Acknowledgements
4. Butulinum toxin
Does local injection of botulinum toxin (BTX) lead to functional or symptomatic improvements in adults with spasticity?
Intramuscular BTX injections can be used to selectively weaken overactive, spastic muscles by preventing the release of acetylcholine from presynaptic nerve endings [51]. The effect takes approximately 2 weeks to develop and lasts for 2–6 months, but the maximum dose that can be administered at any one time is limited. Preparations of two serotypes are currently available (in UK: Type A Botox® and Dysport®, Type B Neurobloc®), but the doses of the different formula-tions (even of the same serotype) are not equivalent. A good therapeutic outcome depends on careful selection of target muscles and a realistic appraisal of the possible rehabilitation goals (often requiring a detailed, multi-disciplinary assess-ment) [52]. Electromyography (EMG) or ultrasound local-ization can improve injection accuracy.
The placebo-controlled RCT evidence for the use of BTX in adult spasticity is summarized in Table 11.4. All studies to date have used BTX Type A, except Ref. [53] which used Type B. These studies showed good evidence that BTX Type A can lead to improvements in PROM (and functions such as passive dressing), together with some evidence for improve-ments in spasticity-related pain and spasms, and active 90 Part 2: Neurological symptoms/problems
Chapter 11: Central and spinal spasticity91 Table 11.1 Physical interventions for spasticity and other upper motor neurone phenomena.
Reference Study type Patients (n) Intervention Intensity Improvement in active Improvement in Reduction in Reduction in
(reference) voluntary movement PROM spasticity-related spasms
pain
[11] RCT SCI (14) Passive stretching of 30 min daily No No
Single blind one ankle versus other
ankle not stretched
[12] RCT crossover TBI (9) Ankle casts and stretching 7 days each arm Yes
Single blind versus no casts Torque-controlled
PROM
[13] RCT crossover TBI (15) Serial elbow and/or 1 month No Yes
wrist casts versus Goniometry
traditional therapy
[14] RCT crossover Stroke (44, 21 Bobath versus 20 sessions Bobath was superior at Single blind with spasticity) orthopaedic physiotherapy over 4 weeks motor assessment and
approach stroke impact scales
[15] SR of 6 RCTs MS (164) Exercise therapy versus Strong evidence for
normal activity mobility-related activities
Moderate evidence for arm/hand use
[16] SR of 11 RCTs Stroke (458) Treadmill training with No
body weight support Walking speed
versus usual activity Walking dependence
[17] RCT Stroke (28) Functional electrical 30 min daily for Yes Yes
Single blind stimulation (UL) versus 3 weeks Upper extremity Higher functioning
usual activity functioning test group only
Drawing Test Ashworth score
Motor activity log
[18] RCT Stroke (32) Functional electrical 12 sessions of Yes Yes
stimulation (LL) versus physiotherapy to Walking speed Wartenberg usual activity train use of FES Physiological cost index pendulum test
UL: upper limbs; LL: lower limbs; SCI: Spinal cord injury; MS: Multiple sclerosis; PROM: Passive range of movement; SR: systematic review; TBI: traumatic brain injury.
Part 2: Neurological symptoms/problems
Table 11.2 Oral drug treatments for spasticity.
Reference Study type Patients (n) Intervention Improvement in active Improvement in PROM Reduction in spasticity- Reduction in
voluntary movement related pain spasms
[20] RCT Stroke (20) Baclofen (30 mg) Yes
versus placebo Ashworth
[21] RCT crossover MS (23) Baclofen (up to 80 mg) Yes Yes Yes
versus placebo Unvalidated score
[22] Four-way crossover study MS (38) Baclofen (20 mg) and/or Yes
with no washout period stretching exercises Ashworth score and
between treatment arms angle of flexion
[23] RCT MS (166) Baclofen (60–80 mg) Yes Yes
versus placebo Unvalidated score
[24] RCT crossover Stroke (38) Dantrolene (50–200 mg) No No
versus placebo
[25] RCT Stroke (18) Dantrolene (average Yes
dose 165.4 mg/day) Novel spasticity grading
scale
[26] RCT Spinal cord Dantrolene (up to 400 mg) Yes Yes Yes
disease (25) versus placebo Walking speed only Unvalidated tone score
[27] RCT Various with Tizanidine (up to 10 mg/day)
spastic versus placebo
paraparesis (13) No
[28] RCT crossover Stroke (9) and Tizanidine (up to 36 mg) Yes Yes
TBI (8) versus placebo Ashworth score For LL only
[29] RCT SCI (124) Tizanidine (4–36 mg) versus Yes Yes
placebo Ashworth score
[30] RCT MS (257) Tizanidine (2–36 mg) versus No No No No
placebo
[31] RCT MS (187) Tizanidine (up to 36 mg) No Yes No No
versus placebo Composite Ashworth
score
[32] RCT MS (66) Tizanidine (up to 36 mg) No Yes in some muscle No No
versus placebo groups
Unvalidated tone score
_4_011.qxd 2/7/07 2:48PM Page 92
Chapter 11: Central and spinal spasticity93
[33] RCT crossover MS (16) Cannabinoids versus placebo No No
Worsening in timed walk and 9-hole peg test in THC treated group
[34] RCT crossover with no MS (24) and Cannabinoids versus placebo No Yes Yes
washout period SCI (4) VAS VAS
[35] RCT MS (611) Cannabinoids versus placebo Yes No Yes Yes
Timed walk in THC group
[36] RCT crossover with MS (50) Cannabinoids versus placebo Yes No Yes in those who
unequal treatment periods Mobility in those who received90%
received90% prescribed dose
prescribed dose
[37] RCT MS (160) Cannabinoids versus placebo No No
[38] RCT crossover Stroke (19) Diazepam (6–15 mg) versus No No
placebo Grip strength worse
[39] RCT crossover Stroke (12) Diazepam versus placebo No Yes
Knee passive movement [40] RCT Stroke (120) Tolperisone (300–900 mg) ? Yes for walking distance Yes
versus placebo (graph but not statistics Modified Ashworth score shown)
[41] RCT crossover SCI (6 Clonidine (0.1–0.5 mg) Yes – in only 1 Yes in 5 of 9
paraplegic, 3 versus placebo paraparetic patient Ashworth score paraparetic)
[42] RCT crossover with SCI (25) Gabapentin (2400 mg) Yes Yes
2-day treatment periods versus placebo Ashworth score
[43] RCT crossover MS (22) Gabapentin (900 mg) Yes Yes Yes
versus placebo Ashworth score
LL: lower limbs; TBI: traumatic brain injury; SCI: Spinal cord injury; MS: Multiple sclerosis; PROM: Passive range of movement; VAS: Visual analogue scale.
Part 2: Neurological symptoms/problems
Table 11.3 Intrathecal baclofen treatment for spasticity.
Reference Study type Patients (n) Intervention Improvement in active voluntary Improvement in PROM Reduction in spasticity- Reduction in spasms
movement related pain
[45] RCT Hemiplegia due to TBI Test dose of IT baclofen Yes Yes
or CVA (6) versus saline Ashworth score Penn scale
[46] RCT Stroke (21) Test dose of IT baclofen Yes Yes
versus saline Ashworth score Penn scale
[47] RCT Spinal spasticity (93) Test dose of IT baclofen Yes (88 responded, but
versus saline outcome measure results
not reported) [48] RCT Spinal spasticity (22) Infusion of IT baclofen
versus saline for 13 weeks Mobility subscale of sickness Yes (effect size 1.40) Yes (effect size 0.94) Slight (effect size
Impact profile Modified Ashworth 10-point scale 0.20)
score Penn scale
TBI: traumatic brain injury; CVA: cerebrovascular accident; IT: intrathecal.
_4_011.qxd 2/7/07 2:48PM Page 94
Chapter 11: Central and spinal spasticity95 Table 11.4 Intramuscular botulinum toxin injections for spasticity.
Reference Study Patients (n) Intervention Improvement in active Improvement in PROM Reduction in Reduction in
type voluntary movement and function spasticity-related spasms
pain
[55] RCT CVA (39) BTX versus placebo for arm and forearm No Yes No
spasticity Ashworth in 300 units
group only
[56] RCT CVA or TBI (21) BTX versus placebo for arm and forearm No Yes
spasticity Ashworth
Finger curl distance PROM at wrist but not fingers
[57] RCT CVA (82) BTX versus placebo for arm spasticity No Yes – for all doses
Modified Ashworth
[58] RCT CVA (40) BTX versus placebo for arm and forearm No Yes No
spasticity Ashworth
Disability and carer burden scales
[59] RCT CVA (59) BTX versus placebo for arm spasticity No Yes No
Modified Ashworth Elbow PROM
[60] RCT CVA (126) BTX versus placebo for forearm spasticity No Yes Yes
Ashworth
Disability assessment scale
[53] RCT CVA (15) BTX Type B versus placebo for arm and No No No
forearm spasticity Ashworth
[61] RCT CVA (91) BTX versus placebo for arm and forearm No Yes No
spasticity Ashworth
[62] RCT CVA (50) BTX versus placebo for arm and forearm Yes Yes Yes
spasticity with some residual active Action research arm test MAS VAS
movement (500 unit group only)
[63] RCT MS (74) BTX versus placebo for hip adductor Yes
spasticity Distance between knees for
highest dose (1500 units Dysport) only
(Continued p. 96)
Part 2: Neurological symptoms/problems
Table 11.4 (Continued.)
Reference Study Patients (n) Intervention Improvement in active Improvement in PROM Reduction in Reduction in
type voluntary movement and function spasticity-related spasms
pain
[64] RCT Chair or bed BTX versus placebo for hip adductor No Yes No
bound spasticity Adduction angle Nursing
MS (9) care
[65] RCT (23) 19 CVA 4 TBI BTX versus placebo for Yes for active dorsiflexion Yes
crossover foot spasticity Reduced use of walking Ashworth
aids in 6 patients
[66] RCT CVA (234) BTX versus placebo for calf spasticity Yes – use of walking aids Yes Yes
only MAS
No – 2 min walking distance or stepping rate
[67] RCT CVA (45) BTX versus placebo for foot spasticity Yes Yes Yes
Gait speed Ashworth
[54] RCT Early after TBI (35) Casting alone versus casting plus BTX Yes – for casting and/or
versus stretches to prevent loss of ankle BTX
dorsiflexion range Ankle PROM
[68] RCT Various (12) BTX versus placebo for UL (8) Yes Yes
crossover or LL (4) spasticity Ashworth
[69] RCT Various (52) BTX versus placebo for UL (32) Yes for LL group Yes
or LL (20) spasticity Rivermead mobility index Ashworth
only Range of movement
TBI: traumatic brain injury; BTX: Botulinumtoxin; UL: upper limbs; LL: lower limbs; MS: Multiple sclerosis; CVA: cerebrovascular accident; MAS: Modified Ashworth Scale; PROM: passive range of movement.
_4_011.qxd 2/7/07 2:48PM Page 96
voluntary movement (walking and UL movement) in some.
Verplancke et al. [54] investigated when BTX should be administered in order to try to prevent biomechanical com-plications developing. This study highlighted that contrac-ture can start to develop within only a few weeks of severe head injury, but this can be reduced by maintaining appro-priate stretch (by splinting) with the addition of BTX injec-tions where necessary.
Conclusion
Successful spasticity management requires multi-disciplinary assessment and treatment, focusing on appropriate and realis-tic goals. Evaluation of physical and medical anti-spasrealis-ticity treatments is hampered by the limitations of individual out-come measures for this complex, multi-faceted problem.
Improvement or maintenance of limb PROM can be achieved by physical measures (stretching, casting and functional elec-trical stimulation), oral drug therapy, intramuscular BTX injec-tions and IT treatment (baclofen or phenol), but oral drug therapy alone is often insufficient. Published evidence indi-cates that improvements in spasticity-related pain and spasms can be achieved by oral drug therapy, BTX injections and IT baclofen or phenol, but the trials of physical interventions included in this review did not assess this outcome. Improve-ments in active voluntary movement often cannot be achieved with physical or medical anti-spasticity treatment, but evi-dence to support such benefit in selected cases exists for phys-iotherapeutic treatment, exercise therapy, functional electrical stimulation, oral drug therapy, BTX injection and IT baclofen infusion. Further work is needed to improve the outcome measures available for use in anti-spasticity treatment trials, to identify the optimal timing and intensity of physical and medical interventions, and to evaluate the cost effectiveness of such an optimal multi-disciplinary management approach.
Clinical service provision should ensure that all the necessary multi-disciplinary elements are available, with the timeliness and intensity of treatment that is required.
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Chapter 11: Central and spinal spasticity 99
Background
Neurological illness and injury are major causes of disability.
With an ageing population and more people surviving what would have until relatively recently been fatal neurological insults, utilizing best evidence for rehabilitation is increasingly important. Rehabilitation emphasizes adaptive and restora-tive strategies across the many aspects of human life and performance. Whilst management and prevention of pathol-ogy and impairment remain crucial, promoting functional improvement, assisting people to participate in a meaningful life and helping them and their families attain or maintain the best quality of life (QoL) are rehabilitation’s real goals.
Data on incidence and prevalence of different neurological disability vary greatly according to the way data are collected.
The USA Centre for Disease Control1suggests 1 in every 10 people has major activity limitation due to a chronic condition with two recent household surveys (in the UK and New Zealand [1,2]) suggesting that around one in every five adults and one in every ten children have some sort of disability, with the most common disability being difficulties resulting from neurological origin. The Neurological Alliance recently esti-mated that around 6% of people have a neurological condition where they need daily help with activities [3]. Disability aris-ing from neurological conditions is therefore no small issue.
Despite some very clear gaps in knowledge, research in rehabilitation has advanced significantly over recent years.
New technologies are being applied (including advanced neuroimaging, robotics and virtual reality) and the critique that rehabilitation interventions have lacked a firm theore-tical basis [4] is increasingly being challenged. For instance, recent advances in motor learning theory are being applied to develop novel physiotherapeutic interventions [5,6], self-regulation theory being utilized to challenge perhaps the most ubiquitous intervention in neurorehabilitation – goal setting [7–10] and neurobiology findings influencing a wide range of developments across conditions and strategies given the emerging potential that neural ‘reorganization’ shows in con-tributing to recovery, restoration and adaptation [11].
Along with technological and theoretical advance, many aspects of rehabilitation now having increasing evidence that
they work: specialized stroke units are effective [12,13]; spe-cialist neurological rehabilitation teams can improve outcome after traumatic brain injury [14]; interventions from specialist rehabilitation teams are beneficial for people with multiple scle-rosis [15,16] as well as younger people with physical and com-plex disabilities [17]. There is also a growing body of evidence for the cost-effectiveness of neurorehabilitation [13,18,19].
Despite these advances, evaluating the impact of rehabilita-tion remains complex [20]. It is not a synonym for any one type of intervention (such as surgery/medication) nor is it the domain of any one health professional group (such as medi-cine, physiotherapy or occupational therapy). Further, rehabil-itation strategies aim to achieve outcomes that are wide ranging and difficult to operationalize and the interventions themselves can be difficult to describe. Subtle differences in the way inter-ventions are delivered may very well influence the impact of those interventions (i.e. the process of care/management [21]).
One of the frustrations for clinicians, patients and their families is that as a result of this complexity, trial data (and therefore meta-analyses) concerning rehabilitation has fre-quently yielded equivocal findings. Whilst improved rehabili-tation trials are a clear priority, it is arguable that in addition, practical tools are required to help determine best practice and best decision making in the absence of ‘gold standard’
results from randomized trials [20,22]. Further, for some questions that need to be confronted, (such as what type of therapeutic interventions are most acceptable to specific popul-ations, what barriers and facilitators exist in relation to pro-moting active engagement in rehabilitation) methodologies including qualitative work have a clear role. With these cau-tions in mind, advances over the very recent past about
‘what works’, mean there is reason to feel optimistic about the knowledge base of neurorehabilitation.