Summary: Progress in the field of insomnia since 2017 necessitated this update of the European Insomnia Guideline. Recommendations for the diagnostic procedure for insomnia and its comorbidities are: clinical interview (encompassing sleep and medical history); the use of sleep questionnaires and diaries (and physical examination and additional measures where indicated) (A). Actigraphy is not recommended for the routine evaluation of insomnia (C), but may be useful for differential‐diagnostic purposes (A). Polysomnography should be used to evaluate other sleep disorders if suspected (i.e. periodic limb movement disorder, sleep‐related breathing disorders, etc.), treatment‐resistant insomnia (A) and for other indications (B). Cognitive‐behavioural therapy for insomnia is recommended as the first‐line treatment for chronic insomnia in adults of any age (including patients with comorbidities), either applied in‐person or digitally (A). When cognitive‐behavioural therapy for insomnia is not sufficiently effective, a pharmacological intervention can be offered (A). Benzodiazepines (A), benzodiazepine receptor agonists (A), daridorexant (A) and low‐dose sedating antidepressants (B) can be used for the short‐term treatment of insomnia (≤ 4 weeks). Longer‐term treatment with these substances may be initiated in some cases, considering advantages and disadvantages (B). Orexin receptor antagonists can be used for periods of up to 3 months or longer in some cases (A). Prolonged‐release melatonin can be used for up to 3 months in patients ≥ 55 years (B). Antihistaminergic drugs, antipsychotics, fast‐release melatonin, ramelteon and phytotherapeutics are not recommended for insomnia treatment (A). Light therapy and exercise interventions may be useful as adjunct therapies to cognitive‐behavioural therapy for insomnia (B).

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.

According to epidemiological studies, insomnia is associated with cardiovascular mortality. However, it is yet to be determined whether this link is mediated by known cardiovascular risk factors. The current study aimed at investigating the association between primary insomnia, defined as subjectively reported sleep disturbance in the absence of any other pathology or substance intake, and alterations in polysomnographically determined nocturnal heart rate (HR) and heart rate variability (HRV). A total of 4 581 nocturnal short-term electrocardiographic recordings (5 min each) from 104 participants (58 with primary insomnia, 46 healthy controls) were evaluated for HR as well as for time and frequency domain measures of HRV. In the primary insomnia group, we found a lower wake-to-sleep HR reduction and a lower standard deviation of RR intervals (SDNN) compared to healthy controls. However, between-group differences in resting HR were not found, and previous results of an increase in sympathovagal balance and a decrease in parasympathetic nocturnal activity in objectively determined insomnia could not be confirmed in our sample of self-report insomnia patients. When restricting our analyses to insomnia patients with objectively determined short sleep duration, we found reduced parasympathetic activity as indicated by decreased high frequency power of HRV, as well as decreased root mean square of successive RRI differences (RMSSD) and percentage of successive RRIs that differ by more than 50 ms (pNN50) values. A lower wake-to-sleep HR reduction and alterations in HRV variables might, at least partially, mediate the increased rates of cardiovascular morbidity and mortality observed in insomnia patients.

Summary: The world‐wide prevalence of insomnia disorder reaches up to 10% of the adult population. Women are more often afflicted than men, and insomnia disorder is a risk factor for somatic and mental illness, especially depression and anxiety disorders. Persistent hyperarousals at the cognitive, emotional, cortical and/or physiological levels are central to most theories regarding the pathophysiology of insomnia. Of the defining features of insomnia disorder, the discrepancy between minor objective polysomnographic alterations of sleep continuity and substantive subjective impairment in insomnia disorder remains enigmatic. Microstructural alterations, especially in rapid eye movement sleep (“rapid eye movement sleep instability”), might explain this mismatch between subjective and objective findings. As rapid eye movement sleep represents the most highly aroused brain state during sleep, it might be particularly prone to fragmentation in individuals with persistent hyperarousal. In consequence, mentation during rapid eye movement sleep may be toned more as conscious‐like wake experience, reflecting pre‐sleep concerns. It is suggested that this instability of rapid eye movement sleep is involved in the mismatch between subjective and objective measures of sleep in insomnia disorder. Furthermore, as rapid eye movement sleep has been linked in previous works to emotional processing, rapid eye movement sleep instability could play a central role in the close association between insomnia and depressive and anxiety disorders.