Snoring Remediation with Oral Appliance Therapy Potentially Reverses Cognitive Impairment: An Intervention Controlled Pilot Study.

Respiration rate (RR) dynamics entrains brain neural networks. RR differences between mild cognitive impairment (MCI) and Alzheimer's disease (AD) in response to oral appliance therapy (OAT) are unknown. This pilot study investigated if RR during stable sleep shows a relationship to pathological severity in subjects with MCI and AD who snore and if RR is influenced following stabilization of the upper airway using OAT. The study cohort was as follows: cognitively normal (CN; n = 14), MCI (n = 14) and AD (n = 9); and a sub-population receiving intervention, CN (n = 5), MCI (n = 7), AD (n = 6) subjects. The intervention used was an oral appliance plus a mouth shield (Tx). RR maximum (max) rate (breaths/minute) and RR fluctuation during 2116 stable sleep periods were measured. The Montreal cognitive assessment (MoCA) was administered before and after 4 weeks with Tx. Baseline data showed significantly higher RR fluctuation in CN vs. AD (p < 0.001) but not between CN vs. MCI (p = 0.668). Linear mixed model analysis indicated Tx effect (p = 0.008) for RR max. Tx after 4 weeks lowered the RR-max in MCI (p = 0.022) and AD (p < 0.001). Compared with AD RR max, CN (p < 0.001) and MCI (p < 0.001) were higher with Tx after 4 weeks. Some MCI and AD subjects improved executive and memory function after 4 weeks of Tx.

Sleep quality changes in chronically depressed patients treated with Mindfulness-based Cognitive Therapy or the Cognitive Behavioral Analysis System of Psychotherapy: a pilot study.

OBJECTIVE: To capture any sleep quality changes associated with group psychotherapy. PATIENTS/METHODS: Physician-referred, chronically depressed patients (n = 25) were randomized to either eight group sessions of Mindfulness-based Cognitive Therapy (MBCT, n = 9) plus Treatment As Usual (TAU), or the Cognitive Behavioral Analysis System of Psychotherapy (CBASP, n = 8) plus TAU, or to TAU only (control group, n = 8). Participants recorded their sleep at home. The primary outcome variables were: stable and unstable sleep, which were assessed using cardiopulmonary coupling (CPC) analysis, and estimated total sleep and wake time (minutes). Cardiopulmonary coupling measures heart rate variability and the electrocardiogram's R-wave amplitude fluctuations associated with respiration. RESULTS: By post-treatment night 6, the CBASP group had more stable sleep (p= 0.044) and less wake (p = 0.004) compared with TAU, and less wake vs MBCT (p = 0.039). CONCLUSION: The CBASP group psychotherapy treatment improved sleep quality compared with Treatment As Usual.

WITHDRAWN: Sleep quality changes in chronically depressed patients treated with mindfulness-based cognitive therapy or cognitive behavioral analysis system for psychotherapy: a pilot study.

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Bupropion response on sleep quality in patients with depression: implications for increased cardiovascular disease risk.

Depression could be an independent risk factor for cardiovascular disease. We assessed bupropion response in depressed patients by polysomnography (PSG) and cardiopulmonary coupling (CPC) variables. Nineteen subjects participated in a two-session, two consecutive night PSG protocol. Participants received either placebo or bupropion-SR 150 mg, orally, in a randomized, double-blind cross-over fashion on night two. Outcome variables were: sleep stages, REM latency, stable, unstable sleep and very low frequency coupling (VLFC). CPC analysis uses heart rate variability and the electrocardiogram's R-wave amplitude fluctuations associated with respiration to generate frequency maps. Bupropion increased REM latency (p=0.043) but did not impact PSG sleep continuity, architecture and CPC variables. A trend (p=0.092) was observed towards increasing VLFC duration. Bupropion increased the number of stable-unstable sleep transitions (p=0.036). Moderate to strong correlations between PSG and CPC variables were found on placebo and bupropion nights. Limitations include a small sample size, limited power to detect CPC changes and lack of normal controls for comparison. Increased stable-unstable sleep transitions and VLFC duration may indicate vulnerability to cardiovascular disease due to their association with low heart rate variability that has been associated with increased mortality raising the question whether the beneficial effects of the antidepressant medication outweighs the impact on cardiopulmonary dynamics.

An electrocardiogram-based analysis evaluating sleep quality in patients with obstructive sleep apnea.

OBJECTIVE: The study compares polysomnography (PSG) and cardiopulmonary coupling (CPC) sleep quality variables in patients with (1) obstructive sleep apnea (OSA) and (2) successful and unsuccessful continuous positive airway pressure (CPAP) response. PATIENTS/METHODS: PSGs from 50 subjects (32 F/18 M; mean age 48.4 ± 12.29 years; BMI 34.28 ± 9.33) were evaluated. OSA patients were grouped by no (n = 16), mild (n = 13), and moderate to severe (n = 20) OSA (apnea-hypopnea index (AHI) ≤ 5, >5-15, >15 events/h, respectively). Outcome sleep quality variables were sleep stages in non-rapid eye movement, rapid eye movement sleep, and high (HFC), low (LFC), very low-frequency coupling (VLFC), and elevated LFC broad band (e-LFCBB). An AHI ≤ 5 events/h and HFC ≥ 50 % indicated a successful CPAP response. CPC analysis extracts heart rate variability and QRS amplitude change that corresponds to respiration. CPC-generated spectrograms represent sleep dynamics from calculated coherence product and cross-power of both time series datasets. RESULTS: T tests differentiated no and moderate to severe OSA groups by REM % (p = 0.003), HFC (p = 0.007), VLFC (p = 0.007), and LFC/HFC ratio (p = 0.038) variables. The successful CPAP therapy group (n = 16) had more HFC (p = 0.003), less LFC (p = 0.003), and e-LFCBB (p = 0.029) compared to the unsuccessful CPAP therapy group (n = 8). PSG sleep quality measures, except the higher arousal index (p = 0.038) in the unsuccessful CPAP group, did not differ between the successful and unsuccessful CPAP groups. HFC ≥ 50 % showed high sensitivity (77.8 %) and specificity (88.9 %) in identifying successful CPAP therapy. CONCLUSIONS: PSG and CPC measures differentiated no from moderate to severe OSA groups and HFC ≥ 50 % discriminated successful from unsuccessful CPAP therapy. The HFC ≥ 50 % cutoff showed clinical value in identifying sleep quality disturbance among CPAP users.

Quantitative measurement of sleep quality using cardiopulmonary coupling analysis: a retrospective comparison of individuals with and without primary insomnia.

OBJECTIVE: The purpose of this study was to determine the utility of a new operator-independent, automated measure of sleep physiology based on cardiopulmonary coupling (CPC) analysis in subjects with primary insomnia vs. good sleepers. PATIENTS/METHODS: The polysomnograms of 50 subjects with primary insomnia and 36 good sleepers were summarized and analyzed from a consecutive two-night protocol. The electrocardiograms (ECG) from adaptation and baseline night polysomnograms were analyzed using CPC analysis. This Fourier-based technique uses heart rate variability and ECG R wave amplitude fluctuations associated with respiration to generate frequency maps of coupled autonomic-respiratory oscillations. The resulting sleep spectrogram is able to categorize sleep as "stable" (high-frequency coupling [HFC], 0.1-0.4 Hz) and "unstable" (low-frequency coupling [LFC], 0.1-0.01 Hz), independent of standard sleep stages. Wake and rapid eye movement sleep exhibit very low-frequency coupling (VLFC, 0.0039-0.01 Hz). Elevated LFC (e-LFC) is a subset of LFC that is associated with fragmented sleep of various etiologies. RESULTS: CPC variables showed a significant multivariate analysis of variance group, night, and group × night main effect, except for HFC by night. Relative to good sleepers, primary insomnia patients on adaptation night had lower HFC, a putative biomarker of stable sleep, and HFC/LFC ratio, an indicator of sleep quality. The primary insomnia group also had higher LFC, an index of unstable sleep, and an increase in VLFC and e-LFC compared to good sleepers on adaptation night. On baseline night, the primary insomnia group had increased LFC, VLFC, and e-LFC and a lower HFC/LFC ratio. Except for HFC, good sleepers had larger CPC variable differences between adaptation and baseline nights compared to the primary insomnia group. CONCLUSION: Primary insomnia subjects have a marked worsening of sleep quality on the adaptation night, which is well captured by both conventional and ECG-derived sleep spectrogram techniques. The larger improvement of sleep quality was found among good sleepers and captured only by CPC analysis. The operator-independent, automated measure of sleep physiology demonstrated functionality to differentiate and objectively quantify sleep quality.

Assessment of therapeutic options for mild obstructive sleep apnea using cardiopulmonary coupling measures.

OBJECTIVES: To examine the efficacy of various therapeutic modalities for mild obstructive sleep apnea using cardiopulmonary coupling variables of sleep quality. METHODS: A 67-year-old Caucasian subject's sleep was recorded at home for 10 nights using a type 3 sleep recording device that measured ECG and body position, followed by generation of the cardiopulmonary sleep spectrogram. Three baseline nights, one night with a sleep jacket containing 3 tennis balls to restrict sleep in the supine position, 2 nights with oxygen only delivered via a nasal cannula at a flow rate of 2 L/minute, 2 nights with a mandible advancing appliance (MAA) only, and 2 nights using oxygen at 2 L/minute with the MAA were compared. RESULTS: Baseline sleep quality estimated using the ratio of high-frequency and low-frequency coupling (1.03) was below the expected normal adult values ranging from 1.67-4.0. The sleep quality ratio was significantly higher (2.08) using the MAA alone compared to baseline, sleep position restriction (1.61), oxygen therapy (0.81), and the combination of MAA with oxygen (1.66). CONCLUSION: Sleep quality measured objectively using cardiopulmonary coupling variables differentiated the efficacy of therapeutic options for mild obstructive sleep apnea. Such an approach may have practical utility.

REM sleep and cortisol responses to scopolamine during depression and remission in women.

Baseline electroencephalographic (EEG) sleep and the EEG sleep response to scopolamine were studied in 10 adult female patients with unipolar major depressive disorder. Subjects were studied twice for two consecutive nights while depressed and, again, during remission. On the second night of each two-night session, normal saline or scopolamine (1.5 microg/kg, i.m.) was administered in a randomized, double-blind, cross-over fashion. Nocturnal urinary free cortisol (NUFC) measures also were collected. Compared to the depressed state, NUFC was significantly lower during remission. In contrast, baseline EEG sleep measures did not differ from episode to remission. Scopolamine suppressed rapid eye movement (REM) sleep to a comparable extent during the depressive episode and in remission. Scopolamine also reduced NUFC secretion during both clinical states, but to a lesser extent than REM sleep suppression. The findings suggest that the dysregulation in cholinergic systems associated with depressive illness may be persistent during remission, at least for some cholinergic systems. The results also suggest that the central cholinergic system(s) that regulate(s) REM sleep may be more sensitive to dysregulation than the cholinergic system(s) that control(s) nocturnal cortisol secretion.