October 2011
Volume 52, Issue 11
Letters to the Editor  |   October 2011
Author Response: Vitreoschisis in Diabetic Macular Edema
Author Affiliations & Notes
  • Avinoam Ophir
    Division of Ophthalmology, Hillel-Yaffe Medical Center, Hadera, Israel.
  • Michael Martinez
    Division of Ophthalmology, Hillel-Yaffe Medical Center, Hadera, Israel.
Investigative Ophthalmology & Visual Science October 2011, Vol.52, 8456-8457. doi:https://doi.org/10.1167/iovs.11-8603
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      Avinoam Ophir, Michael Martinez; Author Response: Vitreoschisis in Diabetic Macular Edema. Invest. Ophthalmol. Vis. Sci. 2011;52(11):8456-8457. https://doi.org/10.1167/iovs.11-8603.

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      © ARVO (1962-2015); The Authors (2016-present)

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We would like to thank Dr. Sebag for bringing up the issue of vitreoschisis (v-schisis) in diabetic macular edema (DME). 
V-schisis is described as splitting within the native multilamellar posterior vitreous cortex (PViC) during an anomalous posterior vitreous detachment (PVD). That definition is similar to that of retinoschisis or iridoschisis, which describe a split in the native relevant tissues. That is different from a split at an hypercellular membrane, which Dr. Sebag and colleagues consider v-schisis as well. 1 Furthermore, v-schisis that was shown histologically in only one eye in their study, 1 did not represent a split at the hypercellular ERM, since fibroblasts were not detectable at the specimen. Further, Dr. Sebag wrote in an earlier article, “It is possible that at least part of the multi-lamellar structure present at the vitreo-retinal interface in pathologic eyes is the internal limiting membrane (ILM) of the retina rather than the PViC alone.” 2 This would obviously have a different effect on decision-making of whether a split involves the ILM. Based on the above, when a split is shown by the OCT as occurring within a hyperreflective, fibrocellular epimacular membrane, we refrain from terming it as v-schisis (also explained in the article). Since the split is not at the native PViC, its exact histologic level is unclear, and the mechanism of that split and its consequences might be different from a split at the native PViC. That is in contrast to Dr. Sebag's approach, in which he interprets the membranous split in Figure 1 of his letter as v-schisis. 
Posterior vitreous detachment most commonly precedes idiopathic epiretinal membrane (ERM) emergence. 3 V-schisis at the native vitreous cortex occurring during an anomalous PVD is hypothesized to be a pathogenesis of less than half of these idiopathic ERMs. In the aforementioned study on idiopathic ERM and macular pucker using the imaging device OCT/scanning laser ophthalmoscopy (SLO), v-schisis that included in definition also eyes with a split at the hypercellular epiretinal membranes associated with the posterior vitreous cortex, was reported to occur in 42% (19/44) of eyes. 1 However, recent studies did not interpret v-schisis as an association between idiopathic ERM and PViC (or, posterior hyaloid) when the PViC was apparent. For example, in Figure 2 of their study, Koizumi et al. 4 describe “a hyperreflective zone of the detached posterior hyaloid to be contiguous with the attached posterior hyaloid and the ERM.” Chung et al. 5 also investigated the morphologic features of idiopathic ERMs in the presence or absence of PVD. V-schisis was not referred to anywhere in these manuscripts that studied idiopathic ERMs. Rather, each figure was described as it was actually seen, similarly to the way we describe our observations on the various associations between the ERM and PViC in the DME eyes, including Figure 3A. 
In his letter, Dr. Sebag writes in paragraph 3, “the findings [in our study] at the vitreoretinal interface are most likely the manifestation of diabetic vitreopathy with vitreoschisis.” First, the words “most likely” direct us to an interpretation. However, we should be attentive to this option, since it might lead us farther from reality, as judged by Socrates and now quoted by Dr. Sebag. Secondly, Dr. Sebag comes to that conclusion by correlating two unrelated data points: (1) 57% of the 23 subjects in our present study had proliferative diabetic retinopathy (PDR); (2) in another study on PDR, 81% of eyes were described to have v-schisis. 6 However, all 81% of these eyes had either traction retinal detachment or combined traction/rhegmatogenous retinal detachment. This is not the case in our series. Furthermore, in another study on PDR, only 17% of eyes were suggested by ultrasonography to have v-schisis 7 ; however, most of these eyes had vitreous hemorrhage as well. Again, vitreous hemorrhage was not the state in our series. In addition, Dr. Sebag et al. 1 recently studied the prevalence of v-schisis in various macular diseases using the OCT/SLO and reported the presence of v-schisis in only 13% of eyes with non-PDR, 1 although without histologic proof in any diabetic eye. Nonetheless, these proposed low prevalences of v-schisis in DME, at 13% and 17%, as detected by OCT-SLO or ultrasound, respectively, 1,7 contradict Dr. Sebag's generalization that our findings at the vitreoretinal interface are most likely the manifestation of diabetic vitreopathy with vitreoschisis. 
In contrast to idiopathic ERM, the posterior vitreous is commonly attached in DME eyes with ERM. 8 However, anomalous PVD can occur without v-schisis. 3 In group A of our DME series 9 (i.e., incomplete papillary PVD), the vitreous at the macula is attached, so the option of v-schisis at the macula does not seem relevant. Yet it is possible that a variant of a v-schisis process took place in some eyes with partial PVD at the macula (group B), as we explain in the manuscript. However, this should be proven in further studies. 
Finally, vascularization associated with the membrane in Figure 2 was detected clinically and is presented now in SD-OCT. 
Gupta P Yee KM Garcia P . Vitreoschisis in macular diseases. Br J Ophthalmol. 2011;95:376–380. [CrossRef] [PubMed]
Sebag J . Vitreoschisis. Graefes Arch Clin Exp Ophthalmol. 2008;246:329–332. [CrossRef] [PubMed]
Kishi S Demaria C Shimizu K . Vitreous cortex remnants at the fovea after spontaneous vitreous detachment. Int Ophthalmol. 1986;9:253–260. [CrossRef] [PubMed]
Koizumi H Spaide RF Fisher YL . Three-dimensional evaluation of vitreomacular traction and epiretinal membrane using spectral-domain optical coherence tomography. Am J Ophthalmol. 2008;145:509–517. [CrossRef] [PubMed]
Chung SE Lee JH Kang SW Kim YT See SW . Characteristics of epiretinal membranes according to the presence or absence of posterior vitreous detachment. Eye. Published online, July 15, 2011.
Schwartz SD Alexander R Hiscott P . Recognition of vitreoschisis in proliferative diabetic retinopathy: a useful landmark in vitrectomy for diabetic traction retinal detachment. Ophthalmology. 1996;103:323–328. [CrossRef] [PubMed]
Chu TG Lopez PF Cano MR . Posterior vitreoschisis: an echographic finding in proliferative diabetic retinopathy. Ophthalmology. 1996;103:315–322. [CrossRef] [PubMed]
Gandorfer A Rohleder M Grosselfinger S . Epiretinal pathology of diffuse diabetic macular edema associated with vitreomacular traction. Am J Ophthalmol. 2005;139:638–652. [CrossRef] [PubMed]
Ophir A Martinez MR . Epiretinal membranes and incomplete posterior vitreous detachment in diabetic macular edema, detected by spectral-domain optical coherence tomography. Invest Ophthalmol Vis Sci. 2011;52:6414–6420. [CrossRef] [PubMed]

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