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Purpose: To report a case of Posner-Schlossman syndrome with retinal arterial tortuosity in a young male. Case summary: A 15-year-old male presented to our department with a halo in his left vision. Best corrected visual acuity was 0.6 and intraocular pressure was 59 mm Hg in the left eye. Slit lamp examination revealed corneal edema, keratic precipitate, deep anterior chamber, anterior chamber cell (1+) and open angle. Fundus examination revealed increased cup/disc (C/D) ratio and retinal arterial tortuosity. After treatment with anti-glaucomatic eyedrops, steroid eyedrops, and nonsteroidal anti-inflammatory drug (NSAID) eyedrops, intraocular pressure decreased to 15 mm Hg and C/D ratio decreased. Conclusions: Posner-Schlossman syndrome can occur even at an early age and must be included in the differential diagnosis of glaucoma in pediatric patients. Additional studies should be conducted regarding the association between retinal arterial tortuosity and Posner-Schlossman syndrome. J Korean Ophthalmol Soc 2014;55(11):1710-1713

Purpose: The purpose of this study was to investigate the prophylactic effect of brimonidine 0.15% on intraocular pressure (IOP) elevation and the risk factors for its elevation after intravitreal triamcinolone acetonide injection (IVTA). Methods: A prospective, randomized clinical trial was conducted on 67 eyes of 64 patients undergoing IVTA. Eyes were randomly divided into two groups, those which had used brimonidine 0.15% (40 eyes) and those which had not used it (27 eyes). IOP was measured preoperatively, at one week, and monthly until six months post-injection in each group. Results: The mean post‐injection IOP at one week was 11.93±3.36 mmHg for the group that had used brimonidine and 13.58±3.25 mmHg for the group that had not used it. The difference between the two groups was statistically significant at one week (p=0.049), but others were not statistically significant. An elevation in the IOP of more than 22 mmHg was seen in 8 eyes (20%) in the group using brimonidine and in 7 eyes (25.9%) in the group not using brimonidine. There was no difference in the incidence of IOP elevation between the two groups. Conclusions: Prophylactic use of brimonidine 0.15% will prevent sudden IOP elevation and will, therefore, prevent damage to the retina and optic nerve. However, in the long term, there is no prophylactic effect of brimonidine 0.15% on IOP elevation because there was no difference in the incidence of IOP elevation of more than 22 mmHg between the two groups.

Purpose: The purpose of this case report is to describe accompanying ocular findings, especially optic neuropathy, in a patient with MELAS syndrome. Methods: A 10-year-old male patient who had lactic acidosis and neurological symptoms (loss of consciousness, vomiting, epilepsy, decreased vision, and constricted visual field), underwent a brain magnetic resonance imaging (MRI) scan and a molecular genetic analysis. Results: A diagnosis of cerebral infarction due to occlusion in the right posterior cerebral artery was made and confirmed by MRI scan. The diagnosis of MELAS syndrome was confirmed by performing molecular genetic analysis demonstrating the transformation of the mitochondrial tRNAleu(UUR) gene (MTTL1) A to G(3243). According to the ocular examinations, the patientꡑs left eye showed decreased vision, hemianopsia, relative afferent pupillary defects, mild swelling of optic nerve, and decreased amplitude on visual evoked potential exam. Conclusions: We encountered a case of MELAS syndrome involving optic neuropathy, which can (although rarely) occur with this syndrome. Therefore, in patients with an optic neuropathy of uncertain etiology, clinicians should consider performing comprehensive ocular exams and molecular genetic exams to rule out the possibility of genetic diseases.