The Management of Spasticity after SCI A
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Transcript The Management of Spasticity after SCI A
THE MANAGEMENT OF
SPASTICITY AFTER SCI
A SYSTEMATIC REVIEW
OF THE LITERATURE, 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
Editor:
Leslie VanHiel, MSPT
Reviewers:
Jennith Bernstein, PT
Amanda Gillot, OT
Ashley Kim, PT
Elizabeth Sasso, PT
Kristen Casperson, PT
Anna Berry, PT
Liz Randall, SPT
Glossary of Abbreviations
General
SCI - Spinal cord injury
ASIA – American Spinal Injury Association
AIS – ASIA Impairment Scale
ISNCSCI – International Standards for the
Neurological Classification of Spinal Cord Injury
Assessment (formerly ASIA exam)
Glossary of Abbreviations
Research Studies and Interventions
RCT – Randomized control trial
LE – Lower extremity
ROM – Range of motion
TENS – Transcutaneous electrical nerve stimulation
rTMS - Repeated transcranial magnetic stimulation
eSCS - Spinal cord electrical stimulation
FES – Functional electrical stimulation
WBV – Whole body vibration
Glossary of Abbreviations
Outcome Measures for Research Studies
AS – Ashworth Scale
MAS – Modified Ashworth Scale
CSS - Composite spasticity score (based on several AS scores)
VAS – Visual Analog Scale
MPSFS – Modified Penn Spasm Frequency Scale
SCATS – Spinal Cord Assessment Tool for Spastic Reflexes
SCI-SET – Spinal Cord Injury Spasticity Evaluation Tool
Hmax/Mmax – Electrophysiological ratio measure of neural
excitability
EMG - Electromyography
Definitions of Spasticity
Involuntary muscle firing
Velocity-dependent
Increase resistance to stretch
Abnormal processing of sensory input within networks of neurons
in the spinal cord networks.
There are many definitions of spasticity, but the most referenced:
Lance, 1980:
“Spasticity is a motor disorder characterized by a velocitydependent 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, withdrawal reflex).
Adams & Hicks, Spinal Cord, 2005
Positive Effects of Spasticity
Spasticity may:
Be
used to help with
transfers, standing,
walking, and ADLs.
Help
prevent muscle
atrophy.
Muscles
may appear to
be healthier compared
to those without
spasticity.
http://www.dinf.ne.jp/doc/english/global/david/dwe001/d
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Negative Effects of Spasticity
However, spasticity may
also lead to:
Decreased range of
motion (ROM)
Inability to position the
limbs safely
Limited mobility
Difficulty performing
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 ADLs
Improve ease of care
Patient
Evaluation
and
Treatment
Planning
Evaluate Patient:
Does spasticity/ overactivity interfere
significantly with function?
No
No treatment
necessary
Measures must include all aspects of
spasticity
Will it lead to musculoskeletal deformity?
Yes
Patient and
Caregiver
Objectives
• Identify patient
and caregiver
goals
Functional Objectives
Technical Objectives
• Improve gait, hygiene, ADLs, pain
relief, ease of care
• Promote tone reduction,
improved range of motion,
joint position
• Decrease spasm frequency & severity
• Decrease spasm frequency
• Decrease hyper-reflexia
Spasticity Management Program
MODIFIED from Spasticity Treatment Planning. WEMOVE.org, 2005.
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
Adjunct
– oral or pump (intrathecal)
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 to the spinal
cord (epidural spinal cord stimulation) and
electromagnetic stimulation to the brain
(transcutaneous magnetic stimulation - TMS) may
mimic the effects of surgical interventions.
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, hyperreflexia, 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.
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 (quick and short
lasting) spasticity of resistance felt when an extremity is moved
quickly
Hypertonia = tonic (longer lasting, co-contraction) 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 (e.g. the knee
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, and
these all differed.
Each of the 7 papers used different outcome
measures of spasticity.
These are ongoing problems with research in this
area.
Study
Definition of Spasticity provided
Aspect of spasticity measured
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
Bowden &
Stokic 2009 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/hyper-reflexia
Flexion withdrawal
Based on Decq, 2003: “…a symptom of upper motor
neuron syndrome, characterized by an exaggeration of
the stretch reflex, spasms, and resistance to passive
Kumru, et al. movement across a joint, secondary to hyperexcitability of
spinal reflexes.”
2010
Velocity-dependent resistance
to stretch
Passive resistance to stretch
Clonus
Spasm frequency & severity
Stretch reflex/hyper-reflexia
Hypertonia
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
hyper-reflexia
Study
Definition of Spasticity
provided
none provided
Velocity-dependent resistance to stretch
Passive resistance
Clonus
none provided
Velocity-dependent resistance to stretch
none provided
Passive resistance to stretch
Stretch reflex/quadriceps hyper-reflexia
none provided
Passive resistance to stretch
Spasm frequency
Stretch reflex/quadriceps hyper-reflexia
Chung &
Cheng 2009
Kakebeeke
TH, et al.
2005
Krause P et
al. 2008
Pinter MM,
et al 2000
Aspect of spasticity measured
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
Study
Design
60 mins active RCT,
TENS or 60
n=18
mins placebo;
over the
common
peroneal nerve
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,
Samso JV, et al.
2010
Intervention
Repetitive
Transcranial
Magnetic
Stimulation
(TMS)
Study
Design
RCT with
cross- over
for sham
group,
n=15
Outcome Measures
MAS
VAS for pain
MPSFS
SCAT
SCI-SET
Hmax/Mmax,
Reflex (reflex
responses on EMG as
indicators of neural
excitability)
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 & nontraumatic 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 stimulation
peripherally (i.e. at the common peroneal nerve or the nerve
innervating the muscle antagonistic to the spastic muscle, Chung &
Cheng, 2009), or electromagnetic stimulation centrally (i.e. over
the primary motor cortex, Kumru et al., 2010) for motor
incomplete injuries led to a significant reduction in several
different aspects of spasticity:
– Velocity-dependent resistance to stretch
– Spasms
– Hypertonia
– Hyper-reflexia
– Clonus
Descriptive Study Design: Longitudinal
Study, Epidural E-stim
Study
Pinter et
al. 2000
Intervention
Study Design
Epidural spinal Longitudinal,
cord electrical n=8
stimulation
(eSCS)
Outcome Measures
EMG during passive
stretch of LE & Pendulum
Test
Ashworth Scale
Clinical rating scale
Participant
Characteristics
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 legs (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
Bowden PharmaM, Stokic cologic,
DS. 2009 intrathecal
baclofen
Study
Outcome Measures
Design
Single
Ashworth Scale
subject Lower extremity strength
case
using ISNCSCI
report
EMG
H-Reflex & H/M ratio
(reflex responses on EMG
as indicators of neural
excitability)
Plantar Withdrawal Reflex
Maximal Voluntary
Dorsiflexion
Participant
Characteristics
1 male
41 y.o.
T11, AIS D
8 years post-SCI
Strength Decreased, BUT Spasticity
Decreased More
Dose-dependent decreases in:
Ashworth
Bilateral
H/M
score (p<0.01)
lower extremity strength (p<0.001)
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
Participant
Outcome Measures
Design
Characteristics
Kakebeeke 30 mins
Pre-Post, Muscle strength testing using 9 male;
et al. 2005 passive lower n=10
isokinetic dynamometry
1 female
extremity
(torque) in sitting & lying;
23-60 y.o.
ergometry
movements of leg at 10°/sec & C6-T12
120°/sec; taken before, after, AIS A, B
& 1 week post passive cycling 1-25 years
session
post-SCI
Study
Intervention
Results: Strength 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
Krause P, Functional
Crosset al.
electrical
over,
2008
stimulation
n=5
cycling, Passive
cycling
Outcome Measures
Modified AS of quads
Pendulum Test of quads.
Also during Pendulum Test:
Peak Velocity (deg/s)
during first swing
Relaxation Index
(A1/(1.6 x A0), where
A1 & A0 = degrees of
first swing in flexion, then
extension, respectively)
Participant
Characteristics
3 male;
2 female
37-66 y.o.
T3-T7, AIS A
3-9 years postSCI
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).
* Participants were not on anti-spasticity medications.
Descriptive Study Design:
Longitudinal, Whole Body Vibration
Study
Intervention Study Design
Outcome Measures
Whole body Longitudinal, Pendulum test
Ness LL,
Field-Foté vibration on n=16
EC, 2009 vibrating
platform
SCI Participant
Characteristics
14 male;
3 female
28-65 y.o.
C4-T8
AIS C, D
> 1 year postSCI
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 antispasticity 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
These 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)
can lead 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).
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 averaged and reported as a
whole.
It remains unknown whether there is a differential response
to the interventions.
Study Limitations
Studies included persons with chronic SCI, who may have
musculoskeletal consequences to chronic spasticity.
Chronic spasticity has musculoskeletal effects, namely
muscle shortening and contractures (Gracies et al., 1997).
Musculoskeletal parameters were not assessed in any of
these studies. Improvements may have been neural or
musculoskeletal or both.
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.
There were no studies addressing the costeffectiveness of treatments for spasticity.
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.
Recommended Future Research
Further study is warranted to determine:
the differential responses to interventions in those with
varying levels of injury, classifications of injury, and
times since injury.
the differential effects of interventions on neural and
musculoskeletal tissues.
the effects of interventions on function.
the long-term effects of these interventions.
the cost-effectiveness of the various treatments for
spasticity.
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