scholarly journals Effects of Sleep Deprivation on Brain Bioenergetics, Sleep, and Cognitive Performance in Cocaine-Dependent Individuals

2013 ◽  
Vol 2013 ◽  
pp. 1-10 ◽  
Author(s):  
George H. Trksak ◽  
Bethany K. Bracken ◽  
J. Eric Jensen ◽  
David T. Plante ◽  
David M. Penetar ◽  
...  

In cocaine-dependent individuals, sleep is disturbed during cocaine use and abstinence, highlighting the importance of examining the behavioral and homeostatic response to acute sleep loss in these individuals. The current study was designed to identify a differential effect of sleep deprivation on brain bioenergetics, cognitive performance, and sleep between cocaine-dependent and healthy control participants. 14 healthy control and 8 cocaine-dependent participants experienced consecutive nights of baseline, total sleep deprivation, and recovery sleep in the research laboratory. Participants underwent[31]P magnetic resonance spectroscopy (MRS) brain imaging, polysomnography, Continuous Performance Task, and Digit Symbol Substitution Task. Following recovery sleep,[31]P MRS scans revealed that cocaine-dependent participants exhibited elevated global brainβ-NTP (direct measure of adenosine triphosphate),α-NTP, and total NTP levels compared to those of healthy controls. Cocaine-dependent participants performed worse on the Continuous Performance Task and Digit Symbol Substitution Task at baseline compared to healthy control participants, but sleep deprivation did not worsen cognitive performance in either group. Enhancements of brain ATP levels in cocaine dependent participants following recovery sleep may reflect a greater impact of sleep deprivation on sleep homeostasis, which may highlight the importance of monitoring sleep during abstinence and the potential influence of sleep loss in drug relapse.

SLEEP ◽  
2020 ◽  
Vol 43 (Supplement_1) ◽  
pp. A114-A114
Author(s):  
D Lawrence-Sidebottom ◽  
J M Hinson ◽  
P Whitney ◽  
K A Honn ◽  
H Van Dongen

Abstract Introduction Total sleep deprivation (TSD) causes profound vigilant attention deficits, with large, trait-like individual differences, as evidenced convincingly by response lapses on the psychomotor vigilance test (PVT). There is debate, however, about the role of vigilant attention deficits in the effects of TSD on other speeded performance tasks besides the PVT. We addressed this issue by testing whether PVT response lapses are related to delays in responding to stimuli under strict deadlines in two decision making tasks. Methods N=54 healthy adults (aged 21-38y; 31 females) completed an in-laboratory TSD study. Following a 10h baseline sleep opportunity, cognitive testing occurred after 25h and 29h of TSD (09:00 and 13:00). Testing included an AX continuous performance task with switch (AX-CPTs), which is a dynamic decision making task requiring subjects to respond to a frequently occurring cue-probe combination; an identical pairs continuous performance task (CPT-IP), which is a 1-back go/no-go task; and a 10min PVT. Lapses (RTs>500ms) on the PVT and target accuracy on the AX-CPTs and CPT-IP were calculated as indices of vigilant attention. Intraclass correlation coefficients (ICCs) were used to quantify the stability of individual differences, and absolute rank-order correlation (|ρ|) was used to compare the three indices. Results The stability of individual differences ranged from fair to substantial (PVT: ICC=0.44; AX-CPTs: ICC=0.73; CPT-IP: ICC=0.31). The rank-order correlation between the AX-CPTs and CPT-IP vigilant attention indices was relatively high (|ρ|=0.44), whereas correlations with PVT lapses were much lower (AX-CPTs: |ρ|=0.14; CPT-IP: |ρ|=0.04). Conclusion Individual differences during TSD were moderately stable for each index of vigilant attention, but the relationships between PVT lapses and the other indices were weak. This suggests that any or all of the indices considered here are not pure measures of vigilant attention, or that vigilant attention may constitute multiple, distinct constructs. Support CDMRP grant W81XWH-16-1-0319


2020 ◽  
pp. 003329411989989
Author(s):  
Janna Mantua ◽  
Allison J. Brager ◽  
Sara E. Alger ◽  
Folarin Adewle ◽  
Lillian Skeiky ◽  
...  

Objective Individuals vary in response to sleep loss: some individuals are “vulnerable” and demonstrate cognitive decrements following insufficient sleep, while others are “resistant” and maintain baseline cognitive capability. Physiological markers (e.g., genetic polymorphisms) have been identified that can predict relative vulnerability. However, a quick, cost-effective, and feasible subjective predictor tool has not been developed. The objective of the present study was to determine whether two factors—“subjective sleep need” and “subjective resilience”—predict cognitive performance following sleep deprivation. Methods Twenty-seven healthy, sleep-satiated young adults participated. These individuals were screened for sleep disorders, comorbidities, and erratic sleep schedules. Prior to 40 hours of in-laboratory total sleep deprivation, participants were questioned on their subjective sleep need and completed a validated resilience scale. During and after sleep deprivation, participants completed a 5-minute psychomotor vigilance test every 2 hours. Results Both subjective resilience and subjective sleep need individually failed to predict performance during sleep loss. However, these two measures interacted to predict performance. Individuals with low resilience and low sleep need had poorer cognitive performance during sleep loss. However, in individuals with medium or high resilience, psychomotor vigilance test performance was not predicted by subjective sleep need. Higher resilience may be protective against sleep loss-related neurobehavioral impairments in the context of subjective sleep need. Conclusions Following sleep loss (and recovery sleep), trait resilient individuals may outperform those with lower resiliency on real-world tasks that require continuous attention. Future studies should determine whether the present findings generalize to other, operationally relevant tasks and additional cognitive domains.


2020 ◽  
pp. 108705471989781
Author(s):  
Orrie Dan ◽  
Ami Cohen ◽  
Kfir Asraf ◽  
Ivgeny Saveliev ◽  
Iris Haimov

Objective: To identify the impact of sleep deprivation on functioning of young adults with or without ADHD on a continuous performance attention task. Method: Thirty-four men ( M age = 25.38) with ( n = 16) or without ( n = 18) ADHD completed a continuous performance task before and after 25 hr of sustained wakefulness in a controlled environment. Results: In both groups, sleep deprivation caused a decline in performance on all variables: omission errors, commission errors, reaction time, and reaction time variability. In addition, the ADHD group made more omission and commission errors, and had greater reaction time variability. Conclusion: Sleep deprivation has a detrimental effect on attention functioning among young adults. In addition, although young adults with ADHD generally perform worse on continuous performance tasks than young adults without ADHD, the groups are similarly affected by sleep deprivation.


2017 ◽  
Vol 114 (16) ◽  
pp. 4243-4248 ◽  
Author(s):  
David Elmenhorst ◽  
Eva-Maria Elmenhorst ◽  
Eva Hennecke ◽  
Tina Kroll ◽  
Andreas Matusch ◽  
...  

Adenosine and functional A1adenosine receptor (A1AR) availability are supposed to mediate sleep–wake regulation and cognitive performance. We hypothesized that cerebral A1AR availability after an extended wake period decreases to a well-rested state after recovery sleep. [18F]CPFPX positron emission tomography was used to quantify A1AR availability in 15 healthy male adults after 52 h of sleep deprivation and following 14 h of recovery sleep. Data were additionally compared with A1AR values after 8 h of baseline sleep from an earlier dataset. Polysomnography, cognitive performance, and sleepiness were monitored. Recovery from sleep deprivation was associated with a decrease in A1AR availability in several brain regions, ranging from 11% (insula) to 14% (striatum). A1AR availabilities after recovery did not differ from baseline sleep in the control group. The degree of performance impairment, sleepiness, and homeostatic sleep-pressure response to sleep deprivation correlated negatively with the decrease in A1AR availability. Sleep deprivation resulted in a higher A1AR availability in the human brain. The increase that was observed after 52 h of wakefulness was restored to control levels during a 14-h recovery sleep episode. Individuals with a large increase in A1AR availability were more resilient to sleep-loss effects than those with a subtle increase. This pattern implies that differences in endogenous adenosine and A1AR availability might be causal for individual responses to sleep loss.


SLEEP ◽  
2020 ◽  
Author(s):  
Erika M Yamazaki ◽  
Caroline A Antler ◽  
Charlotte R Lasek ◽  
Namni Goel

Abstract Study Objectives The amount of recovery sleep needed to fully restore well-established neurobehavioral deficits from sleep loss remains unknown, as does whether the recovery pattern differs across measures after total sleep deprivation (TSD) and chronic sleep restriction (SR). Methods In total, 83 adults received two baseline nights (10–12-hour time in bed [TIB]) followed by five 4-hour TIB SR nights or 36-hour TSD and four recovery nights (R1–R4; 12-hour TIB). Neurobehavioral tests were completed every 2 hours during wakefulness and a Maintenance of Wakefulness Test measured physiological sleepiness. Polysomnography was collected on B2, R1, and R4 nights. Results TSD and SR produced significant deficits in cognitive performance, increases in self-reported sleepiness and fatigue, decreases in vigor, and increases in physiological sleepiness. Neurobehavioral recovery from SR occurred after R1 and was maintained for all measures except Psychomotor Vigilance Test (PVT) lapses and response speed, which failed to completely recover. Neurobehavioral recovery from TSD occurred after R1 and was maintained for all cognitive and self-reported measures, except for vigor. After TSD and SR, R1 recovery sleep was longer and of higher efficiency and better quality than R4 recovery sleep. Conclusions PVT impairments from SR failed to reverse completely; by contrast, vigor did not recover after TSD; all other deficits were reversed after sleep loss. These results suggest that TSD and SR induce sustained, differential biological, physiological, and/or neural changes, which remarkably are not reversed with chronic, long-duration recovery sleep. Our findings have critical implications for the population at large and for military and health professionals.


SLEEP ◽  
2021 ◽  
Vol 44 (Supplement_2) ◽  
pp. A117-A117
Author(s):  
Janna Mantua ◽  
Carolyn Mickelson ◽  
Jacob Naylor ◽  
Bradley Ritland ◽  
Alexxa Bessey ◽  
...  

Abstract Introduction Sleep loss that is inherent to military operations can lead to cognitive errors and potential mission failure. Single Nucleotide Polymorphisms (SNPs) allele variations of several genes (COMT, ADORA2A, TNFa, CLOCK, DAT1) have been linked with inter-individual cognitive resilience to sleep loss through various mechanisms. U.S. Army Soldiers with resilience-related alleles may be better-suited to perform cognitively-arduous duties under conditions of sleep loss than those without these alleles. However, military-wide genetic screening is costly, arduous, and infeasible. This study tested whether a brief survey of subjective resilience to sleep loss (1) can demarcate soldiers with and without resilience-related alleles, and, if so, (2) can predict cognitive performance under conditions of sleep loss. Methods Six SNPs from the aforementioned genes were sequenced from 75 male U.S. Army special operations Soldiers (age 25.7±4.1). Psychomotor vigilance, response inhibition, and decision-making were tested after a night of mission-driven total sleep deprivation. The Iowa Resilience to Sleeplessness Test (iREST) Cognitive Subscale, which measures subjective cognitive resilience to sleep loss, was administered after a week of recovery sleep. A receiver operating characteristic (ROC) curve was used to determine whether the iREST Cognitive Subscale can discriminate between gene carriers, and a cutoff score was determined. Cognitive performance after sleep deprivation was compared between those below/above the cutoff score using t-tests or Mann-Whitney U tests. Results The iREST discriminated between allele variations for COMT (ROC=.65,SE=.07,p=.03), with an optimal cutoff score of 3.03 out of 5, with 90% sensitivity and 51.4% specificity. Soldiers below the cutoff score had significantly poorer for psychomotor vigilance reaction time (t=-2.39,p=.02), response inhibition errors of commission (U=155.00,W=246.00,p=.04), and decision-making reaction time (t=2.13,p=.04) than Soldiers above the cutoff score. Conclusion The iREST Cognitive Subscale can discriminate between those with and without specific vulnerability/resilience-related genotypes. If these findings are replicated, the iREST Cognitive Subscale could be used to help military leaders make decisions about proper personnel placement when sleep loss is unavoidable. This would likely result in increased safety and improved performance during military missions. Support (if any) Support for this study came from the Military Operational Medicine Research Program of the United States Army Medical Research and Development Command.


SLEEP ◽  
2021 ◽  
Vol 44 (Supplement_2) ◽  
pp. A56-A56
Author(s):  
Mark McCauley ◽  
Peter McCauley ◽  
Hans Van Dongen

Abstract Introduction In commercial aviation and other operational settings where biomathematical models of fatigue are used for fatigue risk management, accurate prediction of recovery during rest periods following duty periods with sleep loss and/or circadian misalignment is critical. The recuperative potential of recovery sleep is influenced by a variety of factors, including long-term, allostatic effects of prior sleep/wake history. For example, recovery tends to be slower after sustained sleep restriction versus acute total sleep deprivation. Capturing such dynamics has proven to be challenging. Methods Here we focus on the dynamic biomathematical model of McCauley et al. (2013). In addition to a circadian process, this model features differential equations for sleep/wake regulation including a short-term sleep homeostatic process capturing change in the order of hours/days and a long-term allostatic process capturing change in the order of days/weeks. The allostatic process modulates the dynamics of the homeostatic process by shifting its equilibrium setpoint, which addresses recently observed phenomena such as reduced vulnerability to sleep loss after banking sleep. It also differentiates the build-up and recovery rates of fatigue under conditions of chronic sleep restriction versus acute total sleep deprivation; nonetheless, it does not accurately predict the disproportionately rapid recovery seen after total sleep deprivation. To improve the model, we hypothesized that the homeostatic process may also modulate the allostatic process, with the magnitude of this effect scaling as a function of time awake. Results To test our hypothesis, we added a parameter to the model to capture modulation by the homeostatic process of the allostatic process build-up during wakefulness and dissipation during sleep. Parameter estimation using previously published laboratory datasets of fatigue showed this parameter as significantly different from zero (p<0.05) and yielding a 10%–20% improvement in goodness-of-fit for recovery without adversely affecting goodness-of-fit for pre-recovery days. Conclusion Inclusion of a modulation effect of the allostatic process by the homeostatic process improved prediction accuracy in a variety of sleep loss and circadian misalignment scenarios. In addition to operational relevance for duty/rest scheduling, this finding has implications for understanding mechanisms underlying the homeostatic and allostatic processes of sleep/wake regulation. Support (if any) Federal Express Corporation


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