Association Between the Initial Response After Perturbation to Standing Balance and Spasticity Measurements (1) and Kinematic Response Strategy to Restore Balance (2) in Children With Spastic Cerebral Palsy

Background:

Spasticity is a common impairment following an upper motor neuron lesion, such as cerebral palsy (CP). Children with CP suffer a lot from balance impairments, which will impair their participation in daily life activities. When clinically assessing spasticity, a passive muscle is stretched and spasticity is scored based on the observed resistance against this stretch. Similar muscle stretches also occur when standing balance is perturbed, as for example when standing on a departing bus or walking on uneven terrain.

Maintaining balance involves complex sensorimotor transformations to activate the muscle to produce the required balance correcting response. Sensorimotor processing refers to how the nervous system translates incoming sensory information about body motion into motor commands to activate muscles. In both healthy animals and humans, sensorimotor processes underlying reactive standing balance can be explained by delayed feedback from CoM kinematics. The sensitivity to the CoM disturbance have been shown to be relatively constant within one subject, but change with age, age-related cognitive decline, sensory deficits, and neurological impairments.

Both kinematic and muscle responses to perturbations of standing balance are impaired in children with CP. Children with CP have a higher chance of losing their balance, change to a stepping strategy at lower perturbation levels, and have increased muscle (co-)activation. However, it is unknown whether the underlying sensorimotor transformations are altered in CP and how these changes contribute to the altered balance responses observed in CP. Therefore, the first aim was to understand alterations in sensorimotor processing underlying reactive standing balance control in children with spastic CP.

The increased muscle co-activation that is observed in CP might be a functional compensation strategy to improve balance control. For example, muscle co-activation will increase joint stiffness and therefore resisting movement of the body with respect to the feet during backward translational perturbations. In this case, co-activation will help to maintain balance. However, it is not clear whether children with CP use the increased co-activation as compensation strategy to improve balance control or whether the muscle co-activation is a consequence of impaired balance control. When standing balance is perturbed using rotational perturbations, muscle co-activation will hinder balance control. Increased muscle co-activation and the following increased joint stiffness will couple body movement to platform movement resulting in body tilt. Hence, increasing joint stiffness might not be beneficial during rotational perturbations. Our second aim was to investigate whether children with CP use increased muscle co-activation as a compensation strategy to improve balance control or whether muscle co-activation causes balance control impairments by combining translational and rotational perturbations of standing balance.