In the present study, we compared brain development and metabolism of small-for-gestational-age (SGA) and appropriate-forgestational-age (AGA) infants using proton magnetic resonance spectroscopy ( 1 H-MRS). We tested the hypothesis that intrauterine growth retardation caused by placental insufficiency is associated with changes in cerebral metabolism and is followed by an adverse neurodevelopmental outcome at the age of 2 y. Twenty-six AGA and 14 SGA (birth weight ϽP 2.3) preterm infants with no major ultrasound abnormalities were enrolled prospectively. At 32 and 41 wk postmenstrual age, 1 H-MRS and magnetic resonance imaging were performed. For 1 H-MRS, a volume of interest was placed in the basal ganglia and in the periventricular white matter. Using echo times of 31 and 144 ms N-acetylaspartate/choline (NAA/Cho), lactate/Cho, myo-inositol/Cho (mI/Cho), and glutamate-glutamine-␥-aminobutyric acid/Cho (Glx/Cho) ratios were compared between AGA and SGA groups. Griffiths' developmental quotient (DQ) values were assessed at 24 mo corrected age. Griffiths' DQ (AGA, 104 Ϯ 10; SGA, 99 Ϯ 9) and brain development assessed using magnetic resonance imaging showed no significant differences between both AGA and SGA groups, and NAA/Cho, Lac/Cho, mI/ Cho, and Glx/Cho ratios were not significantly different between the groups. NAA/Cho ratios increased from 32 to 41 wk, whereas mI/Cho ratios decreased in both groups. Preterm infants who are small for gestational age (SGA) as a result of placental insufficiency are at increased risk for adverse neurodevelopmental outcome in comparison with agematched appropriate-for-gestational-age (AGA) neonates (1-4). Placental insufficiency can be demonstrated in these pregnancies using Doppler ultrasonography of the umbilical artery (5). Most of these pregnancies are terminated by cesarean section because of severe fetal compromise with impending hypoxia-ischemia (6).During the past decade, it was demonstrated that perinatal hypoxia-ischemia may have long-lasting effects on cerebral metabolism as has been demonstrated using in vivo cerebral proton magnetic resonance spectroscopy ( 1 H-MRS) (7,8). A decrease of the N-acetylaspartate/choline (NAA/Cho) ratio in asphyxiated full-term neonates predicts an adverse neurodevelopmental outcome (7,9 -11). Elevated levels of lactate (Lac) in the brain of asphyxiated neonates, even months after the hypoxic-ischemic insult, have been shown to be predictive of neurodevelopmental delay (7,8,10,12