{"title":"Visual Loss in Neuro-Ophthalmology","authors":"E. Rath","doi":"10.5772/INTECHOPEN.80682","DOIUrl":null,"url":null,"abstract":"Optic neuropathy is damage to the optic nerve from any cause. Damage and death of these nerve cells lead to characteristic features of optic neuropathy. The main symptom is loss of vision (visual acuity and visual field damages), with colors appearing subtly washed out in the affected eye. The diagnosis is made on clinical examination. The history often points to the possible etiology of the optic neuropathy. In most of the cases, one eye is affected but it could be both. A rapid onset is typical of demyelinating, inflammatory, ischemic, and traumatic causes. A gradual course points to compressive, toxic/nutritional, and hereditary causes. The classic clinical signs of optic neuropathy are visual acuity and field defects, dyschromatopsia, and abnormal pupillary response. There are ancillary investigations that can support the diagnosis of optic neuropathy. Visual field testing, neuroimaging of the brain and orbit are essential in many optic neuropathies including demyelinating and compressive. In the last decade, increase of use new technology for optic neuropathies evaluation including multifocal visual evoked potentials and optic coherence tomography. Long standing of optic neuropathy is described by pale optic disk or optic atrophy, which means damage and death of these nerve cells or neurons. regimen versus 17% of patients in the placebo group. This benefit of treatment was seen only in patients who had abnormal brain MRI at the time of onset of the optic neuritis. The protective effect was short and by 3 years after optic neuritis groups treated with ONTT IV regimen versus placebo groups had equal incidence to develop MS. These findings suggest that a patient with acute optic neuritis who has an abnormal brain MRI may benefit in the short term (2 years) from treatment with the IV/oral steroid regimen.","PeriodicalId":259772,"journal":{"name":"Causes and Coping with Visual Impairment and Blindness","volume":"1 1","pages":"0"},"PeriodicalIF":0.0000,"publicationDate":"2018-09-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Causes and Coping with Visual Impairment and Blindness","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.5772/INTECHOPEN.80682","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 0
Abstract
Optic neuropathy is damage to the optic nerve from any cause. Damage and death of these nerve cells lead to characteristic features of optic neuropathy. The main symptom is loss of vision (visual acuity and visual field damages), with colors appearing subtly washed out in the affected eye. The diagnosis is made on clinical examination. The history often points to the possible etiology of the optic neuropathy. In most of the cases, one eye is affected but it could be both. A rapid onset is typical of demyelinating, inflammatory, ischemic, and traumatic causes. A gradual course points to compressive, toxic/nutritional, and hereditary causes. The classic clinical signs of optic neuropathy are visual acuity and field defects, dyschromatopsia, and abnormal pupillary response. There are ancillary investigations that can support the diagnosis of optic neuropathy. Visual field testing, neuroimaging of the brain and orbit are essential in many optic neuropathies including demyelinating and compressive. In the last decade, increase of use new technology for optic neuropathies evaluation including multifocal visual evoked potentials and optic coherence tomography. Long standing of optic neuropathy is described by pale optic disk or optic atrophy, which means damage and death of these nerve cells or neurons. regimen versus 17% of patients in the placebo group. This benefit of treatment was seen only in patients who had abnormal brain MRI at the time of onset of the optic neuritis. The protective effect was short and by 3 years after optic neuritis groups treated with ONTT IV regimen versus placebo groups had equal incidence to develop MS. These findings suggest that a patient with acute optic neuritis who has an abnormal brain MRI may benefit in the short term (2 years) from treatment with the IV/oral steroid regimen.