Rapid eye movement sleep disturbance in posttraumatic stress disorder

Ross, Richard; Ball, William A.; Dinges, David F.; Kribbs, Nancy Barone; Morrison, Adrian R.; Silver, Steven M.; Mulvaney, Francis D.

doi:10.1016/0006-3223(94)91152-5

Cited by 203 publications

(128 citation statements)

References 20 publications

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“…These questions have tremendous importance for posttraumatic stress disorder (PTSD), which can involve aberrant fear processing, 1 is linked to stress-related alterations in sleep 2,3 and is characterized by continuing disturbances of sleep and arousal. 4,5 There are also implications for other anxiety disorders and depression which are associated with abnormalities in memory 6 and sleep. 7 Rapid eye movement sleep (REM) can be highly affected by stress and fear.…”

Section: Introductionmentioning

confidence: 99%

Brief Optogenetic Inhibition of the Basolateral Amygdala (BLA) in Mice Alters Effects of Stressful Experiences on Rapid Eye Movement Sleep (REM)

Machida

Wellman

et al. 2017

Sleep

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Study Objectives: Stressful events can directly produce significant alterations in subsequent sleep, in particular rapid eye movement sleep (REM); however, the neural mechanisms underlying the process are not fully known. Here, we investigated the role of the basolateral nuclei of the amygdala (BLA) in regulating the effects of stressful experience on sleep. Methods: We used optogenetics to briefly inhibit glutamatergic cells in BLA during the presentation of inescapable footshock (IS) and assessed effects on sleep, the acute stress response, and fear memory. c-Fos expression was also assessed in the amygdala and the medial prefrontal cortex (mPFC), both regions involved in coping with stress, and in brain stem regions implicated in the regulation of REM. Results: Compared to control mice, peri-shock inhibition of BLA attenuated an immediate reduction in REM after IS and produced a significant overall increase in REM. Moreover, upon exposure to the shock context alone, mice receiving peri-shock inhibition of BLA during training showed increased REM without altered freezing (an index of fear memory) or stress-induced hyperthermia (an index of acute stress response). Inhibition of BLA during REM under freely sleeping conditions enhanced REM only when body temperature was high, suggesting the effect was influenced by stress. Peri-shock inhibition of BLA also led to elevated c-Fos expression in the central nucleus of the amygdala and mPFC and differentially altered c-Fos activity in the selected brain stem regions. Conclusions: Glutamatergic cells in BLA can modulate the effects of stress on REM and can mediate effects of fear memory on sleep that can be independent of behavioral fear.

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Section: Introductionmentioning

confidence: 99%

Brief Optogenetic Inhibition of the Basolateral Amygdala (BLA) in Mice Alters Effects of Stressful Experiences on Rapid Eye Movement Sleep (REM)

Machida

Wellman

et al. 2017

Sleep

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“…Mellman, David, et al (1995) reported that the "re-experiencing symptom" item from the PTSD severity scale was significantly correlated with REM density in PTSD patients. However, the reported change of REM sleep across studies has been variable; Engdahl, Eberly, Hurwitz, Mahowald, and Blake (2000), Ross et al (1994b), Ross et al (1999), and Woodward, Murburg, and Bilwise (2000) reported an increased REM sleep percentage; whereas Hefez et al, Kramer and Kinney (1988), Mikulincer et al (1989) reported a decrease in the REM sleep percentage. Four studies reported increased REML (Hefez et al, 1987;Kramer & Kinney, 1988;Mikulincer et al, 1989), and one study reported decreased REML (Greenberg, Pearlman, & Gampel, 1972).…”

Section: Traumatic Stressmentioning

confidence: 99%

The Effect of Psychosocial Stress on Sleep: A Review of Polysomnographic Evidence

Kim

Dimsdale

2007

Behavioral Sleep Medicine

355

250

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This systematic review examines the effect of diverse psychosocial stressors on polysomnographic measures of sleep. Sixty-three articles were located and categorized in terms of the types of stressors imposed. Experimental stress resulted in fairly consistent changes: decreases in slow wave sleep, REM sleep, and sleep efficiency (SE), as well as increases in awakenings. Data were limited in terms of response to non-experimental stressors, except for the case of post-traumatic stress disorder (PTSD) on sleep, where a number of reports suggest that PTSD patients have increased awakenings and decreased SE. Future research needs to define stress more precisely in terms of duration and severity and to measure its impacts on sleep in populations that differ in terms of age, comorbid illness, gender, and so forth. Without such fine-grained analyses, it is difficult to draw definitive conclusions about this important area.Sleep researchers traditionally have focused on primary sleep disorders such as sleep apnea, narcolepsy, or periodic limb movement disorder; but common knowledge has it that the stresses of daily life can perturb even healthy sleep. As Mason (1968) described, psychological stressors are potent stimuli for physiological stress responses. Most studies on psychosocial stress and its physiological effects on sleep are based solely on subjective reports. However, these subjective reports of sleep are not sufficient to evaluate physiological sleep changes as measured by polysomnography (PSG; Akerstedt, Hume, Minors, & Waterhouse, 1994;Schneider-Helmert & Kumar, 1995). What really happens in sleep physiology after exposure to stressors? Although the gold standard of measurement of sleep is PSG, there are relatively little data concerning the effects of ordinary or severe stress on polysomnographically examined sleep. This article systematically reviews the diverse literature in this area.Stress is notorious for being difficult to define. It encompasses all kinds of stimuli of varying amounts of aversiveness and duration (Dimsdale, Irwin, Keefe, & Stein, 2005). Kecklund and Akerstedt (2004b) grouped stressors conceptionally into physical versus psychological or social, acute versus chronic, and high intensity versus low intensity.Copyright © Lawrence Erlbaum Associates, Inc. Correspondence should be addressed to Joel E. Dimsdale, University of California, San Diego, 9500 Gilman D., La Jolla, CA 92093-0804. jdimsdale@ucsd.edu. NIH Public Access Author ManuscriptBehav Sleep Med. Author manuscript; available in PMC 2014 December 15. NIH-PA Author ManuscriptNIH-PA Author Manuscript NIH-PA Author ManuscriptAlthough there are numerous animal models of social stress, it is still challenging to generalize psychosocial stress responses in animals to those in humans. This review focuses on psychosocial stressors; other types of stressors such as environmental manipulations (e.g., temperature), exercise, or intentionally imposed sleep disruption are not covered in this article.It is possible that different types...

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“…Specifically, individuals with PTSD appear to have decreased total sleep time, an increase in rapid eye movement activity, and an increased number of awakenings [38][39][40]. Recent studies have found that the centrally active · 1 -adrenergic antagonist, prazosin, might have some clinical efficacy in alleviating trauma-associated nightmares in individuals with chronic PTSD [41][42][43].…”

Section: Behavioral Correlates Of the Role Of Na In Ptsdmentioning

confidence: 99%

Noradrenergic Mechanisms in the Pathophysiology of Post-Traumatic Stress Disorder

O'Donnell¹,

Hegadoren

Coupland³

2004

Neuropsychobiology

142

106

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Post-traumatic stress disorder (PTSD) is a serious psychiatric illness that may develop in individuals after exposure to a traumatic event. Recent data suggest that trauma and/or long-term stressors can cause alterations in the functioning of neuroanatomical structures and neural networks throughout the central nervous system. Specifically, dysregulation in central and perhaps, peripheral noradrenergic neural networks has been implicated as the cause of specific symptom clusters in the pathophysiology of PTSD. In this review, both clinical and preclinical data are presented to highlight types of noradrenergic dysfunction observed in individuals with PTSD. Additionally, the role of noradrenaline dysregulation in the acquisition/initiation, and maintenance of hyperarousal and reexperiencing symptom clusters in PTSD will be addressed.

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Rapid eye movement sleep disturbance in posttraumatic stress disorder

Cited by 203 publications

References 20 publications

Brief Optogenetic Inhibition of the Basolateral Amygdala (BLA) in Mice Alters Effects of Stressful Experiences on Rapid Eye Movement Sleep (REM)

Brief Optogenetic Inhibition of the Basolateral Amygdala (BLA) in Mice Alters Effects of Stressful Experiences on Rapid Eye Movement Sleep (REM)

The Effect of Psychosocial Stress on Sleep: A Review of Polysomnographic Evidence

Noradrenergic Mechanisms in the Pathophysiology of Post-Traumatic Stress Disorder

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