The brain usually exhibits a severe degree of softening and often is converted into a semi-fluid, deliquescent, "creamy" or "raspberry like" mass; or it contains numerous hamorrhagic foci; or, finally, there may be sclerosis with narrowing of the convolutions and second ary hydrocephalus. Hence, in some eases softening, in others hyper temia may be the chief condition, or a hfemorrhage may be simulated. Histologic examination reveals necrosis, atrophy of the white matter, disappearance of the ganglion cells, accumulations of leucocytes, masses of fatty granules, in some cases a high grade of plethora., hmorrhage, or even a marked proliferation of neurogliar tissue.
The clinical picture is usually that of an extreme febrile symptom complex. The temperature rises rapidly to 40° to 41° C. (104° to 105.S° F.) and continues very high. Disturbance of consciousness occurs early. There is stupor, which is soon replaced by complete coma. Convulsions are always present; they often represent the initial stage of the disease and arc prone to recur again and again. The breathing is superficial. Cheyne-Stokes respiration and attacks of asphyxia occur. The pulse is usually greatly accelerated and feeble. Rigidity of the neck is fre quently- present; bulging of the fontanelle is not always observed. The extremities are rigid, usually in a position of flexion. Strabismus is not uncommon. These severe general symptoms overshadow the localized focal phenomena, which are usually confined to slight paresis or monospasm of individual extremities or of the facial nerve.
The duration of infantile encephalitis is from 1 to 2 weeks; the child ultimately dies of cardiac or respiratory failure.
The differential diagnosis between acute inflammation of the brain substance and simple acute meningitis practically cannot be made by the clinical symptoms. In the presence of a pneumonia or some intes tinal process, and after pertussis the chances are in favor of meningitis. Turbidity, of the cerebrospinal fluid obtained by lumbar puncture also points to inflammation of the meninges.
It is not to be inferred from the above schematic description of infantile encephalitis that acute inflammation of the brain in the early periods of life is always so extensive and necessarily runs a fatal course. It is impossible to make a sharp distinction between diffuse severe forms of encephalitis which have a special tendency to occur in early infancy and the more circumscribed conditions which belong, to the later periods of life; and infantile encephalitis may run a mild COUrSC ending in recovery just as, on the other hand, the disease in older chil dren may be marked by the above-described violent symptoms and end in death. But in order to understand the forms of encephalitis without
autopsy findings which will be discussed presently, a knowledge of the fatal forms of the disease is necessary, because, with respect to the inten sity and extension of the morbid process, these must be regarded as exaggerated forms of the same disease ivhich ends in recovery.
3. Encephalitis in Older Children with a Tendency to Recovery.—ln children between the ages of 2 and 4 acute inflammation of thc brain may run a course similar to that observed in the infant. More fre quently, however, it is circumscribed and the symptoms are not so violent. A large proportion of the cases terminate in recovery with persistence of focal symptoms.
The most frequent causes of encephalitis after the first and second years of life are the infectious diseases—measles, diphtheria, scarlet fever and whooping-cough. Acute meningitis is frequently; followed by a superfieial encephalitis. Many forms of acute inflammation of the brain which, however, are rare in childhood, are caused by intoxication. Aside from these secondary forms of diseases we also have an acute inflammation of the brain occurring primarily like an independent disease. Strumpell must bc given the credit for calling attention to these conditions and his investigations have taught us to regard polio encephalitis or acute inflammation of the brain, poliomyelitis, and possibly also inflammation of the peripheral nerves as different manifes tations of an independent acute disease due to bacterial causes and possessing a special predilection for childhood. The same individual not infrequently presents the remains of both cerebral ancl spinal palsies, and epidemics of acute inflammation of the brain and of the spinal cord in association have even been described (Medin). Head injuries may possibly be capable of producing a simple encephalitis as well as a purulent inflammation, as is shown by the occurrence of inflammation of the brain after severe injuries to the skull and also by animal experi ments, although it is still doubtful whether the contusion itself is the actual cause of the inflammation or only the exciting cause acting on a previous bacterial predisposition.