Cerebral softening foci are an important cause of epilepsy, often arising from damage to the cerebral cortex after trauma, and these epilepsies have been extensively studied [1]. Non-traumatic cerebral softening can also cause intractable epilepsy, and there are few clinical reports on it. The 28 patients who underwent surgical treatment in our department are now reported. Subjects and methods 1. General data From January 2004 to July 2007, we performed surgical procedures on 42 patients with epilepsy associated with cerebral softening foci. 28 cases were included in this study because they needed to meet all of the following conditions: 18 males and 10 females; age 7 to 39 years, mean 18.1 years; age of onset 0 to 16 years, mean 9.2 years; duration of disease 2 to 15 years, mean 8.9 years. There were 9 cases of complex partial seizures, 8 cases of simple partial seizures, and 11 cases of generalized tonic clonic seizures secondary to partial seizures. 12 cases had a history of postnatal hypoxia, 6 cases had been diagnosed with central nervous system infection, 3 cases had a history of gamma knife treatment, and 7 cases had unclear etiology. 2. Preoperative evaluation All patients were questioned in detail before surgery, especially the symptoms of seizures, and the symptomatology of the symptom initiation area of epilepsy was analyzed with the video recording of the seizure period, and cranial magnetic resonance image (MRI), 64-lead video long-range electroencephalography (V-EEG), positron emission topography (PET). VEEG localization of epileptic foci: long T1-long T2 signal or mixed signal on MRI, low signal on diffusion tensor MRI imaging; reduced glucose metabolism on PET during interictal period. The location of the foci is compared. The surgical plan is selected according to the results of preoperative examination, and the surgery is chosen for those with the same basic localization of clinical symptoms, MRI, PET and EEG. If the softening foci were located in the non-functional cortex, intraoperative cortical EEG monitoring was performed to excise the softening foci, including the softening foci and the epileptogenic area. After excision, the local dura was removed and the dura was repaired with a nonbiological neural patch to prevent postoperative meningeal hyperplasia and cortical adhesions. Pathological biopsy of the excised tissue is performed. 4. Postoperative management and follow-up Oral antiepileptic drugs (1-2 antiepileptic drugs taken before surgery were selected) were administered 12 h after surgery, blood concentration and EEG were rechecked 6 months after surgery, and drug adjustment was performed if necessary, and the drug was gradually reduced when there was no seizure for 3 consecutive years. The treatment effect was scored according to Engel classification: grade I: complete disappearance of seizures or aura only after surgery; grade II: seizure count Q3/year; grade III: significant improvement in seizures with R90% reduction; grade 4 no significant improvement with <90% reduction. Results 1. Localization of epileptic foci by MRI, PET and VEEG The location of cerebral softening foci was determined according to MRI and PET. 18 cases were located in a single lobe, another 7 cases were located at the lobe junction, and 3 cases were 2 unconnected softening foci; 17 cases of softening foci were mainly lateral hemispheric non-functional brain areas, and 12 cases were accompanied by hemispheric atrophy. VEEG showed interictal epileptiform discharge (IED) confined to the area of the softening foci in 12 cases, IED distributed between the softening foci and other areas in 11 cases, and IED predominantly in unrelated areas of the softening foci in 5 cases. All three cases with two softening foci showed epileptic discharges originating from a single softening foci. In all cases, MRI showed thickened soft meninges and arachnoid membranes with pale, tough, and tight adhesions to blood vessels, enlarged subarachnoid space, atrophied and narrowed cerebral gyrus, and widened cerebral sulcus; brain tissue was tough, partly yellowish, with incomplete border and easy bleeding during resection. The cystic structure was detected intraoperatively in 8 cases, and the internal fluid was yellowish and transparent, with a dark yellow precipitated layer in the surrounding cyst wall, which was soft and easily removed by suction; in the remaining 3 cases, the cystic fluid was colorless and transparent, with smooth cyst wall. Under the light microscope, the cortical layer of the softened foci was seen to be proliferated with local glial cells and fibrous connective tissue, and neuronal cells were reduced with microvascular malformation. 3. Surgical results All patients were followed up for more than 2 years, and at 2 years after surgery, there were 17 cases of Engel grade, 5 cases of grade II, 4 cases of grade III, and 2 cases of grade IV. Statistical analysis showed that whether the softening foci were located in the functional area or the main area of the IED had no significant effect on whether the seizures continued after surgery, while patients with hemispheric atrophy and a history of refractory hypoxia had a worse prognosis (P<0.05). 4. Surgical complications Five cases developed transient dysfunction after resection of softening foci adjacent to functional areas, including two cases of speech impairment and three cases of unilateral limb weakness, of which four recovered within 2 weeks and one case of limb dyskinesia recovered at 4 weeks postoperatively, without long-term complications. Discussion Cerebral softening foci are an important cause of epilepsy and can be caused by traumatic brain injury, ischemia and hypoxia, and infection. MRI, video EEG and interictal PET are important noninvasive tests for preoperative localization of epileptic foci. Softening foci are caused by atrophy and reduction of neurons in cortical tissue and proliferation of fibrous tissue and glial cells, which can cause epileptiform discharges by igniting excitatory neurons in limbic structures, while alteration of the cortical microenvironment increases excitability of adjacent neurons. Therefore, softening foci are the primary consideration as the responsible foci for epilepsy. In our group, 43% of patients with preoperative EEG could see limited epileptic waves in the softening foci area, while intraoperative cortical EEG in all cases found significant epileptic wave issuance in the softening foci area and surrounding glial cell proliferation zone, and the epileptic waves in the softening foci area disappeared after resection, and the EEG waveforms in the surrounding area improved. Therefore, we believe that intracranial electrode embedding examination is not required when seizure symptoms suggest that the origin of epilepsy is associated with a confined lesion, and the lesion can be removed directly when surgery is required. Even when the epileptic focus and the softening foci are not in the same location, the prognosis is significantly better when the area of abnormal structure alone is removed during surgery than when the epileptogenic area alone is treated. Seizures were reduced by more than 90% in 93% of patients after surgery, while 61% of patients were seizure-free after surgery, suggesting that softening foci are often the main cause of epilepsy and can be effectively controlled after resection. Currently, resection of soft foci in the brain is usually used to treat epilepsy caused by soft foci, but the extent of resection is not clearly defined, especially for soft foci in functional areas. Non-traumatic softening foci are associated with hypoxia and infection, and their pathology is characterized by neuronal atrophy and degeneration, fiber and glial cell proliferation, which may be accompanied by local or even hemispheric cortical dysplasia [7], so the physiological functions of softening foci and glial proliferation zones are often very limited, and resection does not cause significant neurological dysfunction. A few patients in this study experienced postoperative loss of limb muscle strength, but all recovered within 1 month, so that combined softening foci resection and multiple submural transection of the periphery is safe for functional foci. The characteristics of the softening foci are closely related to the prognosis. The cases included in this study were all limited cerebral softening foci with good results after surgery, which was mainly performed by complete resection; however, it should be noted that only 33% of patients with concomitant hemispheric atrophy or dysplasia were seizure-free after surgery, suggesting that patients with concomitant hemispheric or total brain atrophy may have extensive brain functional impairment and factors leading to increased neuroexcitability in addition to softening foci, and this aspect needs This aspect needs further study. The presence of a history of cerebral hypoxia at birth also suggests a poor prognosis, which may be related to the fact that more cases of cerebral hypoxia are associated with hemispheric atrophy. In our group, there were 6 cases of epilepsy caused by limited softening foci associated with encephalitis, and 67% of them reached Engle grade I after surgery. of the diagnosis is not exact. In our case study, we found good results for epilepsy surgery associated with non-traumatic limited cerebral softening, although the chance of seizure-free postoperative epilepsy was lower in those with a history of combined hemispheric atrophy or cerebral hypoxia than in other cases, but these cases were often associated with some mental retardation and frequent seizures. Surgical treatment.