with epilepsy, autism and mental retardation [73]. Tuberous sclerosis nodules were detected in one fetus [12], suggesting that fetal development of subependymal nodules can lead to the early onset of epilepsy that was diagnosed at the age of 14 months in a neuropathologically examined autistic male. The subependymal nodules detected in this autistic male’s brain are partially similar to tubers seen in subjects diagnosed with tuberous sclerosis [24]. The cause of subependymal nodular dysplasia in the examined subject is unknown. In the reported subjects, bilateral periventricular nodules are linked to mutations of the filamin A (FLNA) gene located on chromosome Xp28. Filamin A is an actin-crosslinking protein that is essential for cell locomotion [16], and nodule formation might be related to a defect in cell migration. The presence of miniature nodules that were built of poorly differentiated small neurons within the subependymal cell layer and an increase in nodular size with signs of growth and differentiation of neurons suggests that neurogenesis, differentiation and maturation of neurons were in progress within the subependymal germinal matrix of the 7-year-old autistic child. This interpretation of subependymal nodule genesis is consistent with lineage studies demonstrating that cells in nodules express cellular markers that are
