EEG spectral power and sleepiness during 24 h of sustained wakefulness in patients with obstructive sleep apnea syndrome.
ABSTRACT This study investigated if obstructive sleep apnea syndrome (OSAS) may be associated with higher activity in different frequency bands of the EEG during a sustained wakefulness paradigm.
Twelve OSA patients and 8 healthy controls were studied with the Karolinska Drowsiness Test (KDT) and subjective ratings of sleepiness (VAS and KSS) conducted every hour during 24 h of sustained wakefulness.
The waking EEG activity, mainly in the low (0.5-7.8 Hz) and fast (12.7-29.2 Hz) frequency band, increased as time awake progressed in both groups but more obviously in OSA patients. A similar pattern was observed for rated sleepiness in both groups. Moreover, VAS ratings of alertness were closely related to the awake theta, fast alpha and beta bands in controls but not in OSA patients.
OSAS was associated with a wake-dependent increase in low (0.5-7.8 Hz) and fast (12.7-29.2 Hz) frequency range activity. Variations in behavioural sleepiness measured by VAS ratings closely reflect most of the waking EEG parameters in controls but not in OSA patients.
In a sustained wakefulness paradigm, higher activity in delta, theta and beta bands associated with OSAS indicates that OSA patients show marked signs of higher sleepiness and stronger efforts than controls to stay awake, even though they tend to underestimate their sleepiness.
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ABSTRACT: The main consequence of insufficient sleep is sleepiness. While measures of sleep latency, continuous encephalographical/electro-oculographical (EEG/EOG) recording and performance tests are useful indicators of sleepiness in the laboratory and clinic, they are not easily implemented in large, real-life field studies. Subjective ratings of sleepiness, which are easily applied and unobtrusive, are an alternative, but whether they measure sleepiness sensitively, reliably and validly remains uncertain. This review brings together research relevant to these issues. It is focused on the Karolinska Sleepiness Scale (KSS), which is a nine-point Likert-type scale. The diurnal pattern of sleepiness is U-shaped, with high KSS values in the morning and late evening, and with great stability across years. KSS values increase sensitively during acute total and repeated partial sleep deprivation and night work, including night driving. The effect sizes range between 1.5 and 3. The relation to driving performance or EEG/EOG indicators of sleepiness is highly significant, strongly curvilinear and consistent across individuals. High (>6) KSS values are associated particularly with impaired driving performance and sleep intrusions in the EEG. KSS values are also increased in many clinical conditions such as sleep apnea, depression and burnout. The context has a strong influence on KSS ratings. Thus, physical activity, social interaction and light exposure will reduce KSS values by 1–2 units. In contrast, time-on-task in a monotonous context will increase KSS values by 1–2 units. In summary, subjective ratings of sleepiness as described here is as sensitive and valid an indicator of sleepiness as objective measures, and particularly suitable for field studies.Journal of Sleep Research 04/2014; 23(3). DOI:10.1111/jsr.12158 · 2.95 Impact Factor
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ABSTRACT: OBJECTIVE: To explore the use of detrended fluctuation analysis (DFA) scaling exponent of the awake electroencephalogram (EEG) as a new alternative biomarker of neurobehavioural impairment and sleepiness in obstructive sleep apnea (OSA). METHODS: Eight patients with moderate-severe OSA and nine non-OSA controls underwent a 40-h extended wakefulness challenge with resting awake EEG, neurobehavioural performance (driving simulator and psychomotor vigilance task) and subjective sleepiness recorded every 2-h. The DFA scaling exponent and power spectra of the EEG were calculated at each time point and their correlation with sleepiness and performance were quantified. RESULTS: DFA scaling exponent and power spectra biomarkers significantly correlated with simultaneously tested performance and self-rated sleepiness across the testing period in OSA patients and controls. Baseline (8am) DFA scaling exponent but not power spectra were markers of impaired simulated driving after 24-h extended wakefulness in OSA (r=0.738, p=0.037). OSA patients had a higher scaling exponent and delta power during wakefulness than controls. CONCLUSIONS: The DFA scaling exponent of the awake EEG performed as well as conventional power spectra as a marker of impaired performance and sleepiness resulting from sleep loss. SIGNIFICANCE: DFA may potentially identify patients at risk of neurobehavioural impairment and assess treatment effectiveness.Clinical neurophysiology: official journal of the International Federation of Clinical Neurophysiology 04/2013; 124(8). DOI:10.1016/j.clinph.2013.02.022 · 2.98 Impact Factor
Article: Waking EEG in primary insomnia.[Show abstract] [Hide abstract]
ABSTRACT: Quantitative analysis of the waking EEG has been proposed as an objective method for measuring neurobehavioral impairment in primary insomnia. Thirty six patients with DSM-IV primary insomnia diagnosis (mean age 36 years) and 29 controls, matched for age and education, participated in the study. Waking EEG from 21 scalp electrodes was subjected to spectral analyses using a fast Fourier transform algorithm. Significantly lower values of power in the theta range and higher values of beta power were found in insomniacs as compared to control subjects. This theta power decrease in patients suffering from insomnia was not uniform throughout the brain, but it was pronounced in prefrontal derivations. Lower values of theta power correlated negatively and higher values of beta power correlated postively with Hyperarousal Scale score. Results of the research presented here support the notion of twenty-four hour hyperarousal in primary insomnia. Attenuated theta and enhanced beta power can be electrophysiological correlates of dysfunctional arousal in insomnia. Less waking theta power in insomniacs suggests a decrease in homeostatic sleep propensity.Acta neurobiologiae experimentalis 01/2011; 71(3):387-92. · 2.24 Impact Factor