Wake and sleep EEG provide biomarkers in depression

• Published in: Journal of psychiatric research 2010-03, Vol.44 (4), p.242-252
• Main Authors: Steiger, Axel, Kimura, Mayumi
• Format: Article
• Language: English
• Subjects: Adult and adolescent clinical studies; Animals; Antidepressant drugs; Antidepressants; Biological and medical sciences; Biological markers; Biomarkers; Brain - physiopathology; Depression; Depression - diagnosis; Depression - physiopathology; Disease Models, Animal; EEG; Electroencephalography; Electroencephalography - methods; Humans; Medical sciences; Mood disorders; Neuropharmacology; Pharmacology. Drug treatments; Psychiatry; Psychoanaleptics: cns stimulant, antidepressant agent, nootropic agent, mood stabilizer; Psychoanaleptics: cns stimulant, antidepressant agent, nootropic agent, mood stabilizer..., (alzheimer disease); Psychology. Psychoanalysis. Psychiatry; Psychopathology. Psychiatry; Psychopharmacology; Rapid eye movement sleep; Sleep; Sleep - physiology; Sleep Wake Disorders - etiology; Wakefulness - physiology
• ISSN: 0022-3956; 1879-1379
• DOI: 10.1016/j.jpsychires.2009.08.013

Abstract Both wake and sleep electroencephalogram (EEG) provide biomarkers of depression and antidepressive therapy, respectively. For a long time it is known that EEG activity is altered by drugs. Quantitative EEG analysis helps to delineate effects of antidepressants on brain activity. Cordance is an EEG measure with a superior correlation with regional brain perfusion. Prefrontal quantitative EEG cordance appears to be a predictor of the response to antidepressants. Sleep EEG shows characteristic changes in depression as impaired sleep continuity, desinhibition of REM sleep and changes of nonREM sleep. Elevated REM density (a measure for frequency of rapid eye movements) characterizes an endophenotype in family studies of depression. REM-sleep changes including a more distinct REM rebound after sleep deprivation are found in animal models of depression. Most antidepressants suppress REM sleep in depressed patients, normal controls and laboratory animals. REM suppression appears to be a distinct, but not an absolute requirement for antidepressive effects of a compound. Sleep-EEG variables like REM latency or certain clusters of variables were shown to predict the response to the treatment with a certain antidepressant or even the course of the disorder for several years. Some of these predictive sleep-EEG markers of the longterm course of depression appear to be closely related to hypothalamo-pituitary-adrenocortical system activity.