Modeling of post-stroke stimulation of cortical tissue.

Following a stroke, cortical networks in the penumbra area become fragmented and partly deactivated. We develop a model to study the propagation of waves of electric potential in the cortical tissue with integro-differential equations arising in neural field models. The wave speed is characterized by the tissue excitability and connectivity determined through parameters of the model. Post-stroke tissue damage in the penumbra area creates a hypoconnectivity and decreases the speed of wave propagation. It is proposed that external stimulation could restore the wave speed in the penumbra area under certain conditions of the parameters. Model guided cortical stimulation could be used to improve the functioning of cortical networks.

Sensorimotor mapping affects movement correction deficits in early Huntington's disease.

Huntington's disease (HD) is associated with early voluntary movement problems linked to striatal dysfunction. In pointing movements, HD increases the irregularity of the terminal part of movements, suggesting a dysfunction in error feedback control. We tested this hypothesis in movements requiring continuous feedback control. Patients in the early stages of HD and controls traced as fast and accurately as possible circles within a 5-mm annulus on a digitizing tablet when visual feedback of the hand and the circle was direct or indirect (through a monitor). Patients deviated more often from the annulus and showed larger corrections toward the circle than controls when using indirect visual feedback but not with direct visual feedback. When velocity requirements were removed, patients showed little change in these control problems. These results suggest that HD does not affect error feedback control in all movements and that the striatal contribution to voluntary movement is sensitive to sensorimotor mapping.