Neonatal encephalopathy (NE) following perinatal asphyxia (PA) is considered an important cause of later neurodevelopmental impairment in infants born at term. This review discusses long-term consequences for general cognitive functioning, educational achievement, neuropsychological functioning and behavior. In all areas reviewed, the outcome of children with mild NE is consistently positive and the outcome of children with severe NE consistently negative. However, children with moderate NE form a more heterogeneous group with respect to outcome. On average, intelligence scores are below those of children with mild NE and age-matched peers, but within the normal range. With respect to educational achievement, difficulties have been found in the domains reading, spelling and arithmetic/mathematics. So far, studies of neuropsychological functioning have yielded ambiguous results in children with moderate NE. A few studies suggest elevated rates of hyperactivity in children with moderate NE and autism in children with moderate and severe NE. Conclusion: Behavioral monitoring is required for all children with NE. In addition, systematic, detailed neuropsychological examination is needed especially for children with moderate NE.

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NE has a mildly negative effect on behavioral functioning, but does not lead to elevated levels or specific patterns of developmental psychopathology.

Children with moderate HIE had smaller hippocampal volumes than controls, with a trend toward smaller volumes following mild HIE. Reduced hippocampal volumes were associated with poorer long-term visuospatial memory.

in addition to a global effect on intelligence, NE had a specific effect on verbal working memory, verbal and visuo-spatial long-term memory, and learning, which was associated with degree of NE. Although these memory problems occurred in children without CP, they were more pronounced when children had also developed CP.

ABSTRACT:Magnetic resonance imaging studies have contributed to recognize the patterns of cerebral injury related to neonatal encephalopathy (NE). We assessed whether a smaller corpus callosum (CC) explained the difference in motor performance between school-age children with NE and controls. Frontal, middle, and posterior areas of the CC were measured in 61 9 -10-y-old children with NE and in 47 controls. Motor performance was determined using the Movement Assessment Battery for Children (M-ABC). Linear regression was used to assess whether differences in M-ABC between NE children and controls could be explained by CC size. The CC of 11/30 children with NE type I according to Sarnat (NE I) and 19/36 children with NE type II according to Sarnat (NE II) showed generalized or focal thinning, compared with 8/49 controls. Children with NE II had significantly smaller middle and posterior parts and total areas of the CC. Children with NE scored significantly worse on the M-ABC than controls. The reduction in size of the posterior part of the CC partly explained the mean differences on the M-ABC. Children with NE have poorer motor skills than controls, which is partly explained by a smaller size of the CC. N eonatal encephalopathy (NE) related to perinatal asphyxia has a prevalence of 1-6/1000 live-born, full-term infants (1). Long-term follow-up data of neurodevelopmental outcome are still scarce but have shown significantly more problems at school age in children with moderate NE (NE II) according to the criteria of Sarnat (2) compared with children with mild NE according to the criteria of Sarnat (NE I) and matched controls (3-6). Magnetic resonance imaging (MRI) studies have made a major contribution to recognize the different patterns of NErelated cerebral lesions, which have been shown to be predictive of long-term neurodevelopmental outcome (7-10).The corpus callosum (CC) links associative areas of the two cerebral hemispheres. The genu of the CC is formed between 8 and 13 wk of gestation. After 20 wk gestational age the total CC is formed (11). The CC is among the last structures to be completed during postnatal maturation. Its size increases with age until early adulthood because of the ongoing myelinization process, which begins to appear at about 4 mo of age in the splenium and at 6 mo in the genu (12,13). Due to its longer myelogenetic cycle, the CC is vulnerable to hemorrhage and ischemia (14). Fibers from the frontal lobe and the anterior part of the parietal lobe course through the rostrum and genu of the CC. Fibers from the temporal, posterior part of the parietal and occipital lobe are carried in the caudal portion of the body of the CC and in the splenium (14,15).Several studies have shown a relation between the CC size and motor outcome in preterm infants (16 -18). Maneru et al. (19) demonstrated that the CC was smaller in adolescents who suffered from moderate asphyxia than in controls. The CC measurements correlated with neuropsychological performance.In the present study, we assessed the differ...

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