Summary: This European guideline for the diagnosis and treatment of insomnia was developed by a task force of the European Sleep Research Society, with the aim of providing clinical recommendations for the management of adult patients with insomnia. The guideline is based on a systematic review of relevant meta‐analyses published till June 2016. The target audience for this guideline includes all clinicians involved in the management of insomnia, and the target patient population includes adults with chronic insomnia disorder. The GRADE (Grading of Recommendations Assessment, Development and Evaluation) system was used to grade the evidence and guide recommendations. The diagnostic procedure for insomnia, and its co‐morbidities, should include a clinical interview consisting of a sleep history (sleep habits, sleep environment, work schedules, circadian factors), the use of sleep questionnaires and sleep diaries, questions about somatic and mental health, a physical examination and additional measures if indicated (i.e. blood tests, electrocardiogram, electroencephalogram; strong recommendation, moderate‐ to high‐quality evidence). Polysomnography can be used to evaluate other sleep disorders if suspected (i.e. periodic limb movement disorder, sleep‐related breathing disorders), in treatment‐resistant insomnia, for professional at‐risk populations and when substantial sleep state misperception is suspected (strong recommendation, high‐quality evidence). Cognitive behavioural therapy for insomnia is recommended as the first‐line treatment for chronic insomnia in adults of any age (strong recommendation, high‐quality evidence). A pharmacological intervention can be offered if cognitive behavioural therapy for insomnia is not sufficiently effective or not available. Benzodiazepines, benzodiazepine receptor agonists and some antidepressants are effective in the short‐term treatment of insomnia (≤4 weeks; weak recommendation, moderate‐quality evidence). Antihistamines, antipsychotics, melatonin and phytotherapeutics are not recommended for insomnia treatment (strong to weak recommendations, low‐ to very‐low‐quality evidence). Light therapy and exercise need to be further evaluated to judge their usefulness in the treatment of insomnia (weak recommendation, low‐quality evidence). Complementary and alternative treatments (e.g. homeopathy, acupuncture) are not recommended for insomnia treatment (weak recommendation, very‐low‐quality evidence).

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).

Although commonly observed in clinical practice, the heterogeneity of obstructive sleep apnoea (OSA) clinical presentation has not been formally characterised.This study was the first to apply cluster analysis to identify subtypes of patients with OSA who experience distinct combinations of symptoms and comorbidities. An analysis of baseline data from the Icelandic Sleep Apnoea Cohort (822 patients with newly diagnosed moderate-to-severe OSA) was performed.Three distinct clusters were identified. They were classified as the “disturbed sleep group” (cluster 1), “minimally symptomatic group” (cluster 2) and “excessive daytime sleepiness group” (cluster 3), consisting of 32.7%, 24.7% and 42.6% of the entire cohort, respectively. The probabilities of having comorbid hypertension and cardiovascular disease were highest in cluster 2 but lowest in cluster 3. The clusters did not differ significantly in terms of sex, body mass index or apnoea–hypopnoea index.Patients with OSA have different patterns of clinical presentation, which need to be communicated to both the lay public and the professional community with the goal of facilitating care-seeking and early identification of OSA. Identifying distinct clinical profiles of OSA creates a foundation for offering more personalised therapies in the future.

Summary: The publication of “The Sleep Apnea Syndromes” by Guilleminault et al. in the 1970s hallmarked the discovery of a new disease entity involving serious health consequences. Obstructive sleep apnea was shown to be the most important disorder among the sleep apnea syndromes (SAS). In the course of time, it was found that the prevalence of obstructive sleep apnea reached the proportions of a global epidemic, with a major impact on public health, safety and the economy. Early on, a metric was introduced to gauge the seriousness of obstructive sleep apnea, based on the objective measurement of respiratory events during nocturnal sleep. The apnea index and later on the apnea−hypopnea index, being the total count of overnight respiratory events divided by the total sleep time in hours, were embraced as principle measures to establish the diagnosis of obstructive sleep apnea and to rate its severity. The current review summarises the historical evolution of the apnea−hypopnea index, which has been subject to many changes, and has been criticised for not capturing relevant clinical features of obstructive sleep apnea. In fact, the application of the apnea−hypopnea index as a continuous exposure variable is based on assumptions that it represents a disease state of obstructive sleep apnea and that evocative clinical manifestations are invariably caused by obstructive sleep apnea if the apnea−hypopnea index is above diagnostic threshold. A critical appraisal of the extensive literature shows that both assumptions are invalid. This conclusion prompts a reconsideration of the role of the apnea−hypopnea index as the prime diagnostic metric of clinically relevant obstructive sleep apnea.

The consequences of obstructive sleep apnea (OSA) are largely mediated by chronic intermittent hypoxia and sleep fragmentation. The primary molecular domains affected are sympathetic activity, oxidative stress and inflammation. Other affected domains include adipokines, adhesion molecules and molecules that respond to endoplasmic reticulum stress. Changes in molecular domains affected by OSA, assessed in blood and/or urine, can provide a molecular signature for OSA that could potentially be used diagnostically and to predict who is likely to develop different OSA-related comorbidities. High-throughput discovery strategies such as microarrays, assessing changes in gene expression in circulating blood cells, have the potential to find new candidates and pathways thereby expanding the molecular signatures for OSA. More research is needed to fully understand the pathophysiological significance of these molecular signatures and their relationship with OSA comorbidities. Many OSA subjects are obese, and obesity is an independent risk factor for many comorbidities associated with OSA. Moreover, obesity affects the same molecular pathways as OSA. Thus, a challenge to establishing a molecular signature for OSA is to separate the effects of OSA from obesity. We propose that the optimal strategy is to evaluate the temporal changes in relevant molecular pathways during sleep and, in particular, the alterations from before to after sleep when assessed in blood and/or urine. Such changes will be at least partly a consequence of chronic intermittent hypoxia and sleep fragmentation that occurs during sleep.

The aim was to assess the prevalence of obstructive sleep apnoea (OSA) as defined by an apnoea–hypopnea index (AHI) ≥15 in the middle-aged general population, and the interrelationship between OSA, sleep-related symptoms, sleepiness and vigilance.A general population sample of 40–65-year-old Icelanders was invited to participate in a study protocol that included a type 3 sleep study, questionnaire and a psychomotor vigilance test (PVT).Among the 415 subjects included in the study, 56.9% had no OSA (AHI <5), 24.1% had mild OSA (AHI 5–14.9), 12.5% had moderate OSA (AHI 15–29.9), 2.9% had severe OSA (AHI ≥30) and 3.6% were already diagnosed and receiving OSA treatment. However, no significant relationship was found between AHI and subjective sleepiness or clinical symptoms. A relationship with objective vigilance assessed by PVT was only found for those with AHI ≥30. Subjects already on OSA treatment and those accepting OSA treatment after participating in the study were more symptomatic and sleepier than others with similar OSA severity, as assessed by the AHI.In a middle-aged general population, approximately one in five subjects had moderate-to-severe OSA, but the majority of them were neither symptomatic nor sleepy and did not have impaired vigilance.