A Randomized, Controlled Trial of Corticosteroids in the Treatment of Acute Optic Neuritis

Beck, Roy W.; Cleary, Patricia A.; Anderson, Malcolm M.; Keltner, John L.; Shults, William T.; Kaufman, David I.; Buckley, Edward G.; Corbett, James J.; Kupersmith, Mark J.; Miller, Neil R.; Savino, Peter J.; Guy, John; Trobe, Jonathan D.; McCrary, John A.; Smith, Craig H.; Chrousos, Georgia Antonakou; Thompson, H. Stanley; Katz, Barrett; Brodsky, Michael C.; Goodwin, James; Atwell, Constance W.

doi:10.1056/nejm199202273260901

Cited by 1,185 publications

(770 citation statements)

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“…Intravenous high dose methylprednisolone therapy, 1 g daily for 3 days, followed by oral prednisone therapy (1 mg per kg of body weight per day for 11 days) also accelerates recovery from acute optic neuritis compared to placebo. 24 The optimal dose of i.v. methylprednisolone therapy is unclear.…”

Section: Corticosteroid Therapymentioning

confidence: 99%

“…high dose methylprednisolone, oral prednisone alone in standard (intermediate) doses (1 mg per kg per day for 14 days) has no beneficial effect on acute optic neuritis compared to placebo and may increase the risk of new episodes of optic neuritis. 24 One study has reported that oral intermediate dose methylprednisolone therapy alone for 21 days (48 mg daily for 7 days, followed by 24 mg daily for 7 days and then 12 mg daily for 7 days) is equally as effective as i.v. high dose methylprednisolone therapy (1 g daily for 3 days) for the treatment of acute relapses of MS. 26 The authors recommended that oral intermediate dose corticosteroid therapy be used instead of i.v.…”

Section: Corticosteroid Therapymentioning

confidence: 99%

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Recent progress in the diagnosis and treatment of multiple sclerosis

Pender

1999

Journal of Clinical Neuroscience

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Magnetic resonance imaging (MRI) now provides valuable diagnostic and prognostic information for the management of multiple sclerosis (MS) but the diagnosis still largely rests on the clinical features of central nervous system (CNS) lesions disseminated in time and place. Recent histological and MRI studies indicate that extensive axonal damage can occur in MS, even early in the disease course, and is likely to be an important cause of accumulating disability. Several immunomodulating agents have now been shown to have beneficial effects in MS. High dose intravenous or high dose oral methylprednisolone therapy accelerates recovery from attacks of relapsing-remitting MS, but at present there is no convincing evidence that standard dose (intermediate dose) oral corticosteroid therapy is beneficial for such attacks. Interferon beta, copolymer 1 (glatiramer acetate) and i.v. immunoglobulin therapy each significantly reduce the frequency of attacks of relapsing-remitting MS. Interferon beta also inhibits the progression of disability in relapsing-remitting MS and secondary progressive MS, but its effect on primary progressive MS is unknown. Oral low dose methotrexate therapy slows the progression of disability in secondary progressive MS and possibly in primary progressive MS, but it is likely that the currently used dosage (7.5 mg weekly) is suboptimal. Further research is needed to determine the optimal doses and combinations of the above therapies in MS and to develop better therapies, particularly for primary progressive MS.

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Section: Corticosteroid Therapymentioning

confidence: 99%

Section: Corticosteroid Therapymentioning

confidence: 99%

Recent progress in the diagnosis and treatment of multiple sclerosis

Pender

1999

Journal of Clinical Neuroscience

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“…Among patients with severe ON, an inverse relationship between pRNFL thickness (i.e., optic disc edema) and visual acuity was observed for nontreated patients, which is in agreement with previous findings (Beck et al., 1992; Henderson et al., 2010; Malik et al., 2014). The possible mechanism for the steroid treatment effect may involve a suppression of the inflammation associated with acute ON, which in turn may limit the neuronal damage and accelerate visual function recovery (Beck et al., 1992; Kapoor et al., 1998; Sellebjerg, Nielsen, Frederiksen, & Olesen, 1999).…”

Section: Discussionmentioning

confidence: 99%

“…The possible mechanism for the steroid treatment effect may involve a suppression of the inflammation associated with acute ON, which in turn may limit the neuronal damage and accelerate visual function recovery (Beck et al., 1992; Kapoor et al., 1998; Sellebjerg, Nielsen, Frederiksen, & Olesen, 1999). This is supported by the current study's observation that nontreated patients experienced an early reduction in the pRNFL thickness and a delayed improvement of visual acuity and color mixing.…”

Section: Discussionmentioning

confidence: 99%

“…Optic neuritis has several pathophysiological similarities with MS (Frohman et al., 2008), and treatment with high doses of methylprednisolone (steroid) has been shown to alleviate symptoms and accelerate recovery in both disorders (Beck et al., 1992; Brusaferri & Candelise, 2000; Miller et al., 2000). However, the time of initiation of treatment after symptom presentation may be important for the effect, for instance, the earlier the treatment is initiated there may be a chance for protecting visual function and retinal cell layers (Nakamura et al., 2010; Plant, Sibtain, & Thomas, 2011).…”

Section: Introductionmentioning

confidence: 99%

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Time to steroid treatment in severe acute optic neuritis

et al. 2018

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ObjectivesSteroid treatment can accelerate visual recovery in patients with optic neuritis (ON), but it is unknown whether the timing of the start of treatment influences the outcome. The main purpose of this observational study was to assess the effect of early onset steroid treatment of ON on visual prognosis and retinal morphology.MethodsForty‐nine patients with acute mild/moderate (n = 21) or severe (n = 28) ON, and an equal number of healthy controls were enrolled. Patients with severe ON either received early onset steroid treatment (initiated within 1 week of presentation with visual loss) (n = 9), late‐onset treatment (initiated after 1 week) (n = 13), or no treatment (n = 6). Visual function and retinal morphology was studied after 6 and 12 months.ResultsAll measures of visual function had improved after 6 months (p ≤ 0.03) in the three groups with severe ON. This was not the case for Rayleigh match setting range (SR) in the nontreated group (p = 0.24), or for SR (p = 0.08) and latency to P100 of visual evoked potential (p = 0.08) in the late‐onset treated group. After 12 months, further improvement occurred in the nontreated and late‐treated groups, but not in the early treated group. Macular retinal nerve fiber layer (mRNFL) and ganglion cell plus inner plexiform layer had decreased significantly (p ≤ 0.001) in all three groups with severe ON after 6 months. After 12 months, only mRNFL had further significantly decreased and only in the late‐onset treated group (p = 0.02).ConclusionThe beneficial effects of early onset steroid treatment of ON is limited to a few months whereas the long‐term prognosis is independent of the timing of treatment.

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