The so-called idiopathic type of EMM is caused by glial migration and proliferation from a defect in the internal limiting membrane (ILM) created by a posterior vitreous separation (6). Retinal breaks, retinopexy, photocoagulation, inflammation, and vascular disease (7) can lead to glial proliferation (8, 9, 10, 11, 12) on the retinal surface. Retinal pigment epithelial cells (13,14) can migrate through a retinal break and proliferate on the retinal surface just as they do in proliferative vitreoretinopathy (PVR). EMMs can be thought of as localized glial or retinal pigment epithelium (RPE)-induced PVR.

Hypocellular contraction of the EMM causes nonrhegmatogenous elevation of the macula thought by the authors to be responsible for a major fraction of the associated visual loss. Fluid under the macula is universally seen on optical coherence tomography (OCT). Reversible macular edema secondary to macular separation from the fluid pumping mechanism of the RPE contributes to visual loss as well. Although it is widely stated that traction on the ILM can produce macular edema, it is unclear what the mechanism would be and the concept remains unproven. Although the terms “macular pucker” and “surface wrinkling retinopathy” emphasize retinal distortion, some patients have marked improvement in postoperative vision in spite of persistent retinal distortion and metamorphopsia.

The typical EMM patient experiences a relatively rapid loss of vision accompanied by metamorphopsia over a period of several weeks, followed by relative stabilization of visual function. In spite of this typical history, it is common practice for doctors to advise a patient with a recent history of visual loss to, for example, the 20/50 level that he or she should wait until the vision is reduced to 20/80 or worse before considering surgery. In fact, the vision will usually stabilize at a visual level at or near that noted on initial presentation. Because visual results are better with better preoperative vision and shorter duration, it is better practice to make a decision on surgical intervention on the first visit.

As with all surgical procedures, the decision to operate is a multifactorial process based on symptoms, extent of visual loss, visual needs, status of the other eye, age, duration, medical status, and the presence of other ocular diseases. There is no substitute for ethical, sound clinical judgment in making the decision to operate.

The principal author’s visual acuity threshold for surgery has moved from 20/200 to 20/40 in selected cases, as the methodology has improved. A patient with preoperative vision of 20/40 can and should be operated if the patient is significantly symptomatic, is in good health, is relatively young, and understands the issues. Specific visual acuity
levels are less important than symptomatology and impact on activities of daily living for recommendation of surgery for EMMs. Duration is a relative rather than absolute criterion because cases of 10 years’ duration have had significant visual improvement following surgery. The visual improvement in long-duration cases is presumably because the minimal amount of subretinal fluid present in these cases leads to minimal irreversible photoreceptor degeneration, just as is the case in central serous retinopathy. Macular edema, except in the vascular disease subgroup, is probably secondary to macular elevation, typically reversible and not a contraindication to vitreoretinal surgery. Knowledge that the patient had poor vision before the membrane occurred is an absolute contraindication to surgery. The slow recovery of vision after retinal reattachment surgery coupled with the typical 1-month onset of EMM makes it difficult to make a surgical decision in this situation. Patients with severe hereditary photoreceptor degeneration or a previous central retinal artery occlusion frequently have wrinkling of the retinal surface without an epiretinal membrane because of marked decrease in retinal thickness. Surgery is contraindicated in these situations (15, 16, 17, 18, 19, 20, 21, 22, 23, 24, 25, 26, 27).