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oa Editorial [Hot Topic: New Avenues of Research on Multiple Sclerosis from the Perspective of Chronic Cerebrospinal Venous Insufficiency Paradigm (Guest Editor: Marian Simka)]
- Source: Reviews on Recent Clinical Trials, Volume 7, Issue 2, May 2012, p. 81 - 82
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- 01 May 2012
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Abstract
Multiple sclerosis (MS) is a chronic and debilitating neurological disease characterized by multifocal areas of inflammation, demyelination and neurodegeneration within the brain and spinal cord. At its core MS is still a big enigma and it seems that there is clearly a gap in our knowledge about this disease [1,2]. It is hoped that the discovery of venous lesions associated with MS, the so-called chronic cerebrospinal venous insufficiency (CCSVI) [3,4] will-at least partially-fill that gap. Although it is widely accepted that MS is an autoimmune disorder, which means that the disease is caused by autoimmune attack against nervous tissue antigens, therapeutic strategies that are based on this autoimmune concept fall short of success in the long-run and cannot protect the patients from the accumulation of disability [5-8]. Over the last century alternative causes of MS were discussed, including infectious, environmental, genetic, epigenetic and-importantly-vascular factors. Vascular model of MS has recently been revived by Italian vascular surgeon, Paolo Zamboni. His group demonstrated that majority of MS patients present with obstructive vascular abnormalities in the main veins draining the central nervous system: the internal jugular veins and the azygous vein. Zamboni's venous paradigm claims for significant role of these venous blockages in neurological pathophysiology [9-11]. The idea that MS may be contributable to vascular disorders is not new and stretches much back in time then the Zamboni's discovery [12]. It actually has its roots in the first description of MS by Charcot who depicted plaques characterized by vasocentric localization [13]. However, prior to CCSVI hypothesis, MS has not been suggested to result from impaired venous outflow. It should be emphasized that this new venous model of MS is not necessarily contrary to its currently ruling autoimmune paradigm. The heterogeneity of MS and a relative lack of response to immunomodulatory treatments leads to the hypothesis that the autoimmune and venous disorders may represent two sides of the same coin, with MS being a disease triggered and exacerbated by immune and vascular [14], and possibly also other mechanisms....