The application of transcranial slow oscillation stimulation (tSOS; 0.75 Hz) was previously shown to enhance widespread endogenous EEG slow oscillatory activity when applied during a sleep period characterized by emerging endogenous slow oscillatory activity. Processes of memory consolidation typically occurring during this state of sleep were also enhanced. Here, we show that the same tSOS applied in the waking brain also induced an increase in endogenous EEG slow oscillations (0.4 -1.2 Hz), although in a topographically restricted fashion. Applied during wakefulness tSOS, additionally, resulted in a marked and widespread increase in EEG theta (4 -8 Hz) activity. During wake, tSOS did not enhance consolidation of memories when applied after learning, but improved encoding of hippocampus-dependent memories when applied during learning. We conclude that the EEG frequency and related memory processes induced by tSOS critically depend on brain state. In response to tSOS during wakefulness the brain transposes stimulation by responding preferentially with theta oscillations and facilitated encoding.transcranial slow oscillation stimulation ͉ sleep ͉ plasticity ͉ cortex ͉ tDCS (transcranial direct current stimulation)

Previously the application of a weak electric anodal current oscillating with a frequency of the sleep slow oscillation (∼0.75 Hz) during non-rapid eye movement sleep (NonREM) sleep boosted endogenous slow oscillation activity and enhanced sleep-associated memory consolidation. The slow oscillations occurring during NonREM sleep and theta oscillations present during REM sleep have been considered of critical relevance for memory formation. Here transcranial direct current stimulation (tDCS) oscillating at 5 Hz, i.e., within the theta frequency range (theta-tDCS) is applied during NonREM and REM sleep. Theta-tDCS during NonREM sleep produced a global decrease in slow oscillatory activity conjoint with a local reduction of frontal slow EEG spindle power (8–12 Hz) and a decrement in consolidation of declarative memory, underlining the relevance of these cortical oscillations for sleep-dependent memory consolidation. In contrast, during REM sleep theta-tDCS appears to increase global gamma (25–45 Hz) activity, indicating a clear brain state-dependency of theta-tDCS. More generally, results demonstrate the suitability of oscillating-tDCS as a tool to analyze functions of endogenous EEG rhythms and underlying endogenous electric fields as well as the interactions between EEG rhythms of different frequencies.

Restoring sleep is strongly associated with a better physical, cognitive, and psychological well-being. By contrast, poor or disordered sleep is related to impairment of cognitive and psychological functioning and worsened physical health. These associations are well documented not only in adults but also in children and adolescents. Importantly, adolescence is hallmarked by dramatic maturational changes in sleep and its neurobiological regulation, hormonal status, and many psychosocial and physical processes. Thus, the role of sleep in mental and physical health during adolescence and in adolescent patients is complex. However, it has so far received little attention. This review first presents contemporary views about the complex neurobiology of sleep and its functions with important implications for adolescence. Second, existing complex relationships between common adolescent somatic/organic, sleep-related, and psychiatric disorders and certain sleep alterations are discussed. It is concluded that poor or altered sleep in adolescent patients may trigger and maintain many psychiatric and physical disorders or combinations of these conditions, which presumably hinder recovery and may cross into later stages of life. Therefore, timely diagnosis and management of sleep problems appear critical for growth and development in adolescent patients.

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Sleep problems are common in attention-deficit/hyperactivity disorder (ADHD) to the extent that they mimic or exacerbate daytime symptoms expression. In this review, we advocate the need for a better understanding of sleep alterations in youths with ADHD and their impact on neurobehavioral functions including learning, memory and emotional regulation. An in-depth exploration of existing data showed that although extensively studied, the actual nature of sleep problems in ADHD and their effects on daytime behavior are still less well understood. Important issues, among which developmental changes in sleep architecture and role of subtle sleep electroencephalogram signatures, are generally neglected. Future research of sleep effects on behavior in ADHD would benefit from considering developmental aspects and links between brain activation patterns during sleep and wake.

SUMMAR Y The aim of the study was to characterize the sleep pattern in children with attention deficit/hyperactivity disorder (ADHD). By means of polysomnography (PSG), sleep patterns were studied in 17 unmedicated preadolescent boys rigorously diagnosed with ADHD and 17 control boys precisely matched for age and intelligence. Although ADHD children did not display a general sleep alteration, major PSG data showed a significant increase in the duration of the absolute rapid eye movement (REM) sleep and the number of sleep cycles in ADHD group when compared with controls. In addition, REM sleep latency tended to be shorter in ADHD children. These results suggest that in ADHD children, a forced REM sleep initiation may produce a higher incidence of sleep cycles and may also contribute to an increased duration of the absolute REM sleep. The overall pattern of the findings implies that a forced ultradian cycling appears characteristic for the sleep in ADHD children, which may be related to alterations of brain monoamines and cortical inhibitory control accompanying the ADHD psychopathology.k e y w o r d s attention deficit/hyperactivity disorder children, brain monoamines, cortical inhibition, rapid eye movement sleep, ultradian cycling

ADHD and TD are characterized by specific sleep alterations. When coexisting, the two disorders alter the sleep pattern in an additive manner, suggesting a high impact on clinical and therapeutic perspectives.

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