Cases of localized softening are seen where no cause has been found, except perhaps a thrombus in the heart, which has discharged its softened and puriform contents; and it is probable that the connecting links exist in the form of embolisms so minute as to escape ordinary observation.

The consequences of capillary emboli if they block every minute ramification of an arterial branch must be essentially the same as if the branch itself were stopped; but if only a part are thus affected, the resulting anæmia is not so complete, since the zones of capillary congestion surrounding the part the supply of which is cut off may be sufficient entirely to cover it and make more or less complete compensation. The experimental emboli, in the form of tobacco-seed and other insoluble substances, which have been traced into the brain in considerable numbers, often give rise to no distinct lesions in the cases where the immediate effects are recovered from.

Among the other sources, ulcerative endocarditis may be mentioned as of special importance, not from the size but the character of detached emboli, which will give rise, not to simple anæmia, nor, on the other hand, to merely negative results, but to septic changes at the place of lodgment.

Aside from these conditions, which are almost the same on a small scale as we find with the large emboli, we have several peculiar substances formed in the body and floating in the blood which lodge in the capillaries of the brain. These are pigment, fat, lime salts, and white corpuscles. Every one of these, however, is much better known anatomically than clinically.

Pigment scales, flakes, granules, or cells containing them, are formed in the course of severe malarial fever, and deposits consisting of this pigment are found in the spleen, liver, kidneys, heart, lungs, and lymphatic glands, as well as the brain and spinal cord. The brain, when a deposit of pigment has taken place, is of a slaty-grayish or chocolate color, which is marked only in the cortical substance, the white being unaffected. The pigment is found in the capillaries, and, according to Frerichs, fibrinous coagula are often associated. Punctiform hemorrhages in the brain have been seen, as well as meningeal hemorrhages, in connection with this degeneration.

The point at which these masses are formed is still a matter of theory. If the liver, as has been supposed, is one of the places of formation, or if they originate in the blood, it is of course easy to see how they reach the brain. If in the spleen, they must pass through the wide portal capillaries before they are arrested in the narrower ones of the brain.

It is by no means certain, however, that pigment reaches the brain in the form of emboli. It is quite as probable that it is found in many organs which undergo repeated congestions from the local destruction of blood-corpuscles and changes in their pigment. The very general deposition seems to point to a process of this kind rather than to a local origin and a distribution through the blood. The punctiform extravasations which may be found with deposits of pigment are also found without it.

Minute particles of fat have been found in cerebral capillaries, but are much less common here than in the lungs. They may be derived from the decomposition of a thrombus, as described above, or they may come from a fractured bone, when, of course, only particles fine enough to pass through the pulmonary capillaries can reach the brain. This form of embolism has an interest in connection with diabetic coma.

Collections of white corpuscles in considerable number have been observed to form an embolus. These cannot be considered to differ very widely in character from the ordinary fibrinous embolus, which contains white corpuscles. It is, however, not certain that such emboli are deposited during life.

Calcareous masses formed from the decomposition of bone have been seen in cerebral arteries.