The cause of<unk>  is unclear. It is generally agreed that<unk>  occurs during late neuronal migration (when majority of the neurons arrived at cerebral cortex after their starting points around the ventricular system of the brain) or early cortical organization of fetal development. Evidence for both genetic and non-genetic causes exists. Chromosomal abnormalities have been identified in<unk>  such as 22q11.2 deletion (characterised by bilateral perisylvian<unk> , heart defects, facial dysmorphism, microcephaly) and 1p36 deletion (bilateral perisylvian<unk> , intellectual disability, dysmorphic facial features and microcephaly). Apart from that, mutations in more than 30 genes have been associated with<unk> . Common genes assocciated with<unk>  are TUBA1A and PIK3R2. Association with the gene WDR62 (diffuse or asymmetric<unk>  and SCN3A has also been identified, as well as other ion channels such as KCN, CACNA, GRIN, and GABAR. Other genes implicated are: GPR56 (Bilateral frontoparietal<unk> , TUBB2B (anterior predominant<unk> , NDE1 (Diffuse<unk> , AKT3 (Bilateral perisylvian<unk> , and PIK3CA (Bilateral perisylvian<unk> . Non-genetic causes include defects in placental oxygenation and in association with congenital infections, particularly cytomegalovirus, syphilis, and varicella zoster virus.
Polymicrogyria
Geographic atrophy
Posterior cortical atrophy
Coprolalia
Neurofibrillary tangle
Argyria
Hypermastigia
Fibular hemimelia