Effects of stress hormones on traumatic memory formation and the development of posttraumatic stress disorder in critically ill patients - PubMed

Affiliations

• PMID: 12559838
• DOI: 10.1006/nlme.2002.4083

Effects of stress hormones on traumatic memory formation and the development of posttraumatic stress disorder in critically ill patients

Gustav Schelling. Neurobiol Learn Mem. 2002 Nov.

Abstract

A majority of patients after intensive care treatment report traumatic memories from their stay in the intensive care unit (ICU). Traumatic memories can be associated with the development of posttraumatic stress disorder (PTSD) in a subpopulation of these patients. In contrast to other patient populations at risk for PTSD, patients in the ICU often receive exogenously administered stress hormones like epinephrine, norepinephrine, or cortisol for medical reasons and are extensively monitored. ICU patients therefore represent a suitable population for studying the relationship between stress hormones, traumatic memories, and the development of PTSD. Studies in long-term survivors of ICU treatment demonstrated a clear and vivid recall of different categories of traumatic memory such as nightmares, anxiety, respiratory distress, or pain with little or no recall of factual events. The number of categories of traumatic memory recalled increased with the total administered dosages of stress hormones (both catecholamines and cortisol), and the evaluation of these categories at different time points after discharge from the ICU showed better memory consolidation with higher dosages of stress hormones administered. However, the administration of stress doses of cortisol to critically ill patients resulted in more complex findings as it caused a significant reduction in PTSD symptoms measured after recovery. This effect can possibly be explained by a differential influence of cortisol on memory. Increased serum cortisol levels not only result in consolidation of emotional memory but are also known to cause a temporary impairment in memory retrieval which appears to be independent of glucocorticoid effects on memory formation. Disrupting retrieval mechanisms with glucocorticoids during critical illness may therefore act protectively against the development of PTSD by preventing recall of traumatic memories. Our findings indicate that stress hormones influence the development of PTSD through complex and simultaneous interactions on memory formation and retrieval. Our studies also demonstrate that animal models of aversive learning are useful in analyzing and predicting clinical findings in critically ill humans.

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