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
(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 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?,).
Adams & Hicks, Spinal Cord, 2005
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
• Promote tone reduction,
• Improve gait, hygiene, ADLs, pain
relief, ease of care
improved range of motion,
joint position
• Decrease spasm frequency & severity
• 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
 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 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
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 2008 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
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/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
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 hyperreflexia
none provided
Passive resistance to stretch
Spasm frequency
Stretch reflex/quadriceps hyperreflexia
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
Outcome
Measures
Participant
Characteristics
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 & 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
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
Pinter et Epidural
al. 2000 electrical
stimulation
Longitudinal,
n=8
Outcome Measures
Participant
Characteristics
 EMG during passive
 4 male;
stretch of LE & Pendulum 4 female
Test
 18-34 y.o.
 Ashworth Scale
 C5-T6,
AIS
 Clinical rating scale
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
Bowden PharmaM, Stokic cologic,
DS. 2008 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 postSCI
Strength Decreased, BUT Spasticity
Decreased More

Dose-dependent decrease 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
Intervention
Study
Design
Kakebeeke 30 mins
Preet al. 2005 passive lower Post,
extremity
n=10
ergometry
Outcome Measures
 Isokinetic dynamometry in
sitting & lying; movements of
leg at 10°/sec & 120°/sec;
taken before, after, & 1 week
post passive cycling session
Participant
Characteristics
 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
Outcome Measures
Design
Krause P, Functional
Cross Modified AS
et al.
electrical
over,
 Pendulum Test
2008
stimulation
n=5
 Torque, used to determine
cycling, Passive
peak velocity and
cycling
relaxation index
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).
Note: Participants were not on spasticity
medications.
Descriptive Study Design:
Longitudinal, Whole Body Vibration
Study
Ness LL,
Field-Foté
EC, 2009
Intervention Study Design
Outcome Measures
Whole Body Longitudinal,  Pendulum test
Vibration
n=16
Participant SCI
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
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.
References
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2.
3.
4.


1.
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