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Euretina Lecture focuses on cystoid maculopathies and role of OCT
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NICE, France — The Euretina Lecture this year focused on cystoid maculopathies and the revolution that OCT has brought into the understanding of cystoid macular changes.
The history of cystoid macular edema is closely linked to blood-retinal barrier (BRB) studies and the advent of fluorescein angiography at the end of the 1960s, Alain Gaudric, MD, emeritus professor in the Department of Ophthalmology at the Lariboisière Hospital, University of Paris 7, said.
Alain Gaudric
The advent of OCT in 1995, which allowed the routine measurement of macular thickness, improved the understanding of cystoid macular changes in many ways, showing that CME is not always associated with leakage and BRB breakdown.
Treatments of diabetic macular edema, a major cause of vasogenic macular edema, may have limited functional effects when macular thickening results in relative retinal atrophy after fluid resorption. Atrophy may in fact be hidden in the macular thickening, Gaudric said.
“OCT changed the diagnostic paradigm of CME, which is not limited to BRB breakdown, but includes a broad range of cystoid maculopathies, such as retinal vein occlusion, chronic central serous choroidopathy, epiretinal membranes and vitreomacular traction,” Gaudric said.
For instance, a macular thickening with cystoid spaces may be due to mechanical forces in vitreomacular traction or myopic foveoschisis with no leakage from the macular capillaries.
“This produces what we could call a non-vasogenic macular edema whose en face image is absolutely similar to that of any other cystoid macular edema,” he said.
Other causes of non-vasogenic macular edema include some hereditary retinal dystrophies such as X-linked retinoschisis, enhanced S-cone syndrome and bestrophinopathy. Potentially retinotoxic drugs, such as taxanes, nicotinic acid and tamoxifen, can also lead to cystoid maculopathy.
Finally, primary Müller cell impairment in macular telangiectasia type 2 may result in cystoid maculopathy without macular thickening.
Future treatment strategies will probably be oriented toward an earlier treatment of chronic CME acting on the restoration of the BRB, but possibly also on the restoration of Müller cell function and cell-to-cell adherence, Gaudric said. – by Michela Cimberle
Disclosure: Gaudric disclosed financial support from Bayer and Novartis.