In an earlier study we identified severe Vitamin D deficiency as a problem in institutionalised children with cerebral palsy (CP), which resulted in rickets and a high incidence of fractures. The purpose of this study was to establish whether a cohort of non-ambulatory children with CP, living at home, presented with Vitamin D deficiency. The participants were a consecutive sample (N=100) of non-ambulatory children with CP attending a CP outpatient clinic. Their ages ranged from 2 to 15 years (mean 5.8, SD 3.3 years). There were 57 males and 43 females. Nineteen were on Level IV of the Gross Motor Function Classification System (GMFCS), and 81 were on Level V. 66% were on anticonvulsant therapy (ACT). Basic demographic data was collected, and measurements included blood sample analysis and wrist radiographs. There was radiographic evidence of osteopenia and delayed ossification of the carpal bones.Aim
Method
Osteogenesis imperfecta (OI) is characterised by decreased bone density and increased bone fragility. We studied the effect of bisphosphonates on clinical features and bone mass, enrolling to the study 22 children with OI treated with these drugs. Sixteen of them received continuous oral alendronate and six received cyclical IV pamidronate. Evaluation included mobility score, fracture rate, chemistry of skeletal remodelling, iliac crest biopsy and DEXA assessment of bone mass. After 18 months of bisphosphonate therapy, 10 patients were fully assessed. There was a definite clinical improvement, with significantly improved mobility (p =0.04), a reduction in the annualised fracture rate from 1.27 to 0.44, and significant improvement in bone mass density (p =0.01).
The purpose of this study was to determine factors contributing to the high incidence of fractures in patients with spastic quadriplegic cerebral palsy in residential care, and to assess the effect of vitamin D therapy. Over a period of four years, 20 patients in a cohort of 88 had sustained 56 long bone fractures. We compared them to an age-matched group from the same cohort with no history of fractures. The mobility of patients, who spent their time indoors, was severely restricted in both groups. There was radiological and biochemical evidence of rickets and osteomalacia in both groups, but the disease was more severe in the fracture group. There was a significant relationship between the number of fractures and the use of anticonvulsant therapy. Administration of vitamin D (5 000 IU per day) to both the fracture and control group over three months resulted in a marked increase in mean serum calcium (p =0.01), and a dramatic decrease (p <
0.003) in mean alkaline phosphatase to a level just above normal. All non-ambulatory residents with cerebral palsy now receive a maintenance dose of 50 000 IU of calciferol a month. No further fractures have occurred since vitamin D administration. We recommend vitamin D supplementation for all non-ambulatory children with cerebral palsy in residential care who do not get regular exposure to sunlight.
