Aurora D'Atri

Is Sleep Essential for Neural Plasticity in Humans, and How Does It Affect Motor and Cognitive Recovery?

There is a general consensus that sleep is strictly linked to memory, learning, and, in general, to the mechanisms of neural plasticity, and that this link may directly affect recovery processes. In fact, a coherent pattern of empirical findings points to beneficial effect of sleep on learning and plastic processes, and changes in synaptic plasticity during wakefulness induce coherent modifications in EEG slow wave cortical topography during subsequent sleep. However, the specific nature of the relation between sleep and synaptic plasticity is not clear yet. We reported findings in line with two models conflicting with respect to the underlying mechanisms, that is, the “synaptic homeostasis hypothesis” and the “consolidation” hypothesis, and some recent results that may reconcile them. Independently from the specific mechanisms involved, sleep loss is associated with detrimental effects on plastic processes at a molecular and electrophysiological level. Finally, we reviewed growing evidence supporting the notion that plasticity-dependent recovery could be improved managing sleep quality, while monitoring EEG during sleep may help to explain how specific rehabilitative paradigms work. We conclude that a better understanding of the sleep-plasticity link could be crucial from a rehabilitative point of view.

Topographic electroencephalogram changes associated with psychomotor vigilance task performance after sleep deprivation

OBJECTIVES The psychomotor vigilance task (PVT) is a widely used method for the assessment of vigilance after sleep deprivation (SDEP). However, the neural basis of PVT performance during SDEP has not been fully understood. In particular, no studies have investigated the possible relation between EEG topographical changes after sleep loss and PVT performance. The aim of the present study is to assess the EEG topographic correlates of PVT performance after SDEP. METHODS During 40 h of SDEP, 16 healthy male subjects were evaluated in four sessions performed at the same time (11:00 a.m. and 11:00 p.m.) of the first and second day with: (a) subjective sleepiness recordings by means of the Karolinska Sleepiness Scale (KSS); (b) EEG recordings (5 min eyes-open condition); and (c) PVT. RESULTS SDEP induced a slowing of PVT reaction times (RTs), higher level of subjective sleepiness and an increase of delta, theta, alpha and beta 1 EEG activity. Only slowest PVT RTs were influenced by circadian factors, with longer RTs in the morning. Both fastest PVT RTs and KSS scores were positively correlated with post-SDEP changes in EEG theta activity, mainly in centro-posterior areas, but not with other EEG frequencies. KSS scores and PVT measures were also positively correlated. CONCLUSIONS These findings suggest that SDEP differently affects PVT variables, and that an increase in theta activity may be the principal EEG basis of the post-SDEP slowing of fastest PVT RTs. Similar neural mechanisms seem to underlie both performance deterioration to PVT and the increase of subjective sleepiness.

The Fall of Sleep K-Complex in Alzheimer Disease

Although a slowing of electroencephalographic (EEG) activity during wakefulness and –to some extent- sleep of Alzheimer disease (AD) patients (i.e., increased slow-frequency activity) was documented, recent findings in healthy elderly show a decreased 0.6–1 Hz slow wave activity (SWA) during NREM, which was associated to β-amyloid deposition and impaired hippocampal memory consolidation. We hypothesize that the apparent contradiction may be explained by the partial overlap between 0.6–1 Hz EEG activity and K-Complex (KC). According to this view, we studied both frontal KCs and SWA in 20 AD patients and 20 healthy age-matched controls (HC) during nightly sleep, under the hypothesis that KCs better discriminate patients from healthy elderly than ≤1 Hz SWA. A drastic decrease of KC density during stage 2 NREM was found in AD compared to HC. Patients show more than 40% reduction of the KC density, allowing a correct classification of 80%. On the other hand, ≤1 Hz SWA of AD patients is slightly (not significantly) higher in most cortical areas compared to HC. Although no significant changes of ≤1 Hz SWA are detectable over frontal areas in AD, KC density decreases over the same location, and its decrease is related to the cognitive decline.

Mapping changes in cortical activity during sleep in the first 4 years of life

A coherent body of evidence supports the notion that sleep is a local and use‐dependent process. Significant changes in brain morphology and function occur in the first years of life, revealing a postero–anterior trajectory of cortical maturation. On this basis, a recent study demonstrated that regional cortical maturation between early childhood and late adolescence is reflected in regional changes of sleep slow wave activity (SWA) during non‐rapid eye movement (NREM) sleep. Our hypothesis is that changes of electroencephalogram (EEG) rhythms during sleep from birth to childhood are also mirrored by parallel regional changes in the EEG rhythms of sleep according to the assumption of a postero–anterior gradient in cortical maturation. We studied all‐night EEG of 39 healthy, full‐term, infants and children aged between 0 and 48 months, evaluating regional differences in NREM sleep. We confirmed the strictly local nature of sleep with frequency‐specific regional differences. Specifically, we found a general shift of maxima of the upper alpha activity from occipital to prefrontal regions, expressed mainly by the ~11 Hz frequency. This shift corresponds to a postero–anterior trajectory of the so‐called ‘slow spindles’. The theta and alpha EEG activity of the frontal cortex exhibits a clear, positive, correlation with age. We conclude that specific local differences during NREM sleep, parallel cortical maturation also in the first 4 years of life.

EEG topography during sleep inertia upon awakening after a period of increased homeostatic sleep pressure

OBJECTIVE Behavioral and physiological indexes of high sleep inertia (SI) characterize the awakening from recovery (REC) sleep after prolonged wakefulness, but the associated electroencephalogram (EEG) topography has never been investigated. Here, we compare the EEG topography following the awakening from baseline (BSL) and REC sleep. METHODS We have recorded the EEG waking activity of 26 healthy subjects immediately after the awakening from BSL sleep and from REC sleep following 40 h of prolonged wakefulness. In both BSL and REC conditions, 12 subjects were awakened from stage 2 sleep, and 14 subjects from rapid eye movement (REM) sleep. The full-scalp waking EEG (eyes closed) was recorded after all awakenings. RESULTS Subjects awakened from REC sleep showed a reduction of fronto-central alpha and beta-1 activities, while no significant effects of the sleep stage of awakening have been observed. Positive correlations between pre- and post-awakening EEG modifications following REC sleep have been found in the posterior and lateral cortices in the frequency ranges from theta to beta-2 and (only for REM awakenings) extending to the fronto-central regions in the beta-1 band, and in the midline central and parietal derivations for the alpha and delta bands, respectively. CONCLUSIONS These findings suggest that the higher SI after REC sleep may be due to the fronto-central decrease of alpha and beta-1 activity and to the persistence of the sleep EEG features after awakening in the posterior, lateral, and fronto-central cortices, without influences of the sleep stage of awakening.

In Search of Sleep Biomarkers of Alzheimer’s Disease: K-Complexes Do Not Discriminate between Patients with Mild Cognitive Impairment and Healthy Controls

The K-complex (KC) is one of the hallmarks of Non-Rapid Eye Movement (NREM) sleep. Recent observations point to a drastic decrease of spontaneous KCs in Alzheimer’s disease (AD). However, no study has investigated when, in the development of AD, this phenomenon starts. The assessment of KC density in mild cognitive impairment (MCI), a clinical condition considered a possible transitional stage between normal cognitive function and probable AD, is still lacking. The aim of the present study was to compare KC density in AD/MCI patients and healthy controls (HCs), also assessing the relationship between KC density and cognitive decline. Twenty amnesic MCI patients underwent a polysomnographic recording of a nocturnal sleep. Their data were compared to those of previously recorded 20 HCs and 20 AD patients. KCs during stage 2 NREM sleep were visually identified and KC densities of the three groups were compared. AD patients showed a significant KC density decrease compared with MCI patients and HCs, while no differences were observed between MCI patients and HCs. KC density was positively correlated with Mini-Mental State Examination (MMSE) scores. Our results point to the existence of an alteration of KC density only in a full-blown phase of AD, which was not observable in the early stage of the pathology (MCI), but linked with cognitive deterioration.