The Role of Slow Wave Sleep in Memory Pathophysiology: Focus on Post-Traumatic Stress Disorder and Eye Movement Desensitization and Reprocessing.

Post-traumatic stress disorder (PTSD) is a clinical condition that may develop after a person experienced a traumatic event. PTSD can be considered as a disorder in which a fear conditioned response fails to extinguish, leading to several symptoms such as re-experiencing of the traumatic moment with intrusive thoughts, flashbacks and nightmares, avoidance of situations related to the trauma, negative alterations in cognitions and mood, and hyper-arousal. One important feature of PTSD is the re-experiencing of specific aspects of the traumatic memory. This aspect is related to the fact that, as originally suggested by Van der Kolk (1997; 1998), traumatic memories are encoded differently than memories of ordinary events, including several multisensory fragments that cannot be integrated in a structured meaningful narrative. At a neurobiological level, memories recorded during extreme stressful situations cause a maximal potentiation of amygdalar synapses, assumed to temporarily store the events. This cause the saturation of all amygdalar alpha-amino-3-hydroxy-5-methyl-4-isoxazole (AMPA) receptors-bindings sites, preventing the recorded emotional memory trace to be merged with the cognitive memory trace from the hippocampus (Corrigan, 2002; Harper et al., 2009). Therefore, the fragments of emotionally charged memories remain trapped in the limbic system and cannot be transfer to the cortical areas, where a further processing and integration into already existing networks should take place.