LECTURES 
ON TIIE 
LOCALIZATION 
OF 
SPINAL AND CEREBRAL DISEASES 
Delivered at the College of Physicians and Surgeons during 
the months of December, 18t7, and January, 1878. 
BY 
E. C. SEOUIN, M.D., 
Clinical Professor of Diseases of the Mind and Nervous System in the 
College of Physicians and Surgeons. New York, etc. 
Reprinted from The Medical for distribution 
to the Author's friends. 
NEW YORK: 
1878. L E 0 T TJ R E S 
ON THE 
LOCALIZATION 
OF 
SPINAL AND CEREBRAL DISEASES 
Delivered at the College of Physicians and Surgeons during 
the months of December, 1877, and January, 1878. 
E. C. SEGUIN, M.D., 
Clinical Professor of Diseases of the Hind and Xervous System in the 
College of Physicians and Surgeons, New York, etc. 
Reprinted from The Medical Record for distribution 
to the Author's friends. 
NEW YORK: 
1878. LECTURES ON THE LOCALIZATION OF 
SPINAL AND CEREBRAL DISEASES.* 
Lecture I. 
SUMMARY—INTRODUCTORY REMARKS—HISTORICAL CON- 
SIDERATIONS CONCERNING LOCALIZATIONS IN THE 
SPINAL CORD—PHYSIOLOGICAL ANATOMY, AND PHYSI- 
OLOGY OF THE SPINAL CORD. 
Oentlemen :—The Faculty having again done me 
the honor to assign to me some of the extra Thursday 
Lectures this winter, I have chosen as a subject the 
very practical question of the Localization of Diseases 
in the Spinal Cord and Brain. 
This topic is now engaging the attention of many 
of the best minds in the profession, and it is being 
made the object of careful observation and ardent 
controversy. Well-reported cases bearing on the 
question abound in the current medical literature. 
The subject has two principal aspects. One of 
these, that relating to the doctrine of the localization 
of functions in the brain and spinal cord, is more 
especially interesting to the physiologist and psy- 
chologist. The other aspect, that which concerns us as 
practical physicians, is with reference to the possi- 
bility of making an accurate diagnosis of the seat of 
the lesion in organic diseases of the nervous centres. 
It is this second aspect of the question which I shall 
discuss with you; and I shall endeavor to do it in as 
concise and practical a manner as possible—in such a 
way, in short, as shall enable you to utilize in your 
future daily practice the various principles and propo- 
* Delivered at the College of Physicians and Surgeons during the 
months of December, 1877, and January, 1878. 4 
sitions which I shall have the pleasure of presenting 
to you. 
In other words, the following lectures will be upon 
the rational diagnosis of cerebral and spinal diseases. 
In practice, when we have completed the examina- 
tion of a patient, several questions are put to us by 
the patient, by his friends, or by ourselves. These are 
in chronological order: Is there disease ? Where is 
the disease ? What is the disease ? What are we to 
do for the cure of the disease or for the relief of the 
patient ? Will the patient die or recover ? 
Of these questions the one which our client and the 
world at large consider the most important, is the 
fourth—that relating to treatment and cure. This 
preference is natural, but highly unscientific; it is a 
manifestation of that untrained mental action which 
demands results and scorns methods, which welcomes 
empirical achievements (provided they be agreeable), 
and which conduces to the perpetuation of quackery 
of all kinds. But to the physician who is not a mere 
prescription-writer, who aims at infusing as much 
science into his practice as possible, and who believes 
that he is not in the world for the purpose of gratify- 
ing his patients at so much per visit, but that he owes 
himself a debt of training and self-culture, and who 
has a sincere regard for science—to sucli a physician 
the first three questions assume a justly great import- 
ance. Pray observe that I do not say paramount 
importance, but great importance. And the su- 
periority of the humanitarian over the scientific duty 
becomes less glaring if we bear in mind the truth— 
and I firmly believe it to be such—that success in 
treatment now depends, and in the future will still 
more closely depend, upon the scientific study of the 
human subject in health and disease. In other words, 
I would impress you with my own conviction that the 
best trained and most scientific physician, if he be not 
a closet-student and theorizer, is the best practitioner. 
We occasionally hear of an oyer-fine diagnosis, of 
extreme caution in the treatment of disease, and of 
the sweeping application of physiological laws to 
practice by men who are said to be “ too scientific; ” 
but who can number the errors, nay the sacrifices of 5 
life which must be laid at the door of the falsely so- 
called “ practical men,” who despise learning and 
scientific methods ? Those of us who see something 
of the rarer and more formidable kinds of disease 
fully realize that in medicine, as probably in other 
applicable sciences, ignorance leads to rashness and 
crudity in practice, wfiiile ripe knowledge conduces to 
success, or, at any rate, to caution in prognosis and 
expectancy in treatment. 
Of the three diagnostic questions: Is there disease ? 
Where is the disease ? What is the disease ? the second 
is the one which forms the key-note of these lectures. 
Where is the lesion producing the disordered actions 
or symptoms ? The method to be followed in arriv- 
ing at the solution of this question varies somewhat 
in different departments of medicine. Some lesions 
can be seen by the trained unaided eye, or felt by the 
skilled hand; the seat of others can be determined by 
auscultation and percussion, by the aid of instruments, 
such as the ophthalmoscope, laryngoscope, speculum, 
etc. But in the study of the nervous system greater 
difficulties are met with; we are, to a great extent, 
deprived of these physical aids; we cannot appre- 
ciate the condition of the brain and spinal cord 
directly by our special senses, but only by a proper 
interpretation of the way in which the functions of 
these parts are performed. In other words, the diag- 
nosis must be made chiefly by reasoning. 
What are the conditions or data necessary for cor- 
rect reasoning in nervous pathology ? An enumeration 
of these will be a brief statement of the way in which 
I purpose treating the questions before us. 
First, you should possess a knowledge of the 
physiological anatomy of the parts concerned, viz., 
the brain and spinal cord. You are not obliged, for 
this purpose, to know much of the histology of the 
nervous tissue, but you should understand the ar- 
rangement of its various parts as recently revealed to 
us by perfected anatomy and embryology. 
■ Second, you must be well versed in the mode of 
life and action, or physiology of the cerebro-spinal 
axis. You must understand, as well as the present 
state of science allows, what parts are excitable and 6 
•what inexcitable, which transmit impulses and sensa- 
tions, which receive impressions, which originate the 
motor impulse, and which are endowed with special 
functions. 
Third, you need a thorough understanding of the 
perverted functions of the nervous system, and of 
other systems connected with it—i. e., of the symp- 
toms of nervous disease; you should cultivate semei- 
ology. And it is here more especially that previous 
general medical training is of great aid to the student 
of nervous pathology. 
Fourth, you must have a clear conception of the 
empirical knowledge already gained by numerous 
post-mortem examinations of persons who have died 
with disease in the nervous system. You should not 
accept every proffered autopsy, but critically analyze 
before making use of it. You may demand that it 
shall approximate a physiological experiment in ex- 
actness and in simplicity. 
Fifth, and not least, it is necessary that you have 
and use a keen critical and logical sense in the ap- 
preciation and combination of the above normal and 
morbid phenomena, in order that you may arrive at 
sound inductions. 
The importance of the combination of the above 
notions for the study of nervous diseases is immense. 
Any hypothesis, to be acceptable, must be based upon 
anatomy, physiology, semeiology, and pathological 
anatomy. The various crude theories which have 
reigned awhile in medicine were such as did not ful- 
fil this requirement: some of them were deductions 
from anatomical data, others applications a priori of 
physiological laws to medicine, others still based 
solely upon clinical studies, or upon autopsies. In- 
deed an effort is now being made to break down the 
growing doctrine of localization of lesions and func- 
tions in the brain by just such a one-sided argument. 
It is claimed by a high authority that facts of the 
fourth category (post-mortem contra- 
dict, in a perfectly overwhelming manner, the doc- ' 
trine in question. Now, I trust that, however feebly 
I may handle the subject, I shall yet be able at the 
proper time to give you good reasons why we must 7 
decline to accept and apply that authority’s facts as 
he does. 
Of the few who now deny that we can accurate- 
ly localize disease in small parts of the brain during 
the life of the patient, I would, finally, make this crit- 
ical remark. Their seemingly crushing argument is 
based upon what seems to me a fundamental error in 
the appreciation of natural phenomena, and that is, 
not making allowance for variability and mutability 
in the highly organized human frame. We now, since 
the labors of Darwin more particularly, admit that 
species in the animal and vegetable kingdoms are not 
fixed forms, but that they may pass into one another 
by almost infinitely numerous and delicately graded 
varieties; we know that the ultimate composition of 
high organic bodies (proximate principles like albu- 
men) varies somewhat; we are prepared to occasionally 
find (passing to the human organism) the viscera trans- 
posed, or to meet with an exanthematous fever without 
its rash, with a pneumonia unaccompanied by expec- 
toration, or with a painless peritonitis, etc. ; in other 
words, we are, as naturalists and physicians, ready to 
admit variability and irregularity in the organism. 
Yet, in spite of all this general and special knowledge, 
the opponents of localization maintain that there can 
be no irregularity in cerebral action, and they say, by 
implication at least, that the decussation of the ante- 
rior pyramids must always take place, and be total. 
They demand of those who believe in localization that 
they should be able to make every observed case har- 
monize with their generalizations. Is this reason- 
ing fit to be applied to natural history ? Are we pre- 
pared to make use of the mathematical method in 
pathology ? 
I shall treat, first, of localizations in the spinal cord 
and medulla oblongata; and, second, of localizations 
in the brain proper. 
I take up the spinal cord and medulla first because 
the phenomena are there more simple, and there is less 
controversy about them than there is with reference to 
the brain. 8 
HISTOKICAL CONSIDERATIONS. 
The now voluminous literature of diseases of the 
spinal cord does not teach us much with respect to 
the localization of its diseases. The writers of the 
end of the last century and of the first quarter of this— 
Frank, Sauvages, Rachetti, Abercrombie, Ollivier— 
adopted a pathological classification, which has been 
generally followed in systematic treatises since. Frank 
recognized, in a pretentious section of his great work 
on medicine, only spinal neuralgia (racliialgia), myeli- 
tis and spinitis (rachialgitis), and liydrorachis. Olli- 
vier, in his last edition, 1837, enlarges greatly upon 
this primitive list, and describes at least eleven mor- 
bid conditions of the spinal cord and its membranes. 
Brown-Sequard, in 1861, besides demonstrating, as he 
thought, the existence of reflex paraplegia, treats of all 
diseases of the spinal cord briefly, and makes an at- 
tempt at localizing lesions. He admirably points out 
how we can diagnosticate a lesion occupying one-half 
of the spinal cord (hemi-paraplegia and spinal hemi- 
plegia), and also how the height of a lesion in the cord 
may be estimated. Besides, he makes the first attempt 
at localizing disease in one of the columns of the cord, 
saying that when the anterior columns are alone in- 
flamed there is paralysis without anaesthesia and little 
dysaesthesia. He (not knowing of Turck’s researches) 
doubts the pathological independence of locomotor 
ataxia. 
In 1864 appeared Jaccoud’s excellent book, which 
chiefly treats of semeiology and aetiology of spinal dis- 
eases. He makes an advance upon previous writers, by 
considering the question of diagnosis of location of the 
lesion quite fully, and reaching the following conclu- 
sions: 1. Disease in the antero-lateral columns pro- 
duces palsy without alteration of sensibility; 2. There 
are no symptoms clearly indicating disease of the an- 
terior gray matter alone ; 3. It is easy to recognize if 
the aesthesodic tract is diseased (sclerosis of the pos- 
terior columns) by pain, increased reflex,* and anaes- 
* This word is used in a substantive sense, in imitation of German 
writers, to designate reflex movements. I think that the word is now 
much used orally by clinical teachers in this way. 9 
thesia ; 4. Lesion in one-half of the cord low down 
is indicated by hemi-paraplegia, high up by spinal 
hemiplegia. Leyden, writing in 1874-6, adopts the 
usual pathological classification, and his work is an 
admirable treatise. He in numerous places refers to 
the localization of lesions in the posterior columns, 
the lateral columns, the anterior cornua, the centre of 
the cord, and the nuclei of the medulla oblongata, 
pointing out the diagnosis of each. Hammond, 1876, 
gives a good resume of the state of knowledge on the 
subject, basing his classification in part upon notions 
of localization. 
But it is to monographs that we owe most in this 
branch of pathology. 
In 1851 Tiirck demonstrated the extent and exact dis- 
tribution of descending degeneration in the spinal cord 
secondary to cerebral lesions, and in 1857 he found 
the lesion in locomotor ataxia (then called tabes dor- 
salis) to be sclerosis of the posterior columns; Dr. J. 
Lockhart Clarke discovered the lesion of progressive 
muscular atrophy in 1861-2; Prevost that of in- 
fantile spinal paralysis in 1865; Prof. Charcot that of 
progressive labio-glosso-laryngeal paralysis in 1868; 
in 1865 the same observer published an autopsy of a 
case of sclerosis of the lateral columns (three others 
had been published by Tiirck in 1856), and in 1875 
Prof. Erb, of Heidelberg, and Prof. Charcot delin- 
eated the clinical features of this disease—spasmodic 
tabes, or spastic spinal paralysis. In 1874 Charcot 
described a mixed type, in which disease of the an- 
terior gray matter is combined with sclerosis of the 
antero-lateral column—amyotrophic lateral sclerosis. 
Disease in the central gray matter has been well stud- 
ied by Hallopeau 1869-70, and Schuppel, and by Ley- 
den, 1876. During the present year Prof. Flechsig 
has begun the publication of a series of papers upon 
the systematic diseases of the spinal cord, a work of 
the greatest merit, based in greater part upon the au- 
thor’s own pathological observations, and upon his 
yet more important embryological and microscopical 
studies upon the structure of the spinal cord (1873-6). 
As regards the diagnosis of the location of non-sys- 
tematic lesions (focal lesions) of the spinal cord we 10 
have made no material advance upon the data given 
us by Brown-S6quard in 1861. 
Let us now briefly review so much of the anatomy 
of the spinal cord as is indispensable to the study of 
the localization of its functions and lesions. I shall 
take it for granted that you are acquainted with the 
usual descriptive anatomy of the nervous centres, 
and call your attention chiefly to their physiological 
anatomy. 
The spinal cord is a mass of white and gray ner- 
disposed lengthwise in columnar form, 
and varying in relative proportions at various points. 
This finer arrangement of the gray and white columns 
is'best studied in transverse sections made at different 
heights in the spinal cord—for example, through its 
upper cervical part, through the cervical enlargement, 
through the lower dorsal region, through the middle 
of the lumbar enlargement, and near the end of the 
cord. In every such section we find the same parts, 
white and gray, but the shape of each is very different 
on the various surfaces. In general terms the gray 
substance or vesicular neurine is disposed in the cen- 
tre of the section in the shape of an irregular letter H, 
with clubbed ends forward. These ends, anterior and 
posterior, are called horns ; they are symmetrical on 
either side of one section, and the posterior reach 
out to the very periphery of the cord, dividing the in- 
closing white substance of each half of the section into 
two parts, the posterior column and the antero-lateral 
column. By means of pathological study, by histol- 
ogy, and more especially by means of embryology, 
these white columns have been much more subdivided. 
Following the latest arrangement by Fleclisig, we find 
in each lateral half of a transverse section of the spi- 
nal cord the following parts, proceeding from behind 
forward: 
n, 1. A small triangular column of varying size, lying 
next to the posterior median septum, in contact with 
its fellow of the opposite side, the posterior median 
column, or column of Goll. 
2. Externally to this, lying between it and the inner 
margin of the posterior gray horn, is a broad band con- 
taining the sensory fibres of the posterior roots, the 11 
posterior root zone, or zone radiculaire posterieure 
(Charcot), or column of Burdacli. These two consti- 
tute the posterior column of the simpler classification. 
3. A small zone lying next to the periphery of the 
cord, just anterior to the apex of the posterior horn— 
the direct cerebellar column. 
4. Between that and the body of the posterior horn 
lies an ovoid mass of fibres, the crossed pyramidal 
column—derived from the opposite cerebral hemis- 
phere by way of the anterior pyramid. 
5. Anteriorly to these two, occupying the sides of 
the section and reaching inward to the gray matter, 
we find the lateral columns. 
6. Lying in front of the anterior gray horns, and 
extending forward to the periphery, is the zone radicu- 
laire anterieure (Charcot), or anterior fundamental 
column. 
Fig. 1. 
Transverse section of the spinal cord.—A. Anterior median fissure ; 
P. Posterior median septum ; 1. Columns of Goll; 2. Columns of Ger- 
lach ; 3. Direct cerebellar column ; 4. Crossed pyramidal column ; 5. 
Lateral column : fi. Anterior fundamental column; 7. Direct pyra- 
midal column ; 8. Posterior gray horns ; 9. Anterior gray horns. Stip- 
pled part=gray matter. Shaded part=£esthesodic system. Unshaded 
part=kinesodic system. 
7. A strip of white matter lying on the margin of 
the anterior median fissure, extending quite to its bot- 
tom, is the column of Tiirck, or better, the direct 12 
pyramidal column—derived from the cerebral hemis- 
phere of the same side, by way of the anterior pyra- 
mid. 
The simple division of the gray matter into 8. The 
posterior horn ; 9. The anterior horn, will suffice for 
our purpose. In the accompanying wood-cut the 
above subdivisions are indicated by numbered spaces. 
In an equally aphoristic manner allow me to recall 
to you the chief physiological attributes of the spinal 
cord : 
1. It is an organ for conduction. Conduction 
takes place in two directions, centrifugally for motor 
impulses, and centripetally for sensory impressions. 
The paths (I will not say fibres) for sensory im- 
pressions ascend only a very small distance in the pos- 
terior columns (columns of Burdach) before they enter 
the gray matter, and there at once pass over to the oppo- 
site half of the cord (in man at least). Consequently we 
say that the conductors of sensation decussate in the 
spinal cord throughout its whole extent. Motor paths, 
on the contrary, in the spinal cord proper, remain in 
one-half of the organ white and gray matters; they 
have already decussated (jn part) at the crossing of 
the pyramids. A strange fact to be borne in mind is 
that very little gray matter may suffice to transmit all 
sensations. The illustration (Fig. 2) after 
Brown-S6quard, the course of sensory and motor con- 
ductors. 
2. The excitability of various parts of the spinal 
cord is a point of some interest. It has been quite well 
settled that no part of the healthy spinal cord is ex- 
citable, except the posterior columns; though very 
lately Professor Yulpian has discovered traces of ex- 
citability in the internal part of the anterior column. 
However, in morbid states, a great change occurs, and 
even the unquestionably inexcitable gray substance be- 
comes excitable, giving rise to various morbid sensa- 
tions and to spasm. 
3. The spinal cord has an autonomy of its own. 
giving rise to reflex motor impulses, and producing 
others spontaneously. It is also probable that sen- 
sory impressions are rendered more perfect in the 
spinal gray matter, but I am indisposed to attrib- 13 
ute consciousness to it. This organ furthermore pre- 
sides over (executes) many automatic acts, many of 
them highly complex; such as walking, swimming, 
standing, to a certain extent eating, dressing, playing 
upon musical intruments, etc. Part of the spinal 
gray matter is slowdy and painfully educated to per- 
form these actions, and can afterward do them with- 
out any marked cerebral interventions. 
Fig. 2. 
Course of motor and sensory paths in the spinal cord, after Brown- 
S6quard.—D. Decussation of pyramids ; M. Motor paths ; S. Sensory 
paths. 
4. Besides, the spinal gray matter is supposed to pos- 
sess a trophic function, to preside over the nutrition 
of muscles and other tissues, partly through the 
bloodvessels, and partly directly. This question is 
under discussion, but the fact remains, that disease of 
the anterior gray matter produces marked atrophy of 
muscles, and may cause joint-lesions. The spinal 
cord is also said to embrace several so-called centres; a 
genital or genito-urinary centre in the lumbo-dorsal re- 
gion, a cilio-spinal centre in the lower cervical region, 14 
and various subordinate vaso-motor regions ; of these I 
recognize only one as useful in such a study as the 
one we are beginning, viz., the cilio-spinal centre 
(Budge, Waller, Brown-Sdquard). There is a part of 
the spinal cord (in each of its halves), extending from 
the fifth cervical vertebra to the second dorsal verte- 
bra, which contains vaso-motor nerve-fibres for the 
corresponding side of the neck, face, and eye. It 
also contains fibres whose normal action is to cause 
a dilatation of the pupil. In estimating the height 
of a lesion in the spinal cord a knowledge of 
the location of this cilio-spinal centre is of real 
utility. 
To sum up the physiology and anatomy of the spinal 
cord I may divide its section-surface into two great 
territories, as indicated in Figure 1. The larger part, 
not shaded, embracing the anterior horns and all the 
antero-lateral columns, may be designated as the 
kinesodic system, and the smaller shaded portion, 
including the posterior horns and the posterior col- 
umns, as the sesthesodic system. As the names im- 
ply, the latter system conveys and receives sensory 
impressions, while the former transmits and originates 
motor impulses, and possibly is trophic in function. 
In the next lecture I shall systematically treat of the 
localization of disease in these physiological and 
anatomical subdivisions of the spinal cord ; first in 
the two systems, and second, in each column or horn 
within each system. 
Lecture II. 
SYNOPSIS.—1. SYSTEMATIC LESIONS OP THE SPINAL CORD ; 
LESIONS IN TIIE SYSTEM, LESIONS IN 
THE KINESODIC SYSTEM. 
Gentlemen:—As a basis for our study of the diag- 
nosis of the location of lesions in the spinal cord, I 
offer you the following classification, which I think 
embraces all that sound clinical observation and post- 
mortem examination will justify us in diagnosticating 
with certainty. 15 
I. Systematic Lesions of the Spinal Cord. 
II. Non-systematic or Focal Lesions of the Spinal 
Cord. 
By the former we are to understand pathological 
changes which involve one of the gray or white col- 
umns of the cord for a part or the whole of its extent 
up and down, without extension to adjacent columns. 
Such lesions are almost always symmetrical in the two 
halves of the organ; and occasionally more than one 
such lesion may be present. 
By the second form of lesion we understand a focus 
of disorganization or new tissue growth involving the 
spinal cord in a limited part vertically, and invading 
diverse columns, or even systems, transversely. These 
are the lesions en foyer of French authors. 
The first group may be subdivided as follows: 
I. Systematic Lesions of the Spinal Cord. 
a. Lesions in the /Esthesodic System. 
1. Sclerosis of the Columns of Goll. 
2. Sclerosis of the Columns of Burdach. 
b. Lesions in the Kinesodic System. 
1. Sclerosis of the Anterior Columns. 
2. Sclerosis of the Lateral Columns. 
a, with changes in Anterior Horns. 
3. Degeneration of the Postero-lateral Columns. 
4. Myelitis of the Anterior Horns. 
5. Degeneration of Ganglion Cells of Anterior 
Horns. 
6. Central Myelitis. 
In studying the above forms of disease, I shall apply 
more or less rigidly the following method: 
First, state the general symptoms which indicate 
disease in the part of the spinal cord (the system) 
affected. Second, accurately locate the lesion, and 
state the symptoms produced by it particularly. 
Third, say a few words concerning the disease in 
question. 
a. Lesions in the sestliesodic system are characterized 
by the following symptoms: Pain, usually of a pecu- 
liar kind, hypersesthesia, numbness, and anaesthesia; 
by a peculiar disorder in voluntary movements, viz. : 
ataxia: and, negatively, by the absence of true paraly- 
sis or spasm in the affected limbs. 16 
1. Sclerosis of the columns of Goll, or the posterior 
median columns. Whether in the ascending secondary 
degeneration, or idiopathically produced (one case), 
the lesion occupies the more or less exactly triangular 
space lying between the columns of Burdach. At the 
lowest part of the cord the lesion is hardly visible, 
owing to the smallness of the columns at this point, 
but in the cervical region it is quite large and distinct. 
At the calamus scriptorius the lesion disappears, and 
so far has not been traced higher up. In Pierret’s 
case these columns were sclerosed throughout their 
whole extent. In cases of ascending secondary degen- 
eration they are affected only above the focus of 
disease. 
The common lesion of the columns of Goll (sec- 
ondary degeneration) gives rise, so far as we now 
know, to no symptoms; consequently, we can only 
infer its presence by determining the existence of a 
lesion capable of producing ascending and descending 
degeneration in the spinal cord. 
The symptoms in the single case of idiopathic dis- 
ease of these columns (Pierret’s) are too uncertain and 
too badly reported to be of any use. They consisted 
in numbness, slight anaesthesia, and a tendency to 
retropulsion. 
It is right to conclude that we cannot to-day directly 
diagnosticate disease limited to the columns of Goll. 
2. Sclerosis of the columns of Burdach, or the pos- 
terior root-zones. The lesion begins in the outermost 
portion of these columns, near the inner margin of the 
posterior horns, and, extending forward and inward, 
ultimately occupies the whole of the columns of Bur- 
dach, as shown in the accompanying diagram. 
The section showing this lesion, which I now 
pass around, was taken from the cervical enlarge- 
ment of the spinal cord of a woman who had typical 
locomotor ataxia in the lower and upper extremities, 
gastric crises, diplopia, and amblyopia. In most fully 
developed cases of locomotor ataxia the sclerosis is 
found to occupy the posterior median columns as well, 
i. e., the whole of the posteriorcolumnsare degenerated; 
but, since the researches of Pierret upon the functions 
and pathological anatomy of the posterior median 17 
columns, we must look upon changes in them as sec 
ondary to the sclerosis of the columns of Burdach. 
Fig. 8. 
Location of essential sclerosis in locomotor ataxia. 
In complicated cases of sclerosis of the posterior 
columns there may also be sclerosis of the lateral 
columns, or degenerative changes in the central and 
anterior gray matter. 
The symptoms which are characteristic of sclerosis 
of the columns of Burdach are, in order of importance, 
pain, hyperaestliesia, anaesthesia, ataxic movements. 
I can only in these lectures call your attention to the 
great diagnostic symptoms, and must not attempt to 
delineate the semeiology, etc., of any disease ; yet the 
above symptoms deserve more than a mere mention. 
The pains are peculiarly characteristic—nay, almost 
pathognomonic. They are of several varieties. First, 
sharp, lancinating cutaneous pains, appearing in spots, 
usually circular or oval, in size from one to two 
inches in diameter, in any part of the limbs which are 
afterward to become ataxic. A few shootings may take 
place in one spot, or it may be the seat of pain for 
twelve or twenty-four hours. A capital point is the 
capriciousness with which the pains appear in any and 
all parts of the limbs—toes, thighs, calves, shins, etc. 
They are vagrant or vagabond pains, in sharp con- 
trast to the fixed neurol pain of neuralgia. Second, 
deep, boring pains; and third, tearing or bruising 
deeper pains, affecting the articulations as well. 18 
These pains are also vagabond and capricious in their 
mode of appearance. They may exist for years with- 
out anaesthesia and ataxia showing themselves, and 
both patient and physician are apt to speak of the 
pains as “ rheumatic,” instead of as pathognomonic of 
an incurable disease. Ilypenesthesia accompanies and 
succeeds the pain, more especially in the patches of 
skin which are the sea.t of stabbing pains. During 
the paroxysm, and for hours afterward, the patch or 
patches are exquisitely sensitive, and hyperalgesia 
exists. Anasstliesia is said to be present very early 
in the disease, as well as later. In the former case it 
occupies patches of skin on the legs, arms, and trunk, 
according to the extension of the disease. In the 
second case it is found under the feet, later in the legs, 
and may involve the whole of the lower (and upper) 
extremities toward the close of the disease. 
The ataxic walk consists in a jerky, stamping gait, 
the abductors and extensors acting over-forcibly; 
the want of co-ordination affects large muscular 
' groups, thus differing from chorea, paralysis agitans, 
etc. But a somewhat similar ataxia may be present 
in cases of intra-cranial disease, so that I would 
urge you to fall back upon the sensory symptoms for 
your diagnosis. 
Many practitioners employ what they consider a sure 
and ready test for locomotor ataxia, viz., they bid the 
patient try to stand with his eyes closed. If he stagger 
or fall, he is said to have the disease. Now, I would 
have you all bear in mind that this test is worthless. 
Oscillating with closed eyes is a symptom comjnon to 
many cerebral, spinal, and peripheral morbid states, 
as hysteria, myelitis, etc. I once artificially froze the 
soles of a patient’s feet, and showed him in this am- 
phitheatre with an excellent stagger when his eyes 
were closed. He staggered because his feet were 
anaesthetic, and that is one reason why hysterical 
women and the bearers of myelitis do the same. We 
may safely put it in this way : patients with locomotor 
ataxia, at a certain stage, do stagger when their eyes 
are closed; but, as the bearers of several other spinal 
diseases do the same, the sign has no special value. 
For many years, and even long after the patient is 19 
absolutely unable to stand, there is almost no paresis 
and no diminution of reflex or of electrical excitabili- 
ty in the affected extremities, unless the sclerosis ex- 
tend forward into the gray matter. 
We ought, I think, to be able to correctly diagnosti- 
cate this lesion in its first stage, viz., when only pain 
and hypersesthesia are present. 
Historical Considerations—The clinical history of 
locomotor ataxia has been fairly well known since 
1835 or 1840; German physicians describing it in 
great part under the name of Tabes Dorsualis. Rom- 
berg, in 1853 (and earlier), gave almost a perfect pic- 
ture of the disease ; but it was reserved for Duchenne 
(1859-60) to recognize the value of the pains and of 
the ataxia, as distinguished from paresis, as cardinal 
symptoms. Although Duchenne’s description of the 
affection has hardly been improved upon, it must be 
admitted that he knew nothing of its pathological 
anatomy, and was quite wrong in his explanation of 
the symptoms. Yet the lesion of locomotor ataxia, or 
tabes dorsualis, had already been discovered by Turck 
in 1857. Unfortunately, he buried his remarkable pa- 
per in the Transactions of the Academy of Vienna; 
and Gull (Sir William) independently made the same 
discovery in 1859. In France, Bourdon worked out 
the pathological anatomy in 1861, and since, our know- 
ledge upon the point has grown enormously. The 
anomalies of locomotor ataxia, both semeiological and 
pathological, have been best studied by Charcot and 
his pupils. In 1873, Charcot and Pierret published 
their cases demonstrating that the primary essential 
lesion of locomotor ataxia involves the columns of 
Burdach. 
b. Lesions in the kinesodic system are characterized 
by the following symptoms: paresis or paralysis, 
spasm, and muscular atrophy; and, negatively, by the 
absence of anaesthesia, or of marked and permanent 
pain or numbness. 
1. Sclerosis of the true anterior columns or columns 
of Turck, or, best, the direct pyramidal fasciculi, has 
been known pathologically since the publication of 
Tiirck’s first papers in 1851. Its semeiology is, how- 
ever, unknown. We can infer its existence in those 20 
cases in which we diagnosticate lesion No. 3 (infra), 
because pathological anatomy shows us that the two 
lesions are usually simultaneous. 
2. Sclerosis of the lateral columns. The lesion con- 
sists in an increase of the neuroglia and atrophy of 
nerve-fibres in the lateral masses of white substance 
throughout a greater part or the whole of the spinal 
cord. It may exist alone as a primary lesion, or may 
be associated with other (secondary) morbid processes, 
such as No. 4 (infra). 
The symptoms consist in progressive paresis of the 
lower limbs, and later of the upper, with increased 
reflex, and a tetanoid state of the extremities. There 
is very little sensory disturbance, never anajsthesia; 
the paralyzed and tetanized muscles do not undergo 
atrophy; and the bladder is not in the true sense of 
the word paralyzed. 
These symptoms have been designated by various 
names. Erb calls the symptom-group spastic spinal 
paralysis; Charcot, spasmodic tabes; and I would 
suggest the term tetanoid paraplegia or paralysis. 
Erb in 1875, and Charcot in 1876, Erb again this 
year, have fully described the clinical aspects of the 
disease. 
In 1873 I described, under the title of tetanoid 
pseudo-paraplegia, the symptoms of the semi-devel- 
oped disease, of that transition period when the pa- 
tient is still able to get about upon his morbidly stiff- 
ened limbs. I failed, however, to seize upon the 
whole clinical picture. 
The pathological anatomy of this affection does not 
as yet rest upon a firm basis. Tiirck in 1859 pub- 
lished three autopsies in cases of this sort, but their 
clinical features had not been worked out. In 1865 
Charcot reported sclerosis of the lateral columns as 
the lesion found in a woman who had suffered from 
aggravated hysteria, with contractures of the ex- 
tremities, for many years. In the essays of 1876-7 no 
other autopsies are recorded. 
2 a. Combination of lesion of the anterior horns 
with sclerosis of the lateral columns. Charcot, in 
1874, first called attention to this complex systematic 21 
lesion, and designated the disease as amyotrophic 
lateral sclerosis. 
The cervical enlargement of the spinal cord being 
nearly always the first part affected, we observe that 
the symptoms appear first in the hands; a paralytic 
atrophy setting in with considerable rapidity. Formi- 
cation and fibrillary movements may be present. The 
atrophy resembles more that observed in myelitis of 
the anterior horns (No. 4) than in degeneration of the 
ganglion cells of the anterior horns (No. 5). In a 
short time a degree of rigidity appears in the upper 
extremities, and the legs become first paretic, later, 
rigid and contractured. This contracture may be 
greatly relaxed while the patient is in bed, but is 
exaggerated if he try to stand or walk. In conse- 
quence of great atrophy of the interossei, the “ claw- 
hand ” deformity may appear. As a rule, the muscles 
of the lower limbs do not waste. The bladder and 
rectum are not paralyzed, and no anaesthesia is ob- 
served. If the patient’s life be prolonged, the disease 
invades the nuclei of the motor bulbar nerves, and to 
the above picture we have superadded the symptoms 
of labio-glosso-laryngeal paralysis. 
Cases of this kind had been observed prior to 1874, 
but it is Charcot who in that year first gave us a clear 
statement of the pathological anatomy and semeiology 
of the disease. The connection between the two 
lesions, disease in the anterior horns, and sclerosis of 
the lateral columns, is by no means understood, and 
it may be questioned whether they are pathologically 
related.* 
3. Degeneration of the posterior part of the lateral 
column, or (better) of the crossed pyramidal fascicu- 
lus. The lesion occupies, in a transverse section, a 
* Since this lecture was delivered, Prof. Flechsig, of Leipzig (in 
Archiv de.r Ifeilkunde, 1878, Heft 1), has made an elaborate critique 
of Charcot’s cases and others, and claims that the lesion in the lateral 
columns is chiefly in the postero-lateral columns, as in descending de- 
generation from cerebral lesiou, and that the nature of the lesion 
seems more like a degenerative than a sclerotic one. Flechsig suggests 
that future research may reveal a double lesion in the cerebrum, or, at 
any rate, in the upper part of the intra-cranial motor tract. This view 
seems to me well worthy of consideration, and a careful attempt 
should be made to verify it. 22 
part of the white substance which lies between the 
lateral column and the posterior gray horn. It is 
separated from the periphery of the cord by healthy 
tissue, the direct cerebellar fasciculus. This alteration 
of tissue is secondary to a lesion in parts of the ner- 
vous centres above the decussation of the pyramids; in 
the anterior pyramids, the great motor tract in the 
basis cruris cerebri, the anterior part of the internal 
capsule, the nucleus caudatus, the convolutions com- 
prising the excitable districts of the cerebrum. Le- 
sions of any of these parts cause what is known as 
secondary degeneration throughout the motor tract, to 
the lowest part of the spinal cord. Consequently, the 
lesion in the spinal cord is always (?) on the side oppo- 
site to that on which the primary, supra-spinal disease 
exists. Hence, also, we usually find descending degen- 
eration only in one-half of the cord. It should be re- 
membered, however, that, as a portion of the anterior 
pyramid of the medulla does not decussate, but de- 
scends as the direct pyramidal fasciculus, or column 
of Tvirck, we must expect to find in many cases a sim- 
ilar lesion of this fasciculus on the same side as the 
supra-spinal lesion (No. 1). For example, after a 
lesion involving the great motor tract in the left 
hemisphere, we shall find descending degeneration of 
the crossed pyramidal fasciculus in the right half of 
the cord, and of the anterior column, or direct pyra- 
midal fasciculus in its left half. 
The symptom characteristic of this morbid condi- 
tion is the secondary contracture, or late contracture, 
which so often succeeds attacks of hemiplegia, being 
superadded to paralysis or anaesthesia. This lesion 
may be complicated with No. 4, when atrophy of 
some of the paralyzed and rigid muscles supervenes. 
In briefly mentioning the historical data connected 
with this lesion, I must again mention Tiirck, the 
great pioneer in the pathology of systematic lesions of 
the spinal cord. In 1851 and 1853 he exactly de- 
scribed the crossed part of the lesion. An excellent 
study of this and other forms of secondary degenera- 
tion was made by Bouchard in 18G6, under the direc- 
tion of Profs. Yulpian and Charcot. Last year Flech- 
sig published his remarkable researches upon the ner- 23 
vous centres, and more exactly defined the seat of 
both the crossed and the direct degenerations. To 
Prof. Bouchard is due the credit of completing the 
clinical picture, by pointing out the value of the 
symptom contracture. 
1. SYSTEMATIC DISEASES OP THE SPINAL CORD, CON- 
TINUED; LESIONS IN THE KINESODIC SYSTEM. 2. 
NON-SYSTEMATIC OR FOCAL LESIONS OF THE SPINAL 
CORD ; LESIONS AT DIFFERENT HEIGHTS IN THE 
ORGAN. 
Lecture III. 
Gentlemen:—There remain for consideration a few 
of the systematic lesions of the spinal cord. 
4. Myelitis of the anterior horns, or poliomyelitis 
anterior. Like all affections of the kinesodic tract, 
this affection is characterized by the predominance of 
motor symptoms and the absence of sensory ones. But 
we also meet with great trophic changes—muscular 
atrophy—in this disease. 
The lesion consists, as we know from the autopsies 
by Gombault, by Cornil and Lepine, and by D6j6- 
rine, in an inflammation of the anterior gray horns of 
the spinal cord, leading to atrophy, and even destruc- 
tion of the motor (and trophic ?) ganglion-cells. The 
change in the cells is acute pigmentary degeneration. 
In those regions of anterior gray matter correspond- 
ing to the paralyzed parts, hardly any motor ganglion- 
cells remain. Other lesions are degenerative changes in 
the motor nerves, as far as their termination, and 
muscular atrophy, usually without fatty metamor- 
phosis. 
The symptoms of the affection vary in the three 
varieties : acute, sub-acute, and chronic. 
a. In acute febrile poliomyelitis anterior we observe 
a sharp, remittent or continued fever, lasting one or sev- 
eral days, accompanied in many cases by pains in the 
limbs, and sometimes by slight numbness. This is 
followed, suddenly, as a rule, by extensive paralysis, 
the fever ceasing. The paralysis may affect all the 24 
limbs, or two of them, or one only ; it tends to dimin- 
ish spontaneously to a marked extent. No anaesthesia 
is present, and but little numbness, lieflex move- 
ments are reduced or abolished, the bladder and rec- 
tum act normally, and there is no tendency to bed- 
sore. But other, even more characteristic symptoms, 
soon follow. In a few days the nerve-trunks in the 
severely palsied limbs lose their galvanic and faradic 
excitability, and the muscles, while ceasing to re- 
spond to the faradic current, contract slowly, and 
with abnormal formula, to the galvanic current—we 
have the degeneration-reaction. A little later, after 
two or three weeks, the palsied muscles undergo rapid 
atrophy, an atrophy which is progressive if no recov- 
ery is to take place. Ultimately only one muscular 
group may remain paralyzed and atrophied. 
b. There is a non-febrile acute myelitis anterior. 
The patient, usually a child, is put to bed well, and 
awakes in the morning with one or more paralyzed 
limbs, with the subsequent symptoms as above. 
In these two forms are to be ranged nearly all cases 
of infantile spinal paralysis so-called, and many cases 
of the same disease occurring in the adult. 
c, d. Febrile and non-febrile subacute myelitis of 
the anterior horns differ from the above only in de- 
gree of acuteness and in rapidity of development, and 
need no detailed description. 
e. Chronic myelitis of the anterior horns is often mis- 
taken for progressive muscular atrophy; yet a diagno- 
sis, is, I think, frequently possible. Often in this vari- 
ety of poliomyelitis there occur severe neuralgic pains 
in the limbs which are to undergo palsy and wasting. 
These phenomena, when they appear, weeks or months 
after the first symptoms, attack whole muscular groups 
at once, and we do not observe the fibrillary or fasci- 
cular wasting of progressive muscular atrophy. The 
reactions are like those found in the acute and subacute 
form. No anajsthesia appears. This rare form has 
been observed in children and in adults. 
It is only very recently that we have had a correct 
knowledge, clinical and pathological, of myelitis an- 
terior. Prior to 1865, infantile spinal paralysis, 
though well known clinically (Heine, 1840), was 25 
thought to be due to congestion of the spinal cord, 
etc. ; but in that year Prevost, working with Charcot, 
discovered the lesions in the anterior horns, and since 
numerous autopsies have yielded the same results. As 
regards the disease in the adult, it was correctly ob- 
served and classified as far back as 1847 (Duchenne), 
and in subsequent years by Charcot and others. Its 
pathological anatomy was not discovered until 1873 
(Gombault) and 1875 (Cornil and LGpine). Although 
we need more light upon the intimate nature of the 
pathological changes occurring in this disease, I be- 
lieve it to be now quite firmly established in nosology. 
Its diagnosis should be readily made by all prac- 
titioners. 
5. Degeneration of the ganglion-cells of the an- 
terior horns. As indicated by the name, the lesion in 
this affection is degenerative rather than inflamma- 
tory. This is true in the sense that changes in the 
neuroglia are wanting as a rule, and that the molecu- 
lar death of the ganglion-cells takes place very 
slowly. This is in marked contrast to the suddenness 
and extent of the lesion in No. 4. Ganglion-cells are 
found in every stage of transition from simple increase 
of normal granular contents to mere roundish masses 
of granules—granular bodies; in some parts of the 
anterior horns not even vestiges of cells remain. 
The symptoms of this lesion are fibrillary contrac- 
tions followed by atrophy. Sensory symptoms are 
wholly wanting as a rule, and in a few cases the wast- 
ing limbs are the seat of some neuralgic pains. There 
is at no time a true paralytic condition, since the loss 
of power is precisely in proportion to the destruction 
of muscular tissue. 
The mode of occurrence of the atrophy deserves a 
remark. Whole muscles or muscular groups do not 
waste away rapidly as in No. 4, but the muscular 
tissue undergoes change, bundle by bundle, very slowly. 
It thus happens that we see one or two large fasciculi 
in a muscle quite atrophied, while the adjacent fasci- 
culi of the same muscle are normal, or only show 
fibrillary contraction. Several months may elapse be- 
fore a muscle be wdiolly atrophied. Another feature 
of the atrophy is that it attacks by preference certain 26 
muscular groups, as those of the hand, chest, thighs, 
etc. It also affects simultaneously, or nearly so, parts 
which are symmetrical and homologous. If we ex- 
amine the wasting muscles with the faradic current, 
we obtain yet another diagnostic sign : in this affec- 
tion reaction to the faradic current is lost only in the 
absolutely atrophied muscles or parts of muscles. 
This loss of reaction is in direct proportion to the 
atrophy, w’hereas, in myelitis of the anterior horns 
whole muscles and muscular groups lose their faradic 
reaction en masse, and this, too, often before any 
marked degree of wasting has appeared. By the 
latter test, by the distribution of paralysis and atrophy, 
and by the predominance of neuralgic pains in chronic 
myelitis of the anterior horns, we may nearly always 
distinguish it from progressive muscular atrophy. Of 
course, the two diseases are congeners, and their 
pathological relationship may even be closer than we 
now suspect. 
Cruveilhier, Aran, Duchenne, and Roberts admira- 
bly described the clinical aspects of this disease, and 
its naked-eye pathological anatomy. But it is to the 
very recent labors of Lockhart Clarke (1861-2), and 
of Charcot and his pupils, that we owe the exact de- 
termination of the lesion in the anterior horns of the 
spinal cord. It is also only within the last ten years that 
we have clearly distinguished pure muscular atrophy 
from the various forms of symptomatic atrophy. 
6. Central myelitis. An inflammation of the central 
parts of the spinal gray matter, involving the aesthodic 
and kinesodic tracts, extending in some cases through- 
out the whole length of the organ. The proliferative 
changes and exudations result either in the formation 
of a central plug, or the development of a cavity, 
which is filled with clear fluid. The anterior horns 
and the various columns of the spinal cord are more or 
less involved through extension of inflammatory ac- 
tion, or by compression. As might be inferred from 
the above, the symptomatology of the affection is 
obscure and complex. Early in the disease, disorders 
of sensibility—as numbness, formication, and pain, 
followed by anaesthesia—are prominent. Irregularly 
distributed paralysis, with or without atrophy, is also 27 
present. The diagnosis in this early stage, which may 
last years, is next to impossible. When the disease 
is fully formed, we have quite a distinct symptom- 
group. The arms alone are sometimes paralyzed, atro- 
phied, and anaesthetic, while the legs are the seat of 
abnormal reflex, even to the degree of tetanoid walk. 
In other cases we see a general paralysis and universal 
anaesthesia, with contracture of some muscular groups, 
paralysis of the bladder, and the appearance of bed- 
sores. If the cervical enlargement be the seat of dif- 
fused central myelitis, pupillary symptoms are seldom 
wanting, and the pulse is accelerated. The disease 
is eminently a chronic one, years being required for 
its full development. 
Historical considerations.—Ollivier (1886) observed 
and described central myelitis with formation of cav- 
ities, but not much was learned of the disease and its 
semeiology until Schiippel published his paper (Ueber 
Hydromyelus) in 1865. Hallopeau, in 1871-2, contrib- 
uted a series of elaborate articles upon the subject to 
the Archives Generates de Medecine, and in the last few 
years Westphal and Leyden have paid considerable 
attention to this rather rare form of disease. 
2.—NON-SYSTEMATIC OK FOCAL LESIONS OF TIIE SPINAL 
cord; lesions at different heights in the 
ORGAN. 
A variety of lesions may involve the whole or a large 
part of the spinal cord at a given level, extending 
transversely through its various columns. These are 
focal lesiong, and chief among them we find : injuries 
of all kinds; compression by bone or by a tumor; 
transverse sclerosis; transverse softening; hemor- 
rhage in cord ; tumor in the cord, etc. 
The nature of the lesion is sometimes such (fracture 
of vertebrae) as to indicate at once the seat of in- 
jury to the spinal cord; but in many cases the peculi- 
arity in the symptoms is not due to the nature of the 
legion, but to its location high up or low down. The 
diagnosis of this location is possible only by the aid 
of anatomical and physiological knowledge. 
The following diagram, made from data furnished 28 
by Malgaigne, may assist in estimating the height 
of a lesion. It indicates the point of origin of the 
important nerves and plexuses, and the seat of so- 
called centres relatively to the spinous processes of 
the vertebrae. 
In general terms, we may say, that these focal 
lesions give rise to paralysis, numbness and anaesthe- 
sia, to modifications of the reflex function, usually an 
increase; that they cause paresis or paralysis of the 
bladder and the sphincter ani, and that they set up a 
great liability to bed-sores. This general sketch varies 
greatly from that of the symptoms of any of the sys- 
tematic spinal lesions, except No. 6, central myelitis. 
This great dissemblance is a necessary result of the 
difference in the location of lesions; focal lesions in- 
volving kinesodic, aesthesodic, and trophic parts of 
the cord, and cutting off the inhibitory action of the 
encephalon (Setschenow), upon the spinal cord. 
I shall attempt to make clear to you the diagnosis 
of lesions placed (1) in the lower lumbar enlargement; 
(2) just above the lumbar enlargement; (3) in the 
mid-dorsal region; (4) in the cervical enlargement, 
and (5) in the upper cervical region. 
1. Focal, transverse lesions in the lower part of the 
lumbar enlargement. The motor symptoms produced 
by such a lesion are paralysis of the muscles inner- 
vated by the sciatic nerve—those of the feet, legs, pos- 
terior aspect of the thigh and the nates. The sphinc- 
ter ani will be weak or paralyzed; the bladder 
unaffected. The reflex movements of the paralyzed 
muscles are reduced in force, or absolutely wanting; 
wanting if the whole of the gray matter in the lower 
end of the cord is diseased in such a way as to destroy 
its functions. Dependent also upon this extent of 
lesion downward, is the state of muscular irritability. 
If the condition be as just described, the paralyzed 
muscles undergo atrophy, and lose their faradic con- 
tractility. The sensory symptoms are various; at the 
beginning of the disease (often before paresis) there 
is numbness in the soles of the feet, without anaesthe- 
sia. Later the numbness may appear in the whole 
foot, the calf, the posterior aspect of the thigh, 
and actual anaesthesia may supervene. If the soles of 29 
the feet lose their sensibility, the patient is no longer 
able to maintain his equilibrium when his eyes are 
Medulla. 
Relation of spinous processes of vertebrae to spinal nerves. After 
Malgaigne, Traite d'Anatomie Chirugicale, vol. ii., pp. 32-3. 
Fig. 4. 
closed. Another sensory symptom of importance is the 
cincture or band feeling, which, whether like a cord 30 
or like a belt round about the palsied parts, indicates 
(in accordance with the distribution of sensory nerves) 
the upper limit of the spinal lesion. Thus, in the 
condition we now study, the cincture feeling will not 
be about the waist or groin, but around the ankle, leg, 
or thigh. The above symptoms make up an incomplete 
paraplegia. 
2. Focal, transverse lesions, situated just above the 
lumbar enlargement. Conduction to and from the brain 
is interfered with, but the gray matter of the lumbar 
enlargement retains its functional activity in great 
measure; hence we have a very different semeiology 
from that described above. In addition to weakness 
in the feet, there is developed a more or less complete 
paralysis of the whole of the lower extremities, from 
the pubis down. The rectum and bladder are paral- 
yzed, the latter showing defective action by slow, 
interrupted micturition, or by retention, while con- 
stipation expresses the rectal paresis. The reflex move- 
ments of the paralyzed limbs are usually exaggerated, 
sometimes enormously so. This increase in reflex 
movements gives rise to the combined tonic and clonic 
movements of the paralyzed limbs, which Brown-SG- 
quard years ago designated spinal epilepsy. This 
often seems spontaneous, when the patient is in bed 
for example, but it is certain that peripheral irrita- 
tions, whether from the contact of the bed-clotliing 
or from faeces in the rectum, urine in the bladder, etc., 
always precede and cause it. The preservation and 
increase of reflex is owing to the continued (increased) 
activity of the lumbar gray matter below the lesion, 
and the cessation of cerebral inhibitory action. De- 
pendent upon the former fact also, we observe that the 
paralyzed muscles do not undergo positive atrophy, 
and that their electrical reactions are normal or exag- 
gerated. Erections occur, and coition may be accom- 
plished in these cases and in those to be described in 
the next paragraph. 
As regards sensory symptoms we have, as in No. 1, 
numbness and anaesthesia in the paralyzed parts, ex- 
tending as high upward as the groins or waist. The 
cincture feeling is nearly always present, and is placed 
by the patients round about the body at the level of 31 
the hips, or waist just below the umbilicus. In some 
cases the cincture is incomplete, and the feeling is 
likened to a firm grip in the patient’s side or hip. The 
$bove description is a picture of common, complete 
paraplegia. 
3. Focal, transverse lesions in the middle or upper 
dorsal region. The motor and sensory symptoms 
produced by a lesion so placed are very similar to 
those just described, with the following additions. 
The abnormal reflex movements are often more marked 
than in No. 2, and the cincture feeling, index of the 
upper limit of the lesion, is placed at or above the 
umbilicus, around the lower ribs, or even just under 
the arms. In this condition the rectum and bladder 
may after a while partly regain their functions ; i. e., 
their contents are involuntarily expelled from time to 
time by reflex action. 
If the urine dribbles away it is not because the 
“ sphincter ” (?) of the bladder is paralyzed, but be- 
cause there is retention and overflow—a state de- 
manding the daily use of absolutely perfect and car- 
bolized soft catheters. In the earlier stages of the 
affection, the occurrence of increased reflex action in 
the paretic limbs gives rise to a tetanoid state during 
attempts at standing or walking, and too hasty, quasi- 
involuntarily micturition and defecation. Later in the 
disease the paralyzed limbs may become contractured, 
by reason of secondary changes in the lateral columns. 
4. Focal, transverse lesions in the cervical enlarge- 
ment. According as the lesion suddenly or gradually 
affects the whole of the cord transversely, or accord- 
ing as it is placed on the lower or upper portions of 
the enlargement, somewhat different symptoms are 
obtained. They always, however, bear a general re- 
semblance to those in Nos. 2 and 3. 
a. A partial lesion may for a time produce symp- 
toms, numbness and paresis, in the arms and hands 
alone, the lower limbs being only weak and showing 
increased reflex. Later, as the lesion extends, the legs 
as well as the arms are paralyzed, and the cincture 
feeling exists high up. 
i. A lesion involving the cord at the level of the 
eighth cervical and first dorsal nerves (see sketch) will 32 
give rise to paralysis, often with atrophy and loss of 
faradic reaction in those muscles of the upper ex- 
tremities which are animated by the ulnar nerves, i. e., 
nearly all the small muscles of the hands, and some of 
the flexors of the wrist and fingers. There will be 
sensory symptoms in the same district; and the cinc- 
ture feeling, if present, will be across the upper part 
of the chest. The lower extremities are paretic or 
wholly paralyzed, numb or anesthetic, according to 
the completeness of the destruction of the spinal tis- 
sue. In severe cases nearly all the intercostal muscles 
will also be paralyzed, and thus life will be much 
more jeopardized than by lesions placed lower down. 
The danger is all the greater because the expiratory 
muscles (intercostals, triangularis sterni, abdominal 
muscles) are paralyzed also. 
c. If the lesion be situated in the upper part of the 
enlargement, the motor and sensory symptoms will be 
apparent in nearly the whole of the upper extremities, 
as well as below them. The reflex capacity, the state 
of bladder and rectum, the faradic reactions of mus- 
cles remain substantially as in Nos. 2 and 8. The 
cincture feeling is referred to the level of the clavicles, 
or a little lower, across the chest and the arms below 
the deltoid. The difficulty of breathing is even great- 
er than in &. The symptom-groups produced by le- 
sion No. 4 are often designated by the names of cervi- 
cal paraplegia, or general paralysis. 
In case of lesion in any part of this region (from 
the level of the fourth dorsal to that of the fourth 
cervical nerves) there may be pupillary and facial 
vaso-motor symptoms. If the lesion be of such a na- 
ture as to cause irritation of thecilio-spinal centre, the 
symptoms are dilatation of the pupils and pallor of 
the face, while if there be a loss of the activity of the 
cilio-spinal centre, the pupils are small and the face 
and ears flushed and hot. It must be added that these 
vaso-motor and ciliary symptoms are not by any 
means as frequently observed as theory and experi- 
mentation would lead us to expect. 
The same may be said with reference to some pecu- 
liarities in the action of the heart and variations in the 
bodily temperature which have been observed. In 33 
severe traumatic lesions in this region, we often find 
retardation of the pulse, and great elevation of the 
temperature of paralyzed parts. 
. Focal, transverse lesions in the upper cervical re- 
gion. These, like No. 4, produce cervical paraplegia, 
but a much more complete one. The patient is whol- 
ly paralyzed below the head, and the entire body may 
be anaesthetic. Of necessity the phrenic nerves are pa- 
retic or paralyzed, according to the completeness of 
the injury to the cord, and life is almost immediately 
terminated by asphyxia. Cases of this category are 
nearly always of a surgical character; non-traumatic 
lesions of this region being exceedingly rare. There 
may be ciliary and facial vaso-motor symptoms here 
as in No. 4, and the bodily temperature and pulse- 
rate are variable, Life is preserved too short a time 
to allow of much study of these symptoms. In slowly 
developed lesions we may have phenomena of irrita- 
tion, as hiccough, dyspnoea, acceleration of the pulse, 
together with paretic symptoms in the arms and chest, 
later in the legs. 
Lecture IV. 
2. NON-SYSTEMATIC OR FOCAL LESIONS OF THE SPINAL 
CORD CONTINUED; LESIONS INVOLVING ONE LATERAL 
HALF OF THE SPINAL CORD, IN ITS LOW ER AND UP- 
PER REGIONS ; DIAGNOSIS OF SPINAL HEMIPLEGIA. 
ANATOMY AND DISEASES OF THE MEDULLA OBLONGATA. 
Gentlemen :—When a focal lesion, caused by spon- 
taneous disease, or by traumatism, involves one lateral 
half of the spinal cord more or less exactly, we ob- 
serve striking and characteristic symptoms in the pa- 
tient. Some of these are in relation to the height of 
the lesion in the organ as pointed out in the preceding 
lecture, but the most important ones are dependent 
upon the fact that one lateral half of the cord is in- 
jured in its kinesodic and sesthesodic tracts. A refer- 
ence to Figures 2 and 4 in preceding lectures will facil- 
itate the comprehension of what I shall have to say 
upon these lesions. 34 
" According as the lateral focal lesion is placed low 
down or high up in the spinal cord, we denominate 
the symptom-groups as hemi-paraplegia in the first 
case, spinal hemiplegia in the second. 
a. Hemi-paraplegia. A tumor compressing one 
lateral half of the spinal cord in its dorsal (case by 
Charcot) or lumbar regions, a kDife-cut, a contusion 
by a piece of broken vertebra, or a patch of hemor- 
rhage or softening, will give rise to this symptom- 
group. Let us suppose the lesion to be situated in 
the right half of the spinal cord. As a result (see Fig. 
2) the motor paths from the brain and upper spinal 
cord to the right lower extremity are cut off, together 
with the sensory paths which, crossing the median line 
below the lesion, supply the left lower extremity with 
sensibility. 
In the living human subject we observe motor paral- 
ysis, more or less complete in the right lower extrem- 
ity, and the sensibility of this member is preserved or 
increased. If the lesion be traumatic and quite com- 
plete, hyperaesthesia and increased temperature are 
present. In the left lower extremity, on the contrary, 
we find no paralysis, but more or less complete anaes- 
thesia. It is noteworthy that the so-called muscular 
sense is not abolished in that anaesthetic limb. The 
bladder and rectum may be paralyzed. In some cases 
the distribution of symptoms in the two extremities is 
not as typical and clear as above stated, some paresis 
appearing on the side opposite the lesion, and slight 
loss of sensibility existing on the paralyzed side. 
This, I need hardly say, is owing to the fact that the 
lesion crosses the median line. 
As regards constriction bands, increased reflex, nu- 
trition of muscles, and visceral paralysis, regard must 
be had to the exact height of the lesion in the cord, 
as determined in sections 1, 2, 3 of the preceding 
lecture. 
This form of paraplegia can be exactly repro- 
duced in animals. It is now nearly thirty years since 
Brown-SCquard showed to the Biological Society 
of Paris, animals (Guinea-pigs, etc.), in whom hemi- 
paraplegia had been produced by cutting one lateral 
half of the cord in the dorsal region. The operation 35 
is not very difficult, and the results are always strik- 
ing. 
b. Spinal hemiplegia. A lateral focal lesion in the 
cervical enlargement, or above it, will give rise to the 
following symptoms, more or less exactly distributed. 
If the right half of the organ is the seat of the lesion, 
we observe that the arm and leg on the same side are 
paralyzed, the intercostals usually escaping, while on 
the opposite side there is no paralysis, but more or less 
perfect anaesthesia exists to the median line of the 
body, and as high as the limit of distribution of sen- 
sory nerves coming from the spinal cord just below 
the lesion. The absolute height of the lesion is to be 
determined as in sections 4 and 5 of Lecture III. In 
these cases we nearly always find, on the same side as 
the injury, contraction of the pupil, redness and in- 
creased temperature of the face and ear. These symp- 
toms are due to paralysis of the vaso-motor and cili- 
ary centres in the spinal cord. Often the paralyzed 
limbs are hotter than the anaesthetic. 
In some cases, owing to incomplete destruction of 
one lateral half of the cord, the arms, thorax, and 
face alone exhibit symptoms, the legs remaining 
normal. In other cases various degrees of abnormal 
reflex action are present in the affected lower limbs; 
sometimes more on the anaesthetic side. 
We owe a clear conception of these interesting 
forms of spinal paralysis to Brown-Sequard, although 
some cases of spinal hemiplegia had been placed on 
record before him (Sir Chas. Bell, Ollivier, Or6, and 
others). This distinguished physiologist and physi- 
cian produced spinal hemiplegia and hemi-paraplegia 
in animals from 1849 on, and in 1863-5 published 
elaborate mbmoirs, in which he collected all the cases 
then known, and critically studied their semeiology. 
In 1868 and 1869 the same author published other cases 
and remarks which have placed our knowledge of this 
subject upon a firm foundation. Some doubt exists 
as to the absolute correctness of Brown-SSquard’s 
law of the course of motor and sensory paths in the 
spinal cord in animals, but in man it would seem, 
from the study of many cases, that the law holds 
good. 36 
ANATOMY AND DISEASES OF THE MEDULLA OBLONGATA. 
Leaving the diseases of the spinal cord to proceed to 
the consideration of those of the medulla oblongata, I 
must again refresh your memories upon the physiologi- 
cal anatomy of the parts concerned; mentioning only 
such data as will be of use to us in our diagnosis of 
location of disease. The first, and perhaps the most 
important point I wish to call your attention to is the 
decussation of the anterior pyramids at the junction 
of the spinal cord and medulla. This decussation is 
made up of bundles of nerve fibres coming from the 
anterior pyramids of the medulla, crossing the median 
line, and continuing their way down the cord in each 
of its halves, constituting that part of the lateral col- 
umn known as the crossed pyramidal column. An 
other bundle extends downward, without crossing the 
median line, into the inner part of the anterior col- 
umn, the so-called direct pyramidal column (com- 
pare Fig. 1., Lecture I.). According to the books, 
the uncrossed portion of the pyramidal fasciculus, the 
direct pyramidal column, is much smaller and less 
important than the other bundle of fibres which cross 
the median line. 
Of immense importance for the study of localiza- 
tions in the brain, and particularly for the estimation 
of the symptom hemiplegia, is a knowledge of the 
exact extent and regularity of this decussation, or 
more strictly speaking, semi decussation. If we are 
to follow text-books we shall be led to believe that 
the semi decussation always occurs in about the same 
proportion on the two sides: a view which Brown- 
SSquard and others admit while trying to demonstrate 
that a lesion of the brain may produce paralysis on the 
same side of the body. Still, in past times a few 
facts had been recorded against the constancy of the 
pyramidal decussation, but it was not until Flechsig 
published his embryological researches in 1870, that 
it was known how very variable is this decussation. 
Examining the spinal cord of sixty fmtuses, this in- 
vestigator found that the proportion in the size of the 
crossed and direct pyramidal columns varied almost 
infinitely between the following figures: in one case 37 
the direct pyramidal column was equal to 90, the 
crossed column to 10. In another case at the other 
extreme the proportion was 0 to 100; in other words 
all the pyramidal fibres had crossed the median line. 
There was no case in which there was absolutely no 
decussation, but Fleclisig correctly remarks that there 
is no reason why such a specimen should not be met 
Fig. 5. 
Diagram explicative of pyramidal decussation : p v, pons Varolii 
m o, medulla oblongata; o, olivary body; a P, anterior pyramid; d, de- 
cussation ; s c, spinal cord. The direct and crossed bundles vary very 
much in size, as shown in the following ratios of crossed and direct : 
100 : 0, 92 : 8, 84 : 16, 70 : 30, 52 : 48, 35 : 65, 10 : 90.—{Flechsiq.) 
with. The majority of the foetuses had an ordinary 
semi-decussation, the crossed bundle predominating 
over the direct. The above variations in the pyramidal 
decussation are diagrammatically represented in Fig. 5. 38 
Besides, Flechsig determined that there were other 
irregularities in the proportionate size of the four 
columns (two crossed pyramidal columns, two direct) 
which result from the breaking up of the pyramids, 
but this is not essential to our present study. 
The practical bearing of this discovery is very great, 
for it will be readily understood that in the exceptional 
cases in which the pyramidal decussation is nearly 
wanting, an unilateral lesion of the medulla, pons, or 
brain must give rise to symptoms of paralysis on the 
same side as the lesion. 
Again, in those few cases in which the semi-decussa- 
tion is nearly equal, an unilateral lesion above the 
spinal cord will produce weakness on both sides of the 
body. Lastly, in the immense majority of cases, those 
in which most of the pyramidal fibres cross the median 
line, we obtain the classical crossed hemiplegia. It 
is ignorance of these researches of Flechsig which 
makes that distinguished physiologist, Dr. Brown- 
S6quard, invert the reasoning and draw chaotic and 
iconoclastic conclusions respecting the mode of pro- 
duction of hemiplegia (and other symptoms of brain 
disease). Starting with the generally received doc- 
trine (never proven in a scientific way) that the pyram- 
idal decussation is invariable and nearly total, and 
finding scattered in medical literature more than three 
hundred cases in which paralytic symptoms appeared 
on the same site as the lesion, he concludes that we are 
all wrong in considering hemiplegia to be due to de- 
struction of or pressure upon motor tracts in the brain 
and basis cerebri. 
Bearing in mind Flechsig’s demonstration, the erro- 
neous logic of the above is evident. Besides, these 
exceptional cases, so laboriously collated, should be 
looked at in another way. Most of them are old 
cases, i.e., cases reported before modern cerebral anat- 
omy was understood; many of them are related by 
men utterly or relatively unknown. Furthermore, any 
one who has worked much in the post-mortem room 
will appreciate how easily right is wrongly written, 
when left is meant, as a brain is turned over and around 
for examination. Consequently, we might claim the 
right to reject as worthless many of these three liun- 39 
dred or more cases. Suppose, however, that they are 
accepted as bona fide examples of palsy on the same 
side as an encephalic lesion, and that we compare 
them with the thousands of cases of classical hemiplegia 
on the side opposite the cerebral lesion, do we obtain 
a proportion greater than that observed in Fleclisig’s 
series of foetuses, one to sixty ? I think not. 
I have thus digressed from proper medulla dis- 
eases in order to treat the subject of pyramidal decus- 
sation fully, i.e., anatomically and clinically, in one 
lecture. Having done this will save much repetition 
in treating of lesions above this point. 
The pyramids whose decussation we have studied 
are the direct motor tracts which connect the cerebral 
cortex with the spinal cord. They are externally vis- 
ible on the anterior (inferior) surface of the medulla, 
can be traced in the pons and crura, and thence into 
the internal capsule in the white centre of the hemi- 
spheres, to those parts of the cerebral cortex which are 
now considered as in some way motor. In subsequent 
lectures I shall describe this great motor tract more 
fully, and give you the reasons for believing it to be 
continuous from the cortex to the end of the spinal 
cord. Tiie remainder of the kinesodic system of the 
medulla embraces longitudinal bundles of fibres which 
lie between the two olivary bodies (supposed to be in 
connection with the ganglia at the base of the cere- 
brum) and the various nuclei of motor nerves in the 
floor of the fourth ventricle. These nuclei, or groups 
of motor (and trophic ?) cells, represent the anterior 
horn cells of the spinal cord, strangely thrown back- 
ward and toward the median line. They differ from 
the cell-groups of the anterior horns also in being 
more differentiated in relation to the nerves which 
arise from them. Reckoning from below upward, we 
find the nuclei of origin of the spinal accessory (11th), 
hypoglossal (12th), facial (7th), and abducens (6th) 
nerves. The last two lie on the confines of the me- 
dulla and pons. These nerves and their nuclei must, 
I think, be looked upon as active in three ways; 1, by 
their own (trophic?) neurility; 2, by reflex action 
set up through the adjacent and correlated sensory 
nerves; 3, by impulses coming from supra-bulbar 40 
parts, great basal ganglia, cortex of the brain. This 
last connection is undoubtedly a crossed one, i.e., the 
tibres or paths which transmit the motor impulse down 
to these nuclei cross the median line at some unknown 
distance above them. There is therefore another mo- 
tor decussation besides the great one described above, 
The aesthesodic system of the medulla oblongata oc- 
cupies its lateral portions chiefly, and a part of the 
gray matter under the floor of the fourth ventricle, 
outside of the series of motor nuclei. In this gray 
matter we find, from below upward, the nuclei of origin 
of the pneumogastric (10th), glosso-pliaryngeal (9th), 
and acoustic (8th) nerves. All through the lateral 
region of the medulla posterior to the olivary bodies lies 
the great descending root of the trigeminus (5th) nerve, 
which meets with groups of cells throughout this re- 
gion down to the uppermost parts of the spinal cord. 
These various nuclei and nerves, kinesodic and 
iesthesodic, make up arcs for reflex actions of the most 
important kind, as breathing, swallowing, and (with 
gray matter in the pons) the state of vascular tonus. 
The respiratory centre (so-called) is in the nuclei of 
the pneumogastrics, the vaso-motor centre lies near the 
median line at the junction of the medulla and pons, 
and there are various subordinate foci or centres for 
important morbid actions, as the diabetic centres, the 
albuminuric centre, etc. Besides, the hypoglossal 
nuclei and nerves preside over the movements of the 
chief organ of speech. 
I should add that the medulla oblongata has inti mate 
though ill-understood connections with the cerebellum, 
by means of the restiform and olivary bodies. 
As regards the localization of disease in the medul- 
la, I shall have but little to say, for the reason that, in 
accordance with the terms of the course, I am bound 
to speak of only well-determined clinical forms whose 
lesions can be diagnosticated. Consequently, I will 
say nothing of systematic lesions in the bulbar nesthe- 
sodic system, nothing of bulbar lesions in diabetes 
mellitus, almost nothing of focal lesions of the organ. 
a. Systematic lesions of the kinesodic tract are repre- 
sented by only one typical symptom group, viz. : the 
so-called labio-glosso-laryngeal paralysis, or bulbar 41 
paralysis. The lesion in this disease consists of gran- 
ular degeneration of the ganglion cells of the nuclei 
of origin of the hypoglossus, spinal accessory, and of 
part of the facial nerves. The alteration is very like 
that present in progressive muscular atrophy (syste- 
matic lesions of the spinal cord, No. 5, Lecture III.), 
a molecular death, by degeneration, of ganglion cells. 
The symptoms of typical labio-glosso-laryngeal par- 
alysis are strictly motor, and consist in fibrillary con- 
tractionsin and atrophic paralysis of the orbicularis oris, 
muscles of the tongue and throat, and some muscles of 
the larynx. Labial sounds are interfered with, saliva 
dribbles from the mouth, forcible blowing or whist- 
ling becomes impossible, the tongue plays heavily in 
the mouth as shown by thickness of speech and by 
difficult mastication, the voice becomes nasal through 
palatal paresis, and hoarseness, almost aphonia, is pro- 
duced by palsy of the laryngeal muscles. At the 
same time, in extreme cases, the lower facial muscles 
become inert, the lower jaw hangs down, and an 
abundance of tenacious saliva runs from the patient’s 
mouth ; speech is quite unintelligible, and swallowing 
performed with extreme difficulty. At the close of 
life, if that be not cut short by the lodgment of food 
in the larynx, there are symptoms of injury to the 
pneumogastric nucleus, such as exceedingly rapid 
pulse and sudden stoppage of respiration. 
In certain non-typical cases the lips, tongue and 
throat are affected in very various degrees; in others 
the pneumogastrics suffer early; and in others still 
the symptoms of progressive muscular atrophy, or of 
amyotrophic lateral sclerosis (Lecture II.) set in simul- 
taneously or subsequently. I am disposed to believe 
that we may have many forms of “ bulbar paralysis,” 
and consequently would use the term as a generic 
one, to embrace certain varieties, only one of which is 
now well known. 
[It will be asked wrhy I do not speak at length of 
descending degeneration through the medulla. Thi3 
lesion is the continuation downward of a degenera- 
tive change in the motor tract beginning in the cere- 
bral cortex, the internal capsule, the nuclei of the 
corpus striatum, or in the basis cerebri. 42 
It usually affects only one anterior pyramid, and is 
continued downward into the cord, in its direct and 
crossed pyramidal columns. No symptoms indicate this 
alteration in the medulla, and we infer its existence 
from the diagnosis of descending degeneration in the 
spinal cord (Section 3, Lecture II.). I do not formally 
treat of this systematic bulbar lesion for the reason 
that it has no semeiology.] 
t. With respect to focal lesions. A lesion involving 
one lateral half of the medulla will produce, first, 
symptoms of injury to the kinesodic and aesthesodic 
systems in that half of the medulla, the symptoms 
being on the same side as the lesion; and second, 
hemiplegia of motion (and sensation, if the injury be 
deep enough) in the opposite side of the body. Again, 
a superficial focal lesion involving the anterior (inferior) 
face of the medulla may produce symptoms closely re- 
sembling those of bulbar paralysis of the type labio- 
glosso-laryngeal paralysis; and perhaps the only way of 
reaching a correct diagnosis is by determining the 
presence of the degeneration-reaction in the paral- 
yzed facial and lingual muscles, and by demonstrat- 
ing weakness or positive palsy of the extremities. 
An exceedingly atypical form of bulbar paralysis 
is the one caused by ischaemia of the medulla, owing 
to arrest of circulation in the vertebral and anterior 
spinal arteries. The symptoms are mixed motor and 
sensory (deglutition and articulation impaired, breath- 
ing of the Cheyne-Stokes type, rapid pulse, tottering 
gait or marked general paralysis) and death rapidly 
ensues. 
SUMMARY :—LESIONS OF THE BASIS CEREBRI ; PHYSI- 
OLOGICAL ANATOMY OF THE PARTS INVOLVED. 1. 
LESIONS OF THE PONS VAROLII. 2. LESIONS OF THE 
CRURA CEREBRI. 3. LESIONS OF THE BASAL PARTS 
FORWARD OF THE CRURA ; HEMIOPIA AND NEURO- 
RETINITIS. 
Lecture V. 
Gentlemen:—Leaving the region of the medulla, we 
are brought to those numerous and important parts 43 
which constitute the encephalon. I purpose consid- 
ering in some detail, in this and subsequent lectures, 
the localization of disease in the chief subdivisions of 
this mass, but in this lecture I can only enunciate some 
general pathological propositions relative to the en- 
cephalon as a whole, and study the lesions of one of 
its parts. 
For our purpose I make the following subdivision 
of the encephalon—a semi-physiological classification : 
1. The basis cerebri, including all the parts which 
lie upon the base of the skull, but more especially the 
pons Yarolii, crura cerebri, their attached nerves, and 
the optic and olfactory apparatuses. 
2. The great basal ganglia ; i.e., the thalamus opti- 
cus, nucleus caudatus, nucleus lenticularis, and the cor- 
pus quadrigeminum. 
3. The white substance of the hemispheres, espe- 
cially the internal capsule. 
4. The cortex cerebri. 
5. The cerebellum. 
The general pathological propositions relative to 
these parts are as follows : 
1. Lesions of the basis cerebri, especially if involv- 
ing the pons and crura, give rise to the following 
symptoms: paralysis (often of crossed variety), an- 
aesthesia in the face and limbs, impairment of equi- 
librium, changes within the eyes; no psychical symp- 
toms. 
2. Lesions of the great basal ganglia probably pro- 
duce no symptoms unless by encroaching upon the in- 
ternal capsule which passes near them. An exception 
may be the nucleus caudatus. 
3. Lesions of the white centre of the hemispheres 
produce no symptoms when they do not involve the 
parts composing the internal capsule ; if the anterior 
portion of this capsule be injured, we observe paraly- 
sis, if its posterior part, anaesthesia. 
4. Lesions of the cortex cerebri produce, when lo- 
cated anteriorly, psychical symptoms ; when located in 
the median regions, paralysis of an imperfect kind, 
and when situated posteriorly, no symptoms at all 
(sensory symptoms in animals). 
5. Lesions of the cerebellum produce no symptoms 44 
except by involving adjacent parts containing impor- 
tant motor and sensory tracts; thus giving rise to 
irregular paralyses, changes in the optic apparatus, 
symptoms of irritation of the vagus nerve, etc. 
6. Lesions in one lateral half of any part of the 
encephalon produce motor and sensory symptoms in 
the side of the body opposite to the lesion. When 
the lesion is in one-half of the basis cerebri some 
symptoms (direct symptoms) are found in the side of 
the face and head corresponding to the lesion, others 
in the opposite half of the body (crossed paralysis). 
7. Lesions in the median line cause symptoms to 
appear in both sides of the body. 
8. Any intracranial lesion which acts in such a 
way as to increase the intracranial pressure may pro- 
duce (in addition to other symptoms) the condition 
known as choked disk, or neuro-retinitis. 
With these preliminary general statements, I pass to 
the study of the first of the subdivisions—the basis 
cerebri: 
PHYSIOLOGICAL ANATOMY. 
To be very logical, the medulla oblongata, pons, and 
crura should be grouped together under this denomi- 
nation, but for clinical purposes I leave the medulla 
with the spinal cord, and add to the basis cerebri the 
parts which lie in front of the crura, viz., the optic 
tracts and nerves, and the olfactory apparatus. 
As heretofore, I assume that you are familiar with 
the descriptive anatomy of the parts; and what I wish 
you particularly to understand is the arrangement of 
sensory and motor tracts, of nerves, and of ganglia in 
the basis cerebri. 
The projecting mass we call the. pons is largely 
made up of numerous transverse nerve-fibres which 
connect it with the two halves of the cerebellum, and 
which are not, under our present knowledge, of special 
physiological or pathological importance. In the an- 
terior (inferior) half of the pons, lying under those 
transverse fibres, and partly separated into bundles by 
them, we find the great motor or peduncular tract, the 
continuation upward of the anterior pyramids and of 
the central motor fasciculi of the medulla. This tract 45 
is easily seen with the naked eye, broken up into a 
number of smaller fasciculi by transverse fibres, and it 
can be traced upward a long distance. In the poste- 
rior (superior) region of the pons, under the floor of 
the fourth ventricle, near the median line, there is a 
lengthened mass of motor gray matter, whence arise 
the original fibres of the sixth, seventh, and motor 
root of the trigeminus nerves. Laterally, in the pos- 
terior part of the pons, are sensory tracts, some directly 
continuous with the brain above, others more particu- 
larly in relation with the sensory root of the trigemi- 
nus, which radiates to an immense extent up and down 
in the basis cerebri and below it. 
In the crura cerebri we find substantially the same 
parts not covered over by transverse fibres. The an- 
terior portion of the crura consists of the great motor 
or peduncular tract just issued above from the white 
matter and basal ganglia of the cerebrum. Posterior- 
ly are sensory tracts and masses of gray matter in in- 
timate relation with the thalamus opticus and corpus 
quadrigeminum. The final (upper) extremity of the 
elongated mass of gray matter giving rise to motor 
nerves is found here, posteriorly, just beneath the 
aqueduct of Sylvius, in the shape of the common nu- 
cleus of the third and fourth nerves. Let us finally 
bear in mind that the sixth, seventh, and fifth nerves 
are intimately connected with the pons Varolii; the 
third and fourth nerves, and the optic tracts are associ- 
ated with the crura. 
The posterior portions of the crura and pons consti- 
tute the greater part of what Meynert designates the 
tegmentum cruris cerebri, while their anterior parts con- 
tribute to form his basis cruris cerebri. 
All these parts lie in the middle fossae of the cra- 
nium, the chiasm of the optic nerve occupying their 
forward extremity. In the anterior fossae we find only 
the olfactory commissures and ganglia, together with 
the under surface of the frontal lobes of the cerebrum. 
As regards the physiology of these parts, the mesen- 
cephalon of some authors, we may sum it up as follows: 
The anterior part of the crura, pons (apart from the 
superficial transverse fibres), and medulla oblongata, 
contains the chief motor tract connecting the superior 46 
centres with the spinal cord. This motor tract is 
made up of nerve fibres, which convey excitations 
chiefly in a centrifugal direction; many of them, de- 
rived from the motor regions of the cortex, consti- 
tute the anterior portion of the internal capsule, and 
then enter the crura, traverse the pons, go to make up 
the anterior pyramids of the medulla, partially and 
irregularly decussate at the pyramidal decussation, and 
finally are found in the postero-lateral and anterior 
columns of the spinal cord. This most important 
bundle of nerves may be designated the direct cerebral 
motor tract. Another portion of the anterior region 
of the mesencephalon is likewise motor in function, 
and is made up of bundles of fibres derived from the 
nucleus caudatus and nucleus lenticularis. These 
bundles can be traced downward into the middle 
regions of the medulla, but their connection with the 
spinal cord is yet uncertain. The posterior region of 
the pons and crura, composed largely of gray matter, 
is partly sensory and partly motor. It is motor only in 
so far as it includes the nuclei of origin of the upper 
cranial nerves, the seventh, sixth, motor root of fifth, 
the fourth and third. You will remember that the 
nuclei of these nerves are all to be found near the 
median line, underneath the floor of the fourth ventri- 
cle or its continuation, the aqueduct of Sylvius. The 
sensory parts of the mesencephalon embrace the re- 
gions lying external to these nerves, giving origin to 
the eighth and fifth pairs of nerves; the latter pre- 
senting an enormous expansion in its origin; its upper 
roots extending as high as the region of the corpus 
quadrigeminum, the lowest probably as far down as 
the upper part of the spinal cord. 
The posterior regions of the mesencephalon, the 
tegmentum cruris, are the seat of the reflex actions 
of the most important character, and they probably 
serve also for the elaboration, if not perception of 
sensory impressions from the periphery. At the 
upper part of the medulla and the lower part of 
the pons in this region is a mass of gray matter which 
controls the vaso-motor phenomena throughout the 
body. It is highly probable that some severe convul- 
sive manifestations, such as epileptic and tetanic seiz- 47 
ures, are due to morbid processes in the posterior part 
of the pons and crura. 
Finally, with respect to the physiology of the optic 
apparatus lying at the base of the brain, I will only 
say that I am disposed to accept the doctrine of semi- 
decussation of the optic tracts in the chiasm, and shall 
use this hypothesis in explanation of symptoms. 
SYMPTOMS OF LESIONS OF THE BASIS CEREBRI. 
Before taking up systematically the study of the 
semeiology of basal lesions, allow me to fully discuss 
one of the most frequent symptoms of all these lesions, 
viz., crossed paralysis. I wish to study crossed paralysis 
in general, previous to speaking of it under each head- 
ing of the remainder of this lecture, partly to impress 
you with its importance, and partly to avoid future di- 
gressions and repetitions. By crossed paralysis (paraly- 
sie alterne of the French) is meant a form of paralysis 
in which the symptoms immediately caused by a basal 
lesion are on one side of the face or head and on the 
same side as the lesion, while the bodily symptoms 
are on the opposite side of the median line, viz., on 
the side opposite the lesion. As thus enunciated, in 
principle, it is at once apparent that the phenomena of 
crossed paralysis may, according to the seat of a 
lesion at the base of the brain, involve, on the one 
hand, any one of the cranial nerves, and on the other 
the limbs of the opposite side. This conception 
is verified by clinical and post-mortem experience, 
cases of crossed paralysis of every possible variety 
being on record. The most striking and best known, 
however, are those presenting what I may be allowed 
to term the third nerve and body type, the trigeminus 
and body type, and the seventh nerve and body type. 
It is to the late Prof. Romberg, of Berlin, that we owe 
the exact definition and conception of the principle 
of crossed paralysis, while Prof. Gubler, of Paris, first 
made a thorough study of the seventh nerve and body 
type. 
Diffused lesions of the pons produce, when fully 
developed, partial anaesthesia and paresis on both 
1. LESIONS OF THE PONS VAROLII. 48 
sides of the face, generalized paralysis below the neck, 
with or without anaesthesia, the latter symptom ap- 
pearing only if the deeper, posterior, portions of the 
organ are involved. We also observe inability to 
maintain equilibrium, without ataxia, sometimes con- 
vulsions, or contracted pupils, or neuro-retinitis. If 
the lesion advance forward beyond the pons, new 
symptoms, such as will be described further on, are 
superadd ed. 
Localized lesions of the pons may occupy on either 
side of the median line one of four locations. 
a. In the anterior portions of the pons forward of an 
imaginary transverse line passing through the origin of 
the trigemini. As shown by Gubler, this lesion does not 
produce crossed paralysis of the seventh nerve and 
body type, but both the face and body are para- 
lyzed on the same side, i.e., on the side opposite 
the lesion, just as in cerebral lesions strictly speaking. 
A point for differential diagnosis is that when the 
cerebrum is injured, there is almost invariably conju- 
gate deviation of the head and eyes toward the affected 
hemisphere; in pons lesions nothing of the kind occurs. 
b. A lesion placed so as to injure the anterior 
(inferior) region of the pons on one side, back of 
the imaginary line above mentioned, will cause 
typical crossed paralysis, i.e., the facial nerve w7ill 
be paralyzed on the same side as the lesion, and 
the extremities on the opposite side. For example, if 
the right face and the left arm and leg be palsied in 
a patient, we recognize crossed paralysis of the seventh 
nerve and body type, and may diagnosticate with 
positiveness a lesion placed as above described. There 
is, perhaps, no more positive example of constant re- 
lation of lesion to symptoms in the whole of nervous 
pathology. 
In a and b, if the trunk of the trigeminus be in- 
volved in the disease, the face will be more or less 
anaesthetic and neuralgic on the same side as the facial 
palsy and the lesion. From a study of cases of these 
two kinds, Gubler drew the anatomical conclusion 
that the paths which connect the cerebrum with the 
nuclei of the seventh nerve decussate at about the 
middle of the pons, i.e., some distance above the nuclei 49 
of these nerves. A useful diagram for studying the 
principle of crossed paralysis, and of this type in par- 
ticular, you will find in Dr. Hammond’s Treatise on 
Diseases of the Nervous System, ed. 1876, p. 99. 
c. Lesions occupying the posterior region of the 
pons above its middle. Besides paralysis of the face 
and body on the side opposite the lesion, we are like- 
ly to have anaesthesia of the paralyzed parts, even 
amounting to liemi-ansesthesia (without involvement 
of the special senses.) Other symptoms often pro- 
duced are epileptic convulsions, impairment of sight 
from neuro-retinitis, and various forms of paralysis of 
ocular muscles. 
d. Lesions in the posterior part of the pons, below 
the imaginary transverse line through its equator, may 
likewise, if extensive, without crossing the median 
line, cause hemi anaesthesia of common sensory nerves, 
but will also produce crossed palsy, of face on same 
side as the lesion, of the body on the opposite side. 
As in c, we may have neuro-retinitis, epileptic seizures, 
with, besides, palsy of the sixth nerve, and bulbar 
symptoms if the lesion involve the medulla. 
e. A lesion situated very laterally in the pons, or so 
placed as to irritate the lateral peduncles of the cere- 
bellum, will (as shown by a number of cases) give rise 
to rotatory movements of the patient around the long 
axis of his body toward the side of the lesion. Of 
course this symptom appears with others, which are 
more or less in accord with the above symptom- 
groups. 
2. LESIONS OF THE CRURA CEREBRI. 
a. Lesions of the crus proper on one side of the 
median line. The symptoms of such a lesion are ex- 
ceedingly definite, and might even be designated path- 
ognomonic. The third nerve, its trunk or origin, is 
involved in the disease or compressed, as well as the 
great motor tract which, lower down, is to decussate. 
Consequently we observe a crossed paralysis of the 
third nerve and body type; i. e., if the right motor 
oculi and the left extremities be paralyzed in a patient, 
we may feel sure that he has a lesion under or in the 
right crus cerebri. Prof. Rosenthal, of Vienna, states 50 
that in such cases the electro-muscular contractility (to 
faradism) is reduced in the paralyzed limbs, contrary to 
what obtains in hemispheric lesions. You will re- 
member that the optic tract curves around the crus 
on either side, and it at times happens that symptoms 
characteristic of injury to one optic tract present 
themselves. These symptoms will be considered 
later. 
b. Lesions deeply placed in the crus, on one side 
of the median line. In addition to the above de- 
scribed crossed paralysis, we shall probably observe 
hemi-amesthesia of common sensation only on the side 
opposite the lesion. There may be convulsions, cho- 
reiform spasm, hemiopia, or neuro-retinitis. 
c. Lesions placed in the median line, or involving 
both crura more or less. The symptoms will be, in 
case of lesion situated anteriorly (interiorly), wholly 
motor, viz. : paralysis of both third nerves, and of 
both sides of the body below the neck. In case of 
lesion involving the tegmentum cruris, marked disor- 
ders of sensibility, neuro-retinitis, and convulsions will 
occur. 
Extension of the disease backward to the pons 
will be characterized by symptoms (detailed in first 
paragraph) referable to the trigeminus and seventh 
nerves. 
It has been stated that the bladder is paralyzed in 
severe lesions of the crura, but this lacks confirma- 
tion. 
It might not be ill to add that patients having 
lesions in the locations defined above, do not present, 
strictly speaking, cerebral symptoms. They preserve 
their intellect, are not aphasic, and the special senses 
(except the sense of sight) are not involved. 
3. LESIONS SITUATED AT THE BASE OF TIIE BRAIN 
ANTERIORLY TO TIIE CRURA. 
These are rare, but give rise, when considerable, to 
noteworthy symptoms. 
a. Lesions involving one of the optic tracts posterior 
to the chiasm. A small lesion in this location will 
produce hemiopia, a symptom of such importance and 51 
scientific interest as to require special mention. If 
the lesion extend, it may involve the chiasm of the optic 
nerves, or the tract of the opposite side, or the crura 
cerebri, thus either destroying the special symptom, 
liemiopia, or adding to it the signs of crossed par- 
alysis of third nerve and body type. 
By hemiopia is meant a condition of the organs of 
vision such that only one-half (vertically divided) of 
objects are seen by the patient. In other words, the 
fields of vision of the two eyes are darkened in one of 
their halves. Usually the vertical line of division 
between the lighted and darkened half-fields is ex- 
actly in the centre of vision. The hemiopia affects 
the two eyes always, and is distributed differently in 
each eye under the determining influence of the exact 
location of lesions about the optic tracts and chiasm. 
The immediate cause of hemiopia is interruption in 
the centripetal conducting power of certain bundles 
of nerve-fibres in the optic nerves and tracts; hence 
it has been found necessary to frame a theory of the 
course of fibi’es in the optic apparatus. The hypoth- 
esis of Wollaston, that of semi-decussation, is the 
one which is generally adopted to-day, and I append 
a diagram illustrating it, and the positions of lesions 
producing the varieties of hemiopia. A satisfactory 
anatomical demonstration of the truth of the theory 
of semi-decussation has not yet been given, and some 
few facts and authorities are opposed to it, but I think 
that I can assure you that in the present state of sci- 
ence it is the one which best serves the purposes of the 
physiologist and the clinical observer. 
According to this hypothesis nerve-fibres derived 
from the deep origins of one (the left) optic tract, 
combine to form that bundle and extend undivided 
as far as the chiasm. As shown in Fig. 6 at the chiasm 
some of the fibres of the tract (the external group 
possibly) pass directly into the external portions of 
the left optic nerve, and are distributed to the exter- 
nal (temporal) half of the left retina. The remaining 
nerve-fibres of the left optic tract cross the median 
line in the middle of the chiasm, decussating with the 
similar fibres derived from the right tract, then enter 
the right optic nerve, and are distributed to the inner 52 
(nasal) half of the right eye. Thus it is seen that the 
nasal half of the right eye and the temporal half of 
the left eye are anatomically and physiologically ho- 
mologous. 
The same explanation applies to the course of fibres 
which form the right optic tract. Besides these main 
bundles of fibres, a few filaments are supposed to con- 
nect the two retinae, passing through the optic nerves 
and the anterior border of the chiasm without decus- 
sation, while others connect the two sets of tubercula 
quadrigemina by way of the optic tracts and the pos- 
terior border of the chiasm. These commissural fibres 
may, however, be left out of consideration in the 
study of hemiopia. 
If now we bear in mind this distribution of fibres 
in the optic apparatus we can by the aid of Fig. 6 de- 
monstrate the mechanism of each of the four forms of 
hemiopia, viz.: right and left lateral hemiopia (shaded 
parts a and b), bi-temporal and nasal hemiopia. 
Lateral hemiopia, i.e., that form of hemiopia in 
which the homologous parts of the two eyes (temporal 
half of the left retina and the nasal half of the right) 
lose their function, is invariably produced by a lesion 
destroying one optic tract—the left in the diagram. 
Vice versa, destruction of any part of the right optic 
tract would cause blindness in the temporal half of the 
right retina and in the nasal half of the left. Inas- 
much as all visual rays cross in the eye owing to re- 
fraction in the lens, the hemiopia, i.e., the obscura- 
tion of the half-fields of vision is on the opposite side 
from the blind half-retinae. For example, in the first 
instance described above, and illustrated in the dia- 
gram, the hemiopia is of the form designated right 
lateral (or homonymous) hemiopia, and is produced 
by a lesion involving the left tractus opticus. 
Binocular temporal hemiopia can be caused only by 
a lesion placed (as 1 in Fig. 6) in front of the chiasm, 
cutting off the fibres which supply the two nasal fields. 
Binocular nasal hemiopia is produced by a double 
lesion compressing or destroying the outer parts of the 
chiasm (2 in Fig. 6), which are imbedded fibres sup- 
plying the temporal halves of both retina?. Prof. 
Knapp, of New York, has placed a remarkable case Fig. 6.—Diagram explicative of hemiopia. The shaded intra- and 
extra-ocular parts, a and B, indicate the obscuration in right lateral 
(or homonymous) hemiopia, as caused bv lesion 3, so placed as to 
destroy one optic tract. In that tract are two sets of nerve fibres, 
one represented by a dotted line supplying the nasal half of right 
retina, the other fibres by a broken line supplying the outer or tem- 
poral half of the left eye. As visual lines cross in the eye the obscu- 
ration of the half-fields is the opposite. Lesion No. 1, anterior to 
< hi asm, produces blindness of inner half of each retina, and consequent- 
ly bi temporal hemiopia. Lesions No. 2, pressing upon the sides of the 
chiasm, injure fibres supplying the temporal half of each retina, and 
cause bi-nasal hemiopia. c. q, corpus quadrigeminum, in which Prof. 
Charcot believes a second partial decussation takes place. I c. In- 
ternal capsule containing, on Charcot’s hypothesis, all the fibres com- 
ing from the eye of the opposite side. 4. Lesion of internal capsule 
injuring all the fibres connected with the right retina, and causing am- 
blyopia of the right eye. 54 
of this kind on record, in which the lesion consisted 
of thickened and enlarged internal carotid arteries. 
I need hardly add that lesions involving one optic 
nerve in front of the chiasm cannot give rise to 
liemiopia ; they produce monocular loss of vision. 
It should not be forgotten that lesions lying in 
front of the crura and behind the chiasm may press 
upon the motor nerves of the eye as they traverse the 
middle fossae of the cranium on their way to the sphe- 
noidal fissure, thus producing a variety of paralytic 
symptoms about one or both eyes. 
b. Lesions in the anterior cranial fossa, anterior to 
the chiasma. When unilateral, such a lesion involves 
the olfactory tract and ganglion, thereby producing 
anosmia, or loss of smell, on the same side as the lesion, 
with or without subjective odors. 
If the lesion be large, it may act upon the nucleus 
caudatus or other motor parts of the encephalon, and 
cause common hemiplegia (face and limbs) on the op- 
posite side. Thus we may have a last form of crossed 
paralysis, of the olfactory nerve and body type. With 
a lesion involving both sides of the median line, com- 
plete double anosmia, with or without generalized 
paresis of the extremities, would be met with. 
There is one more symptom common to all lesions 
of the basis cerebri, but produced also at times by any 
intracranial disease which causes pressure. I mean 
neuro-retinitis or choked disks. This is always (?) 
bilateral, though it may be more marked in one eye, and 
is esteemed one of the most important signs of gross 
encephalic disease, especially of tumors. In neuro- 
retinitis, ophthalmoscopic examination shows that the 
optic nerves are swollen, and they may project con- 
siderably (measurably) above the level of the sur- 
rounding retina; the margin of the disk is obscured 
or wholly lost, and no line of demarcation can be 
made out between the nerve and the retina. The 
blood-vessels present striking anomalies, the arteries 
being relatively small, the veins positively enlarged 
and tortuous; there are often small hemorrhages in 
the retina, round about the disk. Strange to say, 
very good sight may coexist with this lesion. This 
condition of choked disks may last a number of 55 
weeks (much longer in cases of tumor of the brain), 
and then subside, giving place to the appearances of 
atrophy of the optic nerves, viz., an unnatural white- 
ness or bluish whiteness of the disk, smallness of the 
retinal vessels, and unusual sharpness of the outline of 
the disk, with impaired vision. 
SUMMARY :—LESIONS OF THE GREAT GANGLIA AT THE 
BASE OF THE BRAIN, AND OF THE WHITE SUB- 
STANCE OF THE HEMISPHERES.—SKETCH OF THE 
PHYSIOLOGICAL ANATOMY OF THESE PARTS : LESIONS 
OF THE GREAT BASAL GANGLIA; OF THE INTERNAL 
CAPSULE, AND OF THE REMAINDER OF THE W'HITE 
SUBSTANCE.—IjESIONS OF THE CEREBELLUM. 
Lecture YI. 
Gentlemen:—The great ganglia at the base of the 
brain are from before backward, the nucleus caudatus 
and the nucleus lenticularis of the corpus striatum (the 
intra- and extra-ventricular portions of the corpus 
striatum, according to English and American books), 
the thalamus opticus, and the corpus quadrigeminum 
(or tubercula quadrigemina). These masses of gray 
matter are of coarse double, i. e., symmetrically ar- 
ranged on either side of the median line. Their rela- 
tions to adjacent portions of the brain are of great 
importance to us, and worthy of a somewhat detailed 
study. 
In very general terms, it may be said that all of these 
bodies have at least a duplex connection, one superior 
with the cortex of the brain, the other inferior with 
the various parts which make up the mesencephalon. 
More particularly, the nucleus caudatus (intra-ven- 
tricular nucleus of the corpus striatum) sends bundles 
of fibres downward into the crura, and the same is 
true of the externally-placed nucleus lenticularis. So 
we say that both parts of the corpus striatum are in- 
timately connected with the basis cruris ceiebri. 
On the other hand, the thalamus and corpus qua- 
drigeminum are intimately united with the nucleus of 
the tegmentum, and send bundles of fibres into and 56 
through it, in the posterior or sensory system of the 
mesencephalon. Physiologically, we may look upon 
the basis cruris and its superadded ganglia as motor 
in function, and upon the tegmentum cruris as sen- 
sory and as the seat of performance of important and 
complex reflexes. 
As regards the other connections of these bodies, 
they are probably connected with their homologues 
across the median line, and superiorly with various 
parts of the cortex. There would seem to be, judg- 
ing from a series of cases of cerebral atrophy, a bun- 
dle of nerve-fibres connecting the nucleus caudatus 
of one side with the opposite half of the cerebellum 
by way of the processus cerebelli ad cerebrum. At 
any rate, great atrophy of the right hemisphere (for 
example) and corpus striatum is usually accompanied 
by atrophy of the left hemisphere of the cerebellum. 
I need hardly remind you of the intimate union be- 
tween the optic tracts and the corpus quadrigeniinum 
and the external portion of the thalamus. 
The white centre of the hemispheres is made up 
of many separable fasciculi, the physiology of many 
of which is as yet obscure. In the first place, we can 
demonstrate in it commissural bundles running in 
various directions: transversely, connecting various 
portions of the cortex of both hemispheres by way of 
the corpus callosum and the so-called commissures; 
others extend longitudinally in one hemisphere, con- 
necting the convolutions of one lobe with those of 
another; yet others simply bind together adjacent 
convolutions Secondly, there are heavy masses of 
fibres extending from the basal ganglia to the con- 
volutions of the hemispheres, constituting a great 
part of what is known as the corona radiata. Third- 
ly, and most important in pathology to-day, is a 
bundle of white substance in each hemisphere, which 
directly unites the cortex of the brain with the crura, 
pons, and spinal cord—the so-called internal capsule. 
This fasciculus appears (upon anatomical and physi- 
ological evidence) to be the continuation of the sen- 
sory and motor tracts which we have studied in the 
basis cerebri. The extension of the sensory tract up- 
ward from the crura into the internal capsule is not so 57 
clear as is the continuity of the motor tract anteriorly. 
This, denominated by some the peduncular tract, 
and designated in Lect. V. as the direct cerebral 
motor tract, can be traced by dissections, by physi- 
ological experiments, by embryology, and lastly by 
the help of pathological processes (descending de- 
generation) from certain convolutions of the cortex 
r Fig. 7.—Diagram of course of sensory and motor tracts in the mesen- 
cephalon and hemispheres, s, sensory tract in posterior region of 
mesencephalon, extending to o and t, occipital and temporal lobes of 
hemispheres; m. motor tract in basis cruris, extending to p and r, 
parietal and (part of) frontal lobes of hemispheres; c C, corpus qua- 
drigeminum ; o t, optic thalamus; n l, nucleus lenticularis; n c, nu- 
cleus caudatus. 
cerebri into the anterior half or two-thirds of the in- 
ternal capsule, into the crus cerebri, the pons, the 
medulla, and (in accordance with the law of decussa- 
tion—vide Lect. IV.), into both halves of the spinal 
cord. The composition and extension of the internal 
capsule is rudely represented in diagram by Fig. 7. 
Its exact position in the hemisphere and its relations 
to other parts of the encephalon is well shown in Fig. 
8, modified from a cut in Prof. Charcot’s Lectures on 
Localization in Cerebral Diseases. This represents 
a transverse vertical section of the hemispheres made 58 
through the middle of the optic thalamus. The inter- 
nal capsule is seen to lie between the external border 
of the thalamus and the nucleus lenticularis of the 
corpus striatum. In this location the bundle is much 
compressed, aud seems to have little or no connection 
Fig. 8.—Modified from Charcot’s diagram, to show position, rela- 
tion, and distribution of the internal capsule as seen in a vertical trans- 
verse section of the brain on a level with the greatest development of 
t o, thalamus opticus, i c, location of internal capsule ; N L, nucleus 
lenticularis: k c, external capsule: d, claustrum ; N c, nucleus cau- 
datus ; M r c, motor regions of cortex cerebri ; 1, fibres representing 
the radiation of the internal capsule vertically to the motor region of 
cortex. 
with the gray bodies just named; it expands in every 
direction after passing them, and its anterior fibres 
are ultimately distributed to the middle regions of the 
cortex cerebri—motor district—embracing the third 
frontal, the posterior extremities of the first and 
second frontal, the ascending frontal convolutions, 
also the ascending parietal and first parietal convolu- 59 
tions; also, lastly, to the continuation upon the inner 
surface of the hemisphere of the ascending frontal 
and parietal convolutions which make up the para- 
central lobule. The posterior third of the internal 
capsule is very probably distributed to the occipital, 
temporal and second parietal convolutions—the sup- 
posed sensory gyri. 
Besides common sensory tracts, the posterior part of 
the internal capsule contains fibres which are directly 
or indirectly connected with the special sense organs, 
viz., the optic, olfactory, gustatory, and acoustic. 
This is shown by the fact that total hemi-anaesthesia 
in man results from lesions involving the internal cap- 
sule; from experiments upon animals, whereby certain 
occipital or temporal convolutions being removed, 
blindness or deafness is caused on the opposite 
side. 
The physiology of the great ganglia, commis- 
sural fibres, and internal capsule is far from satisfac- 
torily marked out. Many glaring contradictions are 
apparently proved by the experiments of different 
observers. It would appear well settled that the 
corpus quadrigeminum and the corpora geniculata 
are a part of the optic apparatus; that the nucleus 
caudatus and the nucleus lenticularis have motor 
functions of some sort. The greatest uncertainty 
exists, I think, concerning the attributes of the thal- 
ami optici. 
On the other hand, we now know pretty positively 
that most of the sensory paths for the body pass in 
the posterior part of the internal capsule, laceration 
of this part in animals being invariably followed by 
hemi-anaesthesia on the opposite side. That the thala- 
mus has anything to do with the perception of sensa- 
tions is rendered doubtful by the occurrence of cases 
in which lesions, strictly limited (i. e., not pressing on 
adjacent parts) to the thalamus have produced no 
special symptoms. The same objection (pathologi- 
cal) can be urged against the view that the nucleus 
lenticularis has important motor functions. That the 
anterior part (two-thirds?) of the capsule consists of 
motor fibres is likewise quite well established by ex- 
periments upon animals and by the study of patho- 60 
logical cases.* What the functions of the various 
commissural fibres may be, is, at the present time, only 
a matter of speculation more or less logically con- 
structed. 
1. LESIONS OF THE BASAL GANGLIA. 
The generally received statements that lesions of 
these bodies produce definite symptoms—lesions of 
the nucleus lenticularis and nucleus caudatus paral- 
ysis, and lesions of the thalamus opticus anaesthesia— 
are, I think, very questionable. From the evidence 
now before us it seems doubtful if lesions of the nu- 
cleus lenticularis, and of the thalamus, produce any 
symptoms except by exerting pressure upon the inter- 
nal capsule lying near by. At any rate, cases of de- 
struction of large parts of these bodies without symp- 
toms are on record. As regards the nucleus caudatus, 
it is possible that its destruction is followed by hemi- 
plegia and secondary degeneration; but on the other 
hand, it must be admitted that almost all lesions of 
this body are so placed, and of such a nature, as to 
cause pressure upon the motor portion of the internal 
capsule. This is especially true of hemorrhage, as 
showm by Prof. Charcot in his recent lectures on the 
brain. 
2. LESIONS OF THE INTERNAL CAPSULE. 
These, on the other hand, produce, as shown by the 
recent study of pathological evidence, and by experi- 
ments upon animals, constant symptoms. If the an- 
terior half or two-thirds of the capsule be injured, we 
have hemiplegia on the opposite side of the body ; 
* Since these lectures were delivered, a brilliant and final proof of 
the motor functions of the anterior part of the internal capsule, and 
of the continuity of the motor convolutions and the direct cerebral 
motor tract has been advanced by the French experimenters, Franck 
and Pitres (Lc ProflrUs Medical, Jan. 19, 1878J. These physiologists 
found that by faradizing those parts of the white centre of the hemi- 
sphere which lie underneath the so-called cortical motor centres, they 
were able to produce definite movements in parts of the body on the 
opposite side. This tract of white matter, constituting the anterior 
portion of the internal capsule, contains physiologically distinct 
fasciculi which are connected on the one hand with the motor dis- 
tricts of the cortex, and on the other hand with peripheral parts of 
the body across the median line. 61 
more or less perfect hemiplegia according to the exact 
seat and size of the lesion. It 'will be readily under- 
stood that lesions (especially haemorrhage and tumors) 
of parts adjacent to the capsule, such as the lenticular 
and caudate nuclei, the white centre of the frontal 
lobe, etc., may by pressure bring about a similar result. 
Besides paralysis, descending secondary degeneration 
is an inevitable result of lesions of the internal capsule. 
This lesion can be traced downward through the whole 
length of the direct cerebral motor tract so frequently 
referred to before, to the lower end of the spinal 
cord. Lesions of the nucleus caudatus are also said 
to produce the same results, but recent researches 
(Flechsig) throw doubt on this. 
If the posterior part of the internal capsule be in- 
jured directly, or indirectly by the pressure of lesions 
in adjoining regions, there is produced anaesthesia, 
more or less complete, on the opposite side, usually 
with only slight paralysis. If the lesion be considerable 
the anaesthesia is absolute; i. e., the special senses and 
common sensory nerves lose their function, or more 
properly speaking, impressions coming through these 
cannot reach the perceptive centres. Hemiopia is 
never (?) thus produced, and Charcot explains this 
by supposing a second semi-decussation to take place 
in some part between the chiasm and the internal 
capsule; probably in the corpus quadrigeminum. A 
reference to Fig. 6, Lect. V., will, I trust, make this 
hypothesis plain. 
Yet a third symptom results from lesions of the 
internal capsule, viz., choreiform movements follow- 
ing hemiplegia and hemi-anaesthesia. These move- 
ments vary in degree and type from true athetosis to 
ataxia, from chorea to tremor, and constitute an in- 
teresting symptom-group, well worthy of further 
study. In my own cases of post-hemiplegic chorea, 
hemi-anaesthesia of slight degree wTas present, and in 
one case lateral hemiopia. 
Extensive lesions of the central parts of the hemi- 
spheres may produce, besides the specific signs named 
above, a number of other symptoms. Thus, sudden- 
ly produced lesions (haemorrhage, softening) will 
nearly always cause conjugate deviation of the eyes 62 
and head. The patient, though insensible, turns his 
eyes and head constantly to one side, toward the 
injured hemisphere, and away from the paralyzed 
side. In spite of a recent attempt to impeach the 
value of this symptom of hemispheric injury, I am 
disposed to attach value to it. Great increase in the 
bodily temperature also follows large injuries. 
Other lesions, sucli as cause pressure, and slowly 
grow to a great size (tumors), cause, in addition to the 
specific signs dependent upon their exact location, the 
change within the eye which we call neuro-retinitis, 
(;vide Lect. V.). They will also usually produce con- 
vulsions. 
As regards the remainder of the white substance, 
such as the central regions of the frontal, occipital, 
and temporal lobes, modern critical study of recorded 
cases would seem to indicate that lesions involving 
these parts in such a way as not to press upon the in- 
ternal capsule and nucleus caudatus, do not give rise 
to any symptoms; e. g., an immense abscess may oc- 
cupy the temporal and occipital lobes, or the anterior 
part of the frontal lobe, without causing paralysis or 
anaesthesia. Anatomy and experimentation, however, 
seem to indicate that lesions of the occipital and 
temporal lobes should give rise to sensory symptoms: 
and a more careful study of cases of disease in these 
parts is just now a desideratum. 
We do not know any more relative to lesion of the 
great commissural bundles which unite the two hemi- 
spheres and different parts of one hemisphere. The 
cases of congenital absence of the corpus callosum on 
record do not teach anything definite. 
I add a few words relative to another terra incognita 
in the brain, the cerebellum. Its situation is known 
to all of you, but there are a few points in its anatomy 
to which I would specially invite your attention. In 
the first place, this great mass of nervous matter is 
closely bound down by a strong fibrous covering (a 
bony septum in some animals), the tentorium cerebelli. 
This fold of dura mater probably serves important 
3. LESIONS OF THE CEREBELLUM. 63 
purposes in health, but in case of disease in the cerebel- 
lum it causes pressure-effects to be transmitted chiefly 
forward and downward. This is important to bear in 
mind when studying the effects of cerebellar lesions. 
Second, the cerebellum is remarkable for its numerous 
connections with other parts of the nervous system. 
Fibres connect each of its hemispheres with the nu- 
cleus caudatus and cerebral hemisphere of the oppo- 
site side, by means of the crura cerebelli ad cerebrum. 
Other fibres, forming heavy bundles, make up the crura 
ad pontem or lateral peduncles of the organ ; extend- 
ing deeply into the white and gray substances of the 
mesencephalon. It is probable that each half of the 
cerebellum is thus connected with the opposite half of 
the pons; possibly some fibres are strictly commissu- 
ral, i.e., unite the two hemispheres of the organ after 
passing over the pons. Lastly, the cerebellum is con- 
nected with the medulla and spinal cord. It forms, 
by means of the crura cerebelli ad medullam, close 
connections with the olivary bodies, and with the ex- 
ternal portion of the lateral columns (near the extrem- 
ity of the posterior horns) in the spinal cord. It has 
been claimed that some cranial nerves (third, fourth, and 
acoustic) have been traced into the cerebellum, but the 
evidence on this point is unsatisfactory. Third, the 
cerebellum overlies highly important organs, and this 
proximity serves to explain much of the semeiology of 
its lesions. In front of it is the corpus quadrigemi- 
num and the tegmentum cruris, with its contained 
vasomotor (and convulsive?) centre; beneath it the 
medulla oblongata, with its floor and such vital nerves 
as the pneumogastric and the spinal accessory. 
The physiology of the cerebellum is at the present 
day quite unknown. That it serves for purposes of 
co-ordination in a direct and positive manner is dis- 
proved by experimentation and pathology ; that it is 
a centre for the movements of the eyeballs (Ferrier) is 
equally doubtful; and so is the view that it is the 
seat of psychical attributes of an emotional character. 
Mitchell’s hypothesis, that it is a store house of nerve 
force for use in emergencies, is plausible but unproven. 
The mechanism and purpose of the cerebellar connec- 
tions is likewise not understood. 64 
As regards the diagnosis of lesions of the cerebel- 
lum, I must admit that in the very numerous symp- 
toms produced by them I do not know of one that is 
characteristic. In other words, lesions strictly limited 
to the substance of the cerebellum produce no definite 
symptoms: and on the other hand, the symptoms 
which we observe in cerebellar diseases are the result 
of pressure-effects upon adjacent parts. Thus, the 
affections of sight so common in cerebellar lesions are 
caused by pressure upon the corpus quadrigeminum 
or the corpora geniculata, and also upon the origins 
of the third, fourth and sixth nerves. The nausea, 
vomiting, and sudden death may be explained by 
irritation and paralysis of the nuclei of the pneumo- 
gastric nerves in the floor of the fourth ventricle; 
convulsions, by pressure upon the tegmentum cruris ; 
the imperfect hemiplegia or general paralysis, by a 
similar action upon the motor regions of the mesen- 
cephalon. The diagnosis (assisted by predominance 
of pain in the occipital region) must be made chiefly 
by exclusion. A symptom of great importance when 
present is titubation. This has been termed cerebellar 
ataxia, but as a descriptive term titubation is better. 
The patient walks with his feet separated, his body 
bent a little forward and swaying, his hands and arms 
in use to preserve his equilibrium. There is no true 
ataxic jerking, no want of harmony between antago- 
nistic groups of muscles, no choreic movements, no 
tremor.* 
* After the delivery of this lecture Prof. H. Nothnagel of Jena, pub- 
lished (in Berliner k linixche Wochenachrift, 1878, No. 15) the results of 
hiB analysis of more than two hundred and fifty cases of cerebellar dis- 
ease. His conclusions, I nm happy to say, are substantially equivalent 
to what has been said above. However, Prof. N. is disposed to admit 
one symptom—cerebellar ataxia—as characteristic of injury to the cere- 
bellum, or more properly, to one of its smaller parts, the superior ver- 
miform process. N. says that by cerebellar ataxia we are to under- 
stand a perversion of equilibrium closely resembling that observed in 
alcoholic intoxication ; the patient titubates, stands with feet wide 
apart: if he be barefooted the toes are seen in active motion ; and in 
walking the body sways a good deal, the foot is brought down with ball 
or with heel first irregularly ; closing the eyes sometimes makes stand- 
ing and walking worse, sometimes not. In the recumbent position 
there is no ataxia. In the large majority of cases the upper extremi- 
ties remain free from inco ordination. 65 
Lecture YII. 
SUMMARY:—ANATOMY AND LESIONS OF THE CORTEX 
OF THE BRAIN.—THE CHIEF CORTICAL MOTOR CEN- 
TRES, AND BROCA’S SPEECH-CENTRE. — LOCALIZED 
LESIONS OF THE CORTEX CEREBRI ; DIFFUSED LE- 
SIONS OF THE SAME. 
Gentlemen: — The cerebral cortex is an immense 
spread-out ganglion, whose functions are not yet fully 
or exactly known. Like all ganglionic masses, it is com- 
posed of ganglion-cells, nerve-fibres, blood-vessels, and 
neuroglia. Its ganglion-cells are generally pyramidal 
in shape, the apex of the pyramids being turned out- 
ward or peripherally. They vary very much in size 
and in precise shape, the largest occurring in convo- 
lutions of the median parts of the hemispheres. 
This gray cortical layer becoming folded through 
the process of growth, ultimately presents irregular 
swellings and depressions of its surface. The swellings 
are called convolutions or gyri; the depressions, fis- 
sures or sulci. Some of the sulci are very deep, and 
receive special names. It should not be forgotten 
that the bottom of every sulcus is formed by the same 
ganglionic gray matter as the prominent parts or 
gyri. 
These gyri are so grouped and separated by large 
sulci, that we are now enabled to make a successful 
topographical study of the apparently confused mass 
of convolutions; and in my brief description of the 
cortex cerebri I shall almost follow Ecker’s classifica- 
tion of its parts. Thus in each hemisphere we have 
four lobes or groups of gyri, viz., the frontal, parietal, 
temporal, and occipital lobes. Separating these lobes 
are three large and constant fissures: the fissure of 
Sylvius, between the frontal and temporal lobes; the 
fissure of Rolando (or central f.), separating the 
frontal and parietal lobes; and the occipito-parietal 
fissure in the inner face of the hemisphere, limiting 
the occipital and parietal lobes. 
Besides, we recognize four lobules, viz., lobulus cen- 66 
tralis (island of Reil at the bottom of the fissure of 
Sylvius), lobulus paracentralis, lobulus cuneus, and 
lobulus quadratus, on the inner surface of the hemi- 
sphere. The paracentral lobule is made up almost 
wholly of the upper (inner) ends of the ascending fron- 
tal and ascending frontal convolutions as they dip 
into the great longitudinal fissure. 
For a full account of these parts I would refer you 
to Ecker’s monograph on the cerebral convolutions, to 
Ferrier’s work on the functions of the brain, and to 
the latest edition of “ Dalton’s Physiology.” A few of 
the convolutions in these lobes and lobules are of im- 
portance in the study of localization, and I must 
briefly describe them. 
First, the third and ascending frontal convolutions. 
The former of these (f. 3, Fig. 9) constitutes the lower 
tier of gyri in the external aspect of the frontal lobes, 
and forms the antero-superior lip of the fissure of Sylvi- 
us. Its posterior part and its continuation into the isl- 
and of Reil certainly have a very close connection with 
the function of written and spoken speech. The as- 
cending frontal gyrus (A, Fig. 9) forms the posterior 
limit of the frontal lobe, and lies against the fissure 
of Rolando. Ecker calls it the anterior central con- 
volution, but in common with Prof. Charcot and his 
pupils, I prefer the former designation. Immediately 
behind the fissure of Rolando, extending almost verti- 
cally, is the ascending parietal gyrus, or the posterior 
central convolution of Ecker. These two gyri, the 
ascending frontal and parietal, are intimately con- 
nected with movements of the face, arm, and leg; so- 
called centres for the face existing in the lower ascend- 
ing frontal, centres for the upper extremities being 
found in its middle portions and in the ascending 
parietal gyrus; while the centres for the movements of 
the lower limbs are in the upper (inner) extremities of 
both these gyri, and in the next parietal convolution 
near the median fissure, viz., the superior parietal (p. 
1, Fig. 9). 
The last gyrus of clinical importance is the next 
below the inferior parietal and its extension toward 
the occipital lobe, the angular gyrus, so-called (P2' 
Fig 9). Some recent clinical and post mortem facts 67 
would seem to connect it with movements of the eye- 
lids and upper face. Besides, the paracentral lobule 
is of importance to us, because we know that its de- 
struction is followed by descending degeneration. 
Fig. 9. 
Modified from Ferrier: letters and figures the same.—S, Fissure 
of Sylvius; c. Fissure of Kolando; po, Parieto-occipital fissure. A, 
Ascending frontal gyrus; B, Ascending parietal gyrus; F3, Third 
frontal gyrus; P3', Gyrus angularis. Circle I„ Seat of lesions which 
(on the left side) cause aphasia. Circle II., Seat of lesions which con- 
vulse or paralyze the upper extremity of the opposite side. Dotted 
Circle III., Seat of lesions which probably convulse or paralyze the face 
on the opposite side. Dotted Oval IV., Seat of lesions which probably 
convulse or paralyze the lower extremity of the opposite side. These 
districts receive their blood-supply chiefly from the middle cerebral 
artery. 
The cerebral convolutions are supplied with blood 
by branches of the anterior, middle, and posterior 
cerebral arteries, and an exact knowledge of the dis- 
tribution of these trunks and their ramification is of 
the utmost importance in the study of localization of 
lesions, inasmuch as one of the most common patho- 
logical processes by which destruction of convolu- 68 
tions is caused, is embolism, or plugging of one of 
these arteries. 
In general terms, the anterior cerebral artery sup- 
plies the inner face of the hemisphere as far back as 
the occipito-parietal fissure; the first, second, and 
(very partially) the ascending frontal convolutions. 
The middle cerebral artery, or the Sylvian artery, is 
the most important physiologically, as it supplies all 
the convolutions mentioned above as concerned in the 
production of voluntary movements, viz., the third 
and ascending frontal, ascending, and first and second 
parietal convolutions. Easily recognized branches of 
the middle cerebral artery furnish blood to the third 
frontal (first branch in the fissure of Sylvius), to the 
ascending frontal, to the ascending parietal; a fourth 
branch extends as far as the angular gyrus, and a fifth 
supplies the first temporal convolution. 
The posterior cerebral artery supplies the remainder 
of the temporal lobe and the whole of the occipital. 
It might not quite be out of place to state here that, 
according to Charcot and Duret, the basal ganglia of 
the brain receive their blood through small branches 
which leave the great arteries very near the origin of 
the circle of Willis. The anterior part of the nucleus 
caudatus is supplied by arterioles derived from the an- 
terior communicating artery, and from the first portion 
of the anterior cerebral artery. The nucleus lenticu- 
laris and the anterior part of the thalamus opticus are 
vascularized by branches of the trunk of the middle 
cerebral artery before it enters the Sylvian fissure. The 
larger part of the optic thalamus is supplied by vessels 
coming from the second portion of the posterior cere- 
bral artery beyond the circle of Willis. Finally the 
inner aspects of the thalamus and the walls of the 
third ventricle receive branches from the posterior 
communicating artery, and from the first portion of 
the posterior cerebral artery within the circle of Willis. 
To return to the arteries of the cortex. Ramifying in 
the pia covering the convolutions, they penetrate the 
nervous tissue in a peculiar manner, in the shape of 
long and straight branches, which supply the various 
layers of the cortex by means of horizontal branches, 
and ultimately, in small numbers, and greatly reduced 69 
in size, reach the white substances. A most important 
peculiarity in the superficial and deep cortical circu- 
lations is the absence of anastomosis between arteries of 
any great size. As to the exact amount of anastomosis 
there is a difference of opinion between the two origi- 
nal observers in this matter—both equally competent 
—Duret, of Paris, and Heubner, of Leipzig. The 
former maintains, and pathology supports him, that 
there is next to no anastomotic circulation upon or in 
the cortex (except through capillaries), while Heubner 
thinks that considerable branches of the great cerebral 
vessels open into one another upon the surface of the 
brain. The importance of this point for the progno- 
sis of embolism of the cerebral arteries is enormous, 
and for my part I would say that I am disposed to 
consider Duret’s statement as more applicable to 
practice. 
I now pass to a very short account of the physiology 
of the cortex. My statements upon this matter wdll 
be all the briefer because an excellent and full ac- 
count of the physiology of the cerebrum is accessible to 
all of you in Prof. Dalton’s “ Treatise on Physiology.” 
Dr. Dalton himself has taken an honorable part in the 
researches which have, in the last five years, revealed 
unsuspected properties in the cortex of the brain. 
First. We now know, since the experimental re- 
searches of Fritsch and Hitzig (1870), and of Ferrier 
(1878), that the cortex of the brain is excitable; i. e., 
that galvanization or faradization of the cortex pro- 
duces muscular movements in the body and limbs. 
This fact, standing out in direct contradiction to the 
teaching of all physiologists from Magendie and Mul- 
ler, is a monumental acquisition to biological science. 
Second. Very numerous researches by Hitzig, Ferrier, 
and a host of others, appear to have established be- 
yond question that a certain relation exists between 
well-defined portions of the cortex of one hemisphere 
and limited muscular groups (almost individual mus- 
cles) in the opposite half of the body. The areas of 
convolutions whose irritation by electricity is followed 
by definite movements of peripheral parts have been 
denominated motor centres, or psycho-motor centres; 
and a large number of these centres have been deter- 70 
mined by Prof. Ferrier and by Prof. Hitzig, upon the 
brains of dogs, cats, and living monkeys whose brains 
bear a certain resemblance to the cerebrum of man. 
While knowing of a few opposing experiments which 
would seem to show that there is no constant relation 
between the spot irritated and the resultant move- 
ment, I am bound, by the weight of evidence and 
by the wonderful accord between the researches of 
various experimenters, to accept the facts as stated 
above. 
Third. The excitable district of the brain is its 
median group of convolutions, including (as sketched 
upon a human brain, after experiments upon monkeys) 
the second, third, and ascending frontal convolutions, 
the ascending and first parietal convolutions. This 
excitable district or zone includes, as you perceive, 
gyri which receive their blood-supply by branches of 
the middle cerebral artery, with the exception of the 
second frontal gyrus. As my chief object is not phy- 
siological teaching, I prefer simply to enumerate the 
cortical centres as laid down by Ferrier, not encum- 
bering the diagram with a representation of them. 
On the posterior extremity of the third frontal gyrus, 
near the fissure of Sylvius, is a centre for the move- 
ments of the lips and tongue (a speech-centre accord- 
ing to the teaching of pathology); this is numbered 9 
and 10 on Ferrier’s plate. Next in order, upon the 
lower part of the ascending frontal convolution are 
centres for movements of the elevators and depressors 
of the angle of the mouth; numbered 8 and 7. Still 
higher on this gyrus is a centre for movements of the 
forearm and hand: numbered 6. Upon the upper 
two-thirds of the ascending parietal convolution are 
several centres for complex movements of the hand 
and wrist; designated by Ferrier, a, h, c, d. Much 
farther forward, upon the hemisphere near the great 
longitudinal fissure, is an extensive region embracing 
the posterior parts of the first and second frontal 
gyri, governing lateral movements of the head, eleva- 
tion of the eyelids, and dilatation of the pupil; num- 
bered 12. Immediately behind this, near the longi- 
tudinal fissure, upon the posterior extremity of the 
first frontal convolution, is a centre for extension and 71 
forward movements of the hand and arm ; numbered 
5. The posterior (inner) ends of the ascending fron- 
tal and ascending parietal convolutions contain cen- 
tres (not clearly differentiated) for complex move- 
ments of the arms and legs together; numbered 2, 3, 
and 4 on Ferrier’s plate. Finally, behind these on 
the superior parietal lobule is a centre for movements 
of the leg and foot; numbered 1. 
The sensory centres of Ferrier occupy various parts 
of the inferior parietal lobule, the gyrus angularis, the 
second occipital, and first temporal convolutions. Al- 
though the experiments of various observers make 
it exceedingly probable that these inferior and poste- 
rior portions of the hemisphere are connected with 
general and special sensory functions, yet, as human 
pathology has so far thrown no light upon these 
questions, I shall hereafter confine myself to the study 
of the motor districts of the convolutions. 
Not to weary you by the citation of the now very 
numerous cases in which localized cortical lesions, 
as tumors, abscesses, clots, softening, pressure-effects 
from bone or thickened meninges, have given rise to 
definite symptoms, in close or even almost exact 
agreement with the data obtained by faradizing the 
cortex, I shall state in a general manner the tendency 
of these recent clinical and post-mortem studies. 
In the first place, it appears almost absolutely cer- 
tain that in man a lesion involving the posterior part 
of the third frontal convolution (on the left side 
usually) causes aphasia; i. e., impairment or loss of 
articulate speech, or even of language in general. It 
would seem, besides, that (1) lesions of the same part 
on either side of the brain produce paresis of many 
muscles concerned in lingual and pharyngeal move- 
ments ; (2) that lesions of the anterior folds of the 
island of Reil, convolutions which are continuous 
with the third frontal, may also produce aphasia; and 
that (3) loss of speech may result from injury to the 
white substance lying between the third frontal gyrus 
and the basis cerebri. I believe, you observe, in a not 
too limited localization of the motor functions exerted 
in language, and would graphically represent this by 
the circle marked I. in Fig. 9. 72 
In the second place, lesions limited to the inferior 
portions of the ascending frontal and parietal gyri 
have produced spasmodic and paralytic phenomena 
limited to the upper extremity of the opposite side. I 
am disposed to admit as highly probable that these 
parts are connected in the healthy living man with the 
various voluntary movements of the arm and hand. 
This zone is represented in Fig. 9 by circle II. 
I am not prepared to go farther in admitting path- 
ologically proved cortical centres, but would add 
that there are some reasons for believing that future 
autopsies will locate one centre for the external facial 
muscles just forward of the two centres named above, 
viz., the region included in the dotted circle III. ; 
and another for movements of the legs upon the 
upper parts of the ascending frontal and parietal, as 
roughly indicated by dotted oval IV. 
As regards sensory cortical centres, I have already 
said that we have as yet no pathological data for their 
study. 
Having thus expressed myself about the question 
of cortical centres in man, I pass to the more clinical 
study of symptoms observed when the cortex is in- 
jured. 
First. What are the symptoms of localized lesions 
involving the cortex alone, or the cortex and a mini- 
mum of subjacent white matter ? The symptoms 
differ vastly in accordance with a rule laid down 
years ago by Brown-SCquard, according as the lesion 
is an irritative or destructive one; and besides, they 
vary according as the lesions are within the excitable 
cortical region (defined supra) or outside of it. We 
can clear the ground pretty safely at once by admit- 
ting that lesions irritating or destroying convolu- 
tions not embraced in the motor zone produce no 
symptoms at all. Large parts of the frontal, tem- 
poral, or occipital convolutions may be injured or 
utterly destroyed without the patient showing during 
life any special symptoms of organic cerebral disease. 
This statement is based upon the study of recent cases 
only, though I doubt not that in the literature of the 
century numerous apparently contradictory cases 
might be collected. In considering this negative 73 
proposition, one proviso must be borne in mind, 
viz., that if the lesions of these unexcitable districts 
involve the dura mater, convulsions and localized 
cephalalgia may occur. Of this I have seen one 
marked example. We are now prepared to study the 
symptoms of lesions in the excitable or motor zone of 
the hemispheres, as indicated by the various circles 
in Fig. 9. 
1. The symptoms of an irritative lesion of these parts 
consist in convulsions, with or without subsequent tran- 
sient paralysis; e. g., such a lesion in circle III. (Hit- 
zig’s case) would give rise to spasmodic movements in 
the superficial muscles of the face on the opposite side, 
with slight paralysis. Irritative lesions of the regions 
inclosed in circles II. and IV. will cause convulsions 
limited to, or first appearing in the hand and arm, or 
foot and leg, of the opposite sides. As regards cir- 
cle I., Broca’s speech-centre, we know little of the 
effects of its pathological irritation. In one case 
which I have placed on record, a thickening of the 
meninges involving the third frontal convolution of 
the left side produced intermittent and incomplete 
aphasia. 
It was by the close study of the clinical and patho- 
logical aspects of cases of localized epilepsy (fingers 
and hands), that Dr. J. Hughlings Jackson was ena- 
bled to form his theory of motorial discharges from 
irritation of the cortex cerebri, and thus pave the 
way for Ferrier’s admirable researches. Dr. Jackson 
must. I think, be considered, after Prof. Broca, as the 
founder of our present growing doctrine of cortical 
localizations. 
2. Destructive lesions of portions of the excitable 
district produce paralysis in peripheral parts across 
the median line. The symptoms will, to a certain 
extent, correspond with the precise location of the 
lesions, very much as in .irritative lesions; e. g., embo- 
lism of the first branch of the middle cerebral artery 
on the left side will cause softening of the posterior 
part of the third frontal gyrus, with the symptom 
aphasia. A destructive lesion of the principal part 
of the motor zone on the right side will produce left 
hemiplegia without aphasia ; bnt if this lesion occupy 74 
the left hemisphere, loss of speech will co exist with 
the paralysis. 
It must be added that secondary descending degen- 
eration ensues after destructive lesions of the motor 
regions of the cortex, and that we have late contracture 
or rigidity of the paralyzed limbs as part of the symp- 
tom-group. ' 
Negative characters of these cortical lesions are pres- 
ervation of sensibility in the paralyzed parts, and (ex- 
cept with epileptic attacks) preservation of conscious- 
ness, and incompleteness of paralysis. 
In the next place, let us inquire what are the symp- 
toms produced by diffused lesions of the cortex. As 
exemplified in acute meningitis, the chief symptoms 
are delirium, convulsions, and pain; evidences of in- 
tense irritation. The coma and paralysis which follow" 
may in some degree be caused by impaired nutrition 
of the cortex, but more probably by circulatory and 
tension-changes in the whole encephalic mass. 
There is a much better disease for studying the 
effects of lesions of the surface of the brain, both irri- 
tative and destructive—I mean general paralysis of 
the insane, or, anatomically speaking, diffused chronic 
meningo-encephalitis. The affection is very common, 
and has been thoroughly studied clinically and patho- 
logically. From these studies wre learn that in the first 
stage of the affection there occur fibrillary contractions 
in many muscles of the tongue, face, and limbs ; that 
speech is made tremulous and jerky ; that there is over- 
ideation and even acute delirium ; that gradually mem- 
ory and judgment become impaired, and a semi-para- 
lytic and semi ataxic condition develops in the limbs. 
Later the mental faculties are abolished ; a stage of 
dementia with occasional gleams of delirium (exalted 
notions), and integrity of the organic functions char- 
acterize the disease. The attempt is now being made 
to show that when the meningo-cortical changes are 
limited to the frontal lobes the symptoms are mainly 
psychical; when the lesion involves the motor dis- 
tricts alone we observe abundant fibrillary tremors and 
pseudo-paralysis; and, finally, if the occipital lobes 
are affected, sensory symptoms (hallucinations) pre- 
dominate. As yet not much support has been ob- 75 
tained for such a distinction, which appears very 
tempting upon physiological grounds. It should 
not be forgotten, in using cases of general paralysis 
for the study of the question of localization, that 
the disease is one in which lesions exist in many 
parts, or almost all the parts of the cerebro-spinal 
axis. 
The question of the localization of functions in the 
cerebral convolutions, and that of the possibility of 
diagnosticating their lesions are as yet in their infan- 
cy ; we need numbers of exact observations to decide 
it one way or the other. Just now, I believe that the 
presumption is in favor of a positive answer; there 
are many facts supporting this affirmative. The clini- 
cal and post-mortem facts have just been referred to, 
and I shall close the lecture by recapitulating the 
various anatomical, physiological, and pathological 
evidence in favor of the existence of motor centres in 
the cortex. 
1. Coarse anatomy enables us. to trace bundles 
of fibres upward from the motor tract of the me- 
dulla and pons, into the internal capsule as far as 
the convolutions which are grouped about the fissure 
of Rolando. By its aid we can also trace sensory 
nerve-fasciculi from the posterior regions of the pons 
to the occipital and temporal lobes, and their cortex. 
Such gross dissections are, however, condemned as 
unreliable by some authorities. 
Microscopic anatomy shows that the so-called 
motor gyri are rich in large cells; nay, that they 
alone contain the “ giant-cells ” of Betz, that is, gan- 
glion-cells, which in size and number of processes bear 
a remarkable resemblance to the unquestionably mo- 
tor ganglion-cells of the anterior horns of the spinal 
cord and the medulla oblongata. In the motor con- 
volutions these giant-cells are found in little clusters 
of three, five, or more, in a section, imbedded among 
the large ganglion-cells of the third layer. 
2. Experimental physiology teaches us that electri- 
cal irritation of this zone, and of this zone only, pro- 
duces muscular contraction in parts on the other side 
of the median line ; and, further, that this zone may be 
divided into a number of “ centres ” for various small 76 
parts, tongue, face, arm, leg, etc.* By experimenta- 
tion we also learn that slicing or burning off these 
cortical centres produces partial paralysis of periphe- 
ral parts on the opposite side of the body, with pre- 
cisely the same correspondence between centres and 
muscular groups as the irritative experiments demon- 
strate. 
By the latter mode of experimenting applied to the 
occipital and temporal convolutions (Ferrier, II. Munk, 
and others), it is made highly probable that there is a 
certain relation between parts of these gyri and the 
organs of special and general sensibility across the 
median line. 
3. Pathological anatomy (recent cases) demon- 
strates (a) that destructive lesions of the motor re- 
gions of the cortex (and of the paracentral lobule) pro- 
duce descending degeneration throughout the direct 
cerebral motor tract extending into the lateral columns 
of the spinal cord; and (ft) that there is a remarkable 
correspondence between certain localized spasmodic 
and paralytic symptoms observed during life, and 
lesions irritating or destroying certain definite spots 
in the motor zone of the cortex. 
Lecture VIII. 
SUMMARY:—SURGICAL ASPECTS OF THE QUESTION OF 
CEREBRAL LOCALIZATIONS—CRANIO-CEREBRAL TOPOG- 
RAPHY, AND ITS UTILIZATION IN DIAGNOSIS AND 
FOR OPERATIVE PROCEDURES. 
Gentlemen :—Tiie question of the utilization of the 
doctrine of localization in surgery remains for study. 
This, the most novel part of the subject, is, I think, 
of great present interest and of much promise in the 
future. Already several brilliant surgical operations 
have been performed upon indications derived from 
* Still more recent researches by MM. Franck and Pitr&s show that 
after removal of the cortex in the excitable zone, faradization of 
those portions of white substances which are then exposed (anterior 
half of the internal capsule) gives rise to similar (in kind and in dis- 
tribution) movements in peripheral parts across the median line. 77 
the newly acquired knowledge of cranio-cerebral 
topography. By this term we mean the determination 
of the relations between the external surface of the 
skull and the principal gyri and sulci of the brain. 
So little was done toward ascertaining these relations 
that up to 1861 the position of the fissure of Rolando 
relative to the coronal suture was wholly unknown. 
In that year Prof. Broca invented a scientific proce- 
dure for the study of the subject; he inserted pegs 
into the cerebral substance through holes drilled 
into the skull at given points, and then, removing 
the skull-cap carefully, was enabled to determine 
exactly what convolutions corresponded to the pierced 
regions of the skull. He thus discovered that the 
parieto-occipital fissure lies under the lambdoid suture, 
and that the fissure of Rolando slopes backward, so 
that its posterior extremity is placed at more than 
forty millimetres behind the coronal suture. Since 
that year the subject has been thoroughly studied by 
Broca, Bischoff, Heftier (1878), Prof. Turner, of Edin- 
burgh (1874), Ch. Fer6 and Broca (1875), and others. 
Perhaps the best and most applicable of these contri- 
butions is that of Fer§, and I shall follow it closely 
in the following remarks. It should be borne in mind 
that for purely anthropological purposes the determi- 
nation of the relation of gyri and sulci to certain su- 
tures or processes of the bare skull is sufficient; but 
that for use in the regional diagnosis of cerebral in- 
juries, and in practical surgery, the cranial landmarks 
should be such as are easily determined upon the scalp 
and face of the living man. The resume of cranio-cer- 
ebral topography which I offer for your guidance is 
based upon the latter principle of study. 
As shown in Fig. 10, I shall sketch the situation of 
the principal convolutions, fissures, and central gray 
bodies of the cerebrum upon an outline figure of the 
profile of a skull. The skull is represented as resting 
upon a peculiar plane, one passing under the con- 
dyles of the occipital bones and the alveolar processes 
of the superior maxillae—the alveolo-condyloid plane 
of Broca. Upon this horizontal line, which can be 
determined with reasonable accuracy in the living 
human being, we erect other lines and measure dis- 78 
tanees which enable us to solve almost the whole 
problem. 
1. A vertical line (a) drawn from the alveolo-con- 
dyloid plane through the external auditory meatus 
upward will pass through or very near to the bregma 
or line of junction of the frontal and parietal bones 
at the vertex; it passes through the anterior (lower) 
extremity of the fissure of Rolando. 
2. If from the upper end of this vertical line A, we 
measure a distance of 45 mm. backward toward the 
occiput and draw a descending vertical line (1-2), we 
mark out the location of two most important parts of 
the cerebrum, viz., the posterior extremity of the fis- 
sure of Rolando, and the posterior limit of the thala- 
mus opticus in the hemisphere [at <?)]. 
3. To conclude with the occipital end of the skull; 
if we can make out with the finger the lambdoid su- 
ture at the median line, we thus learn the situation of 
the subjacent occipito-parietal suture, which separates 
the parietal and occipital lobes. 
4. The last vertical line worth noting is one drawn 
at a distance of 30 mm. forward of the auriculo-breg- 
matic line. This vertical line (3-4) will pass through 
the middle fold of the third frontal convolution (just 
forward of the speech-centre), and will also indicate 
the anterior limit of the central cerebral ganglia, viz., 
the head of the nucleus caudatus in the hemisphere 
[at (<J1 
5. The upper level of the central cerebral ganglia 
may be quite exactly indicated by a horizontal line 
drawn at a distance of 45 mm. below the surface of 
the scalp at the bregma (or 35 below the surface of 
the bare skull at the same point). This line (7-8) also 
extends across the middle regions of the motor district 
of the convolutions, containing centres for the face 
and upper extremities. 
6. The external angular process of the frontal bone, 
not difficult to define in the living subject, is the 
starting-point of another horizontal line (5-6), whose 
posterior extremity passes a little below the lambdoid 
suture. Upon this horizontal line we can, by measure- 
ment, determine the location of certain parts. Thus, 
at a distance of 18 or 20 mm. behind the external 79 
angular process lies the folded part of the third 
frontal convolution (a). This point in many heads 
will correspond with the vertical line 3, 4. 
Fig. 10.—Outline of skull resting upon the alveolo-condyloid plane 
of Broca ; modified from Topinard (Anthropology). Vertical line a, or 
auriculo-bregmatic. Line 9-10 drawn parallel to the plane of Broca. 
Upon this line, at a distance of 45 mm. posterior to the bregma, a verti- 
cal line, 1-2, will pass through the upper (inner) end of the fissure of 
Rolando, b ft, and through the posterior extremity of the thalamus opti- 
cus, c). A third vertical line, 3-4, drawn at 30 mm. forward of the 
bregma, will pass through the fold of the third frontal gyrus, a, and 
through the bead of the nucleus caudatus (d. The horizontal line 7-8, 
at 45 mm. below the bregma (scalp), indicates the upper limit of the 
central ganglia. The third horizontal line 5-6, passing through the 
external angular process of the frontal bone and the occi pi to-parietal 
junction, approximately indicates the course of the fissure of Sylvius, 
and serves for measurements. At 18 or 20 mm. behind the ext. ang. 
process on this line is the speech-centre of Broca : 5 to 8 mm. behind 
the intersection of 3-4 and 5-6, is the beginning of the fissure of Sylvius, 
and at 28 or 30 mm. behind this intersection is the lower end of the 
fissure of Rolando, ft, ft, placed a little too far back in the cut. At 
x (near 6), near the median line, is the location of the occipito-parietal 
fissure. 
7. The situation of the fissure of Sylvius may be ap- 
proximately ascertained in the following manner: Its 
middle portion extends horizontally, almost under the 80 
upper part of the squamous suture, which in the living 
subject is to be found a little below the horizontal 
line 5-6. The anterior extremity or beginning of the 
fissure of Sylvius is a little below this horizontal line, 
at a distance of some 5 to 8 mm. posterior to the inter- 
section of 3-4 and 5-6, and consequently about 22 or 
25 mm. anterior to the auriculo-bregmatic line A. 
Lastly, according to Turner, the parietal eminence 
almost always overlies the supra-marginal gyrus (P2, 
Fig. 9), consequently the posterior extremity of the 
fissure of Sylvius is likewise in this vicinity. 
8. The angular gyrus is to be found below and 
behind the parietal eminence, a little above the hori- 
zontal line drawn from the external angular process 
(5-6). 
9. The anterior (lower) end of the fissure of Rolando 
lies at a distance of 28or 30 mm. behind the line 3-4, 
and a little above 5-6. It is therefore a few mm. an- 
terior to the vertical line A. 
The application of these data to practical medicine 
and surgery is quite obvious. 
In medical cases, when tumors of the skull develop 
externally, we may determine by cranio cerebral topog- 
raphy whether their extension inward can give rise to 
the motor symptoms which are present (convulsions 
and paralysis), according as the excitable districts of 
the brain are threatened by extension of the growth 
from the inner surface of the skull, or not. 
In surgery, the utility of cranio-cerebral topography 
is much greater. 
For example, as far back as 1871, Professor Broca 
wTas able to correctly diagnosticate an abscess of the 
left third frontal convolution, and wras successful in 
trephining directly over it. In 1876, Proust and Lucas- 
Championnifcre successfully trephined the skull, in two 
cases, for the removal of fragments which were com- 
pressing the ascending frontal and parietal convolu- 
tions, and causing paralysis. 
In the case of a patient who is paralyzed on one 
side of the body, after an injury to the skull, the fol- 
lowing considerations might justify, or contra-indicate 
an operation for the removal of bone, of blood, or of 
pus: 81 
1. If the hemiplegia (or hemi-spasm) be very com- 
plete, it is probable that the injury to the brain is con- 
siderable in extent, and extends deeper than the special 
centres for the face, arm, and leg. 
2. If the externally evident injury be over non- 
excitable convolutions, and the paralytic or spasmodic 
phenomena he marked, it is more than probable that 
the brain is torn or compressed at other points than 
under the seat of injury, and an operation is contra- 
indicated. 
3. If the paralytic or convulsive symptoms be on 
the same side as the evident cranial injury, it is proba- 
ble that there are cerebral lesions on the other side 
produced by contre-coup, hence interference will be 
undesirable. 
4. Even if a cranial injury be directly over excita- 
ble convolutions, if the resulting paralysis or convul- 
sions be accompanied by marked anaesthesia, an opera- 
tion cannot be expected to do much good, because 
the presence of anaesthesia makes it highly probable 
that the white substance of the hemisphere (posterior 
half or third of the internal capsule) is involved in 
the lesion. 
5. A favorable indication for trephining is when 
aphasia supervenes immediately, or in a few weeks 
after an injury to the skull in the region of the left 
third frontal convolution (see Fig. 10). It is extremely 
likely, in the first case, that a clot or spiculum of bone 
will be found compressing or lacerating the centre 
for speech; in the second, that an abscess has formed 
in the same part (Broca’s case). 
6. Another combination of symptoms which makes 
an operation desirable, and holds out a hope of its 
being successful, is when an injury to the skull over 
the fissure of Rolando on one side is accompanied by 
slight hemiplegia, or by paralysis of the face, or arm, 
or leg, or of any two of these parts combined, on the 
opposite side of the median line, without anaesthesia. 
Under such circumstances, the probabilities almost 
amount to certainty that the centres for (see Fig. 9) 
the face, arm, and leg are separately or collectively 
involved in the lesion (cases of Proust and Lucas- 
Championnifere). 82 
7. A contra-indication to operative interference, 
even in apparently favorable cases, would be symp- 
toms of basal lesions, such as palsy of cranial nerves, 
neuro-retinitis, Cheyne-Stoke’s respiration, and vomit- 
ing. 
Addendum.—A number of corrections to the propo- 
sitions in these lectures have been suggested by my 
friends, or have occurred to my own mind, but I 
believe that only one is worth inserting here. The 
other corrections-and additions are right enough in 
a theoretical sense, but as I have tried to adhere to 
my rule of making no statement which does not re- 
ceive support from several sources, normal anatomy, 
pathological anatomy, and clinical observation, I pre- 
fer not to publish them. 
The correction which I wish to make is to the 
paragraphs a, b, and c, in Lect. V., p. 103, descriptive 
of the crossed paralysis caused by lesions of the crura. 
It should be added in each of these paragraphs that the 
lower part of the face is usually paralyzed on the 
same side as the body palsy, i.e., on the side opposite 
the lesion. In case of a lesion involving both crura, 
the two halves of the face 'will be paretic.