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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...

Objectives:We aimed to identify the prevalence of circadian phase and phase angle abnormalities in patients with insomnia. Methods: We conducted a cross-sectional, multicenter study at three sleep laboratories in the United States and Australia. Patients with insomnia and healthy control participants completed a sleep log for 7 days. Circadian phase was assessed from salivary dim light melatonin onset (DLMO) time during a 12-hour laboratory visit. Results: Seventy-nine patients meeting the Research Diagnostic Criteria for Primary, Psychophysiological, Paradoxical, and/or Idiopathic Childhood Insomnia (46 females, 35.5 ± 12.3 years [M ± SD]) and 21 controls (14 females, 34.4 ± 11.8 years). As compared to controls, patients with insomnia tried to initiate sleep on average at the same clock time (24:17 ± 1:17 hours vs. 24:13 ± 1:30 hours, respectively; p = .84) but had a later average DLMO times (20:56 ± 1:55 hours, 18:17-01:21 vs. 22:02 ± 2:02 hours, 17:11-04:52, respectively; p = .04). Consequently, patients with insomnia slept at an earlier circadian phase than controls (phase angle, bedtime-DLMO 2:13 hours (± 1:43) vs. 3:10 hours (± 1:08), respectively; p = .008), of whom 10% tried to sleep at or before DLMO (compared to 0 controls), and 22% tried to sleep before or within 1 hour after DLMO (compared to 6% of controls). Conclusions: A substantial proportion (10%-22%) of patients with insomnia initiate sleep at too early a circadian phase, implicating a circadian etiology for their insomnia. Outpatient circadian phase assessments should be considered to improve differential diagnoses in insomnia and to inform the development of appropriately timed circadian-based treatments.

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The last decade has seen a dramatic increase in our understanding of sleep-dependent memory consolidation, moving it from a generally discredited (or at best ignored) concept to a largely accepted tenet among both memory and sleep researchers, even found in undergraduate psychology textbooks. This work has established a firm connection between sleep and memory function. But given the complexity of both sleep and memory, each of which comprise multiple stages and subtypes, even the most basic characterizations of this phenomenon remain unclear. To date, most studies have sought to assign consolidation of particular classes of memory to discrete sleep stages, for example consolidation of procedural memories to REM sleep or declarative memories to slow wave sleep (SWS). But exceptions to this simple dichotomy come close to outnumbering supporting studies.Several new studies, presented here, lead us to now propose a unified sleep-dependent memory consolidation hypothesis, to describe how sleep stages contribute to memory consolidation. We propose that sleep plays a more nuanced role in memory processing than previously considered, with sleep stages being selectively involved not with specific memory types, but with specific components of the memory consolidation process. Specifically, we propose that SWS stabilizes recently acquired declarative and procedural memories, while REM and Stage 2 nonREM sleep subsequently enhance them, selectively reinforcing their most valuable components and integrating them into pre-existing networks of stored information.This new hypothesis is consistent with the growing literature of sleep-dependent consolidation across a range of memory functions, and is strongly supported by new results presented in this talk. These new results, in concert with the unified memory consolidation hypothesis, move the study of sleep and memory beyond a discussion of classical memory consolidation (i.e., stabilization), into the realm of more powerful and valuable forms of sleep-dependent memory processing that (i) enlarge the neural networks in which memories are stored, (ii) extract patterns and rules from large bodies of encoded information (iii) integrate them with other, older memories into rich semantic networks, and, perhaps as a consequence of these other processes, (iv) selectively enhance those aspects of memories of greatest value to the organism.Background: There are few data on the sleep patterns of Australian children, or the associations between sleep and sociodemographic factors [age, sex, socio-economic status (SES)], temporal context (type of day, season), type of day (school day, weekend, holiday), and individual characteristics (weight status). Methods: Between 2001 and 2007, 4,033 9-18 year old Australians reported the time of falling asleep and waking up on 9,053 individual nights. Using a computerised use-of-time recall, the adolescents also reported all activities performed on that day, choosing from 250 different activities and reporting in time slices as fine as 5 minutes. Resul...