Cerebral palsy (CP) is a motor disorder resulting from damage to the foetal or infant brain. With increasing life expectancy, preserving bone and muscle health is key to maintaining independence. In young adults with CP, 40% have documented osteopenia/osteoporosis1, with prevalent fractures in up to 38%2. It is unclear whether low bone mass in adults with CP is predominantly due to less bone accrual during childhood, earlier onset of bone loss or accelerated bone loss in adulthood.
We conducted a retrospective longitudinal study of 45 subjects with CP aged >10 years to investigate changes in areal bone mineral density (aBMD) during adolescence and young adulthood. The effect of ambulation, nutrition and hypogonadism on longitudinal changes in aBMD was also examined.
Mean age at first DXA was 19.4 years (range: 10 - 36 years), 57.8% were male and 80% were non-ambulatory. Mean Z-scores at baseline were <-2.0 at all sites, however these remained stable over time. The median change in aBMD was +1.2 to 1.9%/year in all subjects but in those <20 years of age, the median change was 4 to 8%/year. Peak bone mass was achieved late in the third decade of life/early in the fourth decade and plateaued thereafter. Reduced functional state as measured by the gross motor functional classification scale (GMFCS) had a negative effect on aBMD over time.
Low baseline Z-scores remain stable over time suggesting bone mass deficits occur early in childhood. Bone accrual during puberty and subsequent maintenance parallels that of typically developing adolescents/adults, albeit at a lower set-point. This has important implications for timing of treatment, with early childhood intervention to optimise nutrition, mobility or use of pharmacological therapy likely key to adult bone health. Puberty and its associated changes in bone mass should be monitored and timely pubertal induction given if necessary.