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CHAPTER 1

INTRODUCTION

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The word spasticity originates from the Greek word spastikos meaning to

pull or drag, which is consistent with the definition of spasticity today as an

involuntary velocity-dependent, increased resistance to stretch.20

Spasticity has occupied a substantial amount of the neuroscience and

rehabilitation literature for decades. It is the feature that most occupies the minds of

the clinicians.1

Spasticity is difficult to define comprehensively, presumably because

the neurobiology of the motor system remains largely a mystery. When the

motor system is fully understood, one will be able to explain, name, and

perhaps treat the multiple disorders now grouped together into the syndrome

known variously as spasticity, spastic paresis and the upper motor neuron

(UMN) syndrome. It is important to differentiate among spasticity, spastic

dystonia, and spastic paresis. It is also important to recognize different

clinical syndromes such as cerebral or hemiplegic spasticity versus spinal or

paraplegic Spasticity and to differentiate severe spastic dystonia from

cutaneously induced spasms.2

However as pointed out by Landau (1980), there is a major problem

inherent in this word itself since it is commonly used clinically to signify

many different features associated with brain lesions ranging from loss of

strength to increased tendon jerks, and include the resistance offered to

passive movements, and abnormal patterns of movement and posture .1

Most physicians and therapists working with physically disabled people feel

that they can recognize spasticity when they see or feel it. However, defining it, is

much more difficult.3

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The classical definition of Spasticity is given by Lance (1980):

Spasticity is characterized by a velocity-dependent increase in tonic stretch

reflexes (muscle tone) with exaggerated tendon jerks, resulting from hyperexcitablity

of the stretch reflex, as one component of the upper motor neuron syndrome. 4 This

definition provides a useful basis for measurement and appears to have a

biomechanical interpretation, the complex behavior of the reflex arcs and the wide

variation in the pathology makes a single universal definition impossible.5

Besides, spasticity, as defined by Lance (1980), is but one component of this

syndrome. Whereas spasticity is velocity-dependent and is therefore afferent

mediated, many patients present with continuous muscle contractions that continues

for in the absence of movement. This is referred to as spastic dystonia, which is

thought to arise as a result of continuous supraspinal drive to the spinal motoneurones

and is therefore efferent mediated.6

This widely-accepted definition given by Lance was further broadened by

Young to include other signs such as exaggerated deep tendon reflexes, clonus, flexor/

extensor spasms, the Babinskis sign, exaggerated phasic stretch reflexes, hyperactive

cutaneous reflexes, increased autonomic reflexes, and abnormal postures.7

Although spasticity is the part of UMN syndrome, it is often tied to the other

presentations of the said syndrome. Contracture, hypertonia, weakness and movement

disorders can co-exist as a result of the UMN syndrome.8

Besides, there are clearly different types of spasticity (e.g. the syndrome seen

in cerebral lesion versus that seen with spinal lesions) and of rigidity (e.g. that seen

with Parkinsonism versus that seen with an intrinsic tumor of the cervical cord).2

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Hierarchies of other definitions have been added to broaden Lances classical

definition of spasticity over the time. Yet even these broader definitions do not give

any flavour of bewildering variety of problems that can occur in different individuals

and even in the same individual at the same time. The extent and type of spasticity

can fluctuate widely according to position, fatigue, stress and drugs. One limb may

have one pattern of spasticity whilst another may have different pattern.3

More recently, a European thematic network SPASM (Support programme for

assembly of database for spasticity measurement), as part of a review of spasticity

measurement and evaluation, looked at this definition of Lance in detail. In the light

of recent research three specific areas of Lances definition were felt to require

modification;

1) Velocity-dependent changes in the limb stiffness during passive movement are

not solely due to neural changes but are contributed to by the normal

viscoelastic properties of soft tissues.

2) In addition to hyperexcitable stretch reflexes, activity in other pathways

(Afferent, supraspinal and change in the alpha motor neuron) is also important

in the development of spasticity.

3) Spasticity cannot be exclusively considered a motor disorder, as afferent

activity (Cutaneous and proprioceptive) is also involved.

To reflect these aspects, the EU-SPASM group has proposed a new definition

of spasticity:

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Spasticity: a disordered sensorimotor control, resulting from an upper motor

neuron lesion, presenting as intermittent and sustained involuntary activation of

muscles.23

This term, although broader and less specific, does now allow more aspects of

UMN syndrome to be included under the umbrella term of spasticity, such as clonus

and spasms.19

The most common causes of spasticity are as follows:

(a) Direct injury to motor cortex e.g. cerebral palsy, stroke, infections etc.

(b) Corticospinal tract injury in brain e.g. multiple sclerosis, stroke etc.

(c) Corticospinal tract injury in spinal cord e.g. transverse myelitis, syrigomyelia,

spinal bifida etc.

(d) Rare causes of spasticity includes degenerative central nervous system (CNS)

diseases e.g. tay-sachs disease, rett syndrome etc.

Spasticity is a disabling complication of the CNS insult; with its

neurophysiology little understood it becomes more difficult to treat spasticity, that

is why I am making project on spasticity, so that physiotherapy aspirants know

better about its neurophysiology and treatment.

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C HAPTER 2

NEUROPHYSIOLOGY UNDERLYING SPASTICITY

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In humans, both cerebral and spinal spasticity appear to have a slow time

course of development following the initial insult, except in cases of high brain stem

lesions (e.g., traumatic brain injury), in which there may be an immediate increase in

reflex state. Following stroke, reflex hyperexcitablity (hyperreflexia) may be

clinically evident 4-6 weeks after the lesion.1

According to Chapman and Weisendanger (1982), this slow time course

suggests that plastic changes in synaptic connections may contribute to the

development of Spasticity. They point out that one response to denervation may be

formation of new synaptic connection through axonal sprouting. Since this sprouting

has the same time course for development as that of hyperreflexia, the new, functional

synaptic connections may actually mediate the hyperactive reflexes called as

Sprouting theory.15, 5

Another possible response is an increase and abnormal sensitivity of pre or

post synaptic elements to remaining afferent input, i.e. an increased chemical

sensitivity. A third possibility is that previously inactive synapses may become active.

1

Principally, the studies to understand the pathophysiology of spasticity were

done on animal subjects. But the differences in the motor performances especially of

upper extremity and the erect posture of man accounts for limitation of comparison

between human and animal experiments. 15

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The abnormal types of postural tone and the stereotyped total motor patterns

we see in spastic patients are the result of disinhibition, i.e. of a release of lower

patterns of activity from higher inhibitory control.16

The operation of inhibitory centers in conjunction with excitatory centers

during the performance of motor activities causes the excitatory impulses to be

channeled only to those motor units needed to produce the desired motions.18

Inhibition is a very important factor in the control of posture and movement.

The brain-damaged patient suffers from a lack of inhibitory control over his

movements. This shows itself in the release of tonic reflex activity, i.e. spasticity.16

Pattern of hypertonicity can vary from moment to moment depending on many

factors e.g. the general postion of persons head and body, amount and type of

damage to the neuraxis, function of area involved of nervous system.18

DESCENDING PATHWAYS: UPPER MOTOR NEURONS

The cortical areas concerned with origin of motor signals are the primary

motor area, pre-motor area and supplementary motor area in frontal lobe, and sensory

area in parietal lobe. The cortical areas send their output signals to spinal cord through

corticospinal tracts and to brainstem through corticobulbar tracts. About 30% of the

fibers forming corticospinal and corticobulbar tracts take their origin from primary

and supplementary motor cortex, 30% from premotor area and remaining 40% from

parietal lobe particularly from sensory area.11

All those motor pathways which descend from cerebrum and brainstem to the

spinal cord without passing through the pyramids of the medulla are extrapyramidal

or parapyramidal.4

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Fig2.1:Descending Motor Pathways Involved In Motor Control

Isolated lesions of pyramidal tracts in the medullary pyramids (and in spinal

cord) do not produce spasticity perhaps there are non-pyramidal (parapyramidal)

UMN motor fibers which must also be involve for the production of spasticity.5

BRAINSTEM AREAS CONTROLLING SPINAL REFLEXES

From the brainstem, arise two balanced systems for control of spinal reflexes,

one inhibitory and the excitatory. These are anatomically separate and differ with

respect to suprabulbar control.4

Inhibitory system

The parapyramidal fibers arising from the premotor cortex are cortico-reticular

and facilitate an important inhibitory area in the medulla, just dorsal to the pyramids,

known as venteromedial reticular formation. Electrical stimulation of this area inhibits

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the patella reflex of intact cats. In decerberate cats, the previously rigid legs become

flaccid and muscle tone is reduced in cats that have been made spastic with chronic

cerebral lesion. Stimulation of this region also inhibits tonic vibration reflex (TVR)

and flexor reflex afferents.5

Excitatory area

Higher in the brain stem is a diffuse and extensive area that appears to

facilitate spinal stretch reflexes. Stimulation suggests that its origin is in the sub- and

hypothalamus (basal diencephalon), with efferent connections passing through

receiving contributions from the central grey and tegmentum of the mid-brain, pontine

tegmentum and bulbar reticular formation (separate from the inhibitory area above).

Stimulation of this area in intact monkeys enhances patella reflex and increases

reflexes, extensor tone and clonus in chronic cerebral spastic cats mentioned above

Lesions through the bulbopontine tegmentum alleviate spasticity. Although input is

said to come from SMA (Supplementary motor area) stimulation of motor cortex and

internal capsule does not change the facilitatory effect of this region. 5

The lateral vestibular nucleus is another region facilitating extensor tone,

situated in the medulla close to the junction with the pons. Stimulation produces

disynaptic excitation of the extensor motor neurons.5

Although both areas are considered excitatory and facilitate spinal stretch

reflexes they also inhibit flexor reflex afferent, which mediate flexor spasms. The

lateral vestibulospinal tract also inhibits flexor motor neurons.5

The principal descending motor tracts within the spinal cord in the production

of spasticity is the inhibitory dorsal reticulospinal tract (DRT) and the excitatory

median reticulospinal tract (MRT) and vestibulospinal tract (VST). Thus, spasticity

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arises when the parapyramidal fibres of the inhibitory system are interrupted either of

the cortico-reticular fibres above the level of the medulla (cortex, corona radiata,

internal capsule) or of the DRT (dorsal reticulospinal tract) in the spinal cord. 5

SPINAL INHIBITORY MECHANISMS

Presynaptic inhibition

In presynaptic inhibition, a neurotransmitter e.g. GABA is released on to the

terminals of afferent fibers before they make synaptic contact with the cell. This

produces depolarization of the afferent terminals, thus blocking the transmission of

afferent impulses in the normal state; tendon jerks and H-reflexes are suppressed by

continuous muscle vibration because impulses generated in the Ia afferent endings

inhibit the monosynaptic reflex arc by process of presynaptic inhibition.5

Interneurones mediating presynaptic inhibition are controlled by descending

tracts, making it theoretically possible for a CNS lesion to decrease presynaptic

inhibition of Ia terminals and if one admits that Ia discharge produced by muscle

stretch is normally partially blocked by presynaptic inhibition, reduction of

presynaptic would be the cause of stretch reflex exaggeration (since larger quantity of

impulses than normal would reach alpha motor neurons).15

F

ig 2.2

:

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Presynpatic Inhibition:Illustration of Pathways With Documented Impaired Transmission in

Spasticity, That is, The Presynaptic Inhibition of The Terminals of Stretch Reflex Afferents and The

Postsynaptic Reciprocal Ia Inhibition Between Antagonistic Muscles.

Renshaw cell inhibitory system

Located in the anterior horns of the spinal cord, in close association with the

motor neurons, are a large number of small neurons called renshaw cells. These are

inhibitory cells that transmit inhibitory signals to the surrounding motor neurons.

Thus, stimulation of each motor neuron tends to inhibit adjacent motor neurons, an

effect called lateral inhibition.11 These cells inhibit not only the homologous motor

neuron from which they receive the collateral (recurrent inhibition) but also its paired

gamma motor neurons and the Ia inhibitory interneuorns that mediate reciprocal

inhibition of antagonist motor neurons. Inhibition of renshaw cells was responsible

for an exaggeration on the stretch reflex (at least tonic component): a given discharge

of any motor neuron pool would then be less effectively opposed by recurrent

inhibition and so a greater motor discharge would ensue.15

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Fig2.3: Renshaw Cell Inhibitory System

SPINAL SEGMENTAL REFLEXES

Hyperexcitablity of spinal reflexes forms the basis of UMN syndrome, which

has in common increased muscle activity. These reflexes are divided into two groups,

proprioceptive and nociceptive reflex/cutaneous reflex.

Proprioceptive reflex includes tonic and phasic stretch reflex and positive

supporting reaction. Nociceptive/cutaneous reflex includes flexor and extensor

reflexes including Babinskis sign. Clasp knife phenomenon includes features of both

groups.

Stretch reflex is the simplest manifestation of muscle spindle function is the

muscle stretch reflex. Whenever a muscle is stretched suddenly, muscle spindle

causes reflex contraction of the large skeletal muscle fibers of the stretched muscle

and also of closely allied synergistic muscles.11

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s

Fig 2.4: Stretch Reflex

SPINAL

SEGMENTA

L ACTIVITY

ELECTRPHYSIOLIC

TEST

ABNORMALIT

Y

NEUROTRANSMITTE

R

Ia Presynapticinhibition

Vibratory inhibitionof H-reflex

Reduced GABA(-)

Ia reciprocal

inhibition

Conditioning of H-

reflex

Reduced Glycine

Ib non-

reciprocal

inhibition

Conditioning of H-

reflex

Reduced Glycine

Recurrent

inhibition

Conditioning of H-

reflex

Increased and

decreased

Table1.1: Neurophysiology of Spasticity.

It has both components phasic and tonic. A tonic stretch reflex is one in which

a stimulus produces a prolonged asynchronous discharge of motor neurons causing

sustained muscle contraction for the maintenance or alteration of posture, in contrast

phasic stretch reflex consists of a synchronous motor neurone discharge caused by

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brief stimulation of muscle spindle or their afferent pathways. Tonic stretch reflex

may be divided into a velocity-sensitive (dynamic) and a length sensitive (static)

component.4

The clinical signs arising from hyperexcitablity of phasic stretch reflex include

tendon hyperreflexia, irradiation of tendon reflex and clonus. The stretch reflex

underlying spasticity has been regarded as dynamic, i.e. present only when joint is

moving. The clinical sign arising from hyperexcitablity of tonic stretch reflex is

increased resistance to passive movement.5

THE CLASP KNIFE PHENOMENON

This phenomenon is often seen in pyramidal lesions, characterized by resistance

to passive movement which in initial phase is greatest and then suddenly gives away

in latter phase.12This well known clinical sign has as its basis in hyperexcitable tonic

stretch reflex.5

NON REFLEX CONTRIBUTION TO HYPERTONIA

Changes in soft tissue e.g. muscle and tendon may become stiff and less

compliant or in later stages contracture may develop in the spasticity, resisting passive

movement and manifests as increased tone. Thus in spasticity, neural as well as

biomechanical factors may contribute to increased tone.

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UMN lesion

Abnormal muscle contraction Weakness

Dynamic Static Immobilisation at short muscle length

Spasms Spasticity

Co-contraction Spastic dystonia

Clonus Biochemical Changes

Flexor withdrawal Hypertonia -Reduced compliance

+ -Contracture

Reduced ROM

Abnormal posture

Impaired function

Fig2.5: Interaction of Neural and Biomechanical Components of Hypertonia

EXCITATORY SPINAL ACTIVITY

Alpha motor neurone excitability

Alpha motor neurone become intrinsically more excitable as result of change

in their biophysical properties, their response to afferent stimuli is greater which

account for motor overactivity e.g. hyperexcitable spinal reflexes.

Excitatory interneurone hyperexcitability:

Ia polysynaptic excitatory pathways

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TVR (tonic vibration reflex), which is the sustained high-frequency vibration

of a relaxed muscle producing a slowly rising contraction, believed to involve

polysynaptic Ia afferent pathways. This pathway receives supraspinal facilitation from

brainstem. Rather than exaggerated, it is impaired in spasticity. Antispastic

medication suppresses TVR, which can therefore act as a non-specific gauge of the

effect of these medications on polysynaptic reflexes.

Group II polysynaptic pathway

There is better evidence that Group II mediated polysynaptic activity is

exaggerated in spasticity.5

CONCLUSION

Despite the wealth of clinical research, clear correlation between spinal circuit

and clinical features of spasticity are still lacking. Hence it is fair to say, no one test

accurately reflects the basic pathophysiological substrate of spasticity, and it is quite

probable that condition is a heterogeneous one.

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CHAPTER 3

SPASTICITY-CLINICAL CONSEQUENCE, TYPES, AND

DISTRIBUTION

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CLINICAL CONSEQUENCES OF SPASTICITY

The above description of the different patterns of spasticity makes it clear that

there is potentially wide range of functional problems. In order to draw the discussion

together, the major consequences can be annotated as follows:

Mobility

It is the most common function affected as a consequence of spasticity. The

gait can be clumsy and uncoordinated, and falling can become a common event.

Eventually walking may become impossible owing to a combination of soft tissue

contractures, flexor and extensor spasm and unhelpful associated reactions. Even if

individual is wheelchair bound, Spasticity can cause further immobility.49

Loss of dexterity

The spasticity can cause further difficulties in upper extremities for example;

feeding, writing, personal care and self-catheterization can become a problem for a

person with spasticity due to loss of dexterity. All these problems can slowly lead to

decreased upper extremity independence.5

Trunk problems

Although most of the functional consequences of spasticity occur in arm or

leg, it is worth remembering that truncal spasticity can cause problems while sitting

and maintaining upright posture, necessary for feeding and communication.5

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Bulbar problems

Bulbar problems can give rise to difficulty swallowing, with consequent risk

of aspiration and pneumonia. Further problems can rise with communication,

secondary not only to inappropriate posture but also to spastic forms of dysarthria.5

Pain

It is not widely recognised that spasticity and the other forms of UMN

syndrome can be extremely painful. This is particularly the case with flexor and

extensor spasms, and sometimes treatment is needed simply for analgesia rather than

improvement for function. Abnormal posture can also give rise to an increased risk of

musculoskeletal problems and osteoarthritic change in the joints. Any peripheral

stimuli from problems such as ingrowing of toenails or small pressure sores can, in

turn exacerbate spasticity and a vicious circle of increased pain and increased

spasticity can ensue.5

Caring and Nursing problems

Spasticity is one of the unusual conditions that can sometimes require

treatment of the disabled person for the sake of carer. Individuals, particularly with

advanced spasticity, can be extremely difficult to move and nurse. Transfers from bed

to toilet or bed to wheelchair can be laborious. Hygiene can be a problem with, for

example, marked adductor spasticity, causing problems with perineal hygiene and

catheter care. Flexion of fingers can cause particular difficulties with hygiene in the

palm or hand. Complications of spasticity includes, contractures, decubitus ulcers,

fracture malunion, joint subluxation or dislocation, heterotopic ossification and

peripheral neuropathy.49

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DIFFERENCE BETWEEN SPINAL AND SUPRASPINAL SPASTICITY

The clinical picture of spasticity depends on the location of lesion in the

neuraxis. With cerebral lesions spasticity tends to be less severe and more often

involve the extensors, and posture of lower limb is in extension because of imbalance

of reciprocal Ia inhibition (reciprocal inhibition from flexors to extensors is

diminished and inhibition from extensors to flexor is increased), flexor spasm is rare

and clasp-knife phenomenon is uncommon whereas spinal lesions have severe

spasticity, more often in flexors with dominant posture of lower limb in flexion

(spinal spasticity do not have imbalance of reciprocal Ia inhibition), prominent flexor

spasms because the dorsal reticulospinal system suffers more damage in spinal lesions

and clasp-knife is more common.4,5

DISTRIBUTION OF SPASTICITY

In most neurologic patients, spasticity predominates in the antigravity

muscles, particularly the flexors of the arms, and the extensors of the leg. Because of

the resultant discrepancy in the muscle tone in opposing muscle groups, the involved

limbs tend to assume a typical resting posture and to retain this posture passive

displacement in joints occurs. An alternate patterns of spasticity that occurs in patients

with multiple sclerosis, spinal cord injury and traumatic spinal cord injury consists of

flexor spasticity in lower limbs, often results in flexed resting posture and subsequent

contractures.17

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Upper extremity Lower extremity Shoulder

Adductors

Internal rotators

Elbow

Flexors

Hand

Wrist flexors and adductors

Finger flexors

Forearm

Pronators

Hip

Extensors

Internal rotators

Adductors

Knee

Extensors

Ankle

Planterflexors

Invertors

Table3.1: Classic Distribution of Spasticity

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CHAPTER 4

EVALUATION AND MEASUREMENT OF SPASTICITY

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Spasticity is difficult to characterize than to recognize and still more difficult

to quantify. Spasticity is very easily detectable by clinical examination but there is no

effective method of quantifying muscular tonus inspite of the continuous efforts.

Quantification is important to know the response to medication and evaluate the

progression of the disease.13

The measurement of any variable depends an adequate definition. In case of

spasticity it appears that the complexity of any comprehensive definition makes direct

clinical measurement very difficult.5

Apart from this, assessment procedures should distinguish between spasticity,

contracture or other abnormal tone such as rigidity encountered in Parkinsons

disease.1,5 The common element of all assessment methods is to quantify the

resistance to passive movement but it must be remembered that this can result from

neurophysiological as well as biomechanical factors.1 A uniformly acceptable,

reliable, and practical measure of spasticity still continues to elude the clinician. 22

Fig4.1: Causes of Increased Tone: The Major Contributions to Resistance to Passive Motion

Result From Changes in Both the Reflex Behavior and in the Passive Mechanical Properties

of the Muscle.

24

CNS lesion

Reflex hyperexcitablity

Increased tone or

resistance

Altered muscle

function

Altered mechanical

properties


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Detailed evaluation of spasticity includes clinical, biomechanical and

neurophysiological methods.34

CLINICAL METHODS

The commonly used clinical scale is the Ashworth scale, modified Ashworth

scale, degree of adductor muscle tone, Penn spasm frequency scale, and Tardieu scale

etc.14

Ashworth scale

The most commonly used assessment method, Ashworth scale, has the

advantage of ease of use in clinical setting.14It is simple, requires no instrumentation

and is quick to carry out and has been used in number of studies. 24 However its

reliability depends upon ability of the observer both to control the rate of stretch and

to assess the resistance.Hass et al concluded that the Ashworth scale is of limited use

in the assessment of spasticity in the lower limb.5

Modified Ashworth Scale (MAS)

MAS is the most widely used and accepted scale of spasticity.27However, this

scale is not validated for all the joints.28Apart from this, terminology used in the

description of grades in MAS, in terms like slight increase, minimal resistance,

part easily moved, and considerable increase, may contribute to the interrater

disagreement due to varied interpretation.24

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Score Ashworth scale(Ashworth,

1964)

Modified Ashworth

scale(Bohannon andSmith,1987)

0

1

1+

2

3

4

No increase in tone

Slight increase in tone

giving a catch when the

limb

was moved in flexion or

extension

More marked increase in

tone but limb easily flexed

Considerable increase in

tone passive movement

Difficult

Limb rigid in flexion or

extension

No increase in muscle tone

Slight increase in muscle

tone, manifested by a catch

and release or by minimal

resistance at the end of

the range of motion(ROM) when the affected

part(s) is moved in flexion

or extension

Slight increase in muscle

tone, manifested by a

catch,

followed by minimal

resistance throughout the

remainder (less than half)

of the ROM

More marked increase in

muscle tone through most

of the ROM, but affected

part(s) easily moved

Considerable increase in

muscle tone passive,

movement difficult

Affected part(s) rigid in

flexion or extension

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Table4.1: Ashworth and Modified Ashworth Scale

Penn Spasm Frequency Scale

Other method of observing the spasticity phenomenon is to assess the number

of episodic spasms. The penn spasm frequency scale is an ordinal ranking of the

frequency of leg spasms per day per hour. One problem with this scale is that patients

usually report that the number spasms occurred per hour is often affected by their

activity at the time. Also the duration of spasm is not taken into consideration.14

Score Number of spasms

0

1

2

3

4

No spasms

1 per day

2-5 per day

5-9 per day

>10 per day

Table4.2: Penn Spasm Frequency Scale

Tardieu Scale

Owing to the drawbacks of Ashworth and modified Ashworth scale, Tardieu

scale was designed by Tardieu and colleagues in 1954. Only this scale complies with

the concept of spasticity, since it involves resistance at both slow and fast speeds.29,33

The method is very time consuming, therefore it was simplified to the

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modified Tardieu scale. The modified Tardieu scale only defines the moment of

catch, seen in the ROM at particular joint angle at a fast passive stretch. 31

This test is performed with patient in the supine position, with head in midline.

Measurements take place at 3 velocities (V1, V2, and V3). Responses are

recorded at each velocity as X/Y, with X indicating the 0 to 5 rating, and Y indicating

the degree of angle at which the muscle reaction occurs. By moving the limb at

different velocities, the response to stretch can be more easily gauged since the stretch

reflex responds differently to velocity.5

The affected part is moved in three different speeds:

V1: as slowly as possible

V2: intermediate movement (movement under gravity)

V3: as rapidly as possible

Two parameters are measured:

X: type of muscle reaction

Y: angle of muscular event at the three different speeds31

Grades Quality of muscle reaction

0

1

2

3

4

No resistance throughout the course of

passive movement

Slight increase throughout the course of

passive movement, with no clear catch at

precise angle

Clear catch at precise angle, interrupting

the movement, followed by release

Fatigable clonus (10 seconds when

maintaining pressure) occurring at precise

angle

Table4.3: Tardieu Scale; the Guidelines for Classifying the Quality of Muscle Reactions

(X), When Using Tardieu Scale.

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BIOMECHANICAL METHODS

Since the usual definition of spasticity concerns the relationship between

velocity of passive stretch and resistance to motion, it is logical to investigate

biomechanical approaches to quantification.5

Pendulum test

This test was originally proposed by Wartenberg (1951), in which the knee is

released from full extension and the leg allowed to swing until motion ceases.

Wartenberg observed that in the normal healthy subject the leg would swing

approximately six times after release and proposed a test for the assessment of

spasticity involving counting the number of swings before the limb comes to rest.

The advantages of video motion analysis Pendulum test include the ability to do the

analysis anywhere, and freedom from the attachment of cumbersome recording to the

patient, and processing by a non-biased blinded observer.30

While the Wartenberg pendulum test can be used in cases of relatively mild

spasticity, it is likely to be unsuitable for the commonly occurring clinical situations

in which spasticity prevents true oscillation of the limb.5

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Fig4.2: Pendulum Test: Line Drawing Illustrating Pendulum Test Performed with Subject Supine and

Leg Swinging Freely with Motion Sensors Attached and Weight Secured at Ankle

Isokinetic dynamometry

Isokinetic dynamometers may be of value in assessment and evaluation of

spasticity when an objective and reproducible measure of resistance to passive

movement is needed, such as in relation to research projects and drug evaluation. The

great advantage is that they make a standardization of the applied stretch velocity and

amplitude possible, and thereby are able to quantify the velocity-dependent resistance

in the muscle to passive movement.24

The controlled displacement method is mostly used. In this method, velocity

remains constant and so the displacement. But the torque value varies each time

depending upon the resistance felt while passively moving the limb. Advantage of

controlled displacement method is that the velocity and range of motion can be

standardized and controlled.13

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Future aims may be to develop the methods further and to consider whether it

will be feasible to develop new portable or semi portable devices that are easy to use

in the clinical setting as described recently by Burridge et al. 2

Fig4.3: Isokinetic Dynamometer: Assessing Spasticity in Ankle Plantar Flexors

NEUROPHYSIOLOGICAL METHODS

As spasticity results from altered conduction in the reflex pathways, there have

been numerous attempts to quantify it by investigating the abnormalities in the reflex

pathways (i.e. altered presynaptic inhibition and reciprocal inhibition, excitability in

the Ia afferent pathway and increased Alpha motor neurone excitability). The three

common techniques that have been used for clinical quantification of spasticity are

tendon jerks, H-reflex studies and F-wave studies.35 Neurophysiologic assessment

provide objectivity, enhanced sensitivity and independently confirms the evaluation of

spasticity.36However, there are several problems in such studies as the size of the

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responses measured in EMG depends heavily on factors like the placement of

electrodes, skin resistance, subcutaneous fat, muscle atrophy etc.24

Tendon jerk

Tendon jerks are more readily elicited in people with spasticity, i.e. they can

be elicited with smaller levels of stimuli than normal, and the response to these

stimuli has higher amplitude and is more diffuse. Therefore, it has been hypothesised

that the tendon jerk can be a quantifiable measure of spasticity. However, it is

important to note that increase in tendon jerk is not exclusive to spasticity.5

Fig4.4: Electrophysiological Methods: EMG Used to Measure The Responses Evoked By Either

Stretching of The Muscle (Stretch Reflex), Tendon Tap (T-Reflex) Or Electrical Stimulation of The

Peripheral Nerve Supplying The Muscle (H-Reflex) in Order to Evaluate Whether these Responses are

Exaggerated in Spastic Individuals and Related to the Degree of Spasticity.

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H-Reflex (Hoffman reflex)

H-reflex, first described by Hoffman in 1918, in the soleus component of

triceps surae.31

Fig4.5: Recording of H-Reflex: Method Of H-Reflex Recording, Exploring The Monosynaptic Ia-

Alpha Pathways. (A) Stimulation Of The Tibial Nerve At The Popliteal Fossa (S) And Recording Of

The Motor Response Of The Soleus Muscle (R). B-H: Increasing Stimulation Intensities Resulting In

The Occurrence Of H-Reflex, Which Disappears By Collision In Parallel With The Recruitment Of

Motor Fibers And The Increasing Amplitude Of The Direct Motor Response (M)? R-Recording

Electrodes, S Stimulating Electrodes, G -Ground Electrode.

CONCLUSION

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This detailed study has highlighted the fact that there are considerable

variations of opinion as to what actually constitutes spasticity. This weakness of

definition leads inevitably to variety of measurement approaches and makes the

comparison of research studies difficult, if not impossible. While the definition of

Lance (1990) has become widely accepted by the rehabilitation community, the

various measurement approaches frequently do not adhere to it. It is suggested that, if

spasticity is to be regarded as impairment, then the SPASM Group working definition

may be more appropriate in that it embraces a wider range of reflex associated

disorders and more closely matches clinical practice. However, it may be that it is

inappropriate to regard spasticity as impairment at all and it should be thought of as

an umbrella term embracing a range of more specific terms such as contracture,

hypertonicity, clasp knife phenomenon etc. Further, it may be considered under the

ICF definitions so that each of the three categories can be studied and measured with

less ambiguity.28

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CHAPTER 5

PATHOLOGICAL PHENOMENON ASSOCIATED WITH

SPASTICITY

POSITIVE SUPPORT REACTION

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This term is used primarily by physiotherapists to describe a pathological

extensor response in the lower limb evoked by a stimulus of pressure on the ball of

the foot.6 Others have termed this phenomenon the tonic ambulatory foot response. It

is presumed to be a reflex involving a proprioceptive stimulus elicited by stretch of

the intrinsic foot muscles and an exteroceptive stimulus elicited by contact of the foot

with the ground.5

This response prevents hip extension during the stance phase of the gait, the

patient having to flex forward at the hip to maintain balance.6 There may be extension

of the knee, producing a pattern of extensor thrust of the lower limb.5 Patients with

positive support reaction may develop contractures of all muscle groups held in

shortened position e.g. triceps surae, iliopsoas, rectus femoris, hip adductors.6

Inhibition of this pathological response must incorporate desensitization by

mobilisation of the foot itself. Physiotherapists are often advised to avoid contact with

the ball of the foot. However, in this instance, mobilisation of the foot, the posterior

crural muscle group and the Achilles tendon is recommended to desensitize against

both the intrinsic and extrinsic stimuli.6

FLEXOR WITHDRAWAL RESPONSE

This response occurs as a protective mechanism in normal subjects and may

be observed as an individual withdraws the hand from a hot stove, or the foot when

steeping on a nail. It is determined by the direction of noxious stimuli and therefore

may not necessary be in flexion. Patients with incomplete spinal cord lesions may

demonstrate this response to a fairly innoxious stimulus such as removal of bed

clothes. The withdrawal response in the lower limbs is that of flexion and lateral

rotation of the hip, flexion at the knee and dorsiflexion or plantarflexion at the ankle.

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The foot may be everted or inverted, often being everted with dorsiflexion or inverted

with plantarflexion at the ankle.6

Noxious stimulus on a background of abnormal tone may give rise to this

response. For example, a pressure ulcer, pain or an ingrowing toenail may cause an

increase in hypertonia with flexion of thumb. It is essential to determine if there is an

external cause and to treat this prior to undertaking more radical intervention. The

short term influence of such a stimulus may be readily reversible, but prolonged

exposure may have more residual effects such as the development of contractures.6

The clinical picture of the flexor withdrawal response is most apparent during

the swing phase of gait where there is exaggerated flexor activity. Weight bearing

through the affected limb was previously recommended but this should be carried out

with caution. Attempts to stand the patient on a leg which is contracted into flexion

may further aggravate the situation, not least by imposing an additional painful

stimulus.6

SPASTIC CO-CONTRACTION

Co-contraction refers to the simultaneous contraction of both agonist and

antagonist muscles. Controlled co-contraction thereafter is an important feature of

normal motor function providing postural stability or fixation of a body part, for

example, to stabilize the wrist when hitting a tennis ball. Co-contraction is

dysfunctional when it is inappropriate or excessive and impairs agonist function, also

making the agonist appear weaker than it is. Dysfunctional or pathological co-

contraction is a common feature of dystonia and has been demonstrated more in

cerebral palsy than in adult brain injury.5

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The pathophysiological substrate of co-contraction in dystonia is impairment

of Ia reciprocal inhibition in the spinal cord. Co-contraction should be differentiated

from a hyperactive stretch reflex in the antagonist muscle, that is elicited by the

lengthening, produced by the agonist action. For example, active elbow extension by

triceps will lengthen the biceps and may elicit a stretch response. This will appear as

simultaneous contraction of both muscles but is fundamentally different to co-

contraction produced by simultaneous motor drive to both muscles, a diffusion of

descending commands. 5

SPASTIC DYSTONIA

Patients suffering an UMN syndrome frequently adopt an abnormal posture,

well known to most clinicians as the hemiplegic or decorticate posture. The

hemiplegic posture involves flexion of the elbow, wrist and fingers with adduction of

the shoulder and pronation of the forearm. The leg is extended at the hip and knee,

plantar flexed and inverted at the ankle, with adduction of the hip. This may be

loosely described as dystonia, but the term is confusing when used in the context of

the UMN lesion and spasticity. Spastic dystonia may arise from continuous

supraspinal drive from areas disinhibited by the UMN lesion to the spinal

motoneurones. In addition to stretch, spastic dystonia is altered by postural changes,

presumably through vestibular mechanisms. Another finding in patients with UMN

syndrome is delayed relaxation after voluntary contraction caused by continued firing

of motor units. Some consider this a form of spastic dystonia, unlike most of the other

positive features of the UMN syndrome, the motor drive behind spastic dystonia is not

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a spinal reflex; it is efferentmediated rather than afferentmediated. Soft tissue and

joint pathology may also contribute to sustained abnormal postures.5

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CHAPTER 6

PHYSIOTHERAPY MANAGEMENT

40

Person identified with spasticity


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Fig6.1: Algorithm for Management Of Spasticity

Positioning and Seating

41

Is it useful for function?

YES

Physiotherapy

plan to optimize

management

NO

Does it need treatment?

Is it affecting range, care or function?

NO

Assess

spasticity,

if it

increasesfollow yes

column

YES

Assess spasticity

and record specific

measures

Assess for triggering and aggravating factors

Devise physiotherapy plan

Splinting

Positioning and sitting

Standing programme

Spasticity

still

problematic?

NO

Continue with treatment

plan and regular monitoring

YES

Is it focal or

generalised?

FOCAL

Assess the balance of neural and

non-neural components, if non

neural components consider

physiotherapy intervention e.g.splinting and stretching

GENERALISED

Consider oral drug treatment with ongoing

physiotherapy


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Correct positioning, certainly for the immobile brain injury patient, is an

important aspect of management. Incorrect positioning in bed, is a major cause of

unnecessary spasticity.46

Incorrect positioning, can exacerbate tone by facilitating abnormal postural reflex

e.g. tonic labyrinthine reflex.12

Fig6.2: Positioning: Sitting in Cross Leg Position Applies Slow Static Stretch to the Adductors

and Decrease Spasticity.

Proper seating is vital. The fundamental principle of seating is that the body

should be contained in a balanced, symmetrical and stable posture which is both

comfortable and maximizes function. There are many different types of seating

system. All should have the ultimate aim of stabilization of the pelvis without lateral

tilt or rotation, but with a slight anterior tilt so the spine adopts a normal lumbar

lordosis, thoracic kyphosis and cervical lordosis. The hip should be maintained at an

angle of slightly more than 90, which is often facilitated by a seat cushion with a

slight backward slope. Knees and ankles should be at 90. In people with severe

spasticity, this posture may not be possible or may require a variety of seating

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adjustments such as foot straps, knee blocks, adductor pommels, lumbar supports,

lateral trunk supports and a variety of head and neck support systems.46

Reflex inhibiting postures may be useful to reduce spasticity or maintain

relaxation during treatment. The position adopted when sleeping can be used to reduc

spasticity. For example, sleeping prone for 3 to 4 hours reduces flexor spasticity in the

lower limbs.54

Fig6.3: Bobaths Reflex Inhibiting Posture

Where patients are unconscious or paralysed, muscle length can be maintained

by positioning programme, including sand bags and inflatable splints or by preventive

casting.1

Standing and Walking

Weight-bearing reduces spasticity. However, in some severely spastic cases,

the standing position may be impossible without first reducing the spasticity by some

other means, e.g. passive movements, a passive stretch or hydrotherapy.16

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Splinting and casting

Serial casts combined with stretching are effective in reducing spasticity,

improving range and reducing deformity.12

Fig6.4: Neutral Wrist Splint

It is not known whether this is purely a mechanical effect or whether splinting

actually reduces spasticity. Unfortunately, there is no clear agreement on the most

appropriate design nor the length of time a splint should be applied to give the desired

effect. It is a field that requires much research.3

Fig.6.5: Serial Casting: Serial Knee Casts Keeping Knee In Extension And Ankle In 90 Degree

Flexion

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In order to minimize contractures, it is generally recognized that early aggressive

intervention of orthotics is essential. An orthosis, is designed to realign the skeleton in

a patient early in their rehabilitation.5

Fig6.6: Knee Ankle Foot Orthosis

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Fig6.7: Guidelines For Physical Therapy Management In Spasticity:NMES: Neuromuscular

Electrical Stimulation; TENS: Transcutaneous Electrical Nerve Stimulation

MODALITIES

Neuromuscular Electrical Stimulation

Neuromuscular electrical stimulation (NMES) has been shown to reduce

spasticity and improve motor function.12The NMES therapy, which produces

excitation of sensory afferents along with muscle contraction, may promote cortical

excitability targeting the motor neurons of interest. The heightened excitability could

46

Physical interventions

To improve

muscle length

To improve

motor function

and strength

To improve

body awareness

To improve

sensory receptors

of the skin

-Stretching

-Orthosis

-Splinting

-Casting

-Positioning

-Motor

Learning

methods

-NMES

-Strength

training

-Education

and

advice

-Biofeedback

-Relaxation

and

Body

-TENS

-Cryotherapy


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facilitate recruitment of the desired muscles and thus assist training.54In stroke

patients, therapy that combines Bobath inhibitory technique with electrical stimulation

may help to reduce spasticity. Transcutaneous electrical nerve stimulation (TENS) has

been used to improve motor function and reduce tone in patients with Spaticity.12

Cryotherapy

Ice towels may reduce spasticity when it is associated with contracture, but

they have not proved valuable in treating large muscle groups. 6Cold therapy reduce

spasticity by facilitating the alpha motorneurons and inhibiting the gamma

motorneurons.56

Electromyography-biofeedback (EMGBF)

Debacher has described treatment with EMGBF designed to reduce spasticity.

It utilizes three stages of intervention which includes: 1) Relaxation of spastic muscles

at rest; 2) inhibition of muscle activity during passive static and dynamic stretch of the

spastic muscles, and 3) isometric contractions of the antagonist to the spastic muscles,

with relaxation of the spastic muscles, progressing to prompt muscle contraction and

relaxation of the spastic muscles.57

FES (Functional electrical stimulation)

Functional electrical stimulation has potential for a significant improvement in

spasticity, active range of motion, and recovery in muscle strength after a

cerebrovacular accident (CVA).59

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Fig6.8: Functional Electrical Stimulation

The possible mechanism could be that the electrical stimulation may lead to

generalized desensitization of the spinal pathway, reducing the spasticity of spasm

muscles. Electrical stimulation is reported to affect the nerve fibers to the muscles, but

could also travel to higher brain centers, potentially stimulating reorganization of

neuromuscular activity. A limiting factor of FES is the uncomfortable and painful

sensations experienced when the intensity increases enough to elicit functional

movement.60

EXERCISES

Exercises are the key to lasting improvement in reducing spasticity and

improving motor function.

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Primary function should be on first activating contraction of antagonist

muscles (muscle opposite to spastic muscles) to improve inhibition and lengthen

spastic muscles.

Assistance (rhythmic rotation, active assistive and guided movements) can be

used initially as needed but withdrawn as soon as possible.

Reciprocal actions are attempted. Agonist (spastic muscle) contractions are

initiated first in small ranges progressing to larger arcs of movement. Smooth,

reciprocal movements are practiced.

Highly effortful and stressful activities are avoided as they may reinforce

spasticity.

Important functional skills are targeted for training. For example, reciprocal

reaching etc.

Isokinetic movements are effective in improving function in patients with

spasticity.12

Prolonged passive stretching given manually or by utilizing one of the stretch

positions may reduce spasticity.6 Stretching may change the muscles viscoelastic,

structural, and excitability properties. However, many neural and non neural

responses to stretch, especially in spasticity, remain unclear. The aims of stretching in

spasticity may be to normalize muscle tone, to maintain or increase soft-tissue

extensibility, to reduce pain and to improve function.Stretching programs for people

with spasticity are usually used as a daily or weekly regimen over the long-term

placing large demands on resources.58

Hydrotherapy

Passive movements and swimming exercises in a heated pool may provide

temporary relief for some patients.6

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Neutral Warmth

Wrapping the body parts in ace wraps, towel wraps, or application of snug

fitting clothing causes retention of body heat, which activates tactile and

thermoreceptors. Has both segmental (spinal) and suprasegmental (CNS higher

centers) effects. Thus, causes generalised inhibition of tone and promotes relaxation.12

Slow Stroking

The patient placed in a supported position such as prone, or sitting head and

arms supported and resting forward on a table top, slow stroking is applied to

paravertebral spinal region which activates tactile receptors, having both segmental

and suprasegmental effects.It induces generalised inhibition and calming effect.12

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CHAPTER 7

PHARMACOLOGICAL MANAGEMENT

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The management of spasticity requires a multiprofessional approach and is

based on addressing the troublesome effects of the increased tone. Before considering

treatment to reduce spasticity, a careful assessment should be done weighing the risks

of treatment versus the benefits of reducing the spasticity.43Even when

pharmacological agents are used, physical treatment strategies should be in place and

pharmacological interventions should be regarded as adjunctive rather than as

substitutes for physical management.5

Oral anti-spastic medication can be helpful. Occasionally oral medication can

be all that is required, particularly for milder cases. However, in more severe cases

and for focal spasticity, the side effects, commonly drowsiness and weakness, can

significantly restrict the usefulness of these drugs.37

Most oral antispastic agents can be used in combination with each other. The

only reason for this is to improve the clinical effect and lessen the incidence of side

effects. Combinations of baclofen with dantrolene sodium or benzodiazepines are

probably the commonest, but these are more likely to affect higher cerebral

functioning.5

SPECIFIC TREATMENTS

Botulinum toxin

Botulinum toxin (Botox) is an exotoxin produced by the bacterium

Clostridium botulinum. Seven immunogenitically distinct serotypes have been

identified named A to G. Botulinum toxin A is serotype used clinically with well-

established efficacy. Botulinum toxin works by inhibiting presynaptic acetylcholine

release at the neuromuscular junction causing reversible partial flaccid paralysis of the

muscle in which it is injected.43

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Control of symptoms Reduction in pain frequency of spasm

Functional improvement

Aesthetic

Carers burden

Prevention of complications

Improvement in mobility, dexterity,

preservation of sexual function,

improvement in joint ROM, and

facilitation of orthotic fit.

Improvement in position of limb and

body.

Reduced burden of care with hygiene etc

Prevention of joint contracture and hence,

delay, of corrective surgery.

Table7.1: Goals of Pharmacological Management.

Botulinum toxin type A is better tolerated than phenol. Highly selective

blockade of spastic muscles may be achieved by using electromyography to inject

individual muscles. Once injected into a muscle, botulinum toxin is taken up by the

presynaptic terminal at the neuromuscular junction and cleaved to form an active

compound (in a few days) that interrupts the release of acetylcholine from the

presynaptic terminal. This brings about blockade of the neuromuscular junction with

resultant weakness (reducing muscle tone). After about 3 months the presynaptic

terminal sprouts and re-establishes its communication with the muscle fibre (muscle

tone returns).37 Thus, botulinum toxin type A takes effect about 1 week after injection

and lasts about 3 months, after which muscle tone returns to baseline levels. It is a

relatively safe medication and has few serious side effects.40

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Muscle pain, bruising and transient fever may occur on the day of the injection

but are self-limiting. Drug reactions are extremely rare, especially with the less

antigenic newer products.37

The limited literature available and increasing clinical experience indicates

that botulinum toxin does have a role in the management of other spastic conditions

which are as follows:

Toe clawing

Spastic toe clawing usually involves extension of the metatarsophalangeal

joints of the foot, with flexion of the proximal and distal interphalangeal joints. Toe

clawing can be a nuisance in terms of adequate fitting of footwear or orthotic

appliances, and it can also be painful.5

Spastic shoulder

A typical hemiplegic arm is adducted and internally rotated at the shoulder as

well as being flexed at the elbow, pronated at the forearm and flexed at the wrist and

hand. It can be very painful and give rise to significant functional disability.5

Clawed hand

Quite often the disability associated with flexed fingers and wrist is

compounded by a thumb-in-palm deformity which consists of an adducted, flexed

thumb secondary to overactivity of opponens pollicis and often combined with thumb

flexion due to overactivity of flexor pollicis longus and flexor pollicis brevis.5

Hip flexion deformity

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Hip flexion spasticity can cause significant disability, pain and difficulties in

seating in a wide variety of conditions, particularly after traumatic brain injury, stroke

and in multiple sclerosis.

Associated Reactions

Involuntary movements of a paretic arm during ambulation or other motor

activities are known as associated reactions. These occur in around 80% of people

after stroke with a spastic hemiparesis. The movement can often interfere with

balance and makes walking difficult.

But the high costs of botulinum toxin A and possible short term effects raises

problems for its application.38A physiotherapy programme consisting of strengthening

exercises improves the effect on spastic muscles when combined with botulinum

toxin type A injection.40

Intrathecal Baclofen (ITB)

Baclofen is a gamma-amino butyric acid (GABA) receptor agonist. It binds to

GABA receptors and has presynaptic effect on the release of excitatory

neurotransmitters.6

Baclofen acts primarily at the spinal cord level, but it crosses the blood-brain

barrier poorly. Oral administration at higher doses may result in serious systemic side

effects.52

The most effective treatment, with the least side effects, is intrathecal

baclofen. It is more clinically effective than available oral therapy and can be more

cost effective as well. To be considered for intrathecal therapy, patients should have

spasticity from spinal or cerebral causes that result in significant impairment and is

unresponsive to more conservative therapy.39Baclofen decreased spasticity by

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depression of multiple reflex pathways but also reduced excitability of neural

structures underlying voluntary motor tasks, thereby altering muscle activation

patterns.36 Intrathecal baclofen therapy may be used in selected ambulatory patients

with spasticity and is not associated with loss of ambulatory function. When baclofen

is administered orally, only a small portion of the original dose crosses the blood

brain barrier and enters the central nervous system (CNS) fluid, which is the site of

drug action. In order to bypass the oral route, baclofen may be administered

intrathecally by infusion directly to the CNS.

The battery-powered device contains and delivers drug from the pump

reservoir through the catheter to the intrathecal space by peristaltic action. The life of

the battery is four to seven years.

Due to limited battery life, the initial pump procedure will need to be repeated

every 5-7 years. The dosage of baclofen may be increased due to increased tolerance

of the drug.

Advantages of intrathecal baclofen infusion are:

1. Direct drug administration to the CSF.

2. The central side effects of oral baclofen such as drowsiness or confusion appear to

be minimized with Intrathecal administration. The Intrathecal delivery of baclofen

concentrates the drug in the CSF at higher levels than those attainable via the oral

route.

3. Intrathecal administrations can use concentrations of baclofen of less than one

hundredth of those used orally.

4. Adjustable/programmable continuous infusions make it possible to finely titrate

patients dose and to vary the dose over the hours of the day. For example, the dose

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can be relatively low to give the patients the extensor tone needed for ambulation

during the day, and increased at night, thereby improving quality of sleep.

5. Reversible (in contrast to surgery).42

Fig7.1 Intrathecal Baclofen Administration: Baclofen is Injected Through the Skin into a Reservoir

Placed in the Abdominal Wall. The Reservoir also Contains a Programmable Pump Which is

Connected to the Lumbar Epidural Space Via a Catheter.

Dantrolene Sodium

Dantrolene sodium, 1-[(5-nitrophenyl) furfurylidene] amino hydantoin sodium

hydrate, isahydantoin derative and is the only drug in clinical use for spasticity that

produces relaxation of contracted skeletal muscle by affecting the contractile response

at a site beyond the neuromuscular junction.44 It reduces spasticity by inhibiting

calcium release from thesarcoplasmic reticulum, thus uncoupling electricalexcitation

from contraction. Dantrolene sodium reaches peak blood levels in 3-6 hrs, while its

active metabolite 5-hydroxydantrolene reaches peak levels in 4-8 hrs after oral

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administration. Dantrolene reduces spasticity by inducing skeletal muscle weakness,

which is its most significant side effect.43

Other side effects include weakness, fatigue, drowsiness and diarrhoea.

Hepatotoxicity has been reported with the use of dantrolene, and hepatic function

must be monitored periodically in patients on dantrolene.43

Cannabis

Cannabis is fairly newer anti-spastic agent which is a main psychoactive

constituent of the Cannabis sativaplant, 9-tetrahydrocannabinol (9-THC), acts on

a specific cannabinoid receptor in the brain (the cannabinoid CB1 receptor).

Activation of CB1 receptors decreasesneuronal excitability by activating somatic and

dendritic potassium channels. Using the experimental allergic encephalomyelitis

(EAE) mouse model of MS, cannabinoids have been reported to reduce both

spasticity and tremor; furthermore,changes in CB1 receptors have been found in the

CNS of EAE animals led to the proposal that endocannabinoids provide a natural,

anti-spastic function in the CNS.48

The side-effect profile indicated the long-term safety of the product. However,

the precise place of Sativex in the management of spasticity awaits larger and longer-

term studies.5

Drugs Initial dose Daily

maximum

Mechanism of

action

Common side

effects

Baclofen 5mg/ 3

times daily

80mg (can

be higher

its side

effects arenot a

Centrally acting

GABA analogue.

Binds to the

GABA receptor atthe presynaptic

Day time sedation,

dizziness,

weakness, nausea;

lowers seizurethreshold

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problem).

Best

divided

into 4

doses.

terminal and thus

inhibits the muscle

stretch.

withdrawal

seizures and

hallucination with

abrupt

discontinuation.Dantrolene 25mg 100mg/4

times daily

Interferes with the

release of ca from

the sarcoplasmic

reticulum of

muscle.

Generalised muscle

weakness, mild

sedation, dizziness,

nausea, diarrhoea,

hepatotoxicity(liver

enzymes should be

monitored).

Tizanidine 2-4mg 36mg Imidazole

derivative, with

agonist alpha-2adrenergic

receptors in CNS.

Dry mouth,

sedation, dizziness,

nausea, mildhypotension,

weakness (less

common than

baclofen).

Clonidine 0-05mg twice

daily

0-1mg/4

times daily.

Acts at multiple

levels as alpha-2

agonist in the

CNS.

Bradycardia,

hypotension,

depression, dry

mouth, sedation,

dizziness,constipation.

Gabapetin 100mg/3

times daily

600-800mg

4/times

daily.

GABA analogue.

May have indirect

effect on GABA-

ergic

neurotransmission.

Somnolence,

Dizziness, ataxia

and fatigue.

Table7.2: Antispastic Drugs: Dose, Mechanism of Action and Side Effects of Common Antispastic

Drug

There are now a number of useful agents, but their small therapeutic range

makes them ineffective in some patients before side effects occur. However, they are

essentially safe in most patients, and those with milder forms of spasticity generally

tolerate them well. Such drugs include Diazepam, Benzodiazepines, central alpha-2

adrenergic receptors agonists e.g. Clonidine, Tizanidine, and Cannabis etc.

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NEUROLYTIC BLOCKS

Nerve Blocks

Khalili and co-workers were the first to describe the use of phenol for

selective peripheral nerve block, by a percutaneous approach. A surface electrode is

normally used to locate the peripheral nerve. A needle with insulated shaft is then

used as an exploratory electrode and the needle tip manipulated until a good muscle

contractile response is observed. At this stage the phenol is injected. These nerve

blocks are best used for the treatment of focal spasticity rather than generalised

spasticity.46

Nerve blocks have been used to successfully manage abnormal arm and leg

posture in chronic hemiparesis (> 6 months post-stroke). In the leg, chemodenervation

of the posterior tibial nerve can reduce equinovarus deformity, and in the sciatic nerve

reduces inappropriate knee flexion. The effect may last from a few months to several

years.45

Peripheral nerve blocks should be avoided in the upper limbs because they

may cause loss of skin sensation, dysthesias and also because of the risk of vascular

damage. Botulinum toxin is a useful alternative for the treatment of upper limb

spasticity.5

Whilst the nerve blocks reduce undesirable hyperactivity as occur in

spasticity, they may also lead to joint instability and increased energy expenditure.6

Intra thecal Blocks

Administration of phenol or alcohol into the Intrathecal subarachnoid space is

generally reserved for severe symptomatic cases of lower limb spasticity refractory to

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other methods of treatment.6It may result in serious morbidity and should be avoided

in subjects with a reasonable bladder and bowel control and in ambulatory patients.

Intrathecal blocks are most useful for the treatment of intractable painful muscle

spasticity in paraplegic or tetraplegic patients who have no realistic prospects of

functional recovery, no skin sensation in the lower half of the body and no control

over their bowel and bladder function. Intrathecal block is usually painless because of

the immediate anaesthetic effect of the neurolytic agents.5

CONCLUSION

Antispasticity drugs are first line treatment for the pharmacological

management of generalized spasticity following physiotherapy. As more drugs

become available and as more becomes known about spasticity, health professionals

will become more skilled in utilizing different regimens. Spasticity management is a

team responsibility designed to address the needs of the disabled individuals and the

caregiver. The place of oral antispastic agents has been well established.5

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CHAPTER 8

SURGICAL MANAGEMENT

When spasticity cannot be controlled by conservative methods or by

botulinum toxin injections, ablative procedures must be considered. The surgery

should be performed so that excessive hypertonia is reduced without suppression of

useful muscular tone or impairment of the residual motor and sensory functions.

Therefore, neuroablative techniques must be as selective as possible. Such selective

lesions can be performed at the level of peripheral nerves, spinal roots, spinal cord or

the dorsal root entry zone.5

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Common goals of surgery are usually to increase mobility, decrease the use of

external aids, correct or prevent deformity, and ultimately maximise function.14

Peripheral Neurotomies

Neurotomies are indicated when spasticity is localized to muscles or muscular

groups supplied by a single or a few peripheral nerves that are easily accessible

Selectivity is required to suppress the excess of spasticity without producing

excessive weakening of motor strength and severe amyotrophy.5

Selective Neurotomies are able not only to reduce excess of spasticity and

deformity but also to improve motor function by re-equilibrating the tonic balance

between agonist and antagonist muscles.5

Figure8.1: Obturator Neurotomy: Skin Incision on the Relief of the Adductor Longus Muscle;

Dissection of the Anterior Branch (AB) of Right Obturator Nerve (ON). The Adductor Longus Muscle

(AL) is Retracted Laterally And Gracilis Muscle (G) Medially. The Nerve is Anterior to the Adductor

Brevis Muscle (AB). The Adductor Brevis Nerve (1 And 2), Adductor Longus Nerve (3) and Gracilis

Nerve (4 And 5) is Shown. The Posterior Branch (PB) of the Obturator Nerve Lies Under the Adductor

Brevis Muscle (AB).

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Fig 8.2: Movement Analysis in Spastic Foot (Equinovarus) Before and After Selective Tibial

Neurotomy.

SELECTIVE DORSAL RHIZOTOMY

Selective dorsal rhizotomy (SDR) is a neurosurgical treatment that is mainly

performed at lumbar level in patients with bilateral spasticity. Selective dorsal

rhizotomies are reported to be effective in alleviating spasticity in children with

cerebral palsy. This neurosurgical operation reduces spasticity by cutting selected

posterior nerve rootlets on the basis of intraoperative electrical stimulation and

electromyography recordings.50

For non-ambulatory patients, the operation can increase range of motion;

improve sitting, dressing, and positioning; and may lead to gains in functional

mobility. For ambulatory patients, it can increase stride length and walking velocity;

improve motion about the thighs, knees, and ankles; and ameliorate foot floor contact.

Patients need to be carefully selected with emphasis on ascertaining the clinical

importance of obstructive spasticity. When chronic pain and spasticity complicate the

care of patients with stroke or spinal cord injury, microsurgical lesions at the dorsal

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root entry zone have been shown to be effective in reducing tone and in alleviating

pain.51

LONGITUDINAL MYELOTOMY

The method consists of a frontal separation between the posterior and anterior

horns of the lumbosacral enlargement from T11 to S2 performed from inside the

spinal cord after a posterior commisural incision that reaches the ependymal canal.

Longitudinal myelotomy is indicated only for spastic paraplegias with flexion spasms,

when the patient has no residual useful motor control and no bladder or sexual

function5.

MICROSURGICAL DORSAL ROOT ENTRY ZONOTOMY (MDT)

This method named microDREZotomy (MDT) attempts to selectively

interrupt the small nociceptive and the large myotatic fibres (situated laterally and

centrally, respectively), while sparing the large lemniscal fibres which are regrouped

medially5

MDT was originally developed for the treatment of neurogenic pain,

particularly for those cases secondary to a brachial plexus avulsion.53

Complications after the procedure have been reported to include loss of bowel,

bladder, or sexual function, sensory loss, dysaesthesias, and weakness of the lower

extremities. One serious complication of early dorsal root entry zone surgery is

muscular weakness.53

MDT is indicated in paraplegic patients, especially when they are bedridden as a

result of disabling flexion spasms, and in hemiplegic patients with irreducible and/or

painful hyperspasticity in the upper limb.5

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Apart from these interventions Stereotactic neurosurgery, and cerebellar

stimulation are other surgical procedures used to reduce spasticity, but outcomes are

poor.7

Hemiplegia with Paraplegia with

hypertonicity spasticity

Lower limb Non ambulatory

Patient

Spastic Foot Neurotomy of tibial nerve bed ridden if flexor

spasm

Equinus soleus (Gastrocnemius)

Varus posterior tibialis

Flexion of toes flexor fascicles SDR myelotomy MDT

Hemiplegia with Ambulatory patient

hypertonicity

Upper limb

-entire limb with MDT MDT

proximal predominance

Diffuse

-entire limb with MDT spasticity ITB

Distal predominance with neurotomy of median nerve

(+ ulnar) flexor branches

Fig8.3 Guidelines for surgical management of spasticity: SDR: Selective Dorsal Rhizotomy,

MDT: Microsurgical Dorsal Root Entry Zonotomy, ITB: Intrathecal Baclofen.

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NEURO-ORTHOPEDIC SURGERY

Neuro-orthopedics is the field of orthopaedic surgery that treats limb deformities

resulting from neurological disease or injury. With severe spasticity contractures and

subluxation can occur.49

Orthopaedic procedures can reduce spasticity by means of muscle relaxation

that results from tendon lengthening and may help in restoring articular function when

deformities have become irreducible5

.Contracture release is the most common

orthopaedicprocedure for spasticity. By cutting the tendon of a contractedmuscle, the

surgeon can reposition the joint in a normalangle and cast over it. In a few weeks

when the tendonre-grows, the cast is removed and serial casting is done followedby

rehabilitation for many months. The result shouldbe a more natural joint position and

a better orthotics fit andgait. Hamstring and Achilles tendon release are common.7

Upper extremity Lower extremity

Adducted shoulder

Flexed elbow

Pronated forearm

Flexed wrist

Clenched fist

Thumb in palm

Adducted hip

Flexed hip

Flexed knee

Stiff knee gait

Equinovarus foot

Claw toes or cavus foot

Valgus foot

Table 8.1; Common Motor Neuron Extremity Deformities.

Tendon transfermoves the insertion site of the spastic muscle to a new

location,thus, the spastic muscle no longer pulls the joint into a deformed position.

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After this surgery joints will generally lose active function, but will maintain passive

range and have better anatomical alignment. Split anterior tibial tendon transfer

(SPLATT) is a common procedure for correction of equinovarus deformity.7

Osteotomyis a procedure where part of the bone is removed (wedge shape) to

reshape or reposition the main bony structure and is commonly done in hip

displacement and foot deformity. Osteotomies aim to correct bone deformity resulting

from growth distorsion in a child (e.g. femoral derotation osteotomy to correct

excessive ante version in patients with cerebral palsy) or to treat stiffened joints (e.g.

supracondylar femoral osteotomy for irreducible flexed knee).5

Arthodesis is used when joint fusion limits the ability of a spastic muscle to

pull the joint into an abnormal position. It is most commonly performed on bones in

the ankle and foot.7

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\

REFERENCES

1. Carr J, Shepherd R. Neurological rehabilitation: Optimising Motor

Performance. Butterworth-Heinemann.1998:191-192,198.

69


70/76

2. Young R R. Spasticity: a Review. Neurology. (Suppl.9).1994;44:512-520.

3. Barnes M P. Management of Spasticity. Age and Ageing.. 1998;44: 210-245.

4. Lance J W, Mcleods J G, A physiological Approach to Clinical Neurology.

Third Edition, Butterworth-Heinemann.

5. Barnes M P, Johnson G R. UMN Syndrome and Spasticity: Clinical

management and Neurophysiology. Second Edition. Cambridge University

Press. 2008:4-5, 11, 16, 33-38, 43-45, 69, 110.

6. Bromley I. Tetraplegia and Paraplegia: A Guide for Physiotherapists. Sixth

Edition. Churchill livingstone. 2006: 291-293, 367.

7. Mostoufi S A. Spasticity and its Management. Pain management Rounds.

Issue 5:2005.

8. Ivanhoe CB, Reistetter TA. Spasticity: The Misunderstood Part of UMN

Syndrome. American Journal of Physical Medicine Rehabilitation, 2004 Oct:

83 (10 Suppl): S3-9.

9. Young R R et al. Current Issues in Spasticity Management. The Neurologist

1997 3:261-275.

10. Sternberg T L. Treatment of Spasticity Associated With Spinal Cord injury

and Other Central nervous System Damage. Northeast Florida Medicine. 60:

2009.

11. Guyton A C, Hall E J. Textbook of Medical Physiology, W. B Saunders

Company. Ninth Edition. 1996: 689.

12. OSullivan S.B, Schmitz T J. Physical Rehabilitation: Fifth Edition. F A Davis

Company. 2007: 497-498,519.

13. Supraja M, Singh U. Study of Quantitative Assessment of Spasticity by

Isokinetic Dynamometry. IJPMR 14, April 2003: 15-18.

70


71/76

14. Braddom R L. Physical Medicine and Rehabilitation. Third Edition. Saunders

Publishers. 2007: 657.

15. Delwaide P J, Young R R. Clinical Neurophysiology in Spasticity. Elsevier.

1985: 96-97.

16. Bobath B. Adult Hemiplegia: Evaluation and Treatment. Third Edition.

Butterworth-Heinemann. 2-3.

17. Fredericks C M, Saladin L K, Pathophysiology of Motor Systems, F A Davis

Company. 1996.

18. Smith K L, Weiss E L, Lehmukhl L, D. Brunnstroms Clinical Kinesiology.

Fifth Edition. F A Davis Company. 1996: 119.

19. Stevenson V, Marsden J F. Spasticity management: A Practical

Multidisciplinary Guide. Fifth Edition. Human Press. 2006.

20. Dorland. Illustrated medical Dictionary. Twenty Eighth Edition.W. B

Saunders Company. 1994.

21. Ensberg J R, Olree K S, Ross S A. Quantitative Clinical Measure of Spasticity

in Children With Cerebral Palsy. Archieves of Physical Medicine

Rehabilitation. 1996.

22. Sehgal N, McGuire J R. Beyond Ashworth: Electrophysiologic Quantification

of Spasticity. Phy Med Rehabil Clin N Am. 1998 Nov;9 (4): 949-979.

23. Pandyan et al. Systematically Acting Pharmacological Interventions for

Spasticity After Stroke. Wiley Publishers. 2008

24. Sorensen F B, Nielson J B, Klinge K. Spasticity-Assessment: A review.

International Spinal Cord Society.2006: (44), 708-722.

71


72/76

25. Nuyens et al. Clinical Scales for Assessment of Spasticity, Associated

Phenomenon, and Function: A Systematic Review of Literature. Disability and

Rehabilitation. 2005: 27 (1/2): 7-18.

26. Sherwood A M, Graves D E, Priebe M M. Altered motor Control and

Spasticity After Spinal Cord injury: Subjective and Objective Assessment.

Journal of Rehabilitation and Research and Development. Vol. 37. Jan/Feb

2000: 41-52.

27. Ansari N N et al. Inter and Intrarater reliability of Modified Ashworth Scale in

Patients With Knee Extensor post Stroke Spasticity. Physiotherapy Theory

Practical. Vol. 24. May/June 2008: 205-213.

28. Johnson G R. Spasticity: Perceptions, Definitions and Measurement. 9th

Annual Conference of International FES Society. September 2004.

29. Becker J G et al. Clinical Assessment of Spasticity in Children With Cerebral

Palsy: A critical Review of Available Instruments. Developmental Medicine

And Child Neurology. Vol. 48, 2006: 64-73.

30. Bohannon R W, Harrison S, Kinsella-Shaw J. Reliability and Validity of

Pendulum Test Measures Of Spasticity Obtained With The Polhemus

Tracking Systems From Patients With Chronic Stroke. Journal of

Neuroengineering and rehabilitation. 2009: 1-7.

31. Decq P, Filipetti P, Lefaucher J P. Evaluation of Spasticity in Adults.

Operative Techniques In Neurosurgery. 2005:100-108.

32. Mackey A H, Walt S E. Intraobserver of Modified Tardieu Scale in the Upper

Limb Of Children With hemiplegia. Developmental Medicine and Child

Neurology. 2004: 267-272.

72


73/76

33. Hagh A B, Pandyan A D, Johnson G R. A Systematic review of Tardieu Scale

For the Measurement of Spasticity. Disability Rehabilitation. Jan 2005; 69-80.

34. Burridge G h et al. Theoritical and Methodological Considerations in the

Measurement of Spasticity. Clinical Rehabiliation. 2009:373-383.

35. Voerman G E, Gregoric M, Hermens H J. Neurophysiologic Methods of

Spasticity: The Hoffmann Reflex, the Tendon Reflex, and the Stretch Reflex.

Disability Rehabilitation. 2005: 33-68.

36. Bowden M, Stokic D S. Clinical Neurophysiologic Assessment of Strength

and Spasticity During Intrathecal Baclofen titration in Incomplete Spinal Cord

Injury. The Journal of Spinal Cord Medicine. Vol. 32. Nov. 2009.

37. Satkunam L E. Rehabilitation Medicine: Management of Adult Spasticity.

Canadian medical Association of Journal. Nov. 2003: 1173-1178.

38. Maurtiz K H et al. Botulinum Toxin for Lower Limb Extensor Spasticity in

Chronic Hemiparetic patients. Journal of Neurology and Psychiatry.

1994:1321-1324.

39. Giovanneli M et al. Early Physiotherapy After Injection of Botulinum toxin

increases the beneficial Effects on Spasticity in Patients With Multipe Sc

lerosis. Clinical Rehabilitation. 2006:331-337.

40. Sadiq S A, Wang G C. Long Term Intrathecal Bacolfen Therapy In

Ambulatory Patient With Spasticity. Journal Of Neurology. 2006: 563-569.

41. Medical Advisary Secretariat, Ministry of Health and Long Term Care.

Ontario Health Technology Assessment Series. Vol. 5, 2007.

42. Patel D R, Soyode O. Pharmacologic Interventions in reducing Spasticity in

Cerebral palsy. Indian Journal of Pediatrics. Vol. 72. Oct. 2005: 869-872.

73


74/76

43. Growden J H et al. L-Threonine in the Treatment of Spasticity. Clinical

Neuropharmacology. Vol. 14,1991: 403-412.

44. Bhakta B B. Management of Spasticity in Stroke. British Medical Bulletin,

Vol. 56. 2000: 476-485.

45. Kopec K. Cerebral Palsy: Pharmacologic Treatment of Spasticity. United

States Pharmacology, 2008: 22-26.

46. Smith P F. New Approaches in the Management of Spasticity in Multiple

Sclerosis Patients: Role Of Cannaboids. Therapeutics and Clinical Risk

Management. 2010: 59-63.

47. Gelber D A. Clinical

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