Combined translational and rotational perturbations of standing balance reveal contributions of reduced reciprocal inhibition to balance impairments in children with cerebral palsy
Fig 4
a) Graphical representation of the (extended) sensorimotor response model. Measured muscle activity (black) is reconstructed (red) using delayed feedback of CoM acceleration, velocity, displacement, and stiction (for plantar flexors only) along a balance-correcting pathway (green) and antagonistic pathway (orange; sensitive to CoM movement in the opposite direction). CoM acceleration, velocity, position, and stiction are multiplied by subject specific feedback gains (balance correcting: ka, kv, kd, ks; antagonistic pathway: ka’, kv’, kd’). Note the opposite sign of the CoM kinematics in the balance correcting (green) and antagonistic pathways (orange) of the plantar flexors (top row) and tibialis anterior (bottom row). In the extended model, both pathways are used (balance correcting and antagonistic gains), while in the simple model only the gains of the balance correcting pathway are used. b) Exemplar cases with the extended sensorimotor response model for one child with cerebral palsy (left) and one typically developing child (right) with average co-activation for perturbation level 2. Exemplar cases for children with high and low co-activation are presented in Fig E in S1 Text. Top row: center of mass kinematics; second row: measured (black) and reconstructed (red) muscle activity signals with balance correcting contribution in green and antagonistic contribution in orange; third row: balance correcting gains; bottom row: antagonistic gains (i.e., prime gains). Grey line indicated onset of perturbation. LG = lateral gastrocnemius; SOL = soleus; TA = tibialis anterior.