Spasticity management after stroke
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Transcript of Spasticity management after stroke
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+
Management of spasticity after strokeDr Rosie Belcher
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+Contents
What is spasticity?
Why do stroke patients develop spasticity?
What management options are available? Drugs Botulinum toxin
Cases
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+What is spasticity?
“Spasticity is a motor disorder characterized by a velocity-dependent increase in tonic stretch reflexes (muscle tone) with exaggerated tendon jerks, resulting from hyper-excitability of the stretch reflex, as one component of the upper motoneuron syndrome.”1
This is commonly accepted definition, but multiple definitions exist
Makes some of the literature difficult to apply as differing definitions used
1. Lance Symposium synopsis in Spasticity: Disorder of motor control. 1980
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+Who gets spasticity?
Prevalence estimates vary from 4%-43%1
Differing definitions
Prevalence increases with time
Risk factors include Severe paresis Sensory deficits Stroke related pain Lower Barthel Index
1. Wissel et al. Neurology 2013; 80: S13-S19
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+Pathophysiology
Not entirely known
Imbalance of inhibitory and excitatory inputs resulting in over-activity of alpha motor neuron
Hyperactive stretch reflex arc
Lack of supraspinal inhibition
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+Advantages
Maintenance of tone which assists mobility
Maintenance of muscle bulk Prevention of pressure sores
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+Disadvantages
Reduced range of motion, contractures
Muscle fatigue
Pain
Difficulties with personal care/hygeine
Difficulties with positioning
Increased energy (caloric) needs
Abnormal bone stress
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+Effects of spasticity
Patients with spasticity spend significantly longer in rehabilitation
Costs of care over the first year are correlated with spasticity1
1. Lundstrom et al. Stroke 2010; 41: 319-324
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+Modified Ashworth scale
0 normal
1 slight increase in tone
1+ slight increase in tone throughout ROM
2 moderate increase in tone, PROM easy
3 marked increase in tone, PROM difficult
4 rigid limb
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+Management options
Positioning/splinting
Drugs Baclofen Tizanidine Dantrolene
Botulinium toxin
Phenol/alcohol ablation
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+Positioning and splinting
Does not improve underlying spasticity
Aim Improve position to functionally more useful position or to
facilitate hygeine Prevent contractures
Evidence base limited Mostly small/medium sized RCTs No clear evidence for extending range of motion
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+Drugs: baclofen
GABA analogue
Selectively binds to GABA-b receptors
Cannot cross blood brain barrier
Decreased activation of alpha motor neuron
Reduced excitatory
neuron input
Presynapse: reduces
polarization of
membrane
Postsynapse: Direct
inhibitory action
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+Baclofen: evidence
V little evidence specifically in stroke
Double blind study comparing baclofen with tizanidine 30 pts Improvement in spasticity No functional assessment 20% of pts on baclofen dropped out due to intolerable
adverse effects
1. Medici Curr Med Res Opin 1989; 11: 398
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+Intrathecal baclofen
Small prospective observational trials 17 pts1
26 pts2
Improved Ashworth scores1
Functional Independence Measure scores improved2
Improvement in QoL2
Benefit for lower limb >> upper limb
Evidence in stroke
1. Meythaler Stroke 2001; 32: 20992. Scheiss Neuromodulation 2011; 41: 38
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+Baclofen:
Can be given via PEG (liquid formulation or crush tablets)
Cheap NHS costs ~£23/year
Good evidence for IT baclofen in highly selected populations
Adverse effects common at doses effective for controlling spasticity Drowsiness Confusion/memory
impairments Headache Hallucinations Ataxia
Little evidence of benefit post stroke for oral baclofen
Advantages Disadvantages
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+Drugs: tizanidine
Alpha-2 adrenergic agonist
Decreased activation of alpha motor neuron
Reduced excitatory
neuron input
Presynapse: inhibition of excitatory
spinal interneurons
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+Tizanidine: evidence
Double blind RCT compared with diazepam1
105 pts Titrated up to max dose 24mg tizanidine or 30mg diazepam Increased walking distance Decreased duration and angle of contractures Much better tolerated than diazepam
Open label observational study 47 pts, titrated slowly to max 36mg Reduced MAS score (2.8) Reduced pain intensity Improved QoL scores
1. Bes Curr Opin Res Med 1988; 10: 709
2. Gelber Stroke 2001; 32: 1841
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+Tizanidine
Can be given via PEG (crush tablets)
Better tolerated than baclofen
Adverse effects Hypotension and
dizziness Sedation Dry mouth
More expensive than baclofen NHS costs ~£87/year
Advantages Disadvantages
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+Botulinum toxin
Type A (Botox)
Type B (NeuroBloc)
Injected at target site
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+Botulinum toxin: evidence
Upper limb spasticity Number of trials report improvements in spasticity as
assessed on (modified) Ashworth scale1, 2
Mixed evidence regarding functional improvement1 or pain2
Meta-analysis suggests correlation between improvement in spasticity and function3
Lower limb spasticity Fewer and smaller trials Focus on improving plantar flexion/inversion Improvements in spasticity/facilitation of physiotherapy/gait
pattern No evidence of improvement in global functional measures11. Ozcakir Clin Med and Res 2007; 5: 132-138
2. Olvey Clin Ther 2010; 32: 2282-23033 . Francis JNNP 2004; 75: 1547-1551
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+Botulinum toxin: pros and cons
Safe1
Nausea Dry mouth
Good evidence base in stroke
Not suitable for generalised spasticity due to need for high doses/multiple injections
Needs repeated injections
Advantages Disadvantages
1. Turkel Arch Phys Med Rehab 2006; 87: 786-792
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+RCP stroke guidelines
All pts with weakness should be assessed for spasticity
If spasticity causes concern, start with simple measures and monitor Positioning, active movement
If persistent or progressive focal spasticity and a therapeutic goal is identified, treatment should be with botulinum toxin.
If troublesome generalised spasticity, baclofen or tizanidine should be tried in first instance
Intrathecal baclofen reserved for difficult-to-manage patients under specialist MDT spasticity service (or in clinical trials)
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+NICE guidance on stroke rehabilitation
Expected June 2013
Will specifically include management of spasticity