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Insomnia disorder

Abstract

Insomnia disorder affects a large proportion of the population on a situational, recurrent or chronic basis and is among the most common complaints in medical practice. The disorder is predominantly characterized by dissatisfaction with sleep duration or quality and difficulties initiating or maintaining sleep, along with substantial distress and impairments of daytime functioning. It can present as the chief complaint or, more often, co-occurs with other medical or psychiatric disorders, such as pain and depression. Persistent insomnia has been linked with adverse long-term health outcomes, including diminished quality of life and physical and psychological morbidity. Despite its high prevalence and burden, the aetiology and pathophysiology of insomnia is poorly understood. In the past decade, important changes in classification and diagnostic paradigms have instigated a move from a purely symptom-based conceptualization to the recognition of insomnia as a disorder in its own right. These changes have been paralleled by key advances in therapy, with generic pharmacological and psychological interventions being increasingly replaced by approaches that have sleep-specific and insomnia-specific therapeutic targets. Psychological and pharmacological therapies effectively reduce the time it takes to fall asleep and the time spent awake after sleep onset, and produce a modest increase in total sleep time; these are outcomes that correlate with improvements in daytime functioning. Despite this progress, several challenges remain, including the need to improve our knowledge of the mechanisms that underlie insomnia and to develop more cost-effective, efficient and accessible therapies.

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Figure 1: The relative importance of three types of factors in the course of insomnia.
Figure 2: Indicators of hyperarousal in insomnia.
Figure 3: An overview of the flip-flop switch model.
Figure 4: Central nervous system pathways that are potentially involved in the psychopathology of insomnia.
Figure 5: Main neurotransmitters involved in the ascending reticular activating system.

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Acknowledgements

Preparation of this manuscript was supported in part by grants to C.M.M. from the US NIH (MH-091053) and the Canadian Institutes of Health Research (MOP42504).

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Contributions

Introduction (C.M.M.); Epidemiology (C.L.D.); Mechanisms/pathophysiology (D.R. and K.S.); Diagnosis, screening and prevention (A.G.H. and R.M.); Management (A.D.K. and C.M.M.); Quality of life (C.L.D.); Outlook (C.M.M.); Overview of Primer (C.M.M.).

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Correspondence to Charles M. Morin.

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Competing interests

C.M.M. has served as a consultant for Novartis, Merck and Valeant, has received research contracts from Novartis and Merck, and research grants from the National Institute of Mental Health and the Canadian Institutes of Health Research. C.L.D. has received grants and/or research support from the US NIH, IntelClinic, Merck, Pernix and Teva. He has also served as a consultant for Jazz, Teva and Merck. A.D.K. has received grants and/or research support from the NIH, Teva, Eisai, Sunovion, NeoSync, Brainsway, Janssen, ANS St. Jude and Novartis. He has also served as a consultant for Abbott, Astellas, AstraZeneca, Attentiv, Bristol-Myers Squibb, Teva, Eisai, Eli Lilly, Jazz, Janssen, Merck, Neurocrine, Novartis, Otsuka, Palladin, Pernix, Pfizer, Lundbeck, Roche, Somnus, Sunovion, Somaxon and Vantia. D.R. has served as a consultant for AbbVie. He is also a board member of the Freiburg Educational Institute for Behavioural Therapy (a non-profit institution) and receives honoraria for teaching and supervising psychologists in training to become certified psychotherapists. A.G.H., R.M. and K.S. declare no competing interests.

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Morin, C., Drake, C., Harvey, A. et al. Insomnia disorder. Nat Rev Dis Primers 1, 15026 (2015). https://doi.org/10.1038/nrdp.2015.26

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