Rasmussen syndrome (RE), also known as Rasmussen’s encephalitis, was first reported by Rasmussen in 1958 and has been reported in various countries since then. It is a rare but severe condition that is caused by immune-mediated brain dysfunction resulting in unilateral hemispheric atrophy with progressive neurological dysfunction and refractory epilepsy. The etiology of the disease is still unknown, and some arguments have linked the disease to viral infections, but it has not been determined which viral infections can cause the disease. The disease is characterized by various forms of seizures, progressive hemiparesis, and mental retardation. Symptomatology: Rasmussen’s syndrome has its main onset in childhood, with an average age of 6 years, but can also occur in adolescence and adulthood. The most common first symptom is a myoclonic seizure, but it can also be a simple partial seizure, a complex partial seizure, or a secondary generalized seizure, often presenting as a partial seizure continuum with clear consciousness and involving any small muscle group, such as one side of the mouth, face, fingers, or lower extremities. Seizures, however, are not an obligatory symptom of Rasmussen syndrome. In particular, brain damage caused by AIDS can also manifest as partial status epilepticus. Partial epilepsy can also be seen in forest encephalitis, non-ketotic coma, multiple sclerosis, brain tumors, MERRF, and L-K syndrome. Diagnostic criteria: When a child presents with partial status epilepticus, at least one of the following must be present to make a diagnosis: 1. progressive neurological impairment at the onset of epilepsy or later; 2. progressive hemispheric atrophy with hypointense on CT or abnormal signal on MRI; 3. positive oligoclonal zone on cerebrospinal fluid examination; 4. brain biopsy pathology confirming chronic encephalitis . In addition, Rasmussen syndrome interictal EEG shows diffuse slow waves or multifocal spikes in the contralateral cerebral cortex of the affected limb, and sometimes bilateral independent epileptiform discharge heads can be seen; 5. MRI examination shows atrophy of one cerebral hemisphere, long T2 signals in the frontal, temporal and parietal lobes or partial lobar dysplasia. Therefore, a comprehensive evaluation of the patient’s clinical features, EEG performance, neuroimaging and serological data is crucial for a definitive diagnosis. Treatment: Almost all antiepileptic drugs have no satisfactory efficacy in Rasmussen syndrome. Antiviral drug therapy has also not shown definitive clinical efficacy. However, there are studies using ganciclovir to treat Rasmussen syndrome with 1.5 years of seizure-free follow-up, so it is recommended that antiviral medication should be administered as early as possible when the disease is suspected. Because of the possibility of genetic coupling between epilepsy and immunodeficiency, patients with epilepsy may also develop immunodeficiency after long-term antiepileptic drug therapy, and the antibodies produced lead to immune-mediated damage to the cerebral cortex, so immunomodulation is an important aspect of the treatment of Rasmussen syndrome, and most studies have concluded that immunoglobulin therapy is a treatment approach worth trying, but it is generally There is increasing evidence that lateral hemispherectomy is significantly more effective than partial resection for seizure control, reducing seizures by 60% – 80%. The shorter the duration of the disease and the younger the age, the better the outcome. After years of follow-up, there is further improvement in both psychomotor development and social functioning. Therefore, early surgical treatment is currently considered very important and should be aggressively pursued once the diagnosis is clear, rather than waiting too long for drug therapy alone and delaying the disease.