2.7 Spasticity Post ABI

2.7.1  Definition of Spasticity

Define Spasticity.

  1. Spasticity is a common symptom encountered post acquired brain injury and is an element of the upper motor neuron syndrome 17.
     
  2. Spasticity has been formally defined as “a motor disorder characterized by a velocity-dependent increase in tonic stretch reflexes with exaggerated tendon reflexes, resulting from excitability of the stretch reflex” 18.
     
  3. Common features of spasticity included increased muscle tone, exaggerated tendon jerks, and clonus. 

2.7.2  Treatment of Spasticity

2.7.2.1  Indications for Treatment of Spasticity

When is treatment of spasticity indicated?

  1. Spasticity may require intervention when it interferes with functional abilities such as mobility, positioning or hygiene, or when it is the cause of deformity or pain.
     
  2. Factors that must be taken into consideration when proposing treatment of spasticity include chronicity of the problem, the severity, the pattern of distribution (focal versus diffuse) and even the locus of injury 19.
  • Spasticity is not unique to individuals who have sustained a brain injury.
     
  • Spasticity results in involuntary contractions of synergistic muscles in the extremities, which are clinically manifested as flexor or extensor spasms 20;21.
     
  • Improving patient function is the key to developing any plan to treat spasticity 19.
     
  • For many developing plans to treat their spasticity is done in the early days of rehabilitation, however in those with an ABI, symptoms my not appear for several weeks or months post injury.

2.7.2.2  Treatment Approach to Spasticity Post ABI

Describe a treatment approach to spasticity.

  1. Remove those factors which may increase spasticity.
     
  2. Oral antispastic medications.
     
  3. Botulinum toxin for focal spasticity, when oral antispastic medications are ineffective.
     
  4. Intrathecal baclofen should be used as a last resort for severe spasticity.

2.7.2.3  Oral Antispasticity Drugs Post ABI 

When should oral antispastic drugs be used in the ABI patient, and what are some of the concerns with using these medications?

  1. Oral agents are often used to manage spasticity particularly when a systemic agent to treat upper and lower extremity spasticity is required 22.
     
  2. Although anti-spasticity agents may be used with other medical conditions such as spinal cord injury or multiple sclerosis 23the effectiveness should not be presumed to be similar for brain injury survivors. 
     
  3. One particular limitation is the associated cognitive and behavioral changes associated with brain injury. 

What drugs are available?

  1. Multiple medication have been evaluated to treat spasticity of both cerebral and baclofen, benzodiazepines, dantrolene sodium which affects ion flux and agents that affect alpha-2 adrenocrepeptors such as tizanidine and clonidine.

Oral Tizanidine 

  • One RCT investigated the effect of trizanidine in the management of spasticity on individuals recovering from an ABI or stroke 20.
     
  • A common adverse effect was increased somnolence (41%) compared to placebo (0%).
     
  • Oral tizanidine was found to be effective for improving upper and lower extremity spasticity.

Oral Baclofen

  • Oral baclofen was administeredto patients post ABI to assistin the management of spasticity 24.
     
  • Lower extremity spasticity scoresimproved followingthe administration of baclofen; however, upper extremity spasticitiy scores showed no significant improvement.
     
  • A noted common adverse effect of the oral baclofen was the onset of considerable sleepiness in 6 (17%) patients. 
     

For further details on the effectiveness of oral antispasticity drugs on individuals with an ABI see ERABI/Motor and Sensory Impairments Remediation Post Acquired Brain Injury.

What are some of the concerns when using these medications?

  1. One particular limitation is the associated cognitive and behavioural changes associated with brain injury.

What evidence is there for oral anti-spasticity drugs in ABI?

  1. There is Level 1 evidence that oral tizanidine improves lower and upper extremity spasticity when compared to placebo.
     
  2. There is Level 4 evidence that oral baclofen improves lower extremity spasticity but not upper extremity spasticity

2.7.2.4  Botulinum Toxin Injections for Spasticity Post ABI

How does botulinum toxin work in the treatment of spasticity? 

  1. Botulinum toxin type A (BTX-A) acts at pre-synaptic terminals to block acetylcholine release into the neuromuscular junction.  
     
  2. When selectively injected into a specific muscle, BTX-A is thought to cause local muscle paralysis thereby alleviating hypertonia due to excessive neural activity 25.
     
  3. BTX-A is a relatively new treatment strategy for the management of spasticity in ABI.
     
  4. It has been suggested that BTX-A may be useful in the treatment of localized spasticity if oral treatments such as benzodiazepines, baclofen, dantrolene sodium or tizanidine cause significant adverse effects 22.

When should it be used?

  1. It has been suggested that BTX-A may be useful in the treatment of localized spasticity if oral treatment such as benzodiazepines, baclofen, dantrolene sodicum or tizanidine cause significant adverse effects.

What is the evidence for the use of botulinum toxin to treat spasticity in ABI patients?

  1. There is Level 4 evidence that botulinum toxin A injections may be effective in the management of localized spasticity following ABI.
  • Results of three studies suggest that botulinum toxin type A injections may be effective in the management of localized spasticity following ABI 26-28.
     
  • Yablon et al. 26reported that BTX-A injections into the upper extremities improved range of motion, and spasticity as measured by the modified Ashworth scale (MAS) in 21 ABI patients. 
     
  • Fock et al. 27noted BTX-A injections into the lower extremities improved measures of walking performance including walking speed, stride length, cadence, dorsiflexion on contact with the ground and passive dorsiflexion; however, no significant improvements in overall a spasticity was found.
     
  • van Rhijn et al. 28reported that BTX-A was effective in improving MAS scores (in a pediatric population) up to 5 months post-treatment with concomitant improvements in range of motion.
     

For further details on the effectiveness of botulinum toxin injections on individuals with an ERABI/Motor and sensory Impairments Remediation Post Acquired Brain Injury.

2.7.2.4   Intrathecal Baclofen for Spasticity Post ABI

What is the rationale behind use of intrathecal baclofen?  What are the pros and cons of using it to treat spasticity post ABI?

  1. A limitation of oral baclofen is the inability to achieve sufficient concentrations in the cerebrospinal fluid in order to modify spasticity without first causing significant sedation 23.
     
  2. Intrathecal baclofen refers to direct administration of baclofen into the intrathecal space and cerebrospinal fluid at the lumbar level. For therapeutic treatment, a subcutaneously placed pump is required to provide continuous administration of the medication into the intrathecal space. 
     
  3. This treatment procedure is more invasive and is associated with complications including infection, pump failure and tube complications such as kinking or disconnection 23.

What is the evidence for the use of intrathecal baclofen in the treatment of spasticity post ABI?

  1. There is Level 1 evidence, based on a single RCT, that bolus intrathecal baclofen injections produce short-term (up to 6 hours) reductions in upper and lower extremity spasticity.
     
  2. There is Level 4 evidence prolonged intrathecal baclofen results in longer-term (3 months and one year) reductions in spasticity in both the upper and lower extremities following an ABI.
     
  3. There is Level 4 evidence, based on one study, that intrathecal baclofen results in short-term improvements in walking performance, particularly gait velocity, stride length and step width.
  • Meythaler et al. 29in an RCT, confirmed the effectiveness of intrathecal baclofen to decrease upper and lower extremity spasiticity .
     
  • Subsequent studies, found the effectiveness of intrathecal baclofen for decreasing upper extremity spasticity for up to 3 months 29;30and 1 year 31 duration.
     
  • Investigations carried out by other research groups have reported similar findings 32-36
     
  • Of note: Future studies should be conducted using prospective controlled trials or RCTs that include control or placebo groups to further establish the efficacy of intrathecal baclofen for the management of spasticity.
     
  • Overall, the results from these 10 studies suggest:
  1. bolus injections of intrathecal baclofen produce short-term reductions in upper and lower extremity spasticity post ABI;
     
  2. prolonged intrathecal baclofen reduces upper and lower extremity spasticity post ABI;
     
  3. intrathecal baclofen may cause short-term improvements in walking performance.

     

For further details on the effectiveness of intrathecal baclofen on individuals with an ABI see ERABI/Motor and sensory Impairments Remediation Post Acquired Brain Injury