From January 2004 to July 2005, we admitted 28 patients with focal cortical dysplasia causing intractable epilepsy, and based on morphologic, electrophysiologic, and functional imaging examinations The epileptic lesions were identified, surgical procedures were performed and the outcome was observed, which is summarized here. I. General data From January 2004 to July 2005, 28 patients with focal congenital cortical dysplasia causing intractable epilepsy were admitted to our epilepsy center. Among them, 18 were males and 10 were females; age ranged from 4 to 39 years, with an average of 18.1 years; duration of disease ranged from 2 to 15 years, with an average of 8.9 years. The seizure form included generalized tonic-clonic seizures in 16 cases, complex partial seizures in 8 cases, and simple partial seizures in 4 cases. 12 cases were accompanied by mental retardation. 12 cases had a clear history of obstructed labor. The patients were treated with systemic antiepileptic drugs for more than 3 years and had more than 10 seizures per month, which seriously affected their life safety and life learning. The MRI examination showed that the cerebral gyrus in the cortical dysplasia area was narrower than the contralateral side, the sulcus was deeper and wider, and the gray and white matter boundaries were unclear, and the signal was high in T2WI. The 128-conductor video long-range EEG showed spikes, sharp waves or slow spikes in all hypoplasic cortical areas, which were obvious when symptoms appeared. 16 cases had seizure waves originating from the hypoplasic area during the seizure phase, and then issued to the whole brain. In 16 cases, the seizure waves originated from the area of cerebral hypoplasia, and then issued to the whole brain. According to the three preoperative examinations, craniotomy was performed under general anesthesia with tracheal intubation, and the epileptic foci in the hypoplasia area were removed under cortical EEG monitoring. Cortical thermal cautery and subchondral transection were performed within 3 cm of the epileptic focus. Cranial closure was performed after cortical EEG retest without epileptic waves. All 28 patients in this group underwent focal resection of the dysplastic area, cortical cautery, and submural transection. The abnormal discharges in the dysplastic areas of the cerebral cortex were completely resected, followed by peripheral cortical cautery and submural transection. The thickened soft membranes and arachnoid were carefully peeled off near the important functional areas, and the abnormal cerebral cortex was selected for pathologic biopsy, surrounded by cortical cautery and subhypophyseal transection. Care was taken to protect the surrounding arteries and veins to avoid severe postoperative cerebral edema. The cortical EEG is retested to ensure that no epileptic waves are present around the epileptic focus. The dura mater in the operative area is repaired with a biologic neural patch. Postoperatively, antiepileptic drugs were selected according to the type and dose of preoperative medication, and the blood concentration was checked after 5 d. The number and dose of medication were adjusted according to the blood concentration. The postoperative medication was reviewed for six months, and the medication was gradually reduced if the EEG seizure waves were not obvious, and the antiepileptic medication was continued if the background activity of seizure waves still existed on the EEG. The prognosis was evaluated using Engle’s prognostic grading for epilepsy with a follow-up of more than 1 year. The morphology and pathology of the cortical dysplasia area were found to be thickened, tough and tightly adhered to the blood vessels. 24 cases of cortical dysplasia were found to be harder than normal brain tissue, with mild atrophy of the cerebral gyrus and widening of the cerebral sulcus. 12 cases were found to have abundant veins on the brain surface and easy bleeding after submural transection. The pathological findings showed localized neuronal cell reduction, disturbed gray-white matter boundaries, giant anomalous neurons, microglia hyperplasia, and focal vascular malformations. According to the FCD classification, four cases of cortical dysplasia (AD), eight cases of cytoarchitectural dysplasia (CD), and eight cases of Taylor’s cortiacal dysplasia (TCD) were found. cortiacal dysplasia (TFCD) without balloon-like cells in 10 cases (Figure 2), and TFCD with balloon-like cells in 6 cases. Results Five patients developed postoperative contralateral limb weakness and two developed partial aphasia, all of which gradually returned to normal within 3 weeks. Discharge was arranged after blood concentration was adjusted to the effective range. All patients were followed up for more than 12 months, with a mean follow-up time of 14.6 months and no long-term complications. The treatment effect at 1 year after surgery was graded by Engel: 12 cases of grade I, 9 cases of grade II, 4 cases of grade III, and 3 cases of grade IV. Among the 21 cases with prognosis grade I-II, 6 cases were in the frontal lobe, 9 cases in the temporal lobe, 3 cases in the frontotemporal lobe, and 3 cases in the temporoparietal lobe. Discussion Focal cortical dysplasias (FCD) is a heterogeneous disease of cortical development, which is currently thought to occur due to genetic or environmental factors after partial completion of neuroblastoma displacement. Nearly half of our patients had a clear history of obstructed labor or febrile convulsions, and it is considered that cortical dysplasia may be related to hypoxia and infection in early childhood. The location of the dysplastic region is widely distributed, mainly in the temporal lobe, and may be accompanied by frontal or parietal atrophy, often with localized seizure wave issuance and hypometabolism of neurons, resulting in seizures. However, we found that drug treatment is effective within 3 months, and the effect of drug treatment is poor over half a year, and the seizures often cause irreparable accidental damage, so we believe that if the examination suggests the presence of brain dysplasia, and the EEG and PET localization are consistent with the location of the lesion, we can consider surgery after half a year of drug treatment if it is ineffective. Surgery can be considered after six months of medication. We performed MRI, 128-lead long-range EEG, and interictal PET in 28 patients, and these tests were able to localize the epileptogenic foci in different ways. MRI can detect limited cerebral dysplasia at a rate of 60% to 90%, so it was used as a primary screening test. Long-range video EEG suggested typical epileptic waves in the area of cortical dysplasia during the seizure phase, mostly spreading peripherally and even through the corpus callosum to the contralateral cerebral hemisphere, and significantly reduced neuronal glucose metabolism during the interictal period, which is consistent with other studies. Intraoperatively, the cerebral gyrus in the cortical dysplasia area was slightly narrowed and locally hard in texture. Pathological examination showed a reduction or polarity change of local neurons and proliferation of microglia/oligodendrocytes, which can alter neuronal excitability and predispose to seizures. In conclusion, cortical dysplasia is likely to be an important cause of epilepsy. Removing the epileptogenic focus and blocking the epileptic wave conduction pathway is the key to surgical treatment of epilepsy. The scalp incision should cover as much as possible a 3-cm area around the epileptic focus. After craniotomy, cortical electrodes should be used to detect the brain waves around the cortical hypoplasia area, and if necessary, a meiotic evocation test should be performed to accurately locate the epileptic origin. The portion of the cortex within the cortical hypoplasia area where the epileptic waves are dense should be excised during surgery and surrounded by a subcortical transection. Since nerve cells cannot be regenerated after cortical excision, epileptic foci located in functional areas can be treated with fine cortical thermal cautery and subchondral transection in and around the lesion. Postoperatively, patients may experience decreased muscle strength or aphasia in the contralateral limb, most of which can gradually recover within 1 month and the epilepsy is well controlled with medication. The use of bioartificial dura mater to repair the dura in the surgical area may prevent the development of new epileptic foci by adhesions of the meninges to the brain tissue.Bingaman summarized 105 patients with limited cortical dysplasia secondary to intractable epilepsy who were followed up for 3.4 years after complete focal resection and 25% had complete resolution of symptoms. In our group, 42.8% of patients had good epilepsy control within 1 year after surgery, and further follow-up is needed for long-term outcome. With the continuous improvement of basic research, the clinical surgical treatment results are expected to be further improved.