The paper is aimed at the analysis of the role of the circadian regulation of ghrelin levels in patients with Parkinson’s disease. Based on the literature data, patients with Parkinson’s disease have clinical fluctuations in the symptoms of the disease, manifested by the diurnal changes in motor activity, autonomic functions, sleep-wake cycle, visual function, and the efficacy of dopaminergic therapy. Biological rhythms are controlled by central and peripheral oscillators which links with dopaminergic neurotransmission – core of the pathogenesis of Parkinson`s disease. Circadian system is altered in Parkinson`s disease due to that ghrelin fluctuations may be changed. Ghrelin is potential food-entrainable oscillator because it is linked with clock genes expression. In Parkinson`s disease this hormone may induce eating behavior changing and as a result metabolic disorder. The “hunger hormone” ghrelin can be a biomarker of the Parkinson’s disease, and the study of its role in the pathogenesis, as well as its dependence on the period of the day, intake of levodopa medications to improve the effectiveness of treatment is promising.
The article summarizes the arguments and counter-arguments within the scientific discussion on the impact of sleep disorders on the development of cognitive decline in patients with Parkinson's disease. The main purpose of the study is to study the possibility of predicting the development of cognitive decline by assessing the severity of sleep disorders and their differences in the presence of cognitive impairment. Systematization of literature sources and approaches to solving the problem showed that sleep disorders develop in the early stages of Parkinson's disease and are often accompanied by cognitive impairment. Cognitive decline is manifested throughout Parkinson's disease and ranges from moderate in the early stages to dementia in the late stages. The relevance of the study of the relationship between sleep disorders and cognitive functions lies in the possibility of further improving the prediction of the development of cognitive decline in order to effectively correct it. Treatment of sleep disorders can be accompanied by improved memory and even morphological changes in the brain. Therefore, the question arises about the possibility of correcting cognitive decline by influencing sleep disorders. The methodology of the study included assessment of the overall status of patients on a unified scale of Parkinson's disease, Montreal cognitive rating scale and sleep scale in Parkinson's disease. The duration of the study was 8 months. Patients with Parkinson's disease were selected as the study. The article presents the results of a survey of patients who show that patients with Parkinson's disease and cognitive decline showed a predominance of motor disorders, sleep disorders and the overall score on the sleep scale in Parkinson's disease. In the presence of cognitive decline more pronounced disorders of motor functions in everyday life, which can lead to sleep disorders and its quality. The study empirically confirms and theoretically proves that the assessment of sleep disorders can be used to predict the risk of developing cognitive impairment in patients with Parkinson's disease. The results of this study may be useful for improving the early diagnosis and prevention of cognitive impairment in patients with Parkinson's disease, which, in turn, leads to improved quality of treatment of these patients. Such changes can directly affect the choice of therapeutic tactics and improve the quality of life of patients with Parkinson's disease. The question of the features of various sleep disorders and their prognostic value in relation to cognitive decline in patients with various forms of Parkinson's disease remains open.
The aim was to analyze the contemporary scientific literature on Devic’s opticomyelitis and to present a case report from our clinical practice. Based on the patient’s complaints, case history and features of clinical course, objective neurological status, clinical laboratory and additional examination methods, characteristic MR-patterns, consultations of related specialists and differential diagnostics, we made the clinical diagnosis according to ICD-10: G36.0 Devic’s opticomyelitis, exacerbation, with a sustained bilateral lesion of the optic nerves in the form of retrobulbar neuritis with the development of partial atrophy of the optic nerves in both eyes, spinal cord lesions with common cystic, cicatrical and atrophic alterations at C1-Th8 level with moderate lower paraparesis, expressed by sensory ataxia, sensory disturbances by the descending conductive type from Th10, impaired function of pelvic organs by the type of acute urinary retention, asthenic and neurotic syndrome. Widespread cases of demyelinating pathology in medical practice and complexity of differential diagnostics determine the need for a specific diagnostic algorithm. This algorithm should consider anamnestic data along with the course of the disease, clinical, laboratory and instrumental examination, including neuroimaging, analysis of CSF for oligoclonal bands, analysis for IgG antibodies to AQP4, which will allow to carry out diagnostics and to decide on tactics for further management of patients of this cohort. Further research is needed to conduct additional studies for optimization of tactics for dynamics monitoring and improvement of diagnostic, treatment and rehabilitation measures in patients with Devic’s opticomyelitis, including appropriate immunological control, given the complexity of differential diagnostics and the affinity of this pathology to multiple sclerosis.
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