[Current management of carotid artery stenosis. What does the evidence show us?].

Objective: Surgery of carotid artery stenosis as treatment for acute cerebral vascular accident was most used in the 1980s. This surgical procedure is one of the few to have been 'examined' to demonstrate its usefulness by means of a series of prospective multicentric trials, carried out between 1980 and 1990. This paper aims to show the results of these trials and give useful advice for current management of these patients.

Clinical presentation and management of giant anterior communicating artery region aneurysms.

Object: The authors reviewed their 20-year experience with giant anterior communicating artery aneurysms to correlate aneurysm size with clinical presentation and to analyze treatment methods.

Methods: In 18 patients, visual and cognitive impairment were quantitated and clinical outcome was categorized according to the Rankin scale. Statistical analysis was performed using Fisher's exact test.

Risk factors of moyamoya disease in Canada and the USA.

Over the past 28 years, 39 patients with Moyamoya disease or syndrome defined as spontaneous occlusion of the circle of Willis with extensive basal collateral vessels have been treated by the author in Canada and the USA. All patients presented with clinical or radiologic evidence of hemorrhage (23) or ischemia and infarction (16). A total of 12 patients had associated cerebral aneurysms and seven of these patients with aneurysms presented with subarachnoid hemorrhage.

Giant fusiform intracranial aneurysms: review of 120 patients treated surgically from 1965 to 1992.

The paucity of information about giant fusiform intracranial aneurysms prompted this review of 120 surgically treated patients. Twenty-five aneurysms were located in the anterior and 95 in the posterior circulation. Six patients suffered from atherosclerosis and only three others had a known arteriopathy.

Pseudotumor syndrome resulting from a cerebral arteriovenous malformation: case report.

We report a case of a cerebral arteriovenous malformation presenting as a pseudotumor cerebri syndrome. The lack of mass effect, hemorrhage, or hydrocephalus, in addition to angiographic evidence of high-flow and venous outflow restriction, implicate increased cerebral blood flow and venous hypertension as the mechanism for the papilledema. This case illustrates a pathophysiological mechanism in the development of intracranial hypertension associated with vascular malformations.