The Effects of Total Sleep Deprivation on the Generation of Random Sequences of Key-Presses, Numbers and Nouns

2005 ◽  
Vol 58 (2) ◽  
pp. 275-307 ◽  
Author(s):  
Herbert Heuer ◽  
Olaf Kohlisch ◽  
Wolfhard Klein

According to a recent hypothesis, executive functions should be particularly vulnerable to the effects of total sleep deprivation. Random generation is a task that taps executive functions. In three experiments we examined the effects of total sleep deprivation on random generation of keypresses, numbers, and nouns, in particular on the suppression of prepotent responses and the selection of next responses by way of applying a local-representativeness heuristic. With random key-presses suppression of prepotent responses did not suffer from lack of sleep, but it became poorer at a sufficiently high pacing rate. In contrast, suppression of prepotent responses suffered when numbers and nouns were generated. According to these findings different types of random generation tasks involve different types of inhibitory process. With only four response alternatives, but not with larger response sets, application of the local-representativeness heuristic was impaired after a night without sleep. In terms of a simple formal model, serial-order representations of the preceding responses are used in selecting the next response only for the small response set, and not for larger response sets. Thus, serial-order representations are likely to suffer from loss of sleep. These findings strongly suggest that random generation involves multiple processes and that total sleep deprivation does not impair all sorts of executive functions, but only some.

2021 ◽  
Vol 4 (3) ◽  
pp. 95
Author(s):  
Fani Tuti Handayani ◽  
Pratiwi Nur Widyaningsih ◽  
Fitranto Arjadi

Background: Salivary pH can rise or fall influenced by intrinsic and extrinsic factors. Sleep deprivation is one example of intrinsic factors. Sleep deprivation causes a reduction in sleep time at a certain time. Purpose: Analyze the effect of different types of sleep deprivations and sleep recovery on salivary pH. Method: This study was experimental research with a post-test only with a control group design. Thirty white Wistar strain rats were randomly divided into 5 groups: healthy control group (KI), partial sleep deprivation (PSD/KII), total sleep deprivation (TSD/KIII), partial sleep deprivation, and continued sleep recovery (PSD+SR/KIV) and total sleep deprivation and continued sleep recovery (TSD+SR/KV). The treatment is carried out on a single platform method. Salivary pH was measured with the help of color-coded pH strips that were given grading after the completion of sleep deprivation induction. Result: The mean decrease in salivary pH was highest in the TSD group. One Way ANOVA test showed significant differences (p <0.05) in the control group with PSD and TSD, the PSD group with PSD+SR, TSD group with PSD+SR and TSD+SR. Conclusion: Sleep deprivation is proven to reduce the pH of Saliva. Total sleep deprivation is a chronic condition that has the most influence on decreasing salivary pH. The effect of decreasing salivary pH due to sleep deprivation is proven to be overcome by sleep recovery.


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.


2021 ◽  
pp. 102910
Author(s):  
Binney Sharma ◽  
Trina Sengupta ◽  
Lal Chandra Vishwakarma ◽  
Nasreen Akhtar ◽  
Hruda Nanda Mallick

SLEEP ◽  
2020 ◽  
Vol 43 (Supplement_1) ◽  
pp. A116-A116
Author(s):  
R A Muck ◽  
L Skeiky ◽  
M A Schmidt ◽  
B C Satterfield ◽  
J P Wisor ◽  
...  

Abstract Introduction There are substantial, phenotypical individual differences in the adverse impact of total sleep deprivation (TSD) on vigilant attention performance. Dopaminergic genotypes have been found to contribute to these phenotypical differences. Here we investigated the association between a single nucleotide polymorphism (SNP) of the dopamine receptor D2 (DRD2) gene, C957T (rs6277), on vigilant attention performance measured with the psychomotor vigilance test (PVT) in a laboratory TSD study. Methods N=46 healthy adults (ages 26.0±5.3y; 25 females) completed a 4-day in-laboratory study with a baseline day (10h time in bed: 22:00-08:00), a 38h TSD period, and a recovery day (10h time in bed: 22:00-08:00). DNA isolated from whole blood was assayed for DRD2 C957T genotype using real-time polymerase chain reaction. PVT performance was measured during TSD at 2-4h intervals, and analyzed for genotype using mixed-effects analysis of covariance of lapses of attention (RTs&gt;500ms). Results The genotype distribution in this sample - 28.3% C/C, 50.0% C/T, 21.7% T/T - was found to be in Hardy-Weinberg Equilibrium (X21=0.0008, p=0.98). As expected, there was a significant effect of time awake on PVT performance (F14,602=26.67, p&lt;0.001). There was a significant main effect of DRD2 genotype (F2,602=3.24, p=0.040) and a significant interaction of time awake by DRD2 genotype (F28,602=1.96, p=0.003). Subjects homozygous for the T allele showed greater impairment during extended wakefulness than carriers of the C allele. Genotype explained 7.6% of the variance in the PVT data observed during the 38h TSD period. Conclusion Subjects homozygous for the T allele of DRD2 C957T were considerably more vulnerable to TSD-induced PVT performance impairment than carriers of the C allele. A recent study showed that DRD2 C957T influences PVT performance in interaction with a SNP of the DAT1 gene. Here, DRD2 genotype was by itself also associated with PVT performance impairment during TSD. Support CDMRP awards W81XWH-16-1-0319 and W81XWH-18-1-0100.


2021 ◽  
Vol 89 (9) ◽  
pp. S176
Author(s):  
Jeehye Seo ◽  
Edward F. Pace-Schott ◽  
Mohammed R. Milad ◽  
Huijin Song ◽  
Anne Germain

1990 ◽  
Vol 5 (1) ◽  
pp. 29-30
Author(s):  
F Lang ◽  
J Pellet ◽  
B Estour

SummaryThe authors report the case of a 45-yr-old male who presented from 1979 to 1986 with several severe depressive episodes. The patient fulfilled Feighner criteria for major depression, Newcastle criteria for endogenous depression: the depressive episodes were all classified as severe recurrent depression without melancholia according to DSM III. The patient was resistant to different types of treatment (ECT, tricyclic and MAOI drugs, lithium, sleep deprivation). With a treatment of 10 cg/day of fenetyline, reduced to 5 cg/day after 6 months, (atypical manic episode), the patient improved considerably for 20 rnonths. The therapeutic response decreased after this period but after a month of withdrawal, the patient again responded. The authors cannot explain the duration of this therapeutic response.


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&lt;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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