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Spontaneous brain hemorrhage accounts for about 10% of all strokes and is fatal in about 50% of the cases. Its incidence, in contrast to other types of strokes, has not declined. Hypertension accounts for about half of these hemorrhages; the rest are due to tumors, aneurysms and vascular malformations, inflammatory and degenerative vasculopathies and hematologic and iatrogenic disorders of coagulation. In some patients no cause is ever found. Hypertensive brain hemorrhage occurs in the deep gray nuclei of the hemispheres, the cerebellum, and the pons and results in specific clinical syndromes depending on the location. Computerized tomography has revolutionized the diagnosis of brain hemorrhage and is resulting in the development of rational criteria for medical and surgical management of these lesions. Intensive medical therapy guided by clinical status and continuous monitoring of ICP may improve outcome. Surgical removal of the hematoma is indicated in lobar and putaminal hemorrhages when the patient is deteriorating in spite of vigorous medical therapy. In addition most large (greater than 3 cm) cerebellar hemorrhages, as well as smaller cerebellar hemorrhages that result in significant brain stem compression should be evaluated. The roles of intensive medical therapy, elective late surgery and of immediate operation in improving eventual functional outcome need to be investigated further.

Cerebellopontine angle (CPA) meningiomas constitute about 1% of intracranial meningiomas. The clinical aspects of a series of 32 patients with surgically confirmed CPA meningiomas are analyzed. The most common symptoms at the time of the initial evaluation were from the eighth cranial nerve (unilateral hearing loss--24 patients, vertigo or imbalance--19 patients, tinnitus--11 patients), and the fifth cranial nerve (altered sensation--9 patients, facial pain--5 patients). On examination, the most common findings were absent caloric response (19 patients), nystagmus (16 patients), diminished facial sensation (14 patients), ataxia (13 patients), reduced hearing (9 patients), and facial weakness (9 patients). There was often a long interval from the onset of symptoms to the correct diagnosis of a tumor. Brain stem auditory evoked potentials, blink reflex testing, posterior fossa myelography, computerized tomographic scanning, and angiography were abnormal in all patients in whom the test was done, but all tests were not performed on all patients. Computerized tomographic scanning and angiography are important for definitive diagnosis and for planning surgical treatment. The histopathology of the temporal bone was studied in three patients with meningiomas in the region of the internal auditory meatus.

In 41 cases of verified ruptured saccular aneurysm, we prospectively predicted the presence or absence of delayed symptomatic cerebral vasospasm. CT criteria quantifying the extent and location of subarachnoid blood (developed in our previous retrospective study) were used in this prospective series of patients. Twenty-two patients had recognizable subarachnoid clots larger than 3 X 5 mm or layers of blood more than 1 mm thick (measured on reproduced images). In 20 of the 22 patients with severe significant clot or thick layer, severe vasospasm was correctly predicted and localized (2 false positives). In 19 patients with no blood, or diffuse blood, or blood outside the subarachnoid space, the absence of severe vasospasm was correctly predicted in 14 (5 false negatives). All of the false-positive and false-negative cases could be explained by inadequate CT technique. The data indicate that the extent and location of blood in the subarachnoid space determine the severity and location of vasospasm and that patients in jeopardy of developing symptomatic cerebral vasospasm can now be identified. Early preventive measures may now be assessed more accurately.