Abstract
Myopic traction maculopathy (MTM) is an important treatable condition among individuals with high myopia. It encompasses a spectrum of conditions ranging from retinal retinoschisis to full-thickness macular hole (FTMH). Traction of various kinds, together with the morphologically changes in eyes with high myopia, play a central role in the pathogenesis. Individuals with MTM in the more advanced stage with visual loss or showing significant progression can be treated surgically, while those with early disease and stable visual acuity should be monitored with optical coherence tomography. Pars plana vitrectomy with peeling of the epiretinal membrane and/or internal limiting membrane (ILM) forms the backbone of the treatment. In the absence of macular hole (MH), various modifications of surgical techniques have been suggested to increase the rate of surgical success and to prevent complications, in particular the formation of secondary macular hole. If macular hole is present, on the other hand, surgical adjuncts have been studied to maximize the rate of macular hole closure. These adjuncts include endotamponade, inverted ILM flap or autologous ILM transplantation, autologous blood/platelet concentrate, lens capsular flap transplantation, macular buckle, and autologous neurosensory retinal transplantation. Advances in surgical instruments and skills have shown promises in the management of this challenging condition.
Highlights
As described in the previous chapter, myopic foveal retinoschisis was first described in 1958 [1], by Takano and Kishi in 1999 through the advent of optical coherence tomography (OCT) [2]
Fovea-sparing instead of complete peeling of the ILM and avoidance of gas tamponade could prevent the formation of secondary macular hole in myopic traction maculopathy (MTM)
Central to the pathogenesis of MTM is traction, which was postulated to arise from one or more of the following mechanisms [7]: vitreomacular traction associated with perifoveal posterior vitreous detachment (PVD) [8–10]; relative incompliance of inner retinal structures to the outer retina which conforms to the shape of the posterior staphyloma; and traction exerted by retinal arterioles [14, 20, 21]
Summary
As described in the previous chapter, myopic foveal retinoschisis was first described in 1958 [1], by Takano and Kishi in 1999 through the advent of optical coherence tomography (OCT) [2]. The various pathological effects of traction on the macula in patients with high myopia were collectively termed myopic traction maculopathy (MTM) by Panozzo and Mercanti in 2004 [3]. The term MTM originally encompassed retinal thickening, macular retinoschisis, foveal detachment, and lamellar macular hole with or without epiretinal membrane and/ or vitreomacular traction [3]. It is generally accepted that eyes with complications such as foveal detachment or full-thickness MH with or without retinal detachment, or eyes with significant progression in the extent of macular retinoschisis on OCT should undergo intervention early. An early macular retinoschisis involving only a limited area of the macula with preserved vision should be monitored with OCT for any progression. The principles of the treatment are: (1) to relieve traction, mainly achieved through pars plana vitrectomy (PPV) with or without ILM peeling; (2) to minimize surgical damage to the weakened macula through technique modifications in order to prevent the formation of postoperative MH; and (3) in the presence of full-thickness MH to maximize the chance of hole closure through the use of various surgical adjuncts
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