multi-modal-home-sleep-monitoring-in-older-adults

Multi-Modal Home Sleep Monitoring in Older Adults

The gold standard for sleep monitoring is attended in-lab polysomnography; however, this method may be cost-prohibitive and inconvenient for patients and ...

Washington University School of Medicine

An accurate home sleep study to assess electroencephalography (EEG)-based sleep stages and EEG power would be advantageous for both clinical and research purposes, such as for longitudinal studies measuring changes in sleep stages over time. The purpose of this study was to compare sleep scoring of a single-channel EEG recorded simultaneously on the forehead against attended polysomnography. Participants were recruited from both a clinical sleep centre and a longitudinal research study investigating cognitively normal ageing and Alzheimer's disease. Analysis for overall epoch-by-epoch agreement found strong and substantial agreement between the single-channel EEG compared to polysomnography (κ = 0.67). Slow wave activity in the frontal regions was also similar when comparing the single-channel EEG device to polysomnography. As expected, Stage N1 showed poor agreement (sensitivity 0.2) due to lack of occipital electrodes. Other sleep parameters, such as sleep latency and rapid eye movement (REM) onset latency, had decreased agreement. Participants with disrupted sleep consolidation, such as from obstructive sleep apnea, also had poor agreement. We suspect that disagreement in sleep parameters between the single-channel EEG and polysomnography is due partially to altered waveform morphology and/or poorer signal quality in the single-channel derivation. Our results show that single-channel EEG provides comparable results to polysomnography in assessing REM, combined Stages N2 and N3 sleep and several other parameters, including frontal slow wave activity. The data establish that single-channel EEG can be a useful research tool.

Comparison of a single-channel EEG sleep study to polysomnography.

Sleep disturbances are associated with future risk of Alzheimer disease. Disrupted sleep increases soluble amyloid β, suggesting a mechanism for sleep disturbances to increase Alzheimer disease risk. We tested this response in humans using indwelling lumbar catheters to serially sample cerebrospinal fluid while participants were sleep-deprived, treated with sodium oxybate, or allowed to sleep normally. All participants were infused with  C -leucine to measure amyloid β kinetics. We found that sleep deprivation increased overnight amyloid β38, amyloid β40, and amyloid β42 levels by 25 to 30% via increased overnight amyloid β production relative to sleeping controls. These findings suggest that disrupted sleep increases Alzheimer disease risk via increased amyloid β production. Ann Neurol 2018;83:197-204.

Effect of sleep on overnight cerebrospinal fluid amyloid β kinetics.

In Alzheimer's disease (AD), deposition of insoluble amyloid-β (Aβ) is followed by intracellular aggregation of tau in the neocortex and subsequent neuronal cell loss, synaptic loss, brain atrophy, and cognitive impairment. By the time even the earliest clinical symptoms are detectable, Aβ accumulation is close to reaching its peak and neocortical tau pathology is frequently already present. The period in which AD pathology is accumulating in the absence of cognitive symptoms represents a clinically relevant time window for therapeutic intervention. Sleep is increasingly recognized as a potential marker for AD pathology and future risk of cognitive impairment. Previous studies in animal models and humans have associated decreased non-rapid eye movement (NREM) sleep slow wave activity (SWA) with Aβ deposition. In this study, we analyzed cognitive performance, brain imaging, and cerebrospinal fluid (CSF) AD biomarkers in participants enrolled in longitudinal studies of aging. In addition, we monitored their sleep using a single-channel electroencephalography (EEG) device worn on the forehead. After adjusting for multiple covariates such as age and sex, we found that NREM SWA showed an inverse relationship with AD pathology, particularly tauopathy, and that this association was most evident at the lowest frequencies of NREM SWA. Given that our study participants were predominantly cognitively normal, this suggested that changes in NREM SWA, especially at 1 to 2 Hz, might be able to discriminate tau pathology and cognitive impairment either before or at the earliest stages of symptomatic AD.

Cristina D. Toedebusch

Department of Neurology

Washington University School of Medicine

Multi-Modal Home Sleep Monitoring in Older Adults

Cristina D. Toedebusch

.css-o250i3{font-size:18px;font-family:Open Sans,sans-serif;line-height:21.6px;}Department of Neurology

Washington University School of Medicine

Multi-Modal Home Sleep Monitoring in Older Adults

Department of Neurology