In utero disappearance of the corpus callosum secondary to extensive brain injury.

he corpus callosum is the largest white matter tract connecting the 2 cerebral hemispheres. Its embryologic development has been studied extensively.1 At 11 to 12 weeks’ gestation, axons begin to cross the lamina terminalis to form the corpus callosum. Development generally proceeds anterior to posterior (from genu to body to splenium) with the exception of the rostrum, which forms last. The mature crescentic shape of the corpus callosum is essentially complete by 18 to 20 weeks. As the brain matures, thickening of the corpus continues until after birth. Basic knowledge of normal callosal development is essential to the understanding of callosal abnormalities. If the normal developmental process is disturbed, the corpus callosum may be completely absent (agenetic) or partially formed (hypogenetic). Because of the anterior-to-posterior development process, when the corpus callosum is hypogenetic, it is the posterior portion that is most affected.2 Developmental abnormalities of the corpus callosum may be isolated but more often are associated with other central nervous system anomalies, including Dandy-Walker malformation, holoprosencephaly, Chiari malformation, chromosomal abnormalities, and many other syndrome complexes.3 In addition to developmental abnormalities of the corpus callosum, abnormalities of the corpus callosum in the fetus can be destructive in origin.4 A recent unfortunate case of attempted in utero treatment of a fetus with a large sacrococcygeal teratoma proved that the finding of complete absence of the corpus callosum can be secondary, occurring in the setting of extensive brain injury.