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Figure 36-1 Multiple sclerosis T2-weighted MRIs demonstrating multiple plaques in the periventricular white matter (left), emanating radially from the corpus callosum ( Dawson ngers ) (middle), and cervical spinal cord (right) The radial orientation and periventricular location of cerebral lesions is typical of the disease
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Etiology and Epidemiology
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Cruveilhier (circa 1835), in his original description of the disease, attributed it to suppression of sweat, and since that time there has been endless speculation about the etiology Many of the early theories appear ludicrous in the light of present-day concepts, and others are of mainly historical interest There is little point in enumerating them here; complete accounts are to be found in the reviews of DeJong (1970), Prineas (1970), R T Johnson (1978), and McDonald (1986)
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Although the precise cause of MS remains undetermined, a number of epidemiologic facts have been clearly established and will eventually have to be incorporated in any etiologic hypothesis The disease has a prevalence of less than 1 per 100,000 in equatorial areas; 6 to 14 per 100,000 in the southern United States and southern Europe; and 30 to 80 per 100,000 in Canada, northern Europe, and the northern United States More recently, Mayr and colleagues reported an incidence of 8 and a prevalence of 177 cases per 100,000 in Olmstead County, MN; this prevalence has been stable for approximately 30 years A less well de ned gradient
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exists in the Southern Hemisphere Kurland s studies indicate that there is a threefold increase in prevalence and a vefold gradient in mortality rate between New Orleans (30 degrees north latitude), on the one hand, and Boston (42 degrees north) and Winnipeg (50 degrees north) on the other In Japan there is a similar though less distinct geographic gradient (the prevalence of MS there is much lower than in corresponding latitudes of North America and northern Europe) The increasing risk of developing MS with increasing latitude has been con rmed by J B Barlow and Kurtzke and associates The latter studied a series of unprecedented size (5305 undoubted cases of MS and matched controls) They showed also that in the United States, African Americans are at lower risk than whites at all latitudes, but both races show the same south-to-north gradient in risk, probably indicating the importance of an environmental factor regardless of race Supporting this view are the descriptions, by Kurtzke and Hyllested, of an epidemic of MS in the Faroe Islands of the North Atlantic They found a much higher than expected incidence of the disease, occurring as three separate outbreaks of decreasing extent between the years 1943 and 1973 (It should be pointed out that the largest outbreak consisted of only 21 cases) It was their contention, con rmed by Poskanzer, that the disease was due possibly to an unidenti ed infection introduced by British troops who occupied the islands in large numbers in the years immediately preceding the outbreak Kurtzke and colleagues have also described a similar postwar epidemic in Iceland Several studies indicate that persons who migrate from a highrisk to a low-risk zone carry with them at least part of the risk of their country of origin, even though the disease may not become apparent until 20 years after migration Such a pattern has been demonstrated in both South Africa and Israel Dean determined that the prevalence of MS in native-born white South Africans was 3 to 11 per 100,000, whereas the rate in immigrants from northern Europe was about 50 per 100,000, only slightly less than among the nonimmigrating natives of those countries The data of Dean and Kurtzke indicate further that in persons who had immigrated before the age of 15, the risk was similar to that of native-born South Africans; whereas in persons who had immigrated after that age, the risk was similar to that of their birthplace Alter and colleagues found that in the descendants of European immigrants born in Israel, the risk of MS was low, similar to that of other nativeborn Israelis, whereas among recent immigrants the incidence in each national group approached that of the land of birth Again, the critical age of immigration appeared to be about 15 years These epidemiologic studies and others have shown that MS is associated with particular localities rather than with a particular ethnic group in those localities and again implicate environmental factors in the genesis of the disease Also, a familial aggregation of MS is now well established About 15 percent of MS patients have an affected relative, with the highest risk of concurrence being observed in the patient s siblings (Ebers, 1983) In a large population-based study carried out in British Columbia by Sadovnick and colleagues, it was found that almost 20 percent of index cases had an affected relative, again with the highest risk in siblings In a subsequent study, Sadovnick and colleagues sought to determine the degree of heritability of MS by comparing the risk of disease in the half-sibs (one biologic parent in common) of affected individuals with the risk in full sibs; the risk for full sibs was two to three times greater than for half-sibs and they interpreted these results as largely genetic in basis The case for heritability is supported by studies of twins in
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whom one of each pair is known to have MS In the most extensive of these studies (Ebers et al), the diagnosis was veri ed in 12 of 35 pairs of monozygotic twins (34 percent) and in only 2 of 49 pairs of dizygotic twins (4 percent) Furthermore, in two additional sets of monozygotic twins who were clinically normal, lesions were detected by MRI The concordance rate in dizygotic pairs is similar to that in nontwin siblings Despite these provocative ndings, no consistent pattern of mendelian inheritance has emerged (Of course, one must not assume that all diseases with an increased familial incidence are hereditary in that instances of the same condition in several members of a family may simply re ect an exposure to a common environmental agent Paralytic poliomyelitis, for example, was about eight times more common in immediate family members than in the population at large) Nonetheless, further evidence of a genetic factor in the causation of MS is the nding that certain histocompatibility locus antigens (HLAs) are more frequent in patients with MS than in control subjects The strongest association is with the DR locus on the sixth chromosome Other HLA haplotypes that are overrepresented in MS (HLA-DR2 and, to a lesser extent, -DR3, -B7, and -A3) are thought to be markers for an MS susceptibility gene possibly an immune response gene The presence of one of these markers increases the risk that an individual will develop MS by a factor of 3 to 5 These antigens may indeed prove to be related to the frequency of the disease, but their presence is not invariable and their exact role is far from clear (see Compston) The low conjugal incidence of MS, on the other hand, indicates that any common exposure to an inciting infection or environmental agent must occur early in life In order to test this hypothesis, Schapira and coworkers determined the periods of common exposure (common habitation periods) in members of families with two or more cases From this they calculated the mean common exposure to have happened before 14 years of age, with a latency of about 21 years gures that are in general agreement with those derived from the migration studies quoted above The incidence of MS is two or three times higher in women than in men, but the signi cance of this fact is unclear, the best current explanation being that women are generally more susceptible to immune and in ammatory conditions The incidence in children is very low; only 03 to 04 percent of all cases appear during the rst decade In an analysis of three childhood-onset cases, Hauser and colleagues found no phenotypic differences between childhood and adult cases Beyond childhood, the risk of rst developing symptoms of the disease rises steeply with age, reaching a peak at about 30 years, remaining high in the fourth decade, then falling off sharply and becoming low in the sixth decade It has been pointed out that MS has a unimodal age-speci c onset curve, similar to the age-speci c onset curves of many infectious and connective tissue diseases About two-thirds of cases of MS have their onset between 20 and 40 years of age Of the remainder, most cases begin before the age of 20; in a smaller number, the disease appears to develop in late adult life (late fties and sixties) In the latter patients, early symptoms may have been forgotten or may never have declared themselves clinically (we have several times found the typical lesions of MS in aged autopsied individuals who had no history of neurologic illness) Gilbert and Sadler report ve such cases and from their pathologic ndings declare that the true incidence of MS may be three times higher than stated gures Several studies from northern Europe and Canada have suggested that the likelihood of developing MS is somewhat greater
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