APOPLEXY , the term employed by Galen to designate the "sudden loss of feeling and movement of the whole body, with the exception of respiration," to which, after the time of Harvey, was added "and with the exception of the circulation." Although the term is occasionally employed in medicine with other significations, yet in its general acceptation apoplexy may be defined as a sudden loss of consciousness, of sensibility, and of movement without any essential modification of the respiratory and circulatory functions occasioned by some brain disease. It was discovered that the majority of the cases of apoplexy were due to cerebral haemorrhage, and what looked like cerebral haemorrhage, red softening; and the idea for a long time prevailed that apoplexy and cerebral haemorrhage could be employed as synonymous terms, and that an individual who, in popular parlance, "had an apoplectic stroke," had necessarily suffered from haemorrhage into his brain. A small haemorrhage may not, however, cause an apoplectic fit, nor is an apoplectic fit always caused by haemorrhage; it may be due to sudden blocking of a large vessel by a clot from a distant part (embolism), or by a sudden clotting of the blood in the vessel itself (thrombosis). Owing to the prevailing idea in former times that cerebral haemorrhage and apoplexy were synonymous terms, the word apoplexy was applied to haemorrhage into other organs than the brain; thus the terms pulmonary apoplexy, retinal apoplexy and splenic apoplexy were used.
The term "apoplexy" is now used in clinical medicine to denote that form of coma or deep state of unconsciousness which is due to sudden disturbance of the cerebral circulation occasioned by a local cause within the cranial cavity, as distinct from the loss of consciousness due to sudden failure of the heart's action (syncope) or the coma of narcotic or alcoholic poisoning, of status epilepticus, of uraemia or of head injury.
The sudden coma of sunstroke and heat-stroke might be included, although owing to the suddenness with which a person may be struck down, the term heat apoplexy is frequently used, and, from an etymological point of view, quite justifiably. The older writers use the term simple apoplexy for a sudden attack which could not be explained by any visible disease. Again, congestive apoplexy was applied to those cases of coma where, at the autopsy, nothing was found to account for the coma and death except engorgement of the vessels of the brain and its membranes. In senile dementia and in general paralysis the brain is shrunken and the convolutions atrophied, the increased space in the ventricles and between the convolutions being filled up with the cerebro-spinal fluid. In these diseases apoplectic states may arise, terminating fatally; the excess of fluid found in such cases was formerly thought to be the cause of the symptoms, consequently the condition was called serous apoplexy. Such terms are no longer used, owing to the better knowledge of the pathology of brain disease.
Having thus narrowed down the application of the term "apoplexy," we are in a position to consider its chief features, and the mechanism by which it is produced. Apoplexy may be rapidly fatal, but it is very seldom instantly fatal. The onset is usually sudden, and sometimes the individual may be struck down in an instant, senseless and motionless, "warranting those epithets, which the ancients applied to the victims of this disease, of attoniti and siderati, as if they were thunder-stricken or planet-struck" (Sir Thomas Watson). The attack, however, may be less sudden and, not infrequently, attended by a convulsion; while occasionally, in the condition termed ingravescent apoplexy, the coma is gradual in its onset, occupying hours in its development. Although unexpected, various warning symptoms, sometimes slight, sometimes pronounced, occur in the majority of cases. Such are, fulness in the head, headache, giddiness, noises in the ears, mental confusion, slight lapses of consciousness, numbness or tingling in the limbs. A characteristic apoplectic attack presents the following phenomena: the individual falls down suddenly and lies without sense or motion, except that his pulse keeps beating and his breathing continues. He appears to be in a deep sleep, from which he cannot be roused; the breathing is laboured and stertorous, and is accompanied with puffing out of the cheeks; the pulse may be beating more strongly than natural, and the face is often flushed and turgid. The reflexes are abolished. Although apoplexy may occur without paralysis, and paralysis without apoplexy, the two, owning the same cause, very frequently co-exist, or happen in immediate sequence and connexion; consequently there is in most cases definite evidence of paralysis affecting usually one side of the body in addition to the coma. Thus the pupils are unequal; there may be asymmetry of the face, or the limbs may be more rigid or flaccid on one side than on the other. These signs of localized disease enable a distinction to be made from the coma of narcotic poisoning and alcoholic intoxication. It must be borne in mind that a person smelling strongly of liquor and found lying in the street in a comatose state may be suffering from apoplexy, and the error of sending a dying man to a police cell may be avoided by this knowledge.
If the fit is only moderately severe, the reflexes soon return, and the patient may in a few hours show indications of returning consciousness by making some movements or opening his eyes when spoken to, although later it may be found that he is unable to speak, or may be paralysed or mentally afflicted (see Paralysis). In severe cases the coma deepens and the patient dies, usually from interference with the breathing, or, less commonly, from arrest of the heart's action.
The mechanism by which apoplexy is produced has been a matter of much dispute; the condition was formerly ascribed to the pressure exerted by the clot on the rest of the brain, but there is no increase of intracranial pressure in an apoplectic fit occurring as a result of the sudden closure of a large vessel by embolism or thrombosis. Suddenness of the lesion appears to be, then, the essential element common to all cases of apoplexy from organic brain disease. It is the sudden shock to the delicate mechanism that produces the unconsciousness; but seeing that the coma is usually deeper and more prolonged in cerebral haemorrhage than when occasioned by vascular occlusion, and that an ingravescent apoplexy coma gradually develops and deepens as the amount of haemorrhage increases, we may presume that increase of intracranial pressure does play an important part in the degree and intensity of the coma caused by the rupture of a vessel. Apoplexy seldom occurs under forty years of age, but owing to the fact that disease of the cerebral vessels may exist at any age, from causes which are fully explained in the article Neuropathology, no period of life is exempt; consequently cases of true apoplexy are not wanting even in very young children. Recognizing that there are two causes of apoplexy in advanced life, viz. (1) sudden rupture of a diseased vessel usually associated with high arterial pressure, enlarged, powerfully acting heart and chronic renal disease, and (2) the sudden clotting of blood in a large diseased vessel favoured by a low arterial pressure due to a weak-acting heart, it is obvious that the character of the pulse forms a good guide to the diagnosis of the cause, the prevention and warding off of an attack, and the treatment of such should it occur.
Anything which tends directly or indirectly to increase arterial pressure within the cerebral blood-vessels may bring on an attack of cerebral haemorrhage; and although the identification of an apoplectic habit of body with a stout build, a short neck and florid complexion is now generally discredited, it being admitted that apoplexy occurs as frequently in thin and spare persons who present no such peculiarity of conformation, yet a plethoric habit of body, occasioned by immoderate eating or drinking associated with the gouty diathesis, leads to a general arterio-sclerosis and high arterial pressure. All conditions which can give rise to a local intracranial or a general bodily increase of the arterial pressure, i.e. severe exertion of body and mind, violent emotions, much stooping, overheated rooms, exposure to the Sun, sudden shocks to the body, constipation and straining at stool, may, by suddenly increasing the strain on the wall of a diseased vessel, lead to its rupture.
The outlook of apoplexy is generally unfavourable in cases where the coma is profound; death may take place at different intervals after the onset. If the patient, after recovering from the initial coma, suffers with continual headache and lapses into a drowsy state, the result is likely to be serious; for such a condition probably indicates that an inflammatory change has taken place about the clot or in the area of softening.
Treatment. - The patient should be placed in the recumbent position with the head and shoulders slightly raised. He should be moved as little as possible from the place where the attack occurred. The medical man who is summoned will probably give the following directions: an ice-bag to be applied to the head; a few grains of calomel or a drop of croton oil in butter to be placed on the tongue, or an enema of castor oil to be administered. He may find it necessary to draw off the water with a catheter. The practice of blood-letting, once so common in this disease, is seldom resorted to, although in some cases, where there is very high arterial tension and a general state of plethora, it might be beneficial. Depletives are not employed where there is evidence of failure of the heart's action; indeed the cautious administration of stimulants may be necessary, either subcutaneously or by the mouth (if there exist a power of swallowing), together with warm applications to the surface of the body; a water-bed may be required, and careful nursing, is essential to prevent complications, especially the formation of bedsores.
(F. W. Mo.)
Note - this article incorporates content from Encyclopaedia Britannica, Eleventh Edition, (1910-1911)