Licence: In copyright
Credit: Abcess of the brain / by Heinrich Neumann. Source: Wellcome Collection.
![the usual one. It arises by the coincidence of a pial vein happening to lie across the point of infection, when thrombosis occurs and spreads backwards into the brain substance. It is most liable to happen in connection with a lateral sinus thrombosis. The histological appearances are quite distinct. Here we see a vein filled with breaking-down clot [slide shown], the accompanying artery being patent, and the vessels in the fissure, which we cannot see here, show similar appearances. The degree of surrounding perivasculitis is slight, due merely to the infected thrombus. The area of brain drained by this vessel begins to degenerate owing to interference with its blood supply, and again the part least able to stand up to this is that in which the blood supply is least good, i.e., the avascular zone. Another slide from the same case shows an abscess, again occupying the position of the white core of a folium, with several thrombosed veins on the surface. The cases in this group are more likely to show multiple abscesses and to cause death by meningitis, as they tend to spread towards the surface along the course of the thrombosis and to rupture into the subarachnoid space. The third route requires but brief mention. If an artery is caught in the area of infection, it may become partially or completely occluded by a thrombus, and from this thrombus a small embolus can be shot off. This slide shows a thrombosed artery in the wall of an abscess which was probably occasioned by the thrombosis [slide shown]. The onset of such abscesses due to embolism is typically apoplecti¬ form. and their situation is not necessarily adjacent to the focus of infection. Spread.—Once an abscess has started in the brain substance it tends to increase in size in a fairly constant manner. The grey matter of the cortex is more resistant, by reason of its better blood supply, than the central white matter, and extension therefore occurs at the expense of the latter. In the cerebrum the abscess tends to spread along the course of the vessels towards the lateral ventricle, perforation into which is a not unusual terminal event. Exploration, therefore, should be towards the ventricle, and the operator must have a very clear conception of the position of this structure inside the brain. In the cerebellum extension occurs again at the expense of the white matter, but, in this case, of the white matter forming the centre of a lobule. This central core is gradually destroyed, inwards as far as the central mass of white matter and backwards through the lobule. The central white mass is respected until quite late in the course of the disease. In other words, the ordinary cerebellar abscess, as distinct from the commonly multiple abscesses secondary to a sinus thrombosis, is a single abscess and is nearly always confined to one lobule. That lobule is usually the one immediately below, and sometimes the one immediately above, ■the great horizontal fissure, which is covered by the horizontal part of the lateral sinus. One of these two lobules is the most likely place in which to find a cerebellar abscess in default of any guiding sign, such as a patch of dural thickening. It is, moreover, quite frequently a smooth-walled regular cavity, and not, as often stated, full of nooks and crannies and hence difficult to drain. Capsule.-—A few words about the capsule of the abscess. I use the word because it is part of the usual brain abscess jargon, but it is a complete misnomer. All we mean by it is the wall of the abscess cavity, and it differs in no essential respect from the wall of an abscess in any other part of the body ; it is simply the expression -of the attempt on the part of the body to wall off and limit the spread of an infection. It occurs more slowdy and with more difficulty in the brain, because the neuroglia, being a specialized connective tissue, does not enter into reparative and protective processes with the same zeal as connective tissue in other parts. Thus we have, with a very virulent infection, no evidence of a protective mechanism, but simply an acute spreading encephalitis similar to an acute spreading cellulitis in the arm. At the other end of the scale we have a very chronic abscess with a thick wall, and between the two, all possible gradations. The point of practical importance is . C b cd ' (CD- i t— U_» c3 cd GO cd CD CD CD CD Q- May—Otol. 2 *](https://iiif.wellcomecollection.org/image/b30628313_0017.jp2/full/800%2C/0/default.jpg)
