Presentation on theme: "The Management of Spasticity after SCI A Systematic Review ( )"— Presentation transcript:
1The Management of Spasticity after SCI A Systematic Review (2000-2010)
2Systematic Review – Management of Spasticity Compiled by the Shepherd Center Study Group in Atlanta, GA. Innovative Knowledge Dissemination & Utilization Project for Disability & Professional Stakeholder Organizations/ NIDRR Grant # (H133A050006) at Boston University Center for Psychiatric Rehabilitation.
3Systematic Review – Management of Spasticity A review was conducted using a system for rating the rigor and meaning of disability research (Farkas, Rogers and Anthony, 2008).The first instrument in this system is: “Standards for Rating Program Evaluation, Policy or Survey Research, Pre-Post and Correlational Human Subjects” (Rogers, Farkas, Anthony & Kash, 2008???) and “Standards for Rating the Meaning of Disability Research” (Farkas & Anthony, 2008).
4Shepherd Center Systematic Review Group Leadership Team:Reviewers:Lesley Hudson, MSDavid Apple, MDDeborah Backus, PhD, PTRebecca AcevedoJennith Bernstein, PTAmanda Gillot, OTAshley Kim, PTElizabeth Sasso, PTKristen Casperson, PTAnna Berry, PTLiz Randall, SPTData Coordinator:
5Definitions of Spasticity InvoluntaryVelocity-dependentIncrease resistance to stretchAbnormal processing of intraspinal processing of afferent (sensory) inputTraditional and most referenced: Lance, 1980:“Spasticity is a motor disorder characterized by a velocity- dependent increase in tonic stretch reflexes (muscle tone) with exaggerated tendon jerks, resulting from hyperexcitability of the stretch reflex, as one component of the upper motor neuron syndrome.”
6Other DefinitionsDecq’s definition, 2003 : “…a symptom of the upper motor neuron syndrome characterized by an exaggeration of the stretch reflex secondary to hyperexcitability of spinal reflexes.” It separates:Intrinsic tonic spasticity: exaggeration of the tonic component of the stretch reflex (hypertonia).Intrinsic phasic spasticity: exaggeration of the phasic component of the stretch reflex (hyper-reflexia, clonus, velocity-dependent resistance?).Extrinsic spasticity: exaggeration of extrinsic flexion or extension spinal reflexes (spasms?,).Adams & Hicks, Spinal Cord, 2005
7Patient Evaluation and Treatment Planning Evaluate PatientDoes spasticity/ overactivity interfere significantly with function?Measures must include all aspects of spasticityWill it lead to musculoskeletal deformity?Patient EvaluationandTreatment PlanningNo treatment necessaryNoYesPatient and caregiver objectivesIdentify patient and caregiver goalsFunctional ObjectivesImprove gait, hygiene, ADLs, pain relief, ease of careDecrease spasm frequency & severityTechnical ObjectivesPromote tone reduction, improved range of motion, joint positionDecrease spasm frequencyDecrease hyperreflexiaSpasticity Management ProgramMODIFIED from Spasticity Treatment Planning. WEMOVE.org, 2005.
8Spasticity and its management in SCI is multi-faceted. Spasticity is no longer just an extremity’s resistance to quick movement.It includes spasms, overall hypertonia, and clonus.The optimal treatment for each of these different aspects of spasticity is not yet clear.The literature related to spasticity has not been evaluated in terms of what is meaningful to persons with SCI.
9Positive Effects of Spasticity Spasticity may:Be used to help with transfers, walking, ADL.Help keep the muscles from decreasing in size.Muscles may appear to be healthier after SCI.
10Negative Effects of Spasticity Spasticity may also lead to:Decreased range of motion (ROM)Inability to position the limbs safelyLimited mobilityDifficulty maintaining personal hygieneDiscomfort and painandgodlaughs.blogspot.com
11Is Treatment Necessary? If mild, wait and see?Questions to ask:Does it cause pain?Interfere with sleep?Make function unsafe?Cause secondary issues of -Poor posture / asymmetric seating?Pressure sores?Make care difficult?Affect hygiene?Will treatment improve quality of life and safety?
12Treatment Goals Relieve signs & symptoms Decrease frequency and severity of spasticityImprove functionGaitPostureReach and grasp for ADLImprove ease of care
13Spasticity is an ongoing problem, despite treatment options. Traditional and surgical treatment options are routinely used to decrease spasticity…Yet, many persons with SCI continue to have problems related to spasticity:More than half of all persons surveyed with chronic SCI report symptoms and sequelae of spasticity (Sköld, et al ; Maynard, et al. 1990).Persons with cervical and motor incomplete injuries seem to have spasticity that is more frequent and more severe.
14Conservative Treatment Options Pharmacological ManagementBaclofen – oral or pump (intrathecal)Adjunct Dantrolene, Zanax, or ValiumPhysical and Occupational TherapyRange of motion (ROM) exercises & prolonged stretchingCasting or splintingElectrical stimulation - transcutaneous nerve stimulation (TENS)AcupunctureMassage
15If other options don’t work… Surgery involves cutting pathways in the nervous system thought to be involved in spasticity.However, forms of electrical stimulation of the spinal cord (epidural spinal cord stimulation) and brain (transcutaneous magnetic stimulation - TMS) may mimic the effects of surgical interventions.
16Purpose of ReviewTo evaluate all published research from the past 10 years related to the management of spasticity after spinal cord injury (SCI) to determine which evidence may be:Meaningful to persons with SCI who have spasticity (e.g. includes level and completeness of injury).Related to any type of spasticity a person may experience (velocity-dependent resistance, spasms, hypertonia, clonus).
17Definitions of types of spasticity used in this review Velocity-dependent resistance = phasic spasticity of resistance felt when an extremity is moved quicklyHypertonia = tonic spasticity of increased resistance to movement throughout rangeSpasms = phasic spasticity of body movement into a flexor or extensor patternClonus = phasic spasticity of repeated movement of a body part when positioned with the muscle stretchedHyper-reflexia = increased reflex response
18The Review Conducted by 7 clinicians. Included all articles published between 2000 and related to the treatment of spasticity in persons with SCI.All articles rated on quality of the science & meaningfulness to persons with SCI, or their caregivers and clinicians, or payers.Any article of high quality that was meaningful was considered for this summary.
19Study Designs Accepted for Review Experimental: Employed methods including a random assignment and a control group or a reasonably constructed comparison group.Quasi-experimental: No random assignment, but either with a control group or a reasonably constructed comparison group.Descriptive: Neither a control group, nor randomization, is used. These included case studies and reports, studies employing repeated measures, and pre-post designs.
20Search Results Of 49 papers reviewed: Seven papers met criteria of quality and meaningfulness.Only 3 of the 7 papers defined spasticity.Each of the 7 papers used different outcome measures of spasticity.Ongoing problems with research in this area.
21Definition of Spasticity provided Aspect of spasticity measured StudyDefinition of Spasticity providedAspect of spasticity measuredBowden & Stokic 2008Based on Lance, 1980: “…a motor disorder characterized by a velocity-dependent increase in tonic stretch reflex with exaggerated tendon jerks, resulting from hyperexcitability of the stretch reflex, as one component of upper motor neuron syndrome”; “…include clonus, involuntary muscle contractions or spasms, and muscle co-contraction.”Passive resistance to stretchSpasm frequency & severityStretch reflex/hyperreflexiaFlexion withdrawalKumru, et al. 2010Based on Decq, 2003: “…a symptom of upper motor neuron syndrome, characterized by an exaggeration of the stretch reflex, spasms, and resistance to passive movement across a joint, secondary to hyperexcitability of spinal reflexes.”Velocity-dependent resistance to stretchClonusStiffnessNess & Field-Foté 2009Own definition: “…spastic hypertonia with increased reflex excitability and disordered motor output (i.e. spasticity, clonus, spastic gait patterns)…”Stretch reflex/quadriceps hyperreflexia
22Definition of Spasticity provided Aspect of spasticity measured StudyDefinition of Spasticity providedAspect of spasticity measuredChung & Cheng 2009none providedVelocity-dependent resistance to stretchPassive resistanceClonusKakebeeke TH, et al. 2005Krause P et al. 2008Passive resistance to stretchStretch reflex/quadriceps hyperreflexiaPinter MM, et al 2000Spasm frequency
23Experimental Study Design: Overview 2 of 7 studies used a randomized controlled trial (RCT).Both of these studies used electrical stimulation for the treatment.2 studies were longitudinal cohort designs.1 study was a case study.1 study used a pre-post design.1 study used a cross-over design.
24Experimental Study Design: RCT of TENS InterventionStudy DesignOutcome MeasuresParticipant CharacteristicsChung BPH, Cheng BKK 200960 mins active TENS or 60 mins placebo; over the common peroneal nerveRCT,n=18Composite Spasticity ScoreFull range passive ankle dorsiflexionAnkle clonus14 male; 4 female24-77 y.o.C4-T12AIS A, B, C, D4 weeks to 364 weeks (approx. 5.5 years) post-SCI
25Results: Reduction in Resistance and Clonus with TENS TENS group showed significant decrease in:Composite Spasticity Score (29.5%, p=0.017)Resistance to full passive range at ankle dorsiflexion (31%, p=0.024)Ankle clonus (29.6%, p=0.023)Notes:Anti-spasticity medications were allowed.No significant differences between groups at baseline.Chung & Cheng 2009
26Experimental Study Design: RCT of TMS InterventionStudy DesignOutcome MeasuresParticipant CharacteristicsKumru H, Murillo N, Samso JV, et al. 2010Repetitive Transcranial Magnetic Stimulation (TMS)RCT with cross- over for sham group,n=15MASVASMPSFSSCATSCI-SETHmax/Mmax, T Reflex & Withdrawal Reflex12 male; 3 female15-68 y.o.C4-T12AIS C, D2-17 months post-SCI
27RCT of TMS: Sample Notes 11 of 15 using Baclofen4 of 15 on no anti-spasticity medsNot all traumatic SCIs:4 of 15 etiology = tumor4 of 15 etiology = myelitisKumru et al., 2010
28Results: Decrease in Some Spasticity, Motor Control Still Disordered Neurophysiological function did not change.TMS group, but not sham group, significantly decreased:MAS score (p<0.006)not significantly different between those with traumatic & non- traumatic SCIMPSFS (p=0.01)SCATS (p<0.04)SCI-SET (p=0.003)MAS, SCATS, & SCI-SET results maintained one week after last session (p=0.049).Kumru et al., 2010
29Results (cont.):14 of 15 reported significant improvement in pain on VAS (p<0.002).Was maintained in 13 of 15 at end of the week after TMS (p=0.004)No significant change in measures when sham only.Kumru et al., 2010
30Experimental Study Design: Summary of RCTs In persons with acute or chronic, motor complete or incomplete, paraplegia or tetraplegia, applying electrical stim peripherally (i.e. at the common peroneal nerve or the nerve innervating the muscle antagonistic to the spastic muscle, Chung & Cheng, 2009) or centrally (i.e. over the primary motor cortex, Kumru et al., 2010) led to a significant reduction in several different aspects of spasticity:ClonusHypertoniaHyper-reflexiaVelocity-dependent resistance to stretchSpasms
31Descriptive Study Design: Longitudinal Study, Epidural E-stim InterventionStudy DesignOutcome MeasuresParticipant CharacteristicsPinter et al. 2000Epidural electrical stimulationLongitudinal,n=8EMG during passive stretch of LE & Pendulum TestAshworth ScaleClinical rating scale4 male; female18-34 y.o.C5-T6, AIS A, B, C19-94 months post-SCI
32Results: Epidural Stim Reduced Some Aspects of Spasticity Significant reduction in:EMG activity in left and right LEs (p=0.004, p=0.0035, respectively).Except for quadriceps when analyzed independentlyAshworth score (p=0.0117)7 of 8 participants discontinued anti-spasticity medication.Pinter et al., 2000
33Descriptive Study Design: Case Study with Baclofen InterventionStudy DesignOutcome MeasuresParticipant CharacteristicsBowden M, Stokic DS. 2008Pharma-cologic,intrathecal BaclofenSingle subject case reportAshworth ScaleLower extremity strength using ISCSCIEMGH-ReflexPlantar Withdrawal ReflexMaximal Voluntary DorsiflexionMale41 y.o.T11, AIS D8 years post-SCI
34Strength Decreased, BUT Spasticity Decreased More Dose-dependent decrease in:Ashworth score (p<0.01)Bilateral lower extremity strength (p<0.001)H/M ratioEMG amplitude and duration of the plantar withdrawal reflexDecrease in strength was less than decrease in spasticity.After withdrawal of medication, the rebound in spasticity was less than increase in strength.
35Descriptive Study Design: Pre-Post with Passive LE Cycling InterventionStudy DesignOutcome MeasuresParticipant CharacteristicsKakebeeke et al. 200530 mins passive lower extremity ergometryPre-Post,n=10Isokinetic dynamometry in sitting & lying; movements of leg at 10°/sec & 120°/sec; taken before, after, & 1 week post passive cycling session9 male; female23-60 y.o.C6-T12AIS A, B1-25 years post-SCI
36Results: Torque Same, BUT Reports of Reduced Spasticity No change in elicited peak torque before, immediately after, or one week after passive cycling.6 of 10 participants reported reduced spasticity immediately after cycling.Kakebeeke et al., 2005
37Descriptive Study Design: Cross-over, FES & Passive Cycling InterventionStudy DesignOutcome MeasuresParticipant CharacteristicsKrause P, et al. 2008Functional electrical stimulation cycling, Passive cyclingCross- over,n=5Modified ASPendulum TestTorque, used to determine peak velocity and relaxation index3 male; female37-66 y.o.T3-T7, AIS A3-9 years post-SCI
38Results: Both Active & Passive Cycling Show Some Effects Greater & significant increase in relaxation index (RI) after FES cycling (68%) than after passive cycling (12%) (p=0.01).Peak velocity (PV) significantly increased after FES cycling, unchanged after passive cycling (p=0.01).MAS decreased significantly for both FES cycling (p<0.001) and passive cycling (p<0.05).Note: Participants were not on spasticity medications.
39Descriptive Study Design: Longitudinal, Whole Body Vibration InterventionStudy DesignOutcome MeasuresParticipant SCI CharacteristicsNess LL, Field-Foté EC, 2009Whole Body VibrationLongitudinal,n=16Pendulum test14 male; female28-65 y.o.C4-T8AIS C, D> 1 year post-SCI
40Results: Long Lasting Effects with WBV Significant reduction in quadriceps spasticity (p=0.005).Significant reduction within session (range p= to for weeks 1,2,4).No significant difference between those on anti- spasticity meds and those not.Effects lasted at least 6-8 weeks post-intervention.Ness LL, Field-Foté EC, 2009
41Medications Varied 7 of 16 on Baclofen 1 of 16 on Tizanidine 9 of 16 on no spasticity medicationNess LL, Field-Foté EC, 2009
42Descriptive Study Design: Summary of Studies Studies provide further support that:stimulating the nervous system (e.g. electrical stimulation), ORaltering the excitability in the nervous system (e.g. Baclofen)leads to a reduction in spasticity in persons with complete or incomplete tetraplegia or paraplegia.
43Methodological Considerations Definitions of spasticity differ:A motor disorder characterized by a velocity-dependent increase in tonic stretch reflex, exaggerated tendon jerks; includes clonus, involuntary muscle contractions or spasms, and muscle co-contraction (Lance, 1980)Includes intrinsic tonic spasticity (i.e. the exaggeration of the tonic component of the stretch reflex, hypertonia), intrinsic phasic spasticity (i.e. the exaggeration of the phasic component of the stretch reflex or hyper-reflexia and clonus), and extrinsic spasticity, (i.e., the exaggeration of extrinsic flexion or extension spinal reflexes, spasms) (Adams & Hicks, 2005).Should also consider the musculoskeletal effects of spasticity, namely muscle shortening and contractures (Gracies et al., 1997).
44Study LimitationsStudies included persons with chronic SCI, who may have musculoskeletal (MS) consequences to chronic spasticity.MS parameters were not assessed in any of these studies. Further study is warranted to determine if there are long-term effects of these interventions and if these effects include both neural and musculoskeletal effects.Improving one and not the other may preclude maximal improvements.
45Study Limitations There were no functional assessments. Whether reducing spasticity is necessary and sufficient for improving motor control and function remains unclear.
46Study LimitationsSpasticity syndrome may be worse in people with cervical and incomplete injuries than those with thoracic and complete Injuries.(Kirshblum, 1999; Maynard et al, 1990; Sköld et al, 1999).Even though studies included persons with complete and incomplete paraplegia and tetraplegia, as well as acute and chronic injuries, results were reported as a whole.It remains unknown whether there is a differential response to the interventions.Further study is warranted to determine the response in those with different levels, classifications, and time since SCI.
47RecommendationsAny stakeholder interested in the evidence related to the management of spasticity after SCI should consider:Outcome measures differed across all studies.Different aspects of spasticity may be affected by a given intervention.For instance, if spasms are the worse aspect of spasticity, rTMS, eSCS, or baclofen (all with evidence of reducing spasms in persons with SCI) may be pursued.Those with velocity-dependent resistance to stretch may choose TENS or rTMS, but rTMS may give the best results overall if there are multiple areas related to spasticity.
48RecommendationsIt is unknown from these studies:How each intervention affects spasticity in persons with different levels, completeness, and acuity of injury.How each intervention affects musculoskeletal tissues.Neural changes without accompanying musculoskeletal changes may preclude functional improvements.
49ReferencesAshworth B, Preliminary trial of carisoprodol in multiple sclerosis. Practitioner, 192:Bovend'Eerdt TJ, Newman M, Barker K, Dawes H, Minelli C, Wade DT, The Effects of Stretching in Spasticity: A Systematic Review. Arch Phys Med Rehabil, 89(7):Bowden M, Stokic DS, Clinical and Neurophysiologic Assessment of Strength and Spasticity During Intrathecal Baclofen Titration in Incomplete Spinal Cord Injury: Single - Subject Design. J Spinal Cord Med, 32(2):Chung BPH, Cheng BKK, Immediate effect of transcutaneous electrical nerve stimulation on spasticity in patients with spinal cord injury. Clinical Rehabilitation, 24(3):Farkas, M., & Anthony, W., Standards for Rating the Meaning of Disability Research. Boston: Boston University, Center for Psychiatric Rehabilitation.Farkas, M., Rogers, E., & Anthony, W., Systematic review procedures for rating the rigor and the meaning of disability research. Boston: Boston University, Center for Psychiatric Rehabilitation.Kakebeeke TH, Lechner HE, Knapp PA, The effect of passive cycling movements on spasticity after spinal cord injury: preliminary results. Spinal Cord, 43(8):Katz RT, Rovai GP, Brait C, Rymer WZ Objective quantification of spastic hypertonia: correlation with clinical findings. Arch Phys Med Rehabil, 73(4):Kirshblum S, Treatment alternatives for spinal cord injury related spasticity. J Spinal Cord Med. 22(3):Krause P, Szecsi J, and Straube A, Changes in spastic muscle tone increase in patients with spinal cord injury using functional electrical stimulation and passive leg movement. Clinical Rehabilitation, 22(7):Kumru H, Murillo N, Samso JV, et al, Reduction of Spasticity with Repetitive Transcranial Magnetic Stimulation in Patients with Spinal Cord Injury. Neurorehabilitation and Neural Repair, 24(5):Lance JW, Spasticity: disordered motor control (Year Book). In: Feldman R, Young R, Koella W, eds. Symposium Synopsis. Chicago, IL: Medical Publishers,
50References (cont.)Levin MF, Hui-Chan CW, Relief of hemiparetic spasticity by TENS is associated with impromvement in reflex and voluntary motor functions. Electroencephalogr Clin Neurophysiol, 85(2):Marino R, editor , Reference manual for the international standards for neurological classification of spinal cord injury. Chicago, IL: American Spinal Injury Association.Maynard FM, Karunas RS, Waring WP 3rd , Epidemiology of spasticity following traumatic spinal cord injury. Arch Phys Med Rehabil, 71(8):Ness LL, and Field-Foté EC, Effect of whole-body vibration on quadriceps spasticity in individuals with spastic hypertonia due to spinal cord injury. Restorative Neurology and Neuroscience, 27(6):O'Dwyer NJ, Ada L, Neilson PD, Spasticity and muscle contracture following stroke. Brain, 119(Pt 5):Pinter MM, Gerstenbrand F, Dimitrijevic MR, Epidural electrical stimulation of posterior structures of the human lumbosacral cord: 3. Control of spasticity. Spinal Cord, 38(9):Rogers, E., Farkas, M., Anthony, W., & Kash, M, Standards for Rating Program Evaluation, Policy, Survey, Pre- post, or Correlational Human Subjects Studies. Boston: Boston University, Center for Psychiatric Rehabilitation.Sköld C, Levi R, Seiger A, Spasticity after traumatic spinal cord injury: nature, severity, and location. Arch Phys Med Rehabil. 80(12):Sköld C, Spasticity in spinal cord injury: self- and clinically rated intrinsic fluctuations and intervention-induced changes. Arch Phys Med Rehabil, 81(2):Taricco M, Pagliacci MC, Telaro E, Adone R, Pharmacological interventions for spasticity following spinal cord injury: results of a Cochrane systematic review. Eura Medicophys. 42(1):5-15.