Sleep electroencephalography as a biomarker in depression

Abstract

Abstract:The sleep electroencephalogram (EEG) provides biomarkers of depression, which may help with diagnosis, prediction of therapy response, and prognosis in the treatment of depression. In patients with depression, characteristic sleep EEG changes include impaired sleep continuity, disinhibition of rapid-eye-movement (REM) sleep, and impaired non-REM sleep. Most antidepressants suppress REM sleep in depressed patients, healthy volunteers, and in animal models. REM suppression appears to be an important, but not an absolute requirement, for antidepressive effects of a substance. Enhanced REM density, a measure for frequency of REM, characterizes high-risk probands for affective disorders. REM-sleep changes were also found in animal models of depression. Sleep-EEG variables were shown to predict the response to treatment with antidepressants. Furthermore, certain clusters of sleep EEG variables predicted the course of the disorder for several years. Some of the predicted sleep EEG markers appear to be related to hypothalamic-pituitary-adrenal system activity.

Heart rate variability and cordance in rapid eye movement sleep as biomarkers of depression and treatment response

“…Actually, biomarker properties of HRV in REM sleep did resemble REM density. The latter is considered a trait marker of MDD, with high values indicating increased risk of depression (review: Steiger et al, 2015). In our study, both, HRV and REM density separated between patients (total group at week 1 and 4; responders and non-responders at week 4) and matched controls but they did not predict response.…”

“…Accordingly, we compared HRV in REM sleep with previously established REM sleep-derived biomarkers of depression, such as REM density and cordance. Elevated REM density (a measure of rapid eye movement frequency during REM sleep) is an endophenotype of depression (Lauer et al, 1995;Modell et al, 2005;Steiger et al, 2015), and indicates an increased risk of depression recurrence (Hatzinger et al, 2004). Further, in a sub-sample of this study population, we have previously shown that the quantitative electroencephalography (QEEG) biomarker cordance could predict antidepressant treatment response in MDD patients.…”

“…As HRV changes between sleep stages and correlates with brain activity during sleep (Spiegelhalder et al, 2011), we further proposed that REM sleep would be the ideal sleep stage to refer to HRV and depression: REM sleep is characterized by high activity of the mPFC, which influences the ANS and may amplify differences in HRV between depressed patients and controls (Desseilles et al, 2011). Moreover, as REM sleep is commonly disinhibited in depression (Steiger et al, 2015), we expected that REM sleep derived HRV would separate between patients and healthy controls distinctively.…”

Sleep, Cognition and Cortisol in Addison’s Disease: A Mechanistic Relationship

“…This pattern points to a reciprocal interaction between sleep architecture and hormones of the hypothalamic-pituitary-somatotrophic (HPS) and HPA systems. Confirming the sleep-promoting role of GHRH and the sleep-disrupting effect of CRH, in older adults the typical age-related reduction in GH levels is accompanied by reduced SWS, whereas in both older adults and in depressed younger adults increased CRH levels contribute to the typically-observed sleep disruptions (27,42).…”

Chronobiology, sleep-related risk factors and light therapy in perinatal depression: the “Life-ON” project

“…Objective sleep markers in depressed patients concern sleep disturbances such as prolonged sleep latency (SL), increased wake after sleep onset (WASO), increased early morning wake time, decreased total sleep time (TST), decreased sleep efficiency (SE = percentage of sleep on the total bed time), decreased slow waves sleep (SWS), decreased REM sleep latency, increased REM amount [30]. Nevertheless, mood disorders are also commonly found in patients affected by sleep disorders (i.e.…”