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.
Download ReportTranscript 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.
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
Leadership Team:
Lesley Hudson, MS David Apple, MD Deborah Backus, PhD, PT
Data Coordinator:
Rebecca Acevedo
Reviewers:
Jennith Bernstein, PT Amanda Gillot, OT Ashley Kim, PT Elizabeth Sasso, PT Kristen Casperson, PT Anna Berry, PT Liz Randall, SPT
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
Decq’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
Patient Evaluation and Treatment Planning Evaluate Patient
Does spasticity/ overactivity interfere significantly with function?
Measures must include all aspects of spasticity Will it lead to musculoskeletal deformity?
Yes No 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
MODIFIED from Spasticity Treatment Planning. WEMOVE.org, 2005.
Spasticity 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.
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 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.
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.
Study Definition of Spasticity provided Aspect 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
Chung & Cheng 2009
Definition of Spasticity provided
none provided
Aspect of spasticity measured
Velocity-dependent resistance to stretch Passive resistance Clonus Velocity-dependent resistance to stretch Kakebeeke TH, et al. 2005 none provided none provided Krause P et al. 2008 none provided Pinter MM, et al 2000 Passive resistance to stretch Stretch reflex/quadriceps hyperreflexia 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
Study
Chung BPH, Cheng BKK 2009
Intervention
60 mins active TENS or 60 mins placebo; over the common peroneal nerve
Study Design
RCT, n=18
Outcome Measures
Composite Spasticity Score Full range passive ankle dorsiflexion Ankle clonus
Participant Characteristics
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
Study
Kumru H, Murillo N,
Intervention
Repetitive Transcranial Samso JV, et al. Magnetic 2010 Stimulation (TMS)
Study Design Outcome Measures
RCT with cross- over for sham group, n=15 MAS VAS MPSFS SCAT SCI-SET Hmax/Mmax, T Reflex & Withdrawal Reflex
Participant Characteristics
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
Study
Pinter et al. 2000
Intervention Study Design
Epidural electrical stimulation Longitudinal, n=8
Outcome Measures Participant Characteristics
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
Study
Bowden M, Stokic DS. 2008
Intervention
Pharma cologic, intrathecal Baclofen
Study Design
Single subject case report
Outcome Measures
Ashworth Scale Lower extremity strength using ISCSCI EMG H-Reflex Plantar Withdrawal Reflex Maximal Voluntary Dorsiflexion
Participant Characteristics
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
Study
Kakebeeke et al. 2005
Intervention
30 mins extremity ergometry
Study Design
Pre passive lower Post, n=10
Outcome Measures Participant Characteristics
Isokinetic dynamometry in 9 male; sitting & lying; movements of leg at 10 ° /sec & 120 ° /sec; taken before, after, & 1 week post passive cycling session 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
Study
Krause P, et al. 2008
Intervention
Functional electrical stimulation cycling, Passive cycling
Study Design
Cross over, n=5
Outcome Measures
Modified AS Pendulum Test Torque, used to determine peak velocity and relaxation index
Participant Characteristics
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
Study
Ness LL, Field-Foté EC, 2009
Intervention Study Design
Whole Body Vibration Longitudinal, n=16
Outcome Measures
Pendulum test
Participant SCI Characteristics
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
1.
Studies provide further support that: 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.
References
3.
4.
1.
2.
3.
4.
1.
2.
5.
6.
Ashworth B, 1964. Preliminary trial of carisoprodol in multiple sclerosis. Practitioner, 192: 540-542.
Bovend'Eerdt TJ, Newman M, Barker K, Dawes H, Minelli C, Wade DT, 2008. The Effects of Stretching in Spasticity: A Systematic Review.
Arch
Phys Med Rehabil, 89(7):1395-1406.
Bowden M, Stokic DS, 2009. 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):183-90.
Chung BPH, Cheng BKK, 2010. Immediate effect of transcutaneous electrical nerve stimulation on spasticity in patients with spinal cord injury. Clinical Rehabilitation, 24(3):202-210.
Farkas, M., & Anthony, W., 2008. Standards for Rating the Meaning of Disability Research. Boston: Boston University, Center for Psychiatric Rehabilitation.
Farkas, M., Rogers, E., & Anthony, W., 2008. 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, 2005. The effect of passive cycling movements on spasticity after spinal cord injury: preliminary results. Spinal Cord, 43(8):483-488.
Katz RT, Rovai GP, Brait C, Rymer WZ. 1994. Objective quantification of spastic hypertonia: correlation with clinical findings.
Arch
Phys Med Rehabil, 73(4):339-347.
Kirshblum S, 1999. Treatment alternatives for spinal cord injury related spasticity.
J Spinal Cord Med. 22(3):199-217.
Krause P, Szecsi J, and Straube A, 2008. Changes in spastic muscle tone increase in patients with spinal cord injury using functional electrical stimulation and passive leg movement. Clinical Rehabilitation, 22(7):627-634.
Kumru H, Murillo N, Samso JV, et al, 2010. Reduction of Spasticity with Repetitive Transcranial Magnetic Stimulation in Patients with Spinal Cord Injury. Neurorehabilitation and Neural Repair, 24(5):435-441.
Lance JW, 1980. Spasticity: disordered motor control (Year Book). In: Feldman R, Young R, Koella W, eds. Symposium Synopsis. Chicago, IL: Medical Publishers, 485-500.
References (cont.)
11.
12.
13.
14.
15.
16.
17.
18.
19.
20.
Levin MF, Hui-Chan CW, 1992. Relief of hemiparetic spasticity by TENS is associated with impromvement in reflex and voluntary motor functions. Electroencephalogr Clin Neurophysiol, 85(2):131-142. Marino R, editor , 2003. 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 3 rd , 1990. Epidemiology of spasticity following traumatic spinal cord injury. Arch Phys Med Rehabil, 71(8):566-569.
Ness LL, and Field-Foté EC, 2009. Effect of whole-body vibration on quadriceps spasticity in individuals with spastic hypertonia due to spinal cord injury. Restorative Neurology and Neuroscience, 27(6):621-631.
O'Dwyer NJ, Ada L, Neilson PD, 1996. Spasticity and muscle contracture following stroke. Brain, 119(Pt 5):1737 1749.
Pinter MM, Gerstenbrand F, Dimitrijevic MR, 2000. Epidural electrical stimulation of posterior structures of the human lumbosacral cord: 3. Control of spasticity. Spinal Cord, 38(9):524-531.
Rogers, E., Farkas, M., Anthony, W., & Kash, M, 2008. 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, 1999. Spasticity after traumatic spinal cord injury: nature, severity, and location.
Phys Med Rehabil. 80(12):1548-1557.
Arch
Sköld C, 2000. Spasticity in spinal cord injury: self- and clinically rated intrinsic fluctuations and intervention-induced changes.
Arch
Phys Med Rehabil, 81(2):144-149.
Taricco M , Pagliacci MC , Telaro E , Adone R , 2006. Pharmacological interventions for spasticity following spinal cord injury: results of a Cochrane systematic review. Eura Medicophys. 42(1):5-15.