Structural MRI studies demonstrate the global and widespread impact of prenatal alcohol exposure, but also implicate some specific brain areas that may be particularly vulnerable. For example, evidence continues to accumulate indicating that the caudate may be one such region. Disproportionate reductions [11] or deformation [26] of the caudate have been recently reported. Caudate volume has also been shown to predict neurobehavioral disruption [28]. DTI studies are linking the alcohol-induced white matter microstructural changes to specific deficits, most recently oculomotor control [34]. Furthermore, recent evidence demonstrates that the developmental trajectory of both cerebral cortex volume and white matter microstructure is altered [37, 38]. Continued longitudinal research examining brain development over the lifespan is necessary. Longer latencies between sensory stimulus presentation and cortical activation detected with MEG demonstrate deficits in auditory processing in young children and visual stimulus processing in adolescents [40, 71]. BOLD changes during cognitive tasks continue to reveal differing activation patterns between alcohol-exposed youth and more typically developing controls [44]. Further, the BOLD activation patterns among individuals with FASD are also at least partially distinct from contrast groups,
