 Hello everyone, I am Dr. Labya Ayesha, junior resident department of radio diagnosis in MJ Medical College in Hospital Navi, Mumbai, presenting our case series on Neuronal Migration Disorders and Overview under the guidance of Dr. Ashutosh Chitnis. Neuronal Migration Disorders are a group of disorders caused by insults to migrating neuroblast during the third to fifth month of gestational age, resulting in developmental delays, seizures and abnormal motor skills. In this study we review the salient features of these anomalies, their MR appearances, relationship of pathologic anatomy and theories of pathogenesis. Aim of the study is to study the utility of MRI as a method of imaging, to diagnose patients with Neuronal Migration Disorders and our objectives are to study the characteristics and salient features of Neuronal Migration Disorders and their appearances on MRI and to differentiate these disorders from each other on the basis of ability of MRI to exceptionally differentiate gray and white matter and to study the relationship between pathologic anatomies of these disorders and their theories of pathogenesis. This is a retrospective study done in MJ Medical College in Hospital Navi, Mumbai in a review of 300 MR studies in the pediatric age group, three patients with migrations anomalies were identified, patients presenting with seizures, develop mental delay or mental retardation were referred for imaging and the patient's ages range from five years to 20 years, all patients were scanned on Toshiba 1.5 Tesla MRI machine. Migration anomalies were diagnosed from the characteristic MR morphology of the affected brains. These cases include three cases consisting of one case of lesion kipali, one case of season kipali and one case of purin kipali. Case number one, a six year old male patient presented with complaints of seizures and developmental delay. Here is the T2 axial image of the MRI brain showing diffuse thickening and broadening of gyri with shallow sulci involving the right hemisphere showing poor differentiation of subparticle white matter and mild paucity of underlying white matter. Here also the T1 chagatal image showing diffuse thickening and broadening of gyri with shallow sulci. This is the characteristic appearance of lesion kipali patchy gyria spectrum. Now moving to case number two, a five year old female patient came with complaint of spastic hemiplegia, seizures and developmental delay. Here is the T1-T2 axial image of the MRI. There is evidence of cleft following CSF intensity with focal pointed nipple like out pouching extending from ependymia or body of right lateral ventricle up to the pyl cortical surface of right parietal lobe. The lips of cleft are closely opposed with dysplastic heterotopic grey matter lining the cleft on either side. There is absence of septum pelocidum. However corpus callosum appears normal. Here also the T1 chagatal image showing the cleft and corpus callosum appearing normal. This is the characteristic appearance of closed lip unilateral season kipali. Now moving to case number three, a twenty year old male patient presented with history of seizures, inappropriate behavior and mental retardation. T1-T2 axial image of MRI showing CSF signal intensity cystic lesion in left temporal lobe which is seen to be communicating with adjacent subarabic night space surrounding incafalo-Malaysia noted involving left parieto-oxypetotemporal region. T1-T2 axial image showing the cystic lesion lined by encephalo-Malaysia. This is the characteristic appearance of porine kipali involving the left temporal lobe. Normal cerebral cortex is six layer consisting of marginal layer, external granular layer, external pyramidal layer, internal granular, internal pyramidal and fusiform layer. Terrible cortex develops in three stages proliferation, migration of neuronal fibroblast along the process of previous glia and post-migrational development. Cells resulting from abnormal proliferation often neither migrate nor organize properly and the abnormalities of neuronal migration disorders are characterized by ectopic location of neurons in the cerebral cortex. And these conditions are associated with intractable epilepsy, major psychomotor developmental disorder. The common underlying feature of migration abnormalities is abnormal location of neurons and thickened cortex by a large disorganized layer of neurons and subcortical white matter layer is thin because of the absence of post-migrational organization. And the faulty cytodifferentiation and programmed cell death play important roles in generation of dysplasia. Lezen kipali consists of four layer cerebral cortex instead of normal six layer cortex. There is the cell sparse zone which is the area of lamina necrosis secondary to metabolic insult during migration phase and degeneration occurs in the neurons that have already migrated but have their axonal and dendritic connections interrupted within the layer of necrosis. The subcortical white matter is thin because the organizing neurons with established dendritic and axonal corrections are micrally reduced. Sheezing kipali consists of bilateral or unilateral full thickness clefs of cerebral hemisphere. Pathologically these clefs are characterized by an infolding of cortical gray matter along the clef with a fusion of pyrilining of brain and deep endima of ventricle. And the clefs are lined by dysplastic gray matter, porine kipali is the presence of intracerebral fluid fill cyst within the CSF lined by white matter. Now the conclusion, recognition of neuronal migration disorders depend on awareness of the characteristic appearance of the entities and use of proper imaging technique. MRI remains the best investigation to identify the anomalies of neuronal migration because of its exceptional ability of better differentiation of gray matter from white matter. And more sensitive and detecting sheezing kipali by recognizing the presence of gray matter lining the cleft is critical to differentiate it from porine kipali which is lined by white matter. And in detecting patching area where critical details of cortical architecture are obscured on CT due to overlying bone, MRI should be primary mode of investigation in infants presenting with seizures and developmental delay. And lastly the references.