Multiple Sclerosis Flashcards
immune mediated destruction of CNS w/ secondary loss of axons
MS
classic MS lesion
demarcated white matter plaques, have a periventricular prominence
initial step in pathogenesis
lymphocytes and macs penetrate BBB
MS vs other leukodystrophies (demyelinating dzs)
MS gives autoimmune destruction of myelin
leukodystrophies have abnl myelin produced (defective synthesis)
MS affects people from what location
born and raised in temperate latitudes or global zones father from the equator (maybe related to lower vit D levels?)
“risk factors” for MS
genetically susceptible
exposure to triggering factors (maybe virus)
live in temperate zones
amount of inc risk for siblings of MS patient
20-fold inc risk
MS population
young adults 20-40 y/o
F:M ratio for MS
2:1
first course of MS
80% relapsing-remitting
20% primary progressive
2nd phase for MS pts who started relapsing-remitting
secondary progressive phase - less recovery
primary progressive MS pathogenesis
different from relapsing-remitting type, doesn’t respond well to immunomodulators
cause of death for MS
infection, malnutrition, and pulm emboli –> complications of immobility
initial sxs of MS
optic neuritis, sensory/motor deficits in lower limbs, internuclear opthalmoplegia
MLF lesion
aka internuc opthalmoplegia - blurry vision/diplopia
Lhermitte’s sign is due to
due to short circuiting w/in posterior columns of C spine from MS plaques, Vit B12 deficiency, or compression of spinal cord
electric shock/tingling down spine into arms/legs provoked by neck flexion
Lhermitte’s sign
MS “attack”
aka relapse/exacerbation
lasts 24+ hrs
no fever/infection
MS pseudo-exacerbation
looks like recurrence but is due to infection (inc temp causes impaired depol/conduction thru a remyelinated region)
historic dx for MS
sxs disseminated in time and space w/ no other identifiable cause
current dx for MS
use MRI (high sensitivity, but not specific, for white matter lesions)
monophasic mimics of MS (aren’t “disseminated in time”)
post-infectious encephalomyelitis
aging of lesions via MRI
acute/new lesions enhance (inflamm), chronic/inactive lesions don’t enhance
CSF for MS
oligoclonal bands
inc Ig synthesis
MS evoked potentials
delayed cortical response to stimuli
MS tx for acute aggressive attack
IV high dose steroids (methylpred 500-1000 mg/day x 3-5 days +/- prednisone taper)
method to”help prevent “MS flare” sxs
fever control
tx to reduce severity/frequency of MS attacks
DMT - beta IFN or glatiramer acetate
protein that inc suppressor T cell fxn, dec lymphocytes entering CNS, dec antigen presentation, dec cytokine production
beta IFN
Betaseron
IFN beta-1b
subq injection every other day
Avonex
IFN beta-1a given IM weekly
Rebif
IFN beta-1a given subq 3x/wk
Glatiramer acetate (aka Copaxone)
polypeptide resembling myelin basic protein (byproduct of myelin destruction) , given subq daily
MS tx to dec limb spasticity
Dilfampridine (4-aminopyridine)
Dilfampridine (4-aminopyridine)
K channel blocker
inc walking speed
Natalizumab (Tysabri)
interferes w/ binding of lymphocytes to CNS vasc cell adhesion machines
complication of Natalizumab
reactivation of JC virus
other oral meds for MS
fingolimod (Gilenya), teriflunomide (Aubagio) and dimethyl fumarate (Tecfidera)
