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.

Despite the recent reports of the potential association between semaglutide and nonarteritic anterior ischemic optic neuropathy (NAION), available evidence remains inconclusive. We aimed to evaluate the relative effect (RE) of NAION in individuals treated with semaglutide compared to the control group. The results of this systematic review and meta-analysis were reported according to the PRISMA guidelines. The study protocol was prospectively registered in PROSPERO with ID: CRD42025649542. A systematic search was performed on the PubMed, Embase, and Cochrane Library databases until May 18, 2026. Meta-analysis of REs with 95% confidence intervals (CI) was calculated using random-effects models. Eight observational cohort studies, involving a total of 5,916,559 participants, were included in the meta-analysis. Of these, 1,870,346 patients received semaglutide treatment, while 4,046,213 were administered non-semaglutide treatment. Compared to non-semaglutide-treated patients, semaglutide users had a higher risk of NAION (RE, 1.93; 95% CI, 1.22-3.08; I2, 91%; P  =  .01). There was a significant association between NAION risk and semaglutide use in individuals with diabetes (RE, 1.84; 95% CI, 1.21-2.80; I2, 88.26%; P  < .01). However, the results were non-significant among overweight or obese individuals (RE, 1.68; 95% CI, 0.72-3.91; I2, 83.98%; P  =  .23). The current meta-analysis suggests a possible association between semaglutide and risk of NAION. Further randomized clinical trials are required to draw a clear conclusion.

This article describes a technique for biomechanical testing of human extraocular muscle samples based on the principle of nanoindentation. The technique involves both static and dynamic testing of tissue samples. The study determines a set of biomechanical parameters that characterize the viscoelastic properties and stiffness of various areas of muscle tissue. The obtained data can serve as a basis for establishing normative biomechanical parameters of human extraocular muscles, as well as for subsequent assessment of pathological changes in various forms of strabismus.

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.

Pneumosinus dilatans (PSD) is a rare expansile disorder characterized by enlargement of an aerated paranasal sinus beyond its normal anatomic boundaries while preserving bony integrity. We report a 26-year-old man with progressive unilateral proptosis presenting 18 years after severe craniofacial trauma complicated by permanent sixth and seventh cranial nerve palsies. Examination demonstrated 5 mm axial left proptosis with paralytic lagophthalmos, lower eyelid retraction, and exposure keratopathy. Computed tomography revealed marked left frontal sinus enlargement (62.7% volumetric increase) with intact bony walls, consistent with frontal PSD. This case demonstrates the importance of objective exophthalmometry and orbital imaging in distinguishing true space-occupying sinus-related proptosis from smaller anterior globe displacement and periocular changes associated with facial nerve palsy alone. Management consisted of orbital decompression combined with upper and lower eyelid rehabilitation. Hertel asymmetry improved from 5 mm to 1 mm with satisfactory functional and cosmetic outcomes. The case emphasizes that careful imaging is essential when evaluating globe prominence in the setting of facial asymmetry.

Adenoid cystic carcinoma (ACC) with intracranial metastasis and sixth cranial nerve (CN VI) palsy, spinal metastases, and malignant spinal cord compression is an uncommon clinical entity. We present a case of a patient exhibiting this constellation of findings secondary to the parotid ACC. A 55-year-old man with no identifiable risk factors for ACC presented with a 10-year history of a left parotid tumor. He underwent two surgical resections and received one cycle of chemotherapy. Subsequently, his disease progressed locoregionally and systemically. He developed diplopia due to left sixth cranial nerve palsy caused by an intracranial metastatic lesion, together with complete spinal cord syndrome secondary to thoracic spinal metastases with malignant spinal cord compression. The patient was treated with whole-brain radiotherapy for intracranial metastasis and palliative spinal radiotherapy for spinal cord compression, achieving neurological stabilization without further deterioration. Systemic therapy with a tyrosine kinase inhibitor was subsequently initiated (lenvatinib 24 mg QD). The lungs are the most common site of distant metastasis in ACC, followed by bone and liver involvement. However, intracranial dissemination may occur rarely and should be considered in the clinical evaluation of these patients.

Bell's palsy is the most common cause of acute unilateral lower motor neuron-type facial nerve paralysis and is generally managed with early administration of corticosteroids, with or without antiviral therapy. Although most patients experience substantial recovery, a clinically meaningful subset-including older adults, individuals with delayed presentation, and those with comorbid medical conditions-may be left with incomplete resolution, with persistent facial weakness, asymmetry, or synkinesis. Electroacupuncture (EA) has been proposed as an adjunctive treatment modality for facial nerve recovery, with hypothesized mechanisms including enhanced neuromuscular activation, improved regional blood flow, modulation of local inflammatory responses, and facilitation of peripheral nerve regeneration. However, robust clinical evidence and detailed case-based documentation remain limited. We report the case of an 81-year-old male patient who presented with acute left-sided lower motor neuron-type facial paralysis. The diagnosis was consistent with Bell's palsy, after a cerebrovascular accident was excluded, and neuroimaging demonstrated no acute intracranial pathology. An integrative treatment approach incorporating acupuncture with low-frequency electrical stimulation was initiated on day 17 post-onset, targeting facial and cranial acupoints. EA treatment was administered twice weekly for seven weeks and was supplemented with conservative home-based interventions. Facial nerve function improved from House-Brackmann Grade IV at presentation to Grade I-II. While this case suggests that EA may have a role as an adjunctive therapy in Bell's palsy, including in patients with delayed presentation and less favorable prognostic features, its interpretation is limited by the single-case design and the known potential for spontaneous recovery. Accordingly, controlled prospective studies are warranted to further evaluate the efficacy, optimal timing, and clinical utility of EA in the management of acute facial nerve paralysis.

Trigeminal neuralgia (TN) is a neuropathic pain disorder characterized by recurrent, unilateral, electric shock-like facial pain, with trigger zones representing one of its most distinctive clinical features. These localized hypersensitive regions can be reliably activated by innocuous mechanical stimuli such as light touch, speech, or chewing, and their distribution provides important guidance for localizing the affected trigeminal branch and directing treatment decisions. Current evidence suggests that trigger zone formation involves peripheral nerve hyperexcitability driven by upregulation of voltage-gated sodium channels, mechanical sensitization from adjacent facial and masticatory muscle activity, and central sensitization within the trigeminal brainstem complex. At the brainstem level, abnormal activation of wide dynamic range neurons results in the misinterpretation of innocuous tactile input as pain. Clinically, systemic sodium channel blockers remain the foundation of initial treatment, while trigger zone-targeted interventions including peripheral nerve blockade, botulinum toxin type A injections, and minimally invasive ablative techniques have emerged as important adjunctive approaches. The absence of standardized objective assessment criteria and insufficient comparative clinical evidence remain key limitations in the field. A more thorough understanding of trigger zone pathophysiology may ultimately support the development of precision-based, individualized management strategies for TN.

Spaceflight-Associated Neuro-Ocular Syndrome (SANS) has remained poorly understood throughout the history of human spaceflight despite being classified as the largest physiologic barrier that astronauts face. Existing mechanistic explanations of SANS are limited in accounting for its tissue specificity, interindividual heterogeneity, and persistence beyond return to Earth, which has left countermeasure development without a coherent biological target. Through integration of tissue-resolved murine spaceflight transcriptomic datasets with human retinal ganglion cell models of Leber Hereditary Optic Neuropathy (LHON), we define a share pattern of injury underlying SANS. Across all datasets, suppression of mitochondrial oxidative phosphorylation (OXPHOS) consistently preceded innate immune, interferon, and PANoptotic activation, establishing metabolic collapse as the initiating event rather than a downstream consequence. Strain-dependent divergence in mitochondrial resilience between BALB/c and C57BL/6 J mice onboard the International Space Station (ISS) supports a threshold-dependent susceptibility model, and cross-species convergence with LHON-derived retinal ganglion cells identifies shared molecular signatures linking spaceflight neurodegeneration with terrestrial mitochondrial optic neuropathies. These findings support reclassification of SANS as a mitochondrial-inflammatory optic neuropathy, spaceflight-associated optic neuropathy (SAON), providing the first mechanistically complete basis for countermeasure development, risk stratification, and an evolution from syndromic classification towards a defined disease framework.