Thyroid-related ophthalmopathy, currently defined as an autoimmune disease. The cause of pathogenesis is unclear. The pathogenesis is not clear. The literature shows that 90% of patients with thyroid-related ophthalmopathy have combined hyperthyroidism, 5% have combined hypothyroidism, and 5% have normal thyroid function. Of these patients with combined hyperthyroidism, 40% have hyperthyroidism followed by ocular disease, 40% have both hyperthyroidism and ocular manifestations, and 205 have ocular disease followed by hyperthyroidism. The classic diagnostic criteria for thyroid-related eye disease are: 1) hyperthyroidism combined with ocular abnormalities; 2) normal thyroid function combined with upper eyelid recession. However, in patients with combined upper eyelid recession, I prefer to diagnose normal thyroid function ophthalmopathy in the absence of abnormal thyroid function. The treatment of thyroid-related ophthalmopathy begins with a determination of the severity and activity of the patient’s condition. The severity is most commonly determined clinically by the NOSPECS index, with N being no discomfort that the patient can subjectively feel; O being only subjective discomfort such as eye swelling, eye pain, and head discomfort; S being visible ocular abnormalities such as eyelid edema, eyelid congestion, and conjunctival congestion; P being visible eye protrusion; E being the appearance of restricted eye movement; C being the appearance of corneal changes; and S being the appearance of visual acuity change. Determination of activity: 1. Eyelid edema. 2. Eyelid congestion. 3. Conjunctival edema. 4, Conjunctival congestion. 5, tear mound edema. 6. Resting pain in the eye. 7. Painful eye movement. However, the determination of activity is still difficult. When the doctor is confronted with a patient, the patient’s condition is static relative to the doctor and relies more on the patient’s narrative, such as abnormal changes in the eye in the last period of 3 months. Because activity itself is a process that changes over time. Treatment principles: Mild patients in the stationary phase are given only supportive symptomatic treatment, such as with sunglasses and glasses to correct diplopia; moderate to severe patients can consider surgical decompression, surgical repair cosmetic surgery. Active patients are preferred to hormone therapy, such as high-dose hormone shock therapy, oral hormone therapy, and local post-ocular injection for those who cannot tolerate hormone. Radiation therapy is currently limited to active moderate to severe patients, and radiation therapy for mildly active patients is still controversial. Most patients treated with radiation therapy are relapsed patients after hormone reduction and patients who cannot tolerate hormone side effects. Chemical immunosuppressive therapy currently has clinical applications. The above briefly describes the rationale and the current basic situation in clinical work. Medicine itself is a practical science, and the mechanisms of development of many diseases are unclear, thyroid-related eye disease being an example. The current treatment is basically symptomatic, and because the pathogenesis is unclear, the cure still needs to be studied diligently. The development of modern medicine and diligent physicians will eventually unravel its mysteries.