THE LOCALIZATION OF LESIONS IN THE NERVOUS SYSTEM.
BY E. C. SEGUIN, M.D.
There are two ways in which this important subject may be treated. Of these, the more interesting and logical would be to systematically expose the results of anatomical researches and of physiological experiments which tend to demonstrate the organic independence and the functions of various parts of the nervous system, and to give a classified series of results of autopsies bearing on localization. This would be all the more satisfactory because the questions involved, although of much importance in practice, are in reality physiological. The localization of functions being known, the physician could from the symptoms (i.e. perverted or abolished functions) present make a deductive diagnosis of great exactness. A treatise on medicine, however, cannot allow the space necessary for such a treatment of the topic which is best suited for monographic writing. The other method of exposition, the one we will follow, is that of summary statement of the association of the symptoms with definite lesions, with occasional anatomical and physiological explanations. This will, after all, be a series of diagnostic propositions stated as concisely and classified as practically as possible. With this end in view we divide the subject into five parts:
The localization of lesions in the peripheral nervous system (including the cauda equina);
The localization of lesions in the spinal cord;
The localization of lesions in the medulla oblongata;
The localization of lesions in the encephalon.
Cranio-cerebral topography.
I. Localization of Lesions in the Peripheral Nervous System.
In general terms, it may be said that lesions of peripheral (cerebro-spinal) nerves give rise to various sensory symptoms in the area of cutaneous distribution of the affected nerves, and to a flaccid atrophic paralysis in muscles supplied by the same nerves. These muscles almost always exhibit the De R. in varying degrees, and other trophic and vaso-motor symptoms are common. Many of these symptoms also occur in cerebral and spinal diseases, so that, after all, the diagnosis of peripheral localization depends largely on a correct knowledge of the course and distribution of nerves; of the relative distribution of the sensory and motor filaments of nerve-trunks; and of the frequent anomalies which occur. The subject of collateral innervation at the periphery must also receive attention, as involving a source of error.
Of extreme importance is the law of the relative distribution of motor and sensory filaments derived from one nerve-trunk. This, Van der Kolk's law,1 has hardly received the attention it deserves from practical neurologists. Briefly stated, it is that of the two sorts of fibres in a mixed nerve the sensory filaments go to those parts which are moved by muscles innervated by the motor filaments of the same nerve. The reader can verify for himself the exactness of this law by making sketches of an extremity and tracing the motor and sensory distribution of its various nerves. There are partial and apparent exceptions to the formula, but this objection applies to almost all our medical laws. In the cranial system of nerves it is necessary to consider the trigeminus as the sensory companion of the six anterior motor nerves; the pneumogastric as the associate of the spinal accessory (in part).
1 Van der Kolk, On the Minute Structure and Functions of the Spinal Cord, etc., p. 7, New Sydenham Soc. transl., London, 1859; Hilton, On Rest and Pain, p. 101, Am. ed., N. Y., 1879.
(a) Irritative lesions of nerves, as tumors, punctured wounds, perineuritis, moderate pressure, etc., are indicated by pain, numbness, and other paræsthesiæ in their cutaneous distribution, and of spasm or cramp with paresis only, in the associated muscles. Pain is the most prominent symptom by far, and many cases of so-called neuralgia belong to this category. As a rule, there is no anæsthesia, and the electrical reactions of nerves and muscles remain normal, or at least they do not present De R. In some cases vaso-motor spasm (coldness, white or bluish appearance of parts) shows itself in the most peripheral distribution of the nerve. The cutaneous and tendinous reflexes are variable, but usually preserved.
(b) Destructive lesions of nerves, by section, severe pressure, true neuritis, etc., are characterized by anæsthesia with or without paræsthesiæ, by motor and vaso-motor paralysis, and by loss of superficial and deep reflexes. Later, there occurs degenerative atrophy of the paralyzed muscles with fully-developed De R., and dystrophic changes in the skin, etc. supplied by the sensory filaments of the injured nerve. In these anæsthetic parts ulceration is easily caused by traumatism and want of cleanliness.
The abnormal electrical reactions of the paralyzed muscles are of much importance for the diagnosis of the amount of injury done to the nerve and for the purpose of prognosis. They may be summarized as follows, assuming a case of complete section of a nerve-trunk:
α. The Faradic Reactions diminish rapidly in degree in both nerve and muscles from the third or fourth day, and in the nerve they are, as a rule, completely lost at the end of from ten to fifteen days. In the muscles complete loss of faradic reaction is noted only somewhat later, and is absolute. A return of musculo-faradic contractility is a most positive sign of recovery of the nerve.
β. The Galvanic Reactions.—In the nerve, distal of the lesion, the result is similar to that stated above—viz. after a few days (from five to fifteen) all reaction disappears. The anatomical cause of the complete loss of the faradic and galvanic reactions in the nerve is its disintegration by the Wallerian degeneration. In the attached muscles the phenomena are widely different, and present interesting and complicated variations. In the first place, during a variable number of days there is increased excitability—i.e. the paralyzed muscles, deprived of innervation, contract to a much weaker current then do the homologous normal muscles. This is best shown in cases of peripheral facial paralysis (Bell's palsy) in the second and third weeks, by placing the electrodes in the median line, one upon the cervical vertebræ, the other (a small testing interrupting electrode) on the chin; on closing a very weak current of from four to eight elements it will be seen that the muscles on the paralyzed side of the face (the lower muscles) contract distinctly, while those on the normal side remain quiet. In the course of time, many weeks usually, the excitability diminishes, and falls below the normal, and in some cases ultimately disappears. These are known as the quantitative changes in musculo-galvanic reactions. During the long period preceding recovery, or without it, various qualitative changes are also observed in the reaction. The normal general formula of CaCC > AnCC (with rapid, jerking and full contractions of the muscle) becomes CaCC = AnCC or CaCC < AnCC. Often, too, distinct opening contractions occur, usually AnOC. The muscular contractions also tend to the tonic type or tetanus, expressed as CaDT or AnDT, etc.
The form of the contractions obtained is much altered. Throughout a practically endless period in some cases, or until regeneration of the nerve takes place in others, it is observed that musculo-galvanic contractions are delayed, are slower, less jerking, or assume an undulating wave-like character, easily passing into tetanus. This change from the rapid, jerky, and full normal muscular contraction to one which is slow and wave-like we consider to be the most positive and reliable evidence of neuro-muscular degeneration and of the cutting off of the spinal-cord influence. Fig. 4 shows the characters of a human degenerative myogram contrasted with a normal one, Fig. 3.
FIG. 3.
Contraction of Normal Abductor Indicis, CaCC, with strong current (Amidon2).
FIG. 4.
Contraction of Paralyzed Muscle on thirty-first day of Bell's palsy of the face. CaCC. 20 El. (Amidon). Shows retarded contraction and slow contraction, with tendency to tetanus.
2 “The Myography of Nerve-degeneration in Animals and Man,” Archives of Medicine, viii., No. 1, 1882.
In the period of recovery or regeneration of the nerve the musculo-galvanic reactions slowly reacquire their normal characters; the normal suddenness and completeness of the contractions gradually appear, and faradic excitation causes slight responses. Lastly, the nerve also begins to exhibit excitability under galvanism and faradism. These various abnormal electrical reactions, also frequently observed in diseases of the spinal cord, constitute the so-called reaction of degeneration, or De R. The subject is one of much practical importance, and for details the reader is referred to the treatises on electro-therapeutics of Erb and De Watteville.
Just as we depend upon the De R. to prove interruption of motor nerve-fibres (or, in other cases, destruction of ganglion cells in the anterior horns of the cord), so do we rely upon the demonstration of complete anæsthesia to prove interruption of sensory fibres. In seeking for the area of anæsthesia several points must be borne in mind: (1) The normal distribution of the principal nerve-trunks as taught by ordinary anatomical works; (2) the remarkable anomalies of distribution which sometimes occur; (3) that many nerves near their endings exchange filaments in very variable numbers; loops for collateral innervation, which will supply some sensibility to parts which, judging by ordinary anatomical rules, should be made anæsthetic by section of a given nerve-trunk; (4) another consideration is the degree of anæsthesia. Before pronouncing upon the complete and fatal division of a nerve-trunk (by injury or by disease), absolute anæsthesia should be demonstrated in its area of principal and isolated distribution. Ordinary tests are not, as a rule, sufficient for this purpose. The best means in our experience consists in the use of a very strong induction (faradic) current, as follows: The skin of the suspected region to be thoroughly dried and rubbed with chalk or powdered starch; one pole, consisting of an ordinary wet electrode, to be applied just above the part to be tested, and the other pole, consisting of a single wire, with which different parts of the anæsthetic area are to be touched. By this means partially insensible regions, not responding to pricking and burning, may be made to yield reaction, and the area of absolute anæsthesia be thereby much reduced. Malingering may also be readily exposed by this test, which presents another advantage—viz. of not causing local injury or scars as burning will.
It follows from the preceding statements that in cases of limited atrophic paralysis with De R. the diagnosis between a central lesion (destruction of ganglion cells of the anterior horns of the cord) and a strictly peripheral (or neural) lesion is to be chiefly based upon two considerations: (1) The distribution of the paralysis, which in the first case affects muscles which are physiologically grouped or associated, while in the second case the simple law of anatomical associations or grouping is observed; (2) by the state of sensibility, which is normal in disease of the anterior horns of the cord, and is frequently impaired or abolished in nerve lesions.
Lesions affecting the cauda equina cause all the above-mentioned symptoms of peripheral lesions in a limited (partial) paraplegic distribution. If the lesion or injury be in the sacro-coccygeal region, the symptoms will, as a rule, be found confined to parts below the knee, occasionally also involving the muscles on the posterior aspect of the thigh (flexors of the leg). Below the knees we find an atrophic paralysis with De R., anæsthesia of the foot and part of the leg, loss of plantar and achillis reflexes, and the sphincter ani will be paralyzed. The patellar reflex is preserved or exaggerated. In case the lesion be in the lumbar region, below the first lumbar vertebræ, the symptoms will be found to extend as high as the groin, involving also the buttocks and sphincter ani; state of the bladder variable. All reflexes will be lost in the paralyzed extremities, except in some cases the cremasteric reflex.
Strange as it may appear, physicians do not always remember that there is practically no lumbar spinal cord (vide [Fig. 2.]), and that injuries, etc. of the lumbar vertebræ and dura tend to affect nerves, and not a nervous centre.
II. Localization of Lesions in the Spinal Cord.
Diseases of the spinal cord are distinguished by the following general characters, positive and negative:
Positive Characters.—Tendency to primary bilateral or paraplegic distribution of all the symptoms. In the majority of cases preservation of electro-muscular excitability, and in one well-defined group of cases De R. more or less typically developed in the paralyzed parts. Frequent vesical and rectal paralysis, either of the retaining or of the ejecting apparatus. Pains and other paræsthesiæ in the extremities, the pains often possessing the electric or fulgurating character. Anæsthesia of paraplegic distribution. Sensations of constriction or cincture about a limb or about the body at various levels. Occurrence of ataxia without paralysis. Progressive muscular atrophy without actual paralysis. Easy production of eschars (bed-sores).
Negative Characters.—Absence of typical hemiplegic or monoplegic distribution of symptoms. Rarity of head symptoms, as headache, vertigo, mental disturbance; of lesions of the optic nerve. Absence of epileptiform convulsions. Absence of such grouping of motor and sensory symptoms as would exactly correspond to the area of distribution of one or more large nerve-trunks.
The above symptomatic indications are, of course, of the most general meaning only, and are liable to exceptions and subject to varying conditions.
The DIAGNOSIS of the exact localization of lesions in the spinal cord, considered from the clinical standpoint, is perhaps best arrived at by following an anatomical and physiological order of subdivision of the problem into three questions, as follows:
FIRST QUESTION.—BEING GIVEN SYMPTOMS INDICATING DISEASE LIMITED TO ONE OR MORE SYSTEMS OF THE SPINAL CORD, TO DECIDE WHICH ARE AFFECTED.
Physiology and the results of embryological and pathological researches justify us in making a general division of the spinal cord, for purposes of diagnosis, into two great systems, whose limits are fairly well known—viz. the æsthesodic or sensory system, and the kinesodic or motor system. The following outline diagram (Fig. 5) of section through the spinal cord exhibits the ascertained limits of the two systems.
FIG. 5.
Diagram of a Transverse Section of the Spinal Cord through the Cervical Enlargement: The æsthesodic system is shaded, the kinesodic system unshaded. Parts of the æsthesodic system: (1) Posterior nerve-roots; (2) posterior gray horns; (3) fasciculi cuneati (columns of Burdach, inclusive of posterior root-zones); (4) fasciculi graciles (columns of Goll or posterior median columns); (5) ascending cerebellar fasciculi; (6) columns of Clarke. Parts of the kinesodic system: (7) Anterior roots; (8) anterior columns (inclusive of anterior root-zones); (9) anterior gray horns; (10) crossed pyramidal fasciculi; (11) direct pyramidal fasciculi (columns of Türck); [10 and 11 are the intraspinal prolongation of the cerebral motor tract]; (12) lateral columns, of ill-defined limits and unknown functions; P. R., posterior roots; P. S., posterior septum; A. R., anterior roots; A. F., anterior fissure.
A. Lesions of the Æsthesodic System.—Limits of the Æsthesodic System.—By this term we mean that combinations of ganglion-cells and nerve-fibres whose functions are locally sensory, and of those fibres which transmit impressions centripetally (frontad) to the encephalon. The following are the recognized parts of this system, as outlined on the diagram: (1) the posterior (dorsal) nerve-roots and attached ganglia; (2) the posterior gray horn and central gray substance to an unknown distance ventrad; (3) the fasciculi cuneati (columns of Burdach), whose lateral parts are more particularly designated as posterior root-zones; (4) the fasciculi graciles (columns of Goll) or posterior median columns; (5) the fasciculi ad cerebellum; (6) the vesicular columns of Clarke (most developed in the dorsal part of the cord). All of these parts have sensory functions, or at least transmit impressions centripetally, and they undergo secondary (Wallerian) degeneration toward the encephalon—i.e. frontad of a transverse lesion of the cord.3
3 There are some results of physiological experiments and a few isolated pathological facts which would seem to point to the existence of other sensory (centripetal) fasciculi in the lateral columns, but it would be wholly premature to make use of these facts in a practical consideration of the subject.
At the present time there is only one lesion of the æsthesodic system which can be diagnosticated during the patient's life from positive symptoms.
(a) Lesions of the fasciculi cuneati (posterior root-zones, 3). The symptoms of lesion (usually sclerosis) in this region are wholly sensory and ataxic. At an early stage acute pains, fulgurating pains, occur in the extremities; later paræsthesiæ, anæsthesia, and ataxia. The fulgurating pains caused by the slowly-progressive lesion of the posterior root-zones are very peculiar, and almost pathognomonic (vide preceding article for their description). In some cases paræsthesiæ precede the pains, which inversion of the usual order must be due to a difference in the starting-point of the sclerosis within the large fasciculi cuneati. Tendinous reflexes (especially the patellar) are lost at an early period in the disease, and by noting the disappearances of the different reflexes we can trace with some accuracy the longitudinal extension of the sclerosis (vide [Fig. 2]). In many cases the pupillary reflex is also abolished, constituting the Argyll-Robertson pupil.
As negative characters of lesions of the posterior root-zones (and of the rest of the æsthesodic system) we note absence of paralysis, contracture, atrophy, and De R.
In the present state of our knowledge of spinal physiology and pathology we think that a lesion in this location should be recognized by the physician early and positively—in some cases years before ataxia and other grosser symptoms make the diagnosis of locomotor ataxia obvious even to a layman's eye.
(b) Lesions of the fasciculi graciles (column of Goll, 4) cannot, we believe, be recognized directly by positive symptoms. There are a few cases on record of primary (?) sclerosis of these columns, in which during life vague sensory symptoms had been noted, but we cannot build upon such data. Indirectly, however, we can in many cases diagnosticate degeneration of these fasciculi, reasoning from the data of pathological anatomy. Thus, for example, in advanced cases of sclerosis of the fasciculi cuneati (posterior spinal sclerosis) we know that in the dorsal and cervical regions of the cord the columns of Goll are in a state of secondary degeneration. After complete transverse division of the cord by injury, extreme pressure, or focus of myelitis, etc. the same (centripetal) degeneration exists above the lesion.
The same remarks apply fairly to our clinical knowledge of the remaining parts of the æsthesodic system, columns of Clarke (6), and fasciculi ad cerebellum (5). We know absolutely nothing of lesions of the posterior horns (2) in their clinical and diagnostic relations.
B. Lesions of the Kinesodic System.—Limits of the Kinesodic System.—In general this includes the antero-lateral parts of the cord. In a trans-section of the cord (vide Figs. 5 and 6) the following columns and fasciculi are recognized, their location and limits being made known to us by embryology, descriptive and pathological anatomy: (7) The anterior (ventral) nerve-roots emerging from (8) the true anterior columns or anterior root-zones; (9) the ventral (anterior) gray horns with their groups of ganglion cells; (10) the crossed pyramidal fasciculus, which is the caudal continuation of the cerebral motor tract of the opposite hemisphere; (11) the direct pyramidal column (column of Türck), which is the caudal continuation of the cerebral motor part of the hemisphere on the same side; (12) the antero-lateral column. Fasciculi 10 and 11 bear an inverse relation to each other—i.e. 11 is larger in proportion as 10 is smaller.
FIG. 6.
Diagram of a Transverse Section of the Spinal Cord through the Lumbar Enlargement: The æsthesodic system is shaded; the kinesodic system unshaded. Parts of the æsthesodic system: (1) Posterior nerve-roots; (2) posterior gray horns; (3) fasciculi cuneati (columns of Burdach, inclusive of posterior root-zones); (4) fasciculi graciles (columns of Goll, or posterior median columns); (5) ascending cerebellar fasciculi; (6) columns of Clarke. Parts of the kinesodic system: (7) Anterior roots; (8) anterior columns (inclusive of anterior root-zones); (9) anterior gray horns; (10) crossed pyramidal fasciculi; (11) direct pyramidal fasciculi (columns of Türck) [10 and 11 are the intraspinal prolongation of the cerebral motor tract]; (12) lateral columns of ill-defined limits and unknown functions; P. R., posterior roots; P. S., posterior septum; A. R., anterior roots; A. F., anterior fissure.
In a general way it may be stated that lesions of the kinesodic system are characterized positively by the isolated existence or predominance of motor symptoms, by impairment of muscular nutrition, and by De R.; also by contractures. The reflexes are almost never normal, being either exaggerated or lost. Negative symptoms are—absence of sensory symptoms, of ataxia, and of vesical or rectal symptoms.
(a) Lesions of the anterior gray horns (9) are revealed by most definite and characteristic symptoms. There occurs a flaccid paralysis involving more or less extensive groups of muscles in the extremities, rarely truncal muscles, and never those of organic life. In a few weeks the paralyzed muscles undergo atrophy, sometimes to an extreme degree, and various degrees of De R. are present. Cutaneous and tendinous reflexes are abolished. The bladder and rectum are normal. Sensory symptoms absent, and if present consist only of mild paræsthesiæ, which are probably due to postural pressure upon nerve-trunks or to disturbance of the peripheral circulation. There is no tendency to the formation of bed-sores, but circulation and calorification are reduced in the paralyzed members. It should be remembered that paralysis due to systematic lesion of the anterior gray horns is never typically paraplegic, with horizontal limit-line of sensory symptoms, a cincture feeling, and vesical paralysis.
The above symptom-grouping is characteristic of lesion of the anterior horns en masse; in other words, of poliomyelitis. In that form of systematic disease of the anterior horns which consists primarily and chiefly of a degeneration or molecular death of the ganglion cells there is no true paralysis; the atrophy of muscles is infinitely slower, and it proceeds in various muscles fasciculus by fasciculus, the wasting being usually preceded by fibrillary contractions, and being almost always symmetrically located on the two sides of the body (affecting analogous or homologous parts). The electrical reactions are abnormal, in that musculo-faradic reaction is lost in exact proportion to the wasting; so that in a large muscle one part may contract normally, while the adjacent fasciculi do not. It is as yet uncertain whether De R. occur in this disease (progressive muscular atrophy). Calorification and circulation are much less impaired than in poliomyelitis; the negative symptoms are much the same.
It is sometimes difficult to distinguish poliomyelitis from generalized neuritis. The diagnosis is to be made by the presence in the latter disease of marked sensory symptoms—neuro-muscular pains, numbness, slight anæsthesia—and by a grouping of symptoms coinciding with the distribution of nerve-trunks and branches. No assistance can be derived from electrical tests, as both diseases yield more or less typical De R.
(b) Lesions of the spinal pyramidal tract (of fasciculi 10 and 11) are followed by motor symptoms only—viz. paralysis and contracture—or, in other words, by a spastic paralysis. Sensibility is unaffected; the bladder, rectum, and truncal muscles are not distinctly paralyzed; the reflexes are much increased, and ankle-clonus is often present. The electrical reactions of the paralyzed muscles are normal, qualitatively at least. The diagnosis of localization may be pushed still farther by the following considerations:
(1) When the condition of spastic paralysis is unilateral, of hemiplegic distribution, and follows an attack of cerebral disease of some sort, we may feel sure that both the crossed and the direct fasciculi of the pyramidal (10 and 11) belonging to one cerebral motor tract are degenerated throughout the length of the spinal cord, the crossed fasciculus on the paralyzed side and the direct on the healthy side (same side as injured hemisphere). It would thus appear that lesion of the direct pyramidal fasciculus (11) produces no symptoms,4 except, of course, in those rare cases in which it is larger than its associated crossed fasciculus.
4 Unless it be the increase of reflexes which is so often observed on the non-paralyzed side in hemiplegics.
(2) The above symptoms may be bilateral, as observed in children as a congenital or early-acquired condition. In such cases the four fasciculi of the motor tract are degenerated or undeveloped, in correspondence with a symmetrical bilateral lesion of the motor area of the cerebrum—imperfect development or early destruction.
(3) When the legs alone are the seat of spastic paralysis, with increased reflexes, spastic or tetanoid gait, without sensory symptoms, the diagnosis of a primary sclerosis of both lateral columns (inclusive of 10) of the spinal cord is justified.
(c) Lesions of antero-lateral columns of the cord (8 and 12), primary and independent of lesions of the anterior horns or of the crossed pyramidal fasciculus, cannot now be diagnosticated during life. These large masses of fibres include fasciculi whose functions are probably motor; others (especially in 12) whose functions, according to recent experiments, may be sensory; and still others which are associating or commissural.
(d) Various combinations of the above lesions occur, and may be recognized positively during life: (1) Combined sclerosis of the posterior columns and of the crossed pyramidal fasciculi (3 and 10), indicated by ataxia with paralysis, absence of patellar reflex, tendency to contracture, pains, and anæsthesia less marked than in typical posterior spinal sclerosis. This symptom-group is usually found in children; it is pre-eminently a family disease, and is known as Friedreich's disease. Similar cases also occur in adults as a strictly personal disease. (2) Secondary degeneration of the pyramidal tract (10 and 11), with more or less localized atrophy of cells in the anterior horns (9) coexists in two forms: First, in a few cases of cerebral hemiplegia with contracture, and pathological atrophy of various muscles on the paralyzed side; second, as a distinctly spinal bilateral affection, characterized by a spastic or tetanoid state of the lower extremities, and a mixture of atrophic paralysis (vide (a)), with contracture in the arms and hands. This latter form is the amyotrophic lateral sclerosis of Charcot.
SECOND QUESTION.—BEING GIVEN SYMPTOMS INDICATING A TOTAL TRANSVERSE LESION OF THE SPINAL CORD, ONE INVOLVING ITS VARIOUS SYSTEMS AT A CERTAIN LEVEL, TO DETERMINE THE ELEVATION OR FRONTO-CAUDAL SITUATION OF THE LESION.
This question is usually easy of solution by the following method: Since a transverse lesion of the spinal cord gives rise to both motor and sensory symptoms of horizontal, paraplegic distribution caudad of the lesion, the first thing to do is to determine accurately the upper level of the symptom, either the line of anæsthesia or the limit of paralysis. The former is always much more definite than the latter, and usually serves as the guide to diagnosis, indicating accurately the uppermost part of the lesion. In the thorax the levels of sensory and motor symptoms nearly coincide, but in the extremities the operation of Van der Kolk's law of distribution of motor and sensory fibres of nerve-trunks must be borne in mind, although it does not apply as strictly in this case as in nerve lesions strictly speaking. Gowers's diagram will prove very serviceable in making a diagnosis of transverse lesions, and will also prove of use in the study of vertebral injury and disease, as it indicates with sufficient accuracy the relation between vertebræ (spinous processes) and segments of the spinal cord. (Vide [Fig. 2.])
The following are the principal transverse localizations of disease which are usually recognized during life by the above procedure:
(a) Lesions of the cauda equina (by tumors, caries, or fracture of the bones, etc.) produce paralysis, anæsthesia, atrophy of muscles, with De R., in the range of distribution of the sciatic nerves mainly. The sphincter ani is paralyzed and relaxed, while the bladder remains normal as a rule. In all essential respects this paraplegiform, but not paraplegic, affection resembles that following injury to mixed nerve-trunks. It is in reality an intra-spinal peripheral paralysis. The more exact location of the lesion, in the absence of external physical signs (fracture, etc.), may be approximately determined by a study of the distribution of the symptoms and their relation to nerve-supply.
(b) Lesions of the lower end of the lumbar enlargement, or conus medullaris, behind the first lumbar vertebra, will give rise to the same symptoms as (a). The expression, lumbar part of the spinal cord, should be more carefully used than it is at present in the discussion of spinal injuries and spinal-cord diseases, disease of the lumbar enlargement being common enough, but disease of the lumbar part of the cord very rare. In the discussion of railway cases, more especially, it is often forgotten that the spinal cord practically ends behind the first lumbar vertebra.
(c) Lesions of the middle and upper parts (segments) of the lumbar enlargement are evidenced by true paraplegia, without paralysis of the abdominal muscles. In some cases the quadriceps group, supplied by the crural nerve, is not paralyzed. The constriction and the limit of anæsthesia are about the knees, at mid-thigh, or near the groin in different cases. The paralyzed muscles, as a rule, retain their irritability and show normal electrical reactions; the cutaneous and tendinous reflexes are preserved or increased. The sphincter is usually paralyzed, while the bladder is relatively unaffected.
(d) Transverse lesion of the dorsal spinal cord produces the classical type of paraplegia—i.e. paralysis and anæsthesia of all parts caudad of the lesion. The limit of anæsthesia and the constriction band are nearly horizontal, and their exact level varies with the height of the lesion, from the hypogastric region to above the nipples. Below the level of anæsthesia, which indicates by the number of the dorsal nerve the upper limit of the cord lesion, there are complete paralysis, retention of urine, constipation with relaxed sphincter ani, greatly exaggerated reflexes in the lower extremities, even to spinal epilepsy; the muscles preserve their volume fairly well, and their electrical reactions are normal—sensibility in all its modes is abolished; bed-sores are easily provoked. Retention of urine is an early symptom in lesion of the middle dorsal region of the cord—sometimes, in our experience, preceding symptoms in the legs.
(e) A transverse lesion of the cord at the level of the last cervical and first dorsal nerves—i.e. in the lower part of the cervical enlargement—gives rise to typical paraplegia with a sensory limit-line at or just below the clavicle, but also with some very peculiar symptoms superadded. These characteristic symptoms are in the upper extremities, and consist of paralysis and anæsthesia in the range of distribution of the ulnar nerves. In the arms the anæsthesia will be found along the lower ulnar aspect of the forearm, the ulnar part of the hands, the whole of the little fingers, and one half of the annuli. There will be paralysis (and in some cases atrophy with De R.) affecting the flexor carpi ulnaris, the hypothenar eminence, the interossei, and the ulnar half of the thenar group of muscles, producing in most cases a special deformity of the hand known as claw-hand or main-en-griffe. Another important symptom of a transverse lesion in this location is complete paralysis of all the intercostal and abdominal muscles, rendering respiration diaphragmatic and making coughing and expectoration impossible. The breathing is abdominal in type, and asphyxia is constantly impending.
(f) A transverse lesion of the upper part of the cervical enlargement, below the origin of the fourth cervical nerve, gives rise to symptoms designated as cervical or total paraplegia. The lower extremities and trunk are as in (d) and (e), but besides both arms are completely paralyzed and anæsthetic. The limit of anæsthesia usually extends along the clavicles to the acromion processes, or a little below, near the deltoid insertions. All reflexes caudad of this line are vastly increased, either with tonic or clonic contractions. In some cases of pressure upon the cervical cord by tumors, caries of vertebræ, etc. the tetanoid or spastic state of the extremities (the lower more especially) may precede paralysis for a long time; as the compression increases paralysis becomes more and more marked, while the reflexes remain high. This constitutes the clinical group we described in 1873 as tetanoid pseudo-paraplegia.
(g) Transverse lesions of the spinal cord from the decussation of the pyramids to the fourth cervical nerve are very rare, and usually of traumatic origin. They produce complete paralysis of the entire body, and also of the diaphragm (third and fourth cervical nerves), thus causing death by apnœa in a very short time.
(h) In ascending paralysis (Landry) the above symptom-groups, excepting (a), (b), are met with at successive stages of the disease, often by almost daily accession, until finally respiration ceases.
(i) The height of a transverse localized lesion (e.g. a stab-wound) of one lateral half of the spinal cord is to be determined by the various groupings of symptoms stated in the preceding paragraphs, the chief guide being the limit-line between the sensitive and anæsthetic portions of the body, measured vertically. The symptoms are, however, distributed in a very remarkable manner on either side of the median line. The paralysis will be found on the same side as the lesion, often accompanied by hyperæsthesia, vaso-motor paralysis, and loss of muscular sense, while the anæsthesia is on the other side of the body. When such a lesion occurs below the first dorsal nerve, the symptom-group is designated as hemiparaplegia; when the lesion is higher up, so as to paralyze the arms, the affection is termed spinal hemiplegia (Brown-Séquard).
Above the decussation of the pyramids total transverse lesions are practically unknown, so that the second question need not be followed farther.
By means of the data above given we are also enabled to determine the length—i.e. fronto-caudal extension—of the systematic lesions of the cord.
The symptoms of transverse lesions of the spinal cord are not exclusively caudad of the lesion, and some very striking ones are observable in the head. In lesions of the upper part of the dorsal cord and of the cervical enlargement (e, f, g) we observe vaso-motor and pupillary symptoms, due to injury of the spinal origin of the cervical sympathetic nerve; the pupils are contracted; the cheeks and ears congested and unnaturally warm; the cutaneous secretions are increased. In other words, the symptoms about the head, frontad of the lesion, are the same as those we produce experimentally in animals by section of the cervical sympathetic or of the lower cervical cord. In hemi-lesion of the cord, in man as in animals, these symptoms are unilateral, on the same side as the injury.
Another point to be remembered in the study of transverse lesions of the spinal cord is that the lesion may involve enough of the anterior gray horns to give rise to atrophic paralysis with De R. in some few muscles deriving their motor innervation from the focus of disease. This is not rarely seen in cervical paraplegia.
THIRD QUESTION.—BEING GIVEN VERY LIMITED MOTOR OR SENSORY SYMPTOMS OF SPINAL ORIGIN, TO DETERMINE THE EXACT LOCATION OF THE FOCAL LESIONS CAUSING THEM.
(a) In the range of sensory disturbances this question rarely presents itself for solution. Localized anæsthesia and pain of spinal origin (except the fulgurating pains of tabes) are rare, and we do not know the relation of cutaneous areas with the spinal segments as well as we know the motor innervations. It should be stated here, however, that the location of a fixed pain and of a zone of anæsthesia is often of great value in determining what spinal nerve is affected, just outside of the cord itself, by such directly-acting lesions as vertebral caries, spinal pachymeningitis, tumors upon the spinal cord, etc. Among the various symptoms of Pott's disease of the spine, fixed pains in one side of the trunk, in one thigh, or in the upper occipital region, etc. is a sign against which the physician should always be on his guard, as it is a very early and valuable indication of the existence of an affection which requires special treatment as soon as a diagnosis can be made.
(b) Localized motor symptoms of spinal origin calling for a diagnosis of the focal lesions causing them are frequent, and are mostly met with in two affections—viz. progressive muscular atrophy and poliomyelitis. The problem is now capable in many cases of an approximately exact solution by the deductive application of our knowledge of the intimate connection between certain muscles and muscular groups and limited portions or segments of the spinal cord (anterior gray horns more especially). This knowledge has been accumulated and organized from ordinary anatomy, physiological experiments, and more especially from carefully-made autopsies with microscopic examination of the cord. We cannot present this subject better than by reproducing a tabular statement of these results prepared by M. Allen Starr.5 Future autopsies may correct this table, and in making use of it the occurrence of anomalous nerve-distribution should be remembered:
LOCALIZATION OF FUNCTIONS IN THE VARIOUS SEGMENTS OF THE SPINAL CORD.
5 “The Localization of Functions of the Spinal Cord,” American Journal Neurology and Psychiatry, iii., 1884.
The above table should be studied in connection with Gowers's diagram of the vertebral column and spinal cord ([Fig. 2, p. 53]), for the thorough study of cases of neural and spinal localization. Additional details of much value with respect to the peripheral nerve distribution are accessible in the works of Ranney6 and Ross7.
6 The Applied Anatomy of the Nervous System, N. Y., 1881, p. 355 et seq.
7 Handbook of Diseases of the Nervous System, Am. ed., Philada., 1885, p. 356 et seq.
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. SYSTEMATIC LESIONS OF THE OBLONGATA.—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 lips and cheeks, the intrinsic lingual muscles, the laryngeal and pharyngeal muscles. Later, the masseters, temporals, and pterygoids are sometimes involved; and, finally, extremely rapid action of the heart with pneumonic symptoms indicates the gravest extension of the morbid process. An early symptom in such cases is abnormal salivation. These affections, generally designated as varieties of bulbar paralysis, subacute or chronic, are usually readily recognized intra vitam, and recent discoveries in morbid anatomy have enabled us to correctly diagnosticate the seat of the lesion in its various extensions. The laryngeal paralysis represents disintegration (atrophy) of ganglion-cells in the bulbar origin of the spinal accessory nerve; lingual atrophic paralysis indicates the same lesion in the nuclei of the hypoglossal nerves; the labio-buccal symptoms are produced by lesion of the facial nerve nucleus (inferior facial nucleus of older writers); the paralysis of the muscles of mastication is due to extension of cell-degeneration to the motor nucleus of the trigeminus in the pons; and the final cardio-pulmonary symptoms indicate an extension of the lesion into the sensory (?) origin of the pneumogastric nerves.
It is evident that this systematic lesion of the oblongata is the equivalent or analogue of the various acute and chronic lesions of the anterior horns of the spinal cord, described supra, and in practice we sometimes find these bulbar and spinal lesions associated: progressive muscular atrophy of the extremities and amyotrophic lateral sclerosis being complicated with bulbar paralysis.
B. FOCAL LESIONS OF THE MEDULLA OBLONGATA, as at present known, occur mostly in the kinesodic system, but may also involve several fasciculi and nuclei at one time. The symptoms of such lesions are grouped in two principal types:
(a) Single symptoms, such as atrophy or atrophic paralysis of some one muscle or muscular group innervated by the hypoglossal, facial, or spinal accessory nerves. For example, unilateral atrophy of the tongue, when not due to neural injury, is quite surely the representative of destruction of one hypoglossal nucleus. It is possible that some cases of peripheral facial paralysis, so-called, or Bell's palsy, and cases of paralysis of the sterno-mastoid and trapezius, are not due to neural lesion, but to primary disease of the nuclei of the facial and spinal accessory nerves, either as poliomyelitis or as progressive cell-degeneration and atrophy.
A similar reserve must be used in speaking of the localization of small lesions in the oblongata, causing diabetes mellitus, polyuria, albuminuria, and salivation. From experiments upon animals and a few post-mortem examinations in human cases we know that such lesions may occur and cause the symptoms, but their recognition during the patient's life is at the present time next to impossible.
(b) The symptoms may be complex and belong to the general class of crossed paralysis, the mouth, face, tongue, and larynx being paralyzed (often with anæsthesia of the face) on one side, while the extremities are paralyzed on the other side. Such a symptom-group would indicate a large lesion (tumor) in one lateral half of the oblongata, more especially in its ventral aspect. These localizations will be studied more in detail farther on, under the general head of Crossed Paralysis due to Lesions of the Base of the Brain.
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
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 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.
FIG. 7.
Horizontal Section through the Centre of the Right Cerebral Hemisphere: M, median line; Nc, nucleus caudatus; Nucleus lent., nucleus lentiformis with its three segments; To, thalamus opticus; c. i., internal capsule with its frontal division, its bend or knee, and its caudal division. 1, mass of fibres destined for pons and others forming a part of the corona radiata, non-pyramidal fibres; 2, knee of the internal capsule, containing fasciculus from cortical centre for the face to the nucleus of facial nerve (non-pyramidal fibres); 3, fasciculus for the tongue and throat to nucleus of hypoglossus, etc. (non-pyramidal fibres); 4, fasciculi from the pre- and postcentral gyri and the paracentral lobule to the pyramid of the oblongata (the true pyramidal fasciculus, continued in the cord as fasciculi, 10 and 11 of Figs. [5] and [6]); 5, the caudal third of the internal capsule, containing fasciculi destined to the sensory cortical centres.
(c) Lesions of cortical areas connected with fasciculi of the sensory part of the internal capsule (c. i. 5).
(α) Lesion of the cortical area or centre for smell cannot at present be diagnosticated. From the results of experiments upon higher mammals we would expect such a centre to be in the cortex of the mesal gyri of the temporal lobe.
(β) Lesions of the cortical centre for taste are equally unknown; it is probably situated in the meso-basal aspect of the temporal lobe.
(γ) Lesions of the acoustic centre are somewhat better known, at least as far as the function of hearing language-sounds (psychic hearing) is concerned. A number of recently-published cases9 have quite positively 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.
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-examination10 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.
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 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:
FIG. 8.
Diagram of Visual Paths, designed to illustrate specially Left Lateral Hemianopsia from any lesion. L. T. F., left temporal half-field; R. N. F., right nasal half-field; O. S., oculus sin.; O. D., oculus dexter; N. T., nasal and temporal halves of retinæ; N. O. S., nervus opticus sin.; N. O. D., nervus opticus dext.; F. C. S., fasciculus cruciatus sin.; F. L. D., fasciculus lateralis dext.; C., chiasma, or decussation of fasciculi cruciati; T. O. D., tractus opticus dext.; C. G. L., corpus geniculatum laterale; L. O., lobi optici (corpus quad.); P. O. C., primary optic centres, including lobus opticus, corp. genic. lat., and pulvinar of one side; F. O., fasciculus opticus (Gratiolet) in the internal capsule; C. P., cornu posterior; G. A., region of gyrus angularis; L. O. S., lobus occip. sin.; L. O. D., lobus occip. dext.; Cu., cuneus and subjacent gyri, constituting the cortical visual centre in man. The heavy or shaded lines represent parts connected with the right halves of both retinæ. The reader may place the lesion as he pleases.
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
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 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
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.
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 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.
FIG. 9.
Longitudinal (sagittal) Section through the Brain, to show the distribution of the fasciculi of the internal capsule. Fasciculi of motor tract in dotted lines, to fronto-parietal convolutions. Fasciculi of sensory tract in full lines, to temporo-parieto-occipital convolutions: N. C., nucleus caudatus; N. L., nucleus lentiformis; T. O., thalamus opticus. 1, level of crus cerebri; 2, level of pons; 3, level of oblongata. (This diagram is to be used in conjunction with [Fig. 7.])
The location of two other motor centres—one for the movement of the eyeballs in or near the gyrus angularis, and one for vocal laryngeal movements in the base of the right third frontal gyrus (homologous to the speech-centre in the left hemisphere), is problematical, or at least not well enough established to be recognized in a practical treatise.
Recent experimental researches have shown that to electrical excitation at least the fasciculi for the tongue, face, arm, and leg yield the same distinct reaction (isolated muscular contractions) as do their respective centres or cortical areas; perhaps they are more excitable.
When these cortical areas are destroyed by disease, or when their connected fasciculi are severed, secondary degeneration takes place and extends to the end of the respective bundles, even to the lower extremity of the spinal cord.
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 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).
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 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 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.
FIG. 10.
FIG. 11.
2. FOCAL LESIONS OF THE CEREBELLUM.—(a) Lesions strictly limited to one lateral lobe or hemisphere of this organ do not give rise to any characteristic symptoms—in some cases, indeed, to no symptoms at all. When the lesion tends basad, irritating and compressing the subjacent pons and oblongata on one side, incomplete paralysis appears in the limbs opposite the lesion, the face usually remaining normal. Occipital 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 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.
(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.
FIG. 12.
Topographical Lines applied to the External Contour of the Head.
From this line (1-1) a vertical line, or one exactly perpendicular to the first, is drawn through the external auditory meatus. At the top of head this line—the auriculo-bregmatic line (A A)—indicates the bregma or true vertex, which important landmark is to be marked with carmine or aniline upon the scalp. Upon the top of the head an imaginary horizontal line (4-4), parallel with the alveolo-condyloid plane, is projected, and upon it we measure backward a distance of 50 mm. (2 inches), and then draw a second vertical line (B B). At the point where this line reaches the convexity of the head is the Rolandic point (R), under which, 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 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).
FIG. 13.
Topographical Lines applied to Henle's Figure of the Skull. Location of the Rolandic point. Rolandic line, motor-centres, and the branches of the middle meningeal artery.
Having exactly determined and marked the situation of the Rolandic point and of the inferior termination of the fissure of Rolando above the ear, these two points are to be connected by a line, which is represented on the diagram by a black bar. This, the Rolandic line, is the guide for nearly all operations for the relief of spasm or paralysis of traumatic origin, or of such as may be caused by tumors, abscesses, etc. It is surrounded by the so-called motor centres for the face, arm, and leg (?) as demonstrated by experiments upon animals and by now numerous autopsies in human cases of injury and disease.
Other relations of interest are the apex of the temporal lobe, a little beneath the line (2-2) and at about 10 to 15 mm. posterior to the external angular process of the frontal bone; the situation of the occipito-parietal fissure, almost immediately under the posterior end of the line (2-2) at its junction with the lines (E E), which indicate the posterior extremity of the cerebrum; the anterior end of the brain being marked off by the line (D D).
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.
FIG. 14.
The same Topographical Lines applied to the Left Cerebral Hemisphere in Henle's Skull. The motor centres are approximately indicated by dotted lines. (The leg centre should be reduced in size as it lies near to and in the longitudinal fissure.) The Rolandic line is placed a little behind the fissure for the sake of clearness.
The location of the middle meningeal artery, which so often furnishes the blood that compresses the brain after various injuries to the head, is surgically of great importance. The course of its two principal branches is approximately indicated upon Fig. 13 by the branching lines drawn on the anterior inferior angle of the parietal and the upper part of the squamous portion of the temporal bone. In the living subject the main trunk of the artery would be found under the horizontal line (2-2) a little posterior to the speech-centre, about 30 mm. behind the external angular process, and in front of the beginning of the fissure of Sylvius.
Upon the shaven head of a patient seated in a chair or lying in bed the principal landmarks and relations above defined can be mapped out with sufficient approximation to accuracy by the use of a ruler to mark 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.
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, 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.