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Cerebral palsy: phenotypes and risk factors in term singletons born small for gestational age.
BACKGROUND AND OBJECTIVES: Children born small for gestational age (SGA) are at increased risk of developing cerebral palsy (CP). The pathophysiology behind this association remains unclear. We compare the clinical profile of children with CP born SGA to other children with CP. We hypothesize that differences noted will support antenatal causes of CP in children born SGA.
METHODS: We conducted a retrospective cohort study of term singletons with CP, extracting data from the Canadian Cerebral Palsy Registry. SGA was determined as birth weight for gestational age and sex below the tenth percentile.
RESULTS: Mothers of children with CP born SGA were more likely to be of African-American ethnicity (RR 2.54, 95% CI 1.20-5.39), have intrauterine infections (RR 2.22, 95% CI 1.09-4.50) and have gestational hypertension (RR 1.78, 95% CI 1.06-3.00). Children with CP born SGA had smaller head circumferences at birth (p < 0.001) and higher frequencies of emergency cesarean-section (RR 1.53, 95% CI 1.22-1.92), birth asphyxia (RR 1.53, 95% CI 1.0-2.32), and placental abnormalities (RR 1.45, 95% CI 1.00-2.10). Children with CP born SGA had greater fine motor (RR 1.46, 95% CI 1.02-2.11), gross motor (RR 1.53, 95% CI 1.12-2.10) and communication impairment (RR 1.24, 95% CI 1.10-1.40), and a higher frequency of cognitive impairment (RR 1.33, 95% CI 1.06-1.69).
CONCLUSION: Children with CP born SGA have different clinical factors and phenotypic profiles than other children with CP. These differences support the hypothesis of antenatal and perinatal causes of CP in children born SGA. Future case control studies would be desired to further define this causal pathway.
METHODS: We conducted a retrospective cohort study of term singletons with CP, extracting data from the Canadian Cerebral Palsy Registry. SGA was determined as birth weight for gestational age and sex below the tenth percentile.
RESULTS: Mothers of children with CP born SGA were more likely to be of African-American ethnicity (RR 2.54, 95% CI 1.20-5.39), have intrauterine infections (RR 2.22, 95% CI 1.09-4.50) and have gestational hypertension (RR 1.78, 95% CI 1.06-3.00). Children with CP born SGA had smaller head circumferences at birth (p < 0.001) and higher frequencies of emergency cesarean-section (RR 1.53, 95% CI 1.22-1.92), birth asphyxia (RR 1.53, 95% CI 1.0-2.32), and placental abnormalities (RR 1.45, 95% CI 1.00-2.10). Children with CP born SGA had greater fine motor (RR 1.46, 95% CI 1.02-2.11), gross motor (RR 1.53, 95% CI 1.12-2.10) and communication impairment (RR 1.24, 95% CI 1.10-1.40), and a higher frequency of cognitive impairment (RR 1.33, 95% CI 1.06-1.69).
CONCLUSION: Children with CP born SGA have different clinical factors and phenotypic profiles than other children with CP. These differences support the hypothesis of antenatal and perinatal causes of CP in children born SGA. Future case control studies would be desired to further define this causal pathway.
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