scholarly journals Depression and sleep: pathophysiology and treatment

2006 ◽  
Vol 8 (2) ◽  
pp. 217-226 ◽  

This review examines the relationship between sleep and depression. Most depressive disorders are characterized by subjective sleep disturbances, and the regulation of sleep is intricately linked to the same mechanisms that are implicated in the pathophysiology of depression. After briefly reviewing the physiology and topography of normal sleep, the disturbances revealed in studies of sleep in depression using polysomnographic recordings and neuroimaging assessments are discussed. Next, treatment implications of the disturbances are reviewed at both clinical and neurobiologic levels. Most antidepressant medications suppress rapid eye movement (REM) sleep, although this effect is neither necessary nor sufficient for clinical efficacy. Effects on patients' difficulties initiating and maintaining sleep are more specific to particular types of antidepressants. Ideally, an effective antidepressant will result in normalization of disturbed sleep in concert with resolution of the depressive syndrome, although few interventions actually restore decreased slow-wave sleep. Antidepressants that block central histamine 1 and serotonin 2 tend to have stronger effects on sleep maintenance, but are also prone to elicit complaints of daytime sedation. Adjunctive treatment with sedative hypnotic medications--primarily potent, shorter-acting benzodiazepine and gamma-aminobutyric acid (GABA A)-selective compounds such as zolpidem--are often used to treat associated insomnia more rapidly. Cognitive behavioral therapy and other nonpharmacologic strategies are also helpful.

Author(s):  
Amit Chopra ◽  
Ramya Bachu ◽  
Michael J. Peterson

Depressive disorders are commonly associated with sleep disturbances including insomnia, hypersomnia, and nightmares. Based on shared neurobiological mechanisms, a bidirectional link exists between sleep disturbances and depressive disorders. Presence of sleep disturbance is not only associated with increased depression severity but also portends a poorer prognosis with increased suicide risk in patients with depressive disorders. Polysomnographic findings such as reduced slow-wave sleep, decreased rapid eye movement (REM) sleep latency and increased REM density are associated with major depression. Comorbid primary sleep disorders such as obstructive sleep apnea, restless legs syndrome, and circadian rhythm disorders not only increase the risk but also complicate the treatment of major depression. It is imperative to comprehensively assess and treat sleep disturbances, either due to depression or due to co-existing primary sleep disorders, to optimize remission, prevent relapse, and reduce the risk of suicide in patients with depressive disorders. Medications, chronotherapies, and behavioral approaches alone or in combination may prove to be effective in treating sleep disturbances associated with depressive disorders; however, more research is warranted in this area to determine the optimal management strategies. Cognitive behavioral therapy for insomnia, a promising treatment for management of insomnia comorbid with major depression, needs wider implementation and more research to establish its efficacy in preventing suicide.


2021 ◽  
pp. 003329412110484
Author(s):  
Julie K. Staples ◽  
Courtney Gibson ◽  
Madeline Uddo

Insomnia can be a serious problem diminishing quality of life for Veterans and military populations with and without posttraumatic stress disorder (PTSD). Sleep disturbances are one of the symptoms of PTSD but even after evidence-based PTSD treatments, insomnia symptoms often remain. The primary approaches for treating insomnia are cognitive behavioral therapy for insomnia (CBT-I) and pharmacotherapy. However, each of these treatments has drawbacks. Complementary and Integrative Health (CIH) approaches such as mindfulness meditation, mantram meditation, yoga, and tai chi may provide alternative treatments for insomnia in military populations. This paper provides a brief review of studies on CIH interventions for sleep disturbances in Veterans. It also proposes possible mechanisms by which CIH practices may be effective, including increasing hippocampal volume and gamma-aminobutyric acid acid (GABA). Finally, the acceptability of CIH approaches among Veterans is discussed.


2021 ◽  
Vol 7 (23) ◽  
pp. eabe2626
Author(s):  
Mireia Coll-Tané ◽  
Naihua N. Gong ◽  
Samuel J. Belfer ◽  
Lara V. van Renssen ◽  
Evangeline C. Kurtz-Nelson ◽  
...  

Sleep disturbances in autism and neurodevelopmental disorders are common and adversely affect patient’s quality of life, yet the underlying mechanisms are understudied. We found that individuals with mutations in CHD8, among the highest-confidence autism risk genes, or CHD7 suffer from disturbed sleep maintenance. These defects are recapitulated in Drosophila mutants affecting kismet, the sole CHD8/CHD7 ortholog. We show that Kismet is required in glia for early developmental and adult sleep architecture. This role localizes to subperineurial glia constituting the blood-brain barrier. We demonstrate that Kismet-related sleep disturbances are caused by high serotonin during development, paralleling a well-established but genetically unsolved autism endophenotype. Despite their developmental origin, Kismet’s sleep architecture defects can be reversed in adulthood by a behavioral regime resembling human sleep restriction therapy. Our findings provide fundamental insights into glial regulation of sleep and propose a causal mechanistic link between the CHD8/CHD7/Kismet family, developmental hyperserotonemia, and autism-associated sleep disturbances.


SLEEP ◽  
2021 ◽  
Vol 44 (Supplement_2) ◽  
pp. A335-A335
Author(s):  
Fayruz Araji ◽  
Abha Patel

Abstract Introduction Somnambulism is a parasomnia occurring in non-rapid eye movement sleep, and is characterized by ambulation as a disorder of arousal regulation. Sleep deprivation, alcohol abuse, fragmented sleep and certain medications can increase the risk of sleep walking. Report of case(s) Here we present a 35-year-old man with multiple triggers for sleep walking, resulting in recurrent parasomnia events over fifteen years. He had a history of bipolar disorder, post-traumatic stress disorder (PTSD), chronic insomnia, moderate untreated obstructive sleep apnea (OSA), anxiety with violent daytime behaviors, and prior alcohol abuse status post six years of sobriety. He was sent to our clinic due to increased frequency and severity of events, with nightly events for the last five years. Episodes were characterized by walking around the home, leaving the home, and driving on occasion. He reported at least one minor car accident as a result of sleep driving. He also reported an injury resulting from a fall in his home while sleep walking. Several security measures were implemented, including door gates, door alarms, and hiding car keys. His family slept in different bedrooms with locked doors for safety. The patient’s chronic insomnia improved with cognitive behavioral therapy, leading to an average sleep time of five hours per night with no reported hypersomnia or daytime fatigue. After his initial evaluation, he was referred for a mandibular advancement device for treatment of his OSA, due to prior poor compliance with positive airway pressure therapy related to his PTSD. Optimizing his OSA helped decrease arousals that might trigger sleep walking events. He also maintained close follow up with mental health for pharmacotherapy and psychological therapy. Treatment with clonazepam 0.25 mg at bedtime was initiated given the severity of his somnambulism. Conclusion The use of a benzodiazepine can reduce slow wave sleep duration by its effect on the inhibitory neurotransmitter gamma aminobutyric acid (GABA). Our patient had multiple risk factors for parasomnias, with severe, frequent episodes of sleepwalking leading to self-injury. His treatment involved both pharmacotherapy as well as optimization of underlying triggers. Support (if any):


2018 ◽  
Author(s):  
Lampros Perogamvros

Based on past literature, it is here supported that insomnia, and parasomnias such as sleepwalking, sleep terrors and nightmares, reflect an evolutionary survival mechanism, which has threat-related origins and which, in some vulnerable individuals, becomes persistent due to failure of a fear extinction function. Genetic determinants, personality traits and sleep disturbances seem to determine whether the individual will resume normal sleep after the acute phase (return to safety) or will develop the pathological condition of chronic insomnia, persistent sleepwalking in adulthood and nightmare disorder. Possible treatments targeting fear extinction are proposed, such as pharmacotherapy, cognitive behavioral therapy and targeted memory reactivation during sleep.


2020 ◽  
Vol 19 (2) ◽  
pp. 210-232 ◽  
Author(s):  
Theodora A. Manolis ◽  
Antonis A. Manolis ◽  
Evdoxia J. Apostolopoulos ◽  
Helen Melita ◽  
Antonis S. Manolis

: Sleep is essential to and an integral part of life and when lacking or disrupted, a multitude of mental and physical pathologies ensue, including cardiovascular (CV) disease, which increases health care costs. Several prospective studies and meta-analyses show that insomnia, short (<7h) or long (>9h) sleep and other sleep disorders are associated with an increased risk of hypertension, metabolic syndrome, myocardial infarction, heart failure, arrhythmias, CV disease risk and/or mortality. The mechanisms by which insomnia and other sleep disorders lead to increased CV risk may encompass inflammatory, immunological, neuro-autonomic, endocrinological, genetic and microbiome perturbations. Guidelines are emerging that recommend a target of >7 h of sleep for all adults >18 years for optimal CV health. Treatment of sleep disorders includes cognitive-behavioral therapy considered the mainstay of non-pharmacologic management of chronic insomnia, and drug treatment with benzodiazepine receptor agonists binding to gamma aminobutyric acid type A (benzodiazepine and non-benzodiazepine agents) and some antidepressants. However, observational studies and meta-analyses indicate an increased mortality risk of anxiolytics and hypnotics, although bias may be involved due to confounding and high heterogeneity in these studies. Nevertheless, it seems that the risk incurred by the non-benzodiazepine hypnotic agents (Z drugs) may be relatively less than the risk of anxiolytics, with evidence indicating that at least one of these agents, zolpidem, may even confer a lower risk of mortality in adjusted models. All these issues are herein reviewed.


SLEEP ◽  
2021 ◽  
Vol 44 (Supplement_2) ◽  
pp. A140-A141
Author(s):  
Emma Zhao ◽  
Afik Faerman ◽  
David Spiegel

Abstract Introduction Hypnosis-based interventions have been shown to have a positive impact on several dimensions of sleep health. However, current evidence is limited as only a paucity of studies included populations with sleep complaints. Here we present a pilot data set to demonstrate the feasibility of developing a hypnosis-based adjunctive treatment for subjective sleep complaints. Methods Eleven adults (42% female; mean age 45±16.87 years) who sought treatment at the Stanford Sleep Medicine Center or Center for Integrative Medicine for subjective sleep complaints received hypnosis as adjunctive treatment. Self-report questionnaires were used to assess the weekly frequency of subjective sleep disturbances experienced before and after treatment, as well as 5-point Likert scale ratings of perceived qualitative improvement in symptom severity and overall sleep quality. Results Five participants (45%) reported a reduction in symptom frequency and severity after hypnosis treatment. All five participants attributed at least some of the improvement to hypnosis treatment. Most participants (63%) observed post-treatment improvements in their overall sleep quality. No participants reported adverse effects of hypnosis. Conclusion Results suggest hypnosis-based adjunctive treatment may be effective for alleviating subjective sleep disturbances. The findings serve as preliminary support for further randomly controlled trials in larger samples. Support (if any):


2013 ◽  
Vol 27 (2) ◽  
pp. 138-154 ◽  
Author(s):  
Lynndall Dwyer ◽  
Sara Olsen ◽  
Tian Po S. Oei

Recent literature has shown that group cognitive-behavioral therapy (CBT) is effective for individuals with heterogeneous anxiety disorders. However, these studies have used a narrow range of outcome measures, and have not included global measures such as quality of life. In addition, heterogeneous mood disorders have not been well researched. The aim of this study was to replicate and extend on previous studies by assessing the effectiveness of group CBT treatment programs designed for use with heterogeneous anxiety or depressive disorders. Global outcome measures of quality of life and social functioning were assessed in addition to outcome measures of anxiety and mood symptoms. There were 173 patients who completed either group CBT for anxiety disorders or for depressive disorders. Symptom measures and quality of life measures were used to determine treatment effectiveness. Results demonstrated that the treatments were effective in reducing overall symptom severity and improving quality of life. Treatment gains were maintained to 12 month follow-up. However, the degree of change was considerably lower than that found in comparable trials with diagnostically homogenous samples. Overall, group CBT for heterogeneous diagnostic populations was effective but requires further investigation and refinement.


2001 ◽  
Vol 15 (6) ◽  
pp. 1089-1091 ◽  
Author(s):  
ARTUR MAYERHOFER ◽  
BARBARA HÖHNE-ZELL ◽  
KATIA GAMEL-DIDELON ◽  
HEIKE JUNG ◽  
PETER REDECKER ◽  
...  

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