Siobhan Banks

University of South Australia , Adelaide, South Australia, Australia

Are you Siobhan Banks?

Claim your profile

Publications (21)86.42 Total impact

  • Article: Implications of Sleep Restriction and Recovery on Metabolic Outcomes.
    Roo Killick, Siobhan Banks, Peter Y Liu
    [show abstract] [hide abstract]
    ABSTRACT: Context:Alongside the growing epidemics of obesity and diabetes mellitus, chronic partial sleep restriction is also increasingly common in modern society, and the metabolic implications of this have not been fully illustrated as yet. Whether recovery sleep is sufficient to offset these detriments is an area of ongoing research.Objective:This review seeks to summarize the relevant epidemiological and experimental data in the areas of altered metabolic consequences of both shortened sleep and subsequent recovery sleep.Data Acquisition:The medical literature from 1970 to March 2012 was reviewed for key articles.Data Synthesis:Epidemiological studies suggest associations between shortened sleep and future obesity and diabetes. Experimental data thus far show a probable link between shortened sleep and altered glucose metabolism as well as appetite dysregulation.Conclusion:Sleep often seems undervalued in modern society, but this may have widespread metabolic consequences as described in this review. Acute sleep loss is often unavoidable, but chronic sleep restriction ideally should not be. Understanding the implications of both sleep restriction and recovery on metabolic outcomes will guide public health policy and allow clinical recommendations to be prescribed.
    The Journal of clinical endocrinology and metabolism 09/2012; · 6.50 Impact Factor
  • Article: Sleep deprivation and stressors: Evidence for elevated negative affect in response to mild stressors when sleep deprived.
    [show abstract] [hide abstract]
    ABSTRACT: Stress often co-occurs with inadequate sleep duration, and both are believed to impact mood and emotion. It is not yet known whether inadequate sleep simply increases the intensity of subsequent stress responses or interacts with stressors in more complicated ways. To address this issue, we investigated the effects of one night of total sleep deprivation on subjective stress and mood in response to low-stress and high-stress cognitive testing conditions in healthy adult volunteers in two separate experiments (total N = 53). Sleep was manipulated in a controlled, laboratory setting and stressor intensity was manipulated by changing difficulty of cognitive tasks, time pressure, and feedback about performance. Sleep-deprived participants reported greater subjective stress, anxiety, and anger than rested controls following exposure to the low-stressor condition, but not in response to the high-stressor condition, which elevated negative mood and stress about equally for both sleep conditions. These results suggest that sleep deprivation lowers the psychological threshold for the perception of stress from cognitive demands but does not selectively increase the magnitude of negative affect in response to high-stress performance demands. (PsycINFO Database Record (c) 2012 APA, all rights reserved).
    Emotion 02/2012; 12(5):1015-20. · 3.88 Impact Factor
  • Source
    Article: Impact of five nights of sleep restriction on glucose metabolism, leptin and testosterone in young adult men.
    [show abstract] [hide abstract]
    ABSTRACT: Sleep restriction is associated with development of metabolic ill-health, and hormonal mechanisms may underlie these effects. The aim of this study was to determine the impact of short term sleep restriction on male health, particularly glucose metabolism, by examining adrenocorticotropic hormone (ACTH), cortisol, glucose, insulin, triglycerides, leptin, testosterone, and sex hormone binding globulin (SHBG). N = 14 healthy men (aged 27.4±3.8, BMI 23.5±2.9) underwent a laboratory-based sleep restriction protocol consisting of 2 baseline nights of 10 h time in bed (TIB) (B1, B2; 22:00-08:00), followed by 5 nights of 4 h TIB (SR1-SR5; 04:00-08:00) and a recovery night of 10 h TIB (R1; 22:00-08:00). Subjects were allowed to move freely inside the laboratory; no strenuous activity was permitted during the study. Food intake was controlled, with subjects consuming an average 2000 kcal/day. Blood was sampled through an indwelling catheter on B1 and SR5, at 09:00 (fasting) and then every 2 hours from 10:00-20:00. On SR5 relative to B1, glucose (F(1,168) = 25.3, p<0.001) and insulin (F(1,168) = 12.2, p<0.001) were increased, triglycerides (F(1,168) = 7.5, p = 0.007) fell and there was no significant change in fasting homeostatic model assessment (HOMA) determined insulin resistance (F(1,168) = 1.3, p = 0.18). Also, cortisol (F(1,168) = 10.2, p = 0.002) and leptin (F(1,168) = 10.7, p = 0.001) increased, sex hormone binding globulin (F(1,167) = 12.1, p<0.001) fell and there were no significant changes in ACTH (F(1,168) = 0.3, p = 0.59) or total testosterone (F(1,168) = 2.8, p = 0.089). Sleep restriction impaired glucose, but improved lipid metabolism. This was associated with an increase in afternoon cortisol, without significant changes in ACTH, suggesting enhanced adrenal reactivity. Increased cortisol and reduced sex hormone binding globulin (SHBG) are both consistent with development of insulin resistance, although hepatic insulin resistance calculated from fasting HOMA did not change significantly. Short term sleep curtailment leads to changes in glucose metabolism and adrenal reactivity, which when experienced repeatedly may increase the risk for type 2 diabetes.
    PLoS ONE 01/2012; 7(7):e41218. · 4.09 Impact Factor
  • Source
    Article: Auditory evoked potentials remain abnormal after CPAP treatment in patients with severe obstructive sleep apnoea.
    [show abstract] [hide abstract]
    ABSTRACT: To assess the effects of 3 months of optimal CPAP treatment on auditory event related potentials (AERP) in patients with severe obstructive sleep apnoea (OSA) compared with healthy controls. Auditory odd-ball related N1, P2, N2 and P3 AERP components were assessed in 9 severe OSA subjects and 9 healthy controls at baseline evaluation and at ∼3 months follow-up in both groups, with OSA subjects treated with continuous positive air-way pressure (CPAP) during this period. Severe OSA subjects showed significantly delayed, P2, N2 and P3 latencies, and significantly different P2 and P3 amplitudes compared to controls at baseline (group effect, all p<0.05). At follow-up evaluation P3 latency shortened in treated OSA patients but remained prolonged compared to controls (group by treatment interaction, p<0.05) despite high CPAP compliance (6h/night). The earlier AERP (P2 and N2) components did not change in either controls or OSA patients at follow-up and remained different in patients versus controls. This study demonstrates that in severe OSA patients AERP responses show minimal or no improvement and remain abnormal following 3 months of optimal CPAP treatment. Persistent cortical sensory processing abnormalities despite treatment in severe OSA may have implications for daytime neurobehavioral performance and safety in OSA patients. AERP responses may help identify residual performance deficits and risks.
    Clinical neurophysiology: official journal of the International Federation of Clinical Neurophysiology 08/2011; 123(2):310-7. · 3.12 Impact Factor
  • Article: Emotional expressiveness in sleep-deprived healthy adults.
    [show abstract] [hide abstract]
    ABSTRACT: The purpose of this study was to evaluate the influence of sleep deprivation on emotional expression and subjective emotional experience in a highly controlled, laboratory setting. Twenty-three healthy adult participants watched positive (amusing) and negative (sad) film clips before and after they were randomly assigned to a night of sleep deprivation or a normal sleep control condition. The intensity of their facial expressiveness while viewing the films was coded by human judges and compared to their subjective emotional responses. Relative to the control group, sleep-deprived participants demonstrated less expressiveness, especially in response to positive stimuli. Subjective responses were not significantly different between the sleep-deprived and control groups. These preliminary results suggest that sleep deprivation is associated with attenuated emotional expressiveness in healthy adults.
    Behavioral Sleep Medicine 01/2011; 9(1):5-14. · 1.55 Impact Factor
  • Source
    Article: Catechol-O-methyltransferase Val158Met polymorphism associates with individual differences in sleep physiologic responses to chronic sleep loss.
    [show abstract] [hide abstract]
    ABSTRACT: The COMT Val158Met polymorphism modulates cortical dopaminergic catabolism, and predicts individual differences in prefrontal executive functioning in healthy adults and schizophrenic patients, and associates with EEG differences during sleep loss. We assessed whether the COMT Val158Met polymorphism was a novel marker in healthy adults of differential vulnerability to chronic partial sleep deprivation (PSD), a condition distinct from total sleep loss and one experienced by millions on a daily and persistent basis. 20 Met/Met, 64 Val/Met, and 45 Val/Val subjects participated in a protocol of two baseline 10h time in bed (TIB) nights followed by five consecutive 4 h TIB nights. Met/Met subjects showed differentially steeper declines in non-REM EEG slow-wave energy (SWE)-the putative homeostatic marker of sleep drive-during PSD, despite comparable baseline SWE declines. Val/Val subjects showed differentially smaller increases in slow-wave sleep and smaller reductions in stage 2 sleep during PSD, and had more stage 1 sleep across nights and a shorter baseline REM sleep latency. The genotypes, however, did not differ in performance across various executive function and cognitive tasks and showed comparable increases in subjective and physiological sleepiness in response to chronic sleep loss. Met/Met genotypic and Met allelic frequencies were higher in whites than African Americans. The COMT Val158Met polymorphism may be a genetic biomarker for predicting individual differences in sleep physiology-but not in cognitive and executive functioning-resulting from sleep loss in a healthy, racially-diverse adult population of men and women. Beyond healthy sleepers, our results may also provide insight for predicting sleep loss responses in patients with schizophrenia and other psychiatric disorders, since these groups repeatedly experience chronically-curtailed sleep and demonstrate COMT-related treatment responses and risk factors for symptom exacerbation.
    PLoS ONE 01/2011; 6(12):e29283. · 4.09 Impact Factor
  • Source
    Article: Effects of sleep restriction on adiponectin levels in healthy men and women.
    [show abstract] [hide abstract]
    ABSTRACT: Population studies have consistently found that shorter sleep durations are associated with obesity and cardiovascular disease, particularly among women. Adiponectin is an adipocyte-derived, anti-inflammatory hormone that is related to cardiovascular disease risk. We hypothesized that sleep restriction would reduce adiponectin levels in healthy young adults. 74 healthy adults (57% men, 63% African American, mean age 29.9years) completed 2 nights of baseline sleep at 10h time in bed (TIB) per night followed by 5 nights of sleep restricted to 4h TIB per night. An additional 8 participants were randomized to a control group that received 10h TIB per night throughout the study. Plasma adiponectin levels were measured following the second night of baseline sleep and the fifth night of sleep restriction or control sleep. Sleep restriction resulted in a decrease in plasma adiponectin levels among Caucasian women (Z=-2.19, p=0.028), but an increase among African American women (Z=-2.73, p=0.006). No significant effects of sleep restriction on adiponectin levels were found among men. A 2×2 between-group analysis of covariance on adiponectin change scores controlling for BMI confirmed significant interactions between sleep restriction and race/ethnicity [F(1,66)=13.73, p<0.001], as well as among sleep restriction, race/ethnicity and sex [F(1,66)=4.27, p=0.043)]. Inflammatory responses to sleep loss appear to be moderated by sex and race/ethnicity; observed decreases in adiponectin following sleep restriction may be one avenue by which reduced sleep duration promotes cardiovascular risk in Caucasian women.
    Physiology & Behavior 12/2010; 101(5):693-8. · 2.87 Impact Factor
  • Article: DQB1*0602 predicts interindividual differences in physiologic sleep, sleepiness, and fatigue.
    [show abstract] [hide abstract]
    ABSTRACT: The human leukocyte antigen (HLA) DQB1*0602 allele is closely associated with narcolepsy, a neurologic disorder characterized by excessive daytime sleepiness, fragmented sleep, and shortened REM sleep latency. We evaluated whether DQB1*0602 was a novel marker of interindividual differences by determining its relationship to sleep homeostatic, sleepiness, and cognitive responses to baseline and chronic partial sleep deprivation (PSD) conditions. Ninety-two DQB1*0602-negative and 37 DQB1*0602-positive healthy adults participated in a protocol of 2 baseline 10 hours time in bed (TIB) nights followed by 5 consecutive 4 hours TIB nights. DQB1*0602 allelic frequencies did not differ significantly between Caucasians and African Americans. During baseline, although DQB1*0602-positive subjects were subjectively sleepier and more fatigued, they showed greater sleep fragmentation, and decreased sleep homeostatic pressure and differentially sharper declines during the night (measured by non-REM EEG slow-wave energy [SWE]). During PSD, DQB1*0602-positive subjects were sleepier and showed more fragmented sleep, despite SWE elevation comparable to negative subjects. Moreover, they showed differentially greater REM sleep latency reductions and smaller stage 2 reductions, along with differentially greater increases in fatigue. Both groups demonstrated comparable cumulative decreases in cognitive performance. DQB1*0602 positivity in a healthy population may represent a continuum of some sleep-wake features of narcolepsy. DQB1*0602 was associated with interindividual differences in sleep homeostasis, physiologic sleep, sleepiness, and fatigue-but not in cognitive measures-during baseline and chronic PSD. Thus, DQB1*0602 may represent a genetic biomarker for predicting such individual differences in basal and sleep loss conditions.
    Neurology 10/2010; 75(17):1509-19. · 8.31 Impact Factor
  • Source
    Article: Time of day effects on neurobehavioral performance during chronic sleep restriction.
    [show abstract] [hide abstract]
    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
  • Source
    Article: Neurobehavioral dynamics following chronic sleep restriction: dose-response effects of one night for recovery.
    [show abstract] [hide abstract]
    ABSTRACT: Establish the dose-response relationship between increasing sleep durations in a single night and recovery of neurobehavioral functions following chronic sleep restriction. Intent-to-treat design in which subjects were randomized to 1 of 6 recovery sleep doses (0, 2, 4, 6, 8, or 10 h TIB) for 1 night following 5 nights of sleep restriction to 4 h TIB. Twelve consecutive days in a controlled laboratory environment. N = 159 healthy adults (aged 22-45 y), median = 29 y). Interventions: Following a week of home monitoring with actigraphy and 2 baseline nights of 10 h TIB, subjects were randomized to either sleep restriction to 4 h TIB per night for 5 nights followed by randomization to 1 of 6 nocturnal acute recovery sleep conditions (N = 142), or to a control condition involving 10 h TIB on all nights (N = 17). Primary neurobehavioral outcomes included lapses on the Psychomotor Vigilance Test (PVT), subjective sleepiness from the Karolinska Sleepiness Scale (KSS), and physiological sleepiness from a modified Maintenance of Wakefulness Test (MWT). Secondary outcomes included psychomotor and cognitive speed as measured by PVT fastest RTs and number correct on the Digit Symbol Substitution Task (DSST), respectively, and subjective fatigue from the Profile of Mood States (POMS). The dynamics of neurobehavioral outcomes following acute recovery sleep were statistically modeled across the 0 h-10 h recovery sleep doses. While TST, stage 2, REM sleep and NREM slow wave energy (SWE) increased linearly across recovery sleep doses, best-fitting neurobehavioral recovery functions were exponential across recovery sleep doses for PVT and KSS outcomes, and linear for the MWT. Analyses based on return to baseline and on estimated intersection with control condition means revealed recovery was incomplete at the 10 h TIB (8.96 h TST) for PVT performance, KSS sleepiness, and POMS fatigue. Both TST and SWE were elevated above baseline at the maximum recovery dose of 10 h TIB. Neurobehavioral deficits induced by 5 nights of sleep restricted to 4 h improved monotonically as acute recovery sleep dose increased, but some deficits remained after 10 h TIB for recovery. Complete recovery from such sleep restriction may require a longer sleep period during 1 night, and/or multiple nights of recovery sleep. It appears that acute recovery from chronic sleep restriction occurs as a result of elevated sleep pressure evident in both increased SWE and TST.
    Sleep 08/2010; 33(8):1013-26. · 5.05 Impact Factor
  • Source
    Article: Sleep restriction is associated with increased morning plasma leptin concentrations, especially in women.
    [show abstract] [hide abstract]
    ABSTRACT: We evaluated the effects of sleep restriction on leptin levels in a large, diverse sample of healthy participants, while allowing free access to food. Prospective experimental design. After 2 nights of baseline sleep, 136 participants (49% women, 56% African Americans) received 5 consecutive nights of 4 hours time in bed (TIB). Additionally, one subset of participants received 2 additional nights of either further sleep restriction (n = 27) or increased sleep opportunity (n = 37). Control participants (n = 9) received 10 hr TIB on all study nights. Plasma leptin was measured between 10:30 a.m. and 12:00 noon following baseline sleep, after the initial sleep-restriction period, and after 2 nights of further sleep restriction or recovery sleep. Leptin levels increased significantly among sleep-restricted participants after 5 nights of 4 hr TIB (Z = -8.43, p < .001). Increases were significantly greater among women compared to men (Z = -4.77, p < .001) and among participants with higher body mass index (BMI) compared to those with lower (Z = -2.09, p = .036), though participants in all categories (sex, race/ethnicity, BMI, and age) demonstrated significant increases. There was also a significant effect of allowed TIB on leptin levels following the 2 additional nights of sleep restriction (p < .001). Participants in the control condition showed no significant changes in leptin levels. These findings suggest that sleep restriction with ad libitum access to food significantly increases morning plasma leptin levels, particularly among women.
    Biological Research for Nursing 05/2010; 12(1):47-53. · 1.28 Impact Factor
  • Article: Total sleep deprivation, chronic sleep restriction and sleep disruption.
    Amy C Reynolds, Siobhan Banks
    [show abstract] [hide abstract]
    ABSTRACT: Sleep loss may result from total sleep deprivation (such as a shift worker might experience), chronic sleep restriction (due to work, medical conditions or lifestyle) or sleep disruption (which is common in sleep disorders such as sleep apnea or restless legs syndrome). Total sleep deprivation has been widely researched, and its effects have been well described. Chronic sleep restriction and sleep disruption (also known as sleep fragmentation) have received less experimental attention. Recently, there has been increasing interest in sleep restriction and disruption as it has been recognized that they have a similar impact on cognitive functioning as a period of total sleep deprivation. Sleep loss causes impairments in cognitive performance and simulated driving and induces sleepiness, fatigue and mood changes. This review examines recent research on the effects of sleep deprivation, restriction and disruption on cognition and neurophysiologic functioning in healthy adults, and contrasts the similarities and differences between these three modalities of sleep loss.
    Progress in brain research 01/2010; 185:91-103. · 3.04 Impact Factor
  • Source
    Article: PER3 polymorphism predicts cumulative sleep homeostatic but not neurobehavioral changes to chronic partial sleep deprivation.
    [show abstract] [hide abstract]
    ABSTRACT: The variable number tandem repeat (VNTR) polymorphism 5-repeat allele of the circadian gene PERIOD3 (PER3(5/5)) has been associated with cognitive decline at a specific circadian phase in response to a night of total sleep deprivation (TSD), relative to the 4-repeat allele (PER3(4/4)). PER3(5/5) has also been related to higher sleep homeostasis, which is thought to underlie this cognitive vulnerability. To date, no study has used a candidate gene approach to investigate the response to chronic partial sleep deprivation (PSD), a condition distinct from TSD and one commonly experienced by millions of people on a daily and persistent basis. We evaluated whether the PER3 VNTR polymorphism contributed to cumulative neurobehavioral deficits and sleep homeostatic responses during PSD. PER3(5/5) (n = 14), PER3(4/5) (n = 63) and PER3(4/4) (n = 52) healthy adults (aged 22-45 y) demonstrated large, but equivalent cumulative decreases in cognitive performance and physiological alertness, and cumulative increases in sleepiness across 5 nights of sleep restricted to 4 h per night. Such effects were accompanied by increasing daily inter-subject variability in all groups. The PER3 genotypes did not differ significantly at baseline in habitual sleep, physiological sleep structure, circadian phase, physiological sleepiness, cognitive performance, or subjective sleepiness, although during PSD, PER3(5/5) subjects had slightly but reliably elevated sleep homeostatic pressure as measured physiologically by EEG slow-wave energy in non-rapid eye movement sleep compared with PER3(4/4) subjects. PER3 genotypic and allelic frequencies did not differ significantly between Caucasians and African Americans. The PER3 VNTR polymorphism was not associated with individual differences in neurobehavioral responses to PSD, although it was related to one marker of sleep homoeostatic response during PSD. The comparability of PER3 genotypes at baseline and their equivalent inter-individual vulnerability to sleep restriction indicate that PER3 does not contribute to the neurobehavioral effects of chronic sleep loss.
    PLoS ONE 02/2009; 4(6):e5874. · 4.09 Impact Factor
  • Article: American time use survey: sleep time and its relationship to waking activities.
    [show abstract] [hide abstract]
    ABSTRACT: To gain some insight into how various behavioral (lifestyle) factors influence sleep duration, by investigation of the relationship of sleep time to waking activities using the American Time Use Survey (ATUS). Cross-sectional data from ATUS, an annual telephone survey of a population sample of US citizens who are interviewed regarding how they spent their time during a 24-hour period between 04:00 on the previous day and 04:00 on the interview day. Data were pooled from the 2003, 2004, and 2005 ATUS databases involving N=47,731 respondents older than 14 years of age. N/A. Adjusted multiple linear regression models showed that the largest reciprocal relationship to sleep was found for work time, followed by travel time, which included commute time. Only shorter than average sleepers (<7.5 h) spent more time socializing, relaxing, and engaging in leisure activities, while both short (<5.5 h) and long sleepers (> or =8.5 h) watched more TV than the average sleeper. The extent to which sleep time was exchanged for waking activities was also shown to depend on age and gender. Sleep time was minimal while work time was maximal in the age group 45-54 yr, and sleep time increased both with lower and higher age. Work time, travel time, and time for socializing, relaxing, and leisure are the primary activities reciprocally related to sleep time among Americans. These activities may be confounding the frequently observed association between short and long sleep on one hand and morbidity and mortality on the other hand and should be controlled for in future studies.
    Sleep 10/2007; 30(9):1085-95. · 5.05 Impact Factor
  • Article: Behavioral and physiological consequences of sleep restriction.
    Siobhan Banks, David F Dinges
    [show abstract] [hide abstract]
    ABSTRACT: Adequate sleep is essential for general healthy functioning. This paper reviews recent research on the effects of chronic sleep restriction on neurobehavioral and physiological functioning and discusses implications for health and lifestyle. Restricting sleep below an individual's optimal time in bed (TIB) can cause a range of neurobehavioral deficits, including lapses of attention, slowed working memory, reduced cognitive throughput, depressed mood, and perseveration of thought. Neurobehavioral deficits accumulate across days of partial sleep loss to levels equivalent to those found after 1 to 3 nights of total sleep loss. Recent experiments reveal that following days of chronic restriction of sleep duration below 7 hours per night, significant daytime cognitive dysfunction accumulates to levels comparable to that found after severe acute total sleep deprivation. Additionally, individual variability in neurobehavioral responses to sleep restriction appears to be stable, suggesting a trait-like (possibly genetic) differential vulnerability or compensatory changes in the neurobiological systems involved in cognition. A causal role for reduced sleep duration in adverse health outcomes remains unclear, but laboratory studies of healthy adults subjected to sleep restriction have found adverse effects on endocrine functions, metabolic and inflammatory responses, suggesting that sleep restriction produces physiological consequences that may be unhealthy.
    Journal of clinical sleep medicine: JCSM: official publication of the American Academy of Sleep Medicine 09/2007; 3(5):519-28. · 3.23 Impact Factor
  • Source
    Article: The Maintenance of Wakefulness Test and driving simulator performance.
    [show abstract] [hide abstract]
    ABSTRACT: It has been suggested that the Maintenance of Wakefulness Test (MWT) may be clinically useful to assess fitness to drive, yet little is known about the actual relationship between sleep latency and driving performance. This study examined the ability of 2 MWT trials to predict driving-simulator performance in healthy individuals. Experimental. NA. Twenty healthy volunteers (mean age 22.8 years; 9 men). NA. The MWT and driving-simulator performance were examined under 2 conditions-partial sleep deprivation and a combination of partial sleep deprivation and alcohol consumption. Each subject was studied a week apart, with the order randomly assigned. Subjects completed a nighttime 70-minute AusEd driving simulation task and two 40-minute MWT trials, 1 before (MWT1) and 1 after (MWT2) the driving task. In the sleep-deprived condition, the MWT1 sleep latency was inversely correlated with braking reaction time. During the partial sleep deprivation and alcohol condition, the number of microsleeps during the driving task, steering deviation, braking reaction time, and crashes all negatively correlated with the MWT1 sleep latency. Additionally, construction of a receiver-operator characteristic curve revealed that MWT1 sleep latency in the partial sleep deprivation plus alcohol condition significantly discriminated subjects who had a crash from those who did not. These results indicate that sleep latency on the MWT is a reasonable predictor of driving simulator performance in sleepy, alcohol-impaired, normal subjects. Further research is needed to examine the relationship between daytime MWT results and driving simulator performance in sleepy patients (eg, those with obstructive sleep apnea) and in experimentally sleep-deprived normal subjects.
    Sleep 12/2005; 28(11):1381-5. · 5.05 Impact Factor
  • Article: Efficacy of positive airway pressure and oral appliance in mild to moderate obstructive sleep apnea.
    [show abstract] [hide abstract]
    ABSTRACT: The efficacy of currently recommended treatments is uncertain in patients with mild to moderate obstructive sleep apnea (apnea-hypopnea index [AHI], 5-30). A group of 114 sleep clinic patients with an AHI of 5-30 have participated in a randomized controlled crossover trial of 3 months of treatment with each of nasal continuous positive airway pressure (CPAP), a mandibular advancement splint, and a placebo tablet. Outcomes were sleep fragmentation and hypoxemia, daytime sleepiness, quality of life, neurobehavioral function, and blood pressure. Both active treatments improved sleep outcomes, but positive airway pressure had a greater effect. The quality of life, symptoms, and subjective but not objective sleepiness improved to a similar degree with both treatments; however, many of the improvements seen in neuropsychologic function and mood were not better than the placebo effect. Some aspects of nocturnal blood pressure were improved with the splint but not with CPAP. This study has shown that although both CPAP and mandibular advancement splint effectively treated sleep-disordered breathing and sleepiness, the expected response in neurobehavioral function was incomplete. This may be due to the splint having a lesser therapeutic effect and CPAP being poorly tolerated and therefore used less in this patient group.
    American Journal of Respiratory and Critical Care Medicine 10/2004; 170(6):656-64. · 11.08 Impact Factor
  • Source
    Article: Low levels of alcohol impair driving simulator performance and reduce perception of crash risk in partially sleep deprived subjects.
    [show abstract] [hide abstract]
    ABSTRACT: Partial sleep deprivation and alcohol consumption are a common combination, particularly among young drivers. We hypothesized that while low blood alcohol concentration (<0.05 g/dL) may not significantly increase crash risk, the combination of partial sleep deprivation and low blood alcohol concentration would cause significant performance impairment. Experimental Sleep Disorders Unit Laboratory 20 healthy volunteers (mean age 22.8 years; 9 men). Subjects underwent driving simulator testing at 1 am on 2 nights a week apart. On the night preceding simulator testing, subjects were partially sleep deprived (5 hours in bed). Alcohol consumption (2-3 standard alcohol drinks over 2 hours) was randomized to 1 of the 2 test nights, and blood alcohol concentrations were estimated using a calibrated Breathalyzer. During the driving task subjects were monitored continuously with electroencephalography for sleep episodes and were prompted every 4.5 minutes for answers to 2 perception scales-performance and crash risk. Mean blood alcohol concentration on the alcohol night was 0.035 +/- 0.015 g/dL. Compared with conditions during partial sleep deprivation alone, subjects had more microsleeps, impaired driving simulator performance, and poorer ability to predict crash risk in the combined partial sleep deprivation and alcohol condition. Women predicted crash risk more accurately than did men in the partial sleep deprivation condition, but neither men nor women predicted the risk accurately in the sleep deprivation plus alcohol condition. Alcohol at legal blood alcohol concentrations appears to increase sleepiness and impair performance and the detection of crash risk following partial sleep deprivation. When partially sleep deprived, women appear to be either more perceptive of increased crash risk or more willing to admit to their driving limitations than are men. Alcohol eliminated this behavioral difference.
    Sleep 09/2004; 27(6):1063-7. · 5.05 Impact Factor
  • Source
    Article: The maintenance of wakefulness test in normal healthy subjects.
    [show abstract] [hide abstract]
    ABSTRACT: The Maintenance of Wakefulness Test (MWT) examines an individual's ability to stay awake in an environment of decreased sensory stimulation. Only 1 previous study has systematically examined the MWT in normal healthy subjects. Sleep disorders unit laboratory 31 subjects (mean age 48.5 years, SD 9.6; 8 women) were randomly selected via the telephone directory within a 30-km radius of the test centers. They answered a general screen for health complaints (respiratory, cardiovascular, and psychiatric disorders) and sleep difficulties (snoring). N/A. Overnight polysomnography and a 40-minute MWT the following day were performed on all subjects. Mean sleep latency to the first epoch of unequivocal sleep during the 40-minute trial MWT was 36.9 +/- 5.4 (SD) minutes. The lower normal limit, defined as 2 SD below the mean, was therefore 26.1 minutes. Mean sleep latency for the first 20 minutes of the trial (with sleep latency defined as time to the first appearance of 1 epoch of stage 1 sleep or a 10-second microsleep) was 18.6 +/- 2.3 minutes, with a lower normal limit of 14.0 minutes. The mean results are consistent with previously published normative data. However, the SDs found in this study are smaller, and, thus, the lower normal limit suggested here is 4 to 6 minutes longer. The subjects in this study were randomly selected from the general population and may, therefore, be a truer representation of the normal population than in the previous study in which subjects were recruited via hospital advertisements and word of mouth.
    Sleep 07/2004; 27(4):799-802. · 5.05 Impact Factor
  • Source
    Article: Factors associated with maintenance of wakefulness test mean sleep latency in patients with mild to moderate obstructive sleep apnoea and normal subjects.
    [show abstract] [hide abstract]
    ABSTRACT: This study investigated the possible factors related to the Maintenance of Wakefulness Test (MWT) mean sleep latency. A second analysis explored the characteristics of subjects who had discrepant Epworth Sleepiness Scale (ESS) and MWT scores. A total of 151 subjects (110 mild to moderate obstructive sleep apnoea (OSA) patients and 41 control subjects) were recruited for the study. The subjects completed an overnight Polysomnography (PSG), MWT, cognitive, performance and vigilance tasks and answered self-report questionnaires on mood and sleepiness. A forward stepwise multiple regression was performed on MWT mean sleep latency. The predictor variables age (r = 0.28), subjective sleep history for 1 week prior to MWT (sleep diary; r = 0.19) and number of >4% SaO2 Dips during the PSG (r = -0.21) best explained the MWT results, but only accounted for 12.8% of the variance in the test. It was found that 33% of subjects had discrepant ESS and MWT scores. A new variable was created to analyse these subjects (MWT/ESS discrepancy score; MED). A forward stepwise multiple regression analysis found that depression, performance errors and sleep disordered breathing explained 13.4% of the variance in MED scores. The MWT is a complex behavioural test whose scores do not seem to have a very robust relationship with potential predictors and co-correlates. Further comprehensive study is needed if the test is to be used in a diagnostically meaningful way.
    Journal of Sleep Research 03/2004; 13(1):71-8. · 3.16 Impact Factor

Institutions

  • 2010–2012
    • University of South Australia 
      • Centre for Sleep Research
      Adelaide, South Australia, Australia
    • Beth Israel Deaconess Medical Center
      • Department of Neurology
      Boston, MA, USA
  • 2011
    • University of Pennsylvania
      • Department of Psychiatry
      Philadelphia, PA, USA
    • Repatriation General Hospital
      Adelaide, South Australia, Australia
  • 2004–2010
    • Hospital of the University of Pennsylvania
      • Department of Psychiatry
      Philadelphia, PA, USA