Репозиторий Университета

© 2018, Springer Science+Business Media, LLC, part of Springer Nature. Purpose of Review: Sleep-wake disorders (SWD) are common not only in the general population but also in stroke patients, in whom SWD may be pre-existent or appear “de novo” as a consequence of brain damage. Despite increasing evidence of a negative impact of SWD on cardiocerebrovascular risk, cognitive functions, and quality of life, SWD are insufficiently considered in the prevention and management of patients with stroke. This narrative review aims at summarizing the current data on the bidirectional link between SWD and stroke. Recent Findings: Several studies have demonstrated that sleep-disordered breathing (SDB) is an independent risk factor for stroke and has a detrimental effect on stroke recovery. Short and long sleep duration and possibly other SWD (e.g., insomnia, circadian rhythm disorders) may also increase the risk of stroke and influence its outcome. Data on SDB treatment increasingly indicate a benefit on stroke risk and evolution while treatment of other SWD is still limited. Summary: A systematic search for SWD in stroke patients is justified due to their high frequency and their negative impact on stroke outcomes. Clinicians should actively consider available treatment options.

The article analyzes the anatomy, morphological and neurochemical connections and functions of the brain histaminergic system, one of the leading systems in the mechanism maintaining wakefulness. The possibilities of histaminergic system modulating for the treatment of various sleep/wake cycle disorders are discussed. The data of clinical trials on the influence of the histamine H1 receptor antagonist doxylamine on sleep in healthy volunteers and patients with insomnia are considered. The evidence-based efficacy of the drug in sleep disorders is discussed.

The most frequent among the symptoms and syndromes, which are comorbid to panic disorder, are sleep disorders, primarily, insomnia, persisting in 60-80% of patients in this category. Panic disorder and insomnia have bilateral relationships. On one hand, there is a clear correlation between disease severity and accompanying sleep disorders. On the other, the conditionality of sleep disturbances with pathological anxiety has been demonstrated. Treatment of insomnia in panic disorder includes a set of measures aimed at harmonizing the emotional state and stopping insomnia as a syndrome. A comprehensive approach, which includes, along with adequate pharmacotherapy, a wide range of methods of psychotherapeutic treatment, is the key for the success of therapy for sleep disturbances in panic disorder.

Physiology of breathing during sleep predisposes to the development or worsening of the respiratory disorders in patients with chronic obstructive pulmonary disease (COPD) even if waking respiratory function remains relatively normal. Physicians, who assess patient's state only during the day, in some cases can underestimate this problem. Respiratory abnormalities can provoke insomnia, which additionally affects patient's quality of life. Supplemental oxygen and pressure support ventilation improve blood gases during sleep, but in many cases, insomnia persists. In many cases, such patients need the treatment with hypnotics. Widely used drugs in insomnia are benzodiazepines. They are rather effective but can cause respiratory depression and respiratory failure in patients with COPD. Z-hypnotics are comparable to classical benzodiazepines but much more safe and rarely worsen respiratory parameters. Melatonin and melatonin receptor agonists, antihistamines, antidepressants and neuroleptics can be effective in some patients with insomnia, but insufficient data about their safety in case of respiratory pathology restrict the use of these drugs in patients with COPD. The orexin receptor antagonist suvorexant is a novel hypnotic with the potential benefits for patients with COPD because it strongly improves sleep but does not depress respiration and has a minimal negative impact on daytime cognitive function.

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. This review provides information on prospects for using the antidepressant agomelatine in neurological practice. The drug has a unique receptor profile, being a melatonin receptor type 1 and 2 agonist and a serotonin receptor subtype 2C antagonist. Due to this and in addition to antidepressant action, the drug has a number of other effects, such as analgesic, anti-apathetic, anti-asthenic, procognitive, anxiolytic, and sleep-normalizing ones, which are of great importance in the treatment of neurological diseases. There are clinical and experimental data that prove the high efficiency and safety of agomelatin in the follow-up of patients with post-stroke depression, Parkinson's disease, Alzheimer's disease, Pick's disease, Huntington's disease, chronic fatigue syndrome, and pain syndromes.

© 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.