The role of slow wave sleep in memory pathophysiology: Focus on post-traumatic stress disorder and eye movement desensitization and reprocessing
Description
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 et al. (1997); Van Der Kolk (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 causes 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 transfered to the cortical areas, where a further processing and integration into already existing networks should take place. [Excerpt]
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 et al. (1997); Van Der Kolk (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 causes 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 transfered to the cortical areas, where a further processing and integration into already existing networks should take place. [Excerpt]
Format
Journal
Language
English
Original Work Citation
Carletto, S., Borsato, T., & Pagani, M. (2017, November). The role of slow wave sleep in memory pathophysiology: Focus on post-traumatic stress disorder and eye movement desensitization and reprocessing. Frontiers in Psychology, 22(8), 2250. doi:10.3389/fpsyg.2017.02050
Citation
“The role of slow wave sleep in memory pathophysiology: Focus on post-traumatic stress disorder and eye movement desensitization and reprocessing,” Francine Shapiro Library, accessed May 10, 2024, https://francineshapirolibrary.omeka.net/items/show/24708.