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PURPOSE OF REVIEW: Cerebral palsy is the most common and visible motor disability of childhood. Its aetiology remains a topic of hot debate between those who see it as a reflection of medical mismanagement of an avoidable complication and those who see its origins in the development of the fetal brain affected at many points along a causal pathway to damage. This review outlines the themes of research publications over the year 2004/2005. RECENT FINDINGS: The review looks at recent findings relating to epidemiology, infection and inflammation, prematurity, multiple pregnancy, thrombophilias, genetics, placenta, neuroimaging and rescue therapies in cerebral palsy. SUMMARY: Papers this year have helped clarify risk groups and identify some areas (e.g. the management of thrombophilias and the potential of induced hypothermia) with the potential to be rapidly introduced into clinical practice. In this enigmatic and multifactorial condition, however, progress remains slow. New tools such as magnetic resonance imaging are providing valuable insights into the lesions that result in cerebral palsy but the pathways to injury remain unclear. The future of cerebral palsy research lies in understanding the complex interactions of multiple factors on the road to cerebral palsy or in looking for final common pathways such as inflammation which may be amenable to manipulation.

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Between June 1993 and December 1996, 276 term newborn infants with encephalopathy and 564 randomly selected term controls were enrolled in a population-based study of moderate and severe term newborn encephalopathy (NE) in Western Australia. During comprehensive neurobehavioural and cognitive follow-up of all patients and controls at 3 years and again at 5 years of age we found an unexpected but strong association between NE and autism spectrum disorders (ASDs). A diagnosis of ASD by age 5 years was reached using criteria according of the Diagnostic Statistical Manual, 4th edition. Linking records to the Western Australian Disability Services Commission Register ensured that no child in the study with ASD was missed. By age 5 years, 37 (13.4%) infants with NE and one (0.2%) control had died. Among the 239 survivors of NE, 12 (5%) were diagnosed with an ASD. Of these, 10 (4.2%) met the full criteria for autism, one had pervasive developmental disorder-not otherwise specified, and one had Asperger syndrome. Among the 563 surviving controls, five (0.8%) were diagnosed with an ASD: three with autism, one with autism/possible Asperger syndrome, and one with Asperger syndrome. Compared with the controls, the children who had experienced NE were 5.9 times (95% confidence interval 2.0-16.9) more likely to have been diagnosed with an ASD.

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Cerebral palsy (CP) can occur in term infants with or without preceding newborn encephalopathy. We compared the type and severity of CP and associated disability in these two groups. Participants from a population-based case-control study of term newborn encephalopathy were followed up for 6 years and linked to the Western Australian Cerebral Palsy Register. The remaining term infants with CP for the same period were also identified from the Cerebral Palsy Register. 13% of neonatal survivors of term newborn encephalopathy had CP, a rate of 116 per 1000 term live births. Overall, 24% of term infants with CP followed newborn encephalopathy. CP following newborn encephalopathy was more likely to: affect males (72% vs 56%); be severe (47% vs 25%); and be of spastic quadriplegia or dyskinetic types. Cognitive impairment was more common (75% vs 43%) and severe (41% vs 16%), as was epilepsy (53% vs 29%) in survivors of encephalopathy. These children were also more likely to: be non-verbal (47% vs 22%); have a severe composite disability score (47% vs 26%); and die between time of diagnosis of CP and age 6 years (5-year cumulative mortality 19% vs 5%). Children born at term who develop CP following newborn encephalopathy have a poorer prognosis than those with CP who were not encephalopathic in the first week of life.

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OBJECTIVE: The aim of this study was to ascertain the early developmental status of children who have a history of newborn encephalopathy. METHODS: A longitudinal follow-up was conducted of a population-based, case-control study of children born in Western Australia between June 1993 and December 1996. The study included 276 term children (>/=37 weeks' gestation) with moderate or severe newborn encephalopathy and 564 unmatched term control subjects. The Griffiths Mental Development Scales was used to ascertain developmental status and a General Quotient (GQ) score. Outcome measures were the Griffiths developmental subscales, GQ, diagnosis of cerebral palsy, and mortality. RESULTS: Thirty-four patients and 1 control subject died before reaching assessment. Between June 1994 and December 1999, 195 (81%) eligible patients and 445 (79%) eligible control subjects were assessed. Statistically significant differences were found between patients and control subjects for GQ and all developmental subscales. Overall, 39% of patients had a poor outcome as defined by death, cerebral palsy, or a significant degree of developmental delay, compared with 2.7% of control subjects. Furthermore, 62% of those with severe encephalopathy had a poor outcome compared with 25% of those with moderate encephalopathy. Patients with a history of seizures were 3 times more likely to develop cerebral palsy than patients without. Overall, 28 (10.1%) of patients have cerebral palsy. CONCLUSIONS: These data provide important prognostic information regarding survival and serious disability and indicate that newborn encephalopathy places children at significant risk of developmental delay by their second year. These findings also suggest that comprehensive clinical and educational assessments are required to enable appropriate educational provisions as these infants approach school entry.

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