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Non-Pharmacological Interventions for Spasticity/Passive Stretching

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.

Robot-Assisted

There is level 1b evidence from two RCTs (Fang et al. 2015; Mirbagheri et al. 2015) robot-assisted exercise appears to decrease all components of spasticity (isometric torque, reflex and intrinsic stiffness).

Functional Electrical Stimulation

There is level 2 evidence from 2 studies, also supported by level 4 evidence, that single bouts of FES-assisted cycling ergometry, with a single level 2 study also showing that similar passive cycling movements are effective in reducing spasticity over the short-term although FES is more effective than passive movement.

There is level 1 evidence from 1 study, with conflicting evidence across two level 4 evidence studies, that show FES cycling decreases spasticity over the long-term.

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), however, a level 2 study showed no reduction across several lower limb muscles when considering an overall sustained effect.           

There is no evidence to describe the optimal length and time course of FES-assisted walking for reducing spasticity.

Effects of Standing

There is level 2 evidence (from one prospective controlled trial; Sadeghi et al. 2016) that dynamic and static standing training does not reduce spasticity.

Body Weight Support Treadmill Training versus Tilt Table Standing

There is level 2 evidence (from one RCT; Manella & Field-Fote 2013) that electrical stimulation treadmill training and LOKOMAT robotic-assisted training decreases ankle clonus.

There is level 4 evidence (from one pre-post study; Adams et al. 2011) that use of tilt-table standing decreases extensor spasms and body-weight support treadmill training results in a reduction in passive resistance to movement and flexor spasms.

Dynamic Standing

There was level 4 evidence (from one pre-post study; Boutilier et al. 2012) that showed use of a Segway device for dynamic standing results in a reduction of spasticity.

Exoskeleton

There is conflicting level 4 evidence (from two case series; Kressler et al. 2014; Del-Ama et al. 2014) that use of an exoskeleton walking device results in a reduction in spasticity.

Upper Limb

There is level 4 evidence (from one pre-post study; Cortes et al. 2013) that use of robotic training of the wrist does not improve upper limb spasticity.

Hydrotherapy

There is level 4 evidence (from one pre-post study; Kesiktas et al. 2004) that hydrotherapy is not more effective in producing a short-term reduction in spasticity than conventional rehabilitation alone.

Direct Muscle Electrical Stimulation

There is level 2 evidence (from two prospective controlled trials and one pre-post study; Van der Salm et al. 2006; Seih et al. 1994; Robinson et al. 1988a) 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).

There is level 4 evidence (from one pre-post study; Robinson et al. 1988b) that a long-term program of muscle stimulation does not reduce muscle spasticity and may even increase local muscle spasticity.

There is conflicting level 4 evidence (from two pre-post studies; Cart et al. 2013; Tancredo et al. 2013) that use of neuromuscular electrical stimulation decreases spasticity.

Taping

There is level 1b evidence (from one RCT; Tamburella et al. 2014) that kinesio tape has short-term effects of decreasing spasticity and improving balance and gait in individuals with chronic SCI.

TENS

There is level 1a evidence (from three RCTs; Oo 2014; Chung & Cheng 2010; Aydin et al. 2005) that an ongoing program of TENS acts to reduce spasticity as demonstrated by various clinical and electrophysiological measures.

There is level 1b evidence (from a single RCT; Aydin et al. 2005) that reductions in spasticity with ongoing programs of TENS may persist for up to 24 hours.

There is level 1a evidence (from two RCTs; Oo 2014; Aydin et al. 2005) that a single treatment of TENS acts to reduce spasticity but to a lesser degree than that seen with ongoing programs of TENS.

Penile Vibratory Stimulation

There is level 1b evidence (from one RCT and one pre-post study; Laessoe et al. 2004; Alace et al. 2005) 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.

Helium-Neon Irradiation

There is level 2 evidence (from one RCT; Walker 1985) that helium-neon irradiation of sensory nerves may suppress ankle clonus for up to 60 minutes following 40 seconds of stimulation.

Electrical Nerve Stimulation

There is level 4 evidence (from one pre-post study; Halstead et al. 1993) that several sessions of rectal probe stimulation reduces lower limb muscle spasticity for up to 8 hours.

There is level 4 evidence (from one pre-post study; Van der Salm et al. 2006) that electrical stimulation of the triceps surae does not significantly reduce spasticity.

Vibration

There is level 5 evidence (from one observational study; Ness & Field-Fote 2009) that whole body vibration results in reduced quadriceps spasticity over the short term.

There is level 4 evidence (from one pre-post study; Murillo et al. 2011) that vibration over the rectus femoris muscle results in reduced knee spasticity and increased knee range of motion.

Massage

There is level 4 evidence (from one pre-post study; Goldberg et al. 1994) 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.

Cryotherapy

There is level 4 evidence (from one pre-post study; Price et al. 1993) that cryotherapy may reduce muscle spasticity for up to 1 hour after removal of the cold stimulus.

Extracorporal Shock Wave Therapy

There is level 4 evidence (from one pre-post study; Altindag & Gursoy 2014) that three sessions of extracorporal shock wave therapy may reduce muscle tone over the short term.

Direct Spinal Cord Stimulation

There is level 4 evidence (from three pre-post studies and one case series; Hofstoetter et al. 2014; Pinter et al. 2000; Barolat et al. 1995; Dekopov et al. 2015) that ongoing spinal cord stimulation may provide some relief from otherwise intractable spasticity.

There is level 4 evidence (from one pre-post study and one case series; Hofstoetter et al. 2014; Midha & Schmitt 1998) that the beneficial effects of spinal cord stimulation may subside for most initial users over a short period of time. This, combined with the potential for equipment failure and adverse events, suggests that spinal cord stimulation may not be a feasible approach for ongoing management of spasticity.

Repetitive Transcranial Magnetic Stimulation 

There is level 1a evidence (from two RCTs and one case control; Nardone et al. 2014; Benito et al. 2012; Kumru et al. 2010) that rTMS decreases spasticity and improves walking speed.

Neurosurgical Intervention

There is level 2 evidence (from one RCT and one case series; Livshits et al. 2002; Putty & Shapiro 1991) 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.

T There is level 2 evidence (from one RCT; Livshits et al. 2002) that Pourpre’s technique for dorsal longitudinal T-myelotomy is more effective in maintaining reduced levels of spasticity than the Bischof II technique.

Oral Baclofen

There is Level 1a evidence that oral baclofen improves muscle spasticity secondary to SCI. This conclusion is based on the results from five positive small-scale RCTs (Chu et al. 2014; Nance et al. 2011; Aydin et al. 2005; Duncan et al. 1976; Burke et al. 1971) although is minimally muted by a single negative finding from one small RCT (Hinderer et al. 1990) with an overall lack of homogeneity in outcome measures and study participants. Additional evidence from a prospective controlled trial (Dicpinigaitis et al. 2000), a cohort (Veerakumar et al. 2015) and pre-post study (Nance 1994) also provide support for the use of oral baclofen in reducing spasticity.

Intrathecal Baclofen

There is level 1a evidence (from six small-sample RCTs; Ordia et al. 1996; Nance et al. 1995; Coffey et al. 1993; Hugenholtz et al. 1992; Loubster et al. 1991; Penn et al. 1989) that bolus or test dose intrathecal baclofen decreases spasticity.

There is level 4 evidence (from several studies; see Table 13) that support the use of long-term intrathecal baclofen to decrease spasticity.

There is conflicting level 4 evidence (from several studies; see Table 15) that intrathecal baclofen may improve functional outcomes.

There is level 1b evidence (from two RCTs; Ordia et al. 1996; Nance et al. 1995) that intrathecal baclofen is a cost-effective intervention for treating post SCI spasticity.

There is level 4 evidence (from several studies; see Table 13) 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 one case series; Meythaler et al. 2003) that adding cyprohetptadine to baclofen and benzodiazepines may be useful for the treatment of intrathecal baclofen withdrawal.

Tizanidine

There is level 1a evidence (from two RCTs and one prospective controlled trial; Chu et al. 2014; Nance et al. 1994; Mirbagheri et al. 2013b) to support the use of tizanidine in reducing spasticity.

Clonidine

There is level 1b evidence (from one RCT, two prospective controlled trials; Stewart et al. 1991; Malinovsky et al. 2003; Remy-Neris et al. 1999) supported by 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 and less than robust study designs.

Fampridine (4-Aminopyridine)

There is level 1a evidence (from two large-scale RCTs; Cardenas et al. 2014; Cardenas et al. 2007) that indicate no significant anti-spasmodic effects of Fampridine-SR compared to placebo; however, this is tempered by positive findings from level 1b evidence (from one small RCT and one pre-post study; Potter et al. 1998a; Potter et al. 1998b) on the beneficial anti-spasmodic effects of Fampridine-SR. Study results must be interpreted with caution given that spasticity results were secondary outcomes of all studies except the phase 3 clinical trial results from Cardenas et al. (2007).

There is conflicting level 1b evidence (from one RCT and one pre-post study; Donovan et al. 2000; Hayes et al. 1994) that intravenous administration of Fampridine has no significant anti-spasmodic effect. Study results must be interpreted with caution given that spasticity results were secondary outcomes of the studies.  

Cyproheptadine

There is level 1b evidence (from one RCT and one pre-post study; Thompson et al. 2013; Nance et al. 1994) that supports the use of cyproheptadine in the treatment of spasticity in patients with chronic SCI.

There is level 4 evidence (from one case series; Meythaler et al. 2003) supporting the use of cyproheptadine (along with baclofen and diazepam) as an adjunct treatment of acute intrathecal baclofen withdrawal syndrome.

Gabapentin

There is level 1b evidence (from one RCT; Gruenthal et al. 1997) that supports the use of gabapentin for SCI-related spasticity. Despite the robust study design and validated outcome measures, no confidence intervals were reported and the sample size was relatively small.

Other Anti-Spasmodics

There is level 1b evidence (from one RCT; Liu et al. 2014) that traditional Chinese medicine is a safe, effective and economical long-term treatment for spasticity in SCI.

There is level 2 evidence (from one prospective controlled trial; Casale et al. 1995) for short-term use of intravenous orphenadrine citrate for treatment of spasticity secondary to SCI.

There is level 1b evidence (from one RCT; Theiss et al. 2011) that riluzole is effective in treating spasticity post SCI.

There is level 1b evidence (from one RCT; Lee & Patternson 1993) that L-threonine produces minimal anti-spasmodic effects post SCI.

There is level 4 evidence (from one pre-post study; Brackett et al. 2007) that naloxone causes a profound increase in spasticity in individuals with SCI.

There is level 1b evidence (from one RCT; Finnerup et al. 2009) that Levitiracetam is not effective for treating spasm severity in SCI.

Continued use of diazepam and dantrolene for reducing SCI-related spasticity is not supported with up to date evidence and would benefit from new controlled comparison studies. Whether effective or not, replicating results in well-designed trials is warranted before alternative recommendations for new or older treatments will be accepted into current practice.

Cannabinoids

There is level 1b evidence (from one RCT; Pooyania et al. 2010) that nabilone is effective in reducing spasticity in both the involved and overall muscles.

There is level 2 evidence (from one compromised RCT; Hagenbach et al. 2007 and supported by one pre-post study; Kogel et al. 1995) to support the use of oral delta-9-tetrahydrocannabinol (dronabinol) in reducing both objective and subjective measures of spasticity.

Botulinum neurotoxin

There is level 1b evidence (from one RCT, two pre-post studies, and one case series; Richardson et al. 2000; Spiegl 2014; Bernuz et al. 2012; Hecht et al. 2008) that botulinum toxin type A improves focal muscle spasticity in SCI. It is important to note the RCT included just 6 of 52 subjects with spasticity of confirmed spinal cord origin.

Phenol

There is level 4 evidence (from one case series; Uchikawa et al. 2009) that phenol neurolysis improves pain, range of motion and function related to shoulder spasticity for individuals with tetraplegia in SCI.

There is level 4 evidence (from one pre-post study and two case series; Ghai et al. 2013; Ghai et al. 2012; Yasar et al. 2010) 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 SCI.