Multiple sclerosis (MS) has long been classified as an autoimmune disease. However, in recent years, several researchers have published studies suggesting otherwise. One of the most prominent theories revolves around the idea that a toxic or infectious injury or assault to the nervous system is responsible for the pathology in MS. According to this theory, the immune system, in turn, responds to the nervous system injury.
Experimental Autoimmune Disease
One of the criteria for an autoimmune disease is that the disease can be reproduced in animal models by injecting them with the autoantibodies responsible for the disease. However, no specific autoantibody or autoreactive T-cell directed against a self-antigen in the nervous system can passively transfer MS to experimental animals. Another requisite for a disease to be considered autoimmune is the improvement seen when immunosuppressant drugs are administered. This does not hold true in experimental MS. Nor do immunosuppressants typically result in long-term remission in patients with MS although there may be a reduction in inflammation.
Disease Course in Multiple Sclerosis
The disease course in MS is highly variable and depends on which nerve fibers are affected. Symptoms range from mild muscle weakness, fatigue and mild gait disturbances to visual disturbances (ocular myasthenia gravis), cognitive changes, emotional disturbances, and paralysis. While most patients experience cycles of relapse alternating with periods of remission, some patients experience a rapidly progressive disease course.
Rarely, sudden death can occur during the early stages of relapse. Sudden death can occur in MS if the damage (or lesion) to nerve fibers occurs in parts of the brain that control vital functions such as breathing and blood flow.
Pathology in Multiple Sclerosis
Multiple sclerosis is a neurological disorder of the nerve fibers of the central nervous system, including the brain and spinal cord. Scar tissue in the white matter of the brain leads to the formation of lesions known as plaques, which are accompanied by inflammation. John Prineas, in his studies, which began at the University of New Jersey in Newark, has demonstrated that the first stage of MS involves the destruction of the oligodendrocyte brain cells that produce myelin. Myelin is a protein that normally forms an insulating sheath around nerve fibers. Myelin facilitates the movement or conduction of electrical messages through nerve fibers. In the absence of myelin, scar tissue forms around and damages the nerve fibers.
By studying the lesion responsible for the death of a teenager with MS, Prineas and his colleagues were able to demonstrate that the lesion occurred first and the immune system changes resulted as a response to the neurological injury. In the post-mortem examination, Prineas noticed that the myelin in the lesion was still intact, and there was no evidence that the typical armada of immune system cells and molecules had migrated into the area yet. In addition, oligodendrocyte cells in various stages of cell death were observed.
Infectious Origin and Toxins
The development of multiple sclerosis tends to have a genetic predisposition, occurring more often in patients with a family history of multiple sclerosis. An environmental trigger is also suspected since most people with a family history of MS do not develop MS. Whether the trigger destroys myelin as suggested by Barnett and Prineas's observation, or launches an autoimmune response, certain environmental agents are highly associated with MS.
Suspected environmental triggers include infectious agents including mycotoxins, adenovirus (cause of the common cold), Borrelia, Epstein-Barr virus, cytomegalovirus, para-influenza viruses, and others; dietary factors, such as eating smoked meats and other products with a high nitrite content, and nutrient deficiencies, particularly low vitamin D3 levels; latitude and geographical location; and chemicals such as aspartame in artificial sweeteners, vaccines, industrial cleaners, and pesticides.
Resources:
Michael H.?Barnett, and John W. Prineas, Relapsing and Remitting Multiple Sclerosis:? Pathology of the Newly Forming Lesion, Annals of?Neurology online edition; February 23, 2004, accessed May 20, 2007.
Elaine Moore, Autoimmune Diseases and Their Environmental Triggers, Jefferson, NC: McFarland Publishing, 2002.