High‐dose intravenous methylprednisolone in the treatment of multiple sclerosis

Durelli, Luca; Cocito, Dario; Riccio, Anna Maria; Barile, Carmen; Bergamasco, B.; Baggio, Gianfranco; Perla, Francesco Massimo; Delsedime, M; Gusmaroli, Graziano; Bergamini, L

doi:10.1212/wnl.36.2.238

Cited by 169 publications

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“…High dose methylprednisolone therapy accelerates recovery from relapses of multiple sclerosis (Durelli et al, 1986;Milligan et al, 1987). In optic neuritis, low-dose oral prednisone does not accelerate clinical recovery and may lead to an increased risk of relapse, whereas treatment with high dose methylprednisolone accelerates recovery and may reduce the risk of relapse (Beck et al, 1992).…”

Section: Discussionmentioning

confidence: 99%

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

McCombe

Nickson

Tabi

et al. 1996

Journal of Neuroimmunology

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We have studied the effects of corticosteroid treatment on the numbers of lymphocytes obtained from the spinal cords of Lewis rats with acute experimental autoimmune encephalomyelitis (EAE) induced by inoculation with myelin basic protein (MBP) and adjuvants. Flow cytometric studies showed that treatment with dexamethasone (4 mg/kg) 8-12 h prior to study on day 14 after inoculation resulted in a reduction in the numbers of CD5 + , TCR + and V 8.2 + cells in the spinal cord. Limiting dilution analysis indicated that dexamethasone treatment 12 h prior to study on day 12 after inoculation reduced the frequencies of MBP-reactive and interleukin-2-responsive lymphocytes in the spinal cord to low levels, but reduced the frequency of concanavalin-A-responsive lymphocytes to a lesser extent. Using propidium iodide staining of nuclear chromatin we also studied lymphocyte apoptosis. Greater numbers of apoptotic cells were found in the cells extracted from the spinal cords of rats, examined on day 14, that had been treated 1-12 h previously with dexamethasone, than in saline-treated controls. This increased level of apoptosis was observed in the CD5 + and TCR + cell populations. At 1-4 h after dexamethasone treatment there was a reduction in the selective apoptosis of V 8.2 + cells that normally occurs during spontaneous recovery from EAE. Therefore apoptosis of V 8.2 + cells cannot explain the reduction in the numbers of V 8.2 + cells and MBP-reactive cells in the CNS after dexamethasone treatment. By 8-12 h after dexamethasone treatment the selectivity of the apoptotic process was restored. These studies suggest that a reduction in the number of T-lymphocytes in the central nervous system contributes to the beneficial effects of corticosteroids in EAE.

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Section: Discussionmentioning

confidence: 99%

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

McCombe

Nickson

Tabi

et al. 1996

Journal of Neuroimmunology

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“…Durelli et el. 23 have also shown that i.v. high dose methylprednisolone therapy accelerates recovery from attacks of relapsing-remitting MS, but they used a more complicated regimen of 15 mg per kg per day for 3 days followed by i.v.…”

Section: Corticosteroid Therapymentioning

confidence: 91%

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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“…Synthetic IV steroids, and rarely oral forms, are the most commonly used drugs in MS relapse. There is Level I evidence regarding accelerated clinical improvement in MS relapse provided by steroids (50,51,52).…”

Section: Adrenocorticotropic Hormone and Steroidsmentioning

confidence: 99%

Relapses in Multiple Sclerosis: Definition, Pathophysiology, Features, Imitators, and Treatment

Sevim¹

2016

tnd

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Relapse in multiple sclerosis (MS) is defined as a neurologic deficit associated with an acute inflammatory demyelinating event that lasts at least 24 hours in the absence of fever and infection. Myelinoclasis and axonal transection occur in relapses. Diagnosis, prognosis, treatment, and many other features of the disease are directly related to the relapses. MS starts as the relapsing-remitting (RRMS) form in 85% of patients. A large number of relapses in the first years, polysymptomatic relapses, and pyramidal system, brain stem, and spinal cord involvement are signs of a poor outcome. The average frequency of relapses is approximately one per year during the first years of RRMS. The frequency of relapses increases during systemic infections, psychological stress, and in the first 3 months after birth. Seventy-five percent of relapses are monosymptomatic. Pseudo-relapses and paroxysmal symptoms are distinguished from relapses by their sudden onset, sudden termination, and shorter duration. Contrast enhancement is valuable in imaging, but undetectable in most relapses. The regression in the first few weeks of relapses is explained by reduction of the edema, and by remyelination in the following months. Relapses and their features are also among the main determinants of treatment. High-dose methylprednisolone and early treatment with adrenocorticotropic hormone reduce post-relapse disability and shorten the duration of relapses. Plasmapheresis is a good option for patients who do not respond to steroid treatment. Identification of relapses by patients and physicians, distinguishing them from imitators, proper evaluation, treatment when necessary, and monitoring the results are of great importance for patients with MS. The educational levels of patients and physicians regarding these parameters should be increased. Well-designed studies that evaluate the long-term effect of relapse treatment on disability are needed. Keywords: Multiple sclerosis, relapse, definition, features, treatmentMultipl sklerozda (MS) ateş ve enfeksiyon yokken en az 24 saat süren akut enflamatuvar demiyelinizan süreçle uyumlu nörolojik defisitler atak olarak tanımlanır. Ataklarda miyelin yıkımı ve aksonal transeksiyon oluşur. Hastalığın tanısı, seyri, tedavisi ve diğer birçok özelliği ataklarla doğrudan ilişkilidir. MS hastaların %85'inde atak ve düzelmelerle giden formda başlar. İlk yıllarda atak sayısının fazla olması, atakların birden çok semptomla ortaya çıkması, motor sistemi içermesi, beyin sapı ya da spinal atak formunda olması kötü prognoz göstergeleridir. Atak ve düzelmelerle giden formun başlangıç yıllarında yıllık ortalama atak sayısı 1'dir.Sistemik enfeksiyonlar, psişik stres ve postpartum 3 aylık dönemde atak sıklığı artar. Atakların %75'i monosemptomatiktir. Yalancı ataklar ve paroksismal bulgular genellikle ani başlayıp ani sonlanmalarıyla ve kısa sürmeleriyle ataklardan ayrılır. Görüntülemede kontrast tutulumu değerlidir, ancak atakların çoğunda saptanamaz. Ataklarda ilk birkaç hafta içindeki düzelme ödem etkisinin azalması...

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High‐dose intravenous methylprednisolone in the treatment of multiple sclerosis

Cited by 169 publications

References 0 publications

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

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

Recent progress in the diagnosis and treatment of multiple sclerosis

Relapses in Multiple Sclerosis: Definition, Pathophysiology, Features, Imitators, and Treatment

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