Guillain-Barré syndrome (GBS) and chronic inflammatory demyelinating poly-(radiculo)neuropathy (CIDP) are immune-mediated disorders with a variable duration of progression and a range in severity of weakness. Infections can trigger GBS and exacerbate CIDP. Anti-ganglioside antibodies are important, but there is debate on the role of genetic factors in the pathogenesis of these disorders. Randomized controlled trials (RCT) have shown that intravenous immunoglobulin (IVIg) and plasma exchange (PE) are effective in both GBS and CIDP. Most CIDP patients also improve after steroid therapy. Despite current treatment options, many patients have residual deficits or need to be treated for a long period of time. Therefore, new treatment trials are highly indicated. This review focuses on the current and possible new treatment options that could be guided by recent results from laboratory experiments.
[Show abstract][Hide abstract] ABSTRACT: Inflammatory demyelinating diseases comprise a spectrum of disorders affecting the myelin of the central and peripheral nervous system. These diseases can usually be differentiated on the basis of clinical, radiological, laboratory and pathological findings.
Recent studies have contributed to current awareness that inflammatory demyelinating diseases are not restricted to the adult age group, but are more common in pediatric age than previously believed. Some of pediatric inflammatory demyelinating diseases carry an unfavorable long-term prognosis but appropriate treatments can improve the outcome. The possibility of physical and cognitive disability resulting from these diseases, highlights the urgent need for therapeutic strategies for neurorehabilitation, neuroregeneration, and neurorepair.
This review discusses characteristics of primary demyelinating diseases more frequently observed in childhood, focusing on epidemiology, clinical aspects and treatments.
DNA research: an international journal for rapid publication of reports on genes and genomes 06/2010; 8(2):135-48. DOI:10.2174/157015910791233141 · 3.05 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: Conventional treatment options, including corticosteroids, intravenous immunoglobulin, or plasma exchange, often fail to treat dysimmune neuropathies, such as chronic inflammatory demyelinating polyneuropathy, multifocal motor neuropathy, and monoclonal gammopathy with its subtypes. Therefore, a significant percentage of patients require adjunctive immunosuppressive therapies. Considering that even immunosuppressive agents often are ineffective and/or associated with significant toxicities, the need for the development of safe and effective new treatment options is rising. Currently, several monoclonal antibodies (MAbs) have been tested in open-label small-sized studies or even in single cases so as to establish future directions in the therapy of diseases of the peripheral nervous system (PNS). Rituximab, an MAb targeting against the B cell surface membrane protein CD20, is the most widely used and promising MAb for the treatment of dysimmune neuropathies, especially for those in which immunoglobulin M (IgM) autoantibodies are pathogenetically involved. The efficacy of alemtuzumab, bevacizumab, and etanercept to treat various forms of dysimmune neuropathies is currently under investigation. This review looks critically at recent developments in molecularly targeted therapies for dysimmune neuropathies and also highlights areas of future research to pursue.
Molecular Medicine 05/2012; 15(7-8):283-7. DOI:10.2119/molmed.2009.00041 · 4.51 Impact Factor
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