Діагностика та лікування немоторних порушень при хворобі Паркінсона

Удосконалення методів ранньої діагностики та підвищення ефективності лікування немоторних порушень на основі комплексного обстеження при хворобі Паркінсона. Вираженість депресій і больового синдрому. Зменшення прогресування патологічного процесу.

Рубрика Медицина
Вид автореферат
Язык украинский
Дата добавления 30.07.2015
Размер файла 281,1 K

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Ключевые слова: болезнь Паркинсона, немоторные проявления, нейрон-специфическая энолаза, альдегидфенилгидрозоны, кетонфенилгидрозоны, ГАМК/глутаматная диссоциация, амантин, проноран.

Summary

Kutsak A.V. Diagnostics and treatment of non-motor disorders in Parkinson's disease. - The manuscript.

Dissertation on competition of scientific degree of candidate of medical sciences on speciality 14.01.15. - Nervous Diseases. - National medical academy postgraduate education P.L.Shupika of Ministry of Health of Ukraine, Kyiv, 2011.

Dissertation is devoted the improvement of methods of early diagnostics on the basis of complex examination and increase efficiency of treatment of non-motor disorders in Parkinson's disease (PD).

In-process first certainly, that the level of neuron-specific enolase (NSE) of more than 30 мg/L is associated with the high estimations of non-motor manifestations of PD, in a greater degree cognitive disorders. It is set from data of regressive analysis, that the presence of non-motor manifestations influences on life quality in patient with PD, expressiveness of depressions and pain syndrome. As a result of the conducted research the original discriminant model of neuro-psychological examination is offered with a high sensitiveness which allows it is enough exactly to diagnose and determine authenticity of unfavourable clinical course of PH, and also in good time to develop strategy, with the purpose of diminishing of progress of pathological process and prevention complication.

It is first found out, that basic predictors of motion deficit in PH were carbonyl stress with activating of freely radical oxidization (increase of aldehydic and ketonic forms of phenylhydrazones) from GABA/glutamate by dissociation, and pathological changes in a power homoeostasis from elevation of proapoptotic markers and damage of homocysteine with a thiol-disulfide disbalance were anymore related to non-motor (especially cognitive) fluctuations. For patients with PD by the study of levels of spontaneous and metal-induced of oxidizing modification of protein after the levels of aldehyde- and keto-phenylhydrazones the state of activating of free-radical processes is certain depending on the stages of pathological process. It is found out, that a level of blood homocysteine of more than 20 мg/mL is predictor and by the non-invasive marker of cognitive disorder progress in PD.

Possibility of pharmacological correction of non-motor manifestations is first well-proven for patients with PD by an antagonist NMDA-glutamate receptors amantin or dopaminergic agonist pronoran on a background base levodopa therapy due to normalization of different neuromediatory and oxidative-antioxidative systems, power exchange of neurons, decline of neurodegeneration intensity and, as a result, reduction of blood level of NSE. It is shown, that during the expressive activating of oxidative stress, in comparing to the power deficit, more effective was amantin therapy, and pronoran therapy is clinically approved for the prophylaxis of transformation of some non-motor disorders to dementia, that also improved life quality in PD at more expressive cognitive deviation.

Keywords: Parkinson's disease, non-motor disorders, neuron-specific enolase, aldehydephenylhydrazones, ketophenylhydrazones, GABA/glutamate by dissociation, amantin, pronoran.

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