Neuronal migration anomalies are developmental malformations of brain tissue of varying degrees, including anencephaly, megalencephaly, gray matter heterotopia, cerebral fissure malformation, multiple microcephaly, hemimegalencephaly, and localized cortical dysplasia, due to various reasons that block the migration of adult neuronal cells from the embryonic germinal matrix to the surface of the brain during cortical development. Each type has a specific etiology, pathological changes and imaging features. Macrocephaly is caused by laminar necrosis of cortical cells due to brain metabolic disorders, and the necrotic area acts as a barrier so that late migrating neurons are blocked from forming a normal cerebral cortex, resulting in thickening of the cerebral cortex, widening of the gyrus, shallowing of the sulci; thinning of the medulla and mild to moderate enlargement of the ventricles. In complete gyral agenesis, the surface of the brain is smooth, which is called anencephaly, while incomplete gyral agenesis, which only shows a decrease in the number of gyri but an increase in volume, is called megalencephaly. Macrocephaly is an incomplete cerebral gyrus deficiency, which is characterized by a decrease in the number of participating gyri and an increase in their size. In severe cases, only the major gyrus may be present. Megalimbic gyrus malformations are often combined with anencephaly. Megalimbic gyrus malformation is the result of brain development remaining in the primitive stage, the germinal layer. The developmental disorder occurs before the second month of embryonic life. Microscopic surgery reveals that the 4-layer cellular structure of the primitive cortex is still preserved, the cortical structure is incomplete, and the neural cells are immaturely differentiated. Due to impaired peripheral migration of neuroblasts, ectopic neuroblasts are often found in the white matter, sometimes in groups present in a nodular pattern. Ectopic gray matter masses can be found in the hemianopia, cerebellar white matter, and brainstem. MR shows moderate to severe enlargement of the affected cerebral hemisphere; cortical hypoplasia, wide gyrus, shallow sulci, and thickened cortex; and heterogeneous white matter signal, suggesting gray matter ectopic and dysplastic neurons and glia. The shape of the lateral ventricle in a typical patient is characteristic: it is enlarged in proportion to the enlargement of the affected hemisphere, with the frontal horn straightened and pointing anteriorly and superiorly. The affected hemisphere has a large multifunctional deficit and can be the cause of epilepsy. MRI is the gold standard for the diagnosis of the disease and can be used both for diagnosis and as a reference for treatment. Since the disease is resistant to antiepileptic drugs, early surgery is the best treatment for this condition. Surgical options include hemispheric resection, hemispheric cortical resection and partial cortical resection. An hourglass configuration is visible, perpendicular to the lateral fissure of the brain (shown by the red arrow in the figure); a smooth-edged, markedly thickened cortex is shown by the yellow arrow; a wide, flat cerebral gyrus is shown by the green arrow; and a clear gray-white matter junction line. Anencephaly Anencephalic gyrus: only a few shallow sulci are seen in the cranium, with marked cortical thickening ranging from 12 to 20 mm (normal 3 to 4 mm) and scattered subcortical cyst formation. The surface of the cerebral cortex was smooth, the sulci were absent, and only a few broad, flat, and thick cerebral gyri remained. The cerebral gray matter was thickened, the white matter was thinned, and the gray-white matter partition interface was abnormally smooth, with no white matter protruding into the gray matter. The insula is absent. The ventricular wall may have a nodular appearance due to the presence of abnormal gray matter. Anencephaly is often associated with abnormal changes such as hyaline septal space, enlarged ventricles, and marked widening of the subarachnoid space. The lateral fissure of the brain is significantly widened and shallowed, giving the brain an “hourglass” appearance. The most common symptom is seizures. Children with anencephaly have a high mortality rate. Children with milder forms of anencephaly have better motor and cognitive function and a longer survival time. Hemimegalencephaly is a rare congenital disorder that results from a combination of abnormal proliferation of progenitor cells and disrupted apoptosis of normal posterior neural cells. It often involves the entire cerebral hemisphere and occasionally the cerebellum. Large lobar or focal involvement is rarely seen. Clinical features: symptoms of macrocrania, developmental delay, and intractable seizures can be seen from early childhood. The diagnosis: 1. atypical cortical hyperplasia and thickening, including multiple gyrus, giant gyrus, fusion of gyrus and shallow sulci; 2. usually enlarged lateral ventricles; 3. straight and sharp anterior horn of the lateral ventricles; 4. impaired myelin formation or neuromyelin formation causing white matter T2-weighted signal variability; 5. cortical dysplasia causing blurring of the gray-white matter junction; 6. frequent foci of dystrophic calcification in the lesion area; 8. white matter hypertrophy; 9. White matter hypertrophy; 9. hypoglycemia (50% of cases). Case sharing: Case 1: A child aged 8 months with recurrent, intractable seizures since birth. Case 2: Male child, 6 years old, with refractory seizures with left-sided limb weakness.