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JOURNAL ARTICLE
REVIEW
Advances in understanding the pathophysiology of headache.
Neurology 1992 March
Recent evidence suggests that migraine may not be due to vasoconstriction followed by reactive vasodilation, and tension-type headache may not be due to excess muscle contraction. The prodromes of migraine may have a hypothalamic origin, and the aura and changes in cognition may have a cortical neuronal origin. The pain of migraine and tension-type headache may be generated centrally or enhanced or generated by neurogenic inflammation. Drugs used to treat headache frequently interact with serotonin receptor subtypes: abortive drugs at the 5-HT1 receptor and preventive drugs at the 5-HT2 receptor.
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