FIG. 1.
Reflex arc
Diagram illustrating the Arc for Reflex Action. The centripetal and centrifugal paths, the receptive and terminal organs of the arc, are shown connected with the spinal centre, which is a portion of central gray matter containing ganglion cells. The inhibitory cerebral influence is constantly exerted in health to moderate reflexes.
In the healthy animal body many important functions are performed under the law of reflex action; for example, many organic or secretory functions, the movements of hollow viscera, vascular movements, muscular tonus, defensive and expressive muscular movements. In the process of education many acts which at first must be learned by oft-repeated efforts, such as walking, playing upon musical instruments, etc., later become habitual and automatic, and are then largely executed by reflexaction unconsciously, co-ordinated by the spinal (?) apparatus. Much of our intellectual activity is governed by the same law operating between the psycho-sensory and the psycho-motor apparatus.
Reflex actions are only to a moderate extent under the control of volition—indeed, most of them are subconscious—but a strong restraining action is unconsciously exerted by the cerebrum (vide Fig. 1) upon the spinal reflex centres. This is the so-called inhibitory cerebral influence. The existence of such an influence is shown by experiments upon animals, and by human cases in which, the cerebral activity being reduced or abolished, we observe a great increase in the frequency and extent of reflex movements, particularly in the common muscular apparatus.
Clinically, we distinguish cutaneous or superficial, tendinous or deep reflexes, according to the seat of the original excitation or testing-point. Cerebral or psychic reflexes are, however, also to be borne in mind. These reflexes may be abolished or increased.
(a) Diminution and abolition of reflex action are frequent symptoms of disease of the nervous system. The fault or break may be anywhere in the reflex arc, so that each case must be analyzed by itself. Let us consider the phenomena as exhibited by two widely distant and different apparatuses.
First, in the eye. In case of atrophy of the optic nerve the pupillary reflex is lost, the reflex action failing because the receptive surface and efferent nerve are injured. In certain cases of spinal disease (posterior spinal sclerosis) the same pupillary immobility is observed (theArgyll-Robertson pupil); and in this case the lesion either affects indirect efferent spinal fibres destined for the iris, or it is situated in the centre for the reflex action—viz. the gray matter of the lobus opticus. There may be loss of pupillary reflex due to injury of the direct efferent fibres of the arc (paralysis of the motor oculi, N. iii.). Lastly, the iris itself may be so diseased as to be incapable of contracting, though it receive the reflex impulse properly; the lesion is then in the terminal organ of the arc.
Second, the patellar tendon reflex. In a healthy individual, sitting at ease with one leg thrown over the other (knee over knee), upon tapping the ligamentum patellæ of the overhanging or free leg a contraction of the quadriceps muscle occurs, causing a visible forward movement of the leg and foot. This is the well-known patellar reflex or knee-jerk. The arc in this case consists of the ligamentum patellæ with its included sensory fibres as receptive organs, sensory (afferent) fibres of the crural nerve, a segment of the lumbar gray matter of the cord as centre, motor (efferent) fibres of the crural nerve, supplying the quadriceps extensor femoris, which is the terminal organ. Theoretically (vide Fig. 1), we can conceive of numerous abnormal conditions of parts of this arc which would lead to abolition of the patellar reflex, but in practice the following are the principal lesions to be thought of: Disease (sclerosis) of the posterior root-zones of the lumbar enlargement of the cord, as exhibited in the pre-ataxic stage of tabes; disease of the posterior roots themselves through meningitis or meningo-myelitis, as in diphtheritic ataxia; lesion of the nervous centre, as is frequently observed in cases of infantile poliomyelitis; a lesion of the crural nerve, involving its efferent or afferent fibres, or both sets of fibres, would produce the same result, as would also, lastly, a severe myositis or cancerous infiltration of the quadriceps muscle.
It is therefore evident that there is, or can be, nothing pathognomonic in the loss of a given reflex: it simply indicates a break in the reflex arc, the seat and nature of which remain to be determined in each case. The topographical study of reflexes in disease is of very great importance, more especially as a help to the correct location and extent of neural and spinal diseases. To assist this study, and for use more especially in connection with the ensuing sections on localization, Gowers's excellent diagram and table are reproduced in Fig. 2.
FIG. 2.
Spinal nerves and sensory and reflex functions
Diagram and Table showing the Approximate Relation to the Spinal Nerves of the Various Sensory and Reflex Functions of the Spinal Cord (after Gowers).
(b) Exaggeration of reflex actions. This is due, theoretically, to any condition which increases the excitability of the reflex arc, but practically and usually the cause of the increase is more or less complete removal of the inhibitory supraspinal or cerebral influence. The reflex arc itself remains structurally sound, but its function is abnormally active. Thus, we meet with the most exquisite exhibition of exaggerated reflexes in the paralyzed part after a transverse lesion of the dorsal part of the cord. The lesion cuts off all communication between the lumbar enlargement and the brain; no sensations pass to consciousness, and no volitional influence can be exerted upon the legs; yet the legs are abnormally active, the least touch on or pricking of the skin, tapping a tendon, handling a joint, the pressure of feces in the rectum, etc., produce more or less violent spasmodic movements of mixed clonic and tonic forms (spinal epilepsy). Increased knee-jerk, foot-clonus, and epileptoid trepidation are also present. Other proofs that removal of the inhibitory cerebral influences is the chief cause of increase of spinal reflexes are given by thehistory of various cerebral diseases. Thus, in hemiplegia with secondary contracture the cutaneous and tendinous reflexes on the paralyzed side are much exaggerated; in dementia paralytica, as a rule, the patellar reflex is increased on both sides; and in cerebral neurasthenia all reflexes are often extremely great.
A variety of increased tendon reflex is known as clonus—a series of rhythmic clonic muscular contractions set up by stretching the body and tendon of a muscle. This is best studied at the ankle. By holding the patient's leg nearly extended upon our left hand, and rather suddenly forcing back the foot (dorsal flexion) by pressing under the ball of the foot with our right hand, a series of oscillations or to-and-fro movements of the ankle-joint are produced for a few moments (ankle- or foot-clonus). Sometimes the same rhythmic clonic contractions may be produced in the quadriceps by quickly pulling down the patella with the leg semi-extended.
In some instances, together with great increase of tendon reflex, we observe a transfer of the centrifugal impulse to other nerves of the same extremity, or across the spinal cord to nerves and muscles of the homologous limb.
Another interesting manifestation of morbid reflex movements is the defensive tonic spasm of muscles about a diseased joint (of the hip-muscles in coxitis, of vertebral muscles in Potts' disease). This constitutes a valuable symptom for the differential diagnosis between articular and neural diseases in certain cases.
Clinically, increase of reflex action is not as valuable an indication as its absence, many healthy persons having high reflexes. Still, when studied comparatively as to topography (comparing the two sides of the body) and as to variations at different times in a given case, the symptom is of considerable assistance.
IV. Trophic Symptoms.
IV. Trophic Symptoms.
Our present knowledge of this great group of symptoms of nervous disease is in a somewhat chaotic state; and although we possess a large accumulation of facts of this category, their classification is incomplete and their explanation is for the most part theoretical and unsatisfactory. The following subdivisions may be made to include all the phenomena, and is sufficient for clinical purposes:
1. DEGENERATIVEATROPHY, as distinguished from the simple atrophy of insufficient nutrition, of disuse of the parts, and of retarded growth, includes all those trophic symptoms in which, under the influence of nervous disease, the solid tissues exhibit histological and chemical alterations as well as reduction of volume. The principal factor of this group is—
(a) Muscular atrophy due to lesions of some part of the nervous apparatus (thus excluding directly traumatic or inflammatory atrophy), as seen in the course of progressive muscular atrophy, of various forms of poliomyelitis, of lead paralysis, of neuritis, and injuries of nerves. These muscular atrophies are characterized by reduction in the size of the affected muscles, by altered electrical reactions, and by histologicalchanges. Reduction in size may affect one muscle or a muscular group shortly after paralysis (as in poliomyelitis, lead paralysis, affections of nerve-trunks), or without evident paralysis it may involve only small fasciculi of a muscle at a time (as in progressive muscular atrophy); so that we speak of diffused and fascicular atrophy, of secondary (post-paralytic) and primary atrophy. In some cases the wasting proceeds to such a degree that apparently no muscular tissue remains, and the skin seems to rest directly on the bones; in others the reduction in bulk is moderate, and is compensated by increase in the intra- and extra-muscular fat (thus in stout children the atrophy of severe poliomyelitis may be quite masked to the eye); in still another category the increase in connective tissue with fatty accumulation overbalances the muscular wasting, and we have the pseudo-hypertrophic condition. Alterations in electro-muscular contractility are most important signs of impaired muscular innervation and nutrition. They present numerous and somewhat complicated variations of value for diagnosis and prognosis, but which cannot here be noticed at length. The general principle underlying these variations is this: that a muscle deprived of its normal innervation (centrifugal or motor) soon loses its capacity to respond to the induced (faradic) current, and reacts in an abnormal way to the galvanic current. This constitutes the reaction of degeneration of Erb.6The chief abnormality in the galvanic reaction of a paralyzed and diffusely atrophied muscle is its slow or wave-like contraction, which on a graphic, or even to the observer's eye, presents a striking contrast to the sharp, jerking, complete contraction of a healthy muscle. Besides, the reactions to the two poles become equal, or even reversed, so that we may obtain in testing by the polar method such formulas as CaCC = AnCC, or CaCC < AnCC. With reference to the failure of atrophied muscles to respond to the induced or faradic current, this qualification must be added: If the poles are applied on the moistened skin, as usual in testing or treating cases, no reaction occurs even with most intense currents; but if a needle be made one pole of the battery and inserted into the affected muscle, slight and limited contractions may be obtained with a moderate current for many months. Of this we have repeatedly satisfied ourselves in cases of poliomyelitis, lead paralysis, and traumatic peripheral paralysis. In the later stages of diffused paralytic atrophy, after an uncertain number of years, no reaction can be obtained with either electrical current. In fascicular non-paralytic muscular atrophy (as in progressive muscular atrophy) the loss of faradic contractility is only demonstrable in the affected fasciculi, good contractions being obtained in adjacent healthy fasciculi of the same muscle. The amount or extent of contraction varies pari passu with the progress of the atrophy. The galvanic reactions of this form of muscular atrophy are not yet well established. Muscles and muscular groups in a condition of impaired nutrition exhibit at an early period an interesting condition—viz. that they no longer contract by reflex excitation. Thus in a case of infantile poliomyelitis with paralysis of the muscles of the leg, these muscles no longer contract when the sole of the foot is tickled, and if the thigh-muscles are affected even so slightly as to appear of normal size and consistence, the patellar reflex is found wanting. In these and in traumatic cases thereflex act is prevented by lesion of the centrifugal motor nervous apparatus, and perhaps also by the associated muscular trophic alterations.
6Conveniently expressed by the symbol De R.
Histological changes in atrophied muscles vary somewhat in character in different diseases, and vary much in degree at different periods of the atrophy. An early appearance is the presence of proteinaceous and of fatty granules or molecules in the sarcous substance. Later, the muscular fibres become reduced in size, lose their striation, and show inequalities; the interstitial connective tissue becomes active and increases in amount, at the same time that fat is deposited. The fatty change in some cases, in others the granular or proteinaceous transformation, ultimately completely destroys the muscular substance, so that in the place of a muscle we find abnormal connective and fatty tissues, blood-vessels, fatty and proteinaceous débris, the whole presenting a pale yellowish-white aspect. It is in this final stage of degenerative atrophy that all electrical reactions are lost. In the pseudo-hypertrophic state the interfibrillary and interfascicular connective-tissue growth is much more active, and the wasting muscular fibres are buried in masses of wavy and fatty connective tissue. In this condition also electrical reactions may be wholly absent.
(b) Atrophy due to defective innervation sometimes affects the skin and bones. In the former, after nerve-injuries more especially, we observe loss of thickness, glossiness, and perverted circulation and secretion; the hairs may fall out or grow abnormally; the nails are slow of growth, thick, rugose, incurvated, and brittle. In other cases, as in cerebral and spinal paralyses, the skin of the paralyzed part is abnormally dry, rough, and furfuraceous, and it loses its elasticity. In some varieties of so-called skin diseases the patches of altered nutrition (eczema, bullæ, herpes, psoriasis, leucoderma, scleroderma, etc.) are often, probably, dependent upon nervous lesions.
In the very rare disease known as progressive facial atrophy the skin, subcutaneous areolar tissue, and the bones undergo extreme atrophy. The initial lesion is usually a patch of scleroderma with or without neuralgic phenomena; the skin is thin, darker and smoother than normal; it soon adheres to the subjacent bone (maxilla or zygoma), which itself steadily diminishes in size. Almost the entire half of the face (including the palate and tongue) may ultimately show the atrophic changes. We are not yet prepared to state the causal nerve-lesion in this disease.
The bones are abnormally fragile (fragilitas ossium) in some nervous diseases, more especially in dementia paralytica and posterior spinal sclerosis; but whether this condition is due directly to the nervous disease or is the expression of more general malnutrition is now undecided.
The complex lesions of joints observed in the course of posterior spinal sclerosis, the spinal arthropathies of Charcot, probably belong to this category. The affected joint (knee, shoulder, or ankle) rather suddenly swells, and the swelling usually invades the rest of the member or extends to the next distal joint; it is a hard, semi-elastic swelling unlike common œdema. After its gradual subsidence it is found that changes have taken place in the articulation itself, and later distinct evidences of destructive disease, such as erosion of cartilages, relaxation of ligaments, swelling, are observed. In many cases extra-articular lesions appear in the shape of osteophitic formations from the adjacent bones. The hydrarthrosis may persist or disappear. So complete may be the destruction ofthe joint that—for example, in a case of arthropathy of the knee—the leg may be twisted about in all directions, and even over-extended so as to lie upon the anterior surface of the thigh. Examination of the joint post-mortem reveals non-suppurative destruction of all its component parts, cartilages, ligaments, and epiphyses; the eroded, deformed ends of the bones rub against one another in a false joint-cavity formed of the skin, connective tissue, tendons, and remains of ligaments. The absence of pain and tenderness in the course of arthropathies is a striking feature—so much so that when, in an adult patient, it is observed that manipulation or puncture of a diseased joint is painless, special inquiry should be made for symptoms of posterior spinal sclerosis.7
7We have known one case in which the diagnosis of tabes dorsalis was made (and verified after death) in this way, after the surgeon in charge of the patient had mentioned the fact that puncturing a swollen diseased knee-joint was painless.
(c) Under the head of degenerative atrophies should be included the secondary changes which affect certain nerve-tracts within the nervous system itself. It is impossible in this introduction to treat fully of this interesting category of trophic changes; the following summary must suffice: (1) When the cerebral motor cortex or any part of the associated pyramidal (or motor) tract is destructively injured, there occurs, in from three to six weeks, a degeneration of the whole tract caudad of (below) the brain. The myeline becomes granular and disappears, the cylinder-axes are broken up and vanish, the connective tissue (neuroglia) increases in amount; the atrophied and degenerated area appears in a transection rather translucent in contrast to the pearly white of the normal medullary tissue, and when the preparation is stained with carmine the patch takes up an abnormal amount of pigment. This is the so-called descending degeneration, or centrifugal atrophy of the central nervous system. (2) After total transverse lesions of the spinal cord, besides the above-described centrifugal degeneration caudad of the lesion, we observe frontad of (above) it similar changes in the posterior median columns, and in the direct cerebellar tracts—centripetal degeneration. At present we have no knowledge of centripetal (ascending) degenerations in the cerebrum and in nerve-trunks; and if the results of von Gudden's experimental method be cited against this statement, it must be replied that its effects are best seen in newly-born animals, and that its pathology is yet unknown. (3) Lesions of the anterior gray matter (ventral cornua) of the spinal cord, and of mixed nerve-trunks produce only centrifugal or descending degeneration. All the nerve-fibres deriving their innervation from the injured area in the cord, or in case of nerves all fibres below the injury, perish—i.e.their myeline breaks up and undergoes granular and fatty degeneration, their cylinder-axes are segmented and disappear, while at the same time the connective tissue of the nerve becomes abnormally active and increases. Furthermore, in cases of this category there are, inevitably, degenerative and atrophic changes in the attached muscles, and peculiar electro-muscular reactions (vide supra). All these central and peripheral nervous degenerations, due to a local lesion, are conveniently grouped under the name of Wallerian degeneration.
2. ERUPTIONS ANDULCERATIONS.—(a) The cutaneous eruption about whose nervous origin there is the least doubt is that known as herpes orzona. This manifests itself, with or without paræsthesiæ (pain, itching, formication, etc.), as vesicles upon deeply-inflamed spots of skin distributed in the territory of one or more sensory nerves, and almost always unilaterally. The destructive process in the derma is so profound as to leave scars which are indelible as a rule. In general terms it might be stated that herpes may occur in the range of any sensory nerve distributed to the skin or mucous membranes. The neuralgia attending its development may be severe, and in some cases lasts for years after the healing of the eruption. The pathology of this affection appears to be inflammation of the ganglion of the posterior root of one or more spinal nerves (including the trigeminus and glosso-pharyngeal) or of their trunks. Herpes may appear in the course of spontaneous and traumatic neuritis; and in the last-named conditions a variety of eruptions have been observed in the area supplied by affected nerves, such as eczema, bullæ, etc.
(b) That ulceration may result directly from a nervous lesion is shown by the history of herpes, where a destructive process takes place in the derma under such conditions as to exclude the action of external agencies. But the same cannot be said of the ordinary ulcerations and gangrenous lesions observed in a number of nervous diseases, as the bed-sores of myelitis or of spinal injuries, the ulceration of the cornea in trigeminal anæsthesia, the digital ulcers and gangrene of lepra, asphyxia of the extremities, and nerve-injuries. As regards all these, the proper explanation is, it seems to us, that the anæsthesia existing as a predisposing cause (leading to imperfect protection of the part), the ulceration itself, is directly, actively caused by external agencies. Let me briefly cite a few instructive experimental and pathological facts bearing on this question.
It is well known that in animals and man lesions of the trigeminus nerve sufficient to produce anæsthesia (of its first branch more especially) are frequently, if not invariably, followed by ulceration and perforation of the cornea and phthisis bulbi. These were long held to be true dystropic changes, but about thirty and twenty years ago Snellen and von Gudden demonstrated independently and by different methods that these ocular lesions could be entirely prevented by absolute closure (perfect protection) of the eyelids prior to the experiment on the trigeminus. Not long afterward Brown-Séquard showed that the sloughing ulcers which occur about the foot of an animal whose sciatic nerve has been cut may be entirely prevented by care, cleanliness, and soft bedding. The conclusion to be drawn from these observations is that in almost all cases the ulcerations and sloughing observed in man during the course of a nervous disease sufficient to produce anæsthesia, such as traumatic neuritis, lepra anæsthetica, traumatic or simple myelitis transversa, disease of the trigeminal nerve, etc., are in reality produced by external agencies, injuries to the cuticle, action of filth, and, we think, the entrance of bacteria, which are well known to possess extraordinary powers of penetration into tissues whose protecting epithelial layer is removed. Clinical observation corroborates this view, for, with strict antiseptic treatment and under sealed dressings (collodion to ulcerated finger-tips), these ulcerations heal rapidly and completely, while the anæsthesia remains unchanged and the nervous lesions may even progress. At the sametime, while we believe the above to be the pathology of so-called trophic ulcers, we would admit the possibility of spontaneous neuritic ulceration and gangrene, as shown more especially in herpes.
3. ALTEREDSECRETIONS.—Under the influence of disordered innervation secretions may be altered in quantity and in quality. Symptoms of this class may be caused by neural or by central lesions, and the mechanism of their action may be direct or reflex.
(a) After section or lesion by disease of the cervical sympathetic nerve we observe increased activity of the entire skin in the affected area of the head and face: there is more perspiration, lachrymation, and more cerumen is found in the ear. In cases of lesions of a certain part of the oblongata we find one result to be polyuria. In many cases of nerve-injuries the sweat-glands and hair-follicles of the parts supplied by the affected nerve appear to be sometimes abnormally active, or in other cases inactive. In some rare cases of insanity profuse salivation and extraordinary growth of hair are striking symptoms. Lastly, in some functional nervous affections the various secretions and excretions may be altered to extraordinary extremes (e.g.the polyuria and anuria of hysteria).
(b) Qualitative modifications of secretions also occur, as exhibited in the many variations in the composition of the urine in various neuritic conditions, the watery urine of hysteria, the phosphatic urine of neurasthenia. Injuries of a part of the floor of the oblongata (and very probably other lesions of the nervous system) give rise to the appearance of sugar, and sometimes of albumen, in the urine. Under the influence of disease or of an emotion the breast-milk may become toxic to the nursing child, causing diarrhœa, convulsions, etc. In some forms of nervous dyspepsia large quantities of acid or of alkaline fluid may be rapidly poured out into the stomach as a result of disturbed glandular and vaso-motor action. In a few cases of neurosis malodorous or perfumed perspiration has been observed.
In a general way it may be stated that, inasmuch as the normal function of glands is largely, if not exclusively, under direct and reflex nervous control, their secretions may be quickly altered in quantity or quality by rapid nervous disease or by functional disorders. It is probable that much of our future progress in the semeiology of nervous diseases will be in this direction by the aid of improved medical chemistry.
4. ASSIMILATION, METAMORPHOSIS OFFOOD, TISSUE-LIFE, and BLOOD-MAKINGare probably under nervous control to a certain extent, but our knowledge is not now in a state to speak positively and definitely of alterations in these processes as symptoms of nervous disease.
Having in the preceding pages surveyed the field of neurological semeiology in an analytical way, it remains to briefly indicate how far and in what manner these data can be best utilized for logical diagnosis in the present state of science. If we may be allowed an illustration, wewould say that the foregoing sections contain a nearly complete vocabulary of the language of nervous diseases, and that the following pages express an attempt at formulating its grammar.
In the first place, it is important to classify the symptoms observed according to their probable immediate cause in the nervous organs, whether they are due to irritation or to the destruction of parts. The extreme value of such a distinction in practice was first emphatically brought forward by Brown-Séquard in his famousLectures on the Physiology and Pathology of the Central Nervous System(Philada., 1860); and to the observance of this law of genesis of symptoms we believe that a large part of the subsequent extraordinary progress of neurological science is due.
The symptoms produced by irritation of nervous organs are usually hyperkineses or paræsthesiæ in their various forms. The symptoms, spasm, pain, or numbness, are usually, though by no means always, intermittent. That paralysis and anæsthesia may occur from irritation, by an inhibitory process, is not to be denied, yet we must maintain the extreme rarity of such a mechanism. The phenomena of inhibition are so prominent in the normal nervous system that a physician who looks at nervous diseases from the standpoint of the physiologist may well be excused for seeing morbid inhibitory processes where others do not.
The symptoms due to destructive lesions—i.e.those indicating destruction of parts of the nervous system—are paralysis, hyperkinesis, and anæsthesia, of absolutely or relatively constant presence. Thus, for example, the paralysis of common hemiplegia due to destruction of the motor part of the internal capsule is constant and permanent, while the accompanying tonic spasm (late contracture), which is considered an even more positive sign of serious destructive injury to the cerebral motor tract, is permanent, but intermittent—i.e.it is absent in profound sleep, and reappears as soon as the patient awakes.
The association of symptoms of irritation and those of destruction is frequent but variable. In many cases, as in cerebral tremor and posterior spinal sclerosis, spasm and paræsthesiæ precede paralysis, anæsthesia, and ataxia. In other cases (in many at a certain period) they coexist. In a small group of cases the irritative symptoms follow those indicating destruction, sometimes occurring years afterward, as in post-hemiplegic epilepsy and neuralgia due to cicatrices. We would repeat that very often, more especially in organic nervous affections, much light is thrown on the diagnosis by careful noting of the topographic distribution and chronological order of appearance of the symptoms.
In the second place, it is necessary to group the symptoms of disease of the nervous system in two great classes—viz. those representing demonstrable lesions, macro- or microscopic, and those dependent upon perverted functions or molecular malnutrition of the nervous organs or elements. The first group is designated as organic diseases; the second as functional affections. Mental diseases, so called, can also be classified, according to their symptoms, in either of these groups.
The symptoms of the first group, that of organic nervous diseases, are characterized by definiteness of distribution, by permanency, by relative invariability, and by the predominance of objective signs. Another important characteristic of organic diseases is their progressive or fataltendency, either with reference to life in general or to that of parts or organs. A third peculiarity of these diseases is that they do not occupy the patient's attention as strongly or as constantly as neuroses: in other words, the Ego is less involved.
The symptoms of the second group, that of functional nervous affections (neuroses and psychoses), are characterized by generality and indefiniteness of distribution, by relative variability, by easy removal or spontaneous disappearance, and by the preponderance of subjective symptoms. The affection may endure for many years or for a lifetime without fatal result and without special aggravation. The Ego is very strongly and deeply affected, fear, depression, and constant dwelling upon the symptoms being prominent features.
These are general statements intended to serve as guides for the preliminary study of a case. It must be remembered that they are all liable to exceptions, and that each patient must be separately considered. It should be borne in mind that what to-day appears as a functional affection, chiefly indicated by subjective symptoms, may in a few months present distinct signs of organic changes in the nervous system. Also, it must be added that in the present state of knowledge we sometimes are not sure as to the presence or absence of organic changes even after careful study of a case; as, for example, in some epilepsies and neuralgias.
Furthermore, allowance must be made for the following sources of error:
Anatomical variability; as, for example, in the distribution of peripheral nerves and in the amount of decussation of fibres of the pyramids;
The coincidence of diseases and multiplicity of lesions;
The toxic effects of drugs taken by the patient previous to our examination; as, for example, bromism.
I. The Diagnosis of Organic Diseases of the Nervous System.
I. The Diagnosis of Organic Diseases of the Nervous System.
This should invariably consist, in the observer's mind at least, of three separate diagnoses, each formed by the application of widely different sources of knowledge, and each requiring a different logical process. One diagnosis forms the indispensable preliminary to the others, and the last one, when correct, demonstrates that the neurologist is a physician as well as a specialist. A further utility of this procedure by the method of the threefold diagnosis is, in our opinion, that it constitutes the sure inductive reasoning to be employed in the search after the pathology of new diseases, and must prove of help in the future growth of neurological medicine.
These diagnoses are—
The diagnosis of the symptoms or symptom-group;
The diagnosis of the location of the lesion;
The diagnosis of the nature of the lesion or of the functional disorder.
1. The diagnosis of the symptom or symptom-group is to be made by—(a) careful inquiry into the manner of appearance, development, and chronological order of the symptoms as related by the patient or by his friends, and more especially by (b) an exact, and in some directionsminute, determination of the symptoms, obvious or latent, present in the patient. This valuable method of exact observation is sometimes, no doubt, carried to a ridiculous extreme, entailing much loss of time without corresponding results; but in medical practice, as in all forms of professional work, there enters a sort of genius, partly innate, but largely developed by cultivation, which enables the observer to seize at once, apparently by intuition or in the course of a few minutes of study, the really valuable and suggestive phenomena; and it is in this line, the line of important and correlated facts, that observation cannot be too minute and exact. In following this method technical terms must be correctly used and definitions rigidly adhered to, as superficial and loose records nearly always mislead. Sometimes in the course of the examination a symptom is discovered or a hint is thrown out by the patient which suggests new lines of inquiry, and occasionally necessitates an entire rearrangement of the data obtained. Consequently, it is important that the observer should approach a case tabula rasa, and should, as far as possible, prevent his being biassed by anticipations of, and immature guesses at, the third or final diagnosis.
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.
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).
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:
(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.