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Purpose: Reports of atypical cases have increased awareness that Leber's hereditary optic neuropathy (LHON) is not solely a disease of young men. Here, we present a case of a 70-year-old woman who presented with bilateral sequential loss of vision, and, after several diagnostic dilemmas, was ultimately found to have LHON. Observations: Our patient presented with a one-month history of progressive central vision loss in the right eye. Her visual acuities were 20/200-1 and 20/25-2. She had no afferent pupillary defect and intraocular pressures were normal. Fundus examination revealed cup-to-disc ratios of 0.9 and 0.7 with an inferior notch on the right. Visual fields showed superior arcuate and cecocentral depressions on the right and an inferior nasal step on the left. Ocular coherence tomography showed bilateral, superior and inferior retinal nerve fiber layer thinning. She was diagnosed with normal-tension glaucoma. Laboratory studies and neuroimaging were unremarkable. One month later, she presented with new central vision loss in the left eye. Ocular coherence tomography revealed new, mild optic nerve swelling in the left eye. Due to concern for an acute-on-chronic process, she was hospitalized and treated with intravenous steroids and later plasmapheresis with modest improvement. An extensive laboratory evaluation, lumbar puncture, temporal artery biopsy, and PET CT were normal. Mitochondrial genetic testing was ordered. After a six-week delay, the results revealed a pathogenic variant at mitochondrial position 11778, consistent with a diagnosis of LHON. She began treatment with idebenone. At the most recent visit, her vision had improved to 20/40 and 20/30. Conclusions and importance: LHON is typically not part of the initial differential diagnosis of an optic neuropathy in patients outside the typical demographic. As genetic testing has become more widely available, clinicians should consider including LHON in their differential diagnosis of any optic neuropathy, especially if other, more common causes have been ruled out.

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A 37-year-old, never-smoker, pregnant woman diagnosed with Graves' disease who had stable thyroid eye disease (TED) before pregnancy presented with aggravated proptosis and eyelid swelling at 13 weeks of pregnancy. Despite the administration of local triamcinolone and 3 cycles of corticosteroid pulse therapy from 25 to 28 weeks, the patient's visual acuity decline necessitated postpartum orbital decompression surgery. Although TSH receptor antibody (TRAb) levels decreased during the mid- to late term of pregnancy, the TED worsened. This finding suggests that factors other than anti-TSH receptor antibodies may have a significant effect on disease severity.

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PURPOSE: To study the vitreopapillary interface in non-arteritic ischemic optic neuropathy (NAION) for features that may predispose to optic nerve perfusion defects. DESIGN: Case-control study. PARTICIPANTS AND CONTROLS: Patients with NAION (Study group) were compared with healthy non-NAION patients with crowded discs (Control group I) and non-crowded optic discs (Control group II). METHODS: The vitreopapillary interface was studied in 32 eyes with NAION using high-resolution OCT scans. Results were compared with two control groups consisting of age, sex, and refraction-matched non-NAION individuals with crowded optic discs (Control Group I: 31 eyes) and non-crowded optic discs (Control Group II: 32 eyes). MAIN OUTCOME MEASURES: The incidence of total posterior vitreous detachment (PVD), vitreopapillary and vitreovascular attachments, and epipapillary membranes. RESULTS: The rate of PVD over the macula was similar among groups (NAION: 62.5%, Control I: 61.3%, and Control II: 65.6%, p=0.93) while the posterior hyaloid remained attached to the crowded discs at a significantly higher rate (NAION: 81.2%, Control I: 83.9% and Control II: 43.7%, p=0.0005). A higher rate of focal vitreopapillary attachments on crowded discs than on non-crowded discs was noted (NAION: 72.2%, crowded control I: 58.7%, and non-crowded control II: 19.1%, p=0.007). Vitreovascular attachments (NAION: 69%, crowded control I: 3% vs non-crowded control II: 6%, p=0.00001) and dense epipapillary membranes were observed in NAION eyes. CONCLUSIONS: Crowded discs may have stronger vitreopapillary attachments. A close relationship of these attachments with optic nerve vessels may lead to the transmission of strong tractional forces by a syneretic vitreous gel, especially after macular PVD. This transduced mechanical force may contort the vessel wall and disrupt the blood flow in NAION.

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Leber's hereditary optic neuropathy (LHON), a maternally inherited ocular disease, is predominantly caused by mitochondrial DNA (mtDNA) mutations. Mitochondrial tRNA variants are hypothesized to amplify the pathogenic impact of three primary mutations. However, the exact mechanisms remained unclear. In the present study, the synergistic effect of the tRNAGlu 14693A>G and ND6 14484T>C mutations in three Chinese families affected by LHON is investigated. The m.14693A>G mutation nearly abolishes the pseudouridinylation at position 55 of tRNAGlu, leading to structural abnormalities, decreased stability, aberrant mitochondrial protein synthesis, and increased autophagy. In contrast, the ND6 14484T>C mutation predominantly impairs complex I function, resulting in heightened apoptosis and virtually no induction of mitochondrial autophagy compared to control cell lines. The presence of dual mutations in the same cell lines exhibited a coexistence of both upregulated cellular stress responses to mitochondrial damage, indicating a scenario of autophagy and mutation dysregulation within these dual-mutant cell lines. The data proposes a novel hypothesis that mitochondrial tRNA gene mutations generally lead to increased mitochondrial autophagy, while mutations in genes encoding mitochondrial proteins typically induce apoptosis, shedding light on the intricate interplay between different genetic factors in the manifestation of LHON.

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Familial dysautonomia (FD) is a rare genetic neurodevelopmental and neurodegenerative disorder. In addition to the autonomic and peripheral sensory neuropathies that challenge patient survival, one of the most debilitating symptoms affecting patients' quality of life is progressive blindness resulting from the steady loss of retinal ganglion cells (RGCs). Within the FD community, there is a concerted effort to develop treatments to prevent the loss of RGCs. However, the mechanisms underlying the death of RGCs are not well understood. To study the mechanisms underlying RGC death, Pax6-cre;Elp1loxp/loxp male and female mice and postmortem retinal tissue from an FD patient were used to explore the neuronal and non-neuronal cellular pathology associated with the FD optic neuropathy. Neurons, astrocytes, microglia, Müller glia, and endothelial cells were investigated using a combination of histological analyses. We identified a novel disruption of cellular homeostasis and gliosis in the FD retina. Beginning shortly after birth and progressing with age, the FD retina is marked by astrogliosis and perturbations in microglia, which coincide with vascular remodeling. These changes begin before the onset of RGC death, suggesting alterations in the retinal neurovascular unit may contribute to and exacerbate RGC death. We reveal for the first time that the FD retina pathology includes reactive gliosis, increased microglial recruitment to the ganglion cell layer (GCL), disruptions in the deep and superficial vascular plexuses, and alterations in signaling pathways. These studies implicate the neurovascular unit as a disease-modifying target for therapeutic interventions in FD.

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Leber's Hereditary Optic Neuropathy (LHON) is a rare, maternally inherited eye disease, predominantly due to the degeneration of retinal ganglion cells (RGCs). It is associated with a mitochondrial DNA (mtDNA) point mutation. Our previous study identified that the m.15927G > A homoplasmic mutation damaged the highly conserved base pairing (28C-42G) in anticodon stem of tRNAThr, caused deficient t6A modification and significantly decreased efficiency in aminoacylation and steady-state levels of tRNAThr, and led to mitochondrial dysfunction. Meanwhile, mechanisms underlying mtDNA mutations regulate intracellular signaling related to mitochondrial and cellular integrity are less explored. Here, we manifested that defective nucleotide modification induced by the m.15927G > A mutation interfered with the expression of nuclear genes involved in cytoplasmic proteins essential for oxidative phosphorylation system (OXPHOS), thereby impacting the assemble and integrity of OXPHOS complexes. As a result of these mitochondrial dysfunctions, there was an imbalance in mitochondrial dynamics, particularly distinguished by an increased occurrence of mitochondrial fission. Excessive fission compromised the autophagy process, including the initiation phase, formation, and maturation of autophagosomes. Both Parkin-mediated mitophagy and receptor-dependent mitophagy were significantly impaired in cybrids haboring the m.15927G > A mutation. These changes facilitated intrinsic apoptosis, as indicated by increased cytochrome c release and elevated levels of apoptosis-associated proteins (e.g., BAK, BAX, cleaved caspase 9, cleaved caspase 3, and cleaved PARP) in the mutant cybrids. This study demonstrates that the m.15927G > A mutation contributes to LHON by dysregulating OXPHOS biogenesis, aberrant quality control, increased autophagy, inhibited mitophagy, and abnormal apoptosis.

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OBJECTIVE: This study aimed to develop and test a model for predicting dysthyroid optic neuropathy (DON) based on clinical factors and imaging markers of the optic nerve and cerebrospinal fluid (CSF) in the optic nerve sheath. METHODS: This retrospective study included patients with thyroid-associated ophthalmopathy (TAO) without DON and patients with TAO accompanied by DON at our hospital. The imaging markers of the optic nerve and CSF in the optic nerve sheath were measured on the water-fat images of each patient and, together with clinical factors, were screened by Least absolute shrinkage and selection operator. Subsequently, we constructed a prediction model using multivariate logistic regression. The accuracy of the model was verified using receiver operating characteristic curve analysis. RESULTS: In total, 80 orbits from 44 DON patients and 90 orbits from 45 TAO patients were included in our study. Two variables (optic nerve subarachnoid space and the volume of the CSF in the optic nerve sheath) were found to be independent predictive factors and were included in the prediction model. In the development cohort, the mean area under the curve (AUC) was 0.994, with a sensitivity of 0.944, specificity of 0.967, and accuracy of 0.901. Moreover, in the validation cohort, the AUC was 0.960, the sensitivity was 0.889, the specificity was 0.893, and the accuracy was 0.890. CONCLUSIONS: A combined model was developed using imaging data of the optic nerve and CSF in the optic nerve sheath, serving as a noninvasive potential tool to predict DON.

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Jansen metaphyseal chondrodysplasia (JMC) is an ultra-rare disorder caused by germline heterozygous PTHR1 variants resulting in constitutive activation of parathyroid hormone type 1 receptor. A description of ocular manifestations of the disease is lacking. Six patients with JMC underwent a detailed ophthalmic evaluation, spectral-domain optical coherence tomography (OCT), visual field testing, and craniofacial CT scans. Five of 6 patients had good visual acuity. All patients had widely spaced eyes; 5/6 had downslanted palpebral fissures. One patient had proptosis, and another had bilateral ptosis. Two patients had incomplete closure of the eyelids (lagophthalmos), one had a history of progressive right facial nerve palsy with profuse epiphora, while the second had advanced optic nerve atrophy with corresponding retinal nerve fiber layer (RNFL) thinning on OCT and significant bilateral optic canal narrowing on CT scan. Additionally, this patient also had central visual field defects and abnormal color vision. A third patient had normal visual acuity, subtle temporal pallor of the optic nerve head, normal average RNFL, but decreased temporal RNFL and retinal ganglion cell layer analysis (GCA) on OCT. GCA was decreased in 4/6 patients indicating a subclinical optic nerve atrophic process. None of the patients had glaucoma or high myopia. These data represent the first comprehensive report of ophthalmic findings in JMC. Patients with JMC have significant eye findings associated with optic canal narrowing due to extensive skull base dysplastic bone overgrowth that appear to be more prevalent and pronounced with age. Progressive optic neuropathy from optic canal narrowing may be a feature of JMC, and OCT GCA can serve as a useful biomarker for progression in the setting of optic canal narrowing. We suggest that patients with JMC should undergo regular ophthalmic examination including color vision, OCT, visual field testing, orbital, and craniofacial imaging.

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(1) Background: To investigate the risk factors associated with optic neuropathy (ON) and validate the hypothesis that concomitant isoniazid use and other causes of toxic ON affect the development of ON in ethambutol users. (2) Methods: This cohort study identified ethambutol users who initiated ethambutol therapy between January 2015 and December 2021 and had no ON prior to ethambutol therapy. ON incidence up to 31 December 2022 was evaluated. The users were grouped on the basis of the presence of ON. Demographic and clinical characteristics were investigated for risk factor analyses of ON. Odds ratios (ORs) were calculated using multivariate logistic regression analyses. (3) Results: Among 204,598 ethambutol users, 5277 (2.6%) patients developed ON over the study period. Patients with ON included a higher percentage of women and had a higher mean age than patients without ON. In the multivariate analyses, the risk factors for ON and visual impairment included sex, age, cumulative dose, extrapulmonary indications for ethambutol use, and systemic conditions such as diabetes, hypertension, hyperlipidemia, diabetes, kidney disease, and liver disease. Malnutrition or nutritional disorders significantly increased the risk of ON (OR = 1.27, 95% confidence interval [CI] = 1.19-1.34), whereas concomitant isoniazid use decreased the risk (OR = 0.78, 95% CI = 0.72-0.86). (4) Conclusion: An increased risk of ON in patients with systemic diseases and nutritional deficiency was identified, whereas concomitant isoniazid use was associated with a decreased risk of ON. Patients with these risk factors should be carefully monitored to minimize the vision-threatening ON.

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Leber's hereditary optic neuropathy (LHON) is a maternal inherited disorder, primarily due to mitochondrial DNA (mtDNA) mutations. This investigation aimed to assess the pathogenicity of m.3635G>A alteration known to confer susceptibility to LHON. The disruption of electrostatic interactions among S110 of the MT-ND1 and the side chain of E4, along with the carbonyl backbone of M1 in the NDUFA1, was observed in complex I of cybrids with m.3635G>A. This disturbance affected the complex I assembly activity by changing the mitochondrial respiratory chain composition and function. In addition, the affected cybrids exhibited notable deficiencies in complex I activities, including impaired mitochondrial respiration and depolarization of its membrane potential. Apoptosis was also stimulated in the mutant group, as witnessed by the secretion of cytochrome c and activation of PARP, caspase 3, 7, and 9 compared to the control. Furthermore, the mutant group exhibited decreased levels of autophagy protein light chain 3, accumulation of autophagic substrate P62, and impaired PINK1/Parkin-dependent mitophagy. Overall, the current study has confirmed the crucial involvement of the alteration of the m.3635G>A gene in the development of LHON. These findings contribute to a deeper comprehension of the pathophysiological mechanisms underlying LHON, providing a fundamental basis for further research.

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Objective: Traumatic optic neuropathy (TON) refers to a pathological condition caused by direct or indirect injury to the optic nerves. In the case of patients with traumatic brain injury, adequate vision evaluation is difficult in many cases due to altered mentality. In order to address this problem, we investigated preoperative pupillary light reflex in TON patients as a predictive factor of surgical outcomes after optic nerve decompression. Methods: From April 2020 to September 2022, we enrolled patients who were diagnosed with TON and underwent endoscopic optic nerve decompression at our institution. Vision and pupil reflex tests were performed by an ophthalmologist before and after surgery. Results: Seven patients were enrolled. Their ages ranged from 9 to 78 years and all were male. Among the 7 patients, the patient whose pupillary light reflex was 6mm with sluggish and 7mm with fixated pupil before surgery showed no improvement in vision. Patients with some response to direct reflex or contralateral indirect reflex testing preoperative showed vision improvement postoperative. Conclusion: Direct and indirect pupillary reflexes can be important factors determining treatment for TON. In unconscious patients with a fracture involving the optic canal, timely surgical intervention based on pupillary reflex can prevent permanent loss of vision.

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PURPOSE: To compare blood flow (BF) impairment patterns in different optic neuropathies using laser speckle flowgraphy (LSFG). METHODS: This retrospective study enrolled 24 eyes of 24 patients with non-arteritic anterior ischemic optic neuropathy (NAAION), 59 eyes of 59 patients with optic neuritis (ON), 677 eyes of 677 patients with open-angle glaucoma (OAG), and 110 eyes of 110 controls. The patient backgrounds of all groups were compared. Ophthalmologic findings were evaluated, adjusting for age, sex, blood pressure, pulse rate, and underlying systemic diseases with 1:1 optimal propensity score matching. We used LSFG to obtain optic nerve head (ONH) vessel-area mean blur rate (MBR; ONH-MV), ONH tissue-area MBR (ONH-MT), and choroidal MBR. The NAAION and ON groups were compared with the control and OAG groups. RESULTS: Best-corrected visual acuity was worse in the NAAION, ON, and OAG groups than in controls (p < 0.001). Circumpapillary retinal nerve fibre layer thickness was higher in the NAAION and ON groups and lower in the OAG group than in controls (p < 0.001). Compared to controls, the NAAION and OAG groups had significantly lower ONH-MV, ONH-MT, and choroidal MBR (p < 0.05). Additionally, the NAAION group had lower ONH-MV and choroidal MBR than the OAG group (p = 0.003 and p < 0.001, respectively) but no difference in ONH-MT (p = 0.857). The ON group had significantly lower ONH-MV and choroidal MBR compared to the controls (p < 0.001 and p = 0.022, respectively) but no difference in ONH-MT (p = 0.773). CONCLUSION: Optic neuropathies showed different patterns of ocular BF impairment. Therefore, LSFG can be a useful tool for differentiating optic neuropathies.

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PURPOSE: The role of carotid artery disease (CAD) in the development of various types of ocular arterial occlusive disorders has often been reported. This systematic review aims to evaluate and review the current evidence regarding the role of CAD and the subsequent carotid artery hemodynamic alterations in the development of non-arteritic anterior (NA-AION) and posterior (NA-PION) ischemic optic neuropathy. METHODS: We systematically reviewed studies following Preferred Reporting Items for Systematic Reviews and Meta-Analysis guidelines. We systematically searched PubMed, Embase, and Scopus databases for relevant studies that clearly assessed the role of CAD and the subsequent carotid artery hemodynamic alterations in the development of NA-AION and NA-PION. All studies that examined the associations between CAD and the development of NA-AION and NA-PION in adults aged 18 years or older were synthesized. Quality assessment using the Newcastle-Ottawa Scale (NOS), and Joanna Briggs Institute (JBI) Critical Appraisal Checklist for Case Reports and Case-Series were also conducted. RESULTS: Our search identified 1933 manuscripts published in the English language. The number of participants with non-arteritic ischemic optic neuropathy (NA-ION) ranged from 1 to 191, with a total of 478 patients experiencing either NA-AION (410 out of 478), NA-PION (13 out of 478), or a combination of thereof (1 out of 478). The number of participants with NA-ION due to atherosclerosis ranged from 1 to 191, with a total of 376 patients. CONCLUSIONS: Although carotid artery disease may rarely contribute to the development of NA-ION, it should be considered as a possible cause of NA-ION.

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Introduction: Neuromyelitis optica spectrum disorder (NMOSD) is an autoimmune disorder that principally targets the central nervous system, specifically the spinal cord and optic nerves. NMOSD is often associated with thyroid pathologies such as Graves' disease or Hashimoto's thyroiditis. Thyroid eye disease (TED) is an autoimmune condition characterized by inflammation and hypertrophy of the extraocular muscles. Dysthyroid optic neuropathy (DON), a critical complication of TED, may lead to irreversible visual loss. We report a case of DON complicated by NMOSD. Case Presentation: We report a case of an autoimmune disease presenting as DON in a 44-year-old Japanese woman with a history of Graves' disease, who experienced reduced visual acuity and orbital pain. Brain magnetic resonance imaging disclosed hypertrophy of the rectus muscles, compressing the optic nerve bilaterally. Consequently, she was diagnosed with DON and underwent three courses of steroid semi-pulse therapy and left orbital decompression surgery, alleviating optic nerve compression. Nevertheless, the visual prognosis remained poor. A subsequent serological test showed positive for aquaporin-4 antibody. Treatment with satralizumab, an interleukin-6 receptor monoclonal antibody, was initiated in conjunction with steroids to suppress the autoimmune response and reduce NMOSD relapse risk. Following this treatment, no NMOSD recurrences were reported. Conclusion: This case highlights the necessity of considering the possible coexistence of DON and NMOSD in patients with autoimmune diseases.

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Leukaemic optic neuropathy is an uncommon cause of visual loss which represents a neuro-oncological emergency with the potential of irreversible blindness if untreated. It can be difficult to diagnose, often presenting with normal neuroradiological and cerebrospinal fluid findings. We present the case of a 26-year-old woman with T-cell acute lymphoblastic leukaemia with optic neuropathy secondary to leukaemic infiltration, who demonstrated features on optical coherence tomography that aided the diagnosis of this condition. This included the presence of numerous, small, hyperreflective opacities erupting from the optic nerve head, which improved following treatment with radiotherapy and chemotherapy, and later recurred when the condition relapsed. This finding may help clinicians differentiate between other causes of optic neuropathy as well as assessing response to treatment and monitoring for recurrence.

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Ocular involvement is not uncommon in patients with COVID-19. However, the incidence of COVID-19 ophthalmopathy in COVID-19 patients is still not clear. In this prospective case series study, we recruited 2445 consecutive cases presenting at Neuro-ophthalmology clinic of our Eye Center during the last resurgence of SARS-CoV-2 infection from 8 December 2022 to 15 March 2023 in China, 149 cases were diagnosed as COVID-19 ophthalmopathy, 87 cases were female, with a mean age of 43.2 years, and the mean follow-up time was 15.4 weeks. One hundred and twenty of 149 cases suffered from systemic symptoms mostly manifesting as fever, cough and muscle pain prior to or soon after ocular involvement. The most common COVID-19 ophthalmopathy was optic neuritis (51/149), followed by acute zonal occult outer retinopathy complex disease (31/149), uveitis (17/149), ocular mobility disorder-related (third, fourth, or sixth) cranial nerve neuritis (15/149), anterior ischaemic optic neuropathy (9/149), retinal artery occlusion (8/149), retinal microangiopathy including retinal haemorrhage and cotton wool spot (8/149), viral conjunctivitis (7/149), retinal vein occlusion (3/149), viral keratitis (2/149), ptosis (2/149), and other rare ocular diseases. Except 5 cases with central retinal artery occlusion, other 144 COVID-19 ophthalmopathy cases showed good response to steroid therapy. Our study revealed an incidence of 6.09% for COVID-19 ophthalmopathy in outpatients at our Neuro-ophthalmology clinic during last resurgence of COVID-19 in China, and demonstrated that SARS-CoV-2 infection could induce an initial onset or a relapse of ophthalmic diseases, and that ocular involvement might manifest as the initial or even the only presentation of COVID-19.

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BACKGROUND: To investigate the peripapillary retinal nerve fibre layer (RNFL) thickness changes and analyse factors associated with visual recovery of G11778A Leber hereditary optic neuropathy (LHON) patients. METHODS: Patients diagnosed with G11778A LHON between July 2017 and December 2020 in Tongji hospital were included in this follow-up study. Patients were grouped according to disease duration. Variations in the RNFL thickness in each quadrant at different disease stages were characterised using optical coherence tomography. According to the absence or presence of significant visual acuity improvements, LHON patients of disease duration ≥ 6 months were divided into two groups. A bivariate logistic regression model was constructed to analyse the potential factors associated with spontaneous visual recovery. RESULTS: This study included 56 G11778A LHON patients (112 eyes) and 25 healthy controls (50 eyes), with a mean follow-up of 5.25 ± 1.42 months. All quadrants and mean RNFL thicknesses of LHON patients first increased and then decreased, except for the temporal RNFL. As the disease progressed, RNFL thinning slowed; however, gradual RNFL thinning occurred. Logistic regression revealed that baseline best corrected visual acuity was related to spontaneous visual recovery of LHON patients with disease duration ≥ 6 months. CONCLUSION: The pattern of RNFL involvement could be helpful in the differential diagnosis of LHON and other optic neuropathies. LHON patients with better vision are more likely to experience some degree of spontaneous visual acuity recovery after the subacute phase.

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Neuro-ophthalmic manifestations of Wernicke encephalopathy (WE) are uncommon and vary from nystagmus, oculomotor palsies, anisocoria, and optic disc edema to vision loss. We describe a case of a 53-year-old woman presenting with subacute bilateral painless vision decline, lower-extremities weakness with impaired ambulation, headache, and abdominal pain. Neurological examination was pertinent for confabulation, bilateral decreased visual acuity with an absent blink to threat, absent afferent pupillary defect and fundus abnormalities, and significant allodynia in bilateral lower extremities. Besides elevated inflammatory marker with an erythrocyte sedimentation rate (ESR) of 130 mm/hr, her infectious, autoimmune, paraneoplastic, and neuromyelitis optica work-up was overall unremarkable. Brain MRI showed abnormal fluid-attenuated inversion recovery (FLAIR) signaling in bilateral mammillary bodies and around periaqueductal gray matter concerning WE. Due to concerns of Wernicke-Korsakoff syndrome (WKS), parenteral high-dose thiamine was initiated with significant clinical improvement. The patient was also later found to have a positive anti-myelin oligodendrocyte glycoprotein (MOG) antibody, which was deemed false positive given the atypical phenotype and symptomatic improvement with thiamine supplementation. This case encourages the consideration of vision loss as a manifestation of WKS, especially in patients who have risk factors. Testing serum levels of thiamine is strongly encouraged; however, initiating empiric treatment is advocated for high clinical suspicion due to its reversible nature and minimal risk for side effects.

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INTRODUCTION: This study investigated the effect of pars plana vitrectomy (VIT) versus pars plana vitrectomy combined with radial optic neurotomy (RON) on recent onset non-arteritic anterior ischemic optic neuropathy (NAION). METHODS: In this prospective interventional case series, individuals with recent-onset NAION, lower than one month and low vision (lower than 20/200) were recruited. Patients randomly underwent either VIT, or RON. RESULTS: 34 eyes of 34 patients were included in this study. 10, 9, and 15 eyes were randomly included in VIT, RON, and control groups, respectively. The BCVA of the VIT group improved significantly from 1.84 ± 0.5 logMAR at baseline to 1.29 ± 0.67, 0.93 ± 0.53, and 0.77 ± 0.47 logMAR at 1, 3, and 6 months, respectively (Ps < 0.05). The corresponding values for RON group were 1.73 ± 0.53 logMAR at baseline, which improved to 1.04 ± 0.65, 0.64 ± 0.28, and 0.61 ± 0.26 logMAR at the same follow-up visit times (P < 0.05).The corresponding values for the control group were 1.6 ± 0.58 log MAR at baseline, which improved to 1.03 ± 0.29, 1.00 ± 0.32, and 0.32 ± 0.83 log MAR at the same follow-up visit times. There was no significant statistical difference in BCVA between the three groups. However, both interventions resulted in statistically significant improvement in mean deviation (MD) of visual field (VF) compared with the control group at the end of 6 months (VIT P = 0.006, RON P = 0.043). RNFLT decreased from baseline 235.3 ± 44.01 to 75.6 ± 17.68 at 1 month in the VIT group (P < 0.001), from baseline 268.22 ± 65.9 to 76.67 ± 10.59 at 1 month in RON (P < 0.001), while it decreased from baseline 179.48 ± 39.02 to 112.92 ± 44.51 at 1 month in the control group. CONCLUSION: VIT and RON showed promising results in terms of MD of VF, and optic disc edema resolved faster in these groups compared to the control group in recent onset NAION. A larger sample size study is deemed necessary to generalize the results of this study.