for all pediatricians

1. Cereberal Palsy
(little's disease)
By
Dr Hussein Abass
Consultant of Pediatrics
2019

2. Cerebral palsy (CP) is a diagnostic term used to describe a group of
permanent disorders of movement and posture causing activity limitation that
are
attributed to nonprogressive disturbances in the developing fetal or infant brain.
The motor disorders are often accompanied by disturbances of sensation,
perception, cognition, communication, and behavior as well as by epilepsy and
secondary musculoskeletal problems. CP is caused by a broad group of
developmental, genetic, metabolic, ischemic, infectious, and other acquired
etiologies that produce a common group of neurologic phenotypes. CP has
historically been considered a static encephalopathy, but some of the neurologic
features of CP, such as movement disorders and orthopedic complications,
including scoliosis and hip dislocation, can change or progress over time. Many
children and adults with CP function at a high educational and vocational level,
without any sign of cognitive dysfunction.

4. 1- William John Little (1810–1894) was an English surgeon who is credited with
the first medical identification of spastic diplegia, when he observed it in the 1860s
amongst children. While spasticity surely existed before that point, Little was the
first person to medically record the condition in writing. Thus, for many years,
spastic diplegia was known as Little's Disease; only later did the name change. Also,
Little founded the Royal Orthopaedic Hospital of London.
Cerebral palsy is a diagnosis that has had a constantly evolving definition since
it was first mentioned in the medical literature as “Cerebral Paralysis” by Dr.
William Little in 1843. Currently, the most widely accepted definition, from a
2004 international workshop in Bethesda, Maryland, is that Cerebral Palsy

5. Cereberal Palsy
1- Definition
2- Normal Brain Development
3- Causes
4- Pathophysiology
5- Types
6- Clinical Manifestations
7- Complications
8- Investigations
9- Differential Diagnosis
10- Management
11- Prevention
12- Prognosis

7. CP Definition
A group of permanent disorders of movement and posture causing activity
Limitation Resulting from non-progressive lesions to the developing fetal or infant
brain Affecting mainly the motor centers; cerebral cortex , cerebellum , and basal
ganglia .
OR Static, non progressive disorder of CNS secondary to an insult to immature brain,
resulting in varying degrees of motor milestone delay and dysfunction .
- CP is a disorder of tone, posture or movement
- It results in paralysis, weakness, in coordination or abnormal movement
With frequent Neurologic Associations including:
1- Mental retardation
2- Epilepsy
3- Impaired hearing ;deafness
4- Impaired vision
5- Emotional disturbances
6- Behavioral disturbances

9. Core Problem in Cerebral Palsy
Because of the defect in the brain, muscles are mainly hypertonic and occasionally
hypotonic. Hypertonic muscles are relatively short. This results in a decrease in
range of movement at the adjoining joint.
Stimulus for muscle growth include stretching during rest and movement. Children
with
spastic muscles are unable to stretch them during rest. Motion which occurs in
activities of daily living and play are also restricted. Hence growth of muscles is
progressively hampered in children with CP.
The basis of most of the therapies in CP are based on increasing stretching or
enhancing motion.
Stretching is done by passive range of movement exercises and splinting.
Movement is improved by reducing spasticity (antispasticity drugs, botox injections
and
dorsal rhizotomies), physical aids (crutches) and surgeries (tendon lengthening).

10. Static Encephalopathy, although commonly used as a synonym for cerebral
palsy, is actually a broader term including all individuals with a static injury of
the central nervous system. For example, an individual with intellectual
disability possessing no fine or gross motor deficits would have a diagnosis of
static encephalopathy but not cerebral palsy.
Cerebral palsy is, therefore, a subgroup of static encephalopathy, including only
patients who have accompanying motor system deficits.

11. Definitions of CP adopted for European classification of cerebral palsy :
1- Spastic CP is characterized by at least two of the following:
Abnormal pattern of posture and/or movement
Increased tone (not necessarily constant)
Pathological reflexes (increased reflexes: hyperreflexia and/or pyramidal signs e.g. Babinski response)
Spastic CP may be either bilateral or unilateral
2- Spastic bilateral CP is diagnosed if:
Limbs on both sides of the body are involved
3- Spastic unilateral CP is diagnosed if:
Limbs on one side of the body are involved
4- Ataxic CP is characterized by both:
Abnormal pattern of posture and/or movement
Loss of orderly muscular coordination so that movements are performed with abnormal force, rhythm, and
accuracy
5- Dyskinetic CP is dominated by both:
Abnormal pattern of posture and/or movement
Involuntary, uncontrolled, recurring, occasionally stereotyped movements
Dyskinetic CP may be either dystonic or choreo-athetotic
6- Dystonic CP is dominated by both:
Hypokinesia (reduced activity, i.e. stiff movement)
Hypertonia (tone usually increased)
7- Choreo-athetotic CP is dominated by both:
Hyperkinesia (increased activity, i.e. stormy movement)
Hypotonia (tone usually decreased)

12. incidence
Cerebral Palsy is the most common of all childhood disabilities, affecting approximately
three live births out of every thousand in the United States.
- Cerebral Palsy occurs in 2.3 to 3.6 out of every 1,000 children
Spastic Cerebral Palsy is most common, making up 61 percent to 76.9 percent of all
Cerebral Palsy cases
Male:Female ratio of 1.4 : 1
USA
About 764,000 children and adults currently have Cerebral Palsy
About 500,000 children under age of 18 currently have Cerebral Palsy
About two to three children out of every 1,000 have Cerebral Palsy (United States studies
have yielded rates as low as 2.3 per 1,000 children to as high as 3.6 per 1,000 children)
About 10,000 babies born each year will develop Cerebral Palsy
Around 8,000 to 10,000 babies and infants are diagnosed per year with Cerebral Palsy
Around 1,200 to 1,500 preschool-aged children are diagnosed per year with Cerebral
Palsy
17 Million people with CP All over the world

13. 2- Normal Brain Development
1. Neurulation,
2. Regionalization,
3. Neurogenesis,
4. Migration,
5. Differentiation,
6. Apoptosis,
7. Axon guidance,
8. Synapse formation and Pruning,
9. Myelination
10. Cortical folding.

14. Critical Periods of Brain growth
1 month – neural tube
4th month – All the lobes and major divisions complete
1 year post-natal – 2/3 adult size
2 years age – 75% adult size
5 years – 90% adult size
Potential for Neurogenesis [new brain cell formation] (peaks in utero) and
Synaptogenesis [new connection formation] (peaks by 5 years) continues
throughout life.

15. Prenatal Growth
3 main periods of prenatal development
1- Germinal Period (1st two weeks after conception): Rapid cell division and
beginning of cell differentiation
2- Embryonic Period (3rd through 8th week): Basic forms of all body structures
develop
3- Fetal Period (9th week until birth): Fetus grows in size and matures in
functioning

17. The Human Brain consists of 100 Billion neurons that connect with more than 100 Trillion synapses.
Normal neuronal development can be divided into a series of key steps:
1- neurulation, 2- regionalization, 3- neurogenesis, 4- migration, 5- differentiation,6- apoptosis,
7- axon guidance, 8- synapse formation and pruning, 9- myelination, and 10- cortical
folding. In these 10 steps, cells go from unspecified ectodermal constituents to
highly differentiated neurons for which connections are being fine-tuned at the
synaptic level. Neurodevelopment, however, does not stop with birth and
extends through childhood, in fact likely throughout the whole life span.

19. Prenatal Growth of the Brain
Just 25 days after conception (a), the central nervous
system is already evident. The brain looks distinctly
human by day 100 (c). By the 28th week of gestation
(e), at the very time brain activity begins, the various
sections of the brain are recognizable. When the fetus
is full term (f), all the parts of the brain, including the
cortex (the outer layers), are formed, folding over one
another and becoming more convoluted, or wrinkled,
as the number of brain cells increases.

23. Developmental Milestones for a Normal Child
• Primitive reflexes (disappear by 3-4 months)
• Neck control 3-4 months (earlier in African children)
• Sitting 5-6 months
• Rolls 7 months
• Crawls 7-8 months
• Stands with support 10 months
• Walks 12 months
• Climbs up and down stairs 20 months

24. 3- Aetiology
1- Pre-natal (80%)
- Maternal infection and toxins (TORCHES).
-Fetal exposure to drugs and alcohol through maternal .(cocaine, heroin ,marijuana)
-Congenital malformations of the brain that occur during early pregnancy.
-Rhesus blood group incompatibility resulting in kernicterus.
-Maternal health problems. ex: RF-Infections.
-Prenatal chorioamnionitis and maternal infections and placental abnormalities.
2- Natal (10%)
-Anoxia as a result of perinatal complications.
-Fetal distress.
-Premature delivery.
-Sepsis in neonatal period.
-Bronchopulmonary dysplasia and prolonged ventilation in preterm infants.
-Heart surgery before the age of 1mnth.
3- Post-natal (10%)
- VLBW with intracranial hemorrhage
- Meningitis, encephalitis
- Metabolic e.g. phenyle ketonuria
- Hypoglycemia
- Hyper bilirubinemia
- Hydrocephalus.

25. •Fetal stroke, or that which occurs between 14 weeks of gestation and the
onset of labor resulting in delivery, has been associated with postnatal epilepsy,
mental retardation, and cerebral palsy. The entity is caused by antenatal
ischemic, thrombotic, or hemorrhagic injury. We present seven new cases of fetal
stroke diagnosed in utero and review the 47 cases reported in the literature.
Although risk factors could not be assigned to 50% of the fetuses with stroke, the
most common maternal conditions associated with fetal stroke were alloimmune
thrombocytopenia and trauma. Magnetic resonance imaging was optimal for
identifying fetal stroke, and prenatal imaging revealed hemorrhagic lesions in
over 90% of studies; porencephalies were identified in just 13%. Seventy-eight
percent of cases with reported outcome resulted in either death or adverse
neurodevelopmental outcome at ages 3 months to 6 years. Fetal stroke appears
to have different risk factors, clinical characteristics, and outcomes than other
perinatal or childhood stroke syndromes. A better understanding of those risk
factors predisposing a fetus to cerebral infarction may provide a basis for future
therapeutic intervention trials. Ozduman K, Pober BR, Barnes P, Copel JA, Ogle EA,
Duncan CC, Ment LR. Fetal stroke.

26. proportion of CP is related to Birth Asphyxia
In contrast with popular perception, large clinical epidemiologic and longitudinal
studies indicate that
perinatal asphyxia is an important—but relatively minor—cause. Estimates range
from a low of 3% to a high of 21%. In most cases, the events leading to CP occur in
the fetus before the onset of labor or in the newborn after delivery.
CPoften is caused by brain damage that happens before or during a baby's
birth, or during the first 3-to-5 years of a child's life.

27. Apgar score correlation with the development of CP
Large studies have mixed results. A 1981 study of 49,000 infants found that a low
Apgar score
correlated poorly with the development of CP. Of term infants with scores of 0 to 3
at 1 or 5 minutes,
95% did not develop CP. Conversely, nearly 75% of patients with CP had 5-minute
Apgar scores of 7 to 10. More recent studies have found a stronger association
between low Apgar scores and cerebral
palsy in term infants, but there is no clear association for low birth weight or
premature infants.
A 2010 population study of over 500,000 Norwegian infants found an association
between an
Apgar score <4 at 5 minutes and cerebral palsy, which was strongest for infants
with normal birth weight and for patients later diagnosed with quadriplegia.

28. About 80% of CP is antenatal in origin due to cerebrovascular haemorrhage or ischaemia, cortical migration
disorders or structural maldevelopment of the brain during gestation. Some of these problems are linked to gene
deletions. Other antenatal causes are genetic syndromes and congenital infection.
Only about 10% of cases are thought to be due to hypoxic-ischaemic injury before or during delivery and this
proportion has remained relatively constant over the last decade. About 10% are postnatal in origin.
Preterm infants are especially vulnerable to brain
damage from periventricular leukomalacia secondary
to ischaemia and/or severe intraventricular haemorrhage
and venous infarction. The improved survival of
extremely preterm infants has been accompanied by
an increase in survivors with CP, although the number
of such children is relatively small.
Postnatal causes are meningitis/encephalitis/
encephalopathy, head trauma from accidental or
non-accidental injury, symptomatic hypoglycaemia,
hydrocephalus and hyperbilirubinemia.
MRI brain scans may assist in identifying the cause
of the CP, in directing further investigations and in supporting
explanations to the parents, but is not required
to make the diagnosis.

29. • Cerebral palsy is caused by an abnormality or disruption in brain development,
usually before a child is born. In many cases, the exact trigger isn't known. Factors
that may lead to problems with brain development include:
• Mutations in genes that lead to abnormal brain development
• Maternal infections that affect the developing fetus
• Fetal stroke, a disruption of blood supply to the developing brain
• Infant infections that cause inflammation in or around the brain
• Traumatic head injury to an infant from a motor vehicle accident or fall
• Lack of oxygen to the brain (asphyxia) related to difficult labor or delivery,
although birth-related asphyxia is much less commonly a cause than historically
thought

30. Risk factors
• A number of factors are associated with an increased risk of cerebral palsy.
• Maternal health
• Certain infections or health problems during pregnancy can significantly increase cerebral palsy risk to the baby.
Infections of particular concern include:
• German measles (rubella). Rubella is a viral infection that can cause serious birth defects. It can be prevented
with a vaccine.
• Chickenpox (varicella). Chickenpox is a contagious viral infection that causes itching and rashes, and it can cause
pregnancy complications. It too can be prevented with a vaccine.
• Cytomegalovirus. Cytomegalovirus is a common virus that causes flu-like symptoms and may lead to birth defects
if a mother experiences her first active infection during pregnancy.
• Herpes. Herpes infection can be passed from mother to child during pregnancy, affecting the womb and placenta.
Inflammation triggered by infection may then damage the unborn baby's developing nervous system.
• Toxoplasmosis. Toxoplasmosis is an infection caused by a parasite found in contaminated food, soil and the feces
of infected cats.
• Syphilis. Syphilis is a sexually transmitted bacterial infection.
• Exposure to toxins. Exposure to toxins, such as methyl mercury, can increase the risk of birth defects.
• Zika virus infection. Infants for whom maternal Zika infection causes microcephaly can develop cerebral palsy.
• Other conditions. Other conditions may increase the risk of cerebral palsy, such as thyroid problems, intellectual
disabilities or seizures.

31. Infant illness
Illnesses in a newborn baby that can greatly increase the risk of cerebral palsy
include:
Bacterial meningitis.
Viral encephalitis.
Severe or untreated jaundice.

32. • Other factors of pregnancy and birth
• While the potential contribution from each is limited, additional pregnancy or birth
factors associated with increased cerebral palsy risk include:
• Breech births. Babies with cerebral palsy are more likely to be in a feet-first position
(breech presentation) at the beginning of labor rather than headfirst.
• Complicated labor and delivery. Babies who exhibit vascular or respiratory problems
during labor and delivery may have existing brain damage or abnormalities.
• Low birth weight. Babies who weigh less than 5.5 pounds (2.5 kilograms) are at higher
risk of developing cerebral palsy. This risk increases as birth weight drops.
• Multiple babies. Cerebral palsy risk increases with the number of babies sharing the
uterus. If one or more of the babies die, the chance that the survivors may have
cerebral palsy increases.
• Premature birth. A normal pregnancy lasts 40 weeks. Babies born fewer than 37 weeks
into the pregnancy are at higher risk of cerebral palsy. The earlier a baby is born, the
greater the cerebral palsy risk.
• Rh blood type incompatibility between mother and child. If a mother's Rh blood type
doesn't match her baby's, her immune system may not tolerate the developing baby's
blood type and her body may begin to produce antibodies to attack and kill her baby's
blood cells, which can cause brain damage.

33. The prevalence of CP has increased somewhat as a result of the enhanced
survival of very premature infants weighing < 1,000 g, who go on to develop CP
at a rate of approximately 15 per 100. However, the gestational age at birth adjusted
prevalence of CP among 2 yr old former premature infants born at 20-
27 wk of gestation has decreased over the past decade. The major lesions that
contribute to CP in preterm infants are intracerebral hemorrhage and
periventricular leukomalacia (PVL). Although the incidence of intracerebral
hemorrhage has declined significantly, PVL remains a major problem. PVL
reflects the enhanced vulnerability of immature oligodendroglia in premature
infants to oxidative stress caused by ischemia or infectious/inflammatory insults.
White matter abnormalities (loss of volume of periventricular white matter,
extent of cystic changes, ventricular dilation, thinning of the corpus callosum)
present on MRI at 40 wk of gestational age in former preterm infants are a
predictor of later CP.

34. Multiple pregnancy
was also associated with a
higher incidence of CP and 12% of the cases in the European CP study resulted
from a multiple pregnancy, in contrast to a 1.5% incidence of multiple pregnancy
in the study. Other studies have also documented a relationship between multiple
births and CP, with a rate in twins that is 5-8 times greater than in singleton
pregnancies and a rate in triplets that is 20-47 times greater. Death of a twin in
utero carries an even greater risk of CP; it is 8 times that of a pregnancy in which
both twins survive and approximately 60 times the risk in a singleton pregnancy.

35. Classification
• 1- Clinical (spastic [too stiff], flaccid [too soft], extra-pyramidal [moving without
control or abnormally positioned] and mixed).
• 2- Anatomical (number body parts [limbs] affected)
• 3- The Gross Motor Function Classification System (GMFCS), a recently
developed system, classifies children with CP by their age specific motor activity.

38. Topographic Classification:
(distribution of motor defect)
1- Monoplegia --Only one limb is affected
2- Hemiplegia--Upper and lower limbs on one side are affected
3- Diplegia--All limbs are affected, the lower more affected than
the upper limbs
4- Paraplagia--Only both lower limbs are affected
5- Quadriplegia--All the four limbs are affected

39. 5- Types

42. Types of CP :
1• Spastic (Quadriplegia, Diplegia, Hemiplegia)
2• Dyskinetic (Athetoid, Choreoathetoid, and Dystonic )
3• Ataxic
4• Mixed

43. Causes and Risk Factors
Cerebral palsy is a catch-all term for developmental movement disorders caused by a brain injury. Each type of
cerebral palsy is caused by damage to a specific part of the brain.
Spastic cerebral palsy is caused by damage to the motor cortex and the pyramidal tracts of the brain, which connect
the motor cortex to the spinal cord. Understanding the function of the motor cortex and pyramidal tracts helps to
explain how damage to these systems affects movement in those with spastic CP.
Damage to the Motor Cortex
The motor cortex is located in the cerebral cortex, which is the largest part of the brain. The motor cortex is
composed of several parts that are responsible for relaying signals to other parts of the brain to control movement.
The most important aspect of the motor cortex in relation to cerebral palsy is its regulation of voluntary movement.
Damage to this region of the brain makes voluntary movement harder to control and less fluid, or “spastic”.
Damage to the Pyramidal Tracts
The pyramidal tracts in the brain are the roads of communication between the cerebral cortex and the nerves in the
spinal cord. If pyramidal tracts are damaged, the motor cortex can’t send proper signals to the spinal cord. The
spinal cord is one half of the central nervous system, with the other half being the brain and brain stem. These parts
of the brain are essential for sensory functions such as sight, touch and movement.
The motor cortex and pyramidal tracts may be damaged by:
1-Prenatal brain hemorrhage or infection
2-Lack of oxygen to the brain during birth
3-Brain trauma or infection after birth
Several risk factors may increase the likelihood of a developmental brain injury occurring. Poor maternal health and
a low birth weight are just some of the risk factors for any type of cerebral palsy.

44. Spastic CP
• Spastic (or pyramidal) CP: Characterized by neurologic signs of upper motor
neuron damage with increased “clasp knife” muscle tone, increased deep tendon
reflexes, pathologic reflexes, and spastic weakness.
• Spastic cerebral palsy is a developmental disorder caused by damage to the brain
before birth, during delivery, or within the first few years of life.
• This condition prevents the normal development of motor function.
• Spastic CP is characterized by jerky movements, muscle tightness and joint
stiffness.
• This type of cerebral palsy often makes simple tasks more challenging, such as
walking or picking up small objects. Some children with spastic CP also develop
co-occurring conditions as a result of their brain injury. These coexisting
conditions can range from attention deficit hyperactivity disorder (ADHD) to
epilepsy.

45. Types of Spastic CP
There are 3 main types of cerebral palsy, and each CP diagnosis can be further broken
down to more accurately describe one’s brain damage and related symptoms. The various
types of spastic cerebral palsy are classified based on the location of movement issues.
For example, children with spastic CP may have muscle stiffness in one arm, both legs or
one full side of their body.
Spastic Diplegia
Muscle stiffness occurs primarily in the legs. This type of CP may also slightly affect
mobility in the child’s arms. (more common in the premature infant)
Spastic Hemiplegia
One side of the body is affected by movement problems, with the arm typically being
stiffer than the leg.
Spastic Quadriplegia
All four limbs are affected, as well as the torso and face. Children with quadriplegia often
have co-occurring disorders, such as epilepsy.

46. Dyskinetic Cerebral Palsy (also includes athetoid, choreoathetoid, and dystonic cerebral
palsies) Characterized by prominent involuntary movements or fluctuating muscle tone,
with choreoathetosis the most common subtype. Distribution is usually symmetric
among the four limbs.
People with dyskinetic CP have problems controlling the movement of their hands, arms,
feet, and legs, making it difficult to sit and walk. The movements are uncontrollable and
can be slow and writhing or rapid and jerky. Sometimes the face and tongue are affected
and the person has a hard time sucking, swallowing, and talking. A person with dyskinetic
CP has muscle tone that can change (varying from too tight to too loose) not only from
day to day, but even during a single day.
Ataxic Cerebral Palsy
Primarily cerebellar signs (including ataxia, dysmetria, past pointing, nystagmus)
People with ataxic CP have problems with balance and coordination. They might be
unsteady when they walk. They might have a hard time with quick movements or
movements that need a lot of control, like writing. They might have a hard time
controlling their hands or arms when they reach for something.
Mixed Cerebral Palsy
Some people have symptoms of more than one type of CP. The most common type of
mixed CP is spastic-dyskinetic CP.

47. Signs and Symptoms :
The signs and symptoms of spastic cerebral palsy are different for every child. Differences in symptoms
depend on the severity of the child’s brain injury and any co-occurring disorders that may be present.
In general, the most common symptoms of spastic CP are:
Stiff, tight muscles (hypertonia) on one or both sides of the body
Exaggerated movements
Limited mobility
Abnormal gait
Crossed knees
Joints don’t full extend
Walking on tiptoes
Contractures
Abnormal reflexes
Co-occurring issues may also present themselves, such as hearing and vision impairment, but these aren’t
directly related to the cerebral palsy; they are caused by the initial birth injury.
In the first years of a child’s life, it can be very hard to recognize the signs of cerebral palsy. This is because
symptoms typically do not present themselves until a child begins missing developmental milestones.
During toddlerhood, many children tend to exhibit some of the same jerky reflexes associated with spastic
CP. It can take up to 5 years of age before a full cerebral palsy diagnosis is reached.

48. 6- Clinical Manifestations
• Signs and symptoms can vary greatly. Movement and coordination problems associated with cerebral
palsy may include:
• Variations in muscle tone, such as being either too stiff or too floppy
• Stiff muscles and exaggerated reflexes (spasticity)
• Stiff muscles with normal reflexes (rigidity)
• Lack of muscle coordination (ataxia)
• Tremors or involuntary movements
• Slow, writhing movements (athetosis)
• Delays in reaching motor skills milestones, such as pushing up on arms, sitting up alone or crawling
• Favoring one side of the body, such as reaching with only one hand or dragging a leg while crawling
• Difficulty walking, such as walking on toes, a crouched gait, a scissors-like gait with knees crossing, a wide
gait or an asymmetrical gait
• Excessive drooling or problems with swallowing
• Difficulty with sucking or eating
• Delays in speech development or difficulty speaking
• Difficulty with precise motions, such as picking up a crayon or spoon
• Seizures

49. Evaluation
Diagnosing..
Obtaining a complete history (birth history, birth weight, complications following
birth..)
Asking about the child’s preferential use of one hand or leg.
Related medical conditions (seizures, speech disorders)
Physical examination..
Increased muscle tone.
Deep tendon reflexes are increased.
Fine motor activities testing.
Retained infantile reflexes.
Balance, sitting and gait of child.

50. Diagnosis :
• A thorough history and physical examination should preclude a progressive
• disorder of the CNS, including degenerative diseases, metabolic
• disorders, spinal cord tumor, or muscular dystrophy. The
• possibility of anomalies at the base of the skull or other disorders
• affecting the cervical spinal cord needs to be considered in patients
• with little involvement of the arms or cranial nerves. An MRI scan of
• the brain is indicated to determine the location and extent of structural
• lesions or associated congenital malformations; an MRI scan of the
• spinal cord is indicated if there is any question about spinal cord
• pathology. Additional studies may include tests of hearing and visual
• function. Genetic evaluation should be considered in patients with
• congenital malformations (chromosomes) or evidence of metabolic
• disorders (e.g., amino acids, organic acids, MR spectroscopy). In addition
• to the genetic disorders mentioned earlier that can present as CP,
• the urea cycle disorder arginase deficiency is a rare cause of spastic
• diplegia and a deficiency of sulfite oxidase or molybdenum cofactor
• can present as CP caused by perinatal asphyxia. Tests to detect inherited
• thrombophilic disorders may be indicated in patients in whom an
• in utero or neonatal stroke is suspected as the cause of CP.
• Because CP is usually associated with a wide spectrum of developmental
• disorders, a multidisciplinary approach is most helpful in the
• assessment and treatment of such children.

51. • Investigations :
• 1- MRI Brain & Spinal Cord
• 2- ultrasound/CT brain
• 3- Coagulation studies
• 4- Lab tests (blood work, urinalysis or genetic testing)
• 5- Metabolic screen
• 6- EEG
• 7- EMG
• 8- evaluations (mobility, gait, speech, hearing, vision, feeding and digestion,
cognitive and rehabilitation needs)

52. • What are the Most Common Brain lesions seen on Magnetic Resonance Imaging
(MRI) in children with cerebral palsy? Periventricular Leukomalacia
• Periventricular white matter lesions are the most common and can be seen in
19% to 45% of children
• with CP (particularly formerly premature infants). Other common lesions include
gray matter injuries of the
• basal ganglia and thalamus (21%), developmental cortical malformations (11%),
and focal cortical infarcts
• (10%). Up to 15% of cases of CP do not have an identifiable lesion on MRI. The
varied MRI findings are
• believed to be emblematic of the neurodevelopmental heterogeneity of CP.
• Hadders-Algra M: Early diagnosis and early intervention in cerebral palsy, Front
Neurol 5:185, 2014.

55. Diagnosis
Diagnosing cerebral palsy (CP) at an early age is important to the well-being of
children and their families. Diagnosing CP can take several steps:
1- Developmental Monitoring
2- Developmental Screening
3- Developmental and Medical Evaluations

56. • 1- Developmental Monitoring
• Developmental monitoring (also called surveillance) means tracking a child’s
growth and development over time. At each well-child office visit, the doctor
monitors the child’s development. The doctor does this by asking parents if they
have any concerns about their child’s development, taking or updating the child’s
developmental history, and watching the child during the exam to see how he or
she moves.
• It is important for doctors to monitor the development of all children, but
especially those who are at a higher risk for developmental problems due to
preterm birth or low birthweight.
• If any concerns about the child’s development are raised during monitoring, then
a developmental screening test should be given as soon as possible.

57. • 2- Developmental Screening
• During developmental screening a short test is given to see if the child has specific
developmental delays, such as motor or movement delays. Some developmental screening
tests are in the form of interviews or questionnaires completed by parents, others are tests
that the doctor gives to the child. The American Academy of Pediatrics recommends that all
children be screened for developmental delays during regular well-child office visits at:
• 9 months
• 18 months
• 24 or 30 months
• When a child is 9 months of age, many issues involving movement can be seen easily. However,
mild movement delays that were not found at the 9-month screening might be easier to see
when the child is 18 months of age. By the time the child is 30 months of age, most movement
delays can be found.
• A developmental screening test also can be given whenever the child’s parents or doctor or
others involved in the care of the child have concerns about the child’s development. If the
results of the screening test are cause for concern, then the doctor will make referrals for:
• Developmental and medical evaluations
• AND
• Early intervention or early childhood services

58. • 3- Developmental and Medical Evaluations
• The goal of a developmental evaluation is to diagnose the specific type of disorder that affects
a child. To evaluate movement or motor delays, the doctor will look closely at the child’s motor
skills, muscle tone, reflexes, and posture, and take a careful medical history from the parents.
The doctor will try to rule out other disorders that could cause similar problems.
• Because many children with CP also have related developmental conditions such as intellectual
disability; seizures; or vision, hearing, or speech problems, it is important to evaluate the child
to find these disorders as well.
• The developmental evaluation can be performed by the primary care doctor or by a specialist.
Specialists who can do this type of developmental evaluation include:
• Developmental pediatricians or neurodevelopment pediatricians (doctors with special training
in child development and in evaluating with children with developmental problems).
• Child neurologists (doctors with special training in childhood diseases of the brain, spine, and
nerves).
• Pediatric physiatrists or pediatric rehabilitation doctors (doctors with special training in physical
medicine and rehabilitation for children).
• In addition to the developmental evaluation, additional tests can be done to look for a cause of
CP. Specialists might suggest brain imaging tests, such as x-ray computed tomography (CT scan)
or magnetic resonance imaging (MRI). An electroencephalogram (EEG), genetic testing, or
metabolic testing, or a combination of these, also might be done.
• CP generally is diagnosed during the first or second year after birth. But if a child’s symptoms
are mild, it is sometimes difficult to make a diagnosis until the child is a few years older.

59. Levine (POSTER) Criteria for the Diagnosis of CP
1• Posturing/abnormal movements
2• Oropharyngeal problems (e.g., tongue thrusts, swallowing abnormalities)
3• Strabismus
4• Tone (hypertonia or hypotonia)
5• Evolutional maldevelopment (primitive reflexes persist or
protective/equilibrium reflexes fail to develop [e.g., lateral prop, parachute reflex])
6• Reflexes (increased deep tendon reflexes/persistent Babinski reflex)
Abnormalities in 4 of these 6 categories strongly point to the diagnosis of CP.

60. Why CP difficult to be diagnosed clinically during the 1st year of life?
Unlike adults with acute neurologic deficits, which may be focal, young children may manifest generalized
and nonspecific neurologic dysfunction following an acute neurologic insult:
• Hypotonia is more common than hypertonia in the first year following an acute insult and spasticity
typically develops later, both of which makes the prediction of CP difficult. Hypertonia, especially in
the antigravity muscles, develops to compensate for weakness. Initial hypertonia may be seen with a
basal ganglia insult.
• The early abundance of primitive reflexes (with variable persistence) may confuse the clinical picture.
• An infant has a limited variety of volitional movements for evaluation.
• Substantial myelination takes months to evolve and may delay the clinical picture of abnormal tone
and increased deep tendon reflexes.
• Most infants who develop CP do not have identifiable risk factors; most cases are not related to labor
and delivery events (intrapartum).
Most cases of cerebral palsy can be diagnosed by 18 to 24 months of life.

61. What behavioral symptoms during the 1st year should arouse suspicion about
thepossibility of CP?
• Excessive irritability, constant crying, and sleeping difficulties (severe colic is
noted in up to 30% of babies who are eventually diagnosed with CP)
• Early feeding difficulties with difficulties in coordinating suck and swallow,
frequent spitting up, and poor weight gain
• “Jittery” or “jumpy” behavior, especially at times other than when hungry
• Easily startled behavior
• Stiffness when handled, especially during dressing, diapering, and handwashing
• Paradoxically “precocious” development, such as early rolling (actually a sudden,
reflexive roll rather than a volitional one) or apparent early strength, such as the
stiff-legged “standing” with support of an infant with spastic diplegia .

62. • Differential Diagnosis :
• 1- Degenerative nervous disorders
• 2- Genetic diseases
• 3- Muscle diseases
• 4- Metabolism disorders
• 5- Nervous system tumors
• 6- Coagulation disorders
• 7- Other injuries or disorders which delay early development, some of which
can be “outgrown”

63. Problems are Commonly Associated with CP
• Mental retardation: Two-thirds of total patients; most commonly observed in children with spastic
quadriplegia
• Failure to thrive, growth retardation
• Feeding problems (including dysphagia, sialorrhea [excessive salivation])
• Gastrointestinal problems (gastroesophageal reflux, constipation)
• Learning disabilities
• Ophthalmologic abnormalities (strabismus, amblyopia, nystagmus, refractive errors)
• Hearing deficits
• Communication disorders
• Epilepsy: One-half of total patients; most commonly observed in children with spastic hemiplegia
and related to the degree of neuroimaging abnormality.
• Behavioral and emotional problems (especially attention-deficit hyperactivity disorder,
depression, sleep problems)
• Urinary problems (incontinence, voiding dysfunction, urinary tract infections)
• Spinal column changes (kyphosis, scoliosis)
• Respiratory problems (upper airway obstruction, chronic aspiration)

64. 7- Complications
• Muscle weakness, muscle spasticity and coordination problems can contribute to a number of
complications either during childhood or later during adulthood, including:
• Contracture. Contracture is muscle tissue shortening due to severe muscle tightening (spasticity).
Contracture can inhibit bone growth, cause bones to bend, and result in joint deformities, dislocation or
partial dislocation.
• Malnutrition. Swallowing or feeding problems can make it difficult for someone who has cerebral palsy,
particularly an infant, to get enough nutrition. This may cause impaired growth and weaker bones.
Some children may need a feeding tube for adequate nutrition.
• Mental health conditions. People with cerebral palsy may have mental health (psychiatric) conditions,
such as depression. Social isolation and the challenges of coping with disabilities can contribute to
depression.
• Lung disease. People with cerebral palsy may develop lung disease and breathing disorders.
• Neurological conditions. People with cerebral palsy may be more likely to develop movement disorders
or worsened neurological symptoms over time.
• Osteoarthritis. Pressure on joints or abnormal alignment of joints from muscle spasticity may lead to
the early onset of painful degenerative bone disease (osteoarthritis).
• Osteopenia. Fractures due to low bone density (osteopenia) can stem from several common factors
such as lack of mobility, nutritional shortcomings and antiepileptic drug use.
• Eye muscle imbalance. This can affect visual fixation and tracking; an eye specialist should evaluate
suspected imbalances.

65. Therapies are used to treat the Spasticity and Dystonia of Cerebral Palsy
1- Casting: Serial “inhibitive” casting can reduce tone and allow improved gait and
weight-bearing activities
2- Nerve blocks, motor point blocks, botulinum toxin: Injected to target spasticity
in particular muscle groups
3- Oral and intrathecal medications: Including baclofen, dantrolene, carbidopa-
levodopa, clonazepam
4- Tendon-lengthening surgeries: At ankle, knee, wrist, or elbow to prevent or
delay joint contractures
5- Selective dorsal rhizotomy: A neurosurgical procedure that interrupts the
afferent component of the deep tendon (stretch) reflex .

66. Treatment of CP
1- Physical Therapy as early as possible
2- Occupational Therapy
3- Speech Therapy
4- Devices
5- Drugs
6- Surgery
7- Casting

67. •The goals of treatment that have linked to
productive lives as adults are:
Communication, education, mobility and
ambulation.

68. •Casting
•Short leg casts are applied with extended toe plates, careful
molding of the heel and metatarsal head control.
•For a period of time varies but usually a minimum of 6 weeks.
and is followed by the use of orthoses.
•There is a limited role for casting in patients with cerebral palsy.

69. Treatment for Spastic Cerebral Palsy
Treatment for spastic CP varies with each case. The severity of symptoms, the
location of movement problems and any secondary conditions are the biggest
factors in outlining treatment. However, there are five main routes of treatment for
CP: physical, occupational and speech therapy, medication and surgery.
1-Physical therapy
The first type of treatment prescribed to children with spastic CP is typically
physical therapy. The goal of physical therapy is to provide as much independence
to the child as possible. This treatment is centered on flexibility exercises and
stretching out stiff muscles.
Physical therapists will typically use daily range-of-motion (ROM) and stretching
exercises to improve mobility of joints and soft tissues. Physical therapists often
use age-appropriate toys and games to make the therapy enjoyable for the child.
This type of therapy can help improve overall motor function and prevent any
future complications.

70. Physical therapy..
Often the first rendered to the child with cerebral palsy.
No controlled studies have confirmed that regular physical therapy improves
the out come of the child with cerebral palsy.
The approach to physical therapy is to establish a therapy to monitor the
developmental milestones of the very young child around the age 2-3 years.
Therapy continue if gains are being made in attaining ambulation.

71. Orthoses
Can be helpful in improving gait in
ambulatory patient with cerebral
palsy.
Ankle-foot orthoses are most
commonly prescribed to assist the
child with positioning of the ankle
and foot during gait.

72. 2- Occupational therapy
Another form of therapy used to treat children with spastic CP is occupational
therapy. The goal of occupational therapy is to improve a child’s ability to perform
daily tasks and activities independently in the home, school, work and public
environments.
Occupational therapists perform exercises that target certain muscles in the wrist,
forearm, thumb and upper body. This treatment is beneficial for spastic CP
because it focuses on improving motor control, bilateral coordination and upper
body strength. Occupational therapists can also assess the need for various
assistive devices, such as adaptive scissors or writing utensils.

73. 3- Speech therapy
Speech therapy is used to improve oral movements in children with spastic CP. The
objective of speech therapy is to strengthen the muscles used for speech, which
helps with articulation and coordination. Some children with this type of CP may
experience drooling or difficulty swallowing or speaking. Performing exercises that
incorporate assistive communication devices can help improve motor and cognitive
abilities, as well as confidence.
Speech therapy provides the tools for children with spastic CP to clearly
communicate their thoughts and socialize with others. This form of therapy can
also help make chewing, breathing and swallowing less difficult, allowing for
normal growth and development.

74. Drug Therapy

75. 1- Anticonvulsants are prescribed for patients with cerebral palsy
Topamax
Lamictal
Tegretol
Dilantin
Zonegran
Zarontin
2- Muscle Relaxers
Baclofen
Dantrolene
Tizanidine
Flexeril
Diazepam
3- Anticholinergic Medications
Robinul
Sinemet
Benztropine mesylate
Trihexyphenidyl hydrochloride

76. 4- Antidepressants
Celexa
Paxil
Prozac
Cymbalta
Lexapro
Zoloft
5- Pain Control Medication
Nonsteroidal anti-inflammatory drugs (NSAIDs)
Steroids
6- Complementary and Alternative Medication
Biologically-based supplements
Homeopathic medicines
Herbal medicines

77. Medications :
• Medication is used to alleviate cerebral palsy symptoms and prevent
complications. Several classes of drugs provide relief for cerebral palsy patients,
including these medications:
• Dopaminergic drugs – This medication, commonly used to treat Parkinson’s
disease, raises the body’s dopamine level, leading to less rigidity and better
muscle control.
• Muscle relaxants – Stiff, spastic musculature plagues cerebral palsy patients, so
medications are used to relax muscle groups. Drugs like baclofen can be taken
orally or administered by an automatic, metered pump.
• Benzodiazepines – Relaxants, such as Valium, work on brain chemistry to ease
certain CP conditions.
• Glycopyrrolates – Helps to releive stomach and abdominal pain. Belongs to a
class of drugs known as “Anticholinergics”.

78. • Spasticity and Drug Therapy Medications for Cerebral Palsy
• The most widely diagnosed form of cerebral palsy, spastic cerebral palsy is
characterized by tight, stiff muscles in the arms and legs. Patients can be
impacted on one or both sides, with more pronounced symptoms in the lower
extremities.
• When muscles remain tight over time, contracture can occur, bending joints into
rigid, fixed positions. The condition interferes with mobility, causing pain and
complications in many cases. Treating spasticity is a fundamental concern for
specialists working with cerebral palsy patients. Principal medications for
treating spasticity include:

81. • Baclofen – This muscle relaxant is often prescribed to treat spasticity resulting from cerebral
palsy. The drug can be taken orally, and since 1996, is also available in a pump delivery system,
which administers the medication directly to the spinal cord. Individual doses may cause
sleepiness, nausea, headache, and lightheadedness, which can often be remedied by adjusting
dosing. Baclofen helps to provide long-term reductions in muscle spasticity. Baclofen also is
there to help improve speech, movement, swallowing, and alertness.
• Dantrium/Dantrolene – Severe spasms are treated with this muscle relaxant, which relieves
pain and can help CP patients achieve greater range of movement. The drug can make users
feel dizzy, drowsy, fatigued or weak, and serious liver damage may occur with long-term use.
The drug has not been approved for children under 5. Dantrolene is most frequently
administered orally, but other options are available during surgery.
• Diazepam/Valium – Drugs like Valium serve as general relaxants, relieving widespread CP
symptoms. In addition to easing muscle tension, diazepam may help with seizures. Side effects
may include drowsiness, headache, depression and dizziness.
• Botox – Direct injections to affected muscles can ease spasticity, reducing muscle contractions
from cerebral palsy. Headache and muscle ache are common side effects. Botox injections into
the affected muscles usually last 12-16 weeks providing reduced muscle spasticity.
• Flexeril – A well knows muscle relaxant that works to block nerve impulses the body sends to
the brain. This drug is commonly known for short term use when suffering from muscle injuries
or spasms. Flexeril is less commonly used for cerebral palsy patients compared to other
working drugs. Some side effects include dizzy spells, insomnia, and drowsiness.

82. Baclofen
Dosage Forms & Strengths
Tablet 10mg , 20mg
intrathecal solution 50mcg/mL , 500mcg/mL
Dose :
Spasticity
1- <2 years: 10-15 mg PO divided q8hr; increase dose q3Days by 5-15 mg/day; 40 mg/day maximum
2- Age 2-8 years: 10-15 mg/day PO divided q8hr; increase dose q3Days by 5-15 mg/day; 40 mg/day maximum
3- >8 years: 10-15 mg/day PO divided q8hr; increase dose q3Days by 5-15 mg/day; 60 mg/day maximum
Spasticity (Intrathecal Administration)
Screening phase
Test bolus: 50 mcg intrathecal by barbotage over 1 minute; if inadequate response within 8 hours, 75 mcg 24 hours later; if still inadequate, 100 mcg 24
hours later
May start with 25 mcg dose for small patients
Patients who do not respond to a 100 mcg intrathecal bolus should not be considered candidates for an implanted pump for chronic infusion
Titration (after initial 24 hr)
Initial implant dose: 2 times screening dose that gave positive effect (or screening dose if effect lasted >8 hr) administer over 24 hr period
After the first 24 hours, the daily dose should be increased slowly by 5-15% only once q24hr, until desired clinical effect is achieved
Maintenance
Maintenance dose: Same as adult with spasticity of cerebral origin (average dose usually lower than adult)
Increase by 5-20% or decrease by 10-20% during periodic pump refills
Average daily dose for patients <12 years was 274 mcg/day, with a range of 24-1199 mcg/day

83. Botox
AbobotulinumtoxinA (Dysport®) - Upper and lower limb spasticity, cervical dystonia, and
moderate-to-severe glabellar lines in adults; it is also indicated for lower limb spasticity in
children aged 2 years or older
IncobotulinumtoxinA (Xeomin®) - Upper limb spasticity, cervical dystonia, blepharospasm,
moderate to severe glabellar lines, chronic sialorrhea
RimabotulinumtoxinB (Myobloc®) - Cervical dystonia

84. Botulinum Toxin = Botox
Intramuscular injection of a small amount of botulinum toxin type A into a muscle inhibits
the release of acetylcholine at the neuromuscular junction causing a chemical denervation.
The aim is to reduce excessive muscle activity without excessive weakness.
It is used to
1. Improve function
2. Cosmesis
3. For ease of nursing care.
Indications for use
When there is hypertonia (persistent or dynamic) in absence of significant fixed deformity).
Indications in upper limb
1. Persistent thumb in palm or thumb adduction
2. Wrist posture preventing effective hand use
3. Tight elbow flexion.
Indications in lower limb
1. A dynamic equinus persistent throughout the gait cycle
2. A dynamic knee flexion angle greater than 20° during the gait cycle or interfering with
gait
3. Significant scissoring and adduction at the hips.

85. Dosage of Botox
There is no fixed dose recommended. It depends on the size of
the muscle. The aim is to
get clinical response without excessive weakness.
Dose is around 1-2 U/kg (small muscles),
4-6 U/kg (large muscles); maximum 12 U/kg
(not to exceed 400 U/kg).
May need to be repeated every 4-6 months when effect wears
off.

86. Alcohol and Phenol Blocks
It is a cheaper alternative to botulinum toxin. Alcohol or phenol is
injected into the selected
peripheral neuron. It inhibits gamma motor neuron inhibition for 3-12
months. Common
nerves injected include obturator, posterior tibial and median.

87. Seizure Medication for Cerebral Palsy Patients
Estimates vary, but it is thought as many as 50% of those diagnosed with cerebral
palsy experience seizures. A 2008 CDC study, for instance, returned data indicating
41% of cerebral palsy patients evaluated in four US states had co-occurring
epilepsy. The condition occurs when excessive and irregular brain cell activity
causes electrical impulses to misfire.
When seizures happen, patients are typically affected for a short time, succumbing
to various symptoms, which can include loss of consciousness. There are often few
signs present between episodes. Certain medications can help manage CP-related
seizures:

88. • Depakene – Also known as “Valproate” or “Valreease”. This medication is not exactly known how it treats seizures, but has
been used to treat both petit mal and grand mal seizures.
• Petit mal seizures – Also known as “Absence” seizures involve quick, sudden lapses of consciousness. Petit mal seizures are
more commonly experienced with children. The most commonly known symptom may appear if the individual is staring into
space for a select few moments. This form of seizure rarely leads to physical damage.
• Grand mal seizures – Also known as a “General Tonic-Clonic Seizure”. Grand mal seizures are known to produce heavy muscle
contractions and frequent loss of consciousness. Caused by abmormal electrical activity in the brain, grand mal seizures usually
only happen once to an individual. Anti seizure medications and therapy are able to control this type of event from producing
itself again.
• Diazepam – Also known as “Valium” this drug is a sedative, anti-convulsant and muscle relaxant. Also used for anxiety and
minor surgeries, Diazepam is most commonly known to relieve seizures, relieve muscle spasms and spasticity for cerebral palsy
sufferers. Some side effects are drowsiness, depression, headaches, lethargy, confusion, and dizziness.
• Dilantin – Another medication used to prevent and control seizures. Dilantin can be given in multiple forms: by mouth,
injection, liquid, or intravenously. This drug is best known for helping to reduce and control seizures more affectively than
other medications on the market.
• Epival – Also known as “Divalproex”, another drug known to help control seizures for individuals with cerebral palsy. Epival is
given orally only, and should not be given to children under the age of 2.
• Klonopin – Also called Rivotril, is a “anticonvulsant” drug used to treat both forms of seizures. One benefit to this medication is
that you can combine with other seizure medications to improve overll effectiveness for individuals with cerebral palsy.
• Tegretol – Is known to treat all types of seizures along with pain caused by nerve damage or developmental disorders. Tegretol
is available in both tablet and liquid form to help relieve pain caused by neurological disorders. Some side effects include
swelling, increased blood pressure, and leg cramps.
• Zarontin – Also known as “Ethosuzimide” is primarily known to treat petit mal seizures only. Zarontin can be taken in both
capsule and liquid form which can help control or eliminate petit mal seizures completely. Common side effects include
lethargy, stomach aches, and confusion.

89. • Other Options for Cerebral Palsy Patients
• Effective cerebral palsy treatment uses medication in combination with therapy,
surgery and other forms of intervention. Because cerebral palsy treatment
begins at a very young age, some parents and doctors share concerns about the
side effects of long-term prescription drug therapy. A healthy diet, physical
therapy and other treatment options can reduce reliance on medication.
• Maintaining a special diet, rich in certain fats, may have anti-seizure benefits for
children with cerebral palsy. The ketogenic diet allows patients to consume few
carbohydrates, so the body must use fat to generate energy. The process creates
“ketones”, which protect the body from seizures. A high fiber diet, with adequate
fluid intake, is another example of preventative nutrition, which can keep
patients regular and in control.
• Various forms of therapy help cerebral palsy patients – without the use of
pharmacological agents. However, physical, occupational, and other therapies
may be more effective when paired with medication.

90. 6- Surgery
Selective posterior rhizotomy
• Achilles tendon lengthening
• Adductor tenotomy.
Surgery may be a large part of treatment for children with spastic cerebral palsy.
There are several types of surgeries that are used to correct joint dislocations,
shortened muscles and sensory impairments that hinder normal motor function.
Selective Doral Rhizotomy (SDR) is a common surgery associated with children who
have spastic cerebral palsy. The goal of this surgery is to relax the muscles and
improve mobility in various areas.

92. 11- Prevention
• Most cases of cerebral palsy can't be prevented, but you can lessen risks. If you're
pregnant or planning to become pregnant, you can take these steps to keep
healthy and minimize pregnancy complications:
• Make sure you're vaccinated. Vaccination against diseases such as rubella may
prevent an infection that could cause fetal brain damage.
• Take care of yourself. The healthier you are heading into a pregnancy, the less
likely you'll be to develop an infection that may result in cerebral palsy.
• Seek early and continuous prenatal care. Regular visits to your doctor during your
pregnancy are a good way to reduce health risks to you and your unborn baby.
Seeing your doctor regularly can help prevent premature birth, low birth weight
and infections.
• Practice good child safety. Prevent head injuries by providing your child with a car
seat, bicycle helmet, safety rails on beds and appropriate supervision.

93. 12- CP Prognosis
• Children with mild forms of cerebral palsy have a normal life expectancy. For
example, a two year-old child with mild palsy has a 99% chance of living to the
age of 20, compared with a patient who has severe disease, where the figure may
be as low as 40%.
• If a child is able to sit up unaided at the age of 2, they will eventually be able to
walk. If the child is incapable of sitting upright by the age of 4, there little chance
that he or she may walk.
• Children with impairment of movement of all four limbs (quadriplegia), severe
epilepsy, severe mental retardation and other medical complications like reflux
and pulmonary disease have a worse outcome.

94. Factors that affect life span :
1- key disabilities and the number of impairments
2- level of severity of impairments
3- level of restricted mobility
4- severity of feeding difficulties
5- presence of seizures
6- vision problems
7- intellectual capabilities and severity of mental retardation
8- respiratory functions

95. Improving quality of life and increasing life span
To improve the quality of life as well as increase life span in a child with
cerebral palsy certain goals need to be adopted. These include:
-improving mobility
-improving and maximizing independence in daily activities and fostering self
care
-controlling pain
-improving social and peer associations and interactions
-improve speech skills and communication
-treating associated conditions like epilepsy
-treating complications associated with cerebral palsy
-improving feeding abilities and nutrient intake
-improving learning potential
-improve quality of life

96. Life with CP
Every child with CP is different, and some require more treatment than
others. All parents should have the same goal when it comes to
treatment, which is to give their child the best life possible. There is help
available for parents exploring treatment options and the costs
associated with their child’s condition.

97. Sources :
• http://www.ncbi.nlm.nih.gov/pubmed/18282633
• http://ucp.org/wp-content/uploads/2013/02/cp-fact-sheet.pdf
• http://www.cdc.gov/ncbddd/cp/data.html
• http://www.aacpdm.org/
• http://www.healthychildren.org/English/health-issues/conditions/developmental-disabilities/pages/Cerebral-Palsy.aspx
• http://cpdailyliving.com/
• http://nichcy.org/disability/specific/cp
• http://www.cpirf.org/
• http://www.ucp.org/resources/one-stop-resource-guide
• http://www.thearc.org/
• http://www.nlm.nih.gov/medlineplus/cerebralpalsy.html

98. Thank You