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Assessment & Treatment of

Spastic Muscle Overactivity

Cori Ponter, PT, MPT, NCS

Gerard Francisco, MD

TPTA SED Meeting

March 29, 2012

2

Objectives

Participants will be able to:

Identify types of muscle overactivity and their clinical

presentations

Discuss the pathophysiology and origins of spastic

muscle overactivity

Identify and differentiate various assessment tools

used in assessing muscle overactivity

Discuss various treatment options for spastic

muscle overactivity, including medical management

and therapeutic management

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What is “Spasticity?”

Most Common Definition:

Spasticity is “…a motor

disorder characterized by

velocity dependent increase

in tonic stretch reflexes with

exaggerated tendon jerks,

resulting from hyper

excitability of the stretch

reflex…

(Lance, 1980)

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What is “Spasticity?”

Clinically:

Most “talked about,” but other types of overactivity are

usually grouped together as “spasticity.”

Just one type of muscle overactivity that occurs with

CNS lesions.

By itself, may not cause a high level of

disability

Triggered by stretch and velocity

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Other Types of Muscle Overactivity in CNS lesions

Muscle overactivity present at rest, which is spontaneous and has no primary triggering factor; causes deformation of joints and body postures. Frequently produces twisting or repetitive movements.

Spastic Dystonia

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Hypertonic Rigidity Similar resistance is felt with PROM regardless of the

speed or direction of movement

Spastic Co-Contraction Unwanted activity of antagonistic muscle group during

voluntary agonistic movements (ex: activation of triceps

during voluntary elbow flexion).

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Contracture

Fixed resistance to passive

stretching of muscles due to

shortening or wasting (atrophy)

of muscle fibers or the

development of scar tissue

(fibrosis) over joints. Not

technically muscle over-

activity, but can be confused

with over-activity. This is non-

neural, but can be caused by

neural components.

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Pathophysiology

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Damage to CNS

Paralysis

Contracture

Immobility

Flaccidity Plastic

Changes

Spinal

Overactivity

Supraspinal

Spasticity, Dystonia, Rigidity,

Co-Contraction, etc

Immediate Delayed

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Pathophysiology of Spasticity & Other Muscle Overactivity

Immediate paralysis, leading to immobility

Active and passive tissue changes:

Type I fibers (slow/tonic) change to Type II (fast twitch/fatigable)

Muscle extensibility decreases due to a decrease in the # of

sarcomeres and connective tissue accumulation in extrafusal

fibers

These tissue changes lead to increases in stretch transmission

to muscle spindle

Plastic changes within the CNS

Rerouting at spinal level

Recruitment of new motor pathways

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How Does Spasticity Develop?

Possible mechanisms of spasticity

Increased neuronal excitability

Enhanced excitatory synaptic

input

Segmental afferents

Regional excitatory

interneurons

Descending pathways, i.e.,

lateral vestibulospinal tract

Reduced inhibitory synaptic

input

Renshaw cell recurrent

inhibition

Ia inhibitory interneurons

Ib afferent fibers

Change in intrinsic electrical

properties of the neuron

Change in passive membrane

electrical properties

Change in voltage sensitive

membrane conductance

Enhanced stretch-evoked

synaptic excitation of neurons

γ efferent hyperactivity

Excitatory interneurons more

sensitive to muscle afferent

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Major Descending Pathways Controlling Spinal Reflexes

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Origins of Muscle Overactivity

Spinal - SCI, MS

Inhibitory message is sent but cannot be

received due to disruption of spinal cord

Cerebral -

BI, CVA, CP, MS

Lack of inhibition messages

being sent

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Cortical vs Spinal Spasticity

Muscle tone is affected

by:

the absence of an intact

corticospinal system

An imbalance of inputs

from reticulospinal and

other descending

pathways to the motor

and interneuronal circuits

of the spinal cord

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Indirect cortical

pathways to spinal cord

(e.g., cortico-

reticulospinal) pathways

usually has inhibitory

influence on muscle

tone, especially limb

extensor tone

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Loss of descending tonic or phasic excitatory and

inhibitory inputs to the spinal motor apparatus

Alterations in the segmental balance of excitatory and

inhibitory control

Denervation supersensitivity

Neuronal sprouting

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Cortical Spasticity

Selective damage to area 4

in the cerebral cortex of

primates produces paresis

that improves with time, but

increases in muscle tone are

not a prominent feature

Lesions involving area 6

cause impairment of postural

control in the contralateral

limbs

Combined lesions of areas 4

and 6 cause both paresis

and spasticity to develop

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Spinal Changes

During the development of spasticity, the spinal cord

undergoes neurophysiologic changes in the excitability

of motor neurons, interneuronal connections, and local

reflex pathways

The excitability of alpha motor neurons is increased, as

is suggested by enhanced H-M ratios and F-wave

amplitudes

Judged by recordings from Ia spindle afferents, muscle

spindle sensitivity is not increased in human spasticity

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Flexor vs Extensor Spasticity

Reticulospinal tract flexion, typically

Vestibulospinal tract extension, typically

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Pathophysiology of Spasticity

Imbalance between excitatory and inhibitory impulses

to the alpha motor neuron in the spinal cord

Due to a loss of descending inhibitory input to the

alpha motor neuron due to injury to the cortical spinal

tracts

Descending

Inhibition Sensory

Excitation

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Treatment Options

20

Botulinum

Toxins

Physical

Modalities

and Therapy

Intrathecal

therapies

Phenol

and

Alcohol

injections

Surgery

Oral

Drugs

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Considerations for Management Choices

✦When considering management choices for Cerebral

Origin muscle overactivity, we need to be aware of the

effect of the medications on the brain’s recovery process

✦Many oral anti-spasticity medications have the side

effect of making people sleepy, slowing cognitive

processes, and may ultimately slow the recovery of

function

✦ The challenge is to

manage abnormal tone

without interfering with

brain healing/recovery

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Best Practices Spasticity Management

EFFECTIVE APPROACH

An integrated and

multidisciplinary program

of physical and medical

interventions

A clear individualized

patient management

strategy

WHEN AND HOW TO TREAT

Significance, i.e. disabling

Distribution of spasticity

Chronicity, severity, and

cause

Concomitant conditions

Cost

It’s never too late to treat

spasticity

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How can tx of spasticity facilitate motor recovery?

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Brunstromm Stages of Recovery

STROKE

I

Flaccidity

II

Synergies

Some spasticity

III

Marked

spasticity

IV Out of synergy Less spasticity V

Selective control of movement

VI

Isolated/coordinated

movement

Reversed “maladaptive plasticity”?

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Goal-Setting

PRIMARY EFFECTS

• Focus • Tone reduction

• Spasm reduction

• Locus • Central

• Peripheral

SECONDARY

EFFECTS

• Symptom Relief

• Correct Deficit • Exercise

• Compensation

• Restitution

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Goal-Setting

Spasticity is not the reason for treatment.

Instead, it is the impact of spasticity on a

person’s well-being

Significance, not severity, of

spasticity should dictate need for

treatment

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Management Starts with Goal-Setting

TECHNICAL

Decrease hypertonia

(Ashworth)

Decrease spasm

frequency and severity

Increase range of motion

FUNCTIONAL

“PASSIVE”

Facilitating wearing of

splints

Decreasing pain

associated with abnormal

posture and spasms

Improve nursing care

“ACTIVE”

Increase performance

OTHERS

Improve body image

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Spasticity Management Interdisciplinary Approach

Pharmacologic

Functional Re-training

Physical Intervention

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Spasticity Management

Assessment Goal-Setting Choice of Treatment

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Management Options - Therapy

✦Therapeutic

Interventions: ✦Weight bearing

✦Serial Casting/Splinting

✦Locomotor Training

✦Positioning

✦E-stim

✦Strengthening

Medical Management should always be

supplemented by therapeutic management for

optimal improvement!

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Assessment of Muscle Overactivity

Assessment What are we assessing?

Ashworth/Modified Ashworth Resistance to passive range of motion (including,

but not exclusive of, resistance due to spasticity)

Tardieu/Modified Tardieu Scale Spasticity angle, Quality of movement at multiple

velocities

Passive Range of Motion Amount of passive movement allowed by the joint,

soft tissue, muscle, etc. Goal is to assess without

eliciting a stretch reflex

Active Range of Motion How much active movement can be performed

against the spastic antagonist (NOT strength!).

Functional activities Quality of movement, speed of movement,

postural alignment, energy expenditure, etc.

Patient/caregiver report Pain, ease of care, transfers, quality of life, etc

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Ashworth/Modified Ashworth Scales

0 No increase in tone

1 Slightly increased tone, with a catch & release or

minimal resistance at terminal ROM

1+ Slight increase, catch followed by minimal

resistance throughout the remainder of the range

(<1/2 of the ROM) (only in MAS)

2 Marked increase through most of the ROM, but

affect part is easily moved

3 Considerable increase, passive ROM difficult

4 Affected part is rigid

Passive movements of muscle groups should be

performed over a one-second time frame

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Ashworth/Modified Ashworth Scales

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Ashworth/Modified Ashworth

Variable reliability

Author Subjects Results/Findings

Sloan et al

34 hemiplegic “MAS has acceptable interrater reliability for testing of upper limb spasticity,

but not so for testing of the lower limb spasticity.”

Nuyens,et al 30 MS “AS more reliable for muscles of the ankle than for muscles of the knee, and

least reliable for muscles of the hip.”

Haas, et al 30 SCI Interrater reliability varied between AS and MAS, between muscle groups

(hip adductors > hip extensors/flexors > ankles plantarflexors), and between

limbs. Recommended for both to be used with caution when assessing LE

spasticity with SCI patients

Allison et al 30 TBI Low interrater reliability for ankle plantarflexors, and argued that there was

no support for continued use of MAS to assess PFs in pts with TBI.

Gregson, et al 32 acute CVA Intra/inter-rater reliability found to be “good to very good for the elbow, wrist

and knee, but less satisfactory over the ankle.”

Blackburn et al 36 CVA Acceptable intra-rater reliability, but poor inter-rater reliability for MAS. Most

agreement was with scores of “0,” so conclusion was that reliable

measurements could be obtained to determine whether normal or low

muscle tone is present or not.

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“The results...are clear and tell us the Ashworth Scale has insufficient

validity and reliability to be used as a measure of spasticity. However, we

are left with the problem of how to measure spasticity in a valid and

reliable way. The quest for this holy grail is ongoing.”

- Katharina S Sunnerhagen

So what else can we use??

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Modified Tardieu Scale

Developed by Tardieu as a way to assess the velocity component of

spasticity in 1950s, modified by Boyd and Graham

Measures spasticity using two parameters

The spasticity angle

The spasticity grade

May be more useful to clinicians in

assessing functional implications of

spasticity, as well as effects of treatment

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Tardieu Scale – What does the evidence say?

More likely to identify

presence of contractures

than MAS/AS (Patrick,

2006)

More likely to correctly identify

presence [but not severity] of

spasticity than MAS when

confirmed with EMG (Patrick, 2006)

Very good intra-rater reliablity

across 2 sessions in elbow flexors

and ankle plantarflexors (Singh,

2011)

“In patients with severe

brain injury and impaired

consciousness the

Modified Tardieu Scale

provides higher test retest

and inter-rater reliability

compared with the

Modified Ashworth Scale

and may therefore be a

more valid spasticity scale

in adults.” Mehrholz, 2005

Variable reliability, which increases

with training – – StrokEdge review

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Tardieu Scale – Spasticity Angle

Range of motion measured at two different velocities

V1 – Slow as possible (R2)

V2 – Fast as possible (R1)

R2 R1 Spasticity Angle

Large spasticity angles indicate a large dynamic

component (spasticity), whereas small

differences indicate predominantly muscle

contracture

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R1/R2

R2 R1

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Tardieu Scale – Spasticity Grade

0 No resistance throughout passive movement

1 Slight resistance throughout passive movement

2 Clear catch at precise angle, interrupting passive

movement, followed by release

3 Fatigable clonus (<10 s when maintaining pressure)

occurring at a precise angle, followed by release

4 Unfatigable clonus (>10s when maintaining

pressure) occuring at a precise angle

Notes:

If spasticity angle = 0, grade must be a 0 or 1 by definition

If spasticity angle > 0, grade must be at least a 2, even if no definite “release” felt

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Active Range of Motion

Objective measure of how much the agonist can move against

the overactive antagonist

Example – To assess overactive biceps, we could measure the

degrees of active extension that a patient can achieve.

NOT looking at the strength of the extensors, but rather how

much the overactivity of the flexors can be overcome

Following treatment, would want to reassess to see if the

patient can achieve more active movement,

May be a more functional measurement than passive

measurements

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Functional Evaluation

Ask Questions! How is this impacting their lives? Severity ≠ Significance

What are their goals of treatment?

Observe! Watch them walk, transfer, propel w/c, eat, dress, etc

How are they positioned?

Video, video, video!!

Be Objective when you can! Use measures such as 10MWT, Gaitrite

asssessment, Modified Frenchay Arm Test, Disability

Assessment Scale

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Other Assessments

Penn Spasm Frequency Scale

Timed repeated contractions

Barry Albright Dystonia Scale

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Summary

Clinicians often focus on the direct effects of spasticity;

however, it is the indirect/disabling effects of spasticity

that most impact patients’ daily life

Effective rehabilitation consists of appropriate

assessment, and an individualized, interdisciplinary

approach that may incorporate both pharmacologic and

nonpharmacologic treatments

Spasticity and other chronic stroke complications should

be assessed and managed on a continual basis to

sustain functional gains

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