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Advances in understanding the pathophysiology of headache.

Abstract
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.
AuthorsS D Silberstein
JournalNeurology (Neurology) Vol. 42 Issue 3 Suppl 2 Pg. 6-10 (Mar 1992) ISSN: 0028-3878 [Print] United States
PMID1557193 (Publication Type: Journal Article, Review)
Chemical References
  • Serotonin
Topics
  • Headache (physiopathology)
  • Humans
  • Migraine Disorders (drug therapy, physiopathology)
  • Serotonin (physiology)
  • Vascular Headaches (physiopathology)

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