Toxic Optic Neuropathy Research Articles

Optic Neuropathy Related to Hydrogen Peroxide Inhalation

Optic neuropathy related to toxins is a complex, multifactorial disease potentially affecting individuals of all ages. We report a case of presumed toxic optic neuropathy secondary to H2O2 exposure. This has not been previously reported, and the temporal relationship of the exposure to the optic neuropathy is compelling, although not definite, evidence of a causal relationship.

Myopathy with Ezetimibe Monotherapy; Statin-Associated Pancreatitis; Linezolid Associated Toxic Optic Neuropathy; Hiccups and Dopamine Agonists; SIADH and Seizures in a Patient Treated with Duloxetine; Prevention of a Well-Known Adverse Drug Reaction

The purpose of this feature is to heighten awareness of specific adverse drug reactions (ADRs), discuss methods of prevention, and promote reporting of ADRs to the FDA's medWatch program (800-FDA-1088). If you have reported an interesting preventable ADR to medWatch, please consider sharing the account with our readers.

Ethambutol-associated Optic Neuropathy

Ethambutol is used in the treatment of tuberculosis, which is still prevalent in Southeast Asia, and can be associated with permanent visual loss. We report 3 cases which presented with bitemporal hemianopia. Three patients with ethambutol-associated toxic optic neuropathy are described. All 3 patients had loss of central visual acuity, colour vision (Ishihara) and visual field. The visual field loss had a bitemporal flavour, suggesting involvement of the optic chiasm. Despite stopping ethambutol on diagnosis, visual function continued to deteriorate for a few months. Subsequent improvement was mild in 2 cases. In the third case, visual acuity and colour vision normalised but the optic discs were pale. All 3 patients had some permanent loss of visual function. Ethambutol usage is associated with permanent visual loss and should be avoided if possible or used with caution and proper ophthalmological follow-up. The author postulates that in cases of ethambutol associated chiasmopathy, ethambutol may initially affect the optic nerves and subsequently progress to involve the optic chiasm.

Corneal honeybee sting

Background: We report the complications and management of a retained bee sting injury to the cornea.The case highlights the acute and chronic management of an uncommon injury and its pathogenesis. Methods: A 67-year-old man was attacked by a swarm of bees and was referred for severe Chemosis on the right eye. A retained corneal bee stinger (ovipositor) was seen but removal was only partially successful. He subsequently developed a large corneal epithelial defect, anterior uveitis, intractable glaucoma, traumatic cataract, toxic optic neuropathy, and corneal scarring.We reviewed the literature on corneal bee sting injuries and their complications. Results: Inflammation was controlled with topical steroids and the patient underwent a combined phacoemulsification and trabeculectomy with mitomycin-C for uncontrolled glaucoma. However, optic neuropathy did not resolve. Interpretation: Corneal bee sting injuries are uncommon but can result in severe sight-threatening complications such as toxic optic neuropathy. Early recognition of the possible complications and appropriate treatment may help to prevent permanent loss of vision. Removal of a retained corneal bee stinger remains controversial.

Optic neuropathy associated with linezolid treatment

Two patients undergoing long-term treatment with linezolid for pneumonia had decreased visual acuity, dyschromatopsia, and cecocentral scotomas characteristic of toxic optic neuropathy. Visual function slowly recovered 3 to 4 months after discontinuation of the antibiotic treatment in both patients. Toxic optic neuropathy may occur from linezolid. Early withdrawal of the antibiotic may be associated with visual recovery.

Optic Neuropathy Associated With Linezolid Treatment

Two patients undergoing long-term treatment with linezolid for pneumonia had decreased visual acuity, dyschromatopsia, and cecocentral scotomas characteristic of toxic optic neuropathy. Visual function slowly recovered 3 to 4 months after discontinuation of the antibiotic treatment in both patients. Toxic optic neuropathy may occur from linezolid. Early withdrawal of the antibiotic may be associated with visual recovery.

Mecanismos de expresión proteica en el nervio óptico de la rata: Modificaciones por exposición al alcohol

Previous work from our group demonstrated that regular high consumption of ethanol during pregnancy induces a delay in growth and structural changes in the developing eye and vision (Pinazo-Duran et al., Teratology '93; Eur J Ophthalmol '97; Stromland and Pinazo-Duran, Teratology '94; Alcohol Alcoholism '02). Our main goal is to study at a cellular and molecular level, whether or not the prenatal alcohol exposure may change the development of the glial cells and inducing the optic nerve dysmorphogenesis. We have used key protein markers to analyse the expression in the rat optic nerve throughout the pre- and postnatal periods. To better understanding the actions of ethanol on optic nerve development in alcohol-induced and control dams, these were fed a liquid diet during gestation and lactation, containing either ethanol (5% w/, 35% of the daily food intake) or isocaloric carobydrates (35% of the daily food intake). Eyes were enucleated and processed to immunocytochemical and morphological tecnhiques and western blot approaches, using antibodies against the glial fibrillary acidid protein (GFAP), neurofilament protein (NFP) and myelin basic protein (MBP). Three main observations were made in the ethanol-exposed and control groups: 1) the optic nerve size was significantly lower in the ethanol group than in the control group, 2) there were statistically significant changes in optic nerve astrocytes and oligodendrocytes, optic axons and myelin sheaths and 3) a delay and altered expression of developmental proteins. All data support our earlier studies confirming the deleterious effects of ethanol on the developing visual system. We suggest that ethanol may alter the expression of precise genes involved in eye development and posterior remodelling. These results can be extrapolated to clinical advances in fetal alcohol syndrome and toxic optic neuropathies.

Optical coherence tomography can measure axonal loss in patients with ethambutol-induced optic neuropathy

To map and identify the pattern, in vivo, of axonal degeneration in ethambutol-induced optic neuropathy using optical coherence tomography (OCT). Ethambutol is an antimycobacterial agent often used to treat tuberculosis. A serious complication of ethambutol is an optic neuropathy that impairs visual acuity, contrast sensitivity, and color vision. However, early on, when the toxic optic neuropathy is mild and partly reversible, the funduscopic findings are often subtle and easy to miss. Three subjects with a history of ethambutol (EMB)-induced optic neuropathy of short-, intermediate-, and long-term visual deficits were administered a full neuro-ophthalmologic examination including visual acuity, color vision, contrast sensitivity, and fundus examination. In addition, OCT (OCT 3000, Humphrey-Zeiss, Dublin, CA) was performed on both eyes of each subject using the retinal nerve fiber layer (RNFL) analysis protocol. OCT interpolates data from 100 points around the optic nerve to effectively map out the RNFL. The results were compared to the calculated average RNFL of normal eyes accumulated from four prior studies using OCT, n=661. In all subjects with history of EMB-induced optic neuropathy, there was a mean loss of 72% nerve fiber layer thickness in the temporal quadrant (patient A, with eventual recovery of visual acuity and fields, 58% loss; patient B, with intermediate visual deficits, 68% loss; patient C, with chronic visual deficits, 90% loss), with an average mean optic nerve thickness of 26+/-16 microm. There was a combined mean loss of 46% of fibers from the superior, inferior, and nasal quadrants in the (six) eyes of all three subjects (mean average thickness of 55+/-29 microm). In both sets (four) of eyes of the subjects with persistent visual deficits (patients B and C), there was an average loss of 79% of nerve fiber thickness in the temporal quadrant. The OCT results in these patients with EMB-induced optic neuropathy show considerable loss especially of the temporal fibers. This is consistent with prior histopathological studies that show predominant loss of parvo-cellular axons (or small-caliber axons) within the papillo-macular bundle in toxic or hereditary optic neuropathies. OCT can be a valuable tool in the quantitative analysis of optic neuropathies. Additionally, in terms of management of EMB-induced optic neuropathy, it is important to properly manage ethambutol dosing in patients with renal impairment and to achieve proper transition to a maintenance dose once an appropriate loading dose has been reached.

Optic neuropathies caused by toxins and adverse drug reactions.

Toxic optic neuropathy refers to the ingestion of a toxin or an adverse drug reaction that results in vision loss from optic nerve damage. Patients may present with bilateral sudden loss of vision in the setting of an acute intoxication or an insidious asymmetric loss of vision from an adverse drug reaction. Toxins and drugs associated with a toxic optic neuropathy may directly harm the optic nerve; however, some drugs are associated with an ischemic optic neuropathy or optic neuritis, in which optic nerve damage is an indirect effect of the causative agent. The most important aspect of treatment is recognition and drug withdrawal. Patients need to be appropriately counseled, particularly in the setting of amiodarone-associated optic neuropathy.

Linezolid-Associated Toxic Optic Neuropathy: A Report of 2 Cases

We describe 2 cases in which the prolonged use of linezolid to treat complicated methicillin-resistant Staphylococcus aureus infections was followed by acutely developed blurred vision and progressive loss of vision and color perception during the ensuing few weeks. Both patients received a diagnosis of toxic optic neuropathy, and linezolid therapy was stopped. The patients experienced an initial rapid partial improvement and a subsequent gradual, almost complete, recovery over many months.

Toxic optic neuropathy.

Toxic optic neuropathy is a complex, multifactorial disease potentially affecting individuals of all ages, races, places, and economic strata. Etiology includes nutritional, environmental, toxicologic, and genetic factors. Most cases of nutritional amblyopia are encountered in disadvantaged countries. However, toxic amblyopia related to drug treatment or alcohol abuse is also encountered in the Western world. Typically, toxic and nutritional optic neuropathy is progressive, with bilateral symmetrical painless visual loss causing central or cecocentral scotoma. There is no specific treatment for this disorder. Nevertheless, early detection and prompt management may ameliorate and even prevent severe visual deficit.

Best catch from NANOSNET.

Best catch from NANOSNET.

Metabolic optic neuropathies

Metabolic optic neuropathies form a rubric of disease characterized by bilaterally symmetrical visual impairment with loss of central visual acuity, dyschromatopsia, centrocecal visual field defects, temporal optic disc atrophy, and specific loss of the nerve fiber layer in the papillomacular bundle. The three subcategories of metabolic optic neuropathies are heredodegenerative (such as Leber's hereditary optic neuropathy), nutritional deficiencies (such as vitamins B12 or folic acid), or toxicities (such as ethambutol or cyanide). It's interesting to note that the first of these three is a congenital cause of mitochondrial impairment, whereas the latter two are acquired injuries to mitochondria. Hence, most if not all causes of metabolic optic neuropathies are, in fact, related to mitochondrial impairment. At the present time there is no effective treatment for heredodegenerative optic neuropathy. Nutritional deficiency metabolic optic neuropathies are treated by giving supplements of the appropriate nutrient or vitamin, whereas toxic metabolic optic neuropathies are treated by removing or preventing exposure to the toxin in question.

Optic nerve degeneration and mitochondrial dysfunction: genetic and acquired optic neuropathies

Selective degeneration of the smallest fibers (papillo-macular bundle) of the human optic nerve occurs in a large number of optic neuropathies characterized primarily by loss of central vision. The pathophysiology that underlies this peculiar pattern of cell involvement probably reflects different forms of genetic and acquired mitochondrial dysfunction. Maternally inherited Leber’s hereditary optic neuropathy (LHON), dominant optic atrophy (Kjer disease), the optic atrophy of Leigh’s syndrome, Friedreich ataxia and a variety of other conditions are examples of inherited mitochondrial disorders with different etiologies. Tobacco–alcohol amblyopia (TAA), the Cuban epidemic of optic neuropathy (CEON) and other dietary (Vitamins B, folate deficiencies) optic neuropathies, as well as toxic optic neuropathies such as due to chloramphenicol, ethambutol, or more rarely to carbon monoxide, methanol and cyanide are probably all related forms of acquired mitochondrial dysfunction. Biochemical and cellular studies in LHON point to a partial defect of respiratory chain function that may generate either an ATP synthesis defect and/or a chronic increase of oxidative stress. Histopathological studies in LHON cases and a rat model mimicking CEON revealed a selective loss of retinal ganglion cells (RGCs) and the corresponding axons, particularly in the temporal-central part of the optic nerve. Anatomical peculiarities of optic nerve axons, such as the asymmetric pattern of myelination, may have functional implications on energy dependence and distribution of mitochondrial populations in the different sections of the nerve. Histological evidence suggests impaired axonal transport of mitochondria in LHON and in the CEON-like rat model, indicating a possible common pathophysiology for this category of optic neuropathies. Histological evidence of myelin pathology in LHON also suggests a role for oxidative stress, possibly affecting the oligodendrocytes of the optic nerves.

Optic neuritis: historical aspects.

Optic nerve disorders were not reliably diagnosed until the late nineteenth century when ophthalmoscopy became part of the ophthalmic examination. By the early 1900's, all of the salient clinical features of optic neuritis and its relationship to "systemic sclerosis" were recognized, but there was much controversy and misunderstanding about its differential diagnosis, pathogenesis, and possible treatment. During the twentieth century, physicians began to distinguish optic neuritis from infectious, hereditary, toxic, nutritional, and ischemic optic neuropathies. The development of magnetic resonance imaging and the results from recent clinical trials have enhanced our understanding of the relationship between optic neuritis and multiple sclerosis. The next decade holds the promise of further elaborating the pathogenesis and treatment of optic neuritis.

Practice parameter: the role of corticosteroids in the management of acute monosymptomatic optic neuritis. Report of the Quality Standards Subcommittee of the American Academy of Neurology.

Optic neuritis (ON) is an inflammatory disorder of the optic nerve. Most cases are idiopathic or associated with MS. ON can be associated with a variety of systemic or ocular disorders and is the most common acute optic neuropathy in adults younger than 46 years. Among high-risk populations for MS, the incidence of ON is about 3 per 100,000 population per year, whereas in other areas the incidence is about 1 per 100,000 population per year.1-13 Acute ON often presents as an isolated clinical event without contributory systemic abnormalities (monosymptomatic ON). Clinical features include periocular pain, abnormal visual acuity and fields, reduced color vision, a relative afferent pupillary defect, and abnormal visual evoked potentials. The fundus may appear normal or demonstrate edema of the optic nerve head (papillitis).12-18 MRI white matter abnormalities identical to those seen in MS are found in 50 to 70% of monosymptomatic ON cases.19-22 The visual deficit of ON may worsen over 1 to 2 weeks and usually begins improving over the next month. Lack of improvement in visual function by 30 days is unusual.23 However, most patients have some residual visual function deficit, even if visual acuity improves to 20/20.1-18 Differential diagnosis includes compressive, ischemic, hereditary, toxic, or other inflammatory optic neuropathies (e.g., sarcoid). These conditions usually do not exhibit the same clinical pattern (table 1) or rate of recovery as monosymptomatic ON.1-13 View this table: Table 1. Features of acute demyelinating monosymptomatic optic neuritis Treatment of monosymptomatic ON has included oral, retrobulbar, and IV steroids, immunoglobulin, and acupuncture.23-77 Monosymptomatic acute ON is not rare and because the usefulness of oral prednisone in this disorder has recently been questioned,23,78-82 this practice parameter was developed to provide …

Statistics of optic neuropathy in Seoul Municipal Boramae Hospital in Korea

In order to investigate the causative mechanisms of optic neuropathy, retrospective clinical studies including ophthalmologic examination, imaging study, and molecular biologic analyses were performed on 435 patients with optic neuropathy. The causes of optic neuropathy included optic neuritis (92 patients, 21%), hereditary optic neuropathy (85 patients, 20%), traumatic optic neuropathy (59 patients, 14%), ischemic optic neuropathy (57 patients, 13%), compressive optic neuropathy (41 patients, 9%), and toxic optic neuropathy (38 patients, 9%). In 27 patients with bilateral optic atrophy and 26 patients with unilateral optic atrophy, the causative mechanisms remained unknown. In conclusion, optic neuritis and hereditary, traumatic, and ischemic optic neuropathies were the leading causes of optic neuropathy in this study. The importance of meticulous history taking and molecular biologic testing should be stressed in the differential diagnosis of optic neuropathy.

Chiasmopathy?

A 57-year-old man presented with progressive visual loss in both eyes, bitemporal field defect, and a history of poor nutrition, alcohol abuse, and excessive cigar smoking. Magnetic resonance imaging was normal. The visual acuity and field defect improved with supplementation with vitamins and reduction of alcohol and tobacco consumption. A diagnosis of toxic optic neuropathy was made. The authors discuss the differential diagnosis of bitemporal/pseudobitemporal field defects and the diagnosis and treatment of toxic optic neuropathy.

Toxic Optic Neuropathy After Concomitant Use of Melatonin, Zoloft, and a High-Protein Diet

Melatonin is a neuromodulating hormone found in the pineal gland and retina. It is involved in light-dark circadian rhythms and mediates retinal processes in a manner antagonistic to that of dopamine. Zoloft (sertraline) is an antidepressant drug that blocks the reuptake of serotonin at the neural synapse. Serotonin is the natural precursor of melatonin. A 42-year-old woman sought treatment for visual acuity loss, dyschromatopsia, and altered light adaptation. Neuro-ophthalmologic examination was otherwise normal except for evolving bilateral cecocentral scotomas. She had taken Zoloft for 4 years and began a high-protein diet with melatonin supplementation 2 weeks before onset of visual symptoms. Visual acuity and color vision improved within 2 months after melatonin and the high-protein diet were discontinued. Combined use of melatonin, Zoloft, and a high-protein diet may have resulted in melatonin/dopamine imbalance in the retina, manifesting as a toxic optic neuropathy. Physicians and patients should be alerted to this potential drug interaction.

Nutrition and the eye.

The topic "nutrition and the eye" cannot adequately be covered in a single review article; indeed, dozens of books and hundreds of articles have been written on the subject. This review concentrates on three areas in which specific nutrients are known or theorized to have a major impact on vision and the visual system: vitamin A deficiency; antioxidants and their proposed role in the prevention of age-related cataract and macular degeneration; and nutritional optic neuropathies, including those of the recent Cuban epidemic. In addition, this article touches on nutritional treatments that have been suggested for several less common eye diseases and, finally, considers several less prevalent conditions in which deficiency of or excess exposure to a particular nutrient has been associated with ocular pathology.