Landon Carter Gray.

A treatise on nervous and mental diseases: for students and practitioners of ... online

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lesion may seem to a superficial observer to leave the mind unim-
paired, when careful examination of the patient will show that this is
only seemingly so. Nevertheless, it remains true that lesion of the
frontal lobe anterior to the motor area and the third frontal convolution
produces only mental symptoms, and not physical ones. Some cases,
notably the celebrated crowbar case, have been vaunted as showing

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that the lesion of the frontal lobe may sometimes not even produce
mental symptoms ; but an analysis of the crowbar case has shown
that there were mental changes sufficient to prevent the individual
from following his occupation, whilst subsequent cases have abund-
antly proved 5ie statements that I have just made.


The centrum ovale, it should be remembered, is nothing more than
the nerve strands coming down from the cortex to pass to the sub-
lying ganglia, and lesions, therefore, of the centrum ovale do not
differ from lesions of the cortex except in the fact that the deeper the
level of the lesion, the more convergence and interlacing will there
be of different nerve fibres coming from different cortical centres.
Thus, a lesion just below the centre for the leg and sufficiently
localized to affect only the nerve strands coming from this centre
for the leg, would cause exactly the same symptoms as a lesion of
th^ leg centre itself — viz., paralysis or convulsion, or both, of the
leg. If the lesion were still deeper-seated, so as to implicate the
nerve strands coming from the leg and the arm centres and converg-
ing so as to reach the internal capsule, the symptoms produced would
be that of simultaneous affection of the arm and the leg centres^
namely, paralysis or convulsion, or both, of the arm and leg. The
deeper down we go in the centrum ovale, therefore, the more
complex will be the symptoms. It is often extremely difficult to
make a diagnosis between a cortical and a subcortical lesion, and we
are generally obliged to seek aid from clinical facts as well as ana-
tomical ones. Thus, if there is a monopl^ic paralysis and convul-
sion at the start, and this paralysis and convulsion remain mono-
pl^ic through months, there is a greater probability of the lesion
being cortical than of its being subrortical, for the reason that there
would be more space in the cortex for the lesion to develop and
affect only one limb than there would be in the centrum ovale.
Again, if the diagnosis of a tumor can be made, and the symp-
tom is a paralysis or convulsion which has remained mono-
plegic for months, the probability is greatest of the lesion in the
cortex, because a tumor in the centrum ovale would be likely to im-
plicate nerve fibres from other centres more quickly in its growth.
Again, if the lesion has been a trauma of the skull, the probability
is greatest of the trauma having impinged upon the cortex rather
than upon the subcortical regions. Again, if a diagnosis has been
made of a meningitis, it is certain that the cortex would be affected
by the meningitis long before the subcortical tissue was implicated.
Again, if a diagnosis can be made of an arterial lesion, as in a con-
dition of general endarteritis and atheroma or embolism, the proba-
bilities are far greater of the centrum ovale being implicated, because
the vessels from the pia mater inosculate freely in the cortex, whilst
the subcortical matter is fed with relative sparseness by long, straight
arterial branches dipping down into it. (Fig. 53.) When, how-
ever, the paralysis is not monoplegic, as when both limbs are affected,

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or when there is an affectioD of one or more limbs, or the muscles of
the head and trunk and coincident aphasia, it may be a very diffi-
cult matter to make the diagnosis between a cortical and subcortical
lesion, and in most cases it is almost impossible. To sum up, there-
fore :

1. A cortical lesion is most probable when one centre alone
is affected, and remains affected. Thus, if there should be
paralysis of one arm, with or without convulsion, limited to
that one arm or starting in it, the probability would be exceed-
ingly great that there was a lesion in the middle third of the
motor area. So also when there is a paralysis and convulsion of one
leg, or of the muscles of the head and face, or aphasia alone, or word-
deafness alone, or agraphia alone, or hemianopsia alone, it would be
extremely probable that the lesion was cortical in the respective cen-
tres. If, moreover, there should be a paralysis of a few muscles in
one limb, as of the thumb, and this paralysis should remain for some
time before other symptoms supervened, the probability would pass
into certainty of there being a cortical lesion.

2. A cortical lesion would be rather more probable than a sub-
cortical lesion when there were persistent attacks of loss of con-
sciousness with the localized lesion, although, as I have said, the
weight to be attached to this loss of consciousness is rather prob-

3. A cortical lesion is most probable when one centre is aflTected
first, and then, a distinct interval of time having elapsed, another
centre is affected, and still more if there is a progression of symp-
toms to a third centre, and so on. But this must be nevertheless
taken into consideration : If centres are closely approximated, as are
the arm and leg centres, the centres for the head and neck, and the
centres of motor aphasia and aphasia of conduction, the subcortical
nerve strands from these centres are also close together, so that
a growing lesion could readily extend subcortically as well as
cortically. But if centres as far apart as are the centre for the
leg and the centre for hemianopsia should be affected in progres-
sion, it would then be most probable that the lesion in both cases
was in the cortex, because it would be impossible to conceive of a
subcortical lesion that should extend from beneath the upper third of
the motor area away back to just beneath the occipital lobe without
causing enormous general symptoms, not only of implication of the
whole cerebrum from such a large lesion, but also from impairment
of various nerve centres between the two main ones which we have

4. Meningitis and traumata are more likely to affect the cortex
than the centrum ovale.

5. Tumors are somewhat less likely to affect the centrum ovale
than the cortex, although subcortical tumors are found oflen enough
to prevent this fact from being conclusive.

6. Cortical tumors and meningitis, so far as we now know, are
alone capable of causing a distinct rise of cerebral temperature,
as indicated by my cerebral thermometry. This fact, it should be

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borne in mind^ has only the positive value of making a distinct rise
of cerebral temperature probably indicative of a tumor or meningitis,
but, conversely, the absence of rise of cerebral temperature is of no
value for or against.

This difficulty of diagnosis between a cortical and a subcortical
lesion is of very great importance to the surgeon, because in any
case in which the differential diagnosis canuot be positively made, the
surgeon will save himself many a sore disappointment by carefully
explaining to the patient and his friends the uncertainty of the
localization of the lesion. To this difficulty should be added the
further one of finding the exact site of a lesion, even when it has
been localized in the centrum ovale. This, however, will be dwelt
upon fully in the chapter upon intra-cranial growths (Chap. VII.).


Lesions of the internal capsule are alaiost invariably due to
arterial trouble, either of the nature of endarteritis, embolism, or
thrombosis. In Fig. 52 it has been shown how the terminal
arterioles coming off from the Sylvian artery supply the internal
capsule. At page 38, the location of the different nerve strands in
the internal capsule has been described. Just behind the knee or genu
(Fig. 20) lie the fibres from the motor area, the so-called pyramidal
tract. Immediately in front of them run the nerve strands from the
fecial and byp<^lossus centres, which probably are situated, as we have
seen in Fig. 7, in the lower portion of the ascending frontal convolu-
tion. Behind the pyramidal tract in the posterior third of this portion
of the internal capsule run the sensory fibres, which are on their way to
the t^mentum. Back of the sensory fibres are the optic-nerve fibres
coming in from the occipital lobe. Somewhere in this region are also
fibres from the temporal lobes to the auditory nuclei, aud others from
the olfectory lobes ; but it must be remembered that anatomically the
auditory and olfactory fibres have not been traced, and we are aware
of their existence in this site only by means of clinical facts. Besides
these main motor and sensory fibres there are other short fibres whose
existence we know of anatomically, the lesions of which produce
symptoms that are not known to us; anteriorly to the knee or
genu, there are fibres from the frontal lobe to the pons, and from
the cortex to the optic thalamus ; whilst in the posterior or sensory
portion of the internal capsule, behind the genu, are fibres to the
optic thalamus that are probably sensory, and from the temporo-
oecipital cortex to the pons. Lesions, therefore, of the internal cap-
sule produce either motor symptoms or sensory symptoms, or com-
mingled motor and sensory symptoms. In the majority of cases,
however, the symptoms are motor and but slightly sensory, and the
portion of the internal capsule affected is that supplied by the lenticulo-
striated artery. (Fig. 52.) The form of paralysis is hemiplegic, i 6.,
paralysis of motion or sensation, or both, most frequently motor
alone, of the upper and lower extremity and of the lower part of the
feoe, the eyelids and eye muscles being unaffected. The diagnosis of a

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lesion of the internal capsule is readily made. As has been said,
the paralysis is generally motor only, though sometimes both motor
and sensory ; the onset is relatively acute, being either sudden or
extending over a few hoars or a day ; and in the vast majority of
cases the lesion is one due to some arterial trouble such as an
endarteritis, embolism, or thrombosis. The lesion, therefore,
occurs mainly in certain classes of individuals: first, those who
have the chronic endarteritis of middle age, associated with general
atheroma, hypertrophied heart, and chronic degenerative kidney
lesion; second, those who have au intra-cranial syphilis producing
syphilitic endarteritis ; third, children who have hemiplegia, either
without mental defect or with very slight mental defect; fourth,
in rare cases those who have a premature endarteritis from alcohol-
ism ; fifth, those who have the endarteritis that is associated with
nephritis. Tumors of the internal capsule hardly ever occur, and
traumata impinging only upon this narrow strait of the internal
capsule are equally rare, except where there is existing arterial disease
that renders the arterioles excessively fragile.




These cannot be diagnosed. It is possible, however, that the recent
localization by Ott of a heat centre (see p. 83) in the optic thalamus
will be the means of our making a diagnosis, although as yet this
has not been done, and the heat centre has only been localized in
the dog and the rabbit.


As has been seen in Figs. 21, 24, 27, 29, and 34, the quadrigeminal
bodies are in close relation to the optic-nerve fibres, to the t^mentum,
to the superior and middle cerebellar peduncles, to the pineal gland,
to the pulvinar of the optic thalamus, and also to the nuclei and nerve
fibres of the ocular nerves. It can well be seen, therefore, how much
doubt there is as to whether the symptoms are due to lesion alone
of the quadrigeminal bodies or to associated lesion of the surrounding
structures. Such cases, however, as have so far been published, some
twenty in number, would seem to show that the symptoms are : first,
an unsteady, reeling gait appearing early in the course of the
symptoms ; second, ophthalmopl^ia of the muscles of both eyes, but
not quite symmetrically, nor implicating all the muscles in equal
degree. Nothnagel believes that the reeling gait is due to the quad-
rigeminal lesion alone, as several cases have been reported in which
the cerebellar peduncles were not affected. Thus Feilchenfeld,
Pontoppidan, and Fischer have reported three cases of tumor of the
pineal gland alone, with pressure upon the quadrigeminal bodies,
whilst Massot has reported a case of a tumor of the pineal gland in -
which the quadrigeminal bodies were not compressed and there was no
reeling gait. The reeling gait is like that of cerebellar lesion, and con-

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sists of a stumbling or titubation similar to that of a drunken man^ and
it is entirely dissimilar to the ataxia of locomotor ataxia^ in which
the patient walks erectly but brings his heels down with a stamp or
a tendency to a stamp, and the upper extremities are not affected at all.
The ocular muscles which are most prone to be affected are those sup-
plied by the third pair, although, as has been already stated, other ocular
muscles may be affected so as to give rise to an ophthalmoplegia. The
lesion of the ocular muscles is due to compression or extension of the
quadrigeminal lesion to the nuclei and nerve fibres of the ocular
nerves. As has been said, this ophthalmoplegia is not apt to be com-
plete or bilateral. Thus, when the third nerve is affected, it is generally
the superior and inferior recti which are paretic or paralyzed, or the
lateral movement of the eye may be abolished, or ptosis may be the
most marked symptom ; and although ophthalmoplegia occasionally
occurs, it is seldom as complete as when the nuclei themselvesare affected
(see Prc^ressive Ophthalmoplegia). Nystagmus alone, or in conjunc-
tion with paralysis of ocular muscles, may occur. It has also been
claimed that the trochlear or abducens nerve alone can be affected, and
it was at one time thought that this was a diagnostic symptom, but it
has not been proven. Nothnagel has recently expressed the belief
that lesion of the quadrigeminal bodies may leave the vision entirely
unimpaired, but in .making this statement he does not seem to have
taken account of any other impairment of sight than amblyopia
or amaurosis^ the cases which he cites do not seem to have been
definitely examined for hemianopsia, and in other cases he admits
that choked disc and optic neuritis were present in such degree as to
make it impossible to thoroughly examine the visual acuity ; more-
over, the recent experiments and cases of von Monokow have proven
that the anterior quadrigeminal bodies, together with the lateral
geniculate body, are connected with the optic nerve fibres. Diag-
nosis of a lesion of the quadrigeminal bodies may therefore be made
by means of the reeling gait, associated with ophthalmoplegia or
isolated paralysis of the trochlear or abducens nerve, or with
nystagmus, and also by the absence of other motor, sensory, or vaso-
motor symptoms. I think it is probable that the future will show
that hemianopsia is associated with these symptoms, especially when
the anterior quadrigeminal bodies are implicated ; and it must not be
forgotten that the posterior quadrigeminal and middle geniculate
bodies have been shown by von Monokow and Spitzka to be con-
nected with hearing, so that deafness may prove to be a sign of lesion
in this region (see page 55).


Homen, Meyer, and Spitzka have carefully studied cases of lesion
of the pons.^ Of these three, the most minutely and therefore thor-
oughly described is Spitzka^s. In these three cases the age was forty-

* Hom^n : Virchow's Archiv, 1882, B. Ixxxviii., H. 1, p. 61. Meyer : Arch. f.
Psych. iL Nervenkrankheiten, xiii., H. 1, p. 63. Spitzka: Journal of Neurology
and Psychiatry, November, 1883.

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eight, forty-eight, and fifty-eight, respectively, and the lesion was an
arterio-sclerosis causing either hemorrhages or softening. Meyer's
case was not diagnosed during life, but this diagnosis was made by
Hom6n and Spitzka. It must be remembered that, as has been
shown in Figs. 21, 22, 24, and 27, the pons is a very complicated
structure, containing motor and sensory fibres passing from the cortex
down to the spinal cord, as well as nerve fibres and nerve nuclei of the
different cranial nerves, the cerebellar peduncles, and transverse fibres
connecting the two lobes of the cerebellum. The exact lesions, there-
fore, will vary to some extent according to the level of the pons
that is aflected, but these three cases of Hom^n, Meyer, and
Spitzka, together with the knowledge gained from other sources,
have enabled us to speak with some certainty of the main diagnostic
symptoms. In the former there were : 1. Paralysis of the tongue,
which deviated to the side of the lesion; 2, hemiansesthesia of
the opposite side ; 3, constant dizziness ; 4, ataxia of the limbs of
the opposite side ; 5, exa^erated knee-jerk of the opposite side ; 6,
diminution of cutaneous reflex of the opposite side ; 7, subjective
sense of muscular cramping of the extremities of the opposite side
The hemiansesthftsia consisted of impairment of touch, temperature,,
sense of weight, and muscular sense — the latter to a slight d^ree..
The ataxia was greater on closing the eyes, but was not increased by
placing the feet close together. In Meyer's case there was a loss ot
faradic excitability of nerve and muscle in the face, and of galvanio
excitability of the nerve in the same r^on. Meyer's case had also
contracture, muscular atrophy, and trophic disturbances of the arm
opposite to the lesion. In Spitzka's case the pupil became somewhat
contracted nearly three years after the first symptoms appeared, whilst
in Meyer's case the pupil was unaliected ; and this is a contradiction
of the prevailing view that a lesion of the pons must be necessarily
accompanied by a contracted pupil, although cases do occur in w^hich
there may be myosis, at the same time that other cases have been
observed in which they have been found dilated. The reaction of
the pupils to light is an equally unreliable symptom for purposes ot
diagnosis. The lesion in Hom^n's, Meyer's, and Spitzka's cases
implicated the lemniscus, and in Spitzka's case it was about at the
level that is figured in Figs. 31 and 32, about at Im and extending

Lesions of the pons may be diagnosed by the following symp-
toms : 1. Paralysis of sensation or motion, or both, of the side of the
body opposite to the lesion ; 2, paralysis of the trigeminal, ab-
ducens, facial, or hypoglossal nei'ves, and possibly also of the auditory,
all upon the same side of the body as the lesion ; 3, vertigo ; 4, exag-
gerated knee-jerk on the side of the body opposite to the lesion ;
5, subjective sense of cramping of the extremities of the side of the
body opposite to the lesion; 7, absence of mental disturbances;
8, possibly conjugate deviation of the eyeballs and head toward the
side of the lesion ; 9, difficulty of deglutition and articulation ; and ] 0,
ataxia of the opposite limbs. As we have already seen, the pupillary
conti'action is an unreliable sign, although it is probably of value in

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the diagnosis of a sudden hemorrhage into the pons^ when it has been
frequently observed as a temporary symptom. If disease should be
situated high in the pons, however, near where the cms passes into
it, there would be a unilateral paralysis, t. e., the cranial nerves and
the limbs would be affected upon the same side— opposite to the lesion.
This can be readily understood when we remember that the nerve
fibres from the different cranial nerves have here reached the side
upon which they are going up to the cortex, just as they have in the
internal capsule. (Figs. 21 and 35.)


Lesions of the medulla oblongata assume either the form of pro-
gressive ophthalmopl^ia or labio-glosso-laryngeal paralysis, which
are treated of in separate chapters. Lesions of the individual nerve
nuclei are difficult to diagnosticate, unless symptoms of impairment
of a cranial nerve are observed in the course of one of these symptom^
groups, or of a prc^ressive muscular atrophy.


The dia^osis of cerebellar lesions is a very difficult matter. It
was formerly supposed that a swaying, staggering gait was pathogno-
monic, but since it has been shown to be present in the two care-
fiiUy observed cases of pons lesion recorded by Spitzka and Meyer,
this view is no longer tenable. When, however, to the staggering,
swaying gait there is added a marked tendency to staggering per-
sistently in one particular direction, this would be indicative of lesion
of the cerebellar peduncles, and therefore the probability of a coinci-
dent cerebellar lesion would become stronger. These movements in
one particular direction may consist of staggering to one side, or
backward, or forward, or in a semi-rotary movement around a circle.
A peculiar condition of the eyes was observed in one case of Monat's :
they were motionless, and one looked downward and outward, the
other upward and inward. In three cases of my own I have also
observed a symptom to which I have seen no allusion, namely, a pecu-
liarly tight drawing of the scalp over the skull during the paroxysms of
headache and dizziness. Many cases of disease of the cerebellum
and its peduncles have been latent so far as r^ards symptoms. It
is, therefore, a matter of considerable doubt as to whether we can
positively make a diagnosis between lesion of the cerebellum and its
peduncles and that of the pons ; although the probability would be
strongly in favor of a disease of the cerebellum or its peduncles when
there existed a swaying, staggering gait, especially when this was
accompanied with forced movements in certain directions, and when
there was no motor or sensory paralysis of the extremities and no
implication of cranial nerves.

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Tlie symptoms of lesious at the diflFerent levels of the cord can be
ascertained by means of the table upon page 64. The localization
of symptoms in the various portions of the gray matter and white
matter can only be made to a limited extent. Thus, motor paralysis
with muscular atrophy and entire absence of sensory symptoms
would indicate that the anterior cornua of the cord are implicated, as
in poliomyelitis anterior and some forms of progressive muscular
atrophy ; and a lesioo may be localized in the lateral pyramidal
colunm when there are exaggerated tendon-reflexes, contracture, and
hasty micturition, as in secondary descending degeneration of this tract
from some higher level in the cord, pons, or cerebrum. But a disease
of the posterior cornua cannot be diagnosed, nor of such white
strands of the cord as the columns of Goll, Burdach, Spitzka-Lissauer,
direct cerebellar and Gowers' columns, and the anterior fundamental
column. It has been supposed that the posterior columns of Burdach
and the columns of Goll contained the tactile and muscular sense
nerve fibres, and the column of Clarke, or the vesicular column, the
vasomotor and trophic nerve fibres, but many clinical observ^ations
have failed to prove this view, as well as the belief that lesions of
the direct cerebellar columns are always the cause of ataxia in spinal


Lesions of the peripheral nerves can be diagnosed by the symp-
toms that will be detailed in the chapter upon Neuritis.


At the outset of this subject it should be clearly understood that
there is a technical difference in the meaning of the two words
hemianopsia and hemiopia, although their etymological derivation is
almost tlie same {tide pp. 27 and 46). Hemiopia is the blindness
of bilateral halves of the retina. As is well known, the rays of light
coming from the outside cross in the optic lens, and therefore a person
who has a left-sided hemiopia will fail to see objects to the right side

Online LibraryLandon Carter GrayA treatise on nervous and mental diseases: for students and practitioners of ... → online text (page 11 of 84)