MS, GBS, ALS Flashcards

1
Q

MS disease type

A

autoimmune: CNS

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2
Q

MS pathology, upper or lower

A

UMN

Demyleination of CNS axons

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3
Q

MS who is impacted

A
More F (except in progressive MS, more M)
Young onset (20-30 yr)
Caucasian – vitamin D deficiency?
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4
Q

how is MS diagnosed

A

Combo: MRI (lesions), CSF (increase of antibodies), brain’s electrical activity, patient report

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5
Q

outcomes MS

A

Progressive (all 4 types)
Rarely fatal
Lower life expectancy by a few years
Infections

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6
Q

types of MS

A

– Relapsing – remitting (most common)
– Secondary progressive
– Primary progressive
– Progressive - relapsing (very rare)

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7
Q

etiology of MS

A

Environment: distance from equator/Vit D; smoking, past virus/bacterial infection (EBS). Unknown

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8
Q

symptoms MS

A

Fatigue, vision problems, muscle weakness, pain, decreased sensation, numbness, bladder problems, tingling, difficulty walking, dizziness, sexual dysfunction

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9
Q

medical treatment or management of MS

A

Treating attacks: corticosteroids, plasmapheresis
Progression: interferon beta medications, glatiramer acetate, ocrevus
System specific meds: pain, spasticty, fatigue, incontinence

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10
Q

What symptoms might require other medication (and considerations for rehab team)? MS

A

Pain, depression, sleep, fatigue, spasticity

Avoid heat

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11
Q

eval/assessment MS

A

Expanded Disability Status Scale (0-6 still walking; 7 in w/c; 9 in bed)
MS Functional Composite
Timed 25 foot walk test
9 Hole peg test – fine motor
Paced audiroy serial addition test (PASAT)
6 min walk test - endurance

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12
Q

therapeutic goals and tx options MS

A

Promote independence and QOL, decrease symptoms and/or compensatory strategies, EBP

Varies from individual based on type, age, stage, etc. Treat symptoms. Avoid heat. Compensatory strategies for symptoms and energy conservation. Therapeutic Exercise. Caregiver training. Adaptive equipment education. Psychosocial.

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13
Q

GB disease type

A

Autoimmune, Acute polyneuropathy

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14
Q

GB pathology and upper/lower

A

Demyelinating, lower motor neurons

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15
Q

who is impacted GB

A

Equal affect M vs. F

Extrememly rare

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16
Q

how is GB diagnosed

A

Max weakness 2-3 weeks after onset of symptoms
Symmetrical symptoms, absent reflexes
Higher levels of protein in CSF (>.55g/L), <10 WBCs per mm
NCS and EMG are not required, but can help differentiate

17
Q

outcomes of GB

A

2-5% die from respiratory paralysis or cardiac arrest
Most have full recovery 6-12 mo
30% have residual weakness

18
Q

etiology of GB

A

Often follows: GI infection (gastroenteritis from campylobacter jejuni), respiratory infection (cytomegalovirus, Epstein-barr virus)

19
Q

symptoms of GB

A

Symmetrical paresthesia that worsens to paralysis: ascending (starts in feet); respiratory; BP issues such as orthostatic hypotension; arrhythmias

20
Q

medical tx GB

A
Plasmapherisis (plasma exchange)
Immunoglobulins from donors
No corticosteroids! 
IV antibiotic therapy
Manually move limbs, prevent DVTs
21
Q

What symptoms might require other medication (and considerations for rehab team)? GB

A

ANS dysfunction: urinary retention, flushing face, cardiac arrhythmias
Respiratory therapist

22
Q

eval for GB

A

Occupational profile, COPM, ROM, MMT, Barthel ADL index, Activities Specific Balance Confidence Scale, Sensory testing, 9-hole peg test

23
Q

goals and tx options for GB

A

Prevent DVTs, decrease symptoms, promote independence and QOL, increase strength
Anti coagulative therapy for DVTs, move limbs
Energy conservation, therapeutic exercise, adaptive equipment, strength training

24
Q

ALS disease type

A

Progressive neuromuscular disease

25
Q

pathology of ALS and upper/lower

A

Progressive degeneration of both upper and lower motor neurons

26
Q

who is impacted ALS

A

Mostly 40-60 y.o., but may vary; 60% male, Vets have higher incidence

27
Q

how is ALS diagnosed

A

Symptom history
EMG of muscle fibers
Nerve conduction study (NCS), MRI for brain/sc, muscle biopsy

28
Q

outcomes of ALS

A

Fatal (usually 3-5 yrs; can vary)

29
Q

etiology ALS

A

Genetics: 20 genes implicated (5-10% are familial)
Environmental factors: smoking, lead exposure, electromagnetic fields
(90-95% are sporadic)

30
Q

symptoms of ALS

A

UMN: weakness, spasticity, hyperreflexia
LMN: weakness, atrophy, fasciulations, hypotinia, areflexia, dysphagia and dysarthria

No sensory involvement

31
Q

medical tx for ALS

A

No known cure or effective pharm. tx
Riluzole – slow progression of the disease for some people
Edaravone – slow decline of fx

32
Q

What symptoms might require other medication (and considerations for rehab team)? ALS

A

Respiration, speaking/communication, eating

33
Q

eval for ALS

A

Occupational profile, COPM

34
Q

ALS goals and tx options

A

Ambulation, promote independence in ADLs
Prevention of contractures

Energy conservation and breathing, therepautic exercise, ROM, stretching, introduce adaptive equipment