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Purpose: To report two cases of vitreous hemorrhage caused by avulsed retinal vessel syndrome (ARVS), one of which was successfully treated without vascular occlusion. Observations: A 62-year-old female presented with vitreous hemorrhage of unknown origin. We performed vitrectomy and found a detached and ruptured retinal vein below the optic nerve head. After coagulating the peripheral side of the blood vessel, we were able to prevent the recurrence of vitreous hemorrhage. However, she developed branch retinal vein occlusion and subsequently macular edema. In the other case, a 71-year-old woman also had vitreous hemorrhage, but the fundus was partially visible. The retinal vein in the superior nasal quadrant was detached from the retinal surface and bled into the vitreous cavity. We performed vitrectomy to relieve the vitreous traction. Although we did not coagulate the vein, there was no recurrence of vitreous hemorrhage after surgery. Conclusions and Importance: By releasing the vitreous traction with vitrectomy, we were able to treat the patient with ARVS without vascular occlusion.

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AIMS/INTRODUCTION: In older patients, the management of diabetic macular edema (DME) can be complicated by comorbidities, geriatric syndrome, and socioeconomic status. This study aims to evaluate the effects of aging on the management of DME. MATERIALS AND METHODS: This is a real-world clinical study including 1,552 patients with treatment-naïve center-involved DME. The patients were categorized into 4 categories by age at baseline (C1, <55; C2, 55-64; C3, 65-74; and C4, ≥75 years). The outcomes were the change in logarithm of the minimum angle of resolution best-corrected visual acuity (logMAR BCVA) and central retinal thickness (CRT), and the number of treatments from baseline to 2 years. RESULTS: From baseline to 2 years, the mean changes in logMAR BCVA from baseline to 2 years were -0.01 in C1, -0.06 in C2, -0.07 in C3, and 0.01 in C4 (P = 0.016), and the mean changes in CRT were -136.2 µm in C1, -108.8 µm in C2, -100.6 µm in C3, and -89.5 µm in C4 (P = 0.008). Treatments applied in the 2 year period exhibited decreasing trends with increasing age category on the number of intravitreal injections of anti-VEGF agents (P = 0.06), selecting local corticosteroid injection (P = 0.031), vitrectomy (P < 0.001), and laser photocoagulation outside the great vascular arcade (P < 0.001). CONCLUSIONS: Compared with younger patients with DME, patients with DME aged ≥75 years showed less frequent treatment, a lower BCVA gain, and a smaller CRT decrease. The management and visual outcome in older patients with DME would be unsatisfactory in real-world clinical practice.

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BACKGROUND/AIMS: To investigate the yearly change of real-world outcomes for best corrected visual acuity (BCVA) after 2-year clinical intervention for treatment-naïve diabetic macular oedema (DMO). METHODS: Retrospective analysis of aggregated, longitudinal medical records obtained from 27 retina specialised institutions in Japan from Survey of Treatment for DMO database. A total of 2049 treatment-naïve centre involving DMO eyes of which the initial intervention started between 2010 and 2015, and had been followed for 2 years, were eligible. As interventions, antivascular endothelial growth factor (VEGF) agents, local corticosteroids, macular photocoagulation and vitrectomy were defined. In each eye, baseline and final BCVA, the number of each intervention for 2 years was extracted. Each eye was classified by starting year of interventional treatment. RESULTS: Although baseline BCVA did not change by year, 2-year improvement of BCVA had been increased, and reached to +6.5 letters in the latest term. There is little difference among starting year about proportions of eyes which BCVA gained >15 letters, in contrast to those which lost >15 letters were decreased by year. The proportion of eyes receiving anti-VEGF therapy was dramatically increased, while those receiving the other therapies were gradually decreased. The proportion of eyes which maintained socially good vision of BCVA>20/40 has been increased and reached to 59.0% in the latest term. CONCLUSION: For recent years, treatment patterns for DMO have been gradually but certainly changed; as a result, better visual gain, suppression of worsened eyes and better final BCVA have been obtained. Anti-VEGF therapy has become the first-line therapy and its injection frequency has been increasing.

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BACKGROUND/AIMS: To investigate real-world outcomes for best-corrected visual acuity (BCVA) after 2-year clinical intervention for treatment-naïve, centr-involving diabetic macular oedema (DME). METHODS: Retrospective analysis of longitudinal medical records obtained from 27 institutions specialising in retinal diseases in Japan. A total of 2049 eyes with treatment-naïve DME commencing intervention between 2010 and 2015 who were followed for 2 years were eligible. Interventions for DME included anti-vascular endothelial growth factor (VEGF) therapy, local corticosteroid therapy, macular photocoagulation and vitrectomy. Baseline and final BCVA (logMAR) were assessed. Eyes were classified by the treatment pattern, depending on whether anti-VEGF therapy was used, into an anti-VEGF monotherapy group (group A), a combination therapy group (group B) and a group without anti-VEGF therapy (group C). RESULTS: The mean 2-year improvement of BCVA was -0.04±0.40 and final BCVA of >20/40 was obtained in 46.3% of eyes. Based on the treatment pattern, there were 427 eyes (20.9%) in group A, 807 eyes (39.4%) in group B and 815 eyes (39.8%) in group C. Mean improvement of BCVA was -0.09±0.39, -0.02±0.40 and -0.05±0.39, and the percentage of eyes with final BCVA of >20/40 was 49.4%, 38.9%, and 52.0%, respectively. CONCLUSION: Following 2-year real-world management of treatment-naïve DME in Japan, BCVA improved by 2 letters. Eyes treated by anti-VEGF monotherapy showed a better visual prognosis than eyes receiving combination therapy. Despite treatment for DME being selected by specialists in consideration of medical and social factors, a satisfactory visual prognosis was not obtained, but final BCVA remained >20/40 in half of all eyes.

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BACKGROUND: We report an unusual case of Wernicke's encephalopathy presenting with transient upbeat nystagmus that changed to a persistent downbeat nystagmus. CASE: A 27-year-old man presented with upbeat nystagmus. Three months earlier, he had been diagnosed with Wernicke's encephalopathy after fasting for a month. OBSERVATIONS: This diagnosis was supported by his symptoms (ataxia, a confused state). Clinical recovery followed thiamine therapy. His upbeat nystagmus had linear slow phases with average amplitude and frequency (+/-SD) during fixation straight ahead of 2.8 +/- 0.7 degrees and 4.6 +/- 2.2 Hz, respectively. Two months later, the primary position upbeat nystagmus had diminished and downbeat nystagmus (0.9 +/- 0.5 degrees and 3.2 +/- 0.7 Hz on average) for a 20 degrees downward gaze had developed. Then, 8 months later, he showed only downbeat nystagmus, which obeyed Alexander's law. His primary position downbeat nystagmus was completely suppressed by clonazepam, a gamma-aminobutyric acid (GABA) agonist. CONCLUSIONS: Owing to an underlying central vestibular imbalance, even after the recovery of acute neurological symptoms, Wernicke's encephalopathy can be complicated by persistent downbeat nystagmus, which can be treated by a GABA agonist.

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PURPOSE: To investigate the effects of horizontal disparity on torsional optokinetic nystagmus (tOKN) in humans. METHODS: Ten healthy human subjects were selected for this experiment. Monocular eye movements were recorded three-dimensionally using dual-search coil methods. Torsional OKN was induced by a rotating random-dot pattern (22 degrees in diameter, constant angular velocity: +/-54 deg/s) projected on the virtual screen of the optical see-through, head-mounted display (HMD). The optical distance of the HMD's virtual screen was 2 m. A red LED that could be fixated through the virtual screen of the HMD was located near the center of the rotating random-dot pattern. Horizontal disparity was induced by changing the distance between the fixated target and the subject systematically (1, 1.5, 2, or 3 m; five subjects) or by the prism (+1.5, +0.5, 0, or -0.5 prism-diopter [PD] in each eye; five subjects) in front of the HMD. RESULTS: The average gain with zero horizontal disparity (0.022 +/- 0.008/0.025 +/- 0.014, fixated target at 2 m/fixated target with the plain glass) was significantly higher than the gain with crossed disparity (0.017 +/- 0.003/0.019 +/- 0.008, target at 3 m/with the prism of -0.5 PD) and uncrossed disparity (0.017 +/- 0.002, target at 1 m/with the prism of +1.5 PD; one-way ANOVA, P <0.05). CONCLUSIONS: The horizontal disparity of optokinetic stimulus affects tOKN. Nonzero horizontal disparity decreases the gain of tOKN.

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PURPOSE: To confirm the idea that sole contraction of the superior oblique muscle causes attacks of superior oblique myokymia (SOM). DESIGN: Observational case report. METHODS: A 43-year-old man presented with episodic monocular oscillatory eye movements. Three-dimensional eye movements were recorded using the magnetic search coil system and analyzed as rotation vector. The attacks of SOM consisted of intorsional, depressive, and abductive fast phases and their exponential decaying slow phases. RESULTS: Average direction of rotation axis for the fast phases while fixating straight ahead was 51.5 +/- 5.4 degrees from depression axis in vertical-torsional plane, 78.7 +/- 4.4 degrees from abduction axis in horizontal-torsional plane, and 76.3 +/- 4.3 degrees from abduction axis in horizontal-vertical plane (+/-SD, n = 50). Time constants of slow phases were less than 0.1 second. CONCLUSIONS: Quantitative three-dimensional analysis of SOM directly confirmed that the fast phases of SOM attacks were induced by the sole contraction of the superior oblique muscle.

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