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Myopic traction maculopathy: pathogenic mechanisms and surgical treatment.

To this point, we have been talking about clinical problems that are caused primarily by the process of posterior vitreous detachment (PVD). Now, we are moving to a series of three clinical problems that are not primarily caused, but may be exacerbated, by vitreous traction complicating early stages of PVD. Myopic traction maculopathy (MTM) is an extensive schisis-like thickening in the outer retina of highly myopic eyes with posterior staphyloma. In addition to the schisis-like thickening, there may be other findings, including inner retinal fluid, foveal detachment, and lamellar or full-thickness macular hole. This disorder goes by a number of names, including myopic foveoschisis, and it occurs in a reasonably high percentage of patients with pathologic myopia. The pathoanatomical features were not characterized before optical coherence tomography (OCT), and the pathogenesis is not completely understood. Myopic traction maculopathy virtually always occurs within a posterior staphyloma. The pathoanatomy intuitively suggests a gradual stretching or splitting of the retina over time, likely caused by relative tautness of the inner retina compared with the outer retina within the concavity of a posterior staphyloma. The precise cause of traction is still debated (Figure 1). Some authors argue for a preretinal structure, such as partial PVD with vitreomacular traction, a remnant cortical vitreous layer after PVD, or obvious epiretinal membrane (ERM) (Figure 2A). Others have argued that MTM is caused by something intrinsic to the retina, notably the internal limiting membrane (ILM) or the stiffness of retinal arterioles (Figure 2B). In a recent article, we presented evidence that the cause of the inner retinal noncompliance in MTM is not uniform but varies from one eye to another and that surgical repair can be tailored successfully to the specific pathologic mechanism(s) effective in a given eye. We identified four major traction mechanisms: • Vitreomacular traction (from perifoveal PVD) • Remnant cortical vitreous layer (after PVD) • Epiretinal membrane • Intrinsic noncompliance of the ILM.