3. Among extra-nterine causes, head injuries involving the skull or accompanied by subdural htemorrhage may lead to cerebral infantile palsy. Circumscribed encephalitis, which may develop spontaneously (polieneephalitis, Strumpell) or in the wake of some infectious disease (measles, scarlet fever, varicella, intestinal catarrah, pnemnonia and the like) is a very important cause of cerebral infantile palsy, particu larly the unilateral variety. Sinus thrombosis and embolism may produce the same clinical result; the emboli in most eases are probably of infectious or septic nature and are comparatively rare in otherwise uncomplicated cases of endocarditis.
To what extent syphilis may be responsible for the production of cerebral infantile palsy is difficult to say. This etiologic relation was formerly regarded as very rare (Sachs, Kfinig), but more recent observa tions (Rolly, Konig, Fournier, Erlenmeyer and others) tend to show that permanent cerebral symptoms occur more frequently in hereditary. syphilis than was formerly believed. The diagnostic difficulty arises from the impossibility, in tbe cases of children with hereditary syphilis present ing symptoms of a cerebral palsy, of determining with certainty whether one is really dealing with the remains of ft former pathologic process (that is to say, a cerebral infantile palsy, as defined above) or with a temporarily permanent stage of a still active brain lues.
In a large number of cases all we can learn about the beginning of the disease is that the palsy developed within the first two or three years of life after convulsions, which in most cases are said to have been uni lateral. Sometimes it is stated that the child had repeated attacks of convulsions before it became permanently paralyzed. In these cases it is not proven that the convulsions produced an alteration in the brain (Inemorrhage) which led to the paralysis; it is quite possible that (prenatal, natal, intrapartum) changes were already present in the brain at an early date and that the motor region became involved secondarily (Freud. Rie).
Finally, there are plenty of cases of cerebral infantile palsy in which, either owing to the indifference of the parents or the very mild character of the initial symptoms, it is impossible to elicit any definite history, so that w e can form no conclusion in regard to the date when the palsy began. The existence of this group of cerebral infantile palsy alone precludes a complete etiologic classification of these conditions.
For the study of the pathologic anatomy of cerebral infantile palsy we have at our disposal the terminal conditions of those pathologic processes which represent the foundations of the disease that ultimately leads to cerebral infantile palsy. It must be remembered that various
diseases are capable of producing the same permanent changes in the brain. The initial lesions, as has been stated, may owe their origin to several different causes, most important among which are meningeal cere bral h(emorrhage, embolism, encephalitis, and intra-uterine diseases or injuries. As a rule, the changes produced by these diseases can no longer be distinguished w hen the cases of cerebral infantile palsycome to autopsy.
The changes observed at the autopsy of individuals with cerebral infantile palsy, which represent the final results of the morbid process, are: Porencephalus.—This may he congenital and the expression of a true malformation of the brain or of an intra-uterine disease on the one hand, or may be the result of some process acquired in later life. The defect is found chiefly in the area supplied by the middle cerebral artery and by the artery of the fissure of Sylvius, particularly in the central and temporal convolutions. The time when a given defect in the brain was produced is sometimes very difficult to determine. Either asso ciated with porencephalus or as an independent condition, we also find in cases of cerebral infantile palsy, diminution in the size of the convolutions Onicrogyria), which in turn is due either to arrested de velopment or to a former inflammatory process. Sachs employed the term agenesia corticalis, based on microscopic findings. It is probable that many of these cases are clue to secondary changes in the cortex, the result of meningeal hmmorrhages (Oppenheim). Another pathologic condition that belongs under this head is unilateral atrophy of the brain, which is due to sclerosis of one cerebral hemisphere. The his tologic changes consist in diffuse sclerosis with proliferation of the neurogliar tissue, thickening of the vessel walls, hypertrophy of the perivascular connective tissue, and diminution of the nervous elements. Diffuse sclerosis may- also be bilateral. It has been described as a separate clinical entity which we have already discussed in section V. Localized sclerosis, with bosselated thickening of certain portions of the cerebrum (tuberous sclerosis), has been found at the autopsies of cases of cerebral infantile palsy. The cerebral sclerosis probably repre sents the end-product of vascular disturbances (occlusion of vessels, inflammation), but gives no clue to the original disease.