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Bradykinesia in Alzheimer’s disease and its neurophysiological substrates
Clinical Neurophysiology ( IF 4.7 ) Pub Date : 2020-04-01 , DOI: 10.1016/j.clinph.2019.12.413
Matteo Bologna 1 , Andrea Guerra 2 , Donato Colella 3 , Ettore Cioffi 3 , Giulia Paparella 2 , Antonella Di Vita 3 , Fabrizia D'Antonio 3 , Alessandro Trebbastoni 3 , Alfredo Berardelli 1
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OBJECTIVE Alzheimer's disease is primarily characterized by cognitive decline; recent studies, however, emphasize the occurrence of motor impairment in this condition. Here, we investigate whether motor impairment, objectively evaluated with kinematic techniques, correlates with neurophysiological measures of the primary motor cortex in Alzheimer's disease. METHODS Twenty patients and 20 healthy subjects were enrolled. Repetitive finger tapping was assessed by means of a motion analysis system. Primary motor cortex excitability was assessed by recording the input/output curve of the motor-evoked potentials and using a conditioning-test paradigm for the assessment of short-interval intracortical inhibition and short-latency afferent inhibition. Plasticity-like mechanisms were indexed according to changes in motor-evoked potential amplitude induced by the intermittent theta-burst stimulation. RESULTS Patients displayed slowness and altered rhythm during finger tapping. Movement slowness correlated with reduced short-latency afferent inhibition in patients, thus suggesting that degeneration of the cholinergic system may also be involved in motor impairment in Alzheimer's disease. Moreover, altered movement rhythm in patients correlated with worse scores in the Frontal Assessment Battery. CONCLUSION This study provides new information on the pathophysiology of altered voluntary movements in Alzheimer's disease. SIGNIFICANCE The study results suggest that a cortical cholinergic deficit may underlie movement slowness in Alzheimer's disease.

中文翻译:

阿尔茨海默病中的运动迟缓及其神经生理学底物

目的 阿尔茨海默病的主要特征是认知能力下降;然而,最近的研究强调在这种情况下会发生运动障碍。在这里,我们调查运动学技术客观评估的运动障碍是否与阿尔茨海默病中初级运动皮层的神经生理学测量相关。方法 招募了 20 名患者和 20 名健康受试者。通过运动分析系统评估重复的手指敲击。通过记录运动诱发电位的输入/输出曲线并使用调节测试范式来评估短间隔皮质内抑制和短潜伏传入抑制,从而评估初级运动皮层兴奋性。根据间歇性 theta-burst 刺激引起的运动诱发电位幅度的变化,对类似可塑性的机制进行了索引。结果 患者在手指敲击过程中表现出缓慢和节律改变。运动缓慢与患者的短潜伏期传入抑制减少相关,因此表明胆碱能系统的退化也可能与阿尔茨海默病的运动障碍有关。此外,患者运动节律的改变与额叶评估电池的较差分数相关。结论 本研究为阿尔茨海默病患者随意运动改变的病理生理学提供了新信息。意义 研究结果表明皮质胆碱能缺陷可能是阿尔茨海默病运动缓慢的基础。
更新日期:2020-04-01
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