ABSTRACT
Cerebral palsy (CP) is the term applied to a heterogeneous group of permanent disorders of the development of movement and posture, causing limitation of activity, that are attributable to non-progressive disturbances that occurred in the developing fetal or infant brain. The motor disorders are often accompanied by disturbances of sensation, perception, cognition, communication and behaviour, epilepsy and secondary musculoskeletal problems.1,2
CP constitutes the most common cause of chronic childhood disability, with the prevalence estimated to be between two and three per 1000 live births.3 The aetiology includes congenital brain malformations (5-15%); prenatal causes (50-70%), such as intra-uterine infections, placental malformations, complications of prematurity, brain haemorrhages and stroke (pre-or neonatal); perinatal causes such hypoxic-ischaemic encephalopathy (10%); and post-natal causes (10-25%), such as head injury, metabolic encephalopathy, hyperbilirubinaemia and infections. CP may result from the interaction of multiple risk factors, and, in some cases, there may not be an
identifiable cause. Prematurity is the most common risk factor for CP owing to the fragile cerebral vasculature, immature autoregulation of cerebral blood flow and the vulnerable cerebral parenchyma. Other risk factors include low birth weight, multiple births, intra-uterine infections, Apgar scores <5 at 5 minutes, post-natal hyperbilirubinaemia and maternal disorders (e.g. diabetes). A number of genetic disorders (Rett syndrome, fragile X syndrome, familial or hereditary spastic paraparesis) and metabolic disorders (mucopolysaccharidoses, phenylketonuria, etc.) can masquerade as CP.
