spasticity management

SPASTICITY MANAGEMENT

Presented By: Jwanika Vansiya 1st Year MPT

Guided By: Dr. Ravi Shah

Spasticity is a hypertonic motor disorder characterized by velocit-dependent resistance to passive stretch.

Spasticity arises from injury to corticospinal pathways(pyramidal tracts) and occurs as a part of upper motoneuron (UMN) syndrome.

The signs and symptoms of UMN syndrome include hyperactive

stretch reflexes, involuntary flexor and extensor spasm, clonus, Babinski’s sign, exagerated cutaneous reflexes.

What is 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 reflex that are mediated by muscle spindle stretch receptors.

• Decreased threshold of the alpha lower motor neurons.

Mechanism of spasticity

What is stretch reflex?

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Spasticity resulted from a loss of descending, fascilitatory inhibitory influences that act on Ia interneuron inhibition.

Resiprocal inhibition mediated through Ia interneuron inhibition requires fascilitation from higher centres. With injury to CNS the interneuron is unable to shut off antagonist muscle firing with resultant increased velocity dependent resistance to movement.

The combination of both decrease inhibition, increased depolarization state of cell membrane, decrease action potential threshold for nerve signal conduction thus increase activity of structures innervated by the affected nerves.

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Stroke Multiple Sclerosis Traumatic Brain Injury Acquired Brain Injury Spinal Cord Injury Cerebral Palsy

Examples of UMN Lesions

Spasticity: Consequences

Pain and discomfort Contractures Increased energy cost of

movement Skin breakdown-shear Interferes with breathing Hampers gait and transfers

Interferes with hygiene More work for caregiver Poor safety Sexual difficulties Insomnia Poor posture

ASSESSMENT

GOAL SETTING

CHOICE OF TREATMENT

SPASTICITY MANAGEMENT

Patient report Deep tendon reflexes Passive range of motion Test for clonus Functional observation -Assess interference with function(gait) and effect of stress and/or fatigue -Assess adaptive shortening of muscles vs. irreversible contracture Consider aggravating factors(e.g., UTI, infection, excessive

activity, strengthening exercises) Modified ashworth scale

Spasticity: Assessment

Sample passive and active goals of spasticity management

Passive

Improved hygiene Ease of care Positioning Facilitate casting Reduce pain Ease of dressing Improvement of orthotic

fit

Active

Improvement of transfer Improvement of ADLs Improved mobility Decrease spasms Reduce contraction during

voluntary movement Improvement of foot

position during stance phase of gait cycle

The treatment of spasticity almost always multidimensional or multimodality therapy that includes followings:

Treatment

Oral medications

Parenteral medications

Surgical procedure

Physiotherapy

management

Oral medications Oral medication rely on two common mechanism to reduce

spastic symptoms throughout the body often in combination. I. Compensating for reduced GABA or other inhibitory neurotransmitters

in the brain or spinal cord.II. Reducing the amount of excitatory neurotransmitters through direct

inhibition or activation of inhibitory interneurons.

Pharmacological management

Most common medications are followings;

Benzodiazepines: • Facilitates the binding of existing GABA to the GABA-A receptor

found in high concentration in the reticular formation and polysynaptic spinal tracts.

• GABA-A receptor is ionotropic its activation results in the increase in cell permeability of cl- causing hyperpolarization. This hyperpolarization increases presynaptic inhibition and reduces monosynaptic and polysynaptic reflexes throughout the spinal cord.

• Benzodiazepam has demonstrated improvements in pain , hyperreflexia, and passive ROM.

• Side effects: sedation, hypotension, incoordination, depression, confusion may occur.

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Baclofen

• Baclofen binds to GABA-B receptors and blocks release of substance-P , an excitatroy neurotransmitter from primary afferent terminal.

• Both monosynaptic and polysynaptic reflexes are affected by its action, resulting in a decrease in clinical menifestation.

• Side effects- orthostatic hypotension, and withdrawal symptoms such as seizures, fever, hallucination .

Tizanidine • Reduction in excitatory neurotransmitter.• Tizanidine is an alpha-adrenergic agonist that acts throughout the CNS

to reduce excitatory amino acid release from spinal interneuron.• side effects: nausea, vomitting, sedation and hypotension.

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Dentrolene

• it affects the release of calcium from the sarcoplasmic reticulum in skeletal muscle and , therefore reduces muscle contraction.

• Dentrolene decreases muscle tone, clonus, spasm with minimal CNS side effects.

• Side effects: It affects all skeletal muscles, therefore may cause generalized weakness, including respiratory muscle weakness.

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The advantage of local injections include selectively, greater intensity of effect, reversibility and avoidence of systemic side effects.

Disadvantage includes pain with injections, impracticality for a large number of muscles, and the anatomic inaccessibility of some muscles(e.g. subscapularis)

Agents used for injection:1. Phenol block2. Botulinum toxin

Local injections

Phenol block

• Phenol is a carbolic acid.• When phenol is in contact with motor nerves, it produces

demyelination , destruction of axons and an immediate decrease in spasticity.

• It takes 3-6 months for walerian regeneration and during this period spasticity is controlled.

• Side effects: local pain, fibrosis at injection site and swelling,dysesthesias

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Botulinum toxin:

• Derived from clostridium botulinum bacteria.• It acts by cleavage of polypeptides required for exocytosis at NMJ.• Cleavage of these peptides prevents the release of acetylcholine

into NMJ, relieving focal muscle hypertonia. Injection procedure:• Injected near motor points of muscles.• Multiple injections per muscle.• Peak effect begins 7-10 days after injection.• Should not be reinjected before 90 days.

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Intrathecal baclofen pump:• Drug administered directly into subarachnoid space of CNS with a

programmable pump.• Improvement in walking speed, functional mobility without

impairing uninvolved extremity.• Fewer systemic side effects because not circulating in blood

stream.

Surgical management

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Advantages of ITB

• Non-destructive and reversible• Potential for fewer side effects as compared to oral baclofen.• Dose can be adjusted to optimal effect.• May decrease spasticity related pain

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Potential risks of ITB

• Side effects: weakness, drowsiness, nausea, headache, dizziness.• Overdose leads to respiratory depression, loss of consciousness,

coma and in extreme cases may be life threatening.• Infection• Abrupt discontinuation can result in high fever, altered mental

status, worsened spasticity, and muscle rigidity.

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Neurosurgery• Severe and painful spasticity, irreversible.Dorsal root rhizotomies.• Cuts dorsal cords and grey matter from upper lumber (L2) level to

upper sacral (S2) root level.• Normally these fibers carries excitatory signals from the muscle to

spinal cord and descending inhibitory input from brain to counterbalance them for control muscle tone.

• If this delecate balance is lost due to CNS injury one way to avoid excess sensory input via rhizotomy.

• Performed mostly on children with spastic diaplegic cerebral palsy.

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Orthopedic procedures

• More prevalent compare to neurosurgical procedure.

• Target tissues are bone, joint, ligament, muscle, tendon.

• Goals includes reduce spasticity, improve range of motion, improving fit of orthoses, reducing pain.

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Tendon lengthening- • Allow full passive range with some residual muscle tension.• Hamstring and achilles release are common.Tendon transfer• Split anterior tibial transfer is a common procedure for correction

of equinovarus deformity.Osteotomy• For skeletal deformityArthrodesis• Joint fusion• Stabilize unstable joint,most common in ankle and foot.

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It includes followings:• Avoiding noxious stimuli• Physical modalities• Static stretch• Positioning• Reflex-inhibiting movement patterns• Relaxation• Bio-feedback• PNF techniques• Slow rhythmic passive movement

Physiotherapy management

Spasticity and overactivity have been shown to be increased as a result of this noxious stimulation.

Stimulation of the flexor reflex afferents may lead to an increase in pathologic activity.

The term noxious stimulation encompasses a wide variety of conditions such as a pressure ulcer, ingrown toenail, contracture, kinked catheter, urolithiasis, UTI, DVT

Reduction of noxious stimulation

Proper positioning is an important component of spasticity management. Poor positioning can result in an increase spasticity and decrease ROM, contractures, increased noxious stimulation, pain and exacerbation of a vicious cycle that can lead to worsening spasticity.

Positioning improvement in body alignment and greater symmetry.

Posture that should be avoided include a leg scissoring posture , windswept position and frog leg position which can exacerbate the spasticity.

positioning

Different physical modalities use for spasticity management are followings:

Ultrasound• Ultrasound therapy is assumed to have a viscoelastic changes in

spastic muscle but also decreases the sensitivity of the muscle spindle to stretch and alpha motorneuron excitability by increasing the tissue temperature.

• 10 minutes sessions of continuous ultrasound therapy for 5 weeks• Frequency 1 MHz , intensity 1.5 W/cm2

Physical modalities

Cryotherapy• Local muscle cooling has been described to temporarily decrease

spasticity and clonus mainly by reducing the sensitivity of the muscle spindle to stretch.

• Skin cooling to have an antispastic effect by increasing pain threshold and consequently reducing receptor sensitivity of low threshold afferents.

• Average application time is 20 mins.• Cooling have been describe last only for two hours after

treatment.

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Thermotherapy

• Thermotherapy decrease muscle tone, reduce muscle spasms and increase the pain threshold in patient with spasticity.

• It causes relaxation muscles and decreases gamma afferent fiber activity that would lead to a decrease in impulses from the muscle spindles with a consenquent inhibition of alpha fibers.

• 20 mins and 75 C hot pack application prior passive stretching increases muscle extensibility.

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Neuromuscular electrical stimulation.• NMES reduce spasticity and improve motor function.• Application to tibialis anterior muscle or to the common paroneal

nerve have been shown to reduce spasticity in platerflexor muscles and ankle clonus.

• Faradic stimulation to forearm muscles has been shown to reduce flexor tone and posturing of the hand by reciprocal inhibition.

Biofeedback• Biofeedback is the use of an electrical monitor that creates a

signal, usually a sound, as a spastic muscle relax.In this way the person with spasticity may e able to train himself to reduce muscle tone consciously.

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Spasticity and muscle overactivity also play a part in muscle shortening.

Stretch has the advantage of being a focal treatment that can combat the development of the muscle shortening and increase in spindle sensitivity.

Benefits from the brief stretch is short lived so stretch needs to be applied for a longer period of time for functional benefit.

Chronic stretch via casting or splints changes reflexive activity and reduces the stretch reflex.

Stretch and casting

• Chronic stretch via casting or splints changes reflexive activity and reduces the stretch reflex.

• Serial casting is indicated when an individual presents with range of motion limitation due to contracture or the potential of developing contracture as a result of spasticity.

• The sustained position produces relaxation of the spastic muscles, thought to be the result of GTO autogenic inhibition and adaption of stretch receptors.

• Orthoses• Adjustable orthoses also have been used to provide passive

sustained stretch with added benefits of easy removal for hygiene .

casting

Dynamic orthoses primarily used on elbow or knee flexion contractures, uses a spring loaded or hydrulic mechanism to provide nearly constant pressure.Ex –AFO, KAFO

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Decrease spasticity and maintain limbs in optimal tone-reducing position during functional training.

Inflatable pressure splint

Reflex inhibiting movement pattern Prolong pressure to long tendons inhibits the hypertonicity of a

muscle. Firm pressure can be applied manually or by body weight. Weight bearing postures are used to provide inhibitory pressure,

such as ~ quadruped or kneeling used for inhibition of quadriceps and long finger flexors. ~ sitting, with hand open, elbow extended, and upper extremity supporting body weight can be used to promote inhibition of long finger flexors.

Inhibition techniques

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Rhythmical , slowly performed passive movements through normal patterns may also be helpful and in the more moderate cases patients may subconsciously join in and by his own activity a reduction in spasticity may occur.

Deep rhythmic massage Pressure over the muscle insertion can be given to reduce

spasticity. Slow stroking

Relaxed passive movement

Slow repetitive rocking movements; assisted rocking in weight bearing position, for example

Low intensity vestibular stimulation such as slow rocking produces generalized inhibition of tone.

- rocking in chair - swiss ball - equilibrium board - hammock - slow rolling movement

Slow maintained vestibular stimulation

Immersion in water can enhance treatment of neurologically impaired individuals with both therapeutic, physiological and social benefits.

Hydrotherapy is the term used for exercise in warm water and is a popular treatment for patients with neurologic and musculoskeletal conditions.

The goal of this therapy are muscle relaxation, improving joint motion and reducing pain.

Hydrotherapy

Technique used:a. Rhythmic in initiation- voluntary relaxation followed by passive

movements through increments in range, followed by active movements progressing to resisted movements using tracking resistance to isotonic contractions.

b. Rhythmic rotation- Voluntary relaxation combined with slow, passive, rhythmic rotation of the body or body part around a longitudinal axis, followed by passive movement into the antagonist range.

Proprioceptive neuromuscular techniques

Contract relax active contraction- isotonic movement in rotation is performed followed by isometric hold of the range limiting muscles in the antagonist pattern against slowly increasing resistance followed by voluntary relaxation and active movement into the new range of the agonist pattern.

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PHYSICAL REHABILITATION- Fifth edition (Susan B. O’Sullivan, Thomas J. Schmitz ) DELISA’S PHYSICAL MEDICINE AND REHABILITATION- Fifth edition PRINCIPLE OF NEUROLOGICAL SURGERY- Third edition(Richard G. Ellenbogan, Saleem I. Abdulrauf, Laligam N. Shekhar ) PHYSIOTHERAPY IN NEURO-CONDITIONS ( Glady Samuel Raj)

REFERENCES

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