Chapter II: Front Matter (2)

DOUBLE CONSIOUSNESS is a rare condition, in which the subject appears to have separate forms or phases of consciousness, one normal, the other morbid. This occurs in hypnotic and somnambulic states, probably also in certain cases of insanity and epilepsy. The current of normal consciousness is suddenly broken; the patient enters into the second or abnormal state, in which he acts, writes, speaks, moves about with seeming consciousness; but after a variable time a return to normal consciousness reveals a break in the continuity of the memory: the patient has no recollection whatever of what he did or said in the morbid period. In the hypnotic state subjects may show increased power of perception, and are strangely susceptible to suggestions or guidance by the experimenter. In a second attack the patient often refers back to the first, and does things in continuation or repetition of what he previously did, apparently taking up the same line of thought and action. The morbid states, long or short, are joined together by memory, but are wholly unknown in the normally conscious states. In other words, the patient leads two (or three, according to a few observations) separate lives, each one forming a chain of interrupted conscious states. In epilepsy we observe remarkable breaks in normal consciousness: the patient goes through certain acts or walks a distance or commits a crime in a dream-like state, and suddenly, after the lapse of a few minutes, hours, or days, becomes normally conscious and has no recollection of what he did with such apparent system and purpose during the seizure. It might, perhaps, be as well to classify these phenomena under the head of amnesia. A case is on record where a man travelled, seeming normal to fellow-travellers, from Paris to India, and who was immensely astonished on coming to himself (return to common consciousness) in Calcutta. Many murders have been committed with apparent design and with skill by epileptics, who upon awaking from their dream-like state were inexpressibly horrified to hear of their misdeeds.

AMNESIA, or loss of memory, may vary in degree from the occasional failure to remember which is allowed as normal, to the absolute extinction of all mental impressions or pictures. This word and the expression memory are here used in a restricted sense, reference being had only to purely intellectual and sensorial acts related to intellection. If we take the general or biological sense of the term memory as meaning the retention of all kinds of residua from centripetal impressions and of motor {29} centrifugal impulses, including common sensory and visual impressions, special sense impressions, all unconsciously received impressions, emotional, intellectual, and motor residua, we should consider amnesia in a correspondingly general way. This, however proper for a physiological study, would be far too complex and premature for an introduction to practical medicine. Recognizing memory, therefore, as a universal organic attribute—a capacity to retain impressions—we will treat of it only in the commonly-accepted sense referred to supra.

Failure of memory may be real or apparent. In the latter sense amnesia is induced by diversion of the attention into a channel different from that in which the line of inquiry is conducted. A normal example of this is seen in the state known as preoccupation, where a person intent upon a certain thought or action forgets who is about him, where he is, and if asked questions fails to answer or answers incorrectly. In pathological states, as in acute curable insanity, apparent loss of memory is often caused by the domination of an emotion or of delusions. In both cases, if the subject can be roused or brought to himself, he remembers all that we inquire about and is amused at his previous false answers or silence. Real amnesia consists in the actual blotting out of recollections or residua in a partial or general manner, for a time or permanently. These differences serve as the basis of a complicated subdivision of amnesia which it is not necessary to fully reproduce here.

Temporary partial amnesia is a variety which is frequently observed in normal persons, even the most gifted. A word or fact escapes us, seems wholly lost for a few minutes, hours, or days; the more we strive to recall it, the less we succeed; yet later, when not sought for, the fact or word appears in our consciousness as if spontaneously, but more probably by some effect of the law of association. Such partial and momentary forgetfulness may assume proportions which render it pathological. What is known as transitory aphasia may be classed in this group. In a few minutes or hours a person without apoplectic, epileptic, or paralytic phenomena loses all power to express his thoughts by speaking or writing; there is verbal amnesia and agraphia. The subject is conscious of his condition and of the wholly futile or incorrect attempts he makes to communicate with others.

Temporary complete amnesia is almost equivalent to loss of consciousness, yet not strictly so. For example, after a sharp blow upon the head a person may perform complicated acts, reply to questions, and apparently act normally, yet after a variable time he will declare that he remembers absolutely nothing of the injury and what he did or said for hours or days afterward. The same phenomenon is observed in the course of psychoses, neuroses (epilepsy), in some acute diseases, and in certain states of intoxication.

Permanent partial amnesia occurs in states of dementia, such as senile dementia, paralytic dementia, and in certain cases of aphasia. Great gaps exist in the patient's memory; some things are well recalled, others wholly and for ever effaced. The psychological law governing the failure of memory in these cases is that the earliest and strongest impressions survive, while recent and less forcible (_i.e._ less interesting) ones are lost. Substantives or names are especially liable to obliteration, as are also many of the delicate residua which lie at the basis of the subject's ethical conceptions and acts.

{30} Permanent complete amnesia is observed at the end of degenerative cerebral diseases, as organic dementia, whether of the form termed secondary or that designated as paralytic. Sometimes after acute general diseases the memory may be a perfect blank for a considerable length of time, and education has to be repeated. Memory may be so completely absent that cases are known in which the patient gave a fresh greeting to the asylum physician every two or three minutes indefinitely, as if each were a first meeting. Momentary perception and automatic (reflex) response are there, but no impression is made; there is no residuum left in the cortical centres. In these cases amnesia is accompanied by degeneration of the visual, auditory, etc. cortical areas or centres.

An interesting form of amnesia, not generally recognized as such, is the loss of acquired skill in muscular movements, such as are necessary for writing, for using tools, and for doing various delicate professional movements. Here the motor residua acquired by laborious education or training are gradually lost without actual paralysis or ataxia. This variety is exquisitely illustrated by certain cases of dementia paralytica where long before marked intellectual symptoms occur there is loss of skill in mechanical arts and in handwriting.

In testing a subject's memory due attention should be paid to the law of the survival of older and more interesting residua, as well as to the power of the law of association. Such questions should be asked as pertain to recent events in the patient's experience, and about matters which are not closely related logically. A patient who might tell us nearly all about his early personal experiences, his business and family relations, incidents of his childhood, etc., would fail to remember what he had for breakfast, what he did the day before, etc.

The physiological cause of real amnesia is impairment in the vitality (nutrition) of ganglion-cells in the various cerebral sensory areas or centres, and of the motor area as well (motor residua). In cases of transitory amnesia we suppose this to be due to the action of toxic agents, to anæmia, and impaired molecular or chemical nutrition, as after acute diseases, in extreme debility, in psychoses, etc. In cases of terminal permanent dementia, autopsies afford us evidence of degeneration and disappearance of ganglion-cells: we find granular and fatty pigmentation, atrophy, calcarous degeneration of these bodies, thickening and shrinkage of the neuroglia, and degenerative changes in blood-vessels. Doubtless degeneration or destruction of association fasciculi of nerve-fibres in the cortex cerebri or in the white substance plays a considerable part in the production of permanent amnesia, but we are as yet unable to give a clear demonstration of this. Theoretically, we may admit an organic loss of memory with the following conditions of the brain: (1) diseased perceptive (sensory) centres or motor area with normal association fasciculi; (2) normal perceptive centres and motor area with degenerate or broken association fasciculi, connecting these parts with one another and with the more strictly ideational or expressive (centrifugal) areas and parts of the brain and spinal cord.

Amnesia—or, more properly speaking, dulness of perception and feebleness of retention of residua—occurs as a strictly congenital condition from imperfect cerebral development, or a little later in life from infantile diseases, constituting one of the aspects of idiocy.

{31} WORD-DEAFNESS is a special morbid psycho-sensory state in which the sounds of language lose their significance for the patient. The sense of hearing is preserved for common sounds, and even music in certain cases; words are heard, but not understood. A patient of mine having this symptom used to say, “If I go to a lecture or hear a sermon, I hear the speaker, but what he says is all Greek to me.” On the other hand, this gentleman could go to a concert and understand the musical notes. This condition occurs as a part of the symptom-group aphasia, or it may show itself independently in the course of limited cerebral cortical degenerations. The lesion causing word-deafness is usually found in the left hemisphere, in the first and second temporal gyri, or it may be in the inferior parietal lobule and gyrus supra-marginalis, penetrating deeply enough to injure fasciculi going into the temporal lobe. It would appear, from the evidence now before us, that the centre for psychic hearing is in the caudo-dorsal part of the temporal lobe.

WORD-BLINDNESS, or alexia, is another special morbid psycho-sensory state, in which the visible signs of language lose their significance for the patient. Usually there is no impairment of sight; the patient can see the letters and words as objects, but he cannot read them at all, or must do so letter by letter. Even numerals and pictures of objects in some cases become unintelligible. In testing for this condition a possible confusion with verbal amnesia must not be forgotten. In such a case the patient knows the word or object, but cannot name it; usually he can, however, inform us by signs or indirect expressions that he takes proper cognizance of the object. Alexia is present in a certain proportion of cases of aphasia, and it may be complicated with lateral hemianopia. The exact seat of the lesion producing alexia is at present unknown. Theoretically, however, we must place it in the course of paths from the cortical visual area (cuneus and adjacent gyri) to the general speech-centre. Psychic blindness for objects in general (soul-blindness of the Germans) is now quite conclusively proved to be due to degeneration of both occipital lobes, more especially their mesal gyri, where the visual centres are. This psycho-sensory state, with the accompanying cortical changes, has been demonstrated in cases of dementia paralytica.

APHASIA, or loss of the faculty of language, is so important a symptom as to deserve elaborate consideration in a separate article of this volume; and to it the reader is referred. Suffice it here to state that aphasia may be classified into three forms: (1) Sensory aphasia, in which there is primary disorder of the psycho-sensory (perceptive or centripetal) part of the complex central mechanism for speech; (2) Motor aphasia (including ataxic aphasia), in which the primary lesion affects the motor (expressive or centrifugal) parts of the mechanism; (3) Amnesic aphasia, in which loss of memory (effacement of residua) of words and signs is the prime condition.

II. Sensory Symptoms.

HYPERÆSTHESIA is a condition of exalted excitability in the various parts of the sensory apparatus: terminal nervous organs, nerve-trunks, central gray matter. We may admit such a state as existing {32} independently of consciousness, as where a lesion cuts off communication between the perceptive cerebral centres and the periphery, but in practice we consider only conscious hyperæsthesia. In this state the subject may be able to perceive (feel) slighter impacts than would affect a normal individual, or he receives an exaggerated, usually unpleasant, impression from ordinary excitations. It may also be said that hyperæsthesia exists as a purely subjective state, psycho-sensory hyperæsthesia, without external mechanical excitations.

(_a_) Hyperæsthesia of common tactile sensibility in the skin and mucous membranes is frequent. The least touch is felt with unpleasant acuteness and causes unusual reactions of a reflex order; frequently, but not necessarily always, a sensation of pain is produced at the same time. It has been claimed that in certain cases the points of the æsthesiometer could be perceived (distinguished as two points) at smaller distances than the average normal, but I have never been able to demonstrate this to my satisfaction. The simplest form of tactile hyperæsthesia is met with in persons of a highly nervous organization, in those under the influence of strong emotions, in the hypnotic state, and while intoxicated. The common pathological conditions in which increased sensibility is found are meningitis (cerebral and spinal), hydrophobia, tetanus, neuritis, dermatitis, hysteria, and spinal irritation; also in connection with inflammations and traumatisms.

(_b_) Hyperalgesia, often coinciding with (_a_), is that condition in which pain is produced by excitations so slight that they would not affect a healthy nervous apparatus: it is commonly designated as tenderness. Acute and dull, superficial and deep tenderness should be sought for and distinguished, as having different values in diagnosis. A type of deep tenderness is that found upon pressing steadily upon a diseased nerve-trunk. Acute superficial hyperalgesia is best studied in cases of trigeminal neuralgia and spinal irritation. Occasionally, universal hyperalgesia is met with, usually in hysterical women.

(_c_) Hyperæsthesia to thermal impressions is ordinarily shown with reference to cold. In cases of neuralgia or neuritis cold is felt excessively and painfully; in some cases of posterior spinal sclerosis there is the greatest dread of draughts of cold air, and patients protect their legs in an extraordinary manner.

(_d_) Hyperæsthesia of the muscular sense.[3] The special sensations or notions of muscular states and activities which we possess may be considerably exalted, as shown by greater delicacy and rapidity of movements, and by the abnormally acute way in which perceptions of form and dimensions are obtained by the subject without assistance from other senses. Examples of this condition are met with in hysteria and hypnotism.

[Footnote 3: This term is employed as clinically sufficient. It is impossible in this article to enter into a consideration of the various theories held with reference to the function in question, whether it be psycho-motor, psycho-sensory, or a true muscular sensibility. It certainly differs much from the various forms of common sensibility, and has special paths.]

(_e_) Visceral hyperæsthesia is chiefly shown by abnormal consciousness of the presence and action of an organ. Visceral pain usually accompanies this, and is the more prominent symptom.

(_f_) Increased reflex actions (emotional, motor, vaso-motor, and {33} secretory) rarely fail to accompany hyperæsthesia in its various forms. In the hypnotic exaltation of muscular sense remarkable psychic effects may be induced, partly in a reflex way, but perhaps chiefly through the law of association.

PARÆSTHESIÆ are sensations which arise centrally in nerve-fibres or nervous centres, and are projected outward and referred to the periphery or surface by consciousness, in obedience to the general law of outward projection of sensations in the Ego. They may be produced by external agencies or arise centrally without demonstrable cause. Their number and variety are very great, varying somewhat with the descriptive powers and self-consciousness of the patient, the chief being pain, formication, numbness, coldness and heat, constriction and distension, malposition, imaginary movements, etc. etc.

(_a_) Pain, the most distinct and frequent of paræsthesiæ, is by most authors classed as a hyperæsthesia, yet a careful analysis will show the difference. Pain and hyperæsthesia often coexist and are inseparable, yet in a large proportion of cases of nervous diseases the former sensation occurs independently, sometimes in regions where absolute anæsthesia exists (anæsthesia dolorosa), and even apparently in lost parts (neuralgia after amputations). We are consequently justified in considering most pains as paræsthesiæ. Pain assumes many forms, some real and typical, others as various as the lively imagination of nervous patients can make them. Thus we have sharp, cutting, darting pains in neuralgia, posterior spinal sclerosis, etc.; aching, throbbing, pounding pains in cephalalgia, inflammatory and traumatic conditions; boring, crushing, distending, constricting, burning pains, etc. etc. In some cases the sensation is only semi-painful, and more akin to paræsthesia (neuritis, parenchymatous lesions).

(_b_) Numbness, prickling, and formication usually coincide. They may easily be produced experimentally by pressure upon a nerve-trunk or by the exhibition of aconitia, so that any one may study these sensations for himself. By taking one-fiftieth of a grain of Duquesnel's crystallized aconitia the experimenter will soon find himself the possessor of intense subjective sensations of prickling, numbness, vibrations, and cold, lasting several hours. He will be able to satisfy himself that though the finger-tips feel numb, as if there was a coating or layer of something interposed between the skin and objects, he can distinguish tactile perceptions very well. In the more serious experiment of compression of a nerve-trunk a most interesting succession of phenomena will be observed: the first effects of pressure are various paræsthesiæ in the parts supplied by the nerve; then these sensations (prickling, numbness, swelling, vibration, heat, and cold) cease; paralysis and anæsthesia occur. If the compression be now interrupted, after a few moments the paræsthesiæ reappear, more intensely, as a rule, and as they gradually fade a normal state of sensibility is re-established. By making such experiments it is easy to convince one's self that anæsthesia and numbness are different conditions: indeed, during the stage of recovery from nerve-pressure distinct hyperæsthesia may be demonstrated. These results throw much light on the origin and diagnostic value of paræsthesiæ as expressions of irritation, central or neural, of nervous elements. At the same time, in practice, we occasionally meet with slight dulness of tactile sensibility in numb {34} parts. Another point to be remembered is that while patients usually complain loudly of paræsthesiæ, they are sometimes wholly unaware of anæsthesia (hysterical analgesia, for example); therefore sensibility should be tested even if the patient does not mention sensory disturbances.

Numbness, formication, etc. occur in a vast number of nervous affections—in cerebral and spinal organic lesions, in neuritis, in toxic conditions, and in neuroses. The distribution of paræsthesiæ is a valuable index to the seat of the lesion.

(_c_) Cutaneous itching and prickling may occur independently of any other skin lesion, constituting true or nervous prurigo. This may be universal and last for years.

(_d_) Paræsthesiæ of pressure are felt either as expansive or constrictive. The part appears swollen to consciousness, or it seems to be tightly compressed. Both these sensations are often felt about the head in a variety of pathological states, and an absurd and dangerous fashion has arisen of looking upon a sense of fulness in the head as indicative of hyperæmia. The sense of constriction may show itself around one toe, a leg, the trunk, around the neck, etc.; it may be narrow, like a cord, or broad and extensive, like a stocking or corset. Sometimes it is localized, and likened to the grasp of a hand or a spot-pressure. Not infrequently, especially in cases of paraplegia, the sensation of pressure is combined with subjective cold, the legs feeling as if tightly encased in ice.

(_e_) Subjective sensations of heat and cold are often of the strongest kind, and are very distressing. A part whose real objective temperature is normal may appear to the patient's consciousness as icy cold or burning hot, even to the degree of apparent contact of fire (causalgia of Mitchell). We observe such sensations in posterior spinal sclerosis, myelitis, neuritis, injuries to nerves. In some functional cases complaint is made of patches of hot or cold skin, not relieved by cold or heat.

(_f_) Odd sensations, such as rolling or longitudinal motion of something under the skin, general or local throbbing, coition movements, are described, especially in functional or hysteroid cases.

(_g_) Sensations of hunger, thirst, dyspnœa, defecation, micturition, the sexual feeling, may all appear in an abnormal or unprovoked manner, and are to be classed as visceral paræsthesiæ. An important paræsthesia of this variety is met with in cases of hypochondriasis and melancholia; it is a sense of indescribable distress, with constriction, usually at the epigastrium and about the heart—the precordialangst of the Germans, or, as we would term it, præcordial anguish.

(_h_) Paræsthesiæ of the muscular sense occur. The subject has a feeling as if a part were lying in an unnatural position, or as if it were being pulled or twisted in various ways, and he is sometimes obliged to assure himself by the use of sight and by tactile examination that the sensation is illusory.

(_i_) Hallucinatory paræsthesiæ are those which are so well defined and strong as to need the aid of other senses and reasoning to convince the patient of their unreality. A peculiar example of this is what occurs after amputation of a limb: for days or weeks the lost member is felt with the utmost distinctness; the absent fingers or toes may be moved in imagination and their position described.

(_j_) Delusional paræsthesiæ are such in which the patient (usually {35} insane), no longer correcting his sensations by the use of other senses and by reasoning, firmly believes in their reality—_i.e._ externality. For example: in such patients visceral sensations give rise to the belief that there is a foreign body or an animal inside the patient, or that parts are misplaced or wrenched and beaten. Pains are thought to be due to blows received or to the bites of animals or projectiles thrown upon the patient. With perversions of muscular sense an insane patient may believe that he is flying or floating in the air.

In hypochondriasis many of the symptoms complained of are nothing but paræsthesiæ exaggerated by a morbid state of the mind, and sometimes created (projected) by expectant attention. The hallucinations of the insane are in great measure phenomena of this group, the projections, though special and common, never being so strong and definite as to acquire apparent objectivity.

The auræ of epilepsy are paræsthesiæ. For example: a sensation in the epigastrium preceding a fit indicates an irritation at the origin of the vagus nerve and its projection as a subjective sensation at the distribution of the nerve. An auditory or visual aura similarly represents a discharge or projection from the acoustic and visual cortical areas respectively.

In most cases of malingering, and in some cases of so-called railway spine, the symptoms so loudly complained of belong to the two classes of hyperæsthesiæ and paræsthesiæ; they are undemonstrable and non-measurable; only the patient himself can vouch for their reality. A diagnosis in such cases, without objective symptoms indicating well-known lesions, should be very reserved.

ANÆSTHESIA, or loss of sensibility, may exist in every degree, from one so slight as to be hardly demonstrable by delicate tests to the most absolute loss of all feeling. It manifests itself in various modes corresponding to the normal physiological varieties of sensibility; in most cases the loss of feeling involves all of these, but in others they are separately affected, and we observe the following types, pure or combined:

(_a_) Tactile Anæsthesia. The capacity to perceive superficial and gentle impressions upon the skin and mucous membrane, and the ability to locate and separate such impressions, may be lost, while other modes of sensibility remain normal.

(_b_) Analgesia is that condition in which painful impressions are not perceived, though common, caloric, or muscular sensibility may be normal or nearly so. Pricking, cutting, and bruising are unperceived. This, the most common variety, is usually met with in hysterical cases; it occurs at a certain stage of general artificial anæsthesia, in chronic alcoholism, extreme emotional states, and in hypnotism. Though a very striking symptom, it is not one of as serious meaning as loss of tactile or thermic sensibility. Often the patient is unaware of analgesia until tests reveal its existence.

(_c_) The sensibility of the skin to caloric is usually the last to disappear in the progress of an organic lesion, so that in certain cases (injury to nerves or spinal cord, myelitis, etc.) testing by ice or by a burning object is a sort of last resort. Before deciding in a given case that there is a complete break in the sensory tract, this test should be used as well as the application of the most intense induced electric current delivered upon the dry skin by a wire end.

{36} In some cases of partial anæsthesia (_e.g._ in posterior spinal sclerosis) cold may be felt as heat and vice versâ, or pinching may be felt as burning, and be quite persistent.

(_d_) The so-called muscular sense may be greatly impaired or lost without ordinary anæsthesia. In such a case the subject is no longer directly and spontaneously aware of the exact position of his limbs, of passive motions done to them, and he executes voluntary movements with uncertainty. He is also unable to judge correctly of differences of weight in objects successively placed in his hand or hung from his foot. He needs the aid of sight to guide the affected limb and to judge of its position, etc. The awkwardness and uncertainty in voluntary movements by impairment of muscular sense must not be confounded, as is sometimes done, with ataxia, in which the attempted volitional movement is jerky and oscillatory, owing to the inharmonious action of antagonistic muscular groups.

(_e_) When a strong induced electrical current is passed through a muscle by means of wet electrodes applied to the skin, so as to cause a strong contraction, a special quasi-painful feeling, akin to that of cramp, is experienced in the contracting muscle, and is clearly distinguishable from the cutaneous sensation. This, the electro-muscular sensibility, may be lost independently of other modes of feeling and without loss of contractile power.

(_f_) Some observers claim that a special mode of sensibility exists in the skin by which varying degrees of pressure are estimated, independently of traction upon tendons and muscles (muscular sense), and that this may be separately impaired or lost.

(_g_) Visceral anæsthesia shows itself in the ordinary way by loss of that feeble degree of common sensibility which the internal organs possess, and also by impairment of their special functions, giving rise to anorexia, hydroadipsia, retention of feces and urine, loss of sexual feeling (without progenital anæsthesia). Of course, these symptoms may be due to other conditions, and each case must be carefully studied. In the insane, visceral anæsthesia gives rise to delusions of emptiness, destruction of organs, and even, if coinciding with general cutaneous anæsthesia, to the notion that the body is dead or absent.

A singular phenomenon often witnessed is retardation in the transmission of an impression (usually a painful one). Thus, in testing the sensibility of the skin of the legs in tabetic patients, it is observed that instead of the normal, almost instantaneous, appreciation of the impression made by a needle-point, there is a lapse of two, five, ten, or even sixty seconds between the pricking and the signal of sensation by the patient. It should always be determined in such cases whether the retardation is peripheral and actual, or central and due to psychic conditions (dementia, absorption in a delusional state). Thus, in a case of profound melancholia we may observe extreme slowness and dulness of sensory impressions or complete anæsthesia; but the symptoms would have a very different significance, diagnostic and prognostic, from the same noted in a mentally clear patient.

An important result of impairment of sensibility is a reduction or loss of reflex movements originating from the area or organ which is anæsthetic. This is shown in anæsthesia of the distribution of the trigeminus {37} when the reflex protecting movements of the eyelids no longer take place, in atrophy of the optic nerve when the pupillary reflex actions are lost. In posterior spinal sclerosis we see several illustrations of this law: progressive degeneration of nerve-fibres in the posterior root-zones of the spinal cord, causing loss of patellar reflex, of vesical, rectal, and sexual reflexes, and in most cases of cilio-spinal reflexes and of muscular tonus. In these and analogous conditions one arc of the reflex mechanism is deranged, centripetal conduction is interfered with, and the reflex motor discharge can no longer be evoked.

That a similar pathological condition occurs in the cerebral mechanism, and may serve to explain many psychic symptoms, is very probable.

On the other hand, a destructive lesion may be so placed in the spinal cord or brain as to allow centripetal impressions to reach healthy spinal gray matter in the normal way, but preventing their passage frontad (upward) to be recognized by consciousness. In such a case we observe normal, or more commonly exaggerated, reflex action in parts which are insensible in the ordinary sense of the term. Indeed, in many cases the disconnected caudal portion of the spinal cord is in a state of vastly exaggerated reflex activity, as shown by the tetanoid and convulsive involuntary and reflex movements which take place in completely paralyzed and anæsthetic limbs (paraplegia from transverse myelitis). In general terms, it may be stated that when anæsthesia is due to lesions of peripheral nervous endings, of nerve-trunks, and of the posterior root system of the spinal cord, reflexes are diminished or lost.

It is often stated that anæsthesia causes ataxia of movement. This, from the results of experiments on animals and from clinical study, we believe to be a gross error. In animals and in man loss of sensibility gives rise to awkwardness or uncertainty in movement (increased if the eyes be closed) which is properly to be classed as a special variety of inco-ordination; but it is not from ataxia, in which irregular, jerky, oscillating motions occur when a volitional act is attempted, these movements resulting from want of harmony in the action of antagonistic muscles which in the normal educated state automatically act together to produce the desired result. Besides, we occasionally observe cases of typical spinal ataxia in which no impairment of sensibility can be observed.

THE TOPOGRAPHICAL DISTRIBUTION of alterations of sensibility requires careful determination in practice, as from it we obtain most valuable aid in diagnosis. The following are the principal types observed:

(_a_) Alterations of sensibility in one lateral (vertical) half of the body and head. We thus have hemihyperæsthesia, hemiparæsthesia, or hemianæsthesia, and the special senses on one side are frequently involved. This clearly hemi-distribution indicates that the lesion or functional disorder is in the cerebral hemisphere of the opposite side, more especially in the caudal segment of the internal capsule or in its areas of cortical distribution (occipital, temporal, and parietal lobes). The distribution of hemianæsthesia, etc. from organic disease in these parts is identical with that observed in some functional (hysterical) cases; we can make the diagnosis only by the help of other data.

If the sensory disorder does not affect the head, but is limited to one {38} lateral half of the body, it is, if due to organic disease, quite certainly of spinal origin.

(_b_) Two homonymous extremities or the two lateral halves of the body may exhibit opposite states of sensibility—anæsthesia on one side and hyperæsthesia on the other. This rare condition is witnessed in hysteria and in some forms of injury to the spine (lesion of one lateral half of the cord at a certain level). In the latter case paralysis is usually present on the hyperæsthetic side: the symptoms constituting, with some others, Brown-Séquard's spinal hemiplegia or hemiparaplegia.

(_c_) Alterations of sensibility in one caudal (horizontal) half of the body are said to have a paraplegic distribution, and are usually due to lesions of the spinal cord. The upper level of the symptom may be at any point between the neck and the toes; and the frontal (upper) level indicates, due regard being had to the origin and oblique distribution of the spinal nerves, the highest limit of disease in the nervous centres. Very often, in organic disease especially, this is also indicated by the presence of a cincture feeling (paræsthesia) at the frontal (upper) limit of the anæsthesia, etc.

(_d_) Disorders of sensibility may be limited to one extremity. This very rarely depends upon cerebral disease, and in such a case the anæsthesia, etc. is evenly distributed throughout the member, being most intense at its extremity, and being without sharp, distinct limits near the trunk. When due to diseases of the spinal cord, the cerebral (upper) limit of the symptom is usually clearly defined in accordance with the distribution of sensory nerves from the other (healthy) parts of the cord: a constriction band often marks the limit. Sometimes the peripheral anæsthesia, etc. is more or less in the territory of certain nerve-trunks. When we find the distribution of the sensory symptoms to coincide exactly in the areas supplied by the large nerves of the limb, without cincture feeling, it is certain that the lesions affect one or more of these nerve-trunks or the plexus above. In not a few cases the symptoms are due to hysterical or dyscrasic conditions, and the seat of the lesions (dynamic or molecular lesion) is uncertain. In judging of the distribution of anæsthesia, etc. in a limb due regard must be paid to variations in nerve-branching and to collateral nerve-supply.

(_e_) Alterations of sensibility occurring in well-defined areas of the hand, trunk, or extremities, corresponding to the known distribution of nerves, almost always indicates disease of the nerve itself, much more rarely disease in the spinal cord at the origin of the nerve. The reflexes are then diminished or lost. In judging such cases Van der Kolk's law of the distribution of the motor and sensory filaments of nerve-trunks should be remembered: it is, that of the two sets of fibres in a mixed nerve, the sensory fibres are distributed to parts which are moved by muscles which receive the motor fibres of the same nerve. Thus, in nerve lesions the chief sensory symptoms are always peripheral or distal from the chief motor symptoms.

(_f_) Disorders of sensibility sometimes appear in patches or irregular areas whose nervous connections are indefinite. Such patches of anæsthesia, hyperæsthesia, or paræsthesia sometimes indicate foci of disease in the spinal cord (and brain?); as, for example, the pains, etc. of posterior spinal sclerosis. These patches may also occur in consequence of {39} interference with local circulation of peripheral parts; and we meet with them in such conditions as hysteria, neurasthenia, alcoholism, etc.

(_g_) Universal hyperæsthesia, paræsthesia, and anæsthesia may be observed. The last condition, in the insane, is very apt to give rise to delusions of non-identity and death of the body.

THE SENSORY DISTURBANCES OF THE SPECIAL SENSES are well worth separate consideration.

(_a_) Optic Apparatus.—Hyperæsthesia of the retina shows itself directly in photophobia, and indirectly (reflexly) by lachrymation and involuntary closure of the eyelids. Paræsthesiæ of the optic nerve and retina show themselves as flashes or projections of white or colored light in the visual field. These may be irregularly or generally distributed in the field, or appear as hemiopic (vide infra), or sector-like forms. Phenomena of this order may be experimentally produced by pressure on the eyeball or by the application of electricity over or near the eye. Photopsiæ of most varied sorts, as flashes, colored scotomata, or quasi forms may immediately precede epileptic seizures or attacks of migraine, constituting an optic aura. In some cases this assumes a definite picture form, when it partakes of the character of an hallucination. Anæsthesia of the optic nerve and retina varies infinitely in degree, from slight blurring or veiling of vision (amblyopia) to complete blindness (amaurosis). Another result is sluggishness or complete immobility of the iris under the action of light. As regards distribution, optic anæsthesia may affect the visual fields uniformly and generally, or it may assume definite geometric forms, or may appear in irregular patches (scotomata).

The definite geometric defects are classed under the general head of hemianopsia, by which term is meant that one horizontal or vertical half of the visual field is obscured. (1) Horizontal hemianopsia is not bounded by a very sharp or straight boundary-line, and is almost always due to intraocular disease (retinal lesions, embolism of one large branch of the retinal artery, injuries, etc.). (2) Vertical hemianopsia is usually marked by a sharply-defined vertical limit in the visual field, passing through the point of fixation, or a little to one side of it more usually, leaving central vision very acute. (_α_) Temporal hemianopsia, in which the temporal halves of the visual fields are dark, represents anæsthesia of the nasal halves of the retinæ, and is usually caused by a lesion of the chiasm of the optic nerve, so placed at its frontal or caudal edge as to injure the fasciculi cruciati. This variety is usually bilateral, but a lesion might be so situated as to affect only one fasciculus cruciatis. (_β_) Nasal hemianopsia, in which the inner (nasal) halves of the visual fields are dark, represents anæsthesia of the temporal halves of the retinæ, and is caused by a lesion injuring one fasciculus lateralis or both fasciculi. In the former case the nasal hemianopsia would be unilateral; in the second case, bilateral or symmetrical, (_γ_) Lateral or homonymous hemianopsia is that condition in which physiologically similar halves of the visual field are darkened; for example, the temporal half-field of the left eye and the nasal half-field of the right. This represents anæsthesia of the nasal half of the left retina and of the temporal half of the right. The patient can only see, with one or both eyes, the right half of any object held directly in front of him. In such cases the lesion is always caudad of the chiasm, and may consist in interruption of the right optic tract, {40} of disease of the primary optic centres (corpus geniculatum laterale and lobus opticus) on the right side, of the caudo-lateral part of the right thalamus, of the caudal extension of the internal capsule or optic fasciculus within the right occipital lobe, of the right superior parietal lobule or gyrus angularis penetrating deep enough to interrupt the optic fasciculus; or, finally, the lesion may injure the visual centre itself—viz. the cortex of the right cuneus and fifth temporal gyrus (of Ecker). Hemianopsia of any type may be incomplete or only sector-like—_i.e._ involving only a quadrant or less of one visual field or of both fields. (Vide article on Localization).

Perception of color may be reduced, confused, or abolished in the retina, either a diffused general way, throughout the field of vision, or following the laws of hemiopic distribution. In cases of hysteria, achromatopsia is not rarely met with, affecting the eye corresponding to the side on which the skin is analgesic or where paralysis exists. Hysterical achromatopsia may be transferred from one eye to another by the application of metals, by hypnotic manipulations, etc.

Hemianopsic phenomena may be functional and transient, as witnessed just before attacks of migraine or sick headache.

Attempts recently made, from purely theoretical considerations, to locate centres in the occipital cortex for perception of light, form, and color separately, are wholly unjustified or at least premature.

Loss of reflex pupillary movements is a symptom of much importance. It occurs chiefly under these conditions: (1) with paralysis of the iris due to lesion of the third cerebral nerve; (2) with amaurosis or anæsthesia of the retina; (3) with posterior spinal sclerosis. The last condition is distinguished from the others by the fact that while the reflex iritic movements are lost, the quasi-voluntary movement of accommodation efforts is preserved. This condition is known as the Argyll-Robertson pupil.

Diplopia, or double vision, is due to paresis or paralysis of one or more of the ocular muscles, and as such is to be classed under motor symptoms.

Megalopsia (apparent enlargement of objects) and micropsia (apparent reduction in size of objects) are sometimes due to disorder of the accommodation apparatus within the eye, and to local diseases causing displacement of the rods and cones of the retina; but they are often, no doubt, fanciful (in neurasthenia and hysteria). The same remarks apply to monocular diplopia.

(_b_) Acoustic Apparatus.—We know less of the sensory disturbances in the organs of hearing. Hyperæsia shows itself by undue (painful) sensitiveness to sounds, and by the ability to perceive sounds which are inaudible to normal persons. In meningitis, hydrophobia, the hypnotic state, etc. this condition is observed. Paræsthesiæ are very common, appearing as subjective noises or musical tones (tinnitus aurium) of the most varied kinds (roaring, hissing, blowing, tinkling, whistling, crashing, bell-sounds, etc.), which seem to the subject to be in his ear or in his head. In the present state of our knowledge it is impossible to positively distinguish tinnitus due to local non-nervous ear disease from that which is strictly neural or cerebral in origin. Certainly, intense tinnitus may coincide with complete anæsthesia of the acoustic nerve and a {41} normal state of the middle ear. Theoretically, we may admit tinnitus (corresponding to photopsia in the optic apparatus) as due to an irritative lesion of various parts of the acoustic terminal nervous organ, the acoustic nerve, or the acoustic centre. An acoustic aura (subjective blowing, hissing, etc.) may immediately precede an epileptic attack. Subjective noises may be produced by excitation of the acoustic nerve and terminal organs by the galvanic currents; these galvanic acoustic reactions are regular in the normal condition, and are fully stated in works on electro-therapeutics. Anæsthesia of the acoustic system by peripheral, neural, or central (?) destructive lesions is frequent, and is distinguished from other forms of deafness chiefly by the fact that a sound transmitted through the bones of the cranium (as by a vibrating tuning-fork held against the upper teeth or above the ear) is not heard on one or both sides. Although in a few rare cases the attempt has been made to define nervous deafness for certain sets of notes or as limitations at either end of the musical scale, yet we are not prepared to recognize in neurological practice a condition of partial acoustic anæsthesia corresponding to hemianopsia or achromatopsia. We believe that this progress will be made, however, thus enabling us to locate disturbances in parts of the organ of Corti and in the cortical centre for hearing.

(_c_) Olfactory Apparatus.—Hyperæsthesia of this sense is at present considered more a personal peculiarity than as a symptom of disease. Paræsthesiæ show themselves as subjective odors of various sorts, and when transient may be an olfactory aura preceding epileptic attacks. In conditions of organic disease subjective odors may coincide with complete loss of smell. Anæsthesia of the olfactory nervous apparatus may be due to (1) strictly local disease in the nose, catarrh, etc.; (2) to anæsthesia of the trigeminus nerve and consequent local lesions; (3) to a truly nervous lesion affecting the olfactory nerves, the olfactory bulbs, the olfactory tracts, or, lastly, the cortical centre for smell (at present unknown in man). The two last morbid conditions are usually unilateral, and coexist with subjective odors.

(_d_) Gustatory Apparatus.—In this sense hyperæsthesia is clinically unknown, though as a result of education extreme delicacy of taste, a relative hyperæsthesia, may be produced. Paræsthesiæ are rare. In two cases in which we have observed the symptom (one of neurasthenia, the other of hypochondriacal melancholia) it consisted in a constant and most distressing sweet taste. The application of the galvanic current at the base of the brain, under the jaw, on the cheeks, and within the mouth produces subjective tastes of an acid or metallic nature. Anæsthesia of the gustatory nerve occurs after section of the lingual branch of the trigeminus—an operation sometimes done for lingual neuralgia, in which case the frontal two-thirds of the tongue on one side loses its property of perceiving taste. As the result of central disease next to nothing is known of this symptom. It is probable that sweet and acid tastes are perceived in the mouth and forward part of the tongue; bitter tastes on its caudal (posterior) third and in the throat (glosso-pharyngeal nerve). In the insane, paræsthesiæ and anæsthesia give rise to a great variety of delusions about the state of the parts, the nature of their food, poison in the food, etc.

As a part of typical complete hemianæsthesia the special senses are {42} involved. When of hysterical origin the whole retina of one eye is generally devoid of sensibility, or it does not perceive colors. When the hemianæsthesia is due to a lesion of the caudal part of the internal capsule (organic anæsthesia), we should expect to find lateral hemianopsia, with dark half-fields on the same side as the cutaneous anæsthesia. We would not be understood as claiming that this point of distinction is as yet positively determined, but would advance it suggestively, subject to the result of observations on new cases.

III. Motory Symptoms.

PARALYSIS, or AKINESIS, is a condition in which loss of voluntary or involuntary muscular movement occurs through defective innervation. Such a strict definition is desirable, as excluding cases in which motion is abolished by local or general morbid states not essentially nervous, as in acute articular rheumatism, ruptures of muscles or tendons, fractures, extreme asthenia, etc.

Paresis is a term often employed to designate a paralysis partial in degree; it does not mean an essential muscular paralysis.

Paralysis varies infinitely in extent and distribution, yet certain types are recognized as having diagnostic value, and their exact determination is of great importance in practice.

(_a_) Hemiplegia, or paralysis of many muscular groups in one lateral half of the body.

(_α_) Common Hemiplegia.—In this, the most frequent form, we find loss of voluntary motion in many muscles of one side of the face and body. This condition may or may not be preceded by apoplectic or epileptic symptoms: it may occur gradually or suddenly. Although it is customary to say that in hemiplegia a patient is paralyzed on one side, this is not strictly correct, as careful observation shows that (1) in the face only the lower facial muscles are distinctly affected; the tongue itself is rarely paralyzed, but its projecting muscular apparatus is, so that when protruded it deviates as a whole toward the paralyzed side; the eye-muscles and masticatory muscles are unaffected; (2) in the extremities the loss of power is greatest in the hand and foot, less so in the arm and thigh, very slight in the muscular groups of the shoulders and hips; (3) the muscles of the neck and trunk, the respiratory muscles, and in general the muscles of the vegetative life are practically unaffected. These facts may be summarized by the statement that in common hemiplegia the greatest paralysis is shown in those muscular groups whose action is most independent on either side of the body; or, in other words, in those whose functions are most highly differentiated and whose innervation is most cortical (from the motor centres in the cerebral cortex). Those muscular groups, on the other hand, whose action is usually or necessarily simultaneously bilateral or associated across the median line—or, in other words, whose innervation is largely spinal or subcortical—are least paralyzed; while the purely automatic or reflex muscular apparatuses, those having a strictly spinal or sympathetic innervation, are not at all affected.

Common hemiplegia is rarely accompanied by hemianæsthesia.

{43} It must not be forgotten that double hemiplegia may occur, in which case the symptoms are simply duplicated.

As regards the seat of the lesion in common hemiplegia, it may here be said, in general terms, that it is in the cerebral hemisphere opposite to the paralysis (with excessively rare exceptions which are susceptible of explanation), in its motor cortex, in the subjacent associated white fasciculi, or in the knee and caudal part of the internal capsule; the lesion may directly injure those parts or act upon them by compression.

(_β_) Crossed Hemiplegia (hémiplégia alterne).—In this form there is paralysis of many muscular groups on one side of the body, while the facial nerve or some other cranial nerve (or several cranial nerves together) show loss of innervation on the other side of the median line. Theoretically, therefore, there may be as many varieties of crossed hemiplegia as there are cranial nerves, but, practically, we meet only with a few forms, of which the following are the most common: (1) motor oculi (N. iii.) on one side, and body and face on the other; (2) facial nerve (N. vii.) on one side, and body on the other; (3) trigeminus nerve (N. v.) on one side (anæsthesia of face, paralysis of masticatory muscles), and body on the other; (4) abducens (N. vi.), facial (N. vii.), and acoustic (N. viii.) together on one side, and the body on the other. (5) With symptoms of No. i. we may have lateral hemianopia, dark half-fields on the same side as paralyzed extremities.

In crossed hemiplegias anæsthesia is more common; there is a strong tendency to bilateral extension of the paralysis, and neuro-retinitis is seldom absent before the close of life.

As regards the location of the lesion in crossed hemiplegias, it may be stated, in a general way, that it is in the base of the brain on one side of the median line, so placed as to directly injure one or more cranial nerves at their origin, and to compress or destroy the cerebral motor tract (pyramidal tract) above its decussation-point, and in some cases also the sensory tract in the crura, pons, and oblongata.[4]

[Footnote 4: For a statement of the exact seat of the lesion causing various forms of crossed hemiplegia, vide article on the LOCALIZATIONS OF LESIONS IN THE NERVOUS SYSTEM.]

(_b_) Spinal Hemiplegia.—In this type the face and head are normal, excepting in some cases the iris; the extremities and trunk are more or less paralyzed on one side, the loss of power being more evenly distributed (_i.e._ less distal) than in hemiplegia of cerebral origin. Often there is also anæsthesia, and this is always on the other side of the median line, involving more or less of the whole side. The coincidence of these symptoms below the head indicates positively that the lesion is in the spinal cord, involving one of its lateral halves. Where there is no anæsthesia, care must be taken not to confound the condition with that in which a cerebral lesion causes paralysis of one arm and leg (combined brachial and crural monoplegia).

(_c_) Paraplegia.—The loss of voluntary power involves one transverse half of the body, usually the caudal. When only the lower extremities are affected, the condition is designated simply a paraplegia; when all the parts below the head are paralyzed, the term cervical paraplegia is employed. Frequently, the bladder and rectum are paralyzed, and in some cases the thoracic muscles also, leaving inspiration to be performed by the diaphragm alone. Often there is coextensive anæsthesia.

{44} Hemiparaplegia is a rare variety in which one lower extremity is paralyzed while the other is anæsthetic.

The location of the lesion in paraplegias is in the spinal cord at various levels and in various portions of the gray and white columns. Theoretically, we may now again admit the old proposition that a paraplegia may be of cerebral origin: in such a case the loss of power should follow the laws of distal prevalence (vide (_α_)); there should be no anæsthesia or vesical paralysis, and the lesion ought to be one involving the paracentral lobules of both hemispheres (meso-vertex at fissure of Rolando).

(_d_) Monoplegia, or paralysis of one extremity or of one side of the face, is not rarely observed. It may be caused by central lesions in the brain or spinal cord, or by an affection of the nerve-trunks of the part. Cerebral monoplegias are of great importance in diagnosis, and may be distinguished from others by—(1) loss of power is greatest in the distal part of the affected member; (2) the precedence or coincidence of spasm (usually clonic or epileptiform) in the limb; (3) the absence of marked anæsthesia; (4) the preservation of muscular nutrition.