This document discusses current trends in the management of spasticity in hemiplegic patients. It defines spasticity as a velocity-dependent increase in muscle tone caused by damage to the central nervous system. Spasticity can range from mild muscle stiffness to severe, painful muscle spasms. If left untreated, spasticity may lead to muscle contractures, deformities, and other complications. Common treatments discussed include oral medications, botulinum toxin injections, physical therapy, and the modified Ashworth scale for assessing spasticity severity.

1. CURRENT TRENDS IN THE MANAGEMENT
OF
SPASTICITY IN HEMIPLEGIC PATIENT.
A SEMINAR PRESENTATION
BY
ELOCHUKWU, PEACE UJUAKU
(BMR)PT

2. INTRODUCTION
DEFINITION OF SPASTICITY:
 Spasticity is a motor disorder characterized by a
velocity-dependent increase in tonic stretch reflexes
(muscle tone) with exaggerated tendon jerks,
resulting from hyperexcitability of the stretch reflex.
 Spasticity is a feature of altered skeletal muscle
performance in muscle tone involving hypertonia;
 It is also referred to as an unusual "tightness",
stiffness, and/or "pull" of muscles.
 The word spasm comes from the Greek word,
σπασμός (spasmos), meaning to ‘pull or drag’.

3.  Spasticity is a physiological consequence of an insult to
the brain or spinal cord, that can lead to life-
threatening, disabling and costly consequences (Ward
2008)
 It is characterised by muscle over activity which, if left
untreated, may lead to muscle and soft tissue
contracture.
 Clinically, spasticity is defined as velocity dependent
resistance to stretch, where a lack of inhibition results
in excessive contraction of the muscles, ultimately
leading to hyperflexia (overly flexed joints).

4.  It mostly occurs in disorders of the central nervous
system (CNS) -seen in persons who have had
damage to their central nervous system. That
means damage to the spinal cord or brain.
 Damage to the muscles themselves or to the
peripheral nerves in the limbs does not produce
spasticity.
 In fact, peripheral nerve damage produces the
opposite of spasticity, a condition known as
'flaccidity' which means loose, flabby muscles.
 When damage to the central nervous system
produces spasticity, it also produces weakness, loss
of dexterity or other trouble controlling the
muscles. These are called paresis or palsy; they
produce almost all the handicap or functional
deficit.

5. Classification:
 Spasticity is frequently classified by its presentation
and divided into:
 Generalised
 Regional and
 Focal

6. EPIDEMIOLOGY
 There are varied figures for prevalence of spasticity in
different conditions (Sommerfeld et al. 2004, Pfister et
al. 2003).
 This may be due to the presence of many patients with
mild spasticity for whom little or no treatment is
required for their condition.
 An early brain injury study in the UK estimates that
16% and 18% of first time stroke sufferers and patients
following traumatic brain injury respectively require
spasticity treatment (Verplancke et al. 2005).

7.  In a Swedish study (Lundstrom et al. 2008), the
observed prevalence of any spasticity one year after
first ever stroke was 17% and of disabling spasticity was
4% and
 An American study showed a prevalence of 35% among
adults living in a developmental centre.
 Among all ages, the estimated annual incidence of
ischaemic and haemorrhagic stroke is 183 per 100,000
in the US. (Hirtz et al, 2007)

8. PATHOPHYSIOLOGY
 The pathophysiology is obscure, findings on examination are
inconsistent, and treatment is not always successful, hence spasticity is
managed and not treated.
 Understanding the physiology of normal movement may help the
physician in the understanding of pathophysiology of spasticity.
Physiology of movement
 Afferent input from the internal organs, the musculoskeletal Afferent
input from the internal organs, the musculoskeletal system, and the
skin converge on the medulla spinalis, activates the stretch reflex, both
directly and through neural pathways regulating muscle contraction i.e
the interneuron, and this results in a reflex motor response.
 The same afferent information goes to the cerebellum and the somato-
sensory cortex.
 It is processed in those centers as well as in the basal ganglia.
 The resulting motor response is relayed to the lower motor neuron
through the pyramidal and extrapyramidal system tracts.

9.  The pyramidal tracts go directly to the lower motor
neuron whereas the extrapyramidal tracts end at the
interneuron.
 The cerebellum, basal ganglia, and extrapyramidal
system nuclei modify the motor response as it goes to
the medulla spinalis.
 In this way all motor output is influenced by the
incoming sensory input and converges on the lower
motor neuron.
 The interneurons in the medulla spinalis regulate the
activity of the motor neuron.

10.  Spasticity arises from prolonged dis inhibition of
spinal reflexes as a result of UMN lesion.
 These spinal reflexes include stretch, flexor and
extensor reflexes and are under supraspinal control by
inhibitory and excitatory descending pathways.
 Stretch reflexes are proprioceptive reflexes, and are
either phasic or tonic.
 The tonic stretch reflex arises from a sustained muscle
stretch and is the cause of spasticity (Sheean 2002).
 Damage to pyramidal tracts alone does not result in
spasticity.
 It occurs only when the lesion involves pre-motor and
supplementary motor areas.

11. The motor cortex is responsible for pla
voluntary movement.
The nerve imp
motor cortex is
basal ganglia a
system nuclei.
The basal ga
correct the ti
movement.
s carry movement
or neuron.
The extrapyramidal system
corrects
the force of contraction of the
muscles
involved.
The cerebellum coordinates
the speed and direction of
movement
Muscle spindles in the contracting m
organs in the tendons and mechanoc
send information on the degree of co
medulla spinalis, cerebellum and the
cortex.
nds contraction
ugh the peripheral
mon pathway
s send
ses to the lower
ulate its activity
rective impulses
midal system are
e
ons in the
pinalis

12. Upper Extremity Spasticity

13. Lower Extremity Spasticity

14. SYMPTOMS
 Spasticity can range from mild muscle stiffness to
severe, painful and uncontrollable muscle spasms.
 It is associated with both positive and negative
components of upper motor neuron syndromes.
 Positive components include muscle overactivity, flexor
and extensor spasm, hyperreflexia, athetosis, spastic
dystonia, clonus, and an extensor plantar response.
 Common negative symptoms comprise weakness/
paralysis, early hypotonia, fatigue and loss of dexterity.

15.  Spasticity can be distinguished from rigidity by its
dependence on the speed of muscle stretch and
characteristic distribution in antigravity muscle
groups.
Spasticity does not always cause harm and can
occasionally assist in the rehabilitation process by
enabling a patient to stand when their limb weakness
would not otherwise allow it.

16. Clinical and functional problems associated with severe Spasticity
 Physical :
Non- specific pain
· Discomfort
· Painful muscle spasm
· Difficulties with activities of daily living. e.g. washing, dressing,
eating, toileting, maintaining hygiene, sexual activity
· Problems with posture and mobility
· Physical deformity and long
term contracture
· Pressure ulcers
Emotional/Social:
· Emotional e.g. low mood, distorted self image, impaired
motivation
· Impact on fulfilment of life roles as a partner or a parent
· Sleep disturbance – due to pain and discomfort
· Vocational- impact on employment or education
· Social isolation – due to restricted mobility

17. Vicious cycle of spasticity

18. Complications of spasticity
Spasticity is in itself can be disabling and, if left untreated or
sub-optimally treated, may lead to consequences, such as:
 Muscle contractures (leading to abnormal body segment loading
and sensory change),
 limb deformity and altered body mechanics,
 altered body image,
 the need for special wheelchairs and seating and pressure-
relieving equipment,
 loading on pressure points,
 pressure sores,
 difficulty in the management of pressure sores,
 pain from muscle spasms,
 degenerative joint disease,
 loss of function, and
 mood problems and inability to participate in rehabilitation.

19. Treatment of spasticity
Assessment of spasticity:
Before any intervention is undertaken to modulate
hyper tonicity or spasticity, it is important to attempt
to assess the severity of spasticity.
 Many grading scales are used to quantify spasticity.
These address the degree of muscle tone, the
frequency of spontaneous spasms and the extent of
hyper reflexia.
 Goniometry, Ashworth scale, Tardieu Scales, Goal
attainment scale are only a few of these scales. One of
the most widely used scales is the modified Ashworth
scale.

20. Ashworth scale
 This scale is based on the assessment of resistance to stretch when a
limb is passively moved. It was originally validated for patients with
multiple sclerosis and was validated by Ashworth (1964). Its reliability
is questioned by the subjectivity required by the observer to carry out
the test and by the fact that it measures multiple aspects of limb
stretch. However, it is in general use and has good inter-and intra-rater
reliability (Ashworth 1964). The original Ashworth scale is only
validated for measuring spasticity in the lower limb (Lee et al. 1989). In
addition, it does not distinguish between increased neurogenic muscle
tone and mechanical limb stiffness.
 Despite this, it has nonetheless become the measure against which all
other measures are compared. The major modification (Modified
Ashworth Scale) was proposed to differentiate between mild and
moderate spasticity, as discrepancies appeared in clinical judgement at
the lower end of the original scale. Bohannon validated the scale in
elbow flexion in post-stroke patients and attempts have been made to
widen the validity (Bohannon and Smith 1987). A grade 1+ was added
and the top of the scale was reduced from 5 to 4.

21. Score Ashworth (Ashworth 1964)
Modified Ashworth (Bohannon and
Smith 1987)
O
No increase in tone No increase in tone
1
Slight increase in tone giving a catch
when the limb is moved in flexion/
extension
Slight increase in tone giving a catch,
release and minimal resistance at the
end of range of motion (ROM) when the
limb is moved in flexion/extension
1+ Slight increase in tone giving a catch,
release and minimal resistance
throughout the remainder (less than
half) of ROM
2 More marked increase in tone, but
the limb is easily moved through its
full ROM
More marked increased in tone through
most of the ROM, but limb is easily
moved
3 Considerable increase in tone –
passive movement difficult and ROM
decreased
Considerable increase in tone – passive
movement difficult
4
Limb rigid in flexion and extension Limb rigid in flexion and extension

22. Tardieu scale
 The angle at the point of resistance is noted by stretching a
limb passively.
 This is performed during as slow a movement as possible
(V1), under gravitational pull (V2) and at a fast rate (V3).
 The examiner will feel a catch in a muscle under the
influence of an overactive stretch reflex.
 Five levels have been described at the point of this catch to
capture the quality of the muscular reaction.
 In essence the scale assesses dynamic and static muscle
length as well as joint range of motion.
 The inter and intra-rater reliability is generally good
(Gracies 2001), but the technique does require training to
achieve this.

23. Stretch Velocity
 V1 Slow as possible
 V2 Speed of limb falling under gravity
 V3 Fast as possible
Y Angle (Dynamic Range of Motion)
 R2 Slow Velocity: Passive joint range of motion or
muscle length
 R1 Fast Velocity: Movement through full range of
motion

24. Quality of Muscle Reaction
Course of Passive Movement
 0 No resistance
 1 Slight resistance
 2 Clear catch at precise angle, then release
 3 Fatiguable clonus at precise angle
 4 Unfatiguable clonus at precise angle
 5 Rigid limb & joint

25. Wartenberg Pendulum Test
 In this, the leg moves under gravity and the observer
measures the pendular activity of a spastic limb as it
relaxes. It is best carried out on the lower limb, for it is
not so reliable for other limb segments.
 Other methods for evaluating or assessing spasticity
include muscle grading, deep tendon reflexes and
Range of Motion measuring, bilateral adductor tone
score, visual analogue scale, spasm frequency score,
torque devices and electrophysiological studies
(including dynamic multichannel EMG, tonic
vibratory reflexes and electrical tests related to the H
reflex and F wave). Most of these methods are time
consuming, expensive, require specialised equipment
and are used mainly in research

26. Management of Spasticity
 It is also important to remember that not every “tight”
muscle is spastic. The clinically detectable increase in
muscle tone may be due to spasticity, rigidity or a fixed
muscle contracture.
 The key to successful spasticity management is education
of the patient and carers with both verbal and written
information.
 This allows them to understand, appreciate and be fully
involved in the management plan.
 All patients with spasticity should be followed up by a
coordinated multidisciplinary team, which allows more
timely intervention and close monitor of the progress.
 This helps to deliver a more consistent approach to the
individual over time.

27.  The first step in the management of spasticity is to
identify the key aims and realistic goals of therapy.
 Understanding the underlying pathology and possible
prognosis is helpful in planning these goals .
 Other key points to consider are:
· Identification and management of any trigger or
aggravating factors-
 Initial assessment should exclude any co -morbidity
that may worsen spasticity such as pressure sores,
chronic pain, infection (commonly urinary tract
infection), constipation etc.
 Instigation of an effective and realistic physical
therapy programme including attention to posture and
positioning should also be noted.

28. General aims of management
1. Improve function- mobility , dexterity etc
2. Symptom relief such as
· Relief of pain
-prevent deformity e g muscle shortening,
· -decrease spasms
3. Correcting postural body image
4. Decrease carer burden- Care and hygiene,
positioning, dressing
5. Optimise service responses- facilitate other therapy,
delay/prevent surgery

29. General Management of spasticity
 This includes the medical and pharmacological
management of spasticity and they are as follows:
 A) Pharmacological:
1. The oral agents:
Although different categories of drugs are available, those
most commonly used to treat spasticity are baclofen,
tizanidine, dantrolene, diazepam, gabapentin, botulinum
toxin injection etc Botulinum toxin is the most widely used
treatment for focal spasticity in conjunction with
physiotherapy.

30. 2. Nerve block:
Peripheral nerve blockade/ Regional blocks/ Neurolytic
blockadeare another therapeutic possibility in the
treatment of spasticity. This can be done with the help of
fluoroscopy or nerve stimulation.
 Chemical neurolysis by phenol/ alcohol is irreversible and
can be used at several sites. Blocks are applied most often
to 4 peripheral sites: the pectoral nerve loop, median,
obturator, and tibial nerves.
 The main indication is debilitating or painful spasticity.
Peripheral blocks with local anaesthetics are used as tests
to mimic the effects of motor blocks and determine their
potential adverse effects. Peripheral neurolytic blocks are
easy to perform, effective, and inexpensive.

31.  3. Surgical technique:
Most surgical procedures are irreversible. This means
that realistic goal setting between the health care
provider, family and patient is critical. Neurosurgical
techniques have been proven useful in conditions like
cerebral palsy.

32. Physiotherapy Management
Basic goals of management of spasticity:
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 and normal
movement with the contra-lateral limb
 Facilitate normal movement patterns in the affected limbs

33. A. 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
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
effect of the reflex activities then he can be gradually
be introduced to the use of positions which make
suppression of reflex activity more difficult.

34.  Side lying position well supported by pillows is very
convenient since it avoids stimulation of the tonic
labyrinthine reflex .
 Also, as head and trunk are in alignment, the stimulation
of the asymmetrical tonic neck reflexes 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 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
possible.
 These two positions are helpful if there is flexor spasticity.

35. B. 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.
C. Pressure under surface of the 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 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.

36.  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 motor neurone pools are already in
an excitatory state and any volitional effort is likely to act as a
triggering mechanism to those motor neurone 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, over exertion should
also be avoided as it may increase spasticity.

37. D. 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, golgi tendon organs
which are sensitive to length changes.
 It inhibits or dampens muscle contraction and tone
due largely to peripheral reflex effects.

38.  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

39.  E. 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 ease pain.
 It activates thermoreceptors.
 It decreases neural, muscle spindle firing and provides
inhibition of muscle tone.
 Techniques used
- Immersion in cold water
 ice chips
 - Ice towel wraps
 - Ice packs
 - Ice massage
 - Ice application with exercises

40. F. 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: towel wraps
- Application of snug fitting clothing (gloves, socks,
tights) or air splints
- Tepid baths

41. G. Relaxed passive movements:
 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.
H. Deep Rhythmical Massage (Tendon Rolling):
 Deep rhythmical massage with pressure over the muscle
insertions can be given to reduce spasticity.
I. Biofeedback:
 Biofeedback is the use of an electrical monitor that creates
a signal—usually a sound—as a spastic muscle relaxes.
 In this way, the person with spasticity may be able to train
himself to reduce muscle tone consciously.

42. J. 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.
 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 to
promote 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.

43. K. 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.

44. L. Tone Reducing Orthosis:
 These are plastic AFO’s in which foot plate and broad
upright are designed to modify reflex hypertonicity by
applying constant pressure to the plantarflexors and
invertors.
 They control the tendency of the foot to assume an
equino-varus posture.
 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.

45. M. 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
- Slow rolling movements

46. N. Proprioceptive Neuromuscular Techniques:
 Techniques used
- Rhythmic 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.
- 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.
- 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.

47. THANK YOU AND
MERRY CHRISTMAS IN
ADVANCE

48. References
 Hirth D, Thurman D J et al, How common are the common neurologic
disorders Neurology 2007 68: 326-327
 Pandyan AD, Gregoric M, Barnes MP, Wood D, Van Wijck F, Burridge J,
Hermens H, Johnson GR, Spasticity: clinical perception, neurological
realities and meaningful measurement. . Disability and Rehabilitation
2005; 27(1/2):2-6
 Bohannnon, R.W and Smith M.B, Modified Ashworth scale, (1986).
Physical therapy 67, 206-7
 Burridge J, Taylor P, Hagan S, The effects of common peroneal
stimulation on the effort and speed of walking: a randomised
controlled clinical trial with chronic hemiplegic patients. Clin Rehabil
1997;11:201–10
 Campistol J. Orally administered drugs in the treatment of spasticity
Rev Neurol. 2003 Jul 1-15;37(1):70-4
 Rode G, Maupas E, Luaute J, Courtois-Jacquin S, Boisson D Medical
treatment of spasticity, Neurochirurgie. 2003 May;49(2-3 Pt 2):247-55
 Taricco M, Pagliacci MC, Telaro E, Adone R.Pharmacological
interventions for spasticity following spinal cord injury: results of a
Cochrane systematic review. Eura Medicophys. 2006 Mar;42(1):5-15

49.  Sommerfeld DK, Eek EU, Svensson AK, Widén
Holmqvist L, von Arbin MH. 2004. Spasticity after
stroke: Its occurrence and association with motor
impairments and activity limitations. Stroke 35:134-
140.
 Ward AB. 2008. Botulinum toxin in post-stroke
spasticity in adults. Journal of Neural Transmission 115
(4): 607-616.
 Verplancke D, Snape S, Salisbury CF, Jones PW, Ward
AB. 2005. A randomised controlled trial of the
management of early lower limb spasticity following
acute acquired severe brain injury. Clinical
Rehabilitation 19:117-25.
 Young RR. 1994. Spasticity: a review. Neurology 44:
512-520

50.  Pfister AA, Roberts AG, Taylor HM, Noel-Spaudling S, Damian
MM, Charles PD. 2003. Spasticity in adults living in a
developmental center. Archives of Physical Medicine and
Rehabilitation 84(12):1808-1812.
 Lundstrom E, Terent A, Borg J. 2008. Prevalence of disabling
spasticity 1 year after first-ever stroke. European Journal of
Neurology 15: 533–539.
 Lance JW. 1980. Symposium synopsis. In: Feldman RG, Young
RR, Koella WP, editors. Spasticity: Disordered control. Chicago:
Yearbook Medical. p 485-494.
 Sheean G. 2002. The pathophysiology of spasticity. European
Journal of Neurology 9 (Suppl 1):3-9.
 Nathan P. 1973. Some comments on spasticity and rigidity. In:
Desmedt JE, editor. New developments in electromyography and
clinical neurophysiology. Basel, Karger, p 13-14. 2002
 Buckon CE, Thomas SS, Harris GE, et al ‘Objective measurement
of muscle strength in children with spastic diplegia after
selective dorsal rhizotomy’ Arch PhysMed Rehabil 83(4):454-60