MS, GBS, ALS Flashcards
MS disease type
autoimmune: CNS
MS pathology, upper or lower
UMN
Demyleination of CNS axons
MS who is impacted
More F (except in progressive MS, more M) Young onset (20-30 yr) Caucasian – vitamin D deficiency?
how is MS diagnosed
Combo: MRI (lesions), CSF (increase of antibodies), brain’s electrical activity, patient report
outcomes MS
Progressive (all 4 types)
Rarely fatal
Lower life expectancy by a few years
Infections
types of MS
– Relapsing – remitting (most common)
– Secondary progressive
– Primary progressive
– Progressive - relapsing (very rare)
etiology of MS
Environment: distance from equator/Vit D; smoking, past virus/bacterial infection (EBS). Unknown
symptoms MS
Fatigue, vision problems, muscle weakness, pain, decreased sensation, numbness, bladder problems, tingling, difficulty walking, dizziness, sexual dysfunction
medical treatment or management of MS
Treating attacks: corticosteroids, plasmapheresis
Progression: interferon beta medications, glatiramer acetate, ocrevus
System specific meds: pain, spasticty, fatigue, incontinence
What symptoms might require other medication (and considerations for rehab team)? MS
Pain, depression, sleep, fatigue, spasticity
Avoid heat
eval/assessment MS
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
therapeutic goals and tx options MS
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.
GB disease type
Autoimmune, Acute polyneuropathy
GB pathology and upper/lower
Demyelinating, lower motor neurons
who is impacted GB
Equal affect M vs. F
Extrememly rare
how is GB diagnosed
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
outcomes of GB
2-5% die from respiratory paralysis or cardiac arrest
Most have full recovery 6-12 mo
30% have residual weakness
etiology of GB
Often follows: GI infection (gastroenteritis from campylobacter jejuni), respiratory infection (cytomegalovirus, Epstein-barr virus)
symptoms of GB
Symmetrical paresthesia that worsens to paralysis: ascending (starts in feet); respiratory; BP issues such as orthostatic hypotension; arrhythmias
medical tx GB
Plasmapherisis (plasma exchange) Immunoglobulins from donors No corticosteroids! IV antibiotic therapy Manually move limbs, prevent DVTs
What symptoms might require other medication (and considerations for rehab team)? GB
ANS dysfunction: urinary retention, flushing face, cardiac arrhythmias
Respiratory therapist
eval for GB
Occupational profile, COPM, ROM, MMT, Barthel ADL index, Activities Specific Balance Confidence Scale, Sensory testing, 9-hole peg test
goals and tx options for GB
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
ALS disease type
Progressive neuromuscular disease
pathology of ALS and upper/lower
Progressive degeneration of both upper and lower motor neurons
who is impacted ALS
Mostly 40-60 y.o., but may vary; 60% male, Vets have higher incidence
how is ALS diagnosed
Symptom history
EMG of muscle fibers
Nerve conduction study (NCS), MRI for brain/sc, muscle biopsy
outcomes of ALS
Fatal (usually 3-5 yrs; can vary)
etiology ALS
Genetics: 20 genes implicated (5-10% are familial)
Environmental factors: smoking, lead exposure, electromagnetic fields
(90-95% are sporadic)
symptoms of ALS
UMN: weakness, spasticity, hyperreflexia
LMN: weakness, atrophy, fasciulations, hypotinia, areflexia, dysphagia and dysarthria
No sensory involvement
medical tx for ALS
No known cure or effective pharm. tx
Riluzole – slow progression of the disease for some people
Edaravone – slow decline of fx
What symptoms might require other medication (and considerations for rehab team)? ALS
Respiration, speaking/communication, eating
eval for ALS
Occupational profile, COPM
ALS goals and tx options
Ambulation, promote independence in ADLs
Prevention of contractures
Energy conservation and breathing, therepautic exercise, ROM, stretching, introduce adaptive equipment
