Toxic Optic Neuropathy Research Articles

Anterior Optic Neuropathies without Optic Disc Edema

Anterior optic neuropathies in which the optic discs appear normal include nutritional optic neuropathy, vitamin B12 or folate deficiencies, toxic optic neuropathy due to drugs and heavy metals, and hereditary optic neuropathy. When these conditions become chronic, optic atrophy can occur. Treatment of these diseases, which can cause dramatic vision loss, should be done quickly and permanent neuronal damage should be prevented as much as possible. Therefore, this group of diseases should always be kept in mind by clinicians in cases of unexplained visual loss.

Toxic And Nutritional Optic Neuropathies

Nutritional and toxic optic neuropathies belong to the group of metabolic mitochondrial optic neuropathies together with hereditary optic neuropathies. Nutritional and toxic optic neuropathies are grouped together because they have many common signs and symptoms. Mitochondrial oxidative phosphorylation dysfunction leads to dysfunction of the papillomacular bundle, resulting in optic neuropathy. Common clinical findings include dyschromatopsia, painless bilateral progressive visual loss, central or cecocentral visual field defects, and progressive optic disc pallor. A toxic substance or lacking vitamins and elements critical for mitochondrial function can cause optic neuropathy.

Infective pulmonary diseases and the eye: a narrative review.

Several infectious pulmonary diseases affect the eye. An understanding of the association between infectious pulmonary and ocular diseases is pivotal to their successful management. We aimed to review the infections affecting both the lungs and the eye. The electronic database PubMed and the search engine Google Scholar were searched for relevant articles. Ocular tuberculosis (TB), usually not associated with clinical evidence of pulmonary TB, can affect almost all the ocular structures. Confirmation of the diagnosis of ocular TB requires demonstration of Mycobacterium tuberculosis in ocular fluids/tissues. Among the drugs used to treat TB, ethambutol, isoniazid, and linezolid may cause toxic optic neuropathy. Elderly, those with renal disease, diabetes mellitus, malnourished, alcoholics, and those who will receive ethambutol at doses greater than 15 mg/kg/day and for prolonged periods are at high risk of developing toxic optic neuropathy. These individuals should be referred to an ophthalmologist before initiating ATT for a baseline ophthalmic evaluation. Linezolid may also cause toxic retinal neuropathy. Rifampicin may cause yellowish-orange discoloration of tears and contact lenses. Adenovirus, coronavirus, influenza virus, respiratory syncytial virus, and rhinovirus exhibit both pulmonary and ocular tropism. Pneumocystis jirovecii choroiditis is rare and mainly seen when aerosolized pentamidine is used for pneumocystis pneumonia prophylaxis. Further research is needed to develop non-interventional strategies to diagnose ocular TB. Biomarkers for early detection of toxic optic neuropathy are a need of the hour. Genetic factors and mechanisms behind the development of ethambutol, isoniazid, and linezolid-induced toxic optic neuropathy need further study.

Voriconazole-induced central nervous system toxicity: a pharmacovigilance study based on FDA adverse event reporting system (FAERS) database

ABSTRACT Background This study aims to evaluate the relationship between voriconazole (VRC) and central nervous system (CNS) toxicity based on the real world data. Research design and methods The reports of FAERS from January 2004 to March 2022 were included in our study. The CNS toxicity events were identified by using Medical Dictionary for Regulatory Activities terms. Reporting odds ratios corresponding to 95% confidence intervals were employed to quantify the signals of VRC-associated CNS events. Results The overall RORs (95%CI) for psychiatric disorders, nervous system disorders, and eye disorders were 1.84 (1.70, 2.00), 1.09 (1.01, 1.18), and 3.84 (3.48, 4.23), respectively (p < 0.05). The median time to the CNS events of VRC was 1(IQR 0–5) day. Top six signals were macular opacity, chloropsia, scintillating scotoma, toxic optic neuropathy, corneal bleeding, and dyschromatopsia, all of them grouped as eye disorders. Compared with itraconazole, fluconazole, posaconazole, and isavuconazole, VRC shows significant relationship and higher incidence rate of psychiatric disorders, nervous system disorders, and eye disorders, respectively (p < 0.05). Conclusions VRC was significantly associated with the CNS toxicity. Dosing adjustment, model-based individualized treatment project, and the therapeutic drug monitoring-guided individualized medication regime could be good strategies for efficacy improvement and the adverse events of reducing of VRC.

Erythropoietin for the Treatment of Methanol Toxic Optic Neuropathy: Does It Really Work? A Case Series

ABSTRACT Erythropoietin (EPO) has demonstrated neuroprotective properties and has been used in small case series to treat methanol optic neuropathy. This study aims to evaluate the effectiveness of EPO. This retrospective case series included data from patients diagnosed with methanol optic neuropathy between November 2022 and December 2023 from two centers in Jeddah, Saudi Arabia. Demographic information, time of consumption of methanol to EPO treatment, and other treatments administered were collected. Vision assessment was performed before and after EPO treatment. A total of 8 male patients were included, with an average age of 38.25 ± 7.15 years. The median duration of the follow-up was 66 days, ranging from 13 to 660 days. The means of vision in the logMAR of both eyes before EPO treatment was 1.98 ± 1.08, which changed to 1.87 ± 0.89 after EPO treatment. Patient’s presenting vision before EPO treatment is a significant positive predictor for the vision after treatment with coefficient = 0.782 and 95% CI = 0.349, 0.936. Time to EPO treatment was not statistically significant in defining end vision. Treating methanol optic neuropathy is challenging and time sensitive. In this case series, EPO and adjuvant steroids showed variable effects on visual improvement. Although the vision improved after the treatment, these differences were not statistically significant. Repeat EPO did not give better outcomes. Long-term follow-up is needed to determine the overall impact of EPO treatment.

Risk Factors of Optic Neuropathy in Ethambutol Users: Interaction with Isoniazid and Other Associated Conditions of Toxic Optic Neuropathy.

(1) Background: To investigate the risk factors associated with optic neuropathy (ON) and validate the hypothesis that concomitant isoniazid use and other causes of toxic ON affect the development of ON in ethambutol users. (2) Methods: This cohort study identified ethambutol users who initiated ethambutol therapy between January 2015 and December 2021 and had no ON prior to ethambutol therapy. ON incidence up to 31 December 2022 was evaluated. The users were grouped on the basis of the presence of ON. Demographic and clinical characteristics were investigated for risk factor analyses of ON. Odds ratios (ORs) were calculated using multivariate logistic regression analyses. (3) Results: Among 204,598 ethambutol users, 5277 (2.6%) patients developed ON over the study period. Patients with ON included a higher percentage of women and had a higher mean age than patients without ON. In the multivariate analyses, the risk factors for ON and visual impairment included sex, age, cumulative dose, extrapulmonary indications for ethambutol use, and systemic conditions such as diabetes, hypertension, hyperlipidemia, diabetes, kidney disease, and liver disease. Malnutrition or nutritional disorders significantly increased the risk of ON (OR = 1.27, 95% confidence interval [CI] = 1.19-1.34), whereas concomitant isoniazid use decreased the risk (OR = 0.78, 95% CI = 0.72-0.86). (4) Conclusion: An increased risk of ON in patients with systemic diseases and nutritional deficiency was identified, whereas concomitant isoniazid use was associated with a decreased risk of ON. Patients with these risk factors should be carefully monitored to minimize the vision-threatening ON.

Optic neuropathy from hypovitaminosis A in a series of children with severe dietary restrictions.

Hypovitaminosis A is a leading cause of preventable childhood blindness, especially in developing nations. Vitamin A is a fat-soluble essential micronutrient that serves vital functions in the visual system and in regulating bone resorption. We report on a series of four children with mixed nutritional and compressive optic neuropathy and provide a review of the literature. A retrospective observational study of four males (ages 9-12), three with autism spectrum disorder who presented with loss of vision and multiple vitamin deficiencies including hypovitaminosis A. Patients presented with unexplained visual loss or a change in visual behaviour. All patients had severely restricted diet comprising of predominantly carbohydrates. Two of the four cases demonstrated optic nerve pallor at initial presentation with marked optic atrophy developing in all patients over time. Electrophysiology available in two patients demonstrated optic nerve dysfunction with preserved retinal function. Extensive investigations revealed profound deficiency in multiple vitamins including vitamin A (<0.1-0.2 μmol/L, normal = 0.9-1.7 μmol/L). Three patients also had low vitamin B12 (90-111 pmol/L, normal = 170-800 pmol/L) with normal folate. All four cases had radiological evidence of skull base thickening indicative of low vitamin A. Genetic testing did not find any relevant pathogenic variants. Hypovitaminosis A is a crucial form of nutritional deprivation that results in significant visual loss with potential hyperostosis and optic nerve compression exacerbating nutritional optic neuropathy. Additional micronutrient deficiencies usually co-exist and may contribute. Extra vigilance in vitamin replacement is required of clinicians with patients with autism who have restricted diets.

Visual evoked potential as an early assessment tool in ethambutol-induced toxic optic neuropathy during treatment of tuberculosis

Visual evoked potential as an early assessment tool in ethambutol-induced toxic optic neuropathy during treatment of tuberculosis

Toxic Optic Neuropathy Due to Chronic Arsenic Exposure.

Toxic Optic Neuropathy Due to Chronic Arsenic Exposure.

Maculopapillary Bundle Degeneration in Optic Neuropathies.

Degeneration of the maculopapillary bundle (MPB) is a prominent feature in a spectrum of optic neuropathies. MPB-selective degeneration is seen in specific conditions, such as nutritional and toxic optic neuropathies, Leber hereditary optic neuropathy (LHON), and dominant optic atrophy (DOA). Despite their distinct etiologies and clinical presentations, which encompass variations in age of incidence and monocular or binocular onset, these disorders share a core molecular mechanism: compromised mitochondrial homeostasis. This disruption is characterized by dysfunctions in mitochondrial metabolism, biogenesis, and protein synthesis. This article provides a comprehensive understanding of the MPB's role in optic neuropathies, emphasizing the importance of mitochondrial mechanisms in the pathogenesis of these conditions. Optical coherence tomography studies have characterized the retinal nerve fiber layer changes accompanying mitochondrial-affiliated optic neuropathies. Selective thinning of the temporal optic nerve head is preceded by thickening in early stages of these disorders which correlates with reductions in macular ganglion cell layer thinning and vascular atrophy. A recently proposed mechanism underpinning the selective atrophy of the MPB involves the positive feedback of reactive oxygen species generation as a common consequence of mitochondrial dysfunction. Additionally, new research has revealed that the MPB can undergo degeneration in the early stages of glaucoma, challenging the historically held belief that this area was not involved in this common optic neuropathy. A variety of anatomical risk factors influence the propensity of glaucomatous MPB degeneration, and cases present distinct patterns of ganglion cell degeneration that are distinct from those observed in mitochondria-associated diseases. This review synthesizes clinical and molecular research on primary MPB disorders, highlighting the commonalities and differences in their pathogenesis. 1.Temporal degeneration of optic nerve fibers accompanied by cecocentral scotoma is a hallmark of maculopapillary bundle (MPB) degeneration. 2.Mechanisms of MPB degeneration commonly implicate mitochondrial dysfunction. 3.Recent research challenges the traditional belief that the MPB is uninvolved in glaucoma by showing degeneration in the early stages of this common optic neuropathy, yet with features distinct from other MPB-selective neuropathies. 4.Reactive oxygen species generation is a mechanism linking mitochondrial mechanisms of MPB-selective optic neuropathies, but in-vivo and in-vitro studies are needed to validate this hypothesis.

Toxic optic neuropathy due to methanol: About two cases

Toxic optic neuropathy due to methanol: About two cases

To study visual evoked potential in patients with optic nerve diseases

Background: To study Visual Evoked Potential in patients with Optic Nerve diseases. Study design and settings: Cross – Sectional study. Material and Methods: 72 patients were included in our study, aged 12 years and above, diagnosed as optic nerve diseases like optic neuritis, Nonarteritc ischemic optic neuropathy (NAION), hereditary, nutritional and compressive optic neuropathy etc. Flash and Pattern VEPs were used. VEP amplitude and latency were noted. Results: Out of total 144 eyes, 107 eyes were affected. Ethambutol induced Toxic optic neuropathy was the most common etiology, followed by secondary optic neuropathy, idiopathic, traumatic optic neuropathy, optic neuritis, NAION, compressive and post CRAO (Central Retinal Artery Occlusion) optic neuropathy. Mean latency of all affected eyes was 132±22.5 msec. mean amplitude of the all affected eyes was 6.36±2.1 microvolt. Latency was moderately delayed (110-140 msec) in 45.8%, while severely delayed (&gt;140 msec) in 40.3% of total eyes. Amplitude was reduced in 36.5% of total eyes. Prolonged latency with normal amplitude was found in most of the eyes with optic neuritis while latency was also prolonged in fellow eyes of optic neuritis. In case of NAION prolonged latency and reduced amplitude was found in all eyes. Conclusion: Flash or pattern VEP can be used as an important tool for diagnosis of optic neuropathies or revealing of recurrence of disease and for follow up. VEP can also be used to detect subclinical damage in the fellow eyes of optic neuritis and also useful in differentiating the optic neuritis from ischemic optic neuropathy.

Ocular toxicity of daily anti-tubercular treatment regimen: A prospective observational study

Context: India carries a significant burden of TB which is the commonest cause of infectious disease-related mortality. Anti-tubercular drugs can cause serious ocular toxic effects. Optical coherence tomography (OCT) can be used as a valuable tool in the quantitative analysis of anti-tubercular treatment (ATT)-induced toxic optic neuropathy. Aims: To study the changes in visual parameters in patients on ATT and to analyze the OCT changes in patients by taking measurements once before initiation of treatment and once during ongoing treatment (between three and six months). Settings and Design: Tertiary care center, Prospective observational study. Methods and Material: A prospective observational study was conducted in 140 eyes of 70 subjects undergoing ATT as per the latest RNTCP guidelines where the following determinants were examined, and the corresponding values were taken once before initiation of treatment and once during ongoing treatment (between three and six months) and results were analyzed. Around 90% of the subjects were examined at the end fourth month. Visual acuity was taken using the Log Mar chart, color vision using Ishihara’s chart, and slit lamp examination and fundus evaluation using a 90 D lens. OCT was done and average nasal, temporal, superior, and inferior quadrant retinal nerve fiber layer (RNFL) measurements were taken. Perimetry was also done; however, findings were not included in this study. Statistical Analysis Used: Frequency and percentage were applied to study the changes in visual parameters in patients on ATT. A paired t-test was applied for numerical variables to analyze the OCT changes in patients undergoing ATT. A P value &lt; 0.05 was considered statistically significant. Results: Despite a near-normal appearance of the fundus on ophthalmoscopy, OCT clearly demonstrated and quantified the loss of retinal nerve fibers. Statistically significant RNFL thinning (P value &lt; 0.001) was noted in the superior, temporal, and inferior quadrants and least in the nasal quadrant (P = 0.005). Significant deterioration in visual acuity was observed following three months of ATT (P = 0.001). Red-green color vision abnormalities were detected in 14 out of 140 eyes (10%). Conclusions: RNFL thickness was reduced on OCT. RNFL thickness quantification and assessment of other visual parameters especially color vision help in the early diagnosis of ocular toxic effects of ATT. Hence, awareness and active screening are imperative in preventing visual impairment and blindness.

Optic Neuropathy Secondary to Linezolid for Multidrug-resistant Mycobacterial Tuberculosis

Abstract&#x0D; Introduction : Toxic optic neuropathy is well known side effect of medications, including linezolid in patients with MDR-TB. We present 2 cases of patients with linezolid associated ON.&#x0D; Case Illustration : A 28 year pld man (case 1) and a 50 year old woman complained bilateral progressive visual loss after long term use of linezolid (both 8 months). On initial visit, case 1 presented with 0.1 visual acuity and case 2 presented with counting finger visual acuity. Both have hyperemic optic disc. OCT showed optic disc edema. Both patients showed generalized visual field defect on the Humphrey test. We immediately stopped the linezolid treatment.&#x0D; Discussion : The exact mechanism of linezolid induced ON is still unclear. It may be caused by impaired mitochondrial function for adenosine triphosphate (ATP) synthesis within retinal nerve fiber layer. Duration of linezolid therapy affects the prognosis for linezolid ON.&#x0D; Conclusion : Both Ophthalmologist and Physicians must be aware that visual function monitoring and early recognition of toxicity linezolid. Immediate cessation of linezolid has favorable visual recovery

HISTOLOGICAL FEATURES OF ETHAMBUTOL INDUCED MICE EYES: A PRE- EXPERIMENTAL STUDY ON TOXIC OPTIC NEUROPATHY CASE

Abstract&#x0D; Introduction &amp; Objectives : Toxic Optic Neuropathy (TON) is a visual disease caused by toxic substances damaging the optic nerve. It can be caused by inflammation, infection, or long-term drug use. Over 10% of ethambutol- treated optic neuropathy patients developed major complications. Cellular changes should be observed histologically. This study examines ethambutol-induced mice's eye histology in the fibrous, vasculous, nervous tunica, optical media, and optic nerve tissue.&#x0D; Methods : This pre-experimental study used 20 eyes of 10 white mice aged 1-2 weeks weighing 50-65 grams. Group 1 consisted of healthy mice without therapy and group 2 received 35 mg/kgBW/day of ethambutol for 60 days. (group 2). Hematoxylin eosin staining was used to observe binocular experimental animal eyes after enucleation. All measurements used Olympus® CX-20 microscope with 40x objective resolution.&#x0D; Results : The average thickness of the cornea was 72.238 ± 10.542 and 60.572 ± 10.25, while the sclera was 336.533±40.851 μm and 331.339±34.219 μm. In groups 1 and 2, no significant changes were foundin the cell layer morphology of both tissues (p &gt; 0.05). Iris, ciliary body, and choroid were observedin the tunica vasculosa. Groups 1 and 2 had eye and ciliary body lengths of 595.148±137.805 μm and 497.705±213.866 μm, respectively, and choroid thicknesses of 161.369±37.925 and 162.605±25.160 (p&gt;0.05). Group 1 had 402.268±55.666 μm retinal thickness in the tunica nervosa, while group 2 had 399.854±27.585 (p&gt;0.05).&#x0D; Conclusion : Ethambutol-induced and normal experimental animals had substantial histological differences in optic nerve thickness, but no significant difference in the other ocular structures.

DERAJAT APOPTOSIS SEL GANGLION RETINA PASCA PEMBERIAN TAMBAHAN EKSTRAK MORINGA OLEIFERA ORAL DIBANDINGKAN DENGAN TERAPI STANDAR Studi Eksperimental pada Tikus Wistar Model Methanol Toxic Optic Neuropathy

Abstract&#x0D; Introduction &amp; Objectives : Methanol toxic optic neuropathy can lead to retinal ganglion cell apoptosis which causes visual disturbance. Moringa oleifera has been reported to have an anti-inflamatorry effect that can prevent inflammatory mediators from being relased in methanol toxic optic neuropathy&#x0D; Methods : Twenty-one Wistar methanol toxic optic neuropathy were divided into 3 groups, namely base line group, control group that given intravenous methylprednisolone 4.5mg/6 hours for 3 days, and given standard theraphy and additional administration of oral Moringa oleifera 300mg/kgbodyweight/day for 4 weeks. Assessment of the degree of apoptosis by Anatomical Pathology with histopatolocigal scaoring. The study used Mann Whitney comparative hypothesis test (Significant p&lt;0.05)&#x0D; Results : The degree of retinal ganglion cell apoptosis was significantly lower in the treatment and standard therapy groups compared to the base line group. The treatment group compared to the standard therapy group was not significantly different (p = 1,000)&#x0D; Conclusion : The degree of retinal ganglion cell apoptosis in rat model methanol toxic optic neuropathy was not significantly different between the group that was given additional oral Moringa oleifera extract compared to the standard theraphy group

EFFECT OF MEMANTINE AS N-METHYL D-ASPARTATE RECEPTOR ANTAGONIST ON CASPASE-9 LEVEL OF RETINAL GANGLION CELL IN METHANOL TOXIC OPTIC NEUROPATHY RAT MODEL

Abstract&#x0D; Introduction &amp; Objectives : Methanol toxic optic neuropathy (MTON) remains as a health issue in developing countries and there are no current definitive treatments. Accumulation of formic acid as metabolite of methanol causes mitochondrial dysfunction that can reduce ATP synthesis rate, disrupt axoplasmic transport, and elevate the reactive oxygen species (ROS). All of these mechanisms lead to the death of retinal ganglion cell (RGC) and optic nerve. RGC destruction in MTON has similar patterns with those that have been observed in glaucoma, ischemia, and trauma cases, that is through excessive activation of glutamate neurotransmitter via N-Methyl D-Aspartate receptors (NMDAR). Memantine is a NMDAR antagonist that inhibit the ion channel of NMDAR. This inhibitory effect of NMDAR by memantine is expected to reduce intracellular calcium level, prevent apoptosis of RGC, and prevent further mitochondrial dysfunction. Caspase-9 is essential to eliminate cells by executing apoptotic Objective: To observe the effect of Memantine on Caspase-9 level of RGC in Methanol-Intoxicated Rats.&#x0D; Methods : This experimental study was performed on 28 Methanol-Intoxicated Rats that are assigned into four treatment groups: K1 (MTON;enucleated day-3), K2 (MTON+Memantine; enucleated day-3), K3 (MTON; enucleated day-7), and K4 (MTON+Memantine; enucleated day-7). During the experiment, all groups were exposed to N2O:O2 gas and were given methanol orally. Caspase-9 level of RGC were measured immediately after enucleation.&#x0D; Results : The average of Caspase-9 level (ng/ml): K1=197,88±33,98; K2=205,64±63,66; K3=243,15±40,13; K4=150,08±119,60. The Caspase-9 level was significantly lower in K4 compared to K3 (p value =0.038).&#x0D; Conclusion : Memantine decrease the level of Caspase-9 of RGC in Methanol Toxic Optic Neuropathy rat model.

An analysis of the etiology composition and clinical characteristics of bilateral optic disc swelling

Objective: To investigate the etiology composition and clinical characteristics of bilateral optic disc swelling(ODS). Methods: The medical records of all newly diagnosed bilateral ODS patients admitted to the neurology ward of Beijing Tongren Hospital from January 2017 to June 2021 were retrospectively searched to classify the etiology, obtain demographic and clinical information, and compare the differences in clinical characteristics. Results: A total of 131 patients with bilateral ODS were included, including 56 males and 75 females, aged 15-73 (39±14) years. The most common cause of the bilateral ODS was increased intracranial pressure (ICP)(56/131, 42.7%), followed by optic neuritis (ON)(40/131, 30.5%). Other causes included vascular optic neuropathy (13/131, 9.9%), pseudopilledema (9/131, 6.9%); uveitis (6/131, 4.6%), toxic optic neuropathy (3/131, 2.3%) and unknown causes (4/131, 3.1%). Idiopathic intracranial hypertension (IIH) (43/56, 76.8%) was the most common etiology for papilledema. In the comparison of the two main causes of intracranial hypertension and the clinical characteristics of ON in ODS, there was no statistically significant difference in the incidence of age, gender, complaints of ocular pain or headache, and hemorrhage of optic disc(P>0.05). Visual acuity abnormalities and low vision were more common in ON group than the increased ICP group[36/40(90%) vs 33/56(58.9%), P=0.001; 35/80(43.8%) vs 22/112(19.6%), P<0.001], while severe papilledema was more common in increased ICP group[38/112(33.9%)vs 9/80(11.3%), P<0.001]. Conclusions: The most common cause for bilateral ODS is increased ICP, but it can also be triggered by a variety of other causes. Optic neuritis(ON) is the most important differentiating disease in the study of Chinese patients.

Clinical profile and incidence of toxic optic neuropathy (TON) in patients receiving anti tuberculous therapy: A prospective study

Clinical profile and incidence of toxic optic neuropathy (TON) in patients receiving anti tuberculous therapy: A prospective study

Impacts of climate change on ocular health: A scoping review

Climate change represents a significant global health crisis, characterized by a complex interplay of environmental shifts and interconnected phenomena. These alterations have given rise to a multitude of health implications, notably impacting ocular health. Our comprehensive review delineates a spectrum of eye conditions associated with climate change-related variables. Extremes in temperature and weather events have been observed to affect the ocular surface, resulting in an increased incidence of conjunctivitis, keratitis, dry eye disease, and pterygium. Furthermore, climate change is linked to a rising occurrence of cataracts, glaucoma, periocular tumors, and infections. Prolonged food insecurity, stemming from droughts, has been associated with nutritional optic neuropathies and consequent vision loss. Elevated temperatures have also been correlated with a heightened risk of retinal detachments necessitating urgent surgical intervention to enhance prognostic outcomes.This review also outlines the influence of climate-warming pollutants on a diverse array of eye conditions, manifesting as ocular surface infections, degenerative changes like pterygium, cataracts, refractive errors (myopia), blepharitis, meibomian gland infections, glaucoma, and vascular retinal occlusions.Mitigating the effects of climate change is an urgent global imperative necessitating collaborative efforts, encompassing research and education, to devise sustainable solutions that safeguard human health and well-being. This review seeks to delineate the current extent of available research, identify gaps in the existing literature, and chart the course for future studies in this intriguing association.