Follow-up Of Unoperated Idiopathic Macular Holes

Idiopathic macular hole ( IMH) is one of serious retinopathies which leads to the patients'visual acuity declining severely and is common in old people from 60 to 70 years old. Although the case of macular hole had been firstly reported by Knapp in 1869, the idiopathic macular hole was known mainly till 1980s.There are three major theories of the formation of macular hole. (1) Ocular trauma. (2) Cystoid macular degeneration. (3) Vitreomacular traction syndrome. After 1980s, more and more evidences show the relations between the formation and vitreomacular traction in the process of idiopathic macular holes along with the improvement of clinical equipments and observation techniques. But how vitreous body brings into effect on traction is disputed. In 1988, Gass proposed a new hypothesis to explain the formation of macular holes. It is the contraction of the preofoveolar vitreous cortex that leads to the foveal detachment. Then the tangential traction cause to gradually the formation of holes. Gass outlined the following classification of stages in the development of idiopathic macular holes based on biomicroscopic observations and presumed anatomic changes: Stage 1-foveal detachment; Stage 2 -early full-thickness hole(<400um); Stage 3-mature full-thickness hole(>400um); Stage 4-full-thickness macular hole of any size with posterior vitreous detachment. Recently as a result of the application of optical coherence tomography(OCT),the relation of vitreous and retina is increasing known, then we understand newly the mechanism of idiopathic senile macular holes. Posterior vitreous detachment occurs around fovea, due to the tightjoining of posterior vitreous and fovea. The contraction of the vitreous will lead to fovea centralis flatten out and cysts appear. Cysts may form full-thickness hole for unceasing traction. As further known, degenerative changes of the müller cell cone vitreous cortex interface and müller cell invasion and proliferation within the prefoveal vitreous cortex are the initial changes that lead to contraction of the prefoveal vitreous and retinal dehiscence of the umbo. Although numerous studies have reported outcomes after surgical management of macular holes, few studies have addressed the clinical course of unoperated macular holes. We have collected 43 eyes which are diagnosed idiopathic macular holes in the clinic department of our hospital from December 2002 to February 2004, and followed up them for 18-26 months. The clinical course of unoperated macular holes is addressed by the observation of anatomic changes and visual acuity.We examine the changes of macula lutea with the appliance of direct and indirect ophthalmoscope. The progresses of different stages are compared by the fundus color photography. Follow-up of unoperated macular holes demonstrates a progress in the course and increase in the diameter of the hole. The hole enlargement and vision loss occur more commonly among patients with stage 2 holes than among patients with stages 3 and 4 macular holes, which is significant. Clinical features associated with macular hole are observed, such as cystoid macular edema which appears commonly in stage 1 and decreases along with the course, operculum and epiretinal membrane which appear in stage 3. The pigmentary macular changes are found in all stages. Multiple yellow nodular opacities are found at a rim of holes. Follow-up of unoperated macular holes demonstrates a redistribution and reduced number of yellow nodular opacities, and development of a bull's-eye macular appearance resulting from retinal pigment epithelium(RPE)atrophy surrounding the macular holes. Follow-up of unoperated macular holes demonstrates declining in visual acuity in all stages. Vision loss generally stabilized at the 0.1 to 0.04 level. The vision loss occurs more commonly among patients with stage 2 holes than among patients with stages 3 and 4 macular holes. By the examination monocular fixed vision and visual field, we found the visual acuities in stage 1 are still central visions, some of them in stage 2 are central visions, some of them in stage 2 are periphery visions. All of them in stage 3 and 4 are all periphery visions .There is negative relation of the stages ,the diameter of the hole,the location of the hole and visual acuity. The visual acuity and the associated clinical features at baseline aren't significantly associated with visual outcome at final follow-up. There are following factors that influent visual acuity: (1) the location of the hole. (2) the diameter of the hole .(3) the area of photoreceptorsatrophy. As follow-up, there are two cases spontaneous closure of idiopathic macular holes. One is stage 2 hole, and the diameter of hole is very small. When posterior vitreous detachment happened, the glial cells proliferate and RPE cells move from each bank of the hole's edge to fill the hole's bottom and close the hole. If vision is central vision before the closure, visual acuity will be improved after the closure. The other is stage 3 hole .The epiretinal membrane that forms around the hole's edge contracts, and the glial cells proliferate and RPE cells move from each bank of the hole's edge, so let the hole close. Visual acuity is still periphery vision after closure because vision has been periphery vision before the closure. These guesses need be proved with pathological anatomy and more cases. The result demonstrates that surgery may be most beneficial for those patients with stage 2 macular holes...