Neurocognitive Consequences of Sleep Deprivation

Emory University, Atlanta, Georgia, United States
Seminars in Neurology (Impact Factor: 1.79). 04/2005; 25(1):117-29. DOI: 10.1055/s-2005-867080
Source: PubMed


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.

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Available from: Jeffrey S Durmer, Aug 29, 2015
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    • "Sleep loss not only increases the negative emotional response but also decreases the response to positive events (Boivin et al., 1997). Sleep is an adaptive function of humans, during which the restoration of brain processes, including strengthening of the immune system, growth, major metabolic processes, memory consolidation and brain plasticity, occurs (Durmer and Dinges, 2005; Maquet, 1995; Stickgold et al., 2001). REM (rapid eye movements) sleep might be particularly important in processing and emotional modulation (Cartwright et al., 2006; Walker, 2009). "
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    ABSTRACT: Aim: To compare patterns of sleep and the presence of sleep disturbances in individuals in at-risk mental states (ARMS) for psychosis and bipolar disorder (BD) with a healthy control (HC) group. Methods: This was a comparative study involving 20 individuals in ARMS for psychosis or BD, according to the Comprehensive Assessment of At-Risk Mental States, and 20 age- and sex-matched healthy controls. Quality of sleep in the previous month was assessed using the Pittsburgh Sleep Quality Index, diurnal somnolence was evaluated using The Epworth Sleepiness Scale, and chronotype was determined using the Questionnaire of Morningness/Eveningness (QME). All of the participants underwent polysomnography (PSG) during the entire night for two consecutive nights. The first night aimed to adapt the subject to the environment, and only the data from the second night were used for the analysis. Results: Compared with the HC group, individuals in the ARMS group reported significantly worse sleep quality, as measured by the Pittsburgh Sleep Quality Index. Both groups had scores consistent with daytime sleepiness on the Epworth Sleepiness Scale, and there were no differences with regard to chronotype between the groups, with a predominance of the indifferent type in both groups. In the PSG assessment, we observed increased Sleep Latency (SL) and increased Rapid Eye Movement Sleep Onset Latency (REMOL) in the ARMS group, compared to the HC group. Conclusion: The results of this study indicated that sleep abnormalities could be found early in the course of mental diseases, even in at-risk stages, and support the further investigation of their predictive value in the transition to psychosis and BD.
    Schizophrenia Research 09/2015; DOI:10.1016/j.schres.2015.08.023 · 3.92 Impact Factor
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    • "People are experiencing sleep loss and sleep deprivation (SD) because extended work hours have become a normal state of everyday life (Harrison and Home, 2000; Lockley et al., 2004; Durmer and Dinges, 2005). Except for cognitive deficits, SD can also cause negative emotional and affective reactions, which may adversely impact brain function and result in human errors and accidents (Scott et al., 2006; Franzen et al., 2008; Gujar et al., 2011; Anderson and Platten, 2011). "
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    ABSTRACT: The superficial amygdala (SFA) is important in human emotion/affective processing via its strong connection with other limbic and cerebral cortex for receptive and expressive emotion processing. Few studies have investigated the functional connectivity changes of the SFA under extreme conditions, such as prolonged sleep loss, although the SFA showed a distinct functional connectivity pattern throughout the brain. In this study, resting-state functional magnetic resonance imaging (rs-fMRI) was employed to investigate the changes of SFA-cortical functional connectivity after 36 hr of total sleep deprivation (TSD). Fourteen healthy male volunteers aged 25.9 ± 2.3 years (range 18-28 years) enrolled in this within-subject crossover study. We found that the right SFA showed increased functional connectivity with the right medial prefrontal cortex (mPFC) and decreased functional connectivity with the right dorsal posterior cingulate cortex (dPCC) in the resting brain after TSD compared with that during rested wakefulness. For the left SFA, decreased connectivity with the right dorsal anterior cingulate cortex (dACC) and right dPCC was found. Further regression analysis indicated that the functional link between mPFC and SFA significantly correlated with the Profile of Mood State scores. Our results suggest that the amygdala cannot be treated as a single unit in human neuroimaging studies and that TSD may alter the functional connectivity pattern of the SFA, which in turn disrupts emotional regulation. © 2015 Wiley Periodicals, Inc.
    Journal of Neuroscience Research 09/2015; 93(12). DOI:10.1002/jnr.23601 · 2.59 Impact Factor
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    • "Sleep is a complex and critical biological process that is impacted by both genetic and non-genetic factors in humans. Inadequate sleep can lead to several health issues such as impaired immune function [Aldabal and Bahammam, 2011], increased risk for type II diabetes and obesity [Knutson et al., 2007], and cognitive impairment [Van Dongen et al., 2003; Durmer and Dinges, 2005]. Furthermore, sleep deprivation is associated with common psychiatric conditions such as anxiety and depression [van Mill et al., 2010]. "
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    ABSTRACT: Sleep is critical to health and functionality, and several studies have investigated the inherited component of insomnia and other sleep disorders using genome-wide association studies (GWAS). However, genome-wide studies focused on sleep duration are less common. Here, we used data from participants in the Coriell Personalized Medicine Collaborative (CPMC) (n = 4,401) to examine putative associations between self-reported sleep duration, demographic and lifestyle variables, and genome-wide single nucleotide polymorphism (SNP) data to better understand genetic contributions to variation in sleep duration. We employed stepwise ordered logistic regression to select our model and retained the following predictive variables: age, gender, weight, physical activity, physical activity at work, smoking status, alcohol consumption, ethnicity, and ancestry (as measured by principal components analysis) in our association testing. Several of our strongest candidate genes were previously identified in GWAS related to sleep duration (TSHZ2, ABCC9, FBXO15) and narcolepsy (NFATC2, SALL4). In addition, we have identified novel candidate genes for involvement in sleep duration including SORCS1 and ELOVL2. Our results demonstrate that the self-reported data collected through the CPMC are robust, and our genome-wide association analysis has identified novel candidate genes involved in sleep duration. More generally, this study contributes to a better understanding of the complexity of human sleep.
    American Journal of Medical Genetics Part B Neuropsychiatric Genetics 09/2015; DOI:10.1002/ajmg.b.32362 · 3.42 Impact Factor
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