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Aetna Aetna
Clinical Policy Bulletin:
Spasticity Management
Number: 0362


  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) rhizotomy*

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

    * 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.

  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.

See also CPB 0113 - Botulinum ToxinCPB 0161 - Infusion Pumps, and CPB 0677 - Functional Electrical Stimulation and Neuromuscular Electrical Stimulation.


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 (i) clonus, (ii) contraction of ipsilateral muscles not normally innervated by that nerve, (iii) contralateral muscle contraction, (iv) clinical or EMG contraction that continues after the cessation of stimulation, and (v) 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.

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.

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.: (i) 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 (ii) 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 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 range of motion (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.

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.

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 cerebral palsy 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, 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 postoperatively. At 2 years after the initial operation, all the children improved on their previous functional level; 34 children improved by one GMFCS level, and 5 children improved by two GMFCS levels. The overall improvement in mean GMFM scores was from 71.19 to 83.19.

CPT Codes / HCPCS Codes / ICD-9 Codes
CPT codes covered if selection criteria are met:
64708 - 64714
64600 - 64640
CPT codes not covered for indications listed in the CPB:
HCPCS codes not covered for indications listed in the CPB:
C1767 Generator, neurostimulator (implantable), non-rechargeable
C1778 Lead, neurostimulator (implantable)
C1816 Receiver and/or transmitter, neurostimulator (implantable)
C1883 Adapter/extension, pacing lead or neurostimulator lead (implantable)
G0295 Electromagnetic therapy, to one or more areas, for wound care other than described in G0329 or for other uses
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
Other HCPCS codes related to the CPB:
J0475 Injection baclofen, 10 mg
J0476 Injection, baclofen, 50 mcg for intrathecal trial
ICD-9 codes covered if selection criteria are met:
781.0 Abnormal involuntary movements [refractory spasticity]
728.85 Spasm of muscle [refractory spasticity]
ICD-9 codes not covered for indications listed in the CPB:
330.0 - 330.9 Cerebral degenerations usually manifest in childhood [progressive neurological disorders]
331.0 - 331.9 Other cerebral degenerations [progressive neurological disorders]
333.0 - 333.89 Other extrapyramidal diseases and abnormal movement disorders [progressive neurological disorders]
340 Multiple sclerosis
342.1 Spastic hemiplegia
718.40 - 718.49 Contracture of joint
728.87 Muscle weakness (generalized) [profound in lower extremity muscles]
72982 Cramp of limb
736.71 Acquired equinovarus deformity
737.30 - 737.39 Kyphoscoliosis and scoliosis
737.43 Scoliosis associated with other conditions
754.51 Talipes equinovarus [congenital]
805.00 - 806.9 Fracture of vertebral column [not covered for whole-body vibration]
952.00 - 952.9 Spinal cord injury without evidence of spinal bone injury [not covered for whole-body vibration]
Other ICD-9 codes related to the CPB:
343.0 - 343.9 Infantile cerebral palsy
344.00 - 344.89 Other specified paralytic syndromes
781.2 Abnormality of gait
781.3 Lack of coordination
There are no specific CPT/HCPCS codes for kinesiotaping:
ICD-9 codes not covered for indications listed in the CPB:
781.0 Abnormal involuntary movements
781.2 Abnormality of gait
Focal muscle vibration:
No specific code
ICD-9 codes not covered for indications listed in the CPB:
438.20-438.22 Hemiplegia/hemiparesis
438.30-438.32 Monoplegia of upper limb
728.85 Spasm of muscle [limb spasticity]
781.0 Abnormal involuntary movements[limb spasticity]
Percutaneous Myofascial Lengthening - no specific code:
ICD-9 codes not covered for indications listed in the CPB:
330.0 - 330.9 Cerebral degenerations usually manifest in childhood [progressive neurological disorders]
343.0 - 343.9 Infantile cerebral palsy
Focal Muscle Vibrations - no specific code:

The above policy is based on the following references:
  1. Brown E. Dorsal rhizotomy. JAMA. 1990;264:2569-2574.
  2. Park TS, Owen JH. Surgical management of spastic diplegia in cerebral palsy. N Engl J Med. 1992;326:745-749.
  3. Albright AL, Barry MJ, Fasick MP, Janosky J. Effects of continuous intrathecal baclofen infusion and selective posterior rhizotomy on upper extremity spasticity. Pediatr Neurosurg. 1995;23(2):82-85. 
  4. Craft S, Park TS, White DA, et al. Changes in cognitive performance in children with spastic diplegic cerebral palsy following selective dorsal rhizotomy. Pediatr Neurosurg. 1995;23(2):68-74; discussion 75. 
  5. Nishida T, Thatcher SW, Marty GR. Selective posterior rhizotomy for children with cerebral palsy: A 7-year experience. Childs Nerv Syst. 1995;11(7):374-380. 
  6. Wright FV, Sheil EM, Drake JM, et al. Evaluation of selective dorsal rhizotomy for the reduction of spasticity in cerebral palsy: A randomized controlled trial. Dev Med Child Neurol. 1998;40(4):239-247. 
  7. Subramanian N, Vaughan CL, Peter JC, Arens LJ. Gait before and 10 years after rhizotomy in children with cerebral palsy spasticity. J Neurosurg. 1998;88(6):1014-1019. 
  8. Engsberg JR, Olree KS, Ross SA, Park TS. Spasticity and strength changes as a function of selective dorsal rhizotomy. J Neurosurg. 1998;88(6):1020-1026. 
  9. Abdennebi B, Bougatene B. Selective neurotomies for relief of spasticity focalized to the foot and to the knee flexors. Results in a series of 58 patients. Acta Neurochir. 1996;138(8):917-920. 
  10. Feve A, Decq P, Filipetti P, et al. Physiological effects of selective tibial neurotomy on lower limb spasticity. J Neurol Neurosurg Psychiatry. 1997;63(5):575-578. 
  11. Msaddi AK, Mazroue AR, Shahwan S, et al. Microsurgical selective peripheral neurotomy in the treatment of spasticity in cerebral-palsy children. Stereotact Funct Neurosurg. 1997;69(1-4, Pt 2):251-258. 
  12. Chambers HG. The surgical treatment of spasticity. Muscle Nerve Suppl. 1997;6:S121-S128. 
  13. Sindou M, Jeanmonod D. Microsurgical DREZ-otomy for the treatment of spasticity and pain in the lower limbs. Neurosurgery. 1989;24(5):655-670. 
  14. Sindou M. Microsurgical DREZotomy (MDT) for pain, spasticity, and hyperactive bladder: A 20-year experience. Acta Neurochir. 1995;137(1-2):1-5. 
  15. Laha RK, Dujovny M, Osgood CP. Dorsal longitudinal myelotomy. Paraplegia. 1976;14(3):189-194.
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  17. Fogel JP, Waters RL, Mahomar F. Dorsal myelotomy for relief of spasticity in spinal cord injury patients. Clin Orthop. 1985;192:137-141. 
  18. Putty TK, Shapiro SA. Efficacy of dorsal longitudinal myelotomy in treating spinal spasticity: A review of 20 cases. J Neurosurg. 1991;75(3):397-401. 
  19. Midha M, Schmitt JK. Epidural spinal cord stimulation for the control of spasticity in spinal cord injury patients lacks long-term efficacy and is not cost-effective. Spinal Cord. 1998;36(3):190-192. 
  20. Institute for Clinical Systems Improvement (ICSI). Dorsal rhizotomy and intrathecal baclofen for lower extremity spasticity associated with cerebral palsy. Technology Assessment Report. Bloomington, MN: ICSI; 2000.
  21. Jacobs JM. Management options for the child with spastic cerebral palsy. Orthop Nurs. 2001;20(3):53-59.
  22. Narayanan U, Howard A. Selective dorsal rhizotomy in the management of children with spastic cerebral palsy (Protocol for Cochrane Review). Cochrane Database Syst Rev. 2001;(3):CD003360.
  23. Lazorthes Y, Sol JC, Sallerin B, et al. The surgical management of spasticity. Eur J Neurol. 2002;9(Suppl 1):35-41; discussion 53-61.
  24. McLaughlin J, Bjornson K, Temkin N, et al. Selective dorsal rhizotomy: Meta-analysis of three randomized controlled trials. Develop Med Child Neurol. 2002;44(1):17-25.
  25. Salame K, Ouaknine GE, Rochkind S, et al. Surgical treatment of spasticity by selective posterior rhizotomy: 30 years experience. Isr Med Assoc J. 2003;5(8):543-546.
  26. Ashworth NL, Satkunam LE, Deforge D. Treatment for spasticity in amyotrophic lateral sclerosis/motor neuron disease. Cochrane Database Syst Rev. 2006;(1):CD004156.
  27. Haselkorn JK, Balsdon Richer C, Fry Welch D, et al. Overview of spasticity management in multiple sclerosis. Evidence-based management strategies for spasticity treatment in multiple sclerosis. J Spinal Cord Med. 2005;28(2):167-199.
  28. Maarrawi J, Mertens P, Luaute J, et al. Long-term functional results of selective peripheral neurotomy for the treatment of spastic upper limb: Prospective study in 31 patients. J Neurosurg. 2006;104(2):215-225.
  29. National Institute for Health and Clinical Excellence (NICE). Selective dorsal rhizotomy for spasticity in cerebral palsy. Interventional Procedure Guidance 195. London, UK: NICE; November 2006.
  30. Centonze D, Koch G, Versace V, et al. Repetitive transcranial magnetic stimulation of the motor cortex ameliorates spasticity in multiple sclerosis. Neurology. 2007;68(13):1045-1050.
  31. Valle AC, Dionisio K, Pitskel NB, et al. Low and high frequency repetitive transcranial magnetic stimulation for the treatment of spasticity. Dev Med Child Neurol. 2007;49(7):534-538.
  32. Nordmark E, Josenby AL, Lagergren J, et al. Long-term outcomes five years after selective dorsal rhizotomy. BMC Pediatr. 2008;8:54.
  33. Taira T, Hori T. Selective peripheral neurotomy and selective dorsal rhizotomy. Brain Nerve. 2008;60(12):1427-1436.
  34. Marz-Loose H, Siemes H. Repetitive peripheral magnetic stimulation. Treatment option for spasticity? Nervenarzt. 2009 Dec;80(12):1489-1495.
  35. Ness LL, Field-Fote EC. Effect of whole-body vibration on quadriceps spasticity in individuals with spastic hypertonia due to spinal cord injury. Restor Neurol Neurosci. 2009;27(6):621-631.
  36. Schyns F, Paul L, Finlay K, et al. Vibration therapy in multiple sclerosis: A pilot study exploring its effects on tone, muscle force, sensation and functional performance. Clin Rehabil. 2009;23(9):771-781.
  37. Deltombe T, Gustin T. Selective tibial neurotomy in the treatment of spastic equinovarus foot in hemiplegic patients: A 2-year longitudinal follow-up of 30 cases. Arch Phys Med Rehabil. 2010;91(7):1025-1030.
  38. Karadag-Saygi E, Cubukcu-Aydoseli K, Kablan N, Ofluoglu D. The role of kinesiotaping combined with botulinum toxin to reduce plantar flexors spasticity after stroke. Top Stroke Rehabil. 2010;17(4):318-322.
  39. Bollens B, Deltombe T, Detrembleur C, et al. Effects of selective tibial nerve neurotomy as a treatment for adults presenting with spastic equinovarus foot: A systematic review. J Rehabil Med. 2011;43(4):277-282.
  40. Ashworth NL, Satkunam LE, Deforge D. Treatment for spasticity in amyotrophic lateral sclerosis/motor neuron disease. Cochrane Database Syst Rev. 2012;2:CD004156.
  41. Caliandro P, Celletti C, Padua L, et al. Focal muscle vibration in the treatment of upper limb spasticity: A pilot randomized controlled trial in patients with chronic stroke. Arch Phys Med Rehabil. 2012;93(9):1656-1661.
  42. Mitsiokapa EA et al. Selective percutaneous myofascial lengthening of the lower extremities in children with spastic cerebral palsy. Clin Podiatr Med Surg, 27(2): 335-43  2010.

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