Management of Spasticity

in Children With Cerebral Palsy

Ann Tilton, MD
Spasticity and other forms of muscle overactivity caused by cerebral palsy may impair
function or ease of care or may cause discomfort or poor body image. The treatment
program for a child with spasticity may include allied health therapy, exercise, casting,
constraint-induced therapy, oral medications, chemodenervation, intrathecal baclofen, selective dorsal rhizotomy, and orthopedic surgery. Techniques may be combined for greater
efficacy and better tailoring to the needs of the child. This article provides an overview of
each approach, with a review of significant research findings in support of each.
Semin Pediatr Neurol 16:82 89 2009 Published by Elsevier Inc.

roperly defined, spasticity is a motor disorder characterized by a velocity-dependent increase in tonic stretch
reflexes (muscle tone) with exaggerated tendon jerks, resulting from hyperexcitability of the stretch reflex, as one component of the upper motor neuron syndrome.1 Along with
the other positive motor phenomena of the upper motor
neuron syndromeincluding phasic stretch reflexes (clonus
and hyperreflexia), flexor and extensor spasms, cocontraction, dystonia, and associated phenomenaspasticity can
have a significant functional impact on a child with cerebral
palsy (CP). These various forms of muscle overactivity (for
which spasticity is often a convenient, although overly simplified, shorthand term) represent important therapeutic
targets in the attempt to provide functional gains for the
child. Nonetheless, it is important to realize that the negative
symptomsweakness and lack of dexteritymay be far
more functionally disabling and are far less amenable to treatment. Even so, tone reduction in the properly selected patient can lead to important gains, and acceptance of the limits
is not a reason to avoid trying therapy.
The range of treatments for excess tone is large, from simple stretching exercises to oral and injectable therapies to
surgeries. In this article, we review treatment planning for
spasticity in CP and provide an overview of treatment options.

Department of Neurology, Louisiana State University Health and Sciences

Center, New Orleans, LA.
Address reprint requests to Ann Tilton, MD, Louisiana State University
Health and Sciences Center, New Orleans, LA 70,118. E-mail: atilto@
aol.com

82

1071-9091/09/$-see front matter 2009 Published by Elsevier Inc.

doi:10.1016/j.spen.2009.03.006

Evaluation and
Treatment Planning
The treatment program begins with a careful and thorough
evaluation to determine whether muscle overactivity is interfering with some aspect of function, comfort, cosmesis, or
care. If it is not, no treatment is necessary, and it should not
be undertaken. Additionally, whether the patients spasticity
is aiding functionfor instance, whether lower extremity
stiffness actually improves transfer ability in the face of underlying leg muscle weaknessshould be determined. Reduction of such useful spasticity may possibly be counterproductive; on the other hand, when combined with muscle
strengthening and appropriate orthotics, reduction of spasticity may lead to overall functional benefit and therefore can
be contemplated. Thorough evaluation requires the input of
the entire spasticity management team, including the patient
and caregivers, physicians, physical and occupational therapists, nurses, orthopedists, and orthotists, as well as surgeons
and other professionals in some cases. Psychologists, social
workers, and educators may round out the team.
Spasticity in CP can be classified by affected body region:
Spastic diplegia (both legs involved, more than arms)
Hemiplegia (involves an arm and a leg on the same side
of the body)
Double hemiplegia (both arms involved, more than
legs)
Tetraplegia and/or quadriplegia (all 4 limbs involved,
usually severely)
Within this broad scheme, it is important to document the
particular pattern of spastic involvement (eg, scissoring
thighs, adducted shoulder) and the degree of severity.2,3

Management of spasticity in children with CP

Tone is typically measured with the Ashworth Scale, a subjective but nonetheless useful and easily administered clinical
scale that rates tone from 1 (no hypertonia) to 4 (rigid in
flexion or extension).
Evaluation includes not only measurement of tone with
the Ashworth Scale, but also one or more measures of motor
performance and functional ability, such as the Gross Motor
Function Measure (GMFM), the Functional Independence
Measure, or the Barthel Index. Such measures should be chosen not only for their relevance to the clinical picture and
treatment plan but also for their ease of use, keeping in mind
that a measure is only as good as the consistency with which
it is used during follow-up.
In the broadest terms, the goals of any spasticity treatment
plan are to maximize active function, ease care, and prevent
secondary problems such as pain, subluxation, and contracture. Compromises are often required to navigate among
multiple potentially conflicting goals. Because the patient
may have goals and dreams and because the caregiver plays
the central role in the day-to-day management of the child,
each should be a central figure in setting treatment goals.
When setting treatment goals, it is often vital to temper the
caregivers overly ambitious hopes and to focus on realistic,
attainable goals. This may become even more important after
a successful round of treatment, when excitement over improved function leads to unrealistic expectations for further
improvement. At each stage of goal setting, treatment planning, and plan modification, it is vital to obtain full information from the caregiver regarding the effects of previous treatments and the details of the childs current situation. To
develop the best treatment plan, these details must go beyond
a strictly clinical picture to include how the child is functioning in the home and school, interests of the child (eg, sports
or other activities) that may be affected by treatment, and
other factors important to the childs life. Equally important,
the needs of the caregiver must be considered in formulating
treatment. For instance, the tone reduction that will improve
ease of hygiene is likely to be greater than that which will
improve transfers.
Multiple other factors influence treatment plan and timing.
The age of the child, presence of comorbidities such as seizures or cognitive impairment, the ability of the family to
carry out home treatments or return for regular follow-ups,
financial concerns, and other issues are all considered in
determining the best treatment.
Although every case is unique, several broad parameters
can help shape decision making.3 Orthopedic surgery should
be delayed until the gait is mature. Meanwhile, stretching,
physical therapy (PT), and orthotics are used to maintain
range of motion. Oral medications, botulinum toxin injections, intrathecal baclofen, and/or rhizotomy may also be
appropriate. When gait is mature (between ages 6 and 10),
gait analysis and clinical examination can be used to determine whether surgery is necessary. To avoid multiple surgeries and periods of immobility, one should try to perform all
surgery at one time and remobilize the child as soon as possible. Continued stretching and medical treatment are used
as needed to maintain range of motion and mobility.

83

PT and Orthoses
The importance of regular stretching in maintaining full
range of motion and preventing contracture cannot be overstated. Luckily, children want to move, and much of the need
for range-of-motion exercises can be met by the daily activities of a reasonably active child. However, when impairments
are dealt with by compensatory strategies that minimize
movement of the affected joint, the potential for contracture
increases. Thus, regular stretching of all affected limbs is
generally prescribed. Stretching can reduce severity of tone
for several hours, providing a short-term, but not long-term,
antispasticity action.
PT for the child with CP may encompass a regular exercise
program,4 horseback riding,5 and a variety of modalities, including biofeedback6 and electrical stimulation.7-10
Spastic muscles are often weak. The efficacy of lower limb
strength training has been examined in several controlled
clinical trials.11-14 The results of these trials suggest that when
added to a well-designed PT program, strength training can
improve gait parameters without worsening spasticity.
The intensity and constancy of PT needed to maximize
gains have been the subject of several studies. Bower et al
compared the effects of the usual amount of PT to intensive
therapy (1 hour per day, 5 days per week) over 6 months in
children between ages 3 and 12.15 They found no significant
difference between the groups in either function (as measured by the GMFM) or performance (measured by the Gross
Motor Performance Measure) at the end of the 6-month treatment, though inclusion of age and severity covariates suggested a trend toward significance. Six months after the end
of the trial, there was no significant difference between
groups, even with inclusion of these covariates. The authors
concluded that such intensive therapy was not superior to the
normal therapy that children were already receiving, at least
in its long-term effects. A similar result was shown by Weindling et al, who compared 6 months of standard PT, standard
PT plus extra PT delivered by a trained assistant for 1 hour
per week, and standard PT plus a home visit from a family
support worker. They found no evidence that additional PT
affected motor function, developmental status, or adaptive
function. Moreover, there was no benefit seen from intervention from the family support worker on parental stress or
family needs. The authors concluded that extra intervention
is not necessarily beneficial, although they recognized that
research is still needed to determine what constitutes adequate intervention for children of different needs.16 Christiansen et al compared 2 regimens of PTintermittent (4
times a week for 4 weeks, alternating with a 6-week hiatus) or
continuous (once or twice a week, every week) both for 30
weeks.17 They found no difference in GMFM between the 2
regimens and noted that compliance was higher in the intermittent group.
Constraint-induced therapy (also called forced-use therapy) has received much attention during the past decade. In
this protocol, a hemiparetic childs better-functioning upper
extremity is constrained to force use of the more poorly functioning one. This is believed to lead to plastic changes in the

A. Tilton

84
brain that improve the function of the less able limb. Randomized trials have shown the potential of this therapy for
increased acquisition of new motor skills and increased dexterity that may last for at least 6 months.18-22 Compliance may
be a significant issue, one addressed by Charles et al, who
tested a child friendly schedule of 6 hours per day of constraint for 10 of 12 consecutive days.19 They found this regimen was effective in ways similar to a more restrictive one.
These results were retained over the long term and could be
improved upon by a further course of treatment.23
Ankle-foot orthoses (AFOs) are commonly used to treat
dynamic equinus in CP. Carlson et al have shown with gait
analysis that AFOs could significantly reduce ankle excursion
and increase dorsiflexion angle at foot strike, as well as provide other benefits, although neither stride length nor
walking speed were improved.24 AFOs can also improve the
sit-to-stand transition in preambulatory children whose
standing is impaired by equinus.25 Bjornson has suggested
that dynamic AFOs are most effective in younger children.26
One cautionary note is in order: the patient or caregiver
may expect use of any of the new modalities, such as botulinum toxin, intrathecal baclofen, or selective dorsal rhizotomy, to substitute for an individualized PT program. Experience has shown that patients who do not continue with a
program of strengthening and stretching do not realize the
potential benefits of the intervention.

Oral Medications
Oral antispasticity agents have the advantage of ease of use
but the disadvantages of systemic effect and significant side
effects. Thus, they are most appropriate in children for whom
only mild tone reduction is needed or in whom spasticity is
widespread. Unfortunately, most studies on the efficacy of
these agents are old, did not address measures of function,
and employed trial designs less rigorous than the best practices of today. In addition, most antispasticity trials have been
carried out in adults with spastic disorders, and relatively few
trials have been conducted in children. Thus, the choice of
agent is more a matter of personal experience and trial and
error than of rigorous, evidence-based medicine. Continued
use of any particular agent must be justified by clear benefit to
the patient.

Baclofen
Baclofen is a GABA-B agonist, and oral baclofen is often the
drug of choice for spasticity of spinal cord origin in adults. It
may be useful in selected pediatric patients, although little
research has been conducted to support use in this population, and it does not have Food and Drug Administration
approval for use in CP. Milla et al showed in a double-blind
crossover trial that baclofen reduced spasticity significantly
better than placebo and improved both passive and active
movement.27 More recently, Scheinberg et al showed that
whereas there was no effect on spasticity as measured by the
Modified Tardieu scale or on the Pediatric Evaluation of Disability Inventory, there was improvement vs placebo on the

Goal Attainment Scale, a functional assessment tool.28 The

tendency of Baclofen tendency to cause confusion and sedation limits the dose, although these effects may improve over
several weeks of treatment. A typical starting dose in a child is
2.5 mg/d, which can be gradually titrated up to a maximum
of 20-60 mg/d, depending on body size.29 Weaning off of
Baclofen must be gradual to avoid a withdrawal syndrome.

Tizanidine
Tizanidine is a centrally acting alpha-2 noradrenergic agonist
that has been shown to reduce tonic stretch reflexes and to
enhance presynaptic inhibition in animals. A Russian study
in 30 diplegic children of tizanidine dosed at 6 mg/d reported
improved motor ability, which was confirmed with electroneuromyography.30 Side effects were reported to be well tolerated. To date, no clinical trials of this agent in children have
been published in the English-language literature. Sedation
and the requirement for frequent dosing have been limiting
factors in tizanidine use. Nevertheless, the sedative quality
can be an advantage when the medication is delivered at
night. Improved initiation of sleep and reduced tone are potential benefits.

Diazepam
Diazepam is a benzodiazepine that facilitates the postsynaptic action of GABA. A series of trials in the 1960s demonstrated its ability to reduce spasticity in children with CP.31-35
More recently, Mathew et al showed the ability of diazepam
to reduce muscle overactivity in comparison to placebo in a
randomized trial of 180 children.36 Diazepam has also been
compared with and used in conjunction with dantrolene sodium;37 in the same small trial, the 2 agents appeared to be
equally effective, and the combination was more effective
than either alone. The daily dose of diazepam is usually 0.120.8 mg/kg, divided into 3-4 doses. The known sedation profile of this class of medications must be considered. Diazepam at bedtime may aid sleep without carry-over daytime
sedation.38

Dantrolene Sodium
Unlike other oral antispasticity agents, dantrolene sodium
works at the muscle level, inhibiting calcium release from the
sarcoplasmic reticulum, causing muscle weakness. In double-blind crossover studies, it has been shown to reduce spasticity in children with CP.37,39 It can cause global weakness
and, despite its peripheral mode of action, sedation. It also
has the potential for hepatotoxicity in approximately 1% of
patients. It does not have long-term stability in liquid form,
which limits its administration primarily to children able to
take capsules.
In general, the cognitive and sedative side effects of oral
medications can be said often to overshadow any improvement in spasticity, leaving the patient with minimal global
gain in function. Thus, other types of treatments often play a
more important role in tone management in the child with
CP. Oral agents may be most useful as adjuncts in children
with seizures, sleep disturbance, or other conditions in which

Management of spasticity in children with CP

the other effects of these medications, besides the antispastic
effects, are useful.

Botulinum Toxin,
Phenol, and Alcohol
Chemodenervation (also called neurolysis or neuromuscular
blockade) refers to the use of an injectable therapy to prevent
nerve-muscle transmission. Two strategies are in current use:
perineural injection of phenol or ethyl alcohol and intramuscular injection of botulinum toxin (BoNT). All 3 are appropriate for focal spasticity or for targeting specific problem
muscles in more generalized spasticity.
Both phenol and alcohol have been used in children with
CP, although neither has been widely or rigorously tested.
Phenol is typically injected at a concentration of 3%-6%
aqueous solution, whereas absolute alcohol is diluted to
30%-50%. The target nerve is identified with electrical stimulation, a procedure that may be poorly tolerated in children,
making sedation or anesthesia necessary. The agent is injected perineurally, where it promotes denervation via axonal
degeneration. The effect is not permanent, with functional
reinnervation occurring over months to years. Studies have
shown the benefits for spasticity in CP of both alcohol40 and
phenol.41,42 Benefit ranges from a few weeks to 2 years or
more, with no factors conclusively identified in the literature
as determining the duration. Adverse effects of both agents
include a significant risk of pain or paresthesia when targeting a mixed nerve, which may persist. This, combined with
the high degree of skill required to target the nerve and the
availability of botulinum toxin as an alternative, has kept
phenol and alcohol from assuming a larger role in focal spasticity management. Nonetheless, the absence of immunogenicity and the lower cost compared to BoNT make these
agents more attractive in some settings.43
Botulinum toxin is an exotoxin produced by Clostridium
botulinum, the same organism responsible for tetanus. There
are 7 naturally occurring serotypes of the toxin, A-G, all of
which are zinc proteases that target the synaptic vesicle fusion machinery at the neuromuscular junction. Denervation
occurs because vesicles cannot fuse with the synaptic membrane, and therefore, acetylcholine cannot be released. The 7
serotypes differ in the specific component of the fusion machinery they target, their duration of action, their unit potency, and their immunogenic potential. Two serotypes, A
and B, are commercially available. BoNT-A is marketed under the trade names Botox (Allergan; throughout the world),
Dysport (Ipsen; in Europe and elsewhere), and Xeomin
(Merz; in Europe and elsewhere). BoNT-B is marketed by
Elan Biopharmaceuticals in the United States as Myobloc and
in Europe as NeuroBloc. At effective antispasticity doses, all 4
types have roughly the same duration of clinical action, approximately 3 months. Potency is expressed in mouse units,
the amount of toxin required to kill 50% of mice in a standardized assay. Because of differences in molecular formulation and other variables, the potency of a single unit varies
greatly among the commercial types. Although a unit of Bo-

85
tox is roughly as potent as 1 unit of Xeomin, 4 units of
Dysport, and 40-50 units of Myobloc, it is important to recognize that there is not a simple ratio of dosing equivalencies.
Because of these differences, it is critical to specify the commercial brand when discussing units for dosing recommendations.
Most published research in CP has been conducted with
BoNT-A, although a small number of studies have examined
the effect of BoNT-B in this population. Sanger et al injected
BoNT-B into the biceps and brachioradialis or 1 or both arms
in 7 children with CP and upper extremity dystonia. In this
open-label trial, reaching speed improved in response to
treatment, although no dose-dependent effect was observed.44 BoNT-B and BoNT-A have both been combined
successfully with phenol injection, allowing an increase in
the number of treated muscles per injection session.45
BoNT-B has a tendency to cause more autonomic side effects
than BoNT-A, and should be used with this caution in
mind.46
Although earlier studies of BoNT-A concentrated mainly
on demonstrating spasticity reduction via lowered Ashworth
scores,47,48 more recent work has focused on determining the
functional benefit from injections. Fehlings et al showed that
upper extremity injections of BoNT-A plus occupational
therapy were superior to occupational therapy alone on the
Quality of Upper Extremity Skills Test,49 an effect they correlated with preinjection grip strength.50 Lower extremity
function has also been shown to improve significantly;51-53
however, this may not correlate with an improvement in
health-related quality of life.54
Injections can also ease pain55 and have been shown by
one group to be equivalent to fixed casting for improvement
of dynamic calf tightness 56 but inferior to casting by others.57,58 The 2 can be combined, which some studies have
shown to produce better results than either alone.59-62 Casting is usually delayed until the peak effect of the toxin, about
2-4 weeks after injection, which produces superior results to
immediate casting.63
The functional improvements seen in randomized trials
are somewhat modest, but this may be more attributable to
limitations of study design than to the limitations of the therapy itself. Focal improvements in spasticity are difficult to
capture with global measures of function such as the GMFM,
and the individualized dosing and injection patterns that
optimize therapy are usually not possible in rigorous trials.
Practitioners and caregivers usually agree that the benefits
they see from BoNT injection are greater than those revealed
in clinical trials, although family satisfaction may not always
accompany measurable functional gains.64 Even though
there may be no progressive improvement over the course of
repeated injection cycles, the benefits of a single injection
seen early in treatment can persist for many injection cycles
without waning.65
Dosing guidelines for BoNT-A as Botox, for adults and
children, have been developed by consensus.3,66 With time,
the recommended ceiling doses used by experienced practitioners have increased from 4 to 16 U/kg (Botox) in some
cases. In children, maximum dosing should take into consid-

A. Tilton

86
eration the childs weight, muscle bulk, and degree of spasticity. The lowest effective dose with an injection interval of at
least 3 months or more should be used to minimize the risk of
antibody development. Children may need a topical anesthetic or light sedation during injection. Electromyography
(EMG) or electrical stimulation is sometimes used to help
target difficult-to-localize muscles, such as in the upper
extremities, although clinical examination is sufficient for
determining affected muscles in many situations. Injection of
the psoas requires visualization by ultrasound or other
means. Some injectors potentiate the effects of injection with
neuromuscular electrical stimulation applied over the injection site for the first 3 days after injection. The family can be
instructed to perform this.
Adverse effects of injection are usually mild and transient,
consisting of pain on injection, occasionally a mild flulike
syndrome, and excess weakness.67,68 The botulinum neurotoxin complex is immunogenic, and repeated exposure can
lead to immunoresistance. Rates of immunoresistance in
spasticity treatment have not been published, but the accepted rate in adults with dystonia is approximately 3%.
Recently, Allergan introduced a new batch of Botox to replace
the original commercial batch that had been the source of all
commercial Botox until then. Initial reports indicate that the
new batch may be less immunogenic.69 If immunoresistance
develops, it is possible to switch serotypes, although immunoresistance to the second may develop more quickly than to
the first.70

Rhizotomy
Selective dorsal rhizotomy (SDR) was introduced in North
America in the early 1980s, and has since become a commonly used treatment for reduction of moderate to severe
lower-extremity spasticity. During the procedure, the patient
is positioned prone and the dural sac is exposed so that nerve
roots from L2 to S2 can be identified. Individual nerve rootlets are identified and stimulated independently. Those afferent rootlets that elicit excessive activity, monitored via EMG
and visual observation, are cut. Typically 25%-50% of rootlets are cut.71 Controversy exists about how accurately EMG
identifies the appropriate rootlets. Hays et al found no consistent relationship between the proportion of abnormally
responding rootlets and the degree of spasticity and gross
motor abnormality. They concluded that EMG monitoring as
it is typically performed is unlikely to identify accurately
those neural elements that contribute to spasticity in children
with CP.72
Results from clinical trials of SDR have indicated that it
reduces spasticity, although the magnitude of the effect may
be variable. Engsberg et al showed that ankle spasticity could
be reduced almost to normal by SDR, although the standard
deviations were large, indicating high response in some patients and minimal response in others.73 The same group
obtained similar results in a measure of hip spasticity conducted later.74 In a prospective study, Buckon et al demonstrated that SDR and orthopedic surgery can each contribute

significantly to improvements in movement over the long

term.75
The relationship of spasticity reduction to functional improvement has also been controversial with this treatment, as
with others, and 2 investigator-masked trials of similar design have reached opposite conclusions. Both groups randomized candidates to receive surgery plus PT or PT alone.
Both groups quantified functional changes with the GMFM
and used a variety of measures to quantify spasticity changes.
McLaughlin et al76 included 21 surgical and 17 PT-only patients, with a 24-month follow-up, whereas Wright et al77
included 12 surgical and 12 PT-only patients, with a 12month follow-up. Evaluators in both studies were blinded
to surgical status. They differed in one significant aspect:
McLaughlin et al sectioned a mean of 25% of rootlets vs
approximately 50% for Wright. In addition, patients in the
Wright study were significantly more functionally impaired
at baseline than those in the McLaughlin study. Both groups
showed significant postoperative reduction in spasticity with
SDR plus PT compared to that with PT alone, which, in the
words of McLaughlin, was judged by blinded investigators to
be clinically obvious and meaningful. However, in that
study, no long-term functional differences were seen between the 2 groups, despite a 24-month follow-up in which
spasticity reduction might have been expected to afford the
SDR group an advantage. In contrast, Wright et al showed a
7.7 point difference in GMFM scores after 12 months that
favored the rhizotomy group. Further studies will be needed
to determine whether the different outcomes in these 2 studies were attributable to differences in patient population, surgical technique, or some other variable.
Reduction in strength following SDR has historically been
a concern, although more recent studies have not found objective loss of strength.73,74,78 A retrospective study of 158
children who underwent SDR in a single center showed that
postoperative complications occurred in up to 30% of patients. Approximately 10% of patients had back pain starting
6 months or more after surgery, sensory changes, and neurogenic bladder or bowel problems.79
In our experience, the best candidates for SDR are children
from ages 4-8 for whom spasticity is more significant in the
legs than in the arms, with reasonably well-preserved leg
strength and mobility, and whose spasticity is interfering
with that mobility. SDR is followed by intensive PT to remobilize the child and improve strength. Despite best management, most children who require SDR will also eventually
require orthopedic surgery to correct spasticity-induced deformities. However, SDR may reduce the number of such
surgeries required.80 Overall, the use of SDR has declined
with the expanding indications for intrathecal baclofen.

Intrathecal Baclofen
Intrathecal baclofen (ITB) is delivered to the intrathecal space
via a catheter attached to an implanted pump. Because of
direct delivery to the central nervous system, the required
dose is less than 1% of that delivered orally, thus limiting the
side effect of lethargy, which is especially of concern in this

Management of spasticity in children with CP

population. ITB has been shown to reduce spasticity in CP in
several large trials.81-83 Some functional improvement has
been demonstrated as well.83,84 ITB is expensive, but a recent
modeling of cost-effectiveness indicated that over a 5-year
period, ITB, despite increasing cost of care by $49,000 compared to alternative treatment, added 1.2 quality-adjusted
life-years, which is considered good value for the money.85
ITB is typically indicated for patients with lower-extremity
spasticity, although studies have shown significant benefit on
upper-extremity spasticity as well. The dimensions of the
pumpabout the size and shape of a hockey pucklimit the
use of ITB in the very young children, although a smaller
pump is available and has been implanted in children as
young as age 3. Typically, candidates are screened with a
bolus injection of baclofen delivered via lumbar puncture. A
catheter trial with incremental dosing over several days is
beneficial in certain patients, especially those with dystonia
or other movement disorders. A negative response is an indication that further clinical evaluation may be necessary, for
instance, to rule out fixed contracture as the source of muscle
tightness.
The pump is implanted subcutaneously or subfacially in
the abdomen, and the catheter is advanced to the high thoracic region. The pump contains a refillable reservoir, and an
alarm sounds when the reservoir is low. Refills, delivered
transcutaneously, are required every 2-3 months. The pump
is programmable via a telemetry wand, and the dose may be
adjusted to serve different functions over the course of the
day, for instance, increasing at night to aid in comfort for
sleep and decreasing in the morning to aid transfers.
Chronic ITB use carries a small but significant risk of serious complications. Overdose from a programming error is
possible, and may lead to respiratory depression and coma.
Abrupt withdrawal caused by emptying of the reservoir,
pump failure, or catheter withdrawal, kinking, or breakage is
more common. More than a dozen cases of a withdrawal
syndrome and 6 deaths have been reported in the literature.86
Symptoms develop over 1-3 days and include prodromal
itching or paresthesias, rebound spasticity, priapism in men,
tachycardia, hypotension or labile blood pressure, dysphoria
evolving to decreased consciousness, and the potential for
seizures. The most effective treatment is the prompt restoration of ITB therapy. Intravenous benzodiazepines and highdose oral or enteral baclofen, along with life-support measures, may be needed until restoration is possible.

Orthopedic Surgery
Despite best medical and rehabilitation management, children with spastic CP will often eventually require orthopedic
surgery to correct deformities induced by muscle overactivity. Uncorrected deformities can cause pain, interfere with
mobility or care, and lead to subluxation. It is estimated that
hip subluxation or dislocation occurs in up to 25% of children with CP.87 Correction typically involves multiple tenotomies and transfers of the thigh adductors and, in severe
cases, femoral osteotomy. Equinovarus foot is the most common deformity seen in CP, resulting in a flexed ankle and

87
turned-in foot, sometimes with toe curling. Treatment often
involves tendon lengthening. An advance is the SPLATT
split anterior tibial transferin which the tendon is split
along its length and the distal end of the lateral half is transferred to the cuneiform and cuboid bones, where it can exert
a corrective pull across the joint. This procedure is typically
combined with Achilles tendon lengthening and toe flexor
release. Treatment may also be prescribed for the knee and
the upper extremities, depending upon the degree of deformity in these joints.
Orthopedic procedures are best performed sometime after
gait has matured, usually between the ages of 6 and 10. As far
as possible, the multilevel procedures are performed all at
once to minimize postsurgical recovery times, and the child is
mobilized as quickly as possible. PT remains a central part of
treatment to strengthen and improve range of motion in
newly realigned limbs.

Conclusions
Muscle overactivity can be a significant source of functional
disability in a child with CP. Treatment planning is centered
on improving function, comfort, and care; reducing pain;
and preventing or correcting deformity. Oral medications,
chemodenervation, rhizotomy, intrathecal baclofen, and orthopedic surgery may all play a role in treatment of the properly selected child. Physical and occupational therapy are
central to any treatment plan.

Acknowledgments
The author thanks Richard Robinson for his assistance in
preparing this manuscript.

References
1. Lance JW: Symposium synopsis, in Feldman RG, Young RR, Koella WP
(eds): Spasticity: Disordered Motor Control. Chicago, Yearbook Medical, 1980, pp 485-494
2. Mayer NH, Esquenazi A, Childers MK: Common patterns of clinical
motor dysfunction, in Brashear A, Mayer NH (eds): Spasticity and
Other Forms of Muscle Overactivity in the Upper Motor Neuron Syndrome: Etiology, Evaluation, Management, and the Role of Botulinum
Toxin. New York, WE MOVE, 2008, pp 27-38
3. Russman BS, Gormley ME Jr, Tilton A, et al: A rational approach to a
treatment protocol, and the role of botulinum toxin in treatment, in
Brashear A, Mayer NH (ed): Spasticity and Other Forms of Muscle
Overactivity in the Upper Motor Neuron Syndrome: Etiology, Evaluation, Management, and the Role of Botulinum toxin. New York, WE
MOVE, 2008, pp 179-192
4. Verschuren O, Ketelaar M, Gorter JW, et al: Exercise training program
in children and adolescents with cerebral palsy: A randomized controlled trial. Arch Pediatr Adolesc Med 161:1075-1081, 2007
5. Sterba JA: Does horseback riding therapy or therapist-directed hippotherapy rehabilitate children with cerebral palsy? Dev Med Child Neurol 49:68-73, 2007
6. van Dijk H, Jannink MJ, Hermens HJ: Effect of augmented feedback on
motor function of the affected upper extremity in rehabilitation patients: A systematic review of randomized controlled trials. J Rehabil
Med 37:202-211, 2005
7. Ozer K, Chesher SP, Scheker LR: Neuromuscular electrical stimulation
and dynamic bracing for the management of upper-extremity spasticity
in children with cerebral palsy. Dev Med Child Neurol 48:559-563,
2006

88
8. van der Linden ML, Hazlewood ME, Aitchison AM, et al: Electrical
stimulation of gluteus maximus in children with cerebral palsy: Effects
on gait characteristics and muscle strength. Dev Med Child Neurol
45:385-390, 2003
9. van der Linden ML, Hazlewood ME, Hillman SJ, et al: Functional electrical stimulation to the dorsiflexors and quadriceps in children with
cerebral palsy. Pediatr Phys Ther 20:23-29, 2008
10. Khalili MA, Hajihassanie A: Electrical simulation in addition to passive
stretch has a small effect on spasticity and contracture in children with
cerebral palsy: A randomised within-participant controlled trial. Aust J
Physiother 54:185-189, 2008
11. Dodd KJ, Taylor NF, Graham HK: A randomized clinical trial of
strength training in young people with cerebral palsy. Dev Med Child
Neurol 45:652-657, 2003
12. Patikas D, Wolf SI, Mund K, et al: Effects of a postoperative strengthtraining program on the walking ability of children with cerebral palsy:
A randomized controlled trial. Arch Phys Med Rehabil 87:619-626,
2006
13. Unger M, Faure M, Frieg A: Strength training in adolescent learners
with cerebral palsy: A randomized controlled trial. Clin Rehabil 20:
469-477, 2006
14. Scholtes VA, Dallmeijer AJ, Rameckers EA, et al: Lower limb strength
training in children with cerebral palsyA randomized controlled trial
protocol for functional strength training based on progressive resistance exercise principles. BMC Pediatr 8:41, 2008
15. Bower E, Michell D, Burnett M, et al: Randomized controlled trial of
physiotherapy in 56 children with cerebral palsy followed for 18
months. Dev Med Child Neurol 43:4-15, 2001
16. Weindling AM, Cunningham CC, Glenn SM, et al: Additional therapy
for young children with spastic cerebral palsy: A randomised controlled
trial. Health Technol Assess 11:iii-x, 1-71, 2007
17. Christiansen AS, Lange C: Intermittent versus continuous physiotherapy in children with cerebral palsy. Dev Med Child Neurol 50:290-293,
2008
18. Taub E, Ramey SL, DeLuca S, et al: Efficacy of constraint-induced
movement therapy for children with cerebral palsy with asymmetric
motor impairment. Pediatrics 113:305-312, 2004
19. Charles JR, Wolf SL, Schneider JA, et al: Efficacy of a child-friendly
form of constraint-induced movement therapy in hemiplegic cerebral
palsy: A randomized control trial. Dev Med Child Neurol 48:635-642,
2006
20. Deluca SC, Echols K, Law CR, et al: Intensive pediatric constraintinduced therapy for children with cerebral palsy: Randomized, controlled, crossover trial. J Child Neurol 21:931-938, 2006
21. Gordon AM, Chinnan A, Gill S, et al: Both constraint-induced movement therapy and bimanual training lead to improved performance of
upper extremity function in children with hemiplegia. Dev Med Child
Neurol 50:957-958, 2008
22. Sung IY, Ryu JS, Pyun SB, et al: Efficacy of forced-use therapy in hemiplegic cerebral palsy. Arch Phys Med Rehabil 86:2195-2198, 2005
23. Charles JR, Gordon AM: A repeated course of constraint-induced
movement therapy results in further improvement. Dev Med Child
Neurol 49:770-773, 2007
24. Carlson WE, Vaughan CL, Damiano DL, et al: Orthotic management of
gait in spastic diplegia. Am J Phys Med Rehabil 76:219-225, 1997
25. Wilson H, Haideri N, Song K, et al: Ankle-foot orthoses for preambulatory children with spastic diplegia. J Pediatr Orthop 17:370-376,
1997
26. Bjornson KF, Schmale GA, Adamczyk-Foster A, et al: The effect of
dynamic ankle foot orthoses on function in children with cerebral
palsy. J Pediatr Orthop 26:773-776, 2006
27. Milla PJ, Jackson AD: A controlled trial of baclofen in children with
cerebral palsy. J Int Med Res 5:398-404, 1977
28. Scheinberg A, Hall K, Lam LT, et al: Oral baclofen in children with
cerebral palsy: A double-blind cross-over pilot study. J Paediatr Child
Health 42:715-720, 2006
29. Gracies JM, Nance P, Elovic E, et al: Traditional pharmacological treatments for spasticity. Part II: General and regional treatments. Muscle
Nerve Suppl 6:S92-S120, 1997

A. Tilton
30. Brin IL, Kurenkov AL, Gotlib VI: [the use of sirdalud in cerebral palsy in
children]. Zh Nevrol Psikhiatr Im S S Korsakova 99:30-33, 1999
31. Engle HA: The effect of diazepam (Valium) in children with cerebral
palsy: A double-blind study. Dev Med Child Neurol 8:661-667, 1966
32. Holt KS: The use of diazepam in childhood cerebral palsy. Report of a
small study including electromyographic observations. Ann Phys Med
Suppl:16-24, 1964
33. Hiller CJ, Mason JL Jr: Therapeutic test of diazepam (valium) in cerebral palsy. J S C Med Assoc 62:306-309, 1966
34. Carter CH: Evaluation of diazepam in skeletal muscle hypertonicity in
cerebral palsy. Arch Phys Med Rehabil 49:519-523, 1968
35. Marsh Ho: Diazepam in incapacitated cerebral-palsied children. JAMA
191:797-800, 1965
36. Mathew A, Mathew MC, Thomas M, et al: The efficacy of diazepam in
enhancing motor function in children with spastic cerebral palsy. J
Trop Pediatr 51:109-113, 2005
37. Nogen AG: Medical treatment for spasticity in children with cerebral
palsy. Childs Brain 2:304-308, 1976
38. Mathew A, Mathew MC: Bedtime diazepam enhances well-being in
children with spastic cerebral palsy. Pediatr Rehabil 8:63-66, 2005
39. Haslam RH, Walcher JR, Lietman PS, et al: Dantrolene sodium in children with spasticity. Arch Phys Med Rehab 55:384-388, 1974
40. Tardieu G, Tardieu C, Hariga J, et al: Treatment of spasticity in injection
of dilute alcohol at the motor point or by epidural route. Clinical
extension of an experiment on the decerebrate cat. Dev Med Child
Neurol 10:555-568, 1968
41. Spira R: Management of spasticity in cerebral palsied children by peripheral nerve block with phenol. Dev Med Child Neurol 13:164-173,
1971
42. Yadav SL, Singh U, Dureja GP, et al: Phenol block in the management
of spastic cerebral palsy. Indian J Pediatr 61:249-255, 1994
43. Tilton AH: Injectable neuromuscular blockade in the treatment of spasticity and movement disorders. J Child Neurol 18:S50-S66, 2003
(Suppl 1)
44. Sanger TD, Kukke SN, Sherman-Levine S: Botulinum toxin type B
improves the speed of reaching in children with cerebral palsy and arm
dystonia: An open-label, dose-escalation pilot study. J Child Neurol
22:116-122, 2007
45. Gooch JL, Patton CP: Combining botulinum toxin and phenol to manage spasticity in children. Arch Phys Med Rehabil 85:1121-1124, 2004
46. Dressler D, Eleopra R: Clinical use of non-A botulinum toxins: Botulinum toxin type B. Neurotox Res 9:121-125, 2006
47. Corry IS, Cosgrove AP, Walsh EG, et al: Botulinum toxin A in the
hemiplegic upper limb: A double-blind trial. Dev Med Child Neurol
39:185-193, 1997
48. Koman LA, Mooney JF III, Smith BP, et al: Management of spasticity in
cerebral palsy with botulinum-A toxin: Report of a preliminary, randomized, double-blind trial. J Pediatr Orthop 14:299-303, 1994
49. Fehlings D, Rang M, Glazier J, et al. An evaluation of botulinum-A toxin
injections to improve upper extremity function in children with hemiplegic cerebral palsy. J Pediatr 137:331-337, 2000
50. Fehlings D, Rang M, Glazier J, et al: Botulinum toxin type a injections in
the spastic upper extremity of children with hemiplegia: Child characteristics that predict a positive outcome. Eur J Neurol 8:145-149, 2001
(Suppl 5)
51. Love SC, Valentine JP, Blair EM, et al: The effect of botulinum toxin
type A on the functional ability of the child with spastic hemiplegia
a randomized controlled trial. Eur J Neurol 8:50-58, 2001 (Suppl 5)
52. Ubhi T, Bhakta BB, Ives HL, et al: Randomised double blind placebo
controlled trial of the effect of botulinum toxin on walking in cerebral
palsy. Arch Dis Child 83:481-487, 2000
53. Steenbeek D, Meester-Delver A, Becher JG, et al: The effect of botulinum toxin type A treatment of the lower extremity on the level of
functional abilities in children with cerebral palsy: Evaluation with goal
attainment scaling. Clin Rehabil 19:274-282, 2005
54. Redman TA, Finn JC, Bremner AP, et al: Effect of upper limb botulinum
toxin-A therapy on health-related quality of life in children with hemiplegic cerebral palsy. J Paediatr Child Health 44:409-414, 2008

Management of spasticity in children with CP

55. Barwood S, Baillieu C, Boyd R, et al: Analgesic effects of botulinum
toxin A: A randomized, placebo-controlled clinical trial. Dev Med Child
Neurol 42:116-121, 2000
56. Flett PJ, Stern LM, Waddy H, et al: Botulinum toxin A versus fixed cast
stretching for dynamic calf tightness in cerebral palsy. J Paediatr Child
Health 35:71-77, 1999
57. Ackman JD, Russman BS, Thomas SS, et al: Comparing botulinum
toxin A with casting for treatment of dynamic equinus in children with
cerebral palsy. Dev Med Child Neurol 47:620-627, 2005
58. Kay RM, Rethlefsen SA, Fern-Buneo A, et al: Botulinum toxin as an
adjunct to serial casting treatment in children with cerebral palsy.
J Bone Joint Surg Am 86-A:2377-2384, 2004
59. Glanzman AM, Kim H, Swaminathan K, et al: Efficacy of botulinum
toxin A, serial casting, and combined treatment for spastic equinus: A
retrospective analysis. Dev Med Child Neurol 46:807-811, 2004
60. Desloovere K, Molenaers G, Jonkers I, et al: A randomized study of
combined botulinum toxin type A and casting in the ambulant child
with cerebral palsy using objective outcome measures. Eur J Neurol
8:75-87, 2001 (Suppl 5)
61. Bottos M, Benedetti MG, Salucci P, et al: Botulinum toxin with and
without casting in ambulant children with spastic diplegia: A clinical
and functional assessment. Dev Med Child Neurol 45:758-762, 2003
62. Booth MY, Yates CC, Edgar TS, et al: Serial casting vs combined intervention with botulinum toxin A and serial casting in the treatment of
spastic equinus in children. Pediatr Phys Ther 15:216-220, 2003
63. Newman CJ, Kennedy A, Walsh M, et al: A pilot study of delayed versus
immediate serial casting after botulinum toxin injection for partially
reducible spastic equinus. J Pediatr Orthop 27:882-885, 2007
64. Bjornson K, Hays R, Graubert C, et al: Botulinum toxin for spasticity in
children with cerebral palsy: A comprehensive evaluation. Pediatrics
120:49-58, 2007
65. Moore AP, de-Hall RA, Smith CT, et al: Two-year placebo-controlled
trial of botulinum toxin A for leg spasticity in cerebral palsy. Neurology
71:122-128, 2008
66. Brashear: A, Mayer NH: Dosing and administration of botulinum toxin
for muscle overactivity in adults with an upper motor neuron syndrome, in Brashear A, Mayer NH (eds): Spasticity and Other Forms of
Muscle Overactivity in the Upper Motor Neuron Syndrome: Etiology,
Evaluation, Management, and the Role of Botulinum toxin: New York,
WE MOVE, 2008, pp 207-218
67. Boyd RN: GJNGeal Medium-term response characterisation and risk
factor analysis of botulinum toxin type A in the management of spasticity in children with cerebral palsy. Eur J Neurol 6:S37-S45, 1999
68. Delgado MR: The use of botulinum toxin type A in children with
cerebral palsy: A retrospective study. Eur J Neurol 6:S11-S18, 1999
(suppl 4)
69. Jankovic J, Vuong KD, Ahsan J: Comparison of efficacy and immunogenicity of original versus current botulinum toxin in cervical dystonia.
Neurology 60:1186-1188, 2003

89
70. Dressler D, Bigalke H, Benecke R: Botulinum toxin type B in antibodyinduced botulinum toxin type A therapy failure. J Neurol 250:967-969,
2003
71. Smyth MD, Peacock WJ: The surgical treatment of spasticity. Muscle
Nerve 23:153-163, 2000
72. Hays RM, McLaughlin JF, Bjornson KF, et al: Electrophysiological
monitoring during selective dorsal rhizotomy, and spasticity and
GMFM performance. Dev Med Child Neurol 40:233-238, 1998
73. Engsberg JR, Ross SA, Park TS: Changes in ankle spasticity and strength
following selective dorsal rhizotomy and physical therapy for spastic
cerebral palsy. J Neurosurg 91:727-732, 1999
74. Engsberg JR, Ross SA, Wagner JM, et al: Changes in hip spasticity and
strength following selective dorsal rhizotomy and physical therapy for
spastic cerebral palsy. Dev Med Child Neurol 44:220-226, 2002
75. Buckon CE, Thomas SS, Piatt JH Jr, et al: Selective dorsal rhizotomy
versus orthopedic surgery: A multidimensional assessment of outcome
efficacy. Arch Phys Med Rehabil 85:457-465, 2004
76. McLaughlin JF, Bjornson KF, Astley SJ, et al: Selective dorsal rhizotomy: Efficacy and safety in an investigator-masked randomized clinical
trial. Dev Med Child Neurol 40:220-232, 1998
77. Wright FV, Sheil EM, Drake JM, et al: Evaluation of selective dorsal
rhizotomy for the reduction of spasticity in cerebral palsy: a randomized controlled tria. Dev Med Child Neurol 40:239-247, 1998
78. Buckon CE, Thomas SS, Harris GE, et al: Objective measurement of
muscle strength in children with spastic diplegia after selective dorsal
rhizotomy. Arch Phys Med Rehabil 83:454-460, 2002
79. Steinbok P, Schrag C: Complications after selective posterior rhizotomy
for spasticity in children with cerebral palsy. Pediatr Neurosurg 28:
300-313, 1998
80. Chicoine MR, Park TS, Kaufman BA: Selective dorsal rhizotomy and
rates of orthopedic surgery in children with spastic cerebral palsy.
J Neurosurg 86:34-39, 1997
81. Albright AL, Cervi A, Singletary J: Intrathecal baclofen for spasticity in
cerebral palsy. JAMA 265:1418-1422, 1991
82. Gilmartin R, Bruce D, Storrs BB, et al: Intrathecal baclofen for management of spastic cerebral palsy: Multicenter trial. J Child Neurol 15:7177, 2000
83. Van SP, Nuttin B, Lagae L, et al: Intrathecal baclofen for intractable
cerebral spasticity: A prospective placebo-controlled, double-blind
study. Neurosurgery 46:603-609, 2000
84. Awaad Y, Tayem H, Munoz S, et al: Functional assessment following
intrathecal baclofen therapy in children with spastic cerebral palsy.
J Child Neurol 18:26-34, 2003
85. de Lissovoy G, Matza LS, Green H, et al: Cost-effectiveness of intrathecal baclofen therapy for the treatment of severe spasticity associated
with cerebral palsy. J Child Neurol 22:49-59, 2007
86. Coffey RJ, Edgar TS, Francisco GE, et al: Abrupt withdrawal from
intrathecal baclofen: Recognition and management of a potentially lifethreatening syndrome. Arch Phys Med Rehabil 83:735-741, 2002
87. Cornell MS: The hip in cerebral palsy. Dev Med Child Neurol 37:3-18,
1995