prognosis is not good; however, if noninduced seizures occur after the primary dis­ease improves, chronic epilepsy can develop. Therefore, the recurrence of epilepsy is a key factor affecting the overall prognosis. Among 194 patients with acute symp­tomatic seizures reported by Grau-Lopez etal. [154], 56 (29%) had a second seizure during a 2-year follow-up, indicating that 29% of patients with acute structural brain injury may develop epilepsy. Among 54 patients with cerebral venous throm­bosis described by Pais-Cunhaz etal. [155], 3 experienced seizures. Among 346 patients with acute symptomatic seizures described by Tsur etal. [159], 29.2% experienced recurrent seizures during follow-up. Rodrigo-Gisbert etal. [167] con­ducted a study on 230 patients with SE and reported that 198 patients (86.1%) had acute symptomatic epileptic status, 55 patients (23.9%) of whom later experienced seizures. Rodrigo-Gisbert etal. [168] followed 360 patients after their rst onset of SE for 1.8years and reported that 109 patients (30.3%) experienced seizures during the follow-up period, suggesting that 5–30% of patients with acute symptomatic seizures with brain injury develop chronic seizures within 1–3years. (2) Factors related to the development of chronic epilepsy: not all acute symptomatic seizures evolve into chronic epilepsy requiring treatment, so predicting the development of chronic epilepsy has become important for improving patient prognosis. Grau­Lopez etal. [154] conducted a study on 194 patients with acute symptomatic sei­zures due to acute structural brain injury and found that signicant epileptiform discharge on EEG and SE were important markers for epilepsy recurrence within 2years and progression to chronic epilepsy. Lopez-Espejo etal. [163] studied 207 children and newborns and reported that patients with acute symptomatic SE, abnormal EEG activity, and cortical lesions were more likely to experience epilepsy recurrence. In a prospective cohort study of EEG monitoring of 81 patients with ischemic stroke, Tatillo etal. [169] also reported that patients with highly suggestive rhythmic or periodic patterns on EEG and no delta region attenuation which is an important indicator for predicting the progression of chronic epilepsy, had a greater likelihood of epilepsy recurrence. It is suggested that continuous EEG monitoring can provide useful information for identifying patients at greater risk of epilepsy after stroke, which can aid in individualized treatment and care. Rodrigo-Gisbert etal. [167] studied 198 patients with acute symptomatic SE and reported that etiol­ogy, time to start treatment, EEG pattern, and nonresponsiveness were strong pre­dictors of epilepsy formation after new SE.These studies have shown that SE, epileptoid discharge on EEG, and progressive aggravation of etiology (such as tumor, autoimmune encephalitis, and progressive brain injury) are strong predictors of the progression of acute symptomatic epilepsy to chronic epilepsy [170].

symptomatic epilepsy needs to be treated with medication has always been contro­versial. Acute symptomatic seizures are a symptom of the primary disease, and as the primary disease improves, most seizures stop on their own. Considering the side effects of drugs and treatment uncertainty, the use of ASMs is not necessary. Kim etal. [165] reported that 54 (2.3%) of 2312 stroke patients had acute symptomatic seizures. They found that seizures could increase NIHSS scores but had no effect on treatment, and the prognosis of patients with epilepsy was the same as that of patients with or without treatment. Tyvaert et al. [171] suggest that epilepsy of immune origin can be divided into two types: acute symptomatic seizures secondary to autoimmune diseases and autoimmune-related seizures; the latter refers to chronic seizures and requires long-term treatment, while the former only refers to acute symptomatic seizures, for which the use of ASMs has little effect [172]. However, Byrnes etal. [173] conducted a study on 465 stroke patients, 101 of whom used ASMs for a long time, mainly due to the abnormal EEG data of the patients. Therefore, they suggested that acute symptomatic epileptic seizures with risk fac­tors still need to be treated with ASMs. Sortino etal. [174] also advocated the selec­tion of ASMs. A comparison of phenobarbital, midazolam, valproic acid, and other drugs revealed that lidocaine and levetiracetam may be more effective for treating acute symptomatic epileptic seizures in children. (2) Primary prevention: Zaccara et al. [175] reviewed the literature on the need for primary prevention of acute symptomatic seizures and found that the evidence supporting primary prevention of acute symptomatic seizures was limited and of low quality, which was not enough for routine recommendation. (3) Secondary prevention: Whether ASMs are needed to prevent acute symptomatic seizures from progressing to chronic seizures has not been determined. A total of 75.7% of the 346 patients described by Tsur etal. [159] took ASMs, and the authors speculate that ASMs are benecial for reducing sei­zures during follow-up. Qiang etal. [176] studied 488 patients, 58 (11.9%) of whom had seizures 3years after intracerebral hemorrhage. They did not nd that preven­tive use of ASMs had an effect on patient seizures, suggesting that secondary pre­vention of seizures was not necessary, and Zaccara etal. [175] did not recommend secondary prevention of acute symptomatic seizures. (4) Discontinuation of ASMs: Although acute symptomatic epilepsy is unlikely to be followed by chronic epi­lepsy, secondary prevention has no denite efcacy. Byrnes et al. [170] reported that most patients with acute symptomatic epilepsy were still taking ASMs after discharge, and their survey of clinics specializing in acute symptomatic epilepsy management also revealed that 27% of patients continued to take ASMs even when they did not have seizures or seizure-like abnormalities. Herzig-Nichtweiß etal. [30] reported that acute symptomatic epilepsy is very common in neurological intensive care. To prevent subsequent seizures, long-term treatment with ASMs is often prescribed despite a lack of supporting evidence. It has also been argued that the selective use of ASMs may be appropriate for patients with acute symptomatic seizures with risk factors, so ASMs are chosen [159, 173]. Therefore, patients tak­ing ASMs need to receive personalized management to achieve safe withdrawal of drugs. An online survey showed that the majority of neuro-intensivists suggest that the use of these ASMs should generally not be for more than 3months [177].

The use of epilepsy detection devices to understand the occurrence of systemic tonic–clonic seizures, respiratory and heart rate monitoring devices to detect cardio­pulmonary distress, prevention of airway obstruction (safety pillow), and the use of drugs to reduce central ventilation deciency may also have preventive effects on SUDEP [209]. In addition, studies in animal models of SUDEP have revealed that a variety of neurotransmitters, including 5-HT and adenosine, may be involved in the pathophysiological mechanism of SUDEP, and these neurotransmitters may become targets for future SUDEP drug intervention [209].