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Neuro > MS and Spasticity > Flashcards

MS and Spasticity Flashcards

1
Q

Multiple Sclerosis refers to (two)

A
  • multiple neurologic symptoms that accrue over time
  • characteristic plaques or sclerosed areas that are seen in numerous areas of the brain and spinal cord
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1
Q

are men or women more commonly affected?

A

women

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2
Q

MS primary risk factors

A

geography, age, environmental influences (smoking or vit D deficiency) and genetics

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3
Q

Why is cigarette smoking a risk factor?

A

the lung is a critical site for the activation of pathogenic T lymphocytes responsible for autoimmune demyelination

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4
Q

Genetic association

A

HLA DRB11501 and Interleukin-2alpha/7alpha

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5
Q

etiology

Microbrial theory

A
  • a direct attack on myelin/oligodendrocytes
  • may stimulate autoimmune response causing demyelination
  • increased IgG synthesis in CNS as well as antibody titers to certain viruses
  • gut microbes may alter microglia functioning resulting in increased activity of astrocytes
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6
Q

What viruses could cause MS?

A

HCV, herpes, human endogenous retrovirus, Epstein-barr

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7
Q

etiology

autoimmune theory

A

attack against myelin and oligodendrocytes, myelin basic proteins may serve as an autoantigen

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8
Q

Which cell is the key initiator

A

TH1 (t helper cells) are activated in the periphery by interacting with antigen presenting cells and then cross the blood brain barrier and attack myelin

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9
Q

what breaks down the blood brain barrier for t-cells to pass through?

A

MMP: matrix metalloproteins

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10
Q

Th17 cells

A

potentially activated inside the blood brain barrier and move from ventricles through choroid plexus

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11
Q

Th2 or Treg

A

usually supresses T cell activation, but in MIS it is impaired or there are less

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12
Q

what cytokines are involved in the inflammatory response?

A

VEGF-B, TNF-alpha, INF-gamma, IL-2

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13
Q

what are the modulators (good guys) of the immune response?

A

TGF-beta, TGF-alpha, and IL-10 can down-regulate immune response

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14
Q

B cell involvement

A

traffic into CNS and activate pro-inflammatory T cells to promote secretion of pro-inflammatory cytokines
also involved in autoantibody production against myelin

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15
Q

What is the pathologic hallmark of MS?

A

stripping of the myelin sheath around CNS neurons

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16
Q

disruption of nerve impulse transmission leads to

A

neurologic symptoms
- increased refractory periods delaying impulse conduction
- hyperpolarization due to altered potassium channels

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17
Q

neurodegeneration

A

cumulative axonal and neuronal loss is the most important contributor to irreversible neurologic disability and progressive symptoms

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18
Q

Relapsing Remitting MS

A

clear relapses with either full recovery or will partial recovery and lasting disability.* between attacks there is no progression or worsening of disease*
most common

19
Q

Primary Progressive MS

A

steady progression or worsening from onset with only occasional plateus or minor recovery

20
Q

Secondary Progressive MS

A

begins with clear-cut relapses and recovery but becomes steadily progressive over time with continued worsening between attacks

21
Q

Progressive-Relapsing MS

A

steadily progressive from onset but also has clear acute attacks
rare

22
Q

Spasticity

A

stiff or rigid muscles - unusual tightness or increased muscle tone due to upper motor neuron deficit/dysfunction

23
Q

Upper motor neuron and Inhibitory interneurons neurotransmitters?

A

Upper: Glutamate
Inhibitory: GABA

24
Q

Upper Motor Neuron Deficit

A

normally after a muscle stretch/contraction, the upper motor neuron will release glutamate which activates the inhibitory interneuron to release GABA and cause relaxation at muscle
- when deficient: glutamate not released so prolonged muscle contraction and spasticity

25
Q

When are glucocorticoids used? (methylprednisone, prednisone, dexamethasone)

A

used to manage either first attack or acute exacerbations (antiinflammatory)
they can reduce severity and duration of attacks

26
Q

Interferon-beta1a

A

Avonex, Plegridy (pegylated form)

27
Q

Interferon-beta1b

A

Betaseron

28
Q

Interferon-beta MOA

A
  1. augmenting suppressor cell function and reducing IFN-gamma(pro-inflammatory) secretion by activated lymphocytes
  2. macrophage activating effect
  3. downregulate expression of IFN-gamma-induced MHC gene producted on antigen presenting glial cells
29
Q

Glatiramer acetate (Copaxone) MOA

A
  • may mimic antigenic properties of myelin basic proteins and therefore inhibit binding of the actual MBP
  • induces Th2 anti-inflammatory lymphocytes to reduce inflammation, demyelination, and axonal damage
  • neuroprotective effects by inducing brain-derived neurotrophic factor
30
Q

Mitoxantrone (Novantrone) MOA

A

DNA reactive agent: intercalates into DNA, causing crosslinks and strand breaks resulting in cytocidal effects
- suppresses proliferation of macrophages, t cells, b cells but seems to enhance t-cell suppressor functions

31
Q

Sphingosine-1-Phosphate Receptor Modulators

A

Ponsimod (Ponvory), Fingolimod (Gilenya), Ozanimod (Zeposia) and Siponimod

32
Q

Sphingosine MOA

A

immunosuppressants via sequestration of circulating lymphocytes and macrophages into secondary lymphoid organs which block their ability to merge from lymph nodes and reduce their infiltration into CNS/inflammation

33
Q

Teriflunomide (Aubagio) MOA

A

active metabolite of leflunomide (immunosuppressant)
inhibits dihydroorotate dehydrogenase (an enzyme required for pyrimidine synthesis) to prevent proliferation of peripheral T & B cells

34
Q

Natalizumab (Tysabri) MOA

A

Partially humanized monoclonal antibody directed at the cell surface adhesion molecule alpha4beta-integrin, it attaches and blocks its interaction with VCAM-1 on BBB endothelial cells
prevents entry of activated lymphocytes in the CNS

35
Q

Fumerate derivatives and MOA

A

dimethyl fumarate (tecfidera), diroximel fumerate (vumerity), and monomethyl fumerate (bafiertam)
activates nuclear factor Nrf2 pathyway and independent pathways to be anti-inflammatory and cytoprotective
- been linked with progressive multifocal leukoencephalopahty risk

36
Q

Alemtuzumab-Lemtrada MOA

A

humanized monoclonal antibody against CD52, a glycosylphosphatidyllinosital anchored protein expressed in high levels on T and B lymphocytes
- causes depletion of CD52 positve cells

37
Q

Ofatumumab (Kesimpta), Rituximab and Ocrelizumab MOA

A

monoclonal antibody targeting CD20-positive B cells
- binds to cell surface of CD20 protein preventing B cell from causing myelin and axonal damage

38
Q

Cladribine (Mavenclad) MOA

A

Purine nucleoside analogue (antimetabolite)
a prodrug which is activated by phosphorylation and converted into the active moiety Cd-ATP. Incorporates into DNA to result in breakage of DNA strand and shut down of synthesis/repair

39
Q

Agents used for Spasticity

A

Benzos, Tiagabine, Gabapentin, Pregabalin, Baclofen, Tizanidine, Dantrolene Sodium, Botox, Delfampridine

40
Q

Baclofen MOA

A

GABA B receptor agonist
causes closure of presynaptic Ca2+ channels and increases postsynaptic K+ conductance
enhances spinal inhibitory interneurons and decreases activity of alpha motor neurons

41
Q

Tizanidine (Zanaflex) MOA

A

significant alpha2-adrenergic agonist reducing spasticity at doses that cause few CV effects
increases inhibitory action of spinal interneurons acting both pre and post synaptically

42
Q

Dantrolene Sodium (Dantrium) MOA

A

works locally at the muscle to impair Ca2+ release from SR by binding to the ryanodine receptor RyR1 to block opening of the channel
- minimal effects on cardiac and smooth muscle RyR2

43
Q

Botox MOA

A

produces chemodenervation and prevents release of Ach by interfering with vesicle fusion by proteolytically cleaving SNAP-25

44
Q

Dalfampridine (Ampyra) MOA

A

long acting broad spectrum K+ channel blocker

Neuro (4 decks)

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