Although MS was first described over 130 years ago, the exact cause(s) still remain a mystery, and there is no known cure. The term "multiple sclerosis" refers to two characteristics of the disease: the numerous affected areas of the brain and spinal cord producing multiple neurologic symptoms that accrue over time, and the characteristic plaques or sclerosed areas that are the hallmark of the disease. MS is usually diagnosed in individuals between the ages of 20 and 45 years (although cases in children have been reported), with peak incidence occurring in the fourth decade.(1)

MS is, in general, a disease of temperate climates. Interestingly, in both hemispheres, its prevalence increases with distance from the equator. The highest known prevalence (250 per 100,000) occurs in the Orkney Islands, located north of the mainland of Scotland. Multiple sclerosis is also common in Scandinavia and throughout northern Europe.(2) Prevalence seems to be higher in Caucasians than other racial groups. MS is extremely rare in Japan and in black Africans; however, Japanese Americans and African Americans are at a significantly higher risk for developing the disease, with respective prevalence rates estimated at one-fourth and one third that of Caucasians.

There are several theories about the cause of MS. One is the autoimmune theory. In the autoimmune theory, MS results from the immune system's attack against the individual's own myelin which is a fat-like substance that forms a sheath around part of the nerves. What actually causes this to happen has not been clearly established, but it has been attributed to several factors that are involved in what the body needs to accomplish in fighting the disease.(3)

T-helper cells appear to be key initiators of myelin destruction. These cells are activated in the periphery, possibly after viral infection, and recognize myelin-associated proteins as antigens or substances that usually activate the creation of antibodies. This cellular recognition creates an inflammatory cascade where the T-helper (CD4) cells are activated. Activated T cells are able to cross the blood brain barrier and produce the autoimmune response that leads to the destruction of myelin. It is also probable that the chemicals responsible for growth regulation called cytokines are involved in the pathology of MS. A large number of pro-inflammatory cytokines have been detected in the brain, cerebrospinal fluid (CSF), and peripheral blood of MS patients. Another theory posits that a virus or combination of viruses may play a role in MS. There are several ways in which a virus could play a role in the pathogenesis of MS, including either a direct attack on myelin or stimulation of an autoimmune response.(1, 3) Antibodies to a variety of viruses such as measles, herpes simplex, and rubella have been found in the blood and of patients with MS. Recently, HHV-6, or human herpes virus-type 6, has been reported to be found in MS plaques. To date, however, no virus has been isolated consistently.

As with many of the autoimmune disorders, a look into environmental influences may play a key role in uncovering the contributing initiators to the disease process. This could include environmental toxins such as heavy metals, endotoxins from various infections, stress response, genetics, nutrient status, or any combination of the above. When damage occurs to the myelin sheath, this causes disruptions in the transmission of nerve impulses. This leads to symptoms which reflect the area of the brain that is being affected. The symptoms that result vary with individuals and with the progression of the disease.

The course of MS can take several paths, and progression of the disease is roughly divided into four categories. The first is the most benign, and is characterized by unpredictable recu