Practice question

Facial dysmorphology and microcephaly hallmark fetal alcohol syndrome originate primarily from injury to two populations. Cranial neural crest cells arising at dorsal neural tube edges migrate into frontonasal prominence contributing to facial skeleton highly sensitive to oxidative apoptosis, impaired L1 adhesion and reduced sonic hedgehog trophic support after ethanol. Depleted crest leads to midfacial hypoplasia. Simultaneously ventricular zone neuronal progenitors and postmitotic neurons undergo ROS-mediated apoptosis and cell cycle arrest, reducing brain volume and cortical complexity. Liver, lung less affected. Combined neural crest and neuronal cell loss explains neurocristopathy features central to fetal alcohol syndrome presentation.