This work was supported by USPHS Grant NS09287.
Hemicranial Disorder of Vasomotor Adrenoceptors in Migraine and Cluster Headache
Version of Record online: 22 JUN 2005
Headache: The Journal of Head and Face Pain
Volume 20, Issue 6, pages 321–335, November 1980
How to Cite
Yamamoto, M. and Meyer, J. S. (1980), Hemicranial Disorder of Vasomotor Adrenoceptors in Migraine and Cluster Headache. Headache: The Journal of Head and Face Pain, 20: 321–335. doi: 10.1111/j.1526-4610.1980.hed2006321.x
- Issue online: 22 JUN 2005
- Version of Record online: 22 JUN 2005
- Accepted for Publication: March 11, 1980
- Cited By
Regional cerebral blood flow (rCBF) and cerebral vasomotor responses to 5% CO2 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 CO2 responses were greatest on side of headache. After peripheral μ-stimulation, peripheral μ-blockade, peripheral β-stimulation or blockade, CO2 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 CO2 responses. There appears to be an asymmetrical adrenoceptor disorder in M and C possibly due to sympathetic denervation-hypersensitivity.