Neuronal migration anomalies are abnormalities of the brain tissue that result from the blockage of the migration of adult neuronal cells from the embryonic germinal matrix to the surface of the brain during cortical development, including anencephaly-megalencephaly, gray matter heterotopia, cerebral fissure malformation, polymicrocephaly, hemimegalencephaly, and local cortical dysplasia. Each type has a specific etiology, pathological changes and imaging features. So, what is its etiology? The causes of neuronal migration anomalies are described below. Anencephaly-megalimbic gyrus malformation is a disorder that occurs early in the migration of primitive neurons. Anencephaly is the complete absence of gyrus, also known as “smooth brain”, often accompanied by giant gyrus; megalencephaly is the reduction, widening and shallowing of the gyrus. Both of them belong to the same type of neuronal migration lesion with different degrees, so some people call megalencephaly a special type of anencephaly. The anencephalic gyrus shows cortical thickening, white matter thinning, and vertical lateral fissures on cranial MRI, while the megalencephalic gyrus shows thick, sparse gyrus and shallow sulci on cranial MRI. Both have cortical thickening, white matter reduction, and loss of gray-white matter junction. There are three types of anencephalic gyrus malformations. Type I is a typical anencephaly with a smooth brain surface, lacking sulci and gyri, and mostly accompanied by giant gyrus. It is due to the slowing down or delaying of neuronal migration. Histologically, the cerebral cortex is divided into four layers: the molecular layer, the outer cellular layer (with cone neurons), the sparse cellular layer (containing myelinated fibers and few neurons), and the inner cellular layer (a thickened layer of disordered neurons), in order from the outside to the inside. This type of anencephaly has microcephaly and/or abnormal facial morphology. Common facial morphological abnormalities include high forehead, small jaw, low ear position, collapsed nasal bridge, wide eye spacing, and posterior forehead tilt. The occurrence of these abnormalities is associated with certain genetic factors, such as Miller-Dieker syndrome, Norman-Roberts syndrome, and Neul-axova syndrome. Type II is also called “cobblestone-like anencephaly”, in which the surface of the brain is smooth and nodular, resembling a cobblestoned road. It is a complex brain malformation, including cobblestone-like cortex, white matter abnormalities, enlarged ventricles, brainstem and cerebellar atrophy, and cerebellar gyrus. It is currently believed to be caused by excessive neuronal migration, as the rupture of the soft membrane-glial boundary membrane causes cells to migrate beyond their normal position and enter the soft meninges, forming a neuronal layer mixed with the soft meninges on the surface of the brain. Histologically, the cortex is seen to consist of two layers: the outer layer consists of disorganized neurons, neuroglia, collagen bundles, and blood vessels; the inner layer consists of residual cortical plates containing disorganized neurons. This type lacks facial morphological abnormalities and is commonly seen in a group of disorders associated with congenital myotonic dystrophy and ocular malformations. (microphthalmia, glaucoma, retinal developmental anomalies, etc.), associated disorders such as Walker-Warburg syndrome, myo-ocular-encephalopathy and Fukuyama type congenital myotonic dystrophy, all autosomal recessive, often combined with agenesis of the corpus callosum, hindbrain malformation, microcephaly and Dandy-Walker malformation. Type III is an isolatedlissencephalysequence (ILS), which is genetically related. Recent studies have confirmed that two genes are associated with ILS, including the [ILS] gene on chromosome 17p13.3 and the XLIS (DCX) gene on chromosome Xq22.3-q23. However, the majority of anencephaly is caused by mutations in the LIS1 gene, and in males and some females, it can be caused by mutations in the XLIS gene. Most anencephalic gyrus malformations are more severe in the hindbrain than in the forebrain, and these malformations are associated with mutations in the LIS1 gene on 17p13.3. A few anencephalic gyrus malformations are more severe in the forebrain than in the hindbrain, and these malformations are associated with mutations in the XLIS gene on Xq22.3-q23.