|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)|
|Neurodevelopmental outcome of small-for-gestational-age infants|
The relationship of SGA to minimal neurologic dysfunction (MND) is clearer than its relationship to cerebral palsy, predominantly because MND is more common, occurring in 10 to 35% of SGA populations, and very large sample sizes are not necessary to define this relationship (Chiswick, 1985). On the other hand a major problem in quantifying the relationship is that MND is not very well defined, and the term is used differently in different studies. In one of the first studies to evaluate outcome of SGA infants, Fitzhardinghe and Steven (1972) found very high rates of MND in a group of SGA children, but did not have appropriate controls. Hadders-Algra et al (1988), evaluated MND in four groups. Fifteen percent of full term AGA infants had MND compared to 24% of full term SGA infants. Preterm AGA infants had a 26% rate of MND while 37% of preterm SGA infants had MND. In a later study, Hadders-Algra and Touwen (1990) found little difference in the rate of MND between term AGA infants (16%) and the less severe term SGA infants (22%). On the other hand, the most severe SGA infants had more than double the rate of MND (41%) compared to the term AGA infants (16%). In comparison, both the preterm AGA infants (30%) and the preteen SGA infants (40%) had higher rates of MND.
Ounsted et al (1984), found decreased verbal ability, practical reasoning and motor coordination in SGA infants compared to AGA infants, and, interestingly, found less of these conditions in LGA infants. Therefore, there appears to be a continuum in teems of infant size in relationship to MND. On the other hand, Low et al (1978; 1982; 1992), reported no significant differences in motor, cognitive handicap or developmental delay between term SGA and control infants. Martikainen (1992) found that preterm SGA infants were at a two-fold greater risk for abnormal neurologic development than term infants, and symmetric SGA infants were at greater risk for MND than asymmetric infants. Evaluating hypotonia as the outcome, Touwen et al (1988), found this condition in 11% of full-term SGA children at age six, but in none of the control term AGA children. Walther (1988), found a moderate increase in school failure in SGA infants, probably secondary to 'soft' neurologic signs and behavioral characteristics such as hyperactivity, poor concentration and clumsiness.
Veelken et al (1992), found an increase in minor neurologic abnormalities in < 1500 g SGA infants compared to control infants. Similarly, Smedler et al (1992), studying 15 < 1500 g SGA infants at 10 years of age, found that these infants scored significantly lower on measures of visio-spatial ability, non-verbal reasoning, strategy formation and gross motor coordination. Low et al (1992), evaluating learning deficits at 9-11 years in both term and preterm SGA infants, found an approximate doubling of learning deficits compared to gestational age matched controls.
Spinillo et al (1993, 1995), in a series of studies, found that SGA infants of hypertensive mothers were snore likely to have mild neurologic findings such as hypotonia than idiopathic SGA infants. Severely SGA term infants (mean birthweight 1947 g) had more transient neurologic signs than less severely SGA infants. In a very interesting study of Israeli Army recruits, those born SGA had about a 50% increase in minor neurologic abnormalities even after adjustment for socioeconomic status, birth order and intrapartum events (Paz et al, 1995). In many studies, the severity of school problems in SGA children was influenced by the child's social class, sex, parental abilities, home environment, and preschool education (Parkinson et al, 1981). We interpret these studies to indicate that SGA infants, whether at term or preterm, are more likely to be diagnosed with various components of minimal neurologic dysfunction than non-SGA infants.