Circadian Phase and Phase Angle Disorders in Primary Insomnia.

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.

Neurobehavioral performance impairment in insomnia: relationships with self-reported sleep and daytime functioning.

STUDY OBJECTIVES: Despite the high prevalence of insomnia, daytime consequences of the disorder are poorly characterized. This study aimed to identify neurobehavioral impairments associated with insomnia, and to investigate relationships between these impairments and subjective ratings of sleep and daytime dysfunction. DESIGN: Cross-sectional, multicenter study. SETTING: Three sleep laboratories in the USA and Australia. PATIENTS: Seventy-six individuals who met the Research Diagnostic Criteria (RDC) for Primary Insomnia, Psychophysiological Insomnia, Paradoxical Insomnia, and/or Idiopathic Childhood Insomnia (44F, 35.8 ± 12.0 years [mean ± SD]) and 20 healthy controls (14F, 34.8 ± 12.1 years). INTERVENTIONS: N/A. MEASUREMENTS AND RESULTS: Participants completed a 7-day sleep-wake diary, questionnaires assessing daytime dysfunction, and a neurobehavioral test battery every 60-180 minutes during an afternoon/evening sleep laboratory visit. Included were tasks assessing sustained and switching attention, working memory, subjective sleepiness, and effort. Switching attention and working memory were significantly worse in insomnia patients than controls, while no differences were found for simple or complex sustained attention tasks. Poorer sustained attention in the control, but not the insomnia group, was significantly associated with increased subjective sleepiness. In insomnia patients, poorer sustained attention performance was associated with reduced health-related quality of life and increased insomnia severity. CONCLUSIONS: 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.

Improved neurobehavioral performance during the wake maintenance zone.

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, specifically 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 influence of the WMZ on neurobehavioral performance under normal conditions and following sleep deprivation. METHODS: Thirty-one adults (8 F; 18-29 y) completed an in-patient 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 significantly 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 circa-dian 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.

Fatigue and sleep disturbance following traumatic brain injury--their nature, causes, and potential treatments.

BACKGROUND: Although fatigue and sleep disturbance are commonly reported following traumatic brain injury (TBI), understanding of their nature and treatment remains limited. OBJECTIVES: This article reviews a series of investigations of the nature and causes of fatigue and sleep disturbance following TBI. METHODS: A large cohort of community-based patients with TBI, recruited from a TBI rehabilitation program, completed measures of subjective fatigue and sleep disturbances, as well as attentional measures. A subgroup of participants completed polysomnography and assessment of dim light melatonin onset. RESULTS: Fatigue and sleep disturbance are common. Both are associated with anxiety, depression, and pain. However, fatigue is also associated with slowed information processing and the need for increased effort in performing tasks. Sleep disturbances contribute to fatigue. Objective sleep studies show reduced sleep efficiency, increased sleep onset latency, and increased time awake after sleep onset. Depression and pain exacerbate but cannot entirely account for these problems. There is increased slow-wave sleep. Individuals with TBI show lower levels of evening melatonin production, associated with less rapid-eye movement sleep. CONCLUSIONS: 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.

Searching for the daytime impairments of primary insomnia.

Primary insomnia is a sleep disorder where the subjective complaint of initiating or maintaining sleep, or the experience of sleep that is non-refreshing, cannot be directly attributed to a comorbid medical or psychiatric disorder. For a diagnosis of primary insomnia, a patient must also report that the nighttime sleep disturbance is impacting upon daytime functioning. Yet, while subjective complaints of impaired wake-time functioning are well documented, consistent objective evidence of these impairments has proved elusive, particularly with regard to cognitive functioning. We aimed to review the body of literature examining neurobehavioural impairments in primary insomnia to identify which cognitive domains appear to be most consistently impaired in this group. The relatively few studies that have investigated neurobehavioural performance deficits in patients with primary insomnia have produced inconsistent and sometimes conflicting findings. It is suggested that methodological limitations, including heterogeneous test populations, variable testing protocols and conditions as well as unsuitable cognitive tasks have contributed to our inability to describe unequivocally the daytime impairments associated with insomnia. Based on our review, it appears that the deficits associated with insomnia are relatively subtle and may be qualitatively different to those that result from other sleep disorders and from imposed sleep deprivation. Attention tasks, which have a high cognitive load, and working memory tasks appear to show performance deficits more often than not in insomnia patients. It is important to more definitively characterise the daytime impairments associated with primary insomnia so that the efficacy of treatments to remedy the wake-time consequences of the disorder, in addition to the nighttime symptoms, can be investigated.