Gangliogliomas are rare benign tumors of the central nervous system containing neoplastic ganglion and low grade glial cells. In studying 10 surgically treated cases, we evaluated the clinical, pathological, radiological, and immunocytochemical features, with follow-up. Ranging from 18 to 58 years in age, 7 patients were women, and 3 were men. The most common presenting symptom was seizure. Computed tomographic scan showed a low density enhancing mass in 8 and calcification in 5. Six had minimally abnormal vascularity on angiography. Seven patients had total and 3 had subtotal resections of the tumor. The temporal lobe was the location of the tumor in 6 cases. All of the cases met the histological criteria of Russell and Rubinstein for ganglioglioma. Four patients received postoperative radiotherapy because of subtotal resection or aggressive histological makeup. On follow-up, from 2.5 to 7 years, 8 patients are alive and tumor-free, and 7 are also seizure-free. Two died after operation: one immediately and the other of a glioblastoma that developed 5 years later. Our study confirms that ganglioglioma is a distinct histological entity, anatomically localized, with characteristic clinical and radiological findings and long term survival. Aggressive histological makeup is not a definite indication of malignant potential. The definitive role of follow-up radiotherapy for this tumor needs further study. Malignant evolution is rare, but warrants follow-up.

Ten cases of sporadic cerebral amyloid angiopathy (CAA) were seen as intracranial hemorrhage. CAA was seen as a stroke or catastrophic intracranial hemorrhage in all cases. CAA complicated by intracranial hemorrhage carried a high mortality; 9 of 10 patients died in spite of aggressive medical or surgical treatment. Senile dementia of Alzheimer's type was an associated finding in only 1 patient. Computed tomographic scanning in 4 patients initially was not diagnostic for hemorrhage. Lambda chains and amyloid P protein were demonstrated in the areas of amyloid angiopathy immunocytochemically. The pathogenesis of hemorrhage in CAA could be either increased fragility of amyloid-laden blood vessels or rupture of microaneurysms. Surgical treatment of intracranial hemorrhage in CAA should therefore be undertaken with caution.