Chapter V: Front Matter (5)

(_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.

(_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:

{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.

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. 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.

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.

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).

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.

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).

(_d_) In the very rare cases in which paralytic phenomena are found on the same side as the evident cranial injury, it would be proper to trephine on the opposite side of the skull in search of fracture or hemorrhage, the result of contre-coup.

(_e_) In chronic epilepsy after traumatism of the head the indication for trephining is present, but it is seldom a specific indication connected with the subject of localization. Lesions of any part of the skull and dura may be a cause of epileptic attacks, irrespective of motor centres.

(_f_) In cases of tumor in the motor centres, if there be not symptoms of tumors in other parts of the brain (multiple tumors) or of penetration of the tumor to the central parts of the brain, we believe trephining not only justified, but demanded in the present state of science.

Some of the contraindications to trephining may be thus stated:

(_a_) Whenever in apparently favorable cases there are signs of injury to the base of the brain, such as paralysis of cranial nerves, {98} neuro-retinitis, and Cheyne-Stokes respiration (although the last symptom may occur from simple compression).

(_b_) When hemispasm or hemiplegia is accompanied by hemianæsthesia, thus making it probable that the lesion is deeper and farther back.

It should be added, in conclusion, that these indications and contraindications are formulated from the standpoint of the neurologist.

{99}

MENTAL DISEASES.

BY CHARLES F. FOLSOM, M.D.

DEFINITIONS OF INSANITY.—The term insanity conveys quite different meanings to the community, to lawyers, and to physicians. From the three points of view its definition has been constantly widening for the past century. A great part of the alleged recent increase in insanity is due to the fact that its definition is applied to more people. Our insane asylums are more quiet and orderly, not only because of the more humane treatment of the inmates, but largely also because quieter and less insane people are now sent there than formerly. Doubtless the mistake is sometimes made of going so far, in zeal for science and philanthropy, as to make the definition of insanity too broad; and in a refined civilization the nice adjustment of complicated social relations, or even a fastidious taste, requires people to be sent to insane asylums who in simpler states of society would be cared for at home.[1]

[Footnote 1: The physician in general practice is referred to Clouston's _Clinical Lectures on Mental Diseases_, and to Part 1 of Spitzka's _Manual of Insanity_. For those who wish to study insanity thoroughly the literature is rich and its bibliography is readily available. Of many parts of the subject only an outline, of course, can be given within the limits of the present paper.]

The popular idea of insanity is of wild, incoherent, or crazy conduct. If maniacal, the timid or frightened young girl who would not hurt a fly, and the tottering, harmless old man if confused and partly demented, are hurried off to the asylum with the use and show of force suitable for a desperate criminal, while the victim of overwhelming delusions, because he seems clear, logical, and collected, is vigorously defended against the physician's imputation of insanity until he commits an offence against the laws, when he is fortunate if he is not treated as a criminal. It is often impossible for judges, juries, counsel, and even medical experts, to wholly divest themselves of the popular notions of insanity in cases appealing strongly to the passion or prejudice of the day. Cases involving the question of responsibility for crime are decided against science and the evidence because of certain preconceived notions upon insanity which no amount of skilled opinion can controvert. Jurors, and less often judges, make up their minds what a sane man would do under given conditions, and of what an insane man is capable, judging from the facts within their own experience; and in forming their decisions it is the act itself, and not the man, diseased or otherwise, in connection with the act, that chiefly governs them. Often they are right, not seldom wrong. Strange, apparently purposeless, illogical, inconsistent action is frequently attributed to the author of it being insane on that subject, whereas he may be {100} simply acting from strong impulse or emotion, and may be by no means insane. On the other hand, because a man knows right from wrong in the abstract, and can ordinarily behave well, the very characteristic workings of his insane mind are often seized upon as unquestionable proof of sanity, even when they admit of no other explanation to the skilled physician than that of insanity. There is no doubt of the fact that the whipping commonly used in the treatment of the insane by the monks several centuries ago put an end to much insane conduct; and in insane asylums now, in spite of the best efforts of the medical staff to the contrary, a brutal, bullying patient is sometimes struck by another patient or an attendant in return for some unusually exasperating and cruel conduct, with the result of making him behave well in the future. It is with reference to this class of cases that the crowd oftenest errs in its definition of insanity. Society claims a voice in the enforcement of the laws for its own protection, assuming to know who could control themselves from crime and who not, and naturally wishes the standard of responsibility to be kept high. Of course its sympathies and prejudices largely govern its voice in the matter.

With precisely the same degree of insanity and the same power to control their actions two murderers may be sentenced, one to death for an act where the motive and method were those of the criminal, and the other to an insane asylum for killing a person under circumstances which are not explainable by sane reasons. The Pocasset Adventist who sacrificed his loved child, as he thought, by the Lord's command, would probably have been hanged if he had committed a crime similar to John Brown's, Wilkes Booth's, Orsini's, or Guiteau's. Sometimes the accused gets the benefit of the doubt, and sometimes society, according to the view of the merits of the case taken by the judge in his charge or by the jury in their verdict.

To the lawyer insanity means only a condition of mind with reference to certain conduct. An insane man is simply non compos mentis. Insanity is irresponsibility. The whole question to the lawyer is with regard to a certain act or series of acts. The lawyer's definition is narrower than that of the physician. In wills and contracts the course is usually clearer than when there is a question of serious crime, and even an insane person in an asylum may be a party to a valid contract or make a will that will hold in law. It is not necessary that a will or contract be such as would be made by a just man or a reasonable man, but simply that it fairly represent the wishes and character of the man making it, uninfluenced by any insane delusion or prejudice caused by mental impairment; that the will or contract in itself bear evidence of a correct appreciation of the circumstances and conditions of the case; and that the mind be able to act independently enough, with a reasonable knowledge of the duties of the individual and the just rights of others. An unsound mind, as defined by the physician, would cover a large portion of the convicts in our workhouses and prisons to-day if they could be critically examined, but the lawyers and courts would not find many of them insane. A man is not insane in law unless his act is traceable to, or its nature has been determined by, mental disease affecting his free agency; in other words, unless insanity caused his act either wholly or in great part.

{101} In the partly irresponsible condition of mind often produced by grave hysteria, so-called nervous prostration, and the general mental and moral demoralization often seen in seduced and abandoned women, or after exhausting illness, or following apparent recovery from cerebral hemorrhages or embolism, blows upon the head, sunstroke, chronic alcoholism, syphilis, etc., there may be loss of self-control and a distinct moral perversion or decided change of character without very evident mental impairment; and the courts recognize a diminished capacity, as the result of disease, to appreciate and follow what is right and just and to avoid what is wrong or unjust, and yet not complete irresponsibility. In this connection the fact should be borne in mind that a very little mental disease can make bad people criminals, and may not take others beyond the bounds of propriety. A criminal may become insane and be still pretty much the same kind of a criminal as before. Morality, too, is relative, and many criminals, like children, know almost nothing of abstract truth, justice, or virtue, because they have never been taught them; and there are many cases where the perverse or criminal actions of people may be about equally explainable on the theory of insanity or wickedness. The criminal, a creature of his surroundings and associations, may often not be discriminated from the man with mental disease. Indeed, it is not difficult to take the philanthropic position that all criminals are insane because they are not in sympathy with the moral conceptions of their time, or, to use the fashionable expression of the day, because they are not in harmony with their environment. Such a view of crime, however, leads to only one of two conclusions—either that insanity is no sufficient defence for wilful violation of the laws, or that all criminals should be treated as persons of unsound mind.

The free agency of the individual is affected or modified in many different ways by the different diseases of the mind, and the question of responsibility will often be found to be one of the most perplexing problems with which the physician has to deal. If well-marked forms of insanity alone were to be investigated, the matter would be comparatively a simple one; but such is far from always being the case. The insane man often commits certain crimes precisely as an ordinary sane criminal would do the same thing. Often the evidence is contradictory, the testimony as to previous life and character conflicting, and the disease of so obscure a stage or type that it is almost impossible to form a clear opinion. The determination of a man's degree of free agency is no simple affair which can be decided in all cases by a few or a few dozen interviews. Not seldom the mystery remains unsolved after the autopsy. Man's free will is not the property of any substance which can be demonstrated by chemistry, physiology, or microscopical research, but it is the result of the combined action of a whole group of functional activities the very relations of which to each other are as unknown as their method of action. No stethoscope or ophthalmoscope can reveal its morbid action, which can only be inferred indirectly from the operations of the mind.

The cases in which the physician is called upon to define insanity as the term is used by the lawyers are (1) to secure limitation or control of an individual's actions, usually by a guardianship; (2) to control him absolutely in an asylum; (3) to estimate his culpability or criminality, or {102} his capacity to make a will or contract or to transact business. It is quite important, therefore, that the medical man should understand that there may be, as regards some particular person, a wide difference between medical insanity or mental disease and legal insanity or irresponsibility. He does most wisely when he confines his testimony to an explanation of the changes caused by disease in the particular case, and to the effect of such changes upon the mind, leaving to the judge's charge and the jury's verdict the questions of guilt and responsibility.

Insanity may be of congenital origin or slowly developed from early childhood, but usually it indicates a change caused by disease, so that the person alleged to be insane must, as a rule, be compared with himself at some previous time, and not with some ideal standard of mental health which does not exist. Indeed, if we could measure nicely no two of us could be fairly held to precisely the same degree of accountability. The knowledge of right and wrong is not a fair criterion, as many insane men possess that knowledge well enough in the abstract. The ability to distinguish right from wrong in the particular act is possessed by some insane persons whose will and power of self-control have become so limited by disease that they cannot avoid what they know to be crime. Delusion overpowering the mind is sufficient evidence of irresponsibility, but all delusions are by no means so powerful that they cannot be resisted, and many must be classed as simply false beliefs or mistaken views which could be, and should be, controlled. In case, therefore, of alleged delusions not manifestly insane further evidence of insanity is required, and the way in which a man believes or does anything may be more of an indication as to the soundness or unsoundness of his mind than what he believes or does. A crime committed under the influence of maniacal delirium, acute delirious mania, epileptic furor, uncontrollable impulse, alcoholic insanity, or hysterical mental disease will usually explain itself, while a demented insane person is so characteristic an object that his crime cannot well be mistaken for that of a responsible agent.