II. Sensory Symptoms.
II. Sensory Symptoms.
HYPERÆSTHESIAis 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 existingindependently 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.3The 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.
3This 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, andsecretory) 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.
PARÆSTHESIÆare 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 numbparts. 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 (usuallyinsane), 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.
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 trigeminuswhen 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.
THETOPOGRAPHICALDISTRIBUTIONof 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 onelateral 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 ofinterference 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.
THESENSORYDISTURBANCES OF THESPECIALSENSESare 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,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 anormal 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 areinvolved. 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.
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.
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
4For a statement of the exact seat of the lesion causing various forms of crossed hemiplegia, vide article on theLOCALIZATIONS OFLESIONS IN THENERVOUSSYSTEM.
(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.
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.
(e) Localized Paralysis.—The extreme types of this form of paralysis are paralysis of one external rectus and of one superior oblique. These muscles are each supplied by one whole nerve, and may therefore exhibit isolated paralysis. In the rest of the body, however, localized paralysis shows itself in groups of muscles as innervated by nerve-trunks or by certain so-called centres in the spinal cord. As examples of the former variety may be cited common facial paralysis (Bell's palsy) and paralysis of the extensor muscles of the hand by injury to the musculo-spinal (radial) nerve, of the foot and leg from lesions of the sciatic nerve. As examples of the second variety we have the irregular paralysis of anterior poliomyelitis (infantile spinal paralysis). In localized paralyses due to lesion of the nerve-trunks anæsthesia is usually present, whereas it is not common in the second variety. The determination of the seat of lesion in neural localized paralysis is much facilitated by bearing in mind Van der Kolk's law of the distribution of the motor and sensory fibres of a nerve-trunk.
Pseudo-paralysis—i.e.conditions in which voluntary motion is lost without defect in innervation, as from muscular disease, injuries, inflammations, etc.—is usually localized or irregularly distributed.
(f) The various internal organs, the viscera, supplied with striped or unstriped muscular fibres, may be paralyzed.
(g) The muscular coat of the vascular system beyond the heart may be paralyzed in extensive or limited areas—the so-called vaso-motor paralysis. This may assume hemiplegic or monoplegic or localized forms.
SPASM, or HYPERKINESIS, consists in abnormal and often violent involuntary muscular contractions, with or without loss of consciousness.
1. A purely mechanical classification of spasms into tonic and clonic forms is generally admitted as serviceable for clinical description, though we have as yet no positive knowledge of their relations to pathological conditions.
(a) Tonic or tetanic spasm is one in which the muscular contraction is continuous or constant for a measurable length of time. Thus, in some cases of petit mal there is a momentary stiffness or rigidity of the entirevoluntary muscular apparatus (respiratory muscles included): the patient sits or stands with staring eyes as if petrified. In tetanus and local tetanoid seizures the muscles of large regions or of a part of a limb may remain contracted for many minutes; in the disease called tetany this condition may endure days and weeks—in hysteria and in some paralyses dependent upon organic disease for years or permanently. Prolonged tonic spasms occurring in chronic diseases are designated as contractures, and the affected parts are said to be tetanoid or spastic. A tonic spasm of long duration may show itself in involuntary muscles, as in the arteries, causing vaso-motor spasm and ischæmia; in the ciliary muscle, causing spasm of accommodation; in the urethra, œsophagus, etc.
A tonic muscular contraction accompanied by intramuscular pain is termed cramp.
Under this general head may also be classed the emotional or dramatic expressive spasms of hysteria and hystero-epilepsy—a condition in which the emotions or ideas occurring in the patient's mind are involuntarily translated externally into attitudes or gestures:e.g.anger, fear, disgust, amorous and religious feelings, etc.
(b) Clonic spasms are those which consist in rapidly intermittent muscular contractions, local or general. These may be rhythmical in time or form, as in paralysis agitans, or wholly irregular, as in chorea. Jerking is a quasi-popular designation of clonic spasms.
Tremor, or trembling, observed in persons during repose in any attitude, consists in small, wholly involuntary muscular contractions of sufficient extent to communicate to the parts a visible to-and-fro movement which is very often rhythmical. In order to distinguish this from any form of inco-ordination it is necessary that the observed movement should occur independently of all volitional effort. Thus in the senile state, in chronic alcoholism, in paralysis agitans, and in dementia paralytica we observe trembling of the facial and lingual muscles, of the extremities, and even of the whole body in some cases. These are usually conditions of permanent or chronic tremor, but the symptom is sometimes observed as a transient phenomenon, as after violent muscular effort, after excesses of various sorts, under the influence of emotions, etc. Occasionally, persons are met with who have trembled from childhood or early years without actual disease of the nervous system. It is clinically useful to divide tremor into varieties, as rhythmical and irregular, fine and coarse, constant and occasional. These terms define themselves sufficiently, so that no further statement is necessary, but we would repeat that it is of much advantage in diagnosis to determine accurately the characteristics of tremor.
2. A much more useful classification of spasms, and to a certain extent a physiological one, is into types according to their distribution in the body, following exactly the classification of paralyses. There are few topics of more utility for the physician to study, in our opinion, than that of monoplegias and monospasms, of hemiplegias and hemispasms in their genesis, mutual relations, and diagnostic significance.
(a) Hemispasm of cerebral origin, tonic or clonic (or both forms associated), may affect the face and limbs on one side of the body, with or without paralysis. As in hemiplegia, the morbid phenomena are greatest in the most distal muscular groups or in those whose innervation is mostcortical. Very often hemispasm precedes, immediately or remotely, hemiplegia in the same parts. In other cases the relation is inverse, as when, after a severe hemiplegia, we find the paralyzed muscles in a state of nearly constant tonic contraction (secondary contracture), or when hemi-epilepsy follows a cerebral lesion. In the former case the spasm, clonic or tonic, is designated as pre-paralytic; in the second case, as post-paralytic. These terms are useful, because they are associated with laws of diagnosis and prognosis.
(b) Conjugate deviation of the eyeballs and head is an important symptom of gross cerebral lesions, and may be considered here, although it is probably due to paralysis. Still, the deviation itself always strikes the observer as a spasmodic effect. The symptom consists in a steady turning of the eyes, face, and head toward one or the other side, and may be best described by likening it to the normal act of looking at an object which is on one side or a little back of us. In one form—that due to an irritative lesion of the motor cortex of one hemisphere—the conjugate deviation forms a part of the hemiplegic epileptiform convulsions (mixed tonic and clonic) which are produced: the deviation is away from the lesion. In a second form, where severe hemiplegia is produced by an acute lesion of the motor area and the subjacent fasciculi of one hemisphere, whether the patient be comatose or semi-conscious, the deviation, of paralytic origin, is away from the paralyzed side of the body and toward the injured hemisphere: the patient is said to be looking at his lesion. In a third form, when the lesion is in one side of the base of the brain (more particularly of the pons), the deviation, again paralytic, is away from the lesion, as a rule. In some cases conjugate deviation exists only as a tendency to look to either side. It is always a valuable symptom in severe cerebral affections, more especially the apoplectic state.
(c) Paraplegic spasm is also shown in tonic and clonic forms. Partial tonic spasm of this distribution, with paresis of the legs, causes the gait or attitude known as tetanoid or spastic. The four extremities may be in this state of mixed paresis and contraction, as observed in some very young children whose cerebral motor area is probably undeveloped or ill-developed, or which has been damaged shortly after birth by meningeal hemorrhage.
(d) Monospasm, spasm affecting one side of the face or one extremity, may be of cerebral, spinal, or neural origin. Very often monospasm of clonic form serves to indicate with wonderful precision beginning disease (irritation stage) in limited parts of the cerebrum (in cortical centres and in the connected fasciculi for the face and limbs). Cerebral monospasms are sometimes combined so as to almost constitute hemispasm—i.e.brachio-facial or brachio-crural monospasm. Monospasm may precede or succeed monoplegia.
(e) Universal spasms, tonic, clonic, or mixed, occur in numerous diseased states—in hysteria, epilepsy, chorea, tetanus, toxic conditions, etc. A universal tonic spasm may last long enough (tetanus, epilepsy) to kill by apnœa.
(f) Localized spasms, not monoplegic, are observed. For example, the orbicularis palpebrarum may be the seat of clonic spasm, or the masseters of tonic spasm for long periods of time; the œsophagus or urethra may be temporarily closed by constriction; chorea may affect a small musculargroup. A rhythmic spasm limited to a single muscle is termed myoclonus; the use of this term should not lead one to forget the nervous origin of the spasm. A localized tonic arterial spasm may be so severe and prolonged as to produce great ischæmia, even gangrene of the affected part.
(g) Fibrillary contractions, non-rhythmic contractions of fasciculi in muscles, spontaneous or provoked by direct mechanical excitation, may be considered as hyperkinesis. Subjectively, fibrillary contractions are felt as a quivering or as if a worm moved under the skin; objectively, they appear not unlike the rising and falling of a cord under the cutaneous covering. They unquestionably occur frequently in muscles which are undergoing degenerative or atrophic changes (progressive muscular atrophy), but they are also met with in cases of lead paralysis, neurasthenia, etc.
INCO-ORDINATION, or DYSKINESIS, is the condition in which volitional movements are not performed with normal precision and steadiness. Several varieties are recognized.
(a) Ataxic tremor is distinguished from common or spasmodic tremor by the fact that it is developed during the performance of a volitional act in parts which are quiet when not used. Thus, tremor appears in speaking, putting out the fingers, using the hands, etc. in the muscles actively employed, and occasionally also in others at the same time. This form of tremor is well seen in dementia paralytica, where in certain cases the patient's muscles are still until we induce him to make voluntary movements or provoke expression movements. In cases of disseminated sclerosis the same phenomenon is a characteristic symptom, a coarse tremulous ataxia or oscillatory trembling appearing whenever volitional acts are attempted. In looking, there appears nystagmus, a rhythmic ataxic tremor of some of the ocular muscles; in speaking, an irregular, jerky, slow, or syllabic speech is heard; and when the hand is carried to a given object or pointed the extremity exhibits oscillatory trembling. Common and ataxic tremors may coincide, as in some cases of dementia paralytica and in alcoholism.
(b) Ataxia is a symptom of the utmost importance, and its strict definition should be maintained. It is that form of inco-ordination in which there is want of harmony in the action of the various muscular groups employed in the voluntary performance of a given act. The simplest movement of an extremity (and more complicated ones a fortiori) is made up of simultaneous contractions of flexor and extensor muscles, often also of adductors and abductors in due proportion, so as to produce a steady position and movement of the parts. This is not accomplished by the will acting directly on the different muscles themselves, but through the medium of a co-ordinating mechanism which is strictly spinal (including the intracranial expansion of the cord as far frontad as the third ventricle), and which is educated or trained from the first days of life. We will the action and set the co-ordinating mechanism going, so that the movement is in a certain sense indirectly accomplished. Yet volition does interfere directly to a certain extent by estimating through the muscular sense, and by exerting the proper amount of force required, and by guiding the movement in a general way. The most striking peculiarity about ataxic movements is the defect in the harmonious action of the various(antagonistic) muscles employed, resulting in jerky, oscillatory, but non-rhythmic movements, constantly made worse by greater tension of the will. In simple tremor volition may for a few moments stop the movements (as best shown in paralysis agitans), while in ataxia the more the patient tries to achieve the act, the greater becomes the disorder. The anatomical fault is mostly in the spinal co-ordinating mechanism; the long-established motor and sensori-motor associations are interrupted or confused, and in some cases besides the muscular sense is impaired.5The idea that ataxia results from faulty centripetal impressions due to various degrees of anæsthesia is certainly erroneous and misleading. In the first place, there are cases recorded in which typical ataxia of the extremities occurred without the slightest impairment of sensibility; and, secondly, neither in animals (section of posterior roots of spinal nerves) nor in man does ataxia appear as a result of anæsthesia. In this condition there is inco-ordination, to be sure, but not ataxia in the strict meaning of the term. Ataxia is nearly always a symptom of organic disease of the spinal cord, more especially posterior spinal sclerosis and diphtheritic myelitis. It may also occur from disease of the oblongata, pons, and crura cerebri. In certain cases of lesion in caudo-lateral part of the thalamus involving the caudal part of the internal capsule (irritation or partial destruction), we observe various forms of irregular movements which have been designated by Weir Mitchell as post-paralytic chorea. We long ago became satisfied that this term included quite a number of forms of inco-ordination, some cases showing choreiform and trembling movements, others ataxic tremor, true ataxia, and athetoid movements (also the true athetosis of Hammond?). It seems probable that diseases of the cerebellum, by exerting pressure on or by irritating subjacent parts, may sometimes cause pure ataxia of the extremities on the side opposite the lesion. That a strictly localized cortical lesion can give rise to ataxia we are not now prepared to admit.
5Ataxia is greatly aggravated by closing the eyes.
(c) Uncertainty in voluntary movements is sufficiently defined by the term employed and by the absence of ataxia. This is well illustrated in those rare cases in which the muscular sense is impaired or lost: in such a case volitional movements, such as placing the fore finger on an object or fastening a button, are fairly well done with the aid of sight, but without it the hand and fingers grope almost or quite hopelessly about the object. It is important to note that persistent trying to do the act does not aggravate the disorder, but that, on the other hand, success is often achieved after feeling about. In certain cases of blindness irregular movements of the eyeball are observed, due to semi-voluntary efforts to look or to direct the eyeballs in the direction of a person or object. In states of cutaneous anæsthesia when the eyes are closed the same disorder appears in muscular movements. Claude Bernard many years ago showed that section of the posterior roots of spinal nerves in an animal was followed, not by ataxia, but by vague inco-ordination and staggering. In human cases we find that where the sensibility of one hand is lost or greatly impaired, without paralysis, there is extreme awkwardness and uncertainty in delicate muscular movements, but no ataxia. The staggering exhibited by patients having plantar anæsthesia is largely of this type: they stand fairly well while their eyes are open, but oscillate orfall when they are closed. This variety of inco-ordination may result from toxic conditions (alcohol), peripheral, neural, or central nervous disease. A few cases are on record which would seem to show that there is a centre for muscular sense in the cortex of the brain, in a part intermediate between the caudal sensory area and the central motor one—viz. in the inferior parietal lobule, supramarginal gyrus (and angular gyrus?). It has also been shown (by Spitzka and others) that there is a conduction tract for muscular sense, dorsad of the pyramidal tract in the pons and oblongata (in the stratum intermedium and interolivary tract), lesions of which produce inco-ordination (ataxia?) without marked paralysis or anæsthesia.
(d) Titubation, or staggering, is the inability to stand erect or walk straight because of impaired equilibrium. There is neither tremor nor ataxia present, and paralysis and anæsthesia are not necessary factors. It is distinguished from vertigo and dizziness by absence of subjective sensations of movement. Staggering may show itself in a general way or in the shape of latero-, retro-, or propulsion (disease of the internal ear, paralysis agitans). A well-defined variety of staggering is the wrongly-termed cerebellar ataxia. In this the patient, having disease of the cerebellum involving its vermis superior, stands with feet widely separated to increase his base of support; the body is bent somewhat forward, and the arms and hands are used as balancing-rods to maintain a sort of equipoise. In walking, this attitude is exaggerated, and if the feet be bare it will be seen that the toes are unconsciously clutching the floor for support; there is no outward jerk of the leg or stamp of the heel as in the ataxic gait, and closing the eyes does not aggravate the attitude or walk. Besides, if the extremities be separately tested, it is found that with closed eyes the patient can perfectly well place his fore-finger on his nose or one heel on the opposite patella (lying down). The proper term for the disorder is cerebellar titubation. Yet it must be remembered that titubation also occurs from disease of the oblongata and pons, from lesions of the base of the brain in general, and from alcoholic, etc. intoxication. In many cases titubation occurs in connection with vertigo or dizziness.
(e) Inco-ordination more or less of the ataxic form often affects the muscles of articulation, phonation, and deglutition, giving to the symptoms dysarthria, dysphonia, and dysphagia. Dysarthria and dysphagia are probably often caused by lesions of the insula and subjacent white substance, as well as by those affecting the oblongata. There are two recent autopsies which would indicate that there may be a cerebral cortical centre for phonation laryngeal movements: in the ventral extremity of the right third frontal gyrus—a part homologous to the speech centre on the left side of the brain. In some cases, however, dysphonia and aphonia indicate a lesion of the laryngeal nerves or of the oblongata (nucleus of NN. x. and xi.).
(f) Doubtless the internal muscular organs and the blood-vessels are frequently the seat of inco-ordinate or quasi-ataxic movements, but our present knowledge of these conditions amounts to very little.
It may be permissible to consider vertigo under the general head of inco-ordination, because it usually finds a motor expression, either actual or subjective. Subjective vertigo consists in a sense of whirling or horizontal movement which is clearly referred to the brain by the patient. Thesensation is variously expressed: in some the head seems to whirl around; in others external objects seem to whirl about the patient horizontally or vertically; in others still there is a sensation of falling in a given direction or of dropping into a hole. Dizziness is a minor degree of subjective motion conjoined with more or less confusion and other paræsthesiæ in the head. Static vertigo is that form in which there is actual loss of equilibrium, or falling. It is observed more especially in diseases of the internal auditory apparatus, and it may be produced artificially by galvanization of the brain. If the electrodes are placed exactly on the median line, and the current passed fronto-caudad through the brain, no loss of equilibrium or vertigo is produced. If, however, the current is passed transversely through the brain, there is produced at the moment of the closure and opening of the circuit a distinct tendency to fall or an actual fall to one side: in closing the current the fall is always away from the negative pole or cathode. The greatest amount of disturbance is produced when the electrodes are placed on the mastoid processes or near them. Whether the disturbance of equilibrium is caused by a change in electrotonus in the hemispheres, or by a change in the vascular supply of the hemispheres (in one anæmia, in the other relative hyperæmia), is uncertain. A third explanation is equally plausible—viz. that the vertigo is caused by unequal excitation of the internal acoustic organs and the two halves of the cerebellum. This view would be supported by the fact that in animals and man a lesion of the acoustic nerve and of the processus ad pontem on one side produces strong rotary movements about the long axis of the body.
ABNORMALREFLEXMOVEMENTS.—Some reference has already been made to absence or exaggeration of reflexes in the preceding paragraphs, but the importance of these symptoms demands that they should be separately considered.
A reflex action, in its simplest conception, is a movement (muscular, vascular, or psycho-motor) or a secretion which is the result of the transformation of a centripetal impression into a centrifugal impulse. The apparatus required for the accomplishment of the reflex action consists essentially of a sensitive surface of skin or mucous membrane, of tendinous or other deep structure, to receive the impression; a sensory afferent nerve to convey it; a nervous centre of the simplest structure (one or two ganglion cells) to receive and transform it; a motor or efferent nerve to transmit the resulting impulse to a common muscle, to the vascular wall of a vessel or viscus, or to a gland. These various terminal organs execute their normal functions in response to the centrifugal impulse, and thus give external or tangible evidence that the reflex action or reflex is completed. This mechanism, the reflex arc, is illustrated by the diagram (Fig. 1), which will also serve for the explanation of many of the morbid reflex states.