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CERTIFIED MULTIPLE SCLEROSIS
SPECIALIST EXAM PREP Questions and
Correct Answers/ Latest Update / Already
Graded
Pathophysiology: Immune Dysfunction
Ans: 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 cell s 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:
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Destruction of Myelin and Axonal Damage or Loss
Ans: 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.
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
Ans: Increased susceptibility is present in families in which MS
already occurs
High genetic susceptibility observed in monozygotic twins
(20%-40%)
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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
Ans:
Theories of Etiology: Other
Ans:
Epidemiology: Geographic Distribution
Ans: 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
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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
Ans: Females have 3>1 greater risk of developing MS (70 -75%)
PPMS = 50/50
Epidemiology: Age of Onset
Ans: 10-59 years, highest incidence between 20-40 years
Average age of onset is 28-30 years
All rights reserved © 2025/ 2026 |
CERTIFIED MULTIPLE SCLEROSIS
SPECIALIST EXAM PREP Questions and
Correct Answers/ Latest Update / Already
Graded
Pathophysiology: Immune Dysfunction
Ans: 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 cell s 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:
All rights reserved © 2025/ 2026 |
, Page |2
Destruction of Myelin and Axonal Damage or Loss
Ans: 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.
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
Ans: Increased susceptibility is present in families in which MS
already occurs
High genetic susceptibility observed in monozygotic twins
(20%-40%)
All rights reserved © 2025/ 2026 |
, Page |3
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
Ans:
Theories of Etiology: Other
Ans:
Epidemiology: Geographic Distribution
Ans: 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
All rights reserved © 2025/ 2026 |
, Page |4
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
Ans: Females have 3>1 greater risk of developing MS (70 -75%)
PPMS = 50/50
Epidemiology: Age of Onset
Ans: 10-59 years, highest incidence between 20-40 years
Average age of onset is 28-30 years
All rights reserved © 2025/ 2026 |
