Many of the symptoms of cerebral abscess—prominently those attending the rapidly-developed forms and the exacerbations of the chronic form—are due to cerebral compression. It is the pulse and pupils, above all, that are influenced by this factor.
In an affection having so many different modes of origin as cerebral abscess, and occupying such a wide range of possible relations to the cerebral mechanism, it is natural that there should exist many different clinical types. So far as the question of the diagnosis of localized cerebral abscesses is concerned, I would refer to the article dealing with cerebral localization, in order to avoid repetition. With regard to the etiological types, they will be discussed with the respective causal factors.
ETIOLOGY.—Abscess of the brain is so frequently found to be due to metastatic or other infectious causes that it is to be regarded as highly improbable that it is ever of idiopathic occurrence. The most frequent associated conditions are—suppurative inflammation in neighboring structures, such as the tympanic cavity, the mastoid cells, the nasal cavity, or inflammation or injury of any part of the cranium and scalp. The connection of these structures with the brain through lymphatic and vascular channels is so intimate that the transmission of a pyogenic inflammatory process from the former to the latter is not difficult to understand. But disease of far distant organs, such as gangrene of the lung, and general affections, such as typhoid fever, occasionally figure among the causes of cerebral abscess, particularly of the miliary variety.
Among the commonest causes of cerebral abscesses are those which the surgeon encounters. The injury may be apparently slight and limited to the soft parts, or the bone may be merely grazed. Gunshot wounds are particularly apt to be followed by a cerebral abscess; and it has been noted that those which granulate feebly, whose base is formed by a grayish, dirty, and fetid material, are most apt to lead to this ominous complication. The symptoms do not usually develop immediately, and after the surgeon is led to indulge in the hope that danger is past, proper reaction sets in, healthy granulations develop—nay, the wound may close and be undergoing cicatrization—then the patient complains of feeling faint or drowsy, and with or without this premonition he has convulsive movements of one side, sometimes involving both extremities and the corresponding side of the face. Consciousness is usually preserved, but the spells recur, and the patient is noted to be absent-minded during and after the convulsive seizure. On some later day he is noticed to become pale, as in the initial stage of a true epileptic seizure; total abolition of consciousness follows, and the clonic spasms, affecting the same limbs and muscles involved in the first seizures, now recur with redoubled violence. After such an attack more or less paresis is observed in the muscles previously convulsed. A number of such seizures may occur, or a fatal issue terminate any one of them. Not infrequently the field of the involved muscles increases with each fit. Thus the thumb or a few fingers may be the first to show clonic spasm; in the next fits, the entire arm; in succeeding ones, the leg and face may follow suit. In such a case the periphery first to be convulsed is the first to become paralyzed, thus showing that where the disease began as an irritative lesion the cortex is now destroyed, and that around the destructive focus as a centre the zone of irritation is spreading excentrically, first to irritate and then to destroy seriatim the functions of the various cortical fields in their order. According to the teachings laid down in the article on Localization, the order of invasion and extension, as well as the nature, of the focal symptoms will vary. Finally, the attacks become more severe and of longer duration; the patient does not recover in the intervals, but complains of nausea, pain, confusion, and head-pressure. He is noted to be dull, his temperature is slightly raised (100° F.), and the speech may be affected. Several attacks may occur in a day, each leaving the patient more and more crippled as to motility and mind. He is delirious and drowsy at intervals; his temperature may rise after an attack from one to four degrees, usually remaining near 103°–104° F. in the evening; and, coma developing, death occurs, the convulsion or paralytic phenomena continuing at intervals during the moribund period, and the temperature and pulse sometimes running up rapidly toward the last. On examining the parts, it is found that the bone is necrotic at the point of injury, usually only in its outer table, but sometimes in its entire thickness. In exceptional cases the normal continuity of the entire table is not interrupted to all appearances, and a small eroded spot on the inner table is found bathed in pus, or a detached necrotic fragment may be found in the latter. Corresponding to the purulent focus on the inner table the dura mater is detached, discolored, and perforated in one or more places with irregular rents or holes which have a greenish or blackish border. An abscess is found in that part of the brain which corresponds to this opening. There is no question that it was caused by direct infection from the necrotic spot.
Cases have been noted,55 apparently of idiopathic origin, in which a sudden paralysis of a few fingers was the first symptom produced by the development of a cerebral abscess. In a few days such a paralysis extends to the other fingers and to the forearm. Occasionally no convulsive phenomena are noted, or choreic movements indicate, in their place, that the cortical field is irritated. Such cases usually run a rapidly fatal course.
55 Arthur E. W. Fox, Brain, July, 1885.
The most frequent cause of cerebral abscess in civil practice is suppurative inflammation of the middle ear. It may be safely asserted that the person suffering from this affection is at no time free from the danger of a cerebral abscess, a purulent meningitis, or a phlebitic thrombosis of the sinuses. Cases are on record where the aural trouble had become chronic, and even quiescent, for a period of thirty years, and at that late date led to abscess with a fatal termination. Of 6 cases of this character in my experience, 4 of which were verified by anatomical examination, not one but had occurred at least four years after the commencement of the ear trouble, and 1 happened in a man aged fifty-four who had contracted the latter affection in childhood. In 2 there was in addition diffuse purulent meningitis, limited on the convexity to the side where the abscess was situated.56 In 4 the abscess was in the temporal lobe, 1 of them having in addition an abscess in the cerebellar hemisphere of the same side; in a fifth the abscess was in the deep white substance of the cerebral hemisphere, opening into the lateral ventricle, and in the sixth it was in one cerebellar hemisphere alone.
56 One of these was seen during life by J. R. Pooley; the other was a paretic dement at the New York City Pauper Asylum.
The course of this class of abscesses is usually obscure: focal symptoms are not commonly present, and the constitutional and local symptoms usually appear as a gradual outgrowth from the aural troubles. Thus there is at first usually little fever, vertigo, and chilliness, but considerable tinnitus, and sometimes pain in the ear. Occasionally local signs of a septic metastasis of the otitis, such as œdema over the mastoid or painful tumefaction of the cervical glands, are visible. The pain previously referred to the region of the ear now becomes general; commonly—even where the abscess is in the temporal lobe—it becomes progressively aggravated in the frontal and sometimes in the nuchal region, and under an increase of the febrile phenomena death may exceptionally occur without further complication. Even large abscesses in one half of the cerebellum occur without producing Ménière's symptom—a fact which leads to the suspicion that the purulent deposit must have been of slow and gradual development. In one case distinct symptoms indicating an affection of the subcortical auditory tract were observed. As a rule, this class of abscesses are accompanied toward the close by active general symptoms—convulsions, coma, narrowing and impaired light-reaction of the pupils. Delirium, when a prominent symptom from the beginning, indicates the probable association of meningitis with the abscess.57 Occasionally severe pain, rigor, high temperature, and paralysis may be absent even with rapidly-developed abscess from otitis.58
57 The same is probably true of oculo-motor paralysis, which Ross (loc. cit., vol. ii. p. 735) refers to uncomplicated abscess.