CEREBRAL PALSY

I. DEFINITION/ DESCRIPTION

Cerebral palsy is one of the most complex of the common permanent disabling conditions.

 Cerebral palsy is a disorder of movement, muscle tone or posture that is caused by damage

that occurs to the immature, developing brain, most often before birth.

II. INCIDENCE

The incidence of cerebral palsy have not changed in more than 4 decades, despite significant
advances in the medical care of neonates.

 In developed countries, the overall estimated prevalence of cerebral palsy is 2-2.5 cases per
1000 live births.
 In the developing world, the prevalence of cerebral palsy is not well established but
estimates are 1.5-5.6 cases per 1000 live births.
 Lower socioeconomic status and male sex may be increased risk factors for cerebral palsy.
 Approximately 30-50% of patients with cerebral palsy have mental retardation, depending
on the type.
 Approximately 15-60% of children with cerebral palsy have epilepsy, and epilepsy is more
frequent in patients with spastic quadriplegia or mental retardation.

III. RISK FACTORS

Some events or medical problems during pregnancy can increase the risk of congenital cerebral
palsy. These risk factors include

 Low birth weight or preterm birth. Infants born preterm (defined as before 37 weeks of
pregnancy) and infants who weigh less than 5.5 pounds at birth are at greater risk of
cerebral palsy than are early term (defined as 37 weeks to 38 weeks of pregnancy) and full-
term (defined as 39 weeks to 40 weeks of pregnancy) infants and those who are heavier at
birth. The earlier the birth and the lower the infant’s birthweight, the greater the risk.
 Multiple gestations. Twins, triplets, and other multiple births are at higher risk of cerebral
palsy. The risk is also greater for an infant whose twin or triplet dies before or shortly after
birth.
 Infertility treatments. Infants born from pregnancies resulting from the use of certain
infertility treatments are at higher risk for cerebral palsy than are infants born from
pregnancies not related to infertility treatments. Much of this increased risk may be due to
the fact that infertility treatments are more likely to result in preterm delivery and multiple
gestations.
 Infections during pregnancy. Toxoplasmosis, rubella (German measles), cytomegalovirus,
and herpes can infect the womb and placenta, leading to brain damage in the fetus.
 Fever during pregnancy. Sometimes fever in the mother during pregnancy or delivery can
lead to brain damage in the fetus, resulting in cerebral palsy.
 Blood factor between mother and fetus does not match. Those who have a certain protein
found on red blood cells—abbreviated Rh—are Rh positive; those who do not have the
protein are Rh negative. If a mother’s Rh factor is different from that of the fetus, her
immune system may attack the blood cells of the fetus, including blood cells in the brain,
which can lead to brain damage.
  Exposure to toxic chemicals. If a mother is exposed to a toxic substance, such as high levels
of methyl mercury (found in some thermometers and in some seafood), during pregnancy
the fetus is at higher risk of cerebral palsy.
 Maternal medical conditions:
o Abnormal thyroid function
o Intellectual and developmental disability
o Too much protein in the urine
o Seizures
 Complicated labor and delivery. Infant heart or breathing problems during labor and
delivery and immediately after birth increase the risk of cerebral palsy.
 Jaundice (pronounced JAWN-dis). Jaundice, which causes an infant’s skin, eyes, and mouth
to turn a yellowish color, can be a sign that the liver is not working normally. Jaundice occurs
when a substance called bilirubin (pronounced BIL-uh-roo-bin) builds up faster than the liver
can clear it from the body. This condition is common and is usually not serious. However, in
cases of severe, untreated jaundice, the excess bilirubin can damage the brain and cause
cerebral palsy.
 Seizures. Infants who have seizures are more likely to be diagnosed with cerebral palsy later
in childhood.

IV. MANIFESTATIONS

Several major types of cerebral palsy occur; each has distinctive clinical manifestations.

 Spastic type- is the most common type and is characterized by a hyperactive stretch reflex,
clonus (rapid involuntary muscle contraction and relaxation, contractures, scissoring (when
scissoring is present, the child’s legs are crossed and the toes are pointed down.
 Athetoid type- is marked by involuntary, uncoordinated motion with varying degrees of
muscle tension; children with this disorder are constantly in motion, and the whole body is
in a state of slow, writhing muscle contractions whenever voluntary movement is
attempted.
 Ataxic type- is essentially a lack of coordination caused by disturbances in the kinesthetic
and balance senses; ataxic cerebral palsy may not be diagnosed until the child starts to walk;
the gait is awkward and wide-based.
 Rigidity type- is uncommon and is characterized by rigid postures and lack of active
movement.
 Mixed type- Children with signs of more than one type of cerebral palsy, turned mix type,
are usually disabled; the disorder may have been caused by postnatal injury.

Signs of cerebral palsy include the following:

 Developmental delay. History of gross motor developmental delay in the first year of life.
 Abnormal muscle tone. The most frequently observed symptom; the child may present as
either hypotonic or, more commonly, hypertonic, with either decreased or increased
resistance to passive movements, respectively; children with cerebral palsy may have an
early period of hypotonia followed by hypertonia; a combination of axial hypotonia and
peripheral hypotonia is indicative of a central process.
 Hand preference. Definite hand preference before age 1 year: A red flag for possible
hemiplegia.
 Problems in crawling. Asymmetrical crawling or failure to crawl.
  Growth disturbance. There is a growth disturbance especially in failure to thrive.
 Increased reflexes. Indicating the presence of an upper motor neuron lesion; this condition
may also present as the persistence of primitive reflexes.
 Problems in reflexes. Underdevelopment or absence of postural or protective reflexes.

V. MANAGEMENT
 LAB EXAM / DIAGNOSTIC PROCEDURE
The diagnosis of cerebral palsy is generally made based on the clinical picture; there are no definitive
laboratory studies for diagnosing the condition, only studies, including the following, to rule out
other symptom causes:

 Thyroid function studies. Abnormal thyroid function may be related to abnormalities in

muscle tone or deep tendon reflexes or to movement disorders.
 Lactate and pyruvate levels. Abnormalities may indicate an abnormality of energy
metabolism (ie, mitochondrial cytopathy).
 Ammonia levels. Elevated ammonia levels may indicate liver dysfunction or urea cycle
defect.
 Organic and amino acids. Serum quantitative amino acid and urine quantitative organic acid
values may reveal inherited metabolic disorders.
 Chromosomal analysis. Chromosomal analysis, including karyotype analysis and specific DNA
testing, may be indicated to rule out a genetic syndrome if dysmorphic features or
abnormalities of various organ systems are present.
 Cerebrospinal protein. Levels may assist in determining asphyxia in the neonatal period;
protein levels can be elevated, as can the lactate-to-pyruvate ratio.
 Cranial ultrasonography. Can be performed in the early neonatal period to delineate clear-
cut structural abnormalities and show evidence of hemorrhage or hypoxic-ischemic injury.
 Computed tomography scanning of the brain. In infants, helps to identify congenital
malformations, intracranial hemorrhage, and periventricular leukomalacia or early
craniosynostosis.
 Magnetic resonance imaging of the brain. The diagnostic neuroimaging study of choice
because this modality defines cortical and white matter structures and abnormalities more
clearly than does any other method; MRI also allows for the determination of whether
appropriate myelination is present for a given age.

 TREATMENT/ PHARMACOLOGIC MANANGEMENT

Treatment of cerebral palsy focuses on helping the child to make the best use of residual abilities
and achieve maximum satisfaction and enrichment in life.

 Physical therapy. Methods must be suited to the needs of each child, as well as the general
needs arising from the condition; these methods are based on principles of conditioning,
relaxation, use of residual patterns, stimulation of contraction, and relaxation of antagonistic
muscles.
 Orthopedic management. Braces are used as supportive and control measures to facilitate
muscle training, to reinforce weak or paralyzed muscles, or to counteract the pull of
antagonistic muscles; orthopedic surgery sometimes is used to improve function and to
correct deformities, such as the release of contractures and the lengthening of tight heel
cords.
  Technological aids. Devices range from simple items, such as wheelchairs and specially
constructed toilet seats, to completely electronic cottages furnished with a computer, a tape
recorder, a calculator, and other equipment that facilitates independence and useful study
or work; feeding aids such as spoons with enlarged handles for easy grasping or with bent
handles that allow the spoon to be brought easily to the mouth.

Pharmacologic Management

Numerous medications, including the following, may relieve the movement difficulties associated
with cerebral palsy:

 Botulinum toxin with or without casting. Botulinum toxin (Botox) type A may reduce
spasticity for 3-6 months and should be considered for children with cerebral palsy with
spasticity.
 Phenol intramuscular neurolysis. This agent can be used for some large muscles or when
several muscles are treated, but phenol therapy is permanent.
 Antiparkinsonian, anticonvulsant, antidopaminergic, and antidepressant agents. Although
antiparkinsonian drugs (eg, anticholinergic and dopaminergic drugs) and antispasticity
agents (eg, baclofen) have primarily been used in the management of
dystonia, anticonvulsants, antidopaminergic drugs, and antidepressants have also been
tried.

 NURSING RESPONSIBILITIES
1. Ensure therapeutic communication. To ease the change of environment, the nurse needs to
communicate with the family to learn as much as possible about the child’s activities at
home.
2. Enhance self-esteem. Assist the patient to increase his/her personal judgment of self-worth.
3. Provide emotional support. Provide of reassurance, acceptance, and encouragement during
times of stress.
4. Strengthen family support. Utilize the family’s strengths to influence patient’s health in a
positive direction.
5. Prevent injury. Prevent physical injury by providing the child with a safe environment,
appropriate toys, and protective gear (helmet, kneepads) if needed.
6. Prevent deformity. Prevent physical deformity by ensuring the correct use of prescribed
braces and other devices and by performing ROM exercises.
7. Encourage mobility. Promote mobility by encouraging the child to perform age-and
condition-appropriate motor activities.
8. Increase oral fluid intake. Promote adequate fluid and nutritional intake.
9. Manage sleep and rest periods. Foster relaxation and general health by providing rest
periods.
10. Enhance self-care. Encourage self-care by urging the child to participate in activities of daily
living (ADLs) (e.g. using utensils and implements that are appropriate for the child’s age and
condition).
11. Facilitate communication. Talk to the child deliberately and slowly, using pictures to
reinforce speech when needed; encourage early speech therapy to prevent poor or
maladaptive communication habits; and provide means of articulate speech such as sign
language or a picture board.
 12. Enforce therapeutic measures. Assist in multidisciplinary therapeutic measures designed to
establish locomotion, communication, and self-help, gain optimal appearance and
integration of motor functions.

REFERENCES:

Retrieved from www.nurseslab/cerebral-palsy, retrieved on February 1, 2020