Traumatic epilepsy is a serious complication of craniocerebral injury and can occur at any time after the injury. It is divided into immediate seizures, early-onset seizures, and late-onset seizures according to the latency period of seizure onset (the time between injury and the first seizure). Epilepsy caused after cranial surgery can also fall under the category of traumatic epilepsy. 1, immediate post-traumatic seizures Immediate seizures are rare and often occur within seconds or hours after craniocerebral trauma. The reason is that the original convulsive threshold of brain tissue is low, and the direct mechanical stimulation during trauma causes seizures, which is a non-specific response. Early-onset post-traumatic epilepsy occurs within 2 weeks (some think 1 week) after traumatic brain injury, and is more common in adults, with an incidence of 20%; the incidence is higher in infants, and is particularly likely to occur in those with perinatal brain injury. Seizures occurring within 24 hours of trauma account for approximately 50% of early-onset epilepsy. It is thought that 1/3 of seizures occur within 1 hour after trauma, 1/3 occur within 24 hours, and the remaining 1/3 occur between 1 and 14 days. The mechanism of early-onset posttraumatic epilepsy may be due to biochemical changes in brain cells, such as a transient increase in acetylcholine release, or to inhibition dysfunction, resulting in hyperexcitability of nerve cells. Pathology can be seen as cerebral edema, intracranial hemorrhage, cerebral contusions, and brain cell necrosis. Skull fractures are common in pediatric patients, with up to 24% reported. Compared with adults, early-onset post-traumatic epilepsy in children has two characteristics: first, very mild brain injury can induce seizures; second, they are prone to seizure continuity, the incidence of which can be as high as 22%, twice as high as in adults, and occur mostly within 1 hour after trauma. Seizures are generally generalized, but they can also be seen as one-sided or partial seizures. 3. Late onset post-traumatic epilepsy is epilepsy in which the symptoms occur after 2 weeks (some consider 1 week) after trauma. The onset of late onset post-traumatic epilepsy can vary between months and years after injury, with the vast majority occurring between 6 months and 3 years after injury, with 57% occurring within a year. The majority of children with late-onset epilepsy do not have significant functional abnormalities at the time of trauma. Pathological and electrophysiological examinations suggest that seizures are associated with neuronal necrosis, degeneration, glial cell phagocytosis, and glial cell proliferation and cerebral and meningeal scar formation at the site of brain injury. Contusions and cortical tears caused by trauma can cause extravasation of erythrocytes, and with hemolysis and deposition of hemoglobin in the neurofibrillary network, iron ions are freed from the hemoglobin to form the typical iron-containing hemosiderin (hemosiderin), which shows high-density areas in MRI, a permanent histological feature of traumatic epilepsy in humans. The epileptic foci are actually located around scar tissue in what appears to be largely normal brain tissue. This is because the scar tissue itself does not produce abnormal electrical emissions, whereas the neurons within the brain tissue surrounding the scar are the sites that actually produce epileptiform discharges. Factors contributing to the development of late onset traumatic epilepsy in pediatric patients include subdural hematoma at the time of trauma, cranial hematoma, depressed skull fracture, cerebral contusion, cerebral edema, intracranial infection, or previous early onset traumatic epilepsy. It has been reported that the incidence of late onset epilepsy is 25% to 30% in those with early onset epilepsy after trauma, while the incidence of late onset epilepsy is only 3% in those without early onset epilepsy after trauma. However, it has also been suggested that there is no correlation between early-onset and late-onset traumatic epilepsy in pediatric patients. Whether the site of brain injury is associated with the development of late-onset traumatic epilepsy has not been determined, but most authors suggest that trauma to the parietal, anterior temporal lobe, and medial aspect appears to predispose to late-onset traumatic epilepsy. The clinical form of seizures varies from case to case and may be generalized, partial seizures or partial seizures with secondary generalization, and partial seizures may have motor or sensory aura. Traumatic epilepsy generally does not manifest as aphasic seizures. 4. Post-surgical epilepsy The incidence of post-surgical epilepsy is related to the primary etiology, nature, lesion site, surgical route and the extent of surgical trauma. The incidence of post-operative epilepsy in the following order: brain abscess (45%-72%), meningioma (17%-29%), glioma (19%-36%), and supratentorial aneurysm (14%-7%). Surgery with a large range of trauma to brain tissue is prone to postoperative epilepsy; surgery with a smaller range of trauma (e.g., ventricular puncture and drainage) has a low incidence of postoperative epilepsy. Injury to any part of the brain can cause epilepsy, but tumors or other lesions on the convex surface of the brain or in the parsagittal sinus are more likely to cause epilepsy after surgery because this area is closest to the cortical area of the central anterior-posterior gyrus of the brain, and the excitation threshold in this area is low. In addition, history of epilepsy and family history are also associated with the incidence of postoperative epilepsy. The high incidence of postoperative epilepsy in those with preoperative seizures and a family history of epilepsy suggests that the individual’s pre-existing epileptogenic characteristics and genetic factors play an important role.