Fetal alcohol spectrum disorders (FASD) is diagnosed by prenatal alcohol exposure, characteristic facial dysmorphology (small eye, smooth philtrum, thin upper lip), growth deficiency and cognitive disabilities with organic brain damage.
The study found a significant difference in the neuropsychological function in various domains in FASD subjects compared to control matched subjects. The FASD subjects and the normal control subjects had a similar pattern of cortical thickness variation. But the FASD had additional areas of thinner cortex in Frontal lobe, Pre and Post central gyrus,Temporal lobe particularly the inferior temporal lobe and the superior parietal lobule.
There was an age related decrease in the thickness of cortex in FASD, similar to that seen in control subjects except that the study subject group had extra areas showing more thinning compared to controls including inferior temporal lobe, Fusiform gyrus etc. Incidentally, they couldn't find any corelation between the cortical thickness variation and the cognitive abilities in these children.
The study found a thinner cortex and no area of thicker cortex shown by the previous study. Opens up a few questions- whether thicker/thinner cortex in FASD? What is the cause for a selective involvement of brain structures in prenatal alcohol exposure? Effect of confounding variables? Age related difference in cortical thickness and how it translates at a functional level?