Kognitive Testung in Laborstudien: Motivationsverlust oder Last Test Effect?

Fragestellung Wenn Probanden in Laborstudien längerer Dauer eine Vielzahl kognitiver Testbatterien wiederholt durchführen, wird häufig befürchtet, dass sich ein Motivationsverlust der Probanden einstellen könnte, die Tests mit immer gleichem Engagement durchzuführen. Zudem ist fraglich, ob die letzte Testung durch die Aussicht auf das bevorstehende Studienende beeinflusst und somit in ihrer Aussagekraft eingeschränkt wird. Diese beiden Themen wurden anhand einer Laborstudie untersucht. Methoden Die kognitive Leistung von 47 gesunden Probanden (mittleres Alter 27 ± 5 (SD) Jahre, 21 Frauen) wurde in 3-stündigen Intervallen während eines 12-tägigen Studienprotokolls getestet so dass insgesamt 65 Tests eines Psychomotorischen Vigilanztests (PVT) und eines Hand-Auge-Koordinationstests (UTT) absolviert wurden. Nach Basismessungen (8 Stunden Schlafzeit) wurden drei Schlafentzugsbedingungen in einem balancierten cross-over Design dargeboten. Nach jeder Intervention erholten sich die Probanden während zwei Nächten und Tagen. Am letzten Studientag wurden 24 Probanden im Vorhinein darüber informiert, dass es sich bei Test 65 um den letzten Test handelte, während 23 Probanden davon ausgingen, dass sich drei Stunden später noch ein weiterer Test anschließen würde. Ergebnisse Eine mixed ANOVA, die die kognitive Leistung am Basistag und am jeweils 2. Erholungstag berücksichtigte, ergab, dass sich die Geschwindigkeit (p=0,3475) und Lapses (p=0,2429) im PVT im Studienverlauf nicht veränderten. Der UTT (p=0,0211) verbesserte sich. Eine 2-way mixed ANOVA mit den Faktoren Gruppe (wissend/unwissend) und Test (Basis/Test 65) sowie deren Interaktion zeigte, dass im Vergleich zum Basistag die letzte Testleistung im PVT besser (Geschwindigkeit: p0,5). Schlussfolgerung Die Ergebnisse legen nahe, dass es möglich ist, die Motivation und das Engagement der Probanden für immer wiederkehrende kognitive Testverfahren über einen längeren Zeitraum aufrechtzuerhalten. Es ergaben sich keine Hinweise auf einen ‚Last Test Effect‘

Impact Of Sleep Restriction And Recovery On Motivation During Repeated Cognitive Performance Testing

Introduction: Both motivation and sleep deprivation affect cognitive performance. Especially during long-lasting studies with repeated cognitive performance tasks there is concern that subjects will lose motivation over time. Results may be confounded due to changes in motivation. Methods: In an ongoing study, 29 healthy volunteers performed 55 cognitive performance tasks at three-hourly intervals in a 12-day inpatient study. After two baseline nights with 8 h time in bed (TIB) the intervention group (N=20; mean age 26 ± 4 years, 9 females) underwent chronic sleep restriction for 5 nights (5 h TIB) with a following recovery night of 8 h TIB. The control group (N=9; mean age 25 ± 5 years, 3 females) had the opportunity to sleep 8 hours every night. Participants completed the Karolinska Sleepiness Scale (KSS) and a questionnaire about their motivation (from 1=very little/not motivated to 5=very motivated) at 6 p.m. on all days. Results: Wilcoxon signed-rank tests showed a significant decrease in motivation (p=.0439) and a significant increase in subjective sleepiness (p=.0184) from baseline (motivation: 2.8 ± 0.6 (SD), sleepiness: 3.2 ± 1.2) to the last day of chronic sleep restriction (motivation: 2.2 ± 0.5, sleepiness: 5.1 ± 1.8) for the experimental group. Motivation remained low after recovery sleep (2.2 ± 0.8; p=.0198). Sleepiness and motivation scores showed a significant Spearman correlation (r=-0.43, p<0.001). Discussion: Chronic sleep restriction for five days leads to an increase in sleepiness and a decrease in motivation. One night of recovery is insufficient to reverse the motivation loss, contrasting with the beneficial effect on sleepiness. During chronic sleep restriction conditions subjective motivation seems to decrease as a function of subjective sleepiness

Residents’ negative attitude towards air traffic is associated with impaired objective sleep quality

Objectives: Nocturnal aircraft noise induces sleep disturbances and is associated with impaired quality of life. The magnitude of physiological and psychological responses to noise varies among individuals. Stable individual vulnerabilities have been reported for aircraft noise induced awakenings. To date it is unknown, whether the subjective attitude towards air traffic and residents' sleep quality impact on each other. Methods: Seventy-four out of 81 investigated residents around Frankfurt Airport (Germany) rated their attitude towards air traffic (from 1 = negative to 5 = positive; negative attitude: score ≤ 2, N=28, mean age 44 ± 16 years; moderate to positive attitude: score > 3, N=46, mean age 44 ± 15 years) and evaluated its necessity (from 1 = not necessary to 5 = highly necessary; no to moderate necessity: score ≤ 3, N=22, mean age 45 ± 10 years; high necessity: score > 3, N=52, mean age 43 ± 17 years). In addition, polysomnographical recordings were obtained in residents' home environment. These investigations were part of the NORAH sleep study in 2012. Results: Significant impairments in sleep quality (prolonged sleep onset latency, increased wake after sleep onset, reduced sleep efficiency, and less deep sleep) were found for participants with a negative attitude towards air traffic. The judgement of no or moderate necessity of air traffic was associated with a significantly reduced deep sleep duration. Conclusions: Residents' subjective attitude towards air traffic and their objective sleep quality are related. Cause and effect in this relationship remain to be identified

Interindividual variabilities in cognitive performance degradation after alcohol consuption and sleep loss are related

Introduction The sleep inducing effects of alcohol as well as the increase in sleep propensity and sleepiness after sleep loss have been linked to the adenosinergic system in the brain. While the performance impairing effects of ethanol have partly been related to the inhibitory effects of cerebral adenosine, sleep loss has been found to increase adenosine receptor density. The interindividual variability of cognitive performance impairments after alcohol intake as well as after sleep loss is extensive. Thus, we examined in humans whether performance degradations resulting from sleep loss and alcohol consumption are related. Methods Performance in a 10-min Psychomotor Vigilance Task (PVT) was tested in 47 healthy volunteers (mean age 27 ± 5 (SD) years, 21 females) at 6 pm 1) after an 8 hour control night, 2) after alcohol consumption (aiming at a blood alcohol concentration (BAC) of 0.08%), and 3) after 35 hours of total sleep deprivation. After alcohol intake, 35 of the participants reached a BAC of more than 0.06% prior to the performance testing (mean BAC 0.074%, SD 0.009%, min. 0.063%, max. 0.095%) and were included in the analyses. Two recovery nights were scheduled between conditions. Results Performance impairments due to acute alcohol intake and due to 35 hours of sustained wakefulness were calculated as differences from performance under control conditions. The degree in performance degradation correlated highly between both conditions (i.e. 10% slowest reaction times: Pearson’s r=0.73, p<0.0001; standard deviation of reaction times: r=0.75, p<0.0001; mean reaction time: r=0.59, p=0.0002). Conclusions Participants whose PVT performance proved to be vulnerable to the effects of alcohol consumption were also vulnerable to sleep loss, whereas individuals who were resilient against the effects of alcohol were also less susceptible to the impact of sleep deprivation. These results suggest that the effects of alcohol and sleep deprivation on performance are mediated – at least in part – by a common pathway that may involve the adenosinergic system in the brain

Are you vulnerable to sleep loss? Association between a priori self-assessed sensitivity to sleep deprivation and waking EEG dynamics

1. Objectives: Sleep deprivation leads to EEG power increases especially in lower frequency bands. Inter-individual differences exist in neurocognitive consequences of sleep loss. We aimed at developing a questionnaire that identifies individuals who are vulnerable to sleep loss. Here we investigated whether a priori self-assessed sensitivity to sleep loss is related to the changes in waking EEG power between a sleep deprived and a well-rested state. 2. Methods: 17 healthy men (M = 27 years) were sleep deprived for 58 h. In the beginning of the study, participants rated their sensitivity to sleep deprivation. Every 6 h during wakefulness participants performed a test battery (waking EEG, Karolinska Sleepiness Scale (KSS) and cognitive tests). EEG power density after 50 h was expressed as a percentage of power after 2 h of wakefulness following 14 h of recovery sleep, and correlated with the results from the sensitivity questionnaire and the KSS (2-50 h). 3. Results: Self-assessed sensitivity to sleep deprivation correlated with the change in theta power (rs (15) = -.52, p = .046) and delta power (rs (15) = -.57, p = .026). The KSS did not correlate with theta or delta power. 4. Conclusions: Individuals with lower sensitivity to sleep deprivation showed a greater decline in waking EEG theta and delta power between sleep deprivation and recovery, suggesting that they recover faster than individuals with high sensitivity. Individuals might be able to predict their vulnerability to sleep loss based on their recovery experience

A priori self-assessed sensitivity to sleep deprivation correlates with individual cognitive Performance Impairment during prolonged Wakefulness

Research question: Differences exist in the individual susceptibility to performance impairments induced by sleep deprivation. Identifying people who are at high risk for such impairments prior to exposure to prolonged wakefulness would offer the possibility to increase safety. This study investigated the relationship between cognitive performance impairment during 58 h of sustained wakefulness and self-assessed sensitivity to sleep deprivation based on prior experience. In addition, cognitive performance impairment was compared with subjective fatigue and sleepiness during the sleep deprivation. Methods: 17 healthy, male volunteers (mean age 27 ± 5 SD, age-span 19-36 years) participated in the study. At the beginning of the study, participants answered a self-assessment questionnaire about their sensitivity to sleep deprivation. During sleep deprivation, fatigue and sleepiness were assessed in 6-h-intervals by the Fatigue Checklist and Karolinska Sleepiness Scale, respectively; cognitive performance was measured by the sum of correct responses in the N-Back Task. The differences in the aforementioned measures between 2 and 50 h of wakefulness and the self-assessed sensitivity to sleep deprivation were used for correlation analysis. Results: The decrease of correct responses in the N-Back Task showed a significant correlation with the sensitivity to sleep deprivation (Spearman’s rs (17) = .59, p = .01) which was based on prior experience. There was no significant correlation between cognitive performance impairment and either fatigue (rs (17) = .19, p = .46) or sleepiness (rs (17) = -.00, p = .99). Conclusion: Participants who rated themselves as sensitive to sleep deprivation performed worse in the cognitive test than those who rated themselves as less sensitive. Whereas acute performance impairments during prolonged wakefulness were not paralleled by changes in subjective fatigue and sleepiness, individuals appear to be capable of predicting such impairments based on prior experience with exposure to sleep deprivation. Possibly, performance under sleep deprivation can be predicted on the basis of a few questions on sensitivity to sleep deprivation