Sleep and REM sleep disturbance in the pathophysiology of PTSD: the role of extinction memory
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CitationPace-Schott, Edward F., Anne Germain, and Mohammed R. Milad. 2015. “Sleep and REM sleep disturbance in the pathophysiology of PTSD: the role of extinction memory.” Biology of Mood & Anxiety Disorders 5 (1): 3. doi:10.1186/s13587-015-0018-9. http://dx.doi.org/10.1186/s13587-015-0018-9.
AbstractPost-traumatic stress disorder (PTSD) is accompanied by disturbed sleep and an impaired ability to learn and remember extinction of conditioned fear. Following a traumatic event, the full spectrum of PTSD symptoms typically requires several months to develop. During this time, sleep disturbances such as insomnia, nightmares, and fragmented rapid eye movement sleep predict later development of PTSD symptoms. Only a minority of individuals exposed to trauma go on to develop PTSD. We hypothesize that sleep disturbance resulting from an acute trauma, or predating the traumatic experience, may contribute to the etiology of PTSD. Because symptoms can worsen over time, we suggest that continued sleep disturbances can also maintain and exacerbate PTSD. Sleep disturbance may result in failure of extinction memory to persist and generalize, and we suggest that this constitutes one, non-exclusive mechanism by which poor sleep contributes to the development and perpetuation of PTSD. Also reviewed are neuroendocrine systems that show abnormalities in PTSD, and in which stress responses and sleep disturbance potentially produce synergistic effects that interfere with extinction learning and memory. Preliminary evidence that insomnia alone can disrupt sleep-dependent emotional processes including consolidation of extinction memory is also discussed. We suggest that optimizing sleep quality following trauma, and even strategically timing sleep to strengthen extinction memories therapeutically instantiated during exposure therapy, may allow sleep itself to be recruited in the treatment of PTSD and other trauma and stress-related disorders.
Citable link to this pagehttp://nrs.harvard.edu/urn-3:HUL.InstRepos:17295758
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