Siobhan Banks

Bio: Siobhan Banks is an academic researcher from University of South Australia. The author has contributed to research in topics: Sleep deprivation & Alertness. The author has an hindex of 32, co-authored 110 publications receiving 5123 citations. Previous affiliations of Siobhan Banks include Repatriation General Hospital & Australian National University.

Behavioral and physiological consequences of sleep restriction

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 traitlike (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. Citation: Banks S; Dinges DF. Behavioral and physiological consequences of sleep restriction. J Clin Sleep Med 2007;3(5):519-528.

Efficacy of positive airway pressure and oral appliance in mild to moderate obstructive sleep apnea.

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 time use survey: sleep time and its relationship to waking activities.

Abstract: Study Objectives: 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)

Sleep Deprivation and Stressors: Evidence for Elevated Negative Affect in Response to Mild Stressors When Sleep Deprived

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.

Neurobehavioral Dynamics Following Chronic Sleep Restriction: Dose-Response Effects of One Night for Recovery

Abstract: RECOVERY OF NEUROBEHAVIORAL FUNCTIONS FROM CHRONIC CURTAILMENT OF SLEEP DURATION AS A RESULT OF WORK, MEDICAL CONDITIONS, OR lifestyle1 is not well understood. It has been rarely studied, despite the fact that a common sleep pattern for millions of people involves sleep restriction for 5 weekdays/workdays, followed by sleep extension on at least one weekend night (or day off from work).2–4 Much of what is known about recovery from sleep loss has been based on total sleep deprivation experiments, where robust NREM EEG slow wave activity (SWA, 0.5-4.5Hz) responses are the norm.5–9 Experiments in chronically sleep-restricted rats revealed increased recovery sleep duration, NREM and REM sleep durations, and elevated SWA, while only a small portion of the chronically lost sleep was actually recovered.10,11 Experiments in healthy humans have confirmed that chronic reduction of sleep can result in waking neurobehavioral deficits that become progressively worse over days;12–15 that the rate of accumulation of waking deficits is a function of the magnitude of the sleep restriction;12,15,16 and that measures of sleepiness, performance lapsing, and cognitive slowing can accumulate to deficit levels found for total sleep deprivation.15 These findings indicate that waking brain impairment from chronic sleep loss is sleep dose-dependent, that it can be as severe as that resulting from total sleep deprivation, and that the “sleep debt” is a result of prior sleep-wake history extending back in time more than a day. Thus, chronic sleep restriction appears to induce slow changes (spanning days to weeks) in neural processes mediating alertness, attention and other aspects of cognitive functioning, including learning and memory.17 How these slow (cumulative) changes are reversed via the dynamics of recovery sleep is not known. Kleitman suggested “sleep debts” are “liquidated” by extending recovery sleep duration (p. 317).18 However, the primary model of human sleep homeostasis, the two-process model,19,20 posits that the intensity and temporal dynamics of NREM EEG SWA, more so than sleep duration, reflect the recovery process. For example, the two-process model predicts only an initial modest (∼10%-20%) elevation in SWA over the first few days of sleep restricted to 4 h per night, which has been experimentally confirmed,15,21 although increases of 50% have been reported for a broader EEG frequency band (1.25-7.75 Hz).22 The relatively modest increment in SWA during and following sleep restriction is not congruent with the large cumulative neurobehavioral deficits that develop across days of sleep restriction.15 The apparent uncoupling during chronic sleep restriction of the putative marker of homeostatic sleep drive (SWA) and waking neurobehavioral functions suggests that sleep duration and/or other aspects of sleep (e.g., REM sleep) may also have a critical role in recovery of neurobehavioral capability following chronic sleep restriction. On the other hand, the high degree of colinearity among SWA, TST and the duration of sleep stages may prevent attributing recovery from chronic sleep restriction to a specific physiological feature of sleep. The dynamics of recovery of human waking alertness and neurobehavioral functions following chronic sleep restriction have not been systematically investigated. Experiments in healthy adults scheduled to 7 nights of sleep restricted to 3 h-7 h TIB12 or 5 nights of sleep restricted to 4 h TIB22 yielded data suggesting that some neurobehavioral functions may not return to baseline following up to 3 recovery sleep periods limited to 8 h TIB.12,23 Studying the dynamics of recovery from cumulative sleep loss is critical to a range of behavioral guidelines (e.g., days off duty for recovery from work schedules),24 biological questions (e.g., mechanisms and rates of homeostatic sleep drive build-up and dissipation),25 and theoretical issues (e.g., processes to instantiate into mathematical models predicting sleep and alertness).26–28The present experiment was designed to provide the first systematic, randomized, sleep dose-response data on the dynamic recovery of neurobehavioral functions when a single recovery sleep opportunity follows 5 days of nocturnal sleep restriction to 4 h TIB. The study tested the hypothesis that following sleep restriction, recovery of primary measures of neurobehavioral alertness would increase monotonically in relation to the duration of time allowed for recovery sleep. We also sought to determine the features of sleep that parallel this recovery.

About sleep's role in memory

Abstract: Over more than a century of research has established the fact that sleep benefits the retention of memory. In this review we aim to comprehensively cover the field of "sleep and memory" research by providing a historical perspective on concepts and a discussion of more recent key findings. Whereas initial theories posed a passive role for sleep enhancing memories by protecting them from interfering stimuli, current theories highlight an active role for sleep in which memories undergo a process of system consolidation during sleep. Whereas older research concentrated on the role of rapid-eye-movement (REM) sleep, recent work has revealed the importance of slow-wave sleep (SWS) for memory consolidation and also enlightened some of the underlying electrophysiological, neurochemical, and genetic mechanisms, as well as developmental aspects in these processes. Specifically, newer findings characterize sleep as a brain state optimizing memory consolidation, in opposition to the waking brain being optimized for encoding of memories. Consolidation originates from reactivation of recently encoded neuronal memory representations, which occur during SWS and transform respective representations for integration into long-term memory. Ensuing REM sleep may stabilize transformed memories. While elaborated with respect to hippocampus-dependent memories, the concept of an active redistribution of memory representations from networks serving as temporary store into long-term stores might hold also for non-hippocampus-dependent memory, and even for nonneuronal, i.e., immunological memories, giving rise to the idea that the offline consolidation of memory during sleep represents a principle of long-term memory formation established in quite different physiological systems.

Neurocognitive Consequences of Sleep Deprivation

Abstract: Deficits in daytime performance due to sleep loss are experienced universally and associated with a significant social, financial, and human cost. Microsleeps, sleep attacks, and lapses in cognition increase with sleep loss as a function of state instability. Sleep deprivation studies repeatedly show a variable (negative) impact on mood, cognitive performance, and motor function due to an increasing sleep propensity and destabilization of the wake state. Specific neurocognitive domains including executive attention, working memory, and divergent higher cognitive functions are particularly vulnerable to sleep loss. In humans, functional metabolic and neurophysiological studies demonstrate that neural systems involved in executive function (i.e., prefrontal cortex) are more susceptible to sleep deprivation in some individuals than others. Recent chronic partial sleep deprivation experiments, which more closely replicate sleep loss in society, demonstrate that profound neurocognitive deficits accumulate over time in the face of subjective adaptation to the sensation of sleepiness. Sleep deprivation associated with disease-related sleep fragmentation (i.e., sleep apnea and restless legs syndrome) also results in neurocognitive performance decrements similar to those seen in sleep restriction studies. Performance deficits associated with sleep disorders are often viewed as a simple function of disease severity; however, recent experiments suggest that individual vulnerability to sleep loss may play a more critical role than previously thought.

Pathophysiology of Sleep Apnea

Abstract: Sleep-induced apnea and disordered breathing refers to intermittent, cyclical cessations or reductions of airflow, with or without obstructions of the upper airway (OSA). In the presence of an anat...

Behavioral and physiological consequences of sleep restriction

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 traitlike (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. Citation: Banks S; Dinges DF. Behavioral and physiological consequences of sleep restriction. J Clin Sleep Med 2007;3(5):519-528.