Electroconvulsive Therapy and the Long-Term Risk of Dementia: Conceptual Issues, Methodological Issues, and Recent...

Electroconvulsive therapy (ECT) induces changes in brain functioning. It requires a generalized seizure to be effective and is associated with anterograde and retrograde amnestic deficits that are mostly mild and short-lasting. For these and other reasons, the treatment has been claimed to cause brain damage and has fueled the consequent question of whether it increases the long-term risk of dementia. The question related to dementia risk is important because ECT-treated cohorts tend to be older rather than younger. This article examines conceptual issues, methodological issues, and findings related to the long-term risk of dementia in patients treated with ECT. In summary, ECT-associated amnestic deficits bear no resemblance to the chronic, deteriorating, global impairment that characterizes dementia. There is no evidence that ECT is associated with macroscopic, microscopic, or biomarker indices of brain injury. ECT is not associated with cortical atrophy, medial temporal lobe atrophy, white matter changes, or cerebral microbleeds. Rather, ECT increases neuroplasticity; there is a dose-dependent increase in neurogenesis, dendritic arborization, and new synapse formation in the hippocampus. ECT also increases rather than decreases hippocampal volume in depressed patients. As a further consideration, because ECT is an effective treatment, it may favorably modify illness-magnified lifestyle risk factors for dementia. With this background, 4 cohort studies published in the last decade (ECT total, 8,994 patients; control total, 277,871 patients) examined the risk of dementia in ECT-treated patients. These studies had an average of 5-25 years of follow-up, modestly adjusted for confounding, including confounding by indication and confounding by severity of indication, as well as considered death as a competing risk. No study found evidence that ECT was associated with an increased risk of dementia.