Sleep deprivation therapy

Kuhs, H.; Tölle, Rainer

doi:10.1016/0006-3223(91)90255-k

Cited by 113 publications

(32 citation statements)

References 60 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Sleep deprivation in different fashion was widely investigated as part of clinical therapy since it could reverse depressive symptoms in approximately 50-60 % of depressed patients (Gillin 1983;Hemmeter et al 2010;Kuhs and Tolle 1991;Landsness et al 2011;Wirz-Justice and Van den Hoofdakker 1999;Wu and Bunney 1990), showing rapid effect on mood (Selvi et al 2007). However, these are acute effects; relapses usually come with the first episode of sleep, which is associated with a high REMS pressure (Adrien 2002).…”

Section: Discussionmentioning

confidence: 99%

Acute escitalopram treatment inhibits REM sleep rebound and activation of MCH-expressing neurons in the lateral hypothalamus after long term selective REM sleep deprivation

et al. 2013

View full text Add to dashboard Cite

Rationale Selective rapid eye movement sleep (REMS) deprivation using the platform-on-water ("flower pot") method causes sleep rebound with increased REMS, decreased REMS latency, and activation of the melaninconcentrating hormone (MCH) expressing neurons in the hypothalamus. MCH is implicated in the pathomechanism of depression regarding its influence on mood, feeding behavior, and REMS. Objectives We investigated the effects of the most selective serotonin reuptake inhibitor escitalopram on sleep rebound following REMS deprivation and, in parallel, on the activation of MCH-containing neurons.Methods Escitalopram or vehicle (10 mg/kg, intraperitoneally) was administered to REMS-deprived (72 h) or home cage male Wistar rats. During the 3-h-long "rebound sleep", electroencephalography was recorded, followed by an MCH/Fos double immunohistochemistry. Results During REMS rebound, the time spent in REMS and the number of MCH/Fos double-labeled neurons in the lateral hypothalamus increased markedly, and REMS latency showed a significant decrease. All these effects of REMS deprivation were significantly attenuated by escitalopram treatment. Besides the REMS-suppressing effects, escitalopram caused an increase in amount of and decrease in latency of slow wave sleep during the rebound. Conclusions These results show that despite the high REMS pressure caused by REMS deprivation procedure, escitalopram has the ability to suppress REMS rebound, as well as to diminish the activation of MCH-containing neurons, in parallel. Escitalopram caused a shift from REMS to slow wave sleep during the rebound. Furthermore, these data point to the potential connection between the serotonergic system and MCH in sleep regulation, which can be relevant in depression and in other mood disorders.

show abstract

Section: Discussionmentioning

confidence: 99%

Acute escitalopram treatment inhibits REM sleep rebound and activation of MCH-expressing neurons in the lateral hypothalamus after long term selective REM sleep deprivation

et al. 2013

View full text Add to dashboard Cite

show abstract

“…4 Previous studies have demonstrated a single night of monitored sleep deprivation can markedly improve depressive symptoms.…”

Section: A S E R E P O R T Smentioning

confidence: 99%

Intensive Sleep Deprivation and Cognitive Behavioral Therapy for Pharmacotherapy Refractory Insomnia in a Hospitalized Patient

Breitstein

Penix

Roth

et al. 2014

Journal of Clinical Sleep Medicine

View full text Add to dashboard Cite

The case of a 59-year-old woman psychiatrically hospitalized with comorbid insomnia, suicidal ideation, and generalized anxiety disorder is presented. Pharmacologic therapies were unsuccessful for treating insomnia prior to and during hospitalization. Intensive sleep deprivation was initiated for 40 consecutive hours followed by a recovery sleep period of 8 hours. Traditional components of cognitive behavioral therapy for insomnia (CBTi), sleep restriction, and stimulus control therapies, were initiated on the ward. After two consecutive nights with improved sleep, anxiety, and absence of suicidal ideation, the patient was discharged. She was followed in the sleep clinic for two months engaging in CBTi. Treatment resulted in substantial improvement in her insomnia, daytime sleepiness, and anxiety about sleep. C A S E R E P O R T SA pproximately 9% to 12% of the population is affected by chronic insomnia with research exhibiting a strong correlation between insomnia, depression, and anxiety. 1 Treatment of insomnia often involves multicomponent cognitive behavioral therapy for insomnia (CBTi) or sedative-hypnotic medications. 2 CBTi has greater effi cacy in the long-term treatment of insomnia compared to medical therapy, which often loses effectiveness over time. 3 Sleep restriction, a component of CBTi, has been successful for insomnia patients failing chronic sedative hypnotic therapy. 2 Although sleep deprivation may increase affective symptoms and anxiety in healthy adults, sleep deprivation followed by sleep restriction can have antidepressant effects. 4 Previous studies have demonstrated a single night of monitored sleep deprivation can markedly improve depressive symptoms. 5-7 Notably, there is a paucity of literature examining sleep deprivation combined with CBTi in patients with psychiatric disorders who have pharmacotherapy refractory insomnia. This case demonstrates the effi cacy of intensive sleep deprivation followed by sleep restriction and stimulus control in an inpatient. The patient had improved sleep quality, decreased anxiety, and resolution of suicidal ideation, all of which had deteriorated on medical therapy alone. REPORT OF CASEA 59-year-old married woman was admitted to a psychiatric ward for suicidal ideation due to pharmacotherapy refractory insomnia. She developed diffi culties falling and staying asleep after undergoing an uncomplicated hysterectomy 10 weeks prior to admission. As an outpatient her generalized anxiety disorder (GAD) and insomnia was treated with paroxetine 15 mg in

show abstract

“…The observation that partial SD late in the night was followed by response rates similar to those obtained after total SD led to propose it as the SD method of choice [38] , but the issues of efficacy, timing and stress are yet debated [17] . Despite similar overall response rates, studies directly comparing total and partial SD found indeed total SD to be more effective than partial SD [39] .…”

Section: Duration Of Wakementioning

confidence: 99%

Sleep Deprivation in Mood Disorders

2011

View full text Add to dashboard Cite

Growing clinical evidence in support of the efficacy and safety of sleep deprivation (SD), and its biological mechanisms of action suggest that this technique can now be included among the first-line antidepressant treatment strategies for mood disorders. SD targets the broadly defined depressive syndrome, and can be administered according to several different treatment schedules: total versus partial, single versus repeated, alone or combined with antidepressant drugs, mood stabilizers, or other chronotherapeutic techniques, such as light therapy and sleep phase advance. The present review focuses on clinical evidence about the place of SD in therapy, its indications, dosage and timing of the therapeutic wake, interactions with other treatments, precautions and contraindications, adverse reactions, mechanism of action, and comparative efficacy, with the aim of providing the clinical psychiatrist with an updated, concise guide to its application.

show abstract

Sleep deprivation therapy

Cited by 113 publications

References 60 publications

Acute escitalopram treatment inhibits REM sleep rebound and activation of MCH-expressing neurons in the lateral hypothalamus after long term selective REM sleep deprivation

Acute escitalopram treatment inhibits REM sleep rebound and activation of MCH-expressing neurons in the lateral hypothalamus after long term selective REM sleep deprivation

Intensive Sleep Deprivation and Cognitive Behavioral Therapy for Pharmacotherapy Refractory Insomnia in a Hospitalized Patient

Sleep Deprivation in Mood Disorders

Contact Info

Product

Resources

About