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Posttraumatic stress disorder-related sleep disturbances may increase daytime sleepiness and compromise performance in individuals with posttraumatic stress disorder. We investigated nighttime sleep predictors of sleepiness in Veterans with and without posttraumatic stress disorder. Thirty-seven post-9/11 Veterans with posttraumatic stress disorder and 47 without posttraumatic stress disorder (Control) completed a 48-h lab stay. Nighttime quantitative EEG and sleep architecture parameters were collected with polysomnography. Data from daytime sleepiness batteries assessing subjective sleepiness (global vigor questionnaire), objective sleepiness (Multiple Sleep Latency Tests) and alertness (psychomotor vigilance task) were included in analyses. Independent samples t-tests and linear regressions were performed to identify group differences in sleepiness and nighttime sleep predictors of sleepiness in the overall sample and within each group. Participants with posttraumatic stress disorder had higher subjective sleepiness (t = 4.20; p .001) and lower alertness (psychomotor vigilance task reaction time (t = -3.70; p .001) and lapses: t = -2.13; p = .04) than the control group. Objective daytime sleepiness did not differ between groups (t = -0.79, p = .43). In the whole sample, higher rapid eye movement delta power predicted lower alertness quantified by psychomotor vigilance task reaction time (β = 0.372, p = .013) and lapses (β = 0.388, p = .013). More fragmented sleep predicted higher objective sleepiness in the posttraumatic stress disorder group (β = -.467, p = .005) but no other nighttime sleep measures influenced the relationship between group and sleepiness. Objective measures of sleep and sleepiness were not associated with the increased subjective sleepiness and reduced alertness of the posttraumatic stress disorder group.

Sleep-wake disturbances in individuals at clinical high risk (CHR) of psychosis may relate to increased symptom severity and contribute to disease progression. Here, we examined differences in rest-activity rhythms (RAR) measures, derived from actigraphy, and objective sleep outcomes, derived from electroencephalography (EEG), between 12 CHR and 16 healthy comparison (HC) individuals. Further, we examined the relationships between RAR disturbances, objective sleep outcomes and clinical psychosis symptoms (i.e., negative, positive, disorganized, general symptoms). Sleep-wake behaviors were monitored via actigraphy for 3-7 days (CHR: 5.7 ± 1.7 days; HC: 6.3 ± 1.2 days) prior to participants spending a night in the sleep laboratory, which was monitored with EEG. Separate regressions were used to examine the effect of clinical group on RAR measures and objective sleep outcomes after controlling for age and gender. CHR participants were found to be less active, specifically during the evening (17:00-20:00; β = 1.145, SE = 0.362, p = .004) and nighttime (21:00-24:00; β = 1.152, SE = 0.326, p = .002) relative to HC. Further, CHR participants had more fragmented sleep (wake after sleep onset: β = 0.888, SE = 0.395, p = .034) and more hyperarousal during sleep (NREM gamma activity: β = 1.087, SE = 0.348, p = .005), but these sleep disturbances were not related to reduced activity or clinical symptoms, whereas lower nighttime activity was related to more disorganized symptoms (ρ = -.640, p = .025). Thus, increasing activity through behavioral interventions may have additional beneficial effects on CHR clinical symptoms.

Youth at Clinical High Risk (CHR) represent a unique population enriched for precursors of major psychiatric disorders. Sleep disturbances are consistently reported in CHR individuals. However, there is a dearth of studies investigating quantifiable objective measures of sleep dysfunction in CHR youth. In this study, sleep high density (hd)-EEG recordings were collected in twenty-two CHR and twenty healthy comparison (HC) subjects. Sleep architecture parameters, as well as sleep EEG power spectra in five frequency bands, were computed and compared between CHR and HC groups during non-rapid eye movement (NREM) sleep. Furthermore, correlation analyses between sleep EEG power spectra, sleep architecture parameters, and clinical symptoms, assessed with the Scale of Prodromal Symptoms (SOPS), were conducted in CHR participants. Our results show that CHR individuals had more Wakefulness After Sleep Onset (WASO) compared to HC participants. CHR also showed a higher NREM sleep gamma EEG power, which was observed in a large fronto-parieto-occipital area, relative to HC. Additionally, higher NREM gamma activity in lateral fronto-occipital regions was associated with more WASO, and increased NREM gamma power in medial fronto/parietal areas correlated with worse SOPS negative symptoms. Altogether, these findings suggest that topographically specific increases in EEG gamma activity during NREM sleep represent neurophysiological signatures underlying some of the objectively assessed sleep disturbances and clinical symptoms of CHR individuals.