Spasticity Management

Frank S. Pidcock, M.D. Kennedy Krieger Institute Johns Hopkins School of Medicine

Musculoskeletal Clinical Goals
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Reduce pain or spasm frequency Increase ROM Cosmesis Hygiene Fitting for orthosis Postpone or avoid surgery PREVENT CONTRACTURES!

BONE GROWTH AND MUSCLES

Normal stretching needed for proper muscle growth Muscle length increases in response to bone growth Muscle imbalance from spasticity limits the lengthening possible with bone growth

CONTRACTURES PHYSIOLOGY

Mobile tissues usually separated by thin layers of loose areolar connective tissue Immobility causes reorganization of the loose connective tissue Once soft tissues are involved - muscle shortening may follow

DYNAMIC CONTRACTURE

Early finding in cerebral palsy Imbalance between muscles acting on a joint Results in abnormal motion and function Attain normal range with passive stretch Becomes fixed over time

FIXED CONTRACTURES

Often inevitable Require surgical lengthening to restore muscle balance Reoperation is often necessary

Common Clinical Patterns: Lower Limbs

Common Clinical Patterns: Upper Limbs

Surgical and Pharmacologic Treatments
General Oral medications Reversible Intrathecal baclofen Selective dorsal rhizotomy

Permanent Permanent

Chemodenervation
Modified from Graham HK, et al. Gait Posture. 2000.

Local corrective surgery

Focal

Botulinum Toxin

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Clostridium botulinum is a gram + anaerobic rod Produces an exotoxin which blocks ACH release at the neuromuscular junction Eight types: A, B, C1, C2, D, E, F, G Most potent poison known with a lethal dose of 1-2 micrograms Incidence of botulinum poisoning is about 10 cases per year in the USA

Botulinum Toxin Type A Mechanism of Action
COOH NH2
S-S

Light Chain
NH2 S
S

Heavy Chain

COOH

Local, Temporary Cholinergic Chemodenervation

Multiple neurotransmitters/neuropeptides released from vesicle

Regulated Exocytosis

Syntaxin

VAMP/ synaptobrevin SNAP-25
Adapted from Trends in Cell Biology, July 1997.

Ca++ Channels

Considerations in Treatment Decisions

Quality of abnormal muscle tone

Spasticity or dystonia or both

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Duration Severity Distribution
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Diffuse or focal Number of candidate muscles

Clinical parameters

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Usual onset of action = 12 hours to 72 hours Time to peak effect = 7 to 10 days Average Duration of response = 1 to 6 months Reinjection interval = wait at least 12 weeks

What is the evidence for botulinum toxin affecting contractures?

Botulinum Toxin for Spasticity after Stroke

Randomized, double-blind, placebo-controlled multicenter trial Adults with increased wrist or finger flexor tone following stroke Primary outcome measure was a self-reported disability rating 32% dressing, 30% limb position, 26% hygiene, 12% pain
Brashear A et al. NEJM. 347: 395-400, 2002

Brashear et al. Results at 6 Weeks

62% subjects in the BTA group as compared with 27% n the placebo group had improvement in the principal target of treatment ( P<0.001) Score on the DAS was correlated with Ashworth Score, Physician’s Global Assessment, and Caregiver/Patient Global Brashear A et al. NEJM. 347: 395-400, 2002 Assessment (P<0.001)

Good Vs. Poor Candidates

Motor learning

Ceiling around 6 years so treat early Assess active and passive range of motion Adapt goals to cognitive capabilities Avoid unrealistic expectations

Dynamic contractures

Selective motor control

Consensus

Localization
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Inspection EMG guidance Electrical stimulation Ultrasound

Comparison of localization techniques
Method
Inspection EMG signal amplificatio n Electrical Stimulation Ultrasound

Time
Quick <1minute 1-5 minutes >5minutes

Discomfort
Painless Needle stick Needle stick + shock Gel + pressure

Accurac y
Fair Better, nonspecifi c Best, specific Not clear, specific*

Tibialis Anterior –Transverse View

DOES IT HURT?

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Anticipatory guidance Size of the needle Waiting Multiple sites Emla vs. Ethyl chloride spray Versed vs.General anesthesia

Adverse Effects
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No anaphylactic reactions Local weakness which may affect surrounding muscles

urinary or bowel incontinence

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Generalized weakness or lethargy Adverse events including respiratory distress and death

Are Oral Systemic Drugs Noninvasive?
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Misconception Chemicals that are ligands to numerous CNS receptors Alter or depress multiple higher function other than motor circuitry

Gracies et al. in Spasticity: Etiology, Evaluation, Management and the Role of Botulinum Toxin, Sept 2002

General Pharmacologic Points

Mechanisms and site of action not completely understood Most alter the function of neurotransmitters or neuromodulators in the CNS
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Suppress excitation (block glutamate) Enhance inhibition (activate GABA or glycine)

Some work through peripheral mechanisms
 Gracies et al. in Spasticity: Etiology, Evaluation, Management and the Role of Botulinum Toxin, Sept 2002

Altering ion flux

Disruptions to the CNS Are Usually Insidious and Underrecognized
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Cognition Alertness Mood Personality

Gracies et al. in Spasticity: Etiology, Evaluation, Management and the Role of Botulinum Toxin, Sept 2002

Selecting Appropriate Treatment

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Assess passive versus active function goals Prioritize treatment goals Consider patient comfort as a goal Awareness of risk/benefit ratio

Gracies et al. in Spasticity: Etiology, Evaluation, Management and the Role of Botulinum Toxin, Sept 2002

Passive Function

Mainly requires sufficient flexibility and looseness of limbs for caregiver to perform activities that patient cannot perform by themselves

Gracies et al. in Spasticity: Etiology, Evaluation, Management and the Role of Botulinum Toxin, Sept 2002

Active Function
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What the patient can do alone Requires
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Active range of motion Strength Attention Alertness Good mood

Gracies et al. in Spasticity: Etiology, Evaluation, Management and the Role of Botulinum Toxin, Sept 2002

The Problem With Oral Drugs

“While it may be possible to enhance both comfort and passive function with a CNS depressant, it may be more challenging to provide improved comfort and active function”.

Gracies et al. in Spasticity: Etiology, Evaluation, Management and the Role of Botulinum Toxin, Sept 2002

Oral Antispasticity Medications

GABA  Baclofen  Diazepam Norepinephrine

Tizanidine Dantrolene

Other drugs that may be useful  Sinemet  Artane  Neurontin

Ion Flux

And the list goes on and on and on

Sleepiness is often a problem

Central side effects common
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Sedation Dizziness Confusion

Other treatments
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Often novel approaches Many are not covered by insurance Usually involve exercise or movement of some type Examples
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Therasuits Hippotherapy Aquatherapy

Adjuncts to the therapy program and not a substitute for the therapy itself.

Role of therapists

Before treatment
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Assess baseline measurements Establish treatment goals Provide reports about the effects of therapies and medications Continue working to achieve goals

After treatment
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Therapeutic Exercise
• • •

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Stretching and range of motion Myofascial and joint mobilization Active assistive, active and resistive exercise Facilitate useful co-contraction Endurance training

Therapy After Treatment

Gait training

devices, activities, timing splinting,seating,equipment substitutions,exercise,mechanics

Positioning

Education

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