Lennox-Gastaut syndrome (LGS) is a refractory epileptic encephalopathy that mainly affects children, but can also involve adults, and is characterized by multiple seizure types, electroencephalographic (EEG) abnormalities, and mental retardation. This review focuses on the etiology, pathogenesis, diagnostic criteria, and treatment of LGS. In terms of etiology, LGS may be caused by a variety of factors such as abnormal brain development, perinatal brain injury, inherited metabolic diseases, and gene mutations. The pathogenesis involves multiple gene mutations that affect the balance of neuronal excitability and inhibition.LGS is diagnosed on the basis of multiple seizure types with an age of onset of less than 18 years, an EEG that shows widespread slow (1.5~2.5 Hz) spiking slow complex waves, and a triad of intellectual and psychosocial dysfunction. Therapeutically, LGS is treated with antiepileptic seizure medications (ASMs) , including valproate, lamotrigine, and rufinamide, but patients often develop resistance to ASMs. Non-pharmacological treatments include ketogenic diet, vagus nerve stimulation (VNS) , and corpus callosotomy (CC) , which provide palliative treatment options for patients who have difficulty controlling seizures. Despite the variety of therapeutic options, the prognosis for LGS is usually poor, with patients often experiencing intellectual disability and seizures persisting into adulthood. This review emphasizes the importance of further research into the etiology and pathogenesis of LGS and the need to develop new therapeutic approaches to improve patients' quality of life and reduce the burden of disease.
