Summary Insomnia disorder comprises symptoms during night and day that strongly affect quality of life and wellbeing. Prolonged sleep latency, difficulties to maintain sleep and early morning wakening characterize sleep complaints, whereas fatigue, reduced attention, impaired cognitive functioning, irritability, anxiety and low mood are key daytime impairments. Insomnia disorder is well acknowledged in all relevant diagnostic systems: Diagnostic and Statistical Manual of the American Psychiatric Association, 5th revision, International Classification of Sleep Disorders, 3rd version, and International Classification of Diseases, 11th revision. Insomnia disorder as a chronic condition is frequent (up to 10% of the adult population, with a preponderance of females), and signifies an important and independent risk factor for physical and, especially, mental health. Insomnia disorder diagnosis primarily rests on self‐report. Objective measures like actigraphy or polysomnography are not (yet) part of the routine diagnostic canon, but play an important role in research. Disease concepts of insomnia range from cognitive‐behavioural models to (epi‐) genetics and psychoneurobiological approaches. The latter is derived from knowledge about basic sleep–wake regulation and encompass theories like rapid eye movement sleep instability/restless rapid eye movement sleep. Cognitive‐behavioural models of insomnia led to the conceptualization of cognitive‐behavioural therapy for insomnia, which is now considered as first‐line treatment for insomnia worldwide. Future research strategies will include the combination of experimental paradigms with neuroimaging and may benefit from more attention to dysfunctional overnight alleviation of distress in insomnia. With respect to therapy, cognitive‐behavioural therapy for insomnia merits widespread implementation, and digital cognitive‐behavioural therapy may assist delivery along treatment guidelines. However, given the still considerable proportion of patients responding insufficiently to cognitive‐behavioural therapy for insomnia, fundamental studies are highly necessary to better understand the brain and behavioural mechanisms underlying insomnia. Mediators and moderators of treatment response/non‐response and the associated development of tailored and novel interventions also require investigation. Recent studies suggest that treatment of insomnia may prove to add significantly as a preventive strategy to combat the global burden of mental disorders.

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Summary According to the hyperarousal model, insomnia is characterised by increased arousal in the cortical, cognitive, and physiological domains. However, the interaction between these arousal domains is poorly understood. The present observational case–control study aimed to investigate cortical arousal during the night, pre‐sleep cognitive arousal and the relationship between these two domains. A total of 109 patients with insomnia disorder (ID) and 109 age‐and gender matched healthy controls were investigated on two sleep laboratory nights. Electroencephalographic (EEG) spectral power during non‐rapid eye movement (NREM) and REM sleep was analysed as a measure of cortical arousal. In addition, patients completed the Pre‐Sleep Arousal Scale (PSAS), which consists of two subscales, one for cognitive arousal (PSAS‐CA) and one for self‐reported somatic arousal (PSAS‐SA). The relationship between the subscale scores and EEG spectral power was calculated by multi‐ and univariate analyses of variance. During NREM and REM sleep, patients with ID showed significantly increased spectral power in the EEG gamma band. In addition, patients with ID showed significantly increased scores on both subscales of the PSAS. The PSAS‐CA score was significantly associated with increased NREM and REM gamma power, whereas PSAS‐SA was associated with decreases in NREM and REM gamma power. Consistent with our hypothesis, patients with ID showed increased cortical and cognitive arousal. Moreover, there was an association between these two arousal domains, which may indicate that cortical arousal during the night is (at least in part) elicited by pre‐sleep worry and rumination.

SummaryInsomnia disorder is among the most frequent mental disorders, making research on its aetiology and pathophysiology particularly important. A unifying element of many aetiological and pathophysiological models is that they support or even centre on the role of some form of hyperarousal. In this theoretical review, we aim to summarise the current evidence on hyperarousal in insomnia. Hyperarousal is discussed as a state of relatively increased arousal in physiological, cortical and cognitive‐emotional domains. Regarding physiological hyperarousal, there is no conclusive evidence for the involvement of autonomous variables such as heart rate and heart rate variability, whereas recent evidence points to a pathophysiological role of neuroendocrine variables. In addition, current literature supports a central involvement of cortical arousal, that is, high‐frequency electroencephalographic activity. An increasingly important focus in the literature is on the role of other microstructural sleep parameters, especially the existence of microarousals during sleep. Beyond that, a broad range of evidence exists supporting the role of cognitive‐emotional hyperarousal in the form of insomnia‐related thought and worries, and their concomitant emotional symptoms. Besides being a state marker of insomnia, hyperarousal is considered crucial for the predisposition to insomnia and for the development of comorbid mental disorders. Thus, beyond presenting evidence from cross‐sectional studies on markers of hyperarousal in insomnia, hypotheses about the mechanisms of hyperarousal are presented. Nevertheless, longitudinal studies are needed to further elucidate the mechanism of hyperarousal throughout the course of the disorder, and future studies should also focus on similarities and differences in hyperarousal across different diagnostic entities.