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Background Chronic uveitis, a major cause of legal blindness in the United States, often requires long-term immunomodulatory therapy (IMT). This study aims to characterize trends in systemic IMT use among adults with chronic uveitis in United States from 2005 to 2025. Methods This cross-sectional time-series study used the TriNetX Network to analyze adults (ages ≥ 18) with chronic, non-infectious uveitis treated with methotrexate, mycophenolate, azathioprine, cyclosporine, tacrolimus, cyclophosphamide, adalimumab, infliximab and/or etanercept. Data was grouped into consecutive 3-year intervals, and Cochran–Armitage tests assessed changes in the proportion of patients treated with each medication. Results The total population included 12,035 adult patients. Academic and non-academic institutions shared similar trends in IMT usage. Overall, there was a reduction in the proportion of patients on methotrexate (44.2% in 2005–2007 to 37.6% in 2023–2025, p  < 0.0001), azathioprine (15.1% in 2005–2007 to 6.7% in 2023–2025, p  < 0.0001), cyclophosphamide (2.5% in 2011–2013 to 0.8% in 2023–2025, p  < 0.0001), infliximab (18.6% in 2005–2007 to 14.1% in 2023–2025, p  < 0.0001) and etanercept (9.0% in 2005–2007 to 2.0% in 2023–2025, p  < 0.0001). Conversely, treatment with adalimumab rose markedly among patients with chronic uveitis (8.0% in 2005–2007 to 34.6% in 2023–2025; p  < 0.0001). There was no change in the proportion of patients on mycophenolate (14.6% in 2005–2007 to 12.8% in 2023–2025; p  = 0.5963). Conclusion Key shifts in management of chronic uveitis include the emergence adalimumab as a key steroid sparing agent, the continued role of methotrexate as the first-line steroid-sparing agent, and a marked decline in the use of many older immunomodulatory therapies.

Background/Objectives: This retrospective cohort study compared hospitalization and follow-up rates in patients with newly diagnosed proliferative diabetic retinopathy (PDR) versus those without prior diabetic retinopathy (DR) screening. Methods: Using TriNetX, a global electronic health record database, 57,964 patients aged ≥ 40 years with type 2 diabetes and newly diagnosed PDR without diabetic macular edema (DME) requiring panretinal photocoagulation or intravitreal injection were included. Patients were stratified based on the presence or absence of prior DR screening in the last 5 years and balanced using propensity score matching (PSM). Primary outcomes included 30-, 60-, and 90-day hospitalization rates and repeat ophthalmic follow-up as estimated using repeat PDR diagnosis codes and repeat retinal imaging codes, including OCT, fundus photography, and fluorescein angiography. Results: Of 57,964 patients, 25,003 had no prior DR screening and 32,961 had prior DR screening. After matching, 19,316 patients were included per cohort. Patients without known DR screening had significantly higher hospitalization rates at 30 days (RR = 1.78, 95% CI 1.67–1.89), 60 days (RR = 1.59, 95% CI 1.51–1.67), and 90 days (RR = 1.51, 95% CI 1.44–1.58), and lower repeat ophthalmic visits by PDR codes at 30 days (RR = 0.458, 95% CI 0.440–0.476), 60 days (RR = 0.450, 95% CI 0.437–0.463) and 90 days (RR = 0.420, 95% CI 0.408–0.432) or by repeat retinal imaging codes at 30 days (RR = 0.450, 95% CI 0.423–0.478), 60 days (RR = 0.394, 95% CI 0.377–0.411), and 90 days (RR = 0.381, 95% CI 0.366–0.396) (all p < 0.0001). Conclusions: Absence of known prior DR screening in PDR patients is associated with higher hospitalization risk and reduced ophthalmic follow-up, suggesting that a lack of screening indicates broader gaps in healthcare engagement and disease control. Tailored strategies are needed to prevent vision loss as well as systemic complications.

Neurofilament light chain (NfL) is a neuronal cytoskeletal protein that has been identified as a marker of neurodegeneration in diseases of the central nervous system. In this study, we investigated whether NfL in the aqueous humor (AH) can serve as a marker of neurodegeneration in glaucoma in a racially diverse North American population. Single-center, case-control study. We enrolled patients with various types and stages of glaucoma undergoing planned ophthalmic surgery as part of their routine care and compared them with patients without glaucoma undergoing phacoemulsification for age-related cataract. We collected AH from 39 glaucoma patients and 10 patients without glaucoma. AH NfL was quantified using the Single-Molecule Array (Simoa) NF-light assay (Quanterix). Demographic information, such as age, body mass index, sex, and self-reported race, as well as clinical information, such as pre-operative intraocular pressure (IOP), maximum IOP, and number of pre-operative glaucoma medications, was obtained by reviewing the medical record. Levels of AH NfL. In a model controlling for age and body mass index (BMI), NfL was significantly elevated in AH from glaucoma patients (mean: 429 pg/mL; standard deviation [SD]: 1136 pg/mL) compared to AH from patients without glaucoma (mean: 3.1 pg/mL; SD: 1.9 pg/mg): P = 0.002. Higher AH NfL was associated with higher maximum IOP (R = 0.44, P = 0.005), higher pre-operative IOP (R = 0.46, P = 0.003), and more pre-operative glaucoma medications (R = 0.61, P < 0.001). There was no association between AH NfL and Humphrey visual field mean deviation (R = -0.20, P = 0.220), retinal nerve fiber layer thickness as measured with optical coherence tomography (R = 0.07, P = 0.694), or glaucoma stage (R = 0.015, P = 0.935). Our findings suggest that AH NfL may have clinical utility as a marker of glaucomatous neurodegeneration.

Visual imagery comprises object and spatial dimensions. Both types of imagery encode shape but a key difference is that object imagers are more likely to encode surface properties than spatial imagers. Since visual and haptic object representations share many characteristics, we investigated whether haptic and multisensory representations also share an object-spatial continuum. Experiment 1 involved two tasks in both visual and haptic within-modal conditions, one requiring discrimination of shape across changes in texture, the other discrimination of texture across changes in shape. In both modalities, spatial imagers could ignore changes in texture but not shape, whereas object imagers could ignore changes in shape but not texture. Experiment 2 re-analyzed a cross-modal version of the shape discrimination task from an earlier study. We found that spatial imagers could discriminate shape across changes in texture but object imagers could not and that the more one preferred object imagery, the more texture changes impaired discrimination. These findings are the first evidence that object and spatial dimensions of imagery can be observed in haptic and multisensory representations.

Lipid-rich drusen are the sine qua non of age-related macular degeneration (AMD), the leading cause of blindness in older adults in the developed world. Efforts directed at uncovering effective therapeutic strategies have led to the hypothesis that altered lipid metabolism may play a pathogenic role in AMD. This hypothesis is supported by the fact that: (1) drusen, the hallmark histopathologic feature of AMD, are composed of lipids, (2) polymorphisms of genes involved in lipid homeostasis are associated with increased odds of AMD, (3) metabolomics studies show that patients with AMD have alterations in metabolites from lipid pathways, and (4) alterations in serum lipid profiles as a reflection of systemic dyslipidemia are associated with AMD. There is strong evidence that statins, which are well described for treating dyslipidemia and reducing risk associated with cardiovascular disease, may have a role for treating certain cohorts of AMD patients, but this has yet to be conclusively proven. Of interest, the specific changes in serum lipoprotein profiles associated with decreased cardiovascular risk (i.e., high HDL levels) have been shown in some studies to be associated with increased risk of AMD. In this review, we highlight the evidence that supports a role for altered lipid metabolism in AMD and provide our perspective regarding the remaining questions that need to be addressed before lipid-based therapies can emerge for specific cohorts of AMD patients.

Retinal detachment (RD) occurs when the neurosensory retina, the neurovascular tissue responsible for phototransduction, is separated from the underlying retinal pigment epithelium (RPE). Given the importance of the RPE for optimal retinal function, RD invariably leads to decreased vision. There are three main types of RD: rhegmatogenous, tractional and exudative (also termed serous) RD. In rhegmatogenous RD, one or more retinal breaks enable vitreous fluid to enter the subretinal space and separate the neurosensory retina from the RPE. In tractional RD, preretinal, intraretinal or subretinal membranes contract and exert tangential forces and elevate the retina from the underlying RPE. Finally, in exudative RD, an underlying inflammatory condition, vascular abnormality or the presence of a tumour causes exudative fluid to accumulate in the subretinal space, exceeding the osmotic pump function of the RPE. The surgical management of RD usually involves pars plana vitrectomy, scleral buckling or pneumatic retinopexy. The approach taken often depends on patient characteristics as well as on practitioner experience and clinical judgement. Advances in surgical technology and continued innovation have improved outcomes for many patients. However, even if retinal re-attachment is achieved, some patients still experience decreased vision or other visual symptoms, such as metamorphopsia, that diminish their quality of life. Continued research in the areas of neuroprotection and retinal biology as well as continued surgical innovation are necessary to enhance therapeutic options and outcomes for these patients.Retinal detachment describes the separation of the neurosensory retina from the underlying retinal pigment epithelium, leading to impaired vision or vision loss. This Primer discusses the epidemiology, pathophysiology, diagnosis and management of this disorder and highlights future research directions.

Topical therapies targeting Rho-associated protein kinase (ROCK) signalling, including netarsudil (Rhopressa®) and ripasudil (Glanatec®), have become widely adopted as part of standard clinical practice to lower intraocular pressure (IOP) in patients with ocular hypertension or glaucoma. Given the pleiotropic roles of ROCK signalling, ROCK inhibition has the potential to cause unintended ocular side effects beyond IOP lowering in other substructures of the eye, both beneficial and deleterious. Additional experience and observation of patients treated with this class of medications have uncovered both new side effects not reported in the initial clinical trials, as well as potential benefits that have inspired off-label uses and that have been the topic of numerous clinical studies, case series, case reports, and translational studies. Here, we performed a comprehensive systematic review and identified 170 studies describing ocular effects of ROCK inhibition. In addition to describing well-established ocular effects associated with inhibition of ROCK signalling, such as conjunctival hyperaemia, corneal verticillata, and reticular corneal epithelial oedema, we also highlight other effects, such as corneal haemorrhages, changes in corneal contour, anterior subcapsular opacities, contact dermatitis, punctal stenosis, and eyelid wound dehiscence, which have been described in case series and case reports. Finally, we evaluated studies describing potential novel applications of ROCK inhibition for treating disorders affecting the cornea, the retina, and the optic nerve, finding strong evidence in support of a beneficial effect of ROCK inhibitors on corneal oedema due to corneal endothelial cell dysfunction. The other potential applications require further research.

Diabetic retinopathy (DR) is a major cause of blindness in working adults in the industrialized world. In addition to vision loss caused by macular edema and pathological angiogenesis, DR patients often exhibit neuronal dysfunction on electrophysiological testing, suggesting that there may be an independent neuronal phase of disease that precedes vascular disease. Given the tremendous metabolic requirements of the retina and photoreceptors in particular, we hypothesized that derangements in metabolic regulation may accelerate retinal dysfunction in diabetes. As such, we induced hyperglycemia with streptozotocin in mice with monoallelic Nampt deletion from rod photoreceptors, mice lacking SIRT3, and mice lacking SIRT5 and tested multiple components of retinal function with electroretinography. None of these mice exhibited accelerated retinal dysfunction after induction of hyperglycemia, consistent with normal-appearing retinal morphology in hyperglycemic Sirt3 −/− or Sirt5 −/− mice. However, mice lacking both SIRT3 and SIRT5 ( Sirt3 −/− Sirt5 −/− mice) exhibited significant evidence of inner retinal dysfunction after induction of hyperglycemia compared to hyperglycemic littermate controls, although this dysfunction was not accompanied by gross morphological changes in the retina. These results suggest that SIRT3 and SIRT5 may be involved in regulating neuronal dysfunction in DR and provide a foundation for future studies investigating sirtuin-based therapies.

Background and Objective: The aim of this study was to characterize longitudinal trends in intraocular lens (IOL) dislocation in patients after cataract surgery. Patients and Methods: Using the TriNetX network, a retrospective cohort study was conducted of 866,010 patients who underwent cataract surgery from the years 2000 to 2024. Those patients who had experienced IOL dislocation based on International Classification of Diseases, Ninth and Tenth Revision (ICD-9 and -10) codes were identified. Patients with risk factors for IOL dislocation, such as ocular trauma, prior intravitreal injections, prior pars plana vitrectomy, pseudoexfoliation glaucoma, and Marfan syndrome, based on ICD-9/-10 and Current Procedural Terminology (CPT) codes, were also identified. Results: From 2020 to 2024, 9,929 (1.1%) of the 866,010 patients experienced IOL dislocation. Over the past 2 decades, there was a significant monotonic increase in the incidence rate of IOL dislocation (P < .01), as well as ocular trauma (P < .01), intravitreal injections (P < .01), and pars plana vitrectomy (P < .01). Conclusion: IOL dislocation is becoming increasingly common. Practitioners must be prepared to manage these conditions.

Purpose: To determine 1) which components of retinal function are impaired after rhegmatogenous retinal detachment, 2) which outer retinal pathways (rod- or cone-driven) are more severely affected, and 3) whether there is concomitant inner retinal dysfunction. Methods: We conducted a prospective observational study in a large academic institution. We performed preoperative electroretinography on eight patients to assess outer and inner retinal function. In all cases, a comparison between the eye with the detached retina and the control fellow eye was made. Results: Eyes with a detached retina had significantly lower a-wave and b-wave amplitudes with respect to both rod- and cone-dominated testing parameters (P < 0.05) and reduced 30 Hz flicker responses compared to fellow eyes (P < 0.05); the effect size was similar for all significantly reduced parameters (r~0.6). There were no significant differences between eyes with detached retinas and control fellow eyes with respect to b/a-wave ratios, a-wave latencies, or b-wave latencies. Conclusion: Patients with rhegmatogenous retinal detachment have preoperative outer retinal dysfunction equally affecting both rod- and cone-driven pathways, and they have minimal inner retinal dysfunction.