Spasticity Management

Number: 0362

Policy

  1. Aetna considers neurosurgical procedures medically necessary for the management of members with refractory spasticity when all of the following selection criteria are met:

    1. The member has good intrinsic lower extremity motor power, but is limited in ambulation by spasticity; and
    2. The member has the functional capacity and motivation to participate in post-operative rehabilitation; and
    3. The member has tried and failed non-surgical, medical management for spasticity including baclofen or other muscle relaxants.

    Aetna considers the following procedures medically necessary for the management of members with spasticity:

    1. Longitudinal myelotomy
    2. Microsurgical dorsal root entry zone lesion (DREZotomy)
    3. Percutaneous radiofrequency (or thermal) rhizotomy
    4. Peripheral neurotomy
    5. Selective posterior (dorsal) rhizotomyFootnotes*

    Members 2 to 6 years of age are optimal candidates for selective posterior rhizotomy.

    Footnotes* Based on a review of the medical literature, Aetna considers selective posterior rhizotomy experimental and investigational when the member has any of the following contraindications:

    1. Concomitant dystonia or rigidity; or
    2. Profound weakness in lower extremity muscles such that the spasticity actually serves to assist in standing; or
    3. Progressive neurological disorders, choreoathetosis, or cerebellar ataxia; or
    4. Severe damage to basal ganglia; or
    5. Severe fixed joint deformities or scoliosis.
  2. Aetna considers selective posterior rhizotomy experimental and investigational for the treatment of spasticity in children with hemiplegic cerebral palsy because these children are unlikely to benefit from this procedure.

  3. Aetna considers spinal cord stimulation (dorsal column stimulator) or neurectomy experimental and investigational for the treatment of spasticity because the effectiveness of these approaches has not been established.

  4. Aetna considers magnetic stimulation (transcranial or peripheral) experimental and investigational for the treatment of spasticity due to multiple sclerosis and other causes because the effectiveness of these approaches has not been established.

  5. Aetna considers the use of whole-body vibration experimental and investigational for individuals with spasticity associated with multiple sclerosis or spinal cord injury and other indications because its effectiveness has not been established.

  6. Aetna considers kinesiotaping for lower extremity spasticity experimental and investigational because its effectiveness has not been established.

  7. Aetna considers tibial nerve neurotomy experimental and investigational as treatment for spastic equinovarus foot because its effectiveness has not been established.

  8. Aetna considers focal muscle vibration experimental and investigational for the treatment of limb spasticity in persons with chronic stroke and other indications because its effectiveness has not been established.

  9. Aetna considers percutaneous myofascial lengthening experimental and investigational for the treatment of cerebral palsy because the clinical evidence is not sufficient to permit conclusions on the health outcome effects of the use of selective percutaneous myofascial lengthening in the treatment of cerebral palsy.

  10. Aetna considers acupuncture for the treatment of spasticity following stroke or spasticity associated with disorders of consciousness following brain damage experimental and investigational because its effectiveness has not been established.

  11. Aetna considers chemo-denervation with alcohol/phenol experimental and investigational for the treatment of limb spasticity following spinal cord injury because its effectiveness has not been established.

  12. Aetna considers sensory barrage stimulation experimental and investigational for the treatment of elbow spasticity because its effectiveness has not been established.

  13. Aetna considers electrical stimulation as an adjunct to botulinum toxin for the treatment of spasticity experimental and investigational because its effectiveness has not been established.

  14. Aetna considers transcranial direct current stimulation for the treatment of spasticity experimental and investigational because its effectiveness has not been established.

  15. Aetna considers botulinum toxin or thalamic stimulation for the treatment of spasticity associated with disorders of consciousness following brain damage experimental and investigational because their effectiveness for this indication has not been established.

  16. Aetna considers pulsed radiofrequency for the treatment of spasticity in persons with spinal cord injury experimental and investigational because its effectiveness has not been established.

  17. Aetna considers support vector machine-based method with surface electromyography and mechanomyography for evaluation of elbow spasticity experimental and investigational because its effectiveness has not been established.

Background

Cerebral palsy (CP) refers to a wide variety of non-progressive brain disorders resulting from insults to the central nervous system during the perinatal period.  Traditionally, the adverse effects of spasticity such as contractures and bony deformities in patients with CP are managed by means of drug therapy, phenol injections, spinal blocks, physical therapy, bracing, and orthopedic surgeries.  In the last 3 decades, selective posterior rhizotomy (SPR) has been used in the management of these patients for reduction of spasticity which may result in an improvement of their active functional mobility.  The use of total posterior rhizotomies of lumbar and sacral nerve roots in reducing lower limb spasticity commenced approximately 80 years ago.  However, the lack of functional improvement despite a reduction in spasticity as well as the adverse side effects such as stasis ulceration, sensory ataxia, and hypesthesia (sensory loss) stimulated the development of partial rhizotomy and SPR is the most sophisticated version of the partial rhizotomy.  Currently, SPR is increasing being used for the treatment of lower extremity spasticity in patients with CP.

The rationale for SPR is that intra-operative electro-stimulation of spinal nerve rootlets in conjunction with electromyographic (EMG) monitoring and direct observation of muscle activity in the lower extremity allow for the identification of afferent posterior rootlets that terminate on relatively uninhibited alpha motoneurones.  Direct observation allows for identification of the diffusion of contraction to other muscle groups.  If these uninhibited rootlets are severed, spasticity can be reduced without the unacceptable side effects.  This technique employs microsurgical dissection of nerve rootlets from the level of L2 to S1 or S2 (if there is a spastic toe flexion).  Individual sensory rootlets (usually 3 to 8 comprising the posterior roots from L2 to S1) are isolated and electrically stimulated.  Those rootlets which produce an abnormal response are cut, while those generating a normal response are preserved.  Responses which are considered to be abnormal include
  1. clonus,
  2. contraction of ipsilateral muscles not normally innervated by that nerve,
  3. contralateral muscle contraction,
  4. clinical or EMG contraction that continues after the cessation of stimulation, and
  5. an EMG crescendo pattern during the stimulus.

If no abnormal responses are observed, the 30 to 60 % of the rootlets giving the strongest tetanic contraction are severed.  In general, no more than 75 % of the sensory rootlets are sectioned.

There is sufficient evidence that selective posterior rhizotomy is safe and effective for the management of children with CP.  Studies have consistently shown that selective posterior rhizotomy can reduce spasticity and improve motor function.  Additionally, if performed during early childhood, it may prevent the development of muscle contractures and orthopedic deformities.  On the other hand, due to the minimal degree of their impairment, children with hemiplegic CP are unlikely to benefit from this procedure.

In a review published in the New England Journal of Medicine, Park and Owen (2002) concluded that SPR can reduce spasticity and improve motor function, and if the operation is performed during early childhood, it may prevent the development of muscle contractures and orthopedic deformities.  Additionally, a Diagnostic and Therapeutic Technology Assessment of SPR published by the American Medical Association stated that in selected patients who have ambulatory potential, this procedure can reduce spasticity and facilitate walking and other movement (Brown, 1990).

An assessment of SPR by the National Institute for Health and Clinical Excellence (2006) concluded that current evidence on the safety of SPR for spasticity in cerebral palsy "appears adequate; however, there is evidence of only limited efficacy."  The assessment cites the results of a meta-analysis of 3 randomized controlled trials (McLaughlin et al, 2002) comparing physiotherapy and SPR with physiotherapy alone, which found that, compared with physiotherapy alone, gross motor function improved by an additional 4 % with physiotherapy and SPR (8 % and 4 % improvements, respectively; p = 0.008).  The follow-up period in the primary studies was 9 to 12 months.  Specialist advisors to NICE commented that there is some controversy about the role of SPR in relation to other management options for spasticity in CP.  They also commented that a reduction in spasticity does not always improve motor function.  The NICE assessment noted that adverse events seen clinical studies of SPR included bladder and bowel disturbances, severe postoperative pain, and dysthesia.  The specialisty advisors to NICE also noted among adverse events limb weakness, joint subluxation, progressive scoliosis or kyphosis, and sensory disturbance.  Theoretical adverse events included paralysis, dividing the wrong nerve rootlets, hypotonicity, weight gain and death.

Appropriate candidates for SPRs should have tried and failed other more conservative types of medical management for spasticity including baclofen or other muscle relaxants.  In addition, candidates should have good intrinsic lower extremity motor power, but are limited in ambulation by spasticity.  It is also important that candidates  have capacity and motivation to participate in post-operative rehabilitation.  Children 2 to 6 years of age are optimal candidates for this procedure.

Patients with one or more of the following condition(s) are generally not considered candidates for selective posterior rhizotomy: concomitant dystonia or rigidity; severe damage to basal ganglia; severe fixed joint deformities or scoliosis; progressive neurological disorders, choreo-athetosis, or cerebellar ataxia; or profound weakness in lower extremity muscles, and spasticity serves to assist in standing.

Bolster et al (2013) evaluated the long-term effect of selective dorsal rhizotomy (SDR) on the gross motor function of ambulant children with spastic bilateral CP, compared with reference centiles.  The study used a prospective cohort design and subjects comprised 29 children classified using the Gross Motor Function Classification System (GMFCS) in level I (n = 7), II (n = 4), or III (n = 18); 18 males, 11 females; median age at time of surgery 6 years 4 months; range of 2 years 10 months to 12 years 1 month), who were examined 5 years and 10 years after SDR.  These researchers used individual centiles based on Gross Motor Function Measure (GMFM-66) scores and age, corresponding to the GMFCS levels.  Individual improvement or deterioration was defined as a change of more than 20 centiles.  Side effects experienced and additional treatment received after SDR were also recorded.  Five years after SDR, 10 out of 28 children (35.7 %) showed improvement, and 10 years after SDR 6 out of 20 children (30 %) had improved.  Spinal side effects were noted in 2 children and hip subluxation in 3.  Additional treatments included subtalar arthrodesis (n = 13), endorotational osteotomy of the tibia (n = 5), and botulinum toxin treatment (n = 13).  The authors concluded that none of the children showed deterioration of gross motor function based on centile ranking.  Five and 10 years after SDR, gross motor function in some children had improved more than would have been expected according to the reference centiles.  They noted that this suggested, taking the limitations of this study into account, that the applied criteria for selection were adequate.  However, the children still needed additional treatment after SDR.

Valle et al (2007) examined the use of low- and high-frequency repetitive transcranial magnetic stimulation (TMS) for the treatment of spasticity.  A total of 17 subjects (8 males, 9 females; mean age of 9 years 1month) with CP and spastic quadriplegia were randomized to receive sham, active 1-Hz, or active 5-Hz repetitive TMS of the primary motor cortex.  Stimulation was applied for 5 consecutive days (90 % of motor threshold).  The results showed that there was a significant reduction of spasticity after 5-Hz, but not sham or 1-Hz, stimulation as indexed by the degree of passive movement; however this was not evident when using the Ashworth scale, although a trend for improvement was seen for elbow movement.  The safety evaluation showed that stimulation with either 1-Hz or 5-Hz did not result in any adverse events as compared with sham stimulation.  The authors stated that results of this trial provide initial evidence to support further trials exploring the use of cortical stimulation in the treatment of spasticity.

In a randomized sham-controlled trial with a 4-week follow-up, Barros Galvao et al (2014) assessed the effectiveness of inhibitory repetitive TMS (rTMS) for decreasing upper-limb muscle tone after chronic stroke.  Patients with stroke (n = 20) with post-stroke upper limb spasticity were enrolled in this study.  The experimental group received rTMS to the primary motor cortex of the unaffected side (1,500 pulses; 1 Hz; 90 % of resting motor threshold for the first dorsal interosseous muscle) in 10 sessions, 3 days/week, and physical therapy (PT).  The control group received sham stimulation and PT.  Main outcome measure included Modified Ashworth scale (MAS), upper-extremity Fugl-Meyer assessment, FIM, range of motion (ROM), and stroke-specific quality-of-life scale.  All outcomes were measured at baseline, after treatment (post-intervention), and at a 4-week follow-up.  A clinically important difference was defined as a reduction of greater than or equal to 1 in the MAS score.  Friedman test revealed that PT is efficient for significantly reducing the upper limb spasticity of patients only when it is associated with rTMS.  In the experimental group, 90 % of the patients at post-intervention and 55.5 % at follow-up showed a decrease of greater than or equal to 1 in the MAS score, representing clinically important differences.  In the control group, 30 % of the patients at post-intervention and 22.2 % at follow-up experienced clinically meaningful changes.  There were no differences between the groups at any time for any of the other outcome measures, indicating that both groups demonstrated similar behaviors over time for all variables.  The author concluded that rTMS associated with PT can be beneficial in reducing post-stroke spasticity.  However, they stated that more studies are needed to clarify the clinical changes underlying the reduction in spasticity induced by non-invasive brain stimulations.

Ness and Field-Fote (2009) stated that individuals with spinal cord injury (SCI) often have involuntary, reflex-evoked muscle activity resulting in spasticity.  Vibration may modulate reflex activity thereby decreasing spasticity.  These researchers examined the feasibility of using whole-body vibration (WBV) to decrease quadriceps spasticity in individuals with SCI.  Participants were individuals (n = 16) with spastic quadriceps hypertonia due to chronic SCI (greater than 1 year).  Quadriceps spasticity was measured by gravity-provoked stretch (Pendulum Test) before (initial) and after (final) a 3 day/week, 12-session WBV intervention.  In addition, differences between immediate (immediate post-WBV) and delayed (delayed post-WBV) within-session effects were quantified.  Finally, these investigators assessed response differences between subjects who did and those who did not use anti-spastic agents.  There was a significant decrease in quadriceps spasticity after participation in a WBV intervention that persisted for at least 8 days.  Within a WBV session, spasticity was reduced in the delayed post-WBV test compared to the immediate post-WBV test.  The WBV intervention was associated with similar changes in quadriceps spasticity in subjects who did and those who did not use anti-spastic agents.  The authors concluded that vibration may be a useful adjunct to training in those with spasticity.  They stated that future studies should directly compare the anti-spastic effects of vibration to those of anti-spastic agents.

In a randomized cross-over pilot study, Schyns et al (2009) examined the effectiveness of WBV on tone, muscle force, sensation and functional performance in people with multiple sclerosis (MS).  A total of 16 individuals with MS were randomly allocated to one of two groups.:
  1. group 1 received 4 weeks of WBV plus exercise 3 times per week, 2 weeks of no intervention and then 4 weeks of exercise alone 3 times per week, and
  2. group 2 were given the 2 treatment interventions in the reverse order to group 1.  Ten-meter walk, Timed Up and Go Test, Modified Ashworth Scale, Multiple Sclerosis Spasticity Scale (MSSS-88), lower limb muscle force, Nottingham Sensory Assessment and Multiple Sclerosis Impact Scale (MSIS-29) were used before and after intervention.
The exercise program had positive effects on muscle force and well-being, but there was insufficient evidence that the addition of WBV provided any further benefit.  The Modified Ashworth Scale was generally unaffected by either intervention, although, for each group, results from the MSSS-88 showed WBV and exercises reduced muscle spasms (p = 0.02).  Although results for the 10-meter walk and Timed Up and Go Test improved, this did not reach statistical significance (p = 0.56; p = 0.70, respectively).  For most subjects, sensation was unaffected by WBV. The authors concluded that exercise may be beneficial to those with MS, but there is limited evidence that the addition of WBV provides any additional improvements.  They stated that further larger scale studies into the effects of WBV in people with MS are essential.

In a randomized, controlled, pilot trial with 6 weeks' follow-up, Tankisheva et al (2014) examined the effects of WBV training program in patients with chronic stroke.  Adults with chronic stroke (n = 15) were randomly assigned to an intervention (n = 7) or a control group (n = 8).  Intervention was supervised, intensive WBV training.  The vibration group performed a variety of static and dynamic squat exercises on a vibration platform with vibration amplitudes of 1.7 and 2.5mm and frequencies of 35 and 40 Hz.  The vibration lasted 30 to 60 seconds, with 5 to 17 repetitions per exercise 3 times weekly for 6 weeks.  Participants in the control group continued their usual activities and were not involved in any additional training program.  The primary outcome variable was the isometric and isokinetic muscle strength of the quadriceps (isokinetic dynamometer).  Additionally, hamstrings muscle strength, static and dynamic postural control (dynamic posturography), and muscle spasticity (Ashworth Scale) were assessed.  Compliance with the vibration intervention was excellent, and the participants completed all 18 training sessions.  Vibration frequencies of both 35 and 40 Hz were well-tolerated by the patients, and no adverse effects resulting from the vibration were noted.  Overall, the effect of intensive WBV intervention resulted in significant between-group differences in favor of the vibration group only in isometric knee extension strength (knee angle, 60°) (p = 0.022) after 6 weeks of intervention and in isokinetic knee extension strength (velocity, 240°/s) after a 6-week follow-up period (p = 0.005), both for the paretic leg.  Postural control improved after 6 weeks of vibration in the intervention group when the patients had normal vision and a sway-referenced support surface (p < 0.05).  Muscle spasticity was not affected by vibration (p > 0.05).  The authors concluded that these preliminary results suggested that intensive WBV might potentially be a safe and feasible way to increase some aspect of lower limb muscle strength and postural control in adults with chronic stroke.  Moreover, they stated that further studies should focus on evaluating how the training protocol should be administered to achieve the best possible outcome, as well as comparing this training protocol to other interventions.

In a single-center, randomized, and double-blind study, Karadag-Saygi and colleagues (2010) evaluated the effect of kinesiotaping as an adjuvant therapy to botulinum toxin A (BTX-A) injection in lower extremity spasticity.  A total of 20 hemiplegic patients with spastic equinus foot were enrolled into the study and randomized into 2 groups.  The first group (n = 10) received BTX-A injection and kinesiotaping, and the second group (n = 10) received BTX-A injection and sham-taping.  Clinical assessment was done before injection and at 2 weeks and 1, 3, and 6 months.  Outcome measures were modified Ashworth scale (MAS), passive ankle dorsiflexion, gait velocity, and step length.  Improvement was recorded in both kinesiotaping and sham groups for all outcome variables.  No significant difference was found between groups other than passive ROM, which was found to have increased more in the kinesiotaping group at 2 weeks.  The authors concluded that there is no clear benefit in adjuvant kinesiotaping application with botulinum toxin for correction of spastic equinus in stroke.

Morris et al (2013) examined the effect of KTT from randomized controlled trials (RCTs) in the management of clinical conditions.  A systematic literature search of CINAHL; MEDLINE; OVID; AMED; SCIENCE DIRECT; PEDRO; SPORT DISCUS; BRITISH NURSING INDEX; COCHRANE CENTRAL REGISTER OF CLINICAL TRIALS; and PROQUEST was performed up to April 2012.  The risk of bias and quality of evidence grading was performed using the Cochrane collaboration methodology.  A total of 8 RCTs met the full inclusion/exclusion criteria; 6 of these included patients with musculoskeletal conditions; 1 included patients with breast-cancer-related lymphedema; and 1 included stroke patients with muscle spasticity; 6 studies included a sham or usual care tape/bandage group.  There was limited to moderate evidence that KTT is no more clinically effective than sham or usual care tape/bandage.  There was limited evidence from 1 moderate quality RCT that KTT in conjunction with physiotherapy was clinically beneficial for plantar fasciitis related pain in the short-term; however, there were serious questions around the internal validity of this RCT.  The authors concluded that there currently exists insufficient evidence to support the use of KTT over other modalities in clinical practice.

Bollens et al (2011) noted that spastic equinovarus foot is a major cause of disability for neurorehabilitation patients, impairing their daily activities, social participation and general quality of life.  Selective tibial nerve neurotomy is a neurosurgical treatment for focal spasticity, whose acceptance as treatment for spastic equinovarus foot remains controversial.  These investigators performed a systematic review of the literature to evaluate the effectiveness of tibial nerve neurotomy as a treatment for adult patients presenting with spastic equinovarus foot.  They queried PubMed, Science Direct, Trip Database and PEDro databases with the following keywords: "equinus deformity" OR "muscle spasticity" AND "neurotomy".  They selected a total of 11 non-randomized and uncontrolled studies, suggesting that neurotomy could be an efficient treatment to reduce impairments in spastic equinovarus foot patients.  The authors noted that their conclusions were based primarily on case series studies.  The effects of tibial nerve neurotomy had not been compared with a reference treatment through a randomized controlled trial, which would be necessary to increase the level of scientific evidence.  Moreover, further studies using quantitative, validated and objective assessment tools are needed to evaluate the effectiveness of tibial nerve neurotomy accurately based on the International Classification of Functioning, Disability and Health from the World Health Organization.

Bollens et al (2013) noted that selective neurotomy is a permanent treatment of focal spasticity, and its effectiveness in treating spastic equinovarus of the foot (SEF) was previously suggested by a few non-randomized and uncontrolled case-series studies.  This study was the first assessor-blinded RCT evaluating the effects of this treatment.  A total of 16 chronic stroke patients presenting with SEF were randomized into 2 groups:
  1. 8 patients underwent a tibial neurotomy and
  2. the remaining 8 received BTX injections.
The soleus was treated in all patients, and the tibialis posterior and flexor hallucis longus were treated in about 50 % of patients.  The primary outcome was the quantitative measurement of ankle stiffness (L-path), an objective measurement directly related to spasticity.  Participants were assessed by a blind assessor before their intervention and at 2 and 6 months after treatment.  Evaluations were based on the 3 domains of the International Classification of Functioning, Disability and Health (ICF).  Compared with BTX, tibial neurotomy induced a higher reduction in ankle stiffness.  Both treatments induced a comparable improvement of ankle kinematics during gait, whereas neither induced muscle weakening.  Activity, participation, and quality of life were not significantly modified in either group.  The authors concluded that the findings of this study demonstrated that the tibial nerve neurotomy is an effective treatment of SEF, reducing the impairments observed in chronic stroke patients.  Moreover, they stated that future studies should be conducted to confirm the long-term effectiveness based on the ICF domains.

Ashworth et al (2012) systematically reviewed treatments for spasticity in amyotrophic lateral sclerosis (ALS), also known as motor neuron disease.  These investigators searched the Cochrane Neuromuscular Disease Group Specialized Register (July 4, 2011), CENTRAL (2011, Issue 2), MEDLINE (January 1966 to July 2011), EMBASE (January 1980 to July 2011 ), CINAHL Plus (January 1937 to July 2011), AMED (January 1985 to July 2011) and LILACS (January 1982 to July 2011 ).  They reviewed the bibliographies of the randomized controlled trials identified, and contacted authors and experts in the field.  They included quasi-randomized or randomized controlled trials of participants with probable or definite ALS according to the El Escorial diagnostic criteria (or a revised version) or the Airlie House revision.  They included trials of physical therapy, modalities, prescription medications, non-prescription medications, chemical neurolysis, surgical interventions, and alternative therapies.  The primary outcome measure was reduction in spasticity at 3 months or greater as measured by the Ashworth (or modified Ashworth) spasticity scale.  The secondary outcome measures were: validated measures based on history, physical examination, physiological measures, measures of function, measures of quality of life, all adverse events, and measures of cost.  Two authors independently screened the abstracts of potential trials retrieved from the searches.  Two authors extracted the data.  They also contacted the author of the paper and obtained information not available in the published article.  All 3 authors assessed the methodological quality of all included trials independently.  These researchers identified only 1 randomized controlled trial that met inclusion criteria and no further trials were identified in subsequent updates.  The included study was a trial of moderate intensity, endurance type exercise versus "usual activities" in 25 patients with AML.  The risk of bias was high and no adverse events were reported.  At 3 months patients performing the 15-min twice-daily exercises had significantly less spasticity overall (mean reduction of -0.43, 95 % confidence interval (CI): -1.03 to +0.17 in the treatment group versus an increase of +0.25, 95 % CI: -0.46 to +0.96 in the control group) but the mean change between groups was not significant (-0.68, 95 % CI: -1.62 to +0.26), as measured by the Ashworth scale (possible scores 0 to 5, where higher is worse).  The authors concluded that the single trial performed was too small to determine whether individualized moderate intensity endurance type exercises for the trunk and limbs are beneficial or harmful.  No other medical, surgical or alternative treatment and therapy has been evaluated in a randomized fashion in this patient population; more research is needed.

In a pilot randomized controlled trial, Caliandro et al (2012) examined the clinical effect of repetitive focal muscle vibration (rMV) on the motor function of the upper extremity 1 month after treatment in patients with chronic stroke (n = 49).  Patients assigned to the study group (SG; n= 28) received rMV, while patients in the control group (CG; n= 21) received a placebo vibratory treatment; patients and the clinical examiner were blind to the intervention.  The primary endpoint was an improvement of more than 0.37 points on the Functional Ability Scale of the Wolf Motor Function Test (WMFT FAS).  The Modified Ashworth Scale and the visual analog scale were the secondary outcome measures.  All measures were administered before the treatment (t0) and 1 week (t1) and 1 month (t2) after the treatment.  The analysis of variance for repeated measurements revealed a significant difference in the expression of the WMFT FAS score over time only in the SG (p = 0.006).  The treatment was successful for 7 (33 %) of 21 patients recruited in the SG and for 2 (13 %) of 15 patients recruited in the CG.  The relative risk was 2.5 (95 % CI: .60 to 10.39), and the number needed to treat was 5.  The Wilcoxon test showed a statistically significant difference between t0 and t2 in the SG (p = 0.02).  No adverse event was observed in the 2 groups.  The authors concluded that these findings suggested that rMV treatment of the upper limb may improve the functional ability of chronic stroke patients, but a larger, multi-center, randomized controlled study is needed.

The selective percutaneous myofascial lengthening (SPML) procedure involves releasing tight bands of tendon.  This is done where muscle and tendon overlap and the tendon starts to blend into a muscle (myofascial).  When the myofascia is cut, the muscle under it can easily stretch and lengthen.  The SPML procedure uses micro-incisions only about 2-mm long which results in decreased scarring.  Areas where the SPML procedure is performed include the back of the ankle for calf / heel cord tightness and spasticity, behind the knee for hamstring tightness and spasticity and in the groin area for scissoring gait and groin spasticity.

Mitsiokapa and colleagues (2010) published the findings of 58 children with spastic CP who underwent selective percutaneous myofascial lengthening of the hip adductor group and the medial or the lateral hamstrings.  All the patients were spastic diplegic, hemiplegic, or quadriplegic.  The indications for surgery were a primary contracture that interfered with the patients' walking or sitting ability or joint subluxation.  Gross motor ability and gross motor function of the children were evaluated using the gross motor function classification system (GMFCS) and the gross motor function measure (GMFM), respectively.  The mean time of the surgical procedure was 14 minutes (range of 1 to 27 minutes).  All patients were discharged from the hospital setting the same day after the operation.  There were no infections, overlengthening, nerve palsies, or vascular complications.  Three patients required repeat procedures for relapsed hamstring and adductor contractures at 8, 14, and 16 months post-operatively.  At 2 years after the initial operation, all the children improved on their previous functional level; 34 children improved by 1 GMFCS level, and 5 children improved by 2 GMFCS levels.  The overall improvement in mean GMFM scores was from 71.19 to 83.19.

In a Cochrane review, Amatya and colleagues (2013) evaluated the effectiveness of various non-pharmacological interventions for the treatment of spasticity in adults with MS.  A literature search was performed using the Specialised Register of the Cochrane Multiple Sclerosis and Rare Diseases of the Central Nervous System Review Group on using the Cochrane MS Group Trials Register which among other sources, contained CENTRAL, Medline, EMBASE, CINAHL, LILACS, PEDRO in June 2012.  Manual searching in the relevant journals and screening of the reference lists of identified studies and reviews were carried out.  Abstracts published in proceedings of conferences were also scrutinized.  Randomized controlled trials (RCTs) that reported non- pharmacological intervention/s for treatment of spasticity in adults with MS and compared them with some form of control intervention (such as sham/placebo interventions or lower level or different types of intervention, minimal intervention, waiting list controls or no treatment; interventions given in different settings), were included.  Three review authors independently selected the studies, extracted data and assessed the methodological quality of the studies using the Grades of Recommendation, Assessment, Development and Evaluation (GRADE) tool for best-evidence synthesis.  A meta-analysis was not possible due to methodological, clinical and statistical heterogeneity of included studies.  A total of 9 RCTs (n = 341 participants, 301 included in analyses) investigated various types and intensities of non-pharmacological interventions for treating spasticity in adults with MS.  These interventions included: physical activity programs (such as physiotherapy, structured exercise program, sports climbing); TMS (Intermittent Theta Burst Stimulation (iTBS), rTMS); electromagnetic therapy (pulsed electromagnetic therapy; magnetic pulsing device), transcutaneous electrical nerve Stimulation (TENS); and WBV).  All studies scored “low” on the methodological quality assessment implying high-risk of bias.  There is “low level” evidence for physical activity programs used in isolation or in combination with other interventions (pharmacological or non-pharmacological), and for repetitive magnetic stimulation (iTBS/rTMS) with or without adjuvant exercise therapy in improving spasticity in adults with MS.  No evidence of benefit exists to support the use of TENS, sports climbing and vibration therapy for treating spasticity in this population.  The authors concluded that there is “low level” evidence for non-pharmacological interventions such as physical activities given in conjunction with other interventions, and for magnetic stimulation and electromagnetic therapies for beneficial effects on spasticity outcomes in people with MS.  They noted that a wide range of non-pharmacological interventions are used for the treatment of spasticity in MS, but more robust trials are needed to build evidence about these interventions.

In a mono-centric, randomized, double-blind, sham-controlled trial, Krewer et al (2014) investigated short-term and long-term effects of repetitive peripheral magnetic stimulation (rpMS) on spasticity and motor.  Patients (n = 66) with severe hemiparesis and mild-to-moderate spasticity resulting from a stroke or a traumatic brain injury.  The average time ± SD since injury for the intervention groups was 26 ± 71 weeks or 37 ± 82 weeks.  Subjects received rpMS for 20 minutes or sham stimulation with subsequent occupational therapy for 20 minutes, 2 times a day, over a 2-week period.  Main outcome measures included Modified Tardieu Scale and Fugl-Meyer Assessment (arm score), assessed before therapy, at the end of the 2-week treatment period, and 2 weeks after study treatment.  Additionally, the Tardieu Scale was assessed after the first and before the third therapy session to determine any short-term effects.  Spasticity (Tardieu greater than 0) was present in 83 % of wrist flexors, 62 % of elbow flexors, 44 % of elbow extensors, and 10 % of wrist extensors.  Compared with the sham stimulation group, the rpMS group showed short-term effects on spasticity for wrist flexors (p = 0.048), and long-term effects for elbow extensors (p < 0.045).  Arm motor function (rpMS group: median 5 [4 to 27]; sham group: median 4 [4 to 9]) did not significantly change over the study period in either group, whereas rpMS had a positive effect on sensory function.  The authors concluded that therapy with rpMS increases sensory function in patients with severe limb paresis.  The magnetic stimulation, however, has limited effect on spasticity and no effect on motor function.

Park et al (2014) noted that acupuncture has been suggested as a treatment for spasticity in patients with stroke.  These investigators reviewed available literature to evaluate its effectiveness in this situation.  Randomized trials assessing the effects of acupuncture for the treatment of spasticity after stroke were identified by searching the Cochrane Library, PubMed, ProQuest, EBSCOhost, SCOPUS, CINAHL, EMBASE, Alternative Medicine Database, and Chinese and Korean medical literature databases.  Two reviewers independently extracted data on study characteristics, patient characteristics, and spasticity outcomes.  A total of 8 trials with 399 patients met all the inclusion criteria.  Compared with controls without acupuncture, acupuncture had no effect on improving clinical outcomes (as measured by validated instruments such as the Modified Ashworth Scale) or physiologic outcomes (assessed by measures such as the H-reflex/M-response [H/M] ratio at the end of the treatment period).  H/M ratios did decrease significantly immediately after the first acupuncture treatment.  Methodological quality of all evaluated trials was considered inadequate.  The authors concluded that the effect of acupuncture for spasticity in patients with stroke remains uncertain, primarily because of the poor quality of the available studies.  They stated that larger and more methodologically sound trials are needed to definitively confirm or refute any effect of acupuncture as a treatment for spasticity after stroke.

Chemo-Denervation with Alcohol/Phenol

In a systematic review, Lui and colleagues (2015) evaluated the literature on chemo-denervation with botulinum toxin (BoNT) or alcohol/phenol for treatment of limb spasticity following SCI. EMBASE, MEDLINE, CINAHL, Cochrane Database of Systematic Reviews and Cochrane Central Register of Controlled Trials were searched for English language studies published up until March 2014.  Studies were assessed for eligibility and quality by 2 independent reviewers.  No controlled trials were identified.  A total of 19 studies were included: 9 involving BoNT and 10 involving alcohol/phenol.  Owing to the clinically diverse nature of the studies, meta-analysis was deemed inappropriate.  The studies produced level 4 and level 5 evidence that chemo-denervation with BoNT or alcohol/phenol can lead to improvement in outcome measurements classified in the body structure and function, as well as activity domains of the International Classification of Functioning, Disability and Health framework.  The MAS was the most commonly used outcome measure.  All 6 studies on BoNT and 3 of the 4 studies on alcohol/phenol measuring MAS reported a decrease in at least 1 point.  An improvement in MAS was not always associated with improvement in function.  The effect of alcohol/phenol has the potential to last beyond 6 months; study follow-up did not occur beyond this time-point.  The authors concluded that chemo-denervation with BoNT or alcohol/phenol may improve spasticity and function in individuals with SCI.  However, there is a lack of high-quality evidence and further research is needed to confirm the effectiveness of these interventions.

Sensory Barrage Stimulation in the Treatment of Elbow Spasticity

In a randomized, cross-over, double-blind pilot study, Slovak and colleagues (2016) examined the feasibility of using a novel form of multi-channel electrical stimulation, termed sensory barrage stimulation (SBS) for the treatment of spasticity affecting the elbow flexor muscles and compared this with conventional single-channel TENS stimulation. A total of 10 participants with spasticity of the flexor muscles of the elbow of grade 2 or above on the MAS were recruited to this trial.  The participants received 2 intervention sessions (SBS and TENS), 1 week apart in a randomized order.  Both interventions were applied over the triceps brachii on the affected arm for a duration of 60 minutes.  Spasticity was measured using the MAS.  Secondary outcome measures were self-reported change in spasticity, measured on a visual analog scale (VAS, 0 to 100), and therapist-rated strength of elbow extension and strength of elbow flexion.  Measurements were taken immediately before each intervention was applied, immediately after the intervention, and 1 hour after the intervention.  Immediately after stimulation, spasticity showed a significant reduction for both TENS and SBS groups assessed by MAS -0.9 ± 0.2 versus -1.1 ± 0.2 and by VAS -15 ± 3 versus -31 ± 8.  For SBS this improvement in MAS was still present at 1 hour after the stimulation, but not for TENS.  A total of 7 SBS responders and 4 TENS responders were identified.  The authors concluded that the findings of this study demonstrated the feasibility and practicality of applying the new concept of SBS’ promising results indicated it caused a reduction in spasticity.  The preliminary findings of this pilot study need to be validated by well-designed studies.

Transcranial Magnetic Stimulation

Korzhova and colleagues (2016) performed a systematic review and meta-analysis of all available publications evaluating the effectiveness of repetitive transcranial magnetic stimulation (rTMS) in treatment of spasticity.  Search for articles was conducted in databases PubMed, Willey, and Google.  Keywords included "TMS", "spasticity", "TMS and spasticity", "non- invasive brain stimulation", and "non-invasive spinal cord stimulation".  The difference in scores according to the Modified Ashworth Scale (MAS) for one joint before and after treatment was taken as the effect size.  These researchers found 26 articles that examined the TMS effectiveness in treatment of spasticity.  Meta-analysis included 6 trials comprising 149 patients who underwent real stimulation or simulation.  No statistically significant difference in the effect of real and simulated stimulation was found in stroke patients.  In patients with spinal cord injury and spasticity, the mean effect size value and the 95 % CI were -0.80 and (-1.12 to -0.49), respectively, in a group of real stimulation; in the case of simulated stimulation, these parameters were 0.15 and (-0.30 to -0.00), respectively.  Statistically significant differences between groups of real stimulation and simulation were demonstrated for using high-frequency rTMS or intermittent theta burst stimulation (iTBS) mode for the M1 area of the spastic leg (p = 0.0002).  The authors concluded that according to the meta-analysis, the statistically significant effect of rTMS in the form of reduced spasticity was demonstrated only for the developed due to lesions at the brain stem and spinal cord level.  They stated that to clarify the amount of the anti-spasmodic effect of rTMS at other lesion levels, in particular in patients with hemispheric stroke, further research is needed.  They stated that larger placebo-controlled trials could be recommended to increase the degree of evidence.

Leo and colleagues (2017) provided an objective view of the non-invasive neuromodulation (NINM) protocols available for treating spasticity, including rTMS and transcranial direct current stimulation (tDCS).  On the basis of the relevant RCTs, these researchers inferred that NINM is more effective in reducing spasticity when combined with the conventional therapies than used as a stand-alone treatment.  However, the magnitude of NINM after-effects depends significantly on the applied hemisphere and the underlying pathology.  Being in line with these arguments, low-frequency rTMS and cathodal-tDCS over the unaffected hemisphere were more effective in reducing spasticity than high-frequency rTMS and anodal-tDCS over the affected hemisphere in chronic post-stroke.  However, most of the studies were heterogeneous in the stimulation set-up, patient selection, follow-up duration, and the availability of the sham operation.  The authors concluded that the the available data on the usefulness of NINM in reducing spasticity need to be confirmed by larger and multi-center RCTs to gather evidence on the efficiency of NINM regimens in reducing spasticity in various neurologic conditions.  Level of Evidence = V.

Electrical Stimulation as an Adjunct to Botulinum Toxin

Mills and associates (2016) examined the quality of evidence from RCTs on the effectiveness of adjunct therapies following botulinum toxin (BTX) injections for limb spasticity.  Medline, Embase, CINAHL, and Cochrane Central Register of Controlled Trials electronic databases were searched for English language human studies from 1980 to May 21, 2015; RCTs assessing adjunct therapies post-BTX injection for treatment of spasticity were included.  Of the 268 studies screened, 17 met selection criteria.  Two reviewers independently assessed risk of bias using the Physiotherapy Evidence Database (PEDro) scale and graded according to Sackett's levels of evidence.  A total of 10 adjunct therapies were identified.  Evidence suggested that adjunct use of electrical stimulation (ES), modified constraint-induced movement therapy, physiotherapy (all Level 1), casting and dynamic splinting (both Level 2) resulted in improved modified Ashworth Scale (mAS) scores by at least 1 grade.  There was Level 1 and 2 evidence that adjunct taping, segmental muscle vibration, cyclic functional ES (FES), and motorized arm ergometer may not improve outcomes compared with BTX injections alone.  There was Level 1 evidence that casting is better than taping, taping is better than ES and stretching, and extracorporeal shock wave therapy was better than ES for outcomes including the mAS, ROM and gait.  All results were based on single studies.  The authors concluded that there was high level evidence to suggest that adjunct therapies may improve outcomes following BTX injection; no results have been confirmed by independent replication.  They stated that all interventions would benefit from further study.

Intiso and colleagues (2017) examined if ES as an adjunct to BTX-type A (BTX-A) could boost botulinum activity and whether the combined therapeutic procedure is more effective than BTX-A alone in reducing spasticity in adult subjects.  These investigators performed a search in PubMed, Embase, Cochrane Central Register, and CINAHL from January 1966 to January 2016.  Only RCTs involving the combination of BTX-A and ES were considered; RCTs were excluded if BTX plus ES was investigated in animals or healthy subjects; certain techniques were used as an adjunct to BTX-A, but ES was not used; BTX-A or ES were compared but were not used in combination.  Electrical stimulation was divided into neuromuscular stimulation (NMS), FES, and TENS.  Two authors independently screened all search results and reviewed study characteristics using the PEDro scale.  A total of 15 RCTs were pinpointed and 9 studies were included.  Trials varied in methodological quality, size, and outcome measures used. ES was used in the form of NMS and FES in 7 and 2 studies, respectively.  No study investigating BTX-A plus TENS was found.  BTX-A plus ES produced significant reduction in spasticity on the Ashworth Scale (AS) and on the modified AS in 7 studies, but only 4 showed high quality on the PEDro scale.  Significant reduction in compound muscular action potential (CMAP) amplitude was detected after BTX-A plus ES in 2 studies.  The authors concluded that ES as an adjunctive therapy to BTX-A may boost BTX-A action in reducing adult spasticity, but ES variability made it difficult to recommend the combined therapy in clinical practice.  Given the variability of ES characteristics and the paucity of high-quality trials, it is difficult to support definitively the use of BTX-A plus ES to potentiate BTX-A effect in clinical practice.  The authors noted that a wide variety of rehabilitation interventions combined with BTX-A have been provided in reducing spasticity, but the present evidence is insufficient to recommend any combined therapeutic strategy.

Transcranial Direct Current Stimulation

Elsner and colleagues (2016) evaluated the evidence regarding transcranial direct current stimulation (tDCS) and assessed its impact on spasticity after stroke.  The following databases were searched up to January 6, 2016: Cochrane Central Register of Controlled Trials (CENTRAL) (Cochrane Library, latest issue), Medline (from 1948), Embase (from 1980), CINAHL (from 1982), AMED (from 1985), Science Citation Index (from 1900).  One author screened titles and abstracts and eliminated obviously irrelevant studies; 2 authors retrieved the full text of the remaining studies and checked them for inclusion; 2 authors independently extracted data from the studies using pre-defined data extraction sheets.  In case an author of being involved in an included trial, another author extracted data.  A total of 5 trials were included, with a total of 315 participants.  There was moderate-to-low quality of evidence for no effect of tDCS on improving spasticity at the end of the intervention period.  There were no studies examining the effect of tDCS on improving spasticity at long-term follow-up.  The authors concluded that there is moderate-to-low quality evidence for no effect of tDCS on improving spasticity in people with stroke.

Spasticity Associated with Disorders of Consciousness Following Brain Damage:

Martens and colleagues (2017) noted that spasticity is a motor disorder often encountered following a lesion involving the central nervous system (CNS).  It is hypothesized to arise from an anarchic re-organization of the pyramidal and para-pyramidal fibers and results in hypertonia and hyperreflexia of the affected muscular groups.  While this symptom and its management is well-known in patients suffering from stroke, multiple sclerosis or spinal cord lesion, little is known regarding its appropriate management in patients presenting disorders of consciousness (DOC) following brain damage.  These investigators reviewed the occurrence of spasticity in patients with DOC and the therapeutic options in treating these patients.  They conducted a systematic review using the PubMed online database.  It returned 157 articles.  After applying the inclusion criteria (i.e., studies about patients in coma, unresponsive wakefulness syndrome or minimally conscious state, with spasticity objectively reported as a primary or secondary outcome), a total of 18 studies were fully reviewed.  The prevalence of spasticity in patients with DOC ranged from 59 % to 89 %.  Current therapeutic options include intrathecal baclofen and soft splints.  Several therapeutic options still need further investigation; including acupuncture, botulinum toxin or cortical activation by thalamic stimulation.   The authors concluded that the small number of articles available in the current literature highlighted that spasticity is poorly studied in patients with DOC although it is one of the most common motor disorders.  They stated that while treatments such as intrathecal baclofen and soft splints appeared effective, large RCTs have to be done and new therapeutic options should be explored.

In a systematic review, Synnot and associates (2017) the effects of interventions for managing skeletal muscle spasticity in people with traumatic brain injury (TBI).  In June 2017, these investigators searched key databases including the Cochrane Injuries Group Specialised Register, CENTRAL, MEDLINE (Ovid), Embase (Ovid) and others, in addition to clinical trials registries and the reference lists of included studies.  They included RCTs and cross-over RCTs evaluating any intervention for the management of spasticity in TBI.  Only studies where at least 50 % of participants had a TBI (or for whom separate data for participants with TBI were available) were included.  The primary outcomes were spasticity and adverse effects.  Secondary outcome measures were classified according to the World Health Organization (WHO) International Classification of Functioning, Disability and Health including body functions (sensory, pain, neuro-musculoskeletal and movement-related functions) and activities and participation (general tasks and demands; mobility; self-care; domestic life; major life areas; community, social and civic life).  These researchers used standard methodological procedures expected by Cochrane.  Data were synthesized narratively; meta-analysis was precluded due to the paucity and heterogeneity of data.  A total of 9 studies were included in this review that involved 134 participants with TBI.  Only 5 studies reported between-group differences, yielding outcome data for 105 participants with TBI.  These 5 studies assessed the effects of a range of pharmacological (baclofen, botulinum toxin A) and non-pharmacological (casting, physiotherapy, splints, tilt table standing and electrical stimulation) interventions, often in combination.  The studies that examined the effect of baclofen and tizanidine did not report their results adequately.  Where outcome data were available, spasticity and adverse events (AEs) were reported, in addition to some secondary outcome measures.  Of the 5 studies with results, 3 were funded by governments, charities or health services and 2 were funded by a pharmaceutical or medical technology company.  The 4 studies without useable results were funded by pharmaceutical or medical technology companies  .It was difficult to draw conclusions about the effectiveness of these interventions due to poor reporting, small study size and the fact that participants with TBI were usually only a proportion of the overall total.  Meta-analysis was not feasible due to the paucity of data and heterogeneity of interventions and comparator groups.  Some studies concluded that the intervention they tested had beneficial effects on spasticity, and others found no difference between certain treatments.  The most common AE was minor skin damage in people who received casting.  These researchers believed it would be misleading to provide any further description of study results given the quality of the evidence was very low for all outcomes.  The authors concluded that the very low quality and limited amount of evidence about the management of spasticity in people with TBI meant that they were uncertain regarding the effectiveness or harms of these interventions.  They stated that well-designed and adequately powered studies using functional outcome measures to test the interventions used in clinical practice are needed.

Pulsed Radiofrequency for the Treatment of Spasticity in Persons with Spinal Cord Injury:

Chang and Cho (2017) noted that spasticity following SCI results in functional deterioration and reduced quality of life (QOL).  These researchers reported the findings of 2 SCI patients who presented with good response to pulsed radiofrequency (PRF) for the management of spasticity in the lower extremities.  Patient 1 (a 47-year old man) had complete thoracic cord injury and showed a phasic spasticity on the extensor of both knees (3 to 4 beats clonus per every 30 seconds) and tonic spasticity (MAS: 3) on both hip adductors.  Patient 2 (a 64-year old man) had incomplete cervical cord injury and showed a right ankle clonus (about 20 beats) when he walked.  After the application of PRF to both L2 and L3 dorsal root ganglion (DRG) (patient 1) and right S1 DRG (patient 2) with 5 Hz and 5 ms pulsed width for 360 seconds at 45 V under the C-arm guide, all spasticity disappeared or was reduced.  Moreover, the effects of PRF were sustained for approximately 6 months with no side effects.  The authors believed that PRF treatment can be useful for patients with spasticity after SCI.  According to these investigators, this was the first report to show the effective use of PRF for managing spasticity caused by SCI.  However, this study was limited because it was a case study.  They stated that further studies that involve larger case numbers are needed.  Moreover, they noted that to achieve the optimal outcomes of PRF, further studies are needed to iexamine the stimulation duration, mode, and intensity of PRF; furthermore, an evaluation of the action mechanisms by which spasticity is reduced is necessary.

Support Vector Machine-Based Method with Surface Electromyography and Mechanomyography for Evaluation of Elbow Spasticity:

Wang and colleagues (2017) noted that the MAS is the gold standard in clinical for grading spasticity.  However, its results greatly depend on the physician evaluations and are subjective.  In this study, these researchers examined the feasibility of using support vector machine (SVM) to objectively assess elbow spasticity based on both surface electromyography (sEMG) and mechanomyography (MMG).  sEMG signals and tri-axial accelerometer mechanomyography (ACC-MMG) signals were recorded simultaneously on patients' biceps and triceps when they extended or bended elbow passively.  A total of 39 post-stroke patients participated in the study, and were divided into 4 groups regarding MAS level (MAS = 0, 1, 1+ or 2).  The 3 types of features, root mean square (RMS), mean power frequency (MPF), and median frequency (MF), were calculated from sEMG and MMG signal recordings.  Spearman correlation analysis was used to examine the relationship between the features and spasticity grades.  The results showed that the correlation between MAS and each of the 5 features (MMG-RMS of the biceps, MMG-RMS of the triceps, the EMG-RMS of the biceps, EMG-RMS of the triceps, and EMG-MPF of the triceps) was significant (p < 0.05).  The 4 spasticity grades were identified with SVM, and the classification accuracy of SVM with sEMG, MMG, sEMG-MMG were 70.9 %, 83.3 %, 91.7 %, respectively.  The authors concluded that these findings suggested that using the SVM-based method with sEMG and MMG to evaluate elbow spasticity would be suitable for clinical management of spasticity.  These preliminary findings need to be validated by well-designed studies.

Table: CPT Codes / HCPCS Codes / ICD-10 Codes
Code Code Description

Information in the [brackets] below has been added for clarification purposes.   Codes requiring a 7th character are represented by "+":

CPT codes covered if selection criteria are met:

63170 Laminectomy with myelotomy (e.g., Bischof or DREZ type), cervical, thoracic, or thoracolumbar
63185 Laminectomy with rhizotomy; one or two segments
63190     more than two segments
63600 Creation of lesion of spinal cord by stereotactic method, percutaneous, any modality (including stimulation and/or recording)
64708 - 64714 Neuroplasty, major peripheral nerve, arm or leg, open
64600 - 64640 Destruction by neurolytic agent, somatic nerves

CPT codes not covered for indications listed in the CPB:

Pulsed radiofrequency, mechanomyography - no specific code:

27325 Neurectomy, hamstring muscle
27326 Neurectomy, popliteal (gastrocnemius)
28055 Neurectomy, intrinsic musculature of foot
61863 - 61864 Twist drill, burr hole, craniotomy, or craniectomy with stereotactic implantation of neurostimulator electrode array in subcortical site (eg, thalamus, globus pallidus, subthalamic nucleus, periventricular, periaqueductal gray), without use of intraoperative microelectrode recording [for thalamic stimulation for the treatment of spasticity associated with disorders of consciousness following brain damage]
61867 - 61868 Twist drill, burr hole, craniotomy, or craniectomy with stereotactic implantation of neurostimulator electrode array in subcortical site (eg, thalamus, globus pallidus, subthalamic nucleus, periventricular, periaqueductal gray), with use of intraoperative microelectrode recording [for thalamic stimulation for the treatment of spasticity associated with disorders of consciousness following brain damage]
61880 Revision or removal of intracranial neurostimulator electrodes. [for thalamic stimulation for the treatment of spasticity associated with disorders of consciousness following brain damage]
61885 - 61886 Insertion or replacement of cranial neurostimulator pulse generator or receiver, direct or inductive coupling [for thalamic stimulation for the treatment of spasticity associated with disorders of consciousness following brain damage]
61888 Revision or removal of cranial neurostimulator pulse generator or receiver. [for thalamic stimulation for the treatment of spasticity associated with disorders of consciousness following brain damage]
63650 Percutaneous implantation of neurostimulator electrode array, epidural
63655 Laminectomy for implantation of neurostimulator electrodes, plate/paddle, epidural
63661 Removal of spinal neurostimulator electrode percutaneous array(s), including fluoroscopy, when performed
63662 Removal of spinal neurostimulator electrode plate/paddle(s) placed via laminotomy or laminectomy, including fluoroscopy, when performed
63663 Revision including replacement, when performed, of spinal neurostimulator electrode percutaneous array(s) including fluoroscopy, when performed
63664 Revision including replacement, when performed, of spinal neurostimulator electrode plate/paddle(s) placed via laminotomy or laminectomy, including fluoroscopy, when performed
63685 Insertion or replacement of spinal neurostimulator pulse generator or receiver, direct or inductive coupling
63688 Revision or removal of implanted spinal neurostimulator pulse generator or receiver
64550 Application of surface (transcutaneous) neurostimulator
64642 - 64645 Chemodenervation of extremity [with alcohol/phenol]
90867 - 90869 Therapeutic repetitive transcranial magnetic stimulation (TMS) treatment
97014 Application of a modality to 1 or more areas; electrical stimulation (unattended)
97032 Application of a modality to 1 or more areas; electrical stimulation (manual), each 15 minutes
97810 - 97814 Acupuncture

HCPCS codes not covered for indications listed in the CPB:

A4556 Electrodes, (e.g., apnea monitor), per pair
A4557 Lead wires, (e.g., apnea monitor), per pair
A4558 Conductive gel or paste, for use with electrical device (e.g., tens, nmes), per oz
A4595 Electrical stimulator supplies, 2 lead, per month, (e.g. tens, nmes)
C1767 Generator, neurostimulator (implantable), non-rechargeable
C1778 Lead, neurostimulator (implantable)
C1787 Patient programmer, neurostimulator
C1816 Receiver and/or transmitter, neurostimulator (implantable)
C1820 Generator, neurostimulator (implantable), non high-frequency with rechargeable battery and charging system
C1883 Adapter/extension, pacing lead or neurostimulator lead (implantable)
E0720 Transcutaneous electrical nerve stimulation (tens) device, two lead, localized stimulation
E0730 Transcutaneous electrical nerve stimulation (tens) device, four or more leads, for multiple nerve stimulation
E0731 Form fitting conductive garment for delivery of tens or nmes (with conductive fibers separated from the patient's skin by layers of fabric)
E0745 Neuromuscular stimulator, electronic shock unit
E0762 Transcutaneous electrical joint stimulation device system, includes all accessories
E0764 Functional neuromuscular stimulator, transcutaneous stimulation of muscles of ambulation with computer control, used for walking by spinal cord injured, entire system, after completion of training program
E0770 Functional electrical stimulator, transcutaneous stimulation of nerve and/or muscle groups, any type, complete system, not otherwise specified
G0295 Electromagnetic therapy, to one or more areas, for wound care other than described in G0329 or for other uses
J0585 Injection, onabotulinumtoxina, 1 unit
J0586 Injection, abobotulinumtoxina, 5 units
J0587 Injection, rimabotulinumtoxinb, 100 units
J0588 Injection, incobotulinumtoxin a, 1 unit
L8679 Implantable neurostimulator, pulse generator, any type.
L8680 Implantable neurostimulator electrode, each
L8681 Patient programmer (external) for use with implantable programmable neurostimulator pulse generator
L8682 Implantable neurostimulator radiofrequency receiver
L8683 Radiofrequency transmitter (external) for use with implantable neurostimulator radiofrequency receiver
L8685 Implantable neurostimulator pulse generator, single array, rechargeable, includes extension
L8686 Implantable neurostimulator pulse generator, single array, non-rechargeable, includes extension
L8687 Implantable neurostimulator pulse generator, dual array, rechargeable, includes extension
L8688 Implantable neurostimulator pulse generator, dual array, non-rechargeable, includes extension
L8689 External recharging system for battery (internal) for use with implantable neurostimulator
L8695 External recharging system for battery (external) for use with implantable neurostimulator
S3900 Surface electromyography

Other HCPCS codes related to the CPB:

J0475 Injection baclofen, 10 mg
J0476 Injection, baclofen, 50 mcg for intrathecal trial

ICD-10 codes covered if selection criteria are met:

M62.40 - M62.49 Contracture of muscle [refractory spasticity]
M62.830 - M62.838 Muscle spasm [refractory spasticity]
R25.0 - R25.9 Abnormal involuntary movements [refractory spasticity]

ICD-10 codes not covered for indications listed in the CPB:

E75.21 - E75.29 Other sphingolipidosis [progressive neurological disorders]
G20 - G26 Extrapyramidal and movement disorders [progressive neurological disorders]
G30.0 - G32.8 Other degenerative diseases of the nervous system [progressive neurological disorders]
G35 Multiple sclerosis
G45.0 - G45.9 Transient cerebral ischemic attacks and related syndromes[spasticity associated with disorders of consciousness following brain damage]
G81.10 - G81.14 Spastic hemiplegia
I69.898, I69.998 Other sequelae of other cerebrovascular disease [spasticity after stroke]
M21.171 - M21.179 Varus deformitym not elsewhere classified, ankle
M21.541 - M21.549 Acquired clubfoot
M24.50 - M24.576 Contracture of joint
M41.00 - M41.9 Scoliosis
M62.421 - M62.429 Contracture of muscle, upper arm [elbow spasticity]
M62.81 Muscle weakness (generalized) [profound in lower extremity muscles]
M62.838 Other muscle spasm [elbow spasticity]
Q66.0 Congenital talipes equinovarus
R25.2 - R25.9 Abnormal involuntary movements [elbow spasticity]
S12.000A - S12.9xxS, S22.000A - S22.9xxS, S32.000A - S32.9xxS Fracture of vertebral column [not covered for whole-body vibration]
S14.101A - S14.9xxS, S24.101A - S24.9xxS, S34.01xA - S34.9xxS Injury of nerves and spinal cord [not covered for whole-body vibration]

Kinesiotaping:

No specific code

ICD-10 codes not covered for indications listed in the CPB:

R25.0 - R25.9 Abnormal involuntary movements
R26.0 - R26.9 Abnormalities of gait and mobility

Focal muscle vibration:

No specific code

ICD-10 codes not covered for indications listed in the CPB:

I69.051 - I69.059, I69.151 - I69.159, I69.251 - I69.259, I69.351 - I69.359, I69.851 - I69.859, I69.951 - I69.959 Hemiplegia/hemiparesis
I69.031 - I69.049, I69.131 - I69.149, I69.231 - I69.249, I69.331 - I69.349, I69.831 - I69.849, I69.931 - I69.949 Monoplegia of upper and lower limb
M62.40 - M62.49, M62.830 - M62.838 Muscle spasm [limb spasticity]
R25.8 - R25.9 Abnormal involuntary movements [limb spasticity]

Percutaneous Myofascial Lengthening:

No specific code

ICD-10 codes not covered for indications listed in the CPB:

E75.00 - E75.6, F84.2
G31.81 - G31.82, G31.9
G93.89 - G94
Cerebral degenerations usually manifest in childhood [progressive neurological disorders]
G80.0 - G80.9 Cerebral palsy

Sensory Barrage Stimulation:

No specific code

ICD-10 codes not covered for indications listed in the CPB:

M62.421 - M62.429 Contracture of muscle, upper arm [elbow spasticity]
M62.838 Other muscle spasm [elbow spasticity]
R25.2 - R25.9 Abnormal involuntary movements [elbow spasticity]

The above policy is based on the following references:

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