Abstract

Sir, we appreciate the thoughtful comments submitted in response to our recent article describing a new retinal phenotype (microcystic macular oedema) in a subset of patients with multiple sclerosis (Gelfand et al. , 2012). We thank Balk et al. and Abegg et al. for sharing similar observations of microcystic abnormalities of the inner nuclear layer in patients with optic nerve injury in the absence of multiple sclerosis. Clarification of the specificity of microcystic macular oedema will contribute towards understanding its aetiology, its relationship to optic neuropathy and its significance in multiple sclerosis. As discussed in our article, we considered two separate, but not mutually exclusive, mechanisms that could contribute to the development of microcystic macular oedema in multiple sclerosis: retinal inflammation with associated blood-retinal barrier leakage and/or trans-synaptic degeneration. We appreciate the proposition by Balk et al. that distortion or loss of Mueller cells in the inner nuclear layer could be an additional contributory mechanism. This warrants more detailed investigation in future studies. We agree that microcystic changes may occur strictly as a consequence of trans-synaptic degeneration; however, the individual cases highlighted by Balk et al. and Abegg et al. should be interpreted with caution. Balk et al. note an example of microcystic inner nuclear layer changes …

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