Epilepsy, a common neurological disorder, is characterized by a predisposition to seizures. Despite advances in treatment, many cases remain resistant to current therapies. Recent research highlights the role of inflammation in epilepsy, showing that inflammatory mediators from brain and immune cells contribute to seizure generation and epileptogenesis. Inflammation can be both a cause and a consequence of seizures, influencing their occurrence and severity. Evidence from clinical and experimental studies indicates that inflammation is involved in the pathophysiology of epilepsy, with inflammatory processes contributing to neuronal loss and seizure-related damage. Inflammatory mediators such as cytokines and chemokines are implicated in the development and progression of epilepsy. The brain's immune response, involving microglia, astrocytes, and peripheral immune cells, plays a critical role in inflammation. Inflammation can also be neuroprotective in certain contexts, such as during CNS injury. Understanding the complex role of inflammation in epilepsy could lead to new therapeutic targets for antiepileptic drugs. Immune-modulating and anti-inflammatory therapies, such as corticosteroids, ACTH, and IVIg, have shown promise in treating certain forms of epilepsy, particularly those with autoimmune components. The role of inflammation in epilepsy-related comorbidities, such as depression and cognitive impairment, is also being investigated. Future research aims to develop targeted anti-inflammatory therapies and improve treatment outcomes for patients with refractory epilepsy.Epilepsy, a common neurological disorder, is characterized by a predisposition to seizures. Despite advances in treatment, many cases remain resistant to current therapies. Recent research highlights the role of inflammation in epilepsy, showing that inflammatory mediators from brain and immune cells contribute to seizure generation and epileptogenesis. Inflammation can be both a cause and a consequence of seizures, influencing their occurrence and severity. Evidence from clinical and experimental studies indicates that inflammation is involved in the pathophysiology of epilepsy, with inflammatory processes contributing to neuronal loss and seizure-related damage. Inflammatory mediators such as cytokines and chemokines are implicated in the development and progression of epilepsy. The brain's immune response, involving microglia, astrocytes, and peripheral immune cells, plays a critical role in inflammation. Inflammation can also be neuroprotective in certain contexts, such as during CNS injury. Understanding the complex role of inflammation in epilepsy could lead to new therapeutic targets for antiepileptic drugs. Immune-modulating and anti-inflammatory therapies, such as corticosteroids, ACTH, and IVIg, have shown promise in treating certain forms of epilepsy, particularly those with autoimmune components. The role of inflammation in epilepsy-related comorbidities, such as depression and cognitive impairment, is also being investigated. Future research aims to develop targeted anti-inflammatory therapies and improve treatment outcomes for patients with refractory epilepsy.