PurposeTo discuss the unique morphology and origin of epiretinal proliferation associated with macular hole (EPMH) occasionally observed in full-thickness macular hole (FT-MH) or lamellar hole (LH) and to introduce the perifoveal crown phenomenon encountered when removing this unusual proliferative tissue.MethodsSixteen patients showing EPMH in spectral domain-optical coherence tomography were selected from 212 patients diagnosed with MH, LH, FT-MH, impending MH, macular pseudohole, or epiretinal membrane between January 2013 and December 2014. Of the 212 patients included for clinical analysis, 33, 23, 11, 7, and 190 exhibited LH, FT-MH, impending MH, macular pseudohole, and epiretinal membrane, respectively. We reviewed visual acuity, macular morphology, and clinical course. Surgical specimens were analyzed histologically.ResultsEPMH presented as an amorphous proliferation starting from the defective inner/outer segment (IS/OS) junction covering the inner macula surface. Among the 16 patients with EPMH, 11 underwent vitrectomy, and all exhibited the intraoperative perifoveal crown phenomenon. EPMH tissue was sampled in three patients, one of whom had more tissue removed than intended and showed delayed recovery in visual acuity. Despite hole closure, IS/OS junction integrity was not successfully restored in four of 11 patients. Five patients were followed-up without surgical intervention. Visual acuity slightly decreased in three patients and did not change in one patient, while the remaining patient was lost during follow-up. Among the three perifoveal crown tissues obtained, two were successfully analyzed histologically. Neither tissue showed positivity to synaptophysin or S-100 protein, but one showed positivity to cytokeratin protein immunohistochemical staining.ConclusionsEPMH exhibited a distinct but common configuration in spectral domain-optical coherence tomography. An epithelial proliferation origin is plausible based on its configuration and histological analysis. Perifoveal crown phenomenon was observed when removing EPMH during vitrectomy.
Purpose: To investigate the influence of intraocular pressure (IOP)-lowering eye drops on myopic retinoschisis. Methods: We investigated myopic retinoschisis patients with high myopia (defined as a myopic refractive error more than -8.0 diopters or an axial length longer than 26.5 mm), who were suspected of having glaucomatous optic neuropathy, using IOP-lowering eye drops between April 2014 and December 2018. We retrospectively analyzed the changes in optical coherence tomography findings after 6 months using IOP-lowering eye drops. The progression of retinoschisis was assessed by analyzing retinal volume changes. A decrease in the total retina volume and a decrease in volume more than 10% in one section out of five without more than a 10% volume increase in any other section was defined as resolution of myopic retinoschisis. The opposite case was defined as an aggravation. Results: We analyzed 17 eyes of 15 patients with high myopia. Six of 17 eyes (35.3%) showed a resolution of myopic retinoschisis at 6 months after using IOP-lowering eye drops. Of the 17 eyes, two (11.8%) experienced progression of myopic retinoschisis. Seven out of 14 eyes (50.0%) who were followed-up over 1 year showed resolution of myopic retinoschisis, and two eyes (14.3%) experienced progression of myopic retinoschisis. There was no macular hole development or posterior vitreous detachment during the follow-up period in the seven eyes, and there was no significant correlation between the absolute value of the initial IOP, axial length, IOP change, and degree of improvement of myopic retinoschisis. Conclusions: The use of IOP-lowering eye drops on highly myopic eyes with retinoschisis showed a significant improvement of myopic retinoschisis, when compared to previous studies. These findings suggest the possibility of IOP-lowering eye drops delaying or improving the natural course of myopic retinoschisis.
We sought risk factors for the development of persistent or recurrent central serous chorioretinopathy (CSC) in patients under long-term follow-up (>1 year) after photodynamic therapy (PDT). Methods: We retrospectively reviewed the medical records of patients who received PDT to treat CSC from January 2005 to February 2016. CSC was considered persistent if subretinal fluid (SRF) was evident for longer than 3 months or if additional treatment was required before 3 months. Also, CSC was regarded as recurrent when SRF re-appeared after initial complete resorption. Results: We enrolled 73 patients (77 eyes). The mean follow-up period was 48.9 ± 31.3 months (12 to 144 months). The persistent group consisted of 10 eyes (13%) and the recurrent group 17 eyes (22%). The mean time to recurrence was 39.8 ± 23.3 months, ranging from 3 to 91 months. Fifty patients (52 eyes) were enrolled in the treatment-naive group. The persistent group consisted of four eyes (8%) and the recurrent group 10 eyes (19%). The mean time to recurrence was 48.4 ± 30.0 months. On chi-squared analysis of recurrence risk factors in all patients, the odds ratio for eyes with a history of both focal laser and anti-vascular endothelial growth factor treatments prior to PDT was 2.94 (p = 0.031). Conclusions: CSC patients with histories of other treatment are likely to exhibit persistent or recurrent disease after PDT.
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