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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.