What Causes Multiple Sclerosis?

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What Causes Multiple Sclerosis?

As with Parkinson's and Alzheimer's disease, which are also neurodegenerative disorders, it seems likely that MS may result from more than one cause. there is some evidence that it may have a genetic component, since in some instances, more than one close relative may be affected. Sixty years ago, one investigator was able to collect 84 references in the literature to support a familial tendency. It is estimated that up to 10 percent of patients have a near relative with the disease. This is much lower than is seen with other heritable disorders, and its occurrence in successive generations is uncommon. However, in one study, the parents, siblings, nephews and nieces of MS patients had a much higher incidence of other nervous and mental disorders compared to the relatives of a control group admitted for fractures. Perhaps MS is simply one manifestation of some familial neuropathic disorder that is expressed in different ways, depending on the genes that are involved.

Some research studies support the theory that multiple sclerosis can be linked to several genes. In one recent study of 75 families with at least two MS members, American and French researchers identified 19 chromosome locations believed to house the genes that determine who will develop MS and who will not. As the lead author commented "This study demonstrates that there is no one gene responsible for causing multiple sclerosis.....We believe it is the interaction of several genes, potentially triggered by an environmental stimulus." As occurs in many other disorders, that stimulus could be emotional stress, which pulls the trigger of a loaded gun.

However, it might also be an infection, and there is good evidence that a herpes virus may be responsible for some cases. In 1995, researchers first identified traces of herpesvirus 6 (HHV-6) in the genetic material of brain tissue from MS patients. Since then, traces of the active human virus have been found in the spinal fluid of three out of seven patients in one study, and in the lymph nodes of three of four in another. Further support comes from a very recent NIH report showing that 73 percent of patients with chronic MS had an increased antibody response to HHV-6 antigen, compared to only 18 percent of matched controls.

About 30 percent of these MS patients had active virus particles in their blood, while none was found in the other participants. Traces of HHV-6 were detected in the diseased brain plaques of a cadaver with MS, but not in normal (non-diseased) brain tissue. Since experimental HHV-6 infections of the central nervous system have been shown to damage the myelin sheath, there is good reason to suspect a causal relationship.

Herpes infections are extremely common, but these viruses characteristically lie dormant in the cell, and produce no signs or symptoms unless triggered by some stress that lowers the body's resistance. Common examples of this are seen in patients with recurrent herpes of the lips or genitalia. It is estimated that nine out of ten American adults harbor the HHV-6 virus, suggesting that many MS cases could be due to infection with this organism. This might also explain why emotional stress and depression can precipitate or aggravate the disease, since both have been shown to lower immune defenses. HHV-6 infection responds to antiviral medications like acyclovir, and trials are under way to determine whether a course of therapy might result in clinical improvement. If results are positive, a vaccine might be considered.

The participation of the immune system seems clear from microscopic and other studies of MS lesions. They show macrophages, plasma cells, T-lymphocytes, and other immune components in fresh plaque lesions. These characteristics suggest a cell-mediated immune response directed against some protein component of myelin. What initiates this, and why it is not prevented or held in check by suppressor cell activity, or other normal balancing mechanisms remains to be determined. The specific antigen against which the immune response is directed has not yet been identified. In addition, it is not clear whether most or any of these immunological responses are the cause of the damage to myelin or the result of it. Attempts have therefore been made to try to develop an animal model of MS that might clarify these relationships, as has been possible with disseminated lupus erythematous. The difficulty is that it would be extremely difficult to replicate the wide variation in signs and symptoms seen in MS. And drugs that might help some complaints, could aggravate others.

The American Institute of Stress.

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