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Abstract
PATIENTS with hypertension and patients with cerebral arteriosclerosis frequently suffer from recurrent, transient episodes of dizziness, weakness of an extremity or aphasia that suggest focal cerebral anoxemia. The ephemeral nature of many of the attacks and the absence of residual signs or symptoms have been attributed in the past to cerebrovascular spasm. In recent years this explanation has been challenged1 on the grounds that cerebral vessels are not structurally adapted for marked constriction; that cervical sympathetic stimulation constricts pial vessels infinitely less than those of the skin2; and that this unproved functional mechanism need not be postulated to explain . . .
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