Aspects on the pathophysiology of migraine and cluster headache.
The specific cause of migraine headache remains unknown. Current theories suggest that the initiation of a migraine attack involves a primary CNS dysfunction with subsequent activation of the trigeminovascular system. Studies in patients have revealed a clear association between headache and the release of the neuropeptide calcitonin gene-related peptide, probably from C fibres. In cluster headache and in a case of chronic paroxysmal headache there was in addition release of the parasympathetic neuropeptide vasoactive intestinal peptide, which was associated with headache, nasal congestion and rhinorrhea. Triptan administration, activating the 5-HT(1B/1D) receptors, caused the headache to subside and the neuropeptide release to normalise. These data suggest the involvement of sensory and parasympathetic mechanisms in the pathophysiology of primary headaches.[1]References
- Aspects on the pathophysiology of migraine and cluster headache. Edvinsson, L. Pharmacol. Toxicol. (2001) [Pubmed]
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