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Cerebral palsy affects about two in every 1000 liveborn infants, but the birth prevalence is some 20–80 times higher among very low birthweight (VLBW, <1500 g) infants than among infants with a birthweight >2500 g. There is evidence that in industrialised societies the prevalence and severity of cerebral palsy among VLBW infants increased during the 1980s, but both may have fallen since then. With improved neonatal care more VLBW infants have survived. Now data from 16 centres in eight European countries have confirmed the fall in prevalence (Mary Jane Platt and colleagues. The Lancet 2007;369:43–50; see also Comment, ibid: 7–8).
The Surveillance of Cerebral Palsy in Europe (SCPE) network was set up in 1998. Data published in 2002 showed a prevalence of cerebral palsy of 73 per 1000 neonatal survivors among VLBW infants and 1.2 per 1000 among normal birthweight infants. Between 1980 and 1996 the 16 centres reported 7884 children with cerebral palsy from birth, including 2103 (27%) with birthweight <1500 g or gestational age <32 weeks. Infants of birthweight <1000 g who had cerebral palsy were more likely than those of birthweight 1000–1500 g to be female and to have hemiplegic cerebral palsy. Twenty per cent of VLBW infants with cerebral palsy were from multiple pregnancies. The cerebral palsy was spastic in 94% of cases and 24% of spastic cerebral palsies were hemiplegic. The birth prevalence of cerebral palsy among VLBW infants was 61 per 1000 in 1980 and 40 per 1000 in 1996. The fall in prevalence among infants of birthweight 1000–1500 g was from 64 to 29 per 1000 live births, but there was no significant change among infants of birthweight <1000 g. Male infants were more at risk in the higher but not the lower birthweight group.
The decline in cerebral palsy among VLBW infants between 1980 and 1996 was largely due to a decrease in bilateral spastic cerebral palsy among infants of birthweight 1000–1500 g, suggesting a decline in periventricular leukomalacia rather than periventricular haemorrhage which largely causes unilateral cerebral palsy.