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Arterial mechanisms in the pathophysiology of migraine headache—implications for modern therapy
Author(s) -
Thomsen L.L.
Publication year - 1995
Publication title -
european journal of neurology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.881
H-Index - 124
eISSN - 1468-1331
pISSN - 1351-5101
DOI - 10.1111/j.1468-1331.1995.tb00149.x
Subject(s) - migraine , medicine , pathophysiology , vasodilation , anesthesia , nitric oxide , headaches , cortical spreading depression , nociception , cerebral blood flow , mechanism (biology) , neuroscience , cardiology , surgery , receptor , psychology , philosophy , epistemology
Studies of the cephalic vascular system have markedly contributed towards an understanding of the mechanisms of migraine pain. Whereas cerebral blood flow changes, and thereby changes in the arterioles, correlate poorly with migraine headache, abnormal regulation of the large cranial arteries seems to play a significant role in relation to migraine pain. Thus, vasodilation of extra‐ and intracranial conductance arteries has been described both during spontaneous migraine attacks and during experimentally provoked vascular headaches. Whether dilation of these arteries is the key mechanism of migraine nociception or is merely associated with another more important nociceptive mechanism remains to be shown. Studies of vascular regulatory mechanisms have not only pointed towards a possible locus of migraine pain, but have also been helpful in demonstrating a new molecular mechanism of migraine—the key effect of the small messenger molecule nitric oxide. It is likely that nitric oxide is the most important molecule responsible for the induction of migraine attacks.