Multiple Sclerosis Flashcards
what is the hypothesized etiology of MS
autoimmune condition induced by viral or other infectious agent (ie herpes, measles, epstein-barr, chlamydial pneumonia)
- may be a genetic susceptibility to immune system dysfunction
what is the pathophys of MS
- immune system triggers production of T-lymphocytes, macrophages, immunoglobulins
- failure of BBB, allows immune cells to cross and attack myelin sheath
- demyelination accompanied by local inflammation
- gliosis (proliferation of neuroglial tissue) occurs and results in “glial scars” or plaques
- axon becomes damaged, undergoes degen
- axonal loss occurs and interferes w normal conduction of nerve signals & loss of function
what about the pathophys of MS leads to a poorer prognosis
less capability for repair w attack in CNS bc of scarring
peak age onset
30yo
- between 15 and 50yo
what populations at higher and lower risk for MS and what does this indicate
more common in caucasian
more common in women
lower risk in AA, asian, and NA
implies a genetic link bc of racial disparity
why is MS difficult to get a clear definitive dx
d/t variability in periods of flares/remission and in clinical courses
what are methods to medically dx MS
CSF markers
- oligoclonal bands (presence of IgG bands)
MRI changes (w gadolinium contrast)
visual evoked potentials
why are MRIs tricky to use as a diagnostic tool in MS
even tho we know glial plaques are forming anywhere in CNS -> this is very spotty and often not visible early on
gadolinium contrast will inc specificity/sensitivity
why/how is visual evoked potentials used to dx MS
measures time nerve impulse takes to travel from retina to visual cortex
bc optic nerve so long and runs thru entire brain -> common area for plaques to form
- visual disturbances are a common sx
what is the struggle w differential dx
no single, definitive test
plaques can form anywhere, hard to implicate one neuro condition
differential dx list is extensive, and remissions make dx challenging
what is the Poser criteria and what is its purpose
presence of 2 episodes over time and evidence of 2 or more lesions in separate regions of CNS
created to inc speed of dx MS
what are 4 categories of differential dx to consider
autoimmune/inflammatory conditions
CNS infections
metabolic conditions
vascular conditions
what are 6 common sites of MS plaque formation
- periventricular regions of cerebrum
- grey/white matter boundary in cerebrum
- cerebellar white matter
- brainstem
- spinal cord (cervical)
- optic nerve
why is it difficult to give an accurate prognosis for MS
many factors involved and variability
how is variability seen in MS
plaques can be anywhere in CNS therefore any and all neuro s/sx are possible
progression of dz is also highly variable and hard to predict
what can rate of progression of MS be related to
intrinsic factors
- dz expression
extrinsic factors
- lifestyle
- weather
- meds
- exercise
what is an MS exacerbation, relapse, or flare?
new or recurrent sx that lasts more than 24hrs
must be separated from previous flare by at least 30days
what is the most common trigger for both MS pseudoexacerbation and prolonged exacerbations
heat intolerance
what is a pseudoexacerbation
new/recurrent sx that lasts less than 24hrs
what are common triggers for MS exacerbations
stress
infections
excessive fatigue
trauma, surgery
childbirth
decline in health status, infection, fever
heat - fever, exercise, hot bath/shower, hot weather conditions
what are the 4 clinical subtypes of MS
- relapsing-remitting (RRMS)
- primary-progressive (PPMS)
- secondary-progressive (SPMS)
- progressive-relapsing (PRMS)
what is RRMS
defined by acute attacks w full recovery or partial residual deficit
- there is a lack of dz progression in between attacks
what clinical subtype are most people w MS initially dx with and what is the difficulty w this
RRMS
- makes it difficult to dx, while it is good bc of periods of remission
what are the most common first signs of RRMS
optic neuritis (40%)
severe/acute vertigo (48%)
what is SPMS
begins w RRMS course, followed by progression at variable rate
may include occasional relapses, remissions, plateaus
- steady decline of function, inc in neuro sx
- may have periods of more severe flares, then return to previous state
how common is SPMS
50% of those w RRMS develop w/i 10yrs
- 90% w/i 25yrs
why are stats of SPMS dx and development expected to change
new dz modifying drugs available
what is PPMS
characterized by progressive disability from onset, w/o distinct remissions, plateaus, or significant improvement
what is the prognosis of someone w PPMS
tend to respond less favorably to standard MS therapies
how common is PPMS and in what population
10% of people w MS
later age of onset (>50yo)
what is PRMS
progression from onset
clear, acute relapses or exacerbations that may or may not resolve
- cont dz progression in intervals b/w relapses
what subtype of MS is the least common form
PRMS
what is a characteristic of RRMS as the dz progresses
the more flares people have over time, the less likely they will return to baseline
what is the gold standard for medical management of MS
interferons - 1a, 1b
“ABCs of pharm management”
what are the 4 disease modifying drugs
interferon beta 1a
interferon beta 1b
glamtiramer (copaxone)
natalizumab (tysabri)
how do disease modifying drugs work in MS
immunomodulators
believed to dec severity and frequency of attacks, thereby slowing dz process
don’t cure MS
what is often the 1st line of defense for MS
interferons
what are common SEs of dz modifying drugs and why is this significant
malaise, fatigue, pain at injection site
usually taken once a week
-> those SE often present the day after they are taken
what is a potential adverse effect of 1 disease modifying drug and which one? why is this significant?
progressive multifocal leukoencephalopathy (PML)
- often fatal
Tysabri
Tysabri is a last line of defense as a result
what types are immunosuppressants approved for
RRMS
SPMS
what type of MS are there no disease modifying drugs believed to be effective for
PPMS
when is an immunosuppressant appropriate
if pt not tolerating other meds well, give people these
what is an example of an immunosuppressant
chemo agent
- mitoxantrone (novantrone)
what type of MS are immunomodulators appropriate for
RRMS
what are examples of meds used for sx management
pain
- gabapentin, dilantin, tegretol
bowel/bladder function
- detrol, ditropan
mood - SSRIs
fatigue - amantadine
acute flare
- steroids (often hospitalized)
spasticity
- baclofen, dantrium, diazepam, botox, phenol
what are common sx of MS that are w/i scope of PT practice
sensory
motor
visual changes
fatigue
pain
cerebellar dysfunction
autonomic changes
- CV dysautonomia
what are common sx of MS that are outside scope of PT practice
bladder/bowel dysfunction
speech/swallowing
- dysarthria/dysphagia
cog
emotional
sexual
what are the 6 most frequent clinical manifestations of MS
fatigue & heat sensitivity*
gait/balance disturbances
bowel/bladder dysfunction
spasms, stiff, sensory loss, pain
visual disturbances*
emotional and cog changes
what is a helpful about testing for path reflexes (like babinski and hoffmans) in MS
path reflexes to test for UMNL
- can be helpful bc of how spotty MS is
primary vs secondary fatigue in MS
primary:
- caused by effects of demyelination and axon destruction
secondary:
- deconditioning
- infections
- sleep disturbances
- poor nutrition
- med SE (interferon/ABCs)
- heat intolerance***
- depression (psych)
what subtypes of MS is fatigue most frequent and most severe
PPMS
SPMS
describe the pathophys of primary fatigue
dysfunction in circuits b/w thalamus, basal ganglia, and frontal cortex affected by MS lesions and disturbed by inflammation
mismatch b/w internal estimation of neural workload required and real neural work used
-> everything you try to do will take extra activation in brain and nerves to be functional
what are 2 causes for balance deficits in MS
visual disturbances
cerebellar lesions
what are 5 common motor sx seen in MS
weakness (primary & secondary)
balance deficits
coordination deficits (ataxia)
gait abnormalities
hypertonia (spasticity*)
how can spasticity present in MS
can present as “phasic spasms”, painful cramping, and/or clonus
inc ext tone tends to dominate
- lot of ADD in LE too
pathophys of MS that can lead to sensory dysfunction
plaques in parietal lobe (sensory cortex) and anywhere along ALF and DCML tracts
what are the top 3 first signs of MS in general
- visual disturbances **
- vertigo
- paresthesias of limb, face, and trunk
- if paresthesia is the first sign, usually years and years before a MS dx
how does sensory dysfunction usually present
numbness and paresthesias
often in conjunction w other sx
altered sensation occurs at some stage in almost all pts w MS
what are 6 manifestations of pain in MS
neuropathic
(+) Lhermittes’ sign
paroxysmal/intermittent limb pain
HAs
optic neuritis
trigeminal neuralgia
why do you see neuropathic pain in MS
associated w damage to neural tissue
what is (+) Lhermitte’s sign and what does this indicate
neck flexion produces a “shock like” sensation runnign down spine and into LEs
d/t posterior column damage / demyelination
what is optic neuritis and why is this seen in MS
eye pain in addition to visual disturbances
d/t inflammation and demyelination
what is trigeminal neuralgia? why is this seen in MS? how can this be treated?
intractable/severe facial pain
likely d/t pontine plaques
sometimes treated w stereotactic gamma knife surgery to sever CN V
what are 5 cerebellar sx commonly seen in MS
ataxia
postural or intention tremors
hypotonia
asthenia -general ms weakness
vestib sx
what are vestib sx commonly seen in MS and why
vertigo, dizziness, gaze instability
high interconnection b/w vestib inputs and cerebellar outputs
how do visual sx in MS present
usually unilateral
- can progress to bilateral
characterized by:
- eye pain
- loss of vision
- blind spots in visual field
- blurred vision
- nystagmus
what is uhthoff’s phenomena
pseudoexacerbation / reaction in response to an increased core body temp (overheating)
dimming or reduction in vision, and fatigue
what can uhthoff’s phenomena indicate
damage to optic nerve, attributed to fluctuation in axonal conduction
when does uhthoff’s phenomena subside/improve
with minutes to one hour of physical rest and lowering core body temp
what emotional changes are seen in MS and why
depression
affective changes in mood, feelings, emotional expression linked to diffuse, (B) frontal or subcortical white matter dz
what are cog impairments seen in MS
verbal fluency and memory
memory loss
processing speed decline
executive function deficit
- poor planning and reasoning
attention deficit
visuospatial learning difficulties
why can CV dysautonomia be seen in MS and how can it present
bc of ANS involvement
difficulty regulating HR, BP, digestion, temp control
orthostasis
dec or absent sweating response
what are signs of orthostasis d/t CV dysautonomia in MS
lightheadedness
fainting
unstable BP
abnormal HR
malnutrition
why is it especially concerning to see wt loss in someone w MS and what can help
wt loss particularly concerning bc already having ms atrophy and don’t want to exacerbate that
RD can be helpful to manage this and nutrition
why is an attenuated or absent sweating response d/t CV dysautonomia in MS problematic
bc heat sensitive and can’t regulate temp
- Uhthoff’s phenomena and then makes it difficult to be able to exercise
what is the life expectancy of someone w MS
close to gen pop, slightly reduced
what are favorable prognostic factors in MS
female
1 sx at onset
RRMS
young age of dx
few neuro signs at 5yrs
few lesions & no axonal loss on MRI
what is a difficulty in MS that is a significant source of disability and morbidity
difficulty staying in workforce and maintaining relationships
what are 2 significant risk factors for MS
smoking
- inc dz severity, sx, progression
obesity
what are 5 causes of death in MS
pneumonia from aspiration
- esp if bulbar sx
infections
- UTI, URI, pressure ulcers
falls
suicide
heart dz (d/t inactivity)
why is education important in this pt population
lot of different domains and focus on secondary complication prevention
what are MS EDGE recommendations
list of 10 highly recommended standardized tests and measures
what is the gold standard for assessing MS dz severity
expanded disability status scale (EDSS)
what EDSS scores indicates peak fall risk
between 4 and 6
what is the expanded disability status scale (EDSS)
standardized disease specific participation measure that quantifies disability in 8 functional systems
- pyramidal
- cerebellar
- brainstem
- sensory
- bowel
- bladder
- visual
- cerebral
what is the MS functional composite (MSFC)
participation level outcome measure
- LE function/amb, UE function, and some cog
what is the MS quality of life - 54 (MSQOL54)
self report, participation level
SF-36 (generic) plus 18 dz specific items
physical health composite, mental health composite, and composite of both
what is the MS impact scale (MSIS-29)
self report measure, participation
rate how MS has impacted function, mood, activities in past 2 wks to calculate disability
what are 3 balance outcome measures
berg
TUG and TUG cog
dizziness handicap index (DHI)
what are 4 pain outcome measures
numeric pain rating scale
VAS or faces scale
McGill pain Q
Dallas pain Q
what are 4 gait outcome measures
timed 25ft walk test
12-item MS walking scale
TUG and TUG cog
DGI
what are 3 outcome measures for dec aerobic capacity and endurance
fatigue severity scale
RPE scale
6MWT
what are 3 fatigue outcome measures
- modified fatigue impact scale (MFIC)
- subj assess of effects on phys, cog, and psychosoc functioning - fatigue scale for motor and cog function
- dz specific**
- measure fatigue d/t cog and motor tasks - VAS for fatigue
what is the overall goal of PT in MS
individualized POC to maximize functional mobility and independence
- inc aerobic endurance and prevent/dec secondary complications
what has cardiorespiratory fitness in MS been associated with
inc grey matter volume, nc white matter integrity, and preservation of neuronal integrity
what are the benefits of aerobic activity in MS
potential neuroprotective effect
dec inflammation
inc strength, endurance, QOL
restore function by dec disuse atrophy/deconditioning
prevent secondary complication of heart dz
what does emerging evidence say about aerobic activity in MS
regular physical activity can be protective and dec inflammation
- doesn’t matter mode/modality of exercise
what are parameters for aerobic activity in MS
2-3x wk / 60-70% MHR
20-30min
incorporate rest periods
what is an important consideration in choosing the mode of aerobic activity
fall risk and safety
what are precautions for aerobic activity
use of fans/climate control
monitor uhthoff’s
slower progress
consider use of yoga/tai chi
exercise alternate days
don’t exercise to fatigue
primary vs secondary weakness and in what ms groups are each seen
primary
- d/t formation of plaques in motor cortex and descending corticospinal tracts
- common in AG ms (hip flex, knee ext, DF)
secondary
- d/t disuse, deconditioning, spasticity
- common in ankle, hip, and trunk ms
what are general guidelines for strengthening in MS
limit number of reps to avoid fatigue
- use RPE
what are the most common joints for contractures to form in
- ankle
- hip
- knee
what types of MS are contractures more common in
progressive forms
what are the goals of regular stretching in MS
preserve ms length and joint ROM
- loss of flexibility leads to biomechanical changes affecting posture, positioning, balance, and gait
there is evidence supporting what benefits to stretching
dec pain, spasms, pressure ulcer risk
what are recommended guidelines for stretching in MS
daily, slow, pain-free stretching of major ms groups w 20-60sec holds
what are examples of PT interventions targeting balance (4)
static activities
dynamic activities
vestib and gaze stability
education on dec fall risk
what is the most common gait deviation pattern we see in MS
ataxic
what is a consideration if a weighted vest is implemented as a PT intervention for ambulation in MS
a compensatory approach
needs to be consistently used, otherwise will see a sharp decline
what are 5 potential impairments that could impact gait
sensation
hypertonicity
strength
coordination
vision
what is an important component to incorporate in ambulation interventions
vestibular challenges
what can uncalibrated eye mvmts directly lead to in MS
postural instability
dizziness
dec funciton
what are examples of oculomotor and gaze stability training interventions
VOR training
saccades training
VSR/balance training
what should you consider if someone has diplopia or blurred vision
eye patches
what is something to encourage pts to regularly use for their vision and why
sunglasses
- helpful bc of sensitivity to light
what are 3 locations of plaques that can impact a pt’s vision and gaze stability
optic nerve
cerebellum
vestib nuclei
what is pt education to provide about vision/gaze stability
outline steps/pathways w contrast markings
encourage optimal lighting
safety at night or dimly lit areas
what is the theory that supports vestibular rehab in MS
fatigue linked to mismatch b/w visual, vestib, and somatosensory input which leads to inc amt of neuroprocessing needed
what can vestibular exercises improve in pts w MS
fatigue
balance
what does spasticity frequently co-exist with in MS
weakness
what exacerbates spasticity in MS
fatigue
heat
infection
stress
what are tone reduction techniques to implement
PROM/stretching
cryotherapy
RR
LTR
deep pressure on tendon
FES may have some benefit
stretching program for self-maintenance
baclofen vs botox/phenol injections for spasticity management
baclofen (has to be low dose)
- SE of fatigue and weakness
injections - don’t have to worry about additional fatigue
what is a PT intervention for coordination to reduce ataxia
cuff weights
weighted boots/belts/vests
what are 6 PT interventions for coordination
- train limits of stability w wt shifting and “functional reach” activities
- light wts/proprioceptive loading to extremities to compensate
- cuff wts, weighted boots/belts/vests to dec ataxia
- PNF (dynamic reversals) vary speed and emphasize timing
- frenkel’s exercises
- equilibrium coordination (ie tandem gait, braiding, figure 8)
what is the key to PT management of fatigue
regular aerobic exercise
what are 5 PT strategies to better manage fatigue
- regular aerobic exercise
- activity diary
- energy conservation
- ADs
- cooling (ie vest, suit)
why might an activity diary be helpful in managing fatigue
detect patterns and sx that may exacerbate or alleviate and assist w pacing/planning
what are 5 energy conservation techniques for better fatigue management
monitor freq of exercise
body mechanics
doc rest periods
environment modifications
4Ps - pacing, planning, prioritizing, positioning
what is the purpose of a cooling vest and what does the evidence say ab it
people can wear these when exercising or performing tasks that can be fatiguing
shown to have good effects
what are PT intervention considerations to better manage heat intolerance
environmental exposure
exercise under climate controlled conditions
- cool
- loose clothing
- rest after exercise
- morning/evening activity
- cold refreshments
what are 4 PT interventions for pain management
postural re-training
hydrotherapy -lukewarm water
pressure garments
TENS
why is postural re-training a component to pain management
for poor body mechanics and mvmt patterns
why are pressure garments a strategy for pain management
activates more pressure receptors and helps to convert sensation of pain (hyperesthesias and paresthesias) to pressure
how can TENS be used as part of pain management and what does the evidence say
treats neuropathic pain
low level evidence, more research warranted
from a PT perspective, pain management must focus on what
secondary impairments associated w MS, as well as primary - CNS mediated pain
why is skin breakdown a common complication
sensory and motor loss contributing risk factors
what are 5 PT interventions to preserve skin integrity
- regular skin checks
- regular pressure relief and ROM
- repositioning maneuvers
- pressure relieving devices
- pt and caregiver ed
what are common cog deficits seen in MS
dec attention & focus
dec working memory
dec abstract reasoning, verbal fluency, and executive functioning
what is an important consideration if you screen for cog deficits
often not detected by MMSE
- referral to neuropsych is warranted
what are strategies to compensate for cog deficits
break down info
organizational strategies
inc time for task completion
what impact can cog deficts have on PT
difficulty learning new verbal info inc likelihood of missing 1 or more PT appts
dec in working memory and processing speed can dec likelihood of achieving rehab goals
what are higher incidences of depression and emotional lability associated with
relapses, fatigue, or dz burden in general
what are 5 main rehab goals when treating MS
- variable and unpredictable nature of dz
- lack of high quality studies on rehab outcomes
- multiple problems requiring priority
- chronicity of dz w no definitive cure
- lack of insurance-based support for ongoing rehab
