Hyperbaric oxygen therapy (HOT) is usually considered to be effective when initi­ated within 24h of the acute phase of CMP, and the initiation of treatment within 6h can further improve neurologic outcomes at 6months [402]. For those with DEACMP, there seems to be no effective treatment. Leucine-rich repeat and immunoglobulin- like domain-containing protein-1 (LINGO-1), a nerve growth inhibitory factor expressed in the regeneration microenvironment of the CNS, is also highly expressed in a rat model of DEACMP, whereas intraperitoneal injection of retinoic acid (10mg/kg) can suppress the expression of LINGO-1 and ameliorate the clinical symptoms of these rats [403]. ASMs are usually selected for epileptic seizures according to seizure type, according to principles similar to those used for patients with HIE.

The relationship between alcohol consumption and seizures is complex and multi­faceted. The most important risk factor for seizures associated with alcohol con­sumption is withdrawal [406]. Ethanol exerts its neuromodulatory effects primarily through the perturbation of receptor-governed ion channel functions on neuronal membranes. It acts as an antagonist of the N-methyl-D-aspartate (NMDA) receptor, a key receptor for glutamate, thus attenuating excitatory glutamatergic synaptic sig­naling. Ethanol also impedes calcium ion translocation across the NMDA receptor, a process that is dependent on the ethanol concentration. Notably, sustained ethanol exposure precipitates an increase in NMDA receptor activity, a condition posited to underpin the clinical phenomena associated with alcohol withdrawal syndrome. Furthermore, ethanol has been shown to potentiate chloride ion ow through the gamma-aminobutyric acid type A (GABAA) receptor, mimicking the pharmaco­logical effects of benzodiazepines. Adaptations within the CNS to chronic ethanol exposure manifest as tolerance, characterized by quantitative alterations in GABAA and NMDA receptor populations. These adaptations include a decrease in GABAA receptor numbers and an increase in NMDA receptor numbers, coupled with decreased GABAA receptor sensitivity to GABA and increased NMDA receptor sensitivity to glutamate. Additional mechanisms, such as the desensitization of ade­nosine receptor responses during alcohol withdrawal and genetic polymorphisms in the neuropeptide Y-encoding gene, have been proposed to contribute to the patho­physiology of alcohol withdrawal seizures. Evidence supporting a genetic predispo­sition includes studies demonstrating familial aggregation of seizure susceptibility associated with alcohol use.

Heroin-induced spongiform leukoencephalopathy (HSLE) is a toxic encephalopa­thy caused by dermabrasion or intravenous injection of heroin and is characterized by vacuolated spongy degeneration of the cerebral white matter.

The disease was rst described in Amsterdam in 1982 by Woltes etal. [409]. With acute or subacute onset, symptoms of cerebellar injury are usually the rst clinical manifestation. Further aggravation of the disease may result in damage to the pyra­midal and extrapyramidal systems or even coma and decortication, while sensation is often normal. There have been reports of epileptic seizures in patients with HSLE, which are associated with cortical necrosis of the hippocampus [410]. The imaging changes in HSLE are located in the white matter region of the brain, especially the cerebellum, showing extensive and symmetrical alterations. The most characteristic features are symmetrical, round-like or buttery-like lesions on both sides of the cerebellar midline with clear borders, which often show low signals on T1WI and high signals on T2WI, the pathology of which reveals white matter vacuoliza­tion [411].

Lacking appropriate research evidence, the treatment of seizures due to HSLE usu­ally follows the principles of conventional ASM selection, but attention should be given to liver and kidney function, as these patients often have impaired functions due to drug and toxic substance abuse.

There are two main hypotheses for the mechanism of injury in RE: vascular endo­thelial cell damage and loss of the regenerative capacity of brain glial cells. Together, these two mechanisms can cause cerebral ischemia and/or hemorrhage, cerebral

Glucocorticoid therapy, such as dexamethasone, should be used for seizures occur­ring in the early stage of RE (within 6months) [416]. In the majority of patients, remission can be achieved after treatment, and long-term use of ASMs is not neces­sary. Late-onset seizures often require long-term medications. Most patients can be treated by monotherapy with sodium channel blockers such as carbamazepine, oxcarbazepine, and lamotrigine or broad-spectrum ASMs such as valproic acid, levetiracetam, and topiramate. Specically, valproic acid, a histone deacetylase inhibitor, can enhance radiosensitivity in esophageal squamous cell carcinoma [417], and thus, it can not only control seizures but also improve the efcacy of radiation therapy for tumors in such patients.

Organ transplantation is a surgical procedure in which a healthy organ (e.g., kidney, liver, heart, or lungs) is transferred from one person to another, who requires the organ to replace their unhealthy or damaged organ. Kidney transplantation is the most common type, followed by liver, heart, lung, and hematopoietic stem cell transplantation. Approximately one-third of patients who undergo solid organ trans­plants develop neurological symptoms. Epidemiological studies have shown that 2–24% of solid organ transplant recipients experience seizures, compared to 7–27% of hematopoietic stem cell transplant recipients [418]. This makes epilepsy the sec­ond most common central nervous system complication after organ transplantation, following neurotoxicity [419].

Early seizures after heart transplantation are associated with immunosuppressant­induced stroke and reversible posterior encephalopathy (PRES), with relatively few non-immunosuppressant-related factors. Other potential etiologies may include tumors, a history of preoperative seizures, diabetes mellitus, and renal insufciency. Additionally, hypoxic encephalopathy due to cardiac arrest can also induce seizures.

In addition to solid organ transplants causing epilepsy, nonsolid organ trans­plants can also lead to the development of epilepsy. The most common scenario is observed in hematopoietic stem cell transplantation. A retrospective study involving over 1400 hematopoietic stem cell transplant recipients revealed that 7% of patients developed seizures postoperatively, and 40% of these seizures were related to medi­cation administration [427]. The proportion of generalized versus focal seizures in the context of seizures after hematopoietic stem cell transplantation appears to be similar, with the rst seizure after transplantation typically characterized by a focal nonconvulsive seizure.

(4) Cerebrovascular disease: Another risk factor associated with epilepsy develop-

For acute seizures following organ transplantation, such as status epilepticus, intra­venous lorazepam and, if necessary, fosphenytoin may be administered. After achieving seizure control, it is crucial to identify and correct factors associated with toxic calcineurin inhibitor (CNI) levels, electrolyte or glucose abnormalities, and hypertension. When selecting an anti-seizure medication for a solid organ transplant patient, considerations should include the type of seizure, patient safety and tolera­bility, and organ dysfunction, particularly of the liver and kidneys.

Levetiracetam is currently considered the drug of choice for anti-seizure medica­tion selection after solid organ transplantation. It is widely used in infants, children, and adults and is available in various forms, such as tablets, oral solutions, and injections. Levetiracetam is primarily metabolized in the blood and excreted by the kidneys, making it less likely to induce hepatic metabolism and drug–drug interac­tions [446, 447]. The recommended dosage for levetiracetam is considered to be 1000mg/day, with incremental increases of 1000mg every 1–2 weeks, up to a maximum of 3000 mg/day. If administered intravenously, a single injection of 1000mg is typically given, and the effect is generally achieved within 15–60min­utes. No interactions have been identied between levetiracetam and various drug­metabolizing enzymes [448–450]. Furthermore, the impact of levetiracetam on metabolic enzymes has not been observed. Notably, levetiracetam does not affect cyclosporine metabolism [451].

In a study conducted by Chih-Hsiang Lin etal., 15 patients who received leveti­racetam, either intravenously or orally, as a single agent for seizure control after liver transplantation were seizure free during the treatment period. Unfortunately, two patients died during the follow-up period due to severe infection and cancer. Importantly, there were no neurological sequelae that interfered with the patients’ daily activities throughout the course of drug administration. This lack of interfer­ence was not attributed to the inefcacy of immunosuppressant drugs or hepatic