Leg muscle activation during gait in Parkinson's disease: adaptation and interlimb coordination.

Adaptation in leg muscle activity and coordination between lower limbs were studied during walking on a treadmill with split belts in one group of parkinsonian patients and one of age-matched healthy subjects. Four different belt speeds (0.25/0.5/0.75/1.0 m/sec) were applied in selected combinations to the left and right leg. While these walking conditions were easily tolerated by the healthy subjects, the parkinsonian patients usually reached the limits of their walking capabilities. Both groups adapted automatically to a change in belt speed within approximately 20 stride cycles. Healthy subjects adapted by reorganizing their stride cycle with a relative shortening of duration of support and lengthening of the swing phase of the "fast" leg and vice versa on the "slow" leg. The patients showed a restricted range of stride frequencies for the various belt speeds during normal and split-belt walking with consequent deviations in the reorganization of the stride cycle. In both healthy subjects and patients, ipsilateral gastrocnemius and contralateral tibialis anterior electromyographic (EMG) activity increased predominantly with an ipsilateral increase in belt speed. Two main differences were observed in the EMG patterns: (1) In the patients leg muscle EMG activity was less modulated and gastrocnemius EMG amplitude was small during normal and split-belt walking. However, there was no significant difference between the two groups in respect to the reorganization of the EMG pattern required for the various split-belt walking conditions. (2) The amount of co-activation of antagonistic leg muscles during the support phase of the stride cycle was greater in the patients compared to the healthy subjects during normal and split-belt walking. It is suggested that reduced EMG modulation and recruitment in the leg extensors may contribute to the impaired walking of the patients. This in turn is a result of an impaired proprioceptive feedback from extensor load receptors. This defective control is partially compensated for in parkinsonian patients by a greater amount of leg flexor activation which leads to a higher degree of co-activation. Visual input plays a role in the control of this increased activation.