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In a double-blind, placebo-controlled, parallel group trial, recombinant human erythropoietin (rhEPO) (48000 IU) treatment or placebo will be administered weekly i.v. for 24 weeks: weekly for 12 weeks and bi-weekly for 12 weeks. Methylprednisolone (MP) 1 g i.v. will be administered before the first and second EPO/placebo administration. The 24-week treatment period will be followed by a 24-week observation period.
Patients with primary progressive MS or secondary progressive MS without relapses during the last 1 year will be suitable for the trial. In all 56 patients will be enrolled into the study.
The primary outcome measure is the change from baseline to 24 weeks in a composite of maximum gait distance, 9-hole peg test, TRAIL making B comparing the placebo-treatment group with the EPO-treatment group.
Allocation: Randomized, Control: Placebo Control, Endpoint Classification: Efficacy Study, Intervention Model: Single Group Assignment, Masking: Double Blind (Subject, Outcomes Assessor), Primary Purpose: Treatment
Multiple Sclerosis (Primary or Secondary Progressive Phase).
Published on BioPortfolio: 2014-08-27T03:12:55-0400
The primary goal of this study is to evaluate the effects of BAF312 (siponimod) on select immune and neuronal (nerve) cells by examining laboratory specimens (blood and/or spinal fluid) at...
The purpose of this study is to determine whether MIS416 administered once weekly over 12 months is safe, tolerable, and improves a range of signs and symptoms associated with secondary pr...
Preliminary not-controlled clinical studies of the efficacy of monthly intravenous cyclophosphamide administration in secondary progressive multiple sclerosis reported encouraging results,...
The purpose of this study is to study safety and efficacy of natalizumab treatment of primary and secondary progressive multiple sclerosis. This will be done by measuring the effect of tr...
The purpose of this study is to determine whether MBP8298 is effective and safe in the treatment secondary progressive multiple sclerosis. Dirucotide is generic name for MBP8298.
No reliable indicators of the transition to the progressive course in multiple sclerosis (MS) have been identified so far. The main clinical feature of the progressive phase of MS is usually impairmen...
Multiple sclerosis (MS) is a chronic central nervous system immune-mediated disease with an important inflammatory component associated with focal demyelination and widespread neurodegeneration. In mo...
There are limited treatments for progressive multiple sclerosis. Ibudilast inhibits several cyclic nucleotide phosphodiesterases, macrophage migration inhibitory factor, and toll-like receptor 4 and c...
Currently available treatments for secondary progressive multiple sclerosis(SPMS) have limited efficacy and/or safety concerns. Adipose-mesenchymal derived stem cells(AdMSCs) represent a promising opt...
Primary progressive multiple sclerosis (PPMS) causes accumulation of neurologic disability from disease onset without clinical attacks typical of relapsing multiple sclerosis (RMS). However, whether g...
A form of multiple sclerosis characterized by a progressive deterioration in neurologic function which is in contrast to the more typical relapsing remitting form. If the clinical course is free of distinct remissions, it is referred to as primary progressive multiple sclerosis. When the progressive decline is punctuated by acute exacerbations, it is referred to as progressive relapsing multiple sclerosis. The term secondary progressive multiple sclerosis is used when relapsing remitting multiple sclerosis evolves into the chronic progressive form. (From Ann Neurol 1994;36 Suppl:S73-S79; Adams et al., Principles of Neurology, 6th ed, pp903-914)
An autoimmune disorder mainly affecting young adults and characterized by destruction of myelin in the central nervous system. Pathologic findings include multiple sharply demarcated areas of demyelination throughout the white matter of the central nervous system. Clinical manifestations include visual loss, extra-ocular movement disorders, paresthesias, loss of sensation, weakness, dysarthria, spasticity, ataxia, and bladder dysfunction. The usual pattern is one of recurrent attacks followed by partial recovery (see MULTIPLE SCLEROSIS, RELAPSING-REMITTING), but acute fulminating and chronic progressive forms (see MULTIPLE SCLEROSIS, CHRONIC PROGRESSIVE) also occur. (Adams et al., Principles of Neurology, 6th ed, p903)
A non-glycosylated form of interferon beta-1 that has a serine at position 17. It is used in the treatment of both RELAPSING-REMITTING MULTIPLE SCLEROSIS and CHRONIC PROGRESSIVE MULTIPLE SCLEROSIS.
Diseases characterized by a selective degeneration of the motor neurons of the spinal cord, brainstem, or motor cortex. Clinical subtypes are distinguished by the major site of degeneration. In AMYOTROPHIC LATERAL SCLEROSIS there is involvement of upper, lower, and brainstem motor neurons. In progressive muscular atrophy and related syndromes (see MUSCULAR ATROPHY, SPINAL) the motor neurons in the spinal cord are primarily affected. With progressive bulbar palsy (BULBAR PALSY, PROGRESSIVE), the initial degeneration occurs in the brainstem. In primary lateral sclerosis, the cortical neurons are affected in isolation. (Adams et al., Principles of Neurology, 6th ed, p1089)
A rare central nervous system demyelinating condition affecting children and young adults. Pathologic findings include a large, sharply defined, asymmetric focus of myelin destruction that may involve an entire lobe or cerebral hemisphere. The clinical course tends to be progressive and includes dementia, cortical blindness, cortical deafness, spastic hemiplegia, and pseudobulbar palsy. Concentric sclerosis of Balo is differentiated from diffuse cerebral sclerosis of Schilder by the pathologic finding of alternating bands of destruction and preservation of myelin in concentric rings. Alpers' Syndrome refers to a heterogeneous group of diseases that feature progressive cerebral deterioration and liver disease. (From Adams et al., Principles of Neurology, 6th ed, p914; Dev Neurosci 1991;13(4-5):267-73)