Presentations by Eric R. Trumble, M.D.
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.
 
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