l. What is 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 (N-methyl-D-aspartic acid receptor), which is the Chinese name for N-methyl-D-aspartate receptor, is widely distributed in the central nervous system, such as the brain and spinal cord. 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 tests made the two ineffective in differentiating them for a long time, and 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. How are the toxic autoimmune encephalitis antibodies produced? It has been found that a small percentage of autoimmune encephalitis antibodies are produced by benign or malignant tumors in the body (e.g., teratoma can produce anti-NMDA receptor anti-Hu, small cell lung cancer produces anti-Hu antibodies); another percentage of patients have immune dysfunction even though no tumors are found in their bodies. Therefore, while giving immunotherapy to patients, doctors never give up looking for possible hidden tumors in their bodies. The treatment of patients with autoimmune encephalitis is a very difficult process. Patients with autoimmune encephalitis often have severe lung infections and even require ventilator-assisted breathing, while severe psychiatric symptoms make care and attention very difficult. The peak of the disease lasts from a few weeks to several months.