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Pediatric Spasticity

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CURRENT MANAGEMENT STRATEGIES IN THE TREATMENT OF SPASTICITY

Eric R. Trumble, MD

NEUROSURGEONS FOR KIDS

Result!  Why, man, I have gotten a lot of results.  I know several thousand things that won’t work. There is no substitute for hard work.

--Thomas Edison

ETIOLOGIES

Cerebral palsy

Stroke

Multiple sclerosis

Traumatic brain injury

Spinal cord injury

Anoxia

Neurodegenerative disease

PATHOPHYSIOLOGY of SPASTICITY

 

 

ASSOCIATED SIGNS

Abnormal cutaneous reflexes (Babinski sign)

Spastic dystonia

            muscle contraction present at rest, dependent on tonic stretch

            significant contribution to deformity

 Spastic co-contraction

abnormal antagonist contraction present during voluntary agonist effort, dependent  on tonic stretch on antagonist

Extra-segmental co-contraction

            abnormal contraction distant from the muscles involved in a voluntary effort

ASSOCIATED SIGNS …

Other types of muscle overactivity

(present with yawning, breathing etc.)

            Muscle shortening

                        consequence of both immobilization and muscle overactivity

            Motor weakness

                        significant source of disability

DISABLING FEATURES

Muscle shortening, motor weakness, and stretch-dependent muscle overactivity (spastic co-contraction and spastic dystonia) are probably the most disabling features in spastic patients.

Three logical solutions in therapy:

muscle lengthening, motor training,

and local muscle relaxation

ASHWORTH SCALE

No increase in muscle tone (normal)

Slight increase in tone giving a “catch” when affected part is moved in flexion or extension

More marked increase in tone but affected part is easily flexed

Considerable increase in tone; passive movement difficult

Affected part is rigid in  flexion or extension (contracture)

UPPER EXTREMITY SPASTICITY

 

LOWER EXTREMITY SPASTICITY

 

CONSIDERATIONS IN TREATMENT DECISIONS

Chronicity

            acute vs. chronic

Severity

Distribution

            diffuse vs. focal

Locus of CNS injury

REASONS FOR TREATMENT

If spasticity interferes with:

            functioning

            positioning

            comfort

            care

If spasticity is not useful, e.g., during transfers

If treatment is expected to provide meaningful improvement

POSSIBLE TREATMENT GOALS

Increased ROM

Decrease energy expenditure

Decreased spasm frequency

Decreased pain

Improved mobility

Improved gait

Improved orthotic fit

Improved positioning

Increased ease of hygiene

Improved cosmesis

TREATMENT OPTIONS

Rehabilitation

Oral medication

Intrathecal baclofen

Chemodenervation

Orthopedic surgery

Neurosurgery

Medical stabilization and removal of noxious stimuli (infection, stress, etc.) precede other treatments.

REHABILITATION

The next step should include PT, OT, and any other non-invasive/non-pharmocological treatments, e.g. massage therapy.

There is little to no risk with these therapies and a potential for a great deal of benefit.

ORAL MEDICATIONS

Benzodiazepines, e.g Valium, allow decreased resistance to passive ROM and hyperreflexia, a reduction in painful spasms with sedation and reduced anxiety. Adverse effects: sedation, weakness, hypotension, GI symptoms, memory impairment, incoordination, confusion, depression, ataxia

Baclofen causes decreased resistance to passive ROM and hyperreflexia with a reduction in painful spasms and anxiety. Adverse effects: weakness, sedation, hypotonia, ataxia, confusion, fatigue, nausea, dizziness, lower seizure threshold

OTHER ORAL MEDICATIONS

Dantrolene sodium reduces calcium release from sarcoplasmic reticulum, thereby uncoupling excitation and contraction leading to a decreased resistance to passive ROM, decreased hyperreflexia and muscle tone, and a reduction in spasms and clonus. Adverse effects: weakness (including ventilatory muscles), drowsiness, lethargy, nausea, diarrhea, and hepatotoxicity

Tizanidine(Zanaflex) alpha-2 noradrenergic agonist which blocks release of excitatory AAs from spinal interneurons and causes inhibition of facilitory coeruleospinal pathways leading to reduced tone, spasm frequency, hyperreflexia with no decrease in strength. Adverse effects: drowsiness, dizziness, dry mouth, orthostatic hypotension

Clonidine alpha-2 agonist

CHEMODENERVATION

Local muscle weakening

            Injectable therapy

                        Temporary, reversible, titratable

Temporary, reversible, titratable

Phenol

Ethyl alcohol

ORTHOPEDIC OPTIONS

Increase function by:

            maintaining appropriate length of muscles via musculotendinous lengthenings

            providing power via tendon transfers

            improving the mechanics of gait via rotational osteotomies

            providing stability via selective joint fusion

SELECTIVE DORSAL RHIZOTOMY

Interruption of reflex arc

Sectioning of afferent nerve rootlets L-2 to S-2

EMG guidance, selected roots only

Treatment goals: improve gait and mobility; facilitate care; prevent contractures or bony deformities.

INTRA-THECAL BACLOFEN

Pump controlled via radio-telemetry link from an external programmer

Allows control of rate, mode, and pattern of infusion

Dosage titration, schedule revision

Preservative-free, stable in pump for up to 90 days

BACLOFEN PUMP

 

TRENDY TREATMENT OF SPASTICITY

Hyberbaric oxygen – meant to allow penumbra (portion of brain/spinal cord dysfunctional but not permanently damaged) to function better.  No controlled studies to document efficacy.  Little risk.

Craniospinal therapy – manipulation to better align motor/bony function.

Acupuncture – re-align your energy fields.