Abstract

Pathophysiological mechanisms of primary headache remain obscure, despite of numerous hypotheses that have been postulated for either migraine and cluster headache. Human experimental models are not available, however, observation of clinical features of migraine or cluster headache attacks support animal studies documenting the development of neurogenic inflammation in tissues receiving trigeminal innervation. The latter studies provided also the background for better understanding the mechanism of action of aborting drugs such as sumatriptan and dihydroergotamine. The debate is whether the primary cause of migraine and other neurovascular headaches is central or peripheral in origin. Trigger factors (stressful events) and personality traits in migraine patients suggest that activation of neurovascular systems is secondary to more complex events taking place in the central nervous system.

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