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PHTH 551- Neurological Rehabilitation > Neuromuscular Disorders > Flashcards

Neuromuscular Disorders Flashcards

1
Q

What conditions fall under the following categories of neuromuscular disorders?

  1. Peripheral nervous system demyelination
  2. Anterior horn cell and motor neuron
  3. CNS demyelination
A
    • Peripheral Neuropathy
    • GBS: Guillan Barre Syndrome
  2. Post-polio syndrome
    - ALS: Amyotrophic Lateral Sclerosis
  3. Multiple Sclerosis

Muscular Dystrophy also falls under neuromuscular conditions.

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2
Q

What are the 4 Types of Peripheral Neuropathy? What are their characteristics?

A
  1. Generalized peripheral neuropathy (Polyneuropathy): Pattern of nerve damage to multiple areas, often symmetrically. Can be axonal or demyelinating or both, usually in long peripheral nerve fibers. AIDPN-GBS or CIDPN.
  2. Focal peripheral neuropathy: Disorder of a single nerve. ex: Carpel tunnel syndrome.
  3. Mononeuropathy Multiplex: Individual peripheral nerves are involved at several sites giving rise to multi-focal signs and symptoms.
  4. Mononeuropathy Multiplex and polyneuropathy may co-exist
    - Motor (weakness)
    - Sensory (Parenthesis and Hypoesthesia)
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3
Q
  1. What is Guillain-Barré Syndrome?
  2. What causes GBS?
  3. Epidemiology of GBS
A

AIDPN

  1. Body’s immune system attacks part of the PNS
    • Autoimmune disease.
    • Can be post viral or bacterial infection.
    • 5-10% post surgery
    • Myth that it is due to Flu vaccine
  3. I: 3,500/year USA + CAN
    P: 1-2/100,0000
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4
Q

What are the signs and symptoms of GBS?

A
  • Bilateral
  • Rapid onset
  • Paresthesia hands and feet
  • Progressive ms weakness (distal to proximal)
  • Respiratory muscle paralysis
  • Bulbar involvement (swallowing)
  • 1-4 days constant painful ms aching
  • Loss stretch reflex
  • Autonomic involvement (BP)
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5
Q
  1. How is GBS diagnosed?

2. What are the treatment for GBS?

A
  1. -Clinical and medical history
    - Lumbar puncture, increase protein in CSF
    - Nerve conduction velocity tests: Slowed
    • No cure
    • Plasmaphoresis (blood exchange)
    • High dose immunoglobulin therapy
    • Corticosteroid (not recommended primary treatment)
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6
Q

What are the stages of GBS?

A

Acute Decline
Stable Period
Recovery

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7
Q

What is Miller-Fisher Syndrome

A
  • Variant of GBS

- Ataxia, opthmopleygia, areflexia, sever weakness less common

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8
Q

What should at PT assess in terms of body function and structure for GBS?

A
  • Motor weakness (trunk and extremities, pulmonary function tests, swallowing difficulty/facial weakness)
  • Pain
  • Sensory- usually not a complete sensory loss. (stocking distribution, LT, vibration and position sense)
  • Autonomic (BP, arrhythmias)
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9
Q

What should a PT assess in terms of activity limitations for GBS?

A 
Endurance (2 or 6MWT)
Functional status (Gait speed, functional mobility, transfers, ADLs, TUG)
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10
Q

What can a PT expect in term of the recovery timeline for GBS?

A
  • Reach lowest point at 3 wks of dx (80%) in terms of weakness.
  • 2-4 wks: Recovery of muscle strength starts after plateau phase
  • 6 months: most become ambulatory by this point
  • 50% minor neuro deficits
  • 15% persistant residual deficits in function
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11
Q

What are the general intervention goals of PT for GBS?

A
  • Resolve respiratory problems
  • Minimize Pain
  • Prevent secondary effects of immobilization
  • Promote recovery of muscle strength and function
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12
Q
  1. What is really important to consider as a pt during the acute phase of GBS?
  2. What are the goals of PT interventions during the acute phase of GBS?
A

PT usually gets involved right away, pt incubated usually in ICU.
-Do not fatigue the pt

2.

  • Skin protection (mattress, positioning)
  • Prevention of Contractures and DVT (PROM, splints)
  • Pain relief (TENS, med, prom)
  • Maintain pulmonary function (chest PT)
  • Monitor physical status (strength)
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13
Q
  1. How long can the plateau phase last?
  2. What condition is the pt in during plateau?
  3. What PT interventions should be done during this period?
A
  1. few days up to 4-6 wks
  2. May be off ventilator, trach’ed, PEG
  3. Mobilize as tolerate
    - Not fatiguing
    - ROM: Monitor E/F, to gain rom need OP at EOR w/ low tension or load for 2 hr/day 5 day/wk for 4 wks
    - Minimize postural hypotension
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14
Q
  1. What does the pt regain during the recovery phase?
  2. What are the goals of PT treatment at this point?
  3. What are the guidelines for exercise prescription at this point?
  4. What are signs of deterioration?
  5. Will ex impact recovery process?
A
  1. Return ms strength, improve sensory deficits, autonomic stability, stretch reflex (depends on age, severity disease…)
  2. Maintain MSK in optimal state. Pace recovery to maximize function as re-innervation occurs.
    - PNF
    - Endurance training and Cv fitness
    • Short periods non-fatiguing ex
    • Increase activity if no deterioration occurs after 1 wk.
    • Return to previous level if deterioration occurs.
    • Functional ex and specific muscle strength
    • Limit fatiguing ex for 1 yr.
  4. recurring ms tenderness, loss reflexes, paresthesia return, loss of function.
  5. Will not aid or hasten nerve regeneration.
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15
Q

What is post-polio syndrome?

A

Progressive clinical syndrome consisting of new weakness, fatigue and pain in individual who have recovered from past paralytic polio.

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16
Q

What is poliomyelitis?

A

A contagious viral infection.

  • Most sever form can cause paralysis, difficulty breathing and death.
  • Fewer 1% cause paralysis
  • Person may not be infected, but can still be contagious.
  • The infection causes inflammation of the nerve cells in the ventral horn of the spinal cord causing damage to motor neurone (anterior horn cells)
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17
Q

What is the occurrence of polio?

A

Not common any more in developed world b/c vaccine w/ 99% compliance.

Disease of childhood in developing countries (Africa and India)

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18
Q
  1. What does it mean that post-polio syndrome is a diagnosis of exclusion?
  2. What are the criteria for diagnosis?
A
  1. Make sure that there are no other medical disorders that may be producing the new problems (rule out other causes).
    • Previous acute paralytic polio
    • Period of recovery w/ stable neuro and functional status (usually >15 yrs)
    • Gradual or sudden onset of new muscle weakness (plus other symptoms)
    • Symptoms persist for at least 1 yr.
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19
Q

What happens at the level of the motor units (motor neurons and muscle) during:
A. Acute Polio
B. Post Polio Recovery
C. Post Polio Syndrome

  • How does C relate to the etiology of PPS?
  • Contributing factors to PPS
A

A. Virus destroys anterior horn cells, leading to atrophy of denervated muscle fibers.

B. Axons sprout in recovered nerves, w/ reinnervation of the orphaned muscle fibers and subsequent hypertrophy.

C. The axon that sprouted in B lose their function, resulting in less muscle fibers per motor unit and subsequent atrophy.

The posible cause of PPS may be peripheral disintegration of the enlarged post-polio motor units. In polio syndrome the original motor neurons are lost, so the remaining motor neurons sprout new axons to innervate more muscle fibers then the original nerve innervated (100 muscle fibers to 700-200 fibers). Muscles can regain their strength (denervation hypertrophy). Overtime though the the sprouted neurons may be overworked and die.

Factors: normal aging process, overuse, muscle disuse.

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20
Q

What are risk factors for PPS?

A
  • Greater severity of acute paralytic polio
  • Greater recovery after acute episode
  • Older age
  • Longer time period since acute episode.
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21
Q

What other conditions mimic the symptoms of PPS?

A
  • Myasathenia gravis
  • Fibromyalgia
  • Spinal stenosis
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22
Q
  1. What are the key muscle groups to assess the strength of in PPS?
  2. How can the strength be assessed?
  3. What are some trends in ms strength in PPS?
A
  1. UE: Shoulder flex, ext, abd ER, Elb and Wrist flex/ext, grip.

LE: Hip abd
Swing: Hip & knee flex, dorsiflex
Stance: Hip & knee ext, plantar flex

  1. Hand held dynamometer, MMT, fixed dynamometer.
  2. LE weakness predisposes to shoulder overuse symptoms.
    UE&LE swing may get weaker faster than stance phase muscles.
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23
Q

What are the treatment guidelines for ms weakness in PPS?

A

Strength ex: based on MMT >3 (isotonic, isokinetic sub-max 3 sets, low reps 1 min rest), <3 isometric, non-fatiguing.

Functional Ex

Aerobic Ex

Stretching to prevent or decrease contractures.

Avoid muscle overuse (pain, burning, fatigue)

Weight loss
Orthoses
Assistive devices

BE CAREFUL NOT TO FATIGUE

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24
Q
  1. How is fatigue assessed for PPS?

2. How is fatigue treated in PPS

A
  1. Generalized fatigue or specific muscular fatigue?
    FI-Fatiguability index or FSS-Fatigue Severity Scale

Fatiguability is failure to maintain the required expected power output.

Test muscle groups whose fatiguability is interfering w/ function.

  1. Energy conservation
    - Lifestyle changes
    - Pacing (BORG 10-13)
    - Regular rest periods
    - Amitriptyline- sleep
    - Pyridostigmine
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25
Q
  1. How is pain assessed in PPS?

2. What are the guidelines for treating pain in PPS?

A
  1. Determine if muscular or if joint pain.
    - PPS: muscular pain, crams w/ activity
    - Assess w/ VAS
    • Medication (? like Fibromyalgia)
    • Manage jt and soft tissue abnormalities (OA, tendinitis…)
    • Modification of extremity use (less overhead reaching)
    • Physical modalities (Ice, US)
    • Strengthening and stretching
    • Orthoses
    • Assistive devices
    • NSAIDs
    • Steroid injections
    • Sx
26
Q

What are some other problems in PPS that may need to be managed?

A
  • Pulmonary dysfunction
  • Dysphagia
  • Psychosocial Difficulties
27
Q

What is the prognosis for PPS?

A
  • Non life-threatening
  • Pt who adjust lifestyle can improve by increasing strength and stabilizing function
  • Most studies show decline strength overtime.
28
Q

What is multiple sclerosis?

A

An autoimmune disorder, where inflammatory factors attacks the myelin sheath resulting in lesions (plaques) where myelin is lost in the CNS (brain, spinal cord and optic nerve). This leads to impaired neurotransmission.

Etiology: genetic, environment, autoimmune, virus. Women are 2-3X more likely to get it.

29
Q

What are the 4 clinical course of MS?

A

Relapsing-Remitting Multiple Sclerosis (most common): Periods of flare up of symptoms then periods of remission. Can have an increase in disability over time w/ each relapse although symptoms can decrease btwn episodes.

Primary Progressive MS: Gradual deterioration in functioning (increase in disability) over time.

Secondary Progressive MS: Start with periods of flare ups and remissions, then gradual deterioration like PPMS.

Progressive Relapsing MS: Gradual deterioration of function over time with periods of increased exacerbation of symptoms.

30
Q

What are predictors of the outcome of MS?

What is pseudo exacerbation?

A

Favourable:

  • women
  • < 35 y.o
  • Localized vs general attacks
  • Complete recovery between flare ups

Less Favourable:

  • men
  • Brainstem symptoms
  • Poor recovery after attacks, frequent attack.s.

A pseudo exacerbation: when there are conditions that make it seem like there is a flare up, but really the symptoms or just worse b/c of these factors (not true exacerbation): fatigue, trauma, fever, hot weather.

31
Q

What are the criteria for diagnosis of MS?

A
  • Evidence of lesions in CNS (at least 2)
  • 2 distinct episodes of neurological disturbance btwn 10-59 yrs.
  • CSF analysis for gamma globulin useful
  • Gadolinium scans are used to differentiate new and old lesions.
32
Q

What medications are used to manage MS?

A

Interferons: Actually modify disease progression by reducing frequency and severity of relapses and delaying physical disability.

Corticosteroids: used during an acute exacerbation

Chemotherapy: PPMS

Symptomatic Therapy

33
Q

What are the most common symptoms in ms?

A 
Fatigue 
Motor weakness 
Sensory changes
Unsteady gait 
Cognitive and emotional symptoms
Tremors
Visual Changes (Scatoma)
Bowel and bladder problems
34
Q

What are some evidence-informed practices in the rehabilitation management of MS?

A
  • Interdisiplinary approach
  • Clinical practice guidelines for fatigue
  • Inpatient rehab as needed
  • Outpatient PT ongoing basis.
  • Self-efficacy interventions
  • Verbal intelligence and cerebellar function might be important predictors of rehab outcomes.
35
Q

What are the goals of rehabilitation for MS

A

Maximize functional independence
Provide a wellness lifestyle

TO:

  • Improve mobility, ADLs, QoL, safety
  • Prevent complications
  • Optimize health care service utilization
36
Q
  1. How are rehab interventions influenced by the stage of MS?
  2. What are some general trends in the response to PT?
A
  1. Acute flare ups: Short term interventions to lessen impact.

Establish deficits and intervene as needed.

Ensure ongoing continued follow-up during all stages.

  1. Good: Balance, conditioning, mobility

Poor: Coordination, training of non-ambulatory persons.

37
Q

What common PT assessment are done for:
A. Body structure and function?

B. Activity Limitations

C. Participation Restrictions

A

A. -EDSS

  • Ashworth spasticity scale
  • FSS
  • ROM
  • MMT

B. Barthel Activity of Daily Living Index (BI)

  • Nine hole peg test manual dexterity
  • Timed walking test
  • Functional Independence Measure (FIM)

C. Quality of Life measure

38
Q
  1. Why is fatigue a common symptom in MS?
  2. What are the forms of fatigue?
  3. What are the distributions of fatigue?
A
  1. Due to demyelination nerve conduction requires more energy
  2. Primary: Intrinsic to MS- gets worse w/ heat, precedes a relapse

Secondary: reconditioning, sleep problems, depression, meds

  1. Generalized: influenced by temp, time of day. Assess: VAS and FSS

Specific Muscle Fatigue: stronger ms compensate for weaker ms. Assess repeat contraction and hold to determine which muscles fatigue.

39
Q

What is the role of a PT in managing fatigue in ms?

A

Primary: Monitor, energy conservation techniques

Secondary: endurance/aerobic conditioning, determine cause, movement limitations causing inefficiencies like tone, assistive devices.

40
Q
  1. How does muscle weakness present in MS?

2. How PT involved in treatment of muscle weakness?

A
  1. LE affected earlier and more severely. Mild weakness during sustained activity. Worsened by: ataxia, deconditioning, spasticity.
    Assess: dynamometer
  2. Exercise routine, assistive devices, energy conservation.

Guidelines for strength training:

  • Cool temp
  • Consider safety: balance effort and rest to avoid fatigue
  • Realist goals
  • Home program
  • Max strength in unaffected ms
  • Progress slowly (submax resistance w/ frequent reps)
  • Functional ex
  • Strengthen core ms
41
Q
  1. How does spasticity present in ms?

2. How is spasticity managed?

A
  1. Interferes w/ function, increases w/ fatigue. Predominantly w/ UE flexors and LE extensors. Assess: Ashworth scale.
  2. Team approach, meds (baclofen), remove underlying cause, physical means (Stretch, TENS, cold).
42
Q
  1. What influences functional mobility in ms?

2. How can treatment target functional mobility?

A
  1. Age, duration, frequency and severity of relapses, spasticity, weakness, decreased sensation, balance deficits.
  2. Bracing (AFOs) , walking aids, wheelchairs, safe mobility, decrease energy cost, assistive devices, strengthen muscles, improve balance.
43
Q
  1. How can balance and coordination be affected in ms and addressed by PT?
  2. Deconditioning?
A
  1. ex: ataxia, dysmetria, tremor.

Compensatory training: functional sequences of mvmt, progressions.

  1. Improve fitness and education Ex.

Aerobic program.

  • Body temp
  • Fatigue
  • Safety
44
Q

What are some sensory dysfunctions that occur in ms? treatment?

A

Impaired sensation
Pain
Dysesthesia
Assess each sensory modality as necessary

Teach to compensate for loss, educate on loss and adaptations.

45
Q

What psychosocial issues should be considered in ms?

A

Employment
Family coping
Social Life

46
Q
  1. What is ALS?

2. What parts of the nervous systems are affected in ALS?

A
  1. Relentless, progressive disease of the motor system that affects both UMN and LMN. Causes weakness and wasting of all skeletal muscle.
  2. Anterior horn cells of the spinal cord
    Motor neurons of the pyramidal tract
    Descending axons of the corticospinal tract (lateral column of the SC).
47
Q

What are the clinical criteria for diagnosis of ALS?

What is the typical progression?

A
  • Evidence of weakness/wasting
  • Fasiculations (twitch-LMN sign)
  • Babinski signs or clonus (UMN)

Distal to proximal: Lower to upper extremity then bulbar. Death usually btwn 3-5 yrs after diagnosis due to respiratory failure.

48
Q

What is the focus of treatment for ALS?

A

There is no cure, survival rate is 2-5 yrs after diagnosis.
Symptomatic Medical treatment.

So focus is to help pt learn to live w/ ALS rather than die from ALS. Making the most of the time you have (quality).

Immediately after the diagnosis it is important to:

  • Educate and support
  • Treat new medical problems
  • Encourage pts to continue living life to the fullest.
49
Q

How to the goals of PT change as the disease progresses for ALS?

A
  1. Optimize remaining function (maximize)
  2. Maintain functional mobility
  3. Maximize QoL
50
Q

What should be assessed in terms of body structures and function in ALS?

A 
Tone 
ROM 
Strength 
Pain 
Balance 
Pulmonary function
51
Q

What should be assessed in terms of activity limitations and participation restrictions in ALS?

A

AL :

  • Ambulation
  • Balance
  • Bed mobility
  • Stairs
  • ALS Functional Rating Scale

PR:
QoL

52
Q

What does the ALS functional rating scale measure?

A 
Dressing and hygiene 
cutting food
Salivation 
Speech 
Turning in bed 
Walking 
Climbing stairs
Breathing 
Swallowing 
Score from 0 to 40 (best)
53
Q

What are the phases/stages of ALS

A

Phase 1- Independent Ambulation
Stages 1-3

Phase 2- Partially independent, wheelchair dependent
Stages 4-5

Phase 3- Dependent, bedridden
Stage 6

54
Q

What are the patient characteristics and treatment goals during Stage 1?

A

PC:

  • mild weakness
  • Clumsiness
  • Ambulatory
  • Independent in ADLs

TG:

  • Encourage to become more active if sedentary or maintain current levels if active
  • ROM program
  • Strengthening- gentle resistance w/ out overwork fatigue
  • psychosocial support
55
Q

What are the patient characteristics and treatment goals during Stage 2?

A

PC:

  • Moderate selective weakness
  • Slight decrease independence w/ ADLs (climbing stairs)
  • Ambulatory

TG:

  • Continue stretching to avoid contracture
  • Strengthening for muscles
  • Consider orthotic supports
  • Adaptive equipment for ADLs.
56
Q

What are the patient characteristics and treatment goals during Stage 3?

A

PC:

  • Severe selective ms weakness wrist, hands, ankles.
  • Moderate decrease independence ADL
  • Get fatigue easily w/ long distance ambulation
  • Ambulatory
  • Slight increase in resp effect.

TC:

  • Continue stage 2
  • Make sure not to fatigue to the point that they cannot perform ADLs.
  • Keep physically independent as long as possible.
  • Encourage deep breathing, chest stretch postural drainage.
  • Prescribe w/c to allow reclining w/ head rest and leg elevation eventually.
57
Q

What are the patient characteristics and treatment goals during Stage 4?

A

PT:

  • Hanging-arm syndrome w/ shoulder pain and some edema hand
  • Wheelchair dependent
  • +/- spasticity
  • Able to perform ADLs but gets tired easily
  • Neck weakness
  • Severe LE weakness

TG:

  • AAROM
  • Heat to manage spasms
  • sling or w/c support arm
  • Anti-edema
  • Isometric contraction all muscles
  • Neck collar
  • Motorized w/c
58
Q

What are the patient characteristics and treatment goals during Stage 5?

A

PC:

  • Sever LE weakness
  • Moderate to severe UE weakness
  • W/c dependent
  • Increased dependent in ADLs
  • Possible skin breakdown b/c of poor mobility

TG:

  • Teach family transfers, positioning and turning
  • Home modification
  • Electric hospital bed w/ air mattress
  • Adapt w/c to hold respirator unit
59
Q

What are the patient characteristics and treatment goals during Stage 6?

A

PC:

  • Bed-ridden
  • Completely dependent ADLs

TG:

  • Dysphagia: diet modification, PEG, tube feed
  • Decrease flow of saliva: med, suction, surgery
  • Dysarthria: electron speech or eye pointing
  • Breathing difficulty: airway clearance
  • Med to manage dyspnea
60
Q

What are some objective measures used to track ALS evolution?

A 
ALS function rating scale 
Sickness Impact profile 
SF-36
TUG
Gait Speed
Ashworth 
Muscle Testing
PFT

Minimize tests maximize education

61
Q

What are common reasons for hospital admission in ALS?

A

Feeding tube insertion

Respiratory management (BIPAP, ventilator, diaphragmatic weakness)

62
Q

What are the submaximal strength training parameters for NMD?

A

F: 2-3 days/week

I-3 sets

6-15 reps (50-70% 1 RM)

Modify depending on the stage of the disease (slow or fast progression, duration, intensity)

  • Exercise in morning best MS (lower body temp)
  • RT for MS EDSS <7
  • Supervise RT
  • Use machine over free weight
  • Start lower then increase intensity or sets
  • Rest 2-4 min btwn sets
  • Whole body programs of 4-8 ex
  • Exercise order: large then small muscle group exercises. Multi before single joint exercise.
  • MS LE strength should be a priority over LE strength.

PHTH 551- Neurological Rehabilitation (12 decks)

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