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Henry Pelouze de Forest 

Class of 1884 

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

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the United States on the use of the text. 92401 2461 1 1 1 


















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




Copyright, 1898, 





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 


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 


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. 



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 




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 



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 





Malingering 34i 

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

2. Substitution of origin 352 

3. Simulation 357 


Treatment of the traumatic neuroses 394 

Index of names 419 

Index of subjects 422 



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 



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 




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- 


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 


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. 


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 

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. 



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 


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- 

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 


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 



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

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. 


Where, etc. : 

On passenger trains 

On freight trains 

On station grounds, etc 

Postal and expressmen 

Cause : 


Getting on and off moving trains . . 

Getting on and off trains after stop 

Defective and unlighted stations and 


Result : 


Loss of limb 

Loss of finger or toe 

Spinal injury 

Fracture or dislocation 


Cuts and bruises 
































II. 6 
























Table 2. 
Injuries to Employees. 
















































































































14. 1 



lb. 3 




















II. I 












Employment : 









Cause : 



Getting on and off trains 

Caught in frogs and switches . 

Use of tools and machinery. . . 

Fell from cars 

Defective tools and appliances 


Result : 


Loss of limb 

Loss of finger or toe 

Spinal injury 

Fracture or dislocation 


Cuts and bruises 


Table 3. 
Percentage of Results. 






Result : 


Loss of limb 

Loss of finger or toe.. . 

Spinal injury 

Fracture or dislocation, 


Cuts and bruises 


Total : 


Travelers on highway. . 






































































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 


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. 



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. 

Congenital cataracts. 
Pigmentary retinitis. 
. Muscular insufiSciency. 

' Polydactyly. 





^ Excessive length of the arms. 


Malformation of the breasts, thorax. 






Spina bifida. 
' Cryptorchismus. 


Spurious hermaphroditism. 




Anomalies of the body 
in general. 

Anomalies of the genital 



Anomalies of the skin. 

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 

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 


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 



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. 


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 

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

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 



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- 

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 


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 


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- 

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 


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. 

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




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 


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 

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 

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. 


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 



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 



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. 



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 



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 

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. 


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 

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 


■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 


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 



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- 


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. 



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 



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- 

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 


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 



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 


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 


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 


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 

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- 



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

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 



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- 


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- 

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 



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. 


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. 



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- 

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 



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- 

12 3 4 

I 2 3 


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 


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. 



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. 



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 



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- 

2. Mental, which indicate interference with intellectual 

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. 


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 


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 

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 



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 

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. 

© Cortical area for the facial nerve. 

O (3) Motor aphasia. 

X (6) Sensory (auditory) aphasia with 

+ (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. 



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 


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- 


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. 



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 





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 


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


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. 


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 


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 



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 


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- 



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: 


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- 

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 

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 


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 


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 


— 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 


of the injury must be made from the nervous symptoms 

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. 


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 

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. 


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. 


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. 


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 


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 


of excessive violence that acts directly upon the spinal 

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 


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 



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 

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 



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 



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 



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 


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. 


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. 


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 

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. 


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

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 

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


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 


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 


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 

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- 


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 


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 

Does such a condition as spinal concussion exist? In 


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- 


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. 



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 


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, 



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. 


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 



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- 


a VII 


a VI 


\ I 



,„ ^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- 



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 



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. 



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 


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. 


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, 

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 

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. 



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 



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 


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 


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 


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. 


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 

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. . 


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 


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 

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- 


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. 


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 

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, 

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. 


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- 


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- 

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 


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 

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- 



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. 



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 


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. 



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- 

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 


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 

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


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- 


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- 

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 


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. 


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. 



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- 

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 


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 

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. 


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 


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. 



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. 


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 

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. 



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- 


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


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 



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 


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 

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 




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. 


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 

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 

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 

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 
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. — 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. 


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 



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 


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 



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 

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 


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 

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. 


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



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 

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 


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- 



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.) 


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. 


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 

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 


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 


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, 


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- 

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- 



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

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 


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- 



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 


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 



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 


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. 


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— Tabes Dorsalis. 


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 


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 


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 

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 



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. ) 



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- 

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

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 


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. 



^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- 


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 



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 



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 



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 : 


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 

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- 

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 


is very essential that the merits of the question be clearly 

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 

^ 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 



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. 


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 


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- 


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 

^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- 


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 


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- 


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 


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- 


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. 


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. 



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- 



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- 



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 


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. 



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- 


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. 


Paralysis Agitans (Parkinson's Disease — Shaking 


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 


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- 

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 



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- 



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- 

Fig. 41. — Showins Jiaracteristic atti- 
tude in paralysis atfitans. (Vander- 
bilt Clinic.) 


sisted, passing to the leg, and afterward to the limbs on the left 

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 — 


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- 


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- 

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. 



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. 





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 



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 


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 


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 


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 



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. 


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 



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- 


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 


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- 

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- 


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 



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 

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 


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 

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 


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 

The larger number of cases can be made to agree w 


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. 


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. 


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- 

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 


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 



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 

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. 



























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 


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- 


rence of the accident and the appearance of pronounced 

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- 


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. 


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 


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 


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 


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- 

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- 

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 


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 


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 

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. 


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 

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- 



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. 


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 



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 

Palpitation of the heart is particularly frequent in per- 


sons who use to excess tea, alcohol, tobacco, or other stimu- 

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- 



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- 


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. 


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- 


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 

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 


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. 


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, 

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- 


tem, London, 1866 ; ibid.. Spinal Concussion, London, 1875 and 

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, 

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, 


Rumpf, Beitrage zur kritischen Symptomatologie der traumat- 
ische Neurose. Deut. med. Woch., 1895, p. 165. 


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. 



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 




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. 


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 

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 


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, 


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- 

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- 

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 



he told the following story and presented the following symp- 

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 


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. 


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 


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- 

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 


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 


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. 



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 


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 


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- 

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 


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 

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 



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 


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 

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 



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- 

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- 


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- 

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 


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 

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 


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 

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 



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 



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. ) 



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 


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. 


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- 

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 


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 

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- 

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 



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. 


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 



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 


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- 

In neurasthenia the acuity of central vision is not im- 

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- 

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- 


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 

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. 


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 



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 


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- 

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 


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. 


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 

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 


estimate of the percentage of cases which completely re- 

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- 


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 


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- 

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 


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, 



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 

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 

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 


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 



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, 

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. 



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 

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. 



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 


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 

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- 



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 


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. 



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. 


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 



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 



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 


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 


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 

As Briquet very truly says, " hysteria attacks the whole 


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- 

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 


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.) 



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.) 

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 



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- 

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 



■ 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 

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. 


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- 


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 



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 


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 : 


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 


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 


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 


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. 



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 


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 



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 


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- 



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 



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 


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 



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 


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- 

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 


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. 



'^ ^ 





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.) 


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- 

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- 


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 



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- 


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 


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 



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 

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 


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- 

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 

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 



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 

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 : 


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 

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 



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 

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 



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- 

F:g. 54. — Attitude in a case of hysterical coxalgia. 
(After Richer and Berbez.) 



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 


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 

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 


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- 

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. 


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 



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- 

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. 


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- 



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 


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 

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. 


(The reader is especially referred to the comprehensive treatise 
of M. de la Tourette.) 



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,. 

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. 


Mobius, Ueber den Begriff der Hysteric. Neurolog. Beitrage, i, 

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, 

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. 



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- 


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 


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, 


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 


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- 



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- 



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. 


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 



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 

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, 



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- 



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 

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 

Pathology. — From the complexity and peculiar character 


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. 



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 

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 

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 

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. 


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 



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. 




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. 



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 



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. 


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, 



". 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 


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 



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 



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 



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- 



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 


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 



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- 



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 



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 



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- 


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- 



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 



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 



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. 



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 



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. 


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 



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 

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 



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 

The past record, however, the successful simulator may 



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 



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 



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. 


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- 

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- 



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- 



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 



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 

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 



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 

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 


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 



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 



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- 

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- 


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 



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, 



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- 


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 


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 

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 


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 


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- 

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- 


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 

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 

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- 



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 

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 

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 


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- 



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 


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 

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 


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 


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 



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 


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 



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- 



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 

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- 



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. 


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. 


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. 



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. 




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- 



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 



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 


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 



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- 

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 


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 



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 



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 

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- 



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- 

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 


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- 

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 



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. 


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- 


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 

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. 


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 

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. 



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 



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 



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. 


The local douches can not be satisfactorily carried out at 

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 


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 

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 


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 

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- 


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. 



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- 


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. 


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, 

Wetterstrand, Hypnotism. Translated by Petersen, New York 
and London, 1897. 

Winternitz, Vortrage uber Hydrotherapie. 


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; 

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 




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. 



Strauss, 220. 
Stroebe, 118. 
Strumpell, 20, 123, ig5, 199 201, 222, 

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. 



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. 




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, 

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, 

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, 

in malingering, 347. 

in neurasthenia, 241, 265. 



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, 

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. 



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), 

Lead palsy, differential diagnosis of, 167. 
Lightning, cause of nervous disease, 

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. 



Locomotor ataxia, 151. 

setiology of, 157. 

and syphilis, 157. 

bibliography of, 163. 

pre-ataxic period of, 157. 

proof necessary for traumatic origin of, 

trauma as a cause of, 158. 
Lumbago, traumatic, 244. 
Lumbar plexus, palsy of, 117. 

Main en griffe, in ulnar nerve palsy, 

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. 



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, 

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. ' 



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, 

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, 

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, 

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. 



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, 

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, 

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, 

Tumors of nervous system, traumatic 
origin of, 121. 



Ulnar nerve, injury to, io8. 

Ultimate organic effects of injury, lig. 

Unclassified forms of traumatic neuroses, 

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, 

Vascular disturbances, simulation of, 

Vertebrae, fractures of, 72. 
Vision, examination of, 22. 
Vision, field of, 25. 

Wet pack, 408. 
Winged scapulae, 107. 
Wrist-drop, 99. 
Wryneck, hysterical, 311. 






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