Optic neuromyelitis optica is an immune-mediated inflammatory demyelinating disease of the central nervous system with predominant involvement of the optic nerve and spinal cord. It is characterized clinically by severe optic neuritis and long segmental transverse myelitis with longitudinal extension. The disease often begins in young adults, with a female predominance, and has a high recurrence and disability rate. In 2004, Lennon discovered a marker specific for optic neuromyelitis optica, namely antibodies to aquaporin 4 (AQP4-IgG), and in 2015 the Optic Neuromyelitis Optica International Collaborative Group updated the concept and diagnostic criteria for optic neuromyelitis optica spectrum disease to a larger scale, divided into AQP4-IgG positive or negative NMOSD. Clinical manifestations (six core symptoms) 1. Optic neuritis optica. It can be monocular, simultaneous or sequential in both eyes. Most of the disease starts rapidly and progresses rapidly. Visual acuity is mostly significantly reduced and even blind, mostly accompanied by eye pain, and severe visual field defects may also occur. In some cases, the treatment is not effective, and the residual visual acuity is <0.1. 2. Acute myelitis: the onset is rapid, the symptoms are severe, and the acute phase is characterized by severe paraplegia or quadriplegia, urinary and fecal disorders, and the spinal cord damage plane is often accompanied by radicular pain or Lhermitte's sign, and the high cervical medullary lesion can involve the respiratory muscles and lead to respiratory failure in severe cases. Paroxysmal painful or non-painful spasms, prolonged itching and intractable pain are more likely to occur during the recovery period. 3.Last area of medulla oblongata syndrome: It can be a single first symptom, manifested as intractable erratic, nausea and vomiting, which cannot be explained by other causes. 4.Acute brainstem syndrome: dizziness, diplopia, ataxia, etc. Some lesions have no obvious clinical manifestations. 5.Acute mesencephalic syndrome: drowsiness, episodic sleep-like manifestations, hyponatremia, abnormal thermoregulation, etc. Some lesions have no obvious clinical manifestations. 6, brain syndrome: decreased level of consciousness, cognitive language and other higher cortical functions, headache, etc., some lesions without obvious clinical manifestations. Treatment: including acute treatment, sequential treatment (immunosuppressive treatment), symptomatic treatment and rehabilitation treatment. 1. Acute treatment: aimed at reducing acute symptoms, shortening the course of the disease, improving the degree of disability and preventing complications. It mainly includes glucocorticoid therapy, plasma exchange, immunoglobulin and other methods. The principles of glucocorticoid therapy are high-dose shock, slow step-down, and small-dose long-term maintenance. 2. Sequential therapy: aims to prevent relapse and reduce the accumulation of neurological dysfunction. First-line drugs include: azathioprine, morte-macrolide, methotrexate, rituximab, etc. Second-line drugs include cyclophosphamide, tacrolimus, mitoxantrone, cyclosporine, etc. 3.Symptomatic treatment: Clinical attention should be paid to concomitant symptoms such as painful spasm, chronic pain, abnormal sensation, pruritus, intractable eruption, cystorectal dysfunction, cognitive impairment, spastic hypertonia of lower limbs, etc. If necessary, relevant drugs need to be given for symptomatic treatment. 4.Rehabilitation: Rehabilitation treatment for NMOSD is equally important. For patients with limb and swallowing dysfunction, corresponding functional rehabilitation training should be carried out early under the guidance of professional doctors. When applying high-dose hormone therapy, avoid excessive activities to avoid aggravating osteoporosis and weight-bearing on the femoral head. When the hormone is reduced to a small oral dose, activities can be encouraged and corresponding rehabilitation training can be carried out.