Sleep Patterns in Young Depressed Patients

Hawkins, D. R.; Taub, J. M.; Castle, Robert

doi:10.1037/e361062004-010

Cited by 11 publications

(13 citation statements)

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“…Eighty percent of depression patients report insomnia, whereas 15%-35% complain of hypersomnia. 12,13 The characteristic sleep EEG changes (Figure 1) in depressed patients consist of: 1) impaired sleep continuity (increase of sleep latency, elevated number of intermittent awakenings, early morning awakening); 2) disinhibited REM sleep: shortened REM latency, or sleep onset REM period (SOREMP; REM latency 0-20 minutes), prolonged first REM period, and elevated REM density (a measure of the amount of REM), particularly during the first REM period; and 3) changes of non-REM sleep (decreases of SWS, SWA, and N2; in younger patients, SWS and SWA shift from the first to the second non-REM period). 14,15 Sleep EEG is influenced by age and sex in normal subjects and also in patients with depression.…”

Section: Sleep Eeg In Patients With Depressionmentioning

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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Section: Sleep Eeg In Patients With Depressionmentioning

confidence: 99%

Sleep electroencephalography as a biomarker in depression

Steiger¹,

Pawlowski²,

Kimura³

2015

CPT

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“…It has frequently been described that depressed bipolar patients display signs of hypersomnia with increased nocturnal sleep and more napping during the day [Michaelis and Hofmann, 1973;Hawkins et al, 1985].…”

Section: Hypersomnia In Bipolar Disordermentioning

confidence: 99%

Sleep and Sleep-Wake Manipulations in Bipolar Depression

Riemann

Voderholzer

Berger³

2002

Neuropsychobiology

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In the last 30 years, it has been convincingly demonstrated that sleep in major depression is characterized by disturbances of sleep continuity, a reduction of slow wave sleep, a disinhibition of REM sleep including a shortening of REM latency (i.e. the time between sleep onset and the occurrence of the first REM period) and an increase in REM density. Furthermore, manipulations of the sleep-wake cycle like total or partial sleep deprivation or phase advance of the sleep period have been proven to be effective therapeutic strategies for patients with unipolar depression. The database concerning sleep and sleep-wake manipulations in bipolar disorder in comparison is not yet as extensive. Studies investigating sleep in bipolar depression suggest that during the depressed phase sleep shows the same stigmata as in unipolar depression. During the hypomanic or manic phase, sleep is even more curtailed, though subjectively not experienced as disturbing by the patients. REM sleep disinhibition is present as well. An important issue is the question, whether sleep-wake manipulations can also be applied in patients with bipolar depression. Work by others and our own studies indicate that sleep deprivation and a phase advance of the sleep period can be used to treat bipolar patients during the depressed phase. The risk of a switch into hypomania or mania does not seem to be more pronounced than the risk with typical pharmacological antidepressant treatment. For patients with mania, sleep deprivation is not an adequate treatment – in contrast, treatment strategies aiming at stabilizing a regular sleep-wake schedule are indicated.

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“…[15][16][17] Similarly, in both community-based and clin ical samples, depression has been associated with prolonged sleep onset latency, poorer sleep consolidation, extended or delayed sleep duration and phase shifts of the sleep-wake cycle. 14,[18][19][20][21][22][23][24] Compared with age-matched controls, young people with bipolar disorder have longer sleep onset latency and increased nighttime awakenings, and they report worse sleep quality and spending extended time asleep. 25,26 The literature on psych otic disorders is scarcer, but compared with healthy controls, patients with schizophrenia have been found to have longer sleep onset latency, extended sleep duration and time in bed, delayed sleep-wake profiles and higher intraindividual variability.…”

Section: Introductionmentioning

confidence: 99%