Day 6 - Flash Cards (Spasticity & Contracture)
List 4 features that differentiate UMN lesion from a LMN lesion.π
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?
Give 4 signs of corticospinal tract lesion besides loss of voluntary movement and skill
Just another way to ask signs of UMN lesion:
- Spasticity
- Hyperreflexia
- Plantar response
- Hoffman
- Clonus
- Pronator drift
List 4 positive and 4 negative of UMN syndrome.π
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
Describe hoffmanβs reflex.
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.
Define rigidity and mention 2 types. π
Resistance to passive movement that is not velocity dependant
Types: lead pipe, waxy, plastic, cog-wheel
Define dystonia, List 4 types and 4 causes. π
Involuntary sustained or intermittent muscle contractions cause twisting, abnormal postures and/or repetitive movements.
Specific dystonias: βTurn your head right, close eye, vocal cords and hands.β
- Torticollis
- Blepharospasm
- Spasmodic dysphonia
- Writerβs cramp
Causes:
- Idiopathic
- Basal ganglia lesion β tumor, abscess, infarct, CO poisening
- Wilsonβs
- Huntingtonβs
- Parkinsonβs
- Tardive dyskinesia
List 5 domains of spasticity. ππ
- A motor disorder
- Abnormal, velocity-dependent increase in the tonic stretch reflexes (muscle tone)
- Exaggerated phasic stretch reflexes (tendon jerks, clonus)
- Resulting from hyperexcitability of the stretch reflex.
- Component of the UMNS.
List 5 categories/goals of spasticity management. π
- MSK biomechanics: Reduce tone, improve ROM
- Functional: ADLs, upper and lower limb function
- Patient: Pain and discomfort, proper fitting orthosis, wheelchair position
- Caregiver: Personal hygiene, dressing, ambulation
- Preventive: Contracture, pressure ulcer
Ref: Review notes
Educate caregiver patient about difference methods in treating spasticity.π
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
Patient with severe spasticity, oral drugs donβt help. List 5 other treatments.
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
List 5 non-PO (non-oral) treatments for adductor spacticity interfering w/ perineal hygiene.
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
What are the indications for treatment of spasticity?
- decrease pain
- improved nursing care
- imrpoved hygiene
- minimize contractures
- pressure ulcer prevention/healing
- improved seating
- improved gait and transfers
- improved self-care activities (ADL)
Ref: txtbook, rehab of people with TBI.
List 4 drugs used for treatment of spasticity and give their mechanisms of action π
- Baclofen: presynaptic GABA B agonist, centrally acting (spinal cord level) β presynaptic and post synaptic.
- tizanidine: alpha 2 agonist, centrally acting, spinal cord.
- dantrolene: interferes with calcium release at sarcoplasmic reticulum, peripherally acting.
- clonidine: alpha 2 agonist, centrally acting (same as tizanidine).
- gabapentin: GABA A analogue β may have indirect effect on GABA-ergic neurotransmission.
- Benzodiazepine (ie. diazepam): GABA A agonist. Presypantic inhibition by hyperpolarization.
Ref: Delisa pg 1322.
Baclofen side effects and mechanism of action.π
Baclofen is a structural analog of GABA β centrally acting.
SIDE EFFECTS:
- N/V.
- Sedation/ hypersomnolence.
- Decrease seizure threshold (abrupt discontinuation).
- GI symptoms (constipation).
- Hypotension.
- Confusion.
- hallucinations (abrupt discontinuation).
Ref: 2003 β CMAJ β Satkunam β management of adult spasticity.
- impaired walking ability.
- paresthesias.
- impaired attention/memory (elderly pts).
- dizziness.
Ref: 1997 β muscle and nerve β spasticity part 2 management paper.
List 4 consequences of abruptly stopping baclofen.π
- seizures.
- rebound spasticity.
- fever.
- hallucinations.
- altered mental status.
- malignant hyperthermia.
- death.
- tachycardia.
- restlessness.