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ABSTRACT: BACKGROUND: Circadian disturbances may play a key role in the pathogenesis of some forms of mood disorders. Despite marked changes in circadian rhythms during the normal course of adolescence and young adulthood, less is known about changes in the 24-h sleep-wake cycle in young persons with mood disorders. METHODS: Seventy-five young participants with mood disorders (unipolar: n=46, 20.1±4.7 years old; bipolar I or II: n=29, 23.2±4.3) and 20 healthy participants (24.8±2.5 years old) underwent actigraphy monitoring during a depressive phase over seven consecutive days and nights. Sleep phase delay was defined as mean sleep onset ≥1:30am and/or sleep offset ≥10:00am. RESULTS: A delayed sleep phase was found in 62% of participants with bipolar disorders when depressed, compared with 30% of those with unipolar depression (χ(2)=6.0, p=0.014) and 10% of control participants (χ(2)=11.2, p<0.001). Sleep offset times were significantly later in subjects with mood disorders compared to the control group, and later in those with bipolar as compared with unipolar disorders (all p≤0.043). LIMITATIONS: This study was cross-sectional and the depressed groups were somewhat younger compared to the healthy controls. Longitudinal studies are required to determine the predictive significance of these findings. CONCLUSIONS: Young patients with mood disorders, especially those with bipolar disorders, are particularly likely to have a delayed sleep phase. Therapies focused on advancing sleep phase may be of specific benefit to these young persons.
Journal of affective disorders 08/2012; · 3.76 Impact Factor
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ABSTRACT: Schizophrenia is a psychiatric disorder that includes symptoms such as hallucinations, disordered thoughts, disorganized or catatonic behaviour, cognitive dysfunction and sleep-wake disturbance. In addition to these symptoms, cardiometabolic dysfunction is common in patients with schizophrenia. While previously it has been thought that cardiometabolic symptoms in patients with schizophrenia were associated with medications used to manage this disorder, more recently it has been demonstrated that these symptoms are present in drug naive and unmedicated patients. Sleep-wake disturbance, resulting in chronic sleep loss has also been demonstrated to induce changes in cardiometabolic function. Chronic sleep loss has been associated with an increased risk for weight gain, obesity and cardiac and metabolic disorders, independent of other potentially contributing factors, such as smoking and body mass index. We hypothesise that the sleep-wake disturbance comorbid with schizophrenia may play a significant role in the high prevalence of cardiometabolic dysfunction observed in this patient population. Here we present a critical review of the evidence that supports this hypothesis.
Clinical Psychopharmacology and Neuroscience 04/2012; 10(1):1-12.
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ABSTRACT: Naismith SL, Rogers NL, Lewis SJG, Diamond K, Terpening Z, Norrie L, Hickie IB. Sleep disturbance in mild cognitive impairment: differential effects of current and remitted depression.Objective: Although patients with mild cognitive impairment (MCI) commonly report sleep disturbance, the extent to which depressive symptoms contribute to this relationship is unclear. This study sought to delineate the contribution of current and remitted major depression (MD) to sleep disturbance in MCI.Methods: Seventy-seven patients meeting criteria for MCI (mean age = 66.6 ± 8.8 years) were grouped according to those with no history of depression (MCI, n = 33), those meeting criteria for current MD [mild cognitive impairment and meeting criteria for current major depression (DEP-C), n = 14] and those with remitted MD [mild cognitive impairment and remitted major depression (DEP-R), n = 30]. Additionally, 17 healthy controls (CON) participated. Sleep was patient-rated using the Pittsburgh Sleep Quality Index and included assessment of sleep quality, duration, efficiency, disturbances, medications, sleep onset latency and daytime dysfunction. Depression severity was clinician-rated using the Hamilton Depression Rating Scale.Results: Overall sleep disturbance was significantly greater in the DEP-C and DEP-R groups in comparison to the CON and MCI groups (p < 0.001). Only 12% of CON reported sleep disturbance, compared to 30% of MCI, 63% of DEP-R and 86% of DEP-C. Sub-scale analysis showed that the sleep disturbance in depressive groups was most evident across the domains of sleep quality, sleep efficiency, sleep latency and daytime dysfunction.Conclusion: Sleep disturbance in MCI is strongly associated with a current or past diagnosis of MD. The finding that sleep complaints are still prominent in those with remitted depression, suggests that ‘trait’ markers exist that may reflect underlying neurobiological changes within the sleep–wake system.
Acta Neuropsychiatrica 07/2011; 23(4):167 - 172. · 0.58 Impact Factor
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ABSTRACT: Major depression is one of the leading causes of premature death and disability. Although available drugs are effective, they also have substantial limitations. Recent advances in our understanding of the fundamental links between chronobiology and major mood disorders, as well as the development of new drugs that target the circadian system, have led to a renewed focus on this area. In this review, we summarise the associations between disrupted chronobiology and major depression and outline new antidepressant treatment strategies that target the circadian system. In particular, we highlight agomelatine, a melatonin-receptor agonist and selective serotonergic receptor subtype (ie, 5-HT(2C)) antagonist that has chronobiotic, antidepressant, and anxiolytic effects. In the short-term, agomelatine has similar antidepressant efficacy to venlafaxine, fluoxetine, and sertraline and, in the longer term, fewer patients on agomelatine relapse (23·9%) than do those receiving placebo (50·0%). Patients with depression treated with agomelatine report improved sleep quality and reduced waking after sleep onset. As agomelatine does not raise serotonin levels, it has less potential for the common gastrointestinal, sexual, or metabolic side-effects that characterise many other antidepressant compounds.
The Lancet 05/2011; 378(9791):621-31. · 38.28 Impact Factor
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ABSTRACT: Multifactorial strategies that prevent or delay the onset or progress of cognitive decline and dementia are needed, and should include education regarding recognized risk factors. The current study sought to investigate whether older adults "at risk" of cognitive decline benefit from psychoeducation targeting healthy brain aging.
65 participants (mean age 64.8 years, SD 9.6) with a lifetime history of major depression; vascular risk as evidenced by at least one vascular risk factor; and/or subjective or objective memory impairment were allocated to weekly psychoeducation sessions or a waitlist control group. The small group sessions were conducted over ten weeks by a team of medical and allied health professionals with expertise in late-life depression and cognition. Sessions focused on modifiable risk factors for cognitive decline including vascular risk, diet, exercise, depression, anxiety and sleep disturbance, as well as providing practical strategies for memory and cognition. Both the psychoeducation and waitlist group completed a 20-item knowledge test at baseline and follow-up. Participants in the psychoeducation group were asked to complete follow-up self-report satisfaction questionnaires.
Repeated measures ANOVA showed a significant interaction effect depicting improvements in knowledge associated with psychoeducation, corresponding to an improvement of 15% from baseline. Satisfaction data additionally showed that 92.3% of participants rated the program as "good" to "excellent", and over 90% suggested they would recommend it to others.
A group-based psychoeducation program targeting healthy brain aging is effective in improving knowledge. Additionally, it is acceptable and rated highly by participants.
International Psychogeriatrics 04/2011; 23(3):413-24. · 2.24 Impact Factor
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ABSTRACT: Sleep-wake disturbance in older people is a risk factor for depression onset and recurrence. The aim of this study was to determine if objective sleep-wake disturbance in late-life depression relates to neuropsychological functioning.
Forty-four older patients with a lifetime history of major depression and 22 control participants underwent psychiatric, medical and neuropsychological assessments. Participants completed self-report sleep measures, sleep diaries and wore wrist actigraphy for two weeks. Outcome measures included sleep latency, the number and duration of nocturnal awakenings and the overall sleep efficiency.
Patients with depression had a greater duration of nocturnal awakenings and poorer sleep efficiency, in comparison to control participants. Sleep disturbance in patients was associated with greater depression severity and later ages of depression onset. It also related to poorer psychomotor speed, poorer verbal and visual learning, poorer semantic fluency as well as poorer performance on tests of executive functioning. These relationships largely remained significant after controlling for depression and estimated apnoea severity.
This sample had only mild levels of depression severity and results require replication in patients with moderate to severe depression. The inclusion of polysomnography and circadian markers would be useful to delineate the specific features of sleep-wake disturbance that are critical to cognitive performance.
Sleep-wake disturbance in older patients with depression is related to neuropsychological functioning and to later ages of illness onset. This study suggests that common neurobiological changes may underpin these disease features, which may, in turn, warrant early identification and management.
Journal of affective disorders 03/2011; 132(1-2):139-45. · 3.76 Impact Factor
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ABSTRACT: With the increasing aging population, neurodegenerative disorders will become more common in clinical practice. These disorders involve multiple pathophysiological mechanisms that differentially affect cognition, mood, and physical functions. Possibly due to the involvement of common underlying neurobiological circuits, sleep and/or circadian (sleep-wake) changes are also common in this disease group. Of significance, sleep-wake changes are often a prodromal feature and are predictive of cognitive decline, psychiatric symptoms, quality of life, need for institutional care, and caregiver burden. Unfortunately, in neurodegenerative disease, few studies have included detailed polysomnography or neuropsychological assessments although some data indicate that sleep and neurocognitive features are related. Further studies are also required to address the effects of pharmacological and nonpharmacological treatments on cognitive functioning. Such research will hopefully lead to targeted early intervention approaches for cognitive decline in older people.
Progress in brain research 01/2011; 190:21-52. · 3.04 Impact Factor
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Naismith Sl,
Rogers Nl,
Lewis Sjg,
Norrie L Hickie,
Sharon L Naismith, Naomi L Rogers,
Simon J G Lewis,
Keri Diamond,
Zoë Terpening,
Louisa Norrie,
Ian B Hickie,
Sharon Naismith
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ABSTRACT: IB. Sleep disturbance in mild cognitive impairment: differential effects of current and remitted depression. Objective: Although patients with mild cognitive impairment (MCI) commonly report sleep disturbance, the extent to which depressive symptoms contribute to this relationship is unclear. This study sought to delineate the contribution of current and remitted major depression (MD) to sleep disturbance in MCI. Methods: Seventy-seven patients meeting criteria for MCI (mean age = 66.6 ± 8.8 years) were grouped according to those with no history of depression (MCI, n = 33), those meeting criteria for current MD [mild cognitive impairment and meeting criteria for current major depression (DEP-C), n = 14] and those with remitted MD [mild cognitive impairment and remitted major depression (DEP-R), n = 30]. Additionally, 17 healthy controls (CON) participated. Sleep was patient-rated using the Pittsburgh Sleep Quality Index and included assessment of sleep quality, duration, efficiency, disturbances, medications, sleep onset latency and daytime dysfunction. Depression severity was clinician-rated using the Hamilton Depression Rating Scale. Results: Overall sleep disturbance was significantly greater in the DEP-C and DEP-R groups in comparison to the CON and MCI groups (p < 0.001). Only 12% of CON reported sleep disturbance, compared to 30% of MCI, 63% of DEP-R and 86% of DEP-C. Sub-scale analysis showed that the sleep disturbance in depressive groups was most evident across the domains of sleep quality, sleep efficiency, sleep latency and daytime dysfunction. Conclusion: Sleep disturbance in MCI is strongly associated with a current or past diagnosis of MD. The finding that sleep complaints are still prominent in those with remitted depression, suggests that 'trait' markers exist that may reflect underlying neurobiological changes within the sleep–wake system.
Acta Neuropsychiatrica 01/2011; 23:167-172. · 0.58 Impact Factor
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ABSTRACT: Chronic nocturnal sleep restriction results in accumulation of neurobehavioral impairment across days. The purpose of this study was to determine whether time of day modulates the effects of sleep restriction on objective daytime performance deficits and subjective sleepiness across days of chronic sleep restriction.
There were N = 90 healthy adults (21-49 yr; 38 women) who participated in a 14-d laboratory protocol involving randomization to 1 of 18 schedules of restricted nocturnal sleep with and without a diurnal nap for 10 consecutive days. The total time available for daily sleep ranged from 4.2 h to 8.2 h across conditions. Performance lapses on the psychomotor vigilance test (PVT) and subjective sleepiness were measured each day every 2 h during scheduled wakefulness. Nonlinear mixed-effects regression was used to test the hypothesis that there would be an interaction between time of day and the accumulation (slope across days) of neurobehavioral sleepiness.
In agreement with earlier studies, less sleep time resulted in faster accumulation of deficits across days. Time of day significantly affected this relationship for both PVT lapses and subjective sleepiness. The build-up rate of cumulative neurobehavioral deficits across days was largest at 0800 and became progressively smaller across the hours of the day, especially between 1600 and 2000. Following 8 d of sleep restricted to 4 h/d, subjects averaged 8.3 more PVT performance lapses at 0800 than at 1800.
This study provides evidence that the circadian system has a substantial modulatory effect on cumulative impairment from chronic sleep restriction and that it facilitates a period of relatively protected alertness in the late afternoon/early evening hours when nocturnal sleep is chronically restricted.
Aviation Space and Environmental Medicine 08/2010; 81(8):735-44. · 0.88 Impact Factor
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ABSTRACT: Continuous positive airway pressure (CPAP) use is associated with reduced motor vehicle accidents in patients with obstructive sleep apnea (OSA). However, interruption of CPAP therapy is common and is associated with a decline in daytime function.
We hypothesized that the wakefulness promoter, modafinil, would ameliorate this decline.
Patients were admitted to the laboratory for three consecutive nights. CPAP was used for the first night, followed by a baseline day, and was then withdrawn for the two subsequent nights (nasal airflow monitored). On each of the mornings after the two CPAP withdrawal nights, patients received 200 mg modafinil or placebo (n = 21) in a randomized, double-blind, crossover design. Treatment periods were separated by a 5-week washout. Driving simulator performance, neurocognitive performance, and subjective alertness were measured by the AusEd driving simulator, psychomotor vigilance task, and Karolinska Sleepiness Scale, respectively.
During CPAP withdrawal, severe sleep-disordered breathing was evident and administration of modafinil improved simulated driving performance (steering variability, P < 0.0001; mean reaction time, P <or= 0.0002; lapses, P <or= 0.01 on a concurrent task), psychomotor vigilance task (mean 1/reaction time and lapses, both P <or= 0.0002), and subjective sleepiness (P <or= 0.01).
Modafinil prevented the decline in simulated driving performance, neurocognitive performance, and subjective sleepiness in patients with OSA with acutely interrupted CPAP therapy. Clinical trial registered with the Australian New Zealand Clinical Trials Registry at www.anzctr.org.au (ACTRN12606000027516).
American Journal of Respiratory and Critical Care Medicine 04/2010; 181(8):825-31. · 11.08 Impact Factor
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ABSTRACT: In this study, we sought to evaluate the utility of actigraphy for examining symptoms of rapid eye movement sleep behaviour disorder (RSBD).
Twenty-two patients with idiopathic Parkinson's Disease (mean age=63.4 years, SD=7.5) underwent neurological assessment and completed sleep diaries, self-report sleep questionnaires and 2-weeks of actigraphy. They also completed the rapid eye movement sleep behavior disorder questionnaire and were classified as screening negative (RSBD-, n=9) or positive (RSBD+, n=13) for RSBD according to published criteria. Key outcome data were the number of wake bouts and duration of arousals during the sleep interval as determined by actigraphy.
Patients classified as RSBD+ demonstrated a higher number of wake bouts than those who were RSBD- (p=0.011).
These results suggest that actigraphy may be a viable tool to assist in the early identification of RSBD. In turn, this could guide early intervention approaches.
Clinical neurology and neurosurgery 03/2010; 112(5):420-3. · 1.30 Impact Factor
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ABSTRACT: While literature suggests that sleep is important for cognition and mood, and that sleep disturbance is a prominent feature of neurodegenerative and neuropsychiatric disorders, these relationships have not yet been examined in older people ''at risk" of dementia. In this study, 15 older people with the nonamnestic subtype of mild cognitive impairment ([MCI] mean age = 66.7 years, SD = 8.7) underwent psychiatric and neuropsychological assessment. Participants completed sleep diaries, questionnaires, and 2 weeks of actigraphy. Key outcome data during the rest interval were time spent ''awake" or wake after sleep onset (WASO) and the number of arousals/wake bouts. Results showed that even after controlling for age, greater WASO was associated with reduced attention and executive functioning and increased arousals were related to poorer nonverbal learning and problem solving. This preliminary data suggests that sleep-wake disturbance in nonamnestic forms of MCI is related to cognitive functioning and may be indicative of shared neurobiological underpinnings.
Journal of Geriatric Psychiatry and Neurology 03/2010; 23(2):123-30. · 3.07 Impact Factor
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ABSTRACT: Night eating syndrome (NES) is characterized by evening hyperphagia and frequent awakenings accompanied by food intake. Patients with NES display a delayed circadian pattern of food intake but retain a normal sleep-wake cycle. These characteristics initiated the current study, in which the phase and amplitude of behavioral and neuroendocrine circadian rhythms in patients with NES were evaluated. Fifteen women with NES (mean age +/- SD, 40.8 +/- 8.7 y) and 14 control subjects (38.6 +/- 9.5 y) were studied in the laboratory for 3 nights, with food intake measured daily. Blood also was collected for 25 h (every 2 h from 0800 to 2000 h, and then hourly from 2100 to 0900 h) and assayed for glucose and 7 hormones (insulin, ghrelin, leptin, melatonin, cortisol, thyroid-stimulating hormone [TSH] and prolactin). Statistical analyses utilized linear mixed-effects cosinor analysis. Control subjects displayed normal phases and amplitudes for all circadian rhythms. In contrast, patients with NES showed a phase delay in the timing of meals, and delayed circadian rhythms for total caloric, fat, and carbohydrate intake. In addition, phase delays of 1.0 to 2.8 h were found in 2 food-regulatory rhythms-leptin and insulin-and in the circadian melatonin rhythm (with a trend for a delay in the circadian cortisol rhythm). In contrast, circulating levels of ghrelin, the primary hormone that stimulates food intake, were phase advanced by 5.2 h. The glucose rhythm showed an inverted circadian pattern. Patients with NES also showed reduced amplitudes in the circadian rhythms of food intake, cortisol, ghrelin, and insulin, but increased TSH amplitude. Thus, patients with NES demonstrated significant changes in the timing and amplitude of various behavioral and physiological circadian markers involved in appetite and neuroendocrine regulation. As such, NES may result from dissociations between central (suprachiasmatic nucleus) timing mechanisms and putative oscillators elsewhere in the central nervous system or periphery, such as the stomach or liver. Considering these results, chronobiologic treatments for NES such as bright light therapy may be useful. Indeed, bright light therapy has shown efficacy in reducing night eating in case studies and should be evaluated in controlled clinical trials.
Journal of Biological Rhythms 03/2009; 24(1):85-94. · 2.93 Impact Factor
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ABSTRACT: Depression in older adults is associated with neuropsychological dysfunction, fronto-subcortical brain changes and sleep disturbance. Research suggests that adequate sleep is critical for many aspects of cognition including processing speed, verbal skills and memory. However, the association between sleep disturbance and neuropsychological functioning in depression has not been well evaluated. The current study therefore aimed to investigate these relationships.
Forty-eight people (mean age=59.6, sd=8.2) meeting DSM-IV criteria for unipolar major depression were included for analysis. Neuropsychological assessment included assessment of processing speed, learning and memory, verbal fluency and executive functions. Early and late insomnia were defined by scores on the Hamilton Depression Rating Scale.
While early insomnia was related to depression severity and poorer global cognition, late insomnia was associated with later age of depression onset, depression severity, and poorer scores on tests of verbal fluency and memory. The associations between cognition and late insomnia were not accounted for by depression severity or age of onset of disorder.
This study was retrospective in nature, and did not include objective measures of sleep.
This is the first known study to indicate that late insomnia in older people with major depression may be independently and aetiologically linked to neuropsychological performance, particularly verbal fluency and memory. It may also indicate underlying structural and neurochemical changes. Sleep and circadian disturbance may serve as a biomarker for ongoing cognitive decline and may be a potentially modifiable risk factor.
Journal of affective disorders 02/2009; 116(1-2):139-43. · 3.76 Impact Factor
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ABSTRACT: Nocturnal sleep restriction and compensation with daytime naps is common in today's society. In a between-participants design, we examined the effects of chronic (10 nights) sleep restriction on 24 h plasma melatonin profiles in humans. Following a baseline period with 8.2 h time in bed (TIB) for sleep, participants were randomized to a control (8.2 h TIB) or sleep-restriction condition (4.2 h TIB), with and without diurnal naps. Sleep restriction was achieved via delaying bedtime and advancing wake time by 2 h each relative to the baseline sleep period. Participants were maintained in a controlled, time isolated laboratory environment throughout the protocol, with light levels below 40 lx at all times. Twenty-four hour plasma melatonin profiles were assessed at baseline and at the end of the sleep-restriction period, with subjects maintained in a constant posture protocol. Compared with the baseline assessment and the 8.2 h TIB control group, a significant phase delay in melatonin onset (1.2 +/- 0.9 h) occurred in all sleep-restriction (4.2 h TIB) groups (P < 0.05). There was no evidence of a phase advance or shortening of the period of melatonin secretion associated with the advanced waking time. These results suggest that nocturnal light and dark exposure may be more potent in effecting circadian phase shifts than exposure to morning light, at least in conditions of controlled, dim lighting in the laboratory.
Journal of Sleep Research 12/2008; 17(4):406-11. · 3.16 Impact Factor
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ABSTRACT: We hypothesized that individuals with untreated obstructive sleep apnea (OSA) would exhibit greater vulnerability to sleep deprivation than healthy controls, due to the additional neurobiological 'load' of chronic sleep fragmentation. After baseline sleep with 8 h time in bed, participants remained awake for 40 h. Psychomotor Vigilance Task (PVT, mean slowest 10% 1/RT), AusEd Driving Simulator task (steering and speed deviation), and subjective sleepiness (Karolinska Sleepiness Scale, KSS) were assessed every 2 h. Nonlinear mixed-effects models were used to characterize individual differences in baseline/average performance, the linear effect of increasing hours awake, circadian amplitude and phase. Eight participants with untreated OSA with mean (SD) age 44.6 (8.4), apnea-hypopnea index (AHI) 49.8 (24.7), Epworth Sleepiness Scale (ESS) 11.9 (4.8) and nine healthy controls age 27.8 (3.7), AHI 4.5 (2.7), ESS 7.3 (2.1) completed the protocol. Baseline KSS was significantly higher (1.4 units, P = 0.03) in the OSA group and there was a trend toward lower baseline speed deviation on the AusEd (P = 0.05). After adjusting for the significant effects of accumulated time awake, circadian amplitude and phase (all P < 0.005), there was no difference in performance decrements between those with and without sleep apnea in PVT, driving simulator performance and subjective sleepiness (P > 0.5). Random-effects modeling confirmed the presence of significant inter-individual variability in vulnerability to sleep deprivation. Patients with OSA did not respond differently to sleep deprivation than healthy controls. As expected, total sleep deprivation led to significant worsening in performance and subjective sleepiness in both groups.
Journal of Sleep Research 09/2008; 17(3):322-30. · 3.16 Impact Factor
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ABSTRACT: The demands of sustaining high levels of neurobehavioral performance during space operations necessitate precise scheduling of sleep opportunities in order to best preserve optimal performance. We report here the results of the first split-sleep, dose-response experiment involving a range of sleep/wake scenarios with chronically reduced nocturnal sleep, augmented with a diurnal nap. To characterize performance over all combinations of split sleep in the range studied, we used response surface mapping methodology. Waking neurobehavioral performance was studied in N=90 subjects each assigned to one of 18 sleep regimens consisting of a restricted nocturnal anchor sleep period and a diurnal nap. Psychomotor vigilance task performance and subjective assessments of sleepiness were found to be primarily a function of total time in bed per 24 h regardless of how sleep was divided among nocturnal anchor sleep and diurnal nap periods. Digit symbol substitution task performance was also found to be primarily a function of total time in bed per 24 h; however, accounting for nocturnal sleep duration and nap duration separately provided a small but significant enhancement in the variance explained. The results suggest that reductions in total daily sleep result in a near-linear accumulation of impairment regardless of whether sleep is scheduled as a consolidated nocturnal sleep period or split into a nocturnal anchor sleep period and a diurnal nap. Thus, split sleep schedules are feasible and can be used to enhance the flexibility of sleep/work schedules for space operations involving restricted nocturnal sleep due to mission-critical task scheduling. These results are generally applicable to any continuous industrial operation that involves sleep restriction, night operations, and shift work.
Acta Astronautica 02/2008; 63(7-10):833-840. · 0.61 Impact Factor
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ABSTRACT: Shiftwork is a common experience for many workers. There are a wide range of shift systems in use, with a number of general approaches and myriad variations of each one. Many aspects of shift systems have been studied, but attempts to reach definitive conclusions about appropriate designs have been hampered by a number of methodological issues. The aim of this systematic review was to provide evidence-based recommendations on the effect of various shift systems on neurobehavioural and physiological functioning and to identify areas which are lacking in appropriate evidence. Two main aspects of shift design were able to be considered-the direction of shift rotation and extended shift length (mainly 12-h shifts). Other areas for which there was at least one relevant paper of adequate methodology were the use of naps during night shifts, the starting time of shifts, and several other specific shift issues. Overall, the review found there is insufficient evidence to support definitive conclusions regarding any of these factors. However, the analysis provides support for the use of forward rotating shift systems in preference to backward rotating shift systems, at last as far as 8-h shifts are concerned. There are many unanswered questions in shift design. For these questions to be answered, it is important that the methodological shortcomings present in most of the studies published to date be overcome.
Sleep Medicine Reviews 07/2007; 11(3):179-94. · 6.93 Impact Factor
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ABSTRACT: A causal relationship between declining nocturnal core temperature, increasing peripheral temperature, and sleep onset has been reported. The exact trigger for these thermoregulatory changes around sleep onset, however, is unknown. Our aim was to examine one possible trigger: prior knowledge of bedtime. Fourteen young, healthy male subjects (mean age+/-sem: 21.9+/-0.6 years), participated in a randomized, single-blind crossover study, where knowledge of bedtime was manipulated. Following a baseline night, subjects completed three experimental nights: (A) aware of bedtime; (B) no knowledge of bedtime; (C) misinformed about bedtime. In all conditions lights were turned off at each subject's habitual bedtime (determined from sleep diaries), to individually standardize the time of lights off. Polysomnography, rectal and peripheral (foot) temperatures were recorded continuously on each night. There was no significant difference in the time of sleep onset among conditions (mean+/-s.d.: 11:55 h+/-0.73 min), and in all conditions sleep onset occurred at the same rectal temperature. A significant difference in the temperature gradient between rectal and peripheral temperatures among the conditions was evident from 90 min to 40 min prior to sleep onset (P=0.05), with subjects achieving a more rapid rate of temperature change in the B and C condition relative to condition A. The present findings suggest that knowledge of bedtime may modulate changes in temperature around the time of sleep onset. It appears that there is an optimal core body temperature at which to initiate sleep, and changes in the rate of peripheral heat loss may assist in achieving this optimal temperature, and hence facilitate sleep onset.
Physiology & Behavior 04/2007; 90(4):643-7. · 2.87 Impact Factor
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ABSTRACT: Evaluation of sleep in subjects with night eating syndrome (NES).
Polysomnographic and questionnaire comparisons between subjects with NES and controls.
Fifteen women with NES (mean +/- SD = 41 +/- 8 years) and 14 women (comparable age and weight) without NES (39 +/- 10 years) were studied in the laboratory for 3 days.
N/A.
Subjects with NES did not differ from controls in timing of sleep onset or offset. They had less stage 2 sleep than controls (minutes, p = .012; percentage, p = .016) and less stage 3 sleep (p = .023), which contributed to their having a lower total sleep time (p = .05) and reduced sleep efficiency (p = .03). Subjects with NES did not have more awakenings than controls, but 93.3% of them ate on awakening during all 3 nights, while 92.9% of controls did not eat on any night. Logistic discriminant analyses identified a multiple sleep parameter model associated with increased likelihood of NES that had sensitivity of 84.6% and specificity of 76.9%. Patients with NES were more depressed than controls (p < .001) and reported greater sleep disturbance that included lower sleep quality (p < or = .001), reduced sleep duration (p < or = .001), and increased number of awakenings (p < or = .001).
Patients with NES appear to have sleep maintenance insomnia rather than sleep-related eating disorder or a parasomnia. The maintenance of normal timing for sleep-wake behavior in the presence of a phase delay in the timing of caloric intake suggests this disorder reflects a state of internal circadian desynchrony associated with significant sleep complaints. It remains unknown whether the sleep disturbance precedes the abnormally timed eating.
Sleep 07/2006; 29(6):814-9. · 5.05 Impact Factor
