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Hemicranial Disorder of Vasomotor Adrenoceptors in Migraine and Cluster Headache
Author(s) -
Yamamoto Masahiro,
Meyer John Stirling
Publication year - 1980
Publication title -
headache: the journal of head and face pain
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.14
H-Index - 119
eISSN - 1526-4610
pISSN - 0017-8748
DOI - 10.1111/j.1526-4610.1980.hed2006321.x
Subject(s) - medicine , cluster headache , peripheral , migraine , blockade , clonidine , vasomotor , anesthesia , stimulation , propranolol , headaches , surgery , receptor
SYNOPSIS Regional cerebral blood flow (rCBF) and cerebral vasomotor responses to 5% CO 2 inhalation were measured before and after pharmacologic μ‐ or β‐adrenoceptor manipulation in Migraine (M) and Cluster headaches (C). Responses of 77 vascular headache patients (M =66 and C = 11) were compared to those of 15 Muscle contraction headache (MCH) and 64 normal volunteers. Oral drugs were: Peripheral μ‐adrenoceptor stimulator:isometheptene (Midrin(r)), peripheral μ‐blocker:dihydroergotoxin (Hydergine(r)), centrally acting μ‐blocker:clonidine (Catapres(r)), peripheral β‐blocker:propranolol (Inderal(r)), peripheral β‐stimulator:isoproterenol (Isuprel(r)). Peripheral μ stimulation markedly reduced rCBF during headache but effect lessened after headache subsided in M and C. Peripheral μ‐blockade and β‐stimulation increased CBF in M and C. Peripheral β‐blockade markedly decreased CBF during headache in M but caused only small CBF reductions when headache‐free. Peripheral adrenoceptor effects on rCBF in M and C were greatest on most recent headache side. Central effects of clonidine were opposite (greatest on non‐headache side). Excessive CO 2 responses were greatest on side of headache. After peripheral μ‐stimulation, peripheral μ‐blockade, peripheral β‐stimulation or blockade, CO 2 responses were restored toward normal but not after central μ‐blockade. In MCH. contrary to M and C, μ‐stimulation had no effect on CBF or CO 2 responses. There appears to be an asymmetrical adrenoceptor disorder in M and C possibly due to sympathetic denervation‐hypersensitivity.