Kristina Ahlin1, Bo Jacobsson1,2, Staffan Nilsson3, Kate Himmelmann4. 1. Department of Perinatal Center, Department of Obstetrics and Gynecology, Institute for Clinical Sciences, Sahlgrenska Academy, Sahlgrenska University Hospital/Östra, Gothenburg, Sweden. 2. Department of Genes and Environment, Division of Epidemiology, Institute of Public Health, Oslo, Norway. 3. Department of Mathematical Statistics, Institute for Mathematical Sciences, Chalmers University of Technology, Gothenburg, Sweden. 4. Department of Pediatrics, Institute for Clinical Sciences, Sahlgrenska Academy at the University of Gothenburg, Gothenburg, Sweden.
Abstract
INTRODUCTION: Antecedents of accompanying impairments in cerebral palsy and their relation to neuroimaging patterns need to be explored. MATERIAL AND METHODS: A population-based study of 309 children with cerebral palsy born at term between 1983 and 1994. Prepartum, intrapartum, and postpartum variables previously studied as antecedents of cerebral palsy type and motor severity were analyzed in children with cerebral palsy and cognitive impairment and/or epilepsy, and in children with cerebral palsy without these accompanying impairments. Neuroimaging patterns and their relation to identified antecedents were analyzed. Data were retrieved from the cerebral palsy register of western Sweden, and from obstetric and neonatal records. RESULTS: Children with cerebral palsy and accompanying impairments more often had low birthweight (kg) (odds ratio 0.5, 95% confidence interval 0.3-0.8), brain maldevelopment known at birth (p = 0.007, odds ratio ∞) and neonatal infection (odds ratio 5.4, 95% confidence interval 1.04-28.4). Moreover, neuroimaging patterns of maldevelopment (odds ratio 7.2, 95% confidence interval 2.9-17.2), cortical/subcortical lesions (odds ratio 5.3, 95% confidence interval 2.3-12.2) and basal ganglia lesions (odds ratio 7.6, 95% confidence interval 1.4-41.3) were more common, wheras white matter injury was found significantly less often (odds ratio 0.2, 95% confidence interval 0.1-0.5). In most children with maldevelopment, the intrapartum and postpartum periods were uneventful (p < 0.05). Cerebral maldevelopment was associated with prepartum antecedents, whereas subcortical/cortical and basal ganglia lesions were associated with intrapartum and postpartum antecedents. CONCLUSION: No additional factor other than those related to motor impairment was associated with epilepsy and cognitive impairment in cerebral palsy. Timing of antecedents deemed important for the development of cerebral palsy with accompanying impairments were supported by neuroimaging patterns.
INTRODUCTION: Antecedents of accompanying impairments in cerebral palsy and their relation to neuroimaging patterns need to be explored. MATERIAL AND METHODS: A population-based study of 309 children with cerebral palsy born at term between 1983 and 1994. Prepartum, intrapartum, and postpartum variables previously studied as antecedents of cerebral palsy type and motor severity were analyzed in children with cerebral palsy and cognitive impairment and/or epilepsy, and in children with cerebral palsy without these accompanying impairments. Neuroimaging patterns and their relation to identified antecedents were analyzed. Data were retrieved from the cerebral palsy register of western Sweden, and from obstetric and neonatal records. RESULTS:Children with cerebral palsy and accompanying impairments more often had low birthweight (kg) (odds ratio 0.5, 95% confidence interval 0.3-0.8), brain maldevelopment known at birth (p = 0.007, odds ratio ∞) and neonatal infection (odds ratio 5.4, 95% confidence interval 1.04-28.4). Moreover, neuroimaging patterns of maldevelopment (odds ratio 7.2, 95% confidence interval 2.9-17.2), cortical/subcortical lesions (odds ratio 5.3, 95% confidence interval 2.3-12.2) and basal ganglia lesions (odds ratio 7.6, 95% confidence interval 1.4-41.3) were more common, wheras white matter injury was found significantly less often (odds ratio 0.2, 95% confidence interval 0.1-0.5). In most children with maldevelopment, the intrapartum and postpartum periods were uneventful (p < 0.05). Cerebral maldevelopment was associated with prepartum antecedents, whereas subcortical/cortical and basal ganglia lesions were associated with intrapartum and postpartum antecedents. CONCLUSION: No additional factor other than those related to motor impairment was associated with epilepsy and cognitive impairment in cerebral palsy. Timing of antecedents deemed important for the development of cerebral palsy with accompanying impairments were supported by neuroimaging patterns.