Neurocognitive deficits, including acute confusion and memory impairment, remain important effects of electroconvulsive therapy (ECT). Laboratory and clinical research demonstrates interactions among neurocognitive functioning, the hypothalmic-pituitary-thyroid axis, depressive mood, and ECT. Preclinical studies have demonstrated that exogenous triiodothyronine (T(3)) administered to animals receiving electroconvulsive shock (ECS) protects against ECS-related amnesia and accelerates the "antidepressant effects" of ECS, possibly due to alterations in catecholamine and/or indoleamine neurotransmission. Clinical data suggest that combined treatment with T(3) and ECT results in increased clinical efficacy of ECT and diminished neurocognitive side effects.