Understanding postural control in children with spastic cerebral palsy: novel insights from a sensorimotor perspective

Abstract

Everyday activities such as walking down stairs, moving through a dimly lit space, or reacting to an unexpected push all challenge a person's balance in different ways. The ability to maintain, achieve, or restore balance across such situations is known as postural control, and it depends on several underlying systems working together: maintaining spatial orientation, integrating and reweighting sensory information, generating timely and appropriately-scaled movement responses, and controlling balance during gait. In children with spastic cerebral palsy (sCP), postural control difficulties are common and a central focus of rehabilitation, but they vary greatly between children, an inter-individual variability that is not well explained by the primary motor impairments of sCP alone. This thesis therefore examined three crucial yet underexplored contributing factors: lower limb proprioception (the sense of joint position), brain lesion characteristics, and exercise-induced lower limb muscle fatigue. A standardized kinematic-based Joint Position Reproduction protocol was developed and validated to assess proprioception at the hip, knee, and ankle (Chapter 2). Applying this protocol showed that children with sCP have generalized proprioceptive deficits across all three joints compared to typically developing peers. While the overall severity of these deficits was similar between children with unilateral and bilateral sCP, the two groups differed in how deficits were distributed across joints and body sides (Chapter 3). These joint-specific deficits related to postural control in a joint- and system-specific manner: hip proprioception was particularly relevant in children with sCP, relating to postural control across multiple systems, whereas ankle proprioception was primarily linked to reactive movement responses, in both children with sCP and typically developing peers (Chapter 4). Brain lesion extent and the specific structures involved, rather than lesion type, explained which postural control systems were most affected. Involvement of subcortical sensory relay structures, particularly the thalamus and the posterior limb of the internal capsule, was associated with difficulties in spatial orientation and sensory reweighting, while involvement of fronto-callosal motor regions and the brainstem was associated with difficulties in movement responses and maintaining balance during gait (Chapter 5). Exercise-induced lower limb muscle fatigue temporarily worsened both postural control and proprioception, to a similar extent in children with sCP and typically developing peers. This shared pattern suggests a general physiological response rather than one specific to sCP, though it likely carries greater everyday consequences for children with sCP given their pre-existing sensorimotor impairments (Chapter 6). Together, these findings indicate that postural control difficulties in sCP cannot be reduced to a single motor deficit, but arise from sensorimotor limitations that differ between children according to their individual proprioceptive and neuroanatomical profile, and can also fluctuate within the same child depending on neuromuscular state. This explains why postural control difficulties manifest differently across tasks and everyday contexts, and supports a more individualized approach to assessment and rehabilitation in sCP.