Methanol poisoning remains an important cause of severe metabolic and neurologic toxicity, most commonly resulting from ingestion of illicit or improperly distilled alcoholic beverages such as Moonshine. We report a case of acute methanol toxicity following Moonshine ingestion, presenting with central nervous system manifestations and visual symptoms. The patient experienced rapid clinical and visual improvement after timely treatment with fomepizole and emergent hemodialysis. In addition to standard therapy, corticosteroids were administered as an adjunctive treatment for visual involvement. This case highlights the importance of early recognition and prompt extracorporeal clearance in methanol poisoning and explores the potential role of corticosteroids as an adjunct in patients presenting with visual symptoms.

The growing number of omics datasets in public repositories provides an opportunity to enhance data reusability through data integration; however, complex statistical barriers often hinder the effective combination of independent studies. To address this problem, we present MetaOmixTools, an interactive web-based suite that streamlines the meta-analysis of ranked feature lists and functional enrichment profiles. The platform integrates 2 primary modules-MetaRank and MetaEnrich-within a code-free environment. MetaRank generates robust consensus rankings from multiple lists by implementing weighted (e.g., rank product) and unweighted (e.g., robust rank aggregation) strategies, while MetaEnrich performs functional meta-analyses by combining probability values from individual overrepresentation analyses using established statistical techniques. Using case studies, we established consensus rankings for acute spinal cord injury across heterogeneous platforms, identifying conserved inflammatory marker genes in the up-regulated gene list (e.g., Slpi, Ccl2, and Msr1) and synaptic loss genes in the down-regulated gene list (e.g., Kcna2, Dao, and Ppp1r1b), and also characterized inverse functional intersections between melanoma brain metastasis and neurodegenerative diseases. By providing intuitive, real-time visualization and reproducible workflows, MetaOmixTools empowers the research community to extract consistent biological insights from multistudy data. We have made MetaOmixTools freely available at https://bioinfo.cipf.es/metaomixtools/.

Cilioretinal artery occlusion is an uncommon retinal vascular emergency that can cause acute monocular visual loss, particularly when the macular region is involved. Non-arteritic anterior ischemic optic neuropathy is another ischemic disorder involving the optic nerve head and is usually associated with optic disc edema and sudden painless visual impairment. Although both conditions involve vascular territories related to the posterior ciliary circulation, the temporal and pathophysiological relationship between cilioretinal artery occlusion and optic nerve head ischemia remains incompletely defined. This case describes a 62-year-old woman with poorly controlled type 2 diabetes mellitus who presented with acute painless visual loss in the right eye. Initial fundus examination showed optic disc pallor and edema, grayish-white retinal edema extending from the optic disc to the macular region, macular involvement, and arterial attenuation. Multimodal ophthalmic evaluation, including fundus photography, Humphrey visual field testing, optical coherence tomography, visual evoked potential testing, and fundus fluorescein angiography, supported a diagnosis of cilioretinal artery occlusion with concurrent and progressive optic nerve head ischemic involvement, clinically consistent with suspected non-arteritic anterior ischemic optic neuropathy. Because the time window for thrombolysis had passed, conservative management for retinal arterial occlusion was initiated. After progression of optic disc edema and angiographic evidence of optic nerve head leakage, parabulbar triamcinolone was administered after consideration of systemic steroid-related risks. Partial reduction of optic disc edema and limited visual improvement were observed during follow-up; however, the single-case design and concurrent treatments preclude any conclusion regarding treatment efficacy. This case emphasizes that optic disc changes in cilioretinal artery occlusion should be monitored dynamically and interpreted using multimodal imaging rather than assumed to represent a fixed sequential diagnostic pattern.

This review is devoted to Leber's hereditary optic neuropathy (LHON), a rare maternally inherited ophthalmic disorder presenting as optic nerve atrophy and associated with an unfavorable prognosis. LHON is the most common primary mitochondrial DNA disorder, and most patients (more than 90% of cases) carry one of three point mutations. The 11778G>A mutation in the MT-ND4 gene is the most common worldwide and causes the most severe variant of the disease. LHON typically manifests as bilateral, painless, acute or subacute significant vision loss, most often in young men. Environmental factors play a crucial role in triggering LHON and determining its severity. A preliminary diagnosis is based on family history and the initial clinical presentation, whereas genetic testing establishes the definitive diagnosis. Given the availability of specific treatment for LHON, early diagnosis is crucial for ensuring therapeutic effectiveness. The only drug currently approved for the treatment of LHON is the antioxidant, synthetic coenzyme Q10 analogue idebenone. Among alternative therapeutic strategies, gene therapy is at the most advanced stage of development.

Eye pain is a common presentation in outpatient, urgent care, and emergency settings. Causes range from benign to vision-threatening. Family physicians should promptly identify red-flag features that require urgent or emergent ophthalmology referral. A painful eye with vision loss, severe photophobia, proptosis, hyphema, or corneal ulceration is a medical emergency. Patient history should include onset, associated vision changes, contact lens use, trauma, chemical exposure, systemic symptoms, and rheumatologic disease. Physical examination should include evaluation of visual acuity (eg, using a Snellen or Rosenbaum chart), pupillary reactions, and extraocular movements. The eyes should be inspected for redness, discharge, and corneal lesions with fluorescein, if available. Findings of significant photophobia, anisocoria, dendritic corneal lesions, or restricted eye movement should prompt immediate referral. Common emergent causes of eye pain include acute angle-closure glaucoma, orbital cellulitis, infectious keratitis, scleritis, and anterior uveitis. An algorithmic approach that distinguishes urgent vs nonurgent etiologies and ophthalmic vs nonophthalmic causes of eye pain can direct next steps.

Glaucoma, a leading cause of irreversible blindness, is characterized by the progressive loss of retinal ganglion cells (RGCs). Beyond intraocular pressure (IOP)-dependent injury, IOP-independent pathways, specifically the self-amplifying axis between oxidative stress and the necroptotic cascade, are key drivers of disease progression. Mediated by the canonical RIPK1/RIPK3/MLKL signaling, necroptosis serves as a pivotal executioner of RGC loss. Oxidative stress functions as the critical upstream trigger that amplifies this cascade, forging a vicious cycle that demands a dual-targeted intervention strategy. To counteract this pathogenic axis, we developed a hierarchically responsive hydrogel (PD@Gel) by dispersing reactive oxygen species (ROS)-responsive Plantainoside D (PD)-loaded nanoparticles (PD@NPs) within a thiolated hyaluronic acid (HA-SH) precursor. Intravitreal injection triggers rapid in situ elation via dynamic disulfide cross-linking. The HA-SH matrix functions as a "macro-scavenger" to deplete extracellular ROS, while PD@NPs fabricated from thioether-functionalized polymers act as "ROS-capturing tentacles" to eliminate intracellular ROS and release PD. Released PD selectively inhibits the necroptotic cascade. In vitro, PD@Gel preserved mitochondrial membrane potential and attenuated necroptotic signaling, alleviating this vicious cycle. In vivo, a single intravitreal injection improved RGC survival, downregulated key necroptosis markers (p-RIPK1/p-MLKL), and partially restored visual function in a murine retinal ischemia-reperfusion (I/R) injury model. Thus, this macro-to-micro platform interferes with the self-amplifying oxidative stress-necroptosis axis, representing a potential neuroprotective strategy.

Exposure to acute hypoxic environments is associated with several ocular disorders, including high-altitude retinopathy (HAR), optic disc edema, retinal hemorrhage, and temporary vision loss. These alterations arise primarily from hypobaric hypoxia and impaired vascular autoregulation. HAR, in particular, is a key indicator of neurovascular dysfunction during systemic hypoxia, affecting retinal ganglion cells-the main output neurons of the retina-as well as the visual cortex, both of which are highly vulnerable to oxygen deprivation. In this study, we investigated the potential protective role of dexamethasone pretreatment against acute intermittent hypobaric hypoxia-induced cellular damage in the retina and primary visual cortex using a rat model of simulated high-altitude exposure. Hypoxic injury was induced in a hypobaric chamber (FiO2=16.6%, pO2=61 mmHg) for 6 hours during 3 consecutive days. Animals in the pretreated group received intraperitoneal injections of dexamethasone (1 mg/kg) once daily for three consecutive days before each hypoxic exposure session. Following hypoxia, untreated rats exhibited significant elevation in retinal layer thickness, increased numbers of choroidal mast cells along with degranulation in the connective tissue around the eyeball, pronounced Müller cell swelling, and neurodegenerative changes in the visual cortex. In contrast, dexamethasone-pretreated animals showed preserved retinal layer cytoarchitecture, reduced choroidal mast cell number, and decreased neuronal loss in the visual cortex. Overall, these findings demonstrate that dexamethasone pretreatment effectively preserves the structural integrity of both the retina and the visual cortex under acute hypoxic conditions.

Valsalva retinopathy is a recognised cause of acute painless visual loss resulting from a sudden increase in intrathoracic or intra-abdominal pressure, leading to subhyaloid haemorrhage. While most reported cases describe rounded or boat-shaped haemorrhages, atypical morphologies documented with multimodal imaging are infrequently reported. We describe a 45-year-old female with long-standing insulin-treated diabetes mellitus who developed sudden visual blurring following a violent coughing episode. Fundoscopic examination revealed a sharply demarcated, heart-shaped subhyaloid haemorrhage involving the macula, and optical coherence tomography confirmed a subhyaloid haemorrhage. Despite intervention occurring almost three weeks after symptom onset, intravitreal tissue plasminogen activator combined with expansile gas resulted in significant anatomical and functional recovery, with visual acuity improving from 6/36 to 6/9 and sustained improvement on follow-up. This case highlights the importance of recognising atypical haemorrhage morphology, accurately localising haemorrhage depth using optical coherence tomography, and individualising management. It also demonstrates that delayed minimally invasive intervention may achieve excellent visual outcomes, even in the presence of pre-existing retinal disease.

Age-related macular degeneration (AMD), characterized by pathologic choroidal neovascularization (CNV), is a leading cause of vision loss in the elderly. Vascular endothelial growth factor A (VEGFa) antagonists can prevent acute vision loss, but high treatment burden and loss of efficacy with chronic therapy highlight the need to explore alternative mechanisms. Recently, microRNA-34a (miR-34a) has emerged as a key regulator in aging and age-related diseases, but its role in neovascular AMD is unclear. In an injury-induced murine CNV model, we found miR-34a promoted pathological angiogenesis, without altering expression of Vegfa or its receptor Kdr, the canonical regulators of CNV. Mechanistically, miR-34a directly targets and inhibits the transcription factor KLF2, thereby upregulating the proangiogenic factors CXCR4 and CXCL12. Finally, we show miR-34a exacerbates CNV in aged mice and is expressed in CNV lesions excised from wet AMD patients. These findings establish a causal link between the age-related miR-34a and neovascularization in AMD.