BACKGROUND AND PURPOSE: According to the medical literature, it is known that intrauterine growth restriction is associated with abnormal fetal brain findings. The aim of this study was to assess the volume of fetal brain structures in fetuses with intrauterine growth restriction compared with the control group and to examine the effect of intrauterine growth restriction on birth weight in relation to the effect on the volumes of these structures. MATERIALS AND METHODS: This historical cohort study included 26 fetuses diagnosed with intrauterine growth restriction due to placental insufficiency. The control group included 66 fetuses with MR imaging scans demonstrating normal brain structures. The volumes of the supratentorial brain, left and right hemispheres, and the cerebellum were measured using a semiautomatic method. In addition, the cerebellum and supratentorial brain ratio was calculated. The measurements of each brain structure were then converted to percentiles according to growth curves. RESULTS: The absolute volumes and percentiles of all brain structures examined were smaller in the intrauterine growth restriction group. All examined brain structures showed results that were statistically significant (P < .015). There was no statistically significant difference in the cerebellum/supratentorial brain ratio (P > .39). The difference in brain volume percentiles was statistically smaller than the difference in birth weight and birth weight percentiles (Dolberg growth curves) between the groups. CONCLUSIONS: Intrauterine growth restriction affects the volume of brain structures, as measured by quantitative MR imaging. Compared with healthy controls, the effect on birth weight was more prominent than the effect on brain structures, possibly due to the “brain-preserving” capability.

Interstitial deletions of 16q24.1–q24.2 are associated with alveolar capillary dysplasia, congenital renal malformations, neurodevelopmental disorders, and congenital abnormalities. Lymphedema–Distichiasis syndrome (LDS; OMIM # 153400) is a dominant condition caused by heterozygous pathogenic variants inFOXC2. Usually, lymphedema and distichiasis occur in puberty or later on, and affected individuals typically achieve normal developmental milestones. Here, we describe a boy with congenital lymphedema, distichiasis, bilateral hydronephrosis, and global developmental delay, with a de novo microdeletion of 894 kb at 16q24.1–q24.2. This report extends the phenotype of both 16q24.1–q24.2 microdeletion syndrome and of LDS. Interestingly, the deletion involves only the 3′‐UTR part ofFOXC2.