Fetal alcohol spectrum disorders (FASD) represent a significant global health concern and are the leading cause of preventable birth defects, intellectual disabilities, and persistent behavioral deficits. The neurodevelopmental mechanisms underlying FASD are not yet fully understood, but there is growing interest in the role of cortical development in the manifestation of these disorders. The cerebral cortex serves as the master regulator of higher-order functions, including sensory perception, motor planning, decision-making, and general intelligence—processes that are all adversely affected by prenatal alcohol exposure (PAE). Higher-level functions emerge from a complex and intricately interconnected neuronal network that develops through a series of delicate and sequential stages involving neuronal and glial cell generation, proliferation, migration, differentiation, and maturation. Recent evidence suggests that PAE disrupts these developmental processes, leading to impaired cortical structure, altered connectivity, and ultimately, to the neurobehavioral deficits observed in individuals with FASD. Rodent models, along with in vitro approaches, have proven invaluable for elucidating the consequences of PAE on cortical development and the underlying mechanisms associated with PAE-related disorders. Although gaps in knowledge remain, advancing our understanding of the neurodevelopmental basis of FASD is essential for identifying potential therapeutic targets and enhancing early intervention strategies for those affected by FASD in the future.