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Glucocorticoid-induced inhibition of memory retrieval: implications for posttraumatic stress disorder

de Quervain, D J F (2006). Glucocorticoid-induced inhibition of memory retrieval: implications for posttraumatic stress disorder. Annals of the New York Academy of Sciences, 1071:216-220.

Abstract

Posttraumatic stress disorder (PTSD) is characterized by traumatic memories that can manifest as daytime recollections, traumatic nightmares, or flashbacks in which components of the event are relieved. These symptoms reflect excessive retrieval of traumatic memories that often retain their vividness and power to evoke distress for decades or even a lifetime. We have reported previously that elevated glucocorticoid levels inhibit memory retrieval in animals and healthy human subjects. We therefore hypothesized that the administration of cortisol might also inhibit the retrieval of traumatic memories in patients with PTSD. In a recent pilot study, we found the first evidence to support this hypothesis. During a 3-month observation period, low-dose cortisol (10 mg/day) was administered orally for 1 month to three patients with chronic PTSD using a double-blind, placebo-controlled, crossover design. In each patient investigated, there was a significant treatment effect with cortisol-related reductions in one of the daily rated symptoms of traumatic memories without causing adverse side effects. Future studies with more patients and longer treatment periods are required to evaluate the efficacy of cortisol treatment for PTSD.

Additional indexing

Item Type:Journal Article, refereed, original work
Communities & Collections:04 Faculty of Medicine > Institute for Regenerative Medicine (IREM)
Dewey Decimal Classification:610 Medicine & health
Scopus Subject Areas:Life Sciences > General Neuroscience
Life Sciences > General Biochemistry, Genetics and Molecular Biology
Social Sciences & Humanities > History and Philosophy of Science
Language:English
Date:2006
Deposited On:06 Sep 2011 07:13
Last Modified:15 Jan 2025 04:49
Publisher:Wiley-Blackwell
ISSN:0077-8923
OA Status:Closed
Publisher DOI:https://doi.org/10.1196/annals.1364.016
PubMed ID:16891572
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