Stretch reflex excitability in contralateral limbs of stroke survivors is higher than in matched controls

Spasticity, characterized by hyperreflexia, is a motor impairment that can arise following a hemispheric stroke. While the neural mechanisms underlying spasticity in chronic stroke survivors are unknown, one probable cause of hyperreflexia is increased motoneuron (MN) excitability. Potential sources of increased spinal MN excitability after a stroke include increased vestibulospinal (VS) and/or reticulospinal (RS) drive. Spasticity, as clinically assessed in stroke survivors, is highly lateralized, thus RS contributions to stroke-induced spasticity are more difficult to reconcile, as RS nuclei routinely project bilaterally to the spinal cord. Yet studies in stroke survivors suggest that there may also be changes in neuromodulation at the spinal level, indicative of RS tract influence. We hypothesize that after hemispheric stroke, alterations in the excitability of the RS nuclei affect both sides of the spinal cord, and thereby contribute to increased MN excitability on both paretic/spastic and contralateral sides of stroke survivors, as compared to neurologically intact subjects.

We estimated stretch reflex thresholds of the biceps brachii (BB) muscle using a position-feedback controlled linear motor to progressively indent the BB distal tendon in both spastic and contralateral limbs of hemispheric stroke survivors and in age-matched intact subjects.

Our previously reported results show a significant difference between reflex thresholds of spastic and contralateral limbs of stroke survivors recorded from BB-medial (p < 0.005) and BB-lateral (p < 0.001). For this study, we report that there is also a significant difference between the reflex thresholds in the contralateral limb of stroke subjects and the dominant arm of intact subjects, again measured from both BB-medial (p < 0.05) and BB-lateral (p < 0.05).

The reduction in stretch reflex thresholds in the contralateral limb of stroke survivors, based here on comparisons with thresholds of intact subjects, suggests an increased MN excitability on contralateral sides of stroke survivors as compared to intact subjects. This in turn supports our contention that RS tract activation, which has bilateral descending influences, is at least partially responsible for increased stretch reflex excitability, post-stroke, as both contralateral and affected sides show increased MN excitability as compared to intact subjects. Still, spasticity, presently diagnosed only on the affected side, with increased MN excitability on the affected side as compared to the contralateral side (our previous study), may be due to a different strongly lateralized pathway, such as the VS tract, which has not been directly tested here. Currently available clinical methods of spasticity assessment, such as the Modified Ashworth Scale, lack the resolution to quantify this phenomenon of a bilateral increase in MN excitability.