On the pathogenesis of headache following TIA

Twelve out of 49 patients with single or multiple transient ischemic attacks (TIAs) had TIA-related headaches, mostly in close temporal relation to the ischemic onset. Headache predominated in patients taking vasodilators when TIA occurred or with orthostatic hypotension at the first clinical examination, but atrial hypertension or a personal history of migraine were not more frequent in patients with headache. The site of the pain did not correlate with the presumed territory of cerebral ischemia. Pain during TIA is conceivably due to an interaction between cerebral vessels and the surrounding nervous system. Blood vessels have a sturdy physiological role concerning blood flow regulation, with receptors and signaling molecules potentially involved with pain production. Reflex mechanisms should justify pain in other areas.