Transcript Spasticity What Causes it and Can it be Inhibited? Kevin Nhan Kyleigh Short Justin DeLong Eric Atristain Paul Broyer PT 224 March 24, 2010 Learning Objectives At the completion of.

Spasticity
What Causes it and Can it be Inhibited?
Kevin Nhan
Kyleigh Short
Justin DeLong
Eric Atristain
Paul Broyer
PT 224
March 24, 2010
Learning Objectives
At the completion of this presentation, the learner will be
able to:
 Define spasticity
 Describe the neurophysiology of spasticity
 An accepted and validated technique for measuring
spasticity
 Can spasticity be inhibited?
 The effectiveness of treatments to reduce spasticity
What is Spasticity?
“Spasticity is a motor disorder characterized by a
velocity-dependant increase in tonic stretch
reflexes with exaggerated tendon jerk, resulting
from hyperexcitability of the stretch reflex”
- James Lance (1980)
What is Spasticity?

Some of the difficulty for clinicians to understand the
pathophysiology of spasticity is due to the definition of
spasticity.

There is much criticism in definitions.

Definition offered by Lance is generally the most
accepted by physiologist.
[Barnes and Johnson]
Who else defined spasticity?

The following individuals also contributed
to the definition and research of spasticity

Bobath and Bobath (1950)
Levine et al (1954)
Wyke (1976)
Lance (1980)
Lance (1990)
Gottlieb and Myklebust (1993)
Morris (2000)






[Ibuki and Bernhardt (2007)]
Mechanism of Spasticity

So what causes a muscle to become
spastic?
•
The absence of an upper motor neuron’s inhibitory control on the
spinal reflex.
Hyperactive stretch reflexes that are mediated by muscle spindle
stretch receptors
Decreased threshold of the alpha lower motor neurons
•
•
Mechanism of Spasticity

Stretch Reflex

Skeletal muscle contain specialized proprioceptors called muscle
spindles.
Leaving the muscle spindles are Ia sensory axons.
Ia input is very powerful
When the muscle spindles senses a change in length.
The skeletal muscle tends to what to pull back and contract.




Mechanism of Spasticity

Once Central Nervous System Lesion
•
•
Hypotoncity
Alpha Lower motor neuron

Days to weeks later
•
Denervation hypersensitivity
•
Alpha lower motor neurons lower threshold
•
An increase in the number of Ach receptors
Characteristics of Spasticity
Rather then being a specific symptom.
•
•
•
•
Hyperactive stretch reflex
Increased resistance to passive movement
Posturing of extremities
Stereotypical movement synergies
Ashworth Scale


•
•
Physical therapist need clarity to realize how
spasticity can have affects on a patients ability to
move
A valid & reliable measure scale for spasticity
Ashworth Scale
Modified Ashworth Scale
Mock Clinic

Manual Muscle Testing to be valid/invalid
•
Since we can now measure voluntary contractions
“Patients with spasticity have been shown to spend 3 times
longer in rehabilitation units than stroke patients without
spasticity”
[Gilen and Burkhardt]
Physical Therapy Intervention

Can Physical Therapy fix spasticity?
•

No! But they can help with function.
Disorder of upper motor neuron pathways include:
•
•
•
•
•
Stroke
Traumatic brain injury
Multiple sclerosis
Spinal cord injury
Cerebral palsy
Interventions
 Effective
Treatments for
reducing Spasticity






PT Intervention
Electrical and Functional
Electrical Stimulation
Casting
Mental Imagery
Pharmacological Interventions
Surgery
Physiotherapy Intervention
[Richardson (2002)]

Components of PT


3 Broad Approaches




Assess, ID goals, measuring problem, implementation of
intervention, reassessment.
Biomechanical - (Car & Shepherd) - improve strength, task
practice
Neurophysiological (Bobath) - motor hierarchy, not as good as
above.
Cognitive - (Fetters) - dynamic systems approach, motivation.
Modalities


Electrical Stimulation & Functional ES
Ice (30 minutes to reduce for 1-1.5hrs), light touch/brushing.
Physiotherapy Intervention
[Richardson (2002)]

Interventions

Stretching (6hr), splinting, casting.
 Strength training (Shean), a stronger muscle will need less force.

Motor Learning

Cortex remapping.
 Constraint induced therapy.

Patient Educators

Explanations help Pts understand, enables them to help themselves.
 Help with compliance with an agreed upon program.
Electrical Stimulation

[Chen et al. (2005)]

Looked at treating Achilles Tendon with 20 min of E-Stim.



Golgi Tendon Organ Ib neuron diminished after stroke.


ES applied to the muscle tendon junction.
Trying to reestablish 1B inhibitory neuron from GTO.
Possible mechanism contributing to spasticity.
Decreased MAS score and improved 10 m walking time,
after 1 month of treatment.

How its administered important, lasting effects are unknown.
Electrical Stimulation

[Mesci, N. et al. (2009)]

Treatment group received NMES treatment for hemiplegic foot
dorsiflexor muscles for 4 weeks, 5 days a week.

Showed a significant increase in ankle dorsiflexion and a
significant decrease in the level of spasticity.
Electrical Stimulation

[Chung, B., et al. (2009)]

Statistical differences of reduction of Composite Spasticity
Score, Achilles tendon jerks, resistance to full-range passive
ankle dorsiflexion and ankle clonus were calculated.

This study showed that a single session of TENS could
immediately reduce spasticity.

-No long term effects
Electrical Stimulation

Golgi Tendon Organ
Functional Electrical Stimulation

[Krause et al. (2007)]

Used to facilitate movement.


Looked at the difference between active
FES movement and passive movement
Greater decrease in spasticity immediately
after FES TX, lasting 30 minutes to 1 day.
No change a week later.

Benefit of increasing muscle strength for
possible long term effects.
Casting

[Preissner (2001)]

Serial casting is a noninvasive procedure that helps children and
adults improve their range of motion so they can perform daily
activities with less difficulty.

Serial casting may be indicated when an individual presents with
range of motion limitations due to contracture, or the potential of
developing contracture as a result of spasticity.

Serial casting has also been used in cases of heterotopic
ossification, fractures, and ligament injuries, but may not be as
effective for these conditions.
Casting

[Singer et al. (2004)]

Looked at serial casting in
reducing spasticity related
ankle contractures.

Must be able to differentiate
from dystonia.

Serial casting more effective
along with botulinum and
physiotherapy.
Mental Imagery

[Bovend’Eerdt et al. (2008)]

The participants were asked to imagine on the visual and
kinesthetic domain about the task being performed.

Motor imagery appears to be a feasible technique for use during
stretching exercises in individuals with spasticity.
Mental Imagery

[Bovend’Eerdt et al. (2008)]

Is therapeutic stretching with motor
imagery more effective than stretch
alone?

Does it work? Not statistically.

The variability in the population and the
small sample size could be factors
affecting the results of the study.
Pharmacological Intervention

[Ward (2002)]

Generalized spasticity


Regional spasticity


Oral agents
Intrathecal baclofen phenol
nerve block
Focal Spasticity

Botulinum toxin phenol block
Pharmacological Intervention:
Generalized Spasticity

Oral Agents - also administered enterally.

Diazepam


Dantrolne Sodium



Peripherally acting muscle relaxant.
Shown to increase ADL, transfers, hygiene, no LT effects.
Tizanide Hydrocholride



Brainstem reticular formation and spinal polysnaptic
pathways. GABA receptor inhibitor.
Inhibits both pre and post synapses. Fewer side effects than diazepam.
Also functional improvements, ambulation distance on flat ground.
General Side Effects

Fatigue, drowsiness, alcohol-like sedation, reduced motor coordination,
impaired intellect, attention, addiction, weakness.
Pharmacological Intervention:
Regional Spasticity

Intrathecal Drug Therapy - administered directly into subarachnoid
space of CNS with a programmable pump.

Intrathecal Baclofen, Morphine Sulphate (Infumorph), Fentanyl.



Improvement in walking speed, functional mobility without impairing
uninvolved extremity.
Fewer systemic side effects because not circulating in blood stream.
Infection, impaired wound healing, pump malfunction, and catheter
dislocation in 20-25% of cases.
Pharmacological Intervention:
Focal Spasticity

Chemical Neurolytics - destruction of a portion of the nerve.

Phenol Injections - causes chemical (Wallerian) denervation.




Dose dependent, hit proximal muscles first.
Works at alpha motorneurons directly.
Pain at administered site, causalgia w/ sensory nerve injury.
Botulinum Toxin - binds to presynaptic cell and prevents NT release.


Begins 3-7 days and last 2-6 months, specific muscles.
May have diminishing returns (A &B), small muscles..
Pharmacological Intervention
•[Gallichio, (2004)]
Drug
Site of Action
Adverse Effects
Oral Drugs
Diazepam
Brainstem reticular
formation and spinal
polysynaptic pathways
Fatigue; reduced motor coordination,
intellect, attention, memory
Dantrolene Sodium
Skeletal muscle
calcium stores
Hepatotoxicity, generalized muscle
weakness
Oral Baclofen
GABA-b receptors
Drowsiness, confusion, headache, lethargy
Tizanidine Hydrochloride
a2-adrenergic
receptors
Dizziness, sedation, dry mouth
Gaba-b receptors
Pump malfunction/ dislocation
Phenol Injection
Neuromuscular
junction
Causalgia with sensory nerve injury, pain at
injection site, hematoma
Botulinum Toxin
Nerve
Injection site pain, muscle weakness in
injected muscle, hematoma, muscle
necrosis, phlebitis
Intrathecal Drugs
Intrathecal Baclofen
Focal Drugs
Surgical Intervention

[Woo (2001)]

Tendon Lengthening - preferred method



Tendon Transfer - used on children (Shriner’s)


Gait analysis with dynamic electromyographic monitory helps
reduce common errors associated with this procedure.
Osteotomy - for skeletal deformity



Allow full passive range with some residual muscle tension.
Muscle must be immobilized under tension.
Restore boney architecture, muscle-length can be improved.
Used along with tendon lengthening.
Artrhodesis - joint fusion


When the above are prohibited.
Stabilize unstabel joints (subtalar, thumb, wrist).
Surgical Intervention [Lazorthes et al. (2002)]

Neurosurgery - severe and painful spasticity, irreversible.
 Dorsal rhizotomies - Regional spasticity.
 Cut dorsal cords and grey mater (gelatinosa area).
 Can cause decrease in voluntary mobility, sepsis, decreased
lemniscal sensitivity, and death.
 Peripheral neurotomies - Focal spasticity.
 Used if botulinum toxin failed.
 Done distally only reducing the myotatic reflex.
 Cervical Spinal Cord Stimulation - reversible.
 E Stim administered directly to spinal area.
 Intrathecal Baclofen is more commonly used.
Learning Objectives

Turn to the person beside you and review these learning
objectives:





Define spasticity
Describe the neurophysiology of spasticity
An accepted and validated technique for measuring spasticity
The effectiveness of treatments to reduce spasticity
Can spasticity be inhibited?
The End
References





Barnes, M. Management of Spasticity. Age and Ageing. 1998;27:239-245
Bohvend’Eerdt, T. JH., Dawes, H., Sackley, C., Izadi, H., and Wade, D. T.
Mental Techniques During Manual Stretching in Spasticity - a pilot
randomized controlled trial. Clinical Rehabilitation. 2006; 23: 137-145
Chen S-C, Chen Y-L, Chen C-J, Lai C-H, Chiang W-H, and Chen W-L.
Effects of surface electrical stimulation on the muscle-tendon junction of
spastic gastrocnemius in stroke patients. Disability & Rehabilitation. 2005;
27(3): 105-110.
Chung, B. , & Cheng, B. (2010). Immediate effect of transcutaneous
electrical nerve stimulation on spasticity in patients with spinal cord injury.
Clinical Rehabilitation, 24(3), 202-210.
Gallichio, Joann E. Pharmacologic Management of Spasticity Following
Stroke. Physical Therapy Journal. 2004; 84: 973-981
References





Ibuki A, Bernhardt J. What is spasticity? The discussion continues.
International Journal of Therapy and Rehabilitation. 2007;14:391-395
Krause, P., Szecsi, J., and Straube, A. Changes in Spastic Muscle Tone
Increase in Patients with Spinal Cord Injury Using Functional Electical
Stimulation and Passive Leg Movements. Clinical Rehabilitation. 2008; 22:
627-634
Lazorthes, Y., Sol, J-C., Verdie, S., & J-C. The Surgical Management of
Spasticity. European Journal of Neurology. 2002; 9(1): 35-41
Preissner, K. (2001). The effects of serial casting on spasticity: a literature
review. Occupational Therapy in Health Care, 14(2), 99-106. Retrieved from
CINAHL Plus with Full Text database.
Mesci, N. , Ozdemir, F. , Demirbag Kabayel, D. , & Tokuc, B. (2009). The
effects of neuromuscular electrical stimulation on clinical improvement in
hemiplegic lower extremity rehabilitation in chronic stroke: A single-blind,
randomised, controlled trial. Disability & Rehabilitation, 31(24), 2047-2054.
References





Richardson, D. Physical Therapy in Spasticity. European Journal of
Neurology. 2002; 9(1): 17-22
Singer, B. J., Dunne, J. W., Singer, K. P., Jegasothy, G. M., and Allison,
G. T. Non-surgical Management of Ankle Contracture Following Acquired
Brain Injury. Disability and Rehabilitation. 2004; 26(6): 335-345
Verplancke, D., Snape, S., Salisbury, C., Jones, P., & Ward, A. (2005). A
randomized controlled trial of botulinum toxin on lower limb spasticity
following acute acquired severe brain injury. Clinical Rehabilitation, 19(2),
117-125. Retrieved from CINAHL Plus with Full Text database.
Ward A. B. A Summary of Spasticity Management - a Treatment
Algorithm. European Journal of Neurology. 2002; 9: 48-52
Woo, R. Spasticity: Orthopedic Perspective. Journal of Child Neurology.
2001; 16(1): 47-53