This study reports a case of MOG antibody-associated optic neuritis masquerading as acute angle-closure glaucoma in which marked discordance between optic disc cupping and visual field loss prompted magnetic resonance imaging (MRI) and led to the correct diagnosis. A 69-year-old woman presented with acute ocular pain, decreased vision, and intraocular pressure exceeding 40 mmHg in the right eye. Humphrey visual field testing demonstrated nearly complete central visual field loss, whereas fundus examination revealed only mild optic disc cupping. Because the severity of visual field loss was disproportionate to the optic disc findings, concurrent optic neuritis was suspected. MRI demonstrated a hyperintense lesion in the right optic nerve on short tau inversion recovery (STIR) imaging. Intravenous methylprednisolone pulse therapy was initiated, followed by bilateral cataract surgery combined with ab interno microhook trabeculotomy because of persistent angle closure and anticipated prolonged corticosteroid therapy. Subsequent serological testing confirmed myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD). Five months later, visual acuity recovered to 20/20 with substantial improvement in the visual field, and intraocular pressure remained well controlled. Even in patients with markedly elevated intraocular pressure suggestive of acute angle-closure glaucoma, pronounced discordance between optic disc findings and visual field loss should raise suspicion for concomitant optic neuritis or other nonglaucomatous optic neuropathies. MRI can facilitate the diagnosis of underlying MOG antibody-associated disease and guide appropriate neurological and ophthalmic management.

Pseudoexfoliation syndrome is a common cause of secondary open-angle glaucoma but rarely presents with acute angle closure in pseudophakic eyes, where management may be challenging when conventional medical and laser therapies fail. We report the case of an 82-year-old pseudophakic woman with known pseudoexfoliation syndrome who presented with acute right eye pain, visual loss, an intraocular pressure of 65 mmHg, a shallow anterior chamber and vitreous prolapse into the anterior chamber. Medical therapy, anterior vitreous disruption and laser peripheral iridotomy failed to adequately reduce intraocular pressure. Office-based trans-pars plana needle aspiration of liquefied vitreous resulted in immediate deepening of the anterior chamber and reduction in intraocular pressure. Visual acuity recovered fully, and intraocular pressure remained controlled with topical therapy after 7 months. This case suggests that office-based trans-pars plana needle aspiration may represent a useful emergency management option in carefully selected patients with refractory acute angle closure associated with pseudoexfoliation syndrome.

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.

Background: Acute angle-closure glaucoma (AACG) is an emergency requiring rapid intervention to prevent irreversible optic nerve damage and permanent vision loss. Methods: This narrative review synthesizes the systemic medication classes most implicated in medication-induced AACG, outlining their underlying pathophysiological mechanisms, typical timing of onset, and practical risk-reduction strategies. Evidence was collected through targeted searches of the PubMed, Google Scholar, Cochrane Library, and Web of Science databases, focusing on major review articles, pharmacoepidemiologic studies, and clinical consensus guidelines. Source selection and data synthesis followed a narrative approach without formal risk of bias assessment or meta-analysis. Results: The literature consistently implicates sulfonamide derivatives (mainly topiramate), serotonergic antidepressants and triptans, potent systemic anticholinergics, and adrenergic decongestants. Sulfonamides typically precipitate bilateral, non-pupillary-block AACG via ciliochoroidal effusion, secondary anterior displacement of the lens-iris diaphragm, and an acute myopic shift. Conversely, serotonergic, anticholinergic, and adrenergic agents typically trigger classic pupillary-block AACG in anatomically predisposed eyes with pre-existing narrow angles. Adverse events predominantly occur shortly after treatment initiation or dose escalation. Management relies on prompt medication discontinuation and rapid intraocular pressure reduction. Importantly, cycloplegics are preferred over miotics in effusion-induced cases. Given the rarity of these events, brief patient education represents a pragmatic and scalable approach, although its direct clinical effectiveness in reducing event rates has not yet been formally established. Conclusions: A select group of widely prescribed systemic medications are associated with most cases of medication-induced AACG. Improving clinician awareness, providing brief patient counseling on warning symptoms, and ensuring prompt ophthalmic evaluation represent the most practical currently available risk-reduction strategies to prevent vision loss.