L5 MS Intro Flashcards
MS defintion
chronic inflammatory progressive disease of myelin in brain, spinal cord, optic nerve, cerebellum
autoimmune disease with genetic component
onset of MS
average and percentages
mean onset is 30 y/o
70% 20-40
10-20% after 60
MS population
younger adults
F>M
genetic, 1st degree relative
epstein barr exposure, vitamin D/sunshine deficiency, smoking
MS pathology of what cells? (2)
oligodendrocytes which form myelin
microglia release inflammatory agents and autoimmune component
pathophys of MS
inflammation opens gaps in BBB, T cells, B cells, macrophages enter CNS and start autoimmune process, microglia start releasing pro-inflammatory signals
antibodies created by T cells activating B cells, target oligodendrocytes
inflammatory demyelination in MS
caused by depletion of oligodendrocytes which remyelinate cells
damages nerve transmission
reducing inflammation reduces symptoms as remyelination occurs
repeated inflammation leads to irreversible damage and disability
plaques in MS
loss of myelin in one area - plaque
associated with axon loss of function
most in SC, then optic nerve and cerebellum
result in brain atrophy
gray matter dysfunction in MS
because white matter/axons are affected, gray matter gets less nutrition and associated with more disability
epidemiology
3:1 W to M
men have more aggressive version
western european, extreme north/south
migrating from these areas reduces risk
above 45 latitude
classifications of MS
relapsing remitting
secondary progressive
primary progressive
progressive relapsing
benign/CIS
relapsing remitting MS
85% of cases
unpredictable attacks which may/may not leave permanent deficits but go into remission
secondary progressive MS
RRMS that develops into progressive after about 15 years
starts a decline without remission
primary progressive MS
gradual worsening of symptoms without remission
doesn’t respond to standard medical Rx
progressive myelopathy
benign MS
one occurrence with no reoccurence
EDSS
expanded disability status scale
0-9
0-1 no disability
5 disability affecting ADLs
6 assistance to walk
7 wheelchair
8=9 bedbound
diagnosis of MS criteria
two lesions in two separate areas of brain, SC, or optic nerve
AND
evidence of two different points in time
AND
rule out other diagnoses
diagnose MS - differential
LBP
fibromyalgia
cervical spondylosis
herniated disc
mitochondrial disease
diagnose MS - testing
needs multiple tests, no single one
MRI: plaques and lesions
lumbar puncture: elevated protein in CSF during exacerbation
Visual evoked potential: measure electrical activity of optic nerve
initial symptoms of MS
20s female
transient
fatigue
double vision
paresthesia/N/T/weakness
LBP
pain in BL LE
s/s in MS exacerbation
lasting longer than 24 hours
N/T
fatigue
visual changes
weakness
gait changes
brain fog
tremors
incontinence
disease pathway of MS
diagnosis
exacerbation - longer = more damage
remission - no activity
management - reduce flares
smoldering model of MS
continuation of disease process even when in remission with reduced symptoms
explains why pts with MS can be in remission but showing more involvement/more lesions developing
pseudoexacerbation of MS
less than 24 hours
resolves on its own
brought on by stress, heat, over exertion
s/s: fatigue, brain fog, pain
does not mean there is nervous system damage
central MS symptoms
fatigue
cognitive impairments
depression
unstable mood
visual symptoms of MS
nystagmus
optic neuritis
diplopia
speech/throat symptoms of MS
dysphagia
dysarthria
MSK symptoms of MS
weakness
spasms
ataxia
sensory symptoms of MS
pain
hypoesthesia
paresthesia
anesthesia
bowel/bladder symptoms of MS
incontinence
diarrhea
constipation
frequency
retention
fatigue types in MS
primary: damage to axons in brain and spinal cord (muscle fatigue)
indirect fatigue; from med/sleep meds, depression
neurologic fatigue: spasms, weakness, heat exposure, energy failure
correlations with fatigue in MS
stress and increased physical activity associated with more fatigue
positive mood associated with less
heat intolerance in MS
Uhtoff phenomenon: increased core body temp
70% pts
exertion, hot water, weather
does not increase disease, does increase symptoms
resolves when heat source is removed
types of spasms in MS
flexor and extensor, more UE than LE
flexor knees bent, extensor scissoring extended legs
spasticity in MS
triggers, effects, % who have it
effects function and QoL
84% have spasticity
made worse by position changes, noxious stim, physiologic stress, pain, cold weather, tight clothing, increased body temp
can lead to contracture, skin breakdown, infection, pain, sleep disturbances, poor hygiene, decreased mobility
neuropathic pain types in MS
acute: from sensory neuron demyelination
trigeminal neuralgia: stabbing pain in face and jaw, not constant
lhermitte sign: stabbing electric shock through the spinal cord
chronic: brought on by stress, fatigue, illness, overheating
dysesthesias: pain in limbs including N/T
pruritis: itching/burning
MSK pain in MS
tightness
loss of ROM
spasticity
weakness
abn motion
compensatory mvmt patterns
abn use/loading
muscle fatigue
sensory impairments in MS
optic neuritis: double vision/blurry/painful
visual field loss
pupillary deficits
dys/an/parathesia
vestibular dizziness/vertigo
MS problems with postural control
what are the actual problems found on exam?
- delayed response to postural perturbations
- increased body sway to quiet standing
- inability to move outside bos
are bowel or bladder problems more common in MS?
both common, bladder more common
35-68% bowel
53-98% bladder
disease modifying drugs for MS have what effect?
prevent new inflammatory lesions
prevent development of secondary progressive MS
prevent loss of neuroprotection and allow more remyelination
slows progression but is not a cure
clinical isolated syndrome disease course
monophasic episode suggesting MS
30-70% develop MS
if they have optic neuritis, 10-85% develop MS
20-45 y/o
RRMS disease course
85% cases
20-30 y/o
relapse over days/weeks with full/partial remission over months/years
secondary progressive MS disease process
75% RRMS develop into this after 15 years
primary progressive MS disease process
steady functional worsening after onset of disease
15%
later onset
