Computational model of the role of sensory disorganization in focal task-specific dystonia.
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.
Sanger
T D
TD
Keck Center for Integrative Neurosciences, UCSF, San Francisco, California 94143-0732, USA.
Merzenich
M M
MM
D020821:Dystonic Disorders / Q000503:physiopathology*; D006801:Humans; D008959:Models, Neurological; D009044:Motor Cortex / Q000503:physiopathology; D009046:Motor Neurons / Q000502:physiology; D009068:Movement / Q000502:physiology; D009473:Neuronal Plasticity / Q000502:physiology; D009475:Neurons, Afferent / Q000502:physiology*; D011187:Posture / Q000502:physiology; D011597:Psychomotor Performance / Q000502:physiology; D012678:Sensation Disorders / Q000503:physiopathology*; D013003:Somatosensory Cortex / Q000502:physiology*; D014836:Volition / Q000502:physiology