the management of spasticity after sci a systematic review (2000-2010)
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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
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
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 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/david/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 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
StudyDefinition of
Spasticity providedAspect of spasticity measured
Chung & Cheng 2009
none provided Velocity-dependent resistance to stretch Passive resistanceClonus
Kakebeeke TH, et al. 2005
none provided Velocity-dependent resistance to stretch
Krause P et al. 2008
none provided Passive resistance to stretchStretch reflex/quadriceps hyperreflexia
Pinter MM, et al 2000
none provided Passive resistance to stretchSpasm frequencyStretch 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
StudyInterventio
n
Study Desig
n
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
Study Intervention
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
Study Intervention
Study Design
Outcome Measures
Participant Characterist
icsPinter 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
Study Intervention
Study Desig
n
Outcome Measures Participant Characterist
icsBowden 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
Study Intervention
Study Desig
n
Outcome Measures Participant Characterist
icsKakebeeke 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
Study Intervention
Study Design
Outcome Measures Participant Characteristi
csKrause 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
Study Intervention
Study Design
Outcome Measures
Participant 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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