hypoglossal, pneumogastric, spinal accessory, and the motor root of
the trigeminus nerves, giving rise to a classical symptom-group. The
symptoms thus produced are exclusively (?) motor and trophic,
consisting of progressively increasing paresis, with atrophy of the
muscles about the lips {80} and cheeks, the intrinsic lingual muscles,
the laryngeal and pharyngeal muscles. Later, the masseters, temporals,
and pterygoids are sometimes involved; and, finally, extremely rapid
action of the heart with pneumonic symptoms indicates the gravest
extension of the morbid process. An early symptom in such cases is
abnormal salivation. These affections, generally designated as
varieties of bulbar paralysis, subacute or chronic, are usually
readily recognized intra vitam, and recent discoveries in morbid
anatomy have enabled us to correctly diagnosticate the seat of the
lesion in its various extensions. The laryngeal paralysis represents
disintegration (atrophy) of ganglion-cells in the bulbar origin of the
spinal accessory nerve; lingual atrophic paralysis indicates the same
lesion in the nuclei of the hypoglossal nerves; the labio-buccal
symptoms are produced by lesion of the facial nerve nucleus (inferior
facial nucleus of older writers); the paralysis of the muscles of
mastication is due to extension of cell-degeneration to the motor
nucleus of the trigeminus in the pons; and the final cardio-pulmonary
symptoms indicate an extension of the lesion into the sensory (?)
origin of the pneumogastric nerves.
It is evident that this systematic lesion of the oblongata is the
equivalent or analogue of the various acute and chronic lesions of the
anterior horns of the spinal cord, described supra, and in practice we
sometimes find these bulbar and spinal lesions associated: progressive
muscular atrophy of the extremities and amyotrophic lateral sclerosis
being complicated with bulbar paralysis.
B. FOCAL LESIONS OF THE MEDULLA OBLONGATA, as at present known, occur
mostly in the kinesodic system, but may also involve several fasciculi
and nuclei at one time. The symptoms of such lesions are grouped in
two principal types:
(_a_) Single symptoms, such as atrophy or atrophic paralysis of some
one muscle or muscular group innervated by the hypoglossal, facial, or
spinal accessory nerves. For example, unilateral atrophy of the
tongue, when not due to neural injury, is quite surely the
representative of destruction of one hypoglossal nucleus. It is
possible that some cases of peripheral facial paralysis, so-called, or
Bell's palsy, and cases of paralysis of the sterno-mastoid and
trapezius, are not due to neural lesion, but to primary disease of the
nuclei of the facial and spinal accessory nerves, either as
poliomyelitis or as progressive cell-degeneration and atrophy.
A similar reserve must be used in speaking of the localization of
small lesions in the oblongata, causing diabetes mellitus, polyuria,
albuminuria, and salivation. From experiments upon animals and a few
post-mortem examinations in human cases we know that such lesions may
occur and cause the symptoms, but their recognition during the
patient's life is at the present time next to impossible.
(_b_) The symptoms may be complex and belong to the general class of
crossed paralysis, the mouth, face, tongue, and larynx being paralyzed
(often with anæsthesia of the face) on one side, while the extremities
are paralyzed on the other side. Such a symptom-group would indicate a
large lesion (tumor) in one lateral half of the oblongata, more
especially in its ventral aspect. These localizations will be studied
more in detail farther on, under the general head of Crossed Paralysis
due to Lesions of the Base of the Brain.
{81} IV. Localization of Lesions in the Encephalic Mass.
Under this head, to prevent repetition and to facilitate condensation,
we will consider the various localizations which can now be
diagnosticated in the cerebrum, basis cerebri, and cerebellum.
It would be of the greatest advantage to preface these statements by a
full summary of the anatomical and physiological data on which the
localizations rest, but space is wanting for such an exposition, and
the reader who is not already familiar with these branches of medical
science will have to seek information in other accessible works.[8]
[Footnote 8: Ferrier, _The Functions of the Brain_, Am. ed., N. Y.,
1876; Charcot, _Lectures on Localization in Disease of the Brain_, Am.
ed., N. Y., 1878; Seguin, E. C., “Lectures on the Localization of
Spinal and Cerebral Diseases,” _N. Y. Medical Record_, 1878; Ranney,
_Applied Anatomy of the Nervous System_, N. Y., 1881; Meynert,
_Psychiatry: A Clinical Treatise on Diseases of the Fore-brain_, Part
I., Am. ed., 1885.]
In a general way, encephalic lesions are distinguished by the
following:
Positive Characters.—Tendency to strictly hemiplegic or bilaterally
hemiplegic grouping of symptoms; frequency of contracture or of a
spastic state of the paretic muscles; increase of reflexes in the
affected extremities; spasmodic manifestations in remote muscular
groups, but not in areas of nerve-distribution (forms of Jacksonian
epilepsy); the presence of paralytic and anæsthetic symptoms in the
range of distribution of cranial nerves; frequency of neuro-retinitis
or atrophy of the optic nerves; occurrence of lateral hemianopsia;
production of symptom-groups known as varieties of crossed paralysis;
frequency of head symptoms, as headache, vertigo, apoplectic and
epileptic seizures; mental symptoms of various sorts, dementia, coma,
etc.
Negative Characters.—Absence of truly paraplegiform distribution of
symptoms, even when they are bilateral; of cincture feelings; of pain
or other paræsthesiæ and anæsthesia in the distribution of
nerve-trunks; of muscular atrophy and De R. in paralyzed parts. Rarely
do we observe visceral paralysis and bed-sores.
Pathological localizations in the encephalon may conveniently be
grouped under two heads—viz. systematic and focal lesions.
A. SYSTEMATIC LESIONS OF THE ENCEPHALON.—The recent advances of
embryology, anatomy, physiology, and pathological anatomy have
conclusively established the existence, and fairly well defined the
limits, of a sensory (æsthesodic) and of a motor (kinesodic) tract in
the brain; and certain lesions of these tracts produce such precise
symptom-groups that their diagnosis during the patient's life is often
possible, and that, too, with great exactness.
1. SYSTEMATIC LESIONS OF THE ÆSTHESODIC SYSTEM OF THE ENCEPHALON.—The
limits of this system are as follows: Within the oblongata and pons it
occupies a somewhat uncertain (from a clinical standpoint) location,
its fasciculi and ganglia lying in a general way dorso-laterad of the
motor or kinesodic system. In the crus cerebri the fibres of the
sensory tract are more closely packed together, and constitute a dense
fasciculus of white substance in the lateral part of the crus in its
subcerebral extremity, estimated by Flechsig at about one-fifth of the
entire crus, and thence it enters into the composition of what is
known as the internal capsule. This narrow but all-important mass of
{82} white fibres, as revealed by a horizontal section of the
hemisphere (vide Fig. 7), lies between the nucleus caudatus and the
nucleus lentiformis, and between the latter and the thalamus, thus
assuming a V or elbow shape. Of this, the caudal third of that part of
the capsule behind the bend or angle contains all the sensory paths
for the opposite half of the body, reinforced by paths for the special
senses; it is the carrefour sensitif of French writers. From this
region sensory fasciculi radiate to various parts of the cerebral
cortex—in the parietal, temporal, and occipital gyri—in which
physiological experiments and human cases of disease have shown
sensory areas or centres. Of the fasciculi from special sense-organs
which reinforce the internal capsule, the only one which is well
defined and easily traceable is the fasciculus opticus (fasciculus of
Gratiolet), derived in part directly from the optic tract of the same
side and from the primary optic centres (lobus opticus, corpus
geniculatum laterale, and pulvinar), proceeds, along with fibres of
the internal capsule, dorso-laterad of the posterior cornu of the
lateral ventricle, to the mesal aspect of the occipital lobe. A
fasciculus from the olfactory apparatus doubtless also joins the
internal capsule, but its course is unknown.
The following localization diagnoses are now possible in the
æsthesodic system as above defined:
(_a_) A lesion of the internal capsule, just above the crus cerebri,
involving its bend or knee and caudal segment, with or without injury
to the nucleus lentiformis and thalamus, will give rise to the
following symptoms: Complete typical hemiplegia and total
hemianæsthesia on the opposite side of the body; the anæsthesia
involves the special senses as well as the body. Vision is, however,
unaffected, unless the lesion extend far enough back to involve the
pulvinar and fasciculus opticus, when lateral hemianopsia occurs (dark
half-fields on the side opposite the lesion). When this lesion is in
the left hemisphere, sensory aphasia also occurs.
(_b_) A lesion involving the caudal part of the thalamus and of the
internal capsule. With such a lesion the motor symptoms consist in
transient paralysis, with usually persistent post-paralytic chorea or
ataxia. The sensory symptoms are more marked, and resemble those
produced by lesion (_a_). It may be determined with some degree of
accuracy whether the lesion be in the thalamus border, or in the
internal capsule near to the nucleus lentiformis by the absence in the
latter case of lateral hemianopsia.
The topography of such lesions is illustrated by Fig. 7.
[Illustration: FIG. 7. Horizontal Section through the Centre of the
Right Cerebral Hemisphere: M, median line; _Nc_, nucleus caudatus;
_Nucleus lent._, nucleus lentiformis with its three segments; _To_,
thalamus opticus; _c. i._, internal capsule with its frontal division,
its bend or knee, and its caudal division. 1, mass of fibres destined
for pons and others forming a part of the corona radiata,
non-pyramidal fibres; 2, knee of the internal capsule, containing
fasciculus from cortical centre for the face to the nucleus of facial
nerve (non-pyramidal fibres); 3, fasciculus for the tongue and throat
to nucleus of hypoglossus, etc. (non-pyramidal fibres); 4, fasciculi
from the pre- and postcentral gyri and the paracentral lobule to the
pyramid of the oblongata (the true pyramidal fasciculus, continued in
the cord as fasciculi, 10 and 11 of Figs. 5 and 6); 5, the caudal
third of the internal capsule, containing fasciculi destined to the
sensory cortical centres.]
(_c_) Lesions of cortical areas connected with fasciculi of the
sensory part of the internal capsule (c. i. 5).
(_α_) Lesion of the cortical area or centre for smell cannot at
present be diagnosticated. From the results of experiments upon higher
mammals we would expect such a centre to be in the cortex of the mesal
gyri of the temporal lobe.
(_β_) Lesions of the cortical centre for taste are equally unknown; it
is probably situated in the meso-basal aspect of the temporal lobe.
(_γ_) Lesions of the acoustic centre are somewhat better known, at
least as far as the function of hearing language-sounds (psychic
hearing) is concerned. A number of recently-published cases[9] have
quite positively {83} shown that the existence of word-deafness
indicates a destructive lesion of the dorsal gyri (more particularly
the first and second) of the temporal lobe (the left always?). The
lesion may also be in the inferior parietal lobule and gyrus
supramarginalis, penetrating deeply enough to injure the acoustic
fasciculus on its way from the internal capsule to the centre.
[Footnote 9: R. W. Amidon, “On the Pathological Anatomy of Sensory
Aphasia,” _New York Medical Journal_, xl. 113, 181.]
(_δ_) The centre for visual impressions is now the best known of any
of the sensory cortical areas. The experimental studies and
pathological results of the last few years have indicated that the
occipital lobe was probably the seat of higher, organized vision (for
form and color). More recent autopsies and re-examination[10] of the
subject point to the cuneus and adjacent gray matter as the visual
centre. The anatomical arrangement is, however, peculiar and complex,
in that each cortical visual area receives impressions from one
lateral half of both retinæ, through the fasciculus opticus.
[Footnote 10: E. C. Seguin, “A Contribution to the Pathology of
Hemianopsia of Central Origin (Cortex-hemianopsia),” _Journal of
Nervous and Mental Diseases_, 1886, No. 1.]
Destructive lesion of one visual centre is therefore indicated during
{84} life by the symptom lateral hemianopsia alone (the dark
half-fields on the side opposite the lesion).
The accompanying diagram illustrates the course of the visual paths
from the eyes to the cortical centres, and the mechanism of production
of various forms of hemianopsia:
[Illustration: FIG. 8. Diagram of Visual Paths, designed to illustrate
specially Left Lateral Hemianopsia from any lesion. _L. T. F._, left
temporal half-field; _R. N. F._, right nasal half-field; _O. S._,
oculus sin.; _O. D._, oculus dexter; _N. T._, nasal and temporal
halves of retinæ; _N. O. S._, nervus opticus sin.; _N. O. D._, nervus
opticus dext.; _F. C. S._, fasciculus cruciatus sin.; _F. L. D._,
fasciculus lateralis dext.; _C._, chiasma, or decussation of fasciculi
cruciati; _T. O. D._, tractus opticus dext.; _C. G. L._, corpus
geniculatum laterale; _L. O._, lobi optici (corpus quad.); _P. O. C._,
primary optic centres, including lobus opticus, corp. genic. lat., and
pulvinar of one side; _F. O._, fasciculus opticus (Gratiolet) in the
internal capsule; _C. P._, cornu posterior; _G. A._, region of gyrus
angularis; _L. O. S._, lobus occip. sin.; _L. O. D._, lobus occip.
dext.; _Cu._, cuneus and subjacent gyri, constituting the cortical
visual centre in man. The heavy or shaded lines represent parts
connected with the right halves of both retinæ. The reader may place
the lesion as he pleases.]
{85} The following diagnostic propositions are applicable to cases
presenting the symptom lateral hemianopsia:
“1. Lateral hemianopsia always indicates an intracranial lesion on the
opposite side from the dark half-fields.
“2. Lateral hemianopsia, with pupillary immobility, optic neuritis, or
atrophy, especially if joined with symptoms of basal disease, is due
to lesion of the tractus opticus or of the primary optic centres on
one side.
“3. Lateral hemianopsia, or sector-like defects of the same geometric
order, with hemianæsthesia and choreiform or ataxic movements of
one-half of the body without marked hemiplegia, is probably due to
lesion of the caudo-lateral part of the thalamus or of the caudal
division of the internal capsule (vide Fig. 7).
“4. Lateral hemianopsia, with complete hemiplegia (spastic after a few
weeks) and hemianæsthesia, is probably caused by an extensive lesion
of the internal capsule in its central and caudal part.
“5. Lateral hemianopsia, with typical hemiplegia (spastic after a few
weeks), with aphasia if the right side be paralyzed, and with little
or no anæsthesia, is quite certainly due to an extensive superficial
lesion in the area supplied by the middle cerebral artery; we should
expect to find softening of the speech-centre, of the motor zone and
of the gyri lying at the extremity of the fissure of Sylvius—viz. the
gyrus supramarginalis, inferior parietal lobule, and gyrus angularis.
Embolism or thrombosis of the middle cerebral artery would be the most
likely pathological cause of the softening.
“6. Lateral hemianopsia, with moderate loss of power in one-half of
the body if associated with impairment of muscular sense, but without
ordinary anæsthesia, would probably be due to a lesion of the inferior
parietal lobule and gyrus angularis, with their subjacent white
substance, penetrating deeply enough to sever or compress the optic
fasciculus in its way caudad to the visual centre.
“7. Lateral hemianopsia, without motor or common sensory symptoms;
this symptom alone, is due, we believe from the convincing evidence
afforded by Cases 28, 29, 41, and 45, to lesions of the cuneus only,
or of it and of the gray matter immediately surrounding it on the
mesal surface of the occipital lobe in the hemisphere opposite the
dark half-fields. Most surgical cases of lateral hemianopsia come at
once or after convalescence within this rule, or No. 6.”[11]
[Footnote 11: Seguin, _op. cit._]
The cortical visual area, as above defined, is supplied by one large
vessel—viz. the occipital artery, a branch of the posterior cerebral.
Embolism or thrombosis of the former vessel is to be thought of as the
probable cause of a suddenly-developed lateral hemianopsia without
paralysis or anæsthesia.
(_ε_) The cortical centre for sensory impressions of muscular sense,
so called, is probably located in the inferior parietal lobule. The
diagnosis of a lesion so placed, in a case presenting along with other
sensory or with motor symptoms marked impairments of muscular sense in
the arm and leg of one side, is justified by a few recent cases.[12]
Spitzka {86} believes that he has clinically and pathologically
demonstrated a basal path (fasciculus) for this mode of sensibility in
the pons and oblongata, dorsad of the pyramidal tracts.[13]
[Footnote 12: Westphal, _Charité Annalen_, vii. p. 446, 1882; Stenger,
_Archiv f. Psychiatrie u. Nervenkrankheiten_, xiii. p. 240, Case
viii.; Wernicke u. Hahn, _Virchow's Archiv_, lxxxvii. p. 325; Ball and
Seguin, _Archives of Medicine_, New York, v. p. 136.]
[Footnote 13: Spitzka, “A Contribution to the Morbid Anatomy and
Symptomatology of Pons Lesions,” _American Journal of Neurology and
Psychiatry_, ii. p. 617 (1883).]
(_ζ_) Lesions of the cortical area for common cutaneous sensibility
cannot be positively recognized at the present time. By exclusion of
the better-known centres, and from experimental data, we may
approximately locate it in the gray matter lying ventrad of (below)
the inferior parietal lobule, extending to the base, and possibly the
mesal aspect, of the temporal lobe, and possibly also on the lateral
aspect of the occipital lobe.
2. LESIONS OF THE KINESODIC SYSTEM OF THE ENCEPHALON.—The kinesodic
system is far better understood, anatomically and physiologically,
than the æsthesodic. Its limits, beginning from the junction of the
cord and oblongata, are as follows: The pyramids, containing the
fibres of the direct and crossed pyramidal fasciculi of the cord (Fig.
5, Nos. 10 and 11), form the meso-basal aspect of the oblongata,
appearing on either side of the median line as two large distinct
bundles of white substance which enter the pons under its projecting
transverse fibres. Within the pons each pyramid is divided into quite
a number of fasciculi more or less separated by fibres of other
systems. Again collected, these bundles constitute a considerable part
of the crus cerebri—its basal middle two-fifths. (The outer or
latero-dorsal one-fifth part of the crus belongs to the æsthesodic
system, the middle (intermediate) two-fifths are the pyramidal fibres,
and the remaining two-fifths, meso-basal part, contain some fibres
from the direct cerebral motor tract destined for the hypoglossal and
facial nuclei, and also large bundles probably derived from the
nucleus caudatus and frontal lobes). As the crus enters the cerebrum
and becomes what we know as the internal capsule, the pyramidal fibres
occupy the bend or elbow of the capsule and part of its caudal segment
(vide Fig. 7).
From this level the fibres of the internal capsule again diverge, as
fasciculi whose physiological independence has been well determined,
going dorsad and frontad to certain gyri of the cerebral cortex where
their fibres join ganglion-cells. Three large fasciculi and
corresponding cortical areas are recognized as constituting the
pyramidal tract, strictly speaking: (1) A fasciculus which extends
frontad to the base of the second frontal gyrus where it coalesces
with the precentral, the centre and fasciculus for movements of the
facial muscles of the opposite side; (2) a fasciculus which extends to
the precentral and postcentral gyri, more especially in their middle
part, constituting the centre and fasciculus for movements of the arm
and hand; (3) another fasciculus which goes dorso-mesad, almost
vertically in the brain, to join the ends of the pre- and postcentral
gyri at the top of the hemisphere, and their continuation upon its
mesal aspect known as the paracentral lobule, centre and fasciculus
for movements of the opposite foot and leg. Besides these three great
cortical areas and their connected fasciculi of nerve-fibres, which go
to make up the pyramidal tract, we recognize (4) a cortical centre for
speech movement of the tongue and lips in the base of the left third
frontal gyrus over the fissure of Sylvius (Broca's speech-centre),
with a connected white fasciculus which passes into the elbow of the
internal {87} capsule, and can be traced (by means of secondary
degeneration) into the inner part of the base of the crus and into the
pons, but not to the pyramid. Another probable centre (5), for coarse
lingual movements and for the various movements of deglutition, is in
the folds of the insula, its fasciculus not joining the pyramid.
[Illustration: FIG. 9. Longitudinal (sagittal) Section through the
Brain, to show the distribution of the fasciculi of the internal
capsule. Fasciculi of motor tract in dotted lines, to fronto-parietal
convolutions. Fasciculi of sensory tract in full lines, to
temporo-parieto-occipital convolutions: _N. C._, nucleus caudatus;
_N. L._, nucleus lentiformis; _T.O._, thalamus opticus. 1, level of
crus cerebri; 2, level of pons; 3, level of oblongata. (This diagram
is to be used in conjunction with Fig. 7.)]
The location of two other motor centres—one for the movement of the
eyeballs in or near the gyrus angularis, and one for vocal laryngeal
movements in the base of the right third frontal gyrus (homologous to
the speech-centre in the left hemisphere), is problematical, or at
least not well enough established to be recognized in a practical
treatise.
Recent experimental researches have shown that to electrical
excitation at least the fasciculi for the tongue, face, arm, and leg
yield the same distinct reaction (isolated muscular contractions) as
do their respective centres or cortical areas; perhaps they are more
excitable.
When these cortical areas are destroyed by disease, or when their
connected fasciculi are severed, secondary degeneration takes place
and extends to the end of the respective bundles, even to the lower
extremity of the spinal cord.