Репозиторий Университета

© 2020 The Author(s) The aim of this European initiative is to facilitate a structured discussion to improve the next edition of the International Classification of Sleep Disorders (ICSD), particularly the chapter on central disorders of hypersomnolence. The ultimate goal for a sleep disorders classification is to be based on the underlying neurobiological causes of the disorders with clear implication for treatment or, ideally, prevention and or healing. The current ICSD classification, published in 2014, inevitably has important shortcomings, largely reflecting the lack of knowledge about the precise neurobiological mechanisms underlying the majority of sleep disorders we currently delineate. Despite a clear rationale for the present structure, there remain important limitations that make it difficult to apply in routine clinical practice. Moreover, there are indications that the current structure may even prevent us from gaining relevant new knowledge to better understand certain sleep disorders and their neurobiological causes. We suggest the creation of a new consistent, complaint driven, hierarchical classification for central disorders of hypersomnolence; containing levels of certainty, and giving diagnostic tests, particularly the MSLT, a weighting based on its specificity and sensitivity in the diagnostic context. We propose and define three diagnostic categories (with levels of certainty): 1/“Narcolepsy” 2/“Idiopathic hypersomnia”, 3/“Idiopathic excessive sleepiness” (with subtypes).

© 2020 The Author(s) The aim of this European initiative is to facilitate a structured discussion to improve the next edition of the International Classification of Sleep Disorders (ICSD), particularly the chapter on central disorders of hypersomnolence. The ultimate goal for a sleep disorders classification is to be based on the underlying neurobiological causes of the disorders with clear implication for treatment or, ideally, prevention and or healing. The current ICSD classification, published in 2014, inevitably has important shortcomings, largely reflecting the lack of knowledge about the precise neurobiological mechanisms underlying the majority of sleep disorders we currently delineate. Despite a clear rationale for the present structure, there remain important limitations that make it difficult to apply in routine clinical practice. Moreover, there are indications that the current structure may even prevent us from gaining relevant new knowledge to better understand certain sleep disorders and their neurobiological causes. We suggest the creation of a new consistent, complaint driven, hierarchical classification for central disorders of hypersomnolence; containing levels of certainty, and giving diagnostic tests, particularly the MSLT, a weighting based on its specificity and sensitivity in the diagnostic context. We propose and define three diagnostic categories (with levels of certainty): 1/“Narcolepsy” 2/“Idiopathic hypersomnia”, 3/“Idiopathic excessive sleepiness” (with subtypes).

The article reviews the phenomenology of sleep and wakefulness disorders in Parkinson's disease and Alzheimer's disease. Degeneration of sleep and wakefulness centers, secondary effect of other symptoms of diseases and side-effects of drug therapy lead to a widespread prevalence of sleep and wakefulness disturbances in these patients. Along with the review of actual literature concerning mechanisms of development and clinical features of these disorders, the authors discuss principal methods for their treatment.

© 2018 Ima-Press Publishing House. All Rights Reserved. Daytime sleepiness is one of the clinically significant non-motor manifestations of Parkinson's disease (PD). One of its insufficiently studied aspects is a relationship between daytime sleepiness and nighttime sleep disorders. Objective: to clarify the clinical characteristics of PD in patients with different types of daytime sleepiness and to estimate of the ratio of daytime sleepiness to clinical and polysomnographic characteristics of nighttime sleep in patients with advanced stages of PD. Patients and methods: The investigation included 110 patients (56 men and 54 women) (mean age, 63.78±0.6 years) with PD (Hoehn and Yahr stage 2.6±0.2; disease duration, 6.3±3.2 years) without dementia. All the patients received therapy with levodopa at a mean daily dose of 667.8 mg; 98 of them had the drug in combination with dopamine receptor agonists at a stable dose. The unified PD rating scale, the PD sleep scale (PDSS), and the Epworth sleepiness scale (ESS) were applied. Nocturnal polysomnography (PSG) and the multiple sleep latency test (MSLT) were performed. Results and discussion: There was daytime sleepiness in 44% of the patients: permanent sleepiness in 15%, sudden daytime sleep attacks (along with low daytime sleepiness (ESS) in 14%, and permanent drowsiness concurrent with sleep attacks in 15%. The PSG findings showed a decrease in sleep efficiency, an increase in the duration of the first stage of sleep, a reduction in the duration of the second and third sleep stages, an extension of rapid eye movement (REM) sleep latency, and frequent awakenings (sleep fragmentation). PSG also demonstrated REM sleep behavior disorders (RBD) in half of the examinees. Patients with sleep attacks differed from those with permanent drowsiness without sleep attacks with more severe sleep disorders (PDSS) and shorter sleep latency (MSLT). Patients with the RBD phenomenon had shorter sleep latency (MTLS) than those without this parasomnia. Patients with moderate or severe sleepiness (ESS scores of >10) differed from those with milder drowsiness (ESS scores of =10) and a lower representation of the third sleep stage. Conclusion: There is evidence for the association of daytime sleepiness in PD with reduced efficiency, changes in the nighttime sleep pattern, and RBD.