Pharmacological attenuation of electroconvulsive therapy--induced cognitive deficits: theoretical background and clinical findings.

Electroconvulsive therapy (ECT) is an effective treatment for depression and other psychiatric disorders. However, the practice of ECT is limited by memory and nonmemory cognitive adverse effects. Technical strategies such as a preference for unilateralover bilateral ECT and low-dose over high-dose stimulation reduce these cognitive adverse effects but may also be associated with lesser treatment efficacy or slower treatment response. This article therefore reviews the use of psychopharmacological agents in the attenuation of ECT-induced cognitive deficits with 2 objectives: the identification of implicated mechanisms and the identification of putative efficacy in both animal and human studies. Drugs examined include N-methyl-d-aspartate receptor antagonists, cyclooxygenase inhibitors, calcium channel blockers, cholinesterase inhibitors, glucocorticoid receptor antagonists, thyroid hormones, opioid antagonists, NO donors, nootropic agents, and other medications. Although the clinical data at present are sparse and inconsistent, many recently opened lines of research improve our understanding of the mechanisms involved as well as suggest possible avenues for the testing of new treatments with the potential to attenuate the cognitive adverse effects of ECT.