No abstract

No abstract

No abstract

Unlike neurological deficits resulting from intracranial hemorrhage in patients with cerebral arteriovenous malformation (AVM), which have well defined etiology, the pathogenesis and treatment of progressive and/or fluctuating non-hemorrhagic neurological and psychological deficits require clarification. Values for local cerebral blood flow (LCBF) and local partition coefficients (L lambda) were measured by the method using stable xenon (Xe)-computerized tomography (CT-CBF) scanning, and were compared to 133Xe inhalation values using external probes in 16 patients with cerebral AVM's. Values were measured by both methods before and after total excision of AVM's in five cases. Neurological and mental status assessments were compared with LCBF results. Clinical improvement was most evident after total excision of AVM's. Other procedures, such as clipping of vessels, partial excision, and ventriculoperitoneal shunting for hydrocephalus, were associated with frequent complications. Embolization carried risks of cerebral infarction and was not efficacious unless combined with excision. Medical treatment resulted in poor or unsuccessful seizure control, with neurological deterioration despite anticonvulsant therapy. Compared with age-matched normal individuals, LCBF values in patients with AVM's were significantly reduced, particularly adjacent to the AVM's. Mean L lambda values for gray and white matter were normal. After excision, LCBF values in gray and white matter increased significantly up to normal. Due to overestimation of CBF by shunt flow with the 133Xe method of measurement, no correlation was found with results of the CT-CBF method before AVM excision, but significant correlation of the two methods resulted after excision. If accurate LCBF values are obtained by high resolution, direct measurement of tracer clearance from brain tissue, progressive and/or fluctuating neuropsychological deficits correlate with the degree of cerebral steal.

Intracarotid BCNU (100 mg/m2) and cisplatin (60 mg/m2) were administered to 36 patients with malignant brain tumors recurrent or progressive after cranial irradiation. Courses of therapy were repeated at 4-6 week intervals. Of 23 evaluable patients with recurrent glioma, 9 (39%) had tumor regression by CT scan and 3 had stable disease. The median time to tumor progression for responding patients was 37 weeks. For all patients with primary tumors it was 14 weeks. Six of 9 patients with no prior chemotherapy had a response and 1 had stable disease. Of 14 patients who had received prior chemotherapy, 3 had a response and 2 had stable disease. Survival ranged from 9 weeks to 95+ weeks (median 34 weeks) from start of therapy. Six of 23 patients with primary tumors are alive 1 year or more following therapy. Four of 11 patients with brain metastases had a response and 2 had stable disease. Major neurologic toxicity of intracarotid BCNU and cisplatin appeared cumulative and consisted of reversible hemiparesis in 3% of 118 courses, TIA in 1%, expressive aphasia in 9%, lethargy in 3%, seizures in 12%, and reversible confusion in 1%. Retinal toxicity consisted of mild blurring of vision in 4 patients and ipsilateral blindness in 5 patients. Three of 22 patients who had received supraophthalmic infusion later developed evidence of leukoencephalopathy. Intracarotid BCNU and cisplatin appears to have modest increase in activity over intracarotid cisplatin alone (Cancer 54:794, 1984), however, neurologic and retinal toxicity may also be increased.