<unk>  is a disorder of neuronal migration, resulting in structurally abnormal cerebral hemispheres. The Greek roots of the name describe its salient feature: many poly small micro gyri (convolutions in the surface of the brain). It is also characterized by shallow sulci, a slightly thicker cortex, neuronal heterotopia and enlarged ventricles. When many of these small folds are packed tightly together,<unk>  may resemble pachygyria (a few "thick folds" - a mild form of lissencephaly). The pathogenesis of<unk>  is still being researched for understanding though it is historically heterogeneous-4. It results from both genetic and destructive events. While<unk>  is associated with genetic mutations, none of these are the sole cause of this abnormality. The cortical development of mammals requires specific cell functions that all involve microtubules, whether it is because of mitosis, specifically cell division, cell migration or neurite growth. Some mutations that affect the role of microtubules and are studied as possible contributors, but not causes, to<unk>  include TUBA1A and TUBB2B. TUBB2B mutations are known to contribute to<unk>  either with or without congenital fibrosis or the external ocular muscles, as well as bilateral perisylvian. GPR56 protein structuregreen: signal peptideyellow: N-Glycosylation siteblue: GPS motiforange bracket: 108-177 aa STPpink bracket: 27-160 aa Ligand binding domain Referenced article: The gene GPR56 is a member of the adhesion G protein-coupled receptor family and is directly related to causing Bilateral frontoparietal<unk> , (BFPP)-6. Other genes in the G protein-coupled receptor family have effects with this condition as well such as the outer brain development, but not enough is known to carry out all the research properly so the main focus is starting with the specific GR56 gene within this category. This malformation of the brain is a result of numerous small gyri taking over the surface of the brain that should otherwise be normally convoluted. This gene is currently under studies to help identify and contribute to the knowledge about this condition. It is studied to provide information on the causes along with insight into the mechanisms of normal cortical development and the regional patterning of the cerebral cortex using magnetic resonance imagine, MRI. Specifically found to<unk>  due to mutation of this gene are myelination defects. GPR56 is observed to be important for myelinations due to a mutation in this gene results in reduced white matter volume and signal changes as shown in MRI's. While the cellular roles of GPR56 in myelination remains unclear, this information will be used to further other studies done with this gene. Another gene that has been associated with this condition is GRIN1 and GRIN2B.
Polymicrogyria
Geographic atrophy
Posterior cortical atrophy
Coprolalia
Neurofibrillary tangle
Argyria
Hypermastigia
Fibular hemimelia