time from the onset. The paralysis
possesses no progressive character ; it recedes but does not ad-
vance further.

The distribution of the paralysis is exceedingly variable. It
is frequently general, involving the muscles of the four
extremities, as well as a great part of the muscles of the trunk,
especially those of the vertebral column, and sometimes those
of the neck. It also frequently assumes the paraplegic form;
but the upper extremities are probably never exclusively affected.
The disease occasionally presents itself in the form of a hemi-
plegia (Duchenne fils, Barlow), and in these cases the side of the
neck, of the face, and of the tongue may be implicated at first
but do not remain permanently paralysed.

The sensibility is almost entirely unaffected throughout the
whole progress of the disease. At the outset of the affection
patients may complain of pains and paresthesias, but these
symptoms are of short duration. A certain degree of cutaneous

SPINAL CORD AND MEDULLA OBLONGATA. 109

hyperesthesia, or rather hyperalgesia, has been described as
being present during t^ie febrile stage, but the tenderness to
touch described may have been due to affections of deeper
structures, such as rheumatic inflammation of joints.

Reflex action, both cutaneous and tendinous, is completely
abolished in all the muscles which are severely attacked, and it
is much lowered or temporarily extinguished in those muscles
that are only slightly affected.

The functions of the bladder and rectum are rarely affected.
Daring the first days, however, there may be retention of urine,
but more frequently there is incontinence, and the stools may be
passed involuntarily. In young children a slight weakness of
the bladder with occasional incontinence may remain for some
time, but as a rule all disturbances of the bladder and rectum
have disappeared in from three to eight days from the onset of
the disease.

(3) Period of Regression. — After a certain time, which varies
from a few days to a few weeks, a gradual improvement of the
paralysis takes place. This improvement may affect a greater
or smaller number of the muscles involved, and some authors
:hink that all the paralysed muscles may completely recover.
The cases in which complete recovery takes place have been
called temporary spinal paralysis (Kennedy). Dr. Edge, of
Manchester, reports an interesting case which appears to have
belonged to this category. It was the case of a boy, aged ten
I years, in whom the muscles of both extremities as well as those
bf the back were paralysed. Some of the paralysed muscles
i were slightly atrophied, the faradic contractility was diminished,
f:here were no bed-sores, and no disturbances in the functions
bf the bladder or rectum ; but there was transitory impairment
pf cutaneous sensibility in the lower extremities. Recovery
Jwas complete in four weeks from the commencement of the
jittack.

As a rule, however, there is only complete restitution of some
)f the muscles, while the rest remain permanently paralysed.
The mode in which the paralysis recedes is peculiar. In six
3ases of generalised paralysis, which Laborde had the oppor-
tunity of observing accurately from the commencement of the
attack, the paralysis in the upper half of the body began to

110

SYSTEM DISEASES OF THE

improve between the third to the fifteenth day from the
commencement; and it disappeared, rapidly from the neck,
upper extremities, and trunk, and became restricted to
the lower extremities. This improvement Laborde calls the
period of first regression, inasmuch as it is followed after a
variable interval of time by a second, period of amendment
which he calls the second regression. During the second
regression there is a gradual improvement of the paralysis in
both lower extremities, and the muscles of one of them may be
completely restored to full power; but the paralysis becomes
permanently established in one or more groups of the muscles
of the other lower extremity, the anterior and external group
of muscles being those most frequently left paralysed. But,
although the improvement usually takes place from above
downwards, it sometimes occurs in the reverse order, and then
the paralysis becomes permanently localised in a superior ex-
tremity ; and in rare cases it becomes localised in the muscles
of the trunk or neck. In the case of a child two years of age,
under the care of Dr. Simon at the Southern Hospital, the
muscles of the neck alone remained paralysed, and all of these
were completely paralysed and atrophied.

The chiefs facts which concern us in this affection are that
the paralysis reaches its maximum of extent and intensity at
once; that in all cases, without exception, improvement occurs
in some of the paralysed muscles ; that the improvement
proceeds most actively during the first four to eight weeks, and
subsequently at a much slower rate; and that this improvement
may continue for from six to nine months, and under appropriate 1
treatment may go on for one or two years from the commence- •
ment of the attack.

(4) Period of Atrophy and Deformities. — All muscles, in
which motor power is not soon restored, become the subjects of I
a rapidly progressive atrophy ; and even the muscles which I
are but slightly affected emaciate to some extent, but soon:
recover on the restoration of voluntary power.

The atrophy usually begins in the first week of the disease,
and it is generally well marked in the course of a few weeks im
the muscles which are severely affected. The muscles become
more and more flaccid and attenuated, and after a time may:

SPINAL CORD AND MEDULLA OBLONGATA. Ill

lisappear so completely that the skin seems to lie immediately
ipon the bone. But the extent of the atrophy of the muscular
;ubstance is not always exactly measured by the loss of bulk of the
nuscle, inasmuch as the amount of atrophy is frequently masked
yy the accumulation of fat in the connective tissue. At times,
ndeed, the volume of the muscle appears to be increased, owing
,o the fatty accumulation, giving rise to the condition which
Duchenne has called pseudo-hypertrophy ; but in these cases
idvanced atrophy can be readily recognised by the extreme
laccidity and doughy feeling of the affected muscles when
compared with the healthy.

The condition of the electrical irritability of the motor nerves
ind muscles deserves special attention. Duchenne was the first
,o use the faradic current as a test of the degree of alteration
n the muscles; and he found that the faradic irritability of
Doth nerves and muscles begins to sink quickly in those
vhich are severely affected. He found, indeed, that it was
naterially diminished at the end of three to five days, and
mtirely abolished by the seventh day or during the course of
he second week. He also laid down a rule which has been con-
irmed by all subsequent observers, and the practical importance
>f which it is difficult to exaggerate — viz., that all the paralysed
nuscles in which the faradic irritability is only more or less
liminished, but not completely lost, during the course of the
second week, do not remain permanently paralysed, the restora-
tion being the more prompt and complete the less their faradic
rritability has been diminished.

The galvanic irritability was first investigated by Solomon,
who showed that the course of the alteration resembled that
)f severe traumatic paralysis. There is rapid loss of galvanic
rritability in the nerves during the first two weeks of the
i mralysis, and the irritability of the muscles manifests the
qualitative changes which characterise the reaction of degenera-
tion. During the first weeks of the paralysis there is an
ncrease of the galvanic irritability, the contraction on anodal
s stronger than on cathodal closure, and the contraction is
sluggish and protracted, instead of being instantaneous as in
wealth. In the course of two or three months the galvanic
rritability sinks again much below the normal standard, but

112

SYSTEM DISEASES OF THE

retains the characteristic qualitative alterations, and in the
course of one or two years from the beginning of the disease
there is only a trace of it generally left. In the muscles that
do not atrophy, and in those which have regained their motor
power, a greater or lesser diminution in the faradic and galvanic
irritability is generally found, but the reaction of degeneration
is absent.

Arrest of development of the osseous system is an important
symptom to which Duchenne and Yolkmann have directed
special attention. The atrophy of the bones has no necessary
relation with that of the muscles. The greater part of the
muscles may indeed be lost in a limb, while the bones are;
almost entirely unaffected ; and, conversely, a limb may be]
considerably shortened, while only one or two muscles are-
atrophied. Volkmann has indeed described cases in which the
motor paralysis was temporary, and followed after a few days
by a complete return of motor functions, but where the trophic
lesions of the bones persisted during life.

The paralysed leg may after some years be found from two
to six inches shorter than the sound limb ; and the upper ex-
tremity may be similarly shortened, although not generally to
the same degree. The long bones are thinner than normal,
they are porous, friable, and yielding. Their epiphyses and
processes grow smaller and less distinct; the paralysed hand or
foot is shorter, narrower, and thinner than the sound one ; and
even the pelvis may be arrested in its development.

The joints become deformed and unusually movable. The
increased mobility of the joints is caused partly by the dis-
appearance of the articular extremities of the bones, and partly
by relaxation and stretching of their ligaments. The relaxation
of the latter is, indeed, sometimes so great that the patient can
dislocate a joint without experiencing any discomfort.

The skin of the affected extremity becomes flabby; its
loss of elasticity being manifested by long retention of slight'
pressure marks, such as that produced by the stocking. The>
surface of the limb assumes a mottled or bluish colour, and.
it is remarkably cold to the touch ; the reduction of tem-
perature in old-established cases being, according to Heine, at
much as 10° to 12° F., as compared with the corresponding

SPINAL CORD AND MEDULLA OBLONGATA.

113

ealthy limb. The skin is liable to be affected with chilblains,
leers which are slow in healing form on slight provocation,
whilst the defective nutrition and great coldness of the skin
ften cause a certain diminution of cutaneous sensibility. The
utritive and vascular changes in the affected extremity are
ccompanied by diminution in the calibre of the arteries
Charcot).

Deformities. — The various deformities which occur in the
ffected limbs in infantile spinal paralysis furnish very
haracteristic features of the disease. Various opinions have
■een held by different authors with respect to the mechanism
•y which these deformities are produced. Some pathologists
elieve that the healthy muscles are always maintained in a
ondition of moderate contraction, constituting the normal
mus of the muscles, and when this tonus is destroyed by
aralysis in a certain group of muscles, the predominant action
f their healthy antagonists produces a deformity. Volkmann,
owever, denies the existence of muscular tonus, and thinks that
le deformity is mainly produced by the weight of the limb
.self. He points out that in paralytic deformities of the lower
itremities, the position generally assumed by the foot is only
high degree of that which it takes when unsupported and left
ee from the action of the muscles. The weight of the limb
nd the direction in which mechanical forces act upon it during
>comotion are undoubtedly important causes of deformities ;
ut two other co-operating factors may be mentioned. The
paralysed muscles permit the limb frequently to assume a
osition in which the ends of their healthy antagonists are more
f leas permanently approximated, and the latter consequently
ndergo adapted atrophy (Adams), and become permanently
lortened. The second factor consists of an affection of the
aralysed muscles themselves. The atrophied muscles are
robably at times, like the bones, the subjects of arrested
svelopment ; their growth does not keep pace with that of
ie healthy muscles and of the body generally, hence they
ecome permanently shortened. Some have supposed that
roliferation of the interstitial connective tissue and its subse-
uent retraction may occur in the course of the atrophy of the
mscles, and thus lead to permanent shortening in them ; but

IH SYSTEM DISEASES OF THE

this i3 doubtful. Wheu the deformity is oaused by shortening
of the paralysed muscles, the latter are found in the concavity of
the distorted extremity. But whatever may be the mechanism
by which these deformities are produced, it would seem that,
disregarding a certain degree of inequality and disfigurement
caused by the arrest of development of the long bones, paralyse
of certain muscles and groups of muscles, along with relaxation
of the ligaments, is the main cause of the various distortions

°bSomeedof the muscles of one lower extremity suffer more
frequently than others from permanent paralyse ; and of these
the antero-external group of the leg-the long extensor of he
toes, tibialis anticus, special extensor of the great toe, and the
long and short peronei-are those most commonly affected
The most frequent forms of paralytic talipes are, therefore, as
might have been expected, talipes eqninus and equmo-varus
(Plate II 5) When the anterior group and the adductors of the
foot are affected at the same time talipes equino-varus results;*
and when the muscles of the calf are alone affected talipes calca- ;
neus is produced, but this form is exceedingly rare ; andsimple
paralytic talipes varus is of still rarer occurrence. Anot e
common deformity is the « pes cavus"-" talus pied creux of the
FrTcn-in which the sole is hollowed and the instep rendered
prominent. Dnchenne thinks it is caused by a more or lew
complete paralysis of the muscles of the calf, along with
rultaneous contraction of the flexors of the cot, either th
long flexor of the toes or the long peroneus. The great lax tj;
of the ligaments of the foot allows the latter to become ben
upon itself from the transverse tarsal joint, where the foot j
unsupported ; but when it is placed upon the ground it assume

the form of " flat foot." ,.

Various deformities occur in the inferior extremity, accordmH
to the extent and' localisation of the paralysis. The anter oJ
and internal muscles of the thigh are most usually affec to
above the knee, and in that case the predominant action ot W
flexors of the leg on the thigh maintains the former in a pe
manent condition of partial flexion (Genu recurvatum) the
being also abducted. The condition is always assoc.ated w*
talipes equino-varus. All the muscles of both legs are son,

SPINAL CORD AND MEDULLA OBLONGATA.

115

imes paralysed so that the patient is compelled to walk on his
;nees drao-o-incr his small thin legs after him. In still more
i .cwravated cases the muscles of both legs and thighs are per-
nanently paralysed so that the small flexible limbs dangle
,bout like the limbs of a doll (membre de policbinelle).

Paralysis of the muscles of the trunk does not give rise in
his disease to a true active curvature of the vertebral column,
>ut the attitudes imposed by other deformities may produce
ompensatory curvatures. Of the curvatures directly attributable
o the paralysis, lordosis is the most frequent and most im-
tortant. Lordosis is caused by partial paralysis of the sacro-
pinal muscles, and in order to prevent the permanent bending
jrwards of the body by the predominant action of the flexors,
he patient voluntarily throws the trunkbackwards,thus relieving
he weakened extensors and throwing additional weight on the
exors, so that the balance between the action of the two sets
f muscles is re-established. The spinal curvature which results
•om this action differs from other forms of lordosis, inasmuch
3 the pelvis is pushed forwards instead of backwards, and the
.uttocks become less instead of more prominent.

The deformities of the upper extremities are much less
equent and serious than those in the lower extremities. The
mscles of the shoulder, and particularly the deltoid, are the
lost usual subjects of paralysis and atrophy in the upper
stremity. In these cases the shoulder is flattened, and the
rorainence of the deltoid is replaced by a more or less deep
2pression according to the degree of atrophy; the humerus
lecomes separated from the glenoid cavity, so that dislocation
lay occur spontaneously, or is readily produced ; the arm hangs
pwerless by the side ; and, to use the apt comparison of
.eine, dangles about like the loose end of a flail. In excep-
onal cases the forearm and hand may undergo distortion; but
lese deformities are not of sufficient importance or frequency
> require description. All the organic functions are well per-
rmed, and the patient may live to extreme old age, as in the
ise of a patient observed by Charcot, who died at the age of
iventy, carrying with him indelible traces of the disease from
hich he had suffered sixty-five years before.

The muscles are paralysed in infantile spinal paralysis in

116

SYSTEM DISEASES OF THE

groups, in accordance with their association in action. Particular
attention has recently been directed to this point by E. Remak.
In what he calls " the upper-arm type " of atrophic paralysis,
the supinator longus is involved along with the deltoid, coraco-
brachialis, and biceps muscles. In what Remak calls " the
forearm type" of infantile paralysis, as well as in lead paralysis,
the extensor muscles of the hand are paralysed, while the
supinator longus is spared.

Analogous facts have been observed in the various atrophic
paralyses of the lower extremities. Cases of infantile para-
lysis are recorded by E. Remak in which the tibialis anticus
and all the muscles supplied by the crural nerve, with the
exception of the sartorius, were paralysed, and he therefore
conjectures that the spinal nuclei of the former and those
of the latter, with the exception of that of the branch to
the sartorius, lie near each other in the spinal cord, and are
liable to be diseased at the same time. Duchenne has proved
that the sartorius is associated in its functions, not so much
with the quadriceps and adductors, as with the flexors. The
sartorius flexes the leg on the thigh, and the thigh on the pelvis.
Bernhardt has compared the sartorius to the supinator longus,
and it appears also to correspond with the latter in having its
spinal nucleus near that of the flexors, and not of the exten-
sors with which it is in anatomical relation. Cases, however,
have not yet been recorded showing that the sartorius is para- -
lysed along with the flexors of the leg, the extensors being J
spared, corresponding to what occurs with the supinator longus I
in the upper-arm type of atrophic paralysis. The tibialis anticus a
is also frequently spared in infantile paralysis when the other ;
anterior muscles of the leg are implicated. Remak states that,
when lead paralysis affects the lower extremities the peroneal}
group are affected, but the tibialis anticus is spared, and hen
conjectures that the spinal nucleus of the tibialis anticus is on:
a higher level than those of the other muscles of the peroneal
region.

(b) Acute Spinal Paralysis of Adults.
Acute spinal paralysis of adults is essentially the sani'.'
disease as infantile spinal paralysis. The differences between tlv
two affections result from the facts that the brain of the adul

SPINAL CORD AND MEDULLA OBLONGATA. 117

>ffers greater resistance than that of the infant to the initial
listurbances ; that the organism of the former is not so disposed
o fever ; that the growth of the bones is already completed ;
ind that the ligaments and joints are firm and resisting.

The disease begins in the adult by pain in the back and the
extremities, paresthesia?, such as formication or numbness, and
'ever, which at times is very intense. There may be severe
headache, vomiting, somnolency, or even slight delirium, but
convulsions have never been observed.

The paralysis is developed more or less rapidly, generally in
:he course of a few hours, and, as in the case of children, it is
more or less widely spread, complete, and associated with entire
iaccidity of the paralysed muscles. Reflex action is either
much lowered or abolished in the paralysed muscles, but may
De retained in those which are only slightly affected. Tempo-
rary weakness of the bladder may be present at first.

The initial general symptoms pass off in a few days, soon
ifterwards the paralytic symptoms begin to improve, and after
;ome weeks or months restitution of motor power may be
complete. Frey has called this variety temporary 'paralysis,
corresponding to the form of the same name in children,
jrenerally, however, there is only partial restoration of motor
power, some of the muscles remaining permanently paralysed.
The latter muscles undergo rapidly progressive atrophy, as in
the case of children, and afford the usual evidences of the
reaction of degeneration. The skin becomes lax and withered
! and the extremities cold and cyanotic.

The sensory disturbances which may have existed at the
beginning soon subside, and the sensibility becomes normal,
the sexual functions are throughout unaffected, there are no
bed-sores, and the general health is good.

Paralytic contractions supervene with their resulting deformi-
ties, but the latter never attain the same degree as in children,
because the joints and ligaments are firmer in the adult, and
the long bones of the extremities have attained their full
development.

§ 397. Course, Duration, and Terminations. — The ordinary
course of the disease is generally the same as that already

118

SYSTEM DISEASES OF THE

described. Cases of this disease divide themselves into two
classes : (1) Those in which complete recovery takes place, and
(2) those in which the recovery remains incomplete. In the
first variety complete restoration of all the muscles takes place
in the course of a few weeks or months. In the second variety
some of the muscles remain permanently paralysed, and atrophy,
with secondary deformities, results. The paralysis does not
greatly interfere with the general well-being of the patient, and
does not appear to have any influence in accelerating death, at
least directly, although the resulting deformities may do so
indirectly. Persons who have had an attack of spinal paralysis
do not indeed appear to be more liable in later life to other
affections of the spinal cord than healthy persons generally.

§ 398. Morbid Anatomy. — The main pathological change
which have been found in infantile paralysis may be sub
divided into those which have been met with (1) in the muscles,
and (2) in the nervous system. Changes have been found it
the tendons and bones, skin and joints, but these are o
subordinate importance.

(1) Morbid Changes in the Paralysed Muscles. — It is quit

Fig. 159.

a 6 c

Fig. 159 (Young). Muscular Fibres from a case of advanced Infantile Paralysis, i
withdrawn by Leech's trochar. — a, Muscular fibres presenting a more or less
healthy appearance ; b, muscular fibres, somewhat atrophied and with granular
contents ; c, muscular fibres greatly atrophied, but presenting faint traces of I
transverse striation, and having their surfaces thickly studded with nuclei.

SPINAL CORD AND MEDULLA OBLONGATA. 119

.nnecessary to describe at length the changes which occur
|n the paralysed muscles, inasmuch as they have already been
described in the first part of this work (§ 108), along with the
ither trophoneuroses. By the kindness of Dr. Leech, I am,
lowever, enabled to show in Fig. 159 the condition of the
nuscular fibres in advanced atrophy when a portion of the
nuscle is withdrawn by means of Leech's trochar. In almost
ivery instance, Dr. Leech assures me that some of the fibres
ippear more or less healthy {a), while others have lost their
lormal striation, their contents are granular, but they are not
nuch diminished in size (b). A large number are, however,
-educed to slender and transparent fibres; their surfaces are
covered by nuclei; the transverse striation is still distinctly
risible, although it is very faint (c). At times two, or even
;hree, nuclei may be seen close together, suggesting that they
lave been derived by proliferation from one nucleus originally.
The nuclei may also be observed to project distinctly from the
surface of the atrophied fibre, and it is therefore probable that
.hey have been derived either from the nuclei of the sarco-
;.emma or of the endomysium.

(2) Nervous System. — The lesions which have been found
n the spinal cord are undoubtedly the most interesting and
important of all those which have been observed in atrophic
paralysis. For a long time theoretical arguments were adduced
on the one hand to show that this disease was a nervous affec-
tion either of spinal or peripheral origin ; while on the other
hand it was maintained that the seat of the lesion was pri-
marily in the muscles, and hence it was called " essential
paralysis." Heine declared in favour of the spinal theory of
[the disease in 1860, in the second edition of his work. This
view was also adopted by Duchenne, but it was not confirmed
by post-mortem examination until 1864, when Cornil, a pupil of
Charcot, first recognised distinct alterations in the spinal cord,
and drew special attention to the atrophy of the anterior grey
horns. Pre'vost and Vulpian, however, in 1866, were the first
to make the positive observation that the essential anatomical
lesion was situated in the grey anterior horn. This observation
was subsequently confirmed by the observations of Lockhart
Clarke, Charcot and Joffroy, and of many others.

120

SYSTEM DISEASES OF THE

When the anatomical basis of the disease was once established, I
it soon appeared that the affection was not exclusively confined
to childhood. Moritz Meyer was the first to point out that
essentially the same disease was met with in adults, and this
opinion was afterwards confirmed by Duchenne. Reports of
cases have recently accumulated, establishing the occurrence of 1
acute atrophic spinal paralysis in adults (Hallopeau, Gombault,
Bernhardt, Frey, Charcot, Seguin, Erb, Weiss, F. Schultze,
Sturge, and others).

It is unnecessary to enter into a minute description of all the I
published reports of post-mortem examinations in cases of
infantile spinal paralysis. The essential anatomical change con- 1
sists in the destruction of a large number of the ganglion cells
of the anterior horns, and this lesion is the cause of the paralysis ]
and subsequent atrophy. The lesion is generally more or lessa
diffused through the anterior grey horns, but it generally reaches j
its greatest intensity at the cervical and lumbar enlargements, |
and as a rule leaves no permanent alteration except at these I
points. It may extend at certain points somewhat backwards ;J
towards the posterior horns, and also forwards and outwards to t{
the antero-lateral columns, and the anterior roots of the nerves
are usually atrophied, but these are secondary changes and do j
not appear to be necessary to the production of the symptoms.
The observations upon which this conclusion is based may be |
divided into those which have been observed within two years ;
from the beginning of the disease, and those which have been i:j
observed after long intervals of time.

Unfortunately no observations have yet been made with J
respect to the disease during the first few days or weeks, owing to)!
the fact that the disease of itself is not fatal. Dr. Clifford Allbuttt jj
reports the case of an infant seven months old who was sud-- J
denly paralysed in all the extremities. Death resulted in aajl
short time from implication of the respiratory nerves. On ['
post-mortem examination two hsemorrhagic clots were dis- |i
covered in the cervical region, one of small size being situated |;
in the left posterior horn, the other being larger and situated If
in the right posterior horn and lateral column. Dr. Allbutt I,
thinks that if these lesions had been found in the lower dorsa I
region the infant would probably have survived, and the case I

SPINAL CORD AND MEDULLA OBLONGATA.

121

light have been regarded as one of infantile spinal paralysis,
it is, however, much more probable that this was a case of
oematomyelia. An instructive case is reported by Dr.
"harlewood Turner in the Pathological Transactions for 1879.
|L child two and a half years of age fell on her back, but played
bout as usual for a fortnight afterwards, and then became
uddenly paralysed in her lower extremities, and in a few days
.fterwards in her upper extremities likewise. On admission to
he London Hospital, a fortnight after the beginning of the
,ttack, all the extremities were completely paralysed, reflex
,ction in them was also abolished, there was absence of
ensation in the lower extremities, and the stools were passed
nvoluntarily. The child had an attack of measles, and died
Jbout six weeks after the commencement of the paralysis. On
>ost-mortem examination, which was made by Mr. R W. Parker,
hanges were observed in the anterior horns and antero-lateral
olumns throughout the whole length of the cord, these being
nore pronounced on the left than the right side. A patch of
eddened gelatinous-looking matter, about the size of a swan
hot, was observed in the left anterior grey horn about the centre
>f the lumbar enlargement. The margin of the patch was of a
larker colour than the centre, "as from the decolorisation of an
lisemorrhagic extravasation." In the neighbourhood of this
hemorrhagic focus the nervous tissues were completely disin-
tegrated, so that no nerve structure could be distinguished
In the anterior grey horn, the outer part of the base of the
posterior cornua. The whole grey substance was abundantly
Infiltrated with leucocytes, a considerable number of them being
idso observed in the white substance ; while they were massed
n great numbers in the sheaths of the larger arterioles. The
vesicular column of Clarke did not appear to have been any-
vhere affected. In the portions of the cord which were remote
rom the seat of haemorrhage, the nervous structure was not
:ompletely destroyed, although many other evidences of disease
vere observed. This case tends to confirm Dr. Allbutt's theory
)f the origin of the disease. It is, indeed, quite probable that a
small haemorrhage into the substance of the anterior horn may
sometimes be the starting point of the affection.
In the Pathological Transactions for 1879 the case of a child

122

SYSTEM DISEASES OF THE

three and a half years of age, who had suffered from an attack
of infaDtile paralysis at the age of seventeen months, is reported
by Dr. Henry Humphreys. On admission to the Pendlebury
Hospital the child presented well-marked talipes calcaneus of
the left heel. Soon after admission the patient developed a
severe attack of scarlet fever, from which she died. The changes
observed by Dr. Humphreys in the spinal cord were limited
to the lumbar region, and consisted mainly of a remarkable
diminution in the number of the ganglion cells beloDgiug to
the anterior and lateral parts of the left anterior grey horn.
The annexed diagram {Fig. 160) shows the condition of th
anterior cornua at the middle of the lumbar region. Dr
Humphreys examined eighty-seven sections of the lumb
region of the cord, and averaged the number of cells the
contained.

The other most notable cases which have been reported
at an early period of the disease are those of Roger and
Damaschino, Roth, Leyden's second case, Parrot and Joffroy, and
a case briefly reported by Rinecker, which was examined by Von
Recklinghausen. No marked changes were discovered in the

Fig. 160.

Fig. 160 (After Humphreys). The letters a, b, c indicate respectively the central,
anterolateral, and postero-lateral groups of ganglion cells. On the left side
the group b ha3 almost entirely disappeared, causing a marked falling in of the
circumference of the grey matter. The groups a and c are fairly well represented
on the left side, but the cells composing them are not so numerous as on the
right. The internal group has disappeared from both sides.

SPINAL CORD AND MEDULLA OBLONGATA.

123

)rd with the naked eye. In some cases the substance of the
3rd seemed tougher at the level of the cervical or lumbar
□largements, and the antero-lateral column on the side affected
ppeared atrophied and distorted. On transverse section the
nterior grey horns were observed to be more or less discoloured,
'hitish or reddish, sometimes soft, diffluent, and diminished
i volume. The anterior roots at the level of the parts mainly
ffected were found grey, translucent, and atrophied.

On microscopical examination, the main lesions hitherto
bserved have been diffused through the grey substance of the
nterior horns with areas of greater intensity in the cervical and
jmbar enlargements, especially in the latter. In the lumbar
egion, sometimes on one side only, but usually on both sides, an
rea of softening has been found in the anterior grey horn, some-
imes extending the whole length of the lumbar enlargement,
nd sometimes occupying only a portion of it in longitudinal
xtent. The area of softening was sometimes situated towards
le centre, sometimes towards the anterior part of the horn,
eing separated from the surrounding parts by a more or less
.aarp line of demarcation. Similar areas were often also found
ccasionally in the cervical enlargement of the cord, and occa-
Lonally in the dorsal and upper cervical portions. The substance
f these areas was friable, soft, and disseminated with numerous
ranulation cells. The blood-vessels were dilated, there was a
iirge increase of connective tissue, and the nuclei were also
icreased in number. Many of the large multipolar ganglion
ells had disappeared, and of those which still remained a large
■roportion were observed in all stages of degeneration and
trophy. The nerve fibres and axis cylinders within the area
f softening were also found to have entirely disappeared.

Slighter and more diffused changes occur much beyond the
mits of the softened areas. These changes consist of single
ranular cells scattered through the grey substance, multiplica-
lon of nuclei, dilatation of blood-vessels, and disappearance or
egeneration of individual ganglion cells. Similar changes are
i ften observed throughout a greater or lesser portion of the grey
lubstance of the dorsal region. The antero-lateral columns have
I ccasionally been found diminished in size, and the seat of a
light sclerosis. The trabecule are then thickened, and indi-

124

SYSTEM DISEASES OF THE

vidual nerve fibres are atrophied (Joffroy and Damaschino).
The anterior roots are diminished in size, and show signs of
degenerative atrophy when examined microscopically.

Observations have been made from seventeen to sixty-one
years after the origin of the disease, by Cornil, PreVost and
David, Yulpian, Lockhart Clarke, Charcot and Joffroy, Petit-
fils and Pierret, Leyden, Gombault, Dejerine, F. Schultze, and
others.

The morbid changes which have been observed in these cases
are generally the same as in those which have been examined
within two years of the onset of the disease. The anterior horns
are shrunk, and the antero-lateral columns appear to the naked
eye grey, translucent, and atrophied. The posterior columns,
posterior grey horns, and vesicular column of Clarke are almost,
if not quite, normal.

On microscopic examination circumscribed lesions are found
in the anterior horns at the lumbar and cervical enlargements,
and in addition to the main lesions more or less diffused changes
are met with in the grey substance and white columns. The
anterior horns are atrophied and shrunk, and within the diseased
foci which they contain there is a more or less firm, fibrillated
connective tissue, rich in nuclei. The blood-vessels are enlarged,
probably also increased in number, and their walls are thickened.
Granule cells are generally absent, but a large number of corpora
amylacea as well as pigment granules have been found. The
multipolar ganglion cells and nerve fibres are more or less com-
pletely destroyed in the diseased foci, and some of the ganglion
cells which remain are found in all stages of degenerative atrophy,
pigmentary degeneration, and shrivelling. Well preserved gan-
glion cells may be found outside the diseased foci.

In the portions of the grey cornua which are comparatively
healthy, such as the dorsal region, the ganglion cells are less
numerous than normal, the connective tissue is increased, and
the nuclei are abundant.

A greater or lesser degree of sclerosis of the antero-lateral
columns may be discovered, the neuroglia is thickened, and
generally there is some degree of atrophy of the nerve fibres.
The sclerosis may vary greatly in extent. It is sometimes
confined to the immediate vicinity of the anterior horns, and at

SPINAL CORD AND MEDULLA OBLONGATA. 125

ther times it is diffused over the entire anterolateral columns,
le pyramidal tract being specially liable to suffer.

Fig. 161.

'ig. 161 (From Charcots Transverse Section of the Spinal Cord taken from the cer-
vical region of a woman, aged fifty years, who died in the Salpetriere, of
general paralysis of the insane, and who was the subject of infantile spinal
paralysis of the right superior extremity. There was fibroid atrophy of the
right anterior cornu, and atrophy of all the white columns of the corresponding
side.

The annexed diagram (Fig. 161) well illustrates the morbid
alterations which are usually observed. The anterior roots are
hin, grey, translucent, and the greater part of their nerve
ibres are atrophied, the connective tissue is often infiltrated
vith fat cells, its nuclei are abundant, and the walls of the
ressels are thickened. Almost all pathologists now regard
he primary lesion as an inflammation of the anterior grey
10ms, although the cases reported by Drs. Clifford Allbutt and
j. Turner appear to show that a slight hemorrhage into the grey
•ubstance may occasionally be the starting point of the morbid
)rocess. The inflammatory process spreads along more or less
liffusely over the greater part of the anterior horns, but attains
ts greatest intensity in the lumbar and cervical enlargements,
n which localities distinct areas of softening, and destruction
)f the multipolar ganglion cells are produced.

126

SYSTEM DISEASES OF THE

When the inflammation subsides, a gradual improvement
takes place in those places where the destruction of the grey
substance has been incomplete ; but where the nerve structure
has been thoroughly disintegrated there is a gradual develop-
ment of cicatricial connective tissue in its place. The antero-
lateral columns become secondarily affected, and when the
lesion takes place during childhood they become retarded in
their development, appear narrow and atrophied, and cause a
considerable change in the form of the spinal cord.

Whether this affection is to be regarded as a parenchymatous
or an interstitial affection is not yet settled. Charcot and
others support the former view ; while Roger and Damaschino,
Roth and others, are in favour of the latter. Dujardin-
Beaumetz, however, suggests that both tissues become w-m
flamed at the same time, and that the myelitis is both
parenchymatous and interstitial.

The peripheral nerves undergo degenerative atrophy, F.I
Schultze found increase of the interstitial connective tissue, i
with atrophy of the nerve fibres.

The tendons, atrophied and stretched, appear as thin, narrows
bands.

The bones are always retarded in growth when the disease
occurs in childhood, the normal protuberances and processes «j
being less developed, and their epiphyses stunted. The ;jj
medullary portion is relatively increased, its fatty contents are t
more abundant, and the external hard lamella of the bone is s
thin and friable.

The ligaments of the joints are thin and loose, while the
articular extremities of the bones are stunted, ground off, I
eroded, and their cartilages attenuated. The alterations ina
the joints, ligaments, and articular cartilages greatly aid the
muscular paralysis in the production of the different forms of
club-foot, and the various other deformities already described.

The arteries are slightly diminished in calibre, the shin aiid^
internal organs are either normal or only show changes which
have no necessary connection with the spinal disease. The i!
brain is normal. In one case Sander found the two ascending |
convolutions and the paracentral lobule — the motor area oi I
the cortex in relation with the paralysed parts — relatively !

SPINAL CORD AND MEDULLA OBLONGATA.

127

iminished in size, but as the spinal disease was associated
nth idiocy, the connection between the atrophy of the cortex
,nd the spinal lesion may have been merely accidental. Par-
icular attention should be paid to the condition of the cortex
n future post-mortem examinations in cases of the disease.

§ 399. Localisation of the Lesion in the Anterior Horns.

A very interesting case in this reference is described by Prevost and
)avid.* It was that of a man, aged sixty years, who suffered from
abrile and typhoid symptoms, which caused his death. The man had
omplete atrophy of the muscles of the thenar eminence of the right hand,
/hich according to his own account came on in childhood. The anterior
oot of the eighth cervical nerve of the right side was notably diminished
i size, as compared with that of the left side, and the anterior root of the
eventh nerve was also slightly diminished in volume on the right side.
)pposite the atrophied root of the eighth nerve the anterior horn on the
ame side was observed to be sensibly diminished as compared with that of
ae left. The diseased portion had a longitudinal extent of about two
antimetres, and the centre of the lesion was on a level with the atrophied
jot. Its greatest transverse extent was also opposite the diseased root of
ae nerve and it gradually diminished in size, both upwards and downwards,
he author says that in the diseased portions the external or lateral (postero-
iteral) group were represented by a few healthy cells, while the anterior
intero-lateral) and the middle or internal (internal) groups were normal,
udging from the drawing, however, the median and central groups
rere entirely destitute of cells, while the antero-lateral group was only
apresented by one cell.

t A case has recently been described by Kahler and Pick which appears
o determine the localisation, in the anterior horns, of the spinal centres
)r the muscles of the calf of the leg. The case was that of a woman,
wenty-four years of age, who died from an attack of typhoid fever. The
luscles of the calf of the right leg were found almost completely atrophied.
>n examination of the spinal cord the right anterior grey horn was found
trophied through the greater portion of the lumbar enlargement, but the
lost marked changes were observed on a level with the fourth and fifth
acral nerves. The roots of these nerves were also atrophied, there was a
light increase of the interstitial connective tissue, which was especially
'ell marked in some bundles. The central group of cells was mainly
ffected.

t In a case of atrophic spinal paralysis of adults, observed by Schultze
3 a man aged forty-two years, the muscles in the regions of distri-

* Archiv. de Physiologie, Serie II., Tome i., 1874, p. 595.
t Archiv. fur Psychiatrie, Bd. x., 2 Heft, 1880, b. 358.
tVirchow's Archiv., Bd. lxxii., 1878, a. 443.

128

SYSTEM DISEASES OF THE

bution of the sciatic nerve in both legs were completely paralysed,
while those supplied by the obturator and crural nerves were spared.
Schultze found sclerosis of both anterior horns over the whole of the
lower half of the lumbar region, and he consequently concluded that the
crural and obturator nerve nuclei do not lie in the lower half of the lumbar
region of the cord. Eemak, however, thinks that the tibiales autici were
also spared in this case, and placed the nuclei of these muscles in the
upper half of the lumbar region of the cord.

The condition of the upper extremity in Schultze's case was no less
interesting. The muscles of the back from the sixth dorsal vertebra down-
wards were yellow and atrophied. The shoulder muscles and the rhom-
boids of the left side were atrophied, and the left trapezius was degenerated
to a less degree, the left deltoid was completely degenerated, the supi-
nator longus of the left arm was considerably altered, while the biceps and
triceps were said to have been normal, and the coraco-brachialis was not
mentioned. On examination of the spinal cord the left anterior horn, in
the upper segment of the cervical enlargement, was smaller than the right,
and appeared to be reduced to one-third of its volume. A red circum-
scribed spot was observed occupying the lateral part of the anterior horn
(postero-lateral group). The condition of the dorsal region of the cord
is not mentioned, but so far as the case goes it supports the idea that the
muscles of the scapula and shoulder are mainly innervated from the
postero-lateral group.

A case of extreme muscular atrophy is reported by Dr. Zach. Johnson,
which was evidently an example of infantile paralysis, and in which " the
muscles of the shoulder and arm had altogether disappeared. The muscles
of the forearm remained apparently unaffected. The muscles of the ball
of each thumb were almost altogether gone, while the muscles of the
fingers continued to be well developed. The muscles on the dorsum of
each scapula were nearly gone also."* The lower third of the cervical
enlargement was alone sent to Dr. Lockhart Clarke for examination, which
ia a source of quite as much regret to others as it was to Dr. Clarke him-
self. An examination of the careful drawings made by Dr. Clarke, as
well as of his description, shows that the weight of the disease falls upon
the central portion of the grey substance along the distribution of the
median branch of the central artery, and that the postero-lateral group of
cells was the one which was principally injured, This case, then, so far
as it goes, supports the opinion already advanced, that the muscles about
the scapula and shoulder-joint are innervated from the postero-lateral
group of cells in the cervical region. But in this case " the muscles of
the ball of each thumb were almost gone." Are we to believe that
they also are innervated from the postero-lateral group? The case
alone certainly does not prove it. Indeed one of the illustrations
shows distinctly that on one side the disease had spread forwards into
the area of distribution of the anterior branch of the central artery,

* Medico-Chirurgical Transactions, voL li., 1868, p. 249.

SPINAL CORD AND MEDULLA OBLONGATA.

129

| id consequently amongst the median group of small cells, while Dr.
larke makes special mention of a streak of disintegrated tissue which
itended backward along the middle of the posterior horns and hence in
le area of distribution of the posterior branch of the central artery,
here is nothing in this case, therefore, to contradict the opinion that the
uscles of the ball of the thumb are innervated from the median area.

§ 400. Morbid Physiology. — Infantile spinal paralysis is one
t the diseases the morbid anatomy of which largely contri-
uted to clear up our knowledge of the functions of the grey
aterior horns. The multipolar cells probably constitute gan-
lionic centres, both for reflex action and for the transmission of
apulses received through the pyramidal tracts, and when they
:e destroyed both reflex and voluntary actions are impaired or
3olisbed according as the destruction of the cells is complete
■ incomplete. Destruction of these cells is also followed, as
e have seen, by various trophic changes in the muscles, bones,
ndons, and joints.

As already mentioned, I believe that the ganglion cells of the
iterior grey horns which constitute the spinal centre for the
gulation of the movements of a muscle also constitute for it a
ophic centre. Most muscles are, however, connected with
ndamental and accessory ganglion cells, and it is only when
.e connection between the former and the muscle is severed
iat profound effects both upon its motor power and nutrition are
•oduced. The acute nature of the lesion in infantile paralysis,
i well as its localisation, is well adapted to sever the muscles
om their connection with the fundamental cells, even if the
tter were to remain themselves entirely unaffected. In a case
)served by Charcot, for instance (Fig. 162), the lesion occupied a
)sition in which only a few of the fundamental cells would be
jured, yet a large number of fibres, as they converge to pass
it to the anterior roots, must have been destroyed, and the
feet would consequently be very similar to that which would
How a peripheral lesion of the nerve. The similarities be-
ireen the clinical phenomena of infantile spinal paralysis and
jripheral disease of the nerves are too obvious to require
nnting out. The case is wholly different when we have to do
ith a chronic and gradually progressive affection like pro-
essive muscular atrophy, in which the accessory cells are first
J

130

SYSTEM DISEASES OF THE

attacked, and the disease by slow and successive steps graduall
invades the more fundamental cells. In such a disease we ma
expect that the clinical symptoms of paralysis and atrophy will
pursue a totally different course from that which obtains in
infantile spinal paralysis.

Fig. 162.

we \

Fig. 162 (From Charcot). Section of the Spinal Cord in the Lumbar Region, .
a case of infantile paralysis.— A, Left anterior cornu, healthy; a, Healthy
median group of ganglion cells. B, Right anterior cornu ; b, Median group
of ganglion cells. The cells are destroyed, and the group is represented by a
patch of sclerosis.

The fact that the disease occurs in certain circumscribe
areas explains the distribution and extent of the paralysis, ana
the immunity of certain muscles and groups of muscles. Th<
acute inflammatory nature of the process explains the suddei
appearance of the paralysis as well as the fever and othe
violent symptoms which occur at the onset of the diseasi
The resolution of the acute inflammation, in part or in whol'
explains the rapid disappearance of the first severe syrup ton'

SPINAL CORD AND MEDULLA OBLONGATA. 131

nd the partial or complete restitution of the paralysed muscles
hich afterwards takes place.

§ 401. Diagnosis. — The symptoms of acute anterior polio-
lyelitis are so definite and characteristic that it is not easy to
)nfound it with any other disease. We must, however, be
ireful not to regard, as true instances of this affection, every
ise of spinal paralysis which arises in childhood, even if ac-
)mpanied with atrophy.

Bcematomyelia, or haemorrhage into the grey substance, say
F the lumbar region, may produce sudden paralysis, which is
dlowed by muscular atrophy, loss of reflex excitability, and the
jaction of degeneration in the related parts ; but the initial
jver is absent, the invasion is more sudden even than that of
ifantile spinal paralysis, the former being almost apoplectiform
i its onset, and disturbances of sensibility, paralysis of the
)hincters, and bed-sores are present.

In acute central or transverse myelitis, cutaneous anaesthesia,
iralysis of the sphincters, and bed-sores are almost invariably
■'esent ; while reflex excitability is increased in transverse
yelitis, and, as a rule, there is no atrophy,
i In myelitis from compression, disturbances of sensibility,
iralysis of the bladder, tremors of the lower extremities, in-
eased reflex excitability, severe pains, and affections of the
irtebral column are present; the general health usually suffers
'eatly, but there is no muscular atrophy.

i Fi *om cerebral hemiplegia this disease may be distinguished
\j the different commencement of the former disease, by the

.iplication of the facial nerve, and by the circumstance that
cerebral paralysis there is no muscular atrophy, that the elec-
.ical irritability is preserved, that the bones are not affected,
jid that there is increased reflex excitability of the tendons.
I Progressive muscular atrophy develops slowly and gradually,
jid the wasting of the muscula/ tissue precedes the paralysis,
Jhile the electrical irritability is retained.
I Paralysis following obstetric operations is observed imme-
, lately after birth, the initial fever is absent, the seventh nerve
the one most frequently affected, while this nerve is never

irmanently affected in anterior poliomyelitis. When the arm

132

SYSTEM DISEASES OF THE

has been paralysed by pressure of the blades of the forceps on
the brachial plexus, ansesthesia remains with the paralysis.

The spasmodic spinal paralysis of children may be readily
distinguished from anterior poliomyelitis by the slow and
gradual development of the paresis, which rarely goes on to
complete paralysis, by the muscular tension and contraction,
the increased irritability of the tendons, and by the absence of
atrophy and the reaction of degeneration.

Amyotrophic lateral sclerosis begins in the upper extremities,
which become more or less paralysed and wasted, while the
antagonists of the paralysed muscles become rigid and con-
tracted; the arm is held tightly to the body, the forearm is,
flexed and pronated, and the hands and fingers are strongly
flexed. The initial fever is absent, and the subsequent progress
of the disease totally differs from that of anterior poliomyelitis.

The peripheral paralysis of single groups of muscles from
pressure on their nerves by tight bandaging or other causes will
be distinguished from anterior poliomyelitis by the absence of the
characteristic initial stage, the strict limitation of the paralysis
to the area of distribution of a single nerve trunk, the occurrence
of an injury to the nerve, the presence of disturbances of sensi-
bility, and the rapid recovery which generally takes place.

§ 402. Prognosis. — Anterior poliomyelitis does not appear
ever directly to threaten life ; and consequently, so far as life is
concerned, the prognosis is very favourable. Tt is, however,
possible that some of the children who die from convulsions
may be suffering from the initial stage of this affection, although
this opinion has not yet been confirmed by post-mortem
examination.

So far as complete recovery is concerned the prognosis is un-
favourable. In recent cases, therefore, the only prognosis we are
warranted in making is, that recovery will take place to a very
considerable extent, but that a certain amount of permanent
paralysis, with atrophy and deformity, is likely to be left
behind. The electrical reactions of the paralysed muscles form
a valuable aid in prognosis. If the faradic contractility of
certain muscles and nerves is diminished at the end of five
days and abolished during the course of the second week, these

SPINAL CORD AND MEDULLA OBLONGATA.

133

'ill, according to the law of Duchenne, remain permanently
aralysed and atrophied; and, conversely, when it is not
bolished by that time, the muscles will regain their mobility,
nd the restoration will be the more prompt and complete the
ass their faradic irritability is diminished. After the second
reek the galvanic current may be usefully employed to test
he probability of the degree of recovery which may be ex-
acted in the paralysed muscles. So long as a muscle, or even
portion of the muscle, responds in the slightest degree to
ither current, a certain degree of recovery of motor power may
ie expected.

The muscles that do not recover a certain amount of motor
ower during the first few months seldom recover at a later
eriod; and after six months of complete paralysis all hope of
3COvery may be abandoned, although even then slight and
artial improvement may occur under appropriate treatment.

The usefulness of the paralysed limbs may, however, be
reatly improved by means of orthopoedic operations, gymnas-
cs, and electrical treatment. The prognosis in this respect
ill depend upon the degree and extent of the paralysis and
:rophy, the amount of deformity already present, the age of
ie patient, and the duration of the disease at the beginning
t the treatment.

§ 403. Treatment. — The treatment may be subdivided into
lat which is appropriate during the acute initial stage and that
hich is to be adopted during the subsequent stages of paralysis,
trophy, and deformity. During the initial stage, when fever
present, rest in 'bed is absolutely necessary, and leeches may
3 applied over the lumbar and cervical enlargements. Rubbing
i of mercurial ointment and counter-irritation by means of
ncture of iodine and blisters have been recommended, but
iese measures should certainly not be adopted until the
:mperature has fallen to the normal standard. Ergotine has
3en employed subcutaneously in doses of one-fourth of a grain
■r a child from one to two years of age, one-third of a grain
>r one from three to five years, half a grain for children from
' ve t° ten years of age, and a grain for patients upwards of ten
sars of age, repeated either daily or twice a day, according to

134

SYSTEM DISEASES OF THE

the severity of the symptoms as tested by the degree of fever
(Althaus). Belladonna has been employed with apparent
benefit in this stage of the affection. Iodide of potassium
has also been administered, but it is a more appropriate
remedy when the thermometer indicates that the fever has
subsided, and it is then that mercurial inunction and counter
irritation can be employed with benefit. For my own part I
should trust during the feverish stage to the application of ice
along the spine, or the employment of Priessnitz's cold com-
presses about the trunk, and frequently repeated small doses of
aconite, given internally; and when the fever had subsided
I would then give iodide of potassium internally, and use mild
counter irritation along the spine, followed by the application
of mercurial inunction. By the first method I would hope to
arrest the active inflammatory process and limit its extension,
and by the second to aid the removal of the products effused
into the grey substance of the anterior horns, and thus promote
recovery.

Eesolution of the changes within the cord may be advanced
by everything which aids the nutrition and advances the tissue
changes of the body generally. A very nutritious and abun-
dant diet should be prescribed with prolonged sojourn in the
open air; mountainous or sea air is especially useful. The
thermal springs of Wildbad, Teplitz, or Gastein have been
specially recommended.

The constant galvanic current should be used as soon as
the fever has subsided, and it should be made to pass through
the diseased area of the cord. If the leg alone be affected,
the current should be directed to the lumbar enlargement; if
an arm only be affected, the cervical enlargement must be
acted upon ; and if the muscles of the trunk suffer likewise, the (
whole dorsal region of the cord should be included in the circuit.
In order to reach the cord, it is better to place one pole on the i
spine, and to apply the other to the anterior surface of the i
trunk. The electrodes should be large, the one placed over I
the back being large enough to cover the entire diseased area i
(Erb) ; the force of the current should be gentle, and the apph- i
cation continued for from three to ten minutes according to
the extent of the lesion (Althaus). Erb has recommended that ;

SPINAL CORD AND MEDULLA OBLONGATA.

135

<ie current be sent through the cord first in one direction and
len in another, but Althaus prefers the action of the positive
Die alone. The treatment must be continued for a long time,
ad afterwards repeated at intervals for years.
At the later period of the disease, when atrophy of the
aralysed muscles has set in, a peripheral application of the
mstant current and faradisation of the paralysed nerves and
luscles may be combined with the application of the current
> the spine. So long as the nerves and muscles have not
atirely lost their faradic irritability, local application of the
iradic current will be of service. The constant current, how-
ver, is on the whole superior to the induced, even for peri-
heral application, since in the majority of cases it is the only
yent which will produce any muscular response. Appropriate
vmnastic exercises of the muscles, shampooing and friction,
ith or without stimulating liniments, may be employed as
ljuncts to the electrical treatment. When the case comes
nder treatment, six months or longer after the invasion of the
isease, iodide of potassium is useless, and greater benefit may
b expected from phosphorous and cod -liver oil. Arsenic has
so been highly recommended at this stage of the disease,
he use of strychnia has been advocated, especially in the form
: subcutaneous injection, but I have never seen any good
isults from its employment, although I have seen the remedy
ushed to an almost dangerous degree. A strenuous endeavour
lould be made to prevent the occurrence of contractures and
eformities. A great deal may be done in this respect by means
f electrical treatment, gymnastics, and light frictions. In
: uarding against talipes equinus, Volkmann advises, during
i le earliest stages of the disease, that, when the patient is lying
i own, the foot be fastened to a light footboard by means of
flannel bandage, and its extremity drawn up somewhat
i awards the leg. Children should wear stout laced boots, with
steel shank on the outer or inner side, or with the sole slightly
bicker on one side, so that the tendency to the development of
ilipes varus or valgus may be counteracted. The formation of
alipes calcaneus may be counteracted by supplementing the
efective action of the posterior muscles of the leg with a
itrong indiarubber band or ring, which passes from the heel

136

SYSTEM DISEASES OF THE

to a trough-like fixture that is applied to the leg just below
the knee, and which is held firmly in its place by a side-bar
fastened to the shoe. In the severer forms tenotomy and
forcible means of correction must be adopted; but it is no part
of this work to enter into the details of orthopoedic surgery, and
the reader must, therefore, be referred to special works for the
further discussion of the subject.

2. Poliomyelitis Anterior Chronica {Chronic Atrophic

Spinal Paralysis),

§ 404. Definition. — Chronic atrophic spinal paralysis on
adults presents itself as a motor paralysis associated with
muscular atrophy, which begins in the lower extremities, and
gradually progresses upwards until the muscles of the trunk
and upward extremities are involved. The affection may
terminate in death from respiratory paralysis, or in gradual
recovery, the motor power returning in the reverse order to
that in which it was lost.

History. — Duchenne first described this affection in 1849, then va,
1852, and he gave a detailed description of it in the third edition of his
Electrization Localises, in 1872. He believed on theoretical grounds that
the disease consisted in chronic degeneration of the grey anterior horns,
and consequently he designated it " Paralysie generale spinale anterieure
subaigue." Single instances of the disease have since been described by
various authors, such as Poche", Frey, Erb, Webber, Cornil and Lepine,
Klose, Goltdammer, Bernhardt, Aufrecht, and others.

§ 405. Etiology. — The causes of this disease are exceedingly
obscure. All the cases which have been observed occurred
in adults between the ages of thirty and fifty years.

Amongst the exciting causes the most frequent are traumatic
injuries, such as a fall on the back or hip, exposure to severe
cold, damp dwellings, and alcoholic and sexual excesses.
Chronic lead poisoning leads to a condition very similar to
chronic atrophic spinal paralysis.

§ 406. Symptoms. — The first symptoms are usually lassitude,
and fatigue in walking, with pain and stiffness in the loins and

SPINAL CORD AND MEDULLA OBLONGATA.

137

wer extremities, which may be accompanied by slight fever, gas-
sic disturbances, and headache. The patient may also complain

various paresthesias After a time there is distinct muscular
eakness, sometimes only in one, at other times in both legs,
he muscular weakness gradually increases, the movements of
ie ankle-joint being usually more interfered with than those
' the hip-joint. After a time the paresis increases to complete
iralysis of single muscles and groups of muscles, or of the
itire extremity. The muscles are flaccid and soft, and no
distance is offered to passive movements of the paralysed
ctremities. The rapidity with which the paralysis takes place
iries greatly. Sometimes it occurs in a few days, sometimes
3t till after the lapse of many months, or even years.

Soon after the paralysis is established the affected muscles
3gin to waste ; the calves of the legs become converted into
ose, flabby sacks, the muscles of the thigh and gluteal region
•ow thin and soft, and the limbs may ultimately be reduced to
condition in which the skin appears to rest immediately upon
ie bones. Fibrillary twitchings of the muscles usually accom-
iny the earlier stages of atrophy. Reflex action, both cuta-
2ous and tendinous, is completely abolished in the paralysed
uscles.

The sensibility of the skin usually remains normal ; but
:casionally the patient may complain of a slight degree of
isensibility and numbness.

The paralysis gradually spreads to the upper extremities,
leir movements become awkward and feeble, and complete
aralysis of them ultimately supervenes. All the muscles of
ie upper extremities are not simultaneously affected; at times
ie extensor muscles of the forearm are earlier and more
iverely paralysed than the rest; at other times the flexors and
ltrinsic muscles of the hand are the first to be attacked ; and,
J a rule, the fingers and hands are more severely paralysed
lan the forearm and shoulder. The hands assume characteristic

> ositions, and the arms lie flaccid and immovable as they are
laced. Rapidly progressive atrophy ensues, Avhich leads to the

i'.ighest degrees of emaciation, especially in the hands and fore-
rms. Reflex action is generally abolished in the paralysed

huscles, sensation is normal, but the . patient may complain of

138 SYSTEM DISEASES OF THE

numbness in the fingers, and of paresthesia in the region of
distribution of the ulnar nerve.

The muscles of the back and abdomen are occasionally
implicated ; the patients can no longer sit up ; expiration,
coughing, sneezing, and defecation are rendered difficult. The
bladder, rectum, and sexual organs remain entirely unaf-
fected. There are no bed-sores, and the general health is
satisfactory.

The electrical phenomena in the paralysed nerves andj
muscles are the same as in acute anterior poliomyelitis, only
modified slightly in correspondence with the slower develop-
ment of the malady.

Duchenne showed that faradic excitability was diminished
at an early period of the paralysis, and was soon entirely lost.
In a case observed by Erb the nerves did not respond either to
the faradic or galvanic currents, and the muscles manifested
the typical reaction of degeneration.

During recovery the electrical excitability returns to the
normal standard only very slowly and gradually. The further
course of the disease is somewhat variable. In the majority o
cases the paralytic symptoms remain stationary for a time
although the muscular atrophy may continue to advance to somea
extent and moderate "paralytic contractions" to be developed.!
After some weeks or months gradual improvement sets in, whichb
begins in the arms and hands, and as it gradually advances fromr
muscle to muscle the galvanic excitability of the muscles sinks,
more and more, and slowly gives place to the normal reaction,}
while the contractures also gradually disappear.

Recovery is so slow that it is only after the lapse of months
that the patients can feed themselves and perform other actions!
with their hands.

The improvement extends after a time to the lower ex-*
tremities, the movements of the hip -joint first becoming more
powerful than those of the knee-joint, and last of all those ok
the foot and toes, until ultimately recovery may be complete.

More frequently, however, the recovery is incomplete. Cer-
tain sets of muscles, especially those in the region of distributioi
of the peroneal nerve, remain paralysed and wasted, so that tin
patient is partially disabled for life.

SPINAL CORD AND MEDULLA OBLONGATA.

139

In a certain small number of cases the disease progresses up-
suds to the medulla oblongata, when articulation, mastication,
'glutition, and ultimately respiration are interfered with, and
ie patient dies from asphyxia. At other times death super-
;nes from simple exhaustion. The progressive cases terminate
I from one to four years, and the favourable cases generally last
onths or years.

I am indebted to Mr. E. L. Luckman, one of the House
hysicians to the Royal Infirmary, for the notes of the following
ise : — :

Eliza R , aged 15 years, entered the Royal Infirmary on August

ird, 18S0, under the care of Dr. Ross.

History. — She has been weakly from infancy, and has worked in the
ill in a hot room since she was eleven years of age. About six months
o her work caused her an unwonted amount of fatigue, and she soon
terwards noticed that there was distinct loss of power in the left leg and
m, followed after a brief interval of time by weakness of the left leg.
ie weakness of the lower extremities gradually increased, so that in two
onths from the commencement of the attack she was compelled to leave
f work. She states that she has been unable to walk for the last three
Dnths, but it was found that, with assistance, she could make a few steps,
e limbs being, as it were, dragged forward. She has entire control over
e sphincters, and the only sensory disturbances complained of have
en " springing" pains in both legs.

Present Condition. — As she lies in bed she has a suffering, anxious
pression, and the muscles of the trunk and extremities are seen to be
uch wasted. The upper lips are dry and cracked, the teeth are covered
.th sordes, and the tongue has a beef-steak appearance.
' Left arm lies by the side, the elbow being removed two inches from the
>dy. The left forearm is flexed at right angles to the upper arm ; it is
Wrongly pronated, so that the ulnar side of the hand is directed upwards.
I ae hand is slightly extended on the forearm, the first phalanges are semi-
'xed on the metacarpal bones, the second phalanges are semi-flexed on
i e first, and the third on the second. The muscles of the ball of the
". umb are decidedly wasted, and those of the hypothenar eminence are
ho atrophied. The patient cannot produce opposition of the thumb,
jid adduction is feeble. The metacarpal bone of the thumb lies on a
ivel with the metacarpal bone of the index finger. The first phalanx of
lie thumb is extended, and slightly abducted, the second phalanx being
lightly flexed on the first. The general position of the right arm corre-
>onds to that of the left. Abduction of the thumb is, however, much
ore powerfully performed on the right side than on the left side, the
igers of both hands are in a semi-closed position, the index and middle
ss closed than the ring and little fingers. The interossei are atrophied,

140

SYSTEM DISEASES OF THE

causing deep grooves to appear between the metacarpal bones. All the
movements of the different segments of the right arm can be performed,
but supination of the forearm is very feeble, and can only be effected to
a position midway between pronation and supination. The left hand lies
powerless, in the position already described, and can be moved only to a
slight extent.

The lower extremities are almost completely paralysed, and when
the patient is asked to move them only a slight movement occurs, which
is effected by the muscles of the thigh. The anterior muscles of the calf
are quite paralysed. Both feet occupy the position of talipes equinus;
but the deformity can be readily made to disappear by producing
passive dorsal flexion of the foot. The different segments of the lower
extremities can be readily moved upon one another, the muscles are
flaccid, and there is a complete absence of the quadriceps tendo-reflex and
of ankle clonus. There are no tremors or fibrillary contractions of the
muscles of the lower extremity, but a few fibrillary contractions are
occasionally observed in the left hypothenar eminence. .The patient
cannot raise herself in bed, but on being asked to do so the recti muscles
of the abdomen may be felt to contract slightly, but have not sufficient
power to raise the body. With the exception of an occasional dribbling
of urine, the functions of the bladder and rectum are normally performed,
and the abdominal muscles contract slightly during the acts of defecation
and urination. When she is raised in a sitting posture she cannot hold
the body erect.

At the onset of the attack she had some "springing" pains in the
lower extremities, but these abnormal sensations have now disappeared.
She can distinguish two points touching the surface of the outer side of
the leg when two inches apart.

The sense of temperature is very accurate and that of touch good.;
Every form of sensibility is, indeed, perfectly normal all over the body.

The reflex of the sole of the foot, the gluteal, abdominal, epigastric, o
and scapular reflexes are absent.

The faradic contractility of the affected nerves and muscles is entirely;
abolished.

The galvanic current, applied percutaneously, obtains no response from:
the anterior muscles of the legs, even when fifty Leclanche' cells are used.

On the current being applied by electric acupuncture, the muscles o
the anterior part of the leg contract slightly with fifteen cells on cathod
closure, but do not contract on anodal.

When the galvanic current is now applied after the needles have beet,
removed, the anterior muscles of the leg contract distinctly on cathoda
closure with fifty cells.

The extensors of the right forearm contract slightly on cathodal closure
with fifty Leclanche' cells, but give no reaction on anodal closure.

The extensors of the left forearm give no response either on cathoda
or anodal closure or opening when fifty cells are used.

SPINAL CORD AND MEDULLA OBLONGATA.

141

The treatment consisted of the stabile application of the constant
rrent to the spiue for a few minutes daily, the current being also passed
• a longer period daily through the affected nerves and muscles. No
isible alteration took place in her condition until the evening of Sep-
nber 16th, when the breathing was observed to be embarrassed. At
ree o'clock in the morning the hands and lips were livid ; the eyes were
If closed ; her face and body were bathed in cold perspiration ; the voice
ts weak ; the diaphragm had ceased to play, respiration consisting chiefly
an elevation movement, and could not be made to contract by a strong
•adic current passed through the phrenic nerves. She seemed to rally
.ittle for a short time, but the diaphragm remained paralysed.
At nine a.m., September 17th, the surface was bathed in profuse per-
iration ; the skin was cold and clammy, the temperature being 97 6 ;
e lips and hands were livid ; and the pulse was feeble and quick, beating
2 in the minute ; the respirations were slow and ineffectual, but she
mained conscious to the last, and died at eleven a.m.
Autopsy. — Immediatly after death the body was placed face downwards,
e spine was covered with ice until the post-mortem, conducted by
\ Alfred Young, in the evening. No changes worth recording were
served by the naked eye in the brain, or even in the spinal cord. The
ins over the posterior surface of the lumbar region of the cord were
3atly distended. On making transverse sections of the spinal cord at
nervals of a quarter of an inch from above downwards, it was observed
■at definite areas of the white substance were of a grey colour and
latinous appearance. The grey substance of the central columns and
terior horns from the fifth or sixth cervical nerves downwards was
pressed below the white substance in each section, and appeared of
ft consistence, and was intersected in every direction by dilated and
gorged vessels.

Microscopic examination showed that the ganglion cells of the anterior
ey horns had almost completely disappeared throughout the entire length
the spinal cord {Fig. 163, 1 to 4). The central column and anterior horns
! ;re intersected with dilated blood-vessels, the walls of the vessels were
ickened, the nuclei of the neuroglia were greatly increased in number,
. d the tissue was infiltrated with leucocytes. In some sections the cells
: the vesicular column of Clarke appeared smaller and rouuder than
,>rmal, but on the whole this column did not seem to be much affected
th disease. The posterior grey horns appeared normal in every respect,
ae upward continuation of the central grey column in the medulla oblon-
ta {Fig. 163, 5) presented similar morbid appearances to those observed
the grey substance of the spinal cord, and the cells of the accessory
lclei, as well as those of the nucleus of the eleventh nerve, had
sappeared ; but the fundamental cells of the hypoglossal nucleus, instead
being destroyed, were hypertrophied. A few hypertrophied ceils were
■io observed in some sections in the centres of the internal and aiitero-
teral groups in the cord, especially in the cervical region, while others

SYSTEM DISEASES OF THE

were represented by small angular masses
without processes ; but all the accessory
cells, and, indeed, the majority of the funda-
mental cells in the cord, had disappeared!
without a trace of them being left.

On holding a section from the middle
of the dorsal region up to the light, a patch,
which was more highly coloured by carmine
than the surrounding tissue, could be dis-
tinctly observed in the posterior root-zone,
where it adjoins the column of Goll. It
began near the posterior commissure, and
extended backwards towards, although it
did not reach, the posterior surface of the I
cord. The deeply-stained portions were i
symmetrically placed on each side of the :
columns of Goll, and to the naked eye they
presented all the characters of patches of i
sclerosis (Fig. 163 , 2). Similar patches j
were observed in the cervical region, but I
they were more diffused than those in the*
dorsal region, their areas were larger, antii
they did not stain so deeply with carmine*
In many sections the peripheral layer ofg
the cord was deeply stained, this being,|
especially marked in the anterior root-zones 4
and columns of Turck. When the deeply^
stained portions were examined micro-.!
scopically, the connective-tissue septa werer,
found swollen, a few of the nerve fibres^
had disappeared, but the majority ok,
these were normal. The most remarkable ,
morbid alteration, however, observed waa
the great increase in the number of Deitert

cells. '

A large number of the nerve fibres o j
the anterior roots had undergone atrophj.

Us. 163 (Young). Transverse fectMS ofJi
Spinal and Medulla Oblongata at differ*
Zeis, from a case of chrome atrophic
paraiyk showing ^appearance o/^

ffiS^ ^Mid^orthe dorsal regie.,
3 Middle of the cervical enlargement ; 4 ,b&
Son on a level with the origin ot the seco
cervical nerve ; 5 Section of .the medf;
oblongata on a level with the middle third I
the olivary body.

SPINAL CORD AND MEDULLA OBLONGATA. 143

1 some of the bundles were replaced by connective tissue. A consider-
e number of the fibres, however, appeared normal.
Portions of the anterior muscles of the leg, and of those of the hypo-
)uar emineuce, were subjected to microscopical examination by Dr.
ech, who kindly examined those muscles for me, and submitted the fol-
ding report : —

" On transverse section the muscular fibres are seen to be separated
an undue amount of fibrous tissue, while the nuclei of the
iomysium are greatly increased in number. The fibres themselves
:y in diameter, some of them being considerably smaller than others,
I the nuclei beneath the sarcolemma are increased in number,
amiuation of longitudinal sections shows that the muscle corpuscles are
Teased in number, and that the structure of the muscular fibre is
;atly altered in other respects. Many of the muscular fibres are
,nular, their transverse striation is indistinct or wanting, and the
iscle corpuscles are increased in number. The most remarkable changes
served, however, consisted in an alteration of the normal relation of the
ltractile and interstitial discs. The contractile discs seemed to be
irtened, and swelled out laterally. In consequence of this change, the
srstitial discs appeared as transverse, more or less transparent, bands
ween the darker bars formed by the contractile discs, and the former
ng also narrower than the latter, the outline of the fibre has a rugose
serrated appearance.

'" Several nuclei are sometimes observed in the transparent bands,
ile one or more muscle corpuscles are obscurely seen in the darker
•s.

" It is doubtful how far the changes just described are the result of
ease, inasmuch as similar appearances may sometimes be seen, although

> rer to the same extent, in healthy muscle withdrawn during life by the
iscle trocar ; and the autopsy in this case being conducted a few hours

; 3r death, the muscle would have been placed in preservative fluid before

1 >t-mortem rigidity had taken place."

A case of chronic atrophic spinal paralysis has recently been
scribed by Aufrecht, in which a post-mortem examination
i been obtained, and the spinal cord, nerves, and muscles
ejected to careful microscopic examination. The appearances
3erved correspond on the whole pretty closely with those just
scribed. In Aufrecht's case, however, the ganglion cells of
3 anterior horns were by no means changed to anything like the
ne extent they were in the case observed by me. From a
reful examination of Aufrecht's description of the morbid
erations in the anterior horns, it is evident to me that the
idamental cells were hypertrophied, and that some of the

144

SYSTEM DISEASES OF THE

accessory cells were shrivelled, while probably a considerable
number of them had disappeared.

§ 407. Diagnosis. — The chronic may be distinguished from
the acute form of anterior poliomyelitis by the slow and gradual
manner in which the former and the sudden way in which the
latter begins. The subacute or chronic form has for some time
a progressive course, and extends more or less gradually
upwards, and the disease may terminate fatally or advance
slowly towards recovery. The course of this disease, therefore,
differs greatly from that of the acute form.

Progressive muscular atrophy may be distinguished from
chronic atrophic spinal paralysis by the circumstance that in
the former the paralysis and atrophy proceed side by side,
while in the latter the paralysis precedes the atrophy ; again,
in the former the atrophy is partial, and in the latter the
muscle wastes as a whole. In progressive muscular atrophy
the middle form of the reaction of degeneration is met with,
and reflex action is retained ; while in chronic atrophic spinal
paralysis the reaction of degeneration is well marked and reflex
action is abolished; and, lastly, progressive muscular atrophy
runs a slow and always unfavourable course, while chronic
poliomyelitis runs a comparatively rapid course and frequently
ends favourably. It is not improbable that some cases which
are usually classed as partial progressive muscular atrophy, but
which are not progressive, really belong to the category of
chronic anterior poliomyelitis.

Amyotrophic lateral sclerosis resembles chronic poliomyelitis
in the paralysis and atrophy of the muscles of the upper ex-
tremities, but in the lower extremities there is paralysis without
atrophy along with tension of the muscles, contractures, and
increase of the tendon reflexes, and only the middle form of the
reaction of degeneration is met with. The diagnosis between
paralysis ascendens acuta and chronic poliomyelitis will be
subsequently described.

Chronic atrophic spinal paralysis may be distinguished from
transverse myelitis, multiple sclerosis, tabes dorsalis, spastic
spinal paralysis, and all other forms of chronic spinal disease,
if due attention be paid to the state of the sensibility, the

SPINAL CORD AND MEDULLA OBLONGATA.

145

functions of the bladder, the nutrition of the skin, reflex action,
ind the electrical excitability of the muscles.

§ 408. Prognosis. — The prognosis is comparatively favourable.
Recovery takes place in the majority of cases, and improvement,
as a rule, goes much further than in the acute form. At the
;ame time it must be remembered that chronic atrophic spinal
oaralysis is not like infantile paralysis in being free from all
langer to life. The more partial forms of the disease are never
langerous to life, although they may lead to permanent atrophy
>f the muscles affected.

§ 409. Treatment. — The same principles are applicable in the
reatment of this disease as for subacute and chronic myelitis
generally. Antiphlogistic treatment should first be employed,
,nd afterwards the use of the galvanic current and a stimulating
.nd supporting treatment.

3. Progressive Muscular Atrophy.
Progressive muscular atrophy is, as its name implies, a pro-
ressive wasting of the voluntary muscles, which pursues a
ironic course, and attacks successively individual muscles and
roups of muscles.

§ 410. History.— Hippocrates made a distinction between paralysis
ith and without wasting of the limbs, and observed that the former was
curable. Cases of muscular wasting, but without paralysis, were pub-
*hed in the first half of this century by Abercrombie, Darwal, Cooke,
9ll, Romberg, Graves, Dubois, and Duchenne, but the affection was not
cognised as a distinct disease. Duchenne, Aran, and Cruveilhier, in 1850,
dependency of each other, gave more accurate descriptions of the
fection, and recognised . its claims to be regarded as a distinct type of
sease. Dr. William Roberts in 1858 collected all the information
isting on the subject up to that time in an essay entitled " On Wasting
dsy ;" aDd since that time the pathology of the disease has been in-
stigated by Gull, Lockhart Clarke, Luys, Charcot, Hayem, Leyden,
'iedreich, Erb, and mauy others.

| § 411. Etiology. — Hereditary predisposition is a powerful
' ctor in the production of progressive muscular atrophy. Dr.
oberts collected the histories of ten families in which a

146

SYSTEM DISEASES OF THE

tendency to the disease prevailed; but the cases described by Dr.
Meryon, which are included in this list, were probably instances
of the advanced stage of pseudo-hypertrophic paralysis. After
Dr. Meryon's cases are eliminated, it may be stated that out of
the eight families referred to by Dr. Roberts twenty-three indivi-
duals were affected, and of these four only were females.

In a case described by Hemptenmacher, the disease could be
traced amongst the branches of three families, who had re-
peatedly intermarried, and who had sprung from one parentage
a hundred and fifty years ago. In this instance males only were
attacked, but the disease was frequently transmitted through
the female. Friedreich found that the disease was transmitted
by a woman to her children, though they were the products of
three separate marriages. Trousseau mentions a family in which
the great-grandfather, grandfather, father, and son suffered from
the disease, the course of which closely coincided in all the
generations. Eulenburg mentions the case of a family where,
out of seven children, two brothers and two sisters were
attacked, while the remaining three brothers escaped.

The male sex shows a much greater tendency to the disease
than the female sex. Out of 176 cases collected by Friedreich
only 33 were females. The disproportion between the sexes
probably depends on men being much more exposed to the
exciting causes of the disease. Dr. Roberts asserts that women
of the working classes, such as washerwomen, domestic servants,
and sempstresses, are not much less liable to the disease than
men employed in kindred occupations, while on the other hand
females belonging to the middle and upper classes enjoy a
remarkable immunity from the disease. It is difficult to
explain the cases which arise in childhood and in which the
male members of the family alone are attacked. Mr. Darwin,
however, has shown that many variations which first appear in
one sex are transmitted to that sex only. If this fact does not
afford an explanation, it at least merges the special into a
general difficulty. With regard to the influence of age, the
disease is found amongst young adults and middle-aged in-
dividuals ; and where there is a marked hereditary tendency
to the affection, children are not unfrequently attacked. The
development of the disease in advanced life is exceptional.

SPINAL CORD AND MEDULLA OBLONGATA.

147

Progressive muscular atrophy is often developed during con-
valescence from acute diseases, such as typhoid fever, measles,
icute rheumatism, and cholera with protracted typhoid stage;
md Charcot and Joffroy have observed it to occur immediately
ifter childbed. Venereal excess, especially onanism, has been
supposed by many authors to be a fruitful source of the affec-
;ion, although the evidence upon which the opinion is founded
a doubtful. Chronic lead poisoning is not unfrequently
ittended by a diffused wasting of the muscles, closely resem-
bling progressive muscular atrophy ; and a similar wasting also
>ccurs in constitutional syphilis.

Of the exciting causes of the disease unusual muscular
;xertion deserves the chief place. That excessive muscular
efforts tend to develop the disease is shown by the fact that the
itrophy attacks by preference the groups of muscles which
inust be maintained in long-continued contraction with persons
bllowing certain avocations, such as blacksmiths, tailors,
nasons, and shoemakers. Betz observed atrophy of the
nuscles of the right side in smiths and saddlers, who had to
lo heavy work with their right hands, and Gull observed the
,ame in a tailor after excessive exertion. In the case of a
tonemason which came under my notice the atrophy began in
ihe muscles of the right hand. In persons who have to per-
orm manual labour the disease generally begins in the muscles
»f the shoulders, arms, and hands ; and the right side is
generally the first to be affected. In children the atrophy not
infrequently begins in the lumbar muscles, and extends to
hose of the lower extremities, a mode of invasion which is
>robably due to the preponderant use of these muscles in
tanding and walking. I have observed a similar mode of
□vasion in a collier, who was compelled to work in a bent
tosture.

Exposure to cold and wet appears to be of itself sufficient to
•roduce the disease. C. H. Richter saw a total atrophy of the
lands in a man who suffered from severe sweating of the hands
nd who was accustomed to bathe them in ice-cold water and
uow. Dume'nil observed atrophy of the lower extremities
fter long-continued standing in water while fishing ; but in
his case it is doubtful how much of the effect is to be

148

SYSTEM DISEASES OF THE

attributed to exposure to cold and how much to excess of
muscular exertion. The disease is doubtless more likely to
be developed when these causes are combined. Cases arising
from exposure to cold are subject to neuralgic or rheumatic
pains in the affected parts, hence these cases are frequently
assumed to be due to rheumatism. In this class of cases the
invasion is often sudden and accompanied by cramps and mus-
cular twitching (Roberts), and the atrophy is more apt to
extend to the muscles of the trunk than in cases due to
overwork. According to Dr. Roberts, of twenty-five cases
attributed to overwork eighteen were partial and only seven
general ; whereas of the sixteen cases charged to the agency of
cold six were local and ten general.

Injuries of various kinds may be the exciting causes of this
affection. In a youth, under the care of Dr. Roberts, who
ultimately died from implication of the respiratory muscles, the
first symptom of atrophy occurred in the ball of the right
thumb six months after the fall of a bale of cotton on his neck.
Cases similar in essential particulars are recorded by Clarke
and other authors. Local injury to some of the muscles of the
body is sometimes followed by progressive muscular atrophy.
Friedreich relates a case in which the hand had been crushed,
and subsequently the atrophy extended progressively upwards
over the entire upper extremity, and finally led to the com-
plication of bulbar paralysis. At other times the inflammatory
irritation appears to be propagated from neighbouring parts,
such as the shoulder and hip joints, and the disease appears at
times to have been caused by cicatrices or suppurating wounds.
These cases are grouped by Friedreich under the name of
myopathica propagata.

§ 412. Symptoms. — The invasion of the disease is slow and
insidious, and it is usually in existence some weeks or months
before its presence is discovered. The patient first experiences
some difficulty in performing certain movements; and on atten-
tion being directed to the affected limbs, some of the muscles
are discovered to be more or less wasted. At other times,
especially when the disease has been caused by exposure to
cold, the mode of invasion is attended by more prominent

SPINAL CORD AND MEDULLA OBLONGATA. 141)

symptoms. Paroxysmal pains, like those of rheumatism or of
neuralgia, are felt in the affected limb several weeks or months
before the atrophy of the muscles is noticed, and when once
the atrophy begins in these cases it proceeds more rapidly and
becomes more generalised than in the painless variety.

The disease usually begins in one of the upper extremities,
more commonly in the right, either in the interossei, the
muscles of the thenar and hypothenar eminences, or in those
:>f the shoulder. Eulenburg says that when the disease begins
in the hand the interossei (and especially the first interosseus)
ire generally attacked before the muscles of the ball of the
thumb; while the contrary opinion is held by Roberts and
Friedreich. The opponens pollicis and the adductor pollicis
are the first muscles to be affected in the ball of the thumb,
while the extensors, abductor, and flexor of the thumb are
spared for a long time, or may escape.

In some few cases the disease begins in the muscles of the
moulder, and in these the deltoid is almost always exclusively
iffected at first. When the atrophy begins in the lumbar
nuscles and lower extremities children are almost always the
•subjects of the disease, and it then frequently simulates
oseudo-hypertrophic paralysis, which will be subsequently
lescribed. During the progress of the disease certain muscles
or groups of muscles are attacked while their neighbours are
spared, and the healthy or less atrophied muscles overcome
me resistance of those more diseased, so that characteristic
contractions and deformities are produced.

The disappearance of the interossei is shown by the deep
'urrows which appear between the metacarpal bones, the
-henar and hypothenar eminences are flattened, and the dis-
ippearance of the muscles of the palm brings into view the
liverging flexor tendons which are stretched between the wrists
md the bulging bases of the fingers (Roberts). The deformity
produced by paralysis of the interossei gives to the hand the
appearance of the talons of a bird of prey ; hence it has been
called the claw-shaped hand or main en griff e (Fig. 77). This
deformity, however, is not peculiar to progressive muscular
atrophy, inasmuch as it may be caused by injury to the ulnar
nerve. In consequence of the atrophy of the opponens and

15q SYSTEM DISEASES OF THE

adductor pollicis, the thumb is extended aud abducted (Plate

"whence forearm is affected, the anterior, posterior, or
exterior aspect of the limb is flattened according as the flexors,
extensors, or supinators are affected. _

When the muscles of the shoulders are affected, the arms may
hang by the side or rather in front of the patient, as if they were
merely attached to him by strings and did not belong to him ;
the natural rounded configuration of th e shoulders is replaced
by a hollow in which the palm of the hand may be lodged
under the projecting acromial and coracoid processes of the
scapula which stand out in relief. The biceps and the other
muscks of the arm may also waste, so that the limb loses its
ronuduess and becomes flattened, aud the humerus appears
to be surrounded merely by the skin.

When the abdominal muscles are affected, the lumbar curve
is greatly exaggerated by the unopposed action of the erector
PiL the abdomen is loose and protruding, hut the thorax is
held well forwards, so that a plumb-line let drop from the most
prominent of the spinous processes of the vertebra will pass
well within the sacrum, contrary to what occurs when the
lumbar muscles are affected. When the atrophy is unequally
distributed on both sides of the body scoliotic or kyphotic
bending of the vertebral column may be produced. When,
the erector spina, and extensors of the thigh are implicated,,
the deformities produced, as well as the gf\*™ ^
to those seen in pseudo-hypertrophic paralysis, and it is un-
necessary to describe them here.

When the lower extremities are invaded, deformities occur,

corresponding to those observed in the »P^£™
but the former are of much rarer occurrence than the latto
The various forms of club-foot may appear, especially the para,

^ ^l^^piratory muscles, as the pectorahs major,
serratus magnus, trapezius, &c are frequently implicated ; anc
a hou^h the wasting and loss of power of these muscles do n
Z tfy endanger life, yet they may do so indirectly, inasmuc
as a slight intercurrent attack of bronchitis may lead
Iphyxia since the inability to make a strong expiratory effo,

SPINAL COED AND MEDULLA OBLONGATA. 151

prevents the tubes from being effectually cleared of mucus. In
the later stages of the affection, the diaphragm and the inter-
costal muscles become affected, expectoration fails, mucus collects
in the tubes, and the patient dies asphyxiated.

The facial, lingual, and laryngeal muscles, as well as the
muscles of deglutition, are frequently affected towards the ter-
minal period of the disease ; but the symptoms caused by
implication of these muscles will be described as labio-glosso-
laryngeal paralysis.

As the following case, which is carefully reported by Mr.
Cullingworth * affords a good example of progressive muscular
atrophy, where the muscles of the back and some of the
muscular groups of the lower extremities are affected, I shall
quote it at length : —

Charlotte A , aged forty-one, admitted into St. Mary's Hospital,

'Manchester, February 3, 1878. She is married, and has had three living
children, all of whom died in infancy. There is no family history of
nervous disorder or of impairment of power of locomotion. Her father,
an intemperate man, died of chest disease at the age of thirty-six ; her
mother died in her fiftieth year of heart disease. Of six brothers and
i sisters, two died in infancy, one from the consequences of her husband's
ill-treatment, and three are living in good health.

She worked in a factory from the age of nineteen until five years ago,
having had constantly two, and sometimes more, looms under her charge.
The nature of her work necessitated the stooping posture, and for some
years this had been a painful strain to her. She was a long time in
straightening herself when the day's labour was over, and the process was
not only difficult but painful. About six years ago, when she was preg-
nant of her last child, she was suddenly seized with an attaok of uncon-
sciousness while at her work ; she fell down, and was carried unconscious
home. She had other attacks of the same kind both before and after her
confinement, and, indeed, had one shortly before her admission. Her
husband says that there is absolutely no warning, that she frequently
hurts herself in falling, that she foams at the mouth and rolls her eyes,
: but that there is no violent struggling. It was on account of these fits
that her overlooker advised her, for her own safety, to cease work several
u years ago. She cannot tell exactly when the peculiarity in walking was
t first noticed, but is certain that she has had difficulty in rising from a
. chair ever since her last confinement. This difficulty has gradually
i increased.

She is a thin, sallow-complexioned woman, of average height, and of
* The Medical Times and Gazette, vol. ii., 1878, p. 121.

152

SYSTEM DISEASES OF THE

feeble intellectual power. Her lips become markedly livid on the least
exertion or exposure; the whole body is sensitive to cold. There is
nothing abnormal in the condition of the thoracic or abdominal viscera.

Examination while Standing. — The head is erect, and movable by the
patient in all directions ; the shoulders are somewhat higher than usual in
a woman ; the upper part of the spine is carried backwards more than
usual. A plumb-line from the most prominent of the spines of the upper
dorsal vertebrae falls an inch behind and away from the sacrum. The
knees are very slightly bent ; the feet are placed firmly on the ground,
with the heels touching, the toes turned outwards and extended naturally.
The upper extremities present no appearance of muscular deficiency, and
the deltoids are prominent arid well developed. The lower extremities
present this anomaly : that while the thighs are thinner, softer, and more
flaccid than natural, the calves, on the contrary, are of a size quite out of
proportion with the muscular development of the rest of the body. The
following measurements were taken : — Circumference of upper arm below
pectorals, 9Jin. ; forearm at thickest part, 9£in. ; middle of thigh, 16in. ;
thickest part of calf, 14jin. It will thus be seen that the circumference
of the calf is nearly equal to that of the middle of the thigh. This

Fig. 164. Fig. 165.

Fig. 164 shows the position assumed by the scapulae when the arms are extended
forwards. There is a deep sulcus between the two bones, the posterior borders
of which project two inches from the costal wall. The posterior border of the
left scapula is parallel with the median line, having been adjusted by the action
of the serratus magnus, whose fibres (passing downwards, outwards, and for-
wards from the lower angle) are seen contracting beneath a fold of skin. This
movement of adjustment has not yet taken place on the right side, where the
lower angle of the scapula is nearer the vertebral column, a Uttle higher, and
altogether more prominent than on the opposite side, owing to the unopposed
action of the deltoid; the serratus magnus, being in a condition of relaxation, is
much less noticeable on this (right) side. The transverse fibres of the trapezius,
passing from the outer half of the spine of the scapula to the last cervical and
first dorsal vertebrae, are well seen ; with these fibres the upper and unaffected
half of the muscle abruptly terminates.

Fig. 165 shows the appearance of the back when a healthy subject is placed in the
same attitude. The scapulse are applied so closely against the costal wall that,
although the person is by no means stout, the outline of the bone is scarcely
traceable. The lower angle is in the axillary line.

SPINAL CORD AND MEDULLA OBLONGATA.

153

circumstance gave rise to a suspicion of pseudo-hypertrophy, and a minute
oortiou of muscle was withdrawn from the calf by the muscle-trocar, and
dndly examined for me under the microscope by my friend Dr. Dreschfeld.
The muscular tissue was not found to have uudergone any change.

As the patient stands at ease, with her back to the observer, attention is
at once attracted to the unusual projection of the posterior borders of the
icapulae. They stand back an inch from the posterior chest-wall, retaining
.heir parallelism with the median line, and leaving a fossa between them four
.nches in breadth and an inch in depth, bounded on each side by a wall of
■ikin, which passes perpendicularly from the scapular borders to the back of
;he thorax. The condition of the inter-scapular muscles can be best studied
vhen the arms are held horizontally forwards {Fig. 164, and Plate II.,
I and 6). The spinal borders of the scapulae then project backwards
■o a distance of two inches from the chest-wall, and approach within an
nch and a half of each other, still preserving their parallelism. Between
■he anterior surface of the scapulae and the chest- wall there is a deep groove
)osteriorly, easily admitting the tips of the fingers when they are bent
>ver the posterior edge of the scapula. The trapezius, perfectly developed
n its clavicular portion and in the upper half of its middle third, ter-
ninates abruptly by a strong bundle of fibres stretching across from the
pinous processes of the last cervical and first dorsal vertebrae to the outer
' <alf of the spine of the scapula. There is not a trace of the muscle to be
alt below this point. Between the posterior border of the scapulae and
he spinal column there are no muscular fibres to be felt, except one little
ihin band passing to the middle of the edge of the scapula. This is all
hat remains of the rhomboids. The latissimus dorsi has also disappeared,
nd there is no response to the strongest faradic current in the course
ither of this muscle or of the lower half of the trapezius, or of the rhom-
oids, except in the slender fasciculus of fibres just named. On the other
.and, the levator anguli scapulae and serratus magnus can be felt to con-
ract forcibly, and they respond readily to a moderate current. The lower
agment of the latter muscle, passing downwards and forwards from the
>wer angle of the scapula to the lower ribs, stands out prominently when
le arms are raised ; and, being uncovered by the latissimus dorsi, can be
rasped underneath the skin, which is raised into a fold by the contraction
f the muscle. The deep scapular muscles (supra-spinatus, infra-spinatus,
ib-scapularis, teres minor, and teres major) are well developed and easily
efined. The pectoral muscles are also unaffected.

The patient cannot elevate her arms vertically ; the nearest approach
) this which she can make is to raise her elbows until they are on a level
ith the ears, at a distance of about nine inches from the head. When
lis position is assumed, instead of the scapula) being closely applied to
ie chest-wall, and rotated so as to bring the lower angle outwards and
>rwards as far as the axillary line, the posterior borders of the scapulae
K re brought into actual contact with each other at their upper extremity,
1 ightly diverging from above downwards, so that the lower angles are two

154

SYSTEM DISEASES OF THE

Fig. 166.

inches apart. The anterior face of the scapula is in the meantime one
inch and three-quarters behind and away from the thorax. When the
arms are stretched out horizontally right and left, the posterior borders of
the scapulse touch each other both at their upper and lower angles, on a
plane one inch and three-quarters behind the chest-wall. If the patient
places one hand upon the opposite shoulder, the scapula assumes the
following position : — The external angle is raised along with the whole
Bhoulder, the internal angle is depressed, the inferior angle is drawn out-
wards, the posterior border projects an inch from the chest-wall and is
distant from the vertebral column three inches at its upper end and four

inches at its lower. When, again, the
shoulders are drawn back, the elbows
placed by the side and flexed, so that
the fingers point upwards, with their
palmar aspect directed forwards, the
posterior borders of the scapulse are
pressed forcibly together, closing over
the vertebral column on a plane two
inches behind it (see Fig. 166).

The patient, in attempting to carry
the arm behind the trunk, cannot
rotate it so as to direct the posterior
aspect of the upper arm outwards, or
carry the upper arm from the plane of
the axilla towards the middle line of
the back.

Walking. — In walking there is &i
general unsteadiness of gait, but no
waddling. The knees are slightly
flexed, and the head and shoulders are
held well back, so that the feet are
always kept in front of the patient.
The mode of progression remains un- j
altered when the patient closes her
eyes. Ascending stairs is a matter of
extreme difficulty, and it is exceed-
ingly painful to witness her condition
of exhaustion and lividity after making
the effort.

Sitting. — When about to sit. down
she steadies herself for a moment,
grasps her thighs firmly with her
hands, and falls suddenly on to the
chair as though the trunk were a dead
weight. At the moment, and in the
act of sitting down, the trunk is in-

Fig. 166 shows the patient, Char-
lotte A , when the shoulders

are thrown back and the scapulse
brought together. The posterior
borders are partially in contact
on a plane two inches behind the
costal wall. The sharp edge of
the unaffected half of the trape-
zius is again clearly seen, as well
as the inferior segment of the
serratus magnus on each side.
The levator anguli scapulas is
acting more powerfully on the
left than the right. This draw-
ing also shows the loss of rotun-
dity in the gluteal region, and
the remarkable contrast between
the hypertrophied calf and the
attenuated muscles of the thigh.

SPINAL CORD AND MEDULLA OBLONGATA.

155

-oluutarily thrown forwards upon the thighs, and it remains in that
•osition until by moving the feet forward and planting them firmly, and
W then grasping the knees, she pushes up the trunk into the erect
>osture " by force of arms."

Rising from the Sitting Posture— She rises from the sitting posture
frith great difficulty, and in the following manner :— Compressing her
lips, she separates the feet widely, and grasps both her knees ; she then
lexes the trunk upon the thighs until the trunk is horizontal, and raises
•he buttocks from the chair by a movement of extension at the knee. In
ihis stooping attitude she shuffles away from the chair until she reaches
omething to lay hold of — mantelpiece, table, or bystander — when, having
ested for a moment, she raises the hands, one by one, from the knees,
nd clutches firmly the object near which she has halted. Then very
lowly and with great effort, keeping the back stiff and straight, she raises
lerself by means of the arms into the upright position. The mode in
?hich she rises from the floor is even more painful to witness. Placing
ier hands on the ground in front of her, she first of all scrambles on to
ier hands and knees. In this posture she makes her way to the nearest
vailable article of furniture, seizing which, she regains her feet. The
runk, however, is still horizontal, and it is the tremendous, and for a long
ime futile, efforts that she now makes to straighten herself that consti-
nte the most distressing part of the performance. Striving to obtain a
rm purchase with her feet, the knees being fully extended, the feet slip
iackwards time after time. Eventually, after violent exertions, which
save her exhausted and breathless, she accomplishes her task.

Flexion of Thigh upon Pelvis, &c. — When lying in bed horizontally
pon the back, she is able to flex the leg upon the thigh, and the thigh
pon the trunk, so long as the heel remains upon the bed ; but when the
3g is fully extended she is unable to lift the heel a single inch from the
lane of the bed. As she sits, with the knees flexed, she cannot raise the
)ot from the ground ; but the movements of adduction and abduction
re accomplished fairly well. She crosses one thigh over the other by the
allowing manoeuvre : — Supposing the right thigh is to be crossed over the
?ft, the left knee, bent to an acute angle, is adducted and pushed under
be right knee, which latter is thus lifted up and carried over to the left
ide, resting upon its fellow.

Ankle. — The movements at the ankle-joint are performed without
ifficulty.

Owing to the kindness of Mr. Cullingworth I have had
epeated opportunities of examining this woman, and the only
ddition I should like to make to his valuable report of the
ase is to draw attention to the gait of the patient, especially
oting the points in which it differs from the gait characteristic
f pseudo-hypertrophic paralysis.

156

SYSTEM DISEASES OF THE

In the case of this woman the feet are held close to each other, and, as
Mr. Cullingworth observes, the gait is not waddling. In walking the head
does not deviate laterally from the middle line during the transference of
the centre of gravity from the active to the passive leg, but it may be
observed to advance by a series of vertical curves. In his remarks on the
case Mr. Cullingworth observes that the patient is unable, when lying
horizontally on her side with the legs extended, to separate her thighs,
thus showing that the gluteus medius and minimus are, at least to some
extent, affected by paralysis. On placing one's own hands over the pelvis
of the patient, one being held on each side immediately above the tro-
chanter of the femur, it is felt that the gluteus medius on the side of the
active leg does not contract during locomotion. The consequence is that,
instead of the pelvis on the side of the passive leg being slightly elevated
as in health, by the contraction of the gluteus medius of the opposite
side, so as to allow the leg to swing forwards, it is distinctly felt to drop
on that side to a lower level. The pelvis, therefore, forms a more or less
acute angle with the active leg instead of, as in health, forming an obtuse
angle with it. It is, however, maintained in a nearly horizontal position I
by the fact that the active leg itself slants downwards and inwards from I
the hip-joint. The line of gravity passes through the pelvis about its j
middle ; and in order that it may pass through the arch of the foot of
the active leg, the latter must occupy a position directly below the middle
of the pelvis, and consequently the hip of that side projects outwards.
The passive leg is prevented from swinging forwards with the normal I
pendulum motion, inasmuch as the hip-joint on that side becomes lower
when the leg is raised off the ground, instead of being elevated by con-
traction of the gluteus medius of the opposite side as in health. The
necessary elevation of the passive foot is obtained by strong flexion of
the thigh upon the body, so that the legs, as described by Mr. Culling-
worth, appear to be in advance of the body. The alternate projection of
the hip on the side of the active leg, and the alternate falling down of
the hip on the side of the passive leg during successive steps, render the
gait of this patient totally unlike that which is so characteristic of pseudo-
hypertrophic paralysis.

The loss of muscular power keeps pace with, the atrophy, and
is, as a rule, directly in proportion to the degree of the latter,
and so long as any muscular fibres are left, they can be made
to contract by voluntary effort. For a very long time, indeed,
the various movements are capable of being performed, although
with much diminished power, and it is only in the last
stage of the affection that complete immobility of the limb is
produced.

At times the loss of motor pow.er apparently much exceeds

SPINAL CORD AND MEDULLA OBLONGATA.

157

the loss of muscular substance ; but in these cases the bulk of
he muscles is maintained or even increased by an interstitial
atty hyperplasia, while the individual muscular fibres are
itrophied, so that the disproportion between the loss of mus-
clar power and the loss of muscular substance is only apparent
md not real. This condition will be more fully described when
he closely-allied disease called pseudohypertrophic paralysis
omes under consideration.

The reflex movements are occasionally exaggerated, but this
iiodification is not constant (Jaccoud).

The electrical reaction of the atrophied muscles, as a rule,
orresponds closely with the diminished volume of the muscles
nd the loss of voluntary power. The normal faradic contrac-
ility is maintained until the muscle has undergone a high
egree of atrophy, and it is only in the last stage of muscular
trophy that the excitability is diminished or abolished. It
eed scarcely be added that, although the faradic excitability is
ot diminished, yet the energy of contraction becomes weaker
and weaker in proportion as the contractile elements of the
mscle disappear. The faradic excitability of the nerve-trunks
retained longer than that of the muscle, and both disappear
>me time before complete loss of voluntary power occurs,
alvanic muscular contractility usually remains normal for a
»ng time, although the energy of the contraction diminishes
i proportion to the degree of atrophy, so that stronger
irrents are required to produce a minimum contraction
^ulenburg). The galvanic excitability of the nerve-trunks
•so remains unimpaired for a long time. Rosenthal has directed
Mention to the fact that the nerve-trunks behave differently
, different points in their course, so that while electric stimu-
tion applied to a portion situated near the centre may pro-
ice normal effects, its results may be less than normal, or
itirely wanting when a more peripheral tract is stimulated,
ight qualitative changes in the muscular reaction may attend
ie ultimate stage of atrophy.

Fibrillary contractions of the affected muscles are fre-
during the entire active stage of the disease,
hese consist of vibratory tremors or quivering of the muscular
3res. They occur spontaneously, but may be provoked by

158

SYSTEM DISEASES OF THE

gently tapping the surface, by exposing to the air parts which
are usually covered, by electrical excitation, and by active or
passive movements of the affected muscles. These fibrillary
contractions are sometimes the earliest symptoms of a fresh
advance of the disease into parts previously unaffected, and
they disappear altogether when the atrophy has reached an
extreme degree, or when its progress is arrested (Roberts).

Occasionally clonic or tonic contractions of entire muscles, or
groups of muscles, may occur, accompanied by intense pain,
analogous to the well-known cramp of the calf.

The sensibility, as a rule, is entirely unaffected. In some
cases, however, the atrophy of the muscles is preceded by
paroxysms of pain in the affected parts. At times the pains
follow the course and distribution of single nerve trunks, as;
that of the median and ulnar nerves ; but at other times the
pains appear to have their origin in the sensory nerves of
the muscles. In the latter case compression of the affected
muscles, as well as active and passive movements of them, pro-
vokes or aggravates the pain, and in some cases the electro-
muscular sensibility seems to be increased. In the later stages
of the affection a moderate degree of angesthesia may be present,
especially in the hands and tips of the fingers, in the form of
blunting of common sensation. The farado-cutaneous sensi-j
bility may also be diminished, and complete analgesia of
circumscribed areas is not uncommon. Sensations of cold and
numbness in the finger tips, formication, and other sensations
are frequently observed.

Vaso-motor disturbances of various degrees and extent may
occur in the affected regions. In the beginning the temperature
of the affected extremities is increased. Baerwinkel found an
elevation of 1° in one case, and Frommann found in the side
first attacked a rise of 0"2° or 03° C, as compared with the
opposite side. In more advanced stages the temperature is
not raised, and at a still later period a distinct lowering occurs,
which, according to Rosenthal, may amount to 4° C, and
according to Jaccoud to 3 or 4j° C. below the normal.

The affected parts are cold and pale, and this is especially
likely to be the case in the hands. This local ischaamia is
followed by relaxation of the vessels, and consequent warmth

SPINAL CORD AND MEDULLA OBLONGATA.

159

and redness of the affected part. An excessive sweating
(hyperidrosis) of a generalised character occurs in the later
stages of the affection, but whether this is due to vaso- motor
disturbance is unknown (Frommann, Friedreich).

Trophic disturbances occur at times in other tissues in addi-
tion to the muscular affection. The skin is not unfrequently
implicated ; and in these cases both the epidermis, cutis, and
subcutaneous tissues are affected. The affection of the skin
may be entirely wanting, and scarcely ever reaches a high
ie°ree, even where the muscular disease is far advanced.
Painful swellings of the joints have been observed in the early
stages of the disease (Remak). These swellings (arthritis
nodosa) generally occur in the phalangeal joints, and are in all
probability closely related to the arthropathies of tabes dorsalis,
rxcept that the latter are more frequent in the large than in
;be small joints.

Oculo-pupillary symptoms are on rare occasions observed in
his disease. They consist of flattening of the cornea (Voisin),
ind contraction and sluggish reaction to light of one or both
)upils (Voisin, Baerwinkel, Schneevogt, Rosenthal). These
"symptoms are in all probability due to paralysis of ' the
sympathetic fibres of the iris.

In the early stage of progressive muscular atrophy the
oatient may complain of chills, and there may be a continuous,
hough slight, increase of temperature, which lasts for days or
nonths. This febrile condition may sometimes be associated
vith arthritis nodosa, and may probably be due to the affection
•f the joints (Remak). In the later stages of the disease
ransitory or permanent elevations of temperature may occur,
vhich. are perhaps due to such complications as diseases of
ahe lungs or acute bed-sore. No constant changes have been
ound in the urine.

§ 413. Course and Duration. — The course of progressive
tiuscular atrophy is essentially chronic. It may at times be
•ormanently arrested after a certain group of muscles is de-
; troyed, but it may progress steadily until nearly all the voluntary
nuscles are implicated and the unfortunate patient is reduced
o such utter helplessness that he cannot raise a hand to feed

160

SYSTEM DISEASES OF THE

himself or turn himself in bed. The advance of the disease is I
seldom continuous even when it is progressive, but is interrupted
by repeated remissions. These may extend over a few weeks,
months, or years. Dr. Roberts thinks that the cases caused
by over exercise of the muscles nearly always terminated in
permanent arrest of the affection after the destruction of one
or more groups of muscles ; while cases which were caused
by exposure to cold, or in which a decided hereditary
predisposition could be traced, showed a greater tendency to
a progressive course and a fatal termination * In some few
cases the atrophied muscles may by treatment be restored to
their former bulk, but the affected muscles usually remain
disabled to a more or less extent for the remainder of life.

The duration of the disease is very variable and uncertain.
In twenty-eight cases analysed by Dr. Roberts the mean dura-
tion was thirty-eight months ; of these four cases ended in
recovery, their mean duration being fourteen months ; in
thirteen cases the disease was arrested with a mean duration
of twenty-seven months, and the remaining eleven cases died *
with a mean duration of the disease of upwards of five years.

§ 414. Morbid Anatomy. — The essential anatomical changes
found on post-mortem examination of those who have died
from progressive muscular atrophy are confined to the muscles
the spinal cord, and the nerves.

The muscles of the affected regions are wasted in various
degrees, and even different parts of the same muscle may
present differences in the degree to which the atrophy has
extended. A small portion of an affected muscle may, indeed,
retain its normal bulk and appearance, while the rest is
reduced to a fibrous band. The altered muscles are generally
of a pale red or rose colour, while at other times they may he ]
buff or ochre, and streaks of adipose tissue may be seen to run
in lines between the fibres.

The early investigators (Meryon, Duchenue, Cruveilhier,
Wachsrnuth, and Yalentiner) regarded the muscular changes
as being the result of fatty degeneration of the fibres, with
secondary disappearance of the sarcolemma ; but the labours of

* Reynolds' System of Medicine, Art. Wasting Palsy, vol. ii., p. 172.

SPINAL CORD AND MEDULLA OBLONGATA.

161

recent investigators (Robin, Friedberg, Foerster, Schueppel,
ilayem, and Friedreich) have shown that the fatty meta-
norphosis of the primitive fibres is a secondary result of a
>revious inflammatory change. The first changes begin in the
lerimysium internum, as a hyperplastic growth of the interstitial
onnective tissue in its finest ramifications among the single
urinative bundles. Swelling and multiplication of the muscular
orpuscles, along with proliferation of their nuclei, may be
bserved, and at times parenchymatous granular cloudiness of
he transverse striped fibrillary substance. Friedreich says that
.e has observed hypertrophied muscular fibres along with a
ichotomous or trichotomous division of their fibres. Wasting
f the muscular substance goes on side by side with increase of
he interstitial tissue, a process which ultimately leads to a
brous degeneration or true cirrhosis of the muscle. A develop-
lent of fat may take place within the hyperplastic connective
issue, leading to a pseu do- hypertrophy of the muscle.

The condition of the spinal cord and of the anterior spinal
erve roots has been examined, according to Eulenburg, in
Drty-nine cases, and out of these positive changes have been
>und in thirty-four, while in fifteen the results were negative. If,
owever, the special methods and special skill which are required
>r conducting the examination of the spinal cord be taken into
msideration, too much weight need not be attached to the
egative statements. In the hands of experts in* the present
ay changes are almost always found in the cord, hence the
egative results of the older observers may be fairly attributed
) defective methods. Cruveilhier was the first to draw atten-
on to the condition of the anterior roots of the nerves in
ais disease. In the body of the showman, Le Compte, who
ied from progressive muscular atrophy of five years' duration,
3 found that the anterior roots, especially in the cervical region,
ere remarkably small as compared with the posterior roots ;
id in a second case, observed by him, a similar condition was
>und. In these cases the brain, cord, and posterior roots were
ated to be normal. Atrophy of the anterior spinal roots,
ther with or without other morbid changes, has since that
me been found by various competent observers, amongst
hom may be mentioned Clarke, Vulpian, Luys, Rosenthal,

162

SYSTEM DISEASES OF THE

Hayem, Charcot, Joffroy, Friedreich, and many others. The
anterior nerve roots have in some cases been found normal
by Clarke, Frommann, Gull, Friedreich, Tiirck, Von Reckling-
hausen, Joffroy, and Frerichs. It may, therefore, be concluded
that the atrophy of the anterior roots is not the essential morbid
change. Yalentiner, in 1855, found a central softening of the
grey matter in the neighbourhood of the lowest cervical and
the uppermost dorsal nerves; and Schneevogt also found a
softening of the cord from the fifth cervical to the second
dorsal nerves. Frommann observed changes in the anterior
column and anterior commissure extending from the medulla
oblongata downwards.

Luys, however, was the first to direct attention to the morbid
changes in the grey substance. A man, the subject of advanced
atrophy of the muscles of the left hand and forearm, along with
slight atrophy of the muscles of the right hand, having died
of pneumonia, the spinal cord at the autopsy appeared healthy
to the naked eye, but microscopical examination showed increase
of the capillary vessels in the grey substance of the cervical
enlargement. The walls of the vessels were thickened and sur-1
rounded with granular exudation, which extended into the
adjacent tissues. Many corpora amylacea were scattered
through the grey substance. A considerable number of the
ganglion cells of the anterior horns had disappeared in the
part affected, and were replaced by granular masses, and of the
remaining cells some were in a condition of degeneration, of a
brownish colour, full of dark granules, and destitute of pro-
cesses. The degeneration affected principally the left anterior
cornu, corresponding with the seat of the muscular atrophy.
The anterior nerve roots on the left side, corresponding to
the disease in the anterior horn, were atrophied. Six cases
have since been described by Lockhart Clarke, confirming, in
a,ll essential respects, the observations of Luys; and similar
observations have been made by Dume'nil, Schueppel, Hayem,
Charcot, and Joffroy.

In a case described by Charcot the ganglion cells of the left
anterior grey horn (Fig. 167, A) could still be distinguished,
but were observed to be in an advanced stage of atrophy. I"
the right anterior grey horn (Fig. 167, B), however, the cells

SPINAL CORD AND MEDULLA OBLONGATA. 1G3

:ould only be distinguished in one group — the postero-lateral
Fig. 167, b) — while the cells of the remaining groups were
:ompletely destroyed. It has appeared to me, however, that
oo little attention has hitherto been paid to the condition of

Fig. 167.
A B

to. 1G7 (Charcot). Transverse Section of the Cervical Region of the Spinal Cord,
from a case of progressive muscular atrophy.— A, Left anterior grey horn ; the
ganglion cells have persisted, but are much altered in appearance. B, Right
anterior grey horn, almost complete atrophy of the cells, one group only (b)
having persisted.

ie central column. In the annexed diagram, from Charcot
fig. 167), the central column, especially the left one, is seen to
} intersected by enlarged vessels, and that of itself affords
me evidence that thi3 column was not free from disease in the
ction from which the drawing was taken. It seems to me,
deed, that the morbid process begins on each side of the
ntral canal, probably in the tissues immediately adjoining
e central artery, and that it extends outwards and forwards
well as upwards and downwards from this point as a centre
' i a transverse section of the middle of the cervical enlargement
• my possession, from an advanced case of progressive muscular
rophy. the material of which I owe to the kindness of
r. Dreschfeld, it was unmistakable that the central grey

164

SYSTEM DISEASES OF THE

column was more severely diseased than any other portion of
the section. The central column was traversed by enlarged
vessels, and almost all structure was obliterated, while the
various groups of ganglion cells in the anterior horns were dis-
tinctly recognisable. The cells of the median area were, indeed,
completely destroyed, so that not a trace of them could be seen,
and a large number of the marginal cells of the other groups
were also destroyed, so that the groups themselves were separated
by unusually large spaces which were destitute of cells (Fig. 168)
The cells of the centres of the groups were, however, distinctly
recognisable, although all of them were observed to be in a

Fig. 168.

Fig. 168 (Young). Transverse Section from the Middle of the Cervical Enlargement
of the Spinal Cord, from an advanced case of progressive muscular atrophy.—
cc, Central canal; t, Internal, al, Anterolateral, and pi, Postero-lateral
groups of ganglion cells.

state of pigmentary atrophy (Fig. 144, 8). I have also observed i
in one of my sections a streak of degeneration to pass along the
posterior branch of the central artery (Fig. Ill, 1") into the
substance of the posterior grey horns, and this may explain why
analgesia of patches of the skin is frequently associated with

SPINAL CORD AND MEDULLA OBLONGATA.

165

progressive muscular atrophy. In the accompanying woodcut
(Fig. 169), borrowed from Leyden's great work on the diseases
jf the spinal cord, it may also be distinctly recognised that the
liseased portions occupy mainly the central columns of the
sord, and that there are lateral extensions of the disease towards
:he anterior grey horns and between the groups of ganglion cells.

Fig. 169;

i'lG. 169 (From Leyden). Transverse Section of the Spinal Cord from the Middle of
the Cervical Enlargement, showing that the central column and a large portion of
the anterior grey horns are diseased.

A case of progressive muscular paralysis has been recently
escribed by Erb and Schultze, in which the erector spinas
hroughout their entire extent, the trapezius on both sides, the
ruscles connected with the shoulder blades, those of the upper
rm, the pectorals, the gluteal muscles, and the flexors of the
3gs on the thighs were atrophied.. The case, indeed, appears
) have been, so far as the distribution of the paralysis is con-

srned, very like that of Charlotte A , already described. The

atient died from an attack of syncope, but without any trace
f bulbar symptoms, and a microscopical examination of the
oinal cord showed that the most pronounced changes were
>und in the " central region of the grey substance." It is also
lentioned that in the lower half of the lumbar and cervical
alargements the ganglion cells had disappeared from the
I median (central) group. The cells of the other groups were

166

SYSTEM DISEASES OF THE

degenerated. The whole microscopical report of the case,
indeed, bears out the idea that the disease began in the central
column, and extended forwards into the anterior horns.

The nature of the disease in the cases just described appears to
have been a chronic inflammation of the grey matter, but in
another series of cases the affection of the grey matter is caused
in a different way.

In the annexed woodcut {Fig. 170), borrowed from Leyden's
work, a section of the cervical enlargement of the spinal cord,
from a case of syringomyelia, is represented. It will be recog-
nised that the destruction of the ganglion cells of the anterior
horns takes place in this case much in the same way as in cases
of chronic inflammation already described, but in which distinct
cavities are not observed. It is indeed doubtful whether any
essential difference exists between the two classes of cases,

Fig. HO.

Fig, 170 (From Leyden). Transverse Section of the Spinal Cord from the Middle of i B.
the Cervical Enlargement, from a case of Syringomyelia, shoicing a cavity behind fill
the posterior commissure, and destruction of a large portion of the ganglion edit t
of the anterior grey horns.

inasmuch as the cavities probably result either from iuflamma-
tion of the tissue of the central grey column and of the adjoin-
ing white substance, or of the walls of the central canal.

In a case observed by Sir William Gull, a considerable dilata-
tion of the spinal canal was found in the cervical region, between
the fifth cervical vertebra and the origin of the third and fourth i\ \
dorsal nerves. The cavity was full of serous fluid, and, with the
exception of a thin layer which surrounded it, and could beM^
stripped off like a membrane, the grey substance had dis- th,
appeared, while the white substance and the anterior nerve 1 1^,

SPINAL CORD AND MEDULLA OBLONGATA.

167

oots seemed normal. In a case observed by. Schueppel, the
ivdromyelia extended down to the tenth dorsal vertebra,
jrrimm also found considerable enlargement of the central
iavity at the expense of the grey substance, the latter being
llattened by pressure to a ring-shaped plate, but in this case
(he cord in the lower cervical and upper dorsal regions pre-
ented a fusiform swelling, caused by the growth of a medul-
ary sarcoma. In the latter series of cases, the destruction of
[he ganglion cells appears to have been caused indirectly by
he pressure of the fluid which had distended the central canal.

The result, however, in both series of cases, is the same, the
ganglion cells being destroyed. Progressive destruction of the
ells seems then to be the essential feature of the morbid
.natomy of the disease. It is right to add that some competent
observers (Lichtheim) found the anterior grey horns normal,
>ut it is probable that, in the earlier observations at least, the
hanges in the ganglion cells had been overlooked. The posterior
olumns, the posterior horns, the posterior roots, and the inter-
ertebral ganglia have been found in a state of degeneration,
Ip addition to the affection of the anterior horns.

Schneevogt found the sympathetic in the neck diseased in a
Lase examined by him. The cervical sympathetic was converted
lmost into a fatty cord, in which the nerve fibres were pressed
side by fat cells, which contained beautiful crystals. The cer-
ical ganglia were almost entirely changed into fat cells, and
he thoracic part of the sympathetic also abounded in fat. Two
imilar observations were made by Jaccoud, and he inferred
L"om the appearances present that the disease began in the
ympathetic and spread along the rami communicantes to the
ord and along the peripheral nerves to the muscles. Changes
1 the sympathetic have been found by Swarzenski and by
)ume'nil ; while other observers as Landry, Frommann, Hayem,
Charcot and Joffroy, and Friedreich have found the sympa-
he-tic healthy.

The peripheral nerves distributed to the affected muscles
ave also been found affected by Schneevogt, Trousseau,
rirchow, Freidberg, Hayem, Charcot and Joffroy, Bamberger,
losenthal, Friedreich, and others. The degenerations were
ometimes limited to the finer intra-muscular nerve branches,

168

SYSTEM DISEASES OF THE

and at other times they existed in the large nerve trunks and
in the plexuses. The changes observed were hyperplasia of
the neurilemma, multiplication of nuclei, and fibrillary thicken- 1
ing of the sheath of Schwann. Friedreich also found varicose
dilatation of the medullary sheath with secondary atrophy off
the nerve fibres. In some few cases examination of the peri-
pheral nerves gave negative results.

§ 415. Morbid Physiology. — Various theories have from time
to time been advanced to account for the symptoms of progressive
muscular atrophy. The theory of Cruvielhier, who regarded
atrophy of the anterior roots as the essential morbid alteration, as
well as the views of those authors who believe that the symptoms
are caused by disease of the peripheral nerves, antero-lateral
columns, or posterior columns of the cord, is definitely abandoned
by all pathologists in the present day. The theoiy first advanced
by Schneevogt, and afterwards elaborated by Jaccoud, which at- ^
tributes the disease to a morbid change of the sympathetic, now
reckons only few adherents. In the first place, the sympathetic is
by no means regularly affected in progressive muscular atrophy ;
and when it is implicated the morbid change is declared by the
superadded symptoms, which may be briefly summed up as
oculo -pupillary phenomena. In short, the disease of the sym- |
pathetic is an occasional concomitant affection ; and in these
cases the morbid changes appear to be propagated from the
anterior horns along the rami communicantes to the cervical
and dorsal portion of the sympathetic trunk and ganglia. It
is not impossible that a reverse process may take place, but
even in that case the disease of the anterior horns, so far as I
the nervous system is concerned, would be the fundamental
lesion of the affection.

These theories being disposed of, two only remain — theHitrj
myopathic theory, of which Friedreich is the declared champion,
and the neuropathic theory, of which Charcot may be mentioned
as the most prominent advocate. Aran first advanced the myo- ]
pathic theory, but in his day the constant changes which have
since been found in the nervous apparatus had not been disco-
vered. No one denies the reality of these changes at present, the
only question which arises is whether the muscular alteration pre- •

SPINAL CORD AND MEDULLA OBLONGATA.

169

edes the morbid changes in the cord, or whether the former are
econdary to and caused by the latter. Progressive muscular atro-
•hy, according to Friedreich, begins as a primary chronic myositis,
lie intra-muscular nerves are secondarily implicated, and a
hronic neuritis ascends along the course of the nerve trunks

0 their roots. The neuritis may then extend in the cord itself,
•roducing a chronic myelitis, which may spread in various
irections. This change may extend to the anterior cornua,
■ut the nutrition of the peripheral nerve fibres and of the
anglion cells of the grey anterior cornua of the cord is also
ffected by the disturbed motor functions, caused by the disease
q the muscles. Various objections may be urged against this
heory, not the least important of these being the fact that the
•eripheral nerves and anterior nerve roots have been found
uite normal in a considerable number of cases.

Friedreich would supplement the theory of neuritis ascendens
y the subordinate theory that simple suspension of muscular
ction would of itself cause atrophy of the ganglion cells. But
ae changes observed in the anterior horns of the cord in the
ase of amputated limbs do not equal in severity those found

1 progressive muscular atrophy. This theory also utterly fails
) account for those cases in which the destruction of the grey
latter of the anterior horns is produced by slow compression
"om gradual distension of the central canal by fluid. Various
ther objections might be urged against the myopathic theory,
ut enough has been said to show that it at least presents
'ide gaps which must be filled up before it can be considered
stablished.

The neuropathic theory has at least the merit of being
mple, and of presenting fewer difficulties. According to it,
ae atrophy is due to the progressive changes, primarily of an
•ritative character, of the ganglion cells of the anterior horns,
'rogressive bulbar paralysis, which is so frequently associated
'ith progressive muscular atrophy, is an analogous affection
msed by morbid changes in the groups of motor cells lying in
ae floor of the fourth ventricle, the reason that the two diseases
re so frequently associated being merely that the morbid
rocess extends from the anterior horns by continuity to the
lotor centres in the floor of the fourth ventricle. The dis-

170

SYSTEM DISEASES OF THE

tinction between the two diseases is, indeed, dependent upon the
locality of the lesion in each case. In both these diseases the
nature of the lesion which destroys the ganglion cells is of little
importance. Much the same results (except probably in respect
to the rapidity with which the atrophy is developed) follow
ordinary grey degeneration, chronic induration, myelitis, red
softening, Clarke's granular degeneration, or isolated pigmentary
degeneration of the cell elements.

On the supposition that the disease begins in the central grey
column and extends outwards and forwards into the anterior grey
horns, it may be readily explained why the groups of muscles
engaged in special actions are usually the first to be affected.
We have already seen that the central column is the embryonic
area of the grey substance, and that the median area of the
anterior horns in the lumbar and cervical enlargements, and the
medio-lateral areas in the dorsal and upper cervical regions of
the cord, may be regarded as outgrowths of the central column.
The median and medio-lateral areas will consequently be the
first portions of the anterior horns to be affected, and the por-
tions which contain the fundamental cells will be the last to
become diseased. When, therefore, the lumbar and dorsal
regions of the cord are affected, the muscles which maintain the
erect posture in man will be those most liable to be affected,
as will be more fully pointed out with regard to pseudo-hyper-
trophic paralysis. Again, when the cervical enlargement is the
first to be affected, the morbid process will extend more readily
forwards to the median area than in any other direction, and
the small muscles of the hand will be first affected. It will
hereafter be pointed out that when the medulla oblongata is
first affected the disease begins in the upward continuation
of the central column, and that the accessory nuclei will be
liable to become first diseased ; and hence it is that the com-
plicated movements of articulation are generally the first to be
affected.

On the supposition that the morbid process begins in the
central column, it may also be readily explained why muscles
innervated' from different levels of the cord may be affected,
while muscles innervated from the intervening portion are
spared, without our being obliged to assume that the morbid

SPINAL CORD AND MEDULLA OBLONGATA.

171

>rocess in the cord has started from two or more centres of
>rigio. The morbid process may, for instance, extend forwards
nto the median area in the cervical enlargement, while it may
>ass upwards through the upper cervical region and keep
imited to the immediate neighbourhood of the central canal,
sphere it would produce no symptoms, and then on reaching
he medulla oblongata extend to the accessory nuclei, and thus
jroduce the symptoms of bulbar paralysis.

§ 416. Diagnosis. — The partial form of the disease is liable to
>e confounded with muscular atrophy caused by direct mechanical
njury to the muscle, or with the various diseases of the peri-
meral nerves. If the disease remain confined to the muscles
triginally affected, or to the region of a single nerve trunk,
)rogressive muscular atrophy can be excluded ; and muscular
-trophy resulting from disease of a mixed nerve is usually
ccompanied by loss of sensation.

The disease may also be confounded with lead palsy; but in
iie latter the invasion is comparatively sudden, the paralysis
jeing at its height in a week or a fortnight at most ; while the
lectric contractility is diminished or lost at an early period,
in the former the paralysis precedes the atrophy ; while in
he latter the loss of muscular power is almost always directly
q proportion to the wasting of the muscular masses, and the
I lectric contractility is maintained so long as any muscle is
reserved. The general symptoms which characterise lead
•oisoning will also assist the diagnosis.

Ordinary general paralysis of central origin may be distin-
guished from progressive muscular atrophy by the fact that in
he former the paralysis occurs as an early symptom, and it is
are that the muscular emaciation bears any proportion to the
oss of power. Progressive muscular atrophy attacks the muscles
a separate groups, dissecting out either individual muscles or
roups of muscles from amongst others which remain healthy,
nd does not attack at the same time extensive regions or the
entire body.

The diagnosis between progressive muscular atrophy and
ofantile paralysis has been mentioned already.

172

SYSTEM DISEASES OF THE

§ 417. Prognosis. — Progressive muscular atrophy is always
very intractable, and when the muscles of the trunk are invaded
it always progresses slowly towards a fatal termination. In the
partial forms, when the disease is limited to one or two ex-
tremities, there is no danger to life, but the limbs are, as a
rule, permanently damaged. In many cases the advance of the
disease may be checked, and, so long as voluntary motion and
the electrical reactions are not completely lost, some hope
may be entertained that partial restoration of the affected
muscles may take place. The most unfavourable cases are
those which begin in a multiple form and spread rapidly. The
cases in which the disease begins in the thorax or shoulder are
unfavourable, because the affection is very liable to implicate
the respiratory muscles. When bulbar symptoms supervene
the prognosis is specially unfavourable, and when the muscles
of respiration are invaded a fatal termination may be expected
within a short time. When the disease can be traced back to a
hereditary predisposition it manifests a greater tendency to
become generalised, and consequently the prognosis is more
unfavourable. The prognosis, on the other hand, is more
favourable when the affection is caused by overwork and when
it is confined to the hands and forearms.

§ 418. Treatment. — An attempt must first be made to remove
the cause. When the disease, for instance, is caused by a syphilitic
taint the usual antisyphilitic treatment must be adopted. When
overwork of the affected muscles appears to have been the
exciting cause of the disease, they must be allowed to rest.
When a decided hereditary predisposition to the affection is
manifested in a family, prophylactic measures may be employed,
such as a regulated course of gymnastics. The members of
such families should also be shielded from deleterious influ-
ences, especially those which are known to excite the disease.

The direct treatment of the established disease embraces the
employment of hygienic measures, such as baths, methodical
exercise, change of air and good diet, and the employment of
galvanism and friction to the affected muscles. No medicine
has hitherto been found of any use in the treatment of this
disease. Tonics, as iron and quinine, may be useful adjuncts m

SPINAL CORD AND MEDULLA OBLONGATA.

173

he treatment, and the nitrate of silver, arsenic, phosphorus,
!nd iodide of potassium have been employed, but with doubtful
uccess.

Thermal and sulphur baths have been recommended, and the
yaters of Aix-la-Chapelle have been much praised, but appa-
ently on insufficient evidence. The cold water cure, conducted
|u a good hydropathic establishment, may occasionally be found
isefoL

Galvanism is undoubtedly the most efficient remedy for the
isease. The local use of the faradic current was applied by
)uchenne, who obtained favourable results from it, but the
galvanic is probably more efficient than the faradic current.
?he local use of both currents alternately has given good results.
Vhen the muscular excitability is very low, strong currents are
equired, and their effects should be intensified by inter-
ruptions and reversals, but as the excitability returns, weaker
urrents should be employed. I have observed favourable
Bsults from the use of electric acupuncture. Suitable gym-
astics, to call forth the activity of the affected muscles, passive
•lotion, shampooing, and friction, are all useful in the treat-
lent of the disease. When the muscular atrophy is associated
l ath neuralgia the subcutaneous injection of morphia may be
I m ployed. Dr. Roberts recommends an injection to be given
i the morning, and he states that it often enables the patient
d pursue his employment with comfort during the day.

4. Primary Labio-Glosso- Laryngeal Paralysis.

{Chronic Progressive Bulbar Paralysis. — Wachsmuth.)

§ 419. Definition. — Labio-glosso-laryngeal paralysis consists
f a progressive paralysis and atrophy of the muscles of the
ongue, lips, soft palate, pharynx, and larynx.

§ 420. History. — A. brief report of a case of this affection was sent to
ur Charles Bell in 1825 by Dr. F. W. Robinson, and Trousseau wrote an
ccurate account of the symptoms of the affection in 1841, but did not
ublish his observations. The individuality of the disease was, however,
ot distinctly recognised until 1861, when Duchenne described the affection
nth his usual exhaustiveness and thoroughness.

174 SYSTEM DISEASES OF THE

§ 421. Etiology. — It does not appear that heredity exercises
any influence in the production of labio-glosso-laryngeal paralysis.
It occurs most frequently between the fortieth and seventieth
years of age, and only exceptionally before the fortieth year.
The disease attacks men more frequently than women, the
proportion being two of the former to one of the latter (Dowse).
All ranks of society from the highest to the lowest, and every
profession, appear to be liable to the affection.

Of the exciting causes, the most frequently mentioned are
exposure to cold, traumatic influences, as a blow on the back of
the neck, violent and continuous mental excitement, excessive
mental activity, straining of the muscles affected, as in singing
and speaking, and bad and insufficient food. Syphilis is not
an unfrequent cause of the disease ; but the authors who regard
this affection as being almost always of syphilitic origin are
undoubtedly in error.

§ 422. Symptoms. — Slight premonitory symptoms usually
precede the full development of the disease, but they are often
entirely wanting and are not in any way characteristic of the
affection. These consist of pain in the head and back of the
neck, slight dizziness, and great diminution or complete loss
of the reflex irritability of the larynx, oesophagus, and pharynx.
The reflex insensibility of the mucous membrane of the fauces,
epiglottis, and pharynx is sometimes so great as to lead to a; J
certain amount of dysphagia, and the passage of food into the
larynx for a considerable time before any actual paralysis is li
observed (Krishaber).

The disease may begin suddenly with difficulty in the move-
ments of the tongue and lips, and of deglutition ; but in these
cases it is probable that a slight haemorrhage has occurred in fbi
the medulla, and consequently they cannob be regarded as true
instances of the primary disease.

The symptoms of the true progressive disease creep of
gradually and stealthily. A slight affection of speech is usually
the first symptom to attract attention. Utterance is less distinct,
the pronunciation of certain letters presents special difficulty,
and the tongue and lips are soon fatigued, so that prolonged
reading aloud or speaking is impossible.

SPINAL CORD AND MEDULLA OBLONGATA.

175

This is followed by a gradual weakness in the lips and palate,
'he expression of the face is altered, the voice becomes nasal,
nd fatigue of the muscles of mastication and deglutition is
3adily induced, so that the patient is soon compelled to eat
nly pulpy food, and is unable to swallow much at one meal.

The paralytic symptoms may at times begin in the lips and
alate instead of the tongue, and then the order of succession
? the symptoms will differ to some extent from that just
escribed.

The initial period of debility and fatigue of the affected
mscles may extend over a period of years before the stage of
.stinct paralysis is reached. When once distinct paralysis is
itablished, the disease assumes a more progressive character,
id advances steadily and surely to a fatal termination.

When the affection begins in the tongue, the patient expe-
ences an ever-increasing difficulty in pronouncing the dental
id guttural sounds which are respectively produced by
iproximation of the tongue to the teeth or hard palate, and

the root of the organ to the soft palate. Since the vowel i
quires the greatest raising of the tongue for its production,
h pronunciation is the first to suffer; and then the pronuncia-
on of the consonants r, s, 1, k, g, t, and lastly d and n, becomes
fficult, imperfect, and finally impossible.
After a time the patient is unable to effect the coarser and
ast complicated lingual movements. He may at first be able

protrude the tongue, but not to raise the tip towards the
;ird palate or towards the nose after protrusion; while ina-
lity to move the tip laterally indicates a still greater degree

paralysis. As the paralysis increases the tongue cannot be
ngthened into a point, or made hollow in the centre; and,
lally, protrusion is impossible, and the organ lies behind the
wer row of teeth completely helpless and motionless, or main-
ined in constant vibration with fibrillary twitchings.
The tongue may maintain its normal aspect, or become large
id flabby; but much more frequently it is sodden, grooved
: Qgitudinally, wrinkled, and shrunken, while simultaneous
< rophy of the papillae gives to the surface a glazed ap-
;arance.

At an early stage of the affection deglutition is rendered

176

SYSTEM DISEASES OF THE

difficult, simply by the increasing weakness of the tongue.
Great difficulty is experienced in collecting the food in the
mouth so as to form it into a bolus, and in pressing it back
against the soft palate and into the pharynx ; and the patient
adopts various devices in order to supplement the deficiencies
of the first stage of deglutition. He takes care, as Trousseau
remarks, to chew well what he eats, and to facilitate its gliding
down by drinking and throwing his head backwards, while at I
other times he assists the imperfect movements of the tongue
with his fingers, using them to extract the food which has
lodged between the teeth and cheeks, and to push the bolus to
the back of the tongue till it is caught by the reflex move-
ments of deglutition.

The muscles which pass from the inferior maxilla to the
hyoid bone, and which elevate the larynx as well as the base of
the tongue during deglutition, are implicated in the paralysis
along with the intrinsic muscles of the tongue; hence it may
be observed that the larynx does not rise so readily as in health]
during the second stage of deglutition. The root of the tongue
cannot, therefore, be brought during deglutition over the de-
pressed epiglottis, the glottis is not completely closed, particles
of food and fluids easily find their way into the tracbeea, and
cause distressing paroxysms of cough and dyspnoea.

The saliva cannot be swallowed and accumulates in the
mouth, and owing to the advancing paralysis of the orbicularis
oris flows from it in an almost continuous stream. Of the
muscles innervated by the facial nerve the orbicularis oris is the
first to suffer. With the increasing weakness of this muscle
the patient becomes unable to whistle, blow, compress his lips,
or kiss. The patient experiences difficulty in pronouncing the
vowels o and u ; and with the advance of the paralysis the labial
consonants p, f, b, and m, become increasingly difficult to
articulate.

Paralysis of the palate renders the formation of the explosive
labial consonants still more difficult ; since the current of air
necessary to force the lips suddenly asunder escapes through
the nose, and the consonants p and b are consequently turned
into me and ve. Duchenne has shown that if the patient's nose
be closed these letters are much better pronounced. Paralysis

SPINAL CORD AND MEDULLA OBLONGATA.

177

)f the palate also gives a nasal resonance to the voice, and
Dermits food and fluids to escape readily through the nose
luring efforts at deglutition. When the muscles of the tongue,
ips, and palate are simultaneously paralysed, speech becomes
nore and more indistinct, and the patient can only give utter-
ance to inarticulate and grunting sounds. The vowel a, how-
ever, can still be pronounced, inasmuch as it is a purely
laryngeal sound, and quite independent of the articulatory
novements of the tongue and lips.

But although the orbicularis oris suffers more profoundly
han the other facial muscles, the quadratus and levator menti
re more or less implicated in the paralysis. The muscles of
he palpebral and nasal regions are never affected, and even the
levators of the superior lip, as well as the levator menti and
buccinators, are only on rare occasions involved in the paralysis.
Che paralysed muscles are almost always distinctly atrophied,

0 that the lips look thin, sharp edged, and furrowed, and fribril-
ary contractions are not unfrequently observed in them. The

| >atient now presents a very striking and characteristic appear-
nce. The lower lip hangs loose and pendulous, the mouth
annot be closed, it is somewhat increased in breadth, and the
I aso-labial folds become marked, and give to the patient a
j ichrymose expression. During states of emotional excitement
Ijhe lower part of the face remains comparatively motionless,
I nd contrasts strongly with the vivacious movements of the
jrpper half of the face, and with the brightness and activity
I f the eyes.

The saliva now flows from the mouth in a continuous stream,
Ind causes much annoyance to the patient, inasmuch as it soaks
1 irough the pillow at night and requires to be constantly wiped
| -om the lips with a handkerchief during the day. The saliva
) ppears to be secreted as a rule in normal quantity, but in
|Dme cases the amount of secretion is very largely increased.

1 chulz estimated in one case that the secretion was six or eicdit
Junes the normal amount, and Kayser found that he could
sl acrease the flow by reflex irritation, and arrest it temporarily
t y means of atropine.

Mastication, as already mentioned, is impaired at an early
9 :age of the affection from the difficulty of moving the tongue,
11

178

SYSTEM DISEASES OF THE

aDd the condition becomes aggravated when the lips and buc-
cinators are simultaneously paralysed. But the difficulty of
mastication is greatly augmented when the motor division of
the trigeminus is involved in the disease. The pterygoid
muscles are usually the first of the masticatory muscles to be
affected, and paralysis of them abolishes the power of effecting
the lateral movements of the lower jaw. With the advancing
paralysis of the remaining muscles of mastication, the power of
chewing the food becomes increasingly difficult, feeble, and
finally impossible.

The difficulty of deglutition, caused by paralysis of the
tongue, lips, and soft palate, is greatly augmented when the
pharyngeal muscles and those which close the larynx are in-
volved in the disease. When the pharyngeal muscles are
paralysed particles of food are apt to lodge in the pharynx, and
this increases the risk of foreign particles entering the larynx.
At other times the whole bolus gets fast on a level with the
glottis, causing danger of instant suffocation.

But when the muscles which close the glottis are .paralysed,
the danger of swallowing either solids or fluids becomes greatly
intensified. Particles of food passing into the larynx produce
distressing paroxysms of coughing and dyspnoea, and by passing
into the bronchi often cause pneumonia. When the paralysis
extends to the oesophagus deglutition becomes impossible, and
to survive the patient must be fed by the stomach pump. When
the nucleus of the spinal accessory nerve is involved in the
disease the laryngoscope reveals paresis or paralysis of the vocal
cords, the voice becomes hoarse and feeble, until finally there is
complete aphonia. The power, not of articulation only, but of
phonation also, is now abolished, the loss of this function being
manifested by inability to pronounce the vowel a. The loss
of phonation does not necessarily interfere with the respiratory
functions, but as the disease advances disorders of respiration
and circulation supervene, which soon prove fatal.

Not much is known with respect to disorders of the circula-
tion in the early stages of the affection. There is no trustworthy
record of retardation of the pulse which could with probability
be referred to irritation of the vagus, but a pulse rising before
death from 130 to 150, or even higher per minute, has been

SPINAL CORD AND MEDULLA OBLONGATA. 179

frequently recorded, and is probably caused by paralysis of the
vagus. In the terminal period of the disease patients often
suffer from fainting fits, accompanied by great anxiety and a
sensation of impending death, and, indeed, death may result
from an attack of syncope. These phenomena are probably
paused by the cardiac centres of innervation having become
involved in the disease.

When the respiratory mechanism is affected a fatal termi-
jaation is near. The respiratory movements become feeble, and,
owing to the implication of the spinal accessory nerves, the
auxiliary muscles of respiration are paralysed, and superior
thoracic breathing is impossible. The inefficiency of the respi-
ratory movements renders the breathing shallow, and all
utempts at coughing or blowing the nose are weak and
powerless. Patients complain of a feeling of constriction,
accompanied by an oppressive feeling of want of breath.
Vfter a time the pneumogastric nerve appears to become ind-
icated in the disease. Paroxysms of dyspnoea, with a tendency

0 syncope, supervene, but these must not be confounded with
•he suffocative attacks which occur at an early period from the
accidental introduction of foreign bodies into the larynx. The
attacks of dyspnoea become more and more frequent as the
lisease progresses, and the breathing power feebler and feebler,
intil ultimately the patient dies from asphyxia. Death may,
ndeed, be caused at an early period of the affection by a slight

isease of the respiratory organs, such as a bronchial catarrh

r pneumonia.

Atrophy of the 'paralysed, muscles is one of the most constant
md striking symptoms of this affection. It is usually most
larked in the tongue, and the lips also become emaciated and
lin, and both are often kept in constant movement by fibrillary
mtractions. Atrophy of the soft palate has not yet been
scorded, and cannot probably be recognised with certainty.

Atrophy of the paralysed muscles is not an early symptom of
ie disease, and does not run a parallel course with the paralysis,
'he tongue may, however, retain a normal appearance and
| olume, and yet exhibit, on microscopical examination, exten-

1 ve degeneration of its muscular fibres (Charcot).

Local atrophy and fibrillary contractions of the small muscles

180

SYSTEM DISEASES OF THE

of the hand are sometimes observed indicating a complication
with progressive muscular atrophy.

The electric excitability is generally said not to undergo any
noteworthy changes, but Erb states that he found the most
marked " reaction of degeneration" on direct irritation of the
muscles of the chin, lips, and tongue. The electric irritability
of the nerves was, however, normal, or but slightly diminished.

The sensibility remains, as a rule, unaffected throughout the
whole course of the disease, and even taste is only altered on
rare occasions. Affections of the auditory nerve, consisting of
buzzing of the ears and deafness, have occasionally been
observed. The trigeminus is sometimes implicated, the
symptoms observed being a furry feeling and anaesthesia on
both sides of the face, and want of common sensation in the
tongue, and in some cases pain has been felt in the occipital
and upper part of the cervical region (Trousseau).

The intelligence remains quite clear to the last, the temper
is somewhat excitable, and patients often manifest an inclina-
tion to laugh on slight provocation.

Reflex irritability is, as already mentioned, sometimes
greatly diminished or abolished in the tongue, soft palate,
pharynx, and even in the larynx before the appearance of any
other symptoms, but on the other hand it is often retained in
these parts until a late period of the disease. Even when the
reflex irritability is lost the patient can feel and localise each
touch quite distinctly.

Vaso-motor disturbances have not been recorded, and there
is no fever during the whole course of the disease.

General nutritive disorders occur sooner or later in the
course of the affection. These are in large part due to the
insufficient quantity of food taken, and which ultimately pro-
duces a vState of inanition. The helplessness of the patient is
greatly aggravated by his inability to close the glottis, and
thus all forcible expiratory actions are rendered impossible.
Duchenne thought, probably on insufficient grounds, that the
constant loss of the saliva exercised a deleterious influence on
digestion, and consequently contributed to produce the general
debility. But whatever may be the causes which co-operate to
produce the state of emaciation and marasmus into which the

SPINAL CORD AND MEDULLA OBLONGATA.

181

patient falls, the debility at last becomes so great that he is
unable to get up. He sits in bed, with the upper part of the
body propped up, and with the head resting on pillows and
inclined to one side, in order to let the saliva flow out of the
-.mouth, and death soon supervenes, either during a paroxysm of
dyspnoea or suddenly and quietly from arrest of the heart's
action.

§ 423. Course, Duration, and Terminations. — The course of
bulbar paralysis is always slow and chronic, but surely progressive.
There is seldom a remission of long duration ; any degree of
improvement is still rarer, and recovery has never been observed
when the diagnosis of a primary affection was beyond question.
Death usually results in from one to five years.

§ 424. Complications. — Progressive muscular atrophy is the
most important and frequent complication of bulbar paralysis.
Labio-glosso-laryngeal paralysis may either be the primary affec-
tion, or it may merely be a terminal phenomenon supervening in
the course of progressive muscular atrophy, and caused by exten-
sion of the morbid process in the anterior grey horns of the cord
to the motor nuclei of the medulla. The two affections are
indeed essentially the same disease, both as regards the clinical
symptoms and the anatomical changes found after death.

Amyotrophic lateral sclerosis is another important com-
plication of progressive bulbar paralysis, and the latter may
either be the primary or secondary affection. Amyotrophic
lateral sclerosis occurs not unfrequently in the later stages of
bulbar paralysis. The disease is then characterised by the
symptoms of progressive muscular atrophy in the superior and
those of spastic spinal paralysis in the inferior extremities. A
number of cases described as bulbar paralysis or progressive
muscular atrophy belong to this class. The disease is no doubt
due to extension of the morbid process in the medulla to the
anterior grey horns of the cervical enlargement and to the
antero-lateral columns of the cord.

§ 425. Morbid Anatomy. — The first observations with respect
the morbid alterations of the nervous system were conducted

1S2

SYSTEM DISEASES OF THE

without careful microscopical examination of the medulla and
pons. In a complex case of paralysis of the tongue, lips, and
veil of the palate, combined with general muscular atrophy,
recorded by Dr. Dumenil, the roots of the hypoglossal, facial,
and spinal accessory nerves, as well as the anterior spinal roots,
were found wasted, the atrophy also extending to the trunks
of the nerves themselves. Trousseau found increased consis-
tency of the medulla oblongata and thickening of the dura
mater of the medulla ; but he regarded the atrophy of the roots
of the bulbar nerves as the essential morbid alteration in this
disease.

The close anatomical connection which the researches of
Lockhart Clarke and others have proved to exist between the
nuclei of origin of the nerves implicated in this disease, as well
as the discovery which had already been made that the allied
affections of progressive muscular atrophy and infantile spinal
paralysis were due to disease of the ganglion cells of the ante-
rior grey horns of the cord, had led pathologists to suspect that
the essential anatomical changes in this disease would be found,
not in the roots of the nerves, but in the ganglion cells of their
nuclei of origin. It was in reference to this expectation that
Dr. Wilks wrote : " The anatomist and the physiologist have
in fact informed the clinical physician of the precise spot
which is affected, and it only remains for the pathologist to
prove it."

About the time that this sentence was being uttered by Dr.
Wilks the opportunity for making the necessary verification
of the hypothesis presented itself to the ever-vigilant eye of
Charcot, and his observation was soon afterwards confirmed by
Duchenne and Joffroy. The essential anatomical changes in
the affection appear to consist of a degenerative atrophy of the
ganglion cells in the grey nuclei on the floor of the fourth
ventricle. The cells shrink and become filled with yellow or
brown pigment, their nuclei disappear, and finally the cells
themselves are only represented by angular, glistening pig-
mented masses.

In some cases the surrounding tissue was found to contain
corpuscles of Gluge in varying quantity, increase of connective
tissue and in the number of nuclei and of Deiter's cells, and

SPINAL CORD AND MEDULLA OBLONGATA. 183

iypertrophy and fatty degeneration of the vascular walls. The
lerve fibres themselves were found atrophied, the medullary
heath had disappeared, and in chronic cases the axis cylinders

dso.

The nucleus of the hypoglossal nerve appears to be the
tarting point of the disease, and the nuclei of the spinal
accessory and vagus are next attacked, while the disease does
lot extend in all cases to the nucleus of the glosso-pharyngeal

Fig. 171.

'ig. 171 (From Leyden). Portion of the Grey Substance on the floor of the fourth
ventricle on a level with the middle of the Hypoglossal Nucleus, from a case of
Progressive Muscular Atrophy with Bulbar Paralysis, showing the destruction of
the Ganglion Cells of the nuclei of the Hypoglossal and Pneumogastric Nerves ( NH/.
R, Median raphe ; H, H, Fibres of the hypoglossal nerves. The accessory
nuclei have evidently disappeared.

; erve. The nuclei of the facial are attacked at a very early
tage, especially those which are connected with the inferior
ranches of the nerve, and which I have named the accessory
uclei of the facial. The annexed diagram {Fig. 171), borrowed
com Leyden, represents the morbid changes observed in the
aedulla oblongata in bulbar paralysis. Remnants of the fun-
amental cells of the hypoglossal nuclei may still be observed,
fhile every trace of the accessory nuclei has disappeared.

The motor nucleus of the trigeminus has been found affected,
>ut the nucleus of the abducens and the acoustic and trigeminal

184

SYSTEM DISEASES OF THE

sensory nuclei appear never to suffer. Other changes have been
described, but they appear to be quite secondary to the altera-
tions in the ganglion cells. The pyramidal tracts have often ]
been found diseased, and the degeneration could generally be 1
traced into the pons and downwards into the antero -lateral
columns of the cord ; but such cases are not pure examples of the
disease. The bulbar affection is often associated with diseases of i
the spinal cord, such as progressive muscular atrophy and amyo-
trophic lateral sclerosis. The roots of the bulbar nerves are
almost always atrophied, and degenerative changes have been
found in the nerves themselves. The muscles atrophy and
undergo the same degenerative changes which are observed in
progressive muscular atrophy. When the disease extends into
the spinal cord, the ganglion cells of the anterior cornua are
diseased in the same manner as in progressive muscular
atrophy. When the cord is affected the spinal nerves issuing
from the diseased portions and the muscles to which they are
distributed are involved in morbid action.

§ 426. Diagnosis. — When bulbar paralysis is fully developed, [
the symptoms are so characteristic that it is hardly possible
to mistake them, but the onset of the disease is often very
insidious. The patient may complain of a feeling of pressure
and traction in the back of the neck, and a slight nasal
resonance of the voice, these being frequently the first
symptoms to attract attention. On closer examination it may
be observed that there is a slight alteration in the expression
of the face, and a certain degree of stiffness of the lips, causing
some imperfection of articulation, and that the tongue trembles
on protrusion.

In the fully established disease the difficulty is to distinguish
between the primary and secondary forms of the affection. The
diagnosis must be made from a careful investigation into the
history of the case, and the order of development of all tbe
symptoms. The manner in which the disease begins is the
best guide to distinguish it from embolism, thrombosis, and
haemorrhage in the medulla. These lesions always commence
suddenly, and the resulting paralysis is frequently unilateral
or more pronounced on one side than on the other, while pro-

SPINAL CORD AND MEDULLA OBLONGATA.

185

jressive bulbar paralysis is always gradual in its onset, and the
[ taralysis is uniformly bilateral.

§ 427. Treatment. — The treatment of true progressive bulbar
>aralysis has hitherto proved of little avail, but much may be
lone to add to the comfort of the patient and probably to delay
he progress of the disease. Nothing should be left undone
vhich tends to improve the general health of the patient.

The special remedies which have been employed in the
xeatment of the disease are nitrate of silver, iodide of potas-
iium, iodide of iron, chloride of gold and sodium, ergotine, and
)elladonna; but unless there is any special indication for the
id ministration of iodide of potassium I should, myself, follow
,he advice of Dr. Dowse, and trust to phosphorous, iron, and
:od-liver oil.

The galvanic current should be used. Erb advises the
tabile application of the current transversely through the
nastoid processes, and longitudinally through the skull ; also
galvanism of the cervical sympathetic, by placing the anode on
he nucha while the cathode is run rapidly over the lateral
urface of the larynx, twelve to twenty movements of degluti-
ion being induced at each sitting. The galvanic or faradic
:urrent may be applied to the tongue, lips, and palate.

As the power of deglutition becomes more and more impaired,
he food must be carefully selected and finely divided, and
inally the patient must be fed through a tube. Care should be
■aken to wash the mouth after eating, and to remove particles
)f food which lodge about the pharynx and underneath the
ongue.

5 . Pseudo - Hypertrophic Paralysis.

[Atrophia Musculorum. Lipomatosa.)

§ 428. Definition. — This disease is characterised by feebleness
)f the muscles of the lower limbs and of the erector muscles of
-he spine, gradually extending to those of the upper extremities.
The paralysis is accompanied by atrophy of some of the muscles,
ind by an apparent increase in the volume of others.

§ 429. His tory.— Isolated ase.s of this disease were described many years
' by several authors. A case was reported by Sir Charles Bell in 1830,

186

SYSTEM DISEASES OF THE

one by Coste and Gioja in 1838, and a well marked case by Mr. Partridge
in 1847. But Dr. Meryon, in 1852, was the first to draw attention to the
clinical features of this affection, and Oppenheim, in 1855, described a well '
marked group of cases. The disease was thoroughly investigated by
Duchenne. His friend, M. Bouvier, sent to his clinique in 1858 a child,
who had been suffering from an unusual form of paralysis, and during
the subsequent three years Duchenne collected other cases, which were
similar to the one sent by Bouvier, and yet did not correspond to the
description of any known disease. Duchenne described the principal
clinical characters of the disease in the second edition of bis work on
Localised Electricity (Paris, 1861), but it was not until 1868 that he
published in the "Archives Gdnerales de Me'decine" a full account of his !
investigations into the nature of the affection. He then gave detailed
descriptions of thirteen cases, which had come under his own observation,
and incorporated with these fifteen cases published up to that date by
other observers. So thoroughly was the work done by this distinguished
physician that nothing essential has since been added to our knowledge
of the course and progress of the disease. Cases have been described in
this country by Mr. William Adams, Dr. Langdon Down, Dr. Ord, Mr.
Kesteven, Drs. Bussell and Balthazar Foster (Birmingham), Dr. Barlow
(Manchester), Dr. Davidson (Liverpool), Dr. Clifford Allbutt, while Dr.
Gowers has written an able monograph on the disease.

§ 430. Etiology. — This affection is almost but not exclusively
confined to infancy. The first symptoms are frequently noticed
at the time when the child ought to begin to walk, although it
is very probable that the disease is established before that time.
The disease begins in a considerable proportion of cases between
the ages of five and thirteen years, and cases are recorded where
adults have been attacked. It may, however, be doubted
whether many of the latter are genuine examples of the disease.
In the case described by Auerbach, for instance, the hyper-
trophy was first noticed in the right arm, and microscopical
examination of the affected muscles showed that the disease
was more like true hypertrophy. In the case described by
Eulenburg, where the patient, a female, was forty-four years of
age when the first symptoms appeared, the paralysis began in
the right arm, in the form of progressive muscular atrophy,
and although there was apparent hypertrophy of the muscles
of the lower extremities, the course and progress of the case
was different from those of a case of true pseudo-hypertrophic
paralysis. In an undoubted instance of the disease under my

SPINAL CORD AND MEDULLA OBLONGATA.

187

re at present the patient is forty-seven years of age, but the
fection be<*an at the age of ten. It is much more common
boys than girls. Of the thirteen cases collected by Duchenne
ily two were girls, of forty-one cases collected by Webber only
re were females, and of twenty-three cases mentioned by Dr.
Dwers only five were females. Out of a total of 220 cases
therto published 190 were males and thirty females (Gowers).
le disease also appears to pursue a more chronic course in
rls than in boys.

Hereditary predisposition to the disease frequently exists.
>vo children in the same family are often attacked, as in the
ses related by Wernich, Heller, and Kesteven, and sometimes
-en eight children of the same family have been affected, as in
e cases related by Meryon. Lutz met with two sisters, a
aternal uncle and aunt, and a maternal half-sister, issue of a
st marriage, affected with the disease. In another example,
ree maternal uncles and aunts were affected ; in a second, a
iternal uncle and a half-uncle ; in a third, three maternal
,lf-brothers; and in a fourth instance, a maternal half-brother,
ree maternal uncles, and other members on the mother's side
oore). It is curious to notice that, although the disease is
linly confined to the male sex, yet the descent, so far as is
town, is always through the mother's side. This disease is
t, as a rule, transmitted directly from parents to offspring;
ice by far the greater number of its victims are attacked at
early age, and therefore do not become parents, and this
nsideration also precludes the idea that it is an example of
ivism. A certain predisposition is, therefore, transmitted,
lich, with the concurrence of other unfavourable circumstances,
2h as an eruptive fever, develops the disease.
The exciting causes of the disease are by no means clear,
.posure to cold and damp appears to be occasionally the
termining cause, while at other times it has followed an
lptive fever, variola, or measles, and several cases have been
hered in by convulsions.

§ 431. Symptoms. — Feebleness of the lower extremities is
ually the first symptom to attract attention, and when the
*ease begins during infancy it is difficult to fix the exact date

188

SYSTEM DISEASES OF THE

of its origin. The attention of the parents is not directed to the
condition of the child until he arrive at the age when otheB
children begin to walk. At this period it is noticed that when the
child is placed on his feet he does not instinctively move his
legs to walk, but immediately falls down, and in other cases
he may have begun to walk, but is soon fatigued and can
no longer stand steadily or walk without stumbling. At
other times the child may be late in attempting to walk,
and is obliged to support himself by holding on to the
nearest article of furniture. The parents are not readily
alarmed at the inability of the child to walk, inasmuch
as the limbs appear to be so well developed. When
standing or walking the feet are widely separated from one
another, and when they are made to approach each other
walking is rendered difficult, and the child may fall. In
walking, the body is inclined from side to side, so that the
gait resembles the waddling of a duck. . When the feet are
kept widely apart the centre of gravity at each step must be
carried well over to the side of the active leg, in order that
the line of gravity may pass through the centre of the arcb [
of the foot planted on the ground. Duchenne thought that the
oscillation of the body in walking depended upon weakness of

the gluteus medius. But in the case of Charlotte A , already

described (§ 412), the gluteus medius on both sides was
paralysed, yet instead of the waddling gait so characteristic of
pseudo-hypertrophic paralysis, the head and body were moved
forwards during locomotion in a straight line without the
normal lateral inclination of them being observed.

In several cases of pseudo-hypertrophic paralysis which I
have examined with reference to this point, on placing one of
my hands on each side of the pelvis immediately above the
trochanters, the gluteus medius on the side of the active leg
could be distinctly felt to contract at each successive step.
The patients also, when lying on one side, with legs extended,
are able to raise the upper leg away from the other, without
much apparent difficulty, and when the hand is placed over
the gluteus medius during this movement the muscle may
be felt to contract powerfully. In an advanced case of the
disease which I saw recently along with my friend Dr. John

SPINAL CORD AND MEDULLA OBLONGATA.

189

•own, of Burnley, the patient could not stand or sit erect, yet
nen lying on his side he could abduct the upper leg, and on
acing my hand above the great trochanter of the femur the
uteus medius was felt to contract. This muscle was, therefore,
>t likely to have been affected at an early period of the affec-
m. The oscillation of the body in walking, therefore, instead

being caused by paralysis of the gluteus medius, is, in my
>inion, mainly effected by contraction of this muscle. The
teral inclination of the body appears, indeed, to be rendered
icessary in the early stage of the affection partly by the legs
;ing held widely apart, and partly by the inability of the
itient to produce dorsal flexion of the foot so as to allow the
issive leg to swing forward in locomotion.

In the second stage of the disease, when double talipes
[uinus and dorsal curvature are established, other factors co-
>erate in the production of the alternate balancings of the
•dy. When talipes equinus is once formed, the body at each
ccessive step must be delicately balanced so that the line of
avity will pass through the ball of the foot, and consequently
e slightest displacement of the centre of gravity would cause
e patient to fall. It is therefore necessary that at each step
e body should be inclined well over to the side of the active
y, and the patient aids himself in balancing the body on the
.11 ot the foot on the side of the active leg by moving his
ms about like a rope dancer.

When the patient is laid down or falls, he raises himself in a
aracteristic manner. If any object be near which he can
uveniently grasp, such as a chair or other article of furniture,

drags himself up by his arms. When the patient has to get
> without extraneous aid, he first raises himself on his hands
d feet. In the first position which he assumes the patient's
?t are planted on the ground, the different segments of the
>ver extremities are slightly flexed upon one another, the
dy is flexed on the lower extremities, and the head directed
•wn wards, and the tips of the fingers of both hands rest on the
ound a little in front of the toes (Plate III., 1). The patient
;xt raises his hand, say the left, and places it above

e left knee. The body is now drawn over to the opposite
le so that its weight rests mainly on the right leg, by one

190

SYSTEM DISEASES OF THE

vigorous push of the left arm the left knee-joint is thrust back-
wards, and the leg and thigh are thus extended one upon
another, while the body is at the same time thrust upwards.
The feeble extensors of the body on the thigh are now brought
into action, and the trunk is partly raised upwards by their
contraction, and partly pushed upwards by the left upper
extremity, while the right may not require to be placed over
the right knee in the early stage of the affection.

But even in the early stage of the disease the action of the
extensors of the body on the thighs is greatly aided by the abduc-
tors of the thighs, and the patient may be observed to elevate the
trunk by a kind of rotatory movement, the body being drawn
first to the one side and then to the other.

The following case has afforded me an opportunity of studying
the different movements which are made in the act of attaining
the erect posture, inasmuch as these are slowly performed; and
as the case is of interest in other respects, I shall describe the
symptoms in detail. I have received valuable assistance from
Dr. A. H. Young in describing the different groups of muscles
which are brought into action by the patient in attaining the
erect posture.

Peter P forty-five years of age, was admitted to the Koyal Infirmary,

Manchester, February 12th, 1880. He was quite healthy until la
years of age, when he had an attack of typhoid fever. During the attack
of fever he suffered from bed-sores, and his recovery was slow and pro-
tracted. Subsequent to this period he could ascend a stair without
difficulty, and could carry weights like other people. He thinks, however,
that his mode of walking was peculiar, and that he was weak on his legs^
He could not join in games which required active exercise, as running, aua
the other boys at school amused themselves by pushing against him aua
throwing him down. At fifteen years of age he was apprenticed to a joiner,
and was then able to ascend a ladder and perform the ordinary work U
was not, indeed, until he was thirty years of age that his present symptom
be-an to attract attention. At this time his master observed that he wa
unable to get through his work like the other men, and consequently Ue
was the first to be discharged when work was scarce. The first symptom
which attracted his attention was that he was unable to ascend a stair .
without placing his hand on his knee, while holding on to the bams er j
the other hand. From that time up to the present, a period of thirt
years, he has become gradually and slowly worse. He was married
teen years ago, and has three children, all of whom are healthy

Present Condition.- The patient seems fairly well nourished and health

SPINAL CORD AND MEDULLA OBLONGATA. 191

here is a cicatrix two inches in diameter on the prominent part of the
crura, and a smaller one over the great trochanter of the femur, on each
ie, these being left by the bed-sores from which he suffered when ill of
phoid fever.

As the patient stands on the floor in the erect posture his feet are
t inches apart at the heels and 10 inches at the toes. The heels scarcely
uch the ground ; when he stands on his naked feet a piece of cardboard
u be readily passed between the heels and the floor. When he raises his
ot off the ground it assumes the position of talipes equino- varus, and he
uuot produce dorsal flexion of the foot, but there is no deformity of the
es. When the patient is staudmg the muscles of the calf are hard, tense,
mparatively large, and well formed. The muscles of the thigh are small,
ft, and flabby, so that the comparatively slender thighs offer a striking
utrast to the large and well formed calves. The buttocks are somewhat
ittened, and fibrillary movements are observed in the erector spinse and
e muscles of the back of the thigh. The scapular muscles are unaffected,
e deltoids are prominent, and act with great energy on voluntary effort,
ie pectoral muscles are decidedly atrophied, and the triceps, biceps, and
e coraco-brachialis are wasted to so marked a degree that the slenderness
the arm offers a strong contrast to the full and rounded shoulder caused
the prominence of the deltoid. The muscles of the forearm are not
rophied, and they stand out prominently under the skin, and feel hard
d tense when the patient grasps anything strongly, yet his grasp is
markably feeble. Dr. Leech, who has made a microscopic examination
portions of these muscles withdrawn by his trocar, assures me that
3y exhibit morbid changes, but he is unable to say that they are the same
those which characterise pseudo-hypertrophy of muscle.
The following measurements were taken : Height 5ft. 7in., circumference
the chest 32in., abdomen 3l£in., upper part of each thigh 16f in., middle
each thigh 13in., each calf 13^in., upper arm 7jin., forearm 9jin. The
cumference of the calf exceeds that of the middle of the thigh, while
3 circumference of the forearm greatly exceeds that of the upper arm.
hile standing the pelvis is inclined well forwards, his abdomen is some-
iat protuberant ; while the upper part of his body is dragged backwards,
that a deep curve, with its concavity directed backwards, is formed in
3 lumbo-dorsal region A plumb-line, let fall from the most prominent
the spinous processes of the upper dorsal vertebra), falls three iuches
hind the sacrum.

Walking. — The gait of the patient is peculiar and characteristic ; the
dy is alternately drawn from side to side, giving to the walk a duck-like

waddling movement. The patient, as already remarked, can neither
ice the two heels firmly on the ground at the same time, nor elevate the
3s by producing dorsal flexion of the foot, and consequently the passive
; cannot swing forwards with the normal pendulum movement.
The difficulty of moving the passive leg forwards is, indeed, increased

the fact that the predominant action of the muscles of the calf extends

192

SYSTEM DISEASES OF THE

the foot on the leg when once it is raised off the ground, so that the limb
is lengthened instead of being shortened by dorsal flexion of the foot, as
in normal locomotion. Under these circumstances the toes of the passive
leg are made to clear the ground by a different mechanism from that
which obtains in health. The feet are, as already described, held widely
apart ; and when the passive leg, say the right, is to be moved forwards
the body is dragged well over to the left. This movement is mainly
effected by the abductors of the thigh on the side of the active leg, and
the gluteus medius on that side is felt strongly contracted on placing the
hand over it. But the centre of gravity is not only drawn over to the
side of the active leg, but it is also drawn somewhat backwards by the
action of the gluteal and probably also the hamstring muscles, and the line
of gravity in passing through the arch of the left foot approaches the heel,
and the latter is now felt to be firmly planted on the ground. During
this double but combined movement the line of gravity is in danger of
being carried too far to the left and backwards, hence the right arm is
thrown outwards and forwards so as to maintain the centre of gravity as
far to the right and forwards as possible. During the lateral movement
of the body towards the side of the active leg the pelvis on the side of the
passive leg is elevated, and thus the length between the head of the femur
and ground is increased, and during the backward movement of the body
the pelvis is made to assume a more vertical position, so that the flexors of
the thigh on the body can act more efficiently on the passive leg. The
thigh of the passive leg is now flexed on the body, the abductors also
contracting and giving to the thigh an outward inclination, the leg is
slightly flexed on the thigh, and the foot is moved slowly forwards and
outwards, and when the step is completed the toe comes first to the
ground.

The forward and outward projection of the passive leg tends to counter-
act the tendency of the line of gravity to pass too far to the side of the
active leg and backwards. When the passive leg is placed on the ground
the abductors of the thigh on that side contract, the body is drawn over
to the right, and the line of gravity is slowly transferred to the leg that
was passive and which now in its turn becomes active.

Attaining the Erect Posture. — On rising from the recumbent position
the patient first gets on his hands and knees, and placing his right foot on
the ground, he rests his right elbow above the knee, and inclines his trunk
to the right so that the centre of gravity passes through the right foot.
When he leans well forwards in this position and presses his right elbow
downwards and backwards, it will tend to drag the trunk and with it the
right hip-joint forwards, but inasmuch as the right knee is at the same
time pressed downwards and backwards, any forward movement of the
hip-joint must be accompanied by elevation. Ihe weight of the trunk is,
therefore, so applied that it tends to drag the hip-joint forwards and
upwards, and thus to extend the trunk on the thighs and to push the right
knee-joint downwards and backwards, and thus to extend the leg upon

SPINAL CORD AND MEDULLA OBLONGATA.

193

the thigh, so that the weight of the trunk is so applied as to aid the
extensors in erecting the body.

The exten-or muscles are now brought into action, and the trunk is
slowly elevated to what I may call the second position. In this position
the various segments of the right lower extremity are slightly flexed upon
oue another, the trunk is directed forwards horizontally, and the right
elbow rests above the knee, while the left thigh is directed vertically
downwards, the left leg is inclined downwards and backwards, and the toe
rests ou the ground considerably behind the right foot, while the left hand
rests lightly on the left thigh immediately above the knee.

After a momentary pause the patient proceeds to attain the third posi-
tion. The abductors of the right thigh contract and rotate the pelvis so
that the left hip-joint is slightly elevated. This movement brings the line
of gravity well within the right foot, and takes the weight of the trunk
entirely oflfthe left lower extremity. The left foot is now drawn forwards
and placed on the ground in a line with the right foot, but slightly removed
from it laterally, while the left hand at the same time grasps the left thigh
immediately above the knee. By a contraction of the abductors and ex-
tensors of the left thigh the line of gravity is now transferred from the
right to the left foot, the right shoulder is elevated, and the right hand
is quickly transferred to the position previously occupied by the elbow ;
the abductors and extensors of the left thigh now relax, until the line of
gravity passes between the feet, and the third position is attained.

In this position the two sides are symmetrically placed. The feet are
placed on the ground and somewhat removed from one another, but the
heels do not quite touch the ground ; the legs are slightly flexed on the
| feet, the thighs on the legs, and the trunk on the thighs ; both arms pass
downwards and backwards, each hand grasping the thigh of the corre-
sponding side close above the knee. When the patient is viewed laterally,
the thigh, arm, and trunk are seen to form the three sides of a triangle
(Plate III., 3), and the weight of the trunk applied through the arms
must tend to push both knees downwards and backwards, while at the
same time tending to elevate the hip-joints. The body is inclined
forwards and upwards, but owing to the deep dorso-lumbar curve the
vertical axis of the pelvis occupies a more horizontal position than might
be expected from the upward inclination of the body. The line which
joins the anterior superior spine of the ilium and the head of the
femur forms nearly a right angle with that which joins the head of
the femur and the centre of the arch of the foot ; and, consequently, were
the gluteus medius and minimus of both sides now to contract, they would
act mainly as flexors of the pelvis on the thighs.

The patient, after a little pause to take breath, prepares for a further
elevation of the body, the great difficulty he has to encounter is to erect
the pelvis on the thighs, while at the same time extending the various
segments of the lower extremities upon one another. By transferring the
line of gravity from one foot to the other he takes the weight of the body
N

194

SYSTEM DISEASES OF THE

off each foot alternately, and in this way he is enabled to slip by turns
each hand further up the thighs until he grasps them about the junction
of the middle with the lower third. The trunk is now dragged over to the
left, so that the line of gravity passes through \he left foot, and the right
hand is removed from the right thigh (Plate III., 4). The right foot is
shuffled outwards and backwards, so as to allow the leg to be fully extended
on the thigh. This movement is performed with great deliberation, and
after it is effected the patient rests for a moment as if to assure himself
that the right foot, which now rests on its inner edge considerably behind
and removed from the left foot, is firmly planted so as not to slip. The
final effort now begins. Apparently by a combined action of the inward
rotators of the left and of the outward rotators of the right thigh the
pelvis is rotated obliquely from before backwards and from right to left.
By this movement the right hip-joint is brought well forwards, and the
pelvis is probably also, by a simultaneous action of the extensors of the
body on the thigh, made to assume a more vertical position. But what-
ever may be the nature of the muscular action concerned in this move-
ment, when it is completed the head of the right femur is placed almost
vertically below the anterior superior spine of the ilium, instead of being
on the same horizontal plane with it as in the third position. The line
which joins the anterior superior spine of the ilium and the great tro-
chanter now forms a very obtuse angle with that joining the great
trochanter and the middle of the arch of the foot, and in this position the
gluteus minimus and medius will act mainly as extensors, of the pelvis on
the thighs. The great effort of the patient is now directed to transfer the
line of gravity from the left to the right foot. This is effected by the
trunk being dragged over in a diagonal manner from before backwards
and from left to right, partly by the conjoined action of the extensors and
abductors of the right thigh, and partly by the left shoulder being pushed
upwards and to the opposite side by forces acting upon it from below
through the arm. The elevation of the left shoulder is effected by the
extension of the different segments of the arm upon one another, and by
the elevation of the heel and consequently of the knee by contraction of
the muscles of the calf. The upward movement of the left shoulder is
not one of simple elevation, but is indeed a very complex act. The left
knee is not only elevated by contraction of the muscles of the calf, but a
strong contraction of the adductors of the thigh prevents it from being
thrust out laterally. The inward rotators of the left arm (the latissimus
dorsi, teres major and minor, and infraspinatus), and the abductors of the
arm, especially the posterior third of the deltoid, enter into strong con-
traction. The tendency of the combined action of these muscles is, the
arm being fixed by the hand grasping the knee, to thrust the left shoulder
to the opposite side, and to rotate the body, so that the left shoulder is
pushed forwards in advance of the right one. We have already seen that
the pslvis was rotated in such a way that the right was placed in advance
of the left hip-joint, and now the left is pushed forwards in advance of

SPINAL CORD AND MEDULLA OBLONGATA.

195

the right shoulder, and consequently the upper part of the body is being
rotated in the opposite direction to the lower part ; or, in other words, the
pelvis is being rotated from right to left through the hip-joints, and from
left to right through the vertebral column, the power in the latter case
being applied on a level with the brim of the pelvis. If the forces which
tend°to rotate the pelvis from right to left, and those which tend to rotate
it from left to right were applied on the same level, they would tend to
neutralise one another, and the pelvis would remain more or less fixed.
But, inasmuch aa the forces which rotate the pelvis from right to left
are applied through the hip-joints, and those which tend to rotate it from
left to ri<mt through the vertebral column, the consequence is that the
former will tend to push the head of the right femur forwards, while the
latter will tend to carry the brim of the right ilium backwards. It will
be thus seen that the forward rotation of the left shoulder will tend to
carry the anterior superior spine of the right ilium backwards, and there-
fore assists the action of the gluteus medius and minimus of the right side
as extensors of the body on the thigh. It may, indeed, be said that the
double rotation just described twists or screws the pelvis into a more or
less erect position with reference to the right lower extremity, around the
hip-joint of which all the movements of the body at present centre.

As the line of gravity approaches the right foot, the left lower extremity
is becoming more and more inclined forwards and outwards, its different
segments become extended upon one another, and the toe rests on the
. ground. "When once the line of gravity passes through the right foot, the
extensors and abductors of the right thigh relax somewhat, while those of
the left now suddenly contract ; the pelvis is rotated once more in such a
way that the head of the left femur is brought forwards under the pelvis.
During this movement the left hand is removed from the thigh, the
muscles of the calf relax, the heel comes to the ground, and the line of
gravity is for a moment transferred to the left foot, but immediately after-
wards the weight of the body is borne by both feet, the line of gravity
falling between them, and the erect posture is attained.

When the patient reclines on one side he can raise the uppermost leg
away from the other with a considerable degree of force, and during this
action the gluteus medius can be felt strongly contracted.

When sitting he can cross one leg over the other readily, abduct and
adduct his legs with considerable force against a resisting object, but he
can only produce dorsal flexion of the foot to a slight extent.

Owing to the feebleness of the gluteus maximus, the patient
experiences great difficulty in getting up steps, and the manner
in which he ascends a stair is as characteristic as that in which
he attains the erect posture. He lays hold of the railing with
one hand, say the right, and by the contraction of the muscles
of the right upper extremity he drags his body upwards at each

196

SYSTEM DISEASES OF THE

step. The right arm is, however, assisted by the left. The J eft
hand is planted above the left knee, and each time the left leg
is raised a step the body is thrust upwards by the various
segments of the left arm being extended upon one another.

One of the most constant symptoms of the disease is the
existence, during standing or walking, of a remarkable curva-
ture of the spine in the lumbo-sacral region. The shoulders
and upper part of the vertebral column are carried backwards,
so that a plumb-line let fall from the most prominent spinous-
process of the vertebrae falls behind the sacrum. I have, how-
ever, observed an undoubted example of the disease in which:
the plumb-line did not clear the sacrum. Duchenne attributes:
this incurvation to weakness of the erector muscles of the spine:
but, as pointed out by Dr. Gowers, weakness of the extensors oi
the pelvis on the thighs contributes to the formation of th
lordosis. Weakness of the extensors allows the pelvis, an
with it the lowest lumbar vertebras, to incline forwards in tried
erect posture, and a compensatory backward inclination of the-:
dorsal spine is necessary in order to keep the centre of gravit]
in the normal position.

Another important feature of the disease is that the patiem
has . a difficulty in bringing his heels to the ground ; and, as th.<
case advances, a permanent condition of talipes equinus, o
equino-varus, is established. The foot becomes more hollov-
from increase of the plantar arch, while paralysis of the inter:
ossei causes the first phalanges to be maintained in a state cd
exaggerated extension on the metatarsal bones, and the tw
distal phalanges to be flexed, so that the toes assume thh
peculiar clawlike appearance, which Duchenne has called grit
des orteils.

The apparent hypertrophy of the muscles, which is the mo?:
characteristic symptom of the disease, generally begins by ei
largement of one calf, the other also becoming affected befon
very long. This is the usual mode of invasion, but sometim
the muscular enlargement begins in the muscles of the upp
extremities, as ia a case related by Duchenne, where tl
deltoids had begun to enlarge many months before the gastr
cnemii. The gluteal muscles become affected soon after tho
of the calf, and then the disease extends in succession to t.

SPINAL CORD AND MEDULLA OBLONGATA.

197

lumbo-spinal muscles and to some of the muscles of the thigh,
trunk, and upper extremities. Of the muscles of the upper
extremities the deltoids are usually the first to suffer. In one
case related by Duchenne the apparent hypertrophy had become
so general that, with the exception of the pectoral muscles, the
latissimus dorsi, and the sterno-mastoids, all the muscles of the
limbs, trunk, and even those of the face, especially the tem-
porals, were successively invaded. In a case related by Weir
Mitchell not only the muscles of the face, but even those of
the tongue, were hypertrophied.

The affected muscles may attain an enormous volume, and
stand out so prominently under the skin that Duchenne uses
the term " hernial protrusions " to describe their appearance.
The muscles also feel hard and resisting to the touch, so that
the whole appearance of the child often suggests the idea of
Herculean strength instead of the great feebleness which in
reality exists. Bat even amidst all this apparent development
of muscular power there are not wanting visible indications of
the real nature of the malady. Some of the muscles are always
found atrophied, their wasted condition contrasting strongly
with the excessive size of the others. Even in the case related
by Duchenne, where the child looked like a young Hercules,
the pectorals and latissimus dorsi were atrophied. In the
majority of cases the muscles of the calves and buttocks, and
probably also the deltoids, are enlarged, while the remaining
muscles of the arm, forearm, shoulders, and trunk are atrophied;
so that the slenderness of the upper part of the body offers a
strong contrast to the abnormal development of the inferior
extremities. We see, therefore, that all the paralysed muscles
do not undergo augmentation of bulk; in fact, atrophy of some
of the muscles is a constant symptom of the disease. Another
circumstance worth noting is that the degree of paralysis has
no direct relation to the amount of hypertrophy. This is well
illustrated in the leg where the action of the extensors of the
foot, although these are much enlarged, predominates over that
of the flexors, as evinced by the elevation of the heel.

The disease now becomes more or less stationary for two or
three years, and sometimes for a much longer period, and as
the general health is good and the muscular development

198

SYSTEM DISEASES OF THE

apparently very powerful, the parents cannot believe that the?
affection is incurable. This illusion is, however,, after a time.;
destined to be dispelled. The feebleness of the lower extre-
mities gradually increases, so that the child cannot maintain,
the erect posture, while the muscles of the superior extremities.-
also become both paralysed and atrophied ; and even the hyper--
trophied limbs begin to waste, and to diminish rapidly in size. .
The patient, now arrived at adolescence, may live on for several]
years in a condition of almost complete paralysis, until finally
death takes place from exhaustion, implication of the respirator^
muscles, or more usually from some intercurrent affection.

There are still some minor features of the disease wbicl
deserve attention. The statements of different observers, witl
respect to the electro-muscular contractility, are somewhat con
tradictory. Except in the very early stages of the disease, th<.
faradic contractility is diminished, while the galvanic contrac
tility may be normal or increased. In the second stage of th<
disease the quadriceps tendon-reflex is completely abolished.

Very frequently the skin over the affected parts presents j
peculiar mottled appearance, the colour varying in different
cases, and in the same case according to the degree of exposure!
Sometimes it is described as of a roseate hue, again as brighba
red, and at other times as consisting of patches of purplis- 1
colour alternating with white. All of these phenomena, howvl
ever, indicate capillary congestion, the result of vaso-motor diri.J
turbance. This supposition is still further strengthened by thbl
fact that the superficial temperature of the inferior extremiti( f
is frequently higher than that of the trunk.

This disease is often associated with a certain amount <<1
mental incapacity. In several instances the subjects of it haw|
been noticed to be slow in acquiring the power of speech, othesB
are described as being obtuse in intelligence, and a considerab I
number have been idiots. The disease is not accompanied tl 1
any suffering, there is no alteration of sensibility, and the fun
tions of the bladder and rectum are not interfered with, whi J
the general health is not much affected until near the termin I
period of the affection.

§ 4*32. Course and Duration. — The disease is essential I

SPINAL CORD AND MEDULLA OBLONGATA.

199

chronic. It begins without fever or marked derangement of
the functions of digestion, respiration, or circulation. As
already stated, it consists of a first stage in which there is
progressive enfeeblement of the lower extremities, saddle-back,
and waddling gait. This stage may last a few weeks, months,
or even a year before the commencement of the next stage.
The second period is characterised by apparent hypertrophy of
a certain number of muscles, usually beginning in those of the
calf, and extending gradually to other muscles of the trunk
and upper extremities. Increase in the volume of some muscles
is always accompanied by atrophy of others. This stage of
muscular hypertrophy continues to increase progressively, and
attains its maximum in degree and extent about eighteen
months from the beginning of the second stage of the disease ;
the symptoms then remain stationary for two, or three, and
sometimes for many years.

The third stage of the disease is now ushered in by a still
further enfeeblement of the muscles already affected, and by
the extension of the paralysis to the superior extremities. Ab-
duction and elevation of the arm is at first rendered difficult,
then impossible, and by-and-by the paralysis gradually im-
plicates the other movements of the arm.

The child, now probably arrived at the age of puberty, enters
upon the last stage of the disease. The slight power of move-
ment of which he was capable during the previous period
becomes gradually lost, so that he can only sit in a chair or
recline on a couch. The patient may continue to live for a
long time in this condition, but eventually death supervenes
from exhaustion or some intercurrent malady.

§ 433. Diagnosis. — When the disease is thoroughly estab-
lished there can scarely be any possibility of mistaking it for
any other affection. The diseases which are most nearly related
to it are infantile paralysis and progressive muscular atrophy
in the infant. True muscular hypertrophy may also be mis-
taken for the disease, and a likely condition to be confounded
with it is a late development of the power of muscular co-
ordination and walking in children, especially when combined
with a cerebral lesion, as in cases of idiotcy.

200

SYSTEM DISEASES OF THE

The invasion of infantile paralysis is sudden and accompanied
with fever, and the distribution of the paralysis is totally different
from that of the pseudo-hypertrophic variety. Sometimes the
paralysis is limited to a few muscles or to an entire limb, at
other times it is hemiplegic, crossed, paraplegic, or general.
The muscles which are least injured recover completely, while
others atrophy, and in the latter there is very early and
decided diminution of electro-muscular contractility.

Progressive muscular atrophy in the child usually begins
between the age of five and seven. Some of the facial
muscles, principally the orbicularis oris and zygomatici, become
atrophied. After a stationary period of some years the atrophy
extends successively to the muscles of the upper limbs and
trunk, and the lower extremities are not affected until a more
advanced period. The muscles are invaded irregularly, and .
as the degree of paralysis is always proportional to the amount .
of atrophy this gives rise to various deformities of the trunk .
and limbs. When the atrophy attacks the extensor muscles of:
the trunk and some of the muscular groups of the lower ex- ■

tremities, as in the case of Charlotte A , already described, 1

progressive muscular atrophy is by no means easy to distinguish i
from pseudo-hypertrophic paralysis.

In making a diagnosis, the main reliance must then be
placed on the history of the case, the progress of the symptoms, .
and a microscopic examination of portions of the muscles of:
the calf withdrawn by the trocar.

Simple muscular hypertrophy may be distinguished from
pseudo-hypertrophic paralysis by the history of the case, the ab- -
sence of paralysis and of the special symptoms of the latter disease, >,
and if necessary by a microscopic examination of the muscle.

In late development of the muscular co-ordination in
children the feet are not planted widely apart, and there is noc
saddle-back or waddling walk. When want of co-ordination is i
combined with idiotcy there is a flow of saliva from the half-;
open mouth, and the tendinous reflexes are generally exag-
gerated in the lower extremities.

§ 431'. Morbid Anatomy. — The first examination of the con-
dition of the muscles in this disease was made in Germany by

SPINAL CORD AND MEDULLA OBLONGATA.

201

Greisinger and Billroth, who excised in a young living sub-
ject a portion of the left deltoid which was completely paralysed
and hypertrophied. Duchenne, however, not liking to under-
take such a serious operation, invented a small instrument,
which he called his " Emporte piece histologique," and which
enabled him to obtain minute portions of muscular tissue from
the living subject. A modification of this instrument, first
proposed by Dr. Ord (Med. Chir. Transac, vol. lvii., 1874), and
made by Hawksley, London, is generally used in this country
for the purpose. But after repeatedly using Dr. Ord's trocar in
various diseases, I am quite satisfied that the relations which
the different elements of the diseased muscle bear to one
another are not always accurately represented by the fragment
of tissue withdrawn by the instrument. Charcot indeed sug-
gests that Duchenne's instrument will withdraw islets of con-
nective tissue, inasmuch as it will seize the fat cells with
greater difficulty; and, judging from my experience of Dr.
Ord's trocar, the objection is valid.

The happy idea occurred to Dr. Leech that an instrument
might be constructed which would withdraw a portion of the
muscle by cutting instead of by tearing; and Hawksley has
made one at his suggestion, which answers the purpose
admirably. The first muscular change which takes place in
this disease consists of an increase of the connective tissue
which separates the muscular bundles from one another, so that
the sheaths of the muscular bundles become greatly thickened.
There is also a corresponding increase of the connective tissue
which passes between the fibres themselves. The compara-
tively thick masses of tissue which now separate the fibres from
one another consist of fibres arranged parallel to the long axes
of the muscular bundles, mixed with a considerable number of
embryonic cells. In this early stage the muscular fibres them-
selves do not appear to undergo any very manifest changes,
except that, according to Duchenne, their transverse striation
becomes fainter, while the longitudinal striation becomes
more marked. The transverse striation is, however, generally
quite distinct until a late period of the disease. Duchenne
regarded the proliferation of the connective tissue as the chief
cause of the increased size of the muscle ; hence he called the

202

SYSTEM DISEASES OF THE

disease "paralysie myoscUrosique ;" but other authors believe
that the muscle does not increase much in volume until the
second stage of the change occurs. This stage consists of the
development of fat cells in the connective tissue and also in the
newl}T-formed fibrous tissue, whereby the muscular fibres become
widely separated from one another. The muscular fibres now
become atrophied and begin to disappear. They become nar-
rower, and indeed a single fibre varies in diameter at different
points in its length. The transverse striation may sometimes
disappear in the narrower fibres, and be replaced by granules
distributed uniformly through them. Much of the fibrous tissue
surrounding the fibres contains oat-shaped nuclei, which are sup-
posed by some to be derived from the empty sheaths of muscular
fibres (Clarke, Gowers). After a time both the muscular fibres
and the newly-formed fibroid tissue completely disappear, and
the entire muscle is represented by fat cells like those of an ordi-
nary lipoma. The fat may subsequently become absorbed, and
connective tissue, with perhaps a few traces of muscular fibres,
is all that is left.

Condition of the Nervous System. — The brain and spinal
cord have been examined in several patients who died from this
disease, but the examinations possess no real value except in
two or three instances. Even in the case reported by Eulenburg,
where the cord was examined with great care by such a com-
petent observer as Cohnheim, it has been justly objected by
Charcot that delicate lesions like atrophy of the motor cells
might escape detection, inasmuch as the cord was examined in
the fresh condition, or only after imperfect hardening. If this
objection be valid, when urged against an examination con-
ducted by Cohnheim, how much more true does it become when
either no microscopic examination or only a very imperfect one
was made. In one of the cases collected by Duchenne the
patient died in February, 1871, and his brain and spinal cord
were carefully examined, both in the fresh state and after
hardening in chromic acid. Portions were forwarded to Charcot,
Vulpian, and Lockhart Clarke, and no abnormal appearances
were detected. A large number of sections of the cord, at
different levels of the cervical and dorsal regions, were made by
M. Pierret, and coloured by carmine, but neither Charcot nor

SPINAL CORD AND MEDULLA OBLONGATA.

203

he could detect any trace of disease. M. Barth examined the
cord in the case of a man forty-four years old, who suffered
from muscular pseudo-hypertrophy, and found partial de-
generation of the antero-lateral columns, and diminution of the
number of ganglion cells in the anterior horns of the cord.
Charcot, however, justly points out that the clinical characters
of this case were more like amyotrophic lateral sclerosis than
pseudo-hypertrophic paralysis.

The most important case hitherto examined is the one
reported by Drs. Lockhart Clarke and Gowers, in which
" varied and extensive " lesions of the cord were found. These
lesions were so numerous that only the most important of them
can be mentioned here. The changes began on a level with
the origin of the second cervical pair of nerves, and consisted
of " disintegration of the lateral grey network which is so con-
spicuous in the region between the caput cornu posterioris and
the tractus intermedio-lateralis, and through which the spinal
accessory nerve makes its way into that tract." "One- half of
the anterior white commissure was entirely destroyed." In the
lower part of the cervical region there was disintegration of
some of the " posterior nerve roots near the entrauce into the
caput cornu posterioris," and both the lateral and posterior
white columns were in many sections damaged by sclerosis.
In the upper portion of the dorsal region " the changes were
less frequent and extensive, but here and there the anterior
white commissure was partially destroyed." The lesions were
" most extensive and striking" at the lower part of the dorsal
region and the commencement of the lumbar enlargement.
The central and lateral parts of the grey substance on each
side were severely damaged by softening and disintegration.
In the middle part of the lumbar enlargement the lesions
were less serious, but in the lower portions and in the conus
medullaris the lesions of the grey substance were again more
extensive and severe. " The central part of the anterior cornu
and the outer part of the cervix cornu posterioris were very
much damaged by continuous disintegration." The large nerve
cells in the anterior cornua were much diminished in number,
and the few remaining cells were atrophied and contained an
excess of pigment.

204

SYSTEM DISEASES OF THE

The following abstract of an important case of this disease,
in which a post-mortem examination was obtained, I owe to
the kindness of Dr. Leech, who is preparing a series of in-
teresting cases of this disease for publication.

R. J , aged seven, came under Dr. Leech's care at the Manchester

Infirmary on the 20th of September, 1877, with the well-known symptoms
of pseudo-hypertrophic paralysis. His walk and method of rising from
the recumbent posture were quite characteristic, and lordosis was well
marked. The calves of the legs were unduly large and firm, the arms
and thighs thin, distinctly atrophied, the other parts of the body were
badly nourished though not definitely wasted. The pectoral muscles were
the most reduced in size and strength, whilst the deltoids were firm and
large as compared with the other muscles of the shoulder and arm.

The boy could stand, though not without difficulty, for the heels could
only be brought to the ground with effort ; his power of locomotion was of
course limited, yet he could easily walk across a wide ward without
falling. The boy had appeared quite healthy till he began to walk. When
two years old it was noticed that he was not so firm on his legs as his
brothers and sisters had been. As he advanced in age muscular weakness
became more apparent. He fell constantly and had difficulty in rising ;
he could only get upstairs with the aid of his arms. At three years of
age the boy's limbs had lost their plumpness. The increase in the size
of the calves of the legs was not noticed till six months before he came
into the Infirmary. It does not appear that any other member of the
family had been similarly affected.

The boy continued under my care two years, and then died of bron-
chitis. A slight amount of wasting went on in all parts of the body during
this time, and the loss of muscular power was considerable.

Eighteen months before he died he became unable to walk or stand,
and the rest of his life was passed in a chair or lying down. For the last
six months he was unable to extend fully his legs, and sat in a bowed
position owing to the weakness of the muscles of his back. The calves
of his legs decreased slightly in size, but continued large as compared
with the other parts of the body.

A post-mortem was made thirty-six hours after death. The muscles
had, for the most part, lost their normal appearance, and were of a light
yellowish brown colour. In some places it was difficult to distinguish
them from connective tissue. This was specially the case with the pectoral
muscles. The gastrocnemius looked on section like dark-coloured fatty
tissue. In taking out the spinal cord a very distinct difference was
noticed between the condition at the erector spinoe in the lumbar and
upper dorsal region. In the former the muscles had a connective-tissue-
like appearance ; towards the mid-dorsal region they became darker and
redder, and in the upper dorsal region had the ordinary appearance of
muscular tissue.

SPINAL CORD AND MEDULLA OBLONGATA.

205

The muscles in the cervical region had the same appearance as those
in the upper dorsal. The rhomboids, levator anguli scapulae, and tra-
pezius were distinctly altered in colour and texture, the upper part of
the trapezius being the least affected.

The microscope seemed to show that nearly all the muscular tissue in
the body was affected, for even in that taken from the upper dorsal region
which looked healthy a distinct increase of connective tissue between the
fibres was evident.

In the muscles which appeared to the naked eye most changed, such
as the pectorals, the new connective tissue growth was very much more
extensive, all the fibres of the primitive fasciculi being separated by it,
whilst here and there single fibres ran alone widely separated by connec-
tive tissue from their companions.

Here and there rows of fat cells appeared sometimes between muscular

Fig. 172.

Fig. 172 (Young). Muscular Fibres in various stages of degeneration, from a case of
Pseudo- hypertrophic Paralysis. — a, Muscular fibre only slightly changed
showing increase of the muscle corpuscles, and indistinctness of the transverse
striation in certain parts of its Jength; b, the same as a, but more atro-
phied ; c, muscular fibre greatly atrophied, and presenting nuclei at intervals •

d, atrophied muscular fibre, with its transverse striation unusually distinct •

e, atrp-phied fibre surrounded by a fibrillated connective tissue rich in
nuclei ; /and g, muscular fibres from the erector spinre, which manifested the
greatest changes to the naked eye. These fibres appear to have undergone a
hyaline change, but their transverse striation is still faintly visible. The fibres
often tapered to a point, sometimes at one and sometimes at both ends.

206

SYSTEM DISEASES OF THE

fibres, sometimes surrounded by connective tissue, and in places accumu-
lations of fat cells were met with instead of single rows.

In the gastrocnemius muscle the same condition was present, but the
fat cells were much more abundant and formed loose accumulations of
adipose tissue amid the muscular fibres and connective tissue.

In all the muscles the fibres were distinctly narrowed, and the nuclei
of the sarcolemma were greatly increased in number, but the striation of
the fibres was for the most part not interfered with and was often unusually
distinct, even in fibres which had undergone a high degree of atrophy
{Fig. 172, c, d). The annexed diagram {Fig. 172) represents the more
usual appearances presented by the altered muscular fibres.

In very few of the fibres was granular change met with, whilst hardly
any good examples of true fatty change were seen.

The decrease in the diameter of the muscular fibre seemed most marked
in the muscles which were most changed to the naked eye. In the erector

Fig. 173.

Fig. 173 (Young). Transverse Section from the lower half of the Lumbar Enlarge-
ment of the ISpinal Cord, from a case of Pseudo-hypertrophic Paralysis. — A,
Anterior grey horn ; P, Posterior grey horn ; cc, central canal ; i, internal,
a, anterior, al, antero-lateral, pi, postero-lateral, c, central group of ganglion
cells ; m, median area.

spinse from the upper dorsal region, for example, it was hardly manifest ;
whilst many of the fibres of the pectoral muscle were reduced to one-sixth
of their normal diameter. The narrowing of the musoular fibres seemed
indeed proportionate to the extent of the development of the new con-
nective tissue.

SPINAL CORD AND MEDULLA OBLONGATA. 207

Dr. Leech kindly sent the spinal cord to me for examination. In the
lumbar region the normal loose and spongy texture of the central column
was replaced by a somewhat dense and fibrillated tissue, in which no trace
of ganglion cells could be found. The blood-vessels were enlarged, and
their walls thickened. In the anterior grey horns the ganglion cells had
completely disappeared from the median area, the anterior group, and the
margins of all the other groups {Fig. 173). The ganglion cells could be
distinctly seen in the internal group {Fig. 173, i), but they were atrophied,
and only a few of their processes could be discovered, and the central
group {Fig. 173, c) presented one or two cells only which were not distinctly
atrophied. The central portions of the anterolateral and postero-lateral
{Fig. 173, al, pi) groups, however, contained some cells which appeared

Fig. 174.

« • ^0U Transverse Section from the middle of the Dorsal Region of the
bpmal Cord from a case of Pseudo-hyper trophic Paralysis.— vc, The vesicular
column of Clarke. The other letters indicate the same as the corresponding
letters in Fig. 173. * °

in every respect normal, but others contained an excess of pigment, while
the marginal cells were decidedly atrophied.

In the dorsal region the central column presented the same general
appearances as in the lumbar enlargement. The disease extended into
the anterior grey horn in the dorsal region chiefly in the area which
lies between the antero-lateral and postero-lateral groups {Fig. 174, al,pl)~
medio-lateral area. The ganglion cells of the postero-lateral 'group
were atrophied and destitute of processes to a very marked degree. The

208

SYSTEM DISEASES OF THE

cells could not be seen, in the anterior {Fig. 174, a) nor in the central group,
but those of the internal and antero-lateral groups were distinctly visible.
Many of the latter, however, contained an excess of pigment, and appeared
to have lost a considerable number of their processes. The cells of the
vesicular column of Clarke appeared normal or only slightly altered.

In the cervical region the central column also presented the same
general appearances as the other portions of the cord just examined. In
the lower half of the cervical enlargement, however, the median area of
the anterior horns contained beautiful healthy cells, and it contrasted
strongly in this respect with the median area in the lumbar enlargement.
The internal group of cells were also healthy, while healthy celLs were
seen in the anterior group. The marginal cells of the central, antero-
lateral, and postero-lateral groups were, however, atrophied, while many
of them had disappeared. In the upper end of the cervical enlargement
the central and antero-lateral groups appeared to have been more diseased
than any other portion of the anterior horn {Fig. 175, c, al).

Fig. 175.

Fig. 175 i Young). Transverse Section from the upper half of tlie Cervical Enlargement
of the Spinal Cord, from a case of Pscudo-hypertrophic_Paralysis. The letters
indicate the same as the corresponding letters in Fig. 173.

§ 435. Pathology. — This disease is so frequently associated
with obtuseness of the mental faculties, or with idiotcy and cre-
tinism, that Duchenne was at first inclined to believe that the •
muscular changes resulted from cerebral disease. More extended I

SPINAL CORD AND MEDULLA OBLONGATA.

209

observation, however, soon showed that this affection frequently
exists independently of any cerebral lesion. The dilatation of
the capillaries of the skin over the affected muscles, and the
frequent elevation of the superficial temperature of the limbs,
as compared with that of the trunk, have led some pathologists
to think that the primary lesion is situated in the vaso-motor
nervous system, but no additional facts have been discovered
to verify this supposition. There still remains the question,
whether the disease is primarily in the muscles, or in that
part of the nervous system which controls their nutrition.
Charcot and Friedreich regard the muscular lesion as the
essential one. Friedreich, however, looks upon progressive
muscular atrophy also as primarily a muscular disease; and,
indeed, he considers the two diseases as essentially the same,
although each is somewhat modified by circumstances.

Charcot, on the other hand, who believes that progressive
muscular atrophy is primarily a nervous disease, regards pseudo-
hypertrophic paralysis as a primary disease of the muscular
tissue. Charcot grounds his opinion mainly on the fact that he
could detect no lesion, in the cord which he had examined for
Duchenne ; and considering how thoroughly competent he is to
decide such a point, it must be admitted that the objection
against regarding the disease as of nervous origin is an ex-
ceedingly strong one.

Passing over the case observed by Barth, as not being an
undoubted example of the disease under consideration, the case
observed by Drs. Lockhart Clarke and Gowers speaks strongly
in favour of the nervous origin of the affection. It is evident,
from the description, that extensive changes had occurred in
the central column, and the postero-lateral group of cells of the
anterior cornua, throughout the greater part of the lumbar
enlargement and lower dorsal region of the cord. I observe,
however, that even Dr. Gowers has abandoned the nervous
theory of pseudo-hypertrophic paralysis, and we must leave the
question an open one at present.

In any subsequent case the condition of the ganglion cells of
the postero-lateral and medio-lateral groups in the lumbar and
Jorsal regions of the cord should be carefully examined. In the
spinal cord which I examined the changes found in the central
o

210 SYSTEM DISEASES OF THE SPINAL COED.

grey column and anterior grey horns corresponded so closely
with those observed in progressive muscular atrophy, that I see
no reason to question the essential unity of the two diseases.

Even if pseudo-hypertrophic paralysis were proved, beyond
doubt, to be a primary disease of the muscular tissue, yet the
clinical affinities between it and progressive muscular atrophy
are so numerous as to justify us in considering the diseases in
the same category.

§ 436. Prognosis. — In two cases under the care of Duchenne,
the disease was arrested in its first stage by treatment. This
shows that the prognosis is not absolutely hopeless. When, how-
ever, the second period, or that of apparent hypertrophy of the
muscles, has set in, the case is in all probability beyond the
reach of treatment, and it is still more surely progressive and
fatal in the period of atrophy.

§ 437. Treatment. — Duchenne relied mainly on the faradic
current in the two cases which he cured. Baths, friction, and
shampooing were also employed as subsidiary means. The gal- [
vanic current applied over the sympathetic nerves has beeu
recommended by Benedikt, but this method has not been found
to possess any advantage in the hands of others. An improvement
in motor power took place in a case under the care of Rosenthal
by the application of the constant current several times a week
to the nerves of the hypertrophied muscles, along with the
daily use of rubbing and the cold plunge bath. Gymnastics
and mountain air aided the treatment. The iodides of iron
or of potassium, or when there are cerebral symptoms the
bromide of potassium may be tried ; but the remedies which
promise to do most good are the so-called tonics, Arsenic,
Parrish's chemical food, phosphorus, and cod-liver oil, and in
some cases strychnia or nux vomica, may be tried.

211

CHAPTER IV.

I.— SYSTEM DISEASES OF THE SPINAL CORD AND
MEDULLA OBLONGATA.

(II.) LEUCOMYELOPATHIES.

1. Progressive Locomotor Ataxy.

(Tabes Dorsalis ; Grey Degeneration, or Sclerosis of the Posterior Columns.)

§ 438. Definition. — Locomotor ataxy is a chronic disease,
characterised by the progressive abolition of the power of
co-ordinating the general movements concerned in locomotion,
and other voluntary actions, but without distinct loss of mus-
cular power.

§ 439. History. — An accurate knowledge of this disease, which is now
so well known, is of comparatively recent date, although obscure inti-
mations of tbe affection may even be found in the writings of the Greek
physicians. In 1679 Bonnet appears to have revived the name of tabes
dorsalis, which had fallen into disuse, and he also associated the symptoms
with anatomical changes, principally atrophy of the spinal cord. Indi-
vidual observations of the disease may be found in the works of Ollivier,
Cruveilhier, Hutin, and Stanley, and the phenomena of ataxy were
described with great accuracy by Bell, Nasse, and Landry ; but W. Horn
was the first to give an accurate account of the course and symptoms of
ataxy, and to recognise it as a distinct type of disease. Horn's description
xppeared in 1827, and the classical monograph of Romberg was published
in 1840, while the anatomical investigations of W. and E. Horn, Jacoby,
Froriep, and, above all, the microscopic researches of Rokitansky and
Tiirck proved that the symptoms were caused by grey degeneration of
the posterior columns of the cord. The disease was most accurately
described in England in 1847 by Todd, who directed special attention
to the fact that the characteristic symptoms were due to want of power
m co-ordinating movements, and not to deficiency of voluntary power.
French physicians had completely neglected the affection until Duchenne

212

SYSTEM DISEASES OF THE

published his memoir in 1858, and so profound was the impression pro-
duced by the exhaustive analysis and accurate descriptions of this author
that he was for a long time regarded as the discoverer of the disease.
The writings of Duchenne and Trousseau contributed more than any
others to obtain for this affection the recognition of the profession.
Duchenne did not make any contribution to the pathological anatomy of
the disease, but he thought that the deficiency of motor co-ordination
must be dependent upon some structural or functional lesion of the
cerebellum. He suggested that the central morbid process began in the
motor nerves of the eye and the corpora quadrigemina, from which it
extended to the superior peduncles of the cerebellum, and lastly to the
cerebellum itself. This view was combated by Eisenmann, and a lively
discussion ensued which had the effect of settling definitely that the most
constant anatomical lesion in locomotor ataxy is grey degeneration or
sclerosis of the posterior columns of the spinal cord. Amongst the
authors who contributed to establish this view may be mentioned
Dumenil, Bourdon, Oulmont, Marrotte, Charcot and Vulpian, Luys and .
Carre' in France ; Bindfieisch, Westphal, Friedreich, and Leyden in Ger- •
many ; and Lockhart Clarke in England. In its clinical relations the
disease has been investigated amongst others by Jaccoud, Topinard, .
Axenfeld, Remak, Spaeth, Cyon, Benedikt, and many other authors.

The name of the disease has also undergone frequent changes in accor-
dance with the prevailing doctrines with regard to its nature. When iti
was regarded as being due to atrophy of the spinal cord, it received theo
name of "Atrophia Medullse Spinalis," a name which had to be abandoned'.!
on more accurate histological investigation. Wunderlich called it " Pro->-
gressive Spinal Baralysis," but this name became untenable when it waa-
found that the symptoms did not depend upon paralysis but on want ofr
co-ordination. In the present day three names are employed indifferently^
to designate the disease. These are " Grey Degeneration or Sclerosis ol
the Posterior Columns of the Cord," " Progressive Locomotor Ataxy," and*
"Tabes Dorsalis." None of these names are- entirely free from objections?
but they have got possession of the field, and it would occupy space tc
very little advantage to discuss here all objections which might be urgec?
against them.

§ 440. Etiology. — The etiology of the disease is very obscure
and in many cases no definite cause of it can be traced.

Hereditary predisposition undoubtedly exercises a certai
amount of influence in its production. Locomotor ataxy i -
frequently met with in individuals whose nearest relative
are liable to suffer from other nervous diseases, such £
monomania, hypochondriasis, epilepsy, migraine, mental dii
eases, or violent fits of anger and drunkenness. Troussea

SPINAL CORD AND MEDULLA OBLONGATA.

213

mentions the case of a patient suffering from advanced
locomotor ataxy, whose uncle and aunt were insane, and who
had one brother ataxic and another hemiplegic. He also
mentions the case of another patient who had been ataxic
for upwards of twenty years, but whose intellect was perfectly
clear. His father committed suicide; aDd his two sons laboured
under peculiar nervous affections, one having singular muscular
spasms, and the other being irresistibly compelled to shriek in
a most extraordinary manner nearly all day. In other cases
the influence of heredity is direct from the parent. Friedreich
met with three different families in which several brothers
and sisters were attacked with the disease at almost the same
age, while the parents themselves were healthy. Carre was
informed by an ataxic patient that seventeen other members of
her family were affected by the same disease. Dr. Dreschfeld
has recorded an instance of a family in which five out of fifteen?
and Dr. Gowers one in which five out of nine children were
affected with locomotor ataxia. In many cases of tabes no
hereditary neuropathic tendency can be traced.

The male is much more liable to be affected with the dis-
ease than the female sex, no doubt greatly owing to the fact
that men are much more exposed than women to the most
powerful exciting causes of the affection, such as exposure to
cold and sexual excesses. Out of 149 cases collected by
Eulenburg 128 were males and 21 only females, so that the
number of the latter affected in proportion to the total number
was barely 14 per cent. The following table, given by Eulen-
burg, shows not only the proportion between the number of
males and females, but the number which occurred at various

Male.

Female.

From 0 to 10 years ...

» 10 „ 20 „

... 2 ...

» 20 „ 30 „

... 35 ...

... 12

» 30 „ 40 „

... 39 ...

... 7

„ 40 „ 50 „

... 47 ...

» 50 „ 60 „

... 5 ...

After 60 years

128

From this table it will be readily seen that locomotor ataxy
a disease of youth and middle age, by far the largest number

214 SYSTEM DISEASES OF THE

of cases occurring from thirty to fifty years of age. The disease
is rare before the twentieth and after the fiftieth year.

Those who from the nature of their occupation are obliged to
expose themselves to cold and wet and to other bodily hardships,
such, for instance, as commercial travellers, engineers, soldiers,
and sailors, are very liable to be affected with locomotor ataxy.
It is notorious that soldiers are particularly liable to be affected
with the disease after bivouacing on damp ground.

Severe bodily and mental exertion both predispose to the
disease and act as exciting causes in its production. The severe i
struggle for existence to which the inhabitants of large towns i
are subjected explains, perhaps, why the disease is relatively
more frequent in large cities than in the country. The largest : j
number of cases of tabes are probably caused by excessive bodily 1 j
exertion and subsequent exposure to damp and cold, hence the i
frequency with which tabes occurs in soldiers after forced i
marches in cold weather.

Emotional disturbances, such as sudden fright, continued
anxiety, and repeated anger, appear occasionally to be capable I
of being the starting point of tabes.

Locomotor ataxy is an occasional sequel of acute diseases,
such as typhus, articular rheumatism, acute pneumonia, and
above all diphtheria ; but it is difficult to determine whether
these affections act as predisposing causes or whether they take e
a direct part in setting up nutritive changes in the cord.
Difficult labours and repeated abortions, severe puerperal
affections, copious haemorrhages, and long-continued lactation
are mentioned as other causes of this affection. Syphilis is
a frequent cause of locomotor ataxy, although probably not so
frequent as was at one time supposed.

At one time sexual excess and onanism were regarded a?
almost the only causes of tabes, and the unfortunate victims of
the disease were often unjustly suspected of leading secretly
immoral lives. That sexual excess, however, is a very important
exciting cause of the affection is shown by the frequency with
which it occurs in men during the period of their greatest
sexual activity, as well as by the fact that the disease has
been known to follow immediately upon great sexual excesses.
Frequent pollutions and spermatorrhoea often precede the

SPINAL CORD AND MEDULLA OBLONGATA. 215

outbreak of tabes, but whether these are the cause of the
disease or mere results of the primary sensory disturbances
which are so common in the early stage of the affection is
difficult to determine.

Various traumatic injuries may be the starting point of loco-
motor ataxy, and instances are recorded in which the disease
soon followed a fracture of the thigh, a fall upon the belly, the
shock of a gunshot wound, and concussion of the spinal cord
(Schulze). Some think that the disease may also be caused by
excessive tobacco smoking, but the statement appears to be
unfounded. In a great number of cases of tabes no recognisable
cause can be traced after the most careful investigation.

§ 441. Symptoms. — Locomotor ataxy generally begins with
a premonitory stage, which may extend over months or years.
The most constant and characteristic premonitory symptoms are
pains of a very peculiar and distressing kind, which are not only
present during the initial stage, but usually accompany the
disease throughout its entire course, and which may last for
years without any other symptoms being present.

These pains have been described under the names of general
neuralgia or neuralgic rheumatism, and are compared by the
patients to forked lightning darting through the body (Light-
ning Pains, § 53). The pains are at other times of a burning
character, and are not un frequently confined to a small well-
defined spot of the skin (Hypersestbetic Spots, § 52). Some-
times the pains may be deeply situated in the soft parts or in
the bones, or they may follow certain definite nerve tracts, and
are often regarded as rheumatic. The nerve trunks may be
sensitive to pressure during a paroxysm. The intensity of the
pain varies in different cases, and at times patients suffer the
greatest torture from them.

Pain in the back is met with occasionally in tabes, and at
times points painful to pressure may be found on the spinous
or transverse processes of individual vertebra, but those are
rare, and appear also to be quite unimportant. Whenever
there is prolonged or severe pain in the back, it may be suspected
that the disease is complicated by spinal meningitis.

The feeling of a tight girdle round the thorax or abdomen,

216

SYSTEM DISEASES OF THE

which is so frequent a symptom of many spinal affections, is also
a frequent symptom of locomotor ataxy (Girdle Sensation, § 51).
Girdle pains may also be felt round the joints of the lower
extremities, and it is sometimes described as a feeling like that
caused by a garter tied tightly below the knee. Sensations
of formication, numbness, or of burning or coldness of the skin
are frequently complained of. Some patients feel as if they
were walking on wool, cork, or felt soles; while others feel
as if they were walking on bladders of water. These parass-
thesiae belong to the earliest stage of locomotor ataxy, and
one or other of them is almost constantly found in the initial
stage of the affection. Hyperaesthesia of the skin is not un-
common in tabes; and at times there may be hyperaesthesia
towards impressions of temperature and anaesthesia of touch,
and at other times anaesthesia of the sense of touch may be
accompanied by a high degree of hyperaesthesia towards im-
pressions of pain.

But anaesthesia is a much more common symptom of loco-
motor ataxy than hyperaesthesia. There may be a high degree
of anaesthesia without the patients being aware of it ; but after >
a time they find that they no longer feel the floor distinctly,
that all articles which they touch have a velvety feel, or that
they cannot hold small objects in their fingers. If there is a
high degree of anaesthesia, the patients cannot judge of the
position of their legs when in the dark. Anaesthetic patches
may be found on the soles of the feet, the toes, and back of the
feet, and they may be so limited that they can only be recog-
nised by the most careful examination. As a rule, however,
the diminution of sensation extends to the thigh, and even the
trunk and portions of the upper extremities, although it is
generally most marked on the legs. But the cutaneous
anaesthesia in locomotor ataxy hardly ever reaches the high
grade observed in the later stages of transverse myelitis, and
slow compression of the cord.

Every variety of paralyses of sensation and every combination
of them are met with in the later stages of the affection;
but probably analgesia is the most frequent. Occasionally,
however, the sensibility to pain is retained, or even increased,
while there is a diminution of sensibility to some or all varieties

SPINAL CORD AND MEDULLA OBLONGATA.

217

of touch; and, again, partial paralysis of the sense of touch may
be combined with analgesia and hyperalgesia, or with hyper-
esthesia towards impressions of temperature. At a late period
of the disease a distinct retardation of the conduction of sensa-
tions, especially of impressions of pain, is observed, and this may
also be found in the earlier stages of the affection. The
prick of a needle frequently gives rise to a double sensation,
the first being one of touch which is conveyed with normal
rapidity, and the second of pain owing to the slowness with
which the impression is conveyed. Hertzberg has demonstrated
that in some cases the sensations of touch and of temperature
are also retarded, although to a less degree than that of
pain. The sensation of pain also continues for a relatively
Ion? time, even when the cause which has induced it has been
of momentary duration, and the highest degree is not reached
until several seconds after the pain has begun (§ 49). Fischer
has recently observed that in certain circumscribed cutaneous
areas of the foot the patient may feel two points when one only
is touching the skin, and when two points are in contact with
it four or five may be felt (Polysesthesia, § 50). Disturbances
of the muscular sensibility and muscular sense are frequently
observed in this affection. In the first stages the alteration
of the muscular sensibility consists of a feeling of unrest in
the limbs, which prevents the patient from lying down or
sitting still for any length of time, a feeling which has been
graphically called the fidgets. It is probable that the feeling
of fatigue, which is so frequent at the beginning of the disease,
is a parasthesia of the sensitive nerves of the muscles. It
must, however, be remembered that even in the early stage of
the disease the locomotive movements require a greater amount
of attention on the part of the patient, and that a much greater
effort is expended in walking than in health.

As the disease advances, the muscular sense becomes
diminished, and consequently the power of recognising what
muscles are thrown into action is lessened in corresponding
degree. When the paralysis of the muscular sense attains a
high degree, the patient does not know the position of his
lower extremities when his eyes are closed, and is also uncertain
with regard to the extent and direction of the movements he

218 SYSTEM DISEASES OF THE

undertakes; hence these movements, not being under due con-
trol, become excessive. This condition must, however, be care-
fully distinguished from the ataxic movements about to be
described.

Although disturbances of sensibility are much more constant
and marked in the lower than in the upper extremities, yet the
latter are frequently involved, especially in the advanced period
of the disease. Cases of pronounced ataxia have been described
by competent observers, in which the most careful investigation
failed to. detect the slightest trace of any disturbance of cuta-
neous or muscular sensibility. On the other hand, cases have
been observed in which a high degree of anaesthesia was present,
but in which the ataxic symptoms were either entirely absent
or little pronounced, so that it may be concluded that there is
no constant relation between the degree of ataxy and that of
cutaneous or muscular anaesthesia.

The motor disturbances constitute by far the most charac-
teristic features of locomotor ataxy. The motor disturbances
were for a long time thought to be of a truly paralytic nature,
but Todd and subsequently Duchenne showed that the charac- [
teristic gait of ataxy was due to a want of certainty and pre-
cision in the execution of movements, especially of combined
and complicated movements ; while the strength and certainty
of simple movements is not at all, or only slightly, diminished.
Duchenne indeed gave the name of ataxy to the disease from
the recognition of the circumstance that the characteristic gait
depends on a want of co-ordination of muscular action and
not upon true paralysis. The motor disturbances almost always
begin in the lower extremities, and are at first so slight that
they can only be recognised by careful examination.

Static Ataxia. — During the early stage of the disease special
tests, which have the power of increasing the motor inco-
ordination, are very valuable in enabling us to determine the
true nature of the affection. If the patient be asked to stand up
and keep his feet closely applied together along their inner
edges, he may manage to maintain the erect posture with
moderate steadiness when his eyes are open ; but when they
are closed, he immediately oscillates from side to side, and would
fall unless he open his eyes or be supported. As the disorder of

SPINAL CORD AND MEDULLA OBLONGATA. 219

muscular co-ordination increases, standing without support, even
when the eyes are open, becomes increasingly difficult, and
station becomes by-and-by impossible without the aid of sticks
or crutches. When at this stage the patient stands by the sup-
port of two sticks, it may be observed that all the extensor
muscles of the body are in a state of powerful tonic contraction.
The muscles of the calf are strongly contracted and extend the
leg upon the foot, so that they form an obtuse angle with.
the other, the extensors of the leg are contracted and ex-
tend the thigh on the leg, the flexors of the thigh are also
contracted, and the foot being fixed, they tend to extend the
trunk on the thigh, this tendency being greatly increased by
contraction of the gluteal muscles and of the erector spinse. It
is evident that if the contractions of these muscles were un-
antagonised, the patient could not for a moment maintain the
erect posture but would fall backwards. The tendency to fall
backwards is counteracted by what appears to be a voluntary
contraction of the muscles which flex the trunk on the thighs.
By this means the body is bent forwards, and the line of gravity
falls in front of the line joining the centre of the arches of the
feet, while the tendency to fall forwards is counteracted by the
support of the two sticks. The attitude assumed by the patient
under these circumstances is characteristic. The legs are drawn
backwards so as to form an obtuse angle with the feet, the
thighs are extended on the legs, and a plumb-line let fall from
each trochanter falls considerably behind the heel, while the
forward inclination of the body causes the buttocks to project
backwards in a marked manner.

Ataxic Gait. — In the early stage of the disease the patient
may be observed to stagger a little on getting up, especially
after sitting for a long time, the staggering being greatly in-
creased when the patient is in the dark, closes his eyes, or has
to turn abruptly round. These phenomena were demonstrated
to me in a striking manner a few weeks ago. I was walking
on a moonlight night in a garden with a friend who has suffered
for upwards of twelve years from the lancinating pains of the
disease, and who is now manifesting slight ataxic symptoms.
Our walk terminated under the shadow of a high wall and tree
covered with thick foliage. So long as my friend was in the

220

SYSTEM DISEASES OF THE

moonlight he walked steadily enough, but when once we got
under the deep shadow the staggering became very apparent,
and was much aggravated when we turned round.

In order to test at this early stage the degree of precision
with which the muscular adjustments of the lower extremities
can be performed the patient may be asked to stand on one leg,
to run, or to hop, these movements being more difficult to execute
than simple walking. He may also be requested to perform
some complicated movement with the extremity, such as to
describe the outline of a circle on the floor with the toe.

When the ataxia becomes more pronounced, the gait becomes
so characteristic that it can be readily recognised without the
application of any special tests. The patient has now to direct
his eyes to the ground and to his feet while walking, and were
he to close them the movements of the legs would become dis-
orderly, and walking would be impossible. The patient assumes
in the erect posture the attitude already described, in which the
trunk is bent forwards on the thighs, the feet are held well in
advance of the buttocks, and the legs are extended on the thighs.
It is impossible in this position to advance the passive leg with
the pendulum movement characteristic of normal locomotion.
And, indeed, owing to the strong tonic contraction of the muscles
of the thigh and the extensors of the foot which is present, the
various segments of the passive leg cannot be flexed upon one
another so as to enable it to clear the ground during its forward
movement. Under these circumstances the passive leg is pro-
jected forwards in one piece by strong contraction of the flexors
of the thigh on the trunk, aided by contraction of the abductors
of the thigh. The consequence is that the passive foot is flung
forwards and outwards with a rapid jerk, being subsequently
brought down with a thump. During this movement the heel
is generally the last to leave the ground and the first to touch
it. The heel is, 'however, sometimes lifted from the ground
before the toe, as occurs in a case under my care at present.
As the passive foot is being elevated a slight flexion occurs at
the knee-joint and the heel is elevated before the toe, but no
sooner is the latter removed from the ground than the leg
becomes suddenly extended on the thigh, the foot is projected
forwards and outwards, and the heel is subsequently brought

SPINAL CORD AND MEDULLA OBLONGATA. 221

down with a thump in the usual manner. In order to
enable the passive leg to clear the ground during its forward
movement, the abductor muscles of the thigh on the side of the
active leg enter into strong contraction, and consequently elevate
the pelvis on the side of the passive leg. So strong, indeed,
does the contraction of the abductors of the thigh on the side
of the active leg become that the patient is in danger of carrying
his centre of gravity too far to that side. In order to counteract
this tendency the upper part of the body is curved to the
opposite side by contraction of the erector spinae, and when the
patient is able to walk without sticks, by the arm on the side
of the passive leg being thrust out laterally, and during the
alternate transference of the line of gravity from one foot to
the other in walking, the trunk is moved from side to side and
the arms flung about like those of a rope dancer in order to
assist the patient to maintain his equilibrium. When the
patient walks by the aid of sticks the tendency to too great a
lateral displacement of the centre of gravity towards the side of
the active leg is counteracted by the patient giving an outward
inclination to the sticks, so that he obtains a lateral support from
them. Patients who have suffered from a high degree of ataxia
have been known to walk long distances without fatigue.

When, however, the disease has made considerable progress,
the irregularity and violence of the movements soon exhaust
the patient's strength, and he cannot take many steps without
panting and being covered with profuse perspiration. After a
time the want of co-ordination becomes so great that the main-
tenance of the erect posture and walking become impossible.
If the patient be supported by two persons under the arms
whilst he tries to walk, his legs are thrust backwards and
forwards to the right and to the left with the utmost
disorder, so that they are incapable of giving the least support
to the body ; they move, as Trousseau remarked, like those of
a puppet or a marionnette. The muscles of the trunk may now
become affected, the patient is unable even to sit in a chair,
and remains confined to his bed. But even in these advanced
cases, the patient when laid down may be able to resist passive
movements of the limbs, and to perform the simple movements
of flexion and extension with scarcely diminished power. When,

222

SYSTEM DISEASES OF THE

under these circumstances, the patient . attempts to touch an
object with the tip of the foot, the line of motion is irregular
and zigzag, and disturbed by lateral movements, while it is quite
impossible for him to execute more complicated movements —
such, for instance, as are required in describing an imaginary
circle with the tip of the great toe.

At a later period the ataxy appears in the upper extremities,
and cases have been described by Friedreich in which the
ataxy appears in the upper simultaneously with or soon after
its first manifestation in the lower extremities. In the more
usual form of the disease, however, ataxy of the upper
extremities is rare, and belongs to the later manifestations of
the affection. Ataxy of the upper extremities first manifests
itself in complicated and special movements, such as those
required for writing, playing the piano, and other movements
requiring delicacy of manipulation. These movements become
difficult and uncertain, and the irregularity becomes greater if
an attempt is made to perform the necessary actions without
the guidance of the eyes. At a later stage the simpler move-
ments also become irregular and ataxic. If the patient now
attempts to grasp an object before him, it can only be reached
in a roundabout way and with jerky interruptions, and the act
of grasping is performed in an uncertain and spasmodic manner.
The slighter shades of ataxy of the upper extremities may be
tested by instructing the patient to touch with closed eyes some
part of the surface of the body, such as the forehead or tip
of the nose by the point of the forefinger of each hand alter-
nately, when the ataxic symptoms declare themselves by the
inability of the patient to touch the intended spot until after
repeated trials. A similar uncertainty of movements is observed
when the patient is asked to transfer a small object from one
hand to the other. Static ataxy at a later period may be
present in the upper extremities, so that the patients can no
longer hold their arms still when stretched out horizontally,
and are unable to exert uniform pressure with their hands.
In a still higher grade patients can no longer dress nor feed
themselves, inasmuch as they cannot perform such simple move-
ments as are requisite for carrying a spoon to the mouth, but
even under these circumstances they may be able to exert great
muscular power in resisting passive movements.

SPINAL CORD AND MEDULLA OBLONGATA. 223

The ataxy may also invade the muscles of the trunk, so that
the body makes irregular, swaying movements, owing to the
impossibility of maintaining the due balance between the
various muscles, contraction of which is necessary for maintain-
ing the erect posture. The muscles of the neck may also be
implicated, and the head become the subject of irregular and
shaking movements. Speech is sometimes also interfered with.
At first the ataxy declares itself by a somewhat indistinct pro-
nunciation of words, but when the affection is more advanced,
there is an irregular, stuttering interruption of speech. At
times whole sentences are uttered rapidly, and then there is a
slight stuttering, and this is repeated in an irregular manner;
while the voluntary movements of the lips and tongue are
apparently quite unaffected. In the highest grades of the affec-
tion articulation may become so defective that speech becomes
almost incomprehensible.

The third and final stage of the disease is characterised by
decided paralysis, although a certain amount of motor weakness
may be shown to be present in the majority of cases of tabes
even at a moderately early stage of the ataxic period. Partial
and temporary paralysis in the domain of single nerves in the
extremities is not of rare occurrence. In the later stages of the
i disease true motor paralysis increases and ultimately becomes
the predominant symptom. The muscles undergo atrophy,
or contractures set in, and they finally become more or less
completely paralysed. With the appearance of the paralysis
the ataxic symptoms are thrown more and more in the back-
i ground.

Symptoms indicative of motor irritation are not prominent
i features of locomotor ataxy. In the earlier stages of the disease
i fibrillary contractions and spasms of single muscles, with slight
| jerking of a limb, may be observed. At times twitch ings of
I entire extremities may occur in connection with the lancinating

pains, and are doubtless reflex in nature.

Muscular tension is also entirely absent from true cases of
I tabes ; the limbs are limp and do not offer the least resistance

to passive movements. When, however, the paralytic symptoms
j supervene muscular tension and contractures also arise, and may
! ultimately reach so high a grade that the limbs remain im-

224

SYSTEM DISEASES OF THE

movable in the position of extension or flexion as they do in
the later stages of other chronic spinal diseases.

The electrical reactions vary at different stages of the disease,
and the statements made by different authors with regard
to them are not in accord with one another. Erb found the
faradic and galvanic excitability to be quite normal in respect
both to quality and quantity. In another series of cases he
found a slight increase in the faradic and galvanic excitability
in the anterior muscles of the leg, without any qualitative
alterations, while in other cases he found a more or less distinct
diminution of electrical excitability in the anterior muscles of
the leg, without qualitative changes. From these cases Erb
draws the general conclusion that in the earlier stages of the
disease there is an increase and in the later stages a diminution
of the electric contractility. But, as Erb confesses, no great
advantage is to be gained either for diagnosis or prognosis from i
electrical examinations.

Reflex Action. — The cutaneous reflex is usually unaffected I
in locomotor ataxy, at least until a late period of the disease. .
In some cases, however, the normal interval between the cuta-|
neous excitation and the resulting contraction may be greatlyr
prolonged (Fischer). The absence of the reflex action of the
tendons (§ 78) constitutes, as has been pointed out by
Westphal, one of the most remarkable features of the affection.i
The patelJar-tendon reflex is usually absent in the premonitory)
stage of the disease, and often long before the ataxic symptoms:
make their appearance, and it is consequently one of the mosfei
valuable signs of the disease which we possess. It must, how-r
ever, be remembered that the absence of the patellar reflex if
not absolutely pathogonomic of the disease. Erb found thi;
reflex absent in forty-eight out of forty-nine cases examined bj
him, but in the one exception the reaction was very lively,
have at present under my care a woman, who developed symp:
toms of ataxia somewhat suddenly two years ago after a mis
carriage, and in whom the patellar-tendon reflex is in excess,
have seen another case, which will be subsequently mentioned
where symptoms of ataxia were associated with excessive reactio
of the patellar-tendon reflex, but the subsequent course of th
case showed that it was one of insular sclerosis. I thought fc I

SPINAL CORD AND MKDULLA OBLONGATA. 225

some time that the case of the woman just alluded to would
turu out to be of the same character; but after watching the pro-
gress of her case now for eight or nine months, I can come to no
other conclusion than that it is one of true locomotor ataxy. The
, ataxic gait and swaying movements on closing the eyes are
I well marked in her, it is true that she has not suffered much
from lancinating pains, but there is decided diminution of
tactile sensibility in the skin over the external aspect of both
legs, there has been some dribbling of urine, and there is com-
plete absence of paralysis and muscular tension. But not only
does the patellar-tendon reflex remain unaffected or even in
excess in cases of true tabes, but it is sometimes absent in those
who are otherwise typically healthy, so that some degree of
caution is necessary in accepting the absence of this phenomenon
as a sign of ataxia. With these reservations, however, the
absence of this reflex is a most valuable sign of locomotor
ataxy.

§ 442. Occasional Symptoms.

Paradoxical Contraction. — Attention has recently been
drawn by Westphal to a curious phenomenon, which may be
regarded as the opposite of the tendon-reflex contraction of
the muscle. As this symptom was unfortunately overlooked by
me when the first volume of this work was passing through
the press, I shall describe it in detail in this place: —

It consists in the contraction of a muscle induced by suddenly approxi-
mating its points of origin and insertion. The curious circumstance that
a sudden relaxation of a muscle causes it under certain circumstances to
contract has led Westphal to name this phenomenon paradoxical con-
traction. This symptom is best studied in the tibialis anticus, which
may in certain diseases of the central nervous system be made to contract
by producing sudden or sometimes a gradual dorsal flexion of the foot.
When the patient is laid on his back in bed, and the muscles are relaxed,
especially if they be paralysed, the feet occupy the position of extension
or plantar flexion. If dorsal flexion of one foot be now produced, the
tibialis anticus, under certain circumstances, contracts, its tendon becomes
prominent, and the foot is maintained for some minutes, sometimes even
, as long as twenty-seven minutes, in the position of dorsal flexion and
1 adduction. When the muscle is made to contract by direct or indirect ex-
citation or by voluntary effort, the foot may remain in a state of dorsal
flexion long after the stimulus has ceased to act, and a constant current
P

226

SYSTEM DISEASES OF THE

passed through it does not produce relaxation. Distinct resistance is also
offered to the passive production of plantar flexion. After a variable length
of time the muscle relaxes, either gradually and continuously, or with
several intermissions, and the foot falls by its own weight to the position
of plantar flexion. The paradoxical contraction sometimes extends to the
extensor communis digitorum and extensor brevis pollicis. In one case
observed by Westphal, the biceps femoris was seen to contract on the leg
being suddenly flexed on the thigh. This kind of contraction may be
present when the tendon reflexes are absent or normal, and probably also
when they are slightly exaggerated ; but the presence of distinct ankle
clonus will, of course, prevent the foot from becoming fixed. The pheno-
menon may also be observed when the cutaneous sensibility of the lower
extremities is normal or lowered, and in the absence of any excess of the
cutaneous reflex excitability. Paradoxical contraction is generally asso-
ciated with paresis of the lower extremities, but a spastic rigidity of the
muscles is never present, although a slight degree of resistance may be
felt to passive movements of the leg and foot. This form of contraction
may extend to the muscles of the upper extremities, and in a case
observed by Westphal, in which some of them were affected, a certain
amount of rigidity subsequently appeared in the muscles of both upper
and lower extremities. It is a remarkable circumstance that the para-
doxical contraction occurs in muscles like the tibialis anticus, which
probably never contract when their tendons are struck ; and, conversely,
the paradoxical contraction has never been observed in muscles like the
quadriceps femoris, which manifest readily the tendon-reflex contraction.
Whether the paradoxical contraction is caused by reflex or direct excitation
is not known. This phenomenon is sometimes a symptom of locomotor
ataxia, but probably never of uncomplicated cases of the disease. Its
presence may, perhaps, be regarded as a sign that the lesion in the pos-
terior columns is extending to the lateral columns, and that the paralytic
stage of the disease is approaching. This contraction has also been
observed by Westphal in paralysis agitans, and in a case of hsematomyelia
at present under my care, in which both lower extremities are completely
paralysed, paradoxical contraction is readily induced in the tibialis anticus
of the right, but not in that of the left leg.

Paralysis of the Ocular Muscles. — One or more of the
ocular muscles are not unfrequently paralysed in tabes dorsalis,
and this symptom also is of great value because it may
precede by many years the motor inco-ordination of the lower
extremities. The motor oculi and abducens are more frequently
affected than the trochlear nerve. The paralysis of the ocular
nerves is usually transient, and generally lasts for a few >
days or months. The paralysis, however, often recurs after
a longer or shorter time, and may become permanent towards

SPINAL CORD AND MEDULLA OBLONGATA.

227

;he later stages of the disease. The temporary paralyses of
:he ocular muscles in locomotor ataxy often do not give rise
:o any apparent squint, but cause double vision (diplopia),
which is either constantly present, or only when the eyes are
turned in particular directions. Distinct squint and ptosis are,
however, present in some cases. Out of 64 cases recorded by
Eulenburg, 25 had strabismus; of these 25, 19 had divergent
strabismus, and 4 had in addition paralytic ptosis, while 6 had
convergent strabismus. When paralysis of the third or sixth
nerve occurs syphilis is generally suspected to be the cause,
and if the paralysis disappear in a few days or weeks under
treatment, the diagnosis seems to be placed beyond doubt.
Paralysis of these nerves may, however, be the first symptom
)f locomotor ataxy. In a case of my own, paralysis of the
rixth nerve appeared to have been promptly cured by iodide of
ootassium, and it was not until eighteen months afterwards
;hat the ataxic symptoms declared themselves and the true
lature of the case was made apparent.

Mydriasis. — Dilatation of the pupil was observed by Eulen-
burg in 9 out of 64 cases. In 3 the dilatation was double, in
t single, and in 2 accompanied by myosis of the other eye.
There is no defect of accommodation accompanying this con-
lition ; hence it would seem that the pupil is dilated not from
paralysis of the third nerve, but from irritation of the cilio-
ipinal nerves. The pupil frequently dilates during severe
mroxysms of lancinating pains (Charcot) and during gastralgic
ittacks (Grainger Stewart).

Myosis. — Eulenburg found contraction of the pupil in 2.8 out
>f 64 cases, 21 showing double and 7 single myosis. The two
mpils are indeed seldom of the same size, and the degree of
contraction varies greatly in different cases and in the same
ase at different times. Inequality of the pupils is common in
l he early stage of the disease ; and on the side on which the
contraction of the pupil is the more marked there may be
; edness of the cheek, congestion of the conjunctiva, and local
nlevation of temperature (Charcot). These symptoms indicate
I'aso-motor paralysis, and prove that the myosis is due to
• paralysis of the cilio-spinal nerves.

The Argyll-Robertson Symptom. — This symptom, as already

228

SYSTEM DISEASES OF THE

mentioned (§ 225, 11), consists in the absence of any contraction
of the pupil on exposure of the eye to light, while contraction
with the accommodation is normally retained. The symptom
is generally, although not invariably, associated with myosis.

Nystagmus is, as Friedreich has shown, occasionally present
in locomotor ataxy; although, contrary to what occurs in multiple
sclerosis, it is an exceedingly rare symptom. The nystagmus
only appears when attempts are made to fix the eye on an object.
The movements of the nystagmus in tabes do not succeed one
another with the same rapidity as the movements in ordinary
nystagmus, dependent upon disease of the eye. The move-
ments are, indeed, purely ataxic, and only occur on a voluntary
effort at fixation being made. Ataxic nystagmus only occurs
in certain cases which possess marked clinical peculiarities, and
it is always a late symptom of the disease.

Atrophy of the optic nerve is a frequent and distressina
complication of locomotor ataxy. The affection begins with
slowly or rapidly advancing diminution in the acuteness of
vision, which soon terminates in amaurosis. Colour blind-
ness can usually be demonstrated prior to any limitation I
in the field of vision. The perception of green is first lost,
then that of red, yellow, and blue in succession, although
deviations from this order may occasionally occur (Erb). The
pupils are usually contracted in such cases and they do not :
react to light. The blindness is caused by white atrophy of the !
optic nerve. The rapidity with which blindness supervenes 9
is very variable. At times total blindness may supervene
in a few weeks, *while at other times years may elapse before
the loss of sight is complete, and occasionally the affection may j
cease to progress after it has lasted for a comparatively long £
time. The disease may be limited to one eye, but usually both I
eyes are simultaneously attacked. Atrophy of the optic nerve
appears in about thirty per cent of all cases of locomotor
ataxy. It is frequently one of the initial symptoms of the
disease, and sometimes even precedes the lancinating pains.
The amaurosis has been known to have existed ten years before
the other symptoms of tabes have made their appearance.

Disturbances of hearing are occasionally observed in tabes.
The defect of hearing is sometimes a purely accidental circum-

SPINAL CORD AND MEDULLA OBLONGATA.

229

stance, but at other times it probably depends upon atrophy
of the auditory nerve, analogous to that of the optic nerve.

Disturbances of taste and smell have also occasionally been
observed, but are of subordinate importance.

The trigeminus at times manifests signs of irritation, giving
rise to pain and paresthesias, or it may be either partially or
completely paralysed, giving rise to a sense of numbness, or to
anesthesia, Disturbances of taste and smell are always asso-
ciated with an abnormal condition of the trigeminus.

The facial nerve is very rarely implicated, but irregular
twitchinsrs of the facial muscles have occasionally been observed.

The hypoglossal nerve has been rarely affected. The pneumo-
gastric and glosso-pharyngeal nerves are very seldom implicated,
unless, indeed, the gastralgic troubles, which are so frequent
and distressing in tabes, are the result of irritation of the
pneumogastrics.

Psychical disturbances are but seldom observed. Westphal
: has, indeed, shown that the majority of patients who suffer from
progressive paralysis of the insane appear to have degeneration
:>f the spinal cord chiefly limited to the posterior columns. The
symptoms of progressive paralysis of the insane may precede
the tabes for many years, or may become associated with it after
it has existed for many years, or may not arise until the terminal
period of locomotor ataxy. In all these cases the tabes is only
3ne of the manifestations of a more widely-diffused degenerative
process, j ust as ataxia may be one of the symptoms of multiple
sclerosis.

There are other symptoms of locomotor ataxy which do not
form such prominent features of the disease as those already
described, but are not on that account less remarkable or of
i.ess importance. These are what may be denominated visceral
symptoms.

Affections of the Bladder and Rectum. — During the early
itage of the disease the patient often suffers from frequent and
painful micturition, along with neuralgic pains in the depth of
the pelvis, in the perineum, or the neck of the bladder. At
i later stage of the disease signs of paresis of the bladder make
their appearance, so that emptying the bladder takes a longer
Lime, and there is some subsequent dribbling, or there maybe a

230

SYSTEM DISEASES OF THE

moderate degree of incontinence ; but complete paralysis of the
bladder is exceedingly rare, and only occurs in the last stage of
the disease. A certain degree of vesical catarrh may be present
during the terminal stages of tabes, but it is seldom of a severe
character.

Patients also complain during the early stage of tabes of
very peculiar sensations in the rectum. These sensations are
at times described by the patient as a feeling similar to that
which might be produced by the forcible introduction into the
anus and rectum of a long and voluminous body (Charcot).
This sensation appears suddenly and soon disappears, and it is
usually accompanied by a strong desire to evacuate the contents
of the bowels, and occasionally an involuntary evacuation of
fecal matters occurs. At a more advanced period of the disease
anaesthesia of the anus may be present, so that the patients
lose the feeling of approaching evacuations, and hence not ; ;
unfrequently dirty themselves. True paralysis of the sphincter :
is rare and only occurs in the terminal period of the disease.

Disturbances of the Sexual Functions. — A certain amount of
disturbance of the genital organs is rarely absent in tabes. In ^
the early period of the disease symptoms of irritation are present.
Trousseau observed in certain cases a singular aptitude for
repeating the venereal act a great many times within a short
period, and he mentions the case of a man who was able to
have connection as many as eight or nine times in one night.
In these cases the appearance of excessive virile power is already
conjoined with symptoms indicative of weakness. Very often
this excessive desire has been preceded by a certain amount of
incontinence of urine and involuntary seminal emissions, and
the erections are often imperfect and accompanied by premature
ejaculation. Charcot and Bouchard have observed symptoms of
genital irritation in women. As the ataxic symptoms manifest
themselves weakness of the sexual functions set in, which soon
develop into complete impotence, although some tabetic patient
retain their sexual power undiminished for a very long time.

A permanent acceleration of the pulse has been mentionec
amongst the symptoms of locomotor ataxy. The temperature o
the body is often increased during the attacks of lightning pains

Oastralgic attacks, described by Charcot under the name o

SPINAL CORD AND MEDULLA OBLONGATA.

231

crises gastriques, are frequently observed in the early stage of
tabes. I know a gentleman who suffered from these attacks,
and lancinating pains, ten years before the appearance of the
ataxic symptoms. The gastralgic attack generally begins sud-
denly during a paroxysm of the lancinating pains. The patient
complains of pain, which starts from the groins and appears to
pass up each side of the abdomen, so as to become fixed in the
epigastric region. At the same time severe pains are felt
situated between the shoulders, which radiate round the base of
the thorax, under the form of lightning pains. As a rule, the
action of the heart is violent, and accelerated during the attacks,
which are generally accompanied by extremely painful and in-
cessant vomiting. The food is rejected, then a quantity of
watery mucus, which is at first colourless, but may ultimately
become mixed with bile and blood. A profound malaise and
vertigo are conjoined with the vomiting, while the lightning
pains are unusually severe, so that the sufferings of the patient
may become truly agonising. These attacks may last without
respite for two or three days, and may recur every two weeks ;
but usually the interval between the attacks is not less than a
month. During the interval the functions of the stomach are
entirely unaffected. The gastralgic attacks may begin at an
early stage of the disease, and may constitute for many years,
along with the lightning pains, the only symptom of the
approaching malady. These attacks do not, however, always
disappear on the ataxic symptoms being established, but may
continue to recur until the fatal termination of the disease.

Nephralgia attacks have recently been described by Raynaud
which present symptoms almost entirely similar to renal colic,
only that there is entire absence of calculi, gravel, or blood
from the urine.

Bronchial attacks have been described' by Fdreol under the
name of " bronchial crises," consisting of paroxysms of spas-
modic cough, difficulty of breathing and swallowing. In cases
described by Friedreich vertigo has been a very prominent
symptom.

Voxo-motor Disturbances. — Vaso-motor disturbances are not
prominent features of locomotor ataxy. Patients not unfre-
quently complain of cold feet ; and sometimes there is a great

232 SYSTEM DISEASES OF THE

tendency to the formation of cutis anserina. The skin is at',
times mottled, and there may be increased or diminished cuta-
neous secretion. A curious case has recently been described by
E. Kemak, in which the ataxic symptoms began in the right
upper extremity. The muscles of the forearm were somewhat
wasted, but there was no distinct loss of motor power, yet the
hand was rendered practically useless from the disorderly move-
ments which occurred when any attempt was made to use it.
Serious sensory disturbances were observed in the extremity
affected with ataxia, and slight analgesia of the sole of the right
foot. There were also slight swaying movements on closing the
eyes, and the patellar-tendon reflexes were absent, but there
were no lancinating pains and no ataxic or paralytic symptoms
in the lower extremities. In addition to these symptoms, the
patient suffered from unilateral hyperidrosis limited to the right
side, redness and slight relative increase of temperature of the
right half of the face and side of the head, and myosis of the
right pupil, the latter becoming more marked with the increase
of the secretion of sweat, and frequently disappearing altogether
with complete rest. The secretion of sweat was increased on the j
right side when the patient took any acid substance into his I
mouth, and also by faradic excitation of the tongue and mucous I
membrane of the mouth, or of the skin of the cheek, and trunk :
of the facial nerve. The conjunctiva is said by Trousseau to be i
frequently congested in locomotor ataxia.

Trophic Disturbances. — The most common trophic affections ;
are eruptions of the skin, such as herpes, lichen, or the forma-
tion of bullae, like those of pemphigus. Bed-sores usually,
belong to the terminal period of the disease only. Dr. Buzzard I
reports a case of locomotor ataxy, in which an eruption of herpes 5
occurred in the right gluteal region during every paroxysm of t
lightning pain. The patient stated that he must have suffered I
from fifty or sixty attacks of herpes during the four years pre- •
vious to the report of his case. The nutrition of the muscles s
remain for a long time unaffected; and, indeed, the muscles of
the lower extremities may undergo a certain amount of hyper-
trophy during the early part of the ataxic stage, owing to the*
excessive activity to which they are subjected. During thee
paralytic stage the muscles may waste rapidly, simply from

SPINAL CORD AND MEDULLA OBLONGATA. 233

disuse, and not from any active atrophy. Occasionally, how-
ever, the disease becomes complicated at a comparatively early
period with atrophy of certain muscles, such as those of the
calves of the legs, or those of the thighs, ball of the thumb, or
of one-half of the tongue; and in these cases the atrophy con-
sists of active degeneration, and not merely of the passive
degeneration which is caused by functional inactivity. The
most remarkable trophic disturbances which occur in tabes are
the affections of the joints, which have been described by
Charcot under the name of arthropathies des ataxiques. It is
possible to meet with joints deformed with rheumatic gout, and
dry arthritis coincidently with tabes, but the arthropathies of
locomotor ataxia develop themselves quite independently of any
general affection. This affection always appears during the
early stage of tabes, usually during the stage of the lightning
pains, although many cases seem to contradict this rule. The
joints of the upper extremities may, for instance, become affected
at an advanced period of the disease. The disease has, however,
only reached an advanced stage in the lower extremities; while
the upper extremities are only just beginning to manifest the
initial stage of the affection. The joint most frequently affected
is the knee-joint; and then in a descending order of frequency,
the shoulder, elbow, the hip-joint, and the wrist in succession.

Various luxations of the joints ensue, producing notable
deformities.

In locomotor ataxy the bones also sometimes become abnor-
mally friable, so that spontaneous fractures may occur, a change
which is no doubt of similar origin to the joint affection.

The following case, reported by Dr. Dreschfeld, will illustrate
the arthropathies of locomotor ataxy : —

B- W , aged fifty, mechanic, married, with no history of either

syphilis or alcoholism, had always enjoyed good health till fifteen years
ago, when the first symptoms of locomotor ataxy came on. These symp-
toms consisted in the inability to walk in the dark, and in the presence of
lightning-like pains in the legs, in consequence of which he was soon
obliged to give up his work. Seven years ago the pains in the right thigh,
without losing their lightning-like character, became suddenly much more
persistent, and obliged the patient to take to his bed, and to remain in bed
for a month, when they left him as suddenly as they came. On trying to
get up he found now that his right leg was much shorter thau the left,

234

SYSTEM DISEASES OF THE

and that there was a projection on the right hip, which occasionally would ]
suddenly disappear with a peculiar noise. Any movement of the thigh or j
leg would, however, make this projection very soon reappear. Three years |
ago the left knee began to give way without any exacerbation of pain, or ]
any sudden swelling of the joint, and very gradually assumed its present
position, that of extreme backward dislocation. In consequence of these
joint affections, walking, which was already difficult before, became
only possible with the help of two sticks. The general health of the
patient had remained very good throughout, his eyesight had been bad
for some years, but he had never suffered from vomiting or any bladder
troubles.

On admission patient looked well and healthy ; the thighs were con-
siderably wasted, but the rest of the body was not emaciated. The chest
and abdominal organs were perfectly healthy. There was no affection of '
any of the cerebral nerves, except marked white atrophy of both of the
discs. The pupils were contracted and reacted to accommodation, but
not to light. The upper extremities were perfectly normal. The lower I
extremities showed the chief symptoms, and here, as regards (1) sensation,
there were diminution of tactile sensibility, analgesia of certain spots, ,
and retardation of sensibility. The sense for temperature and weight was •
normal ; the muscular sense was considerably affected. The patellar-ten- -
don reflex was quite absent. Both lower extremities were often the seatti
of the lightning pains. As regards (2) trophic changes, (a) the muscles ^
of both thighs were flabby and atrophied, but especially the muscles of the^
left thigh. (6) There was marked dislocation backwards of the left thigh, .
so that when the patient stood the upper surface of the tibia couldi
distinctly be felt under the skin. There was no atrophy of either of thet
articulating surfaces, nor any new deposit of bone round the joint as farr
as could be made out on manual examination. The head of the right t
femur was dislocated on to the dorsum of the ilium, and could be felt as a a
distinct round projection ; it was freely movable and could easily bet
reduced, but very soon slipped out again from the acetabulum on to thd
dorsum. Owing to this dislocation the left knee was situated four inches-
lower than the right knee, which difference disappeared as soon as the;
reduction of the head of the femur was effected (Plate IV. 1, 2). The head, i
of the dislocated femur did not seem to be atrophied, nor were there anj j
bone deposits to be felt about the joint cavity. A mass of bone, however -
of more than one inch in length was felt, situated in the sheath of th<
sartorius muscle, totally unconnected with the joint, but moving freeb
with the muscles during this contraction. As regards (3) motility, then
was considerable diminution of motor power in both legs, but more in tb
right than in the left ; the patient was, however, able to stand and to wall
with the help of two sticks ; his walk was characteristically ataxic ; h
was unable to walk with his eyes shut, and with his eyes open his gai
was very unsteady, owing to the ataxy and the dislocations.

Plate iv

SPINAL COED AND MEDULLA OBLONGATA.

235

§ -143. Varieties. — The largest number of cases of locomotor
ataxy follow a very uniform course, which may therefore be
regarded as forming the type of the disease. The symptoms,
however, may deviate considerably from their usual course, or
the affection may be observed in combination with other allied
forms of disease. Locomotor ataxia may, therefore, be divided
into the following varieties (Erb) : —

(1) The Regular Typical Form oj Tabes— It usually attacks men during
middle age. It begins with lancinating pains, disturbances of the nerves
supplying the ocular muscles and 'of the optic nerves, disturbances of sen-
sibility of the extremities, such as paresthesia, slight ansesthesia, feeling
of a tight girdle, great feeling of fatigue, motor disturbances in the lower
extremities, such as swaying on closing the eyes, and disturbances of the
urinary and genital organs.

During the second stage of the disease the symptoms of the first stage
gradually increase, and now become associated with characteristic ataxia.
Patients become more and more helpless, there are well marked distur-
bances of sensibility, such as partial anaesthesia, retardation of the per-
ception of pain, abolition of tendon-reflex along with increase of vesical
and sexual weakness.

In the third or terminal stage true paralysis gradually supervenes in the
form of paraplegia ; there are also contractures, muscular atrophy, bed-
sores, and progressive cachexia.

(2) The Form of Tabes described by Friedreich. — Family predisposition
forms a prominent feature of the disease, and the female members of these
families manifest a tendency to be attacked by preference. The disease
generally begins between the age of twelve and eighteen years. Lanci-
nating pains are rare at the beginning, but, on the other hand, the ataxia
begins early, and rapidly spreads from the lower to the upper extremities,
and sometimes even arises simultaneously in the upper and lower extremi-
ties. Co-ordinating disturbances of speech and ataxic nystagmus are
generally present. Disturbances of sensibility are absent or insignificant ;
the sensibility of the skin and muscles remains unaffected for many
years. No swaying on closure of the eyes. Tendon-reflex abolished. No
disturbances of the bladder or bed-sores, and no psychical disturbances,
tremor, or amaurosis. Muscular atrophy, paresis, contractures, weakness
of the bladder appear only in the last stage. The affection is usually of
remarkably long duration, extending sometimes over thirty-two years.

(3) Anomalous Forms. — Sometimes the degenerative changes do not
remain limited to the posterior columns, but extend to other segments of
the cord, giving rise to a combination of the symptoms of locomotor
ataxy with those of one or more of the other systematic diseases of the
cord.

23G

SYSTEM DISEASES OF THE

(4) Paraplegic Form.— In a certain number of cases manifestations of
motor weakness come into prominence at an early period of the disease,
so that the tabetic symptoms become obscured. The symptoms may in
such cases suggest paraplegia, and emaciation and atrophy of the legss
may seem to confirm this opinion. In these cases the degenerative,
changes have no doubt extended to the pyramidal fibres of the lateral,
columns and to the anterior horns of the grey substance.

(5) Neuralgic Form.- In other cases the lancinating pains constitute
the most prominent, and for a long time, sometimes upwards of twenty,
years, the only symptoms of the disease. This form has been called tabea
dolorosa."

(6) Meningitic Form.-kt times locomotor ataxy becomes complicate
with spinal meningitis, and such cases may offer a very variable combinai
tion of symptoms. Circumscribed or diffused cutaneous hyperesthesia,
pain in the back, and spinal tenderness are some of the symptoms which arr
most commonly present. Locomotor ataxy may also be complicated wit-
various psychical disturbances, and these must be subjected to a specii
investigation.

§444. Course, Duration, and Termination. — The usua;
development of the locomotor ataxia is slow and chronic, er.
tending over months or years, although cases have beet
described under the name of acute ataxia which run a rap
course. As a rule, single symptoms arise which remain isolate
for a long time, and with which others become after. a tun
associated until in the course of months or years the picture
the disease is complete. The ataxic symptoms, as already me
tioned, usually begin in the lower extremities, but a few cas
are reported in which the upper extremities were first affect.
Occasionally a unilateral development has been observed.

When the disease is fully developed the intensity of tt
symptoms progressively increases, new symptoms arise, and 1
condition of the patient gradually grows worse. The dise,
may, however, remain stationary, or even undergo a marl
improvement for months or years; but after a time an n
favourable change usually takes place. The patients feel bet
in summer and worse in winter, but they generally lose m
in cold than they gain in warm weather. In rare cases
improvement may progress to complete recovery. The durat •
of the disease is always to be counted by years, and sometn I
by decades. Even the initial stage, with lancinating pains, iif

SPINAL CORD AND MEDULLA OBLONGATA.

237

last over twenty years. In the majority of typical cases of the
disease the average duration of life appears to be from eight to
twelve years, and in these cases death is caused by bed-sores,
cystitis, or bulbar symptoms, or the spinal affection renders the
patient less capable of surviving intercurrent attacks of disease,
such as pneumonia, the exanthemata, or other fevers.

Recovery is not unusual in the initial stage under appro-
priate treatment; and even when the disease is fully developed,
recovery, or an improvement bordering on recovery, may take
place. Often, however, patients must be content with a
moderate improvement, or an arrest of the malady. As a rule,
the disease is of a progressive character, and the most judicious
treatment may fail to bring about even a temporary improve-
ment. A fatal termination may be brought about in various
. ways. The disease may lead to paraplegia, cystitis, and bed-
sores, and the patient dies from the usual symptoms of severe
spinal paralysis. During the last few days cerebral symptoms,
tas coma and delirium, may supervene. The morbid process

• may, in progressing from below upwards, involve the medulla

• oblongata, and cause death by interfering with respiration or

I with the act of deglutition. Very frequently some intercurrent
I affection, such as typhus, pneumonia, diphtheria, and phthisis,
J causes a fatal termination.

II § 445. Morbid Anatomy. — The spinal pia mater is often
I thickened, cloudy, and connected by numerous adhesions to the
i dura mater. The change in the pia mater is generally confined

to the posterior aspect of the cord, being circumscribed by the
| posterior roots on each side. Occasionally, however, the pia
I mater appears altered over a larger area, and the spinal fluid
|is almost always increased in quantity. The spinal cord is
i generally altered in form, being flattened from before back-
j wards over a considerable portion of its extent, caused by a
i diminution of the volume of the posterior column. On making
i transverse sections at different levels of the cord, a grey or
i greyish-yellow discolouration may be observed along the pos-
i tenor median fissure, extending almost the entire length of the
J cord. The consistence of the cord is usually increased, but

occasionally it may be diminished.

238 SYSTEM DISEASES OF THE

The posterior roots are discoloured, grey, translucent, and
atrophied, this condition being particularly well marked m
the cauda equina. Dr. Carter, of Liverpool, exhibited the
spinal cord from a case of locomotor ataxy at a recent medical
meeting in Manchester, in which the ganglia of the posterior
roots of° the sacral and lumbar nerves were greatly enlarged.

The degeneration is not, as a rule, uniformly distributed over
the whole° transverse section of the posterior columns. The
columns of Goll are usually affected over their entire length,
and the posterior root-zones are always affected to a more or
less extent, although they are not often degenerated throughout
the entire length of the cord. In the inferior portion of
lumbar enlargement there is frequently only a slight grey
discolouration in the external half of the posterior columns;
but on ascending it increases in width, so that m the upper
half of the lumbar enlargement the discolouration embraces
the entire transverse section of the posterior columns. The 1
whole of the posterior columns are usually affected throughout
the entire length of the dorsal region, but its extent diminishes
a^ain in the cervical portion, and the degeneration becomes
limited in the upper cervical region to the columns of Goll.
As a rule, the intensity and extent of the morbid process is
greatest in the upper lumbar and the dorsal portions, dimi-
nishing both upwards and downwards from these points.

The morbid changes may extend upwards into the me-
dulla oblongata, along the ascending root of the trigeminus
(Pierret) The posterior horns of grey matter often appear of
a dark grey colour, shrivelled, and distorted, and the vesicular
columns of Clarke have been found altered. The discolouration
may also extend forwards from the posterior horns to the direct
cerebellar fibres and the pyramidal fibres of the lateral column.
Such, then, are the morbid appearances which are found in
fully-developed cases of the disease, but in cases which have
died from an intercurrent affection during the early stages ot
locomotor ataxia the morbid appearances met with are some-
what different. Charcot and Pierret have shown that, although
the columns of Goll are usually implicated in locomotor ataxy,
the ataxic symptoms may be present in a high degree m
the entire absence of any affection of these columns. Sclerosis

SPINAL CORD AND MEDULLA OBLONGATA.

23!)

t»f the posterior root-zones is, according to these authors, the
essential morbid alteration of locomotor ataxia, and even the
vhole width of these zones need not be implicated. A certain
.mount of alteration of these zones may be detected by micro-
copic examination, if not by the naked eye, even in those cases
hat have died by an intercurrent disease during the stage of
he lancinating pains before the ataxic symptoms had made
heir appearance. And on the other hand, in a woman in whom

Fig. 176.

'ig. 176 (Charcot and Pierret). Transverse Section of the lower portion of the
Lumbar Enlargement, from a case of Locomotor Ataxia. — A, Posterior roots ;
B, Internal radicular fasciculus, the sclerosis being limited to its course ; C,
Right anterior grey horn in a state of atrophy.

he disease appeared in a generalised form, the superior, as well
s the inferior, extremities being the subject of the lightning
iains and motor inco-ordination, the posterior root-zones were
Dund affected the whole length of the cord, while there
fas complete absence of any affection of the columns of Goll
Fig. 176, B).

In very old and protracted cases long portions of the spinal
ord appear hardened and atrophied in its entire thickness.
)n making a transverse section, the whole is found transformed
nto a grey translucent mass, in which it is difficult to recognise
:ven the distinction between grey and white matter.

The microscopical changes in the cord consist in the early stage
>f thickening of the interstitial tissue, increase in the number

240

SYSTEM DISEASES OF THE

of nuclei along with the formation of enlarged and highly- j
developed Deiter's cells.

The nerve fibres dwindle gradually and ultimately disappear. 1
The medullary sheath does not usually undergo fatty degenera- |
tion or break down, and no swelling of the axis cylinder is
observed ; there is simple atrophy and disappearance of the
nerve fibres, and numerous granule cells are found. In recent
cases the vessels are generally thickened, the nuclei are increased
in number, and corpora amylacea are scattered throughout the
tissue in greater or lesser number. In the later stages the prin-
cipal mass of the structure is composed of a firm fibrillar, often
wavy, connective tissue, which contains numerous nuclei and is
disseminated with innumerable corpora amylacea. Most of the
nerve fibres have disappeared, but even in advanced cases some
well-preserved but isolated fibres may still be seen scattered
through the firm connective tissue. ,

The posterior roots, in their passage through the posterior
root-zones to the posterior grey horns — the inner radicular :
fasciculus — are involved in the degenerative process. Their t
fibres are broken down and atrophied, some are completely .*
destroyed, while the remains of those left are separated from i
one another by broad bands of connective tissue.

The posterior horns of grey matter are also implicated in
the degeneration. There is thickening of the connective tissue,
disappearance of nerve fibres, and the ganglion cells are pig-:
mented but not much changed in other respects. Clarke's •
columns are also frequently implicated, although their ganglion ,
cells remain tolerably intact.

Sometimes the degenerative process extends to the anterior
horn3 of grey matter, injuring the large ganglion cells, and
then the muscles innervated from the diseased grey matter are
always in a state of atrophy. This alteration stands, according
to Pierret, in connection with sclerosis of the inner radicular
fasciculus, and extends from those along the bundles of fibres
that radiate into the anterior grey horns. In the annexed diagram
the ganglion cells of the right anterior horn {Fig. 177, D) ar(
in great part destroyed, and the muscles of the upper and lower
extremities of the same side were atrophied.

SPINAL CORD AND MEDULLA OBLONGATA.

241

Most recent observers are of opinion that the degenerative
rocess begins within the cord itself, and not in the posterior
>ots. Leyden thinks that the process from beginning to end
msists of a degeneration; while Charcot, Friedreich, and others
•ok upon the degenerative changes as the result of chronic
trlammation. All, however, are agreed that the process
9gins in the nerve elements themselves, and extends from
lem to the interstitial tissue. The disease may, however,
egin at times in the pia mater, and spread thence to the
jsterior root-zones and columns of Goll.

Fjg. 177.

'r}l {CJ.harcot,an<l Pierret). Transverse Section of the Lumbar Region, from a
case of Locomotor Ataxia, complicated with Muscular Atrophy. — A, A, Sclerosis
of the posterior root-zone; 0 Left anterior grey horn, healthy ;D j35
anterior grey horn in a state of atrophy. * ' '* fc

The posterior nerve roots are atrophied in the late stages of
e disease. They appear as flat, grey, translucent bands, and
nibit degenerative atrophy of the nerve fibres and prolifera-
'n of connective tissue.

The peripheral nerves, the anterior nerve roots, the sympa-

242

SYSTEM DISEASES OF THE

thetic system, and the muscles are generally quite normal. The '
spinal gauglia of the posterior roots have, however, been found
diseased (Carter). Some of the cranial nerves have also been
found diseased, grey degeneration of the optic nerves being the
most frequent change observed. Morbid changes have been
found on rare occasions in the oculo-motorius, abducens, and
hypoglossus. The nuclei of these nerves, on the floor of the
fourth ventricle, also appear sometimes to be affected.

When arthropathies form a part of the disease there is j
disappearance of the articular cartilages, and the articular ends
of some of the bones are eroded. There is little or no tendency ;
to exostosis. - In more recent cases the amount of articular fluid
is greatly increased, points of thickening and fungosities are
found on the synovial membrane, the surrounding soft parts*
are swelled and suffused with fluid.

The changes in the skin and viscera are the same as in
chronic myelitis.

I ;

§ 446. Morbid Physiology. — The general opinion amongstejli
pathologists at present is that sclerosis of the posterior root-zone;
of the spinal cord for a considerable portion of their longitudinal 4 ;
extent is the essential morbid alteration in locomotor ataxia i
As the disease extends horizontally towards the posterior mediae jj \
fissure, the columns of Goll become implicated, and when onc.J$ ::
the fibres of these columns become interrupted in any part ( ft :
their course the portions above the seat of lesion undergo L J
degeneration, so that sclerosis of the columns of Goll througl; j :i
out their entire length is usually present, although it does n<
appear to constitute a necessary part of the morbid change, j
the sclerosis spreads outwards, the inner radicular fascicul
and posterior grey horns become occasionally affected; and
many cases, as already remarked, the disease extends to t
anterior grey horns and lateral columns.

The lancinating pains may be explained by irritation of t
posterior nerve roots, and their prolongations through the pf
terior columns, while the subsequent ansesthesia is caused
destruction of the posterior root fibres. The absence of 1
'patellar-tendon reflex is caused by disease of the affern
portion of the reflex arc in its passage through the poster

>. j:

SPINAL CORD AND MEDULLA OBLONGATA. 243

columns. It is probable that irritation of these fibres may in
;he early stage of this disease give rise to excess of the tendon
'eflex.

Retardation of painful impressions and analgesia are caused
oy disease of the grey substance of the posterior horns. Irrita-
tion of the grey substance of the posterior horns occasions the
cutaneous trophic disturbances. When the morbid change ex-
:ends to the ganglion cells of the anterior horns, atrophy of the
aiuscles supplied from the diseased part results, and it is also
probable that the arthropathies of locomotor ataxia are caused
jj disease of the ganglion cells of the anterior horns. Disease
)f the automatic centres in the lumbar region occasions the
vesical and sexual disturbances. When the pyramidal tract
Decomes implicated in the morbid change the paralytic stage
)f the affection becomes established. Implication of the direct
I ;erebellar tract is not known to produce any symptoms.

It remains now to connect the swaying movements on closing
,he eyes and the ataxia with the morbid changes in the cord.
I \.rewe to connect the motor disturbances in locomotor ataxy with
klisease of the posterior root-zones themselves, or with disease
fti the fibres of the posterior roots and of the posterior grey
biorns with their consequent sensory and reflex disturbances ?
Svrierordt and Heyd have shown that when the soles of the feet
In healthy persons are rendered anaesthetic by chloroform or
Bee, the amplitude of the oscillations of the body is increased,
t This shows that loss of cutaneous sensibility must exercise some
Influence in the production of the motor disturbances of loco-
I motor ataxia, and this influence becomes still greater when, as
frequently happens, the sensibility of the muscles and articula-
: lions is lost.

But there is no constant relation between the degree of

-taxia and that of cutaneous and muscular anaesthesia. Nume-
rous cases are recorded in which a high degree of ataxia was

present in the absence of any disorder of cutaneous or muscular
i . ensibility, and when both symptoms are present they do not

mrsue a parallel course. It must, therefore, be concluded that
'■ <he ataxia is not caused by disease of the fibres of the posterior

>oots of the posterior grey horn, and that it is caused by disease
[ j)f the posterior root-zones themselves. These zones, as already

244

SYSTEM DISEASES OF THE

mentioned, consist of looped fibres which co-ordinate afferent
impulses before they are transmitted upwards to the cephalic ;
ganglia. But the motor disturbances of locomotor ataxia do
not, as we have just seen, result from arrest of cerebro-afferent
impulses (anaesthesia), and it may therefore be concluded that
it is caused by disease of cerebello-afferent fibres.

§ 447. Diagnosis. — Typical cases of locomotor ataxy are easy
to> recognise ; but in those cases in which the morbid process
extends beyond its usual limits, the diagnosis is surrounded by
many difficulties, and it can only be made by one who has a
clear and distinct knowledge of the history of the case and of
the symptoms which implication of each segment of the cord
occasions. It is also very difficult to diagnose tabes at its com-
mencement, and yet it is of great importance not to overlook
the true nature of the case in the initial stage. The most
trustworthy symptoms are the lancinating pains, the feeling of I
a tight girdle, paralysis of the ocular muscles, myosis with the
Argyll-Robertson symptom, amaurosis with white atrophy of
the disc, parsesthesise in the region of the ulnar nerve, great j
sense of fatigue on slight exertion, slight swaying of the body
on the eyes being closed, failure of the patellar-tendon reflex,
slight weakness of the bladder, and disturbances of the sexual
organs.

The following are the chronic spinal affections which are
most likely to be mistaken for tabes : —

Common transverse myelitis, as a rule, presents no difficulties.:
Paralysis of all the spinal functions, botb motor and sensory,*
characterises this affection, and there are no lancinating pains
in the initial stage.

Multiple sclerosis may sometimes be very similar in its
symptoms to locomotor ataxy. The following symptoms may;
be regarded as significant of multiple sclerosis: Great dizziness-
headache, psychical disturbances, early nystagmus, the charac-
teristic tremor on voluntary effort, paralysis, muscular tensions
contractures, increased reflex actions of tendons in the loweh
extremities, and apoplectiform and epileptoid attacks.

Spasmodic spinal paralysis (lateral sclerosis) is characterises
by paresis and paralysis with muscular tension and contractures

SPINAL CORD AND MEDULLA OBLONGATA.

245

reatly increased reflex action of the tendons, absence of ataxy,
nd of sensory and vesical disturbances, lancinating pains, and
Sections of the cranial nerves.

Affections of the cerebellum may sometimes give rise to
prnptoms closely simulating locomotor ataxy. The signs of
arebellar disease are severe headache especially in the back of
le head, occasional vomiting, general convulsions, staggering
ait like that of a drunken man or an impulse to fall back-
wards, and amaurosis, while there is an absence of lancinating
ains or other disturbances of sensibility, and of the vesical
nd sexual functions.

Chronic spinal meningitis is sometimes complicated with
ibes. The symptoms of meningitis are pains and stiffness in
he back, sensitiveness in the spinous processes to pressure, a
ertain amount of sensory and motor weakness, and the absence
f ataxy.

I Progressive cerebral paralysis is distinguished from tabes by
l le presence of disorders of speech and psychical disturbances.

. § 448. Prognosis. — Locomotor ataxy is a serious disease,
? Ithough the prognosis is not always so serious as it was once
fought to be. A certain small per centage end in recovery,
tind in many instances the disease may be arrested for years.
Its duration is, as a rule, always prolonged, and usually many
'■ ears elapse before the fatal termination.

The prognosis is favourably influenced by the absence of any
iereditary predisposition to the disease, or of a neuropathic
iDnstitution, by a slow development and moderate intensity of
he symptoms, especially of the sensory disturbances, by the
jatient being in a comfortable position in life, and by the
jivourable effect of treatment. If, on the other hand, there be
i pronounced hereditary predisposition, if the symptoms make
1 ipid progress, and there be severe paroxysms of pain, rapid
iiiaciation, serious implication of the genito-urinary organs,
rthropathies or other trophic disturbances, and implication of
ie cranial nerves, the prognosis is unfavourable.
The prognosis of individual symptoms is very various,
he disturbances of sensibility usually readily improve, but
he prognosis of the ataxy is unfavourable. The lancinating

246

SYSTEM DISEASES OF THE

pains and the sexual weakness are usually very obstinate, but
the vesical troubles may disappear. The prognosis in paralysis
of the muscles of the eye is favourable, but the amaurosis, due
to atrophy of the optic nerve, is quite hopeless.

§ 449. Treatment. — When there is a manifest predisposition
to locomotor ataxy, the members of the family should be sub-
jected to a careful regimen with the view of preventing the
development of the disease. Members of such families should
be cautioned against exposing themselves to the exciting causes
of the disease, such as cold and damp, venereal excesses, and
onanism.

Antiphlogistic treatment may be useful in the very early
stage of those cases which are complicated by spinal meningitis,
but it does no good in any other case. Counter-irritants have
been greatly employed in the treatment of tabes, but they have ■
never been found to be of any use, except probably in those i
cases which were complicated by spinal meningitis. Thermal I
baths have been much used at one time, but they are probably •
injurious instead of being beneficial, except in those cases which j
are attended by lancinating pains of unusual severity, and in
which there are general excitability, sleeplessness, and other r
symptoms of irritation. The temperature should never her
above 90° F., and the patient should not remain in the bath:
longer than from fifteen to twenty minutes, and it should be
used only once in two or three days (Erb).

Sulphur baths have been much used in France, and thej>
-effects obtained from them have been favourably reported on
They have only, however, been used as adjuncts along witfc
other agents, so it is impossible to tell how much of the effec
is to be attributed to them.

Saline thermal baths appear to act favourably on the disease
Rheims has long enjoyed a reputation in the treatment of tahef I
and Erb reports favourably of Nanheim. Chalybeate and mxv I
baths have been employed in the treatment of the disease, bu I
it is doubtful if they possess any special advantages.

The cold-water cure, in well-conducted hydropathic establisl I
ments, is probably one of the very best methods of treating tl"
disease. Almost all authorities on nervous diseases, with tl

SPINAL CORD AND MEDULLA OBLONGATA.

247

ixception of Leyden, speak most favourably of the beneficial
ction of hydro-therapeutics, and Erb recommends his patients
:o use the cold sponge bath at home all winter. The wet pack
mould be used with caution, beginning with a temperature of
38° F. and going down to 77° F. Wet rubbings, beginning at a
temperature of 77° F. and going down to 65° F. do good. The
institutions to which patients affected with tabes are sent
should be situated in mountainous regions and provided with
convenient walks. Patients should be sent there in the be-
ginning of summer with instructions to remain till autumn.

Electro-therapeutics unquestionably exercise a favourable
influence on the progress of the disease. The constant current
is usually employed. Both electrodes should be placed on the
vertebral column — one in the lumbar region, and the other at
the nucha. The direction of the current appears to be an in-
different matter, but an ascending current is generally preferred.
One pole, say the lower, should be fixed, and the other slowly
moved along the back so as to come in contact with every part
of the vertebral column ; then the upper pole should be fixed,
while the lower one should be slowly moved along the back.
Peripheral galvanisation of the nerves of the lower extremities
by cathode labile currents may be combined with the galvanic
treatment of the spine. In irritable persons with severe pains
the currents employed should be very weak, and strong currents
should be avoided on all occasions. The galvanic current should
be employed daily, but each sitting should not be for more than
from three to six minutes' duration. Galvanic treatment should
be discontinued if the patients feel fatigued after each sitting,
if the pains increase, and if the condition of the patient becomes
gradually worse.

Of internal remedies the nitrate of silver has acquired the
greatest reputation in the treatment of tabes, and most authors
are agreed that it frequently produces a beneficial effect.
Friedreich has recently drawn attention to the fact that its
loDg-continued use may induce albuminuria, but moderate
doses may be taken for a considerable time without producing
any deleterious effect. It should be given in doses of one-sixth
to one-third of a grain three times a day. It may be continued
I for three weeks at a time, and then after an interruption for two

248 SYSTEM DISEASES OF THE

weeks its use may be resumed for another three weeks. The ;
use of the medicine may be continued in this way with repeated
interruptions for many months without producing any delete-
rious effects. If the skin shows the slightest discolouration, the I
medicine must, of course, be interrupted for a longer period.

The iodide- of potassium given in large doses has sometimes
been found of benefit, especially in those cases which are com-
plicated with meningitis. The bromide of potassium in large
doses is also said to be of use in mitigating the pains.

Belladonna and ergot of rye have been tried in tabes, but
neither of them appear to have been productive of good ; and
the same may be said of arsenic, chloride of gold and sodium,
and chloride of barium. Strychnia should on no account be
administered, as it always appears to do harm. Phosphorus
has been found to have a beneficial effect occasionally, especially
in cases where the sensibility is greatly affected.

God-liver oil is strongly recommended by many authors, and
in many cases its employment is attended with great benefit.

Esmarch made a communication of great importance at a
recent surgical congress at Berlin. In a case which was 1
diagnosed by Professor Quinke as locomotor ataxia, and in which I
the lancinating pains attained their greatest severity in the
forearm, Crede, of Dresden, stretched the nerves in the axilla,
and the pains and ataxic symptoms disappeared.

The diet and method of life should be carefully regulated
in tabes. Patients should have as much fresh air as possible, .
especially mountain and sea air, and that of forests.

Patients should be particularly careful not to over-exert
themselves, although a certain amount of graduated muscular r
exercise has a beneficial effect. Patients must of course be i
carefully guarded against exposure to cold and damp ; and I
should, therefore, be particular to wear warm clothing and;
flannel next to the skin. In old cases patients should be dis-
couraged from all useless attempts at curative treatment. Thet
existence of the patient must be rendered as pleasant as pos-
sible, and the treatment may be directed to sustain the general:
health, but it is quite useless to adopt any special' treatment.

In such a long and tedious illness symptomatic treatment
will have to be adopted in the course of the disease. For the

( 5

D 0

SPINAL CORD AND MEDULLA OBLONGATA. 249

•loyed at various times. Amongst these may be mentioned
ynapisms, blisters, warmth, Priessnitz's cold-water compresses,
■elladonna plasters, rubbing with chloroform, faradisation or
galvanisation (stabile anode) of the hyperaesthetic spots, sub-
utaneous injections of morphia, large doses of the bromide of
mtassium, of the hydro-bromide of quinine, and, when there is
neningitis, large doses of the iodide of potassium.

Electricity is the only remedy for cutaneous anaesthesia,
notor weakness, and atrophy of the muscles.

In vesical weakness faradisation of the bladder, either
vith or without the aid of the bladder electrode, is useful.
Cystitis must be treated in the same way as chronic myelitis.
Tor the amaurosis no treatment appears to be of any avail.

Constipation is sometimes a very troublesome symptom.
I ?he diet should be carefully regulated, with the view of acting
ipon the bowels, and enemata may be employed as aids to
| reatment. If necessary, mild aperients may be used; but all
I »urgatives should, as far as possible, be avoided.

In obstinate cases faradisation of the bowels may be of great
rise.

2. Sclerosis of the Columns of Goll.

(a) Primary Sclerosis of the Columns of Goll.

§ 450. The most notable example of primary sclerosis of the
:olumns of Goll is a case observed by Pierret. The following is a
>rief abstract of the symptoms recorded : — Margaret Magnaigat,
et. 30 year.?, experienced numbness, formication, sensations of
leat, and deep-seated pain in the limbs, more especially in the
ipper extremities. There were also obstinate headache, pains in
he loins, and a sense of constriction of the thorax. In 1860 she
lid not feel the ground distinctly with her feet, and she was
bliged to walk with a cane, and three years later she entered
he Salpetriere under the care of Charcot. Tactile sensibility
vas then diminished in the sole of the feet, which she detached
vith difficulty from the ground. These symptoms were especially
narked in the left foot, and she could not walk without the. use
>f a crutch under the right axilla. When she wished to advance
he felt as if she were being drawn backwards, but once started

250

SYSTEM DISEASES OF THE

she was impelled forwards by a force she could not control. She
could maintain the erect posture with closed eyes, but felt ready
to fall at every instant. In 1866 she complained of girdle sen-
sations, and lightning pains passing round the body and down

the anterior part of the thighs, while she was readily fatigued,
but the muscular sense was unaffected. She died in 1871 from
an attack of pneumonia. At the autopsy Pierret found sclerosis
of the columns of Goll, and he thinks that disease of these
columns explains the tendency to propulsion and retropropulsion
experienced by the patient as well as the uncertainty felt in
maintaining the erect posture. The posterior root-zones were
to some extent implicated in the lesion in the dorsal region, and
I should say, from the careful drawings which accompany the
case, in the lumbar region also. Implication of the posterior
root-zones doubtless explains the lightning pains and other
sensory disturbances present during the progress of the case.
A case of primary sclerosis of the columns of Goll has been re-
corded by Ducastel and another by Gowers, but in neither were
there symptoms during life which could with probability be
attributed to disease of these columns.

(6) Secondary Sclerosis op the Columns op Goll.

§ 451. Secondary sclerosis of the columns of Goll occurs in
connection with transverse myelitis, and it is then called ascend-
ing sclerosis (§ 390, a). It is also, as we have just seen, usually
associated with sclerosis of the posterior root-zones in locomotor
ataxia, and is often observed in many of the compound lesions
of the cord. In none of these cases, however, has the affection i
of the columns of Goll ever been connected with any definite i
symptoms.

3. Sclerosis of the Direct Cerebellar Tracts.

§ 452. Sclerosis of the direct cerebellar tracts is, so far aa
is known, always secondary and ascending. It occurs in trans-
verse myelitis along with sclerosis of the columns of Gol
(§ 390, a). These tracts are also diseased in cases of meningo-
myelitis, or what is called cortical or ring-shaped sclerosis
Disease of these tracts has never been connected with an;
symptoms during life.

SPINAL CORD AND MEDULLA OBLONGATA.

251

4. Lateral Sclerosis.

(a) Primary Lateral Sclerosis.

Tabts Dorsalis Spasmodica (Charcot). Spasmodic Spinal Paralysis.

§ 453. Definition. — The disease is characterised by a
)rogressive paresis advancing gradually from below upwards,
tccompanied by muscular tension, contractures, and increase of
he tendinous reflexes, along with entire absence of sensory and
mtritive disturbances.

§ 454. Etiology. — No very decided hereditary tendency to the
iffection has as yet been made out. It appears to occur rather
more frequently in males than females.

With respect to age, by far the largest number of cases begin
between the ages of thirty and fifty. The disease is occasionally
observed in childhood, a fact which might suggest the existence
of a congenital defect of some parts of the spinal cord.

The exciting causes of the affection are unknown, although it
is very probable that exposure to cold, injuries to the spine,
lead poisoning, and syphilis may co-operate as factors in the
production of the disease.

§ 455. Symptoms. — The first and for a long time the only
symptom is a paresis of the inferior extremities, which may be
equal in both or more pronounced in one of them, and the only
effect of which is to render walking somewhat difficult, especially
immediately on getting out of bed in the morning. The patients
complain that they are soon fatigued, that their limbs are heavy,
and their gait becomes dragging and difficult. It is only in the
later stages of the affection that the paresis increases to com-
plete paralysis. Manifestations of motor irritation now ally
themselves with the motor weakness. On lying down and
especially in bed at night, or after being fatigued, the legs
become subject to clonic or tonic spasms. The former produce
tremors, which sometimes remain limited to the extremities
but are at other times so violent as to be communicated to
the entire body. These may be readily excited by pushing
against the toes so as to produce dorsal flexion of the foot
(Ankle Clonus, § 80). After a time distinct muscular tension
is developed. On passive movements of the lower extremities

252

SYSTEM DISEASES OF THE

the muscles become tense, but in the early stages of the
affection the muscular tension can be readily overcome by
increasing the pressure, while it can be considerably diminished
by repeated movements. The muscular tension soon shows itself
on voluntary movements being made, rendering them difficult
and uncertain, and making the degree of paresis appear greater
than it is in reality.

After a time the muscular tension increases to permanent,
rigidity, and a high degree of contracture results. The legs are
maintained in a position of rigid extension, the thighs being
also held rigidly together by contracture of the adductors, the
feet are in a position of extreme talipes equino-varus, and the
toes are generally strongly flexed. The rigid immobility of the
feet is now and then interrupted by clonic trembling, which
may extend to the entire leg. The trembling may appear to
arise spontaneously, but is nearly always caused either by a
reflex or voluntary movement of the foot.

The Spasmodic Gait or Spastic Walk — The combined
paresis, stiffness, and tremors of the lower extremities render
the gait quite characteristic. The foot seems to cling to the ^
ground, from which it is detached with difficulty, and as it is
made to slide forwards it produces a characteristic scraping
noise ; while the toes find an obstacle in every elevation of the
ground, and the patient readily stumbles and falls. Owing to
the contracture of the extensors of the lower extremity the
limbs are held in a rigid condition at all the articulations, so
that the necessary elevation of the passive leg is obtained by
an upward rotation of the pelvis, caused by contraction of the
abductors of the thigh on the side of the active leg. The body
is consequently strongly inclined at each step to the side of I
the active leg. The movement of the passive foot is not, how-
ever, directly forwards. The predominant contraction of the
adductors of the thigh over the abductors causes the legs to be
drawn energetically towards one another, while the foot is
sometimes though not always inverted, owing to the strong con-
tracture of the inward rotators of the thigh. The consequence
is that the toe of the leg about to be moved forwards often gets
entangled against the heel of the active leg, and the trunk has ,
to be strongly inclined towards that side so as to give additional

SPINAL CORD AND MEDULLA OBLONGATA.

•urchase to the abductors of the opposite thigh, and thus
liable them to move the foot outwards and away from the
ther. The passive leg is, therefore, moved outwards and
orwards in a semicircle, and when it is brought to the ground
t generally crosses over to the opposite side in front of the
•ther foot. It will be observed that at each step the body is
trongly inclined towards the side of the active leg, and con-
equently the gait is somewhat " waddling," and is in this
espect, as Hammond remarks, like that of a woman with a
vide pelvis..

At this period the weight of the body suffices to arrest the
Ionic contractions of the muscles of the calf of the active leg,
>ut the passive leg is often agitated by tremors, which greatly
idd to the difficulty of progression. As the disease, however,
ncreases, the spasmodic rigidity of the muscles of the calf be-
omes so great that the patient rests upon the tips of his feet;
rhile the body is inclined forwards, the arms being propped up
>y crutches, or supported by two sticks, which are held well in
ront of the patient with an outward inclination. The contrac-
ure of the muscles of the calf is now so pronounced that the
/eight of the body does not suffice to prevent ankle clonus from
uking place, and, consequently, when the patient first attains
he erect posture, his heels become strongly elevated, probable
o the extent of 6 inches from the ground. After the first
ilevation the heel is in some cases almost immediately lowered
o the extent of about 1 to 1^ inches, and this in its turn is
ucceeded by another elevation and so on in rhythmical sequence.
?he heels and with them the whole body are thus elevated and
lepressed 7 or 8 times or more in rapid succession, the number
'f these elevations which take place in a second of time corre-
ponding to those of the ankle clonus already described.

After a time the upward and downward movements of the
>ody cease, the heels come closer to the ground although
| hey do not come in contact with it, and the patient now
•ndeavours to move forwards one leg, say the right. The first
tep may be performed with tolerable facility, but when once
he right foot is projected forwards it crosses over to the other
ide, and is brought to the ground in front of the left foot.
When the left has now to be advanced the greatest difficulty is

254

SYSTEM DISEASES OF THE

experienced in disengaging the toe from the heel of the right
foot, and in the effort to do so the muscles of the calves of both
legs become strongly contracted, the patient is elevated on tip-
toes, and every effort to abduct the left foot so as to move it
away from the other may induce clonus of the right ankle, and
consequent elevations and depressions of the body. When at ]
last the left foot is disengaged, and is being moved forwards
in the semicircular manner already described, it is generally
seized with trembling (partly consisting of ankle clonus and
partly of tendinous reflex contractions of the' muscles), which
extends to the trunk, and throws the whole body into violent
agitation. This description only applies of course to the severer
cases, and if the muscular contracture increases beyond this
point walking becomes impossible. In less aggravated cases
one sudden elevation of the heel of the active leg may be
followed by a depression without subsequent elevation, so that
the gait has a peculiar hopping character.

The disease extends slowly and gradually upwards until the
superior extremities are implicated. The lumbar and abdominal
muscles are also affected, the abdomen becomes prominent, hard,
and separated from the base of the thorax by a horizontal fold I
of more or less depth, while at the same time a kind of lordosis
is produced.

When the upper extremities are affected, the paretic con-
dition of the hands manifests itself by the inaptitude of the
patient to seize small objects. The digits from time to time
become flexed involuntarily into the palm of the hand; while
at a later period of the disease the fingers become perma-
nently flexed. The muscles acting on the wrist and elbow
are successively affected, and the forearm and hand become e
rigid in a condition of extension and pronation. The superior
extremities are now rigid and immobile, and more or less -
strongly drawn to each side of the body, but the tremors are (
never so pronounced in them as in the lower extremities.?
Although this is the usual course of the disease, yet. occasionally,
the symptoms are developed in a different order. At times the
affection passes first from one lower extremity to the upper
extremity of the same side, and this hemiplegic condition may
persist for many years before the other lower extremity is

SPINAL CORD AND MEDULLA OBLONGATA.

255

ittacked. Sometimes the disease begins in the upper extre-
mities, progresses downwards, and does not involve the lower
ixtremities until a later period.

The paralysis after a time becomes complete, the contractures
.ncrease in intensity, the patients grow stiff and immovable,
ind are doomed to keep their beds. But even in patients who
are bedridden for years the general health is good, and it does
not appear that the disease ever directly causes death, which
generally results from an intercurrent affection.

The tendinous and periosteal reflexes are greatly exaggerated
in this disease. The patellar-tendon reflex and ankle clonus
can be elicited in the usual way with undue readiness. The
quadriceps femoris and the adductors of the thigh may be
excited to contract by tapping the broad upper end of the tibia,
and the contractions may extend even to the adductors of the
opposite thigh. The adductors of the thigh may also often be
made to contract by tapping over the region of the lumbar
vertebrse. Tendon reflexes also occur in the tibialis posticus,
semi-tendinosus, and other muscles.

The tendon reflexes are in like manner increased in the upper
extremities when they become implicated. They can be elicited
in the biceps and triceps by striking the tendons, while the former
may be made to contract by tapping the lower end of the radius,
and the latter by tapping the lower end of the ulna. The pos-
terior portion of the deltoid often contracts along with the triceps,
when the lower end of the ulna is lightly struck. The flexors of
the fingers, the extensors of the wrist, and the supinator longus
can each be made to contract by tapping their tendons at the
wrist ; while the interossei may sometimes be made to contract
by tapping the ends of the metacarpal bones. The deltoid may
be made to contract by tapping the spine of the scapula, and the
pectoralis major by tapping the sternum.

The cutaneous reflex appears to be occasionally increased,
but it is generally normal or diminished.

The electrical excitability of the motor nerves may manifest
slight quantitative but never any qualitative changes. The
faradic and galvanic excitability of the muscles is generally
diminished (Erb).

Sensory disturbances are entirely absent in this disease,

256

SYSTEM DISEASES OF THE

the various forms of cutaneous and muscular sensibility being
normal. The patient does not complain of paresthesias, girdle
sensations, lancinating pains, or the affections of the cranial
nerves, which are so common in locomotor ataxia. The func-
tions of the bladder, rectum, and sexual organs are entirely
unaffected. Vaso-motor disturbances are absent, and there are
no nutritive affections of the muscles or skin, and no bed-sores.

§ 456. Course, Duration, and Terminations. — The course o
the disease is generally very chronic. It comes on in a ve.j
insidious manner, and months or years may elapse before the
affection can be recognised with certainty. Occasionally the
symptoms become developed in a "typical manner in a com-
paratively brief space of time, and it may then remain stationary
for a long period.

The duration of the disease is nearly always long, extending
over many years. Complicated cases may run a comparatively
rapid course.

The disease occasionally terminates in recovery. Heuck
reports a case of spastic spinal paralysis which began suddenly
with acute and violent pains in the back, and terminated, after
a duration of five weeks, in complete recovery. Death generally
occurs from accidental causes or intercurrent diseases.

(6) Compound Lateral Sclerosis,
(i.) amyotrophic lateral sclerosis.

ScUrose Zatdrale Amyotrophique (Charcot).

§ 457. Symptoms. — Spasmodic spinal paralysis may be com-
plicated with every degree of progressive muscular atrophy;
but the highest degree of this combination is presented by those
cases which have been described by Charcot, under the name
of scUrose late'rale amyotrophique.

The disease generally begins, according to Charcot, in the
upper extremities by motor weakness, accompanied by a rapid
muscular wasting, which extends uniformly to all the muscles
of the affected limbs. The symptoms of paresis may be pre-
ceded by formication and numbness in the upper extremities,-
and the atrophy is accompanied by fibrillary twitchings of the

SPINAL CORD AND MEDULLA OBLONGATA.

257

ffected muscles. Muscular tension and contractures are soon
uperadded to the paresis and atrophy, and the affected ex-
remities are brought into permanently deformed positions,
'he arm is applied to the trunk, the forearm is semi-flexed and
ronated, and it is not possible to supinate or extend it without
mploying a considerable degree of force and causing pain, the
and is flexed on the forearm, and the different segments of the
ngers are flexed upon one another and upon the metacarpal

Fig. 178.

Fig. 178 (After Charcot). Attitude of the Hand and Forearm in
Amyotrophic Lateral Sclerosis.

ones. When the patient elevates the arm by a voluntary
ffort, the extremity becomes agitated by tremors, not unlike
hose which occur in sclerosis in patches. In advanced cases
jhe thenar and hypothenar eminences become flattened, the
• aim of the hand becomes excavated, and the muscular atrophy
lay proceed so far that the forearm and arm are reduced almost
y> a skeleton. Under these circumstances the spasmodic rigidity
tecomes less pronounced, but the limbs may even then main-
tain the forced attitudes in which they have been held so long.

In some patients the head is fixed by spasmodic rigidity of
he muscles of the neck so that they cannot move it in any
irection. The contracture may also extend to the temporal
mscles so that the mouth can only be opened to a limited
egree (Charcot). The muscular atrophy may occasionally be
|iasked by a pseudo-hypertrophy of the affected muscles.
R

258

SYSTEM DISEASES OF THE

After a period of from two to six or nine months the lower
extremities become affected, first by paresis, which may be pre-
ceded or accompanied for a longer or shorter time by formication
and numbness of the limbs. The paresis of the lower extremi-
ties is not, as occurs in the upper extremities, necessarily accom-
panied by atrophy of the muscles. It is, however, accompanied
by muscular tension, permanent contractures which maintain
the extremities rigid in the position of extension, by tremors,
ankle clonus, and increased reflex action of tendons. These
symptoms are, indeed, those which have already been described
as belonging to primary lateral sclerosis, and they soon increase
to such a degree in the amyotrophic varieties as to render
walking impossible.. At first the muscles of the lower extremi-
ties are tense and firm, and do not show any trace of atrophy,
but after a time fibrillary contractions occur, diffused atrophy
of the muscles supervene, and the contractures diminish.

The third stage of the disease is characterised by the appear-
ance of bulbar paralysis, consisting in paralysis of the tongue
and lips, and of the pharyngeal and laryngeal muscles. The
nuclei of the pneumogastric nerves appear finally to be in-
vaded, giving rise to disturbances of circulation and respiration
which before long induce death. The disease develops rapidly,
and, according to Charcot, always causes death in from one to
three years ; differing in this respect greatly from progressive
muscular atrophy, which may extend over a period of from
eight to twenty years.

(ii.) COMBINED SCLEROSIS OF THE POSTERIOR. AND LATERAL COLUMNS.

-§ 458. The symptoms of locomotor ataxy and of primarj
lateral sclerosis may be present in every possible combination
those of the former predominating at one time and of the latte"
at another. The symptoms which indicate that the latera
columns are being gradually invaded in locomotor ataxy an
spontaneous jerkings in the lower extremities, gradual loss c
power to perform simple movements of extension and flexioi
muscular tension, and contractures.

When, on the other hand, the symptoms of lateral scleros
predominate, the signs by which a complication of locoinot<

SPINAL CORD AND MEDULLA OBLONGATA.

259

ixy may be suspected are the presence of lancinating pains,
•die pains, and other sensory disturbances, vesical weakness,
ght swaying on closing the eyes, and, above all, the absence
the patellar-tendon reflex and ankle clonus.

§ 459. Lateral sclerosis occurs as a secondary disease in
insverse myelitis and in various diseases of the medulla
longata, pons, and brain. It always occurs below the seat of
e lesion, and pursues a descending course (§ 390, b). The
mptoms caused by secondary lateral sclerosis are the same as
ose caused by the primary form of the affection, being only
Ddified by the symptoms of the primary lesion with which it
associated. These symptoms are, briefly, voluntary paralysis,
iscular tension and contracture, excess of the deep reflexes,
d generally also of the cutaneous reflexes. The symptoms
secondary degeneration of the pyramidal tracts will be more
nutely described when the primary lesions with which it is
>ociated are under discussion.

§ 460. Morbid Anatomy.~The morbid anatomy of primary
,eral sclerosis has given rise to a good deal of discussion, and

post-mortem examination of an uncomplicated case of the
sease has hitherto been published. But what we know

the functions of the lateral columns renders it probable
at the anatomical basis of the affection consists of sy ra-
dical sclerosis of the lateral columns. Leyden has, however,
vanced powerful arguments against this opinion. Two cases
ve been published by Charcot and Pitres, one of which was
ignosed during life as amyotrophic lateral sclerosis, and
3 other as primary lateral sclerosis, and the post-mortem
imination showed that both were anomalous cases of sclerosis

patches. The French authors, however, acknowledge that

the case which was diagnosed during life as primary lateral
erosis the symptoms were not quite characteristic. Symptoms,
• instance, of vesical weakness and slight sensory disturbances
;re present, and the authors think that had sufficient weight
en given to the presence of these symptoms the diagnosis of

260

SYSTEM DISEASES OF THE

primary lateral sclerosis would not have been made. And,
again, although a focus of disease was found in the posterior
columns in the cervical region of the cord, the other foci were j
found in the pyramidal tracts in their passage through the I
crusta, anterior pyramids of the medulla, and lateral columns I
of the cord. Charcot, therefore, thinks that this case confirms to i
some extent the theory of symmetrical sclerosis of the lateral
columns. Dr. Carl Ritter von Stofella has published a case in
which the typical symptoms of spasmodic paralysis were present
during life. The autopsy was conducted by Prof. Klob, who i
found symmetrical sclerosis of the posterior portion of the
lateral columns. Prof. Klob, however, mentions that the
sclerosis extended in the thoracic and lumbar regions to the t
pia mater, so that, as pointed out by Ley den, the direct cere-
bellar tract must have been affected, and the case cannot he
quoted as an example of symmetrical sclerosis of the pyramidal
tracts. No microscopic examination of the cord was made, and
this fact of itself would render the case almost valueless with
respect to the morbid anatomy of the affection.

Dr. R. Schulz communicates three cases in which the.
symptoms of spasmodic paralysis were present during life, but
in which the post-mortem examination decided against a priman
sclerosis of the pyramidal tracts. In the first case a tumour o
the medulla oblongata was found, accompanied by descendiD;
sclerosis of the pyramidal tracts ; in the second a tumour wa
found between the right lobe of the cerebellum and pons, bu
without a trace of descending sclerosis; while the third cas
was one of chronic hydrocephalus internus, also without a trae
of descending sclerosis of the cord.

A patient under the care of Dr. Morgan, in the Manchesfr
Royal Infirmary, who presented the typical symptoms of prima,
lateral sclerosis, died from- some intercurrent disease. U
spinal cord having been hardened in bichromate of ammom
symmetrical sclerosis of the pyramidal tracts of the late:, I
columns of the cord, from the medulla oblongata to the cor
medullaris, was found.

Dr. Dreschfeld, who made a microscopic examination of 1
cord, assures me that no other lesion exists in the cc
Aufrecht has recorded a somewhat similar case.

SPINAL CORD AND MEDULLA OBLONGATA.

201

In the amyotrophic variety of the affection Charcot has
veral times proved the presence of symmetrical sclerosis of
e pyramidal tracts of the lateral columns of the cord, and of
e anterior pyramids of the medulla oblongata, along with
igenerative atrophy of the anterior grey horns and loss of the
rge ganglion cells of the cord and of the motor nuclei in the
edulla oblongata. The condition of the bulbar nuclei in this
fection is represented in Fig. 179, borrowed from Charcot, the
seased nuclei being shown to the left of a fictitious line (R, R'),
id the healthy one, for the sake of comparison, to the right of
tat line. The part which Charcot calls the fasciculus teres
■ally consists of a group of small cells, and is the same as that
hich I have called the external accessory nucleus of the facial.

is seen to be diseased on the left side (D') of the figure. The
ternal accessory facial nucleus is, however, apparently healthy,
hese observations have also been confirmed by Joffroy,
omboult, and others. Valuable contributions to the morbid

Fig. 179.

% Srtt

179 (From Charcot). Transverse Section of the Medulla Oblongata on a level
with the middle of the Nucleus of the Hypoglossal. -R, R', median raphe" • A B
t!K en.t8ithe, normal condition, and A', B' the parts as they appear in amvo-
SS\latei;al «cleros"8; 0, C, the floor of the fourth ventricle ; V avTssel
5SSS,lSQ?dS *he nucl^s of the hypoglossal anteriorly and externally • D
Ktfci fe3f ?nd D- the corresponding part on the diseased side- A
heSJK nUC!eUS rf ^e hyP°glossal; and A', the diseased nucleus, b' the
eased LS™!.0 the Pneumo&'^ric nerves ; and B', the nucleus on the dis-
eased side, which is seen not to be much affected.

262

SYSTEM DISEASES OF THE

anatomy of the cord, in cases where the symptoms of loco-
motor ataxy and of spasmodic paralysis were combined, have
been made by Westphal and others.

§ 461. Morbid Physiology. — Little need be added to what
has already been said with regard to the connection which
exists between the morbid anatomy and the symptoms in
this disease. The fibres of the pyramidal tract convey volun-
tary impulses from the cortex of the brain ; and, consequently,
when these fibres are diseased, and conduction through them is
interrupted, voluntary paralysis must result. It is more difficult i
to explain why voluntary paralysis should be associated with h
muscular tension and contractures, but I agree with those -,
pathologists who believe that these symptoms are caused by *
the unantagonised influence of the cerebellum on the paralysed
muscles.

§ 462. Diagnosis. — Spasmodic spinal paralysis is liable to be
mistaken for transverse myelitis, inasmuch as the lateral column.?
are generally implicated in the latter disease. In transverse-
myelitis there are various disturbances of sensibility, vesica'
weakness, and bed-sores, the paraplegia is developed more rapidlj
and completely, while the upper boundary of the paralytii
manifestations remains stationary. Reflex action of the skin it
as a rule, considerably increased.

In the cases of locomotor ataxy which are complicated witl
sclerosis of the lateral columns, the diagnosis must largel
depend upon the history of the case, especially with respect t
the sensory disturbances.

This disease may be distinguished from poliomyelitis
anterior chronica by the fact that in the latter the paralyse
muscles become rapidly atrophied, the reflex action of th
tendons and the faradic excitability of the muscles are lost, th
muscles generally manifest the reaction of degeneration, an
the deformities are of the nature of paralytic contractions.

When multiple sclerosis first makes its appearance in 1 1
lateral columns, it may be impossible for a time to distingui.
between it and spasmodic spinal paralysis. As the forff: ,
disease progresses, its symptoms become so characteristic tl
the diagnosis between the two diseases is easy.

SPINAL CORD AND MEDULLA OBLONGATA. 263

Spasmodic spinal paralysis may be distinguished from
aralyses arising from lesions of the cauda equina and other
eripheral paralyses by the absence in the former of disturb-
nces of sensibility and muscular atrophy, the retention of
lectrical excitability, and the increase of the reflex action of
he tendons.

The hemiplegic form of primary lateral sclerosis may be
oistaken for hemiplegia of cerebral origin. In the former
lisease the lower extremity is first affected, and the paralysis
»nly advances very slowly to the upper extremity, and mus-
clar tension and contractures are early developed. There are
10 disturbances of sensibility and no symptoms referable to the
;erebrum or to the cranial nerves. A focal lesion affecting the
Dyramidal tract symmetrically in the anterior pyramids of the
nedulla oblongata, followed by descending sclerosis, may cause
iymptoms which cannot perhaps be distinguished from those
)f primary lateral sclerosis.

§ 463. Prognosis. — Spasmodic spinal paralysis is probably
he most protracted of all the chronic affections of the spine.
Uncomplicated cases do not appear to shorten life at all, owing
:o the entire absence of disturbances of the bladder, bed-sores,
md any affection of the respiratory centres. In some few cases
the disease is capable of considerable improvement or even
complete recovery.

Where the disease is complicated with muscular atrophy and
bulbar symptoms, the prognosis is of course very grave.

§ 464. Treatment. — The treatment of spasmodic spinal para-
lysis is generally the same as that of chronic myelitis and of tabes.
The galvanic current is by far the most trustworthy remedy.
Carefully conducted hydropathic treatment may be beneficial,
and gaseous thermal springs have been employed with apparent
advantage. The nitrate of silver has been used internally, but
it does not appear to be so useful in this affection as in tabes.

The rules with regard to diet, exercise, and general regimen
are the same as for other forms of chronic myelitis.

264

CHAPTER V.

IL — MIXED DISEASES OF THE SPINAL CORD AND
MEDULLA OBLONGATA.

(I.) PARALYSIS ASCENDENS ACUTA.

Aeute Ascending Paralysis — Landry's Paralysis.

§ 465. Definition. — Acute ascending paralysis is characterised
by a motor paralysis which generally begins in the lower ex-
tremities, spreads pretty rapidly over the trunk to the upper
extremities, and usually involves the medulla oblongata, the
general sensibility and also slightly the functions of the bladder
and rectum; but there is no decided atrophy of the muscles
and no alteration of their electrical excitability. I

§ 466. History. — Cases of this disease were described by Ollivier,
"Watford, and others, and it appears that Cuvier died of it in 1832.
The disease, however, was not recognised as a separate affection until
1859, when Landry described some cases under the name of " Paralysie
Ascendante Aigue." Kussmaul also described two cases in the same year.
Since Landry's publication reports of cases have multiplied ; although at
times instances of other diseases, such as of acute central myelitis, and of i
subacute anterior poliomyelitis, have been described under this name.

§ 467. Etiology. — Very little is known with respect to the
causation of this disease ; and at times it arises in the absence
of recognisable predisposing or exciting causes. Most of the
reported cases have occurred between the ages of twenty and
forty, and men are more frequently attacked than women.

Exposure to cold is probably the most frequent exciting cause.t
Some cases have occurred during convalescence from acute
diseases, as typhoid fever, pleurisy, or variola, and a few have
followed suppression of the menses. Various authors regard

MIXED DISEASES OF THE SPINAL COHD. 265

pbilis as a frequent cause of the disease, but it is doubtful
)\v far tbis opinion is correct. In the case of a woman of
renty years of age, who died of tbe disease in the Royal In-
mary, within a week from the commencement, there were
:ep cicatrices in the left groin, but no further evidence of
philis could be detected. The interior of the uterus was lined
ith a layer of blood. I did not see the case during life, but
te symptoms as reported to me were very characteristic.

§ 468. Symptoms— The paralytic phenomena are generally,
ough not always, preceded by various premonitory symptoms,
ch as slight fever, shooting pains in the back and limbs,
rmication and numbness in the feet and finger tips, and a
; eling of great weariness, debility, and general discomfort,
hese may last for one or several days, and they have occa-
, anally existed for six weeks.
The characteristic symptoms of the disease now make their
ipearance. Great weakness of the lower extremities is soon
i mplained of, which increases to such an extent as to render
; indiDg and walking impossible. The patient can for a short
i.ne execute when lying down the individual movements of the
gs, but this power is soon lost. The paralysis appears first
the muscles which move the feet, then in those which move
le legs, and at last in the muscles of the thighs, and thus, in
e course of a few days, the lower extremities may be cem-
etery paralysed. The legs now lie flaccid and powerless, there
no resistance to passive movements of them, and there is
mplete absence of muscular tension and contractures.
The paralysis advances steadily upwards, the muscles of the
:iink are invaded, and sitting up is rendered impossible; while
j.e acts of coughing, sneezing, and defecation are weak and
effective through paralysis of the abdominal muscles,
j The muscles of the upper extremities are now attacked ;
ley are implicated, indeed, before the abdominal muscles, and
on become completely paralysed. The hands first grow
eak, and finer actions, as writing, become impossible. The
Jovements of the forearm become more and more difficult, and
nose of the shoulder-joint are soon implicated, the arms, like
'e legs, being completely relaxed and immovable.

266

MIXED DISEASES OF TELE

Disturbances of respiration now appear, owing to paralysis
of the intercostal and other respiratory muscles of the trunk..,.

The disturbances of sensibility are quite subordinate to the
motor paralysis, although they are not entirely wanting.
Patients frequently complain of numbness and formication in
the fingers and toes, a diminution of feeling in the soles of the
feet, extending occasionally over, the whole of the lower extre-
mities, and pain may be complained of at the beginning of the
disease, although it is never a prominent symptom. Cutaneous i
sensibility is usually normal, but occasionally it is distinctly
lowered towards the periphery of the extremities, and in some i
few cases there is almost complete anaesthesia, while rarely i
hyperalgesia has been observed.

A considerable amount of emaciation may appear just as occurs
during the course of any other acute disease, but the paralysed
muscles do not undergo rapidly progressive atrophy, and the
electrical excitability of the paralysed nerves and muscles
remains normal. The nutrition of the skin is not affected, and
bed-sores do not occur.

In a case reported by Eisenlohr transitory oedema of the.
skin with redness of the integument over various joints is men-1
tioned as having been present, and in some other cases s
profuse secretion of sweat has been noticed, but no other vaso-
motor disturbances.

Keflex action is preserved during the first few days of th>
disease, it then diminishes more or less rapidly, and is finall
extinguished. In Eisenlohr's case an increase of reflex actio:
was observed. In one case examined by Westphal the reflei<
excitability of the tendons was abolished as well as that <
the skin.

The functions of the bladder and rectum are usually ui
affected. In some few cases slight disturbances of the bladd',
have been met with, but the severe paralysis of the bladder an
rectum, which occurs in other forms of central myelitis, h
never been observed. The bowels are usually constipated.

The general health is as a rule good, and in the majority
cases there is no fever. In some, however, the general heal
is disturbed, and febrile symptoms appear, which occasiona
may be severe. The brain is entirely unaffected throughoj

SPINAL CORD AND MEDULLA OBLONGATA. 267

ie whole course of the disease ; even the cerebral motor nerves
re not implicated until the terminal period.

As the disease advances upwards, patients complain of pain
ud stiffness in the neck, and the muscles of that region
ecome paralysed, and sometimes there is paresis of the facial
mscles. The medulla oblongata is soon implicated, and then
he functions of articulation, mastication, deglutition, and ulti-
mately respiration are interfered with; evidences of hyperemia
nd hypostatic congestion of the lungs appear, and the patient
des from asphyxia. Sometimes the pupils have been unequal,
,nd the pulse may become very frequent.

The duration of the disease is somewhat variable. In some
ases it runs its course and ends in death in two or three days,
vhile occasionally it lasts from two to four weeks. The average
luration of fatal cases is from eight to twelve days.

But the disease may end in recovery. It may cease to pro-
gress at any stage of its development. This usually takes place
I >efore the nerves of the medulla oblongata are involved, but
ecovery has been known to take place even after disturbances
»f respiration, deglutition, and mastication had commenced.

In cases which run a favourable course improvement takes
)lace at an early period of the disease, the parts last attacked
)y the paralysis being the first to show signs of improvement.
The patients first begin to use their hands, after a time they
ire able to sit up, and finally after another considerable interval
hey are able to stand and walk. The period of recovery occu-
Dies many weeks, although the duration varies much in indi-
vidual cases. Fluctuations and relapses may occur during
'ecovery, and the patients complain for a long time of debility.
The disease occasionally begins in the bulbar nerves, and the
Daralysis progresses downwards within the cord. Cuvier, as
-eported by Pellegrini-Levi, died of this acute descending
paralysis.

The following, according to Landry, is the order in which the
muscles are affected by paralysis : —

1. The muscles which move the toes and foot, then the
posterior muscles of the thigh and pelvis, and lastly the
anterior and internal muscles of the thigh.

268

MIXED DISEASES OF THE

2. The muscles which move the fingers, those which move?

the hand, and the arm upon the scapula, and lastly the
muscles which move the forearm upon the arm.

3. The muscles of the trunk.

4. The muscles of respiration, then those of the tongue,

pharynx, and oesophagus.

It will thus be seen that although the paralysis pursues a
general ascending course, yet the various groups of muscles are
not affected in the same relative order in which they are in- I
nervated from the cord. The muscles of the hand, for instance,
are paralysed before those of the abdomen, yet the former are
innervated from the cervical and the latter from the dorsal
region of the cord.

§ 469. Diagnosis. — It may not be possible to arrive at a
positive diagnosis during the first days of the disease, but when .
it is fully developed the diagnosis presents no difficulty.

Acute anterior poliomyelitis may be distinguished from this
affection by the circumstance that it has no progressive character,
rarely attacks the medulla, and hardly ever directly causes death. 1 ;
It is also ushered in by fever, and there is rapid muscular
atrophy and loss of faradic excitability. Even the temporary
form of acute anterior myelitis may be distinguished from acute
ascending paralysis by the loss of reflex excitability and lowering
of faradic excitability, and by the fact that the paralysis is not
progressive.

Subacute anterior poliomyelitis, when it pursues a tolerably
rapid ascending course, may very readily be mistaken for acute i
ascending paralysis, but the latter disease is not attended with :
muscular atrophy, and electrical excitability is preserved. In:
subacute anterior poliomyelitis reflex action is earlier abolished
than in this affection, there is almost entire absence of dis-
turbances of sensibility and the functions of the bladder, and
bulbar symptoms only appear at a late period, and the disease-
is never so rapidly fatal.

In acute central myelitis there is always a high degree ol
disturbances of sensibility, reflex action is early abolished, and
in addition, there is paralysis of the sphincters, fever, acute bed

SPINAL CORD AND MEDULLA OBLONGATA. 269

>res, a lowering of faradic excitability, and a rapidly fatal
irmination.

The spinal form of syphilis, when it assumes the form of
cute ascending paralysis, may be distinguished by the previous
istory or evidences of still existing syphilis, and by the results
f antisyphilitic treatment.

Acute multiple neuritis may be distinguished from acute
scending paralysis by the severe pains limited to single nerve-
Dots, by the limitation of the anaesthesia and paralysis, and by
he rapid lowering of electrical excitability.

§ 470. Morbid Anatomy. — All the examinations which have
itherto been made have yielded completely negative results
>oth as regards the spinal cord, medulla oblongata, brain, sym-
athetic nerves, peripheral nerve trunks, and muscles. The
ames of Vulpian, Cornil and Ranvier, Bernhardt, Westphal,
)ejerine, and Goetz, who have conducted the examinations,
[ifficiently attest the competency of the observers. Dejerine
nd Goetz state that they observed changes in the anterior
oots of the nerves. The altered fibres presented the ordi-
nary characteristics of parenchymatous neuritis or degenerative
trophy, such as are observed in the peripheral segment of a
1 terve after section.

The following case appears to me to have been an example
>f Landry's paralysis; but, as I did not see the patient during
ife, the diagnosis must, perhaps, be regarded as somewhat
loubtful. The symptoms were reported to me by Mr.
Vartenburg, who was then House Surgeon at the Royal
nfirmary, and who took charge of the case in the absence of
he House Physician : —

Henrietta R , set. twenty-one years, was admitted into the Royal

infirmary, under the care of Dr. Browne, on January 26th, 1877, and died
J he following day. On admission the lower extremities were completely
paralysed, and there was partial paralysis of the upper extremities. The
!>aralysis of the upper extremities became rapidly more pronounced, the
espiratory muscles were soon implicated, and the patient died from
■sphyxia about thirty hours after admission. No sensory disturbances,
iculo-pupillary phenomena, vesical troubles, or bed-sores were noted. The
nstory obtained on admission was that the patient had had a slight blow
>n the back of the neck four days previously, and that bhe soon afterwards

270

MIXED DISEASES OF THE

became paralysed in the lower extremities. There were no contusions or
other signs of injury.

The autopsy was conducted by me thirty-six hours after death, and the
following is an abstract of the report : Three linear and deep cicatrices
are observed in the left groin. The skin over the sacrum and trochanters
is not ulcerated ; the muscles are plump, and none of them present any
signs of atrophy. The spinal cord was somewhat softer than usual in the
lower half of the cervical and dorsal regions, and in the lower half of the
lumbar enlargement and conus medullaris, the remaining portions being
normal. The other morbid appearances noted were unimportant. I have
repeatedly examined sections of the spinal cord, and always found the
greater portion of the ganglion cells of the anterior horns so beautifully
defined and healthy that I came to regard the cord as being typically
healthy. I observed decided pathological changes in the central column,
but regarded them as accidental, or at least of no importance so far as the
functional disturbances present during life were concerned. When, how-
ever, embryological considerations forced upon me the conclusion that the
central columns were endowed with important functions, my judgment of
the significance of the morbid changes observed in this cord became
altered. A section of the dorsal region is represented in Fig. 180; the

Fig. ISO.

Fig. 180 (Young). Section of the Upper Dorsal Region of the Spinal Cord, from
case of Acute Ascending Paralysis.— A, Anterior horns ; P, posterior horns; c
central canal ; vc, vesicular column of Clarke ; i, internal, al, antero-latera-
pi, postero-lateral group of cells ; ml, the medio-lateral area. The disease
portion is represented by the lightly-shaded area which occupies the centr
grey column and its extensions between the antero-lateral and postero-later.
groups, and between the internal and antero-lateral groups.

SPINAL CORD AND MEDULLA OBLONGATA.

271

ernal, anterolateral, and postero-lateral groups are normal, while the
ltral column and medio-lateral area are diseased. A section of the
ddle of the cervical enlargement is represented in Fig. 181 ; the internal,
terior, anterolateral, and postero-lateral groups are normal, while the
itral column, the median area, and the central group of ganglion cells
5 diseased. The diseased areas showed granular degeneration of Ger-
:h's nerve network, complete disappearance of the ganglion cells, increase
nuclei, and dilatation and congestion of blood-vessels.

Fig. 181.

o. 181 (Young). Section of the middle of the Cervical Enlargement of the Spinal
Cord, from a case of Acute Ascending Paralysis.— c, Central group, and a, anterior
group of ganglion cells ; m, median area. The remaining letters indicate the
same aa the corresponding letters in Fig. 180. The diseased area is represented
by the lightly-shaded portion which represents the central grey column and its
extensions into the median area (m), between the anterolateral and postero-
lateral groups of cells, and round the central group.

§ 471. Morbid Physiology. — The pathology of this affection
exceedingly obscure, and Westphal considers it probable that
e disease is due to some intoxication, and a similar opinion
.d been maintained by Landry. In many respects this disease
like tetanus. Acute ascending paralysis manifests itself, as
; name implies, by loss of motor power, while tetanus is mani-
?ted by symptoms of motor irritation, but both affections
e similar in their mode of invasion, in their rapid course, and
jquently rapid fatal termination.

272

MIXED DISEASES OF THE

§ 472. Prognosis. — The prognosis is always very serious.
The more rapid the ascending course of the disease, the earlier
respiration has been attacked, and the more pronounced the
signs of bulbar paralysis, the graver does the prognosis become.
When once the progress of the disease is arrested and improve-
ment begins, the prognosis becomes more hopeful, but even
then there is danger of a relapse.

§ 473. Treatment. — At an early stage of the affection Chap-
man's ice-bag may be applied to the spine. The constant
current has been employed in the later stages of the cases
which have terminated favourably.

(II.) ACUTE DIFFUSED MYELITIS.

Acute Diffused Inflammation of the Spinal Cord.

§ 474. Definition. — Acute diffused myelitis comprises all the
affections of the spinal cord which are attended by fever, and
which lead in a short time to serious functional disturbances, e
with the exception of the acute system diseases of the cord
which have just been considered.

§ 475. Etiology. — Many cases apparently originate spon-
taneously without any recognisable exciting cause. The male sex
appears to be more subject to the disease than the female sex.
The greater number of cases occurs between the ages of ten and
thirty, with the exception of infantile spinal paralysis. Sexua
excesses, and severe bodily exertion, act as predisposing cause:
of the disease.

The most usual exciting causes of the affection are injurie
such as those produced by puncturing and cutting instrument'
fractures and luxations of the vertebrae, contusions, slow con:
pression of the cord, and inflammatory processes transmitte
from neighbouring organs. Exposure to cold, especially whe
the body is overheated, or after severe bodily exertion, an
sleeping on the damp earth or in snow, are the most frequeii
causes of the affection.

Acute myelitis is not un frequently developed as a complicate I

ft
k

SPINAL CORD AND MEDULLA OBLONGATA. 273

sequel of acute diseases, such as typhus, the acute exanthe-
ita, acute rheumatism, severe puerperal diseases, and more
pecially of variola.

Myelitis, running a very rapid course, is observed with un-
ual frequency amongst syphilitic patients. Suppression of
e menses and hsemorrhoidal bleeding play a more or less
ubtful role in the etiology of the disease.
Violent emotions appear sometimes to have caused the
iection, and several cases are recorded in which the first
mptoms of myelitis showed themselves immediately after
eat fright, anxiety, or anger.

Irritative lesions of peripheral organs give rise to acute
yelitis. A proportion of the so-called reflex paraplegias, which
e developed in connection with diseases of the digestive and
nito-urinary organs, or the joints, should be classed as acute
pelitis. Feinberg has recently succeeded in exciting an acute
iammation of the spinal cord in rabbits by varnishing the
in, but the mechanism of its production is unknown.

§ 476. Symptoms. — The symptoms of acute diffused myelitis
fer greatly in each individual case, so that it is difficult to
1 3cribe the generic features of the affection. The onset of
2 disease is very variable. It is sometimes preceded by
neral malaise, slight pyrexia with or without a feeling

chilliness, and the usual febrile accompaniments, headache,
neral depression, aching pains in the limbs, and loss of
petite. In many cases the spinal symptoms make their
pearance at once, disturbances of sensation being those
l lich usually first attract the attention of the patient. The
nptoms of sensory irritation assume the greatest prominence,
t in some few cases they are entirely wanting, and the vio-
:it shooting pains of meningitis are rarely present. The pains
I myelitis consist of neuralgic pains surrounding the trunk
) a variable height like a girdle, dragging, tearing, boring,

burning sensations in the limbs which are not increased by
pssure or movement, and pain in the back extending over a
pre or less extensive area. Several of the spinous processes
p often tender to pressure. The tender spot can sometimes

best elicited by passing hot and cold sponges or the cathode
s

274

MIXED DISEASES OF THE

of the galvanic current along the vertebral column. Various
parsesthesiae are almost constantly present in the disease, the
most common and constant of these being the sensation of con-
striction, like a girdle, which is felt both in the trunk and in the
extremities and joints. Feelings of tension or swelling, and of
cold or heat, or pricking sensations and formication are experi-
enced over more or less extensive areas of skin, especially that of
the lower extremities. True hyperesthesia is rarely present in i
acute myelitis, and when it occurs it is probably due to a com-
plication with meningitis. It, however, occurs on the same -
side as the motor paralysis in unilateral circumscribed myelitis. •
As the disease advances the feelings of numbness and furriness •
become more and more prominent, and these are soon followed
by the diffused painful and vibratory sensations which Charcot
has named dysesthesia?, and which are produced by touching
the skin of circumscribed areas, or of the entire surface of one
or both extremities.

As the disease advances, the feelings of numbness and furri-
ness give place to complete loss of sensation. The anaesthesia
may be partial, or may manifest itself in the form of retardation-:
of sensory conduction. At other times it may be more or less1
diffused and complete, although the parts deprived of sensa-
tion may be subject to severe pains — ancestJiesia dolorosa
Shooting pains and spasmodic twitchings of the muscles an
very common in the paralysed parts. Patients complain a
times of painful, dragging sensations in the bladder and rectim
gastralgic attacks, and neuralgic pains in the other viscera I'
all severe cases there is complete anaesthesia of the lower ha.
of the body up to a certain height, the anaesthetic being rnarke
off from the normal skin by a pretty sharply denned line.

The motor disturbances consist of both irritative and paralyl
phenomena. In children the onset of the disease is mark*-
by general convulsions. The symptoms of motor irritation
spinal origin are twitchings of individual muscles or of enti
extremities, while at times the spasmodic contractions of t
muscles may increase to a condition of tetanic rigidity. 1
paralytic symptoms are, however, much more constant a
important. They may sometimes be developed with su-
rapidity that we speak of apoirtectiform myelitis. In soi

SPINAL CORD AND MEDULLA OBLONGATA.

275

ses the paralysis may be developed in the course of a night,
even in less than an hour, while in the hemorrhagic form it
ly develop in the course of a few minutes. When the para-
tic symptoms are rapidly developed the muscles are perfectly
,ccid, and offer no resistance to passive movements of the
.nts, and when the limbs are raised, they fall like those of a
ad body. Symptoms of motor irritation may reappear in the
jected limbs at a later period of the disease, if the patient
rvive. Isolated spontaneous twitchings of the muscles may
en be observed in the paralysed limbs, these being generally
companied by severe shooting pains.

Spasmodic tonic contractions of the muscles occur, which
e excited by a voluntary effort to move the affected limb,
by irritation of the sensitive nerves. Ultimately severe
ntractures are produced, which fix the legs in an extended or
xed position, and are frequently rendered more intense by
;empts at active or passive movements of the paralysed
abs. These symptoms are, however, more frequently ob-
:ved in the subacute and chronic than in the acute forms of
felitis.

The most common forms of paralysis are paraplegia, hemi-
raplegia, monoplegia, and paralysis of the cervical muscles,
rile complete paralysis of all four extremities and of the
eater number of the muscles of the trunk not unfrequently
curs.

The reflex excitability varies according to the seat of the
iease. The reflex activity of both the skin and muscles
iy be diminished, destroyed, or increased. In some cases
is abolished at an early period of the disease, and im-
idiately after the development of the paralysis, so that
lex actions cannot be excited even by severe irritants. At
aer times it is not entirely abolished, but a longer time is
[mred for the production of reflex movements; while in other
pes it undergoes a considerable increase, so that slight irri-
tions call forth active reflex muscular twitchings, which may
urease to a convulsive jerking of the paralysed parts. In
her cases the reflex excitability is unaltered, or it is slightly
creased for a time and then begins to diminish and gradually
] comes weaker, and finally disappears.

27G

MIXED DISEASES OF THE

The sphincters are frequently involved. Vesical paralysis may
be one of the earliest, or even a premonitory symptom of acute
myelitis. In severe cases complete retention of urine is usually
present, so that the use of the catheter is rendered necessary.
In other cases there is merely incontinence of urine, while in
the beginning the symptoms are those of irritation, such as
spasmodic closure of the sphincter, with increased desire to
urinate. In severe cases the urine after the seventh or eighth day
becomes alkaline and sometimes bloody ; it contains numerous
crystals of the triple-phosphates, and there is a muco-purulent
deposit. Paralysis of the sphincter ani is generally present.
Priapism is a not uncommon symptom in acute myelitis, the
erections generally being incomplete, but often persisting for
days, with slight variations in degree.

The vaso-rnotor disturbances are variable. Engelken found
in one case a rise in the temperature of the paralysed parts,
but most authors speak of the extremities as being cold
Diffuse oedema of the paralysed lower limbs is often ob-
served. The perspiration is sometimes increased, some- :
times diminished. The trophic disturbances consist of gan-
grenous inflammation of the skin over the sacrum, trochanters
and other exposed situations, and these usually progres:
rapidly and prove fatal by septic fever. When the lesion i
unilateral the bed-sore is situated on the opposite side of th
body to the motor paralysis. Acute bed-sore may make it
appearance as early as from the second to the fifth day of th
disease.

The case may terminate so rapidly that there is no ti;
for the development of trophic changes in the nerves an»
muscles, but traces of degenerative atrophy have been four
even in rapidly fatal cases of central myelitis. The atrophy |
the muscles is generally well marked when the disease has be*
of somewhat longer duration. In these cases there is loss s
faradic irritability of the muscles and nerves along with t
development of the reaction of degeneration. There are cat;
of acute myelitis, however, in which there is no change in t
electric irritability, and others in which only slight quantitafc
changes such as slight increase or diminution can be deni';
strated.

SPINAL CORD AND MEDULLA OBLONGATA. 277

Cerebral phenomena are not often present in acute myelitis,
t in children there may be headache, delirium, and general
lvulsions at the beginning. Headache and delirium some-
les occur in the adult, but they are probably due to the
:ompanying fever or to the simultaneous presence of sep-
aemia or uraemia.

When the inflammatory process extends to the brain graver
ebral symptoms become developed. In cervical myelitis
llo-pupillary symptoms are sometimes observed, and when
3 medulla oblongata is implicated speaking and swallowing
ly be interfered with. Disturbances of the optic and ocular
rves, such as occur in cases of locomotor ataxia, have not
3n observed.

The bowels are obstinately constipated, and at a later period
: 3 abdomen may be greatly distended with flatus.
The pulse is increased in frequency, and when the myelitis
:ends to the cervical portion of the cord the acceleration of
5 pulse may be very great. Many patients suffer from palpi-
ion and irregularity in the action of the heart, accompanied
unpleasant sensations in the cardiac region,
i When the abdominal muscles become paralysed, all forcible
oiratory acts, as coughing, are rendered feeble, and conse-
• ently the air passages cannot be cleared of mucus. The
j:ctores spinas are probably paralysed even before the ab-
minal muscles.

As the disease ascends still further the intercostal muscles
30 me paralysed, and the patients breathe only with the
iphragm. When the latter muscle is involved in the para-
!is the dyspnoea becomes intense, inspiration being only
j-ried on by means of the cervical muscles, and death by
nhyxia is imminent.

The formation of bed-sores and cystitis cause sleeplessness
■\i loss of appetite, which are soon followed by marked dis-
tance of nutrition, great emaciation, and exhaustion.
Fever is generally present in the commencement of acute
relitis. It may at times run very high and remain per-
tently high throughout the entire course of the disease. At
ter times it occurs in isolated sharp attacks, and an excessive
e of temperature is not unfrequently observed immediately

278

MIXED DISEASES OF THE

before death. In other cases the fever is slight, never attains
a high grade, and may disappear entirely during the subsequent
course of the disease. An exhaustive symptomatic fever occurs
in the latter stages of the affection, caused by the bed-sores,
cystitis, pyelo-nephritis, and consequent septic infection.

§ 477. Course, Terminations, and Duration. — The course
of acute myelitis is exceedingly variable, but it is always •
rapidly developed, and it is this feature which entitles it to be i
regarded as an acute affection. Cases which take more than
ten days to develop may be regarded as subacute. The
paralysis may at times be developed in an apoplectiform manner
almost without premonitory symptoms, and it may attain con- 1
siderable intensity in an hour or even less. As a rule, however,
there is a premonitory stage of variable length, and days may
elapse before the paralysis develops into pronounced paraplegia
At times the development of the disease is interrupted by
remissions instead of being continuous.

In central myelitis and hsematomyelitis the paralysis rapidly
ascends, symptoms of asphyxia appear, and death takes place
in a few days ; or the fatal termination is brought about by the1
violent fever and septicaemia caused by the acute bed-sores anc
cystitis, and life may then be prolonged for a period of a few
weeks. In the less severe cases, particularly when the entire
lumbar enlargement is affected with or without the dorsal por
tion of the cord, the course is somewhat slower. There, is comi t
plete paraplegia with paralysis of the bladder, cystitis, decubitu
fever, cachexia, and exhaustion, and the patient succumbs aftej
several weeks or months.

In all other cases chronic myelitis is developed, and tl
symptoms are then complete motor paralysis with incomple
paralysis of sensation and of the bladder. The syrupton? |
may then remain stationary for months or years. After tl |
disease has persisted for a variable time cystitis and bed-sor
may develop, but they never become very severe and a
susceptible of being at least partly cured. Death finally resu
from exhaustion or from some intercurrent disease.

In other cases the disease ceases and the general healtb
soon completely restored. The disorders of sensation and

SPINAL CORD AND MEDULLA OBLONGATA. 279

bladder, and the trophic disorders of the skin, are usually
-irely wanting. The disease then terminates in imperfect
overy, the only traces left being paralysis and atrophy of
i or more muscular groups.

Complete recovery takes place in rare cases, and in these
nptoms of improvement set in early. After paralysis, fever,
J other symptoms of a mild attack of acute myelitis have
rsisted for one or two weeks they undergo a slow and gradual
xooression, and in a few weeks all the functions of the body
; completely restored, although convalescence is somewhat
Dtracted.

§ 478. Morbid Anatomy. — After acute inflammation the
: inal cord is generally softened, but the appearances presented
the diseased parts differ according to the stage of the mye-
is. Leyden divides the inflammatory softenings of the spinal
:d into (1) red, (2) yellow, (3) white, (4) grey, and (5) green
purulent softening.

(1) Red Softening. — The stage of hyperemia and com-
mcing exudation is not often met with post mortem. It
>y, however, be observed in cases of traumatic and central
r^elitis which run a rapidly fatal course. The affected spot

ay be found swollen, the transverse markings on section
ing blurred and indistinct, and the cut surface presenting' a
riegated marbled appearance. The colour may vary from a
3y injection to a deep red, reddish brown, or chocolate colour,
d numerous capillary haemorrhages may be observed. The
flamed spots are moist and soft, and swell up above the level
the cut surface, and at times the tissue becomes diffluent,
rare instances a slight increase of consistency is observed in

: e stage of hyperemia. The membranes in the neighbourhood

! the affected spot also frequently present the signs of hyper-

mia and inflammation.

< (2) Yeltow Softening. — As the disease progresses the affected
irta become paler and softer, hence this stage may be called

at of yellow softening. The change of colour from red to
hllow is due partly to the diffusion and alteration of the
I'louring matter of the blood, and partly to the fatty degene-
'.tion of the medullary sheaths, and the formation of masses

fat-granules.

282

MIXED DISEASES OF THE

which undergo a granular degeneration and are finally absorbed.
The axis cylinders are swollen, often attaining enormous dimen-
sions. They present large spindle-shaped swellings, appear
cloudy, and are in a state of granular degeneration.

In the second stasre the nerve fibres are broken down into
fragments, the medullary sheath is in a state of fatty degenera-
tion, and the axis cylinders altered or destroyed.

(4) The Ganglion Cells. — The nerve cells are involved in the
• inflammatory changes. They are swollen, often to a consider-
able size, their substance is clouded, and the nucleus and
nucleolus may at times be observed in process of division,
while at other times they undergo vacuolation. Their processes
are also swollen, cloudy, irregular in shape, and in part destroyed.
At a later period the cells shrivel, lose their processes, and become
reduced to small angular masses without structure, while some
may entirely disappear.

When a cicatrix has formed, the affected spot is occupied by
a dense connective tissue containing numerous nuclei and neu-
roglia cells ; numerous Deiter's cells may be observed, and they
are often large and possess numerous processes. The vessels
are dilated, their walls are thickened, and the ganglion cells, if
any remain, are atrophic. When cysts are formed they are sur-
rounded by a more or less dense layer of connective tissue, and
they are generally traversed by a loose connective tissue net-
work. Nothing can be detected in the fluid except detritus.
When the case has become chronic and sclerosis has occurred,
the increase of the interstitial tissue becomes particularly dis-
tinct. This condition will, however, be described under chronic
myelitis. The peripheral nerves have been found in different
stages of degenerative atrophy, more especially in central mye-
litis. The muscles also manifest the characteristic appearances
of the first stage of atrophy.

The mucous membrane of the bladder is often found swollen
and covered with mucus. Hemorrhagic spots are frequently
observed in it, or it may present sloughs, or be covered with
diphtheritic exudation. Similar changes are often found in the
ureter, extending to the pelvis of the kidney. The kidneys are
filled with metastatic abscesses. The lungs are frequently con-
gested, and often present the appearances which characterise

•

SPINAL CORD AND MEDULLA OBLONGATA. 283

pneumonia ; the pleurae and pericardium are generally studded
with small haemorrhagic spots.

The large sloughs characteristic of acute bed-sores are usually
found on the parts exposed to mechanical pressure, as the
sacrum, nates, and trochanters.

§ 481. Morbid Physiology. — The initial symptoms of irrita-
tion must be ascribed to the increase of the irritability of the
nerve cells and fibres, caused by increased nutritive activity
during the early stages of the inflammatory process, and the
later symptoms of paralysis to the destruction of these elements
and their compression by the inflammatory exudation. The
girdle pains depend upon implication of the posterior roots in
the inflamed focus, and the parsesthesiaB and neuralgic pains of
the inferior half of the body by irritation of the sensory tracts
situated in the grey substance and in the posterior white
columns of the cord. Since the sensory tracts either lie within
the grey substance or pass through it for a certain distance the
intense anaesthesia in acute central myelitis may be readily
accounted for. In the circumscribed, disseminated, and cortical
forms of myelitis, the degree of disturbance of sensation will
depend solely on the extent to which the posterior roots and
sensory tracts are involved in pathological changes.

The motor disturbances are first caused by irritation and
subsequently by loss of function of the motor centres and con-
ducting fibres in the cord. When the anterior horns of grey
matter are affected, paralysis ensues with complete flaccidity of
the limbs. When the pyramidal tract is affected, loss of volun-
tary power ensues, followed, if the patient survive some weeks,
by muscular tension and contractures.

The condition of the reflex excitability furnishes a valuable
indication of the state of the grey substance. So long as the
grey substance is unaffected, so long is there a continuance of
reflex actions, unless indeed the reflex arcs be interrupted in
their passage through the posterior and anterior roots and their
continuations through the white columns to reach the grey
suostance. When a portion of the grey substance is separated
from its connection with the brain by a myelitis situated higher
up the cord, reflex actions become increased. In transverse

284 MIXED DISEASES OF THE

myelitis of the dorsal region, the lumbar portion of the grey
matter is separated from the brain, but being itself healthy
the reflex of the sole is increased. When the disease is situated
in the cervical region, the cremasteric, gluteal, abdominal, epi-
gastric, dorsal, and scapular reflexes are increased. When
the grey substance is destroyed by disease, the reflexes are
abolished, hence their disappearance in myelitis of the lumbar
enlargement, and more especially in diffuse central myelitis,
in which all reflex action is usually abolished from the very
commencement. When inflammation gradually extends down-
wards, the reflex activity, which may have been normal or
increased at first, subsequently becomes weaker and gradu-
ally disappears. Important conclusions can be drawn from the
condition of the reflex excitability with regard to the localisation
of the myelitis in the grey substance. The reflex actions can
also be modified by disease of the anterior roots, and disease of
the lateral columns appears also to exert an important influence
on them, especially on the tendon reflexes.

When the myelitis affects the lumbar region, the sphincters
of the bladder and rectum become involved, beginning with
spasmodic closure of them and ending in paralysis. The priapism
which is so often present must be regarded as a sign of irritation
produced either by irritation of the nerve tracts passing from
the brain to the lumbar portion of the cord, or by reflex excita-
tions proceeding from the bladder or skin.

The trophic affections of the muscles and bones are caused
by lesion of the ganglion cells of the anterior horns, while the i
cutaneous trophic affections and bed-sores appear to be caused i
by disease of the posterior horns. The vaso-motor disturbances i
are caused by interference with the vaso-motor centres of the
cord, but the mechanisms in the cord which preside over these j
functions are not yet clearly ascertained.

§ 482. Varieties of Acute Diffused Myelitis.

The following forms of acute diffused myelitis may be distin-
guished : — 1, Acute central myelitis; 2, Hyper-acute central,
myelitis or hsematomyelitis ; 3, Acute bulbar myelitis ; 4, Acute,
transverse myelitis; 5, Acute hemilateral myelitis; 6, Acute
myelo-meningitis ; 7, Acute disseminated myelitis.

SPINAL CORD AND MEDULLA OBLONGATA.

285

L Acute Central Myelitis.— This affection begins suddenly by disturb-
ances of sensation, which are soon followed, often in the course of a few
hours, by complete anesthesia and paralysis of the lower extremities, with
flaccidity of the limbs, and paralysis of the bladder and rectum. The
reflex excitability is abolished, and the paralysed muscles undergo early
and rapid atrophy, with loss of faradic contractility. The further progress
of the disease is marked by acute bed-sores, cystitis, and ammoniacal urine,
oedema of the paralysed limbs, arthropathies, more or less intense fever'
progressive advance of the paralysis upwards, and early death by asphyxia!

Morbid Anatomy.— In this form of myelitis the softening affects prin-
cipally the grey substance, which often' flows out or becomes depressed
under the surface of section when the cord is divided transversely. On
microscopic examination the disease is seen to extend in the lumbar region
forwards from the central column into the anterior grey horns, the gan-
glion cells of which may be entirely destroyed, and also backwards into
the posterior grey horns. In the cervical and upper dorsal regions of
the cord and in the medulla oblongata, however, the disease is restricted
to the central grey columns, and the accessory cells of the anterior horns
and their continuations through the medulla, while the fundamental cells
in these regions may be almost entirely unaffected.

2. Exmatomyelitis is a variety of acute central myelitis, and is distin-
guished from the latter clinically only by the sudden onset of the
symptoms. In hematomyelitis the .paralysis becomes complete in the
course of a few minutes, or at most in the course of an hour or two, and
the more rapid is the development of the disease the more predominant
13 the hemorrhagic element in the morbid process likely to be. Hemato-
myelitis can only be distinguished from hemorrhage into the substance
ol the cord in those cases in which the paralytic symptoms are preceded
Dy paresthesia, girdle sensations, vesical weakness, muscular twitching
and lever. & '

Morbid Anatomy.-Tho morbid anatomy is the same as that of acute
ceo r«l myehto, except that io haematomyelitis the central softened mass
assumes a hemorrhagic character.

J\jTfthUr.^ditis--Thia dkease always bogi-" suddenly by
toes * ,Z u"' 6 T33' TOmiti"& di^'"g Mccough, various panes-
■ rvedt T 7 m,S"a'l0win8 and "P-Kiog. Consciousness is, however,
«me sale , "h?1"«™ in « aP°P>«* attack. Afir a shor

<Ce Ti„ 1 T?u°ml °f bulbar Para,y3is make their France. The
a fso t It"" mUSCleS °f the faoe' th0 »™*» °f «» tongue

affel caa Di \ T °f d,eg'Utiti0n ^ affeCted ~™3 Sreatb/in
the disease Th Dl8turba°ces of respiration appear at an early period of

™all,quickeaehd^e T °°' d78P"C°a' a0d CyanMis- The P^"
q ' and lrre8ular> or mtermittent. When the anterior pyramids

286

MIXED DISEASES OF THE

are affected, one, two, or all four extremities may be paralysed, or there
may be complete absence of paralysis of the limbs. The patient may
complain of pains and formication in the limbs, but there is no anaesthesia.
The bladder and rectum may become paralysed towards the terminal
period of the disease. The disturbances of circulation and respiration in-
crease, the patient becomes unconscious, and death results from asphyxia.

Morbid Anatomy. — In three cases of acute bulbar myelitis, observed
by Leyden, small centres of softening without definite boundaries were
found in the medulla oblongata. In two cases the centres of softening
occupied the internal portion of the medulla from the floor of the fourth
ventricle to the anterior pyramids ; while in the third a small centre of
softening was found situated between the restiform and olivary bodies,
and roots of the hypoglossal nerve.

4. Acute, Transversa Myelitis. — This variety of acute inflammation of
the cord is represented by the form of the disease which develops after
severe injuries of the spinal cord and vertebral column. The symptoms
vary greatly according to the level at which the cord is diseased. For
practical purposes acute transverse myelitis may be subdivided into:
(a) Acute dorso-lumbar transverse myelitis ; (6) Acute dorsal transverse
myelitis ; and (c) Acute cervical transverse myelitis.

(a) Acute Dorso-lumbar Transverse Myelitis. — This variety usually
begins by fever, formication, numbness, and pain in the lower extremities.
These symptoms are accompanied or soon followed by startings of the
limbs, but the phenomena of sensory and motor irritation soon give place
to those of paralysis. The paralysed limbs are, rigid, and the reflexes
both cutaneous and deep, are exaggerated, and there is a tonic spasm of
the sphincters. After a time the urine becomes altered, acute bed-sores
appear over the sacrum and trochanters, intermittent fever supervenes,
and the patient dies from marasmus.

Sometimes the onset and progress of the disease is so rapid that it
deserves to be called hyper-acute or apoplectiform. Hayem has reported
two cases, in which death occurred in the one in five days, and in the
other in twelve.

(6) Acute Dorsal Transverse Myelitis. — This form of the disease is the
least dangerous of the three. The sensory and motor disturbances are
more or less similar to those which occur in the dorso-lumbar form. In
acute dorsal transverse myelitis, however, there is complete absence of
bed-sores, the bladder is unaffected, and consequently the septicaemia and
marasmus are absent. Cases of this kind may completely recover, but,
as a rule, the affection assumes the chronic form. A large number of
cases of chronic paraplegia belong to this variety.

The patient may at times recover from a first attack, and may even
partially recover from a second and third attack, and ultimately succumb
to the disease many months after the first attack (Pierret).

SPINAL CORD AND MEDULLA OBLONGATA.

2«7

generally begins with pain in the back of the neck, followed by spasmodic
rigidity of the muscles of the back of the neck, which may at times be
more pronounced on one side, so that the head is rotated as well as
retracted. The pain and spasmodic contractions soon extend to the upper
extremities, and these symptoms are succeeded by paralysis, muscular
atrophy, and various other trophic disturbances, such as codema and
arthropathies. The hands assume characteristic positions, but these will
be subsequently described when we come to speak of the chronic varieties
of the disease. The lower extremities become implicated after a time, and
if the case do not terminate fatally in a brief space of time, the muscles
become the subjects of contractions, and the deep reflexes are exaggerated.
The pupils are in some cases contracted, in others dilated, and there may
be great pallor or flushing of the face, but in other cases oculo-pupillary
and vaso-motor phenomena have been absent.

The paralytic phenomena may be preceded for some time by anomalous
symptoms, such as coughs, dyspnoea, sweats, wasting, pains between the
shoulders, severe attacks of vomiting recurring at regular intervals, diffi-
culty of deglutition, hiccough, and great slowness of the pulse, which may
fall to twenty-eight beats (Gull), or even to fifteen beats per minute
(Eulenburg). The inflammatory process generally ascends to the medulla,
and death results from arrest of respiration.

Morbid Anatomy. — Little need be said with regard to the morbid
appearances presented in cases of acute transverse myelitis. The main
centre of the lesion is found in various stages of softening, and the cord
may be so diffluent that the softened mass flows out on section. If the
case has assumed a more or less chronic form, the usual ascending and
descending degenerations are observed above and below the primary seat of
disease.

In cases which are rapidly fatal there is no time for the secondary
degenerations to occur ; but I have always observed that the central grey
substance is affected both above and below the primary lesion. In the
neighbourhood of the primary lesion all the ganglion cells of the anterior
horns may be destroyed; but in the portions of the cord remote from
the latter, the disease of the grey substance becomes more and more
limited to the central grey column, and the margins of the groups of
the ganglion cells of the anterior horns. Although Fig. 146 has been
taken from a somewhat protracted case of myelitis, I have observed
similar appearances in the cervical region of the cord from a case of
fracture of the vertebral column in the dorsal region, which proved fatal
in five days. The continuation of the central column upwards into the
medulla, and the accessory nuclei of the latter, are generally implicated.

5. Acute Hemilateral Myelitis. — When the lesion is limited to one-half
of the cord there are motor paralysis, hyperesthesia, and elevation of
temperature on the side of the lesion, and more or less antesthesia on the
opposite side. The symptoms and morbid anatomy of this affection will
be more fully described hereafter.

288

MIXED DISEASES OF THE

6. Acute Myelo-Meningitis.-A.cute myelitis is frequently complicated
with meningitis. We shall hereafter speak of those cases in which
myelitis is developed simultaneously with or as a complication of acute
meningitis, but at present we wish to limit our remarks to the cases in i
which meningeal changes are superadded to acute myelitis. This compli-
cation is not very important, since the addition of meningitis to an acute
inflammatory affection of the cord does not appear to add to the gravity
of the latter. The symptoms which indicate meningitis are pain and stiff- :
ness in the hack and neck, pronounced hypersesthesia, and diffused pains. -
"When these symptoms are superadded to those of acute myelitis, the case •
is likely to be one of myelo-meningitis.

Morbid Anatomy.— When, the membranes are affected they become
congested, and sometimes capillary extravasations may be observed in
them, or they are infiltrated with serum and cellular elements, the spinaU
fluid is increased in quantity, is cloudy or reddish, and in more protracted i
cases the membranes become thickened and loosely adherent. On micro-
scopical examination the membranes are found thickened and infiltrated
with cellular elements, while in the cortical layer of the spinal cord itself
a large number of the nerve fibres are destroyed, the connective tissue
septa being thickened, and a great increase in the number of Deiter's cells
having taken place. In carmine preparations, after hardening, the cord
is surrounded by a highly-stained border which extends into the substance.,
of the cord to a greater or lesser depth, according to the extent of the.
disease. This form of disease has consequently been called peripheric or I
cortical myelitis.

7. Acute Disseminated Myelitis .—The symptoms of this affection are
paraplegia, sometimes associated with spastic symptoms. The bladder;
is generally paralysed. The state of the sensibility is variable, but it is
generally more or less impaired. The reflex and electric excitability is
also variable, both being generally diminished. The grouping of the
symptoms and the exacerbations show sometimes during life that several-
centres of disease exist. The disease may be suspected if the symptoms
of acute myelitis supervene during an attack of variola, or if they develop
suddenly in phthisical patients.

Morbid Anatomy.— This form of myelitis occurs in small spots scattered
through the substance of the cord, and appears to form an intermediate,
grade between the acute and chronic forms of myelitis. The essential
characteristic of the morbid process appears to be an increase in the inter-;
stitial tissue, which becomes unusually dense, and rich in nuclei. The
septa are swollen, the walls of the vessels thickened, and some granule
cells are observed. The consistence of the cord is often increased.

§ 483. Diagnosis.— Typical cases of acute myelitis are easil}
recognised, but the less pronounced cases and those compHcatec
by the presence of other affections are difficult to unravel. Th<

SPINAL CORD AND MEDULLA OBLONGATA. 289

characteristic symptoms are, the sudden onset of the affection,
the presence of more or less marked signs of sensory and motor
itation, the rapid development of complete paralysis of some
of the limbs and of the bladder, the rapid formation of bed-
ores, and the presence of fever.
Acute myelitis may be mistaken for the following diseases : —
Acute ascending paralysis resembles diffuse central myelitis
50 closely that it is scarcely possible to distinguish the two
fections. Landry's paralysis is characterised by the absence
f convulsive movements at the onset of the affection, absence of
ophic disturbances, slight degree of sensory disturbances, and
he preservation of the faradic contractility of the paralysed
uscles.

Acute meningitis of the cord is characterised by high fever,
evere pain, dorsal and cervical rigidity, contractures, slight
mptoms of paralysis, especially of the sphincters, absence of
evere trophic disturbances, and pronounced hyperaesthesia.
he two diseases are often combined, and then the difficulties
f diagnosis become greater.

Hcematomyelia or simple haemorrhage into the spinal cord is
ery difficult to distinguish from central myelitis, especially
om the hsemorrhagic form of the affection. In the former the
aralysis is developed suddenly without fever or prodromata,
d the paralysis is stationary instead of being progressive as
the latter.

Hczmatorrhachis or haemorrhage into the meninges of the
rd is characterised by a very abrupt development without
emonitory symptoms or fever, symptoms of severe meningeal
tation, violent pains, dorsal rigidity, a comparatively slight
gree of paralysis, and particularly by the slight intensity of
e anaesthesia.

Hypevwmia of the cord is characterised by the absence of
ver, the slight intensity of the sensory and motor disturbances,
ie frequent and rapid variations in the symptoms, and the
sence of vesical weakness and of bed-sores.
The diagnosis of hysterical paralysis from acute myelitis will
reafter be considered. Several poisons produce symptoms
hich resemble closely those of acute central myelitis.

290

MIXED DISEASES OF THE

The seat of the disease in the cord and its extension in the
transverse and vertical directions can be determined from the
area of the paralytic phenomena, the state of the reflex irrita-
bility, and the trophic disorders.

§ 484. Prognosis. — The prognosis is generally unfavourable,
but there are exceptions to this rule. Perfect recovery is rare.
In many cases a chronic disease is induced ; whilst in others
there is arrest of the disease, but incurable defects remain.

The prognosis depends on the locality and extent of the in-
flammatory process. The higher up the disease is situated in
the dorsal and cervical regions, the greater the liability of the
respiratory tracts to become affected and the greater is the danger
to life. Dorsal myelitis is, however, other things being equal,
more favourable than dorso-lumbar myelitis, because the genito-
urinary automatic centres are unaffected in the former.

The prognosis is the more unfavourable the greater the extent
of the transverse section of the cord involved in the process. It
is rendered very unfavourable when the central and posterior
portions of the grey substance are involved, owing to the con-
sequent cystitis and acute bed-sores. It is doubtful how far
implication of the white columns influences the prognosis.

The prognosis also becomes worse in proportion to the
longitudinal extent of the disease. A circumscribed transverse
myelitis is not so dangerous as the same affection when it
extends over a greater length of the cord. The progressive
ascending forms of the disease, and particularly of central
ascending myelitis, have a particularly unfavourable prognosis.
A longitudinal extension of the disease in the white columns is
not so dangerous.

A rapid development and great intensity of the paralysis,
complete paralysis of the sphincters, early formation of acute
bed-sores, progressive advance of the disease upwards, high fever,
impairment of the general health, dyspnoea, cyanosis, and other
disorders of respiration influence the prognosis unfavourably.
A moderate degree of paralysis, absence of trophic and sensory
disturbances, implication of the bladder to only a slight extent,
absence of fever and of marked impairment of the general
health, and commencing improvement of some of the nervous

SPINAL CORD AND MEDULLA OBLONGATA.

291

symptoms are all favourable signs. The nature of the causes
of the affection and the possibility of their removal, the
occurrence of relapses, the state of the general health, and the
effects produced by treatment are other elements which should
be taken into account in forming a prognosis.

§ 485. Treatment — In acute diffused myelitis the patient
should maintain absolute rest in bed, and lie as much as pos-
sible on his side or abdomen, while Chapman's ice-bag is applied
to the spine. It is also desirable to place the patient on a water
! bed, and the parts exposed to pressure should be sponged with
brandy or whisky, and dusted with an absorbent powder, in
order to prevent, if possible, the formation of bed-sores.

Internal remedies do not appear to be of much use in the
treatment of acute myelitis ; but ergot or belladonna is supposed
to do good in the early stage of the disease, and iodide of potas-
sium may be given to promote absorption when the fever has
subsided. A saline mixture may be given in order to maintain
the activity of the skin and kidneys, while the bowels should be
gently acted on by mineral waters containing sulphate of mag-
nesia, or by senna, rhubarb, or castor oil. When myelitis
becomes developed in the course of syphilis, energetic mer-
curial treatment in combination with large doses of iodide of
potassium is to be adopted.

Counter irritation to the spine should be used in great
moderation, for fear of favouring the formation of bed-sores.
In cases where the disease is situated in the dorsal and upper
I cervical regions a blister may be applied, or a hot iron may be
I used ; but counter irritants should never be applied in cases
I where the skin is anaesthetic, and all the parts exposed to con-
I tinuous pressure should be avoided in their application.

The galvanic current should never be employed in the acute
I stage of myelitis, but it is useful in the treatment of the
I sequelae of the affection, and in the treatment of the more chronic
forms. The diet should be easily digestible and nourishing,
\ and no tea, coffee, or alcohol should be allowed.

Great care should be used in introducing the catheter for
I fear of setting up or aggravating the cystitis. The catheter
t should always be washed in carbolic acid lotion, and lubricated

292

MIXED DISEASES OF THE

with carbolic oil, in order to prevent the introduction of bacteria
into the bladder. When the disease has become subacute or
chronic, the treatment must be modified accordingly.

(III.) CHRONIC DIFFUSED MYELITIS.

Chronic Inflammation of the Spinal Cord.

§ 486. Definition. — Chronic diffused myelitis comprises all
those slowly-developing and diffused processes in the spinal
cord which run a lingering course without fever, and which are
at present ascribed to chronic inflammation.

§ 487. Etiology. — It is very probable that individuals in-
heriting a neuropathic constitution are predisposed to myelitis,
but no statistical proof has as yet been forthcoming. The other
predisposing causes of the disease are mental and bodily over-
exertion, dissipation, sexual excesses, syphilis, emotional excite-
ment, especially the depressing emotions. The disease is most
common during youth and middle age, and in the male sex.

Chronic myelitis can develop from the acute form, although
the former can be produced primarily from the same causes as
the acute.

The following are the usual exciting causes of the affection : —
Exposure to cold, long sojourn in damp and cold localities,
sleeping on damp earth, bodily over-exertion, especially when
combined with exposure to cold, as occurs during campaigns.
Simple concussion of the cord, without direct injury, and gradual
compression, may also give rise to chronic myelitis, and sexual
excess may act both as a predisposing and exciting cause.

Syphilis is a fruitful source of chronic myelitis. Syphilitic
neoplasms are not here in question, but cases of chronic myelitis
which arise in the course of secondary syphilis, or in persons
who had previously suffered from the disease, and where no
specific lesion can be discovered to account for the affection.
It is probable, therefore, that we have here- to do with simple
myelitis in persons predisposed by syphilis to chronic in-
flammations.

Chronic myelitis is occasionally developed as a sequel of
various acute and chronic diseases, such as lepra, chronic

SPINAL CORD AND MEDULLA OBLONGATA. 293

alcoholism, and chronic lead poisoning. It may also be developed
from irritation and diseases of peripheral organs, and most of
the cases called reflex paralysis belong to the category of sub-
acute and chronic myelitis.

§ 488. Symptoms. — All the diseases comprised under the
term chronic myelitis cannot be included in one general descrip-
tion. The following description applies more particularly to
transverse myelitis, where one large focus of disease exists at
any height in the cord, or where there are several foci, one of
which, however, determines the chief clinical features of the
affection. In the majority of the cases belonging to this class
the symptoms develop slowly and gradually. Sensory disturb-
ances are first complained of, consisting of abnormal sensations
and anaesthesia in the lower, more rarely in the upper extremi-
ties, and these may entirely disappear for a time. They are
frequently accompanied by a girdle sensation in the trunk, or
perhaps also in the extremities. Painful sensations, severe
pains, and hypersesthesia are rarely complained of. The symp-
toms are variable and inconstant, and only attain a high degree
of intensity very slowly and gradually.

Of the motor disturbances which occur in the early stage of
the affection those of motor irritation are of subordinate im-
portance. These usually consist of slight twitching movements
of the legs, or the patient may experience slight muscular
contractions and trembling of the legs after prolonged exertion.
The paralytic symptoms are usually more prominent and im-
portant. The first motor symptoms to attract the patient's
attention are a feeling of weakness and heaviness of the limbs
and an undue sense of fatigue on slight exertion. These
symptoms may at first be relieved by walking, patients often
feeling stiffer and more fatigued at starting than after they
have walked for some time. The affection occasionally begins
by vesical weakness manifested by slight incontinence or reten-
tion, while on rare occasions the onset may be marked by
pronounced paralysis of the bladder.

As the disease advances the symptoms become slowly and
progressively aggravated, or become suddenly worse under the
influence of one of the exciting causes of the affection.

294

MIXED DISEASES OF THE

The stiffness and weakness of the lower extremities now
become more marked, the legs feel as if they were made of lead,
and the feet are slowly dragged along the ground, the toes
catching readily in every inequality. The movements of the
toes, and of the fingers if the upper extremities be implicated
in the paralysis, are slowly performed, each of them being
accompanied by a large number of associated movements. The
paralysis generally assumes the typical form of spinal paraplegia,
although occasionally it appears as spinal hemiplegia, and still
more rarely the arms may be paralysed, while the legs remain
very little or not affected.

Ancesthesia of varying forms and degrees of intensity, usually
involving the lower extremities and the trunk up to a variable
height, is rarely wanting. Retardation of sensory conduction
and various parsesthesise are often observed, and the patients
occasionally complain of dyssesthesige.

The reflex activity is increased in the majority of cases, and
a variety of reflex movements may be produced by irritation of
different sensitive surfaces. Tickling the soles of the feet causes
active jerking and kicking movements in the paralysed legs ;
while the introduction of a catheter, or the act of dressing a
bed-sore, may also excite movements in them. Evacuation of
urine may be produced by irritating the skin of the feet or by
introducing the finger into the rectum, erections may be pro-
duced by rubbing the inside of the thighs, and a discharge of
fceces often occurs during the dressing of a bed-sore.

The tendon reflexes are as a rule abnormally active, the
reactions obtained being similar to those described under
spastic spinal paralysis. In some cases the various reflexes are
diminished or even entirely abolished. In these cases the grey
substance is extensively involved, or the conducting fibres of
the various reflex arcs are destroyed as they pass through the
nerve roots.

The vaso-motor disturbances are as a rule not very prominent.
The patients complain of coldness of the feet, and the limbs
are often of a cyanotic or bluish-red colour.

The electric irritability of the nerves and muscles is generally
preserved, both quantitatively and qualitatively, when the reflex
actions persist, and in some cases both faradic and galvanic

SPINAL CORD AND MEDULLA OBLONGATA.

295

irritability may be increased. When the reflexes, however, are
abolished, in consequence of extensive destruction of the grey
matter, the muscles undergo atrophy accompanied by loss of
their faradic excitability and the reaction of degeneration. The
distribution of the atrophy is very variable. At times the upper
extremities are alone or chiefly affected by the atrophy, the
lower limbs presenting simple paralysis without atrophy.

In transverse myelitis bed-sores are sooner or later developed
in the usual places. The bed-sores usually assume the chronic
form, although they may occasionally pursue an acute course.
In some rare cases large sloughs may become permanently cica-
trised, even though there be no noticeable improvement in the
other symptoms of the disease.

The sphincters are almost always involved to a more or less
extent, and the vesical functions are particularly liable to be im-
paired at an early period, but there are some exceptional cases
in which the bladder remains unaffected thoughout the entire
course of the disease.

Sexual power is usually impaired at an early period. It
diminishes with more or less rapidity, and finally disappears
entirely. In cases of incomplete paraplegia sexual power may
be preserved for a long time.

The general health may remain perfect for a long time ; but
in all the more severe cases a constantly increasing dis-
turbance of general nutrition is observed, which becomes more
marked as soon as cystitis and bed-sores are developed. Loss
of appetite, fever, progressive emaciation, and exhaustion con-
stitute the final symptoms, provided life be not terminated
sooner by some acute intercurrent disease.

The cerebral nerves are, as a rule, not implicated in cases of
chronic transverse myelitis, except towards the termination of
the disease. In some cases the morbid process ascends until it
at last reaches the medulla oblongata, giving rise to disorders
of deglutition, speech, circulation and respiration, and ulti-
mately causing death by asphyxia.

§ 489. Course, Duration, and Terminations.— When the
chronic is preceded by the acute form, the onset of the disease
is of course sudden. In most cases, however, the disease super-

296

MIXED DISEASES OF THE

venes slowly and gradually, so that the first symptoms attract
little or no attention. The development, instead of being
continuous, is sometimes marked by intervals of more or less
improvement, which alternate with exacerbations and slight
relapses.

The disease on attaining a certain height may remain sta-
tionary for many months or even years, or it may slowly progress
and terminate in different ways. The duration of the affection
generally extends over many years, and in some cases it may
last a lifetime without producing dangerous symptoms.

Complete recovery is rare, and even in those rare cases
relapses are liable to occur. Various symptoms, such as para-
lysis, atrophies, partial anaesthesias, deformities, vesical dis-
orders, and other affections, often remain behind permanently.
The usual course of the disease is a slowly progressive one,
leading gradually and in different ways to a fatal termination.
The process may slowly creep upwards until disturbances of
deglutition and respiration occur, and death results from
asphyxia. At other times the secondary affections caused by
the myelitis, such as bed-sores, cystitis, pyaemia, and septicaemia,
destroy the vital powers of the patient and lead to death by
exhaustion and marasmus. In a large number of cases death is
caused by an intercurrent affection, such as pneumonia.

§ 490. Morbid Anatomy. — The morbid appearances pre-
sented by the spinal cord are often so slight that they cannot
be detected by the naked eye. In many cases, however, changes
occur in the consistence, colour, and form of the cord, which can
be readily detected.

It is unnecessary to repeat here what has already been said
with regard to sclerosis or grey degeneration (§ 387). It will
suffice to remind the reader that in subacute cases, or in the
earlier stages of a chronic myelitis which has developed from
the acute form, the tissue, instead of being found in a state of
sclerosis or grey degeneration, may have -undergone softening,
or the morbid process may have led to the formation of cavities.
It must also be remembered that a chronic myelitis often ter-
minates by an acute attack, and that softening may be found
associated with sclerosis.

SPINAL CORD AND MEDULLA OBLONGATA.

297

In chronic myelitis the cord undergoes various changes of
form, according to the extent and localisation of the lesion.
An increase of volume of the whole or circumscribed parts of
the cord is rare, but a diminution of volume or atrophy is
common. The atrophy may be general and affecting the trans-
verse area of the cord equally in all directions, or it may take
place in particular directions. The cord may be flattened in
the antero-posterior direction, so that it presents the appearance
of a band, or the surface may be depressed the entire length
of certain columns, as the posterior columns in locomotor ataxy,
or the surface may be depressed in isolated and circumscribed
spots.

Microscopic Examination. — Changes have been observed in
the (1) connective tissue, (2) the nervous tissues, and (3) in the
blood-vessels.

(1) Connective Tissue or the Neuroglia. — The connective
tissue septa become thickened, the neuroglia cells enlarge and
their nuclei undergo proliferation, while Deiter's cells become
greatly increased in size and number. After a time the normal
neuroglia becomes converted into a dense, fibrillated connective
tissue in which a large number of nuclei may be observed.

(2) Nervous Tissues. — The nerve fibres undergo changes
wh ich correspond to some extent with the secondary degeneration
of the fibres of peripheral nerves. The medullary sheath becomes
irregularly thickened, then undergoes granular and fatty degene-
ration, and is finally absorbed. The axis cylinders become at
first much swollen, so that they may attain two or three times
their normal dimensions, but when they are viewed longitudi-
nally they are seen to present spindle-shaped enlargements.
After the disappearance of the medullary sheath the naked
axis cylinders may often be observed for a considerable time
longer, but after a time they also undergo atrophy and dis-
appear, so that nothing remains but a dense fibrillated connec-
tive tissue. The ganglion cells are cloudy and swollen at first,
but after a time they undergo various forms of atrophy and
vacuolation.

(3) Changes in the Vessels. — The walls of the small arteries
and veins, and probably of the capillaries also, become thickened,
while their calibre is lessened. The walls of the vessels are

298

MIXED DISEASES OF THE

often adherent to the indurated connective tissue, so that the
lymph spaces are destroyed. In other cases the perivascular
spaces contain collections of fat and pigment granules, and
occasionally granule ceils also. Granule cells and corpora
amylacea are observed scattered through the diseased tissue.

§ 491. Morbid Physiology. — The connection between the
morbid lesions and the symptoms is the same in the chronic as
in the acute varieties of myelitis, so that it is .unnecessary to
repeat what has already been said with regard to the morbid
physiology of the disease.

§ 492. Varieties of Chronic Diffused Myelitis.

The following varieties of chronic diffused myelitis may be
distinguished : — 1, Chronic central myelitis ; 2, Chronic trans-
verse myelitis ; 3, Universal progressive myelitis ; 4, Chronic
bulbar myelitis ; 5, Chronic myelo-meningitis ; and 6, Chronic
disseminated myelitis or multiple sclerosis.

1. Chronic Central Myelitis. — (a) The subacute general spinal para-
lysis of Duchenne is probably a typical example of inflammation of the
central grey column, with, extensions of the process into the anterior horns,
and pursuing a gradually ascending course. Chronic atrophic paralysis is,
indeed, closely similar in its symptoms to Landry's paralysis, of which it
may be regarded as the chronic form. Hallopeau has shown that this
form of paralysis sometimes pursues a descending course. In these cases
the upper extremities, especially the muscles of the forearm, become first
paralysed ; they undergo atrophy soon afterwards, and the hands assume
deformed postures. It is often seven or eight months or longer before
either of the lower extremities are affected, and it may be several months
longer before both of them are implicated in the paralysis. But even in
these cases the disease pursues an ascending course as well, bulbar
symptoms supervene after a time, and death results from paralysis of the
respiratory centres.

(b) Peri-ependymal Myelitis — the " myellite pe'ri-e'pendymaire " of Hal-
lopeau— is another variety of chronic central myelitis. The symptoms
are characterised by paralysis followed by diminution of the faradic con-
tractility, and atrophy of the affected muscles.

The paralysis comes on somewhat suddenly ; the patient finds that he
is not able to move the fingers, hands, or more rarely the entire limb.
After a time the muscles lose their faradic contractility and become
atrophied, so that the affected extremities assume deformed positions.
Fibrillary contractions are either absent or only present in a slight

SPINAL CORD AND MEDULLA OBLONGATA. 299

degree. The patient may complain of vague pains along the vertebral
column, but other sensory disturbances are usually absent. Tlie
sphincters also remain unaffected. The course of the affection is slow, and
it may be temporarily arrested for a long time. The muscles most
frequently affected are the flexors of the foot on the leg, and of the thigh
on the pelvis in the lower extremities ; and the extensors of the fingers
and of the hand, then the muscles of the hand, and lastly the flexors and
other muscles of the arm and shoulders. This affection may pursue a
descending or an ascending course, and in the latter cases bulbar paralysis
supervenes and death is caused by respiratory paralysis. Many cases of
syringomyelia and hydromyelia are only forms of chronic central myelitis.
Peri-ependymal myelitis is closely allied, on the one hand, with the sub-
acute general spinal paralysis of Duchenne, and with progressive muscular
atrophy on the other. And if we compare the symptoms of Landry's
paralysis, subacute general spinal paralysis, peri-ependymal myelitis, and
progressive muscular atrophy, it is impossible not to be struck with the
essential unity which underlies them, while their differences are no less
instructive.

All these diseases are characterised by a progressively-invading para-
lysis, which may pursue an ascending or a descending course, and by
almost entire absence of sensory disturbances, bed-sores, and paralysis of
the sphincters. The most striking differences between them are found in
the time occupied in development of the symptoms, and in the course of
the disease. Landry's paralysis is sudden in its onset and rapid in its
progress ; while, on the contrary, progressive muscular is gradual in its
; onset and slow in its progress, and the other two diseases occupy inter-
mediate positions between these with respect to their development in
time. In Landry's paralysis there is no decided muscular atrophy, and the
faradic contractility is nearly normal ; in subacute general spinal paralysis
there is decided muscular atrophy, rapid loss of faradic contractility, and
the reaction of degeneration ; in peri-ependymal myelitis there is also pro-
nounced atrophy, and the faradic contractility becomes slowly and gradually
diminished, while in progressive muscular atrophy the atrophy and para-
lysis proceed usually side by side, and the faradic contractility is generally
normal so long as any muscle remains.

We shall hereafter show that the morbid anatomy of these diseases
tends to explain the differences just described, on the supposition that all
are only different kinds of inflammation of the central grey columns
of the cord, with anterior and lateral extensions of the disease into the
anterior grey horns.

(c) Chronic Central Dorso-Lnmbar Myelitis. — In this variety of the
disease the symptoms correspond to the affection already described as acute
central myelitis. The lower extremities are paralysed, the limbs are
flaccid, the muscles undergo atrophy, and the faradic contractility of
the paralysed muscles is soon lost ; the reaction of degeneration is present,
and the paralysis may gradually ascend to the muscles of the trunk and

300

MIXED DISEASES OF THE

those of the upper extremities. So far then the symptoms of this affectionj
correspond to those of subacute general spinal paralysis of Duchenne, butt
other symptoms are observed in the former which do not occur in thee
latter. These symptoms are oedema of the lower extremities, paralysis off
the sphincters, bed-sores, and arthropathies. Sensory disturbances also,
exist, consisting of various parsesthesiae and hyperalgesia, followed by>
varying degrees of analgesia. If the myelitis be limited to the grey sub-
stance, tactile sensibility and the sense of locality and of temperature;
remain unaffected. If the lower portion of the cord be not implicated in:
the disease, the reflex of the sole may be exaggerated in the early stage of I
the disease. This form of myelitis is seldom if ever chronic from the I
commencement, and results usually as the sequel of an acute attack.

Morbid Anatomy. — It is unnecessary to say much at present with I
regard to the morbid anatomy of the chronic forms of central myelitis..!
It appears to. me that Landry's paralysis, chronic atrophic spinal paralysis, .1
peri-ependymal myelitis, progressive muscular atrophy, and what I have-l
termed chronic central dorso-lumbar myelitis are only different forms of f
inflammation of the central grey column of the cord. In Landry's i j
paralysis the inflammatory process is very acute, and keeps limited to the I \
central column and the embryonic areas (the medio-lateral area in the-l
dorsal and upper cervical regions, and the median areas and margins of :'
the groups of ganglion cells in the lumbar and cervical enlargements) 1 1
of the anterior grey horns. The muscles thus still maintain their 4
connection with the fundamental cells, and their faradic contractility • j
and nutrition remain comparatively unaffected. In chronic atrophic J
paralysis the morbid process pursues the same ascending or descending U
course, but the fundamental ganglion cells are invaded and destroyed, . j
hence muscular atrophy and loss of faradic contractility result. Peri-
ependymal myelitis pursues a somewhat similar course, but the funda- j
mental cells are not invaded at so early a period as in the chronic |
atrophic variety. Progressive muscular atrophy pursues a still more t
chronic course. The disease, indeed, appears to be a parenchymatous one, j
and to spread from fibre to fibre and from cell to cell. It appears to begin j
in the small cells and fine fibres which lie near the central artery, and to f
spread gradually upwards and downwards and laterally. In its lateral I
extension the ganglion cells which were last developed become first i
affected, and the process gradually spreads to the more fundamental cells.
It will be apparent that in such a gradual process as this the muscular
paralysis and atrophy will pursue a parallel course, and that the faradic
contractility will be maintained so long as the fundamental cells are able
to perform their functions even imperfectly, and long after they have
become partially diseased.

In the form of the disease which I have named chronic central
dorso-lumbar myelitis the affection apparently begins as an acute
central myelitis,- and then assumes a chronic form. It pursues an
ascending course, but is not so surely invading as Landry's paralysis and

SPINAL CORD AND MEDULLA OBLONGATA.

301

chronic atrophic paralysis. The morbid process, on the other hand,
extends backwards to the posterior grey horns, and thus gives rise to
analgesia ; but, if it remain limited to the grey matter, the tactile sensi-
bility is comparatively unaffected. The sphincters also become para-
lysed, and bed-sores appear on the sacrum. Recovery may take place
even after bed-sores have formed ; but if the affection has become chronic,
many of the muscles of the lower extremities remain permanently atro-
phied. The disease may extend in the lumbar region into the white sub-
stance ; and if death supervenes, a transverse myelitis, with ascending
sclerosis of the columns of Goll, and the direct cerebellar tract and
descending sclerosis of the pyramidal tracts, will be found associated with
the morbid appearances usually observed in central myelitis. Such were
the conditions observed in a case under the care of Dr. Simpson, in which
I conducted the post-mortem examination. The prominent symptoms
during life were paralysis with fiaccidity of limbs, muscular atrophy, and
loss of the faradic and reflex excitability, ultimately associated with
anaesthesia and paralysis of the sphincters. At no time did the symptoms
indicate a spastic condition of the muscles. On microscopic examination
the lower dorsal region of the cord was disorganised in the whole of its
■transverse diameter, there was ascending sclerosis of the columns of Goll,
and of the direct cerebellar tracts, while the pyramidal tracts were
sclerosed in the lumbar region. The central grey column was diseased
from the conus medullaris up to the lower end of the medulla. In the
upper dorsal and cervical regions, however, the fundamental cells appeared
quite healthy, while the accessory cells had disappeared. The condition
,of the grey substance in this cord in the cervical region is, indeed, repre-
sented in Fig. 146.

In a case of what I must regard as in the main a central myelitis, under
the care of Dr. Morgan, the morbid appearances discovered differed from
those observed in Dr. Simpson's case. The patient under Dr. Morgan
was run over and had his sciatic nerve injured. This was followed by
paraplegia, characterised by fiaccidity of limbs, and muscular atrophy. A
few weeks after the accident spontaneous fracture of the neck of the right
femur occurred. After a time there was anaesthesia of the lower extre-
mities, paralysis of the sphincters, bed-sores, and death from pyaemia and
peritonitis. The posterior columns of the cord could be seen with the
naked eye to be gelatinous in appearance. On microscopic examination
the presence of sclerosis of the posterior columns of the cord was con-
firmed. The portion of the posterior columns which adjoins the posterior
commissure was healthy in the lumbar region, the whole of the columns
were diseased in the dorsal region, but in the lower cervical region the
portions which adjoin the posterior grey horns were healthy, and the
healthy areas gradually increased in size until in the upper cervical region
the sclerosis was limited to the columns of Goll. In addition to the
sclerosis of the posterior columns, the central grey columns were found
diseased throughout the entire length of the cord, accompanied with the

302

MIXED DISEASES OF THE

usual lateral extensions into the embryonic areas of the anterior grey,
horns. I have observed similar morbid appearances — posterior sclerosis
and central myelitis — in a case of tumour pressing upon the cauda equina.

2. Chronic Transverse Myelitis — The symptoms vary according to
the level at which the cord is diseased. This affection may be subdivided
into (a) chronic dorso-lumbar, (b) chronic dorsal, (c) chronic cervical
transverse myelitis, and (d) compression myelitis.

(a) Chronic Dorso-Lumbar Transverse Myelitis. — The paralytic symp-
toms are often preceded by girdle pains, formication, numbness, and
various other paraesthesiae, and by lancinating pains in the lower extre-
mities. The patient often complains of muscular cramps, especially in
the calves of the legs ; he is soon fatigued, and the movements are stiff
and constrained. After a time the lower extremities become rigid by con-
tractures, the gait assumes the spastic form, and both the superficial and
deep reflexes are exaggerated. If the lesion be situated below the origin of
the sixth lumbar nerves the patellar-tendon reflex is abolished. The
sensory disturbances also increase, the patient cannot feel the floor, and
he finds it necessary to direct his eyes to the ground ; tactile sensibility
and the sense of locality and temperature are generally impaired, while
in advanced cases there may be retardation of sensory conduction and
analgesia. The general health may be unaffected for a long time, but by-
and-by the paraplegia becomes complete, and the various forms of sensi-
bility become more profoundly affected, so that at last there may be
complete anaesthesia of all forms of sensibility. Muscular atrophy,
accompanied by loss of the reflex and faradic contractility, may now
supervene, the sphincters are paralysed, bed-sores form over the parts
exposed to mechanical pressure, and the patient dies from pyaemia and
marasmus.

(b) Chronic Dorsal Transverse Myelitis. — In this form both the sensory
and motor paralysis extends higher than in the dorso-lumbar variety. The
condition of the lower extremities with regard to paralysis, contractures,
spastic walk, and exaggerated reflexes is the same as in the dorso-
lumbar form of the disease. When the lesion is situated in the upper
portion of the dorsal region, the muscles of the back and abdomen are
involved in the disease. The paralysis of the abdominal muscles renders
urination, defecation, and forcible expiratory acts difficult, so that the
patient is much troubled by constipation, and he cannot clear the bron-
chial tubes thoroughly from mucus. Death is therefore liable to be caused
by slight bronchial catarrh. Valuable information may be obtained with
regard to the level at which the cord is diseased by an examination of the
cremasteric, gluteal, abdominal, epigastric, dorsal, and scapular reflexes.
Erb has recently described a case in which a spontaneous subacute dorsal
transverse myelitis was preceded by double optic neuritis.

(c) Chronic Cervical Transverse Myelitis. —The initial symptoms now
generally begin in the upper extremities which become paralysed some

SPINAL CORD AND MEDULLA OBLONGATA.

SOS

time before the lower extremities. As the disease increases all the four
extremities become paralysed. The muscles of the upper extremities after
a time become atrophied and lose their reflex and faradic contractility,
while those of the lower extremities are in a state of contracture, their
faradic contractility being preserved and the superficial and deep reflexes
increased. Various oculo-pupillary symptoms are also commonly present.
When the upper cervical region of the cord is diseased, all four extremities
are affected, but the nutrition of the muscles of the upper as. well as those
of the lower extremities remains unaffected, and their reflex activity is
increased. The diaphragm becomes paralysed, and the patient suffers
from dyspnoea, impairment of speech, vomiting, and hiccough.

Morbid Anatomy. — The morbid anatomy of chronic transverse myelitis
varies according to the level at which the cord is affected. At the level
of the principal focus of disease both the grey and white substances are
affected, and this portion of the cord may be softened instead of being in a
state of sclerosis. Above the level of the main lesion the columns of Goll
and the direct cerebellar tracts undergo ascending sclerosis ; while the
pyramidal tracts undergo descending sclerosis below the level of the lesion.
If the lesion is situated low down, the ascending sclerosis may be limited to
the columns of Goll and the descending to the pyramidal tracts of the
lateral columns. If, on the other hand, the lesion be situated high up in
the cord, both the columns of Goll and the direct cerebellar tracts are
affected with ascending sclerosis, and the pyramidal tracts and the columns
of Tiirck with descending sclerosis. Jn addition to these changes trans-
verse myelitis is frequently accompanied by central myelitis, which may
extend up into the medulla oblongata. Near the main lesion the central
myelitis may extend forwards so as to destroy all the ganglion cells of the
anterior horns, but in the upper portion of the cord and in the medulla
oblongata the accessory ganglion cells are alone destroyed, while the
fundamental cells remain more or less healthy.

(d) Compression Myelitis. — This is a very common form of myelitis, and
may occur along with any disease of the vertebral column or membranes
which causes a slow compression of the cord. The symptoms of this
affection correspond in the main with those of spontaneous transverse
myelitis. The characteristic feature of the affection is the existence of
symptoms which indicate local disease of the cord for some time previous
to the development of definite paraplegia. The most usual of these
symptoms are severe pains along the course of nerves which issue from
a particular level of the cord, cramps in the muscles supplied by those
nerves, local paralysis and muscular atrophy, local hyperesthesia or
anaesthesia, and pain and stiffness of the back.

Morbid Anatomy. — The morbid anatomy of compression myelitis is the
same as that of the transverse varieties. The structure of the cord is
destroyed at the level where the compression has been applied ; while
there is ascending sclerosis above the level of the lesion, and descending
sclerosis below it. Central myelitis is frequently present also.

304

MIXED DISEASES OF THE

3. Universal Progressive Myelitis. — In this form of the disease the
myelitis gradually extends until it involves the whole breadth of the cord.
It is characterised by progressive weakness of the muscles of the lower ex-
tremities followed by complete paralysis. The disease generally begins in
the lower extremities, and pursues an ascending course ; but occasionally
it begins in the upper extremities, and then its course is descending.
There may at first be contracture of the muscles, and this is followed by
gradual atrophy as the grey substance becomes involved. The reflexes
and the faradic contractility also gradually diminish and ultimately dis-
appear. There may be more or less violent pains in the back, trunk, and
extremities, the patient complains- of parsesthesiee and dysesthesia?, and
after a time there is complete anaesthesia, paralysis of the sphincters, and
bed-sores.

Morbid Anatomy. — In the lumbar and lower dorsal regions the entire
transverse area of the cord is diseased, but in the upper dorsal and cervical
regions the sclerosis may be limited to the columns of Goll and the direct
cerebellar tract, associated sometimes with more or less of chronic central
myelitis.

4. Chronic Bulbar Myelitis. — The most characteristic form of
chronic bulbar myelitis has already been described as chronic progressive
bulbar paralysis, but cases of bulbar paralysis are occasionally observed
which do not possess a distinctly progressive character. When the latter
class of cases is caused by a bulbar myelitis, the affection is probably in
alb cases produced by the extension of inflammation from morbid changes
taking place in the neighbourhood of the grey nuclei of the medulla
oblongata. Inflammation of the bulbar nuclei may in this manner be set
up by tumours of the neighbouring structures, or they may be involved in
the inflammatory zone which frequently surrounds haemorrhagic foci and
centres of necrotic softening.

5. Chronic Myelo-meningitis. — This form of myelitis has been termed
peripheric or cortical myelitis by Vulpian, because it consists of a chronic
inflammation of the cord extending inwards from the pia mater. It is
not easy to recognise this form of myelitis during life ; but its presence
may be suspected when the symptoms .of chronic meningitis are accom-
panied by an unwonted degree of both sensory and motor paralysis. The
paralysis is generally of the spastic variety and muscular atrophy does
not occur. It may, however, be assumed that, should the anterior roots
become involved in the disease, muscular atrophy will inevitably take
place. In some cases the posterior columns are more involved than the
lateral tracts, and then ataxic symptoms predominate over those of
paralysis.

Morbid Anatomy.— -The most characteristic feature of the morbid ana-
tomy of this affection is that the affected portion of the cord is surrounded
more or less completely by a ring of sclerosis. Sometimes, however, the
sclerosis appears to spread inwards in the posterior columns to a greater

SPINAL CORD AND MEDULLA OBLONGATA.

305

lextent than elsewhere, while at other times the anterior are affected to a
[greater degree than the posterior or lateral columns.

6. Chronic Disseminated Myelitis. — As this disease is not usually
limited to the spinal cord, but extends as a rule to the cerebrum and cere-
bellum, its description will fall more naturally with the encephalo-spinal
than the spinal diseases.

§ 493. Diagnosis. — Simple chronic transverse myelitis is cha-
racterised by slow development of paraplegia with relatively
slight irritative motor symptoms, and by the presence of more
or less marked sensory and vesical disturbances, contractures,
increased reflexes, and bed-sores. The affection is but slightly
progressive in character, and runs a tedious course. Transverse
myelitis can as a rule be readily distinguished from the syste-
matic affections of the cord. In some cases of the latter, how-
ever, the lesion of one of the functional systems of the cord
extends to neighbouring systems, and combinations are thus
produced which are sometimes very difficult to distinguish from
transverse myelitis. Numerous combinations of the system-
diseases are possible, and every case of the kind requires sepa-
rate study and a special diagnosis.

§ 494. Prognosis. — The prognosis is generally unfavourable in
simple transverse myelitis. The affection is always severe and
dangerous, and the most that can usually be hoped for is arrest of
the morbid process with considerable loss of power in the lower
extremities. Complete recovery is exceptional.

A slow progressive course must be looked for in the majority
of cases, and the disease generally terminates in death in a few
years. The prognosis will be determined by the ascending
tendency of the disease, the occurrence of relapses, and by the
presence or absence of cystitis and bed-sores.

§ 495. Treatment. — The treatment of the early stages of
chronic myelitis must be conducted on the same general prin-
ciples as are applicable to the acute varieties. So long as any
active symptoms of irritation are present, the patient should
maintain the recumbent posture, while all the usual precau-
tions against the formation of bed-sores and cystitis must be
u

306

MIXED DISEASES OF THE

adopted. Ergot, belladonna, and the iodide of potassium aro
the internal remedies which have been found of most use. I
syphilis be suspected, active antisyphilitic treatment must be<
employed. Nitrate of silver was first recommended by Wun-i
derlich in the treatment of chronic myelitis, but it is probabl}
of more use in locomotor ataxia than in any other variety oi
the disease. It should not be administered in cases associated I
with spasmodic rigidity of the muscles. Arsenic, phosphorus- 1
and cod-liver oil may sometimes be found useful, but strychnines
is positively injurious.

Counter irritation was at one time used too indiscriminately,]
and the results obtained were not very gratifying. The use off!
the milder counter-irritants, such as flying blisters, may be;
employed with advantage. Brown-Se'quard praises highly the;!
application of a hot douche, from 98° to 104° F., for two on
three minutes at a time. The stream should be nearly an inch:
in diameter. The greatest reliance must be placed on baths, |
hydropathy, and galvanism.

Baths. — Erb strongly recommends the thermal brine baths J
(Rehme, Nanheim). The temperature should not be above I
86° — 78° F., and the immersion not too prolonged, and the 1
water should not contain an excessive quantity of carbonic acid. J
Ordinary brine baths, chalybeate, and mud baths are much j
extolled by many authors.

Cold-water cure is very useful. All severe and strongly-
exciting procedures, such as the use of water at a very low tem-
perature, cold douches, and sharp slappings, should be avoided,
and even wet packs of the entire body have proved injurious
(Erb). Simple rubbing with wet-cloths, foot-baths, sponging the
back, hip-baths, and local compresses to the back left on till
they become warm, appear to be the most useful measures. The
treatment should begin with baths of moderate temperatures
(68°— 77° F., never below 60°— 53° F.), and should not be too
prolonged. When an insufficient reaction follows a bath, and
chilliness and discomfort are produced, the treatment should be
discontinued.

The galvanic current is one of the most important therapeutic
agents for the treatment of chronic myelitis. The electrodes
must be applied differently according to the differences in the

SPINAL CORD AND MEDULLA OBLONGATA. 307

'•' position and extent of the forms of disease. It is best to let
both poles act successively, either with a stabile or with a slowly
labile current. The currents used should not be very strong,

I and each application should be of short duration. The treat-
ment should be continued for months, being occasionally inter-
rupted only to be recommenced after a brief pause. It is
expedient to alternate or combine galvanisation with other
methods of treatment. Some few cases do not bear well the
application of galvanism, and with these the use of it must be
discontinued.

The general management, the diet, and the mode of life
of the patient are of the utmost consequence. Rest and
a regular mode of life are essential. Over-exertion of any
kind, mental as well as bodily, must be avoided. Sexual
intercourse should be confined within the strictest limits or
completely stopped. All excitement and violent emotions must
be prevented as much as possible. The diet must be simple,
nutritious, and easy of digestion, and cod-liver oil is often bene-
ficial. Alcoholic beverages, coffee, tea, and tobacco should be
used with great moderation. Residence in a mountainous region
at a moderate elevation, or at the sea-side, will be useful; and
it is advisable that the winters should be passed in the south.

When the patient is completely paraplegic, a wheeled chair
may be used so as to permit the enjoyment of fresh air, and when
patients are bedridden, care should be taken that the recum-
bent posture is not always maintained, but occasionally replaced
by the lateral or abdominal position.

Pain must also be relieved by various means, the subcutaneous
injection of morphia being the readiest and most effectual
method. Other serviceable drugs are bromide of potassium,
quinine, bromide of quinine, zinc, and valerian. Cutaneous
irritation, electricity either in the form of the faradic brush or
galvanic current, Preissnitz's compresses, applications of chloro-
form, and frictions with veratrine ointment and similar agents,
often do good service. For the paralysis, atrophies, and anaes-
thesia, which persist after the disease has run its eouFse,
electricity is the best remedy.

308

MIXED DISEASES OF THE

(IV.) MYELOMALACIA.

§ 496. Simple Softening of the Spinal Cord, — Softening off
the spinal cord may result from non-inflammatory processes.

§ 497. Symptoms. — The symptoms of simple softening are J
exceedingly obscure. The patient first complains of feelings of:
numbness and feebleness, generally of the lower extremities,,
which gradually increase in severity, until ultimately anaesthesia
of the lower extremities and paraplegia are fully established ; :
the reflex excitability is also gradually diminished and ultimately
abolished. To these symptoms are added progressive paralysis J
of the sphincters of the bladder and anus, and in the final stage •
bed-sores, marasmus, and pyaemia.

Brown-Sequard and Hammond assert that at no time in the
course of the disease are there any pains, hyperesthesia, spasms,
or increase" of the reflex excitability.

^ § 498. Morbid Anatomy. — The post-mortem appearances of
simple softening are similar to those of white softening caused
by previous inflammation. When fatty degeneration assumes
special prominence, the softened spot may assume a yellowish j
colour, and present the appearances of yellow softening. The j
softened spot usually merges imperceptibly into the normal
tissue. The microscopical characters are not well known ; but
it may be presumed that the nuclei of the neuroglia do not
multiply to such an extent, and that the corpuscular elements
and granule cells are less abundant in simple than inflammatory
softening.

§ 499. Morbid Physiology.— -The symptoms of simple soften-
ing are caused by the gradual destruction of the nerve elements
without previous irritation. Softening is probably in all cases
caused by disease of the vessels, thrombosis, and embolism.

§ 500. The diagnosis must rest mainly on the absence of
all symptoms of sensory and motor irritation during the entire
course of the affection. The prognosis of the affection is de-
cidedly unfavourable when the centres of softening are at all
extensive.

SPINAL COED AND MEDULLA OBLONGATA. 309

, ft 501 The treatment must be carried on according to the
rules laid down for the chronic forms of myelitis. Brown-
Sequard recommends, besides iron and quinine iodide of
potassium in a bitter infusion, and strychnine used with th
greatest caution, while he avoids ergot and belladonna. He
also thinks that the cold douche or shower bath to the bacK
is indicated, and maintenance of the dorsal position The food
should be abundant and nourishing, and when possible moderate
exercise should be taken. The use of the galvanic current will
be found advantageous.

310

CHAPTER VI.

Ill— VASCULAR DISEASES OF THE SPINAL CORD AND
MEDULLA OBLONGATA.

(I.) ANiEMIA, THROMBOSIS, AND EMBOLISM OF THE SPINAL
CORD AND MEDULLA OBLONGATA.

1. Ancemia of the Cord.

§ 502. Ansemia of the spinal cord consists of a diminution
in the amount of blood contained in it. This condition may
be due to causes special to the cord itself, and then it is
called spinal isehmmia; or to general causes, such as oligsemia
and hyrdsemia, and then it is called dyscrasic spinal anaemia
(Jaccoud).

§ 503. Etiology. — The predisposing causes of spinal ansemia
are congenital narrowness of the calibre of the vessels, weakness
of the heart, and undue excitability of the vaso-motor nerves.
The female sex is strongly predisposed to spinal ansemia.
Diseases of the vessels of the cord, such as atheroma or the
fibrosis which accompanies Bright's disease, also produce spinal
anaemia. The exciting causes of the affection are arrested or
diminished circulation, as may be produced by compression,
thrombosis, or embolism of the abdominal aorta above the
point of origin of the lumbar arteries.

Owing to the numerous anastomoses of the spinal arteries,
thrombosis and embolism of one or more of them only lead
to circumscribed ischsemia. It is probable that a considerable
number of the so-called reflex paralyses are caused by a reflex
spasm of the spinal arteries, and direct irritation of the vaso-
motor conducting paths in the cord may likewise produce spasm
of these vessels.

VASCULAR DISEASES OF THE SPINAL CORD.

311

I The cases of spinal anaemia which arise from general causes
Ihave been described by Jaccoud under the name of parapUgies
myscrasiques.

Spinal paralysis occurs only rarely in dyscrasic anaemia of
the cord, but paraplegia has been known to follow great losses
of blood, as in parturition, menorrhagia, and haemorrhage from
the kidneys and intestines ; and weakness of the lower ex-
tremities is a not unfrequent symptom of chlorosis and severe
acute diseases.

§ 504. Symptoms. — It has been proved experimentally in
animals that, when the aorta is compressed, motor and sensory
paralysis of the lower extremities immediately occurs, the reflex
acts cease, and the bladder and rectum are paralysed. When
the circulation is restored, improvement in the symptoms is
slow in proportion to the duration of the compression. The
same symptoms occur in man after embolism of the aorta.
Gull observed paralysis to occur in a few minutes from embolism
of the abdominal aorta in a case of aneurism. If the con-
traction of the aorta occurs gradually, the symptoms develop
gradually, and are less severe in nature. They consist of a
feeling of numbness and weakness of the lower extremities,
which become easily fatigued on slight exertion. Nothing is
known of the symptoms caused by ischaemia of the cervical
region of the cord.

Vaso- motor ischaemia or anaemia from reflex irritation is
characterised by the same kind of symptoms as those caused
by aortic obstruction, although they are much less severe in the
former than in the latter. In vaso-motor ischaemia some source
of peripheral irritation can be discovered, and the paralytic
symptoms generally disappear if the source of irritation can be
removed. The intensity of the paralytic symptoms is said to
vary in degree according to the severity of the peripheral
irritation.

In the spinal anaemia produced by general causes, motor
weakness, tremor on the slightest exertion, and in some cases
complete paralysis are the most . constant symptoms. These
symptoms begin in the lower extremities, and extend to the
trunk and arms. The sensibility is usually intact, but paraes-

312

VASCULAR DISEASES OF THE

thesiae, pain, hyperesthesia, and even slight anaesthesia may
occasionally be present. The reflex actions are often exaggerated,
and the sphincters are not, as a rule, affected. It is said that
the symptoms improve on lying down, and, on the contrary,
are made worse when the patient assumes the erect posture.
The paralytic symptoms are associated with the usual signs of
general anaemia or of chlorosis.

§ 505. Course, Duration, and Termination. — The disease
may begin suddenly when it is caused by severe haemorrhage or
embolism, but the onset is more gradual when it results from
thrombosis and chlorosis. The patient often recovers rapidly
by the establishment of collateral circulation. At other times
recovery is slow and gradual, and in cases of embolism the cord
may undergo softening, so that recovery becomes impossible.

§ 506. Pathological Anatomy. — Anaemic portions of the
cord look pale and bloodless. The grey substance is dull in
colour, and sinks below the level of section ; while the white is
soft, and protrudes slightly above the surface of the section.
The membranes are pale, and their vessels are empty. The
anaemic portions contrast strongly in colour and consistence with
those which are healthy. In thrombosis and embolism of the
small spinal vessels it is often possible to find the point of
occlusion. Ked softening exists in the region supplied by the
plugged artery and collateral fluxion in its vicinity. If the
ischaemia be protracted, white and yellow softening of the cor-
responding portion of the cord may occur.

§ 507. Diagnosis. — The diagnosis must rest mainly on the
concomitant symptoms. The symptoms of the acute ischaemic
form resemble those due to spinal haemorrhage, and anaemia
can only be inferred to be the cause when the aorta is known to
be obstructed or a great loss of blood has recently occurred.

The chronic forms of spinal anaemia resemble chronic myelitis
or chronic meningitis, but when severe general anaemia exists
it may be inferred that the disease is caused by it. The fact
that the horizontal position relieves the symptoms may afford
valuable aid in forming a diagnosis (Hammond).

SPINAL CORD AND MEDULLA OBLONGATA.

313

8 508. Prognosis. — Spinal anaemia is not a serious disease
taken in itself, but in some of the severer cases softening may
occur, and then the prognosis becomes unfavourable.

§ 509. Treatment — The causes of anaemia of the cord must
first be removed. This must be done by a tonic and stimu-
lating treatment.

The patient should be laid on his back with his head and
legs raised, and this position should be maintained in the night
and for a considerable portion of the day.

Special stimulants of the cord itself may be administered,
the most powerful and reliable of them being strychnine. The
constant current should be applied daily to the vertebral column,
especially in the form of the ascending stabile current. Warm
applications should be made to the back, such as hot sand bags,
or Chapman's spinal bags filled with hot water.

The diet should be generous and moderately stimulating.

2. Ancemia of the Medulla Oblongata — Thrombosis and
Embolism — Necrotic Softening.

§ 510. — Anaemia of the medulla oblongata is generally accom-
panied by anaemia of the brain and spinal cord. Some of the
symptoms, however, which occur in general anaemia are probably
caused by anaemia of the medulla oblongata.

Thrombosis and embolism of the vessels supplying the me-
dulla are not very rare, and the anaemia in such cases is so great
that, unless the circulation be quickly restored, the part soon
undergoes softening.

Thrombi and emboli generally occur in the vertebral and
basilar arteries (§§ 353, 354). This subject has received much
attention in recent years, and in consequence cases which were
at one time classed together as apoplectic bulbar paralysis are
now known to have been produced by embolism or thrombosis
of the arteries of the medulla oblongata.

§ 511. Symptoms. — The symptoms of simple anaemia of the
medulla do not require to be separately considered, as they are
merged in the symptoms of anaemia of the cord.

314

VASCULAK DISEASES OF THE

The symptoms produced by obstruction of the arteries differ
according as the main arteries or the small branches are affected.

The following general symptoms are commonly observed
when one or both vertebral arteries, or the basilar artery, are
obstructed by thrombosis or embolism. A more or less complete
bulbar paralysis occurs suddenly or in a very short time, and
without loss of consciousness. The soft palate and tongue are
paralysed, the power of articulation and of deglutition is lost,
and there is partial paralysis of the muscles supplied by the in-
ferior portion of the facial nerve. These symptoms are some-
times accompanied by paralysis of the ocular and masticatory
muscles, dulness of hearing, and noises in the ears. Respiratory,
circulatory, and vocal disorders are also of frequent occurrence.
Paralysis of one or all of the extremities is simultaneously
developed. As a rule, a certain degree of anaesthesia is
present.

If death from respiratory paralysis does not at once ensue,
the disease is not of a progressive character, and at most only
a slight change for the worse takes place during the first few
days.

In some cases gradual improvement may take place, the
paralysis partially disappears, the muscles of the extremities
undergo various degrees of contracture, and the tendon reflexes
are exaggerated, but life may be preserved for a comparatively
long period.

§ 512. Varieties.

(1) Obstruction of the basilar artery, as a rule, produces bilateral symp-
toms, paralysis of all four extremities, and of both sides of the face. But the
most important symptom is the cessation of the functions of the vagus and
glosso-pharyngeal nuclei, causing severe respiratory disorders, dyspnoea,
cyanosis, and usually a rapid death from asphyxia. A rapid and complete
obstruction of the basilar artery generally produces profound coma and rapid
death. If life last for a few hours complete paralysis of all four extremities
is observed.

(2) If the obstruction extend only to a small portion of the basilar, or if
the thrombosis be merely attached to the walls of the vessel and only cut
off the blood from a few branches, the symptoms are often less threatening.
Individual cranial nerves are paralysed, and there is weakness or paralysis
of the extremities ; some of the ocular muscles may be paralysed, as well
as those supplied by the facial and trigeminal nerves. If, however, the

SPINAL CORD AND MEDULLA OBLONGATA. 315

Circulation continue in the posterior portion of the basilar artery and in
She vertebral arteries, respiration is not arrested.

(3) Simultaneous obstruction of both vertebral arteries produces exactly
Ahe same effects as thrombosis of the basilar artery. The life of the patient
lis not in such immediate danger if the thrombosis be slowly developed so
las to allow time for collateral circulation to be established. Joffroy
|attaches some importance to the lockjaw which has been observed in such
leases.

(4) Obliteration of one vertebral artery produces symptoms which assume
■ to some extent the hemiplegic form. The lesion is more frequent in the

I left artery, from which the anterior spinal artery is often exclusively or in

II great part given off. The inferior cerebellar artery is also obstructed.

The hemiplegia may either be on the same side as the lesion or on the
' opposite side, a matter that depends on variable conditions, such as the
: situation of the obstruction, the point of origin of the anterior spinal
artery, the completeness of the decussation of the anterior pyramids, and
other circumstances. The hypoglossal and spinal accessory nerves may be
paralysed, causing disorders of articulation and deglutition and aphonia,
and in addition there may be paralysis of the inferior branches of the facial,
and partial paralysis and ansesthesia of the soft palate. These symptoms
may be to some extent bilateral, but are generally more pronounced on one
side of the body.

The successive occlusion of the different arterial territories may be
recognised by the grouping of the symptoms and the order in which they
follow one another.

The larger the vessel obstructed, and the more complete the occlusion,
the quicker does death ensue. If the circulation can be quickly restored
by the disintegration or displacement of the thrombus or embolus, or by
sufficient collateral branches, improvement in the symptoms and partial
recovery may take place.

(5) Occlusion of the small arteries of the medulla oblongata can
never be diagnosed with certainty from the symptoms. But as these
vessels are terminal their obliteration is surely followed by necrosis of
the parts affected, and it only depends on the territory of such artery
whether we get symptoms or not. Obstruction of the smaller vessels
may produce partial paralysis of the tongue, difficulties of articulation and
swallowing, unilateral paralysis of the facial and abducens nerves, respira-
tory disorders, and perhaps even fits of asthma.

(6) Obstruction of the superior cerebellar artery produces paralysis of the
third nerve on the side of the occluded vessel and hemiplegia of the
opposite side.

§ 513. Morbid Anatomy. — Either one or both vertebral
arteries may be completely obliterated, and the thrombosis may-
extend from them into the basilar artery. The basilar artery

316

VASCULAR DISEASES OF THE

may be obstructed, either from one end to the other or for a
short distance in its anterior, median, or posterior division, and
any one or all of the branches given off from the main arteries
may be partially or wholly obstructed by thrombosis.

Most of the arteries of the medulla oblongata are terminal
arteries, hence obstruction of one of them always occasions
grave disorders of nutrition. The immediate result is to pro-
duce intense ansemia in the vascular territory affected. The
second stage consists of engorgement, accompanied by effusion of
blood (hsemorrhagic infarct), which leads to red and afterwards
yellow and white softening. The final stage often consists in
the formation of a cavity of variable size in the medulla. The
walls of the cavity are formed of a soft reticular connective
tissue, while delicate threads of the same traverse the interior.

If the obstruction take place in one of the smaller vessels, a
number of small wedge-shaped centres of softening or hsemor-
rhagic infarcts are found, having their apices directed forwards
and their bases towards the floor of the fourth ventricle.

§514. Diagnosis. — When a bulbar paralysis, accompanied
either by hemiplegia or paraplegia of the extremities, occurs
suddenly, our attention should at once be directed to the pons
and medulla oblongata. In fulminant and extremely rapid
cases, when the patient sinks into deep coma and universal
paralysis sets in with threatening asphyxia, we can only make
a guess with regard to the nature and situation of the lesion.

Even when it is possible to determine that the lesion has
occurred in. the medulla oblongata, it is not always easy to
decide whether a hsemorrhage or an embolus has taken place,
and the question must be determined from general considera-
tions. When the symptoms come on, one after another and
not all at once, obstruction of a vessel must be presumed.
Epileptoid convulsions are more frequent in hsemorrhage
than in embolus and thrombosis. It is only when the basilar
is completely occluded that we meet with a severe apoplectic
attack.

The symptoms of embolism are often of a definite character,
owing to the regular distribution of the vessels; whilst those of
apoplexy are more dependent on chance, so that we meet with

SPINAL CORD AND MEDULLA OBLONGATA.

317

ia repetition of exactly the same group of symptoms more
frequently in cases of embolus than we do in extravasation.

Striking and rapid improvement, with total disappearance of
complete groups of paralytic symptoms, seldom occurs in cases
of hcemorrhage. The frequent anomalous distribution of the
vessels often renders it impossible to diagnose the particular
artery which has been obstructed. Other symptoms may help
us to a diagnosis. An unusually full pulse in the carotids is
said to point to obstruction of the basilar artery.

§ 515. Prognosis. — The prognosis is always of the gravest
character, and sudden and complete obstruction of the basilar or
of both vertebral arteries is almost invariably fatal. A slowly-
developing occlusion of one or more of the large vessels in this
region also terminates in death within a short period. Life
may be prolonged and partial recovery take place in cases of
relatively limited obstruction which happen to affect the least
dangerous parts of the medulla, or when a considerable collateral
circulation is established.

§ 516. Treatment — Stimulants and tonics are plainly in-
dicated when one of the bulbar arteries are obstructed ; but
unfortunately the diagnosis is so uncertain in many cases that
it is difficult to follow out any definite course of treatment.
At a later period electricity may be applied with the greatest
hope of success.

IH.) HYPEREMIA AND HEMORRHAGE OF THE SPINAL CORD
AND MEDULLA OBLONGATA.

1. Hypercemia of the Spinal Cord and its Membranes.

§ 517. It is impossible to separate hyperemia of the spinal
cord and of the spinal membranes, either clinically or anato-
mically, hence the two must be considered together. By hyper-
emia of the cord and its membranes, therefore, is understood
an increased supply of blood in the structures contained within
the vertebral canal.

§ 518. Etiology. — Hyperemia of the cord is produced by
excessive functional activity, such as occurs in severe exertion

318 VASCULAR DISEASES OF THE

or violent sexual excitement. Congestion is also present in the
early stages of inflammation of the cord, so that all the causes
of myelitis are likewise causes of hyperaemia of the cord. *
Hy perse mia of the spinal cord may also be caused by various i1
toxic agents, such as strychnia, carbonic oxide, and alcoholic
excess. Exposure to cold is probably the most common cause i1
of spinal hyperaemia, but it may be produced by the suppression b
of accustomed discharges, and by concussion and traumatic c<
injuries of the vertebral column, while it is a frequent sequel of f
the specific fevers and malarial infection.

Passive hyperaemia is generally caused by the conditions i;
which favour general venous congestion or stasis, such as i i
diseases of the heart and lungs, or diseases like tetanus and i
eclampsia.

§ 519. Symptoms. — The most prominent symptoms of spinal
hyperaemia are pains in the loins and along the spine of a dull, , :
oppressive character, which are not increased on pressure. The ■ •
patient complains of tingling, formication, and tearing pains in .9:
the lower extremities, and a slight degree of hyperaesthesia of il;
the skin, a girdle sensation, and a moderate increase of reflex M
activity may be present. The motor symptoms consist offBi
transitory jerking of the muscles and trembling of the limbs, lH
and Rosenthal says that the electrical excitability is increased. .1

Depressive symptoms may likewise appear at an early period il
of the disease. A sensation of numbness is felt in the lower :\m
extremities and there may be also a slight degree of anaesthesia. .9

The patient complains of fatigue on slight exertion, the limbs >tl
feel heavy and feeble, but it is probable that complete para--|«
plegia never occurs in simple hyperaemia.

Paresis of the bladder is rare, but has been occasionally met:i A
with, and Hammond has observed erection of the penis.

The symptoms are almost always bilateral and are limited to) J
the lower half of the body, or at least they begin in the lower r| >vi
extremities. Occasionally the affection may extend to the upper rl
extremities, and in those cases the respiration is said to have?' °4
been disturbed.

Brown-Sequard says that the symptoms are aggravated by 1
lying on the back, with the head and legs raised, while they

SPINAL CORD AND MEDULLA OBLONGATA. 319

are relieved by lying on the face or by standing or walking,
and the patients are also said to feel worse in the morning
while in bed. When serous effusion has taken place, it collects
in the lower part of the spinal canal on the patient assuming
the erect posture, and consequently the patients are then better
in the horizontal position. There is no fever, and the pulse may
be either quick or slow if the hyperemia extend to the spinal
centres of cardiac innervation. The general health suffers to a
! greater or lesser degree.

It is very difficult to distinguish between active and passive
hyperemia, but if the irritative phenomena predominate, it
may be presumed that the case is one of active hyperemia ;
and if depressive symptoms predominate, that it is one of
passive hyperemia.

§ 520. Course. — The development is at times sudden, and
then the disease runs through an acute course, and is soon
terminated. At other times the course of the affection is slow ;
it gradually increases in severity, and then continues for days,
weeks, or months, with varying degrees of intensity. The disease
generally ends in recovery, but relapses are not rare. Recovery
is often favoured by critical haemorrhages. It is probable that
simple hyperemia never ends fatally.

§ 521. Diagnosis. — The diagnosis of hyperemia of the struc-
tures within the spinal canal is based on the slight and transi-
tory nature of the sensory and motor disturbances, and upon
the frequent and rapid changes in the symptoms, the absence
of increase of temperature, the short and favourable course of
the symptoms, and the success of treatment calculated to relieve
congestion.

Concussion of the cord may be distinguished from hyperemia
by the history of an injury.

In spinal meningitis the prominent symptoms are spasm of
the back and neck, pain on moving the limbs, and high fever —
symptoms which are absent in simple hypersemia.

Acute myelitis may be recognised by the presence of fever,
severe paralytic symptoms, contractures, paralysis of the
bladder, and bed-sores.

320

VASCULAR DISEASES OF THE

Spinal apoplexy begins suddenly, the paralytic symptoms
are severe, and more or less lasting.

Spinal anwmia is distinguished from hyperaemia by the fact
that lying on the back gives relief to the symptoms of the
former, while they aggravate those of the latter.

§ 522. Prognosis. — The prognosis is on the whole favourable;
but the affection, if unchecked, is liable to cause haemorrhage
or inflammation of the cord, and then the prognosis becomes
serious.

§ 523. Morbid Anatomy. — After death the arteries con-
tract and empty their contents into the veins, so that even when
active hyperaemia has existed during life it may occasion no cha- ■
racteristic appearances after death; while, on the other hand, .
vessels may become much congested in consequence of a pro- •
longed death struggle, or of hypostatic congestion after death. .
In active hyperaemia the grey substance often appears of a rose
or scarlet colour, and the white substance of a reddish tinge, .
the blood-vessels are tortuous and congested, and on microscopic :
examination the smaller arteries and capillaries are seen to be:
enlarged and unusually distended with blood. In severe cases*
punctiform extravasations and ecchymoses may be seen dotted
over the membranes, and in the substance of the cord. The.
spinal fluid is usually increased in quantity, and is of a muddy
or reddish colour (Erb).

In passive hyperaemia the extra-meningeal plexuses of veins
are especially distended with blood ; the individual veins ar
enlarged and tortuous, and the whole cord presents a dar
blue colour. The spinal fluid is almost always increased, an
ecchymoses may also be present.

In chronic and frequently-repeated hyperaemia the pia mate
and arachnoid are thickened and opaque, and highly pigmented

§ 524. Treatment. — The most favourable cases of activ
hyperaemia are those which arise from the suppression of a
habitual discharge or from exposure to cold. The patient
should be directed to lie on the side or face, with the extremitie
as low as possible. Venesection may be practised in robus

SPINAL CORD AND MEDULLA OBLONGATA.

321

persons when the symptoms are violent, but as a rule it is
preferable to draw blood by leeching. The leeches may be
ipplied to the region of the spinal column, anus, vagina, or
:ervic uteri, according to the nature of the case.

I have seen an aggravated case of spinal hypersemia recover
in a few days under the care of my colleague, Dr. Simpson.
The treatment consisted in the application of Chapman's ice-
bags to the spine, while the patient was ordered to lie with
his face directed downwards. The application of cold affusions
and douches, cold packing, and sea baths may take the place of
the ice-bag.

A saline purgative may be of use by unloading the vessels
and lowering arterial tension. Ergotin and belladonna are the
favourite internal remedies, but it is very doubtful how far they
are of use.

The diet should be plain and nourishing, but unstimulating,
and everything which might increase the hypersemia, such as
sexual and alcoholic indulgence, must be avoided.

2. Hcemorrhage into the Substance of the Spinal Cord.

Hcematomyelia—Sjrinal Apoplexy.

§ 525. Definition. — Spinal apoplexy consists of haemorrhage
into the substance of the cord.

§ 52G. Etiology. — Contrary to what occurs in cerebral disease,
spinal apoplexy is more common in youth and middle age than
in old age. Men are more subject to the affection than women.
Chronic affections of the cord are often brought to a sudden
close by haemorrhage, owing doubtless to coincident changes
occurring in the walls of the vessels. Amongst the exciting
causes are traumatic injuries, active congestion of the cord, and
anything that produces a want of equilibrium between the
pressure within and without the blood-vessels. It is doubtful
how far excessive cardiac action in the absence of degeneration
of the vessels can give rise to haemorrhage. Haemorrhage may
occur in connection with tumours, or any morbid process which
occasions softening of the substance of the cord.

§ 527. Symptoms. — The attack generally begins suddenly
v

322

VASCULAR DISEASES OF THE

with fulminant symptoms. The patient complains of violent
pains, and becomes suddenly paraplegic, but without loss of
consciousness. The disease may be preceded by premonitory
symptoms, consisting either of those indicative of spinal conges-
tion or of the symptoms which precede acute central myelitis,
and these may last from a few hours or several days. But
even in the cases in which the affection is preceded by pre-
monitory symptoms, the onset of the characteristic symptoms
is always sudden, and complete paraplegia develops in the
course of a few minutes, or at most an hour. During the
development of the paralysis the patient complains of violent
pain, either localised or extending over the entire spinal column,
but usually disappearing when the paralysis has become com-
plete. When the cervical region is implicated, the paraplegia
extends to the upper extremities, the respiratory muscles are
, affected, and the patient breathes laboriously by the aid of the
diaphragm.

The paralysed muscles are flaccid, and more or less complete
ansesthesia of every form of cutaneous sensibility having the
same distribution as the motor paralysis is present. Paralysis
of the rectum and bladder occurs ; at first there is retention of
urine and afterwards various degrees of incontinence.

Vaso-motor disturbances are generally present. Levier found
the temperature of the paralysed extremities, as compared with
that of the axilla, increased from 0*2° to 2°0 C.

The reflex actions vary much according to the seat of the
lesion. When the grey matter is infiltrated down to its lowest
point, they are completely abolished. When the seat of the
haemorrhage is higher up, reflex actions disappear for a short
time, owing to the shock ; but they may afterwards reappear in
an exaggerated form. In most cases, however, the reflex actions
disappear after a time. Priapism is mentioned as a symptom
in a few cases. The paralysed muscles undergo atrophy, they
lose their faradic excitability, and manifest the reaction of
degeneration. At a later period, when secondary changes
occur in the cord, a few of the muscles may become rigid and
contracted. The symptoms of secondary myelitis may be super-
added and give rise to violent pains, twitching movements and
jerkings of the extremities, and the formation of contractures.

SPINAL CORD AND MEDULLA OBLONGATA.

323

Throughout the whole course of the disease symptoms of
motor irritation are almost entirely absent. During the first
moments of the haemorrhage slight muscular twitching and
partial spasms may occur, but these phenomena soon give
place to paralysis. Spasmodic symptoms may also occur at a
later period, but they are caused by secondary degeneration.
Tingling and other paresthesia? may occasionally be felt in the
paralysed parts, but, as a rule, these symptoms are wholly
absent, and the patients do not feel their limbs.

After a few days or weeks, according to the severity of the
case, gangrenous bed-sores appear on the sacrum, trochanters,
heels, and other places exposed to pressure. Paralysis of the
bladder leads to alkalescence of the urine, cystitis, pyelitis, and
their sequelae, and the patient dies in a state of great marasmus.
" The symptoms, of course, vary greatly according to the
cause, extent, and situation of the haemorrhage. In small
haemorrhages the symptoms are so destitute of any dis-
tinguishing features as to render the diagnosis a matter of
great uncertainty. When the haemorrhage is limited to the
anterior cornua, the symptoms produced will be mainly those
of local paralysis ; while if it be limited to the posterior cornua,
the symptoms will be extremely indefinite.

If the lumbar region of the cord be affected, the symptoms
of paralysis and anaesthesia are restricted to the lower extremi-
ties, bladder, and rectum; reflex actions are absent, and rapid
atrophy of the muscles and bed-sores occur at an early period
of the disease.

If the dorsal region be affected, the paralysis extends higher
up. The expiratory muscles and those which compress the
abdomen are paralysed, but reflex actions may be retained for
a long time, and atrophy of the muscles is slow.

If the cervical region be implicated, all the four extremities
are affected, a portion of the inspiratory muscles are paralysed,
oculo-pupillary symptoms may be present, and the implication
of the reflex processes and nutrition depend on the downward
progress of the lesion. If the haemorrhage occur above the
origin of the phrenic nerve, rapid death by asphyxia is inevitable.
In a few cases the haemorrhage has been found limited to one
half of the cord.

324

VASCULAR DISEASES OF THE

§ 528. Course, Duration, and Termination. — The course
depends on the cause of the disease and the extent and locality
of the haemorrhage. In severe cases of diffuse central bleeding
a fatal termination occurs soon through paralysis of respiration,
or death results from acute bed-sores, pyaemia, and septicaemia.
If the haemorrhage be small the case may be very protracted,
but death ultimately results from bed-sores, cystitis, fever,
marasmus, and other complications.

The lesion in the cord sometimes cicatrises, and partial
recovery occurs even after cystitis and bed-sores have made
their appearance ; but in these cases some muscles or group of
muscles usually remain paralysed and atrophied. Complete
recovery is only possible when the clot is small.

The duration of the disease varies greatly. Rapid cases
terminate in a few minutes, hours, or days ; while in less severe
ones, weeks, months, or even years may elapse before death
occurs.

§ 529. Morbid Anatomy. — The bleeding is generally limited
to the grey substance, and may involve the cornua or the entire
grey substance, and may extend to various distances longitu-
dinally. Two kinds of extravasation may occur : the haemor-
rhagic or apoplectic clot, and the haemorrhagic infiltration or
softening.

The hemorrhagic or apoplectic clot varies in size from that
of a pea to that of a hazel-nut, and its longitudinal is generally
longer than its transverse diameter. The clot is often seen
through the pia mater as a bluish nodule, while the pia is
sometimes ruptured, so that blood makes its way into the
subarachnoidal space. The clot is surrounded by ragged walls
formed by disintegrated nerve tissue. The haemorrhage may
pass for a considerable distance between the bundles of white
fibres, and a large portion of the grey substance may be de-
stroyed, giving rise to what is called a " tubular haemorrhage."
The portions of the cord most usually affected are the cervical
and upper dorsal regions.

The clot after a time undergoes a series of further changes.
It either slowly dries up to a crumbly, caseous mass of a dark
colour, containing crystals of haematoidin, or undergoes a pro-

SPINAL CORD AND MEDULLA OBLONGATA.

325

cess of softening, with subsequent absorption, so that at last a
capsule of connective tissue is left, filled only with a serous
fluid. When the extravasation is small it may be absorbed, so
as to leave only a small cicatrix of connective tissue.

Secondary disease of the cord is very often found in the
neighbourhood of the clot. This generally consists of softening,
which extends to a variable distance both upwards and down-
wards. The grey matter often undergoes haemorrhagic softening,
and is sometimes converted into a softened mass of a reddish
black or chocolate colour, while white softening may be observed
in the neighbourhood of the clot. In old-standing cases secondary
ascending and descending sclerosis occurs.

Hemorrhagic infiltration or softening occurs in the grey
substance exclusively. It is limited to one or more of the grey
horns, or extends over the whole of the grey matter, but rarely
spreads to the white substance. It may extend longitudinally
a few centimetres only, or the whole length of the cord. The
grey substance is changed into a reddish-brown mass dotted
with dark red points. The microscope shows elements like
those in the clot, but with the addition of granular corpuscles
and degenerative changes in the nerve fibres and ganglion cells.

The usual evidences of acute central myelitis may be observed
far beyond the limits of the haemorrhagic infiltration.

§ 530. Diagnosis. — The diagnosis is chiefly based on the
sudden and very rapid invasion of paraplegia without much
irritation, and the immediate severity of the symptoms. It is
distinguished from cerebral apoplexy by the retention of con-
sciousness, the absence of all symptoms of paralysis of cerebral
nerves, the paraplegic form assumed by the paralysis, and by
the presence of paralysis of the sphincters.

In meningeal haemorrhage there are active symptoms of irrita-
tion, hyperesthesia and pain, violent spasms, while paralysis is
less prominent, the disturbances of sensibility are slight, and
the course of the attack is rapid and comparatively favourable.

Acute central myelitis is very similar in its symptoms to
spinal apoplexy. In myelitis the paraplegia requires hours or
days for development. It begins with symptoms of irritation,
such as pain and slight spasm, the vertebral column is sensitive

326 VASCULAR DISEASES OF THE

to pressure, fever may be present, and anaesthesia and par.
aesthesiae are prominent symptoms, while partial paralysis and
weakness of the bladder precedes the occurrence of severe
paraplegia. The ascending progress of central myelitis mav
hL^^f Stati°nary nature of the symptoms in

Poliomyelitis anterior acuta in adults is often like haemato
myelia. It may be distinguished by the presence of fever at
the commencement, the absence of sensory disturbances, and of
palsy of the bladder and bed-sores.

The isehcemic paraplegia caused by embolism of the aorta
can alone be mistaken for haemorrhage, and this accident may be
recognised by absence of the femoral pulse and other attendant
symptoms.

§ 531 Prognosis.-The prognosis is always grave. Large
central haemorrhages and those which are seated at a hie* level
are necessarily fatal. The prognosis becomes more hopeful if the
nrst tew days and weeks pass without bringing severe compli-
cations, but complete recovery is rarely to be expected. Small
circumscribed haemorrhages are less dangerous, but it is rare
tnat the diagnosis of such cases amounts to anything like
certainty.

§ 532. Treatment. ~ Prophylactic treatment should be
adopted, such as removing retained or suppressed menses, or
alleviating heart disease and congestion of the cord When
the symptoms are related to a central myelitis, a very active
antiphlogistic treatment should be adopted. Chapman's ice-
bag should be applied to the back, but after the acute stage
is over a more stimulating treatment may be adopted. For
the haemorrhage itself little can be done beyond relieving the
congestion of the cord by the employment of local bleedino-
tree application of ice, and maintenance of the horizontal
position upon the side or abdomen, with the- internal use of
digitalis or ergot, purgatives, and application of warmth to the
extremities.

Trophic disturbances, cystitis, and bed-sores must be sub-
jected to the usual treatment. If the first weeks pass without

SPINAL CORD AND MEDULLA OBLONGATA.

327

serious results, iodide of potassium may be administered to
promote absorption. Warm spring and brine baths, or a
moderate hydropathic treatment, and the constant current may
all be occasionally of use.

3. Hyperemia and Haemorrhage of the Medulla Oblongata.

§ 533. Hyperaernia strictly limited to the medulla must be
an extremely rare occurrence, and in the majority of cases it is
nothing more than part of a general hyperaernia of the brain or
spinal cord.

§ 534. Haemorrhage of the medulla is more closely related
to the vascular diseases of the brain than to those of the cord,
and the frequency of the occurrence of haemorrhage is greater in
the cerebral than in the spinal end of the medulla. Kupture
of a vessel is on the whole a rare occurrence in the pons and
medulla oblongata. The pathology of haemorrhage of the
medulla is the same generally as that of haemorrhage of the
cord. Disease of the vessels, such as miliary aneurisms,
atheroma, fatty degeneration, and capillary dilatation resulting
from processes of softening, is the most important con-
dition which leads to the production of haemorrhage. Cases
of atheroma and aneurism of the basilar artery are often
accompanied by haemorrhage from the smaller branches in the
medulla and pons. Bright's disease is a very important cause
of haemorrhage into the medulla. Caries of the cervical ver-
tebrae, purulent basilar meningitis, and tumours in or around
the medulla predispose to haemorrhages by impairing the nutri-
tion of the walls of the vessels.

Haemorrhage is also produced traumatically through injuries
to the skull and back of the neck. Westphal produced capillary
haemorrhage in the medulla of the guinea-pig by light blows of a
hammer on the head. In extensive cerebral haemorrhage, which
breaks through into the ventricles, the fourth ventricle often
becomes filled with blood through the aqueduct of Sylvius.

§ 535. Symptoms. — Very little is known of the symptoms of
active hyperaernia in the medulla, but it is probable that some
of the symptoms of general cerebral hyperaernia are due to

328

VASCULAR DISEASES OF THE

congestion of the medulla. These symptoms are dyspnoea, slow
pulse, vomiting, general convulsions, and certain defects of
speech. Certain initial symptoms of acute bulbar disease, such
as pains in the head and back of the neck, spasms in the face
and tongue, and formication in the region supplied by the fifth,
are probably caused by congestion of the medulla oblongata.

Haemorrhage into the medulla, even of limited extent, is
always exceedingly dangerous. It commences generally with
the most alarming symptoms, and not unfrequently causes
instant death. In these cases the patients fall down with
a cry or in epileptiform convulsions, and die instantaneously.
Large effusions of blood into the hemispheres and basal
ganglia sometimes reach the fourth ventricle ; they irritate and
oppress the medulla, quickly producing death, preceded by
vomiting, convulsions, coma, and general paralysis.

Slight haemorrhage into the medulla generally produces
symptoms of an alarming and very threatening nature, and
these are more grave the nearer the effusion is to the respira-
tory centre, for when the latter is affected instant death
ensues. In cases which survive a longer time the patients utter
a loud cry, or are attacked by buzzing in the ears, dizziness,
sudden headache, vomiting, or convulsive spasm of the body,
followed by coma. Epileptiform convulsions have been observed
amongst the initial symptoms of haemorrhage into the medulla
and pons.

The motor paralysis varies greatly in extent, sometimes
attacking the lower extremities only, sometimes only the upper,
and at other times causing hemiplegia. In most cases all four
extremities are either completely or partially paralysed. Some
of the bulbar nerves are always more or less affected. The
hypoglossal, facial, spinal accessory, and trigeminus are usually
more or less completely paralysed, and sometimes the nerves of
the orbit also. When there is a hemiplegia, the paralysis of
the extremities occupies the side of the body opposite to the
extravasation, while paralysis of the bulbar nerves occurs on the
same side, giving rise to a characteristic hemiplegia altemans.

Paralysis of sensation when present follows the same rule
as that of motion, but is not usually so well developed.
When coma is present, it is impossible to ascertain anything

SPINAL CORD AND MEDULLA OBLONGATA. 329

Ivith respect to the condition of sensation. When the affection
I s unilateral, the sensory disturbances are also crossed ; but owing
|:o the peculiar course of the sensory fibres in the medulla, we
ban hardly expect a sharply-defined anaesthesia.
I Respiratory disturbances are the most important and
characteristic symptoms of the affection. If fatal asphyxia
does not ensue at once, the respiration is impaired, becoming
lirregular, stertorous, often intermittent, and accompanied with
great dyspnoea. The Cheyne-Stokes respiration is frequently
observed; the breathing then becomes more and more em-
barrased till death from asphyxia results. Alterations in the
action of the heart are generally less prominent, but the pulse
is usually frequent, irregular, and intermittent.

Vaso-motor changes have not been often described, but in
the period immediately succeeding the haemorrhage, unilateral
or bilateral rise of temperature of the skin has been noticed.
A considerable rise of temperature occurs during the death
agony, as occurs in other forms of apoplexy.

Disturbances of speech and deglutition and unilateral or
bilateral paralysis of the soft palate result from the parti-
cipation of the bulbar nerves in the paralysis. Deafness
and buzzing of the ears are also frequently observed from
implication of the auditory nerves. Frequently recurring vomit-
ing and a continuous troublesome hiccough have been observed
as symptoms. Potain found polyuria present in one case.
Mader and Desnos found albumen in the urine in a case where
the kidneys proved to be normal at the autopsy.

In cases where life is prolonged the electric reactions remain
normal in the extremities, but there may be loss of faradic
contractility and the reaction of degeneration in the muscles
supplied by the paralysed cranial motor nerves.

§ 536. Course. — The disease is either fatal at once from
paralysis of the respiratory centres, or death does not result
for a few hours or days, but there is general paralysis and
profound unconsciousness ; or life may be maintained for a
considerable time. In the latter case the patient gradually
recovers his consciousness, some of the paralytic and other
symptoms disappear, and nothing remains but hemiplegia or

330

VASCULAR DISEASES OF THE

partial paraplegia, and more or less difficulty in articulation
and deglutition. In such cases contractures are very liable to '
ensue, just as occurs when the pyramidal tract is interrupted in
any other part of its course. Very little is known of the symp-
toms of small capillary haemorrhages in the medulla, but they
are probably similar to those produced by emboli of the nutrient
arteries of the bulb.

§ 537. Morbid Anatomy. — Hyperemia of the medulla is?
characterised by the same anatomical appearances as cerebral \
hyperaemia, and requires no further description. A similar -
remark applies to haemorrhage of the medulla. A clot goes i
through the same changes in the medulla as in the brain, .
and unless it is rapidly fatal it ends in the formation of a i
contracted scar or of a small cyst. Secondary degenerations of
the pyramidal tracts are generally developed. Extravasations
are usually of small size, except when the pons is simul-
taneously affected, and then they may be large ; they are
roundish, resembling an olive or bean, but frequently irregular.
Near the median line we meet with small triangular spots of
haemorrhage, with the apex pointing forward, corresponding to
the territory of a median bulbar artery.

§ 538. Diagnosis. — It is probably impossible to make a
special diagnosis of hyperaemia of the medulla oblongata. Loss
of consciousness, epileptiform convulsions, and sudden death
are sufficiently characteristic symptoms of severe cases of hae-
morrhage into the substance of the medulla. In cases of less
severity the onset may be attended by general epileptiform con-
vulsions, vomiting, hiccough, more or less threatening respiratory
disorders, dysphagia, disorders of speech, paralysis of the tongue
and soft palate, of the inferior branches of the facial and of
the abducens oculi, the presence of albumen and sugar in the
urine, a final rise of temperature, the extension of paralysis
to all four extremities, the unequal degree of paralysis in the
extremities of one side and the face and tongue on the other
side, and the abolition of all reflexes in the regions supplied
by the paralysed bulbar nerves. It may be concluded that the
lesion is limited to the anterior half of the floor of the ventricle

SPINAL CORD AND MEDULLA OBLONGATA.

331

■vhen we see paralysis of the abducens, facial, and trigeminus,
■Jono- with aural disorders and sugar and albumen in the
Birine. Haemorrhage in the posterior portion of the rhomboid
Minus produces paralysis of the hypoglossus, facial, and trige-
Mninus, and of the spinal accessory and vagus, accompanied by
rrave respiratory disorders and usually by paralysed extremities,
md it is a symptom of some importance when these latter
ilternate with paralysis of the tongue. Alternate paralysis of
m upper and lower extremity probably indicates that the lesion
is situated in the centre of the decussation of the pyramids.

§ 539. Prognosis. — The prognosis is very unfavourable, and
when the haemorrhage is of large dimensions the lesion is
invariably fatal. There is only hope in cases of very limited
haemorrhage, or when the localisation is very favourable, espe-
cially when it is far removed from the respiratory centres. The
patient's condition may then improve gradually and partial
recovery take place.

§ 540. Treatment — The rules of treatment are the same
for hyperaemia and haemorrhage as for the same processes in
other parts of the brain. Venesection, combined with active
stimulants, is the most suitable treatment in severe cases
I when respiration is threatened ; the latter must be inj ected
! per rectum, as the patient cannot swallow.

In chronic cases, when paralysis continues and when speech
and deglutition are impaired, a suitable application of electricity
is indicated.

332

CHAPTER VII.

IV.— FUNCTIONAL AND SECONDARY DISEASES OF THE
SPINAL CORD AND MEDULLA OBLONGATA.

(I.) SPINAL IRRITATION.

§ 541. Definition. — This disease generally occurs in the:
female sex, and is characterised by great irritability of the
sensory functions, along with motor weakness.

§ 542. Etiology. — The female sex predisposes to the disease,
although it occasionally occurs in men. The greater number of
cases are met with between the fifteenth and thirtieth years,
and more frequently in neuropathic constitutions.

Everything which weakens the nervous system may act as
an exciting cause, as emotional disturbances, excessive bodily
exertion, severe marches, sexual excesses, bad food, exhausting
diseases, intoxication with alcohol or opium, traumatic agencies,
and exposure to cold.

§ 543. Symptoms. — The disease generally begins with ill-
defined pains in the back, especially between the shoulder-
blades, the patient also complains of excentric pains, increased
nervous irritability, and general loss of power, these symptoms
gradually increasing in severity until the disease is fully
developed. In some cases the development occurs quickly, it
may be in a few days.

When the affection is fully developed the patient complains
of a general feeling of illness, and displays increased mental
irritability. One of the most prominent symptoms is pain in
the back, situated in various spots, most frequently betweeu

FUNCTIONAL DISEASES OF THE SPINAL CORD.

333

.he shoulder-blades, in the back of the neck, and less frequently
m the loins. The pain is aggravated by exertion, and the
vertebral column is exceedingly sensitive to pressure, the
lightest tap over some of the spinous processes calling forth
expressions of pain. Certain spots are found to be very sensi-
tive when a hot sponge or the cathode of a galvanic battery
is passed along the spine. The patient complains of neuralgi-
form pains in various parts of the body. These pains are felt
in the upper extremities, occiput or face, lower extremities,
pelvic region, bladder, genitals, or viscera. Paresthesias, such
us tingling, formication, and feelings of heat or of cold, are
frequently associated with the neuralgiform pains. Actual
anaesthesia is seldom observed. The patient feels weary and
exhausted on slight exertion, and walking soon becomes im-
possible owing to the intolerable pain caused by it. Most
patients soon come to remain on their backs, and even move-
ments of the upper extremities may be avoided owing to the
pain occasioned. Real paralysis does not exist, although in a
few cases a certain amount of paresis may be present.

Spasmodic symptoms in the form of fibrillary twitchings,
spasms of some muscles, choreic movements, and hiccough
are observed. Even permanent contractures and epileptic
attacks are said to arise from spinal irritation.

Vaso-motor disturbances are frequent. Most patients suffer
from coldness of the hands and feet, which are often cyanotic,
and the patients easily turn red or pale, owing to undue irrita-
bility of the vaso-motor nerves.

Functional disturbances of the viscera are generally present.
The most common symptoms are eructations, nausea, vomiting,
palpitations, asthmatic breathing, spasmodic cough, vesical
spasms with increased desire to urinate, and abundant discharge
of pale urine, but actual paralysis of the bladder or rectum
does not occur. Increased mental irritability and depression,
along with sleeplessness, are almost constant symptoms. There
are also noises in the ears, dizziness, and inability to read con-
tinuously owing to the occurrence of muscae volitantes, and
other disturbances of vision.

§ 544. Varieties of Spinal Irritation. — The disease may be

334s FUNCTIONAL AND SECONDARY DISEASES OF

divided into three classes, according as the symptoms point tc
the upper, middle, or lower parts of the cord.

(1) When the cervical portion is affected, the pain and sensitiveness ara
localised in the cervical vertebrae, and the prominent symptoms are ther •
referred to the head. These symptoms are giddiness, sleeplessness, dis
turbances of the special senses, pain in the occiput, and pains in the areeJ
of distribution of the nerves of the brachial plexus. In addition to theseJ
nausea, vomiting, palpitation, and hiccough, and impairment of powei i
in the upper extremities may be complained of.

(2) If the dorsal portion of the cord be affected, the symptoms are locaaj
tenderness of the dorsal portion of the vertebral column, intercostal neuul
ralgia, gastralgia, nausea, dyspepsia, and motor and sensory disturb™
ances in the lower extremities.

(3) When the lumbar portion of the cord is affected, the symptoms arc
neuralgia in the lower extremities and pelvic organs, spasm or paresis oc
the bladder, cold feet, and weakness of the legs.

§ 545. Course, Duration, and Terminations. — The course-
of the disease is usually fluctuating, and relapses occur withoui
apparent cause. Some cases run a comparatively acute course*
but the duration generally extends over a period of months oo
years, and some patients suffer from occasional attacks all theii
lives, although most of them ultimately recover.

Nothing is known with regard to the morbid anatomy cc
spinal irritation. It is probably a functional disturbance of tha
cord, accompanied by alternating conditions of hyperemia and
anaemia.

§ 546. Diagnosis. — Spinal irritation is very difficult to diss
tinguish from bypersemia of the cord. In severe hypergemii
distinct paralysis is rarely absent, and the duration of thh
disease is not as long as that of spinal irritation. Hammona
says that strychnine injected subcutaneously does good in spina
irritation, and harm in hyperemia. Spinal irritation resembkt
in some respects spinal meningitis, but in the latter there an
stiffness and painful tension of the muscles of the back, ana
fever. ,

The first stage of meningeal tumours is very similar to spina
irritation, but in the former only deep pressure on the spinoii
processes is painful, and there is no circumscribed hyperesthesia i
in the vertebral region.

THE SPINAL CORD AND MEDULLA OBLONGATA.

335

It is impossible to diagnosticate spinal irritation from hysteria
1 many cases, and indeed the two affections have been regarded
s identical.

§ 547. Prognosis. — The disease is always chronic and may
ist for months or years, but the prognosis is generally favour-
,ble, and life is never in danger, although a great deal of
uffering is produced.

§ 548. Treatment — The treatment of spinal irritation offers
lifficulties from the great mental irritability and changeable-
less of the patient.

The first endeavour must be to remove the cause of the
liseases when this is possible. The next endeavour must be
:o improve the general nutrition, and to direct special treat-
nent to the spinal cord. A tonic regimen must be adopted,
i full and stimulating diet, as well as moderately free use of
wine or even in some cases brandy or whisky. Active and
passive exercise in the open air must be taken, but fatigue
should be avoided, and the patient should frequently rest in
the recumbent posture. The air of mountains and forests is
useful, as well as a moderate hydropathic treatment.

The most useful remedies in the treatment of the affection
are quinine, iron, zinc, and strychnine. The ascending stabile
[constant current passed through the vertebral column, including
the painful portions between the poles, may be of service. Each
! sitting should be short, and the strength of the current moderate.
The negative pole acting directly on the painful vertebrae has
often done good. Many patients of this class are benefited by
general faradisation and central galvanisation.

Counter-irritants applied directly over the painful portion of
the spine often effect wonders. Various symptoms, such as
neuralgiform pains, require treatment as they arise.

(II.) FUNCTIONAL WEAKNESS OF THE SPINAL CORD.

Neurasthenia Spinalis.

§ 549. Definition. — Neurasthenia spinalis is observed in per-
sons who are subject to the general symptoms grouped under

336

FUNCTIONAL AND SECONDARY DISEASES OF

the popular name of "nervousness," but in it the functions of
the cord are affected in a special degree.

§ 550. Etiology. — The affection generally occurs in neuro-
pathic families, and the male is more liable to be attacked than
the female sex. Youth and middle age suffer most from the
disease, and it is more common in the upper than in the lower
classes. The exciting causes are excessive mental or bodily
exertion, the depressing emotions, and sexual excess.

§ 551. Symptoms. — Patients complain chiefly of great weak-
ness of the lower extremities, accompanied by an intense feeling
of fatigue on slight exertion. A dull feeling of weariness is,
indeed, often felt by the patient in the lower extremities in the
morning before rising. After prolonged exertion this feeling
may be accompanied by occasional tremors of the legs, and a
remarkable stiffness and pain of the muscles of the lower extre-
mities, similar to that produced in a healthy man by prolonged
marching. Symptoms of rapid exhaustion and fatigue may be
observed in the arms also, but never reach the same intensity
as in the legs.

The sensory disturbances consist of pain in the back, which is
aggravated by the movements of the muscles. The pain is not
intense, and varies greatly in its time of occurrence and position.
It is increased or brought on by slight exposure to cold, and by
venereal and other excesses.

A diffused sensation of burning in the skin of the back is
often observed, especially between the shoulder-blades, which is
usually accompanied by sensitiveness of some of the sj)inous
processes, as in spinal irritation. Neuralgiform pains may be
present in the extremities ; they are never of long duration,
but often recur after unusual exertion. The patient also com-
plains of numbness and formication, especially in the lower
extremities, of cold hands and feet, and occasionally there is a
burning feeling in the feet.

The sexual functions are generally more or less interfered
with, there is diminished power of erection and premature
ejaculation, and the act of coition is followed by remarkable
prostration and restlessness of the limbs.

THE SPINAL CORD AND MEDULLA OBLONGATA. 337

There may be a little dribbling of urine, but the functions
)f the bladder are usually normal. The patient is much
roubled with sleeplessness, and feels particularly prostrate in
the morning, he complains of a sense of constriction of the head,
S self-conscious and timid, and manifests a strong tendency to
shed tears. Vertigo is usually absent, and the special senses
and higher mental faculties remain unaffected.

Dyspepsia, along with constipation, flatulence, and palpitation,
is frequently present. The patients are generally hypo-
chondriacal, and live in constant dread of tabes dorsalis, or
some serious affection of the cord. The general nutrition is
generally impaired, the patient loses flesh, acquires a sallow
look, and becomes ansemic. There is always great sensitiveness
to cold and changes of weather.

The objective symptoms are almost entirely negative. The
closest examination reveals no trace of motor disturbances or
want of co-ordination. The sensory disturbances are equally
slight. There is no great sensitiveness of the spinous processes,
the reflex functions of the skin and tendons are normal, there is
no muscular atrophy, and no change in the electrical reactions
of tlue muscles.

§ 552. Course, Duration, and Termination. — The disease
may occasionally begin rapidly, but, as a rule, it develops
gradually and increases in severity for weeks or months, and
then remains more or less stationary. Slight fluctuations in the
intensity of the symptoms are common. Under proper treat-
ment the disease begins to improve, but months or years may
pass before complete recovery occurs, and relapses are common.
Intercurrent febrile affections often appear to influence the
affection favourably. In some cases the patient is compelled to
relinquish business on account of the affection.

§ 553. Morbid Physiology. — The simultaneous occurrence of
sensory and motor disturbances of the legs, and the affections of
the bladder and sexual organs, show that the disease is of spinal
origin, while its favourable course, and the absence of the usual
objective symptoms indicative of organic disease of the cord,
show that it is a functional affection. It is probable that a
w

338

FUNCTIONAL AND SECONDARY DISEASES OF

certain amount of anaemia of the cord exists combined with an
irritable condition of the nervous tissue itself, leading to a ready
discharge of nervous force and subsequent exhaustion. It may •
also be assumed that repair of the exhausted tissues does not
take place promptly and rapidly as in health.

§ 554. Diagnosis— -The diagnosis will be based on the great '
disproportion between the acute subjective complaints of the
patient and the almost negative result of objective examination.!.
The diagnosis becomes clearer when in addition there exists-
general nervous weakness and sleeplessness, and the causes are
present which induce the disease.

This affection might be mistaken for the early stage of tabes;
dorsalis, but in the latter the presence of the lancinating pains s
and other disturbances of sensibility, the girdle sensation, anddj
especially the ataxic symptoms ought to render the diagnosis*,
easy.

Nervous weakness of the cord may be distinguished fromai
active hyperemia by the absence in the former of pain, cuta-a
neous hyperaesthesia, and symptoms of motor irritation. It may*
be distinguished from passive hyperaemia by the absence of t j »
paretic symptoms and by the feeling of heaviness in the legs.

It may be distinguished from incipient myelitis by the?
absence of paraesthesiae and anaesthesia, of paresis or paralysis of|
the limbs and of pronounced weakness of the bladder.

From spinal irritation it may be distinguished by the facti
that in the former the sensory disturbances, as dorsal pains,
neuralgias, and sensitiveness of the spines of the vertebrae, are the?
most prominent symptoms, while fatigue on exertion and sexual! I
weakness are the main symptoms of the latter.

§ 555. Prognosis.-* The patient generally recovers after a.v
time, when the causes of the affection are removed and a suit-'
able treatment adopted. Kelapses are, however, of frequent:
occurrence when the patient remains exposed to the exciting:
causes of the disease.

§ 556. Treatment. — Particular attention must first be directed
to remove the exciting causes of the affection. Great attention1.

THE SPINAL CORD AND MEDULLA OBLONGATA. 330

lust be paid to the regimen and diet of the patient. His
■ork should be light and agreeable, and he should retire to
Mst at an early hour. His food must be nourishing and easily
Bgestible. Alcoholic beverages may be allowed in moderation,
■id open-air exercise, short of fatigue, should be enjoined,
sexual excess must be carefully avoided, although coition need
lot be entirely forbidden.

With regard to the special treatment, a moderate hydropathic
Ireatment has been found useful. Change of air to a mountainous
listrict is also exceedingly useful in promoting recovery,
Switzerland and the Tyrol being very suitable places.

An ascending stabile galvanic current, of moderate intensity,
should be applied to the vertebral column. Iron, quinine, and
strychnine are the most useful internal remedies. Chalybeate
baths are useful for anaemic persons, but patients who are sen-
sitive to cold should at first be sent to the thermal brine baths.
Sea baths are useful in the after-treatment.

Such symptoms as sleeplessness, pain, spermatorrhoea, im-
potence, and digestive disorders must be treated in the
usual way.

(III.) REFLEX AND SECONDARY PARAPLEGIA.

§ 557. It has long been known that paralysis of the lower
extremities is frequently associated with genito-urinary diseases.
These affections were at one time grouped together under the
name of urin ary paraplegice. Bro wn-Sequard, however, showed
that essentially the same symptoms might be set up by irrita-
tive diseases of the intestines, and other organs, and on the
supposition that the paralytic phenomena were caused by a
reflex spasm of the spinal vessels he named the affection reflex
paraplegia. The paraplegia which is associated with diseases
of the urinary organs and other viscera appears to consist of
several varieties. The following may be distinguished : (1)
Secondary myelitis, caused by an ascending neuritis of the
nerves of the diseased organ ; (2) Functional paralysis, caused
by some mechanism not yet accurately determined, but which
in the meantime may be called reflex paraplegia; and (3)
Paralysis, caused by direct propagation of inflammation from

340 FUNCTIONAL AND SECONDARY DISEASES OF

the nerves of the urinary passages to the lumbar and sacral,
plexuses : — ,

(1) Secondary Myelitis. — The diseases which usually cause secondary
myelitis are gonorrhoea, stricture of the urethra, chronic cystitis, prostatic
abscess, pyelo-nephritis associated with calculus, and nephritis. As a rule,
spinal paralysis occurs only in chronic affections of the urinary passages. •

, The symptoms are usually those of a subacute transverse myelitis,h
situated at the superior part of the lumbar enlargement. They
are, briefly, formication and numbness in the lower extremities, girdle
sensation, and later anaesthesia or analgesia. Paraplegia is soon established,
with excess of the reflex actions, but these become diminished and ulti-
mately lost as the lumbar enlargement is involved, cystitis and bed-sores«
then form, and soon cause death. Inflammatory action may at times ex-,
tend upwards and involve the upper extremities in the paralysis. It has.'
been proved experimentally that inflammation of the sciatic nerve may;,
cause myelitis (Tiesler), and several cases are recorded in which injuryj
of it has been followed by myelitis in man. A case is recorded by*
Cornil in which tumour of the cauda equina produced a myelitis of th<
central grey substance of the cord, along with sclerosis of the posterior:
columns, and similar cases have been recorded by Simon, Lange, and
Leyden ; a case of the kind has come under my own observation,
In the case already mentioned, under the care of Dr. Morgan,;
a severe injury to the sciatic nerve was followed by the symptoms of
subacute central myelitis. After death a microscopical examination:
showed perineuritis of the injured sciatic nerve, central myelitis, reaching;: ;
up the whole length of the cord, along with grey degeneration of thed
posterior columns in the lumbar and dorsal regions, but limited|j
to the columns of Goll in the cervical region, the portion which adjoinsti
the posterior commissure being healthy too in the lumbar region.

In a case related by Dume'nil, a neuritis of the sciatic nerve was- i
followed by paraplegia, and at a later period by paralysis of one of!
the upper extremities. The paralysed muscles became atrophied withi^
diminution of their faradic contractility. At the autopsy the greyp
matter was found diseased, while the white substance was unaffected.
Charcot describes a case in which lesion of one of the nerves of thee!
forearm was first followed by inflammation of the peripheral portion off |
the nerve, atrophy of the muscles of the hand, and pemphigoid eruptions,;. ,
while at a later period the arm of the opposite side was affected with
atrophy and anaesthesia.

(2) Reflex Paraplegia. — In this form of the disease the paralysis never
extends to the upper extremities, while the lower extremities are onlj
paretic, and never completely paralysed. There is also complete absence
of pains in the loins, girdle pains, dyssesthesice, anaesthesia, muscularr
tension, and contractures, paralysis of the bladder, bed-sores, andl
other trophic disturbances. The paralytic symptoms are variable kd

THE SPINAL CORD AND MEDULLA OBLONGATA.

341

their intensity, and may improve rapidly if there be an amendment of
the peripheral lesion which is the cause of the affection.

Brown-Soquard observed that ligature of the hilus of the kidney in
animals produced spasm of the vessels of the spinal cord, and he argued
that the paralysis which is caused by diseases of the urinary organs is
occasioned by anaemia of the spinal cord. Charcot, on the other hand,
believes that the peripheral irritation produces an inhibitory effect on the
spinal cord. In chronic Bright's disease the fibroid changes, which the
spinal, like the other vessels of the body undergo, must cause anajmia
of the cord, which may, in exceptional cases, reach such a degree as to
cause some amount of paralysis.

(3) Peripheral paralysis from extension of neuritis from the nerves of
the urinary organs is rare. Kussmaul reports a case in which inflamma-
tion of the urinary passages had given rise to a neuritis, which extended
to the nerves of the sacral and lumbar plexuses. During life, the patient
complained of shooting pains along the course of the sciatic nerves, while
there was paresis of the lower extremities. Pelvic abscesses may cause
inflammation of the sacral plexus, and thus occasion paralysis and anaes-
thesia of one or both the lower extremities (Adams).

(IV.) SALTATORY SPASM.

§ 558. Bamberger first described in 1859, under the name of
saltatory spasm, two cases in which, as soon as the patients
set their feet on the floor, the lower extremities became the
subject of such strong clonic convulsions that the patients
were thrown repeatedly into the air. Similar cases have been
reported by P. Guttmann, and A. Frey has recently communi-
cated a case and examined the subject in detail.

The common characteristic of all the published cases of
the affection is that there is a great increase of reflex
excitability in certain nerve tracts, so that on the sole of the
foot being placed on the floor a singular spasm occurs, which
has the effect of throwing the patient repeatedly into the air.
These spasmodic contractions continue as long as the patient
maintains the erect posture, and they cause the patient to hop
and jump on the floor, and render him quite unable to stand
still for an instant. When the patient sits or lies down the
movements disappear, but can be instantly made to reappear
by tickling, or pressing on the soles of the feet.

In saltatory spasm the reflex mechanism of the cord is
alone affected, and there is complete absence of paralysis.

342

FUNCTIONAL AND SECONDARY DISEASES OF

In some of the reported cases other spasmodic manifestations
are mentioned, but the spasm which causes the patient to hop
on assuming the erect posture is by far the most characteristic-
feature of the disease.

It was demonstrated in Frey's case that the reflex actio
did not begin in the skin, and he regards the symptom
being due to tension and stretching of the muscles, and it is no
by any means improbable that the spasms are really due
to increase of the reflex excitability of the tendons. Ba
berger's first case appears to show that the reflex action ma-
originate in the skin. His second case was associated witl
hysteria, and therefore allied to so-called chorea major. If
Frey's case paresis, contractures, and atrophy were present, an
consequently the saltatory spasm was to be regarded as
symptom of chronic myelitis. The distribution of the spas
varies greatly in individual cases. They are at times limit
to the legs, while at other times they extend to the muscles c
the back, face, neck, and pupils, but the arms always remain u
affected. Mental influences have been found to aggravate t1
spasm in some cases, and to arrest it in others. The diagnos!
of the affection is easy on account of the very characterise
hopping movements as soon as the feet touch the floor.

§ 559. Treatment — In Bamberger's first case the admi
stration of morphia appeared to have a beneficial effect, but |
is doubtful how far treatment has been attended by good resul
The agents most worthy of trial are bromide of potassiu
Calabar bean, ergotine, conia, and atropia.

(V.) TONIC SPASMS IN MUSCLES CAPABLE OF VOLUNTARY

MOVEMENT.

§ 560. In this affection, if it can be called a separate affe
tion, the voluntary muscles become the subjects of increase
tension and tonic spasms the moment any attempt is made \
move them. Such cases manifest a marked hereditary ter
dency. The most remarkable cases of this kind are recordc-t
by Dr. Thomsen, who had himself been subject to the diseas
since childhood. The disease appeared in his children, brother
and sisters, and could be traced through four generations of hb

THE SPINAL CORD AND MEDULLA OBLONGATA.

343

ancestors. The disease begins in early life, and Dr. Thomsen
was able to recognise it in his children even in the cradle.

The disturbance of movement consists in a peculiar stiffness
and rigidity of the muscles on voluntary movement, and this may
increase to a regular tonic cramp, so that intended movements are
entirely prevented and the patients fall to the ground. Volun-
tary contraction of the muscles occurs very slowly ; but when
once it has begun it persists long and terminates only very
gradually, so that patients cannot at once let go articles they
have firmly seized. When, however, after a powerful voluntary
exertion the muscles are got to act, the movements are effected
with increasing freedom and ease, so as to be little distinguished
from healthy movements. Emotional disturbances, increased
attention directed to the movements, and cold, all act unfavour-
ably on the condition. The muscular system in these patients
is well developed ; they are capable of performing a large
amount of labour, and their general health and mental func-
tions are unaffected.

§ 561. Morbid Physiology. — Thomsen thought that the
affection was mainly of psychical origin, but there is not suffi-
cient evidence in support of this opinion. The view ultimately
adopted by Seeligmuller, that it arises from a congenital or
inherited affection of the pyramidal tracts of the cord, appears
more likely to prove correct. The question, however, can only
be decided by further observations.

§ 562. Treatment — No treatment has hitherto been of any
service.

(VI.) INTERMITTENT SPINAL PARALYSIS.

§ 563. One of the most remarkable of the manifestations of
malarial infection is the occurrence of intermittent attacks of
paraplegia.

In the recorded cases (Hertz, Romberg, Hartwig) paraplegia
became rapidly developed and advanced steadily to complete
motor paralysis. The paralysis of the lower extremities may
or may not be accompanied by anaesthesia and paralysis of the

344

FUNCTIONAL AND SECONDARY DISEASES OF

sphincters. The paraplegia usually disappears in the course of
a few hours, and gives place to an almost complete intermission,
accompanied by the appearance of a critical sweat. This pro-
cess is repeated, in a more or less regular manner, in the
quotidian, tertian, or quartan type, and the affection is either
cured or favourably influenced by quinine.

§ 564. Morbid Physiology. — All we know about the patho-
logy of this affection is that it is in all probability due to the
malarial poison acting on the spinal cord, but of its mode of
action we know nothing.

§ 565. Diagnosis. — The intermittent character of the affec-
tion renders the diagnosis easy, and the treatment is the same
as that which is applicable to all forms of intermittent fever.

(VII.) TOXIC SPINAL PAEALYSIS.

§ 566. Opium, belladonna, arsenic, phosphorus, lead, mercury,
carbonic oxide, sulphide of carbon, tobacco, camphor, ergot,
alcohol, absinthe, mushrooms, copaiba, and many other toxic
agents induce various forms of motor paralysis, such as para-
plegia, paralysis of groups of muscles, or of single extremities,
and general paralysis.

Permanent paralysis is only caused as a rule by these agents
when the organism is exposed for a long period to their
influence, although occasionally paralysis may result from a,
temporary poisoning.

Absolutely nothing is known with regard to the nature and .
locality of the lesion caused by the majority of these agents.
Landouzy has recently collected all the various forms of para- •
lysis which occur in the course of or subsequent to infective and !
other acute diseases, but inasmuch as many of these are not of
spinal origin, it will be well to defer their consideration at;
present. This subject will be subsequently treated in greater:
detail.

(VIII.) HYSTERICAL PARAPLEGIA.

This form of paralysis will be described at greater length
hereafter, and is mentioned in this place only with the view

THE SPINAL CORD AND MEDULLA OBLONGATA. 345

of reminding the reader to be carefully on his guard lest hys-
terical paralysis be mistaken for more serious disease. In
hysterical paraplegia, the lower extremities are generally main-
tained in a condition of rigid extension, while the feet are in
the position of extreme talipes equino-varus. As a rule, how-
ever, there is no muscular atrophy, the electric reactions are
normal, and the limbs become quite relaxed when chloroform is
administered.

346

CHAPTER VIII.

V.— TRAUMATIC DISEASES, TUMOURS, AND ABNOR-
MALITIES OF THE SPINAL CORD AND MEDULLA
OBLONGATA. .

(I.) WOUNDS OF THE SPINAL CORD AND MEDULLA

OBLONGATA.

The affections comprised in this section are acute traumatic
lesion of the substance of the cord and medulla oblongata.

§ 567. Etiology. — In fractures and luxations of the spinal
column the injured vertebras may be so displaced as to cause
compression and crushing of the cord.

Gunshot wounds often injure the spinal cord either by the
entrance of the bullet into the spinal canal or by fracture of the
vertebras. Stabs and cuts of the spinal cord are rare ; but sharp
instruments have been known to enter the cord, the point of the
instrument having entered the canal either by dividing the
vertebral arches or by passing through the intervertebral
spaces.

Injuries of the medulla oblongata may be produced by a
sharp instrument piercing between the occiput and altas, by
bullets, splinters of bone, blows on the back of the neck without
fracture, and on the top of the head by contre coup. Fractures
and dislocations of the first two cervical vertebras are also
important causes of wounds of the medulla oblongata. Dis-
location of the first vertebra, or rupture of the odontoid
ligament, is accompanied by a backward displacement of the
odontoid process, which presses against the anterior surface of
the medulla, and causes instant death.

TRAUMATIC DISEASES OF THE SPINAL CORD.

347

§ 568. Symptoms.

1. Wounds of the Spinal Cord.

The symptoms may be subdivided into those which are
caused by (a) comparatively slight injuries of the cord, such as
simple incised and punctured wounds ; and (b) those which
arise from the more serious lesions, such as compression, crush-
ing, and tearing of the cord.

(a) The symptoms which indicate that an injury by cutting or
stabbing in the neighbourhood of the spine has penetrated the
cord will at first be those caused by loss of conduction to and
from the brain in the portions situated below the seat of the
injury. At the moment the injury is received there is usually
motor paralysis of various extent in the form of paraplegia,
hemi-paraplegia, or general paralysis. If the cord be com-
pletely divided, there is complete anaesthesia of the paralysed
parts; but if only one-half of the cord be divided, the sensory
paralysis is situated on the side opposite to the injury and to
the motor paralysis. The anaesthesia is sometimes partial, and
if the lesion be very restricted, hyperesthesia in the form of a
girdle is present. If the injury be of any considerable extent,
paralysis of the bladder and rectum occurs, and there is also
vaso-motor paralysis with increased temperature and redness of
the regions affected by the motor paralysis. The reflex actions
are usually abolished at first owing to the shock ; but if the
lesion be situated in the dorsal or cervical regions, they may
after a time be exaggerated.

Girdle pains, caused by irritation of the posterior roots at the
seat of injury, are usually present. After a time the symptoms
of secondary traumatic myelitis complicate those caused by the
primary lesion. The symptoms of irritation now appear, such
as girdle pains, active pains in the paralysed parts, cutaneous
hypersesthesia of variable extent, and twitchings and spasms of
single muscles and groups of muscles.

When the inflammatory action spreads through the whole
thickness of the cord, the paralysis extends in the transverse
direction, so that even when the wound has only injured a small
portion of the transverse diameter of the cord, complete para-
plegia, para-ansesthesia, and paralysis of the vaso-motor paths,

348 TRA.UMA.TIC DISEASES AND ABNORMALITIES OF

bladder, and rectum may occur. When the lesion is situated
high up, disturbances of respiration become prominent, and
various oculo-pupillary phenomena and vaso-motor disturbances
of the head and face may be present. At a later period bed-
sores, cystitis, pyaemia, and septicaemia supervene with all their
deleterious consequences.

(6) The symptoms which indicate that the cord is crushed
or torn in severe injuries of the spine are complete paralysis
and anaesthesia of the portion of the body below the seat of
injury. The reflex actions are abolished, there are retention of
urine, involuntary evacuations with constipation and meteorism,
painful erections, and elevation of the temperature of the body
below the lesion. The local symptoms of injury to the spine
and of displacement of the vertebrae are of course present.
The symptoms of acute traumatic myelitis appear in a few
days, consisting of bed-sores and pyaemia, with their usual con-
sequences.

If the lumbar region be crushed, there is rapid atrophy of the
muscles of the legs, with loss of electrical contractility, and
cystitis. When the cervical region is injured, the temperature
may rise to an excessive height (43° — 44° C.) (109° — 111° F.).
In some cases, when the dorsal region has been injured, the
temperature has been abnormally low for some days before
death (Nieder). The severer cases are rapidly fatal by paralysis
of respiration, while death is caused in other cases by acute
bed-sores and pyaemia. In partial crushing of the cord the
symptoms run a milder course.

§ 569. Varieties. — The symptoms vary according to the level
at which the lesion is seated.

If the cord be injured at the level of the first or second cervical
vertebra, death usually occurs at once ; and when the lesion is situated
above the origin of the phrenic, nerves, respiration is only maintained
by the forced action of the auxiliary muscles of inspiration, and the case
terminates fatally in a brief space of time.

If the lesion be situated in the cervical region below the origin of the
phrenic nerves, the arms are partially and the legs completely paralysed,
anaesthesia being also partial in the former and complete in the latter ;
inspiration is performed by the diaphragm, expiratory acts are feeble,
painful erections are often present, and life may be prolonged for some
time.

THE SPINAL CORD AND MEDULLA OBLONGATA.

349

If the lesiou be situated in the dorsal region, the arms remain un-
affected, the muscles of the trunk and lower extremities are paralysed
below the seat of the lesion, the reflex actions soon become exaggerated,
painful erections are rare, the bladder and rectum may after a time become
paralysed, and bed-sores supervene with their usual consequences, or the
myelitis assumes an ascending course, and the patient dies from asphyxia.

If the lesiou be situated in the lumbar region, the arms and the greater
portion of the trunk are unaffected, the legs, bladder, and rectum are totally
paralysed, reflex actions of all kinds are abolished, there are no erections,
and the muscles of the lower extremities undergo rapid atrophy, with ex-
tinction of their electrical reaction. The symptoms arising from lesion of
the cauda equina are somewhat similar, but iu it the region supplied by
the lumbar plexus is unaffected.

2. Wounds of the Medulla Oblongata.

§ 570. If the injury to the medulla be a severe acute one,
the patient collapses as if struck by lightning, and dies instan-
taneously. Sometimes he gives utterance to a piercing cry
before falling, or death may be accompanied by a few transitory
convulsions. All this results from sudden paralysis of the
respiratory centre and complete interruption of all the con-
ducting paths between the spinal cord and the brain.

When the wound is less severe, or when the medulla is only
partially lacerated, the affection may last for some time, but these
cases too, as a rule, terminate suddenly. It is probable that
patients sometimes survive very small injuries to the medulla,
but this is difficult to prove. Sudden death may perhaps some-
times occur from simple concussion of the medulla in the entire
absence of any serious lesion.

§ 571. Morbid Anatomy.

Simple incised or punctured wounds produce injuries of
various size and depth. The edges of the wound project at
first beyond the pia and the wound is closed with coagulated
blood. In a few days the edges are still further protruded,
while the neighbouring parts of the cord are more or less
softened, and the membranes are reddened and inflamed and
covered with fibro-purulent exudations. In animals at least,
and probably also in man, if life be preserved, the edges of the
wound heal, and a cicatrix of connective tissue is formed.

Crushing produces softening and disintegration of the cord,

350 TRAUMATIC DISEASES AND ABNORMALITIES OF

along with congestion and hemorrhage into the membranes.
The crushed • spot is usually flat and thin, and the medullary
substance is changed into a dark red or chocolate coloured mass
composed of blood and the de'bris of nerve -substance. The
adjoining parts become congested and subsequently undergo
inflammatory softening. The microscope shows granular cor-
puscles, detritus of myeline, decomposed blood corpuscles,
pigment and blood crystals, and remnants of ganglion cells,
along with inflammatory swelling and disintegration of nerve
fibres and axis cylinders. In a few weeks the cord for a con-
siderable distance, both above and below the injury, undergoes
softening, and this is specially apt to occur in the lower part of
the cord. Ascending and descending secondary degeneration
occur when life is prolonged, and in several cases fatal within
a few days from the date of injury I have found decided evi-
dences of a central myelitis up to the medulla oblongata.

If the patient live, the destroyed nerve tissue becomes
absorbed, and a kind of cicatrix is formed, which may enclose
cystic cavities containing clear fluid. Regeneration of nerve
substance is not known to occur in man.

Complete severance of the cord occasionally occurs, and then
the pia is also torn, and the two ends of the cord are separated
by a considerable space. The spinal dura mater may remain
uninjured. Inflammatory softening occurs as after crushing,
and extends more or less upwards and downwards.

The anatomical changes found in the medulla when it is
wounded, lacerated, or crushed resemble the acute injuries of
the spinal cord.

§ 572. Course, Duration, and Termination. — In simple
incised wounds of the cord a comparative cure may be effected,,
and life retained for many years. Physiological experiment
shows that animals may be kept alive for a long period even,
after complete division of the cord, and it is quite possible that:
lesions of moderate severity may undergo repair. As a rule,
however, the secondary myelitis set up continues to increase, .
the paralysis becomes more complete, bed-sores with all theirr
attendant evils make their appearance, and the patient dies;
after protracted suffering. The severe forms of injury to the:

THE SPINAL CORD AND MEDULLA OBLONGATA.

351

spinal cord are always fatal. Death may take place a few hours
or days after the injury from shock or paralysis of respiration,
but in some cases life may be protracted for many months.

Acute severe injury to the medulla oblongata causes instant
death, and slight injuries are exceedingly dangerous, because
the inflammatory action set up by them generally leads rapidly
to a fatal termination.

^ 573. Diagnosis. — In the case of a wound of the pia mater
the occurrence of meningeal haemorrhage might give rise to the
idea of injury of the cord. In meningeal haemorrhage, however,
the symptoms of irritation are very prominent at the outset,
while those of paralysis are less severe than in injury of the
cord.

Hcematomyelia induces a certain amount of crushing of the
cord, and gives rise to similar symptoms, but in it there is
usually no history of external injury, and when there is, the
diagnosis between the two affections is not of much consequence.

Cases of severe concussion of the cord may usually be
recognised by the absence of a clear demarcation of the
anaesthesia and paralysis, and by the absence of bed-sores, and
other trophic changes. If dislocations of the vertebrae are found
to exist, crushing of the cord is more probable.

§ 574. Prognosis. — In all the severer forms of injury the
prognosis is exceedingly unfavourable, but in cases of partial
injury and simple incised wounds a certain amount of recovery
may take place. Sudden injury to the medulla oblongata is
almost uniformly fatal.

§ 575. Treatment. — The associated traumatic myelitis must
be treated according to the principles applicable to other forms
of acute inflammation of the cord.

(II.) SLOW COMPRESSION OF THE SPINAL CORD AND
MEDULLA OBLONGATA.

§ 576. In all the lesions comprised under this section an
external force slowly and gradually compresses the cord or

352 TRAUMATIC DISEASES AND ABNORMALITIES OF

medulla oblongata in a limited longitudinal extent, giving rise
to characteristic groups of symptoms.

§ 577. Etiology. — Any circumstance which gradually narrows
the spinal canal and leads to a slowly increasing compression
of the cord may become a cause of myelitis by compression.
Such compression may be caused by meningeal, perimeningeal,
and intramedullary tumours, inflammatory and haemorrhagic
processes, aod parasites. Diseases of the vertebral column,
especially caries of the vertebrae, constitute the most important
causes of compression of the cord, and may produce pressure on
the cord in several ways. The wasting and sinking of the bodies
of the vertebrae produce kyphosis, which may narrow the ver-
tebral canal to such an extent as to compress the cord.

In caries of the vertebrae, however, compression of the cord is
generally produced by the extension of the inflammatory process
in the bone to the spinal membranes. The irritation caused by
the diseased vertebrae and especially by accumulations of pus
produce a pachymeningitis, so that the outer layers of the dura
are changed into a thickened mass of young fibro-plastic tissue,
which either surrounds the dura like a ring or presses it from
one side. The nerve roots are also involved in the morbid
process, and become more or less thickened, swollen, and in-
flamed. The cause of pressure may be deposits of caseous
pus, displaced fragments of bone, or protruding intervertebral
cartilages.

Carcinoma of the vertebrae, whether primary or secondary,
causes compression of the cord when it grows into the ver-
tebral canal. The form of compression myelitis known as
'paraplegia dolorosa with most acute pains is then developed.

Amongst other diseases of the vertebrae which occasionally
cause compression of the cord may be mentioned exostoses,
syphilitic new formations, dry arthritis of the vertebras, and
thickening of the odontoid process of the axis.

External tumours of all kinds, such as carcinomata, sarco-
mata, aneurisms, and echinococci, growing against the verte-
bral column and entering the vertebral canal, occasion com-
pression of the cord. When the gradual compression gives
rise to transverse myelitis, another characteristic group of

THE SPINAL CORD AND MEDULLA OBLONGATA. 353

symptoms appears, which constitutes the second stage of the
affection. The irritation caused by tumours may produce
myelitis in the absence of any compression. If the compression
be not soon relieved, secondary ascending and descending
degenerations of the cord supervene, and then another group of
characteristic symptoms develop, constituting the third stage
of the disease.

Slow compression of the medulla oblongata is caused by
tumours growing from the bones, periosteum, meninges, or in
the surrounding parts of the brain and growing in the direction
of the medulla, or by tumours growing in the substance of the
pons or medulla itself, and aneursims of the arterial trunks.
Caries of the occipital bone or of the first two cervical vertebrae
with consequent exudation, abscess, or dislocation of the
odontoid process may also produce gradual compression of the
medulla oblongata.

The medulla is often compressed, too, by abnormalities in
the shape and size of the bones, such as contraction of the
foramen magnum and enlargement of the odontoid process.
Arthritis deformans in the articulations between the occiput
and altas would appear to be a very rare cause of compression
of the medulla.

§ 578. Symptoms.
1. Slow Compression of the Spinal Cord.

The symptoms of compression myelitis may be divided into
(a) extrinsic and (6) intrinsic symptoms.

(a) The extrinsic or prodromal symptoms are, in addition
to the signs of Pott's curvature or tumour, phenomena of irri-
tation of the roots of the spinal nerves. The first symptoms
generally consist of severe girdle pains, hyperesthesia of the
skin corresponding to the distribution of the pain, and eccen-
tric neuralgiform pains generally fixed to one particular spot.
Other symptoms generally present are severe pain in the back,
local stiffness, and tenderness of the spinous processes. The
neuralgic pains are often accompanied by herpetic or bulbous
eruptions of the skin. Phenomena of motor irritation are
superadded to the sensory disturbances in the distribution of
x

354 TRAUMATIC DISEASES AND ABNORMALITIES OF

the nerves whose roots were first implicated. These consist
of twitchings, spasms, and contracture of the muscles supplied
by the affected nerves. The irritative motor symptoms are
soon followed by weakness and paralysis, which is limited to
single muscles or groups of muscles, and often accompanied by |
atrophy and loss of electrical excitability. In the paralysis
caused by pressure on the roots of the nerves reflex actions are
abolished. The initial stage may last months or years, and
always precedes for some time that of compression of the cord.
The irritative symptoms are absent in cases of intra-medullary
tumours.

(b) The Intrinsic Symptoms. — The second stage of the
disease is generally ushered in by paralysis of more or less-
rapid development, usually in the form of paraplegia. The
paralysis may at times begin as hemiplegia, and afterwards-
develop into paraplegia. The paralysis may be preceded for a i
short time by pargesthesise in the lower half of the body, such as I
tingling, furriness, sensations of burning or coldness, and girdle
sensations. The order in which the sensory and motor symptoms •
appear depends on the direction in which the pressure is made.
The paralysed muscles are at first flaccid and offer no resistance
to passive movements, but the cutaneous reflex actions are
increased in the lower extremities, except when the lumbar
enlargement is subjected to pressure.

Paralysis of the rectum and bladder occurs sooner or later
when there is a considerable degree of compression, but it is
usually a late symptom when the lesion is situated in the dorsal
or cervical regions. As the disease progresses the muscles become
gradually tense and rigid, and are affected with twitchings or
transient tonic spasms. Contractures appear, which are at first
temporary, but soon become permanent. The lower extremities
continue in a permanent position of extension, which may sub-
sequently give place to flexion.

The cutaneous and tendinous reflex actions are now greatly
exaggerated, and slight dorsal flexion of one foot may produce
active clonic movements, or convulsive tremors in both the lower
extremities. The reflex actions originating in other parts are
also increased. The introduction of a catheter or the evacuation
of the bladder or rectum may cause active jerkings of the limbs,

THE SPINAL CORD AND MEDULLA OBLONGATA.

355

and irritation of the inner side of the thigh has been known
to produce erections of the penis.

The sensory disturbances are not usually so well marked
as the motor, and complete anaesthesia of the paralysed
parts is rare in vertebral caries. Cancer of the vertebral
column, growing into the spinal canal, is, however, accompanied
by pains of intense severity (Charcot). These pains consist
of a severe girdle pain and pain radiating along the distribu-
tion of certain nerves, as the crural and sciatic nerves when
the lumbar vertebras are affected. The skin to which the
affected nerves are distributed is intensely hypersesthetic, so
that the slightest touch is painful. The pains are constantly
present but are liable to paroxysmal exacerbations of intense
severity, which are difficult to allay even by large doses
of narcotics. Patches of anaesthesia may be observed in the
skin to which the affected nerves are distributed, while the pain
still continues unabated (ancesthesia dolorosa). The symp-
toms of compression of the cord are after a time superadded to
these sensory disturbances, and then the condition has been
called paraplegia dolorosa. On local examination of the ver-
tebral column an excurvation of the spine may be observed,
and the spinous processes in this region may be exceedingly
tender to pressure or percussion. Inasmuch as cancer of the
vertebral column is always secondary, the presence of a can-
cerous tumour in some other part of the body, or of the can-
cerous cachexia, greatly aids the diagnosis.

Trophic disturbances are not prominent in compression
myelitis. When the lumbar or cervical enlargement is affected,
or when secondary inflammation of the grey substance extends
upwards or downwards to these parts, the muscles of the cor-
responding extremities undergo rapid atrophy, attended by loss
of faradic contractility and the reaction of degeneration. In
some cases a few of the muscles become atrophied, while others
undergo contracture. An eruption of herpes sometimes en-
circles one-half of the body on a level with the lesion. In
severe cases, and in the terminal period of ordinary cases,
bed-sores and cystitis supervene, with their usual deleterious
consequences.

The subsequent course of the disease is not uniform. The

356

TRAUMATIC DISEASES AND ABNORMALITIES OF

less severe cases continue for a long time without change, but
afterwards improvement may gradually take place. The anaes-
thesia first diminishes, the functions of the bladder are better'
regulated, and after a time motor power gradually returns. In:,
severe cases the symptoms grow worse, the paraplegia becomes
complete, the bladder and rectum are paralysed, cystitis, bed-
sores, and pyaemia supervene, and soon cause death.

§ 579. Varieties. — The symptoms differ considerably accord- -
ing to the situation of the lesion.

(a) Compression of the Cervical Region of the Spinal Cord. — When the !
upper part of the cervical region is affected the disease often begins by I
pain in the occiput, stiffness of the whole neck, obliquity of the head, and
inability to nod or to rotate the head. The paralysis often begins in the •
upper extremities, while the lower are wholly or comparatively unaffected ;
but at a later period the extremities become paralysed, the reflex actions
being exaggerated in all the extremities. Paralytic myosis or spastic
mydriasis may be present on one or on both sides. Other symptoms which
have been observed are repeated vomiting, difficulty of swallowing, inces-
sant hiccough, retardation of the pulse, which may beat only 48 to 20 times
in the minute, fainting fits with temporary arrest of the heart's action,
and occasionally epileptic attacks.

If the cervical enlargement be affected, the initial symptoms of pain,
anaesthesia, spasm, paralysis, and atrophy are localised in the upper
extremities, and tbe symptoms appear in the lower extremities at a later >
period. Oculo-pupillary symptoms, disturbances of respiration, and
retarded pulse may also occur. Reflex action may be abolished in the
upper extremities.

(b) Compression of the Dorsal Region of the Cord. — The dorsal region is
the most frequent seat of compression. The symptoms are girdle pains,
intercostal neuralgia at different levels of the trunk, paraplegia up to the
corresponding level, reflex actions in the lower extremities retained or
increased, and the nutrition of the muscles and their electrical excitability
normal.

(c) Compression of the Lumbar Region of the Cord. — If the lumbar
region be affected, the paralysis is confined to the lower extremities,
bladder, and rectum. The initial symptoms are localised in the lower
extremities, where reflex actions are abolished, and the muscles are per-
manently relaxed and atrophied and exhibit the reaction of degeneration.
If one lateral half of the cord be compressed, the characteristic symptoms
of Brown Se'quard's unilateral lesion appear.

THE SPINAL CORD AND MEDULLA OBLONGATA. 357

2. Slow Compression op the Medulla Oblongata.
The initial symptoms are caused by irritation and subsequent
paralysis of the roots of the nerves of the medulla and pons.
Those of irritation first show themselves, consisting of neural-
giform pains in the region of the trigeminus, either on one or
both sides, and buzzing in the ears. The motor irritative symp-
toms consist of twitchings of the facial muscles, transitory
cramps in the tongue and lips, and occasionally clonic or tonic
contractions in the extremities. When the medulla oblongata
is seriously compressed, epileptiform convulsions, vomiting, diz-
ziness, and hiccough are produced. The second stage is ushered
in by paralysis of the sensory and motor nerves. There may
be anaesthesia in the region of the trigeminus, often accom-
panied by intense pain and neuroparalytic ophthalmia. There
may be loss of taste, or deafness on one or on both sides, and
one or more of the cranial motor nerves may be paralysed, while
tbe paralysed muscles undergo atrophy, lose their faradic con-
tractility, and manifest the reaction of degeneration. After a
time a true bulbar paralysis appears, the extremities become
paralysed, and disorders of respiration supervene. The symp-
toms begin sometimes so suddenly as to simulate embolus or
thrombosis. These acute symptoms are caused by a rapidly
developing bulbar myelitis, or by oedema, thrombosis, or haemor-
rhage. The optic nerves are not affected unless the tumour
be of large size, and probably then only when it is accompanied
by effusion into the ventricles of the brain.

§ 580. Course, Duration, and Termination. — The course
of the disease depends on the nature of the primary lesion.
Meningeal and intra-medullary tumours, as well as carcinoma
or other malignant tumours of the vertebrae, are always fatal.
In most cases of vertebral caries, on the other hand, the course
is comparatively favourable. Many cases, however, progress
slowly with remissions and exacerbations to a fatal termination.
In other cases the recovery is incomplete, partial paralysis,
contractures, muscular atrophy, and anaesthesia remain, and
relapses are frequent.

§ 581. Morbid Anatomy. — The meninges are often hyper-

358 TRAUMATIC DISEASES AND ABNORMALITIES OF

gemic, opaque, and adherent to the neighbouring parts, or
covered with deposits of various thickness. The nerve roots .
may be closely united with the tumour or exudation. At first
they are swollen and hyperaemic, and their fibres are in a
state of fatty degeneration. At a later period the roots are
atrophied, pale grey, degenerated, and nearly reduced to con-
nective tissue.

The substance of the spinal cord is rendered more or less flat
and thin at the point compressed, and it maybe reduced to the
size of a small quill. The compression is sometimes greater
anteriorly, sometimes greater posteriorly, at other times from
one or other side, so that the cord assumes a distorted and
irregular appearance. The compressed spot varies in length,
and is usually softened, although it may be sclerosed in long-
standing cases. In chronic cases the usual ascending and
descending changes occur above and below the level of the
lesion.

A microscopical examination of the spinal cord reveals the
appearances which usually characterise a chronic interstitial
myelitis. In addition to the characteristic phenomena of
ascending and descending sclerosis, a myelitis of the central
grey substance may often be discovered for a considerable dis-
tance above and below the seat of lesion. In favourable cases
restoration and almost complete recovery may take place, and
consequently the nerve elements must be to some extent restored
at the point of compression. Charcot and Michaud examined a
case, fatal from other causes, in which recovery from compression
myelitis had occurred. The transverse section of the cord
at the seat of compression was much smaller than the other
portions "of the cord, and looked grey and degenerated.
Microscopical examination showed that there was an excess of
connective tissue at the seat of compression, through which a
considerable number of normal though slender nerve fibres
passed. The grey substance was much reduced in size, but
some healthy ganglion cells were observed in it. It is probable
that the axis cylinders of all the fibres were not destroyed, and
that they had assumed anew medullary sheath on the pressure
being removed.

The medulla oblongata may be flattened, either on one or

THE SPINAL CORD AND MEDULLA OBLONGATA. 359

both sides, turned on its axis, and distorted in virion, ways.
The tissue of the medulla is anemic and softened, while extra-
vasations of hlood are often observed. The roots of the cranial
nerves may be compressed and flattened, and the nerves then
undergo degenerative atrophy. The pyramidal tracts of the
lateraf columns and the columns of Tnrck may undergo
descending degeneration throughout the entire length of the
spinal cord.

8 582. Diagnosis.— The initial symptoms caused by com-
pression of the roots of the nerves are of importance m the
diagnosis of the affection, and in ordinary cases confirmation of
the° diagnosis will be obtained from the external appearances
presented by the primary disease. In Pott's curvature the
aradual formation of angular kyphosis, and the history of the
case generally, afford indications of the nature of the affection
which are unmistakable.

In carcinoma of the vertebrae the girdle sensation and other
eccentric pains are of the most agonising severity ; they occur
m nocturnal paroxysms, and great hyperesthesia usually exists
in the painful region. If primary cancer can be found m
another organ, or there be a general cachexia, the diagnosis will
be less difficult.

The recognition of the rarer causes of compression of the cord,
such as exostoses, syphilitic new formations, and aneurisms, is
made from the general symptoms of the respective diseases.

Slow compression of the medulla oblongata may be suspected
when symptoms of irritation in the regions of distribution of
some of the bulbar nerves are followed by those of sensory or
motor paralysis, and when electrical examination shows that
the motor paralysis is of peripheral origin. The diagnosis is
still further confirmed when the patient suffers from giddiness,
violent headache, severe vomiting, epileptoid convulsions, and
when twitching and subsequent paralysis and contractures occur
in the extremities, more especially when the distribution of these
in the latter is unsymmetrical. Cases of compression of the an-
terior pyramids of the medulla may closely resemble spastic
spinal paralysis. The points of distinction between the two
affections are that the paralysis begins suddenly in compression,

360 TRAUMATIC DISEASES AND ABNORMALITIES OF

the upper extremities are usually affected before the lower,
and bulbar paralysis sooner or later supervenes ; while in spastic
paralysis the commencement of the paralysis is slow and
gradual, the lower extremities are usually affected before the
upper, and bulbar symptoms probably never appear in primary
lateral sclerosis.

§ 583. Prognosis. — In most cases of slow compression of the
cord the prognosis is unfavourable. Cases due to the pressure
of syphilitic formations, peri-meningeal exudations, and verte-
bral caries often recover. In young, well-nourished persons,
who are not scrofulous, recovery with slight deformity of the
vertebral column generally takes place. In many cases, how-
ever, recovery is imperfect, and a certain amount of paralysis of
the lower extremities with contractures remains.

The prognosis of slow compression of the medulla oblongata
is always unfavourable.

§ 584 Treatment. — In severe cases the treatment must be
altogether palliative, and directed to the relief of pain and
other discomforts.

The most promising cases for treatment are those of Pott's
disease. In them rest in bed for months is necessary, in order
to maintain the spine in a condition of repose. Yarious kinds
of apparatus have been used for the support and protection
of the spine. The best apparatus consists of the plaster of
Paris bandage, introduced by Dr. Sayre, but I must refer the
reader to surgical works for a full description of the method
of application.

The internal treatment should be that adapted to scrofulous
patients generally, consisting of fresh air, cod-liver oil, cream,
iron, and quinine. The hot iron has been recommended by
Charcot and others to be applied every two weeks on each side
of the curvature.

In slow compression of the medulla oblongata, treatment is
of very little avail, unless the case be one of caries, or syphilitic
tumour.

THE SPINAL CORD AND MEDULLA OBLONGATA. 3G1

(III.) HEMIPLEGIA ET HE MIPAR APLEGI A SPINALIS.

Unilateral Lesion of the Spinal Cord.

Brown-S4quard"s Spinal Paralysis.

§ 585. Definition. — The symptoms which are grouped to-
gether under the name of unilateral spinal paralysis are mainly
characterised by unilateral motor paralysis and hyperesthesia
on the side of the lesion, anaesthesia on the opposite side, and
local symptoms caused by implication of the roots of the nerves
on a level with the primary lesion.

§ 586. Etiology. — The symptoms depend not upon the nature
of the lesion, but upon its localisation in one lateral half of the
spinal cord, so that it is unnecessary to give a detailed account
of all the causes of the affection. The penetration of the ver-
tebral canal by pointed instruments constitutes the most fre-
quent cause. Compression of the cord from meningeal tumours,
fractures or dislocation of the vertebras, meningeal haemorrhage,
intra-medullary tumours, haemorrhage into the substance of the
cord, and circumscribed sclerosis may also give rise to the
symptoms of unilateral spinal paralysis.

§ 587. Symptoms. — The symptoms of unilateral spinal
paralysis may be developed insidiously and gradually, or quite
suddenly, the mode of invasion depending of course on the
nature of the lesion. The most prominent feature of the
affection is a motor paralysis, which is unilateral, and which
may only involve one leg (hemiparaplegia), or, if the lesion
be situated high up, may also implicate the arm of the same
side (spinal hemiplegia). The muscles on the paralysed side
usually undergo early and rapid atrophy, and their faradic
excitability is diminished. The side opposite to the seat of the
lesion is either free from paralysis or is only affected to a slight
degree.

Evidences of vaso-motor paralysis are generally found on the
side of the lesion, especially if the affection has been rapidly
developed. The temperature of the paralysed limbs is usually
raised to the extent in 1*8° F. or more, although it may be lower
than natural when the disease has existed for some time.

362 TRAUMATIC DISEASES AND ABNORMALITIES OF

Muscular sensibility and muscular sense are usually dimi-
nished on the affected side, but all forms of cutaneous sensibility,
instead of being diminished, are greatly increased. Impressions
of touch, temperature, and pain are felt with great acuteness, and
there is an increased power of localising tactile sensations. At
times, however, the hyperesthesia is limited to a few only of the
forms of cutaneous sensibility. The hyperaesthetic region of skin
is usually bounded by an anaesthetic zone, which corresponds with
the height and longitudinal extent of the lesion in the spinal
cord ; and. a narrow hyperaesthetic zone which extends to the
opposite side may sometimes be detected above the anaesthetic
belt. The state of reflex action on the paralysed side varies.
It has been found increased by Paoluzzi and JEUegel, and
diminished by Brown-Se'quard, Bazire, and others. Not many
observations have hitherto been made with respect to the state
of tbe reflex irritability of the tendons, but Erb found it in-
creased in one case.

There either are no motor disturbances, or they are only of
slight degree on the side opposite the lesion, and both the
muscular sense and the electro-muscular sensibility are retained.
There is more or less complete anaesthesia of the skin. Some
forms of sensibility may at times be involved to a greater
extent than others. The anaesthesia extends to the median
line of the body, and it is often bounded above by a slightly
hyperaesthetic region, corresponding to a similar zone on the
opposite side. There are no vaso-motor disturbances on this
side, and reflex action is usually normal, although it has occa-
sionally been found increased (Brown-Sequard). The patient
sometimes complains of a painful feeling of constriction on a
level with the lesion, along with various painful sensations, such
as burning, darting, and boring pains, which may at times be
more prominent on the anaesthetic, at other times on the hyper-
aesthetic and paralysed side, and occasionally occurs on both
sides. Acute traumatic cases are usually associated at first
with retention or incontinence of urine, but after a time only
a certain amount of weakness of the sphincters of the bladder and
rectum remains. The sexual functions are at times unaffected,
and at other times more or less weakened.

Acute bed-sore may appear on the anaesthetic, and inflam-

THE SPINAL CORD AND MEDULLA OBLONGATA. 3G3

mation of the knee-joint on the paralysed side, while well-
marked ataxia may be observed on the return of motor power
in the paralysed leg (Joffroy and Solmon).

§ 58S. Varieties of Unilateral Paralysis.
The symptoms differ considerably, according to the level at
which the lesion is situated in the cord.

(1) In a unilateral lesion of the lumbar enlargement of the cord an
anesthetic zone may be found on the paralysed side, corresponding to the
area of distribution of one or more of the lumbar nerves, in addition to the
other characteristic unilateral symptoms. This area is not always in the
form of a belt, and may be situated round the abdomen, in the region of the
groin, or over the anterior surface of the thigh, so that from an imperfect
examination one might be led to believe that the anaesthesia was diffused
over the lower extremities.

(2) Unilateral lesions of the dorsal portion of the cord give rise to the
most characteristic symptoms of the disease, as already described.

(3) In unilateral lesions of the cervical portion of the cord the grouping
of the symptoms varies greatly, according to the level at which the lesion is
situated and its longitudinal extent. It is manifest that the distribution
of the motor and sensory disturbances will differ according as the upper or
lower roots of the brachial plexus are involved in the lesion, and according
as the cilio-spinal region is or is not implicated.

In the lower extremities and trunk the motor and sensory disturbances
are the same as when the dorsal portion is implicated. In the upper ex-
tremities on the side of the lesion a certain number or all of the muscles
are paralysed, there is hypercesthesia of certain parts of the skin mingled
with anaesthesia of other regions or for certain varieties of sensation.
On the side opposite to the lesion there is no paralysis, but there is more
or less complete anaesthesia over the whole skin below the lesion, or over
special territories.

The neck and head on the side of the lesion manifest anaesthesia and
hyperaesthesia of certain areas of the skin and paralysis of the vaso-motor
and oculo-pupillary fibres, giving rise to increased temperature of that
side of the head and body, heightened sensibility, narrowing of the palpe-
bral fissure, and contraction of the pupil. On the side opposite the lesion
there is usually anaesthesia of the neck, along with a narrow zone of hyper-
aesthesia, and a normal condition of the face and eye.

§ 589. Morbid Physiology. — It is almost needless to mention
that unilateral section will divide the columns of Tiirck, the
anterior root- zones, the pyramidal tracts and direct cerebellar
fibres of the lateral columns, the posterior root-zones and the

364 TRAUMATIC DISEASES AND ABNORMALITIES OF

Fig. 182.

columns of Goll, and the anterior and posterior horns of grey
matter; and when the lesion is of considerable longitudinal I
extent a considerable number of the anterior and posterior
nerve roots may be destroyed.

Division of the pyramidal tracts in the anterior and lateral
columns will sever the muscles below the point of the lesion
from the cortex of the brain, hence there will be complete loss
of voluntary power below and on the same side as the lesion.
When the lesion is permanent, the pyramidal tracts undergo
secondary descending degeneration, and, after a time, increased

muscular tension and contrac-
tures are superadded to the
motor paralysis. Recent in-
vestigations have apparently
proved that the vaso-motor
tracts also run in the lateral
columns, thus division of these
would produce vaso-motor dis-
turbances on the side of the
lesion.

Division of the anterior root-
zone and direct cerebellar tract
is not known to give rise to any
symptoms, probably because
the result of injury to these
parts is masked by the presence
of motor paralysis. Similar
remarks apply to injury of the
columns of Goll and the pos-
terior root-zones, but it is in-
teresting to find that Joffroy
and Solmon observed the occur-
rence of well-marked ataxy on
the return of motor power in
the paralysed extremity, caused
doubtless by the injury of the
posterior root-zone of that side.

Division of the grey matter
of the one half of the cord

Fig. 182 (After Erb). Diagram of the
Course of the principal Conducting
Paths within the Cord. — 1 and 1',
The motor and vaso-motor tracts,
passing through the anterior root (v),
and remaining on the same side of
the cord ; 2 and 2', Tracts which
conduct the muscular sensibility,
also passing through the anterior
roots, and remaining on the same
side, of the cord ; 3 and 3', The tracts
which conduct sensory impressions
of touch, temperature, pain, and
tickling. These enter the cord
through the posterior roots, and
cross to the other side, and pursue
their course upwards on that side.
Section of the right half of the
cord (a) must interrupt conduction
through the motor, vaso-motor, and
musculo-sensory tracts (] and 2) on
the right side, and the cutaneous
sensory tracts on the left side (3') .

THU SPINAL CORD AND MEDULLA OBLONGATA.

305

produces anaesthesia of one half of the body below the level of
the lesion on the opposite side, showing that the sensory
fibres cross over to the opposite side soon after their entrance
into the cord. The fibres conducting impressions of touch,
temperature, pain, and tickling decussate with those of the
other side very near their point of entrance into the spinal
cord, and run to the brain in the opposite side of the cord.
Those concerned in the phenomena of muscular sense are
supposed to enter the cord with the anterior roots, and, like the
motor tracts, run through the cord on their own side of the
body.

Brown-Se'quard states that Fig. 183.

the conducting tracts of the
various forms of cutaneous
sensibilitv cross at different

heights, those concerned in
the sensation of temperature
crossing somewhat earlier than
the rest. He also thinks that
they are separated from one
another in their further course,
each lying in certain definite
segments of the cord, and that
the sensitive tracts of the
lower extremities lie behind
those of the upper in the
cervical portion of the cord.
The centripetal fibres con-
cerned in reflex action have a
crossed course within the cord
(Miescher).

It is evident, therefore, that
section of one half of the spinal
cord must cause anaesthesia of
the opposite side for sensations
of touch, pain, temperature,
and tickling, and loss of the
muscular sense, and motor
paralysis on the same side.

FIG. 183 (After Erb). Diagram of the
cutaneous symptoms in unilateral
lesion of the dorsal portion of the
spinal cord on the left side. — The
diagonal shading (a) signifies motor
and vaso-motor paralysis ; the verti-
cal shading (b, d) signifies cutaneous
anaesthesia ; the dotted shading (a, c)
indicates hyperaesthesia of the skin.

366 TliAUMATIC DISEASES AND ABNORMALITIES OF

The phenomena which result from section of one half of the
spinal cord are well illustrated by Fig. 183.

Anatomists have described a middle and a superior crossing of sensory '
fibres, both of which are supposed to take place in the medulla oblongata.
The sensory decussation of the pyramids described by Meynert consists of
fibres which issue from the nuclei of the cuneate and slender fasciculi.
These fibres pursue an arcuate course around the central grey column, aud
become mixed with the crossing fibres of the lateral column. Flechsig,
however, asserts that these fibres curve round the olivary body of the
same side and .enter into its substance. The most recent researches with .
regard to the sensory crossing have been undertaken by MM. Debove
and Gombault. Their observations were made in a case of amyotrophic
lateral sclerosis, in which the motor fibres of the anterior pyramids of the

Pig. 184.

FlG. 184 (After Debove and Gombault). Section of the Anterior Pyramid (P) of
the Medulla Oblongata, on a level with the middle part of the crossing of the
Sensory Fibres. — FS, Sensory fibres ; FSA, Posterior and external sensory-
fasciculus which does not penetrate into the substance of the pyramid ; E,
Crossing of the sensory fibres ; O, Nucleus of the pyramid ; Z, Stratum zonale.

medulla had undergone degeneration. The sensory fibres become sub-
divided into small fasciculi, which penetrate into the posterior and
external portion of the anterior pyramids. The fibres then curve upl
wards and become inseparably mixed with the motor fibres. A little higher
up some of these fibres become mixed with the fibres of the stratum
zonale. These fibres are very well seen in some of my sections of the
medulla oblongata from a nine months human embryo, but I have always
regarded them as being derived from the external portion of the inner
division of the inferior peduncle of the cerebellum, and I am by no
means satisfied that their functions are sensory.

The relations of reflex action to unilateral section of the cord are not
.yet well ascertained, and the condition appears to vary in different
animals. According to the experiments of Woroschiloff, it would appear
that the fibres which check or control reflex action in a lower extremity

THE SPINAL CORD AND MEDULLA. OBLONGATA.

run their course principally in the same half of the cord, while those
which call forth reflex action run chiefly in the opposite half. When
the lesion extends longitudinally, so as to destroy several of the posterior
root fibres before their crossing, there will be au anaesthetic zone on the
paralysed side lying above the hypera)sthetic region, and corresponding in
width to the number of fibres destroyed by the lesion. Implication of
the cilio-spinal region causes vaso-motor disturbances in the face and
side of the head, paralytic myosis, and narrowing of the palpebral fissure on
the side of the lesion.

The narrow hypera)sthetie zone sometimes observed above the anaes-
thetic belt is explained by Brown-Sequard on the ground that the des-
cending fibres of the posterior roots fall within the range of the lesion,
tie has, however, recently obtained a curious result by making a section
of one half of the pons in animals immediately in front of the middle
peduucle of the cerebellum, followed after a time by section of the other
half. After section of the first half of the pons, there is hyperesthesia of
one half of the body, on the side of the lesion, and anaesthesia of the
opposite half, the sensory disturbances being specially well marked in the
lower extremities. In an -animal which had undergone hemisection of the
right side of the pons, and which was consequently hyperaesthetic on the
right side, hemisection of the left side of the pons produced a reversal of
the sensory phenomena, so that the left half of the body became hyper-
aesthetic and the right anaesthetic. This curious result shows that the
phenomena of sensory conduction are by no means so definite or so well
ascertained as those of motor conduction.

The existence of cutaneous hyperaesthesia on the side of the lesion is
usually explained on the supposition that it is a phenomenon of irritation
caused by the secondary inflammation surrounding the lesion ; but after
the result obtained by Brown-Se'quard it will probably be better to suspend
our judgment with regard to it in the meantime. It does not, however,
appear to me that much light is thrown upon the point by postulating^
like Brown-Se'quard, the existence in the cerebro-spinal axis of special
centres possessed of inhibitory and dynamogenic functions.

§ 590. Course, Duration, and Termination. — The course of
the symptoms depends chiefly upon the nature of the lesion
which has caused the affection and varies greatly in different
cases. The lesion as a rule extends both longitudinally and
transversely, and only remains stationary in rare cases. When
the lesion extends transversely, paraplegia and the other symp-
toms of transverse myelitis result. As the inflammation sub-
sides the symptoms of the unilateral lesion may recur, and may
then continue unchanged for many years. Complete recovery
has occasionally been observed in traumatic unilateral lesions, and

368 TRAUMATIC DISEASES AND ABNORMALITIES OF

according to Brown-Se'quard the motor disturbances disappear
earlier and more completely than those of sensation. In tumour
the disease generally extends transversely, giving rise to para-
plegia.

§ 591. Diagnosis. — Hemiparaplegia, from lesion of one side
of the cauda equina, may be distinguished from that caused by
unilateral lesion of the cord by the circumstances that in the
former the paralysis and anaesthesia are on the same side, and
that, as a rule, only certain nerve territories of the lower extre-
mities are affected.

The hemiplegic form of lateral sclerosis is readily recognised
by the absence of all disturbances of sensation and of any
disorder of the bladder or rectum. Cerebral hemiplegia, may
be distinguished from the spinal form by the fact that in the
former there is either no disturbance of sensation or that it is
to be found on the same side as the paralysis, and that there is
unilateral paralysis of the face and tongue. The nature of the
lesion is not readily ascertained in the absence of any distinct
inj ury, and consequently the diagnosis must rest upon general
pathological principles.

§ 592. Prognosis. — The prognosis depends entirely upon the
nature of the lesion which causes the symptoms. The rnajority
of traumatic cases end in recovery with proper care and treat-
ment.

§ 593. Treatment. — The treatment is generally the same as
that which is applicable to wounds of the spinal cord and to
chronic myelitis.

(IV.) CONCUSSION OP THE SPINAL CORD.

(Commotio Spinalis.)

§ 594. Definition. — Concussion of the spinal cord includes
cases in which traumatic injuries occasion severe functional
disturbances without the production of recognisable changes.

§ 595. Etiology. — The most usual causes of spinal cot*-
cussion are falls upon the feet, or buttocks, and blows over the

TEE SPINAL CORD AND MEDULLA OBLONGATA. 369

back. Another common cause of the affection is the shock to
the whole body, occasioned by the sudden arrest of its motion
when it is passing at a rapid rate through space, such as occurs
in railway collisions. The persons who sit with their backs
towards the direction from which the shock comes suffer most
from spinal concussion in railway accidents.

The concussion may be limited to a portion of the cord when
the vertebral column has been struck, but in eases of shock to
the body the greater portion of the cord or the whole is affected.
Violent mental excitement appears to produce symptoms of
concussion of the cord, and lightning passing through the body
causes a general shock in which the spinal cord participates.

§ 596. Symptoms. — The symptoms vary according to the
nature of the injury, the degree of individual resistance, and
various other circumstances. The most usual symptoms of the
affection are feebleness of the extremities, amounting in some
cases to decided paralysis, parsesthesise of various kinds, pain
in the neck, loins, or along the spinal column, tenderness on
pressure of some of the spinous processes, some degree of cuta-
neous hyperesthesia, or more often anaesthesia, weakness of the
bladder, and considerable emotional disturbance.

§ 597. Varieties of Spinal Concussion. — The following
varieties may be distinguished : —

(1) Severe, form of Shock, giving rise to Aggravated Symptoms at once,
and Death in a short time. — The patient after the injury is found compa-
ratively paralysed in all his extremities, with distinct anaesthesia, great
prostration, and confusion of ideas or complete loss of consciousness and
involuntary evacuations. • The pulse is small, weak, and slow, the skin is
cool and pale or slightly cyanotic, and there may be respiratory distur-
bances amounting sometimes to dyspnoea. In a few hours or days death
occurs amid general prostration and paralysis of the respiration.

(2) Slight Shock causing Severe Symptoms at the moment of injury,
but soon ending in Recovery. —The patient is found immediately after the
accident more or less paralysed in the lower extremities and sometimes in
the upper also, and complaining of severe and general pain in the body or
in the lower half of it. Some degree of antesthesia is usually present, but
is not often complete, and the bladder is not always paralysed. Soon
after the accident the reflex functions, especially the tendinous reflex
actions, may be found exaggerated, and the electrical reaction in the

370 TRAUMATIC DISEASES AND ABNORMALITIES OF

paretic parts may be increased or depressed. Improvement begins in a
few days. The patient is able to stand and walk, at first slowly, feebly,
and with tremor ; the pains disappear, and recovery is complete in a few i
weeks.

(3) Severe Symptoms at first, followed by Protracted Illness of some
years' duration ; Recovery in most cases. — The patient complains of motor •
weakness soon after the accident, which gradually increases until the
extremities are paralysed. He also complains of painB •which are some
times more or less diffused, but are often situated in the back of the neck,
loins, or along the vertebral column. Various paraesthesise are com-
plained of, but anaesthesia is not usually well marked. Retention of '
urine sometimes occurs. There may be vomiting and loss of consciousness
at first, and patients often manifest a high degree of mental irritability
for a long time. The extremities are cold and livid, and the vertebral
column is tender on pressure and often excessively sensitive. Gradual
improvement now occurs, but the patient complains of great weakness ;
there may be slight atrophy of some of the muscles, and complete recovery
may not take place for several years, and the patient may remain irritable
and sensitive long after all the paralytic symptoms have disappeared.

(4) Very Slight Symptoms at tlie beginning, but after a longer or shorter
time a Severe Progressive Spinal Disease develops ; the Result is Doubtful.
These cases are usually caused by a railway collision, and the symptoms
are generally insignificant immediately after the injury. The patient
has a sensation of having been severely shaken, suffers from momentary
weakness and slight confusion of mind, but soon recovers, picks himself
up, and walks about. On the next day, or several days, weeks, or even
months later, more threatening symptoms set in. Pain appears in the
back and limbs, and gradually increases in intensity ; the patient feels
feeble, suffers from mental depression and sleeplessness, with a strong
tendency to emotional weakness, and cannot attend to his business.
He also often complains of noises in the ears, and there may be slight
deafness, and on attempting to read, the letters become confused. The
subsequent course of the disease varies greatly in individual cases, but the
following are the most usual phenomena observed : The gait is uncertain,
straddling, stiff, and dragging, indications of disturbed co-ordination are
present, and the legs become progressively feebler. There is stiffness of
the back and of the general attitude. The back is painful when moved,
and some of the spinous processes are tender on pressure. Girdle
sensations, parsesthesise of all sort3, anaesthesias in varying degrees and
in different situations, or hyperaesthesiae, may be present. Weakness
of the bladder and diminution of sexual power are generally present. The
expression of the countenance is changed, the complexion becomes pale
and sallow, and the general nutrition impaired. Marked atrophy occurs
in individual muscles and groups of muscles, and it may at times be ex-
tensively distributed. Disturbances of circulation manifest themselves in
the form of cold extremities and bluish complexion. The patient is irri-

THE SPINAL CORD AND MEDULLA OBLONGATA.

371

table and timid, suffers from a feeling of constriction of the head, sleep-
lessness, weakness of memory and intelligence, impaired power of work,
and in fact his whole character has undergone change.

The symptoms point to a meningo-myelitis, associated with more or
less considerable disturbances of the cerebral functions. The subsequent
course of the affection varies. Periods of apparent improvement and com-
parative health alternate with those of downward progress, but on the
whole a favourable termiuation is seldom witnessed. Cases, however,
occur in which the disease ceases to progress, and in which considerable
improvement may take place.

§ 598. Morbid Anatomy. — In cases which have terminated
fatally at an early period small extravasations of blood have been
found in the cord and its membranes, but it is probable that
these are of secondary importance to the molecular disturbance
of the whole substance of the cord produced by the shock. It
is probable that chronic meningitis and myelitis may develop
out of concussion, and then the usual appearances which dis-
tinguish these affections will be found after death.

§ 59.9. Diagnosis. — Cases of concussion in which severe symp-
toms develop immediately after the injury may be mistaken
for crushing or contusion of the cord, hsematomyelia, or hsetna-
torrhachis. The course of concussion, however, is much more
rapid and favourable. It may be inferred, when a severe para-
plegia comes to a favourable ending in a few days or weeks
without bed-sores or other grave symptoms, that the case is one
of concussion.

The initial symptoms are more severe in concussion than in
haematorrhachis, and in the latter affection the preponderant
symptoms are those of pain and spasm, and the paralysis is
slight, while in the former the opposite conditions obtain.

Cases of concussion, in which the symptoms are slight at first
and gradually increase in severity, are not essentially different
from myelitis and meningo-myelitis with a slow beginning, and
the diagnosis must depend in great measure on the connection
of the affection with an injury.

Crushing of the cord and concussion are frequently combined,
so that it is almost impossible to distinguish between the symp-
toms which are due to the one and those due to the other,

372 TRAUMATIC DISEASES AND ABNORMALITIES OF

and the diagnosis can only be made after the disappearance of [
the symptoms of concussion.

§ 600. Prognosis. — In the severest form of concussion known
as shock the prognosis is always grave, but the slighter cases of
the kind generally recover. Compared with the severity of the
symptoms the prognosis is good, and indeed the severe initial
symptoms seem to be the very cases to warrant a favourable
prognosis as compared with those the development of which is
slow.

Even in cases where symptoms of meningitis or myelitis
appear, the prognosis is not absolutely bad, but when, after one
or two years of rational treatment, no further progress is made,
recovery is hardly to be expected.

§ 601. Treatment. — The treatment must vary according to
the form assumed by the affection.

In cases with severe initial symptoms the treatment must
be first directed against the shock. The patient must be placed
in the recumbent posture, and warmth applied to the body, and
full doses of some stimulant, such as wine, coffee, tea, hot
spirit and water, or drugs like aromatic spirit of ammonia
ether, musk, and camphor, must be at once administered.

Symptoms of reaction must be treated by absolute rest
in a suitable position. If the patient cannot bear lying on his
face or side, Erichsen recommends him to lie on his back on a
couch tilted at its foot. The usual remedies for myelitis must
now be employed.

(V.) TUMOURS OF THE SPINAL CORD AND MEDULLA

OBLONGATA.

§ 602. Tumours are rarely found in the substance of the
spinal cord, but are more frequent in the medulla oblongata.

§ 603. Varieties of Tumours found in the Spinal Cord
and Medulla Oblongata. — The following are the more usual
tumours found in the substance of the cord and in the medulla
oblongata : —

1. Gliomata. — The tumour is generally of a rounded or more or less

THE SPINAL CORD AND MEDULLA OBLONGATA. 373

elongated shape, but at other times it may extend the whole length of the
spinal cord, as in a case recorded by myself.

2. Myxo-Cdiomata. — This form of tumour is only a variety of Glioma.

3. Olio-Sarcomata, Myxo-Sarcomata, Sarcomata, and Carcinomata are
only rarely found in the substance of the cord and the medulla oblongata.

4. Fibromata have been observed in the medulla oblongata, either
growing from the ependyma or in the medullary substance.

5. Solitary Tubercle. — This is one of the most frequent tumours of the
spinal cord. It may appear at any period of life, but is relatively more
frequent in youth than in old age. The favourite sites of solitary tubercles
are the cervical and lumbar enlargements, especially the latter. They
may be situated either in the grey or white substance, and vary in size
from that of a hemp-seed to a hazel-nut. Solitary tubercle may attain
to the size of a walnut in the medulla oblongata.

6. Gummata or Syphilomata. — These tumours are on the whole rarely
fouud in the cord and medulla oblongata.

7. The cystic dilatations, which have been called hydromyelus or
syringomyelia, may be reckoned amongst the tumours of the spinal cord
when they compress the nervous substance ; they are often associated
with new growths, such as gliomata, myxo-gliomata, and myxo-sarcomata.

§ 604). Etiology.— -The causes of tumours of the spinal cord
and medulla oblongata are very obscure, but it is probable
that injuries, such as blows or jars of the spinal column, may
act as exciting causes.

§ G05. Symptoms.

(1) Symptoms of Tumours of the Spinal Cord. — The symp-
toms caused by the growth of a tumour within the substance
of the cord are very variable, but are generally the same as
those of compression myelitis. They are paraplegia, anaes-
thesia, increased reflex action, paralysis of the bladder and
rectum, muscular atrophy, and bed-sores. The development of
paraplegia may be preceded by shooting pains in the limbs,
girdle pains, and various paresthesia?. Indefinite initial symp-
toms may persist for a long time, and then paralysis develop
suddenly, occasioned by an acute attack of transverse myelitis
or haemorrhage into the substance or neighbourhood of the
tumour. The development of paralysis proceeds at other times
more slowly. One limb, probably an upper extremity, becomes
first affected, the other extremities becoming gradually impli-
cated until the paraplegia is complete.

374 TRAUMATIC DISEASES AND ABNORMALITIES OF

In slowly-growing and dense tumours the nerve fibres appear
to be thrust aside without being ruptured, and extensive changes ]
may sometimes be found after death in the cord while only
very slight and indefinite symptoms existed during life. In a |
few cases the symptoms are caused by a diffused ascending:
myelitis, while in occasional instances the disappearance of the
reflex excitability and the occurrence of extensive muscular i
atrophy indicate that the grey substance has been destroyed I
by a secondary descending myelitis or by a descending exten-
sion of the new growth.

Various other symptoms may appear in the course of the
disease, according to the situation of the tumour and the direc-
tion in which it is growing. The chief groups of symptoms
which may be thus caused are progressive muscular atrophy,
ataxia, and spastic paralysis.

(2) Symptoms of Tumours of the Medulla Oblongata. —
Tumours in the substance of the medulla oblongata may
remain latent for a long time, and may either cause no
recognisable symptoms during life, or not until a few hours or
days before death, which results from asphyxia.

The most prominent of the initial symptoms are paroxysmal
attacks of headache, situated in the occiput or nucha," dizziness,
violent vomiting, tinnitus aurium, hiccough, and occasionally
epileptoid attacks. These symptoms persist and grow worse,
while others are soon superadded to them, the latter being
caused by compression of some of the fibres of the bulbar
nerves as they pass through the medulla, or by destruction of
portions of the bulbar nuclei. The most usual symptoms
caused by compression of the fibres of the nerve roots are
distortion of the face, unilateral and bilateral paralysis of the
tongue, internal squint, disorders of articulation, vocalisation,
and deglutition, a nasal tone of voice, and disorders of circu-
lation and respiration. There may also be more or less ex-
tensive paralysis of the extremities, consisting of unilateral
or bilateral paresis, with or without contractures. Hemiplegia,
alternating with paralysis of the facial, abducens, or hypo-
glossal nerves, forms a characteristic symptom. Reflex action
is often increased in the extremities.

Disorders of motor co-ordination have sometimes been

THE SPINAL CORD AND MEDULLA OBLONGATA.

375

observed, which may resemble those of locomotor ataxia, but
more commonly a cerebellar reel (§ 8G), probably caused by
interference with the peduncles of the cerebellum.

The sensory are not so well marked as the motor disturbances.
They generally consist of pain, and paramnesias in the nucha,
back, and extremities, and anaesthesia may occasionally be pre-
sent in the trunk and extremities. When the tumour or the
inflammatory action which surrounds it extends into the pons,
there may be paralysis of the masticatory muscles, hyperoes-
thesia, neuralgic pains, and subsequently anaesthesia of one or
both sides of the face, while one or both eyes may suffer from
neuroparalytic ophthalmia. Deafness on one or both sides may
be met with, and double optic neuritis, amblyopia or amaurosis
are almost constant accompaniments of the presence of tumour
within the cranial cavity.

Glycosuria and polyuria may be present, and the temperature
of the body is generally persistently depressed.

Psychical disturbances, such as loss of intelligence and
memory, have occasionally been observed at an early period, and
are almost constantly present towards the termination of the
disease. These symptoms are probably caused by the hydro-
cephalus internus which almost always accompanies tumours of
the medulla. The effusion into the ventricles may be, to some
extent, caused by the pressure of the tumour on the veins,
especially the venae galeni ; but probably depends rather upon
the hindrance offered by the tumour to the return of the cerebro-
spinal fluid into the sub-arachnoid space.

As the disease advances, the headache and paralytic symp-
toms grow worse, the vomiting and hiccough may become
incessant, epileptic attacks occur more frequently, coma super-
venes, and the patient dies from asphyxia.

§ 606. Localisation of the Tumour in the Cord and Medulla

Oblongata.

1. Tumours of ike Spinal Cord. — The level at which the cord is affected
can generally be made out by the height to which the paralysis extends,
and by the condition of the various cutaneous and deep reflexes. The
extent to which the grey substance is diseased, either by the invasion of
the tumour or by secondary myelitis, can be ascertained by the muscular
atrophy and other trophic affections associated with the paralysis ; while

376 TEAUMATIC DISEASES AND ABNORMALITIES OF

implication of the posterior or lateral columns may be respectively
recognised by the presence of ataxia or spastic paralysis.

2. Tumours of the Medulla Oblongata. — (a) Tumours in the anterior i
pyramids of the medulla produce unilateral or bilateral paralysis of the
muscles of the extremities and trunk, accompanied by contractures and
increased tendon reflexes. Paralysis of the bladder is sometimes super-
added, but sensibility remains unimpaired. In the later stages of the
disease the symptoms of bulbar paralysis are superadded.

(b) Tumours on the floor of the fourth ventricle may cause vomiting,
hiccough, glycosuria and polyuria, slow pulse, and respiratory disorders.
The symptoms which indicate paralysis of cranial nerves may be present,
but paralysis of the extremities if present at all is a late symptom. Sen-
sory disorders are rare, but some degree of ataxia or reeling may be present.

(c) Tumours of the restiform body may give rise to sensory disorders in
the extremities, unilateral anaesthesia in the face, auditory troubles, and
ataxic walk, but our knowledge of the symptoms caused by these tumours
is not sufficiently accurate.

(d) Tumours of the formatio reticularis and olivary bodies cause no
symptoms by which their presence can be recognised, except those com-
mon to intracranial growths. When, however, these tumours increase
to such a size that they compress the bulbar nuclei, the fibres of the bulbar
nerves in their passage through the medulla, or the anterior pyramids, the
grouping of the symptoms may be such as to render it possible to make
an accurate diagnosis of the localisation of the lesion. The following case,
for the notes of which I am indebted to Mr. Hodgson, who was then one
of the House Physicians of the Eoyal Infirmary, well exemplifies the
grouping of the symptoms which may take place from a tumour com-
mencing in the formatio reticularis : —

"William B , set. eight years, was admitted February 17, 1880, into

the Eoyal Infirmary, under the care of Dr. Ross. He is a well-nourished
boy for his years, and his mental faculties do not appear to be in any
way impaired. He complains of headache, and the occipital region is
sensitive to touch. Both eyeballs are inverted, the external recti muscles
being completely paralysed. The right pupil measures 5 and the left 3
mm., but both contract readily to light. There is slight facial paralysis
on the right -side extending to the eyelid of the same side, which cannot
be closed. The soft palate is loose and pendulous, and the uvula occupies
the middle line, until a reflex contraction of the palatal muscles is excited
when it assumes a curved form, the point being directed to the right
and the convexity to the left. There are no sensory disorders of the face or
body, no loss of taste, deafness, paralysis of the tongue, or recognisable
paralysis of the extremities. The reflex contractility of the right facial
muscles is diminished, but they still contract to a faradic medium current.
The galvanic contractility is also somewhat diminished, but there are no
qualitative changes. When the child stands his head is inclined to
the left, but it is difficult to know whether this attitude is due to

THE SPINAL CORD AND MEDULLA OBLONGATA. 377

paresis of the right sterno-cleido-mastoid muscle, or to a voluntary
effort to correct the false images caused by the double internal squint.
When he walks his gait is staggering, and he manifests a constant
tendency to fall towards the right side, yet there is no paralysis of the
right lower extremity. The cervical glands at the angles of the jaws
and along the sterno-mastoid muscles on both sides are slightly enlarged.
The heart and lungs are healthy. The urine is acid, s.G. 1026, contains no
albumen or sugar, and is normal in quantity. The reflex of the sole,
and the cremasteric, abdominal, epigastric, gluteal, and interscapular
reflexes are normal.

March 22. When the patient stands he reels from side to side, and
manifests a greater tendency to fall to the left than the right, and the
patellar-tendon reflex is more marked in the left than right leg. There is
also decided paresis of both the lower and upper extremity on the left
side. Ophthalmoscopic examination reveals double optic neuritis.

April 9. The left half of the body is distinctly paralysed, with mus-
cular rigidity, the right arm is feeble, and the patient cannot stand.
The face is now symmetrical, and there is decided loss of expression,
while both eyes remain open during sleep, and the patient cannot close
them. The power of articulation is interfered with, and the food has
to be placed far back on the dorsum of the tongue in order to secure
deglutition. The masticatory muscles are feeble, the jaw hangs loose,
the mouth is half open, and saliva dribbles constantly from the mouth.
The simple movements of the tongue can still be readily effected.

The mental faculties are becoming blunted, but so far as can be judged
the senses of taste and hearing are unimpaired, while even the sense of
sight is fairly good. Sensibility to pain and touch are impaired on both
sides of the face and in the limbs.

May 11. Since last report the paralytic phenomena have become
gradually worse. The left arm and leg are now completely paralysed,
while the right limbs are very feeble. There is double facial paralysis,
masticatory paralysis with contracture of the muscles so that the jaws
are held close together, and increasing difficulty of articulation and
deglutition. The right conjunctiva has been for some time red, and
covered by tenacious secretion, and the cornea is now becoming cloudy.
The patient has had an attack of severe vomiting about two weeks ago,
but it has not recurred.

May 20. Since last report the symptoms have become gradually worse.
All the limbs are paralysed, the right cornea is ulcerated, while the left
conjunctiva is injected and covered by tenacious secretion. Inability to
swallow was manifested this morning, and he died in the afternoon from
arrest of respiration.

At the autopsy no changes worth noting are observed in the nervous
system with the exception of the medulla oblongata and pons. On the
fourth ventricle being exposed, a tumour is observed to project from its
surface on a level with the striae medullares. It is about the size of a

378 TRAUMATIC DISEASES AND ABNORMALITIES OF

pigeon's egg, and the greater portion of it lies to the right of the median
raphe*, while it projects forwards into the substance of the medulla and
pons. Two tumours, each about the size of a hazel-nut and occupying
symmetrical positions on each side of the middle line, are observed in
the upper part of the ventricle immediately under the valve of Vieussens.
A few scattered miliary tubercles are found in the apices of the lungs.
The tumours in the pons were tubercular.

Dr. Leech, who kindly transferred this case to my care, told me that
the symptoms began by internal squint of the right eye, and staggering
gait, with a tendency to fall to the right side, these symptoms being
followed by right facial paralysis. The symptoms were so definite in this
case that an accurate diagnosis could readily be made. The headache,
gradual invasion of the symptoms, and the presence of double optic neuritis,
showed that the case was one of intracranial tumour, while the swelled
glands in the neck, and other circumstances, indicated its probable
tubercular nature. The succession of the various groups of bulbar
symptoms were so definite that there could be no possibility of mistaking
the localisation of the main focus of disease. The early paralysis of the
external rectus of the right side showed that the primary focus began on
a level with the sixth nerve, and to the right of the median raphe.
Suppose, then, that the tumour began to grow in the formatio reticularis
on the right side {Fig. 185, ar) on a level with the sixth nerve (rvi), and

Fig. 185.

Fig. 185. Transverse Section of the Pons on a Level with the Points of Origin of the
Sixth and Seventh Nerves. (See Fig. 126, p. 40.)

THE SPINAL CORD AND MEDULLA OBLONGATA. 379

that it grew equally in all directions. It would first produce paralysis of the
right external rectus, and as it grew forwards it would press on the trans-
verse fibres of the pons, and produce reeling, with a tendency to fall to
the ri^ht, or the symptoms which would have been caused by disease of the
middle peduncle of the cerebellum. As the tumour enlarged to the right
it would press on the fibres of the seventh nerve (itvn), and cause
paralysis of the right muscles of the face, having the characters of a
peripheral paralysis. As it grew towards the left it would press on the
left sixth, and then on the left seventh nerve, causing successively in-
ternal squint of the left eye and left facial peripheral paralysis. As it
grew still further forwards it would compress the fibres of the pyramidal
tract, first on the right side, causing crossed paralysis of the left ex-
tremities, and then on the left tract (Fig. 185, P, p), causing paralysis
of the extremities on the right side.

Again as the tumour extended downwards it would compress the ninth,
tenth, twelfth, and probably also the eleventh nerves, and so give rise to the
more purely bulbar symptoms present, such as the vomiting, and disorders
of articulation and deglutition. As it extended upwards it would compress
the motor and to some extent the sensory divisions of the fifth nerves,
causing the masticatory paralysis, the facial sensory disturbances, and the
neuro-paralytic ophthalmia. Not only was an accurate localisation of the
lesion capable of being made in this case, but we were even able to anticipate
to a large extent the later symptoms which supervened. When paralysis
of the left rectus occurred, we were able to foretell that it would soon be
followed by peripheral paralysis of the left side of the face. It was also
possible to anticipate that left hemiplegia would supervene, which
would end in general paralysis if the patient survived long enough,
and that the upward and downward extensions of the tumour would give
rise to motor and sensory disturbances in the region of the fifth on the one
hand, and difficulties of articulation and deglutition on the other.

§ 607. Course, Duration, and Terminations. — The course
of intramedullary tumour is usually very protracted, and the
patient may live for many months after complete paraplegia
is established. Intramedullary tumours are, with the exception
of gummata, uniformly fatal. Death may be caused by cystitis,
bed-sores, and their consequences, arrest of respiration when the
myelitis takes an ascending course, or intercurrent disease.

Tbe course of tumours of the medulla oblongata is probably
uniformly fatal. The disease may, however, extend over a
period of years, with considerable variations in the intensity of
the symptoms, but, as a rule, it proceeds uninterruptedly to a
fatal termination.

380

TRAUMATIC DISEASES OF THE SPINAL CORD.

§ 608. Diagnosis. — It is not always possible to make a decided
diagnosis; but the presence of a tumour may be suspected
when the intensity of the paralytic symptoms fluctuate, or
when symptoms of central myelitis or hsematomyelia supervene
upon those of a long-continued and insidious spinal affection.
Evidence of scrofula, tuberculosis, or syphilis may greatly aid
the diagnosis. The initial symptoms of irritation are generally
of less intensity in intramedullary than meningeal tumour, and
the former is more apt to give rise to an ascending myelitis
than the latter.

Tumour of the medulla oblongata may be recognised with
some certainty when the general symptoms of an intracranial
growth are accompanied by signs of local irritation or paralysis
of some of the bulbar nerves, and when in addition there are ob-
stinate vomiting, hiccough, glycosuria, or polyuria. When ataxia
or reeling is a prominent symptom of tumour of the medulla
oblongata, or when tumours of the cerebellum implicate the
medulla secondarily, it may be impossible to distinguish
tumours in the two regions. If, however, the patient has been
under observation from an early period of the disease, the
mode of invasion and succession of the symptoms generally
enables the diagnosis to be accurately made.

In progressive bulbar paralysis the regular symptoms of
tumour of the medulla oblongata, such as headache, vomiting,
hiccough, disorders of hearing, glycosuria, amblyopia, epilepti-
form convulsions, and double optic neuritis, are never present.

It may be impossible to distinguish tumours in the substance
of the medulla from those which grow in the membranes or
surrounding bones, but signs of irritation and paralysis in the
region of distribution of the cranial nerves are probably less
prominent in the former than in the latter.

§ 609. Prognosis. — Except in the case of syphilitic gummata,
the prognosis is absolutely unfavourable.

§ 610. Treatment. — It is only when syphilis exists that treat-
ment is of any avail, when large doses of iodide of potassium
should be promptly administered. In other cases the treatment
should be the same as that of acute and chronic myelitis.

381

CHAPTER IX.

DISEASES OF THE MEMBRANES OF THE SPINAL CORD
AND MEDULLA OBLONGATA.

(I.) VASCULAR DISEASES OF THE MEMBRANES.

1. Hypercemia of the Spinal Membranes.

§ 611. Hyperaemia of the spinal membranes cannot be sepa-
rated from hyperaemia of the spinal cord, and has already been
sufficiently considered.

2. Hazmatorrhachis — Meningeal Apoplexy.

§ 612. Haematorrhachis implies any effusion of blood in,
about, or between the spinal meninges.

§ 613. Etiology. — The disease is more frequently observed
in men than women, but very little is known with respect to
the predisposing causes of the affection.

The most usual exciting causes are injuries of the spinal
column, such as fractures and contusions. Caries of the
vertebrae has in some cases led to injuries of the vessels of
the cord and to haemorrhage from them. Excessive bodily
exertion, the violent spasms of epilepsy, eclampsia, and tetanus,
the sudden suppression of accustomed discharges, and all the
circumstances which induce spinal hyperaemia may act as exciting
causes of meningeal apoplexy.

Meningeal haemorrhage may occur in scorbutus, purpura
haemorrhagica, smallpox, and typhoid fever and other acute
infectious diseases. Aneurisms have been frequently known to
rupture into the vertebral canal, and blood effused into the
brain or cerebral membranes may sometimes pass down into
the spinal canal.

382

DISEASES OF THE MEMBRANES OF THE

§ 614. Symptoms. — The disease begins suddenly. The pa-
tient is attacked with violent pains and falls down, but generally
without loss of consciousness. The development of the disease is
occasionally slower and more gradual, and premonitory symp-
toms, such as lumbar pains and headache, may then be present.
The severity of the symptoms may increase after a few hours
or days.

The characteristic symptoms are those of irritation and sub-
sequent paralysis. The phenomena of irritation consist of a
violent pain, localised at a spot corresponding to the seat of the
haemorrhage and radiating in various directions along the dis-
tribution of the nerves, the roots of which are first implicated.
Eccentric sensations, such as pain, formication, burning, and
tingling, are associated with the local pain, and hyperassthesia
is also mentioned as being occasionally present.

The chief symptoms of motor irritation are spasmodic jerking
of the muscles which may sometimes increase to general con-
vulsions, trembling of the extremities, and tonic spasm and
contracture of various groups of muscles. During this stage the
vertebral column is stiff and painful, so that it is impossible for
the patient to raise himself in bed or to assume the sitting
posture.

Paralytic symptoms, however, soon supervene in the lower ex-
tremities, but seldom amount to complete paraplegia. There
is also a more or less distinct anaesthesia of the lower extremi-
ties, associated with feelings of furriness and numbness, as well
as with sensations of swelling and heaviness in the limbs and
trunk. The distribution of the symptoms depends upon the
seat of the lesion.

Reflex excitability is said.to be depressed in some cases, but
probably this only occurs in the regions supplied by the nerve
roots directly affected. Weakness of the bladder and rectum is
rarely mentioned, but maybe present in severe cases. Fever is
absent at first, but may occur during the irritative reaction
which sets in on the second or third day.

§ 615. Varieties of Meningeal Hcemorrhage.

(1) "When the cervical region is affected, the attack begins with pain in
the arms and shoulders, stiffness in the neck, and pain in the occiput.

SPINAL CORD AND MEDULLA OBLONGATA.

383

The anresthesia and paralysis are most marked in the upper extremities,
and oculo-pupillary symptoms, difficulty of breathing, and a retarded and
weak pulse may be present.

(2) When the dorsal region is affected, there is pain in the back and
abdomen, girdle-pain, stiffness in the dorsal part of the spine, paralysis
of the legs and abdominal muscles, while the reflex excitability is retained
iu the lower extremities.

(3) When the lumbar region is affected, there are pain and stiffness in
the loins, tearing pains in the lower extremities, perinaourn, bladder, and
genitals, well marked paralysis of the lower extremities with loss of reflex
activity, and paralysis of bladder and rectum.

§616. Course and Terminations — The symptoms remain
stationary for some time, but improvement usually sets in
sooner or later. The symptoms of inflammatory reaction are
seldom prominent or soon disappear. The disease usually runs
a favourable course when it is uncomplicated, and in a few weeks
or months a tolerably good recovery may be anticipated. Death,
however, is not a rare occurrence when the haemorrhage occurs
at a high level so as to affect the respiratory centres. If the
extravasation be large, the severity of the compression may lead
to complete paraplegia, cystitis, bed-sores, and their usual con-
sequences.

§ 617. Diagnosis. — The diagnosis must be founded on the
sudden occurrence of the illness, the peculiar combination of
phenomena of irritation and paralysis, the absence of severe
cerebral symptoms, the paraplegic character of the symptoms,
the speedy improvement, and usually favourable termination.
Meningeal haemorrhage may be distinguished from concussion
of the spinal cord by the absence of spasm and other symptoms
of irritation in the latter. From spinal apoplexy the meningeal
affection may be distinguished by the severity and suddenness
of the paralysis and the high degree of anaesthesia in the former.

Both meningitis and myelitis develop more slowly than
meningeal haemorrhage, and both are accompanied by fever.
In central spinal myelitis marked anaesthesia is never wanting,
and paralysis is usually complete from the beginning.

§ 618. Prognosis. — The prognosis is always doubtful; but if
the extent of the haemorrhage be not great, and if it be not

384

DISEASES OF THE MEMBRANES OF THE

caused by a permanent lesion, such, as the growth of a tumour,
improvement and complete recovery may take place. When
the haemorrhage is considerable, or when it is situated in the .
cervical region, or if the symptoms of myelitis supervene, the
prognosis becomes unfavourable. When, on the other hand,
the haemorrhage is small, the reaction moderate, and the patient
young, the prognosis is favourable.

§ 619. Treatment. — When the symptoms of meningeal
haemorrhage have occurred, absolute rest in the horizontal
posture, with the patient lying on his side or face, should
be maintained. The primary object is to prevent the bleeding
from extending, the most usual remedy being application of ice
to the vertebral column, and ergot may be given internally
when symptoms of inflammatory reaction set in. Leyden recom-
mends mercurial inunction and repeated small doses of calomel.
When the period of reaction has passed, absorption may be
promoted by the external and internal use of iodine, and the
galvanic current.

(II.) INFLAMMATION OF THE SPINAL DURA MATER.

Pachymeningitis Spinalis. Peri-meningitis.
§ 620. Pachymeningitis may be subdivided into two varieties :
(1) External pachymeningitis, when the morbid products are
deposited in the loose cellular tissue between the dura mater
and vertebrae; and (2) Internal pachymeningitis, when the
inner surface of the dura mater is attacked.

(i.) Pachymeningitis Spinalis Externa. Peri-pachxmeningitis.

External pachymeningitis consists of inflammation of the
outer layers of the dura mater and the cellular tissue sur-
rounding it.

§ 621. Etiology. — Various diseases in and about the verte-
bral column, such as vertebral caries and bed-sores, constitute
the most frequent causes of the affection.

§ 622. Symptoms. — Pain in the back, which varies in its seat
and extent according to the locality of the lesion, is one of

SPINAL CORD AND MEDULLA OBLONGATA.

385

the most constant and important symptoms of the affection.
Rigidity of the back, which renders it difficult and painful for
the patient to sit up, spasm of various groups of muscles, eccen-
tric pains in the form of a girdle or shooting into the extremi-
ties, formication and slight hyperesthesia of the skin, are the
usual symptoms complained of.

After a time symptoms of compression of the cord are gradu-
ally superadded. Both sensory and motor paralysis may occur
slowly or suddenly, and muscular tension, increased reflex action,
especially increased tendon reflex, paralysis of the sphineters, and
bed-sores appear after a time. These symptoms are caused
partly by local compression of the cord and partly by myelitis
and secondary degenerations.

The symptoms may develop in an acute or chronic form. In
the acute purulent forms the prominent symptoms are caused
by irritation, while in the chronic fibrinous form the symptoms
of compression and paralysis of the cord predominate.

§ 623. Course. — When pachymeningitis externa accompanies
caries of the vertebrae the disease is frequently arrested and the
paralytic symptoms disappear. In the severer cases its course
may vary, but is usually protracted, and only after the lapse of
many weeks is there a termination in recovery or death.

§ 624. Morbid Anatomy. — The essential nature of the
affection consists of an inflammation of the outer layers of the
dura mater and surrounding cellular tissue, with exudation of a
purulent, plastic, or tuberculous nature. The exudation has
been found as much as half an inch in thickness. The inner
surface of the dura is also thickened and opaque, and frequently
covered with a thin fibrinous deposit. The pia mater and
arachnoid do not often participate in the affection, but they
have at times been found adherent to the dura, opaque, and
infiltrated with pus. The morbid changes are usually limited
to a small portion of the cord, even when they extend over the
greater part of the dura mater.

The cord itself is more or less compressed, flattened, anaemic,
and often softened. Ked softening and hyperaemia are found
in the neighbourhood of the compressed portion, and in chronic
z

386

DISEASES OF THE MEMBRANES OF THE

cases ascending and descending secondary degenerations are
observed. The nerve roots which pass out at the seat of the
pachymeningitis are compressed and atrophied, or inflamed and '
soft. The primary lesion which has produced the pachymenin-
gitis will of course be found on post-mortem examination.

§ 625, Diagnosis. — The diagnosis is chiefly founded on the
slowly-increasing symptoms of meningeal irritation and of com-
pression of the cord. Valuable aid to diagnosis may be obtained
by the discovery of abscess or the other morbid changes near
the vertebral column.

§ 626. The Prognosis depends upon the nature of the
primary lesion which has caused the pachymeningitis.

§ 627. Treatment.— The first aim of treatment is to remove
the effects of the original lesion. The use of brine baths, iodide
of potassium and iodide of iron, frictions with mercurial oint-
ment, and various other remedies have been employed, and
Charcot recommends the use of the cautery for obstinate cases.

(ii.) Pachymeningitis Interna (Hypertrophica et Hemorrhagica).
§ 628. Definition. — Internal pachymeningitis is an inflam-
mation chiefly of the inner surface of the dura mater, with
deposition of morbid products between the dura mater and
arachnoid. There are two forms of the disease : (1) Pachy-
meningitis interna hypertrophica, consisting of thickening of
the dura mater; and (2) pachymeningitis interna hemorrhagica,
or hematoma of the spinal dura mater, consisting of the forma-
tion of successive pseudo-membranous layers, between which
blood is effused.

§ 629. Etiology. — -The causes usually assigned to the hyper-
trophic form are exposure to cold and damp, and excessive use
of alcohol.

The hemorrhagic form often accompanies hematoma of the
cerebral dura mater, and is produced by the same causes. It is
often associated with dementia paralytica and other mental dis-
orders. It appears sometimes to result from alcoholic excess,
and Leyden has described a traumatic form.

SPINAL CORD AND MEDULLA OBLONGATA.

387

§ 630. Symptoms. — The hypertrophic form usually occurs
in the cervical region, and has been described by Charcot
under the name of pachyme'ningite cervicale hypertrophique.
During the first stage of the disease, which lasts two or three
months, the symptoms of sensory irritation predominate. The
most usual of these symptoms are neuralgiform pains in the
neck and head, which extend to the shoulders and arms, and
a painful sensation in the upper part of the chest, as if the
patient were bound by a tight cord. The muscles of the neck
are in a state of spasmodic rigidity, the patient often complains
of formication and numbness of the upper extremities, and
cutaneous trophic disturbances, such as vesicular and herpetic
eruptions, may make their appearance on the upper extremities.

The transition to the second stage is characterised by the
gradual development of paralysis and muscular atrophy. At
first there is simply paresis of the extremities, which after a
time becomes developed into a more or less complete paralysis,
with flaccidity of the affected muscles. In the upper extremities
the paralysis often predominates in the muscles supplied by the
ulnar and median nerves, while those supplied by the musculo -
spiral nerve are comparatively spared. The consequence of
this mode of distribution of the paralysis is that the hand is
maintained in the position of exaggerated extension, the
phalanges are flexed on the metacarpal bones and upon one
another, so- that the fingers are held like claws, and the thumb

Fig. 186.

Fig. 186 CAfter Charcot), Attitude of the Hand in Pachymeningitis Cervicalis
Hypertrophica, when the disease is situated on a level with the lower half of the
cervical enlargement of the spinal cord.

388

DISEASES OF THE MEMBRANES OF THE

is extended (Fig. 186). This position of the hand is not, how-
ever, so much a sign of the disease as it is of its locality.
When this deformity is present, the lesion is situated in 1
the lower half of the cervical enlargement of the cord, and
the distortion indicates that the roots of the ulnar and me-
dian nerves stand at a lower level in the cord than those of
the musculo-spiral nerve. When the disease is situated in the
upper cervical region and implicates the upper portion of the
cervical enlargement, the resulting deformity differs greatly from
that just described. The distortion of the hand present under
those circumstances is shown in (Fig. 187), taken from a
photograph, of a remarkable case under the care of Dr. Leech.
The arm is held close to the side, the forearm is extended on
the arm and strongly pronated, the hand is flexed on the
forearm, the fingers are in a line with or only slightly extended
on the metacarpal bones, and the phalanges are extended upon
one another, while the thumb is flexed into the palm (Fig. 187).

Fig. 187.

Fig. 187. Attitude of the Hand in Pachyvieninyitis Cervicalis Hypertrophica, when
the lesion is situated on a level with the upper half of the cervical enlargement.

All the muscles of the forearm and hand were no doubt more
or less paralysed in this case, but it will be seen that the
muscles supplied by the musculo-spiral nerve were on the
whole more affected than those supplied by the ulnar and
median nerves.

The paralysis is accompanied by marked atrophy and loss of
the faradic contractility of the affected muscles. After a time

SPINAL CORD AND MEDULLA OBLONGATA.

389

muscular tension and contractures appear in the paralysed
muscles, and circumscribed areas of ana3sthesia may be ob-
served in the skin of the upper extremities. At a later period
the lower extremities become paralysed, and contractures with
increase of the tendinous reflexes appear after a time in the
muscles, similar to that which occurs in primary lateral sclerosis.
The muscles of the lower extremities do not undergo atrophy
like those of the upper extremities, or at least not until a late
period of the disease. In severe cases complete paraplegia, with
marked anaesthesia, paralysis of the bladder, and bed-sores
arise, leading to a fatal termination.

The symptoms are at first due to compression of the cord by
the dura mater contracting around it and to transverse myelitis
at the spot compressed, and at a later period to descending
degeneration of the pyramidal tracts. This form of the disease
has a resemblance to progressive muscular atrophy, amyotrophic
lateral sclerosis, and other diseases attended by atrophy. The
most important points of distinction are the stage of pains, the
partial anaesthesia, and the paraplegia without atrophy.

In hcemorrhagic pachymeningitis interna the symptoms are
very obscure, and usually complicated with those of co-existing
cerebral disease. They point to a slow meningitis, and consist
of pains in the loins and back, tearing pains in the extremities,
stiffness of the vertebral column, increasing muscular weakness
which may gradually develop into complete paraplegia, contrac-
tures, various degrees of cutaneous hypersesthesia and anaes-
thesia, and weakness of the bladder. If a patient with these
symptoms be at the same time suffering from cerebral para-
lysis and chronic alcoholism, haemorrhagic pachymeningitis may
be suspected.

The diagnosis is not readily made in this form of the affection.

§ G31. Morbid Anatomy. — In the hypertrophic form the
dura mater is much thickened and consists of a large number of
concentric layers of cicatricial connective tissue. The pia mater
and arachnoid are also thickened and adherent to the dura
mater. The thickened membrane may compress the cord on one
side, or from behind forwards, but usually embraces it like a
ring. The compressed portion of the cord is pale and soft, and

390

DISEASES OF THE MEMBRANES OF THE

generally presents all the characteristics of transverse myelitis.
The nerve roots on a level with the lesion are compressed, and
the muscles supplied by the nerves issuing from them are in a
condition of degenerative atrophy.

Fig. 188.

Fig. 188 (From Charcot and Joffroy). Transverse Section of the Middle of the Cer-
vical Enlargement, from a case of Hypertrophic Cervical Pachymeningitis. — A,
Hypertrophied dura mater; B, Roots of the nerves traversing the thickened
membranes ; C, Pia mater adherent to the dura mater ; D, Lesion of chronic
myelitis ; E, Cystic formation in the grey substance.

In the hcemorrhagic form a portion of the dura mater is
covered by a soft, rusty-brown exudation composed of fibrine
and connective tissue, and studded with numerous hsemorrhagic
extravasations. The exudation contains numerous blood-crystals,
pigment, detritus of decomposed blood, and is only slightly
adherent to the dura mater or arachnoid, so that it is readily
stripped off.

§ 632. Treatment. — The treatment is the same as that of
meningitis in general.

In the chronic form counter irritation, preparations of iodine,
galvanism, and the use of baths or the cold water treatment
deserve a trial.

(III.) INFLAMMATIONS OF THE PIA MATER AND SPINAL

ARACHNOID.

Leptomeningitis Spinalis — Perimyelitis and Arachnitis.

§ 633. Spinal leptomeningitis presents many varieties, but
for practical purposes it is sufficient to subdivide the disease
into the acute and chronic forms.

SPINAL CORD AND MEDULLA OBLONGATA.

391

(i.) Leptomeningitis Spinalis Acuta.

The acute variety begins suddenly with violent sensory dis-
turbances, attended by marked fever.

§ 634. Etiology. — The predisposing causes of the affection
are a scrofulous or tubercular constitution, insufficient food,
damp dwellings, and sexual and other excesses. The disease
attacks by preference children, young persons, and the male sex.

The most important of the exciting causes are exposure to
cold, wounds and injuries of the vertebral column, and exten-
sion of inflammation from neighbouring structures. Tubercular
basal meningitis is usually accompanied by a spinal affection
of the same nature. Spinal meningitis may occur along with
or during convalescence from pneumonia, acute articular rheu-
matism, and other febrile and infectious diseases. Epidemic
cerebro -spinal meningitis will be subsequently described.

§ 635. Symptoms. — Acute spinal meningitis is generally
complicated by a simultaneous affection of the cerebral pia
mater, so that it is not always easy to separate the purely
spinal from the cerebral symptoms.

The disease begins suddenly, but the outbreak of the cha-
racteristic phenomena may be preceded by premonitory symp-
toms, such as general heaviness and depression, slight chilliness,
gastric disturbances, transitory pains in the head and back,
restlessness, and sleeplessness.

The characteristic symptoms of the disease are ushered in
by a rigor followed by pyrexia of irregular type, and if the pia
mater of the brain be affected, vomiting and severe cerebral
symptoms are also present. The patient now complains of an
intense, deep-seated, boring pain in the loins, back, or nape of
the neck, corresponding to the localisation of the lesion. The pain
is increased by movements of the vertebral column and by pres-
sure on the spinous processes. The pain is subject to remissions,
followed by exacerbations of great severity, and radiates from
the vertebral column round the trunk, shooting in all directions
through the extremities.

The muscles of the vertebral column are in a state of spas-

392

DISEASES OF THE MEMBRANES OF THE

modic rigidity. When the inflammatory process is limited, the
rigidity may be limited to certain portions of the vertebral
column corresponding to the situation of the lesion, but the 1
spasm may extend over the whole length of the spine, so as to
resemble a tetanic seizure.

The muscles of the extremities are also subject to painful
tension and spasm. The limbs are then rigid and immovable
or the subjects of painful twitchings.

Cutaneous and muscular hypersesthesia is often present in
the extremities and trunk in places corresponding to the areas
of distribution of the nerves whose posterior roots are involved
in the inflammation. Reflex activity is at first increased and
subsequently diminished.

Functional disturbances of the bladder and rectum appear at
an early period of the disease, probably owing to a spasm of the
sphincters. When the cervical part of the cord is involved in
the inflammation the muscles of respiration become rigid and
painful, producing difficulty of breathing, which may increase
to such an extent as to cause asphyxia.

When the cerebral pia mater is implicated the patient may
suffer from vertigo, violent headache, delirium, unconsciousness,
and coma. These may occur at an early or late period of the
disease, and usually indicate a fatal termination.

As the disease progresses symptoms of sensory and motor
paralysis supervene, although those indicative of irritation may
for a time be variously combined with them. Cutaneous
sensibility becomes diminished and complete anaesthesia may be
established, while the extremities manifest various degrees of
motor weakness up to complete paralysis. When the lesion is
situated high up, paralysis of the respiratory mechanism may
lead to a fatal termination, and the Cheyne-Stokes respiration
has been repeatedly observed towards the fatal termination.
The pupils may be contracted, dilated, and unequal. In fatal
cases deep coma supervenes, accompanied, by a rapid elevation
of temperature.

At other times deceitful signs of temporary improvement
appear, but paralysis and bed-sores supervene, and death follows
after long suffering. Sometimes, however, there is real improve-
ment, and slight cases may speedily recover, but in most instances

SPINAL CORD AND MEDULLA OBLONGATA. 393

convalescence is slow and the symptoms of sensory and motor
irritation only disappear after a long period.

Incurable defects are often left behind, such as anaesthesia
of variable degree and extent, and paralysis of individual
muscles, groups of muscles, or of entire extremities. The
muscular paralysis may be associated with atrophy and con-
tractures. The symptoms which indicate sclerosis of single
columns of the cord, such as ataxia and spastic paralysis, may
sometimes become permanently established.

If the inflammation extend to the medulla oblongata or to the
base of the cranium, the characteristic symptoms, vomiting, head-
ache, delirium, and paralysis of the ocular muscles, supervene.

§ 636. Course, Duration, and Termination. — In cerebro-
spinal meningitis death occurs early, occasionally within a few
hours, but more usually it is postponed for a few days. In less
violent cases the duration may be two or three weeks, and the
severity of the symptoms fluctuates greatly.

In other cases the acute symptoms subside and the disease
assumes a chronic form which is usually associated with mye-
litis. Cystitis and bed-sores supervene, and the patient dies
from exhaustion.

In mild cases the threatening symptoms may disappear
rapidly and the patient speedily recover. But convalescence is
as a rule protracted even when the patient ultimately makes
a complete recovery, but in a large number of cases a certain
amount of paralysis and anaesthesia remains.

§ 637. Morbid Anatomy. — The morbid changes found in
acute spinal meningitis may be subdivided into three groups,
according to the period of the disease : — (1) A stage of hyper -
aemia and commencing exudation; (2) a stage of serous, purulent,
or fibrinous exudation ; (3) a stage in which chronic changes are
established.

(1) In the first stage the pia mater is congested, of a rosy
or a dark red tint, and dotted with haemorrhagic extravasations.
The tissue is swollen, infiltrated with serum, and the cerebro-
spinal fluid is slightly turbid. The arachnoid is also congested,
and the hyperaemia extends to the cord and to the dura mater.

394

DISEASES OF THE MEMBRANES OF THE

(2) In the second stage the spinal fluid becomes more and
more turbid, and fibrinous flakes and plates are found in the
subarachnoid tissue or adhering to the surface of the dura mater. ,
The pia mater becomes more and more opaque, and the sub-
arachnoid tissues are transformed into a gelatinous mass. The
exudation becomes more and more purulent, and at last the
whole pia mater and subarachnoid tissues are infiltrated with
pus. The spinal fluid assumes a sero-purulent appearance and
contains numerous flakes of fibrin e.

Small miliary nodules maybe found in some cases distributed
along the course of the vessels of the pia mater, constituting
tubercular spinal meningitis.

The distribution of the exudation varies greatly. It usually
covers the greater part or the whole of the cord, but the posterior
surface is affected in a greater extent than the anterior, and
the changes are sometimes limited to a small portion of the
cord. The exudation not unfrequently extends from the spinal
canal into the brain, and the arachnoid is always involved in
the inflammatory action. It is thickened, opaque, infiltrated
with serum or pus, and often abounds with grey miliary tubercles,
while the subarachnoid tissue is similarly affected.

The dura mater is often hyperaemic, opaque, and covered with
thin fibro-purulent exudation. The nerve roots are almost
always involved, they are enveloped in thick masses of exuda-
tion, and are often swollen and softened. The cord itself is pale
and cedematous, or congested, and is usually softened either at
limited spots or diffusely.

(3) In the third stage chronic changes supervene and become
permanent, the most common of these being opacity and
thickening of the spinal membranes, adhesions, accumulations
of fluid in the arachnoidal space (hydrorrhachis), and sclerosis
and atrophy, either diffused through the cord or affecting
isolated portions or systems. In cases where absorption has
taken place, there is, of course, no third stage.

§ 638. Morbid Physiology. — The pains in the back, eccen-
tric pains in the extremities, hyperassthesia, and muscular rigidity
and twitchings are caused by irritation of the posterior and
anterior roots of the nerves. The sensory and motor paratysis

SPINAL CORD AND MEDULLA OBLONGATA. 395

which characterises the second stage of the disease is caused
by the compression of the nervous tissues occasioned by the
exudation. Implication of the anterior roots and anterior grey
horns explains the muscular atrophy which is sometimes
observed, while affection of the posterior grey horns in the
lumbar region accounts for the paralysis of the bladder and
rectum, cystitis, and bed-sores which are sometimes present, while
extension of the morbid process to the upper part of the cervical
region causes the disturbances of respiration which occur.

§ 639. Diagnosis. ^The general evidences of the disease
are fever, pain and rigidity of the back, stiffness of the neck,
muscular spasms, cutaneous hyperesthesia and paresthesia,
pains in and paralysis of the limbs, retention of urine, consti-
pation, and dyspnoea.

When the membranes of the brain are implicated, the cerebral
symptoms will of course constitute the most prominent feature
of the disease.

It is not always possible to distinguish acute spinal meningitis
from acute myelitis, inasmuch as the two affections are often
combined. Stiffness in the back and neck, eccentric pains in
the limbs, and hyperesthesias are characteristic of acute spinal
meningitis ; while sensory and motor paralysis predominate in
myelitis.

In tetanus cerebral symptoms are always absent, there is
no hyperesthesia of the skin, and reflex excitability is very
greatly exaggerated. The presence of the risus sardonicus and
the early occurrence and severity of the tetanic spasm in
tetanus render the diagnosis between it and spinal meningitis
as a rule easy.

The diagnosis of the tubercular form of the disease must rest
chiefly on general considerations, such as the evidence of scrofula
or tuberculosis of other organs. It is probably always associated
with tubercular basilar meningitis ; so that the presence of the
cerebral symptoms characteristic of that affection may be of
use in clearing up the diagnosis of the spinal disease.

§ 640. P rognosis. — The prognosis varies greatly in different
cases. Hyperacute and tubercular meningitis, and that caused

390

DISEASES OF THE MEMBRANES OF THE

by deep bed-sores, are always fatal. The prognosis is more
favourable in rheumatic and traumatic cases. The prognosis \
is unfavourably influenced by the following circumstances : very '
young or advanced age, implication of the cervical portion of '
the cord, early symptoms of paralysis, signs of exhaustion, high
fever, progressive rise of temperature and frequency of pulse,
great difficulty of breathing, and severe cerebral symptoms.

§ 641. Treatment. — In the early stage of the affection energetic
antiphlogistic treatment must be adopted. The main remedies
of this class are blood-letting and the application of cold. Local
blood-letting will generally suffice, and cold must be applied
sedulously by means of Chapman's ice-bags. A smart purgative,
such as the compound jalap powder or the aperient saline waters,
may also be administered.

When the temperature has fallen slightly blisters may be
applied along the spine, and in the milder cases weaker counter-
irritants may be adopted. Mercury is very useful in the treat-
ment, the inunction being the best method of application. From
fifteen grains to a drachm of the ointment should be rubbed
daily into the back and extremities. The patient should be
placed in a quiet, airy, moderately-warmed room, and kept lying
in the recumbent posture on his side and face, and should be
prevented from using any exertion. Nourishment should be
fluid, easily digestible at first, but care must be taken to allow
a more generous diet at an early period of the disease.

Various symptoms require to be treated during the course of
the affection. Sedatives are required in order to relieve pain,
sleeplessness, and hyperesthesia, and for this purpose large
doses of opium and subcutaneous injections of morphia are best.
Warm baths afford great relief, and moist packing of the whole
body often soothes and induces sleep.

When the affection has assumed the chronic form, large doses
of iodide of potassium should be administered. The sequelse,
such as paralysis, atrophy, anaesthesia, and weakness of the
bladder, must be treated with baths and electricity.

(ii.) Leptomeningitis Spinalis Chronica.
§ 642. Etiology. — The disease frequently develops from the

SPINAL CORD AND MEDULLA OBLONGATA. 397

acute form and then has the same causes. The acute form is
more apt to degenerate into the chronic variety in debilitated
and badly-nourished subjects, or in those who are addicted
to alcoholic and other excesses.

§ 643. Symptoms. — The symptoms are, on the whole, the
same as those of the acute variety, but they develop more
gradually, and are slower in their progress. When the disease
develops from the acute form the violent symptoms disappear,
but the pain, stiffness, abnormal sensations, and paralysis
remain for a longer time, and the disease passes on to become
chronic.

In the majority of cases the disease begins in an insidious
manner, the commencement being marked by abnormal sensa-
tions in the lower extremities, gradually increasing pain and
stiffness of the back and neck. The pain in the back is described
as a feeling of drawing and pressure in the loins, and is aggravated
by movements of the vertebral column, though not increased by
pressure on the spinous processes.

A girdle sensation, as well as shooting and boring pains, is
felt in the trunk, on a level with the morbid lesion. The patient
complains of tingling, formication, and a feeling of coldness
in the limbs, which feel weak and heavy. These abnormal
sensations may be accompanied by tearing or shooting pains,
either limited to the region of some nerve trunk, or changing
from one place to another.

The eccentric symptoms are limited to the region of distri-
bution of the nerves whose roots originate in the part chiefly
affected, and they are more marked as a rule in the lower
extremities, although the upper are not unfrequently affected.

Symptoms of motor irritation are of subordinate importance
in chronic meningitis, although some are almost always present.
A certain degree of stiffness of the back and neck and involun-
tary drawing up or extension of the limbs are rarely absent.

The heaviness and weakness of the limbs gradually increase,
but the paraplegia in spinal meningitis is seldom complete and
fluctuates in its intensity from day to day. If there be a con-
siderable effusion of spinal fluid the paralysis increases when
the patient stands; but at other times the paralysis increases

398

DISEASES OF THE MEMBRANES OF THE

when the patient is lying on his back, and then it is probable
that the cord is liable to become passively congested.

Hypersesthesia is a frequent symptom, but anaesthesia is rare.
There is usually only slight blunting of the cutaneous sensi-
bility, limited to the feet and lower part of the legs.

In severe cases the muscles may undergo atrophy with loss of
electric excitability. Anaesthesia is developed, the reflex actions
are abolished, bed-sores and cystitis appear, and the patient
dies from pyaemia and marasmus.

§ 644. Course, Duration, and Results. — The disease is always
slow, and extends over a period of months or years. Some cases
recover, but the return to health is slow, and often interrupted
by relapses. The sensory disturbances are the first to disappear,
the motor persisting longer. In many cases recovery is only
partial, and paralysis of. some muscles or extremities, with or
without atrophy, circumscribed anaesthesia, weakness of the
bladder, and other symptoms remain permanently. In the great
majority of cases chronic meningitis ends after a time fatally.
The symptoms which precede and cause death are usually para-
plegia, paralysis of the bladder, cystitis, bed-sores, and marasmus.
In other cases the morbid process extends to the cervical region,
giving rise to difficulty of breathing. At other times death is
brought about by an acute attack of purulent meningitis super-
vening on the chronic form. Death may also be caused by \
many other complications and accidents.

§ G45. Morbid Anatomy. — The pia mater and arachnoid in
chronic spinal leptomeningitis are congested, thickened, opaque,
often pigmented, and closely adherent to the dura mater on the
one side and the cord on the other. The spinal fluid is usually
in excess ; it is generally turbid, tinged with blood, or mixed
with an abundant fibrinous exudation. Numerous thin and
small calcareous plates may be observed on the arachnoid,
especially in the lumbar region. The cord is usually implicated
in the morbid changes. Transverse myelitis, or cortical, syste-
matic, or disseminated sclerosis may be observed.

§ 646. Diagnosis. — The diagnosis of chronic spinal lepto-

SPINAL CORD AND MEDULLA OBLONGATA.

399

meningitis presents no difficulty when the disease is fully
developed and uncomplicated, but is difficult during the first
obscure symptoms of the affection, and when it is complicated
with chronic myelitis.

Pain and stiffness in the back, eccentric pains in the extre-
mities, girdle pains, and other symptoms caused by irritation
of the roots of the nerves, a slight degree of paralysis with
fluctuations in its intensity, especially when the last varies
according as the patient is in the prone or erect posture, hyper-
esthesia or a slight degree of anaesthesia, normal or absent
tendon reflexes, and painful muscular jerkings point strongly
to spinal meningitis.

When severe paralysis and anesthesia are present, the pains
slight, and the tendinous reflexes exaggerated, the presence of
myelitis may be inferred.

Spinal meningitis may be readily distinguished from loco-
motor ataxy, but it must be remembered that the two diseases
are often combined.

§ 647. Prognosis. — The prognosis is always grave, although
many apparently hopeless cases have been known to recover ;
as a rule, some permanent damage to the cord is generally left
behind.

§ 648. Treatment. — The acute form should always be sub-
jected to energetic treatment, with the view of avoiding the
establishment of the chronic variety. Active antiphlogistic
treatment does no good in the chronic form of the disease.

Counter-irritation along the vertebral column is one of our
best means of treatment. Repeated large blisters to the back
are the most effectual of this class, although the milder counter-
irritants may be sufficient in some cases.

Iodide of potassium in moderate doses is the only reliable
internal medicine. Mercury should not be administered unless
the presence of syphilis be suspected. Ergot and belladonna
are of no use. The patient should be kept warm, and warm
baths of all sorts are efficacious.

400

DISEASES OF THE MEMBRANES OF THE

(IV.) TUMOURS OF THE SPINAL MEMBRANE.

§ 649. The tumours which are found within the spinal canal
usually develop from the spinal membranes. The majority of'
them spring from the dura mater, but some originate from the
arachnoid and pia mater, and remain limited to these mem- •
branes. Morbid growths may also arise from the neighbouring |
structures and extend towards the canal so as to involve the
membranes secondarily.

§ 650. Etiology. — The causes of meningeal tumours are
obscure. Many cases have been observed where the first symp-
toms occur after a fall or blow on the back or spine ; in many
cases the commencement of the disease dates from childhood.
Disease of the vertebrae, the tubercular and scrofulous diathesis,
syphilis, and probably an inherited tendency to the formation
of carcinomatous and other growths are the main predisposing
causes.

§ 651. Symptoms. — The symptoms may be divided into two
groups — (1) those caused by local irritation and compression of
the nerve-roots and membranes first involved in the tumour ;
and (2) those caused by irritation and compression of the cord
itself, and by consecutive myelitis.

The symptoms of the first group may precede those of the
second by many years. They are very variable, as might be
expected, when it is considered that they must largely depend
upon the locality of the tumour, and the direction and rate of
its growth.

Violent Pains of a lancinating, tearing, and boring character
are complained of, and these may remain confined to a single
point, or attack a nerve trunk. They either surround the
trunk like a girdle at various levels, or invade the upper or
lower extremities of one or both sides. They may also extend
gradually or suddenly into neighbouring nerve districts. They
are often increased by movement of the spinal column, and,
like all neuralgic pains, are made worse by sudden changes of
weather.

Parcesthesice, such as tingling, formication, numbness, either

SPINAL CORD AND MEDULLA OBLONGATA.

401

in the form of a girdle or limited to certain regions of the
extremities, are observed.

Twitchings and Spasms of individual muscles may appear
when the motor roots are first subjected to the pressure of the
tumour.

These symptoms are almost always accompanied by local
pain, and stiffness of the spine in the neighbourhood of the
tumour.

Symptoms of both sensory and motor paralysis appear sooner
or later, but these are at first limited to the region of distribu-
tion of the nerves which take origin from the part of the cord
affected. These symptoms consist of circumscribed anaesthesia,
often associated with pain (anaesthesia dolorosa), and local
paresis or paralysis of the corresponding muscular groups,
followed by atrophy and the reaction of degeneration.

If the cervical portion be the seat of the affection, an upper
extremity may first be seized by pains, paresthesias, partial
paralysis, and atrophy before the symptoms of compression of
the cord appear. When the dorsal region is the seat of the
tumour, the illness is introduced by intercostal neuralgias and
herpes zoster. Neuralgias and trophic changes in the district
of the lumbar or sacral plexuses indicate that the lumbar region
is involved.

After a period of weeks, months, or years, according to the
rate of growth of the tumour, the symptoms due to compression
and myelitis appear either gradually or suddenly. When para-
plegia occurs suddenly, or in a period of a few hours, it is
generally caused by secondary myelitis. If the paraplegia
result from the compression caused by the slow growth of the
tumour, one lateral half of the cord may be subjected to pres-
sure, or the compression may occur on the anterior or posterior
surface of the cord. Motor phenomena predominate when the
anterior surface is chiefly affected, and sensory phenomena when
the posterior is principally involved. When the cord is com-
pletely compressed, or transverse myelitis occurs, the whole of
the body below the seat of the tumour becomes more or less
completely anaesthetic and paralysed, and the bladder and
rectum are paralysed, while cystitis and bed-sores with their
consequences supervene.
AA

402

DISEASES OF THE MEMBRANES OF THE

Symptoms of motor irritation often accompany those of
paralysis. These usually consist of muscular twitching and:
transient spasms, and after a time secondary degeneration'
occurs, causing contracture of the extremities.

The reflex actions, both superficial and deep, are usually
increased, but when the grey substance becomes secondarily
diseased, or when the tumour is situated in the lumbar region,
the reflexes are abolished.

Muscular atrophy may at first be limited to the area of dis-
tribution of the nerves, the anterior roots of which are compressed
by the tumour; but after a time all the paralysed muscles
undergo rapid atrophy, and their faradic contractility disap-
pears. Death is generally caused by cystitis and bed-sores,
but when the tumour is situated nigh up death may be caused
by arrest of respiration. Death not unfrequently results from
an intercurrent attack of pneumonia, or spinal meningitis.

§ 652. Course, Duration, and Termination. — The first stage
of the disease is very insidious and may extend over many years.
When once paraplegia makes its appearance the progress is
usually more rapid; but even then years may pass before death
occurs. The symptoms fluctuate greatly in severity, and the
entire duration of the affection varies from eight months to four
or five years ; although cases are known which have extended
over a period of fifteen years. The disease generally ends
fatally, but in the case of syphilomata, scrofulous tumours, and
inflammatory new formations, complete or partial recovery may
take place.

§ 653. Diagnosis. — During the first stage of the disease it
may be inferred that there is a circumscribed lesion of the cord,
but it is not possible to make an accurate diagnosis of tumour.
When symptoms of a slowly-developing compression of the cord
are present, and when these have been preceded by symptoms
of irritation or compression of the nerve roots, a tumour may be
suspected.

The diagnosis of tbe nature of the tumour must be made by
a careful examination of all the circumstances of the case.
When Pott's disease or marked scrofula exists, a peri-menin-

SPINAL CORD AND MEDULLA OBLONGATA.

403

gitic exudation may be inferred ; and when there is primary
cancer of the vertebra? or of some other part, a carcinomatous
tumour may be considered probable ; while if there be other
evidences of syphilis a gummatous tumour is to be expected.
Echinococcus may be inferred to be present when the parasite
has been found in other organs, and neuroma if neuromata are
found on the peripheral nerves.

§ 654. Morbid Anatomy.
Fibroma and fibrosarcoma are usually small, oval tumours,
3 to 5 cm. long and 2 to 4 cm. thick. They spring from the
dura or pia mater, and may be situated either within or without
the sac of the dura. They consist of connective tissue, with
more or less abundant spindle or round cells.

Sarcoma occurs in every possible form, as hard and soft,
fibrous or cellular, and often as a cystosarcoma. It generally
originates from the inner membranes, and is usually of an
elongated form, and frequently lobular.

Myxoma almost exclusively originates from the arachnoid or
pia mater. It is a soft, juicy, lobulated tumour of moderate
size, and pale colour.

Psammoma appears in the form of a small roundish or oval-
shaped smooth or lobed tumour, and generally originates in the
soft membranes. It is really a sarcomatous tumour with
granular concretions of lime imbedded in its substance.

Lipoma has repeatedly been found in the vertebral canal,
and may originate either in the fatty tissue outside the dura
mater or from the soft membranes.

Enchondroma, of the size of a hazel-nut, and firmly adherent
to the dura mater and connected vertebrae, has been found by
Virchow.

Osteoma, in the form of so-called cartilaginous discs, is very
common in the arachnoid, and diffuse ossification of the dura
mater also occurs, but neither of these can be regarded as
proper tumours.

Multiple Fibrous Melanoma has been found in the spinal
canal by Virchow and Sander.

Neuromata have been found on the nerve roots, especially of

404

DISEASES OF THE MEMBRANES OF THE

the cauda equina. They are generally false neuromata, and are
either multiple, or occur singly.

Carcinoma springs very rarely from the spinal membranes. '
These tumours are almost always developed secondarily by
extension from the vertebras or neighbouring parts, or by
metastasis from other organs.

Miliary tubercles are found in the soft membranes, and
closely allied to these are tumours which originate from inflam-
matory, hsemorrhagic, and other processes in the spinal mem-
branes or the neighbouring parts, such as peri-pachymeningitic
exudations, circumscribed masses of a purulent or caseous
nature, scrofulous exudations between the dura and vertebral
column, and hsematoma.

Syphilomata usually consist of gummata of the dura or pia
mater.

Parasitic growths are rarely met with in the vertebral canal.
Cysticercus cellulosse bas been found by Westphal, and echino-
coccus has been occasionally observed.

§ G55. Prognosis. — The prognosis is always very serious, and
the more quickly the symptoms have developed the worse it is.
The presence of carcinoma warrants the worst prognosis. Iu
the inflammatory, syphilitic, scrofulous, and hsemorrhagic forms
the prognosis is more favourable. If paraplegia be complete
the prognosis is hopeless.

§ 65Q. Treatment. — The internal remedies from which most
is to be expected are iodide of potassium and mercury.

The painful and other distressing phenomena must be relieved
by suitable remedies.

(V.) DEFORMITIES OF THE SPINAL MEMBRANES.

§ 657. Spina Bifida consists of an abnormal accumulation
of fluid within the cavity of the dura mater in connection with a
greater or lesser deformity of the vertebral column. It presents
itself as a sac-like dilatation and pouching of a more or less
circumscribed portion of the cavity of the dura mater, which is
generally associated with deficiency or absence of one or more
vertebral arches. The sac protrudes like a hernia through the

SPINAL CORD AND MEDULLA OBLONGATA.

405

cleft, and raises the skin in the form of a tumour of variable
size. The seat of the tumour is generally in the sacral and
lumbar regions, and more rarely in the dorsal or cervical por-
tions of the cord. It is almost always situated in the middle
line and seldom deviates to either side. As a rule there is only
one tumour, but several are occasionally present. They vary
in size from a hazel-nut to that of a child's head, and are
usually round or elliptical in form, but at times may extend
over a large portion of the spinal column. The tumour is
either sessile or pedunculated, and sometimes subdivided into
two or lobulated.

The skin over the tumour may be normal, or stretched
thin, red, and ulcerated, and at times an umbilicated depression
may be seen at some point on the surface of the tumour, caused
by the insertion of the end of the cord in the interior of the sac.

The dura mater is either thickened or thin and stretched,
and usually lies immediately beneath the skin. The arachnoid
usually encloses the fluid, and if hydromyelia exist, the pia mater
takes part in the formation of the sac. The neck of the sac is
more or less narrow, and communicates with the spinal canal.
Occasionally it may be closed by adhesions, so that the external
sac forms a cystic tumour.

The condition of the spinal cord varies in different cases.
As a rule the cord is normal and takes no part in the deformity
except that its lower extremity may be adherent to the sac.
The cord may be lengthened, and rendered thin and flat by its
extremity being drawn out of tbfe vertebral canal. In these
cases the nerve roots return along the walls of the sac or through
the fluid. When a hydrorrachis interna exists along with the
spina bifida, the lower portion of the cord is more or less de-
stroyed, atrophied, and the cavity of the sac communicates
directly with the dilated and open central canal of the cord.

The contents of the sac consist generally of a light colourless
and clear fluid, identical with the normal cerebro-spinal fluid,
and its quantity may amount to from 3oz. to 21b. or more.

§ 658. Symptoms. — The most marked symptom at birth
consists of a tumour over the vertebral column, usually seated
in the sacral or lumbar region, and occasionally at a higher

406

DISEASES OF THE MEMBRANES OF THE

point of the spinal column. When the tumour is large the sac
may burst during birth, and the child then generally dies from i
asphyxia a few hours or at most a day or two after birth. The'
tumour may remain stationary or increase in size. In rare cases-
it may develop for the first time after birth.

The tumour is tense, elastic, fluctuating, and when the skin i
is thin and stretched it may appear translucent. At times the
skin may be ulcerated, so that the wall of the sac is constituted
by the distended spinal membranes. The sac can be emptied
by slow and gradual pressure except in those cases in which
communication of the spinal canal has been cut off by closure
of the sac ; and if there be coincident hydrocephalus, pressure
on the tumour causes swelling and protrusion of the fontanelles.
The swelling also increases on assuming the erect posture, and
during coughing and sneezing. The tumour is sometimes sensi-
tive on pressure. It may remain stationary and give rise to no
other symptoms, and the patient may arrive at maturity without
developing any serious symptoms. As a rule, however, it in-
creases in size and produces pressure on the lower part of the
cord and the cauda equina, so that the children affected soon
suffer from paraplegia, incontinence of urine and faeces, and bed-
sores, and the case soon terminates fatally. When there is
coexistent hydrorrachis interna, paraplegia and paralysis of
the sphincters are present from the beginning, and death
speedily results.

Rupture of the sac may be caused in various ways, and is
followed by purulent inflammation which usually extends from
the sac into the spinal canal, and a purulent spinal meningitis
results, which terminates fatally in a few days. When the per-
foration is very minute and the fluid flows out very slowly, the
case has been known to terminate favourably and to lead to
the cure of the disease. When the opening is large and the
fluid is rapidly evacuated, death may follow very quickly pre-
ceded by general convulsions.

§ 659. Diagnosis. — The diagnosis is as a rule exceedingly
easy, and presents no difficulty except when the tumour is small
and when the orifice of communication is small or entirely
closed. The characteristic signs of the disease may be gathered

SPINAL CORD AND MEDULLA OBLONGATA.

407

from the symptoms already described. The sacral tumour,
resulting from the displacement of the abdominal and pelvic
viscera, can as a rule be readily distinguished from the tumour
of spina bifida, and the malformations and defects which not
rarely coexist with spina bifida, such as hydrocephalus, deformi-
ties of the lower extremities, anomalies of the genital apparatus,
inversion of the bladder, with congenital fissure of the abdominal
walls, can be readily recognised.

§ 660. Prognosis. — The prognosis is as a rule very unfavour-
able. The majority of the children die either from accidental
opening of the sac, progressive growth of the tumour, or in
consequence of operations undertaken to effect a radical cure.
The larger the tumour and the higher its situation the more
unfavourable is the prognosis. The prognosis is also bad when
the orifice of communication is large, when hydromyelia and
hydrocephalus are associated with it, and when the constitution
of the child is feeble.

§ 661. Morbid Physiology. — The origin of spina bifida is
still doubtful. Some regard it as being due to dropsy of the
subarachnoidal space, or as a primary dropsy of the central
canal, with disappearance of the cord and secondary widening
and distention of the spinal membranes. If these changes take
place before the vertebral arches are closed, a cleft of the ver-
tebral column may be induced. Others think that the cleft of
the vertebral column is the primary part of the process and the
hydrorrachis is developed at a subsequent period.

§ 662. Treatment. — The surgical operations which have been
attended with the best results are methodical compression of
the tumour, simple and repeated puncture of the sac, and
puncture with subsequent injection of iodine.

Simple puncture may be performed repeatedly, and it is
best effected by means of the hypodermic syringe. The sac
should not be completely emptied, and pressure should be after-
wards lightly applied. For the details of the treatment of spina
bifida surgical works must be consulted.

409

Part IV. — DISEASES OF THE ENCEPHALON.

CHAPTER I.

ANATOMICAL AND PHYSIOLOGICAL INTRODUCTION.

The encephalon is invested with three membranes continuous
with those of the spinal cord. They are named (1), dura mater ;
(2), arachnoid ; and (3), pia mater.

§ G63. Dura Mater. — The cranial part of the dura mater is
adherent to the inner table of the skull, especially along the
lines of the sutures and the margins of the foramina. Strong
flattened prolongations from the inner surface of the dura mater

Fig. 189.

Fig. 189 (From Turner). Dura Mater and Cranial Sinuses. — 1, Falx cerebri ;
2, Tentorium ; 3, 3, Superior longitudinal sinus ; 4, Lateral sinus ; 5, Internal
jugular vein; 6, Occipital sinus ; 7, 8, Veins of Galen ; 9 and 10, Superior and
inferior petrosal sinus ; 11, Cavernous sinus ; 12, Circular sinus, which connects
the two circular sinuses together ; 13, Ophthalmic vein, from 15, the eyeball ;
14, Crista galli of ethmoid bone.

410 ANATOMICAL AND PHYSIOLOGICAL INTRODUCTION.

form partitions between divisions of the encephalon. These
partitions are respectively named the falx cerebri, tentorium
cerebelli, and falx cerebelli. ,

The cranial dura mater is mainly composed of two layers of
fibrous tissue, which separate from each other along certain
lines, so as to form tubular passages, named sinuses; these
transmit the venous blood returning from the brain.

The sinuses usually pass from before backwards, and several
join opposite the internal occipital protuberance at a spot which
is called the torcular Herophili. The blood is drained from
the torcular by the lateral sinuses, which terminate in the
internal jugular veins. The minute structure of the membranes
of the brain is the same as already described in the case of the
spinal membranes.

§ 664. The Arachnoid. — The arachnoid is a delicate and
transparent membrane, and between it and the dura mater is a
space, containing a small quantity of limpid serum, which
lubricates the smooth opposed surfaces of the two membranes.
This space is regarded as equivalent to the cavity of a serous
membrane, and is named the arachnoid cavity or sub-dural
space. The arachnoid and pia are separated by a distinct space
called the sub-arachnoid space. The space contains a limpid
cerebro spinal fluid, varying in quantity from two drachms to
two ounces.

Pacchionian Bodies. — Clusters of granular bodies are
observed on each side of the longitudinal sinus imbedded in
the dura mater, named Pacchionian bodies. These bodies spring
from the arachnoid membrane, a^nd sometimes attain a relatively
large size.

§ 665. Pia Mater. — The pia mater closely invests the whole
outer surface of the brain, and dips in the fissures between the
convolutions, differing in this respect from the arachnoid, which
passes from the summit of one convolution to that of another.
A wide prolongation of this membrane passes into the interior
of the cerebrum, named the velum interpositum. The pia
mater is prolonged along the roots of the cranial and spinal
nerves and filum terminale. It is the vascular membrane of

ANATOMICAL AND PHYSIOLOGICAL INTRODUCTION. 411

the brain, and the arteries which pass from it into the
substance of the latter are invested by it with a loose
funnel-shaped sheath, which opens into the sub-arachnoid
space, and contains cerebro-spinal fluid (Key and Ketzius). The
ventricles of the brain are also supposed to be in free commu-
nication with the sub-arachnoid space.

THE BRAIN OR ENCEPHALON.
The part of the central nervous axis, which is contained
within the cavity of the skull, is termed the brain or encephalon.
The brain is conveniently divided into (1), the medulla ob-
longata; (2), the pons variolii; (3), the cerebellum; and (4), the
cerebrum.

§ 666. The Medulla Oblongata. — The medulla oblongata is
the expanded upper end of the spinal cord, and has already
been described.

§ 667. The Pons Variolii. — The pons rests on the dorsum
sellae of the sphenoid bone, and is marked on its inferior aspect by
a median longitudinal groove, in which the basilar artery lies; its
posterior surface receives the pyramidal tracts and the upward
continuation of the anterior root-zones, and the grey matter of
the cord; its anterior surface gives origin to the two crura
cerebri ; each lateral surface is in relation to a hemisphere of
the cerebellum ; the superior surface forms in part the upper
portion of the floor of the fourth ventricle, while the corpora
quadrigemina rest upon its anterior half.

Structure of the Pons. — The pons consists of grey and white matter.
The greater portion of the grey matter of the pons is an upward continua-
tion of the grey matter of the spinal cord and medulla oblongata, which
has been already described. In addition to the grey matter on the floor
of the fourth ventricle, there is a considerable quantity interposed between
the transverse fibres of the pons. The transverse fibres derived from each
lateral lobe of the cerebellum appear to terminate in the interposed grey
matter of the opposite half of the pons.

The white matter of the pons consists of longitudinal and transverse
fibres. The longitudinal fibres are the upward continuations of the
anterior pyramids of the medulla, the anterior root-zones of the cord,
and probably also fibres ascending from the olivary body. The longi-
tudinal fasciculi are also reinforced by fibres arising in the pons itself.

412 ANATOMICAL AND PHYSIOLOGICAL INTRODUCTION.

The transverse fibres go from one hemisphere of the eerebellum to that'
of the opposite side, although the fibres are probably interrupted in the
pons by interposed grey matter. These fibres, therefore, constitute the,
commissural or connecting arrangement, by means of which the two
hemispheres of the cerebellum become anatomically continuous with one
another.

THE CEREBELLUM.

§ 668. — The cerebellum occupies the inferior occipital fossae.
It consists of two lateral hemispheres joined together by ai
median portion called the vermiform process. On the superior r
surface of the cerebellum this is a mere elevation, but on its i
inferior surface it forms a well-marked projection, named the
inferior vermiform process. This process lies at the bottom
of a deep fossa (vallecula), which is prolonged to the posterior
border of the cerebellum, and forms there a deep notch, in
which the falx cerebelli is lodged.

The Peduncles. — The cerebellum is connected below with the
medulla oblongata by the two restiform bodies which form its
inferior peduncles. The crossed connection of the fibres of the
inferior peduncles of the cerebellum with the olivary bodies
has already been described. The cerebellum is connected with
the corpora quadrigemina and crura cerebri by two superior
peduncles. The greater portion of the fibres of the superior
peduncles decussate in the upper end of the pons and in the
tegmenta, the fibres of one side becoming connected with the
red nucleus of the tegmentum of the opposite side. The trans-
verse fibres of the pons form the middle peduncles of the
cerebellum.

Folia. — The surface of the cerebellum consists of numerous
laminae or folia, which are separated by fissures or sulci of diffe-
rent depths.

Fissures. — The great horizontal fissure begins behind the
middle peduncles, passes horizontally backwards round the
circumference of the cerebellum, dividing its tentorial and
occipital surfaces. From this primary fissure numerous others
proceed, and some that are constant in their position and deeper
than the rest have been described as separating the cerebellum
into lobes.

Lobes. — The tentorial surface is subdivided into two smaller

ANATOMICAL AND PHYSIOLOGICAL INTRODUCTION. 413

lobes, named anterior superior and posterior superior. On
the occipital surface each hemisphere is subdivided from behind
forwards into the posterior inferior lobe, the slender lobe,
the biventral lobe, and the flocculus. Immediately internal
to the biventral lobe is the amygdala or tonsil, which forms the
lateral boundary of the anterior part of the vallecula. The infe-
rior vermiform process is subdivided into a posterior part or
pyramid, an elevation or uvula situated between the two tonsils,
and an anterior pointed process or nodule. Stretching between
the two flocculi, and attached midway to the sides of the nodule,
is a thin, white, semi-lunar-shaped plate of nervous matter, called
the posterior medullary velum, whilst the layer of grey matter
stretching between the uvula and tonsil on each side is called
the furrowed band.

§ 669. Internal Structure. — The cerebellum consists of both grey and
white matter. The grey matter forms the exterior or cortex, while the
white forms the interior of the organ. A vertical section through the
cerebellum presents an arborescent appearance known by the name of
arbor vita. Independent masses of grey matter are found in the interior
of the cerebellum. If the hemisphere be cut through to the outer side of
the median lobe, a nucleus of grey matter is observed similar in its arrange-
ment to the olivary body, and named the corpus dentatum. It encloses

Fio. 190.

Fig. 190 (From Turner). The Occipital Surface of the Cerebellum.— a, Vallecula;
b. Pyramid ; c, Uvula ; d, Nodule ; e, e, Margin of tentorial surface ; /, /,
Great horizontal fissure ; g, g, Posterior inferior lobes ; h, k, Slender lobes ;
k, k, Biventral lobes ; I, Tonsil ; in, Flocculus ; n, Posterior medullary velum ;
o, Cut surface from which the left tonsil has been detached.

414 ANATOMICAL AND PHYSIOLOGICAL INTRODUCTION.

white fibres which leave the interior of the corpus at its inner and lower
sides. Stilling has described two grey masses situated in the anterior
end of the inferior vermiform process which he named roof nuclei. ,

The white matter is for the most part continuous with the fibres of the '
peduncles of the cerebellum. The fibres of the inferior peduncles pass
upwards to join the grey matter of the superior surface of the cerebellum, .
especially in the median lobe. They are also connected with the corpus •
dentatum and roof nuclei. Those of the superior peduncles descend from
the corpora quadrigemina and reach the grey cortical matter, more espe- •
cially that of the inferior surface of the cerebellum, and they are also con-
nected with the corpus dentatum. The fibres of the middle peduncles
terminate chiefly in the cortex of the lateral lobes. The cerebellum also •
contains fibres which connect different parts of its grey matter with one
another, named fibrce propria. Stilling describes a median fasciculus, the
fibres of which connect the superior and inferior vermiform processes.
Other fibres cross the median plane to unite symmetrical regions of the
lateral lobes. Meynert describes a cerebellar origin of the auditory and
fifth nerves.

Minute Structure. — The grey matter of the cortex is divided into an
external grey or cellular layer, and an internal rust-coloured layer of about
equal thickness. The external layer consists of a delicate matrix contain-
ing cells and fibres. Most of the fibres have a direction at right angles
to the surface, the majority of them being the processes of Purkinjd's
cells, to be immediately described. Of the cells some are small, and
appear to belong to the connective-tissue matrix, while others are larger,
and probably connected with the processes of Purkinje's cells. The
inner part of the external layer contains fibres which run parallel with
the surface.

Tlie inner or granule layer consists of granule-like corpuscles, which ;
lie in dense groups in a gelatinous matrix, containing a plexus of fine
nerve fibres. Some are round, while others are angular and possess a
protoplasmic envelope with processes, which are supposed to be connected
with the plexus of fine nerve fibres amongst which they lie.

The cells of Purkinje lie in a single layer, between the outer and inner
layers of the cortex. Most of them are flask-shaped bodies, containing a
spherical nucleus and nucleolus. The long axis of the cell is generally
directed at right angles to the surface. From the external surface of tbe
cells two processes are given off ; these pass out towards the surface and
divide repeatedly in their course. The finer subdivisions of these pro-
cesses have been said to curve back towards the granule layer, where,
according to Boll, they form a network of extreme minuteness, from which
it is believed that nerve fibres arise. From the inner end of the cell
another fibre is given off ; it is unbranched, passes into the granule layer,
and is supposed to be continuous with the axis cylinder of a nerve fibre.

The medullary centre consists of nerve fibres arranged in parallel or
interlacing bundles. They form the central stem of the folia, whence

ANATOMICAL AND PHYSIOLOGICAL INTRODUCTION. 415

they radiate into the cortex. They disappear in the granule layer, and
are commonly believed to be continuous with the inner processes of
Purkinje''s cells.

THE CEREBRUM.

§ 670. The cerebrum constitutes the largest division of the
encephalon, and lies above the level of the tentorium. It con-
sists of a narrow constricted portion — the crura — of certain
basal ganglia — the corpora quadrigemina, optici thalami, and
corpora striata — and of an upper expanded portion — the cere-
bral hemispheres.

§ 671. Exterior of the Cerebrum. — The cerebrum is ovoid in
shape and presents superiorly, anteriorly, and posteriorly a deep
median longitudinal fissure, which subdivides it into two
hemispheres. The two hemispheres are connected across the
median plane by the corpus callosum. The outer surface of
each hemisphere is convex, and adapted in shape to the con-
cavity of the inner table of the cranial bones. Its inner sur-
face is flat, and is separated from the opposite hemisphere by
the falx cerebri. The under surface, where it rests on the tento-
rium, is concave, and is separated by that membrane from the
cerebellum and pons. From the front of the pons two strong
white bands, the crura cerebri or cerebral peduncles, pass for-
wards and upwards to enter the basal ganglia of their respective
hemispheres. The optic tracts wind round each crus, and con-
verge in front to form the optic commissure from which the two
optic nerves arise. The crura cerebri, optic tracts, and optic
commissure enclose a lozenge-shaped space which includes from
behind forwards the posterior 'perforated space, the corpora
albicantia, and the tuber cinereum, from which the infundi-
bulum projects to join the pituitary body. Immediately in
front of the optic commissure is a grey layer, the lamina
cinerea or lamina terminalis of the third ventricle; and between
the optic commissure and the inner end of each Sylvian fissure
is a grey spot perforated by small arteries, the anterior per-
forated space.

The peripheral part of each hemisphere consists of grey
matter, and exhibits a characteristic folded appearance, known
as the convolutions or gyri of the cerebrum. The convolutions
are separated from each other by fissures or sulci, some of

416 ANATOMICAL AND PHYSIOLOGICAL INTRODUCTION.

which are considered to subdivide the hemispheres into lobes,
whilst others separate the convolutions of each lobe from each |^i<
other.

Fig. 191.

Fig. 191 (From Henle's Anatomie). Base of the Brain. — P, Pons; Tho, Optic

thalamus ; Lpp, Posterior perforated space ; Jn, Island of Beil.
Tbo, Olfactory bulb. Cc, Corpora albicantia.

Let, Lamina cinerea. Tc, Tuber cinereum. Gf, Gyrus fornicatus.
Ccl2, Knee of the corpus callosum. T, Tegmentum.

Pec, Peduncles of the corpus callosum. B, Crusta.

Cba, Commissure of the corpus callosum. Sr, Substantia reticularis.
Spa, Anterior perforated space. Mo, Medulla oblongata.

The Roman letters indicate the corresponding cranial nerves : I, Olfactory
nerve ; I1, Olfactory bulb ; II, Optic nerve ; II1, Optic tract ; *, Sylvian fissure ;
**, the point of the temporo-sphenoidal lobe drawn back to show the continuity of
this lobe with the posterior convolution of the Island of Reil.

ANATOMICAL AND PHYSIOLOGICAL INTRODUCTION. 417

§ 672. Lobes of tlie Cerebrum. — They are five in number,
named respectively frontal, parietal, occipital, temporo-
sphenoidal, and central. The divisions between these lobes
are marked partly by certain conspicuous fissures, and partly by
artificial lines.

§ 673. The Primary Fissures. — The Sylvian fissure is the
first to appear in the development of the hemisphere. It passes
obliquely along the outer surface of the hemisphere from before
backwards, and upwards. In man it divides into two rami —
the posterior or horizontal (Fig. 192, S'), and the ascending or
anterior (Fig. 192, S"). The portion included between these
two branches receives the name of the operculum, and forms
the roof of the central lobe or Island of Reil. Below the fissure
of Sylvius lies the temporo- sphenoidal lobe, and above and
in front of it the parietal and frontal lobes. The frontal is
separated from the parietal lobe by the fissure of Rolando
(Fig. 192, c) or Central Sulcus. It extends from the longitu-
dinal fissure obliquely, downwards and forwards, along the outer
surface of the hemisphere towards the Sylvian fissure. The
parietooccipital fissure commences at the longitudinal fissure,
about two inches from the posterior end of the hemisphere. It
passes down the inner surface of the hemisphere, and also trans-
versely outwards for a short distance on the outer surface, and
separates the parietal and occipital lobes from each other.

§ 674. Secondary Fissures and Convolutions. — The temporo-
sphenoidal lobe presents on the outer surface of the hemispheres
three parallel convolutions, named the superior (Fig. 192, Tl),
middle (Fig. 192, T2), and inferior temporo-sphenoidal (Fig.
192, T3) convolutions. — The fissure which separates the superior
and middle of these convolutions is called the parallel fissure.

The occipital lobe also consists of three parallel convolutions,
named superior (Fig. 192, 01), middle (Fig. 192, 02), and
inferior (Fig. 192, 03) occipital convolutions.

The frontal lobe consists of three convolutions arranged in
parallel tiers from above downwards, and named superior (Fig,
192, Fl), middle (Fig. 192, F2), and inferior (Fig. 192, F3)
frontal convolutions. These are prolonged anteriorly to the

418 ANATOMICAL AND PHYSIOLOGICAL INTRODUCTION.

orbital surface of the frontal lobe, and terminate posteriorly in
the convolution which forms the anterior boundary of the
fissure of Rolando, named the ascending frontal convolution,
(Fig. 192, A).

The secondary fissures which separate the superior, middle,
and inferior frontal convolutions from one another are the
supero- frontal (Fig. 192, /l), and the infero -frontal (Fig.

Fig. 192.

Fig. 192 lEcker). Lateral View of the Human Brain. — F, Frontal lobe. P,
Parietal lobe. 0, Occipital lobe. T, Temporo-spbenoidal lobe. S, Fissure
of Sylvius, S' Horizontal, S" Ascending ramus of the same, c, Sulcus cen-
tralis, or fissure of Rolando. A, Anterior central or ascending frontal con-
volution. B, Posterior central or ascending parietal convolution. Fj Superior,
F2 Middle, and F3 Inferior frontal convolutions. /x Superior and /2 Inferior
frontal sulcus ; /3 Sulcus prse-centralis. Pj Superior parietal or postero-parietal
lobule ; P2 Inferior parietal lobule, viz. P2 Gyrus supra-marginalis, P2' Gyrus
angularis. ip, Sulcus intra-parietalis. cm, Termination of tbe calloso-marginal
fissure. 0, First, 02 Second, 03 Third occipital convolutions, po, Parieto-
occipital fissure, o, Sulcus occipitalis transversus ; o2 Sulcus occipitalis longi-
tudinalis inferior. Tl First, T2 Second, T, Third temporo-sphenoidal convo-
lutions, f j First, £2 Second temporo-sphenoidal fissures.

ANATOMICAL AND PHYSIOLOGICAL INTRODUCTION. 419

192, /2), while the continuity of the three frontal convo-
lutions with the ascending frontal one is interrupted by the
antero-parietal sulcus, or Sulcus Prce-centralis (Fig. 192, /3).
The ascending ramus of the fissure of Sylvius (Fig. 192, S") also
interrupts the continuity of the inferior frontal with the ascend-

ing frontal convolution.

Fig. 193.

Fig. 193 (After Ecker and Duret). View of the Brain from below.

Fl, Gyrus Rectus.

F2, Middle frontal convolution.

F3, Inferior frontal convolution.

/4, Sulcus olfactorius.

fb, Sulcus orbitalis.

T2, Second or middle temporo-sphe-

noidal convolution.
T3, Third or inferior temporo-sphe-

noidal convolution.
T4, Gyrus occipito-temporalis lateralis

(lobulus fusiformis).
T5, Gyrus occipito-temporalis medialis

(lobulus lingualis).

<4, Sulcus occipito-temporalis inferio
t'i, Sulcus temporo-sphenoidalis inferior.
t2, Sulcus temporo-sphenoidalis me-
dialis.

po, Parietooccipital fissure.
oc, Calcarine fissure.
H, Gyrus hippocampi.
U, Gyrus uncinatus.
Ch, Optic chiasma.
cc, Corpora albicantia.
KK, Crura cerebri.
C, Corpus callosum.

420 ANATOMICAL AND PHYSIOLOGICAL INTRODUCTION.

The orbital surface or orbital lobule presents two fissures —
the olfactory sulcus, which runs parallel with the longitudinal
fissure and lodges the olfactory bulb, and the orbital mlcus i
{Fig. 193, /5), which lies in the centre of the lobule and. is ofteD
triradiate, The straight convolution {Fig. 193, Fl) lies between
the longitudinal fissure and the olfactory sulcus, and is con-
tinuous at its anterior extremity with the superior frontal
convolution. Three convolutions are sometimes described as
lying around the orbital sulcus, named, according to their
positions, the internal, the anterior, and the posterior orbital
convolutions.

The 'parietal lobe presents several convolutions. The most
anterior is the ascending parietal convolution {Fig. 192, B),
jjvhich lies immediately behind the fissure of Eolando, and is
bounded posteriorly by a sulcus termed the imtra-parietal
sulcus {Fig. 192, ip). The postero-parietal convolution or
superior parietal lobule {Fig. 192, PI) springs from the upper
end of the back of the ascending parietal convolution, and forms
the boundary of the longitudinal fissure, extending as far back
as the parieto-occipital fissure. The supra-marginal convo-
lution {Fig. 192, P2) springs from the lower end of the ascend-
ing parietal convolution at its posterior aspect, and arches round
the posterior extremity of the Sylvian fissure. The angular
gyrus {Fig.l92,T?2/) is continuous with the supra-marginal con-
volution, and bends round the posterior extremity of the parallel
fissure. The supra-marginal convolution and angular gyrus have
together been described as the inferior parietal lobule (Ecker),
or the convolutions of the parietal eminence (Turner). They
occupy the hollow in the parietal bone which corresponds with
the parietal eminence.

The occipital is connected with the parietal lobe by two
annectant or bridgimg gyri. The superior annectant gyrus
passes between the postero-parietal and the superior occipital
convolutions, whilst the second annectant gyrus connects the
middle occipital with the angular gyrus. Two annectant gyri
also pass from the inferior occipital convolution to the lower
convolutions of the temporo-sphenoidal lobe.

The central lobe, or Island of Reil, lies deeply within the
fissure of Sylvius, being invisible except when the lips of the

ANATOMICAL AND PHYSIOLOGICAL INTRODUCTION. 421

fissure are separated. It consists of about six short, straight
convolutions (gyri operti), which radiate outwards from the
anterior perforated space. The anterior convolution is con-
tinuous with the adjacent posterior orbital convolution, while
the posterior convolution joins the temporo- sphenoidal lobe.
Externally, the island of Reil is separated by a deep sulcus
from the contiguous convolutions of the operculum, and it
covers the lenticular nucleus of the corpus striatum.

The small convolutions which lie behind the parieto-occipital
fissure form the internal convolutions of the occipital lobe,
named the internal occipital lobule, or cuneus (Fig. 194, Oz).
Those which lie immediately in front of the internal part of
the parieto-occipital lobule and between it and the curved
posterior extremity of the calloso - marginal fissure are called

Fig. 194.

A c b
_ \\l

Fig. 194 (Ecker). View of the Median Aspect of the Right Hemisphere of the Human
Brain.— CC, Corpus callosum, longitudinally divided. Gf, Gyrus fornicatus.
H, Gyrus hippocampi, h, Sulcus hippocampi. U, Uncinate gyrus, cm,
Sulcus calloso-marginalis. Fi, Median aspect of the first frontal convolution,
c, Terminal portion of the sulcus centralis, or fissure of Rolando. A, Anterior ;
B, Posterior central convolution. Pi", Precuneus. Oz, Cuneus. Po, Parieto-
occipital fissure, o, Sulcus occipitalis transversus. oc, Calcarine fissure,
oc', Superior ; oc", Inferior ramus of the same. D, Gyrus descendens. T*,
Gyrus occipito-temporalis lateralis (lobulus fusiformis). T*, Gyrus occipito-
temporalis medialis (lobulus lingualis).

422 ANATOMICAL AND PHYSIOLOGICAL INTRODUCTION.

the praicuneus or quadrilateral lobule (Fig. 194, Pi»). The
paracentral lobule lies immediately in front of the precuneus.
It consists of the upper extremities of the ascending frontal I
and parietal convolutions, viewed from the internal surface of
the hemisphere. It is cutomary to name the convolution which

1 3 Com

Fig. 195 ( From Henle's Anatomie ). Internal View of the Hemisphere of

the Cerebrum.

Ftp, Posterior transverse fissure.
Vq, Fourth ventricle.
Mo, Medulla oblongata.
P, Pons.

Cca, Corpora caudicantia.
Tc, Tuber cinereum.
H, Pituitary body.
II1, Optic tract.
II, Optic nerve.
Let, Lamina cinerea.
Coa, Anterior commissure of the third
ventricle.

Cba, Commissure of the corpus cal-

losum.
Ccl1, Rostrum.

Ccl2, Knee of the callosum.

Ccl3, Corpus callosum.

Ccl4, Splenium of the corpus callosum.

SI, Septum lucidum.

Com, Median commissure of the third

ventricle.
SM, Sulcus Monroi.
Cop, Posterior commissure of the third

ventricle.
Cn, Pineal gland.
Lq, Corpora quadrigemina.
A, Aqueduct of Sylvius.
Fta, Anterior transverse fissure.
Vma, Anterior medullary velum.
Cbl, Cerebellum.

I ANATOMICAL AND PHYSIOLOGICAL INTRODUCTION. 423

. t -u f„,m the parietooccipital fissure along the
extends ^ ^udinal fissure to the anterior extremity
STbiSJrS wHch then turns hack to the anterior
perforated space, the marginal convolution.

The internal is not divided into lobes like the external
surface but the convolutions may be studied in connection
^ the corpus callosum and with certain fissures situated ,n

^pZieto-occipital fissure (Fig. 194, Po) is continuous with
the fissure of the same name on the external surface. It ex-
d ownwards and forwards, and blends with the calcarine
fissure. The adcarine fissure (Fig. 194, oc) commenc » £the
posterior extremity of the hemisphere, usually in . » , bi fu cated
manner and extends forwards to terminate beneath the poa
"extremity of the corpus callosum. It marks the position
of the calcar avis or hippocampus minor in the posterior coma
of the lateral ventricle. The calloso-margmal fissure (F*.
194 cm) commences beneath the anterior extremity of the
corpus callosum, and passes forwards, upwards, backwards,
round the corpus callosum, terminating behind the superior
extremity of the ascending parietal convolution.

The convolution which immediately bounds the corpus
callosum is termed the gyrus fornicatus (Fig. 194 Gf). It
begins at the anterior perforated space, turns round the an-
terior end of the corpus callosum, extends parallel to its upper
surface, and then turns round its posterior end It is sepa-
rated from the corpus callosum by the callosal fissure and
from the marginal convolution by the calloso-margmal fissure.
The posterior end of the gyrus fornicatus curves downwards
and then forwards under the name of gyrus uncinatus, or
gyrus hippocampi (Fig. 194, H), to the tip of the inner sur-
face of the temporo-sphenoidal lobe. The uncinate gyrus ends
anteriorly in a crook-like extremity, or crochet, named the
mums gyri fomicati, or mbiculum comtt «— (*V
194 U) The gyrus is separated anteriorly by a narrow-curved
fissure, called hippocampal or dentate fissure, from a white
band named the tcenia hippocampi. This band possesses a
free-curved border, round which the pia mater enters the
lateral ventricle through the great transverse fissure of the

424 ANATOMICAL AND PHYSIOLOGICAL INTRODUCTION.

cerebrum. The grey matter of the gyrus hippocampi termi-
nates at the bottom of the hippocampal fissure in a well-defined
dentated border named the fascia dentata. The hippocampal 1
fissure marks the position of an eminence in the descending
cornu of the ventricle called the hippocampus major.

"Running along the internal aspect of the occipital and tem-
poro-sphenoidal lobes is a fissure termed, the collateral, which
marks the position of the collateral eminence in the lateral ven-
tricle. It separates two convolutions from each other which
connect the occipital and temporo-sphenoidal lobes with each
other, and are therefore named the occipitotemporal convo-
lutions (Fig. 194, T4, T5). The upper of these is termed the
gyrus occipito-temporalis medialis, or lingual lobule (To);
while the lower is named the gyrus occipito-temporalis
lateralis, or lobulus fusiformis (T4).

§ 675. KELATIONS OF THE CONVOLUTIONS TO THE SKULL.

The relations of the primary fissures and convolutions of the
brain with, relation to the skull bave been investigated by
Broca, Fdre, Turner, and others. The following is an abstract
of Turner's conclusions : —

Definite Landmarks on the Surface of the Skull. — The following struc-
tures and markings are easily recognised on the skull. The external
occipital protuberance (Fig. 196, o), the parietal (P) and frontal (F) emi-
nences, and the external angular process of the frontal bone (A), the
coronal (c) and lambdoidal (I), squamous (s), squamoso-sphenoid (ss),
and parieto-sphenoid sutures (ps), and the curved line of the temporal
ridge (t).

Primary Areas of the Skull. — The coronal suture (c) forms the posterior
boundary of the frontal area. A vertical line (Fig. 196, 2) drawn from the
squamous suture (s) upwards through the parietal eminence (P) to the
sagittal suture lies almost parallel to the coronal suture, and subdivides
the parietal region into an antero-parietal (Fig. 196, SAP + IAP)
and a postero-parietal area (Fig. 196, SPP + IPP). The occipital region
lies between the lambdoidal suture (I) and the occipital protuberance (o),
with the superior curved line extending from it {Fig. 196, o).

Secondary Areas of the Skull— These four primary divisions of the skull
may be subdivided into secondary areas. The temporal ridge (Fig. 196, t)
starting from the external frontal process curves backwards across the
frontal (A), antero-parietal, and post-parietal areas to the internal angle of
the occipital bone, and subdivides each of these regions into an upper and

ANATOMICAL AND PHYSIOLOGICAL INTRODUCTION. 425

a lower area. The upper frontal area, which includes all the frontal regions
above the temporal ridge, is again divided by a line drawn vertically
upwards and backwards from above the orbit through the frontal eminence
to the coronal suture {Fig. 196, c). This line divides the upper frontal
area into a supero- frontal (SF) and a mid-frontal area (MF).

Two other areas remain to be described. These are concealed by the
temporal muscle, and are limited superiorly by the scpaamoso-parietal,
sphenoido-parietal, and fronto-sphenoidal sutures. The lines of the sutures
naturally divide this area into a squamoso- temporal (Sq) and ali-sphcnoidal
area (AS).

The following then are the secondary areas of the skull : Superior
Frontal (SF), Middle Frontal (MF), Inferior Frontal (IF), Upper
Antero-Parietal (SAP), Lower Antero- Parietal (IAP), Upper Postero-
Parietal (SPP), Lower Postero- Parietal (IPP), Occipital (0), Squamoso-
Temporal (Sq), and Ali- Sphenoidal (AS).

Fig. 196.

Fig. 196 (Ferrier). Lateral View of the Human Skull.— A, The external angular
process of the frontal bone. F, The frontal eminence. P, The parietal eminence.
o, The occipital protuberance, c, The coronal suture. I, The lambdoidal
suture, s, The squamous suture, t, The temporal ridge, fs, The f ronto-sphenoid
suture, ps, The parieto-sphenoid suture, ss, The squamoso-sphenoid suture.
pm, The parieto-mastoid suture. 1, Frontal line. 2, Parietal line. SF, MF,
IF, The supero-, mid-, and infero-frontal subdivisions of the frontal area.
SAP, The supero-antero-parietal area. IAP, The infero-antero-parietal area.
SPP, The supero-postero-parietal area. IPP, The infero-postero-parietal area.
O, The occipital area. Sq, The squamoso-temporal area. AS, The ali-sphenoid
area.

426 ANATOMICAL AND PHYSIOLOGICAL INTRODUCTION.

RELATIONS OF THE CONVOLUTIONS AND FISSURES OF THE
BRAIN TO THE AREAS OF THE SKULL.

§ 076. The fissure of Sylvius {Fig. 197, SS) commences I
behind the posterior border of the lesser wing of the sphenoid,
and courses upwards and backwards below the greater wing of
the sphenoid, where it articulates with the anterior inferior
angle of the parietal bone, and then appears in the lower part
of the inferior antero-parietal region. The fissure of Rolando
{Fig. 197, R) lies in the antero-parietal region, both in its
superior and inferior divisions, its upper extremity being as
much as two inches and its lower one and a half inch behind
the respective ends of the coronal suture. The coronal suture
does not, therefore, correspond to the boundary between the
frontal and parietal lobes of the brain.

The parieto-occipital fissure is situated on an average about
0'7 to 0'8 inch in front of the apex of the lambdoidal suture
{Fig. 197, PO).

Contents of the Respective Areas.

The frontal area is occupied by the frontal lobe, but does not cover
the whole of it, the posterior extremities of the three frontal convolutions
lying behind the coronal suture. The frontal area therefore corresponds
to the part of the frontal lobe supplied by the anterior cerebral artery,
and which is not excitable to stimulation. The superior, middle, and in-
ferior frontal areas of the skull correspond respectively to the superior,
middle, and inferior frontal convolutions, with the exception of their
posterior extremities.

The upper antero-parietal area {Fig. 197, SAP) contains the upper
two-thirds of the ascending frontal (AP) and ascending parietal (S) con-
volution, and the posterior extremities of the superior (l-2in.) and middle
frontal (l"3in.) convolutions. At the upper posterior angle of this area
part of the postero-parietal lobule is visible, and below this, part of the
supra-marginal lobule may appear.

The lower antero-parietal area {Fig. 197, IAP) contains the lower third
of the ascending parietal (lin.) and ascending frontal (AP) convolutions,
and the posterior extremities (lin.) of the inferior frontal convolution.
A small portion of the supra-marginal gyrus is visible at the upper
posterior angle of this area, and below it a small portion of the superior
temporo-sphenoidal convolution.

The upper postero-parietal area {Fig. 197, SPP) contains the greater
part of the postero-parietal lobule. Below it lies the upper portion of the
angular gyrus (SPP), and part of the supra-marginal gyrus ( X ). Poste-
riorly the annectant gyri blend with the occipital lobe.

ANATOMICAL AND PHYSIOLOGICAL INTRODUCTION. 427

The lower postero-parietal area {Fig. 197, IPP) contains part of the
supra-marginal gyrus, and hehind it part of the angular gyrus, and below
this the posterior or upper ends of the temporo-sphenoidal convolutions.

The occipital area {Fig. 197, 0) indicates the situation of the occipital
lobe, but is not co-extensive with it, inasmuch as a portion extends ante-
riorly beyond the lambdoidal suture into the postero-parietal area.

The squamoso-temporal area {Fig. 197, Sq) contains the greater portion
of the temporo-sphenoidal convolutions, but the superior temporo-
sphenoidal convolution ascends into the lower parietal areas.

Fig. 197.

Fig. 197 (Turner). Diagram showing the Relations of the Convolutions of the Skull.
R, The fissure of Rolando, which separates the frontal from the parietal lobe.
PO, The parieto-occipital fissure between the parietal and occipital lobes.
SS, The fissure of Sylvius, which separates the temporo-sphenoidal from the
frontal and parietal lobes. SF, MF, IF, The supero, mid-, and infero-frontal
subdivisions of the frontal area of the skull ; the letters are placed on the
superior, middle and inferior frontal convolutions. SAP, The supero-antero-
parietal area of the skull : S is placed on the ascending parietal convolution,
AP on the ascending frontal convolution. IAP, The infero-antero-parietal
area of the skull : I is placed on the ascending parietal, AP on the ascending
frontal convolution. SPP, The supero-postero-parietal area of the skull : the
letters are placed on the angular convolution. IPP. The infero-postero-parietal
area of the skull : the letters are placed on the mid-temporo-sphenoidal convo-
lution, x , The convolution of the parietal eminence, or supra-marginal gyrus.
0, The occipital area of the skull : the letter is placed on the mid-occipital
convolution. Sq, The squamoso-temporal region of the skull : the letters are
placed on the mid-temporo-sphenoidal convolution. AS, The ali-sphenoid
region of the skull : the letters are placed on the tip of the supero-temporo-
sphenoidal convolution.

428 ANATOMICAL AND PHYSIOLOGICAL INTRODUCTION.

The ali-sphenoidal area (Fig. 197, AS) contains the lower or anterior
extremity of the temporo-sphenoidal lobe.

The central lobe, or Island of Reil, does not come to the surface, but
lies deep in the fissure of Sylvius, and is concealed by the convolutions •
which form the margin of that fissure anteriorly. It lies opposite the
upper part of the great wing of the sphenoid and its line of articulation .
with the anterior inferior angle of the parietal and the squamous part of
the temporal.

The convolutions situated on the internal aspect of the hemisphere are
altogether out of relation to the surface of the skull.

The deep-seated position and direction of the hippocampal region are
superficially indicated by the convolutions of the temporo-sphenoidal lobes,
contained chiefly in the inferior postero-parietal, squamoso-temporal, and
ali-sphenoidal areas.

§677. INTERNAL PARTS OF THE CEREBRUM.

The anatomy of the cerebrum is most conveniently studied
by successive horizontal sections.

Centrum Ovale. — A horizontal section made half an inch
above the corpus callosum displays the white matter of each
hemisphere surrounded on all sides by the grey matter of the
convolutions. The white central mass in each hemisphere was
named by Vicq. d'Azyr the centrum ovale minus. A section
made at the level of the corpus callosum shows that the white
substance of that part is continuous with the central white sub-
stance of each hemisphere. The large white medullary mass
thus displayed is named the centrum ovale majus.

The Corpus Callosum connects the centres of the two
hemispheres, and it approaches nearer their anterior than
their posterior extremities. It terminates behind in a free
rounded end — the splenium, whilst in front it forms a knee-
shaped bend, and passes downwards and backwards as far as
the lamina cinerea. It is thicker behind than in front, the
middle part being the thinnest. It consists of bundles of nerve
fibres, almost the whole of which pass transversely between the
two hemispheres. The fibres may be traced into the white
cores and grey matter of the convolutions, and apparently
connect corresponding convolutions in the opposite hemispheres.
A few fibres run longitudinally on the surface of the corpus
callosum, named the striae longitudinales or nerves of Lancisi.

Topography of the Centrum Ovale. — A systematic nomen-

ANATOMICAL AND PHYSIOLOGICAL INTRODUCTION. 429

clature of the various parts of the centrum ovale has been
devised by Pitres. His system consists in making vertical
sections of the brain at definite points, and naming the various
parts of the medullary substance exposed in each section. A
vertical section of the hemisphere at right angles to its longi-
tudinal axis in the pra3-frontal region gives the prce-frontal
section {Fig. 198). The next section is made two centimetres

Fig. 198.

Fig. 198 (After Pitres). Prce-frontal Section.—!, 2, 3, First, second, and third
frontal convolutions. 4, Orbital convolutions. 5, Convolutions on the internal
aspect of the frontal lobe. 6, Prae-frontal fasciculi of the centrum ovale.

Fig. 199.

Fig. 199 (After Pitres). Pedunculo-frontal Section.— 1, 2, 3, First, second, and third
frontal convolutions. 4, Anterior extremity of the insular lobe. 5, Posterior
extremity of the orbital convolutions. 6, Superior pedunculo-frontal fasciculus.
7, Middle pedunculo-frontal fasciculus. 8, Inferior pedunculo-frontal fasciculus.
9, Orbital fasciculus. 10, Corpus callosum. 11, Caudate nucleus. 12, Internal
capsule. 13, Lenticular nucleus.

430 ANATOMICAL AND PHYSIOLOGICAL INTRODUCTION.

in front of the fissure of Rolando and passes through the bases •
of the three frontal convolutions, and is named the pedunculo-
frontal section (Fig. 199). The medullary substance in this |
section is subdivided into a superior, middle, and inferior
pedunculo-frontal fasciculus, corresponding with the respective
frontal convolutions. The next section is 'made through the
ascending frontal convolution, parallel with the fissure of
Rolando, and is named the frontal section. It also passes
through a small portion of the sphenoidal lobe. The medullary
substance of this section is also subdivided into superior, middle,
and inferior frontal fasciculi (Fig. 200). The fourth section

Fig. 200.

Fig. 200 (After Pitres). Frontal Section. — 1, Ascending frontal convolution.
2, Insular lobule. 3, Sphenoidal lobe. 4, 5, 6, Superior, middle, and inferior
frontal fasciculus. 7, Sphenoidal fasciculus. 8, Corpus callosum. 9, Caudate
nucleus. 10, Optic thalamus. 11, Internal capsule. 12, Lenticular nucleus.
13, External capsule. 14, Claustrum,

is carried through the ascending parietal convolution, and is
named the parietal section. It is subdivided into superior,
middle, and inferior parietal fasciculi (Fig. 201). The next
is the pedunculo-parietal section, made by dividing the hemi-
sphere three centimetres behind the fissure of Rolando, and
cutting the superior and inferior parietal lobules. It is sub-

ANATOMICAL AND PHYSIOLOGICAL INTRODUCTION. 431

Fig. 201.

■ j

Fig. 201 (After Pitres). Parietal Section. — 1, Ascending parietal convolution.
2, Insular lobe. 3, Sphenoidal lobe. 4, Superior parietal fasciculus. 5, Middle
parietal fasciculus. 6, Inferior parietal fasciculus. 7, Sphenoidal fasciculus.
8, 9, 10, 11, 12, 13, 14, as in the preceding figure.

Fig. 202.

Fig. 202 (After Pitres). Pedunculo-parietal Section.— 1, Superior parietal lobule.
2, Inferior parietal lobule. 3, Sphenoidal lobe. 4, Superior pedunculo-parietal
fasciculus. 5, Inferior pedunculo-parietal fasciculus. 6, Sphenoidal fasciculus.
7, Corpus callosum. 8 and 10, Caudate nucleus. 9, Optic thalamus.

432 ANATOMICAL AND PHYSIOLOGICAL INTRODUCTION.

divided into superior and inferior pedunculo-parietal and
sphenoidal fasciculi {Fig. 202).

• The last is the occipital section {Fig. 203) in which no
separate fasciculi are distinguished.

Fi<*. .203.

Pig. 203 (After Pitres). Occipital Section.— -1, Occipital convolutions. 2, Occipital

fasciculi of the centrum ovale.

Lateral Ventricles. — The lateral ventricle is divided into a
central space or body, and three curved prolongations or cornua.
The anterior comu extends forwards and outwards into the
frontal lobe, the posterior curves backwards, outwards, and in-
wards into the occipital lobe, and the descending comu curves
backwards, outwards, downwards, forwards, and inwards, behind
and below the optic thalamus into the temporo-sphenoidal lobe.

On the floor of the central space may be seen from before
backwards the caudate nucleus, and to its inner and posterior
part a small portion of the optic thalamus, whilst between the
two is a curved flat band, the tcenia semicircularis. The
choroid plexus rests on the upper surface of the optic thalamus,
and immediately internal to it is the free edge of the fornix.

The anterior end of the caudate nucleus projects into the
anterior cornu, while the posterior cornu has an elevation on its
floor, named the hippocampus minor, and the eminentia col-
lateralis lies between the posterior and descending cornua. The
hippocampus major extends along the floor of the descending
cornu, and terminates below in a nodular end, the pes hippo-
campi. Along its inner edge is a narrow white band prolonged
from the posterior pillar of the fornix, named the tcenia hippo-
campi. If the taenia be drawn aside the hippocampal fissure

ANATOMICAL AND PHYSIOLOGICAL INTRODUCTION. 433

is exposed, at the bottom of which the grey matter of the gyrus
hippocampi may be seen to form a serrated border, named the
fascia dentata. The choroid plexus enters the descending
cornu through the great transverse fissures of the brain between
the taenia hippocampi and optic thalamus. The lateral ven-
tricle is lined by cylindrical epithelium, which rests on a layer
of neuroglia, and is in many parts ciliated. This lining is con-
tinuous with that of the third ventricle through the foramen of
Monro, the lining of the latter being continuous with that of the
fourth ventricle through the aqueduct of Sylvius. A little fluid
is contained in the cerebral ventricles.

Septum Lucidum. — If the corpus callosum be divided trans-
versely about its middle, and the two halves reflected forwards
and backwards respectively, the fornix and septum lucidum
are exposed. This septum extends vertically between the corpus
callosum above and the fornix below. It consists of two layers
of grey matter, having an interval between them containing
fluid, and covered by an epitheliated membrane. This space
is the fifth ventricle.

The fornix is an arch-shaped band of nerve fibres which ex-
tends in the antero-posterior direction, its anterior end form-
ing the anterior pillars, its posterior the posterior pillars,
and its body the summit of the arch. It consists of lateral
halves, but at the summit of the arch the two are joined
together to form the body. The anterior pillars are separate
from one another ; they descend in front of the third ventricle
to the base of the cerebrum, where they form the corpora
albicantia, and then enter the substance of the optic thalamus.
The posterior pillars are also separate ; each curves downwards
and outwards into the descending cornu of the ventricle, and
forms the free border of the hippocampus major, which is
named the tcenia hippocampi.

The velum interpositum is a fold of pia mater which passes
into the interior of the hemispheres through the great trans-
verse fissure. It is triangular in shape, the base is in a line
with the posterior end of the corpus callosum, the lateral mar-
gins are fringed by the choroid plexuses, and the apex, where
the choroid plexuses blend with each other through the foramen
of Monro, lies behind the anterior pillars of the fornix.
CC

434 ANATOMICAL AND PHYSIOLOGICAL INTRODUCTION.

The choroid plexuses consist of highly vascular folds of I
membrane, and the epithelium of the ventricles is continued
over their surface. These plexuses contain the small choroidal I
arteries, and supply the corpora striata, the optici thalami, and
corpora quadrigemina, the blood from these bodies being re- •
turned by the veins of Galen. If the velum interpositum be
raised from before backwards, the optic thalami, third ven-
tricle, pineal gland, and corpora quadrigemina are exposed
(Fig. 204).

The third ventricle is a cavity situated in the mesial plane,
between the optici thalami ; its roof is formed by the velum
interpositum and the body of the fornix, its floor by the pos-
terior perforated space (pons Tarini), the corpora albicantia,
the tuber cinereum, infundibulum, and optic commissure ; its
anterior boundary by the anterior commissure and laminse
cinerea ; its posterior boundary by the corpora quadrigemina
and. posterior commissure. The cavity of the ventricle is small,
and it is crossed at its middle by the middle or soft commis-
sure, which consists of grey matter and connects the two inner
surfaces of the optici thalami together. If the anterior pillars of
the fornix be separated, the anterior white commissure may be
seen entering the lenticular nuclei. The white fibres of the
posterior commissure pass across between the two optic
thalami in front of the corpora quadrigemina.

BASAL GANGLIA,

§ 678. The ganglia of the base of the cerebrum are the
corpora striata, the optici thalami, the corpora geniculata, the
corpora quadrigemina, and the locus niger.

(1) The corpora striatum is situated in front and to the
outer side of the optic thalami, and consists of two masses of
grey matter, separated from each other by bands of medullated
fibres, which pass from below upwards through its substance.
The upper mass projects into the lateral ventricle, and is called
the intra-ventricular portion or caudate nucleus.

The caudate nucleus consists of a club-shaped portion directed forwards,
and a slender tail-like extremity directed backwards, the two together
forming almost a complete ring, which encircles the optic thalamus and
internal capsule, like a loop or surcingle. The body of the nucleus grows

ANATOMICAL AND PHYSIOLOGICAL INTRODUCTION. 435

smaller as it extends backwards in the upper part of the ventricle, and
soon runs into the tail-like prolongation ; when the latter reaches the
posterior end of the optic thalamus it curves downwards into the inferior
horn of the ventricle and runs forward to its anterior extremity, when it

Fig. 204.

Fig. 204 (From Henle's Anatomie,'

Ccl2, Knee of the corpus callosum.
Cs, Corpus striatum.
Vsl, Ventricle of the septum lucid um.
Cf, Crura of the fornix.
Sf, Taenia semicircularis.
Ts, Anterior tubercle of the optic tha-
lamus.

Basal Ganglia viewed from above.

Com, Cop, The middle and posterior

commissures respectively.
Tfo, Taenia thalami opt.
Pv, Pulvinar.
Tho, Optic thalamus.
Cn, Pineal gland.
Pen, Peduncles of the pineal gland

436 ANATOMICAL AND PHYSIOLOGICAL INTRODUCTION.

terminates in an enlarged extremity almost exactly opposite the point
where it started in the anterior horn. The head of the caudate nucleus
is continuous with the lenticular nucleus and with the grey matter of the
anterior perforated space. The extremity of the surcingle, ou the other
hand, is connected with a deposit of grey matter forming the anterior
wall of the inferior horn of the ventricle, named the amygdala. The
taenia semicircularis accompanies the concave border of the surcingle, and
runs forwards along the roof of the inferior horn of the ventricle to its
anterior end, and there terminates in the amygdala (Dalton). In a vertical
transverse section of the brain through the optic thalamus the superior
portion of the surcingle is visible above the lenticular nucleus and internal
capsule, while the inferior portion appears as an isolated mass of grey
matter below the level of the lenticular nucleus and near the outer part
of the inferior horn of the ventricle.

Fig. 205 (After Dalton). Longitudinal and Vertical Section of the Might Hemisphere,
showing the Cavity of the Lateral Ventricle and the Caudate Nucleus.— G, Head
of the caudate nucleus. S, Surcingle. V, Ventricle. A, Amygdala. 1, Parieto-
occipital fissure. 2, Calcarine fissure.

The lower extra-ventricular portion, or lenticular nucleus, is separated
from the intra-ventricular part by a layer of white substance named the
internal capsule, while it is separated from the Island of Reil by a layer of
white substance named the external capsule, and a grey lamina termed the
claustrum. The lenticular nucleus, as its name implies, is of the form of
a bi-convex lens on horizontal section, but on a vertical section through
its middle it appears triangular, the apex being directed inwards. Two
white bands which run parallel to the outer surface of the nucleus or the
external capsule divide it into three zones named from within outwards
the first, second, and third divisions of the lenticular nucleus.

ANATOMICAL AND PHYSIOLOGICAL INTRODUCTION

(2) The optic thalamus is of an oval shape and rests on the
Icrus cerebri of the same side. It is bounded externally by the
corpus striatum and taenia semicircularis. The upper surface
is free and is partly seen in the lateral ventricle, and is partly
(covered by the fornix, the former being called the anterior
tubercle and the latter the posterior tubercle or pulvinar.

Sra

Fig. 206 (From Henle's Anatomie). Vertical Section of the Brain immediately
behind the Anterior Commissure of the Third Ventricle. — Ccl3, Corpus callosum ;
Vsl, The fifth ventricle ; Ls, Lamina of the septum lucidum ; Cs, Caudate
nucleus ; B', Internal capsule ; St, Tsenia semicircularis ; Nl. Lenticular
nucleus ; Cls, Claustrum ; In, Island of Reil ; Cf, Interior pillars of the
fornix ; Cp, External capsule ; Coa, Anterior commissure of the third ven-
tricle ; Coa', Anterior commissure as it winds back beneath the lenticular
nucleus to reach the convolutions of the cortex ; Am, Descending horn of the
lateral ventricle ; Sra, Substantia retic. alba. ; II', Optic tract ; Tc, Tuber
cinereum.

438 ANATOMICAL AND PHYSIOLOGICAL INTRODUCTION.

The posterior surface is also free and projects into the descend-
ing cornu of the lateral ventricle. The inner surfaces of the
two thalami form the lateral walls of the third ventricle, and
are connected together by a transverse portion which forms the
middle or soft commissure of the third ventricle. Tb.e inner
surface is lined by grey matter which, according to Meynert, is
distinct from that of the interior of the thalamus, and is pro-
bably the upward continuation of the central grey substance of
the spinal cord.

The internal capsule consists of a thick band of medullated
fibres, which separates the lenticular nucleus on the one hand
from the caudate nucleus and optic thalamus on the other. On
horizontal section the internal capsule is seen to consist of an
anterior and posterior division, which form an obtuse angle
with one another, the latter being called the knee of the
internal capsule. The anterior division lies between the
anterior and internal margin of the lenticular nucleus and the
head of the caudate nucleus, and the posterior division between
the posterior and internal margin of the lenticular nucleus and
the optic thalamus ; while the knee of the capsule is directed
inwards towards the third ventricle, and forms by its projection
a partial separation between the caudate nucleus and optic
thalamus.

The external capsule consists, as already mentioned, of a
thin band of white substance which bounds the lenticular
nucleus externally and lies between it and the claustrum.

(3) The corpora geniculata consist of two small oblong and
flattened eminences connected with the posterior extremity of
the optic tract, named respectively corpus geniculatum ex-
ternum and internum.

(4) The locus niger is a dark mass of grey matter which
lies between the crust and tegmentum in the cms cerebri. It
occupies nearly the whole diameter of the crus and extends
from the anterior edge of the pons to the corpora albican tia.

The pineal body or gland is a reddish body, enveloped by
the velum interpositum, and situated upon the anterior eleva-
tions of the corpora quadrigemina.

The peduncles of the pineal body, by means of which it is connected with
the rest of the cerebrum, pass forwards, one on the inner side of each optic

ANATOMICAL AND PHYSIOLOGICAL INTRODUCTION. 439

halamus, to join, along with the taniia semicircularis, the anterior pillar
f the fornix of its own side.

(5) The corpora quadrigemina or optic lobes are situated
behind and between the optici thalami, and rest upon the
posterior surface of the crura cerebri. These bodies are divided
into four eminences by a longitudinal and transverse fissure, the
anterior pair beiDg named nates, and the posterior testes. From
eaeh testis a white cord, the superior peduncle of the cere-
bellum, passes backwards to the cerebellum, while the valve
of Vieussens, or anterior medullary velum, stretches between
the pair of cerebellar peduncles.

The aqueduct of Sylvius is a narrow canal which passes
beneath the corpora quadrigemina, and connects the third with
the fourth ventricle. It is lined by a ciliated cylindrical epi-
thelium

DISTRIBUTION OF THE ARTERIES OF THE BRAIN.

§ 679. The arteries of the brain are derived from two great
trunks — the vertebral and internal carotid arteries. The branches
of the vertebrals and of the basilar trunk formed by their union
supply the posterior and lesser portion of the brain, while the
terminal branches of the internal carotid arteries supply the
anterior and greater part of the brain. The branches distri-
buted to the brain from the vertebral arteries may be called
the posterior or vertebral, and those derived from the internal
carotids the anterior or carotid arterial system.

The posterior cerebral arteries are the terminal branches of
the basilar trunk. Each artery winds round tlie eras cerebri to
reach the occipital lobe, and gives off a number of twigs — the
posterior median group (Fig. 211, 2) — which pierce the pos-
terior perforated space, and supply the internal surface of the
optic thalamus, and the walls of the third ventricle.

Branches. — A choroid branch is given off to the velum interpositum,
and small twigs pass into the substance of the crus cerebri as the vessel
winds round it. A number of small branches, the postero-lateral group
(Fig. 211, 4), enter the base of the brain behind the posterior border of the
crus cerebri, and pass into the optic thalamus and corpora quadrigemina.

The cortical branches are three in number ; the first, or anterior tem-
poral artery, being distributed to the anterior part of the uncinate gyrus

440 ANATOMICAL AND PHYSIOLOGICAL INTRODUCTION.

and its vicinity ; the second, or posterior temporal artery, to the posterior
part of the uncinate gyrus and the lower part of the temporo-sphenoidal
lohe ; and the third, or occipital artery, to the inner and outer surfaces of
the occipital lobe.

Fig. 207.

Fig. 207 (After Ecker and Duret). View of the Brain from below.

DISTEIBUTION OF VESSELS.

The region bounded by the line (• ) represents the territory over which the

Internal and Inferior Frontal Branches of the Anteeiob Ceeebbal Abtebt are
distributed.

The regions bounded by the line ( — — ) represent the territories over

which the branches of the Postebioe Ceeebbal Abtebt are distributed.

I. Is the region of the Anterior Temporal Artery.
II. Posterior Temporal Artery.

III. „ Occipital Artery.

The internal carotid artery reaches the base of the brain
close to the outer side of the optic commissure, and immediately
breaks up into two branches — the anterior and middle cerebral
arteries.

ANATOMICAL AND PHYSIOLOGICAL INTltODUCTION. 44-1

The anterior cerebral artery (Fig. 211, C A) runs forwards
in the longitudinal fissure, and, turning round the corpus
callosum, is distributed to the anterior part of the cerebrum.
The arteries of the two sides are united at their commencement
by a short transverse branch, the anterior communicating
artery.

Fig. 208.

A e B

Fig. 208 (After Ecker and Duret). Inner Surface of Bight Hemisphere.

DISTRIBUTION OF VESSELS.

The regions bounded by the line ( ) represent the territories over which the

branches of the Anterior Cerebral Artery are distributed.

I. Is the territory of the Interior and Anterior Frontal Artery,
II. Internal and Middle ,, ,,

III. ,, ,, Internal and Posterior

The regions bounded by the line ( ) represent the territories over

which the branches of the Posterior Cerebral Artery are distributed.
II. Is the territory of the Posterior Temporal Artery.
III. ,, „ Occipital Artery.

Branches. — The anterior median group {Fig. 211, 1) are given off from
the anterior communicating and the commencement of the anterior cere-
bral arteries ; they supply the anterior part of the head of the caudate
nucleus. The cortical branches are four in number — the first ' being dis-
tributed to the two internal orbital convolutions ; the second to the ante-
rior extremity of the marginal convolution, and to the superior and anterior
portions of the middle frontal convolutions on the outer surface ; the

442 ANATOMICAL AND PHYSIOLOGICAL INTRODUCTION.

third to the inner surface of the hemisphere as far as the extremity of the^
calloso-margmal fissure ; and the fourth to the quadrate lobule, the lastt
supplying a branch to the corpus callosum.

The middle cerebral or Sylvian artery {Figs. 210, 211 S)
runs in the fissure of Sylvius, and is the largest and most
important branch of the internal carotid artery. It gives small
branches— the antero-lateral group (Fig. 211, 3)— which pierce
the anterior perforated space, and supply the corpus striatum
and anterior part of the optic thalamus.

Fig. 209.

Fia. 209 (After Ecker and Duret). Outer Surface of the Left Hemisphere.

m. . , , , , DISTRIBUTION OP VESSELS.

1. Is the region of the External and Inferior Frontal Artery. '
jit.' >> >i Anterior Parietal Artery.
Y±' » » Posterior Parietal Artery.
1V* » j» Parieto-sphenoidal Artery.
Ihe posterior and inferior region bounded by the line ( _ \

ISiVaLtuteT °Ver WhiCh branChCS °f the P0STEKI0R Cerebral

F ANATOMICAL AND wnS.OL0O.CAl .NTUOOUCT.ON. 443

i ■ • nff' ftither bv the middle cerebral
Brano^.-A choroid branch » g en oB. corel)ri „ reaoh

or internal carotid arter.es, winch ^ tnmk divides into

Fig. 210.

Fig. 210. Z>^ *

S Sylvian or middle cerebral artery ; P, ^ert oral! ng ^ branch

frWal branch; 2, Ascending , frontal ^^^^a, Ending frontal
d and 5 Parieto-sphenoidal and spnenoiaai ui*u , First, second,

convolution; B, Amending parietal convolution F,,^, 1^ tMrd ietal
and third frontal third temporo-sphenoidal con-

convolutions; 1 1> Vi' iT
volutions ; OL, Occipital lobe.

■m its distribution to the outer part of ^^^^
inferior or third frontal convolution. The «f ^ and

the chief part of the ^»«"« paaae3 into the fissure of Rolando, and
atcmding parietal artery {FV 210, 3), passes' d; ietal con.

supplies the rest of the ^^t\^V^7^ The

4 an^sl suppiy the inferior parietal lobule and the superior tenaporo-
sphenoidal convolutions.

The posterior communicating artery is a long and slender

vessel watch connects the internal carotid with the posterior

cerebral arteries.

444 ANATOMICAL AND PHYSIOLOGICAL INTRODUCTION.

The circle of Willis is formed by the union of the anterior
and posterior arterial cerebral systems by means of the posterior
communicating arteries. The free anastomosis which is thus
formed enables the circulation of blood in the brain to be carried
on when one of the main trunks is obstructed.

Fig, 211.

Pig. 211 (After Charcot). Diagram of the Distribution of the Vessels at the base erf
the Cerebrum. — CA, Anterior cerebral artery. S, S, Sylvian arteries. V, Vr
Vertebral arteries. B, Basilar. CP, CP, Posterior cerebral arteries. 1. 2,

3, 3, 4, 4, Groups of nutritive arteries. The line limits the ganglionic

vascular area.

The following parts of the encephalon are situated within
this vascular area : the optic commissure, lamina? cinerea. in-
fundibulum and tuber cinereuru, corpora albicantia, posterior
perforated spot with part of the crura cerebri, and the origin of
the third pair of nerves.

Cortical System of Arteries. — The arteries which supply the cortex of
the brain ramify in the pia mater and are distributed to the grey matter
of the convolutions and subjacent white matter. The terminal ramifica-

ANATOMICAL AND PHYSIOLOGICAL INTRODUCTION.

445

r, h« rikpn as the type of the distribution of
,ons of the Sylvian -J^**^ artery divides into the five
the cortical system of • described, and each of these

secondary branches which have £ toady ^ ^ tertiarj brand

agin subdivides into into primary (K* M ^

(Fig. 212 A) of the nm. tery thege ^ ^ ^ pia mater a

and secondary twigs (Fig. 213, U, W f th brain are

territories, but the primary and secondary twigs 01 tnese
anastomose amongst themselves.

Fig. 212;

«. n. « A TWtiarv branch of the main artery. B, Primary
Fl<yi! lAc"c SSStaT^ JgHV Cortical arteries. 3, 1«k of cort.ca,
arteries in the cerebral tissues.

Nutritive Arterits of the Brain.
The nutritive arteries are derived, not only from the extremities of the
prima y and secondary twigs, bnt a large number issue from the sides of
"wigs, as weli as from the sides of the tertiary branches o the -
ar toryY^ 212, I, 2). The nutritive arteries are of two kinds_(«) the
* •> K , „ anA (h\ ihr short or cortical arteries.

ovale for a distance of three or four centimetres They do not oommu-
°L to with each other in their course except by fine capillaries, and con-
rquentty constitute so many small independent vascular tomtoms. The
erminations of these vessels approach the upward continuation of tbe gang-

446 ANATOMICAL AND PHYSIOLOGICAL INTRODUCTION.

lionic system of vessels, but the two systems do not appear to anastomose
with, one another. In a section of a convolution, twelve or fifteen medul-
lary arteries may appear ; three or four of these pass into the free surface
of the convolutiou {Fig. 213, 1), and pursue a vertical course; those which
enter the sides of the convolution pursue an oblique course through it,
while those which pass into the bottom of the fissure again become vertical.

Fig. 213.

Fig. 213 (After Duret). — 1, 1, Medullary arteries. 1', Group of medullary arteries
in the fissure between two neighbouring convolutions. 1", Arteries of the system
of arcuate fibres. 2, 2, 2, Arteries of the grey substance of the cortex, o, A
large meshed capillary network situated under the pia mater, b, A smaller
meshed capillary network situated in the middle layers of the cortex, c, Some-
what larger network in the internal layers adjoining the white substance.
d, Capillary network of the white substance.

(6) The cortical nutritive arteries arise from the vascular network of
the pia mater in the same way as the long arteries, but the former are
thinner than the latter and pursue a shorter course. Some of these
vessels pass through the whole thickness of the grey substance, and give
small capillaries to the centrum ovale, while others terminate in the sub-
stance of the cortex. The vascular network in the convolutions possesses
the following characteristics : — In the first layer, about one-half milli-
metre in thickness, the meshes of the network are large (Fig. 213, a); in

ANATOMICAL AND PHYSIOLOGICAL INTRODUCTION. 4 47

the second, corre.sponi.liig to two layers of ganglionic cells, a very close
ud tine vascular network is formed {Fig. 213, b) ; in the third, corre-
ponding to the internal layers of the cortex, a larger and coarser vascular
etwork exists (Fig. 213, c); aud in the fourth layer, or medullary sub-
stance, a still larger and coarser vascular network is observed.

The Central or Ganglionic System of Arteries.

These arteries cousist of small branches which are given off from the
trunks of the chief cerebral vessels; they pierce the base of the brain
perpendicularly to reach the substance of the basal ganglia. These
arteries form six main groups, which may be named the anterior and
posterior median (Fig. 211, 1 and 2), the right and left antero-lateral
(Fig. 211, 3, 3), and the right and left postero-lateral (Fig. 211, 4, 4) groups.
An imaginary line passing round the circle of Willis, at a distance of two
centimetres external to it, would completely surround all these vessels,
and the area so limited may therefore be called the ganglionic vascular
area (Charcot). All these vessels are terminal arteries. Some of these
vessels are of sufficient importance, owing to their liability to rupture, as to
deserve special description. The vessels derived from the middle cerebral
artery — the antero-lateral group— after piercing the anterior perforated

Fig. 214.

Fig. 214 (From Duret). Transverse Section of the Cerebral Hemispheres, about 1 cm.

behind the Optic Commissure.
Arteries op the Corpus Striatum. — Ch, Chiasma ; B, Section of the
optic tract ; L, Lenticular nucleus ; /, Internal capsule ; C, Caudate nucleus ;
E, External capsule ; T, Claustrum ; R, Island of Reil ; V, V, Section of the
lateral ventricle ; P, P, Anterior pillars of the fornix ; 0, C-rey substance of
the third ventricle.

Vascular Areas.— I, Anterior cerebral artery ; II, Middle cerebral
artery; III, Posterior cerebral artery. — 1, Internal carotid artery ; 2, Sylvian
artery ; 3, Anterior cerebral artery ; 4, 4, External arteries of the corpus
striatum (lenticulo-striate artery) ; 5, 5, Internal arteries of the corpus striatum
(lenticular arteries). The opto-striate artery is not represented in the figure.

448 ANATOMICAL AND PHYSIOLOGICAL INTRODUCTION.

apace, ascend vertically to supply the corpus striatum, the internal capsule,
and a portion of the optic thalamus. The following branches may be
distinguished : — ,

(a) Lenticular branches consist of two or three small twigs, which
ascend vertically and enter the substance of the lenticular nucleus, and
are distributed to its two inner divisions and the adjoining portion of the
caudate nucleus {Fig. 214, 5).

(b) The lenticulo-striate branch is much larger than either of the pre-
ceding arteries. It ascends along the external surface of the outer division
of the lenticular nucleus, traverses the superior part of the internal cap-
sule, and then passes from behind forwards into the substance of the
caudate nucleus. It gives branches to the outer division of the lenticular
nucleus, the internal capsules, and the caudate nucleus {Fig. 214, 4).

(c ) The lenticulo-optic branch passes, like the lenticulo-striate artery,
al6ng the external surface of the outer division of the internal capsule,
passes through the posterior part of the internal capsule, and terminates
in the anterior and external part of the optic thalamus. The anterior
median group of vessels derived from the anterior cerebral and anterior
communicating arteries are small arteries ; they supply the anterior part
of the caudate nucleus, and derive their chief importance from the fact
that haemorrhage from them may rupture into the ventricles and thus cause
rapid death.

The posterior cerebral artery gives rise to two branches, which deserve
special mention, (i.) The posterior internal artery of the optic thalamus,
which is derived from the artery near its point of origin from the basilar,
and is distributed to the internal surface of the optic thalamus. Haemor-
rhage from this vessel often finds its way into the ventricular cavity,
(ii.) The posterior external artery of the optic thalamus is derived from the
posterior cerebral artery after it has wound round the peduncle. It passes
upwards in the crus to the posterior part of the optic thalamus, where it
terminates. It supplies the external geniculate bodies.

INTERNAL STRUCTURE OE THE CEREBRUM.

§ 680. The cerebrum is made up of (1) grey and (2) white
matter.

(1 ) The grey matter is disposed in three great groups : (a) the
grey matter which forms the central end of the cerebro-spinal
tube ; (&) the grey matter of the basal ganglia ; (c) the grey
matter of the cortex of the hemisphere.

(a) The grey matter which forms the central end of the
cerebrospinal tube has already been described up to the level
of the opening of the aqueduct of Sylvius into the third ven-
tricle, and the grey matter which surrounds the third ventricle

ANATOMICAL AND PHYSIOLOGICAL INTRODUCTION. 449

ifiay be regarded as the upward continuation of the central
Jube. The grey matter of the third ventricle consists of a
well-defined layer covering the inner wall of each optic
jlhalamus and the masses situated at the base of the brain
letween and in front of the crura cerebri ; viz., the posterior
jherforated space (pons Tarini), tuber cinereum, lamina cinerea,
Slnfundibulum, and part of the pituitary body.

(6) The basal ganglia consist of the locus niger, red nucleus
[fof the tegmentum, corpora quadrigemina, the corpora genicu-
filata, the optic thalami, and corpora striata.

The locus niger lies between the crus and tegmentum, and
j extends the whole diameter of the crus, and from the anterior
Sedge of the pons to the corpora albicantia. It consists of nerve
{.cells of various forms containing much dark pigment.

The red nucleus of the tegmentum is a round, reddish-grey
centre, in structure somewhat similar to the olivary body of the
medulla oblongata.

The corpora quadrigemina consist of grey and white matter,
the former being continuous in front with the grey matter of
the optic thalamus, and behind with that of the pons, and by
means of the nucleus of the roof of the fourth ventricle with
the corpus dentatum of the cerebellum.

The Corpora Geniculata. — The external geniculate body is
; densely filled with large branching and fusiform cells, and
; the fibres of the outer portion of the optic tract pass through it.
The internal geniculate body contains numerous small nerve
cells similar to those of the corpora quadrigemina.

The optic thalamus is composed of interlacing fibres mingled
with grey matter. The nerve cells in the grey matter are both
multipolar and fusiform.

The middle or grey commissure, connecting the two thalami,
consists of small cells containing yellow pigment.

The corpus striatum is arranged in two chief masses, named
respectively the caudate and lenticular nuclei. The caudate
nucleus is connected below with the lamina cinerea, the anterior
perforated space, and that part of the grey matter of the optic
thalamus which is seen in the third ventricle. It contains large
and small nerve cells, both possessing many branched processes.

450 ANATOMICAL AND PHYSIOLOGICAL INTRODUCTION.

No axis-cylinder process has been observed springing from the
cells of the caudate nucleus.

The lenticular nucleus is continuous below with the caudate
nucleus, and with the grey matter of the anterior perforated
space. The two innermost zones contain numerous large
branching nerve cells with yellow pigment. The cells are
smaller in the outer division of the nucleus.

The claustrum is made up of fusiform and bipolar cells,
somewhat resembling the cells of the vesicular column of Clarke
on the one hand, and those of the fifth layer of the cortex on
the other.

The amygdaloid nucleus is a small, round mass of grey matter,
connected with the inferior part of the claustrum. It lies in
front of the anterior extremity of the descending horn of the
lateral ventricle, and is composed of fusiform cells similar to
those of the claustrum.

(c) The Grey Matter of the Cortex. — When a convolution is
divided vertically the grey matter is seen to be confined to
the surface and to enclose a white core. The cortical substance
consists of cells and fibres embedded in a matrix similar to the
neuroglia of the spinal cord.

The cells are of various forms, the most usual forms being
spherical, stellate, pyramidal, and fusiform. The fibres radiate
into the grey cortex from the white centre of each convolution,
their course being vertical to the free surface of the convolution.
They are arranged in bundles as they pass through the grey
substance, and this gives to the nerve cells a columnar arrange-
ment. The radiating fibres are wanting in the sulci between
the convolutions, but the internal layer of the grey substance
of the cortex generally contains fibres which pursue an arciform
course and connect adjacent convolutions. Fibres pass in all
directions through the grey substance connecting its several
layers, and forming a dense network, like that of Gerlach in
the spinal cord.

Layers of the Cortex. — The cortex of the cerebrum is divided
into several layers, each of which possesses a definite histological
character. The most commonly distributed form of structure
is what Meynert has called the "five laminated type." The
external layer consists of neuroglia and a layer of delicate

ANATOMICAL AND PHYSI

nerve tubes, along with a few
scattered small nerve cells
which are destitute of pro-
cesses. The next layer is com-
posed of small angular or
pyramidal nerve cells with
branching processes. The
third layer contains large and
■small pyramidal cells with
branching processes, arranged
with 'their pointed extremi-
ties towards the surface of
the convolutions, and sepa-
rated into groups by bundles
of the radiating fibres. In the
innermost portion of this layer
the pyramidal cells are larger
than in the remaining portions,
and it has therefore been de-
scribed as a separate layer by
Dr. Lockhart Clarke. In the
cortex of the occipital lobe the
deeper cells of the third layer
are pyramidal in form, with
their bases turned inwards
towards the medullary sub-
stance, but their basal pro-
cesses are directed laterally so
as to connect adjacent cells,
and none of them appear to be
directed inwards to connect
the cells with the fibres of the
medullary substance. In the
anterior portion of the frontal
convolutions the disposition of
these cells is somewhat similar,
but a distinct basal process has
occasionally been observed,
which is directed towards the

INTRODUCTION. 451 .
Fig. 215.

Fig. 215 (After Meynert). Transparent
Section of a Furrow of the Third Cere-
bral Convolution of Man. Magnified
100 decimeters. — 1, Layer of the scat-
tered small cortical corpuscles ; 2,
Layer of close-set, small pyramidal
corpuscles ; 3, Layer of large pyra-
midal cortical corpuscles (formation
of the comu Ammonia) ; 4, Layer of
email, close-set, irregular-shaped cor-
tical corpuscles (granule-like forma-
tion) ; 5, Layer of fusiform cortical
corpuscles (claustral formation) ; m,
the medullary lamina.

452 ANATOMICAL AND PHYSIOLOGICAL INTRODUCTION.

medullary substance of the convolution, and which afterwards
becomes continuous with one of the fibres of the centrum i
ovale.

In the central convolutions of the brain Betz and Mezier-
jewski have discovered cells which are two or three times the
size of the pyramidal cells of the other regions of the cortex,
and they have consequently named them giant-cells. Ia

Fig. 216.

Fig. 216. Pyramidal Giant-Cell. — n, Nucleus ; a, a, a, Branched processes ;

c, Unbrauched basal process.

addition to the branched protoplasmic processes (Fig. 216, a, a)
which connect neighbouring cells with one another, these cells
possess a distinct axis-cylinder process (Fig. 216, c). The latter
is always unbranched, and after becoming surrounded by a
medullary sheath it forms the axis cylinder of a nerve fibre of
the centrum ovale. Giant-cells have been observed in the para-
central lobule and in a portion of the postero-parietal, as well as
in the ascending frontal and parietal convolutions, and posterior
extremities of the three frontal gyri. These cells are disposed

ANATOMICAL AND PHYSIOLOGICAL INTRODUCTION. 453

in groups, and correspond in position to the motor centres of
physiologists. The giant-cells vary greatly in size, the largest
being found, as we have already seen, in the paracentral lobule,
which may be regarded as the upper extremity of the ascending
frontal and parietal convolutions. Large pyramidal cells are
also found in the upper part of the ascending frontal convolu-
tions, but Dr. Bevan Lewis has found that they diminish in size
from the upper extremity until at the lower extremity they
are but half the size. The pyramidal cells of the posterior
extremities of the frontal convolutions are on the whole smaller
than those of the ascending frontal, and the cells also diminish
from above downwards, those in Broca's convolution being the
smallest.

The fourth layer consists of closely-set angular corpuscles
with fine processes, placed irregularly and not distinctly sepa-
rated into groups.

The fifth layer consists of medium-sized, fusiform, and
bipolar cells. The long diameters of these cells run parallel
to the layers of the cortex, and are associated with the system
of fibres which connects different convolutions of the same
hemisphere with one another.

(2) The ivhite matter of the cerebrum consists of (a) trans-
verse or commissural fibres ; (b) longitudinal or collateral fibres ;
and (c) ascending or peduncular fibres.

(a) The transverse or commissural fibres consist of the
following : —

(i.) The transverse fibres of the corpus callosum pass transversely from
one side to the other, and connect corresponding convolutions in the
hemispheres. These fibres lie on a plane superior to those of the corona
radiata, and consequently the two systems of fibres interlace on their way
to the convolutions.

(ii.) The fibres of the anterior commissure wind backwards through the
lenticular nuclei to reach the convolutions around the Sylvian fissure.

(iii.) The fibres of the posterior commissure run through the optic thalami.

(6) The longitudinal or collateral system of fibres are the
following : —

(i.) Arcuate fibres or fibra? propria, which are situated immediately
beneath the inner surface of the cortex, and connect together the grey
matter of adjacent convolutions.

454 ANATOMICAL AND PHYSIOLOGICAL INTRODUCTION.

(ii.) Fibres of the gyrus fornicatus take a longitudinal course imme-
diately above the corpus callosum and form the white matter of that
convolution. In front they bend round the corpus callosum, and become ,
connected with the anterior perforated space. Behind they turn round
the back of the same body, and are said to pass forwards to reach the
anterior perforated space, so that these fibres completely surround the
corpus callosum. Offsets from these fibres pass upwards and backwards
to reach the summits of the secondary convolutions derived from the gyrus
fornicatus near the longitudinal fissure.

(iii.) Longitudinal septal fibres lie on the inner surface of the septum
lucidum and extend into the gyrus fornicatus.

(iv.) The fasciculus uncinatus passes across the bottom of the Sylvian
fissure, and connects the convolutions of the frontal and temporo-
sphenoidal lobes.

(v.) The longitudinal inferior fasciculus connects the convolutions of
the occipital with those of the temporal lobe.

(vi.) The longitudinal fibres of the corpus callosum (nerves of Lancisi)
connect, the anterior and posterior ends of the callosal convolution.

(c) The Ascending or Peduncular Fibres. — The fibres which
connect the central grey tube with the encephalon have already
been traced as far as the crura. The upward continuation of
the fibres of the anterior root-zones of the cord terminate in
the optic thalamus. The posterior longitudinal fasciculus lies
in front of the nucleus of origin of the third nerve, and when
the aqueduct of Sylvius opens into the third ventricle, the
fibres of the fasciculus bend outwards in the posterior commis-
sure of the third ventricle to reach the inner wall of the optic
thalamus, where they appear to terminate. Meynert describes
these fibres as passing downwards and outwards to form part of
the fillet of the crus cerebri, but examination of the crus in the
embryo does not bear out this statement. The fibres of the
posterior longitudinal fasciculus are medullated at an early
period of embryonic life, but in a nine months embryo no
medullated fibres having the course described by Meynert can
be seen in the crus cerebri. The fibres of the posterior com-
missure, on the other hand, are the first fibres of the cerebrum
to assume a medulla (Mechsig). The upward continuation of
the external portion of the anterior root-zone of the cord lies
in the crus cerebri to the outside of the third nerve and poste-
rior longitudinal fasciculus, and the fibres of this area are con-
tinued upwards into the optic thalamus, where they form a thin

ANATOMICAL AND PHYSIOLOGICAL INTRODUCTION. 455

Stratum of fibres which separates the grey matter which lines
the third ventricle from the rest of the optic thalamus. A
|portion of the upward continuation of the external part of the
anterior root-zone of the cord bends backwards in the pons to
reach the corpora quadrigemina.

Fig. 217.

Fig. 217 (From Henle's Anatomie). Vertical Section of the Brain parallel to the
course of the Ascending Fibres of the Right Cerebral Peduncle. — *, Great longi-
tudinal fissure ; 1, Left ; and 2, Right hemisphere ; Lq, Lamina quadri-
gemina ; Cn, Pineal Gland ; Ccl8, Corpus callosum ; Tho, Thalamus : Sz,
Striatum zonale of the thalamus ; Cs, Caudate nucleus ; Nl, Lenticular
nucleus ; Tbo, Tuber olfactorium ; Cls, Claustrum ; Sn, Locus niger ; Ntg,
Red nucleus of the tegmentum ; Fqs and Fqi, Superior and inferior transverse
fibrea of the pons ; IT, Optic tract.

The corpora quadrigemina are connected with the optic
thalami by nervous tracts, named brachia. The cerebellum is
connected with the corpora quadrigemina by the superior
peduncles. A large number of the fibres of the superior
peduncles of the cerebellum decussate in the tegmentum, so
that the fibres of the one side cross to become connected with
the red nucleus of the opposite side. Some of these fibres

456 ANATOMICAL AND PHYSIOLOGICAL INTRODUCTION.

probably terminate in this nucleus, while others appear to
pursue an uninterrupted course to the brain. The course of the
fibres of the superior peduncles of the cerebellum is not well |
ascertained beyond the red nucleus. Some anatomists think
that these fibres terminate in the optic thalamus, while others
believe that they pass uninterruptedly as a thin stratum of :
fibres between the optic thalamus and the internal capsule,
and through the corona radiata to reach the grey matter of the
central convolutions.

Fig. 218.

Cgi

Fig. 218 (From Henle's Anatomie). Horizontal Section of the Hemisphere of the
Brain, close to its Inferior Surf ace. — Lq, Lamina quadrigeniin a; A, Aqueduct
of Sylvius ; Ntg, Eed nucleus of the tegmentum ; Rdf, and Raf, Descending
and ascending roots of the fornix; Co, Optic commissure, seen through the
floor of the third ventricle ; Cs, Caudate nucleus of the corpus striatum ; Nl,
The lenticular nucleus ; *, Division between the two nuclei of the corpus
striatum ; Spa, Anterior perforated space ; In, Island of Reil ; Coa', Anterior
commissure ; Sn, Substantia nigra ; B', Transverse section of the crusta ; IF,
Optic tracts ; Cgl, External geniculate body.

ANATOMICAL AND PHYSIOLOGICAL INTRODUCTION. 457

The Internal Capsule and Corona Radiata.-The crust of
the cerebral peduncle consists of bundles of longitudinal fibres
which have ascended mainly from the anterior pyramid of the
medulla. The crust of the peduncle is, however, much larger

Fig. 219.

Fig. 219 (From Henle's Anatomie). Transverse Section of the Hemisphere of the
Brain at >a little higher elevation than Fig. 218.-Cp, External capsule; Cls,
Claustrum. The remaining letters indicate the same as Fig. 218.

458 ANATOMICAL AND PHYSIOLOGICAL INTRODUCTION.

than the anterior pyramid, hence the fibres of the latter must
have been reinforced in their ascent through the pons.
The crust of the peduncle is quadrilateral in form, but in as- . •)
cending to the hemispheres it becomes flattened from above
downwards, and from within outwards, and the fibres spread
out like a fan, the edges of which are directed forwards and j

Fig. 220.

Fig. 220 (From Flechsig). Horizontal Section of the Brain of a Child nine months
of age, the right side being at a somewhat lower level than the left half. — F, Frontal,
TS, Temporo-sphenoidal, and 0, Occipital lobes; Op, Operculum; In, Island of
Eeil ; Gls, Claustrum ; /"', Third frontal convolution ; Th, Optic thalamus ;
NG, Caudate nucleus ; NG', Tail of caudate nucleus ; LN, Lenticular nucleus ;
I, II, III, First, second, and third divisions of the lenticular nucleus ; EE,
External capsule ; IE, Posterior division, IE', Anterior division, and E, Knee
of the internal capsule ; ah, ph, Anterior and posterior horns respectively of the
lateral ventricles ; gec, Knee of the corpus callosum ; sp, Splenium ; mc, Middle
commissure ; /, Fornix; si, Septum lucidum ; a, Cornu Ammonis.

ANATOMICAL AND PHYSIOLOGICAL INTRODUCTION. 459

lackwards. The fan formed by these fibres is bent into the
lorm of an incomplete hollow cone, having its concave surface
llirected downwards and outwards, and its convex upwards and
Inwards. As the fibres ascend they pass at first between the
Lptic thalamus and lenticular nucleus, but higher up they pursue
Iheir course beneath and to the outside of the thalamus and
baudate nucleus, and over the lenticular nucleus. On horizontal
Lection of the hemisphere, close to the inferior surface of the brain,
the crusta is seen to be of an irregularly quadrilateral form,
with its long axis directed from before backwards and from
within outwards (Fig. 218, B'). At a higher level the crust, or
what may now be regarded as the internal capsule, is of the
same general form as in the preceding section, but its long axis
is somewhat lengthened in proportion to its short axis (Fig.
219, B'). Still higher up the internal capsule has spread out
from before backwards, while the anterior half forms an obtuse
angle with the posterior. The angle where the halves meet is
called the knee (Fig. 220, K), while the divisions themselves
are called the anterior (Fig. 220, IK') and posterior segments
(Fig. 220, IK) of the internal capsule.

Corona Radiata. — On emerging from the basal ganglia the
fibres of the internal capsule radiate in all directions to reach
the cortex of the hemisphere, hence these have been described
by Reil under the name of corona radiata, and the point at
which the fibres emerge from between the ganglia is called the
foot of the corona radiata.

The following fibres may be distinguished in the crusta and
internal capsule: —

(1) The sensory peduncular tract and optic radiations of Gratiolet, the
latter joining the internal capsule from the optic thalamus; (2) the
pyramidal tract ; (3) fibres in the crust connecting the central grey tube
and the corpus striatum ; (4) fibres issuing from the external surface of
the optic thalamus to join the internal capsule ; (5) fibres issuing from
the external surface of the caudate nucleus ; (6) fibres ascending from the
superior and internal surface of the lenticular nucleus ; (7) fibres already
described ascending from the superior peduncle of the cerebellum ; (8)
fibres from the corpus callosum (Wernicke).

(1) Sensory peduncular fibres and optic radiations of Gratiolet. — The
posterior root-zones and columns of Goll terminate, as we have already
seen, in the triangular and clavate nuclei ,* and the connection between

460 ANATOMICAL AND PHYSIOLOGICAL INTRODUCTION.

these nuclei and the olivary body, and of the latter with the cerebellum, has
already been sufficiently described. It has also been seen that the sensory
fibres cross in the spinal cord, but Meynert describes a sensory crossing
which takes place in the lower part of the medulla oblongata. According to
this author, fibres issue from the nuclei of the cuneate and slender fasciculi
which pursue an arcuate course round the central grey column, and become
mixed with the fibres of the lateral column as they bend forwards to
decussate. As already noticed, Flechsig thinks that these fibres curve
round the olivary body of the same side, and enter its substance, while
Meynert thinks that they form the outer fasciculus of the anterior pyramid
of the medulla oblongata, and ascend with the latter up through the pons
to reach the crus cerebri. Debove and Gombault describe an additional
crossing of sensory fibres higher up in the medulla. These fibres pursue
an arcuate course from the triangular and clavate nuclei, pass forwards to
the outside of the olivary body, and then become subdivided into small

Fig. 221.
b' Cs

Fxg. 221 (Prom Henle's Anatomie). Transverse and Oblique Section of the Basal
Ganglia slanting upwards and forwards from the anterior edge of the Pons (P). —
B, Crust of the crus cerebri ; B', Radiation of the peduncular fibres into the
hemisphere ; Sn, Locus niger ; Ntg, Red nucleus of the tegmentum ; *, Upper
portion of the formatio reticularis; Tho, Thalamus opticus; Cs, Caudate
nucleus; II', Optic tract; Hp, Hippocampus.

ANATOMICAL AND PHYSIOLOGICAL INTRODUCTION. 461

fasciculi, which penetrate into the posterior and external aspects of the
Interior pyramid, and finally curve upwards, becoming mixed with the
notor fibres. It is very probable that these sensory fibres occupy the
posterior and external portion of the pyramidal tract in its ascent through
;he pons, inasmuch as bundles of fibres exist here which are not so dis-
tinctly medullated in a nine months human embryo as those lying in

Fig. 222.

Fig. 222 (After Debove and Gombault) -Section of the Anterior Pyramid (P) of
the Medulla Oblongata, on a level with the middle part of the crossing of the
Sensory Fibres.— FS, Sensory fibres ; FSA, Posterior and external sensory
fasciculus which does not penetrate into the substance of the pyramid ; E,
Crossing of the sensory fibres ; 0, Nucleus of the pyramid; Z, Stratum zonale.

front of them. It has been at least ascertained that the sensory fibres
occupy the external fourth of the crusta, and about the posterior third of
the posterior segment of the internal capsule in their ascent towards the
cortex of the brain. These fibres do not appear to be in any way con-
nected with the optic thalamus and lenticular nucleus, but pass onwards
between them to reach the cortex of the brain. In the posterior third of
the posterior segment of the internal capsule the sensory fibres bend
abruptly backwards, and then radiate to reach the convolutions of the
occipital and temporo- sphenoidal lobes. The fibres of this tract are never
medullated in an embryo of nine months, and can be readily traced
upwards in the outer segment of the crusta and posterior segment of the
internal capsule. In addition to the fibres which ascend from the spinal
cord, medulla oblongata, and pons, the sensory tract in the internal capsule
contains fibres which connect the first and second cerebral nerves with
the cortex of the brain.

The optic tracts take origin in the basal ganglia by an internal, middle,
and external root.

The internal root consists of a bundle of fibres which passes between
the external geniculate body and outer edge of the crusta, and penetrates
into the substance of the internal geniculate body, appearing to end in
the anterior pair of corpora quadrigemina. Huguemin has recently main-

462 ANATOMICAL AND PHYSIOLOGICAL INTRODUCTION.

tained that this root is connected with the posterior pair of corpora ir •'
quadrigemina, either directly or through the medium of the external :P
geniculate body.

The middle root terminates in the external geniculate body.

The external root passes to the outside of the external geniculate body .- $
and penetrates the inferior peduncle of the optic thalamus about ] 2mm. in
front of the posterior border of the pulvinar. By extirpating the eyeballs
of young hares Gudden found that, when the animals were killed some
months subsequently, the anterior pair of corpora quadrigemina, the optic
tbalami, and the external geniculate bodies were atrophied; while the
posterior pair of corpora quadrigemina and the internal geniculate bodies
were unaffected. In man, however, both the anterior and posterior pair
of corpora quadrigemina have been found diminished in size in cases of
long standing atrophy of the optic nerves.

These various roots of the optic nerves appear to be connected with
the cortex of the brain by means of the fibres which have been named
the optic radiations of Gratiolet. This bundle of fibres issues from the
posterior and external border of the optic thalamus and is closely applied
to the peduncular sensory tract in its passage through the internal cap-
sule ; these fibres radiate backwards and upwards to be connected with
the convolutions of the occipital lobe.

The olfactory lobe, according to Meynert, divides in front of the anterior
perforated space into an internal and external olfactory convolution. The
external convolution coalesces with the temporal extremity of the gyrus
fornicatus or the subiculuni cornu ammonis. The internal convolution is
continuous with the frontal end of the gyrus fornicatus, beneath which it
may be recognised for some distance as a distinct longitudinal elevation.

A considerable portion of the white substance of the olfactory lobe
traverses the corpus striatum until it meets the anterior commissure
coming in the opposite direction. The olfactory fibres are supposed to I
cross in the anterior commissure, corresponding to the crossing of the fibres
of the optic nerves in the chiasma. After crossing these fibres appear to
ascend upwards and backwards and to join the fibres of the optic radiations
of Gratiolet, and pass along with them to- the convolutions of the cortex
of the occipital or temporo-sphenoidal lobe. The posterior third of the
posterior segment of the internal capsule, therefore, contains the peduncular
sensory fibres and the fibres which connect the optic nerves, and the olfac-
tory bulb with the cortex of the brain.

(2) The Pyramidal Tract. — The course of the fibres of the pyramidal
tract has already been traced upwards through the spinal cord, medulla
oblongata, and pons. It remains to trace the course of these fibres through
the crusta, internal capsule, and corona radiata to their destination in the
convolutions of the cortex. "We have also found that the greater number
of the fibres of the pyramidal tract in the cord are medullated in a nine
months human embryo, while a large proportion of the fibres which join
the tract in the medulla oblongata and pons are non-medullated. The ex-

ANATOMICAL *AND PHYSIOLOGICAL INTRODUCTION. 403

Jerual portion of the anterior pyramids of the medulla contains on tho^ne
laud medullated without any admixture of non-medullated fibres, the
Internal and anterior margin of the pyramid on the other hand contains
Sion-medullated without any admixture of medullated fibres, while an area
lies between these in which the two kinds of fibres are mixed. The first

Fig. 223.

Fig. 223 (Modified from Krause). Transverse Section of the Crus Cerebri on a level
with the anterior pair of Corpora Quadrigemina, from a nine months embryo. —
cc, crusta ; P, fundamental, P', mixed, and p, accessory portion of the pyra-
midal tract ; LN, locus niger ; MN, red nucleus of the tegmentum ; L, posterior
longitudinal fasciculus ; ar and ar1, upward continuation of the internal and ex-
ternal portions respectively of the anterior root-zone of the spinal cord ; in,
third nerve ; ill', nucleus of the third nerve ; IV, fourth nerve ; iv', nucleus of
the fourth nerve ; iv", crossing of the fibres of the fourth nerves to opposite
sides ; dt, descending root of the trigeminus ; cc, aqueduct of Sylvius ; x, cross-
ing of the fibres of the superior peduncles of the cerebellum ; pf, fasciculus of
medullated fibres proceeding to the anterior pair of corpora quadrigemina.

of these regions may be called the fundamental, the second the accessory,
and the third the mixed area. We have already seen that in the pons the
accessory portion of the pyramidal tract lies internal to the fundamental
portion, and in the crusta they occupy the same relative positions. The
fundamental portion of the tract occupies the greater portion of the middle

464 ANATOMICAL AND PHYSIOLOGICAL INTRODUCTION.

thirjl {Fig- 223, P), and the accessory portion the larger part of the internal
third of the crusta {Fig. 223, p). The mixed area of the tract lies partly
in the middle third of the crusta between the fundamental area and the
locus niger, and winds round to the inside of the fundamental and '
between it and the accessory area {Fig. 223, P'). Speaking broadly, the
fundamental fibres ascend in the middle {Fig. 224, P) and the mixed
fibres in the anterior third of the posterior segment of the internal capsule
{Fig. 224, P'), while the accessory fibres ascend in the anterior segment of
the capsule {Fig. 224, p).

Fig. 224.

Fig. 224. Horizontal Section of the Basal Ganglia and Internal Capsule of a Nine
Months Embryo. — LN, Lenticular nucleus ; II, III, Second and third segments
of the nucleus respectively ; NC, Caudate nucleus ; Th, Optic thalamus ; In,
Island of Reil ; ps, Peduncular sensory tract and optic radiations of Gratiolet ;
P, Fundamental, P', Mixed, and p, Accessory portion of pyramidal tract ; C,
Fibres from the corpus callosum (?).

The fibres of the pyramidal tract, on emerging from between the basal
ganglia, ascend in the corona radiata, and are distributed to the convo-
lutions of the cortex in the following manner : — The fundamental fibres
pass to the central convolutions near the margin of the great longitu-
dinal fissure. These convolutions are, briefly, the parietal lobule, the
paracentral lobule, the superior extremities of the ascending frontal and
parietal convolutions, and probably also the posterior extremity of the
first frontal convolution. These convolutions are, as we have already
seen, those in which the largest pyramidal cells of the fourth layer of

ANATOMICAL AND PHYSIOLOGICAL INTRODUCTION. 405

Le cortex have been found. The accessory fibres are distributed to the
Evolutions that constitute the operculum. These convolutions are the
Uterior extremity of the third frontal and the inferior extremities of
he ascending frontal and parietal convolutions, and correspond to those
fu which the smaUer^ed pyramidal cells with axis-cylinder processes
Lave been observed. The mixed pyramidal tract is distributed to the
evolutions between the two other areas. These convolutions are the
Lsterior extremity of the second frontal and the middle of the ascending
End parietal convolutions. What connection exists between the pyramidal
iract and the supra-marginal and angular gyri has not been ascertained.

(3) Fibres connecting the Central Grey Tube with the Corpus Stnatum..-
TV first and second divisions of the lenticular nucleus are connected with
the crusta by a band of radiating fibres, which in their ascent are disposed
in two thin bands, named the strice medullares, and which run parallel to

Fig. 225.

■11 0

-Com.

Rd£

Cca,

Fig. 225 (From Henle's Anatoinie). Transverse and Vertical Section of the Basal

Ganglia on a level with the Corpora Caudicantia.

Cca, Corpora albicantia. Nl, Lenticular nucleus.

Rdf, Descending roots of the fornix. Cat, Corpus subthalamicum.

Com, Anterior commissure. II', Optic tracts.

Tto, Tamia of the optic thalamus. B, Crust of the cerebral peduncle.
Cs, Caudate nucleus.

466 ANATOMICAL AND PHYSIOLOGICAL INTRODUCTION.

the outer surface of the nucleus, and divide it into three zones. Many
of these fibres terminate in the substance of the nucleus, while others
pass through it probably without interruption. A large number of these
fibres at least pass transversely through the internal capsule, interlacing
with its ascending fibres, and becoming connected with the optic thalamus
and caudate nucleus. Fibres appear to enter the crusta from the locus
niger, and it is not improbable that the latter nucleus is to be regarded
as the means of communication between the anterior root-zone of the
spinal cord and the corpus striatum.

(4) Fibres issuing from the External Surface of the Optic Thalamus to
join the Internal Capsule. — The optic radiations of Gratiolet already
described belong to this system of fibres, inasmuch as they issue from the
external surface of the posterior portion of the thalamus. Other fibres
issue from the external surface of the anterior two-thirds of the thalamus
and join those of the pyramidal tract on their way to the cortex.
The anterior radiating fibres of the thalamus are probably distri-
buted to the convolutions of the frontal lobe, and the central radiating
fibres to the convolutions of the parietal lobe, while as we have already
seen the posterior radiating fibres are distributed to the convolutions of
the occipital lobe.

(5) Fibres issuing from the External Surface of the Caudate Nucleus. —
These fibres are described as issuing from the external surface of the
caudate nucleus, and as passing into the corona radiata immediately above
and internal to the radiating fibres of the optic thalamus.

(6) Fibres issuing from the Superior and Internal Surface of the Lenticular
Nucleus to join the Ascending Fibres of the Internal Capsule. — A large num-
ber of fibres issue from the superior and internal surface of the lenticular
nucleus, and pass transversely through the internal capsule, interlacing
with its longitudinal fibres. Other fibres are described as pursuing an
ascending course parallel with the longitudinal fibres of the internal cap-
sule. The latter fibres are supposed to radiate in all directions on gaining
the corona radiata to become connected with the cortex. It is right,
however, to add that the latest anatomical researches throw considerable
doubts upon the existence of the radiating fibres which anatomists have
described as connecting the caudate nuclei and the third division of the
lenticular nucleus with the cortex. "Wernicke states that neither the
caudate nucleus nor the third division of the lenticular nucleus are directly
connected with the cortex by radiating fibres, and he thinks that they
must be regarded as independent ganglia, like the grey matter of the
cortex itself. The first and second divisions of the lenticular nucleus
form ganglia of interruption, which connect the caudate nucleus and the
third division of the lenticular nucleus with the central grey tube.

(7) Fibres Ascending from the Superior Peduncle of the Cerebellum.—
The red nucleus of the tegmentum is connected, as already described, with
the fibres ascending in the superior peduncle of the cerebellum of the
opposite side. Fibres appear to ascend from the red nucleus to the

ANATOMICAL AND PHYSIOLOGICAL INTRODUCTION. 4G7

optic thalamus, and Flechsig supposes that some of the fibres of the
superior peduncle of the cerebellum of the opposite side pass uninter-
ruptedly through the red nucleus and along the internal surface of the
fibres of the pyramidal tract to be distributed to the central convolu-
tions of the cerebrum.

(8) Fibres issuing from the Corpus Callosum and Descending into the
Internal Capside.— Wernicke states that the fibres of the corpus callosum'
which form the anterior wall of the anterior horn of the lateral ventricle
wind backwards along the external border of the caudate nucleus, where
they become mixed with the longitudinal fibres of the internal capsule
He is unable to trace them further.

(9) Fibres of the External Capside.— -The fibres of the external capsule
either ascend from the crusta, pass along the inferior surface of the
lenticular nucleus, and bend abruptly upwards round its inferior external
angle to reach the external surface, or they take origin in the cells of the
nucleus, and after issuing from its inferior surface pursue the course just
described. These fibres ascend along the external surface of the lenticular
nucleus forming the thin stratum of white matter between it and the claus-
trum (Fig. 220, EE), and on reaching the corona radiata they radiate to
reach the convolutions of the cortex. The external surface of the lenticular
nucleus and the external capsule are simply in contact with one another,
and there appear to be no connections formed between the fibres of the
one and the cells of the other. The two surfaces are, indeed, separated in
some places by blood-vessels ascending from the middle cerebral artery.

Besides those of the internal capsule and corona radiata, other
fibres connect the basal ganglia and the cortex of the brain.
These fibres consist of the fornix, tcenia semicircular is,
pedunculus septi, and a considerable proportion of the fibres
which constitute the collar or fillet of the crus.

The fornix arises in the optic thalamus. Its fibres of origin are
connected with the tcenia semicircidaris and the peduncles of the pineal
gland. They descend to the under surface of each thalamus, and after
forming a loop in the corpora albicantia they ascend upwards and forwards
in the walls of the third ventricle as the anterior pillars of the fornix.
The fibres of each crus then pass backwards in the body of the fornix,
and end as the ta3nia hippocampi in the gyrus of the same name.

The tcenia semicircular is connects the apex of the temporal lobe with
the whole length of the internal margin of the caudate nucleus. The fibres
which penetrate into the anterior region of the head of that nucleus are
named strice cornea.

The pedunculus septi connects the cortical substance of the septum
lucidum with the basal mass of the corpus striatum.

The Collar or Fillet of the Crus Cerebri.— A. bundle of fibres forms at the

4G8 ANATOMICAL AND PHYSIOLOGICAL INTRODUCTION.

posterior, inferior, and external angle of the optic thalamus, which winds
downwards, outwards, and forwards round the posterior margin of the
ascending fibres of the crusta. These fibres are named the inferior peduncle
of the optic thalamus, and constitute the posterior portion of the collar
or fillet of the crus ; they spread out on the roof of the descending cornu
of the lateral ventricle and pass forwards to the convolutions of the
anterior extremity of the temporo-sphenoidal lobe. It is probable that
some of them also radiate backwards to reach the convolutions on the
inferior surface of the occipital lobe. Other fibres appear to issue from
the anterior, inferior, and external angle of the thalamus, which wind
round the anterior border of the crusta, and terminate in the lenticular
nucleus, or pass to the convolutions of the temporo-sphenoidal lobe.
These fibres form the anterior portion of the collar of the crus.

§ 681. Development of the Brain. — The cerebral end of the cerebro-
spinal tube is at first uniform in appearance with the spinal part, but it
soon expands into three vesicular dilatations— the primary cerebral vesicles.
These vesicles are named, from their relative positions, anterior, middle,
and posterior, and the structures which go to form the several sub-
divisions of the encephalon are produced in their walls.

* The posterior cerebral vesicle first bends forwards to form the medulla
oblongata, and then backwards to form the cerebellum, the pons being
developed at the angle where these two parts are continuous with one
another. The cerebellum consists at first of a central lobe, and the
lateral lobes are only developed in the mammalia.

The middle cerebral vesicle bends forwards from the posterior one, its
central hollow becoming the aqueduct of Sylvius ; the optic lobes are
formed in its roof, and the crwra cerebri in its floor.

The anterior cerebral vesicle bends downwards from the middle vesicle,
and its central hollow becomes the third ventricle. The optic thalami
form in its lateral walls, and the pineal body in its upper and posterior
wall. The lamina cinerea closes the vesicle in front. The posterior part
of the anterior vesicle gives off from each side a flask-shaped prolongation —
the primary optic vesicle — which subsequently forms the optic tract with
the optic nerve and retina.

The antero-lateral part of the cerebral vesicle is prolonged forwards
into two hollow processes, the hemisphere-vesicles, from which the cerebral
hemispheres are subsequently developed. These vesicles are separated
from one another by a median longihidinal fissure, whilst the hollow in
the interior of each forms the lateral ventricle. On the floor of this
vesicle a grey mass forms which may be named the basal nucleus, and
which subsequently develops into the corpus striatum. The remaining
portions of the walls of the vesicle form the cortex of the brain, the
basal nucleus and cortex being continuous in the part which subsequently
forms the anterior perforated space. When after a time fibres shoot
down from the cortex to reach the central grey tube, and shoot upwards

ANATOMICAL AND PHYSIOLOGICAL INTRODUCTION. 409

from the central grey tube, corpora quadrigemina, and optic thalamus
to reach the cortex, they pursue the shortest course by passing
through the basal nucleus, so that the latter becomes divided into
an inferior and external (the lenticular), and a superior and in-
ternal portion (the caudate nucleus), the two being continuous with one
another and with the cortex of the cerebrum in the anterior perforated
space. The development of the basal nucleus therefore renders it probable
that the corpus striatum is a modified portion of the cortex of the brain,
. thus confirming the view recently adopted by "Wernicke. The fibres of
which the fornix consists now appear on the inner wall of the hemisphere-
vesicle, while the transverse fibres of the corpus callosum pass above
the plane of the fornix to connect the cortex of one hemisphere with
that of the other. Between the corpus callosum and the upper surface of
the fornix, anteriorly, two thin layers of grey matter belonging to the inner
surface of each hemisphere- vesicle are enclosed. These together form
the laminae of the septum lucidum, and the cavity which separates them
becomes the fifth ventricle. Each hemisphere-vesicle gives off from its
anterior part a hollow process which develops into the olfactory bulb.

The longitudinal or collateral system of fibres, which connects the
occipital lobe on the one hand and the temporal and frontal lobes on
the other, form a relatively thick white layer in their passage through the
middle lobe, which cuts off the fifth from the remaining layers of the cortex
of the Island of Reil, the detached portion being known as the claustrum.
It consists, as we have seen, of fusiform cells analogous to those found in
the fifth layer in other areas of the cortex, and which are probably asso-
ciated in the latter with the system of arcuate fibres.

The Convolutions. — The walls of the cerebral hemispheres consist at
first of two smooth shell-like lamellae which include the cavities afterwards
named the lateral ventricles. The first traces of the convolutions appear
about the fourth month, the primary sulci appearing as slight depressions
on the smooth surface. The Sylvian fissure begins as a cleft between the
anterior and middle lobes about the fourth month, and is the first fissure
to make its appearance after the great longitudinal fissure. Soon after-
wards the fissure of Rolando appears ; it is followed by the parietoocci-
pital, and at a somewhat later period by the calloso-marginal fissure.
After the fifth month, the secondary fissures develop rapidly, and all
the convolutions and fissures make their appearance towards the seventh
and eighth months. The hemispheres do not cover the optic thalami
until the third month, at the fourth they reach the corpora quadri-
gemina, and at the sixth month they cover a great part of the cerebellum.

The convolutions of the human brain are divided into primary or fun-
damental and secondary or accessory. The disposition of the fundamental
convolutions is fixed, and corresponds closely with the arrangement of the
convolutions in the brain of the monkey ; but the disposition of the acces-
sory convolutions is variable, and they must be regarded as being super-
added to the former in the course of evolution. The arrangement of the

470 ANATOMICAL AND PHYSIOLOGICAL INTRODUCTION.

convolutions of a human embryo at the sixth month corresponds closely
to that of the brain of the adult monkey.

The fundamental convolutions are distributed along the margin of the
great longitudinal and other primary fissures, while the accessory convo-
lutions border the secondary fissures.

The grey matter of the accessory is connected with that of the funda-
mental convolutions by means of arcuate fibres, while the former is not
directly connected with the ascending and radiating fibres of the internal
capsule.

Another circumstance worth observing is that the grey matter of the
summits of the convolutions is developed before that at the bottom of the
fissures (Broad bent). It must be remembered that the growth of the brain
is restrained at an early period of embryonic life by the skull. The distri-
bution of the blood-vessels to the brain is such that the surface of the
hemisphere must be more freely supplied with blood than the medullary
substance, and consequently the former will grow at a more rapid rate
than the latter. If then the cortex grow at a more rapid rate than the
medullary substance, and be at the same time restrained from growing
freely outwards by the skull, the surface of the organ must be thrown into
folds. The young nerve cells and fibres grow in the neighbourhood of the
vessels and the older ones are thrust away from them. It follows that
when two vessels run a more or less parallel course on the surface of the
brain the younger nerve cells and fibres lie near each vessel, while the
older ones occupy a position midway between them. If the surface of the
brain were free to grow in all directions like the skin, the vessels them-
selves would be thrust further apart during growth and the surface would
remain more or less smooth ; but as the surface of the brain grows under
pressure, the vessels cannot be thrust from each other at a sufficiently
rapid rate to keep progress with the growth of nerve tissue between
them. The consequence is that either the growth of the nerve tissue
between the two vessels must be arrested, or a fold must be formed so
that the grey matter between them may pursue a curved instead of a
straight course. If this be an approximately accurate account of the way
in which the cerebral convolutions are formed, it will be readily seen that
the earlier-formed nerve cells and fibres occupy the summits of the convo-
lutions, while the later-formed cells and fibres occupy the bottom of
the fissures. It may be noticed, in confirmation of this view, that the
summits of the convolutions are alone directly connected with the pedun-
cular and radiating fibres, while the grey matter of the fissures is only
connected with them indirectly through that of the sumnits by means of
arcuate fibres. The depth of the fissures may, therefore, be taken along
with the complexity of the arrangement of the convolutions and other
circumstances as a measure of the degree of development of the brain.
The distribution of the blood-vessels of the cortex would also lead us to
expect that the superficial layer next the pia mater is the embryonic
layer of the grey matter, while the earlier-formed portions occupy the

ANATOMICAL AND PHYSIOLOGICAL INTRODUCTION. 471

position furthest removed from the vessels, and consequently consist of
the internal layers with caudate cells.

§ 682. Differences between the brain of tlie adult man and that of the higher
mammalia and human infant.— The usual information given in auatomical
works with regard to the size and weight of the human brain as compared
with that of animals will be passed over here in order to insist upon less
conspicuous, but probably not less important, differences. 0

There has been a widely-spread belief that the large development of the
frontal lobes is peculiarly characteristic of the brain of man, but some
years ago Dr. Carpenter drew attention to the fact that in the lower forms
of auimals the cerebellum is entirely uncovered by the cerebrum, that it
is only partially covered by the posterior lobes in the more intelligent
animals, such as dogs and monkeys, and that it is only in man that the
posterior lobes of the cerebrum completely overlap the cerebellum. Dr.
Carpenter argued from this that the increase of the posterior lobes is more
characteristic of advance in development than that of the anterior lobes.
But he ignores the fundamental facts of development, while regarding
superficial appearance. If we take the fissure of Rolando, or the central
sulcus in animals, as the line which separates the frontal from the
parietal lobe, it will be noticed how small a portion of the brain lies
anterior to the sulcus in such animals as the rabbit (Fig. 226, r), which

Fig. 226.

Fig. 226 (Modified from Ferrier). Brain of Rabbit. — O, Olfactory bulb ; r, Central
sulcus ; x , Parallel sulcus ; M, Motor area ; A, Anterior or psychical area ;
P, Posterior or sensory area.

is one of the lowest animals in which the sulcus is developed. Even in
the dog and monkey only a relatively small part of the brain lies anterior
to this sulcus compared to the large mass which lies behind it. And
a study of the development of the human brain shows that the occipital
and parietal lobes increase rapidly at an early period in the develop-
ment of the embryo, while the frontal lobes increase chiefly during
the later months of fcetal life. The portion which lies in front of
the sulcus of Rolando in a six months human footus (Fig. 227, r) is
small, while the sulcus itself is directed vertically upwards in a line
with the anterior ascending limb of the fissure of Sylvius ; the superior
extremity being somewhat anterior to the inferior extremity. In the brain
of the human adult the superior extremity of the sulcus of Rolando is
pushed backwards, owing to the great increase of the frontal lobes, so

472 ANATOMICAL AND PHYSIOLOGICAL INTRODUCTION.

that a vertical line drawn from it would pass through the posterior ex-
tremity of the horizontal limb of the Sylvian fissure. During the develop-
ment of the human brain the superior extremity of the sulcus of
Rolando therefore suffers a backward displacement in order to make room
for the increasing size of the anterior area of the cortex ; and, similarly,
in the evolution of the human brain from the simian type the occipital
lobes have undergone a posterior displacement in order to make room for
the relatively, large increase of size of the frontal lobes, hence the covering
of the cerebellum is not caused directly by an increased size of the occi-
pital, but indirectly by an increased size of the frontal lobes.

Fig. 227.

Fig. 227 (From Quain, after Wagner). External Surface of the Fatal Brain at Six
Months. — F, Frontal lobe. P, Parietal lobe. O, Occipital lobe. T, Temporal
lobe, a, a, a, Slight appearance of the several frontal convolutions. S, Sylvian
fissure ; S', its anterior division. C, Convolutions of the island, r, Fissure of
Rolando, p, External part of the vertical fissure.

Another remarkable feature in which the human brain differs from
that of animals is the manner in which the Island of Reil is completely
surrounded, and hidden out of view by deep convolutions. This is brought
about by the large development of the posterior extremity of the inferior
frontal, the inferior extremities of the ascending frontal and parietal
convolutions, and of the supra-marginal, angular, and inferior temporo-
sphenoidal gyri. It appears to me that the cortex of the central lobe,
starting from the grey matter of the anterior perforated space, is the
embryonic portion of the cortex of the brain, just as the central grey
column is the embryonic portion of the grey matter of the spinal cord.
The anterior perforated space is a point where the grey matter of the two
nuclei of the corpus striatum and of the cortex of all the lobes of the
brain meet, and it may therefore be regarded as the starting point of the
whole of the grey matter derived from the primary cerebral vesicles.
On the supposition that the portion of the central lobe which lies in
the line of distribution of the Sylvian artery is the embryonic portion of the
convolutions of the central or motor area of the brain, it may be expected
that the earlier-formed portions of Hhese convolutions will be thrust up-
wards towards the great longitudinal fissure, while the later-formed por-
tions approach nearer and nearer to the root of the artery. According to

ANATOMICAL AND PHYSIOLOGICAL INTRODUCTION. 473

this supposition therefore the fundamental portions of tho convolutions
supplied by the Sylvian artery will be found near the great longitudinal
fissure, and the accessory portion low down, near the root of the artery,
the latter corresponding to the convolutions named the operculum,
which is so highly developed in man.

The great development of the supra-marginal and angular gyri is also a
characteristic feature of the brain of man.

FUNCTIONS OF THE ENCEPHALON.
The functions of the medulla oblongata have already been
described in detail, and those of the pons, corpora quadri-
gemina, and crura cerebri in a general way.

§ 683. Functions of the Cerebellum. — The cerebellum is,
according to the view adopted in these pages, an organ of com-
pound co-ordination in space, and regulates the continuous
muscular actions which are necessary for the maintenance of
certain attitudes in space. Flourens observed that when a
small portion of the cerebellum was removed from a pigeon, the
animal's gait became unsteady, and that when larger portions
were taken away, the movements became much more disorderly.
Section of the middle peduncle gives rise to a forced movement,
the animal rolling round its. longitudinal axis, and the rotation
being generally towards the side operated upon. Injury of the
lateral lobe of the cerebellum, and probably of the fibres of the
peduncle as they pass transversely through the pons, produces
the same forced movements as section of the middle peduncle.
Nothnagel concludes from experiments on rabbits that lesions
which injure the fibres uniting the two sides of the organ
occasion the greatest amount of motor disturbance.

Ferrier found that electric stimulation of the cortex of the
cerebellum in animals caused movements of both eyes, with
associated movements of the head, limbs, and pupils.

§ 684. Functions of the Basal Ganglia. — The most generally
received hypothesis, especially in England, with respect to
the functions of these ganglia is that the optic thalami are
concerned in the upward transmission and elaboration of cen-
tripetal impulses; and the corpora striata in the downward
transmission and elaboration of centrifugal impulses. The

474) ANATOMICAL AND PHYSIOLOGICAL INTRODUCTION.

impulses elaborated by the thalami may either be transmitted
anteriorly and laterally to the corpora striata, or upwards to the
grey matter of the cortex, while the incitement to action may
come to the corpora striata either from the thalami directly or
from the cortex. When the impulses are transmitted directly
from the thalami to the corpora striata, and from the latter
downwards to the cord, then the basal ganglia may be regarded
as the superordinates of the central grey tube ; but when the
impulses are transmitted from the thalami to the cortex, and
from the latter to the corpora striata, the basal ganglia, although
still the superordinates of the central grey tube, are the subor-
dinates of the grey matter of the cortex.

Very serious objections have been urged against the view that the
thalamus is the sensory ganglion of the opposite half of the body, but
these have been fairly answered by Dr. Broadbent, to whose writings
we are indebted for two most fruitful discoveries in the application of
physiological principles to the elucidation of the phenomena of diseases
of the nervous system.

The first objection is, that lesion of the thalamus does not impair sen-
sation in the same degree that motor paralysis is caused by injury of the
corpus striatum ; but the reply is, that centripetal currents are more
diffusely conducted than centrifugal currents, and that this feature is as
characteristic of the grey matter of the posterior horns of the cord as it
is of the thalamus. Another objection is, that if the thalamus be the
common sensory ganglion, lesion of it ought to cause not only hemi-
aneesthesia, but also unilateral blindness and deafness. To this objection
Dr. Broadbent replies by extending his principle of the bilateral association
of the nerve-nuclei of muscles bilaterally associated in action to the func-
tions of the nerves of special sense. Bilateral association of sensation ought
to involve fusion of sensory nuclei, and the combination of sounds reach-
ing the ears, and of light reaching the retinae, being completely fused into
one sensation, the two auditory and the two optic nuclei ought to be fused
practically into one, so that unilateral deafness or blindness from injury
to one thalamus becomes thus impossible. Another objection to this
view is, that while lesion of the thalamus is frequently unaccompanied by
complete hemiansesthesia, it is sometimes accompanied by motor paralysis
of the opposite side of the body ; from this it has been argued that the
thalamus is a superior centre for reflex action (Crichton Browne). It
must, however, be remembered that the pyramidal fibres of the internal
capsule lie almost immediately external and inferior to the thalamus, so
that disease of the latter may readily implicate the former, and then
paralysis of the opposite side result.

The hypothesis, therefore, that the thalamus is a centre for the com-

ANATOMICAL AND PHYSIOLOGICAL INTRODUCTION. 475

pound co-ordination of centripetal impulses is not open to any insuperable
objections, and accords better with facts than any other theory of its
function. The compound co-ordinated centripetal impressions may be
transmitted directly to the corpus striatum, and reflected downwards to
the anterior horns and anterior root-zones of the cord, thus causing a
compound reflex action, or upwards to the cortex of the brain, where the
impressions become correlated with feeling. There are no sufficient grounds
for believing that the activity of the thalamus implies consciousness, even
of the most rudimentary kind. A compound differs from a simple reflex
action not only as being more complex, but also as consisting of a suc-
cession of different actions. The act of sucking in an infant is a complex
act, but it consists of a series of similar complex actions in response to a
series of similar impressions, and this action may be taken as a good
example of reflex actions in general. But when a chicken has just burst
the shell, and almost immediately begins to pick grains of food off the
ground, the necessary actions are not only complex, but consist of a
succession of different complex actions in response to different complex im-
pressions. There is no reason to believe that the latter action is a con-
scious one, any more than that of sucking in an. infant ; but while the
latter is a simple reflex action, and co-ordinated in the central grey tube,
the former is a compound reflex action, and co-ordinated in the basal
ganglia acting in association with the central grey tube and probably also
with the cerebellum. When impressions are made upon a large number
of the end organs of the afferent nerves, these, after being first co-ordinated
in the posterior part of the grey matter of the central grey tube, undergo,
on ascending, a second co-ordination in the thalami, whereby they are
integrated in various ways, and reduced to something like serial order.
When the centripetal impulses so arranged are transmitted to the corpora
striata, and reflected downwards, they give rise to a succession of muscular
contractions ; when again they are transmitted to the cortex — which is, as
we have already remarked, the organ of doubly compound co-ordination in
time — their serial order adapts them for evoking the rhythmical sequences
of centrifugal impulses which regulate complex psychical actions.

The corpus striatum, on the other hand, is a centre for the
compound co-ordination of centrifugal impulses for the opposite
half of the body. When it acts in obedience to impulses received
from the optic thalamus, it is an organ of compound reflex action.
All the actions which are regarded as inherited instincts, or
which through long-continued repetition have assumed the cha-
racter of acquired instincts, are of the nature of compound reflex
actions; they are or have become independent of conscious-
ness, and are co-ordinated in the basal gaDglia. But the corpus
striatum is supposed to act in obedience to impulses received

476 ANATOMICAL AND PHYSIOLOGICAL INTRODUCTION.

through the cortex of the brain. We have already seen that
there is an uninterrupted connection between the cortex and
grey matter of the cord by means of the pyramidal fibres, and
we must now endeavour to differentiate the functions of the
cortex when it acts through the latter fibres and through the
corpus striatum respectively. A simple illustration will make
this clear. When a child is learning to write, the muscles of
the thumb, index, and middle fingers are moved in separate
groups, so that the fingers are ultimately brought to a proper
attitude for holding the pen. Subsequently the separate
groups of muscles are brought successively into action,
whereby the point of the pen is moved upwards, downwards,
and laterally, so as to produce the elementary strokes of
writing. These actions, described in subjective terms, are
not simply conscious, but involve that active consciousness
which constitutes attention, and they are also deliberate, the
outward sign of deliberation being slowness of execution. The
centrifugal impulses which initiated these movements may be
presumed to have passed through the pyramidal fibres. After
long-continued habit, however, the actions involved in writing
are to a large extent, if not wholly, unconscious, and demand
no deliberation, and this absence of deliberation is accompanied
by extreme rapidity of execution. The centrifugal impulses
regulating these actions are co-ordinated in the corpus striatum,
under the guidance of a relatively small number of impulses
from the cortex. This illustration also shows that the progress
of education is from actions which are at first regulated through
the pyramidal fibres, to actions which are regulated through the
corpus striatum.

The characteristics of the actions regulated through the pyramidal
fibres are, that they are complex, slowly executed, and grouped in an un-
usual manner ; while the characteristics of the actions which are regulated
through the corpus striatum are, that they are quickly executed, and
arranged in frequently repeated combinations. Now, the slowly executed
movements grouped in unusual ways precede in the order of development
the quickly executed and habitual movements, and the structural corre-
lative of this fact is, that in the course of development the pyramidal
fibres assume a medullary sheath some time before the fibres in the crusta
which connect the cord with the corpus striatum. All the complex move-
ments which animals manifest in response to emotional disturbances are

ANATOMICAL AND PHYSIOLOGICAL INTRODUCTION. 477

organised in the corpora striata. The attitude expressive of fear and anger
assumed by a cat when threatened by a dog may be taken as a familiar
example of such actions. Mr. Darwin's description of this attitude is that
the cat " arches its back in a surprising manner, erects its hair, opens its
mouth, and spits." The regulation of the muscular movements concerned
in producing this attitude is organised mainly in the corpora striata, but
the incitement to the action of these centres in such a case comes from
the cortex.

My friend Dr. Noble, of Manchester, whose work " On the Human
Mind in its relations with the Brain and Nervous System V was so much
in advance of the time in which it was written, was the first to suggest
that the movements which are in relation with the desires and emotions
are regulated through the basal ganglia acting in subordination to the
cortex of the brain ; but this view, like many of his other opinions, did
not then attract the attention it deserved.

To illustrate the functions of the basal ganglia, let us suppose that an
impression is made on the retina by a minute object, such as a fly,
approaching the eye. The eyelids immediately close. This action is
purely reflex, and is determined by the corpora quadrigemina and cord,
uninfluenced by the basal ganglia. Part of the disturbance, however, is
conveyed to the optic thalami, and by them co-ordinated in such a way
that on reaching the cortex of the brain they give rise to a sensation, or
even to an indistinct perception, but the closure of the lids is quite
independent of, and prior in time to, the sensation or perception. Let
us now suppose that the impression on both retinoe is made by a larger
body, such as a cricket-ball, at a considerable distance from the eyes, but
moving towards them. The disturbances produced are conducted inwards
by the optic nerves and the afferent nerves of the ocular muscles, and after
being elaborated by the sensory part of the grey matter of the pons and
corpora quadrigemina, some of them pass upwards to reach the cortex
through the sensory fibres of the internal capsule, while others are con-
ducted to the thalami, and after having undergone a second elaboration
and reduction to something like serial order, they also are transmitted
to the cortex. The mental correlative of the cortical disturbance is a
perception of the object and of its position in space, and of the rate
and direction of its motion. Centrifugal impulses may now be sent
from the cortex to the inferior centres, which will eventuate in a series
of movements, either to catch the ball or to avoid collision with it.
One man, in whom no special aptitude has been organised with respect
to the motion of the ball, may simply move his head to one side to
avoid collision. The slower the execution is the more sure we are that
it has not been frequently repeated in the previous experience of the
individual, and that it has been determined by conscious and volitional
mpulses. In such a case the volitional or centrifugal impulses are con-
ducted outwards through the pyramidal fibres, and the corpora striata
have had nothing to do with it. Another man, or rather a woman, on

478 ANATOMICAL AND PHYSIOLOGICAL INTRODUCTION.

seeing the ball may exhibit the outward manifestations of alarm by
facial expression or screaming, and execute a series of locomotive actions
far greater than necessary to avoid collision with the ball, and the greater
these outward manifestations are, the more certain we may be that the
sensory impressions on reaching the cortex have caused a profound
emotional disturbance, and that the centrifugal impulses reach the
periphery through the corpora striata. But a third man, instead of
endeavouring to avoid collision, may put up both hands so as to catch
the ball. Now, the centrifugal impulses may pass in this case either
through the pyramidal fibres or corpora striata, according to circum-
stances. If the action have been frequently repeated so that it be
done with precision, and without a feeling of conscious effort, its regula-
tion is organised in the corpora striata ; and if it be done awkwardly, and
with the inward feeling and outward manifestation of a conscious effort,
then the centrifugal impulses have passed through the pyramidal fibres.

It must, however, be admitted that the foregoing account of the func-
tions of the basal ganglia is by no means fully established. We have
already stated that the internal surface of the optic thalamus is lined by a
layer of grey'substance which represents the upper end of the central grey
tube, and that the upward continuations of the anterior root-zone of the
cord terminated in this ganglion, and consequently it must be presumed
that a portion at least of the thalamus is endowed with motor functions.
The opinion that the optic thalami is a high reflex centre has been ably
sustained by Dr. Crichton Browne on pathological grounds. The
anatomical difficulties which stand in the way of regarding the corpus
striatum as an intermediate ganglion between the cortex of the brain and
the central grey tube are also very great. The latest researches of Wer-
nicke appear to show, as we have seen, that neither the lenticular nor the
caudate nucleus possess radiating fibres ; and if this be the case, the corpus
striatum must be regarded as a nerve centre co-ordinate with and not
subordinate to the cortex. Ferrier observed that when the corpora striata
were stimulated by a strong interrupted current, the muscles of the oppo-
site side of the body became strongly contracted ; but it is impossible to
prevent even weak currents through the corpus striatum from affecting the
fibres of the internal capsulej and the spasm of the opposite side would be
probably caused by irritation of the fibres of the pyramidal tract. We shall
hereafter see that when hemiplegia occurs from haemorrhage into the corpus
striatum, the patient recovers if the fibres of the pyramidal tract remain
uninjured. Nothnagel found that destruction or injury to a particular
part of the caudate nucleus gave rise in the rabbit to remarkable forced
movements.

§ 685. Functions of the Cortex of the Cerebmrn. — The cortex
of the cerebrum is, probably the exclusive seat of psychical action,
arid there seem to be no grounds for believing that the activity of
any other portion of the encephalon is necessarily connected with

ANATOMICAL AND PHYSIOLOGICAL INTRODUCTION. 479

even the crudest consciousness. But before we can refer certain
states of consciousness to definite processes in the cortex of the
cerebrum, it is necessary to have a classification of mental
phenomena, for no decided progress can be made in interpreting
the results of experiments on the cortex of the brain until the
true nature of a psychical action is defined and some rational
classification of psychical states is adopted by physiologists.

Nature of Psychical Actions. — We have already seen that
simple reflex adapted actions consist of a series of similar complex
movements evoked by a series of similar impressions, and that
compound reflex adapted actions consist of a series of different
complex movements evoked by a series of different impressions ;
and we must now endeavour to show wherein true psychical
action differs from simple and compound reflex actions. Reflex
actions, both simple and compound, consist of three factors :
(1) conduction to a nerve centre of an impression made on the
surface; (2) reduction to order of these impressions in the
centre ; and (3) conduction of these outwards, with the muscular
contractions resulting from them. But, as has been frequently
stated by Mr. Herbert Spencer, four factors may be distinguished
in every psychical action. To quote Mr. Spencer's own language,
" there is (a), that property of the external objects which
primarily affects the organism — the taste, smell, or opacity;
and, connected with such property, there is in the. external
object that character (b) which renders seizure of it, or escape
from it, beneficial. Within the organism there is (c), the im-
pression or sensation which the property (a) produces, serving
as stimulus; and there is, connected with it, the motor change
(d), by which seizure or escape is effected. Now psychology
is chiefly concerned with the connection between the relation
ab, and the relation cd, under all those forms which they
assume in the course of evolution. Each of the factors, and
each of the relations, grows more involved as organisation
advances. Instead of being single, the identifying attribute a,
often becomes, in the environment of a superior animal, a
cluster of attributes, such as the size, form, colours, motions,
displayed by a distant creature that is dangerous. The
factor b, with which this distant combination of attributes is
associated, becomes the congeries of characters, powers, habits,

480 ANATOMICAL AND PHYSIOLOGICAL INTRODUCTION.

which constitutes it an enemy. Of the subjective factors, c
becomes a complicated set of* visual sensations co-ordinated
with one another and with the ideas and feelings established
by experience of such enemies, and constituting the motive to
escape ; while d becomes the intricate, and often prolonged,
series of runs, leaps, doubles, dives, &c, made in eluding the
enemy."

Classification of Psychical States. — Various classifications of
mental states might be adopted, but the best is clearly that
which involves the fewest assumptions and theoretical implica-
tions, and which will enable us at the same time to connect
mental phenomena with the facts of development and experi-
mental physiology.

" It would be the greatest benefit to mental science," says Max
Miiller, " if all such words as perception, intuition, remember-
ing, ideas, conception, thought, cognition, senses, mind, intellect,
reason, soul, spirit, etc., could for a time be struck out of our
philosophical dictionaries, and not be admitted again till they
had undergone a thorough purification." This passage expresses
a state of mind which has been felt by almost everyone who
has seriously engaged in psychological study ; and Mr. Herbert
Spencer, whose great. works have formed an era in philosophy
and psychology, has, with' his usual breadth of treatment,
adopted a classification which does in a great measure avoid
the use of these words, except indeed where the use of them
admits of accurate definition. We shall avail ourselves of this
classification in our future remarks.

Mr. Spencer subdivides all mental states into volitions, cog-
nitions, and feelings ; and the first of these subdivisions may
be disposed of in a few words. " Will," says Mr. Herbert
Spencer, "is a simple homogeneous mental state, forming the
link between feeling and action, and not admitting of sub-
divisions."

" Cognitions," says Mr. Spencer, " are those modes of mind
in which we are occupied with the relations that subsist among
our feelings." They are divisible into four great sub-classes.

(1) " Presentative cognitions, or those in which conscious-
ness is employed in localising a sensation impressed on the
organism."

ANATOMICAL AND PHYSIOLOGICAL INTRODUCTION. 481

(2) " Presented ive -representative cognitions, or those in
which consciousness is occupied with the relations between
a sensation or group of sensations and the representations of
those various other sensations that accompany it in experience"
(perceptions).

(3) " Representative cognitions, or those in which conscious-
ness is occupied with the relations among ideas or represented
sensations, as in all acts of recollection" (concrete ideas).

(4) "Re-representative cognitions, or those in which the occu-
pation of consciousness is not by representation of special rela-
tions that have before been presented to consciousness, but those
in which such represented special relations are thought of
merely as comprehended in a general relation — those in which
the concrete relations once experienced, in so far as they become
objects of consciousness at all, are incidentally represented along
with the abstract relation which formulates them" (abstract
ideas). " It is clear," Mr. Spencer adds, " that the process of
representation is carried to higher stages as the thought becomes
more abstract."

Feelings, or those modes of mind in which we are occupied,
not with the relations subsisting between our sentient states,
but with the sentient states themselves, are divisible into four
parallel sub-classes.

(1) Presentative feelings are those in which a corporeal im-
pression is regarded as pleasure or pain (sensations).

(2) Presentative-representative feelings are those in which a
sensation or a group of sensations arouses a vast group of repre-
sented feelings (emotions).

(3) Representative feelings, comprehending the ideas of the
emotions when they are called up, apart from the appropriate
external excitements, such as the emotions excited by a vivid
description.

(4) Re-representative feelings are those more complex sen-
tient states that are less the direct results of external excite-
ments than the indirect or reflex results of them, such as the
love of property, which consists of the represented advantages
of possession in general, which is not made up of certain con-
crete representations, but of the abstracts of many concrete
representations.

F F

482 ANATOMICAL AND PHYSIOLOGICAL INTItODUCTION.

" The classification," Mr. Spencer proceeds, " here roughly-
indicated, and capable of further expansion, will be found in
harmony with the results of decided analysis aided by develop-
ment. Whether we trace mental progression through the
grades of the animal kingdom, through the grades of mankind,
or through the stages of individual growth, it is obvious that
the advance, alike in cognitions and feelings, is, and must be,
from the presentative to the more and more remotely represen-
tative. It is undeniable that intelligence ascends from those
simple perceptions in which consciousness is occupied in locali-
sing and classifying sensations, to perceptions more and more
compound, to simple reasoning, to reasoning more and more
complex and abstract, more and more remote from sensation.
And in the evolution of feelings there is a parallel series of
steps. Simple sensations ; sensations combined together ; sen-
sations combined with represented sensations; represented sen-
sations organised into groups in which their separate characters
are very much merged ; representations of those representative
groups in which the original components have become still more
vague. In both cases the progress has necessarily been from
the simple and concrete to the complex and abstract ; and as
with the cognitions so with the feelings, this must be the basis
of classification."

It is not, perhaps, possible in the present state of our know-
ledge to separate the cortex of the brain into areas exactly
corresponding to the various subdivisions of Mr. Herbert
Spencer's classifications. The cortex may, however, be sub-
divided into areas which will' correspond with the leading
features of this classification.

1. The cortex of the brain must maintain some connection with
the surface of the body, by means of which impressions made
on the latter occasion molecular changes in the former. The
parts at which the cortex is connected with the centripetal
system of nerves maybe called sensory inlets, and if the portion
of the cortex containing these inlets can be isolated from the
remaining portions of the cortex, there can be no serious
objections to calling it the sensory area of the cortex. And,
indeed, if the inlets from the various senses can be more or
less isolated from one another, each may be called a

ANATOMICAL AND PHYSIOLOGICAL INTRODUCTION. 483

sensory centre. We have already seen that the posterior third
of the posterior division of the internal capsule contains cen-
tripetal fibres for the opposite half of the body, and that these
radiate in the centrum ovale to terminate in the convolutions
of the occipital and temporo- sphenoidal lobes, or the area of
the cortex, which is supplied by the posterior cerebral artery.

That the fibres of the tract which ascends in the external
third of the crusta and posterior part of the external capsule
are sensory has been proved by the experiments of Veyssiere,
and confirmed by Carville and Duret, Raymond, and others.
Veyssiere showed that section of the posterior part of the in-
ternal capsule lying between the lenticular nucleus and optic
thalamus was followed by hemiansesthesia of the opposite side
of the body.

Fig. 228.

Fig. 228 (After Carville and Duret). Transverse Section of the Brain of a Dog on a
level with the Corpora Albicantia.—0 , O, Optic thalami; S, S, Caudate nuclei ;
L, L, Lenticular nuclei ; P, P, Posterior region of the internal capsule ;
x, Section of the posterior part of the internal capsule determining hemi-
anesthesia ; A, A, Cornu Ammonis.

'2. The cortex of the brain must be connected with the
muscular system, in order that the reactions of the organism
Upon its environment may be regulated in correspondence with
the impressions made upon it. The parts at which the cortex
is connected with centrifugal fibres may be called motor outlets,
and if the portion of the cortex which contains these can be
isolated from the remaining portions of the cortex it may be
called the motor area. And if the motor outlet for a particular
movement can be isolated from the outlets for other movements
there can be no great harm in calling it a motor centre.

484 ANATOMICAL AND PHYSIO LOGICAL INTRODUCTION.

A cortical motor centre then constitutes the link between
cortical activity on the one side, and voluntary muscular con-
tractions on the other ; and volition being the link between
feeling and action, the cortical motor centres may be regarded
as the structural counterparts of volitions.

We have already seen that the pyramidal tract contains the
centrifugal fibres from the cortex of the brain, and this has also
been determined experimentally by Veyssiere, who found that
section of the anterior two-thirds of the internal capsule was
followed by hemiplegia of the opposite side, unaccompanied by
sensory paralysis.

Tig. 229.

Pig. 229 (After Carville and Duret). Transverse Section of the Brain of the Dog,
five millimetres in front of the optic commissure.— S, S, The caudate nuclei of
the corpora striata ; P, P, Peduncular fibres (the internal capsule) ; L, Lenti-
cular nucleus ; B, Stylet, by means of which Veyssiere produced section of the
internal capsule at (x).

But the pyramidal tract is not, according to most anatomists, the only
outlet from the cortex of the brain. Leaving out of account the centri-
fugal fibres which probably connect the cortex of the cerebrum with the
cerebellum, there still remain the fibres which connect the cortex of the
cerebrum with the central grey tube through the intermediation of the
corpus striatum. The cortical actions which are regulated through the
corpus striatum and pyramidal tract are often, although not always, an-
tagonistic to one another. The excitation of the cortex which is the cor-
relative of feeling, whether the latter be pleasurable or painful, always
tends to find a vent in immediate action, while a great portion of our
voluntary efforts are directed to restrain action, and to postpone the ini-

ANATOMICAL AND PHYSIOLOGICAL INTRODUCTION. 485

mediate gratification of the feelings in order to accomplish remote ends.
Excitation, for instance, of the cells in the cortex which are in immediate
contact with the terminations of the centripetal nerves in the summits of
the convolutions of the posterior area of the cortex tends to be conducted
immediately outwards along the centrifugal fibres which connect these
convolutions with the corpus striatum. If these excitations are conducted
at once outwards, they give rise to movements which have been named
se)isori-motor; but if the excitations, instead of being conducted at once
outwards, pass from the cells in connection with the termination of one
bundle of centripetal fibres (vision) to those in connection with another
bundle (tactile), so that the relation between the two feelings comes
into prominence, then a presentative cognition is formed. When,
for instance, the centripetal impulse received in a convolution from the
irritation caused by a thorn in the finger is brought into connection with
the impressions received through the optic and other centripetal nerves,
and which, on reaching the cortex, becomes the correlative of the con-
sciousness of the finger itself, then a cognition of the relationship of pre-
sentative feeling is formed. Now, a presentative cognition does not
usually, like a presentative feeling, immediately result in action. The
excitation expends itself in the former in producing excitation of other
groups of cells in the cortex, the transition from one group to another
giving rise to other presentative and representative cognitions, until finally
the motor area is reached, and the excitation passes out along the pyramidal
fibres. Subjectively considered, the cognition of the thorn and finger would
call up other cognitions connected with these by previous experiences, as
that of a pin, and probably the highly representative cognitions of the
general properties of the lever, until finally the pin is voluntarily grasped
and rightly applied for the removal of the thorn. This action is very
different from that which impels a dog to lick with his tongue the foot in
which a thorn is lodged. The latter is a sensori-motor or doubly compound
reflex action, and in immediate relation with the cortical excitation which
causes the feeling of pain, while the former results from a series of com-
plex cortical excitations, some of which check the tendency to immediate
action, until by-and-by complex actions result which are guided by wide
experience and adapted to remote ends. The movements which result
immediately from the feelings have been called sensori-motor, percipio-
motor, and ideo-motor, on the supposition that they occurred in response
to the cognitions ; but it would be better to call the movements which
result from a presented feeling a doubly compound reflex action, that from
a presentative-representative feeling a trebly compound reflex action, and
that from a representative feeling a quadruply compound reflex action,
and so on in an ascending scale, according to the degree of the complexity
of the feeling. When, however, a series of cognitions intervene in the
mental operations between the feeling which prompts a movement and
the movement itself, the resulting muscular adjustment is a voluntary
one, and is regulated through the pyramidal fibres. When, for instance,

486 ANATOMICAL AND PHYSIOLOGICAL INTRODUCTION.

Leverrier, prompted by the highly representative feeling of a desire for
discovery, directed his telescope to a certain spot in the heavens, and dis-
covered Neptune, the requisite muscular adjustments necessary for carry-
ing out this action were preceded in his mind by a long series of involved
and highly representative cognitions; and these muscular adjustments
themselves were, to a large extent, voluntary.

3. The region of the cortex supplied by the anterior cerebral
artery still remains to be connected with some kind of mental
activity. We have seen that the area supplied by the posterior
cerebral artery is the sensory area, and consequently excitation
of this area is the correlative of the presentative and presenta-
tive-representative cognitions and feelings, while excitation of
the area supplied by the middle cerebral artery is the cor-
relative of volition. Excitation of the cortical area supplied by
the anterior cerebral artery is the correlative again of the
representative and re-representative cognitions and feelings. It
is somewhat difficult to find a name which will be expressive of
the functions of this area, and if we consent to call it the
ideational area, it must be remembered that it is no less likely
to be the anatomical substratum of the higher emotions than
of the higher intellectual operations.

§ 686. Anatomical Substratum of Consciousness. — It is well
recognised that a large number of psychical actions may take
place in an unconscious manner. Leaving out of consideration
the phenomena of dreaming and somnambulism, we may in-
stance such a familiar fact as that a man may read aloud whole
pages of a book while his mind is engaged in solving a difficult
problem, and he is wholly unconscious of what he is saying, yet
the muscular movements engaged in reading are co-ordinated
in the cortex of the cerebrum. If, under these circumstances, the
eye falls on an unusual word, consciousness is directed to it for
a moment, and the reading may then go on unconsciously as
before. It would therefore appear that impressions which have
been frequently repeated in experience may pass up to the cortex
and give rise to complicated motor impulses from the cortex
without being attended by consciousness; but that when the
impressions made on the sensory organ present an unusual
combination, consciousness is aroused. Unusual combinations

ANATOMICAL AND PHYSIOLOGICAL INTRODUCTION. 487

of sensory impressions are, therefore, probably cond acted to
and through the cortex in channels which are only partially
open, while the habitual combinations pass in channels
which are open and well defined. In intellectual efforts the
highest consciousness is aroused when the mind is contem-
plating new combinations of presentative and representative
impressions, or, to translate this into the language of physics,
when the organism is adjusting itself to new combinations of
circumstances and events. In other words, the highest intel-
lectual consciousness is aroused during the time that a new
organisation in the cortex of the brain is being superadded to
the existing one, while excitation of the portion of the cortex
which is already thoroughly organised is attended by little
or no consciousness.

It cannot be supposed that the large cells, with the distinct
processes and definite connections found in the internal division
of the third layer of the cortex, will readily undergo structural
changes in the healthy adult, and it is much more probable
that any new alteration of structure in the cortex will proceed
from the small cells of the external layers of the cortex. The
first layer may probably be regarded as an embryonic layer
without any active nerve functions, and consequently the second
layer and external portion of the third layer of the cortex, the
cells of which do not possess definite connections with one
another or with nerve fibres, must be regarded as the areas,
excitation of which is attended by the highest consciousness.

Experiments on animals have proved, as we have seen, that
the fibres which pass through the posterior third of the posterior
division of the internal capsule are sensory, but the sensory area
of the cortex is also connected with the periphery, through the
optic thalamus and its radiating fibres. It is probable that
impressions which have been frequently repeated in experience
pass through the optic thalamus and its radiating fibres, and
that they give rise to little or no consciousness on reaching
the cortex. It may be presumed, on the other hand, that
unusual combinations of impressions are conducted through the
posterior fibres of the internal capsule, and give rise on reaching
the cortex to distinct consciousness.

488 ANATOMICAL AND PHYSIOLOGICAL INTRODUCTION.

§ 687. Experimental Determination of the Functions of
the Cortex of the Brain.
1. Motor Centres.

Experiments by Stimulation. — When the cerebrum is removed slice by
slice there is a gradual loss of intelligence and volition, and consequently
Flourens, who conducted these experiments, concluded tbat the brain
acted, as a whole, without any special functions being assigned to special
parts. Hughlings-Jackson, however, drew attention to the fact that focal
disease of the cortex of the brain may occasion epileptiform convulsions,
localised to particular groups of muscles. Hitzig and Fritsch showed that
the local application of the galvanic current to particular parts of the
cerebral convolutions gives rise to definite movements of various groups of
muscles. These experiments were extended and rendered more definite
by Ferrier, who used the faradic instead of the galvanic current as a
means of stimulation. The motor centres as determined by Ferrier in
the monkey are represented in Figs. 230 and 231, while the corresponding
parts in the human brain are shown in Figs. 232 and 233.

Fig. 230.

Fig. 230 (After Ferrier). The Left Hemisphere of the Monkey.

Burdon-Sanderson states that the motor reactions to cortical stimulation
are not prevented from taking place by a horizontal incision carried some
distance from the surface. This simply shows that a faradic current
applied to the surface of the brain is conducted into the centrum ovale
and stimulates the ends of the divided pyramidal fibres, but it does not
show that the cortex is non-excitable.

Burdon-Sanderson also found that local stimulation of the white matter
immediately surrounding the corpus striatum produces localised move-
ments similar to those caused by stimulation of the corresponding cerebral
surface. This experiment, like the last, shows that the fibres of the
pyramidal tract are excitable, but it proves nothing with regard to the
excitability or non-excitability of the cortex. If the motor area of the

ANATOMICAL AND PHYSIOLOGICAL INTRODUCTION. 489

cortex be removed, excitation of the subjacent white .substance causes the
same movements as excitation of the motor centro itself. In such a case
the ends of the fibres of the pyramidal tract which issued from the motor
centre are now exposed, and excitation of them causes the same kind
of motor reaction as that caused by excitation of the motor centre
itself. If the auimal, however, survive the operation, the pyramidal fibres
undergo secondary descending degeneration, and excitation of the scar or

Fig. 231 (After Ferrier). Upper Surface of the Hemisphere of the Monkey.
L Advance of the opposite leg as in walking.

2, Complex movements of the thigh, leg, and foot, with adapted movements of

the trunk.

3, Movements of the tail.

4, Retraction and adduction of the opposite fore limb.

5, Extension forward of the opposite arm and hand, as if to reach or touch

something in front.

Circles (a), (6), (c), (d\ Individual and combined movements of the fingers and
wrists, ending in clenching of the fist.

6, Supination and flexion of the forearm, by which the hand is raised towards

the mouth.

7, Action of the zygomatics, by which the angle of the mouth is retracted and

elevated.

8, Elevation of the ala of the nose and upper lip, with depression of the lower

lip, so as to expose the canine teeth on the opposite side.

9, Opening of the mouth with protrusion of the tongue.

10, Opening of the mouth with retraction of the tongue.

11, Retraction of the angle of the mouth.

12, Eyes opening widely, pupils dilating, head and eyes turning towards the

opposite side.

13 and 13', Eyeballs moving to the opposite side. Pupils generally contracting.

14, Sudden retraction of the opposite ear.

15, Subiculum cornu Ammonis. Torsion of the lip and nostril on the same side.

Fig. 231.

490 ANATOMICAL AND PHYSIOLOGICAL INTRODUCTION.

its neighbourhood no longer produces the particular movements charac-
teristic of the destroyed area (Albertoni and Michieli).

Experiments by Destruction of Portions of the Cortex. — It has been
observed that removal or destruction of a motor centre is followed

Fig. 232.

Figs. 232 and 233 (After Ferrier). Side and Upper Views of the Brain of Man.

The figures are constructed by marking on the brain of man, in their respective
situations, the motor areas of the brain of the monkey as determined by experiment,
and the description of the effects of stimulating the various areas refers to the brain
of the monkey.

1 (On the postero-parietal lobule), Advance of the opposite hind limb as in
walking.

2, 3, 4 (Around the upper extremity of the fissure of Rolando1, Complex move-
ments of the opposite leg and arm, and of the trunk, as in swimming.

a, b, c, d (On the ascending parietal convolution), Individual and combined
movements of the fingers and wrist of the opposite hand. Prehensile
movements.

5 (At the posterior extremity of the superior frontal convolution), Extension

forward of the opposite arm and hand.

6 (On the upper part of the ascending frontal convolution), Supination and

flexion of the opposite forearm.

7 (On the median portion of the ascending frontal convolution), Retraction and

elevation of the opposite angle of the mouth by means of the zygomatic
muscles.

8 (Lower down on the same convolution), Elevation of the ala nasi and upper

lip with depression of the lower lip, on the opposite side.

ANATOMICAL AND PHYSIOLOGICAL INTRODUCTION. 491

by inability to execute the movements assigned to the area (Hitzig,
Ferrier), but it has subsequently been found that the paralytic symptoms
disappear when the animal operated upon survives some days (Nothnagel,
Hermann, Goltz). Hermann removed cortical motor centres from dogs,

Fig. 233.

9, 10 (At the inferior extremity of the ascending frontal and posterior extremity
of the third frontal convolution), Opening of the mouth with (9) protrusion
and (10) retraction of the tongue. Region of Aphasia.

11 (At the inferior extremity of the ascending parietal convolution), Retraction

of the opposite angle of the mouth, the head turned slightly to one side.

12 (On the posterior portions of the superior and middle frontal convolutions),

Eyes opening widely, pupils dilating, and the head and eyes turning
towards the opposite side.

13, 13' (On the supra-marginal lobule and angular gyrus), The eyes moving
towards the opposite side with an upward (13) or downward (13') devia-
tion. Pupils generally contracting. (Centre of vision. )

14 (On the infra-marginal or superior temporo-sphenoidal convolution),
Pricking up of the opposite ear, head and eyes turning to the opposite
side, and pupils dilating largely. (Centre of hearing.)

Ferrier moreover places the centres of taste and smell at the extremity of the
temporo-sphenoidal lobe, and that of touch in the gyrus uncinatus and hippo-
campus major.

492 ANATOMICAL AND PHYSIOLOGICAL INTRODUCTION.

and found that tho paralysis, which immediately followed the operation,
disappeared in a few days. These results were afterwards confirmed by
Carville and Duret, who also found that the restoration of motor power
could not have been due to the corresponding centre of the opposite
hemisphere, inasmuch as subsequent destruction of the latter produced
the usual paralysis on the side opposite to the lesion, but did not cause a
repetition of the paralysis oq the side opposite to the first lesion. These
authors suppose that portions of the same hemisphere took up the func-
tions of the destroyed centre.

Fig. 234.

Fig. 234 (After Broca and G-omier). External Convex Surface of the Brain of the
Adult Monkey . — Fissures: R, Fissure of Rolando : Sf, Fissure of Sylvius ; pf,
Parallel fissure ; pof, External perpendicular or parieto-occipital fissure ; pcf,
Prae-central fissure. Convolutions: A, Ascending frontal convolution; B,
Ascending parietal convolution; Fi, Fa, Fs, First, second, and third frontal
convolutions ; ag, Angular gyrus ; inig, Infra-marginal gyrus ; hi, Horizontal
lobule ; ol, Occipital lobe. Motor Centres : 1, Movements for rotation of bead
and neck ; 2, Movements of muscles of tbe face ; 3, Movements of tbe tongue
and jaws; 4, Movements of anterior extremity; 5, Movements of posterior
extremity ; 6, Movements of tbe ocular muscles ; 7, Movements in relation
with sense of bearing.

Goltz removed parts of the cerebral surface by washing the nervous
substance away by a stream of water, and he came to the conclusion that
the paralytic phenomena did not depend so much upon the locality as the
extent of the injury. He also found that the paralysis disappeared in a
short time, whatever might be the portion of brain removed. He was able
in one case to remove the greater part of one hemisphere, and yet recovery
of motor power took place, clumsiness in the execution of certain move-
ments alone remaining ; this Goltz attributed to a deficiency of tactile
sensibility. He thinks that the paralytic phenomena are caused by an
inhibitory action produced by the injury on lower centres, similar to the

ANATOMICAL AND PHYSIOLOGICAL INTRODUCTION. 493

temporary paralysis of the automatic centres in the lumbar portion of the
spinal cord produced by section in the dorsal region.

But examples of a localised destroying lesion of the cortex of the brain
in man have now multiplied to such an extent that there is no room for
doubt with regard to the main symptoms caused by them, whatever may
be the interpretation. When a patient has been unable to move his right
arm and hand for months, and when after death a destructive lesion of
the cortex of the opposite hemisphere is observed strictly limited to the
middle of the ascending frontal and parietal convolutions, and when cases
of this nature occur with sufficient frequency to show that the connection
between the lesion and symptoms during life is not accidental, it is idle
for any physiologist to deny that the paralysis was due to destruction
of the cortex in that area, inasmuch as only temporary paralysis would be
caused by a similar lesion in the dog. The fact that paralysis following
cortical lesions in the dog is only temporary shows that differences must
exist with regard to the relation which obtains between the highest nerve
centres and muscular movements in man and the dog respectively.
And it is not difficult to point out where some of these differences lie.

Fig. 235.

Fig. 235. External Convex Surface of the Human Brain. — Fissures : R, Fissure of
Rolando ; S/, Fissure of Sylvius ; pf, Parallel fissure ; ipf, Interparietal fissure ;
pof, External parietooccipital fissure. Convolutions and Lobules : A, Ascending
frontal; B, Ascending parietal convolutions; Fi, F*, Fa, First, second, and
third frontal convolutions; Pi, Superior parietal lobule; Pa, Supra-marginal
gyrus ; Ps, Angular gyrus ; Oi, 0», Oa, First, second, and third occipital con-
volutions ; Ti, T«, Ta, First, second, and third temporo-sphenoidal convolu-
tions. Motor Centres : 1, Movements for rotation of head and neck ; 2, Move-
ments of the upper facial muscles ; 2', Movements of the lower facial muscles ;
3, Movements of the tongue and jaws ; 4, Movements of superior extremity ;
5, Movements of inferior extremity ; 6, Movements of the ocular muscles ; 7,
Movements in relation with the sense of hearing.

•

494 ANATOMICAL AND PHYSIOLOGICAL INTRODUCTION.

We have already seen that paralysis of the external rectus muscle of the
one side and of the internal-of the other occurs in most cases of Budden
hemiplegia in man, causing a conjugate deviation of the eyes away from
the paralysed side. This paralysis disappears in a few days, and is
almost exactly similar to what occurs in the paralyses of cortical lesions
caused in the dog. And even injury to the deep-seated parts of the
brain in the dog, such as the crus cerebri, does not cause a hemiplegia
at all comparable to the hemiplegia which occurs in man. In lesion
of the right crus cerebri in the dog there is only a very partial hemi-
plegia. When standing the animal carries his body towards the right,
his eyes are directed to the right, and his head is also rotated to the right,
and if the animal move he goes round in a circle after his tail (Broadbent).
It would not be more preposterous to tell us that because injury of the
crus cerebri causes a mouvement de manege in the dog it cannot therefore
cause hemiplegia in man, as to say that because rapid recovery from the
paralysis caused by cortical lesions takes place in the dog the affections
caused by similar lesions in man is not due to the destruction of a
cortical centre. The disappearance of paralysis of the limbs in the dog
corresponds exactly to the disappearance of conjugate deviation of the
eyes in man, and the explanation which suffices for the one will probably
suffice for the other (§ 90). But even Goltz admits that some movements
in the dog become more or less permanently paralysed. For instance, he
may use his forepaw to drag bones and other morsels of food from under
a table, and he may also be taught to perform special tricks with his paws ;
all such special movements become more or less permanently lost after
portions of the cortex have been removed. This shows that the purely
voluntary actions are more or less permanently lost, while paralysis of
the automatic actions concerned in ordinary locomotion rapidly disappears.
Goltz found that the animals operated on could after a time be trained
or educated to perform special actions with their paws, a fact which shows
that a new organisation takes place more readily in the brain of the dog
than in that of man, but it is quite probable that new structural arrange-
ments may also take place to a certain extent in the brain of man after
partial injury.

2. Sensory Centres.

It has already been seen that the centripetal fibres terminate amongst
the cells of the second and third layers of the cortex without forming any
direct connection with them, while the fibres of the pyramidal tract take
origin in the axis-cylinder processes of the giant-cells of the internal
portion of the third layer. It may, therefore, be suspected that the cen-
tripetal currents will pass in a much more diffused manner through the
cortex than the centrifugal, just as it is found that the former pass in a
more diffused manner through the spinal cord than the latter. It is not
therefore likely that the sensory inlets are as definitely localised as the
motor outlets.

ANATOMICAL AND PHYSIOLOGICAL INTRODUCTION. 495

Experiments by Stimulation. — On stimulating the angular gyrus
Ferrier obtained various movements of the eye and associated move-
ments of the head, and he regarded the phenomena observed as
being " merely reflex movements on the excitation of subjective visual
sensation." He, therefore, concluded that the angular gyrus and sur
rounding grey matter constituted the centre of vision. On somewhat
similar grounds he placed the auditory centre in the superior temporo-
sphenoidal convolution, the centres of taste and smell at the extremity of
the temporo-sphenoidal lobe, and that of touch in the gyrus uucinatus
and hippocampus major. But these experiments, although exceedingly
interesting and important as being the first to break ground in a new
territory, are by no means conclusive. Dr. Ferrier himself, indeed, did not
rest satisfied with them, but proceeded to verify his hypotheses by the
extirpation or destruction of the portions of the cortex which he supposed
to be the sensory centres.

Experiments by Extirpation or Destruction of Sensory Centres. — The
most remarkable result obtained by Ferrier in his first experiments
was afforded by destruction of the angular gyrus. When the angular gyrus
of the left hemisphere was destroyed, it was found that the animal was
blind on the right eye soon after the operation, but recovered sight com-
pletely on the following day. In another case the angular gyri of both
hemispheres were destroyed and the animal became completely blind in
both eyes. In no case was any motor paralysis observed.

The admitted objections to these experiments are that Ferrier did not
keep his animals alive a sufficiently long time to ascertain if a return of
vision occurred. Goltz found in his experiments that when a considerable
portion of the cortex of the brain was removed the animals, although not
blind, manifested a peculiar imperfection of vision. The animal operated
upon could use his sight in avoiding obstacles, but often failed to recognise
his food, and appeared quite indifferent when threatened with the whip.
He also found that recovery from this condition was possible, at least to a
considerable extent, by means of educational exercises.

Munk believes again in the existence of a " visual area," situated in
the occipital lobes, and of much larger extent than that of Ferrier. He
maintains that removal of this area causes blindness, and that extirpa-
tion of small portions of it gives rise to blindness of localised areas of
the retina. He believes that there are three visual spheres in the cortex
of the occipital lobe corresponding to three visual areas in the retina.
The external part of the retina of the left eye is connected with the
external part of the cortical visual centre in the left hemisphere, while
the internal and central portions of the retina of the right eye are respec-
tively connected with the internal and central portions of the visual
centre of the opposite or left hemisphere. He also thinks that the
upper part of the retina is connected with the front, and the lower part
with the posterior aspect of the visual centre of the opposite side.
Removal of both visual centres causes, according to this observer, complete

496 ANATOMICAL AND PHYSIOLOGICAL INTRODUCTION.

or absolute blindness. Partial removal of these areas on the other hand
gives rise to the visual defect called attention to by Goltz, in which the
animal can see and avoid objects, bnt does not recognise his food as such.
This Munk calls psychical blindness (Seelenlahmungen, Seelenblindheit).
He finds that after a time the animals recover from psychical blindness,
provided the whole visual area be not removed. He thinks that the
recovery is due to a process by which there is a deposition of new visual
experiences in the rest of the visual area. The physical part of the
restoration might probably be spoken of with greater justice as the
formation of new structural arrangements in the visual areas. Munk
describes an auditory area, which however differs from that of Ferrier, and
he regards the whole front part of the brain as forming a large " sensory "
area, in which separate sensory centres may be distinguished.

Fig. 236.

Fig. 236 (After Munk). Upper Surface of the Brain of the Monkey. — Sensory Areas :
A, of the eyes ; B, of the ears ; C, of the sensibility of the lower extremity ;
D, Anterior extremity ; E, Head ; F, Ocular muscular apparatus ; G, Region
of ears; H, Neck; I, Body.

An elaborate paper on the cerebral visual centres was read before
the physiological section at the meeting of the British Medical Association,
at Cambridge, in August last, by Professors Ferrier and Gerald F. Yeo.
Large portions of the brains of monkeys were removed, the operations
being conducted antiseptically, so that there was a total absence of
encephalitis. The following is an abstract of the chief results obtained : —

1. Removal of both occipital lobes did not cause any recognisable dis-
turbance of vision, or other bodily or mental derangement, provided the
lesion did not extend beyond the parieto-occipital fissure.

2. Complete destruction of one angular gyrus causes temporary loss of
vision of one eye, lasting only a few hours. The restoration of vision is

ANATOMICAL AND PHYSIOLOGICAL INTRODUCTION. 407

not due to the integrity of the other angular gyrus. If both angular gyri
be destroyed simultaneously total blindness ensues in both eyes, but does
not last more than three days, although vision may be impaired for
months. If the angular gyri be destroyed successively, several weeks
elapsing between the operations, the animal sees quite well with both eyes
in a few hours.

3. Simultaneous destruction of the angular gyrus and occipital lobe on
one side causes evident loss of vision in both eyes towards the side oppo-
site the lesion (hemiopia), but recovery from this condition takes place at
the end of a week.

4. Destruction of the left angular gyrus (recovery), and subsequently of
the right angular gyrus and occipital lobe, produces left hemiopia, from
which the animal recovers in a fortnight.

5. Destruction of both occipital lobes, followed after a time by destruc-
tion of the left angular gyrus, causes transient blindness followed by
indistinctness of vision of right eye, with subsequent complete recovery.

6. Destruction of both angular gyri and occipital lobes causes total and
permanent blindness in both eyes, without any impairment of the other
senses or of motor power.

3. Prce-frontal or Ideational Area of the Cortex.

Experiments by Stimulation. — Electrical irritation of the prae-frontal
region of the cortex in the monkey causes no motor reaction (Ferrier).

Experiments by Extirpation. — Complete destruction of the prse-frontal
lobes in the monkey causes no paralysis of motion and no sensory dis-
turbance, but the character of the animal suffers great deterioration sub-
sequently to the operation. " Removal or destruction by the cautery of
the antero-frontal lobes," says Dr. Ferrier, " is not followed by any definite
physiological results. The animals retain their appetites and instincts,
and are capable of exhibiting emotional feeling. The sensory faculties —
sight, hearing, touch, taste, and smell — remain unimpaired. The powers
of voluntary motion are retained in their integrity, and there is little to
indicate the presence of such an extensive lesion, or a removal of so large
a part of the brain. And yet, notwithstanding this apparent absence of
physiological symptoms, I could perceive a very decided alteration in the
animal's character and behaviour, though it is difficult to state in precise
terms the nature of the change. The animals operated on were selected
on account of their intelligent character. After the operation, though
they might seem to one who had not compared their present with the
past fairly up to the average of monkey intelligence, they had undergone
a considerable psychological alteration. Instead of, as before, being
actively interested in their surroundings, and curiously prying into all
that came within the field of their observation, they remained apathetic
or dull, or dozed off to sleep, responding only to the sensations or impres-
sions of the moment, or varying their listlessness with restless and
purposeless wanderings to and fro. "While not actually deprived of
GG

498 ANATOMICAL AND PHYSIOLOGICAL INTRODUCTION.

intelligence, they had lost to all appearance the faculty of attentive and
intelligent obeservation." The conclusions which Dr. Ferrier has drawn
from his experiments on animals are fully borne out, as we shall subse-
quently see, by the results of diseases and injuries of the prse-frontal lobes
in man. The whole evidence shows that, although destruction of these
lobes is not followed by decided sensory or motor disturbances, yet that
the later evolved (representative and re-representative) cognitions and
emotions are seriously impaired.

§ 688. Localisation of the Mechanisms which regulate the Fundamental and

Accessory Actions.

We have already seen that the fundamental portions of the convolutions
of the motor area of the brain are found near the great longitudinal fissure,
while the accessory portions of these convolutions are found in the convo-
lutions of the operculum ; and it may therefore be expected that the funda-
mental motor actions will be regulated from the former, and the accessory
functions from the latter. Several lines of evidence converge in support
of this view. The large giant-cells are found in the convolutions near the
great longitudinal fissure, while these cells diminish in size as we descend
towards the convolutions of the operculum. But we have already seen that
the size of the motor ganglion cells of the anterior grey horns of the cord
is determined by the size of the muscles whose movements they regulate
more than by any other circumstance, and it is very likely that a similar
relation exists between the giant-cells of the cortex and the muscles with
which they are connected. But the fundamental actions are, as a rule,
produced by the contractions of large muscles, such as those of the trunk
and lower extremities, and consequently we may expect that they will be
regulated by means of the large cells of the central convolutions near the
great longitudinal fissure ; while, on the other hand, the accessory actions
are produced by small muscles, such as those of the hand, larynx, and
face, and we may expect that they will be regulated through the smaller
cells of the convolutions of the operculum. Again, the fibres of the
pyramidal tract, which are medullated in a nine months embryo —
the fundamental fibres — are connected with the central convolution
near the great longitudinal fissure ; while the non-medullated fibres —
the accessory fibres of the tract — are connected with the convolutions
of the operculum. The fibres which connect the posterior portion of the'
third frontal convolution with the internal capsule and crusta are not me-
dullated before fourteen weeks after birth (Flechsig). We have already
seen that a large proportion of the accessory fibres of the pyramidal
tract terminate in the medulla oblongata, and in all probability the
majority of them are concerned in regulating the special movements of
articulation and facial expression. A glance at Dr. Ferrier's diagrams
{Figs. 232 and 233) of the motor centres of the human brain shows that
the movements of the trunk and lower extremities are regulated from the
central convolutions near the great longitudinal fissure ; that those of the

ANATOMICAL AND PHYSIOLOGICAL INTRODUCTION. 409

arms are regulated from the middle of the ascending frontal and parietal
convolutions ; and that those of the face, tongue, and hand are regu-
lated from the convolutions of the operculum. The facts of development
and of experimental physiology, therefore, concur to show that the funda-
mental actions are regulated from the central convolutions near the great
longitudinal fissure, and the accessory functions from the convolutions of
the operculum. It must also be remembered that the grey matter at the
bottom of the fissures is developed subsequently to that of the summits, and
consequently the former represents an organisation which has been super-
added to the latter in the course of evolution. But the portion of the cortex
of the Island of Reil which adjoins the convolutions of the operculum is the
great area in which new structure is superadded to the motor region of the
cortex. As the grey matter in the neighbourhood of the anterior perforated
space increases in superficial extent, the external aspect of the cortex of
the central lobe is thrust upwards and outwards so as to develop the
convolutions of the operculum ; and each addition of grey matter to the
latter convolutions represents an additional complexity in the pre-existing
structure corresponding to an additional complexity of previous muscular
adjustments. Each increment which is added to the inferior extremities
of the central convolutions by the upward growth of the cortex of the
Island of Reil increases the length of the former ; but as their upper ex-
tremities are prevented from moving freely upwards by the skull, their
lower extremities are thrown into a fold, and consequently the depth of
the sulcus which separates the Island of Reil from the convolutions of the
operculum may be accepted as an indication of the degree of development
of the accessory portion of the motor area of the cortex.

§ 689. Localisation of the Cortical Centres of General and Special Sensations.

We have seen that in the spinal cord the conducting paths of the
common sensations passed directly into the posterior grey horn, through
the middle of the fan formed by the fibres of the posterior roots on their
entry into the cord ; while, on the other hand, the conducting paths of
the special cutaneous sensations are thrust inwards and outwards, so
as to occupy positions outside the margins of the posterior horns. A
somewhat similar process appears to take place during the development
of the cortex in relation to the common and special cutaneous sensations
and the special senses. According to the latest experiments of Ferrier
and Munk the centre of vision — the most special of all the senses — is
situated on the outer convex burface of the occipital lobe in the area of
the terminal distribution of the posterior cerebral artery, while the centre
of tactile sensation is situated in the hippocampal region, close to the root
of the same artery. It is probable that the sensation of pain is too much
diffused in the cortex to admit of any definite localisation. Both the
auditory centre — the superior temporo-sphenoidal convolution — and the
olfactory centre — the subiculum cornu Ammonis — although situated
nearer the root of the artery than the visual centre, yet occupy positions

500 ANATOMICAL AND PHYSIOLOGICAL INTRODUCTION.

near the terminal distribution of some of the branches of the posterior
cerebral artery, and certainly further removed from its root than the
centre of tactile sensation.

§ 690. Localisation of Function in the Prcs-frontal Area of the Cortex.

If the higher mental operations be carried on in the anterior area of
the cortex, this region must contain the plexuses of cells and fibres, which,
when excited, become the correlatives of the representative and re-
represehtative cognitions and feelings. No progress has been made
in localising the functions of this area of the cortex. It is, however,
probable, that the later-acquired emotions and cognitions will be repre-
sented in the cortex by the grey matter in the bottom of the fissures, and
by the grey matter of the convolutions of the orbital surface which
adjoins the anterior perforated space and which are situated close to
the root of the anterior cerebral artery. Pathological observation
bears out the idea that disease of the cortex of the orbital surface
produces much less mental disturbance than disease of the superior
convex surface of the prae-frontal area. And this is only what might be
expected if the former is developed at a later period than the latter. The
convolutions of the orbital surface would then represent the later-acquired
cognitions and emotions, and abolition of them would cause less mental
disturbance than abolition of those which are earlier acquired but more
fundamental. A man, for instance, may live what is regarded as a
respectable life when he is destitute of all reverence, and is wholly in-
capable of doing an unselfish action, while the only self-restraint he
places over his appetites and passions is that which the most calculating
selfishness suggests. Yet reverential feeling, unselfishness in action, and
self-restraint are the latest acquisitions in the development of the human
mind. If, however, a man, instead of being lacking in reverential feeling,
becomes openly profane, and instead of not being unselfish he commits
deeds of violence in order to deprive others of their rightful property, and if
instead of curbing his passions even by a calculating selfishness he gratifies
them without shame and regardless of consequences, it is gvident that a
lower stratum of mental degradation has been reached, and the portion of
the cortex now diseased is a more fundamental one, which must have been
developed at an earlier period than that which was diseased in the first
instance.

.301

CHAPTER II.

MORBID ANATOMY AND CLASSIFICATION OF THE DISEASES

OF THE ENCEPHALON.

(I.)— MORBID ANATOMY OF THE ENCEPHALON.

The operation of the law of evolution having been already
traced in the construction of the brain, we must now endea-
vour to trace the action of the. law of dissolution in the
breaking down of structure the result of disease.

§ 691. Histological Morbid Changes. — The histological
changes which occur in the tissues of the brain during diseased
processes are essentially the same as those which have already
been described in the case of the spinal cord (§ 387), and it is,
therefore, unnecessary to repeat the description.

§ 692. Morbid Alterations of the Circulation within the
Cranium. — It was first pointed out by the second Monroe that
the circulation within the cranium differs from that of other
parts of the body. The cranium forms a bony case, capable of
resisting the atmospheric pressure, and no substance can be
dislodged from it without some equivalent taking its place;
while, on the other hand, no substance can be added to the con-
tents of the cranium without dislodging an equivalent bulk of
some other substance. This opinion was experimentally tested
by Kellie, and defended by Abercrombie, Reid, and Watson.
Dr. Burrows endeavoured to combat this opinion, but he only
showed, what was never denied, that the quantity of blood in
the brain could be increased or diminished by various circum-
stances. The doctrine of Monroe simply asserts that if the
quantity of blood in the cavity of the cranium be increased,

502

MORBID ANATOMY AND CLASSIFICATION

some other fluid must be dislodged; while if the quantity of
blood be diminished, some other fluid must fill up the vacant
space. The quantity of blood in the brain can undoubtedly
be increased or diminished, but this can only take place by a
corresponding diminution or increase in the quantity of the
cerebro-spinal fluid and of the fluid contained in the peri-
vascular lymph spaces. When, however, the intracranial pres-
sure is rendered still greater, as by extravasation of blood
from rupture of a blood-vessel, room is made for the sub-
stance superadded to the contents of the cranium by a certain
quantity of blood being squeezed out of the intracranial
arteries, veins, and sinuses, in addition to the displacement of
the cerebro-spinal fluid. The circulation within the cranium is
liable to be disordered by occlusion or rupture of one or more
of the intracephalic vessels, but the reader is referred to the
sections on embolism, thrombosis, and cerebral haemorrhage for
detailed descriptions of these processes.

Tumours. — The growth of intracranial tumours of all kinds
must necessarily be attended by great disturbance of the cere-
bral circulation. In order to make room for the increasing bulk
of the tumours the cerebro-spinal fluid, as well as the fluid of
the perivascular lymph spaces, is first squeezed out, the blood
is then compressed from the intracranial blood-vessels, so that
the whole brain is rendered ansemic.

§ 693. Secondary Degenerations. — Long-standing hemor-
rhagic and other diseased foci give rise to various secondary
changes not only in the surrounding tissues, but also in distant
parts. These changes are of two kinds : firstly, those which
involve the entire mass of the brain ; and secondly, those
limited to certain tracts of conducting fibres which are inter-
rupted in their course by the haemorrhage.

(1) General Atrophy. — With regard to the former of these
kinds, it is found that the brain frequently undergoes, even
after an insignificant haemorrhage, a slow and general atrophy
which occasionally affects both hemispheres. This condition is
especially common after extravasations into the cortex. A per-
sistent alteration of one hemisphere of the brain may after
a time induce atrophy of the opposite hemisphere of the
cerebellum.

OF THE DISEASES OF THE ENCEPIIALON.

503

(2) Systemic Degeneration. — As has been frequently staled,
whenever the fibres of the pyramidal tract are injured in any
part of their course from their origin in the cortex of the brain
down to their termination in the spinal cord, the portions below
the seat of injury undergo descending degeneration.

A focal lesion, limited to the middle third of the posterior segment of
the internal capsule {Fig. 237, F), is followed by descending degeneration
[ of the fibres of the middle third of the crusta (Fig. 238, L), and of a
portion of the longitudinal fibres of the pons and anterior pyramid of the
medulla.

In the lower end of the medulla the greater part of the degenerated fibres
cross over to the lateral column of the opposite side of the cord (Fig. 239,
A), while some of them pass clown the column of Tiirck of the same side
. (Fig. 239, B). The course pursued by the secondary degeneration in the case

Fig. 237.

Fig. 237 (Charcot). Horizontal Section of the Eight Hemisphere parallel with the
Fissure of Sylvius.— Nc, Caudate nucleus ; Sa, Anterior segment of the in-
ternal capsule; Nl, Lenticular nucleus ; G, Knee of the internal capsule ; Sp.
Posterior segment of the internal capsule ; Co, Optic thalamus ; F, A focal
lesion in the middle third of the posterior part of the internal capsule.

504? MORBID ANATOMY AND CLASSIFICATION

Fig. 238.

T
I

Fig. 238 (Charcot). Horizontal Section of the Crura Cerebri in a case of Secondary
Degeneration. — T, Tegmentum; F, Crusta of the healthy side; L, Locus
niger; D, The degenerated fibres, occupying about the middle third of the
crusta; P, The fibres which undergo secondary degeneration only when the
fibres of the anterior segment and the knee of the internal capsule are diseased.

Fig. 239.

Fig. 239 (Charcot). Transverse Section of the Cervical Region of the Sjrinal Cord,
from a case of lesion of the motor area of the cortex of the opposite hemisphere. —
A, Degeneration of the pyramidal tract ; B, Degeneration of the direct fibres ;
C, Direct cerebellar tract ; D, Intermediate region between the posterior grey
horn and the pyramidal tract, the fibres of which do not undergo descending
degeneration.

OF THE DISEASES OF THE ENCEPHALOX.

505

just described corresponds to that of the fundamental libres of the pyra-
midal tract during their development (Figs. 223 and 224). A case has
been described by Brissaud in which, along with extensive recent softening
of one hemisphere, an old focus of softening was observed limited exactly
to the knee of the internal capsule {Fig. 240, D). A streak of degeneration

Fig. 240.

Fig. 240 (Brissaud). Recent Softening of the Frontal Lobe, the Island of Reil, and
Middle Third of the Lenticular Nucleus. — D, Old focus of softening occupying
the knee of the internal capsule; A, Caudate nucleus; B, Optic thalamus ;
C, Anterior, and E, Posterior division of the internal capsule.

was observed lying between the internal and middle thirds of the crusta,
being the anterior portion of the area which has already been described as
the mixed area of medullated and non-medullated fibres in a nine months
embryo (Fig. 223). According to Brissaud degeneration occurs in the knee
of the internal capsule in cases of long-standing aphasia.

Another important case has been observed by Brissaud in which an
old focus of softening was found in the anterior half of the lenticular
nucleus, destroying also the anterior segment of the "internal capsule
(Fig. 241, F). A streak of degeneration was observed in the internal
third of the crusta (Fig. 241, P), but all the fibres of this area were not
implicated in the degeneration, a small bundle of the innermost fibres
remaining normal. The degenerated fibres in this case corresponded very
nearly to those which we have described as the accessory fibres of the tract.
Degeneration of the internal tract of the crusta, according to Brissaud,
appears to be always connected with intellectual disorders.

506

MORBID ANATOMY AND CLASSIFICATION

The following bundles of fibres may, therefore, be distinguished in the
internal capsule (Brissaud) : —

(1) A posterior or sensory fasciculus (occupying the external third of the
crusta), which is never the seat of secondary degeneration.

(2) A middle fasciculus (occupying the middle third of the crusta),
which is the usual seat of secondary degeneration.

(3) A geniculate fasciculus (occupying the point, of union of the middle
and internal thirds of the crusta), which has erroneously been regarded as
incapable of degeneration. This fasciculus contains fibres which are dis-
tributed to the bulbar centres, and are concerned in the production of the
voluntary movements of the face and tongue.

(4) An anterior fasciculus (occupying the internal third of the crusta),
degeneration of which appears only to be associated with intellectual
disorders.

Fig. 241.

Fig. 241 (Brissaud).— A, Caudate nucleus ; B, Optic thalamus ; C, Posterior and
healthy part of the lenticular nucleus ; D, Posterior segment of the internal
capsule ; E, Lesion of the anterior segment of the capsule ; F, Cyst pre-
senting the form of the lenticular nucleus; P, Degeneration of the internal
fibres of the crusta.

OF THE DISEASES OF THE ENCEPHALON.

507

' § G94. Congenital Malformations of the Skull and Brain.

(1) Anencephalia— In this condition the upper portion of the skull and
brain is entirely absent. This condition is sometimes associated with
amyelia, a condition in which the vertebral column remains unclosed, and
the spinal cord is wanting (Forster).

(2) Hemicrania.— The anterior portion of the skull is absent and the
brain deficient.

(3) Hemicephalia.— The lateral half of the brain and skull is deficient.

(4) Notenceplialus.— The upper part of the skull is deficient, and the
vertebral column is not entirely closed in, while the brain develops in the
vertebral canal instead of the skull.

(5) Hydrencephalocele— In this condition the bones of the skull are
deficient, an opening being left, generally at one of the fontanelles, through
which a soft, fluctuating tumour projects. The tumour contains fluid, and
can generally be emptied by steady pressure. The walls of the tumour
consist of the soft coverings of the skull, and the distended membranes of
the brain. The tumour communicates with the general ventricular cavity
of the brain.

(6) Encephalocele. — The bones of the skull are again deficient at some
part in this condition, but through the opening formed a portion of the
brain itself projects, forming a broad, flat, solid tumour. The tumour
frequently occupies the forehead, orbit, or side of the nose.

§ 695. The Law of Dissolution. — Although the law of disso-
lution is probably destined at some future time to throw more
light on the morbid anatomy of the brain than on that of any
other organ of the body, yet it must be admitted that up to
the present very little progress has been made in this direction.
The law has been applied by Dr. Hughlings-Jaekson with
much ingenuity and success to the interpretation of disordered
cerebral functions, but it has yet to be applied to the eluci-
dation of morbid cerebral structures. The histological elements
of the brain doubtless conform to this law in their degene-
rations in a manner similar to that already described with
regard to the histological elements of the spinal cord. And
even when the disease is diffused in the neuroglia the small
cells and thin fibres of the accessory portion of the brain
must suffer injury more readily than the large cells and thick
fibres of the fundamental portion. This a priori necessity has
not, however, been verified as yet by a posteriori observations.
Even in such a coarse lesion as that caused by occlusion of one
of the cerebral arteries — say the inferior frontal branch of the

508

MORBID ANATOMY AND CLASSIFICATION

left Sylvian artery — the operation of this law may probably be
traced. If, as we have already endeavoured to prove, the later-
formed cells and fibres of Broca's convolution lie near the root
of this artery, while the earlier-formed cells and fibres are
thrust upwards and forwards towards the terminal twigs of the
vessel, it is manifest that the earlier is in a much more favour-
able position than the later developed portion to obtain nourish-
ment from the neighbouring vascular territories. But this con-
clusion, although there is much probability in its favour, has
not yet been confirmed by careful dissection. These brief
and imperfect remarks are all that we feel justified in making,
in the present state of our knowledge, with regard to the
applicability of the law of dissolution to the structural altera-
tions produced by disease in the brain.

(II.) -CLASSIFICATION OF THE DISEASES OF THE
ENCEPHALON.

It is impossible to give a full and scientific classification
of the diseases of the encephalon, inasmuch as a large propor-
tion of them are beyond the scope of this work. It is not our
intention to enter upon the discussion of the wide class of
diseases of the brain comprised under the general term insanity,
and yet no classification of the diseases of the encephalon can
be considered satisfactory which does not comprise them. In
endeavouring to classify the diseases which remain, we shall
proceed on the principle of considering first those which give
rise to the fewest, and leaving to the last those that occasion
the most numerous and complicated symptoms. Now as disease
of the membranes can hardly ever exist without producing
secondary disease over a large area of the surface of the brain,
the symptoms characterising the former may be expected to be
on the whole more complicated than those of the latter, and
consequently the diseases of the encephalon will be considered
prior to those of the membranes. Of the diseases of the
encephalon, the lesions which give rise to the least complicated
symptoms are the focal, and those which give rise to the most
complicated symptoms are the diffused lesions. It is known
that a focal lesion, as a tumour, may by increasing the intra-
cranial pressure and in other ways give rise to diffused effects,

OF THE DISEASES OF THE ENCEPHALON.

509

and that a diffused disease like encephalitis may by terminating
in abscess occasion local symptoms. The division into focal and
diffused lesions is, therefore, not a scientific but a practical dis-
tinction, and must be judged entirely from a practical stand-
point. The symptoms caused by focal diseases depend partly
upon the nature and partly upon the locality of the lesion.
Cerebral hcemorrhage, for instance, occasions a grouping of
symptoms which enables the affection to be readily distinguished
from the symptoms produced by the slow growth of an intra-
cranial tumour ; yet the symptoms caused by destruction of a
certain portion of the internal capsule, for instance, is the same
whether the injury be caused by haemorrhage or by the growth
of a tumour. The focal diseases, therefore, admit of considera-
tion under two aspects: (I.) according to the symptoms common
to the pathological state in general; and (II.), according to the
special functions of the region affected. With these few
remarks the following classification may be allowed to explain
itself : —

A. Diseases of the Enceyfhalon.
I. Focal diseases.

(i.) General consideration of focal diseases, according
to the nature of the lesion.

1. Occlusion of intracranial vessels.

2. Intracranial haemorrhage.

3. Intracranial tumours.

(n.) Special consideration of focal diseases, according
to the localisation of the lesion.

1. Affections of peduncular fibres and internal capsule.

a. Affections of the pyramidal tract.

(i.) Hemiplegia,
(ii.) Hemispasm.

b. Affections of the sensory peduncular fibres and optic

radiations of Gratiolet.
(i.) Hemianesthesia.

2. Lesions of the cortex of the brain and of the subjacent

portion of the centrum ovale,
a. Lesions in the area of the middle cerebral artery,
(i.) Unilateral convulsions, and monospasms,
(ii.) Monoplegia).

(iii.) Cortical affections of speech.

510 CLASSIFICATION OF DISEASES OF THE ENCEPHALON.

b. Lesions in the area of the posterior cerebral artery.

c. Lesions in the area of the anterior cerebral artery.

3. Lesions in the basal ganglia, external capsule, claustrum,

and base of the brain.

4. Lesions localised in the structures situated below the

tentorium.

a. Lesions in the pons and peduncles of the cerebrum.

b. Lesions in the peduncles of the cerebellum.

c. Lesions in the cerebellum.

II. Diffused diseases of the encephalon.

(i.) Anaemia and hypersemia of the brain,
(il.) Atrophy and hypertrophy of the brain,
(ill.) Shock, and concussion of the brain,
(iv.) Encephalitis.

1. General encephalitis. „

2. Partial encephalitis.

a. Acute encephalitis, complicating affections of the

petrous portion of the temporal and other bones
of the skull.

b. Acute pysemic encephalitis.

c. Encephalitis secondary to other cerebral lesions.

d. Chronic abscess of the brain.

B. Diseases of the Membranes of the Brain.

I. Diseases of the dura mater.

(i.) External pachymeningitis.
(II.) Internal pachymeningitis.

II Diseases of the pia mater.

Acute inflammation of the pia mater.

t. Leptomeningitis Infantum.

2. Tubercular meningitis.

3. Meningitis of the base of the brain.

4. Meningitis of the convexity of the brain.

5. Metastatic meningitis.

6. Traumatic meningitis.

511

CHAPTER III.

( I. ) GENERAL CONSIDERATION OF FOCAL DISEASES,
ACCORDING TO THE NATURE OF THE LESION.

L OCCLUSION OF THE INTRACRANIAL VESSELS.

The arteries, veins, sinuses, and capillaries of the brain are
liable to become occluded, a circumstance which gives rise to
various pathological changes. The occluding body may be
formed on the spot, constituting thrombosis ; or may be carried
from distant parts, constituting embolism.

(a) Occlusion of the Cerebral Arteries.

§ 696. Etiology. — Emboli consist of fibrinous masses washed
away from the left cavities of the heart, the aortic and mitral
valves, the arch of the aorta, and occasionally from the pulmonar}'
veins. In cases of carcinoma of the lungs, a cancerous mass
may possibly be carried from the pulmonary veins and pass
into the cerebral vessels.

Arterial thrombosis is determined partly by general causes
tending to diminish the force of the heart's action and to alter
the quality of the blood, and in part by local degenerations of
the coats of the vessels themselves. During convalescence from
acute diseases and other exhausting processes, the heart is weak,
and the blood becomes so altered in quality that it is specially
prone to coagulate. This process is, of course, much favoured
if the heart have undergone dilatation without proportionate
hypertrophy/ The local causes of thrombosis are alterations of
the walls of the arteries, whereby their lining membrane is
roughened and their calibre is narrowed. The coagulation of
fibrine is favoured by changes in the walls and internal surface
of the vessel, such as those due to atheromatous and calcareous

512

FOCAL DISEASES, ACCORDING TO

degenerations. Thrombosis is particularly liable to occur when
general causes and local degeneration act together.

.Thrombosis may take place in any of the arteries at the base
of the brain, or in several of them at the same time. A thrombus
not unfrequently forms in one of the internal carotid arteries,
and the clot then often extends into the middle and anterior
cerebral arteries of the same side, and sometimes even into the
posterior communicating and the posterior cerebral artery.

Of the predisposing causes of cerebral thrombosis age is
probably the most important. Thrombosis occurs more fre-
quently in advanced age, owing to the degenerative changes
in the vessels, although it may occur at all ages. Embolism,
on the other hand, is met with in relatively young persons,
although it may also occur in persons of advanced years.

§ 697. Symptoms-. — The symptoms which characterise the
later stages of thrombosis and embolism are the same, but those
of the early period differ considerably.

The symptoms of embolism are very sudden in their onset,
and are not preceded by any premonitory signs. The patient is
suddenly attacked with dizziness, utters an involuntary cry, or
complains momentarily of headache, and then almost imme-
diately loses consciousness. The symptoms occasioned by
embolism of a cerebral artery are in their general characters
and mode of onset almost identical with those of cerebral
haemorrhage, but the unconsciousness caused by embolism is,
as a rule, more transient than that produced by haemorrhage.

In many cases there is no coma, but only some dizziness or
slight confusion of mind for a minute or two, along with the
sudden advent of paralysis. The attack is sometimes ushered
in by epileptiform convulsions, which may sometimes be general
like an ordinary epileptic attack, but are at other times limited
to one-half of the body, to one extremity, or one-half of the face.

When general convulsions are present they ^occur simul-
taneously with the loss of consciousness, and are followed by
paralysis immediately, while unilateral and partial convulsions
may recur repeatedly before paralysis is fully established. In
some cases the attack is accompanied by vomiting, and Hammond
reports a case in which active delirium, and another in which

THE NATURE OF THE LESION.

513

hallucinations and delusions were present for some hours after
a sudden attack of hemiplegia. The presence of disease of the
aortic and mitral valves in Hammond's cases rendered the
diagnosis of embolism very probable.

In many cases sudden speechlessness, a condition which will
be subsequently described as aphasia, constitutes the only
symptom of the affection, and in these cases the symptom may
disappear in a few days when collateral circulation is estab-
lished. As a rule, however, the aphasia is associated with
right-sided hemiplegia, which possesses the same general
characters as that which results from haemorrhage into the
lenticular nucleus and neighbouring parts. The right side is
more frequently affected with paralysis than the left, owing to
the greater liability of the left middle cerebral artery to be-
affected by embolism. The state of the pupils during the onset
of the attack has been variously described, and it probably
varies in ditfeient cases. Erlenmeyer states that the pupils
remain sensitive, being neither contracted nor dilated, while
Hammond has found dilatation, contraction, or irregularitv.

The symptoms of thrombosis are, as a rule, more gradual in
their development than those of embolus. The more usual
premonitory symptoms of thrombosis of a cerebral vessel con-
sist of headache, which may be diffused through the entire
head or referred to the neighbourhood of the morbid process
(Hammond), dizziness, and a sense of general confusion. The
patient may complain of numbness, coldness, or formication in
one extremity or throughout the distribution of one nerve
or in the entire half of the body. At times there may be
considerable mental disturbances, and failure of memory is
often a marked symptom. Motor disturbances are usually of
the nature of more or less extensive paresis, but occasionally
the loss of motor power is preceded by slight convulsive move-
ments. Paralysis may occasionally supervene suddenly, but, as
a rule, its development is slow and gradual, its progress being
marked by successive remissions and exacerbations. This mode
of development appears to be due to the fact that thrombosis
has a tendency to extend backwards and to implicate more and
more of the arterial branch, in whose ultimate twigs the process
may have first begun. The duration of the prodromal stage

514

FOCAL DISEASES, ACCORDING TO

may vary from a few hours to several months, and occasionally
apoplectic symptoms may come on suddenly, as in embolism.
When once the vessel has become completely occluded, the
further progress of thrombosis is like that of embolism in the
same situation.

When softening occurs the temperature, according to Bourne-
ville, rises on the second or third day after the attack, and in
two or three days may be as high as 40° C. (104° F.). In a few
days longer the temperature sinks rapidly, its decline being
more rapid than that which takes place after the period of re-
action in cases of haemorrhage. When once softening has
become thoroughly established the symptoms are those which
result from localised cerebral disease generally, and indeed the
symptoms of softening and of haemorrhage when regarded as
localised diseases are often identical.

Contractures of the paralysed limbs are not so common in
cases of occlusion of vessels as in cases of haemorrhage, but they
occur sufficiently often to make their presence or absence
destitute of diagnostic significance.

The sensory, trophic, and vaso-motor disturbances, as well
as the affections of the special senses, with the exception of
vision, are the same as those which occur in connection with
cerebral haemorrhages. In some cases of embolism the ophthal-
mic artery has become occluded, giving rise to sudden amaurosis.
On ophthalmoscopic examination the arteries of the retina are
seen to be empty ; they appear like fine threads, but still re-
tain their red colour. The veins are not much diminished in
size, and are filled with dark blood. The retina presents a
greyish or. white opacity which is most marked around the
macula lutea, but the fovea centralis remains of a bright red
colour, forming a marked contrast with the pallor of the sur-
rounding portion of the retina.

Various disturbances of the mental faculties may result from
embolic softening. Probably the most interesting of these is
aphasia, which results from embolism of the middle cerebral
artery generally of the left side, but this condition will be dis-
cussed at greater length in a future chapter.

In some cases of qcclusion of cerebral arteries the symptoms
begin to improve at an early period, and the patient may

THE NATURE OF THE LESION.

515

ultimately recover completely. In these cases it is evident
that the collateral circulation has been established before
softening has commenced. In other cases the patient, after
partial or complete recovery, is attacked again with embolism,
and there may be a second recovery. In some cases of throm-
bosis the first symptoms may be of moderate severity, and may
afterwards become by sudden accessions more and more severe.

In some few cases death may follow immediately, but as a
rule it is not so sudden as in haemorrhage.

Diseases of the mitral or aortic valves, aortic aneurism,
ulcerative endocarditis, and. inflammatory or syphilitic affec-
tions of the muscular substance of the heart are the compli-
cations usually met with. In cases of thrombosis evidences of
degeneration of the vascular system can usually be detected in
the radial and other arteries. Important symptoms may arise
from embolism in the spleen, the kidneys, and the arteries of
the extremities.

§ b'98. Diagnosis. — The problem of diagnosis is to distin-
guish cerebral embolism, thrombosis, and haemorrhage from
one another. This must be done, not so much by means of
the cerebral as of the associated symptoms.

When sudden hemiplegia occurs in a young or middle-aged
person who is suffering from valvular disease of the heart or
aneurism, the symptoms are in all probability due to embolism.
The probability of embolism of a cerebral artery is rendered
still greater if there be a history of previous seizures in the
brain or other organs. "Right-sided hemiplegia, with aphasia,
results more frequently from embolism of the left middle cerebral
artery than from any other cause, and consequently in such
cases the presumption is always in favour of occlusion of the
vessel rather than haemorrhage, provided there be the necessary
conditions for its occurrence. There are no absolute means of
distinguishing between haemorrhage and thrombosis, and it is
needless to discuss the various diagnostic signs which have from
time to time been proposed.

§ 699. Morbid Anatomy. — Embolism affects certain vessels
with special frequency. The mode of origin of the left carotid

516

FOCAL DISEASES, ACCORDING TO

directly from the arch of the aorta, and the angle at which it
leaves the arch, very much favour emboli being carried into
it. These emboli usually pass the circle of Willis and. make
their way into the left middle cerebral artery, which is the
direct continuation of the internal carotid, and, consequently,
this artery is more frequently occluded by an embolus than
any other vessel of the brain.

Thrombosis does not appear to have a special preference for
any one artery. The middle and posterior cerebral, and verte-
bral arteries are equally liable to be occluded by thrombosis.

When one of the cerebral arteries — the left middle cerebral
artery, for example — is obstructed close to the circle of Willis,
the circulation through the nutrient arteries supplied, by it to
the basal ganglia is arrested, and as these are terminal arteries
rapid softening occurs. When one of the vessels of the brain
is obstructed on the cardiac side of the circle of Willis, the free
anastomosis of the latter re-establishes the circulation so quickly
that no pathological changes occur in the brain. If, again, the
embolus be carried forwards past the basal portion to the arterial
system of the cortex, it is quite possible that the free anasto-
mosis of the latter may prevent decided pathological changes
from taking place. In many cases, however, a certain amount
of softening does occur under such circumstances, because the
anastomosis is not always so free as to compensate for the
blocking up of a large branch of the artery. When the
embolus is lodged in one of the terminal arteries of the basal
arterial system softening always occurs, owing to the absence
of anastomosis with neighbouring arteries.

The first effect produced by occlusion of a terminal artery is oedema of
the part supplied by it. The venules and arterioles of the part are imper-
fectly nourished so that their walls dilate and frequently rupture, giving
rise to hyperemia attended by oadematous swelling and hseniorrhage. The
tissues, not being supplied with nourishment, break down and undergo
softening. When the softened tissues become mixed with extravasated
blood, they give rise to red softening. The hyperaemia and hemorrhage
may fail to occur, and then simple necrobiosis results from the occlusion
of the vessel, giving rise to a softened mass of a yellowish- white or white
colour. These changes generally begin in the course of the second twenty-
four hours after the obstruction has occurred, although cases are reported
in which the consistence of the brain tissue was normal after the lapse of
two days.

THE NATURE OF THE LESION. 517

Microscopic examination reveals the presence of a large number of
red blood corpuscles, which is the only abnormal appearance observed
during the first twenty-four hours. At a later period the nerve elements
undergo gradual degeneration. The most prominent microscopic pecu-
liarity consists of granular corpuscles, which are probably derived from
degeneration of neuroglia and ganglion cells of the grey substance, and
various other sources.

Experimental Investigations.— -The first experimental researches with
respect to the emholic process was undertaken by Virchow, and great
additional light has been thrown upon the subject by the important ex-
perimental and microscopic investigations of Cohnheim. Panum studied
experimentally the results of occlusion of cerebral vessels with the view of
determining the manner in which death is caused. B. Cohn investigated
experimentally various clinical and anatomical points ; Feltz studied the
results of capillary embolism ; while Prevost and Cotard made a series of
experiments with the view of determining the relation of occlusion of
cerebral vessels to softening.

§ 700. Morbid Physiology. — The most difficult problem to
solve with respect to the morbid physiology of the affection is
how occlusion of only one of the cerebral arteries produces loss
of consciousness. Brown-Se'quard has recently dwelt upon the
fact that local lesions exert an influence over remote parts of
the nervous system, and the sudden arrest in the circulation in
one of the arteries of the brain is likely to produce widely-
spread effects. Heubner and Duret have shown that although
the abundant anastomoses between the arteries of the cortex
after a time establish a collateral circulation, yet at the
moment of obstruction great disturbances of the circulation
and marked changes in pressure may occur in and around the
implicated region. We have already seen that sudden depriva-
tion of nourishment increases the irritability of nerve fibres,
and it is probable that the abrupt arrest of the arterial circu-
lation induces a powerful outgoing discharge from the cortex.
That this occurs in certain cases is undoubted, inasmuch as
the onset of the attack is marked by general convulsions. A
powerful discharge of this kind would be followed by exhaustion,
and temporary loss of function, or in other words the attack
would be characterised by loss of consciousness. In those cases
in which there is an absence of convulsions the cortical dis-
charges may be supposed to neutralise one another in the
nervous system without producing their usual visible effects.

518

FOCAL DISEASES, ACCORDING TO

§ 701. Prognosis. — Both embolism and thrombosis are
always serious affections. When embolism occurs in a young
person recovery from the immediate effects may be rapid and
complete, but the underlying affection to which the attack was
due will still be present and may cause a similar attack in
the future or give rise to other grave symptoms. Thrombosis
is usually associated with advanced age, enfeeblement of the
heart's action, and degeneration of arteries, and during the
attack there is great danger, however slight the symptoms may
at first appear, that the occlusion will become more and more
extensive.

§ 702. Treatment. — Prophylactic measures can only be
adopted when premonitory symptoms are present for a long time
in connection with a slowly-forming thrombosis. In such cases
the heart should, according to theory, be stimulated by digitalis,
ammonia, and alcoholic stimulants ; but since it is impossible
to diagnose this condition during life from haemorrhage, it will
be better to be content with adopting the same treatment
as that recommended for haemorrhage. During the stage of
coma also the same means should be used as in haemorrhage.

(b) Thrombosis of the Cerebral Sinuses.

§ 703. History. — Special attention was first directed to the subject of
thrombosis of the cerebral sinuses by the observations of Tonnele. Many
valuable clinical observations with regard to the disease were made by
Puchelt, and the attention of Lebert was also directed to it. The treatises
of Von Dusch, B. Cohn, and of Lancereaux helped greatly to extend and
to systematise our knowledge with respect to this thrombosis ; and in
more recent times our knowledge has been further increased by the
labours of Gerhardt, Griesinger, Corazza, Heubner, and Hugnenin.

§ 704. Etiology. — Thrombosis of the sinuses may be divided
into two groups : the first comprising the cases which arise in
the absence of any affection of the walls of the veins, and the
second those which originate from phlebitis.

The cases of the first group arise in conditions of marasmus,
in which the quality of the blood is altered and the circulation
enfeebled. Under such circumstances coagulation of the blood
is specially prone to occur in the sinuses, inasmuch as they are

THE NATURE OF THE LESION.

519

rigid tabes and incapable of collapsing ; they are also destitute
of muscular walls, and are traversed by bands of connective

tissue. I

Thrombosis of the sinuses from marasmus is particularly
apt to occur in children, especially during the first six months
of life, when they are liable to suffer from collapse induced by
severe diarrhcea. It also occurs in adults, in consequence of
profuse suppuration, cancer, senile marasmus, and other con-
ditions of debility. This form of thrombosis occurs with special
frequency in the longitudinal and lateral sinuses. Obstruc-
tion to the return of the venous blood towards the heart
increases the liability to the formation of thrombosis of the
sinuses, but it is not likely that venous stasis can give rise to
it in the absence of other favouring conditions.

The second group of thromboses is caused by inflammation
of the sinuses, the result generally, probably always, of disease
or injury of the cranial bones. Caries of the petrous portion
of the temporal bone is by far the most common cause of
inflammation of the sinuses ; the lateral and petrosal sinuses,
which lie in the vicinity of the temporal bone, are then
particularly liable to be affected, although the process may
implicate the circular and cavernous sinuses as well as the
upper part of the internal jugular vein. In most cases a real
phlebitis is induced, followed by the formation of purulent
thrombi. Thrombosis of the sinuses also frequently follows
blows on the head, or inflammatory conditions of the scalp
and cranial bones. Erysipelas of the head and face, and
furunculus of the face, especially of the upper lip and fore-
head, not unfrequently give rise to thrombosis of the sinuses.
Cohn observed a case in which suppurative phlebitis of the
cavernous sinuses occurred in connection with purulent inflam-
mation of the deep muscles of the neck.

§ 705. Symptoms. — The symptoms of thrombosis of the
cerebral sinuses are generally marked by complicating diseases,
so that it is rarely possible to diagnose the affection during
life. The symptoms also vary greatly, both according to the
seat of the occlusion and according as the thrombosis is or is
not the result of phlebitis.

520

FOCAL DISEASES, ACCORDING TO

Thrombosis of the sinuses in children almost always arises
during the marasmus, caused by exhausting diarrhoea, and the
symptoms produced are the same as those of cerebral anaemia,
being such as Dr. Marshall Hall described under the name of
hydrencephaloid disease. In addition to the collapse, somno-
lence, and coma of pure cerebral anaemia, motor disorders, as
convulsions or paralysis, are generally present. Rigidity of the
muscles of the neck, sometimes also of those of the back and
even of the limbs, occasionally nystagmus, strabismus, ptosis,
and paresis of the facial muscles have been observed.

Thrombosis of the sinuses resulting from marasmus in adults
gives rise to very various and indefinite symptoms, and at times
a slight degree of apathy and general depression are the only
symptoms observed. The patient at the outset may complain
of headache, nausea, and vomiting, but these soon give place
to coma, while in a few cases loss of consciousness may be pre-
ceded by delirium, which may assume a maniacal character.
The condition of the pupils is variable.

Motor disturbances are usually present, the most usual being
strabismus, trismus, contractures which may involve one-half of
the body, or both legs and both arms, tremors, and epileptiform
convulsions, either limited to one or involving the four extremi-
ties. The motor disorders may assume the form of paresis or
paralysis, which may be limited to the facial nerve or to the
motor oculi, or may involve one-half or both sides of the body.
At other times both paralysis and convulsions may be asso-
ciated, one extremity being the seat of contracture and the
other of paralysis. These symptoms may, however, be present
in cases of cerebral anaemia or of venous hyperemia of the
brain.

A valuable .sign of the disease is sometimes afforded by
swelling of the veins outside the skull which are in commu-
nication with the obstructed sinus. The superior longitudinal
sinus, for instance, communicates directly with the veins of the
nasal cavities and with those on the upper surface of the skull.
The occurrence of epistaxis, therefore, favours the idea of
obstruction of this sinus, and in children the presence of
.distended vessels running to the anterior fontanelle from the
neighbourhood of the temples and ears on both sides of the

THE NATURE OF THE LESION.

521

head also favours the same view. Cyanosis of the face limited
to the part supplied by the anterior facial veins is also, according
to Gerhardt, of diagnostic significance.

The lateral sinus communicates with a small vein which
traverses the mastoid process, and in thrombosis of the sinus
localised oedema behind the ear may make its appearance.
This sign is occasionally valuable, but is rarely met with.
Simultaneous occlusion of both lateral sinuses gives rise to the
same symptoms as occlusion of the superior longitudinal sinus.

The cavernous sinus communicates with the ophthalmic
veins, and in thrombosis of this sinus venous hypera3mia of the
fundus oculi has been observed, as well as oedema of the eye-
lids and conjunctiva and prominence of the eyeballs, due to
congestion of the retrobulbar veins and of the frontal vein.
Paralysis of the motor nerves of the eye, trigeminal neuralgia,
and neuroparalytic ophthalmia, may also be present, owing to
the disturbance in the nutrition of the nerves which pass along
the side of the cavernous sinus.

In thrombosis of the sinuses in infants the fontanelle is
depressed, and at times the edges of the bones pushed one over
the other ; but during the progress of the disease the fontanelle
may again become tense and prominent, and the cranial bones
pressed apart (Gerhardt). This increase of the contents of the
skull is caused either by effusion of serum from the tense veins
giving rise to a species of hydrocephalus or to extensive
meningeal or intra-cerebral hemorrhage resulting from throm-
bosis of the sinuses.

The phlebitic variety, as already remarked, is generally
caused by otitis interna or injuries to the head. These affec-
tions also give rise to meningitis and cerebral abscesses as
well as to purulent thrombosis, and inasmuch as these patho-
logical conditions are frequently combined, it is very difficult
to distinguish clinically between them. In a few reported
cases, however, suppurative thrombosis was alone present
uncomplicated by meningitis or by lesions of the cerebral sub-
stance. The affection sometimes pursues a latent course, and
is only discovered after death. The symptoms are usually
similar to those observed in cases of septicaemia with specially
prominent cerebral symptoms. The attack frequently begins

522

FOCAL DISEASES, ACCORDING TO

with chilliness, which generally recurs repeatedly during the
course of the disease, and the patient has a characteristic typhoid
look, with dry tongue, loss of appetite, and mental confusion.
After a time the patient falls into a somnolent condition, which
gives place to complete coma, terminating in death. Mild
delirium is present in a few cases, and more rarely the delirium
assumes an active form.

Suppurative thrombosis is frequently associated with motor
and sensory disturbances caused by the accompanying menin-
gitis. These consist of pain in the head, hyperalgesia, paresis,
paralysis, and convulsions.

§ 706. Diagnosis. — When a patient, suffering from caries of
the internal ear, furunculus in the face, or who has received an
injury to the head, develops symptoms like those of pyaemia,
with marked disturbance of the cerebral functions, purulent
thrombosis of the sinuses may be suspected. The diagnosis
will be further corroborated by the disturbances of the circu-
lation, which have already been described from the thrombosis.

§ 707. Course and Prognosis. — The duration of the disease
is difficult to determine, and it may probably extend occasionally
over several weeks, although usually terminating in a much
shorter time.

The prognosis is very unfavourable, but recovery is said
occasionally to take place (Se'dillot, Lebert, and Griesinger).

§ 708. Morbid Anatomy. — Any sinus may become the seat
of thrombosis, but some of them are much more liable to be
affected than others. The superior longitudinal sinus is the
one which is usually implicated in cases of thrombosis from
marasmus, and the sinuses in the neighbourhood of the petrous
bone in the phlebitic variety. The veins which empty them-
selves into the sinuses become enlarged and gorged with
blood, and are often filled with thrombotic masses, so that they
look like large earthworms when lying on the surface of the
brain. Ruptures of the vessels not unfrequently occur, causing
meningeal haemorrhage, but sometimes consists only of small
hemorrhagic spots, while at other times may amount to pro-

THE NATURE OF THE LESION.

523

fuse hemorrhage. The cortex of the brain is also frequently
the seat of capillary haemorrhages, and Lancereux has described
small spots of softening. The phlebitic variety is frequently
accompanied by meningitis, caused by the primary lesion.

§ 709. Treatment. — No treatment has hitherto been found
of any avail.

§ 710. Experimental investigations have shown that marked
disturbances of the cerebral functions may be caused by occlusion
of the cerebral capillaries, and clinical records also point to the
same conclusion.

§ 711. Etiology. — In severe cases of malarial and intermit-
tent fever the cerebral capillaries are liable to be obstructed by
dark masses, a condition which has been called 'pigment em-
bolism. The cerebral capillaries may also be obstructed by
drops of fat. The fat is usually swept into the blood current
by the breaking up of atheromatous formations in the interior
of the larger blood-vessels. In cases of injury to bone the
fatty tissue of the marrow may be carried into the blood-vessels,
giving rise to emboli in the lungs and possibly in the brain.

Chorea has been supposed to be due to capillary embolism,
but the subject will be subsequently discussed. The cerebral
capillaries are said to be occluded by lime becoming deposited
in their walls, a process named by Virchow lime metastasis.
Some disease of bone is usually associated with this condition,
and Virchow thinks that the lime is first absorbed from the
diseased bone, and afterwards deposited in the vessels.

§ 712. Symptoms. — The experiments of Feltz, and of PreVost
and Cotard show that extensive embolism of very fine particles
may rapidly induce death in animals by causing diffuse anaemia
of the brain. Nothing analogous to this is known to take place
in diseased conditions. If the embolic masses are few the
symptoms which they give rise to are so slight as not to be
recognisable during life. Such is known to be the case in
certain instances of fat embolism. In other cases a considerable

524

FOCAL DISEASES.

territory of the brain may be suddenly deprived of its nutriment,
and apoplectic symptoms may then be produced, followed by the
usual symptoms of a localised cerebral disease.

The symptoms, however, are usually such as arise from
diffused cerebral disease, the more common of them being
dizziness, headache, nausea, trembling, and weakness in the
extremities, and mental disturbance, as marked loss of memory
and other signs of mental decay.

§ 713. Morbid Anatomy. — Capillary occlusions are, of course,
only to be detected with the microscope. Delacour says that
in cases of lime metastasis a resistance is felt to the knife in
cutting through the brain, and rough prominences may be felt
on the surface with the finger.

The nature of the secondary changes in the brain varies
according to the number of the vessels obstructed, and it is
only when a large number are occluded that disturbance of the
circulation will not be compensated, structural changes then
occurring analogous to those following obstruction of the large
arteries. Experimental investigation has shown that the first
effect of the occlusion is to cause anaemia, and in the further
progress of the affection the various stages of necrobiosis may
supervene, ending in complete softening. The centres of
softening are often of small size, but several are usually
present.

§ 714. The course and prognosis depend upon the extent
and nature of the occlusion. Isolated capillary embolisms are
of no significance ; but if they are numerous the resulting dis-
turbances are in every respect similar to the corresponding
secondary effects of the occlusion of the larger arteries.

§ 715. Treatment. — The treatment must be conducted on
general principles.

CHAPTER IV.

(I.) GENERAL CONSIDERATION OF FOCAL DISEASES,
ACCORDING TO THE NATURE OF THE LESION
(Continued).

2. INTRACRANIAL HAEMORRHAGE.

Intracranial haemorrhage may be divided into (a) cerebral,
and (6) meningeal haemorrhage.

(a) Cerebral Haemorrhage.

§ 716. Definition. — By cerebral haemorrhage is here meant
an extravasation of blood into the substance of the encephalon
or into the ventricles of the brain.

§ 717. History. — Hemorrhage into the substance of the encephalon is
frequently termed apoplexy. The word ano-nXi) o-o-w means " 1 strike down,"
and a person who had suddenly fallen down insensible was said to be in a
condition of It was pointed out by Wepfer that this condition

was frequently caused by cerebral haemorrhage, and after a time the name
of the group of symptoms which signified sudden unconsciousness was
transferred to the anatomical condition which was the most frequent cause
of that occurrence. The process did not stop here ; during the course of
investigation it was seen that haemorrhage into the substance of other
organs was not uncommon, and after a time the meaning of the term was
extended so as to include these haemorrhages also. The term therefore
having come to signify conditions so different, it will be well to avoid
its use as much as possible.

§ 718. Etiology. — The circumstances which predispose to
cerebral haemorrhage are — (1) Disease of the vessels, (2) In-
crease of the arterial tension, (3) Disease of the tissues
surrounding the vessels, and (4) Certain diseases of the blood
itself.

526

FOCAL DISEASES, ACCORDING TO

(1) Disease of the Vessels. — The great majority of massive haemorrhages
into the substance of the brain are due to fatty degeneration of
branches of the Sylvian artery, which pass through the anterior
perforated space to reach the corpus striatum. Fatty degeneration of
arteries may be primary or secondary. Primary fatty degeneration
is a passive process, not being preceded by any increased nutritive
activity of the affected parts, but the secondary form of the process
is preceded by an inflammatory cellular infiltration of the sub-
endothelial connective tissue of the vessels, and constitutes atheroma.
It was formerly believed that when the arteries at the base of the
brain were found in a condition of atheromatous degeneration the
existence of a similar condition of the vessels in the interior of the
brain might be inferred, and that intracerebral haemorrhages might
in most instances be attributed to the brittleness of the vessels.
The belief is now growing that the influence of atheromatous disease
in the causation of cerebral haemorrhage is indirect rather than direct.
Atheroma of the vessels may occasionally lead to aneurisms of the larger
vessels at the base of the brain, but they are not often the cause of
haemorrhage. Besides, rupture of an aneurism of one of the larger vessels
would give rise to haemorrhage between the meninges, and not into the
substance of the brain. Atheromatous degeneration may, however, cause
haemorrhage indirectly by rendering the walls of the larger vessels rigid,
so that the pulse wave reaches the arterioles without being modified by
the normal elasticity of the arteries.

By far the most frequent cause of intracerebral haemorrhage is that
condition of the arterioles which has been described by Charcot and
Bouchard as miliary aneurisms. These aneurisms are situated on the
arterioles, are of a reddish colour, and vary in size from that of a millet-
seed to a pin's head. Sometimes a few only are found in the vicinity of
the ruptured vessel, while at other times they are scattered in large
numbers throughout the whole brain. The parts of the brain in which
they are situated, taken in the order of their decreasing frequency, are
the lenticular nucleus, the optic thalami, the pons, the convolutions, the
caudate nucleus, the cerebellum, the medulla oblongata, the middle
peduncles of the cerebellum, and the centrum ovale.

Miliary aneurisms occur rarely before the fortieth year, but are found
with increasing frequency after that age. They result, according to
Charcot and Bouchard, from a kind of arterial sclerosis of the nature of a
chronic periarteritis. This alteration consists in multiplication of the
nuclei of the lymph-sheaths and adventitia, a process which is generally
accompanied by atrophy of the muscular coat. When atrophy of the latter
occurs without a compensatory thickening of the adventitia, rupture of
these aneurisms very readily takes place.

The part which primary fatty degeneration of the vessels plays in the
causation of cerebral haemorrhage has been insisted upon by Paget. This
condition of the vessels is found at all ages, and in cachectic children even

THE NATURE OF THE LESION.

527

more frequently than among aged persons, so that care must be taken not
to over-estimate its influence in the production of haemorrhage. Billroth
has also shown that in a large number of cases this form of fatty degenera-
tion of the small vessels is secondary to disease of the nervous tissues.
Even after making these deductions from its importance as a predisposing
cause, there can be no doubt that this condition does increase the liability
to cerebral hiemorrhage.

(2) Vascular Tension.— It is very doubtful whether increase of the
arterial tension ever gives rise to cerebral haemorrhage without disease of
the vascular walls; but when the latter are degenerated then sudden
increase of tension becomes a powerful predisposing cause of haemorrhage.
Sudden exposure to cold may increase the arterial tension by inducing ex-
tensive contraction of the cutaneous arteries. During the winter months
it is very common for individuals to be found in an apoplectic condition on
the streets, and taken up by the police supposed to be drunk. Such cases
occur usually in persons beyond middle age, their breath may smell of
alcohol, and they may even be known to have been drinking during the
evening. The evening has been spent in a heated apartment, where, under
the conjoined influence of a high temperature, alcohol, and emotional
excitement of various kinds, the cutaneous vessels have become dilated, the
skin bathed in perspiration, and the cardiac action increased. On going
out into the cold air the surface becomes suddenly chilled, the cutaneous
vessels contract, the arterial tension becomes immediately greatly in-
creased, the internal organs become gorged with blood, and if, as is
frequently the case, the walls of the cerebral vessels are weakened by
disease, rupture takes place (Fothergill).

The hypertrophy of the left ventricle which is associated with con-
tracted kidney takes a more active part in the production of cerebral
haemorrhage. Avoiding as much as possible controversial points, it is
beyond question that contracted kidney is associated with a general con-
dition in which the walls of the arterioles of the entire body become
thickened, inelastic, and the lumina of the vessels themselves much dimi-
nished in size. This condition greatly obstructs the flow of blood from
the heart towards the capillaries, and the left ventricle becomes the
subject of compensatory hypertrophy, with the effect of producing a
permanent increase 'in the arterial tension. And whatever may be the
nature of the primary change in the arteries, whether a hypertrophy of
the muscular coat, or sclerosis of the external coat, or both combined, the
walls of the vessels undergo in long-standing cases degenerative changes
which render them brittle and easily ruptured.

Obstruction to the return of the venous blood from the brain probably
also predisposes to haemorrhage, but its direct effect must be small.
The obstruction may be temporary or permanent. Temporary in such
actions as coughing, sneezing, laughing, or straining at stool, and per-
manent in affections of the mitral and tricuspid valves, obliteration
and compression of the cerebral sinuses, compression of the jugulars and

528

FOCAL DISEASES, ACCORDING TO

superior vena cava, and affections of the lungs as emphysema and fibroid
phthisis.

(3) Condition of the Tissues. — Eochoux advanced the theory that spon-
taneous haemorrhage is generally preceded by a process of softening of the
cerebral tissue, to which he gave to this process the name of ramollissement
himorrhagipare. In consequence of the change of consistence of the
nervous tissue, the small vessels lose their natural support, and become
unable to resist the pressure of the blood. It is now generally believed
that the softening is a secondary process, the result partly of the imbi-
bition of blood serum, and partly of inflammation excited by the ex-
travasation in the surrounding tissues. Haemorrhage may, however, occur
as a result of softening of the tissues in cases of embolism and thrombosis,
but this condition will be noticed hereafter. Some authors think that
haemorrhage is due occasionally to atrophy of the cerebral substance, and
believe that the vessels then rupture in consequence of their becoming
dilated in order to fill the vacuum. But the reduction in the size of the
brain proceeds far too slowly for much dilatation of the vessels to result
from it; and the atrophy is compensated to some extent by thickening of
the skull and increase in the size of the frontal sinuses, but chiefly by
increase of the cerebro-spinal fluid.

(4) State of the Blood. — Various diseases, the essential condition of
which appears to be caused by some change in the composition of the
blood, occasionally lead to cerebral haemorrhage. Cerebral haemorrhages
have been observed in pyaemia, in the typhoid state, scorbutus, purpura,
chlorosis, leucocythaemia, pernicious anaemia, and icterus, but are excep-
tionally met with in these diseases.

§ 719. Other Predisposing Causes. — Some families exhibit
a predisposition to cerebral haemorrhage, hence it has been
assumed that the disease is hereditary. The action of heredity
in predisposing to haemorrhage is, however, only an indirect
result of the inherited tendency to arterial degeneration. It
was formerly believed that some individuals inherited an apop-
lectic constitution. This was supposed to be characterised by
broad chest, short neck, large abdomen, powerful muscular
system, and florid complexion. Exact statistics, however, prove
that cerebral hsemorrhage does not spare any constitution,
and that poorly-nourished, thin persons are as frequently
attacked as the plethoric.

One of the most important predisposing causes of the disease
is age. Cerebral haemorrhage is rare before the fortieth year,
relatively frequent afierwards. It must not be forgotten that
the disease attacks young persons, and it has been observed in

THE NATUBE OF THE LESION.

521)

infants and even at birth. Meningeal haemorrhage is relatively
common in early childhood.

Sex undoubtedly exercises a certain degree of influence in
predisposing to cerebral haemorrhage, probably owing to the
fact that men are more frequently exposed to the exciting
causes of the disease. The proportionate frequency with which
men and women are attacked has been variously estimated by
different authors, but it may safely be asserted that the ratio
of 21 rather under than overstates the proportion.

The influence of occupation in predisposing to cerebral
haemorrhage has not yet been satisfactorily determined, and the
same may be said with regard to the influence of climate, since
the immunity from the disease once attributed to warm climates
has recently been called in question. In Europe the disease is
most common in winter, then in autumn and spring, and least
so in summer. Altitude appears to exert some influence in the
production of the affection, since it is very common in the
elevated regions of Mexico, of the Cordilleras, and the Andes.
Certain substances, as alcohol, predispose to haemorrhage by
inducing fatty degeneration of the vessels.

§ 720. Symptoms. — The symptoms vary greatly according to
the situation and extent of the lesion ; but the mode of onset
being sudden and the lesion of a destructive character, the
initial group of symptoms bear a general similarity to each
other in all cases.

1. Premonitory Symptoms. — The attack is frequently
ushered in without any premonitory symptoms, and in no
instance can any symptom be relied upon as an invariable
antecedent of haemorrhage. Premonitory symptoms may, how-
ever, manifest themselves days and even weeks before the
actual onset of the attack, and these are no doubt frequently
caused by rupture of minute vessels prior to the graver event
which ushers in the apoplectic condition. The usual fore-
runners of the apoplectic attack are dizziness, headache, ringing
in the ears, muscse volitantes, numbness in the hand or foot,
muscular twitchings of the face or of some portion of the
upper or lower limbs, especially of the fingers or toes, mistakes
in talking or writing, vomiting, mental irritability and drowsi-
1 1

530

FOCAL DISEASES, ACCORDING TO

ness. These symptoms may appear separately or variously
combined, and although, all of them may occur without being
followed by an apoplectic attack, yet in the old and middle
aged, especially when the arteries are degenerated, they should
be regarded as warnings.

2. Modes of Onset. — For facility of description the mode of
onset of cerebral hsemorrhage may be divided into three prin-
cipal classes: (i.) The apoplectiform onset; (ii.) the epileptiform
onset; and (iii.) the simple mode of onset (Bastian).

(i.) Apoplectiform Onset. — This mode of onset is characterised
by sudden loss of consciousness with resolution of the limbs, and
what is popularly termed " apoplexy." In a small number of
cases the onset may be instantaneous. In the midst of apparent
health the patient may fall insensible to the ground. In such
cases the lesion, which need not necessarily be large, is usually
found in the pons or medulla. The attack usually begins more
gradually. The patient suffers from dizziness, abnormal sen-
sations or pain in the head, mental confusion, difficulty of
speech, drowsiness, nausea and vomiting, or a sense of great
exhaustion ; and after some of these symptoms have con-
tinued for a few minutes or longer the stage of unconsciousness
comes on.

When the apoplectic attack is well marked the patient lies
in a state of profound coma, and is insensible to all kinds of
stimuli. The face is usually flushed and swollen, though occa-
sionally it may be pale and clammy, the lips are livid, the head
and neck feel warm and are bathed in perspiration, the carotids
and other arteries throb violently, the eyelids are closed, the
conjunctivae injected, the eyeballs fixed, the pupils sluggish to
light, the respiration is usually deep, with or without ster-
torous inspiration and protrusion of the cheeks during ex-
piration, the pulse is generally full and slow, and there is either
complete muscular resolution, so that the limbs when raised
drop like inert bodies, or the resolution is more marked on one
side of the body than on the other. In the severest cases
there is not only complete absence of voluntary motion, but
all the reflex movements are abolished, with the exception of
the cardiac and respiratory movements, and those concerned in

TIIE NATURE OF THE LESION. 531
\

deglutition, the latter being generally retained as regards the
pharyDX and oesophagus.

When this condition has been brought about by a severe
lesion of the brain, the patient may die after a few minutes, a
few hours, or a few days. Tn the slighter forms, however,
the apoplectic state may last only a short time, and then
gradually give place to other related symptoms. When the
coma is not very profound, powerful irritations cause reflex
movements, and in the lesser degrees of the apoplectic state,
the patient, when loudly spoken to, raises his eyelids for a
moment or two, and may even reply in a monosyllable when
loudly pressed with any question. In such cases a difference
can be detected between the two halves of the body; the ex-
tremities of one side offer a certain resistance to passive
motion, while those of the other sink, when unsupported, like
inert masses ; the corner of the mouth on one side is lower
than on the other, and the opposite naso-labial fold is strongly
marked.

(ii.) The Epileptiform Onset. — The epileptiform is a mere
variety of the apoplectiform mode of onset. The patient,
either with or without prodromata, drops down insensible in a
kind of epileptic fit, and after a time it is discovered that the
patient is paralysed on one side of the body. Temporary
hemiplegia may follow severe attacks of unilateral convulsions
due to a molecular lesion of the cortex, but in the cases under
present consideration, the haemorrhage destroys a certain por-
tion of the brain, and the paralysis initiated is more or less
persistent. Although prodromata may be absent altogether,
yet the epileptic attack is very frequently preceded either by
pains in the head or by muscular twitchings, or the initial
attack may be characterised by unilateral convulsions, and in
these cases the half of the body convulsed corresponds with
that which is subsequently paralysed. But when convulsions
occur after paralysis has become established, it usually happens
that the non-paralysed side is the one which is affected with
clonic spasms, and in these cases there is probably co-existing,
but unequal, damage to both hemispheres of the brain.

Some of the patients whose hemiplegic condition is ushered
in by convulsions speedily die, whilst others remain liable to

532 FOCAL DISEASES, ACCORDING TO

a recurrence of epileptiform attacks at variable intervals ; in
many cases no subsequent attack occurs, even though the
patient live for many years. Another remarkable peculiarity
with respect to cases initiated by convulsions is, that the
period of stupor or partial unconsciousness may be prolonged
for three, four, five, or even six weeks, and yet the patient may
recover. In these cases, however, the patient is not deeply
comatose, but lies in a somewhat lethargic condition, with
eyes closed or only half open, and takes no notice of anything
that is going on around him. A patient, on the other hand,
who continues deeply comatose for forty-eight hours very rarely
recovers.

(iii.) Simple Onset. — In the simple mode of onset the patient
may suddenly fall owing to paralysis of an inferior extremity,
but the fall is not accompanied by any loss of consciousness.
The patient may experience no pain, but usually complains of
a feeling of " numbness " in the paralysed side of the body.
This mode of invasion is very frequent in the slighter forms of
hemiplegia.

Temperature. — The variations of the temperature of the body
in cases of apoplexy have been studied with great care by
Bourneville. The temperature is at first lowered in all cases,
sometimes reaching 96'5° F., and in the fulminating form of the
disease it remains low until death. If life continue for ten or
twenty hours the initial sinking gives place to a marked eleva-
tion of temperature. If the primary depression is followed by
a steady and continuous rise of temperature it is a very un-
favourable sign, and in these cases the pyrexia may reach
108° F. before death. In the more favourable cases the initial
lowering is followed by a stationary period, during which the
temperature varies between 99° F. and lOO'S0 F., and continues
to oscillate rather irregularly for from two to four days. If the
case be going to terminate in recovery, and supposing there be
no inflammatory complications of other organs, the temperature
gradually falls to the normal standard, and there remains.
When, however, the case is to terminate fatally in the course
of a day or two more, the stationary period is followed by a
rapid and continuous rise of temperature, which is a not less
unfavourable sign than when the same occurs after the period
of initial lowering.

THE NATURE OF THE LESION.

Conjugated deviation of the eyes, ivith rotation of the
head away from the paralysed side and towards the hemi-
sphere which is the seat of disease, usually occurs as a tem-
porary symptom in all cases of severe cerebral haemorrhage
(§ 90). The eyes are usually fixed, but occasionally exhibit
slight nystagmus. When the disease is situated in the posterior
half of the pons the rotation is directed towards the paralysed
side (Pre'vost, Grasset). The rotation may completely disappear
when the patient falls asleep.

3. Permanent Symptoms. — The permanent symptoms caused
by cerebral haemorrhage consist of paralysis of voluntary motion,
generally limited to one side of the body (hemiplegia) ; various
tonic or clonic spasmodic affections, also generally limited to one
side of the body (hemispasm) ; and unilateral sensory disturb-
ances, including affections of the special senses (hemianaesthesia).
As these affections are not, however, peculiar to haemorrhage,
we reserve consideration of them for the present.

§ 721. Disturbances of the Mental Functions. — The majority
of those who have been attacked with cerebral haemorrhage do
not regain their full mental vigour. Memory usually fails, more
especially for* recent events. In the daily affairs of life the
judgment of the patients may not appear to have suffered, but
they are unequal to any unusual intellectual effort; and at
times the intellect may progressively decline, reducing the
patient to a state of childishness or pronounced dementia. At
other times they become peevish, whimsical, irritable, or
give way to outbursts of passion. The mental affections con-
nected with disturbance of speech (aphasia) will be hereafter
considered.

Trophic and Vaso-motor Disturbances. — Immediately after
an attack the paralysed limbs of a hemiplegic patient are
frequently redder and warmer than the corresponding healthy
limbs. The difference in temperature may vary from a fraction
of a degree to as much as two degrees. These symptoms are
no doubt due to paralysis of the sympathetic. About twenty-
four hours after the beginning of an attack the paralysed limbs
may become swelled owing to a certain amount of subcutaneous
oedema. The temperature of the paralysed limbs gradually

534

FOCAL DISEASES, ACCOEDING TO

decreases, and is eventually lower than that of the sound side.
When no cedema exists the skin may be dry and scaly.

Acute Bed-sore. — This is an acute process of sloughing, which occasionally
occurs over the centre of the gluteal region on the paralysed side, after
cerebral haemorrhage or softening. The affection has already been
sufficiently described (§ 114).

Congestions and Haemorrhages. — Congestions and actual ha2morrhages
into the substance of the lungs, extravasations in or beneath the pleura,
endocardium, and the mucous membrane of the stomach, as well as
into the substance of the supra-renal capsules and kidneys, frequently
accompany cerebral haemorrhage. Schiff and Brown-Se'quard produced
experimentally hyperaemia, or haemorrhage of the pleura and lungs, by
certain lesions of the pons, middle cerebellar peduncles, and the optic
thalami and corpora striata. These hypersemic conditions and haemorrhages,
whether in the lower animals or in man, are sometimes confined to the
paralysed side of the body. The diminution of the contractile power
of the walls of the arterioles on the paralysed side often gives rise to a
perceptible difference between the radial pulses of the two sides.

Inflammation of the Joints. — Some of the joints of the paralysed side
of the body may become the subjects of a subacute inflammation, which
usually begins from the third to the sixth week after the hemiplegia,
although sometimes the joints inflame at a still later period after the
beginning of the attack, and occasionally the affection shows itself as
early as the fifteenth day. There are the two varieties of this articular
inflammation, the one acute and the other chronic. In the first variety
the joint becomes red, hot, swollen, and, after death, acute synovitis, fre-
quently with considerable exudation, is discovered. This form almost
exclusively attacks the larger joints. A chronic joint affection has been
described by Hitzig which seems to be peculiar to the shoulder. The
joint is almost immovable, painful on pressure, and, owing to paralysis of
the muscles, the humerus semi-dislocated.

Changes in Nerve Trunks. — Cornil has shown that in a certain number
of cases there is a sub-inflammatory hypertrophy of the nerves or of their
sheaths, and in such cases there is pain on pressure of the paralysed
limb, especially marked along the course of the principal nerve-trunks.
At other times the whole paralysed side may be generally tender, without
any special limitation of the tenderness to the joints and large nerves.

Muscular Atrophy. — In some rare cases an early and rapid wasting
takes place in the muscles of one or both limbs a few weeks after the
onset of the paralysis, but in these cases there is reason to believe that
the fibres of the pyramidal tract have undergone secondary degeneration,
and that the motor cells of the anterior horns of the cord have become
implicated in the process.

Arrest or Retardation of Growth in Paralysed Limbs. — When hemi-
plegia occurs in childhood, the arm and leg, or the arm only, on the para-

THE NATURE OF THE LESION.

535

lysed side grow more slowly than on the sound side, so that as growth
advances the limbs of the paralysed remain permanently smaller than
those of the opposite side. The arm is more frequently affected than the
leg, and there is always a certain amount of muscular rigidity of the
affected extremity.

Skill, Hair, and Nails. — The skin of the paralysed side sometimes
undergoes trophic changes, which involve the cutis and subcutaneous
tissue, so that a fold pinched up by the fingers feels thicker than normal.
The hair grows better on the affected side, and the nails become yellowish,
marked with ridges, brittle, and curved.

§ 722. Morbid Anatomy. — Morbid anatomists usually divide
cerebral haemorrhage into two varieties, named respectively
punctiform and massive haemorrhages.

Punctiform haemorrhages occur in the form of a number
of minute points of the size of a pin's head, or even smaller.
They result from rupture of capillary vessels, and are invariably
multiple. Capillary haemorrhages are observed in the tissues
surrounding massive haemorrhages, or in parts which are the
seat of softening, and they are met with in considerable numbers
in the cortex of the brain in consequence of thrombosis of the
venous sinuses. At other times extravasations of blood are
found in the lymph sheaths of the vessels, and they must then
be regarded as minor degrees of the massive haemorrhages.

Massive haemorrhages may be of various sizes, being
sometimes as small as a pea, at other times large enough
to destroy almost an entire hemisphere. The hemorrhage
may either separate the nerve fibres of the white substance or
rupture them, the latter event being by far the more frequent.
When the nerve fibres are pushed aside by the haemorrhage
without rupture the form assumed by the clot will be deter-
mined by the direction of the fibres, but when the fibres are
ruptured the clot is round or oval. In the cortex the form
assumed by the haemorrhage is largely determined by the dis-
position of the convolutions and membranes, so the effusion
usually spreads out laterally and assumes an irregular form.
Massive haemorrhages are, as a rule, single, although several
foci may occasionally be observed, and it is not unusual to find
traces of many extravasations of various ages in the same brain.

Haemorrhagic foci may occupy any part of the brain, but

536

FOCAL DISEASES, ACCORDING TO

they are much more frequent in certain parts. The favourite
seats are the caudate and lenticular nuclei, and the optic
thalami.

Recent Focus. — In the recent condition the apoplectic focus
forms a dark red. clot, which is soft and uniform in character
throughout. It is frequently mixed with the de'bris of the
substance of the brain. The internal surface of the cavity is
irregular and consists of torn shreds of cerebral tissue. This is
surrounded by a zone of variable thickness, averaging a few
lines in depth and gradually merging into the healthy tissues,
composed of softened tissue saturated with blood serum, and
frequently the seat of punctiform hgemorrhages. If the nerve
fibres have been simply separated from one another without
rupture, then the detritus of cerebral tissue in the internal
surface of the walls of the cavity is absent, and the softening
and punctiform hgeniorrhages of the surrounding tissues are
much less marked. If the clot be floated out under water, it is
sometimes possible to detect the miliary aneurism from which
the primary extravasation took place.

Period of Absorption and Repair. — If the hemorrhage
does not end fatally after a few hours structural changes take
place, both in the clot and surrounding tissues, which lead
to the absorption of the former and to a certain amount
of repair in the latter. The blood-clot after coagulation
parts with its serum, and the injured tissues surrounding the
clot become softened, partly by imbibition of serum, but
chiefly owing to a retrograde fatty metamorphosis of the
torn fragments of brain tissue. The softened tissues become
mixed with the clot so as to form a dark, chocolate-coloured
mass, of the consistence of gruel, the more fluid constituents
of which are soon absorbed. The h 33 matin e is dissolved, and
soaks into the tissue round the clot to a considerable distance,
until it is absorbed. As a result of this process the pulpy material
filling the cavity passes from its first dark red to a brighter red,
and finally to a saffron colour. A reparative process now begins,
by means of which the hemorrhagic focus is converted into a
cyst. The first step in the reparative process is the formation of
a fibrinous capsule round the entire periphery of the clot. It is
at first a line or more in thickness, soft as jelly, and of a trans-

THE NATURE OF THE LESION.

537

lucent yellowish tint. At a later period this capsule becomes
converted into a much thinner but stronger layer of fibrillar
connective tissue, which permanently shuts off the apoplectic
deposit from the surrounding substance of the brain. The
fluid contained in the cyst is at first turbid, but after a time
becomes transparent and limpid. These cysts, however, contain
not fluid merely but also a loose spongy connective tissue, which
is suspended in the fluid like a film. But the reparative pro-
cess does not always end here ; the whole of the fluid may
become gradually absorbed, and the opposite walls of the
cavity may ultimately come into contact, and adhere to one
another by a connective tissue, which usually contains a consider-
able amount of pigment. This constitutes the haemorrhagic or
apoplectic cicatrix, which consists merely of a thin strip of con-
nective tissue. Superficial foci in the cortex pass through similar
phases, and after cicatrisation they appear as yellow indurated
spots which have been taken for vestiges of encephalitis.

Duration of the Reparative Process. — The clot is soft and
homogeneous during the first three or four days. At this time
the process of softening and separation of the internal surface
of the cavity, and the absorption of the fluid contents, reach
their maximum activity at the eleventh or twelfth day. The
reparative process which leads to the formation of the capsule
begins usually from the seventh to the ninth, the cyst is com-
plete about the twentieth, and the lining membrane is organised
from the thirtieth to the fortieth day.

Circumstances which prevent the Reparative Process. —
Various circumstances delay or entirely prevent the reparative
process. The principal of these are, a too extensive sero-san-
guineous infiltration of the surrounding tissues followed by a
co-extensive area of softening, an excess of the irritative pro-
cess necessary to repair, which gives rise to secondary encepha-
litis, a fresh haemorrhage and dropsy of the cyst, leading to
distention and consequent pressure on the surrounding tissues.
Repair of injury to the brain from haemorrhage may be pre-
vented, like repair of injuries of every part of the body, by
the general state of the health in various conditions of debility.

§ 723. Prognosis. — The prognosis in any given case depends

538

FOCAL DISEASES, ACCORDING TO

upon the opinion formed of the extent and situation of
the lesion taken in conjunction with the age and previous
state of health of the patient. Death not unfrequently takes
place during the apoplectic condition. If the patient cannot be
roused at all, if there be no signs of reflex activity when the
conjunctiva is touched, while there is involuntary passage of
faeces and urine, and well-marked stertor, the patient may die
rapidly within a few hours, or even a few minutes ; and the
persistence of a slighter degree of these symptoms without
abatement is a sign of great gravity. Laboured respiration and
quickness with marked irregularity of the pulse, are also un-
favourable signs. A marked and persistent depression of the tem-
perature is regarded by Charcot as an almost certainly fatal sign.
If the patient has recovered from the apoplectic condition, then
the prognosis will greatly depend upon the age and general
condition. Granular disease of the kidneys, a general state
of malnutrition, or evidences of senile degeneration of the
arterial system, will render the ultimate prognosis grave
in cases where the extent and situation of the haemorrhage
itself would cause no danger to life. A sudden rise of tempera-
ture in cases of cerebral haemorrhage is a very grave indication,
unless some inflammatory complication be present to account
for it. A sudden depression of temperature, with increase or
renewal of a pre-existing comatose condition, indicating as it
does the occurrence of a fresh haemorrhage, is also of serious
import.

Acute sloughing of the buttock on the paralysed side, com-
mencing within a few days after the onset of the apoplectic
attack is, according to M. Charcot, of fatal significance. Decided
difficulty of deglutition and articulation is also a serious
symptom, being indicative of marked interference with the
functional activity of the medulla and pons. When the patient
has outlived the apoplectic attack, the period of reactive inflam-
mation brings new dangers, when death may result.

When the inflammatory period is passed there is compara-
tively little reason to expect a fatal result from the brain lesion
itself or from its more immediate complications. In middle-
aged and old people, however, there is a constant danger of a
recurrence of the haemorrhage. The dangers of the apoplectic

THE NATURE OF THE LESION.

539

attack having been surmounted, the point which has to be
determined is the degree of improvement likely to take place
in the patient's mental faculties, in his power of articulation
and speaking, and as regards the probability of restoration of
motor power to his paralysed limbs.

In the majority of instances when the first loss of conscious-
ness has passed away, the patient is left free from any very
decided meutal defect, except a certain amount of mental weak-
ness and a tendency to emotional displays. In rare cases the
hemiplegic attack is followed by a chronic maniacal condition,
which may pass into a state of complete dementia. This
condition is apt to follow limited cortical haemorrhage of the
occipital lobes, especially in elderly people, but the haemorrhage
may itself be only an effect of previously-existing degenerative
changes.

Large lesions occurring in infancy or at the time of birth,
either in the substance or on the surface of the brain, often
induce a semi -idiotic condition.

§ 724. Treatment. — The aims of treatment are (1) to avert a
threatened attack; (2) to treat the apoplectic condition; (3) to
allay excitement during the stage of inflammatory reaction ; and
(4) to restore power to the paralysed limbs, and to improve the
other morbid conditions which accompany the hemiplegic state.

(1) Prophylaxis. — In devising measures to prevent a threa-
tened attack, each case must be made the subject of special
study; and much depends for the success of these on the age,
general state of health, and hereditary tendencies of the patient.
Bodily and mental rest are absolutely necessary. The patient
ought to be kept cool, with his head and shoulders well raised.
If the patient be beyond middle age, with signs of arterial
degeneration and a weak intermittent action of the heart,
stimulants, cardiac tonics, and the frequent administration of
easily-assimilated fluid nutriment is necessary. In the presence
of a moderate amount of granular disease of the kidneys with
cardiac hypertrophy and high arterial tension, saline purgatives
are indicated.

(2) Within the last few years our treatment of the apoplectic
condition has undergone a great change. Bleeding was regarded

540

FOCAL DISEASES, ACCORDING TO

as the great remedy for the apoplectic condition from the time
of Hippocrates down to within a few years ago, when the
teachings of Todd and Trousseau produced a reaction in the
opposite direction. When, however, hemorrhage takes place
in a case associated with high arterial tension, a small bleeding
may, by lowering the blood pressure and thus diminishing the
intracranial pressure, avert for a time threatening s}?mptoms.
If the heart be feeble, with compressible pulse, then bleeding
is entirely inadmissible.

If there be much heat of the head, with violent throbbing
of vessels, pounded ice in a bladder or india-rubber bag, or
evaporating lotions should be applied while the head and
shoulders are raised, and everything about the neck loosened.
In the present day it is superfluous to condemn the barbarous
practice of applying mustard plasters to the calves of the legs.

A stimulating treatment is required when the heart's action
is feeble and the respiratory centre is threatened. In such a
case the patient's face is cold and clammy, the pulse feeble,
and the respiration hesitating and intermittent, or it may be
assuming the Cheyne-Stokes character.

If the disease be characterised by recurring epileptiform
attacks, bromide of potassium may be administered, and if there
be a restless condition, with more or less of delirious wandering,
the same drug or bromide of camphor may .be useful. If the
bowels be constipated, an enema containing castor oil or castor
oil and turpentine may be administered, or two drops of croton
oil may be given. The state of the bladder must also be
attended to, and a catheter used if necessary. In many cases no
drugs are required during the apoplectic stage, and purgatives
should not be resorted to on all occasions as a routine treatment
irrespective of the nature of the case.

(3) If the patient survive the first shock of the apoplectic
attack the less we interfere during the first few days the
better. He must be kept as quiet as possible both in body
and mind, and his diet and secretions must be carefully
regulated. When the reactive febrile symptoms appear cold
should be applied to the head, but the old practice of bleeding
at this stage is to be strongly condemned. If headache be pre-
sent along with persistent wakefulness or delirium, it may be

THE NATURE OF THE LESION.

541

necessary to administer a full dose of bromide of potassium or
even an opiate or chloral. During this time great care must be
taken to prevent bed-sores on the paralysed side, by paying
constant attention to the state of the bedding and securing ex-
treme cleanliness. In severe cases the patient should be placed
on a water bed from the first where this is possible.

(4) The most efficient means of promoting the improvement
of the condition of the paralysed nerves and muscles is a
thorough attention to the general health of the patient. The
treatment which it will be necessary to adopt will depend on
the age, habits, and constitution of the patient, and on the pre-
sence or absence of any special concomitant disease. The
general principles of treatment, however, are to take care that
the patient has easily-digestible and nutritious food ; that all
circumstances which might cause mental excitement are avoided;
and that the patient has a due amount of repose and sleep. In
the hemiplegias of elderly people, which are usually associated
with miliary aneurisms, great care must be taken that the cir-
culation is not subjected to any sudden strain, and with this
object it is necessary to take care that the bowels do not become
constipated, lest the straining at stool should induce another
attack. Iodide of potassium is often beneficial. The patient
should also take open-air exercise in a chair or carriage when-
ever the weather is suitable; and much good may be done
at a later period of the disease by sponging with salt water,
either tepid or cold, or even by shower baths. When there is
advanced degeneration of the arteries or high arterial tension,
great caution is necessary in the use of cold sponging and
shower baths, since the sudden impression on the cutaneous
surface will be followed by contraction of the arterioles dis-
tributed to the surface of the body, and this will be followed
by sudden increase of the arterial tension, and consequent risk
of the rupture of another vessel. It may indeed be laid down
as a rule that hemiplegic patients should only use baths of
moderate temperature.

These general measures should after a time be followed
by local treatment of the paralysed limbs. The first local
measures to be resorted to are passive movements of the
paralysed limbs, and friction of the skin by means of a

542

FOCAL DISEASES, ACCORDING TO

flesh brush, flannel, or the palm of the hand. When a
paralysed limb is painful, gentle rubbing is very soothing and
grateful to the patient. The patient may be directed to make
voluntary efforts to move the limbs. Electricity is one of the
most valuable agents we possess in the treatment of paralysed
limbs. Both the faradic and galvanic currents have been
employed, but the latter appears to be the more generally
useful. The constant current has been employed in three
different ways. According to one method the current is passed
through the brain, in a second it is passed through the cervical
sympathetic, while in a third it is directly applied to the
paralysed limbs.

The practical rules which must be observed in carrying out
the treatment are the following : —

(a) This method of treatment should not be adopted in the early stage
of hemiplegia, as injury may be done by over-stimulation of the brain.

(&) The duration of each application through the brain ought to be
short, not exceeding three minutes.

(c) The current should be weak, more especially in the case of elderly
people — such, for instance, as that derived from five to ten or at most
fifteen Leclanche's cells.

(d) The electrodes are to be placed on the mastoid processes, or one
on the mastoid process and the other on the back of the neck.

(e) The electrodes should be placed in position when the index is at
zero, and the current is then gradually increased and, after two or three
minutes' application, gradually diminished before the electrodes are re-
moved. Sudden interruptions and*rapid reversals of the current ought to
be avoided.

In the second method the current is -passed through the cervical
sympathetic. In this method the electrodes are placed over the course of
the sympathetic in the neck, and it appears to be indifferent whether the
anode is above and the cathode below or the reverse. The currents em-
ployed may be stronger than when the brain was directly acted upon.
From fifteen to twenty-five Leclanch6's cells may be used.

In the third method the electrodes are used along the course of the
nerves, the negative pole being placed near the plexus to which the affected
nerve belongs, or over the corresponding part of the vertebral column, and
the positive pole over the trunks of the nerves. Some, however, recom-
mend descending instead of ascending currents, but it does not appear to be
of much consequence which is used. The current from thirty Leclanche:s
cells may be used for about eight minutes, and in order to increase its
stimulating action the intensity may be alternately increased and clinii-
nished, while the circuit is kept closed. Interruptions and reversal of the

THE NATURE OF THE LESION.

543

current should only be used for the purposes of diagnosis. This mode of
applying galvanism to the paralysed limbs does good in cases of clonic
spasm after hemiplegia, and in some cases of " late rigidity ;" but when
the contracture has become permanent, so that it does not intermit
during sleep, it is hopeless to expect any benefit from treatment.

Faradic currents have been employed in contractures for the
purpose of acting, not on the contracted muscles, but upon their
antagonists, but it does not appear that much benefit has ever
resulted from this treatment. The disturbances of sensibility
on the paralysed side do not usually require any special treat-
ment, since the measures which are directed to mitigate the
motor paralysis exercise a favourable influence on any existing
sensory impairment. If there be hemianaesthesia, metallo-thera-
peutics, as employed by Charcot, which will be described in the
section on hysterical hemiansesthesia, may be adopted, but our
knowledge of this subject is too recent and too imperfect to
enable us to form a definite opinion of its merits.

(b) Meningeal Hcemorrhage.

Definition. — By meningeal haemorrhage is here meant an
extravasation of blood between the membranes or on the surface
of the brain.

§ 725. Etiology. — The most frequent causes of meningeal
apoplexy are injuries of the skull, by means of which the main
meningeal arteries, the sinuses, or the vessels of the pia mater
are ruptured, but this subject belongs to surgery.

Aneurisms of the arteries at the base of the skull may by
rupture give rise to meningeal haemorrhage. In a case which
came under my observation, a large meningeal haemorrhage
was caused by rupture of an aneurism, about the size of a
pea on the left Sylvian artery, about an inch from its origin.
Another aneurism unruptured, symmetrical with it in size and
position, was found on the right Sylvian artery. Next
to the middle cerebral, the basilar artery is most frequently
affected with aneurism. Haemorrhage may also take place from
the veins, and large meningeal haemorrhage may result from
thrombosis of the sinuses, especially the superior longitudinal
sinus. Blood may make its way from the substance of the brain
into the meninges through rupture of the cortex. Meningeal

544

FOCAL DISEASES, ACCORDING TO

haemorrhage may result in the course of infectious diseases, and
chronic dyscrasiae, and frequently occurs in the course of the
chronic degeneration of the cortex of the brain, which underlies
progressive paralysis of the insane.

The meningeal apoplexy of new-born children is caused by
certain accidents attending childbirth.

§ 726. Symptoms. — It will suffice if we point out here the
differences which exist between the symptoms of cerebral and
meningeal haemorrhages. The clinical history of meningeal
haemorrhages of traumatic origin is usually complicated with
other cerebral symptoms directly resulting from the injury,
such as concussion, and the same may be said with regard to
the cases where an intracerebral haemorrhage has made its
way to the surface of the brain, as well as with regard to the
haemorrhage which accompanies general paralysis. Haemorrhage
caused by rupture of an aneurism forms, the least complicated
class of cases.

In severe cases the patient becomes suddenly apoplectic
without any warning, or with only slight premonitory symptoms,
such as headache, dizziness, and vomiting. The paralysis is
commonly general, affecting all four extremities uniformly, and
only in rare cases is hemiplegia met with. Epileptiform convul-
sions are also frequent in meningeal haemorrhage, and vomiting
is another sign often observed. These cases are accompanied
by profound coma, and death results in a few hours, or at most
a few days.

In less severe cases the patient may partially recover after a
few hours from the apoplectic state, and then may complain of
headache, be delirious or somnolent, until he becomes finally
comatose.

In other cases the patients do not become immediately apop-
lectic, but complain of headache, dizziness, weakness or numb-
ness of the extremities, on one or on both sides; there is also
more or less stupor, but the fatal coma may not supervene for
a long time. In these cases the haemorrhage appears to be
small at first and gradually to increase.

If an aneurism of considerable size have existed for some
time before the occurrence of haemorrhage, the apoplectic

THE NATURE OF THE LESION.

545

attack may be preceded by some of the symptoms which in-
dicate the existence of a cerebral tumour. The more usual of
these symptoms are headache, double optic neuritis, paralysis of
the facial nerve in aneurism of the internal carotid, of the third
nerve in aneurism of the posterior communicating artery, and
vomiting, epileptiform convulsions, and disorders of deglutition,
speech, and respiration in aneurism of the basilar artery.

In the meningeal haemorrhages of the new-born, the children
are either born dead or in a condition of asphyxia, and die soon
afterwards. If respiration be established the infant remains
weak, somnolent, or comatose, and dies after a few days from
convulsions. Sometimes the children are weak and somnolent
at birth, and remain in this condition from one to three weeks,
when vomiting, dyspnoea, convulsions, and coma supervene and
soon prove fatal.

§ 727. Morbid Anatomy. — The blood may make its way
into the arachnoid space in consequence of injury to the dura
mater, or from the vessels of the pia mater, or from the cerebral
vessels and subsequent rupture of the pia mater. When the
extravasation is large the haemorrhage spreads extensively
through the arachnoid space, so that an entire hemisphere,
or exceptionally the surfaces of both hemispheres, may be
covered with a thick layer of blood. When a large collection
of blood has formed at the base and around the pons varolii, it
may make its way into the ventricles through the great trans-
verse fissure, and pass down through the aqueduct of Sylvius to
the fourth ventricle. The quantity of the effused blood may
vary from a few drops to half a litre or more. The pigmented
spots sometimes found on the meninges and surface of the
brain seems to indicate that small meningeal haemorrhages may
be absorbed, but large haemorrhages invariably prove fatal.

The appearances presented by the brain vary greatly, accord-
ing to the amount and seat of the haemorrhage and the time at
which death takes place. Haemorrhage from the dura mater, if
large, compresses without rupturing the brain. In such a case
the gyri are found flattened and the substance of the brain pale.
Haemorrhage from rupture of the vessels of the pia mater
or of the brain itself, and especially rupture of an aneurism
J J

546

FOCAL DISEASES.

of the larger sized arteries at the base of the brain, may cause
considerable destruction of cerebral tissue.

§ 728. The prognosis is more unfavourable in meningeal
than intra-cerebral haemorrhage, inasmuch as it is apt to be
more copious, but the treatment of the two affections is similar.
Trephining may possibly be of use in some cases of meningeal
hsemorrhage.

547

CHAPTER V.

(I.) GENERAL CONSIDERATION OF FOCAL DISEASES,
ACCORDING TO THE NATURE OF THE LESION
(Continued).

3. INTRACRANIAL TUMOURS.

§ 729. Definition. — Intracranial tumours consist of circum-
scribed pathological growths situated within the cavity of the
skull.

§ 730. Etiology. — Tumours of the brain arise from similar
causes to those which give origin to tumours in other localities.
For the sake of convenience, cerebral tumours may be divided
into (a) New formations ; (b) Vascular tumours ; (c) Parasites.
Hereditary predisposition plays an important part in the pro-
duction of new formations. Cancerous and tubercular tumours
and syphilitic gummata depend upon a general constitutional
taint, and it is also probable that glioma, sarcoma, and other
tumours are more liable to arise in some families than in others.
Cancer is one of the most common tumours of the brain, and
is generally primary. When secondary it often follows cancer
of the orbit. It is a disease of adult and advanced age, the
largest number of cases being found between the ages of thirty
and sixty years. Tubercle on the other hand is rarely primary,
but is generally associated with tubercle of the lungs or cheesy
glands; it is essentially a disease of youth, being most common
between the ages of three and thirty years. It is probably
the most frequent of all cerebral tumours. Syphilitic gummata
may be met with at every period of life.

Cerebral tumours are more frequent in men than in women.
Out of 329 cases of cerebral tumours of all cases collected by

548

FOCAL DISEASES, ACCORDING TO

Ladame 208 were male, 95 female, and in 26 the sex was not
stated, so that, according to this computation, the proportion
is rather more than two to one. Injuries of the skull act as
exciting causes in the production of cerebral tumours. Several
cases have come under my own observation in which the disease
dated from a blow on the head, and the tumour in these cases
frequently grew at a place corresponding to the seat of injury.

Vascular tumours consist of aneurisms of the cerebral
arteries and erectile tumours. Aneurisms are observed at all
ages, but they are more common between the ages of forty and
sixty years, when the vessels begin to undergo atheromatous
degeneration ; the causes of erectile tumours are unknown.

The parasites met with in the brain are the cysticercus and
echinococcus.

§ 731. Symptoms. — Headache is one of the earliest and most
striking of the initial symptoms of intracranial tumours.
Ladame found this symptom in two-thirds of the cases collected
by him. Headache is more violent in intracranial tumour than
in any other disease except meningitis and the uraemia of
chronic Bright's disease ; it consists of an acute lancinating or
severe boring pain, which may continue many weeks without
intermission, and is aggravated by impressions of light, noises,
and all movements of the head. The pain sometimes occupies
the occipital and at other times the frontal or temporal regions;
but its seat has no necessary relation to the situation of the
tumour, although constant occipital pain is often associated
with cerebellar tumour. Neuralgic headache from irritation of
the fifth may be associated with the more profound headache
of general pressure. Tenderness on percussing the skull may
sometimes be observed at a point corresponding to the situation
of the tumour (Ferrier).

Dizziness is a frequent initial symptom, and it may be
present with or without cephalalgia. Paroxysms of head-
ache and dizziness may be the only symptoms present for
months, and the patient may feel well in other respects.
Dizziness is probably caused by alterations in the circulation
of the brain induced by the growth of the tumour; but the
insecurity on assuming the erect posture, which is one of the

THE NATURE OF THE LESION.

549

main elements of vertigo, is frequently caused by pressure on
the labyrinthine fibres of the auditory nerve.

Sensory disturbances are generally ushered in by hyper-
esthesia or some other irritative phenomena, which are after a
time followed by anaesthesia. Wandering pains, formication,
tinodinof, and numbness alternate with one another before there
is a distinct diminution of sensation, and these symptoms do
not entirely cease until complete anaesthesia is established.
La dame found cutaneous anaesthesia in one-seventh of his
cases.

Neuralgia of the trifacial nerve arises from a variety of
causes, but when all the three divisions of the nerve are simul-
taneously affected the presence of intracranial tumour is to be
suspected. The pain occurs in paroxysms, and is usually asso-
ciated with numbness, formication, itching, and the feeling of
the part being swollen. When sensation is diminished on the
painful side the pressure of a tumour on the nerve may be
suspected, and the diagnosis is rendered more certain if dis-
turbances of other cranial nerves are present.

Motor disturbances are generally ushered in by phenomena
of irritation, to be followed by paralysis. The irritative
symptoms are cramps of various parts or tremor of one of the
extremities or of half the body. The cramps may vary from
slight spasmodic twitches of the muscles of the face or of other
special groups of muscles, to persistent tonic, clonic, or choreiform
muscular spasms in the extremities ; or there may be epilepti-
form convulsions, accompanied by unconsciousness. After a
longer or shorter duration the irritative motor symptoms give
place to paralysis, which creeps on gradually, and does not
become complete for a comparatively long period. Hemiplegia
is the more frequent form of paralysis, being present in a third
of Ladame's cases. Permanent contractions of the paralysed
extremities occur when the pyramidal tract is pressed upon or
otherwise injured, but the spastic condition of the limbs is
seldom so pronounced in intracranial tumours as in other focal
diseases of the brain. The paralysed muscles atrophy apparently
simply from disuse, and retain for a long time their electric
excitability.

Affections of the Special Senses. — With respect to the affec-

550

FOCAL DISEASES, ACCORDING TO

tions of the special senses, those of sight are by far the most
important. Calmeil found amblyopia in two-fifths of his cases,
and Ladame found amaurosis in one-fifth. The optic disc may
present the appearance known as " choked disc " (Stauungs-
papilla), or there may be neuritis (§ 207). The former is
by far the most important sign of cerebral tumour, as it is
generally present whenever there is increased intracranial
pressure ; and although this condition is said occasionally
to accompany fluid effusion, yet the usual cause is a solid
growth.

It is of the utmost importance for regional diagnosis to
examine carefully for contractions of the field of vision, and for
the different varieties of hemiopia. Diplopia is also a frequent
symptom of tumours at the base of the brain, caused by an
affection at the origin or pressure in the course of the third,
fourth, or sixth cranial nerves.

The pupils vary; they may occasionally be contracted or
unequal, but when by the growth of the tumour the intracranial
pressure becomes great, they are always dilated and react feebly
to light.

The sense of hearing is also frequently affected. Calmeil
found some disturbances of hearing in one-ninth of his cases ;
Ladame says that the sense of hearing is affected only one
half as often as the sense of vision. The auditory disturbances
usually consist of dulness of hearing and rushing noises, but
complete deafness is sometimes observed.

The injection experiments of E. Weber have shown that
there is a communication between the arachnoid cavity and the
labyrinth by means of the aqueduct of the cochlea, and con-
sequently increased intracranial pressure may produce an
affection of the auditory apparatus similar to that which occurs
in the eyes under the same circumstances. Alterations of
hearing may likewise be caused by pressure on the trunk of
the auditory nerve or on its nuclei of origin in the medulla and
pons. Pressure on the labyrinthine fibres of the auditory nerve
may occasion vertigo and disorders of motor co-ordination similar
to those observed in Meniere's disease.

The sense of smell is relatively seldom affected in cases of
tumour of the brain. The number mentioned in literature, how-

THE NATURE OF THE LESION.

551

ever, is not a true criterion of the real number affected, since the
patient is very apt not to mention the loss of smell unless it
be entirely lost, and the physician is apt not to make any
special investigation of it. Ladame found the sense of smell
distinctly diminished or entirely lost in ten only of his collected
cases, and never present as the only symptom.

The sense of taste is likewise only rarely affected. In
Ladame's collected cases mention is made of alterations of this
function only seven times, once the affection was unilateral,
and the sense was only rarely completely lost. There are good
grounds, however, for believing that if taste were carefully
tested in all cases of cerebral tumours, alterations would be
more frequently found.

The organic functions always become more or less injured
in intracranial tumour. The intense cephalalgia alone prevents
the patient from sleeping, and the continual wakefulness reacts
on the general health.

Vomiting is frequently associated with paroxysms of head-
ache and vertigo, but it may occur independently of these.
It is often extremely obstinate and may continue for hours, and
when it recurs frequently the general nutrition suffers greatly.
Constipation is usually present, but in some cases it may alter-
nate with diarrhoea. Irregularity of the heart's action and
slowness of the pulse have been frequently observed, probably
from irritation of the vagus. Towards the end, however, the
pulse becomes very frequent.

The respiratory function is not often disturbed, but the
rhythm may be quickened by irritation, and rendered slower by
pressure, of the brain. Vierordt and Hegelmaier, by recording
the movements of the superior abdominal region of rabbits on
the drum of the kymograph, found that a moderate artificial
pressure on the brain diminished the respirations by one-half,
while they were increased in number by a stronger pressure.
With moderate pressure the inspirations were fewer and the
expirations longer.

Polyphagia is an occasional symptom of cerebral tumour,
but it does not prevent the progressive emaciation. Rosenthal
mentions a case where the polyphagia was accompanied with
diabetes mellitus.

552

FOCAL DISEASES, ACCORDING TO

Polyuria and saccharine urine, either separately or com-
bined, are frequently met with. In these cases it is almost
certain that there must be irritation of the floor of the fourth
ventricle, but the irritation need not be direct. Rosenthal relates
the history of a case where diabetes was caused by tumour of
the pituitary body, and I have seen a case where polyuria was
occasioned by a tumour situated at the base of the skull over
the right cavernous sinus.

Fever is not a usual symptom, but it is sometimes present
during an attack of cerebritis, these complications being most
frequently observed in the incipient stage of tubercular tumour.

The nutritive disturbances do not maintain a due pro-
portion to the gravity of the cerebral phenomena, nor does
the nature of the tumour appear to exert a marked influence
on the general health. Cases have been observed in which
cancer of the brain had existed for some months without pro-
ducing a perceptible influence on the nutrition of the body,
and those suffering from sarcoma may even manifest a tendency
to obesity. As a rule, however, the subjects of tubercle and
cancer sooner or later exhibit traces of cachexia. Tumour of
the brain may act injuriously on nutrition in several ways. A
state of great marasmus is sometimes induced by frequently
recurring vomiting, while at other times the vital powers of the
patient become exhausted by incessant headache and sleep-
lessness.

Psychical disturbances are frequently observed in cerebral
tumour, but the statements of authors differ considerably with
respect to the relative frequency of the symptom. Andral and
Durand-Fardel assert that mental disturbances occur very seldom,
while Calmeil observed psychical disorders in one-half, Friedreich
in 43 per cent, Lebert in one-third, and Ladame in rather more
than a third of their cases. Symptoms of mental irritation fre-
quently precede those of depression. The irritative symptoms
consist of mental excitement and those emotional disturbances
which are usually known as hysterical, ideas of grandeur, with
consequent extravagance, halluciuations, delusions, and out-
bursts of passion which may amount to maniacal fury. The
symptoms of depression consist of drowsiness, apathy, loss of
speech, and imbecility. The affections of speech which occur

THE NATURE OF THE LESION.

553

in cerebral tumour are variable in character. Ladame found
affections of speech in 45 of his collected cases.

Terminal Phenomena. — As the tumour grows in size the
brain becomes compressed to such an extent that its functions
become gradually abolished, and the terminal phenomena of
the affection are ushered in. These consist of extreme emacia-
tion, widely spread anaesthesia, blindness and diminution or loss
of one or more of the other special senses, motor paralysis
often implicating all the extremities, imbecility and. deep and
enduring coma.

§ 732. Morbid Anatomy. — The morbid growths which con-
stitute intracranial tumours are very variable, and, regarded
from the standpoint of pathological anatomy, have little or no
affinity with each other, but are conveniently grouped together
for practical purposes on account of their clinical affinities.
The brain is surrounded by unyielding osseous walls, and the
development of any foreign body within the cranium encroaches
upon the space occupied by it, and consequently tlrere is a
close similarity in the symptoms caused by intracranial tumours
however different in nature.

(a) Varieties of Intracranial Neiv Formations.

(1) Glioma. — The gliomata form tumours which vary in size from a
cherry-stone to that of the closed fist ; they are vascular, of a white or
greyish-red colour, and are never distinctly circumscribed from the tissues
of the brain, the grey matter of which they much resemble in consistence
and colour. The hemispheres of the brain are the favourite seats of
gliomata, although they may appear in any part of the brain or spinal
cord. Gliomata are composed of a matrix, which varies in consistence,
and an abundant admixture of cells and nuclei. The cells vary in shape
and size ; they are sometimes round or oval, with granular contents and
one or two nuclei ; at other times spindle-shaped or stellate, and provided
with fine processes, which are continuous with those of adjoining cells.
There are two principal varieties of gliomata, the hard and the soft. In
the hard gliomata the cells are scanty, and usually contain several nuclei.
The matrix is formed of fine fibrilla), which are more or less parallel to one
another, and can sometimes be isolated into long threads. In the hardest
forms the matrix is no longer formed of long, separable fibrilla?, but of a
finely reticular substance, which can only be separated into short stiff'
fibres. At times part only of the tumour is hard, and it then contains
one or more hard kernels, which may equal in density fibro-cartilaginous

554,

FOCAL DISEASES, ACCORDING TO

tumours. True cartilaginous structure has, however, never been found
in these tumours. The hard gliomata are allied in general characters to
the fibromata, and intermediate forms are met with which are termed
fibro-cjliomata. .

In the fibro-cjliomata the matrix consists of fibres forming thick bundles,
or exhibiting a stratiform arrangement enclosing here and there nucleated
cells.

The soft gliomata contain more cells than the hard ; the cells vary con-
siderably in size and form, but are generally small and deficient in plasma.
The matrix consists of a fibrillary network, in the interstices of which the
cells are imbedded.

Transitional forms between the soft gliomata and other tumours are
met with. "When , the number and size of the cells are increased, the
tumours are allied to the sarcomata, and are therefore called glio-sareomata ;
and when the matrix assumes a mucoid character, the tumour resembles
the myxomata. The gliomata are sometimes richly supplied with rela-
tively large blood-vessels, constituting what Yirchow has named telean-
giectatic glioma. This form is characterised by the tendency to haemorrhage,
which always occurs in the centre of the tumour, and the appearances
presented may closely resemble simple apoplexy. Hseniorrhagic glioma
usually occurs in the white substance of the hemisphere, where simple
apoplexy is rarely seen; and in the former, even when the tumour is
largely destroyed by haemorrhage, a narrow zone surrounds the clot, which
is sufficient to reveal the origin of the mischief.

Gliomata grow slowly, and the tumour generally attains a large size.
That these tumours undergo retrogressive changes is shown by the fre-
quent occurrence of fatty degeneration in their interior, but the changes
instead of leading to a curative process are much more likely to cause
haemorrhage as soon as the absorption of the fatty debris lowers and
removes the pressure on the vessels in the interior of the' tumour. By
fatty metamorphosis and softening of the intercellular substance cavities
form which may be distinguished from cysts by their irregular and uneven
walls. In the vicinity of tumours where the tissues are reddish and
softened, fatty granules, cholesterine crystals, neuroglia nuclei, and frag-
ments of axis cylinders may be found.

(2) Hyperplasia of the pineal gland is, both in external characters and
in the nature of its elements, very similar to glioma. Virchow says that
it forms a solid, greyish-red, slightly lobulated, or a smooth round tumour,
which may grow to the size of a walnut or even larger. On section it
exhibits the well known grey, moist, vascular tissue of the pineal gland,
and in old persons a large number of the sand-like bodies are rarely
absent. Histologically, the cell elements are somewhat larger and firmer
than in the normal gland. These tumours produce pressure on the cor-
pora quadrigemina and venae niagnoe Galeni, and that on the latter in its
turn may give rise to secondary hydrocephalus.

(3) Myxoma is rarer in the brain than in the spinal cord and peripheral

THE NATURE OF THE LESION.

555

nerves. It takes its origin, like glioma, from an overgrowth of the
neuroglia, and extends uniformly in all directions by infiltration.

(4) Solitary Tubercle, which is by far the most common tumour of the
brain, is regarded by Rindfleisch as a product of the neuroglia, and as
being allied to the fibromata. They consist of hard nodules, varying in size
from a pea to a pigeon's egg, and sometimes even larger, of grey, yellow,
or yellowish-white colour and globular form. On section the interior of
the nodule is yellowish and cheesy, while the outer cortex is of a reddish-
grey colour, and very vascular. The thickness of the cortical layer is
inversely proportional to the size of the tumour ; in a tumour the size of a
hazel-nut which I saw lately it was a line in thickness, and in another of
the size of a walnut it was not much thicker than brown paper. The
cortical tissue is continuous with the cheesy nodule on the one side and
with the healthy brain matter on the other. These tumours are met with
in all parts of the brain and cord, but their favourite seat is the cortical
substance of the cerebrum and cerebellum, close upon the cortico-medullary
boundary. This tumour is frequently multiple, and then each nodule is
usually small ; but when there is only one tumour it may attain a con-
siderable size. Rindfleisch distinguishes a tubercular and a non-tubercular
variety of the solitary cheesy nodule.

In the non-tubercular variety the cortex of the nodule consists of a
round-celled embryonic tissue, in which nothing peculiarly tubercular
can be detected. The layer of nervous matter surrounding the nodule is
also infiltrated with corpuscular elements, and thus the nodule increases
steadily in size. Within the zone of proliferation there is found a large
development of fibres between the corpuscular elements of the embryonic
tissue, rendering it dense, while the cells are entirely replaced by fibres in
the centre.

The small cheesy nodules are usually multiple, and prove on minute
examination to be really tuberculous. The grey zone of proliferation
which surrounds them is seen with the naked eye to consist of spherical
nodules, each of which corresponds in shape and size to a miliary tubercle,
while the interior of the nodule consists of tubercles which have under-
gone the cheesy transformation. The young granules are continually pro-
duced at the circumference, and the tumour grows by the constant addition
of these. When the nodule has attained a considerable size, the process
of growth stops, and a fibrous envelope gradually forms round the mass,
so as to completely isolate it from the surrounding brain tissue, and this
condition has led some pathologists to believe that all tubercles occur
in an encysted condition in the brain. The centre of the nodule some-
times softens, and occasionally the whole contents of an encysted tubercle
may undergo this change. Very rarely the tubercular nodule has been
found to have undergone a process of cretification. The cortex of the
tumour consists of giant-cells, each being surrounded by lymphoid cells
imbedded in a fibrillated reticulum.

(5) Carcinomata. — Cancer of the brain frequently appears as fungus

556

FOCAL DISEASES, ACCORDING TO

nematodes of the dura mater. When it originates from the outer surface of
the dura mater it forces its way along the vessels into the compact tissue
of the bones, and ultimately perforates them, protruding as a fungoid
tumour, and pushing the scalp before it.

Simple cancer of the brain generally grows from the under surface of
the pia mater, and even such tumours as appear to he free in the substance
of the brain are usually connected at some point or other with the pia
mater lining an adjoining sulcus. Isolated tumours, however, do exist,
but they are always secondary. Cancer is one of the most frequent of in-
tracranial tumours. It is generally primary, and, as a rule, remains long
isolated. According to Lebert, out of 48 cases 45 were primary, and of
these 13 exhibited simultaneously carcinoma of other organs. Primary
cancer of the substance of the brain is generally single, but occasionally
there is a symmetrical appearance of a tumour in corresponding parts
on each side of the brain. Several tumours are generally found in the
brain in the secondary form, but these are usually small. The smallest
cancerous tumours are generally found embedded in the hemispheres of
the brain, in the pons, base of the brain, and the medulla oblongata.
Cancer rarely occurs in the medulla oblongata, crura, and corpora quad-
rigemina, relatively more frequent in the optici thalami, corpora striata,
and cerebellum. *

Cancerous tumours destroy the neighbouring tissues by pressure and
infiltration. They are surrounded by a zone of softened tissue of about
a line in breadth, in which active growth proceeds. The microscope dis-
plays large cells rolled into nests, and crowded together in a matrix of
fibres and blood-vessels.

Many cancers, especially those connected with bone, exhibit a calcifi-
cation of their stroma. The medullary forms undergo a cheesy meta-
morphosis, which may lead to their being mistaken for tubercle of the
brain.

(6) Cholesteatoma, or pearl cancer, according to Eindfleisch, " combines
the structure of an epithelioma with the harmlessness of a wart or fibroid
thickening." It appears to be derived from the pia mater, and is usually
situated in some hollow at the base of the brain. It develops from iso-
lated growths of the size of a mustard-seed, which blend to fomi masses
of the size of a walnut. The tumour is enclosed by a delicate, inchstinctly
fibrous capsule ; it has an irregular form, and its surface presents a beau-
tiful mother-of-pearl lustre. The tumour on section is hard, pearly, non-
vascular, and composed of epidermic cells arranged in concentric layers,
which have undergone partly horny and partly fatty transformation.
These tumours grow very slowly, and consequently may remain for a long
time without giving rise to symptoms, and they only excite irritation
in the neighbouring tissues in the later stages.

(7) Papilloma of the pia mater is occasionally met with ; and a second
variety of this tumour, in which there is an abundant production of mucus
from the surface of the papilla?, is said by Eindfleisch to be frequently

THE NATURE OF THE LESION.

557

mistaken for myxoma, and he proposes to call this variety papilloma
myjcomatudes.

(8) Si/pkilomata are usually found near the surface of the brain and
develop from the perivascular sheaths. They may reach the size of a
walnut or even a hen's egg. In their interior there are usually several
cheesy patches, while the circumference is made up of soft jelly-like and
very vascular tissue. Syphilitic gummata are made up of highly cellular
embryonic tissue, with an abundant mucoid basis-substance, the cells being
concentrically arranged round the vessels. Other signs of the syphilitic
dyscrasia are generally found at the autopsy.

(9) Sarcomata occur in all varieties in the brain, and grow from the
free surfaces of the interstitial spaces. They appear as hard, slightly
vascular, round, somewhat nodulated tumours. The soft, cellular sarcomata
present many transitions to other forms of tumour indicated by the names
glio-sarcoma, myxo-sarcoma, &c. One form of spindle-cell sarcoma grows
by preference from the dura mater at the base of the brain, forming
tuberculated masses near the sella Turcica, and compressing the adjacent
parts of the brain and the cranial nerves at their points of exit. In some
sarcomatous tumours the spindle-cells are arranged in concentric layers
forming nests. This form has been named " nested sarcoma" by Dr.
Gowers.

(10) Lipoma has occasionally been met with on the inner surface of
the dura mater and on the ventricular ependyma.

(11) Psammomum is a tumour with a basis of connective or sometimes
of mucoid tissue, distinguished by its containing calcareous concretions.
It usually grows from the membranes of the brain, and especially from
the choroid plexus, in which situation it often contains numerous cysts.
According to the most recent investigations psammomum is to be regarded,
not as a distinct kind of tumour, but as a calcareous deposit in tumours
of widely different structure (Dreschfeld).

(12) Osteomata. — If we exclude the calcifications of other tumours,
true formations of bone are the rarest of all intracranial growths. Osseous
formations in the dura mater, after injuries, are more common. Syphilitic
exostoses, although for the most part arising from the external table, yet
sometimes spring from the internal surface of the skull, and cause pres-
sure on the brain like other tumours in the same locality.

(13) Cystic growths in the brain are not so common as was formerly
supposed. They are most common in the pituitary body.

(14) A ngiomala generally occur in the brain as a complication of other
tumours, such as glioma. The growths on the inner surface of the dura
mater, described under the name of pachymeningitis hEeniorrhagica breg-
matica, belong to this class.

(b) Aneurisms.

Aneurisms of the cerebral arteries are not rare. They are of various
sizes, but only those which arise from the larger vessels, chiefly at the

558

FOCAL DISEASES, ACCORDING TO

base of the brain, will come under consideration at present. They gene-
rally arise in consequence of atheromatous degeneration of the vessels.
The common termination is in rupture.

The animal parasites which occur in the cranial cavity are (]) Cysti-
cercus cellulosse, and (2) Echinococcus hominis.

(1) Cysticercus Cellulosce. — Cysticerci of the brain generally occur,
according to Kosenthal, in the parts which are richly supplied by vessels,
such as the ventricles, the ganglia and their commissures, the pia mater,
and the cortex of the brain. They were found 23 times in the meninges,
especially the pia mater, 59 times in the cortex, 32 times in the basal
ganglia and adjacent commissures, 18 times in the ventricles, 18 times in
the cerebellum, 4 times in the pons, and twice in the medulla oblongata
(Eosenthal). The parasite is sometimes found in other parts of the body
as well as in the hrain. Out of 88 cases collected by Kuechenmeister,
the cysticerci were found 1 1 times in other parts of the body. Cerebral
cysticerci are usually enclosed in a soft capsule, in which the animal may
be seen with the naked eye as a small white tubercle ; while its neck, with
the characteristic hooklets, may be discovered on microscopic examination.
Cerebral cysticerci occur with greatest frequency in places where cows
pasture in fields strewn with the excrement collected in cities (Cobbold).

(■2) Echinococcus Hominis. — Echinococcus cysts often reach a large size.
In a case reported by Dr. Morgan, the cyst was as large as a walnut, and
weighed 647 grammes. Of forty observations collected by Dr. Morgan,
the cyst was situated 10 times in the cerebral lobes, 8 times in the cere-
bellum, 4 times in the ventricles, twice in the ventricles, and once in the
pons. The cysts attain their greatest size in the hemispheres, and in the
lateral ventricles, especially in children before the fontanelles are closed.
The cyst is composed of an external fibrous membrane which encloses the
parasites ; its internal surface is lined by small buds, each about the size
of a millet seed, and provided with the characteristic ring of hooklets.
The cavity of the cyst is usually filled with a liquid, which is either clear
or contains floating ddbris and secondary vesicles, the buds of the latter
being destitute of hooks, and called acephalocyst.

§ 733. Morbid Physiology. — The only part of the physiology
of cerebral tumours with which we are here concerned is to
connect the symptoms with the effects produced by the
growth upon the nervous tissues. The tumour grows from a
minute point, and gradually increases in circumference, so that
it is at first almost entirely latent, or only gives rise to
indefinite symptoms. As the tumour increases in size it pro-
duces progressive general compression of the whole brain. In

THE NATURE OF THE LESION.

559

order to make room for the increasing size of the tumour, the
cerebro-spiual fluid is first removed, the blood is then squeezed
out of the vessels, and the whole substance of the brain suffers
pressure. It is evident, therefore, that a process of this nature
will ultimately lead to gradual abolition of the functions of the
brain.

But not only is the brain subjected to general compression,
but the tissues surrounding the new growth are liable to special
pressure, which soon leads to their destruction. The tumour
itself must probably always be regarded as a destroying lesion,
and consequently its direct tendency, as a local growth, is to
give rise to depressive symptoms. It must, however, be remem-
bered that the abolition of the function of a higher centre
may leave the functional activity of a lower centre more unre-
strained.

But although the direct tendency of the tumour is to destroy
the surrounding tissues, yet its indirect effect is often irritative.
The tumour acts as a foreign body, and is liable to cause hyper-
emia and inflammation of the surrounding tissues. Intercurrent
attacks of irritative symptoms are therefore very liable to take
place in the course of cerebral tumour, but they are generally
followed by a further extension of those of depression. It must
also be remembered that irritation of a higher centre may pro-
duce an inhibitory action on a lower centre. But the processes
set up in the surrounding tissues are not always of an irritative
or inflammatory nature. An artery may be compressed and
the tissues to which it is distributed may undergo ischsemic
softening. The veins in the vicinity of the tumour may be
compressed, giving rise to effusion of serum either into the sur-
rounding tissues or into the ventricles of the brain. Softening
as well as oedema of the surrounding tissues, in whatever way
produced, must be regarded as a destroying lesion, and the
symptoms depend upon the situation and not the nature of
the lesion.

§ 734. Grouping of the Symptoms. — A review of the symp-
toms of intracranial tumours shows that, although they are
very numerous and variable, they admit for practical purposes
of the following arrangement : — (1) General and initial symp-

FOCAL DISEASES, ACCORDING TO

toms, which may be present in every kind of intracranial
tumour, whatever its position; (2) Symptoms caused by the
localisation of the lesion ; (3) Intercurrent symptoms depend-
ing on accessory lesions ; (4) Terminal phenomena.

(1) The general and initial symptoms consist of headache, dizziness;,
restlessness, and mental irritability, parsesthesise, various disturbances
of the special senses, and convulsions. These symptoms may be present
individually or in various combinations, and for a long time they may be
the only symptoms complained of.

* (2) The symptoms which depend upon the localisation of the tumour
do not differ essentially from the symptoms caused by other focal diseases
of the brain. They result from destruction of the surrounding parts of the
brain ; they are essentially paralytic in their character, although the loss
of function may occasionally be preceded by transitory irritative phe-
nomena. These symptoms will be more fully described hereafter.

(3) The accessory lesions which give rise to intercurrent symptoms are
hypertemia and inflammation of the surrounding tissues. The chief
symptoms caused by these lesions are hallucinations, maniacal and con-
vulsive paroxysms, and attacks of apoplexy and meningitis.

(4) The terminal symptoms are caused by gradual and increasing
compression of the brain, and consist of the progressive abolition of the
mental faculties, and general sensory and motor paralysis, ending in coma.
In many cases of cerebral tumours death results from an intercurrent disease,
from an attack of cerebral haemorrhage, or from sudden paralysis of the
respiratory centre when the tumour is situated in the pons or upper end
of the medulla, or when the ventricles are distended with serum. The
intensity of the symptoms is by no means proportional to the size of
the tumour, inasmuch as a growth may sometimes attain a large size
without giving rise to marked symptoms, while at other times a small-
sized tumour may give rise to intense disturbances.

The following are the conditions on which the differences in the in-
tensity of the symptoms appear to depend : — (a) Idiosyncrasies of the
patient ; (b) the position of the tumour ; (c) the nature and rate of growth
of the tumour ; (d) the changes set up in the surrounding tissues ; and
(e) the presence of several tumours, or the existence of complications.

(a) Idiosyncrasies of the Patient. — It is well known that some men
react much more actively than others to the same degree of irritation. A
degree of irritation, for instance, which would not produce an appreciable
effect on adults may occasion violent convulsions in children.

(b) Position of the Tumour— -Some parts of the brain are tolerant and
others are very intolerant of displacement or any interference from without.
The white substance of the hemispheres and the occipital lobes belong to
the first category ; the medulla, pons, and the internal capsule of the
lenticular nucleus to the second.

THE NATURE OF THE LESION.

561

(c) Nature of the Tumour and its Rate of Growth. —It may be laid down
as a general ride that the intensity of the symptoms is in direct pro-
portion to the rapidity of the growth of the tumour. The slow-growing
cholesteatornata, for instance, usually attain a considerable size before
giving rise to any distinctive symptoms. When the growth is rapid there
is a greater flow of blood to the part, and the surrounding tissues are more
liable to undergo irritative changes, while the brain has no time to accom-
modate itself to the new disturbance. The increased bulk of the tumour
is sometimes caused not by growth of its tissue elements, but by oedema
or haemorrhage, and then it produces all the effects of a sudden injury
to the brain. Conducting fibres which, if pushed aside by a slow-growing
tumour, would maintain for a long time their functional integrity, are now
suddenly stretched, ruptured, and irremediably damaged. Retrogressive
changes within the tumours may, according to their nature, cause great
variations in the symptoms. Sometimes these changes may lead to haemor-
rhage and all its consequences ; while at other times the tumour may by
these changes become diminished in bulk, thus relieving the pressure on
the brain and leading to a temporary amelioration of the symptoms.

(d) Morbid Changes in the Surrounding Tissues. — The changes set up in
the tissues surrounding the tumour may either constitute discharging or
destroying lesions. It is not possible to draw a clear line of demarcation
between these two kinds so far as the symptoms are concerned, since the
effect of a destroying lesion in the immediate vicinity of the tumour may
be obscured by those of discharging lesions in remote parts. In the early
stages of the growth of the tumour the discharging lesions predominate.
The tumour acts as a mechanical irritant or foreign body, and it may
directly irritate the part in which it is situated, or indirectly irritate remote
parts by reflex action, or again its effects may be more or less diffused
and general.

It is very important to observe that the symptoms of intracranial
tumours frequently intermit in the early stages of the disease, and only
become permanent and continuous in the latter stages when the whole
brain is subjected to pressure. The reasons for this intermittence of
symptoms are not far to seek. A large discharge of nervous energy is
followed by exhaustion, so that the discharging lesions caused by the local
irritation of the tumours are followed by exhaustion, accompanied by tem-
porary subsidence of the active symptoms. At other times the symptoms
may be caused not so much by the size of the tumour as by oedema and
inflammation of the surrounding tissues, and when the latter subside the
symptoms disappear for a time, although the primary lesion still persists.

(e) The Presence of several Tumours and Complications. — The variety
and complication of symptoms are very much increased when several
tumours are present, or when symptoms of tumour are associated with
cerebral disturbance caused by an independent affection, such as Bright's
disease.

K K

562

FOCAL DISEASES, ACCORDING TO

§ 735. Diagnosis. — Intracranial tumours may be confounded
with other cerebral lesions, and indeed at an early stage it is
almost impossible to be sure of the diagnosis. The most
important symptom of tumour is to be found in the optic discs.
Many cases are recorded in which the presence of double optic
neuritis was the only symptom that could lead one to the
suspicion of cerebral tumour, and in which the diagnosis was
subsequently justified by the progress of the case. Two cases
of this kind have come under my own observation, and the
occurrence of such cases has led Dr. Hughlings-Jackson to insist
on the routine use of the ophthalmoscope in the examination
of patients.

In tubercle the disease of the brain is generally associated
with tuberculous affections of other organs, and a hereditary
predisposition to the disease can usually be ascertained.

Hydrocephalus, in its chronic form, is a frequent accompa-
niment of tumour, especially when the latter is situated under
the tentorium, where the growth is liable to produce pressure
on the venas Galeni magna?, or to prevent the return of the
cerebro-spinal fluid into the spinal canal.

Apoplexy occurs in advanced age, its onset is sudden, and
it is usually associated with disease of the heart, atheroma
of the vessels, and granular kidney ; while the paralysis is
sudden, without premonitory symptoms, and frequently followed
by late rigidity in the extremities. Tumour, on the other hand,
occurs at every time of life without being necessarily associated
with other diseases, while the paralysis comes on slowly and
increases gradually, and is preceded by other symptoms, such
as violent cephalalgia, vomiting, vertigo, and neuralgia, and it
is rarely followed by late rigidity. They may be further dis-
tinguished from each other by the double optic neuritis of
cerebral tumour, in opposition to the rarer unilateral embolic
amaurosis of apoplexy. Care, however, must be taken not to
confound one form of albuminuric retinitis with the optic
neuritis of cerebral tumour.

In chronic softening the paroxysms of headache are less fre-
quent and intense than in tumour, while affections of the special
senses and anaesthesia of the cephalic nerves occur more fre-
quently in tumour than in softening; on the other hand the

THE NATURE OF THE LESION.

5G3

occurrence of sudden and complete hemiplegia and aphasia is
more common in softening than in tumour. Alternate and
bilateral paralysis occur, according to Hasse, frequently in
tumour and only exceptionally in softening.

Abscess of the brain is to some extent similar to tumour in
its physical relations, inasmuch as it may produce increase of
intracranial pressure, and, like tumour, the tissues surrounding
the diseased focus are often affected by inflammatory attacks.
Abscess usually occurs as the direct consequence of an injury,
such as fractures of the skull and concussions of the brain, or
associated with some other disease, such as caries of the petrous
portion of the temporal bone, ozsena, foci of suppuration, diseased
vessels, or valvular diseases of the heart; while tumour is never
more than a remote consequence of an injury. In tumour the
cephalalgia is severe, the various symptoms assume a progressive
character, and there is usually a gradual extinction of the
functions of the brain; or apoplexy may occur, but meningitis
is rare.

Atrophy of the brain produces an early destruction of the
mental activities which passes gradually into imbecility. The
presence of tremors of the lips, tongue, and limbs, of epilepti-
form convulsions, hemiplegia or paraplegia, and loss of mental
power, form a group of symptoms so characteristic that they
cannot well be mistaken for those of tumour.

Hypertrophy of the brain of children gives rise to symptoms
as cephalalgia and epileptiform convulsions somewhat similar
to those of tumour. The large circumference of the great
fontanelle, with its strong pulsation, the slow dilatation of
the head, the distinct traces of rickets in the skeleton, and
spasms of the larynx combine to prevent this disease from being
mistaken for cerebral tumour.

Syphilis of the brain may give rise to symptoms closely
simulating those of cerebral tumour, and indeed the presence of
a distinct gumma induces symptoms which are identical with
the symptoms of other forms of tumour. The history of the
case, permanent traces of the disease such as cicatrices, the
peculiar pains of the nerves and bones, epileptiform convulsions,
and evidences of the presence of more than one focus of disease,
are amongst the signs to be made use of in forming a diagnosis.

564

FOCAL DISEASES, ACCORDING TO

§ 736. Diagnosis of the nature of the Tumour. — It is not
always possible to diagnose the nature of the tumour, although
this may be done sometimes with a considerable degree of cer-
tainty. The development of glioma is frequently preceded by
an injury to the skull, the progress of the symptoms is slow,
and the illness is consequently of comparatively long duration.
Haemorrhage not unfrequently occurs into the substance of the
tumour or into the surrounding tissues, and the patient is,
therefore, liable to suffer from intercurrent attacks of apoplexy.

Turbercular tumour may be suspected when the symptoms
of intracranial tumour occur in childhood, and when a heredi-
tary predisposition to tubercle can be traced. The diagnosis is
rendered more certain when evidence of tuberculosis in other
organs or cheesy degeneration of the glands can be detected.
The tumour is also more likely to be of a tubercular nature
when the symptoms indicate that it is situated in the cere-
bellum, or that multiple lesions are present. Tubercular
tumour often begins after an acute febrile disease, as measles
or scarlet fever, while its progress is frequently complicated by
slight attacks of meningitis.

Carcinoma of the brain is characterised by the rapid pro-
gress of the symptoms, and the presence of the cancerous
cachexia or evidence of the deposition of cancer in other organs.

Sarcomata are not easily diagnosticated during life, but when
the most prominent symptoms are afforded by compression of
the nerves at the base of the brain sarcoma may be suspected.

Syphilomata of the brain will be subsequently described in
detail.

Oysticercus cellulosai, when situated in the brain, often re-
mains latent for a comparatively long period. The more usual
symptoms of the affection are headache and vertigo, followed
by muscular spasms, epileptiform convulsions, and various
mental disturbances, but distinct paralysis is rare. The con-
vulsions caused by the presence of the parasite may at first-
be similar in every respect to those of idiopathic epilepsy, but
in the terminal period the attacks increase in number and
violence, as many as 80 to 100 daily having been known to
occur during the week previous to death (Rosenthal). The
psychical disturbances consist at first of illusions, delirium,

THE NATURE OF THE LESION.

565

maniacal attacks, followed by melancholy, somnolency, and
stupor. The diagnosis of the presence of cysticerci is rendered
more probable if, in addition to the symptoms just described,
the history of the case show that the patient had previously
suffered from taenia, or if the patient be a butcher or pork
dealer.

Echinococcus hominis, when found in the brain, does not
give rise to characteristic symptoms. The most constant symp-
toms are headache, vertigo, vomiting, tremors, epileptiform
attacks, and the usual evidences of the presence of an intra-
cranial tumour in the optic discs. In the cases collected by
Dr. Morgan the duration of the symptoms averaged one and a
half years. The tumour may sometimes make its way through
the cranial bones. In Keeb's case it made its way through
the parietal bone, while in a case observed by Westphal two
openings were found in the frontal bone through which the
tumour projected ; an incision having been made 90 vesicles
flowed through the opening, and the case terminated in recovery.
Westphal states that the diagnosis of the presence of echino-
cocci in the brain must be made from the general symptoms of
intracranial tumour appearing and disappearing alternately,
oedema of the eyelids, an opening in the cranial bones through
which a fluctuating tumour projects, or exploratory puncture.

Aneurism of the cerebral arteries gives rise to symptoms like
those of other tumours situated at the base of the brain, nor
are there any sure signs by means of which the former may be
distinguished from the latter. Even auscultation of the skull
has not hitherto proved of much use in the diagnosis of intra-
cranial aneurism. If aneurism of any of the other vessels of
the body co-exist with the symptoms of tumour situated at the
base of the skull, then aneurism of one of the cerebral vessels
may be suspected. It is probable that aneurism gives rise to
more pronounced symptoms of irritation, such as intense cepha-
lalgia, paroxysms of severe and intractable trifacial neuralgia,
attacks of mania and other grave psychical disorders, than
solid growths. If a patient, who has been suffering from the
symptoms of tumour situated at the base of the brain, die
suddenly from an attack of ingravescent apoplexy, it may be
conjectured that the tumour was an aneurism rather than a

566

FOCAL DISEASES, ACCORDING TO

new formation. If a case, in which the patient has suffered
from the symptoms of tumour situated in the anterior fossa of
the skull, terminate fatally from a copious haemorrhage from
the nose, it may be assumed with considerable probability that
an aneurism of the anterior cerebral artery has perforated the
cribriform plate of the ethnoid bone. If pulsation and a mur-
mur on auscultation be observed in the orbit immediately after
an injury to the skull, it is probable that a communication has
been established between the internal carotid artery and the
cavernous sinus (Lebert).

§ 737. Prognosis. — With the exception of syphilitic cases,
death is the usual consequence of cerebral tumours. Even a
syphilitic tumour may not be amenable to treatment if it be of
long standing, since irreparable mischief to the brain may have
already been caused by it. Cases of cerebral tumour may some-
times terminate in sudden death through an attack of apoplexy
or of convulsions, or occasionally without evident cause. In
other cases the symptoms may become quiescent, the vomiting
cease, the amaurosis even disappear, and the patient regard
himself cured. After a time, however, the symptoms usually
recur with increased intensity, and lead to a fatal termination.

§ 738. Treatment. — In the large majority of cases very little
can be done by treatment, but even in these unpromising
cases curative efforts should not be abandoned. In the earlier
stages of cerebral tumours the symptoms are generally those of
irritation and of local congestion, and these must be treated by
cold to the head, purgatives, and occasionally by the use of
flying blisters.

The cephalalgia may be combated by ice to the head, and if
no relief be afforded, narcotics are to be cautiously resorted to.
Subcutaneous injections of morphia will be found the most
useful and reliable remedy, although small doses of belladonna
have occasionally been attended with benefit. The chloride of
ammonium may occasionally be found useful.

When convulsions are a prominent symptom, doses of from
half a drachm to a drachm of the bromide of potassium may be
useful.

THE NATURE OF THE LESION.

567

With the view of promoting absorption of the morbid growth,
iodide of potassium has been administered in large doses and
with apparent benefit. For adults half-drachm doses may be
given to begin with, and increased until a drachm is taken
three times a day. Of course if there be evidence of syphilis,
energetic anti-syphilitic treatment by means of mercury and
iodide of potassium is indicated.

568

CHAPTER VI.

(II.) SPECIAL CONSIDERATION OF FOCAL DISEASES,
ACCORDING TO THE LOCALISATION OF THE LESION.

, 1. AFFECTIONS OF THE PEDUNCULAR FIBRES AND
INTERNAL CAPSULE.

a. Affections of the Pyramidal Tract.
(i.) Hemiplegia.

§ 739. Hemiplegia consists of paralysis of one-half of the
body, although many of the muscles are either not implicated or
only temporarily weakened. The paralysis is, as a rule, limited
to the arm, leg, and part of the face.

In facial paralysis of cerebral origin the cheek on the affected
side looks flat, the corresponding naso-labial fold is obliterated,
the upper lip is less arched, and the angle of the mouth is
lowered on the affected side, the distortion becoming more
marked when the facial muscles of the healthy side contract.
Paralysis of the orbicularis oris interferes with the pronunciation
of the labials and with such actions as whistling and blowing
out a candle. The patient can frown as usual, raise his eye-
brow and eyelid and close his eye on the paralysed almost as
well as on the healthy side, but is unable to perform a uni-
lateral action like winking on the affected side. The facial
paralysis begins usually to disappear in a few weeks, and some-
times in a few days, while it may persist for months. The
muscles chiefly affected in facial paralysis of cerebral origin
are the buccinator, orbicularis oris, and the straight muscles
which pass to the angle of the mouth and to the nose on the
paralysed side; while the occipito-frontalis, corrugator super-

FOCAL DISEASES.

5G9

cilii, and orbicularis oculi remain almost entirely unaffected.
In facial paralysis of peripheral origin all the muscles supplied
by the facial nerve below the lesion are equally paralysed.

The hypoglossal nerve is affected in most cases of apoplexy,
as shown by a certain degree of difficulty in executing the
movements of the tongue. On protrusion its point deviates
more or less to the paralysed side, the base being dragged
further forwards on the healthy side. The affection of the
tongue, as a rule, disappears in a short time, but is occasionally
permanent.

Some observers state that the muscles of the trunk are un-
affected in hemiplegia, but the inspiratory muscles undoubtedly
act less freely on the paralysed side for the first few days in
severe cases.

(ii.) Hemispasm.

§ 740. The spasms which occur in connection with focal
cerebral lesions are of three kinds : (a) Tonic, (b) combined
tonic and clonic, and (c) clonic sijasms.

(a) Tonic Spasms. — The tonic contractions which occur in
connection with focal lesions of the brain may be divided into
two classes : (i.) Early and (ii.) late rigidity.

(i.) Early Rigidity. — The contractions which occur in early
rigidity may be subdivided into those which immediately ac-
company the haemorrhage, and those which occur a few days
after the attack. The contractions of the first kind are
probably produced by irritation of the fibres of the pyramidal
tract, occasioned either by rupture or partial injury. The
second form of early rigidity appears in the paralysed parts a
few days after the occurrence of haemorrhage, and during the
time inflammatory changes are taking place in the tissues sur-
rounding the clot. These contractions, therefore, are probably
also the result of irritation of the fibres of the pyramidal
tract. Early rigidity may be so slight as only to be manifest
when passive movement of the paralysed extremity is made.
When the arm is flexed, for instance, if an attempt be made to
straighten it, the biceps offers resistance to the movement;
while at other times resistance is offered to flexion by con-
traction of the triceps.

570 FOCAL DISEASES, ACCORDING TO

The rigidity may sometimes be limited to the fingers, while
at other times the arm is drawn to the side of the chest, the
elbow and wrist are firmly bent, the fingers are flexed upon the
palm, and all attempts to extend the limb increase the con-
tractions, and cause pain as well as some amount of tremor or
slight clonic spasm. The resistance yields occasionally under
steady pressure. This form of rigidity may affect the leg as
well as the arm, and then the thigh becomes flexed on the
trunk, and the leg on the thigh, so that the heel is brought up
to the buttock. Early rigidity generally disappears soon, but
may persist for weeks or months. The affected muscles do
not undergo atrophy, their faradic and reflex excitability is
increased, and they become completely relaxed during sleep,
although the spasm recurs immediately on the patient awaking.
The appearance of early rigidity diminishes the chances of the
patient's recovery, and when it continues for a long time changes
take place in the muscles, tendons, and joints of the affected
extremities, which ultimately leave them permanently contracted
and useless.

(ii.) Late Rigidity. — This form of contracture is caused "by
descending degeneration of the fibres of the pyramidal tract,
and corresponds in its essential character to the spasmodic
rigidity of primary lateral sclerosis. Its most characteristic
feature is the exaggeration of the tendinous and periosteal
reflexes. When the lower extremity is affected the patellar-
reflex is in excess, and ankle-clonus is readily elicited, and
corresponding phenomena may be obtained in the upper ex-
tremity when it becomes the subject of contracture. When
the loss of voluntary power is complete, the rigidity is more or
less constant, although it is in most cases diminished during
sleep and increased during voluntary efforts and emotional
disturbances.

The attitudes assumed by the limbs affected with late
rigidity differ considerably in different cases, but on the whole
they conform to the rule observed in almost all spasmodic
affections, namely, that flexion predominates in the upper, and
extension in the lower extremity. In the most usual attitude
of the upper extremity the arm is drawn towards the trunk by
contraction of the pectoralis major. The forearm is semi-flexed

THE LOCALISATION OF THE LESION.

571

on the arm and pronated, the hand is slightly flexed on the
forearm, and the fingers are closed. In some cases the forearm,
instead of being semiflexed and pronated, is semi-flexed and
supinated. In a few rare cases the forearm is extended upon
the arm, and then the forearm may either be in a state of
supination or pronation (Charcot). Probably the most frequent
attitude of the hand is that in which the fingers are ex-
tended at the metacarpophalangeal and flexed at the phalangeal
joints (Gowers). The inferior extremity is, as a rule, main-
tained in a state of rigid extension, the foot being in the posi-
tion of talipes equino-varus. In some few cases flexion pre-
dominates over extension in the lower extremity, and then the
thigh becomes flexed on the trunk, and the legs on the thigh,
so that the heel touches the buttock. In these cases the con-
tracture is apt to extend to the opposite extremity, and then
station and locomotion are impossible. In some cases the con-
tracture extends to the inferior muscles of the face. The con-
tracture is at first transitory, and only manifested when the
patient laughs or cries, but after a time it becomes permanent.
The angle of the mouth on the affected side is then elevated,
the naso-labial fold is increased in depth, and even the eye of
the corresponding side may be smaller than the healthy eye
(Plate VI, 2, 3, and 4).

After a time, however, the muscles may undergo progressive
atrophy, and the contractures almost entirely disappear, although
the bones and ligaments having become adapted to the form in
which the limb has so long been maintained the deformity
persists. In these cases it is probable that the descending
degeneration of the lateral column of the spinal cord has ex-
tended to the ganglion cells of the anterior grey horns. The
muscles which do not suffer at all, or suffer least, from late
rigidity are those that are bilaterally associated in their actions,
while those acting independently of the corresponding muscles of
the other side are most affected. In accordance with this rule, the
muscles of the trunk remain unaffected, and the muscles of the
lower extremity are less frequently and less profoundly affected
than those of the upper ; the superior muscles of the face
generally escape, while the inferior facial muscles are occasion-
ally attacked. The rigidity, however, is not always so fixed and

572

FOCAL DISEASES, ACCORDING TO

unvarying as that just described. It may never become fully
established, or after having become established may undergo a
considerable amount of improvement. When the rigidity has
never been fully established, it may be observed that the tension
becomes less when the limb is warm and greater when it is
cold ; that it can be diminished by gently rubbing the muscles ;
and that it disappears almost, if not entirely, during sleep. On
the other hand, the rigidity is increased during voluntary efforts
to move the limb, this effect being more marked when the
patient is under observation.

Although rigidity may have become fully established, at the
end of some months it gradually diminishes to such a degree
that Brissaud proposes to call the condition latent contracture.
The patient may perform all the simple movements of the limb,
and probably with undiminished power, but whenever his atten-
tion is specially directed to the movements, as when he wishes
to perform any manual operation requiring a little dexterity,
the muscles instantly become rigid, the fingers are flexed on
the palm, and the deformity which was present during the
period of fixed contracture reappears. It may also be shown
that the tendon reflexes continue exaggerated, although the
muscular tension has in great part disappeared. It is not yet
ascertained whether the disappearance of the muscular tension
is due to a corresponding repair of the fibres of the injured
pyramidal tract on the opposite side, or to the establishment
of new connections with the cortex of the brain on the same
side through commissural fibres in the cord.

(b) Combined Tonic and Clonic Spasms. — The cases just
described, in which a slight degree of muscular tension per-
manently present in the affected extremity is associated with
marked spasm on a voluntary effort being made to move the
limb, form a fitting transition to those cases in which a fixed
tonic contraction of some of the muscles is associated with
clonic contractions of others. In the combined tonic and clonic
varieties of post-hemiplegic motor disorders, the muscular con-
tractions are at first entirely like those which occur in late
rigidity, but after a time some of the muscles implicated
become the subjects of clonic spasm.

Varieties. — The combined tonic and clonic spasms of hemi-

THE LOCALISATION OF THE LESION.

573

plegic limbs consist of the following varieties : — (i.) Intermittent
tremor, and (ii.) Choreiform movements.

(i.) Intermittent Tremor— The most usual form of tremor
observed in hemiplegic limbs corresponds with that which is
observed in spastic spinal paralysis. The tendon reflexes are
exaggerated, and the tremor is induced when the muscles are
put upon the stretch by any attempt at voluntary movement
or otherwise. This kind of tremor is therefore similar to that
described as "spinal epilepsy" in lateral sclerosis of the spinal
cord, and, like the latter, it is associated with descending
sclerosis of the pyramidal tract. The tremor is, like that of
multiple sclerosis, absent during repose.

The muscles of hemiplegic limbs are liable to be affected
with fibrillary contractions similar to those which occur in
progressive muscular atrophy and amyotrophic lateral sclerosis.
It is probable that muscular atrophy is always associated with
these contractions in hemiplegia, and that the descending
changes of the pyramidal tract have extended to the ganglion
cells of the anterior grey horns of the cord.

(ii.) Choreiform Movements. — Clonic choreiform spasms of
the extremities may either precede or follow an attack of hemi-
plegia, the former being named pre-hemiplegic, and the latter
2)Ost- hemiplegic chorea (Weir Mitchell, Charcot). In pre-
hemiplegic chorea the patient complains of a feeling of numb-
ness and feebleness of the extremities of one side, his gait
becomes hesitating and irregular, and the upper extremity of
the affected side is attaked by choreiform movements. These
symptoms may continue for some days, when complete hemi-
plegia, usually associated with hemiansesthesia, is either sud-
denly or gradually established. Post-hemiplegic chorea occurs
in partially but never in completely paralysed limbs, and usually
appears simultaneously with a marked diminution of the para-
lytic symptoms. The clonic spasms as a rule become gradually
established as motor power returns, although they sometimes
supervene suddenly, and appear to be sometimes induced by a
strenuous voluntary effort on the part of the patient to move
the paralysed limb. Clonic spasms occur more frequently in
the arm than in the leg, and when they exist in both they are
more severe in the former, while if the leg be exclusively affected

574

FOCAL DISEASES, ACCORDING TO

the arm is usually completely paralysed. The muscles of the
face are sometimes affected by those spasms, causing various
distortions, which become greatly increased when* the patient
laughs or cries.

The movements affected by choreiform spasm in the upper
extremity are, in decreasing order of frequency, the special
movements of the fingers and thumb, flexion and extension of
the wrist, pronation and supination of the forearm, extension
and flexion at the elbow, and movements at the shoulder-joint.
The iuterossei are particulary liable to be affected by chorei-
form spasm, and consequently the movements most frequently
observed consist of varying degrees of flexion and extension at
the metacarpo-phalangeal articulations, associated respectively
with extension and flexion at the phalangeal articulations. The
movements induced by these spasms are of wider range than
those of hemiplegic tremor, resembling in this respect the
movements of chorea. They are disorderly and irregular, and
may or may not continue during complete repose ; they cease
during sleep, and become much aggravated during voluntary
efforts to perform a definite movement with the affected limb,
such as that of raising a glass of water to the mouth. When
the lower extremity is affected, the whole body may be thrown
into a state of agitation during locomotion.

Two forms of jpost-hemiplegic chorea may be distinguished :
(a) the post-he iniplegic chorea of adults ; and the spastic
hemiplegic of infancy. The spastic hemiplegia of infancy may
consist of a purely tonic spasm of the muscles without any
admixture of clonic spasms, although the choreiform variety is
probably the more common.

(a) Post-hemiplegie Chorea of Adults. — The post-hemiplegic
chorea of adults and the corresponding affection of infancy differ
in various ways. In the former the history of the case shows
that the attack of hemiplegia which preceded the appearance
of the clonic spasms occurred during adult life, or at any rate
not in early infancy. The attack of hemiplegia may have occa-
sionally become gradually established when due to the slow
growth of a tumour, but as a rule it has come on suddenly with
apoplectic symptoms. An examination of the patient may
reveal valvular disease of the heart, or there may be a history

THE LOCALISATION OF THE LESION.

575

of injury to the head. The post-hemiplegic chorea of adults,
apart from the history, differs from that of infancy in the co-
existence of hemianesthesia in the former and its absence in
the latter. The anaesthesia extends over the lateral half of the
body ; and all forms of sensibility, including the special senses,
are more or less affected. Three distinct cases of the post-
hemiplegic chorea of adults have come under my own obser-
vation. All the patients were comparatively young men, their
ages ranging from 25 to 33 years. The attack of hemiplegia,
which had preceded the choreiform movements, occurred in
each several years previously to my seeing them. Two of the
patients presented evidence of slight stenosis of the mitral
valve, and in the third the apoplectic attack had been induced
by a fall on the head. The attitude assumed by the affected
arm was very similar in the three cases. There was marked
tonic spasm of the posterior third of the deltoid in all of them,
so that the elbow was abducted from the trunk to the extent of
about two and a half inches, while it was also drawn backwards
considerably behind the posterior plane of the body. The fore-
arm was slightly flexed on the arm and strongly pronated, the
hand was slightly flexed on the forearm, while the fingers were
kept in constant movement by clonic spasms of the interossei
muscles. There- was also a certain degree of spasmodic pro-
nation and supination of the forearm and flexion and extension
of the hand in all; while in one, irregular jerking movements
of the forearm, hand, and fingers occurred when the patient
attempted to grasp any object with the paralysed hand. A
marked feature presented by these cases was the fact that each
patient carried the affected hand in the out pocket of his coat,
in order to arrest its disorderly movements. In this position
the upper arm was directed downwards, outwards, and back-
wards from the shoulder, the elbow being considerably removed
from the trunk and behind its posterior plane, the forearm was
slightly bent on the arm, and the back of the hand was pressed
closely against the hip.

In the three patients referred to the tactile sensibility of the
palm and fingers of the affected hand was remarkably deficient.
When the patient was asked to close his hand on a coin placed
on the palm, with his eyes closed, he could not say whether he

576

FOCAL DISEASES, ACCORDING TO

had or had not the coin in his grasp; and when the coin was
withdrawn before the closure of the fingers, it was amusing to
observe his puzzled expression on opening his eyes and hand
when he found the latter empty. The patients could be pricked
with a pin over half the face, trunk, and over extremities on
the affected side almost without pain. In one of these cases
all forms of cutaneous sensibility, and the muscular sense, were
diminished over half of the body on the affected side, the senses
of taste and smell were also diminished on the corresponding
side, but the senses of hearing and sight were not affected to
an appreciable extent.

Spastic Hemiplegia of Infancy. — In the spastic hemi-
plegia of infancy the lesion which determines the paralysis
occurs during birth, or in early infancy. The paralysis
appears sometimes to have become established before birth,
but cases of this kind are exceptional. It is, however, not
uncommon to ascertain, on inquiry from the parents, that the
patient who is affected with the spastic hemiplegia of infancy
suffered from repeated convulsions accompanied by uncon-
sciousness for the first two or three days after birth, although
it may not be observed that the child is paralysed on one half of
the body till some time subsequently. In the majority of these
patients, however, the onset of the disease dates from the age
of two to three months to that of four or five years. The most
usual history is that after an illness of indefinite character ex-
tending over a few days, or without any warning, the child has
been taken with convulsions. These convulsions, as a rule, have
recurred repeatedly for some hours or days, the child remaining in
the meantime in a state of unconsciousness. In many cases this is
the only history which can be obtained, but where the parents
are intelligent it may be ascertained that the convulsions
were limited to the side of the body which had subsequently
become paralysed. Many infants doubtless die during these
convulsions or a few days after, but in the cases which
survive it is soon observed that one half of the body is
paralysed. The hemiplegia in these cases pursues the usual
course, contractures become established, and choreiform move-
ments may or may not make their appearance during partial
recovery, but when once these movements appear they remain

THE LOCALISATION OF THE LESION.

577

permanent. So far, then, these cases present nothing peculiar
except that the disease dates from childhood, that it is ushered
in by convulsions and profound unconsciousness, and that the
motor paralysis is not accompanied by hemianesthesia.

In the spastic hemiplegia of childhood, however, it is soon
observed that the intellect of the patient, however bright the
child may have been previous to the attacks of convulsions
which marked the onset of the disease, has become markedly
defective. This form of hemiplegia is, indeed, nearly always
associated with some degree of idiocy.

Another marked peculiarity of the affection is that at a cer-
tain age the hemiplegia becomes associated with epilepsy. The
epileptic attacks generally begin when the patient is from seven
to fifteen years of age, and at first are usually limited to the
paralysed side of the body, and may not be attended by decided
loss of consciousness. In the case of a well-developed girl four-
teen years of age, under my care, suffering from the spastic
hemiplegia of childhood, the epileptic attacks began when she
was eight years of age. The right half of the body was
paralysed, the arm being more paralysed than the leg, both
limbs were somewhat rigid, but neither manifested any chorei-
form movements. The epileptic attack always began by move-
ments of the paralysed arm ; these soon extended to the muscles
of the mouth on the same side, and then to the paralysed leg.
In most attacks this patient became unconscious for a few
moments, and then got up and walked about as if nothing
had happened. In some, however, the convulsions were
limited to the paralysed arm, with probably a slight exten-
sion of them to the angle of the mouth, but the leg remained
free, and there was no loss of consciousness. The patient was
once reported by the nurse to have walked across the ward
during an attack, holding down the convulsed and paralysed
arm with the opposite hand. In old-established cases the con-
vulsions may become general, but it may be observed that they
retain a unilateral character at the commencement of the attack,
and the patient usually describes a unilateral aura.

The aura is often described as a sensation beginning in the
paralysed hand, and ascending along the arm to the shoulder
and head, when unconsciousness supervenes. At other times

578

FOCAL DISEASES, ACCOEDING TO

the sensation begins in the paralysed leg, and ascends succes-
sively to the arm and head. In several cases under the care oi
Mr. Hardie, which I examined recently in Crumpsall Workhouse,
three of which are represented in Plate VI., Figs. 2, 3, and 4, the
patients could not give any account of an aura; and so far as I
could judge from the account given by their attendants, the con-
vulsions did not assume a unilateral character. In all these
cases marked idiocy was present, so that the presence of an aura
could not be determined from the inability of the patients to
describe it. In one case of the kind, with choreiform move-
ments of the paralysed hand, sent to me by Mr. Cullingworth,
the patient had an epileptic attack once while I was examining
her. I could not observe that the convulsions assumed a pro-
nounced unilateral character at any time during the attack. On
cross-examining her with respect to the aura, she positively
denied that she had had any warning whatever of impending
attacks; but after a time she volunteered the statement,
" When the fits began first I used to have a creeping feeling
in the leg, which came up to the arm," at the same time
pointing successively to the paralysed leg and arm.

These patients also present other phenomena which are
worthy of notice, the most remarkable of which is an arrest
of development of the paralysed limbs, generally implicating
the corresponding side of the face. The circumference of the
paralysed extremities is usually less than that of corresponding
parts of the opposite limbs, although not always so. Where a
limb is subject to violent choreiform movements, the muscles
may become hypertrophied so that its circumference exceeds
that of the corresponding healthy extremity. But even under
these circumstances it may be found that the circumference of
the bones on the affected side is less than that of the sound
side, and that the enlargement is limited to the muscles. Each
of the long bones of the affected extremities may be from ^in.
to lin. shorter than the corresponding bones of the affected
side, and even the clavicle of the paralysed side may be from
^in. to ^in. shorter than the opposite clavicle. The diminution
of size of half the face may extend to all the features, inclu-
ding the eyebrows, eyelids, half of the nose, the cheek, and half
the mouth. -

THE LOCALISATION OF THE LESION.

579

(c) Clonic Spasms. — The post-hemiplegic motor disorders,
which consist of clonic spasms unaccompanied by tonic con-
tractions of the muscles, are (i.) continuous or remittent tremor,
(ii.) choreiform movements (athetosis), and (iii.) jerking move-
ments on voluutary effort (hemiataxia).

(i.) Continuous or Remittent Tremor. — The tremor which
has already been described as occurring in hemiplegic limbs
was associated with increased muscular tension, excess of the
tendon reflexes, and only occurred when a voluntary movement
of the limb was made. In the form of tremor about to be
described, muscular tension, if present in excess at all, is not a
prominent feature of the case, the tendon reflexes are not
exaggerated, the tremor is continuous at least during waking
hours, and instead of being exaggerated it may be diminished
or arrested by a voluntary effort. We have seen that the first
form of tremor is like that which is observed in sclerosis in
patches; while the second form is in all essential particulars
like the tremors of paralysis agitans. A case of the latter kind
has been described by Grasset. The tremors, which continued
during repose, were accompanied by sensations of heat like
those complained of by patients suffering from paralysis agitans.
A case is described by Leyden in which tremors occurred in the
right arm, momentarily arrested by a voluntary effort, while
there was complete absence of any paralysis or contractures and
of sensory disturbances. A round sarcomatous tumour was found
in the left optic thalamus. By the courtesy of Dr. Leech, I
had an opportunity of showing to the members of the British
Medical Association at the Manchester meeting, a case in which
one-half of the body presented all the characteristics of a
moderately advanced paralysis agitans. The tremors extended
to the right foot, leg, and one-half of the trunk; while the atti-
tude of the forearm, fingers, and thumb was quite characteristic.
The symptoms supervened nine months previously, and were
preceded by a slight attack of confusion, not amounting to un-
consciousness, followed by slight paresis of the right side of the
body.

(ii.) Athetosis. — An affection has been described by Ham-
mond under the name of athetosis, in which the patient is
unable to maintain the fingers or toes in fixed positions. The

580

FOCAL DISEASES, ACCORDING TO

fingers and toes in this affection are maintained in continuous
slow movement, and are made to assume various distorted
positions. These movements are not always limited to the
fingers and toes, but extend to the hand and foot, and occasion-
ally even to the muscles of the neck and face. No motor
weakness has been recognised, the movements are only to a slight
extent under the control of the will, they usually persist during
sleep, and are not accompanied by contractures. Cases of the
affection have been described by Allbutt, Currie Ritchie, Fisher
(Boston, U.S.), Gairdner, and others, while Claye Shaw and
Dreschfeld have drawn attention to the analagous condition
sometimes observed in the limbs of imbecile children. Oulmont
has written a valuable monograph of the whole subject.

The appearance of the clonic spasm is in almost all cases
preceded by a distinct attack of hemiplegia, and when no
decided paralysis can be ascertained to have been present the
history of the case shows that the patient has suffered from an
attack of convulsions and unconsciousness.

Hemianesthesia is described as being present on the affected
side in some of the reported cases, while a certain degree of
numbness of the same side is frequently mentioned. In a con-
siderable number of cases the condition of sensibility is not
mentioned, and probably no special attention was directed to
the point.

The affected extremity usually presents vaso-motor disturb-
ances. It is red or livid, moist, and colder than the corre-
sponding extremity.

The affected hand or foot is also frequently atrophied ;
although the muscles which are affected by the spasm may
undergo a certain amount of hypertrophy. The electric con-
tractility of the affected muscles varies in different cases, being
sometimes normal, at other times enfeebled or increased.

Oulmont has observed an unusual degree of relaxation of the
ligaments and joints of the affected extremities.

A bilateral athetosis has been described by Oulmont. It
does not differ essentially from the unilateral affection, except
that the muscles of the face appear to be more liable to be im-
plicated to a greater extent in the former. The bilateral affec-
tion is generally associated with idiocy, but may occur without

THE LOCALISATION OF THE LESION.

581

this complication. It is not, according to Oulmont, preceded
by apoplexy or hemiplegia, and is unaccompanied by sensory
disturbances.

(iii.) Hemiataxia.—A case has been described by Dr. Gowers
in which there was great inco-ordination of the right arm
during voluntary movement, while there was complete absence
of permanent rigidity and spontaneous spasm. The patient
had suffered from a slight attack of apoplexy followed by hemi-
plegia a year and a half before he came under observation, but
the paralysis had disappeared, a slight weakness of the arm,
leg, and face alone remaining. The ataxic movements of the
arm became exaggerated on the eyes being closed. Tactile
sensibility was diminished in the right arm, but sensibility to
pain was normal. In a somewhat similar case recorded by the
same observer the autopsy revealed "a puckered cicatrix"
passing through the left thalamus from the one side to the other.
A case in which ataxic movements occurred in the right hand is
also described by Grasset. The patient had a series of apoplectic
attacks followed by hemiplegia and a certain embarrassment of
speech. The ataxic movements were limited to the right arm,
the paralysis being more marked in the face and arm than in
the leg. At the autopsy three centres of softening were found
in the left hemisphere. The first occupied the region of the
lenticulo-striate artery ; the second was in the optic thalamus
close to its ventricular border ; and the third was found in the
thalamus close to the posterior portion of the internal capsule.

§ 741. The Hemiplegic Walk — When the muscles of the
paralysed lower extremity have acquired a certain degree of
rigidity, the patient is able to walk by the aid of a stick, even
if the voluntary paralysis of the affected side remain complete.
The patient leans towards the healthy side, but is prevented
from falling over to that side by the support of the stick ; the
pelvis and hip-joint of the paralysed side are elevated by
contraction of the abductors of the opposite thigh, so that the
weight is taken off the paralysed extremity. When the
paralysed lower extremity, say the right leg, is the active one,
the line of gravity is carried over to a slight extent to that
side; but instead of reaching the centre of the paralysed foot,

582

FOCAL DISEASES, ACCORDING TO

it remains midway between it and the end of the stick, so that
the weight of the body is maintained partly by the paralysed
lower extremity and partly by the healthy arm through the
stick. The healthy or left lower extremity is now quickly
moved forwards a step, an unusual degree of flexion of the thigh
upon the body taking place in order to avoid the necessity of
carrying the line of gravity too far to the paralysed side. The
left leg now becomes active, and the paralysed one must be
moved forwards. The manner in which this movement is exe-
cuted depends upon the degree of paralysis and of muscular
rigidity present. If the paralysis be almost complete and the
rigidity not great, the extremity is partly swung and partly
dragged round mainly by the contraction of the inward rotators
of the healthy limb. Contraction of these muscles causes the
pelvis to rotate forwards on the hip-joint of the healthy side, and
consequently the opposite hip-joint, dragging after it the para-
lysed leg, is moved forwards. This forward movement is aided
by a further elevation of the right hip -joint caused by contrac-
tion of the abductors of the opposite thigh, and sometimes by
a slight backward inclination of the trunk by means of which
the distance between the points of origin and insertion of the
flexors of the thigh on the body is increased.

If a high degree of contracture with talipes equinus be pre-
sent, the paralysed lower extremity is moved forwards much in
the same manner as has already been described in the case of
primary lateral sclerosis. When once the weight of the body
is taken off the paralysed extremity the heel becomes elevated,
and the toe during the forward movement, which takes place in
a semicircular manner, makes a characteristic scraping noise.

If tremors or choreoid movements be present in the paralysed
lower extremity, the hemiplegic walk may become modified in
such numerous ways as to render it impossible to comprise the
different varieties which may be presented in a single description.

b. Affections of the Sensory Peduncular Tract and
Optic Radiations of Gratiolet.

HEMIANiESTHESIA.

§ 742. — In cerebral hemiansesthesia the affection develops
suddenly after an attack of apoplexy, or gradually as the result,

THE LOCALISATION OF THE LESION.

583

for instance, of the progressive growth of a tumour. The
sensibility is diminished over the whole of one-half of the
body, face, and extremities, including the accessible mucous
membranes as well as the skin. The abolition of sensation
is sometimes incomplete, and then cutaneous analgesia or
thermo-anaesthesia may be present, while tactile sensibility
remains unaffected. At other times the anaesthesia of the skin
and mucous membranes is complete, and even muscular sen-
sibility and muscular sense are abolished. The patient, for
instance, does not feel deep pressure, strong contraction of the
muscles may be produced by the faradic current without
causing pain, and when his eyes are closed he is unable to
describe the position in which the affected extremities may be
placed by passive movements, and is not aware when his
attempted voluntary movements are forcibly prevented. The
patient can walk without difficulty when his eyes are closed,
but by slight pressure upon the affected side he may be easily
induced to walk in a circle while under the impression that he
is walking in a straight line.

One-half of the mucous membrane of the tongue, mouth,
and veil of the palate, and the conjunctiva of the same side,
are insensitive, but the cornea retains its sensibility.

The affected side is colder, and the prick of a pin does not
bleed so readily as on the opposite half of the body.

The cutaneous reflex actions may be abolished on the side
affected, while the deep reflexes are retained.

The senses of taste and smell are both abolished on the
affected side.

The sense of hearing is also diminished, and in some cases
there may be complete unilateral deafness.

The sense of sight is impaired but not abolished, but hemi-
opia has not been observed when the lesion is limited to the
internal capsule. The acuteness of vision may be tested in
the usual manner by Snellen's scale. There is also concentric
restriction of the field of vision, and the perception of certain
colours may entirely cease (dyschromatopsia).

§ 743. Morbid Anatomy and Physiology. — It is impossible
to separate lesions of the internal capsule and crusta from

584

FOCAL DISEASES, ACCORDING TO

those of the ganglia by which they are surrounded. Since the
days of Willis and Morgagni up to a few years ago, paralysis of
one-half of the body has been associated with disease of the
corpus striatum. This doctrine had indeed received a shock
upwards of twenty years ago, from the observations of Tiirck,
who showed that hemianesthesia of the opposite side of the
body might result from disease situated in the posterior part
of the lenticular nucleus. It was also suggested by Meynert
and Broadbent that some of the fibres of the crusta passed
upwards to reach the cortex of the brain without being in any
way connected with the basal ganglia; and Charcot, with his
usual readiness and skill in utilising the details of anatomical
research for clinical purposes, suggested, and soon proved by
observation and analysis of cases, that both hemiplegia and
hemianesthesia are caused by injury of the direct fibres which
lie between the basal ganglia, and not by lesions of the ganglia
themselves. We have already seen that the fibres of the
posterior third of the posterior segment of the internal capsule
are sensory ; that those of its middle third connect the mecha-
nisms in the cortex of the brain and spinal cord which regulate
the fundamental actions ; that those of the anterior third of the
posterior division connect the mechanisms which regulate the
specialised actions ; and that those in the knee and the anterior
segment of the capsule connect the mechanisms which regulate
the most specialised actions. Speaking broadly, it may be said
that the fibres of the middle third of the posterior segment of
the capsule are concerned in regulating the actions of the trunk,
lower extremities, and probably the general actions of the upper
extremities ; that the fibres of the anterior third of the posterior
segment are concerned in regulating the more special move-
ments of the hand as an organ of prehension, and probably also
the movements of rotation of the head and neck, along with
the associated ocular movements ; and that the fibres of the
knee of the capsule and the adjoining part of the anterior
segment of the capsule are concerned in the regulation of the
movements of facial expression, articulation, and the most
special movements of the hand, as those of writing.

Of all the arteries of the brain the lenticulo-striate artery
is, according to Charcot, the one which is most liable to rupture.

TIIE LOCALISATION OF THE LESION.

585

This artery lies, as we have seen, between the external capsule
and the external surface of the third division of the lenticular
nucleus. When this vessel ruptures, if the haemorrhage be
small, it may lodge between the external capsule and the lenti-
cular nucleus, and give rise to no symptoms (Charcot). The
vessel, however, beiDg a comparatively large one, the haemor-
rhage, as a rule, extends beyond these limits. It is sometimes
directed upwards between the external capsule and the lenti-
cular nucleus, and may then extend for a considerable distance
into the centrum ovale. Under these circumstances the fibres
of the internal capsule become ruptured at their point of emer-
gence from between the basal ganglia where they form the foot
of the corona radiata. Haemorrhages in this situation may
be so extensive as to extend upwards to the summits of the

Fig. 242.

Fig. 242 (Modified from Charcot). Vertical Section of the Brain a little behind the
Knee of the Internal Capsule, showing the effects of rupture of the lenticnln
striate artery ■ -NC, Head, and NC, Tail of the caudate nucleus; Ch
Chwama ; NL, Lenticular nucleus ; IK, Internal capsule ; Cls, CJaustrum •
h f,, ,5?°? fre1uent Position in which the lenticulo-striate artery is ruptured •
1 ' 1 ' 1 'r * ™gre881ve extension of the haemorrhage producing compression and
rupture of the fibres of the pyramidal tract (hemiplegia) ; 2, Primary focus"n
the internal capsule ; 2', 2", 2"', Successive extension of the clot

586

FOCAL DISEASES, ACCORDING TO

ascending frontal and parietal convolutions, while the cortex of
the Island of Reil is compressed by the clot, but the external
capsule is rarely ruptured. At other times the haemorrhage
is directed inwards through the grey matter of the lenticular
nucleus ; and if it be large, it must impinge upon and rup-
ture the fibres of the internal capsule, and when these fibres
give way the haemorrhage may make its way into the lateral
ventricles, then through the foramen of Monroe into the third,
and through the aqueduct of Sylvius into the fourth ventricle.

If the haemorrhage remain limited to the space between the
external capsule and lenticular nucleus, it produces no symptoms
during life; but when it makes its way into the substance of
the lenticular nucleus, or into the centrum ovale above the
nucleus, the fibres of the pyramidal tract are compressed, and
hemiplegia of the opposite side of the body results. If the
fibres of the pyramidal tract, however, remain intact, the
patient will recover more or less completely from the paralysis.
A case which came under my observation several years ago was
that of an old man who died a few hours after being knocked
down by a cab when crossing a street. The left lenticular
nucleus was completely destroyed, and its usual position was
occupied by a cyst containing serous fluid. No good history of
the case was procurable, but he was not supposed to be suffering
at the time of the injury from any form of paralysis. A still
more striking case will be subsequently described, in which both
lenticular nuclei were converted into cysts, the symptoms during
life being those of bulbar paralysis without any evidence of
paralysis of the extremities. When the haemorrhage remains
limited to the lenticular nucleus, not only does the patient ulti-
mately recover the full use of his limbs, but the apoplectic
symptoms during the attack are slight. The patient complains
of giddiness, there may be vomiting, and confusion of ideas,
but he does not lose consciousness, or the loss is transitory.
When, however, some or all of the fibres of the internal cap-
sule rupture, the larger size of the clot produces a more pro-
found immediate effect, while injury to the fibres of the pyra-
midal tract gives rise to a paralysis which remains permanent.
The degree and extent of the paralysis will, of course, depend
upon the extent of the injury done to the motor tract. It is

THE LOCALISATION OF THE LESION.

587

probable that the first form of early rigidity occurs during the
time the fibres of the tract are being stretched or ruptured by
the haemorrhage; the second form of early rigidity is again
probably caused by irritation of these fibres, caused by inflam-
matory changes in the tissues surrounding the clot ; while late
rigidity is caused either directly or indirectly by descending
degeneration of the ruptured fibres. But if the haemorrhage
make its way either between the ascending longitudinal fibres
of the corona radiata, so that a large clot forms in the centrum
ovale, or if it rupture into the lateral ventricle, profound symp-
toms of coma supervene, and the patient dies in a short time.

We have seen that the comparatively unyielding wall formed
by the external capsule directs haemorrhage from the lenticulo-
striate artery inwards, and consequently the full force of the
blood will impinge against the internal capsule at a point a little
behind its knee, or at the point where embryological considera-

Fig. 243.

Fig. 243. Horizontal Section of the Basal Ganglia and Internal Cavsulc in an
embryo of nine months. -NC, Caudate nucleus; TH, Optic thalamu s • rfv
Island of Eeil; //, ///, Second and third segments of tSl^iSnudff
ps, Sensory peduncular tract ; P, Fundamental, and P', Mixed MrhK'

fnteGraSpsulea8CiCUlU8 °f ^ * AnteS?^^ thJ

588

FOCAL DISEASES, ACCORDING TO

tions had led us to believe those fibres to pass, which connect
with each other the nervous mechanisms in the cortex and spinal
cord that regulate the movements of the hand. In haemorrhage
from this artery, therefore, the upper extremity is more paralysed
than either the lower extremity or face. Rupture of the anterior
branches of the artery may injure the anterior segment of the
capsule to a greater extent than the posterior segment, and
then facial paralysis predominates. The fibres which conduct
those impressions from the cortex which cause rotation of the
head and eyes to the opposite side probably also pass in the
anterior third of the posterior segment of the internal capsule,
and on the side of the capsule which adjoins the lenticular
nucleus, and they also must be ruptured by a moderately-sized

Fig. 244.

Fig. 244 (Modified from Charcot). Vertical Section of the Brain on a level with the
Posterior Part of the Internal Capsule, showing the effects of rupture of the
lenticulo-optic artery (hemiansesthesia). — JVC, JVC, Tail of the caudate nucleus;
NL, Lenticular nucleus ; TH, Optic thalamus ; Cls, Claustrum ; 1, Primary
focus in the posterior part of the external capsule (hemiansesthesia) ; 1', 1", 1"',
Progressive extension of the primary focus causing compression or destruction
of the internal capsule; 2, Primary focus in the internal capsule (hemianses-
thesia) ; 2', 2", 2"', Successive extension of the focus.

THE LOCALISATION OF THE LESION. 589

haemorrhage of the lenticulo-striate artery, but the conjugate
deviation which results is as usual only a transitory symptom
(§ 90). Haemorrhage of the lenticulo-optic artery is also directed
inwards against the fibres of the internal capsule by the un-
yielding walls of the external capsule, and its greatest force
impinges against the posterior half of the posterior segment of
the capsule. It is evident, therefore, that haemorrhage from
this vessel will tend to injure the sensory peduncular fibres and
the fibres of the fundamental mechanism, but inasmuch as the
muscles of the trunk are bilaterally associated, the paralysis
resulting from injury of the latter fibres will be more marked
in the leg than in any other part of the body. An analysis of
clinical records had led Dr. Hughlings-Jackson long ago to con-
clude that the form of hemiplegia in which the leg is more
profoundly affected than the arm is generally associated with
hemianaesthesia. The fibres of Gratiolet are not usually affected
in haemorrhage from the opto-striate artery, and consequently
the special senses are not always implicated in the anaesthesia.

The anterior segment of the internal capsule is frequently
injured by lesions of the head of the caudate nucleus, the
resulting hemiplegia of the opposite side being thus more
marked in the face than arm, and in the arm than leg, while
sensibility is seldom affected.

Cases are recorded of lesions of old date having been found
at the autopsy without paralytic symptoms having been present
during life (Nothnagel, Samt). In a case of this kind recently
described by Honegger there were no descending changes ob-
served in the crusta, medulla oblongata, or spinal cord, although
the fibres of the middle third of the posterior segment of the
internal capsule in the left hemisphere appear to have been in
great part destroyed.

The internal capsule may be injured by lesions of the optic
thalamus. Haemorrhage from the posterior internal optic artery,
if small, does not appear to give rise to any definite symptoms,
and certainly not to permanent paralysis. A large haemorrhage
from the vessel generally makes its way into the cavity of the
ventricle, and death results in a short time. Lesions in the
region of distribution of the posterior external optic artery are
liable to implicate the fibres of the external and posterior

590

FOCAL DISEASES, ACCORDING TO

extremity of the crusta and their continuations through the
internal capsule. The path of least resistance to the passage
of haemorrhage from the vessel appears to be upwards and
inwards ; and as the internal capsule lies below and to the
outside of the thalamus, its fibres are never injured to the
same extent by haemorrhages from this vessel as they are in
those which take place into the lenticular nucleus. Hemi-
plegia is, therefore, not a prominent feature of lesions of the
optic thalamus, and when it occurs it is seldom complete. The
sensory peduncular fibres, and the optic radiations of Gratiolet,
are very liable to be injured by lesions in the region of dis-
tribution of the posterior external optic artery, and conse-
quently complete hemiansesthesia with implication of the
special senses is a frequent symptom. When the lesion occurs
in the pulvinar, the external geniculate body is apt to be impli-
cated, and then bilateral hemianopsia of the opposite side
results. When the lesion is situated more anteriorly close to
the internal capsule, the fibres of the pyramidal tract suffer in-
jury, and hemiplegia results. The hemiplegia is usually asso-
ciated with a certain degree of hemiangesthesia, and after a
time choreiform movements are apt to become established in
the paralysed limbs. In six cases of post-hemiplegic chorea
collected by Kaymond, in which a post-mortem examination
was obtained, the lesion was situated in every instance in the
posterior part of the optic thalamus, and involved the fibres of
the internal capsule; and in two cases of pre-hemiplegic chorea
reported by him, the lesion was situated in the same locality.
In a case of pre-hemiplegic chorea reported since then by
Grasset, several lesions were found in different regions of the
hemispheres, but one of these occupied the external margin of
the optic thalamus close to the internal capsule.

The lesions which have been found to give rise most frequently
to hemichorea are yellow cicatrices, the remains of old haemor-
rhages, or softening from occlusion of the posterior external
optic artery, although choreiform movements have occasionally
been observed during the growth of tumours in this region.
It is evident, therefore, that the symptoms depend, not upon
the nature of the lesion, but on its localisation. The symptoms
do not appear to depend upon lesion of the optic thalamus

THE LOCALISATION OF THE LESION.

591

itself, inasmuch as they are never present, unless some of the
fibres of the sensory-peduncular and pyramidal tracts are
injured, nor does it even appear to be caused by injury of the
sensory fibres, since hemianesthesia with bilateral hemianopsia
may be present without being associated with choreiform move-
ments. It would seem, therefore, that injury to some of the
fibres which lie in front of the sensory peduncular tract is the
cause of hemichorea. That some of the fibres of the pyramidal
tract are always injured in these cases can scarcely be doubted,
inasmuch as the clonic are always associated with tonic spasms,
and exaggeration of the tendon reflexes, the latter symptoms
being those which are always associated with disease of the
pyramidal tract. Two probable explanations of the clonic
spasms present in these cases suggest themselves to my mind.
The first is that fibres connecting the cerebrum with the cere-
bellum are injured by these lesions, so that the normal propor-
tion between the outgoing discharges which regulate the tonic
(cerebellar) and the clonic (cerebral) actions of the body is lost.
The second is that the injured fibres all belong to the pyramidal
tract, and that those which suffer most are related to the more
fundamental and not to the more special functions, as in disease
of the lenticular nucleus. We have seen that the more funda-
mental actions are regulated from the convolutions near the
longitudinal fissure, while the more special movements are
regulated from the convolutions bordering the Sylvian fissure ;
and it is therefore manifest that the fibres which descend in
the corona radiata from the former will pass along the optic
thalamus side of the internal capsule, while those which descend
from the latter will pass on the side of the capsule next the
lenticular nucleus. The effects produced by destructive pro-
cesses in any structure whatever must differ greatly according
as the foundations or the latest-formed portions are the first to
be injured. It appears to me, therefore, that partial injury
done to the fundamental motor mechanism while the acces-
sory one is left unaffected would be very likely to cause the
phenomena of hemichorea. In such an event the usual tonic
contractions and exaggerated tendon reflexes would result from
injury of the pyramidal tract, while the apparatus ef the more
voluntary and special actions, although still uninjured, would

592

FOCAL DISEASES, ACCORDING TO

act in an irregular manner owing to the damage done to the
fundamental apparatus.

The lesions found in cases of unilateral athetosis, although
not always strictly limited to the region of the posterior external
optic artery, have often been in its vicinity. In three cases
of athetosis observed by Charcot the lesion was situated in the
posterior extremity of the optic thalamus in one, the posterior
part of the caudate nucleus in a second, and the most posterior
part of the corona radiata in a third. The lesions of all these
cases were situated in such positions that the same system of
fibres which are implicated in post-hemiplegic chorea would
be likely to suffer damage, and consequently athetosis must
generally be regarded as a minor degree of post-hemiplegic
chorea. In a case observed by Landouzy an old focus of soften-
ing was found in the portion of the lenticular nucleus which
adjoins the internal capsule. In another, observed by Gnauck,
the co-existence of sensory disturbances in the region of distribu-
tion of the fifth nerve on the side opposite to the spasmodic
movements rendered it probable that the lesion was situated
in the lateral half of the pons. It is, therefore, probable that
the lesion in athetosis may occupy different positions in the
vicinity of the pyramidal tract. The position occupied by the
lesion in all cases rendered it probable that the fibres of the
pyramidal tract are never completely ruptured, and conse-
quently there are no descending changes in the cord and no
muscular rigidity during life. The fibres of the tract are, how-
ever, likely to have suffered partial injury by being involved in
a cicatrix or other morbid change, and the impulses which pass
through them become consequently irregular.

Direct Cerebral Paralysis. — Although the paralysis of the
extremities is usually situated on the side of the body opposite
the lesion in the brain, it is occasionally situated on the same
side, and is then called direct paralysis. The most reasonable
supposition in these cases is that the pyramidal tracts do
not decussate as usual in the medulla oblongata. The usual
method of crossing is that from 91 to 97 per cent of the fibres
cross over to the lateral column of the opposite side of the cord,
while from 9 to 3 per cent pass downwards in the columns of
Tiirck of the same side. Flechsig, however, has shown that

THE LOCALISATION OF THE LESION.

593

the proportion of fibres which decussate is very variable, and
he has even found that it occasionally fails altogether. It is,
therefore, probable that the decussation may fail in cases of
direct paralysis, although this has not yet been proved by
dissection.

The lesions observed in the spastic hemiplegia of childhood
scarcely belong to the category at present under consideration,
inasmuch as they primarily involve the cortex of the brain,
while the internal capsule is only secondarily implicated. In
infantile hemiplegia the lesion is situated in the convolutions
of the motor area of the cortex. The primary lesion, consisting
probably of a local encephalitis sometimes following an in-
jury, local softening, or haemorrhage, gives rise to extensive
secondary changes. In some cases a large loss of substance has
been observed, causing various deformities of the skull when it
occurs in early life, or leading to hydrocephalus in order to fill
up the vacant space. At other times a puckered cicatrix may be
found at the seat of the primary lesion, while the hemisphere
has undergone a diffused consecutive atrophy. The fibres of
the pyramidal tract in connection with the diseased focus
undergo descending degeneration, and to it the spastic con-
dition of the paralysed extremities is either directly or in-
directly due. Bilateral athetosis appears also to be due to
partial atrophy of the motor area of the cortex, both hemi-
spheres being probably inplicated. The considerations which
favour this opinion are that the affection is either congenital or
becomes established in early infancy, that it is associated with
some degree of imbecility or idiocy, and that there are no sen-
sory disturbances.

594

CHAPTER VII.

(II.) SPECIAL CONSIDERATION OF FOCAL DISEASES,
ACCORDING TO THE LOCALISATION OF THE LESION
(Continued).

2. CORTICAL LESIONS.

a. Lesions in the Area of the Middle Cerebral Artery.

(i.) Monospasms and Unilateral Convulsions.

§ 744. Irritative lesions of the cortex are characterised by-
unilateral convulsions or monospasms. Lesions of various kinds
may cause irritation of the cortex, the most common of these
being localised meningoencephalitis, tubercle, syphilitic gum-
mata and other tumours, cicatrices of wounds and spicula of
bone, and of these the syphilitic are by far the most frequent
lesions. The tissues in the immediate neighbourhood of the
main focus of disease are maintained in a state of irritation, and
are consequently supplied by an usually large quantity of blood.
The ganglion cells of the grey substance absorb an undue supply
of nutriment, so that they discharge themselves in a sudden and
explosive manner (Hugh lings- Jackson). But we have already
seen that explosive discharges of nervous energy are followed by
exhaustion and consequent paralysis of the muscles implicated
in the convulsion, and accordingly unilateral convulsions are
often followed by temporary paralysis of the convulsed limbs.
It must be remembered that an irritative lesion is frequently
associated with a destroying one. A syphilitic gumma, for
instance, destroys the portion of the cortex in which it is
situated, while it maintains the surrounding tissues in a state of
irritation. It is not, therefore, unusual to find a certain degree
of permanent paralysis associated with unilateral convulsions.

FOCAL DISEASES.

595

Unilateral convulsions were first distinguished clinically and
their varieties accurately described by Bravais, although he did
not recognise their pathological significance. Similar observa-
tions were made by Bright and Wilks, who surmised that
these convulsions were due to local disease. The pathology
of these spasmodic affections was first clearly recognised by
Hughlings-Jackson, and it was in explanation of these convul-
sions that he first suggested the idea of the existence of motor
centres in the cortex, an idea which has been so fruitful to
pathology.

In some cases the spasm is limited to one limb or to the
side of the bead (monospasm) ; in other cases it begins in one
limb (protospasm), and extends to the other or to the head, to
the half of the body, or the convulsions may become bilateral
and generalised. Another characteristic of these convulsions is
that they are either not attended by loss of consciousness or
the convulsion begins before the patient becomes unconscious,
so that he is afterwards able to describe a motor aura.

§ 74-5. Varieties. — The following are the clinical varieties
of unilateral convulsions : —

(a ) Crural monospasm or protospasm, in which the spasms are either
limited to the leg, or begin in it, the arm being next attacked and the face
last.

(6) Brachial monospasm or protospasm, in which the spasms are either
limited to the arm, or begin in the arm, the face being next implicated and
the leg last.

(c) Facial monospasm or protospasm, in which the spasms are either
limited to the side of the face or begin in the face, the arm being next
implicated and the leg last.

(a) Crural Monospasm or Protospasm. — There are not many uncom-
plicated cases on record in which the spasms were limited to the leg, or
invariably began in the leg, and in which a post-mortem examination was
obtained. Ferrier quotes a case recorded by Broca of crural monospasm
caused by injury to the left side of the skull, which was cured by
trephining, but the exact position on the brain is not mentioned.
Charcot and Pitres quote a case from Griesinger of frequently recurring
spasm of the leg and arm. Numerous cysticerci were found in the brain,
the largest of which occupied the superior part of the ascending parietal
convolution of the opposite side. Several small cysts were found on the
frontal and parietal surface of the same hemisphere. Hughlings-Jackson
reports a case in which the fits were often limited to the leg, and always
began there. The leg became gradually weaker after each attack, and

596

FOCAL DISEASES, ACCORDING TO

finally became permanently paralysed. A tumour was found at the upper
and posterior part of the left frontal lobe, about two inches in diameter, ex-
tending from the posterior extremities of the first and second frontal con-
volutions backwards to the fissure of Rolando. In another case recorded
by the same author, the convulsions began in the left great toe, and were
often limited to the left leg. A syphilitic lesion was found at the upper
part of the ascending parietal convolution and over several of the adjacent
convolutions of the parietal lobule. Bourneville describes a case of the
hemiplegia of infancy, in which the convulsions began by tremors and
twitching in the left or paralysed leg. The cortex of the right hemisphere

Fig. 245.

was found atrophied in front of the fissure of Rolando in the superior
half of the ascending frontal, the posterior extremities of the first and
second frontal {Fig. 245), and the whole extent of the paracentral lobule.

(b) Brachial Monospasm or Protospasm. — Several cases are recorded in
which the spasm is either limited to or begins in the arm. Instances
of this kind have been recorded by Dr. Hughlings- Jackaon. In the case
of one man who suffered from repeated convulsions limited to the right
arm with subsequent paralysis, a nodule was found situated at the
posterior extremity of the first frontal convolution of the left hemisphere.
In another case, in which the spasms were almost similar to those observed
in the last nodule was found situated at the posterior extremity of

the first frontal convolution where it joins the ascending frontal. The
spasm in this case began in the shoulder and went down the arm, con-
trary, Dr. Jackson thinks, to the usual order. In a third case the spasm
invariably began in the left thumb, and a tumour of the size of a hazel-nut
was found under the grey matter at the posterior extremity of the third
frontal convolution of the right hemisphere. In a fourth case the spasms
began in the right arm, and occasionally in the right side of the face, and
the patient had suffered from a transitory attack of left hemiplegia. In the
left hemisphere adhesion was found between the dura mater and the brain,
over " the lower part of the ascending frontal and ascending parietal con-
volutions, to a trifling extent to the hinder part of the third frontal and

THE LOCALISATION OF THE LESION.

597

several of the convolutions of the upper wall of the fissure of Sylvius
behind the ascending parietal." In the right hemisphere, the side opposite
the paralysis, a mass was found behind the fissure of Rolando, but has
no bearing upon our present subject. In a fifth case temporary right
hemiplegia supervened after a unilateral convulsion. Convulsions recurred
repeatedly, beginning in the little finger of the right hand, occasionally
in the right side of the face, and always followed by slow and hesitating
speech. A syphilitic tumour of considerable size was found in the cortex
about the junction of the frontal and parietal lobes, surrounded by an area
of softening in the posterior extremities of the frontal, ascending frontal
and ascending parietal convolutions, and partly of the Island of Reil. A
case of partial epilepsy is reported by Ballet and Lalesque in which the
spasms began in the right hand. Paresis of the right arm supervened, the
right side of the face and tongue being also implicated to a slight degree
as the case progressed. Some degree of embarrassment of speech was also
present before death. At the autopsy three small hydatid cysts were
found in the cortex of the left hemisphere, one being situated about the
middle of the ascending frontal convolution, the second at the junction of
the middle and lower thirds of the ascending parietal convolution, and the
third at the posterior extremity of the second frontal convolution.

A case of brachial protospasm, caused by syphilitic disease, has been
recorded by Dr. Dreschfeld, in which I conducted the post-mortem exami-
nation, confirming the diagnosis made by Dr. Dreschfeld during life. The
attacks began "by sudden clenching of the fist, flexing of the wrist, and

Fig. 246.

pronation of the forearm of the left side, the corresponding angle of the
mouth being at the same time drawn downwards. This sudden tonic spasm
lasted for several seconds, and was then followed by a few clonic spasms of
the same extremity and a slight tremor of the arm, the patient being at the
same time agitated and pale, but perfectly conscious." The dura mater was
found adherent to the brain on the right side over the greater part of the
ascending parietal convolution and the supra-marginal lobule {Fig. 246).

598

FOCAL DISEASES, ACCORDING TO

The case of a boy, three months old, is reported by Mr. Cullingworth, who
developed cerebral symptoms somewhat suddenly nearly four months sub-
sequently to an injury to his head. The symptoms began by screaming
and elevation of temperature. A few hours later it was observed that the
left arm and hand were flexed and rigid, and this was soon followed by
conjugate deviation of the eyes to the right. The dura mater was found
thickened and adherent to the bone over a small area of the right hemi-
sphere immediately to the right of the longitudinal fissure. The cortex
underlying the adhesions was reddened and softened, the softened part
involving the upper portion of the ascending frontal convolution. A layer
of pus was found over the whole surface of both hemispheres and the
greater portion of the cerebellum.

Charcot and Lepine describe a case of partial epilepsy beginning in the
left arm in which after death a haemorrhagic focus was found situated in
the posterior part of the first right frontal convolution. In another case
of partial epilepsy beginning in the left arm, described by the same
authors, an old focus of softening was found between the first and second
frontal convolutions of the right hemisphere where they adjoin the
ascending frontal convolution ; while in another case described by them,
the convulsions began in the right arm, and a small focus of disease was
found in the superior part of the ascending parietal convolution of the left
hemisphere. A case is described by Glicky, in which the convulsions
began in the left arm, but subsequently involved the left half of the body ;
a glioma was found which had destroyed the two ascending central convo-
lutions and the paracentral lobule on the right side. Mahot reports a case
of partial convulsions beginning in the fingers of the left hand, in which a
tuberculous mass was observed imbedded in the substance of the right
ascending frontal convolution in its middle third. Berger reports the case
of a woman who suffered from convulsions of the right arm with subse-
quent weakness of the same, the convulsions after a time became general,
and the right arm was completely paralysed, while there was weakness of
the muscles of the leg and face. A sarcoma growing from the dura
mater had penetrated into the cortex of the brain over the left ascending
frontal convolution, opposite the posterior extremity of the second frontal
convolution. Burresi describes a case of partial epilepsy of the left arm
followed by paresis, and at last by complete paralysis ; a tuberculous mass
was found in the fissure of Kolando.

(c) Facial Monosi^asm or Protospasm. — The case of a French soldier is
described by Hitzig, who, two months after a bullet wound on the right
side of the head, suffered from clonic spasms followed by paralysis of the
left side of the face and tongue. An abscess was found in the cortex of
the right hemisphere situated in the inferior part of the ascending frontal
on a level with the third frontal convolution.

"Wernher reports a case in which there were convulsions of the muscles
of the face, neck, forearm, and of the extensors and flexors of the fingers,
all on the right side. The lesion was situated in the cortex of the left

THE LOCALISATION OF THE LESION.

599

hemisphere in the inferior part of the ascending frontal convolution near
the fissure of Sylvius.

The case of a woman is described by Dr. Bramwell, who, after a cranial
injury received some years previously, began to have right-sided convul-
sions. The convulsions always began in the right platysma, and were
often almost entirely confined to this muscle. A spiculum of bone was
found projecting from the inner table of the skull, and causing a limited
lesion of the inferior margin of the ascending parietal convolution {Fig.
247).

Fig. 247.

Seeligmuller describes a case of epileptiform convulsions of the right
half of the face, followed after a time by facial paralysis. At a some-
what later period the right arm became convulsed, and afterwards paralysed.
A sarcomatous tumour was found in the ascending parietal convolution,
which probably began to grow at its lower extremity and progressed
upwards.

These cases tend to show that convulsions, either limited to or begin-
ning in the face, are caused by a lesion situated in the inferior part of the
ascending frontal and parietal convolutions, the portion which adjoins the
fissure of Sylvius.

(ii.) Cortical Paralyses and Monoplegia.

§ 746. It is now well established that destructive lesions of
the cortex of the brain cause permanent paralyses. Destroying
lesions of the motor area of the cortex may be divided into (1)
General lesions, extending over the greater part of the area ;
and (2) Partial or localised lesions, limited to small portions
of it (Ferrier).

(1) General or Extensive Lesions (Hemiplegia). — Extensive

600

FOCAL DISEASES, ACCORDING TO

lesions of the cortex give rise to complete hemiplegia, similar
in all essential particulars to that resulting from disease of the
internal capsule.

A case of complete hemiplegia of the right side of six years' duration
is described by Lepine in which there was total destruction, caused by
yellow softening, of the ascending parietal convolution and partial de-
struction of the Island of Reil, ascending frontal convolution, and of the
anterior part of the superior and inferior parietal lobules of the left

Fig. 248.

hemisphere {Fig. 248). Secondary degeneration was traced in the left half
of the pons and in the left pyramid of the medulla. Duret reports a case
of complete right hemiplegia supervening in the course of a meningo-
encephalitis. A thick fibro-purulent exudation occupied the three frontal
convolutions of both sides, but it extended on the left over the ascending
frontal and ascending parietal convolutions, the lobule of the pli courbe,
and the parietal lobule.

A case of right hemiplegia with aphasia of one year's duration, accom-
panied by late rigidity of the paralysed limbs, is reported by Charcot and
Pitres, in which a patch of yellow softening was found, involving the whole
of the ascending frontal, the base of the third frontal, and the whole of
the ascending parietal convolutions, along with the inferior parietal lobule
and the two posterior digitations of the Island of Eeil in the left hemisphere.
The basal ganglia were normal. Secondary degeneration was observed in
the crus, pons, and anterior pyramid on the same side.

A case is quoted by Trousseau which occurred in the clinique of Charcot,
in which left hemiplegia existed for three months ; the ascending
frontal and third frontal convolutions, and Island of Reil in the right
hemisphere were found softened. Secondary degeneration was traced in
the crus, pons, and pyramid of the same side as the lesion, and on the

THE LOCALISATION OF THE LESION.

G01

opposite side of the spinal cord (Fig. 249). Cases of this kind might be
multiplied, but it would occupy too much space to narrate them. The
following cases are examples of hemiplegia, caused by lesions of the cen-
trum ovale.

Fig. 249.

A case of right hemiplegia, with late rigidity of the paralysed limbs,
is related by Hodgson, in which a cavity of considerable size was found in
the centrum ovale of the left hemisphere, situated between the anterior
horn of the lateral ventricle and the Island of Reil. The rest of the brain
was normal.

Dussaussay describes a case, quoted by Pitres, of right hemiplegia

Fig. 250.

with conjugate deviation of the eyes to the left. A cavity was discovered
in the centrum ovale of the left hemisphere, containing dark, coagulated
blood (Fig. 250). The cavity was limited internally by the grey substance

602

FOCAL DISEASES, ACCORDING TO

of the paracentral lobule, superiorly and externally by the grey substance
of the ascending frontal and parietal convolutions ; in front it extended
to the prse-central fissure, and behind to the posterior border of the ascend-
ing parietal convolution ; while it was separated inferiorly from the corpus
striatum by a layer of white substance lcc. in thickness.

Dr. Ringrose Atkins has recorded a case of right hemiplegia due to
embolism, in which, in addition to a patch of softening at the lower
extremity of the ascending parietal convolution {Fig. 251), there was a

Fig. 251.

focus of softening two inches in diameter in the centrum ovale, extending
from a point 2£ inches behind the apex of the left frontal lobe to a point
3£ inches outward to the apex of the occipital lobe. The basal ganglia
were normal.

(2) Partial or Localised Lesions of the Motor Area of the

Cortex— Monoplegice.

(a ) Crural Monoplegia. — The recorded cases of disease of the cortex in
which the paralysis was limited to the leg are not numerous. A sufficient
number are reported to render the existence of a cortical centre for the
regulation of the movements of the lower extremity more than probable,
even from clinical evidence alone and in the absence of the more elaborate
proof afforded by experiment on animals.

Loffler describes the case of a Danish corporal, who was struck by
a bullet at the superior and posterior extremity of the left parietal bone,
close to the sagittal suture. The right leg was immediately paralysed, and
the right arm on the seventh day after the accident. On trephining,
recovery took place, the arm being first restored and then the leg. In
another case reported by the same author, fracture of the summit of the
right parietal bone was followed by paralysis of the left leg.

The case of a woman, aged 76 years, is reported by Oudin, in which
there was paralysis with contractures and arrest of development of the

THE LOCALISATION OF THE LESION.

003

right lower extremities, dating from the age of nine and a half years, and
following a fall. At the autopsy the median parts of the superior surface
of the hemispheres were found to present a remarkable asymmetry. The
posterior extremity of the first frontal and superior extremity of the
ascending frontal convolution were remarkably atrophied on the left
hemisphere, while the corresponding parts of the right hemisphere were
normal aud of comparatively large size. The superior portions of the
ascending parietal convolutions were atrophied on both sides, although
the atrophy in the left hemisphere was more pronounced than in the
right. The anterior extremity of the superior parietal lobule was also
involved in the atrophy on the left side {Fig. 252) .

Fig. 252.

Dr. Haddon, of Manchester, records a case in which paralysis remained
limited to the left leg for five months, but after a time the left arm also
became paralysed. After death a tumour three inches in diameter was
found connected with the dura mater, situated to the right of the middle
line, compressing the subjacent hemisphere, and destroying the upper ex-
tremities of the ascending frontal and parietal convolutions, as well as
the postero-parietal and paracentral lobules {Figs. 253 and 254). The case
of a man, set. 40 years, is reported by Dr. Ferrier, in which the symptoms
of general tuberculosis were complicated by monoplegia of the left lower
extremity. The paralysis was strictly limited for four days to the left leg,
but subsequently extended to the left arm. The patient died a month
subsequently to the appearance of the paralytic symptoms, and at the

604

FOCAL DISEASES, ACCORDING TO

autopsy the pia mater over the upper margin and internal aspect of the
right hemisphere on both sides of the fissure of Rolando was merged into
a caseous mass, which could not be removed without tearing the cortical
substance. The lesion occupied the quadrilateral lobule on the internal

Fig. 253.

aspect of the hemisphere, and the upper extremities of the ascending
parietal and frontal convolutions on its superior and external aspect, the
portion of the cortex implicated corresponding to the areas marked 1 and 2
on the monkey's brain {Figs. 230 and 231).

Fig. 254.

THE LOCALISATION OF THE LESION.

GO")

(b) Bncchio-crural Monoplegia. — Paralysis of the leg and arm are
frequently associated iu disease of the cortex. Charcot and Pitres de-
scribe a case of paralysis with rigidity of the limbs of three years'
duration, in which a patch of softening was found at the upper extremity
of the fissure of Rolando on the convex surface of the right hemisphere

Fig. 255.

(Fig. 255). Hughlings-Jackson reports a case of paralysis of the left ex-
tremities caused by a glioma situated in the superior part of the fissure
of Rolando, and comprising the ascending parietal convolution and the

Fig. 256.

parietal lobule. A larger number of examples of brachio-crural monoplegia
resulting from cortical disease might be quoted, but these must suffice.
Pitres describes a case of paralysis with unilateral convulsions of the

G06

FOCAL DISEASES, ACCORDING TO

left extremities in which a focus of softening was found, not in the cortex,
but in the centrum ovale, immediately beneath the posterior extremity
of the first frontal convolution {Fig. 256, L), and extending backwards
underneath the superior parietal lobule.

(c) Brachial Monoplegia. — A case of paralysis of the left arm is de-
scribed by Pierret in which a centre of softening was found in the cortex
of the right hemisphere at the point where the second frontal joins the

Fig. 257.

ascending frontal convolution (Fig. 257). Boyer records a case in which the
arm and leg became suddenly paralysed, the paralysis of the arm alone
remaining permanent. Death took place five years subsequently to this
attack, and a patch of atrophy was found on the right hemisphere in the
ascending frontal and parietal convolutions, with an extension of the
lesion to the temporo-sphenoidal lobe.

A case of paralysis of the right hand and arm is reported by Bingrose
Atkins supervening a few days before death in a patient suffering from
general paralysis. The cortex was softened in the middle of the ascending
frontal and parietal convolutions, the lesion also extending backwards
along the anterior edge of the supra-marginal gyrus as shown in Fig. 258.

Fig. 25S.

THE LOCALISATION OF THE LESION.

007

Decaisne has collected a large number of cases of brachial monoplegia?,
but it would occupy too much space to quote more cases at present.

It may be observed in passing that the central convolutions of the oppo-
site hemisphere have been fouud atrophied in cases of long-standing
amputation (Chuquet, Boyer). The results obtained have not, however,
been very definite. Dr. Gowers found in a case of congenital absence of
the left hand the middle part of the ascending parietal convolutions in the
right hemisphere distinctly smaller than the corresponding convolutions
in the left, and a somewhat similar case has been recorded by Bastian.

(d) Brachio-facial Monoplegia. — Paralysis of the face and arm are not
uncommonly associated. When the left hemisphere is the seat of the
lesion, these cases are usually associated with aphasia. Dieulafoy records
a case of paralysis of the face and arm in which the autopsy revealed a
haemorrhagic focus, the size of a nut, situated in the ascending frontal con-
volution on a line with the third frontal convolution. Troisier mentions a
case of paralysis of the arm and face in which tubercular granulations
and congestion were found immediately
posterior to the third frontal convolu-
tion. Landouzy describes a case of slight
paralysis of the inferior facial muscles and of
the arm caused by a spot of tubercular
meningitis occupying the inferior part of
the fissure of Rolando, and the inferior half
of the two ascending convolutions. Pitres
quotes from Anton Frey a case in which there
was paresis of the left arm and of the left
side of the face; the autopsy showed a focus
of softening in the medullary fibres at the
junction of the middle frontal with the
ascending frontal convolutions (Fig. 259).

(e) Facial Monoplegia.— Facial paralysis of cerebral origin is generally
complicated by aphasia or paralysis of the arm, but a few uncomplicated
cases of facial paralysis from diseases of the cortex have been observed.

Fig. 259.

Fig. 260.

G08

FOCAL DISEASES, ACCORDING TO

Charcot and Pifcres describe a case of apoplexy followed by left hemi-
plegia and rigidity of the limbs. The rigidity disappeared after a time and
the paralysis became limited to the lower facial muscles. An extensive
area of softening was found in the cortex of the right hemisphere, invading
the third frontal, the lower extremities of the ascending frontal and
parietal convolutions, and a large extent of the parietal and temporo-
sphenoidal lobes of the Island of Keil {Fig. 260). Although the cortical
lesion in this case was so extensive, it will be seen that disease of the inferior
extremities of the ascending convolutions was the important lesion so far
as the motor area is concerned. Hitzig relates the case of a soldier who
received a bullet-wound on the right side of the head and became affected
two months subsequently with clonic spasms in the left side of the face,
followed by paralysis of those muscles and of the left half of the tongue.
After death an abscess was found in the ascending frontal convolution
between the prae-central fissure and the fissure of Rolando, corresponding
to the seat of injury {Fig. 261).

Fig. 261.

A case of left hemiplegia is reported by Dr. Gowers in which gradual
recovery took place, with the exception of marked paralysis of the inferior
facial muscles. At the autopsy a hemorrhagic extravasation was found
in and beneath the upper half of the prae-central sulcus which had passed
into the substance of the adjoining convolutions, consisting of the posterior
extremities of the middle and superior frontal and corresponding part of
the ascending frontal of the right hemisphere. A large number of cases
might be cited in which right facial paralysis existed, associated with
aphasia, and in which the lesion was situated at the junction of the third
frontal with the ascending frontal convolution of the left hemisphere. The
case of a woman, aged 71 years, is reported by Ballet, who had a slight
attack of apoplexy without loss of consciousness. The permanent symptoms
consisted of paralysis of the left half of the face and of the tongue. There
was also slight feebleness of the left upper extremities, but the lower was
unaffected. There were no sensory disturbances. Towards the evening of

THE LOCALISATION OF THE LESION.

609

the same day the head and neck became deviated to the right and the
paralysis of the left arm became more marked. Death took place from
coma four days subsequently to the beginning of the attack, and at the
autopsy a ha>niorrhagic focus, of the size of a large nut, was found in
the inferior part of the ascending frontal convolution {Fig. 262). The in-
ferior frontal and inferior parietal fasciculi of the white tissue were partially
destroyed, but the basal ganglia were normal.

Fig. 262.

(/) Unilateral Oculo-motor Monoplegia. — It has already been mentioned
that conjugate deviation of the eyes and rotation of the head and neck are
frequent symptoms both of convulsions and of hemiplegia, and that the
deviation in the former is directed away from, and in the latter towards
the hemisphere in which the lesion is situated. In the brain of the
monkey, Ferrier localises a centre {Fig. 232, 12) in the posterior extremity
of the second frontal extremity, irritation of which causes elevation of the
eyelids, dilatation of the pupils, conjugate deviation of the eyes, and
turning of the head to the opposite side ; while, on the other hand,
extensive movements of the eyeballs, along with associated movements of
the head and neck, result from irritation of the supra-marginal and
angular gyri (Fig. 232, 13, 13').

A case is reported by Chouppe which appears to show that the centre
for the production of conjugate deviation of the eyes and rotation of the
head and neck is situated in the posterior extremity of the second frontal
convolution. The case as quoted by Landouzy was that of a young
man, 19 years of age, who presented the ordinary symptoms of tubercular
meningitis, the most striking being a rotation of the head and eyes to the
. right without any other paralysis. After death a superficial focus of
disease, of the size of a franc piece, was found on the posterior extremity
of the middle frontal convolution in the left hemisphere. Other lesions
were found in the superior and lateral part of the sphenoidal lobe of the
right hemisphere. Landouzy thinks that the deviation of the eyes was
caused by an irritative lesion of the posterior extremity of the second
frontal convolution, but it must be remembered that the lesion in the
N N

CIO

FOCAL DISEASES, ACCORDING TO

superior part of the sphenoidal lobe was close to the angular gyrus, and it
is probable that the deviation was due to a destroying lesion in this area.

The case of a child, aged five months, is mentioned by Ferrier, on the
authority of Dr. Carroll, of New York, in which a fracture of the skull
was produced by a fall. When Dr. Carroll saw the patient, the head was
rotated to the right, its range of motion never extending to the left of
the middle line ; the eyes, when at rest, were turned to the right, but could
be voluntarily moved almost to the middle line; pupils, perhaps, a little
dilated, but responsive to light ; upper lids elevated. There was a fracture
in the right parietal region, and a linear fracture could be detected in the
parietal bone, about midway between the squamous and sagittal sutures,
and intersecting a vertical line drawn upwards from the auditory meatus.
The position of the fracture was, as pointed out by Ferrier, such as might
coincide with injury of the posterior extremity of the second frontal con-
volution, the lesion being doubtless of a paralytic nature. It must, how-
ever, be admitted that these two cases are not of themselves sufficient to
prove the existence of a centre for the rotation of the eyes situated in the
middle frontal convolution.

Strong evidence has indeed been recently brought forward by Grasset
to show that when conjugate deviation of the eyes is caused by disease of
the cortex, the lesion is situated in the supra-marginal and angular gyri.
He reports a case of left hemiplegia with conjugate deviation directed to
the right, in which the lesion consisted of disease of the pli courbe of the
right hemisphere (Fig. 263). Liouville describes a case of right unilateral

Fig. 263.

convulsions in which the head was strongly turned towards the right.
The lesion, which consisted of tubercular meningitis, was situated on
both sides of the horizontal limb of the fissure of Sylvius on the left
hemisphere.

Sergiu reports a case of left hemiplegia with contracture of the muscles
of the right side (probably paralysis of the muscles of the left side) of the
neck. The lesion consisted of a meningo-encephalitis in the right middle

THE LOCALISATION OF THE LESION.

611

lobe at the level of the superior part of the fissure of Sylvius. Charcot
and Pitres mention a case reported by Samt, in which there was right
hemiplegia, while the head and eyes were deviated to the left. A focus
of softening was found situated upon the parietal lobe, not quite reaching
the ascending frontal convolution in front, bounded posteriorly and in-
feriorly by the posterior extremity of the parallel fissure, and passing
beyond the interparietal fissure superiorly, but not quite reaching to the
2reat longitudinal fissure. These cases, although many more might be
added, will suffice to show the importance, with regard to conjugate
deviation of the eyes, of the convolutions which border the posterior
extremities of the Sylvian and parallel fissures.

Many cases are recorded in which conjugate deviation of the eyes was
oaused by disease of the centrum ovale, and in these the lesion was, as a
rule, situated between the internal capsule and the supra-marginal and
angular gyri. ProVost reports a case of right hemiplegia with rotation
of the head and eyes to the left. A haemorrhagic focus was found in the
posterior part of the parietal lobe of the left hemisphere. In another case
reported by the same author right hemiplegia, with rotation of the head
and eyes to the left, was caused by a sarcoma, of the size of a pigeon's
egg, situated in the centrum ovale behind the fissure of Rolando, and
along the longitudinal fissure.

It would appear that disease in the neighbourhood of the angular gyrus
and supra-marginal lobule produces at times paralysis of the levator pal-
pebrae superioris of the opposite side, wi thout the other muscles supplied
by the third nerve being implicated (Landouzy).

Lesions may occur in the cortex of the brain in the area of distribution
of the middle cerebral artery without being attended by paralysis. Boyer
maintains that there are two " neutral " zones in the area, the one occu-
pying the superior parietal lobule, and the other the anterior part of the
precuneus and a part of the gyrus fornicatus. A case is reported by Dr.
Ringrose Atkins, in which there was a superficial erosion of the cortex on
the postero-parietal lobule of the left hemisphere without motor disturb-
ance having been present during life. I would suggest that the neutral
zones of Boyer are associated with centrifugal fibres connecting the cortex
of the brain with the cerebellum. Other cases are recorded in which the
cortical motor centre of the leg was found diseased at the autopsy, yet in
which the leg on the opposite side either had never been paralysed or had
recovered. It is probable that in such cases the movements of both lower
extremities were regulated from one hemisphere, the one on the side
opposite the lesion receiving its impulses through commissural fibres in
the spinal cord.

The motor area of the cortex may be compressed by very large tumours
without paralysis being produced. In the Pathological Museum of the
Owens College there is a preparation, presented by Mr. Windsor in 1877,
of a sarcomatous tumour, about the size of the closed fist, which grew
from the dura mater over the vertex, and near to the falx cerebri. The

612 FOCAL DISEASES, ACCORDING TO

underlying hemisphere was compressed and flattened, the motor area of
the cortex being involved, but the patient had no paralytic symptoms
during life. Two cases of a more or less similar kind have been recently
described by Pitres.

Sensory Disturbances. — It has been maintained by Tripier that lesions
of the cortical motor area of the brain are sometimes attended by
hemiansesthesia as well as paralysis of the opposite side of the body,
tactile sensibility being specially affected. He adduces in favour of this
opinion some experimental evidence, and reports of seven clinical cases
in which more or less of hemiplegia was associated with hemiansesthesia,
the lesion in all of them being found limited to the motor area of the
cortex of the hemisphere opposite to the side affected. But hemi-
ansesthesia so frequently results from functional disturbances of the
brain that it would be somewhat hazardous to conclude from these cases
alone that the lesion of the motor area of the cortex was the cause of the
loss of sensibility. Several cases are collected by Nothnagel to show
that diminution of the muscular sense is not unfrequently associated
with motor paralysis from cortical disease. He thinks that the cortical
centres of the muscular sense lie near to, although they are not identical
with, the motor centres.

Yaso-motor and trophic disturbances, consisting of elevation of the
temperature of the paralysed limbs and acute bed-sore, have been
observed in cases of disease of the cortex of the brain, but they do not
possess any value as localising symptoms.

(iii.) Affections of Sfeech feom Cobtical Dtsease.

§ 747. The disorders of speech which are liable to occur in
cortical disease constitute one of the most complicated problems
of neurology; and before proceeding further, it is desirable to
limit our subject so as to separate disorders of speech due to
disease of the cortex of /the brain from other affections of the
nervous system that may resemble them. Language, taken in
its widest sense, consists of the various means by which animals
indicate mental states to one another. Mental states may be,
as we have seen, divided into feelings, cognitions, and volitions.
In one sense language may be said very often, if not always, to
indicate volitions ; but inasmuch as volitions are practically
always determined by what are called motives, or in other words
by the feelings and cognitions, the language of volitions merges
itself into that of the other two mental states. Language may
therefore be divided into that of the feelings or emotional
language, and that of the cognitions or intellectual language
or speech.

THE LOCALISATION OF THE LESION.

C13

But the division between the language of the emotions and
speech is by no means clear and trenchant. When a man
delivers an oration, for instance, only a small part of what he
utters is speech. All the variations of tone, the melodious
voice, the graces of attitude and gesture, the charm of elegant
and rhythmical language, and the thousand other ways by which
a great orator knows how to sway and influence his audience,
belong to emotional and not to intellectual language. Similar
remarks apply to written language. The pleasure we derive
from looking at a clearly-printed volume, and especially from
looking at an illuminated text, the pleasure derived from
looking at a well-executed picture rather than at a diagram,
the methods, as accent, italics, and notes of exclamation,
by which inflection and emphasis and wonder are indicated ;
the rhythm of metrical language, and the diction and imagery
of poetry belong to emotional language. The languages of
emotional and of intellectual gesture are also by no means readily
separated. The gestures of those who retain the full use of
spoken and written language are in great part indicative of the
feelings, but that gesture can be made subservient to intel-
lectual expression is shown by the importance it assumes in the
intellectual training of the deaf and dumb.

Language is the instrument of the social state, and that it
may be the means of intercommunication between animals it
possesses to each a subjective and an objective value, or fulfils
an impressive and expressive function. Each individual of a
social community, in order to become an effective member, must
be able to feel or comprehend the mental states of the others
from watching their gestures and listening to their various
vocalisations, and must also be able by his gestures and vocalisa-
tions to render his own mental states intelligible to the others.

The subjective or impressive function of language, or rather
of speech, with which we are here more immediately concerned,
may be subdivided into receptive and regulative functions.

The receptive department is represented structurally by the
various peripheral sense-organs and the centripetal fibres, or cells
and fibres, which conduct impressions made upon the former to
the cortex. Complete loss of speech from disease of the receptive
apparatus is unknown.

614

FOCAL DISEASES, ACCORDING TO

The vocal speech of a person born blind is almost entirely
unaffected either in its subjective or objective aspects, while
the patient may, by the device of raised letters, be taught to
understand written language. The deaf mute is taught both to
understand and to give expression to a complicated speech by
gesture ; and in recent times such patients have been taught to
use their vocal organs for expression in speech, while they are
made to understand the vocal speech of others by closely ob-
serving the movements of the muscles of articulation.

The remarkable case of Laura Bridgeman, who became blind and deaf
in her second year, while her sense of smell and taste were also very
deficient, shows how much careful training may do in developing language
and thought through the sense of touch. This girl was taught by Dr.
Howe, of Boston, who affixed on a number of common objects labels on
which the name of the article was written in raised characters. After she
had learnt to associate each label with its object, a number of separate
labels were put in her hand, and she was then encouraged to place each
label on its corresponding object. After a time the separate letters were
placed in her hand, and she was then taught to put them together so as to
form the names of common objects. " Up to this," says Dr. Howe, " the
proceeding was only a mechanical one, and the result was about as great
as if one had taught a number of tricks to a clever dog. The poor child
had sat there in mute astonishment, and patiently, imitated everything
that was performed before her. But now the matter seemed to dawn upon
her in its true light, her understanding began to exercise itself, she noticed
that she now possessed the means of arranging for herself symbols of some-
thing that lay before her mind, and of showing this to another mind ;
immediately her countenance beamed with human reason ; she could no
longer be compared to a parrot or dog ; the immortal intellect now seized
greedily upon this new bond of union with other intellects ! I could almost
point out the moment at which this truth dawned upon her and poured
light over her whole face."'

The structural counterpart of the regulative function consists
of that part of the cortex of the brain in which the centripetal
impulses are reduced to such order as is necessary to render
them the correlatives of the cognitions. Now, the cognitions,
as we have seen, express the relations between our feelings, and
all cognitions must be expressed by propositions. The mode of
expression may not always assume a distinct propositional form,
but it must at least possess a propositional value if it convey
distinct knowledge. If I repeat the word " orange " in the
hearing of another, it may, or may not, convey to him distinct

THE LOCALISATION OF THE LESION.

615

information; but. if any information be imparted, the word
must convey to the listener the idea that the object named
"orange" belongs to a class of objects already known to him
under that name, and the word in this sense possesses the value
of a distinct proposition. If the listener has never had any
experience of the object named "orange," it is clear that the
utterance of the name will convey no meaning; but if he has
had experience of other fruits and of colours, distinct information
may be conveyed to him with regard to the object by saying
" an orange is a yellow fruit." The listener will be able to
associate the general properties of fruit and a distinct colour
with the word in future, but the information has been im-
parted by means of a formal proposition. The activity of the
regulative cortical centres of speech have for their functional
correlative the arrangement of the presentative and represen-
tative cognitions into the form of distinct mental propositions.

The objective or expressive function of speech may be sub-
divided into emissive and executive departments.

The emissive department is represented structurally by that
organisation in the cortex of the brain in which the regulative
impulses are finally co-ordinated before being conducted to the
executive department.

The executive department is represented structurally by
groups of nerve cells in the central grey tube, and by the
nerves and muscles concerned in vocalisation, articulation,
the manual operations of writing, and various gestures. Com-
plete loss of speech from disease in the executive structure
is most unusual. The patient, for instance, may lose his
voice in different diseases of the larynx, but he can still arti-
culate; he may lose both voice and articulation in bulbar
paralysis, but is generally able to make known his wants in
writing, and when unable to write from want of previous
education he can make his ordinary wants known by gesture.

Our further remarks must be limited to the derangements of
speech caused by disease of the cortex of the brain. These
consist of disorders of the regulative department of the im-
pressive function, and of the emissive department of the
expressive function; and as the latter is probably the simpler
of the two, we shall deal with it first.

GIG

FOCAL DISEASES, ACCORDING TO

§ 748. (a) Loss or Impairment of the Emissive department
of the Expressive faculty of Speech while the Impressive
faculty is unaffected. (Ataxic Aphasia — Agra/gMa —
Amimia.)

In cases of this kind the patient is 'unable to communicate
his thoughts by words or by writing, while his intellectual pan-
tomime is impaired. He can often utter words, but these may not
possess any intellectual value ; in the words of Dr. Hughlings-
Jackson the patient is speechless but not wordless. The words
which the patient can utter, as a rule, continue the same in the
same patient — " recurring utterances." Or the patient may
under excitement swear, or even utter a phrase appropriate to
the surrounding circumstance, such as " Good-bye," when a
friend is leaving. It will be readily seen that the " recurring
utterances" such as " Yes" or " No," which are repeated on all
occasions whether appropriate or not, do not possess any intel-
lectual value, while of the occasional utterances swearing is a
purely emotional expression, and even the phrase " Good-bye"
must be regarded as expressing a state of mental regret rather
than a purely intellectual appreciation of the surrounding condi-
tions. In some cases, in addition to the usual recurring utter-
ances of " Yes " and " No," the patient repeats such phrases as
"Come on to me" (Jackson), or "I want protection" (Paget). The
man whose recurring utterance was "Come on to me" was a rail-
way signalman, and had been taken ill on the rails in front of his
box, while the man who could only say " I want protection" had
his left cerebral hemisphere injured in a brawl. Dr. Hughlings-
Jackson makes the very probable supposition that in these
cases the recurring utterance constituted the last words spoken
or which were in a state of mental preparation for utterance
when the damage occurred to the brain. It is not improbable
that words uttered or about to be uttered during a period
of great excitement might leave permanent traces which
would render them liable to be subsequently uttered as inter-
jectional phrases during emotional states. That all these words
and phrases must be regarded as expressive of emotional rather
than intellectual states is shown by the fact that the patient is
frequently unable to repeat his favourite oath or his formula

THE LOCALISATION OF THE LESION.

617

of leave-taking, or perhaps " Yes " or " No" when asked to do
so (Broadbent).

The patient, on the other hand, understands all that is said
to him, and remembers what is read to him or what he
reads himself. His articulatory actions are well performed, and
during eating and swallowing his vocal organs act normally,
and he may sing, laugh, smile, and frown as usual. He will
point to objects named and recognise drawings of them, pro-
vided they were known to him before his illness. He is able
to play at cards and other games, and recognises handwriting.
The few words which the patient can use, as yes or no, may be
uttered with such variations of tone and gesture as to indicate
when he is angry or joyful. His use of words is, in accordance
with Mr. Herbert Spencer's theory, more akin to song than to
speech, and belongs rather to emotional than to intellectual
language.

So far we have considered the cases of those patients who are
completely deprived of the power of expressing intellectual
language while retaining the power of understanding it, but we
must now turn our attention to those lesser grades of ataxic
aphasia in which the patient still retains the use of a few words
or phrases of real speech value. We have seen that most
aphasics use words in an interjectional sense, and when excited
oaths or phrases as " God bless me " may be uttered, but
these also must be regarded as compound interjections and as
purely indicative of emotional conditions. Besides the interjec-
tional use of words and phrases, the patient may occasionally
utter a word or phrase which is evidently equivalent to a
distinct proposition. He may, for instance, retain the full
use of the words "yes" and "no," and even when he uses " no"
to express assent as well as dissent, he may be able by the
aid of pantomime to indicate in which sense he intends the
word to be understood. Dr. Hughlings-Jackson mentions the
case of a woman who could only utter the phrase " Yes, but
you know," who was once heard to say " Take care !" when a
child was in danger of falling, but could not repeat the phrase
when asked to do. It cannot be denied that this utterance
possesses an intellectual element, inasmuch as it is an appro-
priate admonition to a person in danger of falling. It must,

618

FOCAL DISEASES, ACCORDING TO

however, be remembered that the phrase, although appropriate
to the occasion, was uttered under circumstances calculated to
induce alarm and excitement, and the same words had probably-
been frequently repeated under similar circumstances. In the
slighter defects of speech the patient can talk, but uses a word
kindred in its meaning with the one intended, as " worm-
powder" for " cough-medicine," or in its sound, as " parasol" for
" castor-oil" (Jackson).

(b) Loss or Impairment of the Regulative department of
the Impressive faculty of Speech, while the Expressive
is either unaffected or only secondarily implicated.
(Amnesic Aphasia.)

(1) Loss of Memory of Names or Nouns. — In many cases
of loss of memory for words the names of things are forgotten,
while the memory for dates, events, and the relations between
these may remain good. Dr. Broadbent mentions the following
case : — An old gentleman, after very slight right hemiplegia,
could give long answers fluently, and volunteer statements, so
long as the phrase did not contain a noun.

" Oh, yes ; I am much better than when you last saw me." " I shall

be 73 on the three — four when he confused himself in trying to find

the word December. He could not name a hand when told to do so, but
in his effort something like a leg was once heard. This gentleman's
memory of facts, events, dates, and faces is very good.

The patient is often enabled to supply the want of a noun
by a paraphrase, as in the following case, quoted by Kussmaul
from Bergmann : —

" A hind, 40 years of age, was unconscious for four weeks after a
severe injury of the head ; he regained his recollection of things and
places, but his memory for names was lost. The nouns had disappeared
from his vocabulary, but he still had command of the verbs. A pair of
scissors he called that with which one cuts ; the window, that through
which one sees, through which the room is illiuninated, &c. He had
forgotten most of his songs and prayers. He recovered subsequently."

Sometimes the initial consonants of words are left out of
words in speaking and writing (Schlesinger), while in a case
recorded by Graves the sight of persons and objects merely
suggested the initial consonants of their names, the rest of the

THE LOCALISATION OF THE LESION.

G19

name not being recalled until the corresponding written word
met the eye.

" A man, 56 years of age, after an apoplectic attack, lost his memory
for proper names and substantives in general, with the exception of
their first letters, although the power of speech was not impaired in
other respects. He prepared for himself an alphabetically arranged
dictionary of the substantives required in his home intercourse, and when-
ever it became necessary for him to use a noun he immediately looked it
out in his dictionary. When he wished to say ' Cow,' he looked under C.
As long as he kept his eye upon the written name, he could pronounce it,
but a moment afterwards he was unable to do so."

(2) Inability to Express the Relations between Things. — Tu
another form of amnesic aphasia the names of persons and
things are more or less remembered, but the memory of words
indicative of relations and attributes is impaired.

In the case of a somewhat complicated disorder of speech mentioned
by Dr. Broadbent the patient could only say : " Brother, brother — New
York — America, two brothers in America — letter." This patient was,
therefore, able to recall the names of the persons and places intended, but
could not express the relations between them so as to construct a sentence.

(3) In another disorder of the receptive faculty of speech the
patient is unable to name any object which he sees, or to read
a single letter, although he may converse fluently and write
correctly (word-blindness — word-deafness). A case related by
Dr. Broadbent is a remarkable example of this affection.

An intelligent man, 59 years of age, after an acute cerebral attack,
lost completely the power to read printed or written words. He was
also unable to recall the name of the most familiar object presented
to him. This man could, however, converse fluently, his vocabulary was
large, and his words well chosen and arranged, although he occasionally
forgot the names of streets, persons, and things. He could also write
easily and correctly both from dictation and spontaneously. He died from
an extensive haemorrhage into the left temporal lobe, with rupture into
the lateral ventricle. Two foci of softening of older date were observed,
one being situated in the temporo-sphenoidal lobe beneath the posterior
end of the parallel sulcus, and the other higher up underlying the angular
gyrus, and between it and the point where the descending horn of the
ventricle is given off.

(4) In a fourth form of amnesic aphasia the patient appa-
rently fails to comprehend written or spoken language, and seems
to be unconscious that his speech, which consists of mere jargon,

620

FOCAL DISEASES, ACCORDING TO

is unintelligible to others. The following brief abstracts of two
cases described by Dr. Broadbent are good examples of this
condition : —

A man, aged 60 years, who had previously been a good talker and
great reader, suffered, after a fit of some kind, from a peculiar affection of
speech, paresis of the right side of the face but no hemiplegia. His speech
was a mere inarticulate jargon. When asked a question he would make a
brief reply as if he understood and answered ; the modulation of the
voice and the emphasis were perfectly natural, and corresponded with the
facial expression and gestures, but, as a rule, there was not the least sem-
blance to words in what he said. His replies were often so suitable in length
and emphasis that it might have been supposed that he had comprehended
the question. When, however, he was told to do anything, it was seen that
he did not understand the simplest phrase. He sat up in bed once or twice
when required to do so, but as this was not made a test question there
would be other indications of what was wanted, and he was extremely ready
in comprehending signs. When told to give his hand he invariably put out
the tongue. A letter addressed to him at the hospital being handed to him,
he took it, appeared to read the name and address, and put it down again.
Not attempting to open it, a piece of paper having " Give me your hand "
written upon it was handed to him. He took it, held it so as to get a good
light on it, and then having apparently read it laid it aside without giving
his hand, though asked to do so by word of mouth as well as in writing.

The patient died somewhat suddenly, and at the autopsy a large focus
of softening was found in the left hemisphere, limited to its posterior half.
Part of the supra-marginal lobule was yellow in colour, shrunken in
volume, and soft. This condition extended upwards and backwards to
within about half an inch of the longitudinal fissure just in front of the
external parieto-occipital fissure, involving, therefore, the postero-parietal
lobule. The morbid change implicated the angular gyrus, and nearly
reached the occipital lobe ; the adjacent parts of the temporo-sphenoidal
lobe, the posterior end of the infra-marginal, and parallel gyri were sofc,
but not wasted or discoloured on the surface.

The affection of speech in the following case reported by
Dr. Broadbent is more complicated than that in the case just
described.

The patient was a well-educated and intelligent young mau, who had
contracted syphilis eight years previous to the date of the report. About
a fortnight before his admission into St. Mary's Hospital he was suddenly
seized with hemiplegia and loss of speech. He appeared to understand
all that was said to him, but could not answer questions at first, although
after a few weeks he improved so much as to be able to reply to questions
requiring brief and simple answers. He was, however, unable to give a con-

THE LOCALISATION OF THE LESION.

621

nected account of anything requiring more than a few words. H is method
of correcting an erroneous statement which had been made that he woke
up from sleep paralysed and speechless was as follows : " No— evening,
evening— put down my cigar, smoking, smoking not a quarter of an hour-
all at once "— iudicatiu g by gestures the loss of power in the limbs and
adding—" Couldn't speak." He lost at first all knowledge of numbers, and
could not tell how many 2 and 2 made ; but by practice he could in a few
weeks multiply by 2 and 3 up to 12.

When a table, glass, inkstand, and violets were pointed out to him, he
was unable to name them, nor could he name his gloves, hat, or a pen.
He named, however, some objects, such as his hand and the fire. He perused
his newspaper regularly, and with all the marks of intelligent interest.
He understood it also, for he went to the sister in a state of great excite-
ment to tell her of the failure of a firm with which he had business rela-
tions, carrying the paper in his hand, and pointing out the announcement ;
and he could always find a given paragraph, when asked to do so as a test.
When, however, he was asked to read aloud, the result was gibberish. The
following passage was selected : — " You may receive a report from other
sources of a supposed attack on a British Consul- General. The affair,
however, is utterly unworthy of consideration. No outrage was even
intended, and the report was due to misrepresentation of the facts. The
Odessa line is again working properly." It was read slowly, and in a
jerky manner, as nearly as it could be ta.ken down thus : — " So sur wisjee
coz wenement ap ripsy fro fruz fenement wiz a seconce coz foz no Sophias a
thee freckled pothy conollied. This affaise eh oh cont oh curly of conse-
quences. Uce sudos val oh es es entain ah thee enepol a oh dee a ah
messequence oh coz foz. The assoil lens a puff pifl miss corres povety. "
It was evidently an effort to read aloud, requiring close attention, and he
read seriously and steadily, apparently unconscious of the absurdity of his
utterances, till interrupted by laughter, which it was impossible to restrain,
in which he usually joined. He was never able to give the simplest
written answer to a question, or to write from dictation, but he signed his
name quite well, and wrote down the names of his brothers, but with the
initial only of the Christian name, the surname in full.

When asked to copy a sentence, he wrote the short words quickly, and
in a good hand ; but a long word he took down slowly, letter by letter,
in large schoolboy characters, usually accurately, but, as he wrote each
letter, he named it aloud, and always wrongly.

§ 749. Morbid Anatomy. — So far as is known of the morbid
anatomy of cortical disorders of speech may be summed up in
a few words. A comparison of a large number of observations
shows that the lesion in ataxic aphasia is situated in the
posterior portion of the third frontal convolution and the ad-
joining portion of the Island of Reil of the left hemisphere. Tn

622

FOCAL DISEASES, ACCORDING TO

exceptional cases the disease of the third frontal convolution
has been found in the right instead of the left hemisphere, and
in these the aphasia was associated with left hemiplegia during
life ; the patients were in most cases known to be left-handed.
In other cases of right hemiplegia., but without aphasia, the
posterior extremity of the third left frontal convolution has
been found disorganised after death, and in such cases also the
patients were left-handed. .,

The portion of the ascending frontal convolution which
adjoins the Island of Reil is often involved in the disease.
The lesion generally consists of occlusion — either by embolus
or syphilitic thrombosis — of the left middle cerebral artery, or
at least of the branch which supplies Broca's convolution.

In amnesic aphasia, on the other hand, the lesion is in the
area of distribution of the posterior and terminal branches of
the left middle cerebral artery, and the region of softening
comprises the supra-marginal and postero- parietal lobules, the
angular gyrus (visual centre), the posterior part of the infra-
marginal convolution (acoustic centre) and the convolutions
bounding the parallel and collateral fissures (Broadbent).

Lesions that damage the fibres of the corpus callosum
which connect the third frontal convolutions of the two sides,
and those which connect the third left frontal convolutions with
the internal capsule, produce, as has been pointed out by Broad-
bent, as permanent an affection of speech as destruction of
Broca's convolution itself.

A man, aged 66 years, whose case is
reported by Pitres, suffered from right hemi-
plegia, with embarrassment, and finally
complete loss of speech. At the autopsy, two
small patches of yellow softening were found
in the cortex of the left hemisphere, one being
situated upon the superior parietal lobule, and
the other upon the lobule of the pli courbe.
No changes were observed in the third frontal
convolution, but a large focus of softening
was observed in the centrum ovale, which
extended anteriorly to the part underlying
the posterior extremity of the third frontal
convolution, and posteriorly beyond the pos-
terior extremity of the optic thalamus {Fig.
264, L).

THE LOCALISATION OF THE LESION.

623

§ 750. Morbid Physiology .—When the structure of the cor-
tex at the posterior extremity of the third left frontal convolu-
tion is thoroughly disorganised, the expressive faculty of speech
is arrested at its origin. The patient can understand everything
that is said to him, he can think and probably clothe his ideas
in suitable subjective language, but the objective or expressive
part of speech is entirely lost. He can understand the thoughts
of others, but cannot communicate his thoughts to others either
by spoken or written language or by gesture. Most aphasics
present apparent exceptions to this rule, inasmuch as the
majority of them are not quite destitute of the power of uttering
words. But, as pointed out by Dr. Hughlings-Jackson, a patient
may be completely speechless though not entirely wordless.
The words that aphasic patients use are recurring utterances
like " Yes " and " No," which are repeated on all occasions,
whether appropriate or not. The patients have only an inter-
jectional and not a cognitional use of these words, and they
must be regarded as part, not of intellectual, but of emotional
language. The patient may be able to swear, oaths being part
of emotional language. Dr. Hughlings-Jackson thinks that
as actions become more and more automatic they tend to
become organised in the right as well as in the left hemisphere,
and he believes that the recurring utterances and phrases used
by aphasics are those which had become automatic either
previous to or during the attack, and consequently organised in
the right hemisphere. The words which become automatic
are those like "Yes" and "No," which have been frequently
repeated in the experience of the individual, and words of
the character of oaths, which, although they may not neces-
sarily have been frequently used by the patient, have been
used under circumstances of excitement and are expressive of
emotional states. In those cases in which the patient can
repeat words in the form of a proposition, such as the man
mentioned by Paget, who was injured in a brawl, and who
could only say " I want protection," it is thought probable by
Dr. Hughlings-Jackson that the patient was about to repeat
the words at the moment of injury. He thinks, therefore, that
these words had become automatic in him by being repeated
under circumstances of great excitement. But whatever may be

624

FOCAL DISEASES, ACCORDING TO

the explanation of the recurrence of such phrases, it is obvious
that they possess no value as a form of intellectual expression,
inasmuch as they are repeated without any reference to their
appropriateness to surrounding circumstances.

But what explanation can be given of the fact that the com-
plex muscular movements which serve for intellectual expression
are organised in one hemisphere only ? Accepting the crossed
connection of the hemispheres of the brain with the muscles
of the trunk and limbs as a fact, there can be no difficulty
in understanding why in right-handed people the more special
muscular adjustments of the hand should be organised in the
left hemisphere. It seems strange, however, that the muscular
movements concerned in articulation should follow the same
rule. It must at least be admitted that it would be an economy
of force if the muscles of the two sides concerned in
articulation were regulated from one hemisphere, and it is
also probable that a greater precision in . the execution of
these movements is obtained by a unilateral organisation. It
is likewise somewhat difficult to understand why in left-handed
people both the structural correlatives of the more special move-
ments of the hand and of the articulatory movements of spoken
language are found together in the right hemisphere. But
whatever may be the explanation, there is abundant clinical
evidence that such is the case.

If then ataxic aphasia be caused by a destroying lesion of
the emissive organisation of speech, it might be supposed that
simple severance of the cortical organisation from the executive
organisation would produce the same effect. In other words,
it may be supposed that disease of the fibres of the pyramidal
tract, which connect the posterior extremity of the third frontal
convolution and the nerve nuclei in the medulla, would produce
the same effect as disease of the cortex itself. When a com-
mander-in-chief, for instance, sends orders to a general of
division to execute a particular movement, the latter cannot
obey the order unless the line of communication between
the two be kept open, no matter how effective may be the
organisation of the emissive department of intelligence at its
central end. But it so happens in war that when the direct
line of communication is cut off, an indirect one may be dis-

THE LOCALISATION OF THE LESION.

625

covered. And something of this nature occurs in aphasia
caused by disease of the pyramidal tract. We have already
seen that the fibres of the knee of the internal capsule connect
the third frontal convolution and the nuclei of articulation in
the medulla, and when these are interrupted on the left side,
the patient suffers from temporary loss of speech. But, as has
been pointed out by Dr. Broadbent, the patient under these
circumstances makes a good and moderately rapid recovery.
The explanation given by Dr. Broadbent of this rapid recovery
is that, although the direct line of communication between the
emissive organisation and the executive is cut off, an indirect
line is readily established.

The usual course is for the message to be conducted
downwards by the fibres of the left pyramidal tract and to
cross over in the medulla to the nuclei of articulation of the
opposite side, and then through commissural fibres to the nuclei
of the same side. But when this channel is interrupted the
message is sent from the left third, frontal convolution through
the fibres of the corpus callosum to the corresponding convolu-
tion of the right side, and from the latter through the right
pyramidal tract to the nuclei of articulation of the opposite side,
and through commissural fibres to the nuclei of the same side
(§ 89). In this way the organisation in the third left frontal
convolution can, after a time, be utilised, but during the time
occupied in opening the new channels of communication the
patient suffers from greater or lesser degrees of disturbances of
speech. But, as has been pointed out by Broadbent, when the
fibres of the pyramidal tract in connection with the hemisphere
and the fibres of the corpus callosum which connect the third
frontal convolutions of the two sides are both interrupted by a
lesion in the centrum ovale, the affection of speech is as perma-
nent as if the third frontal convolution itself were completely
disorganised.

Speech, in its objective or expressive aspect, consists of
highly special and complex movements, and the question arises,
why are cases of aphasia not associated with paralysis of the
muscles of articulation ? The reply is that although there is
not a paralysis of the separate actions of the muscles of arti-
culation, yet there is a paralysis of the combinations of action

626

FOCAL DISEASES, ACCORDING TO

which are necessary for the production of speech. That ataxic
aphasia is of a paralytic nature may be shown in several ways.
The third left frontal convolution, for instance, is situated near
the centres for the regulation of the movements of the inferior
facial muscles and of the muscles of one-half of the tongue, so
that the aphasia caused by disease of Broca's convolutions is
associated with unilateral facial and lingual paralysis even in the
slighter cases in which complete hemiplegia is not produced.
But still more cogent evidence in favour of this view may be
derived from cases of bilateral diseases of the hemispheres, affect-
ing either the third frontal convolutions or the tracts of fibres
which connect these with the nuclei in the medulla, and in
which there is not only paralysis of the special but also of the
general movements of articulation (anarthria). For the follow-
ing example of this affection I am indebted to Dr. Leech, who
kindly transferred the case to me ten days before the patient
died. The notes of the case were taken by Mr. Gordon, when
the patient was under the, care of Dr. Leech, and by Mr.
Luckman after he came under my care.

Joseph C , aged 49 years, was admitted under the care of Dr.

Leech, November 15th, 1880. The patient was healthy until about eleven
months ago, when he began to complain of headache, usually situated in
the temples and occasionally in the back of the head. It was also observed
about this time that his speech was " thick," but no other notable symp-
toms were observed. Four and a half months ago he fell out of bed three
or four times the same night, and was unable to get in again until assisted
by his wife and son. From that time up to the present his speech
appeared to have become more and more unintelhgible, while he com-
plained of general weakness, but there was no distinct paralysis of any of
the extremities.

Present Condition. — The patient is emaciated and feeble, so that he
soon tires on attempting to walk, but there is no paralysis of the extremi-
ties. There is considerable loss of facial expression, and the patient
cannot compress his Hps or whistle, but can blow out a candle with
tolerable facility. He can protrude his tongue, but cannnot curl the
tip up towards his nose, or roU it up laterally so as to render it tubular.
His speech is almost unintelligible, and great attention is necessary in
order to understand the few words he is able to utter. He can pronounce
the separate consonants with tolerable distinctness, but finds difficulty
with the labials and dentals, the letters c, d, f, I, m, n, s, t, x, h, and w '
giving him the greatest difficulty. Food collects between his teeth, viscid
saliva collects in his mouth, which has to be constantly wiped away, and

THE LOCALISATION OF THE LESION.

G27

the power of deglutition is impaired. His arteries are atheromatous,
but no other important geueral symptoms are present.

Nov. 26. He has complained of pain for the last few days over the
temporal region. The nurse reports that he baa been slightly delirious at
times for the last few days, that he got out of bed several times yesterday,
and that on one occasion he fell down and had to be assisted into bed.
During this attack he is reported to have been conscious, but his speech
was greatly affected, and there was some degree of paralysis of both the
lower extremities. There is at present no distinct loss of power in either
the legs or the arms, but his speech is more unintelligible than at any
time since his admission.

Dec. 1. The patient is now suffering from diarrhoea, and there are
marked fluctuations of the temperature curve. The uvula is somewhat
pendulous, although not distorted, and its reflex excitability is dimiiiished.
The fauces and epiglottis can be examined with the point of the finger
without provoking a cough, while the patient exhibits a remarkable toler-
ance to laryngoscopic examination. The vocal cords move normally during
respiration and phonation.

Dec. 10. Since last report the diarrhoea has proved intractable to treat-
ment, and the patient is much feebler, the temperature curve presents
marked variations in the course of twenty-four hours, being at noon yester-
day below 97° F., and at midnight 105° F. During the previous thirteen
days the temperature varied from between 96*5° F. and 97-5° F. in the
morning to between 101 "5° F. and 103'5° F. in the evening. The speech
has been for some days quite unintelligible. The patient now became
gradually comatose, and died in the evening.

The post-mortem examination was conducted by Dr. A. H. Young
twenty-four hours after death. The arachnoid over the anterior part of
the convexity of the brain was opaque, and the subarachnoid tissue
cedematous, but the membranes were healthy posteriorly and over the
base. Each cerebral hemisphere presented a single well-defined cystic
cavity, containing clear straw-coloured fluid, and occupying the positions
of the lenticular nuclei. In the left hemisphere the lenticular nucleus was
simply replaced by the cyst, but in the right the cavity was considerably
larger than the area of the nucleus, extending anteriorly slightly beyond
the anterior extremity of the caudate nucleus, and posteriorly to the wall of
the descending horn of the lateral ventricle, although it did not commu-
nicate with the latter. The claustrum and internal capsule on each side
were unaffected. The ventricles contained a slight excess of fluid. The
arteries at the base of the brain were atheromatous. The mucous mem-
brane of the rectum and descending colon was covered by deep ulcers, with
thickened margins.

Microscopic examination showed that the nerve nuclei in the medulla
were healthy, and no descending changes could be detected in the pyra-
midal tracts in any part of their course.

628

FOCAL DISEASES, ACCORDING TO

Dr. Barlow was probably the first to draw attention to the
fact that lesions, symmetrically situated in the hemispheres,
may produce symptoms closely simulating those of bulbar
paralysis. A boy, aged 10 years, suffering from aortic disease,
had an attack of right hemiplegia with aphasia, from which he
made a good recovery. Four months subsequently he had an
attack of left hemiplegia with aphasia, as well as paralysis of
the muscles of articulation, those concerned in the first act of
deglutition, and of the muscles of mastication. At the autopsy
evidence of an embolus was found in both Sylvian arteries.
The obliteration of the vessel on each side was associated with
a focus of softening, about the size of a shilling, and situated
in the inferior part of the ascending frontal convolution, and
the posterior extremities of the second and third frontal con-
volutions. Soon afterwards an important paper was contri-
buted by Ldpine on this subject. In the case observed by
this author the symptoms were more or less similar to those

just described in the case of Joseph C , but in the former

the difficulty of deglutition was more marked than in the
latter. At the autopsy a diseased focus was found in each
hemisphere, involving the external capsule and the second
and third divisions of the lenticular nucleus, while that
in the right hemisphere extended to the convolutions of the
Island of Reil and the posterior extremity of the third frontal
convolution. Another case of the same kind is quoted by
Ldpine from Oulmont.

Le'pine also refers to a case reported many years ago by
Magnus, in which anarthria was caused by a unilateral lesi6n
of the brain, the disease being situated in the corpus striatum
of the right hemisphere. Another case is reported by Kirchoff in
which bulbar symptoms were caused by a diseased focus situated
in the right hemisphere, the left being healthy. The cases in
which the lesion was unilateral appear to show that the general
or more automatic movements of bilaterally associated muscles
are often regulated almost- entirely from the right hemisphere of
the brain. Cases of this kind suggest the question as to whether
the bulbar symptoms were caused directly by the lesion of the
lenticular nucleus or indirectly by implication of the fibres of
the knee of the internal capsule. In the case observed by me

THE LOCALISATION OF THE LESION.

G29

the most careful microscopical examination of the crusta, pons,
anterior pyramids of the medulla, and spinal cord failed to
detect any descending changes in the pyramidal tracts. The
cysts in the hemispheres were, however, very much distended
with fluid, and it is quite probable that a certain amount of
pressure was thus exercised upon the fibres of the internal
capsule, sufficient to partially interrupt conduction through
them, without being sufficient to cause secondary degeneration.
This question must, therefore, be left for future observations to
determine.

The mechanism by which the different forms of amnesic
aphasia is produced is much more difficult to comprehend than
that of the ataxic variety. In order to facilitate the compre-
hension of the various forms of aphasia, several authors have
constructed diagrams to represent hypothetically the nervous
mechanism concerned in speech. The best of these are the
diagrams of Kussmaul and of Broadbent, and although not
entirely agreeing with either of them, we shall avail ourselves
of the diagrams of the latter. Dr. Broadbent sets out in his
explanation with the proposition " that all muscular movements
are performed under the direction of a ' guiding sensation.' " It
would have been better if he had said under the guidance of
"centripetal impulses" instead of "sensation," inasmuch as
muscular movements take place in the entire absence of sensa-
tion. If, for example, the palm of the hand of a person asleep
be tickled, the hand closes under the guidance of centripetal
impulses, but independently of sensation, the action in this
case being reflex. But when the individual is awake the out-
going portion of the reflex arc can be utilised by the cortex of
the brain, and then voluntary closure of the hand takes place.
The nuclei of the motor fibres of the peripheral nerves in the
spinal cord are, therefore, subservient both to centripetal im-
pulses coming from the periphery, and to centrifugal impulses
coming from the cortex of the brain. But the centrifugal im-
pulses from the cortex are initiated and controlled by centripetal
impulses coming towards the cortex from the periphery. It
thus appears that each movement is represented in the anterior
grey horns of the cord by a group of connected cells, and that
this group may be called into activity by centripetal impulses

630

FOCAL DISEASES, ACCORDING TO

coming from the periphery to the same level of the cord, or by
centrifugal impulses from a higher nerve centre, or, in Dr.
Broadbent's words, " a motor cell-group is formed under the
guidance of a sensory cell-group on the same level, and, when
formed, is made use of by a higher centre."

The "motor cell-group" in the case of speech, which for the
sake of convenience Dr. Broadbent calls a word-group, must
combine into orderly action the thoracic muscles in order to
obtain an expiratory current of air, the laryngeal muscles for
phonation, and the muscles of the lips and tongue for articula-
tion. I shall follow Dr. Broadbent in placing the word- groups
in the corpus striatum, although in my opinion it would have
been better had he discarded this ganglion from the explana-
tion and merely spoken of the cortex and medulla oblongata,
which are connected with one another by straight fibres.

When the cells of the word-group are called into action by
centripetal impulses on the same level, the action is reflex, and
the resulting contraction would simply represent a complicated
muscular adjustment without any reference to intellectual ex-
pression, and it is only when its activity is evoked from the cortex
that the movement becomes subservient to speech. The cortical
outlet for speech is situated in the third left frontal convolution,
while the cortical guiding sensory centre for spoken language is
situated in the superior temporo-sphenodial convolution (auditory
centre). In accordance with the annexed diagram, lesion of S,
the speech centre, will cause ataxic aphasia, and lesion of A, the

auditory perceptive centre, or of
a s, the fibres which connect the
inlets and outlets, will cause dif-
ferent forms of " mistakes in
words." A hypothetical explana-
tion is thus afforded for three
disorders of speech. In lesion of
S the "way out" for all the mus-
cular adjustments concerned in
intellectual expression is de-
stroyed ; in lesion of as, the
line of communication between
the guiding sensory centre and

Fig. 265.

THE LOCALISATION OF THE LESION.

031

the motor outlet is damaged, and mistakes in words recognisable
by the patient occur ; while in lesion of the sensory centre A,
mistakes in words occur, of which the speaker remains un-
conscious.

But in intellectual expression still higher centres are en-
gaged, and diseases of these produce various complicated
disorders of speech. " The formation of an idea of any ex-
ternal object," says Dr. Broadbent, "is the combination of the
evidence respecting it received through all the senses ; for the
employment of this idea in intellectual operations it must be
associated with and symbolised by a name. The structural
arrangement corresponding to this process I have supposed to
consist in the convergence from all the 'perceptive centres' of
tracts of fibres to a convolutional area (not identified), which
may be called the ' idea centre' or ' naming centre.' This will
be on the sensory, afferent, or upward side of the nervous
system ; its correlative motor centre will be the propositionising
centre, in which names or nouns are set in a framework of other
words for outward expression, and in which a proposition is
realised in consciousness or mentally rehearsed. If we are to
have a seat of the faculty of language, it would be here rather
than in the third left frontal convolution, with which, however,
it may possibly be in close proximity. Expressing this by a
diagram, we have V, A, and T, the visual (angular gyrus, Ferrier),
auditory (infra-marginal Sylvian
gyrus), and tactual (uncinate
gyrus), perceptive centres send-
ing converging tracts of fibres,
vn, an, tn, to N, the ' naming
centre.' Here the perceptions
from V and T (smell and taste
are omitted for the sake of sim-
plicity) are combined into an
idea, which idea is symbolised by
the name reaching N through A-
which has always, in the expe-
rience of the individual, been
associated with the object. P is
the propositionising centre in

G32

FOCAL DISEASES, ACCORDING TO

which the phrase is formed, its relations with N and S being
sufficiently clear."

According to this scheme lesion of the naming centre N
would cause loss of the memory of names or nouns, leaving
the patient able to express himself imperfectly in words indi-
cative of relations and attributes.

Lesion of P, the propositionising centre, would render the
patient unable to construct a sentence although retaining the
use of names. This condition is illustrated by the patient who
could say "brother, brother — New York — America — two bro-
thers— America — brother."

Lesion of vn, the channel of communication between the
visual perceptive centre V and the naming centre N, would
explain cases of word-blindness ; while cases in which the lesion
is situated in the auditory perceptive centre A, or its line of
communication (an) with the naming centre, would explain
cases of word-deafness.

When the lesion involves more than one of the sensory
centres or their lines of communication with the naming centre,
it is manifest that complicated disorders of speech will arise,
difficult to analyse into their separate factors. What has here
been said with regard to spoken speech may be extended to
written speech and intellectual pantomime, inasmuch as all
forms of intellectual expression are usually involved in the
disorder.

I have so far endeavoured to give a succinct account of
Dr. Broadbent's theory of aphasia, while making use as much
as possible of his own words. It would be comparatively easy
to criticise this scheme, but not so easy to construct a better. I
do not, for instance, like Dr. Broadbent's use of the phrase,
" perceptive centre." If I look at a patch of yellow colour
before me and perceive that it is caused by what I know as an
" orange," it is because along with a vivid sensation of colour I
feel a faint revival of tactual, gustatory, and other sensations
previously experienced in conjunction with a similar sensation
of colour. If I stretch out my hand and find that the faint
tactual sensation I feel along with the visual sensation cannot
be converted into a vivid sensation, I call the patch of
colour, not an orange, but an illusion, and I begin to think

THE LOCALISATION OF THE LESION.

633

that my senses have played me false. The physical corre-
lative of a perception must, therefore, be excitation of a
portion of the cortex of the brain in which all the sensory
inlets are variously combined, and would, therefore, correspond
in the diagram to Dr. Broadbent's naming centre, while his
perceptive should be described as sensory centres. On the
other hand, I see no good grounds for postulating the existence
of a naming as distinct from a perceptive centre.

The process of naming demands a large increase in the size
of the perceptive centre, but not the existence of a separate
centre. Suppose, for instance, again, that I have an ocular
perception of an orange, the presentative element in the cog-
nition is a vivid feeling of a yellow colour, and the repre-
sentative elements faint revivals of previously experienced
feelings of touch and taste. I now close my eye and hear the
word " orange" spoken, the sound of the word forms the presen-
tative element of the cognition aroused, while the representative
element as before consists of faint revivals of touch and taste,
and of sight also now. The process of naming is, therefore, a
method by means of which artificial symbols are linked on to
groups of previously experienced feelings, and although the
exercise of this function demands a great extension and com-
plication on the perceptive centre of animals, yet it does not
demand the formation of a separate centre for its exercise.
Again, I hardly think that Dr. Broadbent has shown sufficient
grounds for assuming the existence of a distinct propositionising
centre, but I prefer not to enter upon a criticism of this portion
of his scheme.

b. Lesions in the Area of Distribution of the Posterior

Cerebral Artery.
The posterior cerebral artery supplies, as we have already
seen, the temporo-sphenoidal and occipital lobes, with the ex-
ception of the superior temporo-sphenoidal convolution, which
receives branches from the Sylvian artery. The experiments
of Ferrier and others appear to show that the functions of
the cortex of these lobes are purely sensory, and that it is
directly connected with centripetal fibres, and only indirectly
with centrifugal fibres through the cortex of the parietal lobes.

634

FOCAL DISEASES, ACCORDING TO

Disease of the cortex of the temporo-sphenoidal and occipital
lobes, however, does not give rise to localised motor disturbance,
and, contrary to what the results of experiments on animals
would lead us to expect, distinct sensory disorders are also
wanting. Lesions of these lobes rule, latent

Lesions of the Occipital Lobes. — Ferrier quotes a case reported by
Vauttier of yellow softening of the right occipital lobe and of the internal
aspect of the left lobe (quadrilateral lobule). There was neither disorder of
motion nor sensation, and, with the exception of considerable hebetude,
there were no symptoms of a cerebral affection. Pitres reports a case
in which an abscess, the size of a billiard-ball, formed in the posterior-
inferior aspect of the brain. There were no sensory or motor disorders,
mental obtuseness being the only indication of a cerebral lesion. In a
case which came to the post-mortem table, when I was pathologist to the
Manchester Royal Infirmary, a traumatic abscess, about the size of a
hen's egg, occupied the right occipital lobe, destroying nearly the whole
of its white substance. Dr. Dreschfeld, who saw the patient during life,
assured me that, with the exception of temporary hypersesthesia of the
left side of the body, there was no disorder of the general or special
senses. The patient suffered from delirium and general convulsions, but
these symptoms were probably due to the presence of meningitis, which
had spread over the occipital and parietal lobes of both hemispheres.
Many similar cases are recorded (Gull, Rodocalat, Pitres). Marce records
a case of contusion of the right occipital lobe, followed by effusion into the
membranes and softening of the cortex, without any sensory or motor
disorders.

In a case reported by Sestie* there was an abscess in each occipital
lobe, but no sensory disturbances were present during life. Charcot
has observed cutaneous formication and other paraesthesiae in cases of
softening of the occipital lobes, while Hughlings-Jackson and Bastian
believe that disease of the posterior lobes is more frequently associated
with mental derangement than disease of other parts of the brain.
Hughlings-Jackson also thinks that discharging lesions of the right
occipital lobe are more apt to give rise to coloured vision and other
ocular spectra than disease of the left lobe. Ferrier quotes the
following case from Abercrombie. A boy suffered from an injury of
the head causing depression of a considerable portion of the right
parietal bone, the depressed portion being forced through the dura mater,
and driven inwards upon the brain. He had paralysis of the left side
and amaurosis of the left eye. On the depressed portion being removed,
the paralysis was greatly diminished, and the eye recovered a considerable
degree of vision. On the third day after the operation, the wound in the
dura mater was inflamed, with considerable tumefaction, and immediately
the left leg and arm became paralysed, the paralysis being preceded by

THE LOCALISATION OF THE LESION.

635

convulsions, and the left eye again became amaurotic. He had frequent
convulsions of the affected extremities for several days, the right side not
being in the least affected, when, suppuration having taken place, all the
symptoms subsided. It is very probable that the depression of the skull
in this case had extended beyond the motor area of the cortex to the
angular gyrus, and compression of the latter would probably suffice to
explain the temporary amaurosis of the opposite eye.

It has been stated by Bastian that vision is apt to be impaired on the
side of the motor paralysis in cases of thrombosis of the posterior cerebral
artery. Fiirstner has observed unilateral affections of sight in cases of
general paralysis of the insane in which the occipital lobes were specially
involved in the disease. A most important case in this connection has
been reported by Glynn, in which the patient became suddenly and
completely blind, and in which a clot was found occluding the posterior
cerebral artery of the left side, causing extensive softening of the left
occipital and temporo-sphenoidal lobes. In the case of word-blindness
observed by Broadbent, and which we have already reported in full, the
important lesion was found in the region of the angular gyrus and supra-
marginal lobule (Fig. 267).

Fig. 267.

Several cases are mentioned by Nothnagel in which disease of the occi-
pital lobe was associated with bilateral hemianopsia, but in most of these
cases the disease of the hemisphere was associated with an affection of
the optic thalamus. But the external geniculate body, in which the optic
tract terminates, is so liable to be implicated in lesions of the optic
thalamus that no case in which the thalamus is extensively involved
along with the occipital lobe possesses any value for the determination of
this cmestion. Even large tumours of the occipital lobe which might
injure the external geniculate body by compression do not afford trust-
worthy evidence. In a case described by Pooley, there was paresis of
the right half of the body, diminished sensibility of the right arm,
and a sharply-defined right-sided hemianopsia of both eyes. A tumour

636

FOCAL DISEASES, ACCOEDING TO

was found in the left occipital lobe ; but, in addition, the left optic
thalamus and the surrounding cerebral substance were completely ■
softened. Another case is described by Hirschberg, in which there
were aphasia, right-sided hemiparesis, and right-sided hemianopsia.
A tumour was found in the left occipital lobe, surrounded by softened
tissue, which extended to the optic thalamus. It is difficult to under-
stand how the external geniculate body could escape being diseased in
such a case. Wernicke reports a case in which the symptoms consisted of
aphasia, agraphia, alexia, and right-sided hemianopsia. Extensive softening
was found in the convexity of the left hemisphere. The area of softening
reached posteriorly 2 cm. behind an ideal line drawn vertically downwards
from the parieto- occipital fissure ; superiorly, it was limited by the intra-
parietal sulcus ; anteriorly, it extended to the ascending parietal convo-
lution above the Sylvian fissure, and involved the superior middle temporo-
sphenoidal convolutions below it. The softening penetrated into the white
substance till it reached the ependyma of the posterior horn of the lateral
ventricle. The left corpus striatum — both the caudate and lenticular
nuclei — was softened ; but the optic thalamus, the geniculate body, the
corpora quadrigemina, and the optic tracts were normal. Baumgarten
mentions a case observed by Jacobson and Jaffe, in which the left
halves of the fields of vision became suddenly lost. The affection of sight
continued unchanged until death, which occurred a few months later from
aortic regurgitation. An apoplectic cyst, about the size of a walnut, was
found in the substanck of the right occipital lobe, and a small hsemor-
rhagic focus in the centre of the right optic thalamus. Nothnagel reports
a case of left brachial monoplegia, with right-sided hemianopsia of both
eyes. The autopsy revealed carcinoma of the pancreas, with secondary
deposits in the liver and stomach. The right hemisphere presented yellow
softening of the middle third of the ascending frontal and parietal con-
volutions, which penetrated deeply into the underlying white substance
and into the superior parietal lobule. About the size of a hazel-nut of
the convolutions on each side of the intraparietal sulcus was of a grey-
yellow colour, while the softening extended in the underlying white sub-
stance down to the wall of the descending horn of the lateral ventricle.
The third occipital convolution of the right hemisphere was also softened.
A spot of red softening, about the size of a hazel-nut, was observed in the
right optic thalamus. In the left hemisphere the posterior extremity of
the second frontal convolution, along with a small part of the adjoining
portion of the ascending frontal convolution, was softened. Another
small focus of softening was found in the anterior part of the superior
parietal lobule, while the whole cortex of the occipital lobe was changed
into a softened mass of a dirty yellow colour. No changes were observed
in the optic nerves or tracts. Softening was observed in the inferior part
of the cervical enlargement of the spinal cord.

Of the cases just mentioned of disease of the occipital lobes, associated
with hemianopsia, only one or two possess real value. In Pooley's case,

THE LOCALISATION OF THE LESION.

G37

the left optic thalamus aud surrounding cerebral substance is described as
being extensively softened, and it is difficult to understand how the
external geniculate body could escape under such circumstances. In
Hirschberg's case, the softening which surrounded a tumour in the occi-
pital lobes extended as far as the optic thalamus ; and, again, the external
geniculate body would be very liable to be diseased. Wernicke's case is,
on the other hand, more convincing, but even in it the corpus striatum is
mentioned as being softened. It is not couteuded that the softening
of the corpus striatum alone would account for the hemianopsia ; but
it must be remembered that the surcingle of the caudate nucleus
passes in close proximity to the external geniculate body. It is,
however, mentioned specially that the geniculate bodies were healthy
in this case, so that it must be held to favour the idea that hemianopsia
may be caused by disease of the occipital lobe. Baumgarten's case also
points to the same conclusion, for although a hsemorrhagic focus was
found in the centre of the right optic thalamus, yet its small size and the
position it occupied renders it improbable that this was the cause of the
hemianopsia. Nothnagel's case is not above suspicion. The red spot in
the thalamus probably occurred, as the author asserts, during the last
stages of life, and could not, therefore, have caused the hemianopsia ; but
the lesions observed were so extensive and complicated that it would not
be safe to attach much importance to the case. Of the cases just de-
scribed, those of Wernicke and Baumgarten, and in a less degree that of
Nothnagel, are the only ones to which any importance need be attached
as indicating that bilateral hemianopsia may result from disease of one of
the occipital lobes, but these cases can only be regarded as affording a
presumption in favour of this opinion. It is right to add that Bellouard,
who has written an admirable monograph on the subject of hemianopsia
from cerebral disease, believes that typical bilateral hemianopsia may be
caused by disease in the posterior part of the hemisphere a short distance
behind the radiations of Gratiolet's fibres. This question must, therefore,
be left for future observations to determine.

Lesions of the Temporo-sphenoidal Lobe. — Lesions of the temporo-
sphenoidal lobe are often latent as regards symptoms. Charcot and
Pitres report a case which presented no sensory or motor disturbances
during life, but in which yellow softening was found after death in the
cortex of the right hemisphere. The diseased area occupied the posterior
half of the Island of Reil, the posterior half of the second and third tem-
poro-sphenoidal convolutions, and the lower two-thirds of the inferior
parietal lobule. Ferrier places the auditory centre in the first and
second temporo-sphenoidal convolutions, but there is no case on record
in which disease of the cortex of the brain has given rise to deaf u ess.
The reason of this is that hearing is bilaterally associated, and so long as
one hemisphere is unaffected the auditory sense remains unimpaired or
only slightly weakened. The condition already described as word-deafness
is, however, associated with disease of the first and a portion of the

638

FOCAL DISEASES, ACCORDING TO

second temporo-sphenoidal convolution. In a case of this kind reported by
Wernicke there was softening from thrombosis of the first and a large por- , I
tion of the second temporo-sphenoidal convolution of the left hemisphere

Fig. 268.

{Fig. 268). Dr. Shuttleworth reports a case of microcephalic imbecility,
in which hearing was dull during life, and at the autopsy congenital defi-
ciency of the occipital and temporo-sphenoidal lobes was found.

The case of a woman, aged 64 years,
is described by Pitres, in which death
occurred a few hours after an apoplec-
tic attack. Although there was almost
complete loss of consciousness from the
first, there was no paralysis of any of t
the limbs, inasmuch as all of them
were moved on being strongly pinched.
There was no rotation of the head or
deviation of the eyes, but the left pupil
was more dilated than the right. At
the autopsy a recent hemorrhage was
found occupying the whole of the white
substance of the sphenoidal lobe {Fig.
269). The basal ganglia were healthy.

Ferrier found that destruction of the
subiculum comu Ammonis causes loss
of smell on the same side, while in
hemianesthesia from disease of the
posterior fibres of the posterior seg-
ment of the internal capsule the loss
of smell is on the side opposite the lesion. As already described, the
olfactory nerve has two roots, one of which passes directly to the subicular
region of the same side, while the other crosses over to the opposite hemi-

Fig. 269.

THE LOCALISATION OF THE LESION.

689

sphere through the anterior commissure of the third ventricle. It is not,
therefore, probable that unilateral cortical disease will cause complete
anosmia of one nostril.

The anosmia of the opposite nostril, the result of disease of the poste-
rior fibres of the internal capsule, is caused partly by the loss of common
sensation in the nose, from severance of the fifth nerve from the cortex,
and partly by destruction of the fibres of the internal root of the
olfactory nerve. Loss of smell, either alone or associated with dimi-
nution of taste, not unfrequently results from blows on the occiput or
vertex of the head. Dr. Ogle has described several cases of this kind,
and he thinks that the symptom is due to injury of the olfactory nerves,
bulbs, or tracts by counterstroke. When the occiput receives a blow,
the skull, being elastic, may yield without fracture, and the whole of the
cerebral mass is then thrust forwards against its anterior wall. The
temporo-sphenoidal lobe must be the firsc to impinge against the wings
of the sphenoid bone, and the forward movement of this lobe is suddenly
arrested, while the upper part of the cerebrum is allowed to move forwards
until it is arrested by the frontal bone. It is evident that the sudden
arrest of the temporo-sphenoidal lobe must tend to rupture the roots of
the olfactory tract. The forward movement of the upper portion of the
cerebrum will also tend to carry with it the olfactory bulbs, and thus to
rupture the olfactory nerves as they pass vertically through the cribriform
plate of the ethmoid bone.

A case of abscess of the temporo-sphenoidal lobe is reported by Dr.
Glynn, in which the most prominent symptom was complete anosmia.
The symptoms consisted of noises in, and partial deafness of the left ear,
amblyopia and dyschromatopsia of the left eye, neuralgic pains over the
temporal region and above the left ear, the scalp being swollen over these
regions, a crop of herpes on the left ala nasi, paresis of the left masseter,
slight facial paralysis of the left side of the body, loss of taste over
the left half of the tongue, ptosis of left eyelid with contraction of the
pupil on that side, double optic neuritis, complete anosmia, and quasi
hysterical attacks. At the post mortem a circumscribed abscess, about
two inches in length, was found situated in the anterior part of the first
temporo-sphenoidal convolution, and extending inwards and downwards
towards the base of the brain. With the exception of the anosmia, the
localising symptoms in this case were caused by compression of the cranial
nerves at the base of the brain in the auterior fossa of the skull. Dr.
Glynn appears to think that the loss of smell was caused by implication
of the cortical centre, but it is more likely to have been caused by com-
pression of the external root of the olfactory tract of the same side at its
point of entrance into the temporo-sphenoidal lobe and of the fibres
which cross in the anterior commissure of the third ventricle.

Ferrier. localises the centre of tactile sensibility in the hippocampal
region, but unilateral lesions of the hippocampal convolutions are not
known to produce anaesthesia. In the cases of disease of the sphenoidal

642

FOCAL DISEASES.

irritative or paralytic disturbances, the muscles of the face and neck being
first implicated, tben those of the arm, and those of the leg last. "When
lesions of the prse-frontal region are attended by active delirium, or con-
vulsions, it is probable that the primary focus is surrounded by a more or
less diffused encejohalitis, or at least by a zone of tissue in a state of irri-
tation, which extends to the cortex of the motor area. The characteristic
features of lesions in the pree-frontal region of the cortex are afforded by
the psychical disturbances, consisting of dementia, apathy, and somno-
lency. When convulsions are present, they are not preceded by an aura,
and the spasmodic phenomena are of short duration, while the stage of
insensibility is comparatively prolonged.

643

CHAPTER VIII.

(II.) SPECIAL CONSIDERATION OF FOCAL DISEASES,
ACCORDING TO THE LOCALISATION OF THE LESION
(Continued).

3. LESIONS OF THE BASAL GANGLIA, EXTERNAL CAPSULE,

AND CLAUSTRUM.

Lesions of the basal ganglia have already been considered
in a general manner along with the affections of the internal
capsule, and little remains but to show that those limited to
the ganglia themselves do not give rise to decided symptoms
during life, or at least that these symptoms are not of an
enduring character.

(a) Lesions of the Lenticular Nucleus.

§ 751. Several cases are now on record in which the lenticular
nucleus had been found at the autopsy converted into a cyst,
containing serous fluid, but in which paralysis of the opposite
side of the body had been completely absent during life (Ldpine,
Charcot, Nothnagel). When a history of the symptoms can be
obtained it is found that the patient had some months or years
previously suffered from an attack of apoplexy, followed by
temporary hemiplegia. The patient, however, makes a good
recovery, and the cerebral attack from which he suffered may
be completely forgotten, so that the lesion of the lenticular
nucleus is revealed quite unexpectedly at the autopsy. A
woman, aged 57 years, suffering from tabes dorsalis, was under
the observation of Nothnagel for six months before her death,
during which time she had no cerebral symptoms, yet a diseased
focus was found in the posterior and inferior angle of the right
lenticular nucleus.

644 FOCAL DISEASES, ACCORDING TO

la the case of pseudobulbar paralysis already described,
which came under my own observation, both lenticular nuclei
were converted into cysts, and yet there was no paralysis of the
extremities during life.

Tumours of the lenticular nucleus generally give rise to
hemiplegia of the opposite side, the paralysis being sometimes
preceded by spasmodic contractions. Speech was affected in
six out of sixteen cases of tumours of the lenticular nucleus
collected by Ladame, but the size of the tumours in some of
these cases precluded the idea that they could have been
limited to the area of the lenticular nucleus. In two cases
there was difficulty of articulation, in three slowness of speech,
and in one only aphasia. The difficulty of articulation pro-
bably depended upon compression of the geniculate tract of the
internal capsule, the aphasia upon simultaneous compression of
the geniculate fibres and those of the corpus callosum which
connect the posterior extremities of the third frontal convolu-
tions with one another, while the slowness of speech might
either be a symptom of general compression of the brain or .of
special compression of the Island of Reil and the posterior
extremity of the third frontal convolution. A large tumour of
the lenticular nucleus might compress the optic tract, either
at its origin in the external geniculate nucleus, or as it winds
round the crus cerebri, and then bilateral hemianopsia of the
opposite side would be present. Tumours, however, which
remain limited to the lenticular nucleus do not give rise to
decided paralysis.

The case of a woman, aged 30 years, is described by Fiirstner, to whom
two grammes of chloral had been given as a hypnotic on account of
puerperal mania, and who suffered from symptoms of chloral poisoning.
She had repeated rigors, lowering of the temperature of the body, palpita-
tion, and acute oedema of the lungs. For some days she complained of
general weakness, while an erythematous eruption appeared over the
body, and a bed-sore over the sacrum. Pneumonia how supervened, and
the patient died seven days after the administration of the chloral. At
the autopsy, besides the usual signs of pneumonia, a telangiectatic glioma
was found symmetrically placed on each side, and occupying the position
of the middle and internal divisions of the lenticular nuclei, the third
division being free on both sides.

Fiirstner ascribes the feeling of general feebleness, of which

THE LOCALISATION OF THE LESION. G45

the patient complained, to the toxic action of the chloral ; and
even supposing that this feeling was a bilateral hemiparesis
caused by the tumours, it must be remembered that the symp-
tom only appeared a week before death ; besides it is probable,
from the position of the tumours, that the fibres of the internal
capsule suffered a certain amount of injury. A somewhat
similar case is described by Rondot.

A man, aged 30 years, complained of pains in the neck and head, and
of a feeling of weakness of the extremities, but was able to walk about.
At no time did the case present any paralysis, contractures, or sensory
disturbances. Death occurred somewhat suddenly ; and at the autopsy
two tumours were foimd, each being about the size of a large hazel-nut,
and symmetrically placed in the hemispheres. A transverse vertical
section showed that each tumour occupied the position of the lenticular
nucleus ; the fibres of the internal capsule were compressed and pushed
inwards, while the cerebral substance was softened to the extent of three
or four mm. in thickness on the external surfaces of the tumours. The
tumours were dense and white, though their peripheral zones were
vascular.

A case of syphiloma of the brain has been observed by
Schiitz, and one of tubercular tumour by Bramwell, in each of
which the tumour occupied the position of almost the whole of
the lenticular nucleus of the left side, and in neither were
there symptoms of a localised cerebral affection. It may,
therefore, be laid down, as a general rule, that acute lesions
limited to the lenticular nucleus give rise to a transitory hemi-
plegia of the opposite side, while this symptom may be entirely
absent in chronic stationary lesions and slow-growing tumours.

(b) Lesions of the Caudate Nudeus.

§ 752. Lesions of the caudate nucleus do not, any more than
those of the lenticular nucleus, give rise to permanent symp-
toms during life, unless the internal capsule be implicated.
Small cystic cavities and foci of softening are frequently found
in the caudate nucleus at a post-mortem examination, in the
absence of all history of cerebral symptoms during life. Other
cases are reported in which a slight hemiplegia had occurred
during life, followed by a speedy recovery, and in which a focal
lesion was subsequently found in the caudate nucleus.

The following case observed by myself illustrates the

640

FOCAL DISEASES, ACCORDING TO

symptoms which may be present during the growth of a
tumour of the caudate nucleus.

Samuel Holmes, set. 7 years, presented himself as an out-patient at the
Southern Hospital, Manchester, on January 26th, 1876.

The following history was elicited from the mother : — He was a bright,
intelligent, and healthy boy until about 15 months ago, when he fell from
a wall, 5 feet high. Soon afterwards he complained of constant headache,
chiefly confined to the forehead. The top of the head was so sensitive
that combing his hair caused him much pain. He could not keep still ;
his legs, especially, were constantly moving, and at meal times he was in
the habit of knocking the table with his right hand, as if from impatience.
About nine months ago the mother noticed that his mouth was slightly
" crooked," and that his left arm hung helplessly by his side. The forearm
was twisted so that the palm of the hand was directed outwards and the
thumb backwards, his fingers were bent, but she thinks his thumb at
first was held straight and drawn away from the fingers. After some
weeks, however, the thumb became bent inwards under the index-finger,
and she had to pare the nail of the thumb frequently to prevent its cutting
the skin of the outside of the middle finger. He now began to drag the
left foot in - walking, and the forearm was gradually drawn up behind his
back, instead of hanging, as at first, by his side.

The mother had had nine of a family, no miscarriages and no still-born
children. One child died from convulsions during teething ; a second child,
who was weakly from birth, died at the age of three months ; and a daughter
has suffered for the last two*years from white swelling of the knee.

On presenting himself at the hospital he was a well-made and fully- J
developed boy for his years. His head was large, but well-proportioned ; [l
face round and plump, although pallid ; his incisor teeth were regular, his
nose was well formed, the muscular system was well developed, and there
was abundance of subcutaneous fat. There was very well-marked left
facial paralysis, so that the left corner of the mouth coidd not be moved.
Both eyes could be closed ; the pupils were large, equal, sensitive to light,
and there was no affection of the special senses. The left elbow was kept
a little behind the "body, and 2 inches from the side ; the forearm was bent
at right angles to the arm, and drawn behind the trunk ; the hand was
strongly pronated ; the thumb was adducted, and the second phalanx
flexed, so that the point rested against the second phalanx of the middle
finger. The first phalanges of the fingers were extended and in a line
with the metacarpal bones, and the second and third phalanges were
flexed. A considerable amount of muscular rigidity was induced on
attempting passive motion at the elbow and wrist joints. By a volun-
tary effort he could raise his elbow to nearly the level of the shoulder,
and then bring the upper arm slowly forwards; but he could neither
extend the forearm, produce supination, nor extend the fingers. The left
leg dragged during walking, but there was no muscular rigidity, and all

THE LOCALISATION OF THE LESION.

047

the movements of the leg could be separately performed. The electro-
cutaneous sensibility of the left half of the body was increased, especially
over the back of the left hand, and the left half of the face and side of the
head. The slightest touch of the skin over the vertex of the head to the
left of the middle hue caused the patient to wince, and the cutaneous
sensibility to pain was increased over the left half of the body generally.
The other organs appeared to be healthy, and there was no albumen or
sugar in the urine. He was ordered four grains of iodide of potassium
three times a day ; but, as no improvement took place, he was admitted
into the hospital on February 28th.

March 10th, 1877.— He was ordered, on admission, fifteen minims of
the syrup of the iodide of iron, to be taken three times a day, and the
daily application of a weak constant current to the paralysed muscles and
nerves. After two applications of the constant current he could extend
his fingers to a slight extent, and in a few days he was able to raise his
hand to the back of his head. It was observed, however, that the most
marked improvement took place at the shoulder-joint ; and that improve-
ment in the movements of the forearm and hand was only to a slight
extent. This improvement was of short duration, and he now looks
decidedly worse than on admission. The pallor of the face is much
increased ; his appetite has failed ; the pulse is 110, weak and irregular ;
and the nurse says that he has become very stupid. Ordered to be kept
in bed, milk diet and a saline mixture.

March 18th. — Since last report he has got steadily worse, has vomited
frequently, and to-day has been seized with general convulsions. The
convulsions frequently recurred during the next two days, consciousness
not being recovered in the intervals, and he died early on March 21st.

Sectio cadaveris, twelve hours after death. — On opening the skull, the
convolutions of the brain presented a flattened and compressed appearance,
and about 2 ounces of fluid escaped during removal. The brain weighed
51 ounces. On slicing the brain to a level with the corpus callosum the
upper surface of a tumour was exposed, which was situated in the centrum
ovale of the right hemisphere, immediately to the right of the corpus
callosum and at the junction of the anterior and middle lobes. On opening
the lateral ventricles, this tumour was felt as a hard nodule, slightly pro-
jecting into the right lateral ventricle, and occupying the position of
the caudate nucleus and anterior portion of the optic thalamus, and only
covered by the ependyma of the ventricle. The tumour measured three-
quarters of an inch in the transverse and an inch in the antero-posterior
and vertical diameters respectively, so that not only the caudate nucleus
and anterior portion of the optic thalamus, but also the anterior two-thirds
of the internal capsule and the anterior portion of the lenticular nucleus
were destroyed by it.

The growth was pretty sharply defined from the surrounding brain-
tissue, and on section it presented an outer grey, somewhat vascular cortex,
about two lines thick, and a central core of a yellow colour, and apparently
destitute of any structure.

648

FOCAL DISEASES, ACCORDING TO

Microscopic examination showed that .the grey cortex of the tumour
consisted of giant cells, each surrounded by lymphoid cells imbedded in u
fibrillated reticulum.

The right lung was closely adherent to the chest wall and to the
diaphragm. The lung itself was congested, but every portion of it floated
in water. No tubercles nor cheesy glands were discovered, and the other
organs were healthy.

Fig. 271.

Fig. 271 (From FlechBig). Horizontal Section of the Brain of a Child nine months
of age, the right side being at a somewhat lower level than tlie left half.—F, Frontal,
TS, Temporo-sphenoidal, and 0, Occipital lobes ; Op, Operculum; 7w,iIslandof
Reil; Cls, Claustrum; /"', Third frontal convolution; Th, Optic thalamus;
NC, Caudate nucleus ; NC, Tail of caudate nucleus ; LN, Lenticular nucleus ;
I, II, III, First, second, and third divisions of the lenticular nucleus ; EK,
External capsule ; IK, Posterior division, IK', Anterior division, and K, Knee
of the internal capsule ; ah,ph, Anterior and posterior horns respectively of the
lateral ventricles ; gcc, Knee of the corpus callosum ; sp, Splenium ; mc, Middle
commissure ; /, Fornix ; si, Septum lucidum ; a, Cornu Ammonis.

THE LOCALISATION OF THE LESION.

G49

The tumour in this case appeared to have commenced growing
in the cau date nucleus (Fig. 271, NO), although it ultimately
extended to the anterior half of the lenticular nucleus (Fig.
271, LN), and completely destroyed the anterior segment of the
internal capsule (Fig. 271, IK'). The most remarkable feature
about the symptoms was that the face was more paralysed than
the arm, and the arm than the leg, this being the order in
which the paralysis might be expected to appear, provided pres-
sure was exerted on the internal capsule from before back-
wards. The hyperesthesia of the head was probably caused
by irritation of the posterior fibres of the internal capsule.

§ 753. The lesions of the optic thalamus by which the fibres
of the internal capsule suffer damage have already been con-
sidered. Acute lesions of the thalamus except those of small
size are associated with more or less paralysis of the opposite
side of the body, but unless the lesion be large the paralysis
is only temporary, and it is probable that when permanent
paralysis results the fibres of the pyramidal tract are always
injured. Lesions of the thalamus are also frequently asso-
ciated with hemianesthesia, but the sensory phenomena are
in nearly all cases caused by injury of the sensory peduncular
tract in its ascent through the internal capsule, and of the
optic radiations of Gratiolet.

Lesions of the optic thalamus are frequently associated with
bilateral hemianopsia of the side opposite the lesion. When
the lesion of the thalamus is of the nature of haemorrhage or
softening, the hemianopsia is probably caused by implication of
the external geniculate body in the diseased focus ; but when
the lesion is a tumour of the thalamus, the defect of sight is
often the result of pressure on the optic tract as it winds round
the crus cerebri

(d) Lesions of the Corpora Quadrigemina.
§ 754. Tumours of the corpora quadrigemina are of .rare
occurrence. Out of the 331 cases of intracranial tumour col-
lected by Ladame only two were situated in the corpora quad-
rigemina. Several cases of disease of these ganglia have been

650 FOCAL DISEASES, ACCORDING TO

recorded since, but in the majority of them the lesion has not
been strictly limited to these bodies. The more usual symptoms . ,
of lesion of the corpora quadrigemina are disturbances of i
muscular co-ordination, disorders of the movements of the eye- I
balls and iris, and defects of vision.

The disturbances of muscular co-ordination consist of stag-
gering and difficulty of maintaining the erect posture, the
symptoms being similar to those caused by disease of the
peduncles of the cerebellum. And, indeed, when the anato-
mical relations between the corpora quadrigemina and the
superior peduncles of the cerebellum are considered, it becomes
doubtful whether these motor disturbances ought not to be
attributed to implication of the latter. The disturbances in
the ocular movements are generally caused by paralysis of
individual branches of the oculo-motor nerves ; and Nothnagel
thinks that those disorders are more likely to occur when the
posterior pair of ganglia are diseased. The retino-pupillary
reflex is also abolished. No definite statement can be made
with regard to the state of the pupils. When the anterior pair
are affected, blindness is apt to supervene at an early period
of the affection, and often precedes the development of optic
neuritis in cases of tumour. In two cases of tumour of the
cerebellum which 1 observed, and in wThich the corpora quadri-
gemina were secondarily implicated, blindness was an early [
symptom, and was complete in both cases before the secondary
atrophy of the discs had advanced far, although not before the
appearance of double optic neuritis.

(e) Lesions of the Claustrum and External Capsule.
§ 755. A case is described by Brault and Beurmann of a man,
aged 71 years, who a few weeks after an injury had an apo-
plectic attack. On the following day there was slowness of
speech, and paralysis of the right half of the body including the
face. Three days after the attack speech was still slow, but the
facial paralysis had disappeared, and the paralysis of the extremi-
ties-was much improved, while every symptom of the attack had
disappeared six days from its onset. A few days subsequently
the patient died from causes unconnected with the apoplectic
attack, and the left claustrum and external capsule were found

THE LOCALISATION OF THE LESION.

851

completely destroyed by a hemorrhagic focus, 3 cc. long, 2\ cc.
in depth, and only 2—3 mm. broad. . The hemiplegia in this
case was doubtless caused by a temporary slight pressure on
the fibres of the internal capsule, while the affection of speech
was occasioned probably by pressure on the Island of Reil,
but none of the symptoms could be attributed to the destruc-
tion of the claustrum and external capsule themselves.

if) Lesions of the Base of the Skull.

(i.) Anterior Fossae op the Skull.
§ 756. Records of lesions limited to the anterior fossae of the
skull are not numerous. Disturbances of smell are not unfre-
quently present in chronic basal meningitis, but the lesion almost
always extends beyond the anterior fossae, and gives rise to com-
plications. The symptoms caused by tumour in this region are
variable, but the most trustworthy is afforded by compression
of the olfactory bulbs or tracts. Several cases of tumour in this
region have been collected by Longet, of which the following
is an example : —

A woman, aged 59 years, suffered from recurrent attacks of dizziness,
feelings of formication, and numbness of the left half of the face. After a
period of four years she began to suffer from epileptiform convulsions,
but enjoyed good health in the intervals. A year later the patient expe-
rienced a peculiar disorder of smell, which she could not accurately
describe, immediately before each attack of dizziness, and this last was
followed by an epileptiform attack. After the expiration of another
year the disorder of smell had became less troublesome and finally disap-
frontal headache, loss of intelligence, and coma. At the autopsy a can-
peared. The terminal symptoms consisted of attacks of severe dizziness,
cerous tumour the size of a duck's egg was found in the anterior lobe of
the left hemisphere, lying on the dura mater of the anterior fossa, and
extending from the lamina cribrosa to the olfactory roots. The left
olfactory tract was completely destroyed.

(ii.) Lesions of the Middle Fossje of the Skull.

§ 757. Diseases situated in the middle fossae of the skull are
liable to implicate many important structures as the olfactory
nerves, the optic commissure and tract, as well as the third,
fourth, fifth, sixth, seventh, and eighth nerves. It will thus be
seen that lesions of this fossa must give rise to very compli-

G52

FOCAL DISEASES, ACCORDING TO

cated symptoms. The following case reported by Ziemssen
illustrates the symptoms caused by basal meningitis, mainly
limited to the pia mater and lying over the middle fossa of the
skull.

A man, aged 33 years, contracted syphilis in 1855, and suffered from
secondary symptoms. On March 9th, 1856, while walking on the street,
he suddenly observed double vision, associated with ptosis of the left eye-
lid, both symptoms remaining constant. In June he complained of intense
headache, the mouth was drawn to the left, and there was difficulty of arti-
culation and deglutition. Great general weakness gradually developed, so
that the patient could not stand alone, and when supported by two
attendants his gait was staggering. On August 11th, the patient was
found in a state of great emaciation ; there was inability to close the right
eye, owing to paralysis of the lower lid ; while the upper lid could be ener-
getically moved, the right eye could be moved upwards, inwards, and down-
wards, but not outwards, and only slightly outwards and downwards. The
pupil was contracted, and reacted feebly to light. In the left eye there
was complete ptosis, and the eyeball was immovable. The pupil was dilated
and fixed. Apart from diplopia, vision in both eyes was good. The right
facial nerve was completely paralysed, and the muscles did not react to
the faradic current; the left facial muscles reacted feebly. The move-
ments of the tongue were normal. The sensory disturbances in the region
of distribution of the fifth nerves, and the senses of taste and smell,
were unaffected. The movements of both the lower and the left upper
extremity were normal, but the grasp of the right hand was feeble, the
power of moving the fingers was incomplete, and the interossei muscles and
those of the ball of the thumb were atrophied. There were no sensory dis-
turbances of the body or extremities. In this case the right facial, left
oculo-motor, right trochlear, and the two sixth nerves were completely
paralysed, while the right oculo-motor and left facial were partially
paralysed. Death took place on August 9th from pulmonary phthisis.
The pia mater corresponding to the middle lobes was thickened, while the
diseased area extended towards the optic coniniissure. The pia mater
was thickened over the left oculo-motor nerve, which was congested,
in some parts thickened and softened, and in others atrophied. In
the thickened parts a microscopic examination revealed fine fat globules,
without a trace of nerve fibres. The right facial and trochlear nerves were
altered in the same manner as the left oculo-motor. A certain degree of '
thickening was found at the origin of the right ocido-motor nerve ; but a
microscopic examination revealed, besides fat globules, healthy nerve fibres.
The left facial and the two acoustic nerves presented morbid appear-
ances similar to those found in the right oculo-motor nerve. Both the
sixth nerves were flattened. The olfactory, optic, trigeminal, hypo-
glossal, spinal accessory, glosso-pharyngeal, and pneumogastric nerves were
normal. The brain was healthy.

THE LOCALISATION OF THE LESION.

653

The changes in this case extended beyond the middle fossa?
of the skull, inasmuch as the facial and acoustic nerves were
implicated in the disease, but it nevertheless affords a good
example of the symptoms caused by a chronic basal meningitis.
In a patient under the care of Dr. Simpson, sent to the Cheadle
Convalescent Hospital a few months ago, the following were
the leading symptoms observed: —

A man, aged 49 years, suffered for some time from headache and
blindness of the right eye. When I examined him in July, 1880, there
was complete blindness of the right eye, with atrophy of the optic disc,

Fig. 272 (From Landois' " Physiologie "). — Schema of the semi-decussation of the
fibres of the Optic Commissure ; b a, Left Optic Tract, the fibres of which are
distributed to the left halves of both retinse ; a' b', the Right Tract, with its
fibres supplying the right halves of both retinae.

complete immobility of the eyeball, ptosis, and exophthalmos from para-
lysis of all the ocular motor nerves. Vision was good in the left eye, the
field of vision in it was not restricted, and there were no changes in the
optic disc The patient had suffered for some time from neuralgic pains
in the region of distribution of the first and second division of the fifth
nerve, and at the time of examination the sensibility of this region was
blunted but not abolished. A tenacious secretion covered the right eye-
ball, but the cornea was not cloudy. The right masseter muscle was feeble
and decidedly atrophied in comparison with the corresponding muscle on
the left. The man died two weeks after my visit, and at the autopsy
Dr. Massiah found the right optic nerve close to the foramen, surrounded
by a ring of dense, apparently cicatricial, tissue. This thickened tissue,
which did not form a distinct tumour, had extended backwards above
the cavernous sinus and spread over the Gasserian ganglion and motor
root of the fifth nerve. The right optic tract {Fig. 272, a' V) was un-
affected.

Tumours of the middle fossa of the skull generally give rise

Fig. 272.

654

FOCAL DISEASES, ACCORDING TO

to still more definite symptoms. The symptoms in the following
case, under the care of Dr. Dreschfeld, deserve to be compared
with those of the case which has just been described. '

A man, aged 40 years, suffered for some time from symptoms of cere-
bral disease. For some weeks before his death his symptoms were blindness
of the right eye with atrophy of the disc, ptosis, immobility of the eyeball,
and paralytic exophthalmos of the right eye ; after a time neuro-paralytic
ophthalmia of the same, right facial prosopalgia, optic neuritis of left disc,
with temporal hemianopsia of the left eye, and polyuria. The post-mortem
was conducted by myself. I found a sarcomatous tumour lying close to
the right optic foramen, and compressing the optic nerve ; it extended
backwards over the cavernous sinus, and compressed all the nerves lying
in its walls, and likewise the right optic tract {Fig. 272, a' b').

Most of the symptoms in this case were so definite that they
scarcely require a word of explanation. The blindness of the
right eye and atrophy of the disc were caused by the injury of
the optic nerve at its point of entrance into the optic foramen,
the temporal hemianopsia of the left eye by compression of the
right optic tract, the optic neuritis of that eye was the usual
form indicative of the presence of an intracranial tumour,
while the paralysis of all the ocular muscles was caused by
compression of the third, fourth, and sixth nerves as they pass
along the wall of the cavernous sinus. The polyuria present
in this case is not an unfrequent symptom of tumours in the •
neighbourhood of the pituitary body, and glycosuria is some- 1
times observed in such cases.

Aneurism of the internal carotid artery at the base of the
skull does not appear to give rise to any characteristic symptoms,
and auscultation of the cranium has not proved of much service.
Besides a constantly recurring and distressing headache, the
more usual symptoms of aneurism of the internal carotid at the
base of the skull are unilateral or bilateral disturbances of
vision from compression of the optic tract or nerve, spasms soon
followed by paralysis of the ocular muscles, hyperesthesia, and .
neuralgia, followed by anaesthesia in the region of distribution; j
of the fifth nerve and great mental disturbances. Paralysis off i
the extremities of the opposite side may occasionally occur fromi
compression of the pyramidal tract on its way through the? t
crusta.

THE LOCALISATION OF THE LESION.

055

(iii.) HEMORRHAGE INTO THE LATERAL VeNTIUCLES.

§ 758. Hemorrhage into the ventricles is followed by deep
coma, and the majority of patients die in the course of the first
or second day ; although occasionally they may live for several
days. Hemorrhage into the lateral ventricles constitutes the
majority of those cases which have been called ingravescent
apoplexy, but some of these are caused by a large haemorrhage
into the centrum ovale, or on to the surface of the brain
from the bursting of an aneurism. When rupture into the
lateral ventricle takes place the corpus callosum and fornix
become partially destroyed, and the haemorrhage makes its
way into the third ventricle and into the lateral ventricle of
the opposite side, and passes through the aqueduct of Sylvius
to the fourth ventricle. The first stage of haemorrhage into the
ventricle may consist of ordinary hemiplegia, commencing with
an apoplectiform, epileptiform, or simple mode of onset. In-
deed, the simple mode of onset is not an unusual one, since
the haemorrhage frequently begins in the head of the caudate
nucleus, lenticular nucleus, or optic thalamus, and the primary
symptoms produced are not well marked. But whenever the brain
substance is ruptured, so that blood is poured in considerable
quantity into the lateral ventricle, a severe apoplectic attack
occurs, characterised by profound coma, general paralysis of the
limbs, and dilated pupils. The rectal temperature sinks several
degrees, and remains depressed for several hours ; but if a fatal
result do not speedily occur the initial depression is followed
by a rapid rise, which continues, in cases about to prove fatal,
till the death of the patient. Haemorrhage into the lateral ven-
tricle is frequently attended with a spasmodic contraction of
the extremities of the opposite side, which may be either tem-
porary or persist until death.

(iv.) TOMOURS IN THE NEIGHBOURHOOD OF THE PITUITARY BODY.

§ 759. Tumours of the pituitary body are usually of large
size. They produce compression of the anterior perforated
space, the olfactory tracts, optic commissures and roots of the
optic nerves, the corpora albicantia, the posterior perforated
space, and when the tumour is large the pons and peduncles of

653

FOCAL DISEASES, ACCORDING TO

Fig. 273.

_ „. TT .>, „ A„„f„miB^ The Base of the Brain and adjoining part

Fig 273 ^.^^L^^'^^^utBi by tbe corresponding

lt.?^tomIfa?Xnr^rPar^ intermedia of the seventh; no I,

First cervical nerve.

THE LOCALISATION OF THE LESION.

657

Fig. 274.

Fig. 274 (From Henle's "Anatomie "). Internal View of the Base of the Skull,
showing the Places of Exit of the Cranial Nerves. -The Nerves are represented
by the corresponding Roman numerals, from I to XII. V1, Vs, Vs, the
first, second, and third divisions of the fifth respectively. V*, the Gasserian
Ganglion. The sensory root is cut short in order to show the motor root of
the fifth as it passes under the ganglion. The dura mater is removed on the
right side, and the nerves may be followed to the various foramina through
which they pass from the skull. The Nerves III, IV, V1, and VI may be
seen passing over the convexity of the curve, which the internal carotid artery
makes in the groove of the sphenoid bone. 1, Anterior clinoid process ;
2, Posterior clinoid process ; 3, Transverse section of the internal carotid
artery. H, Peduncle of the pituitary body ; t, anterior body of the divided
tentorium ; fcb, Falx Cerebelli.

658

FOCAL DISEASES, ACCORDING TO

the cerebellum may be pressed upon and flattened. They may
also encroach upon the cavernous sinuses and sphenoidal fissures
and the nerves which pass through them, while the ventricles
are not unfrequently distorted or obliterated. These tumours
are also very liable to cause softening of the surrounding
cerebral tissue, which may extend to the basal ganglia or the
centrum ovale.

Periodical headache, usually situated in the frontal and tem-
poral regions and extending forwards to one of the eyeballs and
supra-orbital region, is one of the earliest symptoms of tumour
in the neighbourhood of the pituitary body. Blindness occurs
at an early period of the growth of these tumours, owing to
their proximity to the optic commissure. It is important to
remember that pressure on the optic commissure or nerves causes
secondary atrophy of the discs without being preceded by the
" choked disc."

There may also be unilateral or bilateral anosmia due to
injury of the olfactory tracts. When the tumour exercises
pressure on the cavernous sinuses, incomplete or complete para-
lysis of the motor nerves of the eye supervenes on one or both
sides.

Disorders of cutaneous sensibility are rare and generally of
a transitory nature. If the tumour be large, one or more of
the branches of the fifth nerve on one or both sides is first
irritated and then compressed. When a large tumour com-
presses the cerebral peduncles and interpeduncular space, spas-
modic contractions of the muscles of the extremities, followed
by hemiplegia or paraplegia, may supervene.

Two other interesting symptoms are sometimes associated:
with tumours in the vicinity of the pituitary body, the one being;
accumulation of fat in the subcutaneous tissue, and the other:
diabetes. In a case reported by Mohr, as quoted by Ladame;
the patient, who subsequently died from tumour of the pituitary-
body, had become very fat before death ; and in a case under:
the care of Dr. Simpson, in which the symptoms, consisting:
mainly of paroxysmal headaches and blindness, with simple
white atrophy of both discs, pointed to the presence of a tumoun
in this neighbourhood, the patient became very fat after he;
illness. During her residence at the Manchester Royal Ini

THE LOCALISATION OF THE LESION.

659

tirmary she was passing a considerable quantity of pale urine,
being only 1004 in specific gravity. In a case of tumour of
the pituitary body reported by Rosenthal the patient voided
from Slbs. to lOlbs. daily, the specific gravity was from 1038
to 1040, and the urine contained a large quantity of sugar.
Rosenthal conjectures that in cases of this kind the grey matter
lining the third ventricle is first irritated, and that the irrita-
tion travels along the aqueduct of Sylvius to the floor of the
fourth ventricle.

The following case is a good example of the symptoms caused
by tumours in the neighbourhood of the pituitary body, and
possesses a melancholy interest, inasmuch as a respected
member of the medical profession was the victim of the
disease : —

Mr. R , about 34 years of age, consulted me on May 10th, 1878.

He had suffered for some time from frequently recurring attacks of "faint-
ness " and a peculiar defect of vision. He is a tall, dark man, of healthy
appearance, there is a slight depression in the right frontal bone, caused by
a blow received in childhood, but he does not appear to have suffered any
inconvenience from it. During the fainting attacks, one of which I had an
opportunity of observing, there is pallor of the face, the pulse beats from
130 to 140 in the minute, and the patient looks agitated, but there is no
loss of consciousness. The duration of the attack is only about half a
minute. On examining his eyesight he is found to be suffering from double
temporal hemianopsia, the inner halves of the retinae being blind. The
optic discs are perfectly normal, this opinion being confirmed by Mr.
Windsor.

February 7, 1879. The general symptoms continue unchanged, but the
fainting attacks are now accompanied by temporary loss of consciousness.
The patient is now blind on the right eye, while there is temporal hemi-
anopsia of the left. Dr. Little, who made an ophthalmoscopic examination,
reports white atrophy of the right and incipient atrophy of the left
optic disc. The urine is abundant, pale, and of low specific gravity, but
does not contain albumen or sugar. The only psychical disturbance ob-
served was a marked and not unnatural tendency to brood over his own
feelings and symptoms.

The diagnosis in this case presented no great difficulty. It
was manifest that a tumour at the base of the skull was grow-
ing in such a way as to compress the centre of the chiasma at
first, and that it subsequently extended to the right so as to
have compressed the right optic nerve. I saw the patient two

660

FOCAL DISEASES.

or three times subsequent to the last report, but his symptoms
remained unchanged. For the following report of the progress
and termination of the case I am indebted to Dr. M'Fie, of
Bolton.

On the evening of July 3rd, Mr. E was suddenly attacked with

vomiting, followed by an epileptiform seizure, both, symptoms recurring
frequently during a period of an hour and a half. During the convulsive
attacks the spasms were more pronounced on the left than on the right
side. During that night the patient lay in a semi-comatose condition,
hut he gradually regained consciousness on the following day. It was
now noticed that the left side of the face was paralysed, and that there
was some degree of paresis of the left extremities.

August 30. Since last report the patient recovered the use of his
limbs, and, although he has suffered from occasional attacks of sickness,
he has walked about the garden as usual. This evening, however, he has
had another epileptiform seizure.

September AO. Since last report the patient has been downstairs and
walking about the garden, but after partaking of his usual breakfast this
morning he became somewhat suddenly insensible, and died comatose at
night. His temperature immediately before death was 106° F.

At the post-mortem examination the membranes of the brain over the
convexity were found normal. The inner table of the skull and dura
mater were normal at the point corresponding to the external depression
of the right frontal bone. The substance of the brain was observed to be
bulged between the frontal and parietal lobes in the right hemisphere.
On removing the brain a lobulated tumour was observed lying to the right
side of the optic commissure ; the right optic nerve was compressed by it,
but the left nerve occupied its usual position, and did not appear much
altered. The tumour sprang from that portion of the dura mater which
covers the body and basilar process of the sphenoid bone, the body of the
bone being eroded by the growth. The orbital surface of the frontal
lobe of the right hemisphere presented a deep excavation corresponding
to the projection of the tumour, and the nervous tissues in the vicinity
of the growth were somewhat softened. The tumour was niultilobulated
and of the colour of liver.

CGI

CHAPTER IX.

(II.) SPECIAL CONSIDERATION OF FOCAL DISEASES,
ACCORDING TO THE LOCALISATION OF THE LESION
(Continued).

4. LESIONS LOCALISED IN THE STRUCTURES SITUATED
BELOW THE TENTORIUM.

a. Lesions in the Pons and Peduncles of the Cerebrum.

(i.) Lesions in the Pons.

§ 760. Hemorrhage into the Pons. — If the haemorrhage be
of large size, profound apoplexy, with flapping of the cheeks
during expiration, insensibility of the conjunctivae, and strongly
contracted pupils is produced. If the haemorrhage extend
upwards to the grey matter beneath the aqueduct of Sylvius,
the ocular muscles may be paralysed, and the pupils dilated
and fixed. Death occasionally takes place in a few minutes
or in a few hours, although life may be prolonged for a day
or two. Bursting of the haemorrhage into the fourth ven-
tricle is generally attended by convulsious, although convul-
sions may occasionally occur independently of this accident. If
the patient recover from the shock of a central haemorrhage
into the pons, consciousness is gradually regained, but it is
found that all the extremities are paralysed, while cutaneous
sensibility may be more or less impaired. Double facial paralysis
involving the muscles of the eyelids, as well as those of the
mouth, may be present, both sides of the tongue are also para-
lysed, while the patient experiences difficulty in deglutition,
there is a copious flow of saliva from the paralysed side of the
mouth, and the power of articulation is impaired.

If the lesion be situated in the lower part of the lateral half
of the pons, the symptoms may present the appearances charac-
teristic of what Gubler has called alternate hemiplegia. There

662

FOCAL DISEASES, ACCORDING TO

Fig. 275.

is well marked facial paralysis on the side of the lesion, and a
more or less complete motor and sensory paralysis of the limbs
on the opposite side.

If the upper part of the lateral
half of the pons be the seat of the
lesion, the facial paralysis is on the
same side as the paralysis of the ex-
tremities. In order to account for
these phenomena it is necessary to
assume that the fibres of the pyra-
midal tract, which'connect the cortex
of the opposite hemisphere with the
nucleus of the facial nerve in the
upper part of the medulla, cross over
about the middle of the pons, as re-
presented in the annexed figure.

Conjugate deviation of the eyes,
with rotation of the head and neck,
is a symptom of paralysis of the
pons, but the rule with regard to
the direction in which the rotation
takes place is the converse of that
which applies to lesions of the hemi-
spheres. When the lesion is situated
in the hemispheres, the head . and
eyes are turned towards the affected
limbs during convulsions, and towards the side of the lesion in
paralysis ; but in lesions of one lateral half of the pons the
head is turned towards the side of the lesion, if the limbs be
convulsed, and towards the affected limbs when they are
paralysed (Grasset).

Early rigidity of the muscles of the paralysed extremities,
the masticatory muscles, and those of the neck, is often observed
in lesions of the pons.

Disturbances of cutaneous sensibility are frequently met with
in lesions of the pons, wbich become more profound and definite
as the lesion approaches the upper or anterior end of the pons
near the crusta. The sensory disturbances generally consist
of anaesthesia, although unilateral hyperesthesia has occa-

Fig. 275 (From Nothnagel).

L, Left.

R, Eight.

P, Pons.
Mo, Medulla oblongata.
DP, Decussatio pyratnidum.

E, Nerve fibres for the extremi-

ties.

F, Fibres destined for the facial

nerve.

x, Lesion in the upper part of

the pons.
y, Lesion in the lower part of

the pons.

THE LOCALISATION OF THE LESION.

GG3

sionally been observed, and either condition may be accom-
panied by painful sensations in the limbs, or by a subjective
feeling of coldness, even when the temperature of the part is
higher than natural. Implication of the fifth nerve gives rise
to anaesthesia, hyperesthesia, paresthesias, or painful sensations
in the region of distribution of the nerve, as well as to partial
impairment or perversion of taste on the side of the lesion. The
masticatory muscles are often weakened or completely paralysed
on the side of the lesion. Acute lesions of the pons are gene-
rally attended by hyperpyrexia, and the urine is often abundant
and may contain sugar or albumen. These symptoms are
caused by irritation of the grey matter on the floor of the
fourth ventricle.

Three cases have recently been described by Erb, in which,
judging from the symptoms, the primary lesion was situated
in the nerve nuclei of the pons and medulla oblongata. The
affection began with pains in the head and neck, and attained
its full development in the course of a few months. The chief
symptoms consisted of ptosis, paresis, often associated with
atrophy, of the muscles of mastication, tongue, and back of
the neck. There was also weakness of the muscles supplied
by the superior branches of the facial nerve, associated with
phenomena of irritation in them, such as slight clonic spasms ;
but the muscles supplied by the inferior branches were un-
affected. In one case, the movements of the eyeballs were
deficient, but in the other two they were normal. Difficulty of
deglutition was present in two of these cases; buzzing in the
ears, and an abnormal galvanic reaction of the left acoustic
nerve, were observed also in two cases ; while great weakness
of the extremities is mentioned as having been present in two,
and slight weakness of the arms in the remaining case.

One of these cases terminated fatally, but a post-mortem
examination was not obtained. Putting aside the weakness of
the extremities, which was probably caused by implication of
the pyramidal tracts, the other symptoms were evidently due
to disease of the nerve nuclei of the pons and medulla oblon-
gata, or of the fibres of the cranial nerves in their passage
through these structures. It is interesting to observe that the
bulbar nuclei or cranial nerves implicated in these cases are

664

FOCAL DISEASES, ACCORDING TO

those that regulate the actions of muscles which are frequently
associated in their actions. The association of the actions of
these muscles is better observed in animals than in man. Let
us suppose that a dog, for instance, is lying in repose, with his
eyes closed, and that a rabbit or other animal upon which he
preys rushes past to his left. The noise made by the passing
object is conducted to the brain of the dog mainly through the
left ear, and instantly his eyelids open, the eyeballs and the
head are rotated to the left, the mouth opens so as to prepare
for closure of it upon the prey, and the tongue is also ready for
protrusion. It would appear that some of the muscles supplied
by branches of the cervical plexus were affected in these cases
as well as those supplied by the spinal accessory nerve. I would
suggest it as probable that the fasciculus rotundus, the func-
tions of which are not at present known, is the medium of asso-
ciation between the mechanism in the upper end of the pons
and crura cerebri which regulates the movements of the eye-
balls, and the mechanism in the medulla oblongata and upper
end of the spinal cord which regulates the movements of the
neck and head.

Tumours of the Pons. — A slow -growing tumour may be
situated in the centre of the pons, and attain the size of a
hazel-nut, without giving rise to any symptoms.

As in other intracranial tumours, headache is a frequent
symptom of tumour in this region. The headache is sometimes
frontal, sometimes occipital, and at other times general and
deep-seated, but it does not afford any indication of the situa-
tion of the growth.

Motor disturbances constitute the most characteristic features
of tumours of the pons. General convulsions which are not
unfrequently caused by lesions like hemorrhage, which occur
suddenly, are very rare in tumours, and probably never
appear except towards the last few days of life or when the
affection is complicated by meningitis. Even local spasms of
the muscles of the extremities are rare in tumour, inasmuch as
the fibres of the pyramidal tract are slowly subjected to pres-
sure without previous irritation. Paralysis is, therefore, by far
the most important motor symptom observed in tumour of the
pons. When the tumour is situated in one lateral half of the

THE LOCALISATION OF THE LESION. 665

pons, especially in its posterior half, the paralysis assumes the
form of alternate hemiplegia. When, for instance, a tumour is
situated in the right half of the pons on a level with the nucleus

Fig. 276.

Fig. 276 (Modified from Erb). Transverse Section of the Pons on a level with the
Abducens and Facial Roots, from a nine months embryo. — The right half repre-
sents a section made a little lower than the left. P, Pyramidal tract ; p,
accessory portion of the pyramidal tract ; Tr and Tr1, transverse fibres of the
pons ; so, superior olivary body ; ale and pic, anterior and posterior nuclei of the
lateral column respectively, representing the nucleus of the facial nerve ; RVir,
root of the facial nerve ; vi', nucleus of the sixth nerve ; rvi, root of the sixth
nerve ; at, ascending root of the trigeminus. B, The internal division of the
peduncle of the cerebellum as it passes from the cerebellum ; L, posterior longi-
tudinal fasciculus ; ar and ar', the upward continuation of the internal and
external divisions of the anterior root-zone of the spinal cord ; t, fasciculus teres.

of origin of the sixth and seventh nerves {Fig. 276), the extre-
mities and half the tongue on the side opposite the lesion are
paralysed from compression of the pyramidal tract before it has
crossed, while the facial muscles, including those of the eyelid
and eyebrow supplied by the seventh, and the external rectus are
paralysed on the side of the lesion. Under these circumstances
the facial paralysis is caused by compression of the fibres of
the nerve or destruction of the facial nucleus, and the facial
muscles often manifest the reaction of degeneration. In a case

666

FOCAL DISEASES, ACCORDING TO

of this kind under my own observation the reaction to both
currents was diminished in the paralysed muscles, but the
reaction of degeneration never appeared, so that this sign is
not always trustworthy.

It is remarkable how seldom disturbances of the sense of
hearing have been observed in tumours of the pons, weakness
of hearing on the side of the lesion being mentioned a few
times, but unilateral deafness has, so far as I koow, never been
described. Anaesthesia of tHe opposite half of the body and
extremities has been observed only in about one-third of the
reported cases (Ladame), and is never so prominent a symptom
as the motor paralysis. If the tumour be situated in the right

Fig. 277.

^ dt

Fig. 277 (Modified from Erb). Transverse Section of the Pons on a level with the
origin of the Trigeminus, from a nine montlis human embryo. — P, pyramidal
tract ; p, accessory portion of the pyramidal tract ; Tr, Tr', transverse fibres of
the pons ; at, ascending root of the trigeminus and gelatinous substance ; dt,
descending root of the trigeminus ; r, root-fibres of the trigeminus cut trans-
versely ; v, motor nucleus of the trigeminus ; v', middle sensory trigeminal
nucleus ; KV, root of trigeminus ; G, roots of the fifth proceeding from tbe cere-
bellum ; L, Posterior longitudinal fasciculus ; ar and a?1', upward continuation
of the internal and external portions respectively of the anterior root-zone of
the spinal cord.

THE LOCALISATION OF THE LESION. 667

half of the pons on a level with the fibres of origin of the fifth
nerve (Fig. 277), and if it grow forwards so as to compress the
pyramidal tract, the extremities and one-half the tongue are
paralysed on the opposite side of the body, and the face
may still be paralysed on the side of the lesion, either from
compressioD of the fibres of the pyramidal tract belonging to
the facial nucleus after they have crossed in the pons, or from

Fig. 278.

1 cc

Fig. 278 (Modified from Meynert). Transverse Section of the Pons on a level with the
upper end of the Fourth Ventricle, from a nine months human embryo. — P, pyra-
midal tract ; p, accessory portion of the pyramidal tract ; Tr, Tr1, transverse
fibres of the pons ; B, superior brachium of the pons ; L, posterior longitudinal
fasciculus ; ar and ar', upward continuation of the internal and external portions
respectively of the anterior root-zone of the spinal cord ; v', middle sensory
trigeminal nucleus ; dt, descending root of the trigeminus ; IV, nucleus of the
fourth nerve ; cc, aqueduct of Sylvius.

extension of the tumour downwards to reach the fibres of origin
of the facial nerve. The masticatory muscles will also be para-
lysed on the side of the lesion, and various sensory and trophic
disturbances will occur in the region of distribution of the fifth
nerve, such as hyperaesthesia, neuralgic pains, anaesthesia often

668

FOCAL DISEASES, ACCORDING TO

assuming the form of anaesthesia dolorosa, and neuroparalytic
ophthalmia. The taste of the corresponding half of the tongue
is often abolished, while smell is impaired in the nostril
of that side owing to loss of common sensibility. Hemi-
anesthesia of the opposite side may exist, and then the sensory
disturbance presents an alternate distribution like the paralysis.
When the tumour is situated in the middle of the pons from
the first, or extends from one side to the other during its
growth, all the extremities may be paralysed, either simulta-
neously or successively, the muscles of the tongue on both sides
may be weakened, giving rise to difficulties of articulation
(anarthria) and deglutition. There may be double facial
paralysis, complete masticatory paralysis, paralysis of both the
external recti muscles, various sensory and trophic disturbances
in the region of distribution of the fifth nerves, and abolition of
taste on both sides of the tongue. The distribution of the
paralysis may present varieties other than those just described.
Both sides of the face may be paralysed and the extremities on
one side only, or the latter may be unaffected ; on the other
hand, only one side of the face may be affected and the ex-
tremities on both sides. Similar variations may occur with
regard to the distribution of the sensory disturbances, although
they are seldom so well marked. Disorders of motor co-
ordination may be observed in lesions of the pons, especially
tumours, similar to those which will be immediately described
in connection with disease of the peduncles of the cerebellum.

Aneurism of the basilar artery does not appear to cause
symptoms which enable us to distinguish it from a new forma-
tion pressing on the pons in the same situation. It is probable
that unilateral or bilateral deafness is a more frequent symptom
of aneurism than of solid growths.

Psychical disturbances are frequently observed in tumours of
the pons, consisting of loss of memory, apathy, and stupor, all
of them symptoms indicative of compression of the brain.
These symptoms are not, however, directly caused by the affec-
tion of the pons, but by effusion into the ventricles of the brain,
with which the affection of the pons is frequently complicated.

When the lesion implicates, either directly or indirectly, the
pneumogastric nerves or their nuclei of origin, various disorders

THE LOCALISATION OF THE LESION.

609

of respiration and circulation may be present, but these usually
belong to the terminal phenomena.

Albuminuria and glycosuria have been observed in local
diseases of the pons, but by no means with exceptional
frequency.

(ii.) Lesions in the Peduncles op the Cerebrum.
§ 761. The most characteristic features of lesions of the
cerebral peduncle are afforded by an alternate hemiplegia, in
which the extremities, half the face, and half the tongue are

Fig. 279.

Fig. 279 (Modified from Krause). Transverse Section of the Crus Cerebri on a level
with the anterior pair of Corpora Quadrigemina, from a nine months embryo. —
cc, crusta ; P, pyramidal tract ; p, accessory portion of the pyramidal tract ;
ps, Bensory peduncular tract ; LN, locus niger ; UN, red nucleus of the
tegmentum ; L, posterior longitudinal fasciculus ; ar and ar1, upward con-
tinuation of the anterior root-zone of the spinal cord ; in, third nerve ;
in', nucleus of the third nerve ; IT, fourth nerve ; iv', nucleus of the fourth
nerve ; iv", crossing of the fibres of the fourth nerves to opposite sides ; dt,
descending root of the trigeminus ; cc, aqueduct of Sylvius ; x, crossing of the
fibres of the superior peduncles of the cerebellum ; pf, fasciculus of medullated
fibres proceeding to the anterior pair of corpora quadrigemina.

670

FOCAL DISEASES, ACCORDING TO

paralysed on the side opposite, and the oculo-motor nerve on
the same side as the lesion. If the lesion implicate the sensory-
peduncular fibres (Fig. 279, ps), hemianesthesia may be pre-
sent on the side opposite the lesion, but the senses of smell
and sight are not. affected unless neighbouring parts be im-
plicated, or there be secondary atrophy of the optic discs in the
case of tumour. A localised lesion in the superior part of the
crus may give rise to isolated paralysis of the fourth nerve.
Tumours of the crura may paralyse the oculo-motor nerves on
both sides. The form of alternate paralysis just described is only
indicative of lesion of the crus cerebri, when the paralysis of the
limbs and of the motor oculi occur simultaneously. It must
be remembered that multiple lesions in syphilis, situated in dif-
ferent parts of the brain, are very liable to cause a grouping of
symptoms closely simulating those produced by a single lesion
in the Crus cerebri.

b. Lesions in the Peduncles of the Cerebellum.

§ 762. One of the most remarkable examples of haemorrhage
into the middle peduncle of the cerebellum is a case described
by Nonat: —

A woman, about 60 years of age, had an apoplectic attack, charac-
terised by unconsciousness, loss of general sensibility, and paralysis.
The patient lay on her right side, with the head strongly rotated in the [
same direction. The eyeballs were immovable, the right being rotated
downwards and outwards, and the left upwards and inwards. The patient
died on the day following the onset of the attack. At the autopsy a fresh
hseruorrhagic focus, about the size of a chestnut, was found situated in the
right middle peduncle of the cerebellum, extending to some extent into
the corresponding hemisphere. The remainder of the brain and the
membranes were healthy.

Tumours of the middle peduncle pf the cerebellum give
rise to headache and dizziness, trifacial neuralgia, neuro-
paralytic ophthalmia, and partial deafness on the side of the
lesion, and disorders of motor co-ordination, the tendency to fall
being in a lateral direction and towards the side of the lesion.
If the tumour press forwards on the pons, then all the symptoms
of a lesion in the pons itself may be present. Any of the bulbar
nerves may then be implicated according to the position of the

THE LOCALISATION OF THE LESION.

G71

lesion, while compression of the pyramidal tract and of the
sensory fibres may cause hemiplegia and hemianesthesia of the
opposite side. Conjugate deviation of the eyes and rotation of
the head may also under these circumstances take place, the
deviation being directed away from the side of the lesion.
According to Nothnagel, lesions of the superior and inferior
peduncles of the cerebellum do not cause any characteristic
symptoms. He also thinks that stationary lesions of the middle
peduncle do not give rise to symptoms, and that even irritative
lesions only produce them when the connection of the peduncle
with the cerebellum is not completely severed.

c. Lesions in the Cerebellum.

§ 763. Hemorrhage into the lateral lobe of the cerebellum
may or may not occasion loss of consciousness, according to
its extent. The symptoms usually consist of intense cephalalgia,
generally situated in the occiput, but occasionally in the fore-
head ; and vomiting, the latter being probably the most constant
of all the symptoms of cerebellar haemorrhage. Hemiplegia is
not unfrequently present, caused by pressure upon the pons, the
paralysis being sometimes crossed, sometimes direct (Carion).

Spasmodic contractions of the masticatory, facial, or ocular
muscles have occasionally been observed, and marked rigidity of
the muscles of the neck is a more frequent symptom. Paralysis
of the face is exceptional, but when present the orbicular
muscle of the eyelid is implicated, and the paralysis is situated
on the side of the lesion. Strabismus may occasionally be
present owing to compression of one of the motor nerves of the
eyeball. Conjugate deviation of the eyes has been observed, and
it has always been directed away from the lesion. The move-
ments of articulation and deglutition are rarely affected. The
pupils are sometimes dilated, more frequently contracted, and
occasionally insensible to light. In exceptional cases a certain
degree of anaesthesia of the opposite half of the body has been
observed. Blindness has sometimes been observed, as might
have been expected from the proximity of the corpora quadri-
gemina to the cerebellum.

A large haemorrhage into the middle lobe of the cerebellum
may by pressing upon the pons and medulla oblongata cause

672

FOCAL DISEASES, ACCORDING TO

sudden apoplectiform symptoms, speedily terminating in death.
In haemorrhages of smaller size the symptoms are less marked
or wanting. Hemiplegia is not so frequently present as in
lesions of the lateral lobes, and in about one-third of the
reported cases excitation of the genital functions is mentioned
Large stationary lesions may occur in the cerebellum without
giving rise to any recognisable symptoms during life.

Abscesses of the cerebellum have frequently been observed ;
the symptoms on the whole are like those caused by tumour.

Tumours in the cerebellum give rise, in addition to intense
paroxysmal cephalalgia and vomiting, to characteristic motor
disturbances. The most usual of these are a staggering gait,
reeling, or a tendency to fall to one side. When the tumour is
situated in the upper part of the middle lobe, the patient
frequently manifests a tendency to fall backwards, while if it
be situated in the inferior part of the same, it is probable that
the tendency is to fall forwards or to revolve forwards round a
horizontal axis. When the tumour is situated in one of the
lateral lobes, the patient has a tendency to fall towards the side
in which the tumour is situated. If the tumour be growing
slowly, the tendency to fall to one side is counteracted to such
an extent by cerebral action that the symptom is not readily
elicited. A slight stagger may, however, be observed to one
side when the patient is asked to turn round suddenly, and
especially if the eyes be closed. 1

Symptoms of motor irritation are also observed in cases of
tumour of the cerebellum. The most usual of these is a
tonic contraction of the muscles of the neck, causing retraction
of the head. This tonic contraction may extend to the muscles
of the trunk and extremities, giving rise to tetanic seizures
(Hughlings- Jackson). During these attacks the trunk is usually
arched, the head retracted, and the various segments of the
lower extremities extended upon one another and the trunk,
so that the body rests upon the head and heels, as in tetanus.
The various segments of the upper extremities are flexed upon
one another, this being the position occupied by them in tetanus.
The tonic contractions may be more pronounced on one side,
and then the body may be arched towards that side.

Movements of the eyeballs are frequently observed in cases of

THE LOCALISATION OF THE LESIOX.

073

cerebellar tumour. These movements may be vertical, hori-
zontal, or oblique, and are generally parallel (Mackenzie).
Sometimes they are only observed during the convulsive attacks,
but when there is permanent rigidity the eyes may be rotated
in one direction and fixed, or present slight parallel oscillatory
movements.

Tumours of the cerebellum are very liable to be complicated
by effusion into the ventricles of the brain, due either to
pressure on the vena? magna? Galeni or to obliteration of the
communication between the spinal and cerebral subarachnoidal
spaces (S. Mackenzie). This effusion in children gives rise to
enlargement of the head and distension of the fontanelles,
similar to that occurring in chronic hydrocephalus. When the
fontanelles have closed before effusion has taken place, the
head is prevented from enlarging, but in these cases sudden
death is very liable to occur from compression of the floor of
the fourth ventricle, and consequent arrest of the function of the
respiratory centre.

As already remarked, the most marked clinical characteristic
of a tumour of the superior part of the middle lobe of the
cerebellum is a tendency to fall backwards, or to rotate back-
wards round a horizontal axis. In a case under the care of
Dr. Leech, in which this symptom was very marked, and in
which the post-mortem examination was conducted by myself,
a tubercular tumour, the size of a hen's egg, was found in the
right occipital fossa, immediately under the tentorium and close
to the falx cerebelli. In the case of a child, aged 4 years,
under my own care, there was a tendency to fall diagonally
backwards and to the right. I expected to find a tubercular
tumour in the superior surface of the cerebellum, situated be-
tween the right lateral and middle lobes. Instead of that I
found a tubercular tumour, the size of a pigeon's egg, situated
under the tentorium in the occipital fossa to the left of the falx
cerebelli, and a second tumour, about the same size, in the
right middle peduncle. The tendency to fall in a diagonal
direction was evidently the result of a composition of forces,
the first tumour causing a tendency to fall backwards and the
second a tendency to fall to the right.

The following case is an instance of tumour of the inferior
R R

674 FOCAL DISEASES, ACCORDING TO

part of the middle lobe of the cerebellum, although the lesion
was not limited to that region : —

John Thomas Gould, set. 14 years, was admitted into the Royal Infirmary
on March 5, 1877, under the care of Dr. W. Roberts, to whose kindness I
am indebted for permission to publish the case. He was a strong and
healthy boy until a few months ago ; his parents were also healthy, and
there was no family history of consumption or any other constitutional
disease. He was a bricksetter by trade, and three months previously to
admission fell from a ladder and struck the back of his head on the pave-
ment, and since that time he has suffered from more or less constant
occipital headache.

Condition on admission. — As he lies in bed he can move his legs freely
in any direction ; but on attempting to walk, the feet are alternately pro-
jected forwards, the heel coming down forcibly as in locomotor ataxy.
He cannot maintain the erect posture unsupported ; and when all external
aid is momentarily withdrawn, his head shoots downwards and forwards,
as if the body were about to revolve round a transverse horizontal axis.
When the patient is caught in the act of falling and raised again to
the erect posture, he complains of dizziness, and sees objects revolving
from right to left. On directing his eyes to the right, a slight oscillatory
movement of the eyeballs is observed, but there is no nystagmus when
he looks straight in front. The patient is almost quite blind in the left
eye, but can distinguish objects clearly with the right eye.

"When the right eye is fixed on an object, such as a finger twelve inches
in front, a second finger moved laterally and to the right is seen until it is
almost nine inches from the first, showing that the field of vision to the
right is not sensibly diminished. But starting again from the finger on
which the eye is fixed, and moving the second laterally to the left, the
' latter disappears from view when it is from one to two inches removed
from the former. I say from one to two inches, because his replies were not
always the same, thus indicating that the sensitive and blind portions of
the retina are not separated from one another by a sharp and defined
border, but fade insensibly into each other. The ixipils are equal, both
being dilated and very sluggish to light. An ophthalmoscopic examination
reveals double optic neuritis with swollen disc, but there is no atrophy.
The. other special senses and the mental faculties are unaffected, the urine
is free from sugar or albumen, the appetite is good, and all the other
functions of life are normal. He was ordered iod. 'potass., grs. x., to be
taken three times a-day. On March 31, four weeks after admission, it is
evident that the symptoms have altered considerably. The patient now
habitually lies on his back, or slightly inclined to one side. He cannot sit
erect without support, but he has still some degree of voluntary control
over his legs, although the movements are feeble. Cutaneous sensibility
is impaired in the lower extremities ; he can still feel when touched, but
he cannot localise the touch well. Sensibility to variations of temperature

THE LOCALISATION OF THE LESION. 075

and to pain is also impaired. There is complete blindness of both eyes,
but there is only slight atrophy of the optic discs. Two days ago he
passed his urine in bed for the first time. His bowels are very constipated,
and there is general emaciation.

April 15M.— He complains much of frontal headache. There is com-
plete anaesthesia, and entire loss of voluntary motion of the lower extremi-
ties; the stools and mine are passed under him, and there is a large bed-
sore over the sacrum. He cannot hear the ticking of a watch so well with
the left as with the right ear.

May 14^.— There is complete anaesthesia of all parts below a line
passing round the body on a level with the anterior superior processes of
the ilium. Reflex irritability is entirely abolished in the lower extremities,
as tested by tickling, pricking, and the faradic current. The muscles of
the legs and thighs do not react to either the faradic or constant currents.
The calf of the right leg measures 9| and that of the left only 7£ inches.
Each thigh measures 9J inches. The muscles of the thighs and of the
right leg appear only to be emaciated in proportion to the rest of the
body; but it is manifest that the muscles of the left leg are specially
atrophied. There are deep bed-sores over the sacrum, the prominences of
both thighs, the external maleoli of both ankles, and the inside of the left
knee. The intelligence is greatly blunted, and he lies in a half stupor, but
replies readily to any simple question asked him. His pulse is very feeble
and beats about 140 in a minute. His appetite continues remarkably
good. About a week ago it was noticed that the left eyelid was only
half closed when he was asleep, and he could not close it entirely by
a voluntary effort. There was also slight paralysis of the left facial
muscles, so slight that the difference between the two sides could scarcely
be detected when the face was quiescent, but recognisable when the patient
smiled. This affection of the facial nerve only lasted a few days, and has
now entirely disappeared. The condition of his hearing cannot be satis-
factorily tested, owing to the apathetic state of his intelligence.

From this time he lingered on without any further special symptom
manifesting itself. He became more and more apathetic and extremely
emaciated, and died on July 3rd, four months after entering the Infirmary,
and seven months after the fall, to which in all probability the origin of
the disease may be traced.

Sectio cadaveris. — Twenty-four hours after death rigor mortis is mode-
rately well established in both extremities. The body is greatly emaciated.
The calves of the legs each measure 7 inches, and thighs 7£ inches. The
sacrum, both trochanters, and the external malleolus of the left foot are
exposed and denuded in consequence of extensive bed-sores. The tips of
both ears are also ulcerated, as well as the inside of the left knee.

On removing the calvarium the brain appeared to project, and the con-
volutions were flattened. The sinuses and the veins on the surface of the
brain were gorged with blood. The substance of the brain was somewhat
soft, and the ventricles were distended with fluid ; but the cerebrum was

676

FOCAL DISEASES, ACCORDING TO

healthy in other respects. Some grumous turbid fluid escaped from
between the cerebellum and corpora quadrigemina. On inspecting the
cerebellum the edge of a tumour was noticed between the inferior surface i
of the middle lobe at its posterior margin and the superior surface of the
medulla oblongata ; while the anterior end of the tumour could be seen
between the cerebellum and corpora quadrigemina. On making a vertical
section of the cerebellum in the middle line down to the floor of the fourth
ventricle, the tumour was seen to occupy the whole of the anterior part of
the middle lobe of the cerebellum, being somewhat more developed on
the right than on the left side. In consistence the tumour was soft,
of a greyish-red coloiu-, the centre being broken down so as to form a
small cavity from which the turbid fluid already mentioned had escaped.
The tumour was not circumscribed, its margins gradually blending with
the surrounding nervous tissue. The growth passed along the right
superior peduncle of the cerebellum to reach the corpora quadrigemina,
and the latter were somewhat softened and flattened. On opening the
spinal canal the cord was seen to occupy the whole of the cavity trans-
versely, the diameter of the cord being about one-third larger than that
in health. The whole of the cord felt brawny, like bacon. On making
transverse sections, from above downwards, half an inch apart, the mem-
branes in the cervical region were seen to be adherent, slightly thickened,
and the cord was softened ; but in the upper dorsal region the spinal pia
mater, especially on the posterior aspect, was three times as thick as in the
healthy cord. In the middle of the dorsal region the thickened membrane
had developed into a dense well-defined tumour, which pressed on the
cord from behind forwards, so that only a small part of the anterior seg-
ment of the cord was left. In the lumbar region, again, the tumour sur-
rounded the cord, so that a central core, about the size of a goose quill, of.
softened nervous tissue was all that was left to represent the spinal cord.
The tumour was the colour and texture of bacon, and much denser than
that of the cerebellum.

The left lung was adherent to the chest walls. Both lungs were
healthy. The heart was normal. The abdominal organs were healthy.
Microscopic examination showed that the tumour consisted of small
delicate cells imbedded in a finely granular substance. The growth in the
cord presented similar microscopic characters to the cerebellar tumour ;
but contained a larger amount of intercellular substance.

The first time I examined the patient my diagnosis was
"tumour, probably a glioma, situated 'in the inferior portion of
the middle lobe of the cerebellum, and pressing forwards on
the corpora quadrigemina." The reasons for regarding the
case as one of intracranial tumour are so manifest as scarcely
to require mention. They are the history of an injury to the
head, the gradual development and progressive character of the

THE LOCALISATION OF THE LESION.

077

symptoms, the constant headache, and the existence of double
optic neuritis. My reason for believing that the tumour was
situated in the inferior portion of the middle lobe of the cere-
bellum was the remarkable manner in which the head and
shoulders shot forwards and downwards, as if the patient were
about to revolve round a horizontal axis. The circumstances in
favour of the tumour being a glioma were that, if the diagnosis
with respect to the localisation was correct, it probably grew in
the substance of the nervous tissue itself, and not from the
membranes; while the appearance of the patient and the family
history were against tubercle ; there was no evidence of con-
genital syphilis ; and the age of the patient put cancer almost
out of the question.

My reasons for thinking that the tumour pressed forwards
upon the corpora quadrigemina were that I thought this would
to some extent explain the excessive staggering present during
attempts at walking ; but much more that it would explain the
great impairment of vision present at such an early stage of the
disease. But the peculiar character of the disorder of vision
demands an explanation; and for this purpose let us take Char-
cot's scheme of the decussation of the optic tracts as our guide.

In this case, vision was almost totally lost in the left eye,
and the state of vision of the right eye simulated nasal hemiopia.
I say simulated, because it was not a case of hemiopia at all.
The condition of vision in both eyes was that of amblyopia in
its progress towards amaurosis. The amaurotic condition was
nearly reached in both sides of the retina in the left eye; but
in the right eye the right half of the retina had become
amaurotic, while vision was tolerably good in the left half; and
between the halves of the right retina there was a relatively
broad border land, where the comparatively good vision of one
side faded gradually into the blindness of the other. Such a
condition as this could not, therefore, have been caused bv the
pressure of a tumour on the commissure or optic tracts; it was
not likely to have arisen directly from the optic neuritis,
inasmuch as there was no atrophy of the disc ; and it must
therefore have been caused by a lesion interfering with the
optic fibres, either directly or indirectly beyond the termination
of the optic tracts in the external geniculate bodies.

FOCAL DISEASES, ACCORDING TO

It appeared to me very probable that a tumour pressing on
the right side of the corpora quadrigemina, and extending
gradually to the left, would produce the condition of vision met
with in this case. The whirling of objects from right to left
which the patient described showed that there was a greater
amount of irritation of the right than of the left lobe of the
cerebellum, and this rendered it probable that the tumour of
the middle lobe extended farther to the right than to the left.

Suppose, then, that a tumour is pressing on the corpora
quadrigemina from behind forwards, and from right to left, the
fibres (b a) coming from the left eye, and meeting at LOD, would
be first interfered with, then the fibres (a') coming from the
right half of the retina of the right 'eye would be intercepted
in their passage behind the corpora geniculata to the opposite
side. The fibres b' coming, from the left half of the retina of
the right eye would be the last to be injured, so that the con-
dition of vision which was present in this ease would be pro-
duced. It may be urged that Charcot's scheme of decussation is
merely diagrammatic, and that the points LOG and LOD are

Fig. 280.

Fig. 280 (After Charcot). Diagram of Decussation of the Optic Tracts.— T, Semi-
decussation in the chiasma ; TQ, Decussation of fibres posterior to the external
geniculate bodies (OG-) ; a' b, Fibres which do not decussate in the chiasma ;
b' a', Fibres coming from the right eye, and coming together in the left hemi-
sphere (LOG) ; K, Lesion of the left optic tract producing right lateral hemia-
nopsia ; A, lesion in the left hemisphere (LOG), produces crossed amblyopia
(right eye). T, Lesion producing temporal hemianopsia ; N N, Lesion producing
nasal hemianopsia.

TETE LOCALISATION OF THE LESION.

079

supposed to represent positions in the cortex of the hemispheres;
but my reply must be that I am only making a diagrammatic
use of it. If there is a semi-decussation of the optic nerves in
the chiasma, and if the fibres which do not cross in that place
decussate behind the corpora geniculata, then, whatever may be
the further course of these fibres, some such effect as that indi-
cated would be produced by a tumour pressing from behind
forwards, and from right to left on the corpora quadrigemina.
This at least was the process of reasoning by which I came to
the conclusion that the case was one of tumour of the anterior
part of the middle lobe of the cerebellum, inclining to the
right side, and pressing forwards on the corpora quadrigemina,
and this conclusion was verified to a considerable extent by the
post-mortem. One serious objection I always 'had to this view
was, that it was not manifest how the floor of the fourth ven-
tricle could escape under such circumstances; and yet there
was no sugar in the urine, no polyuria, and the breathing was
not interfered with. The autopsy explained this. It showed
that the corpora quadrigemina were probably not so much in-
terfered with by pressure as by extension of the glioma along
the superior peduncle of the cerebellum into the substance of
these bodies.

As the case progressed, it became evident that there was
an independent affection of the cord, as evinced by the com-
plete anaesthesia, and loss of reflex irritability in the lower
extremities, as well as by the trophic changes already described.

Two suppositions could be made with regard to the affection
of the cord. Either that there was tumour pressing on the cord of
the same nature as that in the cerebellum, or that there was
extensive softening in the lumbar region. I must acknowledge
that I felt inclined to adopt the latter view, inasmuch as I was
only thinking of a circumscribed growth, and was not prepared
to find a new formation extending the whole length of the cord.
It is very probable that the new growth had begun to develop
in the spinal cord at the time the patient was admitted into
the Infirmary, and that the symptoms of motor inco-ordination
observed were due, in part at least, to implication of the posterior
root-zones in the morbid process.

In the following case several tumours were found in the cere-

G80

FOCAL DISEASES, ACCORDING TO

brum as well as in the cerebellum, yet it was not difficult to
diagoosticate the presence of a tumour in the latter : —

Louis Ikin, sat. years, entered the Southern Hospital on October
3rd, 1877. His mother stated that he was always healthy until 14 months
ago, when he had an attack of chicken-pox, after which he suffered from
sore eyes. Soon afterwards he began to put his hand to his forehead and
to complain of pain there, and he gradually lost flesh. There was also
some discharge from the right ear. These symptoms continued for about
eight months without any appreciable change; but six months before
admission the mother was awakened during the night by a loud scream
from the child, who was found on the floor, having been apparently-
projected from his bed by the violence of a convulsion. On being picked
up he was found completely paralysed on the right half of the body, and
aphasic.

The paralytic symptoms gradually improved, but convulsions super-
vened, the spasms being hmited to the paretic side, and not attended by
loss of consciousness. He had had the last of those attacks a fortnight
previous to admission. The convulsive movements always began in the
right hand and arm ; but the mother could not be sure whether the right
side of the face or the leg was next invaded. The parents had already lost
one of their children from " water on the brain ; " and another, who had
reached the age of eight years, had never been able to speak more than
a few words (congenital aphasia).

Present Condition. — There is a slight degree of right-sided facial
paralysis, only apparent when the child cries or smiles. There is also
paresis of the right arm and leg ; but he has considerable voluntary power
over both. The fingers of the right hand are semi-flexed, and the thumb
bent inwards on the palm under the fingers. There is some muscular
rigidity on attempting passive movements of the fingers, hand, and fore-
arm, and there is also some degree of rigidity on attempting to move the
right leg and foot. The child, on being placed on his feet, can stand and
even walk a few steps if the upper part of the body be supported, but when
every support is withdrawn his face assumes a frightened expression, and
he would immediately fall on the paralysed side unless prevented. The
act of falling does not consist of a simple yielding of the paretic leg, but
the head and upper part of the trunk shoot laterally to the right, while
the leg of the same side is maintained extended.

His sight is not good. He sees an object held out before him, but on
putting his left hand out to grasp it he has to grope for it. There is
double optic neuritis with commencing atrophy of the discs. His speech
is almost lost, the only word he can say being " Mamma."

November 10th. — About ten days ago he had a convulsion which was
mainly hmited to the left side, this being the first observed since he
entered the hospital.. He has had as many as three attacks in a day,
while some days passed without his having any attack. Altogether he has

THE LOCALISATION OF THE LESION.

081

had about twenty attacks in the ten days. I was not fortunate enough
to see one of these attacks myself, but I gave particular instructions to
the nurse to observe whether the convulsion began in the hand, face, or
leg. The description of the nurse was always to the same effect, that the
attack began with a scream, that the body was bent like a bow, so that
the left ankle and left side of the face nearly met, and that immediately
after the attack the child resumed its usual manner, without manifesting
any tendency to sleep. There is no distinct paralysis of the left extre-
mities.

December 12th.— The child has only had a few convulsive attacks since
the last report, and none at all during the last fortnight. He is now
nearly blind, being able only to see an object placed to the left of the left
eye. There is slight nystagmus. The muscular rigidity on attempting
passive movements of the right arm and leg is now more marked, and the
paralysis on that side is also more pronounced. The lower extremities
are congested, of a blue colour, and cold, but there is no muscular atrophy.
The child eats his food well, and there is a fair amount of subcutaneous
fat. He is becoming apathetic and passes his water and stools under him.

January 28th. — He now lies on his back, and is getting more and more
somnolent and apathetic. The nystagmus is more pronounced and there
is conjugate deviation of the eyes to the left. He screams at night and
disturbs the other children in the ward, on account of which he was dis-
charged.

I continued to visit the patient occasionally at his home, but the only
symptoms of note observed were those of a gradual compression of the
brain, enlargement of the head, separation of the fontanelles, and fluctua-
tion over them. He died on March 13th, 1878.

The post mortem was conducted 24 hours after death. The ventricles
were much distended by a fluid effusion. Four tubercular tumours, each
about the size of a hazel-nut, were found lying along the sulcus of Rolando
of the left hemisphere, one of them being situated at its inferior extremity
close to the posterior extremity of the third frontal convolution. Another
tumour, also about the size of a hazel-nut, was found in the cortex of the
right hemisphere near the superior extremity of the ascending parietal
convolution. A tumour, about the size of a pigeon's egg, was situated in
the left lenticular nucleus, and compressing the internal capsule. The
inferior surfaces of the right and middle lobes of the cerebellum were
occupied by a tubercular mass, which extended also into the left lateral
lobe. A microscopical examination of the spinal cord revealed sclerosis
of the right lateral column.

The first time I examined this child the presence of double
optic neuritis rendered it clear that the case was one of intra-
cranial tumour, the slight stagger to the right and the purulent
discharge from the right ear pointed to a tubercular tumour of

G82

FOCAL DISEASES, ACCORDING TO

the right lobe of the cerebellum ; while the history of unilateral
convulsions beginning in the right arm and the aphasia
pointed to the presence of one or more tubercular tumours
along the sulcus of Rolando. My diagnosis, therefore, was
tubercular tumour situated in the sulcus of Rolando of the left
hemisphere, and another in the right lobe of the cerebellum.
As the case progressed the hemiplegia became so complete that
a cortical tumour would hardly be sufficient to account for it,
and I consequently assumed the existence of another tumour
in the left lenticular nucleus, and compressing the internal
capsule. Had I adhered to this diagnosis it would have been
absolutely accurate up to a certain point. But when the con-
vulsions began in the left half of the body I began to waver in
my previous opinion with regard to the localisation of the
tumours. The unilateral convulsions of the left half of the body
were either due to irritation of the motor area of the cortex of
the right hemisphere, or to irritation of the cerebellum. From
the uniform description of the nurse I came to the conclusion
that these convulsions were of the nature of tetanic seizures,
and therefore due to cerebellar irritation. The unilateral
character assumed by them I explained by supposing that the
tumour was growing in the left lobe of the cerebellum and
causing irritation of the left middle peduncle, but it is of course
doubtful whether there is any justification for such a supposition.
I also thought that the presence of one tumour, situated in the
centrum ovale of the left hemisphere, in such a position as to
interrupt the fibres of the pyramidal tract and the fibres of the
corpus callosum connecting the posterior extremities of the third
frontal convolutions with one another, might account for the
right hemiplegia and aphasia, without assuming the existence
of a tumour in the cortex and another in the lenticular nucleus.
I made a communication to the Manchester Medical Society,
several weeks before the death of the patient, in which these
various opinions were discussed, and, owing to the reluctance I
felt in assuming the existence of five or six tumours situated in
various parts of the cerebral hemispheres and cerebellum, I
came to the conclusion that a tumour in the centrum ovale of
the left cerebral hemisphere and another in the left lobe of the
cerebellum might account for the symptoms. Had I assumed

THE LOCALISATION OF THE LESION.

683

the existence of the Larger number of tumours my diagnosis
would have been almost absolutely correct. I am even now
unable to decide whether the unilateral spasms of the left half
of the body were of the nature of tetanic seizures or were true
cerebral convulsions caused by the irritation of the tumour
found in the cortex of the right hemisphere, near the superior
extremity of the ascending parietal convolution.

In the following case the symptoms pointing to an intracranial
lesion were very obscure, yet the presence of double optic
neuritis and a slight stagger in the gait of the patient rendered
it possible to diagnosticate a tumour of the right lobe of the
cerebellum. For the notes of the case I am indebted to
Mr. Luckman : —

Annie E. M , ret. 21 years, domestic servant, entered the Manchester

Royal Infirmary on October 21st, 1880, under the care of Dr. Ross.
The patient was healthy until about six months ago, when she began to
suffer from a dull headache, occupying the vertex, and extending to either
temple. The headache did not prevent her from sleeping, it was worse, as
a rule, on getting up in the morning, and generally improved after she had
had a warm cup of tea. The headache was liable to intense paroxysmal
aggravation, and during these attacks the patient generally vomited.
About two months ago she felt a little unsteadiness in walking, the head-
aches increased in intensity, and she suffered so much from retching and
vomiting that she was compelled to give up her situation.

On presenting herself at the Infirmary as an out-patient, a week ago,
the only symptoms complained of were intense headache, while there were
great emotional disturbances like those of hysteria. As the patient walked
across the floor a slight staggering towards the right side was observed,
this being especially marked when she turned suddenly round or closed
her eyes. It was not then convenient to make an ophthalmoscopic
examination. When she appeared at the end of a week as an out-patient
the symptoms were still the same, only the hysterical symptoms were
deteidedly more pronounced, and she was admitted as an in-patient.

Present Condition. — On admission an ophthalmoscopic examination
revealed double optic neuritis, but she could read the smallest print. She
never had diplopia, and there was no strabismus or nystagmus. There
was no paralysis, no cutaneous sensory disturbances, and no affection of
the special senses. The patient still suffered from headache, characterised
by remissions and paroxysmal exacerbations, as well as from attacks of
hiccough. In walking a slight stagger is occasionally observed, the tendency
to fall being always towards the right. She also progressed in a slightly
curved line, instead of walking in a straight course. The tendency to
stagger is increased when the patient closes her eyes or turns suddenly
round.

684

FOCAL DISEASES.

November 2nd. — No new symptoms were observed since last report
until 1 o'clock to-day, wben it was noticed that the patient's face and
lips bad become Hvid ; she also complained of a dull, heavy headache
seated on the vertex of the head. At 3 p.m. respiration suddenly ceased,
and Dr. Steele, who was immediately sent for, resorted to artificial
respiration, and maintained the action of the heart for upwards of twenty
minutes, but the pulse ceased to beat four minutes after the artificial
respiration was discontinued. During this time it was noticed that the
right pupil was dilated and the right side of the face slightly paralysed.

The post-mortem examination was conducted by Dr. A. H. Young,
eighteen hours after death. The cerebral hemispheres and basal ganglia
were normal. The ventricles were distended with fluid, and the aqueduct
of Sylvius was considerably dilated. In the cerebellum a well-defined
tumour was found, forming a well-marked projection in the right lateral
lobe. The cerebellar substance appeared prominent in the region of the
foramen magnum, as though pushed out, and seemed to press upon the
floor of the fourth ventricle.

The following case illustrates the movements of the eyeballs
sometimes observed in tumours of the cerebellum : —

In the case of a boy, aged 12 years, under my care at the Southern
Hospital, the symptoms on admission were headache, double optic neuritis,
amblyopia, and a slight stagger on walking, the tendency to fall not being
greater to one side than to the other. He lived in the hospital nearly three
months, and during that time the optic neuritis gave place to atrophy of
the discs, and the amblyopia to amaurosis ; while the change in the other
symptoms consisted of a progressive impairment of the mental faculties
from gradual compression of the brain, the patient ultimately dying coma-
tose. During the last three days of life there was rigidity of the muscles
of the back of the neck along with vertical and parallel movements of the
eyeballs, consisting of an upward alternating with a downward rotation.
The time occupied by each rotatory movement was remarkably uniform,
and as many as twenty of these occurred in a minute. At the autopsy
two tubercular tumours, each about the size of a pigeon's egg, were found
symmetrically situated in the inferior surfaces of the lateral lobes. A
third tumour, about the size of a hazel-nut, was found in the superior
portion of the middle lobe.

G8o

CHAPTER X.

II. DIFFUSED DISEASES OF THE ENCEPHALON.

(I.) ANiEMIA AND HYPEREMIA OF THE BRAIN.

(i.) Anemia of the Brain.

§ 764. History. — Dr. Marshall Hall was one of the first to direct
attention to the symptoms produced by cerebral anaemia, and as these
symptoms in children closely simulate those of acute hydrocephalus he
proposed to call the condition hydrocephaloid or hydrencephaloid disease.
He also pointed out that symptoms which had hitherto been attributed
to cerebral hypertemia were really due to ansemia, and were such as
frequently occurred after exhausting hemorrhages. About the same time
Abercrombie gave a similar interpretation to the symptoms of syncope and
of apoplexia ex inanitione. The study of the effects of ligature of the
carotids by Sir Astley Cooper led the way in the experimental investigation
of cerebral antenna, which was completed in more recent years by the
labours of Schiff, Kussmaul and Tenner, and many others.

§ 765. Experimental Investigation. — When one of the common carotid
arteries is compressed, there is first indistinctness of vision, and after a few
seconds a prickling sensation is felt in half the face, followed by a similar
sensation in the limbs and opposite half of the body. General sensibility
becomes indistinct, the sense of touch is impaired, and even trembling and
convulsive twitchings may occur; but after three or four minutes these
symptoms disappear, because the collateral circulation soon compensates
the effects of the compression. Compression of both carotids is followed
by indistinctness of vision amounting to almost complete blindness, con-
traction followed by dilatation of the pupils, the respiration becomes slow,
deep, and sighing, and there is a sense of oppression about the thorax.
These symptoms are followed by drowsiness, staggering, and loss of con-
sciousness ; and if the compression be continued, universal muscular
twitching, symptoms of choking, and vomiting appear (Schiff).

If the circulation through both carotid and vertebral arteries be sud-
denly interrupted, the pupils first contract, but soon dilate again, the eye-

686

DIFFUSED DISEASES OF THE ENCEPHALON.

balls roll upwards and outwards, the jaws are clenched, and the respiration,
at first short, becomes slow and deep ; these symptoms are soon followed
by general muscular relaxation, loss of consciousness, and general convul-
sions. Similar symptoms attend bleeding to death. If the animal be
previously enfeebled by loss of blood, death results from syncope without
convulsions. The animal may be kept for a short time in a condition
simulating death ; but if artificial respiration be maintained, gradual
recovery takes place when the blood is allowed to flow again through
the vertebral arteries.

It has been found that obstruction of the circulation through the
carotids in animals only causes trifling effects in comparison -with the
symptoms produced in man, showing that the anterior lobes are of much
greater importance in man than in animals.

§ 766. Etiology. — Anaemia of the brain is caused by in-
fluences which act upon the vascular system of the brain alone,
or it may form only a part of general anaemia. The entire brain
may be affected, causing universal anosmia, or it may be
limited to certain parts causing 'partial anosmia. The symp-
toms also differ much according as the anaemia is suddenly or
gradually produced.

Acute universal cerebral anosmia is caused in its most
typical form by a sudden loss of a large quantity of blood.
The most frequent causes of this form of cerebral anaemia are
post partum haemorrhage, haemorrhages from the nose, lungs,
stomach, and intestines, and large losses of blood from external
inj uries. A sudden fall of arterial tension from the relaxation of
large vase alar areas in other parts of the body may also cause
cerebral anaemia. The faintness which frequently accompanies
the rapid withdrawal of ascitic fluid, or immediately after
parturition, is probably caused by the flow of a large quantity
of blood into the relaxed abdominal vessels.

Cerebral anaemia is a frequent accompaniment of organic
diseases of the heart, more especially of aortic regurgitation,
in which death often results from syncope. Weakness of the
muscular walls of the heart, whether temporary as after acute
febrile diseases, or permanent as in fatty degeneration, is apt
to produce faintness from cerebral anaemia. Irritation of the
vagus may cause cerebral anaemia by a temporary arrest of the
heart's action. Fainting, the result of mental impressions, may

DIFFUSED DISEASES OF THE ENCEPHALON. G87

be produced in this way, although spasm of the cerebral vessels
from irritation of the sympathetic nerves may be the cause.

Intense pain may cause faintness or even syncope, which
may result from reflex irritation of the vagus, or direct irri-
tation of the sympathetic. But the direct effect produced
on the nerve-centres must also contribute to the result. The
strong nervous discharges caused by the external injury ascend
along centripetal fibres and produce a corresponding strong
nervous discharge from the higher nerve-centres, . which is
conducted along centrifugal fibres to the periphery, giving rise
to the cries and various bodily contortions which indicate pain.
Again, strong nervous discharges from the higher centres must
be followed by exhaustion and consequent impairment or aboli-
tion of function, just as the discharges of epilepsy are accom-
panied by unconsciousness.

Acute universal cerebral anaemia may probably be caused by
various poisons, although anaesthetic agents, like chloroform and
ether, probably act less upon the circulation of the brain than
upon the cerebral tissues themselves.

Chronic Universal Cerebral Anaemia. — This variety is
caused by any condition which withdraws a large quantity of
the nutrient fluids from the body, such as repeated losses of blood,
severe diarrhoea, chronic suppuration, and all causes of general
anaemia. Chronic anaemia of the brain also occurs in certain
valvular lesions and fatty degeneration of the heart. The intro-
duction of foreign matter into the cavity of the skull, as inflam-
matory exudations in meningitis, the fluid which transudes in
oedema, haemorrhagic foci, and cerebral tumours, may also cause
chronic anaemia of the brain.

Partial Cerebral Anosmia. — Partial anaemia is caused when
one of the vessels of the brain is obstructed, or when external
pressure is exerted by a tumour on a vascular area, but these cases
have already been described. Unilateral anaemia is seen after
ligature of the carotid on one side ; but the symptoms are only
temporary, except in the cases in which there is an impervious
condition either congenital or acquired of the communicating
arteries of the circle of Willis.

688 DIFFUSED DISEASES OF THE ENCEPHALON.

§ 767. Symptoms.

Acute Universal Cerebral Ancemia. — The initial symptoms
are obscuration of the senses, buzzing in the ears, dizziness, con-
traction followed by dilatation of the pupils, imperfect reaction
to external stimuli, and loss of consciousness. The surface
becomes cold and pale, the respiratory movements, accelerated at
first, become slow, and this condition is frequently followed by
general convulsions and coma. The symptoms which are pro-
duced by the temporary ansemia caused by powerful mental
impressions differ considerably from those just described. At
first there is some degree of mental incoherence manifested by
the inability of the patient to direct his attention to a particular
object, a feeling of oppression in the chest, along with a ten-
dency to gape. The face becomes pale, a cold perspiration
breaks out on the forehead and sometimes on the entire body,
and there is general muscular relaxation. There is ringing in
the ears, dimness of sight, nausea, and sometimes vomiting.
The pulse is small, compressible, but regular. The patient may
now begin to recover or fall insensible to the ground, and after
a few moments in the recumbent position he begins to recover.
This constitutes an ordinary fainting-fit or syncope.

Chronic Universal Cerebral Ancemia. — In these cases well-
marked mental irritability is observed, associated with fretful-
ness, restlessness, uneasy sleep disturbed by dreams, and a
certain amount of intolerance of light and sound. These
symptoms are frequently succeeded by the phenomena of
depression, and sometimes the latter predominate from the
first. The patient suffers from almost constant headache,
vertigo, nausea, and faintness. The pulse is small and com-
pressible, the cardiac impulse feeble, and there is great disincli-
nation for either mental or physical exertion.

In the severe forms of chronic or sub-acute cerebral anaemia,
such as that produced by starvation, or that which arises during
the course of exhausting fevers, delirium becomes a promi-
nent symptom. Occasionally delirium comes on after hasmor-
rhage ; but it is generally a late symptom, and occurs more
frequently with robust than feeble people. This symptom
is more common when the ansemia is due to starvation, and
under these circumstances it is called the " delirium of iuani-

DIFFUSED DISEASES OF THE ENCEPHALON. C89

tion." The delirium which comes on after the crisis or during
convalescence in febrile diseases is also to be attributed in
great part to defective nutrition of the brain. During the
delirium of cerebral anaemia the patients are excited and some-
times maniacal ; there are illusions of sight and hearing, and
delusions of persecution. The duration of this condition is
variable ; it may last a few hours or days only, but it sometimes
continues for weeks and occasionally passes into permanent
insanity.

Cerebral anaemia is seen in infants after severe diarrhoea, or
other exhausting disease ; and as this is the form which was
called by Marshall Hall hydrocephcdoid or hydrencephaloid
disease, it demands special notice. The affection may be divided
into two stages — the first, that of irritability; the second, that
of torpor, resembling the first and second stages of hydrocephalus
respectively. In the first stage, the infant is irritable, restless,
with flushed face, warm skin, and frequent pulse ; the patient
starts on being touched or on hearing any sudden noise, sleep
is disturbed and interrupted by sighs, moans, or screams.
During the second stage the countenance becomes pale, the
cheeks and extremities cold, the eyelids are half closed, the
eyes sunk in their sockets, there is frequently slight strabismus,
and the pupils are dilated and do not contract to light. The
breathing is irregular and sighing, the voice husky, and there
is sometimes a teasing cough with rattling in the throat. A
most important symptom which distinguishes this disease from
hydrocephalus is that the fontanelle, instead of being tense as
in the latter disease, is depressed. The child inclines almost
constantly to fall into a sleep, which may pass into coma and
death, but under appropriate treatment gradual recovery
usually takes place.

§ 768. Morbid Anatomy. — The blood-vessels of the mem-
branes of the brain are usually more or less empty, but there
is almost always a certain quantity in the larger veins and
sinuses. A very characteristic appearance is presented by the
pia mater in cases of chronic anaemia associated with condi-
tions which induce general oedema. The pia mater, especially
over the superior surface of the hemispheres, is of a pale colour,
s s

690 DIFFUSED DISEASES OF THE ENCEPHALON.

somewhat opaque, and so oedematous that it pits on pressure.
This condition is especially marked in chronic Bright's disease,
and I have frequently been able to predict on opening the skull 1
at a post-mortem that we should find contracted kidneys. In
these cases the cavities of the arachnoid and the lateral ven-
tricles contain together about two ounces of serous fluid, and
the choroid plexuses are oedematous. At the junction of the
posterior and descending horns of the ventricle the oedema of the
choroid plexuses is so great that it gives the appearance of two
or three cysts, each about the size of a pea, growing from them.
The grey substance is pale, and somewhat decolourised. The
white substance is paler than usual, and there is an absence
of blood-points.

§ 769. Morbid Physiology. — Cerebral anaemia is a complex
condition, depending not merely upon a deficiency of the
quantity of blood supplied to the brain, but also upon a change in
its quality, and upon a diminution in the intracranial pressure.
It is exceedingly difficult to apportion to each, of these their
due share in the production of the symptoms. A glance, how-
ever, at the empirical laws of nerve irritability will afford the
key to the interpretation of the more prominent symptoms of
the disease. When a nerve is imperfectly nourished its irrita-
bility is first increased; or, in other words, a slight degree of its
usual stimulus will cause it to discharge its energy. When the
deficiency of nutrition is continued the increase of the irrita-
bility, which is only a temporary condition, is followed by a de-
crease, and complete withdrawal of nourishment again is followed
by exhaustion. This principle will help to explain the leading
phenomena produced by cerebral ansemia. When a healthy
individual suddenly loses a large quantity of blood, the irrita-
bility of the nervous matter becomes increased, and phenomena
of irritation, such as contraction of the pupils, restlessness, and
ringing noises in the ears, are produced, and there may soon be
a large discharge of nervous energy from the cortex of the
brain, giving rise to general convulsions followed by uncon-
sciousness.

When the anaemia takes place more gradually, the outgoing
discharges will be less powerful, and they will only produce the

DIFFUSED DISEASES OF THE ENCEPH AXON.

GDI

signs of mental irritability, to be followed by a drowsy or som-
nolent condition instead of complete loss of consciousness. If,
on the other hand, the nervous energy of the cortex of the
cerebrum be already exhausted by overwork prior to the loss of
blood, the phenomena of depression may exhibit themselves
from the beginning without being preceded by any signs of
irritation, and under these circumstances unconsciousness may
be produced without being preceded by general convulsions.

§ 770. Course and Duration. — Simple faintness from emo-
tional causes usually soon ends in recovery, although a fatal
case is rarely met with ; but it is probable that in these cases
there is some amount of degeneration of the muscular walls of
the heart. The syncope which attacks patients convalescent
from acute disease, when they assume the erect posture for the
first time, is more dangerous and liable to prove fatal.

§ 771. Diagnosis. — The symptoms of cerebral anaemia are
not unlike those of hyperemia of the brain, and the delirium
from anaemia which arises in the course of acute diseases may
very readily be mistaken for the delirium of active congestion.
Anaemia and hyperaemia of the brain can, indeed, only be dis-
tinguished from one another by careful attention to the con-
comitant symptoms. The cerebral symptoms' themselves are
not to be relied upon, as the delirium in anaemia may be as
violent as in congestion, and the colour of the face is not always
a faithful index of the condition of the cerebral circulation.
The diagnosis must be founded upon the general history of the
case, the nature of the concomitant symptoms, and the treat-
ment which has been adopted prior to the onset of the delirium.
As further aids to the diagnosis, it may be tried whether the
erect or horizontal posture has any influence in aggravating or
diminishing the symptoms, and whether they are increased or
relieved by alcoholic stimulants. The state of the general
circulation must also be carefully examined.

§ 772. The prognosis in a case of hydrocephaloid disease
is generally favourable, provided that the true nature of the
affection be recognised and appropriate treatment adopted.

G92

DIFFUSED DISEASES OF THE EN CEPHALON.

A similar remark may be made with respect to the delirium
of anaemia, although it may sometimes be prolonged and
occasionally prove incurable. The prognosis of the cerebral
antenna caused by heart disease will depend upon the gravity
of the cardiac affection ; and fatal syncope is very apt to- occur
in aortic regurgitation when accompaned by dilatation of the
left ventricle.

§ 773. Treatment. — The treatment must vary according as
the anaemia is acute or chronic, limited to the brain, or affecting
the entire body.

In an ordinary fainting fit the patient should as speedily as
possible be placed in the recumbent posture, and recovery
usually takes place without any further treatment. If the
symptoms are more persistent, some form of cutaneous irri-
tation may be employed. The most usual and readiest method
is to sprinkle the face with cold water, or to fleck the face with
the corner of a towel dipped in cold water. A more efficient
method, however, is the application of the metallic electric
brush if a battery happen to be at hand. Mustard appli-
cations have been employed, but they are too slow in their
action. The preparations of ammonia and other substances,
which irritate the trigeminus and olfactory nerves, are also
useful adjuncts' to the treatment, and stimulating enemata
may be resorted to. As soon as the patient can swallow, and
especially if the heart's action be feeble, stimulants, such as
coffee or brandy, must be administered. The more volatile the
agent the sooner will it be absorbed, hence ether is especially
useful; and the same may be said of champagne, since the
experiments of Bernard have proved that the presence of the
carbonic acid promotes the absorption of alcohoL

In severe cases of cerebral ansemia after profuse haemorrhage,
in addition to the means already mentioned, the body of the
patient ought to be covered with warm blankets or other
clothing and surrounded by bottles containing hot water ; and
in order to increase the flow of blood towards the brain the
head ought to be kept in a low position, while pressure is
maintained over the abdominal and axillary arteries, a pro-
ceeding which will direct the stream of blood towards the

DIFFUSED DISEASES OF THE ENCEPHALON.

C93

carotids and will consequently raise the tension in these vessels.
In cases of severe and prolonged cerebral anaemia from loss of
blood transfusion should be tried as a last resort.

The cerebral anaemia which arises during the course of acute
diseases must be treated by the judicious use of wine and
nourishing diet, and if the case admit of it by such tonics as
quinine and iron. The patient should also be instructed not to
raise his head from the pillow so long as the action is accom-
panied by dizziness or other symptoms indicative of anaemia.
When delirium or other forms of cerebral excitement accom-
panies the anaemia, the great aim of treatment should be to
procure sleep. A full dose of chloral sometimes acts very well
in these cases; but according to my experience an opiate is
much more reliable and efficacious. A single subcutaneous
injection of morphia is frequently followed by calm sleep, and
the patient awakes with restored mental faculties. The dose
should not, as a rule, be more than from one-eighth to one-
fourth of a oraiu.

Hyd/rocephaloid disease must be treated on the same general
principles. The diarrhoea or other disease which has produced
the anaemia must be attended to ; and the case must be treated
by warm applications, appropriate nourishment, and stimulants,
such as wine and musk.

(ii.) Hyperemia of the Brain.

§ 774. Etiology. — Congestion of the brain, like congestion
of other organs, may be either active or passive. The former is
also called the hypercemia of fluxion, and the latter the
hyperemia of stasis.

Active Congestion. — Irritation of the tissues of the brain
causes congestion, but such cases generally terminate in en-
cephalitis, and the congestion is usually more or less local. The
causes of universal active congestion must, therefore, be sought
in the state of the general circulation rather than in the brain
itself. All conditions which raise the arterial tension must tend
to produce congestion of the brain, unless, indeed, the increased
tension be caused, as in chronic Bright's disease, by a diminu-
tion of the lumen of the arterioles all over the body, including
those of the brain. An increased flow of blood to the brain

694 DIFFUSED DISEASES OF THE ENCEPHALON.

may be produced artificially by surrounding one or more of the
limbs by Esmarck's bandages, or by compression of the ab-
dominal aorta, or of some of the large arteries of the body.

Exposure of the surface of the body to cold raises the arterial
tension and occasions congestion of the internal organs, and the
same effect is produced during the cold stage of intermittent
fever, and the rigors which usher in most severe acute diseases.
The sudden arrest of habitual discharges may produce con-
gestion of the brain by increasing arterial tension.

Hypertrophy of the heart does not often cause congestion of
the brain, inasmuch as the hypertrophy is always compensatory
to some resistance offered to the onward flow of blood. Con-
gestion of the brain may, however, be caused by the increased
activity of the heart, which accompanies emotional excitement.
But in such cases the direct excitement of the tissues of the
brain, which underlies the emotional disorder, must co-operate
with the increased activity of the heart as an important factor
in the production of congestion.

Paralysis of the sympathetic or irritation of the inhibitory
nerves of the arteries of the brain may produce cerebral
hypersemia.

Plethoric and nervous individuals, especially of the female
sex, are sometimes attacked with dizziness, headache, and
flushing of the face in the absence of emotional excitement or
disturbance of the circulation generally that would account for
the symptoms, which must, therefore, be referred to derange-
ment of the vaso-motor nerves of the brain. The vertigo and
drowsiness which accompany irritation of the stomach is pro-
bably often caused by cerebral hypergemia. The experiments
of S. Mayer and Pribram have shown that direct electrical or
mechanical irritation of the walls of the stomach produces an
increase of the arterial tension and slowing of the pulse, caused
probably by a reflex contraction of the arterioles of the body
generally. If, under these circumstances, the contraction of
the arterioles of each organ in the body were in a condition of
perfect equilibrium with that of the arterioles of every other
organ, no congestion of any of them would take place. It is
not likely that complete equilibrium can exist between the
contraction of the vessels of all the organs of the body in any

DIFFUSED DISEASES OF THE ENCEPIIALON.

895

case, and it is manifest that the organ whose vessels began
first to dilate must become more or less congested.

Some poisonous agents appear to have the effect of producing
congestion of the brain : most of the narcotics and stimulants
appear to me to act upon the tissues of the brain first, and to
produce congestion as a secondary action. The more diffusible
stimulants, as ether, chloroform, and alcohol, no doubt cause a
certain amount of congestion of the brain, just as they produce
flushing of the face by paralysing the sympathetic ; but nitrite
ofamyl and its allies appear to be the only known agents
which act specially on the vaso-motor system before affecting
the tissue of the cortex of the brain.

The cerebral symptoms in hyperpyrexia and insolation were
at one time referred to congestion of the brain ; but it is much,
more probable that the high temperature acts in a deleterious
manner on the cerebral tissues. The cerebral symptoms of
fevers are probably due quite as much to qualitative as to
quantitative alterations of the blood in the brain.

Active cerebral congestion appears to be more common in
males than in females, and in adults than in either the old or
the young. The statistics of Andral and of Hammond tend to
show that the disease is, as might be expected, more common
in winter than in summer. Heredity undoubtedly exercises
some influence in causing cerebral hyperemia, but it is pro-
bable that the influence is indirect rather than direct, as in the
gouty diathesis.

Passive Congestion. — Venous congestion of the brain may
be only part of venous congestion of the whole body, or it may
be produced by special causes. General venous congestion is
caused by diseases of the heart and lungs ; and for the
mechanism by which this congestion is brought about the
reader is referred to works devoted to diseases of these organs.

Congestion is also caused by all local diseases which retard
the return of blood from the brain.

§ 775. Symptoms. — Congestion of the brain gives rise to
symptoms which vary widely in different cases; but for clinical
purposes three varieties may be described — (a) the slight, (6)
the severe, and (c) the apoplectic form.

696

DIFFUSED DISEASES OF TEE ENCEPH ALON.

(a) In the slight form of congestion the prominent symptoms
are sensory disorders. The patient complains of severe
headache, either deep-seated or lancinating, aggravated by
movement, light, sound, or heat, while all intellectual efforts
become impossible. Patients at the same time complain of
dizziness, tinnitus aurium, and optical illusions. Sleeplessness
is an earl}'- and important symptom. It is accompanied by
restlessness and agitation ; and if sleep do supervene, it is
disturbed by horrible dreams, and the patient awakes un-
refreshed without relief to the headache.

In the arterial variety of congestion the patients are fret-
ful, restless, and excitable; but although they avoid mental
exertion for fear of aggravating their sufferings, their intel-
lectual faculties are not impaired ; on the contrary, there may
be excessive mental activity. There may be some numbness
and formication of the extremities, but there are no motor
disorders. There is generally obstinate constipation. This
form of congestion frequently occurs in plethoric subjects.
The slightest exciting cause, such as a full meal after a
prolonged fast, or unusual mental fatigue, often suffices to
induce an attack, which may last for a few hours only or
persist for some days.

In the venous variety of hyperemia the phenomena of mental
depression are usually more marked than those of excitement.
There is a dull sense of oppression in the head, the face is livid,
there are mental torpor with a tendency to sleep, and a certain
amount of confusion of ideas, especially on awaking after a
short sleep.

(b) In the severe forms other symptoms are added. The
patient suffers so much from vertigo that he is unable to main-
tain the erect posture, and sudden vomiting may occur in the
absence of any gastric irritation to account for it. The pulse
is slow, full, and hard; the arteries of the head and neck beat
forcibly; the face is frequently, although not always, flushed, and
may at times be livid, while a sensation of flying heat shoots
over the head and neck. The pupils are generally contracted,
and there is some degree of intolerance of light and sound.
The patient complains of intense headache, and is the subject
of hallucinations and illusions which pervert the judgment, and

DIFFUSED DISEASES OF THE ENCEPHALON. G97

may lead to strange and disorderly acts. He sometimes en-
deavours to quit his bed, and to pursue or run away from
imaginary objects; he is loquacious or bursts into a flood of
tears, and struggles with and tries to escape from his atten-
dants. After some hours of excitement and struggling the skin
becomes covered with sweat, the pulse is accelerated, the face
of a deep red colour, and the patient presents the leading
symptoms of encephalitis; the thermometer shows that the
temperature, if at all altered, is only slightly above the normal.
If these symptoms persist for some time, the phenomena of
excitement are succeeded by those of depression, the delirium
gradually gives place to mental torpor, the muscular agitation
is replaced by muscular relaxation, the respiration becomes
stertorous, there are involuntary evacuations, and the patient
falls into a state of coma.

In some cases, especially in aged people, the severe form of
congestion declares itself suddenly during the night, as a simple
delirium of action. The patient awakes, does not know where
he is, gets up and performs various disorderly actions of which
he has no knowledge. In the morning he is quiet and sensible,
but is sad, morose, and depressed ; and these phenomena may
be repeated for several consecutive nights, but it generally
ends at last in an attack of delirium similar to that which has
been just described. An abundant secretion from the con-
junctiva and mucous membrane of the mouth is said to be a
frequent symptom of congestion of the brain in old people
(Durand-Fardel.)

Convulsions are the most frequent and most striking symp-
toms of cerebral congestion in infants. It must not, however,
be thought that cerebral congestion always accompanies the
convulsions of children. It is indeed probable that convulsions
from congestion of the brain in children are rare in comparison
with those which are secondary to other diseases. The symptoms
of the cerebral congestion of infancy are similar in many
respects to those of meningitis. Both are attended with partial
or general convulsions, headache, contraction of the pupils,
vomiting, and constipation. The course of the two affections,
however, enables them to be readily distinguished. In conges-
tion the child has been in good health up to the beginning of

698

DIFFUSED DISEASES OF THE ENCEPHALON.

the attack, there is little or no elevation of temperature, and the
disease terminates in recovery in two or three days at most.

(c) The apoplectic form is characterised by sudden and total
loss of consciousness and complete resolution of the limbs, but
reflex excitability is preserved. The patient recovers conscious-
ness in a few hours, and after a short time, two or three days
at most, all the symptoms disappear without leaving a trace
behind. Sometimes, however, after complete restoration to con-
sciousness, a certain amount of muscular paralysis remains in
one limb, or assumes the hemiplegic form and persists for some
time.

§ 776. Morbid Anatomy. — It is necessary to be on one's
guard against certain causes of error with respect to post-
mortem appearances. Both arterial and venous hyperemia
may disappear at death without leaving a trace behind. On
the other hand, when, as is usually the case, the body is
laid on its back, a large quantity of blood may be found in
the veins and sinuses of the occipital fossae, caused by the
influence of gravity after death, aided probably by hypostatic
congestion during the last few hours of death. The act of
dying by respiratory paralysis may also cause a hyperasmia of
the cerebral veins when there were no symptoms of congestion
during the course of the disease.

In pathological hyperaemia, when the calvarium is removed,
the vessels of the diploe are frequently found congested. The
veins of the dura and pia mater are prominent and full of blood,
and so also are the choroid plexuses and sinuses. In the
severer forms of congestion the brain is swollen, and the gyri
are flattened from compression. The grey substance is of a
dark red colour, its consistence is increased, and the cut surface
of the white substance presents a large number of red points,
from which drops of blood exude. The white substance may be
of a yellowish-red colour, while at other times its colour is little
altered.

In chronic congestion the vessels themselves become altered.
In the venous variety the veins, especially those of the mem-
branes, the surface of the brain, choroid plexuses, and velum
interpositum are enlarged and tortuous. In chronic arterial

DIFFUSED DISEASES OF THE ENCEPIIALON. G99

congestion the coats of the arterioles become hypertrophied, and
the smaller vessels may present visible openings after section ;
miliary aneurisms are often discovered by careful examina-
tion, while a certain amount of pigment is found in the peri-
vascular spaces. In very chronic cases oedema of the pia mater
and of the choroid plexuses is found along with increase of the
ventricular fluid, while the brain itself may undergo a certain
degree of atrophy. The 4ktt cribU of Durand-Fardel consists
of a sieve-like appearance of the brain caused by the round or
oval openings of the vessels, some of which are as large as a
pin's head. These openings are supposed by some pathologists
to depend upon dilatation of the perivascular lymph-sheaths.
They are commonly found at the autopsies of elderly people who
have suffered for a long time from cerebral congestion.

§ 777. Morbid Physiology. — In the first stages of active
general congestion the increased quantity of blood within the
cavity of the skull is compensated by displacement of a corre-
sponding quantity of cerebro-spinal fluid, but congestion beyond
a certain degree must augment the intracranial pressure, as may
be readily proved to occur in children by the increased tension of
the anterior fontanelle. During the first stage of active conges-
tion the increased supply of blood to the organ must increase its
functional activity, thus explaining the irritative symptoms ob-
served at the onset of the disease. On the other hand increase
of the intracranial pressure, beyond the point at which it is
compensated by the cerebro-spinal fluid, must compress the
substance of the brain, and so give rise to the phenomena of
depression observed in the second stage of congestion.

In the apoplectic form of congestion, attended by uncon-
sciousness and subsequent paralysis, it is probable that a serous
transudation takes place into the interstices of the tissues.
In venous hypersemia the blood pressure is transferred, so that
increase of venous implies a diminution of arterial tension along
with a superabundance of carbonic acid and a deficiency of
oxygen, conditions which tend to narcotise the brain. The
conditions present, therefore, combine to produce the pheno-
mena of depression and not those of excitement; and the few
symptoms which simulate those of increased excitement, such

700

DIFFUSED DISEASES OF THE ENCEPHALON.

as sleeplessness, restlessness, and mental irritability, are those
which occur in imperfectly nourished brains or in cerebral
anosmia.

§ 778. Diagnosis. — The thermometer may be of use in dis-
tinguishing hyperemia from inflammatory diseases of the brain,
but its indications are not to be too implicitly relied upon.
Congestion may be distinguished from focal disease by the
absence of the usual symptoms of a localised lesion. The apo-
plectic form of congestion is distinguished from true apoplexy
by the transitory nature of the symptoms in the former, but it
must be acknowledged that rupture of a blood-vessel in some
parts of the brain may give rise to symptoms which closely
resemble those of congestion.

The form of congestion attended with delirium may be mis-
taken for delirium tremens ; but the two diseases may be
distinguished by a knowledge of the habits of the patient, and
the circumstances which have preceded the attack. At the
same time the trembling of the lips and hands, the skin
bathed in perspiration, the soft compressible pulse, the timid
and frightened look, and the busy character of the delirium
form a group of symptoms so characteristic that it is difficult
for a practised eye to mistake the alcoholic disease for any
other. A certain kind of delirium may be caused by lead
poisoning, which may simulate that from congestion ; but the
two may be distinguished by the history of the case and by the
condition of the gums.

The respiratory movements and the pulse are retained in
greater integrity in congestive apoplexy than in syncope. The
coma which succeeds an epileptic attack may be mistaken for
the coma of the apoplectic form of congestion. These affections
must be distinguished mainly by the history of convulsions,
and by the fact that the tongue is often bitten during the
epileptic attack.

The lighter forms of congestion may be mistaken for gastric
vertigo, or for the vertigo which is caused by venereal excess.
Gastric vertigo is associated with some forms of dyspepsia, it
often diminishes or ceases after food, and is accompanied by
nausea-

DIFFUSED DISEASES OF THE ENCEPIIALON. 701

After having determined that the symptoms are caused by
cerebral hyperemia* it is then necessary to decide whether the
congestion be arterial or venous, and whether it be primary or
secondary. A careful examination of the lungs, heart, and
blood-vessels, and the condition of the urine, will enable us to
decide whether any mechanical condition is present which
would cause venous or arterial congestion. If none of these
conditions be present, then the congestion must be regarded as
active, and its primary or secondary nature will be revealed
by a knowledge of its cause. The most ordinary causes of
primary congestion are insolation, unwonted mental efforts,
wakefulness, and excess in eating; while the most ordinary
causes of secondary congestion are gout, rheumatism, suppres-
sion of the menses and other habitual discharges, and cerebral
lesions, as tumours of the encephalon.

§ 779. Course and Prognosis. — Great differences exist in the
severity and duration of cerebral congestion. The severer
forms may cause death, and even the lighter forms, if they do
/ not present any immediate danger, are apt to recur and to
produce permanent bad effects.

The prognosis in the severer forms of congestion is grave,
and when delirium is present the case often terminates in
haemorrhage.

Cerebral congestion is most dangerous in old people, because
the degenerated vessels are apt to rupture.

In cases of chronic disease of the brain, as tumour or vascular
degeneration, cerebral congestion may aggravate the symptoms
or prove the immediate cause of death.

§ 780. Treatment. — The treatment of cerebral congestion
will vary according as its cause is found in general plethora,
organic diseases of the heart, vaso-motor disturbances, or a pre-
existing focus of disease in the brain.

During the attack the patient should lie in bed with the
upper part of the body raised, the room darkened, and the
utmost quiet enjoined. If delirium be present and the patient
of a plethoric habit, a small quantity of blood may be drawn
from the arm, followed by the administration of a saline pur-
gative.

702

DIFFUSED DISEASES OF THE ENCEPHALON.

In the congestion of the brain caused by suppression of the
menses, or of hemorrhoidal discharge, leeches may be applied
to the anus or to the upper part of the thigh, and be followed
by a smart purgative. Aloes, or aloes in combination with
sulphate of magnesia, is very useful in these cases.

In the treatment of active congestion with irritative symptoms
from such causes as insolation and excessive fatigue general
bleeding is no longer permissible, and the main reliance must
be placed upon saline or other hydragogue purgatives, mustard
pediluvia, and cold steadily applied to the head by means of
an ice bag or evaporating lotions. If the patient be of a gouty
constitution, a saline mixture with colchicum may be ad-
ministered after the bowels have been acted upon. Aconite is
a useful remedy in many cases.

The diet, of course, must be plain and unstimulating during
the attack. In venous congestion a small bleeding may
occasionally be advisable, inasmuch as the lowering of the ten-
sion within the veins permits the arterial blood to pass more
freely through the capillaries, and the tissues become better
nourished. The main reliance in the treatment of venous
hyperemia of the brain mast be placed upon drastic purgatives,
diuretics, and cardiac tonics as digitalis. Those who have once
suffered from one or more attacks of active cerebral congestion
should adopt certain hygienic precautions to prevent a repetition
of the attack. Their diet should be plain, consisting in large
part of herbaceous vegetables and fruits, and all stimulants, as
wine, tea, and coffee, should be proscribed. They should avoid
everything tending to cause mental excitement, such as public
speaking, theatres and concerts, intellectual efforts, late hours,
and venereal excess.

CHAPTER XI.

II. DIFFUSED DISEASES OF THE ENCEPHALON (Continued).

(II.) ATROPHY AND HYPERTROPHY OF THE BRAIN,
(i.) Atroi-hy of the Brain.
§ 781. Atrophy of the Corpus Callosum. — The corpus cal-
losum begins to develop towards the end of the fourth month
of intra-uterine life by the outgrowth of two lateral stumps
from the internal surface of the hemisphere vesicles. These
grow towards one another, and unite between the sixteenth
and twentieth weeks of iutra-uterine life, the union taking
place from before backwards. The development of the corpus
callosum may be arrested at any period, so that it may be
entirely wanting, or it may grow on each side to nearly the
normal size, but union fails to take place in the middle line.
At other times the union may be partial and the corpus cal-
losum be represented by a rudimentary bridge, or sieve-like
plate of tissue. When the corpus callosum is entirely wanting,
its radiating fibres are also absent, the cavities of the lateral
ventricles are unusually large, they are at the same time filled
with serous fluid, the ependyma is granular and thickened, and
the choroid plexuses are generally found diseased.

§ 782. Symptoms. — Congenital deficiency of the corpus cal-
losum has generally been found associated with idiocy, or at least
with 3ome degree of mental deficiency. The mental defects in
such cases do not present anything characteristic, so that this
condition cannot be recognised during life. Some cases of
arrest of development of the corpus callosum have, however,
been reported in which no marked mental deficiency was ob-
served during life (Paget, Jolly, Malinverni, Eichler).

704

DIFFUSED DISEASES OF THE ENCEPHALON.

§ 783. Atrophy of the Cerebellum. — Slight degrees of atrophy
are often observed, either as complicatioDS of cerebral diseases,
or as consequences of diseased foci in the organ itself, but these
lesions cannot be recognised during life. Cases of uncompli-
cated atrophy of the cerebellum are rare, but the few which
have been observed are important from the light they throw on
the functions of the organ.

§ 784. Etiology. — In the cases reported by Lallement and
Otto, and probably also to some extent in Combette's case, the
atrophy was congenital. In a case reported by Meynert and
another by Pierret, fright is assigned as the cause. In Clapton's
case the nervous symptoms appeared after measles, and gradaully
diminished in severity.

§ 785. Symptoms. — The following were the symptoms in
Combette's case : The girl Labrorse at 12 years was weak-
minded and suffered from epileptic attacks. She could not
stand or walk until five years old. At seven her lower ex-
tremities were feeble, and she often fell. During the last three
months of life she was bedridden and could scarcely move her
legs, and her articulation was imperfect.

Motor disturbances were observed in the cases reported by
Meynert, Pierret, Fiedler, Clapton, Dugnet, and Moreau. Most
authors describe these as those of ataxia; while others state
that the patients could walk, but only slowly and carefully ;
that they fell frequently, especially backwards; and that in
walking they seized hold of objects within their reach. All
these patients had also either persistent or temporary dis-
turbance of speech.

No motor disturbance was noticed by Lallement and Otto.
Otto's patient was impulsive in his movements, but whether
due to psychical causes or disturbance of co-ordination could
not be determined.

Weakness of mind, even idiocy, characterised the patients of
Clapton, Otto, and Fiedler ; while Pierret's case suffered from
weakness of memory.

Epileptiform convulsions are frequently mentioned, but do
not appear to have any special significance.

DIFFUSED DISEASES OF THE ENCEPHALON.

705

Symptoms occasionally noticed are analgesia (Fiedler) and
slight disturbances of sensibility (Pierret).

§ 786. Morbid Anatomy— In Combette's case the entire
organ had disappeared. There was no trace of a pons, although
the cerebral arteries were present and of normal size. In other
reported cases the cerebellum has been found reduced to about
half the normal size.

Lallement mentions a case in which the left lobes of the
cerebellum, including its middle and superior peduncles, was
reduced to the size of a nut, and the transverse fibres of the
pons, the right corpus striatum, and the right olivary body were
atrophied. In Dugnet's case the cerebellum was about half
the normal weight. The atrophy was bilateral and general,
and the substance of the organ showed well-marked sclerosis.
Somewhat similar cases have been reported by Clapton and
Fiedler-Bergmann. No statement is made with regard to the
condition of the pons.

Meynert describes a similar degeneration in the pons, which
he regards as a secondary degeneration, and not as the starting
point of the affection. The cerebellum itself was much altered,
especially on the right side. The posterior pyramids of the
medulla were implicated as well as the pons and the crus
cerebelli ad pontem. In Pierret's case there was an intense
degree of sclerotic atrophy, which affected chiefly the vertical
diameter of the organ, the grey substance being specially
affected. The transverse fibres of the pons and both olivary
bodies were atrophied and replaced by connective tissue. In
Otto's case the left lobe was the more atrophied, and the pons
on the left side was narrower than on the right. The space
usually occupied by the cerebellum was replaced by hyperostosis
of the occipital bone.

§ 787. Complications and Diagnosis. — Atrophy of the
lateral lobe of the cerebellum has been found associated with
atrophy of the transverse fibres of the pons on the same side,
and with atrophy of the olivary body and cerebral hemisphere
on the opposite side. In some few cases the atrophy of the
cerebrum and cerebellum occurs on the same side.

T T

706 DIFFUSED DISEASES OF THE ENCEPHALON.

Atrophy of the cerebellum is difficult to distinguish from
chronic affections of the organ, but headache and vomiting,
which are common in the latter, are rare in the former. The
sensory and reflex disturbances of locomotor ataxia serve to
distinguish it from atrophy of the cerebellum. The symp-
toms of the initial stage of insular sclerosis may be similar to
those of atrophy of the cerebellum, but when the characteristic
tremors of the former appear the diagnosis is easy.

.(ii.) Hypertrophy of the Brain.

Hypertrophy of the brain includes several different morbid
conditions. It' is also usual to include along with hypertrophy a
new formation of cerebral substance within the substance of the
brain itself, a condition which Yirchow has called Heterotopia
of the brain. Hypertrophy may be divided into general and
partial hypertrophy.

§ 788. Etiology. — Hypertrophy of the brain appears to be
generally congenital. Several of the reported cases were
associated with peripheral multiple neuroma (Hesselbach,
Hitchcock, Betz), and both of these conditions are frequent
accompaniments of idiocy or delayed mental development.
The affection is almost always developed soon after birth or
in early infancy. A few cases appear to have developed sub-
sequently to an injury to the head (Tuke, Dance), while the
disease appears to have been a result of chronic lead poisoning
(Andral, Laennec, Bright).

Symptoms. — Severe headache, with remissions or even
complete intermissions, is a prominent symptom of hyper-
trophy of the brain. Epileptiform convulsions, local spasms,
attacks of laryngismus stridulus, and tremors are also com-
monly observed. The pulse is usually retarded, but it may
occasionally be much accelerated (Steiner). The symptoms of
chronic cerebral hypertrophy are not well known. The affec-
tion in children is sometimes associated with premature develop-
ment (Elliotson), or at least a degree of development corre-
sponding to their age. In other cases, again, there is more or

DIFFUSED DISEASES OF THE ENCEPIIALON. 707

less weakness of mind, amounting even to the highest degree of
idiocy. The tongue is often increased in size, and often pro-
trudes from the mouth. Drowsiness is an occasional but by
no means constant symptom. Some of the affected children
are liable to fall frequently, being over-balanced by the great
weight of the head. Disturbances of the nerves of the general
or special senses are comparatively rare. The optic nerve in
particular is seldom mentioned ; Steiner and Ndirenthar alone
speak of the sudden occurrence of blindness, others mention
photophobia. A careful ophthalmoscopic examination of the
optic discs might have given more positive results. Tinnitus
and subjective noises in the head are sometimes present. Death
often results from an attack of convulsions, or in coma due to
cerebral compression, while many of those affected die from
some intercurrent disease.

§ 789. Morbid Anatomy. — The anatomical appearances differ
according as the hypertrophy is partial or general.

General hypertrophy begins in the earlier years of child-
hood, and the skull enlarges just as in hydrocephalus. If the
disease appear for the first time after the bones of the skull
have become ossified, the bones are subjected to compression
from within and undergo atrophy at certain points. It is
probable that this condition is, however, connected with the
changes which the cranial bones are known to undergo in
congenital syphilis.

The cerebral membranes are generally compressed against
and become adherent to each other and to the bones of the
skull. The membranes are thin, their blood-vessels are scarcely
visible, and every trace of cerebral spinal fluid is absent.

The lateral ventricles are compressed so that they either
contain no fluid, or only a small amount. The convolutions are
flattened and so pressed together that the sulci seem entirely
obliterated. The brain substance shows a marked change of
consistency; it is tough, like boiled white of egg or cheese.
Tuke could make no impression on it by a column of water
five feet high.

The brain is, as a rule, found anaemic on section, and the grey
substance so pale that it differs little from the white. This

708

DIFFUSED DISEASES OF THE ENCEPHALON.

extreme anaemia, however, appears to be a terminal phenomena
due to the increased compression.

The average weight of the brain in adults is, according to
Huschke, from 1,500 to 1,600 grammes ; although the weight
of the brains of persons prominent in literature has considerably
exceeded 2,000 grammes. The absolute weight of the brain,
considered without reference to its density and other circum-
stances, only warrants the diagnosis of hypertrophy when the
average is considerably exceeded.

The specific gravity of the cerebral mass should also be taken
into account. Tuke found the specific gravity unchanged on
the diseased side in his case of unilateral hypertrophy, being
1,036 on both sides, but the result differed from that obtained
with normal brains in the fact that it was the same in the grey
as in the white substance.

The cerebrum is as a rule alone affected with hypertrophy,
but there are a few cases in which the cerebellum also is said
to have been affected (Sweatmann).

Yirchow attributes the increased size of the brain to hyper-
plasia of the neuroglia.

Partial hypertrophy is rarer than the general form of the
affection, and even some of the reported cases are not beyond
suspicion, inasmuch as gliomatous tumours were probably
mistaken for partial hypertrophy of the brain. Hesselbach
mentions the case of a man who inherited the disease from his
father, and who, besides multiple neuromata of the peripheral
nerves, presented a considerable enlargement of the sympathetic
ganglia, and of one of' the middle cerebellar peduncles.

§ 790. Course.^- It is very difficult in many cases to estimate
the duration of the disease, inasmuch as even in the cases which
appear to be primarily acute the course may actually have been
protracted, the disease being latent until the space in the
cranium became limited. Many chronic cases suddenly assume
an acute character, and terminate quickly in death. The fatal
termination is often caused by an intercurrent disease, such as
diarrhoea or bronchitis.

Chronic cases may extend over many years, the disease
apparently remaining stationary. A sudden increase in volume,

DIFFUSED DISEASES OF THE ENCEPII ALON . 709

whether in a brain previously healthy or in one already
chronically enlarged, may cause rapid death.

Acute hypertrophy produces the symptoms common to all
diseases causing compression of the brain ; while the chronic
form, especially in children, can scarcely be distinguished from
chronic hydrocephalus.

§ 791. Diagnosis, Prognosis, and Treatment— The diagnosis
is always uncertain, but the possibility of this condition ought
certainly to be borne in mind before puncturing a hydrocephalic
head. The prognosis is always unfavourable, but on account of
the impossibility of making a diagnosis a prognosis cannot well
be given. No treatment is of any avail.

§ 792. Heterotopia of Brain Substance. — This condition was
first described by Virchow, and has hitherto been principally
of interest to the morbid anatomist. Simon found small acces-
sory gyri situated on the summit of the convolutions. Virchow
observed in one case an apparently new formation of gyri within
the white substance of the posterior lobe. He also found a
hyperplastic malformation of the caudate nucleus. Klob found
a mass of white cerebral substance, the size of a bean, hanging
from a pedicle between the optic nerves.

Microscopic examination of the heterotopic grey substance
shows, as a rule, similar elements to those of the normal cortex,
but the ganglion cells in the former are pigmented and fatty.

These conditions have hitherto been found in epileptics,
idiots, or in persons otherwise mentally affected, but their
clinical significance is somewhat doubtful. All authors regard
these malformations as congenital.

710

CHAPTER XII.

II. DIFFUSED DISEASES OF THE ENCEPHALON (Continued).

(III.) SHOCK AND CONCUSSION,
(i.) Shock.

§ 793. Definition. — Shock results from profound bodily or
mental impressions, and appears to depend upon a sudden tem-
porary impairment or permanent extinction of the functions of
the nervous system, the cardiac, vaso-motor, and respiratory
centres in the medulla oblongata being specially affected.

§ 794. Etiology. — Amongst the predisposing causes of shock
may be mentioned constitutional peculiarities or idiosyncrasies.
Some people inherit so unstable a nervous system that an injury
inappreciable to others may produce in them all the phenomena
of shock. The irritability of the nervous system is greater in
youth than in old age, and consequently the phenomena of
shock are produced by slighter causes in the former than in the
latter. The recuperative power, on the other hand, is greater
in youth than in the aged, hence the phenomena of shock,
although less obvious, are more grave in the latter than in the
former. Shock is, as a rule, more easily produced in the female
than the male sex. An undue irritability of the nervous system
is sometimes acquired rather than inherited, and all conditions
which tend to impair the nutrition of the nervous system, as
exhausting diseases, cerebral anseinia from whatever cause
arising, dissipation, prolonged pain, the depressing passions,
predispose to the production of shock. During the stage of
depression of shock the irritability of the nervous system is
nearly exhausted, a greater resistance is thus offered to the con-
duction of impulses from the periphery to the higher nerve-

DIFFUSED DISEASES OF THE ENCEPIIALON. 711

centres, and consequently during this stage a second injury
produces a much less effect than the first. During the stage of
reaction, however, the irritability of the nervous system is ex-
cessive, so that a slight stimulus may produce a profound effect.
In persons of powerful will and stable nervous systems the
effect of an unexpected injury is greater than if the patient
were prepared for its reception; while in emotional patients,
with unstable nervous systems, previous knowledge of an im-
pending injury greatly intensifies its effects. Injuries of the
abdominal viscera, genitals, joints, and bones produce more
profound effects than injuries of other parts of the body.

The excitinsr causes of shock are sudden and severe or ex-
tensive injuries of any part of the body, whether produced by
accidental wounds or burns, or by surgical operations. Shock
is also produced by strong emotional excitement of any kind,
although the depressing passions, as fear and anger, are more
liable to cause it than pleasurable passions, like joy.

§ 795. Symptoms. — Cases of shock may be divided clinically
into two forms — (a) cases in which the symptoms of depression
predominate, and (b) cases in which the symptoms of prostration
are mixed with those of excitement (Travers, Savory). Dr.
Lauder Brunton has proposed to call these forms respectively
torpid and erethismic shock.

(a) Torpid Shock. — In the torpid form of shock the patient
lies utterly prostrate ; the surface of the body is pale, cold, and
covered by a clammy sweat, which collects in drops on the
forehead and eyebrows; the lips are bloodless, the nostrils
dilated, and the countenance of a dull aspect and shrunken,
Avhile the eyes have lost their lustre, are sunk in their sockets,
and partially concealed by the drooping lids. There is complete
muscular relaxation, which may even extend to the sphincters.
If the patient be conscious, he may complain of feeling cold and
faint, while the whole body may tremble. The pulse is frequent,
irregular, unequal, and feeble or imperceptible at the wrist,
although the fluttering action of the heart may be heard on
auscultation. The respiratory movements are irregular and
gasping, or short and feeble, the respirations being sometimes
so superficial that they are scarcely visible, although a slight

712 DIFFUSED DISEASES OF THE ENCEPHALON.

movement of the diaphragm may generally be discovered by
careful observation. The temperature of the body is depressed.
The patient suffers from vertigo and dimness of vision, while in
the less severe cases there is nausea, vomiting, and hiccough.

The psychical symptoms consist of mental depression, restless-
ness, confusion of thought, incoherence, or drowsiness, although
the patient generally gives rational replies to definite questions.
At other times the patient appears singularly calm and rational,
while the various senses remain unaffected, hearing being some-
times unusually acute.

(b) Erethismic Shock. — This form of shock is rare, the
majority of cases in which symptoms of prostration are mixed
with those of excitement being preceded by a distinct, though
it may be transient, stage of collapse. The skin is at first hot
and dry; the face is flushed and wears an anxious expression ;
the pulse is frequent, quick, and bounding, but always com-
pressible; the respirations are hurried, imperfect, and inter-
rupted by sighs; the tongue is tremulous; and the patient
complains of thirst, rigors are occasionally present, while vomiting
is a frequent and sometimes obstinate symptom. The mental
and bodily prostration of collapse is succeeded by tremor and
twitchings of the muscles, there is restlessness, jactitation, pre-
cordial anxiety, and delirium. The psychical disturbances
observed are somewhat variable. At times the patient merely
presents a peculiar irritability of manner, with an increased
disposition to talk, sometimes rationally, occasionally incohe-
rently. At other times the patient has strange illusions, attended
with a peculiar dread of impending evil. In some cases, how-
ever, there is the fiercest maniacal raving, which is most pro-
nounced during the night, or the delirium may assume all the
characteristics of that observed in delirium tremens.

The patient either obtains no sleep, or it is partial, inter-
rupted, and unrefreshing. As the exhaustion increases the
skin becomes covered with a cold, clammy, and often profuse
sweat. The face becomes pale and the expression haggard,
the pulse is frequent, irregular, fluttering, and uncountable.
Subsultus and slight convulsions supervene, and the patient
dies comatose.

DIFFUSED DISEASES OF THE ENCEPHALON. 713

§ 796. Course, Termination, and Duration.— The degree of
shock varies greatly. In the milder forms of the affection the
symptoms are chiefly those of an ordinary fainting fit. Loss of
consciousness is, however, a more marked characteristic of syn-
cope than of slight shock, whilst recovery from the former is
more rapid than from the latter.

In the severest form of shock the functions of the nervous
system are suddenly abolished, and the heart ceases to beat.

Between the slighter forms of shock, which resemble an
ordinary fainting fit, and the severest form, which terminates in
instantaneous death, innumerable transitional forms may be
observed. The medium degrees of shock are known under the
name of collapse.

The slighter degrees of shock terminate speedily in direct
recovery, while the severest form terminates of course in death.
In the intermediate forms recovery may ultimately take
place, but it is preceded by a stage in which the symptoms of
collapse give place to those of excitement, this stage being called
the period of reaction. The period of reaction is characterised
by improved pulse and respirations, restoration of muscular
power, and increase of temperature. Reaction may sometimes
be in excess and febrile symptoms supervene.

The symptoms of the period of reaction may gradually give
place to health, but in some cases relapses are not unfrequent,
and convalescence is then protracted. In other cases the torpid
may be replaced by the erethismic form of the disease. Re-
covery from severe shock is often partial only, the irritability
of the nervous system remains permanently increased, a con-
dition which predisposes to the production of shock from the
application of slight exciting causes.

§ 797. Morbid Anatomy. — No definite changes have been
found in the nervous system in cases of shock. All the cavities
of the heart are usually distended with blood and the venous
system is engorged. Travers, however, relates instances of death
from shock when, on dissection, both sides of the heart were
found empty. Dr. A. H. Young informs me that he has
observed cases of this kind in the post mortem room, and that

714

DIFFUSED DISEASES OF THE ENCEPHALON.

in such cases the abdominal veins have not unfrequently been
enormously eogorged with blood.

§ 798. Morbid Physioldgy. — In its widest acceptation shock
is the sudden impairment or abolition of the functions of
protoplasm by the application of an excessive stimulus. The
functions of the protoplasm of all the organs of the body are
doubtless impaired by severe injuries ; but in the higher animals
the disorder occasioned in the functions of the nervous system
becomes so predominant that the direct effects of injuries on
the protoplasm of the other tissues of the body may be practi-
cally disregarded. The most striking phenomena of shock are
those which cluster around the organs of circulation. The ex-
periments of Goltz, repeated by Brunton, show that shock
probably results from cardiac paralysis and vaso-motor paralysis
of the large vascular trunks of the abdomen. Brunton states
that blows of moderate severity on the abdomen of frogs pro-
duce in some stoppage of the heart, without dilatation of the
abdominal vessels, and in others vascular dilatation, without
arrest of the cardiac pulsations, while severe blows generally
produce both effects simultaneously. The vessels of the ab-
domen are so large that when fully relaxed they are capable
of containing almost all the blood in the body, and con-
sequently the condition resulting from their rapid dilatation
is equivalent to a sudden haemorrhage. This double con-
dition of cardiac failure and vascular dilatation produces
ansemia of the nerve-centres, and this accounts for the pallor
and coldness of the surface of the body, and the weak, com-
pressible, and fluttering pulse. It must not, however, be for-
gotten that the injury which has disordered the functions of the
vaso-motor and cardiac centres in the medulla oblongata must
also have produced a direct deleterious effect upon other nerve-
centres. The disorders of respiration, the cries of pain, and the
various bodily contortions which are caused by bodily injuries,
or severe mental excitement, show that excessive stimuli occa-
sion powerful outgoing discharges from the higher'nerve-centres.
But a powerful discharge from a nerve-centre is followed by
temporary impairment or abolition of its functions, and it is pro-
bable that the arrest of the functions of the higher nerve-centres,

DIFFUSED DISEASES OF THE ENCEPHALON. 715

caused by the application of a sudden and powerful stimulus, is
the most important factor in the production of the phenomena
of shock.

The symptoms of the erethismic variety may be explained
partly on the supposition that the nervous tissues are in the
irritable condition frequently observed when they are imper-
fectly nourished, and partly on the supposition that the
phenomena of excitement are in great part due to the abolition
of the functions of the higher nerve-centres, thus permitting a
greater activity of the lower centres to take place.

§ 799. Diagnosis. — The symptoms of shock may be mistaken
for those of syncope, but the former are more protracted than
the latter. If a history of an injury or of the presence of some
other exciting cause of shock can be ascertained, the diagnosis
is rendered easy. It is not always easy to distinguish profound
collapse from actual death. The difficulty can only arise in
those rare cases of collapse in which the action of the heart
ceases to be heard on auscultation and the respiratory move-
ments fail to be detected, or powerful cutaneous irritants cease
to excite any reflex action. The most certain test consists of
the electrical examination of the muscles and nerves, all re-
action in them ceasing in from one and a half to three hours
after death.

§ 800. Prognosis. — The prognosis depends upon the degree
of shock, and the constitution of the patient. Speaking
broadly, the prognosis is the more favourable the less the
intensity of the shock, and the shorter the time which elapses
before reaction takes place.

§ 801. Treatment. — The treatment of shock is the same
generally as that of syncope, the great aim being to excite
reaction. It must, however, be constantly borne in mind that
reaction, once excited, is apt to become excessive. In the
severer forms of shock the heart must be excited to action.
The mode of procedure to be adopted depends upon whether
the arrest of the heart's action is of purely nervous origin,
or it is complicated or caused by great haemorrhage. In

716

DIFFUSED DISEASES OF THE ENCEPHALON.

the former case the heart is probably distended and the
cervical veins engorged, and consequently venesection from
the external jugular veins should be immediately resorted to
(Savory) ; while in the latter condition the cavities of the
heart are empty, and transfusion of blood appears to be the
only means offering a chance of success. In any case warmth
is indicated, and the patient should be well wrapped up in
warm blankets and surrounded by hot bottles. Stimulants
must now be given internally, brandy being generally the
readiest and best. If the patient be unable to swallow,
ammonia or ether may be administered subcutaneously, or the
former may be injected into a vein, or a stimulating enema
may be given. Tincture of digitalis may be administered in
half drachm doses, but its action is much too slow to be of
much use in the early stage of urgent cases.

(ii.) Concussion.

Concussion is a special form of shock, the disturbance in the
functions of the nervous system being caused by direct com-
motion of the substance of the brain.

§ 802. Etiology. — The exciting causes of concussion are
severe injuries, as falls from a height or blows on the head,
which cause the whole mass of the encephalon to be jolted or
shaken. Concussion may be complicated by fracture of the
skull, and in such cases the effects of the concussion are often
less severe than in uncomplicated cases, apparently because a
certain amount of the applied force is expended in producing
the fracture.

§ 803. Symptoms. — The symptoms of concussion may be de-
scribed under four stages: (a) The stage of collapse; (b) the
stage of rallying or of vomiting ; (c) the stage of reaction ;
(d) the stage of gradual convalescence (Hutchinson).

(a) The Stage of Collapse. — The symptoms during this stage
are very variable both in character and duration. In the slighter
forms the patient suffers from transient confusion of ideas and
slight giddiness. He may feel weak and faint, and be unable
to maintain the erect posture. In the more severe forms the

DIFFUSED DISEASES OF THE ENCEPIIALON.

717

symptoms are those of collapse, with loss of consciousness ; but
paralysis, such as occurs in compression of the brain, is never
present. The patient is semi-conscious or insensible, most
reflex actions are abolished, the skin is cold and pallid, the
respirations superficial and shallow, the pulse feeble or imper-
ceptible at the wrist, whilst the pupils may either be con-
tracted, dilated, or unequal.

(6) The Stage of Rallying or of Vomiting.— After a period
varying from a few minutes even up to days, according to the
severity of the attack, the patient usually begins to show signs of
rallying. This stage is often ushered in by vomiting, or very
occasionally by an epileptiform attack; the pulse improves in
strength, the respirations become less shallow and more per-
ceptible, the body becomes warmer, reflex actions can be excited,
and the patient gives evidence of returning sensibility, while he
may exhibit signs of mental distress.

(c) The Stage of Reaction. — The symptoms of the stage of
rallying are succeeded by those of reaction. In this stage the
phenomena of febrile reaction manifest themselves by the usual
symptoms, hot and dry skin, quick and hard pulse, and scanty
urine ; while the patient is drowsy, yet quite conscious when
roused by a question addressed to him. In some cases these
symptoms gradually develop into those of compression and the
patient dies comatose, while in other cases the symptoms of
reaction give place to those of inflammation of the brain. This
stage may continue from three to twelve days in cases which
recover.

(d) The Stage of Convalescence. — Reaction is followed by a
progressive subsidence of the symptoms, and either by a gradual
restoration of the patient to health, or the establishment of one
or other of several chronic affections of the nervous system.

Cerebral Irritation.— In another form of nervous disturbance
following injuries of the head, and described by Erichsen under
the name of cerebral irritation, the phenomena of cerebral ex-
citement are mixed with those of loss of function. The patient
assumes a peculiar attitude ; he lies with the body bent for-
wards, the knees drawn up on the abdomen, the legs bent on
the thighs, the forearms flexed on the arms, and the hands
drawn. The patient is restless, and frequently changes his

718 DIFFUSED DISEASES OF THE ENCEPHALON.

position, but never stretches himself out nor assumes the supine
posture (Erichsen). The eyelids are firmly closed, the pupils
are contracted, the surface of the body is pale and cold, and the
pulse is small, feeble, and slow, being seldom above 70 beats per
minute. The sphincters remain, as a rule, unaffected.

The patient is indifferent to everything around him, and is
only partially conscious. He may, however, be roused when
addressed in a loud voice, and then looks up, mutters indis-
tinctly, or frowns and turns hastily away. His sleep is not
stertorous.

After a period of from one to three weeks, the pulse
improves, the body becomes warmer, the flexed attitude is
abandoned, and the mental irritability gives place to mental
feebleness and torpidity.

§ 804. Course, Duration, and Terminations. — The mildest
cases of concussion usually make a speedy recovery, although the
patient may suffer for many days from confusion of thought, list-
lessness, and indisposition for mental exertion. In the severest
cases rapid death may occur. Between these extremes every
intermediate degree in the severity of the symptoms is ob-
served. In some cases the patient may never rally, but die after a
more or less prolonged stage of collapse. In other cases the patient
rallies, but the symptoms of reaction are excessive, and followed
either by those of compression or of encephalitis. But even when
the period of reaction is safely passed, serious consequences
may be observed during and subsequent to the period of con-
valescence. In some cases complete recovery may apparently
take place, and the patient resumes his ordinary avocations;
but he remains excitable, and gives way to uncontrollable bursts
of passion. He complains of persistent headaches, his mental
powers are impaired, his speech may be indistinct and stutter-
ing, while vision, smelling, and hearing may be permanently
impaired. The severity of the remote consequences of concussion
do not always bear a direct ratio to the severity of the symptoms
of the first stage of concussion, apparently trivial cases being
sometimes followed by serious consequences.

In cerebral irritation recovery is slow, but may ultimately be
perfect, although remote consequences are not unfrequently
manifested.

DIFFUSED DISEASES OF THE ENCEPHALON. 719

§ S05. Morbid Anatomy. — In most cases of death from con-
cussion the autopsy reveals actual structural changes in the
brain, consisting of superficial lacerations, or of minute
hemorrhagic extravasations, either studded on the surface of
the brain or in its substance, and occasionally of diffused
ecchymosis of the pia mater (Hutchinson). The most common
sites of these superficial hemorrhagic extravasations are oppo-
site bony ridges, and at projecting parts of the brain. In some
cases no structural lesions of any kind have been discovered. It
is probable that in the majority of the cases which recover no
structural changes which could be recognised even by micro-
scopical examination are produced. It is much more likely
that the essential structural alterations in concussion consist
of a molecular disturbance of the substance of the cerebro-
spinal centres.

§ 806. Morbid Physiology. — Various hypotheses have from
time to time been advanced to account for the phenomena of
concussion. Nothnagel thinks that the strong irritation of the
sensory nerves produced by the injury causes contraction of the
vessels of the brain, which in its turn produces anaemia and loss
of function of the cortex. Fischer, on the other hand, attributes
the phenomena with more justice to vascular paralysis; but if
the shock of the blow is sufficient to paralyse the vaso-motor
centres, what is to prevent it from paralysing a more extended
portion of the nervous system 1 By far the readiest way of ac-
counting for the loss of function of the cortex is to assume
that the injury has produced a molecular disturbance of the
protoplasm of the tissues of the brain, which is accompanied
by an impairment or abolition of their functions.

§ 807. Diagnosis. — Concussion may be distinguished from
most other affections by the presence of the symptoms already
described directly following a distinct injury. It is most likely
to be mistaken for compression of the brain. It may be dis-
tinguished from compression by the absence of any obvious cause
of pressure on the brain, of paralysis, and of stertorous breathing.
In compression from haemorrhage a short interval elapses before
the symptoms are developed, and they gradually become more

720

DIFFUSED DISEASES OF THE ENCEPHALON.

profound, while in concussion they immediately follow the injury,
and usually undergo progressive improvement. In compression
the pulse is slow and full, while in concussion it is frequent
and feeble.

§ 808. Prognosis. — The prognosis of concussion is always
grave, even in apparently trivial cases, inasmuch as they may
be followed by serious remote consequences. The prognosis is
also more grave in those who inherit a neuropathic disposition,
or have led dissipated lives.

§ 809. Treatment. — The treatment of concussion consists of
absolute and prolonged rest. One of the most important rules
of treatment is to abstain from giving stimulants, except in un-
usually severe cases, during the stage of collapse. The patient
in this stage should be surrounded by warm blankets, while
hot bottles may be applied to the feet. Absolute rest in a
darkened room should be enjoined until the stage of reaction
is passed, while the diet should be plain and unstimulating,
consisting mainly of milk. During the stage of reaction a
moderate purgative may be given, and ice should be applied
to the head at an early period, if agreeable to the patient.
Even in slight cases prolonged rest should be insisted upon in
order to' prevent, if possible, the development of the remote
consequences of concussion.

§ 810. Contusion of the Brain.

Whenever the skull undergoes a sudden change of form as
the result of external injury, the substance of the brain may
be contused or lacerated. The contusion may be situated
immediately beneath the portion of the skull where the injury
was inflicted, or on the opposite side of the brain as the result
of contre coup, or both these places may be simultaneously
affected.

The morbid appearances presented in contusion of the brain
consist of capillary hsemorrhagic extravasations, which are
usually limited to the cortex of the brain, but may sometimes
extend into its substance. When the injury is limited to a
small portion of the brain, the extravasations may be so closely

DIFFUSED DISEASES OF THE ENCEPHALON.

721

aggregated that the part affected may present the appearance
of a hasmorrhagic infarction. At other times the extravasations
are more diffused. The brain is liable to be lacerated by loose
splinters, or a depression of the bones; and when there is
fracture of the skull, large portions of the brain may be dis-
organised. »

The symptoms of contusion are always complicated by those
of concussion and of compression. The diagnosis of contusion
must be made, in the absence of the signs of a fracture of the
skull, from the presence of symptoms indicative of a local lesion,
as monospasms and monoplegia, in addition to the symptoms
caused by a general injury to the brain.

The prognosis of these cases is usually serious, but not neces-
sarily fatal.

§ 811. Compression of the Brain.

Compression of the brain may occur after injuries from the
pressure of a fractured portion of the bones of the skull, the
presence of extravasated blood, pus formed within the skull, or
of a foreign body lodged there.

The patient becomes unconscious, the breathing is slow, deep,
and stertorous, while the cheeks are puffed out during respira-
tion. The surface of the body is cool at first, but soon becomes
hot and bathed in perspiration. The pupils are dilated or un-
equal, the pulse is slow and full, the fasces pass involuntarily,
and there is retention of urine. This condition of stupor some-
times alternates with paroxysms of delirium, while local spasms
or paralyses are sometimes observed, but it is probable that in
these cases the motor area of the cortex has been lacerated or
contused.

For further information with regard to contusion and com-
pression of the brain the reader is referred to surgical works.

722

CHAPTER XIII.

II. DIFFUSED DISEASES OF THE ENCEPHALON (Continued).

(IV.) ENCEPHALITIS.

Encephalitis consists of primary inflammation of the substance
of the brain followed by softening and in certain instances by
abscess. Two kinds are usually described, namely, (1) diffused
or general ; and (2) 'partial or local encephalitis.

§ 812. Etiology. — The most frequent cause of acute inflam-
mation and abscess of the brain is recent injury. Primary
traumatic encephalitis is most acute when the atmospheric air
is allowed to gain access to the wound, and in such cases it is
associated with meningitis ; but encephalitis may result from
contusions of the brain in the absence of any perforating
wound of the skull, and such cases often terminate in chronic
abscess of the brain.

Affections of the bones of the skull, such as caries and
accumulations of pus in the petrous portion of the temporal
bone, may cause encephalitis, either by an inward extension of
the inflammatory process or by infection. The presence of
tumours gives rise to inflammation of the surrounding brain
tissue, and a certain amount of encephalitis is always met with
in cases of infantile apoplexy.

Multiple cerebral abscesses occur in connection with acute
febrile affections, more especially typhoid fever, and are
generally occasioned by metastasis from other organs. In
scarlet fever abscesses of the brain result from affections of the
internal ear and petrous part of the temporal bone. Localised
inflammatory processes occur in the brain in measles, and

DIFFUSED DISEASES OF THE ENCEPHALON.

723

Westphal found them also in the spinal cord in variola. Cir-
cumscribed affections of the brain are met with in carbonic-
oxide poisoning, but these appear to be of necrotic origin
(Huguenin). Ulcerative endocarditis may give rise to abscess
of the brain by multiple embolism of the cerebral vessels.
Chronic putrid bronchitis and bronchiectasis are especially
liable to produce secondary abscess in the brain, and unhealthy
suppurations in other parts of the body may have the same
result.

Encapsulated abscesses are produced for the most part by
the same causes that give rise to acute abscess. Lebert found
that injury was the cause of encapsulated abscess in about a
sixth of his cases, Schott in thirteen out of forty, Meyer in
twenty-one out of eighty-six, and Huguenin in one case out of
every four. The encapsulated abscess is frequently situated at
a point in the brain opposite to that where the injury was
received.

Abscesses of the brain secondary to affections of the ear are
situated most frequently in the hemispheres, less frequently in
the cerebellum, and in very rare cases in the pons ; the right
hemisphere is oftener the seat of the abscess than the left.
According to Mr. Toynbee, the inflammation of each portion of
the organ of hearing is transmitted to a particular region of
the brain. Affections of the cavity of the tympanum cause
abscess of the cerebrum ; those of the meatus auditorius
externus induce disease of the lateral sinus and of the cere-
bellum; while affections of the labyrinth cause disease of the
medulla oblongata. He also states that when the mastoid cells
are diseased in early life the cerebrum is the part most likely
to suffer; while in later periods of life, the cerebellum is
generally affected.

Inflammation is transmitted in a small number of cases to
the brain from the nose, Antrum of Highmore, and orbit. Polypi
in the nose and frontal sinuses may cause absorption of the
frontal bone, inflammation of the dura mater, and an abscess in
the anterior lobe of the brain. Gull mentions two cases where
the inflammation was transmitted from the nasal to the cerebral
cavity. Caries of the other bones of the skull, especially that
due to syphilis, also gives rise to cerebral abscess.

724 DIFFUSED DISEASES OF THE ENCEPHALON.

Suppuration occurs around tumours, but it is less frequent
than red softening.

The male is more liable to abscess of the brain than the
female sex, probably from the former being more exposed to
injuries, and for a similar reason the greatest number of cases
occur between the twentieth and thirtieth years of age.
Cerebral abscess is very rare after the sixtieth year of age.

§ 813. Symptoms. — No general description of acute encepha-
litis can be given which will apply to all cases. Injuries to the
head are often accompanied by contusions of the brain, which
may be followed by acute localised encephalitis. Superficial
lesions, provided they be exposed to the air, lead to red soften-
ing, with consecutive acute diffused suppuration of the brain ;
while deep contusions may be followed by red softening and
suppuration, which tend to develop into chronic encapsulated
abscesses. The stage of encephalitis without suppuration is
generally transitory, and its symptoms are difficult to recognise,
more especially as the symptoms often commence during the
period of unconsciousness caused by the original contusion.

1. Diffused oe General Encephalitis.

When the contusion is superficial encephalitis is complicated
by meningitis, and it is impossible to distinguish the symptoms
which belong to each affection.

When diffuse meningitis supervenes after injury, local symp-
toms such as isolated spasm, paralysis, or aphasia may occur,
and a distinct spot of red softening be found at the autopsy to
account for them. But when the lesion of the cortex is situated
beyond the motor area, psychical symptoms of a very general
character are alone produced.

2. Partial or Local Encephalitis.
An encephalitic focus in the substance of the brain may also
give rise to localised motor or sensory symptoms when the
pyramidal tract or the sensory peduncular fibres are affected ;
but a focus of • acute inflammation may exist in the frontal,
temporal, or occipital lobes without giving rise to any symp-
toms indicative of localised disease. An acute encephalitis

DIFFUSED DISEASES OF THE ENCEPHALON.

725

following an injury of the head without fracture may conse-
quently run its course without our having a suspicion of its
existence.

When a contusion in the interior of the brain has taken
place, the patient first suffers from the usual symptoms of con-
cussion, and it is only when these have disappeared that the
symptoms of local encephalitis can be recognised. The patient
lies in a semi-conscious condition, and when roused complains
of headache and dizziness, and staggers on attempting to
walk. The pupils are variable in size, generally equal and
reacting slowly to light. The countenance is usually suffused,
but at times turns pale, and the pulse, which was frequent and
irregular during the stage of concussion, sinks to 60 or 70 beats,
and the thermometer may reveal the existence of fever of
remittent type.

The symptoms are at times so insignificant that after a few
days the patient feels quite well, or indefinite symptoms may
continue for two or three weeks.

Suddenly, however, these symptoms become more intense,
the fever increases, but is still of irregular type, the dizziness
and headache become more marked, vomiting is not un-
frequent, the pupils are dilated and fixed, the pulse is slow,
the patient falls into a condition of sopor, which may be
accompanied by delirium, or may pass directly into complete
unconsciousness.

As the case progresses graver symptoms appear in rolling of
the eyes, transitory divergence, sudden permanent paralysis of
the abducens, motor oculi, or facial nerve, and in a few cases
hemiparesis or hemiplegia. Convulsive symptoms are some-
times present, usually consisting of twitchings of both hands,
or there may be clonic convulsions of the limbs. In some cases
a general convulsion occurs which varies greatly in duration
and intensity in different cases. The sopor now grows deeper,
the previously slow pulse becomes quick and irregular, and death
takes place in coma. The course of the temperature varies,
but a continuous elevation until death is exceptional.

The duration of the symptoms is variable. Beck found an
abscess of the brain on the fifth day after an injury of the head,
and Huguenin on the twelfth day. When the air obtains

726

DIFFUSED DISEASES OF THE ENCEPHALON.

access to a peripheral cerebral contusion, and suppuration
occurs, death supervenes more rapidly.

The dangerous symptoms of traumatic encephalitis may
occasionally disappear, and the patient be restored to compa-
rative health. The inflammatory focus may be transformed
into a relatively innocuous condition, but in many cases chronic
changes of a diffused character are occasioned which give rise
to more or less permanent symptoms. The more usual groups
of symptoms caused by these changes are the following: —

(i.) Chronic psychosis in the form of irritable melancholia,
followed by recovery (Huguenin).

(ii.) A psychosis characterised by severe headache, dizziness,
anxiety, and hallucinations ; the intellectual faculties are im-
paired, and there are intercurrent periods of excitement and
constant illusions of the senses. A few cases recover, but in
the majority this condition continues for years, and at last ends
in complete imbecility.

(iii.) Symptoms resembling those of dementia paralytica
supervene at a variable period of weeks or years after the
injury. The development of the disease after an injury is
slow, and the course is protracted.

(iv.) A psychical vulnerability frequently remains, which is
apt to develop into some form of insanity from some slight
exciting cause. In these cases the disposition of the patient is
generally changed, there is great mental irritability and hyper-
sesthesia along with diminution of the power of sustained
thought, and insanity may supervene many years after the
injury.

(v.) Epilepsy is a frequent result of the chronic changes in
the skull that follow an injury. Old depressions of the skull
are often associated with epilepsy.

(vi.) Tumours of the brain have been known to follow injury
(Griesinger, Recklinghausen).

(vii.) Diabetes has supervened immediately after a fall on
the back of the head.

DIFFUSED DISEASES OF THE ENCEPIIALON. 727

a. Acute Encephalitis, complicating affections of the petrous
portion of the Temporal Bone, and of other Bones of the
Skull.

§814. Symptoms. — The symptoms caused by the acute
encephalitis, which accompanies caries of the petrous bone, are
often obscured by co-existing meningitis and thrombosis of the
sinuses. An abscess in the temporal lobe may attain a con-
siderable size, and cause general symptoms of compression
before giving rise to symptoms of local disease, inasmuch as
this lobe does not contain any direct sensory or motor con-
ducting tracts. Acute abscesses of the temporal lobe are con-
sequently seldom recognised during life. Otorrhcea may occur
at all acres, although it is most common in scrofulous children
especially after attacks of scarlet fever; while a purulent dis-
charge from the ear has occasionally been observed immediately
after birth, the affection being then apparently congenital.
Acute cerebral abscess from otorrhoea runs a very rapid course,
its duration being from four to twenty or more days.

The symptoms are those which usually result from a sudden
and progressive compression of the brain, but general convul-
sions may precede the development of complete coma. Fever,
of variable type, is usually present, the pulse is slow, and the
pupils contracted and sluggish.

Severe headache is usually the first symptom of the affection,
but it is soon followed by vomiting, ringing in the ears, con-
fusion of ideas and loss of memory, and mild delirium. As
the disease advances the headache becomes more and more
intense, the patient is delirious and at times unconscious, epilep-
tiform convulsions supervene, and the case soon terminates
fatally amidst profound coma.

In some cases the general symptoms just described are com-
plicated by those of a localised disease. In such cases the
abscess increases rapidly in size, and involves the base of the
lenticular nucleus, compressing the fibres of the internal cap-
sule, and thus causing an incomplete hemiplegia with various
sensory disturbances. It may also compress the cerebral
peduncle, and thus cause paralysis of the oculo-motor nerve,
while paralysis of the facial nerve has occasionally been observed.

728

DIFFUSED DISEASES OF THE ENCEPHALON.

Cases of this kind pursue a rapid course, and terminate fatally
in a short time.

A few cases are associated with acute meningitis or throm-
bosis of the lateral sinus.

b. Acute Pycemic Encephalitis.

The initial symptoms of this affection are somewhat variable
and often masked. There are frequently rigors, but these are
symptomatic of the general disease. The brain affection is
ushered in by severe headache, usually frontal, dizziness, mental
disturbance, slight somnolence, occasionally delirium, unilateral
convulsions in an arm or leg or both, formication and other
forms of dysesthesia, or a slight diminution of sensibility.

The disease usually makes rapid progress, and graver symp-
toms soon supervene. There is intense headache, dizziness is
so great that the patient cannot stand or walk, the mind is
confused, and delirium supervenes, but soon gives place to pro-
found coma.

The local symptoms consist of convulsive movements of the
eyes, face, or of one of the limbs, which may end in unilateral
or general convulsions. There may be at times a considerable
elevation of temperature, but the intensity of the febrile symp-
toms is variable.

c. Encephalitis around pre-existing lesions in the brain, such
as tumours, necrotic softenings, and extravasations of
blood.

(a) Cerebral Hemorrhage. — Within a variable period after
a cerebral haemorrhage, a zone of red softening is found around
the primary focus, in which an abundance of migrated corpuscles
may be. observed. Suppuration, however, is rare, if it ever occur.
Beyond the area of red softening a second zone may be observed
in which the tissues of the brain are unusually dense, owing to
a great increase of the neuroglia corpuscles, while the tissues
surrounding this zone may be extensively cedematous. Secon-
dary haemorrhages may occur in the circumference of the pri-
mary apoplectic focus.

(6) Necrotic Softening from Thrombosis and Embolism. —
The primary focus consists of a hemorrhagic infarct, which is

DIFFUSED DISEASES OF THE ENCEPHALON.

729

followed by inflammation of the surrounding tissues. The in-
farct is thus surrounded by a red areola, studded with capillary
extravasations, which in its turn is surrounded by a yellowish
zone, and the latter by a more or less extensive zone of

cedematous tissue.

The inflammatory process around the focus, as a rule,
gradually ceases, the central portion of the part affected be-
coming transformed into a cyst containing a clear serous fluid,
and sometimes connective tissue septa, or into a number of
small lacunas containing a cloudy serum.

(c) Tumour. — The secondary softening caused by tumours
of the brain is usually most marked around tumours like the
carcinomata, which grow quickly.

The processes around tumours may be divided into several
varieties : —

(i.) Simple softening and oedema of the surrounding tissues,
caused by retardation of the circulation, and probably by
thrombosis.

(ii.) Capillary and larger extravasations, probably due to
fatty degeneration of the walls of the vessels.

(iii.) Genuine encephalitic red softening, accompanied by
rupture of minute vessels, migration of cells, and extensive
oedema of the brain.

(iv.) Suppuration around tumours is occasionally observed.

§ 815. Symptoms.

(a) Cerebral Hemorrhage. — Some of the symptoms which
follow a cerebral haemorrhage must be ascribed to consecutive
encephalitis. The patient may have made a good recovery
from the early symptoms of an apoplectic attack, but several
days afterwards there is a fresh elevation of temperature, and
the pulse becomes hard and frequent. The patient complains of
headache, there may be slight wandering and confusion of ideas,
and he may fall into a somnolent condition. The general are
soon followed by local symptoms, consisting usually of the well-
known secondary contractures. Some patients may manifest
only slight tremor of the paralysed limbs ; in others the flexors
are in a state of contracture, while in a third series of cases

730

DIFFUSED DISEASES OF THE ENCEPHALON.

these conditions alternate. The temperature of the paralysed
side is often considerably elevated, and anomalies in the secre-
tion of sweat are observed. The somnolence may now increase
to a deep sopor, which lasts several days, and may pass into
profound and fatal coma.

In those cases that recover symptoms frequently persist
which show that a chronic encephalitis is established. There
is persistent headache, frequent attacks of dizziness, and the
patient is subject to congestive attacks, each of which ma}'
cause new convulsions in the paralysed limbs. The paralysed
limbs are generally subject to pains of variable character,
situated either in the joints, bones, skin, or muscles. Secondary
encephalitis is also the chief cause of the atrophy of the brain
observed in many of these patients, and which is always
associated with profound psychical disturbances.

(6) Thrombosis and Embolism. — In senile encephalomalacia
the symptoms of secondary encephalitis are caused by an in-
crease of the intracranial pressure on the one hand, and irrita-
tion of the surrounding parts on the other. The symptoms of
inflammatory reaction are slight ; and when a certain degree of
senile atrophy of the brain had existed previous to the occur-
rence of the attack, the mental functions become progressively
abolished without being preceded by symptoms of active irrita-
tion or by those indicative of a gradual compression of the
brain. It frequently happens that, after the formation of a
diseased focus in the brain, a febrile condition, attended by a
drowsy delirium or somnolence, continues for some time, and
either develops into permanent imbecility or gives place to
partial restoration of the mental faculties. When the last result
occurs the mental condition of the patient is characterised by
weakness of memory, irregular and causeless outbursts of temper,
and a disposition to the shedding of tears, and other emotional
displays. The patient is liable to congestive attacks which
occasion temporary unconsciousness, and during these new foci
of softening may be developed in the brain. Couvulsions of the
partially paralysed limbs may occur, and in rare cases general
convulsions.

DIFFUSED DISEASES OF THE ENCEPHALON.

731

encephalitis in the surrounding tissue. The symptoms which
may with probability be ascribed to encephalitis during the
growth of a cerebral tumour are the occurrence of sudden apo-
plectiform attacks, the rapid conversion of slight muscular
weakness into complete paralysis, partial convulsions followed
by paralysis, general convulsions, and the gradual development
of coma. When coma is suddenly developed in the course of the
growth of a cerebral tumour, it is more likely to be caused by
haemorrhage, or sudden oedema, than by encephalitis. Every
secondary encephalitis, however slight, produces violent head-
ache, although such attacks may be due to a congestive swelling
of the tumour itself. Encephalitis around a tumour which
involves the sensitive fibres of the corona radiata is liable to
cause disturbances of sensation in the opposite side of the body.

d. Chronic Abscess of the Brain.
Chronic abscess of the brain may be subdivided into (i.)
primary and (ii.) secondary chronic abscess.

(i.) Primary chronic abscess is usually caused by some
injury of the brain. All the symptoms, or nearly all, may dis-
appear soon after the injury, and a period relatively free from
symptoms may follow, forming the latent stage of chronic
abscess. The average duration of the latent stage is, according
to Lebert, from one to two months, but the period may vary in
individual cases from a few days to years. When once a chronic
abscess is formed, the symptoms caused by it are more or less
similar to those of cerebral tumour; and when the former is
situated in the motor areas of the cortex and centrum ovale,
or injure the sensory peduncular fibres, the symptoms of a
local lesion are present from the beginning. The symptoms
may be divided into those of«(l) the latent, and (2) the ter-
minal stages.

(1) Symptoms of the Latent Period.

(a) In some cases a persistent headache subject to paroxysmal
exacerbations is the only symptom present which could lead to
the suspicion of the existence of an intracranial affection, and
in a few rare cases this symptom may be absent.

(b) In other cases symptoms of a local disease appear which

732

DIFFUSED DISEASES OF THE ENCEPHALON.

make it possible to diagnosticate the locality of the lesion,
while the history of the case and the concomitant phenomena
may place the nature of the lesion beyond doubt. The local
symptoms caused by chronic abscess are the same as those of
all other focal diseases.

(c) In other cases the symptoms of the latent stage are
those of a moderate degree of intracranial pressure. These
consist of constant headache, with paroxysmal exacerbations
accompanied by slight febrile disturbance, dizziness, nausea,
and occasionally vomiting. The headache may be limited to the
spot where the injury was received, or correspond to the part
of the brain where the abscess is situated, the latter being often
at a point of the brain exactly opposite the seat of injury.
Paroxysmal exacerbations of the headache are indicative of
congestion around the abscess, and when these frequently recur
the abscess is likely to prove fatal within a brief space of time.

(d) In a fourth series of cases the symptoms are indicative
of intermittent pressure on the brain, with intervals of com-
parative freedom from all cerebral symptoms. The patient, in
the midst of comparative health, may suddenly complain of
intense headache, he becomes somnolent, and falls into a deep
but transitory coma of several hours' duration, from which he
rapidly recovers. Such attacks are probably due to sudden
pressure on the brain from congestion.

(e) The so-called latent stage is sometimes characterised by
epileptiform convulsions, which may be regarded during life as
true epilepsy (Hutchinson, Jackson). General convulsions are
rare during this stage.

(2) Symptoms of the Terminal Period.

When once the terminal periqd begins, abscess of the brain
generally leads to death in a few days. The symptoms of this
period differ widely in individual cases, and the following groups
may be distinguished : —

(a) Terminal oedema of the brain is the most usual mode of
termination of chronic abscess. In the majority of cases the
tissues of the brain are compressed to such an extent that death
by coma results in two or three days, while in a few cases the
course of the symptoms is characterised by temporary improve-

DIFFUSED DISEASES OF THE ENCEPIIALON.

733

ments and aggravations, so that the fatal issue may be delayed
for some time. In some cases there may be a transitory initial
stage of irritation, characterised by mental irritability, rest-
lessness, illusions, violent delirium, and a slight elevation of
temperature. The irritative symptoms soon give place to
those of depression, the patient complains of headache, the
temperature falls, the pulse is slow, the pupils are dilated and
react feebly to light, there is mental confusion, and the patient
falls into a somnolent coudition, from which he may be roused
temporarily when pressed by questions; but in a short time
coma supervenes, and the case soon terminates fatally, the pulse
becoming small, quick, and irregular before death.

Chronic abscess in the region of distribution of the posterior
and anterior cerebral arteries may run, as we have seen, their
course without giving rise to marked motor or sensory symp-
toms. But even when the abscess is situated in one of these
regions convulsions are not always absent during the terminal
period. An abscess in the pras-frontal region may, for instance,
give rise to partial convulsions, either limited to or beginning
in the face and extending to the arm, these convulsions being
followed by paralysis. General convulsions are sometimes
caused by abscess situated in the latent regions of the hemi-
sphere, and these are usually followed by profound coma. The
symptoms of local disease which may have been present during
the latent stage of the abscess are variously modified in the
terminal stage. Partial convulsions which may have been
present become more violent and are soon followed by para-
lysis, or they may become transformed into a series of epilep-
tiform attacks terminating in coma.

(6) Rupture of the Abscess on the Surface of the Brain. —
When abscesses make their way to the surface of the brain, an
acute and rapidly fatal meningitis generally results. The
symptoms of irritation are at first predominant, consisting of
general convulsions and delirium. The patient, however, soon
becomes unconscious, and dies comatose in a short time.

(c) Perforation of the Abscess into the Ventricle. — This
occurrence causes a group of symptoms which may be recog-
nised, if the existence of an abscess have been previously
suspected. A sudden cerebral attack, attended by bilateral, but

734 DIFFUSED DISEASES OF THE ENCEPHALON.

more or less partial convulsions, such as spasms of both legs, or
of the facial muscles on both sides, is an indication of rup-
ture into the ventricles, provided the patient be not already in
an unconscious condition. General convulsions have sometimes
been observed. Clonic spasms of the ocular muscles soon
appear, caused probably by irritation of the corpora quad-
rigemina. The patient becomes rapidly unconscious, hemiplegia
and death in profound coma take place generally in from four
to twenty -four hours after the rupture of the abscess.

(d) Abscess of the cerebellum may terminate suddenly from
arrest of the respiratory functions produced by pressure on the
medulla oblongata.

(e) Occasionally the brain is found in a condition of remark-
able anaemia, and in such cases the immediate cause of death
is not evident.

(ii.) Secondary Chronic Abscess of the Brain. — Secondary
chronic abscesses are generally caused by affections of the inner
ear. The diagnosis of the presence of chronic abscess of the
brain is difficult, inasmuch as only a small proportion of such
cases give rise to characteristic symptoms. When the abscess
is encapsulated it may remain latent for a long period, so that
no disease of the brain is suspected until the terminal period.
Even the terminal symptoms present varieties which tend to
obscure the diagnosis, these symptoms sometimes resembling
those of diffuse meningitis, and at other times those of throm-
bosis of a sinus.

§ 816. Varieties. — The following varieties of chronic abscess
secondary to disease of the ear may be distinguished : — (a)
Chronic abscess with distinct typical course ; (6) Chronic abscess
with terminal stage alone distinct; (c) Chronic abscess with
thrombosis of the lateral sinus ; (d) Chronic abscess compli-
cated during the terminal period by meningitis.

(a) In affections of the inner ear abscess may form in the
temporo-sphenoidal lobe. In a long-standing case of disease
of the internal ear, where rigors and other general inflam-
matory symptoms are associated with severe pain in the head,
vomiting, convulsions, and other cerebral symptoms, the forma-

DIFFUSED DISEASES OF THE ENCEPHALON. 735

tion of an abscess in the brain may be suspected. These
symptoms may pass oft', and the patient enjoy apparent
health for months, with probably occasional headaches. The
terminal stage is announced by intense headache and dizziness
soon followed by loss of consciousness and stertorous breathing.
Consciousness may be partially restored in a few hours, and
the patient then surfers from intense headache and vomiting.
After a short time the patient lapses a second time into a semi-
conscious condition, and convulsions, generally unilateral, super-
vene. Spasm followed by paralysis of the ocular muscles is
not an unfrequent symptom, and when the abscess is so large
that it extends to the lenticular nucleus and compresses the
internal capsule, or the fibres of the pyramidal tract in the
crusta, a certain degree of hemiplegia may be present.

(6) Chronic abscess of the brain is sometimes observed in
cases of caries of the petrous bone, in which the terminal
symptoms have not been preceded by those indicative of irri-
tation or encephalitis.

(c) Chronic abscess of the brain sometimes precedes, at other
times succeeds to thrombosis of the lateral sinus. The chief
initial symptoms are, besides those of the ear affection, dizziness,
intense headache, and occasionally transitory delirium, followed
by somnolence. The patient suffers from frequently-repeated
rigors if the temperature of the body be raised, and the fever
assumes a remittent type. In the further progress of the case
the symptoms may pursue either of two directions. The
symptoms may be those of progressively increasing pressure
upon the brain, ending in coma, or the general symptoms
indicative of compression may be associated with those of a
localised disease, provided the abscess has attained a sufficient
size to press upon the internal capsule. General convulsions
may occur immediately before death.

(d) Chronic abscess of the brain may be complicated during
the terminal period by meningitis, and when the initial stage
of the former is latent, the terminal symptoms may be so similar
to those of primary acute meningitis that the two affections
cannot be distinguished from one another during life.

736

DIFFUSED DISEASES OF THE ENCEPHALON.

§ 817. Morbid Anatomy. — In encephalitis the affected tissue
assumes a reddish colour, and is studded by a number of capil-
lary extravasations, each about the size of a pin's head, these
being sometimes so numerous that the affected part presents
the appearance of a hsemorrhagic infarct. These capillary extra-
vasations are followed by more or less oedema, which may
extend for a considerable distance into the surrounding tissues.
In consequence of this oedema the affected portion of the
brain becomes voluminous, and the cut surface rises above the
level of the surrounding tissues, the latter of which assume
different shades of colour from the imbibition of the colouring
matter of the blood set free in the central part of the effusion.
When the inflamed focus presents a deep red colour it is sur-
rounded by a red zone, which shades off into brown, then into
yellow, and finally into the normal colour of the cerebral tissue.

The microscopic changes observed in the first stage of
inflammation are great hypersemia and dilatation of the vessels
and capillaries. Hayem asserts that he has seen the vessels dilated
to six times their normal calibre. The vessels are surrounded by
migrated white blood corpuscles and the tissues are infiltrated
by leucocytes, probably derived from multiplication of the nuclei
of the neuroglia and proliferation of the cellular elements of
the walls of the vessels. A large number of granule cells (Gluge's
corpuscles) may also be observed in the inflamed focus. These
are probably derived from the ganglion cells, the nuclei of the
neuroglia, the nuclei of the capillary vessels, and the endothelial
cells of the sheaths of the vessels. The large size and granular
appearance assumed by these cells are supposed by Hayem to be
due to the absorption of nutriment and to be analogous to the
cloudy swelling of Virchow, but the granular appearance is at
least more likely to be caused by commencing degeneration.
The ganglion cells swell up, their protoplasm undergoes
molecular disintegration, and after the inflammation has ceased
they undergo various degrees of atrophy and sclerosis, and in
chronic cases the calcification and pigmentary infiltration
described by Forster.

§ 818. Further Transformations of the Primary Focus.
The primary focus undergoes various changes according to the extent
and situation of the inflammation. In a large proportion of cases the

DIFFUSED DISEASES OF THE ENCEPHALON. 737

inflammatory process ceases before an abscess forms, and the affected part
presents a strong resemblance to a primary necrosis with subsequent
peripheral encephalitis. The resulting conditions are similar in the two .
affections, although they are essentially different in nature.

(1) An encephalitis of slight intensity and small extent, such as that
caused by traumatic contusion, may undergo complete repair.

(2) After the inflammatory process in the larger foci has ceased a re-
siduum is left behind which undergoes the well-known destructive changes,
followed by absorption of the fluid contents. All the cellular elements
in the focus are transformed into granule cells, which undergo a gradual
disintegration ; the contents of the focus becomes thus converted into a
thick emulsion, coloured brownish or yellowish by the blood pigment. All
the nuclei of the vessels and the neuroglia, and the white blood cells,
which are enclosed in the focus, disappear, and its contents become more
homogeneous. After a time a focus of yellow softening forms which
gradually becomes more colourless, and at last may be transformed into a
cavity filled by a thin milky fluid.

(3) But the focus after a time manifests a delicate stroma supplied with
delicate vessels, the interspaces of which are filled by a thin turbid fluid.
The stroma consists of delicate connective tissue supplied with vessels ;
the formed elements of the fluid consist almost wholly of large quantities
of granular fat and albuminous bodies, together with a little free pigment.
The spaces become gradually larger and the fluid clearer, so that a chasm
remains which is traversed by a number of delicate septa of connective
tissue, and surrounded by somewhat condensed cerebral substance. Apo-
plexy and infarct may terminate in the same way, and the nature of the
preceding affection cannot be positively determined from the study of the
lesions in their later stages.

(4) Local encephalitis may lead to the production of firm sclerotic
cicatrices situated usually near the surface of the brain, more rarely deep
in the interior of the organ. These cicatrices are of a dirty-white colour,
tough, and firm ; the tissue surrounding them is atrophied, so that the
affected hemisphere is less than the other. Even distant portions of the
brain, especially of the cortex, may be found in a state of atrophy. When
the cicatrices are situated deep in the brain, cavities .are found within
them at an early period. At a later period the cicatrix contains a nucleus
differing from the rest, and containing fat and pigment granules, hsema-
toidin crystals, and amorphous detritus.

Such inflammatory processes in the brain very seldom become quiescent ;
they are followed by a gradually progressing atrophy of the entire brain,
which causes symptoms during life that even at the present day are fre-
quently included among those of dementia paralytica. Hasse has also
drawn attention to the fact that an encephalitic cicatrix may excite fresh
inflammation at a later period resulting in the development of a new zone
V V

738

DIFFUSED DISEASES OF THE ENCEPHALON.

of red softening with capillary apoplexy. It may also excite a rapidly pro-
gressive yellow softening, which may prove fatal.

The inflammation excited around embolic foci may give rise to sclerotic
capsules, consisting of a dense fibrous connective tissue. Huguenin
examined one that contained a large number of spindle cells with oblong
nuclei, which he surmised to have been derived from migrated white
blood corpuscles.

(5) The encephalitic focus may be transformed into a collection of pus,
which may be subdivided into recent and old abscesses. An abscess is
said to be new or fresh when it has been developed rapidly and does not
possess a capsule, but this distinction does not hold good in all cases. An
acute abscess has a tendency to spread in every direction and it presents
an irregular cavity in the substance of the brain, whose walls have a
rough, shaggy surface. The shaggy projections consist of shreds of
cerebral tissue, which are attached to the larger blood-vessels. The tissue
around the abscess is in a condition of red softening, and in many places
the softened tissue is of a predominantly yellow colour ; while at a greater
distance from the focus the cerebral tissue is cedematous. As the pus in
the central cavity accumulates pressure is exerted on the whole of the
surrounding tissue, which arrests its circulation and leads to further
destruction, and advance of the abscess.

The abscess by virtue of its tendency to enlarge may reach the surface
of the brain, and as soon as perforation occurs an acute purulent inflam-
mation of the pia mater results.

(6) Old abscesses of the brain possess a fibrous capsule which may attain
a thickness of several millimetres. Eindfleisch affirms that there is a
gradual transition from the capsule to the surrounding nervous tissue, but
the connection is not always very close, inasmuch as the abscess can be
enucleated without much difficulty. The internal surface of the limiting
membrane is smooth, and an opaque yellowish- white appearance is given
to it by a continuous layer of cells in a state of fatty degeneration. Out-
side this there is a layer of embryonic tissue.

The pus of the abscess is of a greenish colour, and greasy consistency,
is odourless, and has an acid reaction. After a variable period of quiescence
the abscess enlarges and produces manifold changes in surrounding parts.
The intracranial pressure becomes increased, the nervous tissue in the
vicinity of the abscess may be compressed so that its nutrition is arrested,
and as a result there follows more or less extensive yellow softening.
Local inflammatory processes in more distant parts are met with.

Accessory Changes in the Brain. — Perforations on the surface of the brain
and into the ventricles occur in connection with encapsulated as with
recent abscesses.

. Extensive acute oedema of the brain often results from abscess, and is
probably clue to the increase in the intracranial pressure.

DIFFUSED DISEASES OF THE ENCEPHALON. 739

Ancemia of the brain, and more especially of the cortex, also results
from the increase of the intracranial pressure.

Chronic internal hydrocephalus results whenever an abscess is situated
in the cerebellum in such a position that it lessens the cavity of the fourth
ventricle or of the Sylvian aqueduct.

§ 819. Diagnosis. — The symptoms of abscess of the brain
are very similar to those of tumour, but the two affections may
generally be distinguished by the history of the case and the
progress of the symptoms. Abscess is more frequently pre-
ceded by a distinct history of injury to the head than tumour,
although the latter also occasionally develops soon after injury
to the skull. The course pursued, however, by the two affections
subsequent to the injury, differs widely. If the symptoms of
acute encephalitis occur immediately after the injury, and be
then followed by a remission or complete intermission and break
out again after a latent period of variable duration, either with
or without the phenomena which indicate a local disease, abscess
may be diagnosticated rather than tumour.

If the other causes which give rise to abscess of the bram,
as chronic otorrhcea, caries of the temporal, frontal, or nasal
bones, bronchiectasis and purulent cavities in the lungs with
putrid secretions, and pysemia are present, along with the symp-
toms of a localised lesion of the brain, then also the existence
of an abscess rather than tumour may be inferred.

The symptoms of tumour are sometimes characterised by
frequent remissions and exacerbations, while in abscess the
symptoms may be latent or stationary for a comparatively
long time, but when the terminal period is ushered in the
remissions are of short duration and never frequently repeated.
In many cases of tumour the course of the disease is con-
tinuous and progressive from the first, and the symptoms
increase not only in intensity but in number and extent,
the general symptoms of headache, dizziness, and vomit-
ing of the first period becoming slowly complicated by local
spasms, unilateral convulsions, pareses passing on to distinct
paralyses, sensory disturbances, slight at first but becoming
more profound, and various disorders of the special senses.
Although these symptoms may all be present at a given time in
the course of chronic abscess, yet they never appear in the same

740

DIFFUSED DISEASES OF THE ENCEPHALON.

progressive manner in the latter affection as they do in tumour.
Repeated chilliness and slight elevation of temperature are
more characteristic of abscess than of tumour, but it must be
remembered that the latter is liable to be complicated by
attacks of acute encephalitis.

In the absence of a distinct history of the case, it may be
impossible to distinguish the terminal period of abscess of the
brain from cerebral haemorrhage, or occlusion of a large vessel ;
but if there be a history of injury to the skull, followed by the
symptoms of acute encephalitis, then the diagnosis is less
difficult. This difficulty is likely to arise when, after a long
latent period, the abscess makes its way into the ventricles, or
when sudden oedema of the brain occurs. When the abscess
ruptures on the surface of the brain the terminal symptoms are
those of acute meningitis, and the diagnosis between primary
meningitis and abscess must again be made from the history of
the case and the symptoms.

Abscess of the brain is difficult to distinguish from necrotic
softening. The diagnosis must be made on the one hand by
the history of an injury to the skull or the presence of one of
the other causes which give rise to abscess ; and on the other
hand by a careful general examination of the patient, especially
of the organs of circulation, to ascertain the presence or not of
the conditions which lead to embolism or thrombosis.

§ 820. Prognosis.

(a) Meningo- Encephalitis. — A superficial contusion of the
brain usually terminates in acute suppuration associated with
meningitis, and the affection is generally fatal. Recovery is
possible only when diffuse meningitis does not take place, and
when the pus is discharged through a wound, produced either
by the original injury or by surgical operation.

(6) Suppurative encephalitis without accompanying me-
ningitis, resulting from contusion of the brain, does not appear
to be capable of spontaneous absorption. Recovery, however,
may take place either from spontaneous perforation externally
or from artificial evacuation. Acute abscess may, instead of
at once terminating fatally, pass into the chronic form.

DIFFUSED DISEASES OF THE ENCEPHALON. 741

A small number of cases have recovered spontaneously after
perforation through the skull. The pus has been evacuated by
fortunate trephining, but the number of cases in which the
patient was saved is small.

(d) Otorrluxal Abscess of the Brain. — Several cases of re-
covery of otorrhceal cerebral abscess are on record in which the
pus made its way through the diseased ear. Acute otorrhceal
abscess of the brain often passes into the chronic form, but the
ultimate prognosis in both varieties is unfavourable.

(e) Pycemic Abscesses of the brain, whatever may be their
cause, are always fatal.

(/) Acute Traumatic Encephalitis without formation of
Pus. — Cases of recovery from undoubted traumatic encephalitis
have been collected by Bruns. The prognosis of encephalitis
around chronic abscesses, tumours, chronic softening, and
apoplexies depends upon the nature and extent of the primary
disease. The prospect is least favourable in abscess and tumour.
The age and strength of the patient is an important factor in
estimating the danger of encephalitis secondary to necrotic
softening and cerebral haemorrhage, but the complication is
always a serious one, and even if the patient survive the
general and local symptoms are usually aggravated by an in-
crease in the destruction of tissue caused by the primary focus.

§ 821. Treatment. — The physician's advice may be sought to
aid the surgeon in determining questions of cerebral localisation,
and the other delicate poiuts of diagnosis which are likely to
arise in the progress of such cases, but the decision with regard
to the treatment to be adopted must rest with him.

The secondary inflammation which is liable to supervene in
the course of necrotic softening, cerebral haemorrhage, and
intracranial tumours is the form of encephalitis which is most
likely to come under the care of the physician. This variety
is best treated by complete rest in a darkened room, mild
purgation, and cold applied to the head ; more active measures
like bleeding and blistering are worse than useless.

Chronic abscess of the brain does not admit of any special
medical treatment, but the general health of the patient must
be attended to, and his diet and habits carefully regulated.

742

DIFFUSED DISEASES OF THE ENCEPHALON.

Paroxysms of severe headache may sometimes be relieved by
chloride of ammonium, while more active symptoms like
delirium may be combated by bromide of potassium, either
alone or in combination with chloral, and an opiate may some-
times be found useful. Drs. Russell Reynolds an^ Hammond
speak favourably of Cannabis Indica in the treatment of the
more active symptoms of suppurative encephalitis.

743

CHAPTER XIV.

DISEASES OF THE MEMBRANES OF THE BRAIN.

I. DISEASES OF THE DURA MATER.

Inflammation of the dura mater may be divided into (i.)
external, and (ii.) internal pachymeningitis.

(i.) ^External Pachymeningitis .
External pachymeningitis consists of inflammation of the
outer lamella of the dura mater.

§ 822. Etiology. — The chief causes of the affection are the
following : —

1. Injuries which detach the dura mater from the inner sur-
face of the skull, and occasion an extravasation of blood
between them. The clot may be so large as to compress the
brain and cause death in a short time. At other times inflam-
mation is set up in the surrounding tissues and the bone is
threatened with necrosis.

2. Perforating injuries of the skull, as incised, punctured,
and bullet wounds, which either directly or indirectly injure
the dura mater.

3. Extension of inflammation from neighbouring tissues.
Caries of the petrous portion of the temporal bone is one of
the most frequent causes of external pachymeningitis, and it
usually gives rise to the suppurative form of inflammation.

Purulent inflammation of the external lamella may also
follow caries of other cranial bones, especially the ethmoid and
the flat bones of the skull, as well as by caries of the upper
cervical vertebras and their ligaments.

744 DISEASES OF THE MEMBRANES OF THE BRAIN.

4. The external layer of the dura mater is subject to chronic
fibrous thickening in old age, and becomes adherent to the bone.

§ 823. Symptoms. — In the traumatic form of external pachy-
meningitis the patient may recover from the immediate effects
of the injury, and appear for a time in perfect health. At
the end of two or three weeks he complains of pain in the
head, is feverish, and should there be an external wound, it
assumes an unhealthy aspect. If the inflammation spread
further, the headache increases in intensity, and the patient
suffers from vertigo, nausea, and vomiting, while monospasms
or unilateral convulsions may occur if the motor area of the
brain be implicated. The internal membranes of the brain
now become affected, the previously convulsed limbs become
paralysed, the patient becomes delirious, and fatal coma soon
supervenes.

When an abscess forms between the dura mater and the
bones of the skull, the symptoms may be those of gradual
cerebral compression, and when it is situated over the motor
area of the cortex, monospasms or monoplegias may result.

The pachymeningitis of old age is often discovered after
death without having been suspected during life. In other
cases the meningitis may have manifested itself merely by a
persistent dull headache. After death atrophy of the brain,
compensatory hydrocephalus, and serous infiltration of the pia
mater are observed.

§ 824. Morbid Anatomy. — The dura mater is at first con-
gested, and presents punctiform extravasations. In a more
advanced stage the membrane becomes swollen and infiltrated
with numerous white blood corpuscles. These cells may after
a time become transformed into spindle cells, and ultimately
developed into bundles of connective tissue. Portions of the
membrane may sometimes become ossified.

If the inflammation progress to actual suppuration, the
white blood corpuscles become more numerous, and make their
way through the internal lamella to the free surface, so that a
purulent internal pachymeningitis is added to the external
pachymeningitis. At times, however, the abscess is cut off

DISEASES OF THE MEMBRANES OF THE BRAIN. 745

from the internal layer by the development of adhesions, and
in that case the external layer becomes disintegrated, soft,
and friable; while the internal layer becomes adherent to the
pia mater and brain. In the large majority of cases the in-
flammation spreads to the internal lamella.

§ 82-5. Prognosis. — The prognosis in traumatic cases turns
on the possibility of the pus finding a free escape. If a free
discharge can be obtained, the affection of the dura mater may
occasion but little trouble ; while, on the other hand, if the
matter is pent up, grave symptoms must result, both on account
of the increased intracranial pressure, and the rapidity with
which the suppurative process spreads. The prognosis of puru-
lent inflammation of the dura mater resulting from caries of
the petrous portion of the temporal bone is very unfavourable.

§ 826. Treatment. — The treatment of the acute stage must •
be conducted according to general principles. The question of
trephining will arise in connection with the formation of an
abscess or extravasation of blood between the dura mater and
the bone, but this belongs to surgery.

(iL> Internal Hemorrhagic Pachymeningitis.
(Hcematoma of the Dura Mater. J

§ 827. Etiology. — Hsematoma is associated with all those
diseases which profoundly affect nutrition, and many of them
are diseases like scorbutus, in which haemorrhages are liable
to occur in other parts of the body. The disease is found in
atrophy of the brain accompanied by oedema of the pia mater
and hydrocephalus internus. On the whole, therefore, it seems
probable that when haematoma of the dura mater does not
result from direct injury, it is caused either by constitutional
disease producing profound alteration in the quality of the
blood, degeneration of the vessels of the brain, or by diseases
associated with passive congestion of the brain. It is not
therefore surprising that the affection should occur chiefly in
old age.

§ 828. Symptoms.— The symptoms of hematoma vary
greatly in different cases, but the following are the more
usual : —

746 DISEASES OF THE MEMBRANES OF THE BRAIN.

Headache is a very constant symptom, being rarely absent.
The pain is described as if something were moving about in the
head, or as a throbbing accompanied by a sensation of pressure
in the head. The pain is not accurately localised, but is some-
times more violent on the side of the hoematoma. It is much
increased when a fresh haemorrhage occurs; but if there be great
atrophy of the brain, as in dementia paralytica and in cases of
senile atrophy, a hsematoma may attain a considerable size
without causing much headache. On the other hand, when
there is no shrinking of the brain a thin layer of blood causes
violent pain.

The motor disturbances consist of muscular twitchingrs of
one or both sides, followed by rigidity. In other cases, paresis
first of one and then of the other extremity of the same side
occurs followed by distinct hemiplegia, the facial and hypoglossal
nerves becoming involved. In some cases the paralysis extends
to the other side, showing either that the affection has spread
to the opposite hemisphere, or that a fresh haemorrhage has
occurred. Impairment of co-ordinate movements frequently
occurs, as uncertainty of gait, difficulty in writing and speaking.
Conjugate deviation of the eyeballs towards the side of the lesion
is not unfrequently observed, but strabismus and ptosis rarely
if ever occur.

Sensory disturbances are not very common symptoms.
Patients sometimes complain of formication and numbness
on the paralysed side, but impairment of sensation in the
absence of paralysis is not met with.

Psychical disturbance occurs in a large number of cases.
This is sometimes due to the primary disease, as in dementia
paralytica, while in other cases it is due directly to the haemor-
rhage. Symptoms of irritation are present in the beginning,
evinced by great mental irritability, abnormal sensitiveness to
light, and ringing in the ears, but these soon give place to those
of compression. In other cases the disease begins by a regular
attack of apoplexy.

Drowsiness is an important symptom, and 'Griesinger has
called attention to its occurrence in connection with contracted
pupils and chronic headache, but at times dilatation of the
pupils is observed.

DISEASES OF THE MEMBRANES OF THE BRAIN. 747

Slowness of the pulse occurs in the majority of cases during
the hemorrhage, but the quickness of the pulse varies, and it
becomes frequent and irregular before death.

The pupils are generally contracted and insensible to light
during the irritative stage, but dilatation predominates when
the symptoms of compression supervene.

§ 829. Varieties. — The symptoms may be subdivided into
several groups, according to the extent and localisation of the
haemorrhage and the diseases with which it is associated.

1. In the first group the haemorrhage is so severe from the beginning
that death soon occurs, and in these cases the symptoms cannot be
distinguished from those of ordinary apoplexy. Contractures of the
extremities and slight transitory twitches are sometimes observed in these
cases, and, as a rule, the pupil is more contracted and fixed in hsematoma
than in intra-cerebral haemorrhage. In a small number of cases the
extravasations on one side cause convulsive movements of the opposite
side; but the compression soon becomes so great that the irritability
of the cortex is abolished.

2. In a certain number of cases extravasations are found after death,
though there had been no suspicion of their existence during life. These
haemorrhages, however, are usually small, and are generally found in
cases of dementia paralytica.

3. In a third series the symptoms are at first slight, but gradually
increase in severity and soon prove fatal. The chief symptom in the
beginning is severe cephalalgia, with or without vertigo, followed by
drowsiness increasing grachially to sopor, and ending in profound coma.
The pupils are contracted in the early stage, but when coma supervenes
they gradually dilate and may become unequal. Hemiparesis generally
shows itself on the side opposite to the lesion, while symptoms of irritation
may appear on the same side, but after a time all the extremities may
be paralysed. Similar symptoms are caused by any meningeal affection,
and especially by tubercular meningitis. In establishing a diagnosis,
therefore, the conditions under which the disease has developed must be
taken into account. Haematoma is more likely to be present in old per-
sons, when atrophy of the brain is to be suspected ; tubercular meningitis,
on the other hand, usually occurs in young persons.

4. In a fourth series of cases recovery takes place from a first haemor-
rhage, but after an interval of apparent health a second occurs which
results in death. In these cases unilocular or multilocular sacs are found
on one or both sides, and one of the subordinate sacs always contains a
considerable effusion of blood which has caused death by compression.

748 DISEASES OF THE MEMBRANES OF THE BRAIN.

§ 830. Course, Duration, and Terminations. — The course of
the affection is extremely variable, but it usually begins with
more or less acute symptoms, followed by an interval of com-
parative health; after a time, however, a fresh acute attack
occurs which may lead to death or be followed by a second
interval.

During the interval the symptoms are those indicating a
lesion which produces a certain amount of irritation along
with compression of the brain. These consist of cephalalgia,
diminution of intelligence, impairment of memory, drowsiness,
partial paralyses, disturbances of speech, and sudden mental
excitement without cause, frequently mixed with symptoms of
dementia paralytica.

The duration of the affection is not well known, inasmuch
as it is not always possible to fix with accuracy its commence-
ment. The majority of cases of pachymeningitis end fatally,
but recovery may take place in many cases, only traces of the
affection remaining, such as a slight degree of paresis, head-
ache, sleeplessness, and some weakness of intelligence.

§ 831. Morbid Anatomy. — Hemorrhagic pachymeningitis
presents itself as an organised mass situated between the dura
mater and surface of the arachnoid, and presenting different
appearances in different cases. Yarious opinions have been
entertained with respect to the seat and nature of the affection,
but the explanation which was first given by Virchow is now
pretty generally accepted by pathologists. According to this
view the pachymeningitis begins with hyperemia of the dura
mater, occupying generally the area supplied by the middle
meningeal artery. The inner surface of the dura mater assumes
a rosy colour, and after a time a loose yellowish coating forms,
which is dotted with a number of confluent or separate heemor-
rhagic points.

This coating can be stripped from the dura mater, tearing
many small vessels which enter its substance. Rindfleisch says
that this membrane is rich in vessels, which are usually three
times as large as capillaries and present varicosities. The
basis substance between the vessels is composed of star-shaped
connective tissue cells. Emigrant corpuscles pass from the

DISEASES OF THE MEMBRANES OF THE BRAIN. 749

blood-vessels of the sub-epithelial layer of the dura mater, and
develop into a loose connective tissue. Haemorrhages, varying
in quantity at different times, take place from the vessels which
enter the false membrane ; the clots become partially organised,
and the delicate capillaries which develop in them become the
source of new haemorrhages, so that a large quantity of blood
may in this manner be poured out between the thickened
membranes. It is right, however, to state that Huguenin be-
lieves that the first stage of haematoma is not the formation of
a false membrane, but simply an extravasation of blood on the
inner surface of the dura mater, which undergoes the changes
which usually take place in a coagulum. This coagulum under-
goes partial organisation so as to form a vascular layer, from
which haemorrhage takes place, giving rise to further extrava-
sation, which in its turn becomes organised.

Pachymeningitis haemorrhagica is most frequently found in
the upper part of the brain along the falx cerebri, spreading
down the curved portion of the frontal and occipital lobes, and
laterally towards the Sylvian fissure. Kremiansky found that
in fifty-four out of sixty-five cases its extent exactly corre-
sponded to the parietal bones. In cases of dementia paralytica,
in which the brain is frequently found shrunk and atrophied,
the blood often extends much further, and may reach the base
of the brain. In rather more than half of the cases described
the haemorrhage extended over the surfaces of both hemispheres,
while in the remainder it was limited to one hemisphere.

Changes in the skull have been described by various authors,
but none of them are constantly present ; some of these, such
as elevation, thinning, and thickening of the bones, are in all
probability anomalies, which are entirely independent of the
haematoma. Osteophytes on the inner surface of the skull
have been described by Rokitansky and Cruveilhier.

The pia mater is often the seat of changes, such as are found
in atrophy of the brain, consisting of slight opacities, oedema,
and small fibrous thickenings.

The substance of the brain is variously affected according to
the thickness of the haematoma. The thin extravasations and
membranes do not cause any marked changes in the brain, but
large haematomata compress it, and produce consecutive anaemia
and atrophy.

750 DISEASES OF THE MEMBRANES OF THE BRAIN.

The brain is often found atrophied and contracted indepen-
dently of the hematoma. The decrease in the size and weight
of the brains of drunkards, and senile atrophy are important
factors in the production of hsematoma. The affection is fre-
quently associated with atheroma and calcification of the intra-
cranial arteries. Diffused sclerosis and the chronic degeneration
which accompanies dementia paralytica are often associated
with hsematoma. A glance at all the varied changes found
associated with hsematoma will show that this affection in the
great majority of cases occurs along with alterations which
occasion a reduction in the size of the brain.

§ 832. Prognosis. — The prognosis depends in great measure
upon the fundamental affection which is present along with
the pachymeningitis. It is always grave, although not neces-
sarily fatal.

§ 833. Treatment. — The treatment of hsematoma of the dura
mater will greatly depend upon the underlying affection, and it
it is consequently desirable to examine carefully for disease of
other organs. If venous stasis be present, a small bleeding or
a smart watery purgative gives temporary relief to the circula-
tion, but energetic antiphlogistic treatment must be carefully
avoided.

During the stage of hsemorrhage ice should be applied to the
head; but counter-irritation, if used at all, should be reserved
for a later period. The patient must, of course, be kept quiet
and all excitement prevented.

751

CHAPTER XV.

DISEASES OF THE MEMBRANES OF THE BRAIN

(Continued).

II. DISEASES OP THE PIA MATER.

Inflammation of the Pia Mater (Leptomeningitis J.

Hyperemia of the pia mater is always accompanied by con-
gestion of the brain, and does not demand separate notice.
Attempts have been made to distinguish inflammations of the
visceral layer of the arachnoid from those of the pia mater,
but anatomists are now agreed that the former membrane is
only the thickened external layer of the latter, and clinical
records show that in the cases of so-called arachnitis the in-
ternal layer of the pia mater is always affected.

L Leptomeningitis Infantum (Hydrocephalus sine Tuberculis).

Acute inflammation of the pia mater may occur in infancy
in the entire absence of tubercle, and the simple like the
tubercular variety is attended by effusion into the ventricles
of the brain. Acute ventricular effusion from simple inflam-
mation of the pia mater is most common in children between
one and two years of age, but sometimes occurs in younger and
sometimes in older children.

§834. Symptoms. — The clinical history of this affection
may vary in no important particular from that of tubercular
meningitis, but the premonitory symptoms are not so well
marked in the former as in the latter.

The symptoms of the period of invasion differ considerably

752 DISEASES OF THE MEMBRANES OF THE BRAIN.

in individual cases. Some cases begin with slight fever, which
may be symptomatic of the meningitis or of another affection,
and the febrile condition may be ushered .in by an attack of
convulsions. In meningitis the symptoms of intense cerebral
hyperemia are soon superadded to those of ordinary pyrexia.
In other cases violent headache is the first symptom, and
vomiting is frequently present. The child is restless, the eye-
lids are only half closed during sleep, the eyeballs roll about,
the pupils are contracted but react well to light, and there may
be slight convulsive twitching of the extremities but tbere is
no paralysis. The children are abnormally sensitive to light
and sound, and tbe lightest touch on the skin may cause pain.
Older children are either unable to stand, or totter when they
attempt to walk, they complain of buzzing in the ears, are
fretful, morose, and taciturn. In younger children the fonta-
nelles may be seen to pulsate strongly, but they are not arched.
The countenance has a vexed or angry expression. The features
are at times distorted, the Torehead is wrinkled, and a distress-
ing moan is frequently uttered.

These symptoms may continue for two or three days, and
then the child may be attacked by convulsions. These begin
by conjugate deviation of the eyes and rotation of the head,
the upper and lower extremities of one side are chiefly affected,
and then the spasms cross over to the opposite side, when the
convulsion becomes general. The state of the pupils vary, but
they are generally dilated and fixed during the convulsions.
The temperature rises during the attack, and may exceed
104° F.

Death may occasionally occur suddenly during the attack,
and when the convulsion is not fatal the subsequent course
of the affection is marked by an aggravation of the cerebral
symptoms. Young children lie in a disturbed sleep, with the eye-
lids tightly closed, and showing evidence of pain by wrinkling
of the brow and moaning, but the pulsation of the fontanelles
may now diminish owing to the distension of the ventricles by
effusion. Older children lie for hours in a state of stupor, they
are listless and indifferent, and do not appear to see distinctly,
or they may be absolutely blind. The pulse is very variable in
rate at different times. The respirations are sighing and

DISEASES OF THE MEMBRANES OF THE BRAIN. 753

irregular. The temperature continues more or less elevated,
but its course is very irregular. Persistent vomiting and
obstinate constipation are common, while the power of deglu-
tition may be impaired at an early period.

The child rapidly emaciates, the skin is dry, with the
exception of that of the face, which may be bathed with per-
spiration.

The patient now sinks into a condition of profound coma,
but tetanic spasms of the muscles of the neck and extremities
may persist for a time.

The temperature often falls below normal before death, but
hyperpyrexia has been observed in rapidly fatal cases. The
pulse then becomes very rapid, irregular, and intermittent.

§ 83.5. Coarse, Duration, and Terminations. — Complete
recovery may take place, probably even after effusion has
occurred, but as a rule recovery is partial, and the patient
subsequently suffers from mental feebleness or depraved moral
character. In the latter case the cortex of the brain has pro-
bably undergone some degree of atrophy from the pressure of
the effusion. The majority of cases terminate fatally in from
nine to fourteen days, some die at an earlier period in an attack
of convulsions, while in other cases the disease may be pro-
tracted beyond thirty days, its course being marked by remis-
sions and exacerbations.

§ 836. Morbid Anatomy. — The cranial bones present dif-
ferent degrees of congestion, and the fontanelles are distended.
The convolutions of the brain are flattened and the sulci oblite-
rated, owing to the pressure exerted by the distended ventricles.
The fluid is never found between the dura and outer layer of
the pia mater, and the outer surface of the latter is usually re-
markably dry.- The cortex and white substance are compressed
and but moderately filled with blood, and no capillary extrava-
sations are found in the cortex. The dilatation of the ventricles
is usually symmetrical, and a considerable amount of softening
not unfrequently exists around the ventricles, but this may be
due to post-mortem changes.

The choroid plexuses are unusually voluminous, they often
W w

754

DISEASES OF THE MEMBRANES OF THE BRAIN.

contain punctiform extravasations, and the aqueduct of Sylvius
and fourth ventricle are often dilated and distended with fluid.
No exudation is found at the base of the brain.

§ 837. Prognosis. — The prognosis is always unfavourable,
although a few cases recover either partially or completely.

§ 838. The diagnosis will be discussed in connection with
tubercular meningitis, and the treatment of the two affections
is the same.

2. Tubercular Meningitis (Acute Hydrocephalus).

§ 839. Etiology. — Most of those who suffer from tubercular
meningitis belong to families in which the tubercular diathesis
is distinctly marked. The influence which improper nourish-
ment, want of pure air and light, exposure to cold and damp;
and neglected hygiene exerts in the production of tuber-
cular affections generally is well known. It is not surprising^
therefore, to find that the largest proportion of cases of tuber-
cular meningitis should occur in crowded populations and large
cities, and amongst the poorest and most neglected part of the
population. Season does not appear to exert any influence in
the production of the disease. Tubercular meningitis may set
in at any age, but it is much more frequent between the ages
of two and seven years. The numbers diminish from the seventh
to the tenth, and in still greater proportion from the tenth to
the fifteenth. It is most common in adults between the ages of
twenty and forty, and occurs very exceptionally after the forty-
fifth year. The male sex appears to be more frequently affected
than the female. In adults the proportion is 51*5 men to 48 5
women (Huguenin) ; and the proportion of males affected in
children is still greater.

§ 840. Symptoms. — Various premonitory symptoms manifest
themselves for a variable period of weeks or months before the
development of the distinctive phenomena of tubercular menin-
gitis. The most constant precursor of the affection is a gradual
loss of flesh without any perceptible cause, and this is more
noticeable in the trunk and limbs than in the face. There is
loss of appetite, the bowels are constipated, or diarrhoea may

DISEASES OF THE MEMBRANES OF THE BRAIN. 755

alternate with constipation, and the patient complains of
weariness and an undefined feeliDg of illness.

The premonitory symptoms are better marked in the case of
children. The child loses his vivacity, becomes sad, fretful,
taciturn, irritable, and wants to be left alone, and in the midst
of play leaves his companions in order to give vent to his
distress in tears. The child sleeps with eyes half open, starts,
and cries out ; he grinds his teeth, and his sleep is disturbed by
muscular twitches and horrible dreams.

Headache is generally present, and after a time a slight febrile
accession is observed towards evening without obvious cause.
In some cases the disease begins with head symptoms of an
inflammatory nature in the midst of apparently good health.
In these cases it may be presumed that cheesy foci exist in
some part of the body in a latent condition, and that the
vessels of the pia mater become rapidly and suddenly invaded
at the time of the outbreak of acute symptoms.

Premonitory symptoms may also be absent when the mem-
branes of the brain become secondarily affected in persons who
are already suffering from acute general tuberculosis, or from
local tuberculosis of the lungs, peritoneum, or other organ.
Under these circumstances the patient may have been sleep-
less, restless, feverish, or delirious, before the pia mater is impli-
cated, so that the brain symptoms make their appearance
without any warning. The first symptoms which indicate an
affection of the pia mater in these cases may be violent
headache, vomiting, or facial paralysis, followed quickly by
unconsciousness.

As the invasion approaches, all the premonitory symptoms,
when present, become more pronounced. Some cases are ushered
in by a chill, accompanied by a rapid rise of temperature, while in
others there are distinct shiverings, violent headache, attacks of
giddiness and vomiting. The disease itself presents (a) an
initial period in which the symptoms may be referred to exci-
tation of the cortex ; (6) a period in which symptoms caused
by excitation are mixed with those due to progressive pressure
caused by effusion and to lesions at the base of the brain ;
and (c) a final period in which symptoms due to pressure caused
by the ventricular effusion greatly predominate.

750

DISEASES OF THE MEMBRANES OF THE BRAIN.

(a) The Period of Invasion. — Vomiting is the most common
special symptom of the period of invasion. It varies greatly
in frequency, but as a rule occurs only twice in twenty-four
hours during the first two or three days of the disease. In
some few cases, however, the child vomits incessantly, whether
food is taken or not. When once the tendency to vomit has
ceased for twenty-four hours it does not ordinarily recur. Con-
stipation is present as a rule throughout the whole course of the
disease. Although there are occasional exceptions the consti-
pation is not often obstinate, and it is generally easy to pro-
cure action of the bowels by ordinary means.

Headache is another important symptom of the first stage of
the disease, and may be of a dull, heavy, or lancinating
character. The headache, although continuous, is subject to
paroxysmal exacerbations. It is sometimes referred to the sum-
mit of the frontal bone, but more frequently the whole head is the
seat of pain. Headache is usually an urgent symptom while
consciousness is retained, and its temporary exacerbations are
made known by moaning or shrieks; while even after uncon-
sciousness has set in the patient puts his hand to his head,
wrinkles his forehead, and distorts his face as if from pain.
Vertigo is always present. Patients feel as if they were falling
in bed, or as if surrounding objects were revolving round them,
and the gait is often reeling and unsteady; but the rapid de-
velopment of severe symptoms soon prevents all attempts at
station and locomotion.

Motor disturbances are almost always present in this stage
of the affection. Spasmodic movements occur in the form of
partial convulsions, giving rise to tremor and conjugate devia-
tion of the eyeballs, strong convergent and divergent squints,
grinning contortions of the muscles of the face, grinding of the
teeth, and rotation of the head and neck. In children epilepti-
form convulsions are not uncommon, but they are rare in adults.
It is very probable that what Trousseau has described as the
hydrocephalic cry, which so commonly occurs during this period
of the disease, is due to spasmodic action of the respiratory
and laryngeal muscles, and is quite independent of conscious-
ness. "It is a single, violent cry," says Trousseau, "resembling
the cry of a person suddenly exposed to great danger; the

DISEASES OF THE MEMBRANES OF THE BRAIN. 757

expression of the face is not that of suffering. Any period of
the disease may be attended by this cry, which may occur every
hour, half-hour, or even every five minutes." Besides spasmodic
movements, spastic rigidity of one or more groups of muscles
may occur, the most important of these being stiffness of the
muscles of the nape of the neck and back, and retraction of
the abdominal muscles. Slight paralysis of some of the facial
and ocular muscles may occur, consisting of inequality in the
pupils, ptosis, strabismus, or slight facial paralysis.

Sensory disturbances are not so well marked, and they are
usually soon obscured by loss of consciousness. At times a
general hypersesthesia of the whole surface of the body may be
observed at the beginning of the disease, while at other times
this condition may be limited. General or partial anaesthesia
is not an unfrequent symptom at an advanced period of the
disease, and it has occasionally been observed as a premonitory
symptom (Dreyfous). Intolerance of sound and light is a pro-
minent symptom : the child is impatient of the slightest noise,
and avoids the light by lying with the face buried in the
pillow or turned towards the wall, keeping the eyelids firmly
closed. In this, the usual attitude of the first period of the
disease, the knees are drawn up towards the abdomen, and
Dreyfous believes that it is not voluntarily assumed in order to
avoid the light, but corresponds to the forced attitudes of
animals arising from experimental injury of the brain.

Psychical disturbances are not always present in the early
period of the affection. The patient cannot, however, form
consecutive trains of ideas, and children soon become somnolent,
lie with their eyes closed, and reply to questions curtly or
merely by a nod. When raised up, they complain much, knit
their brows, throw back their heads, and slip down in bed; they
cannot bear the slightest disturbance, and will clench their
teeth against food. Delirium is of frequent occurrence when
the patient is half asleep; and, in the case of children, the
hydrocephalic cry is not unfrequently heard at this time, being
accompanied by starting up in terror. At other times the
patient may spring from bed, or make defensive movements,
in consequence of hallucinations of sight and of hearing. The
somnolence soon increases, the eyes stare without expression

758 DISEASES OF THE MEMBRANES OF THE BRAIN.

into vacancy, and the patient ceases to speak to his attendants ;
but he talks senselessly with himself, or laughs, sings, whistles,
or shouts, and performs meaningless movements, such as pluck-
ing at imaginary objects, picking the bed-clothes, blowing,
spitting, and grimacing. After a time these disturbances cease,
and the mental faculties may again become completely or
partially clear ; but after a longer or shorter period, new and
more profound disturbances supervene, which increase until the
fatal termination.

Examination of the retina may throw light on the nature
of the affection. When general miliary tuberculosis exists
tubercles of the choroid are frequently found, but they are
absent in tuberculosis affecting the pia mater alone. Marked
stasis is often found even at this early period in the veins of
the disc. So long as the patients are tolerably conscious
derangement of vision is generally absent.

The pulse is, as a rule, slow and full (from 60 — 70 beats per
minute) during the early stage of the affection, but it is subject
to rapid variations during muscular exertion of every kind and
psychical excitement, especially in the case of children. The
pulse is often decidedly irregular even at this stage of the
disease. The temperature is very inconstant, and does not
conform to any type.

The skin is usually dry, and even in those cases where the
tubercular meningitis is associated with phthisis the sweats of
the latter disease usually cease when the meningitis manifests
itself. It has also been observed that the cough, dyspnoea,
and expectoration of phthisis cease, and in the case of intestinal
tuberculosis the diarrhoea is arrested. The injection of the
face and conjunctivas varies frequently without obvious cause ;
lividity of the face belongs to a later period or is dependent on
lung complications.

The average duration of the first stage is about eight days,
but it varies from two days to two or three weeks, and is not
unfrequently followed by a remission which leads the friends of
the patient to hope for a favourable termination.

(b) The second stage is now ushered in with the evideuces of
loss of functional activity. The signs of excitement become less
frequent, and somnolence and mental torpor more prominent.

DISEASES OF THE MEMBRANES OF THE BRAIN. 759

At times a profound coma is rapidly developed, which in children
is frequently ushered in by a convulsion, and which generally
continues unbroken until the fatal termination, but in some
cases there are short clear intervals. The hydrocephalic cry in
the case of children is most frequent at this time, and adults
in the midst of sopor give evidence of severe headache by
groans and gestures.

Spasmodic movements and muscular rigidity are more fre-
quent than in the first stage. Contractions of the ocular
muscles give rise to combined movements of the eyeballs
(nystagmus) and inequality of the pupils, while slight con-
vulsive movements occur in the facial muscles and in those
of the extremities. The automatic movements of chewing,
winking, whistling, or grinding of the teeth are also frequent ;
while tremors of the extremities or of the whole body often
occur. A case is recorded by Dr. Hughlings-Jackson in which
the movements of the extremities and face corresponded exactly
to those of acute chorea. At other times the muscles are main-
tained in a state of cataleptic rigidity, and the extremities may
then assume various forced attitudes.

The stiffness of the muscles of the nape of the neck becomes
more intense, so that the head is drawn back and thrust into
the pillow. The rigidity may also extend to the muscles of the
trunk, so that the body is maintained in a condition of tetanic
rigidity, the opisthotonos either appearing in paroxysms and
lasting only a few minutes at a time, or remaining continuous
until death. Paralyses of various extent and distribution now
make their appearance. Paralysis of the oculo-motor nerve is
common, and gives rise to divergent squint, ptosis, dilatation,
and fixity of one pupil. The trochlear nerve may be paralysed
along with the third, but is never affected alone. Paralysis of
the abducens may, however, occur as a separate affection. The
paralytic form of conjugate deviation of the eyes and rotation of
the head and neck may appear at this period of the disease.

Facial paralysis is manifested by the usual signs of paralysis,
of cerebral origin. In some cases total paralysis of the facial
has been observed, and in these the affection is due to inter-
ference with the nerve by effusion at the base of the brain.
In other cases the ocular and frontal branches were affected

760

DISEASES OF THE MEMBRANES OF THE BRAIN.

while the oral and nasal branches were spared, and in these
cases it is doubtful whether the symptoms are to be attributed
to cortical injury or to partial pressure on the nerve at the base
of the brain.

Paralysis of the hypoglossal nerve is manifested by the
tongue turning towards the paralysed side on protrusion, but
this nerve is not so frequently affected as the facial. Hemi-
plegia and hemiparesis are rare, but monoplegias are frequent.
At times one arm or one leg is paretic or completely paralysed ;
while occasionally the paralysis assumes the paraplegic form,
or a considerable diminution of strength may occur in all four
extremities.

Sensory paralysis also supervenes at this stage of the
affection. At times there is a general diminution of all
forms of cutaneous sensibility, at other times anaesthesia may
be, limited to one or other extremity, or to the region of distribu-
tion of one of the branches of the trigeminus. After a time
every form of sensibility is much weakened or abolished.

The retinse undergo decided changes in this stage of the
affection. The veins are dilated and stand out distinctly on the
swelled papilla. Extravasations of blood occasionally occur in
the retina, but they are usually slight in extent. Symptoms
of neuro-retinitis appear either along with the phenomena of
stasis or apart from them.

Yomiting may occur occasionally in this stage, constipation
continues, the urine is generally passed in bed or there is com-
plete retention.

• The pulse becomes less frequent, and may sink to 60 or still
lower, and is at the same time fuller ; but the slightest excite-
ment may raise the number of beats over 100 per minute, and
it is apt to become irregular. The temperature varies.

The respiration is sometimes normal, at other times irre-
gular, occasionally assuming the character of the Cheyne-Stokes
respiration. Neuro-paralytic oedema of the lungs is liable to
occur at this period of the disease. This period may last about
a week, and then the third stage of the disease is ushered
in by the appearance of persistent coma.

The Third Stage. — The patient is now completely insensible
to most external excitants, although he may still respond to a

DISEASES OF THE MEMBRANES OF THE BRAIN. 7G1

loud voice close to the ear, and most reflex actions are extin-
guished.

Isolated paralyses are not so readily observed, as there is
general relaxation of the whole muscular system. Rigidity of
the masticatory muscles and of the muscles of the back and
extremities is not unfrequently observed. Convulsions are rare
in adults; but in children partial convulsive spasms still occur,
and immediately before death the patient may be seized with
general convulsions. The electric excitabilitv of the muscles to
both constant and induction currents is normal. Every form of
sensibility is now completely abolished. The pupils are dilated
and fixed,the upper lids fall inert and paralysed over the eyeballs,
and an ophthalmoscopic examination reveals signs of marked
stasis and oedema of the optic discs, with neuro-retinitis. In
the case of young children, the pulsations of the fontanelle
become weaker and weaker, and may disappear before death.

The pulse during this period becomes more and more fre-
quent and may be irregular.

The respiration is irregular, and at times so superficial and
feeble that it may escape observation, while at other times it is
forced and deep. Rapid emaciation occurs, especially in the
case of children ; the skin is generally dry and rough, and may
become slightly livid with the decreasing force of the heart ;
occasionally a bed-sore appears. The temperature during this
period varies greatly. In some cases it is below normal, and
immediately before death may sink as low as 95°F. or even 93° F.
In another series of cases a state of moderate fever continues
up to the time of death ; while in a third group the fever
greatly increases before death, and may even continue to in-
crease for some time afterwards.

The urine is generally scanty, with high specific gravity ; its
quantity may be increased, normal, or diminished ; the propor-
tion of chlorides varies greatly, and the phosphates are said
to be increased. A small quantity of albumen is frequently
present, but sugar is rare. The duration of the paralytic stage
is generally three or four days, and seldom reaches a week.

§ 841. Course, Duration, and Terminations. — The course
of tubercular meningitis varies greatly. It has already been

762 DISEASES OF THE MEMBRANES OF THE BRAIN.

mentioned that when the affection of the pia mater is secondary
to phthisis or tubercular peritonitis the disease begins without
any premonitory symptoms, and the symptoms of the first stage
are obscure or entirely wanting. Old affections of the brain,
such as tubercular tumours, also render the course of the disease
variable. Under the latter circumstances tubercular meningitis
is superadded to a long-existing affection of the brain as a
terminal phenomenon, and it is then difficult to diagnosticate
anything beyond a meningitis of unknown cause.

In other cases tubercular meningitis runs a rapid course, and
may terminate in five or six days. In some of these cases ven-
tricular effusion is wanting, and death is due to some acute
process in the' brain itself. Some cases, on the other hand,
have an exceedingly protracted course ; the invasion is slow
and insidious, the symptoms are gradually developed, and the
disease may last from thirty to fifty or even sixty days.

In all cases in which the disease began by sudden paralysis,
or paralysis combined with aphasia, the miliary tubercles have
been found limited to the area of distribution of the Sylvian
artery, while the choroid plexuses have been free from tubercles,
and great effusion absent.

The disease is ushered in by depression of spirits, anxiety,
anguish, hallucinations of hearing, self-accusations, and attempts
at escape from punishment. After about forty-eight hours,
unconsciousness supervenes, ptosis and facial paralysis soon
follow with all the other signs of tubercular meningitis.

Sometimes the course of the disease is very similar to that
of typhoid fever. In other cases, especially in children, un-
consciousness comes on at an early period of the disease, and
constitutes throughout the most prominent sjonptom of the
affection. In these cases large ventricular effusion is found
after death, and the brain has been doubtless subjected to
pressure at an early period.

Some cases are recorded in which every time the patient
attempted to sit up attacks of tetanic rigidity supervened
(Biermer, Gerhardt).

§ 842. Morbid Anatomy. — The morbid anatomy of tuber-
cular meningitis varies with respect both to the appearances

DISEASES OF THE MEMBRANES OF THE BRAIN. 703

found in the brain itself and to morbid changes found in
other organs. Various changes may be found in the cranial
bones, and caries of the petrous portion of the temporal bone
is frequently the primary cause of the disease. On removing
the calvaria tubercles may be found in the dura mater, and
would probably be found more frequently if a careful search
were made. They are sometimes found between the two layers
close to small branches of the middle meningeal artery, while
others appear to be situated in the inner lamella of the dura
mater (Huguenin).

The changes in the pia mater are, (a) those which are
directly connected with the formation of miliary tubercles,
(b) those caused by the inflammation surrounding them, and (c)
those which arise from the effusion into the ventricles.

(a) The pia mater is studded with miliary tubercles. They
appear as greyish-white granulations, varying from a size scarcely
visible to that of a millet seed, while masses as large as a pea
may be produced by aggregation.

The tubercles are always distributed in the neighbourhood of
vessels. In some cases the whole length of an artery from its
origin in the circle of Willis is covered with numerous tubercles,
while in rare cases the granulations are chiefly situated on the
peripheral branches of the vessels. At times all the arteries
given off from the circle of Willis are studded with tubercles,
while at other times particular portions of the surface of the
brain are either exclusively affected or affected to a much greater
extent than the remaining portions.

The territory supplied by the Sylvian arteries is particularly
liable to be affected, and tubercles are also commonly found at
the bottom of the great longitudinal fissure along the vessels
which supply the corpus callosum. At other times the tubercles
are most abundant in the pia mater covering the upper and
under surfaces of the cerebellum, or on the median surfaces and
posterior lobes of the cerebral hemispheres.

The number of tubercles present varies greatly. At times
they may be so limited that a careful search is necessary to find
them, while in other cases they are numbered by thousands.
The granulations may be isolated, or collected in dense groups ;
while occasionally they form, along with the inflammatory

764 DISEASES OF THE MEMBRANES OF THE BRAIN.

products of the pia mater, thick masses which exert pressure
on the brain.

The tubercles are found in all stages of development. At
times all of them consist of the small, grey, miliary granula-
tions, but at other times these are mixed with larger tubercles,
which are yellow at their centres from fatty degeneration.
Callosities mainly composed of connective tissue and enclosing
old tubercles are found on various parts on the surface of the
brain.

(b) The inflammatory changes in the pia mater may or may
not be well marked, according to circumstances. When the
pressure caused by the effusion has been great, the surface of
the pia mater may be dry and its vessels empty. The convo-
lutions are flattened and the sulci more or less narrowed. A
moderate hypersemia of the pia mater is, however, frequently
present, especially at the base, where the vessels are less liable
to be subjected to pressure.

Evidences of suppuration are generally found at the base
of the brain. Under these circumstances the whole tissue is
swollen and yellowish, and cloudy streaks of exudation may ,
be observed passing along the vessels. The convexity is not I
so liable to be the seat of suppuration. In some cases, however,
a sero-purulent effusion is observed in the pia mater of the con-
vexity, while at other times the evidences of suppuration on the
convexity are still better marked. In the latter case the pia has
lost its delicacy and transparency, is inelastic and easily torn,
and is everywhere infiltrated with a sero-fibrinous, yellowish
exudation.

The exudation often extends backwards over the anterior
surface of the pons and medulla oblongata, creeps upwards to
the upper surface of the medulla, and implicates the pia of the
entire cerebellum. The suppurative process may extend from
the chiasma forwards to the under and internal surfaces of the
anterior lobe, along the olfactory lobe and the artery of the
corpus callosum.

The changes are not always symmetrical, but in general it
may be said that the greatest suppuration will be found where'
the tubercles are most numerous.

The inflammation may extend along the processes of pia mater

DISEASES OF THE MEMBRANES OF THE BRAIN.

765

which enter the descending cornua of the lateral ventricles, and
may also be transmitted through the great transverse fissure
to the velum interpositum. At times the choroid plexuses and
velum interpositum may be covered with a yellowish purulent
exudation.

Extravasations of blood, varying in size from minute specks
to a patch an inch or more in diameter, may be found in the
meshes of the pia mater. The growth of tubercle in the walls
of a vessel presses upon the media and intima, and thus dimi-
nishes its lumen. The vessel is thus partially obstructed, and
either a thrombus may form at this point, followed by softening
of the coats of the vessel and extravasation, or the internal
and middle coats of the vessel are perforated directly by the
tubercle.

(c) The ventricles are generally distended with serous fluid,
but effusion is absent in about 20 per cent of all cases. The
septum lucidum is frequently broken down ; while the third
ventricle is distended, but to a less degree than the lateral
ventricles, owing to the resistance offered by the optic thalami.
The soft commissure is generally more or less torn and speckled
with capillary haemorrhages, and the anterior portion of the
ventricle may be so distended that the pia mater covering the
lamina cinerea is exposed. The aqueduct of Sylvius is fre-
quently dilated and the fourth ventricle distended. The fluid
is at times purely serous, while at other times it is cloudy
from the presence of epithelial cells and white blood cor-
puscles, and purulent effusions are occasionally observed. In
some cases the fluid is tinged with blood derived from rup-
ture of small vessels in the choroid plexuses. The choroid
plexuses are hyperaemic, and miliary tubercles may be found in
them, though never in large numbers ; small extravasations
of blood are not uncommon. The ependyma of the ventricles
is sometimes dense and opaque, and when viewed by a side
light its surface looks as if sprinkled with fine dust. At other
times larger granulations may be observed intermediate in size
between the fine dust and miliary tubercles.

The distribution of tubercles, inflammatory changes, and
effusion may be combined in various ways. In the majority of
cases miliary tubercles are distributed over the entire pia mater

766 DISEASES OF THE MEMBRANES OF THE BRAIN.

and choroid plexuses, there is a large ventricular effusion, and
the base of the brain is often covered by a purulent exudation,
which in some cases extends to the convexity of the hemi-
spheres. In a few cases miliary tubercles are scattered in
small numbers over the pia mater, the choroid plexuses are un-
affected, ventricular effusion is absent, and no pus is visible to
the naked eye either over the base or convexity of the brain.
In other cases the tubercles are limited to the region of dis-
tribution of one or more of the arteries of the brain, the terri-
tories of the Sylvian arteries being specially liable to be
affected. The base of the brain and the vascular region in
which the tubercles are developed are covered by a purulent
exudation, and there is a moderate ventricular effusion. In
some cases the evidences of recent tuberculosis are accom-
panied by circumscribed thickenings and laminae of caseous
connective tissue, in which old miliary and caseous tubercles
are embedded.

The brain itself undergoes many important changes. If the
effusion be large the cortex and neighbouring white substance
are dry and anaemic, but when effusion is absent these parts are
congested and cedematous. The cortex is ' often studded byt
punctiform haemorrhages, caused, according to Bindfleisch, by
tubercular degeneration of the nutritive arteries. The vessels
of the cortex are surrounded by clusters of white and red-
blood corpuscles. When the pia mater is stripped off, portions
of the substance of the brain will be found clinging to the
vessels of the cortex, and consequently the surface of the brain
assumes a rough appearance. White softening of the substance
of the hemispheres is often observed. It may involve portions
only of the fornix and corpus callosum, or may extend into the
centrum ovale and basal ganglia.

The cranial nerves may all be affected in greater or less
degree in tubercular meningitis. The inflammatory process set
up at the base of the brain may extend to the sheaths of the
nerves and gives rise to neuritis, and when effusion takes place
they are injuriously affected by pressure.

The spinal cord is not unfrequently affected in tubercular
meningitis. The inflammatory affection' of the pia mater passes
down a varying distance into the spinal canal, and tubercles

DISEASES OF THE MEMBRANES OF THE BllAIN. 767

are found in the spinal pia mater. Tuberculosis of the lungs,
pleune, pericardium, peritoneum, liver, spleen, lymphatic glands,
and kidneys is frequently associated with the affection of the
cerebral membranes. Cheesy degeneration of the mesenteric or
retro-peritoneal glands, or of the bronchial, cervical, or axillary
glands, is almost always found associated with the cerebral
affection. Suppurations of the vertebras, of the bones of the
extremities, and pelvis, affections of the periosteum and
joints, caries of the nasal bones from syphilis, caries of the
clavicle, sternum, and petrous portion of the temporal bone are
some of the most frequent causes of tubercular meningitis.

§ 843. Morbid Physiology. — Miliary tubercles act as foreign
bodies and produce an attack of meningitis. In the early stage of
inflammation the symptoms are mainly those of irritation of the
cortex. It is manifest that the initial symptoms of the disease
must largely depend upon the distribution of the tubercles
and resulting inflammation. If the tubercular infiltration be
mainly limited to one or more of the Sylvian arteries, the disease
will be ushered in by symptoms of motor irritation, such as slight
spasms, unilateral, or even general convulsions. In those cases
which begin with aphasia the lesion is situated, as a rule, along
the left Sylvian artery, the branch which supplies the posterior
end of the third frontal convolution being specially implicated.
In the recorded cases it is not mentioned whether the loss of
speech was preceded by any evidence of irritation of Broca's
convolution. Difficulties in the articulation of words may occur
when there is no aphasia. When the area of distribution of
the posterior cerebral artery is chiefly affected, the initial
symptoms will be sensory disturbances, as hallucinations of
sight and hearing ; while the motor disorders consist of asso-
ciated movements, as those of defence agaiust threatened blows,
or attempts at escape from apprehended punishment. When
the anterior cerebral arteries are mainly affected, the disease
begins by sopor alternating with slight delirious excitement,
and coma usually supervenes at an early period.

When the cerebellar arteries are affected, stiffness of the
muscles of the nape of the neck and back, and tetanic seizures
are prominent symptoms. The various irregularities of gait

768 DISEASES OF THE MEMBRANES OF THE BRAIN.

which are observed during the first stage of the affection may
often be explained by reference to implication of the cerebellum.
Dreyfous attributes great importance to implication of the pons
varolii in the production of forced attitudes and various sensory
disturbances, but it does not appear to me that his reasoning is
conclusive.

Motor paralysis occurs mainly in the second stage, but is
also observed at an earlier period. In the first stage the para-
lyses are probably caused by irritation and subsequent ex-
haustion of a motor centre, but in the second stage they are
caused by destructive changes in the motor area of the cortex.
Peripheral paralysis may be produced by the cranial nerves
becoming implicated in the exudation as they pass along the
base of the brain. The sensory portion of the fifth and the
nerves of special sense as well as the motor nerves may be.
injured by the exudation. •

The final stage of general paralysis of sensory and motor
functions is explained by the gradual compression of the brain,
due to increasing ventricular effusion.

§ 844. Diagnosis. — Tubercular meningitis is liable to be mis-
taken for cerebro-spinal meningitis, simple purulent meningitis,
hypersemia of the brain, the terminal stage of abscess, tumours
of the brain, thrombosis of the sinuses, and leptomeningitis
infantum, but the diagnosis between it and these affections
have either been or will be herafter considered.

Typhoid fever with severe brain symptoms may closely
simulate tubercular meningitis. Difficulties of diagnosis only
arise in the case of aberrant forms of typhoid fever in which the
bowels are confined and empty, the abdominal muscles retracted,
and the spots absent. On the other hand, it must be remem-
bered that diarrhoea may be present in tubercular meningitis,
that haemorrhage may occur from the bowels in cases of general
tuberculosis, and that a roseolar rash may appear on the surface
of the body.

The course of the temperature in typhoid fever is often
variable, and not always to be relied upon as a means of
diagnosis. The diagnosis must be made from a consideration
of all the circumstances of the case.

DISEASES OF THE MEMBRANES OF THE BRAIN. 769

Gastric derangement in young children may cause symptoms
almost identical with those of the earlier periods of tubercular
meningitis ; but the diagnosis is soon cleared up by the progress
of the case.

It should also be remembered that many acute diseases are
attended by cerebral symptoms closely resembling those of the
onset of tubercular meningitis.

§ 845. Prognosis. — The prognosis is in every instance ex-
ceedingly grave. Many presumed instances of recovery are
recorded, but these cases are probably examples of leptome-
ningitis infantum or other affection, and not genuine tuber-
culosis of the pia mater.

§ 846. Treatment — Prophylactic treatment is of the utmost
importance, since the prospects of recovery are so unfavourable
when once the disease is established. The children of scrofulous
parents should be most carefully reared. Mothers of strongly
marked tubercular diathesis should not suckle their children,
and this applies all the more to the case of those in whom
evidences of tubercular or scrofulous diseases are already ap-
parent. The children should be sent to the country, fed with
good milk, and the greatest care taken in attending to the
condition of the digestive organs; the slightest diarrhoea should
receive immediate attention. Change of climate to a moun-
tainous district or to the seaside is sometimes attended by the
most decided benefit. With regard to medicines, iron, iodide of
iron, and cod liver oil must be administered according to the
circumstances of the case.

The children should also be specially guarded from the
infectious diseases to which they are liable ; because an attack
of measles or whooping-cough, or indeed any acute disease,
is apt to lead to irritation of the glands and subsequent cheesy
degeneration, and the degenerated glands in their turn may be
the source of tuberculosis.

When the symptoms of meningitis have once appeared, the
grave nature of the prognosis should not prevent the attendant
from adopting appropriate treatment. There is a possibility
in most cases that the meningitis may not be tubercular,

X X

770 DISEASES OF THE MEMBRANES OF THE BRAIN.

and at any rate attempts should be made to allay inflammatory
action. Local blood-letting often relieves the severe headache
and gives at least temporary relief. The head should be shaved
and ice applied persistently. I. have never seen the slightest
good result from counter irritation, and its use should be aban-
doned. Smart purgatives may be of some use in relieving
symptoms, and senna in conjunction with sulphate of magnesia
or the compound jalap powder answers the purpose well. Pre-
parations of mercury and iodine, and a large number of specific
remedies have been used in the treatment of the affection, but
with questionable success.

When once the progress of the case has rendered the diag-
nosis of tubercular meningitis undoubted, the less energetic
treatment the better. During the second and third stages cold
to the head may be exchanged for warm applications. I have
seen delirium and restlessness much diminished by the use of a
warm fomentation to the head, and one great aim of treatment
is to soothe the sufferings of the patient as much as possible.
With this view, when there is jactitation, delirium, and scream-
ing, small doses of opium or chloral should be administered ;
such stimulants as ammonia or even small quantities of wine
may be of use.

Chronic Hydrocephalus.

§ 847. Definition. — Chronic hydrocephalus consists of an
abundant serous accumulation within the cranium, occupying
the general ventricular cavity. A chronic accumulation of fluid
into the sac of the arachnoid has been described under the
name of external hydrocephalus, but it is doubtful whether the
condition has any real existence.

§ 848. Etiology. — Chronic intracranial effusions in adult life
are probably always the result of intracranial tumours, or of
occlusion of one or both of the lateral sinuses, or prolonged
venous congestion; while in old age it may be compensatory to
the cerebral atrophy occurring after haemorrhage and encepha-
litis. These conditions have, however, been already sufficiently
considered, and we shall here deal exclusively with the chronic
hydrocephalus which is congenital or acquired soon after birth.

DISEASES OF THE MEMBRANES OF THE BRAIN. 771

The etiology of congenital hydrocephalus is not well known;
but hereditary predisposition appears to exert some influence
in its production, for more than one child may be affected in
the same family. Congenital syphilis is probably the most
important predisposing cause, and it is possible that too much
importance has been attributed to rickets in its production. Of
the exciting causes little is known. Chronic hydrocephalus is
sometimes preceded by an attack resembling acute hydro-
cephalus.

§ 849. Symptoms. — Chronic hydrocephalus is generally con-
genital, and cerebral symptoms, such as daily recurring convul-
sions, strabismus, or rolling of the eyeballs, are apparent from
the infant's birth, while in a few days or weeks the head is
observed to undergo progressive enlargement.

Impairment of the general nutrition is one of the first
symptoms ; the child may seem eager for food and suck well,
yet it loses flesh and strength, and the skin hangs in loose folds
on its attenuated limbs. The bowels are generally constipated,
or diarrhoea may alternate with constipation, and the evacua-
tions are always unhealthy. The child is restless and may be
drowsy during the day, but wakeful and fretful during the
night. The fontanelles and sutures are now unusually open,
the anterior fontanelle is tense and pulsates strongly, and the
child is subject to paroxysms of restlessness, during which there
is increased heat of the head.

The sutures become gradually wider with the increase of
effusion, the fontanelles increase in size, the head assumes a
globular form, and the physiognomy of the child soon acquires
the characteristic features of chronic hydrocephalus. As the
fluid accumulates within the cranium, it presses equally in all
directions, and the cavity of the skull must enlarge in the direc-
tion of least resistance. According to West, the great increase
in the size of the head is effected chiefly by enlargement of the
anterior fontanelle and by widening of the sagittal suture,
these being the points which are the last to be ossified, and at
which the bones of the skull are less firmly fixed. The frontal
bones are consequently pushed forwards, rendering the forehead
round and prominent, the parietal bones are pressed backwards

772 DISEASES OF THE MEMBEANES OF THE BRAIN.

and outwards, and the occipital bone downwards and backwards,
sometimes even so far that it assumes an almost horizontal
position. The head is, as a rule, globular and flat at the top,
although it occasionally assumes a conical form. Its size
varies, and it has been known to measure two or even three
feet in circumference. The orbital plates of the frontal bones
are pushed from the horizontal to an oblique or it may be
almost vertical position, and thus encroach upon the cavities
of the orbits. The eyeballs are consequently pressed forwards
and rendered prominent; they are at the same time rotated
downwards, so that the white sclerotica appears below the
upper lids, while the pupils are half hidden beneath the lower
lids. On placing the hand over the open fontanel les and
sutures they are felt tense and fluctuating. The hair grows
scantily over the head, the skin is tense and shining, differing
in this respect from the wrinkled condition of that of the rest
of the^ body, distended veins are seen to ramify over the
scalp, and the enlarged head offers a remarkable contrast to
the small face, which, according to West, retains for a long
time its infantile dimensions. The child has a dull and stupid
expression ; he cannot hold his head up, and is therefore
obliged to maintain the recumbent position or to assume a
half-sitting posture, while his head is supported by his hands
or propped up with pillows. The cerebral symptoms which
appear during the progress of the case are variable, the most
usual being convulsions, attacks of laryngismus stridulus,
paralyses, of varying distribution, with contractures, strabismus,
rolling of the eyeballs, and amblyopia progressing to amaurosis.
Hearing, as a rule, remains unaffected until near the fatal
termination.

§ 850. Course, Duration, and Terminations. — Almost every
case of chronic hydrocephalus proves fatal. A large number
die from some intercurrent disease, others from laryngismus
stridulus, or general convulsions. The disease usually lasts
one to two years, occasionally longer ; exceptionally, patients
affected with chronic hydrocephalus have been known to live
to thirty (Bright) or even to seventy-eight years of age
(Trousseau).

DISEASES OF THE MEMBRANES OF THE BRAIN. 773

§ 851. Morbid Anatomy. — In chronic hydrocephalus the
general ventricular cavity of the encephalon is distended with
serous fluid, which varies in quantity from a few ounces to
many pounds. The ventricular cavities are consequently greatly
enlarged, the openings by which they communicate with one
another are dilated, and the septum lucidum, commissures,
fornix, and corpus callosum are stretched or torn, while the
surrounding cerebral substance may be softened, of normal con-
sistence, or unusually dense. The cerebral hemispheres are
compressed and flattened ; the convolutions are pressed out
and the sulci disappear, the white and grey substances being
scarcely distinguishable. The basal ganglia are pressed down-
wards, the cerebral peduncles are separated, the optic commis-
sure is compressed, the pons varolii and corpora quadrigemina
are distorted, the superior surface of the cerebellum is flattened,
and the nerves at the base of the brain are compressed.

The membranes of the brain are rendered thin and softened,
but the ependyma of the ventricles is sometimes found
thickened, rough, and in a granular condition. The bones of
the skull are generally thin and transparent, but in some cases
they are of normal thickness, while in a few cases they are
thicker than normal, being then unusually dense and resisting.

§ 852. Morbid Physiology. — Many pathologists believe that
the effusion of chronic hydrocephalus is a passive dropsy, but
Rokitansky and others are of the opinion that it results from
a chronic inflammation of the ependyma of the ventricles and
the choroid plexuses. The symptoms are partly due to dis-
placement of the cranial bones, and partly to the compression
of the substance of the encephalon.

§ 853. Diagnosis. — Congenital hydrocephalus may be mis-
taken for encephalocele, but in the latter affection the swelling is
local ; it is doughy and elastic instead of being fluctuating, and
is not transparent. Fungus of the dura mater, that has per-
forated at birth, also forms a local tumour, which appears over
one of the bones perforated by it, and not over the sutures or
fontanelles, while the mass feels doughy, and when pressed
upon symptoms of irritation are produced.

774 DISEASES OF THE MEMBRANES OF THE BRAIN.

The enlargement of the head observed in rickets may be
mistaken for chronic hydrocephalus. In the former the en-
largement of the head follows other evidences of the general
affection, while in hydrocephalus rickets is either absent or
develops subsequently to the enlargement of the head, and this
is never so uniform in rickets as in hydrocephalus.

The enlargement of the head which occurs in hypertrophy
of the brain may be mistaken for hydrocephalus, but in the
former affection the head enlarges at first without producing
symptoms, and when these appear the disease pursues an acute
course and terminates rapidly in death.

§. 854. Prognosis. — The prognosis is always grave, although
isolated cases have been known to live to old age. The
prognosis with regard to the restoration of the mental faculties
is even worse than that as to life.

§ 855. Treatment. — Great attention should be paid to the
general health, but it is needless to expect to obtain absorption
of the fluid by means of internal remedies or the application
of counter-irritants. Methodical compression of the head by
means of adhesive plaster has been recommended, but has not
been productive of any good. The treatment by puncture or
aspiration, advised by Couquet and others, affords a chance of
partial success. The puncture should be made by a fine trochar,
or by the needle of an aspirator, which should be introduced
perpendicularly. " The best spot for puncturing the skull," says
Ramskill, " is about an inch or an inch and a half from the
anterior fontanelle, near the edge of the coronal suture, taking
care to avoid the longitudinal sinus and some of the large veins
which empty themselves into it." Only a few ounces of fluid
should be slowly withdrawn at a time, the skull being at the
same time supported by bandages.

3. Simple Meningitis of the Base op the Brain.
( Basilar Meningitis.)

§ 856. Etiology. — Inflammatory processes at the base of the
brain are frequently caused by fissures, tumours, abscesses, and
other lesions near the base of the brain, but cases of this kind

DISEASES OF THE MEMBRANES OF THE BRAIN. 775

have already been sufficiently considered. That form of basal
meningitis only is to be considered at present which arises
spontaneously or from unknown causes. Nearly all those
affected are from 16 to 30 years of age, and in most of them
hereditary predisposition to tuberculosis is wanting.

§ 857. Symptoms. — When primary basilar meningitis is
diffused and general, the affection begins by languor, mental
depression, chilliness or even rigor, thirst, and the usual symp-
toms of fever. The patient complains of intense cephalalgia
and giddiness, and these are followed by severe attacks of
vomiting.

Motor disturbances may be completely absent throughout the
whole course of the affection. When present, they consist of
spasmodic rigidity of the muscles of the back of the neck, with
retraction of the head, and rarely of rigidity or clonic twitch-
ings of certain groups of the muscles of the extremities. The
patient grinds his teeth during sleep; and in the later stages
of the affection, trismus and hiccough have been observed.
Paralysis of the abducens is not uncommon, but paralysis of
the oculo-motor nerve is rare. Paresis of the facial or hypo-
glossal nerves may occur temporarily during the course of
the affection and subsequently disappear, but complete para-
lysis of them has not been observed. The power of degluti-
tion may be impaired during the course of the affection and
be afterwards regained, and this may increase to complete
dysphagia before death. Paresis of the extremities is occa-
sionally observed, but never complete paralysis.

The sensory disturbances consist of cutaneous hyperesthesia,
especially in the region of distribution of the fifth nerves,
ringing in the ears, scintillations before the eyes, and occa-
sionally hallucinations. Anaesthesia and dyssesthesise have not
been observed. The psychical disturbances are more variable
than in any other form of meningitis. In some cases the
mental faculties are unaffected throughout the whole course of
the disease, while in others they are early involved.. The
mental symptoms usually consist of a mild delirium ; but in

L exceptional cases this may be more active, the patient being
restless, quarrelsome, capricious, and irascible. Active delirium

776 DISEASES OF THE MEMBRANES OF THE BRAIN.

is usually temporary and soon gives place to a milder form ;
the patient after a time becomes somnolent, but may be tem-
porarily aroused by a loud question addressed to him; in a
short time he falls into a state of complete insensibility, during
which the urine and faeces are passed involuntarily. Vomiting
continues to distress the patient throughout the course of the
disease, the bowels are constipated, but the abdomen is not
retracted as in tubercular meningitis.

The temperature curve is very irregular. In the initial
period it may rise as high as 104° F. in the evening and approach
to the normal in the morning. In the later stages of the
disease the temperature remains low, being sometimes sub-
normal. The pulse, as a rule, follows the temperature, being
very frequent in the initial period, and sinking in the course
of the disease to below 60 beats in the minute. Towards the
end of life it again increases, and becomes very frequent,
irregular, and intermittent ; the patient is covered with bed-
sores, much emaciated, and dies in a state of marasmus.

The chronic forms of basilar meningitis may give rise to
localised inflammatory products at the base of the brain, which
cause symptoms scarcely to be distinguished from those of
tumours occupying the same situation. The symptoms are
variable in such cases, the most characteristic being paralyses
of the various cranial nerves. In addition to the headache and
dizziness, there are anosmia, amaurosis, or hemianopsia, ptosis,
paralysis of the motor nerves of the eyeball, sensory distur-
bances in the region of distribution of the fifth nerve, masti-
catory paralysis, paresis of the seventh nerve, and occasionally
paresis of one or more of the extremities. If the inflammation
extend to the lower end of the pons, bulbar paralysis, dysphagia,
and dyspnoea may be present.

§ 858. Course, Duration, and Terminations. — Basilar
meningitis generally begins suddenly without premonitory
symptoms. The course of the affection is variable, being inter-
rupted by remissions and exacerbations. The duration of the
disease extends from a period of seventeen to sixty-four days.
In chronic cases it may be prolonged over a period of months ;
the symptoms are in such cases more or less similar to those of

DISEASES OF THE MEMBRANES OF THE BRAIN. 777

tumour situated at the base of the skull. The affection generally
terminates in death.

§ 859. Morbid Anatomy.— The changes found at the base of
the brain vary according to the rapidity of the process. In the
most acute cases purulent infiltration of the pia mater of the
base from the chiasma to the posterior margin of the pons
has been found. This infiltration may extend along the fissure
of Sylvius for some distance, but does not reach the convexity
of the brain ; on the other hand, it often extends along the
whole transverse diameter of the hemispheres, frequently in-
volving the choroid plexuses and the ependyma of the ventricles.
The ventricles are generally distended with fluid, while the
convolutions are flattened and the sulci pressed together. In
less acute cases the inflammatory exudation induces various
degrees of thickening of the pia mater. The choroid plexuses
are increased in size, indurated, and may at times be covered
with pus.

§ 860. Diagnosis. — Basilar meningitis may run a course so
similar to typhoid fever that the two affections can only be dis-
tinguished by long-continued observation. When the tempera-
ture curves of the two affections are similar, the points to be
relied on in forming a diagnosis are the presence in typhoid form
of diarrhoea, rose-coloured spots over the abdomen, and enlarge-
ment of the spleen.

§ 861. Prognosis. — Most cases end in death, but some are
recorded in which the symptoms corresponded closely with those
of basilar meningitis and which ended in recovery.

§ 862. Treatment. — Counter irritation in various forms has
been employed with good effect, but this remedy should be
reserved for the later stage of the disease. Quinine, mercury,
and iodine have been employed, but with doubtful success.
The headache must be allayed by narcotics. If syphilis be
present, mercurial inunction and iodide of potassium should be
employed.

778 DISEASES OF THE MEMBRANES OF THE BRAIN.

4. Menikgitis of the Convexity op the Beain.
This affection may either be primary or secondary, acute
or chronic.

§ 863. Etiology. — Simple primary meningitis of the convexity
is a rare affection. It may occur at all ages, but chiefly attacks
infants under two years of age, and occurs with decreasing
frequency from this age to puberty, when it becomes more fre-
quent. Acute meningitis is rare in advanced age, but the chronic
form is frequent. Of adults, men are more liable to the disease
than women. The exciting causes are not well known.

Secondary meningitis of the convexity may be produced by
inflammation of the bones of the skull, the usual causes of the
latter being external injury, scrofula, and syphilis. Gummata
may also give rise to this inflammation. Otorrhoea, especially
when complicated by caries of the temporal bone, is one of the
most frequent causes of purulent meningitis, and the affection
may result from puriform softening of a thrombus in one of the
sinuses, erysipelas of the head leading to osteo-phlebitis of the
bones of the skull, carbuncles of the face and neck, suppuration
of the eyeball, and old intracranial diseases like tumours,
abscesses, or necrotic softening.

§ 864. Symptonts. — The course of acute meningitis may be
divided into three stages : (1) The period of excitement ; (2) The
period of transition ; and (3) The stage of collapse.

(1) The Period of Excitement. — Obscure premonitory symp-
toms are sometimes observed, consisting usually of a feeling of
heaviness in the head along with paroxysms of violent cephal-
algia, sleeplessness, irritability of temper, and general malaise.
As a rule, however, the disease begins suddenly by a well-marked
rigor, intense headache, vomiting, fever, and delirium, while in
children it is ushered in by an attack of general convulsions.

The headache may be diffused, or referred to the forehead,
temples, vertex, or occiput ; it is intensified by light and sound,
and by all movements of the head. The patient consequently
shuns the light, and holds his head between his hands, in
order to prevent it from moving. The headache is continuous,
but is marked by exacerbations of intense severity, during

DISEASES OF THE MEMBRANES OF THE BRAIN. 779

which the patient, especially if a child, may utter a loud and
piercing cry.

Vomiting is a very constant symptom of meningitis, and is,
like the vomiting symptomatic of other cerebral diseases, unat-
tended by nausea, and epigastric pain or tenderness. It recurs
frequently during the first forty-eight hours, and may then cease
or occur at intervals throughout the course of the affection.

The motor disturbances in this stage are not well marked,
if the general convulsions which usher in the disease in chil-
dren. and which may also frequently recur in the course of the
affection, be excepted. The patient staggers like a person
drunk when he attempts to walk, and when confined to bed he
is restless and keeps changing his position. Strabismus, slight
twitching of the muscles of the face and limbs, and tooic spasms
of those of the neck and back may also be observed. The
pupils are usually contracted or unequal during this stage, but
react readily to light.

The sensory disturbances consist of buzzing in the ears,
flashes before the eyes, and intolerance of light and sound.
Cutaneous bypersesthesia is not unfrequently present, so that
the slightest touch on the skin may cause pain, and the reflex
excitability is increased.

The psychical disturbances are well marked from the first.
The patient is extremely irritable, and fierce delirium is apt to
occur, the patient shouting and violently struggling with his
attendants. At other times he is morose, and buries his head
under the bed-clothes, obstinately refusing to answer questions.
The temperature of the body is elevated, the pulse beats
from 120 to 140 or more, and the respirations are increased to
30 or 40 in the minute.

(2) The Period of Transition. — During this stage the
furious delirium of the first stage becomes quieter, the patient
lies on his back, with his fingers picking at the bed-clothes or
catching at imaginary flies in the air.

More pronounced motor disturbances now make their appear-
ance, consisting of partial or general convulsions, followed by
paralysis. The muscles most commonly affected by partial
convulsions are those of the eyeballs, producing strabismus; the
same muscles in conjunction with those of the neck causing

780

DISEASES OF THE MEMBRANES OF THE BRAIN.

conjugate deviation of the eyes and rotation of the head; the
muscles of the face ; those of the jaws causing grinding of the
teeth and trismus ; those of the tongue causing various distor-
tions of the organ ; the small muscles of the hand causing
jerking movement of the fingers, subsultus, and tremor of the
hands ; and, lastly, the larger muscles of the extremities giving
rise to various convulsive movements of the limbs. It is
probable that the loud cry which the patient continues to
utter occasionally in this stage is not a voluntary action, but
caused by spasmodic contraction of the associated muscles of
vocalisation. The muscles of the neck and back are liable to
be affected by tonic spasm, causing retraction of the head with
attacks of opisthotonos.

These convulsive symptoms are followed by paralysis, which
is very variable in its distribution, some groups of muscles
being paralysed while others continue convulsed.

The sensory disturbances consist of dimness of vision and of
hearing, ending in blindness and deafness, while the general
cutaneous hypersesthesia of the first stage is replaced by
ansesthesia. The bowels are constipated throughout, and the
abdominal walls are often retracted as in tubercular meningitis.
The respirations are irregular, the pulse frequent and thready,
and there is retention of urine.

(3) The Stage of Collapse. — The third stage of the affection
now becomes established ; the convulsive phenomena give
place everywhere to paralysis, and the patient passes into a
profound and fatal coma.

Symptoms of Secondary Meningitis. — The symptoms of
secondary meningitis differ considerably according to the cause
of the inflammation ; but, inasmuch as inflammation from
caries of the petrous bone is the most usual form of the affec-
tion, it will be useful to describe it first.

The affection may be ushered in by chilliness or a distinct
rigor and feverish symptoms; but intense headache, either con-
tinuous or marked by remissions and exacerbations, is the first
symptom to direct attention to the brain. The headache may
be fixed to a point in the vicinity of the diseased ear, or shoot
from one ear to another, while at other times it is diffused over
the whole head. If the local affection be attended by pain,

DISEASES OF THE MEMBRANES OF THE BRAIN. 781

the commencement of the meningitis is marked by a great
increase of its intensity, and the onset • of the latter may
sometimes be completely masked by an increase of the local
inflammation in the ear. Attacks of dizziness now supervene,
accompanied by nausea and vomiting; the patient complains
of noises in the head, general painful sensations diffused over
the body, and obscuration of the spinal senses.

After a paroxysm of intense cephalalgia, the patient begins
to wander, or becomes actively delirious ; these symptoms
may, however, disappear temporarily. The initial symptoms
are accompanied or preceded by the signs of local disease, con-
sisting of transitory phenomena of irritation followed by those
of depression. The signs of motor irritation are rigidity of
the muscles of the nape of the neck, convulsive twitching of
the facial muscles on the affected side, trismus, grinding of the
teeth, and occasionally spasms of the extremities.

The depressive symptoms consist of paralysis of the facial,
hypoglossal, and glosso-pharyngeal nerves on the same side as
the lesion; while, if the inflammation extend forwards along
the base of the skull, the third, fourth, sixth, and probably the
fifth nerves may become involved in inflammation. The state
of the pupils is variable and liable to frequent changes during
the course of the disease, being generally contracted or unequal
at first, and dilated and fixed when effusion has taken place.
Paralysis of the extremities is rare, but the patient has an
unsteady, staggering gait.

The sensory disturbances consist of marked hyperesthesia
of the skin, joints, bones, and muscles, so that every movement
is painful.

Vomiting generally continues throughout the whole course of
the disease, the bowels are constipated, and the abdominal
muscles are tender to the touch and retracted. The temperature
in acute cases is usually high, but remits in the morning,
although it remains constantly high in some cases.

The pulse as a rule rises and falls in frequency along with
the temperature, except in the cases where symptoms of com-
pression of the brain occur during the first days of the disease.

The urine is often albuminous, and this may or may not be
associated with amyloid disease of the liver, spleen, and kidneys.

782 DISEASES OF THE MEMBRANES OF THE BRAIN.

The optic discs usually present the same appearances as those
observed in tubercular meningitis. The psychical symptoms
are very variable, consisting of jactitation, restlessness, and
confusion of ideas, especially towards the evening when the
temperature rises. After a time the patient falls into a somno-
lent condition, from which he can at first be readily roused by
a loud question, but this state soon gives place to profound and
fatal coma.

§ 865. Course, Duration, and Terminations. — The duration
of simple purulent meningitis is variable, but as a rule the pro-
gress of the case is rapid. The disease may terminate in adults
within a week, and in infants in a still shorter period, but
sometimes it may assume a more or less chronic form, death
resulting after weeks or months.

The duration of purulent meningitis, secondary to disease of
the temporal bone, varies from a period of twenty-four hours
to two or three weeks, and the affection is usually fatal.

§ 866. Morbid Anatomy. — The pia mater is infiltrated with
a fibro-purulent exudation, the convexity being usually in-
volved to a greater extent than the base, although the latter
is generally more or less implicated, and the exudation may
even extend over the pia mater of the cerebellum and medulla
oblongata. The effusion into the ventricles varies in quantity,
and is generally sero-purulent in character. Pus may some-
times be found in the tissue of the choroid plexuses. The pia
mater is usually adherent to the cortex, and on being stripped
off, portions of the latter are torn off with it. Small capillary
extravasations are found in the cortex, or the cortex may be
rendered anaemic by the intra-ventricular pressure.

On microscopic examination, the protoplasm of the ganglion
cells is found to be granular and the cells themselves deformed,
while the vessels are surrounded by emigrant white and red
blood corpuscles. Secondary meningitis presents the same
general morbid appearances as the primary variety, although
its distribution is not always the same.

In the meningitis which results from caries of the petrous
bone, the changes may at times be limited to the pons and

DISEASES OF THE MEMBRANES OF THE BRAIN. 783

neighbouring parts, while at other times the base and the con-
vexity of one or of both hemispheres are implicated. The
inflammation generally begins on the inferior surface of the
temporal lobe, and extends to the superior and inferior surfaces
of the cerebellum, the anterior surface of the pons, and even
into the vertebral canal.

If the meningitis be caused by thrombosis of the sinuses, the
morbid appearances characteristic of the latter affection are
found in addition to those indicative of meningitis.

§ 867. Diagnosis. — Simple purulent meningitis is a rare
disease and occurs most frequently in youth and manhood,
while the tubercular variety is much more common and occurs
most frequently between the second and seventh years of age.
The prodromata in simple meningitis are not well marked;
the disease is suddenly developed in apparently healthy per-
sons, and its onset is marked by rigors, while in the tubercular
form the patient has been losing flesh for weeks before the
commencement of the attack, and the disease is developed
more gradually.

The delirium is, as a rule, more violent in primary than in
tubercular meningitis, while the paralytic symptoms are on the
other hand more pronounced in the latter. Partial convulsions
are more characteristic of tubercular, and general convulsions
of simple purulent meningitis, while rigidity of the muscles
of the neck, and tetanic spasms of the muscles of the trunk
are equally common in both affections, but retraction of the
abdominal muscles is not so marked in simple as in tubercular
meningitis. Cutaneous hyperesthesia is more commonly ob-
served in the simple than in the tubercular form.

Meningitis arising from caries of the petrous bone can hardly
be distinguished from tubercular meningitis associated with
disease of the same bone. Meningitis from thrombosis of the
sinuses must be distinguished by the signs of the latter already
described ; and the diagnosis between purulent meningitis and
abscess of the brain has already been considered.

§ 868. Prognosis. — Several recorded cases appear to show
that recovery may take place in the early stage of simple puru-

784 ; DISEASES OF THE MEMBRANES OF THE BRAIN.

lent meningitis, but in such cases the diagnosis must always
remain doubtful; when the disease is once fully developed,
recovery is probably no longer possible. The prognosis of acute
secondary meningitis is always unfavourable ; in a few fortunate
cases, where the affection is secondary to an abscess, the contents
of the latter may escape and recovery ensue.

§ 869. Treatment. — In the first stage of the disease the usual
antiphlogistic treatment must be adopted, consisting of leeching,
purgation, and cold applied to the shaven scalp. When the
cephalalgia is intense, narcotics may be cautiously administered,
the best being a small dose of morphia, subcutaneously injected.
Chloral hydrate, either alone or in combination with bromide,
of potassium, is useful when there is much restlessness and
mental excitement. Mercury and iodide of potassium have
been given with the view of promoting absorption, but the
affection appears to be much too acute for the action of these
drugs.

5. Metastatic Meningitis.

Metastatic meningitis comprises certain varieties of the
affection, which occur as terminal phenomena in the course of
acute diseases.

§ 870. Etiology. — The diseases with which meningitis is
most frequently associated are pneumonia, ulcerative endo-
carditis, acute rheumatism, purulent pleurisy, pericarditis,
diphtheria, and the acute exanthemata. Although chronic
Bright's disease is liable to be complicated by inflammation
of the serous membranes, meningitis is rare.

§ 871. Symptoms. — The extent and intensity of the inflam-
mation vary greatly in different cases; in some there is little
or no effusion into the ventricles, and the symptoms of com-
pression are absent; the inflammation is sometimes limited to
the convexity, and at other times extends to the base and
upper part of the spinal cord ; and in the meningitis of acute
febrile diseases the symptoms are obscured by the cerebral
disturbance usually observed in all grave acute affections.

DISEASES OF THE MEMBRANES OF THE BRAIN. 785

§ 872. Varieties of Metastatic Meningitis.

Meningitis ivith Pneumonia— Meningitis may appear in
the course of pneumonia from the third to the eighth day or
even later. The most usual symptoms are chilliness, intense
headache, rapidly developed and mild, or occasionally furious,
delirium, a fresh accession of fever, and hyperpyrexia before
death. The delirium gives place at an early period to somno-
lency, ending in coma. A slight degree of rigidity and pain
in the neck is always a valuable sign of meningitis, and
vomiting is a frequent occurrence. The pupils are generally
contracted at first, and may subsequently become unequal. If
the base of the brain be affected, paralysis of the ocular motor
and other nerves at the base of the skull render the nature
of the complication more apparent.

Meningitis with Ulcerative Endocarditis. — The cerebral
symptoms in ulcerative endocarditis are caused by multiple
haemorrhagic infarctions of the cortex of the brain or of the pia
mater, and the symptoms produced are more or less like those
of pyaemic encephalitis.

A rheumatic meningitis has been described, but post-mortem
evidence of its existence is wanting.

§ 873. Morbid Anatomy — The amount of blood in the
vessels of the pia mater and brain is variable. The exudation
on the pia mater is usually purulent, and varies in quantity
from a few specks, scarcely appreciable to the naked eye, to a
layer extensively distributed over the surface of the brain. The
layer of pus may be limited to the convexity, or extend to the
base of the brain. The effusion into the ventricles also varies
greatly botb in quantity and quality. The ependyma and
plexuses are not much changed. It is probable that the sub-
stance of the brain, more especially that of the cortex, is
involved in the inflammatory process.

§ 874. Diagnosis, Prognosis, and Treatment. — The diagnosis
must be made from the presence of symptoms which indicate
a meningitis supervening, in the course of such diseases, as
pneumonia, or ulcerative endocarditis. The prognosis is always

Y Y

786 DISEASES OF THE MEMBRANES OF THE BRAIN.

unfavourable, and the treatment must be conducted on the
same general principles as that of other forms of meningitis.

6. Tkaumatio Meningitis.
In traumatic as in other forms of meningitis the cortex of the
brain is involved in the inflammatory action, so that the con-
dition would be more accurately described as a meningo-
encephalitis.

§ 875. Etiology. — This form of meningitis may appear during
the period of reaction from concussion, or follow a contusion of
the brain. Injury of the scalp, with subsequent inflammation
of the bones of the skull and dura mater, may also give rise to
inflammation of the pia mater and brain. At other times the
inflammatory process is set up by a perforating injury of the
skull either with or without extravasation of blood between the
dura mater and the bone, the effects in such cases being inten-
sified by the admission of air containing germs into the open
wound. In other cases the meningitis is a secondary result of
osteitis, thrombosis of the sinuses probably playing an important
part in its production in such cases. The meningitis at other
times may result after necrosis of the bone has taken place.
Hutchinson thinks that in fractures of the petrous portion of
the temporal bone the inflammation extends along the sheath
of the seventh nerve, and in this way gains access to the sub-
arachnoidal spaces.

§ 876. Symptoms. — This affection may be divided into two
varieties : (a) acute, and (6) chronic or subacute traumatic
meningo-encephalitis (Erichsen).

{a) Acute Traumatic Meningoencephalitis. — The symp-
toms of the onset of the acute form of the affection are modi-
fied by the fact that the inflammatory process usually attacks
a patient already suffering from the symptoms of concussion,
compression, or contusion of the brain. It is impossible to
distinguish between the symptoms of the reaction period of
concussion and those of the early or congestive stage of
true inflammation, so that we are unable to determine when
the symptoms of the former terminate and those of the latter

DISEASES OF THE MEMBRANES OF THE BRAIN. 787

begin. At the onset of the inflammatory attack the patient
complains of severe and continuous cephalalgia ; the carotids
beat forcibly ; the face is suffused and the scalp hot ; the pupils
are contracted ; there are intolerance of light and sound, spectral
illusions, noises in the ears, and general hyperesthesia to
external impressions. The patient likewise suffers from the
usual symptoms of pyrexia; the pulse is full and bounding,
and there is restlessness and wakefulness with delirium of a
violent character. These symptoms may, under proper treat-
ment, gradually subside until health is re-established; but more
commonly the symptoms of the stage of irritation develop into
those of the stage of compression.

During the stage of transition between the early stage of
excitement and the stage of compression of the brain the
symptoms of a localised disease may make their appearance.
Clonic or tonic spasms, followed by paralysis, may occur in
particular groups of muscles. Rigidity of the muscles of the
nape of the neck with retraction of the head is usually present
at this period, and may also extend to the muscles of the back
and give rise to tetanic seizures. Hemiplegia of the side
opposite to the injury is, according to Hutchinson, a constant
symptom of direct traumatic meningo-encephalitis, or, as he
terms it, arachnitis. The abdominal muscles are usually
retracted and the bowels constipated. When the meningitis
is situated at the base of the brain, the cranial nerves in their
passage along the base of the skull may become implicated. The
most usual symptoms produced are ptosis, strabismus, paralysis
of the facial muscles or of half of the tongue, and difficulty of
deglutition.

The symptoms of compression of the brain now become
rapidly developed, the delirium is replaced by stupor, from
which the patient is roused with difficulty; the pupils are
dilated and insensible to light; the breathing is slow and
stertorous; the pulse, retarded at first, becomes feeble and
frequent towards the end ; the skin is hot and bathed in per-
spiration; convulsive twitchings or jerkings of the limbs are
observed, but these soon give place to general muscular relaxa-
tion, and the patient dies in profound coma.

(6) Subacute Traumatic Meningo- Encephalitis. — This form

788 DISEASES OF THE MEMBRANES OF THE BRAIN.

of meningo-encephalitis may come on a few days after the
injury or not until months have elapsed (Erichsen). The
patient has often apparently recovered from the original injury,
but as a rule some of the consequences of concussion remain.
The patient in the interval has complained of headache, im-
pairment of sight and hearing, confusion of ideas, or mental
irritability. The symptoms of the inflammatory attack may be
ushered in by an aggravation of the symptoms, which have
persisted during the interval, or by an epileptic attack. The
pupils are contracted, dilated, or unequal; there are intolerance
of light and sound, convulsive twitchings of the limbs and face,
strabismus, delirium, and the ordinary phenomena of symp-
tomatic fever. After a time the symptoms of compression
supervene, and the patient dies eomatose.

§ 877. Course, Duration, and Terminations. — 'The symp-
toms of acute traumatic meningo-encephalitis sometimes begin
a day or two after the injury, at other times not until several
days have elapsed. In the subacute form of the affection
weeks or months may intervene between the injury and the
meningitis.

The duration of the disease varies within wide limits, the
average being eight to fourteen days.

§ 878. Morbid Anatomy and Physiology. — The surfaces of
the visceral and parietal layers of the arachnoid are covered
with adherent lymph of a greenish-yellow and purulent appear-
ance. A little fluid pus may sometimes be found between the
two layers (Hutchinson). The visceral layer of the arachnoid
is congested, or thickened and semi-opaque. The pia mater is
usually much congested, but it does not appear to be infiltrated
with pus or covered by a layer of lymph like the arachnoid. The
substance of the brain is congested and has a rosy hue, while
the red points are increased in number. The ventricles are filled
with a turbid serum, of a reddish colour. Fracture of the petrous
bone gives rise, according to Hutchinson, to inflammation of the
subarachnoid spaces at the base of the brain. In such cases
the inflammation spreads along the sheath of the seventh nerve,
and in this way gains direct access to the subarachnoid spaces.

DISEASES OF THE MEMBRANES OF THE BRAIN. 789

The effusion begins at the base of the brain, and may extend
upwards over the hemispheres or through the transverse fissure
into the ventricles, and may also extend down the spinal cord
for a considerable distance. The effusion is always underneath
the visceral layer of the arachnoid.

§ 879. Diagnosis and Prognosis. — Traumatic meningo-
encephalitis may be distinguished from the reactive stage of
concussion, and from simple congestion of the brain by the
elevation of the temperature and the persistence and severity
of the symptoms generally. The prognosis is always grave;
and in the cases which are said to recover it is doubtful
whether anything more than intense congestion of the brain
was present. It is, however, important to remember that
all the symptoms of the first stage of traumatic meningo-
encephalitis may have been present, and yet that the patient
may make a good recovery.

§ 880. Treatment. — The treatment of acute traumatic
meningoencephalitis is the same as that of the other acute
forms of meningitis and encephalitis. The patient should be
confined in a quiet and darkened room and removed from all
causes of excitement. The head should be shaved and ice
applied to it. Erichsen recommends bleeding from the arm,
leeches or cupping, free purgation, abstinence, and the ad-
ministration of calomel so as to produce salivation,. As the
case assumes a more chronic form the treatment must be less
energetic, but the patient must be kept for a long time in a
state of complete quietude.

791

Part V. — DISEASES OF THE ENCEPHALO-SPINAL

SYSTEM.

CHAPTER I.

PARALYSIS AGITANS, AND MULTIPLE SCLEROSIS.

(I.) PARALYSIS AGITANS
(Shaking Palsy — Parkinson's Disease).

PARALYSIS agitans is a chronic nervous disease characterised
by continuous tremor of the voluntary muscles, and peculiar
alterations in the attitudes of the body.

§ 881. Etiology. — Paralysis agitans occurs in advanced life,
being rarely observed under forty years of age. Duchenne met
with the disease in a youth of sixteen, and Meschede in a boy
twelve years old as the result of having been kicked by a horse
in the face. Men are more frequently attacked than women ;
hereditary predisposition does not appear to be an important
factor in its production.

Exposure to damp and cold seems to be an exciting cause of
paralysis agitans, the disease being frequently met with amongst
persons living in damp and unhealthy situations. It is some-
times caused by great emotional disturbance, and many cases
follow wounds and other injuries.

§ 882. Symptoms. — The clinical history of paralysis agitans
may be divided into three stages: (1) The period of invasion;
(2) the stationary period ; and (3) the terminal period.

(1) The Period of Invasion. — Paralysis agitans, as a rule,
sets in somewhat slowly and progressively, but occasionally in

792

PARALYSIS AGITANS.

an abrupt manner. In the slow mode of invasion the develop-
ment of the disease may be preceded for some time by premoni-
tory symptoms, such as sleeplessness, mental irritability, and a
transitory feeling of weakness in the limbs. The disease itself
is ushered in by a trembling in one of the extremities, usually
beginning in the small muscles of the hand or forearm. At
this stage the tremors are arrested, on the patient making a
voluntary effort. The tremors may, indeed, cease when the
voluntary effort is unconnected with the members affected ;
thus the act of walking may arrest tremor of the upper
extremities. Even at this early period the tremor presents
characteristic features. If the hand be affected, " the patient,"
to quote Charcot, " closes the fingers on the thumb, as though
in the act of spinning wool; at the same moment the wrist is
bent by rapid jerks on the forearm, and the forearm on the
arm." The tremor increases in intensity, and, instead of being
as at first occasional, it gradually becomes persistent, and
invades by degrees parts which have hitherto remained sound.
The order in which the various muscles are invaded by the
tremor is somewhat variable. The most usual mode of invasion
is that which Charcot has called the hemiplegic type. In this
form the tremor usually begins in the right hand, and after
months or years the lower extremity on the- same side becomes
affected, and after another variable period the left hand and
foot are successively invaded. In other cases both the lower
extremities are first affected, forming the paraplegic type;
while in a few cases the upper extremity of one side, generally
the right, is first invaded, and then the lower extremity of the
opposite side, forming what Charcot calls the decussated mode
of invasion. Charcot states that the muscles of the neck and
head are nearly always unaffected by tremor at every stage of
the disease, a fact which deserves particular notice inasmuch as
it serves to distinguish paralysis agitans from the cerebro-spinal
form of disseminated sclerosis. The tremor may be preceded by
a remarkable feeling of fatigue, or by rheumatoid or neuralgic
pains, and in such cases it is not uncommon to find that the
disease has been occasioned by an injury.

In the abrupt mode of invasion the tremor appears sud-
denly either in one extremity or in all the limbs at once, and

PARALYSIS AGITANS.

793

the disease then usually results from great emotional distur-
bance. The tremor may soon diminish or disappear, but it recurs,
and, after a series of alternate exacerbations and remissions,
becomes permanent. Whatever be the mode of invasion, the
duration of the initial stage varies from one to two or three
years.

(2) Stationary Period.— -When the disease is fully developed
the trembling becomes almost incessant, although it varies in
intensity. It is aggravated by emotional excitement, cold, and
voluntary effort; while, on the other hand, it becomes less
during repose, and ceases during sleep.

The different segments of the hands and fingers undergo
involuntary and rhythmical oscillations, which closely resemble
complicated voluntary movements. " Thus, in some patients,"
says Charcot, " the thumb moves over the fingers, as when a
pencil or paper-ball is rolled between them ; in others, the
movements are more complicated, and resemble what takes
place in crumbling a piece of bread." The handwriting now
assumes special characteristics. At an early stage of the disease
the writing at the first glance presents little change ; but, when
examined with a magnifying glass, inequalities are perceived,
some parts being thicker and heavier than others. As the
disease advances the up strokes become markedly tremulous,
probably owing to the lumbricales and interossei muscles being
most profoundly affected by the tremor.

The muscles of the head and neck, as already stated, usually
remain unaffected. The muscles of the eyeballs are also exempt
from tremor, and consequently nystagmus, which is so prominent
a symptom of disseminated sclerosis, has no existence in para-
lysis agitans. The movements of the eyeballs are, however,
often executed with great slowness (Debove). The muscles of
the face instead of trembling are motionless, the features become
fixed, and the face assumes a mournful, stolid, or vacant ex-
pression. The utterance is slow, jerky, and accomplished with
great apparent effort, soon inducing weariness, and if the tremor
of the body be intense it becomes tremulous and broken, while
in old-standing cases the saliva may dribble from the mouth to
some extent.

After a longer or shorter time the muscular power becomes

794

PARALYSIS AGITANS.

gradually weakened. In many cases, however, motor weakness
is more apparent than real, the phenomena depending upon the
great slowness with which voluntary movements are executed,
the immense effort which all voluntary actions, even speaking,
entail, and the readiness with which fatigue is induced. But
although the muscular power, when measured by the dynamo-
meter, is often retained much longer than might be expected,
yet after a "time motor power becomes gradually diminished,
and paralytic symptoms supervene (Charcot). The paralysis,
however, almost always remains partial, and is irregularly
developed in different groups of muscles; and, as in various
other forms of paralysis, the extensors of the limbs are affected
to a greater extent than the flexors. The trembling often
abates in the muscles as paralysis increases. The bladder and
rectum are only very exceptionally involved in the paralysis.
The muscles react normally to both the faradic and galvanic
currents.

After a time the muscles of the extremities, trunk, and
neck become the subjects of rigidity, at first temporary,
but ultimately becoming permanent, the flexors being affected
to a greater extent than the extensors. The rigidity of the
muscles produces characteristic alterations in the attitudes of
the body. The rigidity of the anterior cervical muscles causes
the head to be strongly bent forwards, and the patient cannot
raise it or turn it to either side without great difficulty. The
body is also inclined forwards when, the patient is standing..
The elbows are habitually held somewhat removed from the
chest, the forearms are slightly flexed on the arms, and the hands
are sometimes flexed, sometimes slightly extended on the fore-
arms, and rest on the epigastrium. The fingers are flexed at the
metacarpo -phalangeal articulations, the index and middle fingers
are extended, but the remaining fingers are slightly flexed, at the
phalangeal articulations, all of them are slightly inclined to the
ulnar border of the hand, and the thumb is extended and op-
posed to the index finger, so that the attitude of the hand and
fingers closely resembles that assumed by them in holding a
pen (Charcot — Fig. 281). In some cases the fingers are alter-
nately flexed and extended at their several articulations so as
to resemble the distortions of arthritis deformans (Fig. 282).

PARALYSIS AGITANS.

795

In paralysis agitans, however, the joints are not swollen and
stiff, and passive movement of the articulations does not give
rise to the creaking sounds observed in the former. The
rigidity of the muscles of the lower extremities is sometimes
so great as to resemble paraplegia with contracture. The spasm
of the adductors of the thighs and muscles of the calf pre-
dominate over their antagonists so that the knees are drawn

Fig. 281.

Fig. 281 (After Charcots Attitude of the Hand in Paralysis Agitans.

inwards, the leg is slightly flexed on the thigh, and the foot
assumes the well-known position of talipes equino-varus.
The toes are extended at the metatarso-phalangeal and flexed
at the phalangeal articulations (Griffe des Orleils).

Fig. 282.

Fig. 282 (After Charcot). Attitude of the Hand in Paralysis Agitans simulating

that of Arthritis Deformans.

In the advanced stage of the disease the patients move all
of a piece, as if their joints were, to use Charcot's expression,
soldered together; the head and body are kept inclined for-
wards, a position which no doubt largely contributes to produce
that tendency to fall forwards manifested when walking (Plate
IV., 3 and 4).

The gait of the patient is now characteristic. The patient
gets up slowly and with difficulty from his seat, and hesitates for
a few moments before starting; when once he has begun to walk,

796

PARALYSIS AGITANS.

he is compelled to run forwards, in order to save himself from
falling. In the language of Trousseau, he looks as if pursuing
his own centre of gravity. This gait has been called •paralysis
festinans or procursoria, or simply propulsion.

The forward running or propulsion is the usual gait of
paralysis agitans, but some patients manifest a strong tendency
to run or to fall backwards, although their bodies are inclined
forwards, a tendency which has been named retropulsion.
Graves mentions the case of a patient who, if arrested in his
forward movement, immediately began to run backwards; and
Charcot could excite the impulse to move backwards in a female
patient by slightly pulling her back by the dress when she was
standing. It has already been mentioned that a few cases of
paralysis agitans are ushered in by rheumatoid or neuralgic
pains, but in the majority of cases pains are absent. The
patient is, however, distressed by disagreeable sensations, as
cramps and sensations of tension and traction in the muscles,
along with a general feeling of weariness and discomfort. These
sensations render the patient restless, and cause him to seek
frequent changes of posture. He complains of a constant sen-
sation of excessive heat, although the thermometer shows that
the temperature of the body is normal. In order to relieve
this feeling, the patient throws off the bed-clothes at night, and
only retains the lightest garments in the day-time (Charcot).
This sensation of heat is especially felt in the epigastrium
and back, but may affect the face and limbs. It is liable to
remissions and exacerbations, and seems to attain its maximum
after a paroxysm of trembling ; it is often accompanied by
profuse perspiration.

(3) Terminal Period. — The course of the disease is very
protracted, and may extend over a period of many years. As the
tremors and muscular rigidity increase in intensity, the patients
are compelled to remain the whole day seated on a chair, or con-
fined to bed. The general nutrition suffers, the muscles become
atrophied, and the paresis of the second stage of the disease
gives place to pronounced paralysis. The memory and in-
tellect are weakened, general prostration sets in, the urine
and fasces are passed unconsciously, bed-sores appear on the
sacrum, and the patient dies from nervous exhaustion and

PARALYSIS AGITANS.

797

marasmus. The tremors disappear entirely a few days before
death, and paralytic symptoms become predominant. In the
majority of cases, however, death results from some inter-
current disease, such as pneumonia or pleurisy.

§ 883. Morbid Anatomy. — In a very considerable number of
cases post-mortem examination has not revealed any lesion of
the nervous system. Charcot examined three well-marked
cases of the disease in which no lesion of the nervous system
could be found, and individual cases have been examined by
Petraeus, Olivier, Th. Simon, and Kuhne also with negative
results. Cohn found in one case well-marked cerebral atrophy,
but the brains of old people are frequently found in this con-
dition in the absence of paralysis agitans. Meschede, Bam-
berger, Lebert, Marshall Hall, and Skoda found sclerotic patches
in various parts of the cord and medulla oblongata, pons,
and walls of the ventricles, but these were, doubtless, cases
not of true paralysis agitans, but of disseminated sclerosis.
Parkinson and Oppolzer found induration of the pons, medulla,
and cervical portion of the cord, but these also were probably
not cases of genuine paralysis agitans. Cay ley and Murchi-
son found sclerosis of the posterior part of the spinal cord,
thickening of the septa, enlargement of the central canal,
and aggregation of leucocytes in spots. In three cases of
paralysis agitans recently observed by Charcot and JofTroy,
a microscopical examination revealed changes in the spinal
cord, consisting of obliteration of the central canal by increase
of the epithelium of the ependyma, and pigmentation of the
ganglion cells, especially of the columns of Clarke. In one
there was a sclerotic spot on the posterior surface of the medulla
oblongata.

Dowse and Kesteven found pigmentary degeneration of the
nerve-cells near the decussation of the anterior pyramids, of
the cells of the olivary body, nucleus of the ninth nerve,
laminae and corpus dentatum of the cerebellum, and anterior
cornua of the spinal cord, along with cortical sclerosis of the
right lateral column of the cord, and miliary changes in the
white matter of the corpus striatum and hemispheres.

798

PARALYSIS AGITANS.

§ 884. Morbid Physiology. — As just observed, not much
light has hitherto been thrown upon the pathology of paralysis
agitans by morbid anatomy. The results obtained, however,
favour the idea that the morbid changes are due to a chronic
degeneration. If the changes begin, as the observations of
Charcot and Joffroy seem to indicate, around the central
canal of the spinal cord, the small cells of the accessory system
may be expected to suffer to a greater extent than the large
cells of the fundamental system; and if the lesion consist in
part of a thickening of the connective tissue septa of the cord,
as was observed in Murchison's case, the small fibres of the
accessory system, which lie near the vessels, will be injured
by the usual cicatricial contraction of the new growth to a
much greater extent than the larger and more resisting fibres
of the fundamental system. . Even aggregations of leucocytes
in the neighbourhood of the vessels, such as were found in
Murchison's case, would damage the accessory cells and fibres
to a greater extent than the fundamental. The results obtained
by Dowse and Kesteven, however, appear to show that the
morbid changes in paralysis agitans are not limited to the
spinal cord, but are widely diffused in the cerebellum and
cerebral hemispheres, as indeed might be expected when it is
considered that the disease occurs almost exclusively during
the degenerative period of life. It is worthy of notice that,
Dowse and Kesteven make special mention of the white matter
of the corpus striatum, probably the internal capsule, as having
undergone morbid changes.

Turning to the clinical history of the disease, the most
prominent symptoms are the tremors, the slowness in the
execution of movements, and the peculiar alteration in the
attitude of the body with its associated muscular rigidity. The
causes of tremor have already been discussed (§§ 68 and 73). It
is probably caused in this affection by a diminution in the con-
ductivity of the fibres of the pyramidal tract, which prevents
impulses from the cortex reaching the muscles in suffi-
ciently close proximity to produce a continuous contraction.
According to this view, the tremors and the slowness in the
execution of movements are merely the first indications of
the more pronounced paralysis which supervenes in the

PARALYSIS AGITANS.

799

terminal period. Another view, which might be adopted
with regard to the origin of the tremors, is that they are caused
by a loss of the balance normally existing between the regu-
lative functions of the cerebrum and cerebellum. The attitude
of paralysis agitans is, as has been pointed out by Hughlings-
Jackson, the opposite of that of tetanus. During a tetanic
seizure the actions of the extensors of the trunk and lower
extremities predominate, and the body is arched backwards; in
paralysis agitans the action of the flexors predominates, so that
the different segments of the trunk and lower extremities are
flexed upon one another. In tetanus the muscles, the actions
of which must have gradually predominated in the course
of evolution, in the attainment of the erect posture, are excited
to increased activity; while in paralysis agitans the same
muscles, speaking broadly, become relatively paralysed, and
there is a gradual reduction of the human to the animal
posture. A patient suffering from paralysis agitans during the
stage of propulsion is, in his attitude, very similar to a dog
attempting to walk on his hind legs. If, then, paralysis agitans
be a disease in which the accessory portion of the nervous motor
apparatus suffers to a greater extent than the fundamental part,
it may be asked how it is that the facial and ocular muscles
escape tremor. I am unable to give a satisfactory answer to
this question; but it must be remembered that, although these
muscles do not suffer from tremor, yet they are affected with
comparative immobility and rigidity at a comparatively early
period of the disease.

The phenomena of propulsion are caused partly by the forced
attitude of the patient and partly by the great slowness with
which his movements are executed. When the heel is once
raised from the ground by contraction of the muscles of the calf,
the patient must in walking balance himself on the ball of the
foot, but in walking the forward inclination of the body tends to
make the line of gravity pass in front of the active leg. The posi-
tion is to some extent the same as that assumed by a person run-
ning. In the latter the centre of gravity is held well forwards, so
that the line of gravity falls in front of the foot of the active leg
during the greater portion of the time it is maintained on the
ground. A healthy runner, however, is able to take a rapid

800

PARALYSIS AGITANS.

and long stride with the passive leg, so that by the time it is
brought to the ground, in order to become active, it is in
front of the line of gravity, and the body is thus kept from-
falling. But it is different in paralysis agitans. The rigidity
of the muscles prevents the patient from taking a long stride,
while the great slowness with which all his movements are
executed renders it impossible for him to plant the leg about to
become active in advance of the line of gravity. In retropul-
sion the line of gravity must ever tend to fall behind the point
of the foot of the active leg, while the other leg cannot be moved
backwards with sufficient celerity to enable the patient to plant
it far enough behind the retreating centre of gravity in order
to arrest the backward movement.

§ 885. Diagnosis. — Paralysis agitans is most likely to be
mistaken for senile or toxic tremor and disseminated sclerosis.
It may be distinguished from senile tremor by the facts that it
occurs before senescence, and that its tremor is of greater inten-
sity; the gait and expression of paralysis agitans are also charac-
teristic. The tremor of mercurial poisoning resembles paralysis
agitans more closely than that of any other form of toxic tremor,
and in distinguishing between them the history of the case will
be of much value. The diagnosis between paralysis agitans and
disseminated sclerosis will be described when the latter disease
is under consideration.

§ 886. Prognosis. — As far as recovery is concerned the
prognosis is absolutely unfavourable, but the patient may live
for a very long period. The disease may, indeed, last thirty
years, and the symptoms of the third or terminal period may
linger on for four or five years. The sooner the muscular
rigidity and paralysis supervene the more unfavourable does
the prognosis become.

§ 887. Treatment. — The treatment of paralysis agitans can
only be palliative. Carbonate of iron, chloride of barium,
hyoscyamus, and the use of the constant current or Pulver-
macher's chain, and warm baths are the agents which have been
vaunted in the treatment of the disease. Strychnine has been

MULTIPLE SCLEROSIS.

801

praised by Trousseau, but Charcot thinks that, instead of calm-
ing, it aggravates the tremor. Ergot of rye and belladonna have
-also been tried, but without success. Morphia and other nar-
cotics are necessary adjuncts of the treatment in the later stages
of the affection when the patient is harassed by restlessness and
sleeplessness, and both chloral and bromide of potassium may
be of use ; none of these remedies appears to produce any action
beyond palliating the symptoms. Eulenburg recommends the
subcutaneous injection of Fowler's solution, and I must say that
I should have more faith in arsenic than in any other remedy
with probably the exception of phosphorus. Quinine, zinc,
nitrate of silver, and chloride of gold have all been tried, but
without producing any marked effect upon the disease.

(II.) MULTIPLE SCLEROSIS OF THE BRAIN AND SPINAL CORD

(Disseminated or Insular Sclerosis).

§ 888. Definition. — Multiple sclerosis is, as its name implies,
a chronic induration disseminated in patches in various parts
of the nervous system ; the affection is characterised clinically
by the presence, in greater or lesser integrity, of a group of
symptoms, the most constant of which are muscular weakness
and tremor on voluntary effort.

§ 889. History. — Disseminated sclerosis was first described by Cruveil-
hier in his " Atlas de l'Anatomie Pathologique," 1835 — 1842. The clinical
histories of two cases of the disease are there given, which, along with the
accompanying plates of the lesions found, leave no doubt as to the nature
of the affection described. Carswell in 1838 accurately represented in his
"Atlas" the lesions observed, while Marshall Hall in 1841 described an
undoubted example of this affection. It was that of a man, aged 28 years,
suffering from tremor of the right arm and leg, who had a peculiar rocking
motion of the eyes, and a degree of stammering and defective articulation.
In Germany, the disease was studied clinically by Frerichs (1849), Valentiner
(1856), and Turck (1856) ; while its pathological anatomy was examined by
Rokitansky, Leyden, Rindfleisch, and Zenker. But this singular affection
has been studied with the greatest success in the Salpetriere by Charcot
and his scholars, and our present accurate knowledge of the disease is
mainly owing to their labours. A valuable paper on the subject has been
contributed by Moxon in this country, and individual cases have been
recorded by many others.

z z

802

MULTIPLE SCLEROSIS.

§ 890. Etiology. — Hereditary transmission has been traced
in several recorded cases of multiple sclerosis, although it is
always indirect rather than direct. Duchenne and Erb have
reported cases of the kind. Frerichs observed the affection
in a brother and sister, and Dreschfeld described two exquisite
examples in brothers.

According to Charcot the female is more frequently affected
than the male sex, but the statistics of others do not bear out
this conclusion. Multiple sclerosis is commonly observed in
youth and middle age, and usually makes its appearance during
the second and third decades of life, and probably never after
45 years of age. In a large proportion of the cases recorded
in England, children under ten years of age have been the
subjects.

The exciting causes are exposure to cold and damp, excessive
mental or bodily exertion, profound emotional disturbances,
and traumatic influences, as blows on the head and concussion
from railway accidents.

§ .891 Symptoms. — Multiple sclerosis has been divided by
Charcot into three varieties : (1) The cerebrospinal, (2) the
cerebral, and (3) the spinal form. Of these the cerebro-spinal
form is by far the most frequent and important.

(1) The Cerebrospinal Form. —■ This form of multiple
sclerosis, clS & rule, develops gradually and insidiously, but
occasionally abruptly. In cases the development of which is
gradual the initial symptoms are very obscure, and may be
referred either to the spinal cord or brain. The spinal symp-
toms which usher in the disease consist of paresis of the lower
extremities with a slow and trembling gait, or ataxia with
various parses bhesiae, neuralgic pains, other disturbances of sen-
sibility in the limbs, and cardial gic attacks accompanied by
urgent vomiting. The more usual cerebral symptoms observed
in the beginning of the disease are vertigo, headache, staggering
gait, tremors, on voluntary effort, impairment of speech, vision
or hearing, paresis of the muscles supplied by one or more of
the cranial motor nerves, and various psychical disturbances.
When the disease begins abruptly, the symptoms are ushered

MULTIPLE SCLEROSIS.

803

in by a convulsive or apoplectiform attack, followed by diplopia,
amblyopia, or nystagmus, and disturbances of speecb.

The first motor symptom to attract attention is usually
paresis or paralysis of certain muscular groups. Weakness
generally begins in one leg, aDd subsequently extends to the
other leg and to the arms, but the order in which the paralysis
of the different muscular groups is developed presents every
imaginable combination.

The gait is usually of the spastic variety, muscular contrac-
tures set in, and the legs are held like rigid bars in the position
of extension and adduction, just as in primary lateral sclerosis.
In the later stages of the disease flexion of the different seg-
ments of the lower extremities may predominate over extension .
The paralysis rarely becomes so well marked in the upper as in
the lower extremities. When the upper extremities are, how-
ever, affected with paralysis and contracture, they are main-
tained in a position of forced extension, and closely applied to
the sides of the body. The affection sometimes begins with
ataxia, but in these cases it may often be noticed that charac-
teristic symptoms of true locomotor ataxia are absent, while
others are present which do not usually belong to it. In a
patient under my care at present, for instance, the symptoms
when I first saw him, upwards of two years ago, were paralysis
of both sixth nerves, and an ataxic gait. But the gait, differing
from that of locomotor ataxia, was somewhat reeling, although
not sufficiently so to be attributed to cerebellar disease, there
were no lancinating pains in the extremities, and the patellar-
tendon reflex was exaggerated in both legs. The patient is now
suffering from the same ataxic gait, the characteristic tremors of
multiple sclerosis, slight nystagmus, and scanning speech, while
the paralysis of the external recti muscles has disappeared.

Intermittent muscular tremor constitutes one of the most
characteristic symptoms of this affection, although it has been
found absent in a few isolated cases. This tremor appears
almost exclusively during voluntary movements, and disappears
during repose. So long as the patient remains seated quietly
the tremor is either entirely absent, or at most there is only a
trifling shaking movement of the head, or a slight oscillation of
the trunk. As soon, however, as he attempts to seize anything

804 MULTIPLE SCLEROSIS.

with his hand the tremor begins, and increases in violence in
proportion to the effort made to execute the movement. Several
devices may be used in order to bring into prominence the
characteristic tremor of multiple sclerosis, such as asking the
patient to seize small objects with his fingers or to stretch out
his arms horizontally before him.

The tremor of this affection differs from that of paralysis
agitans, not only in being intermittent instead of continuous,
but also in having a much wider sweep than that of the latter
affection. It holds an intermediate position between the exten-
sive jerking movements of chorea, and the small and frequent
oscillations of paralysis agitans. The true characteristics of
the tremor of multiple sclerosis is best elicited by asking the
patient to convey a glass of water to his mouth. As the glass
is being carried to the mouth it oscillates from side to side in
the patient's hand, these oscillations appearing to increase in
extent and frequency as the mouth is approached. In aggra-
vated cases the contents of the glass are spilt in every direction;
but in milder cases the patient is able, moving his head down-
wards in order to meet the glass, to apply it to his lips, and
then the trunk, head, and arms begin to tremble violently, so
that the edge of the glass rattles against the teeth, and the
contents are spluttered over the patient's face. When the
patient rises and attempts to walk the tremor involves the
entire body, which may be shaken with such violence that he
is unable to proceed or even to remain standing. As soon as
the voluntary effort is relaxed the tremor diminishes, and as
long as the patient is in the recumbent posture no trace of it
can usually be detected; occasionally the tremor has been
known to persist during repose.

The sensory disturbances are somewhat variable and not
always well marked. They may assume the form of facial
neuralgia, lancinating or diffused pains in the extremities,
hyperesthesia or anaesthesia of variable distribution, girdle
pains, and various parsesthesise felt in different parts of the
body, the latter being the most frequent of all the sensory
disorders.

The reflex actions are variously affected in different cases.
The cutaneous reflexes remain for a long time unaffected ;

MULTIPLE SCLEROSIS.

but the deep reflexes are usually exaggerated, especially in the
lower extremities. In consequence of the increase of the tendon-
reflexes in the lower extremities, the knee-phenomenon and
ankle clonus are usually exaggerated, and the limbs may be
thrown into the state of trembling named spinal epilepsy. This
condition must, however, be carefully distinguished from the
characteristic tremor of multiple sclerosis.

Trophic disturbances are generally wanting for a long time,
but in the later stages various nutritive disorders usually make
their appearance. The sclerotic nodules may encroach on the
anterior grey horns of the spinal cord, and then muscular atrophy
results as in progressive muscular atrophy. Muscular atrophy
may present itself in the upper or lower extremities, neck, face,
tongue, or indeed in any part of the body. The electrical reac-
tions of the nerves and muscles remain normal until the muscular
atrophy begins, and then the electric irritability of both becomes
gradually diminished.

During the terminal period of the disease bed-sores appear
over tbe sacrum and other parts subjected to pressure, and
general nutrition fails.

The bladder and rectum, as a rule, remain unaffected for a
comparatively long time, but their functions are ultimately in-
terfered with as in chronic myelitis. The disorders of the sexual
functions are somewhat variable. In some patients sexual desire
appears to be increased at an early period of the disease, while
in others it is completely abolished. In the majority of cases
the sexual functions remain normal for a comparatively long
time.

Bulbar Symptoms. — Some of the phenomena caused by
implication of the pons and medulla oblongata in the morbid
process are amongst the most important and characteristic
symptoms of the disease. The speech is slow and hesitating,
while each syllable is separately pronounced, presenting a mode
of articulation which has been named the syllabic or scanning.
The voice is weak, low, sometimes whispering, and monotonous,
while it breaks readily when forced efforts are made. Laryngo-
scopy examination shows that the vocal cords move normally,
but their tension is diminished and frequently changes (Leube).
The acts of laughing and crying are often represented by peculiar

MULTIPLE SCLEROSIS.

noisy inspirations. After a time symptoms of true bulbar
paralysis supervene, the movements of the lips and tongue are
impaired, and by-and-by mastication and deglutition become
increasingly difficult, the velum palati is paralysed, speech
becomes inarticulate, and the mouth remains permanently
paralysed, while the saliva dribbles out.

Diplopia with strabismus is a not unfrequent symptom,
although it may subsequentlydisappear as in locomotor ataxia.

Nystagmus is, however, the most important of all the ocular
symptoms, being present, according to Charcot, in about half the
cases. The movements of the eyeballs may be persistent or
occur only during forced accommodation, or when movements
are performed by the extremities. At other times the nystagmus
may not be apparent during the ordinary movements of the
eyeballs, but when the patient is asked to look upwards and
outwards so as to strain the ocular muscles, slight oscillatory
movements may be observed.

Amblyopia is not unfrequently observed. It consists of a
progressive weakness of sight, accompanied by colour blindness
and restriction of the field of vision, and may increase to com-
plete blindness. The development of amblyopia is sometimes
preceded by photopsia; the optic discs may be normal, partially
diseased, or the subjects of white atrophy.

The senses of smell, taste, and hearing are impaired in some
cases, but these disorders are rare.

Psychical disturbances are always observed in multiple
cerebro-spinal sclerosis. They consist of mental irritability,
emotional excitability causing the patient to laugh or to shed
tears without apparent motive, and impairment of memory and
intelligence. At other times the mental disorder assumes the
form of distinct unsoundness of mind. In such cases there may
be melancholia, monomania, with ideas of persecution or of
grandeur, and the patient may fall into a state of complete
dementia.

In the course of the disease, the patient suffers from attacks
of vertigo. This symptom usually comes on at an early period,
and continues to distress the patient throughout. The patients
feel as if they themselves were being turned round, or as if

MULTIPLE SCLEROSIS.

807

surrounding objects were whirling round them. They suffer
greatly from sleeplessness and violent headache.

A poplectiform or epileptiform seizures have been observed
in a small number of cases ; they are apparently analogous to
the apoplectiform attacks, which occur in general paralysis
of the insane. They are characterised by the development
of grave cerebral symptoms, and are accompanied by a
considerable elevation of temperature. After slight premoni-
tory symptoms, such as a feeling of pressure in the head, there
is a partial loss of consciousness, which in a few hours may
develop into coma. The face is red and hot, the pulse is quick,
and the temperature of the body rises to 104° F. or 105° F. In
some cases the loss of consciousness is accompanied by unilateral
convulsions — epileptiform attacks; while in other cases there
are no convulsions — apoplectiform attacks. In most cases hemi-
plegia with muscular flaccidity, and on rare occasions rigidity, is
present from the outset of the seizure. After one or two days
the temperature falls, the patient sinks into a quiet sleep from
which he may be readily roused, and he feels, on awaking,
comparatively well. Hemiplegia, however, persists for a few
days longer and then gradually disappears. These attacks may
be repeated several times in the course of the disease, recurring
in some cases every few months ; but each is followed by an
aggravation of the general symptoms, and death sometimes
occurs during an attack.

(2) Cerebral Multiple Sclerosis. — In this form of the disease,
which is rarely observed, the psychical disturbances are pre-
dominant. The tremor is said to precede the paralytic mani-
festations, but in other respects the course of the affection does
not differ greatly from the cerebro-spinal variety.

(3) Spinal Multiple Sclerosis. — The spinal form of the affec-
tion is characterised by the absence of the cerebral symptoms,
particularly nystagmus, tremor on voluntary effort, vertigo,
apoplectiform attacks, and psychical disturbances. The symp-
toms of the spinal form of multiple sclerosis often simulate
those of primary lateral sclerosis, although in the former some
additional symptoms are usually present. In other cases they
simulate locomotor ataxia, but in multiple sclerosis symptoms
are usually present which form no part of the former.

808

MULTIPLE SCLEROSIS.

§ 892. Course, Duration, and Terminations. — The course of
multiple sclerosis is divided by Charcot into three stages : —

The first stage extends from the beginning of the disease up
to the appearance of marked paralysis with contractures. This
stage may last from two to six years, or longer. Its develop-
ment is generally slow. It sometimes begins with cephalic
symptoms, as headache, vertigo, and unsteady gait ; but more
usually with spinal symptoms, as paresis of the lower extremities,
and in such cases the nature of the disease remains doubtful
until the appearance of the characteristic tremor clears up the
diagnosis.

In other cases the development of the disease is more rapid.
It begins by an apoplectiform attack, or gastralgic disturbances,
while paralyses, disorders of co-ordination, tremor, and other
symptoms are superadded in quick succession. The progress of
this stage is often interrupted by remissions or improvements,
but the nature of the disease is essentially progressive. The
patients become more and more helpless, complete paraplegia
is developed, the legs being maintained in a condition of rigid
extension and adduction ; tremor deprives them of the use of
the hands, and the intellectual power becomes more and more
impaired.

The second stage of the disease is now developed ; it lasts
from four to six or more years. During this period the disease
remains more or less stationary ; the general nutrition is but
little impaired.

The third stage is characterised by impairment of general
nutrition and the appearance of symptoms indicative of ex-
haustion. The patient loses his appetite and becomes emaciated ;
the bladder is paralysed, and cystitis and bed-sores occur, leading
to pyaemia, marasmus, and death.

The increasing bulbar symptoms may threaten life in another
way, while it is not unfrequently cut short by intercurrent
disease, as pneumonia, pleurisy, or pulmonary consumption.

Some cases have terminated fatally in from one to two years
from the commencement, but such cases are rare. The average
duration is from five to ten years, but individual cases have
lived much longer.

The termination of the disease is always in death. During

MULTIPLE SCLEROSIS.

809

the first stage a partial amelioration of the symptoms may
occur, either spontaneously or under treatment, which may
lead the patient and his friends to hope for recovery. The
improvement is, however, deceptive, for the symptoms always
return and ultimately prove fatal.

§ 893. Morbid Anatomy. — The morbid alterations in mul-
tiple sclerosis appear in more or less numerous spots or
nodules, which are scattered in greater or lesser number
throughout the spinal cord, medulla oblongata, pons varolii,
cerebellum, and cerebrum.

The individual nodules, when near the surface of the spinal
cord, may be seen through the pia mater as brown or amber
stains, and in aggravated cases the entire surface of the cord may
be studded with greyish spots. Each spot is, as a rule, sharply
defined from the surrounding tissues and slightly elevated
above the surface of the cord, but it is occasionally atrophic and
depressed or on a level with the normal portions. On transverse
section the nodules appear grey or greyish-yellow, and when
exposed to the air change to a salmon colour ; they are trans-
lucent or opaque, irregular or oval in shape, generally isolated
and circumscribed, but occasionally confluent, and are in consis-
tence dense, tough, even cartilaginous, but rarely semi-fluid and
gelatinous. These nodules vary from the size of a hemp-seed
to that of a bean in the spinal cord, but they often become
confluent and consequently appear to attain a much larger size
in the brain. The distribution of the nodules in the spinal
cord is subject to great variations. On making successive
transverse sections of the cord the nodules will appear in one
or both of the lateral columns at one level, in the posterior
columns at another, and in the grey substance at a third, while
the nodule occupies the greater part of the area of the section
at certain levels. The number of nodules which are present is
variable, a few only being observed in some cases, while in" others
hundreds may be counted.

The cerebral hemispheres usually contain a large number of
nodules, their favourite sites being the white substance of
the centrum ovale, septum lucidum, corpus callosum, basal
ganglia, and walls of the lateral ventricles. The cerebellum

810

MULTIPLE SCLEROSIS.

generally contains a few of them, these being generally found
in the central white substance. The convolutions of the cortex
of the brain, and the cortex of the cerebellum, are usually
exempted. A considerable number of nodules are generally
found in the pons, medulla oblongata, and peduncles of the
cerebrum and cerebellum.

The nerves themselves may be affected by patches of sclerosis ;
the cranial nerves in their passage along the base of the skull
are specially liable to be affected. The anterior and posterior
roots of the spinal nerves have been found diseased.

The membranes of the brain and spinal cord are frequently
normal, but at other times they present evidences of hypersemia
and chronic inflammation. The cerebro- spinal fluid is generally
increased, often cloudy, and the ventricles are dilated. Bed-
sores, pyelo-nephritis, and evidences of pyaemia or of an inter-
current disease are usually observed at the autopsy.

On microscopical examination the sclerosed patch is found to
present the usual appearances of chronic interstitial myelitis.
The trabeculse of the neuroglia are thickened, the nuclei are
swollen and increased in number, while Deiter's cells are nume-
rous,'large, and sharply-defined. The medullary sheath of the
nerve-fibres is gradually destroyed, but the axis-cylinder per-
sists for a long time. Ultimately the nodule consists of a wavy
fibrillated connective tissue, in which all trace of nerve structure
is lost. The walls of tbe vessels are thickened and the lumen
is diminished, while tbe adventitia becomes blended with the
connective tissue, and the surrounding lymph -channels are
obliterated; An infiltration of fat into the lymph -channels
surrounding the vessels has been described, but this appearance
is probably produced by methods of histological preparation.
If the sclerosis extend into the grey substance, the ganglion
cells become degenerated and atrophied.

§ 894. Morbid Physiology . — Multiple sclerosis is a compound
affection, and the implication of several of the functional systems
of the spinal cord affords a ready explanation of a large number
of the symptoms.

The paresis, contractures, excess of the tendon-reflexes, and
the phenomena grouped under the name of spinal epilepsy are

MULTIPLE SCLEROSIS.

811

caused by implication of the lateral columns ; the ataxic symp-
toms are produced by the formation of nodules in the posterior
columns ; muscular atrophy by invasion of the anterior cornua ;
while impairment of speech, disturbances of respiration, diffi-
culty of deglutition, and other bulbar symptoms are caused by
disease of the nuclei in the medulla oblongata and pons. The
nystagmus is caused probably by the presence of nodules in the
corpora quadrigemina or peduncles of the cerebellum ; whilst
impairment of smell and taste, diplopia, facial and other para-
lyses, and amblyopia are often produced by sclerotic patches on
the cranial nerves themselves as they pass along the base of the
skull. Vertigo may be occasionally due to an existing diplopia,
but it is generally the result of nodules in the cerebellum.

The psychical disturbances are doubtless caused by the
development of nodules in the hemispheres of the brain.

The apoplectiform attacks are difficult to explain, but the
most usual explanation is that they are occasioned by attacks
of cerebral congestion. This opinion is, however, opposed by
Charcot, who was unable to discover any evidence of congestion
or oedema of the brain in cases which terminated fatally. He
thinks that these attacks are only observed in cases in which
the pons and medulla oblongata are diseased.

The cause of the characteristic tremor of multiple sclerosis is
very obscure. Charcot attributes it to the long persistence of
the axis-cylinders in the nodules of sclerosis. Conduction
through these may still take place, although when once the
medullary sheath is destroyed the conduction will be so retarded
that the impulses from the cortex do not pass in a sufficiently
quick succession to cause a continuous contraction. On the
other hand, it is asserted that in purely spinal cases the charac-
teristic tremors are absent (Hammond, Ebstein), and that they
are never present unless the pons and the parts of the brain
situated in front of it are affected (Ordenstein). Erb examined
twenty-two recent cases with the view of deciding this question.
In all the cases in which the tremors were present during life,
the pons, medulla oblongata, crura cerebri, and other parts of
the brain were involved in the sclerosis y while in the cases in
which there were no tremors the nodules were absent or only

812

MULTIPLE SCLEROSIS.

present in small numbers in the pons, medulla oblongata, and
cerebellum, although other parts of the brain were affected.

§ 895. Diagnosis — Multiple cerebro-spinal sclerosis and para-
lysis agitans have only been distinguished from one another in
recent years. The tremor of paralysis consists of fine rapid oscil-
lations ; it persists during repose, may be temporarily arrested
by a voluntary effort, and never implicates the muscles of the
head ; while the tremor of multiple sclerosis is more extensive,
ceases during rest, is excited or aggravated by voluntary move-
ments, and invariably implicates the muscles of the head. Para-
lysis agitans is a disease of advanced age, and multiple sclerosis
of youth and middle age. In the former paralysis is not
developed until long after the appearance of tremor; while in
multiple sclerosis the paralysis precedes or soon follows the
tremor. The cerebral symptoms of multiple sclerosis already
described are wanting in paralysis agitans.

The spinal form of multiple sclerosis may be mistaken for
locomotor ataxia ; but in the former disease the ataxic gait
may be associated with excess of tendon-reflex, tremor, early
appearance of paralysis, scanning speech, nystagmus, or other
symptoms which do not belong to locomotor ataxia.

The cases of hereditary ataxia described by Friedreich are,
owing to the presence of nystagmus, very liable to be mistaken
for multiple sclerosis ; but in the latter early paralysis, con-
tractures, excess of tendon-reflex, scanning speech and other
bulbar symptoms, and apoplectiform attacks and other cerebral
disturbances are absent. The spinal form of multiple sclerosis
is most liable to be mistaken for primary lateral sclerosis, and
in some cases a diagnosis is impossible. If, in addition to the
well-known and classical symptoms of lateral sclerosis, other
symptoms, as scanning speech and tremor, be present, then
multiple sclerosis ought to be suspected.

When the grey substance of the spinal cord and medulla
oblongata is involved, multiple sclerosis may be mistaken for
progressive muscular atrophy, progressive bulbar paralysis, or
amyotrophic lateral sclerosis ; but the course and symptoms of
multiple sclerosis render it easily distinguishable from the other
affections.

MULTIPLE SCLEROSIS.

813

Certain affections accompanied by trembling, as senile, mer-
curial, and saturnine tremor, bear some resemblance to
multiple sclerosis; but the diagnosis, as a rule, presents no
difficulty. I have, however, seen a case of mercurial tremor
which could only be distinguished from a moderately ad-
vanced case of multiple sclerosis, by the history of the case
and by the beneficial effects of treatment. Tremor in hysterical
subjects may likewise be mistaken for that of multiple scle-
rosis ; in the former the tremor persists during repose provided
the patient be conscious of being observed, it may disappear for
days or weeks and then recur, and general hysterical symp-
toms are usually present. The disorderly movements of chorea
differ considerably from the tremor of multiple sclerosis, but the
diagnosis is not always easy when, as may occasionally happen,
choreiform movements complicate those proper to multiple
sclerosis.

§ 896. Prognosis. — The prognosis is always unfavourable,
but it must be remembered that the course of the disease is
often interrupted by remissions and partial ameliorations of the
symptoms. The prognosis in each case will depend upon the
presence or absence of bulbar symptoms, apoplectiform attacks,
cystitis, bed-sores, and other symptoms which are known to
threaten life.

§ 897. Treatment. — The treatment of multiple sclerosis is
essentially the same as that of chronic myelitis, our therapeutic
means being even more limited in the former than in the latter
disease. Arsenic, belladonna, bromide of potassium, ergot, and
strychnine have proved useless in the hands of Charcot, while
the disease was aggravated by chloride of gold and phosphate
of zinc. Nitrate of silver appeared to produce a favourable
effect, which, however, was maintained only for a short period.
Hammond recommends three-quarters of a grain of chloride of
barium three times a day. The most promising treatment
appears to be the persistent application of the galvanic current
to the spine, hydropathy, nitrate of silver, phosphorus, cod-liver
oil, and nourishing but unstimulating diet.

814

CHAPTEE II.

CHOREA, AND MENIERE'S DISEASE.

• (I.) CHOREA.

Two forms of chorea are often described, named respectively
chorea major and chorea minor, but the former is only an
aggravated form of hysteria, and consequently the latter alone
will here be described under the name of chorea. It is a disease
which chiefly attacks children, and is characterised by irregular
clonic spasms of certain groups of voluntary muscles.

§ 898. Etiology. — Heredity plays an important part in the
production of chorea, but the transmission is probably always
indirect. The patient may inherit either a susceptible nervous
system, or the rheumatic diathesis — rheumatism being one of
the most frequent and important causes of the disease. Age
is an important predisposing cause of chorea, the disease
generally occurring during the period of bodily development.
Isolated cases of the affection have been observed in infants
at the breast, while it is not uncommon in young women. Se'e
states that three-fourths of the cases observed in the Children's
Hospital in Paris occurred in girls.

Everything which augments the excitability of the nervous
system during the period of sexual development, as premature
excitement of the sexual passion, onanism, or any undue
emotional disturbance, increases the tendency to chorea. The
most usual predisposing causes of the affection in adults are
pregnancy, menstrual disorders, and chlorosis.

Very little is known with regard to the geographical distri-
bution of the disease, or the influence exerted by the different

CHOREA.

815

seasons and atmospheric changes in its production. That some
causal relationship exists between articular rheumatism and
chorea has been known since the beginning of the century,
but the true nature of this relationship is not yet accurately
ascertained. The frequent occurrence of cardiac murmurs in
chorea was noticed by Addison and subsequently by Todd. Out
of 299 cases collected by Hughes and Brown, there were 104
whose history could be carefully ascertained, and of these only
15 had not suffered from rheumatism or had not developed
cardiac murmur. Out of 128 patients suffering from chorea
See found 64 who had suffered from articular rheumatism.
Chorea occurs frequently after scarlatina, a fact which may
probably be explained by the frequency with which the latter
is followed by rheumatism.

The relationship between pregnancy and chorea is very
obscure, inasmuch as it is only in a small number of cases that
the attack has been preceded by rheumatism or endocarditis.
Chorea occurs most frequently during first pregnancies, although
it is sometimes repeated in the same patient in subsequent
pregnancies, and the majority of those affected are from twenty
to twenty-three years of age. It appears more frequently during
the first than the second half of pregnancy, but sometimes it
begins in the later months and may continue up to the time of
delivery or even beyond it.

Of the exciting causes of chorea the most frequent and
important are emotional disturbances, such as fright, sorrow,
and discontent. Hysterical girls and those who are strongly
predisposed to chorea, or who have already suffered from an
attack, may acquire the disease by imitation of those suffering
from it.

§ 899. Symptoms. — The development of the characteristic
phenomena of chorea is generally preceded by various premoni-
tory symptoms for a variable period of days or weeks. The
most usual of these are afforded by changes in the character
and disposition of the patient, who becomes forgetful, inatten-
tive, fretful, and discontented or apathetic, while the intellectual
powers are impaired. The spasmodic movements may in some
cases be preceded by paralytic phenomena. A case under my

816

CHOREA.

care at the Manchester Southern Hospital was admitted as one
of hemiplegia, and it was only two days after admission that
the characteristic choreic movements made their appearance.
The irregular spasmodic muscular contractions of chorea are,
indeed, not unfrequently ushered in by a slight dragging of one
of the lower extremities, with a tendency to walk in a curved
line and liability to let objects fall from the hand. These
manifestations of the approaching- disease are probably due, in
some degree, to irregular muscular contractions, but are largely
dependent upon muscular weakness. The characteristic choreic
movements generally begin in the small muscles of the face
and in those of a hand. They consist at first of grimaces and
other contortions of the face, and slight jerking movements of
the fingers and at the wrist joint, with pronation of the fore-
arm, when the patient is conscious of being observed or is
excited from any other cause ; these soon increase in intensity
and persist during repose.

The irregular contractions soon extend so as to involve all
the voluntary muscles, when the affection may be called
general chorea, or they remain more or less limited to the
muscles of one-half of the body, when the disease is called
unilateral chorea or hemichorea.

General Chorea. — When once the disease is fully established
the symptoms are quite characteristic, and it would be difficult
to find phrases more expressive of the disorderly muscular move-
ments than " insanity of the muscles," adopted by Bellingham,
and " folie musculaire " byt Bouillaud.

The features undergo every variety of contortion. The brow
is knit and immediately expanded; the eyebrows are elevated
and the next moment depressed, or one may be elevated while
the other is lowered ; the eyelids open and close alternately ; the
eyeballs are quickly rotated in different directions ; the labial
commissures are suddenly drawn outwards, and as quickly
retracted. These opposite movements succeed one another with
such rapidity that the face presents in quick succession the
most contradictory expressions, such as those of delight, vexatioD,
and anger.

The tongue is thrust out of the mouth, and quickly retracted
and rolled about from side to side ; the jaws are separated and

CHOREA.

817

closed, it may be with so much violence that teeth are broken,
or the tongue and cheeks are severely bitten ; lateral displace-
ments of the lower jaw are frequently observed, and the head
is jerked suddenly from one side to the other, while the facial
grimaces by which the movements of the jaws, tongue, and head
are accompanied add to the comical appearance presented by
the patient.

The superior extremities execute every variety of movement,
the shoulders are elevated, then lowered, and immediately after-
wards drawn backwards or forwards ; the arm and forearm are
moved at the shoulder and elbow joint in every possible
direction ; the hand is alternately pronated and supinated,
flexed and extended ; and the ringers are at one moment
extended and spread apart and at the next flexed. These
movements are combined in such varied ways that a gesticu-
latory agitation is produced which defies description.

The muscles of the trunk are implicated, and their unequal
disorderly contractions produce sudden lateral and antero-
posterior deviations of the vertebral column, which in certain
cases may be so violent that the patient is thrown from his
chair or out of bed. The muscles of the lower extremities also
undergo irregular contractions, causing eversion and inversion
of the foot and various contortions of the toes, as well as move-
ments at the larger articulations. Choreic movements cease as
a rule during sleep and under the influence of chloroform, but
in aggravated cases they may continue during sleep ; the pupils
are usually dilated, and their reaction to light is diminished.
The respiratory rhythm becomes irregular and jerky, and on
laryngoscopic examination the vocal cords have been observed
to act in an irregular and disorderly manner (von Ziemssen).

Most of the irregular movements just described may occur
during repose, although they are much exaggerated when the
patient is under observation or excited in any way. When,
however, the patient endeavours to execute a voluntary move-
ment, the motor disorder becomes, as a rule, greatly increased.
A distinction has been drawn by Dr. Gowers between the
choreic movements that occur during repose, and the motor
inco-ordination observed during attempts at voluntary move-
ments which may be called choreic ataxia ; but whether this

AAA

818

CHOKEA.

distinction be valid or not, it is undoubted that great motor
co-ordination during attempts at voluntary movement may be
present in cases in which the choreic movements of repose are
slight ; and, conversely, the voluntary in co-ordination may be
slight in cases in which the choreic movements of repose are
excessive. In cases of moderate intensity delicate manual
operations, such as those required for writing, sewing, and
playing upon musical instruments, alone become impossible;
while operations, like eating, requiring less complicated adjust-
ments for their performance, are still effected, although in an
imperfect and round-about manner, and after frequent interrup-
tions from the involuntary contraction of antagonistic muscles.

In aggravated cases it becomes impossible to execute almost
any intended movement. When the patient endeavours to
carry anything to his mouth, such as a glass of water, the
progress of his arm is arrested by a series of jerks and
contradictory movements which may scatter the contents of
the glass in every direction; the patient cannot button and
unbutton his clothes ; the maintenance of the erect posture is
difficult or impossible ; and even in the recumbent posture he
is not free from the danger of being thrust out of bed; his
clothes and linen become worn out by constant rubbing ; and
the skin over the prominent bones becomes erythematous and
may ulcerate.

On the patient being asked to show the tongue he protrudes
it with a jerk, the mouth being opened to an unnecessary
extent ; the tongue is immediately withdrawn, while the mouth
and jaws close upon it with violence. When the patient en-
deavours to speak the convulsive action of the facial muscles
becomes aggravated; his articulation is irregular, jerky, drawl-
ing, or stammering ; his voice is monotonous ; and in aggra-
vated cases his speech is so disordered as to be almost if not
entirely unintelligible. Spasmodic contraction extends to the
muscles of mastication and deglutition, and consequently these
functions are performed imperfectly and with difficulty.

Hemichorea. — The spasmodic phenomena are sometimes
limited to the muscles of one-half the body, the unilateral
variety occurring in about one-fifth of all cases. Some authors
state that the left and others that the right is more frequently

CHOREA.

819

affected, but there does not appear to be a great difference
between their relative liability. Broadbent asserts that the
muscles bilaterally associated in their actions, and which are
comparatively spared in hemiplegia, are affected to some extent
on both sides in hemichorea.

The other symptoms of hemichorea are the same as those of
general chorea, and do not require separate description.

Although spasmodic motor disturbance constitutes the most
characteristic feature of chorea, it must not be forgotten that
a certain degree of muscular weakness is always present, this
being easy of recognition in cases of hemichorea. Indeed,
towards the termination of the affection or during its course,
the choreic movements may be replaced by a more or less
complete hemiplegia or paraplegia, and we have already seen
that paralytic symptoms may precede the development of the
characteristic movements.

The electric excitability of the nerves and muscles is said to
be increased to both currents, a fact more readily proved in
hemichorea than in the bilateral variety (Rosenthal, Gowers).

The reflex excitability is said by some authors to be increased
and by others to be diminished.

Sensory disturbances are not frequently observed in chorea.
Painful points have been found at times in the course of the
nerve trunks of the affected region, while tenderness on pressure
over the spinous processes of some of the vertebrae is occasionally
met with. At other times cutaneous hyperaesthesia or hyperal-
gesia distributed over half or the whole of the body has been
observed, but anaesthesia of like distribution is more common.

Vaso-motor and secretory disturbances are wanting, there are
no special trophic changes, and the general health does not
suffer, except in aggravated and chronic cases, in which the con-
stant agitation and want of sleep induces a condition of anaemia
and general marasmus.

Psychical disturbances are invariably observed in chorea.
The mental depression and irritability with which the disease
begins usually increase during its course. The patient is obsti-
nate, taciturn, and even violent towards parents and attendants.
He suffers from impairment of memory, incapacity for thinking,
and general intellectual weakness. At times there may be

820

CHOREA.

hallucinations of sight, especially at night, succeeded by a
maniacal delirium, and according to the observations of Marcd,
half of the cases, in which this delirium supervenes, terminate
fatally.

The pulse may be irregular, and the patient suffers from
palpitation, while a physical examination of the heart gene-
rally reveals the presence of endocardial murmurs, either arising
from disease of the valves or of functional origin. Chorea is
not usually accompanied by pyrexia, but in severe cases, where
there is violent muscular action, elevation of temperature is not
uncommon. When it is associated with acute rheumatism, more
or less fever is necessarily present.

§ 900. Course, Duration, and Results. — Chorea, as a rule,
runs a chronic course, lasting in the majority of cases from six
to eight weeks ; while aggravated cases may continue for four
to five months. The disease may, indeed, last many years, and
it is probable that such cases are the result of permanent ana-
tomical lesions in the nervous system.

The course of the disease is seldom uniform, and relapses
are frequent ; slight emotional disturbances often aggravate the
symptoms or induce a relapse during convalescence.

Chorea frequently recurs at varying intervals. The recurrent
attack may be induced by emotional disturbance, by pregnancy,
or by the presence of an acute disease. Most of the relapses
occur during puberty, but among persons who were choreic at
or before this period they may appear at from twenty to thirty
years of age or later.

The disease generally terminates in complete recovery, but
a nervous fidgetty manner, exhibiting itself in slight grimaces,
needless haste, and want of precision in executing certain move-
ments, often remains for years.

Termination in imperfect recovery is rare. Sometimes, how-
ever, a few symptoms of chorea may persist, paralysis may
develop in the half of the body which has been most affected,
or permanent mental disease, such as mania, melancholia, or
general paralysis of the insane become established. Death is
extremely rare in children in uncomplicated cases, but when
the disease is complicated with rheumatism and endocarditis it

CHOREA.

821

is not unfrequently fatal. Sde found a mortality of 57 per cent
in the chorea of children ; whilst the statistics of Wenzel give
a mortality of 273 per cent in the chorea of pregnant women.
The cause of death in chorea is generally to be assigned to
various complications, but occasionally to the intensity of the
disease itself. In the latter cases the symptoms are unusually
acute and violent from the first, and attain excessive severity
in a few days ; the choreic movements cease either suddenly or
gradually and collapse sets in, along with complete muscular
relaxation and involuntary evacuations, and death follows
preceded by coma.

§ 901. Morbid Anatomy. — In the old observations of
Cruveilhier, Komberg, and others, foci of softening were found
in various parts of the brain, but the absence of a careful
microscopical examination greatly diminishes the value of these
records. Brown-Se'quard and Gendron observed softening of
the spinal cord. Tuckwell in 1867 found, at the post-mortem
examination of a patient dead of chorea, fibrinous vegetations
on the valves of the heart, a branch of the middle cerebral and
another of the posterior cerebral artery occluded by emboli, and
foci of red softening in the cortex of the brain corresponding to
the distribution of the occluded vessels. It may be noticed in
passing that Kirkes had suggested in 1850 and again in 1863
that the well-known relation between rheumatism and chorea
would be found in the endocarditis caused by the former, giving
rise in its turn to multiple embolism of the vessels of the brain.
Ogle published in 1868 an analysis of ninety-six cases of chorea.
Sixteen of these were fatal, and a post-mortem examination
of them was obtained. Cardiac lesions, consisting of fibrinous
deposits on the valves, were found in ten cases only. In six
congestion of the nervous centres was noted. In a girl of
seventeen who died from maniacal chorea during pregnancy,
hyperemia of the surface and softening of other parts of the
brain were observed. The anterior column of the spinal cord
in the lower dorsal region, on a level with the ninth dorsal
nerves, was swollen and softened. A microscopical examination,
conducted by Lockhart Clarke, revealed softening of the white
substance and extravasations of blood, with granular exudation.

822 CHOREA.

Steiner, in 1868, published the results of the post-mortem
examination of three cases of chorea. He found cerebro-spinal
anaemia, effusion of serum into the spinal canal, and proliferation
of the connective tissue in the upper half of the spinal cord in
one case, and in another hyperaemia of the spinal cord and
brain, including their membranes, and an accumulation of fluid
blood about the roots of the cervical and upper dorsal nerves.
Evidences of endocarditis were found only in one of these cases.
Fatal cases of the chorea of pregnancy, in which no signs
of endocarditis were observed, have been recorded by Wilks,
Lawson Tait, and Barnes. Aitken found the specific gravity of
the corpora striata and optic thalami of a person dead of chorea
much less than that of other parts of the same brain, and of the
same parts in healthy brains. Numerous changes were found
in the brain and spinal cord by Meynert in chorea. The main
changes consisted of hyaline swelling with molecular degenera-
tion of the protoplasm of the cells of the cortex of the brain,
partial sclerosis of the cells of the cortex of the island of Reil
and of the basal ganglia, and multiplication of the nuclei of the
nerve cells. He also found great multiplication of the nuclei of
the neuroglia and swelling of Deiter's cells in the spinal cord. tl
Elischer found, in a pregnant woman dead of chorea, nuclear
proliferation, hyperplasia of the connective tissue, and thickening
of the tunica adventitia of the small vessels in the corpus
striatum, and division of the nuclei of the nerve cells in the
claustrum. The spinal cord presented thickening and nuclear
proliferation in the walls of the vessels, thickening of the epen-
dyma of the central canal, and nuclear proliferation of the con-
nective tissue around the nerve cells of the grey matter. The
cells themselves presented a dull appearance, were destitute of
nuclei, and filled with pigment. The white substance was
hypersemic, and the lateral and posterior columns contained
a fibrillated tissue with abundant nuclei. The fibres in the
peripheral nerves were diminished in number.

A valuable paper on " The Pathology of Chorea" has recently
been contributed by Dr. Dickinson, in which the results of the
post-mortem examination of seven fatal cases of chorea are
recorded. The changes described consist of dilatation of the
medium-sized arteries and veins throughout the substance of

CHOREA.

823

the brain and spinal cord, exudations or small haemorrhages
indicated sometimes by the presence of blood crystals, into the
tissues surrounding: the distended vessels, and in chronic cases
patches of sclerosis in the neighbourhood of the vessels. These
changes were most pronounced in the corpora striata and optic
thalami, the anterior perforated spaces, and at the junction of
the posterior grey horns and central columns of the spinal cord,
especially in the upper dorsal and cervical regions. In one case
the central canal of the dorsal region of the spinal canal was
greatly distended by bloody serum. "Speaking generally,"
says Dr. Dickinson, " the chosen seats of the choreic changes
are the parts of the brain which lie between the beginning of
the middle cerebral arteries and the corpora striata — the partes
perforatae ; and in the cord the central portion of each lateral
mass of grey matter comprising the root of each posterior horn."
It will be evident how these observations of Dr. Dickinson bear
out the theory advanced in these pages as to the great patho-
logical importance of the parts of the nervous system which I
have termed accessory.

A microscopical examination of the nervous system in a case

Fig. 283.

Fig. 283 (Young). Section of the Cervical Region of the Spinal Cord from a case of
Chorea.— cc, Central canal ; A. and P, Anterior and Posterior horns respectively.

824

CHOREA.

of fatal chorea, which I had the opportunity of making, enables
me to confirm to a large extent the statements of Dr. Dickinson.
In the cases he describes periarterial erosions and haemorrhages
occurred around the central artery and its primary branches,
while in my case the most pronounced changes were found in
the anterior and antero -lateral arteries. All the vessels of the
cord were more or less distended with red blood corpuscles, but
in some sections a fibrinous plug was observed in the anterior
or antero-lateral arteries, the vessel being distended by it {Fig.
283). Spots of necrotic softening were observed in the corpora
striata. A section of the spinal cord from a case of chorea was
exhibited by Dr. Bury at the Manchester Microscopical Society,
in which the periarterial exudations and haemorrhages round the
branches of the central artery were distinctly shown (Fig. 284),

Fig. 284.

Fig. 284 (Bury). Section of the Anterior Grey Horn of the Cervical Enlargement of
the Spinal Cord from a case of Chorea that died on the fourth day of Scarlet
Fever. — cc, Central canal ; ac, Anterior commissure ; A, Anterior horn.

and corresponded accurately to the description and drawings of
Dr. Dickinson. But although no decided changes were observed
in the tissues near the central artery of the spinal cord in the
case examined by me, I was struck with the alterations presented
by the accessory cells of the anterior grey horns in comparison
with the fundamental cells. The accessory cells could not be

CHOREA.

825

seen with a low power, and are therefore not represented in
the diagram ; but with a higher power they appeared shrivelled,
their protoplasm was granular, the nuclei were obscure, and
many of the processes were indistinct or absent. The larger
fundamental cells did not appear much altered. Of twenty-
two fatal cases of chorea collected by Dr. Dickinson the heart
was found healthy in five only, and of these one only was a
child. As Dr. Dickinson remarks, endocarditis appears to be an
almost invariable accompaniment of fatal chorea in children,
while beading of the mitral valve with lymph is probably
present in every instance of cardiac complication. In the case
observed by me the free edges of the mitral valve were fringed
by a row of fibrinous beads.

§ 902. Morbid Physiology. — In 1868, Broadbent and
Hughlings- Jackson almost simultaneously advanced the hypo-
thesis that the corpus striatum and optic thalamus are the
main centres in which the lesions in chorea are localised.
Hugh lings- Jackson surmised that the convolutions of the cortex
situated near the corpus striatum were also involved in the
disease. The observations of Meynert, Dickinson, and others
confirmed by the case examined by myself, prove that the
lesions are widely distributed throughout the brain and spinal
cord.

An endeavour has been made to determine the localisation of the
lesion in chorea by experimental investigation. Chauveau divided the
spinal cord close to the skull in a dog suffering from general chorea, and
found that the choreic movements continued unabated until the death of
the animal several hours after the operation. The convulsive movements
of the tail and posterior extremities ceased immediately on the spinal cord
being divided in the dorsal region. From the results of these experiments,
Chauveau concluded that the spinal cord is the seat of the lesion. Similar
experiments were conducted by Longet, Bert, and Carville, and the same
conclusion arrived at.

Legros and Onimus found that irritation of the posterior columns of
the exposed cord with the scalpel increased the twitchings. The choreic
movements ceased on the cord being exposed to a current of cold air,
and reappeared on its being subsequently moistened with warm water.
Section of the posterior roots did not exert any influence on the choreic
movements. Partial removal of the posterior cornua and columns
weakened, and complete excision of them abolished the movements. An

826

CHOREA.

ascending galvanic current through the cord increased the intensity and
frequency of the contractions ; while a descending current weakened
them considerably. The authors conclude from these experiments that
the morbid process in chorea implicates the nerve cells of the posterior
grey cornua of the spinal cord, or the nerve fibres which unite them with
the cells of the anterior cornua. Kosenthal injected fine flower seeds into
zhe left carotid artery of a dog suffering from choreic movements of the
right fore-leg. All voluntary movements were instantly arrested, but
choreic movements became much stronger in the affected extremity, and
involved the eyelids and tail, lasting until the animal died two days
subsequently. The autopsy revealed encephalitis of the left anterior lobe,
softening of the left corpus striatum, and embolism of the left Sylvian
artery. A microscopic examination conducted by Dr. Scheiber showed
spots of proliferated connective tissue in many parts of the brain sub-
stance. Canine chorea is by no means the same disease as that of the
same name in man, and it would be hazardous to attach much importance
to any of these experiments.

The nature of the lesion in chorea has been a subject of as
much controversy as its localisation. The relation between
rheumatism and chorea had been known for a long time, and
Bright went so far as to assert that rheumatic pericarditis was
the most frequent cause of chorea. In 1850, and again in 1863,
Kirkes suggested that endocarditis was the causal link between
rheumatism and chorea. According to this opinion, chorea
was caused by embolic particles washed off from the inflamed
endocardium and arrested in the vessels of the brain and spinal
cord. Hughlings-Jackson adopted this view, and in 1868 he
advanced the opinion that chorea was caused by multiple
embolism of the nutritive arteries of the basal ganglia and
convolutions of the cortex of the brain situated near to the
corpus striatum. It cannot be doubted that embolism of the
vessels of the nervous centres does occur at times in chorea,
inasmuch as some of the vessels of the brain have been found
actually occluded by an embolus in fatal cases, while the con-
dition liable to occasion embolism is present in a very large
proportion of fatal cases. On the other hand, in some fatal
cases there has been an entire absence of cardiac complication.
Again, of the large majority of cases which recover, although a
cardiac complication is frequently present, yet this is by no means
invariable. It may, therefore, be concluded that although chorea
may be caused by multiple embolism of the vessels of the nervous

CHOREA.

827

system, yet the affection may occur in the absence of embolism,
and it is not, therefore, the essential condition upon which the
disease depends. Similar reasoning applies to the opinion of
the humoral pathologists, who believe that chorea is caused
by the rheumatic diathesis, or by the poison of rheumatism
circulating in the blood, producing irritation of the tissues
of the nervous system. Chorea may occur in the absence
of a history of active rheumatism. "We see in chorea,"
says Dr. Dickinson, " a widely distributed hyperemia of the
nervous centres, not due to any mechanical mischance, but
produced mainly by causes of two kinds — one a morbid, pro-
bably a humoral, influence, which may affect the nervous centres
as it affects other organs and tissues ; the other, irritation in
some mode, usually mental, but sometimes what is called reflex,
which especially belongs to and disturbs the nervous system,
and affects persons differently, according to the inherent
mobility of their nature."

To turn to the first factor, it must be remembered that dis-
tension of the blood vessels of the nervous system after death
by no means proves the existence of an active hyperemia during
life. The conditions usually present, such as cardiac disease,
are such as to cause anaemia of the nervous system, and the
phenomena of chorea are best explained on the supposition
that the excess of irritability of the nervous centres is caused
by defective nutrition of their tissues.

With regard to the second factor, the profound mental im-
pression causing chorea is usually fright, one of the depressing
passions, which is certainly more calculated to exhaust the irri-
tability of the nervous system than to maintain it in a state of
continuous activity through irritation. Reflex irritation is also
more likely to act by causing anaemia rather than hyperaemia.

The third co-operating factor — inherent instability of the
nervous centres — is a very important one. It is probable that
the children in some families inherit an unstable nervous sys-
tem, which renders them liable to be directly affected by chorea,
but this has not been definitely proved as yet. It is not doubted,
however, that an inherent tendency to develop the disease
at a certain age exists. As Dr. Dickinson remarks, " Every
period of life has its own regions of nervous susceptibility : in

828

CHOREA.

childhood the motor; in adolescence the emotional; in advan-
cing years the mental, and coevally, or nearly so, that part of
the nervous mechanism which instigates glycosuria. Much the
same mental impression may make a child choreic, a girl hyste-
rical, or a man diabetic." In chorea the sensory and psychical
functions of the nervous centres are disturbed, but the great
weight of the disease falls upon the motor functions, and of the
latter the last-developed co-ordinations of the muscles of the
hand and of the face and tongue are implicated in a special
degree.

We have already seen that the most pronounced lesions in
chorea are found in what I have called the embryonic portions
of the motor area of the cortex and corpus striatum, and of the
motor grey matter of the cord, and consequently whether chorea
be viewed functionally or structurally, it appears to be a widely
distributed disease of the nervous centres, in which the cerebro-
spinal motor functions and mechanisms are specially affected,
the accessory functions and structures being affected at an
earlier period and more profoundly than the fundamental
functions and structures. I came to this conclusion after
making a microscopical examination of the nervous system in
the case above referred to, and was not aware at the time that
Hughlings- Jackson, approaching the subject from the clinical
standpoint, had come to practically the same conclusion upwards
of ten years before. " Since the disorder in chorea," he says, " is
of movements which are acquired, and which are probably only
fully learned by a long apprenticeship, I used to suppose that
the nervous arrangements for these movements were but par-
tially developed in children, and that the motor processes
involved, and their arterial integration, would be, so to speak,
caught in a stage of incomplete development — in short, that
their centres were diseased when /&<x£/-educated." In the same
paper he attributes the symptoms to " under-nutrition" of the
tissues affected.

§ 903. Diagnosis. — The diagnosis of chorea can hardly
present any difficulty. Paralysis agitans occurs in the later
years of life, and the attitude of the patient and his mode of
locomotion are so characteristic that this disease is no more

CHOREA.

829

likely to be mistaken for chorea than is the tremor associated
with old age, and with chronic poisoning by alcohol, lead, or
mercury. The spasmodic movements occurring in groups of
muscles supplied by certain nerves, such as convulsive tic, and
those occurring in definite groups of muscles engaged in per-
forming certain actions, as in the case of writer's cramp, are
also separated from the movements of chorea by broad lines of
demarcation.

§ 904. Prognosis. — The prognosis of chorea is, as a rule,
favourable. It becomes grave, however, when the movements
are so violent as to exhaust the patient, cause sleeplessness, and
prevent sufficient food being taken, or when there is delirium.
The chorea of pregnancy is much more fatal than that which
occurs about and before puberty.

§ 905. Treatment — In the treatment of chorea the diet
should be carefully regulated; and any source of reflex irritation,
such as intestinal worms, should be removed. If anaemia be
present, iron may be given, either alone or along with cod liver
oil ; while if rheumatism complicate the case, salicylate of soda
must be administered. The use of the hot vapour bath has
been much praised in the treatment of chorea, and it is worth a
trial in cases in which a rheumatic diathesis can be traced, even
if there be no active rheumatism at the time of the attack.
The child should be immediately removed from school, all in-
tellectual work suspended, and even bodily exertion avoided in
the early stage of the disease.

The medicines which appear to do most good are the nervine
tonics, and of these arsenic is probably the best. Ziemssen
recommends a dose of from five to eight drops of Fowler's
solution for children, and eight to twelve drops for adults.
Most practitioners will be inclined to begin with a smaller
dose and gradually increase it. Iron may be combined with
arsenic if the patient be anaemic and the stomach bears it well.
If the arsenic has not produced a decided improvement in the
symptoms within a period of a week or ten days, zinc may be
substituted, the sulphate being the most convenient preparation
and as successful as any other. A dose of two or three grains

830

Meniere's disease.

may be given at first three times a day, but this dose must be
gradually increased daily ; if nausea or vomiting be produced,
the dose should be slightly diminished for a few days until
tolerance is established. After this it should be again gradually
increased until the symptoms begin to improve, and then con-
tinued without alteration until improvement ceases or the
disease subsides. The tolerance for the drug becomes so great
after a short time that 15 to 20 grains may be given three
times a day to a patient 15 years of age, without nausea or any
other ill effects being produced. I have made a fair trial of
the valerianate and the bromide of zinc, but have not found
these salts to be in any way superior to the sulphate. Bromide
of potassium does not appear to me to exert any favourable
influence on the progress of the disease, but it may be usefully
administered with or without chloral when psychical distur-
bance and sleeplessness are prominent symptoms.

(II.) MENIERE'S DISEASE.
(Auditory Vertigo.)

§ 906. Definition. — Meniere's disease is characterised by
attacks of vertigo, associated with noises in one or both ears,
and partial deafness.

§ 907. Etiology. — All the causes which produce disease of
the peripheral organ of hearing may occasion auditory vertigo,
and they need not, therefore, be enumerated here.

§ 908. Symptoms. — The characteristic symptoms of Meniere's
disease are sometimes preceded by partial deafness, earache,
and other indications of a local lesion of the peripheral organ
of hearing. In other cases the patient is suddenly attacked
with noises in one ear, and a feeling of giddiness, attended by
faintness, nausea, and vomiting. The attack passes off in a
few seconds or minutes, but recurs after a variable period, the
paroxysms becoming more aggravated and more frequently
repeated as the disease advances.

The noise is sometimes heard in both ears, but it is probably
always more pronounced on one side than the other. It is

Meniere's disease. 831

sometimes compared to the loud whistling of a steam engine,
at other times to a succession of explosions, and it is often
described as a continuous humming or buzzing. The noises in
the ear cease with the attack of vertigo, in recent or slight
cases ; but in aggravated forms of the affection they continue
to distress the patient during the intervals.

The attack of vertigo varies in duration and intensity. In
slight cases it consists of a momentary feeling of swim-
ming in the head, in severe cases each paroxysm may extend
over a period of ten or more minutes, while in still more aggra-
vated cases the feeling of uncertainty and giddiness is never
absent during waking hours, and every effort on the part
of the patient to assume the erect posture determines the
vertigo along with nausea and vomiting. During the paroxysm
the patient feels as if he were falling forwards, backwards,
or laterally, or were rotating round a vertical or hori-
zontal axis ; he staggers and clutches at surrounding objects
for support, or actually falls in a direction corresponding
with his sensations. The patient during the paroxysm feels
faint; the skin becomes pallid, cold, and covered with sweat;
the pulse is feeble and flickering; and there is an intense feeling
of nausea, which often terminates in vomiting, when the
attack usually comes to an end. Actual syncope may occa-
sionally occur, and there may be transitory loss of conscious-
ness, but this is exceptional. The patient, however, during the
paroxysm suffers from confusion of ideas, and* in the worst
cases any unusual intellectual effort may determine an attack
of vertigo.

Oscillatory movements of the eyeballs have been observed by
Schwabach and Hughlings- Jackson during the attack. In the
case observed by Schwabach, as quoted by Hughlings-Jackson,
the eyes were turned towards the affected side and slightly
downwards ; while in the case observed by Hughlings-Jackson
himself, c: each eye was partially and very slightly rotated to
the right in frequent jerks from left to right," the left ear being
the diseased one. During the attacks there was an apparent
displacement of objects with reference to the patient; and in
the case described by Hughlings-Jackson, objects were said
to revolve, contrary to what might have been expected, from

832

Meniere's disease.

left to right, or in the same direction as the rotation of the
eyes. An instructive case of this disease is recorded by Mr.
Lewis Mackenzie and quoted by Hughlings-Jackson, in which
the patient — a medical man — was much distressed by con-
tinuous noises in the right ear, following the discharge of a
heavily-loaded gun near it, and, along with the other more
usual symptoms of auditory vertigo, there was manifested a
constant tendency to walk to the left.

§ 909. Gourse,Duration, and Terminations. — The paroxysms
of vertigo come on at first at irregular intervals ; they increase
gradually in frequency and intensity, and in aggravated cases
the patient suffers continuously from some degree of vertigo,
while he is liable to paroxysmal exacerbations of great severity.
The noises in the ears may cease at first during the intervals,
but after a time become constant. The sense of hearing
becomes gradually diminished, and ultimately complete deaf-
ness of the affected ear is established, when, fortunately, the
paroxysms of vertigo and all the distressing symptoms of the
disease cease.

§ 910. Morbid Anatomy and Physiology. — Several post-
mortem examinations have revealed the presence of inflam-
matory exudation in the semicircular canals. The symptoms
under consideration are, however, often associated with disease
of the middle o'r external ear, but in such cases some indirect
influence is probably exerted on the labyrinth.

§ 911. Diagnosis and Prognosis. — Auditory vertigo is liable
to be mistaken for the vertigo associated with gastric disease or
sexual excess, the diagnosis being rendered more difficult by
the fact that a considerable degree of deafness and noises in
the ears may be present in the latter. In auditory vertigo the
noises are unilateral, the feeling of vertigo is very intense, and
is accompanied by a sensation as if the body had undergone
actual displacement ; these symptoms never occur to the same
degree in the vertigo of dyspepsia or sexual excess. Paroxysms
of auditory vertigo may be mistaken for epileptic attacks,
and can only be distinguished by a careful examination of the

MENIERE S DISEASE.

833

symptoms. The prognosis is grave as far as ultimate recovery is
concerned, but the symptoms disappear when complete deafness
is established.

§ 912. Treatment. — If the symptoms depend upon disease
of the external or middle ear, the patient should be placed
under the care of the specialist, and when the local disease
is not accessible to treatment, relief may be obtained by rest in
the recumbent posture. The administration of four or five
grains of quinine three times a day appears to have produced
great amelioration of the symptoms in several cases (Charcot,
Hughlings- J ackson).

BUB

834

CHAPTER III.

EPIDEMIC CEREBRO-SPINAL MENINGITIS, TETANUS, AND

HYDEOPHOBIA.

(I.) EPIDEMIC CEREBRO-SPINAL MENINGITIS.

§ 913. Definition. — Epidemic cerebro-spinal meningitis is
an acute epidemic fever, characteristic symptoms of which are
caused by a purulent inflammation of the spinal and cerebral
pia mater.

§ 914. History. — This disease probably prevailed in ancient times,
but we have no reliable accounts of it before the present century.
The first epidemic prevailed in Geneva, in the early months of 1805.
Then followed epidemics in Grenoble (1814), Vesoul (1822), and Dorsten
on the Lippe (1833). The disease appeared in Southern France in 1837,
and remained confined for many years to the barracks. About the time
that it attained its highest development in France the epidemic extended
to Italy, and prevailed there from 1839 to the spring of 1845.

In 1844 a transient epidemic occurred in Gibraltar, the following year
in Denmark, and in 1846 it appeared in the workhouses of Ireland, while
a few cases were observed in Liverpool. The disease appeared in Sweden
in 1854 and reappeared in 1861; there was an epidemic in Norway in
1859—1860.

The disease may be traced back in the United States to the beginning
of the century, but it made active progress during the year 1842, and
prevailed with great intensity during the civil war. In the last few years
it has appeared in Canada, and it has never entirely disappeared from
the United States, declaring itself either in sporadic cases or in small
epidemics.

Sporadic cases have been observed in the United Kingdom ; but the
most fatal epidemic began in Ireland in March, 1866, and attained its
chief development in the following winter. Its effects were almost
entirely confined to Ireland, the worst cases occurring in Dublin. In
1876 a slight epidemic occurred in Birmingham.

EPIDEMIC CEREBROSPINAL MENINGITIS.

835

§ 915. Etiology.

Predisposing Causes. — When the disease was first noticed in
Southern France in 1837, and in the subsequent outbreaks up
to 1849, it was almost entirely confined to soldiers. Kaw
recruits were specially liable to be affected, and this liability
was probably largely due to great physical exertion and an
overcrowded condition of the garrisons. In subsequent out-
breaks, however, in France and elsewhere no special liability to
the disease has been manifested amongst those engaged in
particular employments.

In the earlier epidemics males were almost exclusively
attacked ; and, although subsequent observation has not con-
firmed the idea that the disease is peculiar to men, it is much
more common in them. Age does not appear to have any
particular influence in the production of the disease. In some
epidemics children, in others young people, and still in others
adults of from thirty to thirty-five have been attacked in
greatest proportion.

The disease is especially prevalent in the cold months of the
year, and, notwithstanding some apparent exceptions, it is
undoubtedly more prevalent amongst the poor and ill-fed than
the affluent classes. In a large number of epidemics it almost
exclusively prevailed amongst the inmates of prisons, work-
houses, and overcrowded garrisons.

§ 916. Symptoms. — Epidemic cerebro-spinal meningitis may
be divided into four varieties : (1), the simple ; (2) the fulmi-
nant ; (3), the purpuric; and (4), the abortive forms.

(1) Simple Epidemic Cerebro- Spinal Meningitis. — Pre-
monitory symptoms are sometimes observed, consisting of loss
of appetite, lassitude, and neuralgic pains in the back and
abdomen. As a rule, however, the patient is suddenly seized,
while following his ordinary occupations, or at play, with shiver-
ing, vomiting, and headache (Burdon-Sanderson). Profuse and
uncontrollable vomiting is almost a constant symptom, the
ejected matters consisting at first of half-digested food and
subsequently of mucus stained with bile. Delirium now super-
venes, sometimes so violent in character that it is necessary to

836

EPIDEMIC CEREBROSPINAL MENINGITIS.

place the patient under restraint, but he is usually apathetic
and drowsy, and only talks of imaginary objects when roused.

The patient soon complains of an agonising pain in the
occiput and nape of the neck, which may extend along the
spine and is aggravated by movement and pressure. The
abdominal muscles, as well as those of the back and loins,
are acutely painful, and any movement rendering them tense
occasions great pain. The skin becomes extremely sensitive,
and severe pain is felt in the limbs, but it is difficult to deter-
mine how much is due to cutaneous or muscular hyperesthesia.
The head is retracted, partly from spasm of the muscles of the
nape of the neck, but mainly as an instinctive means of relaxing
the muscles in order to relieve pain. In no case coming under
the observation of Dr. Burdon-Sanderson were the contractions
of the muscles of the back of the neck of such a character as to
be correctly called tetanic. " The patients," says Dr. Sanderson,
"invariably lay on their sides, with their knees drawn up so as
to relieve the abdominal muscles, and with the face looking
towards the head of the bed, and excessive pain was produced
whenever the body was moved in such a way as to extend the
painful muscles, and more particularly when the patient was
lifted in bed." The period of invasion lasts from one to three
days, and is then followed by the stage of depression.

The mental confusion and low-muttering delirium, which is
present in the stage of invasion, now gives place to stupor, which
in fatal cases ends in profound coma. The patient lies in a
somnolent condition, although often able to answer questions
when roused. The symptoms are liable to undergo considerable
fluctuations ; at times the sopor predominates, at other times
there are restlessness and nocturnal delirium, and the patient
continues to complain of pains in the back of the neck and in
the loins. Tremors are observed in the extremities, the pulse
is slow, the face is livid, the pupils dilated or contracted,
and strabismus, amblyopia, or deafness is not unusually pre-
sent. In several children seen by Dr. Burdon-Sanderson the
symptoms, shortly after the cessation of the initial period, were
very similar to those of tubercular meningitis. An exanthe-
matous eruption appears about the mouth, either like that of
measles or scarlet fever, and occasionally herpetic in character ;

EPIDEMIC CEREBROSPINAL MENINGITIS.

837

it spreads upwards over the eyelids and ears, and downwards
over the chin and neck.

The degree of pyrexia varies greatly in different cases, but
the temperature usually ranges from 100° F. to 103° F., or in
fatal cases to 105° F. or higher. The tongue may be clean, the
bowels are usually constipated, and the abdomen is retracted.
The urine is frequently albuminous, destitute of chlorides, and
contains a relatively large proportion of urates, while polyuria
and saccharine urine have occasionally been observed.

In unfavourable cases the coma increases and becomes asso-
ciated with more pronounced paralytic symptoms, such as ptosis,
strabismus, and paresis of the extremities. The pulse is feeble,
and irregular or intermittent ; the respiration is embarrassed, a
slow and laboured inspiration being followed by a quick expira-
tion and a long pause (Burdon-Sanderson); the skin is cyanotic,
and covered with a cold sweat as in the algide stage of cholera ;
and the patieDt soon sinks.

The disease frequently terminates favourably, the amend-
ment being indicated by a gradual subsidence of the nervous
phenomena, restoration of the mental faculties, and a steady
fall in temperature. If the progress towards recovery be un-
interrupted, health is re-established in from three to four weeks.
Convalescence is, however, often delayed for a long time by
relapses, and in such cases recovery is often incomplete.

(2) Fulminant Epidemic Cerebro-Spinal Meningitis. — In
this variety the patient falls without any premonitory symptom
into a state of collapse, drowsiness rapidly supervenes, and is
quickly followed by coma. Purpuric spots appear over the
surface of the body generally ; these soon change from a purple
to a black colour, and are often confluent so as to form irregular
patches. Death may ensue in less than five hours, or life may
be prolonged for two or three days ; recovery is not unknown
even in this form.

(3) Purpuric Epidemic Cerebro-Spinal Meningitis. — In
this variety the symptoms which characterise the simple and
fulminant varieties are combined in various proportions. In
the great majority of cases the disease follows at first the
course of the simple variety ; but in from one to four days from

844

TETANUS.

the wounded soldiers, after the heat and fatigue of battle or long
marching, are exposed to cold and other privations during the
night.

Tetanus occurs more frequently in tropical countries than in
the temperate or frigid zones, probably owing to the sudden
alternations of temperature which are liable to occur in the
former, sultry days being often followed by cold nights.

Rose has endeavoured to show that improper treatment of
the wounded increases the proportion of tetanus, and there is
no doubt that the proportion of cases of tetanus amongst the
wounded is much less in the present day than in former times.

The male is more frequently affected with tetanus than the
female sex ; it is more frequent in youth and middle age than
in advanced life, and the robust and muscular are said to be
more frequently attacked than the feeble.

§ 923. Symptoms. — Premonitory symptoms are generally
observed in tetanus consisting of shivering or a distinct rigor,
sensation of dragging in the neck, stiffness in certain muscles,
difficulty of articulation and deglutition, and yawning. In trau-
matic cases the wound may become sensitive, and the patient
complain of shooting pains radiating from it. These symptoms
may occur a few hours or even a few days before the charac-
teristic tonic spasms make their appearance.

The spasms, as a rule, begin in the muscles of the jaw. At
first the jaws can be separated, and the movements of chewing
and swallowing be accomplished, although with difficulty.
Soon, however, the jaws become firmly clenched, constituting
the condition called trismus; spasm of the oesophagus renders
swallowing of even a small quantity of fluid difficult and
fatiguing; articulation is indistinct; and the voice is altered,
partly from the difficulty of moving the tongue, and partly from
implication of the muscles of the larynx in the spasm.

Spasm of the facial muscles gives to the countenance a
characteristic expression. The angles of the mouth are drawn
outwards, being at the same time depressed or elevated, and
the lips are often drawn apart and expose the set teeth, so that
the face assumes a sneering expression, named the "risus
sardonieus." The nostrils are dilated; the eyes are staring

TETANUS.

845

and motionless ; the pupils are generally contracted ; the brows
are wrinkled ; and all the lines of the face become strongly
marked, and give to the patient an aged appearance.

The spasm rapidly extends to the muscles of the back of the
neck, causing retraction of the head ; while the erectores spinas
soon become implicated, and the vertebral column is then
arched backwards ; the chest is projected forwards and rendered
very broad, and the body rests on the back of the head
and sacrum, constituting the condition called opisthotonos.
The epigastrium is sunk, and the abdomen flattened, while the
hardness assumed by the abdominal muscles is characteristic.
On rare occasions the body is said to be bent forwards, the
convexity of the arch being directed backwards, a condition
named emprosthotonos. In a few cases the body is maintained
in a rigid attitude without being curved in any direction, a
condition named orthotonos ; and in some rare cases it is
curved laterally — pleurosthotonos.

The muscles of the extremities are usually not affected to so
great an extent as those of the trunk, neck, face, and jaws.

Fig. 285.

Fiq. 285 (From Spence's Surgery).— Taken from the original painting by

Sir Charles Bell.

The muscles of the lower extremities are, however, generally im-
plicated to a greater or lesser extent ; and during the spasmodic
attack extension, as a rule, predominates over flexion, although
flexion at individual joints has occasionally been observed

844

TETANUS.

the wounded soldiers, after the heat and fatigue of battle or long
marching, are exposed to cold and other privations during the
night.

The spasms, as a rule, begin in the muscles of the jaw. At
first the jaws can be separated, and the movements of chewing
and swallowing be accomplished, although with difficulty.
Soon, however, the jaws become firmly clenched, constituting
the condition called trismus; spasm of the oesophagus renders
swallowing of even a small quantity of fluid difficult and
fatiguing ; articulation is indistinct ; and the voice is altered,
partly from the difficulty of moving the tongue, and partly from
implication of the muscles of the larynx in the spasm.

Spasm of the facial muscles gives to the countenance a
characteristic expression. The angles of the mouth are drawn
outwards, being at the same time depressed or elevated, and
the lips are often drawn apart and expose the set teeth, so that
the face assumes a sneering expression, named the "i^isas
sardonicus." The nostrils are dilated ; the eyes are staring

TETANUS.

845

and motionless ; the pupils are generally contracted ; the brows
are wrinkled ; and all the lines of the face become strongly
marked, and give to the patient an aged appearance.

The muscles of the extremities are usually not affected to so
great an extent as those of the trunk, neck, face, and jaws.

Fig. 285.

Fia. 285 (From Spence's Surgery) .—Taken from the original painting by

Sir Charles Bell.

846

TETANUS.

(Bauer). During the attack the various segments of the lower
extremities are extended upon one another and upon the
trunk, so that the patient rests on the head and heels ; the
toes are extended and spread out, and the feet are everted.
Even in severe cases the muscles of the upper extremities
may remain comparatively unaffected, but if passive motion
of the forearm be attempted, increased muscular resistance
is readily perceived. When the spasm extends to the muscles
of the upper extremities, flexion predominates over extension ;
and during the paroxysms the arms are drawn close to the
chest, the forearm is flexed upon the arm, the hand is flexed
at the wrist, and the fist is closed, the palm being directed
towards the upper arm {Fig. 285).

In some cases the spasm persists continuously from the
beginning to the termination of the disease ; but, as a rule, the
spasmodic rigidity of the muscles occurs in paroxysms with in-
tervals of comparative, but never complete muscular relaxation.
Each paroxysm lasts from a few seconds to several minutes, or
with slight remissions for hours ; while the duration of the free
interval varies from ten minutes to hours, but at other times
the spasms recur and remit with such frequency that they
assume a more or less clonic character. As the disease pro-
gresses, the paroxysms of spasm recur with greater frequency,
and muscular contraction is sometimes so violent that teeth
are broken, long bones, like those of the thigh, fractured, and
large muscles, like the psoas and rectus femoris, torn across.
The paroxysms recur spontaneously, but they are induced by
the most trivial external cause, such as a draught of air, a
sudden noise, or an attempt to swallow or to administer an
injection. Attempts at swallowing may, indeed, provoke an
attack so readily that the disease may bear a certain resem-
blance to hydrophobia. The spasm occasioned by the attempt
may be in the pharynx, gullet, or in the cardiac end of the
stomach, as the oesophagus passes through the diaphragm.
But wherever it may be situated, all attempts at swallowing
are rendered impossible, and fluids introduced are ejected
through the nose and mouth, so that the patient can neither be
fed in the usual way nor by the stomach pump. During the
paroxysm the action of the inspiratory preponderates over that

TETANUS.

847

of the expiratory muscles, so that the act of coughing is ren-
dered impossible, and mucus accumulates in the bronchi. In
severe paroxysms the chest becomes fixed ; the countenance is
livid; the eyes are suffused; the patient foams at the mouth;
and is tormented with a feeling of dread and suffocation.
Arrest of respiration may sometimes be caused by spasm of the
glottis ; but, as a rule, it is the result of spasm of the thoracic
muscles and diaphragm. In the intervals respiration is only
slightly changed in frequency, from twenty to twenty-four in
the minute, but it is accompanied by a painful sensation of
increased resistance, requiring effort. Motor paralysis is a rare
symptom of tetanus. Rose observed paralysis of the muscles of
one side of the face in a case in which the primary lesion was
in the area of distribution of the facial nerve. General mus-
cular weakness, and paralysis of certain groups of muscles are
observed as terminal phenomena; strabismus is, according to
Wunderlich, a precursor of death.

The sensory disturbances in tetanus are such as are usually
produced by intense muscular cramp in the muscles of the calf.
Some observers have noticed an increase of the sensibility to
pain independently of the spasms, while at other times the
acuteness of the senses of touch and temperature may be
diminished. Paresthesia}, such as numbness and tingling,
have occasionally been observed. Pain is sometimes absent
during the tetanic seizures ; and Blane mentions the case of a
patient who only felt a pleasant sensation of tickling during
the severest spasms. Pain at the epigastrium, piercing through
the back, is, according to some authors, a pathognomonic
symptom of tetanus. It is present during both the tetanic
paroxysms and the intervals, and depends most probably upon
spasm of the diaphragm.

Psychical disturbance is generally absent in tetanus. The
mind is almost always clear from the beginning to the end of
the disease, although delirium or coma may supervene a short
time before death, often due to the remedies used. Sleepless-
ness is one of the most troublesome symptoms of acute cases
of tetanus, and even in subacute cases sleep is only obtained at
broken intervals. The spasms cease during sleep and the
narcosis of opium or chloroform. The skin, in the paroxysms

848

TETANUS.

and even intervals, is hot and bathed in perspiration, having
a peculiar pungent smell, while the surface may be covered
by sudamina as in other cases of profuse sweating. In the
majority of cases the temperature ranges from 101°F. to 103° F.,
and may even rise suddenly to 105° F. in cases which recover,
although it is not maintained long at this level only in fatal
cases. In many cases there is hyperpyrexia immediately before
death, the temperature rising to 108° F. or even 110° F., and it
may continue to rise for some hours after death.

The pulse may remain normal during the first stage of
tetanus, but there is a considerable increase in its frequency
during the tetanic seizure, and in the last stage, especially
when there is elevation of temperature, it may beat as often
as 180 in a minute. Liston observed in a case of amputation
during tetanus the vessels so contracted that not a drop of blood
had escaped.

The daily quantity of urine passed in tetanus is usually below
the average in health ; the reaction is strongly acid, the specific
gravity high, and there is generally an abundant deposit of
urates on cooling. Sugar in the urine in tetanus was first dis-
covered by Demme, and its presence has since been detected
by others. Senator found that the excretion of nitrogen was not
increased in tetanus as compared with the amount excreted by
a person fasting. He also states that the creatinine is not
increased. There- may be retention of urine, caused probably
by spasm of the sphincter, while at other times dribbling may
occur during the paroxysm. The bladder is, however, never
affected to so great an extent as in acute spinal meningitis.
Spasm of the sphincter ani is often present, as is proved by
the difficulty of introducing an enema pipe.

The general health of the patient suffers greatly during the
course of the disease. The distorted position of the body, the
persistent sleeplessness, the difficulty of respiration, and the
impossibility of swallowing combine to render the state of the
patient extremely distressing. The bowels are constipated, the
tongue is generally coated, a tenacious viscid saliva accumulates
in the mouth, and the patient may be excessively hungry and
tormented with thirst, yet can neither swallow food nor drink.

TETANUS.

849

§ 924. Course, Duration, and Terminations. — The time
which elapses between the occurrence of an injury and the out-
break of tetanus varies greatly. The average interval is from
five to ten days, but the spasms may begin a few hours after
the injury, or weeks may intervene. Mr. Ward, of Manchester,
has reported a case where the symptoms appeared ten weeks
after the injury.

In tetanus neonatorum the disease appears from four to eight
days after birth, but it may sometimes be delayed until the
fourteenth day.

The intensity of the disease is liable to vary considerably.
The symptoms in slight cases may consist only of trismus and
some stiffness of the neck ; in others they develop rapidly and
prove fatal in a few days, or occasionally in a few hours from
the commencement.

Death takes place in several ways. It frequently occurs
during a paroxysm from asphyxia, caused by rigidity of the
respiratory muscles. In other cases the spasms cease, and death
follows during mild delirium associated with quick pulse,
high temperature, and symptoms of asthenia. At other times
the heart suddenly ceases to beat.

In cases of recovery the convulsive attacks become lighter
and less frequent, and after a time entirely cease; if sleep
return, it is a favourable sign. The rigidity continues for some
time after the paroxysms cease and then gradually disappears,
though not in definite order. Recovery takes place in from
one to eight weeks or even longer, and a certain degree of
weakness and stiffness may remain in the muscles for a
long time.

§ 925. Morbid Anatomy. — Rigor mortis sets in almost im-
mediately after death, probably caused by the strongly acid
reaction in the previously active muscles. It has long been
suspected that the morbid changes in tetanus are to be found
in the central nervous system, and more especially in the spinal
cord. In the earlier records, the changes most frequently men-
tioned are congestion and extravasations of blood into the cord
and its membranes, and occasionally softening of the former.
Rokitansky was the first to subject the spinal cord to micro-
ccc

850

TETANUS.

scopic examination in cases of tetanus. He found an increase
of nuclei, destruction of the medullary substance, agglomerations
of fat granules, and amyloid bodies. He also observed similar
changes in the peripheral nerves. Leyden, however, has since
proved that the changes found by Rokitansky are not constant,
being in great measure due to imperfect methods of pre-
paration. Lockhart Clarke found great hypersemia of the cord
and its membranes, as well as centres of softeniDg, in the grey
and white substance, and similar changes have been described
by Dickson, Allbutt, Coats, and other observers.

In the spinal cord of a patient dead of tetanus, I found
marked softening in the lumbar region. A section from the
middle of the lumbar region is shown in Plate V., fig. 6. A
vessel from the anterior fissure, represented in Plate Y., fig. 7,
was seen to be surrounded by leucocytes, and the whole of both
grey and white substances was densely infiltrated with the same,
although not usually aggregated in the perivascular spaces and
around the vessels as in hydrophobia. Another vessel from the
grey substance, cut obliquely, is shown in Plate V., fig. 8, the
lymph sheath of which is filled with leucocytes. The most in-
teresting changes were observed in the ganglion cells of the
anterior horns. A few cells of normal size were seen in the
portion of the median group nearest the anterior fissure, the
greater portion of the cells of the antero-lateral group and a
few of those of the postero-lateral group were also of normal
size ; but most of the cells of the median group, and the mar-
ginal cells of the other groups, had apparently disappeared,
when the section was examined with a low power. The disap-
pearance of these cells was, however, not real ; under a high
power, they could be seen shrunk in their cavities. Similar
changes, although less in extent, were found in other three cases
examined by me. Shrieking of some of the ganglion cells of
the anterior horns has been recently observed by Dr. Harris
and Mr. Doran.

With respect to the medulla oblongata in the cases examined
by me, the cells in the internal and anterior portions of the
nucleus of the hypoglossal were considerably altered, while those
of the body of the nucleus appeared normal. The cells of the
nuclei of the spinal accessory, and pneumogastric, appeared

TETANUS.

851

always to suffer ; while the longitudinal vessel, which lies in the
deepest part of the floor of the fourth ventricle, is, as remarked
by Dr. Coats, usually surrounded by red blood corpuscles. The
nucleus of the facial, the motor nucleus of the fifth, the nucleus
of the abducens, and that of the third and fourth cranial
nerves appeared normal. A large number of leucocytes were
observed in the olivary bodies, the brachium of the pons, and
between the fibres of the seventh nerves.

In the roots of the fifth nerve, proceeding from the cere-
bellum, large vessels were observed which were distended with
red blood corpuscles, and the whole of the surrounding tissue
was densely infiltrated with leucocytes. The corpus dentatum
of the cerebellum and the white substance subjacent to the
cortex, were also densely infiltrated with leucocytes and inter-
sected with distended blood-vessels to an extent which it is
impossible to regard as other than the result of disease. The
cells of Purkinje were surrounded with leucocytes, but did not
themselves present, any decided morbid appearances.

In traumatic tetanus the older reports state that marked
changes were frequently seen at the seat of the wound. Nerves
were crushed and torn, foreign bodies buried in the nerve trunks,
and inflammation and thickening were found about the injury.
Lepelletier was the first to describe the occurrence of an ascend-
ing neuritis in a patient who died from tetanus. Froriep found
red spots and swellings of the nerves alternating with parts
which remained healthy, these changes extending from the
seat of injury to the spinal cord.

Evidences of inflammation have been described by Aronssohn,
Dupuy, and Andral in the sympathetic nerves, especially in the
cervical and semilunar ganglia.

The voluntary muscles are generally of a pale colour, and
ruptures of bundles of fibres with extravasations of blood have
been found. Fatty degeneration of the muscles has also been
observed.

§ 926. Pathology. — The pathology of tetanus is not very
clear, but a few landmarks for future researches have been
ascertained. Morbid alterations have been found in various
portions of the cord and medulla oblongata. Whatever morbid

852

TETANUS.

process these changes may indicate, they are doubtless accom-
panied by breaking down of the structure of the cord, and
during the disintegrative process the molecules of the proto-
plasm of the cells or of the axis-cylinders, or of both, fall
from an unstable to a stable position, the latent energy
being rendered active. During this process the irritability
of the grey matter and of the nerve fibres is increased, while
there is a decrease of their resistance to conduction. In con-
sequence of the increased irritability and diminished resistance,
the slightest peripheral irritation will determine muscular
spasms by setting free a relatively large amount of energy.
Indeed, Romberg regards the increased reflex irritability as
the chief element in tetanus, but it must be remembered that
spasms may be caused by the pathological process going on in
the cord independently of peripheral irritation.

An ascending neuritis has been found in some cases in the
nerve leading from the wound to the cord ; and it is possible
that in all cases there is a progressive extension of the diseased
process from the external wound towards the centre. But the
morbid changes in tetanus are not limited to the peripheral
nerves, spinal cord, and medulla oblongata, but probably
extend to the cerebellum. I am inclined to believe with
Dr. Hughlings-Jackson that discharges of nerve energy from
the cortex of the cerebellum are the main cause of the paroxysms
of spasm in tetanus, although these discharges may to some
extent be determined by the instability of centres in the medulla
oblongata and spinal cord.

§ 927. Diagnosis. — The diagnosis in well-marked cases pre-
sents no difficulty, but the obscure symptoms of the early
stage may be overlooked or their importance under-estimated.
In the tetanus of strychnia the masticatory muscles are rarely
attacked first, and may possibly escape altogether ; the symp-
toms are well marked at the commencement, and reach their
full development in a few minutes ; opisthotonos is a very early
symptom ; there are usually intervals of complete intermission ;
and death occurs commonly in less than three hours, or else
recovery is very rapid.

Masticatory spasm induced by decayed teeth, hysteria,

TETANUS.

853

and other causes, and stiffness of the jaws from tonsillitis,
parotitis, and disease of the articulations of the jaw, may
be mistaken for the first stage of tetanus ; but even in slight
cases of tetanus the cervical muscles are to some extent affected,
and if attention be paid to the symptoms of the former diseases,
thev cannot well be mistaken for the latter.

Hysterical spasms may sometimes closely simulate tetanus,
but in hysteria an interval of variable duration follows the
paroxysm, in which the muscles are relaxed, and other symptoms
indicative of hysteria are present.

§ 928. Prognosis. — The prognosis in tetanus is always grave.
Most authors regard idiopathic tetanus as being less dangerous
than the traumatic variety.

It may be laid down, as a general rule, that the longer the
interval which elapses between the injury and the appearance
of tetanus the more likely is the disease to become chronic and
to end favourably. Acute cases, in which the spasms supervene
soon after the injury, and recur with increasing violence and
at decreasing intervals, are almost always fatal, death taking
place in a few days, or even hours, from the commencement. The
aphorism of Hippocrates, that tetanus ends in recovery if the
patient survive the fourth day of the disease, may be accepted
as practically true, although there are many exceptions.

Special symptoms are relied upon by some authors in forming
a prognosis. The prognosis is said to be grave when attempts
to swallow during the first few days induce suffocative attacks.
Wunderlich regards the occurrence of strabismus as of fatal
augury, and a frequent pulse and high temperature belong to
the terminal phenomena of the affection.

§ 929. Treatment. — At one time tetanus was regarded as an
inflammatory disease,%nd treated accordingly by so-called anti-
phlogi sties, blood-letting, and mercurials ; but this method of
treatment has been abandoned along with the theory upon
which it was founded. It is needless to point out here how
necessary it is in surgical practice to protect all wounds from
unfavourable influences both in the local treatment of the wound
and in the general surroundings of the patient.

854

TETANUS.

Different expedients have from time to time been proposed
with the view of arresting the peripheral irritation caused by
the primary injury. Amputation of the limb and section of
the nerves, at one time recommended, are now abandoned for
the safer and apparently more successful operation of nerve
stretching.

The next aim of treatment is to diminish the irritability of
the cord. Chloral hydrate is probably superior to any other
remedy for this purpose.

Cannabis Indica has been used, but it is too uncertain in its
results, and its physiological action is not yet well ascertained.
Calabar bean or physostigmin has been employed with occa-
sional success. Tobacco or nicotine is highly recommended by
Curling, but the depression it produces is sometimes alarming
and may be dangerous. Bromide of potassium diminishes
reflex irritability, and may be used either alone or in combina-
tion with chloral.

Curara, belladonna, and prussic acid have been employed in
the treatment of tetanus with the view of controlling the
spasms, but the course of the central disease is unaffected by
arrest of the spasms.

The cold bath and cold douche may be used when there is
a sudden elevation of temperature, and under these circum-
stances the patient may be placed in a bath of about 90° F.,
the temperature of which is rapidly reduced to 60° F. by the
gradual addition of cold water.

In ordinary cases the warm bath is exceedingly soothing to
the patient, and for this reason it forms a pleasant auxiliary
to other treatment. The vapour bath has been used, but is
inferior to the warm bath.

The patient should be protected from every source of irrita-
tion, such as noises, strong light, changes in temperature,
and sudden touching of any part of the body. His strength
should be well supported, and when spasm does not permit
the patient to swallow liquids, food should be introduced by
means of a tube passed through the nose after the patient has
previously been brought under the influence of chloroform.
Nutritive enemata may also be employed.

Constipation' is a troublesome symptom, and ma}' require

HYDROPHOBIA.

855

attention ; but less irritation is caused by the contact of faeces
in the bowels to which they are accustomed than by the irrita-
tion produced by powerful cathartics.

A few trials have been made with electricity in the treatment
of tetanus, but the results have not been encouraging.

(III.) HYDROPHOBIA.
§ 930. Definition. — Hydrophobia is a disease caused by the
inoculation of a specific animal poison contained in the saliva
of animals under its influence, the most characteristic clinical
features in man being excitement and spasms induced by
attempts to swallow fluids.

§ 931. Etiology. — The cause of hydrophobia appears to be in
all cases a specific virus contained in the secretions of the mouth
of the infected animal, and the disease is communicated to man,
and probably to other animals also, only by direct inoculation
through a bite. There are no grounds for believing that canine
rabies ever arises spontaneously, and it is probably in all in-
stances communicated from one animal to another by means of
a bite. The animals which are capable of inoculating man are
the dog, wolf, fox, badger, marten, cat, horse, sheep, pig, and
goat (Gamgee). Only a small proportion of human beings
bitten by rabid animals become affected with hydrophobia, a
proportion which has been variously estimated at from 5 to 50
per cent. The number which become subsequently affected with
the disease is greater when the exposed parts of the body are
bitten. It is probable that the teeth in passing through the
clothes are often cleansed, so that the wound escapes inocula-
tion. It is likely that a considerable proportion of those bitten
are protected by the cauterisation and other local treatment to
which the wound is usually subjected at the time. Some
individuals appear to possess a relative or complete immunity
from the disease, and it is transmitted irrespectively of age, sex>
or constitution.

§ 932. Symptoms. — The period of incubation in hydrophobia
is longer, and liable to greater variations in its duration, than
that of any other specific disease. In the majority of cases the

85G

HYDROPHOBIA.

symptoms manifest themselves from four to eight weeks after
the injury, but they may occasionally appear at the end of the
first week or not until nine months, and on rare occasions not
until several years have elapsed.

The outbreak of the characteristic manifestations of hydro-
phobia is often preceded for a day or two by premonitory
symptoms. The wound inflicted by the bite becomes intensely
painful, and the pains generally extend along the nerves towards
the trunk. If the wound has not healed, it assumes an un-
healthy character ; if it has closed, the cicatrix becomes red and
irritable. During the period of invasion the patient suffers
from chilliness and general malaise, the pulse is rapid, the
respirations are quick and sighing, there is thirst and anorexia,
and even in this stage the patient may manifest a disinclination
to swallow fluids. The face is pale and has an anxious expres-
sion; the patient is fidgetty, restless, and peevish; while de-
pression of spirits is so constant and marked a symptom that
the period of invasion has been called the melancholic stage
of the disease.

At the end of a few hours, or at most a day or two, the
characteristic features of the disease become fully developed.
The patient complains of stiffness about the head and neck, his
mouth and fauces are congested, and he suffers from agonising
thirst, while every attempt to swallow induces a violent spasm
of the pharyngeal and respiratory muscles, which often extends
to the muscles of the entire body, and throws the patient into
a condition of intense excitement and alarm.

The patient at first may be able to swallow some liquid. In
the cases that have come under my observation the patient
in the early stage of the disease on being asked to drink took
hold of the vessel, looked at it doubtfully for some time, and
then, with horror depicted on his face, asked for it to be taken
away. Soon afterwards he would summon up sufficient resolu-
tion to ask to drink again, and after a period of deliberation and
apparent preparation for a supreme effort the vessel was carried
rapidly to the mouth, generally with both hands, and part of its
contents swallowed with the utmost precipitancy and agitation,
the vessel being then almost flung from the hands. This period,
however, is of short duration. Every attempt to swallow liquid

HYDROPHOBIA.

857

is found to induce a severe spasmodic paroxysm, and the
abhorrence of water becomes so intense that the spasm may be
excited by the sight of it, or even by the noise occasioned by
pouring it from one vessel to another. A viscid saliva now
accumulates in the mouth, which the patient is constantly
attempting to spit out, giving rise to the sound which has often
been described as a bark. During the course of the disease
convulsive movements may occur in the face, jaw, neck, trunk,
and extremities, the spasms being sometimes not unlike tetanic
seizures.

The sensory disturbances consist of hyperesthesia of general
sensibility and the special senses. The patient often complains
of the weight of the bed-clothes, he shuns the light or luminous
objects, and is distressed by the slightest noise. Patients also
complain of painful sensations in the head, neck, back, and
epigastrium, as well as in the neighbourhood of the primary
wound.

The reflex excitability is greatly increased, and a draught of
cold air on the surface of the body, especially on the face,
may determine a spasmodic attack of great severity. The
slightest impression on the surface of the body occasions, as
has been pointed out by Dr. Gowers, a spasm of the costo-
superior respiratory muscles and erectores spinas, very similar
to that produced by the cold affusion in healthy individuals.
The pulse is small and frequent from the beginning, and be-
comes thready, irregular, and uncountable towards the fatal
termination; and the urine frequently contains albumen and
sugar. Out of five cases, in the Manchester Royal Infirmary,
and reported by Mr. Southam, the urine was saccharine in three,
and highly albuminous in all of them.

Psychical disturbances are always present in hydrophobia,
although they are much more prominent in some cases than
in others. They vary from a certain emotional excitement
that may be mistaken for ordinary hysteria to a state of acute
maniacal delirium, the latter being specially liable to occur in
children. In the majority of cases the patient has a wild and
agitated look ; his eyes are bright and restless ; his brows
wrinkled ; and his countenance assumes an expression of ex-
treme horror. The patient is restless, sleepless, often loquacious,

858

HYDROPHOBIA.

and all his movements are characterised by great precipitation.
The intellect may remain more or less clear for a time, but
towards the end he begins to wander, and hallucinations or
attacks of violent maniacal excitement supervene, during which
the patient may injure himself or the attendants. In children
the symptoms of acute mania may predominate from the first.
In the case of a child four and a half years of age under the
care of Mr. Ewart, in St. Mary's Hospital, Manchester, the
maniacal symptoms were early manifested. During the maniacal
paroxysms, terror, caused probably by hallucinations of sight,
appeared to be the predominant symptom, and the child
screamed to his mother to save him from the " pussy " that was
threatening to attack him (he had been bitten five weeks pre-
viously in the face by a rabid cat), and struggled violently to
escape from his attendants.

As the disease progresses to a fatal termination all the
symptoms are aggravated, and the pulse becomes rapid, irregular,
and thready; tenacious mucus accumulates in the mouth and
is expelled with difficulty, the voice becomes hoarse, and the
spasmodic paroxysms increase in severity and frequency. An
attack of convulsions or profound coma may precede the fatal
termination, but it is rare to observe a case uninfluenced by
narcotics. Death may take place suddenly from asphyxia during
a convulsive attack, or from exhaustion. In some cases the
spasms gradually diminish and may cease a few hours before
death ; the patient may even become able to drink, but this
comparative calm is deceptive, and, instead of being a sign of
recovery, is only the precursor of death.

§ 933. Course, Duration, Terminations. — When ouce the
disease is fully established it pursues a rapid course, and ter-
minates probably always fatally in from two to four days after
the commencement of the symptoms.

§ 934. Morbid Anatomy. — In the older records of post-
mortem examinations in cases of death from hydrophobia the
cliief alterations of the nervous system mentioned are congestion
of the brain, medulla oblongata, and spinal cord and of their
membranes. In 1869 Meynert made a microscopic examina-

HYDROPHOBIA.

859

tion of portions of the brain and spinal cord of two patients
who had died of hydrophobia; but the changes observed by
him, in addition to congestion of the spinal cord and brain,
were somewhat indefinite. Soon afterwards Dr. Allbutt made
some important observations. " In the cerebral convolutions
the mesocephalon, the pons, medulla, and spine, the vessels," he
says, " were seen in various degrees of distension, and in many
places the walls were obviously thickened, and here and there
in them were patches of incipient nuclear proliferation." These
observations were confirmed by Hammond, who also found
changes in the ganglion cells of the nuclei of origin of the
pneumogastric and hypoglossal nerves, as well as in those of
" the first and second" layers of the cortex of the cerebrum. The
nuclear proliferation described by Dr. Allbutt as occurring in
the walls of the distended vessels consists, as was subse-
quently pointed out by Benedikt, of migrated white blood
corpuscles.

In the brains of dogs affected with rabies, Benedikt found the
white blood corpuscles aggregated around the vessels to such an
extent as to form what he termed a miliary abscess. He found
similar appearances in the brain of a human subject who had
died of hydrophobia. The spinal cord and medulla oblongata
were not examined in these cases. These observations have
been confirmed and extended by Coats and Gowers, who found
accumulations of leucocytes around the smaller vessels of the
medulla oblongata, spinal cord, basal ganglia, and cortex of the
brain. Small extravasations of blood were occasionally observed
in the neighbourhood of the distended vessels, while Coats
found migrations of leucocytes in the salivary glands, mucous
glands of the larynx, and kidneys. Marochetti observed pustules
on the frenum linguae during the first few days of the period of
incubation. In the case of a dog that died of rabies I found
miliary abscesses extensively distributed through the spinal cord,
medulla oblongata, basal ganglia, and cortex of the brain. In
addition to the aggregation of leucocytes around the vessels,
Gowers describes intravascular changes, consisting of the pre-
sence of clots in some of the vessels, which he thinks must
have formed during life.

The following description is derived from my own micro-

860

DESCRIPTION OF PLATE V.
(From Drawings by Dr. A. H. Young.)

Fig. 1. — Section of medulla oblongata from a case of hydrophobia, showing
extensive infiltration of the tissues with leucocytes ; all the cut vessels being
surrounded by them. The nucleus of the hypoglossal nerve is infiltrated with
leucocytes ; but its cells are apparently healthy. Almost all the cells of the
nucleus of the pneumogastric nerve have disappeared, and the nucleus of the
spinal accessory nerve was similarly affected lower down the medulla.

Fig. 2. — Portion of the nucleus of the hypoglossal nerve from same section as
Fig. 1, under a higher magnifying power. The ganglion cells appear healthy,
although they are surrounded by leucocytes. The cut ends of the vessels may be
seen surrounded by numerous leucocytes.

Fig. 3. — Portion of grey matter of olivary body from same section as Fig. 1,
magnified, showing infiltration with leucocytes.

Fig. 4. — Section of the anterior horn of the grey substance of the cervical
enlargement of the spinal cord in a case of hydrophobia, m, Median ; al, Antero-
lateral ; pi, Postero-lateral ; and c, Central group of ganglion cells. Shows
infiltration of the tissues with leucocytes, and the cut vessels surrounded by them.
The ganglion cells have apparently disappeared from the area which lies between
the median and the antero-lateral groups, and only two or three of the cells of
the central group are seen; while some cells have also apparently disappeared
from the margins of the antero-lateral and postero-lateral groups. The central
group was also infiltrated with red blood corpuscles.

Fig. 5. — Portion of the area from which the cells had apparently disappeared
in Fig. 4, magnified. Shows that the cells are still present, although they are
much shrunk, and some of their processes destroyed. The walls of the cavity
surrounding them are infiltrated with leucocytes or covered by nuclei.

Fig. 6. — Tetanus. Section of the anterior horn of grey substance from the
middle of the lumbar enlargement. Showing infiltration of the tissue with
leucocytes, and apparent disappearance of the ganglion cells from the area lying
between the few remaining cells of the median group and those of the antero-
lateral group ; also apparent disappearance of a considerable portion of the cells
of the postero-lateral group.

Fig. 7. — Vessel from the anterior median fissure from the same section as
Fig. 6, surrounded by numerous leucocytes.

Fig. 8. — Vessel cut obliquely from the grey substance from the same section a
Fig. 6, showing its lymph sheath surrounded by leucocytes.

Plate. V

Fijf. 1.

Fig. 2.

RMxntern "hth

HYDROPHOBIA.

8G1

scopical examination of the nervous system from six cases of
hydrophobia : —

The changes observed in the medulla oblongata in hydrophobia corre-
sponded closely to the careful drawings and accurate description of Dr.
Gowers ; except, perhaps, with respect to his description of the clot within
the blood-vessels. The distribution of these vascular and perivascular
changes in the medulla oblongata was, in one of my cases, almost coexten-
sive with the distribution of the vessels. The grey matter on the floor of
the fourth ventricle was most affected, probably because it is the most
vascular ; but similar changes were found in the formatio reticularis,
olivary bodies, restiform bodies, and to a less extent in the anterior pyra-
mids. The condition of the medulla in this case is shown in Plate V., fig. 1.
It will be observed that, although the nucleus of the hypoglossal is infil-
trated with leucocytes, its own cells are not much affected, while scarcely a
trace is left of those belonging to the spinal accessory and pneumogastric
nuclei. The same condition is shown under a higher magnifying power in
fig. 2, in which the cells of the nucleus of the hypoglossal appear healthy,
although the tissue is densely infiltrated with leucocytes. Infiltration of
the grey matter of the oh vary bodies with leucocytes is shown in fig. 3.
Similar vascular and perivascular changes were observed, though to a
less extent, throughout the whole extent of the pons, in the grey sub-
stance suiTOunding the aqueduct of Sylvius, and in the corpora quadri-
gemina, as has already been described by Dr. Coats. The cortex of the
brain and subjacent white substance were infiltrated with leucocytes, and
the pyramidal cells of the fourth layer of the cortex were often partially
filled with small yellow granules. The cortex of the cerebellum and
subjacent white substances were also much infiltrated with leucocytes,
the changes here being almost, if not quite, as marked in extent as in
the brain, and the cells of Purkinje were very granular. It would appear,
therefore, that hydrophobia is a disease of a very diffused character.

The changes found in the spinal cord in hydrophobia deserve special
mention. They are not always well marked, and in three of my cases
might very readily be overlooked, while in the other three, marked
alterations were observed in the upper dorsal region and in the cervical
enlargement. One of the anterior horns, from a section of the cervical
enlargement, is represented by Dr. Young in fig. 4. The whole of
the grey substance is infiltrated with leucocytes, and the vessels on each
side of the central canal are surrounded by them. The branches of the
anterior external and anterior lateral arteries distributed to the grey
substance are surrounded by leucocytes. Three distinct miliary abscesses
were observed in the external margin of the antero-lateral group of cells
in the cord taken from the child, who died of hydrophobia, under the care
of Mr. Ewart.

The most interesting changes probably have occurred in the ganglion
cells themselves. Two or three cells, of normal size, may be observed in

862

HYDROPHOBIA.

the part of the median group which is nearest to the anterior fissure, and
full-sized cells may also be observed in the central portion of the antero-
lateral and postero-lateral groups. When examined under a low power,
all the cells seem to have disappeared from the territory which lies between
the few remaining cells of the median group (fig. 4, m) and the antero-
lateral group (fig. 4, a 1), while the cells of the central group (fig. 4, c)
have also, with the exception of two or three, disappeared, and a con-
siderable number are wanting also along the margins of the antero-lateral
and postero-lateral groups. When the areas from which the cells have
apparently disappeared are examined with a higher power, it is seen that
remnants of the latter are still present. The ceUs are surrounded by a par-
tially empty cavity, the walls of which are covered either by leucocytes or
nuclei, while the cells themselves are shrunk to a very variable extent
(fig. 5). The cell membrane appears to be shrunk around the nucleus and
nucleolus, along with a smaU quantity of granular contents ; but one or more
processes can almost always be detected ; the full-sized cells often contain
yellow pigment granules, and sometimes appear to be increased instead of
diminished in size. A number of red blood corpuscles are infiltrated
into the central group of cells (fig. 4, c) and the cells themselves are much
altered and diminished in size. The vesicular column of Clarke, especially
in the upper dorsal and lower cervical regions, is usually much infiltrated
with leucocytes, and its own cells are often deformed and shrunk. At the
junction of the dorsal and lumbar regions, the cells of this group are
frequently found healthy.

§ 935. Morbid Physiology. — The mode of origin of hydro-
phobia shows that the disease is due to a specific animal poison,
and the anatomical lesions found after death appear to indicate
that the toxic agent, whatever its nature, is conveyed in the
blood to the nervous tissues. There is nothing specific in the
miliary abscesses found in hydrophobia as they are observed
in other diseases. The poison, as was first suggested by
Dr. Allbutt, appears to act first on the nuclei of the medulla
oblongata, and more especially on the respiratory centres ; then
on the grey matter of the spinal cord ; and, lastly, on the cortex
of the cerebrum. That the poison of hydrophobia should act
in this manner on the nervous tissues is not more inscrutable
than that the poison of scarlet fever should produce an erup-
tion on the skin, which first appears on the chest, then extends
to the forearms and lower part of the abdomen, and finally
becomes general.

While examining the spinal cord in cases of hydrophobia
I was much struck by the fact that the cells of the median

HYDROPHOBIA.

863

group and the marginal cells of the other groups of ganglion
cells of the anterior horns were invariably altered, while the
ganglion cells of the centres of the groups were apparently
unaffected. It was in my power to take refuge in the supposi-
tion of a special affinity between the poison and these cells,
but I was met by a similar vulnerability of the same cells in
tetanus, in all central inflammations of the spinal cord, whether
acute or chronic, and even in chorea. It was in this state of doubt
that I came to recognise the significance of two other facts with
regard to the cells in question. The ganglion cells which are most
vulnerable in all affections of the grey substance of the spinal
cord are, speaking broadly, smaller than those which are most
resisting, and the former are developed at a much later period
than the latter. The small size of the cells enables them to
present a large surface to their environment in comparison with
their bulk, and consequently they must absorb a proportionably
larger quantity of nourishment. The cell-membranes of the
last are also likely to be thinner than those of the first
developed cells, and this will increase still further the capacity
of the former for the absorption of nourishment. The ganglion
cells which absorb a large quantity of nourishment in a rela-
tively short time must necessarily suffer at an earlier period in
states of active hyperemia than the cells which absorb a less
quantity, while they will be equally the first to suffer in condi-
tions of anaemia, inasmuch as the want of nourishment must be
first felt in those cells which are undergoing the most active
changes. There are no grounds, therefore, for believing that
the accessory manifest a greater affinity than the fundamental
cells for the virus of hydrophobia, but the conditions under
which nutrition is normally carried on in both are such that
the former suffer in this disease to a greater degree than the
latter.

§ 936. Diagnosis. — The history of a bite from a rabid animal
is generally sufficient to direct attention to the true nature of
the disease. But inasmuch as the animal is generally killed
soon after inflicting the injury, we often cannot be sure that it
was the subject of rabies. On the other hand, those who have
been bitten by dogs or other animals are often haunted by the

864

HYDROPHOBIA.

dread of hydrophobia, and hysterical symptoms not unlike those
of the actual disease may become developed in them. In cases
of the kind, besides globus hystericus, other symptoms are
generally present which render their nature apparent, and,
inasmuch as hydrophobia is almost always fatal within four
days from the commencement, its diagnosis from hysteria cannot
long remain matter for doubt. It must also be . remembered
that tetanus may occur after the bite of an animal just as
after other injuries, and it is not impossible that cases of reported
recovery from hydrophobia have been of the nature of tetanus,
In tetanus the patient is usually calm and the mental faculties
are clear to the last; while there is complete absence of
the emotional excitement, horror, and delirium observed in
hydrophobia.

§ 937. Treatment. — Every effort should be made to prevent
the development of the disease. The tissues surrounding the
wound should be at once excised with the knife, or, if this be im-
possible, destroyed by the actual cautery or powerful caustics, as
potassa fusa or nitric acid. Youatt placed the greatest reliance
on the cauterisation of the wound with the solid nitrate of
silver.

When the disease is established, every effort should be
directed to soothe the sufferings of the patient. In the cases
coming under my observation, subcutaneous injections of
morphia and chloral appeared to be productive of most relief,
inasmuch as several hours of quiet sleep were procured for the
unfortunate patient. Hot-air and vapour baths have been
recommended, and the latter is very soothing to the patient;
but there are no grounds for believing that it can eliminate the
virus.

8G5

CHAPTER IV.

HYSTERIA.

Hysteria is a functional disease of the nervous system charac-
terised by paroxysms of convulsions with apparent loss of con-
sciousness, along with various sensory, motor, vaso-motor, and
psychical disturbances, which may be combined in such mani-
fold ways that the grouping of the symptoms may simulate any
one of the numerous organic diseases to which the nervous
system is liable.

§ 938. Etiology. — Hereditary predisposition exerts a power-
ful influence in the production of hysteria. The transmission of
the disease is sometimes direct, the mother transmitting it to
the daughter, and at other times indirect, the patient inheriting
a neurotic constitution which manifests itself in one member of
a family as hysteria, and in the others as neuralgia, epilepsy
chorea, or insanity.

Hysteria occurs with preponderating frequency, although by
no means exclusively in the female sex. Briquet states that
one out of four of all females are affected with decided hysteria,
and that one-half present an undue impressionability which
differs very little from it, a proportion much too high for this
country. Out of 1,000 cases collected by Briquet, one male
was affected with hysteria in proportion to twenty females.

The disease usually begins in females about the age of
puberty, the first symptoms being manifested in more than half
the cases collected by Briquet between twelve and twenty, and
in a third of them between fifteen and twenty years of age.
The establishment of menstruation does not appear to favour

D DD

866 HYSTERIA.

the development of hysteria, although the affection is frequently
associated with derangement of the function.

Hysteria occurs in children of both sexes under ten years of
age. Briquet states that the first symptoms appeared in children
under ten years in about one-eighth of his cases, a proportion
which is much too high so far as this country is concerned.
Boys from ten to fourteen years of age are not unfrequently the
subjects of hysteria ; cases of the kind have been recorded by
Wilks and Roberts, and I have myself seen several examples.

All causes which lower the nutrition of the nervous system,
as haemorrhages, insufficient nourishment, impaired digestion,
and anaemia, predispose to hysteria.

Hysteria affects the females of the higher classes of society
more frequently than those of the working classes. Young
ladies often lead an utterly aimless existence, periods of idle-
ness alternating with the unhealthy excitement afforded by
balls and theatres. Under such circumstances too little exer-
cise is apt to be taken, the bowels become constipated, digestion
is impaired, and anaemia results ; all of these are conditions
tending to diminish the nutrition of the nervous system. The
mental energies not being expended on any healthy occupation
are apt to be directed inwards to the contemplation of the
patient's own thoughts and feelings; and under these circum-
stances the emotions connected with the gratification of the
sexual impulses are apt to occupy a predominant place in the
thoughts. This mental condition, while strengthening the
lower emotions, weakens the power of the will, and induces
that excessive irritability of the nervous system which under-
lies hysteria.

The depressing passions, as fear, anxiety, jealousy, and remorse,
frequently induce hysteria, while exhaustion from overwork
when combined with anxiety, as in the case of those who have
to nurse sick relatives, is one of the most fruitful causes of the
disease.

All uterine derangements, whether structural or functional,
are apt to be attended by hysteria, and the symptoms are liable
to become aggravated during the menstrual periods in those
who are already hysterical. The name hysteria was, indeed,
given to the disease under the belief that it was always caused

HYSTERIA.

867

by disease of the uterus and its appendages; but this exclusive
view of the origin of the disease is now no longer maintained
by anyone. Hysteria may be acquired by those who are pre-
disposed to it by the imitation of others. Young susceptible
girls are not unfrequently seized with hysteria after being
witnesses of the disease in another. An actual epidemic of
hysteria may occur in public institutions, like hospitals, fac-
tories, and girls' schools, and the convulsive epidemics of former
ages appeared to spread in this manner.

§ 939. Symptoms. — The symptoms of hysteria may be
divided for the purpose of description into : (1), those which
characterise the intervals between the attacks ; and (2), those
which constitute the hysterical paroxysm.

(1) Interparoxysmal Symptoms.

(a) Sensory Disturbances. — Hyperesthesia in some form or
another is seldom absent during the course of hysteria. The
acuteness of the perceptive faculties is sometimes increased, so
that hysterical patients may see, hear, smell, or taste objects
imperceptible to the healthy ; and their sense of touch may
also be preternaturally acute. But disorder of the common or
emotional sensations is much more usually met with than dis-
order of the special or intellectual. Sensations which to others
are indifferent or pleasant produce in the hysterical the highest
degree of discomfort ; and, conversely, sensations disagreeable
to others may be eujoyed by them. Hysterical patients often
complain urgently of neuralgic pains in various parts of the
body in the absence of any recognisable cause.

The senses of touch and temperature are sometimes increased
in acuteness. Some hysterical patients recognise persons and
objects by the sense of touch with an accuracy unknown in the
healthy, while they often complain of pulsation in different parts
of the body, which can only be explained on the assumption of
an increased sensibility.

Cutaneous or deep-seated hyperalgesia is rarely absent in
hysteria, and it may or may not be accompanied by spontaneous
pains in the affected parts. Cutaneous hyperalgesia is some-

868

HYSTERIA.

times widely diffused, so that the slightest movement of the
patient causes discomfort. In most cases, however, the hyper-
algesia is limited to particular portions of the surface or to one
extremity, a circumscribed portion of the trunk, or half the
body, while irregularly circumscribed anaesthetic patches are
sometimes found in the midst of a hyperaesthetic region.

The neuralgiform pains which occur in various parts of the
body are described as of extreme severity. Neuralgia of the
mammary gland is sometimes complained of, especially at the
menstrual periods; while a fixed and severe pain in the left
infra-mammary region — probably an intercostal neuralgia — is
an all but constant symptom of hysteria. The skin over the
mamma? may become so sensitive that the slightest touch or
the contact of the dress may be unbearable, and great sensi-
tiveness to pain is often observed in the neighbourhood of the
ensiform cartilage ; while pains of a dull, heavy character,
accompanied by a feeling of oppression and anxiety, are some-
times experienced at different parts of the sternum;

Severe pain diffused over the whole surface of the abdomen
is a not uncommon symptom of hysteria. The abdominal
pain is usually associated with tympanites, and the sensitiveness
to touch is so great that the patient cannot bear the contact of
the bed-clothes; while deep and continuous pressure, on the
other hand, may cause little or no discomfort, especially if
the attention of the patient be diverted. Hysterical patients
suffer greatly from cardialgia, and when it is associated, as is
frequently the case, with persistent vomiting the symptoms
may be mistaken for those of perforating ulcer of the stomach.
Many hysterical patients suffer from a great craving for food,
leading fchem to eat large quantities ; this condition is probably
caused by a hyperagsthetic condition of the mucous membrane
of the stomach. Ovarian hyperesthesia (§ 345) is sometimes
observed, and, curiously, this condition is usually associated
not with hyperesthesia, but with anaesthesia of the same side.
Hysterical patients often suffer, especially at the menstrual
periods, from irritation and burning at the labia and at the
vaginal orifice, these sensations being not unfrequently asso-
ciated with increased sexual desire. The bladder and urethra
are also excessively sensitive and painful in such cases.

HYSTERIA.

809

Hysteralgia is not an unfrequent symptom of hysteria, inde-
pendently of any local disease ; coccygodynia without local
disease is exceptional.

Hysterical patients suffer from various more or less painful
affections of the back. Cutaneous hypergesthesia is sometimes
present, its favourite sites being circumscribed portions of skin
over and between the scapulas. Tenderness of the vertebras and
surrounding structures is, however, a more frequent symptom,
the sensitiveness being sometimes limited to the spinous pro-
cesses and at other times distributed laterally in the muscles of
the vertebral column ; this spinal tenderness is frequently
accompanied by genuine neuralgia. The affection already
described under the name of spinal irritation consists of
spinal tenderness in association with other aggravated symptoms
of hysteria. Increased sensitiveness of the muscular afferent
nerves probably cause the restlessness frequently experienced
by hysterical patients.

The pains and hyperesthesia frequently occurring in and
around the joints are deserving of particular attention, inasmuch
as they are often mistaken for chronic articular disease. Sir
Benjamin Brodie was the first to direct attention to the fre-
quency of these affections, and he asserted that four-fifths at
least of the joint diseases met with in women of the higher
classes of society are purely hysterical. The hip and knee
joints are most frequently affected; but the ankles, wrists, and
even finger joints may be attacked. In the hysterical affection
pressure upon the joint produces pain, but little or no pain is
caused by forcible apposition of the articular surfaces, especially
if the attention of the patient be otherwise engaged. The
disease may continue for years, and in chronic cases the joint
may become slightly swollen from oedema of the surrounding
soft parts.

The senses of smell and taste are frequently increased in
acuteness, the patients recognising tastes and odours which are
inappreciable to most people. At other times there is a per-
version of these senses, and the patient manifests a preference
for certain tastes and odours which are disagreeable or in-
different to others. In obedience to this morbid craving
hysterical patients sometimes devour chalk, cinders, or even

870

HYSTERIA.

disgusting substances, and exhibit a liking for odours like
those of assafcetida and valerian. Hallucinations also of taste
and smell may be experienced in hysteria.

The sense of hearing often becomes extremely sensitive, but
intolerance of sound is more frequently met with than true
auditory hypersesthesia. Subjective sensations, such as ringing,
blowing, roaring, are sometimes heard, or there may be true
auditory hallucinations.

The sense of sight is sometimes increased in acuteness, but
intolerance of light is more frequent. Under the latter circum-
stances the patient shuns the light, and the power of detecting
objects in the dark is increased. At times the hypersesthesia
only exists with respect to a particular colour, most commonly
red. Sparks aod flashes of light are sometimes complained of,
while at other times there are hallucinations of sight, the objects
seen being often productive of disgust and horror.

Anaesthesia. — Diminution or complete loss of sensibility is a
very frequent symptom of hysteria. It may exist over a large
portion of the surface of the body, and may implicate the
muscles and deeper tissues as well as the nerves of special sense.
Anaesthesia, in some form or another, occurs frequently after a
hysterical attack, and the more severe the attack the more
likely is anaesthesia to ensue; as a rule, it diminishes in the
interval. Sometimes, however, an extensive and persistent
anaesthesia may disappear after a fresh attack, and the
sensibility of the previously affected part may become normal
or exaggerated, or the anaesthesia become transferred to another
portion of the body.

In the majority of cases sensibility to pain is alone altered,
while the other forms of cutaneous sensibility remain normal.
In some cases tactile sensibility is lost, while variations of
temperature are correctly appreciated ; in other cases every
form of cutaneous sensibility, as well as that of the muscles,
bones, and joints, is abolished.

Anaesthesia of the mucous membranes is not of uncommon
occurrence either alone or in connection with cutaneous anaes-
thesia. It is associated with diminution or loss of reflex contrac-
tility, neither reflex spasm, lachrymation, nor reddening being
provoked by the contact of foreign bodies with the affected

HYSTERIA.

871

conjunctiva, nor sneezing by the inhalation of irritating sub-
stances when the nasal mucous membrane is implicated. Sensa-
tion may be abolished in the mucous membranes of the pharynx,
larynx, and respiratory tract generally, and the occasional
retention of urine and faeces in hysterical patients is probably
caused by anaesthesia of the mucous membranes of the bladder
and rectum, inasmuch as in such cases the bladder or rectum
may sometimes be found enormously distended without having
caused more than a trifling amount of discomfort. The mucous
membrane of the genital organs and of the urinary passages
is sometimes found insensible. The mucous membrane of the
vulva and vagina may be completely anaesthetic. This con-
dition is found in highly hysterical married women, and in them
there is an entire absence of sexual desire or pleasure.

The special senses are not unfrequently affected by anaes-
thesia in hysteria, more especially after severe hysterical
seizure. The senses of taste and smell may be lost, the loss
being sometimes unilateral, at other times bilateral. Deafness
of nervous origin is also occasionally observed, and it may be
limited to one ear or affect both.

There may be amblyopia or complete amaurosis of one or
both eyes, unilateral amblyopia being the most frequent
condition. Hysterical amblyopia consists of diminution of the
acuteness of vision, restriction of the field of vision and achroma-
topsia, while sometimes a condition simulating hemiopia may
be present. An ophthalmoscopic examination does not reveal
any changes in the optic discs.

The distribution of the different forms of hvsterical anaesthesia
is very variable. Cutaneous anaesthesia is often limited to
certain circumscribed portions of the surface of the trunk and
extremities ; it may be observed in the region of distribution
of one or more nerve trunks, be limited to one or more extremi-
ties, or be accurately confined to half the body.

In hysterical hemiancesthesia the loss of feeling on the
anaesthetic side frequently affects the superficial parts only;
but at other times the muscles, bones, and articulations are
implicated.

Hemianalgesia is the most common form of the incomplete
variety, the insensibility to pain being sometimes associated

872

HYSTERIA.

with thermo-ansesthesia. In complete hemiansesthesia not only
the skin, but the muscles, bones, articulations, and the special
senses, and even the accessible mucous membranes on the
same side of the body are implicated. Taste is abolished on
the corresponding half of the tongue, the sense of smell is
less acute in the corresponding nostril, and partial deafness and
amblyopia exist on the same side. The anaesthesia, however,
does not appear to extend to the viscera, and complete hemi-
ansesthesia is usually associated with ovarian hyperesthesia.

(b) Motor Disturbances. — Spasms, either tonic or clonic, may
occur in hysteria in every muscle or group of muscles of the
head, trunk, and extremities. Every one of the spasms already
described as occurring in the area of distribution of one or
several of the peripheral motor nerves may appear in hysteria
in the form of a more or less persistent or of recurring contrac-
tions. It is unnecessary to describe them in detail. The facial
muscles are incessantly active in many hysterical patients, so
that the countenance has a restless and unsettled expression,
constituting one of the main characteristics by means of which
the practised physician is enabled to diagnosticate the disease.

Spasmodic closure of the glottis may produce alarming
dyspnoea, and the patients are liable to attacks of convulsive
laughter and weeping, which often arise apparently in the
absence of any emotional disturbance. During hysterical
attacks loud screams are commonly emitted, and in that form
of hysteria named chorea major the patients often imitate the
cries of animals by mewing, barking, or howling. Hysterical
patients often suffer from a temporary acceleration and exag-
geration of breathing without there being any feeling of embar-
rassed respiration, and at other times they suffer from temporary
spasmodic pauses in the respiratory rhythm. Hiccough and
yawning are frequent and sometimes very distressing symptoms.

The pharyngeal muscles are sometimes spasmodically con-
tracted, so that swallowing becomes difficult or impossible.
Spasm of the tongue is not ^infrequently associated with that
of the pharyngeal muscles. At every attempt to move the
tongue it becomes distorted in various directions, so that
articulation and swallowing become greatly impeded. The
sensation of choking in the throat, named globus hystericus

HYSTERIA.

873

(§ 61), is supposed by some to be caused by a spasm of the
oesophagus. The sensation of a foreign body in the throat is
sometimes so real that the patient, after making strenuous
efforts to remove it by swallowing, puts her fingers into her
throat in order to induce vomiting, by which she hopes to eject
it. Actual spasm of the oesophagus may sometimes be so
persistent as to resemble organic stricture.

The stomach is liable to undergo spasmodic contractions,
giving rise to persistent and distressing vomiting. The patient
vomits almost immediately after food is taken, so that the latter
is usually ejected in an undigested condition. Some of the food
is, however, probably retained, as the nutrition of the patient
rarely suffers in proportion to the apparent violence and per-
sistency of the vomiting.

Irregular peristaltic movements occur in various parts of the
intestines, and these may be so energetic that they can be felt
through the abdominal wall. The rolling of the intestines may
convince the patient that a movable body is present in the
abdomen. Spasm of certain portions of the intestines may
be so persistent as to cause temporary stricture, and the
bowels above the constricted portion become greatly distended
with gas, giving rise to what has been called a " phantom
tumour;" or a real obstruction of the bowels may sometimes
be caused by accumulation of fasces behind the constricted
portion. Eructations, borborygmi, and griping pains may also
be caused by irregular peristaltic movements of various portions
of the digestive canal.

Spasmodic retention of urine, generally combined with in-
creased inclination to micturate, occurs in many hysterical
patients; and this condition is sometimes, but not always,
associated with a painful condition of the genitals.

Vaginismus, caused by spasm of the constrictor vaginas, some-
times renders coitus difficult or impossible ; it is generally asso-
ciated with hyperesthesia of the vaginal orifice, the spasm
being induced by reflex action.

Paralyses. — Partial or complete loss of muscular power is a
frequent symptom of hysteria. Briquet found that out of 430
cases of hysteria 120 suffered from paresis or paralysis ; and
Landouzy, out of 370 cases, found 40 similarly affected.

874

HYSTERIA.

The loss of motor power may begin with mere weakness and
heaviness of the limb or limbs, which gradually increase to
complete paralysis. At other times the commencement is
sudden, the paralysis becoming fully developed after a hysterical
attack.

The distribution of the paralysis is very variable. It may
assume the hemiplegic form, and in these cases the paralysis
often supervenes after an attack of hysterical convulsions,
attended with partial loss of consciousness, which may last
for several days, so that the hemiplegia resembles the result
of organic lesion of the brain. In hysterical hemiplegia there
is no distortion of the face, nor deviation of the tongue on
protrusion, phenomena which are almost always present at
first in hemiplegia, due to cerebral lesion. In hysterical hemi-
plegia the paralysis is seldom complete; in the majority of
cases the leg is more profoundly affected than the arm, and
the loss of motor power is liable to considerable variations in
intensity, especially under the influence of emotional excite-
ment. Hysterical hemiplegia is, moreover, generally associated
with the hemianesthesia already described, as well as with
ovarian hyperesthesia, retention of urine, tympanites, and other
symptoms of aggravated hysteria. Another feature worthy of
attention is that the convulsive attack which preceded the
paralysis is always produced by a profound moral shock.

One extremity only is affected, or the upper extremity on
one side and the lower extremity on the other, and total
paralysis of all the extremities is not unknown. The paralysis
may be limited to one or more motor nerves, or to one of the
branches of a nerve. Hysterical paralysis of the ocular muscles
is rare, but paralysis of one or both the levator palpebrse
superioris muscles is not unfrequent, and the well-known
hysterical expression is probably partly due to the drooping
of the upper eyelids, caused by imperfect contraction of these
muscles.

The excitability of the paralysed muscles to both the faradic
and galvanic currents remains unchanged even when the
paralysis has existed for years, a circumstance of great im-
portance in establishing a correct diagnosis. After long
disuse the muscles may indeed undergo a certain amount of

HYSTERIA.

875

atrophy, in which case there may be a slight diminution of
electric excitability, but the "reaction of degeneration" is never
established.

Anaesthesia is frequently associated with paralysis in hyste-
rical patients, although each of these conditions may be present
without the other. When both conditions are combined the
anaesthesia is generally not confined to the skin, but extends
to the muscles, and then "electro-muscular sensibility" is
diminished or abolished. Duchenne regarded this condition
as a very valuable sign of hysterical paralysis, but it must be
remembered that muscular anaesthesia is sometimes absent in
hysterical, and occasionally present in paralysis of apoplectic
origin. Hysterical paralysis is always accompanied by other
manifestations of the disease, such as spasm, hyperesthesia,
and particularly by the characteristic psychical condition.

In doubtful cases a careful observation of the course and
progress of the disease will aid in clearing up the diagnosis.
Hysterical paralysis is generally variable in its duration, con-
tinuing for a few hours, days, or weeks, and then completely
disappearing, perhaps to return after subsequent attacks of
hysteria. The mode of extension of the paralysis is sometimes
characteristic. It may be pronounced at first on one-half of
the body, then quickly disappear from that side and present
itself on the opposite side, or it may be crossed. In some
cases the paralysis continues for years unchanged in extent ;
in these cases hysteria may be difficult to distinguish from
hemiplegia caused by circumscribed lesion of the brain, or from
cerebro-spinal sclerosis and spinal paraplegia.

Contracture not unfrequently becomes developed in the
paralysed extremities. In some cases the contracture appears
simultaneously with the paralysis, while in other cases the
paralysis continues for some time and then contracture super-
venes gradually or suddenly after a fresh attack. In the
upper extremities there is spasmodic flexion of the forearm,
hand, and fingers ; the muscles are in a state of considerable
rigidity, so that it is impossible to obtain complete extension,
or to increase the flexion.

The lower extremity is strongly extended upon the pelvis, and
the leg upon the thigh ; the foot generally assumes the position

876

HYSTERIA.

of talipes equino-varus ; and the knees are drawn inwards by
contraction of the adductors of the thighs.

Contractures may, like paralysis, last for years, and then
suddenly cease, generally under the effect of strong emotional
disturbance. In other cases, when the contracture has continued
for many years, atrophy of the affected muscles may result,
accompanied by the " reaction of degeneration." Under these
circumstances the contracture cannot be overcome under the
deepest chloroform narcosis.

In hysterical contracture with paralysis tremor is sometimes
observed, especially on attempting any movement, just as occurs
in the paralysis with contracture arising from sclerosis of the
lateral columns of the cord.

Charcot relates the case of a woman, the subject of hysteria,
who had suffered from contracture in all the extremities for
ten years. The degree of contracture had undergone many
fluctuations for several years, but ultimately became perma-
nently established, and a post-mortem examination revealed
sclerosis of both lateral columns of the cord. But, as Charcot
remarks, the presence of tremors in cases of hysterical contrac-
ture, which terminate abruptly in recovery, shows that this
symptom cannot always be attributed to a permanent lesion of
the lateral columns.

Tremor may also occur in hysteria independently of paralysis
with contracture, and it then closely resembles the tremors of
paralysis agitans or of cerebro -spinal multiple sclerosis. This
tremor may appear in the muscles of the head, tongue, face, or
hands, and is called forth and aggravated by emotional excite-
ment. It persists during repose, if the patient be conscious of
being observed.

Hysterical aphonia from paralysis of the vocal cords is a very
frequent symptom of hysteria. Aphonia may appear suddenly
after some mental excitement, and disappear with equal celerity.
Difficulty of moving the tongue is sometimes associated with
the laryngeal paralysis, and the patients no longer whisper,
but resort to pantomime in order to make themselves intelligible.
Laryngoscopic examination shows paralysis of the adductors of
the glottis sometimes on one, sometimes on both sides.

Paralysis of the muscles of the pharynx and the oesophagus is

HYSTERIA.

877

not an uncommon symptom of hysteria, and swallowing' may
consequently be rendered difficult or impossible. In such a
case the oesophageal tube passes into the stomach without any
obstruction. Retention of urine is common, and often paralytic
in origin.

Paralysis of the muscular coat of the stomach is partly cause,
partly effect of the general tympanites which is so frequently
met with in hysterical patients. Tympanites may come on
suddenly, in consequence of mental agitation or at the close of
a hysterical attack, and sometimes reaches such a degree that
the patients may be kept afloat in a bath by means of the
gaseous distention. The obstinate constipation which is so
frequent in hysteria is probacy due to paralysis of the muscular
coat of the bowels.

(c) Vaso-motor and Secretory Disturbances. — In the inter-
vals between the attacks of hysteria the action of the heart
and the pulse may be normal, unless indeed some general
disease, like chlorosis, be present. Hysterical patients are,
however, liable to suffer from paroxysms of palpitation. During
these attacks the pulse is at first frequent, small, and hard ;
the skin is pale and cold ; there is a feeling of fulness and
oppression in the chest ; and there may be a degree of mental
confusion. After a time the cutaneous vessels relax and the
surface is reddened and covered with perspiration; the pulse
then becomes slow, full, and compressible. Hysterical patients
are liable to fainting fits, caused doubtless by sudden anaemia
of the brain. The cerebral anaemia may in its turn be produced
either by vaso-motor contraction of the intracranial arterioles,
or by sudden dilatation of the arteries of the body, especially
of the abdominal arteries, permitting the blood to accumulate
in the dependent parts.

Various other alterations of the vascular tonus may occur
in hysteria, independently of the state of the cardiac action.
Patients frequently complain of " rushing of the blood to the
head" and flushing of the face, which may assume an
intensely red colour; the hands and feet are at the same time
pale and icy cold, and the mucous membranes, especially of the
conjunctivae and lips, are anaemic. Hysterical subjects are liable
to become pale and to blush alternately, and the flushing of the

878

HYSTERIA.

face "is often accompanied by profuse perspiration. But the
alternate contraction and dilatation of the vessels is not confined
to the face. In hysterical joint affections Brodie observed that
coldness and pallor of the affected extremity existed for some
hoars daily, to be succeeded by redness, heat, and sweating for
a similar period, the latter symptoms in their turn giving place
to the normal condition. The hands, which are dry and cold
when at rest, often become warm and moist on the slightest
attempt at manual exercise, such as writing, and even the cold
hands of hysterical patients are often covered by a clammy sweat.
The whole body is sometimes prone to perspire, while uni-
lateral sweating is occasionally observed. Neuralgic affections,
sometimes accompanied by herpes, are frequently associated
with local hyperemia of the skin in hysterical subjects.

Charcot has drawn attention to the fact that in the complete
form of hysterical hemiansesthesia the ansesthetic side not only
suffers from comparative pallor and coldness, but bleeds little or
not at all on being pricked with a pin. His attention was first
drawn to this peculiarity by observing, on leeches being applied
to a patient affected with hysterical hemianesthesia,- that
their bites yielded very little blood on the ansesthetic side;
while the healthy side bled as usual. Charcot believes that
hysterical ischaemia may furnish an explanation of certain
reputed miraculous occurrences, as, for instance, of the state-
ment made on good authority that in the epidemic of Saint
Medard the sword blows given to the " convulsionnaires " did
not cause bleeding. The amenorrhcea, so frequently associated
with hysteria, is probably often caused by local ischsemia,
although it sometimes results from the general anaemia which
underlies both affections.

Not less remarkable than hysterical ischcemia is what may
be termed hysterical hypercemia. Hysterical hyperaemia some-
times leads to profuse and frequently repeated menstruation,
although, no doubt, both the menorrhagia and hysteria some-
times result from ovarian disorder. In hysterical ischsemic
amenorrhcea haemorrhages may take place from other organs,
and these are generally regarded as vicarious of menstruation.
The mucous membranes of the nose, throat, stomach, and lungs
are the favourite sites of these haemorrhages; but in rare cases

HYSTERIA.

879

they occur from any portion of the surface of the body, and in
the absence of any recognisable lesion of the skin. Haemorrhages
may occur in the hysterical quite independently of any disorder
of the menstrual functions, and in such cases they are due to
local congestions of the affected organ.

In hysterical hamiatemesis it is very difficult to be certain of
the absence of gastric ulcer, since the presence of hysterical
symptoms does not exclude the co-existence of organic disease.
In the former case, however, the general health does not suffer
in proportion to the apparent gravity of the symptom, the
patient may eat indigestible articles of diet with impunity,
and there may be little or no general gastric disturbance.
Sometimes, however, the diagnosis can be made only after pro-
longed and careful observation. The same remarks apply in
great measure to hysterical haemoptysis. Whenever haemoptysis
occurs in a hysterical patient, the most careful examination
of the chest should be made, and the temperature taken night
and morning for some days.

In the examination of hysterical patients one must be con-
stantly on the alert against deception. Such patients simulate
haemoptysis by sucking and drawing blood from their gums,
and haematemesis by mixing the blood of animals with vomited
matters, or even by drinking the blood first and then irritating
the fauces so as to induce vomiting. What is true with
regard to internal haemorrhages is still more so with respect to
haemorrhages from external surfaces. In the phenomenon known
as stigmatisation, large bullae form on various portions of the
surface, especially on the hands and feet, chest, and forehead.
These bullae are at first filled with clear serous fluid, which
soon becomes of a bloody colour, and then, after subsidence of
the vesicle, a flow of blood takes place from the surface which is
tolerably abundant and may persist for a long time.

There are well authenticated cases of haemorrhage from the
surface of the body. Parrot observed an escape of blood-
coloured fluid from the skin of the fingers, knees, thighs, chest,
and conjunctiva in a patient at different times during general
convulsive attacks. Laycock mentions a case in which there
was bleeding from the nipple, and quotes a similar case from
Sir Astley Cooper, while subcutaneous extravasations have

880

HYSTERIA.

been frequently observed in hysteria. When small bleeding
points are observed on the surface of the body, suspicion of
deception should immediately be aroused. Mention has already
been made of the fact that in hysterical patients ischaemia fre-
quently alternates with hyperemia, and if during the former
stage several pricks were made with a pin in the portion of skin
affected, these would not bleed at first, but might bleed freely
a short time afterwards when the hyperseuric stage supervenes.

Sudden elevation of temperature of the body is one of the
most remarkable phenomena of hysteria. In the case of a
lady who suffered from anomalous nervous symptoms after a fall
from a horse, under the care of Mr. J. Teale, a temperature of
122°F. was recorded. More or less similar cases have been
observed by Dr. Donkin. The following case, reported by Dr.
Steell, is a good example : —

M. M , 20 years of age, a nurse in the Manchester Koyal Infirmary,

first came under medical treatment on the 24th of October last. She had
been out nursing a case of erysipelas, and seemed impressed with the idea
that she had contracted the disease. A slight blush above each ankle and
a transitory and slight pyrexia were, however, all the evidences of disease
she then presented. A few days after admission, when the pseudo-
erysipelas had entirely subsided, retention of urine was complained of,
and it was learned that about a year previously she had been similarly
affected, but had not come under medical supervision. The urine was
drawn off twice daily, and various remedies were employed, without
restoring voluntary micturition. As the case was regarded as essentially
hysterical in nature, she was allowed, to go on duty, care being taken that
no undue distension of the bladder occurred. Her pulse and temperature
at this time were always found to be normal. Abdominal pain was
occasionally present, and, perhaps wrongly, was attributed to distension
of the bladder. Menstruation did not deviate materially from the normal.
Other remedies having failed, faradisation was employed, one electrode
being attached to the stilette of a gum-elastic catheter, which was passed
into the bladder, a sponge electrode being applied externally. Acute
cystitis followed this application on one occasion, and dming the attack
ample evidence was given that the power of voluntary micturition was
entirely wanting. The cystitis passed off in a few days, and did not seem to
have been an unmixed evil, some return of voluntary micturition following
it. For this cystitis she had been again warded on December 8th. About
this time Dr. Thorburn, obstetric physician to the Infirmary, examined
the patient, and found a prolapsed ovary enlarged and very tender. She
stated that she had frequently pain on defecation, and abdominal pain
became a frequent and distressing symptom. This was chiefly referred to

HYSTERIA.

881

the left iliac region, where there was also tenderness on pressure, but not
limited entirely to that spot. Her temperature at this time became
unsteady, as shown by the following observations : December 8th, evening,
100-6°; 9th, evening, 98-6°; averaging 101° from the 11th till the 24th,
when it reached li>3-2° in the morning. This temperature was not
maintained, and the thermometer registered 100'4° on the evening of the
25th. The temperature remained about 101° (reaching the normal,
however, on the morning of the 28th) till the 30th, when the remarkable
abnormity which it is the object of these lines to record began to manifest
itself, temperatures of 105° and 98-6° (the former occurring during a rigor)
being observed the same evening. The temperature after this continued
irregular, as before, till the 3rd of January, when the thermometer in the
axilla registered 106-6° at 10 p.m. during a rigor (pulse 132). On the 8th,
105 "8° was noted under similar circumstances, but shortly after 99*4°.
The following two days it remained normal, and on the 11th rose only to
102-6°, again to fall to normal. I regret that I am unable to furnish an
unbroken curve of temperature observations, but I trust the facts I can
substantiate will lose none of their value on that account. Rigors now
began to occur with increasing frequency, each being accompanied by a
rapid and great rise of temperature. They were irregular in occurrence,
and did not conform to any definite type. Perspiration usually followed.
It will be seen that the general form of the temperature curve would most
closely resemble that of pyaemia, and the possible existence of an abscess
in or about the ovary could not but suggest itself. The general condition
of the patient was at variance with this hypothesis, the well-known
features of intense illness being absent. I shall merely mention some
single observations of temperature, giving the date and time. It may be
taken for granted that the high temperatures were those observed during
or immediately after a rigor.

January 24th, 11 a.m 107-2°

„ 24th, 12 a.m 102-2°

„ 24th, 9 p.m 101°

„ 25th, evening 98'4°

„ 29th, „ 100-8°

„ 30th, morning 97-8°

„ 30th, evening 99*6°

February 4th, „ 105°

„ 5th, „ 105-2°

„ 6th, morning 99*8°

10th, „ 105-4°

16th, „ 99-4°

„ 16th, evening 105-6°

„ 24th, morning...... 98°

„ 24th, 5-35 p.m. ... 108-6°

24th, 10p.m. (?)... 98-4°

26th, 6 p.m 112°

28th, 4-30 p.m. ... 113°

March 1st, morning 98-2°

„ 1st, evening 100°

E E E

March 3rd, 8-45 a.m 111°

„ 3rd, 10-30 a.m 108-2°

„ 3rd, 11-30 a.m 99-2°

„ 4th, 5-15 a.m 107*4°

„ 4th, 8-45 a.m 108°

„ 4th, 4 p.m 112-4°

„ 5th, 8-50 a.m 108-6°

„ 5th, 2-30 p.m 106°

„ 5th, 3-45 p.m 107-4°

„ 7th, 10 a.m 109°

„ 7th, 8-30 p.m 102-6°

„ 8th, 6 p.m

„ 11th, 4-30 p.rn 111-2°

„ 12th, 10 a.m 108°

„ 17th, evening 100'4°

„ 18th, 3-30 p.m 116-4°

„ 19th, 4 a.m 11 6° 4-

„ 19th, 8 p.m 98-6°

„ 21st, 9-30 a.m lll°-f-

„ 23rd, 9-30 a.m 106°

882

HYSTERIA.

During the last few weeks of treatment mental disturbance has
supervened. At first this accompanied the hyperpyrexia only, but
latterly it has been nearly constant. She has no fixed delusion, and what
delusions she has manifested have been clearly founded on recent events
which occurred around her. They tended towards the melancholic type
of insanity. At times she has been exceedingly violent, and always more
or less suspicious. There is no family history of insanity.

I believe that the hyperpyrexial attacks were of very short duration,
and where, by the above figures, a prolonged high temperature is indicated,
it is only apparently so, the observations having been made during the
rigors. All were made in the axilla, and different thermometers were
used, several of which had their registering columns driven into the bulb
at the top (indicated above by the symbol +)• I should mention that
the retention of urine noted at the commencement has continued, with
occasional intermissions of varying duration.

These hues were written towards the end of March, and it remains for
me in a few sentences to narrate the subsequent history of the case. The
attacks of hyperpyrexia ceased (though transient pyrexia occurred from
time to time) on the advent of a new series of phenomena, including
general convulsions of extreme violence, accompanied by opisthotonos,
loss of consciousness, hvidity, &c, and followed by persistent trismus,
simulating in a remarkable way the traumatic form of that affection. [
These severe symptoms gradually diminished in intensity and frequency ?
while general amelioration in the patient's condition set in, so that on the
12th of April she was able to be removed to the Cheadle Convalescent
Hospital. There her convalescence continued with but slight interruptions,
and she is now on full duty as a nurse in the institution.

Hysterical patients suffer from various anomalies of secretion
and excretion. Increased flow of saliva is not an unusual
symptom after a hysterical attack, and it occurs occasionally
independently of the fits. At other times an abnormal dryness
of the mouth, along with great thirst, is present, inducing the
patients to drink large quantities of fluid.

The gastric secretion is sometimes largely increased, and may
take place independently of the ingestion of food. Hysterical
vomiting is sometimes caused by spasm of the muscular coat
of the stomach, but at other times it appears to be determined
by the irritating effect of the excessive gastric secretion upon
the mucous membrane of the organ, while in many cases both
conditions are probably present in co-operation. When the
vomiting is due to excessive secretion, large quantities of fluid
are ejected, even during fasting, and the appetite is sometimes
greatly impaired, and at other times enormously increased.

HYSTERIA.

883

Hysterical vomiting is not often accompanied by much loss
of flesh, but great emaciation may take place in hysteria in
the absence of vomiting or any recognisable lesion to account
for it. This condition has been described by Lasegue under
the name of hysterical anorexia, and by Sir W. Gull as apepsia
hysterica. " These patients," says Dr. Wilks, " declare that
they do not care for food, and so they take less and less until
all appetite has gone, and then, indeed, a loathing may come
on." In a case of this kind, that of a girl aged 18 years, which
came under my observation, the emaciation was extreme, the
skin being stretched over the face so as to reveal all the
depressions and prominences of the jaws and malar bones.
The condition of the patient reminded me forcibly of the
appearance presented by those suffering from chronic starvation,
due to organic stricture of the oesophagus. Some months subse-
quent to my seeing the patient her parents changed their
residence ; she almost immediately began to eat, and became
quite plump in a few weeks.

Hysterical vomiting is sometimes the complement of hys-
terical suppression of urine. In such cases, when the suppression
of urine is complete and of long continuance, the quantity
vomited is large, and in a case observed by Charcot a consider-
able quantity of urea was detected in the vomited matters.
Fernet also found urea in the vomited matters in a case of
this kind. It is therefore probable that the vomiting is caused
by the supplemental elimination of urea by the stomach.

The renal secretion undergoes frequent alterations in hysteria
Hysterical polyuria is a very constant symptom after convulsive
attacks, the urine under such circumstances being pale and of
low specific gravity.

Hysterical anuria, although seldom met with, is a more
interesting phenomenon than polyuria. Almost total suppres-
sion of urine may exist for a period of weeks or months without
giving rise to serious symptoms besides the constant vomiting.
Charcot has shown that this curious phenomenon depends, not
upon a spasmodic condition of the ureter, but upon some dis-
order of the kidneys themselves, probably vaso-motor contrac-
tion of the renal arteries analogous to the hysterical ischsemia
already described as occurring on the surface of the body.

884

HYSTERIA.

Increase of the vaginal and uterine secretions frequently
occurs in hysterical patients. Leucorrhoea, resulting from ute-
rine disease, may sometimes be regarded as a cause of hysteria,
but at other times the local discharge must be attributed to
nervous influence.

(d) Psychical Disturbances. — The chief mental charac-
teristic of hysterical patients is an excessive emotional excita-
bility, unchecked by voluntary effort, which finds expression
in various ways. Both pleasant and unpleasant emotions are
excited in them with unwonted ease, so that, as Reynolds
remarks, " the patient is hurried from one extreme to the other
with ludicrous rapidity ; and often she walks, as it were, on the
narrow line where tears and laughter meet. Laughter and
sobbing not only alternate but co-exist, and often without any
obvious and sufficient reason for either." This excessive emo-
tional activity necessarily induces exhaustion, and an exhausted
nervous system is adapted for the retention of the painful
emotions, so that, as a rule, hysterical patients are irritable,
gloomy, and not only exaggerate bodily ailments which exist,
but imagine those which have no existence.

Another mental peculiarity of hysterical patients — a pecu-
liarity which lies at the root of almost all their other mental
derangements — is craving for sympathy. Sympathy is the
quality of mind which adapts man for the social state, and is
the foundation of all his moral actions ; the highest natures
must necessarily crave for the sympathy of their fellows ; and
the more highly the mind is developed the more deeply rooted
will the craving for sympathy probably become. Persons with
well-regulated minds, however, perceive that those have no
right to claim the regard, esteem, and sympathy of others,
who refuse to be sympathetic in their turn and to perform
the actions which are prompted by an active sympathy with
the feelings and sufferings of others. They are constantly
devising schemes by which they can alleviate the sufferings
of other people, and thus add in some form or another to the
stock of human happiness ; and although they could not bear
with equanimity to be regarded with dislike by their fellows,
especially by those whom they esteem good and wise, yet the
desire for any active demonstration of sympathy is exceedingly

HYSTERIA.

885

small. To think of others becomes a second nature, and the
true method by which to purchase the inestimable boon of
human sympathy. Sympathetic natures of this class are neces-
sarily deeply emotional, but the life of active benevolence
which they lead renders it necessary for them to develop the
intellect in adapting means to ends and the will by the daily
exercise of self-control. Such natures are emotional, but they
are also strong-willed and of vigorous intellect ; in one word,
their minds are well-balanced and healthy.

Contrast these individuals with the habitually hysterical.
Both are emotional, and both crave for sympathy ; but while
the former purchase sympathy by actively bestowing it, the
latter would like to be its recipients while refusing it to others.
The former are unselfish and devoted to the interests of others,
while the latter are selfish and regard themselves as the centre

of the whole world of feeling, thought, and action.

It is this morbid desire for sympathy that prompts hysterical
patients either to exaggerate a real ailment or to feign illness
when they are free from it, or even to inflict bodily injury upon
themselves for the purpose of arousing compassion and attention.
Scarcely a disease can be mentioned which may not be simu-
lated by the hysterical, and the methods they adopt to effect
their object are truly marvellous, and would be utterly incredible
unless attested upon undeniable evidence. In order to excite
compassion, some injure and burn themselves, induce purulent
cutaneous eruptions by the use of irritating ointments, swallow
needles, or even pretend that they are about to commit suicide,
although real attempts at suicide are rare.

The depraved ideas formed by hysterical patients, and the
degrading actions resulting from them, defy all description.
Some have drunk urine and eaten excrement in order they
may vomit them ; others have led their too credulous attendants
to believe that urine issued from their navels, breasts, ears, or
eyes; others, again, have introduced living animals, such as
frogs and worms, into the anus or vagina, so that they might,
by reproducing them, excite wonder, and become objects of
sympathy to their friends.

But there are lower depths of human degradation which
hysterical females do not fail to reach. They sometimes

886

HYSTERIA.

intrigue against their friends, and maintain that they are
persecuted and outraged, and play their part with such con-
summate skill as to deceive experienced physicians and learned
judges. Girls about the age of puberty sometimes commit the
greatest crimes which it is possible to imagine, without any
recognisable motive, and apparently from the sheer love of mis-
chief. " When you see a paragraph," says Dr. Wilks, " headed
' extraordinary occurrence,' and you read how every night loud
rapping is heard in some part of the house, or how the rooms
are being constantly set on fire, or how all the sheets in the
house are being devoured by rats, you may be quite sure there
is a young girl on the premises." .

I have known a young lady at a boarding school tear her
sheets and her own underclothing into shreds, and then endea-
vour to fasten the guilt upon a schoolmate. Another placed
a carving-knife under her pillow, and when it was discovered,
as was doubtless intended, she confessed to an intention of
committing suicide.

These, however, are only a few of the minor vagaries which
may be committed by hysterical girls. A young nurse girl has
not unfrequently been . known to poison the children under her
charge, at other times the attempt is directed against her
mistress, and it is so clumsily carried out that the lives of the
whole family may be endangered. At times a piece of burning
coal may be placed under the infant in the cradle, and repeated
attempts be made to set the house on fire, all this being done
while the girl is treated with the utmost consideration and
kindness by her employers.

The well-known case of Constance Kent testifies to the
frightful crimes which may be perpetrated by young girls in
this strange condition. Dr. Wilks, in alluding to the case,
remarks : " When a few years ago the whole country was
shocked by the news of the murder of a little boy in the middle
of the night whilst surrounded by members of his own family,
the event was enveloped in the darkest mystery, seeing that
the crime was of so extraordinary a character, and was wanting
in all those objects for its commission which are usual in similar
deeds. No adult, especially no man in his senses, commits a
crime except to attain some end ; and, therefore, the very

HYSTERIA.

887

purposelessness of the act (except, perhaps, for revenge) con-
vinced me that it was perpetrated by a young woman. I felt
quite sure in my own mind as to the real criminal, who, even
after her own confession, was considered by many incapable of
such a deed."

It is not unusual for the psychical disturbance of hysteria to
assume an erotic character. Girls may then assert that they
have been ravished, and usually maintain that the most out-
rageous violence was used by the perpetrator of the crime, or
that they themselves were previously drugged. The notes of
the following case have been kindly supplied to me by Mr.
Cullingworth, who was the medical witness called in by the
police to investigate the case after her supposed dying state-
ment had been taken : —

In December, L876, a girl of eighteen was found one evening standing,
with her clothing wet and muddy, and in ah apparently stupefied con-
dition, in the closed doorway of a restaurant in the centre of Manchester,
a few yards from where she was lodging. She was taken home and to
bed, and a medical man was sent for. He found her to all appearance
unconscious of what was going on around her, and uttering some dis-
jointed and incoherent complaints of having been drugged and threatened.
He thought she was recovering from the effects of some narcotic, and did
not at first pay much attention to her story. The following day, however,
she appeared worse, and in the evening her condition was considered so
critical that the police were communicated with, with a view to her state-
ment being taken down. She was visited by two experienced detectives,
who, seeing how matters stood, and having the doctor's assurance that she
was in a dying state, sent at once for a magistrate, before whom she made
a solemn declaration to the following effect : She 'believed herself to be
dying. On the previous evening a solicitor, at whose office she had called
on business, told her that she must go into a convent, and gave her "some
sort of dark, sweet drink," which rendered her senseless. On going down-
stairs from the office she met a Jesuit father, whom she had seen once
before. This gentleman took hold of her and pulled her along the street
to a little house in a court, where there was an upper room with a bed in
it and a cross on the wall. Having got her into this room, he said im-
proper things to her, and gave her a little cake which affected her directly.
The woman of the house came into the room and found her on the floor
after which she somehow got outside, the priest following. He again
dragged her along in the dirt to the street corner, when he ran away.

The solicitor and the priest, both of them well-known and highly-
respected, were thereupon placed under arrest in the middle of the night

888

HYSTERIA.

on a charge of having administered certain poisonous drugs with intent to
murder. The story was proved to be purely imaginary, and the magistrates
dismissed the case.

It is not only the actions which are in immediate relation
with the emotions that are so profoundly disturbed in hysteria,
but grave disorders of the representative feelings and cognitions
occur. Illusions of sight are common in the early stages of
severe hysterical attacks. Charcot has drawn attention to the
fact that in the grave cases of hysteria associated with ovarian
hyperesthesia and hemianesthesia the patients frequently see
rats and other odious animals on the anaesthetic side of the
body, or with the eye suffering from amblyopia. At other
times they have hallucinations with erroneous ideas, and
some of the images that have appeared during the paroxysm are
subsequently considered real. The entire hysterical paroxysm
may consist of a succession of images like that occurring in
vivid dreams, a condition generally described as hysterical
delirium.

If the attacks be transient and occur rarely, the patient may
recover completely from their effects ; but if they recur fre-
quently, persistent mental aberration is after a time established.
The delirium frequently makes its appearance in a perfectly
periodical manner and without any recognisable cause, being
regularly preceded by a condition of ill-humour or mental irri-
tability. In other cases a chronic and continuous form of
mental disturbance is established, which is little affected by
the fits.

One variety of this mental condition assumes the form of pure
melancholy. The patients are anxious, wretched, and incapable
of enjoying the society of others, and under such circumstances
they are subject to uncontrollable impulses which urge them to
commit outrageous actions.

A second form of chronic continuous hysterical mental dis-
turbance corresponds closely to the clinical description of the
so-called folie-raisonnante. Patients affected in this way
pursue their own selfish aims with the greatest perseverance,
although they are unfit for any useful employment; the sexual
appetite is often strongly developed, and not rarely they are
given to drunkenness. . There is complete absence of the moral

HYSTERIA.

880

sense; they are quite unable to curb their inclinations and
impulses ; they are liars, and cheat and steal with the greatest
cunning and dexterity ; and are always ready with plausible
reasons to cloak the perversity of their actions, while they
manifest the utmost confidence in the incontrovertible nature of
their arguments. In these cases the intelligence is profoundly
disturbed, for it is evident that the statement which was at one
time a conscious fabrication to meet an emergency is afterwards
reproduced by them with a full belief in its truth. They fre-
quently suffer from hallucinations, which may gradually become
transformed into established erroneous ideas. They are besides
subject to occasional outbursts of excitement, which after a
time pass into pronounced maniacal states.

(2) Hysterical Attacks.

Hysterical fits are exceedingly variable in the combination of
their symptoms and the degree of their intensity, so that it is
impossible to comprise all the various forms under one general
description. The attacks occur sometimes without any recog-
nisable cause, while at other times they are provoked by
over-excitement or some slight emotional disturbance. The
paroxysm always takes place when someone is present to witness
it, and never during sleep, nor when the patient is alone.

(a) Simple Hysterical Attack. — The attack is preceded by
the sensation of globus along with a feeling of suffocation, a
painful dragging in the extremities, pain and giddiness in the
head, singing in the ears, or darkening of the field of vision.
It is often preceded by a fit of crying or laughing, or a
combination of both ; the patient suddenly screams or makes
a spluttering noise, and falls down in a state of apparent
unconsciousness. The head and extremities become affected
with general rhythmical clonic convulsions, the breathing is
accelerated and exaggerated, irregular, or temporarily arrested.
The loss of consciousness is more apparent than real. The
hysterical patient generally hears what is said by those around
her, and she has almost always time to find a suitable place
upon which to fall; she often throws herself on a couch or
reclines on a sofa, and not unfrequently appears to bestow some
degree of attention upon the propriety and gracefulness of her
attitude.

890

HYSTERIA.

Another peculiarity of the hysteric attack is that the facial
expressions and attitudes assumed are not devoid of meaning,
but are repetitions of those occurring in health under varying
emotioDS. Sometimes the expression is that of great terror, at
other times there is a frown as if of anger, and at still other
times it becomes imploring or beseeching.

Hysterical attacks rarely last more than a few minutes, but
they may recur in quick succession, so that they seem to form
an almost continuous paroxysm, extending over a considerable
period. The hysterical seizure frequently ends in a fit of crying
and sobbing, there is no subsequent coma, and on recovery the
patient generally passes a large quantity of clear and limpid
urine of low specific gravity.

(&) Cataleptic attacks are liable to occur in hysterical
patients; they are of variable duration, disappearing some-
times in the course of a few hours, and being . prolonged at
other times, with slight intermissions, for a period of months.
Cataleptic rigidity is sometimes limited to particular limbs;
but, as a rule, the whole body is implicated, and then all
voluntary movements are suspended and reflex action is dimi-
nished. All the forms of general sensibility are usually lost, but
one or more of the special senses may be retained. The sense
of hearing is probably the one most generally retained, a fact
which should be borne in mind by the attendants.

Sometimes every form of sensibility appears to be completely
abolished, and in such cases the limbs retain the position in
which they are placed. This condition has been called waxy
rigidity, because the limbs can be as it were moulded in almost
any position.

There are cases of complete general muscular relaxation in
which the action of the heart and pulse become almost imper-
ceptible, while respiration may be so feeble that the patient
may seem to be dead. These cases have been described as I
" hysterical trance," and it is possible that patients may have
been buried alive in this condition.

(c) Hysteria in Boys. — Boys, at the approach of puberty, not
unfrequently suffer from hysterical symptoms resembling those
observed in the female sex (Wilks, Roberts). Sometimes the
symptoms may assume the form of globus along with attacks of:

HYSTERIA.

891

causeless weeping and sobbing; at other times there may be
partial spasm of the glottis, a barking cough, attacks of dyspnoea,
or some local sensory or motor disturbance. Psychical pheno-
mena often predominate. In a case which I saw a few months
ago the boy was sometimes found creeping on his hands and
knees and barking like a dog ; another time he jumped like a
frog from the floor on to the table. The depraved form of
hysteria, named chorea major, is often met with in boys. In
this variety of the disease the patients run, dance, jump, or
climb with much greater readiness and dexterity than similar
actions could be performed in health, or they may sing or recite
poetry, even in a foreign language.

The paroxysm of hystero- epilepsy will be subsequently
described.

§ 940. Course, Progress, and Terminations. — The grouping
of the symptoms in hysteria is exceedingly variable, not only
in the case of different individuals, but of the same individual
at different times. It is almost always a chronic disease, which
exists for years, and disappears only at an advanced age. Those
who are strongly predisposed to hysteria are frequently very
irritable and peevish during childhood, although convulsive
attacks do not generally occur until the period of puberty.
When puberty is established the convulsive attacks frequently
disappear, and other symptoms, more especially emotional dis-
turbances, are then apt to become prominent.

In some hysterical patients sensory and motor disturbances
are well marked and persistent, and psychical only present to
a slight extent, while at other times the reverse is the case.
The disease is liable to undergo many variations in its course.
The symptoms may disappear for comparatively long periods,
but are liable to recur on exposure to the slightest excitement.

Hysterical symptoms frequently cease after the climacteric
period, but the higher degrees of mental disturbance sometimes
develop at this age.

Hysterical symptoms may appear at puberty, but subse-
quently become latent to a certain extent, reappearing in a
very pronounced manner at the climacteric period. Hysterical
symptoms may be of every degree of intensity from simple

892

HYSTERIA.

mental irritability up to the profound mental disorders which
border upon insanity, and from slight sensations of globus and
infra-mammary neuralgia to attacks of general convulsions,
and widely spread paralysis and anaesthesia. The cases in which
convulsions, paralysis, anaesthesia, and contractions are associated
with severe psychical disorders constitute the most aggravated
forms of the disease.

Hysteria seldom shortens life. Even cases of persistent
vomiting and copious haemorrhage are relatively innocuous in
comparison with similar symptoms arising from other diseases.
Cases, however, are occasionally observed in which after a severe
moral shock violent hysterical symptoms become developed, and
death may occur within a few days or weeks in the absence of
any recognisable organic change.

In a case of hystero-epilepsy observed by Wunderlich, the
patient suffered from epileptiform attacks, not attended by any
increase of temperature, for more than eight weeks, when sud-
denly, without known cause, the patient became collapsed, and
the temperature rose to 109 4° F. (43° C.) before death. In t
a second case, related by the same author, the patient suffered
for several years from various forms of paralysis, hyperesthesia,
loss of sight and smell; ultimately difficulty of swallowing and
vomiting supervened, and she died with febrile symptoms in a
state of marasmus and emaciation, while post-mortem examina-
tion revealed no changes in the nervous system.

Sometimes death may occur indirectly from hysteria, as in 1
the cases of patients who mutilate themselves, with or without
the intention of committing suicide. Hysterical patients rarely
attempt to commit suicide in earnest, but feigned attempts made
in order to attract attention have sometimes been fatal, and
occasionally suicide has actually been committed.

§ 941. Morbid Anatomy and Physiology. — No constant
anatomical changes have been found in cases that have died
from hysteria. Charcot discovered symmetrical sclerosis of the i
lateral columns extending nearly the whole length of the spinal,
cord in the case of a hysterical woman who suffered, for ten:
years, from paralysis with contracture of all the extremities.
It is, therefore, probable that in cases of hysterical contracture

HYSTERIA.

893

the fibres of the pyramidal tracts undergo morbid changes,
at first temporary, although ultimately becoming permanent.
But even if this be so, the primary change probably occurs in
the motor centres of the cortex of the cerebrum. Indeed all
the phenomena of hysteria may be explained most readily on
the assumption that the irritability of the cortex of the brain
is sometimes in excess and sometimes diminished or abolished.
Increased irritability of the cells and fibres of portions or the
whole of the cortex of the cerebral hemisphere supplied by the
posterior cerebral artery would account for the hyperesthesia of
variable distribution and completeness on the opposite side of
the body ; and, conversely, diminution or loss of the irritability
of those same cells and fibres would account for the various
forms of anaesthesia.

Again increased irritability of the cells and fibres of portions
of the cortex of one hemisphere supplied by the middle cere-
bral, artery would account for spasms of groups of muscles on
the opposite side of the body, while diminution or loss of the
irritability of these cells and fibres would account for the
various forms of paralysis observed. Variations in the degree
of irritability of the cells and fibres of the cortex supplied by
the anterior cerebral artery would account for many of the
psychical disturbances. Even the numerous vaso-motor disorders
observed in the course of hysteria are best explained on the
supposition that they are determined by variations in the
intensity of the nervous discharges from the cortex of the brain
to the nerve centres in the medulla oblongata.

Hemianesthesia from organic lesion is generally caused by
disease of the sensory peduncular fibres and of Gratiolet's fibres
in their ascent through the internal capsule ; and hysterical
hemianesthesia might result from a loss of the irritability of
these fibres without recognisable structural change, while
hyperesthesia of half the body might be caused by excessive
irritability of them. Muscular spasm or paralysis, on the other
hand, might be caused respectively by excess or abolition of the
irritability of the fibres of the pyramidal tract. The fact that
anesthesia is sometimes associated with loss of reflex irrita-
bility shows that the irritability of the nervous tissues is modi-
fied in hysteria in more than one locality at the same time.

894

HYSTERIA.

§ 942. Diagnosis. — When hysteria is fully developed, and
the physician has an opportunity of inquiring into the history
of the case and of watching its progress, the diagnosis presents
no great difficulties. Hysteria may, however, simulate almost
every possible disease, and a physician has to be constantly
on his guard if he would not at some time fall a victim to the
deceptions practised by the hysterical.

Individuals of a nervous temperament sometimes exhibit
the minor characteristics of hysteria, such as great irritability
of temper, exaggerated sensibility to physical impressions, and
even occasionally slight motor disorders. Cases of this kind
bordering upon hysteria demand the same treatment, so that
it is unnecessary to enter upon the diagnosis between the
affections. t

Hysterical arthritic affections are particularly liable to be
mistaken for organic disease of the joints. In the hysterical
affection the pain varies in degree at different times and is
fluctuating in character, the form of the joint is unchanged,
there is no heat or redness, and the pain, like most other
local hysterical pains, is limited to the surface, so that slight
contact may be painful while deep pressure causes no dis-
comfort, especially if the attention of the patient be otherwise
engaged.

Pain and sensitiveness over the spinous processes of the
vertebrae in hysterical subjects have led to the affection being
mistaken for grave organic disease of the spinal cord, but these
symptoms, indeed, are rarely present in the organic diseases.
The exciting causes of hysteria simulating disease of the cord
are usually emotional disturbances, which rarely induce organic
spinal affections.

In hysterical paraplegia the lower extremities are feeble
and give way under the weight of the body, while the feet drag-
on the ground. The paralysis is seldom complete, the patient
is able to move her limbs in bed with comparative ease, and
may even be able to get out of bed ; but after walking two or
three steps the limbs give way, the gait becomes tottering, and
unless supported the patient falls. The electric excitability of
the muscles is usually unaffected in hysteria, and the muscles
do not undergo trophic changes.

HYSTERIA.

895

The concomitant symptoms of hysterical paraplegia are
ana3sthesia of the skin and muscles of the lower extremities,
tympanites, constipation, dysmenorrhea, and retention of urine.
Cerebro-spinal multiple sclerosis sometimes closely resembles
hysteria, and the diagnosis between the two affections is occa-
sionally only practicable in the later stages.

Hysterical hemiplegia differs from hemiplegia due to cerebral
disease, in the following respects : — It is usually accompanied
by well-marked disorders of sensibility ; there is no facial or
lingual paralysis ; the paralysis is scarcely ever complete ; in
the large majority of cases it is worse in the leg than the arm ;
it is liable to sudden variations in intensity under the influence
of emotions ; the electric excitability is unchanged ; and the
muscles do not undergo atrophy.

Hysterical convulsions may be distinguished from epilepsy
by negative characters. The loss of consciousness in the former
is not complete, nor is it so sudden in its onset ; there is no
asphyxia ; the tongue is not bitten ; the attacks last longer
than in epilepsy ; the patient does not on the cessation of the
attack fall into a profound stupor, but only appears exhausted ;
and there is much sobbing and crying.

It is sometimes difficult to distinguish between hysteria and
hypochondriasis. Some, indeed, regard hysteria in the female,
and hypochondriasis in the male, as only different manifesta-
tions of the same disease. The psychical symptoms of the two
diseases are, however, different, and paralyses and convulsive
attacks never occur in hypochondriasis.

Hysterical aphonia is seldom accompanied by a cough as is
laryngitis, the loss of voice is sudden, while in almost all other
forms of aphonia the voice becomes gradually extinct ; a laryngo-
scopy examination shows a total absence of any structural
lesion.

Hysterical neuralgia has not the intensity of the genuine
disease, and there is an absence of " painful spots." The dis-
tribution of pains in hysteria is more diffused than in true
neuralgia, and often not limited to any one nerve territory.

In lead paralysis the affected muscles undergo atrophy and
manifest the reaction of degeneration at an early period of the
disease, phenomena which never appear in hysterical paralysis.

896

HYSTERIA.

§ 943. Prognosis. — So far as life is concerned, the prognosis
is always favourable ; it should not be forgotten, however, that
a fatal issue is possible.

But although hysteria rarely causes death, it is almost equally
rare for complete recovery to take place. The most hopeless
cases are those in which a predisposition to the disease is in-
herited, and in which the symptoms commence in childhood.
In such cases the disease usually becomes exaggerated at
puberty, although considerable remissions often take place after
this period. Many patients get well as age advances, and at
times the climacteric produces a favourable change ; but at
other times this period induces exacerbations, and leads to the
establishment of inveterate forms of mental disturbance.

The most favourable cases are those in which the disease
can be traced to a distinct exciting cause that can be removed,
rather than to rooted mental predisposition. When hysteria
has been induced by affections of the generative organs or
chlorosis, hopes may be entertained that the hysterical symp-
toms will vanish with the removal of these. Occasionally,
however, the altered condition of the nervous system continues
after the exciting cause is removed.

Remissions frequently occur in the course of the disease, and
may last for years, but the symptoms generally recur from time
to time in one form or another.

Sensory and motor disturbances, however severe, may sud-
denly disappear temporarily ; but the symptoms become more
obstinate to treatment every time they are repeated, and
ultimately become persistent.

Transitory psychical disturbances, even when they are very
violent, may not exert an unfavourable influence upon the
progress of the case; and even attacks of ordinary insanity
supervening in the course of hysteria are capable of complete
recovery. When once the mental disturbance has assumed a
chronic form the prognosis becomes extremely unfavourable,
and when the signs of moral depravity, folie-raisonnante, or
fixed erroneous ideas have become established, complete resto-
ration seldom occurs.

§ 944. Treatment — The great aim of treatment should be

HYSTERIA.

897

to prevent the appearance of the aggravated form of hysteria.
With this view the greatest attention should be paid to
the early education of children who inherit a nervous tem-
perament, or who are congenitally predisposed to hysteria.
Such children should be trained to habits of unselfishness, and,
under judicious management, considerable progress may be
made before the child leaves the arms of the nurse. One great
difficulty is often experienced in such cases. When the ten-
dency to the disease is inherited through the mother, she herself
is often irritable and explosive in disposition, at one time un-
necessarily harsh to her children, again unduly indulgent to
them, always capricious and never firm; while the father is too
much occupied with business to be able to counteract the evil
influence of the mother.

Under such circumstances the mother should be advised to
place the management of her children as much as possible in
the hands of some firm and judicious woman, be she nurse,
relative, or governess. To train a child into habits of self-
renunciation is the most difficult of tasks anyone can undertake,
and can only be accomplished by the habitual exercise of self-
control on the part of the teacher.

During the period of bodily development great care should
be taken of the health. The diet should be plain, nourishing
and abundant, the utmost care being taken that the child is
not treated as an invalid, inasmuch as the observance of special
rules with regard to diet is apt to foster that feeling of self-
consciousness which it is so desirable to suppress. Regular
hours for meals, going to bed and getting up, should be
observed as part of general discipline ; plenty of outdoor
exercise should be taken, all the better if it can be made
agreeable, or subservient to some useful purpose to engage the
attention. When the young girl passes into womanhood she
ought to be taught that she has a field for work and a mission
in the world, and that she is surrounded by human suffering
which she can alleviate ; there is little doubt that the more
opportunities of usefulness are multiplied for young ladies the
more the tendency to hysteria will diminish.

But let us now pass to the treatment of the fully developed
disease. The exciting cause can only be removed in a few cases

FFF

898

HYSTERIA.

and even when that is possible the modification of the nervous
system already induced may persist. When ansemia exists the
usual treatment with iron and other tonics should be adopted.
If there be indigestion with flatulence, bismuth, charcoal, alka-
lies, or mineral acids may be administered with or without a
better infusion ; constipation demands the administration of
mild aperients, and atony of the alimentary canal quinine, nux
vomica, or strychnine, while uterine derangements must be
subjected to appropriate treatment. The treatment of disease
or suspected disease of the generative organs in cases of hysteria
requires the greatest tact on the part of the medical attendant.
The introduction of the catheter, or a vaginal examination, if
the patient be unmarried, may lead to an aggravation of all the
symptoms. On the other hand, if real disease exist, local treat-
ment may be indispensable to success. When the cause of the
hysteria is a moral one it is often impossible for the physician
to remove it, but even then much may be done by placing the
patient under conditions as much as possible conducive to her
happiness.

The drugs which have been employed in the treatment of
hysteria are characterised by a pungent and often disagreeable
odour. Assafoetida, galbanum, and valerian are the best known
and most commonly used of this class, and many hysterical
patients come to like both the taste and smell of these nauseous
substances. They do not appear to produce a permanent in-
fluence upon the disease, although they may be of use in
removing flatulence and other troublesome symptoms.

When general hyperesthesia and sleeplessness exist, it may
be necessary to administer narcotics, morphia injected subcu-
taneously being the best. The patients, however, should never
be allowed to take morphia or other narcotic at their own dis-
cretion. Bromide of potassium is a valuable agent in some
cases, and where there is much sleeplessness its efficacy is
increased by being combined with chloral.

The electrical treatment of particular symptoms of hysteria
is sometimes followed by improvement of the general con-
dition. Beard and. Rockwell have recently recommended that
the entire surface of the body be treated, in successive portions,
with tolerably strong induced currents, and this treatment has

HYSTERIA.

899

been found very successful, although its efficiency depends pro-
bably on the mental impression produced rather than on the
local action of the current. The influence exerted by counter
irritation of various kinds appears also to be largely due to the
mental impression made.

The most important part of the treatment of hysteria con-
sists of the moral management of the patient. One of the
first requisites for treatment is that the physician should
possess the entire confidence of the patient and her friends. An
essential condition for success is that the physician be himself
convinced that hysteria is a real and not a sham disease, and
that the treatment prescribed is a real and not a sham treat-
ment. There is probably no disease which a medical man
has to treat which makes so many demands upon his firmness,
self-control, and ingenuity as hysteria. He must be able to
sympathise with the feelings of the patient in order to command
her confidence, but if his sympathy degenerate into false
sentiment or into the slightest exaggeration of manner he will
only be administering to the morbid craving for sympathy which
is at the root of the disease, while on the other hand the
slightest attempt to laugh down the patient's fancies may be
fatal to success. Earnestness of purpose, determination, and
fertility of resource are all called into requisition in the treat-
ment of hysteria. The instructions given to the patient should
be plain and such as can be readily carried out; they ought
at the same time to task to some extent her voluntary efforts.
When once instructions are issued the most implicit obedience
to them should be insisted upon, for laxity in enforcing
observance of rules argues want of confidence in their efficacy.
The voluntary efforts of the patient should be daily exercised
by making progressively increasing demands upon them. And
as the power of will becomes strengthened, emotional excite-
ment will diminish in corresponding degree.

Instead of exciting the dormant will into activity by
graduated exercises, this can frequently be accomplished at
once by anything which acts powerfully on the imagination.
Hysterical patients, who have been bed -ridden for years, have
been known to get out of bed, and walk under the influence of
a strong emotion, or after having the imagination powerfully

900

HYSTERIA.

acted upon, so that the rapid change from utter helplessness
to full motor power appears almost like a miracle. Whatever
may be the reason of it, there can be very little doubt that such
wonderful cures are generally effected by clergymen or irregular
practitioners, and rarely by the sedate, highly respectable,
regular practitioner.

Painful remedies used with moderation and humanity are
sometimes very useful, partly by appealing to the imagination.
Of these remedies, the faradic current is probably the most
generally useful, and a subcutaneous injection of morphia is
for a similar reason more efficacious than the internal admini-
stration. Simple water has been successfully substituted for
the narcotic injection, so great is the influence of mental
impression.

It is sometimes possible to cure severe hysterical symptoms
by means of threats, sudden fright, or moral shock. An un-
expected shower of cold water may have the desired effect,
and at other times the threat of the actual cautery is efficacious.
Charcot mentions the case of a woman who had suffered for
more than two years from permanent contracture of one of
the lower extremities, which suddenly vanished on account
of the moral shock caused by an accusation of theft brought
against her ; a second also in whom contracture of four years'
standing suddenly disappeared in consequence of a stern
admonition given her ; and a third in whom a like condition
vanished on account of a sudden disappointment. Great judg-
ment must be exercised in the employment of such means,
inasmuch as the disease may be aggravated instead of amelio-
rated by them.

Hysterical patients are treated with much greater success
in the wards of an hospital than in their own homes. In
aggravated cases, therefore, the patient should be removed
from her home and relations and placed for a period of some
months either in a public institution, or under the care of
complete strangers.

During hysterical fits the patients usually take care not to
injure themselves, but it is often necessary to prevent respiration
being impeded by clothing. I have always found it better
not to allow a hysterical woman to toss about violently

HYSTERIA.

901

in all directions, but to hold her down gently but firmly, and
to prevent her struggles. The best method of securing the
patient is to place an attendant on each side of her, and to
direct each to grasp one wrist with one hand and to hold the
shoulder firmly down to the bed or floor with the other; if
necessary the patient's legs must be held down. It is remark-
able how soon a hysterical patient ceases to struggle when she
finds that she is held as in a vice. So long as the patient can
shake herself free from her attendants, so long is the struggle
apt to be maintained, but when once she feels that she is
thoroughly restrained, and that her efforts do not find outward
expression, she generally ceases to struggle. The most usual
remedy for arresting the attack is to dash cold water on the
face and neck; although this is a useful method occasionally
it is by no means the best. The plan suggested by Dr. Hare
of forcibly holding the mouth and nose of the patient so as to
prevent her from breathing is very effectual. In my own prac-
tice the administration of an emetic was at one time a favourite
method of arresting an attack. Strong, vigorous servant-maids
sometimes suffer from violent hysterical convulsions, and in
them I was in the habit of giving an emetic dose of the
tartrate of antimony. In most cases, however, the sulphate of
zinc is safer if less efficient.

If the attack be caused by some peripheral irritation, its
removal may arrest it. Severe attacks have sometimes ceased
after the rectification of a misplaced uterus. In cases of hystero-
epilepsy Charcot has succeeded in arresting the attacks by firm
compression of the hypersesthetic ovary, but this does not
appear to be a means applicable for the convulsive attacks of
ordinary hysteria. Large doses of the bromide of potassium
exert a favourable influence on the fits of hystero-epilepsy, but
this remedy is not of much value in the common form of
convulsive attack.

Limited spasms in hysteria are best removed by general
treatment and moral management, although local treatment and
special remedies are occasionally found useful. In the case
of patients suffering from obstinate globus, Erb recommends
the repeated application of the constant current, the anode
being placed at the side of the larynx.

902

HYSTERIA.

For spasms of the stomach and bowels, sometimes warm, at
other times cold applications to the abdomen are useful ; opium,
belladonna, quinine, valerian, or other drugs of the same class
may be given internally.

Yomiting is one of the most troublesome and obstinate
symptoms of hysteria. It is usual to regulate the diet, and
to give only bland and easily digestible substances, such as
milk cooked in various forms, but this method is not always
successful. Sometimes the patients retain highly-seasoned food
better than bland diet, and the vomiting may cease if they
are allowed to eat raw ham or raw mince-meat well peppered.
Care, however, should by taken that the nature of the case is
clear. In spastic as well as in paralytic retention of urine warm
sitz-baths will often bring relief ; when they are unsuccessful
the catheter should be employed in case the bladder becomes
distended.

In hysterical paralysis electricity is the best remedy, and the
application of strong faradic currents to the paralysed nerves and
muscles is, as a rule, successful. Galvanisation of the spinal
cord is useful in hysterical paraplegia. Aphonia may at first be
treated by external faradisation, but in obstinate cases recourse
must be had to the intralaryngeal application.

Passive movements and frictions of the limbs with or without
embrocations are also useful as aids in treatment, and Reynolds
strongly recommends the application of narrow strips of
blister passing completely round the affected limbs. Com-
pression of the larynx with the fingers sometimes temporarily
restores lost speech, and a similar effect may be obtained by
passing a strip of adhesive plaster across the larynx so as to
partially surround the neck. Hysterical tympanites may at
times be dispersed by powerful faradisation of the abdominal
muscles or even by firm compression of the abdomen, but in
aggravated cases the introduction of the intestinal tube may be
necessary.

Hysterical anesthesia is best treated by powerful faradic
currents applied by means of the dry metallic brush. Charcot
has succeeded in removing hysterical hemianaesthesia by applying
various metals to the cutaneous surface. This method of treat-
ment was introduced by Burq, but it would appear that the

HYSTERIA.

903

anesthetic condition is only transferred from the affected to
the opposite side of the body. It is somewhat premature to
pass any opinion with respect to the success of this practice.
So long as certain " passes " over the surface of the body can
induce a condition of general anaesthesia, such as that met with
in the mesmeric state, there is nothing absurd in supposing
that similar passes and the application of coins to the surface
may have a curative effect in conditions of partial anaesthesia.

Hysterical neuralgia and hyperaesthesia demand the employ-
ment of narcotics and anaesthetics. Caffein, guarana, and
chloride of ammonium are useful in hysterical cephalalgia.
Chloral hydrate given in scruple and half-drachm doses to
procure sleep is occasionally useful, and inhalation of chloro-
form may be necessary in order to overcome contractures of
muscles.

904

CHAPTER V.

CATALEPSY, TRANCE, ECSTASY, AND OTHER ALLIED

CONDITIONS.

(I.) CATALEPSY.

Catalepsy is characterised by attacks of partial or complete
loss of consciousness, accompanied by stiffening of the voluntary
muscles, having the peculiarity that the limbs retain for a
relatively long period the positions in which they may be placed
by passive motion.

§ 945. Etiology. — Catalepsy often occurs as one of the many
manifestations of hysteria, while at other times it is caused
by chronic cerebral disease, such as softening, tubercular
meningitis, and tumours. In some cases the cataleptic con-
dition appears to be premonitory of true epileptic attacks.
Some cases, however, cannot be traced to either of these causes,
and then catalepsy may be called idiopathic or essential;
cases of the latter form are observed in families who inherit
a decided neurotic disposition. The disease is most frequently
observed about the age of puberty, but it has been met with
as early as five years of age, and occasionally in advanced age.
The two sexes appear to be equally liable to the idiopathic
variety, but the hysterical is almost exclusively observed in the
female. The exciting causes of idiopathic catalepsy are gastric
and intestinal irritation, and great emotional disturbance.
Malarial infection is said to have caused typical attacks of
catalepsy.

§ 946. Symptoms. — The cataleptic attack is sometimes pre-
ceded by premonitory symptoms, such as headache, vertigo,

CATALEPSY.

905

trembling of individual muscles, and an undefined, sense of
discomfort. As a rule, the attack begins abruptly ; the
movements of the patient are suddenly arrested, it may be
while he is speaking or performing some action ; the face
becomes deadly pale ; the respirations are slow and tranquil ;
the pulse is soft ; and, although consciousness is lost, the atti-
tude of the patient at the time of the seizure is retained.
The muscles in action at the beginning of the attack appear to
be the first to become rigid, but the spasm rapidly extends, as
a rule, to all the voluntary muscles, although occasionally it is
partial or unilateral. The affected muscles feel firm, and offer
resistance to passive movements of the limbs ; when once this
resistance is overcome, the limbs, head, and neck, or features
may be placed in constrained positions, which they retain
for a comparatively long period. After the first resistance of
the muscles has been overcome the limbs possess a flexibility
and pliability, which has been compared to that of soft wax.
It has consequently been named flexibilitas cerea. This con-
dition of the muscles enables the limbs to be moulded in
any position compatible with the rigidity of bones and inex-
tensibility of ligaments, and the constrained attitudes in
which the limbs may be placed are maintained without change
during the whole course of the attack. "I was shown," says
Dr. Wilks, "a man in Morningside whom they could mould in
any position. Whilst in bed on his back they could arrange
his arms and legs in any posture and there his limbs would
remain. Dr. Savage has a case in Bethlem of a young man
who will keep his arm stretched out for two hours, and stand
on one leg for a great length of time. If made to follow
another patient, he will continue to do so until he is stopped."
But even during the cataleptic condition the muscular stiffness
does not persist in its full intensity for a lengthened period.
After some minutes the stiffness diminishes somewhat, so that
the arm, for instance, when raised horizontally falls lower by
its own weight, and the limb undergoes a slight trembling,
indicating the approaching exhaustion of the muscles.

Consciousness is usually abolished, but not in all cases. A
certain amount of consciousness may be retained in the early
stage of the attack or be present throughout, so that strong

906

CATALEPSY.

peripheral irritation may cause pain which will be remembered
by the patient. Reflex irritability is sometimes lost ; at other I
times certain reflex actions, such as closure of the eyelids on
touching the conjunctiva, are retained. The electric contrac-
tility of the muscles remains ; and, according to the observations
of Benedikt, the galvanic irritability of the nerves is increased
during the attack, but becomes rapidly diminished during the
intervals. In one case observed by Rosenthal the electrical
reaction of the nerves to both currents was perfectly normal ;
in another it was increased.

The organic functions are not usually seriously interfered
with. The respiration may be normal, but is generally slow
and shallow. The pulse is slow, soft, and compressible. The
temperature is generally lowered, and at times the surface of
the body becomes icy cold. When the surface of the body
is cold, and the pulse at the wrist and respiration are almost
imperceptible, the condition may be mistaken for real death.

The attack of catalepsy is sometimes very brief, lasting
only a few minutes, at other times several hours or days.
Attacks described as being very protracted are in reality made
up of a succession of these, separated from one another by in-
tervals in which the patients recover either wholly or partially.
The seizures sometimes disappear \ quite suddenly, and the
patients at once recover full consciousness and immediately
resume the actions which had been interrupted. As a rule,
however, recovery is gradual, patients at first being stupefied as
if awaking from a profound sleep, a certain amount of muscular
stiffness remaining for some time, which renders motion difficult
and slow.

In simple catalepsy no mental disorder is observed in the
intervals between the attacks, but when it is merely a symptom
of profound nervous disease the intervals may be characterised
by the occurrence of hysterical convulsions, delirium, maniacal
attacks, and hallucinations, or the catalepsy may be associated
with ecstasy and somnambulism.

§ 947. Course. — The course of catalepsy is usually chronic,
extending over many years. Some individuals suffer only from
a small number of attacks separated by intervals of many years.

TRANCE — ECSTASY.

907

Others, again, have frequent periodical attacks. In hysterical
catalepsy the slightest external influence may suffice to provoke
a paroxysm. Catalepsy of malarial origin follows the regular
course of other malarial neuroses ; they are sometimes accom-
panied by fever and sweating, and generally yield to the usual
antiperiodic remedies. Cases caused by sudden fright or injury
may also run an acute course, the disease terminating after a
single attack or after a series of them. Cataleptic attacks are
hardly ever fatal of themselves.

(II.) TRANCE.

§ 948. In this condition the patient lies for days together
in an apparently insensible condition without eating or drinking.
The state of complete insensibility is not, however, continuous,
inasmuch as there occur periods during which the patient
notices those around her, and may partake of small quantities
of food. The condition of the patient is not, indeed, unlike that
of a hibernating animal. In the state of trance the patient
usually lies in a warm room, well covered with clothing, so
that little heat is lost by radiation ; the mental functions are in
abeyance, indicating that the molecular changes which are the
correlatives of mental actions have ceased ; and all muscular
movements are suspended with the exception of the cardiac
contractions, and slight respiratory movements. Under such cir-
cumstances the amount of waste must be small. If Dr. Tanner
(and there are no grounds for believing that any deception
was practised by him), with all the waste implied by the
possession of active mental faculties, outbursts of temper,
walking and driving in the open air, could live forty days
without food, it may be inferred that persons in the state of
trance might live fasting for a much longer period. The
physician must, of course, be on his guard against deception in
cases of trance.

(III.) ECSTASY.

§ 949. This condition is closely allied to trance, the patient
being insensible to outward impressions in both. In ecstasy
the mind is absorbed with some fixed idea, generally of a

908

SOMNAMBULISM AND HYPNOTISM.

religious character, and the patient becomes oblivious of
surrounding events and objects. The limbs are motionless, and
often fixed in maintaining a particular attitude ; the breathing
is slow and feeble ; the pulse is almost imperceptible ; the eyes
are often bright and animated ; and the countenance has an
expression of rapture (Maudsley).

(IV.) SOMNAMBULISM AND HYPNOTISM.

§ 950. In somnambulism the patients appear to be wholly
unconscious, yet they walk, climb, and avoid obstacles, and may
manifest greater strength, agility, and precision of muscular
adjustments than during waking hours.

Hypnotism or mesmerism is, as Maudsley remarks, a kind
of artificially induced somnambulism. The subject, who is
probably always of a neurotic temperament, is induced to look
steadily at the operator, the latter attracting his attention by
making a few gentle " passes" with his hand. Mr. Braid, of
Manchester, directed the person to look upon a disc or some
bright object held in front of and a little above the level of the
eyes. After a short time there is a slight tremor of the eyeballs
of the subject, his pupils dilate, and he falls into the mesmeric
condition. In this state the mental functions are abolished, and
all the actions of the subject are afterwards determined by
the suggestions of the operator. Under the influence of these
suggestions the subject may sing, recite poetry, and perform
the most absurd and outrageous actions. He may be made to
eat a raw cabbage amidst all the outward signs of enjoyment
to appease a suggested hunger; he may spit out pure water
given him to drink with all the. signs of disgust, on the sugges-
tion that it is bitter and nauseous, or drink infusion of
wormwood with apparent relish on being told that it is an
agreeable beverage ; or he may be made to sneeze violently on
being asked to take a pinch of snuff from an empty box. Hyste-
rical patients may be thrown into a condition of trance or of
catalepsy, or one half of the body may be thrown into trance
and the other half into catalepsy, by being made to look upon a
bright light (Charcot). A condition much resembling the hyp-
notic state is sometimes induced by disease. A curious case of

SOMNAMBULISM AND HYPNOTISM.

909

this kind is transcribed by Dr. Wilks from Galignani, and as
the case is a remarkable one in many ways I quote it at length.

A Living Automaton— A curious patient is just now an inmate of Dr.
Mesnet's ward at the Hopital St. Antoine. His profession was that of a
singer at the Cafe's Chantants. During the war of 1870-71 he was hit
over the left ear by a musket bullet, which carried off about 2£ inches of
the parietal bone, and laid bare the brain on the left side. This led to a
temporary paralysis of the members on the opposite side, as is always the
case ; but he was eventually cured of this, while the tremendous wound
on the skull began to heal, so that after a time he could resume his pro-
fessional duties at the cafes to the satisfaction of the public. Suddenly,
however, he was seized with nervous symptoms, lasting from 24 to 48
hours, and of such an extraordinary nature that it was considered safe to
take him to the hospital. His malady is easier to illustrate by examples
than to define. When he is in his fit he has no sensitiveness of his own,
and will bear physical pain without being aware of it ; but his will may
be influenced by contact with exterior objects. Set him on his feet, and,
as soon as they touch the ground, they awaken in him the desire of walking ;
he then marches straight on quite steadily, with fixed eyes, without saying
a word, or knowing what is going on about him. If he meets with an
obstacle on his way he will touch it, and try to make out by feeling what
it is, and then attempt to get out of its way. If several persons join
hands and form a ring around him, he will try to find an opening by
repeatedly crossing over from one side to the other, and this without
betraying the slightest consciousness or impatience. Put a pen into his
hand ; this will instantly awaken in him the desire of writing ; he will
fumble about for ink and paper, and, if these be placed before him, he will
write a very sensible business letter ; but, when the fit is over, he will
recollect nothing at all about it. Give him some cigarette paper, and he
will instantly take out his tobacco bag, roll a cigarette very cleverly, and
light it with a match from his own box. Put them out one after another,
he will try from first to last to get a light, and put up in the end with his
ill-success. But ignite a match yourself, and give it him, he will not use
it, and let it burn between his fingers. Fill his tobacco bag with anything,
no matter what — shavings, cotton, lint, hay, &c. — he will roll his cigarette
just the same, light and smoke it without perceiving the hoax. But,
better still, put a pair of gloves into his hand, and he will put them on at
once ; this, reminding him of his profession, will make him look for his
music. A roll of paper is then given to him, upon which he assumes the
attitude of a singer before the public, and warbles some piece of his reper-
tory. If you place yourself before him he will feel about on your person,
and, meeting with your watch, he will transfer it from your pocket to his
own ; but, on the other hand, he will allow you, without any resistance or
impatience whatever, to take it back again.

910

SOMNAMBULISM AND HYPNOTISM.

§ 951. Morbid Anatomy and Physiology. — Post-mortem
examinations have only revealed changes in those cases in which
catalepsy and its allies are mere symptoms of grave organic
disease. Schwartz reports the case of a boy who, after an
injury, suffered at first from an affection resembling chorea, and
later cataleptoid attacks, and who, after two years, died from
anaemia and marasmus. The autopsy revealed serous effusion
in the arachnoid, softening of the corpus striatum and optic
thalamus, especially of the left side; and a brownish-red, jelly-
like mass, covering the spinal dura mater along the posterior
surface of the cord from the cervical to the lumbar enlargement.
Meissner examined a man, 47 years of age, who suffered from
catalepsy for six years, and in the three last years of his life
from maniacal and epileptic symptoms, with paralysis of the
right side ; he found an epithelioma growing from the dura
mater in the anterior fossa over the ethmoid bone ; the ante-
rior third of the right cerebral hemisphere, as well as the right
corpus striatum, was much softened. Lasegue found no change
in the brains of two men affected with catalepsy examined
by him.

The information obtained from post-mortem examination is
as yet far too scanty to throw much light on the pathology of
the disease. One noteworthy fact in connection with the
slighter forms of cataleptic attacks is their similarity to some
cases of the petit mat of epilepsy. It is a somewhat significant
fact that in Meissner's case of catalepsy the disease was situated
in the praefrontal region of tbe cerebral hemispheres. A
functional or organic lesion of the cortex of the cerebrum might
no doubt account for the sudden loss of consciousness, but the
most characteristic features of catalepsy — the muscular rigidity
and flexibilitas cerea — are still unexplained. Most authors
believe that the cataleptic rigidity is only an increase of the
normal tonus of the voluntary muscles, and some think that
the diminution or loss of voluntary innervation which occurs in
catalepsy causes an increase in the reflex tonus of the muscles,
just as reflex excitability is increased by the removal of the
cerebral hemispheres in frogs. But no amount of increase of
the reflex tonus would account for the condition known as.
flexibilitas cerea, and what is a still more fatal objection to this

SOMNAMBULISM AND HYPNOTISM.

911

theory is that general reflex irritability, instead of being increased
in catalepsy, is on the contrary often much diminished or
abolished.

We have already seen that complete hemianesthesia is
probably caused by a temporary or permanent arrest of the
functions of the centripetal fibres in their ascent through the
internal capsule, or of that part of the cortex of the brain which
is supplied by the posterior cerebral artery. Suppose now that
a complete bilateral hemianesthesia exists, what would be the
condition of the patient 1 There would be complete loss of every
form of cutaneous and muscular sensibility as well as of sensa-
tion in the bones and joints ; there would be loss of taste on both
sides of the tongue, and of smell in both nostrils ; and instead
of there being amblyopia and partial deafness on one side,
as in hemianesthesia, there would be complete blindness and
deafness on both sides, inasmuch as, according to the hypothesis,
the sensory centres in both hemispheres either have ceased to
act or the impressions made on the peripheral sense organs fail
to be conducted to them. But impressions made on the peri-
phery would, however, reach the cortex of the brain through
the optic thalamus, and the subject of bilateral hemianesthesia,
although effectually cut off from the external world so far as
the anatomical substratum of consciousness is concerned, would
perform various complicated actions in response to peripheral
impressions, but without being attended by consciousness. The
condition would, indeed, be very similar to that observed in
somnambulism, the mesmeric state, and various post-epileptic
and allied conditions.

§ 952. Diagnosis. — During the presence of muscular stiffening
and flexibilitas cerea, the diagnosis can present no difficulties.
Only very cleverly executed simulation could give rise to any
doubt ; and in these cases careful testing of the sensibility, reflex
irritability, and electrical reactions, along with comprehensive
observation of the concomitant symptoms, ought to be suffi-
cient to afford a safeguard against deception.

§ 953. Prognosis. — The prognosis of uncomplicated cases of
catalepsy is always favourable as regards life ; but with respect

912

SOMNAMBULISM AND HYPNOTISM.

to complete recovery it is unfavourable. Cases arising from
malarial infection afford a better prognosis, and the same may
be said with respect to acute attacks occurring in comparatively
healthy persons as the result of injuries and mental shocks.

§ 954. Treatment. — The aims of treatment in catalepsy are
to arrest the attacks and to prevent their return. The latter
indication can be best effected when the cause can be removed ;
in catalepsy due to malaria, quinine alone, or combined with
morphia, may effect a complete cure. Favourable results have
been obtained by the use of tonics, iron, ergot, morphia, the
cold douche, and the faradic current. The galvanic current
has hitherto proved useless.

Attempts to put an end to the attack itself have not been
very successful. A slight peripheral irritation may arouse
patients in hysterical catalepsy, but in the idiopathic form very
strong cutaneous irritation has often no influence. In pro-
tracted cases artificial feeding by the stomach pump and
nutritious enemata must be had recourse to.

Trance must be treated on the same general principles as
hysteria, while those who are liable to attacks of somnam-
bulism ought to have their bedroom windows and doors well
fastened at night.

913

CHAPTER VI.

EPILEPSY AND ECLAMPSIA.

(I.) EPILEPSY.

Epilepsy is a chronic functional disease of the nervous system,
characterised by recurring paroxysms of impairment or loss
of consciousness, accompanied generally by partial or general
convulsions.

§ 955. Etiology. — Hereditary predisposition plays an impor-
tant part in the production of epilepsy. The transmission may
be direct, as when the progeny of an epileptic parent are
affected ; or indirect, when one or more generations escape,
and the disease reappears in the descendants. But in other
cases the hereditary tendency is still more indirect. The
family of the patient may have a proclivity to nervous disease,
declaring itself as insanity in one member, as hysteria in a
second, indulgence in alcoholic excess in a third, neuralgia in
a fourth, and epilepsy in a fifth, while other members may only
exhibit the slighter forms of instability termed nervousness.
A hereditary taint may be traced in rather more than one-third
of all cases (Reynolds, Gowers). The children of consangui-
neous marriages appear to suffer from epilepsy in greater
proportion than other children. All family peculiarities, whether
good or bad, are intensified in the children by intermarriage; and
when both parents inherit an unstable nervous system the
probability of some nervous disorder appearing in the progeny is
greatly increased. Under these circumstances one or more of
the children may suffer from epileptic convulsions when the
parents manifest only nervousness, neuralgia, or hysteria. The

GGG

914

EPILEPSY.

disease is transmitted more frequently through the mother than
the father, and the females of a family are more likely to suffer
than the males (Gowers).

The female is rather more frequently affected with epilepsy
than the male sex, in the proportion of 114 to 100 according
to Dr. Gowers. Females are attacked with hystero-epilepsy in
the proportion of 2 to 1 of males.

Age is an important predisposing cause of epilepsy. Out
of 1,450 cases analysed by Dr. Gowers the disease began under
ten years of age in 29 per cent, between ten and twenty
in 46 per cent, between twenty and thirty in 15 '7 per cent,
between thirty and forty in 6 per cent, between forty and
fifty in 2 per cent, between fifty and sixty in 1 per cent, and
above sixty years of age in £rd per cent. The 'proportion in
which the two sexes suffer varies at different periods of life.
Speaking broadly, of the number attacked under thirty years
of age the males exceed the females, while beyond the pro-
portion is reversed. It has been asserted that when a here-
ditary tendency exists the disease begins before twenty years
of age, but Dr. Gowers maintains that the influence continues
until a late period of life.

Defective nutrition of the body generally, including the
nervous system, such as is met with in anaemia, chlorosis, scrofula,
and rickets, appears to beget a certain instability of the nervous
system which predisposes to the production of epilepsy. Chronic
alcoholism is also often associated with epilepsy, but it is
difficult to determine whether the former is the cause of the
latter, or both result from a hereditary taint.

Of the exciting causes of epilepsy, profound emotional distur-
bance, arising from fright, grief, and anxiety, is the most frequent
and important. The first attack of epilepsy often appears after a
sudden fright. This cause is most frequently in operation under
twenty years of age, and the female sex is especially liable to be
affected by it. Epilepsy is sometimes excited in apparently
healthy individuals by witnessing another in convulsion.
Eccentric irritation is another frequent exciting cause of epilepsy.
Of the cases which date their origin from infancy, the first fits
occur in a large proportion during dentition. It must be
remembered that children who have suffered from eclamptic

EPILEPSY..

915

attacks during dentition frequently develop true epilepsy at
puberty, but it is probable that there exists in such cases a
strong predisposition to the disease.

The influence of sexual excess in the production of epilepsy
is probably over-estimated. Women, the subjects of epilepsy,
not unfrequently suffer from a fit during the menstrual period,
and the disease may be caused by uterine and ovarian derange-
ments and by pregnancy. Among other reputed causes of
epilepsy may be mentioned diarrhoea, dysentery, overloading
the stomach, irritation of the intestinal canal from the presence
of worms, the passage of gall stones, over-exertion, and exposure
to cold.

Epilepsy is also liable to become established in the course of
or during convalescence from acute febrile diseases, a con-
siderable proportion of such cases following scarlet fever. In
these a connection between the eclampsia of scarlatinal nephritis
and the subsequent recurrence of convulsions can only occa-
sionally be traced (Gowers). Chronic lead-poisoning is some-
times attended by recurring convulsions like those of epilepsy.

Injuries to the head and sunstroke are frequently followed
by epilepsy. Cases in which the skull is fractured or coarse
structural changes are set up in the brain are at present excluded
from consideration. Injuries to nerve trunks are liable to be
followed by epilepsy, and the first seizure usually occurs weeks,
months, or even years after the injury. The convulsion is
generally preceded by some peculiar sensation proceeding from
the region of the affected nerve.

§ 956. Symptoms. — The symptoms of epilepsy may be
divided into (1) those which precede the paroxysm, (2) those
occurring during the paroxysm, and (3) those observed in the
intervals between the attacks.

(1) Premonitory Symptoms. — The premonitory symptoms
of the epileptic attack may be subdivided into remote and
immediate warnings, the latter forming the aurcs epilepticce.
The remote warnings may extend over hours or days before
the occurrence of the attack ; they usually consist of such
symptoms as headache, dizziness, confusion of thought, or some
mental change, the patient becoming depressed and morose, or

916

EPILEPSY.

excited, lively, and irritable. In a case recently under my
care the patient stated that for hours before an attack he
became sometimes very much depressed in spirits and sus-
picious that his friends were speaking and plotting against him,
while at other times he was unaccountably joyous. He then
volunteered the statement : "I am expecting an attack to-day,
for instance, I feel so happy and joyous, and there is nothing
in my circumstances to make me so, as I have just lost my
situation through these fits." During examination his right
cheek was suffused with a bright red blush ; while the left one
was, as his face had hitherto always been when I saw him,
remarkably pale. If the cortex of the hemispheres of the brain
were as freely supplied with blood as the right cheek, this
might account for his joyous feelings.

Aurce JEpilepticce. — Our information with regard to the
immediate warning of the epileptic paroxysm consists of the
subsequent account which the patient is able to give of his
feelings before loss of consciousness is complete. In more
theoretical language, the aura is the mental correlative of
the commencing molecular change in the brain, which is
the physical cause of the epileptic attack. Consciousness is
abolished so soon that there is no aura described in about half
the cases.

The aura may be (a) motor, (b) sensory, (c) vaso-motor aod
secretory, or (d) psychical.

(a) Motor Auro3. — It is .not always easy to distinguish
between a motor and a sensory aura. In epileptic seizures,
where consciousness is retained throughout the attack, or lost
only at a comparatively late period, the patient is often able to
describe the convulsions of the limbs in objective language.
He may be able to tell that he first felt the thumb dragged
across the palm and the fingers flexed on the thumb, and that
he had then to hold the convulsed hand with the other one in
order to arrest its movements.

A patient of my own was in the habit of acting before the
students with great fidelity the phenomena of the attack. He
first produced twitching of the muscles of the angle of the
mouth, then rotated his head and eyes, and finally flexed his
fins ers, and shook his arm to show how the convulsions had

EPILEPSY.

917

invaded the upper extremity. The attack in this case was due
to coarse lesion of the cortex syphilitic in origin, and conscious-
ness was only partially suspended towards the termination of
the attack. In idiopathic epilepsy, on the other hand, con-
sciousness becomes confused at such an early period that the
patient is unable to describe his feelings in objective language,
although he may still do so in subjective language. When, for
instance, the convulsion begins in the hand, the patient, instead
of describing the thumb as being drawn into the palm, says
that he feels a dragging sensation in the thumb or a feeling
of creeping, or numbness in the hand, which gradually passes
up the arm. The sensation begins sometimes in the muscles
of the shoulder and passes down the arm; but these cases are
probably always associated with a coarse lesion in the brain.
When the convulsion begins in the lower extremity, the aura
generally begins as a creeping sensation in the big toe, which
passes up the leg and may extend to the arm before uncon-
sciousness supervenes.

The motor aura begins not unfrequently in the side of the
face, and is generally described as a feeling of " the face being
drawn," or it may begin in the side of the tongue, and be
described as a feeling of something crawling. The tongue is
associated in its actions with different sets of muscles, according
as it is engaged in articulation, mastication, or deglutition, and
these associated movements appear to be sometimes dimly
represented by the epileptic aura. In a case mentioned by Dr.
Gowers tingling in the tongue was associated with twitching of
the lips, in another with a sensation of lateral movements of the
jaw, and in a third it was followed by a feeling of sickness,
succeeded by a sensation of something rising in the throat and
then by palpitation of the heart.

The aura consists sometimes of sudden inability to speak —
a temporary aphasia, — or there may be motor aurse referred
to the eyeballs, which are generally described in subjective
language. The patient, for instance, never says that the attack
began by a squint, but states that he suffered from double
vision. On rare occasions the patient may describe that his
eyes were turned in a particular direction ; but, as a rule, the
rotation of the eyeballs is felt by the patient as a displacement

918

EPILEPSY.

of external objects in the opposite direction, and he conse-
quently complains of things whirling round him, of swimming
in the head, or of vertigo and sickness. At times patients see
objects recede from them and become smaller or approach them
and become larger, sensations probably depending upon varia-
tions in the tension of the muscles of accommodation. One
of the most remarkable features presented by motor aurse is
that, as a rule, all of them begin in small muscles, such as those
of the eyeballs, tongue, face, and hands. These muscles are
engaged in the most special actions, and consequently the motor
aurse may be said to begin in the more special and to pass gra-
dually to the more general actions. Sometimes the aura begins
in muscles like those of the shoulder engaged in general actions,
while the muscles engaged in special actions are secondarily
involved. Such cases are probably always due to organic disease
of the brain, the lesion being situated near the longitudinal
fissure and away from the special centres of the operculum.
Sometimes the aura may occur in both hands or both legs
simultaneously, or there may be a sensation of trembling in the
muscles of the back, while at other times general tremor or
jerking of the muscles is complained of.

(6) Sensory Auroe. — The sensory auras may be referred to
any of the centripetal nerves of the body, namely, those of
the skin, muscles, and bones, the nerves of special sense, and
the nerves of the viscera. As already remarked, it is not
always easy to determine whether the sensations referred by the
patients to the extremities are due in any particular case to a
discharge from a sensory or a motor centre in connection with
the part. Dr. Gowers remarks that there are two modes in
which the aura extends from the arm to the leg, the one by
continuity, the sensation passing up the arm and down the
trunk to the leg ; and the other by separate commencement in
the muscles of the lower extremity. The same is also true with
regard to the method of invasion from the lower to the upper
extremity. In the continuous method of invasion, Dr. Gowers
believes that the discharge from the sensory centre takes the
lead, while in the discontinuous mode of invasion the discharge
of the motor centre is primary. The sensory aura sometimes
consists of a feeling of general heat or cold, and at other times

EPILEPSY.

919

is distinctly localised. Besides various sensations, as tingling,
numbness, or pain in the extremities, it may consist of head-
ache, frontal, vertical, or unilateral, or a feeling of pressure in
the head (Gowers).

Aurce of the Special Senses. — The aurae of the special senses
may consist of undeveloped sensations, which Hughlings-
Jackson, following Spencer, has named crude sensations, or of
more elaborate sensory representations. During the former
the discharge is limited to a sensory centre, so that a simple
sensation only is revived ; during the latter the molecular dis-
turbance extends to neighbouring, sensory centres, so that com-
plicated perceptions result.

Visual Auro3. — The aura sometimes consists of sparks,
flashes of light, and coloured vision. In some cases the fit
begins by a coloured vision, followed by spectral faces, the
former being a crude sensation, and the latter revived per-
ceptions. Illusions of sight are not uncommonly observed. In
a case of my own the attack is ushered in by the patient finding
himself surrounded by lions and tigers, ready to spring upon
him. In some cases the fit is preceded by a vision of beautiful
places, but disagreeable objects and scenes are more common.
In many cases the attack is ushered in by sudden blindness of
one or both eyes.

Auditory aurce may consist at times of hissing, ringing, or
explosive noises ; at other times voices are heard, or the patient
hears distinct words and sentences. The patient may hear a
noise in the ear at first, and this be followed by a distinct
vocal utterance, while in other cases music is heard. At times
the attack is ushered in by a sensation of unusual stillness.

Gustatory aurce consist of metallic or other abnormal sen-
sations of taste. The alteration in the sense of taste may
sometimes be manifested by semi-voluntary or automatic
movements. In a case mentioned by Dr. Hughlings-Jackson
the patient " put different substances into his mouth ; at the
seaside, sand ; at school he drank ink ; in the country he bit
pieces of butterflies ; he smacked his lips in the attacks, and
his brother said he had a look of disgust."

Olfactory aurce consist, as a rule, of unpleasant smells,
generally described in subjective language, and only occasionally

920

EPILEPSY.

in objective language. Dr. Hughlings- Jackson mentions the
case of a patient who held his nose when the attack began ;
probably in this case there was an objective sensation of smell.

In glancing over the different sensory aurse, the most remark-
able characteristic presented is that a general sensation, as a
red colour, often precedes the appearance of the more special
sensations, such as are afforded by definite images of persons
and things. With the motor aura we saw that, as a rule, the
special precedes the general ; but it would appear that in the
sensory aurse the general precedes the special.

These facts find their interpretation in inferences already
made from embryological considerations ; namely, that the
special movements are represented in the motor area of the
cortex of the brain by comparatively small and young cells
situated in the neighbourhood of the vessels ; while the special
sensations are represented in the sensory area of the cortex by
comparatively large and old cells thrust away from the vessels
by the growth of young cells, the latter of which represent the
general sensations.

Visceral Aurce. — The most common of all the immediate
warnings of epilepsy are sensations referred to different portions
of the area of distribution of the pneumogastric nerve. Of
these a sensation referred to the pit of the stomach, named the
epigastric aura, is by far the most frequent. It is sometimes
described as pain, at other times as a feeling of "coldness,"
" burning," or as a vague, indescribable sensation. The painful
epigastric feeling is generally fixed ; while the vague sensation
ascends to the throat and causes a feeling of choking, or to the
head, when immediate loss of consciousness ensues (Gowers).
In some cases a feeling of suffocation constitutes the warning ;
in others there may be nausea and retching, a feeling of intense
hunger, or palpitation with or without angina.

(c) Vaso-motor and Secretory Aurce. — The attacks may be
ushered in by a sensation of coldness, or numbness in the fiDgers
and toes, and the affected part becomes pale and cold to the
touch. At other times spots in various parts of the body assume
a red colour, and become the seats of feelings of transient heat.
Faintness, which constitutes a frequent aura, may probably
sometimes be associated with sudden dilatation of the abdo-
minal vessels.

EPILEPSY.

921

(d) Psychical Aurcv. — The immediate warning often con-
sists of intense horror or alarm, and the patient may look
startled, guilty, or frightened. In other cases it consists of
an intellectual perversion. The patient feels as if he were
suddenly in a strange country, or the idea suddenly seizes him
that an object, at which he may be looking and which he has
never seen before, was known to him previously. In many
cases the aura is what Dr. Hughlings-Jackson has named " a
dreamy state" or a "voluminous" mental condition. This
condition is similar to that said to be experienced by persons
in the act of drowning, during which all the past events of
life seem to crowd upon the memory.

Order of Succession of the Phenomena of the Aura. —
This subject is so wide that it can only be briefly indicated here.
We have already seen that when the aura is motor, and the
spasm begins in the muscles of the head, those of the arm are
next invaded and those of the leg last ; when the spasm begins
in the muscles of the hand those of the face are next invaded
and those of the leg last, and when the spasm begins in the
muscles of the leg those of the arm are next invaded and those
of the face last. The order in which the convulsions spread in
these three forms of onset may be readily explained by reference
to the topographical distribution of the motor centres in the
cortex.

An undeveloped or crude sensation of sight, such as a red
light, is sometimes followed by a developed perception, such as
the image of a man ; a confused noise may be succeeded by
strains of music ; a subjective sensation of smell may be followed
by efforts to prevent the effluvia gaining admission to the
olfactory chambers, showing that the sensation had become
objective. It would appear that in all these cases the discharge
begins in the sensory centre, and as it spreads it involves a
portion of the cortex, in which connections are formed with other
sensory centres, so that the discharge is now accompanied by a
perception. This process is, however, soon arrested by the
rapid impairment of consciousness, during which both sensa-
tions and perceptions become fainter and soon disappear. A.
visual is not unfrequently associated with an auditory aura,
sometimes the one and sometimes the other taking the pre-

922

EPILEPSY.

cedence. The association of these sensations is readily ex-
plained by the proximity of the visual and auditory centres as
determined by Ferrier. In some cases the epigastric aura is
followed by an emotion of fear or of anguish, and the patient
may have a facial expression corresponding to it. It has been
suggested by Hughlings-Jackson that there may often be a
determinate relation between sensory and visceral aurse, and
between the "dreamy" state of psychical auras, and post-
epileptic actions; but little or no progress has hitherto been
made in collecting materials to decide the question.

. (2) The Epileptic Paroxysm. — The symptoms of the
paroxysm are very variable, but for purposes of description
they may be divided into (a) epilepsia mitior, or le petit Trial, in
which there is impairment or abolition of consciousness, but
no manifest spasms; (b) epilepsia gravior, or le haut mal,
in which there is loss of consciousness along with general tonic
and clonic convulsions ; (c) epileptiform seizures, in which pro-
nounced spasms are present in half the body, but with only
slight suspension of consciousness.

(a) Epilepsia mitior, or le petit mal. — The description of
the minor attacks of epilepsy need not detain us long. The
attack consists of momentary confusion of thought, or transitory
unconsciousness. The patient, for instance, may be attacked
while speaking ; he becomes suddenly unconscious, there is a
pause probably in the middle of a sentence, but in a few
seconds speech is resumed at the point where it was inter-
rupted and the sentence is finished. At times the attack may
consist of a feeling of fainting, along with confusion of mind.
In other cases there is momentary vertigo, slight pallor of the
face, and transitory unconsciousness. Indeed, any one of the
numerous auras just described may, along with slight confusion
of mind, constitute a minor attack of epilepsy. Many of the
sensations described as immediate warnings may be experienced
in the absence of epilepsy; but if the sensation recur at
periodical intervals, and be attended by some confusion of
thought, the occurrence of genuine epilepsy may be suspected,
although a visual sensation, along with some confusion of
thought, often precedes an attack of migraine. If there be

EPILEPSY.

923

involuntary discharge of urine or fasces during the attack the
affection is undoubtedly epileptic.

In many of these slighter attacks loss of consciousness is
accompanied by minor degrees of muscular spasm. At the
onset of the attacks the countenance becomes ghastly pale, the
pupils contracted, and the eyes fixed and staring, or there may
be slight strabismus or drawing of the month, while in other
cases there may be partial rotation of the head and eyes, chew-
ing movements, or rolling about of the tongue. There may be
again momentary rigidity or slight tremor of all the muscles of
the body, while transitory arrest of respiration is not uncommon.
Sometimes the patient utters a shriek, reels, or walks hurriedly
round the room, and then recovers. At times the unconscious-
ness may last for a considerable period, but the patient may go
on with the work in which he was engaged as if he were con-
scious. In a case mentioned by Trousseau the patient continued
to play the violin with accuracy during short periods of uncon-
sciousnesss. It must be remembered that the slighter attacks
of epilepsy are liable to be followed by the condition named
" epileptic mania," to be subsequently described.

(6) Epilepsia gravior, or le haul Trial. — The epileptic
paroxysm may, for the purposes of description, be divided
into three stages. The first is characterised by loss of conscious-
ness with tonic spasm ; the second, by loss of consciousness
with clonic spasm ; and the third, by cessation of the spasm
and gradual restoration to consciousness. A fourth or after
stage may be added.

(i.) The First Stage. — The true epileptic attack is ushered
in by three prominent symptoms occurring simultaneously.
These are loss of consciousness, sudden falling, and great pallor
of the face, while a fourth symptom is often present in the
form of a loud and piercing cry. The loss of consciousness is
sudden and complete, every form of sensibility and mental
operation being completely abolished, although certain reflex
actions are retained (Romberg). The patient often falls, as if
struck by lightning, either forwards on his face, backwards on
his occiput, or latterly, and so instantaneously that he has no
time to select a place or attitude, and may consequently fall
into fire, water, or from a height. At other times the patient

924

EPILEPSY.

has sufficient warning of the impending attack to enable him. to
sit or' lie down. Pallor of the face is probably always present
at the beginning of the attack, although the symptom is some-
times so transient that it may pass unobserved.

The epileptic cry which the patient often utters immediately
before or during the fall is loud and piercing, and alarms,
according to Romberg, both man and animals. When the
patient falls to the ground he remains for a period of from two
to forty seconds in a rigid condition, caused by a tonic, although
unequal contraction, of all the muscles of the body. Various dis-
tortions are thus produced ; there is conjugate deviation of the
eyes, with rotation of the head and neck ; the pupils are dilated
and insensible to light ; the countenance is variously altered ;
the jaws are firmly closed, and the tongue may be severely
bitten ; there is opisthotonos ; and the different segments of
the lower extremities are extended upon one another and
upon the trunk, the foot being rotated inwards and the toes
widely separated ; the segments of the upper extremities again
are flexed upon one another, the thumb being bent into the
palm, the fingers closed, and the hand pronated ; and the forearm
is flexed or sometimes extended upon the arm. The respiratory
muscles are in a state of tonic spasm, and the breathing is
arrested. The hideous cry uttered as the patient falls is pro-
bably produced by spasm of the expiratory muscles with closed
glottis. The pallor of the face is soon replaced by a dull red or
dusky hue, and the veins of the head and neck become greatly
distended, the carotids throb violently, and the action of the
heart is forcible, although the pulse is small or imperceptible at
the wrist.

(ii.) The Second Period. — After a variable period of from two
to forty seconds, the tonic gives place to clonic spasms, which are
usually more pronounced on one side of the body. The muscles
of the face, tongue, pharynx, and larynx are usually first affected
by clonic spasm, and those of the trunk and extremities are
afterwards invaded.

The patient now presents a hideous appearance, the head is
alternately drawn laterally, or forwards and backwards; the
eyeballs are convulsively rotated in various directions, but
rotation in an upward and outward direction predominates, so

EPILEPSY.

925

that the pupils are hidden, and only the whites of the eyes are
visible under the blinking half-closed lids ; the face is variously
distorted, and the convulsive closure of the jaws is often so
violent that teeth are broken and the tongue severely bitten,
while the blood from the wound, mixing with the saliva, oozes
through the clenched teeth as a sanguineous froth. The trunk
and limbs are variously thrown about, and the contents of the
bladder, rectum, or vesiculse seminales may be evacuated.

The venous hyperaemia reaches its maximum just as the
clonic spasms are beginning to abate in severity ; and the skin is
bathed in sweat, which in some cases has a foetid odour. The
heart beats tumultuously ; the carotids throb ; and the pulse, if
it can be felt, is fuller and more laboured than during the
period of tetanic contractions. The pupils are alternately
contracted and dilated, and are said to be slightly sensible to
light. This stage may last from a few seconds to five or ten
minutes, the average duration being from two to three
minutes.

(iii.) The Third Stage. — During the third stage there is a
gradual return to consciousness and voluntary power. The
convulsions either cease suddenly or wear off gradually, the
period of transition being marked by partial jerkings of some
muscular groups, or by a diffused tremor of the body.

General muscular relaxation is now established, but coma
persists for a short time longer. The patient soon attempts
to change his position ; he opens his eyes and looks around him
with a bewildered expression, and perhaps attempts to speak.

The respiratory movements have become more natural in
rhythm, although they are still somewhat irregular ; the pupils
are contracted ; the pulse is variable, but generally full and
quieter than during the previous stage; the conjunctivae are
injected ; petechias are often observed on the eyelids, forehead,
and temples ; and the patient is exhausted and disposed to
sleep.

The attack is often followed by vomiting, and a large quan-
tity of pale urine is often passed. The temperature of the body
appears to be normal after single attacks of epilepsy.

(iv.) The Fourth or After-Stage. — The after-symptoms of
epilepsy differ greatly in duration, severity, and nature. The

926

EPILEPSY.

patient recovers occasionally in about a quarter of an hour after
the attack, and resumes his previous occupation ; but, as a rule,
recovery is delayed for a much longer period. He suffers from
lassitude and stupor, from which he is aroused with difficulty,
and, if awakened, he is peevish and irritable, while the general
muscular relaxation is occasionally interrupted by momentary
clonic spasms or fibrillary contractions. The average duration
of the stupor is about an hour when the attack occurs during
the day ; but when it occurs in the evening it passes insensibly
into the ordinary nocturnal sleep.

Complications. — Various mental disturbances are by far the
most important of the complications of epilepsy. The patient
sometimes exhibits marked mental derangement immediately
before as well as after the paroxysm, and a maniacal condition
constitutes sometimes the principal feature of the attack. A
person the subject of epileptic vertigo may continue for some
seconds, minutes, or even hours in a dull, half stupid condition.
He may mutter a few incoherent words, or some lewd expression,
no matter how foreign to his habit; he may unbutton his
clothes and expose his person, urinate in a public assembly,
exhibit himself naked to his domestics, or even walk in public
naked unless prevented, and on recovery he has only the
vaguest recollection of what has occurred. These, however, are
only a few of the minor actions which may be done by indivi-
duals subject to epileptic vertigo immediately after the attack.
The most motiveless and atrocious crimes are sometimes com-
mitted in this condition, so that some medical jurists are of
opinion that no epileptic is responsible for his actions. Epileptics
sometimes have a warning of the approaching maniacal state,
so that they can warn their friends to protect themselves ;
but generally the seizure is more or less sudden. There is
every variety of intermediate form between the milder and
severer cases. Reynolds says that epileptic mania occurs in
about one-tenth of all cases of epilepsy, including the minor
attacks of epileptic vertigo ; having occurred in the case of any
one individual, it is apt to appear again, especially when several
fits have followed in rapid succession.

Epileptic delirium is not always furious and dangeiws. It
may appear in the form of preternatural gaiety or illusions

EPILEPSY.

927

of the senses before the attack, or during the intervals.
Meningitis has been known to follow epileptic paroxysms ; but
it is generally the result of an injury inflicted by the fall, and
both apoplexy and permanent paralysis are rare complications
of idiopathic epilepsy. Idiocy and epilepsy are not unfrequently
associated, in which case the former disease is generally con-
genital.

Attacks of Hystero-epilepsy. — Hystero-epileptic attacks are
not often seen in this country in the classical form described
by French authors. The patient in the intervals suffers from
various hysterical symptoms, the most usual of which are
complete or incomplete hysterical hemiansesthesia, and ovarian
hypersesthesia. The paroxysm is always preceded by an aura,
consisting of a sensation proceeding from the region of the
hypersesthetic ovary towards the epigastrium, and ascending
to the throat and finally to the head, when the patient utters
a loud shriek and falls insensible to the ground. All the
muscles of the body now become the subjects of tonic spasm;
the head is retracted, and the body and limbs are arched back-
wards and rigid ; the respirations are stertorous and infrequent ;
and foam, sometimes blood-stained on account of the tongue
having being bitten, generally issues from the mouth. The
tonic stage is followed by a few clonic convulsions, but these
soon cease, and a state characterised by general muscular
relaxation, stertorous respiration, and coma terminates the
portion of the attack resembling the epileptic paroxysm.

The second stage, or what the French call the ''phase des
grands mouvements," now makes its appearance. It is charac-
terised by violent contortions of the body, and gesticulations
having a purposive character. There is opisthotonos, or the
body is bent forwards or laterally ; while at other times it is
maintained in a rigid position, with the lower extremities
extended and the upper stretched out.

The third stage, or stage of emotional attitudes (phase des
attitudes passionelles), now appears, and during its continuance
the patient assumes in rapid succession attitudes and gestures
expressive of various emotions. The first attitude assumed by
the patient is usually a threatening one ; she raises herself in

928

EPILEPSY.

a half sitting posture, the brows frown, the fists are clenched,
and the face presents an angry and menacing expression ; this
attitude, however, soon gives place to an expression of abject
fear, which in its turn makes room for a look of intense happi-
ness and beatitude. But the expression of beatitude is also
fleeting in character, and is succeeded by one of intense volup-
tuousness, followed by gestures which lead to this stage being
called the phase of lubricity. Terror now seizes the patient,
she sees rats and other odious animals that evoke from her
passionate exclamations of dread and disgust, and this is
followed by a stage in which she appears to be labouring under
the idea that she has committed a great offence, and sues for
mercy. The patient now hears strains of music, she looks
pleased, and may join in humming the tune ; but her singing is
soon followed by weeping, broken by reproaches addressed to
her parents as the cause of her misery. This last phase con-
stitutes the stage of recovery, but hallucinations may persist
for some time. The patient can always describe subsequently
the hallucinations to which she was subject, and each of the
attitudes is found to have corresponded to a hallucination.

An attack of hystero-epilepsy may be provoked at any time
by various manipulations, such as "suddenly 'gripping' the
skin of the breast on both sides on a level with the fifth rib,
and midway between the anterior and posterior boundaries
of the axillae."* An attack is also readily induced by pinching
a fold of the skin of the sub-inguinal region, or by slight pres-
sure on the region of the hypersesthetic ovary. Sudden and
firm pressure exerted on the affected ovary, however, instantly
arrests the paroxysm at any stage. When such compression of
the ovary is made, the patient's mouth opens widely, the tongue
is spasmodically protruded, and the convulsions cease.

The phenomena presented by attacks of hystero-epilepsy in
this country are too variable to be comprised under one general
description. In some cases there is a condition of emprostho-
tonos, instead of opisthotonos, during the second stage of the
attack, this form being very liable to occur in boys. In other
cases the legs are alternately flexed and extended, and the

* An Account of the Phenomena of Hystero-Epilepsy, by Arthur G-amgee,
M.D., F.R.S., "British Medical Journal," vol. ii., 1878.

EPILEPSY.

929

patient, who lies on her back, may be propelled from one end
of the room to the other. In still other cases the attack
consists of great difficulty of breathing caused by intense respi-
ratory spasm (Gowers).

(c) Epileptiform Seizures. — This form of epilepsy was first
described by Bravais, but its pathology was fully investigated
by Hughlings-Jackson, and it is consequently named "Jack-
sonian Epilepsy." In it the convulsions are partial, being
limited to one half of the body, and consciousness is either
retained throughout the attack, or lost only at a comparatively
late period. The fits are accompanied or followed by paresis of
the convulsed limbs. These seizures are caused by coarse
disease situated near the cortex of the brain, the most common
lesion being a gumma. The convulsions which supervene upon
the spastic hemiplegia of childhood (unilateral atrophy of the
brain) are at first partial, but after a time become general. An
interesting case of epilepsy in a girl aged 6| years is recorded
by Dr. Sturge, in which the convulsions, which began when the
patient was 6 months old, were at first limited to the left half
of the body, and always began in the left hand after they had
become general. The left half of the body was observed to be
weak for some time after each partial convulsion. The patient
was born with an extensive " mother s mark " on the right side
of the head and face ; it extended to the mucous membrane of
the tongue, uvula, and pharynx on the same side, the sclerotic
coat, retina, and choroid of the right eye being also implicated.
Dr. Sturge makes the very probable conjecture that the attacks
were due to a "port wine mark" on the surface of the right
hemisphere of the brain similar to that on the face.

(3) The Inter paroxysmal Condition — The condition which
exists during the interval between the epileptic attacks was
first fully examined by Dr. Russell Reynolds, and deserves
careful attention. The most important phenomena observed
are those which belong to the mental condition of the patients.
In a considerable number of cases no mental disturbance or
weakness whatever can be discovered in the condition of the
patient between the attacks, and occasionally individuals
possessed of high intellectual powers are the subjects of

HHH

930

EPILEPSY.

epilepsy. The classical cases of Julius Caesar and Napoleon,
both of whom suffered from the disease, may be cited as
examples.

Slight impairment of memory, especially with regard to recent
events, while the remembrance of remote occurrences is intact,
is the most common and generally the first mental change.
The next grade of mental impairment declares itself in a certain
amount of mental dulness and want of apprehension ; while a
still lower degradation is manifested by confusion of ideas,
general want of comprehension, and deficiency in intellectual
activity, associated with a stupid and vacant expression. The
moral nature is almost invariably perverted, the patients being
gloomy, irritable, and distrustful.

One or other of these minor mental defects may continue
to exist without any appreciable change during a series of years ;
but at other times the mental change, beginning with minor
degrees of impairment, passes through lower and lower depths
of deterioration until the patient arrives at a condition of com-
plete imbecility.

The conditions which determine mental failure in epileptics
have been carefully examined by Dr. Russell Reynolds ; the
following are the most important conclusions at which he
arrived. Hereditary taint is without influence, and the same
may be said of the duration of the disease, the state of
the general health, the number of attacks, the nature of the
exciting cause, and the severity of the paroxysm when judged
by the duration of the subsequent coma. Frequency of recur-
rence of the seizures exerts a certain amount of influence in the
production of mental impairment, yet there is no constant con-
nection between the two phenomena. Mental impairment is,
according to Reynolds, more frequently associated with minor
than with major attacks of epilepsy, and appears to be not
in direct but rather in inverse proportion to the degree of
muscular manifestation.

Motor Manifestations. — Some motor disturbances occur in
the intervals between the attacks in the majority of instances.
These appear in the form of simple muscular trembling, or
there may be clonic or tonic spasms in single groups of muscles.
Clonic spasm is the most frequent, and may occur in either of

EPILEPSY.

931

two forms. There may be more or less constant choreiform
movement, which continues during sleep, but is exaggerated
during waking hours, as in the spastic hemiplegia of childhood ;
or there may be violent spasmodic shakings of the limbs or of
the trunk, occurring at irregular intervals, and with special
frequency just as the patient is falling asleep; the muscular
jerking is sometimes so sudden and violent that the patient is
thrown out of bed ; or, if standing, he may be thrown down.
Cramp or tonic contraction is comparatively rare.

Sensory Manifestations. — The sensory disturbances are by
no means so constant and important during the intervals as
the motor. Headache and vertigo are the two symptoms most
frequently complained of, and the latter must sometimes be
regarded in the light of an abortive attack.

State of the General Health. — There is no constant relation
between epilepsy and any particular state of health. It is no
doubt sometimes associated with a feeble state of the general
health, but it is much more frequent to find epilepsy in those
who are in other respects quite healthy, and some epileptics are
remarkable for their Herculean frame and strength. The most
frequent change which Dr. Reynolds observed in epileptics
was subnormal temperature, and the least frequent impaired
nutrition.

Relations between the Symptoms of Epilepsy.

(a) Forms of Attack. — Hereditary taint appears to exert
an influence in predisposing to the severer form of epilepsy,
although milder attacks may be associated with the severer in
the cases where there is a frequent recurrence of the latter.
When epilepsy is developed at an early age, there is a some-
what increased proclivity to the attack in its milder form. When
epilepsy becomes developed in consequence of a peripheral
source of irritation, an interval of weeks or even months elapses
between the time the injury is inflicted and the first seizure.
During this period painful sensations may be felt, or there
may be clonic or tonic spasms in the area of distribution of the
affected nerve, or the two conditions may be combined. After
a time spasmodic seizures appear with loss of consciousness ;
they are ushered in either by a sensory, motor, or vaso-motor

932

EPILEPSY.

aura, which is always of the same kind in the same individual,
and begins in the region of the injured nerve. When a
cicatrix is found in the course of the affected nerve, an attack
may occasionally be produced by pressing upon it. Dr. Ogle
reports a Case in which a seizure could be produced by touching
the upper extremity, but the epileptogenous zone is not usually
distinctly marked.

(b ) Frequency of Attacks. — The paroxysms as a rule recur
very irregularly, but Reynolds thinks that frequently " the
recurrence of attacks has some relation to time, as marked by
its natural division into days, and periods of seven days, and
multiples of seven days. Thus a large number of epileptics
have their seizures every day, every two weeks, three weeks, and
four weeks, while only a much smaller number suffer at such
irregular intervals as cannot be thus expressed."

Sometimes the mode of recurrence is what has been termed
" serial." The patient suffers from two or more attacks in a day,
usually within twelve hours, and then there is a free interval of
from one to several weeks. This mode of recurrence is more
frequent in the female than in the male sex.

The frequency of the paroxysms varies within wide limits,
some patients only having one seizure a year, others having
thousands ; but Reynolds states that half the cases are found to
have a rate of recurrence ranging from one attack in fourteen
to one in thirty days. A high rate of frequency is generally
observed in those who are in more or less robust health; and
a low rate of frequency in those whose general condition has
undergone marked deterioration. Early commencement of epi-
lepsy is commonly, bat not always, associated with a high rate
of frequency of recurrence.

The groups of attacks may be composed of from four to a
hundred or more single seizures in twenty-four hours. This
condition may extend over a much longer period, and Delasiauve
saw in a boy of fifteen, within one month, a "collective seizure"
which was composed of 2,500 "fragmentary seizures." The
French have designated this condition 4tat de mal tyileptique
( status, epilepticus J, and Bourneville has recently drawn atten-
tion to the great increase of temperature which characterises
the condition. The patients lie in profound coma, and the

EPILEPSY.

933

temperature may rise to 10760 F., and still higher in fatal cases.
In favourable cases the temperature gradually falls, but in other
cases a subsequent rise takes place, coma becomes profound,
and the patient dies, often with symptoms of collapse associated
with the formation of acute " bed-sores."

It is well to remember that the attacks frequently occur at
night, and especially is epilepsy apt to commence in this way.
Our attention should be directed especially to this fact if a
previously healthy patient complain sometimes on waking in
the morning of such symptoms as depression, stupidity, and
headache ; the surmise of epilepsy will be rendered certain if
in addition there have been involuntary discharge of urine or
faeces, if the tongue be bitten, or if small haemorrhages into the
skin be found.

§ 957. Course, Duration, and Terminations. — Epilepsy is
essentially chronic and may last for years, and, although death
occasionally occurs during a paroxysm, this is exceedingly
rare. The course of the disease does not appear to be much
influenced by surrounding circumstances, and not nearly so
much as might be anticipated by the health of the patient in
other respects. The abuse of alcoholic liquors aggravates the
attacks, and even drinking a moderate allowance of beer or
wine appears to act unfavourably on the course of the disease.
Excess in eating and drinking tea and coffee also appears to
aggravate the disease. The influence which a moderate indul-
gence of venery exerts upon the course of epilepsy is not well
determined. Many instances are known where a paroxysm
came on during coitus, and venereal excess doubtless aggravates
the disease.

During the course of acute diseases the epileptic paroxysms
usually cease, but generally return during convalescence ; a
similar effect is sometimes produced by external injuries.
Chronic diseases act in different ways, sometimes mitigating, at
other times aggravating the paroxysms, and at still other times
not appearing to exert any influence on the course of the disease.

Mental affections of one kind or another are frequently
associated with epilepsy, but .Reynolds has shown that their
concomitance is not nearly so frequent as was at one time

934

EPILEPSY.

supposed. It appears that some mental affection is found
associated with epilepsy in about one-third of all cases, and
especially in those cases where the paroxysms follow each other
in unusually rapid succession. In some of those cases there is
every reason to conclude that the mental affection and epileptic
attacks are joint effects of one common lesion.

§ 958. Morbid Anatomy. — Post-mortem examination has
revealed the most various anatomical changes after death from
epilepsy in almost every organ of the body, but none of these are
constant and some are quite exceptional. Various irregulaiities
have been found in the structure of the skull, especially if the
disease be hereditary or have existed from an early age. The
bones of the skull may be thickened, and there may be exostoses
on the internal -surface of the skull, or contraction of the carotid
foramen or of the foramen magnum.

The meninges of the brain are sometimes opaque, thickened,
or distorted, especially if osteosclerosis exist at the same time.
Various statements have been made with respect to the weight
of the brain, Eeheverria considering that the brain is increased
in weight, while Meynert found a decrease in weight in epileptic
insanity. Asymmetry of >the cerebral hemispheres has been
observed pretty frequently. Meynert also found a difference
between the two hippocami majores, caused by progressive
atrophy, associated with cartilaginous hardness of one of them,
but he regarded this condition not so much a cause as a result
of epilepsy. An abnormal distribution of the grey substance of
the cerebrum and cerebellum has been met with ; but this
condition has also been found apart from epilepsy. Disease
of the pituitary body is sometimes associated with epilepsy. In
chronic cases microscopical changes have frequently been found
by Schroeder van der Kolk, Echeverria, and L. Meyer in the
medulla oblongata, and also in other parts of the brain and
uppermost part of the cervical region of the cord. The changes
observed consisted of a granular albuminous exudation, granule
cells, dilatation of capillaries, with softening of their walls, and
pigmentation of the ganglion cells, especially in the nuclei of
origin of the hypoglossus and vagus. Analogous changes were
found in various parts of the cerebrum, cerebellum, and basal

EPILEPSY.

935

ganglia. The cortex of the brain is affected, either directly or
indirectly in the large majority of cases of epilepsy. The
primary morbid change may then be found in the skull, dura
mater, pituitary body, the cortex itself, or even the white sub-
stance beneath it ; but it is probable that implication of the
cortex by the lesion is the essential condition in all of them.
In epileptiform seizures, from coarse disease of the brain, the
lesion is always situated in or near the cortex of the brain.

Experimental Researches. — The connection subsisting between general
convulsions and antenna of the brain has already been considered. Kuss-
maid and Tenner found that when the brain in animals is rapidly deprived
of arterial blood, either by bleeding or ligature of the four great arteries
going to the head, general convulsions and loss of consciousness were
invariably produced. They also endeavoured to produce an epileptic
attack by faradisation of the sympathetic, but only succeeded in one case
after both vertebrals and one carotid were ligatured. The experiments of
Brown-Se'quard on guinea-pigs, with the view of determining the nature
of epilepsy, are very important. He found that injury to various parts
of the nervous system developed in these animals an epileptic condition.
Section of some of the larger nerve trunks, such as the sciatic, internal
popliteal, and posterior roots of the nerves of the leg, partial or complete
section of the spinal cord, and wounding of the medulla, crura cerebri, or
corpora quadrigemina are the lesions most surely followed by epilepsy.
After the wounds heal a state of increased excitability persists ; spasmodic
twitches appear first in certain groups of muscles, and after a time the
animals are seized with complete epileptic attacks. He also found that
irritation of the skin over a certain limited area in the antero-lateral region
of the neck — generally the area of distribution of the trigeminus and
occipitalis — determines an epileptic attack, and that a considerable pro-
portion of the subsequent progeny of those animals are epileptics.

At the meeting of the British Association at Liverpool, where I was
present, Dr. Brown-Se'quard exhibited a descendant of a guinea-pig that had
become epileptic from section of the sciatic nerve, and on gently ruffling
the hair at the back of one ear an epileptic attack was induced. The por-
tion of skin, irritation of which causes the epileptic attack, Brown -Sequard
has called the epileptogenous zone, and it is important to notice that it is
slight and superficial irritation of it which provokes the attack ; severe
irritation, like pinching, may even arrest a commencing attack, and if the
skin is burned or cut it loses its epileptogenous character. The skin of the
area is, indeed, to a certain degree ancesthetic, and in the animals which after
a long time recover, as some of them do, the anaesthesia of the epilepto-
genous zone gradually diminishes, and disappears along with the epileptic
tendency.

Another noteworthy circumstance with respect to the epileptogenous

936

EPILEPSY.

zone is that it is always found on the same side as the injury of the nerve
or spinal cord, but on the opposite side to the injury when the crus cerebri
has been wounded.

Westphal found that a light tap on the head of a guinea-pig is followed
by an attack of general convulsions. The animal soon recovers and may
appear well for some weeks, but after a time an epileptogenous zone is
developed, irritation of which provokes epileptic attacks, and the attacks
also occur spontaneously.

■ Hitzig has induced artificial epilepsy by injury to the cortical centre of
the anterior extremity ; and, according to Fender, an epileptic attack may
be induced by passing an induction current of moderate strength through
the cortex of one of the hemispheres. In the case of a woman whose brain
was more or less exposed, in consequence of cancerous ulceration of the
skull, Dr. Bartholow applied an induction current directly to the brain in
the region of the postero-parietal lobe — a proceeding which was followed by
convulsions of the opposite extremities.

Various experiments have been undertaken with the view of determining
the starting point of the general convulsions in epilepsy. The most suc-
cessful of this kind are those of Nothnagel, who proved that general con-
vulsions may be induced by irritation of a circumscribed spot on the floor
of the fourth ventricle, a spot which he calls the " convulsion centre."

§ 959. Morbid Physiology. — la idiopathic epilepsy no con-
stant anatomical lesion has been discovered, and it may
therefore be inferred that the lesion is a molecular one. The
question we have now to determine is whether the lesion is a
diffused one, affecting the whole nervous system, or a local one,
affecting only a definite region. In anaemia, for instance, there
is an excess of irritability of the whole nervous system, rendering
the patients subject to mental irritability, and less able to with-
stand any external causes of irritation. In such cases there is
excess of the irritability of the nervous system generally, but
something more than this is necessary to constitute epilepsy. It is
not sufficient that there should be a diffused excess of irritability;
the nature of the epileptic paroxysm and its periodic recurrence
point to the existence of a rupture of the natural balance
between the degree of irritability of different parts of the
nervous system, or, in other words, to a state in which some
part or parts of the nervous system develop increased irritability,
while the remaining portions retain the normal amount. It now
becomes necessary to determine more minutely the part of the
nervous system where the molecular lesion is situated. Different
regions of the nervous system may be affected in different cases.

EPILEPSY. 937

-:/ In some cases there is an epileptogenous zone, in others it is
j absent ; and in some again the sciatic nerve has been injured,
If and probably remains in a permanently irritable condition.
Injury to the spinal cord, the tissues of which may be presumed
to remain in an abnormal state of irritability, may also be a
source of epilepsy. But the more or less uniform character of
the epileptic paroxysm shows that, no matter what other
regions may be affected, a molecular disturbance must take
place in some one definite region of the nervous system in
every attack. Is it possible to localise this region ? The most
important problems in the pathology of epilepsy cluster around
the answer to this question.

The epileptic paroxysm consists of loss of consciousness and
convulsions, and our problem now is to determine what are the
localities disturbance of which will produce these functional
disturbances. Nothnagel has shown that there is a certain
limited spot in the floor of the fourth ventricle by irritation
of which it is possible to throw the whole of the voluntary
muscles into tonic and clonic spasms, and he has consequently
named it the " convulsion centre." He believes that irritation
of this centre is a necessary concomitant of every epileptic
paroxysm. But although irritation of this centre might
account for the convulsions it would not account for the loss
of consciousness. But the vaso-motor centre which is situated
between the upper part of the medulla oblongata and the pons,
close to the convulsion centre, is also supposed to be implicated
in the molecular disturbance during the paroxysm. Irritation
of the vaso-motor centre causes contraction of all the arteries of
the body, includiug the arteries of the brain, and it is to the
anaemia caused by the contraction of the vessels of the brain
that the loss of consciousness is, according to this theory, to be
attributed. Combined excitation of the vaso-motor and con-
vulsion centres is then, according to Nothnagel's theory, the
necessary pathological condition of the epileptic paroxysm ;
excitation of the former centre induces contraction of the vessels
of the brain and the consequent anaemia causes loss of con-
sciousness ; while excitation of the latter centre induces the
muscular contractions. The muscles of the face and neck are
first attacked by convulsions, and by their contractions the

938 EPILEPSY.

large veins of the neck are pressed upon and the return of\
blood from the brain is thus prevented, so that the anaemia of!
the first moments is succeeded by an intense venous hyper-
emia which augments the irritability of the convulsion centre
and prolongs the convulsion and coma. Kussmaul and Tenner
have shown that when the brain is rapidly deprived of arterial
blood, either by bleeding, ligature, or compression of the four
great arteries going to the head, coma and general epileptic
twitchings are invariably produced. It must be remembered,
however, that they did not succeed in a single instance in
producing loss of consciousness merely by faradisation of the
cervical sympathetics. And if the local contraction of the main
arteries of the brain caused by faradisation of the cervical
sympathetics will not cause loss of consciousness or convulsions,
it is not probable that the contraction of the arteries of the
body generally caused by excitation of the vaso-motor centre
will cause these states, inasmuch as the general arterial tension
will be raised and the more powerful contractions of the heart
which will ensue will maintain the cerebral circulation. This
hypothesis also overlooks the fact that loss of consciousness is
the predominant feature of epilepsy, and not the convulsions.
Some cases of true epilepsy are characterised by slight tem-
porary loss of consciousness without any appreciable motor
disturbance, a state which differs widely from syncope caused
by anaemia of the brain, and is unlikely to be caused by vaso-
motor action.

Dr. Todd was the first to attribute epilepsy to an explosion
of nerve force ; but this theory has assumed definite shape in
the hands of Dr. Hugh lings- Jackson, who suggested that con-
vulsions of all kinds associated with loss of consciousness were
caused by discharging lesions of the cortex of the brain. This
hypothesis has received a considerable amount of experimental
verification. Hitzig was able to determine epileptic paroxysms
by various injuries to the cortex of the brain, and Ferrier
obtained a similar result by passing a faradic current of
moderate intensity through the cortex, the electrodes being
widely separated, so that a large portion of the cortex was
included in the circuit.

A survey of the anatomical changes found in epilepsy has

EPILEPSY.

939

already shown us that, of all the manifold lesions observed,
disease of the cortex of the brain predominates. Other facts
tend to the same conclusion, such as that where epilepsy is
associated with imbecility, structural changes are often found on
the surface of the brain, and that general paralysis of the insane,
a disease in which structural changes are generally found in the
cortex of the prsefrontal region, is very often accompanied by
epilepsy.

According to Todd's theory, as elaborated by Hughlings-
Jackson, the convulsions of epilepsy are due to a large discharge
of nervous energy from the cortex of the brain along the cen-
trifugal nerve paths, and the loss of consciousness is caused by
the temporary exhaustion which succeeds to excessive nervous
discharge. The temporary paralysis of the convulsed limbs
observed after epileptiform seizures is also, according to this
theory, due to temporary exhaustion of nerve force following the ,
excessive discharge. But, if this be so, it may be asked, why are
general convulsions not followed by temporary paralysis? The
reply is that they are so followed. After an epileptic attack
there is complete muscular relaxation, but as the patient is at
the same time unconscious the degree of paralysis present can-
not be estimated. Even after consciousness is regained, general
muscular feebleness often remains for a time, which, although
not called paralysis, is really paralytic in nature (Hughlings-
Jackson). The unseemly and apparently immoral actions per-
formed, and the atrocious crimes often committed by patients
after minor attacks of epilepsy, may be explained on the sup-
position that the inhibitory influence of the highest centres is
temporarily suspended, thus permitting the centres which pre-
side over automatic actions and animal instincts to spring into
greater activity (Anstie). Irritation of the peripheral nerves or
of the floor of the fourth ventricle may determine the nervous
discharge from the cortex which constitutes epilepsy, as well as
direct irritation of the cortex itself.

Epileptiform seizures are always caused by a coarse lesion
situated in or near the area of distribution of the Sylvian artery
to the cortex, and it may, therefore, be inferred that when
attacks of idiopathic epilepsy are ushered in by a motor aura,
the molecular disturbance begins in some part of the motor -

940

EPILEPSY.

area of the cortex. When, on the other hand, the aura consists
of sensory disturbances, the discharge probably begins in the
area of the cortex supplied by the posterior cerebral artery.
When the aura consists of emotional states of fear and anger, it
is probable that the discharge also begins in the area of the
posterior cerebral artery, inasmuch as these emotions are pro-
bably often preceded by hallucinations of the senses, or at least
by some disturbance of the sensory apparatus. When the aura
consists of " dreamy " states, the discharge probably begins
in the region of the cortex supplied by the anterior cerebral
artery, and the cases in which unconsciousness supervenes
suddenly without being preceded by an aura probably also take
origin in a molecular disturbance of this area.

§ 960. Diagnosis. — Epilepsy is often simulated by impostors,
and sometimes so successfully that it is very difficult to detect
the fraud. The physician must take into consideration all
the circumstances of the case, but the symptoms which can
hardly be simulated are pallor of the face, and dilatation
and insensibility to • light of the pupil at the beginning of
the seizure. The slighter attacks of epilepsy are frequently
described by the patient as slight "fainting fits," and it is
somewhat difficult to distinguish the two affections. If the
attacks recur at regular intervals in the absence of any distur-
bance of the circulation to account for them, they must be
regarded as. epilepsy. The diagnosis is rendered clearer if, in
addition, an epigastric or other sensory aura be described, or
if the attack be attended by convulsion, twitching, or impaired
consciousness.

Hysteria in its ordinary form may be readily distinguished
from epilepsy by the history of the case before the attack, and
by the absence of the distortion of the features, dilatation and
insensibility of the pupils. Hysterical attacks are unaccom-
panied by complete loss of consciousness, the tongue is not
bitten, there is no marked asphyxia, and the patient, although
exhausted, does not pass into stupor before recovery. The
diagnosis between hysteria and hystero- epilepsy is readily
made when the patient is seen during an attack. Attacks
of the latter are always preceded by an aura, and there is com-

EPILEPSY.

941

plete, although it may be transitory, loss of consciousness. The
diagnosis between epilepsy and eclampsia will be considered

> when the latter disease is under consideration.

When organic diseases of the nervous system are attended

i with convulsions, they present other symptoms over and above
the fits by means of which they may be distinguished from
epilepsy. The most usual intracranial diseases associated with
convulsions are tumour, chronic softening, and chronic menin-
gitis; but in all these diseases some characteristic symptoms,
such as optic neuritis, paralysis, or persistent psychical distur-

1 bances, are present, which render the diagnosis between them

i and genuine epilepsy comparatively easy.

§ 961. Prognosis. — The prognosis in genuine epilepsy is
unfavourable as regards complete and permanent recovery,
especially if the disease has been established for some time. It
ought, however, to be remembered that a few cases are com-
pletely curable, and that, even when the disease has been of
long standing, a considerable improvement may take place. In
a considerable number of cases, probably the majority, no treat-
ment has hitherto produced any beneficial effect.

The following circumstances influence the prognosis. Here-
ditary taint gives an unfavourable indication ; but an early
commencement of the disease is favourable. Herpin thinks
that when epilepsy begins after the fiftieth year the prospects
are still better. The longer the disease has lasted, the greater
the improbability of recovery. Reynolds thinks that those cases
in which the intervals between the attacks are much prolonged
are less amenable to treatment than are those which exhibit a
more rapid recurrence, while Herpin thinks that the prognosis
becomes more unfavourable in proportion to the number of
seizures suffered in a given time. When the epileptic attacks
are caused by peripheral irritation the prognosis is favourable,
unless the disease has already been long established, while of
course on the other hand central disease renders the prognosis
unfavourable. Mental failure is of evil omen, since it indicates
in all probability that a profound and permanent molecular
change has taken place in the grey matter of the cortex. The
danger to life is remote, since it is rare for an epileptic to die
in one of the attacks.

940

EPILEPSY.

§ 960. Diagnosis. — Epilepsy is often simulated by impostors,
and sometimes so successfully that it is very difficult to detect
the fraud. The physician must take into consideration all
the circumstances of the case, but the symptoms which can
hardly be simulated are pallor of the face, and dilatation
and insensibility to ■ light of the pupil at the beginning of
the seizure. The slighter attacks of epilepsy are frequently
described by the patient as slight "fainting fits," and it is
somewhat difficult to distinguish the two affections. If the
attacks recur at regular intervals in the absence of any distur-
bance of the circulation to account for them, they must be
regarded as. epilepsy. The diagnosis is rendered clearer if, in
addition, an epigastric or other sensory aura be described, or
if the attack be attended by convulsion, twitching, or impaired
consciousness.

EPILEPSY.

941

plete, although it may be transitory, loss of consciousness. The
diagnosis between epilepsy and eclampsia will be considered
when the latter disease is under consideration.

When organic diseases of the nervous system are attended
with convulsions, they present other symptoms over and above
the fits by means of which they may be distinguished from
epilepsy. The most usual intracranial diseases associated with
convulsions are tumour, chronic softening, and chronic menin-
gitis; but in all these diseases some characteristic symptoms,
such as optic neuritis, paralysis, or persistent psychical distur-
bances, are present, which render the diagnosis between them
and genuine epilepsy comparatively easy.

The following circumstances influence the prognosis. Here-
ditary taint gives an unfavourable indication; but an early
commencement of the disease is favourable. Herpin thinks
that when epilepsy begins after the fiftieth year the prospects
are still better. The longer the disease has lasted, the greater
the improbability of recovery. Reynolds thinks that those cases
in which the intervals between the attacks are much prolonged
are less amenable to treatment than are those which exhibit a
more rapid recurrence, while Herpin thinks that the prognosis
becomes more unfavourable in proportion to the number of
seizures suffered in a given time. When the epileptic attacks
are caused by peripheral irritation the prognosis is favourable,
unless the disease has already been long established, while of
course on the other hand central disease renders the prognosis
unfavourable. Mental failure is of evil omen, since it indicates
in all probability that a profound and permanent molecular
change has taken place in the grey matter of the cortex. The
danger to life is remote, since it is rare for an epileptic to die
in one of the attacks.

942

EPILEPSY.

§ 962. Treatment. — The treatment of epilepsy must be
directed to the removal of the conditions upon which the
attacks depend, and to the mitigation or avoidance of the
seizures themselves.

When the attacks are maintained by a peripheral source of
irritation, this must, of course, be removed if possible. Epilepsy
has sometimes been known to disappear after the extirpation of
a cicatrix, the removal of a tumour pressing on a nerve, or the
opening of an abscess; and the same result has been obtained
by the removal of sources of irritation in the alimentary canal,
such as worms. When an aura constantly recurred in the
course of the same nerve, it was formerly the practice to
perform neurotomy, or to amputate a finger or even the arm.
No good results attended this practice, and it is now abandoned.
The practice of trephining was also extensively employed in
former times in every case which resisted medical treatment, and
this treatment may possibly be successfully used in a limited
number of cases of epilepsy from organic disease. It is scarcely
necessary to add that in epilepsy, as in all other chronic diseases,
the general health must be carefully attended to and the diet
regulated. Alcohol, tea, and coffee should be sparingly used as
articles of diet.

Excessive mental effort, emotional excitement, and worry
must be avoided ; but a moderate degree of intellectual work
may be useful, and a certain amount of bodily exercise, short
of fatigue, should be enjoined.

Some epileptics have been much improved by the treatment
adopted in hydropathic establishments. The application of ice
bags along the spine was strongly recommended by Chapman;
but Reynolds, who has given the treatment a fair trial, says
that he has found the results absolutely negative. Electricity
in its various forms has been employed in the treatment of
epilepsy, but with little success.

Counter-irritation was at one time extensively used, but the
prevailing opinion at present is that the practice is useless.
If the presence of an epileptogenous zone be ascertained, a
blister over the sensitive area may be attended with benefit.

Bromide of potassium has been found more generally useful
in the treatment of epilepsy than any other drug ; to do good

EPILEPSY.

943

it must be given in doses ranging from ten to forty grains
three times daily. The results of this treatment are that a few
cases have been completely cured ; in other cases the attacks
have been arrested for varying periods of months or years, but
have recurred on the drug being omitted, and ceased again on
its being readministered. In still other cases the attacks have
been diminished in severity, although not removed ; while in a
few cases the drug does not appear to exert any influence on
the disease. When large doses of bromide of potassium are
administered for some time, it is apt to produce an eruption of
acne, which soon subsides on the drug being discontinued ; or
the eruption may, according to Dr. Wilks, be prevented by
combining arsenic with the bromide. Chloral is sometimes a
useful adjunct to the bromide of potassium. Next to the
bromide of potassium the salts of zinc, especially the oxide,
have proved the most generally useful in the treatment of the
disease. This remedy appears to be more efficient with patients
under twenty years of age than in those of maturer age. The
oxide may be given in doses ranging from two to five grains
three times daily. The sulphate has also been employed in
large doses with frequent success. The sulphate may be given
at first in doses of three grains, and progressively increased to
scruple doses three times a day. The bromide of zinc has been
administered in gradually increasing doses up to a scruple three
times a day.

The oxide of zinc may be combined with the extract of bella-
donna or hyoscyamus, or with the powdered root of valerian.

The ammonio- sulphate of copper was at one time much used
in the treatment of epilepsy, but has lately fallen into disuse.

The nitrate of silver was at one time much relied upon in the
treatment of epilepsy, but confidence in its curative power is
much shaken in the present day. The records of the older
authors, however, amply prove that beneficial results followed
its employment, and it may be worth while to give it a trial
when other methods of treatment have failed.

Belladonna has been long used as a remedy for epilepsy, and
recently its alkaloid, atropine, has been substituted for it. The
judgment formed by Reynolds is now pretty generally endorsed
by authors, namely, that by means of belladonna an amelioration

944

EPILEPSY.

is often obtained for various troublesome concomitant symptoms,
such as disturbed sleep, trembling, and nervous uneasiness.

Digitalis, either alone or in combination with bromide of
potassium, is useful in some cases, especially if there be signs of
cardiac failure.

Indian hemp has been found useful as an accessory in the
treatment of epilepsy, and by its means headache and restless-
ness have been relieved, but it does not appear even to have
appreciably mitigated the disease.

If there be a suspicion of syphilis being the cause of
epilepsy, iodide of potassium should of course be given.

The treatment of the attach should be directed to its preven-
tion, and this is only possible when it is preceded by a distinct
warning. When an " aura " is present, the attack may some-
times be arrested by cauterising or blistering the surface from
which the aura commences, or by applying pressure, as by a
tight ligature, between the starting point of the aura and the
trunk. Some patients are able to arrest the paroxysm by a
strong mental effort to perform a definite action.

When the aura consists of contraction of a definite group of
muscles, the attack may be arrested by forcible extension of
them. There are some grounds for believing that the paroxysm
may be sometimes arrested by a sudden impression on the
surface of the body. Inhalation of chloroform or of ammonia,
or a draught of some diffusible stimulant administered at the
moment of onset, may arrest an attack.

Dr. Crichton Browne was able to ward off several attacks by
causing the patients to inhale nitrite of* amyl when a fit
threatened. The well-known action of this agent, in paralysing
the vaso-motor nerves, supplies the rationale of the treatment.

When the attack is once established, it passes through its
regular phases without being influenced by treatment. Measures
must be adopted for preventing the patient injuring himself.
All tight bands about the throat must be loosened, and a piece
of indiarubber or wood should be passed between the teeth, to
prevent the tongue being bitten.

When the paroxysm is over, the patient ought to be placed
with the head and shoulders raised, and allowed to sleep without
interference.

ECLAMPSIA.

945

If the paroxysm be long continued, so that there is danger
of death supervening from congestion of the lungs, blood-letting
may relieve the circulation so much as to arrest the attack.
When the fits are violent, a careful trial may be made of the
inhalation of chloroform, which is so useful in the treatment of
eclampsia.

(II.) ECLAMPSIA.

§ 963. Definition. — Eclampsia is an acute affection arising
without structural lesion of the nervous system, and charac-
terised by partial or general convulsions, accompanied by a
more or less complete loss of consciousness.

§ 964. Etiology. — Age is a most important predisposing cause
of eclampsia. Convulsions are frequent during the first two
years of life, but become rare after the fifth and exceptional
after the seventh year of life.

The influence of hereditary predisposition in the production
of convulsions is shown by the fact that successive infants of
one family are liable to be attacked with convulsions in the
absence of any definite cause. Bouchut mentions an instance
of a family of ten persons, all of whom had convulsions in
infancy. One of these married and had ten children, and nine
of them suffered from convulsions. The children of parents
who manifest evidences of a neuropathic constitution, as hys-
teria, neuralgia, or epilepsy, are more liable to be attacked by
convulsions than the children of the healthy.

All debilitating causes, as insufficient food, profuse diarrhoea,
copious haemorrhages, malarial cachexia, and various diseases,
greatly increase the tendency to convulsions. Amongst the
debilitating diseases which predispose to convulsions rickets
holds a prominent place. Out of 65 infants attacked with
convulsions, Dr. Gee found that no less than 56 of the number
were rachitic. Convulsions occur more frequently in children
during hot than cold weather, and some authors assert that
they are more frequent in female than in male infants, but the
influence of sex is not well ascertained.

Eclampsia has been divided into several varieties according
to the exciting cause of the convulsions. These are : (1), Idio-

946

ECLAMPSIA.

pathic convulsions ; (2), Reflex convulsions ; (3), Convulsions
of fever ; (4), Convulsions^of asphyxia ; (5), Ursemic convulsions ;
(6), Puerperal convulsions ; (7), Toxic convulsions.

(1) In idiopathic convulsions the exciting is quite subordi-
nate to the predisposing cause. Some children are so pre-
disposed to convulsions that the slightest exciting cause, such
as fear, anger, or a slight colic, may induce a convulsion, while
at other times an attack supervenes in the entire absence of
any appreciable cause.

(2) Reflex convulsions are occasioned by irritation of the
extremities of the peripheral nerves. The nature and situation
of the external irritation varies indefinitely. Amongst the most
usual causes of irritation pricking by pins, wounds and burns
of the surface of the body, retention of urine, the presence of a
calculus in the kidney, foreign bodies in the external auditory
meatus, and irritation of the digestive canal from the presence
of worms or undigested food and of the gums during painful
dentition may be mentioned.

(3) Febrile convulsions manifest themselves at the outset of
acute diseases, more particularly in lobar pneumonia, the erup-
tive fevers, and intermittent fever.

This form of convulsion appears to correspond to the rigor
which ushers in most acute febrile diseases in the adult ; and
if not caused, it is at least accompanied by rapid elevation of
temperature. It must not be confounded with the convulsions
which supervene in the course of febrile diseases, since the
latter are usually symptomatic of cerebral hyperemia, or of
some form of meningitis.

(4) Convulsions due to asphyxia occur in the course of
diseases of the respiratory organs ; they are frequently observed
during severe attacks of whooping cough, and may appear as
. terminal phenomena in most of the diseases of infancy.

(5) Urwmic convulsions in children generally result from
scarlatinal nephritis, but they have been occasionally observed
immediately after birth. These convulsions are also observed
in other forms of both acute and chronic nephritis.

(6) Puerperal eclampsia is, as a rule, merely a form of
uraemic convulsions, although some cases are probably caused
by reflex irritation through the uterine nerves or the sacral
plexus.

ECLAMPSIA.

947

(7) Toxic convulsions might be held to include uremic
convulsions, inasmuch as the latter, according to some patho-
logists, result from the accumulation of urea in the blood, and
its conversion into carbonate of ammonia. This h}'pothesis is,
however, doubtful, and it is therefore better to place uremic
convulsions in a separate category.

Certain metallic and organic poisons and irrespirable gases
give rise to attacks of convulsions. Amongst these agents the
most usual are prussic acid, nicotine, picrotoxine, cenanthe cro-
cata, carbonic oxide, and carburetted hydrogen.

§ 965. Symptoms. — An attack of eclampsia eannot be dis-
tinguished from a true epileptic seizure, and it is therefore
unnecessary to give a minute description of it. Infantile con-
vulsions have been divided into internal and external, the
muscles of the glottis and the respiratory muscles being chiefly
affected by spasm in the former and the muscles of external
relation in the latter.

The symptoms caused by spasm of the glottis have already
been described (§ 279), and we shall consequently limit our
further remarks to the external convulsions of children. An
attack of eclampsia may occur either with or without pre-
monitory symptoms; the invasion without prodromata being,
according to Rilliet and Barthez, the more common.

The premonitory symptoms, when present, usually consist of
sleeplessness, and restlessness or drowsiness for a day or two
before the attack ; while immediately before it the pulse is
often hard and wiry, the countenance assumes a frightened
expression, or the child starts up frightened from a fitful and
uneasy sleep. The convulsion usually begins by conjugate
deviation of the eyes, and slight jerking contractions of the
muscles of the angles of the mouth. The natural look of the
infant is now exchanged for a fixed stare, followed soon after-
wards by an upward rotation of the eyeballs, the latter being in
its turn followed by a fixed stare and that again by an upward
rotation of the globes. The eyeballs are often rotated to the
right or left as well as upwards, and the two are generally
moved unequally, so that a considerable degree of strabismus
may occur. The pupils are sometimes dilated, sometimes con-

948

ECLAMPSIA.

tracted, and when they are completely concealed by the superior
lids, the whites of the eyes being alone visible, the countenance
assumes a frightful and characteristic aspect.

Clonic spasms of the facial muscles produce a series of
grimaces and contortions, in which the labial commissures are
drawn outwards, and at each successive jerk a peculiar sucking
noise is made by the passage of air through the mouth, the
lips being covered by a frothy, and often slightly sanguinolent
mucus. The superior lip is sometimes drawn upwards, so as to
expose the teeth, and the countenance then assumes an almost
savage ^expression. The inferior jaw is sometimes agitated by
clonic spasms, while at other times there is trismus, interrupted
from time to- time by grinding of the teeth. The head is usually
strongly retracted, and sometimes rotated to one side. The
thumb is flexed into the palm, and the fingers are flexed over the
thumb ; the forearm is bent upon the arm and is constantly
agitated by slight movements of semiflexion and semiextension ;
the hand is alternately pronated and supinated ; and the seg-
ments of the superior extremities are contorted into every
imaginable shape. The inferior extremities are affected, in a
similar manner, although to a less degree than the superior
The muscles of the trunk occasionally participate in the clonic
convulsions, but as a rule the trunk is maintained rigid by tonic
contraction of its muscles. The contraction of the muscles of
one-half the body may predominate over those of the opposite
side, and then the child is arched laterally in such a way that
he may be projected out of bed by the convulsion. The
spasmodic contraction of the diaphragm and of the muscles
of the larynx produce a peculiar and characteristic noise when
air is drawn into the chest during inspiration. Involuntary
evacuations may occasionally take place during convulsions.
Deglutition is rarely impossible, although attempts to get the
infant to swallow during the convulsion are attended with
danger.

There is complete loss of consciousness during the attack, but
reflex excitability is partially retained. When the convulsion
is prolonged the face becomes of a violet colour and bathed in
perspiration ; the head is hot and the extremities cold ; the skin
is moist ; the pulse is frequent and difficult to count, owing to

ECLAMPSIA.

949

jerking of the tendons; and the respirations are accelerated,
but stertorous only in aggravated cases.

The ocular muscles and those of facial expression are usually
the first to be affected with clonic spasm, and then the muscles
of the fWers and forearm. In the more severe convulsions the
muscles of the shoulders are affected, but the spasms do not
implicate the muscles of the back and lower extremities except
in very aggravated cases. The great tonic contractions which
form the first stage of the epileptic attack frequently fail
altogether in eclampsia.

§ 966. Course, Duration, and Terminations. — The duration
of an attack of eclampsia varies considerably according to
circumstances. The convulsion may sometimes cease in a few
minutes, while at other times they recur for hours or days,
with only short intervals of calm.

The terminal convulsions of asphyxia are generally partial,
incomplete, and alternate with coma. The initial convulsions
of fever are intense and generalised, but are usually limited to
a single attack. Urcemic convulsions are characterised by their
violence, the frequent repetition of the paroxysm, and the pro-
found coma which alternates with or succeeds the latter. After
violent and prolonged convulsions ecchymoses of the skin,
especially over the face and eyelids, and acute pains of the
affected limbs, are frequently observed. Fractures of long
bones, dislocations, and ruptures of tendons have been rarely
recorded.

An attack of convulsions is frequently followed by complete
and rapid re-establishment of health, but in other cases recovery
takes place slowly. When the convulsion is due to a meningeal
hemorrhage or some other organic lesion of the brain, it
generally assumes a unilateral character, and is followed by
paralysis with contractures, choreiform movements, aphasia, or
idiocy. Essential convulsions sometimes end in death, which
may result after a single violent seizure, or after a series of
them occurring in rapid succession. Death is usually produced
by asphyxia, either occurring suddenly from spasm of the glottis,
or more slowly from coma:

950

ECLAMPSIA.

967. Diagnosis. — In any particular case of eclampsia it is
difficult to decide whether or not the case is one of essential
convulsions, epilepsy, or convulsion symptomatic of organic
lesion of the brain. The chief points which ought to he
attended to in order to arrive at a probable diagnosis are the
age of the patient, the state of the temperature and urine, the
character of the convulsions, and the previous health during
the intervals between the attacks.

Eclampsia is most frequently observed during the first years
of life, and is rare beyond that age, except as the result of
definite causes; such as albuminuria, and the invasion of an
eruptive fever or other acute disease. When the attacks are
repeated beyond two years of age, at irregular intervals of
months or years, epilepsy may be inferred, unless symptoms
pointing to a focal lesion of the brain are present. The state of
the temperature is the best guide in deciding between essential
convulsions and the initial convulsions of acute diseases, the
thermometer being nearly normal in the former and rising to
between 103° F. and 104° F. in the latter. The urine should
always be examined for albumen in cases of convulsions, in
order to determine whether or not the attack depends upon the ]
presence of Bright's disease.

If the convulsions are unilateral in character, or consist of
local spasms without loss of consciousness, they are likely to be I
due to organic disease of the brain or its membranes. Such ]
cases are generally followed by some degree of paralysis with
subsequent contracture. If the convulsion be preceded by a
well-marked aura, if its onset be marked by a sudden pallor and
a piercing cry, and if the first stage be attended by well-marked
tonic contractions, the mouth covered by froth, and the tongue
bitten, the attack is one of true epilepsy. In epilepsy the
return to health after the attack is rapid and perfect, and in
the intervals between the severer paroxysms the patient may
suffer from attacks of petit mal.

§ 968. Prognosis. — The prognosis of eclampsia depends upon
the character of the attacks, and the causes by which they are
produced. *

Frequent repetition of the convulsions, the presence of

ECLAMPSIA.

951

stertor, cyanosis, or spasm of the glottis, and a small uncountable
pulse afford a grave prognosis, whatever may be the cause of
the attack.

Essential convulsions are only grave as indicating a neurotic
disposition, and, when the attacks recur frequently, there is
danger lest they develop into confirmed epilepsy.

Convulsions occurring in cachectic infants and in those
exhausted by profuse diarrhoea are almost always the precursors
of death.

The initial convulsions of fever derive all their significance
from the disease with which they are associated. The convul-
sions which occur in the course of fevers always justify a grave
prognosis.

The convulsions of asphyxia are almost always fatal.
Ursemic convulsions terminate more frequently in recovery
than in death. If the infant survive the first 24 or 36 hours
he may be regarded as safe.

§ 969. Treatment. — The most obvious indication of treatment
is to remove the cause of the attack, and in reflex convulsion the
removal of the cause is often successful. If the gum be tightly
stretched over a tooth it may be scarified, but the tooth should
be near the surface and the gums hot and inflamed before this
practice is adopted. If the bowels be constipated, and especially
if they be tympanitic, an injection of warm water is useful. I
have often seen the convulsions cease immediately on the
bowels being opened after an enema of warm water. If the
convulsions are the result of a smart attack of diarrhoea, and
especially if the fontanelles are depressed, a small starch enema,
with half a teaspoonful of brandy and from 2 to 5 minims of
tincture of opium, may be administered. If there be grounds
for believing that the convulsions are caused by the presence of
worms, an anthelmintic, and if from the presence of undigested
food, a smart purgative should be administered. Predisposing
causes, such as anaemia, insufficient nourishment, and rickets,
must be removed by appropriate treatment.

During the convulsion plenty of fresh air should be admitted
into the room, and all articles of clothing should be removed
from the neck and chest of the infant. A warm bath is often

952

ECLAMPSIA.

useful, but when there is hyperpyrexia, the cold bath should be
used in preference. Compression of the carotids and bleeding
have been recommended as means of arresting the attack, but
the former is ineffectual and the latter only rarely applicable.
The inhalation of chloroform is by far the best method of
treating attacks of eclampsia. This treatment is applicable to
all cases of essential and uraemic convulsions, and is only contra-
indicated in cases where there is a considerable elevation of
temperature, and in which there is a cyanotic tint of counten-
ance and stertorous breathing. No harm results from keeping
the child many hours, if necessary, under the full influence of
chloroform. When once the infant is able to swallow, bromide
of potassium or chloral hydrate may be given either separately
or combined. A grain of the bromide of potassium for each year
of age may be given every four hours, and its efficacy appears
to be increased by adding an equal quantity of chloral to each
dose. If chloral be given alone, a full dose — three grains to a
child one year of age — must be administered.

953

CHAPTER VII.

TOXIC, AND FEBRILE AND POST-FEBRILE NERVOUS

DISORDERS.

(I.) ALCOHOLIC NERVOUS DISEASES.

The subject of acute poisoning by alcohol belongs rather to the
province of the toxicologist than to that of the neurologist?
and will be passed over here. Besides a large number of
nervous disorders produced by the ingestion of alcohol need
not be discussed, inasmuch as alcohol is only an indirect cause
of them. Amongst these may be mentioned apoplectic attacks
caused by degeneration of the vascular system, and chronic
dementia caused by hsematoma of the dura mater.

§ 970. Delirium Tremens. — The symptoms known under the
name of delirium tremens occur in persons after prolonged
indulgence in alcoholic excess, or as the result of a single
debauch. The characteristic features of the affection are pre-
ceded by restlessness, tremor more marked in the hands and in
the morning, and wakefulness at night, while a severe attack
of vomiting is frequent in the morning. The patient is
irritable, suspicious, quarrelsome, and agitated, and the little
sleep obtained is broken by disagreeable dreams. The appetite
fails completely, so that little or no food is taken for several days ;
the breath has a characteristic foul odour ; the tongue is tremu-
lous on protrusion, red and glazed, or more commonly covered
with a thick, creamy fur; the skin is bathed in profuse per-
spiration ; the face is generally flushed, but occasionally pale ;
the pupils are usually dilated, and the conjunctivae injected ;

954

TOXIC, AND FEBEILE AND

the temperature is slightly elevated ; and the pulse is usually
large, soft, and dicrotous.

Tremors are always present, and are only an aggravation of ]
a slighter degree of the same which had existed for months j
previously (Anstie). Hallucinations of special sense now make
their appearance, those of sight being most common. The
patient sees, especially at night when about to go to sleep,
sparks of fire and floating bodies; but soon distinct objects,
especially those productive of disgust or terror, are seen in
broad daylight. The patient sees himself surrounded by insects,
snakes, rats, and monsters of variable shape, and armed men
pursuing him with threatening gestures. He talks incessantly 1
in an incoherent and rambling manner, and looks suspiciously
under the bed, and in every corner of the room, to satisfy himself
that none of the imaginary beings by which he fancies himself 1
surrounded are lodging there. His actions, indeed, appear to I
be largely determined by the nature of his hallucinations. I
At times he will busy himself in endeavouring to catch the
insects which crawl over his bed, or he will get up and search 1
everywhere for something which has disappeared in a corner
of the room; while at other times he will dodge about in order 1
to avert a threatened blow, or endeavour to run or hide in I
abject terror behind an article of furniture, 'in order to escape I
from some pursuing foe. The prevailing mental character I
during the attack is one of terror and cowardice, although the
patient may occasionally turn upon his attendant in the belief
that the latter is plotting against him, or is about to inflict upon
him some bodily injury.

As a rule, the patient is very tractable to his medical atten- 1
dant, and gives ready obedience to his commands during Lis
visit; but he is not unfrequently violent towards his friends,
and especially to his wife.

At the end of three or four days, or at most a week from the
commencement, the patient, when the attack is about to termi-
nate favourably, falls into a quiet sleep and awakes refreshed
and calm. Some cases, especially if the patient have previously
suffered from repeated attacks, terminate fatally by coma or
asthenia. In fatal cases the temperature rises to 103° F. or
104° F. ; the pulse is extremely rapid and feeble ; the tremors

POST-FEBRILE NERVOUS DISORDERS.

955

become general, and associated with subsultus tendinum ;
epileptic convulsions, followed by coma, may supervene and
prove fatal, or bed-sores appear and the patient dies exhausted.
Death is not unfrequently caused by an intercurrent attack of
pneumonia, or some other acute disease.

§ 971. Alcoholic Paraplegia. — Dr. Wilks has drawn atten-
tion to a condition of partial paraplegia associated with
ansesthesia, or pains in the limbs, which is liable to occur in
persons, especially women, who have indulged in alcoholic
excess. Chronic pains in the limbs may be complained of long
before the symptoms of paralysis appear, or there may be a
certain degree of motor inco-ordination. The immoderate use
of chloral hydrate may occasion chronic pains in the limbs
(Anstie), and a distressing case came under my own observation
in which the same symptoms were caused by the prolonged
and intemperate use of chlorodyne. The pains in the limbs
disappeared rapidly when the drug was discontinued.

§ 972. Treatment. — The patient should be placed in a dark
room, and the utmost quiet enjoined. He should be constantly
watched by one or two trustworthy attendants, and the use of
mechanical means to restrain his movements should if possible
be avoided. Nutriment should be frequently administered in
the form of beef-tea, soups, milk, and eggs. A full dose of
chloral, either alone or combined with bromide of potassium,
may be given at once, and smaller doses repeated at stated
intervals. If sleep be not procured on the second night, a full
dose of opium or morphia may be administered on the third and
subsequent evenings at the usual bed time. According to my
experience, opium acts better when given after chloral has been
used than at the outbreak of the symptoms. If symptoms of
asthenia be present, it may be necessary to give a certain amount
of the alcoholic stimulus to which the patient has been accus-
tomed ; but, as a rule, alcohol should be wholly forbidden.

(EE.) SATURNINE NERVOUS DISEASES.
§ 973. It is impossible to enter into a full discussion of all
the deleterious effects produced by the prolonged introduction

956

TOXIC, AND FEBRILE AND

of small quantities of lead into the system ; it must suffice to
mention a few of the leading nervous affections caused by this
poison.

Chronic lead-poisoning at one time frequently resulted from
the use of drinking-water stored in leaden cisterns or conveyed
through leaden pipes, but this seldom happens now. Lead-
poisoning is most frequently met with amongst painters, and
workmen pursuing various trades in which lead is used. The
poison may enter the system by being swallowed along with
the saliva, through the lungs by fine particles of the carbonate
being diffused in the air, or through the mucous membrane of
the nose by the adulteration of snuff with red lead (Winter).
Some individuals are much more susceptible to the action of
lead than others ; and, as was first suggested by Dr. Garrod,
those who inherit a predisposition to gout appear to be parti-
cularly liable to become poisoned by lead.

§ 974. Symptoms. — One of the most valuable indications of
the presence of lead in the system is afforded by the formation
of a blue line along the edges of the gums immediately adjoin-
ing the teeth. The blue line, although situated in the sub-
stance of the gums, appears to be produced by the formation of
a sulphide, the latter being formed by sulphuretted hydrogen
emitted from decomposing matters on the teeth.

Sensory Disturbance. — Phenomena of sensory irritation may
be manifested in the form of hyperesthesia of the superficial
and neuralgia of the deeper parts. Rosenthal states that
cutaneous hyperesthesia often accompanies paroxysms of pain,
and that it may alternate with anaesthesia. Arthralgia, probably
of a neuralgic character, is a prominent symptom of chronic
lead -poisoning. The pains in the joints occur in paroxysms,
and may appear in the upper or lower extremities, or in the
jaws. Lead colic, probably also of neuralgic origin, is one of
the most frequent and important symptoms. The pains are
chiefly referred to the umbilical region; they are liable to
paroxysmal exacerbations of great severity, although a consi-
derable degree of uneasiness or pain remains during the inter-
vals (§ 334).

Cutaneous ancesthesia is, however, much more commonly

POST-FEBRILE NERVOUS DISORDERS.

957

observed than hyperesthesia, and is, accordiDg to Bean, one of
the most characteristic symptoms of chronic lead-poisoning. It
is variable in its distribution, and may be complete or incom-
plete. Tactile anesthesia is often associated with motor para-
lysis, colic, or arthralgia. It is most frequently situated on the
skin of the backs of the hands and forearms, the external
surface of the calves, and the abdomen and chest, the skin over
the epigastrium, however, remaining always free (Bean). Loss
of feeling sometimes extends to the veil of the palate and uvula.
In other cases analgesia, thermo- anaesthesia, and loss of the
sensibility to tickling may be present, while tactile sensibility
remains unimpaired. The electric sensibility is often lost
(Raymond). The anaesthesia is often transitory, and, according
to Renaut, is sometimes caused by cutaneous anaemia, and may
be made to disappear by rubefaciants and profuse diaphoresis.

Deafness, according to Tanquerel, frequently follows an attack
of arthralgia, and diminution of taste on half the tongue, and
of smell in one nostril, has been observed. But the affections
of sight are more frequent and important than those of the
other special senses. These consist of transitory amblyopia
without ophthalmoscopic changes ; persistent amblyopia passing
on to amaurosis of both eyes and rarely of one only, attended
by atrophy of the optic nerve; amblyopia with double optic
neuritis; and amblyopia with albuminuric retinitis, in asso-
ciation with granular kidneys.

Motor Disturbances. — Motor are more commonly observed
than sensory disorders in lead -poisoning. Almost all the
muscles of the body may be affected, although certain groups
are attacked by preference. In partial paralysis the extensor
muscles of the forearm are more frequently affected than any
other group ; and consequently when the arms are held out
horizontally, with the hand in a state of pronation, the hand is
flexed at the wrist and cannot be extended, this condition being
technically called wrist-drop. The common extensors of the
ringers are first attacked, then the extensors of the index and
little fingers, and lastly, in succession, the extensor secundi
internodii pollicis, the extensors of the wrist, the extensor primi
internodii pollicis, and the extensor ossis metacarpi pollicis. The
supinator longus is spared until a comparatively late period of

958

TOXIC, AND FEBRILE AND

the disease, and is never affected, according to Remak, unless
the paralysis extend to the muscles of the upper arm. Some-
times the paralysis begins in the muscles of the upper arm, and
then the deltoid, biceps, coraco-brachialis, and supinator longus
are affected (the upper arm type of Remak) (§ 396). When the
muscles of the inferior extremities are paralysed, the anterior
muscles of the leg are generally the first to be affected ; but the
tibialis anticus is often spared under such circumstances. In
some cases all the muscles of both upper and lower extremities
are paralysed, and on rare occasions the muscles of the thorax
and back, those of phonation and speech, the intercostal muscles
and even the diaphragm have been affected. The sphincters
remain always unaffected in the paraplegic form. Paralysis
of the muscles of the glottis has been observed by Trousseau in
horses employed in red-lead factories. The paralysed muscles
undergo rapid atrophy, and lose their faradic contractility before
voluntary power is completely abolished, while the reaction of
degeneration appears in them at an early period.

The duration of lead paralysis is very variable ; it may last
for a period of weeks, months, or years, and both it and the
colic are liable to recur on renewed exposure to the cause.

Tremor is sometimes observed in lead-poisoning. It is often
limited to the upper extremities, and in aggravated cases
may extend so as to become general. Ataxic symptoms have
occasionally been observed, and are generally associated with
anaesthesia (Raymond). The patients in lead-poisoning suffer
from chronic dyspepsia and occasional attacks of jaundice ;
there is pronounced anaemia ; the arteries undergo various
degenerations ; and chronic Bright's disease, with its associated
effects on the mechanism of the circulation, is frequently
observed. It is scarcely necessary to add that the hemiplegia,
which is apt to occur from rupture of a vessel in the brain
under these circumstances, must be distinguished from true
lead paralysis. Women poisoned by lead suffer from menstrual
disorders and profound anaemia, and, if bearing children, they
frequently abort or have stillborn children ; idiocy, imbecility,
and epilepsy appear to be frequently observed amongst the
children of workers in lead. Impotency is said to occur in
advanced cases.

POST-FEBRILE NERVOUS DISORDERS.

959

Psychical Disturbances. — Before the outbreak of pronounced
cerebral symptoms the patient often suffers from headache,
vertigo, and drowsiness during the day and sleeplessness at
night; or there may be a state of agitation or complete apathy.
Cerebral disturbance sometimes assumes the form of quiet
delirium, accompanied by hallucinations of sight and hearing,
or on the other hand the delirium may be furious. But the
most common cerebral disturbance is convulsions. Sometimes
the loss of consciousness is not complete and the convulsions
may be partial, and limited to the muscles of the face and of
one or more limbs ; or they may be general and represented by
general trembling of the body. At other times the attack
assumes the form of eclampsia. These convulsions are gene-
rally followed by a prolonged stage of unconsciousness, with
stertorous breathing. The patient may be comatose after a first
attack, or after a succession of attacks quickly following each
other, and separated in some cases by intervals, during which
there is furious delirium. The patient generally recovers from
the first attack, but is liable to die in subsequent attacks.
Apoplectiform attacks may occur in the later stage of lead
paralysis, and are accompanied by paralysis of variable distri-
bution ; inasmuch as the patient often recovers motor power
quickly, these attacks cannot always be due to haemorrhage.

§ 975. Morbid Anatomy. — The morbid anatomy of lead-
poisoning has been studied by Lanceraux, Gombault and
Charcot, Westphal, Yulpian and Raymond, Erb, and many
others ; a careful paper on the subject, by Dr. S. Moritz, of
Manchester, has recently appeared in the " Journal of Anatomy
and Physiology." The microscopical changes observed in the
muscles are more or less similar to those already described
as occurring in progressive muscular atrophy (§ 414). The
most important changes observed have been in the intra-
muscular nerve fibres. The connective tissue is thickened, the
sheath of the primitive fibres is also thickened, the nuclei are
largely developed between them ; the axis-cylinders are some-
times distinctly visible, and at other times apparently disappear
(Moritz). The nerves, especially the musculo-spiral, have been
found altered in various degrees. Kussmaul and Meyer observed

960

TOXIC, AND' febrile and

sclerosis of the cceliac and upper cervical ganglia, with prolife-
ration of the connective tissue and deformity of the cells.
Vulpian observed vitreous degeneration and atrophy of the
ganglion cells of the anterior horns of the spinal cord, and a
similar observation has recently been made by Monakow.
Other observers have failed to detect any changes in the
spinal cord.

§ 976. Morbid Physiology. — There can be little doubt that,
as first suggested by Duchenne, the muscular disease in lead
paralysis is secondary to nervous changes. Some observers
believe that the disease begins in the intra-muscular nerve
fibres ; while others believe that the primary disease is situated
in the ganglion cells of the spinal cord. It is at least certain
that the muscles are affected in groups according as they are
associated in their actions, and not according to the distribution
of a particular nerve, such as the musculo-spiral. This mode of
invasion corresponds to what occurs in infantile paralysis and
progressive muscular atrophy, both of them spinal diseases,
and differs from that of paralysis of peripheral origin. These
considerations tend to show that the paralysis is probably of
spinal origin (Remak).

§ 977. Diagnosis and Prognosis — Saturnine neuroses are
generally easily recognised by the knowledge of the occupation
of the patient and the presence of a blue line on the gums.
The prognosis is at first favourable, but if colic have frequently
recurred, or paralysis have existed for a long time, and there be
much muscular wasting and cachexia, it becomes gloomy,
especially when the patient remains exposed to the poison.

§ 978. Treatment — Patients whose occupations expose them
to poisoning by lead should if possible seek other employment.
If this be not possible, the patient ought to be instructed to
observe great personal cleanliness, to wash the teeth daily, and
to rinse the mouth frequently with cold water. The use of
lemonade made with sulphuric acid is said to prevent lead-
poisoning by converting the carbonate of lead in the stomach
into an insoluble sulphate. The most important method used

POST-FEBRILE NERVOUS DISORDERS.

9GX

for procuring elimination of the poison appears to be the
internal administration of iodide of potassium, which is said to
convert the insoluble salts of lead deposited in the tissues into
a soluble double salt, capable of being removed. The warm
bath may be used as an adjunct in treatment; no benefit
appears to result from the addition of a soluble sulphide to
the water.

Lead colic must be treated on the same general principles as
other forms of colic with constipation (§ 336). The paralysed
muscles must be subjected to electrical treatment.

(III.) MERCURIALISM.

§ 979. Chronic mercurial poisoning may be due to the
absorption of mercurial preparations through the skin or mucous
membrane, or to the inhalation of the vapour of mercury. The
workmen engaged in quicksilver mines, and in trades in which
mercury is employed, such as that of gilders and looking-glass
makers, are liable to be affected by it.

§ 980. Symptoms. — The symptoms of chronic poisoning by
mercury often begin by slight numbness in the hands or feet>
and occasional neuralgic pains in certain joints, especially those
of the thumbs, elbows, feet, and knees. These sensory dis-
turbances are accompanied or soon followed by slight tremor,
which may for some time remain limited to the hands and arms.
The tremor, like that of disseminated sclerosis, only reveals itself
when the patient makes a voluntary effort ; but at an advanced
period of the disease it persists during repose, and may even
continue during sleep. The tremor gradually becomes more
pronounced, and extends to all parts of the muscular system.
The lower extremities tremble, especially at the knees, when
the patient stands or walks, and the patient is incapable of
performing any delicate manipulations, while in aggravated
cases he may be unable to carry a glass of water to his mouth,
as in disseminated sclerosis. The head and neck are main-
tained in a state of constant oscillatory movement when the
patient is in the erect posture ; the lips are tremulous ; the
utterance becomes broken and indistinct ; mastication is
J J J

962

TOXIC, AND FEBRILE AND

rendered difficult ; and even respiration becomes irregular and
laboured. The muscles of the eyeballs are said never to be
affected in mercurial poisoning, a fact of great importance in
distinguishing it from cerebro-spinal multiple sclerosis. Mus-
cular weakness is associated with the tremor, but distinct
paralysis does not occur, and there is no loss of sensation.
When the tremors attain great intensity, they persist during
repose, and render the patient restless and sleepless at night ;
the appetite fails ; the pulse, strong and slow at first, becomes
small, feeble, and frequent; while the patient becomes
emaciated, and assumes a cachectic appearance. In the
advanced stage of the disease serious cerebral symptoms super-
vene, such as constant headache, sleeplessness, loss of memory,
epilepsy, and coma.

§ 981. Treatment. — The patient must first of all be removed
from the influence of mercury, whatever be the way in which
he may be exposed to it. Iodide of potassium may be adminis-
tered with the view of converting the mercurial compound
already in the system into a soluble double salt. The affected
muscles are to be subjected to local treatment by galvanism.

i (IV.) SYPHILIS OF THE NERVOUS SYSTEM.

It has been abundantly shown in the course of this work that
syphilis may be a cause of almost all the organic diseases to
which the peripheral nerves, spinal cord, and brain are liable.
Syphilis, indeed, as Mr. Jonathan Hutchinson remarks, mimics
nearly all the organic diseases of the nervous system, as well
as those of other organs. Instead, therefore, of attempting
to write a detailed description of the numerous manifestations
of syphilis of the nervous system, it will suffice here if we
recapitulate briefly the anatomical alterations produced by the
action of the poison, bring into prominence the chief points
which must be attended to in recognising its presence, and
make a few remarks on treatment.

§ 982. Morbid Anatomy. — Syphilis of the nervous system
usually belongs to the later secondary or to the tertiary mani-

POST-FEBRILE NERVOUS DISORDERS.

9G3

testations of the disease, although in rare cases it may appear
in the first few months, or the year following infection. Syphi-
litic growths are sometimes developed in the nervous. system as
many as twenty or even thirty years after the primary infection.
Syphilis of the nervous system occurs with greatest frequency
in middle age. Affections of the nervous system not unfre-
quently occur during the first few years of life as the result of
the congenital disease.

Syphilitic lesions may be subdivided into : (1) Primary, or
those which are directly due to the action of syphilis ; and (2)
Secondary lesions, or those which are indirect and remote con-
sequences of it.

(1) Primary Syphilitic Lesions.

(a) Disease of the Bones and Periosteum. — Syphilitic exos-
toses, periostitis, osteitis, and caries of bones in the neighbour-
hood of nervous structures may implicate the latter in disease.
In this manner the peripheral nerves, as they pass through bony
channels, may be compressed or otherwise injured, the vertebral
canal may be narrowed and the spinal cord pressed upon, and
disease may be set up in the brain and its membranes by
syphilitic affections of the cranial bones.

(b) Formation of Gwmmata. — These have already been
described sufficiently for our purpose (§ 732). Gummata may
grow in the dura mater or pia mater. When a gumma grows
in the dura mater it develops between its two layers and
becomes encapsulated. When it is developed in the subarach-
noid space all the surrounding tissues, including the membranes,
the blood-vessels and nerves which traverse the space, and the
substance of the brain itself, are involved in the lesion. The
majority of cerebral gummata originate from the subarachnoid
space and pia mater, and grow towards the substance of the
brain. If the growth be situated on the convexity and lateral
surfaces of the hemispheres, the dura mater becomes so closely
adherent to the cortex that the former cannot be separated
without producing laceration of the latter. If it be situated
at the base of the brain the dura mater is less frequently
implicated, and the new growth then usually fills the spaces
around the chiasma and infundibulum, the interpeduncular

964

TOXIC, AND FEBRILE AND

space, and the spaces at the anterior and posterior borders of
the pons.

Gummata may also grow between the layers of the dura
mater or in the subarachnoid space in the vertebral canal.
The membranes become adherent to one another, and the
spinal cord is compressed and gradually destroyed at the level
of the growth.

The peripheral nerves may also be affected by a gumma
situated in their neighbourhood, or by the extension of the
infiltration into the substance of the nerve. The cranial nerves
are most commonly implicated at their points of origin and
before they become covered by a prolongation of the dura
mater.

(c) Syphilitic Infiltration. — The gummatous formation
sometimes forms a diffused infiltration in the substance of the
nervous tissues instead of forming circumscribed tumours. A
layer of gummatous tissue may in this manner be formed in the
pia mater on the surface of the convolutions of the brain.

(d) Syphilitic Sclerosis. — It is very probable that syphilitic
sclerosis is always preceded by an infiltration of the nervous
tissues by young cells similar to those observed in the gumma-
tous infiltrations. These cells become infiltrated around the
vessels and in the connective tissue septa and neuroglia, and
subsequently undergo partial organisation and cicatricial con-
traction. This process leads to the gradual destruction of the
nerve elements, just as occurs in ordinary chronic interstitial
inflammation of the brain, spinal cord, and peripheral nerves.

(e) Syphilitic Adhesion and Opacities. — When the cellular
infiltration occurs in the membranes and subsequently under-
goes organisation and retraction, a fibroid tissue is formed which
renders the portion affected dense, opaque, and inelastic; adhe-
sions form between the dura mater and pia mater, and between
the latter and the cortex of the brain or the surface of the
spinal cord. When the membranes over the base of the skull
and brain are affected, the cranial nerves may be surrounded
by cicatricial tissue. When the pia mater becomes indurated,
the calibre of the vessels supplied to the cortex of the brain is
liable to be diminished, and the nervous tissues are thus imper-
fectly supplied with nourishment.

POST-FEBRILE NERVOUS DISORDERS.

9G5

(f) Syphilitic Periarteritis and Endarterites. — It is probable
that the adventitia of the smaller arteries are implicated to a
greater or lesser extent in all the syphilitic processes which
have been described. Medium sized vessels may sometimes
be surrounded by concentric layers of gummatous tissue, which
ultimately compress them so as to cause their partial oblite-
ration. A gumma may, like any other tumour, during its
growth compress and obliterate both arteries and veins in its
neighbourhood. But the walls of the arteries are liable to be
affected in syphilis in a much more direct manner than by
any of the processes just described. The substance of the
walls may be infiltrated with cells, and these may undergo
partial organisation and cicatricial retraction, or form gumma-
tous masses. The infiltration may take place chiefly into the
adventitia of the vessel (periarteritis) or between the intima
and endothelium (endarteritis), but it is probable that in most
cases all the coats are more or less infiltrated. When the
cellular infiltration is diffused throughout all the coats of the
vessel and undergoes partial organisation and cicatricial re-
traction, the walls of the affected artery become inelastic and
brittle, while its calibre is uniformly reduced in size. When,
on the other hand, the infiltration is more limited, hard cir-
cumscribed spots may be found, which project from the ex-
ternal or internal surfaces of the vessel, distorting it in various
ways. It would appear that distinct gummata may form in
the walls of arteries, and either project from its external surface
or into its lumen, and in the latter case may either obstruct
the vessel completely or be washed off to be arrested as an
embolus in one of the smaller branches.

(2) Secondary Syphilitic Lesions..
The processes which result indirectly from syphilis are —
(a) Inflammation ; (b) Partial ischcemia, with necrotic
softening.

(a) Inflammation. — Syphilitic diseases of the bones of the
cranium may set up suppurative arachnitis (Wilks and Moxon),
but the purulent affection is of itself not a syphilitic lesion.
Syphilitic gummata act like foreign bodies on the surrounding
tissues, and consequently the membranes in its neighbourhood

966

TOXIC, AND FEBRILE AND

are usually thickened and adherent, while the cerebral tissue
surrounding it is maintained in a state of irritation. It is pro-
bable that the thickened layer by which a gumma is sometimes
encrusted is formed by partial organisation of inflammatory
products in the tissues immediately adjoining the syphilitic
tissue. Some cases reported appear to show that the presence
of a gumma on the surface of the brain may set up an acute
attack of meningo-encephalitis (Gamel). Acute ascending spinal
paralysis is liable to occur in syphilitic subjects, but in such
cases it is difficult to determine whether or not the lesion is a
primary or secondary result of the syphilitic poison.

When once a sclerosis of nervous tissues is set up by a
syphilitic lesion, it is probable that the process may assume a
progressive character independently of the syphilitic poison.

(&) Partial Ischcemia and Necrotic Softening. — When a
portion of the pia mater undergoes fibroid thickening in
syphilis, the calibre of the vessels which pass through it to
nourish the subjacent nervous tissues is reduced in size, and
these tissues suffer from anaemia. As the fibroid thickening
is probably always local in syphilis, the resulting anaemia is
also local. Much more important, however, is the anaemia
caused by obliteration of vessels. Obliteration of the vessels
may occur in several ways ; but occlusion of an artery by the
formation of a thrombus at a point where its inner surface
has been rendered uneven and its calibre diminished is by far
the most common and important of these. Obliteration of an
artery, in whatever way it may be brought about, is followed
by partial ischaemia, and local softening in those portions of the
brain where the terminal arteries do not anastomose with one
another.

Situation and Mode of Distribution of Syphilitic Lesions.
From what has already been said it will be seen that gummata
as a rule form in the membranes of the brain and spinal cord.
It follows that the cortex of the brain and the white columns
of the spinal cord are especially liable to be affected by gum-
mata. The favourite situations of gummata in the brain are
the base and cortex of the convexity in the region of distri-
bution of the middle and anterior cerebral arteries.

Syphilitic thrombosis, like every other form of obstruction

POST-FEBRILE NERVOUS DISORDERS.

9G7

of arteries, assumes greater importance when it occurs in the
arteries of the brain than in those of other parts of the nervous
system. The middle cerebral artery and its branches are
particularly liable to become occluded in syphilis, hence the
frequency with which hemiplegia with or without aphasia
occurs in syphilitic subjects.

Gummatous growth, whether it form a circumscribed tumour
or be infiltrated, is usually more or less localised, and con-
sequently gives rise to the symptoms characteristic of focal
diseases of the brain.

Syphilitic lesions are very liable to be multiple, or, in other
words, to appear at different parts of the nervous system at the
same time, so that the symptoms produced are such as those
resulting from more than one focus of disease. When the
lesions are bilateral they are seldom symmetrically placed, they
often appear at different times, and frequently differ in kind.
A syphilitic lesion compressing a cranial nerve on one side may
be associated with a gumma of the cortex of the opposite hemi-
sphere, but rarely with a gumma compressing the corresponding
nerve on the opposite side. A syphilitic lesion of one of the
cranial nerves is often associated with syphilitic thrombosis of
cerebral vessels, but these lesions usually appear at different
times, so that there is a history of two separate attacks.

§ 983. Diagnosis. — In some cases constitutional symptoms
are so apparent that the presence of syphilis cannot be -over-
looked. If characteristic cutaneous eruptions and ulcerations,
osseous defects in the nose and palate, be present, the nature
of the case can hardly remain in doubt ; although it must not
be forgotten that persons who have previously suffered from
syphilis are also liable to nervous diseases of non- syphilitic
origin. Nervous affections, as a rule, belong to the later mani-
festations of the disease, and make their appearance long after
the more prominent symptoms of the constitutional disease
have ceased to exist. Search must then be made for cicatrices
on the genitals or on the groins, round pigmented spots on
the skin ; depressed and irregular cicatrices over the forehead
and front of the legs with the integument adhering to the sub-
jacent bones ; radiated cicatrices on the mucous membranes,

968

TOXIC, AND FEBRILE AND

especially of the mouth ; circular depressions on the arches of
the palate or tonsils, which look as if a piece of tissue had
been punched out ; irregular protuberances on the surfaces of
the bones ; a moderate degree of, but hard, swelling of the
occipital, cervical, or cubital lymphatic glands; and enlargement
and knobby induration or atrophy of one testicle. An inquiry
into the history of a case may throw great light upon its nature.
If the patient be a man, it may be asked whether he has ever
suffered from syphilitic infection. In the case of a married
woman, valuable information may be obtained by ascertaining
whether or not she has had miscarriages, if some of her children
were still-born or died soon after birth, or whether they mani-
fest any of the characteristic symptoms of congenital syphilis.

(1) Syphilitic Lesions of the Peripheral Nerves. — Syphilitic
lesions of peripheral nerves, like all other similar lesions, are
manifested by symptoms of irritation, as hypereesthesia, neu-
ralgia, and spasm ; followed by symptoms of depression, as
simple ansesthesia, ansesthesia dolorosa, or paralysis in the
region of distribution of the affected nerve, the symptoms of
depression being much more important and frequent than those
of irritation. Syphilitic disease of the peripheral spinal nerves
may occur ; but the cranial nerves are much more frequently
affected. In syphilitic disease of the motor nerves the paralysis
is sometimes limited to a single muscle; while the other
muscles supplied by the same nerve remain unaffected, or
manifest only a slight degree of weakness. The oculo-motorius
appears to be the most frequently affected of the cerebral
nerves, and ptosis generally precedes paralysis of the recti
muscles. When, therefore, ptosis is suddenly developed without
any apparent cause, syphilis should be suspected. It must
be remembered that paralysis of one or more of the ocular
muscles is liable to appear in the early stage of locomotor
ataxy, and cases presenting these symptoms should, therefore,
be carefully examined to see whether or not lancinating pains,
absence of the deep reflexes, or ataxia be present.

If double optic neuritis, paroxysmal vomiting, and headache
be present along with the paralysis of the third nerve, the latter
is caused by the pressure of a tumour on the nerve at the base
of the brain, but even then the tumour may be of syphilitic

POST-FEBRILE NERVOUS DISORDERS.

9G9

origin. Aneurism of one of the arteries at the base of the
brain may give rise to similar symptoms, but it is frequently
associated with vegetations on the cardiac valves (Ogle, Church).
Basilar meningitis may also paralyse the third nerve ; the
acute form of this disease bears no resemblance to syphilis, but
the chronic form of meningitis may be indistinguishable from
it, except by the fact that treatment is not followed by favour-
able results. The sixth nerve is also frequently affected in
syphilis, either separately or along with the fifth or seventh
nerve on the same side. Syphilitic disease of the fifth is not
unfrequent, and the nerve may be affected at its origin, at the
Gasserian ganglion, or in its separate divisions. Disease of this
nerve first declares itself by neuralgic pains in the region of
its distribution, which are liable to nocturnal exacerbations,
and occasionally anaesthesia may be associated with the pain.
The motor root of the nerve is often affected, and then there is
masticatory paralysis with atrophy and the reaction of degenera-
tion in the affected muscles. The paralysis is sometimes preceded
by spasmodic movements of the affected muscles. When the
Gasserian ganglion is implicated there is lachrymation and
neuroparalytic ophthalmia. Syphilitic affections of the fifth
nerve are probably never bilateral, and if both be paralysed by
the pressure of a tumour at the base of the brain, the growth
is likely to be cancer (Hutchinson).

The seventh nerve is, with the exception of the motor nerves
of the eyeball, more frequently affected in syphilis than any
other cranial nerve. The paralysis may affect all the branches
of the nerve, or, contrary to what occurs in central paralysis of
the facial, the muscles about the eye may be the first to become
paralysed. The hypoglossal nerve is probably never subject to
isolated paralysis in syphilis. The optic nerves, chiasma, or
tracts may be the first to suffer, and unilateral amaurosis with
descending neuro-retinitis, or different forms of hemiopia may
occur according to the situation of the lesion. Some cases of
amblyopia or amaurosis have been recorded in which no
lesion could be detected by ophthalmoscopic examination,
but which were cured by antisyphilitic treatment. Various
forms of neuralgia are held to be of syphilitic origin in the
absence of anatomical proof, because they occur in syphilitic

970

TOXIC, AND FEBRILE AND

subjects and yield to antisyphilitic treatment. The most fre-
quent of these are sciatica, occipital neuralgia, and neuralgias
of the testicle, scrotum, and various viscera.

(2) Syphilitic Lesions of the Spinal Cord and its Mem-
branes.— These form late manifestations of the disease, and, as
a rule, marked cachexia is present before their appearance.
The nervous symptoms are generally preceded by general
languor and a feeling of debility; after a time symptoms of
sensory irritation set in, which may last for months without
paralysis. Pains, increased by pressure, are sometimes situated
at a fixed spot, over the vertebral column, in the cervical, lumbar,
or sacral region. At other times they are situated in the ex-
tremities; at first limited to an arm or leg, but later involving
the other limbs. The pains are more rheumatic than neu-
ralgic in character, and are subject to great variations in
duration and intensity (Heubner). The patient often complains
of parsesthesise, such as formication, tingling, and numbness in
the affected extremity.

After a time motor disturbances appear in the form of rigidity
and temporary spasms of groups of muscles or an extremity.
The symptoms are liable to great fluctuations, and may entirely
disappear for a time, the free intervals being sometimes of
several months' duration. Sooner or later, however, the symp-
toms of irritation give place to those of paralysis. The patient
complains of increasing weakness in one leg or in both the leg
and arm of the same side if the lesion be situated in the cer-
vical region, and* in a short time complete paralysis is developed.
Before long the opposite side of the body is affected, and the
paraplegia becomes complete. The accompanying disturbances
of sensibility do not increase in corresponding ratio as they do
in myelitis or other tumours of the cord. The extent of the
paralysis will depend upon the seat of the lesion. When the
lumbar region is affected both lower extremities will be
paralysed, but one usually to a greater extent than the other,
and the sphincters will also be involved in the paralysis.

After a time the symptoms remain stationary for a consider-
able period, and the patient is confined to bed for weeks or
even months. If energetic treatment be adopted, the case may
slowly improve and terminate in comparative recovery, the

POST-FEBRILE NERVOUS DISORDERS.

971

most favourable cases being those in which the morbid process
is limited to the lowest part of the cord.

Improvement begins in the less affected extremity, which
after a time completely regains its motor power ; but, although
the other extremity improves, a certain degree of motor weak-
ness persists. When the sphincters are affected, bed-sores and
cystitis with their usual deleterious consequences are apt to
develop.

When the cervical region is implicated, and especially the
upper portion, the prognosis is very grave, a condition of general
paralysis being rapidly developed.

But even aggravated cases may improve under energetic
antisyphilitic treatment, although the spinal cord remains to a
greater or lesser extent permanently diseased. If the syphilitic
lesion have extended from the pia mater to the lateral columns a
spastic paralysis, resembling more or less that of primary lateral
sclerosis, is developed ; while locomotor ataxia is simulated if
the lesion be limited to the posterior columns. In the above
cases the syphilitic lesion consists of the formation of a gum-
matous tissue, either in the form of a more or less circumscribed
tumour or diffused infiltration into the spinal cord ; at other
times the lesion appears to assume the form of a chronic
degeneration or sclerosis from the commencement. It is
probable that about half of the cases of locomotor ataxia are
of syphilitic origin (Buzzard, Gowers, Erb), and in most of these
the lesion is probably from the first a chronic degeneration.
The grey matter appears to be primarily affected at other times.
Progressive muscular atrophy is probably sometimes of syphilitic
origin, while labio-glosso-laryngeal paralysis is frequently and
exophthalmoplegia externa is said to be always of syphilitic
origin. A case came under my own observation in which the
symptoms of acute spinal paralysis of adults occurred in a
man at the age of 23, while he was suffering from secondary
symptoms. He was 47 years of age when I saw him, and
the symptoms present were slight ptosis, paralysis of the
superior rectus, and comparative dilatation and sluggish move-
ment of the pupil of the right eye, a slight degree of atrophy
of the right half of the orbicularis oris, paralysis with decided
atrophy of the muscles of the right half of the tongue, and

972

TOXIC, AND FEBRILE AND

complete paralysis and atrophy with loss of the electric con-
tractility of all the muscles which produce dorsal flexion of
the foot. All sensory disturbances were absent. The presence
of multiple lesions in this case points to its syphilitic origin.
It must also be remembered that acute ascending paralysis is
apt to become developed in syphilitic subjects ; but no lesion
which can be regarded as characteristic of syphilis has been
discovered in the spinal cords of such cases.

(3) Syphilitic Lesions of the Brain and its Membranes. —
The outbreak of cerebral syphilis is generally preceded by
premonitory symptoms. Headache is the most constant and
important of these, and it may precede more pronounced cerebral
symptoms by days, months, or even years. It occurs in
paroxysms which are sometimes so intense as to be almost
insupportable. The pain is seldom diffused over the whole
head, but generally occupies the lateral, anterior, or posterior
half, or is limited to a very circumscribed region which is tender
to pressure. The headache is liable to nocturnal exacerbations
of great severity, while there is a remission or complete inter-
mission in the morning ; it may entirely disappear for weeks or
months, without treatment, and afterwards recur with great
severity. Sleeplessness is another important symptom of this
early stage ; it is sometimes but not always the result of the
headache, and may continue during the remissions of the
latter. Other premonitory symptoms of less constancy and
importance are, attacks of dizziness, feeling of fainting,
numbness in the head, shooting pains in the extremities,
general discomfort, slight loss of memory, mental confusion,
great excitability of manner, and irritability of temper. Some
of these symptoms probably occur in every case, but they may
sometimes be so slight and transient that the patient does not
complain of them unless questioned.

The purely nervous symptoms depend upon the nature and
situation of the lesion, and may be divided into the following
varieties : (a) Symptoms caused by the presence of a gumma
within the cranium, (&) those caused by occlusion of one of the
arteries of the brain, and (c) those caused by chronic degenera-
tive changes.

(a) Gumma. — If the gummatous tissue form a distinctly

POST-FEBUILE NERVOUS DISORDERS.

973

circumscribed growth, it gives rise to double optic neuritis, and
the other symptoms which characterise intracranial tumours.
If the syphilitic tissue be infiltrated, the symptoms of a focal
disease are probably present, but without double optic neuritis.
We have already seen that syphilitic growths are situated near
the surface of the brain. When the lesion is situated at the
base of the brain, the most prominent phenomena will be those
of pressure upon the cranial nerves, which have already been
considered. When, again, the growth is situated on the con-
vexity, the most prominent symptoms are due to implication of
the cortex of the brain. The primary lesion of the cortex is
generally irritative ; but, as the growth enlarges, part of the
cortex is injured, so that a destroying lesion is superadded to
the irritative or discharging one. If the lesion be situated in
the area of distribution of the Sylvian artery, the symptoms
begin by a unilateral epileptiform attack, usually followed
by some degree of paralysis of the muscles first implicated in
the convulsions. These epileptiform convulsions (Jacksonian
Epilepsy) have been already fully considered, and it is un-
necessary to describe them further. If the syphilitic lesion be
situated in the region of the anterior cerebral artery, then
psychical disturbances predominate, consisting of a drowsy
delirium followed by a somnolent condition, and more or less
coma.

(b) Neurotic Softening. — Occlusion of a cerebral vessel, as
the result of syphilis, produces all the usual symptoms of that
accident from any other cause. When a vessel is occluded,
unless collateral circulation be soon established, a focus of
softening results, which produces the usual phenomena of focal
disease. If the vessels of the lenticular nucleus are occluded,
hemiplegia may be produced, but the patient recovers ; occlu-
sion of Broca's artery causes ataxic aphasia, and of the posterior
branch of the Sylvian artery, amnesic aphasia ; while softeping
in the area of the anterior cerebral artery gives rise to loss of
memory, confusion of ideas, and other psychical disturbances.
What distinguishes syphilitic thrombosis from other forms of
occlusion of vessels is that it often occurs at a comparatively
early period of life, when atheroma of the arteries is not usually
present, and in the absence of all the conditions which give

974 TOXIC, AND FEBRILE AND

rise to embolism or haemorrhage. Syphilitic thrombosis is
besides often associated with peripheral paralysis of one of
the cranial nerves. It must be remembered that unilateral
amaurosis may occur in syphilis from thrombosis of the central
artery of the retina.

(c). Chronic Degenerative Changes. — In cases of this kind
the course of the disease is more or less like that of general
paralysis of the insane. The symptoms begin insidiously, with
feelings of general uneasiness and discomfort, the health suffers,
there is an unusual degree of mental irritability, or great
mental activity interrupted by attacks of confusion of ideas.
The patient commonly has ideas of grandeur, and may indulge
in extravagance much beyond his means. In cases of the kind
the syphilitic affection is liable to manifest itself by a fresh
attack of constitutional symptoms in the throat, nose, or hands.
After a time new symptoms make their appearance ; the patient
is easily fatigued, he is no longer capable of undergoing sus-
tained exertion, the gait is staggering, and his movements are
uncertain and hesitating. The patient complains of numbness,
formication, and shooting pains in one of his limbs, the speech
is hesitating, and stammering, the tongue trembles, and memory
and intelligence decrease gradually and steadily. Yarious forms
of paralysis now make their appearance ; the gait is ataxic ; the
writing is irregular and ultimately becomes illegible ; and after
a variable period of years the patient dies with cystitis, bed-
sores and their consequences, unless carried off by some inter-
current affection.

§ 984. Treatment — The treatment of syphilitic nervous
affections must be prompt and energetic, inasmuch as delay may
lead to irreparable injury being done to the part affected. If
the presence of a gumma be suspected, the iodide of potassium
shoujd be at once administered in doses of a scruple to half a
drachm three times daily. The iodide may from the first be
combined with mercurial treatment, or the administration of
the latter may be deferred until the former has had time to
dissipate the gumma. The iodide, however, should never be
trusted alone, as the lesion is likely to recur in some other
situation within a period of a few months, unless mercury be

POST-FEBRILE NERVOUS DISORDERS.

975

administered. In aggravated cases from three to four scruples
of mercurial ointment should be rubbed daily over the lower
and upper extremities, the abdomen, and back during the first
fourteen days. If improvement be manifested at the end of
this time, the same quantity should be rubbed in every other
day for several weeks, and then half the quantity at the same
intervals for several additional weeks. The mouth and teeth
should be frequently washed during this treatment, in order to
prevent salivation. In milder cases the internal administration
of mercury is more convenient than the inunction, and equally
efficacious, and no preparation can answer the purpose better
than the bichloride.

In syphilitic epilepsy the bromide of potassium may be com-
bined with the iodide, and to allay neuralgic and other pains
morphia must be had recourse to. In the treatment of painful
affections of the peripheral nerves chloral may, according to
Dowse, be added to the solution of the iodide of potassium.

(V.) FEBRILE AND POST-FEBRILE NEUROSES.

§ 985. Numerous nervous disturbances are liable to occur in
the course of or during convalescence from febrile diseases.
The diseases which are most commonly accompanied or followed
by nervous disorders are typhoid fever, the acute exanthemata,
acute dysentery, pneumonia and pleurisy, nephritis and cystitis,
acute rheumatism, intermittent fever, and, above all, diphtheria.
The nervous disorders of febrile disease are generally the same
as those which arise from other causes, and may affect the
peripheral nerves, the spinal cord, or the brain.

(1) Neurosis of Typhoid Fever. — During the first stage of
typhoid the patient may complain of cutaneous hyperaesthesia,
which may involve a considerable portion of the limbs and
trunk. Hypersesthesia and neuralgiform pains are often pre-
sent in the muscles of the limbs, neck, thorax, and abdomen.
These pains are frequently associated with cutaneous hyperaBS-
thesia ; they cause severe suffering to the patient, and all
movements tending to stretch the affected muscles are avoided.
Anaesthesia, either complete or partial, and of variable distribu-
tion, may appear in the course of the fever, and may be present

976

TOXIC, AND FEBRILE AND

as anaesthesia dolorosa. It may occur during convalescence,
and prove rebellious to treatment. Neuralgic pains often
occur during the first week of the fever in the region of the
occipital, supra-orbital, or other nerve ; during convalescence
similar pains are apt to appear in the loins and along the
vertebral column, or in the region of distribution of one of the
branches of the brachial, lumbar, or sacral plexuses.

The muscles supplied by certain nerves may be paralysed in
the course of typhoid fever. A case is reported by Eisenlohr
in which the muscles of the left lower extremities supplied by
the tibial and peroneal nerves were paralysed during a relapse
of typhoid fever. Electrical examination of the affected muscles
revealed the reaction of degeneration in them. Paralysis of
the abductors of the glottis has been known to occur during
convalescence and to render the operation of tracheotomy
necessary. Paralysis sometimes assumes the paraplegic form.
Cormack records a case in which paraplegia gradually super-
vened about the seventh week from the beginning of an
attack of typhoid fever. The patient also had paralysis of the
external rectus muscle of the left eye, and retention of urine,
but ultimately recovered.

The central forms of myelitis are liable to supervene in the
course of typhoid fever. Leudet observed a case in which
acute ascending paralysis developed during convalescence from
a mild attack, and proved fatal in six days. Another case is
reported by Yulpian in which symptoms of acute myelitis
supervened during convalescence from typhoid fever, and
although the patient ultimately recovered, paraplegia and
atrophy of the muscles persisted for a long time. Progressive
muscular atrophy, ataxia, multiple sclerosis, and other chronic
affections of the spinal cord may become established during
convalescence from typhoid fever.

Cerebral disturbances not unfrequently occur during or sub-
sequently to an attack of typhoid fever. A case of temporary
aphasia is mentioned by Trousseau as occurring during con-
valescence from typhoid. Temporary hemiplegia may super-
vene after an attack of typhoid. In other cases there may be
aphasia, delirium of various forms, or acute insanity.

(2) Nervous Disorders of the Acute Exanthemata. — The

POST-FEBRILE NERVOUS DISORDERS.

977

rachialgia which ushers in an attack of smallpox is no doubt of
nervous origin; it is often accompanied by considerable weak-
ness or even complete paralysis of the lower extremities, the
bladder being sometimes involved in the paralysis. The
paralytic phenomena generally disappear with the rachialgia,
but loss of motor power of a more durable character may
supervene during convalescence. The paralysis is limited to
certain groups of muscles or to one of the extremities, or may
assume the form of paraplegia. Loss of motor power is often
associated with sensory disturbances, and the affected muscles
may undergo atrophy or contracture. Hemiplegia with aphasia
or other severe cerebral symptoms may complicate variola
(Rosenthal). Rubeola, scarlet fever, and erysipelas may be
accompanied or followed by local or general paralysis, or hemi-
plegia with persistent aphasia. Infantile paralysis is very liable
to occur in the course of the acute exanthemata.

Diphtheritic Nervous Disorders. — Paralysis occurs after
diphtheria probably more frequently than after all the other
acute diseases together. An interval of several days or weeks
may elapse between the termination of the general disease
and the appearance of the paralytic phenomena. Diphtheritic
paralysis almost invariably begins in the muscles of the soft
palate and pharynx; it is associated with anaesthesia of the
affected parts and loss of faradic contractility in the muscles
implicated. Motor paralysis is sometimes preceded by violent
vomiting and retardation of the pulse, while death appears to be
sometimes caused by paralysis of respiration (Landouzy). These
phenomena seem to be the result of a primary irritation followed
by paralysis of the vagus, and it is unnecessary to describe
them in detail (§§ 270 to 282). I have known glycosuria to
occur during convalescence from diphtheria, but I am unable
to state whether the symptom was transitory or permanent.
Paralysis may invade various other muscles, such as those of
the vocal cords, tongue, and eyeballs, the muscles of accom-
modation being specially liable to be affected. The paralysis
extends to the muscles of the trunk and extremities ; it is
rarely complete, but the bladder and rectum may be involved ;
Trousseau observed impotence in young men, lasting several
weeks or months. Death has been known to result from

KKK

978

TOXIC, AND FEBRILE AND

paralysis of the diaphragm. The sensory disturbances consist
of hyperaesthesia at first, followed by numbness and anaesthesia.
The sense of taste, smell, or hearing may occasionally be
affected, and disturbances of vision are frequent. The disorders
of sight may be caused by paralysis of some of the external or
internal muscles of the eye ; there may be complete amaurosis,
which may continue during several weeks, no appreciable
changes being present in the discs.

(3) Paralysis of Acute Febrile Diseases. — Acute rheumatism
is sometimes followed by a local paralysis in the region of distri-
bution of one of the peripheral nerves. Pneumonia and pleurisy
are sometimes complicated by paraplegia or hemiplegia, but it is
doubtful whether there is anything more than an accidental
connection between the local disease and the nervous disorders.
The forms of paralysis termed reflex have already been con-
sidered.

(4) Nervous Disorders of Intermittent Fever. — Paralysis
sometimes appears suddenly during the febrile paroxysm, and
ceases suddenly with it ; at other times it constitutes the only
evidence of the presence of malarial poisoning (pernicious para-
lytic fever), and in other cases it assumes a chronic form, and is
associated with great cachexia. Of the forms of paralysis which
occur suddenly, hemiplegia with aphasia is by far the most
usual. In the pernicious paralytic variety paraplegia, with
partial anaesthesia and disturbances of sight and hearing, is
sometimes found associated with aphasia (Vincent).

§ 986. Morbid Anatomy and Physiology. — The changes
which the muscles undergo in acute diseases have been carefully
studied by Hay em, but this subject is much too wide to be
discussed here. The local paralyses associated with anaesthesia
occurring after acute diseases are doubtless of peripheral origin,
and are probably caused by neuritis. Even in paraplegia the
disease in the spinal cord is supposed by some authors to be
secondary to that of the peripheral nerves, and the result of an
ascending neuritis. In diphtheritic paralysis Charcot and Vul-
pian observed degeneration of the motor nerves of the velum
palati. Buhl states that there is a nuclear exudation into the

POST-FEBRILE NERVOUS DISORDERS.

979

sheaths of the paralysed nerves similar to the diphtheritic
exudation occurring into the connective and mucous tissues.
Pierret observed spots of false membrane on the spinal cord
and medulla oblongata, associated with perineuritis of the
roots of the corresponding nerves. Vulpian observed slight
changes in the ganglion cells of the anterior horns in two cases,
but found nothing abnormal in a third. Dejerine found
neuritis of the anterior roots and of the intra-muscular nerves,
along with slight alterations in the grey substance of the
cord ; the posterior roots and white substances were normal.
Westphal found spots of softening disseminated throughout
the spinal cord in a case of paraplegia occurring in the course
of smallpox. It is manifest that various and manifold lesions
may be found in febrile and post-febrile nervous disorders
affecting peripheral nerves, spinal cord, or brain. The nature
of these lesions is probably very various. Sometimes the lesion
consists 6f hyperemia, at other times of ansemia, either general,
or partial from occlusion of vessels, or it may be inflammatory
or degenerative from the first.

§ 987. Diagnosis and Prognosis. — That a nervous disorder
has occurred during the course or shortly after an acute disease
is rendered evident by the history of the case. The chief
problem of diagnosis then is to determine whether or not
the lesion be functional or organic, or localised in the peripheral
nerves, spinal cord, brain, or sympathetic system. In order to
determine the latter question, it is necessary to possess an accu-
rate knowledge of all the diseases, especially all the forms of
paralysis, to which the nervous system is liable. No number
of special diagnostic rules will supply the place of this know-
ledge, and such rules are superfluous to those possessing it.
It is scarcely necessary to remind the reader of the value of
electrical examination of the paralysed nerves and muscles in
determining whether the paralysis be of peripheral, spinal, or
cerebral origin.

The prognosis is, as a rule, favourable in the nervous disorders
occurring in connection with acute diseases. In diphtheritic
paralysis recovery usually takes place in some weeks, but in
severe cases it may be delayed for six months and upwards. The

980

FEBRILE AND POST-FEBRILE DISORDERS.

severity of the primary diphtheritic attack bears no proportion
to the intensity and duration of the subsequent paralysis.

§ 988. Treatment. — The treatment must vary according to
the nature of the lesion and . other circumstances. If there
be evidence of hyperemia of the spinal cord or brain, cold
application should be employed. As a rule, however, tonic and
stimulating treatment is required. If there be no organic
disease strychnia is indicated. The best results are obtained
from electrical treatment, hydrotherapeutics, and change of air
and scene.

981

INDEX.

PAGE.

Abdominal muscles, paralysis of . . . .i. 49S
Abdominal portion of the sympathetic,

diseases of i. 585

Abduceus nerve, deep origin and surface

attachments of i. 2S7

Abducens uerve, paralysis of i. 357

Abscess, chronic, of the brain . . . . 731

primary 731

symptoms of the latent period 731
symptoms of the terminal

period 732

secondary 734

varieties 734

morbid anatomy 736

Achilles-teuilou reflex .. .. .. ..i. 150

Achromatopsia i. 330

Acoustic nerve, diseases of i. 334

Acoustic nuclei 49

Action, automatic 76

reflex 75

voluntary 70

Active cerebral congestion 693

Acute atrophic spinal paralysis . . . . 105

definition, history, etiology.. .. 105

infantile 106

of adults 116

symptoms 106, 116

course 117

morbid anatomy 118

localisation in the anterior

horns 127

morbid physiology 129

diagnosis 131

prognosis 132

treatment 133

Acute ascending paralysis 264

definition, history, etiology.. .. 264

symptoms 265

diagnosis 268

morbid anatomy 269

morbid physiology 271

prognosis, treatment 272

Acute bulbar myelitis 285

morbid anatomy 286

Acute central myelitis 285

morbid anatomy 285

Acute cervical transverse myelitis . . . . 287

Acute diffused myelitis 272

definition, etiology 272

symptoms 273

course 278

morbid anatomy 279

microscopical examination . . . . 281

morbid physiology 283

varieties 281

diagnosis 288

prognosis 290

treatment 291

Acute disseminated myelitis 288

morbid anatomy 288

l'AOR.

Acute dorsal transverse myelitis- . . . . 287
Acute dorso-lumbar transverse myelitis 287

Acute encephalitis 727

Acute hemilateral myelitis 287

Acute inflammation of the grey anterior

horns 105

Acute myelo-meningitis 288

morbid anatomy 288

Acute neuritis i. 293

Acute pysemic encephalitis 728

Acute spinal leptomeningitis 391

Acute transverse myelitis 286

Acute universal cerebral anaemia . . . . 686
Acuteness of vision, diminution of ..i. 315

tests of i. 315

Addison's disease i. 591

Adductors of both thighs, contracture of i. 505

iEsthesioneuroses i. 80, i. 81, i. 90

articular i. Ill

osseous i. Ill

visceral i. 113

Afferent fibres, trophic centre of . .i. 281

After-sensations, persistent i. 101

Agraphia 616

Age as predisposing to disease i. 74

Akinesis i. 86

reflex i. 137

of the voluntary muscles i. 121

associated symptoms i. 122

Alcoholic paraplegia 955

Alcoholic nervous diseases 953

Alternate hemiplegia 669

Amaurosis i. 313

symptoms i. 315

tabetica i. 329

Amblyopia i. 313

symptoms i. 315

Amimia 616

Amoeboid movements i. 7

Amyotrophic lateral sclerosis 256

symptoms 256

Amygdaloid nucleus 450

Amyloid corpuscles 86

Anaemia i. 234

Anaemia of the brain 685

histoiy, experimental investiga-
tion 685

etiology 686

acute universal 686

chronic universal 687

symptoms 688

infantile 689

morbid anatomy 689

morbid physiology 690

cause, diagnosis, prognosis . . . . 691

treatment (592

Anaemia of the medulla oblongata . . . . 813

Anaemia, local, of the skin i. 188

Anaemia of the spinal cord 310

Anaesthesia i. 83

982

INDEX.

PAGE.

Anaesthesia :

acoustic i. 355

auditory i. 355

circumscribed i. 99

cutaneous i. 97

in the form of a girdle i. 99

of the larynx i. 418

muscular i. 110

olfactory i. 308

optic i. 313

partial i. 317

of sexual feelings .. .. ;. ..i. 117

tactile i. 100

thermo . . . . i. 100

in the territory of the vagus . .i. 117

Anaesthesia dolorosa i. 304

Analgesia i. 64, i. 97, i. 100

visceral i. 116

Aneurisms, intracranial 557

Angina pectoris ..i. 577

etiology ... .. . .i. 577

symptoms - i. 578

morbid anatomy .. .. i. 579

morbid physiology ..i. 580

varieties i. 581

diagnosis, prognosis a. 582

treatment i. 583

Angioma ... 557

Angioneuroses JL 182

cerebral 1. 186

cutaneous i. 187

peripheral .i. 185

spinal . .i. 185

visceral i. 189

Angioparalysis i. 185

Angioparesis . .i. 185

Angiospasm i. 185

Anidrosis i. 219

Ankle clonus i. 150

Ankle reflex i. 150

Anosmia i. 308

traumatic i. 309

prognosis, treatment i. 310

Ankle clonus i. 150

Ankle reflex i. 150

Anosmia i. 308

traumatic i. 309

prognosis, treatment L 310

Antagonism between size of unit and

absorption i. 13

Anterior fossae of the skull, lesions in . . 651

Anterior grey horns 8, 33, 37

development of 23

Anterior muscles of the leg, spasm of . .i. 522
Anterior pyramids .. .. i. 52, 33, 65, 69
Anterior root-zones . . 33, 35, 51, 57, 64, 69

Aphasia, ataxic 616

amnesic 618

morbid anatomy 621

morbid physiology 623

mechanism of 629

Aphonia paralytica i. 423

spastica i. 419

Apoplexy, meningeal 3S1

Apoplexy, spinal 321

Apselaphesia i. 97

Arachnitis 390

Arachnoid, cranial part of 3

spinal part of 410

Arcuate fibres 34, 37, 61, 62, 453

Area of anterior cerebral artery. 440, 441, 442

lesions in 640

Area of middle cerebral artery . . 442, 443

lesions in 594

Area of posterior cerebral artery . . 440, 441

lesions in 633

Areas of the skull, respective contents

of 426

Argyll-Robertson symptom i. 356

PAGK.

Arsenic i. 260

Arteries of brain 439

of cerebellum n

of medulla oblongata 15

of pons Varolii 15

of spinal cord 19

Arthroneuralgia i. m

general symptoms i. 112

Articular aesthesioneuroses i. Ill

Arythmia cordis i. 181

Ascending degeneration 95

Aspermatism 3. 118

Assimilation i. 9, i. 11

Associated movements of articulation,

disorders of i. 174

Associated movements of the extremities,

disorders of i, 173

Asthma bronchiale i 429

symptoms i. 430

prognosis, pathology, treatment, .i. 431

Asthma nervosum i. 429

Atavism i. 74

Ataxia, locomotor i. 157

Ataxic gait 219

Ataxy, locomotor, progressive 211

Athetosis 579

Atony i. 17S

Atrophia musculorum lipomatosa . . . . 185

Atrophy of the brain 703

general 50S

Atrophy of the cerebellum 704

Atrophy of the corpus callosum . . . . 703
Atrophy of the face, unilateral, pro-
gressive i. 570

Atrophy of the muscles, simple . . . .i. 204
Atrophy of the nerves . . . . i. 89, i. 299

Atrophy of the optic nerve i. 328

Atrophy, muscular, progressive . . . . 145

Atropine i. 256

Attacks, hysterical 889

hystero epileptic 927

epileptic 922

Auditory anaesthesia i. 335

Auditory hyperesthesia i. 334

Auditory hyperalgesia i. 334

Auditory vertigo 830

Auras epilepticae 916

motor 916

sensory 91S

vasa-motor and secretory . . . . 920

psychical 921

Automatic disturbances :

encephalic i. 160

peripheral i. 156

spinal i. 157

Automatic movements i. S5

Azygos uvulae, paralysis of i. 407

unilateral i. 407

Back, muscles of i. 470

Baraesthesiometer 1. 94

Basal ganglia 434

functions of 473

lesions of 643

Basedow's disease i. 560

Baths i. 261

Bedsores i. 230

Belladonna i. 256

Bell's paralysis i. 36S

Binocular diplopia i. 350

Bladder, neuralgia of i. 594

Blepharospasm i. 365

Blood-letting i. 267

Bones, nutritive affections of i. 222

Brachial plexus, injuries to i. 54:!

nerves of i. 452

Brain of adult men and higher mam-
malia and human infant,
difference between 471

INDEX.

983

PAGE.

Brain, abscess of :

diagnosis 7:!9

prognosis 740

treatment 741

Brain, anaemia of 685

Brain, arteries of 489

Brain, atrophy of 708

Brain, chronic abscess of 731

Brain, compression of 721

Brain, concussion of 716

etiology, symptoms 716

course 718

morbid anatomy and physiology. . 719

diagnosis 719

proguosis, treatment 720

Brain, congenital malformations of . . 507

Brain, contusion of 720

Brain, cortical lesions of 694

Brain, development of .... . . 468

Brain, general atrophy of 502

Brain, hypenemia of 693

etiology 693

symptoms 695

morbid anatomy 698

morbid physiology 699

diagnosis 700

course, prognosis, treatment . . 701

Brain, hypertrophy of 706

etiology, symptoms 706

morbid anatomy 707

course 708

diagnosis, proguosis, treatmeut . . 709

Brain, law of dissolution of 507

Brain, parasites of 558

Brain, tumours of 547

Brain-substance, heterotopia of . . . . 709

Bromide of potassium i. 259

Bronchial branches of the vagus, anaes-
thesia of i. 117

Bronchioles, spasm of i. 429

Bronzed skin i. 212, i. 591

Brown- Sequard's spinal epilepsy .. ..i. 155
Brown-Sequard's spinal paralysis . . . . 361
Bulimia i. 114

Calabar bean i. 256

Capsuie, external 438

lesions of 650

Capsule, internal 438, 457

fibres of 459

lesions of 568

Caput obstipum spasticum i. 433

Carcinoma i. 302, 404

Cardiac plexus, neuroses of i. 433

Cardialgia _ i. 5S8

Caidiac nervous mechanism i. 179

action of i. 179

disturbances of i. 180

Cataleptic attacks 890

Catalepsy 904

etiology 904

symptoms 904

course 906

diagnosis and prognosis 911

treatment 912

Caudate nucleus 434

lesions of 645

Causalgia i. lOt

Cell-contents .. i. 10

Cell-membrane i. 10

Cells of Purkiuje 414

Central grey column 8, 45

development of 30

functions of 79

Central grey tube 8

development of 22

Centrum ovale 428

lesions 594

topography of 428

PACK.

Cephalalgia i. 54:i

Cerebellar projection-system i. 54

Cerebellar rigidity i. 160

Cerebellar tetanic seizures i. 160

Cerebellospinal conducting paths. . ..i. 54

Cerobello-spinal system i. 52

fuuctions of i. 59

Cerebellum .. .. i. 52, 412

Cerebellum, atrophy of 704

etiology, symptoms 704

morbid anatomy 705

complications and diagnosis. . .. 7u5

Cerebellum, crura of i. 52, 412

exterior of 412

fissures of 412

folia of 412

functions of 473

grey matter of . . i. 52, 413

intermediate ganglia of i. 54

internal structure of 413

lobes of 412

peduncles of .. .. 412

white matter of 413

Cerebellum, lesions in 671

Cerebral anaemia 685

Cerebral arteries, aneurism of 5:j>7

Cerebral arteries, occlusion of 512

etiology 512

symptoms 513

diagnosis, morbid anatomy .. .. 515
experimental investigations. . .. 517

morbid physiology 517

prognosis, treatment 518

Cerebral capillaries, occlusion of . . . . 523

etiology, symptoms 523

morbid anatomy, course, prognosis 524

treatment 524

Cerebral eruptions i. 210

Cerebral facial paralysis i. 376

Cerebral haemorrhage 525

Cerebral hyperaemia 693

Cerebral maculae i. IS'.*

Cerebral multiple sclerosis 807

Cerebral new formations 55i>

Cerebral osseous lesions i. 225

Cerebral parasites 558

Cerebral projection-system . . i. 50, i. 51
Cerebral sinuses, thrombosis of .. .. 518

etiology 518

symptoms 519

diagnosis, course 522

prognosis, morbid anatomy . . . . 522

Cerebral tumours 547

varieties 553

Cerebro-spinal system i. 48

functions of i. 59

Cerebro-spinal and cerebello-spinal sys-
tems, co-operation of .. ..i. 59
Cerebro-spinal multiple sclerosis . . . . 802

Cerebrum 415

basal ganglia of 434

convolutions of 417

their development 469

their relations to the skull . . 424
their relations to the areas of

skull 426

cortex of 450

crura of 415

exterior of 415

fissures of 417

their relations to the areas of

skull 426

grey matter of 448

internal parts of 428

internal structure of 448

lobes of 417

peduncles of 415

ventricles of 432, 433

white matter of 453

984

INDEX.

PAGE.

Cervical part of the spinal cord, dis-
eases of i. 543

injury to i. 548

Cervical plexus, nerves of i. 444

Cervical sympathetic, compression of by

tumours i. 541

Cervical sympathetic, injuries to . . . .i. 542
Cervical sympathetic, functional affec-
tions of i. 5+3

Cervico-brachial neuralgia i 455

general characters, etiology . . . .i. 455

symptoms i. 456

concomitant symptoms i. 457

diagnosis, treatment i. 458

Cervico-occipital, neuralgia i. 443

Channels of conduction, pathic .. ..i. 92
tactile .. ..i; 92

Chiasma i. 450

Chloral hydrate i. 258

Chemical poisons i. 77

Chorda tympani, lesions of i. 340

nerve fi bres of .. ..i. 372

Chorea 841

etiology 814

symptoms 815

course, duration, and terminations 820

morbid anatomy 821

morbid physiology 825

diagnosis 828

prognosis 829

treatment 829

Chorea, post-hemiplegic, of adults . . . . 574

Chorea, pre-hemiplegic 573

Choreiform movements 573

Chromatopsia i. 313

Chrornidrosis i. 219

Chronic atrophic spinal paralysis . . . . 136
definition, history, etiology, symp-
toms 136

morbid anatomy . . .... . . 141

diagnostic 144

prognosis, treatment 145

Chronic bulbar myelitis 304

Chronic central dorso-lumbar myelitis . . 299

Chronic central myelitis 298

Chronic cerebral abscess 731

Chronic cervical transverse myelitis . . 303

morbid anatomy 303

Chronic diffused myelitis 292

definition, etiology 292

symptoms 293

course 295

morbid anatomy 296

microscopic examination . . . . 297

morbid physiology 298

varieties 298

diagnosis, prognosis, treatment . . 305

Chronic disseminated myelitis 305

Chronic dorso-lumbar transverse myelitis 302
Chronic dorsal transverse myelitis . . . . 302
Chronic inflammation of the spinal cord. 292

Chronic myelo-meningitis 304

morbid anatomy 304

Chronic neuritis i. 294

Chronic progressive bulbar paralysis . . 173
Chronic spinal leptomeningitis .. .. 396

Chronic transverse myelitis 302

Chronic universal cerebral amentia . . 688

Ciliary muscle, paralysis of i. 355

spasm of .. .. .. . .i. 344

Circulation, intracranial, morbid altera-
tions of 501

Cirrhosis i. 206

Clarke, vesicular columns of 8, 22, 80, 33, 45

Claustrum 438, 450

lesions of 650

Ciavate nucleus 50, 61

Claw-hand i. 4S6

Climate cures i. 267

PAGK.

Clonic spasms i. 130, 569

Coccygeal nerve i. 510

neuralgia of i. 519

treatment i. 519

Coccygodynia L 519

Coeliac plexus, neuroses of i. 585

paralysis in the region of . . . .i. 588

spasm in the region of i. 588

Cognitions . . 480

Cold, as a remedy i. 261, i. 277

Cold, exposure to i. 76

Cold waterpack i. 265

Colic i. 585

Colica saturnina i. 585

Colloid bodies 86

Colour-blindness i. 319

Colour-vision, tests of i. 318

changes in i. 317

Columns, vesicular, of Clarke 8, 22, 30, 33, 45

functions of 77

Columns of Goll .. .. i. 55, 52, 58,59, 60

functions of 83

sclerosis of 249

Columns of Tiirck . . . .i. 52, 52, 59, 65, 67
Common sensations i. 92

test of i. 93

Commotio spinalis 368

Compound lateral sclerosis 256

Compression myelitis 303

Compulsory movements i. 160

Concussion of brain 716

of the spinal cord 36S

Conducting paths, i. 50, L 52, i. 54, i. 56, 64-69.

457-467

Conduction i. 30

CoTiductivity i. 31

Congenital spinal deformities 97

Congestion of the brain, active . . . . 693

passive 695

Conium . . i. 255

Conjugate deviation of the eyes aud rota-
tion of the head and neck . .i. 16S
Connective tissue, morbid changes of . . 86

hyperplasia of 87

hypertrophy of S7

retraction of 87

sclerosis of 87

Consciousness, anatomical substratum *of 486

Continuous tremor 579

Contractility. i. 7

mechanical i. 120

Contraction, ideo-muscular i. 120

Contraction, law of a. 124

Contractions, fibrillary i. 130

Contracture i. 132

myopathic i. 132

paralytic i. 132

primary neurotic i. 132

Convolutions of the brain, development

of i. 469

Convulsion i. 131

relative liability of some muscles

to i. 164

Convulsions, internal i. 419

Convulsions, unilateral 594

varieties 595

Convulsive tic i- 361

Cordis arythmia i. 181

Corona radiata _ . . 459

Corpora dentata i. 54, 413

Corpora geniculata 50, 43S, 449

Corpora quadrigeniina . . . . 50, 439, 449

lesions of 649

view of '. i- 284

Corpora striata 434, 449, 465

Corpus callosum 42S

atrophy of 703

Cortex of the cerebrum, functions of . . 47S
grey matter of 450

INDEX.

98.5

PAGE.

Cortex of the cerebrum :

ideational area of 486

lesions of 594

motor area 48 i

motor centre 483

motor outlets 4S3

sensory area 482

sensory ceutre 483

sensory inlets 482

Cortex of the cerebrum, giant cells of . . 452

Cortical affections of speech 612

Cortical brachial monoplegias 606

Cortical brachial monospasms. . .. 595, 596
Cortical brachial protospasins . . . . 595, 596
Cortical brachio-crural monoplegias . . 605
Cortical brachio-facial monoplegias . . 607
Cortical centres of sensation, localisa-
tion of 499

Cortical crural monoplegias 602

Cortical crural monospasms 595

Cortical crural protospasms 595

Cortical facial monospasms . . . . 595, 598
Cortical facial protospasms . . . . 595, 598

Cortical hemiplegia 599

Cortical mechanisms of actions, localisa-
tion of 498

Cortical unilateral oculo-motor mono-
plegias 609

Cough, spasmodic i. 450

Counter-irritation i. 267

Cramp i. 131

Cramps, co-ordinate .. .. i. 161

Cranial nerves, deep origin and surface

attachments of i. 2S3

place of exit of i. 555

Crico-thyroid muscles, paralysis of. . . .i. 427

Crura cerebri i. 57

collar of 467

crusta of . . 457

Crust of the cerebral peduncle, fibres of 459

Crying-fits i. 450

Cuneate fasciculus 50, 61

Cutaneous anassthesia i. 97

symptoms i. 98

distribution of i. 99

Cutaneous hyperesthesia i. 102

Cutaneous hyperalgesia i. 104

Cutaneous nerves of the trunk . . . .i. 457
Cutaneous nerves of the lower extremity i. 515

Cutaneous paralgesia i. 105

Cutaneous reflexes i. 138

Cutaneous secretory affections i. 217

Cutaneous sensations, common . . . .i. 92

special i. 92

tactile i. 92

Cutaneous trophic affections i. 208

theory of .. .. i. 220

Cycloplegia i. 355

Cysticercus cellulosas 558, 564

Cysts 373, 557

Daltonism i. 319

Deafness i. 336

Decubitus acutus i. 213

chronicus simplex i. 215

Degenerations ,i. 234

secondary 9i, 502

Deiter's cells 7, 87

Delirium tremens 053

Dentate nuclei i. 54, 413

Descending degeneration 95

Deviation, secondary, of the sound eye. i. 172

Diabetes mellitus i. 591

Diagnosis, general, pathological .. ..i. 244

topographical i. 241

Diaphragmatic paralysis i. 451

Diaphragm, clonic spasm of i. 447

treatment i. 448

Diaphragm, tonic spasm of i. 447

PAGE.

Diaphragm, tonic spasm of, treatment i. 447
Diphtheritic nervous disorders . . . . 977

Diplegia facialis i.374

Diplopia, binocular i. 350

Direct cerebellar fibres .. .. i. 56, 51, 64
Direct cerebellar tract, functions of .. 82

sclerosis of 250

Direct cerebral paralysis 592

Disassimilation i. 9, i. 11

Diseases of the encephalou, classifica-
tion of . 509

morbid anatomy of 501

Diseases of the medulla oblongata, clas-
sification of 100

Diseases of the spinal cord, classifica-
tion of .100

Diseases of the nervous system, causes of. i. 73

extrinsic i. 76

intrinsic i- 73

Disseminated sclerosis, see sclerosis, mul-
tiple 801

Dorsal muscles i- 470

paralysis of i. 497

treatment i. 498

Dorsal nerves, diseases of i. 493

Dorso-intercostal neuralgia i. 493

etiology i. 493

syriiptoms i. 494

diagnosis, treatment i. 495

Double painful sensations i. 101

Dura mater, cranial part 409

diseases of 743

Dura mater, spinal part 3

Dura mater, spinal, inflammation of . .i. 3S4

Dynamometer i. 120

Dysesthesia i. 104

Dyscrasic spinal anaemia 310

Dysphagia paralytica i. 411

symptoms i. 411

prognosis, treatment i. 412

Dystrophy, neurotic i. 89

Early rigidity . . . . 569

Ecliinococcus hominis 565 568,

Eclampsia 945

definition 945

etiology 945

symptoms 947

course and duration 949

diagnosis, prognosis 950

treatmeut 951

Eclampsia nutans i. 437

Ecstasy 907

Eczema i. 209

Eighth nerve, origin and attachments of.i. 287

nuclei of 49

Electrical examination i. 124

results of i. 124

Electrical stimuli i. 122

Electricity i. 268

chemical i. 272

induced i. 269

static i. 269

Electricity, uses of i. 275

Elementary motor disturbances, varieties

of i. 86

Elementary symptoms, general classifi-
cation of i. 92

Elephantiatis Grascorum i. 213

Eleventh nerve, accessory nuclei of ..i. 48

diagram of i. 405

origin and attachments of . . . .i. 289

Emboli 313, 511

Embolism i. 235, 313, 511

of cerebral arteries 511

symptoms 512

of arteries of the medulla ob-
longata 313

Emotional sensations i. 81

986

INDEX.

PA OR.

Encephalic automatic disturbances . .i. 160

Encephalitis 722

acute, complicating affections of

the slaill 727

acute pyajmic 728

around extravasations 728

symptoms 729

around necrotic softenings . . . . 728

symptoms 730

around tumours 729

symptoms 730

diffused 722

symptoms 723

local 722

symptoms 723

Encephalon 409, 411

congenital malformations of . . . . 507

diseases of 509

general atrophy of 502

hasmorrhage into 525

general atrophy of 502

law of dissolution of 507

morbid anatomy of 501

secondary degenerations of .. .. 502
systemic degenerations of . . . . 503

tumours of 502, 547, 553

Encephalo-spinal system i. 48

functions of . . i. 57

Encephalo-spinal system, diseases of . . 791

Enchondroma 403

Endomysium i. 201

Endoneurium i. 282

Energy, conservation of i. 4

Enteralgia i. 585

Epilepsy 913

etiology 913

symptoms 915

course, duration, and terminations 933

morbid anatomy 934

morbid physiology 936

diagnosis . . . . 940

prognosis 941

treatment 942

Epileptiform neuralgia i. 394

seizures .'. 929

Epineuriuin i. 282

Erect posture i. 61

act of acquiring i. 66

Erethismic shock 712

Eruptions, cerebral i. 210

spinal i. 210

Erythema i. 208

Examination, electrical i. 124

Exanthemata, acute, nervous disorders of 976

Excitability, electrical i. 123

Extensor digitorum pedis communis,

paralysis of i. 528

Extensor longus pollicis i. 528

External capsule 43S, 467

lesions of 650

External kinesioneurose3 i. 119

External rectus oculi, paralysis of . . . .i. 357
Externa] rectus oculi, tonic spasm of . .i. 347

treatment i. 347

External remedies i. 261

Extremities, iuferior, diffused spasm of..i. 423

treatment i, 423

Eye, healthy fundus of i. 312

Eye, secondary deviation of the sounfi . .i. 172
Eyes, conjugate deviation of and rotation

of the head i. 16S

Eyeball, muscles of i. 345

Face, motor points of i. 379

muscles of i. 363

nerves of i. 3S5

sensory nerves of .. .. ..i. 391

Face, universal progressive atrophy of . .i. 570
history i. 570

PAGE.

Face, universal progressive atrophy of :

etiology, symptoms i. 571

pathology i. 574

diagnosis, prognosis i. 575

treatment i. 576

Facial nerve i. 338

accessory nuclei of 47

diagram of i. 362

diseases of i. 361

paralysis of i. 368

etiology i. 368

symptoms i. 370

course i. 375

diagnosis i. 376

prognosis i. 378

treatment i. 378

Facial nerve, deep origin and surface

attachment i. 287

spasm in area of distribution of i. 361

symptoms i. 364

course, prognosis, diagnosis . .i. 366
morbid anatomy and patho-
logy i. 366

treatment i. 366

False neuroma i. 302

varieties of i. 302

False projection i. 352

Faradic irritability .. i. 123

Faradisation i. 270

varieties of i. 270

Faradism i. 269

methods of application of .. ..i. 269

Fascial reflexes i. 153

Fasciculus ouneatus 61

Fasciculus gracilis 61

Feelings 481

Febrile and post-febrile nervous disorders

953, 975

morbid anatomy and physiology . . 978

diagnosis, prognosis 979

treatment 980

Febrile diseases, acute, paralysis of . . 978

Femoral neuralgia i. 501

diagnosis, treatment i. 502

Femoral region, muscles of . . i. 505, i. 507

Fibrillary contractions i. 130

Fibroma i. 302, 373, 403

Fibro-sarcoma 403

Field of vision, alterations in i. 316

test of i. 317

Fifth nerve i. 338

deep origin and attachments of . .i. 2S5
diagram of 1st division of .. ..i. 344

of 2nd division of i. 392

of 3rd division of i. 392

diseases of . . i. 3S4

functions of i. 3S4

ganglion of i. 2S5

Fifth nerve, anaesthesia of i. 3S6

Bymptoms, diagnosis i. 386

treatment i. 3S7

Fifth nerve, neuralgia of i. 3S7

etiology i. 387

symptoms i. 3SS

varieties i. 390

course, diagnosis i. 395

treatment i. 396

Fifth nerve, neuralgia of the first branch

of i. 390

of the 2nd division of i. 892

of the 3r,d division of i. 394

treatment i. 396

Fifth nerve, paralysis in the region of

distribution of i. 402

etiology i. 402

symptoms i. 403

diagnosis, prognosis, treatment ..i. 408
Fifth nerve, spasm in the region of dis-
tribution of i. 400

INDEX.

987

PAGE.

Fifth nerve, spasm In the region of dis-
tribution of :

etiology, diagnosis i. 401

prognosis, treatment i. 402

Fifth nerve, trophic affections in the

territory of i. S9S

Flexors of the leg, spasms of i. 512

treatment i. 512

Flexor communis diidtorum pedis, para-
lysis of i. 529

Flexor pollicis longus, paralysis of . . . .i. 529

Foot, sole of i. 512

Forced movements i. 102

Forearm, muscles of . . i. 480, i. 4S4, i. 485

surface of i. 490, i. 491

Formatio reticularis . . . . 35, 36, 5G, 6S, 09

Formication i. 105

Fornix 433, 407

Fourth nerve, origin and attachment of.i. 2S5

Fractures, spontaneous i. 224

Framework of spinal coid, composition

of 6

Franklinisation i. 26S

varieties of i. 269

Franklin ism i. 269

Frictions, external i. 267

Functions of the cortex of the cerebrum.i. 478

experimental determination of . .i. 488
Functions, the cortical ideational area . . 486

experimental determination of . . 497
Functions of the cortical motor centres

483, 484

experimental determination of . . 488
Functions of the sensory cortical centres

482, 483

experimental determination of . . 494
Fundus of the eye, ophthalmoscopic

appearance of i. 312

Furrowed band 413

Gait, ataxic 211

hemiplegic 581

spasmodic 251

Galvanic excitability i. 123

Galvanisation i. 273

varieties of i. 273

Galvanism i. 272

methods of application of . . . .i. 273

Ganglion-cells i. 19, 8

apolar i. 19

Beale's i. 21

bipolar i. 19

caudate i. 19

multipolar i. 19

spherical i. 19

Ganglion -cells, morbid changes of,

atrophy of 84, 85

colloid degeneration of 85

hypertrophy of 84

nucleus, multiplication of . . . . 84
pigmentary degeneration of . . . . 85

shrinking of 84

vacuolation of 84

Ganglion-cell groups, longitudinal dis-
tribution of in the spinal cord 31
Ganglion-cell processes, branched . J. 19, i. 20

twisted i. 21

unbranched i. 19, i. 20

Gasserian ganglion i. 285, i. 3;i8

Gastralgia i. 588

Gastric branches of the., vagus, anajs-

thesia of i. 117

Gastric plexus, neuroses of . . i. 433, i. 588

Gastrodynia neuralgica i. 588

General convulsions, theory of. . . . . .i. 294

General diagnosis i. 241

General etiology i. 73

General morbid anatomy i. 2i3

General morbid physiology i. 233

PAGE.

General pathology i. S

General prognosis i. 246

General symptomatology i. 79

Giant-ceUs 452

Girdle sensation i. 108

Glands, trophoneuroses of i. 227

of the digestive tract, tropho-
neuroses of i. 227

of the genito-urinary apparatus, .i. 230

lachrymal i. 228

salivary L 227

of the skin i. 218

Glaucoma simplex i. 399

Glioma i. 302, 372, 373, 553

Glossopharyngeal nerve i. 338

diagram of i. 337

origin and attachment of . . . . i. 288

Glossoplegia i. 382

etiology, symptoms i. 382

diagnosis, prognosis, treatment ..i. 383

Glossy skin i. 212

Glottis, spasm of i. 419

etiology, predisposing causes ..i. 416

occasional causes i. 420

pathology, symptoms i. 420

concomitant symptoms i. 421

course, diagnosis i. 421

prognosis, treatment i. 422

Glottis vocalis i. 413

Glottis respirafuria i. 413

Gluge's corpuscles 86

Gluteal region, muscles of.. . . i. 506, i. 507

Glycosuria i. 191

Goll, columns of i. 55, 33, 60, 61

functions of 83

Graphospasms i. 464

paralytic form, symptoms .. ..i. 466

spastic form, symptoms i. 465

tremulous form, symptoms . . . .i. 465

varieties i. 466, i. 467

etiology i. 467

diagnosis, prognosis, treat-
ment i. 468

Gratiolet, optic radiations of . . . . i. 51, 459

Graves' disease i. 560

etiology, symptoms i. 561

morbid anatomy i. 565

morbid physiology i. 566

diagnosis, prognosis, treatment ..i. 569

Grey degeneration i. 234

Grey matter, composition of 8

of the cerebellum 413

of the cerebrum 448-458

of medulla oblongata, superadded. 50

Grey substance i. 35

of the cerebrum 448-458

of the encephalon i. 48

of the medulla oblongata . . . . 33-50

of the spinal cord 8, 21-23

development of 22-31

rearrangement of 33-37

resistance to disease of 87-92

Growth i. 9

reproduction and action, antago-
nism between i. 12

Gumma . . i. 302, 337, 557

Gustatory nerves, anaesthesia of .. ,.i. 341

diseases of i. 336

distribution of i. 339

hyeraesthesia of i. 340

parassthesia of i. 341

Gymnastics, Swedish i. 268

Hsematomyelia 321

Haamatomyelitis 285

symptoms 285

Hasmatorrhachis 381

etiology 38]

symptoms 382

988

INDEX.

PAOE.

Hajmatorrhachis :

varieties 382

oourse, diagnosis, prognosis . . . . 883

treatment 884

Itfemidrosis i. 220

Haemorrhage into the substance of the

cerebellum 671

Hemorrhage into the substance of the

cerebrum 525

Haemorrhage into the medulla oblongata 327
Haemorrhage into the spinal cord . . . . 321
Haemorrhage of the intracranial meninges 343
Haemorrhage of the spinal meninges . . 381
Hsemorrhagic internal spinal pachy-
meningitis 386

definition, etiology 386

symptoms 889

morbid anatomy 390

treatment 390

Hair, trophic disorders of i. 216

Hand, muscles of i. 363

spasm of interosseous muscles of. .i. 391

Head, muscles of i. 363

Head, sensory nerves of i. 391

Headache i. 543

varieties of i. 544

Healthy muscle, structure of i. 201

Heart, accelerator nerves of i. 181

disorders of the rhythm of .. ..i. 181
inhibitory mechanism of . . . .i. 179

innervation of i. 179

reflex mechanism of i. 179

Hameralopia i. 319

Hemianaesthesia- i. 100

cerebral 582

morbid anatomy 583

Hemianaesthesia, hysterical 871

Hemianopsia i. 319

varieties of i. 320

Hemiataxia 581

Hemiatrophia facialis progressiva .. ..i. 570

Hemicrania i. 547

etiology i. 547

symptoms i. 549

varieties i. 551

courses, diagnosis i. 552

morbid anatomy and physiology, .i. 553

treatment i. 556

Hemiopia i. 319

Hemiparaplegia spinalis 361

Hemiplegia i. 121, 538, 599

alternate 669

facialis i. 368

spinalis 361

Hemiplegia, spastic, of infancy . . . . 576

Hemiplegic walk 581

Hemispasm 569

Hepatalgia i. 590

Hereditary predisposition i. 73

Herpes i. 209

zoster i. 398

Heterotopia of brain substance . . . . 709

Hiccough i. 447

Hip, spastic contracture of i. 504

Hippus i. 348

Histrionic facial spasm i. 361

Hydrate of chloral i. 25S

Hydrocephaloid disease 689

Hydrocephalus, acute 754

etiology 754

symptoms 754

course, duration, and terminations 761

morbid anatomy 762

morbid physiology 767

diagnosis . . . .' 768

prognosis 769

treatment 769

Hydrocephalus, chronic 770

definition 770

PAOE.

Hydrocephalus, chronic :

etiology 770

symptoms 771

course, duration, and terminations 772

morbid anatomy 773

morbid physiology 773

diagnosis 773

prognosis 774

treatment 774

Hydrophobia 855

definition 855

etiology 855

symptoms 855

course, duration, and terminations 855

morbid anatomy 858

morbid physiology 862

diagnosis 863

treatment 864

Hyperaesthesia i. 83

Hypalgesia i. 84

Hyperacute central myelitis 284

Hyperaemia i. 2^4

local, of the skin i. 188

Hyperaemia of the brain 693

of the medulla oblongata . . . . 327

of the nerves i. 292

of the spinal cord 317

of the spinal membranes . . . . 317

Hyperesthesia • ..i. 83

auditory i. 334

cutaneous i. 102

cutaneous thermo i. 103

muscular i. 110

olfactory i. 304

Hyperaesthesia, distribution of .. ..i. 103

Hyperassthetic spots i. 104

Hyperakusia i. 334

Hyperalgesia i. 83

auditory i. 334

cutaneous i. 104

muscular L 110

olfactory i. 307

visceral i. 113

Hyperidrosis i. 218

unilateral . . '. i. 548

Hyperkineses, professional i. 464

Hyperkinesis i. 86

reflex i. 137

theory of i. 305

Hyperkinesis of voluntary muscles . .i. 130

varieties i. 130

concomitant symptoms i. 133

consecutive symptoms i. 134

painful points i. 134

Hyperosmia i. 307

Hyperpselaphesia i. 102, i. 551

Hypertony i. 17S

Hypertrophic internal spinal pachy-
meningitis . . 886

definition, etiology 386

symptoms 3S7

morbid anatomy 389

treatment 390

Hypertrophy, neurotic i. SS

of the brain 706

of the nerves i. 301

Hypnotism 903

Hypogastric plexus, neuroses of .. ..i. 591
Hypoglossal nerve, accessory nuclei of . . 4S

diagram of i. 3S1

origin and attachment of . . . .i. 2S9

Hypoglossal nerve, diseases of i. 380

Hysteria S65

etiology S65

symptoms S67

course, progress, and terminations S91
morbid anatomy and physiology. . S92

diagnosis S94

prognosis 8S6

INDEX.

989

PAGE.

Hysteria :

treatment 896

Hysterical aphonia i. 428

attacks 889

paralysis 873

Hysterical paraplegia 344

Hystero-epileptic attacks 927

Idio-niuscular contraction i. 120

Im potency i. 118

Individual motor mechanisms :

elementary affections of .. ..i. 119
Individual sensory mechanisms :

elementary affections of i. 92

Infancy, spastic hemiplegia of 576

Infantile spinal paralysis 106

Inferior extremities, diffused spasm of. .i. 423

treatment i. 423

Inferior maxillary nerve, diagram of ..i. 393
Inferior obliquus ocali, paralysis of . .i. 355
Inferior rectus oculi, paralysis of . . . .i. 354

Inflammation i. 234

infra-maxillary neuralgia i. 394

Inf ra-orbital neuralgia i. 394

Inhibitory mechanism of the heart . .i. 179

disturbances of i. 180

Insane, osseous lesions in the i. 227

Inspiratory spasm i. 449

Insular sclerosis, see sclerosis, multiple . . 801

Intellectual sensations i. 81

Intermittent tremor 579

Intermittent spinal paralysis 343

morbid physiology, diagnosis . . 344

Internal capsule 43S, 457

fibres of 459

lesions of 508

Internal con vulsious i. 419

Internal organs, sensory affections of . .i. 113
Internal rectus oculi, paralysis of . . . .i. 354

Internal remedies i. 254

Interosseous muscle, attachment of ..i. 462

Intracranial aneurisms 557

Intracranial cerebral haemorrhage . . . . 525
definition, history, etiology . . . . 525

symptoms 529

morbid anatomy 535

prognosis 537

treatment 539

Intracranial circulation, morbid altera-
tions of 501

Intracranial meningeal haemorrhage . . 543

definition, etiology 543

symptoms 544

morbid anatomy 545

prognosis, treatment 546

Intracranial new formations, varieties of 553

Intracranial tumours 547

definition, etiology 547

symptoms 548

morbid anatomy 553

varieties 653

morbid physiology 558

grouping of the symptoms . . . . 559

diagnosis 562

diagnosis of the nature of the

tumours 564

prognosis 566

treatment 566

Intracranial parasites 558, 564, 565

Intracranial vessels, occlusion of .. .. 511
Inward rotators of upper arm, paralysis

of i. 471

Iodide of potassium i. 259

Iridoplegia i. 356

Irritable testis i. 230

Irritability i. 80, i. 30

faradic i. 123

Irritation, local i. 78

spinal 332

PAOK.

Joints, nutritive affections of i. 222

Kinesioneuroses i. 85, i. 91

external i. 119

vascular i. 182

visceral i. 176

Koiliker, central grey nucleus of . . . . 7, 8

Labyrinthine impressions, disorders of. .i. 156
Lachrymal glands, trophoneuroses of . .i. 228

Lancisi, nerves of 428

Landry's paralysis 264

Larynx, muscles of i. 413

view of . . i. 414, i. 415, i. 424, i. 425
Laryngeal branches of the vagus, anaes-
thesia of i. 117

paralysis of i. 423

etiology, symptoms i. 423

diagnosis i. 428

prognosis, treatment i. 429

Laryngeal muscles, actions of i. 413

bilateral paralysis of i. 425

unilateral paralysis of i. 425

mixed paralysis i. 425

phonetic paralysis i. 427

respiratory paralysis i. 426

clonic spasm of i. 416

tonic spasm of i. 419

Laryngeal nerves, diseases of i. 413

Laryngismus stridulus i. 419

Larynx, akineses of i. 418

anaesthesia of i. 418

hyperassthesia of i. 418

hyperkineses of i. 418

paraesthesiae of i. 418

parakineses of i. 418

paralysis of i. 423

sensory affections of i. 41S

Latent lesions 634, 640

Lateral columns, crossing of 33

Lateral cutaneous nerve of the thigh,

neuralgia of i. 501

Lateral sclerosis 251

amyotrophic, symptoms . . . . 256

combined 258

primary 251

definition, etiology 251

symptoms 251

course 256

secondary 259

morbid physiology, diagnosis . . 262

prognosis, treatment 263

Lateral ventricles 432

haemorrhage into 655

Late rigidity 570

Latissimus dorsi, paralysis of i. 471

Laughing fits i. 450

Law of muscular contraction i. 124

Left arm, surface of i. 487, i. 488

Leg, muscles of .. .. i. 527, i. 528, i. 529
Leg, spasm of the anterior muscles of . .i. 522

Leg, spasm of the flexors of i. 522

Leg, surface of . . i. 530, i. 531, i. 532, i. 533

Lenticular nucleus 436, 450, 466

lesions of 643

Lepra anaesthetica i. 213

Lepra nervorum i. 10-i

Leptomeningitis infantium 751-

symptoms 751

course and duration 753

morbid anatomy 753

prognosis and diagnosis 754

Leptomeningitis spinalis acuta .. .. 391

etiology, symptoms 39L

course, morbid anatomy . . . . 393

morbid physiology 35*4

diagnosis, prognosis 395

treatment 396

Leptomeningitis spinalis chronica . . . . 396

990

INDEX.

PAOE.

Leptomeningitis spinalis chronica :

etiology 396

symptoms 397

course, morbid anatomy, diagnosis 398

prognosis, treatmeut 899

Lesions of the nervous system, classifi-
cation of i. 233

Lesions according to the alteration of

function i. 237

depressive i. 237

destroying i. 237

discharging i. 237

irritative i. 237

Lesions according to their form .. ..i. 235

circumscribed i. 235

focal i. 235

diffused i. 235

histological i. 236

molar i. 236

molecular . .i. 236

systematic i. 236

Lesions according to their nature . . . .i. 234

compressive i. 235

degenerative i. 234, i. 245

inflammatory i. 234, i. 245

neoplastic i. 245

toxic i. 235

traumatic i. 234

vascular i. 234, i. 244

Lesions according to their situation . .i. 241

encephalic i. 243

peripheral i. 241

spinal i. 242

Lesions of the reflex mechanism . . . .i. 136

localisation of i. 138

Leucoderma, partial i. 212

Levator anguli scapulae, paralysis of . .i. 471

Levator palati, paralysis of i. 407

Levator palpebree superioiis, paralysis of i. 353

spasm of i. 346

Ligameutum denticulatum 5

Lightning pains i. 105

Lipoma 557

Liver, neurotic enlargement of . . . .i. 192
Living matter, fontamental properties of i. 5

Local irritation i. 78

Locality, test of the sense of i. 95

Locomotor ataxia i. 157, i. 223

symptoms i. 157, i. 223

causes . . . . i. 158, i. 224

Locomotor ataxy, progressive 211

definition, liistory 211

etiology 212

symptoms 215

varieties 235

course 236

morbid anatomy 237

morbid physiology 242

diagnosis 244

prognosis 245

treatment 246

Locus niger 449

Lordosis 115

Lower extremity, cutaneous nerves of . .1 515

Lumbar neuralgia i. 499

etiology i. 499

Lumbar plexus, diagram of i. 500

diseases of i. 493, i. 499

Lumbo-abdominal neuralgia i. 499

Luys, superior olive of 50

Lymph-space, sub-arachnoidal . . 5, 410
sub-dural 5, 410

Maculae cerebrales i. 189

Main en griffe i. 486

Malformations of spinal cord 97

Massage i. 267

Masticatory paralysis i. 402

etiology i. 402

PAOE.

Masticatory paralysis, symptoms .. ..i. 403

Masticatory spasm i. 400

etiology, diagnosis i. 401

prognosis, treatmeut i. 402

MaBtodynia i. 495

treatment i. 490

Mechanical contractility i. 120

Mechanical excitability i. 129

Medulla oblongata 411

accessory nuclei of 47

functions of 70

grey substance of 33, 51

morbid anatomy of 84

special nuclei of 49

structure of 6

superadded grey matter of . . . . 50

view of i. 286, L 288

white substance of 51 — 70

Medulla oblongata, anaemia of . . . . 313

Medulla oblongata, embolism of .. .. 313

symptoms 314

varieties 314

morbid anatomy 315

diagnosis 316

prognosis, treatment 317

Medulla oblongata, hemorrhage of . . y_'7

symptoms 327

cause 329

morbid anatomy, diagnosis . . .. 330

prognosis, treatment 331

Medulla oblongata, hyperaemia of .. .. 327

Medulla oblongata, necrotic softening of. 313

Medulla oblongata, sloiv compression of. 351

etiology 352

symptoms 353

varieties of symptoms 356

cause . . 357

. morbid anatomy 357

diagnosis 359

prognosis, treatment 360

Medulla oblongata, thrombosis of .. .. 313

symptoms 314

varieties 314

diagnosis 316

prognosis, treatment 317

Medulla oblongata, tumours of . . . . 372

■varieties 372

etiology 373

symp'.oms 374

localisation of tumour 376

cause 379

■ diagnosis, prognosis, treatment . . 380

Medulla oblongata, wounds of 346

etiology .'. 346

symptoms 349

morbid anatomy 350

cause 351

diagnosis, prognosis, treatment . . 351

Melanoma, multiple fibrous 403

Meniere's disease S30

definition 830

etiology S30

symptoms S30

course, duration, and terminations S32

morbid anatomy and physiology . . 832

diagnosis and prognosis 832

treatment S3S

Meningeal apoplexy 3S1

Meningeal haemorrhage 548

Meningitis, basilar :

etiology 774

symptoms 775

course, duration, and terminations 770

morbid anatomy 777

diagnosis 777

prognosis "77

treatment 777

Meningitis of the convexity of the brain 77S

etiology 778

INDEX.

991

PAGE.

Meningitis of the convexity of the brain :

symptoms .' . . 778

course, duration, and terminations 782

morbid anatomy 78'2

diagnosis 783

prognosis 783

treatment 784

Meningitis, epidemic cerebro spinal .. 88+

definition 834

history 834

symptoms 835

coarse and duration 838

complications and sequelae . . . . 838

morbid anatomy 839

morbid physiology 840

diagnosis and prognosis 840

treatment 841

Meningitis, metastatic 784

etiology 784

symptoms 784

varieties 785

morbid anatomy 785

diagnosis, prognosis, and treatment 7S5

Meningitis, traumatic 786

etiology 7S0

symptoms 780

course, duration, and terminations 7S8
morbid anatomy and physiology. . 788

diagnosis and prognosis 789

treatment 789

Meningitis, tubercular, see hydrocephalus,

acute 754

Mercurial preparations i. 260

Mercurialism 961

symptoms 961

treatmeut 9 2

Middle commissure 449

Migraine i. 547

Mimic convulsion i. 361

Mimic facial paralysis i. 368

Mixed cranial nerves, diseases of . . . . 384

Mogigraphia i. 464

Monospasms 594

varieties of 595

cortical 594, 595

Mons Veneris, neuralgia of i. 503

Morbid nervous structures and functions,

relations between i. 237

Motor apparatus, methods of examining 119

general examination 119

special examination 120

Motor arresting pressure points .. . J. 134
Motor cranial nerves, diseases of .. ..i. 344
Motor exciting pressure points .. ..i. 134
Movement of the heart, regulating ner-
vous centres of i. 179

Movements, automatic i. 8, i. 85

reflex i. 85

spontaneous i. 8

voluntary i. 85

Multiple sclerosis, see sclerosis, multiple 801

Muscle, healthy, structure of i. 201

Muscles, atrophy of i. 204

with nuclear proliferation .. . .i. 205

Muscles, cirrhosis of i. 132, i. 206

Muscles, electrical examination of.. ..i. 124

Muscles of the arm, spasm of i. 463

Muscles of the calf, spasm of i. 523

Muscles of the eyeball i. 345

attachments and axis of rotation i. 346
Muscles of femoral region .. .. i. 505, i. 507
Muscles of gluteal region . . . . i. 506, i. 507
Muscles of inspiration, paralysis of . .i. 451

varieties i. 451

symptoms i. 454

diagnosis, treatment i. 455

Muscles of larynx i. 413

actions of i. 413

Muscles of leg . . . . i. 527, i. 528, i. 629

PACK.

Muscles moving the soft palate .. ..i. 404

actions of i. 406

Muscles moviug the soft palate, paralysis

of i. 407

diagnosis, prognosis, treatment ..i. 40'.i
Muscles of the pharynx .. .. i. 409, i. 410

actions of i. 410

Muscles of the thumb, insertion of . . ..i. 462

Muscles of the trunk i. 470, i. 472

Muscles, paralysed, histological changes

in i. 204

Muscles.rolative immunityof to paralysis i. 165
relative liability to convulsion . .i. 165
Muscles supplied by the circumflex nerve,

paralysis of i. 478

Muscles supplied by the crural nerve,

paralysis of i. 506

Muscles supplied by the hypoglossal

nerve, paralysis of i. 382

spasm of i. 382

Muscles supplied by the gluteal nerve,

paralysis of i. 507

Muscles supplie 1 by the median nerve,

paralysis of i. 484

Muscles supplied by the musculo cutane-
ous nerve, paralysis of . . . . i. 479
Muscles supplied by the nmsculo-spiral

nerve, paralysis of i. 481

Muscles supplied by the obdurator nerve,

paralysis of i. 507

Muscles supplied by the sciatic nerve,

paralysis of i. 5'2t>

etiology, symptoms i. 526

diagnosis, prognosis i. 532

treatment i. 533

Muscles supplied by the sciatic nerve,

spasm of i. 522

treatment i. 523

Muscular anaesthesia i. 110

Muscular contraction, law of i. 124

Muscular fibre, composition of i. 201

development of i. 203

Muscular fibre, striped i. 201

termination of nerves in . . . .i. 203

Muscular hyperesthesia i. llu

Muscular hyperalgesia i. 110

Muscular neuralgia i. 110

Muscular sense i. )09

tests for i. lo9

Muscular sensibility i. 109

tests for i. 109

Muscular sensory disturbances .. ..i. 109

Muscular trophoneuroses i. 201

Muscular tension i. 132

Mydriasis paralytica i. 355

Myelitis, diffused, acute 272

definition, etiology 272

symptoms 273

course 278

morbid anatomy 279

morbid physiology 2S3

varieties 284

diagnosis 288

prognosis 290

treatment 291

Myelitis, diffused, chronic 292

definition, etiology 292

symptoms 293

course 295

morbid anatomy 296

morbid physiology 298

varieties 20S

diagnosis, prognosis, treatment .. 305

Myelomalacia 308

symptoms, morbid anatomy . . 3u8
morbid physiology, diagnosis .. 308

treatment 3u9

Myoneuralgia i. 110

Myopathic contracture i. 132

992

INDEX.

PAOH.

Myosis i. 122

paralytica ' i. 350

spastica i. 848

Myxo-glioma 873

Myxoma i. 302, 554

Myxo-sarcoma 373

Naevi pigmentosi i. 212

Nails, trophic disorders of i. 210

Neck, muscles of i. 470

Nerve-centres, fusion of i. 45

Nerve degeneration i. 194

theory of i. 199

Nerve-fibres, axis-cylinder of i. 22

connective tissue cells of .. ..i. 25

elementary fibrils of i. 21

Kanviei's nodes of i. 24

Nerve-fibres, afferent i. 30, i. 281

arciform 02

arcuate 34, 01, 02

centrifugal i. 41

centripetal i. 41

commissural i. 41

efferent i. 40, i. 281

of grey matter 8

intercentrai i. 41

medullated i. 22

motor i. 41

non-medullated i. 22

secretory i. 41, i. 87

trophic i. 41, i. 87

varicose i. 24

of white matter 9

Nerve-fibres, alterations in i. 190

Nerve-fibres, functions of i. 29

structure of i. 282

Nerve functions, general theory of . . ..i. 33

Nerve regeneration .. i. 195

Nerve stretching i. 278

Nerves, atrophy of .. .. , i. 299

idiopathic • i. 299

secondary i. 299

symptoms, prognosis, treatment, .i. 300

Nerves, congestion of i. 292

Nerves, cranial, origin and attachments

of i. 283-i. 291

places of exit of i. 555

Nerves diseases, causes of i. 73

predisposition to i. 73

Nerves, electrical examination of .. ,.i. 124

Nerves, hypersemia of- 1 292

symptoms i. 292

Nerves, hypertrophy of i. 301

Nerves, inflammation of i. 292

etiology .. i. 293

symptoms i 293

course i. 295

morbid anatomy i. 290

diagnosis i. 297

prognosis, treatment i. 298

Nerves, neoplastic formations in . . . .i. 301
Nerves of special sense, diseases of. . . .i. 300
Nerves of the upper extremity, paralysis

of . i. 4S9

Nervous asthma i. 429

symptoms .. i. 430

prognosis, pathology, treatment . . i. 43 1
Nervous lesions, classification of .. . .i. 233
Nervous system, accessory portion of . . i. 08

construction of a i. 42

fundamental portion of i. 08

law of dissolution of i. 71

law of evolution of i. 70

Nervous tissues, compression of . . . .i. 235

construction of . . i. ^5

degeneration of i. 234

Neuralgia i. Si, i. 100

general symptoms . . . . i. S4, i. lOo
painful points i. 107

PAGE.

Neuralgia :

points apophytaire i. lOSj

concomitant sensory symptoms . .i. 108
various symptoms i. 108

Neuralgia, ano-vesicalis i. 504

cervico-brachialis i. 455

cervico-occipitalis i. 443

Neuralgia, coiliaca i. 588

cruralis i. 502

Neuralgia, dorso-intercostalis i. 493

etiology i. 493

symptoms L 494

diagnosis i. 495

treatment i. 490

Neuralgia, epileptiform L 395

Neuralgia, femoralis i. 601

Neuralgia, gastrica i. 588.

diagnosis j. 589

prognosis, treatment i. 590

Neuralgia hepatica '. . i. 590

symptoms, treatment L 590

Neuralgia, hypogastric 1 i. 531

infra-maxillaris L 394

infra-orbitalis i 394

Neuralgia ischiadica L 509

etiology i. 509

Bymptoms i. 513

course, diagnosis i. 510

prognosis i. 517

treatment i. 519

Neuralgia lumbaris i. 499

etiology, symptoms i. 499

Neuralgia lumbo-abdominalis i. 499

Neuralgia mesenterica i. 585

etiology, symptoms i. 585

pathology i. 580

treatment i. 587

Neuralgia montis veneris i. 503

muscular L 110

obturator i. 502

ophthalmica i. 390

penis i 503

phrenica i. 445

plantaris i. 517

pudendo hsemorrhoidalis . . . i. 503

scrotalis i. 504

spermatica i. 504

supra-m axillaris i. 392

supra-orbit;dis L 391

Neurasthenia spinalis 335

Neurectomy i. 277

Neuritis i. 292

acute i. 293

symptoms i. 293

chronic L 293

symptoms i. 294

course i. 295

morbid anatomy i. 290

diagnosis i. 297

prognosis, treatment i. 29S

Neuritis nodosa i. 295

Neuroglia 0, 7, S, 9

composition of 6

development of 29

distribution of 7

morbid alterations of 86

Neuromata L 301

true i. 301

myelinicum i. 302

amyelinicum i. 302

false i. 302

varieties of i. 302

etiology i. 303

symptoms i. 304

diagnosis, prognosis, treatment . .i. 305

Neuro-paralytic ophthalmia i. 400

Neurotic atrophy i. S9

dystrophies i. 89

paratrophies i. 89

INDEX.

I'AOE.

Neurotic hypertrophy i. 88

Neurotomy i. 277

New formations i. 246

Ninth nerve i. 838

diagram of i. 387

origin and attachment of . . . . i. 287

Nucleus i. 9

Nucleus eaudatus 432, 434

lesions of 645

Nucleus lenticularia 436, 450

Nyctalopia i. 319

Nystagmus i. 347

etiology, treatment i. 348

Obturator neuralgia i. 502

Obliquus inferior oculi, paralysis of ..i. 355

Occipital lobes, lesions of . . 634

Ocular muscles, paralysis of i. 849

general remarks i. 349

general etiology i. 350

general symptoms i. 350

course i. 357

Ocular muscles, progressive paralysis of,

see Ophthalmoplegia externa i. 360

Ocular muscles, spasms of i. 345

Ocular nerves i. 338

diseases of i. 344

Oculo-motorius, origin, and attachment

of i. 285

paralysis of i. 352

incomplete i. 353

Oesophageal muscles, paralysis of . . . .i. 409

plexus, diseases of i. 404

OZsophagismus i. 114

(Esophagus, paralysis of i 412

Olfactory anaesthesia i. 308

hyperesthesia i. 307

hyperalgesia i. 307

Olfactory lobe 462

Olfactory nerve, diseases of i. 306

origin and attachments of . . . .i. 283

Olivary body 50, 62

superior 50

Onanism i. 75

Operculum 417

Ophthalmic neuralgia i. 390

Ophthalmoplegia externa i. 360

symptoms i. 360

morbid anatomy i. 361

prognosis, treatment i. 361

diagnosis, prognosis i. 358

treatment i. 359

Opium i. 257

Oppression, feeling of i. 116

Optic anaesthesia i. 313

symptoms i. 315

Optic anaesthesia, partial . .i. 319

Optic commissure and tracts, diseases of.i. 319

symptoms i. 319

Optic hyperaeathesia i. 313

Optic hyperalgesia i. 313

Optic lobes 50, 439

lesions of 649

view of i. 284

Optic nerve, atrophy of . . . . i. 323, i. 328

simple i. 329

secondary i. 329

by compression i. 329

symptoms i. 329

to optic neuritis i. 330

to obliteration of vessels ..i. 331
to choroido-retinitis .. ..i. 331
to retinitis pigmentosa .. ..i. 331

by excavation L 331

morbid anatomy, course, prog.

nosis i. 332

treatment i. 333

Optic nerve, diseases of i. 322

simple congestion of i. 324

1'ACIK.

Optic norve, structure of i. 310

Optic neuritis i. 322

etiology i. 322

varieties i. 323

symptoms j. 324

general symptoms .. * i. 326

morbid anatomy i. 326

. treatment i. 328

Optic radiations of Gratiolet .. .. i. 51, 459

lesions of 582

Optic thalami 437, 449, 466

Optic tract 415, 461

chiasma of.. .. ■ i. 284

origin and attachment of . . . .i. 283

vessels of i. 284

Oscedo i. 450

Osmidrosis ... ... i. 219

Osseous lesions in the insane i. 227

Osseous trophoneuroses i. 222

of central origin i. 225

of peripheral origin i. 222

of spinal origin i. 223

Osteoma 403, 557

Osteoneuralgia i. 112

Outward rotators of the upper arm,

paralysis of i. 471

Ovarialgia i. 592

Ovarian hypersesthesia i. 592

Pacchionian bodies 410

Pachymeningitis cerebralis externa . . 743

etiology 743

symptoms 744

nioroid anatomy 744

prognosis, treatment 745

Pachymeningitis cerebralis interna hse-

morrhagica 745

etiology 745

symptoms 745

varieties 747

course and duration 748

morbid anatomy 748

prognosis 750

treatment 750

Pachymeningitis spinalis externa . . . . 384

etiology, symptoms 384

course, morbid anatomy . . . . 385
diagnosis, prognosis, treatment . . 386
Pachymeningitis, spinalis interna hae-

morrhagica 386

symptoms 389

morbid anatomy, treatment . . .. 390
Pachymeningitis spinalis interna hyper-

trophica 386

definition, etiology 386

symptoms .. 387

morbid anatomy 389

treatment 390

Painful points .i. 107

Pains i. 81

Palate, muscles of i. 404, i. 406

Palato-pharyngeus, paralysis of .. ..i. 480

Papilloma 555

Para-anaesthesia, cutaneous i. 99

Paradoxical contraction 225

Paraesthesia i. 84

Paralgesia i. 84

cutaneous i. 105

visceral i. 113

Paralysed muscles, morbid changes in . .i. 178
Paralysed parts, associated movements of.i. 163

Paralysis ascendens acuta 204

Paralysis agitans 791

etiology 79!

symptoms 791

morbid anatomy 797

morbid physiology 793

diagnosis 800

prognosis 800

LLL

994

INDEX.

PAOE.

Paralysis agitans, treatment 800

Paralysis, relative immunity of some

muscles to i 164

Paralytic contracture i. 132

Paraplegia .'. i. 121

Paraplegies dyscrasiquos 311

Parasites, intracranial i 557

Paratrophy, neurotic i. 80

Parolivary body 50

Partial optic anaesthesia i. 319

Partial senaory paralysis i. 97

varieties of i. 100

Partial sensory paralysis i. 97

varieties of i. 100

Passive cerebral congestion 695

Patellar-tendon reflex i. 141

abolished . . . .i. 144

diminished i. 144

exaggerated i. 146

Pathic channels i. 92

Pectoralis major, paralysis of i. 470

minor, paralysis of i. 470

Peduncles of the cerebellum, connections

of 61

lesions of 670

Peduncles of the cerebrum, lesions in . . 669

Peduncular fibres, lesions of 561

Pemphigus i. 211

Penis, neuralgia of i. 503

Peri-ependymal myelitis i. 302

Peri-meningitis i. 384

Peri-myelitis 391

Perimysium i. 201

Peri-neuritis.. i. 296

Peri-osteal reflexes i. 158

Peripachymeningitis : 384

Peripheral facial paralysis i. 376

Peripheral nerves, automatic disturb-
ances of i. 156

diseases of i. 281

hypertrophy of i, 301

trophic affections of i. 193

Peripheral urinary paralysis 341

Peroneus brevis, paralysis of i. 528

longus, paralysis of i. 528

Pharyngeal muscles, actions of .. . .i. 410

paralysis of i. 409

Pharyngeal plexus, diseases of . . . i. 404

Pharynx, muscles of i 409, i. 410

Phonetic laryngeal paralysis, i. 423, i.424, i. 427

Phosphorus i. 260

Photopsia i. 313

Phrenic neuralgia i. 445

Pia mater, diseases of . . 1 751

Pia mater, cranial 410

spinal 4

Pianoforte players' spasm i. 406

Pigmentation of the skin, alterations in. i. 212

Pineal body 438

Plantar Neuralgia , i. 517

Pleasures •. i. 81

Pneumogastric nerve, diagram of . . . .i. 405

diseases of i. 404

origin and attachment of . . . .i. 2SS

Points apophysaire i. 108

douloureux i. 107

painful i. 107

pressure i. 134

Poliomyelitis anterior acuta 105

definition, history, etiology . . .. 105

infantium 106

symptoms 106

adultorum 116

symptoms 116

course 117

morbid anatomy 118

changes in the paralysed muscles 118
localisation in the anterior horns 127
morbid physiology 129

PAGE.

Poliomyelitis anterior acuta :

diagnosis 131

prognosis 132

treatment 133

Poliomyelitis anterior chronica . . . . 136
definition, history, etiology, symp-
toms 136

diagnosis 144

prognosis, treatment 145

Poliomyelopathies 105

Polysesthesia i. 102

Polydipsia i. 415

Polyphagia i. 117

Pons Varolii 411

arteries of 11

grey matter of 411

lesions of 661

special nuclei of 49

structure of 411

white matter of 411

Posterior and lateral combined sclerosis 258

symptoms 258

Posterior columns, grey degeneration of 211

sclerosis of 211

Posterior grey horns 8, 33, 44

development of 30

functions of 77

Posterior roots, functions of 77

Posterior root-zones . . . . L 55, 51, 57, 60

Post-hemiplegic chorea 574

Potassium bromide L 259

iodide L 259

Praefrontal cortical lesions 040

Prsehemiplegic chorea 573

Pressure, continuous i. 277

tests of sense of L 94

Pressure points L 134

Primary labio-glosso-pharyngeal paralysis. 173

definition, history 173

etiology, symptoms 174

course, complications, morbid

anatomy 181

diagnosis 184

treatment 185

Primary lateral sclerosis 251

definition, etiology, symptoms . . 251

spasmodic gait 252

course . . . ; 256

morbid anatomy 259

morbid physiology, diagnosis . . 262

prognosis, treatment 263

Primary neurotic contracture .. ..i. 133
Primary sclerosis of the columns of Goll.. 249

Primordial organisms i. 6

Professional hyperkineses i. 543

Progressive locomotor ataxy 211

definition, history 211

etiology 212

symptoms 215

ataxic gait 219

reflex action 224

occasional symptoms 225

paradoxical contraction . . . . 225

varieties 235

course 236

morbid anatomy 237

morbid physiology 242

diagnosis 244

prognosis 245

treatment . . 246

Progressive muscular atrophy 145

definition, history, etiology . . . . 145

symptoms 148

course 159

morbid anatomy 160

morbid physiology 16S

diagnosis 171

prognosis, treatment 172

Prophylaxis i. 250

INDEX.

995

PAGE.

Prosopalgia i. 36S

Protoplasm i. 7

Protospasms 595

PBammomiuu 557

Pseudo-hypertrophic paralysis . . . . 185

definition, history 185

etiology 186

symptoms 187

course 108

diagnosis 199

morbid anatomy 200

pathology 208

prognosis, treatment 210

Psychical actions, nature of 479

disturbances i. 78

states, classification of 480

Ptosis i. 353

Pulmonary plexus, neuroses of . . . . i. 429

Pyramid, nucleus of 50

Pyramidal column 61

Pyramidal tract . . i. 51, 58, 65-67, 462, 4S4

accessory portion of 68

functions of 83

lesions of 568

Pyrosis i. 113

Quadriceps extensor femoris, spasm of . .i. 505

Race, as predisposing to nervous diseases i. 75

Ranvier's nodes i. 24

Rectum, neuralgia of i. 592

Rectus externus oculi, paralysis of . .i. 357

spasm of i. 347

Rectus internus oculi, paralysis of. . . .i. 354

spasm of i. 347

Rectus superior oculi, paralysis of . . . .i. 353

Recurrent sensibility i. 281

Reeling i. 160

Reflex actions, time required for . . . .i. 136

varieties of i. 138

Reflex akinesis i. 137

hyperkinesis i. 137

Reflex mechanism of voluntary muscles,

disturbances of i. 136

Reflex mechanisms of the heart, disturb-
ances of i. 179, i. 180

Reflex movements i. 85

Reflex paraplegia 339-341

Reflexes, cutaneous, stimuli of .. . .i. 120

deep i. 140

fascial i. 153

periosteal i. 153

superficial i. 130

tendinous, stimuli of i. 120

Reil, island of 420

Remak, fibres of i. 22

Remedies i. 254

external i. 261

internal i. 254

Respiratory laryngeal paralysis . . i. 424, i. 427

Restiform body 62

Retro-bulbar neuritis i. 326

perineuritis i. 326

Rhomboidei, paralysis of i. 470

Rheumatic laryngeal paralysis .. ..i. 428

Rigidity, cerebellar i. 160

early 569

late 570

Rolando, fissure of 417, 426

grey tubercle of 61

substantia gelatinosa of 7

Rotation of he«d and neck i. 169

Sacral nerves, diagram of i. 510

Sacral plexus, neuralgia in the region of i. 509

Salaam convulsion i. 437

Salivary glands, trophoneuroses of. . . .i. 227
Saltatory spasm 341

PAGE.

8altatory spasm, treatment 342

Sarcolemma i. 203

Sarcoma '.. 802, 373, 557

Saturnine nervous diseases 955

symptoms 956

morbid anatomy 959

morbid physiology 960

diagnosis, prognosis 960

treatment 960

Scalp, nerves of i. 385

Schwann, sheath of i. 22

Sciatic nerve, paralysis of the muscles

supplied by i. 526

symptoms i. 526

diagnosis, prognosis i. 532

treatment i. 533

Sciatic nerve, spasm of the muscles sup-
plied by i. 522

treatment i- 523

Sciatica i. 509

etiology i. 509

anatomical changes i. 512

symptoms i. 513

course, diagnosis i. 516

prognosis i. 517

treatment i. 519

Sclerose lateral e amyotrophique . . . . 256
Sclerosis of the columns of Goll . . . . 249
Sclerosis of the direct cerebellar tract . . 250

Sclerosis, lateral 251

Sclerosis, multiple 305, 801

definition 801

history 801

symptoms 802

course, duration, and terminations 808

morbid anatomy 809

morbid physiology 810

diagnosis 812

prognosis 813

treatment . . . . » 813

Scotoma i. 316

scintillating i. 316

Secondary degenerations 93

after amputations 96

ascending 95

descending 95

distribution of 94

history of 94

Secondary lateral sclerosis 259

symptoms 259

Secondary myelitis 340

Secondary paraplegia 339

Secondary sclerosis of the columns of Goll 250
Secretory affections, eutaneous .. ..i. 217

Sensations, cutaneous i. 92

common i. 92

special i. 92

tactile i. 92

Sensations of temperature, tests of ..i. 96

Sense of locality, tests of i. 95

of pressure, tssts of i. 94

of sight, diseases of i. 310

functional affections of . . . .i. 313

Sense of smell, analgesia of i. 308

hyperaesthesia of i. 307

methods of testing i. 306

Sensibility, recurrent i. 281

Sensory apparatus, methods of examin-
ing .. .. i. 93

Sensory conduction, test of rapidity of . .i. 93

Sensory peduncular tract 459

lesions of 582

Sensory paralysis, partial i. 97

. varieties i. 98

total i. 97

Serratus magnus, paralysis of i. 473

symptoms i. 473

treatment i. 478

Seventh cranial nerve i. 338

996

INDEX.

PAGE.

Seventh cranial nerve :

accessory nuclei of 47

diagram of i. 362

diseases of . . . . i. 361

origin and attachments of . . . .i. 287

paralysis of i. 368

spasm in the area of distribution of.i. 361

Sex, as predisposing to disease i. 75

Sexual excesses .. ..i. 75

Sexual feelings, anaesthesia of .. . i. 117

Shoemakers' spasm i. 467

Sick headache i. 547

Silver salts i. 261

Singultus .. :i. 447

Sixth cranial nerve, origin and attach-
ments of i. 287

paralysis of i. 357

Skin, local ansemiaof i. 188

local hyperaemia of i. 188

sensory disturbances of i. 92

sensory paralyses of i. 97

Skin pigmentation, alterations in .. ..i. 212

Skull, areas of 424

contents of the areas of . . . . 426
landmarks on the surface of . . . . 424

Slow compression i. 76

Smell, hallucinations of i. 307

illusions of i. 308

Sneezing, attacks of i. 449

Soft palate, muscles moving the . . . .i. 404

actions of i. 406

Soft palate, paralysis of . . • i. 407

symptoms . . i. 407

diagnosis, prognosis i. 409

treatment . . . . i. 409

Soft palate, spasm of i. 407

Sole of foot i. 512

Spasmodic cough i. 450

Spasmodic spinal paralysis 251

Spasms • i. 130

clonic i. 130

symptoms i. 130

tonic i. 131

symptoms i. 131

concomitant symptoms i. 133

consecutive symptoms i. 134

pressure points i. 134

Spasmus inspiratorius . . . . '. . . i. 449

Spastic hemiplegia of infancy 576

Special sensations i. 92

Speech, disorders of 612

emissive department of 612

executive department of . . . . 615

mechanism of 629

Sphincter iridis, paralysis of i. 355

spasm of i. 348

Spina bifida 404

definition 404

symptoms , . 405

diagnosis 406

piognosis,morbid physiology, treat-
ment .. 407

Spinal accessory nerve, accessory nuclei of 48

diagram of i. 405

diseases of i. 433

origin and attachments of .. ..i. 289
Spinal accessory nerve, paralysis of

external branch of i. 441

etiology, symptoms i. 441

treatment i. 442

Spinal accessory nerve, spasm in the
region of the external branch

of i. 433

symptoms i. 434

diagnosis, morbid anatomy . . . .i. 438

prognosis, treatment i. 439

Spinal apoplexy 321

Spinal arachnitis 390

Spinal automatic disturbances .. ..i. 157

PAGE.

Spinal cord, accessor}' nerve-nuclei of . . 26

Spinal cord, anajruia of 310

etiology 310

symptoms 311

course, pathological anatomy . . 312

diagnosis 312

treatment ... 313

Spinal cord, arteries of 19

Spinal cord, concussion of 368

definition, etiology 368

symptoms 369

varieties 369

morbid anatomy, diagnosis . . . . 371

prognosis, treatment 372

Spinal cord, deformities of 97

Spinal cord, diseases of .. .. .. 100

Spinal cord, distribution of vessels of .. 10

Spinal cord, framework of 6

Spinal cord, functional weakness of . . 335

definition 335

etiology 336

symptoms 336

course, morbid physiology . . . . 337

diagnosis, prognosis, treatment . . 338

Spinal cord, functions of 70

accessory 71

fundamental 74

Spinal cord, haamorrhage into the sub-
stance of 321

definition, etiology, symptoms . 321

course, morbid anatomy . . . . 324

diagnosis 325

prognosis, treatment 326

Spinal cord, hyperaemia of 317

etiology 317

symptoms 318

course, diagnosis 319

prognosis, morbid anatomy, treat-
ment . . . 320

Spinal cord, grey matter of . . . . 8, 21 — 37

Spinal cord, malformations of 97

Spinal cord, membranes of 3

Spinal cord, morbid anatomy of . . . . 84
Spinal cord, neuroglia of . . 6, 7, S, 9, 29, 86

Spinal cord, secondary degenerations of 93

Spinal cord, simple softening of . . . . 308

Spinal cord, slow compression of . . . . 351

etiology 352

symptoms 353

varieties 356

course, morbid anatomy . . . . 357

diagnosis 359

prognosis, treatment 360

Spinal cord, structure of 6

Spinal cord, tumours of 372

varieties 372

etiology, symptoms 373

localisation of tumours 375

course 379

diagnosis, prognosis, treatment . . 3S0

Spinal cord, unilateral lesion of . . . . 361

definition, etiology, symptoms . . 361

varieties, morbid physiology . . 363

course 367

diagnosis, prognosis, treatment . . 368
Spinal cord, white matter of . . . . 9, 51, 60

Spinal cord, wounds of 346

etiology 346

symptoms 347

varieties 34S

morbid anatomy 349

course » • • • •

diagnosis, prognosis, treatment . . 351

Spinal dura mater 3

inflammation of 3S4

Spinal eruptions i. 210

Spinal irritation 332

definition, symptoms- 332

varieties 333

INDEX.

907

PAOE.

Spinal irritation, course, diagnosis . . 334

prognosis, treatment 385

Spinal ischaainia 310

Spiual leptomeningitis 391

Spinal lesions i. 242

Spinal membranes, deformities of . . 405
Spinal membranes, hypenemiii of . . 317, 381
Spinal membranes, structure of .. .. 8
Spinal membranes, tumours of . . . . 400

etiology, symptoms 401

course, diagnosis 402

morbid anatomy 403

varieties 404

prognosis, treatment 404

Spinal meningeal hemorrhage . . . . 881

Spinal pachymeningitis 384

Spinal paralysis, atrophic 105

Brown-Sequard's 361

intermittent 343

spasmodic 251

toxic 344

Spinal pia mater 4

inflammation of 390

Spinal vessels, morbid alterations of .. 87
Spleen, neurotic enlargement of .. ..i. 192

Splenius capitis, spasm of i. 446

Spots, hypenesthetic i. 104

Static ataxia 218

Sternutatioconvulsiva i. 449

Stilling, nuclei of i. 54, 50

Stimulants i. 30

Stimuli i. 7, i. 27, i. 30, i. 32, i. 120

electrical i. 122

Stimulus and contraction, relation be-
tween i. 86

Stimulus and sensation, relation be-

tween i. S2

Strabismus convergens i. 357

deorsum vergens i. 353

divergens i. 354

aursum vergens i. 355

Striae medullare8 465

Striped muscles i. 201

motor disturbances of i. 119

structure of i. 201

Striped muscular fibres, termination of

nerves in . . . . " i. 203

Structure, differentiation of i. 14

integration of i. 16

Strychnine .. .. : i. 255

Subacute general spinal paralysis . . . . 298
Successive impressions, inability to

count i. 102

Superficial reflexes i. 138

varieties of i. 138

Superior cervical ganglion i. 538

Superior olivary body 50

Supra-maxillary neuralgia i. 392

Supra-orbital neuralgia i. 391

Sweat, alterations of i. 217

Sylvius, aqueduct of 439

fissures of 417, 426

Sympathetic superior cervical ganglion, i. 538
Sympathetic system, abdominal part of. i. 540

diseases of i. 585

Sympathetic system, automatic actions

of i. 535

Sympathetic system, cervical part of . .i. 536

diseases of i. 577

Sympathetic system, diseases of .. ..i. 5:i5

functions of .. ..i. 535

reflex actions of i. 535

Sympathetic system, thoracic part of . .i. 540

diseases of i. 577

Synkinesis i. 87, i. 122, i 162

Syphilis of the nervous system .. .. 962

morbid anatomy 962

primary lesions 963

secondary lesions 965

PACK.

Syphilis of the nervous system :

diagnosis 967

lesions of the peripheral nerves 968

lesions of the spinal cord . . 970

lesions of the brain 972

treatment 974

Tabes dorsal is, sec Locomotor ataxy .. 211
Tabes dorsal is spasmodica, see Primary

lateral sclerosis 251

Tactile anaesthesia i. 100

channels i. 92

Tactile and painful impressions, separa-
tion of i. 101

Taotile paralysis, partial i. 97

total i. 97

Tactile sensations i. 92

Taenia semicircularis 467

Tailors' spasm i. 467

Tegmentum, red nucleus of 50

Temperature, tests of sensation of . . . .i. 96
Temporo-splienoidal lobe, lesions of . . 637
Tendinous reflexes, i. 140, i. 141, i. 150, i. 153

Tensor palati, paralysis of i. 407

Tenth cranial nerve, diagram of . . . . i. 405

diseases of i. 404

origin and attachment of . . . .i. 288

Testis, irritable i. 230

neuralgia of i. 593

Tetanic seizures, cerebellar i. 100

Tetanus 842

definition, etiology 842

symptoms 844

course, duration, terminations . . 849

morbid anatomy 849

morbid physiology 851

diagnosis, prognosis 852

treatment 853

Tetanilla i. 523

Tetany i. 523

etiology i. 523

symptoms i. 524

Thalami optici 437, 449, 466

lesions of 649

Thermo-ansesthesia i. 100

Thigh, neuralgia of lateral cutaneous

nerve of i. 501

Third cranial nerve, origin and attach-
ment of i. 285

paralysis of i. 352

Thrombosis i. 235, 313, 511

Tibial nerve, paralysis of . . i. 528

Tibialis anticus, paralysis of i. 527

Tic, convulsive i. 361

douloureux i. 394

Titillation j. 114

Tongue, muscles of i. 410

Tongue, paralysis of i. 382

Tonic cerebral spasms 596

Torpid shock 711

Torticollis i. 433

Toxic nervous diseases 953

Toxic spinal paralysis 344

Trapezius, spasm of i. 434

Traumatic anosmia i. 309

Traumatic influences i. 76

Tremor, a debilitate i. 130

coactus j. 130

Trepidation of extremities .. •.. ..i. 154

Triangular nucleus 33, 50

Trigeminus i. 338

diagram of first division of . . . .i. 344
of second division of .. ..i. 392

of third division of i. 393

diseases of j. 344

functions of i, 344

middle sensory nucleus of . . . . 50
origin and attachment of .. ..i. 285
Trigeminus, anaesthesia of j. 386

9<)8

INDEX.

nerves .
Trophoneuroses

Trigeminus, ana3sthesia of :

symptoms, diagnosis i 386

treatment Y 307

Trigeminus, neuralgia of ! '. \ j 337

etiology \\ ' 'i' 387

symptoms j' 38g

varieties . ' ' Y ,,qq

neuralgia of the first division of .' !i. 890
of the second division of . .i. 392
of the third division of . . .' Y 394.

course, diagnosis !!i395

treatment ' "{ jjqq

Trigeminus, paralysis in the region of'

distribution of i 402

etiology !!i! 402

symptom 8 j, 493

diagnosis, prognosis, treatment . .1 403
Trigeminus, spasm in the region of dis-
tribution of j, 400

etiology, diagnosis !!i401

prognosis, treatment . . . . j. 402
Trigeminus, trophic affections in the

territory of j, 398

Trismus L 400

Trochlear nerve, diagram of Y 344

origin and attachment of . . .' Y 285
Trophic affections of the peripheral '

j jg3

.. i. 80,i.87,'i 91,' i. 193

01 the bones j 222

of the cutis \ "i' 208

of the glands \\ Y 227

of the join ts " \ '{ 222

of the muscles .. .. ' Y 201

True neuroma \\ " Y 302

amyelinicum . . . . ' . " ' "j" 3q2

myelinicum . . . . . " ' Y 302

Trunk^nterior surface of .. " "{ 477

cutaneous nerves of .. . . i! 457

muscles of t '470 Y 479

Tubercle, solitary '„;,
Tubercula dolorosa . i 304

Tumours, intracranial . 547

spinal \ 400

Twelfth cranial nerve, diagram of! .' ' 'i 381

accessory nuclei of ... . 4g

diseases of ' [ " ' " ■ 3g0

origin and attachments . '. " ' V 289

lypuoid fever, nervous diseases of . . . ! ' 975

Unilateral convulsions . . . . gg4

•varieties of . . " " 5g5

Unilateral hyperidrosis .'.' j 534

Unilateral phonetic paralysis . ... . .' " '

tt -i x , i. 423, i. 424, 'i. 427

Unilateral progressive facial atrophy i 570

history r "i 570

etiology, symptoms.. .. ' "i' 571

pathology "i" 574

diagnosis, prognosis .. i 575

treatment Y 576

Unilateral spinal paralysis '.' ■ • 351

etiology, symptoms . . . . " " 361

varieties " 3g3

morbid physiology . . '■ " 353

course " " 367

diagnosis, prognosis.! !! qrh
Unstriped muscles, structure of " "i 201
Upper arm, muscles of " " j

Upper extremity, paralysis of the nerves
of . . j

479

Urinar

Urethra, neuralgia of ! ! " "]' ill

vmS^^ ■■ :: ;;. gS

Vagus, ansBsthesia of bronchial branches

gastric branches of

laryngeal branches of !! ",-'117

vagus, diagram of ?*

117

Vagus, diseases of i 404

neuroses of trunk of " " "{ 432
origin and attachments of " "i' 288
Vagus, paralysis of the laryngeal branches ' •

W j 4o'j

etiology, symptoms . . " i' 423

unilateral and bilateral phonetic '

paralyses j. 424 j. 427

respiratory paralyses, i. 424, i. 426
mixed paralyses . . i. 494 i 49<>
Vaso-motor disturbances ' fs?

varieties . .
Veratrine . J* l°Z

vertigo .. .. ;; ;; ;; ■■

auditory gog

Vesicular column of Clarke 8, 22,' 3o' 33 45
functions of 77
Vessels, intracranial, occlu'sion' of " " 511
Violin players' spasm . . .. \ 466

Viscera, diseases of "j" 78

innervation of . . i 179

Visceral anaesthesia .. .. \\ \\ "i! 117

analgesia .' .' .' \ Y n 6

hyperalgesia \ \\ !!i! 113

paralgesia " "j." i^3

sensory disturbances .. . . !.L 118

trophoneuroses i 9'Jl

Vision, alterations of . . . . \\ \\ ' Y 315
alteration in the field of ! . \ Y 31 g
changes in the colour perception of, i! 317
diminution in the acuteness of i 315

test of the field of j. 317

tests of the acuteness of . . Y 315

V ohtions " ' 4gg

Voluntary movements .. '/ '\ 85
Voluntary muscles, akinesis of - ' Y 121

symptoms ' \ J21

associated symptoms .! " i. 122
electrical tests . . .. " " Y l52

Voluutarymuscles, automaticmechanism, '

affections of ... . j 155

Voluntary muscles, hyperkinesis of ' \ 'i! 130

concomitant symptoms i. 133

consecutive symptoms . . " Y 134
Voluntary muscles, reflex mechanism', '

elementary affections of. . . 'i. 136
Voluntary muscles, tonic spasms in 343
Voluptuous feeling, excess of j_ 115

Wallerian nerve degeneration . . i. 194

Walking "l fi9

Warmth " " "j;^

White matter of the cerebellum ' ' 413

of the cerebrum " 453

of the pons .... . . \\ " 4i 1

of the spinal cord " " 9

White substance " " " j 3£

resistance to disease of ! ! 92
White spinal substance, accessory portion

°f 53

development of ....!! 51

functions of " gn

longitudinal distribution of !

Will

rearrangement of 33

Willis! circle of !! !.' '! 44^

Writers' cramp " ' .'.'j. 464

spastic, symptoms .. .! . . ! Y 465
tremulous, symptoms .. . . Y 465
paralytic, symptoms . . . . ! Y 466
etiology j 467

diagnosis, prognosis, treatment ..i. 468

Wry-neck . .i. 433

symptoms [] " !!i.'434

diagnosis, morbid anatomy . . ! .i. 438
prognosis, treatment L 439

Yawning, attacks of j. 450

Zinc j. 260

ERRATA.

Line 12th from the top, f for " centre " read '" cortex.'
Line 14th from the top,

Volume I.

Page 41. Line 8th from the top, j

„ 48. Line 16th from the top, for " cenereum" read "cinereum."

'„ 48. Line 5th from the bottom, f or " P " read "p."

„ 76. Line 11th from the bottom, for " hoemorrhidal " read " haemorrhoidal."

,, 77. Line 2nd from the top, for " adventitas " read " adventitise."

,, 104. Line 12th from the top, for " cethesice " read " cesthesice."

,, 225. Line 11th from the bottom, for " cullus " read " callus."

,, 258. Line 11th from the bottom, for " becomes " read " become."

,, 449. Line 5th from the bottom, for " Sternatatio " read " Slernutatio."

,, 496. Line 19th from the bottom, for " injection " read " injection of morphia."

,, 559. Line 21st from the bottom, for " nitrate " read "nitrite."

Volume II.

Page 62. Line 11th from the bottom, for " ducussating " read " decussating."
,, 168. Line 10th from the top, for " Cruvielhier " read " Cruveilhier."
,, 201. Line 1st at the top, for " Greisinger " read " Griesenger."
,, 214. Line 1st at the top, for " thirty " read " twenty."
,, 411. Line 11th from the top, for " variolli" read " Varolii."
,, 411. Line 16th from the top, for " Variolii " read " Varolii."
„ 427. Line 19th from the bottom, for " of the Skull " read " to the Skull."
„ 434. Line 10th from the bottom, for "corpora striatum" read "corpus
striatum,"

,, 558. Line 19th from the bottom, for " grammes " read "grains."
,, 641. Line 15th from the top, for " began the " read " began."

MANCHESTER '
PRINTED BY ALEXANDER IRELAND AND CO.,
PALL MALL.

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