RESUMO
Electroconvulsive therapy (ECT) is an efficacious treatment for a variety of neuropsychiatric conditions including major depression, mania, catatonia, Parkinson's disease, and neuroleptic malignant syndrome. However, ECT-induced memory dysfunction complicates the treatment and is a major concern for both patients and providers. We briefly review ECT-induced memory dysfunction and propose a glutamatergic model for it. (Articles examined were retrieved by a Medline search on the terms electroconvulsion and glutamate, with language limited to English.) Specifically, we hypothesize that ECT-induced memory dysfunction results from neuronal insults due to excessive release of excitatory amino acids and activation of their receptors, which produce cation and water flux and reversible oxidative stress. This model offers multiple testable hypotheses; exploring them may help to identify the risk factors for this significant side effect of ECT treatment and may thus yield effective agents for its prevention and treatment.
Assuntos
Eletroconvulsoterapia/efeitos adversos , Transtornos da Memória/etiologia , Receptores de Glutamato/fisiologia , Antagonistas de Aminoácidos Excitatórios/farmacologia , Humanos , Modelos Neurológicos , N-Metilaspartato/farmacologia , Receptores de Glutamato/efeitos dos fármacos , Convulsões/fisiopatologiaRESUMO
This article is third in a series of three articles addressing credentialing to appear in AAOHN Journal. The first article, "Credentialing: Concerns and Issues Affecting Occupational Health Nursing," by Olson, Verrall, and Lundvall, appeared in the May 1997 issue [45(5):231-238]. The second article, "Certification and Occupational Health Nursing: An Historical Perspective," by Verrall appeared in the June 1997 issue [45(6):283-289].