Emerging data has identified a potential association between glucagon-like peptide-1 receptor agonists (GLP-1RAs) and nonarteritic anterior ischemic optic neuropathy (NAION), a typically sudden, painless, and irreversible cause of optic nerve-mediated vision loss. This review synthesizes the current clinical, epidemiologic, and potential mechanism linking GLP-1RA-based therapies to NAION risk, informing balanced risk assessment and interdisciplinary clinical decision-making. A structured PubMed search was performed using terms including "GLP-1 receptor agonist," "semaglutide," "liraglutide," "tirzepatide," and "nonarteritic anterior ischemic optic neuropathy," in addition to NAION risk factors, including disc-at-risk anatomy, type 2 diabetes, obstructive sleep apnea, hypertension, hyperlipidemia, renal disease, and ischemic heart disease. A small cup-to-disc ratio ("disc-at-risk") was found to be the most robust anatomical predictor of NAION. Systemic microvascular disease (diabetes, hypertension, hyperlipidemia) and conditions such as obstructive sleep apnea and end-stage renal disease were also linked to increased susceptibility to optic nerve head ischemia. Although data across electronic health records, national registries, and pharmacovigilance analyses suggest a very low absolute incidence of NAION, the use of GLP-1RAs demonstrates a statistically significant association with NAION development, yielding relative risk estimates between 1.2 and 4.3. At this time, the potential association between GLP-1RA therapy and NAION should be interpreted as a safety signal rather than a contraindication. Screening for disc-at-risk anatomy, consideration of prior NAION history, and patient counseling regarding acute visual symptoms may be warranted prior to initiation of therapy. As evidence evolves, collaboration between endocrinologists and ophthalmologists will be essential to support safe and effective patient care.

Kabuki syndrome, caused by KMT2D or KDM6A mutations, is a multisystem disorder with immune dysregulation. Its association with aquaporin-4 (AQP4) antibody-positive neuromyelitis optica spectrum disorder has not been reported. A 17-year-old male with autoimmune hypothyroidism presented with acute visual loss and was diagnosed with AQP4-IgG-positive optic neuritis. He received corticosteroids, plasma exchange, and rituximab, achieving full recovery and remaining relapse-free during follow-up. Genetic testing showed a likely pathogenic KMT2D variant. This case documents the first association between these conditions, where immune dysregulation, including FOXP3-dependent regulatory T-cell dysfunction and Th17-skewed inflammation, suggests a mechanistic link with implications for diagnosis and management.

Post-stroke movement disorders are uncommon, and hemichorea-hemiballismus is most often associated with lesions involving the basal ganglia or subthalamic region. Thalamic lesions are a recognized but less frequent cause. We report a 78-year-old right-handed woman who developed sudden involuntary jumping and dancing movements of the right foot, which later spread to the right arm. She had no weakness, sensory loss, dysarthria, visual symptoms, headache, or loss of consciousness. Examination showed continuous right-sided hemichorea-hemiballismus with preserved strength and sensation. Non-contrast computed tomography demonstrated a focal acute left thalamic intracerebral haemorrhage, with no additional haemorrhage, mass effect, midline shift, or acute infarction identified on the initial scan. Four-factor prothrombin complex concentrate was administered for reversal of edoxaban-associated anticoagulation, and anticoagulation was initially withheld. Tetrabenazine was started and gradually increased to a maximum of 25 mg three times daily, with substantial improvement in the involuntary movements and participation in rehabilitation. Attempts to reduce the dose were followed by worsening of the movements. At higher doses, however, she developed significant irritability, low mood, and emotional lability. Tetrabenazine was therefore gradually withdrawn, and aripiprazole was started at 2.5 mg daily and increased to 7.5 mg daily. At subsequent follow-up, the hemichorea remained markedly improved, and her mood improved after tetrabenazine was discontinued. Mild choreiform movements persisted beyond 12 months, and aripiprazole was later increased to 10 mg daily. This case shows that a focal thalamic haemorrhage can present with isolated hemichorea-hemiballismus and that symptoms may remain clinically relevant for more than a year. It also highlights the need to balance symptomatic benefit against neuropsychiatric adverse effects when using tetrabenazine and to consider alternative treatment when symptoms persist.

Wernicke encephalopathy (WE) is a severe neurological condition caused by thiamine deficiency that remains underreported in pregnancy. We report a clinical diagnosis of WE in a 41-year-old woman, gravida 2, para 1, at 16 weeks of gestation. She presented with acute, painless visual impairment, severe dietary restriction, and marked weight loss secondary to severe hyperemesis gravidarum (HG). Examination revealed reduced visual acuity, horizontal nystagmus, psychomotor retardation, and an ataxic gait. The initial diagnosis was delayed due to her atypical presentation and the absence of MRI or blood thiamine level confirmation. However, empirical treatment with IV thiamine was followed by rapid visual and cognitive recovery within 24 hours. The pregnancy was subsequently complicated by fetal growth restriction and preterm delivery. This case illustrates the necessity of empirical treatment for WE based on clinical criteria in pregnant patients with HG. Recognizing atypical presentations and administering thiamine promptly are critical because delayed treatment may result in irreversible maternal neurological complications and adverse pregnancy outcomes.

BACKGROUND Central retinal artery occlusion (CRAO) is an ophthalmic emergency and a retinal ischemic stroke. Cilioretinal arteries may remain perfused during CRAO because they arise from the posterior ciliary circulation. Most reported cilioretinal sparing involves papillomacular or foveal preservation; nasal sparing is atypical. We report CRAO with nasal retinal sparing and spontaneous head-turn behavior during screening. CASE REPORT A 55-year-old man presented with a 2-day history of sudden, painless vision loss in the right eye. He had newly diagnosed hypertension and was an active smoker. Visual acuity was 1/200 in the right eye and 20/20 in the left. During emergency-room screening, he spontaneously turned his head left while attempting to read a tumbling-E chart. Examination showed a right relative afferent pupillary defect. Fundus examination revealed a cherry-red spot, diffuse retinal whitening, and a nasally preserved sector. Fluorescein angiography confirmed nasal perfusion from a patent nasal cilioretinal artery. Nasal optical coherence tomography (OCT) showed preserved retinal architecture, whereas vertical macular OCT showed inner retinal thickening and hyperreflectivity. Bedside confrontation testing suggested gross temporal field preservation. CONCLUSIONS Multimodal imaging documented atypical nasal retinal sparing in acute CRAO. Because the nasal retina subserves the temporal visual field, the leftward head turn was anatomically compatible with possible compensatory eccentric viewing toward residual temporal field function. However, formal perimetry was unavailable, and this observation remains hypothesis-generating rather than diagnostic. Correlating patient behavior with multimodal imaging may help localize residual retinal function while reinforcing the need for urgent systemic vascular evaluation.