CME on Management of Spasticity and Functional Implications

SPASTICITY
Dr Chua Zhi Cheng
Rehabilitation Department HSI

Objectives
1) Review the definition, distribution and epidemiology of spasticity
2) Discuss the functional implications of spasticity
3) Briefly review the assessment of spasticity
4) Discuss the management options of spasticity and interdisciplinary approach
necessary to improve function in a patient with spasticity

Spasticity
 What is it?
 Velocity-dependent increase in resistance to passive movement felt by an examiner stretching a
muscle group across a joint, resulting from the hyper excitability of the stretch reflex following damage
to the upper motor neuron system
 Therefore, due to an imbalance of the signals between the central nervous system (CNS) and muscles,
this results in “intermittent or sustained involuntary activation of muscles”
 Spasticity of cerebral origin results from lack of descending inhibitory input from subcortical
nuclei in brain
 Spasticity of spinal origin results from interruption of descending tracts that inhibit or modulate
alpha and gamma motor neurons

Spasticity-related Terms
 Rigidity: is the resistance to stretch that is not velocity dependent—the examiner feels just
about the same resistance to stretch irrespective of the velocity as the muscle group is been
stretched
 Muscle tone: is the resistance of a muscle to passive stretch
 Hypertonia: is the subjective description of tone being greater than normal
 In spasticity, we commonly observe:
 Hypertonia
 ↑ Deep Tendon Reflexes (DTRs)
 Clonus (involuntary rhythmic contractions in response to sudden sustained stretch)
 Spasms (sudden involuntary movements involving multiple muscle groups and joints, repetitive and
sustained, represents an exaggerated reflex withdrawal response to nociceptive stimuli)
 Contractures result when muscles are shortened for an extended period of time

Distribution of Spasticity
 Focal
 Isolated local motor disturbance affecting a single body part
 Regional
 Motor disturbance involving a large region of the body
 Generalized
 Motor disturbance involving widespread regions of the body
 Usually, antigravity muscles are more affected

Epidemiology of Spasticity
Spasticity affects approximately:
o 35% of those with stroke
o more than 90% with CP
o about 50% of TBI patients
o 40% of SCI patients
o between 37% and 78% of MS patients
Rivelis Y, Morice K. Spasticity. InStatPearls [Internet] 2019 Mar 6. StatPearls Publishing.

Explanation of the Motor Neuron Pathway

Gamma-Aminobutyric Acid
(GABA)
GABA is the primary inhibitor of impulses crossing synapses in the central
nervous system (CNS).
When GABA binds to its receptors, channels open allowing chloride ions into
the cell and potassium ions out of the cell.
In spasticity, receptors do not bind GABA effectively and consequently nerve
impulses are not inhibited, leading to over contraction of the muscle.

CME on Management of Spasticity and Functional Implications

Issues that may result due to
Spasticity
 Interferes with function
 Can cause extreme discomfort/pain in patients with intact sensation
 Limb deformity and altered body mechanics
 Interferes with nursing care and hygiene
 Muscle contractures
 Decubitus ulcers (pressure sores)
 In patients with fractures, malunion may occur
 Joint subluxation/dislocation
 Mood problems and inability to participate in rehabilitation

Vicious Cycle of Spasticity
Development of
pressure sores
Prone to infections
Difficulty in maintaining
hygiene
Reduced mobility
Poor nutrition
Increased severity of
spasms and spasticity
May also lead to
contractures
Increased spasticity
leading to difficulty in
sitting or lying

Spasticity is under treated
National Stroke Association survey of 504 stroke survivors
Up to 58% of stroke survivors develop spasticity1
 Of the 292 patients in the study with spasticity:
51% (149 patients) were receiving treatment
49% (143 patients) were untreated

Modified Ashworth Scale (MAS)
 The Modified Ashworth Scale is based upon the assessment of
the resistance to passive stretch by the clinician.
 Steps in performing Modified Ashworth Scale:
 Correct positioning of limbs
 Velocity dependent
 Place the patient in a supine position
 If testing a muscle that primarily flexes a joint, place the joint in a maximally
flexed position and move to a position of maximal extension over one second
 If testing a muscle that primarily extends a joint, place the joint in a maximally
extended position and move to a position of maximal flexion over one second

MAS Asessment reliability
In an effort to improve the reliability of the MAS, Bohannon and Smith (1987) proposed
to:
 Test the patient in the supine position.
 Extend the joint from a position of maximal possible flexion to maximal possible
extension.
 Standardize hand positioning and the resting limb position before stretch.
 Standardize the timing of the extension of the limb: Use a duration of about 1 second
(by counting "one thousand one").
 Keep repeated movement cycles at a minimum. Repeat the measurement 5 to 8 times
and choose the most reliable / consistent measurement.

Modified Tardieu Scale (MTS)
 The Modified Tardieu Scale identifies the point in the muscle’s range where spasticity,
or a “catch”, is occurring.
 First measure: This measures the maximum passive range of movement of the target
muscle group. It is generally referred to as R2.
 Second measure: This measure is then made by moving the muscle group from its
shortest to longest position using a rapid velocity stretch. Known as R1, it measures
the angle at which muscle resistance or “catch” is felt in response to this rapid
stretch.
 A “catch” early in the available range indicates more significant spasticity than a catch
that is toward the end of the Range of Movement (RoM).

 The relationship between R1 and R2, calculated as R2 minus R1, indicates the
‘dynamic’ component of spasticity. A large R2 - R1 difference suggests that there is
potential to successfully treat a person’s spasticity.
 Reliability - a reliable measure can be best achieved by an experienced clinician with
sufficient training and practice. Other ways to obtain the most reliable measures
include having a single rater completing the measurements in a standardized test
environment. This includes the position of the person being tested and the starting
position of each muscle group.

Spasticity Treatment Goals
 Prevention of contracture(s)
 Improve seating position
 Improve hygiene
 Improve mobility
 Improve ADL function
 Decrease pain
 Prevent pressure wounds
 Improve quality of life

What to Keep In Mind When
Treating a Patient with Spasticity
 Identification and elimination of triggers  patient and caregiver
education
 Physiotherapy & Occupational Therapy play important roles in
treatment: passive stretching, therapeutic exercises, posture and
standing, physical modalities
 Pharmacological measures (both oral and injectables) exist as effective
treatments for spasticity
 Orthotics
 Surgical intervention as the last option

Identification & Elimination of
Triggers
 Pressure ulcers
 Ingrown toenails
 Skin infections, UTI
 Injuries
 Constipation
 Deep Vein Thrombosis (DVT)
 Improper seating
 Ill-fitting orthotics

Passive Stretching
 Passive stretching decreases excitability of motor neurons and maintains visco-
elastic properties of muscles and joints
 Prolonged stretching can help to treat contractures
 Stretching can be facilitated by using casts or splints, sometimes used together
with botulinum toxin injections
 No conclusive evidence whether therapy is effective but no evidence that it is
harmful

Therapeutic Exercises
 Improves motor control and cardiovascular fitness in people with UMN
disorders

Posture & Standing
 Proper posturing stretches spastic muscles and decreases the sensitivity of
stretch reflex and brainstem reflexes that trigger spasticity
 Weight bearing and standing also help to improve psychological wellbeing,
improves bone mineral density, facilitates pulmonary drainage, and helps
bladder and bowel functions
 Proper positioning of limbs and trunk is essential to prevent aggravation
spasticity and development of contractures
 Devices such as splints help to position limbs properly

Physical Modalities
 These physical modalities work through either modulating the visco-elastic
properties of muscles and tendons:
 Ultrasound
 Cryotherapy
 Vibration
 Shockwave therapy
 Magnetic stimulation
 TENS (transcutaneous electrical nerve stimulation)

Pharmacological Treatment
– Oral Medications

Principles of Drug Therapy
 Weakness is a side-effect of all anti-spasticity drugs, usually due to unmasking
of underlying UMN weakness
 A ‘start low, go slow’ policy limits these unwanted functional effects
 Patients not responding to 1 drug may respond to another
 Reach maximal tolerated dose for a sufficiently long period before stopping a
drug and labeling it as “ineffective”

Principles of Drug Therapy
 Sudden stopping of even an apparently “ineffective” drug may cause a rebound
increase in spasticity. Thus, it is better to taper down initial drug while
simultaneously introducing the second drug
 Combination of 2 drugs should be tried if the spasticity does not respond to a
single agent
 It is important to time the doses according to the patient’s activities, care and
therapy

Commonly Used Oral Medications
Drug Mechanism of Action Side Effects
Baclofen Structural analog of GABA (inhibitory
transmitter of CNS)
Drowsiness, sedation, muscle
weakness, GI symptoms, tremors,
insomnia
Tizanidine α-2 adrenergic agonist, binds to
spinal receptors to block release of
excitatory neurotransmitters
Drowsiness, dry mouth, weakness,
hypotension, elevated liver function
tests
Diazepam (Valium) Increases effects of GABA at CNS
synapses
Fatigue, drowsiness, reduction in
motor coordination, potential for
abuse
Dantrolene (Dantrium) Acts on skeletal muscles by reducing
strength of contraction (by blocking
calcium release from sarcoplasmic
reticulum)
Decrease in gross motor function,
hepatotoxicity
(less sedation as not centrally acting)

Baclofen
 Most widely used oral anti-spasticity drug
 Mechanism:
 GABA-B receptor agonist
 Reduces calcium influx
 Decreases release of excitatory neurotransmitters
 Down-regulates activity of 1a sensory afferents, spinal interneurons and motor
neurons

Baclofen
 Dose:
 Starting: 5mg TDS
 Maintenance: Increase by 5-10mg weekly, until there is an optimal effect
 Max: 90-120mg per day
 Adverse effects:
 Weakness, drowsiness and dizziness
 Sexual dysfunction & urinary incontinence
 Reduces seizure threshold
 Sudden withdrawal may cause seizures or/and hallucinations, and baclofen withdrawal
syndrome*

Benzodiazepines
 Acts on GABA-A receptors, enhances the presynaptic inhibitory effect of GABA
and decreases spasticity
 Absorbed faster than baclofen, acts faster and lasts longer in the body
 Drowsiness and behavioural side-effects limits its use during the daytime
 Particularly useful to treat spasticity that interferes with sleep
 Clonazepam is useful to treat nocturnal spasms
 Usual starting dose is 0.5mg ON, maximum dose 1mg

Tizanidine
 Mechanism:
 α-2 receptor agonist
 Inhibits excitatory spinal interneurons and tracts from locus coereleus*
 Dose:
 Starting: 2mg ON
 Maintenance: Increase by 2mg weekly to maximum 36mg, divided into 3-4 daily
doses

Tizanidine
 Adverse Effects:
 Dry mouth, GI disturbance, hypotension and acute hepatitis
 Sudden stopping of tizanidine can lead to a hyperadrenergic syndrome (anxiety,
tremors, hypertension and tachycardia)

Dantrolene
 Mechanism:
 Blocks calcium release from sarcoplasmic reticulum and interferes with excitation-
contraction coupling of the skeletal muscle
 Acts directly on muscle thus less sedative
 Dose:
 Starting: 25mg OD x 1 week
 Maintenance: Increase by 25mg weekly to a top dose of 100mg, 3-4x daily

– Chemodenervation

Chemodenervation:
Phenol
 Causes demyelination of the nerve
 5% concentration
 Injected directly into peripheral nerves causing destruction of neural tissue by
protein coagulation
 Immediate onset of relaxation
 Usage:
 Effective in treating spasticity that occurs in large, powerful muscle groups close to
the trunk e.g. thigh adductors
 Blocks to the medial popliteal muscles to aid spastic foot drop
 Obturator nerve blocks either to improve scissoring gait, or to improve perineal
hygiene and seating posture

Chemodenervation:
Phenol
 A neurostimulator with a Teflon-coated needle electrode is used for guidance
 Effects can last up to 36 months (average 6 months), and can be repeated as
necessary
 Nerve sprouting may lead to recurrence of spasticity
 Adverse Effects:
 Nerve injury or neuropathic pain because of sensory fiber damage
 Tissue oedema, venous thrombosis, and compartment syndrome resulting from
large amounts of phenol in constrained space
 If injected intravascular can cause convulsions, CNS depression, cardiovascular
collapse

Chemodenervation:
Botulinum Toxin (Botox)
 Acts at the neuromuscular junction
 Blocks release of acetylcholine from the presynaptic neuron
 Injected with USG (ultrasound guidance)
 Maximum effect in 7-10 days, lasts 3 months
 Complications
 Focal weakness
 Distal spread of toxin

– Chemodenervation
– Intrathecal Therapy

Intrathecal Baclofen
• Binds to GABA receptors in the spinal cord, suppressing
release of excitatory neurotransmitters
• Implanted pump delivers Baclofen to the intrathecal
(subarachnoid) space
• Pros:
• Effective at substantially lower doses than are required orally
• Significantly less sedation seen as compared to oral dosing

Intrathecal Baclofen:
Screening Test
• Trial dose of baclofen is given intrathecally (usually
50mcg)
• PT/OCT exam prior to administration
• PT/OCT exams after administration
• Quantify effects of ITB
• If trial is positive, patient proceeds to implantation

Pump Implantation
– Implanted by a neurosurgeon
– Same day surgery
– Treatment is initiated at the time of implant
– Patient wears an abdominal binder for about a month to
prevent oedema at the pump site
– Begin PT and OCT after the post op visit
– Dosing is adjusted slowly
– Continuous or bolus dosing options

Commitment to ITB Therapy
Frequent PT/OCT sessions
Daily HEP
Daily use of static and/or dynamic bracing
Frequent doctor visits for dose titration
Visits 2-4 times a year for pump refills
Pump replacement every 7 years

Orthotic Management
Orthoses are a fundamental component of the rehabilitation
process; they are designed to support, align, correct, or prevent a
deformity and restore motion.
They are described in terms of the segment of the body they
encompass and the biomechanical control parameters of their
mechanical function.
 E.g. Ankle foot orthosis (AFO), wrist hand orthosis (WHO)

Orthotic Management
Based on their construction and design, they are either classified as
either static or dynamic devices:
 Static: places a body segment at rest through rigid support and possesses
no moving parts
 Static progressive: possesses a variable hold feature on a joint that
permits adjustments for joint-position change
 Dynamic: permits movement of specific joints through various extrinsic
mechanisms e.g. elastic bands, springs and motors; has moving parts to
allow motion control as prescribed

Orthotic Management:
Advantages
Lower limbs: Influences both swing and stance phase of gait.
 Prevent or correct deformity and reduce pain during weight bearing
 Improve efficiency of gait and maintain balance
 Improve base of support / lateral support
 Reduce need for compensation of ipsilateral and contralateral limbs
and secondary pain
 To facilitate training in skills

Orthotic Management:
Advantages
Upper limbs: Can be used after an injury to prevent further injury, or
reduce pain by supporting an injured limb.
Prevent or correct deformity reducing pain and maximizing
function in reach and grasp tasks.
Improve efficiency of reach and grasp tasks
Offload an injured limb to allow healing
Reduce need for compensation of ipsilateral and contralateral
limbs and secondary pain

Summary
 Spasticity occurs as result of damage to the central nervous system
 Spasticity can be present with TBI, SCI, CVA, MS, CP
 Spasticity can develop gradually and can change over time
 Spasticity can limit function, causing difficulty in performing ADLs and mobility skills
 Medical complications of spasticity include contracture and skin breakdown
 Treating spasticity as a part of an interdisciplinary rehab program can lead to
improved function and improved quality of life
 Both pharmacologic and non-pharmacologic measures may be helpful in treating
spasticity
 PT/OCT feedback helps us to make determinations in dosing titration

References
 McCollough, N. C., III. (1985) Biomechanical analysis systems for orthotic prescription, in American
Academy of Orthopaedic Surgeons Atlas of Orthotics: Biomechanical Principles and Application,
2nd ed. CV Mosby, St. Louis, pp. 35–75.
 Mayer, N. H., Esquenazi, A., and Childers, M. K. (1997) Common patterns of clinical motor
dysfunction. Muscle Nerve (Suppl. 6), S21—S35.
 Rosenada, J. P. and Ellwood, P. M. (1961) Review of physiology, measurement and management of
spasticity. Arch. Phys. Med. 42, 167–174.
 Trombly, C. A. (1989) Occupational Therapy for Physical Dysfunction, 3rd ed. Williams and Wilkins,
Baltimore, MD, pp. 329–355.
 Bobath, B. (1978) Adult Hemiplegia: Evaluation and Treatment, 2nd ed. Heinemann Medical Books,
London.
 Johnstone, M. (1983) Restoration of Motor Function in the Stroke Patient, 2nd ed. Churchill
Livingstone, London.

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