Post-traumatic epilepsy is a recurrent seizure disorder caused by craniocerebral trauma, and it should be noted that there is not only a temporal relationship between trauma and epilepsy, but also a causal relationship. According to the time of initial onset, post-traumatic seizures are often divided into: 1. Immediate seizures: seizures within 24 hours after trauma. 2. 2. Early seizures: seizures between 1 day and 1 week after trauma. 3. Late seizures: seizures after 1 week after trauma. Only recurrent late seizures can be called post-traumatic epilepsy. Epidemiological surveys show that the incidence of post-traumatic epilepsy is 4%~10%. The pathogenesis of posttraumatic epilepsy is not fully understood, and Penfield and Erickson suggested that a series of biochemical, electrophysiological, and structural brain changes can occur after brain injury, leading to the formation of epileptic foci. Both primary and secondary damage to the brain following trauma can cause alterations in the neurons themselves or in the surrounding glial cells and blood vessels, thus contributing to excessive firing and abnormal hyper-assimilation of individual brain cells. Such alterations can be localized or widespread. In terms of pathophysiology, the main mechanisms of epileptogenesis are as follows: 1. Erythrocyte extravasation, lysis and deposition of iron-containing heme in the neurofibrillary network after craniocerebral trauma are directly linked to epileptogenesis. The cause of blood-induced seizures is closely related to iron ions, and the oxidation of the paste leads to the generation of oxygen, hydroxyl radicals and hydrogen peroxide, which in turn causes cell membrane rupture and changes in the microenvironment, resulting in seizures. 2. The scar left after traumatic brain injury also plays an important role in the formation of epilepsy. Aluminum powder injected into the rat cerebral cortex can produce epilepsy. And preventing scar formation with prednisolone or vitamin deficient diet can significantly reduce seizures. However, giving prednisolone after epilepsy had been induced did not significantly change the seizure frequency.3 Animal experiments revealed selective loss of neurons in the dentate gyrus portal area and significantly increased excitability of dentate gyrus granule cells in rats after traumatic brain injury. The risk factors affecting seizures: 1. severity of craniocerebral trauma: Annegers conducted a back analysis of 4541 patients with traumatic brain injury and found that the more severe the craniocerebral trauma, the higher the risk of post-traumatic seizures. 2.Length of latency: Those with late seizures had a high risk of post-traumatic seizure occurrence, whereas early seizures did not additionally increase the risk of late seizures. 3. Age: Asikainen studied 490 patients and divided the study population into three groups according to age: the first group was children under 7 years old (including 7 years old), the second group was 8 to 16 years old, and the third group was older than 16 years old. RESULTS: The incidence of early epilepsy was 30.8%, 20.0%, and 8.4% in the three groups, and late epilepsy 32.7%, 31.4%, and 18.9%, respectively. Therefore, it is believed that the younger the age, the more likely it is to have early and late seizures. Similar reports have been made by others. 4. Dural integrity: In patients with multiple severe traumatic brain injury, if the dura is intact, the incidence of epilepsy is 7% to 39%. If there is a break in the dura, it is 20%~57%. 5. Site of injury: Injury to any part of the skull can cause epilepsy, but posterior frontal, parietal and diffuse cortical injuries cause significantly more epilepsy than other parts of the brain. This may be related to the special structure and function of the neurons in the anterior and posterior central gyrus and their projection network. 6, Other risk factors: there are still paracranial amnesia within 24 hours, depressed skull fracture, intracranial hematoma, etc. Symptoms of post-traumatic epilepsy: Post-traumatic epilepsy and other causes of epilepsy are similar in symptomatology, thus various types of simple and complex partial seizures as well as generalized tonic-clonic seizures can occur after trauma. Early seizures are predominantly generalized tonic-clonic seizures, whereas most patients with late posttraumatic seizures have at least one generalized tonic-clonic seizure. Approximately 1 in 4 patients will have complex partial seizures. Ancillary tests for post-traumatic epilepsy: 1. Frontal and lateral radiographs should be taken for suspected skull fractures. In addition, the frontal-occipital position (Tang’s position) film should be taken for occipital force injury, and tangential position film should be taken for depressed fracture. For suspected optic nerve injury, optic nerve foramina should be taken, and for orbital fracture, Kirchner’s view should be taken. 2, lumbar puncture to understand the degree of subarachnoid hemorrhage and intracranial pressure. Lumbar puncture is contraindicated in severe injuries with significant intracranial hypertension or signs of brain herniation. 3, CT scan is currently an important basis for the diagnosis of cranio-cerebral injury. It can show skull fracture, cerebral contusion, intracranial hematoma, subarachnoid hemorrhage, ventricular hemorrhage, pneumothorax, cerebral edema or brain swelling, brain pool and ventricular pressure displacement and deformation, midline structure displacement. CT review should be performed when the condition changes. 4, MRI acute craniocerebral injury patients usually do not MRI examination. However, MRI is often better than CT scan for diffuse axonal injury, hemispheric base, brainstem, focal contusion foci and small hemorrhage foci, isointense subacute intracranial hematoma, etc. in stable conditions. 5. EEG epileptic waves originating from the cerebral cortex are often high amplitude spikes, spines, spikes and slow waves or spikes and slow waves combined, and the loci are usually negative; for deep lesions, the waveforms are mostly spikes or spikes and slow waves combined with lower amplitude, and the loci are sometimes negative and sometimes positive. In addition to the waveform, amplitude and phase, the synchronization of the epileptic waves should be noted. Two or more synchronized epileptic waves, sometimes from the same foci, presenting as bilaterally synchronized paroxysmal slow waves, are generally considered as central systemic seizures, or obsolete epilepsy. Treatment of post-traumatic epilepsy: 1. The prevention of early post-traumatic epilepsy should first remove its triggering factors. This includes timely removal of intracranial hematoma, rectification of depressed skull fractures, and early use of dehydrating agents, hormones, and other measures to reduce cerebral edema. Preventive drug therapy: Many studies have consistently shown that antiepileptic drug therapy (phenytoin sodium, phenobarbital, carbamazepine, sodium valproate) can prevent early seizures but cannot reduce the incidence of late seizures. 3, Drug maintenance therapy: For patients with seizures, they should be treated according to the principles of epilepsy drug therapy. 4.Surgical treatment: The main surgical modalities for post-traumatic epilepsy are: excision of the meningeal-haunted scar and its adjacent epileptogenic foci under cortical EEG monitoring, anterior temporal lobe, hippocampus, amygdala excision, multiple subchondral transverse fiber cut, corpus callosotomy, hemispherectomy.