Abnormalities of resting-state EEG in patients with prodromal and overt dementia with Lewy bodies: Relation to clinical symptoms

ObjectiveHere we tested if cortical sources of resting state electroencephalographic (rsEEG) rhythms may differ in sub-groups of patients with prodromal and overt dementia with Lewy bodies (DLB) as a function of relevant clinical symptoms.MethodsWe extracted clinical, demographic and rsEEG datasets in matched DLB patients (N = 60) and control Alzheimer’s disease (AD, N = 60) and healthy elderly (Nold, N = 60) seniors from our international database. The eLORETA freeware was used to estimate cortical rsEEG sources.ResultsAs compared to the Nold group, the DLB and AD groups generally exhibited greater spatially distributed delta source activities (DLB > AD) and lower alpha source activities posteriorly (AD > DLB). As compared to the DLB “controls”, the DLB patients with (1) rapid eye movement (REM) sleep behavior disorders showed lower central alpha source activities (p < 0.005); (2) greater cognitive deficits exhibited higher parietal and central theta source activities as well as higher central, parietal, and occipital alpha source activities (p < 0.01); (3) visual hallucinations pointed to greater parietal delta source activities (p < 0.005).ConclusionsRelevant clinical features were associated with abnormalities in spatial and frequency features of rsEEG source activities in DLB patients.SignificanceThose features may be used as neurophysiological surrogate endpoints of clinical symptoms in DLB patients in future cross-validation prospective studies.     

EEG and behavioural correlates of mild sleep deprivation and vigilance

ObjectiveThe current study investigated the behavioral, cognitive, and electrophysiological impact of mild (only a few hours) and acute (one night) sleep loss via simultaneously recorded behavioural and physiological measures of vigilance.MethodsParticipants (N = 23) came into the lab for two testing days where their brain activity and vigilance were recorded and assessed. The night before the testing session, participants either slept from 12am to 9am (Normally Rested), or from 1am to 6am (Sleep Restriction).ResultsVigilance was reduced and sleepiness was increased in the Sleep Restricted vs. Normally Rested condition, and this was exacerbated over the course of performing the vigilance task. As well, sleep restriction resulted in more intense alpha bursts. Lastly, EEG spectral power differed in Sleep Restricted vs. Normally Rested conditions as sleep onset progressed, particularly for frequencies reflecting arousal (e.g., delta, alpha, beta).ConclusionsThe findings of this study suggest that only one night of mild sleep loss significantly increases sleepiness and, importantly, reduces vigilance. In addition, this sleep loss has a clear impact on the physiology of the brain in ways that reflect reduced arousal.SignificanceUnderstanding the neural correlates and cognitive processes associated with loss of sleep may lead to important advancements in identifying and preventing deleterious or potentially dangerous, sleep-related lapses in vigilance.     

Ibuprofen treatment modifies cortical sources of EEG rhythms in mild Alzheimer’s disease

ObjectiveNon-steroidal anti-inflammatory drugs such as ibuprofen have a protective role on risk of Alzheimer’s disease (AD). Here we evaluated the hypothesis that long-term ibuprofen treatment affects cortical sources of resting electroencephalographic (EEG) rhythms in mild AD patients.MethodsTwenty-three AD patients (13 treated AD IBUPROFEN; 10 untreated AD PLACEBO) were enrolled. Resting EEG data were recorded before and 1 year after the ibuprofen/placebo treatment. EEG rhythms were delta (2–4 Hz), theta (4–8 Hz), alpha 1 (8–10.5 Hz), alpha 2 (10.5–13 Hz), beta 1 (13–20 Hz), and beta 2 (20–30 Hz). LORETA was used for EEG source analysis.ResultsIn the AD PLACEBO group, amplitude of delta sources was globally greater at follow-up than baseline. Instead, amplitude of delta sources remained stable or decreased in the majority of the AD IBUPROFEN patients. Clinical (CDR) but not global cognitive status (MMSE) reflected EEG results.ConclusionsThese results suggest that in mild AD patients, a long-term ibuprofen treatment slightly slows down the progressive increment of delta rhythms as a sign of contrast against the neurodegenerative processes.SignificanceThey motivate future investigations with larger population and extended neuropsychological testing, to study the relationships among ibuprofen treatment, delta cortical sources, and higher order functions.     

Stacked autoencoders as new models for an accurate Alzheimer’s disease classification support using resting-state EEG and MRI measurements

ObjectiveThis retrospective and exploratory study tested the accuracy of artificial neural networks (ANNs) at detecting Alzheimer’s disease patients with dementia (ADD) based on input variables extracted from resting-state electroencephalogram (rsEEG), structural magnetic resonance imaging (sMRI) or both.MethodsFor the classification exercise, the ANNs had two architectures that included stacked (autoencoding) hidden layers recreating input data in the output. The classification was based on LORETA source estimates from rsEEG activity recorded with 10–20 montage system (19 electrodes) and standard sMRI variables in 89 ADD and 45 healthy control participants taken from a national database.ResultsThe ANN with stacked autoencoders and a deep leaning model representing both ADD and control participants showed classification accuracies in discriminating them of 80%, 85%, and 89% using rsEEG, sMRI, and rsEEG + sMRI features, respectively. The two ANNs with stacked autoencoders and a deep leaning model specialized for either ADD or control participants showed classification accuracies of 77%, 83%, and 86% using the same input features.ConclusionsThe two architectures of ANNs using stacked (autoencoding) hidden layers consistently reached moderate to high accuracy in the discrimination between ADD and healthy control participants as a function of the rsEEG and sMRI features employed.SignificanceThe present results encourage future multi-centric, prospective and longitudinal cross-validation studies using high resolution EEG techniques and harmonized clinical procedures towards clinical applications of the present ANNs.     

Functional cortical source connectivity of resting state electroencephalographic alpha rhythms shows similar abnormalities in patients with mild cognitive impairment due to Alzheimer’s and Parkinson’s diseases

Objective

This study tested the hypothesis that markers of functional cortical source connectivity of resting state eyes-closed electroencephalographic (rsEEG) rhythms may be abnormal in subjects with mild cognitive impairment due to Alzheimer’s (ADMCI) and Parkinson’s (PDMCI) diseases compared to healthy elderly subjects (Nold).

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

ObjectiveBehavioral 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.MethodsWe 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.ResultsSubjects 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.ConclusionsThese 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.     

Daily stress,presleep arousal,and sleep in healthy young women: a daily life computerized sleep diary and actigraphy study

ObjectiveOur study aimed to further elucidate the mediating role of presleep arousal in the relationship between daily stress and sleep by investigating subjective sleep quality and actigraphy-assessed sleep efficiency (SE) on both within- and between-participant levels in a sample of healthy young women.MethodsMultilevel modeling was applied on electronically assessed data comprising 14 consecutive nights in 145 healthy young women to assess the relationship between daily stress, presleep (somatic and cognitive) arousal, and sleep on both levels between participants and within participants across days.ResultsHigher levels of daily stress were consistently and significantly associated with higher levels of somatic and cognitive arousal. Somatic arousal mediated the relationship between daily stress and worsened subjective sleep quality on the between-participant level, while cognitive arousal mediated the relationship between daily stress and worsened subjective sleep quality on the within-participants level. Unexpectedly, healthy young women showed higher SE following days with above-average stress with somatic arousal mediating this relationship.ConclusionsOur data corroborate the role of presleep arousal mediating the relationship between daily stress and subjective sleep quality. Interestingly this effect was restricted to somatic arousal being relevant on interindividual levels and cognitive arousal on intraindividual levels. For young and healthy individuals who experience high stress and arousal, well-established cognitive–behavioral techniques could be useful to regulate arousal and prevent worse subjective sleep quality.     

TNFα G308A polymorphism is associated with resilience to sleep deprivation-induced psychomotor vigilance performance impairment in healthy young adults

Cytokines such as TNFα play an integral role in sleep/wake regulation and have recently been hypothesized to be involved in cognitive impairment due to sleep deprivation. We examined the effect of a guanine to adenine substitution at position 308 in the TNFα gene (TNFα G308A) on psychomotor vigilance performance impairment during total sleep deprivation. A total of 88 healthy women and men (ages 22–40) participated in one of five laboratory total sleep deprivation experiments. Performance on a psychomotor vigilance test (PVT) was measured every 2–3 h. The TNFα 308A allele, which is less common than the 308G allele, was associated with greater resilience to psychomotor vigilance performance impairment during total sleep deprivation (regardless of time of day), and also provided a small performance benefit at baseline. The effect of genotype on resilience persisted when controlling for between-subjects differences in age, gender, race/ethnicity, and baseline sleep duration. The TNFα G308A polymorphism predicted less than 10% of the overall between-subjects variance in performance impairment during sleep deprivation. Nonetheless, the differential effect of the polymorphism at the peak of performance impairment was more than 50% of median performance impairment at that time, which is sizeable compared to the effects of other genotypes reported in the literature. Our findings provided evidence for a role of TNFα in the effects of sleep deprivation on psychomotor vigilance performance. Furthermore, the TNFα G308A polymorphism may have predictive potential in a biomarker panel for the assessment of resilience to psychomotor vigilance performance impairment due to sleep deprivation.     

Dissociable effects of sleep deprivation on functional connectivity in the dorsal and ventral default mode networks

ObjectiveTo examine changes in functional connectivity of the default mode network (DMN) that are induced by sleep deprivation, and to identify individual differences that contribute to the vulnerability of the brain's response to sleep deprivation.MethodsUsing functional magnetic resonance imaging, we scanned 51 healthy young subjects during the resting state. Of these participants, 28 were scanned following 24 h of sleep deprivation, and 23 age- and education-matched control subjects were scanned after being well rested.ResultsIndependent component analysis was conducted to identify the DMN. Unlike previous studies that consider the DMN as one homogeneous network, the present study found a dissociable effect of sleep deprivation on two subsystems of the DMN. Functional connectivity within the dorsal DMN decreased; this was correlated with longer response times in a psychomotor vigilance task (PVT). An enhanced functional connectivity was found within the ventral DMN as well as between two subsystems, after sleep deprivation. In addition, between-subsystems connectivity was positively correlated with working memory and negatively correlated with the response time of PVT, suggesting a possible compensatory effect of enhanced communication across two subsystems.ConclusionsThe present findings suggest a dissociable effect of sleep deprivation on functional connectivity in the DMN. Lower functional connectivity in dorsal DMN was related to impairments of basic cognitive function. Notably, working memory was positively correlated with the putative compensatory enhanced functional connectivity across two subsystems, which in turn correlated with behavioral performance after sleep deprivation; this suggests that good working memory may play a protective role in sleep deprivation.     

Let there be no light: the effect of bedside light on sleep quality and background electroencephalographic rhythms

ObjectivesArtificial lighting has been beneficial to society, but unnecessary light exposure at night may cause various health problems. We aimed to investigate how whole-night bedside light can affect sleep quality and brain activity.Patients and methodsTen healthy sleepers underwent two polysomnography (PSG) sessions, one with the lights off and one with the lights on. PSG variables related to sleep quality were extracted and compared between lights-off and lights-on sleep. Spectral analysis was performed to rapid eye movement (REM) sleep and non-REM (NREM) sleep epochs to reveal any light-induced differences in background brain rhythms.ResultsLights-on sleep was associated with increased stage 1 sleep (N1), decreased slow-wave sleep (SWS), and increased arousal index. Spectral analysis revealed that theta power (4–8 Hz) during REM sleep and slow oscillation (0.5–1 Hz), delta (1–4 Hz), and spindle (10–16 Hz) power during NREM sleep were decreased in lights-on sleep conditions.ConclusionsSleeping with the light on not only causes shallow sleep and frequent arousals but also has a persistent effect on brain oscillations, especially those implicated in sleep depth and stability. Our study demonstrates additional hazardous effect of light pollution on health.     

Age-related changes in slow wave activity rise time and NREM sleep EEG with and without zolpidem in healthy young and older adults

ObjectiveWhether there are age-related changes in slow wave activity (SWA) rise time, a marker of homeostatic sleep drive, is unknown. Additionally, although sleep medication use is highest among older adults, the quantitative electroencephalographic (EEG) profile of the most commonly prescribed sleep medication, zolpidem, in older adults is also unknown. We therefore quantified age-related and regional brain differences in sleep EEG with and without zolpidem.MethodsThirteen healthy young adults aged 21.9 ± 2.2 years and 12 healthy older adults aged 67.4 ± 4.2 years participated in a randomized, double-blind, within-subject study that compared placebo to 5 mg zolpidem.ResultsOlder adults showed a smaller rise in SWA and zolpidem increased age-related differences in SWA rise time such that age differences were observed earlier after latency to persistent sleep. Age-related differences in EEG power differed by brain region. Older, but not young, adults showed zolpidem-dependent reductions in theta and alpha frequencies. Zolpidem decreased stage 1 in older adults and did not alter other age-related sleep architecture parameters.ConclusionsSWA findings provide additional support for reduced homeostatic sleep drive or reduced ability to respond to sleep drive with age. Consequences of reduced power in theta and alpha frequencies in older adults remain to be elucidated.     

Nocturnal cognitive arousal is associated with objective sleep disturbance and indicators of physiologic hyperarousal in good sleepers and individuals with insomnia disorder

BackgroundCognitive arousal is central to models of sleep disturbance and insomnia, but findings remain mixed regarding whether cognitive arousal is associated with objective sleep disturbance and physiologic hyperarousal. This study explored associations of objective nocturnal wakefulness and indicators of physiologic hyperarousal with cognitive arousal in healthy sleepers and individuals with insomnia.MethodsIn sum, 52 adults (51.9% women; 18 with insomnia disorder, 34 healthy sleepers) underwent two overnight polysomnography (PSG) studies (adaptation + baseline nights) and a multiple sleep latency test (MSLT). Baseline depression was assessed and presleep cognitive arousal and somatic arousal were recorded for each night. Multivariate regression was used to evaluate associations of PSG sleep parameters with insomnia, cognitive arousal, and somatic arousal.ResultsAnalyses showed that high levels of nocturnal cognitive arousal were associated with prolonged sleep latency, lower sleep efficiency, and shorter total sleep time by PSG on both nights. An association between nocturnal cognitive arousal and wake after sleep onset was observed on night one only. Moreover, greater nocturnal cognitive arousal was associated with greater likelihood of obtaining short sleep and with longer MSLT sleep latencies. Insomnia diagnosis, depression, and somatic arousal were not associated with PSG sleep parameters or MSLT latency.ConclusionsHeightened cognitive arousal at night is linked to objective sleep disturbances and indicators of physiologic hyperarousal at night and during the day. For patients with insomnia, cognitive arousal may contribute to the 24-hr physiologic hyperarousal. Cognitive arousal may be a critical therapeutic target for severe or treatment-resistant sleep disturbance.     

Sleep Deprivation Affects Somatosensory Cortex Excitability as Tested Through Median Nerve Stimulation

BackgroundChanges of cortical excitability after sleep deprivation (SD) in humans have been investigated mostly in motor cortex, while there is little empirical evidence concerning somatosensory cortex, and its plastic changes across SD.ObjectiveTo assess excitability of primary somatosensory cortex (S1) and EEG voltage topographical characteristics associated with somatosensory evoked potentials (SEPs) during SD.MethodsAcross 41 h of SD, 16 healthy subjects participated in 4 experimental sessions (11.00 a.m. and 11.00 p.m. of the 1st and 2nd day) with: a) subjective sleepiness ratings; b) EEG recordings; c) SEPs recordings; d) behavioral vigilance responses.ResultsA clear enhancement of cortical excitability after SD was indexed by: (a) an amplitude increase of different SEPs component in S1; (b) higher voltage in occipital (around 35–43 ms) and fronto-central areas (around 47–62 ms). Circadian fluctuations did not affect cortical excitability. Voltage changes in S1 were strongly related with post-SD fluctuations of subjective and behavioral sleepiness.ConclusionsSleep may have a role in keeping cortical excitability at optimal (namely below potentially dangerous) levels for the human brain, rebalancing progressive changes in cortical responsiveness to incoming inputs occurred during time spent awake. On the other hand, higher level of cortical responsiveness after sleep loss may be one of the mechanisms accounting for post-SD alterations in vigilance and behavior.     

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

ObjectivesThe 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.MethodsDuring 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.ResultsSDEP 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.ConclusionsThese 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.     

Spindles insufficiency in sleepwalkers’ deep sleep

ObjectivesSleepwalkers have consistently shown N3 sleep discontinuity, especially after sleep deprivation. In healthy subjects, sleep spindles activity has been positively correlated to sleep stability. We aimed to compare spindles density during N3 sleep between sleepwalkers and healthy controls.MethodsTwo cohorts of 10 and 21 adult sleepwalkers respectively controlled with 10 and 18 healthy volunteers underwent one baseline and one recovery sleep recording after 38 h (cohort 1) and 25 h (cohort 2) of sleep deprivation. For the two recordings, we performed an automatic detection of spindles (11–16 Hz) from EEG signal during N3 sleep, restricted to the first sleep cycle and repeated for all cycles. For better interpretation of results, we extended the analysis to N2 sleep and we also measured the density of slow waves oscillation (SWO) (0.5–4 Hz) during the same periods.ResultsCompared to controls, sleepwalkers showed significantly lower spindle densities during N3 sleep considering the first sleep cycle (both cohorts) or all cycles (cohort 1). SWO densities did not differ (cohort 1) or were lower (cohort 2) for sleepwalkers. The effect of sleep deprivation did not interact with the effect of group on spindles and SWO densities.ConclusionThis work suggests that the instability of N3 sleep inherent to sleepwalkers may be underpinned by a specific alteration of spindles activity.     

Sources of cortical rhythms in adults during physiological aging: a multicentric EEG study

This electroencephalographic (EEG) study tested whether cortical EEG rhythms (especially delta and alpha) show a progressive increasing or decreasing trend across physiological aging. To this aim, we analyzed the type of correlation (linear and nonlinear) between cortical EEG rhythms and age. Resting eyes-closed EEG data were recorded in 108 young (Nyoung; age range: 18-50 years, mean age 27.3+/-7.3 SD) and 107 elderly (Nold; age range: 51-85 years, mean age 67.3+/-9.2 SD) subjects. The EEG rhythms of interest were delta (2-4 Hz), theta (4-8 Hz), alpha 1 (8-10.5 Hz), alpha 2 (10.5-13 Hz), beta 1 (13-20 Hz), and beta 2 (20-30 Hz). EEG cortical sources were estimated by low-resolution brain electromagnetic tomography (LORETA). Statistical results showed that delta sources in the occipital area had significantly less magnitude in Nold compared to Nyoung subjects. Similarly, alpha 1 and alpha 2 sources in the parietal, occipital, temporal, and limbic areas had significantly less magnitude in Nold compared to Nyoung subjects. These nine EEG sources were given as input for evaluating the type (linear, exponential, logarithmic, and power) of correlation with age. When subjects were considered as a single group there was a significant linear correlation of age with the magnitude of delta sources in the occipital area and of alpha 1 sources in occipital and limbic areas. The same was true for alpha 2 sources in the parietal, occipital, temporal, and limbic areas. In general, the EEG sources showing significant linear correlation with age also supported a nonlinear correlation with age. These results suggest that the occipital delta and posterior cortical alpha rhythms decrease in magnitude during physiological aging with both linear and nonlinear trends. In conclusion, this new methodological approach holds promise for the prediction of dementia in mild cognitive impairment by regional source rather than surface EEG data and by both linear and nonlinear predictors.     

Challenging the sleep homeostat: sleep in depression is not premature aging

ObjectivesThe close relationship between major depression and sleep disturbances led to the hypothesis of a deficiency in homeostatic sleep pressure in depression (S-deficiency hypothesis). Many observed changes of sleep characteristics in depression are also present in healthy aging, leading to the premise that sleep in depression resembles premature aging. In this study, we aimed at quantifying the homeostatic sleep–wake regulation in young women with major depression and healthy young and older controls under high sleep pressure conditions.MethodsAfter an 8-h baseline night nine depressed women, eight healthy young, and eight healthy older women underwent a 40-h sustained wakefulness protocol followed by a recovery night under constant routine conditions. Polysomnographic recordings were carried out continuously. Sleep parameters as well as the time course of EEG slow-wave activity (SWA) (EEG spectra range: 0.75–4.5 Hz), as a marker of homeostatic sleep pressure, were analyzed during the recovery night.ResultsYoung depressed women exhibited higher absolute mean SWA levels and a stronger response to sleep deprivation, particularly in frontal brain regions. In contrast, healthy older women exhibited not only attenuated SWA values compared to the other two groups, but also an absence of the frontal SWA predominance.ConclusionsHomeostatic sleep regulation and sleep architecture in young depressed women are not equal to premature aging. Moreover, our findings demonstrate that young moderately depressed women exhibit no deficiency in the sleep homeostatic process S as predicted by the S-deficiency hypothesis, but, rather, live on an elevated level of homeostatic sleep pressure.     

Sleep deprivation: effect on sleep stages and EEG power density in man

Sleep was analysed in 8 young adults subjects during two baseline nights and two recovery nights following 40.5 h sleep deprivation. Sleep stages were scored from the polygraph records according to conventional criteria. In addition, the EEG records of the entire nights were subjected to spectral analysis to compute the frequency distribution of the power density in the 0.25-25 Hz range for 0.5 Hz or 1.0 Hz bins. In the first recovery night, the power density in the delta band was significantly higher than baseline for total sleep time as well as for sleep stages 2, 3 and 4, 4 and REM. These changes were not restricted to the delta band, but extended to higher frequency bands. Minor, but significant, effects of sleep deprivation were seen in the power density distribution of the second recovery night. In the baseline nights, a progressive reduction of power density in the delta/theta range was present for successive non-REM-REM sleep cycles for total sleep time and stages 2, 3 and 4, and 4. The results show that effects of sleep deprivation as well as trends within the sleep periods are readily apparent from spectral analysis, but are inadequately reflected by conventional sleep scoring. When the power density values were integrated over the entire frequency range (0.75-25 Hz) for each non-REM-REM sleep cycle, an exponential decline from cycle 1 to cycle 3 was suggested. The present findings support the hypothesis that the EEG power density in the low frequency range is an indicator of a progressively declining process during sleep whose initial value is determined by the duration of prior waking.     

Sleep and wakefulness in somnambulism: a spectral analysis study

OBJECTIVE: The sleep structure and the dynamics of EEG slow-wave activity (SWA) were investigated in 12 young adults and age- and gender-matched controls. METHODS: Polysomnography was performed in subjects with well-documented chronic sleepwalking and in matched controls. Blinded visual scoring was performed using the international criteria from the Rechtschaffen and Kales atlas [A manual of standardized technology, techniques and scoring systems for sleep stages of human subjects. Los Angeles: UCLA Brain Information Service, Brain Research Institute, 1968.] and by determining the presence of microarousals as defined in the American Sleep Disorders Association (ASDA) atlas [Sleep 15 (1992) 173.]. An evaluation of SWA overnight was performed on total nocturnal sleep to determine if a difference existed between groups of subjects, since sleepwalking usually originates with slow-wave sleep. Investigation of the delta power in successive nonoverlapping 4-second windows in the 32 seconds just prior to EMG activity associated with a confusional arousal was also conducted. One central EEG lead was used for all analyses. RESULTS: Somnambulistic individuals experienced more disturbed sleep than controls during the first NREM-REM sleep cycle. They had a higher number of ASDA arousals and presented lower peak of SWA during the first cycle that led to a lower SWA decline overnight. When the investigation focused on the short segment immediately preceding a confusional arousal, they presented an important increase in the relative power of low delta (0.75-2 Hz) just prior to the confusional arousal. CONCLUSION: Sleepwalkers undergo disturbed nocturnal sleep at the beginning of the night. The increased power of low delta just prior to the confusional arousal experienced may not be related to Stages 3-4 NREM sleep. We hypothesize that it may be translated as a cortical reaction to brain activation.     

Emotional memory processing is influenced by sleep quality

ObjectiveThe recall of emotional memory is enhanced after sleep and is hindered by sleep deprivation. We used an emotional memory task to assess whether poor sleep quality, as well as sleep deprivation, may influence the accuracy of memory recognition, but also the affective tone associated with the memory.MethodsSeventy-five subjects, divided into poor sleeper (PS), good sleeper (GS), and sleep deprivation (SD) groups, completed two recall (R) sessions: R1, 1 h after the encoding phase; and R2, after one night of sleep for PS and GS groups and after one night of sleep deprivation for the SD group. During the encoding phase, the participants rated valence and arousal of 90 pictures. During R1 and R2, the participants first made a yes/no memory judgment of the 45 target pictures intermingled with 30 non-target pictures, then rated valence and arousal of each picture.ResultsRecognition accuracy was higher for the PS and GS groups compared to the SD group for all pictures. Emotional valence of the remembered pictures was more negative after sleep deprivation and poor quality sleep, while it was preserved after a good sleep.ConclusionsThese results provide the first evidence that poor sleep quality negatively affects emotional valence of memories, within the context of preserved emotional memory consolidation. It is suggested that low sleep quality and lack of sleep may impose a more negative affective tone to memories. The reported effects are not to be ascribed to depressive mood, but to a specific influence of poor sleep quality.