Jesse D. Cook

Utility of the Fitbit Flex to evaluate sleep in major depressive disorder: A comparison against polysomnography and wrist-worn actigraphy

BACKGROUND Sleep disturbance is a common and important component of affective illness. Fitness activity trackers are emerging as alternative means to estimate sleep in psychiatric patients; however, their ability to quantify sleep in mood disorders has not been empirically evaluated. Thus, this study sought to evaluate the utility of the Fitbit Flex (FBF) to estimate sleep in patients with major depressive disorder (MDD) relative to gold standard polysomnography (PSG) and a widely-used actigraph (Actiwatch-2; AW-2). METHODS Twenty-one patients with unipolar MDD wore the FBF and AW-2 during in-laboratory PSG. Bland-Altman analysis compared sleep variables among devices. Epoch-by-epoch analysis further evaluated sensitivity, specificity, and accuracy for the FBF and AW-2 relative to PSG. RESULTS The FBF demonstrated significant limitations in quantifying sleep and wake, relative to PSG. In the normal setting, the FBF significantly overestimated sleep time and efficiency, and displayed poor ability to correctly identify wake epochs (i.e. low specificity). In the sensitive setting, the FBF significantly underestimated sleep time and efficiency relative to PSG. Performance characteristics of the FBF were more similar to the AW-2 in the normal compared to sensitive setting. LIMITATIONS Participants were young to middle aged and predominantly female, which may limit generalizability of findings. Study design also precluded ability to assess longitudinal performance of FBF. CONCLUSIONS The FBF is not an adequate substitute for PSG when quantifying sleep in MDD, and the settings of the device sizably impact its performance relative to PSG and other standard actigraphs. The limitations and capabilities of the FBF should be carefully considered prior to clinical and research implementation.

Effects of partial sleep deprivation on slow waves during non-rapid eye movement sleep: A high density EEG investigation

OBJECTIVE Changes in slow waves during non-rapid eye movement (NREM) sleep in response to acute total sleep deprivation are well-established measures of sleep homeostasis. This investigation utilized high-density electroencephalography (hdEEG) to examine topographic changes in slow waves during repeated partial sleep deprivation. METHODS Twenty-four participants underwent a 6-day sleep restriction protocol. Spectral and period-amplitude analyses of sleep hdEEG data were used to examine changes in slow wave energy, count, amplitude, and slope relative to baseline. RESULTS Changes in slow wave energy were dependent on the quantity of NREM sleep utilized for analysis, with widespread increases during sleep restriction and recovery when comparing data from the first portion of the sleep period, but restricted to recovery sleep if the entire sleep episode was considered. Period-amplitude analysis was less dependent on the quantity of NREM sleep utilized, and demonstrated topographic changes in the count, amplitude, and distribution of slow waves, with frontal increases in slow wave amplitude, numbers of high-amplitude waves, and amplitude/slopes of low amplitude waves resulting from partial sleep deprivation. CONCLUSIONS Topographic changes in slow waves occur across the course of partial sleep restriction and recovery. SIGNIFICANCE These results demonstrate a homeostatic response to partial sleep loss in humans.

Effects of oral temazepam on sleep spindles during non-rapid eye movement sleep: A high-density EEG investigation.

Benzodiazepines are commonly used medications that alter sleep spindles during non-rapid eye movement (NREM) sleep, however the topographic changes to these functionally significant waveforms have yet to be fully elucidated. This study utilized high-density electroencephalography (hdEEG) to investigate topographic changes in sleep spindles and spindle-range activity caused by temazepam during NREM sleep in 18 healthy adults. After an accommodation night, sleep for all participants was recorded on two separate nights after taking either placebo or oral temazepam 15 mg. Sleep was monitored using 256-channel hdEEG. Spectral analysis and spindle waveform detection of sleep EEG data were performed for each participant night. Global and topographic data were subsequently compared between temazepam and placebo conditions. Temazepam was associated with significant increases in spectral power from 10.33 to 13.83 Hz. Within this frequency band, temazepam broadly increased sleep spindle duration, and topographically increased spindle amplitude and density in frontal and central-posterior regions, respectively. Higher frequency sleep spindles demonstrated increased spindle amplitude and a paradoxical decrease in spindle density in frontal and centroparietal regions. Further analysis demonstrated temazepam both slowed the average frequency of spindle waveforms and increased the relative proportion of spindles at peak frequencies in frontal and centroparietal regions. These findings suggest that benzodiazepines have diverse effects on sleep spindles that vary by frequency and cortical topography. Further research that explores the relationships between topographic and frequency-dependent changes in pharmacologically-induced sleep spindles and the functional effects of these waveforms is indicated.

Objective measures of sleep duration and continuity in major depressive disorder with comorbid hypersomnolence: a primary investigation with contiguous systematic review and meta‐analysis

Hypersomnolence plays an important role in the presentation, treatment and course of mood disorders. However, there has been relatively little research that examines objective measures of sleep duration and continuity in patients with depression and hypersomnolence, despite the use of these factors in sleep medicine nosological systems. This study compared total sleep time and efficiency measured by naturalistic actigraphic recordings followed by ad libitum polysomnography (PSG; without prescribed wake time) in 22 patients with major depressive disorder and co‐occurring hypersomnolence against age‐ and sex‐matched healthy sleeper controls. The major depressive disorder and co‐occurring hypersomnolence group demonstrated significantly longer sleep duration compared with healthy sleeper controls quantified by sleep diaries, actigraphy and ad libitum PSG. No between‐group differences in sleep efficiency (SE), latency to sleep or wake after sleep onset were observed when assessed using objective measures. To further contextualize these findings within the broader scientific literature, a systematic review was performed to identify other comparable investigations. A meta‐analysis of pooled data demonstrated patients with mood disorders and co‐occurring hypersomnolence have significantly greater sleep duration and similar SE compared with healthy controls when assessed using ad libitum PSG. These results suggest current sleep medicine nosology that distinguishes hypersomnia associated with psychiatric disorders primarily as a construct characterized by low SE and increased time in bed may not be accurate. Future studies that establish the biological bases hypersomnolence in mood disorders, as well as clarify the accuracy of nosological thresholds to define excessive sleep duration, are needed to refine the diagnosis and treatment of these disorders.

Effects of oral temazepam on slow waves during non-rapid eye movement sleep in healthy young adults: A high-density EEG investigation

Slow waves are characteristic waveforms that occur during non-rapid eye movement (NREM) sleep that play an integral role in sleep quality and brain plasticity. Benzodiazepines are commonly used medications that alter slow waves, however, their effects may depend on the time of night and measure used to characterize slow waves. Prior investigations have utilized minimal scalp derivations to evaluate the effects of benzodiazepines on slow waves, and thus the topography of changes to slow waves induced by benzodiazepines has yet to be fully elucidated. This study used high-density electroencephalography (hdEEG) to evaluate the effects of oral temazepam on slow wave activity, incidence, and morphology during NREM sleep in 18 healthy adults relative to placebo. Temazepam was associated with significant decreases in slow wave activity and incidence, which were most prominent in the latter portions of the sleep period. However, temazepam was also associated with a decrease in the magnitude of high-amplitude slow waves and their slopes in the first NREM sleep episode, which was most prominent in frontal derivations. These findings suggest that benzodiazepines produce changes in slow waves throughout the night that vary depending on cortical topography and measures used to characterize slow waves. Further research that explores the relationships between benzodiazepine-induced changes to slow waves and the functional effects of these waveforms is indicated.

Ability of the Multisensory Jawbone UP3 to Quantify and Classify Sleep in Patients With Suspected Central Disorders of Hypersomnolence: A Comparison Against Polysomnography and Actigraphy

STUDY OBJECTIVES To evaluate the ability of a multisensory fitness tracker, the Jawbone UP3 (JB3), to quantify and classify sleep in patients with suspected central disorders of hypersomnolence. METHODS This study included 43 patients who completed polysomnography (PSG) and a Multiple Sleep Latency Test (MSLT) with concurrent wrist-worn JB3 and Actiwatch 2 (AW2) recordings for comparison. Mean differences in nocturnal sleep architecture variables were compared using Bland-Altman analysis. Sensitivity, specificity, and accuracy were derived for both devices relative to PSG. Ability of the JB3 to detect sleep onset rapid eye movement periods (SOREMPs) during MSLT naps was also quantified. RESULTS JB3 demonstrated a significant overestimation of total sleep time (39.6 min, P < .0001) relative to PSG, but performed comparably to AW2. Although the ability of the JB3 to detect epochs of sleep was relatively good (sensitivity = 0.97), its ability to distinguish light, deep, and REM sleep was poor. Similarly, the JB3 did not correctly identify a single SOREMP during any MSLT nap opportunity. CONCLUSIONS The JB3 did not accurately quantify or classify sleep in patients with suspected central disorders of hypersomnolence, and was particularly poor at identifying REM sleep. Thus, this device cannot be used as a surrogate for PSG or MSLT in the assessment of patients with suspected central disorders of hypersomnolence.

The 5α-reductase inhibitor finasteride is not associated with alterations in sleep spindles in men referred for polysomnography

Endogenous neurosteroids that potentiate the gamma‐aminobutyric acid type A (GABAA) receptor are thought to enhance the generation of sleep spindles. This study tested the hypothesis that the 5α‐reductase inhibitor finasteride, an agent associated with reductions in neurosteroids, would be associated with reduced sleep spindles in men referred for polysomnography.