Existing literature on reward motivation pays scant attention to the fact that reward potential of the environment varies dramatically with the light/dark cycle. Evolution, by contrast, treats this fact very seriously: In all species, the circadian system is adapted to optimize the daily rhythm of environmental engagement. We used 3 standard protocols to demonstrate that human reward motivation, as measured in the dynamics of positive affect (PA), is modulated endogenously by the circadian clock. Under naturalistic conditions, 13.0% of PA variance was explained by a 24-hr sinusoid. In a constant routine protocol, 25.0% of PA variance was explained by the unmasked circadian rhythm in core body temperature (CBT). A forced desynchrony study showed PA to align with CBT in exhibiting circadian periodicity independent of a 28-hr sleep/wake cycle. It is concluded that the circadian system modulates reward activation, and implications for models of normal and abnormal mood are discussed.

Central control of inspiratory motoneuron output differs from that of tonic and expiratory units during sleep onset, suggesting that the maintenance of airway patency during sleep may become more reliant on the stiffening properties of tonic and expiratory modulated motor units.

Alcohol acts as a sedative that interacts with several neurotransmitter systems important in the regulation of sleep. Acute administration of large amounts of alcohol prior to sleep leads to decreased sleep onset latency and changes in sleep architecture early in the night, when blood alcohol levels are high, with subsequent disrupted, poor quality sleep later in the night. Alcohol abuse and dependence are associated with chronic sleep disturbance, lower slow wave sleep, and more rapid eye movement sleep than normal, that last long into periods of abstinence and may play a role in relapse. The chapter outlines the evidence for acute and chronic alcohol effects on sleep architecture and sleep EEG, evidence for tolerance with repeated administration, and possible underlying neurochemical mechanisms for alcohol’s effects on sleep. Also discussed are sex differences as well as effects of alcohol on sleep homeostasis and circadian regulation. Evidence for the role of sleep disruption as a risk factor for developing alcohol dependence is discussed in the context of research conducted in adolescents. The utility of sleep evoked potentials in the assessment of the effects of alcoholism on sleep and the brain and in abstinence-mediated recovery is also outlined. The chapter concludes with a series of questions that need to be answered to determine the role of sleep and sleep disturbance in the development and maintenance of problem drinking and the potential beneficial effects of the treatment of sleep disorders for maintenance of abstinence in alcoholism.

Aim Existing literature links poor sleep and anxiety symptoms in adolescents. This pilot study aimed to develop a practical method through which a program to improve sleep could reach adolescents in need and to examine the feasibility of a mindfulness‐based, multi‐component group sleep intervention using sleep and anxiety as outcome measures. Methods Sixty‐two grade 9 students (aged 13–15) at a girls’ school were screened with the Pittsburgh Sleep Quality Index (PSQI) and Spence Children's Anxiety Scale (SCAS). Ten participants with self‐reported poor sleep were enrolled into a six‐session program based on Bootzin & Stevens, with added stress/anxiety‐specific components. Sessions covered key aspects of basic mindfulness concepts and practice, sleep hygiene, sleep scheduling, evening/daytime habits, stimulus control, skills for bedtime worries and healthy attitudes to sleep. Treatment changes were measured by pre‐post scores on the PSQI, SCAS and 7‐day actigraphy‐measured sleep. Results The program demonstrated high acceptability, with a completion rate of 90%. Based on effect‐size analysis, participants showed significant improvement on objective sleep onset latency (SOL), sleep efficiency and total sleep time; actigraphy data also showed significantly earlier bedtime, rise time and smaller day‐to‐day bedtime variation. Post‐intervention global PSQI scores were significantly lower than that of pre‐intervention, with significant improvement in subjective SOL, sleep quality and sleep‐related daytime dysfunction. There were small improvements on some subscales of the SCAS, but change on its total score was minimal. Conclusions A mindfulness‐based, multi‐component, in‐school group sleep intervention following brief screening is feasible, and has the potential to improve sleep. Its impact on anxiety needs further investigation.

Summary Women with severe premenstrual syndrome report sleep‐related complaints in the late‐luteal phase, but few studies have characterized sleep disturbances prospectively. This study evaluated sleep quality subjectively and objectively using polysomnographic and quantitative electroencephalographic measures in women with severe premenstrual syndrome. Eighteen women with severe premenstrual syndrome (30.5 ± 7.6 years) and 18 women with minimal symptoms (controls, 29.2 ± 7.3 years) had polysomnographic recordings on one night in each of the follicular and late‐luteal phases of the menstrual cycle. Women with premenstrual syndrome reported poorer subjective sleep quality when symptomatic in the late‐luteal phase compared with the follicular phase (P < 0.05). However, there were no corresponding changes in objective sleep quality. Women with premenstrual syndrome had more slow‐wave sleep and slow‐wave activity than controls at both menstrual phases (P < 0.05). They also had higher trait‐anxiety, depression, fatigue and perceived stress levels than controls at both phases (P < 0.05) and mood worsened in the late‐luteal phase. Both groups showed similar menstrual‐phase effects on sleep, with increased spindle frequency activity and shorter rapid eye movement sleep episodes in the late‐luteal phase. In women with premenstrual syndrome, a poorer subjective sleep quality correlated with higher anxiety (r = −0.64, P = 0.005) and more perceived nighttime awakenings (r = −0.50, P = 0.03). Our findings show that women with premenstrual syndrome perceive their sleep quality to be poorer in the absence of polysomnographically defined poor sleep. Anxiety has a strong impact on sleep quality ratings, suggesting that better control of mood symptoms in women with severe premenstrual syndrome may lead to better subjective sleep quality.