bubble_chart Overview

Post-traumatic epilepsy refers to epileptic seizures secondary to traumatic brain injury, which can occur at any time after the injury and are highly unpredictable. Some may appear immediately after the injury, while others may suddenly manifest years after the head injury has healed. However, not all patients with brain trauma develop epilepsy, with reported incidence rates ranging from 0.1% to 50%, varying significantly due to differing data sources. According to Caveness (1916), who analyzed over a million cases of head injury with brain tissue damage, 30% of patients experienced post-traumatic seizures. Among these, 50% occurred within 6 months post-injury, and about 80% within 2 years. Approximately half of these cases resulted in long-term recurrent seizures, causing immense suffering and danger to patients. Post-traumatic epilepsy is more common in young males, likely due to their higher risk of head injuries. Evans (1963) noted that patients with a family history of epilepsy had a higher incidence of post-traumatic seizures (9%) compared to those without (3%), suggesting a genetic component in the development of post-traumatic epilepsy. Generally, the more severe the brain injury, the higher the likelihood of epilepsy. Open brain injuries are more likely to lead to epilepsy (20–50%) than closed injuries (0.5–5%). Penetrating injuries through the dura mater are 5–10 times more likely to cause epilepsy than non-penetrating injuries, with firearm injuries having an especially high incidence rate of 42.1%, compared to 16.4% for non-firearm injuries.

bubble_chart Pathological Changes

Early epilepsy (immediate or recent onset) refers to seizures occurring within 24 hours after injury, accounting for about 30%, and may be related to brain parenchyma injury, intracranial hemorrhage, depressed fracture compression, local cerebral ischemia, edema, and changes in generation and transformation. Among these, 30% occur within the first hour after injury, especially in children, often presenting as partial seizures. Some believe that early epilepsy often indicates the possibility of developing advanced-stage habitual epilepsy. Intermediate-stage [second-stage] epilepsy (delayed or advanced-stage onset) refers to seizures occurring between 24 hours and 4 weeks after injury, accounting for about 13%, mostly due to pathological changes such as cerebral contusion and laceration, intracranial hemorrhage, cerebral edema, swelling, and softening. Injury to the frontal-parietal central area of the cerebral cortex is particularly prone to epilepsy, followed by injury to the medial temporal lobe, including the hippocampus and amygdala, which are susceptible areas for epilepsy. These injuries can lead to microscopic chemical changes, metabolic disturbances, and electrophysiological alterations in neurons, resulting in seizures. The aforementioned early and intermediate-stage [second-stage] epilepsy mainly stems from acute brain parenchyma injury, intracranial hematomas (especially acute subdural hematomas), or secondary tissue reactions and the healing process following brain injury. These pathophysiological changes can gradually alleviate and recover over a certain period, so they do not necessarily lead to recurrent seizures. They are often partial seizures, and if they respond well to medication or resolve spontaneously, surgical intervention is unnecessary. Administering appropriate antiepileptic drugs for prevention or seizure control is sufficient. Advanced-stage epilepsy (late or habitual onset) refers to post-traumatic epilepsy that appears from 4 weeks to several years or even decades after injury, accounting for about 84%, and often presents as recurrent habitual seizures. The onset of such epilepsy is difficult to predict, with patients experiencing prolonged post-traumatic amnesia or early spasms being more prone to advanced-stage epilepsy. Jennett (1975) noted that 31% of patients with acute intracranial hematomas developed advanced-stage epilepsy, 25% of those with early post-traumatic spasms did so, and 15% of those with depressed fractures did. Open head injuries, especially gunshot wounds, are more likely to cause epilepsy due to the higher likelihood of dural rupture, brain parenchyma contusion, and retained foreign bodies. Over half of advanced-stage epilepsy cases occur within the first year after injury, while about one-fifth of patients experience their first seizure four years post-injury, with the latter often being more refractory. The majority of advanced-stage post-traumatic epilepsy cases present as focal seizures (about 40%), with temporal lobe epilepsy accounting for about 25%. The causes are often related to dural-cerebral scars, intracerebral cysts, porencephaly, brain abscesses, intracranial hematomas, foreign bodies, and fracture fragments. These lesions compress, pull, or irritate adjacent normal or partially injured brain tissue, leading to epileptic neuronal discharges and subsequent seizures.

bubble_chart Clinical Manifestations

Except for minor seizures and severe bilateral myoclonus, any type of epilepsy can occur. Most patients have relatively fixed seizure types, while a few may experience changes. Early and intermediate-stage [second stage] epilepsy may spontaneously resolve and cease in about 25% of patients within 2 years or slightly longer. However, advanced-stage epilepsy often tends to worsen, potentially evolving from focal seizures to generalized seizures. In severe cases, symptoms such as memory decline, personality disorders, and intellectual impairment may manifest. Frontal lobe scars typically cause major seizures without aura. Lesions in the central-parietal region often lead to motor or sensory seizures in the limbs. Temporal lobe damage presents as psychomotor epilepsy, while occipital lobe involvement often includes visual auras. Post-traumatic early epilepsy often follows an initial seizure with a variable interval of weeks or months before the frequency gradually increases. About half of the patients may show improvement or cessation of seizures within 3 to 5 years. Some patients continue to experience seizures, but if the frequency is low and the severity mild, antiepileptic drugs can usually control them. A small number of patients, however, suffer from frequent and highly refractory seizures, resulting in a poorer prognosis.

bubble_chart Diagnosis

Traumatic epilepsy always has a history of head trauma, whether it is closed or open craniocerebral injury. Different types of epileptic seizures occurring at different periods after the injury, especially focal seizures where the site of brain tissue injury matches the epileptic focus in patients with no history of epilepsy before the injury, are not difficult to diagnose. The diagnosis of traumatic epilepsy, in addition to clinical manifestations and characteristics, also relies on electroencephalogram (EEG) examination. Epileptic waves originating from the cerebral cortex are often high-amplitude sharp waves, spike waves, sharp-slow wave complexes, or spike-slow wave complexes, usually with a negative phase. For deep-seated lesions, the waveforms are mostly sharp waves or sharp-slow wave complexes, with lower amplitude and sometimes alternating negative and positive phases. Localization of the epileptic focus, in addition to waveform, amplitude, and phase, should also consider the synchrony of epileptic waves. Two or more synchronous epileptic waves sometimes originate from the same focus, presenting as bilaterally synchronous paroxysmal slow waves, generally considered indicative of central system seizures or chronic epilepsy.

In addition, brain CT or MRI scans can also help determine the location and nature of the lesion, often revealing localized or diffuse brain atrophy, gliosis or cystic degeneration, porencephaly, arachnoid cysts, enlarged cisterns, ventricular traction, depressed fractures, hematomas, abscesses, and foreign bodies.

bubble_chart Treatment Measures

Short-term spasms within the first week after trauma often have no significant clinical implications and do not recur thereafter, thus requiring no special treatment. For recurrent early or intermediate-stage [second-stage] epilepsy, systematic antimicrobial therapy should be administered. Generally, medication is selected based on the type of seizure. For grand mal and focal seizures, the order of preference for antiepileptic drugs is phenytoin sodium, phenobarbital, carbamazepine, primidone, or sodium valproate. For petit mal seizures, sodium valproate, ethosuximide, diazepam, or phenobarbital are commonly used. For psychomotor seizures, carbamazepine is the first choice, followed by phenytoin sodium, phenobarbital, primidone, sodium valproate, or diazepam. For myoclonic seizures, diazepam, nitrazepam, or clonazepam are preferred. The principle of medication is to use the minimal dose that completely controls seizures without causing side effects. Therefore, the dose should start small and gradually increase until seizures are fully controlled, with planned administration based on the timing of the patient's seizures. Once the selected drug proves effective, monotherapy is preferred, and changes should not be made lightly. Blood drug concentration should be monitored, maintaining therapeutic levels until the patient remains seizure-free for 2–3 years. Then, the dose can be carefully and gradually reduced. If no seizures occur after complete discontinuation, the condition can be considered clinically cured. For a minority of refractory advanced-stage epilepsy cases unresponsive to systematic drug therapy, surgical intervention is necessary. Under electrocorticography monitoring, the brain scar and epileptogenic focus are resected, with over half of patients achieving favorable outcomes.

**Surgical Method:** Preoperative localization of the epileptogenic focus is critical. Although post-traumatic brain scars are the pathological cause of traumatic epilepsy, the actual seizure activity often originates from nearby (or occasionally distant) epileptogenic discharge foci, sometimes even multifocal. Therefore, during surgery, not only must the brain scar tissue be removed, but also the seemingly normal epileptogenic foci; otherwise, seizures cannot be controlled. The surgery should be performed under local or intravenous anesthesia to allow intraoperative electrocorticography and electrical stimulation. If the scalp has significant scarring, the surgical incision should account for scalp blood supply and reconstructive design. Craniotomy with a bone flap is preferred for better exposure and accurate localization of epileptogenic foci. If there is a skull defect, the scalp should first be carefully dissected from the dura mater, followed by circumferential dural incision. The dura mater should then be gently separated from the brain tissue to avoid excessive injury to normal cortex. Under electrocorticography guidance, the brain scar and epileptogenic focus are resected, with care taken to preserve critical functional areas. The scarred gelatinous tissue should be excised as much as possible, extending deep to the ventricular membrane without penetrating the ventricle. Cortical epileptogenic discharge foci should be treated with subpial gray matter resection. Based on the electrocorticography-monitored area, the pia mater is coagulated along the midline of the gyrus and incised, followed by removal of the gray matter using a small curette or suction. The preserved pia mater is then repositioned. Electrocorticography is repeated until all epileptiform discharges disappear. Finally, hemostasis is ensured, the dura mater is meticulously repaired, and skull defects are addressed either concurrently or in a staged procedure as needed. The scalp is closed in layers with subcutaneous drainage for 24 hours. Postoperatively, antiepileptic drug therapy should continue for 2–3 years.