Presentation on theme: "THE MANAGEMENT OF SPASTICITY AFTER SCI A SYSTEMATIC REVIEW (2000-2010)"— Presentation transcript:
THE MANAGEMENT OF SPASTICITY AFTER SCI A SYSTEMATIC REVIEW (2000-2010)
Systematic 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.
Systematic 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).
Shepherd Center Systematic Review Group Lesley Hudson, MS David Apple, MD Deborah Backus, PhD, PT Rebecca Acevedo Jennith Bernstein, PT Amanda Gillot, OT Ashley Kim, PT Elizabeth Sasso, PT Kristen Casperson, PT Anna Berry, PT Liz Randall, SPT Leadership Team:Reviewers: Data Coordinator:
Definitions of Spasticity Involuntary Velocity-dependent Increase resistance to stretch Abnormal processing of intraspinal processing of afferent (sensory) input Traditional 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.
Other Definitions Decqs 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
Evaluate Patient Does spasticity/ overactivity interfere significantly with function? Measures must include all aspects of spasticity Will it lead to musculoskeletal deformity? Patient Evaluation and Treatment Planning No treatment necessary Patient and caregiver objectives Identify patient and caregiver goals Functional Objectives Improve gait, hygiene, ADLs, pain relief, ease of care Decrease spasm frequency & severity Technical Objectives Promote tone reduction, improved range of motion, joint position Decrease spasm frequency Decrease hyperreflexia Spasticity Management Program No Yes MODIFIED from Spasticity Treatment Planning. WEMOVE.org, 2005.
Spasticity and its management in SCI is multi-faceted. Spasticity is no longer just an extremitys 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.
Positive 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. http://www.dinf.ne.jp/doc/english/global/davi d/dwe001/dwe001g/dwe00136g06.jpg
Negative Effects of Spasticity Spasticity may also lead to: Decreased range of motion (ROM) Inability to position the limbs safely Limited mobility Difficulty maintaining personal hygiene Discomfort and pain andgodlaughs.blogspot.com
Is 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?
Treatment Goals Relieve signs & symptoms Decrease frequency and severity of spasticity Improve function Gait Posture Reach and grasp for ADL Improve ease of care
Spasticity 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. 1999; Maynard, et al. 1990). Persons with cervical and motor incomplete injuries seem to have spasticity that is more frequent and more severe.
Conservative Treatment Options Pharmacological Management Baclofen – oral or pump (intrathecal) Adjunct Dantrolene, Zanax, or Valium Physical and Occupational Therapy Range of motion (ROM) exercises & prolonged stretching Casting or splinting Electrical stimulation - transcutaneous nerve stimulation (TENS) Acupuncture Massage
If other options dont 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.
Purpose of Review To 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).
Definitions of types of spasticity used in this review Velocity-dependent resistance = phasic spasticity of resistance felt when an extremity is moved quickly Hypertonia = tonic spasticity of increased resistance to movement throughout range Spasms = phasic spasticity of body movement into a flexor or extensor pattern Clonus = phasic spasticity of repeated movement of a body part when positioned with the muscle stretched Hyper-reflexia = increased reflex response
The Review Conducted by 7 clinicians. Included all articles published between 2000 and 2010 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.
Study 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.
Search 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.
StudyDefinition of Spasticity providedAspect of spasticity measured Bowden & Stokic 2008 Based 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 stretch Spasm frequency & severity Stretch reflex/hyperreflexia Flexion withdrawal Kumru, et al. 2010 Based 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 stretch Passive resistance to stretch Clonus Spasm frequency & severity Stretch reflex/hyperreflexia Stiffness Ness & Field-Foté 2009 Own definition: …spastic hypertonia with increased reflex excitability and disordered motor output (i.e. spasticity, clonus, spastic gait patterns)… Stretch reflex/quadriceps hyperreflexia
Study Definition of Spasticity provided Aspect of spasticity measured Chung & Cheng 2009 none provided Velocity-dependent resistance to stretch Passive resistance Clonus Kakebeeke TH, et al. 2005 none provided Velocity-dependent resistance to stretch Krause P et al. 2008 none provided Passive resistance to stretch Stretch reflex/quadriceps hyperreflexia Pinter MM, et al 2000 none provided Passive resistance to stretch Spasm frequency Stretch reflex/quadriceps hyperreflexia
Experimental 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.
Experimental Study Design: RCT of TENS StudyIntervention Study Design Outcome Measures Participant Characteristics Chung BPH, Cheng BKK 2009 60 mins active TENS or 60 mins placebo; over the common peroneal nerve RCT, n=18 Composite Spasticity Score Full range passive ankle dorsiflexion Ankle clonus 14 male; 4 female 24-77 y.o. C4-T12 AIS A, B, C, D 4 weeks to 364 weeks (approx. 5.5 years) post-SCI
Results: 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
Experimental Study Design: RCT of TMS StudyIntervention Study Design Outcome Measures Participant Characteristics Kumru H, Murillo N, Samso JV, et al. 2010 Repetitive Transcranial Magnetic Stimulation (TMS) RCT with cross- over for sham group, n=15 MAS VAS MPSFS SCAT SCI-SET Hmax/Mmax, T Reflex & Withdrawal Reflex 12 male; 3 female 15-68 y.o. C4-T12 AIS C, D 2-17 months post-SCI
RCT of TMS: Sample Notes 11 of 15 using Baclofen 4 of 15 on no anti-spasticity meds Not all traumatic SCIs: 4 of 15 etiology = tumor 4 of 15 etiology = myelitis Kumru et al., 2010
Results: 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 SCI MPSFS (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
Results (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
Experimental 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: – Clonus – Hypertonia – Hyper-reflexia – Velocity-dependent resistance to stretch – Spasms
Descriptive Study Design: Longitudinal Study, Epidural E-stim StudyInterventionStudy DesignOutcome MeasuresParticipant Characteristics Pinter et al. 2000 Epidural electrical stimulation Longitudinal, n=8 EMG during passive stretch of LE & Pendulum Test Ashworth Scale Clinical rating scale 4 male; 4 female 18-34 y.o. C5-T6, AIS A, B, C 19-94 months post-SCI
Results: 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 independently Ashworth score (p=0.0117) 7 of 8 participants discontinued anti-spasticity medication. Pinter et al., 2000
Descriptive Study Design: Case Study with Baclofen StudyInterventionStudy Design Outcome MeasuresParticipant Characteristics Bowden M, Stokic DS. 2008 Pharma- cologic, intrathecal Baclofen Single subject case report Ashworth Scale Lower extremity strength using ISCSCI EMG H-Reflex Plantar Withdrawal Reflex Maximal Voluntary Dorsiflexion Male 41 y.o. T11, AIS D 8 years post- SCI
Strength Decreased, BUT Spasticity Decreased More Dose-dependent decrease in: Ashworth score (p<0.01) Bilateral lower extremity strength (p<0.001) H/M ratio EMG amplitude and duration of the plantar withdrawal reflex Decrease in strength was less than decrease in spasticity. After withdrawal of medication, the rebound in spasticity was less than increase in strength.
Descriptive Study Design: Pre-Post with Passive LE Cycling StudyInterventionStudy Design Outcome MeasuresParticipant Characteristics Kakebeeke et al. 2005 30 mins passive lower extremity ergometry Pre- Post, n=10 Isokinetic dynamometry in sitting & lying; movements of leg at 10°/sec & 120°/sec; taken before, after, & 1 week post passive cycling session 9 male; 1 female 23-60 y.o. C6-T12 AIS A, B 1-25 years post-SCI
Results: 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
Descriptive Study Design: Cross-over, FES & Passive Cycling StudyInterventionStudy Design Outcome MeasuresParticipant Characteristics Krause P, et al. 2008 Functional electrical stimulation cycling, Passive cycling Cross- over, n=5 Modified AS Pendulum Test Torque, used to determine peak velocity and relaxation index 3 male; 2 female 37-66 y.o. T3-T7, AIS A 3-9 years post- SCI
Results: 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.
Descriptive Study Design: Longitudinal, Whole Body Vibration StudyInterventionStudy DesignOutcome MeasuresParticipant SCI Characteristics Ness LL, Field-Foté EC, 2009 Whole Body Vibration Longitudinal, n=16 Pendulum test 14 male; 3 female 28-65 y.o. C4-T8 AIS C, D > 1 year post- SCI
Results: Long Lasting Effects with WBV Significant reduction in quadriceps spasticity (p=0.005). Significant reduction within session (range p=0.005 to 0.006 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
Medications Varied 7 of 16 on Baclofen 1 of 16 on Tizanidine 9 of 16 on no spasticity medication Ness LL, Field-Foté EC, 2009
Descriptive Study Design: Summary of Studies Studies provide further support that: 1.stimulating the nervous system (e.g. electrical stimulation), OR 2.altering the excitability in the nervous system (e.g. Baclofen) leads to a reduction in spasticity in persons with complete or incomplete tetraplegia or paraplegia.
Methodological 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).
Study Limitations Studies 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.
Study Limitations There were no functional assessments. Whether reducing spasticity is necessary and sufficient for improving motor control and function remains unclear.
Study Limitations Spasticity 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.
Recommendations Any 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.
Recommendations It 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.
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