Reduced reciprocal inhibition during passive spasticity assessments is related with increased muscle co-activation during perturbations of standing balance

Abstract

Children with cerebral palsy (CP) often have balance impairments, but little is known about the relation between joint hyper-resistance (i.e., the most common symptom in spastic CP) and balance impairments (1). Both during clinical tests of joint hyper-resistance and when standing balance is perturbed, muscles are stretched. In children with CP, the stretch reflex in response to passive joint rotations is often hyper-excitable and reduced reciprocal inhibition has been observed in the antagonistic muscle (2). Furthermore, children with CP often have increased muscle co-activation during standing balance perturbations (3). Recently, we demonstrated that this increased muscle co-activation is not a useful compensation strategy and might therefore be a consequence of reduced reciprocal inhibition (4). Here, we investigated whether a reduction in reciprocal inhibition between plantarflexors and dorsiflexors in response to a passive stretching of the plantarflexors was related to higher levels of co-activation in response to toe-up rotational perturbations of standing balance. Twenty children with spastic CP participated in the study. We performed an instrumented spasticity assessment of the plantarflexors (5) followed by a standing balance assessment (Fig. 1, row1-2). During the instrumented spasticity assessment, the ankle was rotated as fast as possible from a plantar flexed position until the end of range of motion towards dorsiflexion. At least 7 seconds of rest were provided between different trials, five in total. Reactive standing balance was tested on a moving platform. Participants were instructed to maintain balance without stepping and the platform was rotated such that ankle dorsiflexion was elicited. Perturbations were repeated 8 times. Electromyography (EMG) from gastrocnemius lateralis (LG) and medialis (MG), soleus (SOL) and tibialis anterior (TA) was collected during both assessments. EMG was filtered and normalized to the maximal value across assessments (Fig. 1, row 3). We calculated the co-contraction index (CCI) as the overlap between TA and respectively LG, MG, and SOL EMG (6). We tested the relation between the CCI during passive joint rotations and reactive standing balance. The CCI between the plantarflexors and tibialis anterior during spasticity assessment was moderately correlated with the CCI during reactive balance responses (LG-TA: r=0.55; p= 0.02; MG-TA: r= 0.57, p=0.01; SOL-TA: r=0.54, p=0.02; Fig. 1, row 4). Fig. 1: Correlation between co-contraction index during instrumented spasticity assessment and perturbations of standing balance.Download : Download high-res image (242KB)Download : Download full-size image Our results suggest that deficits in spinal pathways governing the stretch reflex, and more specifically reduced reciprocal inhibition, might hinder reactive balance control. Successful postural control might therefore rely on compensations in supraspinal pathways to generate net balance correcting ankle moments. We need to further explore whether increased co-activation also results in worse balance performance.