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Multiple Sclerosis - 3

Agatha M. Thrash, M.D.
Preventive Medicine

Certainly it would be well to enhance the immune mechanism by whatever means can be safely applied. A hot bath one to five times weekly, a proper diet, proper exercise, and other important aspects of healthful living are certainly worthwhile. Patients should adjust such matters as clothing, housing, and habits of life to stabilize heat loss and to prevent sudden changes in temperature. Changeable weather has been shown to be more important than either hot or cold weather in inducing symptoms. Days with the highest difference between high and low temperatures affect the symptoms greater. A warm climate and freedom from upper respiratory tract infections, coupled with much rest, appear to be helpful in the treatment of MS. Very few persons understand that chilling the extremities reduces the defense mechanisms against infection and weakens the body, increasing inflammation and slowing the body's rate of repair. No patch of chilled skin should be tolerated in a person with MS.

There are certain cells in the brain or spinal cord, known as the astrocytes, which form fibers that make a sort of scar tissue in the central nervous system. These scar cells grow in on a nerve that has had myelin damage. Heat is believed by some to loosen already formed scar tissue, and to reduce the amount of inflammation so that scar tissue formation will be less.

There are some cases of MS, which have been thought to have started during periods of exercising. Yet the benefits of exercise in the treatment of MS have been outlined. We suggest that the patient should not emphasize exercise when the disease is in an acute stage. With chronic disease, however, exercise should be promoted.

THE DIAGNOSIS OF MS

MS is characterized by attacks, which last a few days or a week or so and recur about once a year, tending to be more frequent as the disease progresses. Some individuals will be totally incapacitated within six months of the onset. At the beginning a patient may experience only one "attack" in two or three years. MS does not appreciably shorten the life span in most patients unless a serious complication arises. The average age of onset is 29.9 years. There is no laboratory test that confirms the presence of MS, and the diagnosis is made by the meticulous exclusion of all other disorders that could cause the neurologic defects seen.

MS may be due to a slow virus that acts somewhat after the fashion of polio. In 50 MS patients, exposure to household pets was higher than in 50 control subjects not having MS. Antibodies to canine distemper virus show higher titers in patients with MS than in controls who do not have MS. Canine distemper virus is related to human measles virus. Measles virus particles have been found in some individuals with MS, but most authorities believe there is insufficient evidence for accepting this hypothesis. That virus is involved in the disease, however, seems to be a strong possibility. The use of vaccinations and other sera as a cause of MS has been suggested by the fact that there is often the onset of MS or an exacerbation of MS following the use of a vaccine or some kind of serum.

THE CAUSE OF MS

The rate of MS is higher than as been previously estimated. In Canada the previous estimation was 40 per 108,000 but now appears to be between 110-133 cases per 168,000 population in Vancouver. There are twice as many women as men. Over 50% of the patients first resided on a farm, as compared with 31% in a town and 18% in a city. These percentages correlate fairly well with the expected exposure to milk between rural and urban population groups.

The disease is more common in the higher latitudes. Those parts of Europe and America north of the 40th parallel have more MS. The location of a person's childhood determines the risk one has to develop the disease. Persons habituated to tobacco or those who are exposed to smoke secondhand tend to get some of the central nervous system symptoms of MS.

BIBLIOGRAPHY ON MULTIPLE SCLEROSIS

Modern Medicine, December 15, 1577, p. 11-13.

Journal of the American Dietetic Association, Vol. 36, pp. 322-325, April 1960.

Nutrition Today, November-December 1977, p. 34.

British Medical Bulletin, Vol. 33(1), pp. 47-83, January 1977.

Archives of Neurology, Vol. 23, pp. 460-474, November 1970.

The Lancet, October 5, 1974, p. 831.

British Medical Journal, Vol. 2, pp. 1390-1391, 1978.

Archives of Neurology, Vol. 31, pp. 267-272, 1974.

Postgraduate Medicine, Vol. 59, pp. 219-221, May 1976.

Annals of Neurology, Vol. 6(5), p. 456, November, 1979.

The Physical Therapy Review, Vol. 39(5), pp. 297-299, May 1955.

Mount Sinai Journal of Medicine, (New York), Vol. 41, pp. 127-130, Jan/Feb. 1974.

Brain Research, Vol. 36, pp. 133-151, January 14, 1977.

Physical Therapy Review, Vol. 8, pp. 333-334, May 1958.

The Medical Journal of Australia, October 12, 1963, p. 612-614.

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