Author's Reply.

I warmly thank Dr. Tripathy for his interest and discussion of our recent publication. As he mentioned in his first comment “ Figure 1 is a multicolor image from the Spectralis machine and not an infrared reflectance image, as has been described in the manuscript;” it should be corrected to state that Figure 1[1] is indeed a multicolor fundus image and not an infrared reflectance image. I agree that it would be interesting to analyze color fundus photograph and fundus fluorescein angiogram from the acute phase. Unfortunately, however, our patient was evaluated in a rural part of our country where we did not have access to the multimodal imaging evaluation.

Figure 1

Multicolor fundus and optical coherence tomography (OCT) image of the fellow eye show no signs of optic disc pit and its related maculopathy or juvenile retinoschisis.

At his presentation and during short-term follow-up I did not see any subretinal blood, central retinal arterial/venous occlusion, or pigmentary changes involving the macula. The mentioned unusual feature of rapid foveal atrophy in our patient may be due to macular capillary plexus disruption which could not be documented. During his physical examination, we could not find any signs of optic disc pit and its related maculopathy or juvenile retinoschisis in his fellow eye. As Dr. Tripathy requested, I attach the fellow eye's multicolor fundus image and optical coherence tomography (OCT) image as Figure 1.

I agree that OCT findings in whiplash maculopathy or shaken baby syndrome do not exactly match the findings of the current case. The main point of similarity between these reports and our case is the retinoschisis (retinal splitting), although there are major differences considering the exact level of splitting.

Clear signs of vitreous traction could not be seen on OCT [Figure 2],[1] but retinal disruption is primarily confined between the fovea and optic nerve head region. Firm attachment of the vitreous layers at these two sites and retinal disruption in this confined region may indicate that vitreous traction to these close sites of firm adhesion is one of the main pathogenic mechanisms for the development of retinal splitting in the current case.

Figure 2

Spectral domain OCT imaging after trauma revealed outer retinal swelling with relative preservation of inner retina. Disruption and folding of outer nuclear layer, IS/OS folding and cystic disruption of outer plexiform layer.

As Dr. Tripathy has also indicated, this case is a unique case of traumatic macular retinoschisis, the OCT features of which have not been reported to date to the best of our knowledge.

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