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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
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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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\
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