CERTIFIED MULTIPLE SCLEROSIS
SPECIALIST EXAM PREP EXAM
QUESTIONS AND ANSWERS 100% PASS
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 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 - 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.
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,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%)
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
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, 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 - 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
Epidemiology: Ethnicity - ANS Highest prevalence: White/Caucasian
Lowest prevalence: Japanese
Asians are more likely to have spinal cordoptic nerve disease (older age onset, fewer brain
lesions, more enhancing lesions in spinal cord)
3 @COPYRIGHT 2025/2026 ALLRIGHTS RESERVED.
SPECIALIST EXAM PREP EXAM
QUESTIONS AND ANSWERS 100% PASS
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 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 - 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.
1 @COPYRIGHT 2025/2026 ALLRIGHTS RESERVED.
,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%)
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
2 @COPYRIGHT 2025/2026 ALLRIGHTS RESERVED.
, 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 - 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
Epidemiology: Ethnicity - ANS Highest prevalence: White/Caucasian
Lowest prevalence: Japanese
Asians are more likely to have spinal cordoptic nerve disease (older age onset, fewer brain
lesions, more enhancing lesions in spinal cord)
3 @COPYRIGHT 2025/2026 ALLRIGHTS RESERVED.
