Knapp and Noyes first reported traumatic retinal fissure in the macula in 1869 and 1871 respectively, and Kuhnt first reported non-traumatic macular fissure in 1900, since then, various causes of macular fissure have been recognized one after another. Since then, various causes of macular lacunae have been recognized. The prevalence of this disease is not high, accounting for about 3.3 per 1000 of the population, with idiopathic macular fissures of unknown origin being the most common (about 83%), often occurring in healthy women over 50 years of age (average 65 years, female:male = 2:1), and in 6%-28% of both eyes. It also occurs partially in younger patients. Second, disease classification: 1, according to the etiology of classification: (1) idiopathic macular fissure (2) traumatic macular fissure (3) highly myopic macular fissure (4) other secondary macular fissure 2, according to the form of macular fissure: (1) full macular fissure (2) lamellar macular fissure Third, the cause: In addition to idiopathic macular fissure, other causes are clearer, such as trauma, high myopia cystoid macular edema, inflammation, retinal degenerative diseases, macular anterior membrane and eclipse retinopathy, etc. The understanding of idiopathic macular fissures took more than a century until 1988, when Gass proposed that tangential pulling of the retinal surface in the macula was the main cause of idiopathic macular fissures, providing a theoretical basis for the use of vitreous surgery to treat macular fissures. This theory is based on the anatomical relationship between the vitreoretinal intersection and the vitreous retina, which is due to vitreous liquefaction and the occurrence of posterior vitreous detachment during the aging process of human body. As the vitreous cells in these residual posterior cortices increase in value, the retinal surface in the central macular sulcus forms a traction parallel to the retinal surface, and a small central macular sulcus detachment occurs initially, followed by a central sulcus detachment, and finally a full macular fissure is formed. Pathophysiology: The clinicopathology of macular fissure can be shown as follows: 1. 400-500μm macular hole size; 2. 300-500μm “detachment” around macular fissure; 3. 6.The appearance of pre-retinal astrocytes.