Chapter 6

III. The Localization of Lesions in the Medulla Oblongata.

In general terms, lesions of the oblongata are characterized by the early appearance and prominence of motor symptoms in the mouth, throat, and larynx, and by bilaterality of the symptoms. Remote symptoms consist of disturbances in the cardiac action and in the functions of some intra-abdominal organs. There may also be more or less paralysis of all the extremities. These lesions may conveniently be classified, like those of the cord, into systematic and focal.

A. SYSTEMATICLESIONS OF THEOBLONGATA.—1. Systematic lesions of the æsthesodic system of the oblongata are, for purposes of practical diagnosis, unknown at the present time.

2. Systematic lesions of the kinesodic system of the oblongata, on the other hand, are often positively recognizable during the patient's life.

(a) The most strictly systematic and most frequent of these lesions is that of secondary (Wallerian) degeneration of the pyramids, the prolongation of the cerebral motor tract. This morbid change gives rise to no distinct bulbar symptoms, and it can only be diagnosticated inferentially or inclusively by determining the existence of secondary degeneration of the entire pyramidal tract, from the occurrence of hemiplegia followed by contracture and increased reflexes. If the phenomena present be those of double spastic hemiplegia, there is surely degeneration of both pyramids.

(b) A systematic lesion affects the nuclei (origins) of the facial, 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 lipsand 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. FOCALLESIONS OF THEMEDULLAOBLONGATA, 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.

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

8Ferrier,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. SYSTEMATICLESIONS OF THEENCEPHALON.—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. SYSTEMATICLESIONS OF THEÆSTHESODICSYSTEM OF THEENCEPHALON.—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 ofwhite 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.

FIG. 7.

Horizontal section through cerebral hemisphere

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.5and6); 5, the caudal third of the internal capsule, containing fasciculi destined to the sensory cortical centres.

(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 cases9have quite positivelyshown 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.

9R. 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-examination10of 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.

10E. 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 duringlife 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:

FIG. 8.

Diagram of visual paths

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.

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

11Seguin,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.12Spitzkabelieves 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

12Westphal,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.

13Spitzka, “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 THEKINESODICSYSTEM OF THEENCEPHALON.—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 (videFig. 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 internalcapsule, 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.

FIG. 9.

Fasciculi of the internal capsule

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 withFig. 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.

Before leaving the subject of the composition of the kinesodic system 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. Theimportant 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.14He 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).

14Die 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.10and11, 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.

TheSYMPTOMSof 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 followingDIAGNOSESof 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, butwithout 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. FOCALLESIONS OF THEENCEPHALON.—1. FOCALLESIONS OF THECEREBRUM, OF ITSCORTEX ANDSUBJACENTWHITESUBSTANCE, ANDBASALGANGLIA.—(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.7and9). 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 symptomsof 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.

FIG. 10.

Lateral aspect of the cerebral hemisphere

FIG. 11.

Mesal aspect of the cerebral hemisphere

2. FOCALLESIONS OF THECEREBELLUM.—(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. Occipitalheadache, 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. FOCALLESIONS OF THEBASE OF THEBRAIN, 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 cranialnerves 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 (videFig. 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.

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