Functional outcomes of children with dyskinetic cerebral palsy depend on etiology and gestational age.

Abstract

To elucidate the differences in etiology of dyskinetic cerebral palsy (DCP) between term-born and preterm-born children and its relationship to functional outcomes. We determined the etiology of DCP based on the clinical course and brain MRI of 163 term-born and 136 preterm-born children. Information about genetic abnormality was also collected if available. Functional outcomes were compared between the two major etiologies in each group, i.e., hypoxic ischemic encephalopathy (HIE) and bilirubin encephalopathy (BE), using four standardized classification systems, i.e., Gross Motor Function Classification System (GMFCS), Manual Ability Classification System (MACS), Communication Function Classification System (CFCS), and Eating and Drinking Ability Classification System (EDACS). The most common etiologies were HIE (123/163) in term-born and BE (93/136) in preterm-born children. Genetic mutations were identified in 14 of 30 term-born children with no other known etiology. GMFCS levels of the preterm children with BE were significantly poorer than those of term children with HIE (p<0.01). Both the CFCS and EDACS levels were significantly better in preterm children with BE than in term children with HIE (p<0.01). The most common etiology of DCP is different between term-born and preterm-born children, and the distribution of functional impairment is significantly influenced by etiology and gestational age. The difference should be taken into consideration to allow the provision of adequate interventions.