Before the introduction of accurate methods of examining the diseased brain the term inflammatory softening was used in a much wider sense than it is to-day. Most of the disorders ascribed to inflammatory irritation by writers of the period of Andral and Rush are to-day recognized as regressive, and in great part passive, results of necrotic destruction through embolic or thrombic closure of afferent blood-channels. Two forms of inflammation are universally recognized. One manifests itself in slow vascular and connective-tissue changes and in an indurating inflammation. There are two varieties of it: the first of these, which is associated with furibund vaso-motor explosions and regressive metamorphosis of the functional brain-elements, is known from its typicalassociation with grave motor and mental enfeeblement as paretic dementia or dementia paralytica. The second, which is focal in the distribution of the affected brain-areas, is known as sclerosis. The former is treated of in a separate article; the latter is considered in connection with the spinal affections which either resemble it in histological character or complicate its course. The second form of cerebral inflammation is marked by the formation of the ordinary fluid products of acute inflammation in other organs of the body; this is the suppurative form, usually spoken of as abscess of the brain.
In addition to these two generally recognized inflammatory affections there are a number of rare diseases which are regarded by excellent authority as also of that character. The vaguely-used term acute encephalitis has been recently reapplied with distinct limitations to an acute affection of children by Strümpell. This disease is usually of acute onset, infants under the sixth year of age being suddenly, and in the midst of apparently previous good health sometimes, attacked by fever, vomiting, and convulsions.40Occasionally coma follows, which may last for several days, perhaps interrupted from time to time by recurring convulsions or delirium. The convalescence from this condition is rapid, and in some cases is complete; in others paralysis remains behind in the hemiplegic form. The paralysis is usually greater in the arm than in the leg; in extreme cases it involves the corresponding side of the face, and, as the paralyzed parts are arrested or perverted in growth, considerable deformity, even extending to asymmetry of the skull, may ensue. The deformity is aggravated by contractures. Usually there is some atrophy of the muscles, but in one case I found actual hypertrophy41of some groups, probably in association with the hemiathetoid movements.
40As in my case of infantile encephalitis followed by athetoid symptoms (Journal of Nervous and Mental Diseases).
41This was followed by atrophy. There are never any qualitative electrical changes.
The sequelæ of acute infantile encephalitis present us with the most interesting forms of post-paralytic disturbances of muscular equilibrium. Hemichorea and hemiathetosis, as well as peculiar associated movements and hemicontracture, are found in their highest development with this class of cases. Occasionally epileptiform symptoms are noted,42and in others true epilepsy is developed. It is under such circumstances that imbecility is apt to be a companion symptom or result; and this imbecility is prominently noted in the moral sphere.
42Which in one case of my own disappeared spontaneously.
The grave set of symptoms briefly detailed here are attributed by Strümpell43to an acute encephalitis, analogous, in his opinion, to the acute poliomyelitis of children. Its frequent occurrence after measles and scarlatina, as well as the fact that Ross44in a carefully-studied case arrived at the opinion that the disease was an embolo-necrotic result of endocarditis, would lead to the conclusion that it is a focal affection, probably due to the transportation of infectious elements to the brain through the blood-vessels. Its occurrence in children in the midst of apparent health45is consistent with the fact that rheumatism and an attendant slight endocarditis frequently pass unrecognized in infancy. It is supposed that a diffuse form of inflammatory non-suppurative softening exists by some of the Germans, but the proof advanced in favor of this view is not conclusive.
43As a surmise, for up to his writing no reliable autopsies had been made.
44Brain, October, 1883.
45McNutt (American Journal of Medical Sciences, January, 1885) cites Strümpell as attributing the theory of an inflammatory affection, which is analogous to poliomyelitis in its suddenness and nature, to Benedict, and refers to p. 349 of Strümpell's textbook under the erroneous date of 1864. This work was published in 1883-84, and the theory is advanced by Strümpell as his own. It is only a synonym, hemiplegia spastica infantile, that is attributed to Benedict.
A number of rare forms of interstitial encephalitis have been described. In one, elaborately studied by Danillo, an inflammatory hypertrophy of the cortex, involving the parenchyma as well as the connective and vascular structures, was found in a limited area of the motor province of the right hemisphere. There had been crossed epileptiform convulsions during life.46
46Bulletin de la Société de Biologie, 1883, p. 238.
There is some question among pathologists as to the recognition of Virchow's encephalitis of the new-born. Certainly a part of Virchow's material was derived from the imperfect study of a condition of infantile brain-development which, as Jastrowitz showed, is physiological, and on which Flechsig based his important researches of tract-development. More recent studies, however, demonstrate that there is a form of miliary encephalitis in new-born children due to septic causes, such as, for example, suppuration of the umbilical cord. The demonstration by Zenker of the occurrence of metastatic parasitic emboli in cases of aphthous stomatitis, and by Letzerich of a diphtheritic micrococcus invasion in the brain of his own child, show that the subject of early infantile encephalitis merits renewed consideration.47
47The attempt of Jacusiel to revive Virchow's encephalitis of the new-born (Berliner klinische Wochenschrift, 1883, No. 7) under the title of interstitial encephalitis does not seem to have met with encouragement, for, besides Jastrowitz, Henoch and Hirschberg opposed this view in the discussion.
Strictly speaking, the reactive changes which occur in the brain-substance bordering on tumors, hemorrhagic and softened foci, belong to the domain of encephalitis; but as they are considered in conjunction with the graver lesions to which they are secondary both in occurrence and importance, it is not necessary to more than refer to them here.
As indicated in the last article, there formerly existed much confusion in the minds of pathologists regarding the terms softening and abscess of the brain. As long as softening was regarded as an inflammation, so long was abscess of the brain regarded as a suppurative form of softening. Aside from the fact that there is some resemblance in mechanical consistency between a spot of ordinary softening and one of inflammatory softening, there is no essential similarity of the two conditions. True softening is to-day regarded as the result of a death of brain-tissue produced by interference with the blood-supply; it is therefore a passive process. Inflammatory softening, of which abscess is a form, is due to an irritant, usually of an infectious nature. It is to the results of such irritation that the term suppurative encephalitis should be limited.
MORBIDANATOMY.—In all well-established inflammatory braintroubles the active part is taken by the blood-vessels and connective tissue; the ganglionic elements undergo secondary, usually regressive or necrotic, changes. The brain, considered as a parenchymatous organ, is not disposed to react readily in the way of suppurative inflammation unless some septic elements are added to the inflammatory irritant. Foreign bodies, such as knitting-needles, bullets, and slate-pencils, have been found encapsulated in this organ or projecting into it from the surrounding bony shell without encapsulation and without any evidences of inflammatory change. As a rule, a foreign body which enters the brain under aseptic conditions will, if the subject survive sufficiently long, be found to have made its way to the deepest part of the brain, in obedience to the law of gravity, and through an area of so-called inflammatory red softening which appears to precede it and facilitate the movement downward. This form of softening derives its color from the colored elements of the blood, which either escape from the vessels in consequence of the direct action of the traumatic agent; secondly, in consequence of vascular rupture from the reduced resistance of the perivascular tissue in consequence of inflammatory œdema and infiltration; or, thirdly, in obedience to the general laws governing simple inflammation.
A cerebral abscess may present itself to the pathological anatomist in one of three phases—the formative, the crude, and the encapsulated. In the first it is not dissimilar to a focus of yellow softening, being, like the latter, a diffuse softened area varying from almost microscopical dimensions to the size of a walnut, and of a distinctly yellow tinge. Microscopic examination, however, shows a profound difference. In pure yellow softening there are no pus-cells; in the suppurative encephalitic foci they are very numerous, and congregated around the vessels and in the parenchyma in groups. The crude abscess is the form usually found in cases rapidly running to a fatal termination. Here there is an irregular cavity in the brain, usually the white central substance of the cerebrum or cerebellum, formed by its eroded and pulpy tissue; it is filled with yellow, greenish, and more rarely brownish pus. In the most furibund cases broken-down brain-detritus may be found in the shape of whitish or reddish flocculi, but in slowly-formed abscesses the contents are free from such admixture, and thus the third phase is produced, known as the encapsulated abscess. The cavity of the abscess becomes more regular, usually spheroid or ovoid; the pus is less fluid, more tenacious, and slightly transparent; and the walls are formed by a pseudo-membrane48which is contributed by the sclerosing brain-substance, which merges gradually into the outlying normal tissue. I have seen one acute cerebral abscess from ear disease which might be appropriately designated as hemorrhagic; the contents were almost chocolate-colored; on closer inspection it was found that they were true pus, mingled with a large number of red blood-discs and some small flocculi of softened brain-substance. This hemorrhagic admixture was not due to the erosion of anylarge vessel, for the abscess had ruptured into the lateral ventricle at that part where it was most purely purulent. In a case of tubercular meningitis, Mollenhauer in my laboratory found an abscess in the white axis of the precentral gyrus, with a distinct purulent infiltration following the line of one of the long cortical vessels. The abscess was not encapsulated, the surrounding white substance exhibited an injected halo, and the consistency of the contents was that of mucoid material.
48There is considerable dispute as to the real nature of the tissue encapsulating cerebral abscesses. It is known, through the careful observations of R. Meyer, Goll, Lebert, Schott, and Huguenin, that the capsule may form in from seven to ten weeks in the majority of cases, about eight weeks being the presumable time, and that at first the so-called capsule of Lallemand does not deserve the name, being a mucoid lining of the wall. At about the fiftieth day, according to Huguenin, this lining becomes a delicate membrane composed of young cells and a layer of spindle-shaped connective elements.
In cases where the symptoms accompanying the abscess during life had been very severe it is not rare to find intense vascular injection of the parts near the abscess, and it is not unlikely that the reddish or chocolate color of the contents of some acutely developed abscesses is due to blood admixture derived from the rupture of vessels in this congested vicinity. Sometimes the entire segment of the brain in which the abscess is situated, or the whole brain, is congested or œdematous. In a few cases meningitis with lymphoid and purulent exudation has been found to accompany abscesses that had not ruptured. It is impossible to say whether in this case there was any relation between the focal and the meningeal inflammation, as both may have been due to a common primary cause.49In such cases, usually secondary to ear disease, thrombosis of the lateral sinus may be found on the same side. Where rupture of an abscess occurs, if the patient have survived this accident long enough—for it is usually fatal in a few minutes or hours—meningitis will be found in its most malignant form. A rupture into the lateral and other ventricles has been noted in a few cases.50
49Otitis media purulenta in the two cases of this kind I examined.
50In one, observed together with E. G. Messemer, intense injection of the endymal lining, with capillary extravasations, demonstrated the irritant properties of the discharged contents.
Some rare forms of abscess have been related in the various journals and archives which have less interest as objects of clinical study than as curiosities of medical literature. Thus, Chiari51found the cavity of a cerebral abscess filled with air, a communication with the nose having become established by its rupture and discharge.
51Zeitschrift für Heilkunde, 1884, v. p. 383. In this remarkable rase the abscess, situated in the frontal lobe, had perforated in two directions—one outward into the ethmoidal cells, the other inward into the ventricles, so that the ventricles had also become filled with air. This event precipitated a fatal apoplectiform seizure.
The contents of a cerebral abscess usually develop a peculiarly fetid odor. It has been claimed that this odor is particularly marked in cases where the abscess was due to some necrotic process in the neighborhood of the brain-cavity. The only special odor developed by cerebral abscesses, as a rule, is identical with that of putrid brain-substance, and it must therefore depend upon the presence of brain-detritus in the contents of the abscess or upon the rapid post-mortem decomposition of the neighboring brain-substance.
In two cases of miliary abscess which, as far as an imperfect examination showed, depended on an invasion of micro-organisms, an odor was noticed by me which was of so specific a character that on cutting open the second brain it instantly suggested that of the first case, examined six years previous, although up to that moment I had not yet determined the nature of the lesion.52
52Owing to the lack of proper methods of demonstrating micro-organisms, the first case whose clinical history was known was imperfectly studied; of the second case, accidentally found in a brain obtained for anatomical purposes, the examination is not yet completed.
That form of abscess which, from its situation in or immediately beneath the surface, has latterly aroused so much interest from its important relations to localizations is usually metastatic, and directly connected with disease of the overlying structures, notably the cranial walls. In this case the membranes are nearly always involved. The dura shows a necrotic perforation resembling that found with internal perforation of a mastoid or tympanic abscess. The pia is thickened and covered with a tough fibro-purulent exudation; occasionally the dura and leptomeninges are fused into a continuous mass of the consistency of leather through the agglutinating exudation. The abscess is usually found open, and it is not yet determined whether it begins as a surface erosion, and, bursting through the cortex, spreads rapidly on reaching the white substance, or not. The white substance is much more vulnerable to the assault of suppurative inflammation than the gray, and not infrequently the superficial part of the cortex may appear in its normal contiguity with the pia, but undermined by the cavity of the abscess, which has destroyed the subcortical tissue. Possibly the infecting agent, as in some cases of ear disease, makes its way to the brain-tissue through the vascular connections, which, however sparse at the convexity of the brain, still exist.
CLINICALHISTORY.—The symptoms of a cerebral abscess depend on its location, size, and rapidity of formation. There are certain parts of the brain, particularly near the apex of the temporal lobe and in the centre of the cerebellar hemisphere, where a moderately large abscess may produce no special symptoms leading us to suspect its presence. There are other localities where the suppurative focus53indicates its presence, and nearly its precise location and extent, by the irritative focal symptoms which mark its development and by the elimination of important functions which follows its maturation. It is also in accordance with the general law governing the influence of new formations on the cerebral functions that an acutely produced abscess will mark its presence by more pronounced symptoms than one of slow, insidious development. Indeed, there are found abscesses in the brain, even of fair dimensions, that are called latent because their existence could not have been suspected from any indication during life, while many others of equal size are latent at some time in their history.
53Practically, our knowledge of localization of functions in the human brain begins with the observation by Hitzig of a traumatic abscess in a wounded French prisoner at Nancy named Joseph Masseau. The year of the publication of this interesting case constitutes an epoch in advancing biological knowledge, which will be remembered when even the mighty historical events in which Hitzig's patient played the part of an insignificant unit shall have become obsolete. This, the first case in the human subject where a reliable observation was made was an unusually pure one; the abscess involved the facial-hypoglossal cortical field (Archiv für Psychiatrie, iii. p. 231).
An acute cerebral abscess is ushered in by severe, deep, and dull headache, which is rarely piercing, but often of a pulsating character. The pain is sometimes localized, but the subjective localization does not correspond to the actual site of the morbid focus.54It is often accompaniedby vertigo or by a tendency to dig the head into the pillow or to grind it against the wall. With this there is more or less delirium, usually of the same character as that which accompanies acute simple meningitis. As the delirium increases the slight rise in temperature which often occurs in the beginning undergoes an increase; finally coma develops, and the patient dies either in this state or in violent convulsions. The case may run its course in this way in a few days, but usually one to three weeks intervene between the initial symptoms and death.
54Although Ross seems to be of a contrary opinion, it is the exception for the pain to correspond in location to the abscess.
Between the rapid and violent course of acute cerebral abscess detailed, and the insidious course of those which as latent abscesses may exist for many years without producing any noticeable symptoms whatever, there is every connecting link as to suddenness and slowness of onset, severity and mildness of symptoms, and rapidity and slowness of development and progress. It is the encapsulated abscesses which are properly spoken of as chronic, and which may even constitute an exception to the almost uniform fatality of the suppurative affections of the brain. Thus, the symptoms marking their development may correspond to those of an acute abscess, but coma does not supervene, temporary recovery ensues, and the patient leaves the hospital or returns to his vocation. But all this time he appears cachectic, and there will be found, on accurate observation, pathological variations of the temperature and pulse. The appetite is poor; the bowels are usually constipated; there are frequent chilly sensations and horripilations, and a general malaise. This condition slowly passes away in the few cases which recover; in others relapses occur, usually of progressing severity, and terminate life. The period during which the symptoms of the abscess are latent may be regarded as corresponding to the latent period which sometimes intervenes between an injury and the development of the symptoms of acute abscess, and which, according to Lebert, may comprise several weeks or months. In other words, the morbid process may be regarded all this time as progressing under the mask of a remission. It is this latent period which it is of the highest importance for the diagnostician to recognize. There is usually headache, which is continuous and does not change in character, though it may be aggravated in paroxysms. Usually the temperature rises with these paroxysms, and if they continue increasing in severity they may culminate in epileptic convulsions.
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 frequentassociated 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 examiningthe 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,55apparently 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.
55Arthur 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.56In 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.
56One 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 factwhich 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.57Occasionally severe pain, rigor, high temperature, and paralysis may be absent even with rapidly-developed abscess from otitis.58
57The same is probably true of oculo-motor paralysis, which Ross (loc. cit., vol. ii. p. 735) refers to uncomplicated abscess.
58This was the case with an abscess containing five ounces of pus recorded by C. S. Kilham at the Sheffield Medical Society (British Medical Journal, February 13, 1886). As illustrating what was stated about the non-correspondence of the pain and the location of the abscess, it may be stated that notwithstanding this large abscess was in the temporal lobe, what pain was present was in the forehead.
Ulcerative endocarditis, infectious osteomyelitis, pulmonary gangrene, general pyæmia, and, as is claimed by a few authors, typhoid fever, are often accompanied by multiple abscesses in the brain-substance. Usually the foci are small, as may be readily inferred from the fact that they are of embolic origin, the emboli being usually so small as to lodge in very small vessels, and that the fatality of the primary disease is so great as to cut short life before the abscess can reach larger dimensions. For the same reasons the symptoms they produce are rarely distinctive. In chronic lung affections accompanied by putrescence in bronchiectatic or other cavities cerebral abscesses are not uncommon occurrences. Under these circumstances, although we must assume an embolic origin, the abscess is rarely multiple, and the symptoms are as marked as in the ordinary varieties. Thus a patient suffering from chronic phthisis, with or without prodromal malaise or somnolence, experiences formications and pain in his right leg; he then notices a slight halt in walking; twitches appear in the affected extremity; it becomes distinctly paretic. The arm then becomes affected in like manner; the pupils become unequal; a severe chill occurs, followed by delirium, convulsions, coma, and death.
DIAGNOSIS.—There is little difficulty in recognizing the existence of a cerebral abscess in which well-marked focal and constitutional symptoms coincide, or where a distinct abscess-producing cause, such as an ear trouble, a head injury, or a putrid bronchiectasis, coexists.59But there are a number of cases, varying from the latent form to forms with obscure general symptoms, whose recognition is impossible or at best a matter of conjecture. Such cases may be readily confounded with certain tumors. The existence of febrile symptoms, although not excluding tumor, as some tumors are accompanied by such, is greatly in favor of abscess. On the other hand, choked disc, which is rare with abscess and found only with the very largest, is in favor of tumor.
59Yet a leading and careful authority was misled into making the diagnosis of abscess in a case of ear disease complicated by a cerebral tumor.
PROGNOSIS ANDTREATMENT.—The majority of cerebral abscesses must, from the nature of the case, be regarded as not influenceable by medicinal measures or surgical treatment. The miliary and other abscesses due to general septic causes or to mycotic invasion, being in the nature ofthe case but features of intrinsically dangerous or fatal primary diseases, do not call for special measures. It is different with those due to local trouble about the head and to surgical causes. Remarkable advances have been made in the operative treatment of cerebral abscesses, chiefly owing to the increasing accuracy of the localization of the affected areas through the disturbance of their function, and to the perfection of surgical methods. A number of cases by Gussenbauer, Wernicke, and others have shown that some abscesses may be accurately located during life by the focal symptoms produced by their presence. Wernicke's observation of a large abscess in the occipital lobe showed two facts. First, it permitted the study of the effect of large abscesses on the cerebral movements, as it was found after trephining that the pulsation movement of the brain was lost and the dura tensely bulging, thus indicating a high degree of cerebral pressure. Secondly, the operation showed that an abscess can be emptied of its contents, under moderate aseptic precautions, without provoking contiguous inflammatory reaction or infecting the meninges. Notwithstanding these favorable local conditions, the patient died. Gussenbauer60was more fortunate. He surmised from the fluctuation of some symptoms and the predominance of others that his patient had an abscess in the frontal lobe. The suspicion was verified: an abscess of the size of an apple was found, opened, and emptied of its contents. The patient recovered without any immediate untoward symptom.61
60Prager medizinische Wochenschrift, 1885, Nos. 1, 2, and 3.
61Epileptic and focal spasms subsequently developed, which shows that a new inflammatory or other destructive process may have set in in the vicinity of the emptied sac.
The uncertainties of localization in some districts of the brain are so great that a number of attempts to repeat the explorations and aspiration of Wernicke and Gussenbauer have failed. In one case recently operated on in New York City the aspirating-needle was run into the brain-substance in several different directions without striking the pus. It is a question under such circumstances whether the chances of an abscess becoming latent, minimal though they be in cases with pronounced signs, are not to be preferred to those which an uncertain operation can give. The superficial encephalitic foci offer far better opportunities for surgical triumphs. Here not only the symptoms are much more constant, and point more unerringly to the site of the morbid spot, but there are often other signs, such as the evidences of impaction of a foreign body, local tenderness on percussion, or bone disease, which aid in determining the proper spot for the application of the trephine. Several operations where traumatic encephalitis existed with or without leptomeningitis of the convexity, followed by complete recovery, were performed by Macewen.62
62The Lancet, 1885, vol. i. p. 881.
The medicinal treatment of abscess of the brain is limited to derivative methods, whose aim is the relief of pressure—an aim whose fulfilment is more frequently illusory than otherwise.
Benefit has been claimed from the energetic use of mercury, chiefly in the form of calomel, by older writers; and recently Handfield Jones has endorsed its administration, attributing to it a remission in a case in which it was employed. It must be remembered, however, that remissions occur spontaneously in this disease, and that the purgative action of calomel may act well for the time being in an affection so apt to beassociated with hyperæmia and increased cerebral pressure as is an abscess of the brain.63In the nature of the case, even this latter momentarily beneficial effect is at the best temporary.
63Brain, October, 1884, p. 398.
The prophylaxis of cerebral abscess can be carried out only in cases due to cranial and aural affections. The importance of treating all scalp and cranial injuries under aseptic64precautions is recognized by all surgeons. It is generally admitted that the trephining of a bone suspected to be the site of an ostitic or necrotic process involves fewer risks than the allowing it to remain. Similar principles govern the treatment of the inflammatory involvement of the mastoid cells often complicating otitis media. If trephined at all, these should be trephined at the earliest moment. It was a belief among the older aurists that the sudden cessation of an aural discharge was of evil augury, and that cerebral complications were more apt to follow under such circumstances than when the ear discharged freely. Von Tröltsch, Politzer, Gruber, and Toynbee have opposed the exclusive application of the old dogma. In so far as the older ear-surgeons regarded a profuse aural discharge as an encouraging sign, in this respect they were of course wrong. But their observation of the frequent concurrence of cerebral sequelæ with suppression of discharge is, I think, borne out by a large number of cases. It does not apply, however, to the suppression of discharge by the rational employment of aseptic injections.
64This term is used in its widest sense here.
The spinal cord is found to vary considerably in color in different individuals. To some extent this difference is influenced by the position occupied by the body after death, but not as markedly as in the case of the brain. Thus it will be paler in a body which has been kept in the prone than in one which has been kept in the supine position.65It is usually found more injected in persons who have died of febrile affection than in those who have died of exhausting diseases; notably is this the case with typhus fever and with subjects who die with congestive malarial chill. But the most intense congestion, where the gray substance instead of having the normal rosy hue appears like a blood-soaked sponge, and the white substance instead of the tint to which it owes its name has a pink shade, is found in subjects dying in convulsive disorders complicated by asphyxia, such as epileptic status, tetanus, and certain toxic disorders.
65I have not seen it noticed anywhere, but it is a fact readily demonstrable in any autopsy made in a well-preserved body that when a short segment of cord is observed at the moment of section the section surface appears pale; but if it be again examined after a few moments, it will show a reddish tinge, marked as a faint injection would be; this tinge distinctly deepens under the eye. I have observed this in specimens which were not held in the hand, so that the influence of pressure can be excluded. Nor do I believe that the elasticity of the tissues is such as to account for the phenomenon.
In attempting to apply the fact that varying degrees of vascular injection are found on post-mortem examinations of the spinal cord to the elucidation of certain clinical phenomena, we encounter the same difficulties and sources of error that confronted us in the study of nutritivebrain disorders. The majority of writers have therefore contented themselves with making a careful clinical study of the mostly subjective signs of disorders which, once designated as spinal anæmia and hyperæmia, are now classified under the non-committal titles of spinal irritation and exhaustion (neurasthenia), as in this volume. A number of these disorders, like the so-called anæmic paralysis of Bouchut, Leroy d'Etiolles, Beroliet, Baimer, and Brandis, would to-day be considered as hysterical or reflex; and a few of the instances cited by their contemporaries as cases of spinal hyperæmia have been since demonstrated to resemble the initial phases of organic diseases of the cord.
The causes of active spinal hyperæmia are either direct, as when the spinal centres are overtasked by muscular strain either through over-exertion or through toxic convulsions, surprised by violent shocks, such as concussion accidents, or collateral, as when a physiological discharge (menstruation) or a pathological one (hemorrhoidal flux) is suddenly checked. A few cases are reported where carbonic-oxide-gas poisoning provoked spinal hyperæmia. But, like the alleged cases of spinal hyperæmia after continued and exanthematic fevers, they were probably cases of incipient or established myelitis. Hammond claims that surface chilling exerts the same congesting influence on the cord which he claims for the brain; but no definite observations have been made in this direction.
Passive spinal hyperæmia has been attributed to obstructive cardiac and chronic pulmonary affections. In such cases, as with most causes acting on the circulation of blood in the nerve-centres, the coexisting cerebral congestion usually masks the spinal. It is a question how far the intense hyperæmia of the cord found in some cases of tetanus, strychnia-poisoning, and the condition called hydrophobia66is primary and an indication of neural hyperexcitability, and how far it is secondary to the asphyxia attending the last phases of these convulsive states. The weight of opinion is in favor of an acceptation of the latter as the chief or only factor.
66In a case of hydrophobia clinically as well marked as has been recorded, which I had the privilege of examining through the courtesy of Kretschmar, both brain and cord were found remarkably anæmic.
Over-exertion and sexual excesses are frequently followed by a sensation of fulness and tension in the sacral and lumbar regions, which may be relieved by lying prone, while it is aggravated while lying supine.67From the location of this pain it is evident that it is not due to congestion of the cord or its membranes, but to fulness of the vertebral and spinal veins of the lower segment of the vertebral column. A similar sensation, which may be relieved by the same change in position or by a hemorrhoidal flux, is complained of by patients suffering from portal obstruction. The veritable symptoms of hyperæmia manifest themselves in the parts which receive their nervous supply from the affected districts. The reflexes are usually more active; paræsthesias of different kinds, such as formication, tingling, and creeping sensations, are common; andthere is more or less motor weakness, the limbs feeling heavy and sometimes being the seat of an acute pain. As a rule, these symptoms are limited to the lower half of the body.
67Although this fact has been questioned, I have no doubt whatever that it is true, from a large number of observations. In many subjects suffering from the results of excessive venery or masturbation, an intolerable, sometimes pulsating, feeling in the lumbo-sacral region is only relieved by raising the lower end of the trunk with the back up. This condition is influenced by a change of residence to a district having a different level above the sea, and consequently a different barometric condition.
There is very little question when these symptoms exist for any length of time, and become aggravated, that more subtle nutritive changes than are covered by the single term hyperæmia become responsible for them. In a pure hyperæmia the position-test of Brown-Séquard, which shows relief when the patient is upright or prone and aggravation when he is supine, particularly if the gravitation of blood to the cord be facilitated by raising the head and extremities, ought to yield constant results. But in some cases, particularly those of long-standing, the very opposite is noted: the patient's symptoms are aggravated by standing or sitting up, and relieved by lying down. Here there is probably exhaustion or malnutrition of the nerve-elements, rendering them abnormally sensitive to exertion. This view is supported by the fact that molecular disturbances, such as those which probably accompany simple concussion, predispose the patient to the development of the symptoms of spinal hyperæmia, and aggravate them if established previous to such accident.
Hammond,68who in his chapter on Spinal Congestion and Anæmia follows rather the older authors, such as Ollivier, than the newer and either more cautious or more sceptical writers on the subject, describes the symptoms of congestion as comprising belt sensations, paraplegia, erections of the penis, muscular twitches, loss of expulsive power, and incontinence of the bladder, paralysis of the abdominal muscles, paralysis of the anal sphincter, loss or abolition of reflex excitability, diminution of electro-muscular contractility, and occasionally hyperæsthesia and shooting pains. It is not doubtful for a moment that if such a case were to occur in hospital experience it would be regarded as one of organic disease, and not incipient, but well-established organic disease of the cord. Those making the diagnosis would have their opinion strengthened if, as Hammond states, the process took place with great rapidity and had a tendency to extend itself and eventually involve the whole cord, or if, as Brown-Séquard is by him cited as stating, bed-sores occurred in addition. Although Hammond describes certain anatomical changes, such as increased development of blood-vessels and distension and injection of them, I am unable to find any cases recorded as spinal congestion during life, and carefully examined with a due regard to sources of error after death, in which such changes were found. It is true that after strychnine- and cocaine-poisoning an intense hyperæmia69of the cord is found. In mammals it is of a far more pronounced character than in reptiles, and usually more marked in proportion to the existing asphyxia. That the characteristic toxic effects of these drugs is not to be sought for in their direct or indirect congesting influence is shown by the fact that exsanguinated frogs can be made to undergo strychnine tetanus when their blood is replaced by a saline solution according to the method of Salkowski. Little support, therefore, could be derived from a pretended analogy between toxic andpathological hyperæmias, even if the phenomena of both were similar; which is not the case.
68Diseases of the Nervous System, 7th ed., p. 392.
69It is true that in animals which are so organized that the congestion cannot be attributed to asphyxia, as I showed (Hammond Prize Essay of the American Neurological Association, 1878) in some experiments on strychnine, arterial congestion and small foci of hemorrhage were found in the upper cervical cord of frogs who had been kept in continuous strychnine tetanus for over seventy days.
The introduction of subaqueous caissons for workmen engaged in the building of bridges, in which those employed labor under abnormal atmospheric pressure, has led to the development of a previously-unknown cerebro-spinal affection known as the caisson disease, and in which, it is generally supposed, either congestion or hemorrhage of the spinal cord occurs in consequence of sudden changes of vascular pressure resulting from sudden diminution of the barometric pressure. Clinically, this affection has been studied in England, France, and above all in America in connection with the building of the East River Bridge and the one over the Mississippi at St. Louis.70Experiments by Hoppe-Seyler, Bert, and I. Rosenthal have shown that a sudden diminution of pressure leads to hemorrhages in various tissues, and, according to the two first-named, a development of gas occurs in the vascular and other fluids of the body. A number of peculiar symptoms which do not specially interest us here occur in conjunction with the so-called caisson disease: these are—pain in the ear, with or without otitis sicca; peculiar pains in the joints, which occur on leaving the caisson, and are probably due to hyperæmia of the joint-surfaces and sudden increase of the intra-articular fluid; and retardation of the pulse-rate. In some cases cerebral hyperæmia is added, the patients tottering about as if drunk. The spinal symptoms consist of a paraplegiform affection. The paralysis is usually sudden; in some cases the patient a few minutes after stepping from the air-chamber falls down perfectly helpless as far as the lower half of the body is concerned. The expulsive power of the bladder is usually weakened, and there is anæsthesia to all forms of sensation in the affected limbs, as well as diminished electro-cutaneous sensibility. The patient often complains of a strange feeling, as if the lower half of his body were a foreign substance. With this the electro-muscular reactions are normal. In the majority of cases these symptoms disappear entirely in from three to ten days, but occasionally they remain longer; imperfect recovery of motion and sensation occurs, or, as happened in a few cases, one of which was carefully examined during life by Lehwess and after death by Leyden, death occurs as in myelitis. In the only case where an autopsy and careful microscopical examination were made under these circumstances71peculiar fissures were found in the substance of the spinal cord, surrounded by areas of reactive myelitis and filled with granule-cells. The absence of any pigmentary relics of a hemorrhage induced Leyden to assume that the lacunæ were not of hemorrhagic origin. He inclines to the view that they were due to the escape of gas from the blood-plasma, and consequent multilocular inflation of the tissue. If his observation be confirmed, it constitutes a strong objection to the hyperæmia theory of the caisson disease. There is neither permanent hyperæmia nor congestive or hemorrhagic myelitis developed, as far as the limited material thus far studied permits a conclusion.
70Clark,St. Louis Med. and Surg. Journ., cited from Hammond,loc. cit.
71E. Leyden,Archiv für Psychiatrie, ix. p. 316.
Pure spinal hyperæmia rarely presents itself for treatment. The form due to over-exertion is recovered from by rest in a very short time; that due to suppressed discharges, by the re-establishment of the latter or bythe application of leeches to the lumbo-sacral and iliac region. Ergotin is recommended by Hammond in very large doses. It is a question whether this drug may not exert a bad effect in protracted cases where its use has to be continued for a long time.72In using it, it is well to bear in mind that imperfect nutrition of nerve-elements is perfectly compatible with an increased blood-amount.
72A young physician, who for a long period took ergotin in twelve-grain doses for the relief of symptoms regarded as congestive, acquired a tolerance of the drug such as I have not seen recorded anywhere, and in addition presents some obscure signs of cerebellar disease and initial optic-nerve atrophy.
Strychnia has been given with benefit in the caisson disease—another evidence, as this drug is theoretically contraindicated in true hyperæmia, that this disease is not, as Hammond and the majority of authors with him regard it, essentially a congestive affection. The treatment of those numerous cases in which signs of venous fulness accompany spinal exhaustion and irritation is detailed in the articles dealing with those affections.