6130612 Spas Ti City Management

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SPASTICITY & PHYSICAL THERAPY MANAGEMENT Sagar Naik, PT

Spasticity

Sagar Naik, PTSpasticity is a disorder of the sensorimotor system

characterized by a velocity-dependent increase in muscle tone with

exaggerated tendon jerks, resulting from hyperexcitability of the

stretch reflex. It is one component of the upper motor neuron

syndrome, along with released flexor reflexes, weakness, and loss of

dexterity.

Spasticity is the hypertonicity in the muscle group. It

can be defined as an initial catch or resistance felt by the examiner

when rapid passive movements are performed.

In an upper motor neuron syndrome, the alpha motor neuron poolbecomes hyperexcitable at the segmental level.

Spasticity occurs because the inhibition normally provided by the

suppresser areas of the brain is not present.

Brain lesions disrupt the linkages and upset the balance between

suppresser and facilitory areas of the brain.

The major consequence of the disruption of the balance is the excess

facilitation of gamma motor neurons resulting in hypersensitive

muscle spindles. This results in hyperactive phasic stretch reflexes,

hyperactive tonic reflexes, and clonus. Spasticity caused by spinal cord lesions is often marked by a slow

increase in excitation and over activity of both flexors and extensors

with reactions possibly occurring many segments away from the

stimulus.

Cerebral lesions often cause rapid build-up of excitation with a bias

toward involvement of antigravity muscles.

Chronic spasticity can lead to changes in the rheologic properties of

the involved and neighboring muscles.

The abnormal joint positioning, postures, and unequal distribution of

muscle activity imposed by spasticity can produce profound andlasting changes in joints and muscles.

Stiffness, contracture, atrophy, and fibrosis may interact with

pathologic regulatory mechanisms to prevent normal control of limb

position and movement.

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Mechanism:

Primary afferent Ia fibers surrounding intrafusal fibers of the

muscle spindle are excited when a muscle is stretched.

The Ia fiber makes a monosynaptic excitatory connection with

alpha motor neurons of its muscle of origin, and it similarly

connects with alpha motor neurons of synergistic muscles.

The Ia fiber also monosynaptically connects with an inhibitory

interneuron that projects directly to the alpha motor neurons of

antagonist muscles.

When a muscle is stretched, excitation of homonymous and

synergistic motor neurons, combined with inhibition of

antagonists, subserves the mechanism of reciprocal inhibition.

There is evidence for impairment of this mechanism in the UMNsyndrome.

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Features: Spasticity, spinal model:

Removal of inhibition on segmental polysynaptic pathwaysSlow, progressive rise of excitatory state through cumulativeexcitationAfferent activity from one segment may lead to muscle

response many segments away

Flexors and extensors may be overexcited Spasticity, cerebral model:

Enhanced excitability of monosynaptic pathwaysRapid build-up of reflex activityBias toward over activity in the antigravity muscles and the

development of hemiplegic posture The clinical features of released flexor reflex are:

Big toe extension (principal component of Babinski's sign)Ankle, knee, and hip flexion - contraction of abdominals

Clinical Features: POSITIVE SYMPTOMS

Spasticity

- Increased muscle tone- Exaggerated tendon jerks

- Stretch reflex spread to extensors

- Repetitive stretch reflex discharges; clonus

Released flexor reflexes

- Babinski response

- Mass synergy patterns

NEGATIVE SYMPTOMS

Loss of finger dexterity

Weakness

- Inadequate force generation- Slow movements

Loss of selective control of muscles and limb segments

RHEOLOGIC CHANGES IN SPASTIC MUSCLE

Stiffness Fibrosis

Contracture Atrophy

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Potentially Spastic Muscles in the Common Patterns of Upper Motor Neuron

Dysfunction

The Upper Limbs

The Adducted/Internally RotatedShoulder

- Pectoralis major

- Latissimus dorsi

- Teres major- Subscapularis

The Flexed Elbow- Brachioradialis- Biceps

- Brachialis

The Pronated Forearm- Pronator quadratus- Pronator teres

The Flexed Wrist- Flexor carpi radialis and brevis- Extrinsic finger flexors

The Clenched Fist- Various muscle slips of FDP- Various muscle slips of FDS

The Intrinsic Plus Hand- Dorsal interossei

The Thumb-In-Palm Deformity- Adductor pollicis

- Thenar group- Flexor pollicis longus

The Lower Limbs

The Equino-varus Foot(with Curled Toes or Claw Toes)- Medial gastrocnemius

- Lateral hamstrings

- Soleus- Tibialis posterior

- Tibialis anterior- Extensor hallucis longus- Long toe flexors

- Peroneus longus

Striatal Toe(Hitchhiker's Great Toe)- Extensor hallucis longus

The Stiff (Extended) Knee- Gluteus maximus- Rectus femoris

- Vastus lateralis

- Vastus medialis- Vastus intermedius

- Hamstrings

- Gastrocnemius- Iliopsoas (weak)

The Flexed Knee- Medial hamstrings- Lateral hamstrings

- Quadriceps

- Gastrocnemius

Adducted Thighs- Adductor longus- Adductor magnus

- Gracilis

- Iliopsoas (weak)

- Pectineus (weak)

The Flexed Hip- Rectus femoris- Iliopsoas

- Pectineus

- Adductors longus- Adductor brevis (weak)

- Gluteus maximus (weak)

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Management:

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There are two clinical types of spasticity that can develop in

response to injury to the central nervous systemphasic and tonic.

Phasic spasticity is often the initial manifestation of spasticity and

tonic spasticity may occur months to years later.

The muscle has a normal lengthening reaction in phasic spasticitybut the muscle shows a decreased amount of stretch in tonic

spasticity.

This decreased amount of muscle stretch can lead to the gradual

development of contractures.

Thus, spasticity must be aggressively managed in the early stages

to prevent permanent deformities and joint contracture.

General Considerations:

Carefully assess the extent to which muscle overactivityimpacts patients' function, hygiene, comfort, and care. Target

the patient's most bothersome dysfunction.

Be aware of the complications of spasticity such as pressure

sores, contractures, pain, poor hygiene and deconditioning.

Some degree of spasticity may be beneficial in maintaining

postural control and ambulation, so global reduction of tone

may be destabilizing.

Consider factors that may aggravate spasticity including

intercurrent medical illness, certain classes of medicationsknown to increase muscle tone (e.g. neuroleptic agents) and

finally emotional stressors. Factors like

Urinary tract infection

Urolithiasis

Stool impaction

Pressure sore

Fracture & Dislocation

Ingrown toe nail

Clothing that is too tight

Heterotopic ossification

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Medical Management:

Oral Medications: Benzodiazepines - Diazepam and Clonazepam is

centrally acting agents that increase the affinity of GABA

to its receptor. The clinical effects of diazepam include

improved passive range of motion and reduction in

hyperreflexia as well as painful spasms. These agents also

cause sedation and improve anxiety.

Baclofen is GABA agonist that has presynaptic and

postsynaptic effects on monosynaptic and polysynaptic

pathways. The primary site of action is the spinal cord

where baclofen reduces the release of excitatoryneurotransmitters.

Dantrolene sodium acts peripherally at the level of the

muscle fiber. It affects the release of calcium from the

sarcoplasmic reticulum of skeletal muscle and thus reduces

muscle contraction. Dantrolene sodium is generally

indicated for spasticity of supra spinal origin.

Tizanidine has been used for the treatment of spasticity as

a central alpha 2 - noradrenergic agonist; tizanidine

facilitates short-term vibratory inhibition of the H-reflex,

associated with antispasticity effects without muscleweakness.

Botulinum Toxin Type A: BTX-A affects the neuromuscular junction through

binding, internalization, and inhibition of acetylcholine

release.

It must enter the nerve endings to exert its

chemodenervating effect. Once inside the cholinergic nerve terminal cell, BTX-A

inhibits the docking and fusion of acetylcholine vesicles at

the pre-synaptic membrane.

Duration of effect is usually 3 to 4 months, but can be

longer or shorter.

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Gradually, muscle function returns by the regeneration or

sprouting of blocked nerves forming new neuromuscular

junctions.

BTX-A is dose-dependent and reversible secondary to the

regeneration process.

Intrathecal Baclofen (ITB): Intrathecal baclofen therapy (ITB Therapy) consists of

long-term delivery of baclofen to the intrathecal space.

This treatment can be very effective for patients with severe

spasticity, particularly for those patients whose conditions

are not sufficiently managed by oral baclofen and other

oral medications.

Benefits of ITB Therapy typically include reduced tone,spasms, and pain, and increased mobility.

In addition, many patients, caregivers, family members and

physicians have reported striking improvements in

movement and self-care.

Other benefits may include improved speech, sleep quality,

bladder control, and self-image.

The efficacy of ITB Therapy in controlling spasticity

typically allows patients to decrease and often discontinue

other spasticity medications.

Surgical Management:

Neurosurgery for Spasticity:Selective Dorsal Rhizotomy: Selective dorsal rhizotomy (SDR) or selective posterior

rhizotomy in which nerve roots are cut,the fibers lying

just outside the vertebral column that transmit nerveimpulses to and from the spinal cord.

These nerves carry sensory information to the cord from

muscle.

Excitatory signals from these sensory nerves are

counterbalanced by inhibitory signals from the brain,

maintaining normal muscle tone.

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Thus when brain or spinal cord damage upsets this

balance, excess sensory signaling can lead to spasticity.

Hence sensory nerves are targeted.

Favorable selection criteria for selective dorsal

rhizotomy are as follows: Pure spasticity (limited dystonia/athetosis)

Function limited primarily by spasticity

Adequate truncal balance / righting responses

Not significantly affected by primitive reflexes /

movement patterns

Absence of profound underlying weakness

Selective motor control

Some degree of spontaneous forward locomotion

Spastic diplegia

History of prematurity Minimal joint contracture & spine deformity

Adequate cognitive ability to participate in therapy

No significant motivational / behavioral problems

Age 3 8 years

Supportive & interactive family

Myelotomy & Cordotomy:

Myelotomy is complete disruption of some spinal cord

tracts and cordotomy is complete transection of spinal

cord.

These surgeries are advocated as treatment modalities in

most severe cases of spasticity; rarely performed except

occasionally in patients with complete spinal cord

injury.

Side effects of loss of bowel and bladder function,

muscle wasting, and loss of erectile function can be

seen.

Orthopedic Surgery for Spasticity: Orthopedic surgery is the most frequently used surgical

procedure for spasticity. The targets of these surgeries are

the muscle, tendon, or bone in a spastic limb. The goals of

surgery may include

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Reducing spasticity

Increasing range of motion

Improving access for hygiene

Improving tolerability of braces

Reducing pain Orthopedic surgery is done in patients who have been

refractory to more conservative measures and patients

whose recovery after central nervous system insult has

plateaued.

These surgeries alters musculotendinous unit in way that

decreases tension. It is often used when spasticity has

progressed to contracture.

Different techniques include

Tenotomy involves transection of tendon

Neurectomy involves excision of part of nerve Tendon transfer involves moving tendon form one

insertion site to another

Tendon lengthening involves sectioning tendon with

step-like incision and then sewing longest pieces

together, again resulting in increased tendon length

Arthrodesis involves locking joint in fixed position

Bony surgeries, such as rotational osteotomy

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Physiotherapy Management:

When treating a patient who shows spasticity it is necessary to

carry out three important aims:

Inhibit excessive tone as far as possible Give the patient a sensation of normal position andnormal movement

Facilitate normal movement patternsBody Positioning:

In cases of spasticity it is important to facilitate the

patients ability to inhibit the undesirable activity of the

released reflex mechanisms.

The position adopted by the patient is important sincethe head and neck position can elicit strong postural

reflex mechanisms.

Avoiding these head and neck positions can facilitate

the inhibition of the more likely reflexes and if

positions have to be adopted, then help in preventing

the rest of the body from going into the reflex pattern

thus elicited may be required by the patient.

As patient develops control in the suppression of the

effect of the reflex activities then he can be graduallyintroduced to use of positions which make suppression

of reflex activity more difficult.

Side lying position well supported by pillows is very

convenient since it avoids stimulation of the tonic

labyrinthine reflexand also, as head and trunk are in

alignment, the stimulation of the asymmetrical tonic

neck reflexes.

It makes a good resting position for the patient with

spasticity and also is convenient for the application of

rhythmical trunk rotations of both passive and assistedactive form which further helps in reduction of tone.

Side lying is not always desirable because of respiratory

problems in the older patient or because of the need to

obtain a greater range of movement.

Other attitudes are often very satisfactory such ascrook

lying or even with the knees as high on the chest as

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possible. These two positions are helpful if there is

flexor spasticity.

Rotatory Movements:

Trunk rotation produces lower limb to extend, abduct

and externally rotate.

Limb rotations are also very effective in helping to give

a more normal control of muscle tone to the patient.

Pressure over undersurface of Foot:

If the pressure is applied to the ball of the foot it may

well stimulate an extensor reflex in which a

pathological pattern of extension, adduction, and medialrotation of hip is produced together with plantar flexion

of the foot, which is undesirable in case of spasticity.

Ifpressure is applied under the heel of the foot then a

more useful contraction of muscle is likely to occur

giving a suitable supporting pattern.

Normal Movements Patterns & Avoidance of Triggering Factors:

Movement of a normal nature does appear in itself toreduce excessive tone and consequently this should be

encouraged in the patient.

However, care must be taken if conscious volitional

movement is demanded.

Due to reflex release, some motoneurone pools are

already in an excitatory state and any volitional effort is

likely to act as a triggering mechanism to those

motoneurone pools giving associated muscle

contraction in the spastic pattern. Such patients should not be encouraged to make strong

volitional effort since this is inclined to facilitate the

production of spastic patterning.

Other factors such as quick movements, abruptly

performed, noisy surroundings, anxiety, excitement,

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over exertion should also be avoided as it may increase

spasticity.

Slow Sustained Stretching:

Stretching forms the basis of spasticity treatment.

Stretching helps to maintain the full range of motion of

a joint, and helps prevent contracture, or permanent

muscle shortening.

It activates muscle spindles (Ia & II endings), golgi

tendon organs (Ib endings) which are sensitive to length

changes.

It inhibits or dampens muscle contraction and tone due

largely to peripheral reflex effects.

It can be more effective in extensor muscles than flexorsdue to the added effects of II inhibition.

This method does have its dangers since, if stretching is

forced against severe spasticity, the hyperexcitable

stretch reflex reacts even more strongly and damage to

the periosteum of bone may occur where excessive

tension has been applied by the tendons of the stretched

muscles.

Techniques used are

Manual contacts

Inhibitory casting or splinting

Reflex-inhibiting patterns

Mechanical low-load weights

Prolonged Cold Application:

Application of cold packs to spastic muscles (usually for

10 minutes or longer) may improve muscle tone.

While the effect doesn't last long, it may be used to

improve function for a short period of time, or to easepain.

It activates thermoreceptors.

It decreases neural, muscle spindle firing and provides

inhibition of muscle tone.

Techniques used

Immersion in cold water; ice chips

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Ice towel wraps

Ice packs

Ice massage

Ice application with exercises

Neutral Warmth:

Retention of body heat stimulates thermoreceptors,

autonomic nervous system mainly parasympathetics,

which produces generalized inhibition of tone, calming

effect, relaxation and decreases pain.

It should be applied for about 10 to 20 minutes.

Overheating should be avoided as it might increase

arousal or tone.

Techniques used Wrapping body or body parts: ace wraps, towel

wraps

Application of snug fitting clothing (gloves, socks,

tights) or air splints

Tepid baths

Relaxed Passive Movements:

Rhythmical, slowly performed passive movements

through normal patterns may also be helpful and in themore moderate cases patients may subconsciously join

in and by his own activity a reduction in spasticity may

occur.

Deep Rhythmical Massage (Tendon Rolling):

Deep rhythmical massage with pressure over the muscle

insertions can be given to reduce spasticity.

Inhibitory Pressure (Weight-Bearing):

Prolonged pressure to long tendons inhibits the

hypertonicity of a muscle.

It activates muscle receptors (muscle spindles, golgi

tendon organ) and tactile receptors.

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Firm pressure can be applied manually or by body

weight.

Weight bearing postures are used to provide inhibitory

pressure, such as

Quadruped or kneeling postures can be used topromote inhibition of quadriceps and long finger

flexors.

Sitting, with hands open, elbow extended, and upper

extremity supporting body weight can be used to

promote inhibition of long finger flexors.

Biofeedback:

Biofeedback is the use of an electrical monitor that

creates a signalusually a soundas a spastic musclerelaxes.

In this way, the person with spasticity may be able to

train himself to reduce muscle tone consciously.

Functional Electrical Stimulation:

Electrical stimulation may be used to stimulate a weak

muscle to oppose the activity of a stronger, spastic one.

It improves standing, walking, and exercise training as

well as decreases upper extremity contractures. Appears to improve motor activity in agonistic muscles

and reduce tone in antagonistic muscles.

Therapeutic effect may last for less than 1 hour after

stimulation has been stopped, probably because of

neurotransmitter modulation within reflex arc.

Tone Reducing Orthosis:

These are plastic AFOs in which foot plate and broad

upright are designed to modify reflex hypertonicity byapplying constant pressure to the plantarflexors and

invertors.

They control the tendency of the foot to assume an

equino-varus posture.

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Foot plate may be modified which maintains the toes in

an extended or hyperextended position, thus assisting

individual to walk with better foot and knee control.

Slow Maintained Vestibular Stimulation: Low-intensity vestibular stimulation such as slow

rocking produces generalized inhibition of tone.

It facilitates primarily otolith organs (tonic receptors);

less effects on semicircular canals (phasic receptors).

Slow, repetitive rocking movements; assisted rocking in

a weight-bearing position, for example, rocking with

equipments:

Rocking chair Swiss ball Equilibrium board Hammock

Slow rolling movements

Proprioceptive Neuromuscular Techniques:

Techniques used

Rhythmic Initiation Voluntary relaxationfollowed by passive movements through increments

in range, followed by active movements progressingto resisted movements using tracking resistance to

isotonic contractions.

Rhythmic Rotation Voluntary relaxationcombined with slow, passive, rhythmic rotation of

the body or body part around a longitudinal axis,

followed by passive movement into the antagonist

range.

Contract Relax Active Contraction Isotonicmovement in rotation is performed followed byisometric 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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Manipulating Key Points:

For reducing spasticity, manipulating the thumb will

reduce the spasticity. All the movements should be

carried out with thumb in abduction.

Another technique to reduce the spasticity is

manipulating the pelvis which is the central key point.

In sitting, place one hand over the lower back and other

near the xiphoid process. Now move the patient in the

figure of 8 pattern forwards and backwards.

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6130612 Spas Ti City Management

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