Chapter
Cerebral Palsy
45 Advances in Definition, Classification, Management,
and Outcome
Christina A. Buysse and Heidi M. Feldman
Case: Ashley was born precipitously at 27 weeks’
gestation when her mother developed a urinary tract
infection. She required 3 weeks of mechanical ventila-
tion and 4 subsequent weeks of oxygen supplementa-
tion. Ultrasound examination of the brain at age 7
days revealed grade 2 intraventricular hemorrhage
bilaterally. Magnetic resonance imaging at term-
equivalent age revealed mildly enlarged ventricles
and reduced white matter volume. Physical examina-
tion at 4 months of age revealed diffuse hypotonia and
delayed head control with normal cognitive develop-
mental milestones. Examination at 9 months of age
revealed increased tone in the lower extremities and
delayed gross and fine motor milestones. Ashley was
enrolled in physical therapy (PT) and occupational
therapy (OT) at age 11 months. The diagnosis of
diplegic cerebral palsy was confirmed at age 2 years.
At that age, mild delays in cognitive abilities and
communication led to referral for early intervention
services and continued PT and OT. At age 44 months,
she achieved independent mobility. By school age, she
was classified as Gross Motor Function Classification
System Level II and Manual Ability Classification
System Level I. She developed learning disabilities
and weak attention but participated in general educa-
tion with limited support through high school.
Overview
Cerebral palsy (CP) is a group of long-term develop-
mental motor disorders associated with muscle and
movement impairment and mobility disability. It
results from a nonprogressive injury in the brain
that occurs early in life, often in the prenatal or neo-
natal period, though definitive diagnosis is often not
made until children are age 1–3 years. Multiple etiol-
ogies are associated with CP, including prematurity,
low birth weight, multiple-gestation pregnancy, infec-
tion, inflammation, neonatal encephalopathy, and
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genetic factors [1]. Motor abnormalities of CP are
often accompanied by co-occurring disturbances in
cognition, perception, and sensation. The disorders
that are classified as CP represent a wide spectrum of
severity; many individuals with CP, especially those
who have supportive therapies, such as the child in the
opening case, report a good quality of life.
Definitions
In 1843, orthopedic surgeon William John Little first
described spastic rigidity after birth complications,
and in 1889, Sir William Osler labeled the condition
cerebral palsy (CP) [2]. In 1964, Martin Bax described
CP as a disorder of “posture and movement due to a
defect or lesion of the immature brain”[3]. In 2004, an
international workshop on the definition and classifi-
cation of CP at the US National Institutes of Health
revised the definition and classification of CP as
follows:
Cerebral Palsy (CP) describes a group of permanent
disorders of the development of movement and pos-
ture, causing activity limitation, that are attributed to
non-progressive disturbances that occurred in the
developing fetal or infant brain. The motor disorders
of CP are often accompanied by disturbances of sen-
sation, perception, cognition, communication, and
behavior, by epilepsy, and by secondary musculoske-
letal problems [4].
This revised definition carried two new emphases,
aligning it with the International Classification of
Functioning, Disability, and Health (ICF), the World
Health Organization’s framework for assessing health
and disability [5,6]. First, functional and activity limita-
tions must be present for a child to receive a diagnosis of
CP. Second, the new definition recognized that asso-
ciated conditions such as disturbances in communica-
tion and cognition might limit function, daily activity,
and community participation to a greater degree than
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 Section 4 Specific Conditions Associated with Fetal and Neonatal Brain Injury

the motor impairment that defines the disorder.
Together these criteria caused a shift in the conceptual
framework in care of individuals with CP, emphasizing
comprehensive assessment and wide-ranging treatment
targets that could improve overall function rather than
merely assessing neurologic status and motor skills or
aiming in treatment for isolated changes in the move-
ment of physical structures. Though CP results from a
nonprogressive brain disturbance, functional manifes-
tations may change over time and with therapy. For
example, the child in the opening case had early hypo-
tonia that developed into spasticity during her first year
of life. Children with substantial early delays may learn
to walk without assistance or with handheld mobility
equipment. Conversely, spasticity may lead to increas-
ing distal myofascial muscle stiffness, contractures, and
orthopedic deformities that limit mobility [7,8].
Subclassifications Based on
Presentation, Cause, and Severity
CP can be classified several different ways. Table 45.1
summarizes subclassification based on clinical symp-
toms, including definitions and prevalence of the sub-
types [9]. The descriptive terms spasticity, dyskinesia,
and ataxia are defined on the basis of clinical signs
with further specification of the location of extremity
involvement (hemiplegia, diplegia, or quadriplegia).
Muscle tone (isotonic, hypotonic, hypertonic, or vari-
able tone) is used when describing a child’s physical
examination. Spastic CP is the most common subtype
within the spectrum of CP [10,11].
Classification of CP by subtype is helpful in link-
ing symptoms to underlying etiology. The various
causes of CP disrupt the development of neuronal
networks in brain pathways that control movement.
Selective vulnerability during critical periods of brain
development leads to different injuries in different
parts of the brain. Table 45.2 links the timing and
causes of brain insults with the characteristic type of
CP from that cause.
Encephalopathy at birth may be caused by a pri-
mary intrapartum event or be secondary to prenatal
causes. International criteria, including documented
metabolic acidosis at birth and early moderate to severe
neonatal encephalopathy, have been established to help
identify the cases of encephalopathy caused by intra-
partum hypoxia [12]. Intrapartum asphyxia accounts
for 10–20% of cases of CP, and the number is closer to
10% when CP and encephalopathy are carefully

Table 45.1 Subclassification of Cerebral Palsy by Type

Type Clinical findings Associated brain Prevalence in CP

abnormalities and causes (%) [9]
Spastic Increased velocity-dependent Associated with cortical gray 79.2
muscle tone that leads to matter and/or subcortical white
resistance to movement matter injury
Hemiplegia Spasticity affecting left or right Combined gray and white 26.2
side of the body matter injury to one
hemisphere
Diplegia Spasticity affecting lower limbs Injury to bilateral gray and 34.4
periventricular white matter
Quadriplegia Spasticity affecting all four limbs Diffuse injury to multiple brain 18.6
regions
Dyskinesia Distortion or impairment of Injury to basal ganglia 14.4
voluntary movement, including
chorea and athetosis
Ataxic Poor coordination and Injury to cerebellum 3.9
unsteadiness due to
unregulated body posture,
strength, gait, and direction of
limb movements.
Other Mixture of the above — 2.6

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 45 Cerebral Palsy: Advances in Definition, Classification, Management, and Outcome
Table 45.2 Variations in Timing and Nature of Brain Insult in Relation to Type of CP
Timing of insult
First trimester of pregnancy
23–32 weeks of gestation
23–40 weeks of gestation
Third trimester of pregnancy through
infancy
Term gestational age
Term gestational age
Postterm during infancy
defined. In order to attribute neurologic sequelae to
neuronal injury sustained at the time of birth, a sentinel
event such as uterine rupture, placental abruption, or
cord prolapse must also be present [13].
Genetic factors are increasingly thought to contri-
bute to the development of CP and likely are repre-
sented in all phases of neuronal vulnerability. No
subclassification of genetic disorders has been pro-
posed. Several single-gene disorders have been found
to cause CP: for example, mutations in the GPR56
gene cause severe bilateral frontoparietal polymicro-
gyria and CP. Copy-number variants are also asso-
ciated with polymicrogyria and CP. Recent studies
using whole-exome sequencing in cases of sporadic
CP indicate that 14% of participants had likely-causa-
tive single-gene mutations and 31% had clinically
relevant copy-number variants [12].
Another important subclassification is based on
severity. Among children with CP, functional abilities
range from mild hemiplegic gait differences and super-
ior cognitive abilities to nonambulatory quadriparesis
and intellectual disability. Approximately 60% of chil-
dren with CP eventually walk independently, 10% walk
with assistance, and 30% use a wheelchair for mobility
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Etiologic cause of injury to motor Predominant type of CP
pathways
Cerebral malformations, such as Spastic quadriplegia
schizencephaly
Injury to oligodendrocyte cell line Spastic diplegia
from hypoxia, ischemia, and/or
inflammation resulting in
disturbances of white matter
Injury to cerebellum from multiple Ataxic
causes
Vascular instability or hypoxic- Hemiplegia
ischemic injury to watershed regions
resulting in stroke or focal injury
Injury to basal ganglia and thalamus Dyskinesia or dystonia with or
from hypoxia, ischemia, or without spastic quadriplegia
inflammation
Injury to basal ganglia and auditory Dystonia
nerve from kernicterus
Head trauma and meningitis Variable presentations,
depending on brain structures
affected
[11]. The Gross Motor Function Classification System
(GMFCS) is a classification system that describes the
heterogeneity in gross motor skills. It was created in
1997 and revised in 2007 [14]. It uses five levels (I–V) to
describe the gross motor function of children with CP
from birth to age 18 years and has been shown to be
valid, reliable, and stable [15,16]. Use of the system
enables a clinician to establish a prognosis of an indi-
vidual’s later motor functioning because children
rarely cross between levels as they age but continue to
develop within their original GMFCS level. Table 45.3
shows the five levels of the GMFCS for children ages
2–4 years and the corresponding levels for children
ages 6-12 years.[17] A similar classification system, the
Manual Abilities Classification System (MACS), was
designed to measure a child’s ability to manipulate
objects in everyday life [18]. This system also consists
of levels I–V and has been found to be reliable, valid, and
stable (Table 45.4) [19]. The five-level Communication
Function Classification System (CFCS) has been devel-
oped recently to describe the level of communication
function for people with CP. Test-retest reliability has
been excellent, and validity and stability studies are
underway [20].
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 Section 4 Specific Conditions Associated with Fetal and Neonatal Brain Injury

Table 45.3 Gross Motor Functional Classification System: Partial Description of Children at Levels I–V at Ages 2–4 years and at 6–12 Years
[17]

Level Ages 2–4 years Ages 6–12 years

I Children floor sit with both hands free to
manipulate objects; walk as preferred method of
mobility without assistive mobility device.
II Children floor sit but may have difficulty with
balance if both hands manipulate objects, pull to
stand on a stable surface, crawl on hands and
knees with a reciprocal pattern, cruise holding onto
furniture, and walk using an assistive mobility
device.
III Children maintain floor sitting by “W-sitting”
(sitting between flexed and internally rotated hips
and knees), creep on stomach, or crawl on hands
and knees often without reciprocal leg
movements, may pull to stand, cruise or walk short
distances indoors using an assistive mobility device
and adult assistance for turning.
IV Children floor sit when placed, are unable to
maintain alignment and balance without use of
their hands, frequently require adaptive
equipment for sitting and standing, achieve
independent mobility by rolling, creeping on
stomach, or crawling on hands and knees without
reciprocal leg movement.
V Children are restricted in voluntary control of
movement, inability to maintain antigravity head
and trunk postures, functional limitations in sitting
and standing not fully compensated for through
adaptive equipment, no means of independent
mobility.
Children walk indoors and outdoors and climb
stairs without limitations; speed, balance, and
coordination in skills such as running and jumping
are reduced.
Children walk indoors and outdoors and climb
stairs holding onto a railing; limitations in walking
on uneven surfaces and inclines, walking in crowds
or confined spaces, and gross motor skills such as
running and jumping.
Children walk indoors or outdoors on a level
surface with an assistive mobility device, may climb
stairs holding onto a railing, may propel a
wheelchair manually or are transported when
travelling for long distances or outdoors on uneven
terrain.
Children need adaptive seating for trunk control
and to maximize hand function, move in and out of
chair with adult assistance or a stable surface to
push or pull up on with their arms, may walk short
distances with a walker and adult, rely on wheeled
mobility at home, school, and in the community,
may achieve self-mobility using a power
wheelchair.
Minimal developmental change from
characteristics at ages 2–4 years.

Table 45.4 Manual Ability Classification System for Children with CP 4–18 Years of Age: Partial Descriptions of Children at Levels 1–V [18]

Level Characteristic skills

I Handles objects easily and successfully. At most, limitations in the ease of performing manual tasks requiring
speed and accuracy.
II Handles most objects but with somewhat reduced quality and/or speed of achievement. Certain activities
may be avoided or be achieved with difficulty; alternative ways of performance may be used.
III Handles objects with difficulty; needs help to prepare and/or modify activities. Limited success regarding
quality and quantity of movement. Independent performance if activities have been set up or adapted.
IV Handles a limited selection of easily managed objects in adapted situations. Performs parts of activities with
effort and limited success. Requires continuous support and assistance and/or adaptive equipment to
achieve even partial completion.
V Does not handle objects and has severely limited ability to perform even simple actions. Requires total
assistance.

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 45 Cerebral Palsy: Advances in Definition, Classification, Management, and Outcome

Epidemiology and Public Health Issues Clinical Presentation and Establishing

CP has an overall prevalence of 2.1–3.6/1,000 people in the Diagnosis
developed countries [21,22]. Socioeconomic disadvan-
tage is associated with increased rates of CP. Black non- Core Findings
Hispanic children have increased prevalence of CP
CP is diagnosed clinically based on delays in motor
compared with white non-Hispanic children above
development and abnormalities on physical and
and beyond socioeconomic differences; this increased
neurologic examination. In infancy, primitive
risk disappears after adjustment for gestational age and
reflexes, such as the Moro reflex, are integrated into
weight at birth [23]. Males have a slightly higher pre-
voluntary movement patterns as the nervous system
valence than females with a ratio of 1.4:1 [22]. The
matures. Primitive reflexes persisting beyond the
prevalence of CP in developing nations has not been
usual age alert clinicians to an increased risk for
well studied. It is estimated that 80% of children with
CP. As primitive reflexes disappear, postural reac-
CP live in low-resource countries. Though the inci-
tions, such as head righting during tilting and pro-
dence may be higher in these nations, high mortality
tective arm extension to brace falling, develop.
may reduce differences in prevalence between low- and
Absence of these postural reactions raises suspicion
high-resource countries [24].
for CP. Upper motor neuron dysfunction is charac-
In developed countries, CP is highly associated with
terized by spasticity, hyperreflexia, and clonus. Over
prematurity and low birth weight. A meta-analysis
the first years of life, muscle hypotonia may progress
found the prevalence of CP to be 57/1,000 in children
to hypertonia in children with CP, as in the opening
weighing less than 1,000 g at birth, 59/1,000 in those
case. Asymmetries in tone, strength, reflexes, and
weighing 1,000–1,499 g, 10/1,000 in those weighing
coordination on neurologic examination also raise
1,500–2,499 g, and 1.3/1,000 in those weighing more
red flags for CP. CP is not diagnosed at birth because
than 2,500 g. Infants born before 28 weeks’ gestation
the classic diagnostic signs of motor delay and
had a prevalence of CP of 112/1,000, whereas children
impairment do not reveal themselves until the child
born after 36 weeks had a prevalence of 1.35/1,000 [21].
is older. Children with more severe CP are often
Despite the lower incidence, infants born at term
diagnosed in the first year of life, and children with
account for 50–65% of children with CP because 90%
less severe CP are frequently diagnosed in the second
of children are born at term [25].
year of life.
The prevalence of CP has remained relatively
Clinical practice guidelines issued by the
stable over the past 20 years despite many improve-
American Academy of Neurology and the Child
ments in medical care, especially in the developed
Neurology Society in 2004 recommended neuroima-
world [26]. Reduced prevalence would be expected
ging of a child with CP if the etiology has not been
based on several medical advances in treatment of
established. They further recommended magnetic
newborns: (1) widespread rubella vaccination that
resonance imaging (MRI) as preferable to computed
eliminated chronic rubella syndrome as a cause of
tomography (CT) scanning because of greater detail
CP in the United States [27], (2) systematic treatment
and no exposure to ionizing radiation [31]. More
of neonatal jaundice that has dramatically reduced the
than 80% of children with CP demonstrate abnorm-
incidence of kernicterus, (3) cooling for term infants
alities on MRI, though the rest may have a normal
with hypoxic-ischemic encephalopathy that reduces
MRI. Children with a normal MRI often have a
mortality and morbidity [28], and (4) the use of
milder form of CP; children with ataxic and dyski-
antenatal steroids and magnesium sulfate in women
netic CP compared with other subtypes are most
with preterm labor that has decreased the incidence of
likely to have a normal MRI [9]. MRI obtained at
CP and the severity of complications [29,30].
term equivalence has higher predictive sensitivity
Opposing forces, however, have maintained the pre-
than cranial ultrasound [32]. In children with CP,
valence rates: (1) improved survival rates of extremely
white matter injury is found in 19–45% of cases and
low-birth-weight infants, who are more likely to
gray matter injury in 20%. Focal vascular insults and
develop CP than term infants, and (2) increased use
malformations are each seen 10% of the time [33].
of artificial reproductive technologies and multiple-
Figures 45.1 and 45.2 show typical MRI scans of a
gestation pregnancies with associated complications
child with CP.
of low birth weight and preterm birth.

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 Section 4 Specific Conditions Associated with Fetal and Neonatal Brain Injury

(a) (b)

Figure 45.1 The classic appearance of periventricular leukomalacia in an infant with CP. Note the abnormal periventricular white matter
signal, volume loss, and irregular ventricular margins.

Associated Impairments children with CP, evaluation of intellectual function-

ing should use measures that do not require motor
Epilepsy and cognitive, behavioral, and sensory
skills and that avoid the use of timed tests.
impairments may be associated with the motor
Behavioral Disorders. Behavioral and emotional
impairments of CP because the underlying neuro-
disturbances are highly prevalent in children with CP,
pathology puts the child at risk for disorders beyond
ranging from 25% to 40% across studies using differ-
the motor system. The child in the opening case had
ent assessment measures and outcomes. Common
co-occurring cognitive and behavioral conditions.
behavioral problems include difficulties with peer
Rates of comorbidities in prevalence studies may be
interactions, attention problems, hyperactive beha-
somewhat elevated because children with very mild
vior, and emotional dysregulation. The incidence of
CP may be underrepresented.
behavioral problems is increased among the 15–25%
Cognitive and Intellectual Abilities. Studies
of children who also have epilepsy and among chil-
report that almost 50% of children with CP have
dren with severe motor impairment, hearing loss,
some degree of intellectual impairment [26,34,35],
intellectual impairment, and pain [37,38].
though they may not function in the range of intellec-
Approximately 8% of children with CP receive the
tual disability (scores on intelligence tests greater than
diagnosis of autism, frequently diagnosed later in life
2 standard deviations below the mean with compar-
than in children without CP [26].
able adaptive skills). Severity of cognitive impairment
Hearing and Vision. Between 50% and 75% of
often correlates with severity of motor impairment.
children with CP have visual impairment, including
Children with spastic quadriplegia have the highest
refractive errors, strabismus, nystagmus, altered
association with cognitive impairment [36]. The cor-
visual field, and optic atrophy, and 11% are severely
relation between motor and cognitive impairment is
visually impaired [35]. Cortical visual impairment
low in dyskinetic CP. Children with epilepsy and an
plays a large role in the loss of visual acuity and is
abnormal MRI are more likely to have intellectual
most commonly associated with quadriplegia [39,40].
impairment than those without these findings. To
Hearing loss is found in about 12% of children
avoid underestimation of the intellectual abilities of
with CP and is associated with very low birth weight,
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 45 Cerebral Palsy: Advances in Definition, Classification, Management, and Outcome
(a)
Figure 45.2 Sagittal scan of an infant with CP. Note the thin corpus callosum (arrow) and abnormal signal adjacent to the irregular ventricle.
kernicterus, neonatal meningitis, encephalopathy,
and intellectual disability. Approximately 3% of chil-
dren with CP have severe hearing loss [10,41].
Speech, Language, and Communication. Between
31% and 88% of children with CP have a communica-
tion disorder, and 25% of children are nonverbal
[10,20]. Language development in children with CP
correlates strongly with cognitive function. Speech
impairment, such as dysarthria, is independent of cog-
nition and strongly associated with the degree of motor
impairment. Articulation disorders and limitations in
speech intelligibility are seen in 40–88% of children
with CP [42].
Feeding and Growth. Feeding difficulties occur in
30–40% of children with CP and are most common in
children with severe motor impairment. Children
may require help with feeding to allow adequate
weight gain and to avoid choking and frequent vomit-
ing [43]. Approximately 6% of children with CP
require gavage feeding because they cannot safely or
effectively obtain all their nutrition by mouth [10,35].
Pain and Sleep Disorders. Children and adults
with CP experience pain that may decrease their qual-
ity of life and community participation. Pain has
many causes, including spasms, contractures, hip dis-
location, gastroesophageal reflux, skin breakdown
and medical procedures. About 66% of school-aged
children and 75% of teenagers with CP report having
experienced pain in the previous week [44,45].
Up to 50% of children with CP have sleep difficul-
ties, with 25% experiencing a moderate to severe sleep
disorder [46]. Sleep-disordered breathing and difficulty
initiating and maintaining sleep are the most common
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(b)
sleep disorders in this population. Sleep disorders are
often associated with pain, poorly controlled epilepsy,
and behavior disorders [47].
Quality of Life and Life Expectancy. Health-related
quality of life is a multidimensional measure that inte-
grates functional status with services needed, frequency
of treatment, and activity restrictions. Health-related
quality of life is lower in people with CP than in the
general population. Adults with CP report employment
disadvantages, fatigue, pain, and depressive symptoms
[1]. Children with CP have an increased rate of beha-
vioral and psychological difficulties compared with typi-
cally developing peers. Nonetheless, when describing
quality of life, defined as perception of their position in
life relative to their goals and expectations, children with
CP reported quality of life similar to their typical peers,
as the child in the opening case may have [48].
Adolescents with CP relate subjective well-being that is
similar to that of their typical peers in all domains but
social interaction with peers [1,48,49].
Approximately 5–10% of children with CP die dur-
ing childhood, and life expectancy is otherwise near
normal. Most often the children with early mortality
had multiple areas of severe impairment, including
epilepsy and intellectual disability [11]. As children
with CP transition into adulthood, difficulties often
arise in their ability to access healthcare and therapeu-
tic services. Recent advocacy efforts have focused on
ensuring that lifelong care provides rehabilitation that
facilitates societal participation for adults as well as
children with CP. Surveys of young adults with normal
cognition and CP indicate that up to 33% have diffi-
culty performing daily self-care activities and 66% have
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 Section 4 Specific Conditions Associated with Fetal and Neonatal Brain Injury
unmet mobility needs [50]. About 50% of individuals
with CP between the ages of 20 and 24 years are
employed, but 33% of these individuals experience
physical or situational barriers at work [51].
Approximately 75% of young adults with CP and nor-
mal cognition report having experienced dating; 25%
are in a current romantic relationship, and the preva-
lence is unrelated to motor function, education, or
gender [52].
Prevention
Current Approaches to Neuroprotection
A baby born at a gestational age below 28 weeks has
30–80 times the risk of CP as an infant born at term
[53]. Because of this markedly increased risk of neu-
rologic impairment in preterm infants, obstetricians
and neonatologists continue to look for neuroprotec-
tive agents and strategies for high-risk pregnancies
and neonates.
Many studies, including randomized trials, have
found that CP rates are decreased in children prenatally
exposed to magnesium sulfate [29,54]. The American
College of Obstetricians and Gynecologists recom-
mends the short-term use of magnesium sulfate for
fetal neuroprotection for women in preterm labor
under 32 weeks’ gestation [55].
Antenatal corticosteroids also confer neuropro-
tection. Improved neonatal lung maturity leads to
reduced rates of hypoxia and related problems.
Besides improving lung maturity, antenatal steroids
exert potent cerebral vasoconstrictive effects, mini-
mizing fluctuations in cerebral blood flow. Infants
born to women who received antenatal corticoster-
oids during preterm labor have a significantly
decreased rate of CP [30].
Hypothermic cooling in term infants with neona-
tal encephalopathy has become a standard of care. A
meta-analysis examining effectiveness demonstrated
that hypothermia was associated with a reduction in
the composite outcome of mortality or neurodevelop-
mental disability at 18–24 months of age. Seven at-
risk infants must be treated with a hypothermia pro-
tocol to prevent one death or major disability [28].
Emerging Strategies for Neuroprotection
Human erythropoietin (Epo) is the primary regulator
of erythropoiesis and is potentially neuroprotective.
In vitro and in vivo experiments have demonstrated
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anti-inflammatory, antiexcitotoxic, antioxidant, and
antiapopoptic effects of Epo on neurons and oligo-
dendroglia. Recombinant human erythropoietin
(rhEpo) promotes neurogenesis and angiogenesis.
Retrospective reviews of infants treated with rhEpo
for anemia of prematurity revealed improvements in
neurodevelopmental outcomes over infants not
receiving the medication. RhEpo is affordable, easy
to administer, and has been found to be safe in phase
II clinical trials [56]. It may potentiate other therapies,
such as hypothermic cooling.
Inhaled nitric oxide (iNO) is a potent vasodilator
used for the treatment of hypoxic respiratory failure
and pulmonary hypertension. Early investigations
suggest that iNO may decrease rates of severe intra-
ventricular hemorrhage and periventricular leukoma-
lacia and may ultimately reduce long-term disability
rates [57].
Caffeine is a nonselective adenosine receptor
antagonist used widely in the treatment of apnea in
preterm infants. Despite promising early data, an
ongoing randomized, controlled trial (RCT) of chil-
dren receiving placebo or caffeine during the neonatal
period demonstrated inconclusive benefit to neurode-
velopmental outcomes at age 5 years. Data collection
is ongoing [58].
Management of CP
Principles of Management
Care of children with CP requires a team of profes-
sionals working closely with individuals and their
families. Current best practice finds that the primary
care clinician in the medical home is an important
anchor. The team may include members of many
different professional fields: developmental pedia-
trics, neurology, orthopedic surgery, neurosurgery,
physiatry, psychiatry, behavioral management, physi-
cal therapy, occupational therapy, speech and lan-
guage pathology, orthotics, ophthalmology, and
audiology. The spectrum of involvement for indivi-
dual children determines their treatment needs and,
therefore, their treatment team.
Treatment approaches are designed to capitalize
on neuroplasticity. It is generally agreed that neuro-
plasticity is greatest in early childhood and gradually
reduces as children age. Therefore, early intervention
is recommended for children at risk for CP.
A tiered approach typically begins with rehabilita-
tion services (PT, OT, treatment of sensory disorders,
 45 Cerebral Palsy: Advances in Definition, Classification, Management, and Outcome
communication therapy), educational interventions,
and environmental adaptations. Adaptive equipment,
including braces, walkers, and wheelchairs, may
increase functional capacities. As needed, care pro-
gresses to medical treatments and surgical interven-
tions. Outcome goals include improving functional
skills and also preventing complications such as hip
dislocation, deformities, and progressive rigidity.
Overall goals should be broken down into measurable
target objectives in order to inform treatment strategies
and measure and evaluate outcomes. In line with the
International Classification of Function framework,
goals and objectives should emphasize increasing activ-
ity and community participation as well as addressing
motor impairment. The goal is to educate and treat all
children in the least restrictive environment while
addressing their medical, rehabilitative, educational,
social, and personal needs. Scientific evidence suggests
that inclusive education rather than segregated educa-
tion is associated with better outcomes, particularly in
language, social, and emotional domains.
Rehabilitation
The mainstays of rehabilitative therapy of children with
CP are PT and OT. A recent analysis of the literature
suggests that child-active approaches, where the child
practices real-life functional tasks for the purpose of
gaining or consolidating skills, are more effective than
passive approaches, such as stretching by a therapist
[59]. Goal-directed child-active approaches and skills
practice at high rates of repetition are thought to capi-
talize on neuroplasticity. Home programs are an impor-
tant component of effective rehabilitation to increase
opportunities to practice skills. Goals should be achiev-
able for a child at each GMFCS level. For example, a
child classified as GMFCS level IV who is unlikely to
walk independently could learn self-mobility with a
wheelchair. Fitness training has proven effective in
increasing overall fitness in children with CP at all func-
tional levels.
Constraint induced movement therapy (CI) is an
intervention that targets upper extremity motor func-
tion in children with unilateral CP. Systematic reviews
of trials using CI have demonstrated improved hand
function on the affected side after CI [59,60]. The
therapy consists of restraining the unaffected arm via
casting or splinting while training the affected arm.
The two theoretical mechanisms thought to make the
treatment effective are overcoming developmental dis-
regard, the preference to use the unaffected limb
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because of ease, and cortical brain reorganization, the
changes in neural organization that occur when the
limb is used.
Adaptive Devices/Facilitation
Rehabilitative therapists frequently recommend
orthotic devices such as braces, splints, and seating
and standing devices for children with CP. These
devices are used to maintain range of motion, provide
stability, prevent contractures, and improve function.
The ankle-foot orthosis, one of the most commonly
prescribed devices, stabilizes the position of the foot
and stretches the Achilles tendon. Splints are used on
the upper extremity to hold the wrist in a neutral
position and abduct the thumb. Positioning devices
promote skeletal alignment to facilitate independent
function for activities such as eating.
Adaptive equipment, such as walkers, canes, and
wheelchairs, is widely used to promote mobility.
Motorized wheelchairs can be controlled by a switch
that can be activated by the head, mouth, or hand.
Prevention of pressure sores in people with CP with
severe mobility restrictions is an essential element in
the design of adaptive and positioning devices.
Assistive technology is used to promote communica-
tion and improve quality of life for people with CP
and severe dysarthria.
Medical Management
Medical management and secondary prevention inter-
ventions address the child’s health and comorbidities,
which may be more impairing than the motor deficits.
They also strive to prevent worsening of physical dis-
orders, such as contractures or hip dislocations.
Oral Medications. Diazepam has been found to be
effective in reducing spasticity. The evidence regard-
ing the effectiveness of dantrolene in reducing spasti-
city in children with CP is conflicting. At present, the
evidence is insufficient to support the use of oral
baclofen in the treatment of spasticity in children
with CP. Biphosphonates are effective in maintaining
bone density. Anticonvulsant therapy is an important
part of the medical plan for children with seizure
disorders [59,61].
Local Injections. Botulinum toxin A (BTX-A) is a
neuromuscular blocking agent. When used in children
with CP, BTX-A is injected into agonist muscles and
causes transient muscle weakness for several months.
Therapeutic goals include improving function, reducing
733
 Section 4 Specific Conditions Associated with Fetal and Neonatal Brain Injury
pain from spasticity, and reducing joint deformity.
BTX-A has been widely used for over two decades and
has been found to be safe and effective for the treatment
of localized spasticity in the upper and lower extremities
of children with CP, generally leading to improvements
in aspects of gait, such as ankle dorsiflexion and foot
strike [59,61]. Intensive PT and OT after botulinum
toxin injection have been shown to be effective in
improving motor skills acquisition [59].
Orthopedic Management
Because of abnormal muscle tone, children with CP
often develop joint deformities. Orthopedic surgery is
performed to increase the range of motion of a joint
and to treat secondary complications of spasticity.
Serial ankle casting of an affected limb is effective in
maintaining range of motion [59]. Hip dislocation in
CP is potentially preventable if children are included
from an early age in a surveillance program that
includes repeat radiographic and clinical examina-
tions and provided preventive treatment for hips
that are displacing [62]. When necessary, orthopedic
surgery can be effective by lengthening a tendon, cut-
ting through a tendon or muscle (release), or moving
the attachment point of tendon to bone. In children
with spastic quadriplegia, surgery is frequently per-
formed on hyperactive hip adductor muscles to
improve the child’s ability to sit and walk and to
decrease the likelihood of hip dislocation. Hamstring
release surgery may facilitate walking. Achilles ten-
dons are frequently lengthened to improve walking.
When complications such as hip dislocation or pro-
gressive scoliosis occur, orthopedic surgery is
required for correction [7].
Neurosurgical Management
Intrathecal baclofen is often used in children over the
age of 6 years with severe or generalized spasticity or
dystonia. The medication is usually injected via a
subcutaneous pump in the abdomen to a catheter in
the intrathecal CSF compartment. Complications can
include catheter difficulties, meningitis, and CSF leak.
Intrathecal baclofen has been shown to significantly
decrease spasticity in both upper and lower extremi-
ties in children with CP [61].
Selective dorsal rhizotomy interrupts the sensory
component of the deep tendon reflex. It has been
shown to be effective in reducing spasticity in the
lower extremities of children with CP [59].
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Future Treatment Options
Stem cells are multipotential cells that exist in both
adult and developing tissue. True stem cells can dif-
ferentiate into any tissue in the body and have unlim-
ited proliferative and self-renewal capacity. Animal
studies suggest that stem cells mediate neurologic
repair by providing structural support to damaged
tissue, remyelinating damaged axons, and expressing
neurotrophic growth factors. Because true stem cells
have the propensity to form teratomas, experimental
treatment of CP has used partially differentiated stem
cells injected either intravenously or intrathecally.
Preliminary results from a phase I clinical trial using
umbilical cord blood for the treatment of CP suggest
improved cognition, motor function, and brain ima-
ging findings in the stem cell treatment group over
standard rehabilitation alone, but more adverse
events were noted in the treatment group [63].
Further research must be done in this area before
any conclusions about effectiveness or safety can be
drawn. The recent development of “stem cell tourism”
to unregulated clinics in different countries is an
undesirable outcome of the early research in this
field [64].
Clinical Considerations
The medical team in the neonatal intensive care unit
(NICU) is frequently confronted with the difficult task
of counseling families on possible adverse future neu-
rodevelopmental outcomes for a child born preterm
or with medical complications. Qualitative research
has determined that parents want prognostic infor-
mation early in a medical process [35]. This informa-
tion can be particularly difficult to provide to family
members when a child’s medical condition is evolving
and the ultimate diagnoses and prognoses remain
uncertain. Up to 50% of parents of children with
physical disability and 70% of parents of children
with CP express dissatisfaction with the delivery of
their child’s diagnosis by physicians. These data indi-
cate that clinicians must improve how they commu-
nicate potential bad news [65–67].
Qualitative research has found that the best
approach for telling parents bad news is when a sup-
port person is present, the child is present, the clin-
ician uses direct empathic language, and the clinician
indicates a willingness and the time to answer family
questions. Interpersonal physician behaviors such as
empathy, availability for questions, accountability,
 45 Cerebral Palsy: Advances in Definition, Classification, Management, and Outcome
and acknowledging the child as a unique individual
are helpful to parents. Leaving room for hope in the
future has been identified as extremely important,
particularly when outcomes remain uncertain [66].
In general, families are best served by an approach
that balances honesty with hopefulness. An acknowl-
edgment of the difficulty, such as, “How is it for you to
sit with uncertainty?,” can be therapeutic for a parent
faced, for example, with evidence of white matter
damage on their infant’s MRI but without clinical
evidence of neurologic injury. It is important to
arrange referrals for early intervention, rehabilitative
therapy, a pediatrician, and possibly a developmental
follow-up clinic prior to the NICU discharge so that
parents anticipate their child receiving care rather than
simply waiting to learn the outcome. Identifying stra-
tegies for ongoing communication is also important
because questions will inevitably arise after the child
leaves the medical setting. Ideally, a clinician in the
medical home coordinates care with the many specia-
lists on the treatment team and guides the child and
family as they make treatment decisions.
As a child ages, the primary care clinician on the
medical home team assumes an important role in col-
lecting, coordinating, and interpreting information
from the various service providers. Even knowledge-
able parents who have learned medical terminology
may need help in understanding the issues before mak-
ing difficult decisions. Over a child’s lifespan, discus-
sions with families should follow the principles of
family-centered care, the practice of welcoming
families and children as equal partners in the health-
care team. A key tenet of family-centered care is shared
decision making, in which the family is encouraged to
play an active role in helping to formulate the treat-
ment plans for their child. In health conditions such as
CP, where the scientific evidence does not necessarily
dictate the one best treatment course, it is important to
provide the family with unbiased information and sup-
port as they face critical treatment decision points.
Treatment goals should focus not only on improv-
ing a child’s specific body functions but also on allow-
ing a child to be active and to participate in society to
his or her fullest ability. In the traditional medical
model of care, the primary goal is to treat or cure a
patient’s symptoms, such as reducing spasticity or
dystonia in a child with CP. In the social model of
disability, the goal is to increase an individual’s inde-
pendence and participation in the larger community.
Disadvantages experienced by individuals with CP
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may be caused by environmental and social factors
as well as by the health condition. Consider, for exam-
ple, the limitations for an individual who uses a
motorized wheel chair for mobility and lives in a
town without curb cuts to allow the wheel chair to
go from sidewalk to street and back to sidewalk.
Interventions in this situation may be required at the
environmental, social, and even political level. Federal
laws, such as the Americans with Disabilities Act and
the Individuals with Disabilities Educational Act, that
approach disability through the social model have
significantly improved function and access for many
individuals with CP [68].
With advancing medical knowledge and public
awareness, improved functional outcomes are possi-
ble for all people with CP. Early identification and
diagnosis leading to appropriate lifelong interven-
tions and accommodations are all important to
achieving good long-term outcomes for individuals
with CP.
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