Insomnia Patients With Objective Short Sleep Duration Have a Blunted Response to Cognitive Behavioral Therapy for Insomnia

Bathgate, Christina J.; Edinger, Jack D.; Krystal, Andrew D.

doi:10.1093/sleep/zsw012

Cited by 54 publications

(32 citation statements)

References 44 publications

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“…The sleep-onset insomnia phenotype is associated with poor prognosis as it portends a higher likelihood of persistence than the sleep-maintenance or combined (onset and maintenance) phenotypes at the time of disease onset . In addition, preliminary evidence presented in this review suggests that exceptionally high sleep reactivity may underlie the short-sleep insomnia phenotype, which is the most biologically severe and treatment-resistant phenotype (Bathgate et al, 2017;Vgontzas et al, 2013). Recent theories propose that HPA dysregulation, disrupted cortical networks, sympathetic over-activation and parasympathetic under-activation comprise the neurobiological bases of short sleep insomnia (Vgontzas et al, 2013).…”

Section: Insomnia Phenotypesmentioning

confidence: 81%

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The impact of stress on sleep: Pathogenic sleep reactivity as a vulnerability to insomnia and circadian disorders

Kalmbach

Anderson

Drake

2018

Journal of Sleep Research

355

224

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Sleep reactivity is the trait-like degree to which stress exposure disrupts sleep, resulting in difficulty falling and staying asleep. Individuals with highly reactive sleep systems experience drastic deterioration of sleep when stressed, whereas those with low sleep reactivity proceed largely unperturbed during stress. Research shows that genetics, familial history of insomnia, female gender and environmental stress influence how the sleep system responds to stress. Further work has identified neurobiological underpinnings for sleep reactivity involving disrupted cortical networks and dysregulation in the autonomic nervous system and hypothalamic-pituitary-adrenal axis. Sleep reactivity is most pathologically and clinically pertinent when in excess, such that high sleep reactivity predicts risk for future insomnia disorder, with early evidence suggesting high sleep reactivity corresponds to severe insomnia phenotypes (sleep onset insomnia and short sleep insomnia). High sleep reactivity is also linked to risk of shift-work disorder, depression and anxiety. Importantly, stress-related worry and rumination may exploit sensitive sleep systems, thereby augmenting the pathogenicity of sleep reactivity. With the development of cost-effective assessment of sleep reactivity, we can now identify individuals at risk of future insomnia, shift-work disorder and mental illness, thus identifying a target population for preventive intervention. Given that insomniacs with high sleep reactivity tend to present with severe insomnia phenotypes, patient sleep reactivity may inform triaging to different levels of treatment. Future research on sleep reactivity is needed to clarify its neurobiology, characterize its long-term prospective associations with insomnia and shift-work disorder phenotypes, and establish its prognostic value for mental illness and other non-sleep disorders.

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Section: Insomnia Phenotypesmentioning

confidence: 81%

“…Short sleep insomnia is an especially severe and treatment-resistant phenotype of insomnia disorder (Bathgate, Edinger, & Krystal, 2017;Vgontzas et al, 2013). Although reference-standard classification of the short sleep phenotype is recommended via PSG (e.g.…”

Section: Short Sleep Insomnia Phenotypementioning

confidence: 99%

The impact of stress on sleep: Pathogenic sleep reactivity as a vulnerability to insomnia and circadian disorders

Kalmbach

Anderson

Drake

2018

Journal of Sleep Research

355

224

View full text Add to dashboard Cite

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“…This association between the reported subjective and the observed objective neurocognitive deficits may explain the association (Laugsand, Strand, Vatten, Janszky, & Bjørngaard, 2014), reduced productivity and absenteeism from work (Daley, Morin, Leblanc, Grégoire, & Savard, 2009), and the increased risk of serious falls in the elderly with ID (Stone et al, 2014). More importantly, this severe phenotype of insomnia (ID with short sleep duration) is associated with cardiovascular morbidity and mortality , and may have therapeutic implications, as individuals with ID and short sleep duration had blunted response to cognitive behavioural therapy (Bathgate, Edinger, & Krystal, 2017) and responded more to sedating antidepressants .…”

Section: Discussionmentioning

confidence: 99%

Neurocognitive performance in insomnia disorder: The impact of hyperarousal and short sleep duration

Khassawneh

Bathgate

Tsai

et al. 2018

Journal of Sleep Research

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Given the recent evidence on the association between hyperarousal in insomnia disorder and neurocognitive deficits, we aimed to examine the effect of short sleep duration on neurocognitive reaction time tests in insomnia disorder sufferers. We recruited subjects with insomnia disorder (n = 35, mean age = 40.6 years) who scored ≥29 on a Hyperarousal Scale, and a group of controls (n = 54, mean age = 31.5 years) who had no sleep disorders and scored <26 on the Hyperarousal Scale. Participants completed two in-home polysomnograms and four daytime trials of neurocognitive tests, including simple reaction time, choice reaction time, big circle-little circle, rapid visual information processing, attention switching task, and spatial working memory tests. Total sleep time divided study cohorts into subgroups of short (total sleep time <6 hr) and normal (total sleep time ≥6 hr) sleepers. ANCOVA showed a significant interaction between participant type (insomnia disorder versus controls) and sleep duration (short versus normal) for spatial working memory-latency (p = 0.020) and spatial working memory-errors (p = 0.025). The short-sleeping insomnia disorder group had longer spatial working memory-latencies and more spatial working memory-errors than did normal-sleeping controls. Regardless of sleep duration, those with insomnia disorder had more attentional deficits with longer attention switching task-latency (p = 0.011) and more attention switching task-incorrect trials (p = 0.015) than the control group. Normal-sleepers only had longer attention switching task-latency than short-sleepers (p = 0.004). A phenotype of insomnia disorder with hyperarousal and short sleep duration is associated with daytime cognitive deficits in complex attentional and spatial working memory tasks.

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“…The efficacy of sleep opportunity restriction in multiple mutants suggests that, in humans, SRT should be effective across insomnia subtypes, provided there is a mismatch between sleep opportunity and ability. A possible exception is evidence that insomnia patients with objective short sleep duration do not respond as well to CBT-I as those with relatively normal TST 80 . This stands in contrast to our model which explicitly focuses on genetic models of short sleep.…”

Section: Discussionmentioning

confidence: 99%

A Drosophila model of sleep restriction therapy for insomnia

et al. 2019

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Insomnia is the most common sleep disorder among adults, especially affecting individuals of advanced age or with neurodegenerative disease. Insomnia is also a common comorbidity across psychiatric disorders. Cognitive Behavioral Therapy for Insomnia (CBT-I) is the first-line treatment for insomnia; a key component of this intervention is restriction of sleep opportunity, which optimizes matching of sleep ability and opportunity, leading to enhanced sleep drive. Despite the well-documented efficacy of CBT-I, little is known regarding how CBT-I works at a cellular and molecular level to improve sleep, due in large part to an absence of experimentally-tractable animals models of this intervention. Here, guided by human behavioral sleep therapies, we developed a Drosophila model for Sleep Restriction Therapy (SRT) of insomnia. We demonstrate that restriction of sleep opportunity through manipulation of environmental cues improves sleep efficiency in multiple short-sleeping Drosophila mutants. The response to sleep opportunity restriction requires ongoing environmental inputs, but is independent of the molecular circadian clock. We apply this sleep opportunity restriction paradigm to aging and Alzheimer’s Disease fly models, and find that sleep impairments in these models are reversible with sleep restriction, with associated improvement in reproductive fitness and extended lifespan. This work establishes a model to investigate the neurobiological basis of CBT-I, and provides a platform that can be exploited towards novel treatment targets for insomnia.

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Insomnia Patients With Objective Short Sleep Duration Have a Blunted Response to Cognitive Behavioral Therapy for Insomnia

Cited by 54 publications

References 44 publications

The impact of stress on sleep: Pathogenic sleep reactivity as a vulnerability to insomnia and circadian disorders

The impact of stress on sleep: Pathogenic sleep reactivity as a vulnerability to insomnia and circadian disorders

Neurocognitive performance in insomnia disorder: The impact of hyperarousal and short sleep duration

A Drosophila model of sleep restriction therapy for insomnia

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