title: Origin and timing of brain lesions in term infants with neonatal encephalopathy.
abstract: BACKGROUND
  The role of intrapartum asphyxia in neonatal encephalopathy and seizures in term infants is not clear, and antenatal factors are being implicated in the causal pathway for these disorders. However, there is no evidence that brain damage occurs before birth. We aimed to test the hypothesis that neonatal encephalopathy, early neonatal seizures, or both result from early antenatal insults.
  
  
  METHODS
  We used brain MRI or post-mortem examination in 351 fullterm infants with neonatal encephalopathy, early seizures, or both to distinguish between lesions acquired antenatally and those that developed in the intrapartum and early post-partum period. We excluded infants with major congenital malformations or obvious chromosomal disorders. Infants were divided into two groups: those with neonatal encephalopathy (with or without seizures), and evidence of perinatal asphyxia (group 1); and those without other evidence of encephalopathy, but who presented with seizures within 3 days of birth (group 2).
  
  
  RESULTS
  Brain images showed evidence of an acute insult without established injury or atrophy in 197 (80%) of infants in group 1, MRI showed evidence of established injury in only 2 infants (<1%), although tiny foci of established white matter gliosis, in addition to acute injury, were seen in three of 21 on post-mortem examination. In group 2, acute focal damage was noted in 62 (69%) of infants. Two (3%) also had evidence of antenatal injury.
  
  
  CONCLUSIONS
  Although our results cannot exclude the possibility that antenatal or genetic factors might predispose some infants to perinatal brain injury, our data strongly suggest that events in the immediate perinatal period are most important in neonatal brain injury.
authors.affiliation: Department of Paediatrics, Faculty of Medicine, Imperial College, Hammersmith Hospital, London, UK. f.cowan@imperial.ac.uk
authors.forename: Frances
authors.initials: F
authors.lastname: Cowan
authors.forename: Mary
authors.initials: M
authors.lastname: Rutherford
authors.forename: Floris
authors.initials: F
authors.lastname: Groenendaal
authors.forename: Paula
authors.initials: P
authors.lastname: Eken
authors.forename: Eugenio
authors.initials: E
authors.lastname: Mercuri
authors.forename: Graeme M
authors.initials: GM
authors.lastname: Bydder
authors.forename: Linda C
authors.initials: LC
authors.lastname: Meiners
authors.forename: Lilly M S
authors.initials: LM
authors.lastname: Dubowitz
authors.forename: Linda S
authors.initials: LS
authors.lastname: de Vries
mesh_terms: D001921:Brain / Q000473:pathology; D001925:Brain Damage, Chronic / Q000151:congenital* / Q000175:diagnosis; D002544:Cerebral Infarction / Q000151:congenital / Q000175:diagnosis; D020936:Epilepsy, Benign Neonatal / Q000175:diagnosis*; D005260:Female; D005311:Fetal Hypoxia / Q000175:diagnosis*; D005865:Gestational Age; D006801:Humans; D007231:Infant, Newborn; D008279:Magnetic Resonance Imaging; D008297:Male; D011247:Pregnancy; D011379:Prognosis; D012307:Risk Factors