Congenital anomalies in children with cerebral palsy: A population-based record linkage study

Institute of Health and Society, Newcastle University, Newcastle upon Tyne, UK. <>
Developmental Medicine & Child Neurology (Impact Factor: 3.51). 10/2009; 52(4):345-51. DOI: 10.1111/j.1469-8749.2009.03415.x
Source: PubMed


Our aim was to determine the proportion of children with cerebral palsy (CP) who have a congenital anomaly (CA) in three regions (Isère Region, French Alps; Funen County, Denmark; Northern Region, England) where population-based CP and CA registries exist, and to classify the children according to CA subtype.
Data for children born between 1991 and 1999 were linked using electronic matching of cases. All potential matches were checked manually by each centre and verified as true matches.
A total of 1104 children with CP were born during the study period (663 males, 441 females). Of these, 166 (15%; 95% Confidence Interval [CI] 13.0-17.3) children with CP had a CA: 8.8% had a cerebral anomaly, 4.8% had a non-cerebral anomaly, and 1.4% had a non-cerebral-related syndrome or a chromosomal/genetic anomaly.
The prevalence of cerebral anomaly was highest in children with ataxic CP (41.7%) and lowest in those with dyskinetic CP (2.1%). Cerebral anomalies were found in 8.4% and 7% of children with bilateral and unilateral spastic CP respectively. The most frequent cerebral anomalies were primary microcephaly (26.5%) and congenital hydrocephalus (17.3%). The most common non-cerebral anomalies recorded were cardiac (12.6% of children with CP and CA), urinary (5.4%), and musculoskeletal (5.4%). The prevalence of cerebral anomalies was higher among children born at term (13%) than among those born preterm (3.8%). Associated sensorineural or intellectual impairments occurred more often in children with CP and cerebral anomalies. We concluded that cerebral and non-cerebral CA prevalence was higher among the CP population than in the general population of live births.

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Available from: Peter Uldall, Oct 09, 2014
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    • "There is evidence suggesting ataxic CP has different pathologic mechanisms than spastic and dyskinetic forms of CP. There is high proportion of cerebral anomalies associated with ataxic CP, and these often include the cerebellum and its connections, especially white matter (Imamura et al. 1992; Rankin et al. 2010). To highlight the differences in etiology between spastic/dyskinetic CP (mostly disruptive/acquired etiologies) and ataxic CP (genetic etiologies), some authors prefer to use the term ''non-progressive cerebellar ataxia'' instead of ataxic CP (Steinlin et al. 1999). "
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