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At least 19 recordsLinked to original sources
PubMed1998

The predictive value of CSF oligoclonal banding for MS 5 years after optic neuritis. Optic Neuritis Study Group.

The predictive value of CSF oligoclonal banding for the development of clinically definite MS (CDMS) within 5 years after optic neuritis was assessed in 76 patients enrolled in the Optic Neuritis Treatment Trial. The presence of oligoclonal bands was associated with the development of CDMS (p = 0.02). However, the results suggest that CSF analysis is only useful in the risk assessment of optic neuritis patients when brain MRI is normal and is not of predictive value when brain MRI lesions are present at the time of optic neuritis.

Adolescent↗
PubMed1990

Corticosteroid therapy in optic neuritis (optic neuropathy).

Corticosteroid treatment of acute idiopathic optic neuritis is still highly controversial. Controlled studies have indicated that visual acuity has been restored more rapidly after corticoid treatment. Long-term results however do not differ with the untreated control group. Corticoids are essential in the treatment of ischemic optic neuropathy, especially when occurring with auto-immune diseases or giant cell arteritis. Some authors believe that corticoids can be helpful during the acute phase of an idiopathic anterior ischemic optic neuropathy.

Adrenal Cortex Hormones↗
PubMed1992

A randomized, controlled trial of corticosteroids in the treatment of acute optic neuritis. The Optic Neuritis Study Group.

BACKGROUND AND METHODS: The use of corticosteroids to treat optic neuritis is controversial. At 15 clinical centers, we randomly assigned 457 patients with acute optic neuritis to receive oral prednisone (1 mg per kilogram of body weight per day) for 14 days; intravenous methylprednisolone (1 g per day) for 3 days, followed by oral prednisone (1 mg per kilogram per day) for 11 days; or oral placebo for 14 days. Visual function was assessed over a six-month follow-up period. RESULTS: Visual function recovered faster in the group receiving intravenous methylprednisolone than in the placebo group; this was particularly true for the reversal of visual-field defects (P = 0.0001). Although the differences between the groups decreased with time, at six months the group that received intravenous methylprednisolone still had slightly better visual fields (P = 0.054), contrast sensitivity (P = 0.026), and color vision (P = 0.033) but not better visual acuity (P = 0.66). The outcome in the oral-prednisone group did not differ from that in the placebo group. In addition, the rate of new episodes of optic neuritis in either eye was higher in the group receiving oral prednisone, but not the group receiving intravenous methylprednisolone, than in the placebo group (relative risk for oral prednisone vs. placebo, 1.79; 95 percent confidence interval, 1.08 to 2.95). CONCLUSIONS: Intravenous methylprednisolone followed by oral prednisone speeds the recovery of visual loss due to optic neuritis and results in slightly better vision at six months. Oral prednisone alone, as prescribed in this study, is an ineffective treatment and increases the risk of new episodes of optic neuritis.

Acute Disease↗
PubMed2005

The optic nerve sheath on MRI in acute optic neuritis.

Optic nerve sheath dilatation or gadolinium-enhancement on magnetic resonance imaging in acute optic neuritis have been previously reported but have been thought to be rare occurrences. This study recruited 33 patients with acute unilateral optic neuritis. All had their optic nerves imaged with fat-saturated fast spin-echo (FSE) imaging, and 28 had imaging before and after triple-dose gadolinium-enhanced fat-saturated T(1)-weighted imaging. Follow-up imaging was performed on 20 patients (15 following gadolinium). A dilated subarachnoid space at the anterior end of the symptomatic optic nerve on FSE imaging was seen in 15/33 cases. In three of these cases, dilatation was visible on short-term follow-up. Optic nerve sheath enhancement was seen in 21/28 cases acutely: seven at the anterior end of the lesion only, five at the posterior end only and nine at both ends. Optic sheath enhancement was seen in 13 patients on follow-up. This study suggests that optic nerve sheath dilatation on FSE images and optic nerve sheath enhancement on triple-dose gadolinium-enhanced images are common findings in acute optic neuritis. Optic nerve sheath dilatation may be due to inflammation of the optic nerve, with its associated swelling, interrupting the communication between the subarachnoid space of the diseased optic nerve and the chiasmal cistern. Optic nerve sheath enhancement suggests that meningeal inflammation occurs in optic neuritis, in agreement with pathological studies of both optic neuritis and multiple sclerosis.

Acute Disease↗
PubMed2006

The natural history of optic neuritis.

Optic neuritis is a common cause of visual loss in young patients, typically presenting with painful monocular visual loss and decreased color vision. Visual function generally spontaneously improves over weeks, and 95% of patients return to visual acuity of at least 20/40 within 12 months. The initial magnetic resonance imaging (MRI) helps stratify the risk of multiple sclerosis (MS) in patients with acute isolated optic neuritis. In the Optic Neuritis Treatment Trial, the 10-year risk of MS in the group of patients with at least one MRI T2 lesion was 56%, whereas the 10-year risk with a normal baseline MRI was 22%. A normal MRI in concert with painless optic neuritis, severe optic nerve head edema, peripapillary hemorrhages, or a macular star defines a very low MS risk subgroup. High-dose steroids hasten the rate, but not the final extent, of visual recovery in optic neuritis, and the decision to use this therapy is individualized. Interferon beta-1a therapy should be considered in selected high-risk patients.

Disease Progression↗
PubMed2000

Ophthalmology update for primary practitioners. Part I. Update on optic neuritis.

Optic neuritis is a common cause of acute visual loss. It is typified by sudden onset of visual impairment and pain with eye movements, followed by spontaneous recovery of vision over several months. Pathologically, optic neuritis is an acute demyelinating event affecting the optic nerve. Objective physical findings are typically few, including an afferent pupillary defect or Marcus-Gunn pupil, whereas subjective psychophysical findings abound (ie, diminished central visual acuity, color vision, decreased contrast sensitivity, and visual field abnormalities). These characteristics have made the diagnosis of optic neuritis based solely on clinical grounds disquieting to practitioner and patient alike. In addition, the fact that optic neuritis is often associated with multiple sclerosis as the first clinical manifestation of disease gives further reason for both patient and physician anxiety. The serious nature of visual loss and the consequences of making the diagnosis of optic neuritis has given rise to extensive testing and expensive treatments. This review is intended to explore our current state of knowledge with regard to (1) clinical presentation, (2) ancillary testing, (3) therapeutic intervention, and (4) associated disease, specifically the risk for multiple sclerosis in the patient who presents with an acute optic neuritis. Finally, a suggestion guide for informing the patient and addressing his or her concerns will be presented.

Humans↗
PubMed1996

Optic neuritis.

Optic neuritis is an acute inflammation of the optic nerve. It is a common manifestation of multiple sclerosis; it may be the initial expression or occur later in the course of the disease. Approximately 15-20% of cases of definite multiple sclerosis present with optic neuritis; another 40% will suffer an attack at some point. When optic neuritis occurs without antecedent signs of multiple sclerosis, magnetic resonance imaging (MRI) of the brain frequently reveals characteristic signal abnormalities of white matter, and analysis of cerebrospinal fluid often shows oligoclonal bands. Optic neuritis has been considered a forme fruste of multiple sclerosis.

Adrenal Cortex Hormones↗
PubMed1999

mtDNA haplogroup J: a contributing factor of optic neuritis.

Optic neuritis frequently occurs in multiple sclerosis (MS), and shares several similarities with the optic neuritis of Leber's hereditary optic neuropathy (LHON), which is mainly due to maternally transmitted mitochondrial DNA (mtDNA) mutations. Our report shows for the first time that a mitochondrial DNA background could influence the clinical expression of MS. One European mtDNA haplogroup was found only in MS patients with optic neuritis but not in MS patients without visual symptoms. Therefore, we hypothesize that mtDNA haplogroup J might constitute a risk factor for optic neuritis occurrence when it is coincidentally associated with MS, but not be a risk factor for developing MS per se as suggested previously.

Alleles↗
PubMed1997

Visual function 5 years after optic neuritis: experience of the Optic Neuritis Treatment Trial. The Optic Neuritis Study Group.

OBJECTIVE: To assess the 5-year visual course, including the incidence of recurrent optic neuritis, in 454 patients enrolled in the Optic Neuritis Treatment Trial. METHODS: Five-year follow-up vision testing, which included measures of visual acuity, contrast sensitivity, visual field, and color vision, was completed for 397 (87%) of the 454 patients. RESULTS: Visual function test results in the eyes that experienced optic neuritis at study enrollment (affected eyes) were normal or only slightly abnormal after 5 years in most patients; the results did not significantly differ by treatment group (P=.37 for visual acuity). The visual acuity in the affected eyes was 20/25 or better in 87%, 20/25 to 20/40 in 7%, 20/50 to 20/190 in 3%, and 20/200 or worse in 3%. The recurrence of optic neuritis in either eye occurred in 28% of the patients and was more frequent in patients with multiple sclerosis (P=.001) and in patients without multiple sclerosis who were in the prednisone treatment group (P=.004). Most eyes with a recurrence retained normal or almost normal visual function. CONCLUSIONS: Most patients retained good to excellent vision in the 5 years following an attack of optic neuritis, even if the optic neuritis recurred. Recurrences were more frequent in patients with multiple sclerosis and in those treated with oral prednisone alone. The completion of the 5-year follow-up by the Optic Neuritis Treatment Trial cohort has not altered our management recommendations based on the results we reported earlier.

Administration, Oral↗
PubMed1991

The clinical profile of optic neuritis. Experience of the Optic Neuritis Treatment Trial. Optic Neuritis Study Group.

The baseline characteristics of 448 eligible patients entered into the Optic Neuritis Treatment Trial are described in an effort to summarize the clinical profile of acute optic neuritis. A total of 77.2% of the patients were women. Mean age was 31.8 years. Pain accompanied the visual loss in 92.2% of cases. The optic disc appeared swollen in 35.3% of the patients and normal in 64.7%. A wide variety of visual field defects were present. Abnormalities in asymptomatic fellow eyes were noted, particularly on perimetry. Magnetic resonance imaging showed changes consistent with demyelination of the brain in 48.7% of the patients. Magnetic resonance imaging, serologic studies (such as the antinuclear antibody test and the fluorescent treponemal antibody absorption test), chest roentgenography, and lumbar puncture were of limited utility in defining a cause for visual loss other than optic neuritis associated with demyelinative disease.

Adolescent↗
PubMedDate not supplied

Chemical shift selective magnetic resonance imaging of the optic nerve in patients with acute optic neuritis.

Optic neuritis is often the first manifestation of multiple sclerosis (MS). Sixteen patients with acute optic neuritis and one patient with benign intracranial hypertension (BIH) were investigated by magnetic resonance imaging, using a chemical shift selective double spin echo sequence. In 3 of the 16 patients, abnormalities were seen. In one patient with bilateral symptoms, signal hyperintensity and swelling of the right side of the chiasm were found. In another patient the optic nerve was found diffusely enlarged with only a marginally increased signal in the second echo. In the third patient an area of signal hyperintensity and swelling was seen in the left optic nerve. In the patient with BIH the subarachnoid space which surrounds the optic nerves was enlarged. Even using this refined pulse sequence, avoiding the major artefact in imaging the optic nerve, the chemical shift artefact, lesions were only shown in 3/16 (19%) of the patients with optic neuritis. Nevertheless, the presented chemical shift selective double spin echo sequence may be of great value for detection of retrobulbar lesions.

Acute Disease↗
PubMed2002

Management of acute optic neuritis.

Optic neuritis is a common condition that causes reversible loss of vision. It can be clinically isolated or can arise as one of the manifestations of multiple sclerosis. Occasional cases are due to other causes, and in these instances management can differ radically. The treatment of optic neuritis has been investigated in several trials, the results of which have shown that corticosteroids speed up the recovery of vision without affecting the final visual outcome. Other aspects of management, however, are controversial, and there is uncertainty about when to investigate and when to treat the condition. Here we review the diagnostic features of optic neuritis, its differential diagnosis, and give practical guidance about management of patients. The condition's association with multiple sclerosis will be considered in the light of studies that define the risk for development of multiple sclerosis and with respect to results of trials of disease-modifying drugs in these individuals.

Adrenal Cortex Hormones↗
PubMed1991

Optic neuritis.

Optic neuritis can be mimicked by ophthalmologic, neurosurgical, and other conditions. In many if not all cases, optic neuritis may be a manifestation of multiple sclerosis. An ongoing treatment trial may provide answers about whether or not treatment improves outcome.

Adrenal Cortex Hormones↗
PubMed1975

The neuroradiologic evaluation of "optic neuritis".

Optic neuritis, even when clinically typical, cannot be diagnosed with certainty because mass lesions compressing the anterior visual pathways may mimic it. The radiologist is in a position to assist in identifying such lesions or in ruling them out and thus preventing surgical exploration. While every patient in whom the diagnosis of optic neuritis is entertained should have plain roentgenograms of skull, orbits and optic canals, we have developed a schema for detailed neuroradiologic investigation based on clinical and plain roentgenographic findings. A classification of such lesions by location is illustrated.

Adolescent↗
PubMed2004

[Treatment of optic neuritis].

Optic neuritis manifests itself as a reversible loss of vision. It can be a clinically isolated incident or one of the (first) manifestations of multiple sclerosis (MS). Its differential diagnosis is extensive, and management of other disorders can differ radically. In a typical case, treatment with corticosteroids hastens recovery of vision but does not affect the eventual degree of recovery. There is a substantial risk of developing MS after isolated optic neuritis (approximately 50% within 20 years), especially if asymptomatic white matter lesions are found on MRI scanning of the brain. Intravenous treatment with methylprednisolone may delay the onset of MS somewhat, but after three years the benefit of this treatment is lost. Treatment with interferon beta-Ia in high-risk patients also slows down the progression to clinically definite MS, but the long-term benefits are uncertain. MR imaging of the brain has implications for prognosis but not for treatment.

Brain↗
PubMed1978

Visual-evoked response differentiation of ischemic optic neuritis from the optic neuritis of multiple sclerosis.

Fifteen patients with ischemic optic neuritis studied electrophysiologically had a characteristic change of marked reduction in the amplitude of the visual-evoked response even when loss of vision was moderate. The optic neuritis of multiple sclerosis rarely produced this change. Occasionally, small increases in the latent period of the visual-evoked response were recorded from the patients with ischemic optic neuritis. The optic neuritis of multiple sclerosis usually produced significant increases in the latent period. When the normal nerve was tested in patients with ischemic optic neuritis, the visual evoked response was normal. In patients with optic neuritis of multiple sclerosis, stimulation of the "normal" nerve usually produced an increase in the latent period similar to that seen when the involved nerve was stimulated.

Aged↗
PubMed1993

Baseline visual field profile of optic neuritis. The experience of the optic neuritis treatment trial. Optic Neuritis Study Group.

The purpose of the present study was to determine the baseline visual field characteristics in 448 patients with acute optic neuritis who were entered into the Optic Neuritis Treatment Trial. The severity and pattern of visual field loss in both the affected and fellow eyes were classified. For affected eyes, diffuse visual field loss was present in 48.2% of eyes, central or centrocecal scotoma was present in 8.3% of eyes, altitudinal or other nerve-fiber bundle-type defects were present in 20.1% of eyes, and a variety of other defects were present in 23.4% of eyes. Visual field involvement was present in the fellow eye at baseline in 308 (68.8%) of the 448 patients. Evidence of a chiasmal or retrochiasmal visual field defect was present in 2.9% of the patients. Since a wide variety of visual field defects can occur with an acute attack of optic neuritis, the pattern of visual field loss is of limited utility in distinguishing optic neuritis from ischemic optic neuropathy and other optic nerve disorders. Asymptomatic visual field defects in the fellow eye are common.

Acute Disease↗