This document discusses spasticity management. It defines spasticity as a hypertonic motor disorder caused by injury to the corticospinal pathways. Signs of upper motor neuron syndrome include hyperactive stretch reflexes and involuntary flexor/extensor spasms. Spasticity is assessed using measures like the modified Ashworth scale and is treated using a multidisciplinary approach including oral medications, injections, surgery, and physiotherapy. Treatment aims to reduce spasticity and improve function and range of motion.

1. SPASTICITY MANAGEMENT
Presented By: Jwanika Vansiya
1st Year MPT
Guided By: Dr. Ravi Shah

2.  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?

3.  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

4. What is stretch reflex?
.

5.  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.
.

6.  Stroke
 Multiple Sclerosis
 Traumatic Brain Injury
 Acquired Brain Injury
 Spinal Cord Injury
 Cerebral Palsy
Examples of UMN Lesions

7. 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

8. ASSESSMENT GOAL
SETTING
CHOICE OF
TREATMENT
SPASTICITY MANAGEMENT

9.  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

10. 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

11.  The treatment of spasticity almost always multidimensional or
multimodality therapy that includes followings:
Treatment
Oral
medications
Parenteral
medications
Surgical
procedure
Physiotherapy
management

12.  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

13.  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.
.

15.  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.
.

16. 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.
.

17.  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 block
2. Botulinum toxin
Local injections

18.  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
.

19.  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.
.

20. .

21.  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

22. .

23.  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
ad

24.  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.
.

25. 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.
.

26. .

27. 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.
.

28.  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 deformity
Arthrodesis
• Joint fusion
• Stabilize unstable joint,most common in ankle and foot.
.

29. .

30. 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

31.  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

32.  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

34. 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

35. 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.
.

36.  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.
.

37.  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.
.

38.  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

39. • 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

40. 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
.

41. Decrease spasticity and
maintain limbs in optimal
tone-reducing position
during functional
training.
Inflatable pressure
splint

42. 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

43. .

44.  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

45.  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

46.  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

47.  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

48. 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.
.

49.  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

50. THANK YOU