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Autonomic Epilepsy: Clonidine Blockade of Paroxysmal Catecholamine Release and Flushing
- STEWART A. METZ, M.D.;
- JEFFREY B. HALTER, M.D.;
- DANIEL PORTE, Jr., M.D., F.A.C.P.; and
- R. PAUL ROBERTSON, M.D.
Abstract
We studied a 59-year-old man with transient paroxysms of hypertension, tachycardia, and flushing in whom pheochromocytoma was excluded. Although catecholamine excretion was normal, plasma catecholamine levels rose from normal basal levels (282 ±14 pg/ml) to increased levels (585 ±67 pg/ml; ∓ SEM; n= 4) at the peak of spells. Other hormones or substrates expected to rise with nonspecific "stress" did not increase after paroxysms. Therapy with Clonidine (0.2 to 0.4 mg/day) suppressed basal catecholamines to undetectable levels and markedly reduced peak levels during spells (80 pg/ml). An epileptic pathogenesis was suggested by stereotypic olfactory and epigastric prodromata before spells, and abolition of paroxysms with the anticonvulsant carbamazepine. This patient represents a rare case of autonomic epilepsy with the seizure focus in the temporal lobe.
Article and Author Information
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▸From the Division of Endocrinology and Metabolism, Seattle Veterans Administration Hospital; and the Department of Medicine, University of Washington; Seattle, Washington.
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Grant support: in part by U.S. Veterans Administration Research Education Program (MRIS Nos. 7511 and 7155) and U.S. Public Health Service Research Grant AM 12829.
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▸Requests for reprints should be addressed to Stewart A. Metz, M.D.; Veterans Administration Hospital; 4435 Beacon Avenue South; Seattle, WA 98108.
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- Received June 20, 1977.
- Accepted November 10, 1977.
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