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To evaluate whether treatment with Citicoline in oral solution (OS-Citicoline) would increase visual function, retinal ganglion cells (RGCs) function, and neural conduction along visual pathways (neuroenhancement), and/or induce preservation of RGCs fibers' loss (neuroprotection) in non-arteritic ischemic optic neuropathy (NAION), a human model of neurodegeneration. Thirty-six patients with NAION and 20 age-matched controls were enrolled. Nineteen NAION patients received 500 mg/day of OS-Citicoline for a 6-month period followed by 3-month of wash-out (NC Group); 17 NAION patients were not treated (NN Group) from baseline to 9 months. In all subjects at baseline, and in NC and NN eyes at 6 and 9 months of follow-up, we assessed Visual Acuity (VA), Pattern Electroretinogram (PERG), Visual Evoked Potentials (VEP), retinal nerve fiber layer thickness (RNFL-T), and Humphrey 24-2 visual field mean deviation (HFA MD). Mean differences were statistically evaluated with ANOVA between Groups, and linear correlations were analysed with Pearson's test. At 6 months, significant differences between groups for all parameters were observed (ANOVA, p<0.01). In NC eyes, VA increased, PERG responses increased, VEP recordings improved and were significantly correlated with increases in HFA MD (p<0.01), and RNFL-T was unmodified or improved. In contrast, in NN eyes, VA, PERG, VEP responses, RNFL-T, and HFA MD were further worsened. Significant differences were still present at 9-month follow-up in the NN Group and after 3 months of OS-Citicoline wash-out in NC eyes. OS-Citicoline treatment induced neuroenhancement (improvement in RGCs function and neural conduction along visual pathways related to improvement of visual field defects) and neuroprotection (unmodified or improved RNFL morphological condition) in a human model of NAION involving fast RGCs degeneration. ClinicalTrials.gov NCT03758118.

Purpose To determine the clinical effectiveness and potential neuroprotection of levodopa in improving visual acuity, visual field, and retinal nerve fiber layer (RNFL) thickness in eyes affected by NAION. Method Retrospective cohort study involving 59 eyes of 59 participants with NAION who were evaluated within 15 days of NAION onset. Participants received 25 mg carbidopa/100 mg levodopa three times daily with meals for 12 weeks (levodopa group) or were untreated (control group). Best-corrected visual acuity converted to logMAR, mean deviation (MD) threshold sensitivity on automated perimetry, and mean RNFL thickness on optical coherence tomography (OCT) were assessed. The primary outcome was the categorization of eyes into improved visual acuity (by 0.3 logMAR difference), worsened visual acuity (by 0.3 logMAR difference), or no change in visual acuity. The proportions in each category were compared between the levodopa and control groups. Results Among participants with 20/60 or worse initial visual acuity, levodopa-treated participants had significant improvement ( P  < 0.0001) in the mean change from initial to final logMAR visual acuity of −0.74 ± 0.56 (95 % CI, −0.98 to −0.50), while the mean change for the control group at −0.37 ± 1.09 (95 % confidence interval estimate, −1.00 to +0.26) was not significant ( P  = 0.23). A significant difference between groups was observed ( P  = 0.0086) such that 19/23 (83 %) in the levodopa group improved and none got worse, as compared with 6/14 (43 %) in the control group improving while four (29 %) worsened. The change in visual field MD and RNFL thickness on OCT showed no significant difference at P  = 0.23 and P  = 0.75 respectively. No levodopa-treated participant had any adverse event from the levodopa. Conclusions Treatment within 15 days of onset of NAION with levodopa improved central visual acuity by an average of 6 lines on Snellen acuity chart. Levodopa may promote neuroprotection of the maculopapular retinal ganglion cell fibers in NAION.

Purpose There is currently no accepted treatment for Nonarteritic Anterior Ischemic Optic Neuropathy (NAION). One new therapeutic approach involves decreasing optic nerve edema with intravitreal bevacizumab in order to resolve a proposed compartment syndrome. Methods In this non-randomized controlled clinical trial, 1.25 mg intravitreal bevacizumab was compared with natural history. Patients were examined at baseline, 1, 3, and 6 months with a full neuro-ophthalmic exam, automated perimetry, and optic nerve optical coherence tomography (OCT) measurements. The primary outcome measure was change in mean deviation on Humphrey visual field testing. Secondary outcome measures were change in visual acuity and optic nerve OCT thickness. Incidence and type of complications were also recorded. Results Twenty-five patients were enrolled (17 treatment and 8 control). There was no significant effect of treatment on the primary outcome measure of mean deviation score ( P =0.4). There was similarly no effect of group assignment on the secondary outcome measures of change in mean Early Treatment Diabetic Retinopathy Study letters ( P =0.33) or nerve fiber layer thickness on OCT ( P =0.11). In the bevacizumab group, there was one case of a corneal abrasion and two cases of recurrent NAION. No other complications were noted. Conclusions We found no difference between bevacizumab and natural history for change in visual field, visual acuity, or optic nerve OCT thickness. Based on the current evidence we would not recommend the use of intravitreal bevacizumab to treat patients with the new onset of NAION.

Background To evaluate the visual and anatomic outcomes after systemic steroid treatment in non-arteritic anterior ischemic optic neuropathy (NAION). Methods Ten eyes from ten patients diagnosed with NAION and treated during the acute phase with 80 mg daily, tapering-down dose of corticosteroids were compared with a non-contemporary cohort of 27 patients that received no treatment. The visual outcomes of treated and untreated group were compared. Patients underwent complete ophthalmic examination including determination of Snellen visual acuity (VA), visual fields (VFs) (standard automated perimetry, Swedish Interactive Testing Algorithm 24–2 strategy), and optical coherence tomography (OCT) scanning of the optic nerve head at diagnosis, 6–8 weeks and 6 months after presentation. Results No statistical differences were found between steroid-treated and untreated NAION for the median change in VA (Mann–Whitney P =  0.28), median change in VF mean deviation (MD) and median change in VF pattern standard deviation (PSD) (Mann–Whitney P =  0.213 and P =  0.07 respectively). Statistical analysis showed no differences when comparing average RNFL loss ( P  = 0.871) and RNFL loss for superior, nasal, inferior and temporal optic disc quadrants between both groups. Complications occurred in three of the ten treated patients (30%); in one of them, steroid therapy had to be discontinued. Another two patients developed a NAION in their fellow eye after 2 and 3 months while on low-dose prednisone. No complications developed in the control group. The study was interrupted early due to a significantly higher rate of complications observed in the treated group ( P =  0.002) Conclusion High-dose systemic steroid treatment did not show any beneficial effect in visual and anatomic outcomes when given during the acute phase of NAION. Furthermore, it caused serious complications in a third of the patients treated.

AimTo evaluate the effect of intravitreal injection of erythropoietin for the treatment of non-arteritic anterior ischaemic optic neuropathy (NAION).MethodsIn this prospective interventional case series, 31 eyes of 31 patients with NAION were included. Patients received intravitreal injection of 2000 unit (0.2 cm3) of erythropoietin within 1 month of the onset of the disease. Visual acuity and visual field were recorded before injections and 1 week, 1 month, 3 months and 6 months after the injections.ResultsThe mean duration of symptoms before injections was 11.2±5.5 days. Six months after injections, visual acuity improved in 27 eyes (87%), and 17 eyes (54.8%) had ≥3 lines of visual improvement. The mean preinjection visual acuity was 1.01±0.88 logMAR and 0.58±0.58 logMAR (p<0.001) at last follow-up. Visual acuity improvement occurred in 61.2% of patients within the first month. It followed a biphasic pattern in which there was continuous improvement up to 3 months and then started to deteriorate, although it remained significantly better than baseline until the last follow-up. No patient lost any lines of visual acuity compared with the baseline values. The mean of mean deviations of visual field was −19.6±5.7 dB at baseline and −18.6±6.3 dB (p=0.6) at last follow-up.ConclusionsIntravitreal injection of erythropoietin may be safe and effective in the treatment of NAION. The effect may last for a few months and then decline.

Background In non-arteritic anterior ischemic optic neuropathy (NA-AION), no treatments have demonstrated to be effective in recovering visual loss in randomized clinical trials. Oral steroids have been evaluated, and small series of intravitreal triamcinolone acetonide (IVTA) injection in NA-AION have been reported. The purpose of our study was to report the visual outcome and morphological changes in response to a single IVTA injection as a treatment for patients with NA-AION. Patients and methods The charts of 36 patients with visual symptoms and optic disc swelling caused by NA-AION were evaluated. Twenty-one patients had received 4 mg IVTA and were compared with 15 non-treated patients. Visual acuity (VA), retinal nerve fiber layer thickness and static visual field were evaluated after 6 months. Results VA improvement at 6 months is statistically better in the treated group than in the non-treated group ( p  = 0.0035). In the treated group, there was a significant inverse correlation between the delay of the injection and the visual acuity achieved at 6 months (p <  0.0083**, r  = −0.56). A significant improvement of the visual field was noted in the injected group when compared with the non-treated group at 6 months ( p <  0.0028). Discussion In this retrospective study, patients receiving IVTA in the acute phase of NA-AION have better improvement of VA and visual field during the follow-up period of 6 months. However, only a large randomized controlled trial may enable to evaluate the benefits of IVTA Injections on visual outcome in NA-AION.

Neuroprotection may be an option in ischemic optic nerve disease. There have been promising reports about the neuroprotective ability of topical brimonidine in animal studies. Therefore, we tested whether 0.2% brimonidine tartrate could improve the outcome of patients with non-arteritic anterior ischemic optic neuropathy (NAION). The study was stopped after an interim analysis, having not proven its feasibility within practicable time frame. A 3-month, double-masked, placebo-controlled, randomised European multicenter trial conducted according to good clinical practice rules. Thirty-six patients (22 m, 14 f), older than 40 years with first eye involvement and typical signs of NAION were included in the study within the 1st week after visual loss (VA 0.05-1.0) and were randomized to treatment with either brimonidine 0.2% (Alphagan) or placebo. Visual acuity (VA, primary endpoint), visual field (VF, Humphrey 30-2 and Goldmann, quantified by a modified Esterman grid) and automated swinging flashlight test (SWIFT) were performed at baseline, 2 weeks, 4 weeks and 12 weeks after first visit. Primary analysis aimed at intention-to-treat group (ITT, n=29), secondary analysis to the per protocol population (PP, n=25). Tolerability and safety were tested in the safety group (n=36). A two-sample two-sided t-test was used for statistical analysis (alpha level at 0.05). VA did not show statistically significant difference by treatment. There were non-significant trends for better visual field results in the brimonidine group. Adverse events consisting of local irritation were observed six times in the verum and three times in the placebo group. No serious adverse events occurred. In contradiction to an open-labeled, retrospective study published by Fazzone et al., the results of this trial did not indicate any harmful effect of brimonidine in patients suffering from NAION. However, a statistically significant advantage for the patients receiving brimonidine tartrate could not be shown.

Ischemic optic neuropathy is of two types: anterior and posterior. Non-arteritic anterior ischemic optic neuropathy (NA-AION) is the most common type of ischemic optic neuropathy. There are three major misconceptions about NA-AION: (1) that its pathogenesis is not known, (2) that NA-AION and ischemic cerebral stroke are similar in nature, pathogenetically and in management, and (3) that there is no treatment. All these misconceptions are based on lack of in-depth knowledge of the subject. They are discussed in the light of our current scientific knowledge. The pathogenesis of NA-AION is known but is highly complex. NA-AION and ischemic cerebral stroke are very different clinical entities, pathogenetically and in management. Aspirin has no beneficial effect. Corticosteroid therapy during the initial stages can be beneficial. To reduce the risk of development of NA-AION in the other eye or of further visual loss in the same eye, it is essential to reduce as many risk factors as possible. Management of arteritic anterior ischemic optic neuropathy and of posterior ischemic optic neuropathy is discussed.

Objective To review treatment modalities that have been studied in acute non arteritic anterior ischemic optic neuropathy (NAION). Methods We performed a comprehensive literature search of English language publications in the last 5 years, with human species and NAION. Articles were reviewed to identify those that described original research on treatment of acute NAION. Study type, setting, duration, interventions, and results were extracted and articles were reviewed for biases and limitations. Results We identified 22 kinds of treatment varying by compound and modality. These include topical, intravitreal, and systemic drugs as well as surgical approaches. Evidence for efficacy ranges from expert opinion to randomized control trials. Conclusions Although several treatments are utilized in practice, none of these have high quality evidence of efficacy to improve visual outcomes.  Continued collaborative research is necessary to complete high quality studies in order identify effective therapies for this rare and blinding disease.

Ischemic optic neuropathy is a leading cause of sudden vision loss, particularly in elderly individuals, with no available effective treatments. Ischemia-induced irreversible damage to optic nerve fibers highlights the need for novel therapies with neuroprotective potential. Therefore, we investigated the effects of modulating valosin-containing proteins by regulating their intracellular ATPase activity in a rat model of anterior ischemic optic neuropathy. Intravitreal injection of KUS121 (Kyoto University Substance 121), a valosin-containing protein modulator, significantly reduced retinal thinning, retinal ganglion cell death, and optic nerve fiber loss. Morphological and histopathological analyses showed that KUS121 treatment prevented the disorganization, swelling, and loss of myelin. Notably, KUS121 demonstrated strong neuroprotective effects even when administered immediately after the induction of ischemic optic neuropathy. Mechanistically, the neuroprotective effect of KUS121 can be attributed to the suppression of endoplasmic reticulum stress, as evidenced by reduced expression of the C/EBP homologous protein, a marker of endoplasmic reticulum stress, following ischemic injury. Conclusively, KUS121 is promising as a therapeutic option for ischemic optic neuropathy and other ischemia-related neurodegenerative conditions.