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NEURO 210 > Topic 20: Multiple Sclerosis > Flashcards

Topic 20: Multiple Sclerosis Flashcards

1
Q

What is the prevalence of multiple sclerosis around the world?

A

causes decrease toward the equator

due to: European background, lack of sun exposure

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2
Q

What is the most common age of onset of MS?

A

ages 15-25

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3
Q

What is the prevalence of pediatric MS?

A

6% of MS in total

3 to 10% of MS patients onset </= age 18

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4
Q

What is the prevalence of MS based on gender?

A

3:1, female:male

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5
Q

What is relapsing-remitting progression of MS?

A

symptoms then back to baseline

or symptoms that decrease but don’t go fully back to baseline

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6
Q

What is secondary progression of MS?

A

around 70% of the time

no fluctuations, just steady progression?

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7
Q

What is the Expanded Disability Status Scale (EDSS)?

A

evaluating the motor changes, not cognitive ones

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8
Q

What is the pathology of MS?

A

many lesions in the white and gray matter

lesions damage the nerve fibers and tracts

location of lesion causes symptoms

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9
Q

What is the relationship between MS and myelination?

A

demyelination, remyelination, axonal transection

decreased axonal density in MS plaques

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10
Q

What are the causes of MS?

A

genes

environment: infections (EBV, Mono, could bring things to the surface), smoking, sun exposure, sodium (activates the immune system)

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11
Q

What is the genetic contribution to multiple sclerosis risk?

A

no Mendelian relationship

genome wide association studies: HLA or MSC

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12
Q

How can EAE be produced in animals?

A

can be produced by myelin-specific T cells

mice injected with myelin basic protein and complete Frund’s adjuvant develop demyelinating disease (EAE)

the disease is mediated by myelin basic protein-specific T cells

disease can be transmitted by transfer of T cells from affected animal

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13
Q

What is the immunology of EAE?

A
  1. inject MBP
  2. in a pool of naïve T cells there will be a MBP-recognizing cell
  3. MBP-specific T cells cause antigen presentation
  4. there is an expansion of MBP-reactive T cells and they enter the CNS
  5. these cells are reactivated in the CNS, products produce CNS pathology
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14
Q

How is the process of EAE a model of molecular mimicry?

A
  1. virus with molecular similarity to myelin protein (e.g. MBP) interacts with a pool of naïve cells that contains virus-recognizing cells and MBP-recognizing cells
  2. there is antigen presentation of virus to naïve T cells
  3. this causes expansion of virus specific T cells trying to get rid of viruses, and expansion of cross-relative MBP-specific T cells which cause accidental activation which can cause alkaline reaction
  4. these cells enter the CNS, recognize MBP, and initiate inflammatory damage
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15
Q

What do naïve CD4 T cell differentiate into?

A

differentiate into Th1, Th2, Th17, and T regulatory cells

different path based on environment

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16
Q

What is MS pathogenesis based on B lymphocytes?

A

antigen presentation

Breg dysfunction

antibody production

ectopic germinal centers

cytokine activation of astrocytes/microglia

17
Q

What kind of inflammation is seen in MS plaques?

A

peri-vascular inflammation

18
Q

What is the pathogenesis of MS in neurons?

A

astrocyte activation

neuro-axonal degeneration

microglia activation

energy failure

glutamate excitotoxicity

inflammation

ionic imbalance and increased sodium levels

demyelination

activate microglia, axonal death, swelling of axons, demyelination

19
Q

What is immune dependent neurodegeneration in MS?

A

immune dependent, immune system is causing damage, microglia, astrocyte, and B cell caused

20
Q

What is immune independent neurodegeneration in MS?

A

microglia: mtDNA mutation, energy deficiencies, ROS/RNS, mitochondrial injury

astrocyte: demyelination, Fe3+, oxidative stress

B cell: influx of Ca++, glutamate excitotoxicity, ionic imbalance

immune independent due to the swelling, even if inflammation stopped these pathways will continue

21
Q

What is the brain atrophy in MS?

A

enlarged ventricles

damage to white and grey matter

22
Q

What are clinical manifestations of MS?

A

symptoms in almost any area

ocular: blurred vision, diplopia

cerebellar: ataxic walk, vertigo, nystagmus

autonomic: urinary incontinence, sexual disorders

motor: reduced strength and activity, muscle spasms, muscle weakness and loss of strength

sensory manifestations: tuning fork, sensory changes, hypesthesia, progressive sensory loss

23
Q

What is fatigue?

A

a feeling of physical tiredness and lack of energy distinct from sadness or weakness

very difficult for patients or caregivers to describe

severe in up to 74% of patients, worst symptom of the disease in 50-60% of patients

24
Q

What is bladder overactivity?

A

urgency, frequency, urge incontinence

25
Q

What is bladder inefficiency?

A

incomplete emptying, residual, urine

26
Q

What is detrusor-sphincter dyssynergia?

A

co-contraction of bladder and urethral sphincter

27
Q

How many MS patients are affected by bladder dysfunction?

A

about 75%

28
Q

What is persistent neurogenic pain?

A

hard to treat

burning dysesthesia of the limbs and/or trunk attributed to disruption of the spinothalamic pathway usually within the spinal cord

29
Q

What is paroxysmal neurogenic pain?

A

trigeminal neuralgia

episodes of excruciating facial pain

30
Q

How many MS patients are affected by pain?

A

about 40-50%

31
Q

What are treatments of MS in the immune system?

A

existing treatments primarily target the inflammatory component of MS

32
Q

What are treatments of MS in the CNS?

A

there is a need for novel agents that directly target protection and repair of the CNS as well as targeting inflammation

33
Q

What are different therapy options for MS?

A

traditional injections: beta-interferons, glatiramer acetate

oral therapies: dimethyl fumarate (Tecfidera), fingolimod (Gilenya), teriflunomide (Abagio), cladribine

Autologous stem cell transplant (experimental)

chemotherapies: mitoxantrone, cyclophosphamine

monoclonal antibodies: natalizumab (Tysabri), alemtuzumab (Lemtrada), ocrelizumab

34
Q

What are traditional immunomodulatory therapies for treatment of MS?

A

in the 1990’s

interferon (IFN)beta1b: 2 preparations, betaseron, extavia

IFNbeta1a: (sc) and (im) variations

glatriamer acetate (GA): copaxone

35
Q

How does interferon-beta act to treat MS?

A

interferon-beta acts through the interferon-beta receptor and inhibits antigen presentation and T cell activation

reduced the activation of autoreactive T cells

decreases pro-inflammatory Th1 cytokines

36
Q

How does GA act to treat MS?

A

GA is presented as an antigen and generates GA-specific T cells of Th2 bias

GA peptide –> GA specific Th2 cells

37
Q

How does dimethyl fumarate treat MS?

A

dimethyl fumarate activates Nrf2

Nrf2 activates protective response against neurotoxic insult, this increases cell tissue and cytoprotection

Nrf2 ant-inflammatory response, decreases inflammation and tissue damage

38
Q

How does S1P treat MS?

A

the signal mediated through S1P regulated the exit of lymphocytes from lymph nodes

NEURO 210 (23 decks)

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