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Arthur Ecker, MD, PhD
603 Crawford Ave Syracuse, NY 13224

Arch Neurol. 1990;47(9):951.

	Since this article does not have an abstract, we have provided the first 150 words of the full text PDF and any section headings.

To the Editor.

—In his reminiscence, Treatment of Aneurysmal Subarachnoid Hemorrhage, Aring¹ mentions the demonstration of vasospasm in the arteriogram after such hemorrhage.² Since then it has been suggested that such vasospasm may precede and contribute to the development of cerebral arterial aneurysms.^3,4

Most neurosurgeons consider that cerebral ischemia from vasospasm is the major cause of morbidity and mortality in patients with subarachnoid hemorrhage following rupture of a cerebral arterial aneurysm.^5,6 Yet Aring¹ quotes Slosberg⁶ that vasospasm is not a factor in his extensive experience. Slosberg's⁶ management includes prolonged lowering of the patient's blood pressure. Could this program not only prevent secondary hemorrhage but also overcome vasospasm?

However, with another regimen, Heros and coworkers⁷ found that hypotension may precipitate clinical symptoms in a patient who otherwise might have had asymptomatic vasospasm. . . . [Full Text PDF of this Article]

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