Relapsing–Remitting Multiple Sclerosis –Current Treatment Options and Perspectives for the Future
Relapsing–Remitting Multiple Sclerosis –Current Treatment Options and Perspectives for the Future
European Neurological Review, 2010; 5(1): 78–82
US Neurology, 2010;6(1):64–8
Abstract
Multiple sclerosis (MS) is the most prevalent demyelinating condition of the central nervous system and produces significant disability over time. For many years it was considered to be an untreatable disease, but great advances have been made in the treatment of MS in the last 20 years. There are currently six US Food and Drug Administration (FDA)-approved disease-modifying agents for the relapsing form of the disease. We review in detail these medications and the pivotal trials leading to their approval. We will briefly review non-FDA-approved medications already used in MS. We will also discuss some of the medications currently being studied in phase II and III trials that are not yet approved for use in MS.
Keywords
Multiple sclerosis, relapsing–remitting, treatment, clinical trials
Disclosure: Alex Rae-Grant has been a speaker for Biogen Idec, Inc. and Teva Neurosciences within the past year and is participating in several industry-sponsored clinical trials. Daniel Ontaneda has no conflicts of interest to declare.
Received: 4 May 2010 Accepted: 28 June 2010 Citation: European Neurological Review, 2010;5(1):78–82
Correspondence: Alex Rae-Grant, Mellen Center for Multiple Sclerosis, U-10, Cleveland Clinic, 9500 Euclid Ave, Cleveland, OH 44195, US. E: rae-gra@ccf.org
Basic Concepts of Multiple Sclerosis
Multiple sclerosis (MS) is a relapsing inflammatory disease of the central nervous system. It is marked pathologically by discrete areas of demyelinated brain tissue in the white matter with accompanying inflammation.1 It is now evident that axonal loss accompanies demyelination early on in the disease process.2 Cortical pathology may be as important as white-matter changes in MS.3
MS has been modelled as an autoimmune disorder mediated by T-cell responses.4,5 A chemokine response by T cells mediates activation of macrophages and microglial cells, which in turn are the main effectors of myelin destruction.6,7 B-cell activity has also been implicated in the pathogenesis of MS. B cells may sustain T-cell activation.8 Neurodegeneration also occurs, especially in the progressive phase of the disease.9 Different inflammatory and neurodegenerative processes govern tissue injury in MS.10,11 Multiple pharmacological pathways can be targeted to potentially treat MS. It is possible that differing pathological processes in different lesion types explain the variability in clinical response to medications.12 The occurrence of new MS symptoms is thought to be the result of new lesion formation, which has been documented in several serial imaging studies.13 However, there is a discrepancy between the clinical and radiological picture in MS. New magnetic resonance imaging (MRI) lesions form five to 10 times as often as there are new clinical events.14 It is for this reason that MRI has been used as a surrogate marker of efficacy in MS trials.
Clinical Symptoms and Diagnosis of Relapsing–Remitting Multiple Sclerosis
MS can occur in both relapsing and progressive forms. The most common presentation of MS includes an initial relapsing illness followed by a later progressive course.15 Eighty per cent of patients initially diagnosed with MS have a relapsing form.16 Currently, clinical criteria for establishing a diagnosis of relapsing MS require the presence of two episodes of demyelination separated in time and in space.17 Clinical information alone is sufficient to establish a diagnosis; however, when criteria for dissemination in time and space cannot be met on clinical grounds alone, MRI and cerebrospinal fluid (CSF) studies may be used to diagnose MS.
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Multiple sclerosis, relapsing–remitting, treatment, clinical trials
