B7-092 Multiple Sclerosis Flashcards by Felicia Jones

most common demyelinating disease affecting the central nervous system

multiple sclerosis

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CNS myelin comes from

oligodentrites

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PNS myelin comes from

Schwann cells

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what kind of deficit pattern does MS cause?

multifocal

discrete areas of transient inflammatory deyelination

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MS is thought to result from […] response to antigens in myelin

autoimmune

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damaged myelin disrupts […]

saltatory conduction

(slows/stops propagation at nodes of Ranier)

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people living in what areas of the world have the highest risk of getting MS?

temperate zones (northern US, Europe, Canada)

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when migrating from a high-risk to low-risk area, chances of getting MS decrease if migration occurred before what age?

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late infection with […] provides a 3-fold increased risk of developing MS

EBV

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shares epitopes with myelin basic protein

EBV

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theories of geographical distribution of MS [3]

hygiene hypothesis
molecular mimicry (EBV)
low levels of vitamin D

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signs and symptoms of MS are dependent on

location of lesion

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common symptomatic locations of MS plaques [3]

optic nerve
brain stem/cerebellum
spinal cord

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asymptomatic lesions commonly occur where?

cerebral hemispheres

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diagnostic criteria for MS

two or more lesion of the CNS separated in space and time without other explanation

(can use MacDonald criteria to account for radiologic findings)

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supportive findings of MS [3]

multifocal white matter lesions on MRI
CSF oligoclonal bands
CSF pleocytosis <50 cells

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inflammation around penetrating venules that run perpendicular to the ventricles

dawson fingers

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many people have T2 hyperintensities on MRI but without [….], they should not be diagnosed with MS

clinical abnormalities

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what would you expect to seen on CSF analysis in an MS patient

oligoclonal bands
elevated IgG
elevated IgG index
maybe elevated protein
maybe elevated WBC

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85% of MS patients have what type?

relapsing-remitting MS

(50% of these patients develop secondary progressive MS)

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15% of MS patients have what type?

primary progressive MS

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symptoms develop over hours or days
can worsen for several weeks
slowly subside over several weeks or months

relapsing remitting MS

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recurrence of previously experienced symptoms not related to current inflammation
often seen in the setting of systemic infection (UTI, pneumonia)

psedoexacerbation

no steroids

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gradual progression
spinal myelopathy is common

progressive MS

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progressive course following a relapsing remitting course

secondary progressive MS

first presentation of neurological symptoms from inflammatory demyelination

clinically isolated syndrome (often a retrospective diagnosis, can be monofocal or multifocal)

used to guide prognosis of MS

expanded disability status scale (EDSS)

poor prognostic factors for MS [7]

male older age multifocal onset with motor, cerebellar, bladder/bowel symptoms high frequency of relapses severe relapses high lesion load on MRI

used to shorten the duration of relapse

high dose steroids (not used in pseudo exacerbation)

treatment for MS related fatigue

methylphenidate

treatment for MS spasticity

baclofen (oral or pump)

MOA: suppression of gamma interferon

beta interferon

MOA: competes with MBP for antigen presentation

glatiramer acetate

MOA: inhibits pyrimidine synthesis inhibiting clonal expansion lymphocytes

teriflunomide

MOA: decreases lymphocyte proliferation through Nrf2 pathway

dimethyl fumurate

MOA: sphingosine-1-phosphate receptor modulator trapping lymphocytes in lymph nodes

flingolimod/siponimod

MOA: anti-alpha 4 integrin antibody preventing lymphocytes from crossing BBB

natalizumab

MOA: purine nucleoside analog cytotoxic to lymphocytes

cladribine

MOA: anti CD52 antibody causing prolonged lymphocyte depletion

alemtuzumab

MOA: anti CD20 antibody depleting B cells

rituximab/ocrelizumab

side effects: beta interferon

flu like symptoms

side effects: glatiramer acetate

injection site reaction

side effects: teriflunomide

liver dysfunction, hair loss

side effects: dimethyl fumurate

lymphopenia, liver dysfunction

side effects: fingolimod/siponimod

first dose bradycardia herpes virus infections rare PML

side effects natalizumab

higher risk of PML rebound

side effects: cladribine

liver toxicity risk of infection rare PML

side effects: alemtuzumab

risk of autoimmunity infections

side effects: rituximab

infections malignancy rare PML

interferes with antigen presentation

glatiramer acetate

prevent clonal expansion [2]

teriflunomide dimethyl fumurate

prevent the movement of lymphocytes from the lymph node into circulation

fingolimod siponimod

prevent the movement of lymphocytes from the circulation to brain

natalizumab (rebound phenomenon if suddenly stopped since all the lymphocytes can suddenly move in)

kill lymphocytes [3]

cladribine alemtuzumab rituximab

main function of myelin

enable saltatory conduction

[...] loss is a pathological feature of MS

axon

are DMARDs helpful for secondary progressive MS?

what happens to the action potentials where the disease has caused demyelination?

the action potential conduction is slower and can even be blocked when the signal are moving faster (increased temperature)

pathology of what parts of the nervous system can result from MS? [4]

axonal transection brain atrophy demyelination neuronal degeneration

radiographic hallmark of **acute** MS lesion

gadolinium T1 enhancing lesion due to breakdown of the BBB

immunotherapy is effective for what type of MS?

relapsing-remitting

what MRI finding are you less likely to see in progressive forms of MS?

gadolinium T1 enhancement (hallmark of acute lesions)

treatment for secondary progressive MS?

supportive -can use steroids to shorten duration and provide symptom management **DMARDs are not effective**

red flags for psuedo exacerbation [2]

recent infection symptoms they've had before

90% of MS patients will have [...] in the CSF

oligoclonal bands

what feature of MS accounts for reduced processing speeds

demyelination

main pathological feature that leads to demyelination

perivenular inflammation

T2 hyperintensities in the corpus callosum emanting from the ventricles

Dawson's fingers

a few scattered white matter lesions are normal in people over what age?

50 **does not confer risk of MS**

symptoms continuously worsen from onset of disease no history of clear cut attacks

primary progressive MS

A progression of RR-MS characterized by continuous worsening of neurological function that occurs independently of exacerbation events

secondary progressive MS

Exacerbations occur. Symptoms remit almost completely between exacerbations.

relapsing-remitting MS

how long can an MS relapse last?

average 6-8 weeks Note: this is from Dr. Google, I just wanted an idea of when to consider progression, please don't stake your test score on it haha

concordance rate of MS in monozygous twins

30%

represent antibodies generated within the CNS

oligoclonal bands

concordance rate of MS in dizygotic twins

concordance rate of MS in siblings

about 3%