Abstract
Superficial temporal arteries (STAs) are abnormally dilated in the painful side during cluster headache (CH) attacks. We have assessed the possible dysfunction of these arteries by comparing in vitro the reactivity of STAs removed from the painful side of CH patients during a cluster of attacks with that of STAs from patients free of CH. The responses to KCl and norepinephrine (NE) of both types of arteries were similar. Serotonin (5HT) induced a classical dose-dependent constriction in arteries from non-CH patients, but systematically triggered rhythmic contractions in arteries from episodic CH patients. Arteries from chronic CH patients also showed spontaneous rhythmic contractions. In both cases, this activity was stopped by calcitonin gene-related peptide (CGRP) but, even in the presence of CGRP, it could be restored by low concentrations of 5HT. Thus, 5HT, unlike NA, can trigger rythmic activity in STAs of CH patients and may play a major role in CH through abnormal smooth muscle cell reactivity.
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