• Gustav Schelling.
• Department of Anaesthesiology, Ludwig-Maximilians University, 81377, Munich, Germany. gustav.schelling@med.uni-muenchen.de
• Prog. Brain Res. 2008 Jan 1;167:229-37.

AbstractPost-traumatic stress disorder (PTSD) is a well-recognized complication of severe illness. PTSD has been described in patients after multiple trauma, burns, or myocardial infarction with a particularly high incidence in survivors of acute pulmonary failure (Acute Respiratory Distress Syndrome) or septic shock. Many patients with evidence of PTSD after critical illness have been treated in intensive care units (ICUs). 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. A high number of these traumatic memories from the ICU has been shown to be a significant risk factor for the later development of PTSD in long-term survivors. In addition, patients in the ICU are often treated with stress hormones like epinephrine, norepinephrine, or cortisol. The number of the above-mentioned categories of traumatic memory increased with the totally administered dosages of 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. Conversely, the prolonged administration of beta-adrenergic antagonists during the recovery phase after cardiac surgery resulted in a lower number of traumatic memories and a lower incidence of stress symptoms at 6 months after surgery. Findings with regard to the administration of the stress hormone cortisol were more complex, however. Several studies from our group have demonstrated that the administration of stress doses of cortisol to critically ill patients resulted in a significant reduction of PTSD symptoms measured after recovery without influencing the number of categories of traumatic memory. This can possibly be explained by a cortisol-induced temporary impairment in traumatic memory retrieval that has previously been demonstrated in both rats and humans. ICU therapy of critically ill patients can serve as a stress model that allows the delineation of stress hormone effects on traumatic memory and PTSD development. This could also result in new approaches for prophylaxis and treatment of stress-related disorders.

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