Day 6 - Flash Cards (Spasticity & Contracture)

1
Q

List 4 features that differentiate UMN lesion from a LMN lesion.πŸ”‘

A

Remember: Look - Feel - Move

UMN:

  • no atrophy.
  • no fasciculations.
  • increased tone (hypertonia).
  • spasticity
  • babinski response.
  • exaggerated reflexes

LMN:

  • atrophy.
  • fasciculations.
  • hypotonia
  • no spasticity.
  • no babinski response.
  • diminished/absent reflexes.

Ref: GL response, ref?

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2
Q

Give 4 signs of corticospinal tract lesion besides loss of voluntary movement and skill

A

Just another way to ask signs of UMN lesion:

  1. Spasticity
  2. Hyperreflexia
  3. Plantar response
  4. Hoffman
  5. Clonus
  6. Pronator drift
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3
Q

List 4 positive and 4 negative of UMN syndrome.πŸ”‘

A

POSITIVE SIGNS

  • Spasticity
  • Rigidity
  • Spastic dystonia
  • Hyperreflexia
  • Clonus
  • Persistence or re-appearance of primitive reflexes (e.g., positive Babinski response)
  • Athetosis
  • Increased cutaneous reflexes
  • Loss of precise autonomic control

NEGATIVE SIGNS:

  • Muscle weakness
  • Paralysis/paresis
  • Muscle atrophy/wasting
  • Decreased dexterity
  • Loss of voluntary movement
  • Loss of coordination
  • Fatigue
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4
Q

Describe hoffman’s reflex.

A

Signifies presence of UMN lesion from spinal cord compression.

Flip volar or dorsal surface of middle finger; positive test is reflex contraction of the DIP of thumb and index finger; negative is no contraction.

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5
Q

Define rigidity and mention 2 types. πŸ”‘

A

Resistance to passive movement that is not velocity dependant

Types: lead pipe, waxy, plastic, cog-wheel

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6
Q

Define dystonia, List 4 types and 4 causes. πŸ”‘

A

Involuntary sustained or intermittent muscle contractions cause twisting, abnormal postures and/or repetitive movements.

Specific dystonias: β€œTurn your head right, close eye, vocal cords and hands.”

  1. Torticollis
  2. Blepharospasm
  3. Spasmodic dysphonia
  4. Writer’s cramp

Causes:

  1. Idiopathic
  2. Basal ganglia lesion – tumor, abscess, infarct, CO poisening
  3. Wilson’s
  4. Huntington’s
  5. Parkinson’s
  6. Tardive dyskinesia
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7
Q

List 5 domains of spasticity. πŸ”‘πŸ”‘

A
  1. A motor disorder
  2. Abnormal, velocity-dependent increase in the tonic stretch reflexes (muscle tone)
  3. Exaggerated phasic stretch reflexes (tendon jerks, clonus)
  4. Resulting from hyperexcitability of the stretch reflex.
  5. Component of the UMNS.
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8
Q

List 5 categories/goals of spasticity management. πŸ”‘

A
  1. MSK biomechanics: Reduce tone, improve ROM
  2. Functional: ADLs, upper and lower limb function
  3. Patient: Pain and discomfort, proper fitting orthosis, wheelchair position
  4. Caregiver: Personal hygiene, dressing, ambulation
  5. Preventive: Contracture, pressure ulcer

Ref: Review notes

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9
Q

Educate caregiver patient about difference methods in treating spasticity.πŸ”‘

A

Prevention first (non-pharmacological)

  • Remove factors or noxious stimuli that may increase spasticity (UTI, etc).
  • Exercises: positioning, stretching/ROM.
  • Bracing: splinting (static vs dynamic), Serial casting.
  • Modalities: cold, electrical stim, FES

Treating second (pharmacological)

  • oral medications β†’ Baclofen
  • focal treatments β†’ BotoX
  • intrathecal baclofen.
  • surgical options (selective dorsal rhizotomy)..

Ref: http://www.abiebr.com/set/case-study-2/27-spasticity-post-abi

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10
Q

Patient with severe spasticity, oral drugs don’t help. List 5 other treatments.

A

Prevention first (non-pharmacological)

  • Remove factors or noxious stimuli that may increase spasticity (UTI, etc).
  • Exercises: positioning, stretching/ROM.
  • Bracing: splinting (static vs dynamic), Serial casting.
  • Modalities: cold, electrical stim, FES

Treating second (pharmacological)

  • oral medications β†’ Baclofen **SKIP**
  • focal treatments β†’ BotoX
  • intrathecal baclofen.
  • surgical options (selective dorsal rhizotomy)..

Ref: http://www.abiebr.com/set/case-study-2/27-spasticity-post-abi

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11
Q

List 5 non-PO (non-oral) treatments for adductor spacticity interfering w/ perineal hygiene.

A

Prevention first (non-pharmacological)

  • Remove factors or noxious stimuli that may increase spasticity (UTI, etc).
  • Exercises: positioning, stretching/ROM.
  • Bracing: splinting (static vs dynamic), Serial casting.
  • Modalities: cold, electrical stim, FES

Treating second (pharmacological)

  • oral medications β†’ Baclofen **SKIP**
  • focal treatments β†’ BotoX
  • intrathecal baclofen.
  • surgical options (selective dorsal rhizotomy)..

Ref: http://www.abiebr.com/set/case-study-2/27-spasticity-post-abi

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12
Q

What are the indications for treatment of spasticity?

A
  1. decrease pain
  2. improved nursing care
  3. imrpoved hygiene
  4. minimize contractures
  5. pressure ulcer prevention/healing
  6. improved seating
  7. improved gait and transfers
  8. improved self-care activities (ADL)

Ref: txtbook, rehab of people with TBI.

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13
Q

List 4 drugs used for treatment of spasticity and give their mechanisms of action πŸ”‘

A
  1. Baclofen: presynaptic GABA B agonist, centrally acting (spinal cord level) – presynaptic and post synaptic.
  2. tizanidine: alpha 2 agonist, centrally acting, spinal cord.
  3. dantrolene: interferes with calcium release at sarcoplasmic reticulum, peripherally acting.
  4. clonidine: alpha 2 agonist, centrally acting (same as tizanidine).
  5. gabapentin: GABA A analogue – may have indirect effect on GABA-ergic neurotransmission.
  6. Benzodiazepine (ie. diazepam): GABA A agonist. Presypantic inhibition by hyperpolarization.

Ref: Delisa pg 1322.

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14
Q

Baclofen side effects and mechanism of action.πŸ”‘

A

Baclofen is a structural analog of GABA – centrally acting.

SIDE EFFECTS:

  1. N/V.
  2. Sedation/ hypersomnolence.
  3. Decrease seizure threshold (abrupt discontinuation).
  4. GI symptoms (constipation).
  5. Hypotension.
  6. Confusion.
  7. hallucinations (abrupt discontinuation).

Ref: 2003 – CMAJ – Satkunam – management of adult spasticity.

  1. impaired walking ability.
  2. paresthesias.
  3. impaired attention/memory (elderly pts).
  4. dizziness.

Ref: 1997 – muscle and nerve – spasticity part 2 management paper.

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15
Q

List 4 consequences of abruptly stopping baclofen.πŸ”‘

A
  1. seizures.
  2. rebound spasticity.
  3. fever.
  4. hallucinations.
  5. altered mental status.
  6. malignant hyperthermia.
  7. death.
  8. tachycardia.
  9. restlessness.
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16
Q

List 4 conditions for which botulinum toxin could be used other than spasticity. πŸ”‘πŸ”‘

A
  1. Chronic migraine headache prophylaxis
  2. Blepharospasm
  3. Strabismus
  4. Primary axillary hyperhydrosis
  5. Cervical dystonia
  6. Detrusor overactivity
17
Q

What is the effect of botulinum toxin A on muscle?

A

Presynaptic inhibition of acetycholine release at the neuromuscular junction which results in relaxation of the muscle due to denervation.

18
Q

There are 3 disease interactions with Botox (onabotulinumtoxin A) which include: πŸ”‘

A
  • dysphagia/respiratory disorders
  • infection
  • UTI
19
Q

What potential drug-drug interactions can occur with botulinum toxin?πŸ”‘

A
  1. Aminoglycoside antibiotics.
  2. Magnesium sulfate.
  3. Anticholinesterases
  4. Neuromuscular blocking agents
20
Q

List 3 advantages of botulinum toxin over phenol injections.πŸ”‘

A
  1. reversible effects (not permanent).
  2. less painful injections (no burning with BoNT).
  3. decreased risk long term neuralgia or sensory loss.
  4. no need to localize motor endplate( ease of localization)
  5. not associated with CNS (Seizures) or CV effects with intravascular injections.
21
Q

List 6 reasons why you wouldn’t give Botox in these situation.πŸ”‘

A
  1. patient refusal
  2. interferes with functional goals (eg. Quads used for standing).
  3. contractures instead of spasticity.
  4. BoNT in last 3 months (risk of antibody formation).
  5. previous poor results from BoNT.
  6. adverse events or hypersensitivity.
  7. NMJ disorder (ALS, motor neuron disease, LEMS, MG).
  8. borderline breathing or swallowing dysfunction.
  9. contraindicated medications (eg. Aminoglycosides, spectinomycin).
  10. anticoagulants or bleeding diathesis
22
Q

List 2 advantages and 2 risks of intrathecal baclofen pump (ITB).πŸ”‘

A

ADVANTAGES:

avoids high concentrations of baclofen from reaching brain (less side effects).

baclofen dose can be adjusted to effect individually.

can be turned off when not needed.

improved spasticity control over oral medications.

Ref: Karen Ethans – spasticity presentation 2011.

RISKS

  1. DEVICE failure (battery failure, catheter breakage, blockage, retraction).
  2. Infection risk of catheter (meningitis, encephalitis, implantation site).
  3. DRUG failure (overdose or withdrawal, tolerance).
  4. SURGICAL complications (pneumonia, bleeding, infection, CSF leak, etc).
  5. PATIENT symptom changes (increased back pain, increased bladder symptoms, dyspnea).
  6. Requires follow up.
23
Q

List 3 contraindications to intrathecal baclofen πŸ”‘

A
  1. Poor cognitive function.
  2. Contractures more than spasticity.
  3. UE more than LE involvement.
  4. Unreliable patient (low compliance and adherence)
  5. Geographical barriers.
  6. Early demise expected.
  7. Multiple other medical issues.
24
Q

Gabapentin: MOA and 4 common side effects.πŸ”‘

A

GABA analogue – may have indirect effect on GABA-ergic neurotransmission.

SIDE EFFECTS:

somnolence/drowsy/asleep

dizziness.

ataxia.

fatigue.

25
Q

Define contractures and their pathophysiology.πŸ”‘

A

Fixed loss of passive joint range of movement secondary to pathology of connective tissue, tendons, ligaments, muscles, joint capsules and cartilage.

Etiology: Trauma, inflammation, ischemia, infection cause collagen proliferation.

Ref: http://www.abiebr.com/set/case-study-2/26-contractures-post-abi

26
Q

Male with myotonic dystrophy, post-trauma, list 3 categories & risk factors of contractures.

You have bone - muscle - connective tissue.

A

1- ARTHROGENIC:

  • Congenital deformities
  • Cartilage damage
  • Capsular fibrosis
  • Primarily immobilization

2- SOFT AND DENSE TISSUE:

  • Periarticular soft tissue trauma
  • Tendons and ligaments
  • burns

3- MYOGENIC: Intrinsic

  • Degenerative - muscular dystrophy
  • Ischemic

4- MYOGENIC: Extrinsic

  • Muscle imbalance from dystrophy
  • Mechanical (poor positioning)
  • Primarily Immobilization
  • Spasticity

5- MIXED

  • Combined arthrogenic, soft-tissue, and muscle contractures

Ref: Delisa Table 48.3, p1255

27
Q

Muscles that at risk of contractures.πŸ”‘

A

Two joint muscles: More 1a afferent sensory fibres

  • biceps femoris
  • hamstrings
  • TFL
  • gastrocnemius

Ref: http://www.abiebr.com/set/case-study-2/26-contractures-post-abi

28
Q

What are the common locations of contractures?πŸ”‘

A

LOWER LIMB:

  • ankle PF,
  • hip flexion,
  • knee flexion

UPPER LIMB:

  • elbow flexion,
  • pronation
  • shoulder adduction/IR

Ref: http://www.abiebr.com/set/case-study-2/26-contractures-post-abi

29
Q

How to preform serial casting? List 4 absolute contra-indications. πŸ”‘

A

Methods

  • botox (botulinum toxin)
  • cast after 7 days
  • follow up every 2 weeks, re-cast
  • passive stretching, then cast at end range

Contraindications:

  1. any skin issues (infection, open wounds, etc)
  2. cognitive issues – aphasia, unable to report pain
  3. insensate skin
  4. osteoporosis
  5. unable to follow up with patient 2 weeks
  6. recent fractures
  7. patient does not consent
  8. heterotopic ossification
30
Q

List treatment options for contractures.

A
  1. electrical stimulation
  2. serial casting
  3. dynamic splinting
  4. BoNT injections
  5. intrathecal baclofen
  6. surgical interventions
31
Q

What are the surgical options for treatment of spasticity and contractures? (Spasticity Course)

A
  1. tendon lengthening
  2. tendon transfers (SPLATT)
  3. tendon transections
  4. osteotomies
  5. fusion
  6. joint replacement
  7. capsulotomy (soft tissue releases)
  8. selective dorsal rhizotomy