A variety of interactions between the planes of genome–proteome and metabolome regulate develop­mental processes that ultimately influence the forma­tion and maturation of all organ systems, including the fetal brain. In early fetal life, interference with forma­tion of the telencephalic vesicles (holoprosencephaly), dysgenesis of the corpus callosum, absence of the septi pellucidi, cerebellar dysgenesis, and abnormalities in ventricular shape (colpocephaly and single ventricle) may be visualized through targeted neurosonography. As the brain grows in complexity, abnormalities may extend to involve the gray matter (atrophy of the corti­cal ribbon and basal ganglia), white matter (thinning out or loss of volume, demyelination, or dysmyelination of white matter), encephaloclastic lesions (porencephalic cysts), and neuronal migration defects (pachygyria) and can be identified with the aid of high-resolution fetal magnetic resonance imaging (MRI). Neuronal loss or cell death (neurotoxic or apoptotic) is followed by wallerian (secondary axonal) degeneration, leading to atrophy and volume loss in the gray and white matter. These changes result in ventriculomegaly and a prominence of the extra­axial fluid spaces. Porencephalic cysts are seen secondary to ischemic injury following vascular occlusion and focal neuronal necrosis. Secondary processes such as failure or interference with myelination by glial cells will result in demyelination or dysmyelination.