ON THE EARLY DIAGNOSIS 
OF BGMK 
ORGANIC DISEASES 
OF TH E 
NERVOUS SYSTEM. 
By E. C. SEGUIN, M.D., 
CLINICAL PROFESSOR OF DISEASES OF THE MIND AND NERVOUS. 
SYSTEM IN THE COLLEGE OF PHYSICIANS AND 
SURGEONS, NEW YORK. 
Reprinted from The Medical Record, Fib. 36, 1881- 
NEW YORK: 
TROW’S PRINTING AND BOOKBINDING CO.. 
201-218 East 12th Street. 
1881. ON THE EARLY DIAGNOSIS OF SOME 
ORGANIC DISEASES OF THE NER- 
VOUS SYSTEM. 
Pjkobably no one would deny the desirability and 
utility of making an accurate diagnosis of disease at 
the earliest possible period, and one of the results of 
recent progress in the medical art is increased pos- 
sibility in this direction. We can recognize diseases 
which, though existing, were unknown to practition- 
ers of thirty or fifty years ago, and we can also de- 
termine the existence of some of these affections at a 
much earlier period of their evolution than we could 
ten or even five years ago. The sciences of semeiol- 
ogy and of diagnosis have unquestionably progressed 
greatly in the last generation, and this is more espe- 
cially shown in the history of specialties, as ophthal- 
mology, dermatology, gynecology, and neurology. 
I may be permitted to say that it is a duty and priv- 
ilege of the specialist to inform the profession at large 
of the advances made in his department in diag- 
nosis and therapeutics, in order to enable the gen- 
eral practitioner to apply the new knowledge, or the 
confirmed old knowledge, to the advantage of -his 
patients. 
It is with such a motive that I would call your 
attention to the possibility and desirability of an 
early diagnosis of two or three organic diseases of 
the nervous system. Probably I shall name no new 
symptoms, but will aim to call your attention to the 
really valuable symptoms of these affections, and to 
the significant grouping of these symptoms. 
I have selected three affections which are now 
quite well known to us, and yet which, judging from 
my experience, are frequently ignored during long 
periods of their formative periods : I refer to poste- 4 
rior spinal sclerosis (progressive locomotor ataxia),, 
dementia paralytica, and cerebral tumor. 
I. Posterior spinal sclerosis, or progressive loco- 
motor ataxia. 
While willing to admit the occasional occurrence 
of abnormal cases of this disease, in which ataxia 
appears with little premonition, yet I claim that 
the general practitioner at the present day should 
diagnosticate the disease in the clearly defined first 
stage, or pre-ataxic period, which may last from a 
few months to several years. The vast majority of 
cases exhibit this first stage, and its symptoms are 
peculiarly characteristic, if not pathognomonic. In 
general terms the symptoms of this first stage con- 
sist in peculiar pains, and in reduction or abolition 
of reflex movements in different parts of the body, 
and from a combination of these a diagnosis of great 
probability of accuracy can be made years before the 
patient’s gait becomes disordered. 
If we assume that nineteen out of twenty victims of 
posterior spinal slcerosis pass through this neuralgic 
or pre-ataxic stage, we will not be far out of the way. 
The pains of posterior spinal sclerosis are almost 
pathognomonic, especially when described by an in- 
telligent educated patient. They have the following 
characters: 
a. The pains are vagrant; they occur in innumer- 
able spots in the affected parts—so much so that pa- 
tients who have long had them are unable to fully 
enumerate the localities in which they have suffered; 
or, rather, they can hardly name a region which has 
escaped. 
b. The pains do not, as a rule, occur in the course 
or distribution of recognized nerve-trunks or branch- 
es ; they are local pains, and this peculiarity may serve 
(with a) to distinguish between the pains of sclerosis 
and those of true neuralgia (sciatica, etc.). 
c. The seat of pain is commonly in an area of skin 
varying in size from that of a pea to that of a small 
hand. In many cases pains are also referred to the- 
muscles, to the vicinity of bones, and even to artic- 
ulations and viscera. 
d. The pains are paroxysmal in a completely irreg- 5 
ular manner: they may occur every few moments for 
hours in one spot, or may be altogether wanting for 
weeks; or at times a single pain is the signal that 
the disease is not cured. It seems probable that the 
atmospheric disturbance which precedes a storm 
(areas of low barometer) causes an increase in this 
symptom, or even calls it forth. 
e. The pains are sudden and vary in severity from 
■the sensation caused by the penetration of a small 
knife-blade to wrhat we may imagine to result from 
bearing through the tissues, with a hook or large 
knife ; or the sensation is like a painful electric 
shock. Perhaps most of the pain in such cases is in 
the shape of stabbing pains in an ovoid or round area 
of the skin (foot, thigh, arm, shin, etc.), repeated 
every few seconds for hours or even a day or two. 
The suffering is often such as to make the strongest- 
willed man writhe and shriek. The description of 
the pains, i.e., their comparison with known sensa- 
tions or physical conditions, varies greatly, accord- 
ing to the fertility of the patient’s imagination and 
his command of language. From their suddenness 
and electric character the pains of posterior scle- 
rosis are often called fulgurating or terebrating. The 
seat of pain usually is hyperalgesic, i.e., painful to 
the lightest touch during the paroxysm; yet firm 
pressure sometimes gives relief. 
Second.—Diminution of various reflexes through- 
out the body. 
This is best observed in the iris and at the patellar 
tendon, though the constipation and imperfect mic- 
turition which are such frequent symptoms of the 
disease are phenomena of the same order. 
a. The impairment of iritic reflex action (“pupil- 
lary reflex”) was first intelligently studied in 1869 by 
Dr. Argyll Robertson, of Edinburgh. His observa- 
tions have since been abundantly verified by numerous 
observers, and an exhaustive paper on the subject 
has been published by Prof. W. Erb, of Leipzig, in 
the Archives of Medicine, October, 1880. Robertson 
and others after him noticed that the pupil of tabetic 
patients did not dilate in the shadow and contract in 
the light, as do normal pupils; and they further ob- 6 
served that during the effort of- accommodation there 
occurred a normal pupillary contraction. In other 
words, the reflex iris movements were abolished, while 
its associated quasi-voluntary movements were pre- 
served. These phenomena I have observed in almost 
all my patients suffering from posterior spinal scle- 
rosis, and I am in the habit of calling the attention of 
students to the symptom. In two of the patients now 
under my care this condition is not present, but there 
have been cases of abnormal sclerosis, in which all 
the symptoms appeared, in a most irregular manner. 
The pupils in a suspected case of posterior- 
spinal sclerosis are to be tested in the following 
manner: the patient is placed, seated or standing, 
facing a brightly illuminated window, and told to keep 
his look fixed on some distant object, such as a house 
or tree. By alternately closing and opening the lids, 
or better, by shading the eyes with one’s hand mo- 
mentarily, it is easy to see if the pupils change 
diameter. It is of the utmost importance that the 
patient’s intelligent assistance be secured, in order 
that his gaze shall remain adjusted for distance. In 
a given case the absence of reaction to light having 
been noted, we next hold up one finger or a small 
object within a foot of the patient’s face and bid him 
look at it. At once the pupils contract and do so in 
proportion to the accommodative effort and the coin- 
cident convergence; when the patient looks at the 
distant object, and relatively or absolutely relaxes his 
accommodation, the pupils dilate again. 
The finding of such a condition of the pupil—the 
existence of Robertson pupils, if you will allow the ex- 
pression—is now considered of nearly as much im- 
portance for diagnosis as the occurrence of fulgu- 
rating pains. 
b. Diminution and abolition of reflex action in the 
peripheral apparatuses is best studied at the knee. 
We test the so-called patellar reflex or knee-reflex 
or patellar tendon-reflex in the following ways : the 
patient being seated, is told to cross one leg over the 
other in a natural manner, and to let the muscles re- 
lax ; or seated, we place our left hand under the pop- 
liteal space, tell the patient not to help us, to let the 7 
leg hang loose, or, in popular parlance, “ dead,” and 
lift tlie whole limb so that the foot swings a couple 
of inches above the floor ; then we tap the skin over 
the whole of the region from the insertion of the 
quadriceps femoris to the tuberosity of the tibia, with 
one or two finger-tips applied as in percussion. The 
place whence a reflex quadriceps contraction is most 
apt to occur is about midway between the lower end 
of the patella and the tibial protuberance. The taps 
should be gentle at first, and if these fail, harder ones 
are to be tried. A third mode of procedure, which 
is very good indeed, is to seat the patient on a table 
so that his legs dangle some two or three inches be- 
yond its edge ; then we tap the patellar region as 
above described, without supporting the thigh with 
our left hand. The test may be well done through 
the patient’s clothing, yet it is desirable, especially in 
doubtful cases, to tap the bare skin. Another impor- 
tant precaution is to secure the absolute relaxation 
of the patient’s muscles, and to divert his attention 
from what you are doing. Even with all precautions 
it is sometimes next to impossible to secure this 
indispensable muscular relaxation. In the healthy 
subject this test develops a contraction of the quad- 
riceps extensor femoris and causes an extension of 
the leg, or a sudden Jerk. In a very early stage 
of posterior spinal sclerosis no contraction takes 
place. 
I would also call attention to the occasional occur- 
rence of reflex movements of the thigh produced by 
contraction of the iliac group of muscles during the 
knee-test. I have an example of this distant reflex 
action in a typical case of sclerosis of the posterior col- 
umns, in which the quadriceps does not contract at all. 
While claiming very great diagnostic value for this 
negative symptom, I would not be understood as at- 
taching pathognomonic significance to it, as we all 
know that there are a few seemingly healthy indi- 
viduals in whom the patellar tendon-reflex is lack- 
ing, and also that there are other diseases which 
diminish or abolish it. Indeed, I may say that I 
recognize no pathognomonic symptom, and even in 
attempts to push diagnosis to an extreme delicacy, 8 
would urge that reliance be placed on the grouping 
of symptoms, rather than on any one of the signs, 
however constant and important it may appear. 
Physiologically analogous to this condition of loss 
of tendinous reflexes is the flabby state of the mus- 
cles in the affected parts. This is not due to any 
positive atrophy, as electrical tests show us marked 
departure from the normal reactions ; but to impair- 
ment of what physiologists call muscular tonus, a state 
of partial contraction or tension of muscles which 
is kept up by the inevitable and continued excitation 
of the cutaneous nerves by air, clothing, surrounding 
objects, etc., acting in a reflex way through the spinal 
cord. It has been recently claimed that this loss of 
muscular tonus was the most important factor in the 
production of the ataxic movements which character- 
ize the second stage of the disease. 
The vesical and rectal reflexes are diminished in 
posterior spinal sclerosis. Slow, irregular micturi- 
tion is complained of by most patients, in the first 
stage and in the second. We usually micturate 
without using much volition, but the tabetic patient 
is obliged to strain and to try hard to pass water. 
Defecation is, like micturition, a semi-voluntary act, 
and in the late first stage of the disease in question 
constipation becomes more and more marked, and 
that through loss of the automatic or reflex action of 
the rectum and adjacent muscles. 
The sexual act is, in my experience, frequently im- 
paired and sometimes almost lost before the second 
stage sets in. The acts of erection and emission are 
usually brought about in a reflex manner by irritation 
of the skin and mucous membrane of the genitals. 
As a result of diminished spinal reflex action we have 
imperfect erections, and either premature emission, 
or, what is more common, I believe, very slow pro- 
duction of the orgasm, and impossibility of repetition 
within a reasonable time. 
Some writers admit abnormally great sexual power 
in the early stage of tabes, but I am not sure to 
have met with more than one or two cases in which 
this seemed to be the case. In one of the patients, 
a female, I became convinced that her extraordinary ■capacity for sexual intercourse was not in a strict 
sense pathological or pre-tabetic, but had been 
marked in one shape or another from childhood. 
It seems reasonable at the present time to advance 
this general proposition: that in posterior spinal 
sclerosis the various reflex actions performed by 
means of those portions of the cord which are the 
seat of sclerosis, are diminished or lost; or, to put 
it in another way more useful for practice, it may 
be said that the limitations of loss of reflex action 
in different parts of the body accurately indicate 
the limits of sclerosis in the posterior sensory ap- 
paratus in the spinal axis. 
Third.—The occurrence of paralysis of ocular 
muscles. 
A very large proportion of tabetic patients tell of 
past or present diplopia, and in a certain number 
of cases the ocular paralysis precedes the pains 
.and ataxia by several years. So true is this state- 
ment, that it has become an established practice 
with neurologists and ophthalmologists to suspect 
posterior spinal sclerosis in adults who present 
themselves with strabismus, diplopia, or ptosis. In 
such a case we should carefully question the patient 
about the occurrence of fulgurating pains, test the 
pupillary and tendinous reflexes. I need hardly add 
that another obligatory line of inquiry in such cases 
is with reference to symptoms of syphilis. 
The same remarks apply to atrophy of the optic 
nerve, which is occasionally an early symptom. 
I have not the time to refer to the gastric, laryn- 
geal and rectal crises and the peculiar forms of arthri- 
tis which once in a while occur early in the dis- 
ease. 
It seems to me that, by a critical appreciation of 
the above symptoms in a patient, the diagnosis of 
the first or neuralgic stage of posterior spinal sclero- 
sis is as certain as the diagnosis of any internal dis- 
ease, not excepting such affections as pneumonia or 
valvular cardiac disease. Several autopsies are now 
on record, made during this first stage, and in these 
sections of the cord showed sclerosis of the posterior 
.columns. I have one such observation of my own : 10 
fulgurating pains for about thirty years, absence of 
patellar reflex while under observation (two years), 
dilatation of one pupil, no trace of ataxia. The 
sclerosis of the posterior columns in this patient’s 
spinal cord is visible to the naked eye. 
It is often objected that the pains of ataxia are 
not absolutely reliable for diagnosis. This may be 
true when the patient is stupid, or when the physi- 
cian is not careful to ascertain the precise character 
of the pains. 
The only two conditions in which pains somewhat 
resembling fulgurating pains occur, in my expe- 
rience, are paralytic dementia and gout. In the 
former disease, slight fulgurating pains—“ smaller ” 
pains, if I may be allowed the expression—are de- 
scribed by the patients ; but in many of these cases 
autopsy shows that, besides the cerebral lesions 
proper to the disease, the posterior columns of the 
cord exhibit pathological alterations; so that these 
cases are, after all, gwosi-tabetic. The sharp pains of 
gout are short, stabbing pains in the skin of various 
parts of the body, compared by the patients to the 
prick of a needle, cold or hot. There is no ten- 
dency to repetition of the pain in one spot for hours 
or days; the sensations appear in various parts of 
the body, and are bearable. It is but right to add 
that this statement is based on very few observations, 
and requires verification. 
The differential diagnosis of fulgurating pains 
from the pains of neuralgia, strictly speaking, is very 
easy. In neuralgia the pain is in the course and 
distribution of one or two (seldom) nerve-trunks 
and their branches ; it may be paroxysmal, but does 
not assume the excessive irregularity of the tabetic 
pains—agony for a few hours, and freedom from 
pains for hours, days, or weeks. The hyperesthe- 
sia in fulgurating pains is at the seats of pain. In 
neuralgia we find regular “tender points” along the 
nerve-trunk, or where its branches become superfi- 
cial. The lightest touch causes pain in the painful 
districts in tabes, while the tenderness of nerves in 
neuralgia is usually demonstrable only by firm, lo- 
calized pressure. Further, true neuralgia is seldom 11 
bilateral, while it is the rule for fulgurating pains to 
appear on both sides of the median line—in both 
lower extremities, for example. A last important dis- 
tinction is that neuralgia is relievable or curable, 
whereas fulgurating pains are practically incurable, 
and are fully relieved only by morphia-injections. 
The confusion so often made between “ rheuma- 
tism ” and the first stage of sclerosis is even less 
pardonable. Of course no practitioner would mis- 
take fulgurating pains for articular rheumatism ; the 
error is with respect to “rheumatism,” so-called, af- 
fecting muscular masses, and aponeuroses. In these 
affections the pains are usually dull, nearly constant, 
and distinctly aggravated by movements. Pressure 
must be firmly made upon the parts to produce pain, 
whereas in fulgurating pains the condition is one of 
cutaneous hyperalgesia under a slight touch. Again, 
this “rheumatic” condition is distinctly amenable to 
treatment (counter-irritants, etc.), whereas the pains 
of posterior spinal sclerosis are, in one sense, incur- 
able. 
11. The second disease of the nervous system to 
which I would direct your attention as the object of 
more exact and earlier diagnosis is paralytic dementia. 
By this term is meant the passive form of an affec- 
tion which consists in peri-encephalitis, adhesion of 
the meninges, and various secondary degenerative 
changes in the brain and in the posterior columns of 
the spinal cord. Chronic peri-encephalitis also pre- 
sents itself in an active or delirious form, which is 
known as general paralysis or paresis. In neither 
form is there a positive condition of paralysis at any 
time, except as a complication from the occurrence 
of cerebral hemorrhage or softening. Both the seme- 
iological names, paralytic dementia and general pare- 
sis, are, strictly speaking, misnomers ; yet we accept 
them as sufficient. 
The semeiology of peri-encephalitis is complica- 
ted, and it would be beyond the scope of this essay 
to describe it in detail. I merely wish to call your 
attention to the symptoms which, in my opinion, are 
earliest in their appearance and significant of an in- 
curable disease. These are tremors or fibrillary con- tractions in various muscular groups, especially in 
the tongue, facial, and brachial muscles ; a tremulous, 
thick, and vibratory speech; inequality of the pu- 
pils ; dementia. 
The tremor of paralytic dementia probably first 
makes it appearance in the facial and lingual mus- 
cles. It consists in non-rhythmical contractions of 
small muscles or of fasciculi of muscles, which are 
either present in the quiescent state of the features, 
or are excited by emotion or by the performance of 
a voluntary movement, as showing the tongue or the 
teeth. Sometimes innumerable fine fibrillary tre- 
mors cover the face, while in some cases the move- 
ments are coarser and irregular enough to merit the 
term choreic. The tongue exhibits both sets of tre- 
mors—the very fine fibrillary ones and the large cho- 
reic oscillations. There is also, though usually at a 
later stage, some shrivelling or atrophy of the tongue. 
The hands are tremulous, usually in a fine semi- 
rhythmical way. This trembling is sometimes scarcely 
visible, but is perceptible as a delicate parchment- 
like fremitus on holding up the patient’s extended 
fingers between ours. In the lower extremities the 
tremulousness is not apparent. 
The speech is affected as a result of this tremor 
and as the result of a certain want of co-ordination 
in the muscles of articulation. Words are quickly 
spoken, with some syllables omitted or blurred, or 
with a terminal syllable left off. The articulate 
sounds which are produced are heard as vibratory or 
tremulous, and the speech seems thick. Patients 
semi-unconsciously avoid long or difficult words in 
conversation, and even seek roundabout ways of ex- 
pressing their meaning by shorter words. Besides 
this vibratory tremulousness in articulation there is 
an imperfection in the pronunciation of words, long 
words especially. Remedy is pronounced “ remdy ; ” 
constitution, “ constution; ” infallibility, “ infal- 
liby.” The last syllable may be badly sounded or 
even omitted. I have known this characteristic 
speech to be the only well-marked symptom, and to 
be followed by dementia, exaltation, etc. Occasion- 
ally a patient comes to us complaining of this de- 13 
fective articulation. I now recall two such cases, one 
of which died three years later in a German private 
asylum, with all the symptoms of general paralysis. 
Just as spoken language is affected by the facial 
and lingual tremor, so is the handwriting altered by 
fibrillary contractions in the muscles which govern 
the movements of the fingers. A tremulous, jagged, 
wholly irregular handwriting results, and in some 
cases, where dementia is present, words or syllables 
are frequently omitted in composition. 
The pupils in paralytic dementia are either very 
small or irregular, usually the latter. The reaction 
of the iritio muscle to the influence of light may be 
diminished or abolished. 
I may here say, by way of parenthesis, that small 
and unequal pupils in a person of middle age, from 
twenty-five to sixty, should lead to an inquiry into 
the possible existence of one of three morbid states, 
viz. : paralytic dementia (or general paralysis), scle- 
rosis of the posterior columns, cardiac or aortic dis- 
ease (intrathoracic disease). 
In my experience, the patellar tendon-reflex is 
often increased in paralytic dementia. 
The dementia or failure of mental power is some- 
times impossible to detect until after the more peri- 
pheral, physical symptoms have existed for some 
time. It is possible for the psychical symptoms to 
precede the physical; sometimes the two appear to 
develop simultaneously ; usually, I believe, the phy- 
sical symptoms already studied are apparent for 
months before the mind shows decay. 
Dementia is evidenced by impairment of memory 
for recent events, by loss of the power of compari- 
son, and consequently of judgment. Many of the 
automatic or quasi-automatic acts of every-day life 
which form a part of the patient’s manner and indi- 
viduality are badly performed or omitted. This leads 
to what is known as change of character in the sub- 
ject ; he becomes less neat in his attire or personal 
cleanliness; he loses his table-manners, handling his 
spoon, fork and knife awkwardly, soiling his clothing 
with drippings of food, etc. This impairment of 
judgment is probably one of the factors in the ira- 14 
morality and tendency to alcoholic indulgence which 
are so frequent in this disease. 
Yet, in the midst of this increasing moral wreck, 
so visible to the immediate relatives of the patient, 
there may remain a degree of correctness in thought 
and success in every-day occupation which may im- 
pose upon strangers, and even upon a judge and 
jury. The things which the patient is in the habit 
of doing every day, and about which he has thought 
many years, such as professional work and business 
transactions, may be fairly well executed, while the 
tremors, pupillary irregularity, impaired articulation 
and handwriting, together with alteration of moral 
character, make the medical observer recognize a 
fatal, progressive disease of the brain. These cases 
come more frequently under the observation of gen- 
eral practitioners than under that of the specialist, 
whether asylum physician or neurologist. They are 
very frequently in our midst, and their early recogni- 
tion may save much disgrace and impoverishment to 
families, though, alas ! it does not pave the way for 
more successful therapy. 
I would repeat, that a person exhibiting tremors 
of the facial muscles of the tongue and hand, a vi- 
bratory and slurred speech, angular or tremulous 
handwriting, and irregular, small pupils, should be 
suspected of having chronic peri-encephalitis or par- 
alytic dementia. The addition of gradual failure of 
mind—-dementia—makes the diagnosis certain. In 
case there should be superadded exalted notions, 
with maniacal attacks and epileptiform seizures, the 
case deserves the name of general paresis, and as 
such is the form more usually seen and studied by 
asylum physicians. 
It has been claimed in the last few years by Four- 
nier and others that cerebral syphilis, in the shape 
of arteritis, partial arachnitis and localized peri- 
encephalitis, might give rise to the symptoms of 
paralytic dementia. lam in accord with Dr. Julius 
Mickle and others in believing that it is often 
possible to distinguish the idiopathic from the 
syphilitic dementia. The latter is, comparatively, 
much more acute (or rather less chronic), in its de- velopment; in it we do not observe the very fine 
muscular tremors as an early symptom; the pupil- 
lary disturbance consists usually of mydriasis of one 
side, with or without other signs of third-nerve palsy; 
the speech defect is a coarse thickness in pronunci- 
ation, rather than a vibratory, tremulous sound, 
which, when once heard, can never be forgotten. 
There are well-marked paralytic symptoms, usually 
hemiplegic, and decided epileptic phenomena in syph- 
ilitic cortical diseases. The dementia is seemingly 
more profound, causing an apparent imbecility with 
want of control over the sphincters. Altogether, the 
symptom-group is much more threatening in appear- 
ance, yet great improvement or even apparent cure 
may be obtained in very bad cases by the use of 
mercury and the heroic dosing by iodide of potassi- 
um. This therapeutic proving of a disease is of course 
valuable in practice, but logically it cannot be termed 
a diagnosis, and it is a reproach to the present state 
of our science that in several types of disease we 
should be obliged to resort to it. 
111. The third organic disease of the nervous sys- 
tem which should, it seems to me, sometimes be rec- 
ognized with positiveness much earlier than it now 
is, is tumor of the brain. 
In making this statement I am perfectly aware 
that some cerebral tumors produce no distinct or 
special symptoms during life, and that others pro- 
duce incongruous and apparently paradoxical symp- 
tom-groups. Some years ago, before the physiology 
of the brain was as well understood as it is now, we 
could offer no explanation of these perplexing cases 
which seemed to destroy our rules of diagnosis. To- 
day we have acquired an approximately correct 
knowledge of which portions of the brain (cerebrum 
especially), are excitable and capable of causing 
symptoms, and which are inexcitable, and may be 
the seat of extensive disease without clear indi- 
cations. This I say without reference to the finer 
localization theories of the last five years. We know 
quite positively, for example, that extensive lesions 
may exist in the anterior and inferior portions of the 
frontal lobes, in the sphenoidal lobes, and in the 16 
occipital lobes of the cerebrum, and in one-half 
of the cerebellum, without causing any symptom 
specially useful for diagnosis, such as will be con- 
sidered later on. We have also learned, from Flech- 
sig’s researches, that the decussation of the motor 
tract just below the anterior pyramids of the medulla 
oblongata is variable in amount, and that in some 
cases there may be no crossing of fibres, or hardly 
any. This important law of variability in the pyram- 
idal decussation enables us to correctly appreciate 
the rare cases in which a cerebral lesion produces 
symptoms (paralysis or spasm) on the same side of 
the body as itself—cases which have been so urgently 
pressed upon the profession by Brown-Seqnard in 
the last ten years as proofs that our physiological 
laws of cerebral action and of the productions of 
symptoms were all wrong. These laws stand to-day, 
I believe, only strengthened by the exceptions which 
have been adduced. 
All I wish to say is that tumors located in what 
we now term the excitable region of the cerebrum, or 
the motor zone, are capable of very early recognition. 
The region which receives the name of motor zone 
is irregular in shape, and perhaps its limits are not 
yet well ascertained. In a general way we may say 
that it includes the median region of each hemi- 
sphere, in particular the posterior extremity of the 
third frontal convolution, the upper half of the second 
and first frontal, the ascending frontal and ascending 
parietal convolutions, the anterior gyri of the island 
of EeiL the paracentral lobule on the inner surface of 
the hemispheres, and, perhaps, a large part of the 
upper set of parietal convolutions. These are the 
motor convolutions, and embrace the so-called motor 
centres of Ferrier. Besides, we must include under the 
name of motor zone, or region, those fasciculi of white 
substance which connect the above-mentioned gyri 
with the crura cerebri, constituting the anterior half 
(or less) of the internal capsule as it passes between 
the nucleus lenticularis on the outer side and the nu- 
cleus caudatus and thalamus opticus on the inner side. 
The succeeding remarks apply to tumors which 
involve any of this large expanse of cerebral sub- stance, either in its external gray matter or in the 
fasciculi of white substance lying between the motor 
convolutions and the central gray bodies. 
The symptoms which I think are characteristic 
of tumor in the motor zone of the hemispheres 
are: 
Localized convulsions in peripheral muscles; 
equally localized paralysis of peripheral parts ; neu- 
ro-retinitis or choked disk ; localized headache. The 
symptoms are named in the order of their frequency 
and importance. 
The initial convulsions of cerebral tumor are 
sometimes restricted to one side of the face, one 
hand, or even two fingers, or one leg. The spasm is 
usually tonico-clonic, but may be wholly clonic or 
jerky. In many cases this localized spasm is unac- 
companied by loss of consciousness or vertigo, and 
it may remain localized in the part first affected 
during many attacks, extending over weeks and 
months of time. The patient feels the muscular 
contraction before it becomes evident, thus consti- 
tuting a sort of aura. In some cases almost from the 
first, in nearly all cases after a while, the convulsion 
involves more muscles on one side of the body; it 
seems to ascend or descend, to use the patient’s ex- 
pressions, and there results a hemiplegic epileptic 
attack with loss of consciousness. Again, the at- 
tack may begin in a small peripheral part, involve 
the whole of one side of the body, and later affect 
the opposite side, thus constituting a full epileptic 
attack. The patient is able to watch the progress 
of the spasm for a number of seconds or minutes be- 
fore losing consciousness or being thrown down, and 
we may take advantage of this peculiarity to instruct 
the patient in the use of the tourniquet or bracelet, 
placed on the limb just above the seat of first spasm, 
to cut short the attack by pressure. 
This distribution of spasm, and its possible occur- 
rence without loss of consciousness, are signs which 
most positively distinguish these symptomatic con- 
vulsions from the ordinary epilepsy which we con- 
stantly encounter. 
As early as 1827, a French physician, Bravais, de- 18 
scribed the hemiplegic form of epilepsy and showed 
its relation to gross cerebral disease ; but it is to 
Hughlings Jackson, of London, that we owe the 
physiological study of these eases, and of cases of 
more limited epilepsy, and the first demonstration 
of the dependence of localized spasms upon limited 
lesions of the opposite cerebral hemisphere. 
Indeed, in prosecuting these clinical and post-mor- 
tem studies, Hughlings Jackson laid the foundation 
for the vigorous hypothesis of cerebral localization, 
as Ferrier states in the dedication of his book on the 
“ Functions of the Brain ” to this illustrious physician. 
So far as my own experience goes, autopsies have 
invariably verified the theory of localized epilepsy 
which I have stated, and the journals of the last five 
or six years contain numerous corroborative cases. 
As the evidence now stands, chronic localized con- 
vulsions must be looked upon as almost positive in- 
dications of a localized lesion in the opposite cerebral 
motor zone, most probably a tumor. 
What I have said of localized convulsions applies 
to localized paralysis. It, like spasm, may be limited 
to a small muscular group, or to one half of the 
body ; it may begin in a part and gradually extend. 
In general terms paralytic phenomena follow in the 
wake of the convulsions at a distance of weeks ox- 
months, and have the same distribution. 
Neuro-retinitis, or choked disk, is a frequent re- 
sult of tumor witlxin the cranium, but this symptom 
may, on the one hand, be absent with a large or 
even monstrous cerebral sarcoma, and on the other, 
it does not afford any indication of the locality of the 
tumor. The notion which was current a few years 
ago, that neuro-retinitis was pathognomonic of cere- 
bral tumor, is wholly without foundation. 
From my observations I am led to conclude that 
the occurrence of localized convulsions and paraly- 
sis, without choked disk, is valuable evidence of 
tumor, while choked disk without localized spasm 
and paralysis is merely a basis for suspecting tumor. 
The association of the two sets of symptoms makes 
up almost positive proof of the existence of a neo- 
plasm. A diagnosis based on this symptom-group 19 
is quite as secure as that of any other disease giving 
rise to local physical signs. 
The value of headache, of localized cranial pain 
more strictly speaking, is also variable. By itself it 
is not strictly indicative of tumor, but with either 
the choked disks or with localized motor disturbance 
it becomes highly significant. 
The co-existence of the three symptoms justifies a 
positive diagnosis of cerebral tumor. 
Had I more time I should like to speak of the 
possibility of a still finer diagnosis in cases of tumor 
of motor districts of the brain. We are sometimes en- 
abled, through recent advances in experimental phys- 
iology and pathological anatomy, to localize tumors 
within an inch or two of their actual situation, in the 
regions known as centres for speech, centres for the 
face, centres for the arm and hand, centres for the leg, 
and centres for both arm and leg. The future of neu- 
rological medicine is pregnant with discoveries in this 
direction, which will have very practical application. 
My purpose in embracing the opportunity of ad- 
dressing you was to make a sketch of the scientific 
and logical basis for progress in the direction of early 
diagnosis. 
The affections whose semeiology we have studied 
—cerebral tumor, paralytic dementia, and posterior 
spinal sclerosis—are as yet incurable. Yet, if we can 
ever hope to apply remedies to them successfully, it 
will have to be done at the earliest moment when 
their recognition is possible by the general practi- 
tioner, who naturally has charge of the cases in their 
incipience.