1. Spasticity What Causes it and Can it be Inhibited?
Kevin Nhan
Kyleigh Short
Justin DeLong
Eric Atristain
Paul Broyer
PT 224
March 24, 2010

2. 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

3. 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)

4. 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]
Lance’s definition has been criticized for being too narrow by describing spasticty as only a form of hypertonia. However, this hypertonia is one component of the upper motor neuron syndrome.

5. 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)]

6. 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

7. 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.
These receptors sense a change in length for extrafusal skeletal fibers. Ia enter the spinal cord, via dorsal horn, branch repeatedly and form excitatory synapses on interneurons and alpha lower motor neurons. The Ia fibers are Thick myelinated axons. When the muscle spindles sense a change in length (such as during a pull) the Ia fibers are activated, and send excitatory stimulus to the alpha lower motor neuron. When walking, we stretch muscles upon heel strike and with the inhibitory we don’t have this proble

8. 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
The CNS lesion removed the Upper motor neuron input, thus no input to the lower motor neuron. How come when UMN lesion, but yet still have the LMN and muscle spindles, does spasticity not happen right away? Because of the neuronal changes. 1. Alpha LMN have lowered their threshold. (takes less now for them to reach depolarization. 2. Number of Ach receptors on Alpha LMN have increased. The Alpha LMN need Ach to survive, its not about the vasculature. Its about using it or losing principle.

9. Characteristics of Spasticity
Rather then being a specific symptom.
Hyperactive stretch reflex
Increased resistance to passive movement
Posturing of extremities
Stereotypical movement synergies
One more important thing is that an Arm flexor synergy: Shoulder flexion, adduction, internal rotation; elbow flexion; wrist flexion; finger flexion, is more common in the UE and a Leg extensor synergy: Hip, knee extension; ankle plantar flexion is more common in the LE.

10. 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

11. 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]

12. 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
So, if we want to work on impairments and yet spasticity makes it difficult to intervene. So in order to circumvent a patients spasticity there are certain interventions we can use to temporally reduce spasticity and then hopefully improve function

13. Interventions Effective Treatments for reducing Spasticity
PT Intervention
Electrical and Functional Electrical Stimulation
Casting
Mental Imagery
Pharmacological Interventions
Surgery

14. Physiotherapy Intervention [Richardson (2002)]
Components of PT
Assess, ID goals, measuring problem, implementation of intervention, reassessment.
3 Broad Approaches
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.

15. 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.

16. Electrical Stimulation
[Chen et al. (2005)]
Looked at treating Achilles Tendon with 20 min of E-Stim.
ES applied to the muscle tendon junction.
Trying to reestablish 1B inhibitory neuron from GTO.
Golgi Tendon Organ Ib neuron diminished after stroke.
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.

17. 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.

18. 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

19. Electrical Stimulation
Golgi Tendon Organ

20. 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.

21. 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.

22. 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.
So it was important to be able to identify the different characteristics that are present with both spasticity and dystonia. They also used a scale to measure both spasticity and dystonia. In conclusion the combo of treatments is most effective that way any problems that can occur with muscles or neuro can be suppressed.

23. 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.

24. 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.

25. Pharmacological Intervention
[Ward (2002)]
Generalized spasticity
Oral agents
Regional spasticity
Intrathecal baclofen phenol nerve block
Focal Spasticity
Botulinum toxin phenol block

26. Pharmacological Intervention: Generalized Spasticity
Oral Agents - also administered enterally.
Diazepam
Brainstem reticular formation and spinal polysnaptic pathways. GABA receptor inhibitor.
Dantrolne Sodium
Peripherally acting muscle relaxant.
Shown to increase ADL, transfers, hygiene, no LT effects.
Tizanide Hydrocholride
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.

27. 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.

28. 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..

29. 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
Intrathecal Drugs
Intrathecal Baclofen
Gaba-b receptors
Pump malfunction/ dislocation
Focal Drugs
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

30. Surgical Intervention
[Woo (2001)]
Tendon Lengthening - preferred method
Allow full passive range with some residual muscle tension.
Muscle must be immobilized under tension.
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
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).

31. 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.

32. 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?

33. The End

34. References
Barnes, M. Management of Spasticity. Age and Ageing. 1998;27:
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 ; 23:
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):
Chung, B. , & Cheng, B. (2010). Immediate effect of transcutaneous electrical nerve stimulation on spasticity in patients with spinal cord injury. Clinical Rehabilitation, 24(3),
Gallichio, Joann E. Pharmacologic Management of Spasticity Following Stroke. Physical Therapy Journal. 2004; 84:

35. References
Ibuki A, Bernhardt J. What is spasticity? The discussion continues. International Journal of Therapy and Rehabilitation. 2007;14:
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 ; 22:
Lazorthes, Y., Sol, J-C., Verdie, S., & J-C. The Surgical Management of Spasticity. European Journal of Neurology ; 9(1): 35-41
Preissner, K. (2001). The effects of serial casting on spasticity: a literature review. Occupational Therapy in Health Care, 14(2), 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),

36. References
Richardson, D. Physical Therapy in Spasticity. European Journal of Neurology ; 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 ; 26(6):
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), Retrieved from CINAHL Plus with Full Text database.
Ward A. B. A Summary of Spasticity Management - a Treatment Algorithm. European Journal of Neurology ; 9: 48-52
Woo, R. Spasticity: Orthopedic Perspective. Journal of Child Neurology ; 16(1): 47-53