Spasticity is a common symptom encountered post ABI and is an element of the upper motor neuron syndrome. 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” (Lance 1980). Common features of spasticity include increased muscle tone, exaggerated tendon jerks, and clonus.
Management of spasticity is not unique to brain injury survivors, since it is often associated with other conditions affecting the CNS such as spinal cord injury (SCI) and multiple sclerosis (MS). Spasticity may require intervention when it interferes with functional abilities such as mobility, positioning, hygiene, or when it is the cause of deformity or pain. 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 the locus of injury (Gormley et al. 1997), as well as comorbities. Some studies have found that spasticity of cerebral origin versus SCI respond differently to the same medications (Katz 1993). Typically, the clinical approach to spasticity is to first employ treatments that tend to be less interventional and costly; however, multiple strategies may need to be administered concurrently.
Local nerve blocks may be a potential management solution in circumstances where there is muscle spasticity affecting only a few muscle groups in a focal pattern. Essentially, a nerve block involves the application of a chemical agent to impair nerve functioning. The effect of the chemical agent may be temporary or permanent (Katz & Compagnolo 2000). Temporary acting agents include local anesthetic agents that block sodium ion channels, typically lasting only a few hours. Local anesthetic agents are used for diagnostic procedures or for assistance with activities such as casting (Gracies et al. 1997). Agents used for permanent nerve blocks to treat spasticity include ethyl alcohol (>10%) and phenol (>3%). The duration of effect for these agents is 2 to 36 months. Complications of this type of block have included chronic dysesthesia, pain and permanent peripheral nerve palsies (Gracies et al. 1997).
We identified two studies which evaluated the efficacy of nerve blocks as a treatment for spasticity. Keenan et al. (1990) evaluated the effect of percutaneous phenol block of the musculocutaneous nerve to decrease elbow flexor spasticity. The results indicated that there was improved range of motion of the elbow lasting a mean of five months. In the second study, 11 closed head injury patients with spastic paralysis of the upper extremity were treated with percutaneous phenol injections into the spastic wrist and finger flexors (Garland et al. 1984). The authors reported that relaxation of muscle tone persisted for up to two months following the injections. Furthermore, there was a mean increase in resting wrist angle, active wrist extension, and passive wrist extension with finger flexed of 25, 30, and 5°, respectively (Garland et al. 1984). Evidently, these studies found that percutaneous phenol blocks are effective in temporarily controlling spasticity in patients post TBI.
There is Level 4 evidence that phenol nerve blocks reduce contractures and spasticity at the elbow, wrist and finger flexors for up to 5 months post injection.
Phenol blocks of the musculocutaneous nerve may help decrease spasticity and improve range of motion temporarily up to five months post injection.
Oral Antispasticity Drugs
Oral agents are often used to manage spasticity particularly when a systemic agent to treat upper and lower extremity spasticity is required (Gracies et al. 1997). Although anti-spasticity agents may be used with other medical conditions such as SCI or MS, the effectiveness should not be presumed to be similar for those with brain injury. Multiple medications have been evaluated to treat spasticity of both cerebral and spinal cord origin. The more common medications include GABA agonists that affect ion flux such as baclofen, benzodiazepines, dantrolene sodium, as well as agents that effect α2 adrenal receptors such as tizanidine and clonidine. The use of any of these drugs must be weighed against potential side effects, such as sedation, which are complicated by the cognitive and behavioural changes associated with brain injury.
Meythaler et al. (2004) completed a retrospective study evaluating the use of oral baclofen to manage spasticity in a mixed brain injury and stroke population. Pre and post testing revealed that oral baclofen improved spasticity in the lower extremity assessed using the Ashworth Rigidity Scale (ARS) and Spasm Frequency Scale (SFS); however, no changes for tone, spasm frequency or reflexes were found for the upper extremity (Meythaler et al. 2004). The authors suggest that the lack of effect may be due in part to receptor specificity issues. Of note, a common adverse effect of the oral baclofen was the onset of considerable sleepiness in 17% of patients (Meythaler et al. 2004).
Meythaler et al. (2001) completed a randomized, double blinded placebo controlled cross over trial examining tizanidine for the management of spasticity. This study evaluated both stroke (53%) and TBI (47%) survivors. For both lower and upper extremity, there was a significant decrease in the Ashworth scores on the affected side with the active drug compared to placebo. However, significant differences between treatments were not found for upper and lower extremity spasm and reflex scores. Overall the authors felt that tizanidine was effective in decreasing the spastic hypertonia associated with ABI; however, a common side effect was increased somnolence (41%; Meythaler et al. 2001). Despite the study showing effectiveness, no level of evidence will be assigned for this drug due to more than 50% of the population being stroke.
There is Level 4 evidence that oral baclofen improves lower extremity spasticity but not upper extremity spasticity.
Oral baclofen appears to reduce lower extremity spastic hypertonia.
Oral baclofen did not improve tone, spasm frequency of reflexes in the upper extremity.
Botulinum Toxin Injections
Botulinum toxin type A (BTX-A) acts at pre-synaptic terminals to block acetylcholine released into the neuromuscular junction. When selectively injected into a specific muscle, BTX-A is thought to cause local muscle paralysis, thereby alleviating hypertonia caused by excessive neural activity (Jankovic & Brin 1991). 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 (Gracies et al. 1997).
Five studies examining the effects of BTX-A on spasticity following ABI were identified. Intiso et al. (2014) showed a reduction in spasticity for the upper extremity (elbow, wrist, and hand), as well as ankle joints at one and four months post treatment. Although pain was also significantly reduced, no significant improvements in function were shown, measured by the Glasgow Outcome Scale and the Frenchay Arm Test (Intiso et al. 2014). These findings were similar to those found by Yablon et al. (1996) who reported that BTX-A injections into the upper extremities improved range of motion and spasticity in 21 patients with ABI. These improvements were shown for patients who received the injections within one year of injury and also for those greater than one year post (Yablon et al. 1996). The time between injury and injection was also studied by Clemenzi et al. (2012). The results were similar to the previous study for pain and spasticity; however, the time between onset and injection did have an effect on functional outcomes. Patients with a shorter period of time between their injury and first injection had greater improvements on the Barthel Index (Clemenzi et al. 2012).
For the lower extremity, Fock et al. (2004) reported that BTX-A injections improved measures of walking performance including walking speed, stride length, cadence, dorsiflexion on contact with the ground and passive dorsiflexion. In terms of the administration of BTX-A, Meyer et al. (2008) found that a single motor point injection and multisite distributed injection resulted in similar outcomes, with both groups showing a clinical effect at three weeks post-treatment.
There is Level 2 evidence that botulinum toxin type A injections are effective in the management of localized spasticity following ABI.
There is Level 1b evidence to suggest that patients receiving botulinum toxin type A through a single motor point or through multisite distributed injections both show a reduction in spasticity regardless of the drug administration method.
Botulinum toxin type A injections reduce localized spasticity and improve range of motion following ABI.
Patients receiving botulinum toxin type A through a single motor point or through multisite distributed injections both show a reduction in spasticity.
A limitation of oral baclofen is the inability to achieve sufficient concentrations in the cerebrospinal fluid (CSF) in order to modify spasticity without first causing significant sedation (Gracies et al. 1997). Intrathecal baclofen refers to direct administration of baclofen into the intrathecal space and CSF at the lumbar level. For therapeutic treatment, a subcutaneously placed pump is required to provide continuous administration of the medication into the intrathecal space. This treatment procedure is more invasive and is associated with complications including infection, pump failure and tube complications such as kinking or disconnection (Gracies et al. 1997).
Meythaler et al. (1996) confirmed the effectiveness of intrathecal baclofen in decreasing upper and lower extremity spasticity in a randomized, double blinded, placebo controlled cross-over trial. In subsequent studies, the same investigators went on to demonstrate the effectiveness of intrathecal baclofen for decreasing spasticity for up to three months (Meythaler et al. 1997) and 1 year (Meythaler, Guin-Renfroe, Grabb, et al. 1999). Investigations carried out by other research groups have reported similar findings regarding the efficacy of intrathecal baclofen for the management of spasticity post-ABI (Becker et al. 1997; Dario et al. 2002; Francisco et al. 2005; Hoarau et al. 2012; Posteraro et al. 2013; Stokic et al. 2005). However, a common limitation of these studies is the lack of a control group. Regardless, it appears that intrathecal baclofen is an effective treatment for spasticity; however, some adverse effects such as urinary hesitancy were reported. Hoarau et al. (2012) conducted a 10-year follow up of individuals with dysautonomia and hypertonia treated with intrathecal baclofen therapy. The study found that 62.8% of participants had some type of complication; infections at the operative site was the most frequent complication (20.9%), followed by overdosed with profound flaccidity, sedation, and vomiting (16.3%; Hoarau et al. 2012)
Two studies also evaluated the functional consequences by assessing walking performance, gait speed and range of motion following a bolus injection of intrathecal baclofen (Horn et al. 2010; Horn et al. 2005). Horn et al. (2005) and Horn et al. (2010) found that although the injections produced changes in joint range of motion during gait, only ankles showed a significant result. 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 post ABI.
Based on a single RCT, there is Level 1b evidence that bolus intrathecal baclofen injections produce short-term (up to six hours) reductions in upper and lower extremity spasticity.
There is Level 4 evidence to suggest that prolonged intrathecal baclofen results in longer-term (three months, and one year) reductions in spasticity in both the upper and lower extremities following an ABI.
There is Level 4 evidence, from two studies, to suggest that intrathecal baclofen results in short-term improvements in walking performance, particularly gait velocity, stride length, and step width.
Bolus injections of intrathecal baclofen produce short-term reductions in upper and lower extremity spasticity post ABI.
Prolonged intrathecal baclofen reduces upper and lower extremity spasticity post ABI.
Intrathecal baclofen may cause short-term improvements in walking performance in ambulatory patients post ABI.