Eeg Studies of Sleep and the Dexamethasone Suppression Test in the Diagnosis of Depression

Feinberg, Michael

doi:10.1016/b978-0-08-027987-9.50029-9

Cited by 26 publications

(47 citation statements)

References 9 publications

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“…Previous studies had demonstrated a higher percentage of stage S1 and a reduction in SWS but no differences in sleep stage S2 in dysthymic patients as compared with normal controls [21,23]. Major depressives usually exhibit an increase in light sleep and a decrease in SWS [43,[46][47][48]. When comparing dysthymic and major depressive disorder patients, no significant differences regarding the percentage of S1-4 (including S3 + 4) were observed [24].…”

Section: Discussionmentioning

confidence: 80%

Insomnia Related to Dysthymia: Polysomnographic and Psychometric Comparison with Normal Controls and Acute Therapeutic Trials with Trazodone

et al. 2001

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Utilizing polysomnography (PSG) and psychometry, objective and subjective sleep and awakening quality was investigated in 11 patients (mean age 50 ± 14) with nonorganic insomnia (F 51.0) related to dysthymia (F 34.1) as compared with 11 age- and sex-matched normal controls. Patients demonstrated decreased sleep efficiency and sleep stage S2 as well as increased sleep latency to S1, S2 and S3, wakefulness within the total sleep period, number of awakenings, S1 and REM sleep. There was no intergroup difference in REM latency. Subjective sleep quality and the total score of the Self-Assessment Scale for Sleep and Awakening Quality (SSA) were deteriorated as were evening and morning well-being, mood, affectivity and drowsiness. Noopsychic measures showed deteriorated numerical memory, fine motor activity and reaction time variability. In a placebo-controlled crossover design study, the acute effects of 100 mg trazodone¹, a serotonin reuptake inhibitor with a sedative action due to 5HT₂ and α₁ receptor blockade, were investigated in the patients. As compared with placebo, trazodone induced an increase in slow-wave sleep (S3 + 4), a lengthening of REM latency, a decrease in REM sleep and a normalization of the periodic leg movement (PLM) index. In the morning, there was a minimal increase in somatic complaints and a decrease in critical flicker frequency and systolic blood pressure. In conclusion, our study demonstrated that dysthymia induced significant changes in objective and subjective sleep and awakening quality, which were counteracted by 100 mg trazodone, thus suggesting a key-lock principle in the treatment of nonorganic insomnia related to dysthymia with this drug.

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Section: Discussionmentioning

confidence: 80%

Insomnia Related to Dysthymia: Polysomnographic and Psychometric Comparison with Normal Controls and Acute Therapeutic Trials with Trazodone

et al. 2001

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“…1,27,28 In contrast, Feinberg et al found no relationship between sleep EEG and the severity of depression. 29 In depressed children and adolescents, no sleep EEG changes were found in comparison to age-matched healthy controls in most studies. [30][31][32] In contrast, other studies reported similar changes in depressed adults, children, and adolescents.…”

Section: Controlsmentioning

confidence: 99%

“…117 Two different dose ranges of the CRH-1 receptor antagonist R121919 were given to depressed patients. 29 In a subgroup of these patients, sleep EEG was recorded before treatment, at the end of the first week, and at the end of the fourth week of active medication.…”

mentioning

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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“…Twenty-seven patients with bipolar (combined bipolar I and II patients) Feinberg et al [1982] 18 15 no Feinberg and Carroll [1984] 107 69 no Kerkhofs et al [1988] 90 63 no Lauer et al [1992] 14 10 no Fossion et al [1998] 14 28 no Total 291 215 depression (unmedicated for at least 7 days prior to the study) were available for the analysis. The data were compared to 27 unipolar patients exactly matched for age, gender and severity of depression (description of samples in table 2).…”

Section: Sleep In Bipolar Depressionmentioning

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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Eeg Studies of Sleep and the Dexamethasone Suppression Test in the Diagnosis of Depression

Cited by 26 publications

References 9 publications

Insomnia Related to Dysthymia: Polysomnographic and Psychometric Comparison with Normal Controls and Acute Therapeutic Trials with Trazodone

Insomnia Related to Dysthymia: Polysomnographic and Psychometric Comparison with Normal Controls and Acute Therapeutic Trials with Trazodone

Sleep electroencephalography as a biomarker in depression

Sleep and Sleep-Wake Manipulations in Bipolar Depression

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