Acetylcholinesterase activity in patients with torsion dystonia. Measurement in erythrocyte membranes
W. A. Maltese, S. Bressman, S. Fahn and D. C. De Vivo
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.