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.
Edvinsson
L
L
Department of Internal Medicine, Lund University Hospital, S-221 85 Lund, Sweden. lars.edvinsson@med.lu.se
D001341:Autonomic Nervous System / Q000503:physiopathology; D015740:Calcitonin Gene-Related Peptide / Q000378:metabolism; D002490:Central Nervous System / Q000098:blood supply / Q000503:physiopathology; D003027:Cluster Headache / Q000378:metabolism / Q000503:physiopathology*; D006801:Humans; D008881:Migraine Disorders / Q000188:drug therapy / Q000378:metabolism / Q000503:physiopathology*; D018377:Neurotransmitter Agents / Q000378:metabolism; D012702:Serotonin Antagonists / Q000627:therapeutic use; D014660:Vasoactive Intestinal Peptide / Q000378:metabolism
D018377:Neurotransmitter Agents; D012702:Serotonin Antagonists; D014660:Vasoactive Intestinal Peptide; D015740:Calcitonin Gene-Related Peptide