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Management of spasticity after strokeDr Rosie Belcher

+Contents

What is spasticity?

Why do stroke patients develop spasticity?

What management options are available? Drugs Botulinum toxin

Cases

+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

+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

+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

+Advantages

Maintenance of tone which assists mobility

Maintenance of muscle bulk Prevention of pressure sores

+Disadvantages

Reduced range of motion, contractures

Muscle fatigue

Pain

Difficulties with personal care/hygeine

Difficulties with positioning

Increased energy (caloric) needs

Abnormal bone stress

+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

+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

+Management options

Positioning/splinting

Drugs Baclofen Tizanidine Dantrolene

Botulinium toxin

Phenol/alcohol ablation

+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

+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

+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

+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

+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

+Drugs: tizanidine

Alpha-2 adrenergic agonist

Decreased activation of alpha motor neuron

Reduced excitatory

neuron input

Presynapse: inhibition of excitatory

spinal interneurons

+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

+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

+Botulinum toxin

Type A (Botox)

Type B (NeuroBloc)

Injected at target site

+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

+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

+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)

+NICE guidance on stroke rehabilitation

Expected June 2013

Will specifically include management of spasticity