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close this bookCauses and Consequences of Intrauterine Growth Retardation, Proceedings of an IDECG Workshop, November 1996, Baton Rouge, USA, Supplement of the European Journal of Clinical Nutrition (IDECG, 1996, 100 p.)
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close this folderCurrent growth standards, definitions, diagnosis and classification of fetal growth retardation
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close this folderLevels and patterns of intrauterine growth retardation in developing countries
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close this folderBirth weights and stillbirths in historical perspective
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close this folderBiological mechanisms of environmentally induced causes of IUGR
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close this folderSocioeconomic determinants of intrauterine growth retardation
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close this folderEffects of intrauterine growth retardation on mortality morbidity in infants and young children
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close this folderIntrauterine growth retardation, body size, body composition and physical performance in adolescence
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close this folderNeurodevelopmental outcome of small-for-gestational-age infants
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close this folderSmall for gestational age, term babies, in the first six years of life
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close this folderEffects of intrauterine growth retardation on mental performance and behavior, outcomes during adolescence and adulthood
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View the documentSchool age outcomes of young adolescents with intrauterine growth failure (Table 1)
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close this folderFetal growth and adult disease
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close this folderNutritional interventions to prevent intrauterine growth retardation: Evidence from randomized controlled trials
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close this folderReport of the IDECG group on definitions, classifications, causes, mechanisms and prevention of IUGR
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close this folderReport of the IDECG group on effects of IUGR on infants, children and adolescents: Immunocompetence, mortality, morbidity, body size, body composition, and physical performance
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close this folderReport of the IDECG/IUNS working group on IUGR effects on neurological, sensory, cognitive, and behavioral function
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close this folderReport of the IDECG group on variation in fetal growth and adult disease
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Conclusions

In summary, it appears that, overall, being born SGA is associated with an increase in various measures of MND (Aylward et al, 1989; Breart and Poisson-Salomon, 1988; Allen, 1984; Teberg et al, 1988). Major motor and cognitive disability is rare in SGA infants, but is probably significantly increased when evaluated in large sample sizes. Boys seem to be more affected by being SGA than girls, and children born into the low social classes seem to be more affected than other children. If the SGA develops early so that it affects head growth before 26 weeks, there seems to be more of an impact on neurologic function than SGA which develops later (Harvey et al, 1982). Certainly SGA which is accompanied by asphyxia is more commonly associated with neurodevelopment abnormalities than SGA which is not. There does not seem to be a major relationship between SGA status and vision or hearing deficits, although there are some studies to suggest that SGA infants have more difficulty in achieving 'normal' responses to visual or auditory stimuli than do non-SGA infants.

This review suggests that SGA is a heterogeneous condition, at times but not usually associated with various types of neurodevelopment dysfunction. There are no studies we identified showing that improvements in these neurologic outcomes can be achieved by any particular course of action. Logically, however, preventing asphyxia in SGA infants should reduce the prevalence of major and minor handicaps, especially cerebral palsy and mental retardation, seen in some of these infants, particularly those who are asymmetric and associated with maternal hypertension. It is less clear if interventions directed at the more symmetric or uniformly under-grown infants will be able to improve outcome in the relatively small percentage of these children who have major developmental problems associated with being SGA.

Acknowledgement - This project is funded by the Agency for Health Care Policy Research (AHCPR) Contract #290-92-0055.