Scan0025 (17)

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among very many others, and generally failed to attract any atten-tion. I cite it here in order to higlilight it, and in this way to draw it closer to my appropriate standpoint with regard to MS etiopathogen-esis. However, beforeliand, it seems reasonable tofocus one’s attention on a number of facts originating from the observations furnished by many researcliers. These facts, although sometimes surprising, have not always been evaluated thoroughly, hence many authors’ inąuisi-tions proceeded in directions, which did not contribute to grasping the essence of the issue.

Studying the ąuestion referring to epidemiology of MS, it was found out that there are three areas of risk of contracting MS disease. These are:

1.    high risk area, wherein the incidence of MS exceeds 30 cases in 100.000 inhabitants (HRA),

2.    medium risk area (MRA); 5-29 patients for 100.000, and

3.    Iow risk area (LRA) the number being smaller than 5 patients for 100.000 inhabitants.

Markedly higher indices for the morbidity ratę were encountered, e.g. in Wielkopolska (51 : 10?) [3], in Germany (57 : 10'’ ), in Sweden — in Gótteborg (96 : 10⁵) as well as Orkneys and Shetland (143 : 10⁵). The zonę of HRA includes the not hem and central parts of Europę jointly with Poland, Southern part of Canada, norhtern part of the United States, New Zealand, Tasmania and south-eastern part of Australia. The zonę of MRS embraces, among others, the Southern part of South America, northern Australia, Southern part of Africa, countries of Medit.erranean Sea. basin. LR A appears in almost all countries of Africa, Asia and Caribbean countries, in Mexico [2]. In geographic distribution MS preva.ils in latitude — parallel division of the above zones, among others, along ( a.pproximately) the 40°N parallel of latitude runs the borderline of HRA and MRA zones.

0.6. Demyelina.ting Diseases — a New Presentation

49

Special attention was paid to extremely high MS morbidity ratę on Orkneys and Shetland, which claims even 184-309 : 10⁵ [4]. At fchat, it was notified that no correlation was reveałed with ge-netic factors, particularly in the field of HLA system features. It is well known that among subjects with features: A3, B7, DW‘2, DRW2, DRW3 multiple sclerosis is observed markedly morę frecjuently. There was nothing of this kind. However, a striking correlation was disclosed hetween MS intensity on these islands and occupation of Orkneys and Shetland by British troops during the II World War. Bunnel et. al.

13] link this linding with the transport of dogs, having not been pre-yiously inoculated against canine distemper. They were brought to these Islands by the military Staff. After the withdrawal of troops, no iicw MS cases were recorded. Particularly Iow MS morbidity incidence in evidenced among Japanese although the geographic-climatic zonę they inhabit is the regions, where the people are known to exhibit high or medium high risk of being affected by MS. In my opinion, as I am going to expla.in later, this is connected, first of all, with the Japanese modę of life, particularly with pursuing the life style being hased upon hygiene principles to the possibly highest degree.

Pathomorfological changes which are detectable in MS are \ < ry closely similar to those appearing in postinfectious acute dissem-inated inflammation of the brain, but they are morę often combined with infiltration by mononuclear cells. That can be proven, among nlhers, by suiweying microphotographs inserted in the voluminous work by E. Osetowska of 1974 [5]. Finally, H, Pet te and E. Pitte in ihrir work, .1956, on pathogenesis of post-serum myelo-encephalitis, and in post-vaccinal as well as para-infectious inflammations, do as-• • i l.ain that these are pathological States, nosologically closely re-liited, that lead, independently of the causative factor (sera, Sm ł ines, germs) to uniform, in its essence, inflaminatory reactions iii i ho central nervous system, and uniform clinical images. Thus, a #! 11»•I ion arises whether these related pathological states could not be jgKMHiibled into one common pathogenic factor [6]. All these para-in-■rlious and post-vaccinal myelo-encephalitis look uniform in the