spasticity · spasticity management: goal setting • should be tailored on an individual basis:...

Spasticity

March 5th 2017Cherry Junn, MD

Learning Objectives• Understand definition of spasticity• Identify clinical presentation and evaluation of spasticity

• Discuss spasticity management

Spasticity• One of consequences of the

Upper Motor Neuron (UMN) syndrome– Motor changes produced by

lesions proximal to the alpha motor neuron

– Can result from: stroke, cerebral palsy, anoxia, traumatic brain injury, spinal cord injury, multiple sclerosis, and other CNS neurodegenerative disease

Berker, Nadire, and Selim Yalçın. The help guide to cerebral palsy. 2010.

Upper Motor Neuron Syndrome• Positive

– Spasticity – Athetosis– Dystonia– Rigidity – Clonus

NegativeWeaknessLoss of fine motor control/planningLoss of selective motor controlFatigability

Prevalence• Limited due to the lack of strict definition and clinical measurement

• SCI: 65‐78%• Stroke: 19‐92%

– 37% in first year– Basal ganglia, thalamus, insula, and white matter track are strongly associated

• MS: 85%– Typically develops if plaques affect the corticospinal track, brain stem and callosal radiations

Francisco, Gerard E. "Spasticity." Braddom's Physical Medicine and Rehabilitation. Ed. Sheng Li. 5th ed. Philadelphia: Elsevier Health Sciences, 2016. 487. Web.

Spasticity: definition • “disordered sensorimotor control resulting from an UMN lesion, presenting as intermittent or sustained involuntary activation of muscles”1

• Motor disorder characterized by an abnormal, velocity-dependent increase in the tonic stretch reflexes with exaggerated phasic stretch reflexes

1. Pandyan, A. D., et al. "Spasticity: clinical perceptions, neurological realities and meaningful measurement." Disability and rehabilitation 27.1-2 (2005): 2-6.

Fig. 1: The stretch reflex arc.

Lalith E. Satkunam CMAJ 2003;169:1173-1179

©2003 by Canadian Medical Association

Stretch Reflex Arc• Stretched muscle ‐> an impulse is generated in the muscle spindle and is transmitted via the sensory neuron to the grey matter of the spinal cord

• Sensory neuron synapses with the motor neuron ‐> transmitted impulse results in muscle contraction

• Agonist muscles contract while antagonist muscles via an inhibitory neuron within the spinal cord

PathophysiologyStretch reflex: Passive stretch causes change in

length and rate of change detected by muscle spindles (group Ia afferent and group II afferent)


Fig. 2: Potential spinal mechanisms of suppression of hyperactivity in the final common pathway (alpha motor neuron and muscle).

Lalith E. Satkunam CMAJ 2003;169:1173-1179

©2003 by Canadian Medical Association

Pathophysiology: spinal reflex control

Inhibitory inputs to lower motor neuron is decreased, leading to increase in the excitability


Pathophysiology• Loss of inhibitory control by descending corticospinal tracts

• Increased dependence on rudimentary brainstem‐mediated descending motor tracts

• Increased sensitivity of stretch– actives muscle spindles

• Pathological branching of spinal interneurons• Hyperexcitability of alpha motor neurons

Trompetto, Carlo, et al. "Pathophysiology of spasticity: implications for neurorehabilitation." BioMed research international 2014 (2014).

Pathophysiology of spastic paresis. I: Paresis and soft tissue changes

Muscle & NerveVolume 31, Issue 5, pages 535-551, 15 FEB 2005 DOI: 10.1002/mus.20284http://onlinelibrary.wiley.com/doi/10.1002/mus.20284/full#fig1

http://onlinelibrary.wiley.com/doi/10.1002/mus.v31:5/issuetoc

http://onlinelibrary.wiley.com/doi/10.1002/mus.20284/full#fig1

Pathophysiology of spastic paresis. II: Emergence of muscle overactivity

Muscle & NerveVolume 31, Issue 5, pages 552-571, 15 FEB 2005 DOI: 10.1002/mus.20285http://onlinelibrary.wiley.com/doi/10.1002/mus.20285/full#fig1

http://onlinelibrary.wiley.com/doi/10.1002/mus.v31:5/issuetoc

http://onlinelibrary.wiley.com/doi/10.1002/mus.20285/full#fig1

Pathophysiology: Maladptive Plasticity


Spasticity: Clinical Presentation

Spasticity: Clinical Manifestation• Spastic dystonia:

– Tonic muscle overactivity • Clonus

– Involuntary rhythmic contraction triggered by stretch

• Spasms– Sudden involuntary movements

• Co‐contractions– Abnormal antagonist contraction present during voluntary agonist effort

Nair, K. P., and Jonathan Marsden. "The management of spasticity in adults." bmj 349 (2014): g4737.

Benefits of Spasticity • May help some with ambulation secondary to extensor tone

• May assist in maintaining muscle bulk• May assist in preventing DVT or osteoporosis• Decrease of pressure ulcer formation

Complications of Spasticity • Difficulty in movement• Abnormal posture• Can cause discomfort or pain• Difficulty in sitting and transfers• Difficulty and hygiene and dressing• Increased risk of heterotopic ossification

Spasticity EvaluationClinical Measures Electrophysiological Measures

‐ Range of Motion ‐ The H Reflex

‐ Tone Intensity Measures ‐ Vibration Inhibition Index

A. Modified Ashworth Scale Functional Measures

B. Tardieu Scale - Upper Extremity Function

Mechanical Instruments - Gait (timed walking)

- The Pendulum Test Quality of Life Measures


Modified Ashworth Scale• Measures resistance to passive stretch • Commonly used as a primary or secondary outcome measurement in clinical trials

• The most universally recognized metric • Easy to perform and has a long history of use

Modified Ashworth Scale (MAS)• 0 – no increase in muscle tone• 1 – slight increase in muscle tone with a catch at the end range of motion

• 1+ ‐ slight increase in muscle tone with minimal resistance with catch occurring less than 50% of ROM

• 2 – marked increase in muscle tone but easily moved for more than 50% of ROM

• 3 – considerably increased muscle tone with difficulty but possible passive ROM

• 4 – Rigid with tone but not contracture

Tardieu Scale• Alternative to the Modified Ashworth Scale• Incorporates velocity into the assessment

Tardieu Scale• Assessment: Velocity of stretch

– V1: move limb as slow as possible– V2: allow limb to fall under only gravity– V3: move limb as fast as possible

• Measurements– R1: angle at which catch is felt– R2: angle achieved under V1– R2 – R1 = y angle

Tardieu Scale• 0 – no resistance throughout the course of the passive movement

• 1 ‐ slight resistance throughout the course of the passive movement

• 2 – clear catch at precise angle, interrupting the passive movement, followed by release

• 3 – unsustained clonus (less than 10 sec when maintaining the pressure) occurring at a precise angle, followed by release

• 4 – sustained clonus (more than 10 sec when maintaining the pressure) occurring at a precise angle

Spasticity Management: Goal Setting

• Should be tailored on an individual basis:– Functional Improvement– Symptom relief– Postural improvement– Decrease caregiver burden– Enhanced service activity

Ward, Anthony B., and Surendra Bandi. "Spasticity due to stroke pathophysiology." Spasticity: diagnosis and management. New York: Demos Medical Publishing (2011).

Spasticity Management• When choosing, consider these aspects: reversible, permanent, global, focal

• Nonpharmacological management• Medication

– Oral– Injectable– Intrathecal

• Surgical management

Non‐pharmacological Treatment• Identify and avoid triggers• Physical treatments

– Stretching, splinting• Postural management and standing

– Systems to maintain alignment when sitting, standing, or lying in bed

• Exercises– Strengthening exercises improve motor control and function

• Other modalities:– Electrical, thermal, vibration, biofeedbackNair, K. P., and Jonathan Marsden. "The management of spasticity in adults." bmj 349 (2014): g4737.

Pharmacotherapy • FDA approved oral medication for spasticity due to CNS disorder :– Baclofen– Tizanidine– Dantrolene– Diazepam

PharmacotherapyMedication Mechanism PO dosage Side Effect

Diazepam GABA A hyperpolarization

4 – 60 mg /day

Somnolence , memory impairment

Baclofen GABA B hyperpolarization (GABA mimic)

5 – 80 mg (some report 300 mg/day)

Somnolence , withdrawal seizures

Dantrolene Inhibits calcium release 25 – 400 mg Somnolence, hepatotoxicity

Tizanidine Alpha 2 agonist – central

2 – 36 mg Somnolence, constipation, dry mouth, monitor LFT

Clonidine Alpha 2 agonist ‐ central

0.1 – 0.4 mg Dry mouth, withdrawal after long‐term usage, hypoglycemia

Other pharmacotherapyMedication Mechanism PO dosage Side Effect

Gabapentin Unknown 100 – 2400 mg

Dizziness, somnolence

Lamotrigine or other AEDs (topiramate, phenytoin)

Sodium Channel inhibition

25 – 500 mg Dizziness, rash, Steven Johns Syndrome

Cyproheptadine Nonselective histamine and serotonin antagonist

4 ‐32 mg Sedation

Tetrahydrocannabinol

CB1 and CB2 receptors

Varies Anxiety

Injectable therapy• Appropriate for focal spasticity


Neuromuscular Junction

ChemoneurolysisPhenol Ethyl alcohol

2‐7% concentration 45‐ 100% concentration

Lower concentration: demyelination with little axonolysis

Less commonly used

Higher concentration (>5%) : chemical denervation

Less toxic than phenol

Usually lasts > 6 months

Rapid acting nerve block with long-term efficacyComplication: dysesthesia, pain, systemic reaction

with phenol

Phenol


Botulinum Toxin

Chemodenervation• Botulinum toxin:

– Inhibits acetylcholine release at the neuromuscular junction

– Blocks impulse transmission from the nerve to the muscle

– Reduces tone and improves passive function– Lasts 3‐6 months– Complication: distance spread of toxin affect

Phenol and Botulinum ToxinPhenol Botulinum toxin

Mechanism Denatures protein Inhibitors acetylcholine release

Onset Less than an hour Days

Duration 2–36 months 3–6 months

Dose Depending on concentration, less than 10 mL

400 units and 1 single time recommended by FDA

Precaution Pain, dysesthesia Distant spread

Indication Proximal large musclesMore for hygiene and comfort

Focal spasticity

Technique Stimulation stimulation, ultrasound, palpation

Intrathecal Treatment Agents• Baclofen• Morphine• Clonidine

Intrathecal Treatment• Requires a surgery to place a device under the skin

• Delivers medication close to target receptor sites in the dorsal horn of the spinal cord1

• Decreases systemic side effects • Appropriate for patients with passive or problematic active function

Surgeries• Orthopedic surgery:

– Lengthens, releases, or transfer muscle/tendon– Alternatives length/tension relationship– Reduces efferent signaling from muscle spindles– Split Anterior Tibial Tendon Transfer (SPLATT)

• Treat equinovarus deformity of the foot

SPLATT

Sawyer, J and David D Spence. Cerebral Palsy. Campbell’s Operative Orthopaedics. Chapter 33, 1249‐1303.e9

Surgeries • Neurosurgery: Selective dorsal rhizotomy

– Spinal section of dorsal nerve roots in the lumbosacral spinal cord

– Reduces sensory input into spinal motor neuron pools, reducing excitability

Selective Dorsal Rhizotomy

Park, TS and Brian J Dlouhy. Selective Dorsal Rhizotomy for Spastic Cerebral Palsy. Youmans and Winn Neurological Surgery, 243, 1951‐1959.e2

Treatment Decision Making


Citation• Berker, Nadire, and Selim Yalçın. The help guide to cerebral palsy. 2010.• Brashear, Allison, et al. "Intramuscular injection of botulinum toxin for the treatment of wrist

and finger spasticity after a stroke." New England Journal of Medicine 347.6 (2002): 395‐400.• Francisco, Gerard E. "Spasticity." Braddom's Physical Medicine and Rehabilitation. Ed. Sheng

Li. 5th ed. Philadelphia: Elsevier Health Sciences, 2016. 487‐510. Web.• Gracies, Jean‐Michel. "Pathophysiology of spastic paresis. I: Paresis and soft tissue

changes." Muscle & nerve 31.5 (2005): 535‐551.• Gracies, Jean‐Michel, et al. "Safety and efficacy of abobotulinumtoxinA for hemiparesis in

adults with upper limb spasticity after stroke or traumatic brain injury: a double‐blind randomised controlled trial." The Lancet Neurology 14.10 (2015): 992‐1001.

• Kheder, Ammar, and Krishnan Padmakumari Sivaraman, Nair. "Spasticity: pathophysiology, evaluation and management." Practical neurology 12.5 (2012): 289‐298.

• Nair, K. P., and Jonathan Marsden. "The management of spasticity in adults." bmj 349 (2014): g4737.

• Park, TS and Brian J Dlouhy. Selective Dorsal Rhizotomy for Spastic Cerebral Palsy. Youmans and Winn Neurological Surgery, 243, 1951‐1959.e2

• Sawyer, J and David D Spence. Cerebral Palsy. Campbell’s Operative Orthopaedics. Chapter 33, 1249‐1303.e9

Citation• Satkunam, Lalith E. "Rehabilitation medicine: 3. Management of adult spasticity." Canadian

Medical Association Journal 169.11 (2003): 1173‐1179.• Simpson, D. M., et al. "Botulinum toxin type A in the treatment of upper extremity spasticity

A randomized, double‐blind, placebo‐controlled trial." Neurology 46.5 (1996): 1306‐1306. • Snow, Barry J., et al. "Treatment of spasticity with botulinum toxin: A double‐blind

study." Annals of neurology 28.4 (1990): 512‐515.

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