The increase in slow wave activity (SWA) correlates with cognitive training-induced plasticity in a region known to be involved in working memory performance. Thus, in future, the mapping of sleep SWA may be used to longitudinally monitor the effects of working memory training in children and adolescents with working memory deficiencies.

Aging is associated with marked changes in the timing, consolidation and structure of sleep. Older people wake up frequently, get up earlier and have less slow wave sleep than young people, although the extent of these age-related changes differs considerably between individuals. Interindividual differences in homeostatic sleep regulation in young volunteers are associated with the variable-number, tandem-repeat (VNTR) polymorphism (rs57875989) in the coding region of the circadian clock gene PERIOD3 (PER3). However, predictors of these interindividual differences have yet to be identified in older people. Sleep electroencephalographic (EEG) characteristics and circadian rhythms were assessed in 26 healthy older volunteers (55-75 years) selected on the basis of homozygosity for either the long or short allele of the PER3 polymorphism. Homozygosity for the longer allele (PER3 5/5 ) associated with a phase-advance in the circadian melatonin profile and an earlier occurrence of the melatonin peak within the sleep episode. Furthermore, older PER3 5/5 participants accumulated more nocturnal wakefulness, had increased EEG frontal delta activity (0.75-1.50 Hz), and decreased EEG frontal sigma activity (11-13 Hz) during non-rapid eye movement (REM) sleep compared with PER3 4/4 participants. Our results indicate that the polymorphism in the clock gene PER3 may contribute to interindividual differences in sleep and circadian physiology in older people.

Background: Schizophrenia is a severe mental disorder affecting approximately 1% of the worldwide population. Yet, schizophrenia-like experiences (schizotypy) are very common in the healthy population, indicating a continuum between normal mental functioning and the psychosis found in schizophrenic patients. A continuum between schizotypy and schizophrenia would be supported if they share the same neurobiological origin. Two such neurobiological markers of schizophrenia are: (1) a reduction of sleep spindles (12-15 Hz oscillations during nonrapid eye movement sleep), likely reflecting deficits in thalamocortical circuits and (2) increased glutamine and glutamate (Glx) levels in the thalamus. Thus, this study aimed to investigate whether sleep spindles and Glx levels are related to schizotypal personality traits in healthy subjects. Methods: Twenty young male subjects underwent 2 all-night sleep electroencephalography recordings (128 electrodes). Sleep spindles were detected automatically. After those 2 nights, thalamic Glx levels were measured by magnetic resonance spectroscopy. Subjects completed a magical ideation scale to assess schizotypy. Results: Sleep spindle density was negatively correlated with magical ideation (r = −.64, P < .01) and thalamic Glx levels (r = −.70, P < .005). No correlation was found between Glx levels in the thalamus and magical ideation (r = .12, P > .1). Conclusions: The common relationship of sleep spindle density with schizotypy and thalamic Glx levels indicates a neurobiological overlap between nonclinical schizotypy and schizophrenia. Thus, sleep spindle density and magical ideation may reflect the anatomy and efficiency of the thalamo-cortical system that shows pronounced impairment in patients with schizophrenia.

IntroductionA large number of studies have investigated neural correlates of consciousness in adults. However, knowledge about brain function in children with disorders of consciousness (DOC) is very limited. We suggest that EEG recordings during sleep are a promising approach. In healthy adults as well as in children, it has been shown that the activity of sleep slow waves (EEG spectral power 1–4.5 Hz), the primary characteristic of deep sleep, is dependent on use during previous wakefulness. Thus the regulation of slow wave activity (SWA) provides indirect insights into brain function during wakefulness.MethodsIn the present study, we investigated high-density EEG recordings during sleep in ten healthy children and in ten children with acquired brain injury, including five children with DOC and five children with acquired brain injury without DOC. We used the build-up of SWA to quantify SWA regulation.ResultsChildren with DOC showed a global reduction in the SWA build-up when compared to both, healthy children and children with acquired brain injury without DOC. This reduction was most pronounced over parietal brain areas. Comparisons within the group of children with DOC revealed that the parietal SWA build-up was the lowest in patients showing poor outcome. Longitudinal measurements during the recovery period showed an increase in parietal SWA build-up from the first to the second sleep recording.ConclusionsOur results suggest that the reduced parietal SWA regulation may represent a characteristic topographical marker for brain network dysfunction in children with DOC. In the future, the regulation of SWA might be used as a complementary assessment in adult and paediatric patients with DOC.

Slow waves (1–4.5 Hz) are the most characteristic oscillations of deep non-rapid eye movement sleep. The EEG power in this frequency range (slow-wave activity, SWA) parallels changes in cortical connectivity (i.e., synaptic density) during development. In patients with attention-deficit/hyperactivity disorder (ADHD), prefrontal cortical development was shown to be delayed and global gray matter volumes to be smaller compared to healthy controls. Using data of all-night recordings assessed with high-density sleep EEG of 50 children and adolescents with ADHD (mean age: 12.2 years, range: 8–16 years, 13 female) and 86 age- and sex-matched healthy controls (mean age: 12.2 years, range: 8–16 years, 23 female), we investigated if ADHD patients differ in the level of SWA. Furthermore, we examined the effect of stimulant medication. ADHD patients showed a reduction in SWA across the whole brain (−20.5%) compared to healthy controls. A subgroup analysis revealed that this decrease was not significant in patients who were taking stimulant medication on a regular basis at the time of their participation in the study. Assuming that SWA directly reflects synaptic density, the present findings are in line with previous data of neuroimaging studies showing smaller gray matter volumes in ADHD patients and its normalization with stimulant medication.

In adults, cerebral oxy-([O₂Hb]) and deoxyhemoglobin concentrations ([HHb]) change characteristically at transitions of sleep stages. The aims were to assess these changes in adolescents and additionally to measure tissue oxygen saturation (StO₂) by near infrared spectroscopy (NIRS). Previously it was reported that in adults [O₂Hb] increased and [HHb] decreased at the transition from non-rapid eye movement sleep (NREMS) to REMS and wakefulness. Transitions to NREMS from REMS/wakefulness led to a decrease in [O₂Hb] and an increase in [HHb]. We measured [O₂Hb], [HHb] and tissue oxygenation (StO₂) with NIRS approximately above the left prefrontal cortex in 12 healthy adolescent males (aged 10-16 years). We found comparable signs and magnitudes of changes in [O₂Hb] and [HHb] as observed in adults. StO₂ increased at the transitions from NREMS to REMS and decreased from REMS to NREMS and at sleep onset (all p < 0.01, linear mixed effects model). Changes in oxygen metabolism during sleep transitions are similar in adolescents and adults. In addition, we show for the first time temporal changes of StO₂ at sleep transitions.

How does the oxygen metabolism change during sleep? We aimed to measure the change in brain tissue oxygen saturation (StO2) before and after sleep with near-infrared spectroscopy (NIRS) using an in-house developed sensor. According to the synaptic homeostasis hypothesis [1], synaptic downscaling during sleep would result in reduced energy consumption. Thus, this reduced energy demands should be reflected in the oxygen metabolism and StO2. Thirteen nights of 7 male subjects (age 11-16 years, one subject contributed only one night, all others two) were included in the analysis. We performed NIRS measurements throughout the entire night. The NIRS sensor was placed close to electrode position Fp1 (international 10/20 system), over the left frontal cortex. Absolute StO2 and total haemoglobin (tHb) were calculated from the NIRS measurements using a self-calibrating method [2]. StO2 and tHb during the awake period prior to sleep and after awakening were compared. The subjects were instructed to lie in bed in the same position before and after sleep. Values of the two nights were averaged for each subject. Furthermore, a linear regression line was fit through the all-night StO2 recordings. We found an increase in StO2 by 4.32 ± 1.76 % (mean ± SD, paired t-test p < 0.001, n = 7) in the morning compared to evening, while tHb did not change (1.02 ± 6.81 M p = 0.704, n = 7). Since the tHb remained at a similar level after sleep, this increase in StO2 indicates that in the morning more oxygenated blood and less deoxygenated blood was present in the brain compared to the evening. The slope of the regression line was 0.37 ± 0.13 % h(-1) leading to a similar increase of StO2 in the course of sleep. This may be interpreted as a reduced oxygen consumption or energy metabolism after sleep. Abstract How does the oxygen metabolism change during sleep? We aimed to measure the change in brain tissue oxygen saturation (StO 2 ) before and after sleep with near-infrared spectroscopy (NIRS) using an in-house developed sensor. According to the synaptic homeostasis hypothesis [1] synaptic downscaling during sleep would result in reduced energy consumption. Thus, this reduced energy demands should be reflected in the oxygen metabolism and StO 2 . Thirteen nights of 7 male subjects (age 11-16 years, 1 subject contributed only one night, all others two) were included in the analysis. We performed NIRS measurements throughout the entire night. The NIRS sensor was placed close to electrode position Fp1, (international 10/20 system) over the left frontal cortex. Absolute StO 2 and total haemoglobin (tHb) were calculated from the NIRS measurements using a self-calibrating method [2]. StO 2 and tHb during the awake period prior to sleep and after awakening were compared. The subjects were instructed to lie in bed in the same position before and after sleep. Values of the two nights were averaged for each subject. Furthermore, a linear regression line was fit through the all-night StO 2 recordings. We found an increase in StO 2 by 4.32 ± 1...

Working memory is important for mental reasoning and learning processes. Several studies in adults and school-age children have shown performance improvement in cognitive tests after working memory training. Our aim was to examine not only immediate but also long-term effects of intensive working memory training on cognitive performance tests in children. Fourteen healthy male subjects between 10 and 16 years trained a visuospatial n-back task over 3 weeks (30 min daily), while 15 individuals of the same age range served as a passive control group. Significant differences in immediate (after 3 weeks of training) and long-term effects (after 2-6 months) in an auditory n-back task were observed compared to controls (2.5 fold immediate and 4.7 fold long-term increase in the training group compared to the controls). The improvement was more pronounced in subjects who improved their performance during the training. Other cognitive functions (matrices test and Stroop task) did not change when comparing the training group to the control group. We conclude that visuospatial working memory training in children boosts performance in similar memory tasks such as the auditory n-back task. The sustained performance improvement several months after the training supports the effectiveness of the training.