Prolonged apnea during electroconvulsive therapy in monozygotic twins: case reports

Electroconvulsive therapy (ECT) is considered to be the most powerful antidepressant intervention, and is thus recommended for the treatment of severe pharmacorefractory major depressive disorder (MDD) according to international guidelines. Moreover, ECT is usually well tolerated and the potential risks are mainly limited to anesthesia [1]. With regard to muscle relaxation during ECT, several reports of prolonged apnea due to the extended action of depolarizing neuromuscular blocking agents have been published of late [2-5].Reduction of butyrylcholinesterase (BCHE) activity, as first described by German physician W Karow [6,7], can be induced by several somatic diseases, drugs such as acetylcholinesterase inhibitors, steroids, some antidepressants, oral contraceptives and organophosphate poisoning [4,8,9]. Also, inherited forms of BCHE deficiency are known [7], and affect up to 25% of the Caucasian population [5]. Mutations of the butyrylcholinesterase gene (BCHE; 3q26.1-3q26.2, OMIM 177400) were suspected in patients who experienced prolonged apnea after application of several neuromuscular blocking agents. The most common A (Asp70Gly) and K (Ala536Thr) variants were recently detected in patients with prolonged apnea during ECT [5].Here, we report two cases of monozygotic twins, who both underwent ECT because of treatment-refractory severe major depressive episodes. Both patients showed prolonged apnea during anesthesia.A 55-year-old, married male clerk was admitted for ECT in December 2006 because of medication-resistant psychotic depression according to Diagnostic and Statistical Manual of Mental Disorders, fourth edition (DSM-IV) criteria. After antidepressant medication was tapered off, ECT was delivered three times a week. Right unilateral (RUL) stimulation was administered using a Thymatron IV ECT apparatus (Somatics Inc., Lake Buff, IL, USA). During the first ECT, general anesthesia was carried out with thiopental; for muscle relaxation succinylcholine was g