4.4 Article

Postural Feedback Scaling Deficits in Parkinson's Disease

期刊

JOURNAL OF NEUROPHYSIOLOGY
卷 102, 期 5, 页码 2910-2920

出版社

AMER PHYSIOLOGICAL SOC
DOI: 10.1152/jn.00206.2009

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资金

  1. Korea Institute of Machinery and Materials
  2. second stage of the Brain Korea 21 Project
  3. National Institute on Aging [AG-006457]

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Kim S, Horak FB, Carlson-Kuhta P, Park S. Postural feedback scaling deficits in Parkinson's disease. J Neurophysiol 102: 2910-2920, 2009. First published September 9, 2009; doi:10.1152/jn.00206.2009. Many differences in postural responses have been associated with age and Parkinson's disease (PD), but until now there has been no quantitative model to explain these differences. We developed a feedback control model of body dynamics that could reproduce the postural responses of young subjects, elderly subjects, and subjects with PD, and we investigated whether the postural impairments of subjects with PD can be described as an abnormal scaling of postural feedback gain. Feedback gains quantify how the nervous system generates compensatory joint torques based on kinematic responses. Seven subjects in each group experienced forward postural perturbations to seven different backward support surface translations ranging from 3- to 15-cm amplitudes and with a constant duration of 275 ms. Ground reaction forces and joint kinematics were measured to obtain joint torques from inverse dynamics. A full-state feedback controller with a two-segment body dynamic model was used to simulate joint kinematics and kinetics in response to perturbations. Results showed that all three subject groups gradually scaled postural feedback gains as a function of perturbation amplitudes, and the scaling started even before the maximum allowable ankle torque was reached. This result implies that the nervous system takes body dynamics into account and adjusts postural feedback gains to accommodate biomechanical constraints. PD subjects showed significantly smaller than normal ankle feedback gain with low scaling and larger hip feedback gain, which led to an early violation of the flat-foot constraint and unusually small (bradykinetic) postural responses. Our postural feedback control model quantitatively described the postural abnormality of the patients with PD as abnormal feedback gains and reduced ability to modify postural feedback gain with changes in postural challenge.

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