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The most common form of macular telangiectasia is type 2. It affects middle-aged or older people and can lead to progressive vision loss. There is thickening of the basement membrane with a decrease of endothelial cells and pericytes, very similar to diabetic vascular change. Macular telangiectasia type 2 can be associated with intraretinal neovascularization, subretinal neovascular membrane, exudation, and hemorrhage.1
Foveal cyst formation, absent or minimal macular edema (despite prominent leakage on fluorescein angiography [FA]), intraretinal hyperreflective lesions, and foveal flattening are the most common optical coherence tomographic (OCT) findings in patients with macular telangiectasia type 2. These may represent progressive loss of retinal tissue, possibly due to Müller cell degeneration. Visual loss occurs from atrophy of the foveal retina rather than exudation or retinal edema. A subnormal foveal thickness in macular telangiectasia type 2 may be associated with better macular function as assessed by microperimetry. It is hypothesized that in macular telangiectasia type 2, both primary neurosensory thinning and low-grade macular edema can be involved. The coincidence may result in normal retinal thickness but decreased retinal function. The hyperreflective plaque with shadowing on OCT corresponds to a black foveal or juxtafoveolar pigment plaque.2
Lira RPC, Silva VB, Cavalcanti TM, de Souza ACD, Pinto APDC. Intravitreous Ranibizumab as Treatment for Macular Telangiectasia Type 2. Arch Ophthalmol. 2010;128(8):1075–1078. doi:10.1001/archophthalmol.2010.155
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