When the circulation ceases the substance that should have been nourished loses its firmness and acquires a custard-like consistency. The gray and white substances are no longer so distinct in appearance, the latter losing its milky-white color, the whole surface of a section becoming of a dirty yellowish-white, somewhat shining, and looking as if it contained more moisture than normal. When a considerable portion of the interior of the hemisphere is thus affected, the brain outside, with its membranes, bags down, looks swollen, and feels to the fingers as if there were present a sacful of fluid. The boundaries of such an area of softening are marked off from the healthy substance with some distinctness, though less than that of a hemorrhage. There may be some hemorrhage around the edges or into the cavity, so that the presence of a little blood-pigment is no proof that the original lesion was not softening from occlusion. In the further progress the contents of the cavity become more fluid, and finally a somewhat distinct cyst is formed, not unlike that from a hemorrhage, with an internal areolar structure from the remains of connective tissue, and contents of a slightly yellowish or brownish color, or often of a chalky white. These cysts have little to distinguish them, when old, from similar ones left by hemorrhage, except the much greater amount of pigment in the latter. The smaller spots of softening may after a time lose their fluidity, and remain as yellowish patches as firm as, or firmer than, the surrounding brain. The region of the brain involved becomes atrophied, the convolutions shrink, and the membranes become filled with serous fluid, to compensate for the sinking of the surface.
The microscope shows gradually increasing fatty degeneration, disorganization of the nervous tissue, and degeneration of its elements. The pyramidal cells are sometimes distinctly recognizable by their form, and show gradual transition into the indeterminate round granulation-corpuscles. The vessels exhibit fatty degeneration of their coats, as well as accumulation of fatty granules between the vessel and the lymphatic sheath. The clot which blocks the artery becomes adherent to its walls, and the vessel with its contents forms a round solid cord.
In a few instances the thrombi have become perforated through the centre, so that a channel is formed for a renewal of the circulation. There is no reason to suppose that this takes place soon enough to be of any advantage in restoring the nutrition of the necrosed portions of brain.
The region involved in softening depends upon the artery which is plugged and the location of the obstructing body. The place of election seems to be the carotid near its separation into its large branches, or these branches after the separation, especially the middle cerebral, this being peculiarly liable because it is the largest branch and is the continuation in a direct line of the carotid. It is more frequent upon the left side. Cases have been observed where the whole of one hemisphere was softened from obstruction of the carotid at its bifurcation; which may be accounted for, as Charcot suggests, by an unusual distribution of the arteries, as described above, the posterior cerebral as well as the other two being derived almost entirely from the carotid. In a case recently observed by the writer the whole right cerebral hemisphere, with the exception of the tip of the frontal and tip of the occipital lobes, was softened to the consistency of custard, a thrombus extending from the bifurcation of the common carotid into all the ramifications of the middle cerebral. The most common form, however, is where more or less of the brain around the fissure of Rolando and fissure of Sylvius, with or without the underlying ganglia, is softened. This happens from a lodgment of the embolus in the middle cerebral. If the obstruction be close to the origin of the artery, the corpus striatum suffers, from the mouths of its small nutrient arteries arising in this part of its course being stopped, while if it have passed along a little farther, these remain open, and the cortex, to which the larger branches are distributed, alone is softened.
The anterior cerebral is not infrequently affected, either alone or with the middle, and in these arteries as well as the posterior the embolus, if of small size originally, may penetrate so far as to give rise only to quite a limited anæmia. The basilar is an artery not very rarely occluded, though more commonly by thrombus than embolus. This occlusion may be so limited as to affect only the nutrient arteries of the pons and cause a very limited softening, the parts before and behind it being supplied by the unobstructed portion or by collateral circulation from the carotids. Occlusion of the cerebellar arteries and softening of the cerebellum are among the rarer forms. The vertebrals themselves are sometimes plugged. A thrombosis has been observed in the only inferior cerebellar artery which existed, causing softening in both lobes. There was atheroma of the heart and arteries, and a thick calcareous plate in that which was occluded.31
31 Progrès méd., 1876, 373.
In a general way, it may be said, with many exceptions on both sides, that thrombosis and embolism tend to affect the cortex, and hemorrhage the central ganglia.
What has just been written applies to the simple mechanical action of emboli. If, however, they have a septic origin, as notably in cases of ulcerative endocarditis, the region in which they lodge becomes, instead of a simple spot of necrosis, a septic focus or abscess, with its results of compression or irritation. In such a case there are likely to be abscesses of similar origin in other organs, and the cerebral lesion is only a part of the general pyæmic condition.
ETIOLOGY.—So far as the lodgment of an embolus in an artery is concerned, it can hardly be said that there is any etiology, for the detachment of the plug from its place of origin is purely a matter of accident, and may take place at any time. As to its origin in the form of fibrinous deposit on the valves of the heart or a roughened spot on the aorta, we must refer to the article on General Pathology. The most important condition for embolism is disease of the valves of the heart, rheumatic or otherwise. Next comes arterial disease, producing roughening of the inner coat and subsequent deposition of fibrin. So far as we can tell, the causes leading to endarteritis or atheroma are essentially the same as those which produce the periarteritis described in connection with cerebral hemorrhage, and we may therefore put down old age, alcohol, and strain as among the causes of cerebral embolism. Injuries of the lungs leading to thrombosis of the veins may be considered as possible sources for the formation of an embolus, and we might suppose that phthisis and pneumonia would furnish plugs which would lodge in the brain, though as a matter of fact they seldom do so.
Experience shows that embolism, unlike hemorrhage, is not specially a disease of advanced life, but is distributed over different periods, with preference for old age less marked than with hemorrhage. Andral gives the ages of patients with softening—which, however, includes thrombosis as well as embolism—as follows: the average would undoubtedly be displaced in the direction of youth if thrombosis could be taken out of the list: