Encephalomalacia, or local softening of the brain, is found in ischemia, as a result of arteriosclerosis of the smaller vessels, in thrombosis and embolism, and in meningitis and encephalitis. The brain-substance breaks down and undergoes colliquation necrosis. The areas of softening are usually referred to by the color that they present. They are, however, not different processes, but merely different stages of the same condition.

White softening is a colliquation necrosis occurring when the blood-supply has been completely and permanently cut off. If this area is incised, the contents will escape, leaving an irregular cavity with ragged borders, and in it will be found some nerve-fibers and neuroglia. The escaped contents are composed of degenerated nerve-structures, with fat-droplets, granule-cells, and leukocytes.

Yellow softening may be due to an increased fatty degeneration occurring in white softening or a late stage of red softening.

Red softening is a breaking-down of nerve tissue accompanied by the extravasation of blood. It may be due to a hemorrhagic infarction or to diapedesis. The contents of the involved area are not generally as fluid as in the other forms of softening.

The areas of softening may vary greatly in size and in the time of their formation. The same process, however goes on, the myelin sheaths degenerate, the axis-cylinders may disappear, compound granule-cells appear, and finally the neu-rogliar fibers may soften. The broken-down tissue may be slowly absorbed, leaving a cyst with smooth, well-defined walls, and clear contents. The cysts may become encapsulated, or through absorption scar tissue form.

Encephalitis, or inflammation of the brain-substance, is peculiar on account of the tissue that is involved. It differs from inflammation elsewhere in that conditions of degeneration or softening are associated.

Encephalitis may be acute or chronic, diffuse or circumscribed. The causes of the condition are many. It may result from injury without infection; in this form there is a hemorrhagic extravasation, followed rapidly by necrosis. Around the necrotic tissue is a hyperemic zone in which there is some transmigration of leukocytes, and slight proliferation of the connective tissue of the sheaths surrounding the vessels. Injury with injection generally affects the membranes primarily, but soon involves the brain-substance. There is a marked leukocytic infiltration along the blood-vessels, and the brain-substance undergoes degenerative processes. Inflammation of the brain may also be secondary to infectious disease elsewhere in the body. In hematogenic focal encephalitis specific micro-organisms are brought to the brain by the blood. Numerous areas are found in which the bloodvessels are distended and interstitial hemorrhages are present. The lymphatics contain many leukocytes, and the nerve-tissues rapidly degenerate. If the patient survives long enough, suppurative encephalitis may ensue. This form is generally due to infection by the pneumococcus, streptococcus, or staphylococcus, and true abscesses, either single or multiple, are formed. If the extension has been by the blood, they will be multiple; if by direct continuity, as from middle-ear disease, they will be single. The size may vary greatly - they are generally about as large as a walnut. They are most frequent in the cerebrum, but may be found in the cerebellum and rarely in the pons and medulla. When the acute processes subside, a proliferation of the surrounding neurog-liar tissue may occur and encapsulate the abscess. Toxic encephalitis is caused by the presence, in the circulating blood, of certain substances that act upon the nerve-cells and cause various changes that can be recognized by the employment of special methods of study. These changes are found in the cells of both the brain and spinal cord in diphtheria, tetanus, lead-poisoning, and hydrophobia, also to some extent in alcoholism. Chronic encephalitis or sclerosis occurs in all cases of injury to the brain in which recovery occurs. There is a chronic hyperplasia of the neuroglia, which may be local or diffuse. In multiple localized sclerosis there are numerous scattered foci of degeneration, associated with hyperplasia of the neuroglia. They are sharply defined, slightly dense to the touch, and grayish or pinkish in color. Diffuse sclerosis is characterized by widespread areas of neurogliar hyperplasia. It is more common in children, and does not seem to be due to toxic or inflammatory conditions. It may be sharply circumscribed and resemble glioma. At first the brain may appear hypertrophied, but later, as atrophy of the nerves occurs, it becomes smaller. Certain lobes or convolutions may be involved, and there is always considerable degeneration of the nervous structures.

Tuberculosis of the brain may be primary or be secondary to tuberculosis of the meninges. When secondary, there are generally many small tubercles along the perivascular tissues, particularly along the small vessels of the anterior and posterior perforated spaces. Primary tuberculosis is hematogenic, and occurs as single lesions. It is more common in children. The tubercle gradually becomes larger, and caseous degeneration occurs, is rather dense, yellowish in color, and dry, and sometimes undergoes calcification or again contains a yellowish purulent-like matter. The growth increases in size by the formation and aggregation of new tubercles at the periphery of the original focus. These large areas are called tyromata.

Syphilis of the brain generally appears as a gumma that has originated within the pia and extended to the brain. The gumma is at first grayish or reddish-gray, but very soon undergoes a secondary necrosis and caseation. Recovery takes place with the formation of a dense cicatrix. Syphilitic endarteritis is sometimes found and gives rise to secondary degenerations with softening.