Original Article
A Randomized, Controlled Trial of Corticosteroids in the Treatment of Acute Optic Neuritis
N Engl J Med 1992; 326:581-588February 27, 1992
- Abstract
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. (N Engl J Med 1992; 326:581–8.)
Article Activity
- Article
OPTIC NEURITIS is an acute demyelinating disease of the optic nerve. It may occur in a patient with confirmed multiple sclerosis or as an isolated neurologic finding, in which case it may represent a forme fruste of multiple sclerosis.1 The typical clinical profile consists of sudden loss of vision, which can vary in severity from a slight deficit in the field of vision to complete loss of light perception, followed by spontaneous improvement over several months. Most patients have lasting symptoms of visual impairment, and even when visual acuity returns to normal, abnormalities are common in other aspects of visual function, such as the visual field, color vision, and contrast sensitivity.2 , 3
The efficacy of corticosteroids and corticotropin as treatments for optic neuritis has been debated since these drugs were introduced into clinical practice in the 1950s. Numerous anecdotal reports have suggested that they are effective, but randomized trials have not demonstrated a benefit. Three randomized trials of corticotropin4 5 6 7 and one of retrobulbar triamcinolone8 have been inconclusive primarily because of their small samples of patients. Neither oral nor intravenous corticosteroids have been evaluated in randomized trials. In the past decade, case reports have suggested that intravenous corticosteroids hasten recovery from optic neuritis.9
Despite the paucity of evidence about the efficacy of corticosteroids and their potential for causing adverse reactions, many ophthalmologists and neurologists prescribe them as treatment for optic neuritis. In 1986 a mail survey of ophthalmologists and neurologists in Michigan and Florida indicated that 65 percent of the ophthalmologists and 90 percent of the neurologists prescribed corticosteroids (almost always in oral form) for optic neuritis (unpublished data).
To evaluate corticosteroids as treatment for optic neuritis, we designed a multicenter, randomized clinical trial to answer the following questions: Does treatment with either oral prednisone or intravenous methylprednisolone improve visual outcome in acute optic neuritis? Does either treatment speed the recovery of vision? What are the complications of treatment in relation to its efficacy?
Methods
The design of the study (the Optic Neuritis Treatment Trial) has been described in part previously,10 and details of the criteria for eligibility, treatment protocols, testing procedures, and quality-control measures are given in the trial manual.11
Patient Recruitment and Eligibility Criteria
Physicians in the vicinity of each clinical center were asked to refer patients to the study investigators. Patients were evaluated with ocular and neurologic examinations, visual-function testing, magnetic resonance imaging of the brain, antinuclear-antibody and fluorescent treponemal-antigen determinations, and chest radiography. To be eligible for the study a patient had to be between the ages of 18 and 46 years, have a history consistent with acute unilateral optic neuritis with visual symptoms lasting eight days or less, and have evidence of a relative afferent pupillary defect and a visual-field defect in the affected eye on examination. Patients were excluded if they had previously had optic neuritis in the same eye or had clinical evidence of a systemic disease, other than multiple sclerosis, that might cause optic neuritis. Eligible patients signed a form giving informed consent that had been approved by the investigational review board of each institution.
Treatment Assignment
A permuted-blocks design with a separate sequence for each clinical center was used to assign patients randomly in equal numbers to three treatment groups. The first group received intravenous methylprednisolone (Solu-Medrol, 250 mg every 6 hours for 3 days) followed by oral prednisone (Deltasone, 1 mg per kilogram of body weight per day [rounded to the nearest 10 mg] for 11 days) and is referred to as the intravenous-methylprednisolone group; the second group received oral prednisone (1 mg per kilogram per day for 14 days) and is referred to as the oral-prednisone group; the third group received oral placebo on the same schedule as the oral-prednisone group. Each treatment period was followed by a short period during which the oral dose was tapered, to 20 mg on day 15 and to 10 mg on days 16 and 18. Patients in the intravenous-methylprednisolone group were hospitalized for the three days of treatment. Oral treatment was given in a single morning dose. Patients in the oral-prednisone and placebo groups were blinded to their treatment assignment, whereas those in the intravenous-methylprednisolone group were not.
Compliance in taking oral medication was assessed by counting the number of pills remaining in each bottle when it was returned.
Determination of Outcome
Visual field and contrast sensitivity were the primary measures of outcome; visual acuity and color vision were secondary measures. Unlike visual acuity, which measures the eye's ability to resolve small targets (high spatial frequency), contrast sensitivity as tested in this study assesses the eye's ability to recognize large targets (peak spatial frequency).
Follow-up visits were scheduled on or about days 4, 15, and 30, weeks 7, 13, and 19, months 6 and 12, and then yearly. The data collected at the six-month visit were the major measurements of visual outcome. At each visit, we took an interval history, performed a refraction, and measured visual acuity (with a retroilluminated Snellen ETDRS letter chart), contrast sensitivity (with the Pelli—Robson chart), and visual field (with the Humphrey Field Analyzer). At the six-month visit and all subsequent visits, we also performed the Farnsworth—Munsell 100-hue color-vision test and a neurologic examination.
The personnel assessing visual function were always unaware of whether the patient was assigned to the placebo or prednisone group, and as often as possible they were unaware of whether the patient was receiving methylprednisolone.
Adverse Effects and Intercurrent Events
At each visit the patients were weighed, and on days 4 and 15 they were asked about potential side effects of their medication. A new attack of optic neuritis was diagnosed if a patient reported new visual loss in either eye that was documented on visual-function testing and verified by the study chairman's review of records. Treatment for new attacks was given at the physician's discretion. Multiple sclerosis was diagnosed on the basis of the clinical criteria of Poser et al.12 for definite multiple sclerosis.
Statistical Analysis
The necessary sample size was projected to be 145 patients per group, on the basis of the following assumptions: the proportion of patients in the placebo group with abnormal contrast sensitivity at six months would be 75 percent, the expected reduction in this percentage by treatment would be 30 percent, the alpha error would be 0.02, and the power of the study would be 90 percent. The calculated sample size was increased by 20 percent to allow for withdrawal and noncompliance.
In all analyses, each steroid group was compared with the placebo group. All reported P values are two-tailed. Because of differences between the groups in the degree of visual loss at base line (a strong predictor of visual outcome), all comparisons of visual function were stratified according to base-line visual acuity. All results reported here are adjusted values; the results shown in the tables and figures are both adjusted and unadjusted values. The distributions of the data on visual function in each group at six months were compared by a univariate Wilcoxon rank-sum test,13 and all four measures were combined for the Wei—Lachin test of stochastic ordering.14 The relative risk that each measure would demonstrate recovery of function to normal was calculated from the cumulative incidence of return to normal within the six-month follow-up period with the MantelHaenszel method.15 The rate of recovery was analyzed for the entire six months by life-table analysis with the Kruskal—Wallis test for censored data.16
The treatment groups were compared in terms of the side effects of medication by the chi-square test of association in contingency tables, and in terms of weight gain by analysis of variance with two contrasts (each steroid group vs. the placebo group).
Using all our follow-up data (follow-up, 6 to 24 months for each patient), we assessed the differences between the groups in the rate of new episodes of optic neuritis and the rate of development of multiple sclerosis by the Kaplan–Meier product-limit method17 with a Mantel log-rank test,18 and we calculated relative risks by proportional-hazards analysis.
Results
Four hundred fifty-seven patients were enrolled between July 1, 1988, and June 30, 1991. The number enrolled at individual clinical centers ranged from 15 to 46. The status of all patients and their base-line characteristics are summarized in Table 1Table 1
Randomization, Compliance with Medication, and Follow-up of the Treatment Groups. and Table 2Table 2
Demographic and Clinical Characteristics of the Patients at Study Entry.*, respectively. After randomization, two patients were found to have a compressive optic neuropathy rather than optic neuritis; two other patients who did have optic neuritis were found to have connective-tissue diseases. During the 6 to 24 months of follow-up, no other patients had signs of a systemic disease, other than multiple sclerosis, that could be considered a cause of the optic neuritis (e.g., sarcoidosis, systemic lupus erythematosus, or syphilis).Compliance with Medication and Side Effects
The full course of treatment was completed by all but 3 percent of the patients. An additional 2.4 percent of the patients took at least five pills fewer than prescribed during the entire treatment period (Table 1).
In general, the side effects of the treatments were mild. Two patients in the intravenous-methylprednisolone group had serious adverse side effects: one patient had an acute transient depression that required psychotropic drugs, and the other had acute pancreatitis. In both patients the adverse effect resolved without sequelae. Minor side effects were more common in both steroid groups than in the placebo group. The patients in the steroid groups more often reported sleep disturbance, mild mood change, stomach upset, and facial flushing and had a greater mean percentage of weight gain than did the patients in the placebo group (P<0.001 for each comparison).
Follow-up Visits and Masking
The overall rate of visits missed among the seven scheduled follow-up visits in the first six months was 3.4 percent. When examining visual function in the patients in the intravenous-methylprednisolone group, technicians were unaware of the patients' treatment assignment during 86 percent of all follow-up visits overall and 94 percent of the six-month visits. When examining the oral-prednisone and placebo groups, the technicians were unaware of whether the patients were in the intravenous-methylprednisolone group or one of the other two groups during 85 percent of all visits and 86 percent of the six-month visits.
Visual Outcome
Intravenous Methylprednisolone versus Placebo
Analysis of life-table curves indicated that the rate of return of vision to normal was higher in the intravenous-methylprednisolone group than in the placebo group (P = 0.0001 for visual field, P = 0.02 for contrast sensitivity, and P = 0.09 for visual acuity) (Fig. 1Figure 1
Life-Table Analysis Showing Cumulative Rates of Recovery of Normal Visual Function over the Six-Month Follow-up Period, According to Treatment Group. and Table 3Table 3
Results of Kruskal—Wallis Test Comparing Recovery Rates in the Steroid Groups with Rates in the Placebo Group.). The differences between these two groups in the distributions of measures of visual function were greatest on day 4 and day 15 (data not shown). Although thereafter the differences between the groups decreased, as Table 4Table 4
Distributions of Measures of Visual Outcome at Six Months.* demonstrates, at six months the distributions for contrast sensitivity (P = 0.026), visual field (P = 0.054), and color vision (P = 0.033) were still significantly different, although those for visual acuity were not (P = 0.66). The P value for the stochastic-ordering summary statistic for all four measures was 0.029.Although the 95 percent confidence intervals for the relative risk of recovery of normal function included 1.0 for three of the four measures, the cumulative incidence of recovery was greater in the intravenous-methylprednisolone group than in the placebo group for all four measures (the relative risk was 1.17 for contrast sensitivity, 1.09 for visual field, 1.07 for visual acuity, and 1.21 for color vision). For each of the four measures, the relative risk of recovery was lowest among patients whose vision was 20/40 or better at base line, higher among those whose vision ranged from 20/50 to 20/190, and highest among those whose vision was 20/200 or worse (Table 5Table 5
Relative Risk of Recovery of Normal Visual Function within Six Months.*).Oral Prednisone versus Placebo
When the oral-prednisone group was compared with the placebo group, there were no significant differences in the rate of recovery (P>0.05 for each measure) or the distribution of any of the outcome measures at six months (P = 0.54 for contrast sensitivity, P = 0.83 for visual field, P = 0.35 for visual acuity, and P = 0.58 for color vision; P = 0.87 for the stochastic-ordering statistic) (Table 4). The relative risk of recovery (oral prednisone vs. placebo) was slightly above or below 1.0 for each of the four measures (Table 5).
Poor Visual Acuity at Six Months
The number of patients in each group who had a poor visual outcome was similar. At six months only 9 patients (6.0 percent) in the intravenous-methylprednisolone group, 11 (7.1 percent) in the oral-prednisone group, and 8 (5.3 percent) in the placebo group had visual acuity of 20/50 or worse.
New Attacks of Optic Neuritis
Twenty patients (13 percent) in the intravenous-methylprednisolone group, 42 (27 percent) in the oral-prednisone group, and 24 (15 percent) in the placebo group had at least one new episode of optic neuritis in either eye during the 6 to 24 months of follow-up. At least one new episode occurred in affected eyes (i.e., those affected at entry) in 14 patients (9 percent) in the intravenous-methylprednisolone group, 23 (15 percent) in the oral-prednisone group, and 16(10 percent) in the placebo group, and at least one occurred in contralateral eyes in 8 (5 percent), 25 (16 percent), and 11 (7 percent) patients, respectively. Analysis of the length of time to the first new episode of optic neuritis in either eye demonstrated that the rate of new episodes was significantly higher in the oral-prednisone group (P = 0.02), but not the intravenous-methylprednisolone group, than in the placebo group (Fig. 2Figure 2
Kaplan–Meier Curves Showing Cumulative Incidence of New Episodes of Optic Neuritis in Either Eye, According to Treatment Group.). When compared with the placebo group, the oral prednisone group had a relative risk of a new episode that was 1.79 (95 percent confidence interval, 1.08 to 2.95) for either eye, 1.40 (95 percent confidence interval, 0.74 to 2.65) for the affected eye, and 2.50 (95 percent confidence interval, 1.15 to 5.46) for the contralateral eye. In the intravenous-methylprednisolone group, the relative risk of a new episode was 0.81 (95 percent confidence interval, 0.45 to 1.47) for either eye, 0.86 (95 percent confidence interval, 0.42 to 1.76) for the affected eye, and 0.65 (95 percent confidence interval, 0.23 to 1.81) for the contralateral eye.Development of Multiple Sclerosis
Multiple sclerosis was newly diagnosed during follow-up (6 to 24 months) in 20 patients (14 percent) in the intravenous-methylprednisolone group, 35 (24 percent) in the oral-prednisone group, and 28 (20 percent) in the placebo group. The relative risk of multiple sclerosis was 0.65 (95 percent confidence interval, 0.37 to 1.16) in the intravenous-methylprednisolone group and 1.17 (95 percent confidence interval, 0.71 to 1.93) in the oral-prednisone group, when each group was compared with the placebo group.
Discussion
In our randomized, placebo-controlled trial, patients who received intravenous methylprednisolone followed by oral prednisone recovered vision faster than patients given placebo, but their visual outcome at the end of the six-month follow-up period was only slightly better than that in the placebo group. Oral prednisone alone provided no benefit in terms of either the rate of recovery or the outcome at six months. Unexpectedly, patients in the oral-prednisone group had a higher rate of new attacks of optic neuritis than did patients in the other two groups.
The regimen of intravenous methylprednisolone was generally well tolerated; only two patients had serious side effects, both of which resolved without sequelae. As compared with placebo, methylprednisolone was most beneficial during the first 15 days of follow-up and less so subsequently, so that by the end of 7 weeks the differences between the two groups in visual function were small. At six months, when all improvement due to treatment should have been evident, the intravenous-methylprednisolone group was still slightly better, as compared with the placebo group, in contrast sensitivity, visual field, and color vision but not in visual acuity. This differential effect of treatment on the measures of visual outcome was not unexpected, since contrast sensitivity, visual field, and color vision are more sensitive indicators of optic-nerve function than is visual acuity.2 , 3
When the oral-prednisone group was compared with the placebo group, there were no differences in either the rate of recovery or the visual outcome at six months as assessed by any of the measures of visual function. In view of our sample size of 156 patients in the oral-prednisone group and 150 in the placebo group, frequent follow-up visits, and excellent rate of completion of blinded follow-up visits, we have a high degree of confidence that the use of oral prednisone alone as prescribed in this study has no benefit.
The patients in the oral-prednisone group faced a risk, not previously reported, that we consider serious. New attacks of optic neuritis occurred during the 6 to 24 months of follow-up in 42 patients (27 percent) in this group, as compared with 24 patients (15 percent) in the placebo group and 20 patients (13 percent) in the intravenous-methylprednisolone group. Although we do not have a biologic explanation for the higher rate of new episodes in the oral-prednisone group, the likelihood that this finding was a chance occurrence is small.
There were no significant differences between the placebo group and the steroid groups in the rate of development of definite multiple sclerosis. Our data provided no support for the contention of a previous study that multiple sclerosis may develop at an increased rate among patients with optic neuritis who receive intravenous methylprednisolone.19
For this study, we selected oral prednisone because it is widely prescribed for optic neuritis, and intravenous methylprednisolone because our clinical experience and that of others had suggested that it might be more effective than oral corticosteroids. The total dose of methylprednisolone in relation to body weight was several times greater than that of prednisone; we selected the dose of each to approximate the usual quantities prescribed in clinical practice.
The patients in the intravenous-methylprednisolone group were not masked as to their treatment assignment, because ethical and economic considerations prevented the inclusion in the trial of a treatment group that received intravenous placebo. We consider it unlikely that our finding of differences between the intravenous-methylprednisolone group and the placebo group resulted from the lack of masking of the patients, since the personnel examining visual function were usually unaware of the patients' treatment assignments and the differences between groups were evident in several measures of outcome and over the range of follow-up visits.
Although a more rapid rate of recovery was detected in the intravenous-methylprednisolone group on day 4 — i.e., on completion of the course of methylprednisolone (and in most cases before the initiation of the course of prednisone), we cannot determine whether a group of patients who received methylprednisolone alone would have had the same visual outcome as our group that received both methylprednisolone and prednisone. We also cannot determine whether administering a higher dose of methylprednisolone, such as the dose of 30 mg per kilogram suggested for treatment of acute spinal-cord injuries,20 or initiating treatment sooner after the onset of symptoms might have produced even greater benefit than we found with the dose used in this trial.
The results of our study may have a bearing on the treatment of multiple sclerosis with corticosteroids. There is ample evidence that optic neuritis is a manifestation of multiple sclerosis.1 Measures of visual function, as assessed in this study, are more easily quantified than most other measures of neurologic function used in previous trials of treatment for multiple sclerosis. Previous studies of corticosteroid treatment for this disorder have been inconclusive.21 The results of our study indicate the need for a placebo-controlled trial to assess the efficacy of such treatment.
The demographic characteristics of our cohort are similar to those of previously described groups of patients with optic neuritis22 , 23; most patients with a first episode of acute optic neuritis would meet the criteria for eligibility used in our trial. Therefore, we believe that our results are applicable to the care of most patients with a first episode of optic neuritis who are examined within eight days of the onset of visual symptoms.
Although our study was not designed to evaluate the effects of treatment in subgroups, we believe that treating optic neuritis does not benefit vision if visual acuity is 20/40 or better, assuming that visual-field loss is slight. If vision during the first eight days after the onset of visual symptoms is worse than 20/40, treatment with intravenous methylprednisolone followed by oral prednisone must receive consideration. In deciding whether to prescribe this treatment, physicians should weigh the potential for more rapid recovery of vision and slightly better visual outcome at six months against the small risk of serious adverse effects, as well as the inconvenience to the patient and the cost of treatment, particularly if hospitalization is necessary. Since adverse effects of treatment were uncommon, intravenous therapy on an outpatient basis may be feasible. Future studies should assess the efficacy of intravenous doses given once or twice daily, since such a schedule would enhance the feasibility of outpatient treatment.
Oral prednisone, as tested in this trial, not only is ineffective against optic neuritis but also increases the risk of new episodes. On the basis of our results, we believe that there is no role for oral prednisone alone in the treatment of patients with initial episodes of optic neuritis of presumed demyelinative origin.
Address reprint requests to Dr. Beck at the Department of Ophthalmology, University of South Florida College of Medicine, 12901 N. Bruce B. Downs Blvd., Tampa, FL 33612.
Supported under cooperative agreements (EY07212, EY07460, EY07461, EY07659, EY07671, EY07673, EY07674, EY07675, EY07676, EY07678, EY07679, EY07680, EY07683, EY07685, EY07687, EY07689, EY07694, and EY07695) with the National Eye Institute, National Institutes of Health.
*The major participants in the Optic Neuritis Study Group are listed in the Appendix.
We are indebted to the Upjohn Company (Kalamazoo, Mich.) for supplying all the study medications and to Marian Fisher, Ph.D., for considerable assistance in the preparation of the manuscript.
Appendix
A complete listing of the members of the Optic Neuritis Treatment Trial Study Group has been published previously.10 The following are the major participants in the study group.
Central Units. Study Chairman's Office, University of South Florida, Tampa: R. Beck and B.J. Sellers; Data-Coordinating Center, George Washington University, Biostatistics Center, Rockville, Md.: P. Cleary, J.C. Backlund, D. Kenny, N. Loring, S. Campbell, P. Gilbert, W. Watson, and J. Zablotny; Visual-Field Reading Center, University of California, Davis: J. Keltner, C. Johnson, J. Spurr, and L. Shapiro; Magnetic Resonance Image Reading Center, University Diagnostic Institute, Tampa, Fla.: R. Murtagh and J. Arrington; National Eye Institute, Bethesda, Md.: C. Atwell.
Clinical Centers. University of Arkansas, Little Rock: M. Brodsky, B. Lyon, S. Nazarian, W. Jay, A. Luther, and R. Ford; Cullen Eye Institute, Baylor College of Medicine, Houston: J. McCrary, B. Slight, R. Gross, L. Rolak, and P. Frady; Pacific California Medical Center, Smith—Kettlewell Eye Research Institute, San Francisco: B. Katz, N. Hawker, O. Paul, M. Swenson, N. Loey, and N. Kelly; Duke University, Durham, N.C.: E. Buckley, M. Anderson, Jr., G. Valentine, S. Pollock, W. Massey, L. Duncan, K. Kossover, and L. Griffin; University of North Carolina, Chapel Hill: B. Grimson, N. Tripoli, J. Messenheimer, and D. Fletcher; University of Florida, Gainesville: J. Guy, D. Shamis, S. Zam, L. Hamed, J. Malone, and M. Willingham; Center for Sight, Georgetown University, Washington, D.C.: G. Chrousos, S. Lauber, J. Kattah, and E. Coyle; University of Illinois, Chicago: J. Goodwin, E. Sullivan, C. Winterbotham, J. Nichols, L. Skorin, Jr., P. Bobak, and J. Putz; University of Iowa, Iowa City: J. Corbett, S. Thompson, C. Musser, R. Kardon, P. Johnston, G. Mitchell, J. Delsing, and C. Fountain; Wills Eye Hospital, Thomas Jefferson University, Philadelphia: P. Savino, M. Devlin, R. Sergott, T. Bosley, C. Cantor, K. Santa-Maria, and S. Ward; Wilmer Eye Institute, Johns Hopkins Hospital, Baltimore: N. Miller, C. Krich Putzulo, M. Repka, D. Buchholz, S. Reich, and L. West; Kellogg Eye Center, University of Michigan, Ann Arbor: J. Trobe, C. Caudill, W. Cornblath, L. Kruscke, and B. Michael; Michigan State University, East Lansing: D. Kaufman, J. Froehlich, T. Moore, G. Ristow, B. Zendler, J. Kokinakis, E. Rosick, and M. Barris; New York University, New York: M. Kupersmith, A. Addessi, F. Warren, and S. Wahba; Devers Eye Institute, Good Samaritan Hospital, Portland, Ore.: W. Shults, L. Diehl, R. Dreyer, J. Zilis, R. Wilson, R. Herndon, D. Gibbs, H. Leonard, C. Beardsley, J. Arends, K. Steffen, B. Royce, and D. McKenna; University of Washington, Seattle: C. Smith, P. Ernst, J. Orcutt, R. Mills, W. Longstreth, S. Smith, B. Lawrence, D. Bjorn, and Y. Cady.
Data and Safety Monitoring Committee: M. Fisher (chair), P. Alguire, J. Carl, G. Rubin, J. Weinstein, V. Smith, and J. Dunbar-Jacob.
- References
References
1
Ebers
Web of Science | Medline2
Fleishman
Web of Science | Medline3
Sanders
CrossRef | Web of Science | Medline4
Rawson
CrossRef | Web of Science | Medline5
Rawson
CrossRef | Web of Science | Medline6
Gould
CrossRef | Web of Science | Medline7
Rose
Web of Science | Medline8
Bowden
CrossRef | Web of Science | Medline9
Spoor
Web of Science | Medline10
Optic Neuritis Study Group
Web of Science | Medline11
Optic Neuritis Treatment Trial manual of procedures. Springfield, Va.: National Technical Information Service, 1990. (NTIS accession no. PB90–195728.)
12
Poser
CrossRef | Web of Science | Medline13
Wilcoxon
CrossRef | Web of Science14
Wei
CrossRef | Web of Science15
Mantel
Web of Science | Medline16
Breslow
CrossRef | Web of Science17
Kaplan
CrossRef | Web of Science18
Mantel
Medline19
Herishanu
CrossRef | Web of Science | Medline20
Bracken
Full Text | Web of Science | Medline21
Goodin
Web of Science | Medline22
Visual signs at presentation. In: Perkin GD, Rose FC. Optic neuritis and its differential diagnosis. Oxford, England: Oxford University Press, 1979:43–73.
23
Nikoskelainen
CrossRef | Web of Science | Medline
- Citing Articles (174)
Citing Articles
1
Gabrielle R. Bonhomme, Ellen B. Mitchell. (2011) Treatment of Pediatric Optic Neuritis. Current Treatment Options in Neurology
CrossRef2
Aditya Sudhalkar, Mayuri Khamar, Bakulesh Khamar. (2011) Outcomes of toll-like receptors’ antagonism in steroid-resistant optic neuritis; a pilot study. Graefe's Archive for Clinical and Experimental Ophthalmology
CrossRef3
M-H Sun, H-S Wang, K-J Chen, W-W Su, P-Y Hsueh, K-K Lin, L-Y Kao. (2011) Clinical characteristics of optic neuritis in Taiwanese children. Eye 25:11, 1457-1464
CrossRef4
S. Roesner, R. Appel, J. Gbadamosi, R. Martin, C. Heesen. (2011) Treatment of steroid-unresponsive optic neuritis with plasma exchange. Acta Neurologica Scandinavicano-no
CrossRef5
Simon J. Hickman, Robert L. Tomsak. (2011) The Treatment of Indirect Traumatic Optic Neuropathy with Corticosteroids. Neuro-Ophthalmology 35:4, 175-180
CrossRef6
Yochai Z. Shoshani, Alon Harris, Deepam Rusia, George L. Spaeth, Brent Siesky, Ayala Pollack, Barbara Wirostko. (2011) Contrast sensitivity, ocular blood flow and their potential role in assessing ischaemic retinal disease. Acta Ophthalmologica 89:5, e382-e395
CrossRef7
Kazuhiro Nakaya, Takeshi Oshima, Takayuki Kudo, Ryoukichi Ikeda, Hiroshi Hidaka, Toshimitsu Kobayashi. (2011) Outcomes of surgically treated rhinogenic optic neuropathy. Acta Oto-laryngologica 131:8, 833-839
CrossRef8
Oliver W. Gramlich, Stephanie C. Joachim, Philip F. Gottschling, Panagoitis Laspas, Clemens S. Cuny, Norbert Pfeiffer, Franz H. Grus. (2011) Ophthalmopathology in rats with MBP-induced experimental autoimmune encephalomyelitis. Graefe's Archive for Clinical and Experimental Ophthalmology 249:7, 1009-1020
CrossRef9
Fiona E. Costello, Alexander Klistorner, Randy Kardon. (2011) Optical Coherence Tomography in the Diagnosis and Management of Optic Neuritis and Multiple Sclerosis. Ophthalmic Surgery, Lasers, and Imaging 42:4, S28-S40
CrossRef10
Nicholas J Volpe, Leonard A Levin. (2011) How Should Patients With Indirect Traumatic Optic Neuropathy Be Treated?. Journal of Neuro-Ophthalmology 31:2, 169-174
CrossRef11
Yi Du, Jun Yang, Jing-Jing Li, Rui-Wu Zhou, Jian-Feng He. (2011) Unilateral optic neuritis in a Chinese population in three centers. Journal of Clinical Neuroscience
CrossRef12
Emily Y. Chew. (2011) The Value of Randomized Clinical Trials in Ophthalmology. American Journal of Ophthalmology 151:4, 575-578
CrossRef13
Egemen İdiman, Serkan Özakbaş. (2011) The limited demyelinating diseases: the voyage of optic neuritis and transverse myelitis to multiple sclerosis and neuromyelitis. Expert Review of Neurotherapeutics 11:3, 451-462
CrossRef14
Patrick Yu-Wai-Man, Philip G Griffiths, Patrick Yu-Wai-Man. 2011. Steroids for traumatic optic neuropathy. .
CrossRef15
Dong Min Cha, Seong Joon Kim, Jeong Hun Kim, Ho Kyung Choung, Young Suk Yu. (2011) Clinical Features and the Effect of High-Dose Steroid Therapy in Korean Optic Neuritis Patients. Journal of the Korean Ophthalmological Society 52:9, 1083
CrossRef16
Kristin M. Galetta, Peter A. Calabresi, Elliot M. Frohman, Laura J. Balcer. (2011) Optical Coherence Tomography (OCT): Imaging the Visual Pathway as a Model for Neurodegeneration. Neurotherapeutics 8:1, 117-132
CrossRef17
Dong Hyun Jo, Seong-Joon Kim, Jong Hee Chae, Young Suk Yu. (2011) The Clinical Characteristics of Optic Neuritis in Korean Children. Korean Journal of Ophthalmology 25:2, 116
CrossRef18
Geoffrey A Kerchner, Maria Carmela Tartaglia, Adam L Boxer. (2011) Abhorring the vacuum: use of Alzheimer’s disease medications in frontotemporal dementia. Expert Review of Neurotherapeutics 11:5, 709
CrossRef19
Dinelli M. Monson, Justine R. Smith. (2011) Acute Zonal Occult Outer Retinopathy. Survey of Ophthalmology 56:1, 23-35
CrossRef20
Natalie Cornay, Robin Davis, Meghan Harris, Brian Rabin, Karen Small, Edward Johnson, Eduardo Gonzalez-Toledo, Stephen Jaffe, Alireza Minagar. 2011. Neuromyelitis Optica. , 237-251.
CrossRef21
Andrew P.D Henderson, Daniel R. Altmann, Trip S. Anand, Katherine A. Miszkiel, Patricio G. Schlottmann, Steve J. Jones, David F. Garway-Heath, Gordon T. Plant, David H. Miller. (2011) Early factors associated with axonal loss after optic neuritis. Annals of Neurologyn/a-n/a
CrossRef22
Ming He, Dean Cestari, Mary Beth Cunnane, Joseph F. Rizzo. (2010) The Use of Diffusion MRI in Ischemic Optic Neuropathy and Optic Neuritis. Seminars in Ophthalmology 25:5-6, 225-232
CrossRef23
F. Sellebjerg, D. Barnes, G. Filippini, R. Midgard, X. Montalban, P. Rieckmann, K. Selmaj, L. H. Visser, P. Soelberg Sørensen. 2010. Acute Relapses of Multiple Sclerosis. , 411-419.
CrossRef24
Cord Huchzermeyer, Christian Mardin, Leonard Holbach, Jochen Zwerina, Georg Schett, Jürgen Rech. (2010) Successful remission induction with a combination therapy of rituximab, cyclophosphamide, and steroids in a patient with refractory optic neuritis in Wegener’s granulomatosis. Clinical Rheumatology
CrossRef25
David Clark, Workayehu Kebede, Eric Eggenberger. (2010) Optic Neuritis. Neurologic Clinics 28:3, 573-580
CrossRef26
Anneke Van der Walt, Helmut Butzkueven, Scott Kolbe, Mark Marriott, Estella Alexandrou, Melissa Gresle, Gary Egan, Trevor Kilpatrick. (2010) Neuroprotection in multiple sclerosis: A therapeutic challenge for the next decade. Pharmacology & Therapeutics 126:1, 82-93
CrossRef27
Francesc Fernández Monràs, Pedro Arguis, Antonio Martínez. (2010) Mujer de 36 años con dolor ocular izquierdo y disminución de la agudeza visual. Medicina Clínica 134:8, 355-362
CrossRef28
Devon Conway, Jeffrey A Cohen. (2010) Combination therapy in multiple sclerosis. The Lancet Neurology 9:3, 299-308
CrossRef29
Yan-Ming Chen, Chih-Chao Yang, I-Hua Wang, Fung-Rong Hu, Jieh-Ren Jou. (2010) The effect of interferon β-1a on optic neuritis relapse in patients with multiple sclerosis. Graefe's Archive for Clinical and Experimental Ophthalmology 248:2, 231-235
CrossRef30
Seung Ah Chung, Jin SooK Yoon, Sang Yeul Lee. (2010) Effect of Intravenous Methylprednisolone on Idiopathic Orbital Inflammation. Journal of the Korean Ophthalmological Society 51:10, 1299
CrossRef31
John R Guy, Xiaoping Qi. 2010. Optic neuritis. , 278-288.
CrossRef32
Rima M Dafer, Walter M Jay. (2009) Headache and the eye. Current Opinion in Ophthalmology 20:6, 520-524
CrossRef33
Alexandra Schröder, Ralf A Linker, Ralf Gold. (2009) Plasmapheresis for neurological disorders. Expert Review of Neurotherapeutics 9:9, 1331-1339
CrossRef34
K. M. Myhr, S. I. Mellgren. (2009) Corticosteroids in the treatment of multiple sclerosis. Acta Neurologica Scandinavica 120, 73-80
CrossRef35
Jodie M Burton, Paul W O'Connor, Marika Hohol, Joseph Beyene, Jodie M Burton. 2009. Oral versus Intravenous Steroids for Treatment of Relapses in Multiple Sclerosis. .
CrossRef36
Yen-Ching Lin, An-Guor Wang, May-Yung Yen. (2009) Systemic lupus erythematosus-associated optic neuritis: clinical experience and literature review. Acta Ophthalmologica 87:2, 204-210
CrossRef37
Valérie Biousse, Olivier Calvetti, Carolyn D. Drews-Botsch, Edward J. Atkins, Busaba Sathornsumetee, Nancy J. Newman. (2009) Management of optic neuritis and impact of clinical trials: An international survey. Journal of the Neurological Sciences 276:1-2, 69-74
CrossRef38
Meghan K. Harris, Amir Hadi Maghzi, Masoud Etemadifar, Roger E. Kelley, Eduardo Gonzalez-Toledo, Alireza Minagar. (2009) Acute demyelinating disorders of the central nervous system. Current Treatment Options in Neurology 11:1, 55-63
CrossRef39
Frederick L. Ferris. (2009) Clinical Trials – More Than an Assessment of Treatment Effect: LXV Edward Jackson Memorial Lecture. American Journal of Ophthalmology 147:1, 22-32.e1
CrossRef40
Christian J. Lueck, Helen V. Danesh-Meyer, Faith J. Margrie, Carolyn Drews-Botsch, Olivier Calvetti, Nancy J. Newman, Valérie Biousse. (2008) Management of acute optic neuritis: A survey of neurologists and ophthalmologists in Australia and New Zealand. Journal of Clinical Neuroscience 15:12, 1340-1345
CrossRef41
Christian Confavreux, Sandra Vukusic. (2008) The Clinical Epidemiology of Multiple Sclerosis. Neuroimaging Clinics of North America 18:4, 589-622
CrossRef42
Kenneth S. Shindler, Elvira Ventura, Mahasweta Dutt, Abdolmohamad Rostami. (2008) Inflammatory demyelination induces axonal injury and retinal ganglion cell apoptosis in experimental optic neuritis. Experimental Eye Research 87:3, 208-213
CrossRef43
David B. Sommer, Larry B. Goldstein. 2008. Central Nervous System (CNS). .
CrossRef44
C. Arndt, P. Labauge, C. Speeg-Schatz, L. Jeanjean, M. Fleury, G. Castelnovo, L. Ballonzolli, F. Blanc, B. Carlander, J. de Sèze. (2008) Neuropathies optiques inflammatoires récidivantes. Journal Français d'Ophtalmologie 31:4, 363-367
CrossRef45
Dean M. Wingerchuk, Brian G. Weinshenker. (2008) Neuromyelitis optica. Current Treatment Options in Neurology 10:1, 55-66
CrossRef46
Martin Eggert, Robert Goertsches, Ulrike Seeck, Silvia Dilk, Gunther Neeck, Uwe K. Zettl. (2008) Changes in the activation level of NF-kappa B in lymphocytes of MS patients during glucocorticoid pulse therapy. Journal of the Neurological Sciences 264:1-2, 145-150
CrossRef47
A.-M. Beyer, B. Rosche, U. Pleyer, K.P. Wandinger. (2007) Stellenwert der Uveitis im Rahmen demyelinisierender Erkrankungen des Zentralnervensystems. Der Nervenarzt 78:12, 1389-1398
CrossRef48
Patrick Yu-Wai-Man, Philip G Griffiths, Patrick Yu-Wai-Man. 2007. Steroids for traumatic optic neuropathy. .
CrossRef49
Jeremiah Brown, Henry Hacker, Steven T. Schuschereba, Harry Zwick, David J. Lund, Bruce E. Stuck. (2007) Steroidal and Nonsteroidal Antiinflammatory Medications Can Improve Photoreceptor Survival after Laser Retinal Photocoagulation. Ophthalmology 114:10, 1876-1883
CrossRef50
Elliot M. Frohman, Anjali Shah, Eric Eggenberger, Luanne Metz, Robert Zivadinov, Olaf Stüve. (2007) Corticosteroids for multiple sclerosis: I. Application for treating exacerbations. Neurotherapeutics 4:4, 618-626
CrossRef51
Denise Tischner, Holger M. Reichardt. (2007) Glucocorticoids in the control of neuroinflammation. Molecular and Cellular Endocrinology 275:1-2, 62-70
CrossRef52
Carl A. Germann, Michael R. Baumann, Sirus Hamzavi. (2007) Ophthalmic diagnoses in the ED: optic neuritis. The American Journal of Emergency Medicine 25:7, 834-837
CrossRef53
W.A. Lagrèze. (2007) Steroide bei Sehnerverkrankungen?. Der Ophthalmologe 104:6, 517-520
CrossRef54
Molly E. Gilbert, Robert C. Sergott. (2007) New directions in optic neuritis and multiple sclerosis. Current Neurology and Neuroscience Reports 7:3, 259-264
CrossRef55
Mohammad Reza Motamed, Neda Najimi, Seyed-Mohammad Fereshtehnejad. (2007) The effect of interferon-beta1a on relapses and progression of disability in patients with clinically isolated syndromes (CIS) suggestive of multiple sclerosis. Clinical Neurology and Neurosurgery 109:4, 344-349
CrossRef56
Mahmood F. Mafee. 2007. Eye, Orbit, Ear, Nose, and Throat Studies Using MRI. .
CrossRef57
Loren A. Rolak, John O. Fleming. (2007) The Differential Diagnosis of Multiple Sclerosis. The Neurologist 13:2, 57-72
CrossRef58
Satyanarayana S Vedula, Suzanne Brodney Folse, Robin L Gal, Roy Beck, Robin L Gal. 2007. Corticosteroids for treating optic neuritis. .
CrossRef59
Lin-Chung Woung, Ching-Heng Lin, Ching-Yao Tsai, Ming-Tsu Tsai, Jieh-Ren Jou, Pesus Chou. (2007) Optic Neuritis among National Health Insurance Enrollees in Taiwan, 2000–2004. Neuroepidemiology 29:3-4, 250-254
CrossRef60
Fiona Costello. (2007) Optic neuritis: The role of disease-modifying therapy disease-modifying therapy in this clinically isolated syndrome. Current Treatment Options in Neurology 9:1, 48-54
CrossRef61
Benjamin J. Osborne, Grant T. Liu, Nancy J. Newman. 2007. Cranial Nerve II and Afferent Visual Pathways. , 113-132.
CrossRef62
Michael J. Pro, Mauricio E. Pons, Jeffrey M. Liebmann, Robert Ritch, Samiah Zafar, Daniel Lefton, Mark J. Kupersmith. (2006) Imaging of the optic disc and retinal nerve fiber layer in acute optic neuritis. Journal of the Neurological Sciences 250:1-2, 114-119
CrossRef63
Bryn M Burkholder, Steven L Galetta, Laura J Balcer. (2006) Acute demyelinating optic neuritis. Expert Review of Ophthalmology 1:2, 159-170
CrossRef64
Holger M Reichardt, Ralf Gold, Fred Lühder. (2006) Glucocorticoids in multiple sclerosis and experimental autoimmune encephalomyelitis. Expert Review of Neurotherapeutics 6:11, 1657-1670
CrossRef65
Yangtai Guan, Kenneth S. Shindler, Philomela Tabuena, A.M. Rostami. (2006) Retinal ganglion cell damage induced by spontaneous autoimmune optic neuritis in MOG-specific TCR transgenic mice. Journal of Neuroimmunology 178:1-2, 40-48
CrossRef66
Fiona Costello, Stuart Coupland, William Hodge, Gianni R. Lorello, Jeannie Koroluk, Y. Irene Pan, Mark S. Freedman, David H. Zackon, Randy H. Kardon. (2006) Quantifying axonal loss after optic neuritis with optical coherence tomography. Annals of Neurology 59:6, 963-969
CrossRef67
Yen-Ching Lin, May-Yung Yen, Wen-Ming Hsu, Hui-Chen Lee, An-Guor Wang. (2006) Low Conversion Rate to Multiple Sclerosis in Idiopathic Optic Neuritis Patients in Taiwan. Japanese Journal of Ophthalmology 50:2, 170-175
CrossRef68
Balcer, Laura J., . (2006) Optic Neuritis. New England Journal of Medicine 354:12, 1273-1280
Full Text69
Miho SEKIMOTO, Yuichi IMANAKA. (2006) Evidence-based medicine and evidence-based guidelines. Suizo 21:6, 479-483
CrossRef70
F. Sellebjerg, D. Barnes, G. Filippini, R. Midgard, X. Montalban, P. Rieckmann, K. Selmaj, L. H. Visser, P. S. Sorensen. (2005) EFNS guideline on treatment of multiple sclerosis relapses: report of an EFNS task force on treatment of multiple sclerosis relapses. European Journal of Neurology 12:12, 939-946
CrossRef71
Kayur H. Shah, Ralph D. Levinson, Fei Yu, Raquel Goldhardt, Lynn K. Gordon, Christine R. Gonzales, John R. Heckenlively, Peter J. Kappel, Gary N. Holland. (2005) Birdshot Chorioretinopathy. Survey of Ophthalmology 50:6, 519-541
CrossRef72
Hartmut Lins. (2005) Clinical Add-on: Multiple sclerosis – clinical picture and therapeutic strategies. Signal Transduction 5:5, 266-272
CrossRef73
Ling Chen, Lynn K Gordon. (2005) Ocular manifestations of multiple sclerosis. Current Opinion in Ophthalmology 16:5, 315-320
CrossRef74
M. Tariq Bhatti, Nicholas J. Schmitt, Randall L. Beatty. (2005) Acute inflammatory demyelinating optic neuritis: current concepts in diagnosis and management. Optometry - Journal of the American Optometric Association 76:9, 526-535
CrossRef75
Sanjay Sharma. (2005) LEVELS OF EVIDENCE. Evidence-Based Ophthalmology 6:3, 115-116
CrossRef76
Valerie Purvin, Aki Kawasaki. (2005) Neuro-Ophthalmic Emergencies for the Neurologist. The Neurologist 11:4, 195-233
CrossRef77
Dean M. Wingerchuk, Brian G. Weinshenker. (2005) Neuromyelitis optica. Current Treatment Options in Neurology 7:3, 173-182
CrossRef78
David Miller, Frederik Barkhof, Xavier Montalban, Alan Thompson, Massimo Filippi. (2005) Clinically isolated syndromes suggestive of multiple sclerosis, part 2: non-conventional MRI, recovery processes, and management. The Lancet Neurology 4:6, 341-348
CrossRef79
Johannes RM Cruysberg. (2005) The neuro-ophthalmology of multiple sclerosis. The Lancet Neurology 4:4, 209
CrossRef80
Robert E. Shapiro. (2005) Corticosteroid treatment in cluster headache: Evidence, rationale, and practice. Current Pain and Headache Reports 9:2, 126-131
CrossRef81
Mar Tintor
, Alex Rovira, Jordi Rio, Carlos Nos, Elisensa Griv
CrossRef82
Elliot M Frohman, Teresa C Frohman, David S Zee, Roderick McColl, Steven Galetta. (2005) The neuro-ophthalmology of multiple sclerosis. The Lancet Neurology 4:2, 111-121
CrossRef83
Sanjay Sharma. (2005) LEVELS OF EVIDENCE. Evidence-Based Eye Care 6:1, 5-6
CrossRef84
Carmen K.M. Chan, Dennis S.C. Lam. (2004) Optic neuritis treatment trial:10-year follow-up results. American Journal of Ophthalmology 138:4, 695
CrossRef85
Trevor J Kilpatrick, Helmut Butzkueven, Ben Emery, Mark Marriott, Bruce V Taylor, Niall Tubridy. (2004) Neuroglial responses to CNS injury: prospects for novel therapeutics. Expert Review of Neurotherapeutics 4:5, 869-878
CrossRef86
Douglas S. Goodin. (2004) Disease-modifying therapy in MS: a critical review of the literature. Journal of Neurology 251:S5, v3-v11
CrossRef87
ANDREW E. EPSTEIN. (2004) Jumping in Before the Water Is Hot:. Journal of Cardiovascular Electrophysiology 15:8, 867-869
CrossRef88
Carlo Pozzilli, Fabiana Marinelli, Silvia Romano, Francesca Bagnato. (2004) Corticosteroids treatment. Journal of the Neurological Sciences 223:1, 47-51
CrossRef89
Andrew D. Siderowf. (2004) Evidence from clinical trials: Can we do better?. NeuroRX 1:3, 363-371
CrossRef90
Richard A Rudick, Alfred Sandrock. (2004) Natalizumab: α4-integrin antagonist selective adhesion molecule inhibitors for MS. Expert Review of Neurotherapeutics 4:4, 571-580
CrossRef91
S. Kopke, C. Heesen, J. Kasper, I. Muhlhauser. (2004) Steroid treatment for relapses in multiple sclerosis - the evidence urges shared decision-making. Acta Neurologica Scandinavica 110:1, 1-5
CrossRef92
Geert Craenen, Sandra M. Brown, Kenn A. Freedman, Thomas R. Windisch, Jorge Corona. (2004) Rapid, painless unilateral vision loss in a 37-year-old healthy woman. Survey of Ophthalmology 49:3, 343-348
CrossRef93
S. Feldman-Billard, R. Kassaei, R. Benrabah, B. Lissak, E. Héron. (2004) Tolérance glycémique des bolus intraveineux de méthylprednisolone en milieu ophtalmologique. Journal Français d'Ophtalmologie 27:2, 160-161
CrossRef94
Andrew D. Siderowf. (2004) Evidence from clinical trials: Can we do better?. NeuroRX 1:3, 363
CrossRef95
(2004) Visual function more than 10 years after optic neuritis: experience of the optic neuritis treatment trial. American Journal of Ophthalmology 137:1, 77-83
CrossRef96
Sylvie Feldman-Billard, Bruno Lissak, Rabah Benrabah, Roxana Kassaei, Emmanuel Héron. (2003) Intravenous pulse methylprednisolone therapy in eye disease. Ophthalmology 110:12, 2369-2371
CrossRef97
Elliot M Frohman. (2003) Multiple sclerosis. Medical Clinics of North America 87:4, 867-897
CrossRef98
Daniel M. Jacobson. 2003. Optic Neuritis. , 416-420.
CrossRef99
SJ Hickman, CM Dalton, DH Miller, GT Plant. (2002) Management of acute optic neuritis. The Lancet 360:9349, 1953-1962
CrossRef100
Rod Foroozan, Lawrence M. Buono, Peter J. Savino, Robert C. Sergott. (2002) Acute demyelinating optic neuritis. Current Opinion in Ophthalmology 13:6, 375-380
CrossRef101
Colum A Gorman, James A Garrity, Vahab Fatourechi, Rebecca S Bahn, Ivy A Petersen, Scott L Stafford, John D Earle, Glenn S Forbes, Robert W Kline, Helmut Buettner, Dennis M Robertson, Erik J Bergstralh, Kenneth P Offord, Diana M Rademacher, Nancy M Stanley, George B Bartley. (2002) The aftermath of orbital radiotherapy for graves’ ophthalmopathy. Ophthalmology 109:11, 2100-2107
CrossRef102
R Gal, S Brodney-Folse, R Beck, Robin Gal. 2002. Corticosteroids for treating optic neuritis. .
CrossRef103
Ihab R. Dorotta, Armin Schubert. (2002) Multiple sclerosis and anesthetic implications. Current Opinion in Anaesthesiology 15:3, 365-370
CrossRef104
Alastair Compston, Alasdair Coles. (2002) Multiple sclerosis. The Lancet 359:9313, 1221-1231
CrossRef105
T. Patzold, M. Schwengelbeck, L.-M. Ossege, J.-P. Malin, E. Sindern. (2002) Changes of the MS functional composite and EDSS during and after treatment of relapses with methylprednisolone in patients with multiple sclerosis. Acta Neurologica Scandinavica 105:3, 164-168
CrossRef106
B. Mark Keegan, John H. Noseworthy. (2002) M
ULTIPLE SCLEROSIS . Annual Review of Medicine 53:1, 285-302
CrossRef107
E. M. Martínez-Cáceres, M. A. Barrau, L. Brieva, C. Espejo, N. Barberà, X. Montalban. (2002) Treatment with methylprednisolone in relapses of multiple sclerosis patients: immunological evidence of immediate and short-term but not long-lasting effects. Clinical & Experimental Immunology 127:1, 165-171
CrossRef108
Andrew S. Gurwood, Kelly A. Malloy. (2002) Giant cell arteritis. Clinical and Experimental Optometry 85:1, 19-26
CrossRef109
Gregory P. Van Stavern. (2001) Management of optic neuritis and multiple sclerosis. Current Opinion in Ophthalmology 12:6, 400-407
CrossRef110
Nicholas J. Volpe. (2001) Optic Neuritis: Historical Aspects. Journal of Neuro-Ophthalmology 21:4, 302-309
CrossRef111
Laura J. Balcer. (2001) Clinical Outcome Measures for Research in Multiple Sclerosis. Journal of Neuro-Ophthalmology 21:4, 296-301
CrossRef112
Laura J. Balcer. (2001) Evidence-based neuro-ophthalmology: advances in treatment. Current Opinion in Ophthalmology 12:6, 387-392
CrossRef113
Michael Schumacher, Rachida Guennoun, Gilles Mercier, Franck Désarnaud, Pascale Lacor, Jesus Bénavides, Badia Ferzaz, Françoise Robert, Etienne Emile Baulieu. (2001) Progesterone synthesis and myelin formation in peripheral nerves. Brain Research Reviews 37:1-3, 343-359
CrossRef114
Alexandros Tselis. (2001) Acute disseminated encephalomyelitis. Current Treatment Options in Neurology 3:6, 537-542
CrossRef115
(2001) Interferon β-1a for optic neuritis patients at high risk for multiple sclerosis. American Journal of Ophthalmology 132:4, 463-471
CrossRef116
Jenn-Chyuan Wang, Sharon Tow, Tin Aung, Su-Ann Lim, James F Cullen. (2001) The presentation, aetiology, management and outcome of optic neuritis in an Asian population. Clinical and Experimental Ophthalmology 29:5, 312-315
CrossRef117
Colum A Gorman, James A Garrity, Vahab Fatourechi, Rebecca S Bahn, Ivy A Petersen, Scott L Stafford, John D Earle, Glenn S Forbes, Robert W Kline, Erik J Bergstralh, Kenneth P Offord, Diana M Rademacher, Nancy M Stanley, George B Bartley. (2001) A prospective, randomized, double-blind, placebo-controlled study of orbital radiotherapy for Graves’ ophthalmopathy. Ophthalmology 108:9, 1523-1534
CrossRef118
Laura J. Balcer. (2001) Optic neuritis. Current Treatment Options in Neurology 3:4, 389-398
CrossRef119
Ralf Gold, Frank Buttgereit, Klaus V Toyka. (2001) Mechanism of action of glucocorticosteroid hormones: possible implications for therapy of neuroimmunological disorders. Journal of Neuroimmunology 117:1-2, 1-8
CrossRef120
R Pokroy, G Modi, D Saffer. (2001) Optic neuritis in an urban black African community. Eye 15:4, 469-473
CrossRef121
Danielle T. Long, Roy W. Beck, Pamela S. Moke, R. Clifford Blair, Kevin E. Kip, Robin L. Gal, Barrett J. Katz. (2001) The SKILL Card Test in Optic Neuritis: Experience of the Optic Neuritis Treatment Trial. Journal of Neuro-Ophthalmology 21:2, 124-131
CrossRef122
Mats Soderstrom. (2001) Optic neuritis and multiple sclerosis. Acta Ophthalmologica Scandinavica 79:3, 223-227
CrossRef123
Bertil Lindblom. (2001) Big is significantly more beautiful?. Acta Ophthalmologica Scandinavica 79:3, 221-222
CrossRef124
Heather J. MacLean, Mark S. Freedman. (2001) Immunologic therapy for relapsing-remitting multiple sclerosis. Current Neurology and Neuroscience Reports 1:3, 277-285
CrossRef125
Giancarlo Comi, Massimo Filippi, Frederik Barkhof, Luca Durelli, Gilles Edan, Oscar Fernández, Hans-Peter Hartung, Pierrette Seeldrayers, Per Soelberg Sørensen, Marco Rovaris, Vittorio Martinelli, Otto R Hommes. (2001) Effect of early interferon treatment on conversion to definite multiple sclerosis: a randomised study. The Lancet 357:9268, 1576-1582
CrossRef126
Sanjay Sharma. (2001) Levels of Evidence. Evidence-Based Eye Care 2:1, 5-6
CrossRef127
Stanley H. Shapiro, Charles Weijer, Benjamin Freedman. (2000) Reporting the study populations of clinical trials. Journal of Clinical Epidemiology 53:10, 973-979
CrossRef128
Noseworthy, John H., Lucchinetti, Claudia, Rodriguez, Moses, Weinshenker, Brian G., . (2000) Multiple Sclerosis. New England Journal of Medicine 343:13, 938-952
Full Text129
P. CHETONI, L. PANICHI, S. BURGALASSI, U. BENELLI, M.F. SAETTONE. (2000) Pharmacokinetics and Anti-Inflammatory Activity in Rabbits of a Novel Indomethacin Ophthalmic Solution. Journal of Ocular Pharmacology and Therapeutics 16:4, 363-372
CrossRef130
Denis Wakefield, Angela Jennings, Peter J McCluskey. (2000) Intravenous pulse methylprednisolone in the treatment of uveitis associated with multiple sclerosis. Clinical and Experimental Ophthalmology 28:2, 103-106
CrossRef131
Robert Weinstein. (2000) Therapeutic apheresis in neurological disorders. Journal of Clinical Apheresis 15:1-2, 74-128
CrossRef132
Francois A. Bethoux, Jeffrey A. Cohen. (1999) Diagnosis and Treatment of Multiple Sclerosis. Current Opinion in Orthopedics 10:6, 492-497
CrossRef133
John P. Fang, Rosalind H. Lin, Sean P. Donahue. (1999) Recovery of visual field function in the Optic Neuritis Treatment Trial. American Journal of Ophthalmology 128:5, 566-572
CrossRef134
John P. Fang, Sean P. Donahue, Rosalind H. Lin. (1999) Global visual field involvement in acute unilateral optic neuritis. American Journal of Ophthalmology 128:5, 554-565
CrossRef135
John L. Keltner, Chris A. Johnson, John O. Spurr, Roy W. Beck. (1999) Comparison of central and peripheral visual field properties in the Optic Neuritis Treatment Trial. American Journal of Ophthalmology 128:5, 543-553
CrossRef136
Jonathan D Trobe, Pamela C Sieving, Kenneth E Guire, A.Mark Fendrick. (1999) The impact of the optic neuritis treatment trial on the practices of ophthalmologists and neurologists. Ophthalmology 106:11, 2047-2053
CrossRef137
Curtis E Margo. (1999) The Placebo Effect. Survey of Ophthalmology 44:1, 31-44
CrossRef138
Tsubota, Kazuo, Satake, Yoshiyuki, Kaido, Minako, Shinozaki, Naoshi, Shimmura, Shigeto, Bissen-Miyajima, Hiroko, Shimazaki, Jun, . (1999) Treatment of Severe Ocular-Surface Disorders with Corneal Epithelial Stem-Cell Transplantation. New England Journal of Medicine 340:22, 1697-1703
Full Text139
SCOTT E. LITWILLER, ELLIOT M. FROHMAN, PHILIPPE E. ZIMMERN. (1999) MULTIPLE SCLEROSIS AND THE UROLOGIST. The Journal of Urology 161:3, 743-757
CrossRef140
David I. Kaufman. (1999) Acute optic neuritis. Current Treatment Options in Neurology 1:1, 44-48
CrossRef141
Peter-Brian Andersson, Donald E Goodkin. (1998) Glucocorticosteroid therapy for multiple sclerosis: A critical review. Journal of the Neurological Sciences 160:1, 16-25
CrossRef142
P Baron. (1998) Cultured human monocytes release proinflammatory cytokines in response to myelin basic protein. Neuroscience Letters 252:3, 151-154
CrossRef143
Eoin P. O’Sullivan, Christopher Kennard. (1998) Ocular manifestations of neurological disease. Current Opinion in Neurology 11:1, 25-29
CrossRef144
KHURRAM BASHIR, JOHN N WHITAKER. (1998) Current immunotherapy in multiple sclerosis. Immunology and Cell Biology 76:1, 55-64
CrossRef145
Hayrettin Tumani, Wallace W Tourtellotte, James B Peter, Klaus Felgenhauer, The Optic Neuritis Study Group. (1998) Acute optic neuritis: combined immunological markers and magnetic resonance imaging predict subsequent development of multiple sclerosis. Journal of the Neurological Sciences 155:1, 44-49
CrossRef146
Lyn A Sedwick, MD. (1998) Real People, Real Problems. Survey of Ophthalmology 42:4, 373-377
CrossRef147
Dimitrios M Karussis, Oded Abramsky. (1998) Immunomodulating therapeutic approaches for multiple sclerosis. Journal of the Neurological Sciences 153:2, 239-250
CrossRef148
Wood, Alastair J.J., , Rudick, Richard A., Cohen, Jeffrey A., Weinstock-Guttman, Bianca, Kinkel, Revere P., Ransohoff, Richard M., . (1997) Management of Multiple Sclerosis. New England Journal of Medicine 337:22, 1604-1611
Full Text149
J. L. Frederiksen, T. L. Sørensen, F. T. Sellebjerg. (1997) Residual symptoms and signs after untreated acute optic neuritis. Acta Ophthalmologica Scandinavica 75:5, 544-547
CrossRef150
P. Kivisäkk, W. Tian, S. Fredrikson, H. Link, M. Söderström. (1997) Multiple sclerosis: myelin basic protein induced mRNA expression of proinflammatory cytokines in mononuclear cells is suppressed by interferon-β 1b in vitro. European Journal of Neurology 4:5, 460-467
CrossRef151
Samuel F. Hunter, Brian G. Weinshenker, Jonathan L. Carter, John H. Noseworthy. (1997) Rational Clinical Immunotherapy for Multiple Sclerosis. Mayo Clinic Proceedings 72:8, 765-780
CrossRef152
D Barnes, RAC Hughes, RW Morris, O Wade-Jones, P Brown, T Britton, DA Francis, GD Perkin, P Rudge, M Swash, H Katifi, S Farmer, J Frankel. (1997) Randomised trial of oral and intravenous methylprednisolone in acute relapses of multiple sclerosis. The Lancet 349:9056, 902-906
CrossRef153
T. Corona-Vazquez, J. Ruiz-Sandoval, N. Arriada-Mendicoa. (1997) Optic neuritis progressing to multiple sclerosis. Acta Neurologica Scandinavica 95:2, 85-89
CrossRef154
Michael L. Slavin, David A. Liebergall. (1996) Acute unilateral visual loss in the elderly due to retrobulbar optic neuropathy. Survey of Ophthalmology 41:3, 261-267
CrossRef155
P.A. McCombe, I. Nickson, Z. Tabi, M.P. Pender. (1996) Corticosteroid treatment of experimental autoimmune encephalomyelitis in the Lewis rat results in loss of Vβ8.2+ and myelin basic protein-reactive cells from the spinal cord, with increased total T-cell apoptosis but reduced apoptosis of Vβ8.2+ cells. Journal of Neuroimmunology 70:2, 93-101
CrossRef156
A. Ghezzi, V. Torri, M. Zaffaroni. (1996) Isolated optic neuritis and its prognosis for multiple sclerosis: a clinical and paraclinical study with evoked potentials. CSF examination and brain MRI. The Italian Journal of Neurological Sciences 17:5, 325-332
CrossRef157
S Atkin. (1996) Ocular and systemic manifestations of connective tissue disease: Part II, the seronegative spondyloarthropathies and vasculitides. Clinical Eye and Vision Care 8:2, 85-97
CrossRef158
M. P. Pender. (1996) Recent advances in the understanding, diagnosis and management of multiple sclerosis. Australian and New Zealand Journal of Medicine 26:2, 157-161
CrossRef159
Steven L. Galetta, Grant T. Liu, Nicholas J. Volpe. (1996) DIAGNOSTIC TESTS IN NEURO-OPHTHALMOLOGY. Neurologic Clinics 14:1, 201-222
CrossRef160
Masato Wakakura, Asako Mogi, Yoshiaki Ichibe, Keiko Okada, Haruyuki Hasebe. (1996) Leber's hereditary optic neuropathy triggered by optic neuritis. Neuro-Ophthalmology 16:6, 337-341
CrossRef161
C Dees, R Buimer, A D Dick, S. A. Newman. (1995) Ultrasonographic investigation of optic neuritis. Eye 9:4, 488-494
CrossRef162
Shalini Bansil, Stuart D. Cook, Christine Rohowsky-Kochan. (1995) Multiple sclerosis: Immune mechanism and update on current therapies. Annals of Neurology 37:S1, 87-101
CrossRef163
M. Söderström. (1995) The clinical and paraclinical profile of optic neuritis: A prospective study. The Italian Journal of Neurological Sciences 16:3, 167-176
CrossRef164
Barrett Katz, Jonathan D. Trobe, Roy W. Beck. (1995) The Optic Neuritis Treatment Trial: Implications for Clinicians. Seminars in Ophthalmology 10:3, 214-220
CrossRef165
James J. Corbett. (1994) What have the optic neuritis treatment trial and the longitudinal optic neuritis study shown us?. Journal of the Neurological Sciences 125:1, 1-2
CrossRef166
(1994) Corticosteroids, Optic Neuritis, and Multiple Sclerosis. New England Journal of Medicine 330:17, 1238-1239
Full Text167
Howard B. Dickler, Joseph F. Albright. (1994) Immunosuppression in the treatment of disease. Journal of Allergy and Clinical Immunology 93:3, 669-676
CrossRef168
G.C Ebers. (1994) Treatment of multiple sclerosis. The Lancet 343:8892, 275-279
CrossRef169
Silberberg, Donald H., . (1993) Corticosteroids and Optic Neuritis. New England Journal of Medicine 329:24, 1808-1810
Full Text170
Beck, Roy W.Cleary, Patricia A.Trobe, Jonathan D.Kaufman, David I.Kupersmith, Mark J.Paty, Donald W.Brown, C. Hendricksthe Optic Neuritis Study Group. (1993) The Effect of Corticosteroids for Acute Optic Neuritis on the Subsequent Development of Multiple Sclerosis. New England Journal of Medicine 329:24, 1764-1769
Full Text171
Christine D. Dijkstra, Chris H. Polman, Frank Berkenbosch. (1993) Multiple sclerosis: some possible therapeutic opportunities. Trends in Pharmacological Sciences 14:4, 124-129
CrossRef172
Michèle Grochowicki, Alain Vighetto, Serge Berquet, Christine Pissavin. (1993) Evolutive patterns of the visual field in optic neuritis. Neuro-Ophthalmology 13:5, 269-273
CrossRef173
(1992) Corticosteroids in the Treatment of Optic Neuritis. New England Journal of Medicine 327:4, 281-282
Full Text174
Lessell, Simmons, . (1992) Corticosteroid Treatment of Acute Optic Neuritis. New England Journal of Medicine 326:9, 634-635
Full Text
- Letters
