Sanger T D, Merzenich M M
Keck Center for Integrative Neurosciences, UCSF, San Francisco, California 94143-0732, USA.
J Neurophysiol. 2000 Nov;84(5):2458-64. doi: 10.1152/jn.2000.84.5.2458.
We present a new computational model for the development of task-specific focal dystonia. The purpose of the model is to explain how altered sensory representations can lead to abnormal motor behavior. Dystonia is described as the result of excessive gain through a sensorimotor loop. The gain is determined in part by the sensory cortical area devoted to each motor function, and behaviors that lead to abnormal increases in sensory cortical area are predicted to lead to dystonia. Properties of dystonia including muscular co-contraction, overflow movements, and task specificity are predicted by properties of a linear approximation to the loop transformation. We provide simulations of several different mechanisms that can cause the gain to exceed 1 and the motor activity to become sustained and uncontrolled. The model predicts that normal plasticity mechanisms may contribute to worsening of symptoms over time.
我们提出了一种针对特定任务性局灶性肌张力障碍发展的新计算模型。该模型的目的是解释感觉表征的改变如何导致异常运动行为。肌张力障碍被描述为通过感觉运动环路过度增益的结果。增益部分由专门用于每种运动功能的感觉皮层区域决定，预计导致感觉皮层区域异常增加的行为会导致肌张力障碍。肌张力障碍的特征，包括肌肉共同收缩、溢出运动和任务特异性，可通过环路转换的线性近似特性来预测。我们提供了几种不同机制的模拟，这些机制可导致增益超过1且运动活动变得持续且不受控制。该模型预测，正常的可塑性机制可能会导致症状随时间推移而恶化。
