Ambulatory children with spastic cerebral palsy have smaller bone area and deficits in trabecular microarchitecture.

Abstract

Cerebral palsy (CP) is a non-progressive neurological syndrome resulting in abnormal muscle tone, movement, and posture. It is unclear whether ambulatory children with CP have deficits in bone quantity or quality. Furthermore, the relationship between abnormal muscle tone, altered function, and bone health remains largely unexplored. This observational study investigated bone mineral density (BMD) and microarchitecture in ambulatory children with spastic CP and associations of BMD with function, muscle spasticity, and gait. Children with spasticity in both lower limbs (n = 12) aged 3-8 years were recruited. Areal BMD was measured with dual-energy x-ray absorptiometry (DXA) at the proximal femur and lateral distal femur and compared to normative data. High-resolution peripheral quantitative computed tomography (HR-pQCT) was performed at the metaphyseal tibia and radius in a subset of participants (n = 5) and compared to healthy children (n = 7). Gait pathology and cardiopulmonary function were investigated with the Gait Deviation Index, Edinburgh Visual Gait Score, and energy expenditure index. DXA aBMD Z-scores at the lateral distal femur were within a normal range. Instead, the CP group's median aBMD Z-score at the proximal femur was -1.8 (interquartile range: -2.2, -1.2, p=.03) indicating potential skeletal fragility. Strong correlations were found between gait pathology and DXA-based bone outcomes (correlation coefficient 0.62 (p=.04) to 0.73 (p=.01)) as well as energy expenditure index and DXA-based bone outcomes (correlation coefficient -0.63 (p=.03) to -0.98 (p = <0.001)). At the metaphyseal tibia, children with spastic CP had significant deficits in HR-pQCT-measured bone geometry and trabecular microarchitecture: 35% lower total area, 42% lower trabecular area, and 48% lower trabecular number than controls. HR-pQCT parameters were similar between groups at the metaphyseal radius. These differences in tibial metaphysis size and trabecular microarchitecture are similar to those observed in disuse and thus could be a result of abnormal biomechanics or low levels of physical activity.