The patient. a boy, aged 19 years at the time of death. had had some head ache once or twice a week, with vomit ing. since childhood; but about six months before death the headaches be came severe, and cerebellar gait was ob served. Dizziness was also experienced, especially when the patient laid on his back. This dizziness probably the result of pressure of the distended cere bral ventricles on the cerebellum. Slight exophthalmos was observed. Distinct optic neuritis was present in each eye. The knee-jerks were exaggerated. Death occurred suddenly.
The skull was very thin—hardly thicker than a sheet of paper—at the sides of the ealvarium. The cerebral ventricles were much distended, but the fourth ventricle was of normal size. The aqueduct of Sylvius was entirely occluded when examined by the naked eye, but in microscopical sections a very small opening was found, which may have been absent during life. It is questionable whether any fluid passed through this opening during life. Small groups of epeudymal cells were seen in several places, and these had evidently been separated from the ependymal lin ing by the proliferation of the neu roglia.
Oppenheim (Mona ts. f. Psych. u. Xeurol., March. 1900) has described a case of inyasthenia gravis pseudopara lytica hi which he found bridging over of the aqueduct of Sylvius, and in some sections a third canal. Such anomalies of this region he believed had never pre viously been described. The occlusion in the case of H. C., reported by the writer, must, he believes, be of the same character as the partial occlusion in Op penheim's case, and was probably con genital or acquired early, on account of the history of headache and vomiting dating front childhood. The occlusion must have become complete about six months before the patient's death, when the symptoms became much more in tense than they had been previously. The closure of the aqueduct of Sylvius resembles in the changes of tissue pro duced by it the condition often seen in the region of the central canal of the spinal cord.
The symptoms were exceedingly sug gestive of cerebellar tumor. and in every case where a tumor of this portion of the brain is suspected the possibility of internal hydrocephalus should be borne in mind.
This is by no means the first case in which the symptoms of brain tumor were caused by internal hydrocephalus.
Byrom Bramwell (Brain, Spring, 1399) some years ago reported cases in which the characteristic symptoms of cere bellar tumor were present, but a disten sion of the ventricles, apparently the result of closure of the foramen of Magendie from localized meningitis, was found. IV. G. Spiller (Amer. Jour. Med. Sciences, July, 1902).
The brain-substance is anemic, often there is no line of demarkation between the gray and white matter, and the effects of pressure are evident in bad cases, which show, under the micro scope, marked degeneration of the nerve elements. In lesser grades of effusion the microscopical changes may be scarcely noticeable. The ependyma may be normal in appearance, but is often found thickened, infiltrated with leu cocytes, and granular to the naked eye.
In some cases it has undergone erative changes. In most cases some changes are found in the ependyma, and it is probable that these lesions are often directly responsible for the effusion itself, and that they result from an ante cedent attack of ependymitis, simple or specific in character, and often occurring in foetal life.
The bones of the cranium are more or less widely separated, sometimes to the extent of three inches. More rarely pre mature ossification has occurred, and in these cases the head is not enlarged. The cranial bones are remarkably thinned, and may be almost as thin as paper. Spina bifida is quite frequently associ ated with hydrocephalus, and, less quently, some form of meningocele or encephalocele complicates the case. Prognosis.—Complete recovery is prac tically unknown. In the most favorable cases the enlargement of the head spon taneously ceases after some years, and the patient may live for many years, but with no diminution in the size of the cranium. Mental defects are common in such cases. The majority of cases pro gress more or less rapidly to a fatal end. The rapid cases die within the first year, and it is very uncommon for a case of marked infantile hydrocephalus to live over the sixth year of life. Death usu ally results from marasmus, intercurrent disease, or from convulsions ending in coma from which the patient cannot be roused. Very rarely rupture of the head is a cause of death.