The Natural History of Insomnia: Acute Insomnia and First-onset Depression

Ellis, Jason; Perlis, Michael L.; Bastien, Célyne; Gardani, Maria; Espie, Colin A.

doi:10.5665/sleep.3316

Cited by 61 publications

(53 citation statements)

References 71 publications

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“…Riemann et al. proposed that REM sleep fragmentation may lead to rebounds in REM pressure (↓ REM latency, ↑ REM density) resembling sleep abnormalities in the transition from acute to chronic insomnia (Ellis, Perlis, Bastien, Gardani, & Espie, ) and in depression (Pillai, Kalmbach, & Ciesla, ).…”

Section: The Neurobiology Of Sleep Reactivitymentioning

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

299

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: The Neurobiology Of Sleep Reactivitymentioning

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

299

224

View full text Add to dashboard Cite

show abstract

“…Importantly, insomnia is a significant risk factor for the development of several physical and psychological illnesses—most notably major depression 2 3. Despite advances in non-pharmacological insomnia treatments, specifically a 6–8-week course of cognitive-behavioural therapy for insomnia (CBT-I), significant barriers limit its implementation in primary care.…”

Section: Contextmentioning

confidence: 99%

Simplified sleep restriction impacts objective but not subjective sleep for people with primary insomnia in primary care

Ellis

2015

Evid Based Med

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“…However, in insomnia patients, the daytime effects associated with sleep seem especially important, both in theory [25,31] and to patients themselves [29,32]. Current research is aimed at investigating the etiology of insomnia disorder, for example, the development of chronic insomnia from acute insomnia [33], and this suggests the importance of additional factors in the development of insomnia disorder. For example, insomnia patients might experience the effects of sleep disruption more severely or report more frequent nights of poor sleep [28], and changes in sleep architecture could contribute towards this transition [33].…”

Section: Introductionmentioning

confidence: 99%

“…Current research is aimed at investigating the etiology of insomnia disorder, for example, the development of chronic insomnia from acute insomnia [33], and this suggests the importance of additional factors in the development of insomnia disorder. For example, insomnia patients might experience the effects of sleep disruption more severely or report more frequent nights of poor sleep [28], and changes in sleep architecture could contribute towards this transition [33]. Furthermore, in keeping with a normal distribution [28], some normal sleepers could show evidence of sleep disruption, while not quite endorsing insomnia (eg, Ref.…”

Section: Introductionmentioning

confidence: 99%

How are normal sleeping controls selected? A systematic review of cross-sectional insomnia studies and a standardized method to select healthy controls for sleep research

et al. 2015

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There appears to be some inconsistency in how normal sleepers (controls) are selected and screened for participation in research studies for comparison with insomnia patients. The purpose of the current study is to assess and compare methods of identifying normal sleepers in insomnia studies, with reference to published standards. We systematically reviewed the literature on insomnia patients, which included control subjects. The resulting 37 articles were systematically reviewed with reference to the five criteria for normal sleep specified by Edinger et al. In summary, these criteria are as follows: evidence of sleep disruption, sleep scheduling, general health, substance/medication use, and other sleep disorders. We found sleep diaries, polysomnography (PSG), and clinical screening examinations to be widely used with both control subjects and insomnia participants. However, there are differences between research groups in the precise definitions applied to the components of normal sleep. We found that none of the reviewed studies applied all of the Edinger et al. criteria, and 16% met four criteria. In general, screening is applied most rigorously at the level of a clinical disorder, whether physical, psychiatric, or sleep. While the Edinger et al. criteria seem to be applied in some form by most researchers, there is scope to improve standards and definitions in this area. Ideally, different methods such as sleep diaries and questionnaires would be used concurrently with objective measures to ensure normal sleepers are identified, and descriptive information for control subjects would be reported. Here, we have devised working criteria and methods to be used for the assessment of normal sleepers. This would help clarify the nature of the control group, in contrast to insomnia subjects and other patient groups.

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The Natural History of Insomnia: Acute Insomnia and First-onset Depression

Cited by 61 publications

References 71 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

Simplified sleep restriction impacts objective but not subjective sleep for people with primary insomnia in primary care

How are normal sleeping controls selected? A systematic review of cross-sectional insomnia studies and a standardized method to select healthy controls for sleep research

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