1. Autoimmune encephalitis The human immune system often produces autoantibodies, which are toxic. When autoantibodies damage the central nervous system and neurological and psychiatric disorders occur, it is called autoimmune encephalitis. A variety of antibodies that are neurotoxic and can cause neurological damage have been identified, such as anti-NMDA, anti-Hu, Ma2, CV2 (CRMP5), AMPA receptor 1, AMPA receptor 2, GABAB receptor, LGI1 and Caspr2 antibodies. The NMDA receptor is an ionotropic glutamate receptor with NMDA receptors play important physiological roles in the development of the nervous system (e.g., regulation of neuronal survival, regulation of neuronal dendrites and axons). NMDA receptors not only play an important physiological role in the development of the nervous system (e.g., regulating neuronal survival, regulating the development of dendritic and axonal structures, and participating in the formation of synaptic plasticity), but also play a key role in the formation of neuronal circuits and participate in the regulation of learning, memory, and mental activity. When the human body is in a pathological state, more toxic antibodies against NMDA receptors are produced in the body, and the NMDA receptor structures distributed in nerve cells are the first to be damaged, thus causing a diffuse destruction of the central nervous system, which leads to a series of pathological changes such as electrophysiological disorders of the nervous system and edema of nerve cells. This leads to a series of pathological changes such as electrophysiological disorders of the nervous system and neurocytic edema. As the disease worsens, patients exhibit decreased mental capacity, uncontrollable seizures, vegetative dysfunction (excessive sweating, insomnia), and in severe cases, persistent coma and respiratory abnormalities. Pathologically, anti-NMDA receptor antibody encephalitis manifests as lymphocyte-dominated inflammatory cells infiltrating the brain parenchyma and forming cuff-like structures around blood vessels. The similarity between autoimmune encephalitis and viral encephalitis in terms of pathological manifestations, clinical symptoms and biochemical examinations has made it impossible to effectively distinguish between the two for a long time. It was only after the discovery of anti-NMDA receptor antibodies by the French scientist Dalmau J in 2007 that the medical community began to study the disease pattern of autoimmune encephalitis in depth. 2. anti-NMDA receptor encephalitis In 2007, Dalmau et al. discovered anti-N-methyl-M-aspartate receptor (NMDA) antibodies against hippocampal and prefrontal nerve cell membranes in such patients and proposed the diagnosis of anti-NMDA receptor encephalitis. So far (2010), more than 100 cases of anti-NMDA receptor encephalitis have been reported abroad, while only one case of ovarian teratoma-associated encephalitis has been reported in China, whose clinical manifestations and disease course were similar to those of anti-NMDA receptor encephalitis, but anti-NMDA receptor antibody testing was not performed. Clinical presentation: Anti-NMIA receptor encephalitis is more common in young women (about 91%), but it can be seen in any age group, with the youngest known case being 4 years old, the oldest being 76 years old, and the median age being 23 years. About 59% of patients have tumors, most of which are mature ovarian teratomas and a few are mediastinal teratomas and testicular teratomas. Or even small cell lung cancer or neuroblastoma. In most cases, the tumor is found 3 weeks to 4 months after the onset of neurological symptoms, and the absence of tumor may also be associated with a shorter follow-up period. The clinical presentation of the disease is characteristic. The majority of patients have symptoms that resemble viral infections, such as fever, headache, cough, and malaise. At the beginning of the disease, there are obvious psychiatric abnormalities, including anxiety, agitation, bizarre behavior, delusions or paranoia, hallucinations or hallucinations, and some patients may experience short-term memory loss. Most patients develop epileptic seizures (76%) and reduced level of consciousness (88%) within 3 weeks of onset. Epileptic seizures can be of any type, with generalized tonic clonic seizures being the most common, followed by complex partial seizures. As the disease progresses to a catatonic-like schizophrenic stage, symptoms of agitation alternate with akinesis, with diminished or paradoxical responses to stimuli, and some patients exhibit mumbling or imitative language. During this phase, most patients may experience central hypoventilation (often requiring mechanical ventilation for respiration), dyskinesia, and autonomic dysfunction; the most common dyskinesia is involuntary orofacial movements, where patients may make bizarre faces and compulsively open and close their jaws (which can lead to self-injury of the lips, tongue, or teeth), as well as tardive dyskinesia, myoclonus and myofibrillation, atonia, and rhythmic contractions of the abdominal wall. Autonomic disturbances include arrhythmias, various types of tachycardia or bradycardia, dilated pupils, shortness of breath, sweating, and increased or decreased blood pressure. After this stage most patients gradually recover (75%), with a few remaining with severe disability or death. Some scholars have divided the course of the disease into 5 stages, including prodromal, psychiatric symptoms, unresponsive, hypermotility and gradual recovery, but there is no clear boundary between the stages. Diagnosis: There are no uniform diagnostic criteria for anti-NMDA receptor encephalitis, but the current trend is to diagnose it in young female patients with unexplained clinical psychiatric symptoms with epileptic seizures, memory loss, reduced level of consciousness, motor deficits, or even central hyperventilation, especially in those with ovarian teratoma, and positive cerebrospinal fluid and/or serum anti-NMDA receptor antibodies. Treatment: Treatment of anti-NMDA receptor encephalitis includes a combination of tumor resection and immunotherapy, and early detection and removal of the tumor is the key to treatment of the disease. Seki et al. concluded that early tumor resection is an important measure to promote full recovery of patients with this disease, and that early surgery shortens the duration of hypoventilation and motor deficits compared to patients without tumor resection. Immunotherapy for anti-NMDA receptor encephalitis includes hormone, plasma exchange, and immunoglobulin therapy, etc. Iizuka et al. found that immunotherapy alone may also lead to recovery. Ishiura et al. added rituximab to the combination of hormone and immunoglobulin therapy in a patient with anti-NMDA receptor encephalitis in which no tumor was detected, resulting in gradual improvement of psychiatric symptoms and eventual complete recovery. Therefore, it is proposed that treatment with rituximab may be considered for patients with undetected tumors or poor results of other immunotherapy. Prognosis: Although the symptoms of anti-NMDA receptor encephalitis are generally severe, the prognosis is better than that of other types of paraneoplastic encephalitis; Dalmau et al. showed that the majority of patients (approximately 75%) recovered completely or had only mild disability, while a minority had severe disability or even died, and those with a tumor that was removed within the first 4 months of neurological disease had a better prognosis. About 85% of patients with mild residual disability or eventual basic recovery show signs of frontal lobe dysfunction, including inattention, reduced planning, impulsivity and behavioral disorders; about 27% have significant sleep disturbances, such as hypersomnia and sleep apraxia. Approximately 15% of patients with anti-NMDA receptor encephalitis may experience 1 – 3 recurrences of encephalitis, and recurrence rates are less common in patients who undergo tumor resection early in the disease than in those with late or no tumor resection.