Cortical dysplasia is a general term for a group of focal or diffuse abnormalities of cortical structures, and the name MCD was first introduced by Kuzniecky and Barkovich in 1996. With the development of CT and MRI and the discovery of a large number of “symptomatic epilepsy” cases, the epilepsy caused by MCD is being widely recognized. Different names have been given to MCD from different perspectives, such as cortical dysplasia and neuronal migration disorder, including severe disorders of cerebral gyrus formation such as anencephaly, polymicrogyrus, schizotypal malformation, and gray matter ectopia, as well as focal cortical dysplasia. It is now believed that MCD is a congenital developmental defect that often causes developmental delay, epilepsy, local neurological dysfunction, and mental underdevelopment, and the resulting epilepsy is often difficult to control with medications. In recent years, many epilepsy centers have attempted surgical treatment of MCD, especially FCD, which statistically accounts for 12% to 40% of patients receiving surgical treatment for epilepsy. Clinical presentation: Patients with MCD have approximately the same proportion of males and females, and most have their onset within 10 years of age, with the earliest onset being only 8 days, and the most common onset being at 2 to 5 years of age. Developmental malformations can occur in any part of the cortex, with the frontal lobe being the most common. MCD outside the temporal lobe has a younger age of onset than temporal lobe MCD (2.5 years in the former and 9.1 years in the latter) and more often presents with mental retardation and developmental delay. MCD is the most common clinical manifestation of epileptic discharges in focal epilepsy and is the most difficult to control with medication. 15%-30% of patients will develop persistent status epilepticus at some point in time, and partial status epilepticus may occur when the lesion involves the cortex near the central sulcus. The patient with MCD may also exhibit developmental delay. Patients with MCD may also exhibit developmental delays, mental and intellectual developmental delays, and in some cases, neurological impairment, as well as other severe malformations. Cortical dysplasia is an important cause of refractory epilepsy. Cortical dysplasia is also known as cortical dysplasia, cortical developmental malformations, and neuronal migration disorders. The normal development of the cerebral cortex depends on three overlapping processes, namely neuroblast proliferation, neuronal migration, and cortical formation, any of which can be affected by genetic factors or harmful factors in the surrounding environment leading to cortical dysplasia. Diagnostic tests: High-resolution MRI is an important diagnostic method for MCD, and cortical malformations can be detected by MRI in 60% to 90% of MCD patients. PET, a functional imaging test, has been shown in most studies to be pathologically confirmed in areas of MCD where the cortex is said to be hypometabolic, consistent with areas of abnormal electrical activity. It has also been suggested that PET is more sensitive than MRI in detecting minor cortical developmental abnormalities.MCD lesions are mostly hypometabolic areas on PET, but hypometabolic and mixed metabolic areas are also present. For now, PET has not demonstrated better sensitivity than high-resolution MRI, but still may provide important information for the diagnosis of MCD and localization of epileptogenic foci. SPECT, another functional imaging technique, can detect areas of reduced cerebral blood flow during interictal seizures and increased cerebral blood flow in the same area after seizures, which is important for accurate localization of epileptogenic foci. The difficulty of practical implementation of SPECT during single seizures limits the application of this examination method. At present, SPECT in MCD remains an adjunctive imaging technique for diagnosis and localization. The EEG of MCD has certain characteristics: the interictal period is characterized by rhythmic slow spike and spike waves, which can even be issued continuously and in a more diffuse range; about 67% of patients can record frequent and different frequencies of seizure spike wave strings in the corresponding areas. The range of EEG abnormalities in MCD is much wider than that seen on MRI, PET, and intraoperative lesions, and the application of intracranially embedded electrodes for EEG recording is mainly used for the precise localization of seizure onset and functional areas. Surgery: MCD is highly epileptogenic and the epilepsy it causes is often drug-refractory, and surgery has become an available treatment option. The aim of surgery is to remove the epileptogenic focus identified based on imaging, intraoperative probing, and EEG monitoring. Among the important factors affecting the outcome of surgery are the extent of resection of the epileptogenic focus and the preservation of important cortical functions.