|Causes and Consequences of Intrauterine Growth Retardation, Proceedings of an IDECG workshop, November 1996, Baton Rouge, USA, Supplement of the European Journal of Clinical Nutrition (International Dietary Energy Consultative Group - IDECG, 1996, 100 pages)|
|Effects of intrauterine growth retardation on mental performance and behavior, outcomes during adolescence and adulthood|
In general, the follow-up studies report overall normal intelligence with a trend to lower scores among IUGR subjects. Despite the limitations of the literature reviewed, there is no consistent evidence of a detrimental effect of IUGR on the mental and behavioral outcomes of adolescents or adults. The rates of major handicap are low, although there tend to be higher rates of minimal cerebral dysfunction, as evidenced by learning and subtle neurological and behavioral problems in IUGR children with normal intelligence. Three of the studies noted a decrease in the rates of abnormal neurodevelopment with increasing age (Douglas and Gear, 1976; Hawdon et al, 1990; Westwood et al, 1983) which could be associated with an amelioration of subtle neurological dysfunction after the onset of puberty. Support for this hypothesis is the work of Soorani-Lunsing (1993), who reported that onset of puberty was associated with a decrease in the rates of neurologic dysfunction, including fine manipulative disability, coordination problems, choreiform dyskinesia and hypotonia. She hypothesized that general maturational changes during puberty, as well as specific hormonal changes in estrogen secretion, might play a role in improving outcome.
The review of the literature reveals that ongoing detrimental effects of socio-environmental deprivation throughout the lifespan play a much greater role in determining outcome than any potential effect of intrauterine growth failure on the developing nervous system (Douglas and Gear, 1976; Hawdon et al, 1990; Drillien, 1970; Westwood et al, 1983; Illsley and Mitchell, 1984; Neligan et al, 1976; Low et al, 1992; Martyn et al, 1996; Stein et al, 1972). Warshaw (1985) has suggested that rather than representing serious pathology, IUGR may be an adaptation in which the size of the fetus is maintained appropriate to the availability of nutrients. The most consistent biologic predictors of poor later mental development and behavior in IUGR children are hypoxic ischemic injury and subnormal brain growth (Westwood et al, 1983; Berg, 1989; Ounsted et al, 1988; Harvey et al, 1982; Parkinson et al, 1981). Brain growth, as measured by the sonographic biparietal diameter or by head circumference after birth, is usually less affected than weight or length, resulting in "asymmetric" growth failure (Cooke et al, 1977; Kramer et al, 1989). This "brain sparing" may be protective when growth is restricted in utero, and outcome may be affected when this mechanism fails. This is especially evident when brain growth (head size) fails to catch up during infancy and childhood (Hack et al, 1989, 1991; Babson and Henderson, 1974; Lipper et al, 1981).
Thus, with the exception of extreme IUGR affecting brain growth, and hypoxic ischemic injury, IUGR seems to have little or no measurable effect on mental performance and behavior in adolescence or adulthood. However, since IUGR occurs more often in deprived environmental circumstances, it can serve as a marker for the associated poor outcomes throughout life.