In spite of the many clues which point to dilatation of extracranial or intracranial arteries as essential in the mechanism of migraine headache, the immediate cause of the vasodilatation has not yet been defined.1 This report examines the hypothesis that acetylcholine may be the chemical agent responsible for the relaxation of the arterial wall.
Incentives to search for acetylcholine are certain accessory symptoms and signs which accompany migraine headache in some patients. These clues, often so trivial as to be overlooked, suggest a centrally integrated neural discharge over parasympathetic pathways. Commonest are nasal congestion and excessive lacrimation, probably resulting from impulses over the greater superficial petrosal branch of the facial nerve. Rare, but no less significant, are miosis, more marked on the side of the pain when the headache is unilateral, and bradycardia, presumably mediated by the oculomotor and vagus nerves, respectively. An alternative interpretation, that many of these
KUNKLE EC. Acetylcholine in the Mechanism of Headaches of Migraine Type. AMA Arch NeurPsych. 1959;81(2):135–141. doi:10.1001/archneurpsyc.1959.02340140001001
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