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Neuro Rehab 2 > Multiple Sclerosis > Flashcards

Multiple Sclerosis Flashcards

1
Q

what is the hypothesized etiology of MS

A

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

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2
Q

what is the pathophys of MS

A
  1. immune system triggers production of T-lymphocytes, macrophages, immunoglobulins
  2. failure of BBB, allows immune cells to cross and attack myelin sheath
  3. demyelination accompanied by local inflammation
  4. gliosis (proliferation of neuroglial tissue) occurs and results in “glial scars” or plaques
  5. axon becomes damaged, undergoes degen
  6. axonal loss occurs and interferes w normal conduction of nerve signals & loss of function
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3
Q

what about the pathophys of MS leads to a poorer prognosis

A

less capability for repair w attack in CNS bc of scarring

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4
Q

peak age onset

A

30yo
- between 15 and 50yo

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5
Q

what populations at higher and lower risk for MS and what does this indicate

A

more common in caucasian
more common in women

lower risk in AA, asian, and NA

implies a genetic link bc of racial disparity

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6
Q

why is MS difficult to get a clear definitive dx

A

d/t variability in periods of flares/remission and in clinical courses

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7
Q

what are methods to medically dx MS

A

CSF markers
- oligoclonal bands (presence of IgG bands)

MRI changes (w gadolinium contrast)

visual evoked potentials

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8
Q

why are MRIs tricky to use as a diagnostic tool in MS

A

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

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9
Q

why/how is visual evoked potentials used to dx MS

A

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

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10
Q

what is the struggle w differential dx

A

no single, definitive test

plaques can form anywhere, hard to implicate one neuro condition

differential dx list is extensive, and remissions make dx challenging

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11
Q

what is the Poser criteria and what is its purpose

A

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

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12
Q

what are 4 categories of differential dx to consider

A

autoimmune/inflammatory conditions

CNS infections

metabolic conditions

vascular conditions

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13
Q

what are 6 common sites of MS plaque formation

A
  1. periventricular regions of cerebrum
  2. grey/white matter boundary in cerebrum
  3. cerebellar white matter
  4. brainstem
  5. spinal cord (cervical)
  6. optic nerve
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14
Q

why is it difficult to give an accurate prognosis for MS

A

many factors involved and variability

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15
Q

how is variability seen in MS

A

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

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16
Q

what can rate of progression of MS be related to

A

intrinsic factors
- dz expression

extrinsic factors
- lifestyle
- weather
- meds
- exercise

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17
Q

what is an MS exacerbation, relapse, or flare?

A

new or recurrent sx that lasts more than 24hrs

must be separated from previous flare by at least 30days

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18
Q

what is the most common trigger for both MS pseudoexacerbation and prolonged exacerbations

A

heat intolerance

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19
Q

what is a pseudoexacerbation

A

new/recurrent sx that lasts less than 24hrs

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20
Q

what are common triggers for MS exacerbations

A

stress
infections
excessive fatigue
trauma, surgery
childbirth
decline in health status, infection, fever
heat - fever, exercise, hot bath/shower, hot weather conditions

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21
Q

what are the 4 clinical subtypes of MS

A
  1. relapsing-remitting (RRMS)
  2. primary-progressive (PPMS)
  3. secondary-progressive (SPMS)
  4. progressive-relapsing (PRMS)
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22
Q

what is RRMS

A

defined by acute attacks w full recovery or partial residual deficit
- there is a lack of dz progression in between attacks

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23
Q

what clinical subtype are most people w MS initially dx with and what is the difficulty w this

A

RRMS
- makes it difficult to dx, while it is good bc of periods of remission

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24
Q

what are the most common first signs of RRMS

A

optic neuritis (40%)
severe/acute vertigo (48%)

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25
Q

what is SPMS

A

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

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26
Q

how common is SPMS

A

50% of those w RRMS develop w/i 10yrs
- 90% w/i 25yrs

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27
Q

why are stats of SPMS dx and development expected to change

A

new dz modifying drugs available

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28
Q

what is PPMS

A

characterized by progressive disability from onset, w/o distinct remissions, plateaus, or significant improvement

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29
Q

what is the prognosis of someone w PPMS

A

tend to respond less favorably to standard MS therapies

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30
Q

how common is PPMS and in what population

A

10% of people w MS

later age of onset (>50yo)

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31
Q

what is PRMS

A

progression from onset
clear, acute relapses or exacerbations that may or may not resolve
- cont dz progression in intervals b/w relapses

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32
Q

what subtype of MS is the least common form

A

PRMS

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33
Q

what is a characteristic of RRMS as the dz progresses

A

the more flares people have over time, the less likely they will return to baseline

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34
Q

what is the gold standard for medical management of MS

A

interferons - 1a, 1b
“ABCs of pharm management”

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35
Q

what are the 4 disease modifying drugs

A

interferon beta 1a
interferon beta 1b
glamtiramer (copaxone)
natalizumab (tysabri)

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36
Q

how do disease modifying drugs work in MS

A

immunomodulators
believed to dec severity and frequency of attacks, thereby slowing dz process

don’t cure MS

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37
Q

what is often the 1st line of defense for MS

A

interferons

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38
Q

what are common SEs of dz modifying drugs and why is this significant

A

malaise, fatigue, pain at injection site

usually taken once a week
-> those SE often present the day after they are taken

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39
Q

what is a potential adverse effect of 1 disease modifying drug and which one? why is this significant?

A

progressive multifocal leukoencephalopathy (PML)
- often fatal

Tysabri

Tysabri is a last line of defense as a result

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40
Q

what types are immunosuppressants approved for

A

RRMS
SPMS

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41
Q

what type of MS are there no disease modifying drugs believed to be effective for

A

PPMS

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42
Q

when is an immunosuppressant appropriate

A

if pt not tolerating other meds well, give people these

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43
Q

what is an example of an immunosuppressant

A

chemo agent
- mitoxantrone (novantrone)

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44
Q

what type of MS are immunomodulators appropriate for

A

RRMS

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45
Q

what are examples of meds used for sx management

A

pain
- gabapentin, dilantin, tegretol
bowel/bladder function
- detrol, ditropan
mood - SSRIs
fatigue - amantadine
acute flare
- steroids (often hospitalized)
spasticity
- baclofen, dantrium, diazepam, botox, phenol

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46
Q

what are common sx of MS that are w/i scope of PT practice

A

sensory
motor
visual changes
fatigue
pain
cerebellar dysfunction
autonomic changes
- CV dysautonomia

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47
Q

what are common sx of MS that are outside scope of PT practice

A

bladder/bowel dysfunction
speech/swallowing
- dysarthria/dysphagia
cog
emotional
sexual

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48
Q

what are the 6 most frequent clinical manifestations of MS

A

fatigue & heat sensitivity*
gait/balance disturbances
bowel/bladder dysfunction
spasms, stiff, sensory loss, pain
visual disturbances*
emotional and cog changes

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49
Q

what is a helpful about testing for path reflexes (like babinski and hoffmans) in MS

A

path reflexes to test for UMNL
- can be helpful bc of how spotty MS is

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50
Q

primary vs secondary fatigue in MS

A

primary:
- caused by effects of demyelination and axon destruction

secondary:
- deconditioning
- infections
- sleep disturbances
- poor nutrition
- med SE (interferon/ABCs)
- heat intolerance***
- depression (psych)

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51
Q

what subtypes of MS is fatigue most frequent and most severe

A

PPMS
SPMS

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52
Q

describe the pathophys of primary fatigue

A

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

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53
Q

what are 2 causes for balance deficits in MS

A

visual disturbances
cerebellar lesions

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54
Q

what are 5 common motor sx seen in MS

A

weakness (primary & secondary)
balance deficits
coordination deficits (ataxia)
gait abnormalities
hypertonia (spasticity*)

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55
Q

how can spasticity present in MS

A

can present as “phasic spasms”, painful cramping, and/or clonus

inc ext tone tends to dominate
- lot of ADD in LE too

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56
Q

pathophys of MS that can lead to sensory dysfunction

A

plaques in parietal lobe (sensory cortex) and anywhere along ALF and DCML tracts

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57
Q

what are the top 3 first signs of MS in general

A
  1. visual disturbances **
  2. vertigo
  3. paresthesias of limb, face, and trunk
    - if paresthesia is the first sign, usually years and years before a MS dx
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58
Q

how does sensory dysfunction usually present

A

numbness and paresthesias

often in conjunction w other sx

altered sensation occurs at some stage in almost all pts w MS

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59
Q

what are 6 manifestations of pain in MS

A

neuropathic
(+) Lhermittes’ sign
paroxysmal/intermittent limb pain
HAs
optic neuritis
trigeminal neuralgia

60
Q

why do you see neuropathic pain in MS

A

associated w damage to neural tissue

61
Q

what is (+) Lhermitte’s sign and what does this indicate

A

neck flexion produces a “shock like” sensation runnign down spine and into LEs

d/t posterior column damage / demyelination

62
Q

what is optic neuritis and why is this seen in MS

A

eye pain in addition to visual disturbances

d/t inflammation and demyelination

63
Q

what is trigeminal neuralgia? why is this seen in MS? how can this be treated?

A

intractable/severe facial pain

likely d/t pontine plaques

sometimes treated w stereotactic gamma knife surgery to sever CN V

64
Q

what are 5 cerebellar sx commonly seen in MS

A

ataxia
postural or intention tremors
hypotonia
asthenia -general ms weakness
vestib sx

65
Q

what are vestib sx commonly seen in MS and why

A

vertigo, dizziness, gaze instability

high interconnection b/w vestib inputs and cerebellar outputs

66
Q

how do visual sx in MS present

A

usually unilateral
- can progress to bilateral

characterized by:
- eye pain
- loss of vision
- blind spots in visual field
- blurred vision
- nystagmus

67
Q

what is uhthoff’s phenomena

A

pseudoexacerbation / reaction in response to an increased core body temp (overheating)

dimming or reduction in vision, and fatigue

68
Q

what can uhthoff’s phenomena indicate

A

damage to optic nerve, attributed to fluctuation in axonal conduction

69
Q

when does uhthoff’s phenomena subside/improve

A

with minutes to one hour of physical rest and lowering core body temp

70
Q

what emotional changes are seen in MS and why

A

depression
affective changes in mood, feelings, emotional expression linked to diffuse, (B) frontal or subcortical white matter dz

71
Q

what are cog impairments seen in MS

A

verbal fluency and memory
memory loss
processing speed decline
executive function deficit
- poor planning and reasoning
attention deficit
visuospatial learning difficulties

72
Q

why can CV dysautonomia be seen in MS and how can it present

A

bc of ANS involvement

difficulty regulating HR, BP, digestion, temp control
orthostasis
dec or absent sweating response

73
Q

what are signs of orthostasis d/t CV dysautonomia in MS

A

lightheadedness
fainting
unstable BP
abnormal HR
malnutrition

74
Q

why is it especially concerning to see wt loss in someone w MS and what can help

A

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

75
Q

why is an attenuated or absent sweating response d/t CV dysautonomia in MS problematic

A

bc heat sensitive and can’t regulate temp
- Uhthoff’s phenomena and then makes it difficult to be able to exercise

76
Q

what is the life expectancy of someone w MS

A

close to gen pop, slightly reduced

77
Q

what are favorable prognostic factors in MS

A

female
1 sx at onset
RRMS
young age of dx
few neuro signs at 5yrs
few lesions & no axonal loss on MRI

78
Q

what is a difficulty in MS that is a significant source of disability and morbidity

A

difficulty staying in workforce and maintaining relationships

79
Q

what are 2 significant risk factors for MS

A

smoking
- inc dz severity, sx, progression
obesity

80
Q

what are 5 causes of death in MS

A

pneumonia from aspiration
- esp if bulbar sx
infections
- UTI, URI, pressure ulcers
falls
suicide
heart dz (d/t inactivity)

81
Q

why is education important in this pt population

A

lot of different domains and focus on secondary complication prevention

82
Q

what are MS EDGE recommendations

A

list of 10 highly recommended standardized tests and measures

83
Q

what is the gold standard for assessing MS dz severity

A

expanded disability status scale (EDSS)

84
Q

what EDSS scores indicates peak fall risk

A

between 4 and 6

85
Q

what is the expanded disability status scale (EDSS)

A

standardized disease specific participation measure that quantifies disability in 8 functional systems
- pyramidal
- cerebellar
- brainstem
- sensory
- bowel
- bladder
- visual
- cerebral

86
Q

what is the MS functional composite (MSFC)

A

participation level outcome measure
- LE function/amb, UE function, and some cog

87
Q

what is the MS quality of life - 54 (MSQOL54)

A

self report, participation level
SF-36 (generic) plus 18 dz specific items

physical health composite, mental health composite, and composite of both

88
Q

what is the MS impact scale (MSIS-29)

A

self report measure, participation

rate how MS has impacted function, mood, activities in past 2 wks to calculate disability

89
Q

what are 3 balance outcome measures

A

berg
TUG and TUG cog
dizziness handicap index (DHI)

90
Q

what are 4 pain outcome measures

A

numeric pain rating scale
VAS or faces scale
McGill pain Q
Dallas pain Q

91
Q

what are 4 gait outcome measures

A

timed 25ft walk test
12-item MS walking scale
TUG and TUG cog
DGI

92
Q

what are 3 outcome measures for dec aerobic capacity and endurance

A

fatigue severity scale
RPE scale
6MWT

93
Q

what are 3 fatigue outcome measures

A
  1. modified fatigue impact scale (MFIC)
    - subj assess of effects on phys, cog, and psychosoc functioning
  2. fatigue scale for motor and cog function
    - dz specific**
    - measure fatigue d/t cog and motor tasks
  3. VAS for fatigue
94
Q

what is the overall goal of PT in MS

A

individualized POC to maximize functional mobility and independence
- inc aerobic endurance and prevent/dec secondary complications

95
Q

what has cardiorespiratory fitness in MS been associated with

A

inc grey matter volume, nc white matter integrity, and preservation of neuronal integrity

96
Q

what are the benefits of aerobic activity in MS

A

potential neuroprotective effect
dec inflammation
inc strength, endurance, QOL
restore function by dec disuse atrophy/deconditioning
prevent secondary complication of heart dz

97
Q

what does emerging evidence say about aerobic activity in MS

A

regular physical activity can be protective and dec inflammation
- doesn’t matter mode/modality of exercise

98
Q

what are parameters for aerobic activity in MS

A

2-3x wk / 60-70% MHR
20-30min
incorporate rest periods

99
Q

what is an important consideration in choosing the mode of aerobic activity

A

fall risk and safety

100
Q

what are precautions for aerobic activity

A

use of fans/climate control
monitor uhthoff’s
slower progress
consider use of yoga/tai chi
exercise alternate days
don’t exercise to fatigue

101
Q

primary vs secondary weakness and in what ms groups are each seen

A

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

102
Q

what are general guidelines for strengthening in MS

A

limit number of reps to avoid fatigue
- use RPE

103
Q

what are the most common joints for contractures to form in

A
  1. ankle
  2. hip
  3. knee
104
Q

what types of MS are contractures more common in

A

progressive forms

105
Q

what are the goals of regular stretching in MS

A

preserve ms length and joint ROM
- loss of flexibility leads to biomechanical changes affecting posture, positioning, balance, and gait

106
Q

there is evidence supporting what benefits to stretching

A

dec pain, spasms, pressure ulcer risk

107
Q

what are recommended guidelines for stretching in MS

A

daily, slow, pain-free stretching of major ms groups w 20-60sec holds

108
Q

what are examples of PT interventions targeting balance (4)

A

static activities
dynamic activities
vestib and gaze stability
education on dec fall risk

109
Q

what is the most common gait deviation pattern we see in MS

A

ataxic

110
Q

what is a consideration if a weighted vest is implemented as a PT intervention for ambulation in MS

A

a compensatory approach
needs to be consistently used, otherwise will see a sharp decline

111
Q

what are 5 potential impairments that could impact gait

A

sensation
hypertonicity
strength
coordination
vision

112
Q

what is an important component to incorporate in ambulation interventions

A

vestibular challenges

113
Q

what can uncalibrated eye mvmts directly lead to in MS

A

postural instability
dizziness
dec funciton

114
Q

what are examples of oculomotor and gaze stability training interventions

A

VOR training
saccades training
VSR/balance training

115
Q

what should you consider if someone has diplopia or blurred vision

A

eye patches

116
Q

what is something to encourage pts to regularly use for their vision and why

A

sunglasses
- helpful bc of sensitivity to light

117
Q

what are 3 locations of plaques that can impact a pt’s vision and gaze stability

A

optic nerve
cerebellum
vestib nuclei

118
Q

what is pt education to provide about vision/gaze stability

A

outline steps/pathways w contrast markings
encourage optimal lighting
safety at night or dimly lit areas

119
Q

what is the theory that supports vestibular rehab in MS

A

fatigue linked to mismatch b/w visual, vestib, and somatosensory input which leads to inc amt of neuroprocessing needed

120
Q

what can vestibular exercises improve in pts w MS

A

fatigue
balance

121
Q

what does spasticity frequently co-exist with in MS

A

weakness

122
Q

what exacerbates spasticity in MS

A

fatigue
heat
infection
stress

123
Q

what are tone reduction techniques to implement

A

PROM/stretching
cryotherapy
RR
LTR
deep pressure on tendon

FES may have some benefit

stretching program for self-maintenance

124
Q

baclofen vs botox/phenol injections for spasticity management

A

baclofen (has to be low dose)
- SE of fatigue and weakness

injections - don’t have to worry about additional fatigue

125
Q

what is a PT intervention for coordination to reduce ataxia

A

cuff weights
weighted boots/belts/vests

126
Q

what are 6 PT interventions for coordination

A
  1. train limits of stability w wt shifting and “functional reach” activities
  2. light wts/proprioceptive loading to extremities to compensate
  3. cuff wts, weighted boots/belts/vests to dec ataxia
  4. PNF (dynamic reversals) vary speed and emphasize timing
  5. frenkel’s exercises
  6. equilibrium coordination (ie tandem gait, braiding, figure 8)
127
Q

what is the key to PT management of fatigue

A

regular aerobic exercise

128
Q

what are 5 PT strategies to better manage fatigue

A
  1. regular aerobic exercise
  2. activity diary
  3. energy conservation
  4. ADs
  5. cooling (ie vest, suit)
129
Q

why might an activity diary be helpful in managing fatigue

A

detect patterns and sx that may exacerbate or alleviate and assist w pacing/planning

130
Q

what are 5 energy conservation techniques for better fatigue management

A

monitor freq of exercise
body mechanics
doc rest periods
environment modifications
4Ps - pacing, planning, prioritizing, positioning

131
Q

what is the purpose of a cooling vest and what does the evidence say ab it

A

people can wear these when exercising or performing tasks that can be fatiguing

shown to have good effects

132
Q

what are PT intervention considerations to better manage heat intolerance

A

environmental exposure
exercise under climate controlled conditions
- cool
- loose clothing
- rest after exercise
- morning/evening activity
- cold refreshments

133
Q

what are 4 PT interventions for pain management

A

postural re-training
hydrotherapy -lukewarm water
pressure garments
TENS

134
Q

why is postural re-training a component to pain management

A

for poor body mechanics and mvmt patterns

135
Q

why are pressure garments a strategy for pain management

A

activates more pressure receptors and helps to convert sensation of pain (hyperesthesias and paresthesias) to pressure

136
Q

how can TENS be used as part of pain management and what does the evidence say

A

treats neuropathic pain

low level evidence, more research warranted

137
Q

from a PT perspective, pain management must focus on what

A

secondary impairments associated w MS, as well as primary - CNS mediated pain

138
Q

why is skin breakdown a common complication

A

sensory and motor loss contributing risk factors

139
Q

what are 5 PT interventions to preserve skin integrity

A
  1. regular skin checks
  2. regular pressure relief and ROM
  3. repositioning maneuvers
  4. pressure relieving devices
  5. pt and caregiver ed
140
Q

what are common cog deficits seen in MS

A

dec attention & focus
dec working memory
dec abstract reasoning, verbal fluency, and executive functioning

141
Q

what is an important consideration if you screen for cog deficits

A

often not detected by MMSE
- referral to neuropsych is warranted

142
Q

what are strategies to compensate for cog deficits

A

break down info
organizational strategies
inc time for task completion

143
Q

what impact can cog deficts have on PT

A

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

144
Q

what are higher incidences of depression and emotional lability associated with

A

relapses, fatigue, or dz burden in general

145
Q

what are 5 main rehab goals when treating MS

A
  1. variable and unpredictable nature of dz
  2. lack of high quality studies on rehab outcomes
  3. multiple problems requiring priority
  4. chronicity of dz w no definitive cure
  5. lack of insurance-based support for ongoing rehab

Neuro Rehab 2 (48 decks)

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