Insomnia subtypes characterised by objective sleep duration and NREM spectral power and the effect of acute sleep restriction: an exploratory analysis

Insomnia disorder (ID) is a heterogeneous disorder with proposed subtypes based on objective sleep duration. We speculated that insomnia subtyping with additional power spectral analysis and measurement of response to acute sleep restriction may be informative in overall assessment of ID. To explore alternative classifications of ID subtypes, insomnia patients (n = 99) underwent two consecutive overnight sleep studies: (i) habitual sleep opportunity (polysomnography, PSG) and, (ii) two hours less sleep opportunity (electroencephalography, EEG), with the first night compared to healthy controls (n = 25). ID subtypes were derived from data-driven classification of PSG, EEG spectral power and interhemispheric EEG asymmetry index. Three insomnia subtypes with different sleep duration and NREM spectral power were identified. One subtype (n = 26) had shorter sleep duration and lower NREM delta power than healthy controls (short-sleep delta-deficient; SSDD), the second subtype (n = 51) had normal sleep duration but lower NREM delta power than healthy controls (normal-sleep delta-deficient; NSDD) and a third subtype showed (n = 22) no difference in sleep duration or delta power from healthy controls (normal neurophysiological sleep; NNS). Acute sleep restriction improved multiple objective sleep measures across all insomnia subtypes including increased delta power in SSDD and NSDD, and improvements in subjective sleep quality for SSDD (p = 0.03), with a trend observed for NSDD (p = 0.057). These exploratory results suggest evidence of novel neurophysiological insomnia subtypes that may inform sleep state misperception in ID and with further research, may provide pathways for personalised care.

Effect of Sleep Restriction on Cardiometabolic and Haemoinflammatory Parameters in Adult Male Wistar Rats

Background and Objective: While insufficient sleep remains an under-recognized public health issue across the globe, there is paucity and heterogeneity of data regarding its cardiometabolic and haemoinflammatory implications. We, therefore, aimed to evaluate the impact of chronic sleep restriction on cardiometabolic and haemoinflammatory parameters in rats. Materials and Methods: 16 male Wistar rats (aged 8-10 weeks) were randomly assigned into equal control or sleep restriction groups. Gentle handling was used to induce sleep restriction for six weeks. Fasting weight and blood sugar were obtained and lipids were analyzed using their respective Randox kits. Malondialdehyde (MDA) levels and catalase (CAT) and superoxide dismutase (SOD) activities were assayed. Full blood count and CD4+ T cell count were determined using automated analyzer. Data were analyzed using Student’s t-test, with level of significance set at P ≤ 0.05, via SPSS software. Results: Chronic sleep restriction caused significant initial weight loss, increase in feed consumption, and percentage increase in fasting blood sugar (FBS) (32% vs. 15%). We also noted the triglyceride-glucose (TyG) index of sleep-restricted rats to be significantly higher (6.22) than that of controls (5.62). In addition, a significant reduction in monocyte count, monocyte-lymphocyte ratio (MLR), and absolute CD4+ cell count among the sleep-restricted rats was observed. Conclusion: Our findings have provided objective evidence that, over the course of 6 weeks, 5 hours of sleep restriction had caused body weight gain, hyperglycaemia, insulin resistance, and impairment in immunoinflammatory status; hence, it could be a risk factor for developing cardiometabolic syndrome and immune-related disorders.

Predictors of interindividual differences in vulnerability to neurobehavioral consequences of chronic partial sleep restriction

Interindividual differences in the neurobehavioral response to sleep loss are largely unexplained and phenotypic in nature. Numerous factors have been examined as predictors of differential response to sleep loss, but none have yielded a comprehensive view of the phenomenon. The present study examines the impact of baseline factors, habitual sleep–wake patterns, and homeostatic response to sleep loss on accrued deficits in psychomotor vigilance during chronic partial sleep restriction (SR), in a total of 306 healthy adults that participated in one of three independent laboratory studies. Findings indicate no significant impact of personality, academic intelligence, subjective reports of chronotype, sleepiness and fatigue, performance on working memory, and demographic factors such as sex, ethnicity, and body mass index, on neurobehavioral vulnerability to the negative effects of sleep loss. Only superior baseline performance on the psychomotor vigilance test and ability to sustain wakefulness on the maintenance of wakefulness test were associated with relative resilience to decrements in vigilant attention during SR. Interindividual differences in vulnerability to the effects of sleep loss were not accounted for by prior sleep history, habitual sleep patterns outside of the laboratory, baseline sleep architecture, or homeostatic sleep response during chronic partial SR. A recent theoretical model proposed that sleep–wake modulation may be influenced by competing internal and external demands which may promote wakefulness despite homeostatic and circadian signals for sleep under the right circumstances. Further research is warranted to examine the possibility of interindividual differences in the ability to prioritize external demands for wakefulness in the face of mounting pressure to sleep.

Pain thresholds and suprathreshold pain after sleep restriction in migraine – A blinded crossover study

Objective There is an unexplained association between disturbed sleep and migraine. In this blinded crossover study, we investigate if experimental sleep restriction has a different effect on pain thresholds and suprathreshold pain in interictal migraineurs and controls. Methods Forearm heat pain thresholds and tolerance thresholds, and trapezius pressure pain thresholds and suprathreshold pain were measured in 39 interictal migraineurs and 31 healthy controls after two consecutive nights of partial sleep restriction and after habitual sleep. Results The effect of sleep restriction was not significantly different between interictal migraineurs and controls in the primary analyses. Pressure pain thresholds tended to be lower (i.e., increased pain sensitivity) after sleep restriction in interictal migraineurs compared to controls with a 48-hour preictal-interictal cut-off (p = 0.061). We found decreased pain thresholds after sleep restriction in two of seven migraine subgroup comparisons: heat pain thresholds decreased in migraineurs with lower pain intensity during attacks (p = 0.005) and pressure pain thresholds decreased in migraineurs with higher severity of photophobia during attacks (p = 0.031). Heat pain thresholds tended to decrease after sleep restriction in sleep-related migraine (p = 0.060). Sleep restriction did not affect suprathreshold pain measurements in either group. Conclusion This study could not provide strong evidence for an increased effect of sleep restriction on pain sensitivity in migraineurs compared to healthy controls. There might be a slightly increased effect of sleep restriction in migraineurs, detectable using large samples or more pronounced in certain migraine subgroups.

Concordance of multiple methods to define resiliency and vulnerability to sleep loss depends on Psychomotor Vigilance Test metric

Study Objectives Sleep restriction (SR) and total sleep deprivation (TSD) reveal well-established individual differences in Psychomotor Vigilance Test (PVT) performance. While prior studies have used different methods to categorize such resiliency/vulnerability, none have systematically investigated whether these methods categorize individuals similarly. Methods 41 adults participated in a 13-day laboratory study consisting of 2 baseline, 5 SR, 4 recovery, and one 36h TSD night. The PVT was administered every 2h during wakefulness. Three approaches (Raw Score [average SR performance], Change from Baseline [average SR minus average baseline performance], and Variance [intraindividual variance of SR performance]), and within each approach, six thresholds (±1 standard deviation and the best/worst performing 12.5%, 20%, 25%, 33%, and 50%) classified Resilient/Vulnerable groups. Kendall’s tau-b correlations examined the concordance of group categorizations of approaches within and between PVT lapses and 1/reaction time (RT). Bias-corrected and accelerated bootstrapped t-tests compared group performance. Results Correlations comparing the approaches ranged from moderate to perfect for lapses and zero to moderate for 1/RT. Defined by all approaches, the Resilient groups had significantly fewer lapses on nearly all study days. Defined by the Raw Score approach only, the Resilient groups had significantly faster 1/RT on all study days. Between-measures comparisons revealed significant correlations between the Raw Score approach for 1/RT and all approaches for lapses. Conclusion The three approaches defining vigilant attention resiliency/vulnerability to sleep loss resulted in groups comprised of similar individuals for PVT lapses but not for 1/RT. Thus, both method and metric selection for defining vigilant attention resiliency/vulnerability to sleep loss is critical.

O039 Differential effects of sleep deprivation and sleep restriction on error awareness

Introduction The ability to detect and subsequently correct errors is important in preventing the detrimental consequences of sleep loss. We report the first study to compare the effects of total sleep deprivation (TSD) and sleep restriction (SR) on error awareness. Methods Thirteen healthy adults (11F, age=26.8±3.4y) underwent a 34h TSD protocol, completing the Error Awareness Task (EAT: a combined Stroop/1-back/GoNogo task) at 4h and 27h post-wake. Twenty healthy adults (11F, age=27.4±5.3y) were studied both well-rested (WR: 9h sleep) and following SR (3 nights of 3h sleep), completing the EAT once/day (8-9h post-habitual wake). The EAT required participants to withhold responding to “nogo” stimuli and signal, via a button press, whenever they realised they made an error on these nogo trials. Results TSD did not significantly affect error rate (p=.712) or error awareness rate (p=.517), however, participants were slower to recognise errors after TSD (p=.004). In contrast, SR increased error rate (p<.001), decreased error awareness (p<.001), and slowed recognition of errors (p<.01). Discussion Three nights SR impaired the ability to recognise errors in real-time, despite a greater number of errors being made. Thus, impaired error awareness may be one mechanism underlying increased sleep loss-related accidents and errors in occupational settings, as well as at home. Interestingly, 1-night TSD did not lead to more, or impaired recognition of errors. TSD participants were slower to recognise errors, which may be problematic in safety critical settings. Technological and/or operational solutions may be needed to reduce the risk of errors going unrecognised.