Dim light, sleep tight, and wake up bright - Sleep optimization in athletes by means of light regulation.

Despite an elevated recovery need, research indicates that athletes often exhibit relatively poor sleep. Timing and consolidation of sleep is driven by the circadian system, which requires periodic light-dark exposure for stable entrainment to the 24-hour day, but is often disturbed due to underexposure to light in the morning (e.g. low-level indoor lighting) and overexposure to light in the evening (e.g. environmental and screen-light). This study examined whether combining fixed sleep schedules with light regulation leads to more consolidated sleep. Morning light exposure was increased using light-emitting goggles, whereas evening light exposure was reduced using amber-lens glasses. Using a within-subject crossover design, twenty-six athletes (14 female, 12 male) were randomly assigned to start the intervention with the light-regulation-week or the no light-regulation-week. Sleep was monitored by means of sleep diaries and actigraphy. Due to low protocol adherence regarding the fixed sleep-wake schedules, two datasets were constructed; one including athletes who kept a strict sleep-wake schedule (N = 8), and one that also included athletes with a more lenient sleep-wake schedule (N = 25). In case of a lenient sleep-wake schedule, light regulation improved self-reported sleep onset latency (Δ SOL = 8 min). This effect was stronger (Δ SOL = 17 min) and complemented by enhanced subjective sleep quality in case of a strict sleep-wake schedule. None of the actigraphy-based estimates differed significantly between conditions. To conclude, light regulation may be considered a potentially effective strategy to improve subjective sleep, but less obtrusive methods should be explored to increase protocol compliance.

Effects of Natural Between-Days Variation in Sleep on Elite Athletes' Psychomotor Vigilance and Sport-Specific Measures of Performance.

Performance capacity in athletes depends on the ability to recover from past exercise. While evidence suggests that athletic performance decreases following (partial) sleep deprivation and increases following sleep extension, it is unclear to which extent natural variation in sleep impacts performance. Sleep quantity and, for the first time, sleep stages were assessed among 98 elite athletes on three non-consecutive nights within a 7-day monitoring period, along with performance tests that were taken on standardized times each following morning. Performance assessment included psychomotor performance (10-minute psychomotor vigilance task) and sport-specific tests of fine (e.g., accuracy) and gross motor skills (e.g., endurance, power). Mixed-effects models were employed to assess the effect of sleep quantity (total sleep time (TST), sleep onset latency (SOL), wake after sleep onset, sleep efficiency) and sleep stage duration (light, deep, REM) on performance. Average TST was 7:30 ± 1:05 hours, with a mean variation of 57 minutes across days. Longer TSTs were associated with faster reaction times (p = 0.04). Analyses indicated small and inconsistent effects of sleep quantity (TST, SOL) and sleep staging (light sleep) on gross motor performance, and no effects on fine motor skill performance. Results indicate that natural variation in sleep quantity impacts psychomotor vigilance to a greater extent than athletic performance. Small or absent effects can be a consequence of the rather small variation in non-manipulated sleep. It is suggested that one night of compromised sleep may not be immediately problematic, but that more extreme sleep loss or accumulated sleep debt may have more severe consequences.

Train hard, sleep well? Perceived training load, sleep quantity and sleep stage distribution in elite level athletes.

OBJECTIVES: Sleep is essential for recovery and performance in elite athletes. While it is generally assumed that exercise benefits sleep, high training load may jeopardize sleep and hence limit adequate recovery. To examine this, the current study assessed objective sleep quantity and sleep stage distributions in elite athletes and calculated their association with perceived training load. DESIGN: Mixed-methods. METHODS: Perceived training load, actigraphy and one-channel EEG recordings were collected among 98 elite athletes during 7 consecutive days of regular training. RESULTS: Actigraphy revealed total sleep durations of 7:50±1:08h, sleep onset latencies of 13±15min, wake after sleep onset of 33±17min and sleep efficiencies of 88±5%. Distribution of sleep stages indicated 51±9% light sleep, 21±8% deep sleep, and 27±7% REM sleep. On average, perceived training load was 5.40±2.50 (scale 1-10), showing large daily variability. Mixed-effects models revealed no alteration in sleep quantity or sleep stage distributions as a function of day-to-day variation in preceding training load (all p's>.05). CONCLUSIONS: Results indicate healthy sleep durations, but elevated wake after sleep onset, suggesting a potential need for sleep optimization. Large proportions of deep sleep potentially reflect an elevated recovery need. With sleep quantity and sleep stage distributions remaining irresponsive to variations in perceived training load, it is questionable whether athletes' current sleep provides sufficient recovery after strenuous exercise.

Self-reported sleep quantity, quality and sleep hygiene in elite athletes.

Sleep is essential for recovery and performance in elite athletes. While actigraphy-based studies revealed suboptimal sleep in athletes, information on their subjective experience of sleep is scarce. Relatively unexplored is also the extent to which athletes' sleep is adversely affected by environmental conditions and daytime behaviours, that is sleep hygiene. This study aimed to provide insight in sleep quantity, quality and its putative association with sleep hygiene. Participants were 98 elite (youth) athletes competing at the highest (inter-)national level. Sleep quantity, quality and sleep hygiene were assessed once covering a 1-month period by using established (sub)clinical questionnaires, and repeatedly during 7 consecutive days. Sleep quality was generally healthy, although 41% of all athletes could be classified as 'poor sleeper', and 12% were identified as having a sleep disorder. Daily self-monitoring revealed sleep durations of 8:11 ± 0:45 h, but elevated wake after sleep onset of 13 ± 19 min. Sleep quality, feeling refreshed, and morning vigor were moderate at best. Regarding sleep hygiene, general measures revealed irregular sleep-wake patterns, psychological strain and activating pre-sleep behaviours. At the daily level, blue-light exposure and late-evening consumption of heavy meals were frequently reported. General sleep hygiene revealed significant associations with sleep quality (0.45 < r > 0.50; P < 0.001). Results indicate that there is ample room for optimization, specifically in onset latency and in wake after sleep onset. Subtle improvements in sleep seem possible, and optimizing sleep hygiene, such as regular sleep-wake patterns and reducing psychological strain, may facilitate this sleep upgrading process.

Sleep disturbances are associated with reduced health-related quality of life in patients with substance use disorders.

BACKGROUND AND OBJECTIVES: Sleep problems and substance use are strongly linked. Sleep problems play a role in the etiology of substance use, but also may be a result of it. After detoxification, sleep problems may worsen leading to relapse. Nowadays, most substance dependence treatment programs aim at recovery rather than total abstinence, and in that view health-related quality of life (HRQL) is a relevant construct. This article describes the association between self-perceived sleep problems and HRQL in a naturalistic population of polydrug-using inpatients. METHODS: At the start of treatment, 388 polydrug-using inpatients completed questionnaires concerning their sleep quality and HRQL. Three categories were established based on reported sleep problems: patients without sleep problems (21.6%), those with clinically relevant sleep problems (34.5%), and patients with sleep disorders (43.8%). RESULTS: Mean grades for quality of sleep were M = 7.3 (sd 1.7), M = 6.6 (sd 1.7) and M = 5.3 (sd 1.9) for the three categories, respectively. In addition, patients in the disorder category perceived a lower HRQL than those in the other categories. In the explanation of HRQL, both sleep problems and sleep disorders added significantly to the model when controlling for baseline characteristics. DISCUSSION AND CONCLUSIONS: Our findings stress the need for clinicians to pay attention to the quality of sleep of recovering polydrug users, since this may play an important role in the recovery process. Monitoring sleep during treatment is advocated. This study adds to the knowledge about the way HRQL and sleep are related in a naturalistic sample of substance-dependent patients.

Anxiolytic and antidepressive effects of electric stimulation of the paleocerebellar cortex in pentylenetetrazol kindled rats.

Anxiety and depression are component of interictal behavioral deteriorations that occur as a consequence of kindling, a procedure to induce chronic epilepsy. The aim of this study was to evaluate the possible effects of electrical stimulation (ES) of paleocerebellar cortex on anxiety and depressive-like behavior in a PTZ kindled epilepsy model. Kindling was induced via pentylenetetrazol (PTZ) (25.0 mg/kg IP daily) during three weeks. Locomotion in open field, elevated plus-maze (EPM) and Porsolt forced swimming test have been used for the assessment of anxiety and depression-like behavior. ES (100 Hz) has been delivered to V-VII lobules of vermal cortex of kindled rats. ES of paleocerebellum reversed kindling-induced reduction of crossings of central squares, increased rearings, and decreased the number of defecations in open field. The duration that kindled animals spent in the open arms of the EPM increased in post- ES period, and the number of enterings into the closed arms of the EPM decreased. The duration of the immobility response in the swimming test in kindled rats was reduced after ESs of paleocerebellum. In all: ES of paleocerebellar structures suppressed anxious and depressive-like behavior in PTZ-kindled rats.

Psychometric intelligence and P3 of the event-related potentials studied with a 3-stimulus auditory oddball task.

Relationship between psychometric intelligence measured with Raven's Advanced Progressive Matrices (RAPM) and event-related potentials (ERP) was examined using 3-stimulus oddball task. Subjects who had scored higher on RAPM exhibited larger amplitude of P3a component. Additional analysis using the Standardized Low Resolution Electromagnetic Tomography (sLORETA) revealed that this effect corresponds with stronger activity within the frontal cortex and the cingulate gyrus. High intelligence can also be linked with greater P3b response and stronger activity within the parietal cortex and the posterior cingulate gyrus. It may be concluded that the processes related to the initial stage of attention engagement as indexed by P3a, as well as the later stimulus evaluation and classification reflected in P3b, are more intense in subjects scoring higher on RAPM. The quality of mental abilities can therefore be related to differences of the activity in frontal and parietal brain regions.

Neural generators of the auditory evoked potential components P3a and P3b.

The aim of the present study was to define the scalp topography of the two subcomponents of the P3 component of the auditory evoked potential elicited in a three-stimulus oddball paradigm and to identify their cortical generators using the standardized low resolution electromagnetic tomography (sLORETA). Subjects were presented with a random sequence of auditory stimuli and instructed to respond to an infrequently occurring target stimulus inserted into a sequence of frequent standard and rare non-target stimuli. Results show that the magnitude of the frontal P3a is determined by the relative physical difference among stimuli, as it was larger for the stimulus more deviant from the standard. Major neural generators of the P3a were localized within frontal cortex and anterior cingulate gyrus. In contrast to this, the P3b, showing maximal amplitude at parietal locations, was larger for stimuli demanding a response than for the rare non-target. Major sources of the P3b included the superior parietal lobule and the posterior part of the cingulate gyrus. Our findings are in line with the hypothesis that P3a is related to alerting activity during the initial allocation of attention, while P3b is related to activation of a posterior network when the neuronal model of perceived stimulation is compared with the attentional trace.

Covariation of EEG synchronization and emotional state as modified by anxiolytics.

The relationships between subjective estimation of emotional state and synchronization patterns in cortical emotional systems were investigated. The emotional state varied between groups using diazepam, buspirone, and placebo. The University of Wales Institute of Science and Technology Mood Adjective Checklist was used for the assessment of emotional state in the drug condition, yielding three estimates of emotional state: Energetic Arousal, Tension Arousal, and Hedonic Tone. These measures were correlated with the Synchronization Likelihood index of the resting EEG. Increased affective valence and arousal were related to an increased level of synchronization between frontal and right temporoparietal emotional areas. Two identified centers of synchronization, localized in the temporal and centroparietal regions, appeared to be functionally distinct. Stable relationships between subjective emotional state measures and cortical EEG synchronization patterns were confirmed, especially for the valence and energetic arousal estimation. A higher synchronization is associated with increased emotional valence and arousal, and this can thus be seen as a neural correlate of emotional experiences.

Effects of the use of hypnotics on cognition.

Hypnotic drugs are intended to induce sedation and promote sleep. As a result, they have deteriorating effects on cognitive performance following intake. Most hypnotics are benzodiazepine receptor agonists which can have effects on memory in addition to their sedative effects. Other sedating drugs, such as histamine H1 antagonists or melatonin agonists, may have less effect on memory and learning. Hypnotics with other mechanisms of action are currently being investigated for efficacy and safety. For patients using hypnotic drugs, the effects on cognition are relevant to the extent that a drug dose affects daytime performance. Use of benzodiazepine hypnotics is associated with increased risk of car accidents and falling. Therefore, most hypnotics are studied to determine whether they produce residual sedation and impairing effects on performance the morning after bedtime use. Experimental studies using a standardized driving test clearly show that some drugs and doses produce severe residual effects, whereas others seem to have no or only minor impairing effects on next-day performance. No hypnotic has been found yet to improve daytime performance. Studies on long-term use of benzodiazepine hypnotics suggest that effects on daytime performance may diminish over time due to tolerance. However, there are also studies showing that performance may improve after discontinuation of chronic benzodiazepine use, which suggests that tolerance may not be complete.

Decapitation in rats: latency to unconsciousness and the 'wave of death'.

The question whether decapitation is a humane method of euthanasia in awake animals is being debated. To gather arguments in this debate, obsolete rats were decapitated while recording the EEG, both of awake rats and of anesthetized rats. Following decapitation a fast and global loss of power of the EEG was observed; the power in the 13-100 Hz frequency band, expressing cognitive activity, decreased according to an exponential decay function to half the initial value within 4 seconds. Whereas the pre-decapitation EEG of the anesthetized animals showed a burst suppression pattern quite different from the awake animals, the power in the postdecapitation EEG did not differ between the two groups. This might indicate that either the power of the EEG does not correlate well with consciousness or that consciousness is briefly regained in the anesthetized group after decapitation. Remarkably, after 50 seconds (awake group) or 80 seconds (anesthetized group) following decapitation, a high amplitude slow wave was observed. The EEG before this wave had more power than the signal after the wave. This wave might be due to a simultaneous massive loss of membrane potentials of the neurons. Still functioning ion channels, which keep the membrane potential intact before the wave, might explain the observed power difference. Two conclusions were drawn from this experiment. It is likely that consciousness vanishes within seconds after decapitation, implying that decapitation is a quick and not an inhumane method of euthanasia. It seems that the massive wave which can be recorded approximately one minute after decapitation reflects the ultimate border between life and death. This observation might have implications in the discussions on the appropriate time for organ donation.

Endogenous rhythm of absence epilepsy: relationship with general motor activity and sleep-wake states.

The rhythms of spontaneously occurring seizures (spike-wave discharges, SWD) and motor activity, as well as the relationship between SWD and sleep-wake states were investigated in the WAG/Rij rat model of absence epilepsy. In order to establish whether SWD are controlled by external (Zeitgebers) or by endogenous factors such as circadian influences or the state of vigilance, the study was performed in entrained and constant dim light conditions. EEG and motor activity were recorded in the 12:12 light-dark cycle and in constant dim light conditions. Circadian rhythmicity was found both for motor activity and the occurrence of SWD in conditions of entrainment. In constant dim light conditions also circadian rhythms emerged, however, the change in circadian parameters was opposite for the rhythm of SWD and motor activity. SWD were preceded mostly by passive wakefulness and by slow-wave sleep in both experimental conditions. It can be concluded that the rhythm of SWD seems to be generated and controlled by an endogenous mechanism distinct from that which controls the rhythm of motor activity. The relationship between SWD and sleep-wake states preceding their occurrences appeared to be unchanged, suggesting that the mechanism of generation of SWD is independent of the circadian timing system.

Evolution of wakefulness, sleep and hibernation: from reptiles to mammals.

Thus far, most hypotheses on the evolutionary origin of sleep only addressed the probable origin of its main states, REM and NREM. Our article presents the origin of the whole continuum of mammalian vigilance states including waking, sleep and hibernation and the causes of the alternation NREM-REM in a sleeping episode. We propose: (1) the active state of reptiles is a form of subcortical waking, without homology with the cortical waking of mammals; (2) reptilian waking gave origin to mammalian sleep; (3) reptilian basking behaviour evolved into NREM; (4) post-basking risk assessment behaviour, with motor suspension, head dipping movements, eye scanning and stretch attending postures, evolved into phasic REM; (5) post-basking, goal directed behaviour evolved into tonic REM and (6) nocturnal rest evolved to shallow torpor. A small number of changes from previous reptilian stages explain these transformations.

Thalamic lesions in a genetic rat model of absence epilepsy: dissociation between spike-wave discharges and sleep spindles.

Recent findings have challenged the traditional view that the thalamus is the primary driving source of generalized spike-wave discharges (SWDs) characteristic for absence seizures, and indicate a leading role for the cortex instead. In light of this we investigated the effects of thalamic lesions on SWDs and sleep spindles in the WAG/Rij rat, a genetic model of absence epilepsy. EEG was recorded from neocortex and thalamus in freely moving rats, both before and after unilateral thalamic ibotenic acid lesions. Complete unilateral destruction of the reticular thalamic nucleus (RTN) combined with extensive destruction of the thalamocortical relay (TCR) nuclei, resulted in the bilateral abolishment of SWDs and ipsilateral abolishment of sleep spindles. A suppression of both types of thalamocortical oscillations was found when complete or extensive damage to the RTN was combined with minor to moderate damage to the TCR nuclei. Lesions that left the rostral pole of the RTN and part of the TCR nuclei intact, resulted in an ipsilateral suppression of sleep spindles, but a large increase of bilateral SWDs. These findings demonstrate that the thalamus in general and the RTN in particular are a prerequisite for both the typical bilateral 7-11 Hz SWDs and natural occurring sleep spindles in the WAG/Rij rat, but suggest that different intrathalamic subcircuits are involved in the two types of thalamocortical oscillations. Whereas the whole RTN appears to be critical for the generation of sleep spindles, the rostral pole of the RTN seems to be the most likely part that generates SWDs.

Effect of appetitive Pavlovian conditioning on the N150 of the amygdalar Auditory Evoked Potential in the rat.

A large, negative wave which reaches its peak amplitude around 150 ms after stimulus onset, can be found in the Auditory Evoked Potential (AEP) recorded from the lateral amygdala in the rat. Previous studies in our laboratory have repeatedly shown that this N150 component increases during various aversive conditioning protocols and that this increase is attributable to both increases in emotional arousal that are inherent to aversive conditioning and to the formation of an association between the conditioned stimulus (CS) and the aversive unconditioned stimulus (US). Currently it is not known whether the N150 is also enhanced in conditioning procedures with positive reinforcement. To address this issue, we used a Pavlovian conditioning protocol in which an auditory CS signaled the delivery of a food US in food-deprived rats. AEPs evoked by the CS were recorded from the lateral amygdala while the animals were subjected to this appetitive conditioning procedure. Heart rate and N150 amplitude did not increase during conditioning relative to pre-conditioning baselines. In contrast, heart rate and N150 amplitude increases were present during an aversive conditioning protocol (tone-shock pairings) that was carried out after the appetitive conditioning. The present results suggest that the enhancement of the amygdalar N150 is specific for learning experiences that are accompanied by autonomic arousal and that this arousal is a prerequisite for the enhancement of the N150.

Influence of emotional arousal on the N150 of the Auditory Evoked Potential from the rat amygdala.

This study tested whether a general increase in emotional arousal is a sufficient determinant for the evocation of the N150, a negative wave in amygdalar Auditory Evoked Potentials (AEPs). Rats received one of three conditioning protocols: either conditioned stimulus (CS) presentations alone (Control) CS-shock pairings (Paired) or unpaired presentations of the CS and shock (Unpaired). Amygdalar AEPs were recorded in response to the CS. It was hypothesized that if a state of emotional arousal is a sufficient condition for the manifestation of the N150, its amplitude should be enhanced in the Paired and Unpaired conditions relative to the Control condition, which was indeed found. In addition, it was found that the N150 had a larger amplitude in the Paired than in the Unpaired condition. This suggests that an additional N150 increase is established when animals learn the CS-US association. The results are discussed in relation to literature on amygdala function.

The auditory P3 from passive and active three-stimulus oddball paradigm.

The aim of this study was the comparison of basic characteristics of the P3 subcomponents elicited in passive and active versions of the auditory oddball paradigm. A 3-stimulus oddball paradigm was employed in which subjects were presented with random sequence of tones while they performed a discrimination task in visual modality with no response to the tone (passive task) or responded to an infrequently occurring target stimulus inserted into sequence of frequent standard and rare non-target stimuli (active task). Results show that the magnitude of the frontal P3 response is determined by the relative perceptual distinctiveness among stimuli. The amplitude of frontal component is larger for the stimuli more deviated from the standard in both passive and active tasks. In all cases however, a maximum over central or fronto-central scalp regions was demonstrated. Moreover, amplitude of this component was influenced by the strength of attentional focus--a significantly larger response was obtained in the active session than in its passive counterpart. The apparent parietal P3 responses were obtained only in the active condition. The amplitude of this component is larger for the target than the non-target across all electrode sites, but both demonstrated a parietal maxima. This findings suggest that generation of early frontal P3 could be related to alerting activity of frontal cortex irrespective of stimulus context, while generation of later parietal P3 is related to temporo-parietal network activated when neuronal model of perceived stimulation and attentional trace are comparing.

The P3 produced by auditory stimuli presented in a passive and active condition: modulation by visual stimuli.

The aim of this study was to investigate how the processing of auditory stimuli is affected by the simultaneous presentation of visual stimuli. This was approached in an active and passive condition, during which a P3 was elicited in the human EEG by single auditory stimuli. Subjects were presented tones, either alone or accompanied by the simultaneous exposition of pictures. There were two different sessions. In the first, the presented tones demanded no further cognitive activity from the subjects (passive or 'ignore' session), while in the second session subjects were instructed to count the tones (active or 'count' session). The central question was whether inter-modal influences of visual stimulation in the active condition would modulate the auditory P3 in the same way as in the passive condition. Brain responses in the ignore session revealed only a small P3-like component over the parietal and frontal cortex, however, when the auditory stimuli co-occurred with the visual stimuli, an increased frontal activity in the window of 300-500 ms was observed. This could be interpreted as the reflection of a more intensive involuntary attention shift, provoked by the preceding visual stimulation. Moreover, it was found that cognitive load caused by the count instruction, resulted in an evident P3, with maximal amplitude over parietal locations. This effect was smaller when auditory stimuli were presented on the visual background. These findings might support the thesis that available resources were assigned to the analysis of visual stimulus, and thus were not available to analyze the subsequent auditory stimuli. This reduction in allocation of resources for attention was restricted to the active condition only, when the matching of a template with incoming information results in a distinct P3 component. It is discussed whether the putative source of this effect is a change in the activity of the frontal cortex.

Tracking pattern learning with single-trial event-related potentials.

OBJECTIVE: The main aim was to track the dynamics of pattern-learning using single-trial event-related potentials (ERPs). A new 'learning-oddball' paradigm was employed presenting eight random targets (the 'no-pattern') followed by eight regular targets (the 'pattern'). In total, six repetitions of the 'no-pattern' followed by the 'pattern' were presented. METHODS: We traced the dynamics of learning by measuring responses to 16 (eight random-eight regular) targets. Since this alternation of the 'no-pattern' followed by the 'pattern' was repeated six times, we extracted single-trial responses to all 96 targets to determine if learning occurred more rapidly with each repetition of the 'pattern.' RESULTS: Following random targets, ERPs contained a marked P3-N2 component that decreased to regular targets, whereas a contingent negative variation (CNV) appeared. ERP changes could be best described by sigmoid 'learning' curves. Single-trial analyses showed that learning occurred more rapidly over repetitions and suggested that the CNV developed prior to the decay of the N2-P3 component. CONCLUSIONS: We show a new paradigm-analysis methodology to track learning processes directly from brain signals. SIGNIFICANCE: Single-trial ERPs analyses open a wide range of applications. Tracking the dynamic structure of cognitive functions may prove crucial in the understanding of learning and in the study of different pathologies.

Diurnal spectral EEG fluctuations in narcoleptic patients during rest and reaction time tasks.

Narcolepsy is associated with lowered vigilance. Diurnal variation in vigilance appears altered, but the exact nature of this change is unclear. It was hypothesized that the homeostatic sleep drive is increased in narcolepsy. Decreased levels of vigilance are reflected in low frequency band power in the electroencephalogram (EEG), so these frequencies were expected to be increased in the narcolepsy group. Furthermore, it was expected that low frequency power should increase over the day. Narcoleptic patients and healthy controls participated (36 participants in total); they were not allowed to take medication or naps on the experimental day. EEG was measured at 9:00, 11:00, 13:00, 15:00, and 17:00 hours, during rest and during reaction time tasks. In the narcolepsy group, alpha power was lower at rest at all times. Delta and theta power during rest and task performance increased steadily over the day in this group, from 11:00 hours onwards. Additionally, in the narcolepsy group beta1 and beta2 power during rest appeared increased at the end of the day. The effects in the lower frequency bands strongly suggest that vigilance is low at all times. The progressive increase in low frequency power indicates that the sleep drive is enhanced. It is not clear whether this pattern reflects an extreme state of low vigilance, or a pathological brain condition. The effects in the higher frequencies suggest that narcoleptic patients may make an effort to counteract their low vigilance level.