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Glucocorticoid-induced reduction of traumatic memories: implications for the treatment of PTSD


de Quervain, D J F (2007). Glucocorticoid-induced reduction of traumatic memories: implications for the treatment of PTSD. Progress in Brain Research, 167:239-247.

Abstract

Post-traumatic stress disorder (PTSD) is an anxiety disorder that can occur after a traumatic event such as military combat, terrorist attacks, or accidents. The disorder is characterized by traumatic memories that manifest as reexperiencing symptoms including daytime recollections, traumatic nightmares, or flashbacks in which components of the event are relived. These symptoms result from 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 per 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. Furthermore, we have reported evidence for a prolonged effect of the cortisol treatment. Persistent retrieval and reconsolidation of traumatic memories is a process that keeps these memories vivid and thereby the disorder alive. By inhibiting memory retrieval, cortisol may weaken the traumatic memory trace and thus reduce symptoms even beyond the treatment period. Future studies with more patients and longer treatment periods are required to evaluate the efficacy of cortisol treatment for PTSD.

Abstract

Post-traumatic stress disorder (PTSD) is an anxiety disorder that can occur after a traumatic event such as military combat, terrorist attacks, or accidents. The disorder is characterized by traumatic memories that manifest as reexperiencing symptoms including daytime recollections, traumatic nightmares, or flashbacks in which components of the event are relived. These symptoms result from 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 per 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. Furthermore, we have reported evidence for a prolonged effect of the cortisol treatment. Persistent retrieval and reconsolidation of traumatic memories is a process that keeps these memories vivid and thereby the disorder alive. By inhibiting memory retrieval, cortisol may weaken the traumatic memory trace and thus reduce symptoms even beyond the treatment period. Future studies with more patients and longer treatment periods are required to evaluate the efficacy of cortisol treatment for PTSD.

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36 citations in Scopus®
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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
Language:English
Date:22 November 2007
Deposited On:29 Dec 2008 20:56
Last Modified:16 Aug 2016 10:14
Publisher:Elsevier
ISSN:0079-6123
Publisher DOI:https://doi.org/10.1016/S0079-6123(07)67017-4
PubMed ID:18037019

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