In developing countries like India, Linezolid is widely used for the treatment of Multi drug resistant tuberculosis (MDR-TB) and extensively drug resistant tuberculosis (XDR-TB). Long-term administration of Linezolid is reported to cause toxic optic neuropathy causing bilateral, progressive visual loss in patients. We report case details of three patients on anti-tubercular therapy presented to us with sudden, progressive, painless blurring of vision of both eyes the cause of which was confirmed to be toxic optic neuropathy due to linezolid. Subsequently, cessation of the drug resulted in complete visual recovery in two patients whereas one patient had minimal visual improvement due to secondary optic atrophy. Clinicians and health care workers need to be aware of sight threatening complications of Linezolid.

UNASSIGNED: This report details the characteristics of a case of bilateral optic neuropathy during treatment with oral lorlatinib for ALK-positive metastatic adenocarcinoma of the lung.
UNASSIGNED: A 57-year-old woman with metastatic adenocarcinoma of the lung receiving treatment with lorlatinib presented to the ophthalmology urgent care with bilateral loss of vision that had progressed to no light perception over the previous 2 weeks. She was hospitalized for an extensive autoimmune, infectious, neoplastic, and paraneoplastic workup, which revealed enhancement of both optic nerves extending up to the optic chiasm and an area of restricted diffusion in the splenium of the corpus callosum on MRI. Lorlatinib was discontinued by her oncologist and she received treatment with five days of pulse-dose intravenous solumedrol as well as five days of plasmapheresis with gradual improvement in her vision. In follow-up, her vision had improved to 20/40 and 20/30.
UNASSIGNED: There have been few reports describing vision loss associated with lorlatinib, an ALK/ROS1 targeted tyrosine kinase inhibitor used to treat metastatic lung adenocarcinoma. This report details the characteristics of a case of bilateral retrobulbar optic neuropathy as well as the treatment and recovery of such a case. Further exploration is needed in order to improve our understanding of the pathogenesis of this rare but potentially devastating adverse effect.

Amiodarone is a commonly used antiarrhythmic used to treat atrial fibrillation and ventricular tachycardias. While this agent can present with pulmonary, thyroid, and hepatic side effects, it can also, less commonly cause neurologic toxicity, particularly optic neuropathy. Optic neuropathy can manifest as acute vision loss. The management of amiodarone-associated optic neuropathy (AAON) includes early recognition of symptom manifestation so that the medication can be discontinued promptly. Here, we describe a case of a 64-year-old male who developed acute onset complete left-sided vision loss after initiation of amiodarone.

In the absence of evidence-based guidance on the impact of hydroxychloroquine (HCQ) blood concentration on efficacy and ocular toxicity in systemic lupus erythematosus (SLE), the clinical monitoring of HCQ blood concentration is not yet widely performed, which raised concerns about the necessity of conducting HCQ blood concentration monitoring. In this retrospective study, we consecutively enrolled 135 patients with SLE who received HCQ treatment for more than 6 months from July 2022 to December 2022. Ocular toxicity was evaluated by collecting relevant retinal parameters using optical coherence tomography angiography (OCTA). Therapeutic efficacy was evaluated using the SLE disease activity index (SLEDAI) and relevant clinical parameters. HCQ blood concentration was determined by high-performance liquid chromatography-tandem mass spectrometry (HPLC-MS/MS). Spearman correlation analysis revealed that the cumulative dose of HCQ was positively correlated with the foveal avascular zone (FAZ) perimeter and FAZ area (r = 0.734, P < 0.001; r = 0.784, P < 0.001). Meanwhile, the treatment duration of HCQ was positively correlated with FAZ perimeter and FAZ area (r = 0.761, P < 0.001; r = 0.882, P < 0.001). The univariate and multivariate logistic regression analyses indicated that HCQ blood concentration was associated with the disease activity of patients with SLE (odds ratio 0.994, 95% CI 0.990-0.999). HCQ blood concentration may be an important factor in assessing the therapeutic effectiveness of SLE patients. The HCQ-related ocular toxicity was a long-term effect related to long term exposure, rather than the blood concentration of HCQ at the time of testing. More importantly, when addressing HCQ-related ocular toxicity, it may be crucial to pay attention to the cumulative dose and treatment duration of HCQ.

We report the case of an early adolescent male on lamotrigine and levetiracetam therapy with a 1-month history of progressive, bilateral, painless visual loss which resolved on cessation of lamotrigine. To our knowledge, we present the first case of lamotrigine and levetiracetam dual therapy associated with toxic optic neuropathy, supported by electrophysiology and optical coherence tomography (OCT) changes. Electrophysiology findings were consistent with retinal ganglion cell dysfunction, with bilateral optic nerve involvement. Macula OCT showed mild retinal ganglion cell loss in all inner quadrants bilaterally. This case highlights the importance of asking patients with epilepsy treated with lamotrigine and levetiracetam about visual problems and considering early dose reduction or cessation of treatment.

Tuberculosis (TB) is a global health concern and central nervous system (CNS) TB leads to high mortality and morbidity. CNS TB can manifest as tubercular meningitis, tuberculoma, myelitis, and arachnoiditis. Neuro-ophthalmological involvement by TB can lead to permanent blindness, ocular nerve palsies and gaze restriction. Visual impairment is a dreaded complication of tubercular meningitis (TBM), which can result from visual pathway involvement at different levels with varying pathogenesis. Efferent pathway involvement includes cranial nerve palsies and disorders of gaze. The purpose of this review is to outline the various neuro-ophthalmological manifestations of TB along with a description of their unique pathogenesis and management. Optochiasmatic arachnoiditis and tuberculomas are the most common causes of vision loss followed by chronic papilloedema. Abducens nerve palsy is the most commonly seen ocular nerve palsy in TBM. Gaze palsies with deficits in saccades and pursuits can occur due to brainstem tuberculomas. Corticosteroids are the cornerstone in the management of paradoxical reactions, but other immunomodulators such as thalidomide and infliximab are being explored. Toxic optic neuropathy caused by ethambutol necessitates careful monitoring and immediate drug discontinuation. Cerebrospinal fluid diversion through ventriculo-peritoneal shunting may be required in patients with hydrocephalus in stage I and II of TBM to prevent visual impairment. Early diagnosis and prompt management are crucial to prevent permanent disability. Prevention strategies, public health initiatives, regular follow-up and timely intervention are essential in reducing the burden of CNS TB and its neuro-ophthalmological complications.

Various forms of cancer and chemotherapeutics are associated with optic neuropathy. Cisplatin is a platinum analogue chemotherapeutic commonly associated with ocular toxicity among many other serious adverse effects. Carboplatin is a more chemically stable platinum analogue that is generally better tolerated with a comparatively favorable side effect profile. There are very few reports of carboplatin precipitating optic neuropathy. This case report describes a rare occurrence of carboplatin-induced blinding optic neuropathy. We treated a patient receiving carboplatin for neuroendocrine bladder cancer who developed rapidly progressive bilateral optic neuropathy over the course of three days. Upon evaluation at our clinic, his visual acuity had declined to light perception only and 20/60 in his left and right eye, respectively. Carboplatin therapy was immediately held and steroids were initiated. Despite the intervention, the patient\'s visual deficits have not improved at the one-year follow-up. Although the mechanism by which carboplatin causes ocular toxicity remains speculative, arterial ischemia appears to be the likely mechanism given the irreversible nature of visual decline. As demonstrated by our patient\'s course, irreversible vision loss despite high-dose steroid intervention necessitates expeditious recognition and management of this rare adverse effect. ​​​​​.

OBJECTIVE: We aimed to investigate the visual recovery time in patients with ethambutol-induced toxic optic neuropathy (EON) and identify the factors associated with the visual recovery time.
METHODS: In this retrospective cohort study, we reviewed the medical records of 35 eyes from 35 patients with EON. Visual recovery was defined as a gain of three or more lines from the nadir.
RESULTS: Patients were observed following discontinuation of ethambutol (EMB), with the mean follow-up period of 21.0 ± 16.0 months. The visual acuity at nadir was logarithm of the minimum angle of resolution 1.4 ± 0.4, and the final visual acuity was logarithm of the minimum angle of resolution 0.6 ± 0.5. Twenty-seven eyes (77.1%) showed significant visual recovery. In Kaplan-Meier survival, the mean estimated time for visual recovery was 15.2 ± 3.0 months, and 50% of the patients experienced visual recovery at 8.3 ± 2.2 months following EMB discontinuation. Multivariate Cox regression analysis identified several significant risk factors for delayed visual recovery, including duration of EMB medication ≤6 months, period from symptom onset to EMB discontinuation >14 days, and baseline peripapillary retinal nerve fiber layer thickness >98 μm.
CONCLUSIONS: Our study indicated a mean time of visual recovery of 15 months for EON cases. Therefore, patients diagnosed with EON should be followed up for more than 1 to 2 years to evaluate their visual recovery. Delayed EMB discontinuation, short duration of EMB use, and initial peripapillary retinal nerve fiber layer thickening were associated with delayed visual recovery. Therefore, patients taking EMB should be followed up regularly for early detection of EON and immediate discontinuation of EMB to prevent severe damage to the optic nerve.

OBJECTIVE: To screen patients on ethambutol and evaluate its role on visual functions and toxic optic neuropathy.
METHODS: Retrospective, observational single tertiary centre cohort of 80 patients.
METHODS: A total of 69 from the initial 80 patients with visual complaints were categorised into two groups A and B; ongoing anti-tubercular therapy with ethambutol and having stopped ethambutol for greater than six months respectively. All patients underwent vision (V) testing on ETDRS chart and anterior and posterior segment evaluation. Additionally, patients in group A recorded color vision (CV) on Ishihara chart and visual evoked potential (VEP).
METHODS: P value was calculated using Chi square test (SPSS ver. 20).
RESULTS: Out of 69 patients in our study, 58 (84.05%) patients recorded reduced visual acuity. The mean visual acuity was 0.58 logMAR units. 33 out of our 58 (57%) patients with reduced visual acuity showed normal optic discs while 25 out of 58 (43%) showed altered optic discs. In group B, 14 out of 32 patients with vision of less than 20/20 also had optic disc pallor (p = 0.02). 12 out of 15 patients in group A recorded an altered color vision and also had a vision of less than 20/20 (p = 0.023). 15 patients who recorded altered VEP also had vision of less than 20/20 (p = 0.037).
CONCLUSIONS: Visual acuity, color vision and vep are sensitive and sustainable tools which can be implemented in regular screening. Ethambutol toxicity is a real problem and a collaborative approach is necessary to establish screening protocols and prevent ethambutol induced toxic optic neuropathy.

Anti-human epidermal growth factor receptor 2 (HER2) agents have exhibited pronounced tumor-inhibitory activity, yet the accompanying ocular toxicity has frequently been underestimated. We aim to conduct a comprehensive comparative analysis of ocular toxicity risk related to various anti-HER2 agents. We executed a retrospective pharmacovigilance investigation based on the FDA Adverse Event Reporting System (FAERS) database, covering the period from Q2 2018 to Q1 2023. The disproportionality analysis was performed to assess ocular toxicity risk. Multivariate logistic regression was implemented to mitigate potential biases. Moreover, the time to onset of ocular toxicity was also evaluated. A total of 3467 ocular adverse event (AE) reports concerning anti-HER2 agents were collected. At the preferred term (PT) level, there were 69 positive signals, among which excessive eye blinking, abnormal sensation in the eye, and asthenopia presented a significant risk. In comparison to tyrosine kinase inhibitors (TKIs), antibody drugs were associated with a broader range of ocular disorders at Standardized MedDRA Queries (SMQ)levels, including conjunctival disorders, corneal disorders, ocular infections, ocular motility disorders, optic nerve disorders, and retinal disorders. In terms of onset time, pertuzumab displayed an earlier onset at 21.5 days, while trastuzumab deruxtecan had the latest at 91.5 days. In summary, our study reveals varying degrees of ocular toxicity related to anti-HER2 agents, with a significantly higher risk observed in antibody drugs. Additionally, novel ocular toxicity signals, not documented in product labels, have been detected. In the future, further research will be necessary to validate our findings.