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Objectives: Sleep disturbances commonly follow traumatic brain injury (TBI) and contribute to ongoing disability. However, there are no conclusive findings regarding specific changes to sleep quality and sleep architecture measured using polysomnography. Possible causes of the sleep disturbances include disruption of circadian regulation of sleep-wakefulness, psychological distress, and a neuronal response to injury. We investigated sleep-wake disturbances and their underlying mechanisms in a TBI patient sample. Methods:This was an observational study comparing 23 patients with TBI (429.7 Ϯ 287.6 days post injury) and 23 age-and gender-matched healthy volunteers on polysomnographic sleep measures, salivary dim light melatonin onset (DLMO) time, and self-reported sleep quality, anxiety, and depression.Results: Patients with TBI reported higher anxiety and depressive symptoms and sleep disturbance than controls. Patients with TBI showed decreased sleep efficiency (SE) and increased wake after sleep onset (WASO). Although no significant group differences were found in sleep architecture, when anxiety and depression scores were controlled, patients with TBI showed higher amount of slow wave sleep. No differences in self-reported sleep timing or salivary DLMO time were found. However, patients with TBI showed significantly lower levels of evening melatonin production. Melatonin level was significantly correlated with REM sleep but not SE or WASO. Conclusions:Reduced evening melatonin production may indicate disruption to circadian regulation of melatonin synthesis. The results suggest that there are at least 2 factors contributing to sleep disturbances in patients with traumatic brain injury. We propose that elevated depression is associated with reduced sleep quality, and increased slow wave sleep is attributed to the effects of mechanical brain damage. Neurology ® 2010;74:1732-1738 GLOSSARY AUC ϭ area under the curve; DLMO ϭ dim light melatonin onset; EOG ϭ electrooculogram; ESS ϭ Epworth Sleepiness Scale; HADS ϭ Hospital Anxiety and Depression Scale; MEQ ϭ Morningness Eveningness Questionnaire; NREM ϭ non-REM; PSQI ϭ Pittsburgh Sleep Quality Index; PTA ϭ posttraumatic amnesia; SE ϭ sleep efficiency; SOL ϭ sleep onset latency; SWS ϭ slow wave sleep; TBI ϭ traumatic brain injury; WASO ϭ wake after sleep onset.Sleep disturbances are common following traumatic brain injury (TBI), reported by 30%-75% of individuals and contributing to ongoing disability.

These findings suggest potential treatments including cognitive behavior therapy supporting lifestyle modifications, pharmacologic treatments with modafinil and melatonin, and light therapy to enhance alertness, vigilance, and mood. Controlled trials of these interventions are needed.

We found that insomnia patients exhibit deficits in higher level neurobehavioral functioning, but not in basic attention. The findings indicate that neurobehavioral deficits in insomnia are due to neurobiological alterations, rather than sleepiness resulting from chronic sleep deficiency.

Study Objectives: Although impairment of daytime functioning is a symptom of many sleep disorders, there are limited data on their nature for some patient groups. The role of the circadian system on impaired functioning, specifi cally the wake maintenance zone (WMZ)-a ~3-h window of reduced sleep propensity that occurs shortly before the onset of melatonin synthesis-has received little attention. The study examined the infl uence of the WMZ on neurobehavioral performance under normal conditions and following sleep deprivation. Methods: Thirty-one adults (8 F; 18-29 y) completed an inpatient protocol including a baseline day (8-h sleep:16-h wake) and a ~50-h constant routine (CR), including regular assessment of plasma melatonin and neurobehavioral performance (i.e., auditory and visual psychomotor vigilance tests [aPVT, vPVT], Digit Symbol Substitution Test [DSST], and subjective sleepiness). Results: Performance in the 3 hours before the onset of melatonin secretion (i.e., the expected WMZ) was signifi cantly improved compared to performance during a 3-hour block earlier in the biological day, despite a longer time awake. The improvement during WMZ was most prominent after extended wakefulness (i.e., day 2 of the CR). Conclusions: These results suggest that alignment of circadian phase with respect to sleep-wake timing may affect cognitive performance, particularly when homeostatic sleep pressure is high, and especially when performance is assessed in the evening, near the predicted WMZ. The potential contribution of the WMZ to sleep-onset insomnia complaints should be assessed further, using objective neurobehavioral testing and simultaneous circadian phase measurement. Keywords: Cognition, sleep regulation, circadian, performance, melatonin, two-process model, PVT, DLMO Citation: Shekleton JA; Rajaratnam SMW; Gooley JJ; Van Reen E; Czeisler CA; Lockley SW. Improved neurobehavioral performance during the wake maintenance zone. J Clin Sleep Med 2013;9(4): 353-362. http://dx.doi.org/10.5664/jcsm.2588 S C I E N T I F I C I N V E S T I G A T I O N ST he assessment of daytime neurobehavioral impairments in sleep disordered patients has produced inconsistent results, particularly in patients with insomnia.1 In other sleep disorder populations, such as circadian rhythm sleep disorders (CRSDs), there is a paucity of investigations into the daytime impairments associated with the disorders.2 Yet, reports of daytime impairment are a core symptom in the diagnosis of many sleep disorders. The circadian system is known to modulate alertness and performance patterns, and is known to be dysregulated in CRSD. One mechanism by which the circadian system may manifest in the daytime impairments in these patients is via altered timing or amplitude of the wake maintenance zone (WMZ).The WMZ has previously been described as a 2-to 3-h window of reduced sleep propensity that occurs immediately prior to the evening onset of melatonin secretion and under normal conditions, occurs several hours prior to bedtime. 3,4 This window is c...