The European Insomnia Guideline: An update on the diagnosis and treatment of insomnia 2023.

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).

Obstructive sleep apnea syndrome (OSAS): Pathophysiology in Estonians.

The aim of the study was to clarify the roles of age, obesity, smoking, alcohol, pathoanatomy and -physiology in Estonian's OSAS. For this 164 randomly chosen such patients were selected in different regions of Estonia. They underwent naso-oropharyngeal examination, physical examination of craniofacial abnormalities, and polysomnography. They also completed a self-reported questionnaire about smoking, alcohol use, excessive daytime sleepiness, hypertension, cardiac disorders, headaches, concentration disorders, and recurrent upper-airway diseases. The patients (129 men; 35 women) aged between 19 and 75 years (mean 47+/-12), BMI between 21 and 49 (mean 30.5+/-5.15), AHI between 5 and 105 (33+/-22). The results showed that there was a high percentage of naso-oropharyngeal disorders, such as: recurrent upper-airway diseases (54.2%), nasal breathing disorders (63.5%), and hypertrophy of tonsils (57%). There was also a high percentage of general characteristics, such as alcohol use (64%), excessive daytime sleepiness (85.5%), overweight (63%), and hypertension (51.2%). The regression summary for the dependent variable AHI if p-level=0.0042 (R=0.63347013) included age, BMI, hypertension, cardiac disorders, headaches, nasal obstruction, hypertrophy of pharyngeal muscles, tongue level, submental fat and slow-wave sleep (S3+S4%). In conclusion recurrent upper-airway diseases, nasal obstruction, and hypertrophy of tonsils in combination with smoking and alcohol caused the changes in the pharyngeal and lingual muscles. The latter gives rise to such sleep apnea-related problems as heart complaints, hypertension, headache and shortage of slow-wave sleep (SWS).

Myotonometry demonstrates changes of lingual musculature in obstructive sleep apnoea.

Upper airway dilator muscles are important in the pathogenesis of obstructive sleep apnoea (OSA). Previously, soft palate and tongue muscles of patients with OSA have been studied from a histological point of view. Electromyographic studies revealed increased activity of upper airway dilator muscles. We used computerized endopharyngeal myotonometry (CEM) to measure the biomechanical properties of lingual musculature, mainly the genioglossal muscle, to characterize changes of tongue muscles in patients with OSAS. The method records and analyzes the response of the tongue sublingually after a brief mechanical impact. It enabled us to evaluate the most important parameters of tissue tone--stiffness, which is expressed as a frequency, and elasticity, as a logarithmic decrement of the damped oscillation. The results of CEM indicated that patients with OSAS show an increased stiffness (14.1 +/- 0.7 Hz) of the tongue in comparison with non-snoring subjects (11.5 +/- 0.2 Hz). The elasticity of the tongue is decreased, which is numerically expressed as an increased decrement (4.0 +/- 0.2) in patients with OSA in comparison with non-snorers (2.2 +/- 0.2). Changes in the biomechanical characteristics of lingual musculature during wakefulness could result from pathophysiological processes caused by obstructive sleep apnoea.