There is level 1b evidence from a single study that passive ankle movements may not reduce lower limb muscle spasticity in persons with initial mild spasticity.
There is level 2 evidence from a single study supported by level 4 evidence from another study that hippotherapy may reduce lower limb muscle spasticity immediately following an individual session.
There is level 2 evidence that electrical passive pedaling systems have an effect on spasticity and hip, knee and ankle range of motion.
There is limited level 1b evidence from a single study that a combination of a 6 week course of neural facilitation techniques (Bobath, Rood and Brunnstrom approaches) and Baclofen may reduce lower limb muscle spasticity with a concomitant increase in ADL independence. More research is needed to determine the relative contributions of these therapies.
There is level 4 evidence from a single study that rhythmic, passive movements may result in a short-term reduction in spasticity.
There is level 4 evidence from a single study that externally applied forces or passive muscle stretch as are applied in assisted standing programs may result in short-term reduction in spasticity. This is supported by individual case studies and anecdotal reports from survey-based research.
There is level 2 evidence from a single study that hydrotherapy is effective in producing a short-term reduction in spasticity.
There is level 2 evidence from a single study that single bouts of FES-assisted cycling ergometry and similar passive cycling movements are effective in reducing spasticity over the short-term with FES more effective than passive movement.
There is level 4 evidence from three studies that a program of FES-assisted walking acts to reduce ankle spasticity in the short-term (i.e., £24 hours).
There is no evidence describing the length and time course of the treatment effect related to spasticity for hydrotherapy or FES-assisted walking.
There is level 2 evidence from two prospective controlled trials supported by a single pre-post study that a single treatment of surface muscle stimulation reduces local muscle spasticity with agonist stimulation more effective than stimulation to the antagonist.
There is conflicting evidence for how long the effects of a single treatment of electrical stimulation on muscle spasticity persist, although they appear to be relatively short lasting (i.e., £6 hours).
Based on a single pre-post study, there is no evidence that a long-term program of muscle stimulation has an effect on reducing muscle spasticity and may even increase local muscle spasticity.
There is level 1b evidence from a single RCT and level 4 evidence from a case series that an ongoing program of TENS acts to reduce spasticity as demonstrated by clinical and electrophysiological measures.
There is level 1b evidence from a single RCT that reductions in spasticity with ongoing programs of TENS may persist for up to 24 hours.
There is level 1a evidence from two RCTs that a single treatment of TENS acts to reduce spasticity but to a lesser degree than that seen with ongoing programs of TENS. This evidence is muted somewhat by conflicting results with a null result (level 2) compared with 2 positive results (level 4).
There is level 4 evidence from a single pre-post study that several sessions of rectal probe stimulation reduces lower limb muscle spasticity for up to 8 hours.
There is level 4 evidence from a single pre-post study that short periods of massage (e.g., 3 minutes) of the triceps surae results in reduced H-reflexes with the effect lasting no longer than a few minutes.
There is level 1b evidence from a single RCT supported by a single pre-post study that a single bout of penile vibration acts to reduce spasticity lasting for at least 3 hours and possibly up to 6 hours.
There is level 4 evidence from a single pre-post study that cryotherapy may reduce muscle spasticity for up to 1 hour after removal of the cold stimulus.
There is level 2 evidence from a single low quality RCT that helium-neon irradiation of sensory nerves may suppress ankle clonus for up to 60 minutes following 40 seconds of stimulation.
There is level 4 evidence based on two pre-post studies that ongoing spinal cord stimulation may provide some relief from otherwise intractable spasticity for some time (i.e., months to years).
There is level 4 evidence based on two studies that the beneficial effects of spinal cord stimulation will subside for most initial users. This, combined with the potential for equipment failure and adverse events, suggests that spinal cord stimulation may not be a cost-effective approach for managing spasticity.
There is level 4 evidence based on one study that repetitive transcranial magnetic stimulation may be effective in relieving spasticity.
There is level 2 evidence based on a single low quality RCT supported by a single case series study that dorsal longitudinal T-myelotomy may result in reduced spasticity in those individuals initially refractory to more conservative approaches. These reductions may not always be maintained over the course of several years.
There is level 2 evidence based on a single low quality RCT that Pourpre’s technique for dorsal longitudinal T-myelotomy is more effective in maintaining reduced levels of spasticity than the Bischof II technique.
There is Level 1a evidence that oral Baclofen improves muscle spasticity secondary to SCI. This conclusion is based on the results from four positive small-scale RCTs although is muted somewhat by a negative finding from a low n (5) single-subject design RCT and an overall lack of homogeneity in outcome measures and study participants. Additional uncontrolled cohort and case series studies also provide support for the use of oral Baclofen in reducing spasticity.
There is level 1a evidence from five small-sample RCTs that bolus or test dose intrathecal Baclofen decreases spasticity.
There is level 4 evidence from fifteen studies that support the use of long-term intrathecal Baclofen to decrease spasticity.
There is level 4 evidence from seven studies with some conflicting evidence from 2 studies that intrathecal Baclofen may improve functional outcomes.
There is level 4 evidence from thirteen studies that complication rates with the long-term use of intrathecal Baclofen are relatively low although complications can occasionally be severe.
There is level 4 evidence from two studies that intrathecal Baclofen is a cost-effective intervention.
There is level 4 evidence from one study that adding cyprohetptadine to baclofen and benzodiazepines may be useful for the treatment of intrathecal baclofen withdrawal.
There is level 1b evidence based on a single RCT to support the use of tizanidine for the treatment of SCI spasticity, although it is noteworthy that 34% of subjects who received study treatment and discontinued prematurely due to adverse events, lack of efficacy and other reasons not specified, were not included in the study analysis.
There is limited level 1b evidence based on a single RCT and supported by two prospective controlled trials and several non-controlled studies in favour of using clonidine as a SCI anti-spasmodic although this must be interpreted cautiously given small study sample sizes, inadequate outcome measure selection, occurrence of adverse events (level 2 evidence for sedation) and less than robust study designs.
Limited level 1a evidence based on two RCTs in favour of the anti-spasmodic effects of a sustained-release formulation (Fampridine-SR) of 4-AP is tempered by a negative finding from a single RCT involving IV administration. Study results must be interpreted with caution given that spasticity results were secondary outcomes of the studies. Phase 3 clinical trial results of Fampridine-SR effects on spasticity, as the primary outcome, in chronic SCI are yet to be published.
Limited level 1b evidence supports the use of cyproheptadine in the treatment of spasticity in chronic SCI patients, but results should be interpreted cautiously given the small sample sizes, reliance on non-validated subjective outcome measures and inferiority of cyproheptadine when compared to baclofen.
A single level 4 report supports the use of cyrpoheptadine (along with baclofen and diazepam) as an adjunct treatment of acute intrathecal baclofen withdrawal syndrome.
There is limited level 1b evidence from a single RCT that supports the use of gabapentin in SCI-related spasticity. Despite the robust study design and validated outcome measures, no confidence intervals were reported and the sample size was relatively small.
There is limited level 1b evidence from a single RCT supporting the anti-spastic action of intravenous orphenadrine citrate. Father confirmatory research is needed to support its use.
Very little recent evidence supports current use of diazepam and dantrolene for reducing SCI-related spasticity. An RCT investigating L-threonine for the treatment of SCI spasticity showed only minimal effects on spasticity.
There is limited level 2 evidence based on a compromised RCT and supported by studies of various designs to support the use of oral delta 9 THC (dronabinol) in reducing both objective and subjective measures of spasticity.
Nabilone has been shown to be effective in reducing spasticity but additional research is needed.
Based on 2 case studies and 2 case series, there is level 4 evidence that botulinum neurotoxin improves focal muscle spasticity in SCI. This is cautiously supported by an RCT where only 6/52 subjects had spasticity of confirmed spinal cord origin.
The effect of long-term administration of botulinum neurotoxin is based on the results of a single case study involving 8 treatments over 2 years (level 4 evidence). Tolerance to BTX-A may occur with prolonged administration and requires further study.
Based on 1 case series study there is level 4 evidence that phenol neurolysis improves pain, range of motion and function related to shoulder spasticity in the setting of tetraplegia in SCI.
Based on 1 case series study, there is level 4 evidence that phenol neurolysis reduces hip adductor spasticity in individuals with paraplegia and tetraplegia in SCI.
There is no literature to support the use of focal neurolysis with alcohol in the management of spasticity in spinal cord injury.