Clinical manifestations and mechanisms of formation of neurological disorders in patients with vibration disease

Victoria V. Vorobieva, Olga S. Levchenkova
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Abstract

The review presents an analysis of literature sources devoted to the study of changes in the nervous system in patients with vibration disease. Vibration-mediated cellular hypoxia, which occurs as a result of spastic changes in blood vessels, phase fluctuations in intravascular pressure, impaired blood and lymph outflow, causes suppression of energy metabolism, contributes to disorders at the level of receptor (glutamate, GABA-ergic, dopamine and cholinergic) and synaptic structures, conductors of pain and temperature sensitivity (demyelinization), analyzing neurons in the parietal region of the brain, regulatory proteins of the nervous tissue (NF-200, GFAP S-100). A low-amplitude, irregular, disorganized and sometimes deformed EEG spectrum with a predominance of the alpha wave and a shift of the alpha rhythm to the left reflects changes in the spontaneous electrical activity of brain structures in patients. With an increase in the experience dose of vibration-noise exposure, the dominant alpha activity changes to slow-wave or polyrhythmic. Mild and moderate diffuse changes in the brain become focal in nature, cortical-subcortical relationships are disrupted at the diencephalic level, creating a pathophysiological basis for sensorineural (sensory-neural) hearing loss, especially in patients with a genetic predisposition mediated by genes encoding proteins of the heat shock system. The psycho-emotional status of patients is characterized by a hypochondriacal focus on the state of health, mental disadaptation, psycho-emotional disorders in the form of anxiety, depressive mood. The analysis of literature sources on the mechanisms of the formation of neurological disorders in patients with vibration disease revealed the lack of data on the state of the multicomponent ghrelin system interacting with GHSR-1A and GHSR-1B receptors, which determines a new vector in further experimental and clinical studies.
振动病患者神经功能障碍的临床表现及形成机制
本综述分析了有关振动病患者神经系统变化研究的文献资料。振动介导的细胞缺氧是由于血管痉挛变化、血管内压力相位波动、血液和淋巴流出受损而发生的,导致能量代谢受到抑制,导致受体(谷氨酸、氨基丁酸能、多巴胺和胆碱能)和突触结构、疼痛和温度敏感性传导(脱髓鞘)水平紊乱,分析大脑顶叶区域的神经元,神经组织的调节蛋白(NF-200, GFAP S-100)。低振幅、不规则、无序、有时变形的脑电图频谱,以α波为主,α节奏向左移动,反映了患者脑结构自发电活动的变化。随着振动噪声暴露体验剂量的增加,主导α活动转变为慢波或多节奏。大脑轻度和中度弥漫性变化在本质上成为局灶性变化,皮层-皮层下关系在间脑水平被破坏,为感觉神经(感觉神经)听力损失创造了病理生理基础,特别是在由编码热休克系统蛋白质的基因介导的遗传易感性患者中。患者的心理情绪状态的特点是对健康状况的疑病症关注,精神上的不适应,以焦虑、抑郁情绪的形式出现的心理情绪障碍。通过对振动病患者神经系统疾病形成机制的文献来源分析,发现缺乏GHSR-1A和GHSR-1B受体相互作用的多组分ghrelin系统状态的数据,这为进一步的实验和临床研究确定了新的载体。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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