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MS -- What Is It, Who Gets It, and Why?
If ever a disease could be called fascinating, it would be multiple sclerosis. The volumes of available facts and figures give it an intriguing identity. We know, for example, that in the United States almost triple the number of MS cases are found above the thirty-seventh parallel (running from Santa Cruz, California, to Newport News, Virginia) as are found below it. In certain areas of the world, not a single case of MS has ever been reported. Certain races appear to be relatively immune. Some studies show that women from the upper echelons of society, aged twenty-five to thirty-five, form a noticeably high percentage of MS cases, a fact suggesting that MS is some kind of "elitist" disease. Why do all these facts consistently hold true? Scientists today are closing in on the answers to this and other perplexing questions.
We now know what MS is, who gets it, and when, where, and possibly why. Some aspects of the disease, however, such as its cause, still remain a mystery. In fact, a researcher once compared it to the old Indian legend in which a group of blind men encounter an elephant. They can each describe the part of the animal they have touched, but none of them can explain the total picture. This is the case with MS.
Still, scientists are closer than ever to describing the whole MS elephant. In January 1985 a team of researchers from Stanford University announced that they had wiped out a disease in mice that is similar to MS. We are truly on the threshold of discovery.
Among the general public, MS is one of the most misunderstood diseases. Just think of the public service slogan: MS, the Crippler of Young Adults. That's a pretty gloomy label for a disease where 75 percent of those who have it will never need a wheelchair. Whether you've just been diagnosed as having MS or you've lived with it a while -- or even if the MS patient is someone you happen to care for -- it's important to know that misinformation is a greater enemy than the disease itself. So, while we can't provide you with a cure in these pages, we can give you the best tools to beat MS -- the facts.
The MS story begins almost like a fairy tale, because once upon a time there was no MS -- not a case was known to medicine. Then, in the 1830s, two doctors in Europe began to write of a "new" disease, one never seen before. Jean Cruveilhier, professor of pathological anatomy in the Faculty of Medicine at the University of Paris, is credited with the first clinical report in 1835. During routine autopsies, he observed some "brown patches" in the central nervous system and described them to the medical community. Simultaneously, Robert Carswell was commissioned by the museum at University College in London to show a collection of sketches of the central nervous system that he had drawn as a young medical student. Among the two thousand color pictures he had drawn while observing autopsies were some that included unexplained "spots." In 1838, Carswell published an atlas of his drawings, along with written descriptions. In one chapter he wrote, "The anterior surface of the spinal cord presented a number of spots, from a quarter of an inch to half an inch in breadth."
Both Cruveilhier and Carswell only observed the effects of the disease during autopsies. A German doctor named Friedrich Theodor von Frerichs is given credit for the first diagnosis of the disease in a living subject. In 1849 he published a report more similar to the modern concept of MS. He wrote that it is more common in younger patients, that it is characterized by slow progression, that one side of the body is affected and then the other, and so on.
At about this time, too, reports of this disease started to appear outside medical literature. Perhaps the most famous historical case is recorded in the diary and letters of Sir Augustus Frederick d'Este (1794-1848), a grandson of George III of England and a cousin of Queen Victoria. In his published papers, he described his twenty-five years with recurring symptoms that included blurred vision, loss of balance, numbness in the limbs, and paralysis.
Around the world isolated reports of this odd disease were cropping up, but it is the French neurologist lean-Martin Charcot who is credited with bringing the first clear-cut description of multiple sclerosis to the attention of the medical world. Charcot, the foremost authority on paralysis in Europe, attracted doctors from all parts of the continent to his dramatic lectures and presentations. Among his prominent students was the young Sigmund Freud, who traveled from Vienna to observe Charcot's treatment of patients with "hysterical" paralysis -- those paralyzed by emotional, not physical, problems. Charcot would actually get these patients to walk again by hypnotizing them, tricking them, or frightening them horribly. Freud, who became convinced that there were better ways to treat hysteria, ultimately went off on his own and pioneered psychoanalysis.
Still, what Charcot might have lacked in compassion he made up for in medical genius. In 1868 he identified a new disease that had previously been confused with paralysis. He was able to make his first observations of what would soon become known as multiple sclerosis right under his nose -- his own housekeeper had the disease.
On March 14, 1868, Charcot presented the clinical aspects of three cases to the French Biological Society. Soon after, he presented his own illustrations of the disease -- sketches that would appear in neurology textbooks for many generations to come. Most important, though, he was the first to correlate the "brown patches" discovered by Cruveilhier and Carswell with the symptoms of the disease he called sclérose en plaques, translated as "hardening in patches."
Because of Charcot's reputation and prominence, word of this new disease spread quickly, and the study of neurology would never be quite the same. Unfortunately, he only identified three symptoms of the disease -- the ones he observed in his maid -- and for years this led to very limited diagnosis around the world. In fact, until the 1950s the Japanese were thought to be immune to MS. They weren't immune at all; they had symptoms other than those in Charcot's literature, which was still respected as medical gospel.
The first American reports of MS began with a paper given on December 4, 1867, to the College of Physicians in Philadelphia, called "The Case of the Late Dr. C. W. Pennock." Dr. Pennock had been a physician trained both at the University of Pennsylvania and in Paris. Over a period of twenty-four years, he suffered progressive weakness and numbness in his limbs that left him unable to walk and ultimately to work. Dr. Pennock also noticed that warm weather made him feel weaker. His autopsy report mentioned "spots" that were discovered in the spinal cord. Although no name for the disease was ever given, it is apparent today that the case described was one of multiple sclerosis. It wasn't until 1878 that the term sclerosis appeared in American medical literature.
Our knowledge of MS is fairly new. As we look back now, the question is, Did MS appear out of the blue in the 1830s, or was it an older disease overlooked by doctors who made less acute observations? If it is a relatively new disease, it wouldn't be the first time in medical history a disease has suddenly appeared. Syphilis, for example, was unheard of before 1492, one of the more important dates we learn in elementary school. This is not a coincidence, since it was actually Christopher Columbus and his sailors who brought the disease to Europe. Syphilis was a very mild disease that was common among the women of Haiti. After Columbus's first voyage, he and his sailors returned to Europe via Haiti, where they contracted the disease. Unfortunately, Europeans had no immunity to syphilis, and it spread throughout the continent with very serious consequences.
In more recent times, too, brand-new diseases have appeared seemingly out of nowhere. The first case of Legionnaire's disease appeared in 1977, and the first case of AIDS (acquired immune deficiency syndrome) was diagnosed in the United States in 1980.
Why bother to trace the history of a disease at all? Quite often a little piece of information can help define the cause and lead to a cure or effective treatment. While medical debates still continue over the origin of MS, there is convincing evidence that MS was new on the scene in the 1830s.
WHAT WE KNOW ABOUT MS TODAY
Multiple sclerosis is a disease that strikes only the central nervous system, which consists of the brain and spinal cord. These organs control the movements and functions of the entire body. As the brain sends and receives signals, the spinal cord funnels them in and out, to and from different parts of the body through a network of nerves.
The nerves are surrounded by insulating matter called myelin -- a soft, white, fatty substance that forms a protective sheath for the nerves. The myelin sheath, which develops in the first ten years of life, insulates the nerve fibers and helps conduct signals through the body.
Multiple sclerosis is a disease where the myelin breaks down and is replaced by scar tissue. This demyelination can slow down or even block the flow of signals to and from the central nervous system to the rest of the body, impairing such functions as vision, strength, or coordination. One important characteristic of myelin, however, is that it can repair itself. This ability, called remyelination, is one of the reasons MS is usually associated with many attacks, or exacerbations, and recoveries, or remissions.
No one knows what actually causes MS, but we do know that it is an acquired disease -- you are not born with it. Multiple sclerosis is also an exogenous disease, meaning that it is contracted from the outside. And fortunately, it is not contagious. American researchers have shown that the rate of increased prevalence among husbands and wives is only 1 percent. In England, the prevalence of MS among husbands and wives is less than among the general population, occurring at a rate of 4.9 per 10,000 compared with 5.0 per 10,000.
Multiple sclerosis is often confused with other diseases, most commonly muscular dystrophy (MD) and arteriosclerosis. Multiple sclerosis is not related to either. Muscular dystrophy is a disease of the muscles; arteriosclerosis is a disease that causes hardening of the arteries and blood circulation problems. Because MS is confined to the central nervous system, it has been confused with amyotrophic lateral sclerosis (ALS), also known as Lou Gehrig's disease. Amyotrophic lateral sclerosis is a disease of the nervous system, but it is very different from MS; it has no effect on the myelin sheath but destroys the motor neurons in the central nervous system that directly control muscles.
WHO GETS MS?
The focus of much MS research has been in the area of epidemiology -- the study of diseases in terms of their geographic and ethnic occurrence, with analysis of all factors including environment and heredity. The epidemiology of MS is nothing less than intriguing.
Since World War II more than 250 prevalence studies of multiple sclerosis have been conducted. As seen in much of the medical literature, many of the studies conflict. According to the National MS Society, the number of reported cases of MS in the United States is approximately 250,000. The actual number of Americans with MS, however, may be closer to 500,000. Because many patients with minor symptoms never consult a doctor about them, they often ascribe the condition to stress, nerves, and other self-diagnosed causes. Additionally, with recent technological advances, the number of MS cases may climb even higher. New diagnostic tools are showing that many people have "silent" MS: They have MS lesions throughout their central nervous systems, but they never have a single manifestation of the disease.
There is no question that multiple sclerosis has a specific age of onset when symptoms first appear. MS rarely strikes before age ten or after age fifty, and symptoms generally appear between ages twenty and forty. Statistically, the average age of onset is twenty-eight, and the average age of diagnosis is thirty-three. (The average age of onset is slightly lower for women than men.)
Interestingly, the richest countries, with the highest standards of sanitation, have the highest incidence of MS. The poorest countries, with lower standards of hygiene, have the lowest percentage of MS cases. Two large and carefully conducted American studies, along with another from England, have shown that MS has a predilection for the socially privileged. The evidence suggests that people in less sanitary communities may develop some sort of immunity to MS early in life. Although other studies from Ireland, Israel, the Canadian city of Winnipeg, and the Orkney Islands off northern Scotland do not support these findings, MS has maintained its reputation as a disease of the middle and upper classes.
Worldwide research shows that MS has a definite geographical distribution. It has been long established that MS is more prominent in colder regions and very rare in subtropical and tropical areas -- the farther away from the equator, the higher the incidence of MS. In the United States, the farther north, the more MS. And, in fact, if a line were drawn straight along the thirty-seventh parallel, the incidence above the line,would be almost twice that below it: Canada has twice the MS incidence of the United States.
Around the world, high-density areas of MS (30 cases per 100,000) include northern Europe into the USSR, Canada, the northern United States, New Zealand, and southeastern Australia. Medium-density areas (between 5 and 29 cases per 100,000) include nothernmost Scandinavia, the central USSR, southern Europe, the southern United States, and much of Australia. Low-density areas (fewer than 5 cases per 100,000) include all of Asia and the tropics.
Most evidence suggests that exposure to MS occurs before age eighteen, followed by a latency period (before symptoms appear) of twenty-one years. This has been most clearly documented in migration studies conducted in Israel and South Africa.
In Israel scientists recorded every single case of MS -- the age of onset, where each patient came from, at what age he or she immigrated, and the latency period. They found that MS was unknown among native-born Sabras and immigrants from North Africa and Yemen but high among immigrants from western, northern, and eastern Europe. In fact, the MS frequency among immigrants matched the incidence rates in their native countries.
The MS surveys in South Africa were equally revealing. There the native-born blacks and whites were found to have a very low incidence of MS (only 3 cases per 100,000), while the immigrants, mostly from the United Kingdom and the Netherlands, had a high incidence (50 cases per 100,000). However, studies also showed that when northern Europeans immigrated before age fifteen, they had the same lowered risk of MS as did native South Africans.
Both the Israeli and South African studies suggest that immigrants with MS were exposed to the inciting agent in childhood and developed symptoms many years later. But what were they exposed to in those crucial years? Something in the soil or the water? Or could it be the climate? Hot or cold weather doesn't cause a disease, but it can certainly have an effect on other aspects of life, such as home heating and ventilation, how much time is spent indoors, and what types of food are eaten.
Certain racial groups actually get no MS at all. They are the Eskimos, the Gypsies, the Yakuts in Siberia, and the Bantu in Africa. Among other black groups in Africa, MS is rare. In America blacks have about half the incidence of MS as does the white population. In England blacks also have a much lower incidence than whites. In London a prevalence study was done on black immigrants from the West Indies. More than one hundred cases were predicted for this population, but only eleven cases were ever observed. In the United States black veterans were found to have a 4 percent relative risk compared to that of white veterans. MS is more common, however, among American blacks than it is among African and Caribbean blacks -- a factor possibly arising from environmental factors or reflecting interracial ancestry.
Many Oriental groups in the United States, such as the Japanese and Chinese, have a very low incidence of MS -- calculated as low as one-tenth that of many neighboring white populations. The Japanese are probably the most-studied Oriental population in regard to MS. While the disease is very rare in Japan, it is equally rare in Japanese who immigrate into other countries. In Los Angeles, where the risk of MS is moderate, and Seattle, where it is high, MS remains very rare among the Japanese populations, even among those locally born. These findings lend credence to the theory that some people can have a genetic insusceptibility to MS.
Although the data are not abundant, it also appears that MS is less common among North American Indians, some Indian groups in South America, and among people born in India, Pakistan, Sri Lanka, and Malta.
Surveys of patients all over the world show that more women than men get multiple sclerosis. Two separate studies in the United States reported a female-to-male ratio of 1.8 to 1. A survey in western Australia reported a 2.8 to 1 ratio of women to men; and among those born in South Africa, a female-to-male ratio of 2.5 to 1 is accepted. One broader-based study that actually reviewed fourteen different surveys concluded that the average risk for women as compared to men was 1.4 to 1.
Which survey should be accepted? Perhaps none. Taken on face value, they seem to indicate that MS has a definite preference for women, but other factors must be considered. At great risk of sounding sexist, it is our belief that women, in general, pay more attention to their health and see their doctors much more often than do men. So, although surveys show that more women than men contract MS, it is possible that the statistics are weighted in their favor simply because they make themselves more available for neurological assessments.
WHAT CAUSES MS?
Cruveilhier's original descriptions in the nineteenth century attributed the disease to the suppression of sweat. That theory has long been abandoned, but since then there has been endless speculation as to what causes MS. Some present-day theories are increasingly convincing. But a long process of elimination has narrowed down the field to a few possible causes.
At this point in medical history, scientists acknowledge eleven basic causes of all disease. Every disease known to man is caused by something:
Each one of the eleven basic causes of disease has been scrutinized for MS. Here is how scientists over the last century have pushed closer and closer to pinpointing its cause.
Because of the unique geographical distribution of MS, scientists were naturally drawn to the idea that a toxic agent might cause the disease. Over the decades they have studied soil and water to see if the disease might be related to an excessive content of such minerals as aluminum, copper, manganese, and others. But the enormous variety of toxic elements across latitudes spanning four continents led scientists to rule out a geological factor. Toxins in the diet, even the air, were also evaluated. For instance, high gluten foods such as wheat were once thought to be the possible culprit. But removing gluten from the diet completely did nothing to alter MS statistics. To date, all toxic elements that have been studied, including cosmic rays in the atmosphere, have been ruled out as the cause of MS.
Probably the best argument against a toxic theory comes from studies of an MS "epidemic" in the Faeroe Islands. The Faeroes are a group of fifteen volcanic islands between Iceland and Scotland. Before 1943 not a single case of multiple sclerosis had been discovered among the native Faeroese. Then, between 1944 and 1949, the average annual incidence rate rose to 7.1 cases per 100,000. There is little question among scientists that this development was directly related to the between 1,500 and 7,000 British troops who were stationed in the Faeroes for five years beginning on April 13, 1941. Investigators believe that British troops, who were carriers of an infectious agent but without symptoms, brought MS to the islands.
If the British troops had introduced multiple sclerosis to the islands by introducing a toxin, MS would still be around. But this is not the case. Instead, the disease almost disappeared with the evacuation of the British forces. Two later "epidemics" were attributed to the Faeroese, who were now carriers themselves, but manifested no symptoms.
Although the studies of the Faeroes ruled out a toxic theory, other important conclusions were drawn. These included the following key points:
1. MS is a unique, widespread, specific infectious disease that only rarely causes symptoms.
2. Acquisition will take place at the first sufficient exposure between ages eleven and forty-five.
3. The disease remains systemic, or in the body, but causing no damage. Subsequently it either invades the nervous system or disappears.
4. It may be transmissible from person to person but only during part or all of the systemic phase.
In conclusion, no toxic-agent theory has ever held up under scientific scrutiny. But, even with lack of evidence, it may still be possible that some toxic agent not yet proposed is the cause of MS.
Long ago, doctors suspected that MS was caused by something vascular, or related to the blood circulation. The key theory was that something was wrong with the blood vessels, that myelin lesions were possibly caused by spasms of the arteries. As medical technology progressed and tests such as the angiogram could actually examine blood vessels, doctors were able to see that MS patients had perfectly normal vascular systems.
A metabolic disease would reflect some internal chemical abnormality in the body -- such as a disturbance of hormones, sugar levels, or enzymes. Because the age of onset in women is closely associated with puberty, and the risk of developing MS decreases around the time of menopause, scientists examined a hormonal association. But when no hormonal changes were consistently found in MS patients, this association was soon ruled out. At one time MS was also blamed on high blood sugar. Twenty years ago, a neurology resident gave a diabetes drug called Orinase to an MS patient. (Orinase was also being used at the time to treat acne.) Incredibly, the man's MS went into remission. The resident then gave Orinase to seven other patients who allegedly went into remission, too. After this was published in the highly regarded Journal of the American Medical Association, MS clinics across the country tested very large groups, unfortunately without any scientific benefits. Similarly, other metabolic causes have been considered and rejected. These include dietary and nutritional theories about both excesses and deficiencies.
There is interesting evidence of a slight increase in MS among first-degree relatives -- parents, siblings, and children. The most recent extensive study (Sadovnick and Macleod, 1981), in British Columbia, ascertained a risk factor of from 1 to 3 percent. Other studies show as much as a 4 percent increase in MS among siblings. This slight increase over the general population is attributed to the greater likelihood of common exposure to whatever the mystery MS element may be. If MS is caused by something in the environment, such as a virus (as many scientists suspect), there's a good chance that brothers and sisters are exposed together while growing up. They play in the same school yard, walk the same dog, eat the same foods, breathe the same air, and pass each other the same cold, flu, and measles viruses.
It is also suspected that some family members may even inherit a genetic susceptibility to MS. This is suspected in other diseases, too. For example, if two people each smoke three packs of cigarettes a day, why does one get lung cancer and the other not? A genetic susceptibility is one likely explanation.
A Canadian study of twins published in the New England Journal of Medicine (December 1986) has provided the strongest evidence yet of a genetic link for MS. The study found that in nearly 26 percent of identical twins studied both had MS if one did, while in only 2.3 percent of fraternal twins both had the disease if one did. This was a very significant finding, since identical twins come from a single egg and share all their genes, while fraternal twins come from separate eggs and have different genes. The study also showed that in some cases, the "healthy" identical twin had MS lesions, although the disease had never caused symptoms.
In the last ten years, researchers have found that the white blood cells of some people with MS have different human leukocyte antigens (HLA) than those of people without the disease. The HLA system is thought to be connected to the genes that control the immune system. The patterns of these antigens are inherited and can be traced much like blood types.
In the United States and northern Europe, three different HLA antigens are found in higher levels in people with MS than in those without the disease. MS populations in other parts of the world test higher for other HLA antigens. Obviously, the push is on to find if there is one HLA antigen found in the white blood cells of all people with MS and absent from all those without it. When and if this happens, the "susceptibility gene" will have been discovered.
While it is possible to inherit a genetic susceptibility to MS, it is not possible to inherit the disease. And even people who have all the necessary genes don't necessarily get MS. The disease, experts believe, must be triggered by environmental factors.
For MS to be considered a hereditary disease, the percentage of cases among all siblings, not just identical twins, would have to be 25 percent or more. Since it is not, in spite of the suspected genetic link, MS is not considered a hereditary disease.
A congenital disease is one with which a person is born. But since there has never been any evidence that people are born with faulty myelin, congenital theories have basically been ruled out. If people were born with faulty myelin, it wouldn't take so long to show up. The cause for MS must account for its age of onset.
This is a category of disease in which degeneration occurs in a part of the body due to an unknown cause. An example of a degenerative disease is Alzheimer's, in which brain cells begin to die off for no apparent reason. Although degenerative is a scientifically accepted category, it is basically a wastebasket category for the incurable diseases that have no known cause. MS was once in this category, but an overwhelming amount of evidence now points to the probability that MS is caused by infection or allergy.
A psychogenic disease is one that is caused by an emotional condition or process, such as a skin rash or tension headache caused by stress. Although stress, depression, and other emotional factors can aggravate MS, studies show that they do not cause it.
Tumors have never been found to cause demyelination and therefore have never been suspected of causing MS.
At one time, trauma, or injury, was thought to be the cause of MS. This was based on anecdotal accounts, not scientific evidence. Doctors still see many cases in which a patient has a minor injury, such as stubbing a toe in the middle of the night, and wakes up the next morning with numbness in the entire leg. But since this happens on very rare occasions, scientists consider trauma to be a precipitator of an MS attack rather than a cause of the disease.
From the start, infection, whether bacterial or viral, has been a strong suspect as the cause of MS. At one time tuberculosis (TB), a disease caused by a bacterium, was linked to MS. But since TB has been drastically reduced and MS is still around in stable numbers, we know there is no correlation.
Spirochetes, spiral-shaped bacteria, were another area of investigation. Since one kind of spirochete causes syphilis, a disease that also produces spotty lesions, it was a reasonable hunch. But studies showed no link to MS there, either; other bacterial leads also failed.
Today one of the most popular scientific theories is that MS is caused by viral infection. Actually, for the past one hundred years, scientists have suspected that MS is caused by a virus attack Charcot's student and successor, Pierre Marie, first raised the possibility in 1884, and today many researchers still believe that a viral hypothesis can best explain the results of many MS studies. In other words, the viral theory seems to fit the other pieces of the MS puzzle.
The word virus comes from the Latin for "slimy liquid," "stench," or "poison." Most of us are familiar with acute viral diseases -- such as the flu, a cold, or pneumonia -- that hit and leave fairly quickly. These are not caused by the kind of viruses linked to MS. Research is pointing to "slow-acting viruses" that can stay inside the body for months or years before triggering illness. Three areas of investigation have given credence to this theory:
1. Migration studies indicate that MS is related primarily to environmental exposure in childhood followed by a long latency.
2. Animal studies have documented that viruses can evoke relapsing and remitting courses (often seen in MS) and can cause myelin destruction.
3. Studies of MS patients have consistently shown abnormal levels of viral antibodies, the substances the body produces to fight infection.
If a specific virus causes MS, it has yet to be found. At one time or another almost every virus has been investigated for MS, but research in this area still continues. Since 1946 twenty viruses have been studied, and in eleven, high antibody titers (strengths) have been found in the spinal fluid of people with MS. One of the most scrutinized is rubeola, the virus that causes measles.
Rubeola also causes another neurological disease called subacute sclerosing panencephalitis (SSPE) -- a slowly progressive disease that occurs as a complication after measles but many years later. In SSPE, antibody levels against the measles virus are unusually high, and there is also demyelination.
The obvious question in early research was, If the rubeola virus could cause SSPE, could it cause MS? The plot thickened in 1962, when Adams and Imagawa reported that antibodies against the measles virus were present in the spinal fluid of more than 75 percent of MS patients and absent in the control group. More than thirty other studies confirmed these findings.
The age factor added one more interesting dimension. In three case-controlled surveys, the MS group had a history of measles at an older age (eleven to fifteen) than the general population. This is particularly intriguing since those who acquired SSPE had measles before age two.
As may be imagined, measles has been studied and studied, but unfortunately, MS researchers have only been able to show a circumstantial association. Other reports threw a monkey wrench into the theory. Scientists reported at least four people with MS with no history of measles and no antimeasles antibody.
Scientists looking further into the MS-measles connection hit another dead end when they saw that MS lesions had little resemblance to the damage done by measles in SSPE. Finally, they learned through autopsy studies that although the measles virus is found in the brains of those with SSPE, it has never been found in the brains of MS patients.
For these and other reasons, the measles theory eventually fell by the wayside. But for those who still believe that some relationship exists between MS and measles, there will be a definite answer soon enough. An entire generation of American children has now been vaccinated against rubeola. These children will soon be coming of MS age, and if rubeola is the cause, a dramatic decline and even eradication of MS in the United States should take place very shortly.
It is also possible that MS may be caused or triggered by more than one virus. Studies have already shown high levels of measles antibodies in the spinal fluid of MS patients. Additional studies have found even higher levels of antibodies against other viruses, including herpes simplex, influenza C, Epstein-Barr, and others. In one study, 23 percent of MS patients had abnormal levels of antibodies to two or more viruses. In 1985 researchers at the Wistar Institute in Philadelphia implicated a new retrovirus, human T-cell lymphotropic virus I (HTLV-I), in as many as one-third of people with MS. A retrovirus is a type of virus that invades a cell and, through a very complex process called "reverse transcription," can produce unlimited copies of itself. Japanese scientists also found antibodies for the HTLV-I virus in the blood of eleven out of forty-six people with MS. This report caused a great deal of concern among patients who feared that the HTLV-I virus might somehow be connected to the HTLV-III virus, which causes AIDS. It is not. There is no AIDS-MS connection at all.
Further studies still have to be conducted to see if HTLV-I is really unique to MS or if it is also found in people with other neurological diseases. Although each new report is interesting, each must be greeted with caution. It was as recently as 1982 that scientists claimed the subacute myelo-optic neuropathy (SMON) virus was present in the spinal fluid of people with MS. Soon after, however, this "virus" was also found in the spinal fluid of people with illnesses unrelated to MS. The connection MS. A retrovirus is a type of virus that invades a cell and, through a very complex process called "reverse transcription," can produce unlimited copies of itself. Japanese scientists also found antibodies for the HTLV-I virus in the blood of eleven out of forty-six people with MS. This report caused a great deal of concern among patients who feared that the HTLV-I virus might somehow be connected to the HTLV-III virus, which causes AIDS. It is not. There is no AIDS-MS connection at all.
Further studies still have to be conducted to see if HTLV-I is really unique to MS or if it is also found in people with other neurological diseases. Although each new report is interesting, each must be greeted with caution. It was as recently as 1982 that scientists claimed the subacute myelo-optic neuropathy (SMON) virus was present in the spinal fluid of people with MS. Soon after, however, this "virus" was also found in the spinal fluid of people with illnesses unrelated to MS. The connection between HTLV-I and MS remains to be drawn scientifically. Until then, it must be considered casual.
If multiple sclerosis is caused by a virus, how is it contracted?
Viral infections can be divided into three groups: (1) those transmitted by insects such as mosquitoes, ticks, or biting flies; (2) those transmitted by exposure to or consumption of animals that are host to the virus; and (3)those transmitted from human to human.
Although insects can transmit viruses to humans, it is highly unlikely that MS is transmitted this way. All of the known insect-transmitted diseases, such as encephalitis and yellow fever, are acute virus infections without the latent nature of MS.
Exposure to or Consumption of Animal Carriers
Some of the most emotional arguments concerning MS center around the theory that the disease may possibly be transmitted by dogs and that the virus that causes MS might be canine distemper. Canine distemper is caused by a virus related to measles. It is an acute respiratory and gastrointestinal disease often complicated by a central nervous system disorder that can occur weeks or months later.
It has been proposed that exposure to the canine distemper virus (CDV) or exposure combined with, perhaps, a faulty measles immunity might cause MS. Although these theories rank among the most controversial, they do shed some light on some of the more peculiar MS clusters. One of the most intensively studied is in the Orkney Islands off the northeastern coast of Scotland. In contrast to the Faeroe Islands, which had one major epidemic, the Orkneys have consistently had the world's highest MS rate for the past century. (Prevalence rates have been as high as 309 per 100,000 compared with 58 per 100,000 in the United States today.) Oddly, it was recently discovered that MS incidence rates in the Orkneys have fallen significantly. In the most recent survey, taken on September 21, 1983, the prevalence rate had dropped to 193 per 100,000.
According to recently published research (Neurology, April 1985), the decline of MS in the Orkney Islands is linked to the decline of CDV, which until 1959 was "frequent, severe, and widespread." And, as in the Faeroes, British troops were stationed there during World War II. Veterinarians in the Orkneys reported that as the troops increased (ultimately to 60,000), so did the dog population. Puppies born on farms all across the islands were taken in as pets. It is believed that when the soldiers left, they left their dogs behind, and large numbers of strays roamed the deserted camps. Although CDV was always prevalent before the war, it became much more severe with the increase in the dog population.
Could this also explain the epidemic in the Faeroes? Did the presence of British troops cause an increase in the dog population and subsequent CDV incidence? Proponents of the CDV-MS hypothesis argue a strong connection.
Researchers have also used the CDV-MS hypothesis to explain an MS "time cluster" in Iceland following widespread CDV epidemics in 1921 and 1941. Ten years after each CDV epidemic, the annual incidence of MS increased significantly.
Why, then, does the CDV theory remain so controversial? Because most surveys have failed to show that people with MS include more dog owners or people who have had greater exposure to dogs. Another criticism of the theory is that while MS has a preference for colder climates, CDV occurs everywhere. (On the other hand, some argue, distemper peaks in cold, damp weather conditions, when dogs and people are more apt to be indoors and in close contact, and CDV is also more rapidly inactivated in warm temperatures.)
As the controversy continues, both sides agree to err on the side of caution and make sure dogs are vaccinated against distemper.
Human to Human
Most likely, MS is not transmitted from human to human. If it were, the number of cases would have reached outrageously epidemic proportions. The low incidence of MS among married couples establishes that it is definitely not transmitted from adult to adult. But can it be transmitted from human to human during the vulnerable years? There is very strong evidence against this theory, but like many theories in MS research, it has not been absolutely ruled out. If MS is, indeed, caused by a virus, exposure to it occurs in one of the three ways just explored.
The last consideration is allergy. This would not be an allergy to an environmental substance such as a hay fever attack from pollen or a skin rash from a new soap. What scientists link to this disease is autoimmunity -- when a person becomes allergic to his or her own tissue and produces antibodies that attack healthy cells.
A well-known example of an autoallergy is rheumatic fever, in which the person's own antibodies attack heart valves and joints. Rheumatic fever actually starts with a streptococcus infection (such as strep throat in childhood). The individual produces antibodies against the infection, but later, those antibodies backfire and attack healthy tissues by mistake. This is called an autoimmune reaction.
There are many autoimmune diseases such as rheumatoid arthritis (in which antibodies attack joints), lupus (in which antibodies attack small blood vessels), and myasthenia gravis (in which antibodies attack muscles).
There is very strong evidence that multiple sclerosis is an autoimmune disease in which the body's own defense system mistakenly forms antibodies that attack myelin. Three areas of research support this theory. First, in laboratory animal experiments, scientists have been able to produce antibodies that attack myelin, so they know it is possible. Second, it has been known for thirty-five years that the spinal fluid of people with MS shows an increased level of antibodies called immunoglobulins. And third, treatments directed against the autoimmune process are often effective.
In summary, it seems very likely that the initial event that starts MS is a viral infection, but the autoimmune process is what keeps MS going.
To date, no specific antibody for multiple sclerosis has been identified, and attempts to show response to brain or viral material have failed. So, while all the abnormalities are intriguing, there is no scientific proof as yet. Still, the combination theory of an early virus attack causing a later autoimmune response is, many believe, the most logical explanation.
Copyright © 1987, 1992 by Louis J. Rosner, M.D., and Shelley Ross