SPASTICITY & PHYSICAL THERAPY MANAGEMENT Sagar Naik, PT

Spasticity
Sagar Naik, PT
Spasticity is a disorder of the sensorimotor system

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characterized by a velocity-dependent increase in muscle tone with

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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 pool
4abecomes 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,
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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
y

the involved and neighboring muscles.

The abnormal joint positioning, postures, and unequal distribution of
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muscle activity imposed by spasticity can produce profound and

lasting 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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D Mechanism:

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4a
Primary afferent Ia fibers surrounding intrafusal fibers of the
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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
y

synergistic motor neurons, combined with inhibition of

antagonists, subserves the mechanism of reciprocal inhibition.
There is evidence for impairment of this mechanism in the UMN
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syndrome.

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D Features:
Spasticity, spinal model:
• Removal of inhibition on segmental polysynaptic pathways
• Slow, progressive rise of excitatory state through cumulative

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excitation
• Afferent activity from one segment may lead to muscle

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response many segments away
• Flexors and extensors may be overexcited
Spasticity, cerebral model:
• Enhanced excitability of monosynaptic pathways
• Rapid build-up of reflex activity
• Bias toward over activity in the antigravity muscles and the
development of hemiplegic posture
The clinical features of released flexor reflex are:
4a • Big toe extension (principal component of Babinski's sign)
• Ankle, knee, and hip flexion - contraction of abdominals

D Clinical Features:
POSITIVE SYMPTOMS
y Spasticity
sio
- Increased muscle tone
- Exaggerated tendon jerks
- Stretch reflex spread to extensors
- Repetitive stretch reflex discharges; clonus
y Released flexor reflexes
- Babinski response
- Mass synergy patterns
NEGATIVE SYMPTOMS
y

y Loss of finger dexterity

y Weakness
- Inadequate force generation
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- Slow movements
y Loss of selective control of muscles and limb segments
RHEOLOGIC CHANGES IN SPASTIC MUSCLE
y Stiffness y Fibrosis
y Contracture y Atrophy

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 SPASTICITY & PHYSICAL THERAPY MANAGEMENT Sagar Naik, PT

Potentially Spastic Muscles in the Common Patterns of Upper Motor Neuron

Dysfunction

The Upper Limbs

y The Adducted/Internally Rotated y The Flexed Wrist
Shoulder - Flexor carpi radialis and brevis

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- Pectoralis major - Extrinsic finger flexors
- Latissimus dorsi y The Clenched Fist

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- Teres major - Various muscle slips of FDP
- Subscapularis - Various muscle slips of FDS
yThe Flexed Elbow
- Brachioradialis y The Intrinsic Plus Hand
- Biceps - Dorsal interossei
- Brachialis y The Thumb-In-Palm Deformity
y The Pronated Forearm - Adductor pollicis
- Pronator quadratus - Thenar group
- Pronator teres - Flexor pollicis longus
4a
y The Equino-varus Foot
The Lower Limbs

(with Curled Toes or Claw Toes)

- Medial gastrocnemius
- Lateral hamstrings
y The Flexed Knee
- Medial hamstrings
- Lateral hamstrings
- Quadriceps
- Soleus - Gastrocnemius
sio
- Tibialis posterior
- Tibialis anterior y Adducted Thighs
- Extensor hallucis longus - Adductor longus
- Long toe flexors - Adductor magnus
- Peroneus longus - Gracilis
y Striatal Toe - Iliopsoas (weak)
(Hitchhiker's Great Toe) - Pectineus (weak)
- Extensor hallucis longus
y The Stiff (Extended) Knee y The Flexed Hip
y

- Gluteus maximus - Rectus femoris

- Rectus femoris - Iliopsoas
- Vastus lateralis - Pectineus
- Vastus medialis - Adductors longus
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- Vastus intermedius - Adductor brevis (weak)

- Hamstrings - Gluteus maximus (weak)
- Gastrocnemius
- Iliopsoas (weak)

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D Management:

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4a
sio
y
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 SPASTICITY & PHYSICAL THERAPY MANAGEMENT Sagar Naik, PT

There are two clinical types of spasticity that can develop in

response to injury to the central nervous system–phasic 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 spasticity
but the muscle shows a decreased amount of stretch in tonic

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spasticity.
This decreased amount of muscle stretch can lead to the gradual

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development of contractures.
Thus, spasticity must be aggressively managed in the early stages
to prevent permanent deformities and joint contracture.

Û General Considerations:
Carefully assess the extent to which muscle overactivity
4a impacts 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
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intercurrent medical illness, certain classes of medications
known to increase muscle tone (e.g. neuroleptic agents) and
finally emotional stressors. Factors like
y Urinary tract infection
y Urolithiasis
y Stool impaction
y Pressure sore
y Fracture & Dislocation
y

y Ingrown toe nail

y Clothing that is too tight
y Heterotopic ossification
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Û Medical Management:
M Oral Medications:
Benzodiazepines - Diazepam and Clonazepam is

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centrally acting agents that increase the affinity of GABA
to its receptor. The clinical effects of diazepam include

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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 excitatory
neurotransmitters.
4a 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,
sio
associated with antispasticity effects without muscle
weakness.

M Botulinum Toxin Type A:

BTX-A affects the neuromuscular junction through
binding, internalization, and inhibition of acetylcholine
y

release.
It must enter the nerve endings to exert its
chemodenervating effect.
ph

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.

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M Intrathecal Baclofen™ (ITB):

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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,
4a 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
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other spasticity medications.

Û Surgical Management:
M Neurosurgery for Spasticity:
< Selective Dorsal Rhizotomy:
y

Selective dorsal rhizotomy (SDR) or selective posterior

rhizotomy in which nerve roots are cut, the fibers lying
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just outside the vertebral column that transmit nerve

impulses 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:
y Pure spasticity (limited dystonia/athetosis)

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y Function limited primarily by spasticity
y Adequate truncal balance / righting responses

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y Not significantly affected by primitive reflexes /
movement patterns
y Absence of profound underlying weakness
y Selective motor control
y Some degree of spontaneous forward locomotion
y Spastic diplegia
y History of prematurity
4a y Minimal joint contracture & spine deformity
y Adequate cognitive ability to participate in therapy
y No significant motivational / behavioral problems
y Age 3 – 8 years
y Supportive & interactive family

< Myelotomy & Cordotomy:

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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,
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muscle wasting, and loss of erectile function can be

seen.
ph

M 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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y Reducing spasticity
y Increasing range of motion
y Improving access for hygiene
y Improving tolerability of braces
y Reducing pain
Orthopedic surgery is done in patients who have been

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refractory to more conservative measures and patients
whose recovery after central nervous system insult has

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plateaued.
These surgeries alters musculotendinous unit in way that
decreases tension. It is often used when spasticity has
progressed to contracture.
Different techniques include
y Tenotomy involves transection of tendon
y Neurectomy involves excision of part of nerve
4a y Tendon transfer involves moving tendon form one
insertion site to another
y Tendon lengthening involves sectioning tendon with
step-like incision and then sewing longest pieces
together, again resulting in increased tendon length
y Arthrodesis involves locking joint in fixed position
y Bony surgeries, such as rotational osteotomy
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y
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Û Physiotherapy Management:
When treating a patient who shows spasticity it is necessary to
carry out three important aims:
y Inhibit excessive tone as far as possible
y Give the patient a sensation of normal position and

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normal movement
y Facilitate normal movement patterns

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< Body Positioning:
In cases of spasticity it is important to facilitate the
patient’s ability to inhibit the undesirable activity of the
released reflex mechanisms.
The position adopted by the patient is important since
4a the 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
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effect of the reflex activities then he can be gradually
introduced 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 reflex and also, as head and trunk are in
alignment, the stimulation of the asymmetrical tonic
neck reflexes.
y

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 assisted
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active 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 as crook
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

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and externally rotate.
Limb rotations are also very effective in helping to give

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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 medial
rotation of hip is produced together with plantar flexion
4a of the foot, which is undesirable in case of spasticity.
If pressure 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:
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Movement of a normal nature does appear in itself to
reduce 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
y

likely to act as a triggering mechanism to those

motoneurone pools giving associated muscle
contraction in the spastic pattern.
ph

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.

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Stretching helps to maintain the full range of motion of
a joint, and helps prevent contracture, or permanent

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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 flexors
4a due 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
sio
y Manual contacts
y Inhibitory casting or splinting
y Reflex-inhibiting patterns
y Mechanical low-load weights

< Prolonged Cold Application:

Application of cold packs to spastic muscles (usually for

y

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 ease
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pain.
It activates thermoreceptors.
It decreases neural, muscle spindle firing and provides
inhibition of muscle tone.
Techniques used
y Immersion in cold water; ice chips

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y Ice towel wraps

y Ice packs
y Ice massage
y Ice application with exercises

< Neutral Warmth:

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Retention of body heat stimulates thermoreceptors,

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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
4a y Wrapping body or body parts: ace wraps, towel
wraps
y Application of snug fitting clothing (gloves, socks,
tights) or air splints
y Tepid baths

< Relaxed Passive Movements:

Rhythmical, slowly performed passive movements
sio
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 Rhythmical Massage (Tendon Rolling):

Deep rhythmical massage with pressure over the muscle
y

insertions can be given to reduce spasticity.

< Inhibitory Pressure (Weight-Bearing):

ph

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
y Quadruped or kneeling postures can be used to
promote inhibition of quadriceps and long finger

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flexors.
y Sitting, with hands open, elbow extended, and upper

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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 signal—usually a sound—as a spastic muscle
4a relaxes.
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
sio
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:

y

These are plastic AFO’s in which foot plate and broad

upright are designed to modify reflex hypertonicity by
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applying 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:

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

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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:
9 Rocking chair
9 Swiss ball
4a 9 Equilibrium board
9 Hammock
Slow rolling movements

< Proprioceptive Neuromuscular Techniques:

Techniques used
9 Rhythmic Initiation – Voluntary relaxation
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followed by passive movements through increments
in range, followed by active movements progressing
to resisted movements using tracking resistance to
isotonic contractions.
9 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
y

range.
9 Contract Relax Active Contraction – Isotonic
movement in rotation is performed followed by
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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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< 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

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manipulating the pelvis which is the central key point.
In sitting, place one hand over the lower back and other

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near the xiphoid process. Now move the patient in the
figure of 8 pattern forwards and backwards.

4a
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y
ph

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