A macular fissure is a tissue defect that occurs in the macula from the inner retinal membrane to the photoreceptor cell layer, severely impairing the patient’s central vision.Knapp and Noyes first reported traumatic macular fissures in 1869 and 1871, respectively, and Kuhnt first reported non-traumatic macular fissures in 1900.
I. Disease classification:
1.Classification according to etiology.
(1) Idiopathic macular fissure.
(2) Traumatic macular fissure.
(3) Highly myopic macular fissure.
(4) Other secondary macular fissures.
2.According to the morphology of macular fissure.
(1) full-layer macular fissure.
(2) lamellar macular fissure.
Second, the cause of pathogenesis
Except for idiopathic macular fissure, the causes of 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, on the other hand, took more than a century to develop until 1988 when Gass proposed that tangential pulling of the retinal surface in the macular region was the main cause of the formation of idiopathic macular fissures, providing a theoretical basis for the use of vitreous surgery to treat macular fissures. The theory was proposed based on the ratio-anatomical relationship of the vitreoretinal interfacial interface, which is derived from the liquefaction of the vitreous and the occurrence of posterior vitreous detachment during the aging process in humans. As the vitreous cells in these residual posterior cortices increase in value, they form a traction parallel to the retinal surface in the central macular sulcus, initially resulting in a small central macular sulcus detachment, followed by a central sulcus detachment, and eventually a full macular fissure.
III. Pathogenesis
The pathogenesis of macular lacunae is not fully understood. However, with the increase of case reports, it was found that only about 5%-15% of macular fissures were caused by trauma. At the beginning of this century, some authors suggested that cystoid macular degeneration was the main cause of macular fissure, while others suggested that age-related vascular changes led to macular atrophy and eventually macular fissure formation, but these ideas could not explain the pathogenesis of idiopathic macular fissure. In 1988, Gass revolutionized the pathogenesis of idiopathic macular fissure by suggesting that the tangential vitreous traction in front of the central macular recess was the main cause of idiopathic macular fissure, which provided a theoretical basis for the use of vitreous surgery to treat macular fissure. This provided a theoretical basis for the use of vitreous surgery to treat macular fissures. Since then, the number of reports on vitrectomy for macular fissures has increased. In 1995, through clinicopathological studies and based on the fact that visual acuity could be improved after vitreous surgery, Gass further showed that the formation of idiopathic macular fissures was not accompanied by the loss of retinal nerve tissue in the central sulcus. thus explaining the recovery of visual acuity after surgery.
Pathophysiology
The clinicopathology of macular lacunae can be manifested as follows.
(1) Macular hole size of 400-500 μm.
(2) “Detachment” around the macular hole up to 300-500μm.
(3) Atrophy of photoreceptor cells.
(4) macular cyst-like changes.
(5) Yellow dot-like deposits resembling vitreous warts on the surface of the RPE.
(6) The presence of preretinal astrocytes.