Secondary epilepsy is formed by an abnormal process in which nerve cells and their networks in the brain, which were originally normal, are continuously affected by synaptic contacts with cells damaged by the primary epileptogenic focus, and eventually acquire cellular epileptiform discharges. The causes of epilepsy are generally considered to be traumatic brain injury, tumor, vascular malformation, vascular obstruction, infection, poisoning, and hypoxia. However, not all of the above-mentioned disorders present with epilepsy, so attention should be paid to explore how the above-mentioned disorder areas cause neurons in distant lesion areas to produce epileptogenic damage similar to the primary foci, with similar abnormal discharges and clinical manifestations of epilepsy. These secondary foci, however, represent populations of epileptic-like cells that are not directly affected by the primary lesions described above. The resulting secondary epilepsy is the cause of the presence of seizures that continue to occur or continue to worsen after the primary lesion has been eliminated with treatment. There are three stages in the formation of secondary epileptogenic foci: The first stage is the dependent stage At this point, epileptiform discharges can be recorded locally in the primary epileptic focus and in the contralateral cortex. The two discharges are accompanied by a certain latency period and are positively charged. If there is no discharge in the primary epileptic focus, the secondary focal area has normal EEG activity. When the primary foci are removed or suppressed by pharmacological treatment, the secondary foci discharges then disappear. The second stage is the intermediate stage, when the primary epileptic focus is not discharged, and the secondary epileptic focus area shows paroxysmal abnormal discharges, and spike waves can be recorded on the EEG. At this time, the activity of the secondary epileptic focus is no longer dependent on the primary epileptic focus. However, if the primary epileptic focus is removed immediately, the secondary epileptic focus discharges will gradually disappear after several weeks. Because the neurons of the secondary epileptic foci in the intermediate phase have some ability to discharge synchronously, the secondary epileptic foci can discharge abnormally on their own at this time, although there is no influence of the discharge of the primary epileptic foci. However, the excitability of this discharge is variable. It can gradually disappear on its own in the absence of the continuing driving influence of the primary epileptic focus, and there is a certain degree of reversibility. The third stage is the independent stage characterized by non-dependence of the discharge between the primary and secondary epileptic foci. When the primary epileptic focus is cleared, it does not lead to the disappearance of the secondary epileptic focus. The latter discharges continue to exist or become more frequent, and seizures can continue to occur clinically, even with increasing frequency. This indicates that the brain cells of the secondary epileptogenic focus have caused irreversible and permanent changes. The occurrence of damage to secondary epileptogenic foci is closely related to the contact of axonal projection fibers of neurons in the primary epileptic focus and is proportional to the number of contact fibers. The conduction pathways of secondary epileptic discharges are completely different from the diffusion pathways of Jacksonian localized epileptic discharges, which are localized directly to the adjacent surrounding nerve cells, and very few, if any, are transmitted indirectly through the corpus callosum late in the seizure process. In contrast, secondary epilepsy is mostly transmitted via the long-range intrahemispheric projection fiber pathways of the abundant projection fibers of the corpus callosum, arcuate fibers, and superior longitudinal fasciculus. Multifocal epilepsy can result from multiple independent brain injuries and often presents clinically with more than one form of seizure, with no functional connection between the types. In contrast, there must be an axonal connection between the secondary epileptic focus and the primary epileptic focus, and the seizure forms of both also have a functional axonal connection, e.g., the patient’s primary seizure manifests as a sensory abnormality in the right hand, and the subsequent secondary seizure manifests as a motor or sensory abnormality in the left hand. Therefore, the longer the duration of epilepsy, the greater the likelihood of secondary epilepsy. For example, secondary epileptogenic damage occurs in 35% of patients with brain tumors, with an incidence of 29% in those with a shorter duration of disease than 12 years and 61% in those with a longer duration of disease than 12 years. The younger the age of first-onset epilepsy, the more likely it is to occur. There is a relationship between the age of first-onset epilepsy and the probability of secondary epilepsy. Secondary epilepsy occurred in 10 of 18 cases in those with an age of onset of 0.5 to 25 years, and in none of 12 cases in those with an age of onset of 26 to 60 years. Secondary seizures have diverse presentations and are less likely to occur in patients of advanced age. Therefore, surgical excision of the primary epileptic focus may be considered to prevent secondary epileptic foci when treatment with drugs or when drug therapy is ineffective, and care should be taken to continue treatment of secondary epilepsy after removal of the primary epileptic focus while observing its movement.