Full text of "Accident and injury; their relations to diseases of the nervous system"

See other formats

THIS BOOK IS THE GIFT OF

Henry Pelouze de Forest

Class of 1884

The original of tiiis book is in
tine Cornell University Library.

There are no known copyright restrictions in
the United States on the use of the text.

http://www.archive.org/details/cu31 92401 2461 1 1 1

ACCIDENT AND INJURY

THEIR RELATIONS TO DISEASES
OF THE NERVOUS SYSTEM

PEARCE BAILEY, A.M., M. D.

ATTENDING PHYSICIAN TO THE DEPARTMENT OF CORRECTION

AND TO THE ALMSHOUSE AND INCURABLE HOSPITALS ;

ASSISTANT IN NEUROLOGY, COLUMBIA UNIVERSITY ;

CONSULTING NEUROLOGIST TO ST. LUKE'S

HOSPITAL, NEW YORK CITY

^1^

fea

'/M

K^^l

1^^

PSl?> -

ppp

^1 4

■

^Kmj^jv" '

Pearce Bailey, A.M., M.D.

NEW YORK

D. APPLETON AND COMPANY

1900

PROFESSOR STARR,

IN GRATEFUL RECOLLECTION
OF MANY KINDNESSES.

PREFACE,

The original purpose in this undertaking was to furnish
a systematic description of the nervous affections which
result from injury and fright, and which, under the gener-
ally familiar term of " the traumatic neuroses," exist inde-
pendently of any as yet demonstrated lesion in the nervous
system. These disorders are of sufficiently common oc-
currence to constitute a comprehensive chapter in internal
medicine, and they have obtained a position of legal promi-
nence from the frequency with which they are associated
with questions of liability. Yet, in spite of their impor-
tance, that they are not always clearly understood by
physicians generally is shown by the contradictory views
expressed concerning them when they become the subjects
of litigation.

While it can not be denied that the nature of the trau-
matic neuroses is still in many respects obscure, sufficient
evidence as to their causes and symptoms has now accumu-
lated to permit them to be recognized as definite clinical
types, and to be diagnosticated with reasonable accuracy.
This evidence is, however, more or less inaccessible to gen-
eral readers, existing chiefly as scattered monographs, most
of which are in foreign languages. No single book has at-
tempted, in recent years, to present in detail the enlarging
views, and the deductions from them, concerning these dis-
orders. More than a year ago it appeared to the writer
that an embodiment of such views and deductions, together

yi PREFACE.

with facts of personal experience, might prove of service,
not only to practitioners of medicine, but also to those whose
interest in the questions involved arises from legal rather
than from medical reasons.

This task was accordingly undertaken. As it pro-
gressed it became evident that a treatise on the traumatic
neuroses would be much more useful were it preceded
by some account of injuries to the nervous system of or-
ganic character. A disease can only be diagnosticated
as functional when evidences of organic lesion are absent,
and the physician to recognize the one must be able to
exclude the other. Accordingly, instead of proceeding at
once to the delineation of neurasthenia, hysteria, and allied
conditions, the first parts of the volume are concerned
with the simpler methods of examination, with the causes
and effects of acute organic injuries to the nervous sys-
tem, and with a consideration of in how far accidents may
be held responsible for the appearance of certain chronic
degenerative diseases. The question of malingering is so
intimately connected with the traumatic functional nervous
disorders that its description also was deemed essential.
Treatment does not properly fall within the scope of the
work as indicated by the title, but since it is a subject of
such importance the few words regarding it may be found
not out of place.

In its present form the book might be mistaken for a
general treatise on traumatic diseases of the nervous system.
So comprehensive a purpose it can not aspire to fulfil. It
is merely an attempt to present the views which seem most
tenable as to the part played by injury and shock in the
more important of these diseases. The writer has drawn
freely upon the works of Erichsen, Page, Charcot, Oppen-
heim, Knapp, Dana, Gilles de la Tourette, Striimpell, Heller,
and many others, for which he desires to express his obli-
gations. His warmest thanks are due to Professor Starr

PREFACE vii

for kindly suggestions given during the preparation of the
manuscript, and for his permission to make use of the rich
material of the Department for Nervous Diseases at the
Vanderbilt Clinic ; to Dr. V. H. Norrie for many of the
photographs ; and to Mr. I. Strauss for help in correcting
the proofs and in many other ways.

Pearce Bailey.

60 West Fiftieth Street, New York,
October so, iSgj.

CONTENTS.

PACE

Introduction :

The consideration of the case i

I. — Previous history of the patient 6

II. — History of the accident 7

III. — Physical evidences of predisposition to nervous disease, ii

IV. — The examination for the actual injury .... 18

PART I.

ORGANIC EFFECTS OF INJURY TO THE NERVOUS SYSTEM.

CHAPTER

I. — Injuries to the brain 46

II. — Injuries to the spinal cord 68

III. — Injuries to the peripheral nerves . . .' . . -97

IV. — Ultimate organic effects of injury 119

Epilepsy 126

General paralysis of the insane 137

Locomotor ataxia 151

Progressive muscular atrophy 164

Paralysis agitans 178

PART II.

FUNCTIONAL EFFECTS OF INJURY.

I. — The nervous disorders which most frequently follovit rail-
way AND allied accidents. — THE TRAUMATIC NEUROSES . . l86

History 186

Nomenclature 200

Pathology 202

..Etiology 203

Symptoms 215

II. — Traumatic neurasthenia 226

III. — Traumatic hysteria 270

IV. — Unclassified forms 325

X CONTENTS.

PAGE

PART III.

Malingering 34i

1. Exaggeration of symptoms actually present .... 347

2. Substitution of origin 352

3. Simulation 357

PART IV.

Treatment of the traumatic neuroses 394

Index of names 419

Index of subjects 422

LIST OF ILLUSTRATIONS.

FIGURE PAGE

1. Schweigger's perimeter 24

2. Normal field of vision 25

3. Hand dynamometer 29

4. Krauss's plessimeter 38

5. Method of obtaining triceps and supinator jerks 39

6. Jendrassik method of obtaining the knee-jerk 40

7. Diagram of nerve trunks and motor points for the muscles (opposite) , 43

8. Diagram of degenerative electrical reactions ...... 44

9. Schematic representation of the cerebral cortex and its centers . . 50

10. View of the right cerebral hemisphere 51

TI. Schema of cerebro-spinal motor path 53

12. Schema of the motor neurons 54

13. Photograph shovifing double third-nerve palsy 58

14. Photograph showing palsy of the sixth and seventh nerves ... 59

15. Same patient 59

16. Section through the back at the ninth thoracic vertebra .... 70

17. Crush of spinal cord 72

18. Intradural haemorrhage 73

19. Extradural haemorrhage 73

20. Course of blood in hsematomyelia 74

21. Section showing hsematomyelia 75

22. Sensory distribution of spinal-cord segments (Starr) 91

23. Sensory distribution of spinal-cord segments (Kocher) .... 92

24. Anaesthesia chart. Injury to eighth cervical segment .... 93

25. Anaesthesia chart. Injury to fifth lumbar segment 94

26. Sensory distribution of peripheral nerves (opposite) 106

27. Beginning main en grij'is no

28. Distribution of sensory nerves in the hand in

29. Drop-wrist 113

30. Deformity of the back in syringomyelia 123

xii LIST OF ILLUSTRATIONS.

FIGURE PAGE

31. Acromegaly 125

32. Facial expression in general paresis I39

33. Handwriting in general paresis 145

34. Charcot joint 153

35. Attitude of static ataxia 154

36. Anaesthesia chart. Locomotor ataxia 155

37. Field of vision. Locomotor ataxia 160

38. Progressive muscular atrophy . I74

3g. Same patient 175

40. Facial expression in paralysis agitans ....... 180

41. Attitude in paralysis agitans ......... iSi

42. Attitude in traumatic lumbago 248

43. Field of vision. Shifting type of contraction ...... 255

44. Anaesthesia chart. Injury to Cauda equina and astasia-abasia . . . 278

45. Dragging of the foot in traumatic hysteria 282

46. Anaesthesia chart. Traumatic hysteria ....... 283

47. Field of vision. Traumatic hysteria 284

48. Anaesthesia chart. Hemianaesthesia 293

49. Anaesthesia chart. Disseminated anesthesia 293

50. Field of vision. Concentric contraction 297

51. Footprints in hysterical and organic hemiplegia ..... 303

52. Anaesthesia chart. Hysterical paraplegia 306

53. Hysterical contracture at vprist . 309

54. Attitude in hysterical coxalgia ......... 314

55. Some members of the Freeman family 360

ACCIDENT AND INJURY.

INTRODUCTION.

THE CONSIDERATION OF THE CASE.

No sharp line of demarcation can be drawn between the
disorders of the nervous system which develop as a result
of acutely occurring injuries and those which owe their
existence to causes operating more slowly, or whose clinical
manifestations, although they may appear suddenly, are the
effects of subtle morbid conditions that have been for a
long time active. Yet, as every causal factor adds its spe-
cial cdchet to the conditions it induces, so injury and shock
put their stamps upon the nervous affections which are
their results. It is the effects of traumatisms upon the nerv-
ous system which will be considered in the following pages.
The word traumatic is permitted so many meanings that
its limitations must be clearly understood. In its most re-
stricted sense it applies only to such injuries as are the re-
sults of acutely acting physical violence, while in its widest
meaning it includes any detriment to health which originates
outside of the body. By the first meaning of the term
psychic influences are disregarded ; by the latter interpreta-
tion its scope would be practically unlimited, as it would
include all morbid conditions which owe their existence to
toxic or mechanical causes, such as lead poisoning, alcohol-
ism, or writer's cramp, as well as the crushing of nervous
tissue from the pressure of broken-down protecting struc-

2 INTRODUCTION.

ture, or the disturbance of equilibrium in cerebral processes
brought about by mental shock or fright. For clinical pur-
poses neither of these interpretations of the terra is satisfac-
tory. The first disregards the very important influence of
nervous shock and fright as disease-inducing agents, and
the second renders the word traumatic much more compre-
hensive than is desirable, or than is generally understood.
In the following pages traumatic will be used as indicating
quickly acting physical violence or psychic shock which arises out-
side the body. The functional traumatic nervous disorders
have received careful observation and description by neu-
rologists ; but the behavior of the nervous system under
injuries which directly affect nervous structure has been
too little subjected to special investigation. Most acutely
occurring injuries to the brain and spinal cord are received
in surgical wards, where the exact character of nervous
symptoms and the probable location of lesions only occa-
sionally become the objects of close study. Yet organic
injuries to the nervous system constitute a field of investi-
gation full of fruitful promise. There are constantly occur-
ring in all large cities selective injuries to nervous tissue,
which result from all varieties of causes and which occur
under all possible conditions. Were they systematically
examined at the bedside, and were the clinical picture, when
possible, amplified by a microscopic study of the patho-
logical conditions to which the symptoms had been due,
these injuries could be made to subserve the purposes of
experimental pathology, and could be relied upon to furnish
more valuable results than have been obtained by experi-
ments on animals.

It is from the observations of morbid conditions as they
occur in man that we must look for the answers to such
questions as concussion of the spinal cord, or the localiza-
tion of special functions, or the understanding of the factors
of predisposition to nervous disease, or the indications for

THE CONSIDERATION OF THE CASE. j

operative treatment. That the subject has been, and still
is, treated with less attention than it deserves, there is, un-
fortunately, no question of doubt. Injuries to the spinal
cord are as old as the art of medicine itself ; yet it is only
within the last decade that there has arisen any definite
knowledge as to the localization of function of the spinal-
cord segments. Such knowledge as we now possess is
largely due to the study of traumatic cases.

In many cases of traumatic nervous disease the clinical
picture is so plain that a cursory examination suffices for an
immediate and correct appreciation of the cause, the nature
and the probable outcome of the injury. The ambulance
surgeon can often diagnosticate a fracture of the spine from
the seat of the ambulance, and fractures of the skull are of
so common occurrence in emergency hospitals that experi-
enced surgeons recognize the condition by the general ap-
pearance of the patient alone. Yet from the organic lesions
of the nervous system, whose nature is readily apparent, to
those which require the closest study and rarest skill for
their diagnosis, is not so very long a step. In presumable
brain injuries, when the patient is comatose or delirious,
examination for localizing signs is often unsatisfactory, and
the history of the accident may be unobtainable, or if told
by witnesses unreliable, so that the diagnosis of fracture of
the skull or laceration of the brain, as opposed to some of
the idiopathic forms of coma, is very difficult or at times
even impossible.

In the diagnosis of the puzzling forms of traumatism of
the back — as a result of which, without evidences of lesion
to the vertebras, there are selective symptoms of injury to
the spinal cord — considerable knowledge of the anatomy
and pathology of the nervous system is often necessary.
This fact becomes evident upon the perusal of the works of
Erichsen, the pioneer in traumatic neurology, who failed to
recognize the true condition in many cases of back injury.

4 INTRODUCTION.

Affections so common as traumatic peripheral nerve palsies,
especially those which affect the nerves around the shoulder
joint, can in certain cases be recognized only by careful elec-
trical examination. The diagnosis of the disorders which
must still be known as functional are diagnoses by exclusion,
to make which presupposes a considerable knowledge of the
symptoms of organic nervous injuries.

A functional, as opposed to an organic disease of the nerv-
ous system, is one in which the anatomical integrity of nerv-
ous structure remains unimpaired. There may be serious
or even alarming symptoms, yet the evidences which indi-
cate destruction of special centers or conducting paths are
regularly absent ; also, the course of the disease is benign,
tending to recovery. Although there is no reason to doubt
that every departure from health is a result of changes
of some character in physical structure or composition,
the morbid alterations in nervous tissue which underlie
the functional nervous diseases have hitherto escaped iden-
tification, and until they are identified these affections must
be classed as depending upon no known pathological con-
ditions. They can only be diagnosticated as functional,
however, when careful examination has demonstrated that
there is absence of those symptoms which are the infal-
lible signs of morbid conditions of recognized structural
character.

To the inherent difficulties of diagnosis which are due
to the intricacies of the anatomy and physiology of the
nervous system, the commercial spirit of the times has
added others. The bringing of claims for damages for per-
sonal injuries has reached so exaggerated a degree that it is
no rare occurrence for an injured person to see an attorney
before he sees a doctor; and the story which this latter
hears often speaks more eloquently for the medical knowl-
edge of certain members of the legal profession than for the
veracity of the patient.

THE CONSIDERATION OF THE CASE.

If the injuries are to become the basis for a claim for
■damages, there are many complicating factors. Under
these circumstances, while the account of the resulting
symptoms is to be listened to with attention and respect, it
should be accepted with reserve, and only in so far as it may
seem to be justified by the attendant circumstances. Such
conservatism can not be construed as a reflection upon the
honesty of the patient or of his lawyer. As a rule of clini-
cal medicine it is universally observed, and is necessary for
the avoidance of the deception caused by the misstatements
of ignorance as well as those of intention. The question of
liability, which figures very prominently in many cases, is
one with which the physician has little to do. It concerns
him only in so far as he may be able to show that the physi-
cal or mental condition of the claimant at the time of the
accident was of a character such as to render him unable
to take proper precautions against danger.

In the study of traumatic nervous disease so many
factors enter that it has seemed more advisable to en-
title this introductory chapter, which essays to outline
some of the simpler methods of investigation, a consid-
eration of the case rather than an examination of the
patient. As the most successful physicians are those
who treat patients rather than diseases, so he can give
the most valuable opinion in regard to an injury of the
nervous system who has considered it from every point
of view.

The necessity for a painstaking examination of cases
which are in themselves obscure, or for those in which for
forensic reasons accuracy of diagnosis is especially essen-
tial, needs no emphasis. It is always advisable to put the
results of examination immediately in writing, and in med-
ico-legal cases it is well to have the assistance of a stenog-
rapher, in order that the procedure may not be unneces-
sarily delayed and that as full notes as possible may be

6 INTRODUCTION.

taken. The examination may best be divided into four
stages, viz. :

I. Previous history of the patient (ancestral ; personal).

II. History of the accident.

III. Physical evidences of predisposition to nervous dis-
ease.

IV. Examination for the actual injury.

I. Previous History of the Patient.

In nervous disease originating as the result of injury
the influence of hereditary predisposition is usually not
very evident, and is always difficult to prove. Few nerv-
ous diseases are directly transmitted from parent to child ;
heredity seems rather to act by giving to the offspring
a nervous system whose powers of resistance are dimin-
ished, but in which the development of disease depends
upon the specific action of various exciting causes which
vary with environment. Among the morbid conditions
which render their victims particularly prone to transmit
unstable nervous systems to descendants may be mentioned
alcoholism, insanity, epilepsy, syphilis, hysteria, and tuber-
culosis. If any of them have been present in both parents,
or have been generally disseminated throughout a family,
the chances are all the greater that the offspring will be
endowed with an imperfectly developed nervous system, or
with one which will easily succumb to injurious influences.

The object sought for in traumatic cases in inquiring for
a history of the patient's personal life is to establish whether
he were or were not a healthy man before the accident.
The patient is asked the diseases he has had, the amount
of work he has been capable of, and the kind of life he
has been able to lead. More valuable than his own replies
as to his physical condition are facts concerning his sur-
roundings and mode of life. Age, sex, nationality, and race

HISTORY OF THE ACCIDENT. 7

are considerations of paramount importance, which are de-
scribed in succeeding pages. Certain occupations, notably
those which expose the workman to chronic poisonings, are
important predisponents to nervous disease. On account of
real or assumed ignorance, reliable information concerning
the family or personal history is often difficult to obtain,
and the physician will do well to avoid putting too much
credence in statements which seem at variance with the
actual condition of the patient.

II. History of the Accident.

Definite and reliable information concerning the accident
is often unobtainable. In general accidents, such as railway
collisions, where a large number of persons are involved,
there are usually no spectators. The circumstances which
surround such catastrophes make each individual a partici-
pator rather than a witness; and the suddenness of the
accident and the terror which it causes usually render the
victim unable to give an intelligent account of the way his
own injuries were received. Even if he were not rendered
unconscious, he is rarely able to describe just what befell
him. When, however, statements are obtainable from wit-
nesses, such testimony is often more valuable than that of
the victim himself.

In the absence of information as to the exact details there
is usually no difficulty in learning the general characters
of an accident, from which much may be inferred as to
its probable results. The law of averages, or the "law
of the long run," as Prof. Mendenhall (Science, Decem-
ber, 1895) calls it, holds good herfe as elsewhere, so that
each variety of casualty has its own ratios of character-
istic effects. How unvarying these effects are, when de-
termined by sufficiently extensive observations, is shown
by the following tables, which have been kindly furnished

INTRODUCTION.

me by an officer of one of the largest railway systems of
America.

They relate to accidents and injuries of all characters
which have occurred in the past six years on or about the
railway or in any of the shops of the company. They have
proved to be of invaluable service to the public, to em-
ployees, and to the railway company, for, by showing the
varieties of accident which are most frequent and the con-
ditions under which they are most liable to occur, they call
official attention to faults in construction or operation, and
thus furnish the surest means of diminishing the chances of
personal injury.

Lack of space prevents me from reproducing all the
ratios which this able statistician has generously placed at
my disposal. The three following tables, however, illus-
trate the general character of his work and the inferences
which may be drawn from it :

Table i.
Injuries to Passengers.

Year.

Where, etc. :

On passenger trains

On freight trains

On station grounds, etc

Postal and expressmen

Cause :

Collisions

Getting on and off moving trains . .

Getting on and off trains after stop
made

Defective and unlighted stations and
platforms

Miscellaneous

Result :

Death

Loss of limb

Loss of finger or toe

Spinal injury

Fracture or dislocation

Sprain

Cuts and bruises

Miscellaneous

1891.

87.5
8.2

4-3
14.0

27.6
17.2

3-5

0.8
50.9

5-"
1-5
i-5
4-7
8.6

3-9
48.3
26.5

1892.

90.9
4.0
5-1
6-3

33-8
28.9

7-7

29-5

7.2
2.7
0.4
1.8
5-4
4-5
52.9

25-1

1893.

2.5
8.6
5.0

42.7
10.3

0.2

44.4

7.8
1.8
0.4
2.2
3-5
5-7
63.2

15-3

1894.

83.1
3-8

I3-I
6.1

16.9
27.9

7-9

47-3

10.8
1.6

2.3

II. 6

6.6

34-3
32.8

1895-

80.6
8.6

10.8
2.1

8.0
28.0

10.8

2.1
51-1

1.4
1.4
0.7
0.7
8.6
6.4
55-0
25.8

1896.

79.1
5-3

15.6
4.2

8.0
14.5

8.6

2.2

56.7

9-5
0.6

1.2

8.7

12.3

44-7

23.0

HISTORY OF THE ACCIDENT.

Table 2.
Injuries to Employees.

Year.

I89I.

1892.

1893.

1894.

1895.

5-3

6.4

7.2

7.8

5-0

2.0

2.6

2.9

2.2

2.6

4.2

3-5

5-0

4-4

4.1

45-1

45-8

44-3

39-1

30.8

18.4

16.2

18.8

19.4

28.0

I.O

0.7

0.4

16.0

16.6

13.8

10.8

15.8

8.0

8.2

7-3

15-9

13-3

28.6

27.9

26.3

23.2

17.4

1.9

2.4

3-8

2.5

2.2

7-3

7.2

0-5

8.0

7.0

0.2

0.1

0-3

0.1

7.8

0.6

3-2

13-8

22.3

5-5

4.8

4-9

5.0

4-3

1.8

0.6

1.2

0.5

0.6

49-7

56.4

5S-2

46.1

3-9

4.0

3-0

2-5

1-3

1.4

I.I

1.2

0.4

3-2

3-4

3-3

2.3

0.1

1-3

2.7

0.6

O.I

6.2

6.3

6.0

5-3

4.9

14. 1

13-0

II.

lb. 3

15.2

47-7

50.0

49.6

39-4

50.1

23.4

20.9

23.2

31-4

25-7

1896.

4.8

2.1

4-3
26.0

34-6

0.8

16.7

10.7

II. I
1-3

7-5
0.4

28.0
4.1
1.6

47.6

1.6

0.5

1-3

0.1

3-6

17.3

52.2

23.4

Employment :

Conductors

Enginemen

Firemen

Brakemen

Mechanics

Warehousemen

Laborers

Miscellaneous

Cause :

Coupling

Collisions

Getting on and off trains

Caught in frogs and switches .

Use of tools and machinery. . .

Fell from cars

Defective tools and appliances

Miscellaneous

Result :

Death

Loss of limb

Loss of finger or toe

Spinal injury

Fracture or dislocation

Sprain

Cuts and bruises

Miscellaneous

Table 3.
Percentage of Results.

Year.

1893.

1894.

1895.

1896.

Result :

Death

Loss of limb

Loss of finger or toe.. .

Spinal injury

Fracture or dislocation,

Sprain

Cuts and bruises

Miscellaneous

Total :

Passengers

Travelers on highway. .

Employees

Trespassers

Total

10.3

2.7

3-0

0.4

6.6

10.9

44.9

21.2

257
190

2,488
455

9.0

2.2

3-0

1-3

6.6

10.5

47.2

20.2

221

239

3,105

492

8.5
2.1

2-7

2.7
6.6
9.1

47-4
20.9

281

179

3,087

447

8.6

2-3

2.6

0.6

6-2

13-5

36.6

29.6

130

195

2,339

430

6.1

1.4

2.0

0.2

5-7

13-3

46.5

24.8

139
ig6

3,854
433

5.9
i.o

1-3
0.2
4.8

15-3
48.8
22.7

187

184

3,753

399

3,390

4,057

3,994

3.094

4,6.22

4,523

lO INTRODUCTION.

All these statistics are self-explanatory. The first and
second tables show the distribution of accidents among pas-
sengers and employees respectively ; table 3 shows the per-
centage results of all accidents and the total number of
injured persons upon which the statistics are based.

From the study of .these tables it appears that the larger
number of these casualties are trivial and occur among em-
ployees, and are consequently unattended with medico-legal
questions, so that the percentage of injuries to the nervous
system is very much less than one would suppose by read-
ing court records.

What is true for railway accidents is also true for other
kinds of casualties — namely, that their character determines,
to a certain extent, the nature of the resulting injuries. In
the consideration of individual cases it is, of course, impossi-
ble to rely too largely on generalizations. Although it may
be known that certain causes are usually followed by similar
results, a variation of conditions may bring about excep-
tions. In most cases, however, the character of the accident
is an index of the severity and the nature of the resulting
injuries. In serious general accidents the body may be
subjected to every degree of violence, which may induce
immediate death or cause mutilations of all degrees. The
fate of passengers or employees in any single given collision
or derailment can not, of course, be foretold. On the other
hand, it can be positively stated that the sudden stopping or
starting of a vehicle, by which the passenger may be jarred
but receives no external wound, rarely if ever exerts suffi-
cient force to cause irreparable injury to the nervous system.
In many other forms of mishap we are justified in inferring
that the violence was inadequate to cause structural injury.
Thus, a light pasteboard box falls a few feet and strikes a
young girl on the head without inflicting any serious wound.
She immediately goes into convulsions, and, on regaining
consciousness, it is found that she is insensible on the left side

PHYSICAL EVIDENCES. II

of the body. In such a case it is just to infer at once that the
injury could not have caused any lesion of the brain which
might explain the symptoms, but rather that they were due
to the disordered mental state of the patient, and were the
immediate results of fright.

III. Physical Evidences of Predisposition to

Nervous Disease.

In severe injuries, such as fractures of the skull or of
the vertebrae, the previous condition of the patient is of
secondary importance. A strong man may of course sur-
vive a shock that might prove fatal to the patient whose
recuperative powers had been enfeebled through previous
bad health or excess. Yet such a difference can rarely be
positively proved. The chief forensic importance of previ-
ous condition attaches to those disorders of which the excit-
ing cause has not been immediately dangerous to life, but
has been the alleged starting point of diseases which are
more or less serious though not directly fatal. The possi-
bility of error in ascribing a traumatic origin to a disease
which antedated the injury is considered in Part III. Here
it is necessary to mention only such conditions as furnish a
favorable soil for the development of nervous affections.
There are certain anatomical evidences which are regarded
as indicative of a congenitally defective nervous system
which is consequently less tolerant of injurious influences.
These are the stigmata of degeneration, and, although it
would be beyond the scope of these pages to describe them
in detail, their general character may be seen in the fol-
lowing classification as suggested by Peterson : *

* State Hospitals Bulletin, July, 1896.

INTRODUCTION.

Stigmata of Degeneration.

Anomalies of the eye.

Anomalies of the ear.

Anomalies of the limbs.

Cranial anomalies. \ -r. ,

( Deformities.

„ . , ( Prognathism.

Facial asymmetry, i „ ^, •

■^ ( Retrognathism.

Deformities of the palate.

Dental anomalies.

. ,. r ,, ■ , J ,. ( Harelip and cleft palate not

Anomalies of the tongue and lips, i ...

( certainly stigmata.

Anomalies of the nose.

C Flecks on the iris, strabismus, chromatic
asymmetry of the iris, narrow palpe-
bral fissures.
Albinism.

Congenital cataracts.
Microphthalmos.
Pigmentary retinitis.
. Muscular insufiSciency.

' Polydactyly.

Syndactyly.

Ectrodactyly.

Symelus.

Ectromelus.

Phocomelus.
^ Excessive length of the arms.

Hernias.

Malformation of the breasts, thorax.

Dwarfishness.

Giantism.

Infantilism.

Feminism.

Masculinism.

Spina bifida.
' Cryptorchismus.

Microrchidia.

Spurious hermaphroditism.

Hypospadia.

Epispadia.

Atresia.

Anomalies of the body
in general.

Anomalies of the genital
organs.

PHYSICAL EVIDENCES.

Anomalies of the skin.

{Polysarcia.
Hypertrichosis.
Absence of hair.
Premature grayness.

The practical value of the stigmata of degeneration is
impaired by the fact that they occur chiefly in idiots, luna-
tics, and epileptics, about whose degeneracy there could be
no question. Also, almost any one of them may occur in
persons who never present any other structural or functional
anomalies.

More useful from a diagnostic point of view than these
physical telltales of ancestral faults are such evidences of
acquired predisposition as are left by certain diseases and
by certain poisons. In a general way it may be said that
any disease which impairs the general health makes the de-
velopment of nervous disorders more probable. There are
a few conditions, however, which stand so pre-eminently in
a causal relation to neural diseases that it is very necessary
to determine their existence before attributing too high a
value to any exciting cause. Of these, the most important
are alcoholism, syphilis, and arterio-sclerosis.

Alcoholism. — It is a matter of common remark that
drunken persons who are in serious accidents often escape
without any severe injury, or indeed any subsequent ill-
effects whatsoever. While it can not be denied that the mus-
cular relaxation and mental stupor of alcoholic intoxication
not infrequently furnish a means of escape from physical
injury and psychic shock, this is a very minor considera-
tion when compared with the number of persons who are
killed or injured in accidents which would not have occurred
to an individual who was sober. Alcoholism stands in a
very important causal relation to traumatic diseases of all
kinds, but especially to traumatic diseases of the nervous
system. It is frequently accountable for the accident and
the injury, and always is prejudicial to recovery. After

14 INTRODUCTION.

very slight blows on the head, or after trivial injuries to
other parts of the body, alcoholic persons not uncommonly
develop delirium tremens, pneumonia, or heart failure, or
show in other ways that their recuperative powers have
become impaired by alcohol. The evils of the drinking
habit are so widely disseminated in all classes of society
that it is very essential at the beginning of an examination
of any accident case to determine the presence or absence
of chronic alcoholic poisoning as a complicating factor.
Old and steady drinkers present at all times such unmistak-
able physical stigmata of their vice that there is no difficulty
in doing this. But many persons who have regarded them-
selves as moderate drinkers only, and who present none of
the more evident signs of chronic alcoholic poisoning, after
slight injuries, exhibit symptoms which show that their use
of alcohol has been too free. In such cases the history of
excessive drinking is not necessary for its diagnosis, because
there is so great a variation in the individual tolerance to
the poison that a daily quantity which in one person could
be taken without evil effects of any kind might be sufficient
in some one else to cause acute symptoms, or to render the
organism incapable of overcoming visitations, such as a
healthy man could easily resist. Accordingly, more reli-
ance is to be placed upon those evidences of alcoholism
which the physician may discover, rather than upon the
patient's history. They are usually abundantly and charac-
teristically present, and are both physical and mental.

The physical symptoms consist of tremor, generalized
or most prominent in the face, lips and tongue, and in the
fingers ; the skin may be normal, or may be flabby and pale,
with a peculiar appearance of oedema ; gastric irritability is
common; the heart is usually rapid, and there may be an
impairment of the purity of the first sound at the apex;
the functions of the special senses are often vitiated, and
disturbances of general cutaneous sensation, both objective

PHYSICAL EVIDENCES.

and subjective, are particularly frequent. The mental symp-
toms consist of coma or stupor or delirium and their vari-
ations. The delirium is usually characterized by hallucina-
tions of sight, less frequently of the other senses, which
almost always have reference to living objects, such as ani-
mals or crawling things or strange persons. A common
condition is one of forgetfulness and confusion ; the memory
may be lost for considerable periods of time, or the patient
may be unable to collect himself sufficiently to tell where he
is or how he came there. Two patients whom I recently
saw at the Manhattan Hospital thought they went out every
night, when in reality they both had been in bed for several
weeks. Systematized delusions are not common, although
they sometimes occur in the chronic form of poisoning, and
consist with particular frequency of false beliefs in regard
to marital infidelity.

The fact that the symptoms of chronic alcoholic poisoning
resemble in many respects those of Oppenheim's " traumatic
neurosis" has led Saenger*to suggest the possibility that
many of those cases are in reality cases of chronic alcohol-
ism which have been made worse by injury. The tremor,
amblyopia, impairment of cutaneous sensibility, and rapid
pulse, which are prominent in the "traumatic neurosis," are
all found in ethylism. Whether some of these cases are in
reality nothing but " traumatic alcoholism," or whether the
chronic toxaemia has supplied the foundation upon which
has developed a neurosis or psychosis, we are at present
unable to decide definitely. It is certain, however, that
in many of the cases which will be described later alco-
holism has played a very important r61e.

Syphilis. — The typical history of syphilis is obtainable in
a certain number of the cases of nervous disease. In a
large number there is the admission of a sore on the penis

* Die Beurtheilung der Nervenerkrankungen nach Unfall, Stuttgart, 1896.

1 6 INTRODUCTION.

only, but of no subsequent syphilitic manifestations ; in
many instances the patients deny every symptom which
might have been of specific character. In the absence of
a syphilitic history, there are often discoverable certain
physical defects which indicate that the syphilitic poison
had at one time been active. Of these the most important
are scars on the penis, scars on the legs, adhesions of the
iris, and similar results of syphilitic inflammation. While
these evidences are oftentimes characteristic, it is rarely
possible to assert that they are the results of syphilis and
could be the results of nothing else, although in the clinic
they are accepted, usually correctly, as satisfactory evi-
dences of preceding infection. But any one of them could
owe their existence to other causes, and it is consequently
almost impossible to be certain that syphilis has existed
when all active syphilitic processes have subsided.

The part played by syphilis in the getiology of nervous
disease is of great importance. The venereal disease has
an unquestioned and intimate connection with the causa-
tion of general paresis and of locomotor ataxia. After
acute injuries to the nervous system, latent syphilitic pro-
cesses not uncommonly become active and give the symp-
toms of focal lesions. Syphilis, like alcoholism, is an active
factor in the induction of premature senility. By attacking
the blood-vessels it causes serious disturbances of the circu-
lation, which lead to degenerative changes in various organs,
and which render the organism less resistant to deleterious
influences.

It is also a significant factor in the genesis of such func-
tional disorders as neurasthenia, hysteria, neuralgia, and
epilepsy.

Arterio-sclerosis. — The importance of the relationship
between disease of the arteries and certain symptoms of
disturbances of nervous function can hardly be overesti-
mated. By attacking the coronary arteries, arterio-sclerosis

PHYSICAL EVIDENCES.

causes a degeneration in the muscular mechanism of the
heart with a consequent deficiency of propulsive power in
that organ ; by diminishing the caliber of terminal arteries,
it also offers serious impediments to circulation. The pro-
cess, in whichever way it acts, is a direct obstacle to blood
supply and a menace to nutrition. Its effects are wide-
spread, but particularly disastrous to the nervous system.
It is a well-known fact that arterial degeneration is a com-
mon accompaniment of the retrogressive periods of life, but
it is too little recognized that it is not rare in youth and
middle age. In young subjects especially the effects of
alcohol and syphilis are prominent in its causation. In the
autopsies on the bodies of prisoners who die in the Work-
house on Blackwell's Island, arterio-sclerosis, either gener-
alized or chiefly restricted to the cerebral arteries, is fre-
quently encountered in subjects who are under forty years
of age, but who have led a life of exposure and excess.

Arterial degeneration, either disseminated or limited to
the cerebral arteries, may exist for a long time without
causing any subjective symptoms, or it may be the direct
cause of dizziness, failure of mental power, headache, epi-
leptiform attacks, etc. When existent it is directly unfa-
vorable to recovery from acute injuries, both by reason of
its causing a diminution in recuperative power and because
the patients are particularly liable to such complications
as pneumonia and heart weakness. On both clinical and
pathological grounds it is probable that the disturbances
of cerebral circulation which it causes are often respon-
sible for many nervous symptoms which are classed as func-
tional.

In the examination of an accident case, accordingly, it is
very essential to determine whether the injury has acted
upon a perfectly healthy person or upon one whose arteries
were diseased. This>is not always easy to do. In advanced
stages when there are objective signs, such as thickened

1 8 INTRODUCTION.

peripheral arteries, a hypertrophied and overacting heart
whose second aortic sound is intensified, urine with low spe-
cific gravity and which is, perhaps, slightly albuminous, the
diagnosis is plain. But in the earlier stages one or all oi
these signs may be absent, and, although the previous life of
the patient may have been such as to have caused degenera-
tive vascular changes, there are no objective evidences that
such conditions exist. Even in the absence of objective
signs the physician should hesitate in attributing a purely
functional character to such symptoms as dizziness or
cardiac irregularity in persons whose previous life has
been of a character to bring about degeneration in the
circulatory organs.

IV. The Examination for the Actual Injury.

In addition to the search for nervous symptoms, it would
seem superfluous to emphasize the necessity for a thorough
general physical examination of the patient were it not for
the fact that it becomes so frequently apparent, in both clin-
ical and medico-legal cases, that the examination has been
entirely too superficial to furnish sufficient grounds for a
definite opinion. In cases of organic injury, although the
nature of the case may be plain at the first glance, the more
searchingly the physician pushes his inquiries the more
capable will he be of giving an opinion of value. In func-
tional nervous disease the diagnosis can only be made where
it can be proved that organic disease is in all probability
absent. How serious may be the errors incurred through
superficiality of examination was illustrated by a case to
which my attention has recently been called :

A woman sought advice for a peculiar nervous condition which
ensued immediately after a blow on the head from a heavy bale
of carpets. She asserted that previously to this she had been
healthy in every respect, but that since the accident she had been
nervous, emotional, and unable to concentrate her mind on her

THE EXAMINATION FOR THE ACTUAL INJURY. 19

work. Immediately after the accident she developed huskiness
of speech and an annoying tracheal cough, very similar to hysterical
cough, without any expectoration. The patient was extremely
suggestible, and an attempt at hypnotizing her was successful in
inducing the first degree of hypnosis. The condition was diag-
nosticated by the physician as one of " traumatic neurosis." A
subsequent examination of the chest and larynx, when the patient
was admitted to the hospital, revealed unequivocal evidences of
an aneurism of the aorta. Thus, although the nervous symptoms
were undoubtedly functional, the cough and laryngeal symptoms
were the expressions of a fatal disease whose existence had been
entirely overlooked.

The intimate structural and functional relationship of the
nervous system to every organ in the body, and the fre-
quent association of nervous disease with diseases of other
organs or systems, render any examination of the nervous
system incomplete which has not been preceded by an
investigation of general somatic conditions. Such a pro-
cedure is always essential for purposes of prognosis, and in
many cases is the one means of avoiding diagnostic errors.
To determine the presence of eruptions or cicatrices or
other evidences of present or past lesions of the skin, exami-
nation of the whole cutaneous surface is often necessary ; no
examioation is satisfactory which leaves undetermined the
condition of the heart and lungs ; the urine must be tested
for the presence of albumen or sugar — in fact, most of the
important means of diagnosis must be resorted to before the
physician can hope to obtain a clear comprehension of the
case. It may seem almost elementary to lay stress upon
such self-evident facts, but it is certain that the errors
which are occasionally laid to the neurologist's door most
frequently arise from the lack of thoroughness in this re-
spect.

In some cases, and especially if the patients are women,
it is impossible to obtain consent to a complete examination.
Under such circumstances the physician in his report should

20 INTRODUCTION.

not fail to mention such limitations, and should only give a
conditional opinion.

It is impossible to devise any scheme of examination
which is in every way satisfactory, but I have found the
following, slightly modified from Striimpell's, the most
useful :

General appearance (facial expression, manner, etc.).
Mental state.
' Olfactory nerve.
Eyes — 2d, 3d, 4th, and 6th nerves.
5th.
7th.
8th.
9th.

nerves which include speech, deglutition, secre-
tion of saliva, and taste.

loth.
nth.
I2th.

Paralysis, rigidity, tremor, morbid movements, gait.

Sensation (pain, touch, temperature, muscular sense).

Reflex action (superficial and tendon reflexes).

Trophic disturbances.

Electrical examination.

General Appearance. — In many cases the general man-
ner, the facial expression, the speech, the attitudes, the gait,
point at once to the condition from which the patient is
suffering, and indicate the special functions which should
receive the most careful investigation. Many nervous dis-
eases have characteristic physiognomies, and cause pathog-
nomonic movements. From the manner and facial expres-
sion alone it is often possible to decide as to the existence
of real or supposed pain, of insomnia, or, indeed, if the pa-
tient is seriously ill. The observation of the face in certain
diseases (bulbar palsy, paralysis agitans, general paresis) is
often of itself sufficient for diagnosis. Such indications are
always of value as clinical guides, and may prove to be

THE EXAMINATION FOR THE ACTUAL INJURY. 2 1

important supports of the final diagnosis ; but too much
weight should not be assigned to them until their signifi-
cance has been verified by the results of more extended
■examination.

Mental State. — After organic injury to the spinal cord or
peripheral nerves there are no characteristic mental symp-
toms unless the brain is injured as well. The mental states
in hysteria and neurasthenia will be described with those
-diseases.

After severe head injuries the patient may be in coma
•or be stupid and delirious, and no further evidences of the
mental state are obtainable. If, after slight injuries, there
is decided impairment or perversion of the mental faculties,
there is reason to suspect that some disease or poisoning
affecting the mind had pre-existed. Eccentricities of man-
ner, carelessness or peculiarities of dress, and in many con-
ditions the facial expression, are to be regarded as evi-
dences of mental states.

In accident cases the condition of the memory is, for
many reasons, of special importance. It should be ascer-
tained how much the patient remembers about the accident,
^nd whether he is cognizant of events which occurred just
before it, or during it, or just after it. If he were rendered
unconscious, it should be determined how soon conscious-
ness returned and memory became re-established. The
memory for recent events should be compared with mem-
ory for things of the more remote past. The presence or
-absence of systematized amnesia should also be established.
Next to memor}', the power of fixing the attention is one of
the most important of mental symptoms. In coma and deli-
rium it is of cours'e abolished ; but often, when the patient is
-apparently conscious, he shows b}' inattention or by confu-
sion that he has very little idea of his surroundings. Delu-
sions, illusions, and hallucinations may be elicited by the
physician himself, or may be observed by attendants.

22 INTRODUCTION.

The ability to read, to write, to comprehend, or to re-
peat written or spoken words, to recognize objects by any
of the special senses, gives important information in regard
to aphasia, or psychical speech disturbances. Dysarthria, or
interference with speech through physical causes, becomes
apparent upon examination of the cranial nerves.

The Cranial Nerves.

Smell.^Olfactory Nerve. — The sense of smell is im-
paired or lost in injuries to the olfactory nerves and in
hysteria. It should be remembered, also, that it may be
diminished in diseases of the nose. In testing for it one
nostril should be taken at a time, and the other nostril
tightly closed.

The substances ordinarily used are musk, peppermint,
asafoetida, and acids. They should be in solution, and kept
in bottles with rubber corks.

The Eyes. — Although examination of the eyes includes
the examination of several nerves, they may be most con-
veniently considered together. In all doubtful cases, test-
ing of the various ocular functions should be intrusted to
some one especially familiar with them. Every physician,,
however, ought to be able to examine for and understand
the evidences of prominent ocular symptoms, and should be
able to use both the ophthalmoscope and the perimeter.

The first step in the examination of the eyes is to notice
the size of the palpebral fissure and the prominence of the
eyeball. The condition of the upper lid as to elevation or
drooping (ptosis), the ability to close or to open the eye,,
renders important information regarding, respectively, the
seventh and third nerves. The pupils should be examined
for actual and comparative size one to the other, and for
irregularities of outline, such as may have been caused by
preceding iritis. The contraction of the pupil under the
influence of light is usually tested either by covering the eye

THE CRANIAL NERVES.

and then observing, when it is uncovered, if the pupil grows
smaller;* or, if the iris is very dark, the converse of this
procedure is often easier — i. e., after the eye has been ex-
posed to light, it is covered with a dark object, and it is
then observed if it dilates in the shadow. The power of
accommodation is determined by having the patient alter-
nately look at a near object and then at a distant one, and
observing the change in the pupillary circumference. All
these tests should be tried at first with each eye- separately,
while the other is closed, and then with both eyes open.

The Argyll-Robertson pupil responds during efforts at
accommodation, but not to light. It is one of the most
important signs in nervous pathology, as, when sight is
preserved, it is only found in locomotor ataxia, cerebral
syphilis, and dementia paralytica.

Paralysis of the ocular muscles may be at once apparent
by pronounced deviation of one or both eyes. In slighter
degrees its presence is shown by the patient's inability to
perform the movements controlled by certain muscles. It
is accompanied by double vision.

The information obtained by means of the ophthalmo-
scope is always valuable, and not infrequently permits a
diagnosis which otherwise could not have been made. In
recommending its general use, however, it must be empha-
sized that it is an instrument requiring considerable skill
and constant practice. To understand the significance of
the pictures which it reveals implies its almost daily use in
both health and disease. In the hands of a novice, normal
variations may be regarded as evidences of morbid con-
ditions, and pathological changes, significant even when
slight, may escape detection. Few general practitioners
have the opportunity to acquire the skill which is neces-
sary to obtain reliable results from ophthalmoscopic exami-
nation, and it is accordingly advisable to have their ob-
servations and conclusions submitted to the control of a

INTRODUCTION.

competent ophthalmologist, who shall at the same time
determine refractive errors if they exist, and the presence
or absence of such insufficiencies of the ocular muscles as
only appear by the use of prisms.

The limits of the field of vision are obtained by the
perimeter. The use of this instrument requires no par-
ticular skill. It is, however, a too frequently for-
gotten fact that perimetric examinations are only
of value when supplemented by general examina-
tion of the eyes.

A limitation of the visual fields can only be
diagnosticated as functional
when examination by a com-
petent ophthalmologist has
proved an absence of or-
ganic disease or defects
which might explain it.

There are many varie-
ties of. perimeters, of which
the most useful, from the
neurologist's standpoint, is
the one devised by Schweig-
ger (Fig. i). It can be taken
apart, is easily portable, and
furnishes sufficiently accu-
rate results. This instru-
ment is held by the patient so that the cupped end of the
upright, a, is placed just under the lower rim of the orbit,
and the patient is directed to look through the hole, b.
The movable arc, c, can be placed at will at different
meridians, which are indicated by the pointer, d. The
object carrier, e, is fitted with jaws, into which can be in-
serted the disks containing little squares of different colors
and of white. In examining for the field of vision the eye
not under examination is covered, and the object is removed

Fig. I. — Schweigger's perimeter.

THE CRANIAL NERVES.

from the periphery of the field toward the center. As soon
as it is perceived, the degree is read from the scale and is
marked on the perimetric chart.

As indicated by the chart (Fig. 2), the normal field of
vision for white on the horizontal meridian is 90° on the
temporal side, and 60° on the nasal side ; on the vertical
meridian it is 55° superiorly and 70° inferiorly. The out-
line of the entire field as indicated in the chart is fairly
constant in normal eyes. It is subject to slight variations

J..B.

JiM

Fig. 2. — Normal field of vision.

in different individuals within normal limits, but a diminu-
tion of ten degrees must be regarded as of pathological
significance.

The fields for the different colors are smaller than those
for white. They range in size from the field for blue, the
largest, through those for yellow, orange, red, and green in
the order named, to that for violet, which is the smallest.
It is usually convenient to limit the examination of the color
fields to those for blue and red.

The methods of examination of the other cranial nerves.

26 INTRODUCTION.

with the exception of the eighth and the various gustatory
fibers, will be found in the description of their injuries, so
that they need not be given here. A few words must be
said, however, regarding the senses of hearing and of taste.

Hearing. — Auditory Nerve. — Tests of hearing should
be made for one ear at a time, the other ear being tightly
closed. Lesions of the auditory nerve can be distinguished
from those affecting the external or middle ear by the pres-
ence or absence of " bone conduction." When deafness is
the result of inflammations or defects which affect the ear
without involving the auditory nerve, the patient can hear
the tick of a watch or the sound of a tuning fork when
either of these objects is placed on the mastoid process,
very much better than when it is held directly opposite
the auditory meatus; on the other hand, when the audi-
tory nerve is affected, either in its course or in its termi-
nations within the labyrinth, the deafness is equally pro-
nounced in whichever situation the testing object is held.
In the first case, in which the auditory passages are ob-
structed, the bone conducts the sound to the auditory
nerve ; in the second case it is the nerve itself which is
affected, and deafness consequently exists independently of
conduction.

Taste. — The sense of taste depends upon several nerves,
and it is rarely if ever lost as a result of organic injuries
which do not cause coma or extreme laceration of the
mouth and pharynx. Flavors are recognized by means of
the olfactory nerve. The gustatory function has to do with
the qualities salt, sweet, bitter, and sour, and certain me-
tallic sensations only.

In examination for the sense of taste the test solutions
(sodium chloride, lo per cent ; sugar, 5 per cent ; tartaric
acid, 10 per cent; strychnine, o.i per cent) are applied to
the tongue by means of a glass rod while the patient's eyes
are covered and , his nostrils closed. The tongue is held

PARALYSIS. 27

■outside the mouth, and the examiner places drops of the test-
ing fluids on it and inquires if the patient recognizes them.
The examination is often unsatisfactory. Many normal per-
sons can not taste when the tongue is outside of the mouth,
yet when it is withdrawn it is placed against the palate, and
it is then impossible to localize gustatory abnormities if
any exist. The galvanic current is a preferable means of
testing for disturbances of taste. A very weak current,
such as may be obtained from a single cell, is made to
pass through the tongue from wire electrodes placed a
short distance apart. In this way the situation of any
loss of the ability to recognize the metallic sensations may
be discovered. *

Paralysis. — After the initial shock has passed away,
paralysis from cerebral lesions is rarel}' absolute. Even
when the use of the paralyzed member is very greatly im-
paired, the patient can usually succeed in producing some
slight movement. In injuries to the spinal cord, on the
other hand, complete paralysis is the rule, so that the limbs
lie useless and as though dead. In peripheral nerve lesions
the paralysis is so distributed that some muscles may be
absolutely paralyzed, while the motor power in others is as
good as it ever was. The paralyses of hysteria also have
characteristics of their own.

When the patient is unconscious, the examination for
paralysis must of course be made without his assistance. If
the coma is not profound, he may be seen to move the limbs
of one side while those of the other side remain motionless ;
or the limbs of one side may remain unaffected by such
peripheral irritations as pricking, pinching, or tickling —
annoyances which the limbs of the other side endeavor to
escape. Even when the patient is absolutely comatose, by
observing differences of passive muscular resistance — such
as are shown by the way in which the limbs, when lifted up,
fall again to the bed, or by the condition of the muscles as

28 INTRODUCTION.

revealed by grasping them with the hand — the physician
can usually recognize inequalities of muscular power on the
two sides. When the patient is able and willing to assist the
examiner, the task is much easier. If the loss of power is
complete and generally distributed, it is self-demonstrative ;.
but if partial, or if limited to certain muscles or groups of
muscles, it may require considerable care and skill to elicit,
its exact character. The object may best be accomplished
by directing the patient to perform certain movements and
to repeat them in rapid succession, and to make all the re-
sistance of which he is capable against the force exerted
by the examiner. In this way may be found not only the
situation of the paralysis but also its degree. The methods-
of examination for paralyses of the face and tongue will be
described when speaking of those affections.

The neck is rarely the seat of traumatic paralysis. Its
presence is indicated by an inability to move the head and
neck in the various directions, or by abnormal attitudes.
To detect palsy of the muscles about the shoulder joint, the
patient should be required to make all the movements
possible at this point, such as putting the hand on the head,
the chest, the opposite shoulder, and the back, and the press-
ing of the arm firmly against the side. He should try to
maintain these positions while the examiner attempts to
overcome them. By comparing the two sides in this way,
degrees of relative weakness may be demonstrated. Simi-
lar procedures are applicable at the elbow and wrist joints.
The best means of detecting slight degrees of paralysis in
the extensors and flexors of the wrist and fingers is to have,
the patient rapidly open and close the hands for as long a
time as he is able. By this test is shown unilateral weak-
ness as well as the stiffness of the joints which is so impor-
tant an indication of certain forms of injuries to nervous
structures. The grip may be tested by having the patient
grasp and squeeze with both hands the two hands of the

PARALYSIS.

examiner. Weakness in the interossei and lumbricales is
seen by impairment of the finer movements of the fingers.
The patient has difficulty in buttoning his clothes, in pick-
ing up pins or other fine objects, in the effort necessary to
writing, and in similar movements which require muscular
strength and precision.

The examination of the muscles of the abdomen, back,
and lower extremities is conducted on similar lines. The
patient, when lying at full length, should be requested to
raise himself to the sitting posture without using legs or
arms ; he should be told to " bear down " while the hand
of the examiner is on the abdominal wall ; he should be ob-
served while getting into a chair and while getting out of
it without using the hands. The movements at the hip,
knee, and ankle joints should be carefully noted. Assum-
ing and leaving the " squatting " position tests the muscles
on the front and back of the thigh ; they may also be tested
by stepping with one leg on to and down from a chair

Fig. 3. — Hand dynamometer.

without assistance. The muscles of the legs*may be tried
by forward, backward, and lateral movements of the foot.
For the examination of these motor functions various instru-
ments are employed, notable among which is the hand dy-
namometer (Fig. 3), used to determine in kilogrammes or
pounds the strength of the grip. Dana has devised an ap-

30 INTRODUCTION.

paratus by which the strength of the muscles of the lower
extremities may be similarly measured. While these instru-
ments are often convenient, they are by no means essential
for securing an accurate idea of the muscular power, and,
in my experience, equally reliable results may be obtained
without them.

Rigidity. — The rigidity or spasticity which appears after
lesions of the central neuron, either in the brain or in the
spinal cord, and which eventually leads to contractures,
begins to appear in a few weeks after the receipt of the
injury. It is characterized by a stiffness of all the muscles
and by an overaction of the ones which are the least para-
lyzed. There is a consequent limitation of movement at the
joints, which may ultimately render them absolutely immo-
bile. This late rigidity is unmistakable ; it is shown by the
general stiffness of movement, and especially by the gait.

Acute cerebral lesions which produce paralysis cause ri-
gidity in the paralyzed limbs at once. This is called early
rigidity, and is indicative of an irritative lesion of the upper
motor pathway. When the loss of power is well marked it
can easily be detected that the limbs are paralyzed as well
as stiff ; but it not infrequently occurs that the affected limb
is rigid, and still the patient can move it. It is in such
cases that rigidity is an important diagnostic symptom.
Its existence, if the patient is conscious, can easily be dem-
onstrated by having him execute rapid movements which
require a considerable flexibility in the muscles, and ob-
serving whether they are done with normal ease and speed.
When there is coma, the presence of the rigidity must be
determined by the way the limbs feel. This is easy to do if
the stiffness is pronounced, as the limb then feels abnor-
mally hard and resistant to the touch. But when present in
slight degree only it is usually observed by no one except
by him who looks for it carefully, and who is accustomed
to looking for it.

DISORDERS OF MOVEMENT.

Tremor. — Tremor of the face is observed during the ex-
amination of the head. In the extremities it exists chiefly
in the arms and hands, though it may also occur in the legs.
By causing the patient to stand with his arms stretched out
in front of him and his fingers spread apart, by having him
execute movements with the arms and legs, the distri-
bution and character of the tremor may be ascertained.
Tremor of the hands is further shown by the handwriting;
and of the legs in attempts made by the patient at trying
to touch objects with the toes, or by trying to describe cir-
cles on the floor.

Fibrillary tremor, or fibrillation, is a very fine, rapid,
wavelike contraction of individual muscle fibers. It causes
no movement, and although its occurrence is involuntary
it is often observed by the patient himself. It is seen
chiefly in the face, in the muscles around the shoulders, and
in those around the base of the thumb. Although a nearly
constant symptom in muscular atrophy, and in most atro-
phic spinal cord lesions, it is not pathognomonic of any
disease, as it may occur in asthenic conditions which are
brought on by excesses of any kind.

Morbid Movements. — -Convulsions, athetosis, spasmodic
twitchings, and similar purposeless movements, when re-
sulting from accidents, are symptoms of so pronounced
a character that there is rarely any difficulty in referring
them to the lesions or conditions of which they are the
results. Unless the injury has been extremely severe, the
physician only occasionally has the opportunity of wit-
nessing these symptoms. In making his decision as to
their character, he must depend largely upon information
from outside sources. In hospitals, where the patients are
under the constant observation of the house staff and of
trained nurses, there can be no question as to the reliabil-
ity of the facts reported to him. But in the absence of
observations by skilled assistants he should be extremely

INTRODUCTION.

cautious lest he attribute too much weight to symptoms
he does not see.

Gait. — If the patient is able to walk, valuable and posi-
tive information concerning the condition of the motor
mechanism may be obtained by the observation of the gait.
Aside from such individual peculiarities of locomotion as
are due to disorders of the bones or joints, there are certain
types of gait which are absolutely typical as expressions of
morbid conditions which can never be successfully simu-
lated.

The Ataxic Gait is the most characteristic of these.
It occurs after lesions to certain sensory fibers and is
especially seen in locomotor ataxia. In that disease there
is no loss of motor power, but there is loss of the sense of
position, so that the patient does not walk well because he
does not know where to put his feet. More force than
necessary is used in bringing the legs forward ; the feet are
lifted too high and thrown too far outward, and finally come
down to the floor, the heel first and then the toe, with a
sharp slap. In slight degrees of ataxia, although the patient
may get around fairly well, and can often walk rapidly and
go long distances, there is difficulty in walking in the dark,
or in going downstairs. When the ataxia is more pro-
nounced, the patient walks with his eyes riveted upon his
feet, trying in this way to direct the movements of the legs.
When the ataxia is still more exaggerated the patient is
only able to walk with the assistance of a cane or of an at-
tendant, or locomotion may be altogether impossible.

Gait of Motor Paralysis. — The gait of motor paraly-
sis has essential differences according to whether it is the
central or peripheral motor neuron which is affected.

With injury to the central motor neuron, the paralysis
is usually only partial, and is associated with stiffness ; in
lesions of the peripheral neuron it is more complete, but
the muscles are soft and all rigidity in them is absent.

GAIT 33

The types of gait dependent upon affections of the upper
neuron are hemiplegia and, when both sides are affected,
spastic. The hemiplegia gait is usually spastic, but the
term spastic is generally understood to apply to cases in
which both legs are affected.

Hemiplegic Gait.— In cerebral hemiplegia, after the
acute effects of injury have passed away, the leg ordinarily
regains quickly much of its power, but the descending de-
generation in the motor pathway causes it to become
very stiff. In walking, the patient throws the weight of the
body toward the unparalyzed side and circumducts the
paralyzed leg so that it describes a segment of a circle in
its forward movement. From this peculiarity it is some-
times called the " mowing gait." The foot is dragged at its
tip and inner portions only, and there is little movement at
the knee or ankle joints.

Spastic Gait. — The spastic gait is the gait of double
hemiplegia. It occurs as the result of bilateral lesions of
the brain, or of lesions of the spinal cord above the lower
dorsal region.

Its characters are essentially the same as those of the
hemiplegic gait, except that both legs are involved and that
the degree of paralysis is greater than in hemiplegia. In
walking, the patient stiffly circumducts one leg until the
foot has crossed in front of the foot of the opposite side.
The same thing is then done with the other foot. From this
crossing of one foot in front of the other, the spastic gait is
sometimes called " crossed-leg progression." The soles of
the feet leave the floor but little or not at all, and the power
of locomotion is consequently impaired seriously. If the
patient carries a cane he keeps it in front of him, and leans
on it with both hands.

The Equine Gait is the type of gait in flaccid paralysis
of the anterior tibial group of muscles. It is due to lesion
of the peripheral neuron, and is seen in peripheral nerve

34 INTRODUCTION.

palsies and in injuries of the spinal cord in or below the
lumbar enlargement. It is never associated with rigidity.
As a result of the paralysis, when the lower limb is raised
the foot drops, so that the toe touches the floor. The toe
is then dragged, or the leg is raised higher than normal, in
order that the foot may clear the floor. There is, accord-
ingly, pronounced " knee action," and hence the term stepping
or equine gait.

In addition to these characteristic and constant anoma-
lies of progression there are other disturbances of gait which
are frequently observed and which, when present, are at
once suggestive of the conditions to which they are due.
Of these may be mentioned the careful steps of the patient
with lumbago ; the inert dragging of the feet in hysteria ;
the quick yet careless walk often seen in the early stages of
dementia paralytica ; and the festination of paralysis agitans,
of which Trousseau said that " the patient was running after
his center of gravity."

Intimately allied to the gait is the ability of the patient
to maintain his equilibrium. Normal persons can not hold
themselves perfectly motionless when standing with closed
eyes, but in them the swaying is slight. When the swaying
is pronounced it constitutes a symptom of importance and
is called the Romberg symptom.

If the patient is in bed and unable to use his legs it is, of
course, impossible to make these tests. But many persons
remain in bed for long periods of time, although they are
perfectly able to walk. It is always desirable to have the
patient make the attempt, when possible ; when this is not
possible, much information may be obtained by observing
how the patient lies in bed, how the limbs are held, and
whether their attitude indicates pain.

Sensation. — Although the clinical value of the anomalies
of cutaneous sensation, especially as observed in the func-
tional nervous diseases, has been subjected to much adverse

SENSATION.

criticism, the fact remains that anaesthesia, whether of func-
tional or organic origin, is one of the most valuable aids in
neurological diagncfeis, and no examination of a nervous
case can be regarded as satisfactory in which the presence
or absence of anaesthesia has not been definitely determined.
For sensory examinations there are a variety of instruments
which are of greater service to the anthropologist and ex-
perimental psychologist than to the clinician. It is not only
usually impossible to exercise in the clinic the exactness of
the laboratory, but it is generally true that any deviation
from normal sensibility is of very questionable clinical value
when it is so slight as to require instruments of precision for
its determination.

The aesthesiometer, the instruments for recording de-
grees of pressure, the concealed needles for testing sensi-
bility to pain, and the metal piles for determining the de-
gree of thermo-anaesthesia are rarely if ever necessary in
clinical examinations ; a needle, a piece of cotton, and two
test tubes, one filled with hot and the other with cold water,
are usually sufficient apparatus, and furnish results as reli-
able as those obtained by more delicate instruments.

During the examination the patient's eyes are covered,
and he is asked to indicate when he feels a touch rather than
if he feels it. It is advisable from time to time for the
examiner to pretend to touch the patient without actually
doing so, and then noting whether or not he responds ; for
the patient, although he can not see, may say, on hearing
the rustle of the coat sleeve, that he felt contact when none
was made. It is often impossible or inadvisable to extend
the examination over the whole cutaneous surface ; the re-
port should then state what parts were not examined and
the reasons for the omissions.

The limits of the anaesthesia are usually sharply defined
in organic cases. In functional cases the boundary between
parts which are anaesthetic and those which have retained

36 INTRODUCTION.

normal sensibility is often difficult and sometimes impossible
to accurately determine. Inasmuch as a thorough examina-
tion is fatiguing to both patient and exa'miner, it is advisable
in such cases to be satisfied with an approximation of the
anassthetic limits rather than to overfatigue the patient, be-
cause if he becomes tired his answers are less reliable. The
results of sensory examination are best recorded by anzes-
thesia charts, which are printed on pads with gummed
backs, or which may be stamped out with rubber dies. It
is most convenient to mark the affected areas with ink or
pencil on the patient, and then to transfer them to the
chart. Anassthesia of different characters may be indicated
by vertical or horizontal lines, by crosses or circles, or by
various other devices.

The different forms of sensibility should be examined
sequentially. The condition of the sense of touch of the
skin, as well as the patient's ability to indicate the part
touched, is ascertained by light brushes with the cotton.
The state of the conjunctivae and the lips, tongue, and
throat may be best examined at the same time. Slowed
•conduction is essentially a symptom of chronic processes.

For the sense of pain, examination with a needle fur-
nishes the desired information in most cases, although when
simulation is suspected other devices (see Part III) are some-
times resorted to. In testing the sense of temperature two
test tubes, one filled with cold water and the other with water
at a temperature of between 120° and 130°, will enable the
physician to discover any differences in the perception of
either heat or cold, as well as the patient's inability to distin-
guish between these two varieties of sensory stimulation.

The muscular sense is a complex function, and is usually
abolished when anassthesia is total. It includes the sense of
position of the limb and the appreciation of the amount of
exertion necessary for the performance of voluntary move-
ments. When the muscular sense is lost and motor power

REFLEXES. 37

is retained, the patient, in attempting movements of the
limbs, throws them about, often with great force, but with-
out the ability to properly and quickly direct them toward
the objective point. This condition of ataxia is seen in the
gait of tabes, and may be demonstrated for the upper ex-
tremities by directing the patient to perform definite move-
ments with the hands and observing how accurately he does
them. It may further be brought out by attempts of the
patient to put the limb of one side in a position conforming
to that in which the limb of the other side has been placed
by the examiner, or by his inability to tell with closed eyes
the exact position that a limb is in.

Reflexes. — The condition of the pupillary and palpebral
refiexes are determined at the time of the examination of
the eye ; the pharyngeal reflex at the time the throat is ex-
amined for anaesthesia.

There remain a series of reflexes termed superficial, and
deep or tendon reflexes, which should be examined together.
They are extremely valuable, and often constitute the one
link necessary to complete the diagnostic chain. The most
important superficial cutaneous reflexes are the cilio-spinal,
those of the abdomen, the cremasteric, and the plantar.

The cilio-spinal consists in a dilatation of the pupil when
the skin just above the clavicle is irritated by pinching or
by the faradic brush. Its loss is indicative of lesion to the
cervical sympathetic or to the first dorsal root, or to the
first dorsal segment of the spinal cord. The abdominal re-
flexes are epigastric, abdominal, and hypogastric. Their
action in health is seen by the contractions of the skin in-
duced by quickly stroking these regions of the abdomen
with the head of a pin. The cremaster reflex occurs as the
result of irritation of the inner side of the thigh, either by
striking or by pinching, which causes a contraction of the
cremaster muscle and an ascent of the testicle. In the plan-
tar reflex, irritation of the sole of the foot causes a flexion
4

38 INTRODUCTION.

at the knee and hip joints and a more or less violent agita-
tion of the whole limb.

The most important of the deep or tendon reflexes are
those concerned in the contraction of the triceps, the supina-
tor longus, the biceps, the extensors of the wrist, and the
quadriceps extensor of the leg. For their elicitation it is
necessary that the limb be pendent and free, the muscles
relaxed, and that light taps be applied over the tendons of
these muscles, preferably with a small hammer provided
with a rubber tip, known as the plessimeter (Fig. 4).

Fig. 4. — Krauss's plessimeter ; by unscrewing the caps C and D it
may be used as an sesthesiometer, or as a brush for testing tactile
sensibility.

The triceps, or elbow-jerk, and the supinator and biceps
reflex are not necessarily present in health, although they
may be. Their presence or absence is readily determined
by taps, applied for the former just above the olecranon pro-
cess, and for the latter (Fig. 5) just above the head of the
radius on its outer surface.

The knee-jerk, or patellar or quadriceps reflex, is by far
the most important of all. In health, a light tap upon the
patellar tendon induces a quick but slight extension of the
leg. The action is said to be hypertypical when it can be
elicited by taps on the muscle above the knee. There is no
absolute standard by which it may be determined when a
hypertypical knee-jerk becomes exaggerated. Very great
exaggeration is frequently associated with ankle clonus, and.
even in the absence of clonus, when light taps bring about
quick and forcible muscular contraction, the condition must
be regarded as exaggerated. Since absence of knee-jerk is-

REFLEXES.

occasionally observed in persons who are apparently normal,
this symptom alone is not sufficient for the diagnosis of
disease.

When the examination has not been painstaking it may
be concluded that the knee-jerk is absent, although the em-
ployment of the proper means for its elicitation would

Fig. 5. — Showinp; method of obtaining^ the triceps and supinator jerk.

have demonstrated its presence. Such an error is particu-
larly frequent when the reflex activity is diminished, either
as a personal peculiarity or as a result of disease.

In the larger number of cases this reflex may be obtained
by having the patient sit in a chair, one leg crossed over the

INTRODUCTION.

Other, while the physician taps the patellar tendon. If
there is no response, the Jendrassik (Fig. 6) method of re-
enforcement is resorted to. The patient, having crossed
the legs, pulls forcibly on his closed hands and looks up

Fig. 6.— Showinj; the Jendvassik method of obtaining the Ivnee-jerk.

at the ceiling. Before striking the tendon the examiner
should satisfy himself that the patient's hamstring muscles
are relaxed.

If none of these methods is successful they may be va-
ried by having the patient sit on a table so that the legs
hang over the edge ; or the examiner may place one arm
under the leg to be examined, so that the hand rests on
the knee of the opposite leg. In this way the leg is ele-

TROPHIC DISTURBANCES. 4I

vated from the floor, and at the same time the condition of
the hamstring muscles is ascertained.

If the leg is held perfectly limp and no reflex can be
obtained by any of these methods, it is fair to infer that the
knee-jerk is lost. Such an inference is not justifiable, how-
ever, if the flexor muscles of the legs can not be made to
relax, as sometimes occurs in persons who persistently re-
fuse to understand what is said to them. For such cases
the most that can be said is that the knee-jerk was not ob-
tained.

Foot or Ankle Clonus is usually regarded as an evidence
of degeneration of the pyramidal tracts, although it may
rarely occur in functional cases. In these latter, however, it
does not present the exaggerated characteristics which stamp
it as a symptom of organic disease. To examine for it the
patient sits down and the examiner supports the under sur-
face of the knee with the left hand and grasps the toes with
the right. The foot is then sharply flexed. If ankle clonus
is present, there ensues a series of rapidly alternating con-
tractions of the flexors and extensors of the ankle.

Trophic Disturbances. — Trophic disturbances of the skin
become at once apparent when the cutaneous surface is ex-
posed ; but by inspection alone it is impossible to determine
the presence of atrophy of the muscles, unless it has already
reached a considerable degree of advancement. Under
such circumstances the affected part, as determined by in-
spection or by measurement with a steel tape, is found to be
smaller than that of its fellow of the opposite side ; or, if
both limbs are involved, smaller than there is reason to
suppose they were before the accident. Also, when the
atrophy of muscle is pronounced, the skin over it is loose
and flabby, and there is absent the feeling of firmness and
resistance characteristic of normal muscle ; but in the early
stages such unmistakable evidences of atrophy are often
wanting, and it is necessary to resort to examination by

INTRODUCTION.

electricity. If there are abnormal changes in electrical ex-
citability it follows as an inevitable conclusion that there is
also an atrophy of muscle, although it may have escaped
detection by other methods of examination.

Electrical Examination. — In cerebral injuries it is often
immediately evident that the battery can throw no light
upon the character or situation of the lesion. Electrical
examination is indispensable for all affections of the lower
motor neuron, and no case of paralysis can with justice be
diagnosticated as functional unless such means of investiga-
tion have been employed.

Much information can be obtained from a simple faradic
battery, although it is usually desirable to test with both
the interrupted and the constant current. The sponges in
the electrodes must be kept constantly moist, and one of
them should have a small head and be furnished with an
interrupter. A galvanometer is a useful addition to the
galvanic battery, but it is indispensable only when the pa-
ralysis is bilateral, so that the reactions on the injured side
can not be compared with those of the opposite (normal)
side, and when the increased strength of current needed to
cause contraction is the only index of trophic change.

The reactions of degeneration which occur after lesions
of the peripheral neuron are essentially the same, whether
the injury has occurred in the spinal cord or after the
nerves have made their exit. Degenerative reactions are
the expressions of the abolition of. trophic function whose
center is in the anterior horns, and whether it is the center
itself which is destroyed, or the means of transmission of
its influence, makes no difference as far as the electrical re-
actions are concerned.

To determine the character of these changes it is neces-
sary to examine the nerve trunk and its branches to the
individual muscles. With an electrode on the sternum or
some other indifferent point, the examining electrode is

Superior branch.

Fi L ■ ■ Obic. oris. (.'^

lexor brevis pol, "'^ "4-— -=^-»

)JjJ /_i Inferit

N. Facial.

-Opponens pol,
■- Ab. pol.
^N. Med.

ior branch.
— Masseter.
_- Sternocleido.
Platysma. I r-^/—— Trapezius.

_ , — --^rt ^ •-■{ Erbs point.

Brach.ant -t— V i I N. Phrenic.

-Deitoid.

X s

^ N. Musculo - Spiral.

\ "n / SerratusX
\ . Y\ rnagnus. \

•-V— Triceps, (long head.)

• \

)/' •~-X — Ext. dig. comm.

^N. \A Ext. Carp,
^N ^^^\ rad. long.

"""" — -V^^ Recius.

\ »-V — Ext. min. dig.

>v ■* \

V^ "V Extensor ind.

\ P

'' \ •-V — Ext. long, pol

-- Ab. min. dii

Ext. dig. comm. brev.

lowing the superficial position of the large nerve trunks and the motor points for the muscles.

ELECTRICAL EXAMINATION.

placed over Ihe nerve trunk at some point in its course.
The points of entrance of the branches to the muscles were
first fully ascertained by Erb, and their topographical dis-
tribution is shown in the accompanying chart (Fig. 7).

The variations in the character of electrical responses
depend upon the part examined (nerve or muscle), the
current used, the extent of injury, and the time which has
elapsed since its receipt.

In the trunk- of an injured nerve changed electrical re-
actions are of essentially the same character to both con-
stant and induced current. There may be for a day or two
after the injury an increase of excitability, but this is soon
replaced by a diminished response, and in the course of a
few weeks there may be no response at all. If recovery
occurs (and the loss of electrical excitability in the nerve
trunk does not imply that the degeneration is irreparable),
the reaction to stimulation will be gradually restored.

The abnormal electrical reactions of the nerve termina-
tions in the muscles are found by placing one electrode
over an indifferent point and the examining electrode over
the motor points of Erb, which correspond in position with
the entrance of the nerve ending into the muscle.

At these points the electrical evidence of nerve injury
difters with the two currents. Response to the faradic
current may be hyperactive for a day or two after the
injury, but it then rapidly decreases until about the sec-
ond week ; then there is no longer any response at all.
When regeneration begins, often about the second month
after injury, there occurs a gradual return of faradic excita-
bility.

The galvanic reaction, on the other hand, after a day or
two of normal or increased response, falls with the faradic ;
but instead of becoming extinct, like the faradic, it begins to
rise in the second or third week. The increased response to
galvanism may become and remain so marked that very

INTRODUCTION.

weak currents produce forcible contractions. The increase
of galvanic excitability may persist for many months and
eventually be replaced by total absence of response ; or
about the same time that the muscles show a return of con-
tractibility to faradism the galvanic response decreases until
it reaches and remains at the standard of health.

The accompanying diagram (Fig. 8) may graphically
represent the behavior of the electrical reactions for the
first four weeks after a moderately severe injury of a periph-

IN MUSCLE
12 3 4

IN NERVE
I 2 3

FARADIC

2 3 4

12 3 4

Fig. 8. — Diagram to illustrate tlie electrical reactions occurring in a nerve after a
moderately severe injury.

eral nerve. It is seen that in the muscle the response to
faradism is hyperactive for a few days, then rapidly sinks in
about the second week. The galvanic curve, on the other
hand, after an initial rise and fall, begins to rise after the
second week, and remains for some time above the normal.
In the nerve the behavior of the two currents is seen to be
the same.

These changes in electrical reactions indicate degenera-
tive processes of greater or less severity in the nerve trunk
and nerve endings. They are quantitative. Still more im-
portant are the qualitative changes as seen in the " reaction
of degeneration."

The reaction of degeneration is found in the muscles
only, and consists in a reversal of the normal reaction to
galvanism.

ELECTRICAL EXAMINATION. 45

In health the contraction induced by closing the circuit
is greater when the cathode is over the motor point than
when the circuit is completed with the anode in that situa-
tion. The cathode-closure contraction is greater than anode-
closure contraction, or, graphically :

CaCl > AnCl.
In disease these reactions may be reversed, so that

CaCl = AnCl,
or CaCl < AnCl.

In degeneration of nerves the contractions of the mus-
cles to both galvanic and faradic currents are often slow and
wormlike, instead of being quick and tonic, as in health.
This vermicular reaction, like the reaction of degeneration,
is indicative of serious though not necessarily irreparable
injury. Such are the changes in electrical response most
frequently observed after nerve injuries.

PART I.

ORGANIC EFFECTS OF INJURY TO THE
NERVOUS SYSTEM.

While it is not the chief object of this work to portray
the clinical or pathological conditions which may result
from organic injuries to the nervous system, a brief men-
tion of nervous symptoms as caused by definite lesions seems
imperative as a preliminary to the study of functional de-
rangements. In all cases of traumatic nervous disease the
question at once arises whether there is a lesion destroying
nerve tissue, or whether the symptoms are merely indicative
of a repression or perversion of function of temporary char-
acter occurring independently of known lesion.

In functional cases the evidences of structural lesion are
not present ; to prove them absent, however, requires a
painstaking examination directed toward the whole cerebro-
spinal axis. It is accordingly the object of the three im-
mediately succeeding chapters to briefly describe the symp-
toms which are to be regarded as indicative of acute or-
ganic injury to the brain, the spinal cord, and the peripheral
nerves. In the fourth chapter of this section are considered
the possibilities for a traumatic origin of certain of the
chronic degenerative diseases.

CHAPTER I.

INJURIES TO THE BRAIN.

Contrasted to the cerebral injuries in which there is no

difficulty in deciding upon the character or the approximate

location of the trouble, are cases in which the nature or even

INJURIES TO THE BRAIN. 47

the situation of the lesion can not be determined without an
examination of the whole nervous system, and it is in such
cases especially that the physician needs to be familiar with
the essential characteristics of those symptoms which be-
speak loss of continuity in cerebral conducting paths or in-
jury to cerebral cells.

Even the most scrupulous care and widest experience
are often unavailing for diagnosis, and the nature of the con-
dition does not become plain until recovery stamps it with
characteristics of individual types, or until the pathologist
gives the answer to the riddle which the clinician was un-
able to solve.

The most perplexing cases are those in which unknown
persons are found lying senseless. The presence of scalp
wounds may prove a head injury, such as could have been
inflicted by a blow or a fall ; witnesses are wanting, and the
physician or surgeon must rely upon his own skill to decide
whether the patient lost consciousness as the result of a fall
or blow on the head, or whether the fall resulted from dizzi-
ness or unconsciousness brought about by some purely medi
cal disease.

It is the old and perplexing question of the differential
diagnosis of coma; its consideration here must be limited
to a brief description of those symptoms which are usually
present when it is due to direct injury of cerebral tissue.
They are of three classes :

1. General, which may occur after any severe general in-
jury.

2. Mental, which indicate interference with intellectual
processes.

3. Focal, which are due to lesions of circumscribed areas
of the brain.

I. General Symptoms. — The most important symptom of
general injury, either to the nervous system or to other
parts, is surgical shock.

48 ORGANIC EFFECTS OF INJURY.

It is to be distinguished from psychic or nervous shock,
which is the impression made upon the mind by sudden and
painful emotional influences. Physical or corporeal shock
is a sudden depression of the functional activity of the gen-
eral nervous system. Its pathology is unknown. It is a
constant accompaniment of severe injuries of any part, and
it sometimes follows traumatism of a trifling nature. It
occurs immediately after the accident, and may continue a
varying length of time. Consciousness is not lost, but the
patient is depressed and apathetic. The face is pale, the skin
is moist and cold, the pulse is soft, rapid and feeble, and the
respirations are shallow. Shock often appears to be the sole
determining cause of death.

Among other common general symptoms of lesion to the
brain more suggestive than shock may be mentioned vomit-
ing, slow pulse, stertorous breathing, the tendency to con-
gestion, oedema or consolidation of the lungs, fever, and
incontinence or retention of urine or fasces.

2. Mental Symptoms. — Mental symptoms are naturally
the most prominent evidences of disturbances of the organ
which is the seat of the intellectual faculties. In injuries to
the spinal cord, or to the peripheral nerves, consciousness is
usually retained ; but in all severe cerebral injuries, and in
many which are apparently trivial, it is more or less com-
pletely lost. The term " coma " is applied to the condition
in which the patient is completely unconscious, and can be
aroused but little or not at all by peripheral irritations. In
the milder degrees of insensibility, when he can be made to
answer questions, it is called "stupor." From the presence
of unconsciousness alone, it is usually impossible to deter-
mine whether or not there has been a gross structural lesion
of the brain. After a blow on the head a man may remain
unconscious for several days, and finally recover without
any further evidences of cerebral trouble ; or the coma fol-
lowing a similar accident may be less profound, although

INJURIES TO THE BRAIN. 49

permanent paralysis, mental impairment, or death is to be
the result.

Often, instead of unconsciousness or hebetude, the mental
condition is one of confusion. This may even be the case
after injuries which are soon to prove fatal.

A short time ago I had the opportunity of examining at the
Harlem Hospital a young man who had been struck by a billiard
cue over the right parietal eminence. There was a scalp wound
over the place where he had been hit, but no discoverable evi-
dences of fracture. At the time I saw the patient, two days before
his death and several days after the accident, he was apparently
entirely conscious although very much confused. He under-
stood everything that was said to him, but it was difficult to hold
his attention; when told to put out his tongue or perform other
acts, he obeyed promptly, but he did not seem to know what he
was doing, and had to be spoken to two or three times before he
executed the movement. There was general increase of the deep
reflexes, but there was a total absence of evidences of local injury
to the brain. Soon after this he became comatose and died.
The autopsy showed a fissured fracture of the right parietal bone,
and a large subdural haemorrhage on the opposite side of the
brain.

Delirium is a frequent complication of head injuries,
especially in alcoholic persons. It may be mild or mutter-
ing, or may be attended with hallucinations, delusions, and
impulsive acts.

None of the mental symptoms of head injuries is neces-
sarily indicative of permanent organic brain lesion, although
it is generally true that the more serious the mental symp-
toms the more probable becomes the existence of some
irremediable cerebral condition. In some fatal cases of trau-
matic cerebral haemorrhage mental symptoms exist without
any focal signs.

3. Focal Symptoms. — The most certain and definite in-
formation concerning injuries to the brain is furnished by
the symptoms of lesions confined to circumscribed areas
(see Figs. 9 and 10). Although no individual region of the

ORGANIC EFFECTS OF INJURY.

brain acts independently of other parts, there are certain
districts which have specialized functions, and injury to
these causes definite and constant symptoms. The most

Superior frontal sulcus.

Fissure of Rolando.

Interparietal sulcus.

Ascending ramus

of the fissure

of Sylvius.

Fissure of Posterior ramus of the Superior temporal
Sylvius. fissure of Sylvius. sulcus.

Fig. 9. — Schematic representation of the cerebral corfex and its centers.
(After Tillmanns.)

1. First. 1

2. Second. >• Frontal convolution.

3. Third. )

4. Anterior. I Central convolution.

5. Postenor. )

6. Upper. j

7. Middle. )- Temporal convolution.

8. Lower. )

9. Upper.
10. Lower.

■ Parietal convolution.

11. (iyrus angpularis.

12. Upper. 1

13. Middle. >• Occipital convolution.

14. Lower. )

O In 4 and 5 on both sides of the fissure of
Rolando, motor area for the upper
extremity.

O Motor area partly for the upper and part-
ly for the lower extremity (great toe).

Motor area for the lower extremity.

O Cortical area for the hypoglossal nerve.

O (3) Motor aphasia.

X (6) Sensory (auditory) aphasia with
word-deafness.

+ (11) Aphasia with word-blindness.
• (12) Region of the visual area (see also-
Fig. 10).

sharply limited of these districts are the ones which preside
over the faculty of speech and the ones concerned in vol-
untary motion.

INJURIES TO THE BRAIN.

Speech Disturbances. — Most traumatisms which act on
the brain in a way to abolish or impair the activity of the
centers of speech cause at the same time such pronounced

F.po.

S.h.
Fig. 10. — View of the right cerebral hemisphere from the median side ; B, corpus callo-
sum divided longitudinally; G./.^ gyrus fornicatus ; //, gyrus hippocampi; S. h.^
sulcus hippocampi ; G.u., gyrus uncinatus ; 6'. c. m., sulcus calloso-marginalis ; F. 1,
first frontal convolution; .S'. c, termination of the fissure of Rolando ; in front the
anterior central convolution with the motor area partly for the upper and partly for
the lower extremity, and behind the posterior central convolution with the motor
area for the lower extremity; P, praecuneus ; C, cuneus; F.po , parieto-occipital
sulcus ; /, polus ; F.c.^ calcarine fissure ; in the posterior part of this the visual area
is shown by a red dotted line. (After Tillmanns.)

mental symptoms that examination for the highly specialized
cerebral functions is unsatisfactory or unavailing. How-
ever, as such selective injuries sometimes occur without seri-
ously interfering with general intellectual power, and since,
when the acute general effects of injury have passed away,
there may be left symptoms of focal lesions to parts con-
cerned in the faculty of language, the most common forms
of cerebral speech disturbances must be mentioned.

The best defined of the cerebral centers for speech may
be seen in the accompanying figures 9 and 10. They in-

52 ORGANIC EFFECTS OF INJURY.

elude the second and third left frontal convolutions, injury
to which causes motor aphasia or an abolition of the power
of voluntary speech without paralysis of the muscles of
articulation, or without loss of understanding of spoken or
written language. Motor aphasia is the most common of
the isolated speech disturbances which may be due to trau-
matisms. It is almost always associated with right hemi-
plegia. Injury to the first or second left temporal convolu-
tion causes word deafness or the loss of understanding of
spoken words, without any disturbance of hearing or with-
out serious impairment of the power of speech. Injuries
to the occipital lobes sometimes cause a loss of power of the
understanding of written signs, and if situated unilaterally
near the calcarine fissure, hemianopsia. Mind blindness and
mind deafness are rare conditions, in which, without other
mental defect, there is an inability to recognize familiar ob-
jects or sounds.

Motor Symptoms. — Paralysis. — Loss of power of volun-
tary movement is the most constant and most valuable sign
of focal injury to the brain. It is a very frequent accom-
paniment of cerebral traumata, and, even when slight in de-
gree, its meaning is so unmistakable that examination for it
should be scrupulously made in all cases, although it may
seem at first to be absent. The nature of paralysis may be
best understood by referring to the way in which voluntary
movements are normally performed.

Voluntary movements are presided over by the motor
cells, which are situated in the gray matter around the
fissure of Rolando. It is in the cells of this region that the
motor pathway has its beginning, and the motor pathway
(Fig. ii) is the cerebro-spinal tract of 'which our knowledge
is most complete.

It descends through the brain as a well-defined bundle
of nerve fibers which terminate in the basal ganglia, the
pons, the medulla, and the anterior horns of the spinal cord.

INJURIES TO THE BRAIN.

Before reaching the spinal cord the larger number of these
fibers decussate ; those for the cranial nerves, in the pons
and in the upper part of the medulla, and those for the

lotfer extremity

Fig. II. — Schema illustrating the course of the cerebro-spinal motor path.
(After Van Gehuchten.)

.spinal cord, in the lower part of the medulla. By this cross-
ing, the cerebral fibers for motion have their termination in
ihe opposite side of the cerebro-spinal axis to that from
5

ORGANIC EFFECTS OF INJURY.

CORTEX

CENTRAL

which they came. The continuation of the motor tract front
the gray matter of the brain axis and spinal cord is in the
peripheral nerves, which are distributed to the muscles.

The entire tract for voluntary motion, from cortex to
periphery, is composed of aggregations of nervous units,

which are called
motor neurons. A
neuron, a term pro-
posed by Waldey-
er to include the
nerve cell in its en-
tirety, consists of
the {a) cell body,
the ip) protoplas-
mic processes or
dendrites, which
are generally sup-
posed to convey
impulses to the
cell and are conse-
quently afferent,
and the (c) axis
cylinder of the
cell, or the neurax-
on, which is known
to convey impulses
from the cell and
is consequently efferent. The cerebro-spinal motor path-
way is principally made up of two sets of these neural ele-
ments, which are called respectively central, upper, or sec-
ondary neurons, and peripheral, lower, or primary neurons.
(Fig. 12). The cell body of the central neuron is situated in
the motor cortex of the brain, and its neuraxon descends
through the motor pathway, to be connected by fine ter-
minal filaments with the peripheral neuron. The peripheral

MUSCLE

Fig. 12.— Schema to illustrate the arrangement of the
motor neurons.

INJURIES TO THE BRAIN. 55

neuron connects the gray matter of the brain axis or of the
spinal cord, as the case may be, and the periphery. Its
body is in the gray- matter, where it is closely associated
with the terminations of the central neuron ; its neuraxons
form the motor fibers of the peripheral nerves. A volun-
tary movement is the result of some change, the nature of
which is unknown, in the cortical part of the central neu-
ron, by which an impulse is liberated and caused to de-
scend the neuraxon. Its energy is then transferred by
means of the terminal filaments to the peripheral neuron,
along which it passes to the muscle fiber, which it stimulates
and causes to contract. When for any reason the creative
power of the cell body of the central neuron is abolished,
or the conductivity of its lower part or of the peripheral
neuron is lost, the muscles which are controlled by these ele-
ments can not receive the stimulus necessary for their con-
traction, and are consequently paralyzed.

The clinical manifestations of paralysis vary according
as the lesion exercises its inhibitory or destructive action
upon the central or the peripheral neuron.

SYMPTOMS OF CENTRAL NEURON SYMPTOMS OF PERIPHERAL NEU-
INJURY. RON INJURY.

Paralysis, Paralysis,

Rigidity, Flaccidity,

Increase of tendon reflexes, Loss of all reflexes.

Loss of peripheral reflexes,

Preservation of normal elec- Degenerative electrical reac-

trical reactions, tions.

Atrophy slight or absent. Atrophy early and decided.

Trophic disturbances not promi- Trophic disturbances promi-
nent, nent.

Exception must be made for the distinctive character of
these symptoms in so far as that after acute injuries all re-
flexes may be absent for a time ; paralysis may remain flaccid
for hours or days ; and that at least five days are necessary for
the development of degenerative electrical reactions. The

56 ORGANIC EFFECTS OF INJURY.

pure type of central neuron paralysis is seen only in injuries
occurring in or above the basal ganglia of the brain. In
these situations none of the neuraxons have reached their
lowest destination, and since a peripheral neuron does not
begin until its central neuron ends, there are no peripheral
neurons in the vicinity of the lesion, and the paralysis accord-
ingly corresponds to the central neuron type. The pons,
medulla, and spinal cord, on the other hand, contain such
peripheral neurons as are making their exit from the cere-
bro-spinal axis (cranial and peripheral nerves), and also those
central neurons which are still descending to be connected
with the peripheral neurons which are situated at lower
levels. Consequently, while injuries of the cerebrum pre-
sent symptoms referable to lesions of the central neuron
only, those at the base of the brain or in the spinal cord
usually give evidence of interference with both neurons.
Thus an injury to one side of the pons, in a situation below
the crossing of the facial nerve, causes a facial palsy on the
same side as the lesion (peripheral neuron), while the paraly-
sis of the arm and leg is on the other side of the body, and
of central neuron type.

In addition to the types of paralysis, according as one
or the other neuron is affected, there are certain means of
localization of the injury afforded by associated signs, which
are present when the lesion is in some situations and which
are absent when it is in others.

Cortical injuries commonly cause paralysis of the arm
and leg, less frequently of the arm, leg, and face. When
the cortex is injured, convulsions are common, as is seen in
traumatic epilepsy or in the twitchings of muscles recently
paralyzed ; there may also be a loss of the sense of position
and some disturbance of cutaneous sensation. Monoplegia
rarely results from traumatism of the brain ; when it occurs
it is due to a selective injury to the cortex.

In the tracts below the cortex smaller lesions cause more

INJURIES TO THE BRAIN.

extensiye paralysis, as in those situations the motor fibers are
more closely packed together and the pathway is smaller.

Lesions of the internal capsule cause hemiplegia of the
opposite side; when situated posteriorly, there may also be
diminution of cutaneous sensibility and hemianopsia. Le-
sions at the base of the brain, by pressing upon or destroy-
ing the neuraxons of those central neurons which preside
over voluntary motion in the limbs, may cause paralysis of
them of various distributions. But in addition to the pal-
sies of the limbs, central neuron type, there are usually
palsies of the cranial nerves, peripheral neuron type.

The pons, as well as the cortex, contains a convulsive
center, and consequently lesions at the base of the brain,
which irritate the pontine region, are followed by muscu-
lar twitchings or by general convulsions. Pontine lesions
also usually cause anaesthesia.

If the lesion is in the anterior fossa of the skull, the only
cranial nerves affected are the olfactory and optic.

Symptoms of direct injury to the olfactory nerves are
rare. They consist of disturbances of smell, which are usu-
ally associated with impairment of taste. Fractures at the
base of the skull and penetrating wounds not uncommonly
cause laceration or haemorrhage into the sheaths of the
optic nerves. If either optic nerve is injured in front of the
chiasm, the result is more or less complete blindness in the
eye of the same side. The ophthalmoscope shows optic
neuritis, which may be followed by atrophy.

Injury of the optic nerve at the chiasm causes bilateral
blindness. If the optic tract is injured posteriorly to the
chiasm the result is hemianopsia. Palsy of the third nerve,
either total or in some of its fibers only, is one of the most
frequent evidences of injuries in the vicinity of the orbit and
at the base of the brain. From the controlling influences
which this nerve exercises upon the eyelid, upon most of
the extrinsic muscles of the eyeball, and upon the size of the

58 ORGANIC EFFECTS OF INJURY.

pupil, an abolition of its function causes striking symptoms.
When the nerve is the seat of a complete lesion, there are
ptosis, outward and downward rotation of the eye from the

overaction of the external rectus
and the superior oblique, and dil-
atation of the pupil (Fig. 13). Com-
plete third-nerve palsy, however, is
comparatively rare in acute condi-
tions. More frequently the nerve
shows a partial and selective palsy.
Thus there may be a drooping of
the upper lid, so that the affected

Fig. 13. — Double third - nerve , , . ,

palsy, showing outward and eye can not be opened as wide as
downward deviation of both t^g normal eye ; or there may be

eyes and wrinkling of the fore-
head. (Incurable Hospital.) Only a slight dilatation of the pupil

' on the injured side, so that there

exists an inequality in the size of the pupils, the larger being

on the side of the injury ; or there may be a weakness in the

extrinsic muscles supplied by the third nerve.

Palsy oi.\}a.Q fourth nerve is uncommon, and unless pro-
nounced is only demonstrable by means of prisms.

The fifth nerve usually escapes intracranial lesion and is
never injured alone in this situation. Its affection is re-
vealed by palsy of the masseters and buccinators and by
anaesthesia, with pain over the face and forehead. If the
fibers to the eyeball are involved there results neuropara-
lytic ophthalmia.

The sixth nerve is frequently the seat of traumatic pa-
ralysis. Through the resulting weakness of the external
rectus, the eyeball is turned inward and movements out-
ward are limited or impossible. Pa:lsy of any of the ocular
nerves causes the subjective sensation of diplopia.

Intracranial facial {seventh nerve') paralysis differs from
extracranial facial paralysis in that there may be added dis-
turbances of taste' and of salivary secretion. When of trau-

INJURIES TO THE BRAIN.

matic origin it is invariably unilateral and associated with
disturbances of the auditory nerve, such as deafness, sub-
jective auditory sensations, and dizziness. Palsy of the
nerve will be considered more fully on a later page. By
reason of their situation, the glossopharyngeal, pneumogas-
tric, and hypoglossal nerves are never paralyzed by acute
intracranial injuries, which are not almost immediately fatal.
Sometimes several cranial nerves are paralyzed together.
A characteristic clinical type of such multiple nerve lesions,

Fig. 14. — Photograph showing paralysis ot
the left sixth and seventh nerves, due to
a fracture of the skull. Patient trying
to look straight ahead.

Fig. 15. — Same case,
look toward the
Clinic. )

Patient trying to
left. (Vanderbilt

sometimes seen after fractures at the base, is illustrated by
the following case (Figs. 14, 15).

The patient came to the Vanderbilt clinic complaining of deaf-
ness, double vision, and the drawing of the face to one side. He
told us that twelve weeks previously he fell twelve feet, striking
on the buttocks; he lost consciousness for some time, and on
coming to himself observed the symptoms above mentioned, to-
gether with bleeding from the left ear. Our examination showed:

6o ORGANIC EFFECTS OF INJURY.

partial paralysis of left external rectus (sixth nerve), peripheral pa-
ralysis of left side of face (seventh nerve), deafness in left ear with
loss of bone conduction (eighth nerve). The appearance of the
patient was highly characteristic: the left side of the face was
flattened, a condition which was caused by a contraction of the
muscles of the right side. When the patient looked straight in
front of him there was a left internal squint caused by overaction
of the internal rectus ; when he tried to look toward the left,
the right eye executed the movement normally, but the left
looked straight ahead from inability of the left external rectus
to rotate the eyeball outward.

However, in traumatic affections at the base of the brain
there is only rarely the opportunity for that accuracy of
topographical diagnosis w^hich is so generally possible in
chronic lesions. The former result, in the vast majority of
cases, from fractures at the base of the skull which cause
such extensive haemorrhages or lacerations of the cranial
nerves or of the cerebral substance that it is usually impos-
sible to determine as to the existence of discrete multiple
lesions, and the physician or surgeon generally has to con-
tent himself with making the diagnosis of injury at the base
of the brain, without definitely ascertaining its exact loca-
tion.

The symptoms of injury to the cerebellum are often in-
definate. Lesion of the lateral lobes gives no localizing symp-
toms. If the middle lobe, or worm, is involved, there is the
characteristic cerebellar ataxia, which may be associated
with loss of knee-jerks. Injuries to the medulla are always
immediately fatal.

Sensofy Symptoms. — Pronounced ansesthesia is rarely
if ever observed as a focal symptom of traumatisms of the
brain.

After severe injuries, when the coma is profound, there is
often a generalized diminution or a total loss of cutaneous
sensibility, as is shown by the patient's indifference to the
application of painful stimuli. But this is to be interpreted

INJURIES TO THE BRAIN. 6 1

as a disturbance of the receptive centers, due to abolition of
mental function, rather than as an indication of any interrup-
tion of conducting paths. This assumption receives addi-
tional proof from the fact that sensibility almost invariably
returns with a restoration to consciousness. If there is a
well marked hemiplegia, complaints of subjective sensations
of pricking or numbness in the paralyzed side may be made,
and by examination with the needle or with cotton it may
become evident that there is some blunting of sensibility on
the paralyzed side. But, although the patient does not feel
so well on that side as on the other, he can still distinguish
between hot and cold, can tell when he is touched, and
gives some expressions of pain upon the application of
painful stimuli — evidences of hypsesthesia rather than of
anaesthesia. Hemihypgesthesia, associated with disturbances
of the sense of position, is a not infrequent result of injuries
of the motor cortex.

Lesions which result from external violence and which
affect the cerebral sensory tracts probably never cause
complete hemianassthesia, with involvement of the head,
trunk, and extremities, such as is frequently seen in hysteria.
In cortical injuries the resulting ansesthesia is never total
and is rarely pronounced in degree. Pressure upon the pos-
terior third of the hinder limb of the internal capsule may
bring about complete loss of sensibility to all stimuli on the
opposite side of the body; or pressure upon the pons in the
neighborhood of the fifth nerve may cause " crossed hemi-
anaesthesia " — i. e., loss of sensibility in the distribution of
the fifth nerve on the side of the lesion and anaesthesia of
the arms, trunk, and legs of the opposite side. Cases pre-
senting these symptoms have been reported, but, as far as I
know, they have been the results of tumors or of non-trau-
matic vascular disturbances exclusively. It can not be de-
nied, however, that similar symptoms might result from lac-
eration of the brain, or from haemorrhages into it, which

62 ORGANIC EFFECTS OF INJURY.

were caused by quickly acting external violence, but if such
a possibility exists, evidence in its favor has escaped my
notice ; and, indeed, it seems hardly probable that any trau-
matism could act in a way to produce so small and so selec-
tive a lesion as would be necessary to cause the pure type
of hemiangesthesia, such as is produced by interference with
the sensory tracts in the pons or in the internal capsule,
without at the same time so seriously injuring other parts
of the brain that the unilateral character of the sensory loss
was not maintained, or that the sensory symptoms became
masked by more serious nervous disturbances.

As will be mentioned in succeeding pages, hemianges-
thesia — profound, total, and sharply limited by the median
line of the body — is not uncommonly observed in the victims
of railway and allied disasters. To it Charcot ascribed a
pathognomonic value in the diagnosis of hysteria, a view
which was opposed in Germany. Without entering here
into further discussion of the question, it may be safely
asserted that when pronounced hemianaesthesia appears as
one of the clinical results of an accident it is in all proba-
bility hysterical, and that if this symptom is ever the result
of an organic injury to the brain, the inevitable association
of other symptoms of cerebral lesion will leave no doubt as
to its nature and origin.

Reflexes. — As a rule, after injuries to the head which
have been severe enough to cause profound coma, both the
skin and tendon reflexes are temporarily lost. The general
absence of reflexes indicates that the brain has been seri-
ously injured, but gives no indication as to the seat or the
character of the lesion.

When the initial coma is less profound, or when it is
beginning to pass away, the condition of the reflexes is
capable of furnishing more definite information.

All the reflexes on the paralyzed side may be absent,
while those of the unaffected side remain about normal, or

VARIETIES OF BRAIN INJURIES. g,

— and especially if the examination is made a few days after
the accident — there may be a unilateral increase of tendon
reflex activity on the side of the paralysis, while the abdomi-
nal reflexes of that side remain unelicitable. The unilateral
absence of abdominal reflexes, with increase in the knee- or
wrist-jerk, is one of the most valuable diagnostic signs of
hemiplegia, and may be present when the loss of motor
power is very slight.

Bladder and Rectum.— In deep coma there may be the
retention of urine, or the involuntary passage of urinary
and f^cal discharges, which is the rule. When the patient
is conscious there is usually no loss of control of the blad-
der or rectum as a result of cerebral injuries.

Varieties of Brain Injuries.

The brain is very much less securely protected against
injury than the spinal cord, there bepg wanting the thick
cushions of muscles, and the bones which surround the
encephalon being thinner and less resistant than those which
inclose the spinal cord. A blow which, if applied to the
back, would be followed by no evidences of spinal cord
lesion, might, if applied to the head, cause serious cerebral
injuries. By blows on the head, by falls, or by the entrance
of foreign bodies, the skull may be fractured and the brain
be contused or lacerated, either directly by splinters of
bone or indirectly by transmitted force. Haemorrhage may
occur from vessels which are ruptured, either in the bone,
in the membranes, or in the brain substance, or there may
be generalized oedema or circumscribed oedema which latter
gives focal symptoms.

Without fracture of the skull the intracranial blood-
vessels may be ruptured, or the brain substance or cranial
nerves may be contused or lacerated. While in the major-
ity of cases the skull is fractured, the fracture is often not
recognizable during life, and the diagnosis of the nature

64 ORGANIC EFFECTS OF INJURY.

of the injury must be made from the nervous symptoms
alone.

Concussion. — In the chapter on injuries to the spinal
cord it will be stated that there is still much doubt as to the
existence of any such condition as concussion of that or-
gan. The probability that head injuries may be followed
by pronounced cerebral symptoms without there being any
discernible lesions in the brain is very much stronger.
There is, of course, no question but that after many head
injuries multiple hsemorrhages occur, especially in the gray
matter, which do not give any localizing symptoms, and
that in many of these cases the condition must be diagnos-
ticated clinically as that of cerebral concussion. But the
results of daily clinical experience leave hardly room for
doubt that, after very insignificant head injuries, there occur
unconsciousness and other slight cerebral symptoms of too
trivial a character to be dependent upon any lesion so gross
as hgemorrhage. To cite an example familiar to boxers, a
blow on the point of the jaw may deprive the victim of all
appreciation of his surroundings. Yet in a few moments he
is entirely recovered and ready to continue the fray. He
has suffered temporarily from cerebral concussion. From
these conditions, when the patient is for a few minutes
without consciousness, to those in which he lies for days
in coma, stupor, or delirium, there are various intermediate
stages ; and while, in the severer cases, we may suspect dur-
ing life and be able to prove after death that the symptoms
depended upon multiple though minute haemorrhages and
lacerations, there are many patients who do not die, and
who, by the speediness of their recovery, indicate that the
brain has received no severe injury. In the absence of local-
izing signs we are unable to distinguish between the differ-
ent varieties of cerebral concussion, and we are consequently
obliged to designate by the same term conditions which
may be very different.

VARIETIES OF BRAIN INJURIES. 65

The symptoms of cerebral concussion may be slight or
severe. In consideration of the fact that serious organic
injuries of the brain may for a long time cause no pro-
nounced cerebral symptoms, the physician can hardly be
accused of overcautiousness if he refuses to diagnosticate
cerebral concussion until the patient has been under obser-
vation for several days.

After the injury there may be deep coma or stupor, or
only mental confusion. Delirium is not infrequent, and in
alcoholic patients its occurrence, associated with zooscopic
hallucinations, is the rule.

The patient may be induced to answer questions, but his
mind immediately wanders again; he may seem partially
conscious and yet not recognize his surroundings. The
memory of the accident is often entirely lost. There is
usually headache, which may be very intense, and associ-
ated with intolerance of light and sound. Dizziness, nausea,
vomiting, and convulsions are frequent symptoms. The
pulse is slow and regular, and the breathing is superficial.
The tendon reflexes are exaggerated, especially in severe
cases.

With the exception of nystagmus and alternating strabis-
mus there are no focal signs. As soon as any localizing
signs appear, such as unilateral increase of reflexes, or pa-
ralysis of the limbs, or evidences of injury to the cranial
nerves, the diagnosis of concussion must be changed to that
of a more definite lesion. Consequently the diagnosis is one
by exclusion. Cerebral concussion is an accompaniment of
all severe brain injuries, but under such circumstances its
symptoms are masked by those of the graver conditions.

The duration of the condition depends on its severity.
Usually the patient is able to get up in the course of a few
days, although there may be left evidences of mental impair-
ment which are a long time in disappearing, or which may
not disappear at all.

66 ORGANIC EFFECTS OF INJURY.

Fractures. — In fractures of the cranial vault there are
often external evidences of the condition, such as depres-
sions or fissures in the bones. These may be wanting,
however, and in fractures at the base they are never pres-
ent, so that the diagnosis must be made from the nervous
symptoms alone, or from such signs of leakage as subcon-
junctival ecchymosis or discharges from the ears or nose.

When persons are found unconscious, with paralytic
symptoms, with or without scalp wounds, it is not always
easy to determine whether the coma is apoplectic in origin,
or whether it is a result of a fracture of the skull.

In the summer of 1896 one of the female inmates of the Work-
house, aged sixty, was found on the floor of her cell unconscious,
presumably having fallen from her bunk to the stone floor, a dis-
tance of about four feet. There was a deep scalp wound over the
left parietal eminence. She was transferred to the hospital, and
when I saw her she was in partial coma, with a right hemiplegia
unassociated with aphasia. The question was, Did the patient
fall and receive a scalp wound as the result of an apoplectic at-
tack, or was her condition due to a fracture of the skull, with
resulting injury, or compression of the brain ? There were no
external evidences of fracture. There were no palsies of the
cranial nerves, except that the right pupil was larger than the
left. The hemiplegia, which was complete, involved the arm, leg,
and face ; there were no convulsions, and only slight disturb-
ances of sensation. All these symptoms indicated with proba-
bility, but not with certainty, a primary cerebral haemorrhage
rather than a laceration or traumatic compression of the brain.
The autopsy, held ten days after the accident, confirmed this
opinion. There was a large haemorrhage in the left internal cap-
sule, but no injury to the other parts of the brain, and no fracture
of the skull.

In such cases the absence of all external signs of fracture,
the complete hemiplegia without involvement of the cranial
nerves, and the occurrence at a period of life when apoplecti-
form attacks are common, are suggestive of primary rather
than traumatic brain lesion. But the diagnosis is always
difficult, and in many cases can not with certainty be made.

VARIETIES OF BRAIN INJURIES. 67

There is no domain in medicine or surgery in which
more caution in diagnosis and prognosis is required than
in head injuries.

In fractures of the skull the patient may present no
evidences other than those of concussion for days or weeks,
and then suddenly develops symptoms of an alarming or
fatal character. It is a common occurrence for persons
whose skulls are fractured to walk to hospitals or to be
arrested for disorderly conduct on the street.

In a case communicated to me by Dr. Psotta, House Surgeon
of Roosevelt Hospital, a man fell off a cable car, was rendered
unconscious, and was brought to the hospital. There were no
evidences discoverable of fracture of the skull or of local brain in-
jury, and the next day, as the patient was feeling perfectly well,
he was discharged from the hospital. He continued to feel well
for two weeks, when he suddenly died. An autopsy by the coroner
showed a fracture running transversely for the whole width of
the middle fossa of the skull.

The most that the physician or surgeon can do in these
difficult cases is to ascertain, as nearly as possible, the se-
verity of the accident, and, after severe accidents, to with-
hold an opinion until sufficient time has elapsed to render
the occurrence of further symptoms improbable.

Any head injury is liable to be complicated by intracra-
nial inflammation, and the symptoms of meningitis, abscess,
or encephalitis may be added to those of conditions which
did not at first seem serious.

CHAPTER II.

Injuries to the Spinal Cord.

Although the studies of recent years have cleared
away much of the confusion with which the writings of
Erichsen enshrouded spinal-cord injuries, the terminology
applied to these affections to-day is far from satisfactory.
For this the unfortunate survival of the expression " con-
cussion of the spinal cord " is largely responsible.

As used to-day, this term is extremely indefinite in its
meaning. There is, of course, no longer excuse for apply-
ing it to the forms of nervous disease which are purely
functional in character (traumatic neurasthenia), nor to the
cases in which there may be slight injuries to the verte-
bral joints without affection of the more delicate structures
beneath them (lumbago). But aside from its use, or misuse,
as applying to affections in which there is no disturbance
of the structure of the spinal cord itself, it remains as
a designation of lesions for which the names myelitis,
softening, and haemorrhage are alone permissible. Some
writers call any injury to the spinal cord "spinal concus-
sion " ; others use the term for any spinal affection which
may result from concussion accidents ; still others make it
synonymous with intraspinal haemorrhage, with or without
vertebral lesion. A conservative few restrict it to those
cases in which, with absence of injury to the spinal column,
there may be evidences of focal injury to the spinal cord
which has not been caused by haemorrhage.

Since it is still a matter of doubt that there exists any

INJURIES TO THE SPINAL CORD. 69

pathological condition such as the term spinal concussion
in its most restricted sense would imply, to retain so gen-
erally familiar a designation for a condition which, if it
exists at all, is extremely rare, will certainly prove an
obstacle to the advancement of our knowledge of the
causal relations of traumatism to spinal disease. It is, how-
ever, much easier to object to than to do away with a term
which has gained popularity. I would nevertheless strongly
urge that if " concussion of the spinal cord " is to be re-
tained at all in medical nomenclature, it should be re-
stricted to those cases in which it can be shown that the
nervous elements of the cord have been directly injured,
without having been compressed by bone or by extrava-
sated blood.

The degree of violence necessary to cause injury, either
directly or indirectly, to the spinal cord is very great. No
organ in the body is so strongly secured against danger.
It is held in place above and below by attachments of the
dura mater, and at the sides by its thirty-one pairs of nerves.
Between the two membranes which surround it is a thick
column of fluid that envelops it in its whole extent, and
which acts as a cushion in dissipating the force of any
shocks which may be received by the spine. The vertebrse
(Fig. 16) through which it passes are thick and strong, are'
held in place by tough ligaments, and are everywhere
padded by massive layers of muscles.

The accuracy and compactness of the articulation of its
parts enable the spinal column to withstand great degrees
of strain and force before its own integrity or that of the
spinal cord is disturbed. Yet, notwithstanding the solid
strength of the vertebrse, their nicety of adjustment, the
massed layers of muscles, and its other efficient means of
protection, the spinal cord is not infrequently the seat of
serious injuries. But the injuries which overcome the
barriers by which it is shielded from danger are the results

■JO ORGANIC EFFECTS OF INJURY.

of excessive violence that acts directly upon the spinal
column.

Thus from severe falls or blows upon the head there
may result spinal-cord injury, even though the skull escapes

Fig. i6. — Transverse section of the structures surrounding the spinal cord
at the line of the ninth thoracic vertebra

fracture. Falls on the buttocks, either from heights or,
as occasionally occur in consequence of elevator accidents,
may produce a like result. Penetrating wounds, or blows
on the back from heavy objects, may be immediately fol-
lowed by symptoms of impairment or loss of spinal func-
tion. By very severe and sudden twists or wrenches it is
possible for vertebrae to be dislocated or for some of the
intravertebral structures to be torn. But the violence

INJURIES TO THE SPINAL CORD. 71

which causes these injuries is extreme, and differs both in
character and in degree from such violence as may be re-
ceived by the sudden stopping or starting of a train, or from
slipping on a banana peel, which is not infrequently ad-
vanced as a cause of " spinal " injury.

It is obviously difficult to determine the degree of force
which has been exerted on the spinal column in any given
accident. Yet, to prove the existence of an injury to the
spinal cord, it is necessary to show that the force has in all
probability been sufficient to break through the vertebras
or to cause stretching or laceration of the structures which
they surround. Such proof is established when the symp-
toms are in accord with those we now recognize as indica-
tive of lesion of the spinal cord.

Although it is almost always possible to determine
whether the spinal cord has or has not been injured, the
diagnosis of the exact character of the lesion is more dif-
ficult. That our knowledge of this subject might be very
materially advanced by the careful observation of a large
number of accident cases in accordance with some definite
classification, seems reasonable to expect ; and for the fur-
therance of that object the following classification is pro-
posed :

I. Spinal column injured, by wounds, fractures, and dis-
locations which cause compression of the spinal cord, and,
secondarily, myelitis, softening, or haemorrhage.

II. Spinal column uninjured, but spinal cord the seat of:
r. Compression by blood clots. 2. Haemorrhage into cord
substance. 3. Concussion or commotion.

The clinical applicability of such a classification is, of
course, in the present state of our knowledge, restricted,
since where there are no external evidences of vertebral
injury it is usually impossible to be certain of the exact
character of the cord lesion. From the standpoint of patho-
logical anatomy, however, it is justifiable, and it seems not

ORGANIC EFFECTS OF INJURY.

unreasonable to hope that pathological studies conducted
along its lines, when preceded by accurate clinical observa-
tions, would so much enlarge our comprehension of the
nature of spinal-cord injuries that they could be accurately
diagnosticated during the life of the patient. In accordance
with this classification injuries to the spinal cord will now be
briefly discussed.

I. Spinal Column Injured.

By far the larger number of traumatic lesions of the
spinal cord are secondary to injuries of the vertebras. It
is often impossible to determine dur-
ing the life of the patient whether
fracture or dislocation of the bones
has or has not occurred, because the
integrit}' of the spinal column may
be seriously impaired without there
being any irregularity or abnormal
mobility of the vertebral spines. Ex-
ternal evidences of injury are absent
with particular frequency in fractures
which involve the bodies of the ver-
tebras only, or in the dislocations re-
sulting from sudden twists or wrench-
es, in which the bone or intervertebral
cartilage, after having been momen-
tarily thrust forward so as to crush
the spinal cord, immediately springs
back again into its place without leav-
ing external traces of any change of
position.

Vertebral lesions may cause dam-
age to the spinal cord in a variety of ways. The cord
itself may be cut in two or lacerated or crushed (Fig. 17)
by dislocated bone or by splinters of bone; it may be com-

^
«

Fig. 17. — Crush of the spi-
nal cord, due to fracture
of the cervical vertebrae.
(From a drawing kindly
furnished by Dr. Van
Gieson.)

SPINAL COLUMN INJURED.

pressed by hemorrhage into the spinal canal, coming from
the bone, or from the ligaments, or from the membranes
(hasmatorrhachis) (Figs.' i8
and 19); its blood-vessels
may be so torn that blood
is poured out into the cord
tissue itself (hasmatomyelia).
From any of these lesions
may immediately result soft-
ening or inflammation (mye-
litis), or, secondarily, degen-
erations or gliosis of varying
degrees. The symptoms of
any of these conditions indi-

FiG. 18. — Intraduralhc-emorrhagfe. (From
a specimen kindly furnished by Dr. G.
E. Brewer.)

Fig. 19. — Extradural haemorrhage.
(Roosevelt Hospital. j

cate a focal injury to the spinal cord, and will be described
on page 90.

When the medullary lesion is secondary to injuries to
the bones it is usually impossible to decide during the life

ORGANIC EFFECTS OF INJURY.

Fig. 20. — Diagram to illus-
trate the course of the blood
in a case of hiematomyelia.

of the patient the exact nature of
the pathological condition within
the spinal canal. In such cases the
cord is so seriously crushed or com-
pressed at the seat of the fracture
that the symptoms are simply those
of a transverse lesion, whatever the
underlying conditions may be.

In view, however, of the special
pathological interest which attaches
to hasmatomyelia the following case
may be briefly related here. Al-
though the lesion was too extensive
to permit any inferences as to the
special symptoms of central heemor-
rhage, the disposition of the blood
was characteristic of that condition :

A man fell on his head, fracturing the
cervical vertebrae. He did not lose con-
sciousness, but was immediately para-
lyzed in all four extremities, and died in
a few days. I performed the autopsy at
the City Hospital twelve hours after
death. Brain, normal ; spinal column,
comminuted fracture of the third and
fourth cervical vertebras. On opening
the dura, the outline of the spinal cord
was found to be well preserved, though
there was some tendency to bulging at
the fifth and sixth cervical segments.
On section (Fig. 20) there was a sharply
defined haemorrhage which followed, as
nearly as the naked eye could see, the
gray matter of these two segments. Far-
ther up and down the cord there was a
different disposition of the haemorrhage.
The blood had ascended the posterior
horn on the right side as far as the

SPINAL COLUMN INJURED.

middle part of the third cervical segment. The path of the de-
scending blood followed the left posterior horn of the cord to the
lower part of the seventh cervical segment (Fig. 21). Studied in
microscopic sections, the whole of the fifth and sixth cervical
segments, with adjacent portions of the seventh and fourth, were
found to be in a condition of acute myelitis with its ordinary
appearances — viz., destruction of nerve elements with a cellular
exudate consisting of leucocytes and large granular cells. In
these two segments the blood-vessels were unusually prominent

Fig. 21. — Showing inferior termination of the posterior column of blood in
a case of traumatic haematomyelia. (City Hospital.)

and dilated, while at the same time there were many free red blood
cells. By far the larger number of the red blood cells were col-
lected in the gray matter, so that the outlines of the anterior and
posterior horns and the gray commissure were brought out in
sharp relief. In the other segments the red blood cells were still
more closely confined to the gray matter, though they could be
seen as scattered cells throughout all the sections. With the
exception of the fifth and sixth segments, there was little inflam-
mation or softening, and the nerve fibers were well preserved.

The amount of extravasated blood in this case being so large,
it seems probable, although it can not be positively asserted, that
the haemorrhage resulted directly from the injury, rather than

■j(i ORGANIC EFFECTS OF INJURY.

that it was secondary to the softening and inflammation by which
it had been surrounded.

II. Spinal Column Uninjured.

The cases in which the spinal cord is injured while the
vertebral column remains intact form only a small propor-
tion of the total number of injuries to the spinal cord. It
is consequently in regard to them that satisfactory informa-
tion is difficult to obtain and that our knowledge is most
incomplete. Furthermore, as these cases are naturally less
dangerous to life than the ones in which the cord lesions are
secondary to bone lesions, many of the patients recover more
or less completely, and the nature of the affection remains
largely conjectural. They result from the same kind of vio-
lence as is active in causing fracture and dislocation of the
spinal column. In most of the recorded cases of this variety
of injury which have come to autopsy the lesion has con-
sisted of hagmorrhage.

If haemorrhage is the chief pathological factor, its occur-
rence may be explained by assuming that the physical shock
was sufficient to cause a rupture of some of the blood-vessels
of the spinal membranes or of the spinal cord. Haemor-
rhage may occur without bone lesion (i) within the spinal
canal, so that the cord is compressed by blood clots (hsemat-
orrhachis), or (2) into the substance of the cord (hsemato-
myelia). Concussion or commotion will be discussed after
these hsemorrhagic conditions.

I. Hczmatorrhackis may be illustrated by the following
case, reported by Lambret :

A driver fell from a cart, striking on his head. He immedi-
ately developed symptoms of flaccid paraplegia, with anaesthesia
and loss of sphincter control, and as a result of his injuries died
in a little more than twenty-four hours after the accident. At the
autopsy both skull and spinal column were found to be intact, but
there was a long extradural blood clot in the spinal canal which
had compressed the spinal cord in the upper dorsal region.

SPINAL COLUMN UNINJURED. -jj

2. Hamatomyelia (hgemorrhage into the spinal cord) is
one of the most interesting of the present problems of the
pathology of the nervous system. Although it may occur
either with or without fracture of the vertebrae, its chief
clinical interest centers about the cases in vsrhich the spinal
column remains intact, so that the haemorrhage takes place
independently of crushes of the cord. In hospitals and, less
commonly, in clinics, cases are met with, ninety per cent of
which are traumatic, in which the symptoms, by the sud-
denness of their onset and by their distribution, point to the
existence of this condition. Many of the patients recover
more or less completely, so that the diagnosis remains
unsubstantiated by post-mortem demonstration. In others,
death ensues so rapidly that pathological examination, al-
though showing the anatomical condition, leaves undeter-
mined what the ultimate clinical effects would have been
had the patient lived.

There is considerable anatomical evidence, which is
based upon the course which extravasated blood follows in
the spinal cord, in favor of the view that central haemor-
rhage, if not too extensive, may cause symptoms different
from those of a transverse lesion. The gray matter is the
least resisting portion, and its vessels are the most liable
to rupture ; consequently, in many of the cases of primary
baematomyelia, the hsemorrhage occurs in and remains local-
ized to the gray matter, although it may burrow for long
distances up and down the cord.

The anatomical condition is shown by a case of Thor-
burn's, almost identical with the one already described, ex-
cept that the haemorrhage occurred independently of any
fracture of the spine.

A man received a severe blow between the shoulders and be-
came paralyzed in the muscles of the leg and abdomen and in the
intercostal muscles. After three days of the ordinary symptoms
of severe spinal-cord injury he died with congestion of the lungs.

yS ORGANIC EFFECTS OF INJURY.

At the autopsy, "in the muscles over the lower cervical and upper
dorsal regions was some dark effused blood, but the vertebral
column presented no evidences of injury. The membranes of the
cord were quite normal, as was the external appearance of the
cord itself, but on section there was found to be a dark, black
haemorrhage into the central gray matter in the lower cervical and
upper dorsal regions. This haemorrhage, which measured in its
vertical extent from one and a half to two inches, was, in the
greater part of its extent, situated centrally, occupying the whole
of the central gray matter and extending but little into the white
substance, which in its neighborhood was merely softened and of
a faintly yellow tinge. At the lower part, for a very short dis-
tance, the haemorrhage was limited to the anterior cornu of the
right side, while the corresponding left horn appeared to be per-
fectly healthy ; elsewhere the cord was firm, and presented no
abnormity."

In cases in which the patients have partially recovered,
the blood extravasation has been absorbed, leaving long
cavities in the spinal cord. To such cavities Levier gave
the name of "■Rohrenbildung" ; in an elaborate study of this
condition, as yet unpublished. Van Gieson has individualized
the sequelae of hasmatomyelia under the term " hamatomye-
lopore" as indicating a distinct disease of the spinal cord.

The cord may be hollowed out very quickly, as is shown
by the following case reported by Parkin :

The patient was standing, on March 29th, beneath a lift, when
the chain broke and the lift fell on his head. He was immediately
rendered unconscious, and remembers no more about the accident.
On admission to the hospital there were no signs of paralysis of
the limbs, but in eight or ten hours after admission the left arm
was found to be weak, and rapidly became paralyzed. On March
30th there was. anaesthesia over both legs and arms, said to be only
partial. He could move the right arm a little, but not the left.
Could not pass his urine. Catheter had to be used twice a day.
Motions passed involuntarily. Temperature subnormal. April 2d:
Left arm completely paralyzed. Left leg stiff, but moves a little.
No knee-jerk on left side. Plantar and epigastric reflexes present.
April 6th: Left hemiplegia has become complete; anaesthesia
about the same. April nth: Died in about the same condition.

SPINAL COLUMN UNINJURED. 79

{The gradual extension of paralytic symptoms in this case was
very similar to that frequently observed in haemorrhage of the
brain.)

Post-mortem. — Spinal column intact. No extra-meningeal haem-
orrhage. On making section of the cord at a point two inches
and a half below the apex of the fourth ventricle, it was found to
be hollowed out, having about half an inch of healthy periphery.
The cavity contained soft, grumous material, evidently altered
blood, which escaped on section. The cavity occupied about three
quarters of an inch of the length of the cord.

It still remains to be proved whether these acutely occur-
ring haemorrhagic cavities can cause the symptoms of syrin-
gomyelia, which is a disease characterized by chronic cavity
formation in the gray matter. In cases in which the hasmof-
rhage is associated with a fracture of the vertebrae there is
so much direct injury to the spinal cord in addition to the
haemorrhage, that the symptoms indicate a lesion of both the
white and the gray matter ; and even without bone lesion,
if the blood is poured out so extensively that it seriously
compresses the white matter, the clinical manifestations
will be those of a transverse lesion. But when the white
matter has been affected but little or not at all, and the
hasmorrhage appears in the gray matter alone, it seems
probable that if the patient recovers from the effects of the
acute injury he may present symptoms which are the re-
sults of lesions limited chiefly to the gray matter. These
symptoms will be found in the parts of the body receiving
their nerve supply from the segments affected, and con-
sist in localized paralyses of motion, with loss of reflexes
and degenerative electrical reactions ; atrophy and trophic
changes and dissociated angesthesia, of which the most com-
mon variety is a loss of sensibility to temperature and pain,
while the sensations of touch are normally transmitted and
perceived.

The symptoms of syringomyelia are usually more
marked on one side than on the other, and there occasion-

8o ORGANIC EFFECTS OF INJURY.

ally is seen the Brown-S6quard type, which consists in pa-
ralysis of motion on one side of the body and of sensation
on the other side.

Although no autopsy has as yet proved that a central
haemorrhage of the spinal cord can cause symptoms similar
to those observed in syringomyelia, there are several clinical
cases recently reported which speak very strongly for such
a possibility. Of these, one by Minor may be mentioned :

A man, twenty years of age, previously healthy, fell a dis-
tance of seven and a half feet, and two days later was brought to
the hospital. Examination showed no evidences of lesions to the
skull, brain, or vertebrae, but disclosed symptoms which can best
be explained by a small haemorrhage situated in the gray matter of
the left side of the spinal cord, and extending from the sixth cer-
vical to the first thoracic segment. There was paralysis of the left
arm and leg and paresis of the right arm, with diminution of elec-
trical excitability in both upper extremities. The tendon reflexes
were absent on the left side, but were only diminished on the
right. Trophic disturbances were present about the shoulders.
The sensory abnormities were the most interesting. With com-
plete preservation of the sense of touch over the whole body and
of the sense of pain and temperature over the left side, there was
on the right side from the jaw downward a profound analgesia
and thermo-anassthesia. The patient recovered almost entirely
from the paralysis and from all the other symptoms, with the ex-
ception of the loss of sensibility to pain, which remained as long
as the case was under observation. (It will be observed that the
association of symptoms in this case is very similar to that com-
monly observed in syringomyelia.)

In some cases it may be inferred from the motor symp-
toms alone, even when anassthesia is totally absent, that a
small haemorrhage has occurred and has remained limited to
the gray matter.

The following case, a patient at the Vanderbilt clinic
whom I recently presented at a meeting of the surgical sec-
tion of the New York Academy of Medicine, illustrates this :

The patient, who is seventeen years old, was a strong, healthy
lad until the summer of 1895. Then, in diving from a dock six

SPINAL COLUMN UNINJURED. gl

feet above the water, he went too straight and, .the water being
only four feet deep, struck his head with force against the bottom.
He did not become unconscious, but immediately lost power in all
four extremities. He was pulled out of the water by other boys,
and was taken home and put to bed. For three days he lay in
bed, unable to move the Hmbs at all, with pain in the back of the
neck and at the lower part of the spine. There was retention of
urine and incontinence of faeces. "Pins and needles" in the left
side only. No loss of sensation. No involvement of the face.
After three days the right side began to improve and all the pain
ceased. In four months the patient could walk, and has been
gradually improving ever since. Now (April 7, 1897) there are
weakness and stiffness in the intrinsic muscles of the hands of both
sides, very much more marked on the left. The left hand is in
the pen position through spasm of the interossei, and the interos-
seous muscle of the left little finger is paralyzed. Electrical reac-
tions are normal except for the extensors of the fingers and for
the interossei on the left side; in these muscles electrical ex-
citability is diminished. There is a slight sinking in of the left
interosseous spaces. The other muscles of the arms are normal.
The right leg is perfectly normal, but the left leg is weak, and its
muscles are in a condition of spastic rigidity, with increased reflexes
and ankle clonus. The abdominal and plantar reflexes are lost on
the left side. As the patient walks the left leg is dragged some-
what and circumducted in characteristic hemiplegic style. There
are nowhere any changes in cutaneous sensibility, nor tremor, nor
tenderness of the back, nor external evidences of any injury to
the spine.

Thus the symptoms which remain are: Slight flaccid paralysis
of the intrinsic muscles of the left hand, and to a very slight de-
gree of the muscles of the right hand; spastic paresis of the left
leg, no disturbances of cutaneous sensibility, no evidences of in-
jury to the spinal column.

Such symptoms permit a very exact localization of the lesion.
In this case there is every probability that there was a slight
haemorrhage into the gray matter of the first thoracic segment of
the spinal cord, chiefly anteriorly and on the left side. An oedema
or softening quickly developed, so that for a time the patient pre-
sented the symptoms of a transverse lesion. These soon went
away, however, leaving a focal lesion which involved only slightly
the anterior horn of the right side, but destroyed some of the an-
terior horn ori the left side. The absence of sensory symptoms

82 ORGANIC EFFECTS OF INJURY.

would indicate that the posterior horri and the central canal were
not involved. The haemorrhage must also, either directly or indi-
rectly, have impaired the conducting power of the left pyramidal
tract.

In the cases which have been described here, and in-
deed, as far as I know, in all hitherto published cases of
hasmatomyelia, the haemorrhage has been focal. Although
the blood may have burrowed for long distances up and
down the gray matter of the cord, the columns of blood
have been extensions from one bleeding point, and not dis-
tributed as multiple haemorrhages.

Through the courtesy of Dr. T. J. Larkin, Assistant
Pathologist to St. Francis' Hospital, I have recently had the
opportunity of examining a case of haematomyelia essen-
tially different from any previously described. In this case
there was no single point of extensive hasmorrhage, but
the spinal cord was dotted throughout its whole extent with
microscopic collections of free red blood cells. Although
the spine was fractured at one point, the haemorrhages were
multiple and occurred independently of the bone lesions, so
that the case can be properly described in this section. The
facts are as follows :

A workman, after receiving a severe fall, was picked up un-
conscious and brought to the hospital in deep coma and paralyzed
in all extremities. He died in three hours from respiratory fail-
ure. At the autopsy the skull was found intact, but there was a
haemorrhage in the middle fossa. There was a fracture disloca-
tion of the atlas and axis which had caused extensive mutilation
of the second and third cervical segments of the spinal cord.
There was no haemorrhage in the spinal canal. Except at the
point of compression, the spinal cord looked in every way normal.
The membranes were not lacerated, the contour of the cord was
perfectly preserved, and its substance was firm to the touch. On
section it could be seen that the blood vessels were somewhat
prominent, but the eye could detect no haemorrhage either at the
seat of injury or in lower levels. All the other organs appeared
perfectly normal and free from haemorrhage. Through a misun-

SPINAL 'COLUMN UNINJURED. 83

derstanding on the part of the dead-house attendant, the upper
portion of the cord was thrown away, so that the microscopic ex-
amination was limited to the thoracic region and regions below it.
Sections were made of every segment of the thoracic, lumbar, and
sacral regions, and of the conus terminalis, which had been hard-
ened in Miiller's fluid and formalin, and which were then exam-
ined microscopically by means of the picro-acid-fuchsin method.
The lesions found were generally distributed up and down the
cord, and consisted of recent capillary haemorrhages, which were
so minute that they could not have been detected by the naked
eye. No single haemorrhage contained over two or three hundred
blood cells,^and the majority of them contained fewer. In some
places there were only two or three free cells. In a few sections
the blood lay in little cavities, but the most common distribution
of it was in the form of an infiltration of a small number of blood
cells between the neuroglia and nerve fibers. There was nowhere
any tubular cavity formation. The largest extravasations were
in the pia and around the nerve roots. In the spinal cord, al-
though occurring in the gray matter, they were most frequent in
the white matter, especially in the posterior columns. Nearly every
section contained the haemorrhages, but no section contained very
many, usually not more than two or three. The situation of the
haemorrhages bore little or no relation to the location of the large
blood-vessels. The blood-vessels were prominent and filled with
blood. In all other respects the spinal cord appeared .normal.

Thus, to briefly resume, a healthy man fell with sufficient vio-
lence to break his neck and to cause an intracranial haemorrhage
without fracture of the skull. The force was exerted chiefly on
the atlas and axis, as seen by the injury to these bones. But it
was also adequate to cause throughout the cord punctate haemor-
rhages, which were entirely unassociated with the severe local in-
jury and which were probably due to the general violence to
which the whole spinal cord was subjected. That injury can
cause minute and multiple lesions in the spinal cord, without frac-
ture of the vertebra, has often been assumed, but, as far as I know,
never before been demonstrated.

The proof of such a possibility is of great importance for the
possible explanation of the pathology of the obscure cases of sus-
pected spinal disease in which, after severe accidents, the patients
give symptoms of serious impairment of spinal-cord function with-
out definite signs of circumscribed injury. In the present case the
lesions of vital centers completely masked any clinical symptoms

84 ORGANIC EFFECTS OF INJURY.

which the capillary hsemorrhages might otherwise have caused.
Had the violence acted so that there had been no gross lesions, it
might be that the small haemorrhages would have given rise to
symptoms indicative of multiple and minute foci of structural
damage to the spinal cord.

Concussion or Commotion of the Spinal Cord.

As a designation for a pathological entity, the term con-
cussion or commotion of the spinal cord should be limited
to such conditions as may occur as a result of injuries
to the back, or of general concussion accidents, and which
have not been caused by pressure from displaced fragments
of the spinal column or by haemorrhage in the spinal canal
or into the substance of the spinal cord. The time has
gone by when intelligent physicians were deceived by the
supposed resemblance between such general functional affec-
tions as hysteria or neurasthenia and concussion of the
spinal cord. Concussion, however, continues to be invoked
as an explanation for certain cases of organic paraplegia
which are probably due to lesions much coarser than molec-
ular disarrangement. The pathological condition with which
it is most liable to be confused is haemorrhage, and to at-
tempt to distinguish between conditions so closely allied
may at first seem to be of the nature of a pathological quib-
ble. Recent acquisitions to our knowledge of haematomyelia
have shown, however, that such a distinction is imperative
if we are to get at the truth of the influence of trauma in
the pathogenesis of the obscurer forms of spinal-cord dis-
eases. Haemorrhage usually occurs first in the gray mat-
ter, and generally remains localized there. If fibers are
injured without haemorrhage, as the believers in spinal con-
cussion maintain, it would seem reasonable to suppose that
the resulting symptoms would be different from those of
hsematomyelia.

Does such a condition as spinal concussion exist? In

CONCUSSION OR COMMOTION OF THE SPINAL CORD. 85

Other words, can any violence be sufficiently severe to cause
direct injury exclusively to the essential elements of the
spinal cord ? To this question a positive answer is yet to be
given. As is well known, lesions of all grades of severity
may follow compression by bony splinters or by blood clots,
in the spinal canal, and intraspinal haemorrhage may occur
without there being any discoverable pathological changes
in the nerve fibers, other than those explainable by the effects
of pressure. But these are well-recognized conditions, and
are the results of laceration and compression, and do not re-
quire to be explained by the assumption of concussion.

The question is not whether the fibers which compose
the spinal cord are of different function and amenable to
different laws than are nerve fibers situated elsewhere, but
whether they are not so securely protected that an injury
can not reach them without having first fractured or dislo-
cated bone or having caused rupture of blood-vessels.

The nerve fibers of the spinal cord of course differ in no
essential respects from those of the brain or of the periph-
eral nerves. They serve purposes of conduction and obey
general physiological laws ; yet a blow on the head, with-
out causing fracture of the skull or visible damage to the
brain, may cause symptoms of cerebral concussion, and a
blow on a peripheral nerve is frequently followed by loss of
conductivity in it without there being any gross injury to
its structure. With the spinal cord, however, the case is
different. The back often receives severe injuries without
there resulting any symptoms referable to the spinal cord.
The explanation of the fact that violence applied to the
back rarely if ever results in symptoms of spinal-cord
lesions which can not be explained by laceration or com-
pression, is to be sought for in the immunity from any but
the severest injuries afforded that organ by the protecting
structures which surround it.

Accordingly, while we are not in a position to unquali-
7

86 ORGANIC EFFECTS OF INJURY.

fiedly assert that spinal concussion can not occur, we can say
that if it occurs at all it is certainly one of the rarest of acci-
dents to the nervous system — a fact which is amply estab-
lished by experience, and which may be explained by the
anatomy of the cord itself and of the surrounding parts. la
by far the larger number of cases the spine is fractured, and
the only cord symptoms are those referable to a nervous
lesion in the immediate vicinity of the bone lesion. We
never hear of cases of compression of one part of the cord
and of concussion in a part higher up ; on the contrary,
spinal-cord injuries are characterized by the contrast be-
tween the conditions below the lesion and those above it.

The literature of spinal concussion is voluminous, but
trustworthy facts are few.

In the cases which have been regarded as reliable ex-
amples of the condition by A. Westphal, and by Willard and
Spiller, the vertebree were fractured, and there were cord
lesions with haemorrhages in the immediate vicinity of the
fracture. These investigators maintained -that the cord
lesion was the result of " concussion " and not of compres-
sion by loosened vertebrse. They based their opinions upon
the absence of evidences of external bruising to the cord.

If such proof is to be accepted as evidence the condition
must be regarded as not uncommon, for every pathologist
is famihar with the fact that the spinal cord frequently
retains its normal contour after it has been momentarily
though seriously compressed. That slight and temporary
compression is amply sufficient to cause a loss of spinal func-
tion is shown by the frequency with which complete para-
plegia results from spinal operations when the spinal cord
has been merely touched by the finger of the operator. To
disregard the action of so well-recognised a cause as frac-
ture, as is done by the above-mentioned authors, which was
in their cases present, and to assume the action of another
and unproved cause, appears to me unjustifiable.

CONCUSSION OR COMMOTION OF THE SPINAL CORD.

Gowers is the warmest partisan of the theory of spinal
concussion, and one is tempted to accept as final the opinion
of so illustrious a neurologist. Yet the proofs which he
adduces are far from satisfactory. Most of the cases he
cites date from a period whose neurological contributions
must be accepted with considerable reserve. In one of
the more recent ones (Fischer) there was an extra-dural
haemorrhage, extending from the cervical to the lumbar
regions, of which Gowers makes no mention. Gowers's
own case is so interesting that it is to be regretted that it is
not reported a little more in detail.

" A lady was severely shaken in a railway collision. She
seemed immediately after the accident to have suffered no
injury, but in a few days paraplegia developed, and from
its consequences she died six weeks after the accident.
Throughout the dorsal regions of the cord I found indica-
tions of subacute myelitis chiefly in the white columns,
varying in its extent in different regions, but in most part
confined to the lateral tracts." In the absence of fuller de-
tails, this case can hardly be accepted as proof of spinal
concussion ; the softening might equally well have been the
late results of haemorrhage.

The celebrated researches of Schmaus have been gener-
ally received as finally settling the question. Schmaus re-
ports the microscopic examination of the spinal cords of
four individuals who died from the effects of traumatic para-
plegia. In three the spinal column had not been fractured.
As in all of these cases the patients had survived the injury
and had lived with paralytic symptoms for several months, in
order to discover the early stages of concussion, Schmaus
induced paraplegia in animals by tapping them on the back
with a hammer, without inflicting injury to the spinal col-
umn. As the result of his investigations, he concluded that
" anatomical changes of the specific nerve elements may be
brought about by purely traumatic means ; that swelling and

88 ORGANIC EFFECTS OF INJURY.

degeneration of the axis cylinders, breaking up of myelin,
softening and gliosis, with cavity formation, may result di-
rectly from injury independently of accessory causes. Haem-
orrhage is not concerned in the aetiology, but may appear
as an accidental or secondary accompaniment."

Two objections must be overcome before Schmaus's
conclusions can be accepted, as proving that the human
spinal cord can be concussed. One of them is, that of the
human cases which he examined all presented cavities in
the gray matter ; and inasmuch as they did not come to
autopsy till a long time after the injury, the probability is
very strong that these cavities were not the results of gliosis,
as Schmaus interpreted them, but were spaces which were
left after hgemorrhages that had resulted from the original
injury ; and that the cases were not examples of concussion,
but were forms of myelitis secondary to haeniatomyelia.

Schmaus's animal experimentation seems at first sight
more conclusive. The animals became paraplegic, and after
death, without any haemorrhages, there was a swelling of
the axis cylinders in the parts of the cord opposite the seat
of external injury.

Experience has shown, however, that the utmost con-
servatism is necessary in accepting the deductions from
experiments upon the nervous system of animals as appli-
cable to the nervous system of man. In guinea-pigs and in
rabbits, the animals that Schmaus made use of, the pro-
tection of the spinal cord by skin, muscle, bone, and liga-
ments, after due allowance is made for comparative differ-
ences in size, is very much less secure than in man. And
the possibility of causing paraplegia without gross lesions
in these animals does not justify the conclusion that a
similar result might be expected were man the animal ex-
perimented upon. Schmaus's results, furthermore, are not
identical with those of a subsequent observer, Bikeles, who,
in a series of experiments conducted along similar lines,

CONCUSSION OR COMMOTION OF THE SPINAL CORD.

found that swelling of the axis cylinders, a condition to
which Schmaus attached great importance, was absent.

Were the point at issue one as to whether or not the
fibers and cells of the spinal cord were susceptible of a tem-
porary depression of their function under the influence of
properly applied violence, valuable deductions might be
drawn from animal experimentation. Such, however, as has
already been said, is not the question. The problem has to
do with the structures which protect the human spinal cord
rather than with the functions of the spinal cord itself, and
must consequently find its solution in the hospital, in the
dead house, and in the laboratory of human pathology.

Leyden, who is often quoted as a believer in concussion,
now regards it as secondary to hgemorrhage.

Such is the most important evidence for the existence
of the pathological condition known as concussion of the
spinal cord. The writings of Watson, of Vibert, and of
many others who are frequently cited in this connection,
can not be regarded as having materially added to our
knowledge of the subject. In view of the intense interest
with which the question has been for so many years sur-
rounded, and in consideration of its importance both to
medicine and to law, the facts seem very meager.

To the impartial observer the conviction must be inevi^
table that the evidence is totally insufficient for the question
to be accepted as proved, although the weight of evidence
is against the existence of the condition. When one con-
siders the-volumes which have been written upon the sub-
ject, the medical congresses in which discussion of it has
held the prominent place, the enormous sums of money
which have been paid for it in damage claims, and then
turns to the few published cases which are advanced as
proof, there seems to be a great disparity between the
amount that is known about it and the amount that is talked
about it.

pO ORGANIC EFFECTS OF INJURY.

If traumatisms ever act upon the spinal cord, so that its
essential elements are injured without being compressed by
foreign bodies or by blood, such a lesion is, from the pub-
lished evidence, among the rarest of nervous pathology, and
by no means entitled to the position of prominence it has so
long occupied.

Symptoms of Spinal-cord Injury. — The symptoms of
acute injury to the spinal cord are so generall}' familiar that
they need be but briefly referred to. They result from loss
of conductivity and from disturbance of the reflex functions
situated in that organ. There are, accordingly, paralysis,
almost always bilateral, with atrophy and degenerative elec-
trical reactions, and, as a later result, contractures. At first
the paralysis in the affected muscles is flaccid and usually
complete. When the limb is grasped by the hand of the
examiner there is total absence of all resistance ; if lifted up
and then let fall, it drops like a dead weight. The reflexes
are almost always lost at first. Whether they remain
absent, or return and become exaggerated, depends upon
the altitude and extent of the lesion, ultimate exaggera-
tion of the tendon reflexes being the rule in lesions above
the lumbar enlargement. Priapism is frequent. The feeces
may be passed involuntarily, or there may be constipation.
Similarly there is retention or incontinence of urine. Tro-
phic and vaso-motor disturbances, in the form of bedsores,
cyanosis, and coldness in the extremities, are prominent
symptoms in most cases.

Pain, either at the seat of the injury or radiating down
the limbs, is in my experience only an occasional symptom.
Ansesthesia has always been regarded as a cardinal symp-
tom, but it is through the studies of Starr, Thorburn, Sher-
rington, Head, and still more recently of Kocher, that we
have learned its true value. It has been conclusively shown
that the distribution of anaesthesia due to spinal-cord lesions
is entirely different from that caused by injury to the brain

SYMPTOMS OF SPINAL-CORD INJURY.

or to the peripheral nerves, or from that observed in hys-
teria. This fact is of paramount importance for purposes
of diagnosis between affections of the spinal cord and con-
ditions by which they may be simulated, as well as for the
localization of the site of the injury. In fractures or dis-

•CYI-

a VII

riv

a VI

avi-

\ I

L.111.

L.V

,„ ^rvi CVIVc.VIII

,<{^ ^ en

<y cvii

1 ,

Fig. 22.— Sensory distribution of the spinal-cord segments as determined by
spinal-cord lesions. (After Starr.)

locations of the spine it is usually impossible to determine
from such external evidences as mobility or deformities of
the vertebra3 the exact seat of the lesion in the spinal cord.
But when cutaneous sensibility is lost, as it almost always is
in these cases, the topography of the anaesthesia may be
confidently relied upon to furnish a means for the determi-

ORGANIC EFFECTS OF INJURY.

nation of the highest spinal-cord segment which has lost its
power of transmitting sensory stimuli.

The sensory supply of the spinal-cord segments is so
constant that it is possible to construct charts that indicate

Fig. 23. — Sensory distribution of spinal-cord segments. (After Kocher. )

the distribution of the angesthetic areas which may be ex-
pected in lesions of any one segment. Although the
schemes as elaborated by different observers do not agree
absolutely, the differences are unimportant and may be ex-
plained by the fact that the lesion rarely affects a segment

SYMPTOMS OF SPINAL-CORD INJURY.

exactly according to its anatomical boundaries. Figs. 22
and 23 illustrate the areas of segmental distribution of anses-
thesia as laid down by Starr and Kocher.

A transverse lesion of one segment involves a loss of
conductivity in all the segments below it. Thus Fig. 24
illustrates the areas of sensory loss in a case of fracture of
the cervical vertebrse, seen by me in consultation with Dr.
P. R. Bolton. There was a transverse lesion at the eighth

Fig. 24. — Anaesthesia in a case of fracture of the cervical vertebra, with injury to
the eighth cervical segment of the spinal cord. (Hudson Street Hospital.)

cervical segment, with anjesthesia in the distribution of that
segment and in all segments below it. Similarly, in a patient
of my own who is still living, the angesthesia, as shown in
Fig. 25, indicates a lesion which does not extend above the
fifth lumbar segment. The characters of the anaesthesia after
severe injuries are constant. With the exception that it is
less at the upper limits, the anaesthesia is usually total and
complete, so that sensations of touch, pain, or temperature
are not perceived at all, and that the sense of position is lost.

ORGANIC EFFECTS OF INJURY.

The extent and distribution of the various clinical mani-
festations differ with the extent and character of the lesion.
If the cord has been seriously bruised, or if extensive haemor-
rhage has occurred, the resulting symptoms appear prompt-
ly and are then those of a transverse lesion. If, on the other
hand, the damage to the spinal cord has been slight or par-
tial, the symptoms may be somewhat delayed in appearing
and may be of a more selective character. Anaesthesia is

Fig. 25. — Anaesthesia in a case of a fracture-dislocation of the vertebrae, with injury
to the fifth lumbar segment of the spinal cord. (Incurable Hospital.)

always present in severe injuries, but when the other symp-
toms indicate only a partial lesion anaesthesia may be en-
tirely absent.

Thus, in a case seen in consultation with Dr. G. E. Brewer, the
patient, a man, forty-five years of age, had fallen downstairs,
hitting his back, and being generally shaken up. The left radius
was fractured, but there were no external evidences of injury to
the bones of the spine. The patient walked about for two hours
after the accident, but then " felt his legs giving out." He was
obliged on this account to stay in bed at first, but soon partially

SYMPTOMS OF SPINAL-CORD INJURY. 55

regained the use of his limbs. At the time that I saw him, two
weeks after the accident, he could walk with support ; the knee-
jerks were active, especially the right ; the abdominal reflexes were
absent; there was a large bedsore over the sacrum; there was in-
continence of urine and fseces. The most scrupulous examina-
tion of cutaneous sensibility failed to reveal any abnormal varia-
tion of that function for either touch, heat, cold, pain, or the sense
of position. By many this case would be regarded as an example
of concussion of the spinal cord; but, for reasons already given,
it seems to me more correct to make the diagnosis of compression
from a slight dislocation or fracture, or from haemorrhage.

The character of the lesion in injuries to the spinal cord
may usually be correctly inferred if there are evidences of
fracture of the vertebras. It is when there are no external
indications of injury to the spinal column that it becomes
difficult to determine in what way the function of the spinal
cord has become impaired or lost. We are then unable to
distinguish between compression by bone, or haemorrhage.
We onl)' know that heemorrhage is particularly frequent in
the cervical region, and that a gradual extension of symptoms
may be due to blood finding its way up or down the cord.

Bibliography.

Bailey, Three Cases of Brown-Sequard Paralysis. New York
Med. Jour., March 9, 1895.

Ibid., Severe Injuries of the Spine. New York Med. Rec, May,
1897, li, p. 638.

Bikeles, Ref. Schmidt's Jahrb., 1895, 248.

Kocher, Die Lasionen des mensch. Ruckenmarks bei Verletz-
ungen der Wirbelsaiile, Mitt, aus der Grenzgeb. der M. u. C, 1896,

i. 4.

Lambret, Un cas d'h^matorachis traumatique. Bulletin med.,

189s, p. 865.

Levier, Beit, zur Lehre von der Ruckenmarks Apoplexie.
Dissert., Bern, 1864.

Leyden, Klinik der Ruckenmarks Krank, 1875.

Minor, Klinische Beobachtungen uber centrale Hsematomyelie.
Arch.fiir Psych., 1896.

Parkin, Cases of Hsematomyelia. Guy's Hosp. Reports, 1891,
xlvii.

q6 organic effects of injury.

Pfeiffer, Ueber Riickenmarksblutungen und centrale Haemato-
myelie. Zusammenfassendes Referat, Cblatt. fur allg. Path, und
path. Anat, September 15, 1896.

Schmaus, Beitrage zur path. Anat. der Riickenmarkserschut-
terung. Virchow's Archiv, cii, 1890, p. 326.

Sherrington, Philosoph. Trans., 1893, vol. 184.

Starr, A Contribution to the Subject of Tumors of the Spinal
Cord. Am. Jour. Med Sc, June, 1895.

Thorburn, A Contribution to the Surgery of the Spinal Cord,
London, 1889 ; ibid.. Brain, 1894.

Van Gieson, La Semaine mMicale, 1894; New York Med. Jour.,
1894; Report of New York Neurological Society, 1894.

Vibert, Etude m^dico-ldgale sur les blessures, Paris, 1888.

Watson, Experimental Study of Diseases arising from Severe
Concussions.

A. Westphal, Ueber einen Fall von traum. Myelitis. Arch, fiir
Psych., 1896, xxviii, p. 554.

Willard and Spiller, Concussion of the Spinal Cord. New
York Med. Jour., March 6, 1897.

CHAPTER III.

INJURIES TO THE PERIPHERAL NERVES.

Degeneration and inflammation of the peripheral nerves
may result from a variety of causes, but only those forms of
peripheral nerve disturbance which are the effects of direct
and immediate violence virill be considered here. The path-
ological changes that occur in a nerve which has been di-
vided, and so cut off from its trophic center, can not be
detected with the microscope before the expiration of five
to eight days. Then the myelin surrounding the axis cylin-
der may be seen to be breaking up, a process of degeneration
which progresses, and which may be ultimately associated
with the destruction of the axis cylinder and replacement of
nervous tissue by connective tissue. Such a process, which
may occur in varying degrees as the result of crushes, cuts,
blows, or strains, is degenerative rather than inflammatory,
and it is only by the addition of infectious elements (as may
occur in extensive crushes without external wound, or when
there is a wound of the skin as well as injury to the nerve)
that to the degeneration of nerve fibers are added the ordi-
nary vascular manifestations of inflammation. Nerve disor-
ders which take place under these latter conditions may
properly be called traumatic neurites, but the simple degen-
erative process should be spoken of as nerve degeneration,
or palsy, and not as nerve inflammation.

When nerves are cut, regeneration may occur if the ends
are properly united. Repair in nerves injured by blows or
crushes, but not divided, may ordinarily occur in the course

98 ORGANIC EFFECTS OF INJURY.

of several months. In both these cases there may be resto-
ration of function in varying degrees.

Loss of conducting power is the most important symp-
tom of degeneration of nerves. The anterior and posterior
roots of the spinal nerves conduct impulses of different
kinds, but the union of the motor and sensory roots occurs
so soon after their exit from the spinal cord that most pe-
ripheral nerves and all spinal nerves are mixed nerves, and
consequently peripheral nerve palsies almost always present
symptoms of disorder of both sensory and motor function.
The trophic centers for the posterior roots are in the spinal
ganglia, and so extra-medullary ; those for the anterior roots
are in the anterior horns of the spinal cord. Thus there are
different degenerating paths for the two sets of root fibers.
But these are differences which do not appear in the clinical
picture, because simple traumatic lesions affect the nerves
outside the spinal canal, and consequently external to the
trophic centers for both sensory and motor nerves.

^Etiology. — Nerves may be injured by being cut, lacer-
ated, bruised, stretched, or compressed. The most frequent
injuries are bullet wounds, cuts from sharp instruments or
pieces of glass, falls, excessive muscular action, and pressure
from various causes.

In the severer forms of traumatisms the general condi-
tion of the patient has, of course, but little influence upon
the development of paralytic symptoms. But slight blows,
falls, and pressure effects are very much more likely to be
followed by loss of peripheral nervous function in enfeebled
and alcoholic persons than in persons in robust health. In
pressure palsies, particularly, alcohol is a potent predispos-
ing agent.

Symptoms. — Disturbances of motion are the most impor-
tant symptoms of peripheral nerve injuries, and they are
such as are caused by interference with the lower motor
neuron. Loss of conductivity in the neuraxon abolishes the

INJURIES TO THE PERIPHERAL NERVES. gg

transmission by it of the impulses of motion and nutrition,
so that the muscles are paralyzed and undergo atrophy,
although the celLbody portion of the neuron, situated in the
spinal cord, remains unaffected. Although the motor symp-
toms of peripheral nerve palsy are in many ways similar to
those which may result from disease of the spinal cord itself,
they differ so essentially in distribution and in association
with other symptoms, that there is rarely any difficulty in
determining whether it is the spinal or peripheral part of
the neuron which is involved by the lesion.

Although in all injuries to the spinal nerves there is
usually an association of both sensory and motor symptoms,
motor paralysis is the most pronounced and the most impor-
tant. It occurs immediately or soon after the injury, and is
always flaccid in character. It is limited to the muscles sup-
plied by the injured nerve, although usually all the muscles
are not involved to an equal degree. Complete loss of
power of a whole limb is only observed in cases in which the
injury has been extremely extensive and severe. Muscular
weakness becomes apparent, not only through the inability
to perform certain movements, but through various abnor-
mal positions of parts deprived of their muscular power.
Through continuous overaction of opposing muscles the
paralyzed muscles may eventually become tense and the
tendons of the overacting muscles prominent, thus forming
contractures ; but spasticity, such as is ordinarily seen in
cerebral palsies, never occurs. Deformities may result from
the overaction of the opposing muscles, as is seen by the
drawing of the mouth to one side in facial paralysis, or from
the effects of gravity, as is the case with the drop-wrist of
" Saturday-night " paralysis.

Atrophy in muscles slightly paralyzed often does not ap-
pear at all, but when a nerve has been seriously injured its
occurrence is constant. A gentleman was alarmed con-
cerning atrophy of the interossei of one hand and beginning

lOO ORGANIC EFFECTS OF INJURY.

main en griffe ; the atrophy was very marked, and had all
the appearance of a progressive muscular atrophy, but the
condition was one of pressure palsy of {he ulnar nerve,
due to injury received while the patient was under ether
for an operation for appendicitis a month previously.
After injury to a peripheral nerve the muscles may occa-
sionally very soon lose their firmness and consistency ; it is
usually, however, two or three weeks before the atrophy
becomes apparent to the eye.

Tremor is a frequent symptom of peripheral nerve in-
jury ; it occurs in the smaller muscles of the hand, but more
frequently after traumatisms affecting the muscles around
the shoulder joint. It is fine, fibrillary, and very much in-
tensified by movement and fatigue.

Sensory symptoms are not usually prominent in trau-
matic palsies of nerves ; even when a nerve is divided anaes-
thesia does not invariably result. In very few of the isolated
peripheral palsies which have come to my notice have there
been any sensory symptoms other than tingling and numb-
ness in the areas supplied by the injured nerves. Percep-
tion and localization of touch, pain, and temperature are
usually little or not at all impaired. Ansesthesia may occur
in the regions supplied by the nerve, but it is chiefly found
in cases in which inflammation is added to the degenerative
process, or in which the nerve injury has been particularly
severe. The same is true of spontaneous pain. Neuritis can
cause most intense pain. But in the non-septic palsies of
traumatic origin pain is only an occasional symptom. It is
sometimes, however, the most prominent result, so that the
condition is spoken of as traumatic neuralgia rather than
palsy. This is particularly frequent after injuries to the fifth
and to the sciatic nerves. Tenderness over the affected
nerve trunk and muscles is also occasionally present, and
may be a distressing symptom. In lesions of the sensory
portions of nerves it is the lower sensory neuron, which is

INJURIES TO THE PERIPHERAL NERVES. loi

situated between the posterior spinal ganglion and the pe-
riphery, that is affected. Consequently, when it is injured,
the symptoms of disturbed function occur in the course of
the nerves themselves. From the description of aneesthesia
and paraesthesia resulting from spinal-cord injury, it will
thus be seen that the distribution of sensory symptoms is
entirely different in lesions of the peripheral nerves from
that observed in lesions of the spinal cord.

The tendon reflexes in peripheral nerve palsies usually
remain unchanged, because the muscles concerned in reflex
action are rarely involved in these disorders. There is
never any increase of reflex activity, although a degenerat-
ing muscle may contract to slight mechanical stimuli. The
knee-jerk is the only tendon reflex constantly present in
health, and an isolated peripheral palsy of the extensors of
the leg is extremely rare.

Electricity is the most valuable agent at our disposal for
the diagnosis and prognosis of peripheral nerve injuries. It
is only in disease or injury of the lower motor neuron that
the reaction of degeneration occurs ; in primary disease of
the muscles and in cerebral palsies electrical irritability
remains practicall)' unchanged. All severe injuries of the
peripheral nerves, however, like those of the spinal cord,
are associated with changes in electrical reactions. When
the protoplasmic portions of the neuron (the anterior horn
cells) are extensively destroyed, as in infantile spinal pa-
ralysis, degenerative reactions are constant and occur rap-
idly, but in chronic afTections of the anterior horns — e. g.,
progressive muscular atrophy — the cells degenerate slowly
and individually, and consequently electrical excitability of
the muscles is retained for a long time, and only disappear
when all the muscle fibers have atrophied.

The electrical examination of every case of peripheral
nerve palsy is indispensable for clinical purposes, and should
he carried out with both the faradic and galvanic current.

I02 ORGANIC EFFECTS OF INJURY.

The changes in electrical excitability after injuries to the
peripheral neuron have already been described (page 42).
They vary in character, time of appearance, and duration,
but the variations are usually in direct ratio to the extent of
injury. After severe injuries the initial period of hyper-
excitability is short ; after slight injuries it may continue for
several weeks and then return and remain at the normal.
If after six to eight days there is no decrease of excitability,
we may infer that recovery will be complete and rapid. If
after two weeks the faradic irritability of the nerve is en-
tirely lost, the duration of the paralysis will be long. In
severe. injuries there may be for several months no response
to faradism or to galvanism applied to the nerve, or to fara-
dism applied to the muscle, while the galvanic reactions in
the muscles may be increased or reversed. If after three
or four months these electrical alterations persist, and if at
the same time there has been no improvement in the paraly-
sis, it is always certain that recovery, if it occurs at all, will
not be complete. Very frequently, however, there is a re-
turn of motor power before there is any improvement in
the degenerative reaction. Such a return renders the prog-
nosis more favorable.

Vaso-motor and trophic disturbances are common accom-
paniments of severe injuries to nerves, and consist in the
condition known as glossy skin, in oedema, in the impair-
ment of the growth of the nails, in the lowered vitality of
the skin as shown by the occurrence of cutaneous inflamma-
tion and subnormal temperature, afid by the atrophy of
muscle.

Prognosis. — The prognosis of nerve injury depends upon
the general health of the patient and the extent of injury to
surrounding parts and to the nerve itself.

Regeneration of nerves occurs more quickly in the robust
than in the person exhausted from any cause. Injury to sur-
rounding parts interferes with the reparative process. .

INJURIES TO THE PERIPHERAL NERVES. 103

The extent and character of injury which the nerve
itself receives are naturally the most important prognos-
tic considerations. From the effects of gradual pressure,
as in the " sleep palsies," the nerve usually recovers per-
fectly in a few weeks or months. From the effects of
severe lacerations the return to normal function is slower
and more imperfect. Even from complete nerve section
fairly good recovery is possible, if the ends become ap-
proximated, although it is always tedious.

It is impossible to give a certain prognosis in severe in-
juries to nerves until sufficient time has elapsed to permit
us to be guided by electrical reactions.

The importance of paralysis of the cranial nerves, for
purposes of cerebral localization, has already been men-
tioned. Some of them are, although infrequently, involved
by injuries of the head and neck. Any of the superficial
branches of the fifth nerve may be paralyzed by blows or
cuts on the face. The pneumogastric has been injured,
without life being lost, by stabs and bullets. Paralysis of
the spinal accessory, with consequent loss of power in the
sterno-cleido-mastoid or trapezius muscles, or in both mus-
cles, is an occasional result of stabs in the neck. Lesions
of this nerve may be associated with lesions of the hypo-
glossal or pneumogastric. The facial and hypoglossal are
the most important of the cranial nerves frequently injured,
and consequently they are the only cranial nerve palsies
which will be described in detail.

Facial Nerve. — Traumatic peripheral facial paralysis is
not very common. Blows on the ear or over the mastoid
process, stabs or cuts in this region, or fractures of the
jaw, may cause paralysis in all the peripheral branches of
the nerve. Injury to the face may cause loss of power in
either of the facial branches. A lady was operated upon
by infraorbital incision for rebellious one-sided neuralgia of

104 ORGANIC EFFECTS OF INJURY.

the fifth nerve. When seen, several months afterward, the
neuralgia remained, but to it had been added an incurable
paralysis of the same side of the lips and cheek ; the cervico-
facial branch of the seventh nerve had been cut at the
operation.

The symptoms of facial palsy vary with the extent of in-
jury. A blow on the ear or mastoid may cause paralysis
of all branches. Then the paralyzed side of the face will
be flattened, the prominence of its cutaneous and muscular
folds diminished, and the face drawn toward the sound side.
The eye can not be closed because of loss of power in the
orbicularis palpebrarum, a condition which not uncom-
monly results in a troublesome conjunctivitis and exposes
the eye to injury from foreign bodies. The forehead can
not be wrinkled on the affected side. The mouth, when
closed, is usually drawn toward the sound side, causing an
inequality which becomes still more evident when the
patient laughs or opens the mouth wide. In paralysis of
the lips and cheeks the patient complains that food runs
out of the paralyzed side. He can not close the lips per-
fectly, as may be shown by attempts at whistling, etc. If
the temporo-facial branch alone is affected, the paralysis
will be limited to the forehead and eye; if the cervico-
facial, to the lips, cheek, and platysma myoides. Abnormal
electrical reactions occur very quickly.

Blows around the ear affecting the facial nerve may also
cause deafness, tinnitus aurium, and dizziness, indicating
disturbances of the auditory nerve ; but extracranial facial
paralysis is not associated with symptoms of injury to any
other nerve except the eighth. The taste is not affected ;
impairment of sensation may occur in the posterior auricu-
lar region, but never on the face.

The diagnosis is simple ; cerebral facial palsy never in-
volves the occipito-frontalis to a marked degree and does
not seriously interfere with the muscular movements in-

INJURIES TO THE PERIPHERAL NERVES. 105

volved in the display of the emotions. When a person with
cerebral facial palsy laughs, the innervation of both sides of
the face is usually almost equal, so that the differences of the
facial folds are scarcely perceptible ; also, paralysis of the
seventh nerve, when of cerebral origin, is usually associated
with hemiplegia of the same side. In nuclear disease, or in
injury of the nerve in its course from the pons to the exit
from the skull, there are usually associated symptoms of
palsy of other cranial nerves, as well as disturbances of taste
or salivary secretion.

Hysterical facial paralysis is very rare, and is always
associated with other hysterical stigmata.

The prognosis varies with the character and extent of
the injury. If the nerve has been cut, it will not regenerate
unless the ends become approximated soon after the injury.
Many cases do not entirely recover even after a slight blow.
Gowers reports the case of a boy, who was struck behind
the ear with a book, in whom the resulting facial palsy was
permanent. The prognosis should be very guarded, and
controlled by electrical examination. Cases which show no
sign of improvement after four months will probably never
recover entirely.

Hypoglossal Nerve. — Extracranial traumatic paralysis of
this nerve is usually unilateral and always due to punctured
or pistol-shot wounds. That traumatic paralysis of the hypo-
glossal is rarely observed may be accounted for by the
close anatomical relations of this nerve with the pneumo-
gastric, the internal jugular vein, and the internal and ex-
ternal carotid arteries. Because of this association, most
injuries of the nerve in its deep course prove fatal from in-
volvement of one or other of those important structures.
It is only after it has passed under the occipital artery, to
proceed beneath the stylo-hyoid to the tongue, that it may
be injured without great danger of involving the large
blood-vessels and the pneumogastric.

I06 ORGANIC EFFECTS OF INJURY.

A patient at the Vanderbilt clinic presented classical symp-
toms of left-sided paralysis of the tongue. He had been stabbed
in the neck several years before, and sought medical advice for
an aneurism of the left occipital artery. The stab wound must
have divided the nerve, near the occipital artery, but only have
caused slight injury to the blood-vessel.

Unilateral hypoglossal paralysis abolishes motor power
in the corresponding side of the tongue. When the tongue
is protruded it deviates toward the paralyzed side. Eating
and talking may thus be seriously interfered with. Sensory
and gustatory abnormities do not occur. The affected side
of the tongue diminishes in volume, and its surface is
traversed by deep furrows in which collect epithelium and
dried secretions.

Traumatic hypoglossal paralysis can only be cured by
operation.

Cervical Plexus. — Paralysis of the diaphragm, resulting
from injury to the phrenic nerve, which arises from the
third, fourth and fifth cervical nerve roots, is the one im-
portant symptom of injury to the cervical plexus. The
other branches of the cervical plexus are chiefly sensory ;
their distribution may be seen by reference to the chart (see
Fig. 26). Unilateral paralysis of the diaphragm, although
an unusual accident, may result from shot wounds and stabs
of the neck. The symptoms are dyspnoea on exertion and
unilateral loss of the abdominal type of breathing. Litten
was the first to describe a bilateral wavelike movement
caused by contraction of the diaphragm, which may be seen
on the thorax of normal individuals. The movement, which
is very slight, descends from the sixth rib on inspiration, to
occur again on expiration. It is not visible in paralysis of
the muscle. The prognosis of this condition is grave.

Posterior Thoracic. — This nerve supplies the serratus
magnus. Although isolated paralysis of the posterior tho-
racic is not common, it may result from falls on the shoul-

N. trig,

Piex7is
N. supracla-uic.

N. axill
N. cut. niedialis.

N. cut.

|S). Lumbo-ingr.
N. Ilio-ingr.

N, cut. post.

R, cut, lat.
N. per on,

N. saph.

N, suralis, —

N. plant, lat.

\A^ plant, jned.
nerves for cutaneous sensibility.

N. occip. maj.

N. occip. min. E

N. Auric. tnagn. \ ];

NN. supraclavic. i

N. axili.

N. c«^. tnedialis.
Nn. intercost.

N. r«rf.

N, ca^. medius,

N. muse. cut.
Nn. c«^, ciuntum.

N. P^Kf' l^S' sacro-tub,
.. N. rat/.

N. «/«.

N. -inedian.

INJURIES TO THE PERIPHERAL NERVES. 107

der or from injuries to the neck. A woman at the Vander-
bilt clinic developed it immediately after delivery. Such
occurrences are explained by compression of the nerve
through muscular contraction. Traumatic paralysis of the
serratus magnus is always unilateral. The symptoms are
characteristic. At rest the internal edge of the scapula is
prominent, and its lower angle is nearer the vertebrae than
on the unparalyzed side. When the arm is held forward
the scapula has the peculiar prominent position which has
received the name of " winged scapula." The arm can
only with difficulty be raised above the shoulder.

Recovery is always tedious and may not occur.

Circumflex. — The circumflex nerve supplies the deltoid
and is sometimes paralyzed from injuries around the shoul-
der. As a result the shoulder is flattened, and as move-
ments of the deltoid become impossible, the arm can hardly
be raised at all. If there is much atrophy, a subglenoid dis-
location of the humerus is usually present. The circumflex
also supplies the teres minor, but paralysis of this muscle is
unimportant. The electrical reactions, sensory symptoms,
and prognosis in paralysis of the circumflex are similar to
those of other nerves.

Musculo-cutaneous Nerve. — Isolated paralysis is very
rare. The motor symptoms are referable to the biceps and
the brachialis anticus, and the sensory symptoms to the
sensory distribution of the nerve.

Median Nerve. — Isolated paralysis of this nerve is un-
common, but median-nerve palsy is not infrequently associ-
ated with palsies of other nerves affected by injuries around
the shoulder joint.

The symptoms are paralysis or weakness in the muscles
supplied by the nerve. From paralysis of the pronators, the
arm is slightly rotated outward, and pronation is impaired
or impossible. From paralysis of the flexor carpi radialis,
flexor sublimis digitorum, and of one half of the flexor pro-

Io8 ORGANIC EFFECTS OF INJURY.

fundus digitorum, flexion of the wrist and fingers is inter-
fered with. The nerve supply by the ulnar of the flexor carpi
ulnaris, of the inner half of the flexor profundus digitorum,
and of all the interossei, permits, when the ulnar nerve re-
mains intact, some flexion of the wrist and of the terminal
phalanges of the two inner fingers and flexion of the first
phalanges of all the fingers. Through overaction of the
extensors of the thumb (posterior interosseus) and of the
adductor (ulnar) the thumb assumes the position of exten-
sion and adduction, being in the same plane as the fin-
gers. Sensory symptoms are usually unimportant ; they
occur in the sensory distribution of the nerve. According
to Bernhardt, paralysis of this nerve is frequently associated
with trophic disturbances (atrophy, glossy skin, etc.). The
electrical reactions and prognosis have no individual charac-
teristics.

Ulnar Nerve. — The ulnar nerve arises from the inner
cord of the brachial plexus, derived from the eighth cervical
and first dorsal segments of the spinal cord. From its origin
in the axilla, until it passes through the olecranon groove,
its course is superficial. In the upper part of the forearm
it is covered by the flexor carpi ulnaris, but in the lower
half of the forearm it is covered only by integument and
fascia. Its superficial situation renders it very liable to in-
jury. Paralysis may follow blows, cuts on the arm or fore-
arm, dislocation and fractures of the humerus or clavicle ; it
may be compressed by callus or strained by continued or
sudden forced flexion of the forearm ; it may be dislocated
at the elbow or be involved by fractures and dislocations at
the elbow, in the forearm, or at the wrist. Of the cases of
ulnar palsy recently coming to the Vanderbilt clinic, one
was caused by a piece of steel hitting the inner side of the
arm, and two by falls on the elbow. The records of the
Vanderbilt clinic show that of all peripheral paralyses due
to direct and immediate violence, ulnar paralysis is the most

INJURIES TO THE PERIPHERAL NERVES. 109

frequent. Unlike the musculo-spiral, it is rarely the seat of
pressure or sleep palsy.

The symptoms are chiefly motor, and their distribution
may be readily inferred by recalling the distribution of the
nerve. Loss of power in the flexor carpi ulnaris causes
weakness in flexion of the wrist ; loss of power in the inner
half of the flexor profundus digitorum causes weakness in
flexion of the two internal fingers. In complete ulnar pa-
ralysis the little finger can not be moved at all.

The most characteristic and disabling effect of paralysis
of this nerve is paralysis of the interossei, all of which it
supplies. The interossei flex the first and extend the second
and third phalanges of the fingers, which actions are neces-
sary in writing and in most of the finer movements of the
hand. The loss of them causes very serious inconvenience.
The interossei also adduct and abduct the fingers and ad-
duct the thumb, movements which can no longer be per-
formed when the ulnar is paralyzed.

Atrophy of paralyzed muscles and overaction on the
part of opposing muscles are early complications in ulnar
palsy. In beginning stages the condition is manifested by
slight overextension of the first phalanges of the fingers,
especially the little finger (Fig. 27), and an inabilit}' to
firmly extend the terminal phalanges. If the palsy is
complete and permanent, the deformity becomes very
marked, constituting the claw hand or main en griffe of
Duchenne.

The sensory distribution of the ulnar nerve is limited to
the inner side of the anterior and posterior surfaces of the
hand. Posteriorly it extends a little above the wrist and
includes part of the dorsal surface of the middle finger, and
the ring and little fingers ; anteriorly it is limited to the
hand and two inner fingers.

The sensory symptoms which occur as a result of ulnar
palsy are chiefly subjective — numbness, tingling, and simi-

ORGANIC EFFECTS OF INJURY.

lar sensations. There may be some diminution of cutane,
ous sensibility, but complete anaesthesia is extremely rare,
unless the nerve is inflamed as well as injured.*

Prognosis. — Ulnar palsy, when it occurs as a result of
pressure from dislocated bones, usually recovers in a few

Fig. 27. — Beginning main en gfiffe. From an injury to the ulnar nerve.
(Almshouse Hospital.)

weeks or months, if the dislocation is reduced and if the
nerve is not too seriously lacerated or compressed. In frac-
tures there is more danger of the nerve being lacerated, and
consequently the prognosis should be given with greater re-

* The ulnar nerve seems particularly liable to the somewhat unusual affection
known as ascending neuritis, or neuritis migrans. In this extremely painful dis-
ease a peripheral nerve injury, with external wound, is followed by extensions of
the paralysis and the pain up the course of the nerve or to other ner\'es. In a
patient at the Vanderbilt clinic an ulnar neuritis developed, probably from a cut on
the little finger, and eventually the nerve became paralyzed for all its functions.
The pain was intense, and the swollen nerve could be felt as a round cord in the
whole of its peripheral course.

INJURIES TO THE PERIPHERAL NERVES.

Ill

serve. If the paralysis be due to pressure exerted by callus,
operation will be necessary for complete recovery. Elec-
trical examination may be found useful in deciding upon the
necessity for operation. From ordinary blows the nerve
usually recovers perfectly ; the prognosis when the nerve
has been divided is the same as for other nerves.

Fig. 28.— Distribution of the sensory nerves in the hand. (After Quain.)

Musculo-Spiral. — The musculo-spiral nerve arises from
the posterior cord of the brachial plexus, and carries in its
trunk fibers from all the nerve roots which form the bra-
chial plexus with the exception of those from the first
dorsal and those from the fifth cervical. Fibers from the
fifth cervical are sometimes included (Quain). It is prob-
able that in this nerve, as in many others, the cells from
which the motor fibers of the nerve arise are not limited

112 ORGANIC EFFECTS OF INJURY.

to the spinal cord segment from which the nerve root
springs, but may come from the anterior horn cells of any-
one of several segments.

Its situation in the axilla exposes the musculo-spiral
nerve to injury ; dislocations, and fractures of the humerus
and clavicle, are frequently followed by paralysis of this
nerve. In the arm the most frequent cause of musculo-
spiral palsy is pressure, whether caused by a crutch or
by weight of the body during sleep. Blows and wounds
to the forearm, also fractures of the bones, may abolish its
function. Musculo-spiral paralysis has also resulted from
falls on the hand and from sudden and forcible extension of
the arm.

The symptoms are familiar to every physician. If the
nerve is injured in the axilla or upper part of the arm, there
will be paralysis of the triceps as well as of the muscles
situated lower down. If the nerve is injured below the
branch for the triceps that muscle will escape. The other
muscles involved are the supinators of the arm, the exten-
sors of the wrist and fingers and of the thumb.

Complete musculo-spiral paralysis causes the familar
drop-wrist (Fig. 29). When drop-wrist continues for any
length of time there develops a prominence on the back
of the hand due to thickening of the tendon-sheaths. The
hand hangs helpless, and all efforts on the part of the pa-
tient at extension of the wrist or of the first phalanges of the
fingers are ineffectual. If the hand is supported, thus giv-
ing a point dappui to the interossei, the terminal phalanges
can be extended and the fingers separated. The power of
abduction and extension of the thumb is lost. It frequently
happens that the extensors are not completely paralyzed ;
when this is the case the paralysis is least marked in the
index and little fingers. Paralysis of the supinators, espe-
cially of the supinator longus, causes the arm to pronate
when any efforts at flexion of the wrist or fingers are at.

INJURIES TO THE PERIPHERAL NERVES.

113

tempted. In this way the grip is very much lessened in
force. By paralysis of the supinator longus the power of
flexion of the forearm is diminished. If the triceps is in-
volved, extension of the arm is impaired or lost. The meth-
ods of examination for most of these muscular functions

Fig. 29.- Drop-wrist, from palsy of tlie mu ,culo-spiral nerve. (Vanderbilt Clinic.)

are obvious. The most satisfactory test for weakness in the
supinator longus is for the patient, with the ulnar side
of the forearm resting upon a table, to attempt to raise
the forearm against the resistance of the hand of the ex-
aminer.

The sensory symptoms of paralysis of this nerve are
usually limited to numbness and tingling of the radial side
of the forearm and hand and of the back and outer side of
the arm. The extent of the atrophy depends upon the

114 ORGANIC EFFECTS OF INJURY.

severity of the injury. The electrical reactions are the same
as for the other nerves. In the larger number of cases the
injury is of moderate severity, and so pronounced reactions
of degeneration rarely occur.

The diagnosis of traumatic musculo-spiral paralysis ordi-
narily presents no difficulties except when a history of acci-
dent is unsatisfactory. Then it is well to remember that
lead paralysis is usually bilateral, and only exceptionally
affects the supinator longus and extensor longus poUicis.
Also lead poisoning causes electrical changes of serious im-
port. In progressive muscular atrophy the paralysis is
rarely complete, and its distribution is ulnar as well as radial.
In progressive muscular atrophy the electrical reactions re-
main for a long time normal.

The prognosis of musculo-spiral paralysis is in general
very favorable ; unless the injury has been unusually severe,
recovery is the rule.

Combined Paralyses of the Upper Extremity.

Blows or falls on the neck or shoulder or arm, and dislo-
cations and fractures of any of the bones of the upper ex-
tremities, may cause paralysis in more than one nerve.

Thus a patient capie to the Vanderbilt clinic with paraly-
sis of the musculo-spiral, median, and ulnar nerves, which
came on immediately after a fall on the palm of the hand.

The musculo-spiral and ulnar are the nerves most fre-
quently involved together in injuries around the shoulder
joint, although paralysis of the circumflex, or the median or
the musculo-cutaneous, may be added. The symptoms of
these combined paralyses are the sum of the sj'mptoms of
lesions of the individual nerves. They are usually the
result of severe injuries, and the prognosis is accordingly
serious.

Injuries to the neck, falls upon the point of the shoulder,
and less frequently dislocations of the shoulder, sometimes

COMBINED PARALYSES OF THE UPPER EXTREMITY, i 1 5

cause a peculiarly distributed paralysis, first described by
Erb, and often called Erb's palsy. The muscles most fre-
quently affected are the deltoid, biceps, brachialis anticus,
and supinator longus. In several of the Vanderbilt clinic
cases the supra and infra-spinati were involved as well.
In these cases there is slight inward rotation of the arm.
All these muscles, except the last two, receive their inner-
vation through the fifth and sixth cervical nerve roots. The
suprascapular nerve, which supplies the supra- and infra-
spinati muscles, receives some fibers from the fourth cer-
vical segment, but most of its fibers come from the fifth and
sixth nerve roots, and so it may easily be injured when
those roots are affected.

Hoedemaker has suggested that, in injuries to the shoul-
der, paralysis of these nerves may occur by the fifth and
sixth nerve roots being compressed between the transverse
processes of the sixth and seventh cervical vertebrse and the
middle of the clavicle.

In cases where the paralysis is severe this affection is
very disabling. The arm can not be raised from the side,
and the forearm can not be flexed or strongly rotated out-
ward. From paralysis of the deltoid the shoulder of the
affected side is lower than its fellow, and there may be a
slight subglenoid dislocation of the humerus. Atrophy is
often an early symptom, and there is usually marked fibril-
lary twitching in the muscles, when, if not completely par-
alyzed, they are put in action.

The sensory symptoms are never prominent; there may
be numbness and tingling in the region of the shoulder, or
in the radial distribution of the forearm and hand. The
electrical reactions soon show degenerative changes.

All these muscles may, in health, be made to contract by
applying the electric current at a point in the neck called
Erb's point (see Fig. 7); after injury disordered electrical
reactions soon become manifest at this same point. A Van-

Il6 ORGANIC EFFECTS OF INJURY.

derbilt clinic case after a fall on the right shoulder com-
plained of some weakness in the shoulder muscles of that
side, especially in the morning. The man was left-handed,
and examination showed only a comparative weakness of
the right deltoid, biceps, and supinators. This weakness
might have been a normal difference between the right and
left side, and the diagnosis was not clear. But when the
galvanic response in these muscles, obtained through Erb's
point, was found considerably exaggerated on the right side,
it became evident that the patient was suffering from a very
mild injury to the upper part of the brachial plexus.

The diagnosis of this affection is extremely simple if
the patient is examined for muscular power and by elec-
tricity. In severe cases, in which the deltoid is so re-
laxed that it permits a slight subglenoid dislocation of the
shoulder, the condition is sometimes mistaken for a simple
dislocation. Such errors are the results of superficial Ex-
amination.

The general prognosis of this form of paralysis is good,
in that the patients usually recover. In my experience,
however, such recovery has always been tedious, extending
over many months.

Another form of brachial-plexus paralysis involves the
first anterior dorsal root. Through this root pass the sym-
pathetic fibers for the eye. The condition was first thor-
oughly studied by Klumpke, and is called Klumpke's, or
the lower arm type of brachial-plexus palsy. It consists in
a paralysis of the small muscles of the hand, and evidences
of disturbance of the sympathetic on the same side bf the
face. There are myosis, diminished palpebral fissure, loss
of the cilio-spinal reflex, sinking in of the eye, and flatten-
ing of the face. There are no vaso-motor disturbances.
Klumpke's paralysis, as an isolated paralysis of the brachial
plexus, is a great rarity. It occurs from causes similar to
those already mentioned in lesions affecting the fifth and

COMBINED PARALYSES OF THE UPPER EXTREMITY. 117

sixth cervical roots, causing Erb's palsy. The lower roots
of the brachial plexus are affected hiuch less frequently,
however, than the upper, and Klumpke's paralysis is much
more uncommon than the variety named after Erb.

Klumpke's paralysis is only infrequently seen in its pure form.
It is usually more comprehensive, and differs in other ways from the
-variety of brachial plexus lesion first described by that observer.
Thus, in a case at the Vanderbilt clinic, a man fell on the right
shoulder, fracturing the clavicle. After the bone lesion had
healed the patient presented the following symptoms : Left myo-
•sis without other evidences of sympathetic disturbances ; difficulty
in raising and flexing the arm, and an almost total disability in
performing the finer movements of the fingers and in flexing the
wrist and hand. There was slight anaesthesia along the inner side
of the arm. The deltoid and biceps reacted to faradism, but the
muscles supplied by the median and ulnar nerves presented de-
generative electrical reactions. Thus in this case myosis was the
only evidence of disturbance of the sympathetic, but in addition
to palsy of the circumflex and musculo-cutaneous nerves there
was affection of the median and ulnar.

The paralyses of the lumbar and sacral plexuses are rela-
tively infrequent, and result from causes similar to those
■enumerated for the palsies of the arm. When traumatic,
they are usually the results of fractures or dislocations of the
lumbar vertebrge or of the pelvis. It may be sufficient to
recall that the lumbar plexus supplies the muscles concerned
in flexion and adduction of the thigh, and to a slight extent in
rotation outward, and in extension of the leg. Consequently
the knee-jerk may be lost in paralysis of the lumbar plexus.
The other muscles of the hip and thigh, and all the muscles
of the leg, receive their innervation through the sacral plexus.

Injuries to the lumbar or sacral plexus, or to any of
their ultimate branches, are followed by the same kind of
symptoms as have been described under the palsies of the
cervical and brachial plexus, and may easily be diagnosti-
cated by remembering the distribution of the nerves.
9

Il8 ORGANIC JEFFECTS OF INJURY.

Bibliography. •

Bernhardt, Die Erkrankungen der Peripherischen Nerven.
Nothnagel's Spec. Path, und Therapie, Wien, 1895.

Hoedemaker, Ueber die von Erb zuerst beschreiben combinirte
Lahmungsform an der oberen Extremitat. A}-ch. fur Fsych.,
1879, ix, p. 738.

Howell and Huber, A Physiological, Histological, and Clinical
Study of the Degeneration and Regeneration in Peripheral Nerve
Fibers after Severance of their Connection with the Nerve Cen-
ters. Journal of Physiology, 1892, xiii. No. 5; 1893, xiv, No. i.

Gowers, Diseases of the Nervous System, second edition, Lon-
don, 1892.

Klumpke, Contribution S, I'^tude des paralysies radiculaires da
plexus brachial. Revue de mid., 1885, No. 7.

Litten, Ueber die normaliter bei jeder Respiration am Tho-
rax sichtbaren Zwerchfellbewegungen. Deut. med. Woch., 1892,,
No. 13.

Mitchell, J. K., Remote Consequences of Injuries of Nerves.
Philadelphia, 1894.

Mitchell, S. Weir, Injuries of Nerves and their Consequences.
Philadelphia, 1872.

Quain, The Nerves. London, 1895.

Stroebe, Die allgem. Histol. der degenerativ u. regener. Pro-
cesse im central, u. periph. Nervensystem. Cblatt. fiir allg. Path,
und path. Anat., i895-'96, p. 849.

CHAPTER IV.

ULTIMATE ORGANIC EFFECTS OF INJURY.

While the exact diagnosis of the acute conditions which
have been described in the preceding pages sometimes pre-
sent difficulties, their astiology is in most cases easy of dem-
onstration.

When an organic injury is immediately followed by
symptoms of well-recognized pathological conditions in the
nervous system there is rarely any question as to the. pro-
priety of associating the two occurrences in the direct re-
lationship of cause and effect. The ultimate termination de-
pends upon the nature of the injury and upon the part of
the nervous system which has been affected by it. It is
often difficult to foresee what this termination is to be.

Of cerebral lesions the possible variety of final results is
almost unlimited. Death may ensue instantly or after vary-
ing periods of time, and may be due to the destruction of
vital centers ; or the lesion of the brain may be the one addi-
tional straw which an already enfeebled constitution is un-
able to carry. If the patient lives he may recover from the
immediate effects of the injury, but may remain perma-
nently paralyzed as regards motion or special sense func-
tion, or be left with a serious and incurable impairment of
the intellectual faculties. Dementia, associated or not with
paralysis, is one of the most frequent of the permanent re-
sults of severe injuries to the brain.

This is illustrated by a man at present under my observation,
who at the time of the accident was under the care of Dr. Bolton

I20 ORGANIC EFFECTS OF INJURY.

at the Hudson Street Hospital. The patient was a fireman, thirty-
one years of age, who fell through a hatchway, striking on his
thead and fracturing his skull. When brought to the hospital he
was in a stupor, was very irritable and noisy, and presented evi-
dences of paralysis of the left arm and left leg, and of ptosis on
the right side.

The physical symptoms disappeared in a few weeks, but al-
though it is now several months since the accident, and although
he has regained good general health, the patient remains slovenly,
unable to care for himself, or to talk intelligibly or to understand
what is said to him. He sits quietly in his chair, oblivious to his
surroundings, and though able to perform all movements perfectly
well, he does not move unless told to do so. He is at present
completely demented, and hopes for his recovery do not seem
bright.

Any of the psychoses may develop after severe injuries
to the head, whether the skull has or has not been fractured.
Mania and melancholia are the most common of the trau-
matic psychoses. They may appear weeks or months after
the accident, and usually present no symptomatic differences
from like psychoses of idiopathic origin. Their prognosis
is always grave, although some cases, in which there was
a depressed fracture of the skull, have been benefited by
operation. Neurasthenia and hysteria may also be the re-
sult of severe injuries to the head, although these disorders
more commonly follow accidents of less gravity.

It is often impossible in an individual case to foresee
what the ultimate effects of severe head injuries are to be.
In the cases in which the evidences of extensive haemorrhage
or laceration of the brain are pronounced it is usually ap-
parent that the patient has not long to live ; but when the
symptoms do not unequivocally point to a fatal lesion there
are no means by which it may be foretold how complete
recovery is to be or if it is to occur at all. , Abscess of the
brain may develop after injuries to the head in which the
only immediate symptoms were scalp wounds or in which
any abrasion in the cranial covering was not discoverable.

ULTIMATE ORGANIC EFFECTS OF INJURY. 12 1

In acute traumatism of the spinal cord the prognosis is
bad, both as to life and as regards recovery. Lesions of
spinal-cord structure are irreparable ; if nerve fibers or
nerve cells are destroyed, they are not replaced. The only
hope, in cases of traumatic paraplegia, that the symptoms
may entirely disappear, depends upon the loss of function
being due to some lesion such as extrameduUary haemor-
rhage, virhich temporarily abolishes function without seri-
ously disturbing structure. When the cord is completely
cut across there is no chance for recovery, and the patient
usually dies in a few days as a result of the injury. In
many cases the lesion is not completely transverse, and the
patients regain a certain amount of muscular power, and
control of the sphincters may be restored. Angesthesia fre-
quently disappears almost entirely. In general, any one
who sustains an injury to the spinal cord, if he does not
die, remains more or less of a cripple for life, although this
rule has its exceptions. The nearer to the brain the lesion
is situated the worse is the prognosis for life. Injuries to
the fourth cervical segment, or to segments above it, are
almost immediately fatal. The mortality of all cervical
lesions is very high. The prognosis is somewhat better
when they are in the dorsal region, and is most favorable
for those of the lumbo-sacral region and of the cauda equina.

When there is a time interval between the receipt of any
injury to the nervous system and the appearance of the
symptoms which may be alleged to be its direct result, a
causal connection is much more difficult of proof. The
question of the traumatic origin of tumors of the nervous
system is even more obscure than when new growths de-
velop in other parts of the body apparently as the direct
consequence of injury. According to the theory of Cohn-
heim, tumors have their origin in undeveloped embryonal
cells which remain inactive until, through the agency of
some exciting cause, they are stimulated to a disordered

122 ORGANIC EFFECTS OF INJURY.

growth. The nature of the essential exciting causes is un-
known, but that trauma is one of them is commonly be-
lieved. There is little question as to the possibility of
long-continued irritation inducing malignant neoplasms,
especially in the mucous membranes. To prove that a
single acute injury may bring about such a result is very
much more difficult. As far as the nervous system is con-
cerned, the evidence for the traumatic origin of tumors can
not be regarded as anything more than suggestive.

Thus in a recent autopsy held at the Almshouse upon the
body of a woman, seventy-one years of age, who had never given
any symptoms of cerebral disturbance, there was found a large
endothelioma upon the internal surface of the dura mater, on the
right side of the middle fossa of the skull, lying adjacent to the
squamous portion of the temporal bone just posteriorly to the
greater wing of the sphenoid. On the opposite side of the skull
was an old, undepressed fracture. The question is of course open
as to whether the situation of the tumor were entirely accidental,
or whether at the time of the fracture sufficient force was exerted
by contrecoup to incite to morbid activity embryonal cells in the
dura mater, with the resulting formation of an endothelioma.

A still more suggestive case has been reported by Carara * in
which a man, previously well, received a blow on the head and died
of tumor of the brain within five months. The patient, who was
thirty-nine years of age, was struck with a stick on the left pos-
terior parietal region. The scalp wound healed in about six
weeks, but there soon occurred headache, deafness in the left ear,
and dizziness and numbness of the left side. These symptoms be-
came worse, and the patient entered the hospital, where it was
found that in addition to the symptoms already mentioned there
were a weakness and diminution of cutaneous sensibility in the left
arm and leg. The reflexes were normal. The patient began to have
convulsive seizures, and soon after this he died. The autopsy
showed that the skull was not fractured, but that there was a
glioma in the right side of the brain, in the neighborhood of the
Rolandic fissure. Whatever may be one's opinion, it is impossible
to decide whether the blow on the head was the sole cause, or
whether the tumor had begun to grow before it was received.

* Vierteljahrschrift fiir gerichtliche Medicin, January, i8g6.

ULTIMATE ORGANIC EFFECTS OF INJURY.

123

According to views recently expressed by Striimpell *
as to the pathology of multiple sclerosis, the genesis of that

Fig. 30.— Deformity of the back caused by syringomyelia. (Vanderbilt clinic.)

disease depends upon a morbid activit}- being given to ab-
normal islets of neuroglia tissue scattered throughout the

* Neurologische Centralblatt, 1896, No. 21.

124 ORGANIC EFFECTS OF INJURY.

cerebro-spinal axis. If this theory is correct, the astiologj
of multiple sclerosis is probably similar to that of tumors ;.
yet clinical substantiation that multiple sclerosis arises from
traumatic causes is still slight. This subject will again be
referred to.

So little is known about the pathology of aeromegaly
(Fig. 31), and the disease is itself so rare, that knowledge of
the part played by injury in its causation is still largely
speculative. Unverricht, * however, describes a case of
typical acromegaly in a patient who had received an injury,,
and whom the examining physician had regarded first as a
simulator and later as an example of " traumatic neurosis."
Unverricht adduces several other cases of alleged traumatic
origin.

The relationship of traumatism to diseases of the nerv-
ous system is necessarily so obscure that it can not be even
approximately decided except for those disorders which are
comparatively frequent. Thus, although there is no doubt
but that spinal haemorrhage may give rise to conditions in
the spinal cord similar to those found in syringomyelia,
there is as yet only very meager clinical evidence for the
existence of traumatic syringomyelia.

Laehrf reports two cases, in each of which the disease
already existed at the time of the injury, and Huisman % has
recently described as traumatic a case in which the relation-
ship of the injury to the spinal disease is not clear. A simi-
lar uncertainty exists in regard to the traumatic astiology of
ataxic paraplegia and chronic progressive spastic paraplegia.

There is, however, a group of comparativel)' common
chronic degenerative diseases of the nervous system of
which traumatism is regularly spoken of as a cause, and
which, by reason of the symptoms being often observed for

* Miinchener medicinische Wochenschrift, 1895, xlii, 14.

■f Char. Annalen, 1895, Jahrg. xx.

% Deutsche medicinische Wochenschrift, February, 1897.

ULTIMATE ORGANIC EFFECTS OF INJURY.

125

the first time after some accident, have important forensic
relations. These diseases are epilepsy, general paralysis of
the insane, locomotor ataxia, progressive inusctilar atrophy, and
paralysis agitans. In some of them the occasional occur-

FiG. 31. — Acromegaly. (Photni^raph rif a female patient who died in the
Incurable Hospital.)

rence of trauma as a sole cause seems probable ; in others
the possibility of a traumatic origin is extremely doubtful,
as is indicated by the absence of well-authenticated cases
which have occurred in this way. Epilepsy is the only one
of the group which can be positively proved, both clinically
and pathologically, to owe its development, in certain cases,
solely to trauma.

So many factors must be taken into account in a consid-

126 ORGANIC EFFECTS OF INJURY.

eration of these diseases and their relationship to injury that
they require individual description.

Epilepsy.

Epilepsy is one of the most frequent affections of the
nervous system, and is among the commonest of chronic
diseases. It is estimated as occuring in one of every five
hundred of the population. In the larger number of cases
no cause can be found to explain the convulsions ; then the
epilepsy is called idiopathic and is regarded as a disease
sui generis. In a small percentage of the total number of
cases the convulsions can be shown to depend upon gross
intracranial lesions (Jacksonian epilepsy) or upon the irri-
tation of the cortical cells by toxic substances circulating
in the blood. In such cases the convulsions are the expres-
sions of definite pathological states.

When the attacks occur as the immediate result of phys-
ical injury, epilepsy is called traumatic ; the trauma causes
some morbid alterations in the brain substance which find
their clinical expressions in recurring convulsions.

The frequency of traumatic epilepsy, as compared with
the idiopathic form, is somewhat difficult to determine. If
we are to accept as traumatic every case which has the his-
tory of a fall, or a blow on the head, received years before
the appearance of convulsions which are from the first gen-
eral in character, the category of idiopathic epilepsy would
become very restricted ; for few persons reach adolescence
without a fall or an injury of some kind, and almost every
epileptic patient can be made, if closely questioned, to admit
some such history. According to the books at the Vander-
bilt clinic, a large percentage of all the patients had falls in
infancy, or frights, or other trivial traumatisms, but they are
not regarded as examples of traumatic epilepsy, and it seems
doubtful if even one per cent of the total number of cases of
the disease could be proved, with reasonable probability, to

EPILEPSY.

127

have been the direct result of injury. But whatever the
true cause of epilepsy may eventually be shown to be, our
actual knowledge permits us to recognize as traumatic only
such cases as develop within a reasonable length of time
after a severe injury, or as indicate by their symptoms that
there has been an injury to a limited portion of the brain.

Our knowledge of the pathology of traumatic epilepsy is
much more definite than that of the idiopathic form. It has
been carefully studied by Van Gieson. There is frequently
a fracture of the skull, so that splinters of bone press upon
the cortex; or without fracture there may be an exostosis
beneath the site of the original injury. The membranes may
be adherent to one another, and thus form the starting point
of wedges of connective tissue which grow downward at
the expense of brain tissue. The nerve cells in the affected
area are found in various degrees of degeneration, or they
may have entirely disappeared, having been replaced by
islets of neuroglia which have developed in the course of
the arteries that pass perpendicularly from the surface into
the brain cortex. These morbid changes are fairly constant
in traumatic epilepsy, and are sufficient to permit the disease
to be regarded as due to organic cerebral lesion ; but in
furnishing a pathological anatomy they do not explain the
paroxysmal nature of the symptoms. If the cerebral lesion
is sufficient to cause paralysis, that symptom can very easily
be understood by remembering that injury to the cortex has
injured or killed the cells which are the essential factors in
voluntary motion. But why cells, whether they do or do
not regain the power of causing voluntary movement, should
from time to time become the seat of irritation and thus
cause convulsions, remains unexplained.

^Etiology. — In the astiology of traumatic epilepsy pre-
disposition plays a subsidiary r61e. General convulsions
sometimes develop soon after a slight injury to the head or
to other parts in persons who are hereditarily neurotic, or

128 ORGANIC EFFECTS OF INJURY.

whose nervous systems, as a result of alcoholism or other
forms of chronic poisoning or degeneration, have become
less resistant to injurious influences or stimuli. In such
cases it is often impossible to determine the causal value of
the injury. The general character of the convulsions would
seem to indicate that no one portion of the brain had been
traumatized, but that the whole cerebral cortex was in a
condition of latent disease that required only a slight dis-
turbance of the cerebral equilibrium to become active. We
must know very much more about cerebral pathology than
we do at present before it will be possible to decide whether
such cases can properly be regarded as the direct results of
injury, or whether epilepsy would have eventually devel-
oped as a consequence of some one of the mishaps of daily
life to which every one is exposed.

Of the immediate causes of the disease, injuries to the
head are the most important. The records of the Franco-
Prussian War show that from 8,985 head injuries there devel-
oped 46 cases of epilepsy. The same records show 17 cases
among 77,461 persons wounded in the body or extremities.
Thus head injury is not everywhere regarded as the sole
cause.

It seems, however, extremely improbable that wounds or
injuries by which the brain is unaffected, occurring to per-
sons who were not already doomed to present manifesta-
tions of the disease, can be regarded as causes of epilepsy.
At the Vanderbilt clinic, among the records of over one
thousand cases, injury to the head is the sole form of phys-
ical traumatism which has been alleged as active in the pro-
duction of the disordef. It is possible that injuries to other
parts may be followed by epilepsy, as injury may be followed
by any disease, but in such cases the influence of the trauma-
tism must be regarded as inconsequential.

As regards epilepsy, severity is the most important ele-
ment of a head injury. Blows on the head with clubs or

EPILEPSY.

129

heavy instruments, striking the head in falls or in other
ways, are not uncommonly followed by the disease. In
most of the cases the skull is fractured, either in the internal
or external table, so that the brain is directly pressed upon.
But in some cases Jacksonian epilepsy apparently develops
as a result of an injury to the head which has not fractured
the bone.

Thus in a case reported by Lloyd and Deaver, the patient was
struck on the right side of the head at the age of sixteen ; five
years afterward he began to have fits, which commenced with
numbness and spasm in the left arm, extending to the left side of
the face; consciousness was not often lost during the attack. The
skull was trephined over the hand and arm center ; there was no
fracture, and the brain and meninges appeared normal.

Similarly, in a case of Starr's, the patient was hit on the left
side of the head with a sand-bag, and was rendered unconscious
for twelve days. The skull was not fractured, as was proved by
operation, but in three months the patient began to have attacks
of aphasia and convulsions in the right hand.

Interval. — The fits may ensue almost immediately, or
may be separated from the occurrence of the original injury
by a period often varying from months to years.

Thus in a case of Starr's, a boy eighteen years old, previously
healthy, received a traumatism of the right parietal bone by being
struck on the head by a heavy block of wood. In three weeks he
began to have frequent attacks, which were characterized at first
by tingling and numbness in the left hand, a sensation which ex-
tended up the arm to the shoulder, and then down the trunk and
leg, never involving the face. The subjective sensations were
followed by twitching of the muscles of the arm without involving
other parts and without being accompanied by loss of conscious-
ness. The attacks lasted about a minute, and between them there
was neither paralysis nor anaesthesia. It was not possible to deter-
mine by palpation of the scalp whether the bone was fractured or
not; but an operation showed that there was a linear fracture of
the right parietal bone, and that immediately over the hand center
there was imbedded in the dura a splinter of bone one inch long
and three quarters of an inch wide.

I30 ORGANIC EFFECTS OF INJURY.

In contrast to this case, which developed so quickly, is
another one, equally typical of traumatic epilepsy, but in
which the fits did not appear until three years after the
accident.

A man, twenty-four years of age, sustained a fracture of the
skull on the right side about the middle of the coronal suture.
He recovered from the acute effects of the injury, but three years
later began to have epileptic attacks. The fits began with a
movement of the left hand and v/ith a turning of the head to the
left ; the patient then lost consciousness, and the convulsion be-
came general. Operation over the right arm center showed that
a splinter of bone was indenting the dura, that the dura was thick-
ened, and that the brain was yellower and more oedematous than
usual.

Many cases have been reported as traumatic in which the
time elapsing between the occurrence of the injury and the
first appearance of convulsions has been much longer, being
five or ten or even a greater number of years. In such cases,
inasmuch as the fits are almost always general, it is more
difficult to prove the causal relationship of the traumatism
to the convulsive symptoms. So long an interval, however,
is unusual. Of forty-four cases of traumatic epilepsy which
were operated upon (collected by Mason for Gray), most of
the fits began in a few weeks or months after the injury.
Five cases appeared after an interval ranging from three
and a half to fourteen years, but in all of these, except one,
the convulsions were general and the influence of the trau-
matism consequently obscure. The exception is the case
of Lloyd and Deaver, to which reference has already been
made.

In the interval between the accident and the appearance
of the first fit the patient may be perfectly well after recov-
ery from the acute effects of the injury. If the motor tract
has been directly injured, there may be hemiplegia ; or if the
dura has been irritated, there may be the headaches charac-
teristic of pachymeningitis.

EPILEPSY. 1 2 r

Thus a patient at the Vanderbilt clinic, previously healthy and
without nervous predisposition, vi^hen a boy of eleven years of age
was thrown from a wagon, striking his head. Since that time he
has had severe generalized headaches and petit mal attacks, both
of which later became frequent. The physical examination w.as
negative. There were no scars or evidences of fracture of the
skull, no paralysis or other indication of disturbance of the
motor tract.

Usually, hovvrever, in the cases which give no sign of
direct organic injury, the latent period passes without
symptoms.

Symptoms. — The most common history of traumatic epi-
lepsy is somewhat as follows :

A man", previously healthy, is struck on the head by a
heavy instrument, or falls so that his head receives a severe
blow, which inflicts a scalp wound. He becomes uncon-
scious and may suffer for some time from the symptoms of
cerebral concussion, or from those of compression. He
eventually recovers, and finds that one side of the body
is paralyzed. The paralysis usually rapidly improves, so
that when the patient is finally examined for it nothing
remains except a comparative one-sided weakness or stiff-
ness or a unilateral increase of the deep reflexes. Some
weeks or months after recovery from the effects of the
accident the patient begins to have convulsions in some
portion of the body opposite to that of the head injury.
The twitchings, which are usually preceded by a feeling of
numbness or tingling in the affected' part, begin in a few
muscles and then spread to others. They are expressive of
irritation of a localized portion of the brain cortex and are
called, after their original describer, Jacksonian. In the
early stages of the disease the fits often remain local, but
they have a tendency to progress so that they eventually
involve the whole body, although usually the attack con-
tinues to begin in the part first affected. Consciousness is
not lost in the earlier attacks. The tendency of such a case.

132 ORGANIC EFFECTS OF INJURY.

however, is in all respects progressive, so that after the dis-
ease has existed for a number of months or years the attacks
become exactly similar to the grand mal of idiopathic epi-
lepsy, with the possible exception that they may continue
to begin as a localized spasm.

On examination of the head there may be found the scar
of the original scalp wound and a depression in the skull.
The scar is usually not tender, and pressure upon it does
not cause a fit. The skull may be fractured, however, even
on its convexity, without leaving any sinking in of its sur-
face. When a depression exists, the injured portion of the
brain is not necessarily immediately beneath it. The bone
may be splintered, or haemorrhage may have occurred in
such a way that the cerebral lesion is situated at some dis-
tance from the site of the external injury. The frequency
of this occurrence is fully recognized by surgeons who, in
operating for traumatic epilepsy, open the skull at a point
opposite the portion of the cortex which supplies the mus-
cles that first become the seat of spasm, instead of being
guided by the depression in the bone. They follow the
medical rather than the surgical indications.

The typical symptoms of traumatic epilepsy are subject
to variations. The fits ma}' take other forms than those of
muscular spasm. Petit mal is a common and sometimes the
sole symptom. Attacks of headache may be substituted for
convulsive phenomena, as is shown by the after-history of
Case VI of Starr's (Brain Surgery) :

J. R., aged forty, was struck upon the left temple and sus-
tained a fracture of the skull in August, 1889. When he recov-
ered consciousness he was found to be paralyzed upon the right
side and aphasia. In the course of the following six months the
hemiplegia slowly subsided and the speech gradually improved,
so that he was able to go about, but was still unfit for work.
About a year after the accident he began to have convulsions ;
some of these were general, with loss of consciousness, but later
they became localized and remained so for some time. They

EPILEPSY.

133

increased in frequency until, when seen in December, 1892, the
patient was having several every week. The attacks began with
a twitching of the muscles about the mouth upon the right side;
a drawing of all these muscles toward the right, with twitching
of the eyes, and a gradual extension of the spasm to the right side
of the neck and to the right arm and hand. During the attack
he did not lose consciousness, but he could not speak, and ex-
perienced a sensation of tingling in the face and mouth. After
an attack he appeared to be weak and was not able to talk as well
as before. Examination on December 10, 1892, demonstrated a
slight paresis on the right side of the face, the tongue not deviat-
ing, and some weakness in the right arm, but no affection of the
leg; no disturbance of sensation; increased reflexes upon the
right side. A depressed fracture of the skull, running backward
two inches about over the position of the Sylvian fissure, was
evident upon palpation. The posterior limit of the fracture was
an inch below the location of the motor, area of the face. At the
operation a considerable amount of injury to the meninges and
to the brain substance was found on the left motor region. The
patient was trephined four times.

A note made by me on January 22, 1897, four years later, in
the Vanderbilt clinic records, says that " since the last operation
there have been no convulsive seizures, but six or seven times a
year the patient has attacks of headache which last from five to
•six hours. The pain is intense and consciousness is sometimes
lost temporarily. During one of these attacks the patient at-
tempted suicide on account of the pain.

Traumatic epilepsy usually becomes in time an exact
clinical counterpart of the idiopathic variety, and so w^e may
expect to find in it the various psychical equivalents which
are occasionally encountered when the disease arises from
unknown causes. Still, while somnambulistic attacks, im-
pulsive acts, temporary amnesias, and similar phenomena
may occur, they do not constitute a prominent feature of
the traumatic variety of the disease. Many of the morbid
impulsions of cerebral neurasthenia and some of the symp-
toms of traumatic insanity are epileptic in character, being
transitory and coming on without definite warning ; but
Ainless they have been or are associated with convulsive

134 ORGANIC EFFECTS OF INJURY.

seizures, we are not justified by our present knowledge in
calling them manifestations of epilepsy.

The course of traumatic epilepsy is progressive. The
tendency is for the fits to become uninterruptedly more
frequent and severe and to be coupled with a constantly
increasing failure of mental power. In some cases the dis-
ease appears to remain stationary, and very rarely the fits
are said to have ceased altogether, either spontaneously or
through the influence of drugs. However, until very re-
cent years, recovery was practically hopeless. With the
advances which have been made in cerebral surgery the
prognosis has become somewhat more favorable. Opera-
tions have in certain cases been the means of very materi-
ally lessening the number and severity of the attacks, and
a few patients appear to have been permanently cured by
the removal of sources of cortical irritation. But the re-
sults of trephining for epilepsy, although tangible, have not
been sufficiently brilliant to warrant the disease being re-
garded as anything but a very serious affection, which,
in by far the larger, number of cases, is incurable. The
chances for successful treatment are greatest when the
operation is done immediately after the accident ; then, by
the immediate removal of splinters of bone or blood clots,
the brain will be irritated for as short a time as possible.
In any case in which the fits have once appeared and ex-
isted for any length of time the hopes for recovery are
slight. The disease in itself is not a direct menace to life,
but its victims are in constant danger of accident. They
are "risks" which life-insurance companies regularly re-
fuse to accept.

Diagnosis. — To establish beyond reasonable doubt a
causal relationship in any case- between an injury and the
development of epilepsy may be very easy, or it may be
practically impossible. In persons previously healthy in
whom the skull is shown to have been fractured, there will

EPILEPSY.

135

rarely be any question as to the relationship between the
traumatism and the subsequent convulsions. But if exter-
nal evidences of fracture are not demonstrable, there are
several considerations which must be taken into account be-
fore it can be stated that the epilepsy is in all probability
traumatic :

1. In the first place it must be shown that the patient
had never had general convulsions before the injury, except
such convulsions as may occur in infancy without being
considered as expressions of idiopathic epilepsy. General
convulsions are so common in infancy that it would be
manifestly unjust to regard as epileptic persons who had
had fits in the first year or two years of life, but who had
subsequently been free from them.

2. The general condition of the patient, as regards alco-
holism or other degenerative evidences, immediately before
the accident, must be considered, especially if the injury is
supposed to have been slight.

3. The injury itself is naturally the most important causal
element. If it results in hemiplegia or monoplegia, the
causal connection is plain ; or if the seizures are local, and
so indicative of localized brain lesion, there will rarely be
any question as to their traumatic origin. Localized muscu-
lar spasm as a symptom of idiopathic epilepsy, although it
has been observed, is extremely rare, and it would probably
never occur in a way for it to be mistaken for the local
spasm of traumatic epilepsy. When the seizures are general,
whether they depend upon injury or not must be decided
by those other considerations which have already been
mentioned.

4. The time elapsing between the receipt of injury and
the first epileptic manifestations can not be considered as a
definite guide in diagnosis. The statistics are derived from
those cases which have been operated upon, and in most of
them the paroxysmal symptoms have been delayed for a

136 ORGANIC EFFECTS OF INJURY.

few weeks or a few months after the accident. Some few
cases, which in other respects are satisfactory as illustrative
of traumatic epilepsy, have had no fits until several years
after the receipt of the injury. The most that can be said
in this respect is that the larger number of cases have
developed within a year after the accident, and that most
of the cases which appear after longer periods of time are
in other respects less typical of the traumatic form of the
disease.

5. In doubtful cases the age of the patient may be of
assistance in diagnosis. Idiopathic epilepsy is essentially a
disease which begins in childhood and adolescence. Sixty
per cent of the cases occur before twenty years of age, and
only thirteen per cent after thirty. Traumatic epilepsy, on
the other hand, is almost always one of the penalties of the
exposure to accident which is incident to the active periods
of life. Of course, children may receive severe head inju-
ries, and grown men sometimes develop idiopathic epilepsy.
But the two diseases belong so essentially to different peri-
ods of life that traumatic epilepsy in the child can with jus-
tice be diagnosticated only after elimination of all other
causes and a scrutinizing study of attendant circumstances.
Conversely, the probability is greater that the convulsions
that appear after injury to an adult who has never had fits,
arise as the direct consequence of cerebral injury.

It may be said, in conclusion, that no case of epilepsy in
which there is any question of operation or of medico-legal
inquiry, should be accepted as traumatic without the seizures
having been witnessed by a physician or by some person
trained in the observation of the symptoms of disease. Such
observation can best be carried out in hospitals.

Bibliography.

Gray, Epilepsy. Dercutn's Text -book of Nervous Diseases by
American Authors, Philadelphia, 1895.

GENERAL PARALYSIS OF THE INSANE.

137

Lloyd and Deaver, A Case of Focal Epilepsy Successfully
Treated, etc. , Am. Jour, of the Med. Set., November, 1888.

Starr, Brain Surgery, New York, 1893.

Starr, Familiar Forms of Nervous Disease, New York, 1890.

Van Gieson, A Contribution to the Pathology of Traumatic
Epilepsy. New York Medical Record, i2,g^.

General Paralysis of the Insane— General Paresis
— Dementia Paralytica.

An inquiry which has for its object the determination of
the influence of trauma upon the development of general
paralysis of the insane is beset with many of the difficulties
which are met with in investigations relative to the trau-
matic origin of tabes. General paresis, like tabes, has an
initial stage, that may last for months or years, during
which the patient is not only not incapacitated for work, but
may conduct himself so rationally that no suspicion is enter-
tained that he is already suffering from a disease which is
soon to destroy both mind and body. From the insidiousness
of its onset, it is usually impossible tosdy even approximately
when the morbid process began. In non-traumatic cases,
when the first marked symptoms consist of an attack of
acute maniacal excitement or of acute mental depression or
of some other acute manifestation, there is every reason to
suppose that the disease had already existed, though unsus-
pected, for some time. Similarly, when an injury to the
head is quickly followed by an outbreak of the symptoms of
the disease, it is never possible to say with absolute certainty
that the traumatism did anything more than hasten into ac-
tivity a process which was already existent, and whose ulti-
mate development was inevitable, irrespective of traumatic
agency.

Prodromal Stage. — Inasmuch as it is so often the sub-
ject of medico-legal inquiry, the prodromal stage was called
by Le Grande du Saulle "the medico-legal period." How

ORGANIC EFFECTS OF INJURY.

ly it may pass unsuspected by the general public or by
ical men who are not especially versed in mental dis-
s is shown by an incident related by Le Grande du
lie, and quoted by Hamilton :

:'wo brothers went to the office of a Parisian alienist, and the
: had a private consultation, the result being that he was in-
led that the other had the incipient signs of paretic dementia,
that death would occur in three or four years. They de-
ed, and the result was that a policy of insurance was procured
3ne hundred thousand francs. Three years later the elder
her pocketed the results of the robbery.

The prodromal symptoms of general paresis are both
sical and mental. At first the physical symptoms may
othing more than a slight tremor of the face and tongue

1 some indistinctness of speech. Very commonly there
n early myosis, or a pupillary inequality, or the pupils

show the Argyll-Robertson phenomenon. The knee-
s are lost in about one third of the cases ; in the others
■ may be normal or may, in common with other tendon
xes, be exaggerated. The earliest variations from the
nal mental state are a slight forgetfulness, inattentiveness,
lessness, or irascibility. -The patient's character changes
lOut his noticing it. " Der Kranke wird ein Anderer, und
lerkt es nicht." The delusions of grandeur and extrava-

acts, so common in the more advanced stages, are only
sionally prominent in the beginning of the disease,
"hese mental signs, although they may not pass unnoticed
he associates or by the family of the patient, rarely ex-
any particular remark until they have existed for some
, and have become disagreeably prominent. Then in-
y fails to fix within weeks or even months just when the
ges in personality began.

'o determine the exact part played by any exciting cause
disease whose beginning is practicably never determi-

2 appears well-nigh impossible. By the time the symp-

GENERAL PARALYSIS OF THE INSANE.

139

toms of paresis are sufficiently pronounced for the patient
to be brought (he rarely comes of his own accord) for medi-
cal examination, the disease has already existed for some
time ; just how long a time it is impossible to say, but cer-
tainly long enough for the pa-
tient's own statements to have
become unreliable, and for his
friends to'have forgotten when
they first noticed changes in
his character. Consequently,
whether any alleged cause was
so far responsible for the dis-
ease that, had the cause not
existed, the disease would not
have developed, will be a mat-
ter of individual opinion, and
must be largely determined
for each case. The most that
can be done here in consider-
ing the influence of trauma in
the causation of the disease is
to brieify observe the general aetiology and to review the
evidence for traumatic agency.

General .Etiology. — As the clinician is hampered by be-
ing unable to recognize the disease until it has already ex-
isted for a considerable length of time, and as the pathologist
has failed to reveal the fundamental character or causation
of its morbid anatomy, the setiology of general paresis re-
mains imperfectly understood.

Among the general aetiological factors the influence of
syphilis is the most easily demonstrable. There is a varia-
tion in the observations of different investigators as to the
percentage of general paralytics in whom a history of pre-
ceding syphilis is obtainable, but all agree that the percent-
age is large.

Fig. 32. — Showing characteristic facial
expression in the early stage of gen-
eral paresis. (Vanderbilt Clinic.)

40 ORGANIC EFFECTS OF INJURY.

In Germany it is given by

Mendell and Schnell.. . . '7'^ per cent 1 ^ , ,
T3- „ .< f Quoted by

Binswanger 49-72 ^ Oebeke

Ziehen 33-43 " " )

Gudden I surely 35-7 per cent;

( probably 9-6 per cent.

Hirschl (Austria) 70 to 90 per cent.

56 per cent history of syphilis.
25 per cent syphilis probable.
In France it is given by

Regis 70-90 per cent.

In America it is given by

Peterson 60-70 per cent ;

Bannister 89 " "

The frequency with which syphilis has preceded general
aresis is certainly more than a coincidence, for in other
jrms of mental disease the history of lues is not obtainable
1 over 15 to 20 per cent. In what way the syphilitic poison
auses the cerebral degeneration is unknown. Pathology
as failed to reveal whether it acts simply as a predisponent,
rhich requires the addition of some exciting cause to induce
le disease, or whether the late poisons of syphilis are of
lemselves sufficient. The latter alternative seems the less
robable from the fact that while syphilis is very frequent,
eneral paresis, compared to it, is rare. If syphilis alone
:ere capable of producing general paresis, it would be rea-
anable to suppose that the relative frequency of the occur-
ence of the two diseases would be more equal. Further-
lore, general paresis is different, both clinically and in its
athological anatomy, from the affections of the brain char-
cterized by syphilitic lesions. However, important as is
he relationship between syphilis and paresis, it is not abso-
ite. There are cases which give no evidence or history
f syphilis, and in which the pre-existence of syphilis is not
ven probable. Fournier, who believes syphilis to be the
nle cause of tabes, admits that paresis may occur without
he patient having had the venereal disease.

GENERAL PARALYSIS OF THE INSANE. 141

There are other predisposing factors which must be con-
sidered as affecting causation. Paresis is much more fre-
quent in males than in females (four to one, Mickle). In
women of the higher classes of society it is very infrequent.
The disease is sharply limited by age. An overwhelming
majority of the cases occur between the ages of thirty and
fifty ; the disease is very rare before twenty-five, and rarely,
if ever, occurs after sixty. Heredity may often be found to
be an important factor — not in the sense that general paresis
is directly transmitted, but rather that the individual is pro-
vided with a brain which is particularly liable to succumb to
injurious influences.

The causes which are most commonly regarded as excit-
ing in the aetiology of general paresis are mental excite-
ment, worry, and overwork. The general class of persons
among whom the disease is most common, the greater fre-
quency with which it occurs in the inhabitants of cities, and
the fact that it appears at an age when mental and bodily
strain are at their highest tension, substantiate the hypoth-
esis that these agencies are at least powerful contributing
causes.

Trauma as a Cause. — The influence of accident and
injury is universally regarded as important, and trauma
appears in all books on the subject as one of the principal
exciting agents. General iijjuries are sometimes described
as determining causes, but it seems extremely improbable
that any injury can be regarded as sufficient to induce
general paresis unless the blow was directly applied to the
head, or unless there was a considerable shaking up of the
cranial contents, such as may occur in concussion acci-
dents. In only a few of the reported cases has the skull
been fractured.

The percentage of traumatic cases, as it is given by dif-
ferent observers, to the total number of cases of general
paresis varies greatly. Schlager says, " One seventh of all

142 ORGANIC EFFECTS OF INJURY.

cases of mental disease induced by head injuries are cases
of general paralysis." Meyer found fifteen cases of injury
to the head in seventy-six cases of general paresis, in which
the causes " were clearly made out." In eighty male cases,
Krafft-Ebing found cranial injury to be the cause in six.
Mickle quotes these authors, and from a study of the Eng-
lish Lunacy Reports finds six per cent of the cases in both
sexes as due to head injuries.

Christian observed forty-three cases of general paresis
in one hundred cases of injuries to the skull. In five hun-
dred cases of insanity Schlager ascribed a traumatic aetiol-
ogy to forty-nine, of which seven developed general paresis.

Gudden reports forty-five cases in which a history of
head injury was prominent. In six of these the trauma had
occurred in childhood, years before the symptoms of the
general brain disease. In eighteen the trauma and the par-
alytic symptoms were separated by a period varying from
six months to twenty years ; and in twenty-one the para-
lytic symptoms developed in direct sequence (few months)
upon the head injury. The accident was generally accom-
panied by loss of consciousness, and in four cases the skull
was fractured. Of one hundred and seventy-five cases re-
ported by Hirschl, trauma had exerted an influence in 7.4
per cent.

From the above reports of traumatic general paresis
it appears that the injury was incurred in the great major-
ity of cases by falls or by blows on the head received in
brawls. Now, the disease is characterized by momentary
attacks of dizziness or unconsciousness, which may cause
the patient to fall and strike his head* by an inattention
which exposes him to a variety of accidents, and especially
by an excitable mental state, which frequently leads him into
those animated discussions, as a result of which, somebody's
head is often injured. And, indeed, it seems as though the
receipt of head injury was a result of the disease rather

GENERAL PARALYSIS OF THE INSANE. 143

than the cause of it in by far the larger number of the pub-
lished cases. The following case illustrates a history of the
disease such as is usually described as traumatic, but in
which the patient was undoubtedly suffering from paresis
before the occurrence of the accident :

A. G., forty years of age, came to the Vanderbilt clinic on
December 18, 1893. Syphilis and alcoholism denied. The pa-
tient says he was well until six months previously, when he fell
from a building. He did not lose consciousness, but was in bed
two weeks with a swollen ankle. No paralysis. Two months
later right hemiplegia and motor aphasia suddenly developed,
lasted for two weeks, and then as suddenly disappeared. A simi-
lar attack of paralysis, also temporary, occurred a short time
afterward, and was followed in a few days by an attack of motor
aphasia, unaccompanied by loss of muscular power. The day be-
fore I saw the man he had had convulsions in both arms without
any loss of consciousness. Examination showed no paralysis,
no ataxia, pupils equal and reacting to light, knee-jerks absent.
Temporal limitation of the visual fields; tremor of face, tongue,
and hands very marked ; speech and expression characteristic of
general paresis.

There was no question as to the diagnosis of the disease from
which the patient was suffering, but the apoplectiform character
of its course indicated very conclusively that the fall had not, as
the patient claimed, caused the disease, but had been a result of
•one of the earliest seizures.

How necessary it is to consider every fact^^ before
ascribing to trauma a place in the causatioii""6f general pa-
resis is well shown by the following case. Inasmuch as it
is soon to become the subject of litigation, there will be no
mention of names, dates, or places in describing it:

A man, thirty-three years of age, consulted a physician on
account of an injury which he had received six weeks previously.
The patient denied having had syphilis, and said that he had
always been a strong and healthy man until an accident in which
he was struck on the head and knocked down by a passing vehi-
cle. As a result of the injury he was carried to a hospital, and
lay there unconscious for eight days. He then quickly recovered
and returned to work, although still troubled with the headaches,

144 ORGANIC EFFECTS OF INJURY.

for which he sought medical advice. The examination showed
tremor of the face, lips, and tongue, thickness of speech, inequal-
ity in the size of the pupils, though both responded readily to
light and during efforts at accommodation. All the tendOn re-
flexes were active, but there was no paralysis. The general ap-
pearance and manner were those of a patient with general paresis.
The gait was careless, the memory poor, the attention defective.
The diagnosis and the evaluation of the influence of the injury
were, however, postponed until further information could be ob-
tained.

From the house surgeon of the hospital where the man was
taken after the accident it was learned that on admission the
patient was delirious and was paralyzed in one arm, but had no
external injuries except a slight abrasion on one cheek. The
mental condition resembled that of acute mania, with great excite-
ment, delusions, and hallucinations. These soon passed away,
however, as did also the paralysis of the arm.

Witnesses of the accident said that the man fell against the
vehicle, instead of the vehicle running into him. His wife admit-
ted that for a year before the accident her husband had been for-
getful, irritable, and subject to headaches ; that she had noticed
that one pupil was larger than the other; that there had occurred
from time to time paralysis of one arm or of one leg, or loss of
the power of speech, but that these symptoms would pass away
completely in a day or two. She also admitted that, having
been pregnant seven times, she had never given birth to a living
child, the abortion always occurring in the sixth or seventh month.
These facts, together with subsequent observations of the patient,
during which the symptoms became more marked, left little
doubt as to the correctness of the diagnosis of general paresis ;
but they proved conclusively that it was not traumatic general
paresis. The patient was in all probability syphilitic, as shown
by the barrenness of his wife, who is a strong, healthy-looking
woman ; the mental disease had begun at least a year before the
accident, as shown by the attacks of paralysis, the headaches, the
inequality of the pupils, etc. ; the accident was in all probability
a result of the disease, inasmuch as the witnesses said that the
patient fell and was then hit by the vehicle. Accordingly, in this
case, in the absence of external evidences of injury, it is reason-
able to maintain that the accident exerted little or no influence
upon the course of the disease. It would probably not have oc-
curred to a healthy man, but was one of the unavoidable penal-

GENERAL PARALYSIS OF THE INSANE.

145

ties which are paid by persons who are unable to take care of
themselves.

Cases similar to these have undoubtedly been the cause
of much misapprehension as to the part played by injury in
the causation of general paresis. The patient ma)^ himself
believe in the truth of the history he tells regarding occur-
rence of the traumatism, but the mental state of a disease
which is characterized by delusions, hallucinations, and con-
fusion render untrustworthy all the statements which may
be made by any one suffering from it.

If the disease is sufficiently advanced to be diagnosti-
cated, there is no more reason for the physician to accept

y.^^^<^ O"^ /^

Fig. 33. — " This is a iine day for the first of June." Handwriting of a patient in the
early stage of general paresis. (Vanderbilt Clinic.)

the patient's statements regarding accident or injury than
there is to believe the expressions of grandiose ideas or of
depression, or the assertions of magnificent health in a per-
son who is evidently doomed. Consequently, no case of
general paresis can be reasonably regarded as of traumatic
origin unless the testimony of credible witnesses shows that
the injury was the result of an accident which, as far as the
victim was concerned, was unavoidable.

When it can be shown that the head injury was in no
way the result of the disease, but was the consequence of

146 ORGANIC EFFECTS OF INJURY.

one of the many accidents to which all people are com-
monly exposed, it is necessary to determine as clearly as
possible in how far the traumatism was responsible for the
development of the disease.

The inquiry should be especially painstaking as regards
three points :

1. In the first place, to avoid gross errors in diagnosis,
it must be proved that the course and character of the
symptoms are identical or closely allied with those of gen-
eral paresis. After many head injuries, especially if the
skull has been fractured or there has been intracranial
haemorrhage or brain laceration, there develops a condition
of delirium and excitement, at the subsidence of which the
patient passes into a condition of more or less complete
dementia. Associated with the mental symptoms there
may be the dysarthria, the evidences of localized paralyses,
the tremors, and other signs similar to those which occur
in general paresis. These patients may die, in which event
the lesions found are more localized and more prominent
than those of general paresis ; or they may improve and
live in good physical health, although demented, for many
years. Some of them present such striking similarities to
the cases of general paresis that it is only by the obser-
vation of them for considerable periods of time that it can
be decided that the underlying anatomical process must be
essentially different.

2. The question of predisposition is very important in
cases alleged to have resulted from trauma.

In nearly all the reported cases of general paresis which
have followed injury, in which the receipt of the injury
of itself might not have been regarded as a symptom of
the disease, there was evidence that a strong predisposi-
tion, either hereditary or acquired, had pre-existed. The
hereditary predisposition has been proved by the family
history, by congenital syphilis, or by the stigmata of degen-

GENERAL PARALYSIS OF THE INSANE.

147

eralion. The acquired predisposition has consisted in the
results of preceding syphilis. Of all these factors syphilis
is the most important. In view of the fact that syphilitic
processes become much more active after traumatisms, in-
jury is often regarded as of minor astiological importance
if it is soon followed by paretic symptoms in an individual
who is undeniably syphilitic, although he may never have
presented any cerebral symptoms before the accident.
This is hardly just. To deny a traumatic origin to the
disease because the patient has had syphilis, appears to
me to be equivalent to saying that the patient would have
had paresis whether his head had been injured or not.
Such a view is not warranted by our present knowledge.
Similarly to what will be said concerning locomotor ataxia,
there are so many syphilitic persons who receive severe
head injuries without developing general paresis, that in
any syphilitic person in whom head injury is quickly fol-
lowed by the symptoms of the mental disease it seems
more reasonable to ascribe to the traumatism an influence
at least equal to that of the venereal infection. However,
this matter will always be one of individual opinion. Most
of the cases of paresis occurring after head injury have had
syphilis, and it is never possible to decide positively as to
the relative value of the two factors. The number of re-
corded cases of persons who were syphilitic, yet who pre-
sented no symptoms of brain disease until after the receipt
of a head injury, is not small. Thus,

Mickle tells of the case of a soldier with a long syphilitic his-
tory who suffered a severe injury to the head in July, and on the
29th of that month was admitted to the hospital with maniacal
symptoms. Seven weeks afterward he was discharged to duty,
but was readmitted, in the January following, with general pare-
sis, the onset of which had been characterized by the mental symp-
toms which followed closely upon the cranial injury.

In similar cases the syphilis has preceded the paresis by
a period varying from one to twenty years, and the first

148 ORGANIC EFFECTS OF INJURY.

mental symptom had appeared in a few months or years
after the accident.

3. Can a person who has never had syphilis, or marked
hereditary predisposition, develop general paresis as the
direct consequence of injury to the head?

Dr. L. C. Pettit, of the Manhattan State Hospital, Ward's
Island, New York, whose extensive researches bearing upon
this disease are well known, tells me that "from a study of
two thousand clinical histories he is forced to believe that
traumatism is not to be regarded as a sole cause of the dis-
ease. In over one hundred autopsies made on paretics he
has only once seen anything which seemed to be correlative
to traumatism. In one case, over the region of the right
gyrus occipitalis superior, there was a depression, about the
size of a silver twenty-five-cent piece, of the inner table of
the skull, which was the result of injury. In exactly the
same area on the left hemisphere there was necrosis of the
cerebral cortex."

In reference to trauma as a sole cause, Mickle says : " In
cases which have come under my own observation, where
cranial injury has conduced to general paresis, it has, in the
majority, seemed to play the part of a predisposing rather
than of an exciting cause. In speaking of cranial injury as '
a predisposing cause of general paresis, we may suppose
that, in consequence of latent residual results of the imme-
diate effects of trauma, either the cerebral tissues are simply
less resistant to the influences of the ordinary causes of the
pathological process which underlies general paresis, or that
this process springs more fully into being by assisting in,
and in its turn being assisted by, the intensification and ex-
tension of slight local inflammation or hyperplasia sequen-
tial to the brain injury ; or, again, assisted by morbid vaso-
motor effects of that injury."

The views of these observers seem to be substantiated
by clinical experience. I have been unable to find in all

GENERAL PARALYSIS OF THE INSANE.

149

literature a single case of traumatic general paresis in which
sufficient details were given to justify the absolute conclu-
sion that the head injury was the one cause of the disease.

The number of cases in which there is even a possibility
of traumatism being the exclusive cause is very small. The
most complete one is reported by Fox ; but that observer
himself admitted that the disease might have existed pre-
viously to the receipt of the injury :

" The patient was a man, forty-nine years old, married eighteen
and a half years; eleven children; wife miscarried once with twins.
Family and personal history clear. No syphilis. Formerly a cool,
collected, precise, sober, and particularly neat man, who had al-
ways enjoyed very good bodily health. On December 27th was
thrown out of a trap, striking on his head. His wife asserts that he
was in perfect mental health up to the time of the accident, and that
some unusual irritability which had been noticed was simply due to
a heavy cold, which his previous excellent mental health had un-
fitted him to bear patiently. Whether this was or was not the case,
it is certain that, a day or two after the accident, various symptoms
suggestive of general paresis appeared ; so that, if the disease had
not an exclusively traumatic origin, its development and first mani-
festation at least were determined by accident. The first day after
the fall he complained of pain in his head, but after the first day
made no complaints, but said he was never better in his life."

Sixteen days after the accident, when admitted to the hospital,
the physical and mental symptoms of general paresis were easily
recognizable. The disease pursued a characteristic and fatal course.

Another case is reported by Van Deventer (quoted by
Bechholm :

A stonecutter, thirty years old, father alcoholic, patient himself
slightly alcoholic, but no history of syphilis. He was struck in the
left temple by a piece of marble and lost consciousness momenta-
rily, but continued with his work after a few moments. The next
day he became aphasic for twenty-four hours, restless, and un-
willing to stay in bed. Had headache and insomnia. A few days
later, had an attack of violence and confused ideas of persecution.
He entered the asylum three weeks after the accident, present-
ing symptoms of amnesia, megalomania, with hallucinations and
persecutory ideas. 'Seven months later occurred clonic spasms

150 ORGANIC EFFECTS OF INJURY.

and apoplectiform attacks ; seventeen months later, difficulties of
speech, tremor, inequality of the pupils, and weakness of all the
muscles. The patient died, twenty-five months after the accident,
with symptoms of complete dementia.

Neither of these cases is conclusive evidence for the
existence of traumatism as a sole cause of general paresis,
but they are the best evidence we have.

In default of better proof of the traumatic origin of a
disease which is so common and which has so frequently
been the subject of medico-legal inquiry, the conclusion is
unavoidable that if trauma is ever the sole cause of general
paresis, such a causal relationship is extremely unusual and
difficult of proof, and is only to be accepted after scrupu-
lous inquiries have eliminated all of the many opportunities

of error.

Bibliography.

Bechholm, Maladies mentales d'origine traumatique. Thhe
de Paris, 1896.

Bannister, Am. Jour, of Insanity, i893-'94, p. 477.

Christian, Des traumatismes du crane dans leurs rapports avec
I'alienation mentale. Arch, de neurol., Juillet et Sept., 1889.

Fournier, Gaz. mM. de Paris, November 3, 1894.

Fox, Unusual Cases of General Paresis. Jour. Ment. Science,

1891. P- 393-

Gudden, Zur Aetiologie u. Sympt. der prog. Paralysie mit be-
sonden Beriick. des Trauma, etc. Arch. f. Psych., February, 1894.

Hamilton, System of Legal Medicine, New York, 1894.

Hirschl, Die Aetiologie der prog. Paralyse. Abs. Neurol. Cblatt,
1896, p. 369.

Jacobson, Traumatische Psychosen. Nord. Med. Ark., 1893,
iii, 13, p. 1.

Mickle, General Paralysis of the Insane, London, 1886.

Ibid., General Paralysis from Cranial Injury. Jour. Ment. Sci.,
January, 1883, p. 545.

Oebeke, Zur Aetiologie der a-llgemeinen fortsch. Paralyse.
Zeit. fur Psych., 1891, xlix, p. i.

■ Peterson, Relation of Syphilis to General Paresis. New York
Med. Pec, December 9, 1893.

Rdgis, Manual of Mental Med., Syracuse, 1894. (Trans.)

Schlager, quoted by Hudden. Op cit.

LOCOMOTOR ATAXIA.

Locomotor Ataxia— Tabes Dorsalis.

151

Although locomotor ataxia is one of the commonest of
the chronic degenerative diseases of the nervous system,
there is very little definite knowledge regarding its patho-
genesis, and many difficulties stand in the vi^ay of a complete
understanding of its nature. The disease is not in itself
a direct menace to life, and in the cases which come to au-
topsy the morbid process has existed for so long a time and
has become so advanced and so extensive that it is impossi-
ble to tell when it had its beginning. Until we know which
nervous element is first afTected, we can not hope to know
ver}' much about the etiology of the disease. Another diffi-
culty in the study of its pathology is, that although only cer-
tain portions of the cerebro-spinal axis are involved, there is
nothing about the microscopic appearances of the lesion
itself which are exclusively characteristic. Its funda-
mental anatomical character is a degeneration of the pos-
terior columns in the spinal cord, with which are usually
associated an inflammation of the pia mater and a degenera-
tion of the posterior nerve roots and of the spinal ganglia.
It is essentially a degeneration of nerve fibers and nerve
cells, associated with a growth of connective tissue and
sometimes with degeneration of the walls of the blood-
vessels. All these morbid changes are found in other dis-
eases. Even the clinical fact that syphilis frequently pre-
cedes tabes receives no substantiation from the microscopical
anatomy of the latter disease. From a study of the spinal
cord alone in a case of tabes it would be impossible to say
whether the patient had or had not had syphilis. Whatever
the pathological nature of tabes may be, it is certainly some-
thing more than spinal syphilis. It is conjectured that the
ultimate products of the syphilitic virus exercise a select-
ive action on certain portions of the spinal cord or of its
nerve roots, and that the tabetic degeneration is in reality

152 ORGANIC EFFECTS OF INJURY.

syphilitic. Although this view may be correct, it is largely
speculative and lacks anatomical proof. In the absence of
such proof it is unjustifiable to claim an absolute causative
influence for syphilis.

But though the mdrbid anatomy of tabes has been of
iittle or no service in determining the causation of the dis-
3ase, it has yielded an important result in showing that the
character of the lesion is degenerative rather than actively
inflammatory, and that it requires a considerable time for its
development. The nerve-fiber degeneration, the connective-
tissue growth, the vascular abnormities, all bespeak a pro-
:ess which is essentially slow, and argue against the possi-
bility of the disease reaching a marked degree of develop-
ment within a few days or weeks.

Pre-ataxic Period.

The clinical difficulties which are met with in attempts
to elucidate the mysteries surrounding this disease arise from
the insidiousness of its onset, the extreme chronicity of its
course, and the uncertain character of its causes. Locomotor
itaxia is the most chronic of all degenerative nervous dis-
sases. It may exist without seriously impairing the general
liealth of the patient for ten, twenty, thirty, or even a greater
number of years after its existence has become recognized.
How long it may last before any symptoms become appar-
ent is not definitely known, but certainly for a considerable
length of time. A patient of mine, fifty-two years of age, who
had syphilis thirty years ago, has been in the pre-ataxic state
for five years. Both knee-jerks are absent, there is loss of
sexual power, the'right pupil is larger than the left and pre-
sents the Argyll-Robertson phenomenon, and there is a dimi-
nution of sensibility in the ulnar distribution of both hands.
These, signs are sufficient for a diagnosis of tabes, al-
though, aside from a slight swaying of the body on standing
with closed eyes, there are absolutely no disturbances of

LOCOMOTOR ATAXIA. Ijj

motion, and there have never been characteristic pains. The
patient came to me originally for alcoholism, and the tabetic
symptoms were discovered during the course of a routine
examination.

The pain is usually the cause of the patient seeking med-
ical advice, although there are other frequent initial symp-
toms observed by the patient, such as slight ataxia, difficulty
in urination, and disturbances of vision.

The condition of the bones and joints, which predisposes
them to disease or fracture, is sometimes the means of first
calling attention to the existence of the spinal degeneration.

Some time ago a patient came to the Vanderbilt clinic with
extreme enlargement of the right knee joint, which he said was
the result of a fall received a month previously. Although he
did not know it, the man presented classical symptoms of tabes,

Fig. 34. — Charcot joint, the alleged result of traumatism. (Incurable Hospital.)

which must have e.xisted long before the accident ; and although
the particular lesion, which has proved to be a Charcot joint, may
have been to a certain extent influenced by the injury, it occurred
in an individual predisposed by tabes to its development.

The photograph in Fig. 34 is of a Charcot joint in a patient
who presents nearly all the symptoms of advanced tabes. He
says he was perfectly well until he fell on the right knee, as a
result of which it became enlarged, a condition which was followed
by other characteristic symptoms. As the accident occurred years

154

ORGANIC EFFECTS OF INJURY.

before the patient came under observation, it is impossible to
prove the incorrectness of his behef.

Even in the clinically early stages, during which the
patient is usually conscious of one symptom only, or of no
symptoms at all, a careful examination will show that there
are already present objective evidences of structural disease

of connecting paths
which must have
been present for a
considerable length
of time, and which
must, in all proba-
bility, have ante-
dated any subjec-
tive discomfort. In
default of such ob-
jective evidences,
the diagnosis of ta-
bes can not with
certainty be made.
The most common
of diagnostic signs
are the loss of one
or both knee-jerks,
the Argyll-Robert-
son pupil, and the
Romberg symptom.
One or all of these
three symptoms —
the cardinal symp-
toms — are very con-
stant, and usually
appear early, but
none of them would
be noticed by the

Fig. 35. — Attitude of static ataxia.
(Vandeibilt Clinic. )

LOCOMOTOR ATAXIA.

155

patient, and would ordinarily be overlooked in any med-
ical examination in which a determination of the condition
of the nervous system were not a primary object. Similarly
with tactile anaesthesia of the trunk; the patient is, in early
stages, unconscious of it until it is demonstrated by the phy-
sician. It is often one of the earliest of tabetic manifesta-
tions.

Fig. 36 shows the tactile anassthesia chart of a patient whose
•only other symptoms are slight unsteadiness of gait and loss of
knee-jerk.

That the- early symptoms of tabes are often overlooked is
a fact of common experience, for it occurs not infrequently

Fig. 36. — Tactile anaesthesia in a patient in the early stage of locomotor ataxia.

that persons suffering from incipient tabes, when the only sub-
jective symptoms are pain or perhaps slight unsteadiness of
gait, are seen by physicians who are unfamiliar with the
■diagnosis of nervous diseases and who treat such cases with-
out knowing upon what fundamental conditions the symp-
toms depend. No examination of the knee-jerks or of the

156 ORGANIC EFFECTS OF INJURY.

pupils is made, and the condition is regarded as sciatica or
" spinal congestion." There can be no doubt that in many
cases the cardinal symptoms exist for months or years with-
out the patient's knowledge, and the physician who eventu-
ally finds any one of them finds, not a recent symptom, but
one whose character has permitted it to exist a long time
unsuspected ; or the patient may, while in the pre-ataxic
stage, have consulted a physician for other troubles, but
unless at that time he complained of subjective nervous
symptoms as well, there would probably have been no exam-
ination of the pupillary or patellar reflexes. Without such
examination it would be impossible to assert that the patient
were free from spinal disease. Similarly, the fact that the
patient had been a successful candidate for life insurance
would not be an absolute guarantee that he were at that time
free from beginning posterior spinal sclerosis, because in the
routine examination for life insurance there is no attempt at
examining for nervous symptoms which are not immediately
apparent. On the medical examiner's blank the color of the
eyes is noted, but there is no space left for statements con-
cerning the condition of the pupils, and there are no ques-
tions relative to the knee-jerk.

That an examination by a qompetent physician, who is
also on the alert for nervous disease, is necessary before any
one can be pronounced as free from tabes, may seem equiva-
lent to saying that all men are ataxic until they are proved
not to be so. Extravagant as it may appear, that such a de-
mand is essential in any attempts to fix the beginning of the
disease will be thoroughly indorsed by any one who has
studied the literature of the cases which are said to arise
from injury, or who has had under his care cases of tabes-
which have remained for years in the pre-ataxic stage, with
few or no subjective symptoms, but in which symptoms have
suddenly become active and severe as a result of some slight
injury or shock.

LOCOMOTOR ATAXIA.

IS7

^Etiology. — It is evident that there must be considerable
uncertainty concerning the getiology of a disease which may
be in operation for months or years before its existence is
known. This uncertainty is not materially relieved by what
we know about the causal agents of tabes. Of the various
ones which have been named as responsible for the spinal
degeneration, syphilis is least open to destructive criticism.
But even to the influence of syphilis is attributed a differ-
ent importance by various observers. Erb finds preceding
syphilis in over ninety per cent of his cases ; but of one hun-
dred and eight cases observed in Leyden's clinic, Storbeck
finds only twenty-three who are surely syphilitic, twenty-two
which are doubtful, and sixty-three which are " surely not
syphilitic," though how he may be sure of that is not appar-
ent. However, all writers agree that syphilis, either as a
direct or as a predisposing cause, occupies a prominent
place among the setiological factors of tabes, although it can
not be said that tabes never develops unless the patient has
had syphilis. Such a possibility is, indeed, generally ad-
mitted, and Gowers says that in ten per cent of the cases
syphilis may be excluded with confidence.

Although there can be no doubt as to a relationship be-
tween syphilis and tabes, it is very difficult to determine
whether the venereal disease acts as an exciting or as a pre-
disposing cause of the spinal degeneration. In favor of the
theory that it is an exciting cause is the occasionally observed
fact that tabes follows immediately upon syphilis without
any other causes being discoverable. The evidence for it be-
ing a predisposing cause is, in the majority of cases, much
stronger. Tabes does not usually appear until all distinctive
syphilitic manifestations have ceased. When syphilitic and
tabetic symptoms occur together, specific treatment usually
causes the former to subside, but has no effect on the latter;
the number of persons with syphilis is large, compared with
which the number of persons who develop tabes is ex-

1 58 ORGANIC EFFECTS OF INJURY.

tremely small ; the anatomical character of tabes is entirely
different from that of recognizable syphilis. In the cases
which are presumably free from syphilitic infection, it is
usually impossible to satisfactorily prove any particular pre-
disposition to the spinal disease, or to any disease of the
nervous system. Tabes itself may be said to be never
directly transmitted. Neither is the pathogenesis of this
affection explained by the other setiological factors. The
disease occurs chiefly in the male sex (ten to one), and
most commonly appears in the earlier degenerative decades
of life (thirty to fifty).

Of the various exciting causes w^hich are commonly
mentioned in discussions on the astiology, trauma is the
only one of which we need speak, except to say of the
others that their causal relationship to the spinal disease is
rarely clear. If trauma is a cause of tabes, what would be its
most probable mode of action ? Our ignorance concerning
the factor of predisposition renders any satisfactory answer
to this question impossible. In the surely syphilitic cases, if
the syphilis were considered an exciting cause of tabes, the
action of trauma could only be regarded as an injurious in-
fluence acting upon a disease which was already inevitable.
But if the syphilis had only predisposed the spinal cord to
degeneration, it would be entirely permissible to maintain
that the degeneration would not appear unless some excit-
ing factor were added. Our ignorance in regard to the
nature of the syphilitic factor, and our total inability to ex-
plain the pathogenesis of the cases in which syphilis proba-
bly never existed, render it impossible to tell the part that
trauma might play in the evolution of tabetic symptoms
which had been absent before the injury. With a total
absence of clinical evidence adequate to determine the exist-
ence of tabes as a direct result of injury, speculations as to
the possibility of such a condition are more or less futile. If
it is permissible to reason from analogy and from the study

LOCOMOTOR ATAXIA.

159

of those cases published as traumatic, in which, although
they are incomplete as evidence, the influence of trauma in the
development of the disease can not be denied, it would seem
that, if tabes is to result from injuries at all, it will be found
to be from injuries to the peripheral nerves. It has been
shown by Soukanoff and others that posterior spinal degen-
eration not infrequently develops from disorders which
originally were clinically typical of multiple nerve inflamma-
tion. Now, most of the cases of tabes reported as traumatic,
which, although they do not prove a traumatic origin for the
disease,might have been traumatic, have developed after gun-
shot or other wounds of the limbs, which may have involved
the nerves. It may be possible that injury to a peripheral
nerve can cause a neuritis which ascends to the posterior
spinal ganglion, inducing disturbances there that are to be-
come the starting points of degeneration in the spinal cord.
Such a view of pathogenesis is however purely speculative.
If trauma stands in any causal relation whatsoever to tabes,
such a connection must be very infrequent. Of two hundred
and eighty-one cases of Erb, trauma is mentioned as a sole
cause in only one. Now, tabes has received more careful
attention than almost any other disease of the nervous sys-
tem, and several monographs appear every year on getiology
alone. Yet, among the thousands of cases which have been
reported in detail, there are only a few dozen which are
alleged to have been solely due to injury. Of the one
hundred and eighty-five full clinical histories of the disease
which are recorded in the books at the Vanderbilt Clinic, in
three cases only is there mention of an injury which might
be regarded as causal : of these, one, with the Charcot joint
has already been mentioned ; in another, there was an inter-
val of twenty-nine years between the occurrence of the acci-
dent and the f\rst appearance of spinal sj'mptoms. The
third is unique, and since it presents such evidences as
would be accepted as final by any one unfamiliar with the

i6o

ORGANIC EFFECTS OF INJURY.

insidious character of the onset of the disease, it must be
recorded in detail :

The patient, a railway employee, thirty-nine years of age, fell
off a freight car in October, 1896, striking on his buttocks and sus-
taining a fracture of the pelvis and some injury to the left leg. For
one month he was in bed in the hospital, bolstered up with sand bags,
with an extension splint on the left leg. Then he got up, and in try-
ing to walk around his bed fell to the floor and sustained another
fracture. He was in bed again for four weeks, and when he got up
this time found he could not use his legs properly, a condition which

!..£

B.K

Fig. 37. — Field of vision in a case of locomotor ataxia which developed immediately
after an injury. (Vanderbilt Clinic.)

has remained about stationary. He came to the Vanderbilt Clinic
in July, 1897, presenting the ordinary symptoms of locomotor ataxia
— viz., ataxia and loss of muscular sense in the legs, without motor
paralysis, Romberg symptom, loss of knee-jerks, difficulty in pass-
ing water, and numbness in the legs (no objective ansesthesia). The
left pupil was larger than the right and responded slightly during
efforts at accommodation, but not to light. The right pupil was
immobile. Vision : R. E., ff ; L. E., |f (for field of vision see
Fig- 37). The ophthalmoscope showed pronounced optic-nerve
atrophy in both eyes, most marked on the right side.

When questioned as to possible causes, the patient made the
following replies :

LOCOMOTOR ATAXIA. l6l

Syphilis. — He denied emphatically every symptom of any vene-
real disease. He was married at the age of twenty-four, and
his wife gave birth to two healthy children. One miscarriage
came at the eighth month, but it followed immediately upon a
fall, and consequently can not be regarded as an evidence of
syphilis.

Condition Previous to the Injury. — The patient could not be
made to admit the existence of any tabetic symptom previous
to the injury. He was positive that he had never had any diffi-
culty in walking, either on the street, on the stairs, or in the
dark ; he did not fall ; he never had shooting pains. He said
that for several years before the accident his eyesight had not
been so good as formerly, but he could' read the paper without
difficulty, and that three or four months before the accident he suc-
cessfully passed the examination of the eyes for color perception,
which was demanded by the railway of which he was an employee.
He stated that many of the employees were rejected at this ex-
amination.

After the Accident. — The first symptom he observed was fail-
ure of sight. In a week or ten days after he had been in the
hospital his vision became so poor that he could no longer read
the paper, and since then he has been unable to read any but very
large type. The other symptoms of tabes were only observed
when he left the bed, and are essentially those which have been
enumerated. The patient had never thought of bringing a claim
against the company, and his whole manner spoke against his hav-
ing any desire or motive for telling anything but the truth.

Thus an apparently healthy man, not predisposed to nervous
disease, receives an injury and rapidly develops symptoms of
locomotor ataxia. The accident might be regarded as the sole
cause, were it not that, on account of the latent character of the
disease, no injury can be said to be causal, unless, previously to
its receipt, tabetic symptoms were shown to be absent.

In spite of the absence of adequate and reasonable proof,
in most text-books on nervous diseases trauma receives an
important place among the exciting causes of the disease.
For purposes of scientific interest and also because in
negligence cases injury may be alleged to be the cause of
the disease by persons who, though honest, are ignorant of
symptomatology, or by persons with fraudulent intent, it

1 62 ORGANIC EFFECTS OF INJURY.

is very essential that the merits of the question be clearly
understood.

The subject, has received careful study by Prince, who
criticises all previously reported cases with a view of deter-
mining if in any case the disease could have been reasonably
presumed to be of traumatic origin.

He analyzed the forty cases of tabes which had been pub-
lished as traumatic, and rejected them all as being insuf-
ficient as evidence, although he admits that twelve of them
might have been of traumatic origin. But not a single case
fulfills satisfactoril)' 'the conditions which must be com-
plied with if we are to insist on anything like reasonable
proof.

^ The most important of these conditions is to show that
tabes had not pre-existed. If this can not be done, the in-
sidious character of the disease would place the weight of
evidence with him who claimed that it had antedated the
accident. As has already been indicated, such proof is usu-
ally lacking, yet without it any claim of tabes caused by
injury lacks basis. Prince expresses the opinion, which is
indorsed by Bernhardt, that tabes can not be regarded as
traumatic if the patient has had syphilis. Inasmuch as we
are ignorant of how syphilis acts in the astiology of the
spinal disease, and in the absence of proof that injury can
cause tabes in syphilitic persons, this view appears unwar-
rantable. In regard to the severity and character of the
injury we are equally in the dark. It is generally un-
profitable to speculate as to how the human body will react
to injurious influences if we have no clinical data upon
which to rely.

From general principles it would seem reasonable to
expect that an injury to cause so general a disease as tabes
would have to be physical and reasonably severe. Psychic
shock seems hardly sufficient to induce nerve degeneration.

To be serviceable as evidence, the interval between the

LOCOMOTOR ATAXIA.

163

receipt of the trauma and the first appearance of symptoms
would have to be no longer than a few weeks or months.
If tabes results from nerve injuries, the interval should be
occupied by symptoms of neuritis.

Since the writing of Prince's paper three other cases
have been reported. In one, by Bernhardt, tabes had ex-
isted before the injury, but had been made worse by it; in
another, by Hitzig, there was no examination until a year
and a half after the accident ; and in one, by Craig, there
seems to have been some doubt as to the correctness of the
diagnosis of tabes.

Thus the matter stands as it did in 1895, and we can do
no better than to repeat the conclusion of Prince, that " the
view that locomotor ataxia may be caused by traumatism
per se, irrespective of a direct lesion of the cord, is not sus-
tained by the published evidence thus far adduced. If such
a relation exists, further evidence is required before it can
be accepted."

It seems as though Prince would have been justified in

going even still further, and in saying that, in view of the

large number of published cases of tabes, compared with the

few cases reported as traumatic, and in the total absence Of

any verification of traumatism as a cause, it is improbable

that injury or shock stand in any direct causal relation to

the disease.

Bibliography.

Bernhardt, Zur Lehre von der traum. Tabes. Monats.f. Un-
fallheilkunde, 1895, vol. ii, p. 193.

Craig, Case of Tabes from Injury. Lancet, 1895, vol. i, No. 8.

Erb, Syphilis and Tabes. Berl. klinische Woch., 1896, No. 11.

Hitzig, Ueber traum. Tabes u. d. Pathogenese der Tabes im
Allgemeine. Berlin, 1894.

Prince, Traumatism as a Cause of Locomotor Ataxia. Jour.
Nerv. and Ment. Dis., February, 1895.

Storbeck, Tabes Dors, und Syphilis. Inaug. Diss., Berlin, 1895.

Soukanoff, Contribution a I'^tude des changements du systeme
nerveux dans la polyn^vrite. Arch, de neuroL, 1896, p. 177.

164 organic effects of injury.

Progressive Muscular Atrophy (Creeping Palsy).

Including Amyotrophic Lateral Sclerosis.

The researches of recent years have very much enlarged
the field occupied by the disorders in w^hich vv^asting of the
muscles occurs, so that to-day the term progressive muscu-
lar atrophy might be construed so as to include atrophies
which are progressive, although different in course and pa-
thology from the original disorder described by Duchenne.
There are at present two distinct and well-recognized groups
of muscular atrophies, one of which is spinal" in origin, and
the other of which commences in and remains localized to
the muscles without any involvement of the spinal cord.
The latter variety, more commonly called progressive mus-
cular dystrophy, occurs in families, is a disease of childhood
and youth, has a different muscular localization from the
spinal type, and, as it is rarely if ever suspected of being of
traumatic origin, requires no mention here.

The most prominent anatomical feature of progressive
muscular atrophy (spinal) is a degeneration in all parts of
the peripheral motor neuron, with a resulting wasting
of the muscles. Associated with the degeneration of the
peripheral neural element there almost constantly occur de-
generative changes in the lower portion of the central neu-
ron, which descends from the cortex in the motor tract, and
which is continued through the spinal cord in the pyrami-
dal tracts.

According as the morbid changes are most pronounced
in one or the other of these two neurons, the clinical type
of the disease varies. (Compare page 55.) Thus, if the
primary (or peripheral) neuron is chiefly affected, the atro-
phy and weakness will be extreme and reflex irritability will
be lost, in accordance with the type of pure atrophic paral-
ysis. On the other hand, if it is the pyramidal tracts which
are the more involved, the character of the paralysis will be

PROGRESSIVE MUSCULAR ATROPHY. 165

spastic, with a certain rigidity of the muscles and an in-
crease of the tendon reflexes.

To the spastic form of progressive muscular atrophy has
been given the name of amyotrophic lateral sclerosis. It is
a convenient clinical term, but, in spite of a recent mono-
graph by J. B. Charcot in defense of its autonomy, I have
been unable to convince myself that any differentfation of
the two conditions is justifiable on anatomo-pathological
grounds. In by far the larger number of cases there are
morbid changes both in the anterior horns and in the pj^rami-
dal tracts, and the clinical differences which are observed,
•according as one or the other neuron is the more affected,
seem to be variations from a common condition, rather
than expressions of separate morbid entities. Accordingly,
in speaking of the traumatic origin of progressive muscular
atrophy, the term will be used so as to include the clinical
type known as amyotrophic lateral sclerosis.

Symptoms. — The symptoms of progressive muscular
atrophy consist of atrophy, weakness, and fibrillation of the
affected muscles, with, in the early stages, a slight alteration
of electrical excitability only. Objective sensory symptoms
are never prominent, but there may be pain, especially if
the process is rapid. Pain has usually been mentioned when
the disorder has followed traumatism. The bladder and the
rectum are rarely involved in this disease, and there is al-
most never complete loss of sphincter control.

The symptoms vary with the locality of the lesion,
and several types have been described which depend for
their individuality upon the situation of the muscles that
are first attacked. The type Duchenne-Aran is by far the
most frequent. In it the locations in which the disease first
appears and the order in which it progresses are fairly con-
stant. Beginning on one side in the muscles at the base of
the thumb, and in the interossei, it skips up to the shoulder
to affect the deltoid and perhaps others of the shoulder mus-

l66 ORGANIC EFFECTS OF INJURY.

cles. The muscles of the arm and forearm may next be in-
volved, or the disease may first pursue in the upper extrem-
ity of the opposite side the same course that it followed in
the extremity first attacked. Very frequently the deltoid
is the earliest to waste, the small muscles of the hand
joining in the atrophy at a later period. In more advanced
stages the process may move upward, giving the picture of
glosso-labio-pharyngeal paralysis, or it may descend to in-
volve the legs.

A less frequent type of progressive muscular atrophy is
the " peroneal," called, after its earliest describers, the Tooth
or Charcot-Marie type. Its pathology is obscure, as it still
remains to be conclusively proved that it depends upon dis-
ease of the anterior horns of the spinal cord.

The course of progressive muscular atrophy is chronic,
although very much more rapid than that of locomotor
ataxia. In many cases the progress becomes slower as the
disease advances, and in some it seems to stop altogether.
When complicated by bulbar palsy, death soon ensues from
failure of respiration, or from "foreign body" pneumonia.
If the atrophy remains limited to the hand and shoulder
muscles, the patient may live, incapacitated, for many
years.

^Etiology. — Even less is known about the causation of
progressive muscular atrophy than about that of tabes. Syph-
ilis is spoken of as a cause, but its influence is not proved, and
is certainly very much less important than in tabes. Exposure
to cold and wet, and overexertion have sometimes preceded
the first appearance of the disease. From the fact, as first
shown by Ballet and Dutil and later by Hirsch, that the
chronic disease may first appear in muscles which had been
affected by acute infantile spinal palsy, it seems as though
preceding inflammatory conditions of the spinal cord might
be a predisposing cause.

The causal relation of traumatism to progressive muscu-

PROGRESSIVE MUSCULAR ATROPHY. 167

lar atrophy is fairly well established. A considerable num-
ber of cases are on record in which injury of a limb was
quickly followed by an atrophy of its muscles, a condition
which later became general.

Less .frequently blows on the back or concussion acci-
dents have been the only discoverable cause of the typical
symptoms which shortly after ensued.

Diagnosis. — To prove progressive muscular atrophy to
be in all probability the result of injury it must be shown :
I. That the patient has muscular atrophy. 2. That he were
free from the disease a short time before or immediately
after the accident. 3. That the accident caused a consider-
able shaking of the body or injury to a limb.

I. The first requirement is a question of diagnosis, about
which there is usually little difficulty. If the disease is of
the lower Duchenne-Aran type, the two conditions to be
eliminated are injury to the ulnar nerve and lead palsy. It
will be remembered that the ulnar nerve supplies the inter-
osseous muscles and that injury to it causes main en griffe,
which is also a frequent symptom in progressive muscular
atrophy. If the history told by the patient is reliable, ulnar
n?rve palsy and progressive muscular atrophy will rarely be
confused. In the peripheral lesion the atroph}' develops
very much more rapidly, the loss of muscular power is
greater, and the subjective sensory sensations are more
prominent. The diagnosis may, however, usually be made
by objective signs alone. In any palsy of a peripheral nerve
which is sufficiently severe to cause pronounced atrophy,
the electrical conductivity of the nerve is very much dimin-
ished or lost. In nerve injuries without severe wounds or
fractures, fibrillary twitchings are not marked, and in an in-
jury to the ulnar nerve there is never any involvement of
the deltoid.

The differentiation from lead palsy may be more difficult.
If there are no constitutional evidences of plumbism, it is

1 68 ORGANIC EFFECTS OF INJURY.

sometimes an exceedingly delicate matter to decide between
lead palsy and a progressive muscular atrophy in which the
extensors of the wrist and fingers have become involved on
both sides. In lead palsy the supinator longus and the ex-
tensor ossis metacarpi pollicis escape. But they may also be
the only muscles to escape in the spinal disease. In a recent
case at the Vanderbilt Clinic, in which the wasting and
paralysis were bilateral and which by its course has been
proved to be one of progressive muscular atrophy, these
two muscles were the only ones of the extensor group which
had not been involved by the paralysis. Such cases, how-
ever, are unusual ; most frequently progressive muscular
atrophy is at first unilateral, or very much more marked on
one side than on the other. If it has developed in both
hands, there are also characteristic atrophies about the
shoulder muscles, the extensors of the wrist not being
affected until a later period of the disease.

If traumatic progressive muscular atrophy begins in the
deltoid or other of the shoulder muscles, it may, if the his-
tory be unreliable, be confused with some of the palsies of
the brachial plexus. The distribution of the palsy and the
results of electrical examination, as indicated in Chapter III,
will usually permit a recognition of the two conditions. In-
crease of the tendon reflexes, both at the knee and in the
upper extremity, frequently occurs in progressive muscular
atrophy, but is never a part of the peripheral disorder with
which it might be confused. Its existence is therefore a
valuable aid in diagnosis.

2. The validity of a claim of progressive muscular atro-
phy caused by injury depends very largely upon the ability
of the claimant to prove himself to have been free from the
disease at the time of the accident. Such proof is more
easily attainable than it is for the tabetic to prove that at
any given time he had no symptoms of tabes ; for the
symptoms of progressive muscular atrophy are nearly alto-

PROGRESSIVE MUSCULAR ATROPHY. igg

gether objective, and are of a character to be noticed, not
only by the patient but by his. friends. A marked sinking
in between the first linger and thumb may occur in a
month's time, and although the atrophy is usually more
rapid in its development than the loss of povv^er, even a
weakness of the interossei is so annoying and disabling, and
causes so serious an impairment of those finer movements
of the fingers which are essential for the commonest daily
duties, that it could not exist without becoming the subject
of remark. If a person who develops soon after an accident
progressive muscular atrophy, type Duchenne-Aran, could
prove that he had continued to do manual work satisfac-
torily up to the time of the injury, it would be very good
evidence that he were then at least free from the disease.
In most of the reported traumatic cases the patients were
active workers up to the time of injury.

3. The accident which has most frequently induced the
disease has usually been severe. I know of no case in which
fright alone is said to have been a cause, and in most the in-
jury was very appreciable.

Illustrative Cases. — ^The kind of accident and the mode
of the first appearance of symptoms may be illustrated by
the following cases ; some have been seen at the Vanderbilt
Clinic, and others are derived from various sources. For
two reasons no effort has been made to include all the cases
published as due to traumatism : First, because the clinical
evidence in favor of a traumatic origin of the disease is too
well established to make such a review necessary ; and, sec-
ondly, because many of the cases have been described in a
way that renders it impossible for the reader to determine
whether the disease had been caused by injury, or whether,
indeed, it were unquestionably progressive muscular atro-
phy. The following cases, therefore, have been chosen, in-
asmuch as they seem to prove with a considerable degree of
probability that progressive muscular atrophy may result

I/O ORGANIC EFFECTS OF INJURY.

from injury, and because they illustrate the clinical courses
of such cases :

Raymond quotes from Friedreich the case of a man who,
after a bruise of the right hand, developed an atrophy in
that hand which followed a progressive and ascending
course and was eventually complicated by bulbar palsy.
He also refers to Poncet's report of a soldier who was shot
in the right shoulder. The muscles of the wounded shoul-
der soon became atrophied and the left shoulder became in-
volved later.

Clarke describes a case which, in addition to furnishing
a good example of traumatic progressive muscular atrophy,
illustrates the predisposing influences of certain occupations,
and shows the injurious effect of depressing mental influ-
ences upon the course of the spinal disease :

A woman, thirty-eight years of age, married, seamstress, of deli-
cate constitution, fell downstairs and hurt her right hand and
especially the thumb. One year later there was pain in the right
arm, neck, and shoulder. She was unable to hold her needle, yet
there was no pain in the hand or forearm. At this time the mus-
cles of the arm and forearm began to waste, but improved again
in two months. The sudden death of her husband caused her a
severe mental shock, and she then complained of pain in the neck
and that both the arms and both the legs felt weak, cold, and
sometimes numb. Loss of power of the neck muscles ensued, and
the right arm soon became almost completely useless.

When admitted to the hospital the right arm was paralyzed and
wasted, and the examiner " could feel only fat, skin, and bones."
No reaction to faradism. No stiffness.

JExamination. — Left arm : Little power in the hand. The pa-
tient can extend the fingers slowly and feebly. All the thumb
muscles are wasted. The muscles of the lower two thirds of the
forearm are wasted, as are the supinators. She can wriggle the
arm along the chest. There is a fair quantity of muscle on the
upper arm. Interossei react to a slight current ; extensors feebly.

Neck : Muscles can only bend the head a little. There is slight
power in the left trapezium, but none in the right. Muscles on the
scapulae are gone. The facial muscles act slightly. Palate moves
slightly. Tongue protrudes, but is atrophied on both sides. Deg-

PROGRESSIVE MUSCULAR ATROPHY. 171

lutition imperfect. The right leg is wasted, but retains slight
power of movement. There is considerable strength in the left
leg. Patient died four months after admission to the hospital, and
about two years (?) after the receipt of the injury.

A case of the late Prof. Eisenlohr's is interesting, as it
shows the early appearance of the symptoms of bulbar palsy
after an injury to the upper part of the spinal column, and
follows the clinical type of amyotrophic lateral sclerosis in
the extremities :

A locksmith, forty-nine years of age, asserts that he had been
well previously to the receipt of a blow on the neck in the spring
•of 1877. In July of the same year there appeared a gradual weak-
ness of the arms and hands, which extended two months later to
the legs. In October began disturbances of articulation. Exami-
nation in January, 1878, showed the following conditions :

The lower part of the face is flaccid, the lips are constantly
open, and blowing and whistling are impossible.

The tongue is atrophic and its movements are limited. The
articulation of all consonants is bad.

Movements of the soft palate are very slow. Swallowing and
chewing normal. The shoulder and upper arm muscles are mod-
erately atrophied on both sides. The muscles of the forearm are
markedly atrophied on both extensor and flexor surfaces, the in-
terosseous spaces of both hands are deeply sunken in, and the
thenar and hypothenar eminences are flattened. The hands and
fingers are almost immobile. Great loss of power in both arms.
Sensibility is normal. The reflexes are active. Electrical excita-
bility is diminished. Similar changes, though less marked, are ob-
served in the lower extremities.

Death occurred in a few months as the result of the bulbar
palsy. The autopsy and subsequent microscopical examination
showed a degeneration of the anterior horns of the spinal cord
and of both pyramidal tracts.

Progressive muscular atrophy sometimes results from
head injury, or at least from accidents in which the head was
injured. In such cases there has usually been considerable
general violence, and it is impossible to tell how much of it
has been exerted on the spine.

72 ORGANIC EFFECTS OF INJURY.

Mann reports the case of an Englishman who at the age of
wenty-one fell from the rigging to the deck of a ship. He was
endered unconscious but sustained no fractures of the bones,
'reviously to this accident the patient had been perfectly well.
)enied syphilis or nervous disease in his ancestors. One month
fter the fall the deltoid began to waste, then the biceps and the
3wer arm muscles, and finally the muscles of the legs. One year
Iter he was seen by Sir William Gull, who thought the patient
ould not live twelve months. The disease came to a standstill,
owever, for seventeen years after the accident the patient was.
reated by Dr. Mann for another condition.

In a case of BuUard's, a teamster, sixty-one years of age,,
staging fell and struck the side of his head.

The patient had been in previous good health ; there was no-
yphilis or rheumatism or other causes of constitutional disease
liscoverable, although signs of phthisis appeared while the patient
?as under observation.

There was no loss of consciousness at the time of the accident,
lUt soon after it the patient felt pains in the head, neck, and left
houlder, which were followed by weakness and atrophy of the
luscles of the left arm and hand. Seven months after the injury
e was first seen by Dr. BuUard. The muscles of the shoulder and
f the back on the left side were markedly atrophied, those of the
pper arm less so. The forearm was still less affected. Main en
';riffe. Thenar and hypothenar eminences flattened. In the in-
erossei there was diminished faradic reaction. Fibrillary twitch-
ngs were marked. The patient gradually grew worse and the left
rm became affected. One year later the atrophy in the muscles-
f the upper part of the back and the fibrillary twitchings became
ery marked. Reaction to faradism was diminished, but sensation
emained normal.

A case by Ziehen is less convincing :

Man, twenty-one years of age, healthy, received a severe blow
n the chest and was then thrown into a ditch, where he lay un-
onscious for some time. This was in March, 1888.

He suffered from fatigue off and on, which was increased on
ne occasion especially when he stood for some hours in the river
shing (in July, 1889). He soon became unable to do heavy work,
nd appeared at the clinic in 1890, showing a well-advanced case
i progressive muscular atrophy.

PROGRESSIVE MUSCULAR ATROPHY.

173

Ziehen maintains that the atrophy was caused by the original
injury, and that the standing in cold water only aggravated a
process which had become established. The interval of time,
however, which elapsed between the accident and the date of the
medical examination was too long to permit an inference of any-
thing more than a possible relation between the original trauma
and the spinal disease.

The relationship between preceding inflammations and
the development of progressive muscular atrophy is shown
by the following case :

An electric lineman, thirty-five "years of age, a steady drinker,
who had had the initial lesion of syphilis in 1885, came to the
Vanderbilt clinic on October 30, 1896. He said that in 1888 he
fell forty feet from a pole, landing on the back and buttocks. He
then walked a few steps, but his legs soon gave out from under him
and he was carrie'd to bed, completely disabled in the lower ex-
tremities. For three months he was in bed, unable to move his
legs. The urine had to be drawn with a catheter. He then re-
covered and went back to work, and continued at work until July,
1896. He told us that for the past three months be had noticed a
gradually increasing weakness in the legs and thighs, without pain,
but with soreness across the back and stiffness at the ankle, hip,
and knee joints ; pargesthesia existed in the sole of the left foot
and in the ulnar distribution of the fingers, with considerable
weakness in the left arm — a condition which was also just com-
mencing to be felt in the right hand.

Examination. — Gait is paretic and spastic ; there is atrophy
of the right calf muscles, less marked on the left side. Double
ankle clonus and exaggerated knee-jerks. Atrophy of the first
interossei muscles of both hands and beginning main en griffe.
Fibrillary twitchings on the inner sides of both arms.

At the time of the examination the patient was a good illustra-
tion of the peroneal type of progressive muscular atrophy. The
atrophy and loss of power, which had begun and remained most
marked in the legs, had already involved the small muscles of the
upper extremities. If one be permitted to speculate as to the
probable genesis of the disorder, it would seem not improbable
that the original injury (in 1888), coming so soon after the syphi-
litic infection, had caused haemorrhage, or an outbreak of localized
syphilitic inflammation in the spinal canal in a way to exert pres-

174

ORGANIC EFFECTS OF INJURY.

sure upon the spinal cord. From this condition the patient appar-
ently recovered. There was left, however, a locus minoris resisten-
iiiE, as was shown by the progressive muscular atrophy first ap-
pearing in the muscles which had previously been the seat of the
temporary paralysis.

The following case, which has been under our observa-
tion at the clinic for many months, developed progressive
muscular atrophy three months after a blow on the back :

Fig. 38.— Case of progressive muscular atrophy which began three months after an
injury to the back. The photograph shows the wasting of the shoulder and
chest muscles and the ?nain en griffe. ( Vanderbilt Clinic. )

The patient (Figs. 38 and 39) says that, as far as he knows,
there have never been any nervous diseases in his family, and that
previous to his present illness he himself had always been strong
and well. As a young man he had gonorrhoea, but denies all symp-

PROGRESSIVE MUSCULAR ATROPHY.

175

toms of syphilis. He was married at twenty-nine years of age,
and lias one healthy child. His wife never had any miscarriages.

Fig. 39. — Same patient as in Fig. 38, showing wasting of back muscles.

He is a moderate drinker. At the age of thirty-one, eight years
ago, the patient weighed one hundred and seventy-five pounds,
and was healthy and strong. As the proprietor of a rag shop he

?6 ORGANIC EFFECTS OF INJURY.

IS daily engaged in handling heavy packages, an exercise which
! could perform without unusual effort or fatigue. The man is
telligent and straightforward, has no object to deceive, and every
atement he makes relative to his physical condition previous to
e accident indicates that he was a healthy, active, muscular man.

In 1889 — that is, about eight years ago — while lifting one end
a bale of cotton, weighing eight hundred pounds, he slipped and
11 so that one corner of the bale struck him in the small of the
ick. He suffered no pain, and was able to get up and return to
ark, and for three months observed no ill effects from the acci-
;nt. Then he began to have pain in the small of the back and

the muscles of the right arm, with some loss of power, espe-
ally for movements of extension of the wrist and of the fingers,
he weakness of the right upper extremity soon became so marked
at he had to give up working with it. One year after the acci-
int the left hand and' arm became similarly affected. At this
ne he also noticed the hands were becoming very much thinner
:tween the thumbs and fingers, and that there was a decided
iking in around the thumbs. The fingers became stiff, which
IS observed particularly upon attempts to extend them. He soon
;came so incapacitated that he was obliged to give up all heavy
jrk. With the exception of slight pain, there were never any
nsory disturbances, and the functions of the bladder and rectum
mained normal.

The condition of wasting has been progressive, and to-day the
an presents a picture of progressive muscular atrophy, type
uchenne-Aran, with beginning involvement of the leg. There is
:tensive atrophy of the thenar and hypothenar eminences and of
e interosseotis muscles. Both hands are in the attitude of main
griff e. The dorsal surface of the thumb is in the same plane as
e back of the fingers, and its opposability is lost. There is also
1 atrophy of the flexors and extensors of the wrists, the deltoids,
e pectoral muscles, and the muscles of the back, especially of
e right side. There is also a beginning atrophy of the left an-
rior tibial muscles, so that the patient has the " stepping " or
jquine" gait on that side. The atrophied muscles are the seat

fibrillary twitchings, which become very marked on exertion.
1 the muscles, with the exception of those which are wholly
rophied— as are some of the interossei — and of the ones which
e held stiff by contractures, react readily to faradism. The knee-
rks are present, and there are no sensory disturbances. The
tient is practically deprived of all use of the upper extremities.

PROGRESSIVE MUSCULAR ATROPHY.

177

The paralysis and deformities of the fingers and hands prevent
any fine co-ordinated movements, and, on account of the loss of
power in the shoulder muscles, he can with difficulty lift his hands
to his head, or hold his arms out from his body. As a conse-
quence he can do no manual work, can not dress himself, and can
only with difficulty feed himself. His condition is slowly but
steadily becoming worse, and has recently become complicated by
tubercular disease of the right lung.

The only medico-legal question which might arise in regard to
this case is whether the condition is solely due to the injury.
There can be no doubt as to the correctness of the diagnosis;
every symptom is present, and the patient presents a typical pic-
ture of the Duchenne-Aran type. The symptoms appeared a short
time after injury in a man who had undoubtedly been strong and
well before, and who was in no way predisposed to disease. The
injury was sufficiently severe to cause considerable violence, to
the back, and it seems to me entirely reasonable to believe that
had it not been received the spinal disease would not have devel-
oped.

Bibliography.

Ballet and Dutil. Revue de mddicine, January, 1884.

Bullard, A Case of Progressive Muscular Atrophy following a
Blow on the Head. Boston Med. and Surg. Jour., 1885, p. 369.

Charcot, J. B., Contribution a I'etude de I'atrophie muse, prog.,
Paris, 1895.

Clarke and Jackson, On a Case of Muscular Atrophy, with Dis-
ease of the Spinal Cord and Medulla Oblongata. M edico-Chirurg.
Trans., 1867, vol. 1, p. 489.

Eisenlohr, Klinische und Anatomische Beitrage zur progressive
Bulbarparalyse. Zeit. fiir klin. Med., 1880, vol. i, 3, p. 435.

Hirsch, Amyotrophic Lateral Sclerosis following Old Polio-
myelitis. Med. News., 1895, vol. Ixvii, p. 500.

Mann, A Case of Traumatic Progressive Muscular Atrophy of
Long Duration, complicated by an Attack of Left Hemiplegia, due
to Embolism. Alienist and Neurologist, 1886, vol. vii, p. 430.

Raymond, Atrophies musculaires, Paris, 1889, p. 138.

Ziehen, Aerztliches Gutachten iiber einen forensischen Fall
von progressiven Muskelatrophie. Viertjahrs. fiir gerich. Med.,
1894, vol. viii, p. 286.

178 ORGANIC EFFECTS OF INJURY.

Paralysis Agitans (Parkinson's Disease — Shaking

Palsy).

Examination of the properly prepared brain and spinal
cord of a person dead with paralysis agitans shows degen-
erations in nerve fibers and nerve cells and in connective
tissue. Since, however, disease occurs almost altogether in
persons who have reached the age when such degenerations
often occur without causing the symptoms of an}' distinct
disease, it still remains to be proved whether, in paralysis
agitans, the anatomical alterations are causes or effects, or
simply accompaniments of the malady. But, although the
pathology remains unexplained, the fact that in it the central
nervous system appears differently than in health, together
with the fact that the clinical manifestations indicate the
action of a common structural cause, are sufficient to permit
the disease to be classified without impropriety among the
organic nervous diseases.

The symptoms which are the most constant, and which
give the disease its clinical characters, are tremor, rigidity,
and weakness. The tremor is rhythmical and comparatively
coarse, there being between five and seven excursions in a
second. It continues during rest, ceases during sleep, and
although not at all or only slightly aggravated in intended
movements, it is made very much worse by emotional influ-
ences. The tremor usually originates in the thumb and in-
dex finger of one hand, and from there it spreads to other
fingers. Later it involves the wrist and the muscles of the
whole upper extremity. After it has persisted for a longer
or shorter time in any one part, its usual course is that of
extension. The mode of extension, which is fairly though
not absolutely constant, is from the arm to the leg on the
same side, and then to the arm and the leg on the opposite
side. In the rare cases in which the tremor begins in the

PARALYSIS AGITANS. 1 79

leg, it may follow the hemiplegic type, or it may involve the
opposite leg, before passing up to the arm.

The head and shoulder muscles are rarely involved ; these
parts are caused to oscillate by the transmitted movements
from the limbs, but it is only in very exceptional cases that
they are themselves the seat of tremor.

Muscular rigidity and weakness are symptoms of equal
importance to the tremor, and occasionally cases are met
with in which they are present without the tremor, furnish-
ing the seeming paradox of paralysis agitans without agi-
tation.

In the larger number of cases, however, the rigidity and
weakness develop in the same parts and at the same time as
the tremor. The rigidity consists in a stiffness of the mus-
cles without increase of the reflexes, and is consequently
different from spasticity ; it can usually be overcome with-
out difficulty by the physician. The loss of power is never
absolute, but all the movements of the affected muscles
are slow and uncertain.

When the disease is well developed the muscular condi-
tions give rise to characteristic appearances. The face (Fig.
40) is expressionless and drawn. The eyes are wide open,
and there is very little play of the features in talking or in
emotional expressions. The voice, from stiffness of the
muscles of the larynx, changes its pitch but little and is
monotonous. The head is bent forward (Fig. 41), and there
is frequently a bending forward of the spine. The limbs are
flexed at the large joints ; the fingers are flexed at the first
phalanges, and extended at the second and third (interosseous
position). The gait is shuffling, the patient walking with
short steps, and having difficulty in starting, or, having once
started, in stopping himself. Festination, or the tendency to
constantly increase the rapidity of the gait, and retropulsion
and propulsion, or the tendency to fall backward or forward,
as the result of slight pushes, are common symptoms. There

i8o

ORGANIC EFFECTS OF INJURY.

are no changes in refiex action, no atrophy or disturbances
of sphincter action. Cutaneous sensibility remains normal,
although the patients frequently complain of subjective dis-
turbances of sensation. The disease follows a chronic and
progressive course, and is incurable, although it may last for

t IG. 40. — Showing facial expression and position of the hands in paralysis ag:itans.
(Incurable Hospital.)

an indefinite number of years. The symptoms have been de-
scribed in some detail, because the order of their develop-
ment after injury is our chief proof of the traumatic aetiology
of the disease.

./Etiology. — There are few disorders of the nervous sys-

PARALYSIS AGITANS.

I8l

tem in which predisposition is so seldom demonstrable as in
paralysis agitans. In a small proportion of the cases the
disease itself, or epilepsy, or insanity, may be shown to have
existed in relatives, but gen-
erally persons who become
the subjects of Parkinson's
disease have healthy ances-
tors, and have themselves
been previously healthy. The
disease occurs most common-
ly in the decades of life be-
tween forty and sixty, and is
more frequent in men than in
women (five to three). Ac-
cording to Gowers, exciting
causes can be found in one
third of the cases, of which
the only ones requiring de-
scription here are nervous
shock and physical injury.

Gowers believes fright to
be the essential feature in the
genesis of this disease.

In support of this view he
cites the case of a man who was
waked by a bell on account of a
fire ; for a year and a half the
same bell always caused tran-
sient tremor, which then became
permanent, and passed into the
typical form of paralysis agitans.

Also, the case of a woman
who, at thirty -seven years of
age, was sitting quietly at work,
when a stream of water sudden-
ly flowed from a tap onto her left wrist. She was much startled ;
the left arm immediately began to shake, and the tremor per-
13

Fig. 41. — Showins Jiaracteristic atti-
tude in paralysis atfitans. (Vander-
bilt Clinic.)

1 82 ORGANIC EFFECTS OF INJURY.

sisted, passing to the leg, and afterward to the limbs on the left
side.

That the disease often appears and becomes permanent
soon after a severe shock, without any physical injury, there
can be no doubt, but more frequently there has been phys-
ical injury as well. Of one hundred and thirty-nine cases
observed at the Vanderbilt clinic, fright is assigned as the
sole cause in seven. On the other hand, of twenty-six trau-
matic cases examined by Walz, there is no mention of fright
alone as a cause, when unaccompanied by physical injury.

The injury, which is usually moderately severe, may be
of different kinds. Paralysis agitans has immediately devel-
oped after falls, injuries to nerves, stab wounds, contusions,
fractures, etc. Walz's analysis showed, in twenty six cases,
general concussion, six ; wounds (stabs and cuts), seven ;
burning and freezing, one ; sprains, twists, and fractures,
four ; contusions, eight.

Some connection between the part injured and the local-
ity of the earliest symptoms is almost unexceptional. If the
injury were limited to one hand, the tremor and stiffness be-
gin in that hand; if there were fractures of bone, or contu-
sions or injuries to nerves of one extremity, the symptoms
first appear in that extremity.

Thus a male patient, aged sixty, at the Vanderbilt clinic, was
in a runaway accident and was thrown out, striking the left arm
and shoulder. Tremor began soon after in the left arm, and
eventually extended to the leg.

Such a relationship might be regarded as coincidental if
it were true only of the upper extremity, where the disease
regularly, begins ; but it is also almost always true for those
other parts in which non-traumatic paralysis agitans only
very exceptionally has its initial symptom.

Charcot reports two cases in which the influence of the
injury upon the development of symptoms appears unques-
tionable. In one —

PARALYSIS AGITANS. 1 83

A woman fell out of a wagon and received a contusion of the
left side. She soon had severe pain, referred to the sciatic nerve,
and in a short time the whole limb began to shake. The tremor
was permanent, and extended to all the other members.

In the other case a woman suffered a dislocation of the jaw.
The paralysis agitans, which soon developed and eventually be-
came general, first appeared in the jaw.

When the injury is general, such as a concussion of the
whole body, the symptoms begin in one or both of the up-
per extremities, thus acting similarly to progressive muscu-
lar atrophy wrhen it occurs in those parts which had previ-
ously been affected through spinal injury.

Thus in a case described by Walz :

Male, aged sixty-one years, laborer. No syphilis or alcoholism.
Heredity negative. Was struck on the back of the head by a
package weighing about sixty-five pounds, which had fallen frorrT
a fifth-story window. The patient was knocked down and ren-
dered momentarily unconscious. After ten minutes he got up
and walked home. For two weeks he was in bed, with pains in
the upper extremity from the neck to the fingers, with rhythmical
movements of both hands and of the head. The patient recov-
ered sufficiently to get up, but he could not work, and he was
granted a pension, in accordance with the German law, for " pa-
ralysis agitans, which was the direct result of injury.'' The patient
died from spasm of the respiratory muscles four years after the
accident. The autopsy report says: "There are no local findings,
and certainly no haemorrhages of old or recent date. No marked
atheroma, and nothing abnormal in the dura or bones."

Paralysis agitans often develops at the site of an injury
received years before. Examples of this are very common :

A patient of mine, when a young man, received a severe mu-
tilation of the right hand. The wound healed perfectly, and
although the right hand remained practically useless, the patient
for twenty years had no symptoms of nervous disease. At the
end of that time the right wrist and arm began to shake, and gen-
eral paralysis agitans eventually developed. From the Vanderbilt
clinic records may be quoted the case of a man who, at the age of
forty, cut the ulnar side of his right wrist. Paralysis agitans ap-

1 84 ORGANIC EFFECTS OF INJURY.

peared twenty-two years later ; it began in the right hand. Also
that of a man, three fingers of whose left hand were amputated
at the age of thirty, and in whom the first symptom of paralysis
agitans, coming on at the age of sixty-three, consisted of tremor
in the operated hand.

In such cases, on account of the long-time interval, the
injury can only be regarded as a predisposing cause.

The intermediate or the "bridge" symptoms, which exist
between the receipt of the injury and the appearance of the
symptoms of paralysis agitans, consist in general nervous
shock and in pain, weakness, and some stiffness in the parts
which are to become the seat of the tremor.

They usually appear soon after the injury. To refer
once more to Walz's analysis, tremor appeared at once, or
within a day, in eight ; soon, or in a few days in seven ; after
one to eight months, in seven ; and after one to four years,
in four.

The tremor is the first pronounced symptom to appear ;
the other symptoms are of gradual development and do not
vary essentially in their course from the symptoms of the
disease when it occurs independently of traumatic influ-
ences.

It is impossible to explain the genesis of traumatic paraly-
sis agitans further than to note the sequence of events and
to infer that the injury stands in some causal relation to the
disease. Walz believes that the disease can only appear in
persons whose nervous systems are already deteriorated.
While the truth of such a theory can not be denied, it can
not be proved, because it is rarely possible to demonstrate
any predisposition in the patient.

While it may seem reasonable to suppose, at least after
slight injuries, that the disease would have eventually devel-
oped under any circumstances, there are no means of know-
ing that such would have been the case.

PARALYSIS AGITANS. 1 85

Bibliography.

Charcot, QEuvres completes. Paris, 1891, i, p. 155.

Vandier, De la paralysie agitante de cause traumatique. Thhe
de Paris, 1886.

Walz, Die traumatische Paralysis Agitans. Vierteljahrs. f.
gerich. Med., 1896, xii, p. 323.

Gowers, Diseases of the Nervous System. London, 1893.

PART II.

FUNCTIONAL EFFECTS OF INJURY— THE NERV-
OUS DISORDERS WHICH MOST FREQUENTLY
FOLLOW RAIL WA Y AND ALLIED ACCIDENTS—
THE TRAUMATIC NEUROSES.

CHAPTER I.

INTRODUCTORY CONSIDERATIONS REGARDING THE HISTORY,
NOMENCLATURE, PATHOLOGY, CAUSATION, AND SYMP-
TOMS .OF THE TRAUMATIC NEUROSES.

An eventful pathological history attaches to those nerv-
ous disorders which most frequently follow railway and
allied accidents and in which there is no reason to suppose
that there have been gross lesions to the nervous system.
Explained at first on a theory of disturbance of vascularity
of the spinal cord, they were later thought to depend upon
multiple areas of inflammation disseminated throughout the
whole cerebro-spinal axis. They have been successively re-
garded as nearly altogether organic, nearly altogether func-
tional, or nearly altogether feigned. They have been named
after two men — Erichsen and Oppenheim — who held very
different views as to their nature. They have been, and still
are, called by many different titles, chief of which are rail-
way spine, railway brain, concussion of the spinal cord,
concussion of the brain, spinal anaemia, spinal irritation,
traumatic neurosis, traumatic hysteria, traumatic neurasthe-
nia, and traumatic hystero-neurasthenia. These disorders
have become uninterruptedly more frequent and more im-
portant. They are accident neuroses, and we live in an age

HISTORY OF THE TRAUMATIC NEUROSES.

187

of accidents ; they often result from actionable negligence,
and the frequency of actions brought for personal injuries is
constantly increasing. More intimate familiarity with the
general diseases of the nervous system has perfected our
powers in the diagnosis of all nervous affections, and it now
seems that most of these functional traumatic neuroses can
be properly classified, even though they may not be per-
fectly understood.

Such a classification and description will be the object of
the following pages, and may be best accomplished by first
passing in review the various opinions of men who have
contributed to this subject.

Although concussion of the spine had been described by
Abercrombie, Ollivier, and others, the first important writer
on railway injuries was Erichsen. Erichsen was a surgeon,
and wrote at a time when nervous disease was but little un-
derstood. Gross lesions, such as haemorrhage and acute
softening, were of course recognized, but almost nothing
was known of the microscopical pathology of the nervous
system. Had Erichsen been the most expert neurologist
of his time he could have known the finer anatomy of none
of the degenerative diseases except locomotor ataxia. The
knowledge of nervous symptomatology was corresponding-
ly imperfect. From Erichsen's descriptions it is very hard
to tell what many of his patients suffered from. He evi-
•dently did not recognize the differences between ataxia and
paralysis, for in the case of posterior spinal degeneration,
which will be referred to later, he describes the symptonis
as paralytic when in reality they were ataxic. He says little
about electrical reactions, does not examine the reflexes,
and makes very cursory mention of anassthesia. Erichsen
(I quote from the later edition of his book) recognized that
these disorders were not necessarily the exclusive results of
railway accidents.

Of his fifty-three cases only seventeen were injured on

1 88 FUNCTIONAL EFFECTS OF INJURY.

railways. In most of the others the violence acted immedi-
ately on the spine, as in direct blows, injury to the back by
the falling of trees, etc., or in falls from considerable heights
on the head or on the buttocks.

The violence was generally severe, and entirely capable
of fracturing bone or rupturing ligaments, and not the kind
of violence which is most frequently associated with railway
injuries. Many of his cases give evidence of severe organic
lesion of the nervous system, and would to-day undoubtedly
be regarded as depending upon visible anatomical changes
of a morbid character. They would now be explained, not
as Erichsen explained them, by an assumption of molecular
changes in the spinal cord, but by the occurrence of such
visible damage as may be caused by compression of nervous
tissue from splinters of bone or by heemorrhages resulting
from laceration of blood-vessels, or from the wounding of
any of the intraspinal structures. Of only a few of Erich-
sen's cases can it be said with reasonable certainty that they
were functional — not dependent upon local conditions of an
organic character, but due to a functional disorder of the
whole nervous system. These latter Erichsen did not rec-
ognize for what they really were.

With the exception of one case of syphilis of the nervous
system he apparently did not appreciate the possible influ-
ence of trauma upon hastening the clinical manifestations of
latent nervous disease. He also failed to distinguish be-
tween symptoms of spinal and cerebral origin. For exam-
ple, he reports a case (No. 48) of paraplegia, with involve-
ment of the face, as due to spinal injury.

Confusion will invariably result in the mind of any one
who begins the study of traumatic nervous disease by a
perusal of Erichsen's work. He will there find grouped to-
gether cases which are evidently of very diverse character.
Erichsen makes of concussion both a cause and an effect.
For him, concussion is not only the shock, the jar of the

HISTORY OF THE TRAUMATIC NEUROSES. igg

accident, but it is also the disarrangement of molecular
structure of the spinal cord which may result in alterations
of blood supply (anzemia — hypergemia) sufficient to give
clinical symptoms.

Erichsen's theory of concussion of the spinal cord as a
pathological entity was purely hypothetical. Microscopical
technique is more advanced now than it was at the time he
wrote, yet it has thus far failed to disclose not only molecu-
lar pathology, but any such thing as molecular structure.
Molecular disorders are still in the domain of speculative
science. The significance of local spinal aneemia and hyper-
aemia, to which he ascribed much importance is absolutely
unknown. It is not intended to cast any discredit upon
Erichsen or his work, but, writing at the time he did, it
would have been impossible for him to formulate a theory
which could serve as an authority to-day. The following
case, his one autopsy for the determination of the pathology
of spinal concussion, seems to prove this :

Patient, fifty-two years of age at the time of his death, a man
of active business habits, had been in a railway collision. Imme-
diately after the collision the patient walked from the train to
the station, which was close at hand. He had received no e.xternal
sign of injury, no contusions or wounds, but he complained of a
pain in his back. Being most unwilling to give in, he made every
effort to get about in his business, and did so for a short time
after the accident, though with much distress. Numbness and a
want of power in the muscles of the lower limbs gradually but
steadily increasing, he soon became disabled. His gait became un-
steady, /i&e t/ia^ 0/ a /lalf-infoxkated person. . . . In the latter part
of his illness some weakness of the upper extremities became appar-
ent, so that, if the patient were off his guard, a cup or a glass would
slip from his fingers. . . . There was no paralysis of the sphincter
of the bladder until about eighteen months before his death.

This is apparently the description of a case of locomotor
ataxia, and the autopsy by Lockhart Clarke, instead of fur-
nishing an explanation of the pathology of spinal concussion,
as Erichsen supposed it did, added one more to the list, at

igo FUNCTIONAL EFFECTS OF INJURY.

that time small, of the recorded cases of primary degenera-
tion of the posterior columns of the spinal cord. Dr. Clarke
says in his autopsy report :

The membranes at some parts were thickened, and adherent at
others, to the surface of the white columns. . . . On making sec-
tions ... of all the white columns, the posterior were exclusively
the seat of the disease. These columns were darker, browner,
denser, and more opaque than the antero-lateral, and in their
preparations under the microscope this appearance was found to
be due to a multitude of granular corpuscles and isolated granules
and to an exuberance of wavy fibrous tissue disposed in a longi-
tudinal direction.

Erichsen did not appreciate that many serious disturb-
ances of general nervous function may result from injury
and shock when there has been no local damage to the nerv-
ous system itself.

Thus, Case 6, which he describes as " concussion from
a fall out of a bathing machine," might be construed as a
case of hysterical paraplegia, or of astasia-abasia :

A young lad, fourteen years old, fell in shallow water, striking
the sandy bottom. He received no mark of external injury and
walked home. His legs gradually became weak and numb.
Erichsen found, ten days later, that " he was quite unable to stand,
but when lying in bed could kick out his legs quite in a natural
way." He recovered completely in four months.

Erichsen's work, however, possesses more than a merely
historical value. It called attention to the possibility of
fractures of vertebrae and of tearing of ligaments without
external evidences of injury, and proved that serious nerv-
ous symptoms may result from injuries which at first appear
trivial. But he left almost untouched the complicated ques-
tions involved in the greater number of railway injuries, and,
through a failure to recognize the frequent subjective char-
acter of the symptoms, his work is to be regarded as a con-
tribution to surgery rather than to neurology. It remained
for subsequent writers, more experienced than he in general

HISTORY OF THE TRAUMATIC NEUROSES.

191

nervous diseases, as well as in the forms which most fre-
quently result from railway accidents, to explain the chain
of symptoms which are most commonly recited by injured
persons to claim agents, and which are now called the neu-
roses of traumatic origin.

While Erichsen's book marks the beginning of the study
of the nervous disorders following railway and allied in-
juries, it was a long time before their true nature was un-
derstood. Ten years after Erichsen's first edition, Erb still
believed in molecular disturbance as the chief element of
concussion. Westphal, in 1878, reports three cases, in two
of which the symptoms w^re so widely disseminated and so
pronounced that he ascribed them to multiple areas of cere-
bro-spinal softening.

Rigler, in 1879, thought that in many cases the symptoms
were exaggerated or assumed. In the absence of exaggera-
tion or feigning, he regarded the symptoms as due to or-
ganic lesions.

In America, Hodges was the first to object to Erichsen's
pathological views. In 1880 he read a paper before the
Boston Society for Medical Improvement, in which he said
that " we have no knowledge to justify the proposition that
what is popularly called ' concussion of the spine ' is due to
a molecular disarrangement of the cord by an assumed shake
or jar. That vascular disturbances (aneemia, hypergemia,
haemorrhages, spinal apoplexy) followed by meningitis, mye-
litis, or degenerative changes of the spinal cord, are shown
by experimental pathology, and to a certain extent by post-
mortem examinations, to be the true cause of symptoms
heretofore commonly designated as concussion of the spine."
He thought Erichsen's book " presents an exaggerated pic-
ture of its symptoms and consequences which are not justi-
fied by our present knowledge of the subject." Hodges
also suggested the possible functional character of many of
the symptoms.

192 FUNCTIONAL EFFECTS OF INJURY.

It remained, however, for Page to prove, as conclusively
as such things can be proved, that although falls, jars, and
shocks might cause organic injury to the spinal cord, such
a result is relatively infrequent ; that railway accidents, in
which the factors of concussion and fright are so intimately
mingled, more frequently caused nervous disorders of a
functional than of an organic character. Page was surgeon
to the London and Northwestern Railway of England, and
had had a very large experience in railway cases. His ex-
perience was essentially different from Erichsen's, in that,
as a corporation surgeon, he saw many cases of trifling in-
jury, and had to be constantly omhis guard against impos-
ture and exaggeration. His work bears the marks of in-
telligent and impartial observation, and although he may
have been to a certain extent prejudiced in favor of the rail-
way, many of his views have been substantiated by subse-
quent observers. Page saw the errors of Erichsen's work,
and emphasized the important fact that there had been no
satisfactory pathological proof of disease of the spinal cord
resulting from concussion, as distinguished from recogniza-
ble injury. He showed that the discussions regarding spinal
concussion were entirely empirical, and that there was no
proof to show that such a condition, comparable to the de-
magnetization of a magnet by a blow of a hammer, — a favor-
ite simile of Erichsen's — was ever caused by direct blows
on the back or by a general shaking up of the whole body.
He fully admitted the possibility of intraspinal haemorrhage
without external evidences of violence, but he claimed that
such injuries occurred in a relatively small proportion of
railway cases, and did not need to be explained by any
theory of molecular disarrangement. The larger number
of Page's cases had received slight injuries, and the symp-
toms which came on immediately or soon after the accident
consisted chiefly of pain in the back, associated with the
common subjective disorders of neurasthenia, but without

HISTORY OF THE TRAUMATIC NEUROSES.

193

any of the localizing signs of organic injury. He also rec-
ognized the existence of disturbances of motion dependent
upon idea or loss of will power. His chapter on functional
or neuromimetic disorders gives several interesting cases
which would to-day be called traumatic hysteria. One of
these may be quoted to show the long duration which is
possible in functional paralysis :

" Case of functional motor paraplegia. Extreme emotional dis-
turbances." Man, aged forty-one, who was naturally very excita-
ble, was in a very severe collision in which the carriage he was in
was smashed to pieces. There were no evidences of severe phys-
ical injury, but the patient was very nervous and in bed for sev-
eral days. Complained of pain in the back. No tenderness. He
dwelt on the fear of paralysis, and steadily lost power in the legs.
Eight months after the accident he was quite unable to walk, and
failed entirely to make any requested movements of the legs or
feet during examination. There was no paralysis of bowels or
bladder, and the sensory impairment was at best slight. There
were no bed sores or atrophy of muscles.

Nine months after the accident the patient had a sudden at-
tack of aphonia, which lasted three weeks and disappeared as
suddenly as it came. He was troubled by excessive emotional
irritability. Page's report to the company, nine months after the
accident was, that "the cause of the paralysis seems to lie in the
directing power of the will, rather than in lesion discoverable of
the brain or spinal cord." The man ultimately recovered, but
was ill four to five years. His recovery came suddenly. He had
been unable to get out of his chair without help until one day he
got up without knowing it. His son said to him, "Why, father,
look what you've done!" "Good God," he replied, I have got
up myself ! " From that day he could get up without difficulty.

Page publishes an appendix to his book, in which are
tabulated the ultimate results of two hundred and thirty-four
cases as observed from two to five years after the accident.
He says that most cases recover completely, although re-
covery may be much delayed.

He admits, however, that the injured man may never be
as well as he was before, and that many patients perma-

194 FUNCTIONAL EFFECTS OF INJURY.

nently retain evidences of impaired health. From an exam-
ination of his table it would seem that complete recovery-
did not occur in more than seventy per cent of the cases.

Page's book quickly obtained wide favor, and a second
edition appeared in 1885. At this time, also, the possibility
of hysteria occurring as a result of injury and shock became
recognized, and attention was called to the fact that some
of the cases of " concussion of the spine " were purely hys-
terical. Putnam had an accident case of hysterical hemi-
analgesia and paraplegia, and emphasized the necessity of
looking for hysteria in all concussion cases. Walton re-
ported a case of hysterical anaesthesia brought on by a fall,
and in an article entitled " Spinal Irritation " he suggested
a probable cerebral origin for many of the symptoms of
these disorders, and proposed the term " railway brain " as
a substitute for "railway spine." Dana, in December, 1884,
gave the first complete r^sumi of these disorders. His con-
clusions — which, with very slight modifications, have been
proved to be correct — are : " That the term spinal concussion
is misleading and often incorrect, and the symptoms which
are usually associated with that name are really symptoms
of traumatic neurasthenia, hysteria, and hypochondriasis,
associated more or less with symptoms of injury to the ver-
tebral muscles and ligaments and to the spinal nerves ; that,
in other words, concussion is mental shock and physical
bruising." Dana believed in " concussion of the spine " as
occurring in rare instances, and recognized the possibility of
injuries and jars causing myelitis without there being any
injury to the spinal column.

In the following year, Thomsen and Oppenheim, assist-
ants of Westphal, in support of the theory of an organic
basis for these disorders, maintained that hemianassthesia
was not a pathognomonic symptom of hysteria, but might
result from organic cerebral injury, and consequent!}' could
not be regarded as proof that many of these cases were not

HISTORY OF THE TRAUMATIC NEURONS. 105

organic in character. It must be remarked, however, that
the cutaneous insensibility studied by these authors in pa-
tients suffering from cerebral disease differed in essential
particulars from the hemiangesthesia of hysteria. It oc-
curred as a general hypalgesia, or diminution of sensibility
to pain, which was more marked on one side than on the
other, rather than in the form of the sharply defined uni-
lateral loss of sensation so commonly observed in hysteria.
Also, nearly all the cases examined by them presented
psychical anomalies — hallucinations, apathy, depression, etc.
— conditions which render any examination of sensations,
unsatisfactorj^and unreliable. Consequently, the paper by
these authors can in no way be regarded as overthrowing
the theory of a hysterical character for many of the trau-
matic affections under discussion. In 1885 Oppenheim re-
turned to the views of Westphal — namely, that the symp-
toms of " railway brain " were due to disseminate foci of
inflammation or softening.

Striimpell, writing in 1888, described a general traumatic
neurosis and a local traumatic neurosis.

The general .traumatic neurosis, which is apparently a
mixture of hysteria and neurasthenia, he illustrates as fol-
lows:

A healthy man falls from a height, is unconscious or dazed,
and has to be carried home. There are no serious injuries dis-
coverable. Recovery is very slow, and the patient stays in bed
for some time. Then he finds himself unable to work. He be-
comes very nervous. He is melancholy and depressed, and ceases
to take an interest in his surroundings. He loses his energy and
will power, and becomes agitated on slight provocation. There
may be considerable loss of memory. There is diiiftculty in fixing
and holding the attention. Sleep is disturbed by dreams. There
are cutaneous anaesthesia and hyperaesthesia (especially of the
back), and there may be a dissociation of sensations. The func-
tion of the special senses is impaired.

The motor difficulties consist in weakness rather than pa-
ralysis.

196 FUNCTIONAL EFFECTS OF INJURY.

Tremor and stiffness of the rhuscles are frequently present
The skin reflexes are often absent, and the deep reflexes are gen
erally exaggerated. There are various functional disturbances o
the vegetative organs, and complaints are made of loss of sexua
inclination and power. Many of these cases are incurable.

Under the head of local traumatic neurosis Striimpell de
scribed the various local manifestations, such as paralysis
contracture, hyperassthesia, joint affections, etc., of hysteria

Interest in the causative relation of trauma to nervou!
disease reached its height when, in 1889, Oppenheim pub
lished his celebrated monograph, Die traumatische Neuroser
(The Traumatic Neuroses), a book which has been widel)
read and which has exerted no little influence upon subse
quent discussions of nervous disorders following accidents
Oppenheim did not attempt any description of direct lesion;
of the nervous system. He only delineated the clinical forms
which result from accident and injury and which affect the
nervous system " through sudden vibration or in refles
ways." He admitted the existence of traumatic hysteria anc
traumatic neurasthenia, but to the forms of functional trau
matic disorder, which are not typical for either hysteria 01
neurasthenia, he gave the name of traumatic neurosis.

The symptoms of Oppenheim's traumatic neurosis are
chiefly a combination of the symptoms of severe neurasthe
nia, with some hysterical manifestations. They may develop
immediately after an accident, or their appearance may be
delayed for weeks or months. The first disturbances are
purely subjective, such as pains in the back or headache
anxiety, and restlessness. Depression and general worrj
may amount to hypochondriasis, without, however, direcl
impairment of the mental power. The patients are sleepless
dizzy, and subject to " weak spells " ; they have bad dreams
tremor occurring as a simple vibration, or in the form of tu
convulsif, chorea, epilepsy, etc., are not infrequently observed
Disturbances of voluntary motion may usually be explained

HISTORY OF THE TRAUMATIC NEUROSES.

197

by pain caused by movement, though the muscles are nearly
always weak and may be entirely paralyzed ; there may
be a weakness of all four extremities, or hemiparesis, or
paraparesis, or monoparesis ; the paralysis differs from
■organic paralysis in important particulars, one of which
is a peculiar rigidity of the muscles. The knee-jerks are
frequently exaggerated, but never lost. Atrophy may
•occur.

Disorders of speech are limited to a form of stuttering.
Inequality of the pupils is frequent, but they rarely fail to
react to light. Loss of sensibility of the skin and mucous
membranes occurs, but does not follow the distribution of
■organic anzesthesia. The visual fields may be contracted.
Vaso-motor disturbances are prominent. The bladder is
rarely involved, although there may be difficulty in passing
water, or incontinence or retention of urine. The sexual
iunction is generally impaired. The condition of the skin
reflexes is not constant. They may be active, but are usu-
ally diminished or lost in anaesthetic areas. Cardiac irrita-
bility is frequent. Oppenheim deduces the symptomatology
from forty-two cases which he had observed. Very few of
the patients entirely recovered.

Oppenheim's monograph was followed by the appear-
ance in America of a book by Clevenger, of Chicago, enti-
tled Spinal Concussion. Clevenger proposed the name of
■" Erichsen's disease " for these disorders. He says : " Erich-
sen's disease is a group of mainly subjective symptoms of a
nervous and mental nature, sufficiently characteristic to en-
able it to be recognized as a traumatic neurosis, distinct
from other traumatic neuroses, with which it may or may
not be associated. The most common cause of Erichsen's
disease is a concussion of the spinal column, including its
contents and nearest appendages."

The term " Erichsen's disease " has not met with favor
as a designation for any symptom group, and Clevenger's
14

198 FUNCTIONAL EFFECTS OF INJURY.

work is said by Gilles de la Tourette to be " le triomphe de la
confusion des id^es en pareille matiire."

Since 1889 the neuroses following accident or injury have
been a subject of contention, especially among neurologists.
The views of Striimpell and Oppenheim created much dis-
cussion. By some the existence of a special traumatic neu-
rosis with characteristic symptoms was unreservedly ac-
cepted. Many indorsed the theory with certain modifica-
tions, and a few spoke emphatically against the individuality
of any neurosis which occurs only as a result of injury and
shock.

Eisenlohr and Schultze, especially, questioned the value of
the individual symptoms upon which rested the theory of a
clinical entity for a special neurosis after trauma. Schultze
declared that " while a variety of neuroses and psychoses
may be induced by trauma, the traumatic neurosis as such
has no existence." Bruns also adopted this view, believing
it more correct to make the diagnosis of traumatic hysteria
or traumatic neurasthenia than to speak of a traumatic neu-
rosis. But Bruns admitted that, even after the most careful
efforts at differential diagnosis between the various neuroses
of traumatic origin, there remained a certain number of
mixed forms which can not be satisfactorily classified.

The opposition to the admission into medicine of a trau-
matic neurosis as a distinct disorder became more and more
pronounced. At the Twelfth International Medical Con-
gress, held at Wiesbaden in 1893, it was generally accepted
" that, even after slight injuries, general functional disorders
not infrequently develop. These neuroses are not disease
pictures of any particular variety, but all may be classified
under the name of other well-recognized neuroses, of which
the most important are hysteria, neurasthenia, hypochon-
driasis, and their mixtures."

The literature of the traumatic neuroses is now very large.
Page, in 1891, published a new and shorter book. In this

HISTORY OF THE TRAUMATIC NEUROSES.

country Knapp has embodied the results of his extens
study and experience in an excellent chapter in the Tf
book of Nervous Diseases by American Authors. Dana a
discusses the subject very thoroughly in Hamilton's T«
book of Legal Medicine. Dr. Outten, in Witthaus's Medi
Jurisprudence, writes with an authority acquired throu
large experience as a railway surgeon. Crocq has writ
an essay on the " N6vroses traumatiques," which has b(
crowned by the Belgian Academy. An able summary
the questions involved has been given by Saenger.

Strilmpell recently has cast doubt upon the value
many of the individual symptoms of the traumatic disord
His new position was attacked by the men who took pari
the discussions at Hamburg and Frankfort in the spring i
summer of 1896.

Such is the history of the views regarding the functio
nervous disorders which most commonly follow railway z
allied injuries. From the time that they were recognized
depending upon functional nervous disturbance, of wh
the structural changes are more minute and more baffi;
than the coarse lesions of heemorrhage, softening, or infle
mation, they became the object of study by neurologi
rather than by surgeons.

Discussions concerning them have been held with ad
ity and at times with acerbity. It is not surprising tt
without the guidance of visible pathological anatomy, 1
views of different observers regarding the nature of syn
toms are not entirely unanimous. But the progress of g
eral neurology has been constant, and year by year our 1
derstanding of the genesis and character of these neuro
becomes clearer. To-day, although not perfectly understo
nor classified with absolute security, they have obtainec
firmer foothold in clinical medicine than they ever h
before.

The larger number of cases can be made to agree w

200 FUNCTIONAL EFFECTS OF INJURY,

well-recognized and well-defined clinical types, so that the
course of any individual case can be foretold with a certain
degree of accuracy.

The following is a summary of the present understand-
ing of the essential features of the traumatic neuroses :

Nomenclature. — There is now a nearly complete una-
nimity of opinion that there is no such thing as a special
neurosis excited by trauma. Injury and shock may be fol-
lowed by symptoms of any of the well-recognized neuroses
or psychoses, or the symptoms of one or more of these dis-
orders may be blended in the same case. But the theory of
a special traumatic neurosis lacks clinical foundation and
has been generally abandoned. Even the severe forms of
nervous disturbance which sometimes follow injury, the ob-
servation of which led Oppenheim to coin the term " trau-
matic neurosis," do not need to be explained by assigning
them to a special nosological place of their own. Some of
them are mixtures of hysteria and neurasthenia, and others
may eventually be shown to depend upon structural changes
in the central nervous system, of which the clinical manifes-
tations are associated with symptoms of hysteria and neu-
rasthenia. These cases present no symptoms which can not
be explained on such an hypothesis. There is nothing suffi-
ciently individual about them to warrant the use of the term
" the traumatic neurosis."

If this view is correct, if there is no individual traumatic
neurosis, and if trauma is to be regarded in this connection
merely as an exciting cause of other well-known nervous dis-
orders of functional character, the comprehensiveness of the
term traumatic neuroses might be very much enlarged.
Besides neurasthenia and hysteria with their mixtures and
allies, and possibly some forms of organic disease whose
pathology is still to be explained, it could include neuralgia,
chorea, exophthalmic goitre, or any disease which is a neu-
rosis and which may develop as a result of injury and shock.

NOMENCLATURE OF THE TRAUMATIC NEUROSES.

Such a nomenclature would, however, be entirely at v
ance with the original significance of the term and wo
leave us without any generic designation under whict
classify the forms of functional nervous disease which h
obtained such prominence in medical jurisprudence,
the present, at least, it seems impossible to dispense wit!
expression which, although inexact, has come to be gei
ally recognized as applying only to a particular clas!
cases. But, while retaining "traumatic neuroses " as a g
eric designation, the physician should not be satisfiec
saying of any given case that it is one of the traumatic i
roses, but should continue the examination until he can ;
in all probability at least, which one. It is only by repea
efforts at exclusive diagnosis that the pathology and ch
fication of these disorders will be rendered still more pla

Striimpell has suggested that " traumatic neuroses "
changed to " accident neuroses." Against this may
urged that they do not necessarily result from accide
Injuries received in battle can hardly be called accider
Striimpell's reason for the substitution of " accident "
because a trauma is not always demonstrable. But
wider definition of trauma includes psychic as well as pi
ical injury, and consequentl)' traumatic can be with pre
ety applied to those neuroses which result from psy(
shock as well as from physical injury.

In the following pages these disturbances will be
cussed under the heads of —

1. Traumatic neurasthenia.

2. Traumatic hysteria.

3. Unclassified forms.

In traumatic neurasthenia the mental state is subjec
wide variations. The disorder may take on the type of
pochondriasis, less frequently that of melancholia. Tl
variations will be here described as variations of a comi
morbid condition.

202 FUNCTIONAL EFFECTS OF INJURY.

Hysteria following traumata is not always of the pure
type seen when the affection develops in young women from
non-traumatic causes. When owing its origin to injury or
fright, it is more commonly associated with pronounced
neurasthenic symptoms, such as are usually present in non-
traumatic hysteria occurring in men. Although traumatic
neurasthenia and traumatic hysteria frequently occur to-
gether (traumatic hystero-neurasthenia), for purposes of con-
venience they will be described separately.

The uncertainty regarding the group of cases called un-
classified is explained by the name. Further information is
necessary before they can be assigned to any nosological
category. To the other functional nervous disorders, which
are neuroses, and which may arise from trauma, such as
exophthalmic goitre, chorea, etc., no mention will be made.
They are not included by the general terra " traumatic neu-
roses," and require no description in a work of this char-
acter.

Pathology. — The possibility of injury to nervous tissue
has already been considered in Part I.

The belief, which was first systematically formulated by
Page, has now become general, that in by far the larger num-
ber of litigated cases of nervous disorders which follow rail-
way and allied accidents there is no gross injury to nervous
tissue. Physical concussion may be a cause of subjective
nervous symptoms, and if severe may indirectly cause or-
ganic injury. But the conception of spinal concussion as
a cause for general nervous symptoms and as a pathological
condition is without foundation and has been almost en-
tirely abandoned. By far the larger number of cases of the
traumatic neuroses may be explained by the theory that the
symptoms are those of hysteria or neurasthenia, functional
disorders of which the pathology is unknown. There are,
however, a few cases in which the symptoms are somewhat
different from those of hysteria and neurasthenia, and which

ETIOLOGY OF THE TRAUMATIC NEUROSES.

may depend upon the structural lesions of the brain i
spinal cord, although our knowledge concerning their
thology is still largely speculative.

iEtiology. — There are so many causative factors comn
to all of the neuroses of traumatic origin that they may b
be described in a general way together.*

Accidents which become the subject of medico-legal
quiry are more frequently followed by functional nerve
disorders than by organic injuries to the nervous syste
An analysis of one hundred successive cases which wi
seen by Walton, where nervous symptoms were complair
of and in which the question of damages had arisen or wi
likely to arise, gives the following results. " The date of i
examination was from one week to three and a half ye
after the accident, and the nature of the trauma ranged fr
slight jars and moderate blows on various parts of the bo(
to violent collisions and severe falls. In seventeen ca
there were unmistakable evidences of injury to the spi
cord. In the remaining cases the symptoms, although ofi
in many cases pronounced, differed in essential respects fn
the symptoms of organic nervous diseases."

Although the traumatic neuroses may follow any ac
dent in which injury and shock have been prominent f
tors, they have been chiefly studied in connection with r
way accidents.

Interest in them has advanced with the extension of r;
way travel, and until 1866 little attention had been given
these disorders. It is only in recent years that railw
travel has assumed proportions sufficiently extensive to c
ate for railway injuries a medical literature of their own. I
proved mechanical appliances, perfected systems of siguE
and the enforcement of military discipline among employe

* Causal characteristics special to any individual form will be given under
description.

204

FUNCTIONAL EFFECTS OF INJURY.

all tend to reduce the accident percentage. But these ad-
vances are more than counterbalanced by the constantly
increasing traffic on all kinds of surface vehicles, so that the
number of persons killed and injured becomes constantly
larger.

The following table is taken from the Eighth Annual Re-
port of the Interstate Commerce Commission (Washington,.
1896). It contains the total number of persons killed and
wounded on railways in the United States during the last
eight years :

Comparative Summary of Railway Accidents for the Years ending
June JO, i8gs, 18Q4, l8gj, iSgs, i8gi, i8go, i88g, and 1888.

Year.

EMPLOYEES.

Killed.

Injured.

PASSENGERS.

Killed.

Injured.

OTHER PERSONS.

KUled.

Injured.

Killed.

Injured..

1895
1894
1893
1892
189I
1890
1889
1888

1,811
1,823
2,727

2,554
2,660

2,451
i>972
2,070

25,696
23,422
31.729
28,267
26,140
22,396
20,028
20,148

170

324
299
376
293
286
310
315

2,375
3.034
3.229
3.227
2,972
2,425
2,146
2,138

4.155
4,300
4.320
4.217
4,076
3.598
3.541
2.897

5.677
5.433
5.435
5.158
4,769
4,206

4,135
3,602

6,136
6,447
7,346
7,147
7,029

6.335
5.823
5.282

33.748
31,889.
40,393
36,652
33,881
29,027
26,309.
25,88&

After allowance has been made for the increased number
of accidents in 1893, the year of the World's Fair, during
which travel was very extensive, it will be seen that the total
number of persons killed and injured during the past four
years is considerably larger than during the four preceding
years. Startling as are these figures, many deaths and casu-
alties may properly be classed as occurring on railways,,
which do not appear in this report.

The extension of the means of rapid surface transporta-
tion in recent years has very much widened the conception
of the term railway. It now includes elevated roads, elec-
tric systems of all kinds, cable roads, and to a certain extent
horse-car lines.

Railway collisions or derailments are particularly welt

ETIOLOGY OF THE TRAUMATIC NEUROSES. 205,

adapted to cause every variety of injury. Decapitation,,
dismemberment, bruises and crushes of the fiesh, fractures^
dislocations and twists of the bones and joints, cuts from
broken glass, burns and scalds from fire and escaping- steam,,
may immediately induce death or cause disabilities and dis-
figurements of all degrees. To the physical dangers of such
disasters is added mental shock. It is needless to emphasize
how lasting must be the terrible impression which is made
by the suddenness of the accident, the ibranlement, the crash
of breaking wood and glass, the cries of the wounded, the
noise of escaping steam, and the uncertainty and terror of
such catastrophes. But while death or physical injuries of
every character and degree may result from these acci-
dents, the number of persons who receive in this way or-
ganic injury of the nervous system is not great when com-
pared with the number of persons who, although hurt but
little or not at all at the time of the accident, eventually
develop some nervous symptoms. It is a matter of general
remark that the functional disorders occur most frequently
when there has been no gross physical injury. In railway
accidents there are usually a large number of persons who
neither die nor yet are badly hurt. They may be severely
frightened, and violently thrown about, and receive twists
or wrenches of the spine, or blows upon the back or head.
But whatever physical injury is incurred, it does not cause
them great pain or disability at the time. Yet it is these
persons who were considered, at the time of the accident,
as fortunate in escaping unscathed or with slight injury,
who eventually complain of the symptoms of some one of
the traumatic neuroses. There is no reason to suppose that
in such cases the nervous system has received any structural
damage, for in organic nervous injury there is almost im-
mediate loss of nervous function. In the traumatic neu-
roses, on the other hand, with the exception of some
cases of hysteria, there is an interval between the occur-

2o6 FUNCTIONAL EFFECTS OF INJURY.

rence of the accident and the appearance of pronounced
symptoms.

In many cases actions for personal injuries are brought
when there has not only been no physical injury, but even
when there has been no general accident. The sudden
starting or stopping of a train, the slipping in an aisle or
from steps covered with ice, or similar trivial mishaps, are
alleged as causes of neurasthenic symptoms. A woman in
Brooklyn recently brought suit for ten thousand dollars for
alleged injuries (none were visible) received by being thrown
from her seat to the floor by the sudden stopping of a trol-
ley car.

But although many escape from railway accidents with-
out severe physical injury, few are so fortunate as not to be
very much terrified and dazed. Fright is as fruitful a cause
of some functional nervous disorders as physical injury. It
alone may be sufficient to induce paralysis agitans, chorea, or
exophthalmic goitre, and its influence as a causative factor
in the neuroses which most frequently become the subjects'
of litigation — neurasthenia and hysteria — is very impor-
tant. Any of the manifestations of hysteria may appear
for the first time as a result of fright or nervous shock
alone. As we shall see in speaking of the astiology of trau-
matic neurasthenia, fright is usually associated with some
physical injury in the causation of that disorder, although
the physical commotion or shock may be very slight. Both
traumatic neurasthenia and traumatic hysteria may some-
times seem to be the result of physical injury alone or of psy-
chic shock alone, but in by far the larger number of cases of
these diseases the two causative factors have been active ;
and the fact that in catastrophes which occur on railways
large numbers of persons are subjected to fright and to some
physical commotion, explains in part why railway accidents
are such fertile causes of these disorders.

Although accidents on railways stand in the most con-

ETIOLOGY OF THE TRAUMATIC NEUROSES. 2^

spicuous causal relation to some of the traumatic neuros(
any of these disorders may follow mishaps or catastroph
of diverse character in which the elements of physical coi
motion or injury, and psychic shock, are prominent.

New inventions and elaborated mechanical contrivanc
are constantly supplying additional causative factors. The
may follow accidents in elevators, in theatres, in machii
shops. The introduction of rapid surface transit in the stree
has caused the annual number of these disorders to very m
terially increase.

The rapid development in recent years of the industri
uses of electricity has added another to the already long li
of exciting causes. Electric currents of high potential ai
now of such indispensable service in city life that the dang(
of receiving shocks from street currents, although chief
limited to electric linemen, is one to which every citizen
more or less exposed. It is not probable that electric cu
rents which do not induce almost instant death ever cau;
organic nervous disease. No such case has ever come 1
my personal observation, and a search through literature f(
the record of such a case has proved fruitless. As far as tl
nervous system is concerned, it is the functional affectioi
which result from accidents by electricity, and it is the ge
eral public, rather than the employee of the company, whic
suffers.* The lineman may be seriously burned or be i
stantly killed by touching live wires or by receiving in vai
ous ways currents of high voltage. But he resembles tl
brakeman in this respect, that he receives his injury and di<
of it, or quickly gets over the effects of it. Constant fami
iarity has so eliminated the element of fright that for him
is a physical injury, and rarely is followed by any sympton
of functional nervous disease. In persons unfamiliar wil

* In New York city, the placing of the electric-light wires underground, whi
was brought about largely by the efforts of H. P. Brown, Esq., has very materia
diminished the number of electrical accidents to the general public.

2o8 FUNCTIONAL EFFECTS OF INJURY.

electrical appliances the effects of powerful electrical shocks
are essentially different from those experienced by the em-
ployees of electrical companies. Such a one who touches
or is touched by a conductor which is not insulated, or
which he supposes to be not insulated, receives, independ-
ently of any electric shock, a fright as severe as the fright
caused by a railway collision. Thus a case is reported
by Dana of a patient who had read of the killing of a man
by an electric wire. A few days after, he was walking-
along the street when suddenly a dead wire fell and hit
him on the head. The blow was not very severe, but the
man fell unconscious, and when he was aroused he was
found to have typical hysterical symptoms. Of all the cases
of neurasthenia or hysteria which have followed contact
with wires carrying high voltage currents, in only a few
is there reason to suppose that the full strength of the cur-
rent passed through the body. It is very difficult to de-
termine the exact strength of current necessary to cause ex-
tensive burns or instant death. In the executions at Sing
Sing the currents are not of higher voltage than some of those
which pass through city streets, yet the effects of them on
condemned murderers are not always identical. In some
of the men death has been almost instantaneous, without any
charring or burning of the body. In others the flesh has
been considerably burned before life was pronounced to be
extinct. It is impossible to say, simply from the examination
of a person who has received a strong electric current, how
strong the current was which passed through him. It may
have been weak, and still have caused extensive burns, or
it may have been fatal, without leaving external physical
traces. It is certain that the victim of an accident rarely re-
ceives the full strength of a current of high potential. The con-
tact is usually imperfect and only momentary, and the larger
part of the effects of the electricity are dissipated without
coming in contact with the body at all. Clinical observation

ETIOLOGY OF THE TRAUMATIC NEUROSES. 209

shows that the greater number of persons who develop
neurasthenia or hysteria as the result of accidents with elec-
tric wires have not been seriously injured. There are some-
times burns of the clothing or of the hands, but these are
rarely severe, and more often are entirely absent ; and in
many cases circumstantial evidence, or the evidence of wit-
nesses, proves that the patient received no electric current
at all.

That fright is a most important element for the occur-
rence of the traumatic neuroses appearing as sequelas of
electrical accidents receives additional proof from the almost
universal agreement of opinion that such accidents are most
frequently followed by the symptoms of hysteria, the fright
neurosis /ar excellence. Neurasthenia, however, is sometimes
the result of real or supposed injury from electrical currents.
Knapp reports such a case :

A coachman, forty-two j'ears of age, strong, healthy, coura-
geous, and not at all nervous, was driving a team of horses
which fouled a live wire and were thrown. He got out and freed
the horses, but probably received no physical shock. He was
very much frightened, though he was not thrown down himself,
and walked home. After the accident he slept badly; was nerv-
ous and apprehensive. There was a marked tremor of head
and hands, loss of sexual desire, pain in back, exaggeration
of knee-jerks, and rapid heart action. After a duration of three
months these symptoms entirely disappeared, and the man be-
■eame as well as ever. They were symptoms of essentially neu-
rasthenic character, and, as such, are not of the most common
type observed after electrical accidents.

In gaining new causes, the traumatic neuroses have not
lost old ones. Any one of them may result from a fall from
a horse, from a carriage, or from slippery steps, or falls of
any kind in which the person is frightened and he is hurt
or his back is twisted. They very frequently follow falls in
which the victim strikes on the head, on the back, or on
the buttocks. Blows of any kind, but especially such as

lO FUNCTIONAL EFFECTS OF INJURY.

ill upon the head or the back, are often followed by func-
onal nervous symptoms.

Meteorological disturbances, and especially lightning,
re frequently the cause of nervous manifestations in per-
Dns of a neurotic temperament, and sometimes seem to be
le only getiological factor for well-marked neuroses. What
as been said in regard to the place occupied by powerful
lectric currents among the exciting causes of the traumatic
euroses may, with certain modifications, be repeated for
ghtning. Like high potential currents, it may instantly
ill, or cause extensive burns. But the persons who, after
ghtning strokes, develop any of the traumatic neuroses, of
'hich in this connection hysteria is the most frequent, usu-
lly bear no traces of physical injury and probably have not
een struck at all.

Seismic phenomena are associated with the two factors —
hysical vibration or violence, and fright — most essential for
le occurrence of the traumatic neuroses, and they are fre-
uently followed by symptoms of functional nervous disease.

Charcot observed typical cases of hysteria after the
arthquake in Nice. The earthquake in Charleston, S. C,
nd vicinity, in 1886, was followed by many cases of func-
onal nervous disorder.

Porcher quotes as follows the report which a physician
f Camden, S. C, made to the State Board of Health one
lonth after the earthquake shocks of August 31, 1886:

" They " (the earthquake shocks) " at first naturally cre-
ted much consternation among our population, and have
ndoubtedly had a very deleterious effect upon sick and
;eble persons, being followed by much nervous prostration
nd other unpleasant symptoms. Even upon well, robust
eople their effects have been striking in some instances,
ome have described their sensations as similar to those ex-
erienced after a shock from an electric battery ; others have
xperienced a very marked feeling of debility in their lower

ETIOLOGY OF THE TRAUMATIC NEUROSES. 2II

extremities ; others have had vertigo, nausea, etc. Some,
again, who were not affected by these unpleasant symptoms
in the beginning, are now troubled by them."

From the various medical reports of these earthquake
shocks, it appears that most of the nervous symptoms which
developed as a result of them were neurasthenic in char-
acter.

Hughes observed, after the St. Louis cyclone of 1896,
" cases of paraesthesia, hypersesthesia, analgesia and hyste-
roidal shock, neurasthenia and some of the so-called
traumatic neuroses, and ' railway-spine ' symptoms, such
as follow the perceptibly uninjured after railway acci-
dents."

In addition to the character of the accident there are
several other considerations of importance in determining
the causation of the traumatic neuroses.

Among the factors active in the production of general
nervous diseases, an important place is occupied by predis-
position, either hereditary, or acquired through excesses of
any kind. In neurasthenia and hysteria, originating from
causes other than trauma, it may often be discovered that
previously to the appearance of symptoms the resisting
powers of the nervous system had become enfeebled through
various causes. When these disorders result from traumatic
influences, predisposition to nervous disease, either heredi-
tary or acquired, is often difficult to prove. Traumatic neu-
rasthenia frequently appears in persons previously healthy
and active, and in cases which develop hysteria after trauma
it is often impossible to discover any predisposition. The
question of predisposition is, however, very cursorily treated
in many reported cases of this character, although it is of
the highest importance, both for scientific proofs and medico-
legal purposes, to know whether organic disease or an en-
feebled nervous system had pre-existed. It should make a
great difference in a verdict if an injury had merely caused

12 FUNCTIONAL EFFECTS OF INJURY.

n outbreak in symptoms which had previously existed,
tiough latent.

Occupation and mode of life exert a certain influence on
tie occurrence of these disorders. Railway employees,
nXh. the exception of locomotive engineers and railway
ostal clerks, are less prone than passengers to develop
ysteria or neurasthenia after accidents. This is explained
1 part by the fact that the employee, having become more
r less accustomed to the ordinary mishaps incident upon
ailway travel, can bear with a certain degree of composure
ny accident in which he is not severely injured. Also,
■rhen an employee is slightly injured, his one thought is to
et well and to return to work as soon as possible. For
bvious reasons it is bad policy for him to bring suit against
he company — a limitation which acts to his advantage, for
y means of it his convalescence is not delayed by the anxi-
ty and vexations which commonly attend suits for dam-
ges. Engineers, as distinguished from other railway em-
iloyees, do not share in the comparative immunity from
unctional nervous disorders — an exception which may be
1 part explained by the constant nervous strain to which
heir responsibility exposes them.

Railway postal clerks are frequently victims of neuras-
henia. The character of their work demands that they be
n their feet, subject to the constant vibration, swaying, and
Dlting of the rapidly moving train. At the same time, the
orting of the mail requires close attention and concentrated
lental effort. They are, consequently, exposed to the two
lost fertile causes of nervous exhaustion.

Contrary to the generally received impression, the trau-
latic neuroses are relatively more frequent among the
loorer classes. As a reason for this it may be urged that
iboring men are more constantly exposed to injury. But,
side from this unquestionable fact, it seems as though there
i^ere something in the mode of life of the poorer classes

ETIOLOGY OF THE TRAUMATIC NEUROSES. 213

which rendered them particularly susceptible to evil results
from slight traumatisms. Perhaps faulty hygiene furnishes
the predisposition, of which the existence is so often hard
to prove. Men are more frequently affected than women, a
difference which can be explained by the very much greater
frequency with which men are exposed to accidents of all
kinds.

The, physical condition of the person at the time of the ac-
cident exerts a very important influence. The fact is well
established that those who are asleep, or under the influ-
ence of liquor, experience the fewest serious results, both
physical and mental, from railway and allied accidents. On
the other hand, persons suffering from chronic disease of any
kind, and particularly disease of the nervous system, are
especially susceptible to bad effects from traumatism. The
original disease may be made worse, or to it may be added
symptoms of subjective and functional character.

Thus in an unpublished case of Peterson's, which he kindly
permits me to quote, a lady had suffered for some time from amyo-
trophic lateral sclerosis, although the disease had only annoyed
her by interfering with the finer movements of the hands. One
■day, while sitting in a restaurant, she was struck on the head by a
revolving fan, which had become detached from its support on
the ceiling. As a result of this there supervened a condition of
extreme nervousness, irritability, sleeplessness, and despondency
— symptoms previously absent. Also tremor, of which she had
never complained before, became very marked after any exertion
or fatigue.

The influence of suggestion by physicians is frequently

traceable in the causation both of traumatic neurasthenia

and of traumatic hysteria. In many cases it seems as though

these disorders owe their appearance, in large part at least,

to the fact that the patients jiave been told by physicians

that they may some day have trouble with the spinal cord

as a result of the accident. The examples of the bad effects

of such ill-advised statements are numerous.
15

14 FUNCTIONAL EFFECTS OF INJURY.

Thus, a gentleman was slightly jarred by the sudden stopping
' a sleeping-car, but was not thrown from his berth and felt no
imediate ill effects of the mishap. On general principles, how-
ler, the next morning he consulted a physician, who told him
lat his spine had been concussed and that he might eventually
ive serious symptoms as a result. A few days afterward the
itient began to have pain in the back, and finally became a con-
rmed neurasthenic.

Similarly, a park policeman was thrown from the back
atform of a horse-car, striking upon the pavement with his face.
!e thought his jaw was broken, and immediately sought medi-
il advice. The doctor said that there was no serious injury
30ut the head, but that he feared trouble from the spinal
)rd. A few months after this the patient came to the Van-
;rbilt Clinic, presenting a pronounced picture of traumatic
listeria.

Intimately allied with suggestion as a causative factor of
le traumatic neuroses, and by some considered the most
aportant of all, is the question of litigation. In how^ far
id in what way the hope of compensation for personal in-
tries received in accidents influences the development of
mctional nervous symptoms will be considered in succeed-
ig pages. In speaking here of aetiology, it is sufficient to
ly that there is a far greater probability that functional
;rvous disturbances will appear, or, if they have already
jpeared, that they will be made worse, in any case which
3Comes the subject of medico-legal inquiry. Upon this
Dint all authorities agree. There are still many differences
: opinion in regard to the pathology, symptomatology, and
rognosis of the traumatic neuroses, but the belief in litiga-
on as a very potent causative factor is universal. It sur-
)unds the patient with the influences from which he should
3 free, and prevents him from pursuing the course of treat-
ent best suited to permit a. return of health and of self-
)ntrol. It is the physician's duty to do all in his power to
vor an adjustment of claim, rather than have his patient
in the risk of becoming a chronic invalid through the vexa-

SYMPTOMS OF THE TRAUMATIC NEUROSES.

215

tions and annoyances which are invariably associated with
suits for damages.

Symptoms. — The symptoms of the traumatic neuroses
are essentially those of traumatic neurasthenia and traumatic
hysteria. Inasmuch, however, as these two disorders often
occur together in accident cases, and since there has been so
much discussion relative to the clinical value of their mani-
festations, it will be necessary to make some preliminary
observations on the general character of the symptoms, al-
though they will be fully described in later chapters. Many
of them are purely subjective. In private practice, when
the physician has to deal with subjective symptoms, he is
usually safe in believing that they really are causes of annoy-
ance or suffering to the patient, although it may be evident
that they are to a certain extent exaggerated. When the
question of litigation enters, however, the case becomes en-
tirely different; then, instead of looking for the harmless
exaggeration of chronic invalidism, the examiner must be on
his guard against malingering. To insure correct results
from the examination of litigation cases, it is necessary that
the physician be cognizant of fraud, familiar with the meth-
ods of diagnosis of nervous disease, and aware that the func-
tional disorders may be serious or incurable affections. The
examiner, whether he be an expert called by a claimant, or
be employed by a corporation, should undertake the exami-
nation without prejudice and without bias. His position is
always delicate and often difficult. It would be superfluous
to dwell here upon the moral duties of an examiner in litiga-
tion cases. That is a question in ethics rather than in medi-
cine. The physician owes it to his client to exert every effort
in his behalf. He owes it to himself to give an opinion based
solely upon his own convictions. By whomsoever employed,
he will rarely err if he keeps constantly in mind that his func-
tion is scientific, and that he is not to be influenced by the ef-
fect his opinion will have upon the financial aspect of the case.

l6 FUNCTIONAL EFFECTS OF INJURY.

It is often impossible to decide from a single examina-
ion what the merits of the case really are, and in doubtful
ases an opinion should not be given until after several have
een made. In general practice the physician often finds
imself unable to determine the exact nature of a disease
ntil he has observed it during a considerable period of
ime. How, then, in any accident case, in which the symp-
3ms are almost entirely subjective, and in which exist the
trongest motives for exaggeration or deceit, can he hope to
e always correct in diagnosis and prognosis from examin-
ig the patient once only ? In Germany, laboring men who
re the victims of accidents can be placed in the hospital
ntil the exact nature of the disorder becomes plain. Such
procedure is impossible in America. With us only those
ersons go to the hospital who are seriously injured, and
bout whose injuries there could be no question of doubt,
'he others must, for the greater portion of the time, be free
om medical observation. This fact should render the phy-
cian cautious about too unreservedly accepting the patient's
:atements, or about placing too high a value upon such
i^mptoms as are purely subjective in character. The his-
)ry of how injuries were received, or the accounts of phys-
;al conditions, are often unreliable when told by persons
nfamiliar with the significance of symptoms or with the
eneral workings of pathology. To a certain extent in gen-
:al medical cases, and to a greater extent in functional nerv-
us troubles, when there is no thought of litigation, the phy-
cian must be guided by the results of his own examination
ither than by the description of suffering and discomfort
iven by the patient. In cases in which the strongest mo-
ves for exaggeration and deceit are present, how much
lore conservative must he be about too fully accepting
atements of personal ill health which permit of no ob-
ctive proof !
The history may be unreliable even when the patient

SYMPTOMS OF THE TRAUMATIC NEUROSES.

217

believes it to be true. By constantly rehearsing in his mind
the details of the accident as he remembers them, or as they
have been told him by witnesses, by the sympathetic in-
quiries and solicitations of friends or interested persons,
the patient may come to believe that he knows for him-
self what has in reality been told him or suggested to him
by others.

It is, of course, not meant that the examiner should neces-
sarily disbelieve everything that a claimant tells him. But
the history of the traumatic neuroses has shown, and the
nature of the cases demands, that the statements of patients
in litigation cases should be subjected to some corroborative
proof before they are unreservedly accepted as true. The
proof of the reality of the painful sensations from which the
patient says he suffers may often be found in his manner and
general bearing. His whole appearance may indicate ill
health, although there is no one objective symptom to prove
its existence. It is then that the physician must be guided
by his own experience in nervous disease. But when there
are no physical traces left by the suffering through which a
claimant says he has gone, or to which he asserts he is still
subject, there is no way in which it may be decided as to
the unreality of the symptoms, except in so far as repeated
medical examinations may show their existence to be im-
probable, or in so far as information from outside sources
may prove that the claimant only conducts himself like a
sick man when he is being watched. Thus must be deter-
mined the truth concerning such symptoms as sleeplessness,
spontaneous pain, nervousness, lack of interest, and general
fatigue. Some of the symptoms commonly called objective
are also, in large part at least, subjective.

Excitability of the heart and rapid pulse, although ob-
jective signs, are not in themselves necessarily evidences of
disease.

Palpitation of the heart is particularly frequent in per-

2l8 FUNCTIONAL EFFECTS OF INJURY.

sons who use to excess tea, alcohol, tobacco, or other stimu-
lants.

In most people the heart becomes more rapid at the
time of a medical examination, and in those of a nervous
temperament the heart action may become tumultuous from
very slight excitement. The same observation holds good
for anomalies of respiration.

AncBsthesia is the symptom about the diagnostic value of
which there has been the greatest contention.

It has been urged against it that the symptom is subject-
ive, inasmuch as, with the exception of tests which are pain-
ful, the physician gains his information from the patient,
who, through inattention or through the influence of sugges-
tion, or when actuated by ulterior motives, may make an-
swers which are not true, and thus be credited with symp-
toms which do not exist. Yet, although anaesthesia is a
subjective symptom in the sense that the co-operation of the
patient is often necessary for the establishment of its exist-
ence, it is converted into an objective symptom when the
replies of the person under examination show it to be in
accord with the other disease evidences which may be pres-
ent, and in agreement with the loss of sensibility recognized
as characteristic of definite clinical types. There is no ques-
tion as to the objectivity of anassthesia as observed in spinal-
cord lesions or in classical cases of hysteria. When, how-
ever, the loss of sensibility is slight, occurring in small areas
with indefinite boundary lines, or in the form of a general
blunting of the sense of touch or of pain, its diagnostic value
is not great and can easily be overestimated.

Acuteness of cutaneous sensibility is subject to wide
variations which, clinically at least, must be regarded as
within normal limits. It varies with age, sex, and race,
with different individuals under similar circumstances, and
with the same individual under the changing effects of
weather, time of day, fatigue, and similar temporary condi-

SYMPTOMS OF THE TRAUMATIC NEUROSES.

219

tions. Certain diseases, such as general paresis and chronic
intoxications, notably alcoholism, in which pronounced an-
aesthesia is not usually present, are often accompanied by a
certain degree of blunting of sensibility. When due allow-
ance is made for these variations anaesthesia remains as a
symptom of positive and often of pathognomonic usefulness.
The physician who is familiar with the facts will appreciate
the appropriate value of the symptom, and will not be apt
to ascribe to slight impairment of sensibility an unwarranted
diagnostic importance.

Pain or hypercesthesia is subjective, except in so far as it
leaves unmistakable evidences in disturbances of nutrition.
A test usually considered as of considerable value for the
■determination of the genuineness of pain and for converting
it into an objective symptom has been named, after its origi-
nal describer, Mannkopff, although its applicability in the
traumatic neuroses was first pointed out by Rumpf. It con-
sists in observing the pulse rate before, after, and during
pressure upon an area alleged to be painful. If the pulse
becomes more rapid while the pressure is being made, it is
supposed to be proof that the pain is real and has reflexly
caused the heart to beat more rapidly. The application of
the test is illustrated by Rumpf in the following case :

A man, thirty-three years of age, fell from a roof. After the
various early symptoms of injury had disappeared the patient
•still complained of great weakness and pain in the head, back,
and left breast, which was much increased by any contact. The
pain was entirely subjective, but was converted into an objective
symptom by the Mannkopff test. To avoid confusing the in-
■crease of the pulse rate, due to fear or other psychic influences,
with the increase caused by the perception of real pain, the pulse
was first counted with the patient in the recumbent posture with-
out any pressure being applied to the painful areas. The rate
was : In the first quarter of a minute, 20 ; in the third quarter of
a minute, 24; in the fifth quarter of a minute, 29; in the seventh
quarter of a minute, 26 ; in the ninth quarter of a minute, 26 ; in
the eleventh quarter of a minute, 25. Then firm pressure was ap-

220 FUNCTIONAL EFFECTS OF INJURY.

plied to the alleged painful area in the back, and the pulse at once
increased to 33 beats in the first quarter. On removing the pres-
sure it sank again as follows: In the first quarter of a minute, 32 -^
in the third quarter of a minute, 30 ; in the fifth quarter of a min-
ute, 28, in the seventh quarter of a minute, 27; in the ninth
quarter of a minute, 25. In addition to an increase in rate, the
pulse became smaller and at times irregular.

Rumpf regarded the Mannkopff test as of great value in
the detection of simulation; but observations made by
Strauss, in which the pulse waves were carefully recorded
by means of the sphygmograph, have shown that in many
cases of unquestioned pain, pressure over the painful areas
causes no increase in the heart's action ; so that Strauss's
conclusions, which accord, I think, with those of most clini-
cians, is that the Mannkopff symptom is not constant even
in cases in which there is no reason to doubt the real exist-
ence of pain or hyperaesthesia. If the symptom is present,
as it often is in traumatic lumbago, or as it may be in hys-
teria, it is a valuable aid in diagnosis. But if it is absent, we
are by no means justified in concluding for that reason that
the pain or hyperaesthesia is assumed. In making the test
the pulse should be carefully counted for some little time
before exerting the pressure, in order to eliminate as far as
possible any acceleration which may be due to psychic influ-
ences. This test may be extremely painful.

TAe visual disturbances of the traumatic neuroses have
been the subject of much controversy. There is no reason
to doubt that in neurasthenia there is commonly an asthe-
nopia, which prevents any long-continued use of the eyes,
and that some of the visual anomalies of hysteria, although
very difficult to explain, are pathognomonic of that disease.

The chief contention among neurologists has been in
regard to the diagnostic value of the results of perimetric
examinations. The two conditions most commonly observed
in such examination of cases of the traumatic neuroses.

SYMPTOMS OF THE TRAUMATIC NEUROSES. 221

have been the concentric contraction, without structural
disorder of the eye, and the shifting or fatigue contraction
of the visual fields (see Chapter II). The first of these con-
ditions was originally described by von Graefe and the sec-
ond by Forster.

In regard to both of them arises, as it must arise in
regard to any functional symptom, the question, Do they
occur in normal individuals, and do they occur in other
diseases in a way to impair their diagnostic value for the
traumatic neuroses ?

The recent investigations of Koenig indicate very posi-
tively that concentric limitation of the visual fields is not
found in persons with normal nervous systems. From the
examination of two hundred and sixteen non-nervous cases
and of ten pathological cases, Koenig concludes that it does
not occur in healthy persons, that it may be the only symp-
tom of hysteria, and that, when constant, it is typical of hys-
teria, even when the limitation is only slight in degree.

This ocular condition is observed in many of the disor-
ders of the nervous system, of which the most prominent
are tabes, dementia paralytica, epilepsy, trigeminal neural-
gia, and alcoholism. But occurring in this way, even if the
routine examination of the eye fails to disclose any other
visual defects, the associated symptoms will prevent the
contraction of the visual field being ascribed to hysteria
alone. A consideration of these facts, together with the
great improbability of the simulation of the condition, seems
to justify the acceptance of contraction of the visual field,
when there are no morbid alterations of eye structure, and
when symptoms of other forms of functional or organic dis-
ease are absent, as a pathognomonic symptom of hysteria.

The significance of the shifting type of contraction is not
so well established. Peters has found it present in many
persons presumably healthy. Koenig, however, and still
more recently Miiller, incline to the view that, if at all pro-

222 FUNCTIONAL EFFECTS OF INJURY.

nounced, this symptom is certainly indicative of retinal fa-
tigue ; and that although it may occur in healthy men, in
them it is less constant and less pronounced. As Miiller
says, when it is constantly present at repeated examinations
in persons supposedly healthy, it is time to look for nervous
symptoms.

The tendon reflexes, and especially the knee-jerk, become
the subject of discussion in most accident cases. Loss of
knee-jerk does not occur as the result of functional disease.
Exaggeration, on the other hand, is the rule. Unless asso-
ciated with other symptoms, slight exaggeration can not be
regarded as of any particular pathological significance ;
when associated with ankle clonus, it usually, though not
invariably, indicates organic disease ; when associated with
other symptoms, it lends confirmatory evidence as to the ex-
istence of morbid functional states.

Vomiting or spitting up of blood-stained fluid immediately
after the accident, occurs in a certain proportion of the
cases. While alarming in appearance, this symptom has no
particular significance unless it is the result of injury to the
thoracic contents or to pre-existing disease of the lungs. It
is observed in neurasthenia, but more commonly in hysteria.
The discharge comes from the mucous membrane of the
mouth and throat, and, as Striimpell has shown, is character-
ized by the small number of red blood-cells and by the free
mixture of mucous epithelium and bacteria which are col-
lected in the buccal and pharyngeal mucous membrane.

Glycosuria, as a result of injuries to the nervous system,
is a condition about which more information is desirable.
The most that can be said of it is that, while it may occur as
the result of injuries to the brain and medulla, temporary
glycosuria is occasionally found after injuries whose chief
results are functional.

The other symptoms of the traumatic neuroses will be
so fully described in succeeding pages that they require no

SYMPTOMS OF THE TRAUMATIC NEUROSES. 223

mention here. It is to be remembered, however, that it is
not by the consideration of any one symptom that a com-
plete comprehension of any case of functional nervous dis-
ease following an accident is to be obtained. The case
must be looked at in its clinical entirety. Attention must
be given to the kind of accident and the extent of physical
injury as well as for motives for simulation or exaggera-
tion. It is not sufficient to observe objective symptoms
without inquiring whether they could not have antedated
the accident. It is not possible to form a conclusion from
one subjective symptom.

By refusing to express an opinion without having looked
at the case in every aspect the physician will rarely find
himself in error.

Bibliography.

Abercrombie, Treatise on the Brain and Spinal Cord, 1828.

Booth, Critical Digests in Sajous's Ann. of the Univ. Med. Sci.,
1892, 1893, 1894.

Bruns, Critical Digests in Schmidt's Jahrbiicher, ccxx, p. 142 ;
ccxxi, p. 210; ccxxx, p. 81 ; ccxxxi, p. 21; ccxxxiv,p. 25 ; ccxxxviii
p. 73 ; ccxlii, p. 191 ; cclv, 8.

Clevenger, Spinal Concussion. Philadelphia and London,
1889.

Crocq, fils, Etude pathog^nique et clinique des n^vroses trau-
matiques. Bruxelles, 1896.

Dana, Concussion of the Spine and its Relation to Neurasthe-
nia and Hysteria. N.Y. Med. Record, December 6, 1884; ibid.,
article, Traumatic Neuroses. Hamilton's System of Legal Medi-
cine, New York, 1894.

De la Tourette, Traitd clinique et therapeutique de I'hyst^rie.
Paris, 1891 and 1895.

Discussion iiber Nerven-Unfalls Erkrank. Aerzt. Verein zu
Hamburg. Neurolog. Cblatt., 1896, pp. 569 and 617.

Eisenlohr, Bemerkungen iiber die traum. Neurose. Berl. kl.
Woch., 1889, No. 52.

Erb, Ziemssen's EncyclopcRdia of the Practice of Medicine, New
York, vol. xiii, 1878.

Erichsen, On Railway and other Injuries of the Nervous Sys-

224 FUNCTIONAL EFFECTS OF INJURY.

tem, London, 1866 ; ibid.. Spinal Concussion, London, 1875 and
1882.

Forster, Gesichtsfeldmessung bei Ansesthesise Retinae. Kl.
Monatsbl. Augenheilk. Beilage, 1877.

Graefe, von, Anaesthesiae Retinae mit Concentr. Gesichtfeld-
beschrankung. Kl. Monatsbl. fiir Augenh., 1865, iii.

Hodges, Concussion of the Spine, So called. JSost. Med. and
Surg. Jour., 1880, vol. cii.

Hughes, Cyclone Neuroses and Psychoses. Alienist and Neurol.,
January, 1897.

Knapp, Accidents from the Electric Current. Bost. Med. atid
Surg. Jour., April, 1890, pp. 17 and 24; ibid.. Traumatic Nervous
Affections, an Attempt at their Classification, etc. Am. Jour, of the
Med. Sci., 1892, p. 629 ; ibid.. Nervous Affections Following Railway
and Allied Injuries. Text-book on Nervous Diseases by American
Authors. Philadelphia, 1895.

Koenig, Deut. Zeit. f. Nervenh., 1895, vol. vii, p. 263.

Mannkopf. See Rumpf.

Miiller, Zur Frage der Ermiidbarkeit des Gesichtfeldes. Arch,
fiir Psych., 1896, p. 225.

Nammack, Case of Traumatic Neurasthenia. Trans. N. Y.
Neurolog. Soc, 1895.

OUivier, Traits des mal. de la moelle 6pinifere. Paris, 1837.

Oppenheim, Weitere Mittheilungen iiber die sich am Kopfver-
let'zungen und Erschiitterungen anschliessenden Erkrankungen
des Nervensystems. Arch.f. Psych., 1885.

Oppenheim, Die Traumatische Neurosen. Berlin, 1889 and 1892.

Outten, Railway Injuries. Witthaus's and Becker's Medical
Jurisprudence, Forensic Medicine, and Toxicology, New York, vol. iii,
1894.

Page, Railway Injuries in their Medico-legal and Clinical As-
pects. London, 1883 and 1891.

Peters, Deut. Zeit.f. Nervenh., 1894, 3 and 4.

Porcher, Influence of the Recent Earthquake Shocks in Charles-
ton on Health. Med. News, December 11, 1886.

Putnam, Recent Investigation into the Pathology of so-called
Concussion of the Spine. Bost. Med. and Surg. Jour., September
6, 1883.

Rigler, Ueber die Folgen der Eisenbahnverletzungen. Berlin,

1879.

Rumpf, Beitrage zur kritischen Symptomatologie der traumat-
ische Neurose. Deut. med. Woch., 1895, p. 165.

BIBLIOGRAPHY OF THE TRAUMATIC NEUROSES. 22$

Saenger, Die Beurtheilung der Nervenerkrankungen nach Un-
fall. Stuttgart, 1896.

Schultze, Traum. Neurose. Neurol. Cblatt., 1889, p. 402 ; also,
Saml. kl. Vort. N. F., 14.

Seguin, Critical Digests in Sajous's Ann. of the Univ. Med. ScL,
1889, 1890, 1891.

Strauss, Ueber den Werth des Mannkopffschen Symptomes bei
Nervenleiden nach Trauma. JSerl. kl. Woch., 1892, p. 1222.

Striimpell, Die Traumatische Neurosen. Berliner Klinik,iSi2>?>;
also, Muench. med. Woch., December 3 and 10, 1895 ; ibid., Ueber
Untersuchung, Beurtheilung, und Behandlung von Unfallkranken.
Munich, 1896.

Thomsen and Oppenheim, Ueber das Vorkommen und die Be-
deutung der Sensorischen Anaesthesie bei Erkrankungen des cen-
tralen Nervensystems. Arch. fUr Psych., 1884.

Verh. des XII Internat. Med. Kongress, 1893.

Walton, Spinal Irritation : Probable Cerebral Origin of the
Symptoms. Bost. Med. and Surg. Journal, December 27, 1883.

Walton, Hysterical Ansesthesia brought on by a Fall. Bost.
Med. and Surg. Journal, December 11, 1884.

Walton, Contribution to the Study of the Traumatic Neuro-
psychoses. Journ. Nerv. and Ment. Dis., 1890, p. 432.

Westphal, Einige Falle von Erkrankung des Nervensystems
nach Verletzungen auf Eisenbahnen. Charity Annalen, Berlin,
January 6, 1880.

CHAPTER II.

TRAUMATIC NEURASTHENIA.

Neurasthenia is a condition of irritable weakness of
the nervous centers, as a result of which they become less
tolerant of external impressions and of the effects of fa-
tigue. It is a condition rather than a disease ; but, although
it most commonly occurs without there being any structural
lesion of important organs, its clinical picture is so typical
and its symptoms are so well marked that the disorder,
when pronounced, is usually spoken of as though it were a
disease. The clinical manifestations of neurasthenia are the
results of a loss of potential nervous energy. From what-
ever cause it may have been induced, the patient presents
the symptoms of a diminished power of resistance to the in-
fluences of fatigue and a hyperexcitability of the. nervous
centers. He is quickly exhausted by mental and physical
exertion, and reacts too strongly to all forms of peripheral
irritation. The neurasthenic is incapable of prolonged men-
tal or physical work, and such efforts are quickly followed
by confusion and fatigue. All the receptive centers are hy-
persensitive, so that there is a morbid increase of response
to all peripheral stimuli, and the individual becomes intoler-
ant of such slight irritations as pass in health, if not unob-
served, at least without being followed by sensations which
are painful.

Neurasthenia may exist in varying degrees. Temporary
nervous exhaustion naturally follows excessive work of any

kind. Any one who has become over-fatigued by mental

226

TRAUMATIC NEURASTHENIA.

227

strain or by excessive work, will present most of the symp-
toms of neurasthenia. But in the majority of persons, the
evidences of exhaustion which may be present at night
after a hard day's work, have vanished in the morning
when sleep has permitted a restoration of vigor to the nerv-
ous system. When the overwork is continued for too long
a time, however, or when the rest is inadequate, the symp-
toms, which at first were temporary, may tend to become
more and more permanent ; and the tired man or woman,
instead of presenting such effects of overwork as may be
easily repaired, may become a clinical type of pronounced
neurasthenia — a condition which requires more than ordi-
nary rest for its cure. Under the name of nervous prostra-
tion, neurasthenia has come to be a generally familiar affec-
tion. It is commonly spoken of as a disorder which is
directly amenable to the will, in that a person suffering from
it might be well if he could bring himself to believe that he
were not ill. This is true in part only. The nervous ex-
haustion has to a great extent robbed the patient of the
ability to control his own mental processes ; and to restore
the will power there must be a return of energy to the nerv-
ous centers, by the exhaustion of which it has been lost.

^Etiology. — Since the description of neurasthenia by
Beard, the disorder has been generally recognized. It may
complicate any of the chronic diseases, it frequently results
from overwork, anxiety, and excess of any kind, and in some
cases it develops without apparent cause. The fact that it
may develop primarily as a result of injury and shock has
only been recognized in recent years. When occurring in
this way it is called traumatic neurasthenia, and differs only
in slight particulars from neurasthenia due to other causes.
The back injury and the effects of litigation have given cer-
tain peculiarities to traumatic neurasthenia, but the under-
lying conditions and essential symptoms are the same in all
varieties of the disorder.

228 FUNCTIONAL EFFECTS OF INJURY.

Traumatic neurasthenia is by far the most frequent func-
tional nervous affection which occurs as a result of accident.
Its causation has already been described in a general way.
The disorder is infrequent in the old or in the young, most
commonly occurring in the active periods of life. It has
been reported as occurring in children. Vibert records two
cases of " traumatic neurosis " observed in children aged
respectively three and a half and five years. From Vibert's
description, these cases seem to present the symptoms of
psychic epilepsy rather than those of neurasthenia ; and
the functional nervous disturbances following accidents,
which I myself have observed in children, have been sug-
gestive of a more profound affection of the nervous system
than neurasthenia. Men are much more frequently affected
than women. Nervous predisposition, although demonstra-
ble in some cases, does not appear to be an essential factor
in the development of the disorder.

The accident is the most important causative factor of
traumatic neurasthenia. The fact that it very frequently fol-
lows accidents on railways gained for it the original name
of railway spine.

Although it also frequently follows any of the accidents
in which the factors of fright and physical commotion are
prominent, there is something about a railway accident
which seems particularly well adapted to call into action the
peculiar chain of nervous symptoms which are known as
neurasthenic.

The reasons for this can not altogether be explained by
the medico-legal aspects of railway accidents, although trau-
matic neurasthenia has become more frequent with the con-
stant increase in litigation. It may be in part explained by
physical reasons. Railway collisions and derailments usu-
ally put unusual strain upon the back, and pain in the back
is generally the first and most constant symptom of the dis-
order. In the course of non-traumatic neurasthenia, also, the

TRAUMATIC NEURASTHENIA. 229

backache is a prominent symptom. It may be that a rail-
way accident, in causing strain of the spinal ligaments and
muscles, and consequently pain in the back, furnishes at
the outset one of the most characteristic symptoms of neu-
rasthenia, to which general nervous shock and subsequent
events add others. The fact remains that most railway ac-
cidents do cause back strain, through the violent shaking of
the whole body, and traumatic neurasthenia usually begins
with pain in the back. In severe collisions the victim may
be thrown backward and forward many times before the car
ultimately comes to rest. The legs or the trunk may be
caught and jammed between the seats or other objects, and
the free portions of the body may sustain violent wrenches
and twists, which are felt chiefly in the spine. Even when
the passenger is merely thrown from his seat to the floor, or
pitched against the seat in front of him, the suddenness of
the force and the involuntary resistance which is offered by
the muscles of the trunk and back put considerable strain
upon the spinal ligaments and muscles. The sudden stop-
ping or starting of a train may cause the spine to be con-
siderably wrenched. Thus some cases of back strain occur
when there has been no serious accident. In addition to
the local injury, railway catastrophes usually cause the most
severe mental shock that can be imagined. An association
of these two factors, the physical and the psychical, is the
commonest cause of traumatic neurasthenia.

Can shock alone, when the back is not injured, cause
traumatic neurasthenia ? Such a result is unusual. If a per-
son is very much frightened by any accident he may in
future be morbidly nervous about re-exposing himself to
that especial variety of danger. A victim of a severe rail-
way collision may never again be able to feel at ease while
on the railway, although he may never have been physically
injured in traveling. It is a fact of common experience

that runaway accidents, even when no injury is received,
16

230 FUNCTIONAL EFFECTS OF INJURY.

may cause a timidity about driving which is never over-
come. But the morbid fears that result from accidents in
which no physical injury has been received are, in the ma-
jority of cases, systematized, and relate only to the particu-
lar form of accident by which the person has been fright-
ened.

When general neurasthenic symptoms develop from
fright alone, it is probable, in most cases at least, that the
perspn was in a nervous condition at the time of the acci-
dent, or that some injury was received which passed unob-
served.

However, when the nervous shock is severe, neuras-
thenia sometimes results, although the physical injury be
but trifling. Schaefer relates the case of a locomotive engi-
neer in whom the fear of an impending collision and over-
exertion in stopping the train produced typical symptoms.
In the following case also the physical element must have
been unimportant :

A Russian Hebrew, aged thirty-nine, came to the Vanderbilt
Clinic on June 3, 1896. He said that, until the preceding May,
he had always been healthy, and came of a long-lived and healthy
family. He had no bad habits, was married, and had several
healthy children. Denied venereal disease. He is a furrier by
trade. It is not probable, however, that this occupation had pre-
disposed him, by chronic mercurial poisoning, to nervous disease.
Although some workers in furs become poisoned by inhaling:
the mercury with which furs are prepared, such a result only
occurs when the furs are heated and the mercury is volatilized.
Our patient had been exposed to no such danger, and denied,,
furthermore, all symptoms of hydrargyrism. This man had no
motive for malingering. He has never had any thought or cause
of bringing an action; he is a member of no lodge or society.
When not at work, the only money he gets is drawn from what
little he has saved or what is earned by his wife. Since an acci-
dent, which must have, at best, been attended with slight physical
commotion, he has been totally unable to work. I saw the man
in February, 1897— nearly one year after the accident — when

TRAUMATIC NEURASTHENIA.

231

he told the following story and presented the following symp-
toms:

At the time of a fire at Bleecker Street and Broadway he was
leaning out of a window watching the disturbance. His head and
shoulders were out of the window, the abdomen resting on the
window sill and the feet on the floor.

As a result of the explosion of two boilers which were in the
burning structure opposite, the building in which he was at the
time was jarred, but not enough to break any glass or to cause
the plastering to fall from the walls. The man was very much
frightened, and he felt the concussion through his whole body,
but he was not dislodged from his place. Upon getting out of
the window frame, he fell down, but quickly picked himself up,
and was busy and constantly on his feet for the rest of the day.
That evening he went to bed, and stayed there for two weeks,
feeling weak and sick. Soon after the accident the patient began
to have pain in the back, and has had it ever since. There was
no vomiting, no loss of sensation, no trouble with the bowels or
rectum, and no paralysis. When well enough to leave his bed, he
tried to resume work again, but could not do so on account of
the trembling of the fingers and the pain in the back.

He is a man of fairly good color, but has the anxious, tired
look of neurasthenia. The back is painful in its whole extent —
from the cervical to the lumbar region. Pressure over the spinous
processes is painful, but does not cause the heart to beat more
rapidly. The skin over the whole back is hypersensitive. There
are no evidences of organic disease. The pupils are equal, and
react readily to light. The optic nerves are normal. There is
a slight peripheral limitation of the visual fields, although it is
difificult of determination. There is nowhere any loss of sensa-
tion. There is marked tremor of the face and in the hands, con-
stant, but becoming intensified by movement. The gait is slow
and uncertain ; the knee-jerks are normal. Appetite good ; bowels
regular. During his illness the patient has lost eighteen pounds.

In this case there was some physical shaking, although it must
have been very slight.

In some rare cases there seems to have been no injury at
all. Thus, in a case of Page's :

Neurasthenia induced by fright. Previous anaemia. A lady,
aged twenty-four, was in a collision which took place at night

232 FUNCTIONAL EFFECTS OF INJURY.

without the slightest warning. The baggage fell all over the car-
riage, and her husband was thrown against her, but she herself
was neither thrown from her seat nor injured in any single part.
As soon as she got out she was much alarmed at seeing a carriage
had been smashed to pieces, and then she watched a man being
rescued from the debris in which he was buried. She went on her
journey, and the next day felt, to use her own words, as though
she had passed through something terrible ; and from that time
onward she became sleepless, lost her appetite and strength, suf-
fered from pain in the back of the head and at several spots down
the spine, and was quite upset by any attempts at household work
or by reading and writing. Thinking she had not been hurt, her
friends urged her to do as much as possible, and not to give way,
but she steadily got worse rather than better ; and although not
in the least hysterical, it was not until proper treatment was be-
gun that improvement set in. The case was complicated by
previous dysmenorrhcea and anaemia, both of which were in-
creased for a time by the accident.

These cases show that neurasthenia may result from
fright v^hen the physical injury has been insignificant. It
may, on the other hand, follow traumatisms by which the
patients were hurt before they knew that they were in dan-
ger, and so escaped the fear of impending injury. These
latter cases are unusual, for shaking of the whole body or
injury to the back rarely occurs without there being at the
same time some terrifying factors. Few participators in
railroad accidents escape without being very much fright-
ened ; and when physical injuries are received in any way
there is usually a period, even though it be momentary, of
antecedent alarm. The fright, however, is often trifling,
as when caused by the sudden starting of a train, or a fall
on the sidewalk or from the steps of a carriage. As is well
known, neurasthenia may follow such accidents.

The gravity and duration of the symptoms are not always
in proportion to the severity of the accident, although in
general the more severe the accident the more rebellious
will be the resulting neurosis.

TRAUMATIC NEURASTHENIA. 233

As neurasthenia is a condition, it may exist in very
widely varying degrees of severity. Many persons find
themselves after an accident more nervous and more easily
fatigued than they were before ; but the impairment of
general health or strength may be so slight that they do not
complain, and, by continuing their work and thus keeping
their attention away from their own troubles, they institute
without knowing it the very best treatment they could have.
It is in such cases as these that the anxiety attendant upon
bringing claims or litigation may render very serious a dis-
order which otherwise would have been trivial.

Contrasted with the frequency with which neurasthenia
remains a mild affection, is the fact that it may be very
severe, and render its victim totally incapacitated for work.

In recognizing that many cases are transitory and easily
repaired by proper means, sight should not be lost of the
fact that the disorder may be intractable or even incurable.

Pathology. — Little is known of the pathology of neuras-
thenia. It rarely kills, and there are no recorded autopsies
in which lesions were found sufficiently adequate to account
for the neurasthenic symptoms. In the autopsies which
have been made on persons who died during the course of
the disorder the nervous system has not been examined with
sufficient care to discover any morbid appearances in the
ganglion cells. Hodge and, more recently, Lugaro have
shown, however, that visible alterations of form and struc-
ture occur in the ganglion cells of animals as a result of
fatigue. And since fatigue is the most prominent feature in
the clinical picture of neurasthenia, it is to be inferred that
the pathology of the disorder is to be sought for in the
nutritional disturbances of the ganglion cells. It would be
useless to speculate here as to how these changes are
brought about, or what their essential characteristics are.
It is enough to say that it seems probable that, to explain
the disturbances of function, there are structural changes

234 FUNCTIONAL EFFECTS OF INJURY.

which may eventually be seen and to a certain extent under-
stood. But, until our knowledge regarding the pathology
of neurasthenia is more exact and full, it must continue to
be classed with the functional diseases.

Symptoms. — In describing the symptoms of traumatic
neurasthenia it must be understood that they can only be
regarded as belonging to that category when they can not
be ascribed to organic injury of the nervous system, or to
functional nervous disease more serious than nervous ex-
haustion.

The mode of onset of the symptoms is subject to many
variations. The character of the accident and the influences
by which the patient is surrounded both before and after
its occurrence, cause great differences in their development.
Persons who are asleep when the accident occurs are spared
much of the shock and are less liable to injury. The same
is true for persons who are drunk. The two conditions,
sleep and intoxication, render the development of neuras-
thenia less probable.

Immediately after the accident there may be consider-
able prostration and shock. The patient does not lose con-
sciousness, but is pale, dizzy, tremulous, and nauseated, with
cold skin and rapid pulse. If there is head injury, and
sometimes when the head has not been injured, conscious-
ness may be lost for a variable length of time. If the body
has been severely bruised or lacerated, the earliest symp-
toms may be entirely surgical. The latent period, includ-
ing the time between the accident and the first appearance
of neurasthenic symptoms, varies in duration. It is usually
only a few days, though it may last for several weeks.

The ultimate development of neurasthenic symptoms is
to a great extent modified by those influences which sur-
round the patient immediately after the accident. Those pa-
tients do best who can put themselves immediately in a
physician's hands without thinking too much of claims for

TRAUMATIC NEURASTHENIA. 235

damages. Litigation may help the pocket, but does so at
the expense of health. By avoiding it the appearance of
neurasthenic symptoms may oftentimes be entirely avoided.

The symptoms of traumatic neurasthenia are various and
will require examination in detail. When the disorder dates
from the time of a railway disaster, the story is often some-
what as follows : A previously healthy man while riding in
a railway car is suddenly startled by the screech of the loco-
motive, and almost immediately afterward experiences a
sudden physical shock, is thrown violently from his seat to
the floor, where he is flung backward and forward, receiv-
ing blows upon the head and back. Or he may have been
caught between two seats and his back twisted or wrenched.
When the car has finally come to rest he finds himself very
much dazed and confused, though usually does not suffer
much pain. He frees himself or is extricated from the
wreck, and may assist in rescuing others, or may at once
go to some place of shelter. If there are houses near by he
usually walks to one of them, unless he has been severely
wounded. If the accident has occurred in the open coun-
try, away from any habitations, he may be exposed to the
weather until assistance arrives. He is usually nauseated,
and may vomit, and sleeps badly the following night. In a
day or two he begins to have pain in the back. From that
time on occur, in varying degrees, the symptoms of neuras-
thenia. The history will, of course, vary with the kind of
accident, but the salient features of it are usually that the
patient was at first more frightened than hurt, and that the
symptoms only appeared some time after the accident.

The mental symptoms constitute the most character-
istic feature of the disease. In the milder forms the fret-
ful, querulous invalid may be regarded as hypochondriacal
but not as out of his mind. When the symptoms are de-
veloped in their highest degree they bring the patient
very near to the border land of insanity. The neurasthenic

236 FUNCTIONAL EFFECTS OF INJURY.

is irritable, introspective, depressed, and inattentive ; he
quickly tires of any prolonged effort ; he is emotional and
fearful, and does not sleep well. A previously strong,
healthy, and active man may, after some trivial accident,
become entirely changed. Little things which previously
passed unnoticed become matters of annoyance. Slamming
of doors, loud talking, slight jars and noises, become to him
unbearable. An unexpected sound may cause his heart to
palpitate very violently. Strong light hurts his eyes. He
likes best to sit or lie in a darkened room, removed from all
causes which may irritate him. Some patients take to their
beds almost immediately after the accident, and stay there
for weeks or months. In a case which I saw in consultation
with Dr. A. W. Warden, in reference to a claim on the Met-
ropolitan Traction Company, the patient remained in bed
for many months.

She was a single woman, thirty-eight years of age, of neurotic
temperament, who, previously to the accident had always been rea-
sonably well. On May 13, 1896, an open car in which she was sit-
ting was struck by a cable car. The jar was considerable and
the woman was thrown forcibly against the back of the seat.
She was very much frightened, but was not thrown from the
seat, nor did she experience any severe pain at the time. She
felt sick and faint, but was able to walk. She went immediately
to bed, where she stayed for five months, a prey to the customary
neurasthenic symptoms. Pain in the back, difficulty in urinating
(partly due to a pre-existing retroversion of the uterus), difficulty
in breathing, nausea, vomiting, and flushings of the face were, at
one time or another, prominent symptoms.

Our examination in August failed to detect any evidences of
organic nervous injury. There was no anaesthesia, no limitation
of the visual field, no paralysis, no disturbances of the functions
of the bowels or bladder, except such as might be explained by
the local pelvic conditions. The patient was depressed, tremu-
lous, and anxious. The back was hypersensitive in its whole ex-
tent. Pressure on the vertebral spines in the thoracic and lower
cervical regions caused very decided expressions of pain. The
patient could walk, but was afraid to do so. The gait was slow.

TRAUMATIC NEURASTHENIA.

237

hesitating, and uncertain. She complained of dizziness, but could
stand perfectly well with closed eyes. The after-history is in-
teresting. From the time of the accident until October — five
months — the patient was in bed. In October she began to walk a
little about the house, and in November her claim was satisfac-
torily adjusted. But after receiving the money the improvement,
instead of continuing, stopped, and in February, 1897, Dr. Warden
told me that she was in bed again, worse than she ever had been.

The neurasthenic is fretful, fault-finding, and peevish.
His chief interest is in matters directly connected with his
own condition. He observes all his symptoms, and from
superficial reading of medical books he often thinks himself
the victim of innumerable diseases. While solicitude for
his family or his business is usually not lost, it is made to
yield the foremost place in his thoughts to the anxiety about
his own health.

Introspection is an almost constant symptom. The pa-
tient notes and speculates upon the variations in his feelings.
He talks the most willingly to those who will listen the most
patiently to his complaints. He constantly visits the physi-
cian, though he is rarely satisfied with one, but goes from
one doctor to another. Any one who, even when in fairly
good health, is persistently on the alert for some deviation
from the normal of his own physiology, will rarely fail to
detect it. But the healthy mind can usually satisfactorily
account for and dismiss without thought such trivial symp-
toms as a slight palpitation of the heart or an irregularity
of the digestive apparatus. The neurasthenic thinks over
such symptoms, and through constant attention they are apt
to be made worse. As a consequence, he becomes depressed.
Neurasthenic depression is different from the depression of
melancholia, although these two conditions may occur to-
gether. In neurasthenia the depression is in regard to the
patient's own prospects and chances of recovery. Unlike
the melancholiac, the neurasthenic rarely loses hope of ulti-
mate restoration to health, but he is discouraged at its long

238 FUNCTIONAL EFFECTS OF INJURY.

postponement. Every new symptom, or every aggravation
of a pre-existing symptom, adds to his low spirits. Yet he
rarely becomes absolutely despairing. If suicide occurs, it
is probably the result of something more than traumatic
neurasthenia in a person previously well.

Added to these symptoms are often many others, the
most characteristic of which is mental fatigue. The neuras-
thenic mind usually becomes quickly tired, and is incapable
of prolonged effort. The patient may find it almost impos-
sible to keep his attention for any length of time on any
subject not directly connected with his own state of health.
Many cases are entirely unable to keep at work. When a
neurasthenic begins to read, he soon lays the book aside.
If he plays a game, his interest is not in it and he quickly
wishes to stop. Besides the lack of interest in any mental
effort, protracted intellectual work is followed by an in-
■ crease of the various subjective symptoms of which neuras-
thenics so frequently complain.

The will power may become impaired through the com-
bined influences of fear, lack of interest, and lack of atten-
tion. 'The neurasthenic can ordinarily make the simplest
decisions only after much hesitation and doubt. Important
questions to be acted upon excite him very much, and ne
frequently declares himself incapable of deciding them.
There is, however, no real impairment of intellectual ca-
pacity, except such as may not be explained by hesitancy
and lack of close attention. The memory remains good,
though the patient often believes the contrary. There is
little change in the quality of the reasoning powers, when
the patient can be brought to use them.

Fear is a conspicuous symptom. R6gis classes the whole
group of the morbid fears, which are insane fears, under the
head of cerebral neurasthenia. In traumatic neurasthenia,
however, the fears rarely take systematized forms, except in
so far as all circumstances which relate to the accident are

TRAUMATIC NEURASTHENIA. 239

held in dread. It is unusual to observe fear of any one par-
ticular thing, such as fear of contamination (mysophobia) or
fear of closed places (claustrophobia), or any of the various
systematized forms commonly observed in certain insanities.
In traumatic neurasthenia the condition is one of timidity
and shrinking, rather than of active fear. The patient is
afraid to go out lest he become dizzy ;' he is afraid to meet
people lest they tell him how badly he is looking; he is
afraid of anything which causes his mind to revert to the
accident in which he was injured. If he were injured on a
railway, he is very unwilling to undertake a railway journey.
If in an elevator, he prefers the safer method of walking up-
stairs.

Some head injuries, however, even when there are no
symptoms of fracture of the skull or of cerebral concussion,
are followed by effects similar in many ways to the manifes-
tations of cerebral neurasthenia as described by R6gis.

Dr. Starr has kindly communicated to me the history of a
young man, twenty years of age, previously strong, active, and
healthy, who, during a football game, was thrown on his head.
He was momentarily stunned, but continued playing. The team
of which he was an important member was badly beaten, and its
•defeat was, in part at least, explained by the fact that the injured
man made mistakes in the signals and so broke up the whole sys-
tem of team play. The young man himself remembered nothing
of the latter part of the game. After this injury he slept badly,
was nervous and irritable ; a few weeks later he suddenly dis-
appeared, and nothing was heard of him for four days. When he
returned to his family he could give no clear account of his ab-
sence. He said that he had felt as though some one were after
him and as though it were necessary for him to get out of the
way. He was seen at this time by Dr. Starr, who found him quiet,
composed, with the ordinary symptoms of neurasthenia. A short
time after this the patient had an attack of great excitement, dur-
ing which he felt himself obliged to go out and walk, and felt like
knocking down every one he met in the street.

Since the football game, six years ago, this young and appar-
ently strong man has led a life of invalidism. He has wandered

240 FUNCTIONAL EFFECTS OF INJURY.

about to various water cures without fixity of purpose or power
of concentration. His conduct has been erratic, and he is in con-
stant dread and fear of indefinite things. There have never been
any periods of unconsciousness. He is depressed, hypochondri-
acal, and melancholic, and is said to have attempted suicide.

In neurasthenia the speech is sometimes indistinct and
thick, resembling the speech of the general paralytic. But,
unlike the general paralytic, the neurasthenic can at once
correct his speech defects virhen his attention is called to
them, and then he can articulate perfectly well. The
sleep may remain normal. Ordinarily, however, it is bro-
ken, and in traumatic neurasthenia is frequently attended
with nightmares. The bad dreams often relate to the acci-
dent. Neurasthenics are very emotional. Sudden noises,
the sight of trifling accidents, or even thoughts of the acci-
dent of which they themselves have been the victims, may
be followed by evidences of great excitement. Under such
circumstances the patients become tremulous and confused,
can speak only with difficulty, and are conscious of pras-
cordial oppression and palpitation of the heart. They are
rarely subject to outbursts of laughter, but tears come
easily.

It is only in the severer forms of the neurosis that all of
these symptoms are present. They vary in number and de-
gree in individual cases. But usually the picture of trau-
matic neurasthenia is a picture, as Knapp has said, " of the
complaining, irritable, nervous invalid." When he tries to
work he finds himself incapable of keeping his attention
upon what he has to do. Efforts to concentrate the atten-
tion are followed by an increase of subjective symptoms.
He may be almost constantly a prey to the annoyances of
peculiar subjective sensations, and he describes his suffer-
ings as more severe than they really are. He becomes
alternately hot and cold ; he has flushing of the face, his
ears ring, he gets dizzy, his head aches, and he becomes

TRAUMATIC NEURASTHENIA.

241

confused. As a result of the discomfort from which he con-
stantly suffers, and from a fear that any unusual excitement
may make it worse, he prefers staying at home to going into
crowded places or on the street. He shuns society, and,
after his condition becomes generally known, society, unwill-
ing to listen to constant complainings, is glad to shun him.
In traumatic hysteria the mental state has many characteris-
tics similar to those of traumatic neurasthenia, but there are
also some differences. The hysteric is more silent under
his sufferings, resembling in this respect more closely the
type of melancholia. He broods more, but he talks less.
The hysteric has to be questioned in order to find out the
nature of his mental inquietude. The neurasthenic describes
his sensations and feelings with exaggeration, with an un-
necessary elaborateness of detail, and seeks opportunities to
voice his complaints ; the hysteric talks about them only
when he is interrogated.

That some of the symptoms of neurasthenia might be
controlled there is no doubt. But many of them are be-
yond the control of the patient and cause him much dis-
comfort. Those thoughts must indeed be painful which can
make a man, previously strong, healthy, and active, lose all
inclination and ability for his work, and become more or less
oblivious to the interest of his household.

The facial expression often tells the story. It indicates
not so much bad health, as discouragement, anxiety, and
fatigue. In it can be read the eternal worry and self-ques-
tionings which are going on in the mind. The face may be
pale, though very often if previously the cheeks were red,
they do not lose their color.

It is a fact, which is often hard to bear in mind, that the
complaints and actions of the neurasthenic depend upon
actual disturbances of the nutrition of the ganglion cells, for
which he is largely irresponsible. He makes the complaints
because the ganglion cells are exhausted, and he keeps the

242 FUNCTIONAL EFFECTS OF INJURY.

ganglion cells from being repaired because he so constantly
thinks of his own troubles.

Thus he finds himself in a vicious circle. By constantly
thinking of his own ills he renders his condition worse. Yet
the same fatigue of nervous tissue which has caused the
change in his character and health robs him of his independ-
ence and prevents him from withholding his attention from
the trivial annoyances which are passed over unheeded by
healthy men. It is only by an appreciation of this fact that
the neurasthenic can be treated with the consideration he
deserves, and not summarily dismissed as a person whose
only disease is too much thinking about himself.

Most of the mental symptoms of neurasthenia are sub-
jective. The physician becomes cognizant of them chiefly
through the confidences of his client ; and although an ex-
perienced physician can usually tell in how far the recital is
genuine, he has no means of being positive that all the com-
plaints to which he has to listen are really believed in by the
patient. It is the fact of subjectivity of symptoms which in
negligence cases may tempt men to become malingerers, and
which often gains for the neurasthenic patient the name of
cheat.

Motor Symptoms. — Paralysis does not occur in traumatic
neurasthenia, for gross lesions of brain, spinal cord, or pe-
ripheral nerves are absent, and functional paralyses occur ex-
clusively as a result of hysteria. Yet, although no individual
muscle or group of muscles completely lose their powers, or
present degenerative electrical reactions or atrophy, the
vitality of the whole muscular system is very much lowered.
Muscular force is only slightly impaired. A more striking
symptom is the quickness with which the muscles become
fatigued. Single movements may be performed with nearly all
their original energy, but muscular power rapidly becomes
exhausted. The muscular fatigue can not be referred to the
muscles alone. In every voluntary movement the stimulus

TRAUMATIC NEURASTHENIA.

243

passes from brain cortex along nerve fibers to muscles ; and
in the muscular fatigue of neurasthenia all these elements —
nerve cell, nerve fiber, and muscle cell — share ; so that the
apparent muscular weakness of neurasthenia is only another
expression of the general condition of the nervous system in
that disorder. When the muscles become tired there is in-
variably an increase of other symptoms ; the general nerv-
ousness becomes worse and the subjective discomforts are
intensified. The speed with which the muscles tire may be
seen in many ways. Sometimes on standing only for a few
moments the legs seem to give way, or there is often some
shaking of the body when the eyes are closed. The gait,
except in so far as it is afifected by lumbago, presents nothing
unusual. The patient moves slowly, but he lifts his feet
from the floor and walks steadily. He can not, however,
walk far. A man who before the accident could walk
miles without fatigue, may become extremely exhausted by
the walk of a few blocks. Some patients walk little or not
at all for many months. The muscular efforts necessary for
the performance of the ordinary duties of the toilet are very
fatiguing, and the patient may be obliged to sit down several
times while dressing himself. The finer co-ordinated move-
ments of the fingers are imperfectly performed. There is
difficulty in writing, in buttoning the clothes, etc. This is
partly due to tremor and partly to the rapidity with which
all the muscles, but especially the smaller ones, become ex-
hausted.

Tremor is a frequent symptom. It resembles very closely
the tremor seen in alcoholism or in confirmed tea-drinkers.
It is fine, rapid, and regular, becomes somewhat more pro-
nounced on intended movements, and is much intensified by
emotional influences and by fatigue. At times it disappears
altogether. Its most frequent situations are the tongue, the
face, and the hands. The tremor observed in the eyelids
when they are half closed, commonly spoken of as a neuras-

244 FUNCTIONAL EFFECTS OF INJURY.

thenic symptom, occurs too frequently in normal individuals
to be regarded as a diagnostic sign of any great value.

Sensory Symptoms. — Among the various symptoms com-
plained of in traumatic neurasthenia, pain in the back is the
most frequent and the most prominent. It exists in two
forms : First, it may be of a dull, aching character, nearly
constantly present, and affect the whole back, or, as more
commonly occurs, be limited to the neck or to the lower
part of the spine. Its most frequent seats are in the cervi-
cal and thoracico-lumbar regions. It is extremely indefinite
in character, changing about from day to day. Even at the
time of a medical examination the point of most marked
hypersensitiveness to touch changes its location by several
vertebrae within a few minutes. For example, at the first
examination the tenderest spot may be found over the spi-
nous process of the third thoracic vertebra, and ten minutes
later the seventh thoracic spine is found the most sensitive.
The pain is aggravated by bodily or mental fatigue or by
digital pressure over the vertebral spines, and is generally
similar to the backache frequent in simple neurasthenia.
Pain of this character is in large part an expression of
fatigue, and exists independently of injury to the spinal col-
umn.

Secondly, and more frequently observed in traumatic
neurasthenia, is pain in the back of a different character,
which is due to actual back sprain. Our knowledge of this
condition, in regard to the cases resulting from railway
accidents at least, is largely due to Page. The affection
has come to be known as traumatic lumbago, and merits a
separate description.

Traumatic Lumbago.

Traumatic lumbago, since it depends upon actual injuries
sustained by the vertebral column, can not be classified
among functional nervous diseases. Yet it is so frequent an

TRAUMATIC LUMBAGO. 245

accompaniment of neurasthenia, and so rarely fails to become
complicated by neurasthenic disturbances, that it may best
find its description at this place, among the symptoms of
neurasthenia. Lumbago is usually the first symptom to ap-
pear after the accident, and ordinarily lays the foundation
upon which the functional manifestations are superposed.

The confusion which for so many years existed in regard
to the nature of the nervous disorders which most frequently
follow railway accidents was in large part due to the fact
that traumatic lumbago was supposed to be dependent upon
injury to the spinal cord. Although the symptoms are often
serious, and in some respects similar to those caused by
organic injury to the cord, it has been proved, with a rea-
sonable degree of certainty, that in lumbago the spinal cord
is not injured at all. Injury to the spinal cord is rarely fol-
lowed by complete recovery. Complete recovery is the
rule in lumbago — a disorder which is never fatal. In lum-
bago there is no anaesthesia, no loss of sphincter power, and
no paralysis that the patient can not overcome unless the
nerves have been stretched or torn ; when the spinal cord is
injured some or all of these symptoms are present. There
is also now little reason to doubt that the kinds of injury
which most frequently cause a strain of the muscles and liga-
ments of the back are essentially different from those which
-cause disturbance of the contents of the spinal canal. In-
traspinal haemorrhage, or laceration, or other damage to the
spinal cord is almost exclusively the result of extreme vio-
lence. Yet, since such conditions have occasionally followed
accidents which were apparently trivial, it can not be posi-
tively said in any given case that the spinal cord has escaped
injury until examination has shown that its functions remain
unimpaired.

Traumatic lumbago itself depends upon strain or lacera-
tion of some of the numerous structures which protect the
spinal cord. The vertebrae through which the spinal cord
17

246 FUNCTIONAL EFFECTS OF INJURY.

passes are held in place by many ligaments, and between
each bone is a disk of cartilage. The bones and ligaments
are surrounded by numerous muscles, which give protection,
support, and the power of movement to the spine. The es-
sential characteristics of the vertebral column are flexibility
and strength. Yet, while considerable movement is possible
in the spinal joints, especially in the cervical and dorsal re-
gions, these movements are limited by the spinal ligaments,^
and, if they are carried too far, the ligaments will be strained
or torn.

There is convincing evidence in support of the view that,
traumatic lumbago depends upon more or less extensive
lesion to the ligaments or muscles, or to some ether of the
structures which are in relation with the vertebras. From
the anatomy of the spinal column it is obvious that these
injuries may easily result from sudden twists or wrenches of
the spine, such as are so frequently received in railway and
similar accidents, or as may occur through blows or falls on
the back, or through lifting heavy weights. Also, the clinical
type of the affection is identical, when due allowance is
made for differences in function, with those observed in in-
juries to ligaments, articular surfaces, and muscles situated
elsewhere.

The symptoms of spinal sprain appear soon after the in-
jury, though it is several days before they reach their maxi-
mum intensity. The chief characteristic of the condition,
and indeed the one which is the basis for most of the others,
is pain in the back. The pain is usually not spontaneous ;
that is, if the patient is perfectly motionless he may be fairly
comfortable. But the slightest motion in the affected part
causes the pain to become active. Now, almost every move-
ment of the body causes some motion in the spinal joints.
Most movements of the head and neck, any movements of
the arms, the use of the muscles of the abdomen, chest, or
back to effect changes in position, or for expulsive acts, the

TRAUMATIC LUMBAGO.

247

movements of the legs — all are associated with more or less
extensive changes of position in the spinal column. Simi-
larly, slight jars or shakes are transmitted to the spine, and
by causing movements such as pass unnoticed by healthy
persons, quickly induce an increase of pain in parts which
are affected. Consequently there are very few moments dur-
ing waking hours when these patients are comfortable, be-
cause it is almost impossible for any one to remain perfectly
still voluntarily. The pain is severe and real. At the slight-
est movement the patient cries out. The face is drawn and
expressive of past suffering and of apprehension of suffering
to come. In severe sprains of the back the whole vertebral
column, from the skull to the pelvis, is hypersensitive.
More commonly, however, the pain is limited to certain re-
gions, sucH as the neck or the dorsal region. It may be
limited to the coccyx, causing the condition known as coc-
cygodynia. The skin over the painful places is usually
not hyperassthetic, although sometimes the slightest touches
are badly borne. As Page suggests, it is probable that ex-
treme hypersensitiveness of the skin is due to the fear of
being hurt. Previous examinations have taught the patient
that manipulation of the back is painful, and so he dreads all
contact, and may cry out that the physician has hurt his back
before the back has been touched. Deep pressure, however,
either of the back muscles or of the vertebral spines, almost
always causes pain in traumatic lumbago, although it does
not invariably do so in lumbago which is not of traumatic
origin. The muscles are tender to the touch, probably
through injury to the muscle fibers. When pressure is made
on any of the vertebral spines which are in the painful areas,
pain, often very severe, is felt at the seat of pressure chiefly,
but may also radiate up and down the back. There can be
no doubt of the genuineness of this symptom. If, before the
pressure is made, the finger of the examiner is placed upon
the pulse of the patient, it may sometimes be found that the

248

FUNCTIONAL EFFECTS OF INJURY.

spinal pressure causes a considerable acceleration of the
pulse rate. This test— the Mannkopff test, previously de-
scribed (see page 219) — is utilized for the purpose of de-
tecting simulation, or the voluntary exaggeration of spinal

pain. It is a sign of con-
siderable though not of
unfailing value, and is not
always present in trau-
matic lumbago. If the
heart beats faster when
the pressure is made, it is
certain that there is either
real pain, or that the pa-
tient is genuinely afraid
that he is about to be
made to suffer ; the heart
can not voluntarily be
made to materially in-
crease its rate.

The muscles of the
back are usually in a
state of spasm, a condi-
tion which may be very
marked. In a recent Van-
derbilt Clinic case, illus-
trated in Fig. 42, the back
muscles were so tense that
they felt like boards.

In this case the immobil-
ity of the back was extreme.
The patient had received a
severe fall on the buttocks,
soon after which the symptoms became very marked. Not only
was the whole back held as though in a vise, but all movements
of the head, arms, and legs were reduced to a minimum. In
standing, the body was inclined slightly forward, with the hands

Fig. 42.— Characteristic attitude in traumatic
lumbago. (Vanderbilt Clinic. )

TRAUMATIC LUMBAGO.

249

pressed against the thighs ; there was almost no change of posi-
tion in the trunk when the patient sat down ; and in walking, the
legs were dragged forward in short steps, the feet being watched
with as much care as the rigid position of the head permitted.

The attitude usually assumed by the patient with trau-

matic lumbago is due entirely to the pain. He puts himself
in the position in which he is least liable to receive any jar
or vibration, and which permits the greatest freedom from
movement of the back. Only those voluntary acts which
involve the least change in position of the vertebral joints
are undertaken. The spine is held as rigid as possible,
which results in very characteristic attitudes and move-
ments. In standing, the back is seen to be held perfectly
stiff. It is usually bent somewhat forward, and, from an in-
crease of sensitiveness on one side, there may be a slight
curvature. To look up, down, or around, the patient bends
or turns the whole body, holding the neck stiff. Movements
of the arms are performed very slowly ; if the patient is to
stoop down, instead of stooping in the ordinary way, which
would involve bending of the back, he usually goes down on
one knee, holding the back perfectly straight. In getting
up from a chair, or in changing the position of the body
when sitting or lying down, the hands and arms are called
into service, in order that the muscles of the back and abdo-
men may do as little work as possible. In getting up from
the floor the patient may " climb up the legs with the hands,"
as the patients with progressive muscular dystrophy do. In
getting up from the sitting posture, the hands are placed on
the thighs, and the body assisted up in this way.

From similar reasons there may be striking interferences
with gait. The patient walks with slow, hesitating steps,
lifting his feet but slightly off the ground, and sometimes
actually dragging one or both feet. The interference with
gait, through pain in the back, often has the appearance of
true weakness in the legs, although in reality the legs are as

;o FUNCTIONAL EFFECTS OF INJURY.

Tong as ever, and appear weak only because the patient is
■raid to. move them.

In some patients the power of walking is altogether lost
)r a time, as is shown by the following case which was
jferred to me for examination relative to a claim upon
le Delaware, Lackawanna and Western Railway for injuries
;ceived in a collision on January 15, 1894 :

The patient had been bruised about the back and buttocks,
id for two weeks was in bed hardly able to move his legs at all,
scause every movement caused such severe pain. At the end of
ve weeks he could turn over in bed, and soon after began to get
round on crutches, which he was obliged to use for nine weeks.
[e ultimately made a complete recovery.

The patient often attributes the interference with walk-
ig to spinal disease. Thus a gentleman suffering from
epical lumbago, not of traumatic origin, because he had
oticed that he did not lift his feet from the ground with-
ut pain, thought he was suffering from locomotor ataxia,
laving read a little medicine, he came to me to have his
nee-jerks tested. In traumatic lumbago unaccompanied
y anj'^ injury to the spinal cord or nerve roots, the reflexes
;main unchanged. The leg is often held stiff, but the
nee-jerk ma}' be elicited, although re-enforcement is some-
mes necessary. Disturbances of the functions of the blad-
er and rectum are occasionally observed. They are para-
lic in appearance, but not in fapt. Through the pain
lused by the contraction of the diaphragm and the ab-
ominal muscles, the patient performs the expulsive acts
i infrequently as possible. Constipation and temporary
;tention of urine are the results. It sometimes happens
lat there may be a little dribbling of urine, caused by an
ivoluntary overflow of a too full bladder, which the pa-
ent is afraid to empty on account of the pain. There is
3ver, however, any true incontinence or retention of urine
r incontinence of faeces.

TRAUMATIC LUMBAGO. 25 I

Pain caused by movements may make it difficult for the
patient to go to sleep, or during sleep he may be constantly
aroused by the pain.

The duration of traumatic lumbago is variable. Ordi-
narily the intensity of the pain on movement begins to de-
crease after three or four weeks. But the back usually re-
mains sensitive for a long time, and in many cases the patient
never feels that his back is as strong as it was before the ac-
cident.

A switchman, who was struck in the back by the front plat-
form of a cable car, came to the Vanderbilt Clinic four months
after the accident. He had become entirely free from neuras-
thenic symptoms ; yet the pain in the back, although much better
than it had been, was still very annoying, so that he frequently
had sharp twinges on sudden movements, and could not stoop
down without considerable discomfort.

The severe and persistent character of the pain ren-
ders lumbago a somewhat serious affection. By interfering
with sleep, exercise, and alimentary processes, and by caus-
ing constant suffering, it may make decided inroads on nu-
trition. By impairing the general health and by constantly
calling the patient's attention to his back, it materially assists
in the production of the neurasthenic picture. The patient
becomes unhappy and anxious, broods over his trouble,
thinks that his spinal cord is injured, and believes himself in
danger of becoming paralyzed^ — a fear which is not surpris-
ing when one considers how closely the limitation of move-
ment in lumbago may imitate paralysis.

While lumbago is a particularly frequent accompaniment
of traumatic neurasthenia, its occurrence in that disorder is
not constant, nor is it usually so severe as the picture which
has been drawn would indicate.

But the symptoms are always the same in kind, though
they vary greatly in degree. In its exaggerated form, in
which the back is held absolutely immobile and in which

;2 FUNCTIONAL EFFECTS OF INJURY.

1 the other symptoms are equally pronounced, traumatic
imbago is distinctly rare and only occurs as a result of
!vere injury to the back, such as may cause slight dislo-
ition in the spinal joints, or injury to some of the spinal
;rves.

It is much more common for the clinical picture to be
mited to pain and stiffness of the back, which do not seri-
jsly interfere with nutrition or cause disturbances which
ight be referred to interference with the function of inter-
il organs.

Headache is another common sensory symptom of trau-
atic neurasthenia. It may affect the occipital region, and
then complained of by the patient as " pain at the base of
le brain." Or it may be in the forehead and over the eyes,
milar in situation and character to the pain of constipation,
esides pain there may be various peculiar sensations in the
sad. The patient feels as though there were a tight band
"ound it, or as though he were wearing a heavy cap — the
'sque neurastMnique of Charcot. There are frequently sub-
ctive sensations which are complained of as noises in
le head, or feelings as though the skull were about to fly
jart. The mental confusion from which neurasthenics so
equently suffer is associated with a feeling of lightness and
sculiar sensations in the head. In addition to these some-
hat indefinite pains, people suffering from neurasthenia are
equently subject to neuralgia. The pain under such cir-
imstances is a true neuralgic pain, which follows the course
: the nerve trunks, and presents the painful points and other
^mptoms of neuralgia due to conditions of anEemia or mal-
jtrition.

If, at the time of the accident, any parts other than the
3ad or back were bruised or injured in any way, pain per-
sts in them for a longer time than it would in persons who
e not neurasthenic. The neurasthenic pays so constant an

TRAUMATIC NEURASTHENIA.

255

attention to local troubles that subjective disturbances which
accompany them are intensified and made to last longer than
they otherwise would.

Besides local pain, there is almost constantly present a
general feeling of fatigue which may amount to pain. The
patient says he " feels tired all over," a sensation much ag-
gravated by exertion or excitement. Hyperassthesia is also
common. As has been said, it is usually present in the pain-
ful spots of the back, so that pressure over the vertebral
spines is ill borne and may cause some acceleration of pulse.
The skin around such areas may also be hypersensitive, al-
though, as Page says, this is probably a hyperaesthesia of
education. Other regions of the body may also be the seats
of exaggerated sensibility. The scalp is often very tender.
It is usually a long time before injured parts may be touched
without causing expressions from the patient both of fear
and of acute pain. The muscles of the whole body, espe-
cially those of the chest, back, and legs, are commonly sen-
sitive to the touch and tender. Hypersesthesia becomes
more marked after any fatiguing influences.

Angesthesia does not exist in single traumatic neurasthe-
nia. It is frequent in hysteria, and occurs sometimes in the
serious forms of nerve disturbances, which will be described
as unclassified. For any case in which this symptom is
present, the prognosis is graver than that of simple trau-
matic neurasthenia. Neurasthenic patients often complain
of feelings of numbness, " pins and needles " or tingling, but
the examination shows that the situation of these sensations
is indefinite, and that all forms of cutaneous sensibility are
perfectly preserved. There are also various other subjective
sensations in neurasthenia. The complaint may be that
there is a feeling of shivering without being cold, or as if
cold water were running down the back, or as if electricity
were being applied, or of numbness in the legs or hands, or
other peculiar sensations of indefinite character.

254 FUNCTIONAL EFFECTS OF INJURY.

Special Senses. — Ocular Symptoms. — The visual disturb-
ances of this neurosis are usually considerable, although
there are, apart from possible pre-existing organic defects
or disease, no morbid changes in eye structure. The pupils
respond quickly to light, but the responses become pro-
gressively less prompt and complete by successive stimula-
tion. The pupils may also dilate and contract under psychic
influences. They are usually moderately dilated. When
light is thrown into the eye, the iris contracts and then
dilates again, and repeats this alternating contraction and
dilatation until it finally comes to rest in contraction. In-
equality of the pupils is usually regarded as indicative of
organic disease. Binswanger says, however, that inequality
may exist in neurasthenia without indicating organic dis-
ease if the pupils continue to react promptly to light. The
complaints of the patient relate to various disagreeable sub-
jectives feeling referred to the eyes, such as pain, burning,
flashes of light, black specks, and " everything getting dark
about him." The eyes are generally abnormally sensitive to
bright light, and they soon become painful from use. The
picture of the nervous invalid, sitting with the back to such
light as may be admitted through tightly closed blinds, is
generally familiar.

Asthenopia, or weakness of vision, is the most constant,
visual disturbance of the disorder. The eyes quickly be-
come fatigued, so that the patient no longer sees perfectly.
After short efforts at reading or writing the letters and words
become indistinct. The rapidity with which fatigue follows
any attentive use of the eyes interferes very seriously with
vision. The patient feels as though there were a veil before
the eyes, and he complains that they are blurred. Tests
with the perimeter show that the visual disturbances de-
pend, in part at least, upon fatigue of the retina, especially
in its peripheral portions. By successive or continuous ex-
ercise of its functions the retina loses some of its peripheral

TRAUMATIC NEURASTHENIA.

255

power. Thus the visual field is smaller the second time it
is tested than it was the first, smaller the third time than it
was the second. By repeated tests the field may become
very much contracted, or the patient may lose the power of
concentrating the attention upon the testing object. This
symptom of retinal fatigue has been called by Fbrster the
" shifting type of contraction " (Fig. 43). The most conven-
ient method for its determination has been described by

J..JS. n.B.

Fig. 43. — Shifting type of contraction of the visual fields in neurasthenia. (After Bass.)

Wilbrand and Sanger. By this method the testing object is
moved along the horizontal meridian of the perimeter from
without inward to the center, and is then continued across to
the limit of the field on the nasal side. The horizontal ex-
tent of the field before it has become fatigued is thus ascer-
tained. The object is then moved in the same meridian,
across the field back to the temporal side. If the retina is
easily fatigued, the testing object will on its return outward
have ceased to be perceived before it has reached the tem-
poral periphery of the original field. A similar limitation
will be found on the nasal side when the object is again

256 FUNCTIONAL EFFECTS OF INJURY.

moved inward. The shifting type of limitation is the same
for colors as for form. There is never a reversal of the nor-
mal color fields, such as is found in hysteria.

Limitation of the visual fields through fatigue may occur
to a certain extent in normal individuals, but the rapidity
and extent of the contraction in neurasthenia are charac-
teristic.

In neurasthenia the acuity of central vision is not im-
paired.

Of the other special senses, taste and smell are not af-
fected. Organic disease of the auditory apparatus forms no
part of the neurasthenic picture. Hypersensitiveness of
hearing is, however, a prominent symptom, which becomes
much intensified by any local ear disturbance. The hearing
is often remarkably acute. A neurasthenic patient of Bin-
swanger's is said to have been able, while sitting in the
house with the windows closed, to distinguish her husband's
footsteps from the noises of the street, and to recognize the
individual voices of servants who were talking two stories
below. In many cases of neurasthenia slight noises are
heard so distinctly that they become sources of considerable
annoyance, and may add to the severity of the other symp-
toms.

The ear is also frequently complained of as being the
seat of various abnormal subjective sensations, which are de-
scribed as ringing, buzzing, and other peculiar noises. They
are often very troublesome, and become more intensified by
general fatigue or by any temporary disturbances of health.
Dizziness is another symptom which may be referred to the
ear. It is of nearly constant occurrence in neurasthenia, but
it, too, is subjective rather than objective. The patient
complains that his head feels dizzy, that objects spin around
before him, that he is in constant fear of falling, and that he
is often obliged to sit down or to catch hold of surrounding
objects for support. Yet the objective evidences of dizzi-

TRAUMATIC NEURASTHENIA. 257

ness are usually wanting. When told to walk or stand, the
patient can usually hold himself steadily. Sometimes when
standing with the eyes closed there is some swaying of the
body, but it is never in any degree proportionate to the
amount of dizziness and unsteadiness of which complaint is
made.

Reflexes. — Neither the superficial nor the deep reflexes
^re ever lost in simple traumatic neurasthenia. When the
reflexes are either absent or diminished it should excite sus-
picion of more serious trouble than nervous exhaustion.
The deep reflexes 'may remain normal, but in by far the
larger number of cases their activity is increased. This in-
crease affects the two sides equally. If the refiex of one
side is more active than that of the opposite side, it is sug-
gestive of organic lesion. The knee-jerks are usually very
active, so that a slight tap on the patellar tendon induces
a quick, forcible, and extreme extension of the leg. Ankle
clonus occurs very rarely. It is more commonly a sign of
organic disease, and, although it may occur in slight degree
in neurasthenia, it then lacks the exaggerated character and
prolonged duration of the contractions seen in lesions of
the pyramidal tracts. The tendon reflexes of the upper
extremity — the extensor, supinator, triceps, etc. — are fre-
quently absent in health. In neurasthenia they are often
present or hyperactive. There is no standard by which the
normal activity of the superficial reflexes — cremaster, epi-
gastric, abdominal, etc. — can be determined. Some of them
may be absent in normal persons. In neurasthenia they are
usually lively. If there is pain or hyperaesthesia of one side
of the body, there may be an increase of superficial reflex
activity on that side. The reflexes, both superficial and
deep, share, with the other symptoms of neurasthenia, the
common characteristic of becoming quickly fatigued. With
successive blows on the tendon, the knee-jerk becomes pro-
gressively less, and may finally cease to respond altogether.

258 FUNCTIONAL EFFECTS OF INJURY.

The superficial reflexes also quickly tire in the same way.
Fatigue of reflexes may be induced in health, but in neuras-
thenia it supervenes much more quickly.

Vascular Disturbances. — Very few sufferers from trau-
matic neurasthenia escape some disturbances of the circula-
tion, of which the most common is palpitation of the heart.
This neurasthenic palpitation is not due to disease of the
heart itself, for that organ is normal in size and has no mur-
murs. Attacks of palpitation are sometimes sufficiently
severe to resemble the attacks of angina pectoris, so that dur-
ing them the whole prsecordium is made to vibrate by the
tumultuous action of the heart, and pulsation in the super-
ficial vessels is plainly visible. The pulse beats may be as
frequent as one hundred and thirty to one hundred and fifty
to the minute, or it may even be impossible to count them.
The pulse is quick, soft, and full, often intermittent and ir-
regular, without any increase of arterial tension. Pain over
the heart felt during the palpitation is often very severe.
The patient becomes alarmed, his face is anxious and drawn,,
he gasps for breath, although there is rarely any true dysp-
noea, and he experiences a variety of abnormal sensations
which he refers to the praecordial region.

These attacks occur in varying degrees of severity. It
is only rarely that there is any danger of confusing them
with those of true angina pectoris, a condition due to mor-
bid changes in the arteries or walls of the heart. In true
angina pectoris the patients are usually of an age when
arterio-sclerotic changes are most common, some evidences
of which may often be found. In that condition, also, attacks
come without apparent cause, and the pain, which exists for
some time before there appears any irregularity of the
action of the heart, usually radiates from the left shoulder
down the left arm. In neurasthenia, pain occurs more fre-
quently after than before the palpitation, and for neurasthe-
nic palpitation there can usually be found some immediate

TRAUMATIC NEURASTHENIA.

259

exciting cause, although it is often trivial. Sudden noises,
fright, or any slight mishap often bring on an attack. The
mere thought of the accident often causes the heart to beat
violently, and the patient may awake from a bad dream to
find that even in sleep psychic influences have acted upon
the innervation of the heart. In addition to palpitation the
heart action in neurasthenia may apparently remain accel-
erated for long periods of time, beating ninety or one hun-
dred or even more times in a minute.

In connection with long-continuing neurasthenic tachy-
cardia arises the question. Does it lead to structural altera-
tion in the heart muscle ? Oppenheim reports cases which
seem to have resulted in this way, and Knapp inclines to
this view. That in neurasthenia, even when the patient is
at rest and undisturbed, the heart may beat a little more
rapidly than usual, is possible, although difficult of proof.
But that such an increase in the pulse rate, unaccompanied
by other factors, ever leads to hypertrophy and dilatation of
the heart, seems a matter of considerable doubt. It may as-
sist in the development of a pre-existent tendency to cardiac
degeneration, or it may accentuate symptoms which had
passed unobserved. But it is difficult to believe that a per-
son whose vascular system was previously normal is in any
danger of disease of the heart walls from neurasthenia alone.
Undoubtedly cases occur in which cardiac hypertrophy and
dilatation become apparent while the patient is being
treated for neurasthenia. Disease of the blood-vessels,
which existed before the accident, and which would have
eventually become marked by clinical signs even if the pa-
tient had never become neurasthenic, is the most probable
explanation of such phenomena.

The other vascular symptoms of neurasthenia may be
referred to impairment in the capillary circulation. The
patient is frequently subject to sensations of heat and cold
and to sudden flushings of the whole body. The face may

26o FUNCTIONAL EFFECTS OF INJURY.

be observed to become successively red and pale. The
hands and feet are often cold, and may be blue and feel
numb. Sweat is increased in amount, and the patient may
break out into perspiration as a result of slight excite-
ment.

Digestive Disturbances. — Digestive disturbances are fre-
quent in neurasthenia whatever its origin, and in many cases
it seems as though the nervous symptoms were in large
part due to, or aggravated by, an auto-intoxication from
the absorption of poisonous substances derived from im-
perfect metabolism. In traumatic neurasthenia the appetite
may be impaired for some time after the accident, although
it usually soon becomes restored to the normal standard,
even when the nervous symptoms are getting worse. The
tongue is coated and tremulous and the breath is offensive.
The various symptoms of gastric dyspepsia are frequent.
There are peculiar subjective sensations referred to the
stomach, such as feelings of hunger, or as though the stom-
ach were constantly empty, or as though there were , some-
thing gnawing at it. Gastric pain, particularly after eating,
is the subject of frequent complaint. Vomiting may occur
immediately after the accident, but it rarely continues as a
symptom later in the disorder. There is usually a consider-
able production of gas after eating. The gastric symptoms
are commonly associated with palpitation of the heart. A
full meal may cause the heart to beat violently for a consid-
erable length of time. The skin may be sallow and yellow,
but there is rarely any jaundice. The bowels are consti-
pated as a rule. Constipation niay have originally occurred
as a result of lumbago, but it also exists independently of
lumbago, and may persist after the pain in the back has in
large part disappeared. In rare cases occurring after acci-
dents there is persistent diarrhoea, which can not be ex-
plained by other than nervous causes. In the milder de-
grees of the neurosis the general nutrition is not materially

TRAUMATIC NEURASTHENIA. 261

interfered with. In severe cases, however, there may be
considerable loss of weight.

The remaining symptoms, although they may be much
complained of, are of secondary diagnostic importance. In
the female there may be interference with the menstrual
function. Neurasthenic men commonly notice that their
sexual power is becoming diminished, and the desire for
sexual intercourse is usually lessened. They fear "loss of
manhood." The urine shows no characteristic changes. It
is often neutral or alkaline in reaction, so that the phosphates
precipitate readily. The patient, who observes all his symp-
toms, does not fail to ascribe a sinister meaning to this. He
thinks he has spermatorrhoea or Bright's disease. The urine
may be somewhat lessened in quantity.

Prognosis. — The prognosis of traumatic neurasthenia as
regards life is very good. It is doubtful if a previously
healthy man ever dies from the result of an accident in
which he has received no injury more vital than a sprain
of the back or a nervous shock. In persons whose previous
health was impaired, or who were suffering from actual dis-
ease, the effects of injury and shock are much more serious
and may sometimes prove fatal. Although many patients
have died during the course of traumatic neurasthenia, it
seems more reasonable to suppose that in such cases the ac-
cident added an impetus to the pregress of pre-existing dis-
ease, or that the shock, injury, and resulting exhaustion
proved to be more than a previously enfeebled organism
could combat.

Persons who are diseased or enfeebled from any cause
are heavily handicapped in the struggle for life, and acci-
dents or other injurious influences which may seem to fatally
turn the fate against them must be regarded as contributing
rather than as sole causes. So the prognosis of traumatic
neurasthenia, as far as life is concerned, is generally good,

and only becomes serious in the debilitated or diseased.
18

52 FUNCTIONAL EFFECTS OF INJURY.

It is very difficult to arrive at any satisfactory conclusion
;garding the prognosis for recovery. Different men hold
ififerent views relative to the percentage of complete recov-
ries, and to the average duration of the disorder. The
lilway surgeon regards the prognosis as good in nearly all
f the cases. The neurologist, on the other hand, takes a
raver view of the prospects for a return to health. To see
ow widely opinions on this subject may vary, it is only
2cessary to thru from the writings of Page to those of
•ppenheim. Page believes that most of the patients get
ell upon settlement of claim ; from reading Oppenheim's
Dok one might be led to suppose that recovery was ex-
;ptional. This diversity of opinion may be explained, in
.rge part at least, by the kind of cases seen by the different
bservers.

The corporation surgeon sees hundreds of cases of neu-
isthenia following accidents which terminate in complete
xovery, either spontaneously or after settlement. If re-
jvery occur spontaneously, the surgeon thinks the patient
id little or nothing the matter with him ; if it follows
lyment, he infers, and often correctly, that the symptoms
id been largely exaggerated. Such an inference is by no
leans always justifiable. Neurasthenia generally improves
ter mental anxiety and worry are removed, and relief from
lese factors is in many cases as reasonable an explanation
: recovery as the payment of the claim. Furthermore, the
jrporation surgeon, while he often hears of the miraculous
ires which the company's gold not infrequently induces,
ises from sight the vast majority of the patients whom he
famines. Upon adjustment of the claim they vanish intO'
ascurity, and there is no means of discovering whether
ley continue to be the prey of nervous symptoms or not.
[e infers that their troubles are over, but he can only be
ire of this in a relatively small number of cases. And it
this fact which prevents him from arriving at any definite

TRAUMATIC NEURASTHENIA. 263

estimate of the percentage of cases which completely re-
cover.

Page endeavored to decide the question as to the pro-
portion of recoveries and the duration of symptoms. In his
tabulated list of two hundred and thirty-four patients who
had been injured on the London and Northwestern Rail-
way, the inquiries were not made, in the larger number of
cases, until two years had elapsed after the accident. Some
of the cases he saw himself, some he heard about from other
doctors, or from outside sources. The information regard-
ing many of these cases is too meager to be conclusive. But
from his inquiries it appears that considerably more than
one half of the patients recovered eventually, although re-
covery was often delayed.

Unsatisfactory as are such investigations and uncertain
as are their results, they constitute the only means we have
of determining exactly how serious the condition is. It was
originally the intention of the writer to pursue a similar line
of inquiry regarding the injuries to the nervous system which
have resulted from accidents on American railways ; but,
after considerable reflection, and on the advice from various
railway officials, the plan was abandoned as impracticable.
To insure absolute accuracy of results, it would be neces-
sary to have the records of the examinations of a large
number of patients soon after the accident, as well as thor-
ough personal examinations made after a considerable in-
terval of time.

Such a task, were it undertaken by the railway company,
would require an enormous amount of labor ; it is practi-
cally impossible for a private individual. It constitutes,
however, the one means of determining even approximately
the number of persons who eventually recover entirely from
their injuries. Until some such investigation is carried out,
our views of the prognosis of traumatic neurasthenia must
be based upon personal observation and upon the communi-

264 FUNCTIONAL EFFECTS OF INJURY.

cations of neurologists and surgeons who have the oppor-
tunities of seeing large numbers of these cases.

The position of the neurologist is at the other extreme
from that of the railway surgeon. The persons who come
to him are either claimants seeking an expert opinion or
patients desiring treatment. Whichever they may be, they
usually present evidences of serious disturbance of nervous
function. It is, however, unquestionable that the serious
condition of many of these sufferers is due to the influences
by which they have been surrounded since the accident,
rather than to the effect of the accident itself. The patients
engaged in litigation have become worse through anxiety,
uncertainty, and frequent examinations. Those who come
with the sole object of getting well have usually been sub-
jected to faulty methods of treatment.

This is especially apparent in clinic patients. In my
opinion, treatment in clinics is distinctly prejudicial to neu-
rasthenic patients, and I have no doubt that the severity of
the symptoms in some of the clinic cases which have been
reported to show how rebellious an affection traumatic neu-
rasthenia may be, even when unassociated with litigation, was
in large part due to the injurious influences which every
clinic exerts on such cases. The patient, while awaiting his
turn, discusses his case and his symptoms with other pa-
tients. Through the constant association with disease and
doctors, his attention is continually riveted on personal
troubles, and he thus often becomes an incurable and offen-
sive hypochondriac.

These patients are rarely satisfied with one physician, but
usually try several, either simultaneously or consecutively.
One of them confided to me that he had been at one time
under the care of two doctors, who gave him different medi-
cines. In order to avail himself of the therapeutic skill of
each, he mixed the separate medicines together and took
one half of the amount obtained by adding together the

TRAUMATIC NEURASTHENIA. 265

doses of both medicines ! The evil influences of clinic treat-
ment are less prejudicial than those caused by waiting for
claims to be decided upon, but they are longer continued.
A claim is eventually disposed of, and the patient's anxiety
is then in large part relieved. But as long as the neuras-
thenic has strength to work, or money enough to pay car-
fare, he may prolong his dispensary treatment indefinitely.

However, whatever be the causes of the condition, the
neurologist sees many cases of traumatic neurasthenia
which last for years, and many which seem incurable. Of
twenty-nine cases of " traumatic neurosis " observed by San-
ger some time after the accident, three were entirely well,
seven had only slight subjective symptoms and could work,
eleven were only partially able to work, and eight were in
statu quo. Richter reports three cases resulting from acci-
dents, in which the patients were inmates of the Daildorf
Asylum. All of them had originally been regarded as simu-
lators.

A visit to any large neurological clinic will convince the
most skeptical that a large number of these complaining
hypochondriacal invalids believe themselves to be as ill as
they claim to be. To such a clinic come almost daily men
who give no evidences of having any grave disease of the
nervous system, yet who profess themselves as entirely un-
able to work. In such cases idleness does not result from
any hope of compensation. Persons who have actions to
bring rarely come to dispensaries for the outdoor poor. On
the contrary, inability to work means suffering for them
and their families. Yet many of these men who, previously
to the accident, had been active wage-earners, are unable
during months or years to resume their regular employ-
ment. A locomotive engineer has been coming from time
to time to the Vanderbilt Clinic for over two years. From
the time that he was in a collision he has been unable to re-
turn to his occupation. He is a robust, intelligent man, and

266 FUNCTIONAL EFFECTS OF INJURY.

was not conscious of any injury at the time of the accident,
nor have we ever had reason to suspect that his condition
was anything more than traumatic neurasthenia. Yet on the
slightest excitement or fatigue this man becomes so con-
fused and tremulous that he has abandoned all idea of trying
to work, for the present at least, and has gone to live in the
country for a year, to see if he can get back his former
strength and self-control. Nammack reports the case of a
policeman who in the discharge of his duty was very much
frightened and shaken by a team of runaway horses. The
man was not physically injured, and had, of course, no
thought of making any claim, and yet after two years his
nervous condition would not permit him to return to duty,
and he was eventually pensioned by the police department.
Similar cases are of not infrequent occurrence, and several
examples of them have been mentioned in preceding pages.
f It comes especially to the attention of the neurologist
that the seeming exaggeration of traumatic neurasthenia is
not necessarily dependent upon financial considerations.
Many patients, after their claims have been adjusted and
paid, or their actions have been decided, continue to present,
with very little variation, the same old train of familiar symp-
toms. There may be improvement when all the legal for-
malities are at an end, but not infrequently the symptoms
continue with but little or no improvement.

The case mentioned on page 236 grew worse instead of
better after settlement.

However, it is safe to say that of the total number of per-
sons who develop neurasthenia as a result of accident, the
majority recover sufficiently to return to work.

In many, the restoration to health is complete, so that
they are as well as they ever were. Others find themselves
more irritable and more easily tired than before the acci-
dent. The back may become painful on fatigue or when
suddenly jarred or moved. There is more or less headache,

TRAUMATIC NEURASTHENIA.

267

and the patients do not sleep as well as they formerly did.
Such a condition of nervousness and fatigue may continue
for many years, so that the patient never feels himself " the
man he used to be." However, in the majority of persons
previously healthy such symptoms eventually pass away
entirely.

There are other cases, and the number of these is con-
siderable, in which the patients, from the time of the in-
jury, show evidence of profound nervous disturbances. All
the symptoms of neurasthenia are well marked, and, instead
of getting better as time goes on, the condition remains sta-
tionary, or seems to get worse. The symptoms of trau-
matic lumbago may pass away, but the insomnia, the tremor,
the despondency, and the malnutrition remain. In these
cases the prognosis for ultimate recovery is doubtful, and
many of them are never able to resume their occupations.

The duration of the disorder is consequently variable. It
is essentially a chronic affection, requiring a considerable
length of time for repair. The larger number of cases which
are properly treated can return to work in the course of a
few weeks or months, although a longer time may be neces-
sary before they " feel themselves again." It is uncertain
just how long the symptoms may last before it can be said
that recovery is no longer probable. It varies with individ-
ual cases and with associated circumstances. Knapp be-
lieves the chances of recovery in any case which has existed
over three years are slight.

Several factors very materially affect the prospects of
recover)'. Perhaps the most important of these, and cer-
tainly the one which has received the greatest attention, is
litigation.

The worst possible thing to which the patient with trau-
matic neurasthenia can be exposed are the mental influences
of litigation.

Litigation, much more than merely entering a claim

268 FUNCTIONAL EFFECTS OF INJURY.

with willingness to adjust it, furnishes the very influences
from which a neura,sthenic should be free. The anxiety,
uncertainty, and delay which are the inevitable conse-
quences of lawsuits, prevent the patient from having the
physical and mental rest which are essential to recovery.
His mind is more constantly attracted to self-contemplation ;
he is made to frequently relate his symptoms, and is re-
quired to pass through many medical examinations. From
the nature of the proceedings, he is not urged to go back
to his work, even if he is able to do so.

It is hardly fair to assume that the increase of nervous
symptoms during the time that litigation is pending is en-
tirely due to voluntary exaggeration by the patient, or that
the symptoms improve after settlement because there is no
longer anything to be gained by exaggeration. As has al-
ready been said, it is universally characteristic of neuras-
thenia that the symptoms become worse through disturbing
influences of any character. This is observed in cases in
which the question of litigation does not enter at all ; and
also, the various nervous disturbances may become intensi-
fied by litigation, not simply for forensic purposes, but be-
cause litigation itself provides the very factors most preju-
dicial to the patient. Similarly, if the patient improves
when the suit is settled, it is in part, at least, because the
anxiety and uncertainty and fatigue have been removed, not
necessarily by reason of the financial gain.

Treatment, which can do much to hasten recovery, can
not be properly carried out as long as the patient remains a
plaintiff. The physicians whom the patient sees are experts
rather than therapeutists ; the important question is detailed
diagnosis and evaluation of symptoms rather than cure. As
it is usually months or years before a case is settled, the pa-
tient is obliged to go without proper treatment, and to be
surrounded by unfavorable influences for a long time and
during a period when the symptoms are most amenable to

TRAUMATIC NEURASTHENIA.

269

cure. Isolation and rest, the specifics for neurasthenia, are
impossible in negligent cases.

In conclusion it may be said that the prognosis for more
or less speedy and permanent recovery in any case of neu-
rasthenia is good if the patient has no claim to bring and
can put himself at once under the care of a skillful physi-
cian, although even then recovery is not always assured.

Bibliography. ''

Bass, Das Gesichtsfeld. Stuttgart, 1896.

Beard, A Practical Treatise on Nervous Exhaustion, New
York, 1880.

Binswanger, Die Pathologic und Therapie der Neurasthenic, Jena,
1896.

Forster, Gesichtsfeldmessung bei Anaesthesiae Retinae. Kl.
Monatsbl. f. Augenheilk., Bcilage, 1877.

Hodge, C. F., A Microscopical Study of the Changes due to
Functional Activity in Nerve Cells. Journal of Morphology, 1897

Ibid., A Microscopical Study of the Nerve Cell during Electri-
cal Stimulation. Journal of Morphology, 1894.

Knapp, Traumatic Neurasthenia. Nervous Diseases by Ameri-
can Authors, Philadelphia, 1895.

Lugaro, Sur las modifications des cellules nerv. dans les
divers 6tats fonctionels. Arch. Ital. dc Biol., 1895, xxiv.

Nammack, Trans. N. Y. Neurolog. Soc, 1895.

Oppenheim, Die traumatische Neurosen. 2 Auf. Berlin, 1892.

Page, H. W., Railway Injuries in their Medico-legal and Clinical
Aspects, London, 1887.

R^gis, Practical Manual of Mental Medicine, Utica, 1894.

Richter, Berliner Klinik, August, 1895.

Sanger, Die Beurtheilung der nervenerkrankungen nach Unfall.
Stuttgart, 1896.

Ibid., Neurolog. Centblatt., 1892, p. 121.

Vibert, La N^vrose traumatique. Annales d'hygiene pub. et de
me'd. leg., 1892, vol. xxviii, p. 139.

Wildbrand and Sanger, Ueber Sehstorungen bei functionellen
Nervenleiden, Berlin.

CHAPTER III.

TRAUMATIC HYSTERIA*

It is through the philosophical and clinical studies of
Charcot and his pupils that hysteria has come to be re-
garded as a distinct disease, which, although it may take
many forms and show startling powers of mimesis of other
diseases, has its own identity and limitations. It is true of
hysteria, as of many of the psychoses, that the limitations
are often difficult to determine. The manifestations are
essentially psychical, and, when not pronounced, it is not
easy to decide whether they are to be regarded as symp-
toms of disease or as mental variations within the limits of
health.

Hysteria major and hysteria minor are the divisions of
the disorder as classified by Charcot. Hysteria major, or
la grande hysUrie, is the type characterized by convulsive
attacks ; it is infrequent in America. Hysteria minor em-
braces all the varieties in which there are no attacks. This
term, consequently, is extremely comprehensive, since it
might include not only most of the cases of traumatic hys-
teria, but also those which are characterized by slight men-
tal instability, in which there may never have been any of
the stigmata or accidents of the disease.

Just how comprehensive the conception of hysteria
minor should be it is impossible to determine. Mental sug-

* To the part of this chapter which was submitted as a competitive essay was
awarded the Joseph Mather Smith prize at the annual commencement of the Col-
lege of Physicians and Surgeons, Columbia University, in June, 1897.

TRAUMATIC HYSTERIA.

271

gestibility is the most prominent symptom of hysteria ; but
if we are to class as hysterical all persons who display this
symptom, it will be found that a large part of the world's
population is a victim of the disease.

Different views on this subject are held by different men.
Mbbius says that " hysteria is simply the morbid increase of
a rudiment which is present in all, and that every one is a
little hysterical. If this were not so," he aptly adds, "it
would fare ill with the practice of medicine."

Charcot taught that hypnosis is possible in hysterical
subjects only, and yet Bernheim claims that he can hyp-
notize ninety per cent of the persons he sees. If both
propositions are true, the conclusion is inevitable that hys-
teria is an almost universal disease.

For us it is sufficient to say that although all hysterical
persons are suggestible, all suggestible persons do not pre-
sent other hysterical stigmata, and that more symptoms
than mere mental suggestibility are necessary before we are
justified in making the diagnosis of hysteria.

Inasmuch as we are entirely ignorant of the underlying
anatomical character of the disorder, any definition of hys-
teria is necessarily imperfect. For practical purposes, how-
ever, it may be said that hysteria is a disease of unknown
pathology, affecting the whole nervous system. The symp-
toms, which may be permanent or transitory, are mental and
physical. The mental symptoms are the most important,
and in them are to be sought the explanations of the phys-
ical manifestations. The physical symptoms may imitate
very closely those of. organic nervous disease, but they do
not depend on any structural lesions which have as yet
been recognized. They are involuntary expressions of dis-
ordered mental states. When called into activity by trau-
matic agencies, the affection is called traumatic hysteria.

The symptoms of hysteria have been recognized since
the days of Plato and Hippocrates. For many centuries

272 FUNCTIONAL EFFECTS OF INJURY.

they were supposed to be dependent upon uterine troubles,
and to occur exclusively in the female. Charles Lepois,
writing in 1618, abandoned the uterine theory and admitted
the existence of the disorder in men. The contributions of
Sydenham to the subject of hysteria showed more discern-
ment than any which had preceded them, and were more
valuable than many of those which were to follow. Syden-
ham studied most of the hysterical stigmata. He admitted
the existence of hysteria in the male, giving it the name of
hypochondriasis, and regarded the nervous system as the
seat of the trouble. Brodie, in 1837, recognized that func-
tional paralysis may depend upon impairment of will power.
The first modern treatise on the subject was written by
Briquet, in 1859.

It is to Charcot, however, that we owe the complete pres-
entation of the symptomatology of this disease. His able
mind, comprehensive learning, and extensive experience in
all branches of medicine well fitted him to discern the errors
of previous workers in this department of neurology. His
rare opportunities at the SalpStrifere were so well employed
that he lived to see hysteria occupying a definite and
limited place in clinical medicine. It is chiefly through his
teachings that hysteria has been shown to be not a mixture
of affectation, exaggeration, and deceit, but a condition in
which the symptoms are involuntary expressions of dis-
ordered mental states. These symptoms are not assumed.
The paralyses, anaesthesias, and convulsions of hysteria are
as real to the patient as though they had visible underlying
causes.

The false statements of hysterical persons are not neces-
sarily willful lies, but may originate honestly from halluci-
nations or from losses of memory. Many of the physical
symptoms can be accounted for by impairment of will
power. As Paget aptly put it, in referring to a paralysis
which to-day would be recognized as hysterical, " The pa-

TRAUMATIC HYSTERIA.

273

tient says, ' I can not ' ; it sounds like ' I will not ' ; it really
is, ' I can not will.' "

Brissaud has well said that hysteria is " one and indivisi-
ble," and in employing the term traumatic hysteria there is
no intention to imply that hysteria provoked by trauma has
any essential differences from the disorder when it is due to
other exciting causes. But as all diseases vary under differ-
ent causal conditions, so hysteria following trauma has some
characteristics peculiar to itself. These special characteris-
tics are not sufficiently distinctive to warrant any separation
of traumatic hysteria from the protean affection ; individual
clinical parallels may be found in cases of hj'steria in whatever
way they may have developed. Inasmuch, however, as there
are usually certain circumstances which modify the disorder
when it is of traumatic origin, the following description wijl
be limited to those forms of it which are most frequently
observed as a result of physical injury and psychic shock.

Traumatism as a cause of local nervous disturbance with-
out organic lesion had been recognized by Brodie, Russell
Reynolds, Page, Striimpell, and many others. But to Char-
cot must be given the credit of having established beyond a
doubt the pessibility of the existence of hysteria excited by
injury. He taught that the functional paralyses and anaes-
thesias which sometimes follow traumatisms were identical
with those induced or made to disappear by hypnosis, and
he formulated the theory that in the development of hys-
teria the influence of traumatism is an influence of sugges-
tion. The shock of the injury acts as a hypnotizing agent,
the local pain or discomfort calls the patient's attention to
the part injured and suggests the symptoms of paralysis or
contracture, or anaesthesia, or whatever the symptoms may
be. (Traumatic suggestion.) There are some objections to
this theory, but it is the best which has as yet been offered.

As a distinct disease, hysteria is unfamiliar to most
American physicians. The condition is comparatively rare

274 FUNCTIONAL EFFECTS OF INJURY.

in this country, and only exceptionally occurs in the exag-
gerated forms observed in Europe. As a result, many cases
of hypochondriasis and neurasthenia are classed as hys-
terical when they are not hysterical at all. Also, it too fre-
quently happens that hysterical mimesis is confused with
voluntary simulation, and that true cases of hysteria are re-
garded simply as frauds. With the increasing general inter-
est in neurology and with the more conservative use of the
word " hysterical," hysteria may some day become in
America as well recognized a disorder as it is in Europe.

.etiology — Predisposing Causes. — Charcot taught that hys-
teria is a disease which only shows itself in persons whose
nervous systems are diseased, degenerate, or abused. He
classed it with the diseases of degeneracy, and regarded
ilii, as a child of the neuropathic family. He believed that
predisposition to it depends upon ancestral defects or ac-
quired enfeeblement of the nervous system, and that with-
out such predisposition the disorder could not exist. The
profound disturbances of hysteria which may follow insignifi-
cant exciting causes certainly indicate that the agent provo-
cateur can only produce effects in a nervous system already
prepared for their development. Very much less impor-
tance is attached by the Germans to the necessity of predis-
position in the causation of hysteria, and, indeed, to prove it
is not always easy.

As in other nervous disorders, we may in many cases
discover evidence of a hereditary disposition, yet it often
happens that such proofs are not obtainable. In America,
so many of the poorer classes have immigrated as children,
and know little or nothing about their families, that we
are frequently unable to gather any reliable information
regarding their antecedents. The evidences of ancestral
defects, as shown by stigmata of degeneration, aside from
such stigmata as may properly be regarded as hysterical
symptoms, may be entirely absent.

TRAUMATIC HYSTERIA.

275

Just as the history and evidences of inherited impairment
of the nervous system may be wanting, so hysteria may de-
velop in persons whose personal life seems to have been free
from injurious influences. On the other hand it can some-
times be demonstrated that the resisting powers of the nerv-
ous system have become enfeebled through the effects of
disease or of chronic intoxications. Among the diseases
which predispose to hysteria, nephritis, diabetes, syphi-
lis, the continued fevers, and many of the affections of the
nervous system are prominent; chronic metallic poisoning
is an important astiological factor, and especially poisoning
from lead or mercury, the latter of which seems to be asso-
ciated with such particular frequency with hysterical stig-
mata that many authors believe the tremor mercurialis to be
largely, if not entirely, of hysterical origin ; hysteria is also
very frequently found in victims of chronic alcoholism.
When trauma is the immediate provoking agent of hysteria^
predisposition appears less necessary than when the disease
is of non-traumatic origin. Dana and Knapp both regard
hereditary factors as of less importance when the disease
follows a traumatism than when it is due to other exciting
causes. Of twenty-one cases of traumatic hysteria studied
by Berbez, only nine had undeniable neurotic antecedents.

Exciting Causes {Agents provocateurs). — Of the various,
causes by which hysteria may be excited, trauma and shock
are the only ones which concern us here. Traumatic hys-
teria or hystero-traumatism has only been recognized in
recent years. Although it was previously known that slight
injuries might be followed by functional palsies and contrac-
tures, it was not until 1886 that trauma came to be recog-
nized as one of the most frequent of the agents provocateurs
of hysteria. It was again by Charcot that the causal rela-
tionship was made clear. He also showed that not only was
traumatism to be considered as an aetiological factor, but as.
one of the most frequent causes. According to Berbez, a.

276 FUNCTIONAL EFFECTS OF INJURY.

pupil of Charcot, one fifth of all cases of hysteria are of trai
matic origin.

That an injury without being severe may be followed b
functional paralysis, or contracture, or convulsions, has n
ceived abundant clinical verification.

A coachman fell from his cab, and, though considerably shake
up, received no severe injury; five days later he developed
brachial monoplegia of the side upon which he had fallen. .
glass polisher, soon after a slight injury to the wrist, presented
hysterical contracture of the hand. A mother, in a fit of ange
struck her child with the back of the hand ; the hand which ha
given the blow soon became anaesthetic and powerless. All c
these injuries were too slight and inadequate to cause organi
changes sufficient to account for the startling symptoms whic
ensued. — (Charcot.)

Far more important than the severity of the actual injur
are the circumstances under which it occurs, and the patient'
mental state at the time it is received. All influences whicl
cause excitement and fright very much increase the probabil
ity of hysteria ensuing as a result. If, immediately befor
the accident, the about-to-be victim has an opportunity to bi
frightened by what is going to happen to him, the menta
impression thus received accentuates the effects of the phys
ical hurt. To both of these factors — trauma and fright-
mankind has ever been constantly exposed, and in our me
chanical times the probabilities of injury have become sc
many times multiplied that we are almost constantly ex
posed to terrifying accidents.

Hysteria is frequently the sequel of distressing railwa3
and similar disasters, in which the victim may or may no
have been injured. It is essential for purposes of justice
as well as for correctness of diagnosis, that it be generally
recognized that very startling hysterical symptoms can fol
low accidents which have caused only slight physical com
motion or bruising.

In the hysterical phenomena which follow local injury

TRAUMATIC HYSTERIA.

277

the influence of suggestion is evident. It is the part injured
which becomes the seat of the paralysis, or aneesthesia, or
contracture. A blow on the shoulder is followed by brachial
monoplegia of the same side ; a blow on the hand causes
symptoms in the hand only; if the injury is to the head,
the result may be hemiplegia, not crossed, but on the same
side as the traumatism. The influence of suggestion is par-
ticularly well seen in the cases in which hysterical s)'mptoms
are superimposed upon organic injury. Charcot records
the appearance of hysterical contracture of the forearm and
hand, due to splints which had been applied for a fracture of
the radius. Nerve injuries are frequently associated with
local hysterical manifestations. In the following case, for
the privilege of reporting which I am indebted to Dr. Starr, a
lesion of the cauda equina was complicated by astasia-abasia :

A woman, twenty-seven years of age, was injured in a railway
collision on July 4, 1894. She was much frightened, felt severe pain
in the back, was able to walk for a few minutes, but then the legs
gave way and she sank to the ground. She remained unable to
walk at all for fifteen months, though she recovered the power of
moving her legs in all directions when in bed. Immediately after
the accident there was retention of the urine, and since that time
the control of the bladder has been imperfect. The catheter was
used for eight months. The action of the bowels has also been
irregular. There was considerable numbness in the legs and
back, at first with imperfect power of movement and rather rapid
atrophy in the muscles of the thighs and legs, but strength and
volume have returned to them.

Examination, October 2, 1895, showed areas of anaesthesia
(Fig. 44) around the umbilicus and around the anus. Though
the patient had perfect command of the legs, and could move
them in every direction while lying down, astasia was complete,
and the legs collapsing immediately when any attempt was made
to stand. There were general neurotic symptoms as well. This
condition persisted for a long time after the accident, in spite of
substantial damages. In this case it seems that the astasia was
purely hysterical, while the anaesthesia of the perinaeum and the
bladder, and rectal symptoms were evidences of hasmorrhage or
some organic injury to the cauda equina.
« »9

278

FUNCTIONAL EFFECTS OF INJURY.

One year later the patient was seen again, having in the mean-
time been taught to walk with a roller machine. She then walked
perfectly, had no general hysterical symptoms, but the area of
anaesthesia remained exactly the same as before.

When psychic shock alone is the exciting cause, the
symptoms are usually less localized. Under such condi-
tions the hysterical manifestations are more commonly

Fig. 44. — Anaesthesia in a case of injury to the Cauda equina, associated
with astasia-abasia.

aphonia, or convulsions, or coma. Among the other factors
having certain bearings on the aetiology of traumatic hys-
teria are sex, age, occupation, race, and sometimes litigation.
5^;tr. — Non-traumatic hysteria is much more frequent in
women than in men. The failure to recognize that hysteria,
may occur in man was for a long time an important obstacle
in the progress of knowledge regarding the disease ; but in
the past few years its frequent occurrence in the male has.
become amply demonstrated. This advance was largely due
to the observation of hysterical stigmata which occurred in
men as the results of accidents and injury. Although women

TRAUMATIC HYSTERIA. 279

furnish by far the larger number of examples of non-trau-
matic hysteria, when the disorder first appears as a result
of trauma, it seems as though men were more frequently
affected than women. Berbez, in twenty-one cases of trau-
matic hysteria, found that fourteen, or two thirds of them,
were men. In Knapp's cases the relative number of men
and women was about equal (twenty-five cases — thirteen
women). Greater exposure to traumatic influences, acting
as a predisposing cause, may account for the greater fre-
quency with which traumatic hysteria appears in men than
in women. However, the increased proportion of men to
women is not nearly so large in this disease as it is in trau-
matic neurasthenia.

Age exerts the same influence upon the development 01
traumatic hysteria as upon that of traumatic neurasthenia;
both are essentially disorders of the active periods of life,
although traumatic hysteria may occur at any age, and
sometimes is present in children. Profession and mode of
life, except in so far as they predispose to impairment of
health, seem to exercise less influence than race. The Ameri-
can, who is so subject to nervous exhaustion, less commonly
develops hysteria after accidents. In Europe, and especially
in France, traumatic hysteria is not uncommon. All over
the world, Hebrews are a prey to various neuroses, and hys-
teria is a common disease in male Jews. In fact, the largest
number of the cases of traumatic hysteria which occur in
this country are found in Hebrews or in the foreign-born.

The effects of litigation have a somewhat different bear-
ing upon the course of hysteria than upon that of neurasthe-
nia. In neurasthenia the uncertainty and anxiety of suit
may make a serious affection of what would otherwise be
trivial. In hysteria the symptoms are developed soon after
the accident, independently of any question of damages and
often before there is an opportunity for such a question to
arise. Neurasthenia would in many cases not appear at all

28o FUNCTIONAL EFFECTS OF INJURY.

if the patient could at once be surrounded by proper influ-
ences only; but most commonly, when any one who de-
velops hysteria has once received the fright or the injury,
the mischief is already done, and the disease appears in its
full development. The subsequent course of the case will
depend in large part upon environment, and will be pro-
tracted or made more severe by the evil effects of litigation.
But there are few cases of traumatic hysteria of which it
can be truthfully said that the symptoms would not have
appeared except for the question of damages.

Pathology. — Into theoretical speculation upon the pa-
thology of hysteria it would be useless to enter here.
Nothing is known as to what morbid anatornical changes
are responsible for the symptoms of this disease, and, fur-
thermore, it is improbable that the problem will be solved
by any of the microscopical methods at present at our dis-
posal. As far as is known, the central nervous system in
hysteria is anatomically normal. That some morphological
or chemical changes underlie the alteration in function there
is little reason to doubt ; but the pathology of hysteria will
prove even more elusive than that of neurasthenia. Hys-
teria is a disorder chiefly affecting the mind, and its location
is probably cerebral ; but whether it is entirely cortical or
situated as well in other regions of the brain, it is impossible
to say.

Symptoms. — The symptoms of hysteria are divided into
permanent symptoms, or stigmata, and accidental, paroxys-
mal, or intervallary symptoms. Usually some of the stig-
mata are constantly present during the disease ; they in-
clude the mental state, anassthesia, and the affections of the
special senses. The paroxysmal symptoms, as the name in-
dicates, are only of occasional occurrence, and embrace the
paralyses, the contractures, the convulsions, and similar
manifestations.

As Briquet very truly says, " hysteria attacks the whole

TRAUMATIC HYSTERIA. 28 1

organism." Its symptoms may be those of disturbance of
function of any organ. Some are very much more fre-
quently encountered than others, and certain symptoms are
usually associated. Aneesthesia and contraction of the vis-
ual fields are particularly constant, and are generally com-
bined. Paralysis is more infrequent, yet when it occurs it
is almost invariably accompanied with loss of sensation.
Tremor is common, especially in traumatic hysteria. Occa-
sionally only one hysterical symptom is present, and it is in
such cases that the diagnosis is difficult and uncertain, and
can only be made by the exclusion of other conditions. It
is in mono-symptomatic cases of traumatic hysteria that
the exclusion of simulation becomes sometimes impossible.
Fortunately, for diagnostic ends at least, traumatic hysteria
is most frequently revealed by several characteristic evi-
dences, and often the picture is so clearly defined that there
can be no doubt as to its meaning. In a case which* has been
under my care for some time, the patient tells a characteris-
tic story of hysteria which may or may not be true ; but the
symptoms he presents are unmistakable, and have been
abundantly verified by repeated observations. They are in
so many respects illustrative of traumatic hysteria that an
account of the case may be properly given here :

P. D., forty-seven years of age; alcoholic, as was also his
father; denies all symptoms of nervous disease, except alcohol-
ism, in all the members of his family. Says he is an actor by pro-
fession.

On the 19th of October, 1894, while in the flies of a theater, he
fell twenty-eight feet, " landing on the head and spine." He was
in the hospital for seven weeks, during the first half of which pe-
riod he was unconscious. When he came to himself he found that
he could not move the left side at all, and that the movements of
the right hand were very much impaired. There was no loss of
control of the bladder or rectum. For many months after the
accident he was completely aphonic ; he soon recovered consid-
erable power in the left hand, less in the left leg. He was too
much disabled to work, and having no money, he was sent to the

282 FUNCTIONAL EFFECTS OF INJURY.

Almshouse Hospital. The patient remained in the Almshouse
three months and a half, and durmg that time, the house physi-
cian says, he did not utter a sound of any kind, and invariably

dragged the left leg
in walking. He had
no motives for simu-
lation, and I believe
that the patient was
honest in regard to
his symptoms. Even-
tually leaving the
hospital, this man
was again seen in a
few months at the
Workhouse, where
he had been sent for
drunkenness. The
left leg was still
dragged, but the pa-
tient had recovered
the faculty of speech.
He told us that he
had recovered his
voice as the result
of falling off the rear
platform of a rail-
way car. He had
been considerably
stunned by the acci-
dent, but on regain-
ing consciousness, he
says, he " was scared
to death by finding
that he was talking
to himself." The
aphonia, at least,
had been cured ! The
general condition at this time (October, 1896 — two years after
the original accident) appears, from my notes, to be as follows:
A well-developed man, slightly ancemic. Heart, lungs, and other
vegetative organs apparently sound. There is some weakness of
the left hand, shown on attempts at movement. The movements

Fig. 45. — Traumatic hysteria, showing characteristic
dragging of the foot. (Workhouse Hospital.)

TRAUMATIC HYSTERIA.

283

at the left knee and ankle joints are limited by reason of muscu-
lar weakness, so that the patient can flex and extend both the
foot and the leg to a slight degree only. In walking (Fig. 45),
the left leg is dragged, as though it were an inert mass. The
toe and inner side of the foot scrape along the floor, and the
heel touches the floor only when the patient is standing still.
There is a contracture of the wrist and of the fingers of the right

Fig. 46. — Traumatic hysteria. Paralysis existed in tlie left leg. In the shaded areas,
cutaneous sensibility was diminished ; in the left leg it was totally abolished.
(Workhouse Hospiteil.)

I
hand. The fingers are held in extension and the wrist is slightly
flexed. This contracture may be overcome, but attempts at for-
•cible movement in these joints cause considerable pain. There
are nowhere any wasting of muscles or changes to the normal
reactions of electricity.

From a point a very few inches above the knee, downward, the
left leg is totally anaesthetic. The skin does not bleed to ordi-
nary pin pricks in the anaesthetic area. There is a diminution in
the acuity of cutaneous sensibility over the remaining portion of
the left side of the body (Fig. 46). There is slight deafness in the
left ear. The patient insists that he sees perfectly well, but the
visual fields as marked out by the perimeter (Fig. 47) show a
moderate contraction, which follows the periphery of the normal

284

FUNCTIONAL EFFECTS OF INJURY.

field. It is more marked for the left eye. The color fields are
diminished in extent, but there is no reversal of their normal ar-
rangement.

The patient complains of no pain or hypersesthesia, with the
exception of the pain caused by movements of the right wrist.
He sleeps fairly well. He is a tractable prisoner, and because he
walks better at times than at others, he is generally looked upon
as a " fakir " by the guards.

The mental condition presents nothing particularly character-
istic. There have never been any emotional manifestations, and

I..E.

■xijMl-

■ 270' 310'

Fig. 47. — Field of vision in a case of traumatic hysteria. The contraction is more
marked on the left, which was the side of paralysis and anaesthesia. (W^orkhouse
Hospital.)

although at times the patient appears discouraged and depressed,
the neurasthenic mental state, often present in traumatic hysteria,
is not pronounced in this case. The symptoms did not disappear
when the patient was intoxicated. He once came to my office
very drunk, but was dragging his foot in the same old way. The
long period during which he has maintained the same chain of
symptoms, the absolute lack of motive for deception, and the ab-
sence of all evidences of organic disease, render the diagnosis of
traumatic hysteria incontestable.

There was a predisposition caused by alcoholism, both parental
and personal — a consideration which should have been taken into
account had the case been the subject of medico-legal inquiry.

TRAUMATIC HYSTERIA. 285

Mental Symptoms. — The most prominent feature of the
mental state of hysteria is the causation of physical symp-
toms which imitate conditions such as may be the results of
organic disease. The imitation is sometimes so close that it
is with difficulty that the true nature of the physical dis-
turbances may be appreciated. The mimetic powers of this
affection are far more highly perfected than any to which
the voluntary simulator may hope to attain, and differ from
attempts at fraudulent and voluntary simulation in that they
are, in large part at least, unconsciously performed. In a
disorder which of itself is histrionic and exaggerative the
opportunities for voluntary exaggeration and deceit are con-
siderable, and hysterical symptoms become regularly worse
when they are observed by others. The patients, who are
never so happy as when forming centers of attraction, have
a tendency to embellish such of their clinical manifestations
as are deemed worth}' of special investigation by learned
men, or as are received with interest by audiences composed
of physicians and medical students. It seems probable that
some at least of the astonishing hysterical phenomena which
are reported from certain psychiatrical clinics, if they are to
be considered as genuine products of mental disease, could
only occur under conditions which are most favorable to the
full development of the psychosis. Yet, after due allowance
has been made for errors of interpretation, the fact remains
that psychical mimesis is frequently found in persons who
are ignorant of the existence of any such thing as hysteria,
and who, uneducated and without motive, closely imitate dis-
eases of which they have never heard. That hysteria is dif-
ferent from simulation is proved by the occurrence of hys-
terical phenomena among all peoples and in all times, by the
general uniformity in the character of the symptoms and by
the lack of motive or ability of simulation in the majority of
its victims. Although the disease is essentially simulative
and its manifestations unreal, it occurs not only without in-

286 FUNCTIONAL EFFECTS OF INJURY.

tention, but without the patient knowing that his symptoms
are false. It can best be explained by the theory that it is a
morbid mental state which involuntarily and unconsciously
provokes a mimicry of the symptoms of other diseases. It
is only when the fact is appreciated that hysteria is a serious
disorder affecting the mind that the sufferer from it can be
treated with the consideration he deserves ; even then it is
oftentimes difficult to beheve in the sincerity of a patient
who is seen to move a limb which was apparently para-
lyzed, or who, though nearly blind to usual tests, never pays
the accidental penalties of organic blindness. It can be
proved by optical tests that in hysterical amaurosis sight is
in reality not lost ; in the hypnotic state the patients may
•describe sensations which, while awake, passed apparently
unperceived, or may be made to move muscles which were
paralyzed ; similarly, by hypnosis, memory loss may be
shown to be not genuine.

When it is thus demonstrated that functional activity,
though apparently abolished, exists, we can not suppose that
there are lesions in the organs or in the nerve tracts or in
the perceiving centers themselves. Janet, who has studied
this subject with rare skill, explains the apparent contradic-
tion of hysterical phenomena by the theory of a limitation
of the field of consciousness. Mental actions go on, but are
independent of the patient's personal knowledge. Centripe-
tal stimuli may be perceived by the perceiving centers, but
they are not transferred to the domain of personal con-
sciousness. Centrifugal impulses may be voluntarily liber-
ated, but such volitional impulses originate independently
of the higher Ego. By thus assuming a power of subcon-
sciousness, of which the higher consciousness in normal
minds is only occasionally aware, and to which, in hysteria,
the higher consciousness may become completely oblivious,
most hysterical symptoms can be explained.

In non-traumatic hysteria the mental symptoms are

TRAUMATIC HYSTERIA.

287

somewhat different as they occur in men and in women.
Traumatic hysteria, whether occurring in men or in women,
has the characteristics of male hysteria, in which the purity
of the hysterical picture is blurred by the admixture of
symptoms of neurasthenic conditions, so that it is often a
composite of hysteria and neurasthenia, a circumstance
which has gained for it the name of hystero-neurasthenia.
In traumatic cases neurasthenic disturbances are particularly
prominent during the interval between the occurrence of
the accident and the appearance of typical hysterical mani-
festations. A case of Charcot's well illustrates this :

A man, fifty-three years of age, industrious laborer, witnesses
the suicide of his son. He loses consciousness for several mo-
ments. From that time the father is a changed man. From being
gay and active he becomes sad and bad-tempered. He shuns the
people with whom he used to be on good terms. His sleep becomes
restless and filled with annoying and painful dreams. He thinks
of his son as a happy child, and then sees him bloody and dis-
figured. The memory for recent events fails. The man becomes
distracted. His head feels as though he wore a heavy cap. The
sexual functions are weakened. There are digestive disturbances
after eating. He becomes weak and easily fatigued. These
symptoms are largely neurasthenic in character, and they con-
tinue to be prominent even after the addition of paroxysmal hys-
terical accidents.

Suggestibility is the underlying characteristic of the
hysterical mental state, whether the disorder is induced by
traumatism or by other causes. The patient is constantly
subjected to influences similar to those used in induced sleep.
By Charcot's theory, as we have seen, the accident itself
€xerts its influence by means of suggestion. Hypnotism is
the effect of suggestion upon a hysterical mind, or at least
upon a mind which is morbidly suggestible, a condition
closely allied to hysteria, if not in itself hysterical, and the
mental symptoms of hysteria and the manifestations of pro-
voked hypnosis are closely related, if not identical. By this

288 FUNCTIONAL EFFECTS OF INJURY.

theory may best be explained the genesis of the disorder;
by it also may be best understood those symptoms which are
purely psychical and the rapid alternations in the manifesta-
tions which are physical. The different effects of auto-sug-
gestion under different conditions are well illustrated by the
case to which reference has already been made (page 281):
the actor who fell from the flies of a theater was apparently
but little hurt, but became, a few days later, completely
aphonic. For several months he could not utter a sound,
although he was perfectly well in other ways, aside from the
hysterical symptoms. When he fell from the rear platform
of a moving railway train he again escaped with trifling in-
juries ; but the impression which this accident made upon him
acted in a different way from that of the first, for he imme-
diately began to talk, and has had no difficulty in talking ever
since. In a person once hypnotized, the most trifling occur-
rences may act as suggesting agents, and in hysteria it some-
times seems as though these agents originated in the patient's
own mind, independently of external influences. (Auto-sug-
gestion.) Of similar import are dreams and nightmares
which are frequent symptoms of hysteria. When the disor-
der arises from traumatic causes the details of the accident
may in this way be kept constantly in view. In the daytime
the patient reflects upon what he dreamed at night, thus con-
tinuing the auto-suggestion. Many of the apparently false
statements of hysterical subjects arise from dreams which
the patients fail to differentiate from actual occurrences.

From dreams at night and from reveries through the day
may arise hallucinations. Hysterical hallucinations have
attained medico-legal importance in various criminal inqui-
ries in Europe. They are not frequent in traumatic hys-
teria ; when they occur, they usually, but not always, relate
to the accident.

Hun reports a case in which they were an important
feature :

TRAUMATIC HYSTERIA. 289

A dressmaker, who was sitting in the last car of a railway
train which was standing before the station, saw another train on
the same track rapidly approaching from behind. She was very
much frightened, and in trying to get out she was thrown down
and hurt her back, although she escaped any grave injury. She
was temporarily unconscious, but soon came to herself. In addi-
tion to the ordinary hysterical symptoms of sensorial anaesthesia
and paralysis which resulted from the accident, this patient began
to have recurring attacks in which she shouted and " raved that
she was in a lunatic asylum, and begged not to be sent upstairs to
the noisy ones." She also saw knives and blood on the walls of her
room. The patient was paid eight thousand five hundred dollars
by the railway company, without litigation, but after this the
gradual improvement which had begun did not seem accelerated.
She continued to have from three to six attacks of convulsions
each month, and the right leg remained insensible and paralyzed.
After hospital treatment she was cured of all her symptoms.

Loss of memory often gains for the hysteric the reputa-
tion of a liar and swindler, and renders the history he tells
"the physician unreliable by reason of faulty and contradic-
tory statements. Hysterical amnesia usually differs from
organic amnesia in its periodicity and in its limitation to
certain classes of ideas. Janet classifies it as systematized,
localized, generalized, and continued, though the tw^o latter
forms are rare. In systematized amnesia the memory is lost
for a certain category of ideas, not necessarily acquired at
the same time, but relating to any one thing. Thus a patient
remembered other things, but forgot all circumstances con-
nected with Janet's personality. In local amnesia the for-
getfulness is for certain periods of time. Thus, in traumatic
hysteria, the patient may forget circumstances which oc-
curred immediately before or immediately after the accident,
or may not know that any accident occurred, although other-
wise the memory remains normal.

Hysterical affections of memory are inconstant and con-
tradictory. They are not necessarily attended with deteri-
oration of reasoning power. In traumatic hysteria a frequent

290 FUNCTIONAL EFFECTS OF INJURY.

form of memory loss is due to lack of attention and is con-
fined to recent events. The patient remembers the details
of the experiences of childhood, but forgets the happenings
of yesterday.

Aboulia, or impairment of will power, is a constant men-
tal symptom of the disease whatever its origin. In its most
common form it is manifested by a difficulty in performing
motor or intellectual acts at will. The patient feels himself
incapable of doing the simplest things or of undertakings
the most ordinary intellectual exercise. Diminution of voli-
tion is particularly frequent. Instead of being active and
emotional, the patient is quiet and subdued. There is hesi-
tancy in the performance of voluntary acts, which may
amount to complete loss of will power. Attempts by the
physician to arouse activity of mind or body may be success-
ful, but the patient quickly becomes fatigued and confused
and inattentive.

Some of the more striking psychological accidents, such
as have been frequently described in ordinary hysteria,
are usually wanting in traumatic hysteria. Somnambulism,,
catalepsy, and the like are rarely mentioned as occurring in
cases which arise from injury or fright.

Yet, although the occurrence of exaggerated psychical
disturbances is not the rule when the psychosis is of trau-
matic origin, they are sometimes observed. Laudun has de-
scribed the case of —

A girl, eleven years old, who was very much frightened while
swinging. Soon afterward she had several attacks of coma and
paralysis, with cataleptic flexibility of the muscles. In the first
attack the pupils were widely dilated, and did not respond to light.
After twenty-five hours the patient awoke from the stupor, but the
muscular movements remained for some time hesitating and slow.
The memory for the time which elapsed from the beginning of
the attack until the patient awoke was entirely lost. The suc-
ceeding attacks, of which there were several, lasted a shorter
time. In eight days the patient was entirely well again. During

TRAUMATIC HYSTERIA. 29!

the attacks there was sugar in the urine, which disappeared whea
the patient recovered.

The general appearance and manner of a patient suffer-
ing from traumatic hysteria are the results of the mixture of
hysterical and neurasthenic symptoms. He is inattentive,
inactive, and indifferent, and shows a diminution of interest
in his surroundings. He is credulous and may seem fond of
exaggeration and imposture, but his credulity is childlike
and his exaggeration and deception lacks the cunning of the
paranoiac. He is often pictured as a partial maniac, ever
ready to laugh or weep, or to give evidences of exalted men-
tal states. As a matter of fact, he is moody, introspective,
and depressed, approaching the type of melancholia more
closely than that of mania.

Anaesthesia. — Hysterical anaesthesia is a symptom of
which the patient only rarely complains, and of which he is
often ignorant until its existence is pointed out to him by
medical examination. The subjective difference between
hysterical aneesthesia and anaesthesia of organic origin is
well illustrated by a case related by Janet:

A young girl cut her right wrist with a piece of glass, thus in-
juring the median nerve. There was no paralysis, but she com-
plained of tingling and anesthesia, total in places, over the palm
of the hand and fingers. The physician who examined the case
discovered that there was also a complete left hysterical hemi-
ansesthesia, of which the patient not only did not complain, but
whose existence she did not even suspect. There could be no
more convincing proof of the necessity for thorough sensory ex-
amination in nervous cases.

Ignorance of the existence of hysterical anaesthesia on the
part of the patient is an ignorance of personality only. We
have seen that in hysterical anaesthesia, sensations are really
perceived, although they do not enter the field of conscious-
ness. This fact receives additional proof by the absence of
any injury to regions which are hysterically insensible. It
is almost unheard of for a hand, the seat of the profoundest

292 FUNCTIONAL EFFECTS OF INJURY.

hysterical anaesthesia, to be injured without the patient's
knowledge, by cuts or burns. This is in direct contrast to
the anaesthesia resulting from injury to the peripheral
nerves or spinal cord, lor when complete anesthesia of the
hand is of organic origin, it almost invariably happens that
the patient is unconsciously cut, bruised, or burned.

However, in spite of the fact that until told of it the pa-
tients may be unaware of the existence of autesthesia, loss of
some form of sensibility in the skin or mucous membranes is
by far the commonest symptom of hysteria. Even in Amer-
ica, where the more pronounced hysterical affections are in-
frequent, hysterical anaesthesia is constantly met with. The
anaesthesia is most commonly total, all forms of sensibility
being impaired or abolished. Less frequently the different
sensations may be dissociated. This dissociation may be
similar to that of syringomyelia. Thus, of seventeen cases
of hysterical hemi-thermo-aneesthesia examined by Charcot,
eleven presented the type of total anaesthesia. In six there
was a dissociation of sensations. Two of these six had loss
of temperature sense, with preservation of sensibility to
touch and pain. In the four others the dissociation was
the same as that observed in syringomyelia — i. e., touch
sense preserved, pain and temperature sense lost. Anal-
gesia is the most common of any individual sensory defect.

The different forms of sensibility may be entirely lost or
merely impaired, so that the ordinary stimuli applied to the
skin or mucous membranes pass unperceived, but are recog-
nized when the irritation is intensified. Thus, in hysterical
impairment of touch sense, slight touches may not be recog-
nized, although deep pressure is felt ; or there may be anal-
gesia for ordinary painful stimuli, while strong electrical
currents can not be Well borne.

The limits of cutaneous anaesthesia, in my experience,
have usually been sharply defined. The commonest topo-
graphical distribution of hysterical anaesthesia is unilateral.

TRAUMATIC HYSTERIA.

293

In the clinic it most frequently occurs in the form of a left
hemianassthesia extending from the head to the feet, and
involving the mucous membrane of the eye and mouth of
the affected side (Fig. 48). In traumatic hysteria, however,
in which paralysis is so frequent, the sensory loss commonly

Fig. 48.— The most fre-
quent distribution of hys-
terical anaesthesia.

Fig. 49. — Disseminated anaesthesia.'
(After Pitres.)

coincides in its distribution with that of the parts paralyzed
(morphological anassthesia, see Fig. 46). If there is hemi-
plegia, there will be hemianassthesia ; if paraplegia, the sen-
sory loss will be from the waist down, usually, though not
always, skipping the genital organs. If muscular power is
lost in one limb only, the anassthesia involves the skin which
covers the paralyzed member. When the sensory changes
occur in segments of limbs only, it is called segmetal, a form
which is frequently seen in the involvement of areas of skin
ordinarily covered by gloves and stockings (glove anaesthe-
sia — stocking anaesthesia).

Sensory loss may occur in scattered areas (Fig. 49) over

294 FUNCTIONAL EFFECTS OF INJURY.

the whole body — a form easily overlooked if sensory exami-
nation is not painstaking. Pronounced anaesthesia of the
whole cutaneous surface is usually associated with other
unmistakable hysterical symptoms, and is rarely observed
except in coma.

The topographical distribution of hysterical anesthesia
differs essentially from that due to other causes. It never
follows the distribution of individual nerves. In trans-
verse spinal-cord lesions the resulting loss of cutaneous
sensibility is found in the parts supplied by the injured seg-
ments ; these parts do not correspond to the areas affected
by hysterical anaesthesia. Furthermore, the penis usually
retains its sensibility in hysteria, but never does in lesions
above the fifth lumbar segment. In unilateral spinal-cord
lesions (Brown-S6quard paralysis) paralysis of motion and
sensation are on opposite sides. The topographical distri-
butior^ of the anaesthesia of syringomyelia follows the spinal
segmental type. In organic lesions of the brain the result-
ing anaesthesia is generally slight, and the associated symp-
toms are usually sufficient to permit of a correct diagnosis
(see page 60).

Hysterical anaesthesia may come and go, be permanent
or transitory, or may frequently change its situation. It or-
dinarily disappears during sleep, and may disappear during
the various intoxications. Its locality can frequently be
made to change during the hypnotic sleep, and suggestions
received during waking hours may cause it to disappear or
to assume different topographical distributions.

The various alterations of the sensory functions of the
skin and mucous membranes which take place after the hys-
terical attack, after strong emotions, or after the use of the
magnet, are the results of suggestion. Most of the psychia-
trical clinics of Europe are supplied with huge horseshoe
magnets, which are used to demonstrate the mobility of
hysterical anaesthesia. Since Peterson has shown that there

TRAUMATIC HYSTERIA.

29s

are absolutely no physiological effects from the strongest
magnetic currents, it is an inevitable conclusion that the so-
called magneto-therapy acts solely by mental impressions.

The cutaneous surface is the most frequent seat of anees-
thesia. The mucous membranes, especially those of the eye-
lids and pharynx, the muscles, joints, and viscera, are also
common locations. To the eye and to the touch, hysteric-
ally anaesthetic skin is normal. It is not paler than normal
skin, but for some unexplained reason it has a diminished
tendency to bleed when pricked. In the anaesthetic areas
the muscular sense is regularly abolished.

Hyperaesthesia. — Hypereesthesia is a sensory symptom
of hysteria for which examination is usually unnecessary.
The patients complain of spontaneous pain in the hyperaes-
thetic parts, as well as of the suffering caused by slight jars
or knocks. The pain may be very severe" and lasting, as in
the hysterical joint affections, or it may be transitory and
mobile, like hysterical aneesthesia. Hyperalgesia is more
frequent than spontaneous pain. The slightest contact may
cause expressions of agony, and the patients are very un-
willing to permit any touches on the hypersensitive parts.
In such cases deep pressure is often well borne. The pain
caused by touching the hypersensitive part is much accent-
uated if the patient knows that the test is about to be ap-
plied. It often happens that no pain is felt when the part is
brushed or tapped while the patient's attention is fixed on
something else. «

The value of the Mannkopff sign is questionable in trau-
matic hysteria.

The situation of hyperassthesia is variable. General hy-
peraesthesia is extremely 'rare. Hemihypereesthesia may
occur. Anaesthetic areas frequently contain hypergesthetic
zones. In the male the testicle, and in the female the ova-
rian regions, are common locations of hyperassthesia. In
traumatic hysteria there are usually areas of hyperaesthesia

296 FUNCTIONAL EFFECTS OF INJURY.

which correspond in situation to the seat of the injury.
This is the form of hyperaesthesia described in the local
traumatic neurosis of Striimpell. If the back has been
twisted or injured in any way, there is often the pain of
traumatic lumbago, although the spinous processes of cer-
tain vertebrge are frequently hypersensitive, independent-
ly of lumbago. The clavus hystericus — the sensation as
though a nail were being driven into the head — is a hys-
terical symptom generally familiar. In addition to these
forms of increased sensitiveness, headache and peculiar sen-
sations in the head are common. In paroxysmal hysteria
the areas of hyperaesthesia become hysterogenetic zones —
that is, pressure upon them may induce a paroxysm, or
pressure exerted during a paroxysm may cause it to cease.

Hysterical pain does not usually interfere with sleep, nor
is it accompanied with the nutritional disturbances which
are such common consequences of pain from other causes.
It is a difficult symptom to explain. Janet suggests that it
is entirely due to the ideas aroused by association relative to
contact. Although, psychologically, the pain is probably
not genuine, it is real to the patient, and may cause him
much discomfort and suffering.

Special Senses.

Vision. — Next to cutaneous anaesthesia, disturbances of
vision are the most frequent of the hysterical stigmata.
Apart from any possible pre-existing organic defects or dis-
ease, the eye is found to be anatomically normal. The con-
junctivae are very constantly anaesthetic, and the palpebro-
conjunctival reflex is usually abolished. Examination of the
pupils, of the optic nerves, of the ocular muscles, and of
the refracting apparatus, is, with few exceptions, negative.
Nevertheless, vision may be impaired (amblyopia), or there
may be complete blindness of one eye (amaurosis). Bilat-

TRAUMATIC HYSTERIA.

297

eral hysterical amaurosis, on the other hand, is one of the
rarest of hysterical symptoms.

When the eyes are examined with the perimeter, it is
found that there is a peripheral limitation of the fields.

In the larger number of cases of hysterical amblyopia
the peripheral limitation is slight, not exceeding ten or
fifteen degrees. In some cases, however, it may be very
extensive, the perimeter showing that only a few degrees of

z,.s

Ji.jE'.

Fig. 50. — Extreme concentric contraction of the visual fields.
(After Gilles de la Tourette.)

the field retain their normal seeing power. When slight in
degree, the contraction most commonly follows the pe-
riphery of the normal field, but when it is excessive it is
concentric (Fig. 50). Both eyes usually share in the visual
impairment, though it is customarily more marked in one
eye than in the other. If there is unilateral paralysis
or unilateral cutaneous aneesthesia of the body, the more
affected eye will correspond to the paralyzed or aneesthetic
side. At different examinations, the extent of vision often
varies, but the variation does not follow the regular shifting

2^8 FUNCTIONAL EFFECTS OF INJURY.

type observed in neurasthenia. Several examinations are
advisable, and they should be conducted with a view to
rapidity, rather than to minute accuracy. Since the field
often changes as the result of any of the various hysterical
accidents, or with the general condition of the patient, it
has been called by Janet the " barometer of hysteria."

Frequently associated with this limitation of .vision for
form are characteristic abnormities in the color fields.
With contraction of the visual field for form, the perception
of the most internal colors may be lost, or when the con-
traction for form is only moderate in degree there may be a
reversal of the normal color fields ; thus red is often seen in
a larger field than blue.

Visual disturbances, like those of general sensation, are
frequently discoveries of the examining room. The acuity
of central vision ordinarily remains unimpaired. Subjective
ocular disturbances, such as flashes of light before the eyes,
muscag volitantes, etc., occur, but the patients often neither
complain nor are conscious of any trouble with sight, and
they are not subject to the disabilities resulting from con-
traction of the visual field which are present when it occurs
from organic causes. Hysterical patients in reality see, al-
though visual perception does not become known to the
higher consciousness. Thus hysterical amblyopia, like other
hysterical symptoms, is actually false, although, when the
patient is conscious of it, it is real to him.

Although the patient may be unconscious of any visual
disturbances, examination of the seeing power made of each
eye separately may show that in one eye vision is impaired
or lost. While it seems almost incredible that any one can
be totally blind in one eye without knowing it, examination
of many cases has shown that unilateral hysterical amaurosis
may exist independently of the patient's knowledge. That
the apparently contradictory manifestations of hysterical
amblyopia may be genuine and exist, when the patient has

TRAUMATIC HYSTERIA.

299

no motive to deceive or to be " suggested," has been proved
with certainty by Prince. He recently examined a case in
which, instead of there being anything to be gained by simula-
tion, there were the strongest reasons why the patient should
appear sound in every way, for he was a very zealous appli-
cant for a position on the Boston police force. The ocular
symptoms, together with other hysterical stigmata, were dis-
covered at the time of his medical examination for admission.

Prince also reports unusual symptoms in a man who, as the re-
sult of an accident on an electric street car, developed hysterical
hemiplegia and hemianaesthesia and ocular symptoms. Vision in
the right eye was good, but on the left side (the hemiplegia side)
there were amblyopia, color blindness, contraction of the field of
vision, polyopia, a retraction of the near point, and an approach of
the far point to a distance of about eight feet.

The visual disturbances were noticed only when the right
■(sound) eye was closed.

Disorders of the other special senses are less frequent.
If there is impairment of hearing it is almost always uni-
lateral, corresponding to the anaesthetic side of the body.
Bone conduction is interfered with in such cases. Loss of
smell or taste may be bilateral, and is usually associated
with anaesthesia of the nasal mucous membranes and of the
inner surface of the lips and of the tongue. Impairment of
these functions is found under circumstances similar to
those associated with anaesthesia occurring elsewhere.

In a recent Vanderbilt Clinic case, as a result of a bicycle acci-
dent, a young man lost for several months the senses of smell and
taste. This case is particularly remarkable as none of the more
common hysterical stigmata were present. The visual fields were
not contracted, the cutaneous sensibility was normal, and there
were no paralyses. Inasmuch, however, as there had been no
injury to the mouth or pharynx, or other gross injuries, we were
■obliged to consider the ageusia and the anosmia as functional.

Hyperassthesia of hearing, smell, or taste may also occur,
and is evidenced by subjective disturbances of function of
these senses.

300 functional effects of injury.

Motor Symptoms.

Paralysis. — Paralysis is an hysterical accident rather than
a permanent stigma of the disease. Slight injuries frequently
produce marked local symptoms in persons who are already
affected by the disorder, or, as we have seen in discussing
the eetiology of hysteria, the psychosis may appear for the
first time after any accident in which the factors of fright
and injury are prominent.

In the larger number of cases of traumatic hysteria the
local injury is trifling, or at best not severe. Hysterical pa-
ralysis may, of course, follow grave injuries ; but clinical
experience shows that the trauma itself plays only a subor-
dinate part. The loss of muscular power is particularly
prone to follow accidents in which the emotions have been
actively called into play. This is the " traumatic sugges-
tion " of Charcot. Ordinarily there is some little interval of
time between the occurrence of the accident and the appear-
ance of the paralysis. During this "period of meditation"
the patient reflects upon his injury, and, through pain or dis-
comfort, his attention is directed to the injured part until
gradually or suddenly the power of voluntary motion in it
becomes impaired or lost. The sudden paralysis of trau-
matic hysteria is rarely accompanied by the associated signs
of paralysis due to organic lesions of the brain or spinal cord.
Unless developed during an hysterical seizure, or unless the
shock is extreme, there is no prolonged loss of consciousness.

When there is loss of power in a limb, usually some of the
muscles escape, although all may be paralyzed. It some-
times happens that the paralysis affects certain muscular
functions only, and that the pseudo-paralyzed muscles can
perform other movements perfectly well. This is well illus-
trated by the condition first described by Blocq, under the
name of astasia-abasia. In this condition the patient has en-
tire use of the legs for all movements except those necessary

TRAUMATIC HYSTERIA.

30 r

for standing or walking. He may be able to move the legs
in bed, or to dance, or to hold himself on the toes, while all
attempts at standing or walking prove ineffectual. On at-
tempting them the patient falls immediately to the floor.
This condition differs from most forms of hysterical paraly-
sis in that there is no anaesthesia.

The possible medico-legal importance of astasia-abasia
has been shown by Bremer :

A woman, forty-nine years of age, married, claimed that she
had become paralyzed as a result of injuries received in an elevator.
She asserted that by a sudden stopping of the elevator she had
been thrown forward from the seat, striking her head, and that
since that time her lower extremities were paralyzed. She
brought suit for twenty thousand dollars. The physicians who
appeared on behalf of the plaintiff admitted that there were no in-
terference with the functions of the bladder or rectum, or loss of
sensation ; but they asserted that while the patient was capable
of moving her legs in every direction, ^nd with apparently normal
strength in the sitting or lying position, she was not able to either
stand or walk. The expert for the defense accepted the symp-
toms as described by the plaintiff's physicians. But instead of
attributing this peculiar form of paralysis to an injury to the
spinal cord, he ascribed to it only such importance as belongs to
hysteria. It was then shown that the woman had had previous
hysterical accidents, and that the astasia-abasia was only a new
symptom of the hysteria from which she had been suffering for
years. The jury adopted the views of the expert for the defense,
and gave a verdict favorable to the defendant.

The degree of hysterical paralysis varies. It may amount
to nothing more than weakness which is universally distrib-
uted, a condition to which Charcot gave the name of amy as-
thenia.

Amyosthenia, however, is a permanent stigma rather than
a hysterical accident. It is manifested by general muscular
weakness, such as is seen in neurasthenia, but, unlike neuras-
thenic weakness, it is apparent only. In hysterical paralysis,
the patients in reality retain their muscular power, as may

202 FUNCTIONAL EFFECTS OF INJURY.

be proved b}' the muscular work they do. It is when their
attention is drawn to the movements they are about to per-
form — as in dynamometric tests, or in performing move-
ments at command — that the weakness is chiefly mani-
fested. " It sounds like ' I will not,' but it really is ' I can
not will.' "

The degree of paralysis varies also at different times, be-
ing more marked at one examination than at another. As
long as the disease remains active the loss of power usually
becomes progressively greater. Electrical reactions in the
paralyzed muscles almost always remain normal, although a
few cases with diminished electrical excitability have been
recorded. Atrophy is rarely present, and never reaches an
extreme degree.

The most common forms of hysterical paralysis are hemi-
plegia, brachial monoplegia, and paraplegia.

HEiaiPLEGiA occurs most frequently on the left side. It
has many points of difference from organic hemiplegia — viz.,
the face is practically never paralj'zed, although there may
be an associated spasm of the facial muscles, the leg is more
involved than the arm, the knee-jerks are not morbidly exag
gerated, and foot clonus is absent, except in some cases in
which the foot is contracted in extension. In organic spastic
hemiplegia the mowing gait is a sign which the most inexpe-
rienced may interpret. The leg is circumducted in a very
characteristic way. Even in flaccid hemiplegia, if the pa-
tient can walk at all, some use is made of the paralyzed leg.
But in hysterical paralysis the leg is dragged as though it
were an inert mass. This difference is well seen in the ac-
companying reproduction of footprints (Fig. 5 1). In organic
hemiplegia, anaesthesia is rarely an important symptom (see
page 60), while the anaesthesia of hysterical hemiplegia is
pronounced, involving the whole of the paralyzed half of the
body and usually associated with anaesthesia of the special
sense organs.

TRAUMATIC HYSTERIA.

303

'^ ^

!).

Monoplegia is perhaps the most frequent form of pa-
ralysis observed in traumatic hysteria. The left side is the
one usually affected. The loss of power may involve the
whole limb, or, as is more frequent, only certain segments
or muscles are paralyzed. The
arm is much oftener involved
than the leg ; it may hang down
from the shoulder as an inert
mass, or the shoulder may
escape, and only the movements
of the hands be impaired or lost.
The symptomatology of hysteri-
cal brachial monoplegia has been
established through the work of
Miura, who studied thirty-one
cases in which this condition
was a symptom. In fifteen the
paralysis was of traumatic ori-
gin, and followed the injury
immediately, or was separated
from it by a " meditative " pe-
riod. The extent of the motor
loss varied from weakness of
wrist and fingers to complete
paralysis of the whole arm.
When weakness of the leg was
added to the brachial monople-
gia there was an associated hemianassthesia. In nine cases
there was hemianaesthesia with pure brachial monoplegia.
In other cases the anassthesia was limited to the paral3'zed
arm, so that it was bounded superiorly by a line perpen-
dicular to the long axis of the extremity. In one case there
was no anaesthesia at all.

The following case, reported by Lebrun, is interesting, as
it shows both the possibility of hysterical monoplegia. devel-

Fig. 51. — Impressions which illustrate
the differences in the gait (i and 2)
of hysterical hemiplegia, and {3)
organic hemiplegia of the flaccid
type. (From Blocq, after Gilles
de la Tourette.)

304 FUNCTIONAL EFFECTS OF INJURY.

oping from slight injury, and the occurrence of convulsive
attacks as a complication :

A young man, eighteen and a half years of age, when examined
for military service, was found sound in every way and was enlisted.
A few weeks later, while being vaccinated, he was accidentally
pricked by the lancet on the left elbow. He fell unconscious
almost immediately, and on the succeeding day had several more
attacks of unconsciousness. In a few days after the injury, which
was obviously very trifling, power in the left arm began to fail.
He was released from duty, and, as he was becoming worse, he
voluntarily sought the hospital, where he was seen by Lebrun, who
made the following notes :

" Drooping of left shoulder. The left arm hangs inert ; when
told to move it, the patient lifts it a little, with effort, but lets it
fall again. He can hold nothing in the hand. Electrical reaction
normal. No atrophy. Total anaesthesia of the left arm, extending
superiorly a little above the shoulder. There is a concentric limita-
tion of the visual fields, most marked on the left side. The testi-
cles are hysterogenetic zones. The attacks are ushered in by vio-
lent headache, buzzing in the ears and throbbing of the temples,
and by the globus hystericus. The face becomes congested and
anxious in appearance. Inspiration is prolonged and difficult.
Expiration is short. This, the first period of the attack, lasts
about one minute. It is followed by clonic spasms, the arc en
cercle and other histrionic attitudes and movements. This period
closes by the patient bursting into tears. In these attacks con-
sciousness was only partially lost. The patient understood what
was going on around him, but could not reply."

This patient was apparently a confirmed hysteric, since he had
been paraplegic in childhood as the result of a slight injury, and
had always been suggestible. In his case the slight injury caused
by the lancet was sufficient to call into action the dormant psy-
chosis.

Although the arm is by far the most frequent situation of
hysterical monoplegia, other parts may be the seat of local-
ized paralysis. Hysterical monoplegia of the leg is not
rare. Also a few cases of hysterical paralysis, with anaes-
thesia, limited to the one side of the face, have been ob-
served.

TRAUMATIC HYSTERIA. ,05

Paraplegia. — When hysterical paraplegia results from
injury or shock, its onset is usually sudden. It is particularly
liable to be complicated by the development of contractures,
which may be permanent. The loss of power may involve
the whole of both limbs, rendering ali motion impossible,
although more commonly some motor power is retained, so
that the legs or feet may be moved about in bed.

The reflexes are unchanged, except the plantar reflexes,
which are frequently lost. Gilles de la Tourette says that
incontinence of urine and faeces may occur. This is certainly
very unusual. Ordinarily the patients retain perfect control
of these functions. If control is lost, the presumption of
organic mischief becomes very strong.

The anaesthesia in hysterical paraplegia usually extends
from the waist downward, involving all parts except the
genital organs. This rule is not invariable, for the genital
organs may be hypergesthetic or ansesthetic, or other parts
may retain their sensibility. A case detailed by Souques
illustrates this :

A man, twenty-nine years of age, without discoverable nerv-
ous taint, was very much frightened and then knocked down, by a
horse. He was thrown against the curbstone, thus receiving a
contusion of the hip, and immediately went into coma which lasted
two days. In eight days he was able to walk with difficult)', but
soon went into coma again, which lasted this time five days. He
lost for a time the power of speech. Then he began to have
nightmares and hallucinations relative to the accident.

Physical examination at this time showed complete anaesthesia
(Fig. 52) below the waist, with the exception that there was only
a diminution of sensibility of the genital organs, and parts of
both feet were normally sensitive. The muscular sense was lost.
Movement was almost entirely abolished in the lower extremities.
The patient was unable to flex the thigh or lift the heel from
the bed ; but he could be seen to attempt these movements, and
the muscles also could be seen to contract. Slight power of flexion
and extension persisted in the toes. There was absolutely no re-
sistance to passive movement. The knee-jerks were diminished
but present on both sides. The scalp was hyperaesthetic. Left

3o6

FUNCTIONAL EFFECTS OF INJURY.

glosso-Iabio hemispasm. The superior extremities were weak, but
all movements in them possible. Slight tremor. Limitation of the
visual fields. Loss of the sense of smeH on the right side ; the
sense of taste abolished on both sides. While under observa-
tion this patient had an attack of mutism and dyspnoea.

Fig. 52. — Anaesthesia in a case of hysterical paraplegia. (Souques.)

Polyplegia. — Hysterical paralysis of all four extremities
is unusual, but sometimes occurs.

Serieux reports the case of a young girl, fifteen years of age,
who, after a severe fright, fell into convulsions and hallucinatory
delirium, during which her arms and legs received slight bruises.
A few days later all four extremities became paralyzed, the de-
gree of the loss of muscular power in any limb being proportion-
ate to the severity of the injuries the limb had received during the
convulsive attacks. The paralysis was flaccid and there was a
diminution of electrical reactions and of tendon reflexes. The
muscles were the seats of quick, shocklike contractions, resem-
bling those of electric chorea. Anaesthesia was at first generally
distributed, but was very variable. The visual fields were con-
tracted, and the smell and taste were lost.

The symptoms eventually passed away, except a left hemi-
ansesthesia.

TRAUMATIC HYSTERIA. 307

In parts which are the seat of hysterical paralysis or
ansesthesia the muscular sense is lost, as may be demon-
strated for individual limbs by the ordinary clinical tests.
Unsteadiness of standing or walking is sometimes apparent
at once. This may take the form of ataxic movements of
the leg, such as occur in locomotor ataxia. The ataxia may
be more, or less pronounced than in tabes. On standing
still with the eyes closed, there may be considerable sway-
ing of the body. Some hysterical patients can not stand at
all with closed eyes. In a recent case at the Vanderbilt
Clinic the ataxia was most marked when the patient tried to
get up from a chair. These disorders of movement may
occur independently of paralysis. The ataxic and inco-
ordinated movements seen in hysteria often obscure the
diagnosis, and render a proper comprehension of the case
impossible until examination has shown the evidences of
organic disease to be absent, or has revealed the presence of
some of the hysterical stigmata.

Thus, in a recent Vanderbilt Clinic case, the patient's chief
complaint was of an inability to button his clothes. The move-
ments of the fingers were uncertain and ataxic, resembling in this
respect the inco-ordination seen in general paresis. These symp-
toms had occurred subsequently to a fall from a horse car. Ex-
amination failed to reveal any paralysis or other evidences of
organic disease, but the mental condition of the patient was char-
acteristic of traumatic hysteria, and there was a generalized blunt-
ing of cutaneous sensibility, which in both hands and over the left
side of the body was very pronounced.

Similarly, an active farmer, fifty-five years of age, was thrown
from a trolley car, and soon afterward became depressed, apa-
thetic, and emotional. A suit for a large sum was brought against
the company. My exarnination showed a left hemiansesthesia,
weakness in the muscles of the left side, diminution of the visual
field, and similar manifestations of hysteria. There were no evi-
dences of structural lesion. Uncertainty in movements of the
legs was very marked. The man could not, apparently, walk
straight, but would stagger to the right. On standing with closed
eyes he would fall toward the right, although he never let himself

3o8 FUNCTIONAL EFFECTS OF INJURY.

go entirely. His wife said she had observed him when he was
working in the field, and that he would then stagger to the right,
though he never fell.

Contractures. — In hysteria, tonic and continued spasm
may occur in almost any of the muscles, but is most frequent
in the muscles of the extremities. The contracture may de-
velop suddenly as the result of any provoking agent, but
usually it comes slowly, becoming gradually more and more
extensive and severe. It may complicate paralysis, espe-
cially paraplegia, or may occur when 4here is no loss of
power except such as is imposed by the rigidity of the mus-
cles. Hysterical contracture may so closely simulate the
contractures due to degeneration of the pyramidal tracts
that it is sometimes impossible, from morphological appear-
ances alone, to distinguish between the two conditions.
The state of the muscles themselves, however, is very differ-
ent in the two conditions. In hemiplegia, or in disease of the
spinal cord, the contractures come on gradually ; it is many
weeks before they are very pronounced, and even then they
can be overcome by moderate force. It is common in neu-
rological wards to see a hemiplegiac straightening out the
fingers of his paralyzed and contracted hand ; but in hyste-
ria the contractures are vise-like, not to be overcome by any
moderate degree ,of violence. Both sets of muscles sur-
rounding a joint may be so tense that the joint is held abso-
lutely motionless. Also, in organic injury to the pyramidal
tract, increase of tendon-reflex activit}', with ankle clonus,
is the rule, and often occurs, soon after the accident, on
the unparalyzed as well as on the paralyzed side. On the
other hand, there is rarely any great exaggeration of the
tendon reflexes in hysteria. A still more valuable sign
for differential diagnosis is, that hysterical contracture
may appear after injuries too trifling to induce any mor-
bid conditions of organic character. The appearance of
this form of immobility after a slight injury in a strong and

TRAUMATIC HYSTERIA.

309

apparently healthy man is well shown by a case of Berbez
{Obs. 9) :

The patient was a robust blacksmith, thirty-four years of age,
the father of four children. The man had always been appar-
ently in perfect health. He denied all history of ancestral or per-
sonal nervous stigmata. While at work he was slightly burned on
the left hand and
forearm by a red-hot
iron. The wound
was not deep, but
took six weeks to
heal, and left a scar
ten or twelve centi-
metres long and three

^ . Fig. S3- — Hysterical contracture,

or four centimetres (After Richer and Berbez.)

wide, on the back of

the hand and lower part of the forearm. There was no par-
ticular fright connected with the accident, but three or four days
later the patient found that the fingers of the left hand were get-
ting stiff and beginning to feel numb. This condition of stiffness
and numbness continued for seven weeks, when, on arising one
morning after a rather sleepless night, the patient found his hand
in the attitude of main en griffe. This position was gradually
changed into one of flexion of the wrist and fingers, with prona-
tion of the forearm (Fig. 53).

The shoulder and upper arm were not involved ; the forearm
was pronated. The hand was flexed on the forearm ; the four
fingers were so tightly flexed that the nails dug into the palm of
the hand. The fingers were tightly pressed together, and the
thumb was firmly fixed on the external surface of the second pha-
lanx of the index finger. The contractions, which persisted at
night, were so pronounced that all efforts at reduction were un-
successful. Hysterical stigmata were eventually added to these
symptoms. The left side of the body became the seat of a hemi-
ansesthesia, and the taste, smell, and hearing were much blunted
on the left side. Both visual fields were contracted, but most
markedly on the left side. The color fields were, however, not
reversed.

At first, magneto-therapy was able to induce a return of cuta-
neous sensibility to all of the left side except the parts involved in
the contracture. They remained anaesthetic. A later attempt

3IO FUNCTIONAL EFFECTS OF INJURY.

caused the sensibility to return to the left hand and arm, but was.
followed by a contracture of the sound (right) hand.

Hysterical contractures may exist only for a short time
and disappear suddenly, or they may be persistent and some-
times they are permanent. They do not relax during sleep,,
though they may often be made to do so by suggestion, and
almost always disappear during ether narcosis. When
affecting the arms or legs they usually assume forms dif-
ferent from those of organic contractures. In a common
type of contracture of the arm, when either the arm alone
or the arm and leg are both involved, the arm is drawn
across the chest, the forearm is partly flexed, the wrist is
flexed, and the fingers are tightly closed in the hand. The
hand may assume various positions from the preponderance
of the contracture in certain muscles. The position for
holding the pen, due to spasm in the interossei, is not un-
usual.

When contracture affects the lower extremities, they are
usually held absolutely immobile and straight. Not uncom-
monly a contraction of the calf muscles produces a condition
of equino-varus with flexion of the toes.

Although in paraplegia the legs are most frequently held
in rigid extension and adduction, they may assume the same
type of flexion as is seen in organic disease of the spinal
cord.

In some cases the diagnosis of hysterical contracture is
very puzzling, although it may usually be made by examin-
ing the reflexes (if the contractures do not make this impos-
sible), the condition of the muscles themselves, and by look-
ing for other associated signs of hysteria.

Local and persistent spasms may occur in individual mus-
cles or muscle groups. The extrinsic eye muscles may be
involved. Hysterical blepharospasm, which is not infre-
quent, may be unilateral or occur on both sides. It gives the
appearance of ptosis. Spasm of the muscles of the eyeball is

TRAUMATIC HYSTERIA.

less frequent. One side of the face may be the seat of spasm,
giving rise to the appearance of paralysis of the other side.
Spasm of the tongue occasions difficulties of speech. In the
muscles of the neck it may cause the position of torticollis.
Spasm or contracture of the back muscles may produce con-
siderable spinal curvature. Contracture and swelling of the
abdominal muscles are the causes of phantom tumors.

Tremor is an almost constant symptom of hysteria fol-
lowing accidents. In its most common form it is a fine
rapid tremor of the fingers and hands, such as occurs in
neurasthenia. It may sometimes imitate the tremor of pa-
ralysis agitans or the coarse inco-ordinated movements of
multiple sclerosis. It becomes more marked under the in-
fluence of excitement and fatigue, and usually disappears
during sleep. In location it may be generally distributed,
though it is more commonly limited to certain groups of
muscles.

There are also a variety of morbid movements commonly
regarded as hysterical in character, although in many of
them other hysterical stigmata are absent. Among these
may be mentioned the rhythmical chorea of Charcot, para-
myoclonus multiplex, and a series of inco-ordinated move-
ments of forcible and shocklike character.

In Charcot's rhythmical chorea, or chorea major, there
"are alternating contractions in opposing groups of muscles,
especially in those of the hand and trunk. Another variety
has been called electrical chorea, from the sudden and forci-
ble choreiform muscular contractions. It differs in course
and in geographical distribution from the disorder named,
after its first describer, Dubini's disease.

Schutte has recently reported a case of paramyoclonus
multiplex which seems to have been one of the ultimate de-
velopments of traumatic hysteria, and which shows how
long a time may elapse between an accident and the appear-
ance of exaggerated symptoms :

312 FUNCTIONAL EFFECTS OF INJURY.

The patient was a man, fifty-two years of age, having no heredi-
tary nervous taint, who had always been well and strong. He fell
some little distance, striking his head. The accident was followed
by weakness, dizziness, a feeling of pressure in the head, and simi-
lar subjective symptoms. The patient, soon after the accident,
was pronounced as unable to work, and entitled to the indemnity
which the German law allows in such cases. For eight years he
presented the ordinary symptoms of hystero-neurasthenia. At the
end of this time he was admitted to the hospital, suffering from
the complication of paramyoclonus multiplex. The hysterical
stigmata, which had been previously observed, had now disap-
peared, and the general condition was one of neurasthenia, to
which had been added morbid muscular movements. These move-
ments were more marked in the muscles of the trunk, and con-
sisted of fibrillary twitchings and forcible clonic contractions.
The arms and legs were involved to a less degree. On making
intended movements many muscles not necessary for the move-
ment were called into play. During sleep, and when the patient
was at rest, the clonic spasms ceased, but the fibrillary twitchings
continued. The sleep was disturbed. The tendon reflexes were
active, and there was a slight bilateral foot clonus. It was an ap-
parently typical case of paramyoclonus multiplex, and is one of the
few recorded examples of that symptom-complex resulting from
traumatism.

Hysterical Joints. — Hysterical joint affections were rec-
ognized and described by Brodie, and since his time have
become familiar pictures to surgeons. They are frequently
the sequelae of accidents, after which they may appear imme*
diately, although there is usually the intervening meditative
period. Their development, when it once begins, is usually
rapid. In more than one half the cases the knee is the joint
affected ; after it, in order of frequency, come the hip, wrist,
shoulder, and ankle.

The most prominent manifestation of hysterical joint af-
fections is pain which is very much intensified by any move-
ment. Discriminating examination shows, however, that the
hyperalgesia is in the skin rather than in the joint itself.
The hypersensitiveness is not necessarily limited to the

TRAUMATIC HYSTERIA.

313

region of the articulation, as in organic disease, but may in-
volve the whole limb. The position in which the limb is
held does not always indicate the functional nature of the
trouble.

The skin is not reddened, and oedema is rare.

The muscles around the joint are usually the seat of con-
tracture, with or without paralysis, and in this situation also
there are geometrical areas of anassthesia.

In regard to diagnosis I can not do better than repeat a
remark of Pitres's relative to an hysterical coxalgia : " Ab-
sence of redness and swelling, little or no spontaneous pain,
no sensitiveness on percussing the heel, neither retraction
of the muscles nor morbid positions, which is the organic
lesion that could persist for nearly two years with a similar
category of negative symptoms?"

Hysterical joints are freely movable in ether or chloro-
form narcosis — a fact, however, which can rarely be demon-
strated in medico-legal cases. It is well shown in a case of
Charcot's :

The patient was a man, forty-five years of age, with negative
personal and ancestral history. While working at a circular saw,
the machine got out of order, so that he was tossed fifteen feet in
the air, coming down on the buttocks. There was no loss of con-
sciousness nor fracture or dislocation of any bone. The left foot
was slightly bruised, but the patient got up and walked a short
distance. Very soon, however, he found that he could not touch
the left foot to the floor without much pain in the whole left leg.
The left leg soon became so contracted that the knee-jerk on that
side could not be obtained, and movement at the hip became very
limited. When the patient was sitting, the left lower extremity was
extended, not touching the floor. On attempting to rise, the mus-
cles of the arms were called into play ; in order to avoid movement
of the thigh muscles when standing (Fig. 54), the whole weight of
the body rested on the right leg, causing the left side of the pelvis
to be tilted up. There was also considerable curvature of the spine,
the convexity being toward the right ; the left leg and thigh were
slightly carried forward, so that the great toe of the left side was
twenty centimetres higher than that of the right. Measurement

314

FUNCTIONAL EFFECTS OF INJURY.

showed no real shortening. The movements at the hip joint were
very limited and caused expressions of great pain. The surround-
ing muscles were rigidly contracted, and the overlying skin was
insensible to pricks. There were many other hysterical stigmata.

The man was put
under deep chloro-
form narcosis, when it
was found that all
movement at the hip
could be freely made.
When the patient first
recovered from the ef-
fects of the anaesthetic,
movements at the hip
were painless ; but
when his attention
had rested a short
time on the affected
joint the old train of
symptoms returned.

An hysterical joint
may remain useless
for weeks or months.
When of long dura-
tion the condition is
liable to be seriously
i complicated by or-

ganic anchylosis, so that the joint may remain motionless
through the formation of adhesions, long after all the hys-
terical symptoms have passed away. Under the influence
of emotions, the hysterical joint affections may disappear
suddenly. In such cases relapses are frequent.

Reflexes.— Pathological exaggeration of reflex activity is
not the rule in hysteria, although the tendon reflexes are
often overactive. Foot clonus is extremely rare, yet I have
seen foot clonus in a case of paraplegia which presented
every other hysterical symptom, and which eventually re-
covered.

F:g. 54. — Attitude in a case of hysterical coxalgia.
(After Richer and Berbez.)

TRAUMATIC HYSTERIA.

315

The tendon reflexes may be diminished, though never
lost, in a paralyzed limb. This is particularly frequent
when anaesthesia is present as well as paralysis. The plan-
tar and conjunctivo-palpebral reflexes are commonly absent,
but the abdominal and cilio-spinal are sometimes retained,
•even when there is cutaneous anaesthesia.

Sphincters. — Impairment of sphincter control in hysteria
is very unusual. The paroxysm passes without involuntary
micturition, and the various forms of paralysis are usually
unassociated with either rectal or vesical disturbances.
There may be a frequent desire to urinate, due to psychic
rather than to local conditions, and spasm of the heck of the
bladder, resulting in retention of urine, occurs in some cases
of paraplegia. The mucous membranes of the bladder and
rectum rarely if ever lose their sensibility. If they do, it is
€asy to understand how involuntary passage of urine or
fzeces might occur. But the most competent observers ad-
mit that loss of sphincter control is among the most unusual
of hysterical accidents.

The Hysterical Attack. — The grande attaque of the
French consists of four periods: i, epileptiform; 2, period
of clownism ; 3, period of passionate attitudes ; 4, period
of delirium. Although it has been observed in other
Continental countries, it is only in France that the grand
attack is often seen in its full sequence of development.
Bernheim calls it the "attack of culture." It seems proba-
ble that the aggregation of so many hysterical patients as
are assembled in the SalpStrifere may have furnished sug-
gesting influences for the induction of exaggerated symp-
toms. In this country the hysterical attack is uncommon.
Knapp estimates it as occurring in ten per cent of traumatic
cases. Even then it never follows the complete type, but is
manifested by the epileptiform period alone, or by emotional
excitement, or by other parts of the grand attack. The term
hystero-epilepsy, which has been applied to the convulsions

3i6 FUNCTIONAL EFFECTS OF INJURY.

of hysteria, is a misnomer which has led to much confusion.
The disease is either hysteria or epilepsy, or the two diseases
occurring simultaneously in the same individual. Although
in many cases these two diseases occur together, and al-
though it may be impossible to distinguish between them, it
is better to state that such is the case than to employ a mis-
leading and indefinite nomenclature. There are marked dif-
ferences between epileptic and hysterical fits. In epilepsy
the convulsion is of short duration, is not necessarily pre-
ceded by an aura, and occurs very frequently at night. The
duration of a hysterical attack may be a half hour or more.
An aura is constant, and nocturnal occurrence is exceptional.
Biting of the tongue and involuntary passage of urine, almost
constant phenomena in epilepsy, do not occur in hysteria.
During the seizure the pupil almost always reacts to light in
hysteria, not in epilepsy, and after the epileptic attack the
knee-jerk is lost, which is not necessarily the case in hysteria.

Furthermore, the convulsive movements of hysteria have
an exaggerated character ; the period of tonic contraction is
longer than in epilepsy; opisthotonos is common. At the
expiration of the epileptic attack the patient commonly goes
into the condition known as post-epileptic stupor ; from the
hysterical epileptiform attack the patient usually recovers
immediately.

The attacks of hysteria may follow any of the causes
capable of inducing other hysterical phenomena. They are
sometimes very frequent, occurring many times a day, or at.
certain hours of each day. If they take place once, they
will usually recur. After an attack new symptoms may ap-
pear, or existing stigmata be made worse. Convulsive hys-
teria is a grave form of the psychosis.

A not uncommon equivalent of the hysterical attack is
the so-called hysterical coma. The cases I have seen were
in men who were brought to the hospital absolutely uncon-
scious. They were limp, inanimate masses, incapable of

TRAUMATIC HYSTERIA. 317

being aroused by any stimulation. The vascular and respi-
ratory functions were normal. After a varying number of
hours the patients would wake up and walk home.

From the frequency with which they are found lying
senseless in the street, many of them come to be individu-
ally known to ambulance surgeons, who, when they pick
them up, recognize both the condition and the individual.

Hysterical coma may in many ways resemble apoplexy,
especially if it be complicated by hysterical hemiplegia. The
functional character of the affection, however, usually be-
comes evident if all the factors concerned are carefully ex-
amined.

In a case of Comby's a nervous woman, thirty-eight years of
age, without previous hysterical accidents, fell senseless as a re-
sult of a flash of lightning which killed two of her children who
were standing near her. The woman was comatose for four days.
When consciousness returned she was hemiplegic and hemianaes-
thetic on the left side, a condition which disappeared entirely in
three weeks. Two years after this, during a thunderstorm, the
patient again became comatose for seven or eight hours, awaken-
ing to find herself again hemiplegic and hemiansesthetic. In two
weeks she was again perfectly well. Three years later a similar
sequence of symptoms was observed by Comby. The patient
was picked up unconscious in the street, and brought to the hos-
pital. The coma lasted four hours. Examination then showed :
Facial expression good. No fever. Appetite excellent. The
whole left side was completely paralyzed. The left arm lay immo-
bile by the side of the body and, when lifted up, it fell lifelessly to
the bed. The patient was unable to raise the hand from the bed
or to spread the fingers apart. There was a slight paralysis of
the lower branch of the left facial nerve (this is a rather uncom-
mon though not an impossible symptom of hysteria) ; the move-
ments of the tongue and of other muscles of deglutition and of
articulation were also impaired. Knee-jerks present. No foot
clonus. All forms of sensibility of the skin and mucous mem-
branes were completely abolished on the left side. Vision, hear-
ing, smell, and taste were also absent on the left.

In fifteen days all these symptoms disappeared, and the pa-
tient walked out of the hospital apparently as well as ever.

3l8 FUNCTIONAL EFFECTS OF INJURY.

Deaf-mutism is a rare accident of hysteria. That it may
occur as a result of injury is shown by the following case,
reported by Francotte :

A man, thirty-five years of age, who had previously had hys-
terical accidents, was bitten on the leg by a dog. He was very
much frightened, and so confused that he was taken in charge by
the police. When he arrived at the station he had lost all power
of speech, and was completely deaf. Francotte saw the patient
nine days after the accident. During that time he had uttered no
sound, and could only communicate with others by gestures, or
understand what was addressed to him by writing. The case was
cured by hypnotism.

Hiccough and cough are common symptoms of hysteria.
Blood is sometimes vomited or coughed up immediately
after the accident. Anuria may occur, but the passage of
large quantities of pale urine is more frequently observed.
Ordinarily the urine shows no characteristic chemical
changes, although occasionally temporary glycosuria has
been found. Nutrition may be seriously affected.

The other symptoms of traumatic hysteria resemble those
described under neurasthenia. There may be a variety of
subjective symptoms, of which, perhaps, the commonest is
the globus hystericus. Cardiac irritability and digestive
disturbances are frequently observed. There may be con-
tinued vomiting. Constipation is the rule. The respiration
is ordinarily normal, but becomes very rapid through emo-
tional influence. After nervous shocks, or local irritation of
the throat, the voice may be lost. Either aphonia, in which
the patient loses the power of uttering any sound, or mutism,
in which the power of speech is lost, are frequent hysterical
symptoms. As Pitres has pointed out, hysterical mutism is
often an isolated accident, which may be observed in per-
sons entirely free from previous nervous symptoms or active
hysterical manifestations.

Prognosis. — That death may occur as a result of hysteria
uncomplicated by organic disease, appears to be a matter

TRAUMATIC HYSTERIA.

319

of considerable doubt, although such a possibility is ad-
mitted by most authorities. Gilles de la Tourette quotes
several cases in which hysteria is said to have been the cause
of death. The immediate causes in the cases least open to
criticism were due to spasm of the throat and of the stom-
ach, and from exhaustion induced by long vomiting.

A patient at St. Luke's Hospital several years ago presented
the hysterical symptoms of hemianaesthesia, contraction of the
visual fields, and epileptiform convulsions, but we could discover
no evidences of any organic disease. The man was found one
morning dead in bed. The autopsy revealed no causes such as
are usually regarded as adequate to induce death.

There are, however, so far as I know, no cases of hysteria
reported as fatal in which microscopical examination had
excluded visible pathological alterations of nervous tissue.
That careful and thorough examination in accordance with
modern microscopical methods is necessary before it can be
said that a nervous disease is functional, has been thoroughly
demonstrated by the history of Landry's paralysis, a disor-
der which formerly was thought to be characterized by no
discoverable lesions, but which has recently been shown to
be due to degeneration of the ganglion cells in the spinal
cord and in the brain.

As we have seen, many cases of traumatic hysteria are
somewhat different from hysteria when it occurs from
causes other than traumatisms. In traumatic cases, impair-
ment of general nutrition may render the patient less ca-
pable of resisting the ordinary injurious influences of daily
life. Nevertheless, even in them, the prognosis of hysteria in
regard to life is very good. As regards complete recovery,
it is much less favorable than that of traumatic neuras-
thenia.

The patient with traumatic hysteria may be relieved of
his paralyses or contractures more speedily than the neuras-
thenic is rid of his lumbago. Yet the disease often remains.

320 FUNCTIONAL EFFECTS OF INJURY.

ready to show itself again under the influence of suggestion
or emotion, although its paroxysmal symptoms have disap-
peared. Although some cases get entirely well in a few
weeks or months, never to relapse, there is a general agree-
ment of authority that the disordered mental state of hys-
teria, which is the cause of the symptoms, is an extremely
tenacious condition, and that the prognosis in any given
case is always attended with uncertainty.

There are some considerations, however, which to a cer-
tain extent are of value in reaching a prognosis. ^Among
the most important of these is predisposition, which has oc-
curred through enfeeblement of the resisting powers of the
nervous system by transmitted ancestral defects or by ac-
quired exhaustion. Such predisposition is only occasionally
discoverable in traumatic hysteria, and the chances for re-
covery are naturally best, as in certain forms of insanity, in
the patients whose personal and ancestral record is free from
nervous stigmata. As regards age, it may be said that the
younger the patient the better are the hopes for ultimate
recovery. It must not be forgotten, however, that when
hysteria appears in children there may often be found a
strong hereditary predisposition to nervous disease. This
fact may more than counterbalance the favorableness of the
prognosis caused by youth. Hysteria in men is attended
with a more serious prognosis than in women.

The prognosis is better for the well-to-do classes, for in
them proper treatment can usually be instituted. The treat-
ment, which is a regulation of the mode of life rather than a
treatment by drugs, is expensive, and can only occasionally
be properly carried out in the working classes.

In regard to litigation, what is true for the prognosis of
traumatic neurasthenia may be made still more emphatic for
traumatic hysteria. The constant questionings and exami-
nations by lawyers and doctors are most potent suggesting
influences. They render the consciousness still more lim-

TRAUMATIC HYSTERIA.

321

ited, and give an increased permanency to the fixed ideas of
the hysterical patient.

Repeated examinations of a limb which is the seat of
hysterical paralysis render the loss of power more pro-
found and more permanent ; repeated tests for sensation
cause anaesthesia to deepen, to spread, or to appear in new
places ; it is well known that the symptoms of hysteria often
owe their genesis to the suggesting influences of hospital
life ; all these agencies are most prejudicial to ultimate re-
covery. It is the evil results which attend suggestion of
any kind upon the hysterical mind that has led to the gen-
eral abandonment of the use of hypnotism — a procedure
which may cause a symptom to temporarily disappear, but
which involves the danger of aggravating the mental state.

The hysterical patient is very suggestible even when not
hypnotized, and constant examinations almost invariably
suggest to him that the symptoms remain stationary or be-
come worse.

Recovery from hysteria is possible, even when the dis-
order has occurred in an aggravated form. But, as a rule,
the more numerous and severe the symptoms, the less it is
probable that the patient will ever be free from the disease.

The exaggerated psychical phenomena are of especially
serious import, as they denote a profound distuVbance of
mental function. The attacks, catalepsy, trance, and coma,
indicate that the disease is severe, and .that it has probably
developed in a predisposed brain.

Some of the stigmata, such as the anaesthesias and visual
disturbances, are particularly tenacious.

Recovery from the joint affections is usually slow. They
may frequently relapse or last for several years, and may
eventually cause permanent organic disabilities.

There are no means of foretelling how long a hysterical
paralysis may last.

In a case of Page's, paraplegia existed for four years and

322 FUNCTIONAL EFFECTS OF INJURY.

a half, and in a patient of mine, whom I have mentioned, the
left leg has been paralyzed for two years. Zein reports a
case of hysterical paraplegia in which recovery took place
after nineteen years ; and Morton Prince has seen three cases
of hysterical paralysis (two monoplegias and one hemiplegia
and hemianaesthesia) which began in the War of the Rebel-
lion and which had existed, one for twenty-eight and two
for twenty-nine years.

The brachial monoplegias seem, as a rule, the least per-
sistent of the individual forms of paralysis.

The prognosis of mutism, or aphonia, is nearly always
good ; speech is usually restored in a few weeks or months.
But all of these symptoms are liable to relapse, and it is
never justifiable to consider the hysteria as cured because
all the paroxysmal symptoms disappear.

The relapses, which may be more, or less severe than the
conditions which preceded them, follow very shortly after
apparent cure, or are separated by considerable periods of
time.

The rapidity with which hysterical symptoms may van-
ish, and become re-established, is well shown by a case seen
with Dr. G. E. Brewer at the City Hospital :

A man, thirty-eight years of age, alcoholic, fell in the street
and found Doth legs paralyzed. When brought to the hospital he
presented the classical symptoms of hysterical paraplegia — viz.,
great rigidity of the legs, inability to walk, and anaesthesia, with
perfect control of the bowels and bladder. He was put on appro-
priate treatment, and recovered so completely that in a few days,
he walked out of the hospital in a perfectly normal way. About
ten days later I was asked by Dr. Frank Markoe to see a case in
his wards at Bellevue Hospital. It was of a man who had been
found lying in the street with both legs paralyzed. The patient
was the same man that had been seen at the City Hospital.

Bibliography.

(The reader is especially referred to the comprehensive treatise
of M. de la Tourette.)

TRAUMATIC HYSTERIA.

323

Babinski, Contractures organiques et hystdriques. Soc. mM.
des hdp., Mai, 1893.

Bailey, A Case of General Analgesia. N. V. Med. Record, De-
cember 28, 1895. Ibid., The Diagnosis of Idiopathic Epilepsy.
Am. Med. Surg. BuL, August 8, 1896.

Berbez, Hysteric et traumatisme. Thhe de Paris, 1887.

Bernheim, Hypnotisme, Suggestion, Psychoth^rapie, i8gi.

Bremer, A Case of Hysterical Astasia-abasia suing for Dam-
ages. Journ. Nerv. and Ment. Dis., 1893, p. 13.

Briquet, Trait6 clinique et thdrapeutique de I'hystdrie, 1859.

Biocq, Sur une affection caract^risee par de I'astasie-abasie.
Arch, de neuroL, 1888. Ibid., Les troubles de la marche dans les
maladies nerveuses. Paris.

Brodie, Lectures Illustrative of Certain Local Nervous Affec-
tions. London, 1837.

Charcot, QEuvres completes. Paris, 1890.

Comby, J., Apoplexie hystdrique avec hemipl^gie gauche sur-
venue pour la premiere fois a. la suite d'une fulguration. Union
tn^d., 1894, No. 60.

Dana, C. L., Hamilton's System of legal Medicine, New York,.
1894.

Francotte, Sourd-muettite hyst6rique, etc. Mercredi medical,
1894, No. 40.

Guinon, Les agents provocateur de I'hyst^rie. Paris, 1889.

Hun, Two Cases of Traumatic Hysteria. Medical News, April
II, 1891, p. 403.

Janet, Etat mental des hystdriques. 2 vols, Paris.

Knapp, Traumatic Hysteria. Text-book of Nervous Diseases by-
American Authors, Philadelphia, 1895.

Konig, Weitere Mittheilungen iiber die functionellen Gesichts-
feldanomalien mit besonderer Beriicksichtigung von Eefunden an
normalen Menschen. Deutsch. Zeits.f. Nervenh., 1895, vol. vii, p. 263.

Laehr, Ueber Storungen der Schmerz und Temperaturempfin-
dung in Folge von Erkrankungen des Riickenmarkes. Arch, fiir
Psych., 1896, 3, p. 773.

Laudan, Ein Fall von Catalepsie. Wien. med. Presse, 1894,
Nos. 30 and 35.

Lebrun, Monopl^gie brachiale hystdro-traumatique. Arch,
mdd. Beiges, 1893, vol. i, p. 382.

Lepois, quoted by Gilles de la Tourette, op. cit, i, p. 13.

Miura, Trois cas de monopl6gie brachiale hysterique. Arch,
de Neurol., Mai, 1893.

24 FUNCTIONAL EFFECTS OF INJURY.

Mobius, Ueber den Begriff der Hysteric. Neurolog. Beitrage, i,
894.

Page, H. W., Injuries of the Spine and Spinal Cord, without
apparent Mechanical Lesion and Nervous Shock in their Surgical
nd Medico-legal Aspects. London, 1883. Ibid., Railway Injuries
1 their Clinical and Medico-legal Aspects. London, 1891.

Paget, Clinical Lectures and Essays. Second edition, Lon-
on, 1879.

Peterson, Physiological Experiments with Magnetism at the
;dison Laboratory. N. Y. Med. Jour., December 31, 1892.

Pitres, Le9ons cliniques sur I'hyst^rie et I'hypnotisme. Paris,
891.

Prince, Three Cases of Traumatic Hysterical Paralysis of
"wenty-nine. Twenty-eight, and Twenty-nine Years' Duration
5spectively in Males. Am. Jour, of the Med. Sci., 1892, p. 63.

Ibid., Hysterical Monocular Amblyopia. Am. Jour, of the Med.
'«., February, 1897.

Richer, Etudes cliniques sur la grande hystdrie, etc. Paris, 1885.

Reynolds, Russell, Paralysis and other Disorders of Motion
nd Sensation dependent on Idea. Brit. Med. Journal, 1869,
ol. ii, p. 483.

Schutte, E., Ein Fall von Paramyoclonus Multiplex bei einem
Jnfallskranken. Neurolog. Cblatt., 1897, No. i.

Sdrieux, Note sur un cas de paralysie hystero-traumatique des
uatre membres. Arch, de Neurologie, July, 1891, p. 31.

Souques, Etude des syndromes hyst^riques " simulateurs."
'aris, 1891.

Striimpell, Ueber die traumatische Neurosen. Berlin. Klin.,
888, Heft 3.

Sydenham, quoted by Gilles de la Tourette, op. cit., i, p. 15.

Tourette, de la, Gilles, Traits clinique et th^rapeutique de
hysteric. 3 vols, Paris, 1891 and 1895.

Zein, quoted by Gilles de la Tourette, op. cit., vol. ii, p. no.

CHAPTER IV.

UNCLASSIFIED FORMS.

In the preceding pages it has been repeatedly empha-
■sized that the diagnosis of the traumatic neuroses depends
upon the possibility of a clinical separation between organic
and functional nervous diseases. When an organic lesion is
■caused by injury, certain definite signs, which are ordinarily
absent in functional disorders and which point to injury in
definite areas of nervous tissue, usually present themselves
at once. Yet, while it is generally possible to draw the
<iividing line with reasonable exactness, and to infer from the
•circumstances of the accident and from the character of the
symptoms the probable nature of the pathological process,
there remains a group of cases which can not be satisfac-
torily classified. Although they present many of the symp-
toms of hysteria and neurasthenia, their clinical course is
more serious than is customarily observed in these disorders,
and some symptoms are present which, while not giving
positive evidences of definite focal injury, are different
from those usually brought about by the impaired mentality
of hysteria or the over-fatigue of neurasthenia. These are
transition types, and bear testimony to the artificial charac-
ter of the distinction between "organic "and "functional"
disease. They have received various names, and have been
the object of much pathological speculation. By Dana they
are called the " grave traumatic neurosis," on account of
their unfavorable prognosis. Crocq denominates them as
" the grave traumatic neurosis, with probable organic le-

226 FUNCTIONAL EFFECTS OF INJURY.

sions." Knapp, reasoning from the analogy of the organic
character of some of the symptoms, from certain correlated
experiments on animals and from the results of a few hu-
man autopsies, goes still further, and gives to them the
name of "traumatic sclerosis."

As clinical occurrences they are, in my experience, dis-
tinctly rare. Of the large number of patients with nervous
diseases coming to the Vanderbilt Clinic in the past few
years, none are recorded as belonging to this class. Dana
also considers them infrequent. Knapp, on the other hand,
has met with them more often. Some, but not all, of the
cases recorded by Oppenheim in his Traumatic Neuroses
may properly be classed with these unusual forms. Rela-
tive to frequency it may be remarked that his cases, al-
though they were collected during a period of eight years
from the large nerve clinic of the Charity, in Berlin, were
only forty-two in number. It is partly owing to Oppen-
heim's description that so much confusion has arisen con-
cerning the nature of the conditions which most frequently
result from injury and shock. Many persons have inferred
that the symptomatology, as detailed by the German neu-
rologist, was intended to apply to all the affections em-
braced in the term traumatic neuroses. Such an interpre-
tation, however, was not Oppenheim's intention. Although
cases similar to some of those which he describes are in-
frequent, that they occasionally occur there can be no doubt.
My own experience with them has been slight, and in de-
scribing them I shall be obliged to rely chiefly upon facts
as reported by other observers.

iEtiology. — The accident which gives rise to these cases
has usually been severe. Considerable injury of the body is
the rule. Psychic shock is sometimes, but not always,
present. In a case of Knapp's, which ended fatally, "a
woman was dragged in a railway collision, her head and
back bumping over the sleepers." Such accidents as are of

UNCLASSIFIED FORMS. 327

not uncommon occurrence in factories, in which the body
may be seriousty lacerated by revolving machinery, or tossed
about by explosions, are most frequently followed by the
serious forms. Falls on the head from great heights, or any
accidents in which the victims are subjected to very severe
concussions, contusions, and wounds constitute their most
frequent starting points. From the comparative immunity
from exposure to such injuries among the well-to-do classes,
the grave traumatic neuroses are most commonly observed
in laborers and factory hands, or in persons whose occupa-
tions constantly expose them to danger. For similar rea-
sons these disorders are most frequent in men.

Symptoms. — The onset of the symptoms is in many respects
similar to the onset of simple traumatic hysteria and neuras-
thenia. On account of the severe injuries to the body, there
is an increased frequency in the occurrence of physical shock,
and the patients often remain unconscious for a considerable
length of time after the accident. If there has been exten-
sive laceration of the body, the character of the nervous
symptoms may not show itself until some time after the
wounds have begun to heal. It then becomes evident that it
is more serious than is ordinarily met with in accident cases
in which acute organic injuries to the nervous system are ab-
sent. Of the mental symptoms, depression is often present
in a marked degree. The patient sits immobile and inatten-
tive, with many of the evidences of profound depression.
He apparently takes no interest in his condition, his pros-
pects, or his family. If spoken to, he replies, but his replies
are monosyllabic or brief. He rarely presents the mutism
of severe melancholia, yet he is impatient of all interference,
and wishes to be left quietly alone. He may be seen crying
quietly by himself. Suicide has occasionally occurred. In
some cases the picture resembles dementia rather than
melancholia. The patient becomes apathetic and childish,
with considerable impairment of intellectual capacity,

28 FUNCTIONAL EFFECTS OF INJURY.

aused by loss of memory and lack of attention. The am-
esia is chiefly for recent events, although it may be so pro-
ounced that it is impossible for the patient to distinctly re-
all happenings of previous years. He forgets names and
iTords, but usually remembers faces. AH details of the acci-
ent may be entirely forgotten, especially if the head injury
as been severe. The lack of attention does not appear to
le a lack of attention to outside matters such as is com-
lonly seen in introspective mental states. The patient ap-
lears to be thinking not so much about himself as of noth-
ig at all. It is an inhibition of psychic processes rather
ban a diversion of thought into morbid channels. The
cental state resembles that of hysteria more closely than
: does that of neurasthenia, so that the patient is not the
uerulous, petulant invalid, but presents rather the type of
he apathetic man, prematurely old, who is suffering from a
erious disorder affecting the mind which is characterized
y a limitation of all intellectual processes.

Such a mental state renders the patient incapable of pro-
Dnged mental effort. He is entirely unable to work, and
ften can not keep his attention sufficiently concentrated for
he performance of the simplest tasks.

The psychic condition is often revealed by the facial ex-
ression. The face is pale, often of a grayish appearance,
nd the lines in the face may be drawn. The expression is
idicative of absent-mindedness or of depression.

Disturbances of motion are the most frequent and the
lost pronounced of the physical symptoms.

Tremor is constant, and appears in various ways. It is
sually a tremor which disappears when the muscles are at
est, but is very much intensified during the execution of
itended movements and under the influence of excitement
r fatigue. It may be nothing more than an exaggeration
f the common neurasthenic tremor, in which form it is
lost commonly observed in the hands. The patient finds

UNCLASSIFIED FORMS. 329

it difficult to perform the finer co-ordinated movements ;
the hands may tremble so much that it is only with diffi-
culty that he can button his clothes. Similarly, the hand-
writing is often illegible from the uncertainty and irregu-
larity of the pen strokes. In other cases the tremor of the
hands and arms is so coarse, and the excursions are so ex-
tensive, exaggerated, and jerky, and so much increased by
intended movements, that it is very similar to the tremor
which is seen in multiple sclerosis. If the patient attempts
to touch the tip of the nose with his index finger when his
eyes are closed, he comes very wide of the mark. Tremor of
this character renders the individual seriously incapacitated.
The movements are so uncertain that the ordinary affairs of
daily life can only be performed after deliberation and with
care. There may be considerable difficulty in eating ; in
attempts to raise a glass full of water to the lips, the water
may be spilled on the floor or on the patient. The tremor
is usually most marked in the hands and arms, although
sometimes there is shaking of the head as well.

Nonne has recently reported a number of cases which
presented peculiar and characteristic tremor, and in which
the movements did not affect single muscles or segments of
limbs, but one or both extremities. It was a shaking tremor
which, when sufficiently intense, agitated the whole body,
so that the patient was unable to either walk or stand. The
muscles of the affected extremities had a marked tendency
to contract, so that they stood out hard and tumorlike. This
tremor was therefore distinguishable from that of multiple
sclerosis, of exophthalmic goitre, of paralysis agitans, or
from that due to hysterical, senile, toxic, or other causes.
In slight cases the morbid movements ceased during rest.
In severe cases they continued as long as the patient thought
himself observed or was excited in any way. The gait of
these patients was characteristic from their attempts to
overcome the contractions of the flexor and extensor mus-

330

FUNCTIONAL EFFECTS OF INJURY.

cles of the legs, while these extremities, or even the trunk,
were being violently shaken by the tremor. Cases similar
to those described by Nonne are frequently regarded as
simulators. A man presenting these motor symptoms, who
was for a time under my observation at the Workhouse, was
considered by the guards to be malingering in order to
escape being made to work. In all of Nonne's cases the
symptoms remained unchanged for several years, and the
question of simulation, or even exaggeration, could be ex-
cluded. In one the patient committed suicide, after the
symptoms had existed for six years :

Male, fifty-five years of age. Ancestral and personal history
negative. A previously healthy man. After a fall on the back
and head, by which two ribs were broken, the patient found him-
self unable to walk. There was no trouble with the sphincters.
In six weeks after the accident he could walk a little, but never
was able to return to work.

The patient was examined one year after the accident. He then
walked with legs apart and knees slightly flexed. There was con-
siderable dorsal flexion of foot in walking, and he pushed himself
forward from the hips at the same time, thereby showing vacillation
and coarse, shaking tremor in the trunk and all extremities. On
standing, a slight tremor of the trunk persisted. No Romberg
symptom. On walking, many muscles became the seat of invol-
untary contractions, which the patient could not voluntarily over-
come. There was slight bilateral foot clonus. All the reflexes
were active. The strength was diminished in the upper extremities
and still more so in the lower extremities. There was some diminu-
tion of sensibility in the legs. There was slight lateral nystagmus
and a moderate limitation of the visual fields. Speech was not in-
terfered with. The intelligence was good, and there was no mental
depression. Sleep and appetite normal. The clinical picture, with
the exception of some variations in cutaneous sensibility, remained
unchanged for six years. [However, since at the end of this period
the patient took his own life, it is probable that depression had
displaced the previous normal mental condition.]

Although the gait in the unclassified forms does not pre-
sent the stiff, dragging, spastic character of the gait of mul-

UNCLASSIFIED FORMS.

331

tiple sclerosis, it is rarely the gait of a normal person. The
patients walk slowly and hesitatingly, and may drag their
feet a little, but the gait has no evidences of true paralysis or of
contracture. There may be considerable swaying of the body
on standing with closed eyes. In some cases there are fibril-
lary twitchings in the muscles, a symptom which is especiall}'
frequent in the muscles of the shoulders or of the face. The
tongue is tremulous as a rule, and disturbances of speech are
common. The voice is thick and the enunciation indistinct.
The speech defects differ from those of simple traumatic neu-
rasthenia in that they are more or less beyond the patient's con-
trol. With the best endeavors and closest attention he may
be unable to articulate clearly. The voice also often has a jerky
•character, another symptom common in multiple sclerosis.

Paralysis can not be recognized as a symptom of these
transitional forms. When there occurs a localized paralysis,
it must be explained as a hysterical symptom or as an un-
equivocal indication of organic disease.

Indeed, the characteristic which renders the classification
of these cases so difficult is, that they present no evidences
which permit of the diagnosis of a focal lesion such as may
be made in cases of organic injury to the nervous system,
and that the symptoms differ in character and in association
from those of the functional disorders. Some of the clinical
manifestations of hysteria, such as anaesthesia and contrac-
tion of the visual field, may be found, but paralysis is absent.
Paralysis may occur in certain forms of hysteria which have
other severe symptoms, but in such cases the whole symptom-
complex would be usually explained by the assumption of
hysteria or hystero-neurasthenia.

Although no muscle or muscle groups are paralyzed in
the' unclassified forms, there is a weakness in all the muscles.
The patients are loath to make voluntary movements, they
become tired quickly, and muscular exercise and fatigue
cause an increase in the other symptoms.

32 FUNCTIONAL EFFECTS OF INJURY.

As there is no paralysis, so there is an absence of muscu-
ir atrophy. The whole muscular system may share in the
eneral malnutrition, but there is no selective wasting of
luscles. The electrical reactions usually remain normal,.
Ithough diminished excitability of the muscles to electricity
as been observed.

The deep reflexes as a rule are exaggerated. The knee-
;rks are usually so active that taps on or above the knee
iduce very quick and forcible muscular contractions. In
Dme cases a slight foot clonus has been observed, but this,
j'mptom is rare. A few cases have been described in
7hich the knee-jerks are diminished, but in no case have
tie knee-jerks been said to be lost when Jendrassik's method
f re-enforcement has been used. The superficial refiexes^
sually present nothing characteristic, though they some-
imes give sluggish or imperfect responses to stimulation,
'he abnormal changes in reflex activity affect the two sides
f the body equally.

Sensory symptoms may be similar to those observed in
imple traumatic neurasthenia or hysteria, but they are
luch less prominent. If traumatic lumbago is present it
resents the ordinary symptoms characteristic of that con-
ition ; apart from lumbago, pain in these forms is not very
requently or very emphatically complained of.

Headache is usually present in slight degrees, but it or-
inarily lacks the exaggerated character of neurasthenic
eadache. The patient feels a tightness or constriction
round the head, the existence of which he admits when
uestioned, but of which he only rarely complains. There
> usually some pain in the back, and pressure over painful
reas may be poorly borne ; but a characteristic of the pain
1 these forms is that it is passive rather than active. There
re rarely heard the constant complaints (so common in
eurasthenia) of terrible pain and hyperaesthesia which are
lade worse by every movement and by every jar. If the

UNCLASSIFIED FORMS.

333

patient is asked if he has pain in certain parts, he may reply
in the affirmative, but the complainings of constant pain and
exaggerations of sensibility are usually absent.

Angesthesia, which has frequently been observed, differs
in important particulars from the anaesthesia of typical hys-
teria. In extent, distribution, and selection it resembles the
loss of cutaneous sensibility such as is found in the depress-
ive and demented forms of insanity, more closely than the
typical loss of sensibility commonly occurring in hysteria.
The sensory abnormities are in accord with the mental state
of inattention, indifference, or depression, and most fre-
quently exist as a general blunting of cutaneous sensibility.
Slight touches on any part of the cutaneous surface are im-
perfectly perceived, and pricks with sharp instruments cause
only slight pain.

Less frequently the touch sense may be fairly well re-
tained while there is a generalized analgesia. In some of
Oppenheim's cases the analgesia was limited to the hairy
scalp.

While it is more common for the impairment of sensibil-
ity to be general than for it to be limited to circumscribed
areas, such limitations are occasionally observed. They are
most frequently found on the back and legs, but they are
never sharply defined like the local anesthetic areas of
hysteria. Even in the localized areas of anaesthesia occur-
ring in these rare forms, the sensibility to any of the various
forms of stimuU is rarely completely abolished. It is dimin-
ished rather than lost, and the areas of diminution merge in-
sensibly into the regions where sensations are better per-
ceived. It is consequently very difficult to make diagrams
of anaesthesia in these cases. The patients give unsatisfac-
tory and contradictory answers, and it is oftentimes impos-
sible to determine just where the boundaries of the anaesthetic
areas are.

Symptoms referable to the special senses are common,

334

FUNCTIONAL EFFECTS OF INJURY.

of which the most prominent are disturbances of vision.
Nystagmus, an important symptom in multiple sclerosis, is
not infrequently encountered. It is usually limited to lateral
movements and is rarely pronounced. There may be weak-
ness or paralysis of one or more of the extrinsic ocular mus-
cles, thus causing- double vision. Inequality of the pupils, as
vv^ell as the failure of one or both pupils to contract under
the stimulation of light have also been recorded. The
condition of the pupils is essentially different from that
found in simple traumatic neurasthenia in which the dilata-
tion and the quick response to light and the alternating con-
traction and dilatation are frequent. There is, in many
cases of the unclassified forms, some slight limitation of
the visual fields. Optic atrophy has been rarely observed.
Case X, of Oppenheim's, apparently developed atrophy of
the optic nerve as a result of a railway accident. The his-
tory of the case, briefly told, is as follows :

A man, forty-eight years of age, received in a railway accident
severe injuries of the back of the head and (probably) of the back.
He was rendered temporarily unconscious, but soon came to him-
self and helped in clearing away the wreck. From that time on-
ward he complained of pain in the back of the head and a tired
feeling in the back and a constantly increasing numbness and
weakness of the whole body. A year after the accident the sight
in the right eye became impaired. The patient was first examined
by Oppenheim two years after the accident. The symptoms at
that time consisted of depression, anxiety, diminution of intellec-
tual power, dizziness, and attacks of unconsciousness. The visual
field for the left eye was normal, but the right visual field was con-
siderably contracted. The right optic nerve, seen with the oph-
thalmoscope, showed a pallor of the whole papilla and a narrow-
ing of the retinal vessels.

He was examined again after two years. None of the symp-
toms had improved and some had grown worse. The patient was
very depressed and wished to be alone. There were occasional
temporary losses of consciousness, the exact nature of which are
not evident from the history. The visual impairment was more
marked than at the previous examination, and the optic-nerve atro-

UNCLASSIFIED FORMS.

335

phy had become pronounced, especially on the temporal side.
There was a tremor which had many characteristics in common
with the tremor of multiple sclerosis. The speech was thick-
There were various disturbances of sensory function.

Next to vision, hearing is the most frequently affected of
any of the special senses in the unclassified forms. There
may be dizziness, subjective auditory disturbances, such as
buzzing and ringing in the ears and other annoyances sim-
ilar to those observed in traumatic neurasthenia. Diminu-
tion of hearing is more frequently observed than the hyper-
sensitiveness of the auditory apparatus which is common
in neurasthenia. It may affect one ear more than the
other, or there may be a comparative deafness on both
sides.

Taste and smell are rarely abolished. If these senses are
affected at all, there is usually nothing more than a slight
diminution of their functions.

The general symptoms resemble those of traumatic
neurasthenia. The sleep is interrupted and disturbed by
bad dreams. The patients often have the grayish, lifeless-
color of the skin commonly seen in chronic nervous disease.
The appetite is poor, and there may be a variety of gastric
disturbances. The bowels are constipated. Nutritional
disturbances are often well marked. The patients lose in
weight and sometimes become considerably emaciated. The
vascular symptoms are not constant. The heart may remain
apparently normal in structure and function ; in some cases
there is a persistent tachycardia, and there may eventually
appear evidences of hypertrophy and dilatation of the heart.
The urine shows no characteristic changes. If there is
a marked degree of arterio-sclerosis, the urine may be
pale and of lowered specific gravity. Sexual desire and
power are very constantly diminished and may be entirely
lost.

Pathology. — From the complexity and peculiar character

336 FUNCTIONAL EFFECTS OF INJURY.

of their symptoms, and from the absence of any definite
knowledge regarding their pathology, it seems to me more
advisable to simply record the occurrence of such cases,
without, for the present at least, claiming that they all have a
common pathology, or without insisting too strongly upon
what the most probable nature of their pathology is. Some
of the cases may owe their symptoms to scattered foci of
morbid tissue change in the brain and perhaps the spinal
cord, such as occur in the brain in cerebral endarteritis, or in
the whole cerebro-spinal axis in multiple sclerosis. Most of
the symptoms have occurred in men who are in the middle
or later decades of life, a time when degeneration of the vas-
cular system is encountered with particular frequency. Two
autopsies (Sperling and Kronthal, Bernhardt and Kronthal),
made upon patients who died during the period when these
grave symptoms were marked, have disclosed thickened ves-
sels, with areas of degeneration in the cerebro-spinal axis. It
seems more reasonable to suppose, however, that in these
cases the injury added activity to a process already existent,,
rather than that it caused a sclerosis of vessels which were
previously healthy.

The probability and possibility of the occurrence of intra-
cranial or intraspinal injury, without there being any reason
to suspect gross contusions, lacerations, or haemorrhage, has
already been discussed in preceding pages.

There can be no doubt but that minute and multiple
lesions may acutely occur in the brain as a result of injury,
and that they may furnish the general evidences of cerebral
commotion, without indicating which portions of the brain
are chiefly affected. Of the nature of these lesions we are
ignorant, though it is probable that the larger number of
them are haemorrhagic. That such lesions (see case on page
82) may occur in the spinal cord without causing the death
of the patient still remains to be proved, although there is
reason to suppose that they can.

UNCLASSIFIED FORMS.

337

The existence of disseminated areas of hasmorrhage seems
the most plausible pathological explanation for the types
which present the exaggerated forms of tremor and marked
increase of reflex activity, with notable inhibition of psychi-
cal function.

In other instances it seems as though hysterical and or-
ganic symptoms occurred together. Also many of the cases
of Oppenheim, in which the symptoms both of neurasthenia
and hysteria occur together in severe degrees, may be
accounted for by the simultaneous existence of .those two
disorders.

It is probable that it will some day be possible to make
the group of unclassified forms more exclusive. Some of
the cases may, when our clinical and pathological knowledge
is more advanced, be enrolled as variations of some organic
disorders which to-day are but imperfectly understood ;
others may be shown to be the results of too long exhaustion
of nerve cells, and still others may be found to be consist-
ent with the clinical course of the multiform psychosis
hysteria.

From the observation of the profound nervous disturb-
ances which result after physical injury in heavy drinkers,
and in persons whose vascular systems are in advanced
stages of degeneration, I have become convinced of the
force of Saenger's 'suggestion that some of these forms
may be properly regarded as owing their existence to
organically degenerated nervous systems quite as much
as to the accidents which are supposed to have caused
them.

Diagnosis. — The diagnosis of the unclassified forms is a
diagnosis by exclusion. It can only be made when the symp-
toms are of a character to prevent them from being regarded
as surely indicative of organic disease, or when they present
distinct variations from the more common types of the funC'
tional nervous disorders which follow accidents.

338 FUNCTIONAL EFFECTS OF INJURY.

As has been said, it seems highly improbable that all of
the cases which must for the present remain unclassified have
a common pathology. The symptoms present too wide a
variation to make such a supposition tenable. The mental
state of these cases may be nearly normal, or it may be that
of depression, or intellectual power may be so much dimin-
ished as to give a picture similar to that of senile dementia.
The motor disturbances also vary greatly. In the cases
which most closely resemble multiple sclerosis the symp-
toms are rarely identical with those commonly observed in
multiple sclerosis. In the unclassified forms also diplopia is
uncommon, nystagmus is only slight, and the gait has not the
marked spastic character of multiple sclerosis. In the group
of cases described by Nonne, the motor symptoms differ
essentially from the motor symptoms of any disease hitherto
described. The sensory disturbances of the unclassified
forms resemble those of hysteria, but the}' also differ in
essential particulars from the hysterical aneesthesias which
are commonly met with. Consequently, when we assign any
given case of nervous disease following injury to the category
of unclassified forms, we can go no further than to say that the
case is one of severe nervous disorder. We can not definitely
specify upon what pathological basis it rests, or by what the-
ory its symptoms may best be explained. Nevertheless, al-
though the diagnosis can not, for the present, be precise, it is
usually easy to see that the patient is suffering from an affec-
tion more serious than neurasthenia or hysteria are generally
supposed to be. The "general appearance and manner, and
the exaggerated character of many of the symptoms, indicate
that there exists pronounced disturbance of nervous function.
Until the existence of these forms becomes more familiar
to physicians, many of these patients will continue to be re-
garded as simulators. Such an opinion is manifestly unjust,
as has been amply shown by the long periods of time during
which the symptoms have frequently remained practically

UNCLASSIFIED FORMS.

339

unchanged, and in many cases the entire absence of any
motive for simulation. For certainty of diagnosis it is usu-
ally necessary for the injured person to be constantly under
observation for a considerable length of time. It is only by
such means that error can be avoided in the diagnosis of dis-
orders whose pathology and symptomatology are so uncer-
tain and so variable.

Prognosis. — Of all the factors which are concerned in a
consideration of these unclassified forms, the most secure
place is held by prognosis. It is a fairly well-established
fact that few of these cases recover completely. In trau-
matic neurasthenia most of the patients eventually return to
work, and in traumatic hysteria the individual manifestations
vanish, leaving the patient apparently well, although com-
monly branded with some of the hysterical stigmata. But
it is a fact common to all observers that the patients who
fall within the group of unclassified forms are only occa-
sionally able to resume all the duties which the disorder
obliged them to lay aside. Most commonly the symptoms-
attain a certain degree of development and then remain sta-
tionary. The patient gets neither permanently better nor
rapidly worse. By rest and quiet he may seem to improve,,
but any injurious influence, such as excitement or fatigue,
or attempts to work, cause the disturbances to return with
their former or with an increased intensity. Some of the
patients get progressively worse and die, without any cause,
other than the effect of the accident, becoming apparent. In
several, suicide has been reported as the cause of death. A
good many patients become eventually demented, or show
evidence of other forms of mental disease. Cases have been
reported as chronic lunatics which had previously been re-
garded as simulators.

The prognosis as to recovery is consequently very bad.
The prognosis as to duration or as to life must necessarily
vary with the individual case.

340

FUNCTIONAL EFFECTS OF INJURY.

Bibliography.

Bernhardt and Kronthal, Fall von sog. traum. Neuros. mit
Sect. Bef. Neurolog. Cblatt., 1890, No. 4.

Crocq, Les n^vroses traumatiques. Brussels, 1896.

Dana, The Traumatic Neuroses. Hamilton's System of Legal
Medicine, New York, 1894.

Knapp, Traumatic Sclerosis. Text-book of Nervous Diseases by
American Authors, Philadelphia, 1895.

Nonne, Ueber pseudospastische Parese mit Tremor nach
Trauma. Neurolog. Cblatt., 1897, Nos. 20 and 21.

Saenger, Die Beurtheilung der Nervenerkrankungen nach Un-
fall. Stuttgart, 1896.

Sperling and Kronthal, Eine traum. Neurose mit Sect. Befund.
Neurolog. Cblatt., 1889, Nos. 11 and 12.

PART III.

MALINGERING.

At the present time it is a rule, with few exceptions, that
persons who suffer real or supposed injury in railway or
other accidents demand compensation from the companies
or individuals responsible. Mr. Lawrence Godkin, in Ham-
ilton's System of Legal Medicine, states that " probably half
the jury cases tried in the courts of the State of New York
alone in any one year are actions for personal injuries re-
sulting from alleged negligence."

Mr. E. Parmelee Prentice has recently examined the rec-
ords of the Chicago courts which have jurisdiction of these
cases. The results are somewhat startling. He says : " In
1875 there were altogether about two hundred personal-injury
suits pending in Cook County. During the first six months
of 1890 the number of these suits brought in Cook County
was 346, the total damages claimed being $2,814,860. Dur-
ing the corresponding six months in 1896 the number of
such suits brought in Cook County was 893, and the total
amount of damages claimed was $13,510,000. It would be
reasonable to assume from these figures that there are now
pending in Cook County 3,600 of these cases, and that the
damages claimed are between fifty and sixty million dollars."
It is needless to add that this enormous increase is out of
all proportion to the increase in the number of accidents.

As is well known, the number of suits which come to

trial forms only a small fraction of the fotal number of claims

that are entered. Mr. Prentice estimates that for each claim
23 341

342

MALINGERING.

that appears in court it is probable that eight or ten claims
are settled without suit.

The chances of successful issue, which are notoriously
good, seem to be the most prominent consideration in bring-
ing claims for damages. The extent of injury, or the so-
cial position of the claimant, are matters of secondary im-
portance. The larger number of claims are brought for
trivial injuries, and among the claimants may be found the
poor and the rich, the capitalist and the pauper, men of all
professions, of all creeds, and of all classes of society. An
injury received through another's negligence has come to be
regarded as capital, which is to be converted as soon as pos-
sible into cash. This view has received judicial recognition
in Illinois, for by a recent decision of the Supreme Court of
that State a claim for personal injuries is property, which
may be put on the market and transferred or trusteed.

The larger portion of the population is thoroughly cog-
nizant of its rights, and loses little time after the accident in
calling the attention of the responsible parties to the injuries
which have been received. If no thought of financial recom-
pense occurs to the injured person at first, this is an omission
which will soon be remedied, either by sympathizing friends
or by persons experienced in the value of a personal injury as
the basis for a damage claim. The press exerts an important
influence upon the number of claims and suits for damages.
It is especially noticeable in rural districts, where the publi-
cation of a large verdict rendered in a negligence case is com-
monly followed by a very appreciable increase in the number
of personal-injuries claims brought in the neighborhood of
the original accident. This is partly due to the increased at-
tention given to injuries when it becomes generally known
that they may be so easily turned into financial benefit, and
partly because the lawyers who make a specialty of scanning
the papers in search of casualties have their attention thus
called to a promising field for their activities.

INDUCEMENTS TO MALINGERING. 343

Any press mention of an accident occurring in a large
city is sufficient to secure for the injured person an abun-
dance of gratuitous and unsolicited counsel. A man was
recently injured in New York late in the afternoon. Be-
fore eleven o'clock the next morning eight lawyers had
called at the hospital to see him. The last hours of the
unfortunate man were passed in listening to the arguments
of the attorneys who were going to secure damages for him,
had they gotten the chance.

The prosecution of personal-injury suits has become a
systematized business. Mr. Prentice says that many law
firms and brokers employ " runners," who have business
relations with saloon-keepers, policemen, and surgeons living
in the parts of the city where accidents are frequent. The
runners are constantly on the lookout for accidents, and as
soon as one occurs they discover it themselves, or are noti-
fied by their associates, and lose no time in trying to persuade
the injured person to intrust his claim to the firms or brokers
whom they represent.

In New York city the value of information regarding an
accident is so generally recognized that witnesses carry the
news voluntarily to the offices of " ambulance chasers," sat-
isfied with the small fee which they are almost certain of
receiving in return for their services.

It is, of course, simple justice that persons who have
been injured through the negligence of others should receive
reimbursement for the losses entailed by absence from their
business, and that they should be compensated for the suffer-
ing they have been made to pass through, as well as for any
resulting disability. And if, as sometimes happens, the in-
jured person is ignorant of his rights in such matters, it is
essential and proper that these rights should be explained to
him. Nevertheless, although the larger number of actions
which are brought for personal injuries are in all probability
based upon some actual, though often slight, loss of health,

MALINGERING.

". is inevitable, with the enormous increase in recent years
Q the number of accidents, that many cases which appear in
he courts be attended with a certain amount of absolute
raud. And the number of persons who demand compensa-
ion from corporations for trivial injuries, or whose claims
re absolutely fraudulent, and who, either by compromise or
ly failure to prosecute, or for any other reason, do not ap-
lear in the court, must be very large indeed.

The enormous sums paid every year by large corpora-
ions as indemnity for personal injuries renders the tempta-
ion to this kind of fraud very strong.

The general claim agent of a Western railway whose sys-
em covers about five thousand miles told me that in the
ear 1896 the company paid $350,000 in personal-injury
laims alone. This sum was entirely exclusive of the judg-
ments in cases which were brought to trial and which were
lecided against the company. Another large American
ailway pays between $200,000 and $400,000 damages every
ear for personal injuries.

It is, furthermore, a generally recognized fact that cor-
lorations prefer to settle small claims, even when convinced
hat they are fraudulent, to defending suits. They are forced
adopt the policy of settling claims rather than of letting
hem go to trial, from the well-known attitude of juries
oward the defendant when the latter happens to be a cor-
loration.' It is often flagrantly apparent in such trials that
he jury, in reaching a verdict, has concerned itself less
/ith the evidence than with a consideration of the rela-
ive financial resources of the plaintiff and of the defendant,
^his was recently shown in Brooklyn, when Justice Wilmot
1. Smith set aside the verdict of $1 1,000 obtained by Christian
' . Stark against the City of Brooklyn and the South Brooklyn
'erminal Railroad Company. Stark sued for damages for
ersonal injuries received by falling down an embankment
t Thirty-eighth Street. In a previous trial Stark received

SPECULATION IN DAMAGE CLAIMS. 345

a verdict of $10,000, which also was set aside. Justice Smith
said : " Prejudice or passion must have influenced a verdict
so at variance with a result which should have been reached
upon a sober, impartial, and rational consideration of the evi-
dence. A verdict of a jury should not be disturbed unless
to allow it to stand would result in a clear failure of justice.
I set aside the verdict because of a settled conviction in
my mind that to allow it to stand would be a serious reflec-
tion upon the administration of justice, and a confession that
the courts do not furnish a tribunal to which all citizens may
repair with confidence that their contentions will receive
rational and impartial consideration."

As long as prejudice, in the minds of the jury, against
corporations can be counted upon, the temptation to bring
damage suits upon insufficient grounds will remain very
great. The inducements for exaggeration and deceit which
are brought about by these means are furthered by the
speculation in damage claims, which has become so serious
a sociological problem. Many negligence cases are taken
on the contingent-fee plan by lawyers who associate with
themselves self-constituted medical " experts." The lawyer
supplies the witness, the doctor formulates his opinion, and
the result is one of two : The corporation settles, if it can do
so on not too extravagant terms ; or it decides to " fight " ;
it then engages in an unequal contest.

In this way many claimants and plaintiffs receive much
larger sums than any to which their injuries entitle them, or
are paid by the company even when they are entitled to no
compensation whatsoever.

The rectification of this question lies with the corpora-
tions themselves and, in a way, with the medical profession.

By showing themselves more zealous in promoting the
comfort and privileges of their patrons, and by insisting
upon more courteous behavior on the part of employees,
transportation and other companies which have to do with

346

MALINGERING.

large numbers of the public, have their surest means of
gaining the good will of the community, and of thus doing
away with the general prejudice against them which be-
comes so apparent when they engage in litigation against
private individuals.

The part to be done by the medical profession will only
be possible when legislation has provided an answer to the
vexed question of experts. At present, when there is no
legal criterion by which the value of a medical opinion may
be estimated, the testimony of a charlatan may carry as much
weight to the minds of a jury as that of a physician who has
shown himself skilled in his subject. It is the contradic-
tion of professional opinion in the witness chair which has
brought medical expert testimony into disrepute, and which
has caused it to be so often regarded as of questionable value
as evidence.

With the existing state of affairs it is not surprising that
the feigning of disease alleged to be the result of accidents,
or the exaggeration of symptoms due to actual injuries, are
difficulties against which corporations must constantly con-
tend and are means by which they are not infrequently de-
frauded ; yet from a purely medical point of view it should
be generally easy to unmask the malingerer.

Simulation is of necessity limited chiefly to diseases of
the nervous system. In visible physical injuries there is little
chance for fraud. Fractures, dislocations, and similar purely
surgical affections can not be successfully feigned. Few care
to voluntarily injure themselves in a way to cause any misin-
terpretation. Instances of serious wounds self-inflicted by
malingerers may be found in medical and criminal annals, but
in these cases the underlying motives were stronger than
the hope of financial reward. In litigation cases self-disfig-
urement is limited to abrasions or similar slight personal in-
juries, of which the trivial character is readily apparent and
about the means of whose production there can be no great

EXAGGERATION OF SYMPTOMS ACTUALLY PRESENT.

347

doubt. With the nervous system the case is different.
Nervous structure is hidden and protected ; no part of it
can be felt, and the optic nerve is the only part of it that
can be seen, and then only by means of the ophthalmoscope.
In popular opinion, nervous function is indefinite, and nerv-
ous diseases obey no recognized laws.

It is generally known that participators in accidents often
receive large sums of money for injuries to the nervous sys-
tem, although no visible injury be sustained and although
the claimants present no symptoms more definite than those
popularly supposed to constitute " nervous prostration."
Consequently it is to the imitating of diseases of the nervous
system that the simulator naturally turns, and it is with
them that he has the greatest chance for success. Neurol-
ogy is the most recently developed branch of clinical medi-
cine, and is the one least familiar to physicians generally.
As the study of it becomes more popular, successful simula-
tion will become more rare ; for, notwithstanding the com-
plexity and minuteness of the architecture of the nervous
system, and the mystery which must ever surround nervous
function, nervous disease causes characteristic and fairly
constant symptoms. The detection of simulation depends
upon a knowledge of them on the part of the physician, and
the inability on the part of the malingerer to exaggerate or
create the products of disease.

Fraud is attempted in accident cases in three principal
wa3^s :

I. Exaggeration of symptoms actually present. 2. The
substitution of origin, or the allegation that pre-existing dis-
ease was caused by the accident. 3. Entire simulation.

I. Exaggeration of Symptoms Actually Present.

Of the different ways the first is by far the most common.
It is rarely seen in organic injuries. The patient who has
sustained a fracture of the skull or an injury to the spinal

348

MALINGERING.

cord is too seriously hurt to think about exaggerating his
symptoms. It would hardly seem possible that uncompli-
cated injury to one of the peripheral spinal nerves could in
these days be so construed as to serve as the basis for a
claim that the spinal cord had been injured, and that as a
result the patient was suffering from incurable, progressive,
and ultimately fatal spinal disease. Yet such a case has
recently come to my knowledge. The musculo-spinal nerve
had been injured by a blow which had caused a peripheral
and probalaly temporary weakness of the muscles supplied
by the nerve. The physician for the plaintiff must have
counted upon the incapacity of the experts for the defense
and the gullibility of the jury, or else have himself been very
ignorant of nervous diseases. Fortunately, the injury was
recognized at its true value.

It is most commonly the functional conditions, and es-
pecially neurasthenia, which are fraudulently exaggerated.
The number of persons who appear before a claim agent
professing great suffering and disability, although they know
that there is little or nothing the matter with them, is cer-
tainly large. It is impossible to determine the proportion
of dishonest claims, but it is unquestionably large enough to
make the subject one of the most important in medical juris-
prudence. Many claimants allege injuries so trivial and so
obviously exaggerated, that they are readily persuaded to
withdraw the claim without any medical examination. The
extent and frequency of exaggeration in the cases examined
by the corporation surgeon must be in part determined by
the surgeon himself. It is often a matter very difficult to
decide. When there is no question as to the reality of some
of the symptoms, it is frequently impossible to ascertain just
how far the real symptoms are voluntarily magnified. Al-
though he can not always give reasons for his opinion which
prove satisfactory to juries, an experienced surgeon can
usually tell from the appearance and manner of the pa-

EXAGGERATION OF SYMPTOMS ACTUALLY PRESENT.

349

tient whether he believes himself to be as ill as he claims
to be.

But although voluntary and dishonest exaggeration of
subjective nervous symptoms is frequent, it should be re-
membered that not all neurasthenics who may be suspected
of exaggeration are themselves conscious of any misrepre-
sentation. What appears at first sight as exaggeration may
be only a symptom of disease. This fact is too little recog-
nized outside of the medical profession. The bringing of
claims by persons suffering from slight subjective nervous
symptoms has won for the neurasthenic among claim agents
and corporation lawyers, the name of swindler and extor-
tioner. It is not surprising that a claim agent, whose medi-
cal knowledge must at its best be but superficial, and who is.
so constantly a witness of attempted frauds, should be skep-
tical as to the justice of all claims for injuries which can
not be objectively proved. He is unaware that the same
kind of exaggeration he so often sees in the claim-bureau is
daily observed by physicians in cases which are uncompli-
cated by " litigation symptoms." As has been stated in
previous chapters, the patient with traumatic neurasthenia,
even when he has no claim to bring, describes his symp-
toms as more severe than there is any reason to suppose
they are.

A person who has become neurasthenic is tired and
weak. However robust or careless he may previously have
been, exhaustion of the nervous system has rendered him
easily fatigued and' worried, and fearful about himself. By
the immediate discomfort they occasion, and by arousing
fears of trouble in the future, the pains he feels are double
causes of suffering. He can not keep his mind from his
own sufferings, and thereby makes himself worse, in accord-
ance with the law of psychology that attention causes an
intensification of sensations. Could he divert his thoughts
to other channels he would be on the highroad to recovery..

3 so

MALINGERING.

An individual who is occupied and who has neither time
nor inclination to think about his own physical ailments, is
not worried by such trifling symptoms as cause suffering to
a nervous man who has given up his work and who thinks
only about himself. The tendency of introspection which
is a prominent feature in neurasthenia, and which is invari-
ably detrimental to recovery, is very much increased when
the financial question enters.

Furthermore, a person who is claiming damages for in-
juries can not afford to make light of any symptoms which
he may observe. All the circumstances by which he is sur-
rounded tend to cause him to repress, until the case is de-
cided, any efforts on the part of Nature, or of his physician,
directed to dispel the physical annoyances and suffering to
which he is subjected. By frequently rehearsing his case to
lawyers and to experts he comes to believe that he is seri-
ously injured ; by constantly bewailing the permanency of old
troubles, or the advent of new ones, he concludes that he
is " ruined for life." The symptoms of a patient who has
arrived at this stage are so out of proportion to the physical
injuries he has received that the representative of the cor-
poration which is to settle for them thinks they are volun-
tarily invented, when the patient himself believes in their
reality absolutely.

The discrimination between exaggeration of this charac-
ter, which is the voicing of disease, and consequently sin-
cere, and the variety of exaggeration which is the outcome
of dishonest greed, often can not be effected by the medical
aspects of the case alone.

As has been said in speaking of the symptoms of trau-
matic neurasthenia, the disorder, when well marked, consti-
tutes a fairly typical clinical type. In such cases there is an
agreement between the story the patient tells and the way
he looks and acts which leaves no doubt in the physician's
mind that he is really ill. But in mild cases the examiner

EXAGGERATION OF SYMPTOMS ACTUALLY PRESENT.

351

has to depend solely on the patient's symptoms, a means
none too reliable in litigation cases. It is then usually im-
possible to decide this question from an examination of the
patient alone. If a man claims to have a headache, or a
pain in the back, although he may not present the physical
appearances which ordinarily accompany such disturbances,
it is impossible to prove that his head or his back do not
ache. Even to show him to be a liar in other ways would
not necessarily prove that he was lying about these symp-
toms. It is but natural that the feigning of symptoms of
this character, which are subjective and which do not
necessarily reveal themselves b)'^ objective and tangible evi-
dences, should prove a tempting bait to persons who wish
to turn their presence in an accident to good account, or to
swindlers who may invent the history of the accident as
well as the symptoms.

The decision as to the merits of such cases usually lies
beyond the province of the physician, and must be decided
by means of information from outside sources. It should
be ascertained if the patient conducts himself at all times
in a manner which is consistent with the existence of
the symptoms from which he is alleged to be suffering ; if
he is bringing the claim himself, or if he is the victim of
" speculation." The profession and social position of the
claimant is not always a valuable aid in arriving at a just
conclusion. Physicians, and even the clergy, have been
known to bring claims of more than doubtful justice. An
officer of a large corporation has communicated to me the
case of a priest who was in a collision in which he received
no external injuries whatsoever, and who, although experi-
encing no ill effects immediately after the accident, brought
a claim against the company, alleging various subjective
nervous symptoms. The man's occupation was of a charac-
ter to demand excessive mental and physical work, which
he has continued to do without interruption since the acci-

352

MALINGERING.

dent. An examination by a distinguished neurologist two
years after the accident failed to reveal any evidences of
organic disease, and while the physician could not deny that
the patient was still suffering from the results of the acci-
dent, he stated that there was no proof of injury other than
the claimant's own story.

The same gentleman told me of a clergyman who was
struck in the back by a mail sack, but who received no visi-
ble injury. He threatened suit for five thousand dollars,
and compromised for one hundred and fifty dollars.

The question may be one of extreme difficulty. It is one
thing to say that there are no evidences of disease discover-
able, but it is an entirely different matter to prove that a
man does not suffer. When, however, the physician fails to
find evidence of disease, and when it can be proved that the
patient by his daily life shows himself to be strong and
active, there is every probability that his suffering is slight .
at best.

2. Substitution of Origin.

The allegation that pre-existing disease or deformity were
the direct results of accident or injury is a form of fraud often
difficult of detection. If a person claims that he was in
every way normal prior to an injury, and that only since its
incurrence have been observed the symptoms for which
damages are claimed, the proof of this assertion depends
upon facts relative to his previous physical or mental con-
dition, or, in case such facts are not obtainable, or are unre-
liable, upon whether the disability or disfigurements from
which he suffers are of a character such as may result from
the kind of injury which has been received. The difficulties
in obtaining sufficient knowledge of the claimant's previous
life is illustrated by a case reported by Prentice :

A corporation was presented with a person apparently an
idiot, his condition being represented as the result of a blow

SUBSTITUTION OF ORIGIN.

353

on the head. The company's attorney took the precaution of
having his picture taken. No record of the accident could be
found, and after the man had left the attorney's office he could
not be found. The picture, however, was sent to all parts of this
country and Europe where information might be expected ; de-
tectives were employed in mines in Montana and in cities on the
Atlantic coast, with the final result that the defendants' attorney
learned the man's birthplace in Europe, discovered his name upon
the army registers, with the record of his physical condition, show-
ing that his condition as a youth had been such as it was when he
was presented as a claimant. It was subsequently shown that he
had first come to America six months after the accident.

This case illustrates the difficulties, but still more sig-
nificantly the importance, of obtaining knowledge of the
preceding condition of the patient in accident cases. It is a
necessit)' to which corporations are rapidly becoming alive,
and for which they are, as far as possible, providing. Most
corporations now demand a physical examination of appli-
cants for employment. The adoption of this rule is in large
part due to the unusual frequency in the past with which
hernise have been alleged by employees to have resulted
from blows or falls. The frequency of such claims was so
out of proportion to the percentage of traumatic herniae in
general surgical practice that the companies concluded. that
they often paid for disabilities which had existed for a long
time before the injury, and for which they were not respon-
sible. By adopting the system of physical examination of
proposed employees they have materially diminished the
number of unjust claims which are brought against them,
and have at the same time established means for securing
valuable statistics for traumatic surgery.

It is, however, the chronic degenerative diseases of the
nervous system which are particularly liable to misconcep-
tion as to the influence of trauma in their causation. In
many of them the evidences as to the possibility of a trau-
matic origin are still very slight, although we are unable to

354

MALINGERING.

assert that they can not directly result from injury inde-
pendently of the co-operation of other causes.

In traumatic epilepsy and general paresis, which some-
times develop in immediate sequence to blows on the head,
it may often require both delicacy of diagnosis and a
very full knowledge of the patient's condition prior to the
receipt of the injury, before it is possible to determine the
appropriate causal value which should be ascribed to it. As
has been stated, in these diseases particularly there are
many opportunities for error. If a previously healthy person,
a few weeks or months after a fall on the head, by which the
skull may or may not have been fractured, begins to have
convulsive attacks, which at first are localized to certain
muscles, but which may later become general, it is in entire
accord with our present medical knowledge to assume that
the epilepsy is traumatic, and that the patient would never
have had the disease if his head had not been injured. Very
much more conservatism is necessary in ascribing a trau-
matic origin to general paresis when it first appears after a
head injury. It is essential to have considerable evidence
that before the injury the patient had been free from any
symptoms of either of these disorders ; for epilepsy fre-
quently appears for the first time in adolescence or in early
adult life, and the fall on the head, which is alleged to have
caused it, may be the result of the first epileptic attack ; in
general paralysis, also, even when there is no question of in-
jury, the epileptiform attack may be the first symptom
noticed by the friends of the patient, and it may be by it that
attention is called to the fact that the patient had been for
some time different in many ways from what he used to be.
In such cases, of course, the mental symptoms are not in any
way the results of the fall. The attack and the fall simpfy
form another link in the chain of symptoms.

But if the circumstances of the fall were such as to make
it a negligence case, the claim might be made that the men-

SUBSTITUTION OF ORIGIN. 355

tal disease was traumatic, and that the fall was propter hoc,
when in reality it was post hoc.

If the symptoms of locomotor ataxia or progressive mus-
cular atrophy are observed for the first time after an injury,
it is sometimes claimed that the injury was the sole cause of
the disease.

As has been shown (page 138), there is no evidence that
locomotor ataxia may be entirely due to injury. When
trauma is alleged as a sole cause, there is a far greater prob-
ability that the disease had existed, perhaps unperceived,
before the injury. The affection is always of extremely in-
sidious onset, and is generally unfamiliar, in the earlier stages
at least, to the larger number of American physicians. These
facts should make one chary of too hastily 'Ascribing the
development of any case to traumatic causes alone.

Progressive muscular atrophy has only infrequently be-
come the subject of medico-legal inquiry. The evidence
necessary for the establishment of a traumatic origin of the
disease has already been mentioned (page 167).

In paralysis agitans the chances of error are fewer. Cases
of paralysis agitans which follow injury or fright only ex-
ceptionally reach a rapid general development ; so that, if
a patient has marked tremor or stiffness of the muscles, or
characteristic attitude or expression soon after an accident,
it is highly probable that the disease had existed before.

It must be clearly understood that a person who claims
that any of these diseases is the direct result of injury
may do so with perfect honesty. He may himself have
been ignorant of their pre-existence. Thus, a patient of
Prince's sued for damages, alleging that locomotor ataxia,
from which he was suffering, was the direct result of a fall
from the back platform of a railway car. The plaintiff frankly
acknowledged in the court room that he had suffered from
shooting pains in the legs of a typically tabetic character for
six years previously. By this admission he vindicated him-

356

MALINGERING.

self from any suspicion of fraud, but he also gave almost cer-
tain proof that the disease had antedated the accident.

There is great opportunity for fraud in these cases.
Dr. Peterson has communicated to me a case (already re-
ferred to) of progressive muscular atrophy in which a
woman sued for injuries received by a blow on the head
caused by the falling of a revolving fan. The plaintiff
alleged that since the accident she was nervous, tremulous,
and could not sleep well. She was examined by the defend-
ant's physician, who failed to observe the atrophy and loss
of power in the hands, and apparently found symptoms of
nothing more serious than simple traumatic neurasthenia.
After twelve months, when the case came to trial, the plain-
tiff's counsel fi-ankly admitted that his client had suffered for
several years from a chronic and incurable nervous disease
which had been rendered worse by the accident. There
was, of course, no attempt at deception ; but nothing could
illustrate better the possibility of fraud by claiming that pre-
existing disease had been caused by the traumatism. The
time elapsing between the receipt of the injury and the
trial was long enough for progressive muscular atrophy to
develop, and had this patient been unscrupulous, and her
physician dishonest, she could undoubtedly have recovered
a large sum on the complaint that the chronic spinal disease
had been the direct result of trauma.

What has been said concerning the possible pre-existence
of the chronic organic diseases of the nervous system may
be repeated, with certain modifications, for the functional
nervous disorders. It is very essential to know something
about the previous history of the patient. Neurasthenia
very commonly develops in persons who had given no
symptoms before the accident, but the fact that they were
well before should be proved. It is particularly important
to know if there had been no manifestations of hysteria
before the appearance of the particular ones which were

SIMULATION.

357

complained of soon sffter the accident. Thus, in Bremer's
case (page 301) of astasia-abasia, the woman who sued for
damages, alleging that the paralysis of the legs would not
have occurred had she not been in an elevator accident, was
shown to have been for years a victim of various hysterical
accidents, and to have given many proofs of an extremely
disordered mental state.

3. Simulation.

Much confusion has arisen from an indefinite use of the
term simulation. It has been made to apply to cases which
were exaggerated as well as to those which were entirely
created. It will be used here as a designation for those cases
only in which there is no foundation in fact for the symp-
toms which are alleged.

Frequency. — It is now generally admitted by railway
officials, and believed by neurologists, that it is not very
common for persons who have no symptoms at all to simu-
late disease as a result of accidents, on account of which-
they demand compensation. Simulation of all kinds is fre-
quent in armies, in prisons, and in institutions for insane
criminals, and in the earlier periods of the history of trau-
matic nervous affections it was thought to be very frequently
associated with them. Riegler was the first to observe the
great increase in the number of railway claims after the
passage in Germany of a law by which injured persons were
to receive payments, graded in amounts in accordance with
what they had previously earned, for the time they were
unable to work. He was led to believe that feigning was
very frequent, and he stated that all the nervous symptoms
resulting from railway accidents were either simulated or
else due to organic injury of the nervous system.

The opinions as to the extent of simulation have varied a

great deal in Germany, where the subject has received the

most thorough scientific attention. Hoffman at one time
24

358

MALINGERING.

reported simulation in thirty-three per cent of his cases.
From several of the alleged patients he obtained confessions.
One man had been coached by a physician for the simulation
of epilepsy ; another for the pretense of anaesthesia. Seelig-
miiller found, simulation in twenty-five per cent of cases ;
Oppenheim in four per cent. Shultze regarded it as fre-
quent. In this country absolute simulation is generally con-
sidered as unusual. Knapp, Dana, Putnam, and others agree
in believing that few persons could carry out, under severe
investigation, a system of successful feigning. Judd and
Walton, on the other hand, think the percentage of simula-
tion is not small. However, as Seguin says, in this country
" claimants are very rarely subjected to scientific watching
and to repeated examinations ; the physician or expert is-
expected to deliver an opinion after one or two interviews-
with the patient, so that the chances of detecting simulation,
are much reduced."

But although simulation is probably not very common,,
it is sufficiently frequent for it to be an important factor in
the consideration of accident cases. " ' Drag your leg, you
fool! don't you see the doctor coming?' was called out bj
a workman to his fellow who had been in an accident, and
heard by the doctor as he was crossing the yard to see him."
(Page.) Godkin tells an amusing story of a plaintiff who-
testified " that his right arm had been so injured that he was-
unable to raise it any longer to a horizontal position. Upon
cross-examination the defendant's counsel asked him, to indi-
cate how high he could now raise his arm. ' Only so high,'
replied the witness, lifting his arm with apparent difficulty a
few inches from his side. ' And how high could you raise
it before this unfortunate occurrence?' asked the lawyer
suddenly. ' So high,' replied the witness, raising the same
injured arm above his head with ease."

Not so very long ago a man brought a claim against a
Western railway for injury to the spinal cord, which was.

SIMULATION.

359

the alleged result of a collision. The patient was apparently
paralyzed in both legs, and for two years was never seen to
walk without crutches. One day at the end of this time,
while sitting with the claim agent in the office of the corpo-
ration, a settlement was agreed upon, and the man signed
the release and received his check. He arose briskly from
the chair and commenced to walk rapidly out of the office.
"Hullo!" said the claim agent, "have you not forgotten
something?" The satisfied claimant could not repress a
blush at seeing that he had left his crutches standing idly in
the corner.

That simulation may come to be a systematized occupa-
tion and a means of livelihood is well shown by the Freeman
family. In an interesting and cleverly, written pamphlet
entitled Paralysis as a Fine Art, published in 1895 by the
Association of Railway Claim Agents, some of the adven-
tures of the Freemans are described. The family consisted
of a father, mother, and eight children, English (or Polish)
Jews, all of unsavory reputation (Fig. 55). There is no defi-
nite information concerning the male members ; but the
mother, Mary Freeman, and the two daughters, Jennie and
Fannie, between January, 1893, and December, 1894, entered
no fewer than nine claims for damages against railway com-
panies. That the claim was fraudulent and the pretenses
false in their last attempt each and all swore before a notary
in Chicago at the time of their final exposure. There is con-
vincing proof, also, that all the claims that they ever made
were fraudulent. It may be well to briefly outHne how
these frauds were committed :

Mary Freeman, the rnother, was forty-three years of age, slov-
enly in appearance and dress. " She was dirty and infested with
vermin." Hers was the ruling spirit of the family, and she directed
the operation of all the frauds. She had been several times ar-
rested for theft.

On September 11, 1894, she made claim on the Chicago City

36o

MALINGERING.

Railroad Company for injuries caused to her right arm by the
sudden starting of a car. She received a hundred dollars.

Jennie Freeman, the eldest daughter, was between eighteen

and twenty-two years of age. Her morality was questionable.

She was usually on good terms

with some physi- I [ cian or attorney.

She had been ar- rested for theft.

Her appearance gL and manner were

pleasing and gen- jj9P^ '■'^'

On January 9, BJWI'^'' jk 1893, she made
claim on the Chi- ^ '".J; cago City Rail-
road Company ' "^ ^^-, for injuries re-
ceived in a colli- •■r"*itoyajg|HB|fci^^^ - ^'°" between two
cable cars. " She •'"'si^^^^Rr ■ \-«#r' alleged total pa-
ralysis from the "'^^i ' '' n^'^fF thighs downward,
loss of sensation, want of control
of the bowels and urinary organs,

and pretended that she was a

cripple and ruined Jennie Freeman. for life." The

Esther Freeman. Fannie Freeman.

Fig. 55. — Some members of the Freeman family,

company's physician " thought the girl was shamming, although
the symptoms were so closely simulated that it was apparently a
real case of paralysis." The company gave her five hundred dol-
lars, and Miss Jennie is said to have recovered a few days after
the damages were paid.

SIMULATION. 361

If this paraplegia were genuine, it must have followed a course
of unusual benignity, for on October 5, 1893, the patient made
claim on the Manhattan Elevated Railroad Company, of New
York, for injuries received by falling against the car door of a
Second Avenue train while it was rounding the curve at Twenty-
third Street. Settlement of one hundred dollars to her physician
and one hundred and twenty-five to Jennie Freeman.

On May 16, 1894, claim on the Boston and Maine Railroad of
having been injured by slipping on a banana peel when stepping
out of a car at the Prospect Hill Station. The banana peel was
produced in evidence. Jennie Freeman received one hundred and
twenty-five dollars in respect of these injuries, though the claim
agent suspected fraud. She was next heard of in Chicago, where,
on June 28, 1894, she brought claim on the Illinois Central Rail-
road Company for injury received by being thrown against the
back of a seat through the sudden stopping of a train. " She
alleged total insensibility of the lower portion of the body, prac-
tically amounting to paralysis. Had a sore on her backbone,
immediately above the top of the corsets. Alleged an inability to
control the function of the bowels, etc. The examining physician
made every possible test, but she seemed totally insensible to all
pain. The claimant was settled with for two hundred dollars."

On September 10, 1894, Jennie Freeman alleged to have fallen
from her seat while rounding a curve on one of the lines of the
West Chicago Street Railroad. She represented to the company
through her mother that she was paralyzed. Fraud discovered
by claim agent, who, by an unexpected visit, discovered the
alleged paralytic sweeping her room.

Fannie Freeman, younger than Jennie, was untidy in her dress,
quiet, and had little to say. She had been arrested for theft.

On April 20, 1894, she claimed to have been injured by slipping
on a banana peel on the West End Street Railroad Company's
car in Boston. She complained of paralysis of motion and sensa-
tion from the waist downward, and an inability to control bladder
or rectum. Over the lower thoracic vertebra there were traces
in two places where the skin had been abraded. The company's
physician says, in his report : " Tenderness to pressure and per-
cussion over the lumbar and dorsal vertebrae. Can't stand, walk,
or sit unless completely supported, and then can only be held in
the half-sitting and half-reclining posture, all the time evidencing
great agony. When I stuck pins into her feet and legs, and
touched them with my hands, she declared she could not feel any

362

MALINGERING.

sensation, and I couldn't surprise her into any painful expression."
The prognosis was given as unfavorable, and Fannie Freeman was
paid three hundred and twenty-five [or four hundred and twenty-
five] dollars.

On June 6, 1894, Fannie Freeman, under an assumed name,
made claim on the New York, New Haven, and Hartford Railroad
Company at Boston. This case was an identical reproduction of
the preceding, even to the patient's maintaining that it was " her
first accident." But she was unfortunate in being visited by the
same examiner who had seen her a month previously for the
West End Street Railroad Company. For the physician this
time recognized the fraud, which he had failed to do in the first
instance.

On December 24, 1894, Mary Freeman claimed to the general
superintendent of the Chicago, Rock Island, and Pacific Railroad
Company, Chicago, that her daughter Fannie had been injured by
falling on the back in a car of the company. She alleged that her
daughter was paralyzed from the waist down, and had lost all
sensation in the legs ; that there was no power over the rectum or
bladder, and that the young girl was ruined for life. There were
so many suspicious circumstances about the case that. the family
were .watched. Before the expected visit of the company's doc-
tors the alleged cripple was seen, from a hole through the floor of
a room above hers, to get nimbly out of bed and put her feet in a
tub of iced water, in order that they might feel cold and lifeless
to the examiners.

Some of the results of the medical examination, as embodied
in the surgeon's report, are as follows :

" Pulse at first 104, but it changed so that at the last of the
examination it was 132. Her back was marked by a slight spot
about the top of the sacrum, entirely superficial and movable over
the underlying tissues, which may have been produced by some
injury, or by the abrasion of some part of her clothing. Sensation
existed about halfway down the thighs, but below this point it was
alleged to be absent. There were no evidences observed of in-
continence of urine or fseces, and no girdle sensation was com-
plained of. An unexpected test of raising the foot in the air
caused it to stop there, though tests of physical endurance were
applied and successfully withstood."

The doctors were satisfied of the fraud, and reported that there
were no objeative evidences of the conditions complained of.

The following day the three women were arrested. Fannie

SIMULATION.

363

Preeman, "the paralyzed lady, jumped out of bed, cursed, and
inarched around the room with a tramp like a grenadier."

The Freeman cases have been quoted in some detail
because there seems little reason to doubt that all the claims
were absolutely fraudulent, and that the symptoms in each
case were entirely fictitious.

The cases in which there is a detailed report of the med-
ical examination show how far and in what way the sj^mp-
toms of nervous disease may be simulated. Certain of the
symptoms of the Freemans will be referred to again.

Difficulties. — In accident cases simulation is attempted
with the sole object of gain. Reference has already been
made to the temptations which lead to this particular form
of dishonesty. Yet, while the bait is alluring, the person
who makes a claim for personal injuries, when in reality he
has not been injured at all, sets himself a task of no little
■difficulty. In the first place, he must give some account of
himself and of his social relations. He may be able to satis-
factorily conceal his past if he has anything to conceal. Of
course, a notorious rogue would probably be detected at
once ; and the appearance and methods of an impostor who
has been caught by any large corporation might be recog-
nized when he brings claim against some other company.
Pannie Freeman was on one occasion detected in Boston
because she was examined by the same physician who had
seen her a month previously for another company. Claim
agents also exchange for mutual benefit any information
which they may gather in regard to suspicious characters.
The system with them is not so highly elaborated as is the
system of exchange by life-insurance companies of the
Tiames of rejected candidates, but it is usually sufficient to
brand a man who has been detected shamming several
times.

The past record, however, the successful simulator may

364

MALINGERING.

be able to conceal, if concealment is necessary. It is more
difficult for him to prove himself of a character and position,
the possessors of which do not ordinarily resort to flagrant
and absolute imposture. In this respect the absolute simula-
tor is very different from the person who exaggerates actual
though slight injuries. Symptoms may be, and occasionally
are, dishonestly magnified by persons whose reputations for
integrity have escaped suspicion, and who are regarded as
estimable members of society. But such persons are rarely
absolute simulators. The simulator crosses the border land
of deceit and takes his place among criminals. If he can not
prove himself as following some respectable calling, the suc-
cess of his venture is hazarded. Claim agents show an in-
clination to know as much as possible about personal habits
and modes of life of the claimant before they consider ad-
justment, and the impossibility of furnishing satisfactory
details of this character undoubtedly deters many who
otherwise would cheerfully undertake to defraud by feign-
ing disease.

Even when the simulator is able to furnish satisfactory
proof of his honesty and respectability there still remain for
him serious difficulties. To closely imitate nervous disease
requires no mean order of intellect. A clever simulator
must have quickness in adapting himself to new situations,
a plausible and ingenuous manner, the power of close atten-
tion, a good memory, and some knowledge of the symptoms
of disease of the nervous system. These are mental qualifi-
cations all of which are rarely present in the individuals
who resort to the feigning of disease for financial purposes ;
yet all of them must be present if a physician who is reason-
ably skillful and who is on the lookout for shams is to be
made to believe that the symptoms are genuine when in
reality they are entirely assumed.

The simulator must hold himself ready for examination
at- any time. Examinations made at the most unexpected

SIMULATION.

365

hours or in rapid succession should find him always prepared
to reproduce an essentially unvarying chain of symptoms.
He may be successively submitted to the observation of
physicians of different ability who make examinations of
different characters in diverse ways. To deceive them all,
the simulator must have his wits about him. The general
appearance and manner, which are among the most reliable
signs for medical diagnosis, must to a certain extent cor-
respond with the bearing of persons who really suffer from
the symptoms he is trying to imitate. These evidences are
the outward expressions of the morbid agencies which are
at work ; they are difficult to describe and still more diffi-
cult to counterfeit. A knowledge of their significance and
characteristics in disease is only acquired by long experience
in general medical practice, a fact which constitutes perhaps
the most serious stumbling block to the simulator. Even if
he had the necessary knowledge of the general appearances
in nervous diseases, they are symptoms almost impossible to
successfully imitate. They reveal the condition of the whole
organism and are largely beyond the power of voluntary
control. When the simulator tries to copy them he over-
does it. His manner is exaggerated and theatrical ; his
symptoms are severer than real symptoms usually are ; his
prospects are ruined. Yet with it all are wanting the ob-
jective evidences which almost invariably accompany such
severe symptoms. The eye is bright, and the face, seen in
repose, belies the assertion of constant physical and mental
torture. It is the exaggerated character of the story that
often at once excites the physician's suspicion and leads him
to apply searching tests which result in exposure.

Without remarkable powers of attention the simulator
can not hope to meet with much success. He must be al-
ways ready to be examined and constantly on the alert
even when he does not suspect himself of being observed.
When under direct examination or observation he must be

366

MALINGERING.

ever on his guard not to be caught by tricks nor to be be-
trayed by his own emotions. Page tells of " a man who
based a large demand for compensation from a railway com-
pany on stiffness of the elbow and inability to move the
arm, the result of a collision. A verdict incommensurate
with his expectations having been recorded, he threw up
his arms and exclaimed, ' My God ! I'm a ruined man.' "

To sham any form of disease requires that several symp,
toms must be counterfeited at the same time. To imitate
any one objective symptom successfully for the length of
time usually taken for medical examination requires a very
close attention ; to simulate several simultaneously is for the
majority of persons impossible. To keep constantly before
the mind that the legs must not move, that pin pricks must
not hurt, and that movements of the back are painful, is an
intellectual exercise of considerable activity. If these symp-
toms do not really exist, the attention, while one of them is
being examined, is usually concentrated on it at the expense
of the others. As a result, alleged paralyzed legs may be
seen to move, movements of the back may no longer cause
suffering to the subject, or he may be startled into involun-
tary expressions of pain when pricked in areas said to be
anaesthetic. A long and thorough examination, especially if
the examiner be suspicious of fraud, will usually disclose
some or all of the symptoms to be false. Even when the
simulator is entirely conversant with the character of the
disturbances he is shamming he is rarely able to keep himself
from being confused by their examination in rapid succes-
sion. Fannie. Freeman, who was undoubtedly, by experience
and by teaching, thoroughly conversant with the symptoms
of paraplegia, forgot to let her leg drop when it was lifted
up by the examiner. Instead of falling lifelessly to the bed,
as it should have done, it was held in the air, and, by suc-
cessfully resisting the efforts of the doctors to push it down,
showed a high degree of muscular strength.

SIMULATION. 367

A qualification closely allied to power of attention is a
good memory. It is very essential, if a story is to be be-
lieved, that when retold it remains essentially, though not
minutely the same. Many claimants excite suspicion by the
variations and inconsistencies which appear when they re-
late the details of the accident to different persons. Genuine
symptoms have a certain permanency. A clumsy simulator
will often forget, when talking about his case to one ex-
aminer, just what he has complained of to the claim agent
or to the physician whom he had seen before. On the other
hand, it is not always just to infer, because a history of in-
jury or symptoms is indefinite or contradictory, that the
claimant is an impostor. Both the memory and attention
are impaired to a certain extent in neurasthenia, and still
more so in hysteria; but all such inconsistencies will cause
a claimant to be regarded with suspicion until it can be
proved with a remarkable degree of certainty that they are
not the results of clumsy and voluntary attempts at de-
ception.

Knapp believes that simulation must be rare, because the
larger number of persons who would be willing to fraudu-
lently feign disease are unable to obtain a sufficient knowl-
edge of symptoms to successfully imitate them ; that simu-
lators are of a class rarely able to refer to medical books,
and that physicians who might be able to give instruction
in this kind of fraud could not be persuaded to do so. It
seems to me that lack of medical knowledge, in accident
cases at least, is one of the minor difficulties against which
the simulator has to contend. When a large claim is made
and the company decides to contest it, the chances of suc-
cessful simulation are always small. The simulator fails
then, both because his motives are very thoroughly investi-
gated and because he is subjected to a series of rigid exami-
nations. But in by far the larger number of instances the
case does not come to trial, because the claim made is gen-

368

MALINGERING.

erally small, and the companies find it cheaper to settle it
than to go to the expense of trial and expert opinion. In
this way a simulator, without being particularly expert, may
escape exposure, although both claim agent and physician
suspect him of being a swindler.

The form of disease most commonly simulated is neu-
rasthenia, for which no special knowledge is necessary.
The general symptoms of " railway spine " are familiar to
most physicians, even though they be unacquainted with
general nervous diseases. Physicians can very easily simu-
late railway spine or teach how it should be simulated, and
experience shows that they sometimes do so. The condi-
tion can also be feigned with moderate accuracy by persons
who know nothing of general medicine. There are no
positive objective symptoms by which the fraud can be
discovered, and there are a great many persons who, with-
out any medical degree, have acquired sufficient familiarity
with various forms of disease to give a fairly good reproduc-
tion of the picture of neurasthenia. Inmates, attendants, and
hangers-on of various hospitals and public institutions gen-
erally become, through long experience, w^ell acquainted with
the different forms of human suffering. Page remarks upon
the knowledge possessed by persons in the humbler walks
of life, regarding the history and symptoms of the kind of
injury which is popularly supposed to be inevitable to a rail-
way collision. Knowledge of the symptoms of neurasthenia
may be easily acquired. If the simulator can not learn them
himself, there is little reason to suppose that he would have
any serious difficulty in finding a physician ready and able
to instruct him. Knowledge of the symptoms of organic
nervous disease is more difficult to obtain, and most physi-
cians who would impart it for fraudulent purposes do not
themselves know very much about them. But simulation
of organic nervous disease can only be successful when the
examiner is himself careless or unfamiliar with the symp-

SIMULATION.

369

toms and the means of demonstrating them, for organic
nervous disease can not be feigned with any degree of re-
semblance. With assumed symptoms indicative of organic
disease, if the simulator passes undetected it is less of a testi-
monial to his knowledge, than it is a proof that the examin-
ing physician has been superficial, careless, or ignorant.

Detection of Simulation. — The physician's part in the
detection of simulation is to show that the clinical picture is
not produced, a task that is rendered easy by an appreciation
of the various factors which of themselves make the simula-
tor's part so difficult. While some simulators are so clumsy
that they are immediately turned away from the claim
agent's door, well-trained impostors like the Freemans merit
the best skill of the medical man. For the exposure of such
experienced swindlers as they were, the physician must not
only be on his guard, but he must constantly keep on the
defensive the person he is examining. B3' bearing in mind
the disadvantages under which the simulator is placed the
examiner can, in many ways, render them still more em-
barrassing. The detection of skillful simulation of any one
symptom depends upon diverting the simulator's atten-
tion. He must be taken off his guard. When he does not
know that he is being watched, the phj^sician may find that
the facial expression undergoes a marked change. Com-
plaints of pain may be forgotten if he can be made to talk
of something not directly relating to the accident. If the
examination is sufficiently long, it is generally found that
there are periods during which the expressions of suffering
momentarily cease. These lapses may be short, and the
simulator may soon collect himself again. But a momentary
forgetfulness of this character should at once excite the phy-
sician's suspicion. It is by attracting the patient's attention
away from the symptom, the true nature of which the phy-
sician desires to assure himself, that the fraud frequently
becomes apparent. It is very hard to think for any length

370

MALINGERING.

of time on two things at once, and if the examiner is in real-
ity examining for one symptom while he appears to be test-
ing another, he may often be able to prove that one of the
symptoms exists only when the person under examination
has his attention fixed upon it.

Detection of the simulation of those disorders which may
result from accidents is in most cases possible. Clinical pos-
sibilities are limited, and when a man says he is suffering
from the effects of an accident, the question immediately
arises, What is the pathological condition to which the
symptoms are due? By eliminating disorders with which
the symptoms do not agree at all, the physician who is
familiar with the various morbid conditions which cause dis-
turbance of* nervous function can reduce the possibilities in
any case to the one or two conditions with which the symp-
toms agree most closely. It then remains for him to deter-
mine if the resemblance to either or both of these conditions
is sufficiently close to justify the symptoms being regarded
as genuine and not feigned. For example, an allegation that
the arm is injured is not enough. It should be shown how
it is injured, and if careful examination shows that it is sur-
gically intact, and that the symptoms are at variance with
those of any known variety of nervous condition, it is entirely
justifiable to infer that the arm is not injured at all. Page
reports a case in which the dribbling of urine caused by a
large prostate was alleged to be due to injury to the spinal
cord. The man was not paralyzed, and he was at once
recognized as an impostor, because any injury to the spinal
cord which could cause weakness of the vesical sphincter
would cause paralysis or some other symptom of spinal-cord
injury.

Similarly, Fannie Freeman, in her last attempt, might
have been detected at once, from the fact that she failed to
make her paralysis agree with any known form of paraplegia;
for, with alleged complete loss of power of the lower limbs

SIMULATION.

371

and of the bladder and rectum, the feigned anaesthesia only-
reached to the middle of the thighs. If the paralysis bad
been due to injury to the spinal cord, the anaesthesia would
have had a very different distribution. If the whole condi-
tion had been hysterical, the sphincters would have remained
unimpaired.

The choice of diseases for simulation is restricted, inas-
much as the variety of nervous disorders which may result
from injury is not large. Acute organic injury to the brain,
spinal cord, or peripheral nerves causes symptoms which can
not be feigned. General paresis, progressive muscular atro-
phy, and tabes can not be copied with even a shadow of re-
semblance. Feigned paralysis agitans would quickly be pro-
nounced spurious by any medical student who had examined
one genuine case of that disease. Epilepsy is rarely feigned
in accident cases, and usually appears in the form of a
genuine epileptic alleging that the disease was caused by
injury. If epilepsy is alleged as the result of accident, the
evidence of non-medical witnesses of the fit should be re-
garded as insufficient proof.

Neurasthenic disturbances are the ones most frequently
complained of by simulators, who are quick to take advan-
tage of a condition which is practically devoid of objective
symptoms. It is in these cases especially that, as Page says,
" it is only by a consideration of every feature and aspect of
the case — clinical, pathological, social, and moral — that you
can rightfully estimate the kind of exaggeration or malin-
gering with which you have to do." The physician may
believe that a case of neurasthenia is absolutely feigned ;,
but unless he has some definite proof upon which to base
his opinion he is not justified in calling the man a swindler.
If a claimant restricts himself to assertions of pain in the
back, loss of energy, inability to do his work, and similar
complaints of purely subjective character, the physician
may be sure that the symptoms are exaggerated, but he can

372 MALINGERING.

not show that they are false. The truth in regard to claims
which are based upon symptoms of such a character must
be determined by general considerations and by information
gained from sources other than the medical examiner.
Hysteria is probably never simulated in America.

A claim agent, in telling me of many cases from his experience
in which the symptoms had speedily disappeared after settlement,
said that there was one case he had never been able to understand.
A man had received a slight injury in a collision, as a result of
which he alleged that his legs were paralyzed. ' In spite of many
circumstances which appeared suspicious, the claimant was com-
pensated. But the injured man, instead of getting well, remained
a paralytic, and it became generally believed that his spinal cord
really had been injured. Two years after the damages were paid
he suddenly regained full power of the legs. The fact that this
case was misunderstood is in accord with the common opinion,
both lay and medical, held in America in regard to hysteria.

It is not generally appreciated that hysteria is a disease
and not premeditated swindling. Until the subjective real-
ity of hysterical symptoms becomes more generally believed
in, the disease can not be popular with simulators. To feign
a disease which is itself regarded as fraud would be worse
than useless. But the failure to recognize that symptoms
are hysterical and not voluntarily created may cause much
injustice to the hysterical patient. He may be immediately
branded as an impostor the moment the objective symptoms
are shown not to be organic. There is more probability of
a hysterical person being classed as a simulator than of a
simulator attempting to feign hysteria. The diagnosis be-
tween hysteria and simulation, however, should not be diffi-
cult to any one who is familiar with hysterical symptoms.
Hysteria is the cleverest simulator of all, and is adroit and
consistent when the simulator is clumsy and confused. The
hysteric copies, while the simulator caricatures. Hysteria
causes its victim to involuntarily mimic organic disease
much more closely than organic disease can be imitated

SIMULATION OF INDIVIDUAL SYMPTOMS.

373

voluntarily. But even the mimicry of hysteria is not per-
iect, and by the irregularity and association of its symptoms
it can readily be differentiated from organic disease.

The forms of disease which have been described as
unclassified are accompanied by symptoms too serious to
permit them to be misinterpreted or imitated.

An individual or a corporation which is being sued for
damages for personal injuries should be entitled to ascertain
the character and extent of the injury for which he is held
responsible. Viewed from a purely commercial standpoint,
he has a right to know what he is paying for, or, in other
words, to insist upon a definite diagnosis before payment is
made. Such diagnoses, if they can not be made at once,
usually become possible after the observation of a few days
or weeks. When the possibilities of exactness in diagnosis
of disorders of the nervous system are more generally recog-
nized, and when " shattered nerves," and similar meaningless
designations come to be regarded as insufficient claims in
negligence cases, the detection of simulation will be rendered
very much easier. The simulator would then be forced to
choose some definite condition to feign, and to have all his
symptoms in accord with it.

The symptoms most difficult to simulate, or even to ex-
aggerate, are those known as objective. They are of suffi-
cient importance, however, to be considered in detail.

Simulation of Individual Symptoms.
Motion. — The most difficult objective symptom to coun-
terfeit is the loss of voluntary motor power. If the simulator
decides to enlarge upon the simple complaint of pain in the
back and general nervousness, he is very apt to be led away
by the attractive picture of paralysis. By refusing to move
his limbs, or by giving them the appearance of lifelessness
when they are handled by the examiner, it seems to him

comparatively easy to substantiate the statement that certain
25

374

MALINGERING.

muscles have lost their power of voluntary movement. He
loses sight of the fact, however, that true paralysis has cer-
tain signs which are impossible of voluntary imitation, and
that it is well-nigh useless to attempt to impose in this way
upon a careful physician who is familiar with the various
phases and causes of impairment or loss of muscular power.

There are two reasons which seem to justify the state-
ment that true paralysis can not be well feigned. One is
that the condition of the muscles themselves — the flabbiness,
softness, and lack of tone — can not be voluntarily counter-
feited with any great degree of similarity. The other reason
is that organic paralysis does not occur as an isolated symp-
tom, but is invariably accompanied by others which are com-
pletely beyond the control of the will.

If paralysis is simulated, when the limb is lifted up and
suddenly released it may be held a moment before it is
dropped again ; or if the examiner tries to move the limb,
his hand may detect that there is a moment in which the
muscles are held stiff, although they relax again as soon as
the subject discovers the object of the test ; or the limb may
be seen to move under the influence of painful stimuli, or
when the person under examination forgets to hold it mo-
tionless.

Paralysis is rarely isolated. Appearing acutely it can
only take place as the result of organic injury to the nerv-
ous system or of the fixed ideas of hysteria. If the brain
is the seat of a lesion there may be a resulting hemiplegia
or monoplegia, but the paralysis is ushered in with con-
siderable cerebral disturbance. Paralysis due to primary
intracranial lesions rarely occurs without unconsciousness,
or convulsions or severe headaches, or some similar severe-
cerebral symptoms. The functions of the cranial nerves can
not be voluntarily suppressed. A man may claim that he
does not taste, see, or hear, statements which may be difficult
' to verify ; but he can not voluntarily cause permanent devia-

SIMULATION OF INDIVIDUAL SYMPTOMS. 375

tion of the eyes, such as results from palsy of the nerves to
the ocular muscles, nor can he keep his face drawn to one
side so that it does not become apparent, during movements
of talking or laughing, that the facial nerve is not paralyzed.
Hemiplegia is usually quickly followed by unilateral changes
in reflex activity which, as we shall see, can not be imitated
in a way to deceive any one familiar with these important
evidences. The symptoms of hemiplegia, as the result of
injury, are too complex for the average simulator, and are
pictures with which he is usually unfamiliar. Any attempts
to copy them must be unusual, if they are ever made.

Loss of power in the legs seems to the simulator the
clinical type most consistent with the general theory of pa-
ralysis which follows accidents. Injury to the spine with
resulting paralysis of the legs is a comparatively common
condition, and the average simulator is rarely a sufficiently
profound pathologist to recognize the fact that traumatic
paraplegia is most frequently the result of fracture or dislo-
cation of the vertebras, such as only occur after very severe
accidents. Furthermore, organic injury to the spinal cord is
without exception accompanied by many symptoms which
do not permit of voluntary imitation. Trophic disturbances
are beyond the realm of imitative art ; by soaking the legs
in iced water they may be made to feel cold and look blue,
but there is nothing but actual nerve injury which can cause
the appearance of a beginning bedsore, and the cleverest
actor can not make his muscles waste or his nerves give
degenerative electrical reactions. In recent organic para-
plegias there is a softness and flabbiness of the muscles
which is characteristic ; and as the paralysis of some muscles
passes away, as it usually does in time, they resume their
normal tonic action. But the muscles remaining paralyzed
offer no resistance to their opponents, and contractions
and deformities are the results. Organic paraplegia is usu-
ally accompanied with some trophic symptoms, together

376

MALINGERING.

with anassthesia and changes in reflex activity. Even with-
out the aid of them, it is usually possible in any case to
demonstrate whether the paralysis is true or feigned.

The simulation of organic monoplegia is still more diffi-
cult. It is often alleged that the arm is injured, but these
are cases which are characterized by peripheral rather than
central injuries. The neurologist can at once decide if there
has been any injury to peripheral nerves, and a surgical ex-
amination should quickly discover the integrity of the bones
and joints. In the absence of any such evidences of periph-
eral injury it is justifiable to infer that the case is feigned
or hysterical. Traumatic monoplegia from any cause is
very rare, and as a result of spinal injury it is practically
unknown, which may be explained by the fact that the
spinal localization for the movements of any one limb ex-
tends over several segments of the cord. Any injury which
affects a sufficient number of segments to cause a monople-
gia will be accompanied by paralyses of other parts.

Hysteria can imitate better than any simulator the or-
ganic paralyses and, as has been said, there is more danger
that the involuntary mimicry of hysteria be regarded as de-
liberate imposture than that the impostor who feigns para-
plegia may pass undetected. The decision of the question
between hysterical paralysis and simulation may be very
difficult. If the plaintiff's physician assert that his client is
suffering from organic paralysis, the truth of the statement
may be determined with certainty. But if the claim should
be made (it rarely is) that the paralysis is functional, it may
be impossible to refute it by objective signs. The character-
istics of hysterical paralysis have already been described in
such detail that it will be sufficient to recall the fact that
they differ in essential particulars from the paralyses arising
from organic causes. But the differences are very similar
to those which exist between organic paralysis and feigned
loss of muscular power. The hysteric, like the simulator,

SIMULATION OF INDIVIDUAL SYMPTOMS.

377

suffers neither from bedsores nor from loss of sphincter
control; he drags his foot on the side rather than at the
toe ; there is no circumduction of the leg ; there are usually
no changes in the reflexes ; hysterical symptoms are more
marked when the patient knows that he is being watched.
In a word, although hysteria can not imitate the motor
symptoms which do not permit of voluntary imitation, there
are many cases in which, from the character of the motor
symptoms alone, it can not be inferred whether the condi-
tion is the result of premeditated deceit or of the uncon-
scious mimicry of hysteria. To decide this question recourse
must be had to other symptoms.

In the larger number of the cases of hysteria the asso-
ciated signs are sufficient to permit the disorder to be rec-
ognized. Contracted visual fields, the mental state, and the
anaesthesias, if associated with a paralysis not characteristic
of organic lesion, are sufficient to establish the diagnosis.
But occasionally paralysis occurs as the only symptom of
hysteria, and in such cases the elimination of shamming is
extremely difficult. Hysterical paralysis presents the one
difference that, although it may be shown by hypnotism to
be unreal, it does not fall into the traps which so frequently
catch the simulator. The hysterical patient may move his
leg better when unobserved, but even then there is not the
complete preservation of muscular power which the simula-
tor may be shown to have.

Tremor. — Tremor is a symptom of nervous disease
which is very difficult of simulation. Attempts to imitate
the tremor of multiple sclerosis are overdone. It is doubtful
if the tremor of paralysis agitans can be successfully counter-
feited for any length of time. Even if it were, there are
so many other symptoms which accompany tremor in pa-
ralysis agitans that it may be regarded as practically impos-
sible to feign the complete clinical picture of that disease.
The gait, the facial expression, the voice, the muscular rigid-

3/8 MALINGERING.

ity, are all as important symptoms of paralysis agitans as
tremor. They are too numerous and too complex to permit
of consistent and simultaneous mimicry. The other pro-
nounced tremors, such as are observed in paramyoclonus
multiplex, tic convulsif, etc., are too intricate to be volun-
tarily copied with any degree of similarity. Fine tremor,
either in the face, tongue, or hands, is, a common symptom
of functional nervous disorders. It is almost identical in
character with the trembling observed in alcoholism or in
excessive tea drinkers. Although it can not be voluntarily
imitated with success, it is well to bear in mind, in examin-
ing any case which presents this symptom, that it may de-
pend on conditions which antedated the accident.

Anaesthesia. — In organic diseases of the nervous system
anaesthesia may be a most valuable and certain symptom.
In diseases of the peripheral nerves, in spinal-cord lesions,
and, to a less extent, in cerebral affections, blunting or loss
of one or all forms of sensory function is of the highest
value for purposes of diagnosis and localization. It may
also be a pathognomonic evidence of hysteria. The signifi-
cance of this symptom can, however, be easily misinter-
preted. Loss of cutaneous sensibility is extremely change-
able in functional disorders, and even in organic disease it
may vary considerably, so that examinations on different
days or at different times of the same day do not yield iden-
tical results. The value of anaesthesia as an objective symp-
tom is further impaired by the fact that sensibility varies so
extensively in degree in normal individuals. Women are
less sensitive to pain than men. Analgesia, partial or com-
plete, is not a rare occurrence in apparently healthy crimi-
nals. Certain races, especially the Polish Jews, have a
variety of anomalies in pain perception. In persons who
naturally do not feel pain acutely the simulation of analgesia
becomes a comparatively easy matter. There are also a
good many individuals who can suppress any evidence of

SIMULATION OF INDIVIDUAL SYMPTOMS. 379

pain as long as their attention is fixed upon this object.
Many of the " human pincushions " in museums really feel
pain, but, in consideration of the salary they receive, agree
to permit an inquisitive public to stick hat pins through the
calves of their legs, or resort to similar attempts at causing
them to give expressions of discomfort or suffering. Knapp
quotes from Pitres a case of this kind in which the fraud
was exposed : " A man had for several years taken the part
of the anaesthetic man in a show, enduring pricks, cuts,
etc., without the slightest manifestations of pain. In or-
der to obtain the shelter of hospital life, he feigned a
disease, one symptom of which was anaesthesia ; but when
he was subjected to the unexpected application of pain-
ful stimuli, Pitres proved at once that the angesthesia was
feigned."

Persons whose sensibility to pain seems normally not
highly developed, and those who have educated themselves
to repress any of the ordinary manifestations of pain, have
naturally the best chance of escaping detection in the simu-
lation of anaesthesia, and, when the examination is not thor-
oughly and thoughtfully made, may lead the examiner to
believe that insensibility really is present ; but even for
these cases there are several tests which will generally
prove the unreality of the alleged sensory symptoms.

In all sensory examinations the eyes should be blind-
folded. Tests for analgesia are best made when the subject
thinks he is being examined for something else. Thus, if
the legs are alleged to be ansesthetic, a sudden thrust of
the needle into one leg, while the operator is examining the
other, may cause it to be quickly drawn up. Electrical cur-
rents are usually considered of value for the detection of
feigned analgesia. They may be applied by means of a
strong faradic battery, whose current strength should be
suddenly increased without the knowledge of the subject.
Knapp suggests that this test be applied during the course

38o MALINGERING.

of the ordinary routine of electrical examination of the mus-
cles. The individual muscles may be examined in the usual
way, and then, with one of the electrodes over the alleged
analgesic area, the full force of the battery is suddenly
turned on. Strong faradic currents are very startling and
very painful, and this test usually results in some sudden ex-
pression of surprise and suffering if the insensibility is not
genuine. Detection of shamming of the loss of sensibility
to touch is more difficult. The person whose tactile sensi-
bility is normal will know if there has been no contact as well
as recognize light touches ; but he can deny said sensations
when he really feels them. To prove his statements false is
not always possible. The test usually employed is to mark
out the areas in which insensibility to touch is said to exist,
and, after an interval of a few minutes, to repeat the ex-
amination and note if the results of both examinations agree.
This test appears to me to be of very slight value for the de-
tection of simulation. If the anassthetic areas measured at
different times agree perfectly, it is certain evidence that
there is some serious sensory disturbance ; but it is not a
proof of feigning if the limits of the loss of sensibility to
touch vary somewhat at different times. Any one accus-
tomed to making examinations of cutaneous sensation will
remember how often he has been baffled in trying to make
out the anjesthetic limits in cases of unquestionable organic
disease. They vary so widely at different examinations that
variation alone is not sufficient cause for the assertion that
they are not genuine. Sensation to touch is essentially a
subjective symptom and its reality is very difficult to prove.
Since, however, in simulation its loss is nearly always asso-
ciated with analgesia, if it can be shown that the patient feels
pain when he says he does not, we are justified in assuming
that the loss of touch sense is also false.

Thermo-anassthesia is rarely feigned. To test for its
reality, the patient, while being examined with the test tubes

SIMULATION OF INDIVIDUAL SYMPTOMS. 381

filled with cold water and warm water, may suddenly be
touched with a tube of boiling water.

None of these tests for sensation decide positively be-
tween simulation and hysteria. Through the suggestion
imparted by manipulation and examination, hysterical anges-
thesia may change its boundaries or change its situation,
or entirely disappear.

It can, however, usually be decided in accident cases
whether the aneesthesia be true or false without the employ-
ment of these tests, which are, after all, suggestive of the
methods of the Inquisition.

In every nervous disorder of which it is a symptom, anr
sesthesia has certain peculiarities of character and distribu-
tion as well as of the way in which it is associated with
other symptoms. These are individual characteristics fa-
miliar only to those who have devoted considerable study
to the physiology and disease of the nervous system. Were
a simulator familiar with them — which he rarely is — it is
extremely improbable that he could put his theoretical
knowledge to practical use during a thorough medical ex-
amination.

When anaesthesia follows the course of the peripheral
nerves, or the sensory distribution of the spinal segments,
or occupies areas which are known to be favorite locations
for the insensibility of hysteria, it furnishes by its distribu-
tion very strong presumptive evidence that it is not feigned ;
but when, instead of being characteristic, it assumes a form
not in agreement with the other symptoms present, it should
at once arouse suspicion as to its genuineness. Such a sus-
picion may then be verified by the tests commonly employed
to discover if the anaesthesia is real in the places in which it
is alleged to exist.

The anesthetic areas and the characteristics of anaesthe-
sia resulting from injuries to the peripheral nerves or to the
central nervous system and from the mental state of hyste-

382 MALINGERING.

ria have already been described and illustrated. It has been
emphasized that complete loss of sensibility rarely follows
peripheral-nerve or cerebral injuries. Since the sensory
distribution of the spinal cord has become almost absolutely
established, it is just as possible to tell from the anaesthesia
what segment of the spinal cord is injured in a case of spi-
nal compression as it is to refer the numbness and tingling
which may follow a peripheral injury to the nerve upon
whose lesion it depends.

If in any case, the group of alleged symptoms point to
compression or injury to the spinal cord, it may be regarded
as practically impossible for the simulator to have sensory
motor and reflex symptoms all agree so that they could be
referred to injury of the cord at or below any one segment.
Thus, to again quote Case III of Fannie Freeman the fraud
was evident from the anaesthesia alone, for with alleged
total paralysis of the legs the anaesthesia only reached the
middle of the thighs. Such a localization for insensibility
resulting from any injury to the spine is entirely without
precedent.

The irregular areas of hysterical anaesthesia obey certain
general laws. In traumatic hysteria the loss of cutaneous
sensibility is very commonly found only in limbs which are
paralyzed.

To distinguish between simulation and hysteria by the
examination of sensation alone is often impossible. As in
feigned anaesthetic areas, so in parts hysterically anaesthetic,
the effects of accidental injuries to the skin, so common in
organic anesthesia, are rarely observed. In feigned anees-
thesia the skin bleeds readily ; in hysterical anaesthesia the
skin has little tendency to bleed when pricked. But usually,
by reason of the uncertainty and variability of the sensory
disturbances of hysteria, it is necessary to look for associ-
ated signs before one can be certain that the patient really
believes he does not feel. In traumatic hysteria such addi-

SIMULATION OF INDIVIDUAL SYMPTOMS.

383

tional signs are usually present, and it is by appreciating
the character of hysterical paralysis or contracture, or by
demonstrating a functional limitation of the visual fields, that
the functional character of the anaesthesia may also be made
plain.

Pain and Hyperaesthesia. — It is very difficult to deter-
mine the extent and true character of alleged pain. In
many cases disturbances of nutrition and the general bear-
ing of the patient permit no doubt of its reality ; but be-
cause the visible evidences of suffering are absent it can
not always with certainty be inferred that the patient does
not suffer. If he is so situated that he can be constantly
watched in order that it may be determined whether the
sleep is disturbed or the expressions of pain cease when
the patient thinks himself unobserved, the question may be
decided with certainty. In negligence cases such opportu-
nities are rarely at hand, and to decide how much the pa-
tient suffers (or if he suffers at all), the physician must usu-
ally consider each of the many factors in the case, of which
the possible motive for simulation, the general bearing of
the patient, and the agreement of his description with the
ordinary clinical types of pain, are the most important.
The examination should be as long as is feasible, in order
to find out if the pain appear to be continuous, or if by dis-
traction of the attention the patient can be made to betray
himself.

Hyperaesthesia presents many of the same difficulties of
diagnosis as pain. Even when due to actual nervous dis-
ease, it is more intense when the patient's attention is fixed
upon it. However, when any one who makes assertions of
extreme sensitiveness in any part does not show evidences
of pain when the part is touched without his being fore-
warned, it is very probable that the hyperassthesia is exag-
gerated or feigned, although we can not always deny posi-
tively that it exists because the patient does not cry out

384 MALINGERING.

when the sensitive part is disturbed. The Mannkopff symp-
tom is not sufficiently certain in its action to permit the con-
clusion that pain is not caused by pressure on alleged sensi-
tive parts because it is not followed by an increase in the
heart's action.

Ocular Symptoms. — Visual disturbance is frequently al-
leged by simulators, but they usually limit themselves to the
feigning of general impairment of sight or of blindness in
one eye. In any case in which the question arises as to the
genuineness of blindness, examination by an ophthalmologist
is desirable. Bilateral blindness imparts such characteristic
features of attitude, movement, and facial appearance that a
physician who is at all familiar with morbid ocular conditions
can not be imposed upon for any length of time. It might
be possible for a simulator to imitate the deportment of a
blind man were he permitted to keep his eyes closed, but
this he may not do. Blind men keep their eyes open unless
there is paralysis of the ocular muscles, and a claimant who
kept both eyes closed would immediately arouse suspicion.
Furthermore, in true blindness there are important altera-
tions in the pupillary reflex and in the fundus of the eye.
If both eyes are blind, the response of the pupils to light is
impaired or lost. If one eye is blind, light thrown into it
does not cause the pupil to contract ; but if light is thrown
into the sound eye, the pupil of the blind eye contracts
through the agency of the consensual reflex. The ophthal-
moscope renders valuable information, because total blind-
ness rarely occurs in one or both eyes without there being
some demonstrable lesion of the eye itself. If such a condi-
tion could occur, it would be accompanied by other evi-
dences of disease. Although in locomotor ataxia there may
be loss of perception of light before the optic atrophy be-
comes apparent, examination shows a loss of knee-jerk, or
ataxia, or other signs of tabes.

Atropine or allied drugs are sometimes used by im-

SIMULATION OF INDIVIDUAL SYMPTOMS.

385

posters to cause a dilatation of the pupil or a loss of the
pupillary reflexes. Applied either locally or taken inter-
nally, atropine may cause mydriasis, with immobility of the
pupil to all stimuli, without inducing any constitutional
symptoms. From the paralysis of accommodation, vision
for near objects is lost. The patient can not read, and is
uncertain in gait. The pupils are dilated, and do not change
their size under the influence of light. By the dilatation of
the pupil, however, is furnished an opportunity for the more
thorough examination of the fundus of the eye. Bilateral
mydriasis and pupillary immobility, if not artificially in-
duced, are almost always accompanied with significant
changes in the fundus, discoverable by the ophthalmoscope,"
or by paralysis of the oculo-motorial nerves, or by evidences
of constitutional conditions.

The feigning of monocular blindness may be discovered
in a variety of ways. If, with both eyes open, a prism is
placed before the sound eye so as to cause diplopia, and
the patient admits seeing two objects, it is evident that he
sees one of them with the eye alleged to be blind.

This test may be rendered more delicate by bringing the
edge of the prism over only one half of the pupil of the sound
eye while the other eye is closed. The patient at once ad-
mits seeing double. Then if, after uncovering the alleged
blind eye, the prism is held directly in front of the sound eye,
the patient admits diplopia, it is certain proof that he sees
with the eye alleged to be blind. Again : when in a normal
person, one eye is closed, and a pencil is held two or three
inches from the printed page, a part of the field of vision is
obscured so that he can not read a line of the print con-
tinuously, although with both eyes open, it can be read per-
fectly well ; consequently, if a pencil or a similar object be
held before .the sound eye, and the patient reads the lines
continuously, it may at once be inferred that he sees with the
eye alleged to be blind. Or, again, if, while the patient is

86 MALINGERING.

sading with both eyes open, a strong convex lens be placed
efore the sound eye so that vision with it becomes im-
ossible, sight may be proved to exist in the alleged blind
ye by the person under examination continuing his reading.

There are several tests with colors. Thus, if a patient,
nth both eyes open and with a red glass over the sound
ye, can read a line of letters made with a red pencil on a
i^hite ground, he does so with the alleged blind eye, since
olid red, without individualization of letters, is all that is
een with the sound eye. Similarly, with both eyes open, a
pectacle frame containing red glass on one side and green
lass on the other is placed before the patient's eyes. He is
hen asked to read the test cards on which are alternate red
nd green letters, large at one end and growing small at the
ther, on a black ground. A patient who has binocular vis.
Dn can read these letters continuously, but a patient blind in
ne eye would miss every other letter, the eye which is cov-
red with a red glass seeing only the red letters, the green
2tters being neutralized by the red glass, and vice versa.

There are a number of optical arrangements which are
esorted to for the detection of simulation. The stereoscope
nay prove of service. Also the boite de flies, by which test
he subject looks with both eyes into a box containing an
iptical contrivance by means of which the object that is ap-
tarently seen by the right eye is in reality seen by the left
me, and vice versa; so that a simulator may admit seeing an
ibject which appears to him on the same side as his sound
ye, but which is in reality seen by the eye said to be blind,
f a clever simulator makes a study of any of these tests, he
nay become sufficiently expert to avoid being caught by
hem.

As has repeatedly been emphasized, the sight is in reality
lot lost in hysterical blindness, and the hysterical patient
tiay be regarded as a siniulator because he does not conduct
limself during the above tests as a person would who was

SIMULATION OF INDIVIDUAL SYMPTOMS. 387

really blind. The question arises, How is simulated blind-
ness to be distinguished from hysterical blindness ? It may
often happen that such a diagnosis presents many difficulties,
and depends for its solution upon associated symptoms
rather than upon any local conditions. Interferences of
vision, of which the patient is himself conscious, are among
the more serious incidents of hysteria, and are usually ac-
companied with other pronounced hysterical manifestations.
If in any case of blindness which is not organic in origin
there are associated and well-marked stigmata of hysteria,
we may infer that the blindness also depends upon actual im-
pairment of vision and is not fraudulent ; for to prove fraud
we would have to prove that the general symptoms were
also feigned, and to successfully feign the complicated clini-
cal picture of hysteria may be regarded as impossible.

Limitation of the visual field is an ocular sign of great
diagnostic value in hysteria, and it may properly be regarded
as objective. It is typical of hysteria, and probably, in this
country at least, is never feigned. There has been much
discussion among European neurologists and ophthalmolo-
gists as to the possibility of simulating this symptom. It
seems possible that an old hospital patient who had assisted
at many perimetric examinations, or a physician who had
studied visual disturbances, might feign limitation of the
visual fields. But the perimeter is not generally popular in
this country, and even among neurologists is infrequently
used. It is consequently improbable that any simulator would
take the trouble to learn enough about this symptom to coun-
terfeit it with any degree of success. The characteristics of
hysterical contraction of the visual fields have already been

■y

described, and need not be repeated here. If simulation of
it were attempted, there would probably result irregularity
and inconsistencies which would immediately arouse suspi-
cion that the condition was not genuine. Knapp suggests,
if the case is in any way doubtful, the use of perimeters of

388

MALINGERING.

different diameters, claiming that if by different instruments
the fields remain the same the contraction is not feigned.

If the patient complains that his eyesight is impaired
but not lost, it is more difficult to determine how much
truth there is in these statements. If examination of the
eye, as well as of vision, shows no abnormities, the decision
as to whether vision really is impaired, and if so how much,
must be guided by the other aspects of the individual case.

The truth can usually be arrived at by observing the
behavior of the patient during protracted examination, in
which the various tests for acuity and extent of vision are
repeatedly employed.

Hearing. — Deafness is rarely feigned as one of the various
nervous symptoms which follow accidents. Hysterical deaf-
ness usually occurs in the form of impairment of hearing.
If the patient declares he is absolutely deaf and there are
no evidences of any structural disturbance in the auditory
apparatus, the deafness is either functional or feigned. If
feigned, its character may usually be disclosed by resorting
to the various tests which depend upon confusing the simu-
lator or taking him off his guard. Knapp proposes the
following modification of Coggins's stethoscope test : A bin-
aural stethoscope, with tubes several feet long, is placed in
the ears of the person to be examined. The tubes should
be so arranged that either of them may be closed at the will
of the examiner without the knowledge of the subject. Thus
the sound may be conducted, as the examiner pleases, to
either the normal or the alleged deaf ear, which may lead
the simulator to make contradictory statements.

Convulsive Attacks. — The convulsive attacks of hysteria
are not frequent when the disorder results from traumatic
causes, and when they occur they are accompanied with
pronounced permanent stigmata, and can easily be recog-
nized at their true value. The feigning of epilepsy is a fre-
quent device among criminals, and in a few cases epilepsy

SIMULATION OF INDIVIDUAL SYMPTOMS. 389

has been proved to be simulated in actions for personal in-
juries. There are several characteristics about epilepsy
which make it very difficult to simulate in accident cases.
In the first place, epileptic fits only occasionally occur in
public. Although from ten to fifteen cases of epilepsy are
treated daily at the Vanderbilt Clinic, an epileptic fit rarely
takes place there, and we are obliged to treat many cases of
epilepsy in virhich there is no proof, except the statement of
the patient or his friends, that epilepsy exists. The epileptic
paroxysm follows a regular cycle. The patient falls, irre-
spective of any danger of hurting himself ; the initial mus-
cular contractions are intense ; the face is blue ; the tongue
is bitten ; the pupils do not react to light ; the urine is passed
involuntarily ; and the knee-jerks are lost for some time after
the convulsion is over.

To feign epilepsy, the simulator is forced to have his at-
tacks when he can be observed. That fits can be shammed
so skillfully that they might pass for true epilepsy if made
before a witness who was not a physician, is unquestionable.
In such cases it is impossible to tell whether the person
really has epilepsy without having him observed by some
one familiar with the disease ; then the fraud can usually be
discovered. When the simulator falls he usually falls in
such a way that he is in no danger of being hurt. He takes
good care that his tongue is not bitten ; there are no changes
in the reflexes or in the pupils ; the muscular contractions
are exaggerated and theatrical ; the tonic stage is usually
very short ; and in the clonic stage the movements have a
more varied and unnatural character than in epilepsy.

Vascular Disturbances. — Voluntary control of the action
of the heart is possessed by so few persons and always in so
slight a degree, that the simulation of tachycardia merits no
particular attention. It should be remembered, however,
that rapid and tumultuous heart action is frequently ob-
served in persons who have no serious trouble with the

go MALINGERING.

eart, but results from various emotional and toxic causes,
io many exciting influences attend the physical examination
f the chest, especially in women, that considerable care and
epeated examinations are necessary before any serious sig-
ificance can be attributed to tachycardia when it is unasso-
iated with other symptoms of vascular disturbance. In
imulation, fear of detection may cause the heart to beat
luch more rapidly ; thus, at the end of the last examination,,
''annie Freeman's pulse rate rose to 132 to the minute, al-
hough at the beginning it was only 104.

In all cases in which there is any tendency to rapid or
umultuous heart action the examination should be repeated
fter the patient's first excitement has passed away, or after
est in the recumbent posture has permitted a re-establish-
nent of the normal cardiac rhythm.

The other vascular symptoms, such as flushings, cold-
less, and blueness of the extremities, can not be counter-
eited in a way to deceive an examiner who is on the alert
or deception.

Paralysis of the Sphincters. — A person who has lost
'oluntary control of the bladder or rectum is in so miser-
,ble a condition that a superficial examination is usually
.dequate to reveal the genuineness of the symptoms. Pa-
alysis of the bladder results in retention or incontinence
if urine. In retention the urine collects until it is drawn
iff by a catheter, or until the filling of the bladder causes
, relaxation of the vesical sphincter, so that the urine over-
lows either continuously by drops, or in larger quantities at
hort intervals (overflow incontinence). In incontinence
he lips of the meatus are constantly wet from the continu-
)us dribbling of the urine. Both conditions are liable to be
[uickly complicated by excoriations on the scrotum and
ides of the legs, and in both there is almost unexceptionally
I strong urinary odor about the bedding and about the pa-
ient. These secondary results are usually absent in simu-

SIMULATION OF INDIVIDUAL SYMPTOMS.

391

lation, although of course the simulator may produce them
if he will.

If retention is alleged, it may be impossible to prove it
genuine, unless the patient can be watched for twenty-four
hours, in order that it may be observed whether or not he
passes water involuntarily and exhibits the physical signs of
a distended bladder. Such observation is often impossible.
Without it the absence of the ordinary secondary effects of
urinary incontinence, the absence of distention of the blad-
der as shown by percussion above the pubes, and the in-
congruity of the associated symptoms with the alleged vesi-
cal condition, are usually sufficient for diagnosis.

False incontinence is more easily detected than false re-
tention. In the absence of an almost constant moistening of
the meatus, and without the excoriations and urinary smell,
which are the unavoidable consequences of the incontinence
of urine, the existence of that condition can be positively
denied.

Incontinence of fseces is easily recognized. In addition
to the fcccal odor and frequent soiling of the linen, the anal
orifice is large ; and when the examiner inserts the finger in
the rectum, there is total absence of the normal muscular
contraction of the sphincter.

Reflexes. — The reflexes are beyond voluntary control.
The skin reflexes can not even be modified. In cutaneous
areas which are insensitive to touch or pain through organic
disease or through hysterical ideas the superficial reflexes
are lost. It is this latter fact which reacts to the simulator's
disadvantage, for if they are not lost in places alleged to
be anaesthetic, it should excite suspicion of shamming. The
cilio-spinal reflex and the tendon reflexes, on the contrary,
continue to act, unless their spinal centers or their con-
ducting paths have been destroyed. The tendon reflexes
often appear increased in suspicious cases. The tap on the
patellar tendon or on the wrist may be followed by a con-

;92

MALINGERING.

Taction which is exaggerated beyond the usual limits. If
uch exaggeration is not genuine, it usually is at once ap-
)arent by the momentary pause between the application of
he stimulus and the resulting contraction. A person who
s feigning exaggeration of the tendon reflexes may be at
)nce discovered by testing them when his eyes are covered,
deprived of vision, he can no longer tell when to expect the
ap, and the pause which may have been only momentary
vhen his eyes were open, becomes so apparent, and the con-
raction is so evidently unnatural, that there is no difficulty
a saying that the increase is feigned. It may sometimes
lappen that the tap causes the natural reflex at once, and
hat after a few moments, when the brain has had time to
end its message, a second contraction occurs, which is
nanifestly voluntary. Foot clonus can not be imitated in a
vay to deceive. It must be remembered that in some per-
ons the knee-jerks are naturally very active, and the elbow-
nd wrist-jerks are present ; such an increase is always bi-
iteral and is of little significance.

Like the superficial reflexes, the tendon reflexes can not
>e decreased. In testing for the knee-jerk, if it fails to re-
pond, it will be found that the knee is held immobile by the
nuscles. If such is the case, the flexor tendons of the leg
i^ill be felt firm and hard, preventing any extension of the
2g. The Jendrdssik mode of re-enforcement may overcome
his. If it does not, it must be said that the patient does not
lermit the knee-jerks to be tested, but not that they are lost.

Bibliography.

Bailey, Simulation of Nervous Disorders following Accidents.
^he Railway Surgeon, February 8, 1896.

Dana, op. cit.

Godkin, Accident Cases. Hamilton's System of Legal Mediciru
few York, 1894.

Heller, Simulationen und ihre Behandlung. Leipzig, 1890.

Hoffman, Berl. kl. Woch., June 21, 1891.

SIMULATION OF INDIVIDUAL SYMPTOMS. 393

Judd, Legal Aspects of Spinal Concussion. Boston Med. and
Surg, /our., i8go, vol. cxxiii, p. 219.

Knapp, Simulation in Traumatic Nervous Diseases. Boston
Med. and Surg. Jour., September 28, 1893. Ibid., Feigned Diseases
of the Mind and Nervous System. Hamilton's System of Legal
Medicine, New York, 1894.

Page, op. cit.

Prentice, Speculation in Damage Claims. North Am. Review,
February, 1897.

Prince, Traumatism as a Cause of Locomotor Ataxia. Jour.
Nerv. and Mental Dis., February, 1895.

Schmidt-Rimpler, Zur Simulation concentrischer Gesichtfeld-
einengung mit Beriicksichtigung der traumatischen Neurosen.
Deut. med. Woch., 1892, p. 561.

Schultze, Deut. m.ed. Zeit., October 16, 1891. Ibid., Weiteres iiber
Nervenerkrankungen nach Trauma. Deut. Zeit.f. Nervenh., 1891,

P- 444-

Seeligmiiller, Deutsch. med. Zeit., October 16, 1891.

PART IV.

TREATMENT OF THE TRAUMATIC NEUROSES.

It has been frequently asserted in preceding pages
hat the prognosis of the traumatic neuroses depends in
arge part upon the ability and willingness of the patient to
object himself to proper treatment. Although the present
'olume concerns itself with causes rather than with cures,
t seems so essential that there should be a greater familiar-
ty with methods which can often prevent a reasonably
lealthy man or woman from becoming a permanent invalid,
hat these closing pages may be appropriately devoted to
reatment. As we have seen, these disorders comprise trau-
natic neurasthenia and traumatic hysteria, and mixtures of
he two. The treatment for all is essentially the same. It
lonsists in the regulation of the mode of life in such a way
hat the patient is shielded from those influences which ex-
)erience has shown work him the greatest detriment, and
n supplying, as far as possible, the essentials of normal
lealthy living which, by reason of fatigue or perverted
deas, he can no longer gain for himself. It is the natural
nethod, rather than treatment by drugs, and it is based
ipon principles of physiology and psychology, rather than
ipon any to be found in the materia medica. Under the name
)f the Rest Cure, as described by Weir Mitchell,* one form
)f treatment for neurasthenia and hysteria is generally
amiliar. When these disorders result from injury or shock
t undergoes slight modifications.

* Fat and Blood, sixth edition, Philadelphia, 1891.

394

THE REST CURE.

395

The Rest Cure. — It is by no means necessary for every
case of traumatic neurasthenia or hysteria to be put to bed
for weeks or months. It is advisable for any one who has
been severely frightened or shaken up to rest quietly for a
few days or a week, during which time he may be free from
■effort and annoyance and have his thoughts diverted as
much as possible from the accident. But at the end of that
time, if the shock and bruising were not excessive, he can
usually take up his work again. When, however, neuras-
thenia or hysteria is pronounced, and especially when the
patients have been harassed by frequent examinations and
have found no benefit from various therapeutic methods,
the rest cure, in its most comprehensive extent, remains as
the best means of speedy if not of ultimate recovery.

Before proceeding to an enumeration of the various pro-
cedures incident to the rest treatment, emphasis must be
laid upon the one condition, without the fulfillment of which
success is imperilled or rendered impossible. This condition
is the complete control of the patient by the physician. The
amount of rest, both physical and mental, should be deter-
mined by him, and he should be kept constantly informed
of the most trivial happenings which go on in the sick-room.
He should have within his jurisdiction the regulation of the
patient's whole mode of life ; he should have the right to
•determine whether complete isolation be necessary, or if in-
terviews with friends or with counsel are to be permitted,
and he should decide as to their frequency and their length.

While litigation is pending it is practically useless for
the patient to undertake the rest cure. Under existing con-
ditions any person who is really the worse for an accident
■can usually obtain, by settlement, reasonable compensation
for his injuries without going to court. If the claim for
damages can not be amicably settled without suit, the patient
may as well decide at once between the two alternatives,
viz. — whether he wishes to relinquish the chances of a gen-

396

TREATMENT OF THE TRAUMATIC NEUROSES.

erous verdict, or, secondly, to indefinitely postpone his re-
covery. When the injuries are slight, and the amount
claimed is large, this decision is quickly reached ; but if the
functional disorder is well marked, the patient is often un-
able to decide for himself. Under such circumstances the
most that the physician can do is to explain the nature of
the treatment, and to show how impossible it is to fulfill its
requirements and at the same time to grant to attorneys the
proper facilities for preparing their case. When he has em-
phasized the unquestioned truth that the longer a traumatic
functional disease exists the more difficult it is to cure, when
he has explained that during the months or years that these
suits are dragging through the courts before a final verdict
is reached the disease is taking on a phase for which no
money can be considered adequate compensation — when the
physician has made these facts plainly evident to the patient
and his friends, he can do no more.

Although litigation constitutes the most serious obstacle
to the institution and carrying out of the rest cure, it is not
always easy to convince the patient or his friends of the rea-
sonableness of the method, even when the powerful factor
of litigation is absent. The friends of the patient often re-
gard him as more frightened than hurt, and the patient him-
self resents being deprived of his liberty. He may accede
to the physician's demand for a time, but becoming tired
of forced seclusion, eventually insists either upon returning
home or of undertaking some more radical form of treat-
ment. Or his friends may be unwilling to give him over to
the entire charge of strangers and to place him where he is
no longer amenable to their wishes or the recipient of their
sympathy ; or, having consented to the separation, soon
change their minds and insist upon some less exacting
method. Yet, unless the patient's surrender is uncondi-
tional, and unless he agrees to continue the treatment for a
reasonable length of time, the hopes of cure of confirmed

THE REST CURE.

397

neurasthenia or hysteria are slight. If treatment is begun
and given up at the end of a few days or weeks, the patient
goes back to his original environment or falls into the hands
of quacks, and loses what little he may have gained.

The fundamental principles of the rest cure depend upon
isolation and rest in bed. By means of the first it is intended
to permit a restoration of normal vitality to brain cells,
whose function have become disordered, and by the second
to supply to the whole body the rest it needs, but which,
without artificial means, it does not obtain. These two
means operate conjointly, the action of one enhancing and
supplementing the effect of the other. Isolation, in many
cases, should be so absolute that the nurse, and perhaps the
masseur, are the only persons, except the physician, whom
the patient sees. The most effective method (the one advo-
cated by Dr. Mitchell) is obtained away from the patient's
home. For this purpose quiet hotels or boarding houses, or
private hospitals, or public hospitals in which a quiet room
can be obtained, are frequently utilized. The setting aside
of a room in the patient's own house, to which none but the
physician and his assistants are to be admitted, is sometimes
feasible, although it is rarely advisable when strict seclusion
is to be enforced, and is altogether less desirable than for the
patient to be placed away from familiar sounds and scenes.
If complete isolation is necessary, it should be so effected
that there is no communication whatsoever with the outside
world. Then both family and friends are excluded, and
there is naturally total banishment of all questions of busi-
ness ; the patient neither writes nor receives letters ; the
meals are brought to the door of the room by an attendant
and handed in to the nurse. Such absolute imprisonment is
only occasionally desirable and is rarely necessary for a long
time. The physician must decide by the character of the
patient and by the gravity of the symptoms when to insti-
tute it and when to stop it. He must also use his judgment

398 TREATMENT OF THE TRAUMATIC NEUROSES.

as to the kind of persons he permits the patient to receive,
taking care to admit last such relatives or friends as are con-
spicuous by lack of tact or by emotional tendencies.

The one constant companion of the patient during the
weeks when the isolation is more or less complete is the
nurse. Male nurses are not fitted for this kind of work, and
the female nurse must have some special qualifications, and
if possible some experience in the management of such cases.
It is more important, however, for the nurse to realize that
the neurasthenic patient is really ill than it is for her to be
intimately familiar with every detail of the treatment ; for
the way that the rest cure is to be carried out in an indi-
vidual case, will be indicated to her by the physician when
the treatment begins, but, unless she realizes that the un-
reasonableness, impatience, and fretfulness of the patient are
the voicings of disease, she will be unable to maintain the
gentleness, firmness, and patience upon which qualities of
the nurse the success of the rest cure depends. No task is
more trying than the care of such patients ; it requires good
health and an even temper; it is easiest for those nurses
who are enduring and unemotional, and who by their cheer-
ful manners and ability to talk or read well, or by similar
accomplishments, can make the time pass most pleasantly
and quickly for their bedridden companions.

Next to isolation, and together with isolation, the most
important feature of the rest cure is rest in bed, the com-
pleteness of which varies with the severity of the case. In
grave cases of neurasthenia the patient is kept as nearly mo-
tionless as possible. He is not permitted to feed himself,
and should not even turn over in bed without the assistance
of the nurse. The use of the bedpan and of the portable uri-
nal renders it unnecessary for him to get up to empty the
bowels or bladder. Like isolation, this enforced rest gener-
ally proves disagreeable to the patient for the first few days.
However, he ordinarily becomes soon accustomed to it, and

THE REST CURE.

399

ceases to complain. When the time arrives for complete
inactivity to be abandoned, the change is to be effected
gradually. At first the patient may sit up in bed for a few
minutes at a time ; then sit with the feet out of the bed rest-
ing on a pillow ; then sit in a chair, and gradually begin to
walk, doing a little more each day than he did the day pre-
ceding.

Although the re-establishment of the exhausted nervous
system is best secured by means of isolation and prolonged
rest from voluntary effort, the fact remains that the circula-
tion is more active and nutrition consequently better when
the muscles do some work. To secure muscular activity
without making serious demands upon the nervous system,
the methods at our disposal are massage and electricity.
Massage may be given by the nurse if she is a skillful mas-
seuse, and then no outsider need be introduced, and the iso-
lation of the patient remains undisturbed. To be able to
give massage well, however, is an art in itself, of which only
a few of the graduates of our training schools are mistresses.
The most skillful masseurs and masseuses that we have in
this country have been educated in this special branch in
Sweden, and, in New York at least, confine themselves solely
to giving massage. If the passive movement is to be given
by some one other than the nurse, it adds, of course, addi-
tional expense to the treatment, and diminishes the seclusion
of the patient ; but the value of systematic and skillfully ap-
plied massage is so great that its proper administration more
than counterbalances these drawbacks. Systematic rubbing
of the whole body, for purposes of general nutrition, must be
instituted gradually, as the idea of having the body touched
by others is repulsive to many persons, and most patients
only become accustomed to it after several stances. It is
best to delay it until the treatment has lasted several days,
and to begin it by merely rubbing an arm for a few minutes.
It may then be gradually extended, so that at the end of a

400 TREATMENT OF THE TRAUMATIC NEUROSES.

week or ten days the stances last an hour, and the arms,
legs, abdomen, and back are being systematically exercised
every day.

Electricity is the other means by which the patient may
obtain exercise. Its effects, although less pronounced, are
similar to those of massage. If a good masseur or mas-
seuse can be obtained, there is rarely any necessity for using
electricity. When for any reason, however, it is impossible
to secure the services of a skilled massage operator, the fara-
dic battery can be successfully substituted. It has the ad-
vantage that an intelligent nurse can be easily taught to use
it gently and effectively, and that " electrical treatment "
often has a beneficial mental effect on the patient. The
electrodes should be wet with warm salt water, and as the
sponges get very dirty, it adds a touch of neatness to the
procedure if they are either frequently changed, or else cov-
ered by pieces of white gauze at the time of each application.
At first the current is applied in very weak strengths, and
to small areas of the body ; as the patient becomes used to
its action the current strength may be increased until the
muscles react promptly and all of them are in turn stimu-
lated. The stance should last about half an hour.

The regulation of the diet during the rest cure is con-
trolled by two considerations — viz., that it should be so ar-
ranged that the patient may receive plenty of nourishment
in spite of any gastric irritability that he may have ; and, sec-
ondly, that the amount of food taken should be excessive
and out of proportion to the work which is done (forced
feeding). If at the beginning of the treatment dyspeptic
symptoms — such as anorexia, nausea, vomiting, and eructa-
tions — are present, the alimentation must consist exclusively
of milk, in order that the stomach may be brought as soon
as possible to a condition in which it can retain large quan-
tities of more substantial food. Under these circumstances
the milk is given in very small quantities which are repeated

THE REST CURE.

401

at short intervals during waking hours. Thus, one or two
ounces of milk given every hour, or slightly larger amounts
given every two hours, are sufficient for the first few days.
Administered in this way, milk can be borne by almost any
one, although he may think that it does not agree with him,
and although, if given in larger quantities, it might immedi-
ately induce an attack of vomiting. In rare instances it
may seem necessary to have the milk peptonized. Kouniyss,
on account of the alcohol it contains, is not to be recom-
mended as an exclusive diet. This method of feeding, com-
bined with the rest in bed, is usually sufficient to quiet the
more prominent of the gastric symptoms so that in a very
short time the quantities of milk may be increased, or it
may be alternated with more palatable articles of food. At
the end of a week it is usually possible for the dietary to be
amplified, so that while the patient continues to be fed every
two hours, he receives substitutes for the milk two or three
times a day. These substitutes should at first be limited to
fluids, such as soups or broths, or some of the prepared
foods; but they may very soon be made to include soft-
boiled eggs, custards, and jellies, until finally, by the ad-
dition of chops, steaks, chicken, etc., the patient is receiving
a regular diet. As long as he remains in bed the plan of
some nourishment every two hours should be adhered to,
although no large quantity may be taken at any one time.
Even after he gets up and begins to walk around, and is
taking three fairly full meals a day, he should have some
nourishment between meals, in order that the amount of
food taken remain excessive.

Stimulants should be as far as possible avoided. Tea
and coffee can generally be excluded without difficulty. To
relieve the tedium of the dietary a cup of cocoa or chocolate
may be occasionally permitted. If the patient is markedly
alcoholic, with symptoms of cardiac weakness, it may be
necessary to provide some means for the improvement of

402

TREATMENT OF THE TRAUMATIC NEUROSES.

the heart's action. This may be done by prescribing small
quantities of alcohol, or, better, some of the heart tonics,
such as strychnine, strophanthus, or digitalis. Tobacco,
while the patient remains in bed, is to be avoided. Later
the advisability of its use must be determined by the effect
it has on the individual. If it renders him more nervous,
and if it is desired to use it in excess, it should be cut off
altogether. When, however, its effect is to calm rather
than to excite, one or two cigars a day can with safety be
allowed.

The general management of a neurasthenic man or
woman during the one or two months that the only persons
he or she sees are comparative strangers, is a matter of con-
siderable delicacy. Although the patient is in a certain
sense a prisoner, he has undertaken the treatment of his own
accord, and he can terminate it when he wishes. It must
accordingly be the physician's care to make the period of
confinement as little irksome as is consistent with the ulti-
mate object in view. Every possible latitude and privilege
consistent with the sick man's welfare he should endeavor
to provide. When, however, it has once been decided what
the patient may and may not do, the plan of treatment
should remain unaffected by unreasonable protestations and
complaints. By acceding to demands which are the results
of fretfulness and impatience the physician or nurse will
seriously lose in personal influence, and will postpone the
time when such nervous manifestations are to permanently
disappear. Gentle firmness on the part of both physician
and nurse is essential to the success of this kind of treat-
ment. Objections and complaints are best forestalled and
obviated by instituting at once a daily rigime to which the
patient is to conform as regularly as though he were keep-
ing business appointments. By this means he comes to look
forward to the hours given up to special things with ex-
pectancy if not with pleasure, and the time passes with rea-

THE REST CURE.

403

sonable rapidity. When the daily, or rather hourly, sched-
ule is once determined upon, it should only be changed for
purposes of enlargement. Its special character varies with
individual cases, but its principle remains essentially the
same. Thus, if the patient does not leave the bed at all,
he has milk at seven ; at eight he is assisted at his toilet by
the nurse and receives a sponge bath ; at nine more milk,
and is read to for a short time ; at ten the physician calls ;
at eleven more nourishment, followed by rest and quiet,
and so on throughout the day, there being definitely deter-
mined hours for the physician's visit and that of the mas-
seur, for reading, talking, resting, eating, etc. As the pa-
tient begins to improve, these hours are changed to fit differ-
ent requirements, but the rule of regularity remains un-
disturbed.

The length of time necessary for the observance of the
more stringent requirements of the rest cure is in large part
determined by the rapidity with which improvement results
from the treatment. As a general rule, the more prominent
symptoms begin to yield in a few days or weeks. As a re-
sult of the milk diet the dyspeptic symptoms disappear and
the patient begins to realize that he has an appetite ; the
sleep becomes improved in quality and in duration ; the
pains are less frequently complained of ; the tremor and ex-
citability are less evident ; the nutrition is raised, as is shown
by an increase in the color and the firmness of the skin, and
by a gain in weight. There is no absolute rule by which it
may be determined just when the patient may get up or be-
gin to see his friends again. As in convalescence from
general diseases, this question must be decided by the phy-
sician who has learned the capabilities of the person under
his care, and who, by gradually permitting him to do more
and more, can readily ascertain how rapidly the return to
normal living should be.

Valuable as is the rest cure, it is not infallible ; and the

404 TREATMENT OF THE TRAUMATIC NEUROSES.

question arises, If the patient improves but little or not at
all, how long should the treatment continue ? To this differ-
ent answers are given by various authors. In general it
may be said that if at the end of two months the benefit is
not plainly perceptible, the method of treatment should be
very much modified or changed altogether. The prognosis
for recovery in such cases is far from bright.

When the rest cure is reasonably successful, at the end
of from one to three months the patient is comparatively
free from the distressing symptoms from which he suffered
at its beginning, and can endure a moderate amount of exer-
tion fairly well. He is still somewhat nervous and excitable,
however, and in very much the same condition as many
neurasthenics who are hardly ill enough to need the rest
cure, but who require some special form of treatment for
the re-establishment of health.

Carried out in its most perfected form, the rest cure
is expensive, as it implies that the patient be away from
his work for several weeks or months, that he be con-
stantly under the supervision of a nurse, and frequently
visited by a physician. An effort is being made, how-
ever, to make it more accessible to persons who are in
moderate circumstances. In the Philadelphia Hospital beds
are set aside for this treatment, and some few of the hos-
pitals connected with the railways have recognized its value,
and undertake to treat patients in accordance with its prin-
ciples.

In persons who no longer require the complete rest cure,
and in those who were never ill enough make such a pro-
cedure necessary, rest, more than is necessary for healthy in-
dividuals, is still a primary requisite. This may be secured,
if the patients have no employment, by not rising until after
breakfast, and by lying down for thirty minutes or an hour
two or three times during the course of the day. If it is
necessary that the patient return to his employment — and

HYDRIATRICS.

405

in many cases such a course is extremely desirable — rest
may sometimes be obtained during working hours ; or, if
not, the patient should go to bed earlier than usual, so that
he passes at least ten hours in bed. The whole mode of life
of a neurasthenic should be moderate and equable. He
should shun as far as possible all that may fatigue or excite.
What has been said in regard to litigation in its relations to
the rest cure may be repeated with almost equal force for
the patient who does not need to be isolated or put to bed.
In the first case it is a bar to recovery from a serious condi-
tion ; in the second it exposes the patient, who under proper
conditions might soon be well, to the danger of becoming
an irritable and hopeless invalid.

There are a variety of procedures besides the rest cure
which are efficacious in the amelioration and cure of neuras-
thenic and hysterical conditions. Some of them are ap-
plicable during the rest cure itself, and some are only re-
sorted to as a termination of that form of treatment or in
cases which are not sufficiently severe to demand seclusion
and forced rest. For purposes of convenience they will all
be considered together.

Hydriatrics. — Second only in value to the rest cure in
the treatment of neurasthenia and hysteria is the scientific
application of water. Taken internally, by causing an in-
creased activity in the kidneys and skin, and by diluting the
toxic metabolic products which are circulating in the blood,
it exerts a most beneficent influence upon nutrition. It may
be administered with advantage in large quantities during
the whole course of neurasthenia or hysteria, with the ex-
ception of that period of the rest cure during which the
patient is on a fluid diet. A not unpleasant method is a
glass of very hot water, taken one hour before each meal.
It is the external application of water, however, which is at-
tended with the most brilliant therapeutic results in func-
tional nervous diseases.
27

4o6 TREATMENT OF THE TRAUMATIC NEUROSES.

Thirty years ago the water treatment, whose ignorant
exponents were called " hydropaths," had won a well-de-
served reputation for quackery. To-day, largely through
the researches of Winternitz, of Vienna, and of his pupil,
Simon Baruch, of New York, it has taken its place among
the most efficient of therapeutic agents. Its importance is
universally admitted in Europe, where hydrotherapeutic
establishments are numerous. Among the most prominent
of these may be mentioned : In Austria, Dr. Winternitz's, at
Kaltenleutgeben, near Vienna ; the Centralbad, in Vienna ;
Dr. Koehler's, in Eisenbach ; Dr. Pospischl's, in Krems ; in
Germany, at Elgersberg and Konigstein ; in France, at Di-
vonne and Lamalou ; in England, at Malvern.

In America, although "the recognition of the usefulness
of hydriatrics was less prompt than on the other side of
the ocean, its value is now becoming rapidly appreciated.
Some of the sanitaria in this country are prepared to ad-
minister many of the procedures of the water treatment.
Prominent among these institutions are the ones at Dans-
ville, Clifton Springs, and Watkins, in the State of New
York, and at Battle Creek, Mich. The Hydriatric Insti-
tute in New York city, and two institutions at Louisville,
Ky., are fitted out with complete apparatus for all hydriatric
procedures, the various douches being the chief applications
made in them.

The institutions at Louisville, the Hydriatric Institute
and the Riverside Public Baths in New York, give treat-
ment to ambulant patients who may return to their homes
after each treatment.

The beneficial effects of wisely chosen hydrotherapeutic
measures are especially evident in the functional nervous
diseases. Since the opening of the hydriatric department
of the Riverside Public Baths in New York city, most of
the Vanderbilt Clinic cases of neurasthenia and hysteria are
referred to that institution for cold douches. It is only jus-

HYDRIATRICS. 407

tice to state that our success in the treatment of these con-
ditions is now much more satisfactory than it previously had
been. The improvement in nervous symptoms which often
follows a sojourn in a sanitarium is largely due to the water
treatment received there. Some patients with neurasthenia
and hysteria, in whom but little benefit was derived from
the rest cure, have returned, apparently well in every way,
after a few months' stay at a sanitarium.

The success of hydrotherapy in any case depends in
large part upon whether the proper procedure is chosen for
the individual condition it is meant to benefit, and upon
whether it is properly carried out. The methods which
have proved most successful in the treatment of the func-
tional nervous diseases may be briefly outlined here, al-
though for a thorough comprehension of this important
subject the reader must be referred to special treatises.*

The sponge bath, which is given daily during the period
of the rest cure when the patient is in bed, is chiefly for pur-
poses of cleanliness. Different segments of the body are
sponged off with water at 70° F. and then dried. Each seg-
ment is dried and wrapped up before another segment is
bathed.

The drip sheet is to be used when the patient, after the
rest cure, is beginning to walk around the room. The best
time for its application is upon rising in the morning. It
has the advantage that, as it requires no special apparatus, it
may be given perfectly well at home, and is less alarming
to the patient than some of the more elaborate hydriatric
measures. The sheet, after having been partially wrung
out in water at seventy degrees, is applied as follows : The
nurse, standing behind the patient, whose head has been wet
with cold water, puts one corner of the sheet under the pa-
tient's right arm and carries it across the chest ; the rest of

* See Baruch on Hydrotherapy, in Hare's System of Therapeutics, Philadel-
phia, 1 891.

408 TREATMENT OF THE TRAUMATIC NEUROSES.

the sheet is then carried across the back, over the left shoul-
der, and continued over the front of the right shoulder until
the end can be tucked in at the back, so that the body is en-
tirely covered. By slapping and by light and rapid rubbing
over the sheet, from periphery toward the center, the pa-
tient soon becomes warm. When the reaction is fully estab-
lished, which occurs in one or two minutes, he is dried
off quickly with a towel and returned to bed. In succeed-
ing applications the temperature of the water may be re-
duced a few degrees at a time until it finally reaches fifty
degrees.

The Wet Pack. — The full wet pack is only occasionally
necessary in the functional nervous disorders. When neces-
sary, the patient is wrapped in a sheet wrung out in water
at seventy degrees — which may be daily reduced one degree
in temperature until sixty degrees is reached — and then
rolled in a blanket, in which he is left for an hour or longer.
This procedure is of especial service when insomnia is pro-
nounced or when the nervous symptoms are in large part
dependent upon alcoholism or upon inadequate elimination
by the kidneys, and in erethetic conditions. More frequent-
ly the desired results may be obtained by the local wet pack,
which is one of the most efficient agents for allaying mental
excitement and inducing sleep. It is also often useful in the
treatment of chronic constipation. It is applied by placing
a piece of sheet folded two or three times, which has been
thoroughly wrung out in water at sixty to seventy degrees,
and then folded in the form of a compress across the pa-
tient's abdomen. A piece of flannel bandage of the same
length as the compress, but two inches wider, is then put
around the body, so that it holds the compress in position.
The abdominal compress is usually applied just before going
to bed, and should be left for half an hour. If at the expira-
tion of this time no effects from its use are apparent, the
sheet may be wrung out in cold water and again applied.

HYDRIATRICS.

409

The Foot Bath. — In hydriatric institutions the water for
the foot tub enters and leaves in a constant and rapid stream,
so that there is the stimulus of mechanical irritation as well
as that of heat or cold. In private houses it is usually neces-
sary to be content with an ordinary foot tub filled with
water at the desired temperature. The patient sits with the
feet in the water, which comes above the ankles. Either hot
or cold water may be used, the effects of each being similar.
In the cold foot bath the water is at a temperature of forty
degrees, and the patient rubs the feet energetically one
against the other for about five minutes. By the friction
the feet are kept comfortably warm. While in the water,
and when they are taken out, their capillaries undergo
marked dilatation, as is shown by the rosy color of the skin
and the sensations of warmth in the lower extremities. The
hot foot bath is on the whole less eflficacious, although often
very useful. In it the water is at a temperature of one hun-
dred and ten degrees, and the feet are immersed for five or
eight minutes.

Both the cold and hot foot bath are efficient sleep-induc-
ing agents and are valuable aids for the relief of mental irri-
tability and excitement, and of the disagreeable subjective
cerebral sensations.

The Douche. — The douche excels all other hydriatric
measures in the constitutional treatment of neurasthenia and
hysteria. Although it can not be applied during the rest
cure, it is a seasonable post-graduate course to that proced-
ure, and in many cases of functional nervous disease of mod-
erate severity, when for any reason the rest cure is not
undertaken, the patients recover while taking cold douches,
without their ordinary mode of life being seriously inter-
fered with. For the successful operation of this form of
treatment two conditions must be scrupulously fulfilled.
These relate to temperature and pressure. The tempera-
ture of the water must be accurately regulated by means of

4IO

TREATMENT OF THE TRAUMATIC NEUROSES.

the thermometer, in order that the patient may not receive
too great a shock from the water being too cold, or that he
may not fail to react quickly, as often occurs when the water
is too warm. The force with which the douche is deliv-
ered determines the degree of mechanical irritation, which
is nearly as important a factor as temperature. A douche,
even when of proper temperature, which comes to the pa-
tient with only a few pounds of pressure behind it, is fol-
lowed by a prompt reaction in robust persons only ; in an
aneemic and exhausted individual it is a long time after the
contraction caused by the cold before the capillaries dilate
again ; the desired result of a quick alternation of vas-
cular tone is consequently not obtained. As these condi-
tions are difficult of fulfillment in private houses, it is desir-
able for the patient to receive this treatment in institutions
in which the requirements as to pressure and temperature
can be obtained and the physician's directions can be car-
ried out by skilled attendants. The treatment should be
taken every day, or at least every other day. The ordinary
method in hydriatric establishments is for the patient to be
placed for two to three minutes in a chamber filled with hot
air (130° to 150°). On emerging he immediately gets under
a rain bath of sixty to seventy degrees of temperature and
of thirty to seventy pounds of pressure. The degree of tem-
perature and the amount of pressure will vary according to
the amount of stimulation necessary for the individual case.
The colder the water, and the greater the force with which
it strikes the body, the more pronounced is the effect. The
water is turned off at the end of one or at most two min-
utes ; the patient is then quickly dried by towels and by
rubbing. It is best to send him at once into the open air,
unless he be very feeble, in order to take advantage of the
deepened inspirations which follow the douche. As the
general or rain douche is often too severe at the beginning
of treatment, a way may be paved for it by using for a week

HYDRIATRICS.

411

or two the spinal fan douche, in which the back of the pa-
tient is played upon by water coming from a hose fitted with
a quarter-inch nozzle, the stream being scattered into the
shape of a fan by placing a finger upon the nozzle. The re-
quirements as to temperature, pressure, and duration of the
rain douche and the spinal douche are the same. Although
the spinal douche is local in application, its effects are gen-
eral. When applied to other circumscribed areas, this form
of treatment may be followed by improvement in local symp-
toms. It often acts well in the isolated physical manifesta-
tions of hysteria. Under the local cold douche of twenty
to thirty-five pounds pressure the anaesthesia, paralysis, or
contracture, when of functional origin, often disappears.
Local and general douches may be alternated.

It is so frequently impossible for patients needing water
treatment to have access to properly equipped hydriatric in-
stitutions, that it is often necessary for them to get along
with such facilities as the ordinary dwelling house supplies.
This is only feasible, however, when the nervous disease has
not reached a high degree of development. When the pa-
tient is very anasmic or very much exhausted he is liable
to receive more harm than good from measures which can
not be accurately regulated and whose effects can not be
carefully observed. The cold sheet, the foot bath, and
packs are, of course, given as well at home as anywhere,
provided the nurse is intelligent and skillful. The douche,
however, is rarely practicable in private dwellings, as neither
its temperature nor its force can be properly controlled.
Still, when the patient is reasonably robust, certain substi-
tutes for it are possible. These are the ordinary cold shower
bath, provided it is delivered with considerable force; or
the full cold bath, which may begin with the water at eighty
degrees, a temperature which is gradually lowered ; or, if
the patients react well, the alternate sponging of the nape
of the neck and spine with hot (110°) and cold (65°) water.

412 TREATMENT OF THE TRAUMATIC NEUROSES.

The local douches can not be satisfactorily carried out at
home.

Hypnotism. — If hypnotism is understood to include
every variety of suggestion by which the mind can be in-
fluenced, it is a procedure which will never be eliminated
from the practice of medicine. The effect of mental prompt-
ing is evident in all social intercourse, and the peculiar re-
lations existing between physician and patient necessarily
render it an agent of great power. A medical man is sup-
posed to be acquainted with the solutions of all the prob-
lems of physiology, and the patient is as ready to believe
what the physician says as he is to trust to his own sensa-
tions. On the one hand is a person whose judgment, will,
and self-control have been weakened by illness ; on the other
is a man with unimpaired faculties, conversant with human
nature, and presumably conversant with the character of the
symptoms of which the sufferer complains. Nothing could
be more natural under such circumstances than that the
mental actions of the patient be to a certain extent directed
and controlled by those of the more vigorous personality.
In general diseases, in which the brain is apparently unaf-
fected, the influence of mind upon body is too far reaching
to permit of neglect ; and in the functional disorders of the
nervous system, whose symptoms are in large part mental,
the patient is so susceptible to the appeals to the emotions
and to the suggestions or counter-suggestions of certain
trains of thought, that the physician who neglects these
methods can hardly hope to be successful in his treatment.
Contrasted with this form of suggestion, which every phy-
sician uses almost unconsciously, is that which is made dur-
ing the condition of induced sleep.

By the term hypnosis is usually understood the peculiar
psychical condition brought about by various means, during
which the patient's higher consciousness is in abeyance. In
the hypnotic state the subject may be made to do things of

HYPNOTISM. 41^

which on awakening he has no recollection ; also sugges-
tions made during this state may be subsequently acted
upon independently of his volition. It is largely by means
of hypnosis that the falsity of hysterical symptoms has been
shown.

As a therapeutic measure it has been generally aban-
doned by the school of the Salp^trifere. It is still used in
Germany, but its special European exponents are Bernheim,
of Nancy ; Forel, of Zurich ; and Wetterstrand, of Stock-
holm. In America it has never attained popularity among
the members of the medical profession, partly because few
American physicians have had the opportunity of systemat-
ically studying its modus operandi and its effects, and partly
because in this country it has never been freed from the
reputation of quackery. Whatever may be its efi&cacy
among the ignorant peasantry of Europe, in this country,
whose people are matter-of-fact and comparatively free from
superstition, the therapeutic uses of hypnotism are very re-
stricted. It has no part in the treatment of neurasthenia,
and in hysteria it can only cause a disappearance of the
individual manifestations, without benefiting the funda-
mental conditions from which the morbid mental states
arise. Even did we not accept the theory of Charcot, that
hypnotism is only possible in the victims of hysteria, the
ease with which hysterical persons, who have once been
hypnotized by an operator, can again be brought under this
influence, and the readiness with which auto-hypnosis comes
to take an important place among hysterical manifestations,
are sufficient evidences that in la grande n^vrose the reaction
to suggesting influences occurs more readily and is accom-
panied by more permanent effects than in normal individu-
als. When the physician succeeds by means of hypnosis in
causing a disappearance of any of the physical manifesta-
tions of hysteria, he does so by bringing about an alterna-
tion of personality, during which the subconscious self of

414 TREATMENT OF THE TRAUMATIC NEUROSES.

the patient receives and reacts to impressions which would
not affect the conscious self ; but since the nature of hyste-
ria can best be explained by assuming that the physical
manifestations are dependent upon alternations of person-
ality and upon subconscious mental states, it would seem to
be an unavoidable conclusion that by contributing addi-
tional phases to the underlying morbid psychical conditions
the whole disorder would be rendered worse, even though
the temporary physical manifestations are made to disap-
pear. Consequently hypnotism is to be resorted to only
when other therapeutic means have proved useless. When
the patients have failed to receive benefit from the rest cure,
or from hydriatric measures, or from other forms of treat-
ment, hypnotic suggestion is not only permissible, but re-
mains as the one therapeutic measure from which benefit
may be hoped for. However, as Gilles de la Tourette says,
" Hypnotism is a potent modifier of hysterical strata and
may be dangerous even in skilled hands. It should only be
used when the dangers incurred are less serious than the
symptoms which it is intended to cure."

Drugs. — The use of drugs in the treatment of the neu-
roses is subsidiary to the application of some or all of the
procedures which have been described. The patients are,
however, more contented if they are taking some medicine,
and there are a few drugs which unquestionably render ma-
terial assistance in the treatment of these conditions. To
combat anaemia and for purposes of general nutrition, some
form of iron or arsenic is generally useful. When the gas-
tric irritability is pronounced, these tonics may be adminis-
tered in the form of some of the natural waters, such as
Levico, which contain proportionately large amounts of
these minerals. The most popular nerve tonic is strychnine.
It may be given by mouth in the form of the sulphate,
gr. ^jf to ■^, three times a day after meals, or hypodermatic-
ally, as the nitrate, gr. -^. Strychnine is to be especially

DRUGS. 415

recommended when the clinical manifestations indicate de-
pression, rather than irritability, of the nerve centers. A new
drug, which in many cases yields very satisfactory results, is
the glycero-phosphate of soda. It may be prescribed in
three- or five-grain capsules (Chapoteau), or according to the
following formula:

]^ Glycero-phosphate of soda (Schering) . . 3 vj ;

Distilled water 5 viij.

M. Sig. : One teaspoonful in hot water, three times a day,
half an hour after meals.

The bromides may do a great deal of harm in neuras-
thenia, and their indiscriminate use is to be deprecated. In
small doses they are often efficacious in allaying extreme
nervous excitability, especially when exhibited in conjunc-
tion with ergot. They may also be recommended for the
relief of dizziness and headache. The following prescription
has proved useful in the hands of the writer :

T^ Sodii bromid 3 vj ;

Ext. ergot, fl § j ;

Aq. destil q. s. ad § iv.

M. Sig. : One teaspoonful in hot water half an hour after
meals.

Insomnia can usually be allayed by some of the hydro-
therapeutic measures. When they fail to induce sleep, re-
course may be had to small doses of the bromides, or sul-
phonal, or trional, of which the latter is the most efficient
and least harmful. Morphine has no place in the treatment
of the traumatic neuroses.

For constipation much can be done by massage, although
drugs are often necessary. A teaspoonful of magnesium
sulphate in a full glass of cold water, taken on rising in the
morning, is in many cases sufficient to insure one or two
movements daily. If constipation is rebellious, more active
measures are necessary. When possible, the natural aperi-
ent waters, such as Hunyadi or Francis Joseph, are pref-

4l6 TREATMENT OF THE TRAUMATIC NEUROSES.

erable to other laxatives. The fluid extract of cascara,
gtt. X to XXX once or twice a day, or at bedtime, gtt. xlv,
is often serviceable. When these measures fail, recourse
must be had to the more energetic laxatives or purgatives,
which need not be enumerated. If they are given every
night, it is advisable to have a variety, so that, by taking a
different one each night in the week, the patient does not
come to rely too much on any one of them.

Whatever drugs are used, they should be given for defi-
nite purposes, and should be taken according to implicit
directions. Neurasthenic patients are especially fond of
dosing themselves on the appearance of every new symptom,
and of accepting as genuine, and as applicable to their cases,
the cures effected under this or that specific as recorded in
the advertising columns of the newspapers. To combat this
tendency the patient should be told the nature and the dose
of the drugs he is to take, and when he is to take them ; and
he should be particularly cautioned against taking anything
in the way of medicines without the physician's orders.

Such are the most important of the measures at our dis-
posal for the treatment of the traumatic neuroses. Varying
conditions may occasionally demand additional methods. If
the suffering from lumbago is intense, it may be relieved by
the application of a plaster jacket. It is rarely necessary to
continue the immobilization for more than a week or ten
days. At its termination the muscles of the back should be
actively mass6d. The cautery is often used in this condi-
tion, since it alleviates the pain, but it renders the back
sensitive and postpones the possibility of massage. Except
in so far as it supplies exercise for the muscles, faradism is
of but little service. The indefinite pains are best allayed
by rest and by the general tonic treatment. If true neural-
gia exists, it may be improved by hot fomentations, by
some of the analgesics, by the application of galvanism.

EXERCISE.

417

or, better, by ten-minute daily stances with the sinusoidal
current. Also the vibrator, as devised by Peterson, is use-
ful in some cases.

Passive movements are the most rational means for caus-
ing the disappearance of hysterical paralyses and contracture.
By causing movement in limbs which are apparently para-
lyzed, the patient sees that they are movable, and gradually
comes, when sufficiently encouraged, to move them himself.
In hysterical paralysis of the leg the power of walking may
often be speedily restored by having the patient push a
chair in front of him, or by means of a " roller machine."
By distracting the patient's attention, motion can usually be
obtained in hysterical contractures, and gentle and persistent
passive movements are the most efficacious means of treating
this condition. By massage, also, sensibility may be made
to return to skin which was the seat of hysterical aneesthesia.
These means, the beneficial results of which are often per-
manent, are much to be preferred to those, such as the fara-
dic brush or the horseshoe magnet, which depend for their
action upon fright, or upon utilizing the credulity of the
patient. Some general exercise should be insisted upon as
soon as the patient is able to undertake it. During the
rest cure, as soon as complete rest is abandoned, the patient
should be made to perform light exercises, such as opening
and closing the hands, or flexing and extending the elbows
and wrists, as a part of the daily schedule. Similarly, he
should make use of the legs, practising getting up on and
down from a chair, and walking prescribed distances around
the room at regular times. For the rest-cure patient, as he
gets better, and for all neurasthenic and hysterical patients
who do not go to bed, the exercise may include light gym-
nastics and short walks or drives, but may be gradually ex-
tended until it includes some of the moderate athletic sports
for which the facilities are now becoming so generally ac-
cessible.

4i8 TREATMENT OF THE TRAUMATIC NEUROSES.

Change of climate, involving as it does diversion of
thought and modification of home habits, is almost always
beneficial. As a general rule, the seashore is particularly
adapted for the irritable forms of disease, while patients who
are depressed and apathetic do best in high altitudes, such
as may be found in Colorado or in the elevated regions of
soutliern California.

Bibliography.

Baruch, Hydrotherapy. Hare's System of Therapeutics, Phila-
delphia, 1891.

Bernheim, Suggestive Therapeutics. Translated by Herter,
New York, 1889.

Forel, Der Hypnotismus. Stuttgart, 1889.

Mitchell, Fat and Blood. Philadelphia, 1891.

Peterson, Vibratory Therapeutics. Med. News, November,
1897.

Wetterstrand, Hypnotism. Translated by Petersen, New York
and London, 1897.

Winternitz, Vortrage uber Hydrotherapie.

INDEX OF NAMES.

Abercrombie, 187.

Babinski, 323.

Bailey, 95, 323. 392.

Ballet and Dutil, 166.

Bannister, 140.

Baruch, 406.

Bass, 269.

Beard, 227.

Bechholm, 149.

Berbez, 275, 279, 309.

Bernhardt, 108, 163.

Bernhardt and Kronthal, 336.

Bernheiin, 271, 413.

Bikeles, 88.

Binswanger, 140, 254, 256.

Blocq, 300.

Booth, 223.

Bremer, 301, 357.

Briquet, 272, 280.

Brissaud, 273.

Brodie, 272, 312.

Bruns, 198.

BuUard, 172.

Carara, 122.

Charcot, 62, 182, 2io, 252, i'jo et seq.

Charcot, J. B., 165.

Christian, 141.

Clarke, 170, 189.

Clevenger, 197.

Comby, 317

Craig, 163.

Crocq, 199. 325'

Dana, 2g, 194, 199, 208, 275, 325, 326;

358.
Duchenne, 164.

Eisenlohr, 171, 198.
Erb, 115, 157, 159, 191.
Erichsen, 3.

Fischer, 87.
Forel, 413.
Forster, 221, 255.
Foumier, 140.
Fox, 149.
Francotte, 318.
Friedreich, 170.

Godkin, 341, 358.
Cowers, 87, 157, 181.
Graefe, von, 221.
Gray, 130.
Gudden, 140, 141.
Guinon, 323.

Hamilton, 138.
Head, 90.
Heller, 392.
Hirsch, 166.
Hirschl, 140, 141.
Hitzig, 163.
Hodge, 233.
Hodges, 191.
Hoedemaker, 115.
Hoffman, 357.
Howell and Huber, 118

419

420

INDEX OF NAMES.

Hughes, 211.
Huisman, 124.
Hun, 288.

Interstate Commerce Commission, 204.

Jacobson, 150.
Janet, 286, 298.
Jendrassik, 40.
Judd, 358.

Klumpke, 116.

Knapp, igg, 209, 240, 259, 267, 275, 279,

126. 367. 387, 388.
Kocher, 90.
Koenig, 221, 323.
KrafFt-Ebing, 142.
Krauss, 38.

Laehr, 124, 323.

Lambret, 76.

Laudun, 290.

Lebran, 303.

Le Grande du SauUe, 137,

Lepois, 272.

Levier, 78.

Leyden, 89.

Litten, 106.

Lloyd and Deaver, 129.

Lugaro, 233.

Mann, 172.

Mannkopff, 219.

Mason, 130.

Mendell and Schnell, 140.

Mendenhall, 7.

Meyer, 142.

Mickle, 147, 148.

Minor, 80.

Mitchell, J. K., 118.

Mitchell, S. W., 118, 394.

Miura, 303.

Mobius, 271.

Miiller, 221.

Nammack, 266.
Nonne, 329, 330,

Oebeke, 140.
Ollivier, 187.
Oppenheim, 195, 196, 259, 262, 326, 333,

334, 337-
Outten, 199.

Page, 192, 198, 230, 262, 321, 358, 366.

Paget, 272.

Parkin, 78.

Peters, 22i.

Peterson, 11, 140, 294, 418.

Pettit, 148.

Pfeiffer, 96.

Pitres, 313, 318, 379.

Poncet, 170.

Porcher, 210.

Prentice, 341, 343, 352-

Prince, 162, 299, 322, 352.

Putnam, 194, 358.

Quain, iii.

Raymond, 170.
Regis, 140, 239.
Reynolds, 273.
Richer, 309, 314.
Richter, 265.
Riegler, 191, 357.
Rumpf, 219.

Saenger, 15, 199, 264, 337.
Schlager, 141.
Schmaus, 87.
Schmidt-Rimpler, 393.
Schultze, 198, 358.
Schutte, 311.
Schweigger, 24.
Seeligmiiller, 358.
Seguin, 558.
Serieux, 306.
Sherrington, 90.
Smith, 344.
Soukanoif, 159.
Souques, 305.

Sperling and Kronthal, 336.
Starr, go, 129, 132.
Storbeck, 157.

INDEX OF NAMES.

421

Strauss, 220.
Stroebe, 118.
Strumpell, 20, 123, ig5, 199 201, 222,

273-
Sydenham, 272.

Thomsen and Oppenheim, 194.

Thorburn, 77, go.

Tourette, Gilles de la, ig8, 305, 414.

Unverricht, 124.

Van Deventer, 149.

Vandier, 185.

Van Gehuchten, 53.

Van Gieson, 78, 127.
Vibert, 89, 228.

Waldeyer, 54.
Walton, 194, 203, 358.
Walz, 184.
Watson, 8g.
Westphal, igi.
Westphal, A., 86.
Wetterstrand, 413.
Wilbrand and Sanger, 255.
Willard and Spiller, 86.
Winternitz, 406.

Zein, 322.
Ziehen, 140, 172.

INDEX OF SUBJECTS.

Abscess, cerebral, 120.
Aboulia, hysterical, 2go.
Accident cases, fraud in, 347.

frequency of, 341.
Accident, history of, 7.
Acromegaly, traumatic, origin of, 124.
Alcoholism, predisponent to nervous dis-
ease, 13.

symptoms of, 14.
Amaurosis, hysterical, 296.
Amblyopia, hysterical, 296.
Amnesia in hysteria, 289.
Amyosthenia, 301.
Amyotrophic lateral sclerosis, 164.
Anaesthesia, examination for, 35.

generalized, 218.

glove, 293.

in brain injuries, 60.

in hysteria, 291.

in locomotor ataxia, 155.

in peripheral nerve injuries, 100.

in spinal-cord injuries, 90.

in traumatic neuroses, 218.

in the unclassified forms, 335.
Anaesthesia, general, 294.
Anaesthesia, total, 293.

morphological, 293.

segmental, 293.

simulation of, 378.

stocking, 293.
Analgesia, in hysteria, 292.

in spinal-cord injuries, 80.

in simulation, 378.

tests for, 36.
Angina pectoris, 258.

Ankle clonus, 41,

in hysteria, 314.

in neurasthenia, 257.

in the traumatic neuroses, 222.

in the unclassified forms, 332.

in spinal-cord injuries, 90.
Anuria, hysterical, 318.
Aphasia, 52.

Aphonia, hysterical, 318.
Apoplexy and head injuries, 66.

hysterical, 317.
Argyll-Robertson pupil, 23.

in general paresis, 138.

in locomotor ataxia, 154.
Arterio-sclerosis. as a predisponent to
nervous disease, 16.

pathological significance of, 336.

symptoms of, 17.
Astasia-abasia, 300.
Asthenopia in neurasthenia, 254.
Ataxia, in hysteria, 307.

locomotor, 151.

tests for, 36.
Athetosis, 31.
Atrophy, myopathic, 164.

of optic nerve, 160, 334.

progressive muscular, 164.
Auditory nerve, injury to, 59.
Aura, in epilepsy and hysteria, 316.
Auto-suggestion, 288.

Back, injuries to the, 244.

Back muscles, spasm of, in hysteria, 311.-

spasm of, in traumatic lumbago, 248.
Barometer of hysteria, 298.

422

INDEX OF SUBJECTS.

423

Base of Ijrain, lesions at, 57.
Biceps jerk, 37.

Blepharospasm, hysterical, 310.
Boite de Flees, 386.
Bone conduction, significance of, 26.
Brachial-plexus palsy, lower arm type of,
n6.

upper arm type of, 115.
Brain, abscess of, 120.

centers of, 51.

concussion of, 66.

injuries to, 46.

railway, 186.
Brown-Sequard paralysis, 80.
Bulbar palsy, 171.

Capsule, lesions of internal, 57.
Casque neurasthenique, 252.
Catalepsy, 2go.
Cerebellum, injury of, 60.
Cerebro-spinal axis, 52.
Cervical plexus, injury to, 106.
Charcot joints, 153.
Chorea, electric, 311.
Circumflex nerve, injury to, 107.
Clavus hystericus, 296.
Claw hand. (See Main en griffe.)
Coggin's stethoscope test, 388.
Coma, 48.

hysterical, 316.
Combined palsies of the upper extremity,

114.
Concussion of the brain, 66, 186.

of the spinal cord, 84, 186.
Consciousness, limitation of, 286.
Contracture, hysterical, 308.
Convulsive attacks, differential diagno-
sis of, 315.

in epilepsy, 131.

in hysteria, 315.

simulation of, 388.
Corporeal shock, 48.
Cortical lesions, 56.
Coxalgia, hysterical, 313.
Cranial nerves, examination of, 52.

intracranial lesions of, 57.
Creeping palsy, 164.
Cutaneous reflexes, 37.

Deaf-mutism, hysterical, 318.
Deafness, simulated, 388.
Death in hysteria, 318.
Degeneration, reaction of, 44.

stigmata of, 12.
Delirium, in head injuries, 49.

tremens, 15.
Delusions, of grandeur, 145.

in alcoholism, 15.
Dementia after cerebral lesions, 119.

epileptic, 134.

in the unclassifled forms, 327.

paralytica, 137.
Diarrhoea, nervous, 260.
Diplopia, 23.
Douche, the, 409.
Drip sheet, 407.
Dubini's disease, 311.
Dynamometer, 29.
Dysarthria, 22.

Electric currents as causes of nervous

disease, 207.
Electrical chorea, 311.
Electrical examination, 42.
Epileptic equivalents, 132.

headache, 132.

impulsions, 133.
Epilepsy, traumatic, 126.

aetiology of, 127.

bibliography of, 136.

course of, 134.

diagnosis of, 134.

frequency of, 126.

idiopathic, 126.

Jacksonian, 126.

pathology of, 127.

predisposition to, 127, 128.

symptoms and variations of, 131, 132.
Erb's palsy, 115.

points, 43.
Erichsen's disease, 197.

theory of concussion, 189.

views on spinal injuries, 187.
Exaggeration of symptoms in hysteria,
285.

in malingering, 347.

in neurasthenia, 241, 265.

424

INDEX OF SUBJECTS.

Examination of the patient, plan of, 20.
Eyes, examination of, 22.

Face, spasm of, 311.

Facial nerve, extra-cranial injury of, 103.

intra-cranial injury of, 58.
Facial spasm in hysteria, 311.
Fears in neurasthenia, 239.
Fibrillation, 31.
Field of vision, examination of, 24.

in hysteria, 297.

in locomotor ataxia, 160.

in neurasthenia, 254.

in malingering, 387.

in the traumatic neuroses, 220.

in the unclassified forms, 334.

significance of, limitation of, 25.
Fifth nerve, injury of, 58.
Foot bath, 409.

clonus, 41.
Fourth nerve, injury of, 5S.
Fractures of the skull, 64.

of the vertebrae, 72.
Freeman family, histoiy of, 359.
Frontal lobes, injury to, 52.
Functional disease, definition of, 4.

effects of injury, 186.

Gait, ataxic, 82.

equine, 33.

hemiplegic, 33.

in hysterical paralysis, 302.

in neurasthenia, 243.

in paralysis agitans, 179.

in traumatic lumbago, 249.

in unclassified forms, 329.

of motor paralysis, 32.

spastic, 33.

types of in nervous disease, 32.
General paralysis of the insane, 137.
General paresis, aetiology of, 139.

and syphilis, 139.

bibliography of, 150.

medico-legal periods of, 137.
, percentage of " traumatic " cases, 141.

prodromal stage, 137.

proof of traumatic origin, 146.
Globus hystericus, 318.

Glosso-labio laryngeal paralysis, 171.
Glycosuria, 222.

Haematomyelia and syringomyelia, 79.

disseminated, 82.

with injuiy to spinal column, 74.

without injury to spinal column, 77.
Hsematemesis, 222.
Hsematomyelopore, 78.
Hsematorrhachis, with injury to spinal
column, 73.

without injury to spinal column, 76.
Haemoptysis, 222.
Hallucinations, after head injuries, 49.

hysterical, 288.

in alcoholisni, 15.
Hearing, centers of, 52.

disturbances of, in brain injuries, 59.
in facial palsy, 104.
in hysteria, 299.
in malingering, 388.
in neurasthenia, 256.
in the unclassified forms, 335.
Heart, palpitation of, in neurasthenia,

258.
Hemianesthesia, hysterical, 293.

in brain injuries, 61.

symptomatic significance of, 62.
Hemianopsia, in brain injuries, 52, 57.
Hemiplegia, gait of, 33.

in hysteria, 302.

in injuries to the brain, 57.

in injuries to the spinal cord, 80.

in paralysis agitans, 179.
Haemorrhage, of the brain, 63.

of the spinal cord, 73, 76.
Heredity and nervous disease, 6, 11.
Hydriatrics, 405.
Hydriatric institutions, 406.
Hypnotism and hysteria, 271.

in treatment of traumatic neuroses, 412.
Hypochondriasis and neurasthenia, 235.
Hypoglossal nerve, injury to, 105.
Hysteria, aetiology of, 274.

aboulia in, 290.

amnesia in, 289.

amyosthenia in, 301.

anaesthesia in, 291.

INDEX OF SUBJECTS.

425

Hysteria, ataxia in, 307.

attacks in, 315.

barometer of, 298.

bibliography of, 321.

blepharospasm in, 310.

coma in, 316.

condition of sphincters in, 315.

contracture in, 308.

cough in, 318.

hallucinations in, 288.

hearing in, 299.

hiccough in, 318.

hemiplegia in, 302.

hyperaesthesia in, 295.

joint affections in, 312.

major, 270.

mental symptoms in, 283.

minor, 270.

monoplegia in, 303.

motor symptoms in, 300.

paraplegia in, 305.

paralysis in, 300.

pathology of, 280.

•' period of meditation " in, 300.

polyplegia in, 306.

prognosis of, 318.

reflexes in, 314.

respiration in, 318.

smell in, 299.

special senses in, 296.

symptoms of, 280.

taste in, 299.

traumatic, 270.

tremors in, 311.

vision in, 296.
Hystero-epilepsy, 315.
Hystero^enetic zones, 295.
Hystero-neurasthenia, 186.

Injuries to the back, 244.
Injuries, to the brain, 46.

focal symptoms of, 49.

general symptoms of, 47.

in the cerebellum, 60.

in the cortex, 56.

in the internal capsule, 57.

in the pons, 57.

in the tracts, 56.

Injuries, to the brain, mental symptoms
of, 48.

motor symptoms of, 52.

prognosis of, 120.

reflexes in, 62.

sensory symptoms in, 60.

speech disturbances in, 51.

sphincters in, 63.

varieties of, 63.
Injuries to the peripheral nerves, 97.

aetiology of, 98.

bibliography of, 118.

symptoms of, 98.

prognosis of, 102.
Injuries to nerves, 43.
Injuries to the spinal cord, aetiology of, 70.

bibliography of, 95.

causes of, 70.

classification of, 71.

prognosis of, 121.

symptoms of, 90.
Injury, examination for, 18.

functional effects of, 186.

history of, 7.

immediate organic effects of, 46.

ultimate organic effects of, 119.
Internal capsule, lesions of, 57.
Introduction, i.
Isolation, 397.

Jacksonian epilepsy, 126.
Jendrassik method of re-enforcing knee-
jerk, 40.
Joints, hysterical, 312.

Klumpke's palsy, 116.
Knee-jerk (see also Tendon Reflexes),
38.

Lead palsy, differential diagnosis of, 167.
Lightning, cause of nervous disease,

210.
Litigation and hysteria, 279.

and neurasthenia, 267.

and the traumatic neuroses, 214.

frequency of, in accident cases, 341.
Localization, cerebral, 49.
Local spasms in hysteria, 310.

426

INDEX OF SUBJECTS.

Locomotor ataxia, 151.

setiology of, 157.

and syphilis, 157.

bibliography of, 163.

pre-ataxic period of, 157.

proof necessary for traumatic origin of,
162.

trauma as a cause of, 158.
Lumbago, traumatic, 244.
Lumbar plexus, palsy of, 117.

Main en griffe, in ulnar nerve palsy,
log.

in progressive muscular atrophy, 174.
Magnetic currents, physiological effects

of, 295.
Malingering, 341.

bibliography of, 392.

inducement to, 343.

varieties of, 347.
Mania after head injuries, 120.
Mannkopff test, 219.

in hysteria, 295.

in simulation, 384.

in traumatic lumbago, 248.
Massage, 399.

Median nerve, injury to, 107.
Medulla, injury to, 60.
Melancholia after head injuries, 120.
Memory after accidents, 21.
Mental state, examination of, 21.
Meteorological disturbances as causes of

nervous disease, 210.
Mind blindness, 52.

deafness, 52.
Monoplegia in brain injuries, 56.

in hysteria, 303.

simulation of, 376.
Morbid movements, significance of, 31.
Motor centers of brain, 53.

points of Erb, 43.

pathway, description of, 52.
Multiple cranial nerve injuries, 59.
Multiple sclerosis, traumatic origin of,

123, 338.
Muscular sense, examination of, 36.

in cortical injuries, 56.

in hysteria, 307.

Muscular sense, in locomotor ataxia, 157.

atrophy, progressive, 164.

dystrophy, progressive, 164.
Musculo-cutaneous nerve, injury to, 107.
Musculo-spiral nerve, injury to, ill.
Mutism, hysterical, 318.
Myelitis, 68.

Neck muscles, hysterical spasm of, 311.
Nerves, cranial, 52, 57.

injuries to, 97.
Nervous exhaustion, 226.

prostration, 226.

shock, 48.
Neuralgia, traumatic, 100.

treatment of, 416.
Neurasthenia, traumatic, 226.

aetiology of, 227.

auditory apparatus in, 256.

bibliography of, 269.

digestive disturbances of, 260.

insanity from, 265.

mental symptoms of, 235.

motor symptoms of, 242.

ocular symptoms of, 254.

prognosis of, 261.

reflexes in, 256.

sensory symptoms of, 244.

smell in, 256.

symptoms of, 234.

taste in, 256.

treatment of, 394.

vascular disturbances of, 258.
Neuritis, ascending, no.

migrans, no.

traumatic, 97.
Neuron, description of, 53.
Neurons, central and peripheral, 54.

symptoms of injury to, 55.

Occipital lobes, injury to, 52.
Oculo-motor nerves, examination of, 23.
Olfactory nerves, injury to, 57.
Ophthalmoscope, use of, 23.
Opisthotonos, 316.

Oppenheim's traumatic neurosis, ig6.
Optic nerve, atrophy of, in tabes, 160.
atrophy of, in unclassified forms, 334.

INDEX OF SUBJECTS.

427

Optic nerve, examination of, 23.

injury of, 57.
Optic nerves, injury of, 57.
Optic neuritis in brain injuries, 57.
Optic tracts, injury to, 57.
Orbicularis palpebrarum, spasm of, 310.
Organic effects of injury to the nervous

system, 46.
Origin, substitution of, 352.

Pain and hypersesthesia, simulation of,

383-
Painful points in hysteria, 295.

in neurasthenia, 244.

in traumatic lumbago, 247.
Pain sensibility,' examination of, 36.
Palsy (see also Paralysis).

bulbar, 171.

Bell's, 103.

creeping, 164.

facial, 103.

shaking, 178.
Pareesthesia in neurasthenia, 253.
Paralysis " as a fine art," 359.

bulbar, 171.

examination for, 27.

general, 137.

in brain injuries, 52.

in hysteria, 306.

in peripheral-nerve injuries, gg.

in spinal-cord injuries, go.

in the unclassified forms, 331.

simulated, 373.

types of, 55.
Paralysis agitans, 178.

aetiology of, 180.

anatomy of, 178.

bibliography of, 185.

course of, 180.

symptoms of, 178.

trauma as cause of, 182.
Paramyoclonus multiplex, 311.
Paraplegia, hysterical, 305.

in spinal-cord injuries, go.

simulated, 375.
Parkinson's disease, 178.
Patient, examination of, 6.

general appearance of, 20.

Patient, previous history of, 6.
Perimeter, use of, 24.
" Period of meditation," 300.
Peripheral nerves, injuries to, g7.
Petit mal, 132.
Physical shock, 48.
Plessimeter, 38.
Polyopia, 2gg.
Pontine lesions, 57.

Posterior thoracic nerve, injury to, 106.
Predisposition to nervous disease in epi-
lepsy, 127.

in general paresis, I3g.

in hysteria, 274.

in locomotor ataxia, 157.

in neurasthenia, 228.

in paralysis agitans, 178.

in progressive muscular atrophy, 166.

in the traumatic neuroses, 211.

physical evidences of, II.
Progressive muscular atrophy, 164.

aetiology of, 166.

anatomy of, 164.

bibliography of, 177.

course of, 166.

illustrative cases of, l6g.

symptoms of, 165.

trauma as a cause of, 167.
Psychoses after head injuries, 120.
Ptosis, 58.

apparent in hysteria, 310.
Pupil, Argyll-Robertson, 23.

examination of, 22.
in epilepsy, 316.

state of, in general paresis, 138.
I in hysteria, 296.

in locomotor ataxia, 154.
in neurasthenia, 254.

Railway accidents, U. S. statistics of, 204.

as causes of nervous disease, 204.
Railway injuries, statistics concerning, 8.
Railway spine, 186.

brain, 186.
Reaction of degeneration, 44.
Reflex, abdominal, 37.

cilio-spinal, 37.

cremaster, 37. '

428

INDEX OF SUBJECTS.

Reflex, patella, 38.

plantar, 37.
Reflexes (see also Tendon Reflexes).

superficial, 37.

deep, 38.

tendon, 38.

pupillary, 22.

examination of, 37.

pharyngeal, 37.
Rest cure, The, 395.
Rigidity, significance of, 3a
Rohrenbildung, 78.
Romberg symptom, 34.

in locomotor ataxia, 154
Rhythmical chorea, 311.

Sacral plexus, palsy of, 117.

Saturday-night paralysis, 99.

Scoliosis, hysterical, 311.

Section of nerves, 103.

Seismic phenomena, as causes of nervous

disease, 210.
Sensation, examination of, 34.
Seventh nerve, extracranial injury to,
103.

intracranial injury to, 58.
Shaking palsy, 178.
" Shifting type of contraction " of visual

fields, 255.
Shock, nervous, 48.

physical, 48.
Sight, centers of, 52.
Simulation, 357.

bibliography of, 332.

detection of, 369.

difficulties of, 363.

frequency of, 357.

of anjesthesia, 378.

of convulsive attacks, 38B.

of deafness, 388.

of individual symptoms, 373.

of ocular symptoms, 384.

of pain and hyperassthesia, 383.

of paralysis, 373.

of reflexes, 391.

of tremor, 377.

of vascular disturbances, 389,
Sixth nerve, injury of, 58.

Slowed conduction, 36.
Smell, examination of, 22.
Somnambulism, 133, 290.
Spasmodic twitchings, 31.
Speculation in damage claims, 345.
Speech, centers of, 52.

disturbances of, in brain injuries, 51.
in general paresis, 138.
in hysteria, 318.
in neurasthenia, 240.
in the unclassified forms, 331.
Sphincters, condition of, in brain injuries,
63.

in hysteria, 315.

in simulation, 390.

in spinal-cord injuries,' 90.

in traumatic lumbago, 250.
Spinal anaemia, 186.
Spinal cord, injuries to, 68.

protection of, 6g.

concussion of, 84.

commotion of, 84.
Spine, concussion of, 186.

injury to, 244.

railway, 186.
Sponge bath, 407.
Spinal irritation, 186, 194.
Stepping gait, 34.
Stigmata of degeneration, 12.

of hysteria, 280.
Stupor, 48.

Subconsciousness, 286.
Substitution of origin, 352.

in the chronic degenerative diseases,
354-

in the traumatic neuroses, 356.
Suggestibility in hysteria, 287.
Suicide in neurasthenia, 238.

in the unclassified forms, 339.
Syphilis as a predisponent to nervous
disease, 15.

and tabes, 157.

and general paresis, 139.
Syringomyelia, and hasmatomyelia, 79.

traumatic origin of, 124.

Tabes dorsalis, 151.
Tachycardia, significance of, 217.

INDEX OF SUBJECTS.

429.

Tachycardia, in alcoholism, 14.

in malingering, 389.

in neurasthenia, 258.
Taste, examination of, 26.
Temperature sense, examination of, 36.
Temporal lobes, injury to, 52.
Tendon reflexes, diagnostic value of, 38,
222.

examination of, 38.

in brain injuries, 62.

in general paresis, 138.

in hysteria, 315.

in locomotor ataxia, 154.

in malingering, 391.

in neurasthenia, 257.

in peripheral-nerve injuries, loi,

in spinal-cord injuries, 90.

in the traumatic neuroses, 222.

in the unclassified forms, 232.

in traumatic lumbago, 250.
Thermo-ansesthesia in hysteria, 292.

in spinal-cord injuries, 80.

in simulation, 380.

tests for, 36.
Third nerve, injury of, 57.
Tongue, hysterical spasm of, 311.
Torticollis, hysterical, 311.
Touch, examination of, 36.
Tract, lesions of brain, 56.
Tracts, cerebro-spinal, of motion, 53,
Traumatic, definition of, I.
Traumatic hysteria, 270.
Traumatic lumbago, 244.

duration of, 251.

Mannkopff' test in, 248.

symptoms of, 246.
Traumatic neurasthenia, 226.
Traumatic neuroses, 186.

aetiology of, 203.

anaesthesia in, 218.

bibliography of, 223.

cardiac symptoms in, 217.

classification of, 201.

electricity as a cause of, 207.

glycosuria in, 222.

history of, 186.

lightning as a cause of, 210.

litigation as a causal factor, 215,

Traumatic neuroses, meteorological dis-
turbances as a cause of, 210.

nomenclature of, 200.

occupation as a causal factor, 212.

pain and hypersesthesia in, 219.

pathology of, 202.

physical condition as a causal factor,
213.

predisposition as a causal factor, 211.

suggestion by physicians as a causal
factor, 213.

symptoms of, 215.

tendon reflexes in, 222.

treatment of, 394.

unclassified forms of, 325.

visual disturbances in, 220.

vomiting in, 222.
The traumatic neurosis, 186, 196.
Traumatic suggestion, 273, 300.
Treatment of traumatic neuroses, 394.

bibliography of, 418.

climate in, 418.

diet in, 400.

drugs in, 414.

electricity in, 400.

exercise in, 417.

general management in, 402.

hydriatrics in, 405.

hypnotism in, 412.

isolation in, 397.

massage in, 399.

rest cure in, 395.

rest in bed in, 398.

vibrator in, 417.
Tremor, 31.

alcoholic, 14.

of general paresis, 138.

of multiple sclerosis, 123.

in the unclassified forms, 328.

of paralysis agitans, 178.

hysterical, 311.

neurasthenic, 243.

simulated, 377.
Triceps-jerk, 38.
Trophic disturbances, examination for,

41.
Tumors of nervous system, traumatic
origin of, 121.

430

INDEX OF SUBJECTS.

Ulnar nerve, injury to, io8.

Ultimate organic effects of injury, lig.

Unclassified forms of traumatic neuroses,

325-
aetiology of, 326.
bibliography of, 340.
deep reflexes in, 332.
diagnosis of, 237.
disturbances of motion in, 328.
general symptoms of, 335.
hearing in, 335.
mental symptoms of, 327.
optic atrophy in, 334.
pathology of, 336.
prognosis of, 337.
sensory symptoms in, 332.
special senses in, 335.

Unclassified forms of traumatic neuroses,
symptoms of, 327.
taste and smell in, 335.
vision in, 334.
Upper extremity, combined palsies of,
114.

Vascular disturbances, simulation of,

389-
Vertebrae, fractures of, 72.
Vision, examination of, 22.
Vision, field of, 25.

Wet pack, 408.
Winged scapulae, 107.
Wrist-drop, 99.
Wryneck, hysterical, 311.

THE END.

A TREATISE ON

THE DISEASES OF THE

NERVOUS SYSTEM.

By WILLIAM A. HAMMOND, M. D.,

Surgeon-General U. S. Army (retired list).

With the Collaboration of GRAEME M. HAMMOND, M, D.,

Professor of Diseases of the Mind and Nervous System in the New York
Post-Graduate Medical School and Hospital, etc.

"With 118 Illustrations.
NINTH EDITION, WITH CORRECTIONS AND ADDITIONS.

8vo. 932 pages. Cloth, $5.00 ; sheep, $6.00.

" Dr. Hammond's treatise on the diseases of the nervous system is a work which
has been long familiar to the profession, and has attained a great reputation among
the standard books for reference. In the preparation of the present edition the
author has been aided by his son. A vast amount of clinical material is made use
of, and the results of experimental investigation recorded. The book is written in
a clear and pleasing style, and obscure conditions are dealt with in a manner which
will prove of great assistance in the study of this most interesting class of diseases."
— Ga/nadian Practitioner.

" Dr. Hammond published the first edition of his ' Treatise on Diseases of the
Nervous System ' in 1871. It has therefore been before the profession for twenty
years, and during these years it has continued to grow in public favor, this being
the ninth edition that has been issued. Appreciation of this work has not only
been shown in this country, but abroad, as it has been translated into the French,
the Italian, and the Spanish languages. The present edition has been thoroughly
revised, and several new chapters added. This is a book of such great value, and is
referred to so frequently by the medical press and other medical works, that no
library is complete without it." — Alabama Medical and Surgical Age.

" There are few books, even upon those subjects which are constantly in the
ordinary physician's mind, which succeed as has that of Dr. Hammond ; and when
w^e recollect that when the first edition of this work appeared, neurology in America
was in its very infancy, the rapid exhaustion of its editions is the more remarkable.
In the ninth edition the writer's son has done much toward keeping the work abreast
of the times, and, with more confidence than ever, it can now be regarded as one of
the best and most satisfactory works on nervous diseases, either for the practitioner
or for the advanced student. The book is beautified and its usefulness increased by
a larger number of illustrations than heretofore — among the best from a medical
point of view being those representing syringo-myelia, which have been taken from
the studies of Van Giesen." — Medical Neics.

D. APPLETON AND COMPANY, NEW YORK.

THE DISEASES OF
THE NERVOUS SYSTEM.

a text-book for physicians and students.
By Dk. LUDWIG HIET,

PROFESSOR AT TEE tTNIVEESITT OP BBEBLAU.

second american edition, revised from the second german edition
By august HOCH, M. D.,

ABBISTED BY

FRANK R. SMITH, A. M. (Cantab.), M. D.,

ASSISTANT PHYSICIANS TO THE JOHNS HOPKINS HOSPITAL.

WITH AN INTRODUCTION
By WILLIAM OSLER, M. D., F. R. C. P.,

PROFKSBOR OP MEDICINE IN THE JOHNS HOPKINS XTNITEBSITT, AND PHT8ICIAN IN CHIEF TO THE
JOHNS HOPKINS HOSPITAL, BALTIMORE.

8vo, 715 pages. With 181 Illustrations.
Cloth, $5.00; sheep, $6.00.

" This work possesses many points which are sufficiently novel to justify its transla-
tion and publication in this country. The general practitioner is perhaps more in need
of reliable text-books on diseases of the nervous system than is the specialist. . . . The
volume before us admirably meets his requirements, and to a very great extent covers
those parts of the study which have not been fully presented by former writers. . . .
The work of the translators is perfect, leaving no trace of the German idioms." — Ohio
Medical Journal.

" The profession of this country stands under the greatest obligation to the trans-
lators of this standard work for having thus furnished- the opportunity of making'use of
one of the best works ever published upon the subject. As a work of reference to the
physician it has no equal. To specialists in this branch of diseases it is invaluable. As
features of especial commendation may be mentioned the author's clearness in the ana-
tomical and symptomatological arrangement of diseases." — Nashville Journal of Medicine
and Surgery.

" The translators of this volume have conferred a favor upon English-reading mem-
bers of the profession by their excellent rendering of the work of Professor Hirt. The
text is especially valuable for the clear, accurate, and well-ordered description of
pathological anatomy and symptomatology. As regards treatment, the author may be
accepted as a safe guide. . . . The typography and plates of this work are all that can
be desired." — Medical Bulletin.

D. APPLETON AND COMPANY, NEW YORK.

A New, Thoroughly Revised, and Enlarged Edition of

QUAIN'S
DICTIONARY OF MEDICINE.

BY VARIOUS WRITERS.

Edited by Sir RICHARD QUAIN, Bart, M. D., LL. D., etc.,

Physician Extraordinary to Her Majesty the Queen; Consulting Physician to the Hospital for I)isease5

of the Chest, Brompton, etc.

Assisted by FREDERICK THOMAS ROBERTS, M. D., B. Sc,

Fellow of the Royal College of Physicians, etc. ;

And J. MITCHELL BRUCE, M.A., M. D.,
FeUow of the Royal College of Physicians, etc.

With an American Appendix by SAMUEL TREAT ARMSTRONG, Ph.D., M. D.,

Visiting Physician to the Harlem, Willard Parker, and Riverside Hospitals, New York.

IN TWO VOLUMES. Sold only by subscription.

This work is primarily a Dictionary of Medicine, in which the several diseases are fully
discussed in alphabetical order. The description of each includes an account of its etiology
and anatomical characters ; its symptoms, course, duration, and termination ; its diagnosis,
prognosis, and, lastly, its treatment. General Pathology comprehends articles on the origin,
characters, and nature of disease.

General Therapeutics includes articles on the several classes of remedies, their modes of
action, and on the methods of their use. The articles devoted to the subject of Hygiene treat
of the causes and prevention of disease, of the agencies and laws affecting public health, of
the means of preserving the health of the individual, of the construction and management of
liospitals, and of the nursing of the sick.

Lastly, the diseases peculiar to women and children are discussed under their respective
-headings, both in aggregate and in detail.

The American Appendix gives more definite information regarding American Mineral
Springs, and adds one or two articles on particularly American topics, besides introducing
some recent medical terms and a few cross-references.

The British Medical yournal says of the new edition :

"The original purpose which actuated the preparation of the original edition was, to
quote the words of the preface which the editor has written for the new edition, ' a desire to
place in the hands of the practitioner, the teacher, and the student a means of ready reference
to the accumulated knowledge which we possessed of scientific and practical medicine, rapid
as was its progress, and difficult of access as were its scattered records.' The scheme of the
work was so comprehensive, the selection of writers so judicious, that this end was attained
more completely than the most sanguine expectations of the able editor and his assistants
could have anticipated. ... In preparing a new edition the fact had to be faced that never
in the history of medicine had progress been so rapid as in the last twelve years. New facts
have been ascertained, and new ways of looking at old facts have come to be recognized as
true. . . The revision which the work has undergone has been of the most thorough and
judicious character. . , . The list of new writers numbers fifty, and among them are to be
found the names of those who are leading authorities upon the subjects which have beea
committed to their care."

D. APPLETON AND COMPANY, NEW YORK.

THE

SCIENCE AND ART OF
MIDWIFEEY.

By WILLIAM THOMPSON LUSK, M. A., M. D.,

Professor of Obstetrics and Diseases of Women and Children in the Belleyue

Hospital Medical College ; Obstetric Surgeon to the Maternity

and Emergency Hospitals ; and Gynaecologist

to the Bellevue Hospital.

FOURTH EDITION. REVISED AND REWRITTEN.
With 246 Illusteations.

8vo. Cloth, $5.00 ; sheep, $6.00.

" It was the pleasure of the undersigned to write a review of this most
excellent and masterly work on obstetrics, when it appeared in its first
edition. The present is the fourth, an edition oplarged and revised. It is
a model of recent medical literature in obstetrics, and can not but give
great credit to the author and to American medicine. Model it is of clear,
forcible, and beautiful English, of good arrangement of subject-matter, and
of thoroughness of modern obstetric exposition. The changes which have
taken place in the theory and practice of obstetrics since the issue of the
last edition have made it necessary for the author to present to the pro-
fession what is essentially a new book. Most cheerfully will we recommend
to the students of medicine a study of Lusk. It ranks well with Playfalr,
and is second to no book in our language." — Chauncey D. Palmer, in the
Ohio Medical Journal.

"The book is now beyond criticism, for it has been accepted by the un-
erring judgment of the great body of physicians. We congratulate Dr.
Lusk upon this reward for the immense labor he has bestowed upon it." —
New York Medical Journal. "

"It contains one of the best expositions of the obstetric science and
practice of the day with which we are acquainted. Throughout the work
the author shows an intimate acquaintance with the literature of obstet-
rics, and gives evidence of large practical experience, great discrimination,
and sound judgment. We heartily recommend the book as a fall and clear
exposition of obstetric science, and safe guide to student and practitioner."
— London Lancet.

" It is but a short time since we had occasion to review this work, of
which we were enabled to speak in the highest terms of praise. The rapid
advance of many departments of obstetrics has meantime called for a few
additions. These having been made, it can be confidently said that Lusk's
Midwifery holds a high place among American authors, and deserves to
be extensively employed for reference, and recommended to students as
a reliable and unusually readable text-book." — Canada Medical and
Surgical Journal.

D. APPLETON AND COMPANY, NEW YORK

THE PRINCIPLES AND PRACTICE
OF MEDICINE.

By WILLIAM OSLER, M. D.,

Fellow of the Royal College of Physicians, London; Professor of Medicine in the Johns Hopkins Univer-
sity, and Physician in Chief of the Johns Hopkins Hospital, Baltimore; formerly Professor of
the Institutes of Medicine, McGill University, Montreal ; and Professor of Clinical
Medicine in the University of Pennsylvania, Philadelphia.

THE WORK HAS BEEN REWRITTEN, ENLARGED, ENTIRELY RESET,
AND BROUGHT UP TO DATE IN ALL DEPARTMENTS.

THIRD EDITION.
SOLD ONLY BY SUBSCRIPTION.

8vo, 1181 pages. Cloth, $5.50; sheep, $6.50; half morocco, $7.00.

" With new type, clear paper of the best quality, and a somewhat enlarged page, necessi-
tated by the amount of matter in the very thorough revision of a book whose first edition
appeared six years ago, Osier's Practice comes to us with that handsome entourage its prime
excellence, merit, and true value demand. . . . From first to last, title-page to index, the
work is thoroughly practical, and as a guide in diagnosis, symptomatology, and treatment,
will be found well-nigh incomparable, and can not but be the more appreciated the more its
sound advice and wise counsel are sought, whether by the neophyte in medicine or the most
experienced clinician." — Southern Practitioner.

' ' We have little to add to our notice of the second edition (vide Journal, November 30,
1895, page 966), The criticisms then made hold good now, but we regarded the work as one
of the ablest contributions to the literature of the subject in this country, an opinion which
we still hold." — yournaloftke American Medical Assdciation.

" The first edition was great, the second greater, and this last greatest of all." — Cincin-
nati Lancet-Clinic.

' ' There are few books which receive professional confidence and esteem to the extent of
that received by Dr. Osier's well known work, for three large editions have been presented to
us in a period of about six years." — Therafeutic Gazette.

" The work, like former editions, is thoroughly practical in its character, fully up with the
times and down to date, and is a safe guide to all practitioners who may consult its pages.
The student of medicine, whose time is so much occupied by the tremendous amount of
knowledge he is expected to master before graduation, will find here exhaustiveness without
verbosity and a plain matter-of-fact method of discussing the characters of different diseases,
that can not fail to instruct without wearying." — Journal of Medicine and Science.

D. APPLETON AND COMPANY, NEW YORK.

A SYSTEM OF

GENITO-UEINARY DISEASES,

SYPHILOLOGY, ahd DERMATOLOGY.

CONSISTING OP THREE VOLUMES, AS FOLLOWS:

Vol. I, GENITO-URINARY DISEASES; Vol. II, SYPHILOLOGY;
and Vol. Ill, DERMATOLOGY

BT VARIOUS AUTHORS.

Edited by PRINCE A. MORROW, M. D.

SOI.!) OlftT BT SUBSCKIPTION.

" Volume I, Genito-Urinary Diseases. — The first of these three volumes, which
has recently appeared, gives ample evidence of the liberality and thorough work-
manship of its publishers, and of care and thought on the part of its editor, to
whom great credit is due for the admirable manner in which he has accomplished
the arduous task involved in the preparation and production of such an important
work as this is. . . . Of the work as a whole, we do not hesitate to say that it is
the most complete and best single publication of aU those which profess to
cover the ground of genito-urinary diseases, with which we are acquainted, and
recommend it cordially to the favorable consideration of the profession." — Boston
Medical and Surgical Journal.

" The second volume of this valuable series is before us. It covers fully the
field of Syphilography, and is in itself a complete text-book of nine hundred royal
octavo pages. The editor, with the aid of an able corps of assistants, each eminent
as a specialist, has presented to us a very complete work upon Syphilis and Chan-
croid. The literature of recent years is made tributary to this work. Bacterio-
logical researches are brought to date, and the complexity of the pathological rela-
tions of syphilis as here treated form a most valuable feature of the work. General
practitioners will find this volume especially helpful in the diagnosis and treatment
of syphilis and those affections in which it is an essential factor." — North Amer-
ican Practitioner.

" As a complete and systematic treatise on Syphilis and Chancroid this book is
without a rival. It is in every sense modern and eminently practical. An especial
feature of this work is the large number of excellently executed illustrations. The
work of the publishers has been most creditably performed." — University Medical

" This massive volume of one thousand pages finishes this, one of the most val-
uable series of works ever issued in America. The talented editor has gathered
around him the greatest teachers and writers of the time to aid him in this under-
taking, and the result is a series of works which will stand unrivaled for a long
time. They are complete, comprehensive, and exhaustive. The noted publishers
have printed this in their most excellent style, all the work being first class in every
particular." — New England Medical Monthly.

D. APPLETON AND COMPANY, NEW YORK.

October, 1899.

MEDICAL

HYGIElSriC WOEKS

PUBLISHED BY

D. APPLETON AND COMPANY, 72 Fifth Avenue, New York.

ADLDE (JOHN). The Pocket Pharmacy, with Therapeutic Index. A resume
of the Clinical Applications of Remedies adapted to the Pocket-case, for
the Treatment of Emergencies and Acute Diseases. 12mo. Cloth, $2.00.

BARKER (FORDYOE). On Sea-Sickness. A Popular Treatise for Travelers
and the General Reader. Small 12mo. Cloth, 75 cents.

BARKER (FORDYCE). On Puerperal Disease. Clinical Lectures delivered at
Bellevue Hospital. A Course of Lectures valuable alike to the Student and
the Practitioner. Third edition. 8vo. Cloth, $5.00; sheep, $6.00.

BARTHOLOW (ROBERTS). A Treatise on Materia Medica and Therapeutics
Ninth edition. Revised, enlarged, and adapted to " Tlie Kew Pharmacopoeia.
8vo. Cloth, $6.00 ; sheep, $6.00.

BARTHOLOW (ROBERTS). A Treatise on the Practice of Medicine, for the
Use of Students and Practitioners. Seventh edition, revised and enlarged
8vo. Cloth, $5.00 ; sheep, $6.00.

BARTHOLOW (ROBERTS). On the Antagonism between Medicines and be-
tween Remedies and Diseases. Being the Cartwright Lectures for the Year
1880. 8vo. Cloth, $1.25.

BASTIAN (H. CHARLTON). Paralyses: Cerebral, Bulbar, aud Spinal. A
Manual of Diagnosis for Students and Practitioners. With 136 Illustra-
tions. Small 8vo, 6Y1 pages. Cloth, $4.50.

BASTIAN (H. CHARLTON). Paralysis from Brain Disease in its Common
Forms. With Illustrations. 12mo, 340 pages. Cloth, $1.75.

BILLROTH (THEODOR). General Surgical Pathology and Therapeutics. A
Text-Book for Students and Physicians. Translated from the tenth German
edition, by special permission of the author, by Charles E. Hackley, M. D.
Fifth American edition, revigitd and enlarged. 8vo. Cloth, $5.00; sheep, $6.00.

BOYCE (RUBERT). A Text-Book of Morbid Histology. For Students and
Practitioners. With 130 Colored Illustrations. Cloth, $7.50.

BRAMWELL (BYROM). Diseases of the Heart and Thoracic Aorta. Illus-
trated with 226 Wood-Engravings and 68 Lithograph Plates — showing 91
Figures— in all, 317 Illustrations. 8vo. Cloth, $8.00; sheep, $9.00.

BRYANT (JOSEPH D.). ■ A Manual of Operative Surgery. New edition, reilwd
and enlarged. 793 Illustrations. 8vo. Cloth, $5.00 ; sheep, $6.00.

BURT (STEPHEN S.). Exploration of the Chest in Health and Disease. 8vo,
210 pages. With Illustrations. Cloth, $1.50.

(DAMPBELL (F. R.). The Language of Medicine. A Manual giving the Origin,
Etymology, Pronunciation, and Meaning of the Technical Terms found in
Medical Literature. 8vo, Cloth, $3.00,

OARMICHAEL (JAMES). Disease in Children. A Manual for Students and
Practitioners. Illustrated with Thirty-one Charts. 12mo, 591 pages.
(Stddekts' Sekies.) Cloth, $3.00. '

OHAUVEAU (A.). The Comparative Anatomy of the Domesticated Animals.
Revised and enlarged, with the co-operation of 8. Arloing, Director of the
Lyons Veterinary School. Second English edition. Translated and edited
by George Fleming, C. B., LL. D., E'. R. C. V. S., late Principal Veterinary
Surgeon of the British Ai-my; Foreign Corresponding Member of the
Soci6t6 Royale de M^decine, and of the Soci6t6 Royale de M6decine Pub-
lique, of Belgium, etc. 8vo, 1084 pages, with 685 Illustrations. Cloth, $7.00.

CORNING (J. L.). Brain Exhaustion, with some Preliminary Consideration*
on Cerebral Dynamics. Crown 8vo. Cloth, $2.00.

CORNING (J. L.). Local Anagsthesia in General Medicine and Surgery. Being
the Practical Application of the Author's Recent Discoveries. With IlluB-
trations. Small 8vo. Cloth, $1.25.

CURRIER (ANDREW F.). The Menopause. A Consideration of the Phe-
nomena which occur to Women at the Close of the Child-bearing Period,
with Incidental Allusions to their Relationship to Menstruation. Also a
Particular Consideration of the Premature (especially the Artificial) Meno-
pause. 12mo, 284 pages. Cloth, $2.00.

DAVIDSON (ANDREW). Geographical Pathology: An Inquiry into the

Geographical Distribution of Infective and Climatic Diseases. 2 vols.

8vo. Cloth, $7.00.
DENCH (E. B.). Dis-eases of the Ear. A Text-Book for Practitioners and

Students of Medicine. With 8 Colored Plates and 152 Illustrations in the

text. 8vo. Cloth, $5.00 ; sheep, $6.00.

DEXTER (FRANKLIN). The Anatom.y of tlie Peritonsum. 12mo. With
39 colored Illustrations. Cloth, $1.50.

DOTY (ALVAH H.). A Manual of Instruction in the Principles of Prompt
Aid to the Injured. Including a Chapter on Hygiene and the Drill Regula-
tions for the Hospital Corps, U. S. A. Designed for Military and Civil Use.
Second edition, revised and enlarged. 121 Illustrations. 12mo. Cloth, $1.50.

ELLIOT (GEORGE T.). Obstetric Clinic : A Practical Contribution to the Study
of Obstetrics and the Diseases of Women and Children. 8vo. Cloth, $4.50,

EVANS (GEORGE A.). Hand-Book of Historical and Geographical Phthisi-
ology. With Special Reference to the Distribution of Consumption in the
United States. 8vo. Cloth, $2.00.

EWALD (0. A.). Lectures on the Diseases of the Stomach. By Dr. C. A.
Ewald, Professor of Pathology and Therapeutics in the University of Berlin,
etc. Translated from the German by special permission of the author, by
Morris Manges, A. M., M. D. Second edition, revised and rearranged. Cloth,
$5.00 ; sheep, $6.00. {Sold only hy subscription.)

FLINT (AUSTIN). Medical Ethics and Etiquette. Commentarieg on the
National Code of Ethics. 12mo. Cloth, 60 cents.

FLINT (AUSTIN). Medicine of the Future. An Address prepared for the
Annual Meeting of the British Medical Association in 1886. With Portrait
of Dr. Flint. 12mo. Cloth, $1.00.

FLINT (AUSTIN, Jr.). Text-Book of Human Physiology; designed for the
Use of Practitioners and Students of Medicine. Illustrated with three
hundred and sixteen Woodcuts and Two Plates. Fonrth edition, revised.'
Imperial 8vo. Cloth, $6.00; sheep, $7.00.

FLINT (AUSTIN, Jr.). The Physiological Effects of Severe and Protracted
Muscular Exercise ; with Special Reference to it? Influence upon the Excre-
tion of Nitrogen, ISmo. Cloth, $1.00,

FLINT (AUSTIN, Je.).. The Source of Muscular Power. Arguments and Oon-
clnsions drawn from Observation upon the Unman Subject under Conditions
of Rest and of Muscular Exercise. 12mo. Oloth, $1.00.

FLINT (AUSTIN, Jb.). Physiology of Man. Designed to represent the Exist-
ing State of Physiological Science as applied to the Functions of the Human
Body. Complete in 5 vols., 8vo. Per vol., cloth, $4.60 ; sbeep, $5.60.
*^* Vols. I and II can be had in cloth and sheep binding; Vol. Ill in sheep
only. Vol. IV is at present out of print.

FLINT (AUSTIN, Je.). Manual of Chemical Examinations of the Urine in
Disease; with Brief Directions for the Examination of the most Common
Varieties of Urinary Calculi. Revised edition. 12mo. Cloth, $1.00.

FOSTER (FRANK P.). Illustrated Encyclopsedic Medical Dictionary : Being
a Dictionary of the Technical Terms used by Writers on Medicine and the
Collateral Sciences in the Latin, English, French, and German Languages.
The work consists of Four Volumes, and is sold in Parts; Three Parts to
a Volume. {Sold only ty subscription.)

FOSTER (FRANK P.). A Reference-Book of Practical Therapeutics, by
various writers. In Two Volumes. Edited by Frank P. Foster, M. D.,
Editor of The New York Medical Journal. Oloth, $5.00; sheep, $6.00;
half morocco, $6.50, each volume. {Sold only iy suisaripfion.)

FOURNIER (ALFRED). Syphilis and Marriage. Translated by P. Albert
Morrow, M. D. 8vo. Oloth, $2.00 ; sheep, $3.00.

FRIEDLANDER (CARL). The Use of the Microscope in Clinical and Patho-
logical Examinations. Second edition, enlarged and improved, with a
Chromolithograph Plate. Translated, with the permission of the author,
by Henry 0. Coe, M. D. 8vo. Cloth, $1.00. ^

FUOHS (ERNEST). Text-Book of Ophthalmology. By Dr. Ernest Fuchs,
Professor of Ophthalmology in the University of Vienna. With 178 Wood-
outs. Authorized translation from the second enlarged and improved Ger-
man edition, by A. Duane, M. D. Oloth, $5.00; sheep, $6.00.

GARMANT (JASPER J.). Operative Surgery on the Cadaver. With Two
Colored Diagrams showing the Collateral Circulation after Ligatures of
Arteries of Arm, Abdomen, and Lower Extremity. Small 8vo. Cloth,
$2.00.

GERSTER (ARPAD G.). The Rules of Aseptic and Antiseptic Surgery.
A Practical Treatise for the Use of Students and the General Practitioner.
Illustrated with over two hundred fine Engravings. Svo. Cloth, $5.00 ;
sheep, $6.00.

GIBSON-RUSSELL. Physical Diagnosis: A Guide to Methods of Clinical In-
vestigation. By G. A. Gibson, M. D., and William Russell, M. D. With
101 Illustrations. 12mo. (Students' Seeibs.) Cloth, $2.50.

GOULEY (JOHN W. S.). Diseases of the Urinary Apparatus. Part L Phleg-
masic Affections. Being a Series of Twelve Lectures delivered during the
autumn of 1891. With an Addendum on Retention of Urine from Pro-
static Obstruction in Elderly Men. Cloth, $1.50.

GROSS (SAMUEL W.). A Practical Treatise on Tumors of the Mammary
Gland. Illustrated. 8vo. Cloth, $2.50.

GRUBEB (JOSEF). A Text-Book of the Diseases of the Ear. Translated
from the second German edition by special permission of the author, and
edited by Edward Law, M. D., and Coleman Jewell, M. D. With 165 Illne-
trations and 70 Colored Figures on Two Lithographic Plates 8vo. Cloth,
$6.60 ; sheep, $7.60.

HAMMOND (W. A.). A Treatise on Diseases of tlie Nervous System. With
the Collaboration of Graerae M. Hammond, M.D. With one hundred and
eighteen Illustrations. Ninth edition, with corrections and additions. 8vo.
Oloth, $6.00 ; sheep, $6.00.

HAMMOND (W. A.). A Treatise on Insanity, in its Medical Relations. 8vo.
Oloth, $5.00 ; sheep, $6.00.

HAMMOND (W. A.). Clinical Lectures on Diseases of the Nervous System.
Delivered at Bellevue Hospital Medical College. Edited by T. M. B. Oross.
M. D. 8vo. Cloth, $3.50.

HIET (LUDWIG). The Diseases of the Nervous System. A Text-Book for
Physicians and Students. Translated, with permission of the Author, by
August Hoch, M.D., assisted by Frank R. Smith, A.M. (Cantab.), M. D.,
Assistant Physicians to the Johns Hopkins Hospital. "With an Introduc-
tion by William Osier, M. D., P. R. C. P., Professor of Medicine in the Johns
Hopkins University, and Physician-in-Ohief to the Johns Hopkins Hospital,
Baltimore. 8vo, 671 pages. With 178 Illustrations. Cloth, $5.00 ; sheep,
$6.00. {Sold only iy sulscription.)

HOFFMANN-ULTZMANN. Analysis of the Urine, with Special Reference
to Diseases of the Urinary Apparatus. By M. B. Hoffmann, Professor in
the University of Gratz, and R. Ultzmann, Tutor in the University of
Vienna. Third edition, leTised and enlarged. Svo. Cloth, $2.00.

HOLT (L. EMMETT). The Diseases of Infancy and Childhood. Svo. Cloth,
$6.00 ; sheep, $7.00 ; half morocco, $7.50. (Sold only by subscription.)

HOLT (L. EMMETT). The Care and Feeding of Children. A Catechism for
the Use of Mothers and Children's Nurses. 16mo. Cloth, 60 cents.

HOWE (JOSEPH W.). Emergencies, and how to treat them. Fourth edition,
revised. Svo. Cloth, $2.50,

HOWE (JOSEPH W.). The Breath, and the Diseases which give it a Fetid
Odor. With Directions for Treatment. Second edition, revised and corrected.
12mo. Oloth, $1.00.

HUEPPE (FERDINAND). The Methods of Bacteriological Investigation.
Written at the request of Dr. Robert Koch. Translated by Hermann M.
Biggs, M.D. Illustrated. 8vo. Cloth, $2.50.

JACOOUD (S.). The Curability and Treatment of Pulmonary Phthisis. Trans-
lated and edited by Montagu Lubbock, M. D. Svo. Cloth, $4.00.

KEYE8 (E. L.). A Practical Treatise on Genito-Urinary Diseases, including
Syphilis. Being a new edition of a work with the same title by Van Buren
and Keyes. Almost entirely rewritten. With Illustrations. Svo. Oloth,
$6.00; sheep, $6.00.

KEYES (E. L.). The Tonic Treatment of Syphilis, including Local Treatment
of Lesions. Second edition. Svo. Cloth, $1.00,

LEGG (J. WICKHAM). On the Bile, Jaundice, and Bilious Diseases. With
Illustrations in Chromolithography. Svo. Cloth, $6.00 ; sheep, $7.00,

LORING (EDWARD G.). A Text-Book of Ophthalmoscopy,

Part I. The Normal Eye, Determination of Refraction, and Diseases of the
Media. With 131 Illustrations and 4 Chromolithographs. Svo. Buck-
ram, $5.00.

LORING (EDWARD G.). A Text-Book ol Ophthalmoscopy.

Part II. Diseases of the Retina, Optic Nerve, and Choroid : their Varie-
ties and .Complications. The mannscript of this volume, which the
author finished just prior to his death, has been thoroughly edited and
revised by F. B. Loring, M. D., of Washington, D. C, and is now issued
in the same style as the first volume. Profusely illustrated. Part II,
buckrain, $5.00. Two Parts, bnckram, $10.00.

LUSK (WILLIAM T.). The Science and Art of Midwifery. With 246 Illustra-
tions. Fonrth edition, revised and enlarged. 8vo. Cloth, $5.00 ; sheep, $6.00.

MARCY (HENRY 0.). The Anatomy and Surgical Treatment of Hernia.
4to, with about sixty full-page Heliotype and Lithographic Reproductions
from the Old Masters, and numerous Illustrations in the Text. (Sold only
hy subscription.)

MATHEWS (JOSEPH M.). A Treatise on Diseases of the Rectum, Anus,
and Sigmoid Flexure. 8vo. With six Chromolithographs, and Illustra-
tions in the text. Second edition, (Sold only lyy subscription.)

MILLS (WESLEY). A Text-Book of Animal Physiology, with Introductory
Chapters on General Biology and a full Treatment of Reproduction for
Students of Human and Comparative Medicine. 8vo. With 505 Illustra-
tions. Cloth, $5.00 ; sheep, $6.00.

MILLS (WESLEY). A Text-Book of Comparative Physiology. For Students
and Practitioners of Veterinary Medicine. Small 8vo. Cloth, $3.00.

MORROW (PRINCE A.). A System of Genito-Urinary Diseases, Syphilology,
and Dermatology. By various Authors. In Three Volumes, beautifully
illustrated. Vol. I. Genito-urinary Diseases. Vol. II. Syphilography .
Vol. III. Dermatology, {Sold only by subscription^

THE NEW YORK MEDICAL JOURNAL (Weekly). Edited by Frank P.
Foster, M. D. Terms, $5.00 per annum.
Binding Cases, cloth, 50 cents each. ■

" Self-Binder " (this is used for temporary binding only), 90 cents.
Genbeal Index, from April, 1865, to June, 1876 (23 vols.). 8vo. Cloth, 75 cts.

NIEMEYER (FELIX VON). A Text-Book of Practical Medicine, with particu-
lar reference to Physiology and Pathological Anatomy. Containing all the
author's Additions and Revisions in the eighth and last German edition.
Translated by George H. Humphreys, M. D., and Charles E. Hackley, M. D.
2 vols. 8vo. Cloth, $9.00; sheep, $11.00.

NIGHTINGALE (FLORENCE). Notes on Nursing. 12mo. Cloth; 75 cents.

OSLER (WILLIAM). Lectures on Angina Pectoris and Allied States. Small
8vo. Illustrated. Cloth, $1.50.

OSLER (WILLIAM). Lectures on the Diagnosis of Abdominal Tumors.
Small 8vo. Illustrated. Cloth, $1.50.

OSLER (WILLIAM). The Principles and Practice of Medicine. Designed for
the ITse of Practitioners and Students of Medicine. Second edition, levised
and enlarged. Cloth, $5.50; sheep, $6.60 ; half morocco, $7.00. {Sold only
by subscription.)

PELLEW (C. E.). A Manual of Practical Medical Chemistry. 12mo. With
niustrations. Cloth, $2.50.

PHELPS (CHARLES). Traumatic Injuries of the Brain and its Membranes.
With a Special Study of Pistol-Shot Wounds of the Head in their Medico-
Legal and Surgical Eelations. 8vo, 582 pages. With forty-nine Illustra-
tions. Cloth, $6.00. {Sold only ly subscription.)

PIFFARD (HENRY G.). A Practical Treatise on Diseases of the Skin. By
Henry G. Piffard, A. M., M. £>., assisted by Robert M. Fuller, M. D. With
fifty full-page Original Plates and thirty-three Illustrations in the Text.
4to. {Sold only iy subscription.)

POMEROT (OREN D.). The Diagnosis and Treatment of Diseases of the Ear.
With One Hundred Illustrations. Second edition, revised and enlarged. 8vo.
Cloth, $3.00.

POORE (0. T.). Osteotomy and Osteoclasis, for the Correction of Deformities
of the Lower Limbs. 50 Illustrations. 8vo. Cloth, $2.50.

QUAIN (RICHARD). A Dictionary of Medicine, including General Pathology,
General Therapeutics, Hygiene, and the Diseases peculiar to Women and
Children. By Various Writers. Edited by Sir Richard Qaain, Bart.,
M. D., LL. D., etc. Assisted by Frederick Ihomas Roberts, M. D., B. Sc,
and J. Mitchell Bruce, M. A., M. D. With an American Appendix by
Samuel Treat Armstrong, Ph.D., M. D. In two volumes. {Sold only by
subscription.)

RANNEY (AMBROSE L.). Applied Anatomy of the Nervous System, being a
Study of this Portion of the Human Body from a Standpoint of its General
Interest and Practical Utility, designed for Use as a Text-JBook and as a Work
of Reference. Second edition, rerlsed and enlarged. Profusely illustrated. 8vo.
Cloth, $5.00 ; sheep, $6.00.

ROBINSON (A. R.). A Manual of Dermatology. Revised and coi:rected. Svo.
Cloth, $5.00.

ROSOOE-SCHORLEMMER. Treatise on Chemistry.
Vol. 1. Non-Metallic Elements. 870. Cloth, $5.00.
Vol. 2. Part I. Metals. Svo. Cloth, $3.00.
Vol. 2. Part II. Metals. Svo. Cloth, $3.00.

Vol. 8. Part I. The Chemistry of the Hydrocarbons and their Derivatives.
Svo. Cloth, $5.00.

Vol. 3. Part II. The Chemistry of the Hydrocarbons and their Derivatives.
Svo. Cloth, $5.00.

Vol. 3. Part III. The Chemistry of the Hydrocarbons and their Deriva-
tives. Svo. Cloth, $3.00.

Vol. 8. Part IV. The Chemistry of the Hydrocarbons and their Deriva-
tives. Svo. Cloth, $3.00.

Vol. 8. Part V. The Chemistry of the Hydrocarbons and their Deriva-
tives. Svo. Cloth, $8.00.

ROSENTHAL (I.). General Physiology of Muscles and Nerves. With 75 Wood-
cuts. 12mo. Cloth, $1.60.

S AYRE (LEWIS A.). Practical Manual of the Treatment of Club-Foot. Fonrth
edition, enlarged and corrected. 12mo. Cloth, $1.25.

SAYRE (LEWIS A.). Lectures on Orthopedic Surgery and Diseases of the
Joints, delivered at Bellevue Hospital Medical College. New edition, illus-
trated with 824 Engravings on Wood. Svo. Cloth, $5.00 ; sheep, $6.00.

SCHULTZE (B. S.). The Pattology and Treatment of Displacements of the
DteruB. Translated from the German hy Jameson J. Macan, M. A., etc.;
and edited by Arthur V. Macan, M. B., etc. With one hundred and
twenty Illustrations. 8vo. Cloth, $3.60.

SHIELD (A. MARMADUKE). Surgical Anatomy for Students. 12mo.
(Stddbnts' Sbeieb.) Oloth, $1.Y5.

SHOEMAKER (JOHN V.). A Text-Book of Diseases of the Skin. Six
Chromolithographs and numerous Engravings. Third edition, revised
and enlarged. 8vo. Cloth, $5.00 ; sheep, $6.00.

SIMPSON (JAMES Y.). Selected Works: Anaesthesia, Diseases of Women.
3 vols. 8vo. Per volume, cloth, $3.00; sheep, $4.00.

SIMS (J. MARION). The Story of my Life. Edited by his Sod, H. Marion-
Sims, M. D. With Portrait. 12mo. Cloth, $1.50.

SKENE (ALEXANDER J. C). A Text-Book on the Diseases of Women.
Illustrated with two hundred and fifty-four Illustrations, of which one
hundred and sixty-five are original, and nine chromolithographs. Second
edition. 8vo. {Sold only hy subscription.)

SKENE (ALEXANDER J. C). Medical Gynecology. A Treatise on the
Diseases of Women from the Standpoint of the Physician. 8vo. With
Illustrations. Cloth, $5.00.

STEINER (JOHANN). Compendium of Children's Diseases. A Hand-Book
for Practitioners and Students. Translated from the second German edition,
by Lawson Tait. 8vo. Cloth, $3.50 ; sheep, $4.50.

STEVENS. (GEORGE T.) Functional Nervous Diseases: Their Causes and
their Treatment. Memoir for the Concourse of 1881-1883, Acad6mie Royal
de Mfidecine de Belgique. With a Supplement, on the Anomalies of Re-
fraction and Accommodation of the Eye, and of the Ocular Muscles. Small
8vo. With six Photographic Plates and twelve Illustrations. Cloth, $2.50.

STONE (R. FRENCH). Elements of Modern Medicine, including Principles of
Pathology and of Therapeutics, with many Useful Memoranda and Valuable
Tables of Reference. Accompanied by Pocket Fever Charts. Designed for
the Use of Students and Practitioners of Medicine. In wallet-book form,
with pockets on each cover for Memoranda, Temperature Charts, etc.
Roan, tuck, $2.50.

STREOKER (ADOLPH). Short Text-Book of Organic Chemistry. By Dr.
Johannes Wislicenus. Translated and edited, with Extensive Additions, by
W. H. Hodgkinson and A. J. Greenaway. 8vo. Cloth, $5.00.

STRUMPELL (ADOLPH). A Text-Book of Medicine, for Students and Prac-
titioners. Translated, hy permission, from the sixth German edition
by Herman F. Vickery, A. B., M. D., Instructor in Clinical Medicine, Har-
vard Medical School, etc., and Philip Coombs Knapp, Physician to Out-
patients with Diseases of the Nervous System, Boston City Hospital, etc.
With Editorial Notes by Frederick C. Shattuok, A. M., M. D., Jackson Pro-
fessor of Clinical Medicine, Harvard Medical School, etc. Second American
edition. With 111 Illustrations. 8vo, 981 pages. Cloth, $6.00; sheep,
$7.00.

THAYER (WILLIAM SYDNEY). Lectures on the Malarial Fevers. With
nineteen Charts and three Lithographic Plates showing the Parasite of
Tertian, Quotidian, and iEstivo-Autunmal Fevers, Small 8vo, 326 pages.
Cloth, $3.00,

THOMAS (T. GAILLAED). Abortion and its Treatment, from tlie Stand-
point of Practical Experience. A Special Course of Lectures delivered be-
fore the College of Physicians and Surgeons, New York, Session of 1889-'90.
From Notes by P. Brynberg Porter, M. D. Revised by the Author.
12mo. Cloth, $1.00.

THOMPSON ("W. OILMAN). Practical Dietetics, with Special Reference to
Diet in Disease, tvo. Cloth, $5.00. {Sold only hy subscription.)

THOMSON (J. ARTHUR). Outlines of Zoology. With thirty-two full-page
Hlnstrations. 12mo. (Students' Seeibs.) Cloth, $3.00.

TILLMANNS (HERMANN). A Text-Book of Surgery. Yol. L The Prin-
ciples of Surgery and Surgical Pathology. 8vo. With four hundred and
forty-one Hlustrations. Translated by John Rogers, M. D., and Benjamin
T. Tilton, M. D. Vol. II. Regional Surgery. With four hundred and
seventeen Illustrations. Translated by Benjamin T. Tilton, M.D. Each
volume, cloth, $5.00 ; sheep, $6.00. {Sold only iy subscription.')

ULTZMANN (ROBERT). Pyuria, or Pus in the Urine, and its Treatment.
Translated by permission, by Dr. Walter B. Piatt. 12mo. Cloth, $1.00.

VAN BDREN (W. H.). Lectures upon Diseases of the Rectum, and the Sur-
gery of the Lower Bowel, delivered at Bellevne Hospital Medical College.
Second edition, revised and enlarged. Svo. Cloth, $3.00 ; sheep, $4.00.

VAN BTTREN (W. H.). Lectures on the Principles and Practice of Surgery.
Delivered at Bellevue Hospital Medical College. Edited by Lewis A. Stim-
son, M. D. 8vo. Cloth, $4.00 ; sheep, $5.00.

VOGEL (A.). A Practical Treatise on the Diseases of Children. Translated
and edited by H. Raphael, M. D. Third American from the eighth German edi-
tion, revised and enlarged. Illustrated by six Lithographic Plates. 8vo.
Cloth, $4.50; sheep, $5.50.

VON ZEISSL (HERMANN). Outlines of the Pathology and Treatment of
Syphilis and Allied Venereal Diseases. Second edition, revised by Maximil-
ian von Zeissl. Authorized edition. Translated, with Notes, by H. Ra-
phael, M. D. 8vo. Cloth, $4.00 ; sheep, $5.00.

WEBBER (S. G.). A Treatise on Nervous Diseases: Their Symptoms and
Treatment. A Text-Book for Students and Practitioners. Svo. Cloth, $8.00.

WEEKS-SHAW (CLARA S.). A Text-Book of Nursing. For the Use of
Training-Schools, Families, and Private Students. Second edition, revised
and enlarged. 12mo. With Illustrations, Questions for Review and Ex-
amination, and Vocabulary of Medical Terms. 12mo. Clotli, $1.75.

WELLS (T. SPENCER). Diseases of the Ovaries. Svo. Cloth, $4.50.

WORCESTER (A.). Monthly Nursing. Second edition, revised. Cloth, $1.25.

WYETH (JOHN A.). A Text-Book on Surgery: General, Operative, and Me
ohanical. Profusely illastrated, Thirtf edition, revised and" enlarged, Svo.
{Sold only ly subscription.)

iimiminumtim'H'f'*""""'':

Internet Archive Audio

Featured

Top

Images

Featured

Top

Software

Featured

Top

Books

Featured

Top

Video

Featured

Top

Mobile Apps

Browser Extensions

Archive-It Subscription

Save Page Now

Full text of "Accident and injury; their relations to diseases of the nervous system"

See other formats