Modeling reaching impairment after stroke using a population vector model of movement control that incorporates neural firing-rate variability.
The directional control of reaching after stroke was simulated by including cell death and firing-rate noise in a population vector model of movement control. In this model, cortical activity was assumed to cause the hand to move in the direction of a population vector, defined by a summation of responses from neurons with cosine directional tuning. Two types of directional error were analyzed: the between-target variability, defined as the standard deviation of the directional error across a wide range of target directions, and the within-target variability, defined as the standard deviation of the directional error for many reaches to a single target. Both between- and within-target variability increased with increasing cell death. The increase in between-target variability arose because cell death caused a nonuniform distribution of preferred directions. The increase in within-target variability arose because the magnitude of the population vector decreased more quickly than its standard deviation for increasing cell death, provided appropriate levels of firing-rate noise were present. Comparisons to reaching data from 29 stroke subjects revealed similar increases in between- and within-target variability as clinical impairment severity increased. Relationships between simulated cell death and impairment severity were derived using the between- and within-target variability results. For both relationships, impairment severity increased similarly with decreasing percentage of surviving cells, consistent with results from previous imaging studies. These results demonstrate that a population vector model of movement control that incorporates cosine tuning, linear summation of unitary responses, firing-rate noise, and random cell death can account for some features of impaired arm movement after stroke.
Reinkensmeyer
David J
DJ
Department of Mechanical and Aerospace Engineering and Center for Biomedical Engineering, University of California at Irvine, Irvine, CA 92697, USA. dreiken@uci.edu
Iobbi
Mario G
MG
Kahn
Leonard E
LE
Kamper
Derek G
DG
Takahashi
Craig D
CD
D000200:Action Potentials / Q000502:physiology; D016923:Cell Death / Q000502:physiology; D002470:Cell Survival / Q000502:physiology; D006801:Humans; D008959:Models, Neurological; D009068:Movement / Q000502:physiology*; D009474:Neurons / Q000502:physiology*; D020521:Stroke / Q000503:physiopathology*