Journal of Neuro-Ophthalmology最新文献

Background: According to the World Health Organization, infections, particularly sepsis, are linked to over 20% mortality worldwide and are leading cause of morbidity. A variety of infections have neuro-ophthalmic manifestations. The profile of infectious agents, clinical manifestations, severity, and prognosis of these diseases are highly heterogeneous, and it is therefore difficult to make generalized statements about management.

Evidence acquisition: Available literature with regard to individual infectious agents and their neuroophthalmic manifestations or complications was searched using electronic databases such as PubMed, MEDLINE, Scopus, ProQuest, and Embase. The current study is a review of the literature along with the authors' personal experience in this field.

Results: In this review, we describe the key neuro-ophthalmic manifestations of common bacterial, fungal, viral (except HIV, opportunistic infections, and COVID-19 virus), parasitic, and protozoal infections using illustrative examples.

Conclusions: Infections may involve the afferent and efferent visual pathways, as well as higher order visual processing functions. They can directly invade the eye and the brain or may cause damage due to inflammation, necrosis, vascular compromise, and postinfective demyelination. With the shifting geographic boundaries and widespread international migration, the spectrum of infectious neuro-ophthalmic diseases is expanding. Clinical details, dedicated imaging, biochemical, serological, and at times histopathological confirmation aids in making prompt diagnosis.

Background: Retinal ganglion cells (RGCs) are diverse. Various types play specialized roles in vision, and they may be differentially susceptible in optic nerve disease where their death causes vision loss. RGCs are accordingly compelling targets for novel therapeutic strategies, and so it is clinically imperative to be able to evaluate different types individually in the human eye. This is complex and represents an unmet need for both basic and clinical research. We explore this need, survey emerging approaches, and consider their translational potential.

Methods: We conducted focused searches of online databases (PubMed, Embase, and Google Scholar) using relevant search terms for articles published until January 2025, screened abstracts for relevant publications, and citation searched discovered literature.

Results: Many approaches exist to classify human RGCs into types. Evidence suggests that some types are differentially susceptible to ocular disease, but these patterns are not firmly understood. Methods are emerging to evaluate individual RGC types in the human retina, alongside novel, potentially sight-restoring therapies that will depend on these insights for their full realization.

Conclusions: An integrated classification of RGC types, and refinement of methods to assess their status in the human eye, is clinically vital. Uncovering their roles can inform our understanding of disease biology, nominate biomarkers, and assist the development of therapies that protect, repair, or replace RGCs. The ongoing development of these techniques is imperative to the success of novel therapies for ocular disease.

Background: We investigated the initial macular ganglion cell complex (GCC) changes in a group of patients during the conversion from normal vision to visual loss from Leber hereditary optic neuropathy (LHON).

Methods: Optical coherence tomography scans from 17 eyes of 10 patients with genetically confirmed LHON obtained within 12 weeks of visual symptom onset were analyzed. The thickness of the GCC was measured in 6 macular sectors: superior nasal (SN), inferior nasal (IN), superior temporal, inferior temporal (IT), superior (SUP), and inferior (INF). Receiver operating characteristic (ROC) curves and area under the ROC curve (AUROC) analyses with DeLong comparison were used to evaluate the predictive reliability of GCC thinning in each sector.

Results: Selective, nasal (perifoveal) GCC thinning was observed in most LHON eyes during the early stages, with the SN and IN sectors showing the highest AUROC values. Thinning in these sectors provided significantly greater predictive value for the presence of LHON than other sectors.

Conclusions: Nasal GCC thinning is a reliable early indicator of the conversion from normal vision to visual loss in LHON as demonstrated in 10 of 17 eyes. This pattern of GCC loss provides insights into the disease mechanism and highlights the utility of OCT analysis for early diagnosis. The nasal GCC loss suggests selective vulnerability of ganglion cells serving the foveal region in LHON. Early identification of nasal GCC changes may facilitate timely intervention as gene therapy and other treatments become increasingly accessible.

Background: Ocular myasthenia gravis (OMG) is an autoimmune disease characterized by autoantibodies targeting postsynaptic proteins at the neuromuscular junction, leading to weakness and fatigability of the levator palpebrae superioris, orbicularis oculi and extraocular muscles. Although OMG is primarily a clinical diagnosis, serological antibody testing, predominantly acetylcholine receptor (AChR) antibodies, is usually performed. The clinical utility of muscle-specific kinase (MuSK) antibodies is less well established in OMG. This meta-analysis evaluates the use of anti-AChR and anti-MuSK in patients with OMG and the relative costs of simultaneous vs sequential testing.

Methods: Studies were extracted from Cumulative Index to Nursing and Allied Health Literature (CINAHL), Embase (Ovid), Medline (Ovid), and additional gray literature. A systematic review was conducted using Covidence with 2 independent reviewers for study selection and data extraction. The meta-analysis was conducted with R version 4.4.1 on RStudio, and the meta package. Depending on the level of heterogeneity, either a fixed-effects or random-effects model was used to pool the data. Funnel plots were used to assess publication bias.

Results: The pooled analysis of 44 studies (n = 4,937 patients with OMG) revealed 59% (95% confidence interval [CI]: 52%-66%) positivity for anti-AChR, whereas the pooled analysis of 34 studies with (n = 3,380) showed 5% (95% CI: 2%-9%) positivity for anti-MuSK. From 62 studies (n = 5,180), 4 patients (0.1%) were doubly seropositive for anti-AChR and anti-MuSK. In patients with OMG positive for AChR antibodies, 5 studies (n = 527) reported a thymoma prevalence of 35% (95% CI: 3%-90%), underscoring the clinical value of anti-AChR testing. Four studies (n= 259) showed that anti-AChR positive patients had a 1.82 (95% CI: 1.15-2.88) times greater risk of progressing from OMG to generalized myasthenia gravis.

Conclusions: Almost two-thirds (59%) of the patients with OMG tested positive for AChR antibodies, but MuSK antibodies were only detected in 5% of patients. Positivity for anti-AChR in OMG was associated with a worse prognosis, including a higher prevalence of thymomas and an increased risk of disease generalization. Given the relatively low prevalence of anti-MuSK and the higher cost of anti-MuSK testing, clinicians could consider a stepwise approach to the serological diagnosis of OMG, where anti-MuSK is ordered only if the initial anti-AChR returns negative.