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Total sleep deprivation (TSD) and time-on-task (TOT), especially in combination, increase cognitive instability and cause performance impairment. There are large inter-individual differences in TSD...

Introduction Veterans with chronic pain frequently report comorbid disruptions in sleep and psychological dysfunction. The purpose of this study was to investigate whether psychological function variables mediate the sleep–pain relationship. Knowledge regarding such contributing factors can inform the development and optimization of treatments for sleep disturbances and pain. Materials and Methods In an IRB-approved, registered clinical trial, we collected objective sleep data from U.S. military Veterans with chronic pain (N = 184, ages 23-81) using wrist actigraphy for 7 days and self-reported survey data assessing sleep quality, pain intensity, and psychological function (depression, anxiety, post-traumatic stress disorder, and pain catastrophizing). We investigated the associations between objectively measured and self-reported sleep quality and self-reported pain intensity. In addition, using parallel mediation analyses, we examined whether psychological function variables mediated these associations. Results Actigraphy showed suboptimal sleep duration (less than 7 hours) and sleep fragmentation for most participants. Self-reported poor sleep quality and pain intensity were significantly correlated. Pain catastrophizing was found to mediate the association between self-reported sleep quality and pain intensity. Conclusions Sleep disturbances in this sample of Veterans with chronic pain included insufficient sleep, fragmented sleep, and perceived poor sleep quality. Analyses suggest that poor perceived sleep quality and pain intensity are mediated via pain catastrophizing. The finding highlights the potential importance of pain catastrophizing in Veterans with chronic pain. Future longitudinal research is needed to determine the extent to which treatments that reduce pain catastrophizing might also improve both sleep and pain outcomes.

Introduction Fatigue from sleep loss and circadian misalignment causes automobile driving performance impairment. Metrics based on steering wheel angle, which is straightforward to measure, could be used to quantify this impairment. As the tail of the distribution of steering wheel angles (absolute magnitude of deviation from center) increases with fatigue, we investigated whether driving performance impairment could be quantified based on the prevalence of steering wheel excursions beyond a given angle threshold. We used data from two published laboratory studies of simulated shift work, in which fatigue remained low during day shifts but increased across time awake during night shifts. Methods N=37 healthy adults (ages 26.8±5.2y; 25 men) were assigned to a simulated night shift schedule (awake 20:00-10:00) or day shift schedule (awake 08:00-22:00; study 1 only). After an adaptation period, participants underwent two 5-day shift cycles with an intervening rest period. Driving performance was measured on a high-fidelity simulator during adaptation (data not used) and four times at 3h intervals during each shift day. Every drive involved 30min driving at 55mph, including ten 0.5mi uneventful straightaways being considered here. Steering wheel angle was measured at 72Hz (study 1) or 60Hz (study 2). A total of 1,471 drives (31,394,498 angle measurements) were available for analysis. Results We investigated angle thresholds across 0.01-0.25rad in 0.01rad intervals and counted the corresponding number of threshold excursions in each drive for each participant. For study 1, we applied mixed-effects ANOVA with fixed effects for condition and time awake, and their interaction, and determined the local effect size for interaction. A 0.03rad (1.7°) threshold yielded the greatest effect size, f²=0.031 (small). For this threshold, we repeated the analysis using the data from both studies, controlling for study. The interaction was significant (F[3,1428]=13.23, p Conclusion The prevalence of steering wheel excursions beyond a 1.7° angle threshold yielded sensitivity to fatigue-related driving performance impairment during simulated night shifts. Further research will extend our results to driving through curves and with greater fatigue levels. Support (if any) FMCSA DTMC75-07-D-00006

Introduction There are substantial, phenotypical individual differences in the adverse impact of total sleep deprivation (TSD) on vigilant attention performance. Dopaminergic genotypes have been found to contribute to these phenotypical differences. Here we investigated the association between a single nucleotide polymorphism (SNP) of the dopamine receptor D2 (DRD2) gene, C957T (rs6277), on vigilant attention performance measured with the psychomotor vigilance test (PVT) in a laboratory TSD study. Methods N=46 healthy adults (ages 26.0±5.3y; 25 females) completed a 4-day in-laboratory study with a baseline day (10h time in bed: 22:00-08:00), a 38h TSD period, and a recovery day (10h time in bed: 22:00-08:00). DNA isolated from whole blood was assayed for DRD2 C957T genotype using real-time polymerase chain reaction. PVT performance was measured during TSD at 2-4h intervals, and analyzed for genotype using mixed-effects analysis of covariance of lapses of attention (RTs>500ms). Results The genotype distribution in this sample - 28.3% C/C, 50.0% C/T, 21.7% T/T - was found to be in Hardy-Weinberg Equilibrium (X21=0.0008, p=0.98). As expected, there was a significant effect of time awake on PVT performance (F14,602=26.67, p Conclusion Subjects homozygous for the T allele of DRD2 C957T were considerably more vulnerable to TSD-induced PVT performance impairment than carriers of the C allele. A recent study showed that DRD2 C957T influences PVT performance in interaction with a SNP of the DAT1 gene. Here, DRD2 genotype was by itself also associated with PVT performance impairment during TSD. Support CDMRP awards W81XWH-16-1-0319 and W81XWH-18-1-0100.