Sleep Quality and Electroencephalogram Delta Power

Delta activity on electroencephalogram (EEG) is considered a biomarker of homeostatic sleep drive. Delta power is often associated with sleep duration and intensity. Here, we reviewed the literature to explore how sleep quality was influenced by changes in delta power. However, we found that both the decrease and increase in delta power could indicate a higher sleep quality due to the various factors below. First, the differences in changes in delta power in patients whose sleep quality is lower than that of the healthy controls may be related to the different diseases they suffered from. We found that the patients mainly suffered from borderline personality disorder, and Rett syndrome may have a higher delta power than healthy individuals. Meanwhile, patients who are affected by Asperger syndrome, respiratory failure, chronic fatigue, and post-traumatic stress disorder have lower delta power. Second, if the insomnia patients received the therapy, the difference may be caused by the treatment method. Cognitive or music therapy shows that a better therapeutic effect is associated with decreased delta power, whereas in drug treatment, there is an opposite change in delta power. Last, for healthy people, the difference in delta change may be related to sleep stages. The higher sleep quality is associated with increased delta power during the NREM period, whereas a deceased delta change accompanies higher sleep quality during the REM period. Our work summarizes the effect of changes in delta power on sleep quality and may positively impact the monitoring and intervention of sleep quality.

Insomnia subtypes characterised by objective sleep duration and NREM spectral power and the effect of acute sleep restriction: an exploratory analysis

Insomnia disorder (ID) is a heterogeneous disorder with proposed subtypes based on objective sleep duration. We speculated that insomnia subtyping with additional power spectral analysis and measurement of response to acute sleep restriction may be informative in overall assessment of ID. To explore alternative classifications of ID subtypes, insomnia patients (n = 99) underwent two consecutive overnight sleep studies: (i) habitual sleep opportunity (polysomnography, PSG) and, (ii) two hours less sleep opportunity (electroencephalography, EEG), with the first night compared to healthy controls (n = 25). ID subtypes were derived from data-driven classification of PSG, EEG spectral power and interhemispheric EEG asymmetry index. Three insomnia subtypes with different sleep duration and NREM spectral power were identified. One subtype (n = 26) had shorter sleep duration and lower NREM delta power than healthy controls (short-sleep delta-deficient; SSDD), the second subtype (n = 51) had normal sleep duration but lower NREM delta power than healthy controls (normal-sleep delta-deficient; NSDD) and a third subtype showed (n = 22) no difference in sleep duration or delta power from healthy controls (normal neurophysiological sleep; NNS). Acute sleep restriction improved multiple objective sleep measures across all insomnia subtypes including increased delta power in SSDD and NSDD, and improvements in subjective sleep quality for SSDD (p = 0.03), with a trend observed for NSDD (p = 0.057). These exploratory results suggest evidence of novel neurophysiological insomnia subtypes that may inform sleep state misperception in ID and with further research, may provide pathways for personalised care.

P051 SLEEP SPINDLES AND SWA DIFFERENTIALLY CORRELATE WITH OVERNIGHT EPISODIC AND VISUOSPATIAL MEMORY CONSOLIDATION IN OLDER ADULTS WITH AND WITHOUT MILD COGNITIVE IMPAIRMENT

Introduction Sleep microarchitecture disruption is a feature of ageing that is further altered in neurodegenerative disorders. Sleep-memory links in younger adults have been established, however mechanistic pathways of this uncoupling in ageing is poorly understood. Method Our sample consisted of n=46 mild cognitively impaired (MCI) older adults and n=32 cognitively-intact controls who underwent overnight polysomnography and episodic (Rey Auditory Verbal Learning test) and visuospatial (Rey-Osterrieth Complex Figure task) memory tasks that were administered before and after sleep. We examined group differences in overnight memory % retention and associations with NREM slow oscillations (SO, 0.25–1 Hz), delta power (0.5–4 Hz), N2 spindle events (occurrence [11–16 Hz] and slow [11–13 Hz] and fast [13–16 Hz] spindle density p/min) and REM theta power (4.5–8 Hz). Results Repeated measures ANCOVA, controlling for age, indicated greater memory scores in Controls compared to MCI on the episodic task, F=6.7 (p=.01), and no group differences in the visuospatial task (F=1.8, p=.17). In Controls, greater delta power was associated with increased episodic memory retention (r=.515, p=.006). In the MCI group, episodic memory was associated with fast spindle density (r=-.352, p=.04), and visuospatial memory was also associated with fast spindle density (r=-.385, p=.01) and spindle occurrence (r=-.479, p=.003). Conclusion Sleep spindles appear to be negatively associated with memory retention, specifically in MCI. However, given the heterogeneity of MCI, further analysis of its cognitive subtypes is warranted. Comprehensive cognitive and neural pathophysiology profiling are required to better delineate the function of spindles in ageing.

Insomnia subtypes characterised by objective sleep duration and NREM spectral power and the effect of acute sleep restriction: an exploratory analysis

Insomnia disorder (ID) is a heterogeneous disorder with proposed subtypes based on objective sleep duration. We speculated that insomnia subtyping with additional power spectral analysis and measurement of response to acute sleep restriction may be informative in overall assessment of ID. To explore alternative classifications of ID subtypes, insomnia patients (n = 99) underwent two consecutive overnight sleep studies: (i) habitual sleep opportunity (polysomnography, PSG) and, (ii) two hours less sleep opportunity (electroencephalography, EEG), with the first night compared to healthy controls (n = 25). ID subtypes were derived from data-driven classification of PSG, EEG spectral power and interhemispheric EEG asymmetry index. Three insomnia subtypes with different sleep duration and NREM spectral power were identified. One subtype (n = 26) had shorter sleep duration and lower NREM delta power than healthy controls (short-sleep delta-deficient; SSDD), the second subtype (n = 51) had normal sleep duration but lower NREM delta power than healthy controls (normal-sleep delta-deficient; NSDD) and a third subtype showed (n = 22) no difference in sleep duration or delta power from healthy controls (normal neurophysiological sleep; NNS). Acute sleep restriction improved multiple objective sleep measures across all insomnia subtypes including increased delta power in SSDD and NSDD, and improvements in subjective sleep quality for SSDD (p = 0.03), with a trend observed for NSDD (p = 0.057). These exploratory results suggest evidence of novel neurophysiological insomnia subtypes that may inform sleep state misperception in ID and with further research, may provide pathways for personalised care.

The effect of sleep restriction therapy for insomnia on sleep pressure and arousal: a randomised controlled mechanistic trial

Study Objectives Sleep restriction therapy (SRT) effectively treats insomnia but mechanisms are poorly understood. Theoretical models suggest that potentiation of sleep pressure and reduction of arousal are key mechanisms of action. To our knowledge this has never been directly tested. We designed a randomised controlled trial with embedded mechanistic measurement to investigate if SRT causally modifies multidimensional assessments of sleep pressure and arousal. Methods Participants aged 25-55 who met DSM-5 diagnostic criteria for insomnia disorder were randomised to four weeks of SRT or time in bed regularisation (TBR), a control intervention that involves prescription of a regular but not reduced time in bed. Sleep pressure was assessed through daily diary appraisal of morning and evening sleepiness, weekly Epworth sleepiness scale (ESS) scores, psychomotor vigilance, and NREM delta power (0.75-4.5Hz) from ambulatory polysomnographic recordings. Arousal was assessed through daily diary appraisal of cognitive arousal, the pre-sleep arousal scale (PSAS), and NREM beta power (15-32Hz). Outcomes were assessed at baseline (2-week period prior to randomisation), during the intervention phase (1-4 weeks post-randomisation), and at 12-week follow-up. We performed intention-to-treat analyses using linear mixed models. For continuous daily measures, the treatment period was split into early (weeks 1-2) and late (weeks 3-4) treatment. Results Fifty-six participants (39 females, mean age=40.78±9.08) were assigned to SRT (n=27) or TBR (n=29). The SRT group showed enhanced sleep pressure relative to TBR, reflected in (1) enhanced sleepiness in the evening during early (d=1.17) and late treatment (d=0.92), and in the morning during early treatment (d=0.47); (2) higher daytime sleepiness on the ESS at weeks-1 and -2 (d=0.54, d=0.45); and (3) reduced psychomotor vigilance at week-1 (d=0.34). The SRT group also showed reduced arousal relative to TBR, reflected in lower levels of daily-monitored cognitive arousal during early treatment (d=0.53) and decreased PSAS total score at week-4 and week-12 (ds≥0.39). Power spectral analysis of all night NREM sleep revealed an increase in relative, but not absolute, EEG delta power at week-1 and week-4 (ds≥0.52) and a decrease of relative EEG beta power at week-4 (d=0.11). Conclusion For the first time we show that SRT increases sleep pressure and decreases arousal during acute implementation, providing support for mechanism-of-action.

Dysfunctional Overnight Memory Consolidation in Patients with Schizophrenia in Comparison to Healthy Controls: Disturbed Slow-Wave Sleep as Contributing Factor?

<b><i>Introduction:</i></b> Memory deficiency has been shown in schizophrenia patients, but results on the role of sleep parameters in overnight consolidation of associative verbal memory are still missing. Therefore, the aim of our study was to elucidate underlying processes of impaired sleep-related consolidation of associative word pairs in schizophrenia including standard sleep parameters as well as sleep spindle counts and spectral analysis. <b><i>Methods:</i></b> Eighteen stably medicated schizophrenia patients and 24 healthy age-matched controls performed an associative declarative memory task before and after polysomnographic recordings. Part of the participants expected verbal associative memory testing in the morning, while the others did not. Furthermore, participants filled in self-rating questionnaires of schizophrenia-typical experiences (Eppendorf Schizophrenia Inventory [ESI] and Psychotic Symptom Rating Scale). <b><i>Results:</i></b> Schizophrenia patients performed worse in verbal declarative memory in the evening as well as in overnight consolidation (morning compared to evening performance). While duration of slow-wave sleep was nearly comparable between groups, schizophrenia patients showed lower sleep spindle count, reduced delta power during slow-wave sleep, and reduced spindle power during the slow oscillation (SO) up-state. In healthy but not in schizophrenia patients, a linear relationship between overnight memory consolidation and slow-wave sleep duration as well as delta power was evident. No significant effect with respect to the expectation of memory retrieval was evident in our data. Additionally, we observed a negative linear relationship between total number of sleep spindles and ESI score in healthy participants. <b><i>Discussion/Conclusion:</i></b> As expected, schizophrenia patients showed deficient overnight verbal declarative memory consolidation as compared to healthy controls. Reduced sleep spindles, delta power, and spindle power during the SO up-state may link sleep and memory deficiency in schizophrenia. Additionally, the absence of a linear relationship between sleep-related memory consolidation and slow-wave sleep as well as delta power suggests further functional impairments in schizophrenia. Note that this conclusion is based on observational data. Future studies should investigate if stimulation of delta waves during sleep could improve memory performance and thereby quality of life in schizophrenia.

Altered sleep intensity upon DBS to hypothalamic sleep-wake centers in rats

Deep brain stimulation (DBS) has been scarcely investigated in the field of sleep research. We hypothesize that DBS onto hypothalamic sleep- and wake-promoting centers will produce significant neuromodulatory effects, and potentially become a therapeutic strategy for patients suffering severe, drug-refractory sleep-wake disturbances. We aimed to investigate whether continuous electrical high-frequency DBS, such as that often implemented in clinical practice, in the ventrolateral preoptic nucleus (VLPO) or the perifornical area of the posterior lateral hypothalamus (PeFLH), significantly modulates sleep-wake characteristics and behavior. We implanted healthy rats with electroencephalographic/electromyographic electrodes and recorded vigilance states in parallel to bilateral bipolar stimulation of VLPO and PeFLH at 125 Hz at 90 microA over 24 h to test the modulating effects of DBS on sleep-wake proportions, stability and spectral power in relation to baseline. We unexpectedly found that VLPO DBS at 125 Hz deepens slow-wave sleep as measured by increased delta power, while sleep proportions and fragmentation remain unaffected. Thus, the intensity, but not the amount of sleep or its stability, is modulated. Similarly, the proportion and stability of vigilance states remained altogether unaltered upon PeFLH DBS but, in contrast to VLPO, 125 Hz stimulation unexpectedly weakened SWS, evidenced by reduced delta power. This study provides novel insights into non-acute functional outputs of major sleep-wake centers in the rat brain in response to electrical high-frequency stimulation, a paradigm frequently used in human DBS. In the conditions assayed, while exerting no major effects on sleep-wake architecture, hypothalamic high-frequency stimulation arises as a provocative sleep intensity-modulating approach.

The Antidepressant-Like and Analgesic Effects of Kratom Alkaloids are accompanied by Changes in Low Frequency Oscillations but not ΔFosB Accumulation

Mitragyna speciosa (“kratom”), employed as a traditional medicine to improve mood and relieve pain, has shown increased use in Europe and North America. Here, the dose-dependent effects of a purified alkaloid kratom extract on neuronal oscillatory systems function, analgesia, and antidepressant-like behaviour were evaluated and kratom-induced changes in ΔFosB expression determined. Male rats were administered a low or high dose of kratom (containing 0.5 or 1 mg/kg of mitragynine, respectively) for seven days. Acute or repeated low dose kratom suppressed ventral tegmental area (VTA) theta oscillatory power whereas acute or repeated high dose kratom increased delta power, and reduced theta power, in the nucleus accumbens (NAc), prefrontal cortex (PFC), cingulate cortex (Cg) and VTA. The repeated administration of low dose kratom additionally elevated delta power in PFC, decreased theta power in NAc and PFC, and suppressed beta and low gamma power in Cg. Suppressed high gamma power in NAc and PFC was seen selectively following repeated high dose kratom. Both doses of kratom elevated NAc-PFC, VTA-NAc, and VTA-Cg coherence. Low dose kratom had antidepressant-like properties whereas both doses produced analgesia. No kratom-induced changes in ΔFosB expression were evident. These results support a role for kratom as having both antidepressant and analgesic properties that are accompanied by specific changes in neuronal circuit function. However, the absence of drug-induced changes in ΔFosB expression suggest that the drug may circumvent this cellular signaling pathway, a pathway known for its significant role in addiction.