P e d i a t r i c Ton e

Management
a b c,
Sathya Vadivelu, MD , Anne Stratton, MD , Wendy Pierce, MD *

KEYWORDS
 Hypertonia  Spasticity  Dystonia  Baclofen  Rhizotomy  Neurotomy
 Cerebral palsy  Pediatric

KEY POINTS
 The type of hypertonicity needs to be identified to determine optimal treatment.
 Pediatric tone management involves all individuals caring for that child, including the pa-
tient, family, therapists, and the medical team.
 There are multiple nonsurgical and surgical treatments for hypertonicity.

INTRODUCTION

Tone management is one of the primary roles of a pediatric physiatrist and is a

rewarding but frequently challenging task. Hypertonicity frequently inhibits normal
movement patterns in children with central nervous system (CNS) lesions. At times,
hypertonicity can reinforce muscle group firing and be useful for a child’s function,
such as stabilizing the lower limbs during stand pivot transfers. Hypertonicity can
manifest as spasticity, dystonia, or rigidity, and frequently a combination is present.
The manifestations of hypertonicity, underlying etiologies, and guiding treatment prin-
ciples are reviewed.
Spasticity is probably the most common and easily recognizable form of hyper-
tonicity. Spasticity is defined as increased muscle tone where resistance to externally
imposed movement increases with increased speed of stretch and varies with the di-
rection of joint movement.1 A child may experience difficulty with smooth movements
because of spasticity. The muscle stretch reflex may be inadvertently triggered

Disclosures: None.
a
Division of Pediatric Rehabilitation Medicine, Department of Pediatrics, Rady Children’s Hos-
pital San Diego, University of California San Diego, 3020 Children’s Way MC5096, San Diego, CA
92123, USA; b Department of Physical Medicine and Rehabilitation, University of Colorado,
Denver, CO, USA; c Department of Physical Medicine and Rehabilitation, University of Colo-
rado, 4125 Briargate Parkway, Box 520, Colorado Springs, CO 80920, USA
* Corresponding author.
E-mail address: [email protected]

Phys Med Rehabil Clin N Am 26 (2015) 69–78

http://dx.doi.org/10.1016/j.pmr.2014.09.008 pmr.theclinics.com
1047-9651/15/$ – see front matter Ó 2015 Elsevier Inc. All rights reserved.
70 Vadivelu et al

during activity, and the muscle “catch” may result in loss of postural stability. A
commonly used scale to grade spasticity is the Modified Ashworth Scale using a
range from 0 to 4, indicating no increased tone (0) to complete resistance to move-
ment or rigidity (4).2
Dystonia is a more complicated form of tone. It is characterized as increased muscle
tone due to abnormal involuntary co-contractions in muscle groups causing repeated
abnormal posturing of the neck, torso, or limbs.1 Dystonia is typically characterized as
primary dystonia or secondary dystonia, which is typically due to an underlying
cortical lesion in the thalamus or basal ganglia.3 Functionally, dystonia or dystonic
movements increase when a child attempts to perform a novel or difficult task. Usually
when the child is relaxed, there is no increased tone and all limbs may be freely mobi-
lized. When the dystonia is active, the affected body areas or limbs twist into varied
postures even when the child is performing a task with the unaffected limbs. Severe
dystonia with co-contractions can present at rest with joint rigidity. Dystonia is
commonly measured using the Fahn-Marsden (or Burke-Fahn-Marsden) rating scale
or the Barry-Albright Dystonia Scale. The Fahn-Marsden scale ranges from 0 to 4,
from no dystonia, dystonia with a particular action, dystonia on many actions, to dys-
tonia at rest. Each limb and the trunk, head, and neck are evaluated.4 The Barry-
Albright Dystonia scale also ranges from 0 to 4, but looks at the frequency of dystonia
over 8 body regions.5
A mixture of spasticity and dystonia is frequently present in children with more severe
CNS lesions and is important to consider when treating tone disorders. Spasticity, dys-
tonia, or a combination can lead to limb rigidity, which complicates treatment options.
Many pediatric conditions lead to hypertonicity, including cerebral palsy (CP), ac-
quired brain injury, metabolic disorders, leukodystrophies, hydrocephalus, or spinal
cord injury. CP is the most common condition associated with hypertonicity.
CP “describes a group of permanent disorders of the development of movement
and posture, causing activity limitation, that are attributed to nonprogressive distur-
bances that occurred in the developing fetal or infant brain. The motor disorders of
CP are often accompanied by disturbances of sensation, perception, cognition,
communication and behavior, by epilepsy, and by secondary musculoskeletal prob-
lems.”6 Tone and disorders of movement vary greatly among the CP population but
most have some difficulties with limb hypertonicity.7,8 Cerebral vascular accidents,
hypoxic ischemic events, hemorrhagic events related to extreme prematurity, trau-
matic brain injury, neonatal toxoplasmosis, other (syphilis, varicella-zoster, parvovirus
B19), rubella, cytomegalovirus (CMV), and herpes infections (TORCH) infection, or iso-
lated metabolic derangement injuries can lead to CP, highlighting the heterogeneity of
this diagnosis. Neuronal migration abnormalities, such as schizencephaly, porence-
phaly, and polymicrogyria, may qualify under the CP diagnosis umbrella if no other ge-
netic syndromes are associated.
When evaluating a child with newly noted hypertonicity, brain and spinal cord imag-
ing should be considered to evaluate reversible etiologies. The American Academy of
Neurology published a practice parameter guideline for “Diagnostic assessment of the
child with cerebral palsy.” This guideline summary provides levels of evidence asso-
ciated with workup measures for a child with suspected CP.9
There are many causes of hypertonicity and a multitude of treatments to manage
spasticity and dystonia. Treatment approaches should be individualized based on
functional goals of the child and family, level of impairment, and/or ability to care for
the child. The type, locality, and severity of hypertonicity need to be considered. Treat-
ment plans should be created in collaboration with all individuals caring for the child,
including the patient, family, therapists, and medical team.
 Pediatric Tone Management 71

NONSURGICAL MANAGEMENT OF HYPERTONICITY

Nonsurgical management of spasticity and dystonia ranges from physical manage-

ment to systemic medications and focal injections.

Physical Management of Hypertonicity

Physical management of focal and generalized hypertonicity continues to evolve over
time and includes physical therapy, occupational therapy, orthoses, casting, modal-
ities, and assistive technology. Early-intervention studies found that initiating services
before 6 months of age was most effective.10 The most effective therapy approach for
managing tone and impacting function is still unclear.
Passive stretch is a focal approach to tone management that increases range of
motion and reduces spasticity.11 Spasticity is responsive to sustained stretch over
several hours.12 Orthoses and casts are often used to reduce tone by reducing tonic
stretch reflexes by prolonged static stretch.13,14 Caution should be used with certain
orthoses, such as spring-assisted dorsiflexion, as they may exacerbate rapid stretch,
triggering increased spasticity. Serial casting changes the number of sarcomeres and
cross-bridge attachments in muscle. Serial casting also provides constant sensory
input, which modulates the response of the muscle spindle and potentially decreasing
spasticity.10
Physical and occupational therapy techniques are based on different theories of
motor learning to decrease generalized spasticity.10,15 In 2012, Franki and col-
leagues15 performed a systematic review of therapy techniques for tone management.
They found neurodevelopmental treatment (NDT), functional and task-oriented
training, and therapeutic horse riding or hippotherapy had Level IV evidence, hinting
at the causality of reduction in spasticity. Dimitrijevic and colleagues16 found a statis-
tically significant reduction in spasticity in children with CP who participated in a twice-
weekly aquatic therapy program for 12 weeks. Constraint-induced movement therapy
(CIMT) may show functional benefits, but does not statistically change upper limb
spasticity.17
Modalities and manual therapies also have been used in attempts to reduce focal
hypertonia. Therapeutic heat and ultrasound reduce tone by facilitating uptake of neu-
rotransmitters and return of calcium to the sarcoplasmic reticulum. Therapeutic cold
presumably reduces clonus by acting at the cutaneous mechanoreceptor level, which
impacts interneuron excitatory presynaptic potentials at the spinal cord level.13 Cryo-
therapy reduces compound motor-action potentials, which reduces spasticity, but
also decreases motor performance.10 Vibration, acupuncture, and craniosacral ther-
apy have been used, but there are few data reflecting their efficacy on reduction of
hypertonicity.10 Electrical stimulation produces a statistically significant reduction in
spasticity immediately after stimulation.18 The effect of electrical stimulation on spas-
ticity is thought to be due to secondary relaxation as a result of the habituation of the
muscle spindle to the sensory stimulus.10

Enteral Medications for Management of Spasticity

Benzodiazepines, such as diazepam, facilitate CNS inhibition via potentiation of
gamma-aminobutyric acid (GABA) at the spinal and supraspinal levels, leading to a
reduction in spasticity, hyperreflexia, and muscle spasms.19 Benzodiazepines also
have been reported to help with sleep, decrease anxiety, and aid in management of
seizures.10 Side effects include sedation, difficulty with consolidation and formation
of new memory, urinary retention, liver toxicity, and dependency.10,19 Abrupt cessa-
tion of benzodiazepines may lead to agitation, tremor, muscle fasciculation, nausea,
72 Vadivelu et al

hyperpyrexia, and seizures. It is recommended to start with nightly dosing because of

their sedating effects and titrate up to dosing twice a day to 3 times a day.19
Baclofen binds to GABAB receptors and inhibits release of excitatory neurotrans-
mitters and substance P, resulting in decreased spasms, clonus, and spasticity.19
Side effects include sedation, potential exacerbation of underlying seizure disorder,
hypotonia, fatigue, nausea, and vertigo. Withdrawal from baclofen may lead to
rebound spasticity, hypertension, hallucinations, seizures, and hyperpyrexia.10,19
Although baclofen has been found to be less sedating than diazepam, it is still recom-
mended to begin with nightly dosing and titrate up to dosing twice a day to 3 times a
day.19
Dantrolene inhibits calcium release from the sarcoplasmic reticulum during muscle
contraction. The effects are reduction in clonus and muscle spasms caused by inno-
cuous stimuli.19 Dantrolene can be effective in athetoid CP.10 Side effects include mild
sedation, although much less than diazepam and baclofen, malaise, nausea, vomiting,
dizziness, diarrhea, and paresthesias. Hepatotoxicity can occur, so transaminase
monitoring must be performed and is not dose dependent.
Tizanidine is an alpha-2 adrenergic agonist that acts at the spinal and supraspinal
levels, leading to hyperpolarization of motor neurons to reduce spasticity. Side effects
include sedation, hypotension, dry mouth, dizziness, and hepatotoxicity, so transam-
inase monitoring is recommended.
Tiagabine was originally used as an anticonvulsant, but it has been shown to be
beneficial in reducing painful nocturnal spasms. It should be used with caution in those
with hepatic insufficiency. Its side effects include dizziness, weakness, nausea,
tremor, nervousness, confusion, difficulty with concentration, and abdominal pain. It
is not recommended for children younger than 12 years.

Enteral Medications for Management of Dystonia

Much like spasticity, dystonia may be focal or generalized. Although treatment ap-
proaches for focal dystonia may include medications or focal injections, generalized
dystonias in childhood should begin with a trial of dopaminergic agents. A dopa-
responsive dystonia can be caused by a mutation of the GTP cyclohydrolase I gene
on chromosome 14q, leading to an abnormality in dopamine synthesis. Symptoms
include diurnal variation in dystonia and symptoms of parkinsonism. Dopa-
responsive dystonia typically responds well to carbidopa/levodopa.20 Its side effects
include dyskinesias, bradykinesia, hypotension, hallucinations, confusion, and
memory impairment.19
Trihexyphenidyl can be effective in the management of dystonia. Its side effects
include dry mouth, blurred vision, urinary retention, anhidrosis, tardive dyskinesia,
glaucoma, nausea, dizziness, anxiety, and neuroleptic malignant syndrome.19
Baclofen also is used to treat dystonia, especially when carbidopa/levodopa and
trihexyphenidyl fail to produce an adequate response. Higher doses are generally
required to manage dystonia compared with spasticity.20
Clonazepam, in combination with anticholinergic medications, has been helpful in
treatment of myoclonus-dystonia.20
Tetrabenazine and zolpidem have been trialed in treatment of dystonia. Tetrabe-
nazine is an antidopaminergic drug that has been particularly helpful with tardive
dystonia, but has many side effects, including transient acute dystonic reactions,
insomnia, depression, and akathisia. Zolpidem, which has a high affinity for BZ1 re-
ceptors in the basal ganglia, has been effective in helping with some forms of
dystonia.20
 Pediatric Tone Management 73

Treatment for Focal Hypertonicity

In addition to physical modalities to help manage focal hypertonicity, certain medica-
tions may be injected, producing a neuromuscular blockage or chemodenervation
within specific muscles to reduce focal spasticity or dystonia.
Chemodenervation through axonal degeneration may be accomplished using 3% to
5% phenol or 35% to 65% ethyl alcohol. These medications require localization using
nerve stimulation or ultrasound for accurate perineural localization. The use of electric
stimulation, the amount of time required for localization, and caustic effects of the
medication cause pain and discomfort, especially in children, so sedation is often
used. Care should be taken to avoid sensory and mixed sensorimotor nerves, because
destruction of sensory fibers results in painful dysesthesias and numbness. Chemode-
nervation using phenol or ethyl alcohol is a cost-effective means of managing spas-
ticity for 3 to 12 months with immediate effects.19
Targeted injections of 5 to 10 mL of lidocaine 0.5% may provide temporary relief in
focal dystonias, writer’s cramp, and oromandibular dystonias. The effects may last up
to 24 hours, but can be lengthened to potentially several weeks with the addition of
ethanol to the injection.20
Neuromuscular blockade using botulinum toxin (BoNT) has been effective in man-
aging focal spasticity, cervical dystonia, blepharospasms, oromandibular dystonia,
and task-specific dystonias. The commercially available forms include onabotulinum-
toxinA, abobotulinumtoxinA, incobotulinumtoxinA, and rimabotulinumtoxinB. All
active forms of botulinum toxin are made of a heavy chain that binds to the presynaptic
membrane. A zinc-dependent protease light chain cleaves the SNAP-25 protein in
BoNT-A or the synaptobrevin-2 protein in BoNT-B, preventing acetylcholine vesicles
from docking and releasing.20 Dosing regimens for the commercially available ver-
sions of botulinum toxin are not equivalent. The effects of botulinum toxin may be
seen 5 to 7 days after injection and may last 3 to 6 months. Potential side effects
include transient weakness, flulike symptoms, dysphagia, respiratory difficulties, tran-
sient ptosis, blurred vision, and hypophonia, depending on the sites injected.19,20 It
has been found to have better efficacy when used in combination with other therapies.

Treatment Combinations
In a systematic review by Sakzewski and colleagues21 of intramuscular botulinum toxin
A injections with CIMT, bimanual intensive training, or NDT; no treatment was superior.
BoNT-A combined with other treatment approaches provided supplementary benefit.
This was further demonstrated by Hoare and colleagues22 in 2010, who found im-
provements in range of motion with administration of BoNT-A injections in conjunction
with occupational therapy. In 2007, Ronan and Gold10 found that kinesio-taping in
combination with other tone-modifying agents can influence hypertonicity.

SURGICAL MANAGEMENT OF HYPERTONIA

Surgical management of the hypertonia, as with other forms of management, has to be

goal-based, as mentioned. The goals need to be clearly defined before determining
whether surgery is a viable option. Clearly identifying the type of movement disorder,
spasticity, dystonia, or athetosis, will play a role in surgical outcome. Both orthopedic
and neurosurgical procedures can be therapeutic.

Orthopedic Procedures
Orthopedic surgeries primarily correct the musculoskeletal sequelae of spasticity,
specifically joint contracture, subluxation, dislocation, or rotational abnormalities.
74 Vadivelu et al

Orthopedic procedures improve passive range of motion. The improvement of active

range of motion will depend on the patient’s underlying strength and level of control of
the underlying movement. Current evidence suggests that single-event multilevel sur-
gery provides better quality-of-life outcomes.23
After any tenotomy, there is observed short-term tone reduction. There is fibrosis
and decreased responsiveness of the Golgi tendon organs in rat models.24 Tenotomy
provides an interim solution and additional methods for tone management need to
continue.

Neurosurgical Procedures
Cerebellar stimulation had shown some reduction in tone in approximately 80% of
patients. The theory was that stimulation of these tracts would result in inhibition of
activity. Spinal cord stimulation showed limited success with some dystonias but
with minimal clinical effect.
Percutaneous radiofrequency rhizotomy was attempted in the lumbar spine in the
spinal cord injury population. This provided only temporary results that lasted for
months.
Myelotomy involved making an incision in the gray matter of the spinal cord. This
disconnects the anterior horn cell from the posterior horn, thus interrupting the reflex
arc. This was very effective in patients with spinal cord injury, but patients were reluc-
tant to consent to further damaging the spinal cord. This is not an option in CP or any
acquired brain due to the potential neurogenic bowel and bladder consequences.
Selective peripheral neurotomy was first introduced in the 1980s. Using this
approach, the targeted nerve is dissected; electrical stimulation is then used to identify
the sensory and motor nerve fascicles that result in an increased spastic response.
The technique today is being performed in the sciatic, median, ulnar, musculocutane-
ous, and posterior tibial nerves. Patients who are ideal candidates for this procedure
have primary spasticity versus dystonia.
Berard and colleagues25 published neurotomy outcomes in 13 exclusively pediatric
patients with hemiplegia. Unfortunately, 61% of patients (8/13) had recurrence of
spasticity, with 4 of 13 requiring orthopedic intervention. Of the patients who required
orthopedic intervention, biopsy was performed showing evidence of reinnervation.
Kwak and colleagues26 looked at adults with finger spasticity and followed patients
for up to 42 months postoperatively. They found continued effects from surgery at
follow-up. Only 1 of 22 patients had dysesthesias. Buffenoir and colleagues27 followed
15 patients who underwent tibial neurotomy for 15 months. Ninety percent of patients
had clinical reduction of spasticity. Seventy-eight percent of patients had a reduction
in H responses. Eighty percent had reduction of T responses. One in 15 patients had
transient heel pain that was not clearly explained. Bollens and colleagues28 random-
ized 16 patients for botulinum toxin injections to the soleus, tibialis posterior, and flexor
hallucis longus or for selective tibial neurotomy. Findings at 6 months demonstrated a
higher reduction of viscoelastic stiffness with selective tibial neurotomy, with no signif-
icant differences in gait parameters that were measured. One patient developed hypo-
esthesia around the surgical scar but did not develop neuropathic pain.
Intrathecal baclofen is an approved method of treatment for spasticity as well as
dystonia. The pump is routinely implanted in the abdominal wall but the recommended
location may change depending on the level of central obesity and other factors. The
catheter is inserted into the spinal canal, typically in the lumbar spine. The tip of the
catheter is then advanced superiorly depending on the areas affected by spasticity.
Dosage is titrated to effect by a trained medical professional via programming of
the pump, and the pump reservoir is refilled depending on rate of use of the baclofen.
 Pediatric Tone Management 75

There is more pediatric than adult data available for intrathecal baclofen therapy.
Complication rates published between 2 institutions include mechanical complica-
tions of 15.0% to 19.3% and infection rate of 9.3%–21.8%.29,30 Mathur and col-
leagues31 described a cohort of patients between 10 and 28 years of age who
reported not only reduction in spasm frequency, but also reduction in pain associated
with hypertonia with an improvement in quality of life. Baker and colleagues32 reported
an overall improvement in comfort in pediatric patients 37 months after implantation.
Hoving and colleagues33 conducted a randomized controlled trial where the treatment
group was implanted 1 month after the trial and the control group was implanted
6 months after the trial. Overall, the treatment group not only had reduction of spas-
ticity, but improvement of pain and discomfort associated with spasticity.
Although spasticity is the primary indication for intrathecal baclofen therapy, it is
also an effective method of treating secondary dystonia. The first case report was in
1991 by Narayan and colleagues.34 Motta and colleagues35 reported improvement
in dystonia in 18 of 19 patients.36 They also reported improvement in quality of upper
limb movement in 10 of 11 patients with secondary dystonia due to CP.
Dorsal rhizotomy was first introduced as a treatment for spasticity in 1913. The
selective process to identify the sensory roots was introduced in the 1970s. The ideal
selective dorsal rhizotomy (SDR) candidate is 3 to 6 years old with near-normal cogni-
tive function and spastic diplegia. If the patient is ambulatory, he or she must have
sufficient underlying strength so as to remain ambulatory postoperatively. Patients
with primarily dystonia and athetosis are not good candidates for this procedure.
Complications include transient cerebral spinal fluid leakage, dysesthesias, transient
urinary retention, back pain, sensory changes, and neurogenic bowel and bladder.37
Long-term outcomes for SDR were recently published by Dudley and colleagues.38
Reduction in tone was maintained up to 15 years from the time of surgery. Nordmark
and colleagues39 followed patients for 5 years with gross motor functional classifica-
tion system (GMFCS) scores ranging from I to V. There were some improvements in
the gross motor function measure (GMFM)-66 in those with GMFCS III to V at
18 months to 5 years. Chan and colleagues40 looked at 20 children in Hong Kong
with GMFCS levels I to III. There was an average increase of 3.8 points in the
GMFM and overall improvement in the Pediatric Evaluation of Disability Inventory
following SDR.
Deep brain stimulation (DBS) is a surgical treatment specifically for dystonia. It stim-
ulates areas around the subthalamic nucleus that results in a cascade of events that
modulates the basal ganglia and thalamocortical network. It is a very effective treat-
ment for primary dystonia, Parkinson disease, and essential tremor. There are limited
results in treating secondary dystonia.41 Complications of surgery include intracere-
bral and intraventricular hemorrhage, ischemic infarction, hardware discomfort, loss
of effect, infection, lead malposition, and component fracture and malfunction.42
Fitzgerald and colleagues43 reported on a series of 60 children and adults with
generalized dystonia with no improvement in secondary dystonia. Olaya and col-
leagues44 published a case series of 9 children with secondary dystonia who under-
went DBS implantation in the globus pallidus, demonstrating a reduction in the
Barry-Albright Dystonia Scale and the Burke-Fahn-Marsden Dystonia Rating Scale.
Gimeno and colleagues45 looked specifically at 30 children with dystonia who un-
derwent DBS implantation. Although they reported no significant improvement in dys-
tonia scales, there was improvement in quality-of-life measures.
In conclusion, the patient population requiring tone management is quite diverse.
Patient and family goals, care-team goals, type(s) of tone being addressed, and risks
and benefits should all be carefully considered when making recommendations for
76 Vadivelu et al

management. There are many options available for tone management that frequently
work in combination.

REFERENCES

1. Sanger TD, Delgado MR, Gaebler-Spira D, et al. Classification and definition of

disorders causing hypertonia in childhood. Pediatrics 2003;111(1):e89–97.
2. Bohannon R, Smith M. Interrater reliability of a modified Ashworth scale of muscle
spasticity. Phys Ther 1987;67(2):206.
3. Berardelli A, Rothwell JC, Hallett M, et al. The pathophysiology of primary dystonia.
Brain 1998;121:1195–212.
4. Burke RE, Fahn S, Marsden CD, et al. Validity and reliability of a rating scale for
the primary torsion dystonias. Neurology 1985;35:73–7.
5. Albright MJ, VanSwearigen JM, Albright AL. Reliability and responsiveness of the
Barry-Albright dystonia scale. Dev Med Child Neurol 1999;6:404–11.
6. Rosenbaum P, Paneth N, Leviton A, et al. A report: the definition and classification
of cerebral palsy April 2006. Dev Med Child Neurol 2007;49:8–14.
7. Paneth N, Hong T, Korzeniewski S. The descriptive epidemiology of cerebral
palsy. Clin Perinatol 2006;33(2):251–67.
8. Surveillance of Cerebral Palsy in Europe (SCPE). Prevalence and characteristics
of children with cerebral palsy in Europe. Dev Med Child Neurol 2002;44:633–40.
9. Ashwal S, Russman BS, Blasco PA, et al, Practice Committee of the Child
Neurology Society. Practice parameter: diagnostic assessment of the child with
cerebral palsy: report of the Quality Standards Subcommittee of the American
Academy of Neurology and the Practice Committee of the Child Neurology Society.
Neurology 2004;62(6):851–63.
10. Ronan S, Gold JT. Nonoperative management of spasticity in children. Childs
Nerv Syst 2007;23:943–56.
11. Wusthoff CJ, Shellhaas RA, Licht DJ. Management of common neurologic symp-
toms in pediatric palliative care: seizures, agitation, and spasticity. Pediatr Clin
North Am 2007;54(5):709–33, xi.
12. Pin T, Dyke P, Chan M. The effectiveness of passive stretching in children with
cerebral palsy. Dev Med Child Neurol 2006;48(10):855–62.
13. Parziale JR, Akelman E, Herz DA. Spasticity: pathophysiology and management.
Orthopedics 1993;16(7):803–11.
14. Tardieu C, Lespargot A. For how long must the soleus muscle be stretched each
day to prevent contracture? Dev Med Child Neurol 1988;30(1):3–10.
15. Franki I, Desloovere K, De Cat J, et al. The evidence-base for conceptual
approaches and additional therapies targeting lower limb function in children
with cerebral palsy: a systematic review using the ICF as a framework.
J Rehabil Med 2012;44(5):396–405.
 L, Bjelakovic
16. Dimitrijevic  B, Lazovic
 M, et al. Aquatic exercise in the treatment of
children with cerebral palsy. Srp Arh Celok Lek 2012;140(11–12):746–50.
17. Anttila H, Autti-Rämö I, Suoranta J, et al. Effectiveness of physical therapy inter-
ventions for children with cerebral palsy: a systematic review. BMC Pediatr 2008;
8:14.
18. Suh HR, Han HC, Cho HY. Immediate therapeutic effect of interferential current
therapy on spasticity, balance, and gait function in chronic stroke patients: a ran-
domized control trial. Clin Rehabil 2014;28:885–91.
19. Deon LL, Gaebler-Spira D. Assessment and treatment of movement disorders in
children with cerebral palsy. Orthop Clin North Am 2010;41(4):507–17.
 Pediatric Tone Management 77

20. Jankovic J. Medical treatment of dystonia. Mov Disord 2013;28(7):1001–12.

21. Sakzewski L, Ziviani J, Boyd R. Systematic review and meta-analysis of thera-
peutic management of upper-limb dysfunction in children with congenital hemi-
plegia. Pediatrics 2009;123:e1111–22.
22. Hoare BJ, Wallen MA, Imms C, et al. Botulinum toxin A as an adjunct to treat-
ment in the management of the upper limb in children with spastic cerebral
palsy (UPDATE). Cochrane Database Syst Rev 2010;(1):CD003469.
23. Himpens E, Franki I, Geerts D, et al. Quality of life in youngsters with cerebral
palsy after single-event multilevel surgery. Eur J Paediatr Neurol 2013;17(4):
401–6.
24. Jamali AA, Afshar P, Abrams RA, et al. Skeletal muscle response to tenotomy.
Muscle Nerve 2000;23:851–62.
25. Berard C, Sindou M, Berard J, et al. Selective neurotomy of the tibial nerve in the
spastic hemiplegic child: an explanation of recurrence. J Pediatr Orthop B 1998;
7(1):66–70.
26. Kwak KW, Kim MS, Chang CH, et al. Surgical results of selective median neuro-
tomy for wrist and finger spasticity. J Korean Neurosurg Soc 2011;50:95–8.
27. Buffenoir K, Decq P, Hamel O, et al. Long-term neuromechanical results of selec-
tive tibial neurotomy in patients with spastic equinus foot. Acta Neurochir 2013;
155:1731–43.
28. Bollens B, Gustin T, Stoquart G, et al. A randomized control trial of selective
neurotomy versus botulinum toxin for spastic equinovarus foot after stroke. Neu-
rorehabil Neural Repair 2014;27(8):695–703.
29. Motta F, Antonello CE. Analysis of complications in 430 consecutive pediatric pa-
tients treated with intrathecal baclofen therapy: 14-year experience. J Neurosurg
Pediatr 2014;13(3):301–6.
30. Ghosh D, Mainali G, Khera J, et al. Complications of intrathecal baclofen pumps
in children: experience from a tertiary care center. Pediatr Neurosurg 2013;49:
138–44.
31. Mathur SN, Chu SK, McCormick Z, et al. Long-term intrathecal baclofen: out-
comes after more than 10 years of treatment. PM R 2014;6:506–13.e1.
32. Baker KW, Tann B, Mutlu A, et al. Improvements in children with cerebral palsy
following intrathecal baclofen: use of the Rehabilitation Institute of Chicago
care and comfort caregiver questionnaire (RIC CareQ). J Child Neurol 2013;
29(3):312–7.
33. Hoving MA, van Raak EP, Spincemaille GH, et al, Dutch Study Group on Child
Spasticity. Efficacy of intrathecal baclofen therapy in children with intractable
spastic cerebral palsy: a randomised controlled trial. Eur J Paediatr Neurol
2009;13(3):240–6.
34. Narayan RK, Loubser PG, Jankovic J, et al. Intrathecal baclofen for intractable
axial dystonia. Neurology 1991;41(7):1141–2.
35. Motta F, Antonello CE, Stignani C. Upper limb function after intrathecal baclofen
therapy in children with secondary dystonia. J Pediatr Orthop 2009;29:817–21.
36. Motta F, Stignani C, Antonello CE. Effect of intrathecal baclofen on dystonia in
children with cerebral palsy and the use of functional scales. J Pediatr Orthop
2008;28:213–7.
37. Steinbok P, Schraq C. Complications after selective posterior rhizotomy for spas-
ticity in children with cerebral palsy. Pediatr Neurosurg 1998;28(6):300–13.
38. Dudley RW, Parolin M, Gagnon B, et al. Long-term functional benefits of selective
dorsal rhizotomy for spastic cerebral palsy. J Neurosurg Pediatr 2013;12(2):
142–50.
78 Vadivelu et al

39. Nordmark E, Josenby AL, Lagergren J, et al. Long-term outcomes five years after
selective dorsal rhizotomy. BMC Pediatr 2008;14(8):54. http://dx.doi.org/10.1186/
1471-2431-8-54.
40. Chan SH, Yam KY, Yiu-Lau BP, et al. Selective dorsal rhizotomy in Hong Kong:
multidimensional outcome measures. Pediatr Neurol 2008;39:22–32.
41. Miocinovic S, Somayajula S, Chitnis S, et al. History, applications, and mecha-
nisms of deep brain stimulation. JAMA Neurol 2013;70(2):163–71.
42. Fenoy AJ, Simpson RK Jr. Risks of common complications in deep brain stimula-
tion surgery: management and avoidance. J Neurosurg 2014;120(1):132–9.
43. Fitzgerald JJ, Rosendal F, de Pennington N, et al. Long-term outcome of deep
brain stimulation in generalized dystonia: a series of 60 cases. J Neurol Neuro-
surg Psychiatry 2014. [Epub ahead of print].
44. Olaya JE, Christian E, Ferman D, et al. Deep brain stimulation in children and
young adults with secondary dystonia: the Children’s Hospital Los Angeles expe-
rience. Neurosurg Focus 2013;35(5):E7.
45. Gimeno H, Tustin K, Lumsden D, et al. Evaluation of functional goal outcomes
using the Canadian Occupational Performance Measure (COPM) following
deep brain stimulation (DBS) in childhood dystonia. Eur J Paediatr Neurol
2014;18:308–16.