Reduced REM latency predicts response to tricyclic medication in depressed outpatients

Rush, A. John; Giles, Donna E.; Jarrett, Robin B.; Feldman-Koffler, Frida; Debus, John R.; Weissenburger, Jan; Orsulak, Paul J.; Roffwarg, Howard P.

doi:10.1016/0006-3223(89)90008-5

Cited by 104 publications

(29 citation statements)

References 26 publications

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“…With respect to pharmacological treatment, both uncontrolled and controlled studies indicate that patients with shortened REM latency responded more favorably to AD treatment (Coble et al 1979;Akiskal et al 1980;Svendson and Christensen 1981;Rush et al 1985Rush et al , 1989. In contrast to these findings, Kupfer et al (1981) found that reduced REM latency was associated with poor AD response, whereas Heiligenstein et al (1994) reported that baseline REM latency had no predictive value for AD response.…”

Section: Introductionmentioning

confidence: 87%

Effect of bupropion-SR on REM sleep: relationship to antidepressant response

Ott¹,

Rao²,

Nuccio³

et al. 2002

Psychopharmacology

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Section: Introductionmentioning

confidence: 87%

Effect of bupropion-SR on REM sleep: relationship to antidepressant response

Ott¹,

Rao²,

Nuccio³

et al. 2002

Psychopharmacology

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“…These studies reported an association between shortened REM latency before treatment and response to antidepressant treatment. [47][48][49] The predictive value for response to psychotherapy was reported for a set of disturbed sleep EEG variables (sleep efficiency, REM latency, and REM density). 50,51 In patients who did not respond to psychotherapy, REM density before treatment was elevated, and an increased REM density after psychotherapy was a robust correlate of remission.…”

Section: Controlsmentioning

confidence: 99%

Sleep electroencephalography as a biomarker in depression

Steiger¹,

Pawlowski²,

Kimura³

2015

CPT

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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.

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“…Total time in bed (TIB) was computed as the total time from lights-out to wake-up time. Sleep onset latency was defined as the time elapsed before the first epoch of sleep in a 10-minute segment containing no more than 2 minutes of wakefulness or the time in minutes to the first half-minute of REM sleep, whichever was sooner (Rush et al 1989). Total sleep period (TSP) was defined as the length of time from sleep onset to wake up.…”

Section: Polysomnographic Parametersmentioning

confidence: 99%