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首页> 外文期刊>Clinical neurophysiology >Deficits in sensorimotor control during precise hand movements in Huntington's disease.
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Deficits in sensorimotor control during precise hand movements in Huntington's disease.

机译:在亨廷顿氏病中,精确的手部动作过程中感觉运动控制不足。

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摘要

OBJECTIVES: To investigate the performance of patients with Huntington's disease (HD) while manipulating objects using a precision grip. METHODS: The grip forces developed by the fingers were studied while subjects lifted an object of unpredictable weight in the hand. The ability to stabilize grip force after externally imposed weight change was also studied. RESULTS: Patients used higher grip forces than the normal subjects in both the lifting and holding phases, particularly with a lighter weight. Lift timing was slowed in the patients, most markedly with a lighter weight. Increased levels of inter-trial variation were observed only with a light weight. This indicates that the slowing in HD differs from that in Parkinson's disease, which remains constant regardless of object load, and that the slowing in HD is not due to involuntary antagonist muscle activity resulting from an underlying chorea. The grip force response to sudden weight change was normal, but appeared after a delay which increased at lower rates of weight change. CONCLUSIONS: Disturbances in precision grip timing and magnitude in HD may result from a reduced ability to process relevant tactile afferent input. The delay in the adaptive response suggests an increased threshold for detection of weight change in HD. Alternatively, this delay may arise from mediation of the response over an additional cerebellar pathway to compensate for damage to the basal ganglia.
机译:目的:研究亨廷顿氏病(HD)患者在使用精密握把操纵物体时的性能。方法:研究对象在举起手中重量不可预测的物体时手指产生的抓握力。还研究了外部施加重量变化后稳定握力的能力。结果:在抬起和保持阶段,患者使用的抓地力均比正常受试者高,尤其是体重较轻时。患者的提举时间变慢,最明显的是体重减轻。仅在重量轻的情况下观察到试验间变异的水平增加。这表明HD的减慢不同于帕金森氏病,无论物体负荷如何,HD的减慢均保持不变,并且HD的减慢不是由于潜在的舞蹈症引起的非自愿性拮抗剂肌肉活动。对突然的体重变化的抓地力响应是正常的,但是在延迟之后出现,该延迟以较低的体重变化率增加。结论:HD的精确握持时间和幅度的扰动可能是由于处理相关触觉传入输入的能力降低所致。自适应响应中的延迟提示检测HD体重变化的阈值增加。可替代地,这种延迟可能是由于通过额外的小脑途径介导的反应来补偿对基底神经节的损害而引起的。

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