Chapter IV: Front Matter (4)

Besides exactness of observation, it is necessary that the physician should have a thorough knowledge of nervous nosology in order to complete the first diagnosis: he must be acquainted by book-study and by personal observation with the numerous types of symptom-groups which fill up our present classification of diseases, so that he can at once say, approximately at least, in what category the case before him belongs.

2. The second diagnosis, that of the location of the lesions, is to be arrived at by the application of the observer's knowledge of the anatomy and physiology of the nervous system; and therefore it is here that special training is of the greatest advantage. The anatomy and physiology of use in this connection are not the bare sciences as taught in ordinary text-books, but a higher sort of knowledge, corrected and extended by the teachings of pathology and pathological anatomy. The physician must be well versed in the recent revelations of experimentation and of autopsies bearing upon the architecture and functions of the central nervous system, and should be able to apply this knowledge deductively to the case in hand. In this manner the now abundant material grouped under the term Localization of Cerebral and Spinal Diseases (vide the next article) can be made of the greatest utility in every-day practice. The solution of the problem of localization of the lesion is much simplified if it be first accurately determined whether the lesion is peripheral, spinal, or cerebral.

3. The final diagnosis is with respect to the nature of the lesion. While the second diagnosis may be said to possess the greater scientific interest, this one must be admitted to possess paramount practical importance, as from it we derive the indications for rational treatment and the data of prognosis. The third diagnosis is to be made by the application of the observer's knowledge of general pathology and etiology; hence it is in this field that the best-trained physician succeeds—where the experienced practitioner may sometimes eclipse the brilliant specialist. The truth of this is maintained by those who hold, as we do, that it is unwise to embark in specialism without having had good hospital advantages and extensive general practice.

{63} In order to arrive at the diagnosis of the nature of the lesion we must consider the family history, trace out predispositions, study the various causes of disease to which the patient has been exposed, and by a thorough examination of the various functions and the objective condition of the patient ascertain what pathological processes are active in him. Often the clue to the diagnosis is found in signs afforded by non-nervous organs, as nervous syphilis by nodes and cutaneous cicatrices, cerebral hemorrhage by renal disease and increased arterial tension, cerebral tuberculosis by pulmonary lesions, etc.

A purely empirical form of knowledge of some utility in proving the pathological diagnosis is that of the relative frequency of certain lesions in the two sexes, at different ages, in various professions, etc.—a statistical knowledge which is to be applied deductively to the case under study.

Considerable uncertainty sometimes remains even after the most careful analysis of a case, and often, after stating the first and second diagnoses quite positively, scientific caution and due regard for truth compel us to state the third diagnosis in alternative propositions or as a diagnosis of probability, to be finally settled by the appearance of new symptoms, or in some rare cases only by a post-mortem examination.

II. The Diagnosis of Functional Nervous Affections (Neuroses and Psychoses).

In some diseases of this class—as, for example, epilepsy—it is desirable to make the triple diagnosis as stated supra, but usually the two problems to be solved are—What is the symptom-group? and what is the pathology of the affection? The question of localization is less important and less easy of solution, as the symptoms are more usually generalized, often vague, and sometimes purely subjective.

1. The first diagnosis is to be made in the same manner as already stated, but besides, in many cases, a close psychological analysis is required to ascertain the emotional and mental state of the patient. Not only is this indispensable in cases of insanity, but it is often of great utility in other conditions, as hysteria, hypochondriasis, and simulation. In the course of this study we are frequently brought face to face with a most difficult problem—viz. the correct estimation of the degree of pain experienced by a patient. Is it a quasi-objective, correctly-portrayed sensation? is it magnified by abnormal sensitiveness or by true exaggeration? or is it simulated for a purpose? These questions demand the greatest freedom from prejudice and most delicate tact for their solution, and occasionally the most experienced physician is deceived. More especially are caution and scientific doubt to be exercised when this symptom (pain) stands alone or nearly so, as in some medico-legal cases and in certain hypochondriacal states where self-delusion seems to constitute the only real disease.

2. The diagnosis of the pathological nature of the functional disturbance (functional lesion) is to be made only by an exhaustive study of the patient's personal and family history and of his general condition. The following are the principal lines of inquiry to be followed:

{64} (_a_) As to hereditary predisposition: direct or indirect inheritance of neurotic tendencies, of psychic peculiarities, and as to the presence of the various psychic and physical signs grouped under the term psychic degeneration.

(_b_) As to personal habits: overwork, masturbation, the abuse of tobacco, alcohol, or coitus, injudicious diet, abnormal postures, injurious avocations, etc.

(_c_) As to dyscrasic and hæmic conditions: uræmia, lithæmia, anæmia, malarial and syphilitic infection, etc.

(_d_) As to the condition of important organs: of the eye in connection with headaches and vertigo; of the ear in relation to vertigo and epileptiform attacks; of the heart (and arterial tension) in various head-symptoms; of the sexual organs in hysteria, hypochondriasis, epilepsy, etc.

A serious stumbling-block in this last line of inquiry is the ever-recurring question as to the causal relation between the symptoms observed. Is the asthenopia the cause of the headache, or does the neurasthenia, giving rise to the headache, cause the asthenopia? Does the extremely slow action of the heart in a given case produce the epileptoid attacks, or are both due to a lesion of the medulla? Does ovarian hyperæsthesia and neuralgia (with or without organic changes) cause the hystero-epilepsy, or is the ovaria one of the numerous peripherally projected sensory symptoms of the hysteric state? Does the lithæmia, oxaluria, azoturia, or phosphaturia found in a patient give rise to the nervous symptoms complained of, or are they (the morbid excretions) the result of defective innervation? The candid neurologist, looking at his cases from the standpoint of the general physician rather than from the loophole of narrow specialism, must admit that these questions vex him daily, and that they are often not to be resolved in the present state of knowledge except by a recurrence to the therapeutic test.

For this extremely difficult diagnosis of the pathology of functional nervous affections we would obtain much immediate assistance if observers had the courage to publish their cases in continuous series, instead of giving us successful cases, which often only serve to mislead. For example, how greatly would the question of the relation between ovarian symptoms and epilepsy (also hystero-epilepsy) be advanced if we had the final results of all cases of removal of the ovaries for these diseases at a period not less than one year after the operation! And so with the attempts made to cure headaches by the correction of errors of refraction and weakness of the interni. The profession has a right to demand a frank and full report of the experience of those who practice and teach in these directions.

{65}

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 {66} 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).

[Footnote 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 {67} 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.

).]

[Footnote 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 {68} 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 {69} 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.

; (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 {70} 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]

[Footnote 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 {71} 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.

; (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 {72} 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.

{73} 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.

[Footnote 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 {74} 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 {75} 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 {76} 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 {77} 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.

-----------+------------------------+--------------+---------------
Segment. | Muscles. | Reflexes. | Sensation.
-----------+------------------------+--------------+---------------
2d-3d C. | Sterno-mast. trapezius.| . . . . . . | Neck and back
| Scaleni and musc. of | | of head.
| neck. | |
| Diaphragm. . . . . . . | Hypochon- |
| | drium (?). |
| | |
4th C. | Diaphragm. . . . . . . | Dilatation | Neck.
| | of pupil. |
| Supra- and | On irritation| Upper shoulder.
| infra-spinatus. | of neck. |
| Deltoid. . . . . . . . | 4th-7th C. | Outer arm.
| Biceps and | |
| coraco-brach. | |
| Supinator longus. | |
| Rhomboid. | |
| | |
5th C. | Deep muscles of | Scapular. | Back of should-
| shoulder-blade. . . | 5th C.-1st D.| er and arm.
{78} | Deltoid. . . . . . . | . . . . . . | Outer side of
| | | arm and
| | | forearm.
| Biceps and | | Ant. upper
| coraco-brach. . . . | . . . . . . | two-thirds of
| | | arm.
| Supinator longus. | |
| Pectorales. | |
| Serratus magnus. | |
| Triceps. | Elbow tendon.|
| Rhomboid, teres minor. | 5th-6th C. |
| | |
6th C. | Biceps, brach. antic. | . . . . . . | Outer side of
| | | arm and
| | | forearm.
| Pectorales. . . . . . | . . . . . . | Inner and front
| | | of forearm.
| Serratus magnus. | |
| Triceps. | |
| Extensors of wrist and | Wrist |
| fingers. . . . . . | tendons. |
| Flexors of wrist. . . | Wrist |
| | tendons. |
| Pronators, supinator | 6th-8th C. |
| brevis. . . . . . . | |
| | |
7th C. | Triceps, long head. . | . . . . . . | Inner and back
| | | of arm and
| | | forearm.
| Extensors of wrist and | |
| fingers. | |
| Flexors of wrist and | Palmar. . . | Radial
| fingers. . . . . . | | distribution
| | | in the hand.
| Pronators of wrist. . | 7th-8th C. |
| Subscapular. | |
| Latissimus dorsi. | |
| Teres major. | |
| | |
8th C. | Extensors of thumb. . | . . . . . . | Forearm and
| Flexors of wrist and | | hand, median
| fingers. | | and ulnar
| Intrinsic muscles of | | distribution.
| hand. | |
| | |
1st D. | Extensors of thumb. . | . . . . . . | Ulnar
| Intrinsic muscles of | | distribution
| hand. | | to hand,
| Thenar and hypothenar | | little
| eminences. | | finger.
| | |
2d-12th D. | Muscles of back and | Epigastric | Skin of back
| abdomen. . . . . . | skin. | and abdomen,
| | 4-7 D. | and over
| | Abdominal | upper gluteal
| | skin. | region.
| | 7-11 D. |
| Erector spinæ muscles. | Hypochon- |
| | drium (?). |
| | |
1st L. | Ilio-psoas. . . . . . | Cremasteric. | Skin over groin
| Sartorius. . . . . . | 1st-3d L. | and front of
| | | scrotum.
| | |
2d L. | Ilio-psoas. . . . . . | Patellar | Outer side of
| | tendon. | thigh.
| Sartorius. . . . . . | 2d-4th L. |
| Flexors of knee, | Bladder and |
| Remak (?) . . . . . | sexual |
| | centres. |
| | 2d-4th L. |
| | |
3d L. | Quadriceps femoris. . | . . . . . . | Front of thigh.
| Adductores femoris. | |
| | |
4th L. | Adductores femoris. . | Rectal | Inner side of
| | centre. | thigh and leg
| Extensores femoris. . | 4th L.-2d S. | to ankle.
| Tibialis anticus. . . | Gluteal. |
| Peroneus longus. . . | 4th-5th L. |
| Flexors of knee | |
| (Ferrier (?)). | |
{79} | | |
5th L. | Outward rotators of | . . . . . . | Lower part of
| thigh. . . . . . . | | gluteal
| | | region.
| Flexors of knee | . . . . . . | Back of thigh.
| (Ferrier). | |
| Flexors and extensors | . . . . . . | Leg and foot,
| of toes. | | outer part.
| Peronei. | |
| Muscles of calf of leg.| |
| | |
1st S. | Muscles of calf of leg.| Foot clonus. | Leg and foot,
| Long flexor of great | Achillis | except inner
| toe. . . . . . . . | tendon. | part.
| Intrinsic muscles of | Plantar. |
| foot. . . . . . . . | |
| | |
2d S. | Intrinsic muscles of | Plantar. | Perineum, anus.
| foot. . . . . . . . | |
-----------+------------------------+--------------+---------------

[Footnote 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 Ranney[6] and Ross[7].

[Footnote 6: _The Applied Anatomy of the Nervous System_, N. Y., 1881, p. 355 _et seq._]

[Footnote 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 {80} and cheeks, the intrinsic lingual muscles, the laryngeal and pharyngeal muscles. Later, the masseters, temporals, and pterygoids are sometimes involved; and, finally, extremely rapid action of the heart with pneumonic symptoms indicates the gravest extension of the morbid process. An early symptom in such cases is abnormal salivation. These affections, generally designated as varieties of bulbar paralysis, subacute or chronic, are usually readily recognized intra vitam, and recent discoveries in morbid anatomy have enabled us to correctly diagnosticate the seat of the lesion in its various extensions. The laryngeal paralysis represents disintegration (atrophy) of ganglion-cells in the bulbar origin of the spinal accessory nerve; lingual atrophic paralysis indicates the same lesion in the nuclei of the hypoglossal nerves; the labio-buccal symptoms are produced by lesion of the facial nerve nucleus (inferior facial nucleus of older writers); the paralysis of the muscles of mastication is due to extension of cell-degeneration to the motor nucleus of the trigeminus in the pons; and the final cardio-pulmonary symptoms indicate an extension of the lesion into the sensory (?) origin of the pneumogastric nerves.

It is evident that this systematic lesion of the oblongata is the equivalent or analogue of the various acute and chronic lesions of the anterior horns of the spinal cord, described supra, and in practice we sometimes find these bulbar and spinal lesions associated: progressive muscular atrophy of the extremities and amyotrophic lateral sclerosis being complicated with bulbar paralysis.

B. FOCAL LESIONS OF THE MEDULLA OBLONGATA, as at present known, occur mostly in the kinesodic system, but may also involve several fasciculi and nuclei at one time. The symptoms of such lesions are grouped in two principal types:

(_a_) Single symptoms, such as atrophy or atrophic paralysis of some one muscle or muscular group innervated by the hypoglossal, facial, or spinal accessory nerves. For example, unilateral atrophy of the tongue, when not due to neural injury, is quite surely the representative of destruction of one hypoglossal nucleus. It is possible that some cases of peripheral facial paralysis, so-called, or Bell's palsy, and cases of paralysis of the sterno-mastoid and trapezius, are not due to neural lesion, but to primary disease of the nuclei of the facial and spinal accessory nerves, either as poliomyelitis or as progressive cell-degeneration and atrophy.

A similar reserve must be used in speaking of the localization of small lesions in the oblongata, causing diabetes mellitus, polyuria, albuminuria, and salivation. From experiments upon animals and a few post-mortem examinations in human cases we know that such lesions may occur and cause the symptoms, but their recognition during the patient's life is at the present time next to impossible.