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Neuro Clerkship > Multiple Sclerosis > Flashcards

Multiple Sclerosis Flashcards

1
Q

Multiple Sclerosis:

  • Problem?
  • Age of onset
  • Sex distribution?
  • Which race most affected?
A
  • Autoimmune demyelinating disease of CNS–> focal neurological deficits
  • Presents bw 20-40 yoa
  • Women 4: Men 1
  • Most common and least severe variant in caucasian females
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2
Q

What are some risks that predispose patients to MS (4)?

A
  • Northern climate
  • Vitamin D deficiency
  • Female (2-3x risk)
  • First degree relative (20-40x risk)
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3
Q

What is optic neuritis?
How is it associated with MS (1)?
How does it present (4)?

A

Inflammation of optic nerve; most common presentation of demyelinating disease from MS

Clinical presentation:

  • Afferent pupillary defect
  • Blurry vision (dirty dish water)
  • Pain with EOM
  • Optic disc swelling
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4
Q

How should you work up optic neuritis?

What will you see (2)?

A

Perform MRI with and without gadolinium (contrast):

  • New areas of inflammation/ demyelination will enhance (BBB breakdown)
  • Contrast enhancement = lesion LESS THAN 6 wks old
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5
Q

How do we treat acute MS flare like optic neuritis?

Is treatment curative?

A

Treat with 1 gram IV methyl-prednisone for 3-5 days

This will SPEED UP recovery, but will not CURE lesion–patients with and without treatment will be the same at 3 mos

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6
Q

What is a clinically isolated syndrome?

Should these patients be screened for MS?

A

Demyelination/ neuro deficit that does not meet McDonald Criteria for MS–may be paraviral syndrome, etc.

**Should still screen for MS because 20% risk of developing disease

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7
Q

Give 4 examples of clinically isolated syndromes in order of frequency:

A
  1. Optic Neuritis
  2. Brain Syndrome
  3. Spinal Cord Syndrome
  4. Multifocal/ other

*90% patients will have one of these 4 sx

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8
Q

What should you look for in CSF sample to corroborate dx of MS? (4)

**How commonly does disease manifest in CSF?

A
  • ^ Myelin basic protein
  • Oligoclonal banding
  • ^ IgG/ Albumin ratio
  • ^ IgG synthesis rate

**MOST MS patients have positive CSF findings

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9
Q

Goals of long term MS therapy (3)?

A
  • Reduce relapses
  • Reduce new and enlarging lesions on MRI
  • Reduce disability
  • *Tolerable ADR profile
  • *Safe for long term use
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10
Q

What are the two general types of “platform agents” used to treat MS?

What is the relapse rate associated with each method?

A
  1. Beta interferon (30-35%)

2. Glatiramer Acetate (35%)

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11
Q

List 4 types of Beta interferon.

What are the ADRs associated with treatment (5) ?

A
  1. Avonex (low dose)
  2. Rebif (high dose)
  3. Betaseron
  4. Extava

ADRS:

  • HA, malise, myalgia, fever
  • ^ liver enzymes ***
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12
Q

What are the ADRs associated with Glatiramer/ Copaxone? (4)

A
  • Injection site reactions (lipoatrophy)
  • Chest tightness (w injection)
  • Dyspnea
  • Flushing
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13
Q

What are 5 issues with the platform therapy that make it difficult to use clinically?

A
  • Injection (compliance)
  • Incomplete efficacy
  • ADRs
  • NEUTRALIZING AB formation to IFN over time (esp with smokers)
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14
Q

Who is most likely to develop neutralizing Abs to beta IFN over time?

A

SMOKERS!!!!!

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15
Q

List 3 oral drugs to treat MS + their origin:

A
  • Fingolimod (Gilenya): renal transplant drug
  • Teriflunomide (Augbagio): RA drug
  • Dimethyl fumarate (Tecfidera): MS specific
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16
Q

How does Fingolimod/ Gilenya work?

How does its efficacy compare to low dose IFN?

Why does first dose need to be administered in office/ hospital?

What is the most common ADR?

A

Sequesters lymphocytes in lymph nodes

  • Superior to low dose IFN
  • May cause significant bradycardia or HypoTN
  • # 1 ADR = HA
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17
Q

How does Teriflunomide (Aubagio) work?

A

Inhibits pyrimidine synthesis away in lymphocytes–>
Stop activated B/T cell proliferation–>
Decrease inflammation

18
Q

List two important ADRs associated with Teriflunomide:

A
  • TERATOGEN (Pregnancy X)

- Hepatotoxicity***

19
Q

How does Dimethyl Fumarate (Tecfidera) work?

What are the most important ADRs? How are they managed?

A

Inhibit Nrf2 pway–> No cell response to oxidative stress–> cell death

ADRs: flushing, N/Diarrhea within first few mos; control w coadmin ASA + take w food

20
Q

How does Natalizumab (Tysabri) work?

How is it administered?
How effective is it?
What is one ADR–what are two measures taken to minimize risk?

A

Monoclonal Ab against alpha-4 integrin–> Blocks WBC movement across BBB

  • Monthly infusions
  • So effective failure is considered noncompliance or PML
  • ADR = PML Get JC Ab to predict risk + MRI every 4 mos if hx of chemo
21
Q

How do we treat PML associated with Natalizumab administration? (3)

A
  • High dose steroids
  • PLEX
  • Remove Natalizumab
22
Q

How does Alemtuzumab (Lemtrada) work?

List 4 ADRs:

A

Monoclonal Ab against CD52

  • Infusion related (severe)
  • Thyroid disease
  • ITP
  • Goodpastures
23
Q

What is transverse myelitis?

What are the sx?

A

Demyelination of spinal cord

**Sx vary from incontinence, to sensory or motor deficits–> combo of all

24
Q

What must you always check in the case of transverse myelitis?

A

**Neurogenic bladder (post void residual)

25
Q

Primary Progressive MS:

  • What is it?
  • How is the dx made?
A

MS that fails to respond to disease modifying therapy

**Retrospective diagnosis that follow failure of multiple disease modifying agents

26
Q

Define Neuromyelitis Optica/ Devic’s Disease:

  • What are the clinical sx (3)?

- What is treatment of choice?

A

IgG against Aquaporin 4 Chloride Channel–>
Relapsing inflammatory demyelinating disease

Clinical manifestations:

  1. Sudden (~BL) vision loss
  2. Eye Weakness (~BL)
  3. Loss of bladder fxn/ sensation

Treat with RITUXUMAB (anti CD20–> B cell apoptosis)

27
Q

How does Neuromyelitis optic differ from MS? (5)

A
  • Lesions restricted to optic nerves and spinal cord
  • Attacks are more severe
  • Head MRI normal
  • Cord MRI w/ LONGITUDINAL (vs small scattered) lesions
  • No oligoclonal banding in CSF
  • Higher F:M ratio, frequent coexisting autoimmunity
28
Q

How might spasticity present in a patient w MS (3)

A
  • Spasms
  • Tight muscles–> cant initiate movement
  • Contractures (tendon shortening)
29
Q

What are three drugs used to treat spasms associated with MS?

A
  • # 1 Baclofen (centrally acting, preferred); possible pump
  • BDZs
  • Tizanadine
30
Q

Two non pharmacological treatments for MS related spasticity?

A
  • PT/OT

- Surgical tendon release

31
Q

How do we treat neuropathic pain associated with MS? (3)

A
  • TCAs (Amitriptyline)
  • AEDs (Gabapentin, Pregablin, Carbamazepine)
  • SNRIs (#1 Duloxetine)+ Pregalbin combo
32
Q

What three findings increase likelihood of MS related cognitive impairment?

What is the best treatment for this?

A
  • ^ T2 lesion load
  • ^ T1 + T2 lesion load
  • ^ Juxtacortical lesion load

Treat with STIMULANTS–NOT DEMENTIA DRUGS (i.e. ACEi’s!!

33
Q

How does bladder dysfunction in MS manifest? (3)

A
  • Failure to empty (^ risk infection)
  • Failure to store
  • Combo
34
Q

What are the problems that cause failure to empty the urinare bladder in pt with MS? (2)

Describe the sx of failure to empty the bladder in pt with MS

What will make this patient WORSE?

A
  • large, flaccid bladder
  • can’t relax urinary sphincter

Symptoms:
Urgency, frequency, hesitancy, nocturia, incontience, incomplete emptying, ^ UTIs

**Antispasmotics make these patients worse (oxybutinin, etc.)

35
Q

How do we treat failure to empty the bladder? (2)

A
  • intermittent cath

- alpha blockers (flomax)

36
Q

What are the characteristics of failure to store in the bladder of a patient with MS? (2)

What are the sx?

What are 5 treatments?

A
  • normal to small bladder
  • hypertonic bladder

Symptoms:
- urgency, frequency, incontinence

Treatment:

  • LIKE RUBY*
  • scheduled voiding
  • limit H2O in evenings
  • limit diuretics (caffeine)
  • anticholinergics
  • botox injections
37
Q

Patient with 2 + attacks, 2+ lesions?

A

No requirements for dx–they have MS

38
Q

2+ attacks, 1 clinical lesion

A

Three possibilities for MS:

  • Dissemination in SPACE on MRI
  • CSF markers
  • Await additional attack
39
Q

1 attack, 2 lesions

A

2 Possibilities for MS:

  • Dissemination in TIME on MRI
  • Second clinical attack
40
Q

1 attack, 1 lesion

A

3 possibilities for MS:

  • Dissemination in SPACE and TIME on MRI
  • CSF markers
  • Additional attack
41
Q

0 attacks, 0 lesions

A

2/3 of the following:

  • Positive brain MRI
  • Positive spinal cord MRI
  • Positive CSF

Neuro Clerkship (13 decks)

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