Definition. Causes: Nature: intracranial rupture, with pressure, serous effusion, excessive congestion, experimental cases, anæmia from pressure, comparative immunity of horse, heart disease, Bright’s disease, atheroma, degeneration, emboli, age, blood tension, severe exertion, excitement, concussion, insolation, venous obstruction, toxins, neoplasms. Lesions: blood clots, small and multiple, large and solitary, brain absorption, cavities, cysts. Symptoms: dullness, swaying, trembling, elevation of head, turning in circle, sudden fall, spasms, unequal dilated or contracted pupils, eyes turned to affected side, congested or anæmic mucosæ, stertor, puffing cheeks except in solipeds, pulse slow, soft, full, vomiting, stupor, coma, unconsciousness, paralysis, monoplegia, hemiplegia, sequelæ. Diagnosis: sudden unconsciousness, with little spasm, but paralysis, history, sign of trauma, deep coma, eyes turned to one side, pupils unequal, stertor, slow breathing and pulse; from uræmia, pulmonary apoplexy, œdema or anthrax. Treatment: bleeding, ice pack, snow, cold water, rest, derivatives to limbs, later purge, bromides, potassium iodide, tonics, open air life.
Definition. Cerebral apoplexy has been defined as a sudden loss of sensation and voluntary motion, from pressure originating within the cranium and followed by paralysis, often unilateral. The definition is somewhat insufficient as regards the early symptoms as the same conditions attend on convulsions and epilepsy (haut mal), and it is only by excluding these by their characteristic features of sudden seizure with clonic spasms and their intermittent and paroxysmal habit that we reach an easy and satisfactory distinction. Later the paralysis tends to identify the apoplectic attack.
Causes and Nature. The immediate cause and essential lesion of apoplexy has been generally held to be the rupture of an intracranial artery and the formation of a considerable blood clot which presses upon (and abolishes the functions of) the brain. There are cases, however, in which the characteristic symptoms are present, and yet a complete recovery ensues at an early date, too early to allow for the absorption of a considerable clot. Moreover, in fatal cases perhaps no blood clot is to be found, but in place a serous effusion, or an internal congestion which exercised the fatal pressure on the brain. So far, therefore, as clinical phenomena are concerned, we must allow that apoplexy may arise from any sudden pressure on the brain substance. Pagenstecher produced the symptoms of the disease by injecting, at a regulated pressure, melted wax and tallow between the skull and dura mater in the dog. In the moderate cases there were drowsiness, psychic depression and general muscular weakness. In the more severe ones there were added sleep and unilateral paralysis. In the more extreme cases death followed in a few hours after coma set in, though in some of these a partial recovery ensued if the waxy mass was scooped out before the fatal symptoms appeared. Cases ended fatally only when the injection pressure equalled that of the blood, and convulsions occurred only when the pressure was unsteady. The temperature fell as it does in apoplexy in man, at the outset, but it continued falling to the fatal issue contrary to what takes place in man.
Duret injected water into the cranium of animals so as to produce great tension of the occipito-atloid membrane causing thereby arrest of the respiration and slowing of the heart’s action. On tearing the membrane so as to allow escape of the water, respiration began anew and consciousness was gradually restored.
Edes sustains the view that apoplexy is directly due to anæmia of a lesser or greater portion of the brain substance, and that this need not be in any one particular seat nor of any definite extent. This anæmia is usually induced by pressure and may be caused by effused blood, or serum, or by the extreme congestion due to narcotic poisons, or other cause. Embolism of a cerebral vessel, however, by cutting off the blood from the part of the brain which it supplies may give rise to the apoplectic phenomena.
Friedberger and Fröhner found apoplexy quite frequent in sheep, ox. and dog, and rare in the horse, although more subject to the violent exertion which they put in the front of all causes. It is probable that the sluggish, pampered life of the first three animals, and the tendency to fatty degenerations and heart disease introduces a special predisposition as it does in man, while the horse, inured to an open air life and a vigorous muscular condition, is comparatively immune. Bright’s disease is a common cause in the human subject, with its resulting cardiac hypertrophy. The degenerations attendant on these conditions and especially fatty change (atheroma) in the walls of the cerebral arteries, pave the way for their rupture and for blood effusion. Emboli also carried from the diseased heart not only cut off the blood from the parts supplied by the plugged arteries, but increase the blood tension on the cardiac side of the obstruction and endanger rupture at any weak part. Thus they may cause apoplexy from anæmia without rupture or apoplexy from the pressure of effused blood.
Age which is such a notorious factor in man is not without its influence in the lower animals. It is in the old that we mostly see disease of kidneys and heart and the degenerations of the tissues, including the brain and its vessels; in these, therefore, rupture and extravasation are the most frequent.
The other causes are mostly connected with increased blood tension with or without a debility of the vascular walls. Violent exertions as in racing, coursing, dragging heavy loads up hill or on heavy ground, severe excitement, cerebral concussion, insolation, and intense congestion of the brain substance have all been recognized as causative factors. The compression of the jugulars by a small collar, the violent straining attendant on parturition, or constipation, and even the retrocession of blood from the surface when exposed to extreme cold, may contribute to the final rupture.
In infectious diseases in which the toxic products tend to produce profound modifications in the blood and tissues, extravasations are met with in the brain as in other organs. Thus they are seen in anthrax, Texas fever, petechial fever, etc.
Then the formation of neoplasms in the brain may be the occasion of the rupture of the vascular walls and apoplexy. Hæmatoma of the dura in the dog (Friedberger and Fröhner), cholesteatomata in the horse, and carcinoma may be apparent causes.
The effect of mechanical injury must be admitted, as blows on the head, injuries from an ox yoke, and concussions during the battles of rams and bulls.
Lesions. Blood extravasations may be found at any part of the brain: a. into the brain substance; b. into the ventricles; c. from the pia mater; d. into the arachnoid sac; e. between the skull and dura mater. It is especially common in connection with the ganglia adjoining the ventricles; the corpus striatum, optic thalamus, the corpora quadrigemini, the fornix. In other cases the crus cerebri, pons, medulla oblongata, corpus calosum. In other cases the convolutions of the cerebrum or cerebellum suffer. The amount of effusion may be limited to a few drops or it may cover an extensive area and cause considerable flattening of the brain substance.
When capillary hæmorrhages are present—the size of a millet seed or a pea—Friedberger and Fröhner have usually found them multiple, but when large enough to form distinct clots they are usually single and confined to one side. If a clot, involving the brain substance, is small, it merely separates the nervous fibres, but if larger, the cerebral tissue is broken down in the mass of clot, discolored, torn and softened. If the patient has survived the first attack the clot passes through the different stages of discoloration, brown, brownish yellow, yellow, and may become fibrous forming a distinct cicatrix, with loss of brain substance. In connection with the partial absorption of the effused blood, cavities may be filled with a serous fluid (apoplectic cysts), and these may show multiple loculi. The nerve fibres which lead to an old standing lesion are usually degenerated.
When effused into a ventricle, blood is less readily absorbed and tends to remain as a flattened discolored layer.
Extravasation between the dura mater and the cranium is probably always the result of direct mechanical violence.
Symptoms. Premonitory indications of apoplexy are less commonly recognized in the lower animals than in man, doubtless largely because of the impossibility of appreciating subjective symptoms. The first observed indications are usually dullness, some lack of coördination of movement, swaying, unsteady gait, trembling and a tendency to deviate to one side or to move in a circle. In the majority of cases, however, the first symptoms noticed are a complete loss of consciousness or nearly so, a sudden fall and often more or less convulsive movements of the limbs aggravated by any excitement. The eyes remain dilated, the pupils enlarged or sometimes contracted, and in case of unilateral effusion the axis of vision of both eyes is turned to the affected side, right or left. The pupil of one eye is likely to be more widely dilated than that of the other. Rolling of the eyeballs is not uncommon. Convulsions may occur, the head and hind limbs being drawn back forcibly as in oposthotonos, or the animal may lie flaccid and comatose from the first. The nasal, buccal and orbital mucous membranes are usually congested, deep red or livid, yet sometimes they are anæmic and pale (Shock). The breathing is usually characteristic, being deep, slow, labored, irregular and stertorous and accompanied by puffing out of the cheeks at each expiration (except in solipeds). Yet there are cases in which stertor is absent. The pulse is usually slow, full and soft, and, in the carotids, throbbing, but it may be weak and imperceptible. There may be complete unconsciousness, and again from the first, or nearly so, there may be a slight response to a stimulus, which cannot be referred altogether to reflex action. In vomiting animals, emesis may ensue. Stupor and coma are more or less marked, though liable to intermissions under any cause of irritation.
Along with the above symptoms the spasms and sequent paralysis, are significant. If confined to given muscles or groups of muscles (monoplegia) it usually implies pressure on some special cortical convolutions presiding over these muscles, and convulsions are to be expected. If there is hemiplegia it is suggestive of implication of the medulla or pons on the opposite side, or of a clot on the corpus striatum or extensively on one side of the cerebrum. A clot in the lateral ventricle tends to profound coma. So liable, however, is pressure to be extended from one side of the brain to the other, and irritation on the one side to rouse a corresponding condition on the opposite side, or in related ganglia, that deductions of this kind cannot always be implicitly relied on.
Though an animal should recover from an attack there is liable to remain some modification of the nervous functions, partial anæsthesia, circumscribed paresis, dullness, lack of energy, irritability, or muscular atrophy.
Cerebral embolism and thrombosis and their sequelæ, infarction and softening, give rise to corresponding symptoms, according to the seat of the lesion, and like lesions of the blood vessels predispose to subsequent attacks.
Diagnosis is based largely on the appearance, usually sudden but sometimes slow, of a more or less profound unconsciousness, attended or followed by paralytic troubles. The history of the case may assist, any blow on the head, or sustained by falling, striking a wall or post, or wearing a yoke, is to be noted. Any extraordinary exertion or excitement must be considered. Any sign of injury about the head; the congestion of the cephalic mucous membranes in contrast with the pallor of shock; the onset of the attack without convulsions (or with them as in epilepsy); the deep coma indicating cerebral hæmorrhage or narcotic poisoning; the absence of the odor of alcohol, opium, or other narcotic from the breath; the turning of the eyes to one side and the inequality of the pupils on the two sides; the turning of the head to the same side as the eyes; the slow, labored, usually stertorous breathing; the slow, full, soft pulse; the occasionally rigid condition of the muscles and finally the paralysis, hemiplegic, and less frequently monoplegic or paraplegic, make up the diagnostic picture.
Uræmia and diabetic coma may be excluded by examination of the urine, pulmonary apoplexy or œdema by the predominance of respiratory troubles, and fulminant anthrax by the examination of the blood and by the fact that this disease does not prevail in the locality.
Treatment is very unsatisfactory in the lower animals, as the disease is very fatal, and unless recoveries are complete, they are not pecuniarily desirable. It is only in the slighter cases, therefore, that treatment can be recommended. At the very outset nothing is better than a full bleeding in a large stream from the jugular vein or temporal artery. Ice, snow, or cold water should meanwhile be applied to the cranial region. Absolute rest should be given, any harness that would impede circulation or respiration removed, and hot water or stimulating embrocations applied to the limbs.
When consciousness returns and the patient can swallow, an active purgative may be administered, or barium chloride or eserine may be given subcutem. Any recurring heat of the head may be met by renewal of cold applications, and the force of the circulation may be kept in check by small doses of bromides or aconite. In case of the formation of a clot, iodide of potassium and other alkaline agents may be resorted to. Quiet and the avoidance of all excitement together with a laxative non-stimulating diet must be secured throughout. A course of vegetable or mineral tonics and an occasional blister to the side of the neck may prove a useful sequel.