12
Management of spasticity in children
Rachael Hutchinson and H. Kerr Graham
Introduction
Spasticity can be defined as a velocity-dependent
resistance to passive movement of a joint and its
associated musculature (Lance, 1980; Rymer & Pow-
ers, 1989; Massagli, 1991). Although spasticity is usu-
ally present before contracture in children with cere-
bralpalsy, true muscle shortening or contracture also
appears at an early stage. The majority of children
will have a mixture of spasticity and contracture. Dis-
tinguishing spasticity from contracture is important
from a management point of view.
1. ‘Dynamic’ shortening is most commonly caused
by spasticity but may also be associated with
dystonia and mixed movement disorders. Typ-
ically, ‘dynamic’ contracture is recognized in
younger children with cerebral palsy or spas-
ticity of recent onset. Such children are likely
to exhibit hyperreflexia, clonus, co-contraction
and a velocity-dependent resistance to passive
joint motion. Children who exhibit ‘dynamic’
calf shortening may walk on their toes with an
equinus gait, but on the examination couch the
range of passive ankle dorsiflexion may be full or
almost full.
2. ‘Fixed’ shortening or ‘myostatic’ contracture
describes the typical stiffness found in mus-
cles of older children with cerebral palsy or
spasticity of longer duration. The stiffness

our clinics is cerebral palsy, subsequent discussion
214
Management of spasticity in children 215
Table 12.1. Aetiology of spasticity in 341 children
(cerebral palsy, orthopaedic and spasticity clinics)
Cerebral palsy 79%
Acquired brain injury 6%
Spina bifida 5%
Spinal cord injury 2%
Miscellaneous 8%
on pathology and management focuses mainly but
not exclusively on spasticity in the context of juve-
nile cerebral palsy. The effects of spasticity cannot be
separated from the overall effects of the upper motor
neurone (UMN) syndrome (Fig. 12.1). The child with
diplegia who walks on his toes because of calf spas-
ticity may also be unable to voluntarily control the
dorsiflexors of the ankle during gait. No matter how
effective management of the calf spasticity is, gait
may remain impaired because toe clearance cannot
be achieved during the swing phase of gait (Perry,
1985, 1992). Indeed there is virtually always an effec-
tive solution to calf spasticity/stiffness/shortening,
but inability to control the ankle dorsiflexors dur-
ing swing phase may mean life-long dependence on
an orthosis. Weakness and impaired selective motor
control have a much greater impact on gait and func-
tion than spasticity. They are also more difficult to
manage.
Fixed musculoskeletal pathology in cerebral palsy

Spasticity, dynamic and fixed contractures coexist
in varying proportions in most children. The tran-
sition from dynamic to fixed contracture occurs at
different rates in different topographical types of
cerebral palsy and at different rates in different limb
segments and even in different muscle groups in the
same limb segment. There appears to be a ‘biolog-
ical clock’ running at different speeds for different
muscles in children with cerebral palsy, governing
the timing of the transition from dynamic to fixed
contracture (Eames et al., 1999; Preiss et al., 2003).
In hemiplegia, there is an earlier transition from
dynamic to fixed contracture than in diplegia. The
dynamic component can be exploited by spasticity
management (Eames et al., 1999). In spastic hemi-
plegia, fixed contracture usually develops in the
lower limb earlier than in the upper limb. Spastic-
ity management may be appropriate in the upper
limb at an age when surgery is required for a fixed
equinus deformity. In the hemiplegic upper limb, the
first muscle to develop a fixed contracture is almost
invariably the pronatorteres (Preiss et al., 2003). This
may result more from the absence of active supina-
tion than increased spasticity in the pronator teres.
A useful strategy may be to combine a lengthening
or rerouting of the pronator teres, with spasticity
management of the wrist and finger flexors using
botulinum toxin A (BoNT-A). Recognition of these
types of patterns may greatly improve the outcome
of both spasticity and contracture management and


British Editorial Society of Bone and Joint Surgery.)
Management of spasticity in children 217
Figure 12.2. The stages of lower limb pathology in the child with cerebral palsy. (Modified after Rang, 1990.)
lead to the development of creative strategies to deal
with common clinical presentations (Preiss et al.,
2003)(Fig. 12.3).
Measuring spasticity in children: clinical
The Ashworth scale
There are few useful clinical measures of spastic-
ity and none validated for use in children. The Ash-
worth and modified Ashworth scales are blunt and
unresponsive tools in the assessment of the child
with cerebral palsy (Ashworth, 1964; Bohannon &
Smith, 1987). Their evaluations are subjective and
reliability between investigators may be a problem.
Most muscles in most children are grade 1+ to grade
3. Most useful clinical responses to spasticity man-
agement are within and not across a single Ashworth
grade. Of much greater utility is the measurement of
dynamic joint range, which can be used across most
major joints as a quantitative measure of spasticity
(Tardieu et al., 1954; Fosang et al., 2003).
The dynamic and static joint range of motion
The range of motion of joints in both the upper and
lower limbs is classically used as a proxy measure
of the length of muscles crossing that joint. In the
upper limb, the range of elbow extension is taken to
be a measure of the length of the elbow flexors, the
biceps and brachialis. Loss of elbow extension (fixed

fverskiold test (Silfverskiold, 1924) by Perry has in
our view led to an unwarranted devaluation of this
most useful clinical test (Perry et al., 1974, 1976,
1978).
Dynamic joint range of motion is measured by
provoking a stretch reflex if it is present. Typically
this first catch, or R1, comes in at a repeatable joint
angular position. This is usually 20 to 50 degrees
prior to R2, the static muscle length (Tardieu et al.,
1954). The variation is due to the proportion of
the deformity, which is dynamic, and not fixed. R2
approximates to the degree of ‘myostatic contrac-
ture’ or fixed shortening, which may require tendon
Example 1
A 3-year-old child with spastic diplegia has an equinus gait
affecting both lower limbs equally.
R1: −35 degrees (35 degrees of equinus)
R2: +5 degrees (5 degrees of dorsiflexion)
R2 − R1 = 40 degrees
Spasticity management is likely to be beneficial because
there are 40 degrees of dynamic shortening to be exploited
by spasticity management. Surgical lengthening of the heel
cord is contraindicated because the degree of fixed contrac-
ture is so small.
Example 2
A 10-year-old boy with hemiplegia walks with an equinus
gait on the affected side.
R1: − 30 degrees (30 degrees of equinus)
R2: −20 degrees (20 degrees of equinus)
R2 − R1: 10 degrees

spasticity in children, there is a clear need for objec-
tive measurements with a greater degree of valid-
ity and repeatability. A number of techniques have
been described, and although most are useful within
research settings, none have become popular in clin-
ical practice.
Measurements of muscle stiffness address the
biomechanical rather than the neurophysiologi-
cal components of spasticity. These measurements
may also be obtained on the examination couch
or during walking. Static measurements include
measurements of muscle torque and resonant fre-
quency (Walsh, 1988; Corry et al., 1998; McLaugh-
lin et al., 1998). In a placebo-controlled clinical trial,
resonant frequency was found to be an objective
means to quantify muscle stiffness in the hemiplegic
upper limb. Reductions in resonant frequency were
recorded after injecting the forearm muscles with
BoNT-A (Corry et al., 1997).
Video recording of gait and aspects of the static
couch examination are very useful in clinical prac-
tice. Utility is further enhanced by split-screen, two-
dimensional recording with freeze-frame facilities
(Keenan et al., 2004). Careful editing and archiving
of patient records is also important.
Various scoringsystems or‘physician rating scales’
have been devised to increase the sensitivity and
objectivity of information gained from video record-
ings of children’s gait (Koman et al., 1993, 1994;
Corry, 1994). Although some have been tested for

ties in differentiating between dynamic and fixed
deformities and in measuring functional outcomes
in motor disabled children. Spasticity should not
be treated just because it is present. The natural
220 Rachael Hutchinson and H. Kerr Graham
history of spasticity in children is not sufficiently
well known nor are our present methods of manage-
ment sufficiently safe and effective to warrant such
an approach. Children with severe, ‘whole body’
involvement frequently use spasticity in functional
activities. A total extensor pattern may aid stand-
ing transfers. In this scenario, ‘successful’ spasticity
management, if measured by reduction in tone and
improved range of motion, might reduce rather than
enhance function. Hence the prime goal of spasticity
management must be improved function.
Understanding of motor development and meth-
ods of assessing function in children is also crucial.
A major characteristic of children who have cere-
bral palsy is the delayed acquisition of motor skills
(Rosenbaum et al., 2002). Given that spasticity man-
agement must often be undertaken against a back-
ground of growth and motor development, it is clear
that only controlled clinical trials can reliably sepa-
ratethe effects ofspasticity management on function
from gains made as part of normal motor develop-
ment. It is relatively straightforward to demonstrate
reduction in tone, improved joint range of motion
and improved muscle length after spasticity man-
agement, but evidence of functional gains is much

Botulinum
toxin A
SDRITB
Oral
therapy
Focal
Figure 12.4. The four-way compass of spasticity
management with general versus focal (north and south)
and reversible versus permanent (west versus east).
r
Access to appropriate orthotics
Spasticity management may fail for a variety of
reasons including:
r
Spasticity, too severe and generalized
r
Poor cognitive ability
r
Fixed deformity
r
Poor selective motor control
r
Associated medical disease
r
Inadequate home support
r
No access to appropriate physiotherapy or
orthotics
Methods of spasticity management can be clas-
sified on a four-way compass (Fig. 12.4) according

disciplinary exercise. In many centres, the concept
of a spasticity team and a spasticity clinic are well
developed. At the Royal Children’s Hospital in Mel-
bourne, the members of the team are drawn from the
following backgrounds:
r
Physical Medicine and Rehabilitation
r
Child Development and Rehabilitation
r
Physiotherapy
r
Occupational Therapy
r
Clinical Nurse Coordinators
r
Orthotics
r
Neurosurgery
r
Orthopaedic Surgery
r
Motion Analysis Laboratory
Many children are managed successfully by individ-
ual clinicians. However, there are a sufficient num-
ber of very difficult management problems to justify
a monthly spasticity clinic where the management
of a small number of problem children is discussed
in detail. Often investigations such as gait analysis
or examination under anaesthesia are requested to

tiation of the presynaptic inhibitory effects of GABA
at GABA
A
receptors on spinal afferent presynaptic
terminals. Central effects in the brainstem reticular
formation result in sedation (Costa & Guidoffi, 1979;
Young & Delwaide, 1981a; Davidoff, 1989; Blackman
et al., 1992). Diazepam is rapidly and almost com-
pletely absorbed following oral or rectal adminis-
tration. Intravenous administration is occasionally
used to gain rapid control of muscle spasms in a
child who is excessively anxious and in pain after
orthopaedic procedures, but there is a risk of res-
piratory depression, and this route is not recom-
mended for routine use. Intramuscularinjections are
painful, rarely required and erratic in their absorp-
tion profile. Rectal administration is ideal when chil-
dren are fasting, nauseated or unable to take medi-
cation orally. The half-life in children is shorter than
in adults but still long at 18 hours. There tends to
be a cumulative effect of diazepam and it may take
222 Rachael Hutchinson and H. Kerr Graham
some time to reach the appropriate levels in body
tissues and optimal clinical effect. The drug’s vol-
ume of distribution is large, reflecting its extensive
tissue penetration within the body. It is metabolized
by the liver to pharmacologically active metabo-
lites, including nordiazepam and oxazepam (Green-
blatt et al., 1980). The most common side effects are
excessive sedation, respiratory depression, fatigue

1971; Waterman et al., 1980). The main effect on
skeletal muscle appears to be direct muscle relax-
ation rather than a central or a spinal level of action.
Dantrolene inhibits the release of calcium from
the sarcoplasmic reticulum of muscle cells (Van-
Winkle, 1976; Desmedt & Hainaut, 1979; Molnar &
Kathirithamby, 1979). All muscles, both spastic and
normal, tend to be affected, ranging from relax-
ation through to weakness. Dantrolene is rapidly and
extensively absorbed, but there is a lack of pharma-
cokinetic data in children and especially in children
who have spasticity (Lietman et al., 1974; Young &
Delwaide, 1981a; Lerman et al., 1989). The utility of
dantrolene has been limited by the potential for hep-
atotoxicity (Utili et al., 1977; Wilkinson et al., 1979;
Chan, 1990). Fatal dantrolene-induced hepatitis has
been reported in adults but not in children. In chil-
dren, transaminase levels may rise, leading to a with-
drawal of therapy. Liver function should be assessed
prior to starting dantrolene therapy and at frequent
intervals thereafter (Ried et al., 1998).
A number of studies have been reviewed by Black-
man and colleagues, who note that the numbers of
patients within the published files are small and the
outcome measures not particularly objective (Black-
man et al., 1992). However, most studies do report
that in comparison with placebo, dantrolene has a
positive effect in reducing muscle tone but not nec-
essarily in improving function.
Tizanidine

old between effective reduction in spasticity or mus-
cle tone and side effects such as dizziness, weakness
and fatigue is rather small. However, individual chil-
dren can respond well, and a careful trial of various
dose levels is worthwhile, although the majority will
have their medication discontinued because of side
effects. Hallucinations and seizures may occur with
abrupt withdrawal of baclofen; therefore, as with
diazepam, children who have become habituated to
larger doses should be weaned off the drug slowly. A
double-blind crossover trial of oral baclofen admin-
istration in children documented a decrease in spas-
ticity with little change in functional abilities, such
as ambulation and the performance of activities of
daily living (ADLs)(Milla & Jackson, 1977; Molnar &
Kathirithamby, 1979).
Much interest has been raised by the intrathe-
cal administration of baclofen (Knutson et al., 1974;
Penn & Kroin, 1985). Using this technique, the low
lipid solubility and binding to plasma proteins is
avoided by administration of the drug directly to the
target tissues. As will be seen in a later section, this
introduces a new ‘risk–benefit’ profile with specific
advantages and disadvantages.
Casting and orthoses: temporary/focal
The use of casting and orthoses can be classified as
focal/temporary. Casting, orthoses, neurolytic injec-
tions and physiotherapy are often used in vari-
ous combinations to manage spasticity in younger
children with cerebral palsy (see also Chapter 6).

inite biomechanical benefits, confirmed by motion
analysis (Rose et al., 1991; Ounpuu et al., 1993).
Intramuscular injections: chemoneurolysis:
temporary/focal
Intramuscular injections are focal in nature. The
duration depends on the agent, the concentration
used and the site of injection. ‘Chemoneurolysis’
refers to a nerve block resulting in impaired neu-
romuscular conduction by the destruction of neural
tissue, either temporarily or permanently (see Chap-
ter 8). Injection can be performed at many levels in
the peripheral nervous system from nerve root to
motor end plate (Glenn, 1990). The more proximal
the injection site, the more general and prolonged
the effect. Sciatic nerve block results in a variable
degree of weakness of all of the muscles supplied by
the sciatic nerve in the distal thigh and leg. Injec-
tion of the gastrocnemius muscle affects small local