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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