it is desirable to add a few words concerning the decussation of the
pyramids or distribution of the pyramidal tract in the spinal cord. As
is well known, this is double, a small part of the pyramidal bundle
remaining on the same side of the median line, the so-called direct
pyramidal fasciculus or column of Türck (Fig. 5, No. 11) forming the
mesal edge of the anterior column of the cord. The larger part of the
pyramid crosses the median line at the decussation, and enters the
opposite lateral half of the cord, in which it is found as the crossed
pyramidal fasciculus (Fig. 5, No. 10) in the posterior part of the
lateral column, rapidly diminishing in size in the dorso-lumbar part
of the cord. The {88} important point to bear in mind for the study of
monoplegias and of hemiplegia is that the amount of decussation is far
from uniform. This variability was first demonstrated by Flechsig.[14]
He found in a series of sixty fœtuses such variations in the relation
of the crossed and direct fasciculi as 100:0 (complete decussation),
92:8, 84:16, 70:30, 52:48 (nearly semi-decussation, producing equal
fasciculi), 35:65, 10:90 (almost non-decussation).
[Footnote 14: _Die Leitungsbahnen im Gehirn und Rückenmark des
Menschen_, Leipzig, 1876.]
It should also be added that quite certainly the cerebellum, nucleus
caudatus, nucleus lentiformis, and nucleus pontis form parts of the
complete kinesodic system, but we are as yet ignorant of their exact
connections and functions.
With respect to the anterior part of the frontal lobe, forward of the
oblique line A B across Figs. 10 and 11, the study of human cases of
destructive injury and disease would indicate that it is not
associated either with the kinesodic or with the æsthesodic systems.
The SYMPTOMS of lesions of the kinesodic system, particularly of the
pyramidal tract, are exclusively motor, consisting of spasm and
paralysis. Contracture of the paralyzed parts follows the paralysis
after a few weeks if the lesion be a destructive one.
Clinically, the following DIAGNOSES of localization of lesions in this
system are now possible:
(_a_) Lesion of the speech-centre (4) and of its associated white
fasciculus is indicated by intermittent or constant aphasia of the
motor form, with or without paralysis of the face and limbs (on right
side usually).
(_b_) Lesion of the facial centre (1) and of its associated fasciculus
is characterized by the occurrence of spasm or paralysis, or of both
in rapid succession, in the facial muscles; their electrical reactions
remaining normal.
(_c_) Lesion of the brachial centre (2) and of its associated
fasciculus is made known by spasm or paralysis, or by both in
succession, in the hand and arm. In many cases (tumor especially) the
first symptom is clonic convulsive movements of two or more fingers,
extending to other parts of the arm. Such brachial monospasm or
monoplegia is usually accompanied or followed by incomplete
hemiplegia.
(_d_) Lesion of the crural centre (3) in the paracentral lobule and of
its associated fasciculus of white substance is indicated by priority
and predominance of convulsive and paralytic phenomena in the foot and
leg: a crural monospasm or monoplegia exists with or without
incomplete hemiplegia.
The positive diagnosis of these separate localizations is most
feasible in cases of tumors or of cranial injury where the initial
lesion is limited in extent and where the morbid process is for a time
localized. As a rule, localized spasm (Jacksonian epilepsy) without
loss of consciousness is the first symptom, followed after a time by
localized paralysis (always in the same muscular groups); and later
still the symptom-group becomes obscured by the supervention of other
symptoms indicating extension of disease to other parts of the
kinesodic system, or even to the æsthesodic system.
(_e_) Lesion of the insula and adjacent white substance laterad of the
nucleus lenticularis (5) may be suspected from the rapid or sudden
development of symptoms imitating those of acute bulbar paralysis, but
{89} without bilateral paresis of the body and anæsthesia. Aphasia is
very apt to coexist with the bulbar symptoms if the lesions involve
the left insula, whose frontal folds are continuous with the
speech-centre.
Common hemiplegia with contracture, but without anæsthesia, represents
a gross lesion of the kinesodic system, involving several cortical
centres or the motor part of the internal capsule:
(1) A widely-spread lesion of the cortex of the brain, softening of
the motor zone (centres 1, 2, 3, 4) from embolism or thrombosis of the
middle cerebral artery.
(2) Hemorrhage from vessels of the nucleus caudatus and nucleus
lentiformis compressing or destroying the motor segment of the
internal capsule at various levels. More rarely there is a form of
softening or gliomatous growth involving the same parts. Any of these
lesions may be so localized as to destroy only one fasciculus of the
capsule, giving rise to monoplegia.
The limits of the so-called sensory and motor centres or cortical
areas, and the possible localization of lesions in them, will be
better understood by the help of the accompanying diagrams (Figs. 10
and 11, p. 90) of the lateral and mesal aspects of the hemisphere.
B. FOCAL LESIONS OF THE ENCEPHALON.—1. FOCAL LESIONS OF THE CEREBRUM,
OF ITS CORTEX AND SUBJACENT WHITE SUBSTANCE, AND BASAL GANGLIA.—(_a_)
Focal lesions of the frontal lobe produce no specific symptoms, and
cannot be directly diagnosticated unless they extend as far caudad as
the base of the second and third frontal gyri. The forward mass of the
frontal lobe, including the orbital lobule (vide Fig. 10), appears to
be inexcitable and insensitive. Even psychic symptoms do not
necessarily appear after the loss of considerable amount of cerebral
substance from this region. The diagnosis of tumors, abscesses, etc.
in this part of the brain must be made by taking into consideration
the seat of pain, the presence of cicatrices or other etiological
indications, the general signs of the cerebral irritation and
compression, but, after all, usually by exclusion. In some cases
unilateral anosmia is produced.
(_b_) Focal lesions of the caudal part of the frontal lobes, of the
insula, the pre- and postcentral gyri, and other parts of the motor
zone are usually easy of diagnosis. The symptoms of such lesions have
already been detailed when speaking of lesions of the kinesodic
system.
(_c_) Focal lesions of the parietal, temporal, and occipital lobes of
the brain have the characteristic semeiology of lesions of the
æsthesodic system, considered supra.
(_d_) Lesions of the so-called basal ganglia, the nucleus caudatus,
nucleus lentiformis, and thalamus, usually give rise to motor and
sensory symptoms indirectly by pressure upon or destruction of the
segments of the internal capsule which lie between these bodies (vide
Figs. 7 and 9). Lesions of the nuclei caudatus and lentiformis are
thus more prone to produce purely motor symptoms, while sensori-motor
and ataxic symptoms result from lesion of the thalamus.
The symptoms indicating lesions strictly limited (in extent and in
effect) to these ganglionic bodies are at present practically unknown.
(_e_) Lesions (tumors, etc.) of the lobi optici (tubercula
quadrigemina) are productive of early neuro-retinitis and blindness,
of convulsions, and of diffused bilateral incomplete paralysis of the
body, without symptoms {90} of disease at the base of the brain (vide
infra). The diagnosis intra vitam remains of great uncertainty,
inasmuch as other lesions in the median line, involving parts adjacent
to the lobi optici, may give rise to the same symptom-group.
[Illustration: FIG. 10.]
[Illustration: FIG. 11.]
2. FOCAL LESIONS OF THE CEREBELLUM.—(_a_) Lesions strictly limited to
one lateral lobe or hemisphere of this organ do not give rise to any
characteristic symptoms—in some cases, indeed, to no symptoms at all.
When the lesion tends basad, irritating and compressing the subjacent
pons and oblongata on one side, incomplete paralysis appears in the
limbs opposite the lesion, the face usually remaining normal.
Occipital {91} headache, attacks of vomiting, opisthotonos, or intense
subjective stiffness of the back of the neck, with neuro-retinitis,
would strengthen the diagnosis. If the lesion extend laterad, so as to
involve the processus ad pontem (lateral peduncle), a tendency to
rotate while lying or to deviate in walking toward the side of the
lesion may be added.
(_b_) Lesions of the middle lobe, or vermis superior in particular,
may be positively recognized during life. Besides the above-mentioned
general symptoms of cerebellar and bulbar irritation and
compression—viz. occipital headache, cervical stiffness, attacks of
vomiting, neuro-retinitis, and atrophy of the optic nerve—there is a
very characteristic, almost pathognomonic, symptom. This is cerebellar
titubation, miscalled cerebellar ataxia. The patient, whose
equilibrium may be perfect while lying or sitting, upon rising and
attempting to walk does so somewhat like an intoxicated person: the
head and body are bent forward; the arms and hands held out and moved
as balancing weights; the feet are widely separated, the toes
clutching the floor or carpet; the body oscillating somewhat over its
base of support. There are not the wide excursions of the entire body,
the zigzagging, of alcoholic intoxication, nor is there any of the
stamping or jerky step of locomotor ataxia. If the patient be tested
lying or sitting, it is found that neither in the hands nor in the
legs is there a trace of ataxia: muscular strength and sensibility are
long preserved, and the patellar reflex is exaggerated.
3. FOCAL LESIONS OF THE BASE OF THE BRAIN, either within the nervous
substance or springing from the dura, and acting by irritation and
pressure upon various parts of the basal aspect of the encephalic
mass.
(_a_) Diffused bilateral lesions of this class situated frontad of the
crura give rise to more or less distinct symptoms, and a diagnosis is
sometimes possible. (1) Lesions in the vicinity of the sella turcica
and optic chiasm produce symptoms in the optic apparatus very early,
and these remain prominent throughout the illness. These symptoms are,
irregular (at least not lateral) hemianopsia, neuro-retinitis followed
by atrophy of the optic nerve, temporary or permanent paralysis of one
or several ocular nerves. If these exist without symptoms of lesion of
other parts of the brain (reasoning by the process of exclusion), we
may strongly suspect the seat of the lesion to be in the region named.
Other symptoms are paroxysmal headache and occasional vomiting,
epileptiform convulsions (never Jacksonian in distribution), partial
hemiplegia, or general muscular weakness. By such data we were
recently led to the correct localization of a tumor. (2) If the lesion
be farther frontad—_i.e._ strictly in the orbital areas of the basis
cerebri—anosmia, uni- or bilateral, usually with hallucinations of
smell, will be an early symptom, along with neuro-retinitis and
obscure motor and sensory symptoms (headache and convulsions more
especially).
(_b_) Lesions situated caudad of the infundibulum. (1) Bilateral
lesions give rise to symptoms which are the symmetrical duplication on
either side of the face and body of those to be next described as
characteristic of—
(2) Unilateral focal lesions of the base of the encephalon from the
crura caudad to the pyramidal decussation.
In a general way, the symptoms of these lesions are designated as
varieties of crossed paralysis.
Clinically, a crossed paralysis is one in which one or several cranial
{92} nerves show symptoms of irritation or destruction on one side of
the median line, while body symptoms are present on the opposite side.
Physiologically and anatomically, a crossed paralysis is one in which
the lesion is so placed as to affect a cranial nerve (or more than
one) at a point caudad (below) of the decussation of the fibres which
connect its nucleus with the cerebral cortex, or at its nucleus of
origin, or so as to injure the nerve-trunk itself; while at the same
time the lesion affects the main fasciculus of the pyramidal tract
frontad (above) of its decussation, in the crus, pons, or oblongata.
In many cases of crossed paralysis, besides common motor and sensory
symptoms, there is apt to be neuro-retinitis with its consequences.
The chief forms or types of crossed paralysis are:
(_α_) Lesions involving the meso-ventral aspect of one crus cerebri.
The direct symptoms of such a lesion are in the range of distribution
of the motor oculi (N. iii.), such as ptosis, mydriasis, external
strabismus, and heteronymous diplopia; the crossed symptoms are more
or less complete paralysis of the lower part of the face and of the
extremities on the opposite side (hemiplegia). This relatively
frequent form of crossed paralysis we designate as the eye-and-body
type.
(_β_) The lesion occupies the latero-ventral part of the crus. This
rare localization would give rise to direct paralysis of the fourth
nerve, indicated by homonymous diplopia in the lower inner field of
vision; to lateral hemianopsia with dark half-fields opposite the
lesion, from injury to the tractus opticus (vide Fig. 8); and to a
mixed motor and sensory disturbance in the opposite side of the face
and body, without anæsthesia of the olfactory and auditory apparatus.
A very large lesion involving almost the entire crus would probably
also cause direct paralysis of N. iii.
(_γ_) Lesion of the basal part of the pons frontad of an imaginary
transverse line passing through the apparent origin of the trigemini
(NN. v.). Symptoms: A common hemiplegia of the lower face and
extremities on the opposite side with neuro-retinitis and other
general signs of basal disease. The abducens nerve (N. vi.) would in
some cases be involved in its course frontad over the pons, giving
rise to internal strabismus and homonymous diplopia on the same side
as the lesion.
(_δ_) A focal lesion in the caudo-ventral part of the pons—_i.e._
caudad of an imaginary transverse line passing through the trigeminus
roots—gives rise to highly characteristic symptoms. These are: Direct
paralysis of the face, not (?) affecting all the muscles, but without
De R., and common hemiplegia of the limbs on the opposite side.
If the lesion be strictly basal—_i.e._ one springing from the
membranes or bone, the trunks of the sixth and seventh (facial) nerves
are directly injured, and the resulting facial paralysis is of the
peripheral form, affecting all the muscles and yielding De R. The body
symptoms on the side opposite the lesion are less marked.
In the first category of cases, those in which the lesion is in the
substance of the pons, the motor fasciculus from the cortex cerebri to
the nucleus of N. vii. is injured caudad of (below) its theoretical
decussation-point on the middle part of the pons, while the pyramidal
tract is involved frontad of (above) its decussation.
This symptom-group is known as face-and-body type, or as crossed
hemiplegia, strictly speaking.
{93} (_ε_) A lesion so placed laterally in or on the pons as to affect
the origin of one trigeminus (N. v.) will cause, besides motor
symptoms in the face and body (types _γ_ or _δ_), special direct
symptoms—viz. anæsthesia in the distribution of the fifth nerve and
paralysis of the masticatory muscles opposite to the body symptoms.
This is the trigeminus and body type.
Lesions may be so placed ventrad or laterad upon or in the oblongata
as to give rise to other types of crossed paralysis: these are easily
assumed in a theoretical manner, but in practice such cases are
extremely rare, present a complicated semeiology, and are usually not
correctly diagnosticated during the patient's life.
V. Cranio-cerebral Topography.
The study of cerebral localizations from a diagnostic and practical
point of view would be incomplete without a brief reference to the
relations existing between the various gyri of the cerebrum and the
external surface of the head, in order to render more accurate the
estimation of the actual location of cerebral injuries and diseases.
The surgical anatomy of the head with reference to its contents has
been developed with remarkable completeness during the past fifteen
years, chiefly by the researches of Broca, Bischoff, Heftler, Turner,
and Féré. Acting upon these data, a number of surgeons have
successfully trephined the skull for the result of injuries, for
abscess, and even for tumors.
The location of many convolutions and fissures of the cerebrum can be
accurately mapped out upon the surface of the skull, or even upon the
head of the living subject, from the projections of certain lines and
measurements from points thus obtained, as well as from some natural
landmarks. For the projection of these lines the head is placed in a
particular position, as can easily be done when we operate upon a bare
skull, but which can also be approximated when we deal with a living
subject either sitting or lying in bed. The skull or the shaven head
should be so placed and held that a line passing from the alveolar
process of the superior maxilla and through the lowest part (condyles)
of the occipital bone shall be truly horizontal. The greatest care
should be used to determine this line—the alveolo-condyloid plane of
Broca—for upon it all other projections and measurements are based.
This position of the head and the alveolo-condyloid plane (line 1-1)
are represented in Fig. 12.
[Illustration: FIG.12. Topographical Lines applied to the External
Contour of the Head.]
From this line (1-1) a vertical line, or one exactly perpendicular to
the first, is drawn through the external auditory meatus. At the top
of head this line—the auriculo-bregmatic line (A A)—indicates the
bregma or true vertex, which important landmark is to be marked with
carmine or aniline upon the scalp. Upon the top of the head an
imaginary horizontal line (4-4), parallel with the alveolo-condyloid
plane, is projected, and upon it we measure backward a distance of
50 mm. (2 inches), and then draw a second vertical line (B B). At the
point where this line reaches the convexity of the head is the
Rolandic point (R), under which, {94} in average heads, lie the upper
or posterior extremity of the fissure of Rolando, the upper ends of
the pre- and postcentral gyri, and within the longitudinal fissure the
paracentral lobe, which together constitute the cortical centre for
the leg of the opposite side. The Rolandic point, thus determined,
should be distinctly marked upon the shaven scalp.
A third horizontal line is next to be drawn from the external angular
process of the frontal bone backward, parallel with Broca's plane.
This line (2-2), which may be termed the fronto-lambdoid because its
posterior extremity usually passes at or near the upper angle of the
lambdoidal suture, serves for the determination of several important
parts. In the first place, the line (2-2) passes at about 5 mm. above
the upper border of the squamous suture, or through it, and under this
line, mostly {95} parallel to it, are the anterior two-thirds of the
fissure of Sylvius. Secondly, at about 5 mm. above and behind the
intersection of lines (A A) and (2-2) is the inferior extremity of the
fissure of Rolando, bounded by the pre- and postcentral gyri. In the
third place, upon this line (2-2), at a distance of 18 or 25 mm.
behind the external angular process, is the folded part of the base of
the third frontal gyrus or Broca's speech-centre (F 3).
[Illustration: FIG. 13. Topographical Lines applied to Henle's Figure
of the Skull. Location of the Rolandic point. Rolandic line,
motor-centres, and the branches of the middle meningeal artery.]
Having exactly determined and marked the situation of the Rolandic
point and of the inferior termination of the fissure of Rolando above
the ear, these two points are to be connected by a line, which is
represented on the diagram by a black bar. This, the Rolandic line, is
the guide for nearly all operations for the relief of spasm or
paralysis of traumatic origin, or of such as may be caused by tumors,
abscesses, etc. It is surrounded by the so-called motor centres for
the face, arm, and leg (?) as demonstrated by experiments upon animals
and by now numerous autopsies in human cases of injury and disease.
Other relations of interest are the apex of the temporal lobe, a
little beneath the line (2-2) and at about 10 to 15 mm. posterior to
the external angular process of the frontal bone; the situation of the
occipito-parietal fissure, almost immediately under the posterior end
of the line (2-2) at its junction with the lines (E E), which indicate
the posterior extremity of the cerebrum; the anterior end of the brain
being marked off by the line (D D).
{96} Furthermore, for certain purposes the limits of the basal or
central ganglia may be estimated as follows: Their superior limit is
indicated by a horizontal line (3-3) drawn at 45 mm. below the vertex,
their anterior limit corresponding to the head of the nucleus caudatus
by the vertical line (C C), and their posterior limit, the hinder end
of the thalamus, by the vertical line (B B).
Upon the median line at the top of the head an allowance of full
15 mm. should be made for the width of the superior longitudinal sinus
separating the hemisphere.
[Illustration: FIG. 14. The same Topographical Lines applied to the
Left Cerebral Hemisphere in Henle's Skull. The motor centres are
approximately indicated by dotted lines. (The leg centre should be
reduced in size as it lies near to and in the longitudinal fissure.)
The Rolandic line is placed a little behind the fissure for the sake
of clearness.]
The location of the middle meningeal artery, which so often furnishes
the blood that compresses the brain after various injuries to the
head, is surgically of great importance. The course of its two
principal branches is approximately indicated upon Fig. 13 by the
branching lines drawn on the anterior inferior angle of the parietal
and the upper part of the squamous portion of the temporal bone. In
the living subject the main trunk of the artery would be found under
the horizontal line (2-2) a little posterior to the speech-centre,
about 30 mm. behind the external angular process, and in front of the
beginning of the fissure of Sylvius.
Upon the shaven head of a patient seated in a chair or lying in bed
the principal landmarks and relations above defined can be mapped out
with sufficient approximation to accuracy by the use of a ruler to
mark {97} the alveolo-condyloid plane, and a cardboard cut so as to
stand astride the head in the auriculo-bregmatic vertical. A light
wooden apparatus can easily be made to indicate these two lines, while
the remaining measurements can be made with a steel tape-measure, and
the points marked with carmine ink or an aniline pencil.
The value of cranio-cerebral topography is obvious for ordinary
surgical purposes, but it may in the future prove of great utility in
the treatment of cerebral diseases (tumors, abscesses, etc.) by
surgical means. A bold and nearly successful attempt at removing a
tumor of the brain has already been made,[15] and doubtless there are
surgeons who will not hesitate to follow the path thus opened up when
physicians give them a diagnosis of localized tumor or abscess in
parts of the cortex cerebri to serve as a basis.
[Footnote 15: Bennett and Godlee, _The Lancet_, 1884, ii. 1090; 1885,
i. p. 891.]
The indications for trephining or raising bone after cranial injuries,
for the relief of symptoms of cerebral irritation, compression, or
disorganization, may be provisionally stated as follows:
(_a_) When aphasia supervenes immediately or within a few days or
weeks after an injury of the anterior portion of the head on the left
side. It is extremely probable that in the first case a clot or bony
spiculum will be found compressing the speech-centre; in the second
case, that an abscess has formed in or near it (Broca's case).
(_b_) When simple hemiplegia or hemiplegia with hemispasm follows an
injury, however slight, in the temporo-parietal region. If the
paralysis or spasm be limited to one side of the face or to one
extremity, the indication to operate is even stronger. Even if in such
cases the injury be not immediately over the motor area, the surgeon
is justified in exploring that region.
(_c_) In conditions of stupor and coma after cranial injuries,
sometimes without external wound, in which meningeal hemorrhage is the
cause of impending death, the discovery of slight hemiplegia should
justify trephining planned according to the topographic rules above
laid down (Weir's case, 1882). In some cases latent hemiplegia may be
discovered by the presence of an erythematous flush on one buttock and
of a slightly increased peripheral temperature (taken between fingers
or toes).