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Home > Public Resources > Trauma Blog > 2016 - December > Can sleep enhance the benefits of exposure treatment for posttraumatic stress disorder?

Can sleep enhance the benefits of exposure treatment for posttraumatic stress disorder?

Ihori Kobayashi, PhD & Thomas Mellman, MD

December 9, 2016

People often say “sleep on it” before making an important decision anticipating that sleep will help them sort through their thoughts and memories, add perspective, thereby leading to a better decision. Can this conventional wisdom be applied to treatment of posttraumatic stress disorder (PTSD)? We addressed this question with a novel approach.
 
Sleep has been found to enhance memory processes that are thought to underlie recovery from PTSD such as fear extinction memory (i.e., a newly formed memory of a stimulus that was associated with a fearful stimulus is no longer associated with the fearful stimulus) and its retention and generalization (Pace-Schott, Germain, & Milad, 2015). In addition, there is evidence that rapid-eye-movement (REM) sleep promotes the integration of new information into preexisting semantic networks (Cai, Mednick, Harrison, Kanady, & Mednick, 2009). Such processes appear similar to the adaptive integration of new information into trauma memories that is considered critical to recovery from PTSD (Foa, Hembree, & Rothbaum, 2007). The importance of healthy sleep in preventing and recovering from PTSD has also been suggested by observations of people in close temporal proximity to their trauma experience and over the course of treatment (Bryant, Creamer, O’Donnell, Silove, & McFarlane, 2010; Koren, Arnon, Lavie, & Klein, 2002; Lommen et al., 2015). Pace-Schott and colleagues (2015) suggested improving sleep quality and optimizing the timing of sleep in relation to therapy sessions as potential strategies to enhance benefits of exposure-based treatment.
 
In addition to sleep quality and timing, sleep stages appear to have specific roles in processing trauma memories. REM sleep has been implicated in emotional memory learning (Fu et al., 2007; Wagner, Gais, & Born, 2001). The greater frequency of eye movements during REM sleep was associated with worse response to interpersonal therapy for depression (Buysse, Kupfer, Frank, Monk, & Ritenour, 1992). A recent study showed that slow-wave sleep (SWS, deepest sleep stage) also has a role in processing emotional memory that is synergistic with the role of REM sleep (Cairney, Durrant, Power, & Lewis, 2015).
 
The prior human studies examining roles of sleep in emotional memory processing featured healthy volunteers and relied on disturbing but not PTSD-inducing stimuli from narratives or film clips (Kuriyama, Soshi, & Kim, 2010; Porcheret, Holmes, Goodwin, Foster, & Wulff, 2015; Wagner et al., 2001). We recruited people experiencing significant PTSD symptoms and used written narrative exposure (WNE) as a probe of trauma memory processing. WNE is an established intervention and is considered to bring about therapeutic benefits through adaptive restructuring of trauma narratives (Smyth, 1998).
 
We evaluated the role of sleep timing in emotional memory processing and examined relationships between sleep characteristics and PTSD symptom reduction. Participants were randomly assigned to complete either two 30-minute WNE sessions at 8 PM and 8 AM with intervening sleep, or 8 AM and 8 PM with intervening wake. Participants were assigned to the alternative condition one week later. Each participant wrote in as much detail as possible about their most traumatic experience and provided ratings on his or her distress level at the beginning of WNE and every 10 minutes. PTSD symptom severity was measured through clinical interviews at baseline, one week after the 2nd WNE, and one week after the last WNE. Sleep was recorded using polysomnography at baseline and after the 8 PM sessions.
 
Twenty nine community-recruited adults with full or subthreshold (n = 2) PTSD completed the first two WNE sessions, and 21 completed all sessions. The maximum distress level decreased from the 1st to 2nd session, and PTSD symptoms also significantly decreased from the baseline to the follow-up. However, timing of sleep did not influence the reduction in distress or PTSD symptoms. After the evening WNE session, participants slept more than at baseline (320 vs. 386 minutes) and had more frequent eye movements during REM sleep (1.17/minutes vs. 2.11/minutes). Slow wave sleep (N3) decreased after the evening WNE (35% vs. 26%). Reduction of deep sleep as well as increase in eye movement density (Sanford, Morrison, Ball, Ross, & Mann, 1993) can indicate elevated arousal, and both of these trends for sleep induced by WNE were associated with less improvement of PTSD symptoms.
 
To the relief of some our findings do not support that clinicians should start scheduling therapy sessions in the late evening. Our findings do suggest that preserving diminished arousal during sleep could facilitate emotional processing. Further research examining the effect of maintaining diminished arousal during sleep with behavioral or/and pharmacological approaches on outcomes of exposure-based treatment would be of interest.
 

Reference Article

Kobayashi, I.,* Mellman, T.A.,* Altaee, D., Howell, M.K., & Lavela, J. (2016). Sleep and processing trauma memories. Journal of Traumatic Stress. * IK and TAM contributed equally to the manuscript.
 

Author Biographies

Ihori Kobayashi, Ph.D. is a Research Assistant Professor at Howard University, Department of Psychiatry and Behavioral Sciences and a KL2 Scholar at the Georgetown-Howard Universities Center for Clinical and Translational Science. Her research focuses on sleep in PTSD, pharmacological augmentation of behavioral intervention for PTSD, and animal models of sex differences in sleep and PTSD.
 
Thomas A. Mellman, M.D. is Professor of Psychiatry and Director of the Sleep and Stress Research Program and Clinical Translational Research Center at Howard University College of Medicine. His interests include sleep aspects of PTSD and the role of sleep in the effects of stress on physical and emotional health. 
 

Discussion Questions

  1. What behavioral or pharmacological approaches could be used to maintaining diminished arousal during sleep to enhance the benefits of exposure-based treatment?
  2. What are unique challenges in diminishing arousal during sleep in people with PTSD and how those challenges can be overcome?

References

Bryant, R. A., Creamer, M., O’Donnell, M., Silove, D., & McFarlane, A. C. (2010). Sleep disturbance immediately prior to trauma predicts subsequent psychiatric disorder. Sleep, 33(1), 69-74.

Buysse, D. J., Kupfer, D. J., Frank, E., Monk, T. H., & Ritenour, A. (1992). Electroencephalographic sleep studies in depressed outpatients treated with interpersonal psychotherapy: II. longitudinal studies at baseline and recovery. Psychiatry Research, 42(1), 27-40. doi:http://dx.doi.org/10.1016/0165-1781(92)90036-3

Cai, D. J., Mednick, S. A., Harrison, E. M., Kanady, J. C., & Mednick, S. C. (2009). REM, not incubation, improves creativity by priming associative networks. Proceedings of the National Academy of Sciences, 106(25), 10130-10134. doi:10.1073/pnas.0900271106

Cairney, S. A., Durrant, S. J., Power, R., & Lewis, P. A. (2015). Complementary roles of slow-wave sleep and rapid eye movement sleep in emotional memory consolidation. Cerebral Cortex, 25(6), 1565-1575. doi:10.1093/cercor/bht349

Foa, E., Hembree, E., & Rothbaum, B. O. (2007). Prolonged exposure therapy for PTSD: Emotional processing of traumatic experiences therapist guide. New York: Oxford University Press.

Fu, J., Li, P., Ouyang, X., Gu, C., Song, Z., Gao, J., . . . Hu, B. (2007). Rapid eye movement sleep deprivation selectively impairs recall of fear extinction in hippocampus-independent tasks in rats. Neuroscience, 144(4), 1186-1192. doi:10.1016/j.neuroscience.2006.10.050

Koren, D., Arnon, I., Lavie, P., & Klein, E. (2002). Sleep complaints as early predictors of posttraumatic stress disorder: A 1-year prospective study of injured survivors of motor vehicle accidents. American Journal of Psychiatry, 159(5), 855-857. doi:10.1176/appi.ajp.159.5.855

Kuriyama, K., Soshi, T., & Kim, Y. (2010). Sleep deprivation facilitates extinction of implicit fear generalization and physiological response to fear. Biological Psychiatry, 68(11), 991-998. doi:DOI: 10.1016/j.biopsych.2010.08.015

Lommen, M. J. J., Grey, N., Clark, D. M., Wild, J., Stott, R., & Ehlers, A. (2015). Sleep and treatment outcome in posttraumatic stress disorder: Results from an effectiveness study. Depression and Anxiety, doi:10.1002/da.22420

Pace-Schott, E., Germain, A., & Milad, M. R. (2015). Effects of sleep on memory for conditioned fear and fear extinction. Psychological Bulletin, 141(4), 835-857. doi:10.1037/bul0000014

Porcheret, K., Holmes, E. A., Goodwin, G. M., Foster, R. G., & Wulff, K. (2015). Psychological effect of an analogue traumatic event reduced by sleep deprivation. Sleep, 38(7), 1017-1025. doi:10.5665/sleep.4802

Sanford, L. D., Morrison, A. R., Ball, W. A., Ross, R. J., & Mann, G. L. (1993). The amplitude of elicited PGO waves: A correlate of orienting. Electroencephalography and Clinical Neurophysiology, 86(6), 438-445.

Smyth, J. M. (1998). Written emotional expression: Effect sizes, outcome types, and moderating variables. Journal of Consulting and Clinical Psychology, 66(1), 174-184. doi:10.1037/0022-006X.66.1.174

Wagner, U., Gais, S., & Born, J. (2001). Emotional memory formation is enhanced across sleep intervals with high amounts of rapid eye movement sleep. Learning & Memory, 8(2), 112-119. doi:10.1101/lm.36801