Pathophysiology: cImmune cDysfunction c- cANSWER cAn cimpairment cof
cimmune ctolerance cto ccentral cnervous csystem ctissue cthat cultimately cleads
cto cplaque cformation
The cmost cwidely cbelieved chypothesis cis cthat cit cis ca cvirus-induced cimmune-
cmediated cdisease.
Unusually chigh creactivity cof cimmune csystem cT ccells cto cproteins cof cmyelin
cin cthe cCNS
Overrepresentation cof ccells cthat cenhance cimmune cresponses c(pro-
inflammatory cT chelper ccells)
Presence cof cimmune csystem ccells cin cMS clesions cin cthe cbrain, cspinal ccord,
cand coptic cnerves
B clymphocytes cresponsible cfor cproducing cantibodies
Pathophysiology:
Destruction cof cMyelin cand cAxonal cDamage cor cLoss c- cANSWER cPathology cof
cMS cconsists cof clesions cdisseminated cin clocation cand cof cvarying cage.
Lesions care cpresent cin cboth cwhite cand cgray cmatter, cgray cmatter clesions care
cless cevident.
Oligodendrocytes care cdamaged cin cthis cprocess.
Lesions crange cfrom cacute cplaques cwith cactive cinflammatory cinfiltrates cto
cchronic, cinactive, cdemyelinated cscars.
Slowed cconduction cand cconduction cfailure coccur cin cdemyelinated cfibers.
cConduction cfailure cis cdue cto cfiber cfatigue cor cto can cincrease cin cbody
ctemperature. cOngoing cinflammation, cdemyelination, cand cscarring cultimately
,cresult cin cirreversible caxonal cdamage cand closs.
Acute cMS clesions care ccharacterized cby cT clymphocytes, cplasma ccells,
cmacrophages, cand cbare, cdemyelinated, cor ctransected caxons.
Brain catrophy cin cMS crepresents ca cnegative cpathologic cchange.
Theories cof cEtiology: cGenetics c- cANSWER cIncreased csusceptibility cis
cpresent cin cfamilies cin cwhich cMS calready coccurs
High cgenetic csusceptibility cobserved cin cmonozygotic ctwins c(20%-40%)
Some cgenetically cisolated cgroups cnever cdevelop cMS c(Hutterites cin cCanada,
cEast- cEuropean cGypsies)
, Racial cdifferences cin cMS care clikely cgenetically cbased
Theories cof cEtiology: cEnvironmental c- cANSWER
Theories cof cEtiology: cOther c- cANSWER
Epidemiology: cGeographic cDistribution c- cANSWER cHigh cRisk c(> c30 cper
c100,000): cnorthern cand ccentral cEurope, cItaly, cnorthern cUnited cStates,
cCanada, csouthestern cAustralia, cNew cZealand, cparts cof cformer cSoviet
cUnion
Medium cRisk c(5-29 cper c100,000): csouthern cEurope, csouthern cUnited cStates,
cnorthern cAustralia, cnorthernmost cScandinavia, cmuch cof cthe cnorth
cMediterranean cbasin, cparts cof cformer cSoviet cUnion, cwhite cSouth cAfrica,
ccentral cSouth cAmerica
Low cRisk c(< c5 cper c100,000): cAfrica, cAsia, cthe cCaribbean, cMexico, cnorthern
cSouth cAmerica
In cthe cUS cstates csouth cof cthe c37th cparallel chave ca clower crisk cthan cthose
cnorth cof cthe cparallel
People cwho creside cin ctemperate cclimates cin ceconomically cdeveloped
cwestern ccountries ctend cto chave chigher crate cof cMS
Those colder cthan c15 cwho cmigrate cretain cthe cMS crisk cof ctheir cbirthplace.
cThose cmigrating cbefore cage c15 caquire cthe clower crisk cof cthe cnew cresidence
Epidemiology: cGender c- cANSWER cFemales chave c3>1 cgreater crisk cof
cdeveloping cMS c(70-75%)
PPMS c= c50/50
Epidemiology: cAge cof cOnset c- cANSWER c10-59 cyears, chighest cincidence
cbetween c20-40 cyears
Average cage cof conset cis c28-30 cyears
Epidemiology: cEthnicity c- cANSWER cHighest cprevalence: cWhite/Caucasian
cLowest cprevalence: cJapanese
Asians care cmore clikely cto chave cspinal ccordoptic cnerve cdisease c(older cage
conset, cfewer cbrain clesions, cmore cenhancing clesions cin cspinal ccord)
Diagnosis cof cMultiple cSclerosis:
Diagnostic cCriteria c- cANSWER cMS cis ca cclinical cdiagnosis cbecause cno
cdefinitive claboratory ctest cexists.
cimmune ctolerance cto ccentral cnervous csystem ctissue cthat cultimately cleads
cto cplaque cformation
The cmost cwidely cbelieved chypothesis cis cthat cit cis ca cvirus-induced cimmune-
cmediated cdisease.
Unusually chigh creactivity cof cimmune csystem cT ccells cto cproteins cof cmyelin
cin cthe cCNS
Overrepresentation cof ccells cthat cenhance cimmune cresponses c(pro-
inflammatory cT chelper ccells)
Presence cof cimmune csystem ccells cin cMS clesions cin cthe cbrain, cspinal ccord,
cand coptic cnerves
B clymphocytes cresponsible cfor cproducing cantibodies
Pathophysiology:
Destruction cof cMyelin cand cAxonal cDamage cor cLoss c- cANSWER cPathology cof
cMS cconsists cof clesions cdisseminated cin clocation cand cof cvarying cage.
Lesions care cpresent cin cboth cwhite cand cgray cmatter, cgray cmatter clesions care
cless cevident.
Oligodendrocytes care cdamaged cin cthis cprocess.
Lesions crange cfrom cacute cplaques cwith cactive cinflammatory cinfiltrates cto
cchronic, cinactive, cdemyelinated cscars.
Slowed cconduction cand cconduction cfailure coccur cin cdemyelinated cfibers.
cConduction cfailure cis cdue cto cfiber cfatigue cor cto can cincrease cin cbody
ctemperature. cOngoing cinflammation, cdemyelination, cand cscarring cultimately
,cresult cin cirreversible caxonal cdamage cand closs.
Acute cMS clesions care ccharacterized cby cT clymphocytes, cplasma ccells,
cmacrophages, cand cbare, cdemyelinated, cor ctransected caxons.
Brain catrophy cin cMS crepresents ca cnegative cpathologic cchange.
Theories cof cEtiology: cGenetics c- cANSWER cIncreased csusceptibility cis
cpresent cin cfamilies cin cwhich cMS calready coccurs
High cgenetic csusceptibility cobserved cin cmonozygotic ctwins c(20%-40%)
Some cgenetically cisolated cgroups cnever cdevelop cMS c(Hutterites cin cCanada,
cEast- cEuropean cGypsies)
, Racial cdifferences cin cMS care clikely cgenetically cbased
Theories cof cEtiology: cEnvironmental c- cANSWER
Theories cof cEtiology: cOther c- cANSWER
Epidemiology: cGeographic cDistribution c- cANSWER cHigh cRisk c(> c30 cper
c100,000): cnorthern cand ccentral cEurope, cItaly, cnorthern cUnited cStates,
cCanada, csouthestern cAustralia, cNew cZealand, cparts cof cformer cSoviet
cUnion
Medium cRisk c(5-29 cper c100,000): csouthern cEurope, csouthern cUnited cStates,
cnorthern cAustralia, cnorthernmost cScandinavia, cmuch cof cthe cnorth
cMediterranean cbasin, cparts cof cformer cSoviet cUnion, cwhite cSouth cAfrica,
ccentral cSouth cAmerica
Low cRisk c(< c5 cper c100,000): cAfrica, cAsia, cthe cCaribbean, cMexico, cnorthern
cSouth cAmerica
In cthe cUS cstates csouth cof cthe c37th cparallel chave ca clower crisk cthan cthose
cnorth cof cthe cparallel
People cwho creside cin ctemperate cclimates cin ceconomically cdeveloped
cwestern ccountries ctend cto chave chigher crate cof cMS
Those colder cthan c15 cwho cmigrate cretain cthe cMS crisk cof ctheir cbirthplace.
cThose cmigrating cbefore cage c15 caquire cthe clower crisk cof cthe cnew cresidence
Epidemiology: cGender c- cANSWER cFemales chave c3>1 cgreater crisk cof
cdeveloping cMS c(70-75%)
PPMS c= c50/50
Epidemiology: cAge cof cOnset c- cANSWER c10-59 cyears, chighest cincidence
cbetween c20-40 cyears
Average cage cof conset cis c28-30 cyears
Epidemiology: cEthnicity c- cANSWER cHighest cprevalence: cWhite/Caucasian
cLowest cprevalence: cJapanese
Asians care cmore clikely cto chave cspinal ccordoptic cnerve cdisease c(older cage
conset, cfewer cbrain clesions, cmore cenhancing clesions cin cspinal ccord)
Diagnosis cof cMultiple cSclerosis:
Diagnostic cCriteria c- cANSWER cMS cis ca cclinical cdiagnosis cbecause cno
cdefinitive claboratory ctest cexists.
