STEWART A. METZ, M.D.; JEFFREY B. HALTER, M.D.; DANIEL PORTE Jr., M.D., F.A.C.P.; R. PAUL ROBERTSON, M.D.
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.
METZ SA, HALTER JB, PORTE D, ROBERTSON RP. Autonomic Epilepsy: Clonidine Blockade of Paroxysmal Catecholamine Release and Flushing. Ann Intern Med. ;88:189–193. doi: 10.7326/0003-4819-88-2-189
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Published: Ann Intern Med. 1978;88(2):189-193.
Neurology, Seizure Disorders.
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