Sleep in a community sample of elderly war veterans with and without posttraumatic stress disorder.

BACKGROUND: Although sleep disturbances are commonly reported by individuals with posttraumatic stress disorder (PTSD), objective findings have been inconsistent, due in part to small sample sizes, comorbid psychiatric disorders, variations in the recentness of trauma exposure, and the use of PTSD subjects involved in psychiatric treatment. METHODS: A community sample of elderly males (n = 59) exposed to war trauma 28-50 years ago and free from sleep-affecting medications and disorders other than PTSD completed 3 nights of polysomnography. Of these participants, 30 met criteria for current PTSD; three were receiving supportive outpatient psychotherapy. RESULTS: Two statistically significant differences were observed: Those with PTSD had a higher percentage of rapid eye movement (REM) sleep and fewer arousals from non-REM sleep. The perceptions of sleep quality among the participants with PTSD were lower than the perceptions of non-PTSD participants. Although participants with untreated obstructive sleep apnea and sleep movement disorders were not included in the sample, many cases were detected on initial screening. Treatment resulted in improved sleep and increased feelings of well being. CONCLUSIONS: Alterations in REM and arousals characterized PTSD in this sample. When comorbid sleep disorders were ruled out, sleep was clinically similar across the groups. Trauma-related sleep disturbances that subjects reported as arising early in the course of the disorder appear to have declined over time.     

Sleep in Posttraumatic Stress Disorder

Posttraumatic stress disorder (PTSD) is often associated with sleep disturbances. In this review, we focus on the published literature on subjective and objective findings of sleep in patients with PTSD. Insomnia and nightmares are most commonly reported subjective sleep disturbances. Polysomnographic investigations have frequently reported rapid eye movement (REM) sleep abnormalities in PTSD. However, studies have not been consistent about the type of REM sleep dysfunction in PTSD patients. Antidepressants such as nefazodone, trazodone, fluvoxamine, and imagery rehearsal therapy are found to be beneficial in the treatment of PTSD associated sleep disturbances as well as core symptoms of this anxiety disorder. We propose use of such modalities of treatment in PTSD patients with predominant sleep disturbances. Further studies are required to clarify polysomnographic sleep changes especially role of REM sleep dysregulation and treatment of sleep disturbances in PTSD.     

Polysomnography in patients with post‐traumatic stress disorder

Aims: The purpose of the present study was to investigate sleep structure in post‐traumatic stress disorder (PTSD) patients with and without any psychiatric comorbidities. The relationship between sleep variables and measurements of clinical symptom severity were also investigated. Methods: Sleep patterns of 24 non‐medicated male PTSD patients and 16 age‐ and sex‐matched normal controls were investigated on polysomnography on two consecutive nights. Six PTSD‐only patients and 15 PTSD patients with major depressive disorder (MDD) were also compared to normal controls. Sleep variables were correlated with PTSD symptoms. Results: Compared to the normal controls, the PTSD patients with MDD had difficulty initiating sleep, poor sleep efficiency, decreased total sleep time, decreased slow wave sleep (SWS), and a reduced rapid eye movement (REM) sleep latency. The PTSD patients without any comorbid psychiatric disorders had moderately significant disturbances of sleep continuity, and decreased SWS, but no abnormalities of REM sleep. REM sleep latency was inversely proportional to the severity of startle response. SWS was found to be inversely correlated with the severity of psychogenic amnesia. Conclusions: PTSD patients have disturbance of sleep continuity, and SWS deficit, without the impact of comorbid depression on sleep. The relationship between SWS and the inability to recall an important aspect of trauma may indicate the role of sleep in the consolidation of traumatic memories. The relationship between the severity of the startle response and REM latency may suggest that REM sleep physiology shares common substrates with the symptoms of PTSD.     

Sleep in lifetime posttraumatic stress disorder: a community-based polysomnographic study

BACKGROUND: Sleep complaints are common in posttraumatic stress disorder (PTSD) and are included in the DSM criteria. Polysomnographic studies conducted on small samples of subjects with specific traumas have yielded conflicting results. We therefore evaluated polysomnographic sleep disturbances in PTSD. METHODS: A representative cohort of young-adult community residents followed-up for 10 years for exposure to trauma and PTSD was used to select a subset for sleep studies for 2 consecutive nights and the intermediate day. Subjects were selected from a large health maintenance organization and are representative of the geographic area except for the extremes of the socioeconomic status range. The subset for the sleep study was selected from the 10-year follow-up of the cohort (n = 913 [91% of the initial sample]). Eligibility criteria included (1) subjects exposed to trauma during the preceding 5 years; (2) others who met PTSD criteria; and (3) a randomly preselected subsample. Of 439 eligible subjects, 292 (66.5%) participated, including 71 with lifetime PTSD. Main outcomes included standard polysomnographic measures of sleep induction, maintenance, staging, and fragmentation; standard measures of apnea/hypopnea and periodic leg movement; and results of the multiple sleep latency test. RESULTS: On standard measures of sleep disturbance, no differences were detected between subjects with PTSD and control subjects, regardless of history of trauma or major depression in the controls. Persons with PTSD had higher rates of brief arousals from rapid eye movement (REM) sleep. Shifts to lighter sleep and wake were specific to REM and were significantly different between REM and non-REM sleep (F(1,278) = 5.92; P =.02). CONCLUSIONS: We found no objective evidence for clinically relevant sleep disturbances in PTSD. An increased number of brief arousals from REM sleep was detected in subjects with PTSD. Sleep complaints in PTSD might represent amplified perceptions of brief arousals from REM sleep.     

Chronic Sleep Disruption and the Reexperiencing Cluster of Posttraumatic Stress Disorder Symptoms Are Improved by Olanzapine: Brief Review of the Literature and a Case-Based Series

BACKGROUND: Posttraumatic stress disorder (PTSD) is one of the most prevalent psychiatric disorders in young adults. Early diagnosis and treatment of PTSD are essential to avoid possible long-term neuropsychiatric changes in brain physiology and function. A cardinal symptom of PTSD is chronic sleep disruption, often with recurring nightmares. If untreated, PTSD symptoms often contribute to substance abuse and the development of other comorbid psychiatric disorders. Once PTSD is diagnosed, drug treatment should begin with antidepressant therapy. If antidepressants do not correct the sleep disruption, adjunctive treatment with the atypical antipsychotic olanzapine or other agents should be considered. METHOD: This case series reviews 7 cases of patients with PTSD (DSM-IV criteria) seen in primary care clinics who were successfully treated with olanzapine. In most cases, olanzapine therapy was adjunctive and followed failed treatment with antidepressant monotherapy for sleep disturbances. RESULTS: All patients reported improved sleep with decreased or absent nightmares, as well as improvements in other PTSD symptom clusters. CONCLUSION: Further controlled studies are needed to better characterize and validate this therapeutic indication.     

Sleep in post-traumatic stress disorder and panic: convergence and divergence

Disturbed sleep is a common clinical problem in anxiety disorders, particularly in patients with post-traumatic stress disorder (PTSD) and panic disorder (PD). Several studies have attempted to validate the subjective sleep complaints of these disorders using laboratory polysomnography. These attempts, typically focusing on PTSD or PD independently, have demonstrated inconsistent results. To our knowledge, no such studies have attempted to directly compare and contrast sleep disturbances in PTSD and PD together. Our review of the studies of subjective sleep disturbances, sleep architecture, and sleep-related biologic phenomena suggests that a comparative characterization of sleep disturbances in these two disorders is timely. Such an inference is based on our identification of several areas of convergence and divergence between PTSD and PD found in the published literature, as well as our own preliminary investigations. Specifically, PTSD and PD seem to converge on several sleep-related parameters, namely, sleep quality, presence of episodic parasomnias, and movement time. They also appear to diverge in other important sleep-related areas such as respiratory disturbances and the particular phenomenological nature of episodic parasomnias, namely nightmares or nocturnal panic attacks. Investigations focusing on such overlapping phenomena may provide groundwork for further elucidation of central fear systems underlying these two disorders. Additionally, such sleep studies have the potential to provide important insights into ongoing efforts to develop a cohesive conceptual framework into the patho-physiologies of these disorders.     

Sleep disturbance as the hallmark of posttraumatic stress disorder

The reexperiencing of a traumatic event in the form of repetitive dreams, memories, or flashbacks is one of the cardinal manifestations of posttraumatic stress disorder (PTSD). The dream disturbance associated with PTSD may be relatively specific for this disorder, and dysfunctional REM sleep mechanisms may be involved in the pathogenesis of the posttraumatic anxiety dream. Furthermore, the results of neurophysiological studies in animals suggest that CNS processes generating REM sleep may participate in the control of the classical startle response, which may be akin to the startle behavior commonly described in PTSD patients. Speculating that PTSD may be fundamentally a disorder of REM sleep mechanisms, the authors suggest several strategies for future research.     

Sleep respiratory concomitants of comorbid panic and nightmare complaint in post-traumatic stress disorder

Posttraumatic stress disorder (PTSD) patients with comorbid panic disorder (PD) may express additive symptoms of central fear system disturbance. They endorse elevated levels of sleep and nightmare disturbance [Leskin GA, et al., J Psychiatr Res 2002;36:449-452], and demonstrate movement suppression during laboratory sleep [Woodward SH, et al., Sleep 2002;25:681-688]. We estimated respiratory rate and rate variability separately for rapid-eye movement (REM) and non-rapid-eye movement (NREM) sleep. Subjects were 49 Vietnam combat-related PTSD inpatients (11 with comorbid PD and 38 without) and 15 controls. Computer-based estimates of respiratory rate and variability were derived from 10 to 18 hr of baseline sleep collected over two or three nights. Neither rate nor rate variability distinguished PTSD patients with comorbid PD from those without, or PTSD patients from controls; however, PTSD patients failed to exhibit the expected differences between REM and NREM respiratory rates. Moreover, the difference between REM and NREM respiratory rate was inversely related to a continuous measure of PTSD severity. PTSD patients with trauma-related nightmare complaint exhibited higher sleep respiration rates over both REM and NREM sleep. Conversely, in addition to slowed respiration, nightmare-free patients exhibited reduced respiratory rate variability in REM relative to NREM sleep, which was a reversal of the normal pattern. These finding are discussed in light of known telencephalic regulatory influences upon respiration rate.     

Sleep disturbance in anxiety disorders

Many patients suffering from the majority of anxiety disorders complain about their sleep by reporting difficulties in initiating and maintaining it. Polysomnographic studies have shown that, in comparison to normal subjects, the sleep of patients with panic disorder is characterized by longer sleep latency, increased time awake and reduced sleep efficiency. Sleep architecture is normal and there are no significant changes in REM sleep measures. Nocturnal panic attacks are non-REM-related events and occur without an obvious trigger in 18-45% of panic disorder patients. Regarding generalized anxiety disorder, the patients complain of 'trouble sleeping' in 60-70%, while polysomnography has shown increased sleep latency and decreased sleep continuity measures. The findings in REM sleep and sleep architecture generally do not show any aberration to exist. In patients with obsessive-compulsive disorder (OCD) and post-traumatic stress disorder (PTSD), results from the sleep laboratory do not seem to support the subjective complaints of poor sleep. The early reports of shortened REM latency in OCD could not be replicated by recent studies. A dysregulation of the REM sleep control system has been reported for patients with PTSD. Finally, no significant differences were found in all sleep parameters between social phobia patients and controls.     

Disturbed sleep in post-traumatic stress disorder: secondary symptom or core feature?

Sleep disturbances are often viewed as a secondary symptom of post-traumatic stress disorder (PTSD), thought to resolve once PTSD has been treated. Specific screening, diagnosis and treatment of sleep disturbances is therefore not commonly conducted in trauma centres. However, recent evidence shows that this view and consequent practices are as much unhelpful as incorrect. Several sleep disorders-nightmares, insomnia, sleep apnoea and periodic limb movements-are highly prevalent in PTSD, and several studies found disturbed sleep to be a risk factor for the subsequent development of PTSD. Moreover, sleep disturbances are a frequent residual complaint after successful PTSD treatment: a finding that applies both to psychological and pharmacological treatment. In contrast, treatment focusing on sleep does alleviate both sleep disturbances and PTSD symptom severity. A growing body of evidence shows that disturbed sleep is more than a secondary symptom of PTSD-it seems to be a core feature. Sleep-focused treatment can be incorporated into any standard PTSD treatment, and PTSD research needs to start including validated sleep measurements in longitudinal epidemiologic and treatment outcome studies. Further clinical and research implications are discussed, and possible mechanisms for the role of disturbed (REM) sleep in PTSD are described.     

Effect of illicit recreational drugs upon sleep: cocaine, ecstasy and marijuana

The illicit recreational drugs cocaine, ecstasy and marijuana have pronounced effects upon sleep. Administration of cocaine increases wakefulness and suppresses REM sleep. Acute cocaine withdrawal is often associated with sleep disturbances and unpleasant dreams. Studies have revealed that polysomnographically assessed sleep parameters deteriorate even further during sustained abstinence, although patients report that sleep quality remains unchanged or improves. This deterioration of objective sleep measures is associated with a worsening in sleep-related cognitive performance. Like cocaine, 3,4-methylenedioxymethamphetamine (MDMA; "ecstasy") is a substance with arousing properties. Heavy MDMA consumption is often associated with persistent sleep disturbances. Polysomnography (PSG) studies have demonstrated altered sleep architecture in abstinent heavy MDMA users. Smoked marijuana and oral Delta-9-tetrahydrocannabinol (THC) reduce REM sleep. Moreover, acute administration of cannabis appears to facilitate falling asleep and to increase Stage 4 sleep. Difficulty sleeping and strange dreams are among the most consistently reported symptoms of acute and subacute cannabis withdrawal. Longer sleep onset latency, reduced slow wave sleep and a REM rebound can be observed. Prospective studies are needed in order to verify whether sleep disturbances during cocaine and cannabis withdrawal predict treatment outcome.     

Sleep findings in young adult patients with posttraumatic stress disorder.

BACKGROUND: Laboratory sleep studies in posttraumatic stress disorder (PTSD) have not provided consistent evidence of sleep disturbance, despite apparent sleep complaints. Most of these studies have investigated middle-aged chronic PTSD subjects with a high prevalence of comorbidities such as substance dependence and/or personality disorder. METHODS: Ten young adult PTSD patients (aged 23.4 +/- 6.1 years) without comorbidities of substance dependence and/or personality disorder underwent 2-night polysomnographic recordings. These sleep measures were compared with those of normal control subjects and were correlated with PTSD symptoms. RESULTS: Posttraumatic stress disorder patients demonstrated significantly poorer sleep, reduced sleep efficiency caused by increased wake time after sleep onset, and increased awakening from rapid eye movement (REM) sleep (REM interruption). We found significant positive correlations between the severity of trauma-related nightmare complaints and the percentage of REM interruption, as well as wake time after sleep onset. CONCLUSIONS: The results indicate that trauma-related nightmares are an important factor resulting in increased REM interruptions and wake time after sleep onset in PTSD.     

Actigraphic sleep monitoring in posttraumatic stress disorder (PTSD) patients

Posttraumatic stress disorder (PTSD) patients frequently complain that they suffer from sleep disturbances. To date, the polysomnographic studies that have attempted to study PTSD patients' subjective complaints of sleep difficulties have produced conflicting results. The objective of the present study was to compare PTSD patients' subjective complaints of poor sleep and objective actigraphic recordings of their sleep over a period of several consecutive nights. The results indicate that PTSD patients do not suffer from poorer sleep than a control group, based on actigraphic measures, and that their subjective sleep evaluation is inconsistent with objective sleep measures. These patients fail to correctly estimate their sleep.     

Adjunctive risperidone treatment and sleep symptoms in combat veterans with chronic PTSD

Sleep disturbances are core symptoms of posttraumatic stress disorder (PTSD) and are often resistant to treatment. One reason for the recent use of atypical antipsychotics in PTSD appears to be their effects on sleep. Study objectives were (1) to evaluate preliminarily the sleep effects of adjunctive risperidone, and (2) to evaluate the use of sleep diaries versus the more standard retrospective sleep assessments. This was a pilot, open-label, 12-week, flexible-dose trial of adjunctive risperidone in male veterans with a primary diagnosis of chronic, combat-related PTSD, partially responsive to current medications. Diagnostic interviews were administered at baseline, and PTSD ratings were obtained at baseline and at 6 and 12 weeks. Self-report sleep measures, including morning logs, were obtained at baseline and 6 weeks. Seventeen patients completed at least 6 weeks of the trial. Global ratings of sleep disturbance improved. Changes in frequency of awakenings and reductions in trauma-related dreams were only evident via morning log assessments. Nighttime awakening frequency derived from the sleep logs but not from the Pittsburgh Sleep Quality Index (PSQI) decreased significantly. There were no changes in the PSQI nightmare item; however, sleep log data indicated a reduced proportion of traumatic dreams at 6 weeks. Preliminary results suggest that adjunctive risperidone may benefit sleep disturbances associated with chronic PTSD. Prospective logs may be more sensitive to change than are retrospective scales.     

Dyssomnia in children diagnosed with attention deficit hyperactivity disorder: a critical review

OBJECTIVE: Studies prior to 1999 reported prevalent sleep disturbances in children diagnosed with attention deficit hyperactivity disorder (ADHD). However, these reports were largely inconclusive and inconsistent in their findings, hence the current review based on studies published thereafter. METHOD: An online research of the National Library of Medicine and the Cochrane Library was conducted using the terms 'attention deficit hyperactivity disorder', 'sleep', 'human', and 'English language'. RESULTS: Sixteen articles met the search criteria with 10 reporting objective measures of sleep characteristics (i.e. polysomnography, actigraphy, and/or video recording). These studies confirm an increase of rapid eye movement (REM) sleep latency and a proportional decrease of REM sleep in children diagnosed with ADHD. Stimulant treatment appears to have little effect on sleep quality while parent's reports of poor sleep in their ADHD-diagnosed offspring was largely inconsistent with the objective measures. CONCLUSIONS: The review demonstrated a link between disturbances in sleep architecture and ADHD. Whether this is of an intrinsic or extrinsic cause remains debateable, as both behavioural (parental reporting) and physiological (objective differences in sleep architecture) factors are indicated. The effect of stimulant medication on sleep also requires further research, as current evidence is limited by study design.     

Sleep disturbances and psychiatric disorders associated with posttraumatic stress disorder in the general population

The aim of the study was to assess sleep disturbances in subjects with posttraumatic stress disorder (PTSD) from an urban general population and to identify associated psychiatric disorders in these subjects. The study was performed with a representative sample of 1,832 respondents aged 15 to 90 years living in the Metropolitan Toronto area who were surveyed by telephone (participation rate, 72.8%). Interviewers used Sleep-EVAL, an expert system specifically designed to conduct epidemiologic studies of sleep and mental disorders in the general population. Overall, 11.6% of the sample reported having experienced a traumatic event, with no difference in the proportion of men and women. Approximately 2% (1.8%) of the entire sample were diagnosed by the system as having PTSD at the time of interview. The rate was higher for women (2.6%) than for men (0.9%), which translated into an odds ratio (OR) of 2.8 (95% confidence interval [CI], 1.3 to 6.1). PTSD was strongly associated with other mental disorders: 75.7% of respondents with PTSD received at least one other diagnosis. Most concurrent disorders (80.7%) appeared after exposure to the traumatic event. Sleep disturbances also affected about 70% of the PTSD subjects. Violent or injurious behaviors during sleep, sleep paralysis, sleep talking, and hypnagogic and hypnopompic hallucinations were more frequently reported in respondents with PTSD. Considering the relatively high prevalence of PTSD and its important comorbidity with other sleep and psychiatric disorders, an assessment of the history of traumatic events should be part of a clinician's routine inquiry in order to limit chronicity and maladjustment following a traumatic exposure. Moreover, complaints of rapid eye movement (REM)-related sleep symptoms could be an indication of an underlying problem stemming from PTSD.     

Increased delta power and discrepancies in objective and subjective sleep measurements in borderline personality disorder

BACKGROUND: Previous studies have shown depression-like sleep abnormalities in borderline personality disorder (BPD). However, findings in BPD are not unequivocal for REM dysregulation, as well as for a decrement of slow wave sleep and sleep continuity disturbances. Earlier findings in sleep EEG abnormalities in BPD may have been confounded by concomitant depressive symptoms. METHODS: Twenty unmedicated female BPD patients without current comorbid major depression and 20 sex- and age-matched control subjects entered the study. Conventional polysomnographic parameters and for the first time sleep EEG spectral power analysis was performed on two sleep laboratory nights. Subjective sleep parameters were collected by sleep questionnaires in order to assess the relationship between objective and subjective sleep measurements. RESULTS: BPD patients showed a tendency for shortened REM latency and significantly decreased NonREM sleep (stage 2). Spectral EEG analysis showed increased delta power in total NREM sleep as well as in REM sleep in BPD patients. Subjective ratings documented drastically impaired sleep quality in BPD patients for the two weeks before the study and during the two laboratory nights. CONCLUSION: Not-depressed BPD patients only showed tendencies for depression-like REM sleep abnormalities. Surprisingly, BPD patients displayed higher levels of delta power in the sleep EEG in NREM sleep than healthy control subjects. There was a marked discrepancy between objective and subjective sleep measurements, which indicates an altered perception of sleep in BPD. The underlying psychological and neurobiological mechanisms of these alterations are still unclear and need to be clarified in future studies including interventions on a pharmacological and cognitive-behavioral level.     

Stress-induced changes in sleep in rodents: models and mechanisms

Psychological stressors have a prominent effect on sleep in general, and rapid eye movement (REM) sleep in particular. Disruptions in sleep are a prominent feature, and potentially even the hallmark, of posttraumatic stress disorder (PTSD) (Ross, R.J., Ball, W.A., Sullivan, K., Caroff, S., 1989. Sleep disturbance as the hallmark of posttraumatic stress disorder. American Journal of Psychiatry 146, 697-707). Animal models are critical in understanding both the causes and potential treatments of psychiatric disorders. The current review describes a number of studies that have focused on the impact of stress on sleep in rodent models. The studies are also in Table 1, summarizing the effects of stress in 4-h blocks in both the light and dark phases. Although mild stress procedures have sometimes produced increases in REM sleep, more intense stressors appear to model the human condition by leading to disruptions in sleep, particularly REM sleep. We also discuss work conducted by our group and others looking at conditioning as a factor in the temporal extension of stress-related sleep disruptions. Finally, we attempt to describe the probable neural mechanisms of the sleep disruptions. A complete understanding of the neural correlates of stress-induced sleep alterations may lead to novel treatments for a variety of debilitating sleep disorders.     

Comorbidity, impairment, and suicidality in subthreshold PTSD

OBJECTIVE: Reliance on the categorical model of psychiatric disorders has led to neglected study of posttraumatic sequelae that fall short of full criteria for posttraumatic stress disorder (PTSD). Substantial disability and suicidal risk is associated with subthreshold PTSD, but this association has not been well studied. In addition, no studies have examined the role of comorbidity in explaining disability and impairment in subthreshold PTSD. METHOD: On National Anxiety Disorders Screening Day 1997, 2,608 out of 9,358 individuals screened for affective and anxiety disorders at 1,521 sites across the United States reported at least one PTSD symptom of at least 1 month's duration. Impairment, comorbid anxiety disorders, major depressive disorder, and rates of suicidality were determined and compared for individuals with no, one, two, three, or four (full PTSD) symptoms on a screening questionnaire. Regression analyses examined the relative contribution of subthreshold PTSD and comorbid disorders to impairment and suicidal ideation. RESULTS: Impairment, number of comorbid disorders, rates of comorbid major depressive disorder, and current suicidal ideation increased linearly and significantly with each increasing number of subthreshold PTSD symptoms. Individuals with subthreshold PTSD were at greater risk for suicidal ideation even after the authors controlled for the presence of comorbid major depressive disorder. CONCLUSIONS: Higher numbers of subthreshold PTSD symptoms were associated with greater impairment, comorbidity, and suicidal ideation. Disability and impairment found in previous studies of subthreshold PTSD symptoms may be related in part to the presence of comorbid disorders. However, the presence of subthreshold PTSD symptoms significantly raised the risk for suicidal ideation even after the authors controlled for major depressive disorder. Given the broad public health implications of these findings, more efforts are needed to identify subthreshold PTSD symptoms in clinical populations, epidemiologic surveys, and treatment studies.     

Sleep-specific mechanisms underlying posttraumatic stress disorder: integrative review and neurobiological hypotheses

Posttraumatic stress disorder (PTSD) is a prevalent disorder that is associated with poor clinical and health outcomes, and considerable health care utilization and costs. Recent estimates suggest that 5-20% of military personnel who serve in current conflicts in Iraq and Afghanistan meet diagnostic criteria for PTSD. Clinically, sleep disturbances are core features of PTSD that are often resistant to first-line treatments, independently contribute to poor daytime functioning, and often require sleep-focused treatments. Physiologically, these observations suggest that PTSD is partially mediated by sleep disruption and its neurobiological correlates that are not adequately addressed by first-line treatments. However, polysomnographic studies have provided limited insights into the neurobiological underpinnings of PTSD during sleep. There is an urgent need to apply state-of-the-science sleep measurement methods to bridge the apparent gap between the clinical significance of sleep disturbances in PTSD and the limited understanding of their neurobiological underpinnings. Here, we propose an integrative review of findings derived from neurobiological models of fear conditioning and fear extinction, PTSD, and sleep-wake regulation, suggesting that the amygdala and medial prefrontal cortex can directly contribute to sleep disturbances in PTSD. Testable hypotheses regarding the neurobiological underpinnings of PTSD across the sleep-wake cycle are offered.