Changes in electroencephalographic microstates between evening and morning are associated with overnight sleep slow waves in healthy individuals.

STUDY OBJECTIVES: Microstates are semi-stable voltage topographies that account for most of electroencephalogram (EEG) variance. However, the impact of time of the day and sleep on microstates has not been examined. To address this gap, we assessed whether microstates differed between the evening and morning and whether sleep slow waves correlated with microstate changes in healthy participants. METHODS: Forty-five healthy participants were recruited. Each participant underwent 6 minutes of resting state EEG recordings in the evening and morning, interleaved by sleep EEGs. Evening-to-morning changes in microstate duration, coverage, and occurrence were assessed. Furthermore, correlation between microstate changes and sleep slow-wave activity (SWA) and slow-wave density (SWD) were performed. RESULTS: Two-way ANOVAs with microstate class (A, B, C, and D) and time (evening and morning) revealed significant microstate class × time interaction for duration (F(44) = 5.571, p = 0.002), coverage (F(44) = 6.833, p = 0.001), and occurrence (F(44) = 5.715, p = 0.002). Post hoc comparisons showed significant effects for microstate C duration (padj = 0.048, Cohen's d = -0.389), coverage (padj = 0.002, Cohen's d = -0.580), and occurrence (padj = 0.002, Cohen's d = -0.606). Topographic analyses revealed inverse correlations between SWD, but not SWA, and evening-to-morning changes in microstate C duration (r = -0.51, padj = 0.002), coverage (r = -0.45, padj = 0.006), and occurrence (r = -0.38, padj = 0.033). CONCLUSIONS: Microstate characteristics showed significant evening-to-morning changes associated with, and possibly regulated by, sleep slow waves. These findings suggest that future microstate studies should control for time of day and sleep effects.

Sleep Abnormalities in Different Clinical Stages of Psychosis: A Systematic Review and Meta-analysis.

Importance: Abnormal sleep is frequent in psychosis; however, sleep abnormalities in different stages (ie, clinical high risk for psychosis [CHR-P], early psychosis [EP], and chronic psychosis [CP]) have not been characterized. Objective: To identify sleep abnormalities across psychosis stages. Data Sources: Web of Science and PubMed were searched between inception and June 15, 2022. Studies written in English were included. Study Selection: Sleep disturbance prevalence studies and case-control studies reporting sleep quality, sleep architecture, or sleep electroencephalography oscillations in CHR-P, EP, or CP. Data Extraction and Synthesis: This systematic review and meta-analysis followed Preferred Reporting Items for Systematic Reviews and Meta-analyses (PRISMA) reporting guideline. Stage-specific and pooled random-effects meta-analyses were conducted, along with the assessment of heterogeneity, study quality, and meta-regressions (clinical stage, sex, age, medication status, and psychotic symptoms). Main Outcomes and Measures: Sleep disturbance prevalence, self-reported sleep quality, sleep architecture (total sleep time, sleep latency, sleep efficiency, nonrapid eye movement, rapid eye movement stages, and number of arousals), and sleep electroencephalography oscillations (spindle density, amplitude, and duration, and slow wave density). Results: Fifty-nine studies with up to 6710 patients (n = 5135 for prevalence) and 977 controls were included. Sleep disturbance prevalence in pooled cases was 50% (95% CI, 40%-61%) and it was similar in each psychosis stage. Sleep quality was worse in pooled cases vs controls (standardized mean difference [SMD], 1.00 [95% CI, 0.70-1.30]). Sleep architecture alterations included higher sleep onset latency (SMD [95% CI]: pooled cases, 0.96 [0.62-1.30]; EP, 0.72 [0.52-0.92]; CP, 1.36 [0.66-2.05]), higher wake after sleep onset (SMD [95% CI]: pooled cases, 0.5 [0.29-0.71]; EP, 0.62 [0.34-0.89]; CP, 0.51 [0.09-0.93]), higher number of arousals (SMD [95% CI]: pooled cases, 0.45 [0.07-0.83]; CP, 0.81 [0.30-1.32]), higher stage 1 sleep (SMD [95% CI]: pooled cases, 0.23 [0.06-0.40]; EP, 0.34 [0.15-0.53]), lower sleep efficiency (SMD [95% CI]: pooled cases, -0.75 [-0.98 to -0.52]; EP, -0.90 [-1.20 to -0.60]; CP, -0.73 [-1.14 to -0.33]), and lower rapid eye movement density (SMD [95% CI]: pooled cases, 0.37 [0.14-0.60]; CP, 0.4 [0.19-0.77]). Spindle parameter deficits included density (SMD [95% CI]: pooled cases, -1.06 [-1.50 to -0.63]; EP, -0.80 [-1.22 to -0.39]; CP, -1.39 [-2.05 to -0.74]; amplitude: pooled cases, -1.08 [-1.33 to -0.82]; EP, -0.86 [-1.24 to -0.47]; CP, -1.25 [-1.58 to -0.91]; and duration: pooled cases: -1.2 [-1.69 to -0.73]; EP, -0.71 [-1.08 to -0.34]; CP, -1.74 [-2.10 to -1.38]). Individuals with CP had more frequent arousals vs CHR-P (z = 2.24, P = .02) and reduced spindle duration vs EP (z = -3.91, P < .001). Conclusions and Relevance: In this systematic review and meta-analysis, sleep disturbances were found to be prevalent throughout the course of psychosis, and different psychosis stages showed both shared and distinct abnormalities in sleep quality, architecture, and spindles. These findings suggest that sleep should become a core clinical target and research domain from at-risk to early and chronic stages of psychosis.