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Related Experiment Videos

Cortisol insufficiency caused by electroconvulsive therapy? A case report.

M Thorén, S Werner

    Acta Medica Scandinavica
    |January 1, 1986
    PubMed
    Summary

    Electroconvulsive therapy (ECT) may trigger cortisol deficiency by affecting central nervous system regulation of ACTH secretion, leading to symptoms of adrenal insufficiency. This case highlights a potential long-term endocrine complication of ECT.

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    Area of Science:

    • Neuroendocrinology
    • Psychiatry

    Background:

    • A patient with a personality disorder and depressive symptoms underwent electroconvulsive therapy (ECT).
    • ECT is a recognized treatment for severe depression and certain psychiatric disorders.

    Observation:

    • Following ECT, the patient developed anisocoria, followed by syncope, vertigo, anorexia, and weight loss.
    • These symptoms resolved with corticosteroid administration (cortisone acetate and fluorocortisone).

    Findings:

    • The patient exhibited persistent cortisol deficiency, evidenced by low plasma ACTH, cortisol, and urinary cortisol levels.
    • Hormonal responses to ACTH stimulation and hypoglycemia were normal, suggesting a central regulatory defect.
    • Cortisol deficiency recurred upon attempts to reduce or withdraw corticosteroids, indicating a chronic condition.

    Implications:

    • The findings suggest that ECT may induce or unmask a defect in the central regulation of adrenocorticotropic hormone (ACTH) secretion.
    • This neuroendocrine dysfunction, potentially involving the hypothalamic-pituitary-adrenal (HPA) axis, may be a rare complication of ECT.
    • Further research is warranted to elucidate the mechanisms and prevalence of ECT-induced HPA axis dysregulation.

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