Motor overflow in the lower limb after stroke: Insights into mechanisms.

Motor overflow (involuntary muscle activation) is common after stroke, particularly in the non-paretic upper limb. Two potential cortical mechanisms are as follows: (1) The contralesional hemisphere controls both limbs, and (2) inhibition from the ipsilesional to the contralesional hemisphere is diminished. Few studies have differentiated between these hypotheses or investigated motor overflow in the lower limb after stroke. To investigate these potential mechanisms, individuals with chronic stroke performed unilateral isometric and dynamic dorsiflexion. Motor overflow was quantified in the contralateral, resting (non-target) ankle. Transcranial magnetic stimulation (TMS) was applied, and responses were measured in both legs. Relations between motor overflow, excitability of ipsilateral motor pathways, and interhemispheric inhibition were assessed. Non-target muscle activity (motor overflow) was greater during isometric and dynamic conditions than rest in both legs (p ≤ 0.001) and was higher in the non-paretic than the paretic leg (p = 0.03). Some participants (25%) had motor overflow >4SD above the group mean in the non-paretic leg. Greater motor overflow in the non-paretic leg was associated with lesser inhibition from the ipsilesional to the contralesional hemisphere (p = 0.04). In both legs, non-target TMS responses were greater during the isometric and dynamic than the rest condition (p ≤ 0.01) but not when normalized to background muscle activity. Overall, motor overflow occurred in both legs after stroke, suggesting a common bilateral mechanism. Our correlational results suggest that alterations in interhemispheric inhibition may contribute to motor overflow. Furthermore, the lack of differences in non-target motor evoked potentials MEPs between rest, isometric, and dynamic conditions suggests that subcortical and/or spinal pathways may contribute to motor overflow.