Multiple sclerosis etiology

An inconvenient but more descriptive name for this MS is intermittent, patchy demyelination. This clumsy term makes clear that multiple sclerosis is unlikely to be a single entity in terms of cause (etiology) or disease mechanisms (pathophysiology). In principle, any conditions or combination of conditions that lead to intermittent, patchy demyelination are forms of multiple sclerosis. If a clear cause can be identified, the condition is by convention not referred to as multiple sclerosis. The disease is therefore by definition of unclear etiology. The neurology literature of the last 100 years contains confident declarations that multiple sclerosis has been proven to be a viral disease, that it has been proven not to be a viral disease, that it has been proven to be an immune disease, that immune mechanisms in multiple sclerosis have been shown to be secondary to the disease process, and so on. 

Lucchinetd CF, Briick W, and Lassmann H (2003) Neuroimmuno-logic Mechanisms in die Etiology of Multiple Sclerosis. In Neuroinflammation Mechanisms and Management (Wood PL, ed), pp 359—377. Totowa, N.J. Humana Press. 

Multiple sclerosis (MS) is a disease of unknown etiology that primarily affects the myelin membrane and/or the oligoden-droglia (myeHn-producing cells) within the central nervous... 

Siblerud RL and Kienholz E. 1994. Evidence that mercury from silver dental fillings may be an etiological factor in multiple sclerosis. Sci Total Environ 142(3) 191-205. 

Multiple Sclerosis is a disease of unknown etiology or therapy. The article brought up the other day in the newspaper stating that there may have been established a viral etiology for multiple sclerosis should not be too surprising, in as much as that has been the concept for the past 20 or 30 years. To undertake a treatment using oxidative therapy should not otherwise be too unusual, since oxidative therapy is known to be anti-viral. 

The etiology of multiple sclerosis (MS) is unknown, and currently there is no cure. 

Most patients with overactive bladder and UUI have no identifiable underlying etiology. In fact, the most common cause of bladder overactivity and UUI is idiopathic. Clearly identifiable risk factors for UUI include normal aging, neurologic disease (including stroke, Parkinson s disease, multiple sclerosis, and spinal cord injury), and bladder outlet obstruction (e.g., due to benign prostatic hyperplasia [BPH] or prostate cancer). 

There has been considerable interest in the role of Epstein-Barr virus in the etiology of several autoimmune diseases, particularly systemic lupus erythematosus and multiple sclerosis. Epstein-Barr virus is a common infection. Most people (90% or more) are infected, without symptoms or with only mild, nonspecific symptoms, during childhood. When people are exposed as teenagers or as adults, however, infection may result in mononucleosis. Of importance with respect to autoimmune diseases, Epstein-Barr virus infects B cells and results in a latent infection. A close similarity between a peptide sequence in the Epstein-Barr nuclear antigen-1 and a sequence in the Sm autoantigen, one of the autoantibodies seen in systemic lupus erythematosus, has been reported (Sabbatini et al., 1993). In addition, several epidemiological studies have demonstrated strong associations between exposure to Epstein-Barr virus, as demonstrated by virus-specific IgG or IgA antibodies, and risk of systemic lupus erythematosus in children (James et al., 1997) and adults (James et al., 2001 Parks et al., 2005). 

Sjogren syndrome. Chronic inflammatory autoimmune disease of the exocrine glands of unknown etiology. Its primary symptoms are keratoconjunctivitis sicca and xerostomia. Two types of Sjogren syndrome are distinguished a primary (isolated) type and a secondary type associated with another underlying autoimmune disease (e.g. rheumatoid arthritis, systemic lupus erythematosus, systemic sclerosis, primary biliary cirrhosis, autoimmune hepatitis, multiple sclerosis, thyroiditis, autoimmune, etc.). Ro/SS-A and La/SS-B autoantibodies are used as classification criteria. 

Clinical herbalists have reported differing information on the use of Echinacea species in autoimmune conditions. Exacerbation of symptoms has been reported in systemic lupus, ulcerative colitis (autoimmune etiology uncertain), glomerular nephritis, and multiple sclerosis. In "some" cases, effects reoccurred on rechallenge. In rheumatoid arthritis, treatment with Echinacea species for 10 days did not exacerbate the condition (Upton and Graff 2007). A survey of 25 medical herbalists indicated that 12 had used Echinacea species in persons with autoimmune conditions. Of these 12, 11 indicated a beneficial effect and 1 indicated a worsening of symptoms (Upton and Graff 2007). 

The connective tissue diseases (CTDs) are a heterogeneous group of immuno-logically mediated inflammatory conditions of unknown etiology, accompanied by diverse autoantibodies and affecting multiple organ systems. In adults, the more frequent CTDs comprise rheumatoid arthritis (RA), systemic sclerosis (SSc), Sjogren s syndrome (SjS), systemic lupus erythematosus (SLE), polymyositis/ dermatomyositis (PM/DM), and mixed CTD (MCTD). 

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