Page 1 of 30
CERTIFIED MULTIPLE SCLEROSIS SPECIALIST EXAM PREP WITH
COMPLETE SOLUTIONS
Pathophysiology: Immune Dysfunction - ANSWER-An impairment of immune
tolerance to central nervous system tissue that ultimately leads to plaque
formation
The most widely believed hypothesis is that it is a virus-induced immune-
mediated disease.
Unusually high reactivity of immune system T cells to proteins of myelin in the
CNS
Overrepresentation of cells that enhance immune responses (pro-inflammatory
T helper cells)
Presence of immune system cells in MS lesions in the brain, spinal cord, and
optic nerves
B lymphocytes responsible for producing antibodies
Pathophysiology:
Destruction of Myelin and Axonal Damage or Loss - ANSWER-Pathology of MS
consists of lesions disseminated in location and of varying age.
Lesions are present in both white and gray matter, gray matter lesions are less
evident.
,Page 2 of 30
Oligodendrocytes are damaged in this process.
Lesions range from acute plaques with active inflammatory infiltrates to chronic,
inactive, demyelinated scars.
Slowed conduction and conduction failure occur in demyelinated fibers.
Conduction failure is due to fiber fatigue or to an increase in body temperature.
Ongoing inflammation, demyelination, and scarring ultimately result in
irreversible axonal damage and loss.
Acute MS lesions are characterized by T lymphocytes, plasma cells,
macrophages, and bare, demyelinated, or transected axons.
Brain atrophy in MS represents a negative pathologic change.
Theories of Etiology: Genetics - ANSWER-Increased susceptibility is present in
families in which MS already occurs
High genetic susceptibility observed in monozygotic twins (20%-40%)
Some genetically isolated groups never develop MS (Hutterites in Canada, East-
European Gypsies)
Racial differences in MS are likely genetically based
Theories of Etiology: Environmental - ANSWER-
Theories of Etiology: Other - ANSWER-
, Page 3 of 30
Epidemiology: Geographic Distribution - ANSWER-High Risk (> 30 per 100,000):
northern and central Europe, Italy, northern United States, Canada, southestern
Australia, New Zealand, parts of former Soviet Union
Medium Risk (5-29 per 100,000): southern Europe, southern United States,
northern Australia, northernmost Scandinavia, much of the north
Mediterranean basin, parts of former Soviet Union, white South Africa, central
South America
Low Risk (< 5 per 100,000): Africa, Asia, the Caribbean, Mexico, northern South
America
In the US states south of the 37th parallel have a lower risk than those north of
the parallel
People who reside in temperate climates in economically developed western
countries tend to have higher rate of MS
Those older than 15 who migrate retain the MS risk of their birthplace. Those
migrating before age 15 aquire the lower risk of the new residence
Epidemiology: Gender - ANSWER-Females have 3>1 greater risk of developing
MS (70-75%)
PPMS = 50/50
CERTIFIED MULTIPLE SCLEROSIS SPECIALIST EXAM PREP WITH
COMPLETE SOLUTIONS
Pathophysiology: Immune Dysfunction - ANSWER-An impairment of immune
tolerance to central nervous system tissue that ultimately leads to plaque
formation
The most widely believed hypothesis is that it is a virus-induced immune-
mediated disease.
Unusually high reactivity of immune system T cells to proteins of myelin in the
CNS
Overrepresentation of cells that enhance immune responses (pro-inflammatory
T helper cells)
Presence of immune system cells in MS lesions in the brain, spinal cord, and
optic nerves
B lymphocytes responsible for producing antibodies
Pathophysiology:
Destruction of Myelin and Axonal Damage or Loss - ANSWER-Pathology of MS
consists of lesions disseminated in location and of varying age.
Lesions are present in both white and gray matter, gray matter lesions are less
evident.
,Page 2 of 30
Oligodendrocytes are damaged in this process.
Lesions range from acute plaques with active inflammatory infiltrates to chronic,
inactive, demyelinated scars.
Slowed conduction and conduction failure occur in demyelinated fibers.
Conduction failure is due to fiber fatigue or to an increase in body temperature.
Ongoing inflammation, demyelination, and scarring ultimately result in
irreversible axonal damage and loss.
Acute MS lesions are characterized by T lymphocytes, plasma cells,
macrophages, and bare, demyelinated, or transected axons.
Brain atrophy in MS represents a negative pathologic change.
Theories of Etiology: Genetics - ANSWER-Increased susceptibility is present in
families in which MS already occurs
High genetic susceptibility observed in monozygotic twins (20%-40%)
Some genetically isolated groups never develop MS (Hutterites in Canada, East-
European Gypsies)
Racial differences in MS are likely genetically based
Theories of Etiology: Environmental - ANSWER-
Theories of Etiology: Other - ANSWER-
, Page 3 of 30
Epidemiology: Geographic Distribution - ANSWER-High Risk (> 30 per 100,000):
northern and central Europe, Italy, northern United States, Canada, southestern
Australia, New Zealand, parts of former Soviet Union
Medium Risk (5-29 per 100,000): southern Europe, southern United States,
northern Australia, northernmost Scandinavia, much of the north
Mediterranean basin, parts of former Soviet Union, white South Africa, central
South America
Low Risk (< 5 per 100,000): Africa, Asia, the Caribbean, Mexico, northern South
America
In the US states south of the 37th parallel have a lower risk than those north of
the parallel
People who reside in temperate climates in economically developed western
countries tend to have higher rate of MS
Those older than 15 who migrate retain the MS risk of their birthplace. Those
migrating before age 15 aquire the lower risk of the new residence
Epidemiology: Gender - ANSWER-Females have 3>1 greater risk of developing
MS (70-75%)
PPMS = 50/50
