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

Lesley Hudson, MS David Apple, MD Deborah Backus, PhD,

PT

Rebecca Acevedo

Leslie VanHiel, MSPT

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:

Editor:

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 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, 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/dwe001g/dwe00136g06.jpg

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

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 hyper-reflexia

Spasticity Management Program

No

Yes

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 – 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 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, hyper-reflexia, 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 providedAspect of spasticity

measured

Bowden & Stokic 2009

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/hyper-reflexia

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/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

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 hyper-reflexia

Pinter MM, et al 2000

none provided Passive resistance to stretchSpasm frequencyStretch reflex/quadriceps hyper-reflexia

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

StudyInterventi

onStudy Design

Outcome Measures

Participant Characteristi

csKumru H, Murillo N, Samso JV, et al. 2010

Repetitive Transcranial Magnetic Stimulation (TMS)

RCT with cross- over for sham group,n=15

MAS VAS for pain MPSFS SCAT SCI-SET Hmax/Mmax, Reflex (reflex responses on EMG as indicators of neural excitability)

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 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 Intervention

Study Design

Outcome MeasuresParticipant

Characteristics

Pinter et al. 2000

Epidural spinal cord electrical stimulation (eSCS)

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 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

Study Design

Outcome MeasuresParticipant

Characteristics

Bowden M, Stokic DS. 2009

Pharma-cologic,

intrathecal baclofen

Single subject case report

Ashworth Scale Lower extremity strength using ISNCSCI

EMG H-Reflex & H/M ratio (reflex responses on EMG as indicators of neural excitability)

Plantar Withdrawal Reflex

Maximal Voluntary Dorsiflexion

1 male 41 y.o. T11, AIS D 8 years post-SCI

Strength Decreased, BUT Spasticity Decreased More

Dose-dependent decreases 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

nOutcome Measures

Participant Characteristi

csKakebeeke et al. 2005

30 mins passive lower extremity ergometry

Pre-Post,n=10

Muscle strength testing using isokinetic dynamometry (torque) 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: 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

Outcome MeasuresParticipant

Characteristics

Krause P, et al. 2008

Functional electrical stimulation cycling, Passive cycling

Cross- over,n=5

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)

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).

* Participants were not on anti-spasticity medications.

Descriptive Study Design: Longitudinal, Whole Body Vibration

StudyInterventi

onStudy Design

Outcome Measures

SCI Participant

Characteristics

Ness LL, Field-Foté EC, 2009

Whole body vibration on vibrating platform

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

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 cost-effectiveness 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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