4.3 Spasticity Interventions Post ABI
Spasticity is a common symptom encountered post acquired brain injury and is an element of the upper motor neuron syndrome (1997). 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 included increased muscle tone, exaggerated tendon jerks, and clonus.
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. 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 (Gormley, Jr., et al., 1997). Some studies have found that spasticity of cerebral origin versus spinal cord injury respond differently to the same medications (Katz & Campagnolo, 1993). Typically, the clinical approach to spasticity is to first employ treatments that tend to be less interventional and costly. Management of spasticity is not unique to brain injury survivors, since it is often associated with other conditions affecting the central nervous system such as spinal cord injury and multiple sclerosis. However, interventional strategies may differ between diagnoses based on the location of the spasticity (e.g. paraplegia in SCI versus hemiplegia in ABI) and other co-existing morbidities (e.g. cognitive impairment in ABI). Ultimately, multiple strategies may need to be administered concurrently.
4.3.1 Botulinum Toxin Injections
Botulinum toxin type A (BTX-A) acts at pre-synaptic terminals to block acetylcholine release into the neuromuscular junction. When selectively injected into a specific muscle, BTX-A is thought to cause local muscle paralysis thereby alleviating hypertonia due to excessive neural activity (Jankovic & Brin, 1991). BTX-A is a relatively new treatment strategy for the management of spasticity in ABI. Its 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).
Individual Studies
Table 4.7 Effect of Botulinum Toxin on Spasticity post-ABI
| Author/Year/ Country/Study design/ PEDro and D&B Score |
Methods |
Outcome |
|
Ashford and Turner-Stokes (2009) |
N=16 Study participants were given botulinum toxin type A (BoNT-A/BTX-A) injection along with various therapies to treat spasticity of the shoulder girdle or proximal upper limb. Concurrent therapy included splinting, serial casting, exercise programs, functional electric stimulation, arm supports and patient/career education. |
16 weeks post injection, significant improvements were identified in spasticity (Z=-3.535, p<0.0001), pain (Z=-1.942, 0=0.052) and passive function (Z=-3.172, p=0.002). GAS scores improved in all but one subject, with goals either achieved or over-achieved. |
|
Mayer et al., (2008) |
N=36 Patients were randomly assigned to one of two treatments (the motor point injection technique, or the distributed quadrants technique). Following baseline measures, each elbow was randomized to receive injections of Botox. In total 90 units were given to each group; however the sites and injection techniques varied between the groups. Measures used to assess improvement were: the Ashworth scale, and the Tardieu Catch Angle. |
Overall no significant differences were noted between the 2 groups on any of the outcome measures used to assess improvement; however each group showed significant improvement from baseline (p<0.001) on all outcome measures. |
|
van Rhijn et al., (2005) |
N=21 Pediatric patients (2 yrs 7 months – 19 yrs 8 months) were divided into 3 groups according to impairment severity and treatment objectives. Group 1 (spastic quadriparesis patients with impaired consciousness treated with the primary goal of improving comfort and well-being) received bilateral BTX-A injections with specific targeted muscles of the hip abductors, knee and plantar flexors. Group 2 (upper limb spasticity and normal consciousness treated with primary goal of improving arm functioning) received unilateral BTX-A injections into the elbow, finger and wrist flexors and/or shoulder muscles. Group 3 (lower limb spasticity patients with normal consciousness treated with the primary goal of improving leg function) received BTX-A injections uni or bilaterally to plantar, knee and hip flexors and/or hip adductors. Immediately after injections, all patients received either a cast or an orthosis, intensive physiotherapy, ergotherapy, and functional exercises (Groups 2 and 3 only). |
Baseline, 1, 3 and 5-month pos-treatment assessments were done using joint goniometry, Modified Ashworth Scale (MAS) and video observations. All 3 groups showed improvements in MAS at 1 and 3 months post-treatment, with patients in group 2 showing the greatest overall benefit and a continued improvement seen at 5 months post-treatment. In group 3, patients received most benefit at 3 months post-injection. All groups showed improvements in range of motion, with greatest improvement seen in group 2 who showed a consistent improvement at 1, 3 and 5 months. |
|
Fock et al.,
(2004) |
N=7 TBI subjects received botulinum toxin A (BTX-A) into the lower extremities. Muscles targeted for injections included the gastrocnemius and soleus. The tibialis posterior was also injected in some subjects. Modified Ashworth Scale (MAS) scores, walking speed, cadence, stride length and peak ankle dorsiflexion angle during walking over a 10m level track, passive and active range of movement of the affected ankle using a goniometer were assessed before and at 2 and 12 weeks post-injection. |
12 weeks post-injection, there were significant improvements in walking speed, stride length, cadence, dorsiflexion on contact with the ground and passive dorsiflexion in supine position (all p values < 0.03). None of these measures showed significant changes at 2 weeks post-injection. There were no significant changes in dorsiflexion at mid-stance, active dorsiflexion in supine position, and MAS scores at 2 or 12 weeks post-injection. |
|
Francisco et al., (2002) |
N=15 Subjects received either eight volume doses of BTX-A or low volume doses of BTX-A. Those in the high volume group received 1.2 ml of BTX-A per muscle compared those in the low-volume group who received 0.6ml per muscle. Assessments were made at 4, 8 and 12 weeks post injections. Measures used to assess improvement were the Modified Ashworth Scale (MAS) and the Global Rating Scale. |
Over all it was noted that spasticity was reduced in both groups, but there were no significant differences between the groups. Results of the MAS indicate that within each group there were statistically significant differences noted from baseline to each of the 3 post interjection periods. Results from the Global Rating Scale indicate that the scores on the measures dropped at each assessment period post-baseline. Differences in the scores were not found to be significant. |
|
Yablon et al., (1996) |
N=21 severe (GCS score ≤ 8) TBI Subjects received botulinum toxin A (BTX-A) injections (20-40 units per muscle) into the upper extremity. Muscles targeted for injections were the flexor carpi radialis, flexor carpi ulnaris, flexor digitorum profundus, and flexor digitorum superficialis. Flexor pollicis longus was treated if thumb flexor tone was prominent. Some patients also received injections into the biceps and brachialis due to coexisting spasticity in the elbow flexors. Total dose was determined by spasticity severity and the number of muscles treated. After injection, patients received ROM therapy, therapeutic modalities, and splinting and casting as clinically indicated. Outcomes included the modified Ashworth Scale (MAS) and passive ROM at the wrist with full finger extension as measured by goniometry. Outcomes were assessed before and 2-4 weeks after injection. |
Subjects who were injected within 12 months from injury onset (acute group) showed significant improvements in ROM and spasticity severity, specifically, significant improvements in wrist extension (p = 0.001), and MAS scores (p = 0.001). All patients in the acute group showed an improvement in spasticity and no patient worsened or remained unchanged. Patients who were injected > 12 months from injury onset (chronic group) showed significant improvements in wrist extension (p < 0.001), and MAS scores (p = 0.002). All patients in the chronic group showed an improvement in spasticity, but one patient with pre-existing contracture did not improve or worsen. |
PEDro = Physiotherapy Evidence Database rating scale score (Moseley et al 2002).
D&B = Downs and Black (1998) quality assessment scale score.
Discussion
Six studies examining the effects of botulinum toxin on spasticity following ABI were identified. Ashford and Turner-Stokes (2009) found for patients given BTX-A over a 16 week period, spasticity, passive function and pain improved significantly. For some, improvements were noted within the first 2 to 4 weeks of BTX-A being administered. Yablon et al. (1996) reported 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. (2004) reported that 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, there were no significant improvements in overall a spasticity as measured by MAS scores. In the last study conducted in a pediatric cohort, van Rhijn et al. (2005) reported that BTX-A was effective in improving MAS scores up to 5 months post-treatment with concomitant improvements in range of motion.
In the remaining two RCTs, Francisco et al. (2002) and Mayer et al. (2008) found that although botulinum toxin was effective in reducing the level of spasticity, there were no differences based on the amount of botox given.
Conclusion
There is Level 2 evidence based on one cohort study and Level 4 evidence from 3 studies that botulinum toxin type A injections may be effective in the management of localized spasticity following ABI.
One RCT found that both groups of patients receiving botulinum toxin type A injections did show reduced spasticity, regardless of the method of drug administration.
|
Botulinum toxin type A injections reduces localized spasticity following ABI.
|
4.3.2 Nerve Block
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 et al., 2000). Temporary acting agents include local anesthetic agents that block sodium ion channels with a typical duration of only a few hours. Typically, 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 from 2 to 36 months. Complications of this type of block have included chronic dysesthesia and pain and permanent peripheral nerve palsies (Gracies et al., 1997).
Individual Studies
Table 4.8 Effect of Percutaneous Phenol Block to Reduce Spasticity
| Author/ Year/ Country/ Study design/ D&B Score |
Methods |
Outcome |
|
Garland et al. (1984) |
N=11 closed head injury subjects received percutaneous phenol injections (1-2 ml of 3 or 5% phenol solution) at motor points of spastic wrist and finger flexors identified using a nerve stimulator. Injected muscles were the flexor carpi radialis, flexor carpi ulnaris, flexor digitorum sublimus, flexor digitorum profundus, and flexor pollicis longus. Flexor spasticity was assessed objectively by measuring wrist position in four situations: 1) resting angle of the wrist with elbow flexed to 90 degrees, 2) passive extension of the wrist with the fingers flexed, 3) passive extension of the wrist with the fingers extended, and 4) active extension of the wrist with the elbow flexed 90 degrees. Measures were repeated one week, and then monthly for 3 months following phenol block injections. |
Relaxation of muscle tone persisted for up to two months following the injections. Overall, there was a mean increase in resting wrist angle following motor point injections of 25º. Active wrist extension improved an average of 30º. Mean increase in passive wrist extension with finger flexed of 5º. |
|
Keenan et al. (1990) |
N=17 TBI Subjects (mean age 25 years) received a phenol block (3ml of 5% phenol solution in sterile saline; mean interval 6 months) followed by daily program of active/passive range of motion therapy if experiencing moderate to severe flexor spasticity causing fixed or dynamic flexion elbow deformity, decreased upper extremity function (secondary) and an inability to maintain elbow range of motion using standard PT in any patient still experiencing a spontaneous neurologic recovery. Muscle tone, control and ROM measured pre/post block, 24 hr, then weekly intervals while hospitalized for rehabilitation. Post discharge monthly evaluations until PB effects ended, then followed up for continuing rehabilitation for a minimum of 2 years. |
93% showed a short term decrease in motor tone and improved resting position. Maximum improvements occurred 4 weeks post block. Resting position improved to 69 degrees; Active arc increased to 60 degrees; Passive arc to 118 degrees. Mean block duration was 5 months. |
D&B = Downs and Black (1998) quality assessment scale score.
Discussion
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 5 months on average. 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 5º respectively (Garland et al., 1984).
Conclusion
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 musculoskeletal nerve may help decrease spasticity and improve range of motion temporarily up to 5 months post injection.
|
4.3.3 Electrical Stimulation
Electrical stimulation uses electrical current to directly stimulate skeletal muscle causing contraction (Gregory & Bickel, 2005) or indirectly through electrical stimulation of the nerve supplying that muscle. Electrical stimulation has seen some applications with regards to assisting paraplegic patients with standing and walking (Katz et al., 2000). Reports from spinal cord injured populations, suggest that electrical stimulation can be related to significant reductions in spasticity for up to 24 hours post stimulation (Halstead et al., 1993).
Individual Studies
Table 4.9 Effect of Electrical Stimulation in Reducing Spasticity
| Author/ Year/ Country/ Study design/ D&B Score |
Methods |
Outcome |
|
Seib et al. (1994) |
N=10 5 TBI and 5 SCI patients with a passive ROM of 5 degrees with at least 2.5 degrees of dorsiflexion received 20 minutes of Surface Electrical Stimulation to the ipsilateral (the more spastic side) tibialis anterior or sham stimulation. Parameters: 2 sec rise time, 15 sec on, instant fall, 20 sec off. Rate of stimulation was 30 pulses per second. Intensity varied on subject tolerance. |
Significant ipsilateral effects reduced in 9 subjects following simulation (p<0.05). SCI subjects experienced a decrease in path length vs TBI subjects (p<0.05). Sham stimulation produced no statically significant changes in path length. 24 hours after stimulation, ipsilateral path length (spasticity) reduced significantly in 8 of 9 subjects (p< 0.01). Path length decreased significantly in TBI subgroup. Sham therapy effect was significant in the SCI subgroups. No significant change in path length immediately or 24 hours after stimulation / sham therapy. |
D&B = Downs and Black (1998) quality assessment scale score.
Discussion
One study, Seib et al. (1994), was identified which examined the effects of electrical stimulation applied to the lower extremity in traumatic brain injury and spinal cord injury survivors. In this baseline comparison study, the investigators were able to demonstrate that electrical stimulation significantly decreases spasticity in the stimulated extremity whereas the tone in the non-stimulated contralateral extremity does not change. The effect of one stimulation session can last up to 24 hours.
Conclusion
There is Level 4 evidence that electrical stimulation is effective for decreasing lower extremity spasticity for up to 24 hours.
|
Electrical stimulation decreases spasticity for up to 24 hours.
|
4.3.4 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 spinal cord injury or multiple sclerosis (Gracies et al., 1997), the effectiveness should not be presumed to be similar for brain injury survivors. Multiple medications have been evaluated to treat spasticity of both cerebral and spinal cord origin. The more common medications include GABA agonists such as baclofen, benzodiazepines, dantrolene sodium which affects ion flux, and agents that affect alpha-2 adreno receptors such as tizanidine and clonidine. One particular limitation is the associated cognitive and behavioral changes associated with brain injury.
Individual Studies
Table 4.10 Effect of Oral Anti-Spasticity Agents
| Author/Year/ Country/Study design/ PEDro and D&B Score |
Methods |
Outcome |
|
Meythaler et al., (2001) |
N=17 TBI and stroke subjects between 16 and 75 diagnosed with severe chronic spastic hypertonia in at least 1 lower extremity for at least 6 months that has not responded to therapy were given either 4 mg of tizanidine or a placebo, gradually increased to 36 mg after 6 weeks. Patients tapered off over one week, then crossed over to the other study. Ashworth Rigidity Scores (ARS), Penn Spasm Frequency Scale (PSFS), ROM, Spasm Scores, motor component of the FIM, Deep Tendon Reflex, CHART and Motor Strength scores taken pre and post treatment. |
Maximum tolerated dose achieved at 4 weeks. L.E./U.E. ARS (affected side) and Spasm Scores decreased (p = .0883 /p<.001). No significant changes were found in the, UE spasm and the DTR scores. Medication significantly decreased LE tone (p=.0006) and UE tone (p=.007) compared to placebo. This increased motor strength (p=.0089). |
|
Meythaler et al., (2004) |
N=35 consecutive ABI sibjects (including 22 TBI patients) referred to a spasticity clinic for spastic hypertonia (min. chronicity = 6 months) were placed on an oral baclofen regimen starting at 5 mg tid. Dosage determined by caregiver up to 80 mg after which clinic approval was required. Ashworth Rigidity Scale (ARS), Spasm Frequency Scale (SFS), and deep tendon reflexes (DTR) were taken before treatment, and between 1 and 4 months after treatment was initiated. |
Average dose at follow up was 57 ± 26 mg/day. TBI patients mean dose was 55 ± 28 mg/day. Lower extremity ARS and DTR decreased significantly (p=.0003 & p=.0274). No significant change in spasm score (p>.05). TBI patients saw ARS and DTR significantly decreased (p=.0044 & p=.0003) and no significant change in spasm score (p>.05). Upper extremities showed no significant changes ARS, SFS, DTR (p>.05). |
PEDro = Physiotherapy Evidence Database rating scale score (Moseley et al 2002).
D&B = Downs and Black (1998) quality assessment scale score.
Discussion
Oral Baclofen
Meythaler et al. (2004) completed a retrospective study evaluating the use of oral baclofen to manage spasticity in brain injury survivors. Pre and post testing of spasticity using the Ashworth scale revealed a significant decrease in lower extremity spasticity scores, however, results were not significant for upper extremity spasticity scores or frequency of spasms. A noted common adverse effect of the oral baclofen was the onset of considerable sleepiness in 6 (17%) patients.
Oral Tizanidine
In a separate study Meythaler et al. (2001) completed a randomized, double blinded placebo controlled cross over trial of Tizanidine in the management of spasticity in acquired brain injury. This study evaluated both stroke (53%) and traumatic brain injury (47%) survivors. For both lower and upper extremity, there was a significant decrease in spasticity scores compared to treatment with placebo. However, upper and lower extremity spasm and reflex scores did not improve compared to placebo. A common adverse effect was increased somnolence (41%) compared to placebo (0%).
Conclusions
Based on a single RCT, there is Level 1 evidence that oral tizanidine improves lower and upper extremity spasticity compared to a placebo.
There is Level 4 evidence that oral baclofen improves lower extremity spasticity but not upper extremity spasticity.
|
Oral tizanidine is effective for improving upper and lower extremity spasticity.
Oral baclofen appears to improve lower extremity spasticity.
|
4.3.5 Intrathecal Baclofen
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 (Gracies et al., 1997). 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. 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).
We identified ten studies which investigated the efficacy of intrathecal baclofen for the management of upper and lower extremity spasticity following ABI (Meythaler et al., 1999; Meythaler et al., 1997; Meythaler et al.,1996; Becker et al., 1997; Horn et al., 2005; Stokic et al., 2005; Dario et al., 2002; Francisco et al., 2005; Francisco et al., 2002).
Individual Studies
Table 4.11 Effects of Intrathecal Baclofen in Modifying Spasticity
| Author/ Year/ Country/ Study design/ PEDro and D&B Score |
Methods |
Outcome |
|
Meythaler et al., (1996) |
N=11 ABI (9 MVA, 1 gunshot wound, 1 anoxia) patients suffering from spastic hypertonia unresponsive to oral antispastic medications were randomly assigned to receive a bolus injection of intrathecal baclofen (50 ug) or placebo (normal saline). In a cross over fashion, patients received the other treatment (drug or placebo) at least 48 hours after the administration of the first agent. Ashworth Scale, Spasm Score, and deep tendon reflexes were collected at 1, 2, 4, and 6 hours post-injection by a blind investigator. |
No significant differences between groups in any of the measures at baseline. Significant reduction following baclofen treatment in both lower and upper extremity Ashworth scores (p=0.0032, p =0.0033), Spasm scores (p=0.0033,p=0.0070), and Deep Tendon Reflex scores (p=0.0033, p=0.011). Maximum reduction for all measures occurred 4 hours post-treatment. |
|
Horn et al., (2005) |
N=28 ABI subjects received a single 50-µg intrathecal baclofen bolus injection. Walking Performance, and Ashworth scores to measure lower-extremity spasticity were assessed before and 2, 4 and 6 hours after intrathecal baclofen bolus injection. |
Significant improvements in gait velocity (p<0.001), stride length (p<0.05), and step width (p<0.001). Significant reductions in Ashworth scores at 2, 4 and 6 hours post-injection (p<0.001). |
|
Dario et al., (2002) |
N=14 ABI patients (6 TBI and 8 anoxic ABI) with severe progressive spasticity refractory to medical therapy involving the whole body and interfering with daily care or function received continuous intrathecal baclofen infusions. Outcomes assessed before pump implantation and at last follow-up (mean follow up of 23.5 months, range 6-65 months). Ashworth Scale (AS) for lower and upper extremities, Spasm Frequency Scale (SFS) for lower and upper extremities. |
At last follow up, there was a significant decrease in AS score in both lower and upper extremities (both p<0.05). Significant reduction in SFS scores (p<0.001). Mean daily dose of baclofen was 305 µg (range 90-510 µg). |
|
Becker et al., (1997) |
N=18 Severe ABI patients (9 TBI and 9 hypoxic brain injury) received continuous intrathecal baclofen infusion. Ashworth Scale and Spasm Frequency Scale scores were measured at admission and at discharge. |
In all patients, spasticity was reduced significantly. Mean Ashworth score was reduced from 4.5 to 2.33 and the mean Spasm Frequency score from 2.16 to 0.94. Reduction in spasticity lead to a reduction in pain. |
|
Meythaler et al., (1997) |
N=12 ABI subjects (9 TBI and 3 anoxic) who showed a reduction in muscle tone of at least 2 points on the Ashworth scale or a reduction in the number of spasm following a screening trial using a bolus injection on intrathecal baclofen were surgically fitted with an infusion pump for continuous intrathecal baclofen delivery for 3 months. Outcomes included Ashworth Rigidity Scale scores, Spasm Frequency scores, and Deep Tendon Reflex Scores. |
For both the lower and upper extremities Ashworth scores, spasm frequency and reflex scores significantly decreased after 3 months of treatment (all p<0.05). |
|
Meythaler et al.,(1999) |
N=17 Consecutive ABI patients diagnosed with severe, chronic, lower extremity spasticity and dystonic hypertonia that proved unresponsive to treatment with oral antispasticity medications were surgically fitted with a programmable infusion pump into the lower abdominal wall for continuous administration of baclofen using the same methodology as Meythaler et al. (1997) with the exception that patients received continuous intrathecal baclofen for 1 year. Ashworth Rigidity Scale scores, Spasm Frequency Scale scores, Deep Tendon Reflex scores were assessed at 1, 3, 6, 9 and 12 months. |
1 year of intrathecal baclofen treatment (average dose: 302 ug/day) resulted in a decrease of Ashworth, spasm, and reflex scores in both upper and lower extremities (p<.0001). No cognitive side effects observed after 1 year. |
|
Meythaler et al., (1999) |
N=6 ABI subjects recruited consecutively, with long-standing hemiplegia unresponsive to oral treatments were surgically fitted with a programmable infusion pump into the lower abdominal wall for continuous administration of baclofen using the same methodology as Meythaler et al. (1997). Ashworth Rigidity Scale, Spasm Frequency Scale, Deep Tendon Reflex scores were assessed before and after 3 months of treatment. |
Average baclofen dose at 3 months was 205.3 ± 148 µg/day. Lower extremities showed a significant reduction in Ashworth scores (p<0.0001); affected lower limb reflex score (p=0.0208); normal side (p=0.0051), but not significant changes in affected lower limb spasm score (p=0.5). Upper extremities showed significant reductions in Ashworth scores on affected side (p=0.0002) but were not significant for Biceps Reflex score (affected and normal: p=0.1088 and p=0.0679), or spasm score (affected: p=0.1797). No patient complained of subjective weakness on the normal side. |
|
Stokic et al., (2005) |
N=30 Head injury patients (17 ABI, 4 anoxia, and 9 stroke) received a single 50-µg intrathecal baclofen bolus injection. Ashwroth Scale scored were assessed before, 2, 4, and 6 hours post-injection. H-Reflex from soleus muscle and F waves from abductor hallucis in supine position assessed before and 4 hours post-injection. |
Ashworth score on the more involved side significantly decreased at 4 and 6 hours post-injection (p<0.001) H/M ratio significantly decreased bilaterally (p<0.001). F-wave persistence significantly decreased on the more involved side (p<0.05) with no change in F/M ratio. |
|
Francisco et al., (2005) |
N=14 head injury subjects (6 anoxic encephalopathy, 5 TBI and 3 stroke) who had suffered their injuries no more than 1 years before and who experienced spastic hypertonia unresponsive to other treatment modalities including oral spasmolytics, botulinum toxin, phenol neurolysis and physical therapy were involved in this study. Patients who showed a reduction of at least 1 point on the Modified Ashworth Scale (MAS) or any functional improvement 4 hours following a screening trial using a bolus injection of intrathecal baclofen were surgically fitted with an infusion pump for continuous intrathecal baclofen delivery. . |
Lower and upper extremities MAS scores and Disability Rating Scale (DRS) scores were assessed at baseline and follow up. Period of pump implantation was on average 5.62 months (range 2-12 months) from disease onset. Follow up of participants occurred at a mean of 13.9 months post pump implantation. Significant reductions from baseline to follow up in upper (p<0.001) and lower (p<0.02) extremity MAS scores. Non-significant improvement in DRS scores (p=0.75) |
|
Francois et al., (2001) |
N=4 The use of intrathecal baclofen infusion for the reduction of spasticity was investigated in a collection of case studies of patients with severe ABI (GCS ≤ 4). Treatment was started within 1 month following injury onset. Outcomes included Ashworth scores, frequency and intensity of autonomic disorders. |
Reductions in spasticity, and lower limb Ashworth scores at 6 months post-treatment were reported in three of the four cases. In the last case, a substantial reduction in autonomic disorders and spasticity enabling passive physiotherapy was reported. |
PEDro = Physiotherapy Evidence Database rating scale score (Moseley et al. 2002).
D&B = Downs and Black (1998) quality assessment scale score.
Discussion
In the first study Meythaler et al. (1996), the investigators confirmed the effectiveness of intrathecal baclofen to decrease upper and lower extremity spasiticity 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 upper extremity spasticity for up to 3 months (Meythaler et al., 1996; Meythaler et al., 1997); and 1 year (Meythaler et al., 1999) duration. However, all of these studies used a single group intervention design lacking a placebo control group during the phase when the subcutaneously placed pump was used to provide continuous administration of the medication into the intrathecal space.
Investigations carried out by other research groups have reported similar findings regarding the efficacy of intrathecal baclofen for the management of spasticity post-ABI (Stokic et al., 2005; Becker et al., 1997; Dario et al., 2002; Francisco et al., 2005; Francisco et al., 2002). However, these studies still lacked a control group thereby limiting the conclusions of their findings.
For a total of 154 participants in the nine studies identified by this review, it appears that intrathecal baclofen is an effective treatment for spasticity, however some adverse effects such as urinary hesitancy were reported. Only two of the nine studies examined the long-term effectiveness of the treatment. One study also evaluated the functional consequences by assessing walking performance following a bolus injection of intrathecal baclofen (Horn et al., 2005).
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.
Conclusions
Based on a single RCT, there is Level 1 evidence that bolus intrathecal baclofen injections produce short-term (up to 6 hours) reductions in upper and lower extremity spasticity.
There is Level 4 evidence to suggest that prolonged intrathecal baclofen results in longer-term (3 months, and 1 year) reductions in spasticity in both the upper and lower extremities following an ABI.
Based on a single study, there is Level 4 evidence 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.
|