Dysplasias encompass a spectrum of changes ranging from a mild form of cortical disruption, without cellular abnormalities, to the most severe form with cortical dyslamination, with abnormal morphology of neurons and astrocytes [93, 96, 107]. Focal cortical dysplasias with giant neurons and balloon cells [107, 113] are histopathologically similar to tubers containing giant cells in tuberous sclerosis complex [25, 73], suggesting a common pathogenic basis [113]. However, activation of the mammalian target of rapamycin (mTOR) pathway observed in the tuberous sclerosis complex is not present in focal cortical dysplasia [8, 80]. The giant neurons and ballooned cells, which are histopathological features of tuberous sclerosis and focal cortical dysplasia, were absent both in the subependymal nodules and in the focal cortical dysplasia observed in the examined autistic cohort. These findings suggest that in spite of similarities, the pathomechanisms of developmental alterations are different in the examined autistic subjects than those in tuberous sclerosis heterotopias or focal cortical dysplasia. The development of the giant neuron- and balloon cell-free dysplasias observed in the autistic subjects might be related to differences in cause and/or
