Investigating the relationship between objective measures of sleep and self-report sleep quality in healthy adults: a review.

STUDY OBJECTIVES: Sleep is one of the most common factors related to health, yet a standard definition of sleep quality has not been identified. Polysomnography provides important information about objective sleep variables. However, the relationship between objective sleep variables and perception of sleep quality remains unclear. The purpose of this review was to (1) summarize the current methods of measuring objective sleep macrostructure and microstructure, including electroencephalography arousals, spectral frequency, cyclic alternating pattern, and self-report sleep quality, and (2) investigate the relationship between objective measures of sleep physiology and self-report sleep quality in healthy adults. METHODS: A literature search was conducted using Medline, PubMed, and PsycInfo databases and cited reference searches. Eligible studies included a comparison between self-report sleep quality and polysomnography sleep measures in healthy adults. RESULTS: Thirteen studies were identified. Measurement of self-report sleep quality varied widely across studies. Total sleep time and sleep efficiency were most consistently related to sleep quality, while other objective sleep variables, including electroencephalography spectral analysis, were not reliably predictive of self-report sleep quality in healthy adults. There is preliminary support that microstructural sleep analysis with cyclic alternating pattern may be related to self-reported sleep quality. CONCLUSIONS: Further research is needed to define and standardize self-report measures of sleep quality and investigate the microstructure of sleep. Objective measures of sleep and experiences of "quality" sleep are not as closely related as one may expect in healthy individuals, and understanding this relationship further is necessary to improve the clinical utility of sleep physiology. CITATION: Cudney LE, Frey BN, McCabe RE, Green SM. Investigating the relationship between objective measures of sleep and self-report sleep quality in healthy adults: a review. J Clin Sleep Med. 2022;18(3):927-936.

Cerebral cortical thickness after treatment with desvenlafaxine succinate in major depressive disorder.

Thickness of the cerebral cortex has been previously investigated for its potential as a biomarker in major depressive disorder (MDD). This is the first study to examine the longitudinal effects of a serotonin-norepinephrine reuptake inhibitor, desvenlafaxine succinate (DVS), on whole-brain cortical thickness (CT) in patients treated for MDD. We also aimed to replicate a previous finding of an association between improvement in clinical severity and CT in one of five predefined regions-of-interest (ROI). Twenty-five individuals with MDD received treatment with DVS (50 mg/day) for 8 weeks, with 19 completing the study. We used FreeSurfer 6.0 to compare group differences between MDD and controls (n=23) and between treatment responders, treatment nonresponders and controls. We tested correlations between 8-week change in depression severity and regional CT in five ROIs: the rostral and caudal anterior cingulate cortex, lateral and medial orbitofrontal cortex and inferior temporal gyrus. There were no differences in CT between MDD and controls or DVS responders and controls. There was greater CT in DVS nonresponders in the left pars orbitalis when compared to controls [MNI (X, Y, Z=-38.4, 37.6, -11.1); P=0.027]. There were no significant correlations between change in depression severity and CT in any of the five ROIs. Brain CT does not seem to be a sensitive marker of short-term antidepressant response in MDD, except increased CT in nonresponders. Duration of the intervention and interindividual heterogeneity may impede identification of discriminating features of treatment response as associated to CT.

Biological rhythms are independently associated with quality of life in bipolar disorder.

BACKGROUND: Evidence suggests that patients with bipolar disorder (BD) experience biological rhythm disturbances; however, no studies have examined the impact of this disruption on quality of life (QOL). The aim of this study is to investigate the influence of biological rhythm, depressive symptoms, sleep quality, and sleep medication use on QOL in BD. METHODS: Eighty BD subjects (44 depressed and 36 euthymic) completed questionnaires assessing QOL (WHOQOL-BREF), biological rhythm disruption (BRIAN), depressive symptoms (MADRS), and sleep quality (PSQI). The impact of biological rhythm disturbance, depressive symptoms severity, sleep quality, and sleep medication use on QOL was determined with multiple regression analyses. RESULTS: BRIAN (ß = -0.31, t = -2.73, p < 0.01), MADRS (ß = -0.30, t = -2.93, p < 0.01), and sleep medication use (ß = -0.45, t = -2.55, p < 0.05) were significant predictors of QOL in this model (F 4, 75 = 20.28; p < 0.0001). The relationship of these factors with subdomains of QOL showed that poorer social QOL was associated with greater biological rhythm disturbance (ß = -0.43, t = -3.66, p < 0.01) and sleep medication use (ß = -0.49, t = -2.35, p < 0.01), providing support for the social rhythm theory of BD. Physical QOL was associated with depression (ß = -0.30, t = -2.93, p < 0.01) and biological rhythm disruption (ß = -0.31, t = -2.73, p < 0.01). Main limitations include the cross-sectional assessment and the lack of objective measures of biological rhythms in relation to QOL. CONCLUSIONS: Disruption in biological rhythm is associated with poor QOL in BD, independent of sleep disturbance, sleep medication use, and severity of depression. Treatment strategies targeting regulation of biological rhythms, such as sleep/wake cycles, eating patterns, activities, and social rhythms, are likely to improve QOL in this population.

Emotional memory in pregnant women at risk for postpartum depression.

Postpartum depression (PPD) is associated with debilitating effects on mothers and their infants. A previous history of depression is considered the strongest risk factor for PPD. Depressed individuals recall more negative than positive content and higher levels of stress hormones released during encoding are associated with enhanced recall of emotional stimuli. This study examined the impact of a previous history of major depressive disorder (MDD) and pregnancy on emotional memory. Seventy-seven participants completed the study [44 pregnant women in the second trimester of pregnancy with and without a lifetime history of MDD and 33 non-pregnant women with and without a lifetime history of MDD]. All completed an encoding task and provided salivary cortisol (sCORT) and alpha-amylase (sAA) samples. Participants returned one week later for a surprise incidental recognition memory task. Women with a history of MDD had worse recognition than women without a history of MDD for negative, but not positive images; this effect was independent of sCORT and sAA levels. Pregnancy did not affect emotional memory. Considering that several previous studies found enhanced memory bias for negative content during depressive states, our results suggest that clinical remission may be associated with an opposite cognitive processing of negative emotional content.

Alterations in circadian rhythms are associated with increased lipid peroxidation in females with bipolar disorder.

Disturbances in both circadian rhythms and oxidative stress systems have been implicated in the pathophysiology of bipolar disorder (BD), yet no studies have investigated the relationship between these systems in BD. We studied the impact of circadian rhythm disruption on lipid damage in 52 depressed or euthymic BD females, while controlling for age, severity of depressive symptoms and number of psychotropic medications, compared to 30 healthy controls. Circadian rhythm disruption was determined by a self-report measure (Biological Rhythm Interview of Assessment in Neuropsychiatry; BRIAN), which measures behaviours such as sleep, eating patterns, social rhythms and general activity. Malondialdehyde (MDA) levels were measured as a proxy of lipid peroxidation. We also measured the activity of total and extracellular superoxide dismutase (SOD), catalase (CAT) and glutathione S-transferase (GST). Multiple linear regressions showed that circadian rhythm disturbance was independently associated with increased lipid peroxidation in females with BD (p < 0.05). We found decreased extracellular SOD (p < 0.05), but no differences in total SOD, CAT or GST activity between bipolar females and controls. Circadian rhythms were not associated with lipid peroxidation in healthy controls, where aging was the only significant predictor. These results suggest an interaction between the circadian system and redox metabolism, in that greater disruption in daily rhythms was associated with increased lipid peroxidation in BD only. Antioxidant enzymes have been shown to follow a circadian pattern of expression, and it is possible that disturbance of sleep and daily rhythms experienced in BD may result in decreased antioxidant defence and therefore increased lipid peroxidation. This study provides a basis for further investigation of the links between oxidative stress and circadian rhythms in the neurobiology of BD.