Effect of cognitive arousal on sleep latency, somatic and cortical arousal following partial sleep deprivation

Abstract

SUMMAR Y Emerging research has shown that sleepiness, defined as the tendency to fall asleep, is not only determined by sleep pressure and time of day, but also by physiological and cognitive arousal. In this study we evaluated (i) the impact of experimentally induced cognitive arousal on electroencephalogram (EEG) defined sleep latency, and subjective, somatic and cortical arousal, and (ii) whether experimentally induced cognitive arousal enhances performance on a driving simulator test. Twelve healthy sleepers each spent three nights and the following day in the sleep laboratory: an adaptation, a cognitive arousal and a neutral testing day. In the cognitive arousal condition, a visit of a television camera crew took place and subjects were asked to be interviewed. On each testing day, a 5-min heart rate recording, subjective sleepiness and arousal scales, Multiple Sleep Latency Test and a 25-min driving simulator task were scheduled three times at 2-h intervals. Experimentally induced cognitive arousal resulted in significant increases in objective sleep latency. Significantly elevated levels of subjective and somatic arousal -as indexed by a subjective arousal scale and heart rate -were also evidenced following cognitive arousal induction. A marginally significant trend for increased cortical arousal, measured by EEG beta activity, was also found. No effects were found on driving simulator performance. These findings support the concept of cognitive arousal as a significant component in determining sleep latency. In addition, it was illustrated that cognitively induced arousal can provoke increases in somatic and possibly even cortical arousal in normal sleepers. However, this was not accompanied by an enhanced ability to perform adequately on a driving simulator test.k e y w o r d s arousal, beta electroencephalogram activity, heart rate variability, multiple sleep latency test, sleepiness, stress

Can an inert sleeping pill affect sleep? Effects on polysomnographic, behavioral and subjective measures

“…With regard to this issue, two studies already showed that a quasi-desensitization placebo was associated with improved subjective sleep only when the participants were told that it was beneficial (Steinmark and Borkovec 1974;Carr-Kaffashan and Woolfolk 1979). However, in the present study, the suggestion of the pills' efficacy, although present, was not emphasized, since a stronger suggestion may have induced cognitive arousal resulting in significant increases in objective sleep latency (e.g., De Valck et al 2004). In fact, sleep latency did not change as compared to the BSL night.…”

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“…Kronholm et al, 1995;Pressman and Fry, 1989). Furthermore, several experimental studies Arand, 1998, 2005a;De Valck et al, 2004;Gross and Borkovec, 1982;Haynes et al, 1981;Wuyts et al, 2012) have shown that transient increases in physiological or cognitive arousal before going to sleep result in a prolonged latency of sleep onset, which indicates reduced sleepiness. A potential limitation of these studies is the use of a single or few indicators of arousal, most commonly heart rate, since arousal is a multidimensional construct and the congruence between different measures of arousal is either small or insignificant (e.g.…”

An Exploratory Study on the Effects of Tele-neurofeedback and Tele-biofeedback on Objective and Subjective Sleep in Patients with Primary Insomnia

“…Several studies have already shown its relationship with (optimal) cognitive performance (Vernon et al 2003;Gruzelier 2001, 2004;Sterman 1996;Hanslmayer et al 2005) as well as sleep improvement and sleep spindle density (Sterman et al 1970;Hauri 1981;Hauri et al 1982;Berner et al 2006). Thirdly, high beta power (20-30 Hz), which appears to be linked with cognitive processes (Basar-Eroglu et al 1996;Jefferys et al 1996;Makeig and Jung 1996) and arousal (De Valck et al 2004), and is increased in patients experiencing insomnia during the SOP (Lamarche and Ogilvie 1997) and sleep (Perlis et al 2001), was inhibited. The main goal was not to actively decrease the amount of high beta power, but stabilize the reactivity on arousal and stress reflected by the possible instability of this EEG frequency band.…”

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