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Acetylcholinesterase Activity in Patients With Torsion DystoniaMeasurement in Erythrocyte Membranes
William A. Maltese, PhD;
Susan Bressman, MD;
Stanley Fahn, MD;
Darryl C. De Vivo, MD
Arch Neurol. 1985;42(2):154-155.
Abstract
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• Anticholinergic therapy provides symptomatic relief in many patients with dystonia. The mechanism underlying this therapeutic action is poorly understood; however, one possibility is that the degradation of acetylcholine is perturbed in these conditions. To investigate this possibility, acetylcholinesterase activity was measured in erythrocyte membranes from healthy volunteers and patients with torsion dystonia. Enzyme activities in erythrocytes from 14 patients with adult-onset, childhood-onset idiopathic, and childhood-onset familial dystonias did not differ significantly from activities measured in erythrocyte membranes from 17 healthy volunteers. Moreover, when blood samples from several members of a family with dominant inheritance of dystonia were assayed simultaneously, similar enzyme activities were found in the affected and unaffected individuals. The data suggest that a generalized acetylcholinesterase deficiency is not involved in the pathogenesis of torsion dystonia.
Author Affiliations
From the Pediatric Neurology Divisional Laboratories and the Dystonia Clinical Research Center, Department of Neurology, College of Physicians and Surgeons of Columbia University, New York (Drs Maltese, Bressman, Fahn, and De Vivo); and the New York State Psychiatric Institute, New York (Drs Maltese and De Vivo).
Footnotes
Accepted for publication April 5, 1984.
Reprint requests to Division of Pediatric Neurology, Department of Neurology, College of Physicians and Surgeons of Columbia University, 710 W 168th St, New York, NY 10032 (Dr Maltese).
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