Valmores, Maristela Denise S.

PEDIA- NURSING

BSN 2B May 20, 2023

A. NEURO
CEREBRAL PALSY

I. INTRODUCTION OF THE DISEASE

• The term cerebral palsy (CP) was originally coined more than a century ago and loosely
translates as "brain paralysis." However, cerebral palsy is not a single diagnosis but an "umbrella"
term describing motor or postural abnormalities noted during early development due to
nonprogressive brain lesions. Cerebral palsy has been described as follows:
• "A group of disorders of the development of movement and posture causing activity limitations
that are attributed to non-progressive disturbances that occurred in the developing fetal or
infant brain. The motor disorders of cerebral palsy are often accompanied by disturbances of
sensation, cognition, communication, perception, and/or behavior and/or a seizure disorder."
• Cerebral palsy is the leading cause of childhood disability affecting function and development.
The brain lesions that cause cerebral palsy occur from the fetal or neonatal period to up to age 3
years. Although insults to the brain that occur after age 3 years through adulthood may manifest
clinically similar to cerebral palsy, by definition, these clinical scenarios are not described as
cerebral palsy. In addition, despite the fact that the lesion to the developing brain occurs before
age 3 years, the diagnosis of cerebral palsy may not be made until after that time. Some
authorities advocate not making a definitive diagnosis in selected cases until age 5 years or later.
This approach allows the clinical picture to be clear and potentially allows the exclusion of
progressive diseases. In addition, some children have been diagnosed with cerebral palsy at an
early age, only to have the symptoms resolve later.
• Approximately 30–50% of patients with cerebral palsy have mental retardation, depending on
the type. However, because of oromotor, fine motor, and gross motor difficulties,
communication in these patients may be impaired and expression of intellectual capacity may be
limited. However, if cerebral palsy is approached in a multidisciplinary manner, with physical,
occupational, and nutritional therapy to maximize rehabilitative efforts, patients can be more
fully integrated academically and socially.
• Approximately 15–60% of children with cerebral palsy have epilepsy, and epilepsy is more
frequent in patients with spastic quadriplegia or mental retardation.
II. ANATOMY OF PHYSIOLOGY
III. PATHOPHYSIOLOGY
Preterm infants

The premature neonatal brain is susceptible to two main pathologies: intraventricular hemorrhage (IVH)
and periventricular leukomalacia (PVL). Although both pathologies increase the risk of CP, PVL is more
closely related to CP and is the leading cause in preterm infants. The term PVL describes white matter in
the periventricular region that is underdeveloped or damaged (“leukomalacia”). Both IVH and PVL cause
CP because the corticospinal tracts, composed of descending motor axons, course through the
periventricular region.

Intraventricular hemorrhage (IVH)

IVH describes bleeding from the subependymal matrix (the origin of fetal brain cells) into the ventricles
of the brain. The blood vessels around the ventricles develop late in the third trimester, thus preterm
infants have underdeveloped periventricular blood vessels, predisposing them to increased risk of IVH.
The risk of CP increases with the severity of IVH.
Periventricular leukomalacia (PVL)

IVH is a risk factor for PVL, but PVL is a separate pathological process. The pathogenesis of PVL arises
from two important factors: ischemia/hypoxia and infection/inflammation.

Ischemia/hypoxia: The periventricular white matter of the neonatal brain is supplied by the distal
segments of adjacent cerebral arteries. Although collateral blood flow from two arterial sources protects
the area when one artery is blocked (e.g., thromboembolic stroke), this watershed zone is susceptible to
damage from cerebral hypoperfusion (i.e., decreased cerebral blood flow in the brain overall). Since
preterm and even term neonates have low cerebral blood flow, the periventricular white matter is
susceptible to ischemic damage. Autoregulation of cerebral blood flow usually protects the fetal brain
from hypoperfusion, however, it is limited in preterm infants due to immature vasoregulatory
mechanisms and underdevelopment of arteriolar smooth muscles.

Infection and inflammation: This process involves microglial (brain macrophage) cell activation and
cytokine release, which causes damage to a specific cell type in the developing brain called the
oligodendrocyte. The oligodendrocytes are a type of supportive brain cell that wraps around neurons to
form the myelin sheath, which is essential for white matter development. Intrauterine infections activate
the fetal immune system, which produces cytokines (e.g., interferon γ and TNF-α) that are toxic to
premyelinating oligodendrocytes. Infections also activate microglial cells, which release free radicals.
Premyelinating oligodendrocytes have immature defences against reactive oxygen species (e.g., low
production of glutathione, an important antioxidant). IVH is hypothesized to cause PVL because iron-rich
blood causes iron-mediated conversion of hydrogen peroxide to hydroxyl radical, contributing to
oxidative damage.

Excitotoxicity is a process where increased extracellular glutamate levels stimulate oligodendrocytes to

increase calcium influx, which stimulates reactive oxidative species release. Glutamate is increased
because hypoxia causes white matter cells to reduce reuptake of glutamate due to lack of energy to
operate glutamate pumps. Glutamate is also released from microglial cells during the inflammatory
response.

Term infants

Circulation and autoregulation of cerebral blood flow are similar to that of an adult in a full term infant.
Ischemic and hemorrhagic injuries tend to follow similar patterns of those in adults:

Watershed areas where the three major cerebral arteries end in the cortex. This is the most common
area of injury.

Basal ganglia damage can cause extrapyramidal or dyskinetic CP.

IV. SIGNS AND SYMPTOMS

- Signs of cerebral palsy include the following:

• History of gross motor developmental delay in the first year of life

•
Common clinical presentation:

• Delayed motor milestones

• Asymmetric movement patterns
• Abnormal muscle tone
• Associated problems (poor feeding and irritability)

Signs and symptoms according to motor disorder

Spastic Cerebral Palsy

• Increased deep tendon reflexes
• Tremors
• Muscular hypertonicity
• Weakness
• Characteristic scissors gait with toe-walking
Athetoid or dyskinetic Cerebral Palsy
• Abnormally slow, writhing movements of the hands, feet, arms, or legs that are
exacerbated during periods of stress and absent during sleep
Ataxic Cerebral palsy
• Wide-based gait
• Intention tremors that complicate performance of daily activities requiring fine-motor
function

• 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 hypertonia is
indicative of a central process.

• Definite hand preference before age 1 year: A "red flag" for possible hemiplegia

• Asymmetrical crawling or failure to crawl

• Growth disturbance, especially 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
• Underdevelopment or absence of postural or protective reflexes

• The patient’s overall gait pattern should be observed, and each joint in the lower and upper
extremities should be assessed for signs of cerebral palsy, including the following:

• Hip: Excessive flexion, adduction, and femoral anteversion make up the predominant motor
pattern; scissoring of the legs is common in spastic cerebral palsy

• Knee: Flexion and extension with valgus or varus stress occur

• Foot: Equinus, or toe walking, and varus or valgus of the hindfoot is common in cerebral palsy

V. MEDICAL MANAGEMENT

Laboratory studies

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,
rule out other symptom causes:

• Thyroid function studies: Abnormal thyroid function may cause abnormalities in muscle
tone or deep tendon reflexes or 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 support asphyxia in the neonatal period; protein
levels can be elevated, as can the lactate-to-pyruvate ratio

•
Imaging studies
 • Cranial imaging studies to help evaluate brain damage and identify persons who are at
risk for cerebral palsy include the following:

• 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: Is particularly helpful for imaging of blood,
calcification, and bone, and may be performed quickly in a sleeping infant, but emits
radiation. 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 any other method; MRI also allows for determining whether
appropriate myelination is present for a given age. However, sedation in a young child is
required to prevent motion artifacts.

Other

Additional studies in cerebral palsy can include the following:

• Electroencephalography: Important in the diagnosis of seizure disorders

• Electromyography and nerve conduction studies: Helpful when a muscle or nerve

disorder is suspected

VI. SURGICAL MANAGEMENT

Surgical treatments used in patients with cerebral palsy include the following:

• Intrathecal baclofen pump insertion: To treat spasticity and/or dystonia

• Selective dorsal rhizotomy: To treat velocity-dependent spasticity in the lower extremities
• Stereotactic basal ganglia surgery: May improve rigidity, choreoathetosis, and tremor
• Orthopedic surgical intervention: To treat scoliosis, joint contractures or dislocation
 VII. NURSING MANAGEMENT

The child with cerebral palsy may be seen in the healthcare setting at any age level.

Nursing Assessment

Assessment of the child with cerebral palsy includes the following methods:

• Interview. Interview and observe the child and the family to determine the child’s needs, the
level of development, and the stage of family acceptance and to set realistic long-range goals.
• History. Patient history and maternal history often reveals the possible cause of cerebral palsy.
• Neurologic examination. Neurologic examination may reveal hyperactive deep tendon reflexes
and increased stretch reflexes, rapid alternating muscle contraction and relaxation, and
weakness.

Nursing Diagnosis

Based on the assessment data, the major nursing diagnoses include:

• Risk for injury related to spasms, uncontrolled movements, and seizures.

• Impaired physical mobility related to spasms and muscle weakness.
• Changes in growth and development related to neuromuscular disorders.
• Impaired verbal communication related to difficulty in articulation.
• Risk for aspiration related to neuromuscular disorders.
• Disturbed thought processes related to cerebral injury, learning disabilities.
• Self-care deficit related to muscle spasms, increased activity, cognitive changes.
• Deficient knowledge related to home care and therapeutic needs.
 VIII. DRUG STUDY- CHOOSE AT LEAST THREE DRUGS

DRUG DOSAGE ADVERSE WARNINGS ADMINISTRATION

INDICATION EFFECTS

DIAZEPAM tablet: Schedule Advise both IV administration

IV Frequency Not patients and
Also known as 2mg Defined caregivers about IM administration
“Valium” this 5mg Hypotension risks of respiratory
drug is a 10mg Fatigue depression and Oral
sedative, anti- Muscle weakness sedation when
convulsant and oral solution: Respiratory diazepam is used Rectal
muscle relaxant. Schedule IV depression with opioids; administration
Also used for 1mg/1mL Urinary retention advise patients
anxiety and 5mg/mL Blurred vision not to drive or Intranasal
minor surgeries, rectal gel Dysarthria operate heavy administration
Diazepam is (Diastsat Headache machinery until
most commonly Acudial): Skin rash the effects of
known to Schedule IV Changes in concomitant use
relieve seizures, 2.5mg/0.5mL salivation with the opioid
relieve muscle 10mg/2mL Drowsiness have been
spasms and 20mg/4mL determined
spasticity for injectable Serious
cerebral palsy solution: Neutropenia Use caution in
sufferers. Schedule IV Jaundice COPD, sleep
5mg/mL Local effects: apnea,
intramuscular Pain, swelling, renal/hepatic
device: Schedule thrombophlebitis, disease, open-
IV carpal tunnel angle glaucoma
5mg/mL syndrome, tissue (questionable),
intranasal spray necrosis depression,
(Valtoco): Phlebitis if too suicide ideation,
Schedule IV rapid IV push impaired gag
5mg/0.1mL reflex, history of
7.5mg/0.1mL drug abuse, or
10mg/0.1Ml obese patients
(prolonged action
when
discontinued)
DRUG DOSAGE ADVERSE WARNINGS ADMINISTRATION
INDICATION EFFECTS

DILANTIN capsule, Frequent: Risk of IV administration

immediate- hypotension and
This medicine is release Drowsiness arrhythmias with IM administration
used to control 30mg infusion rates that
seizures. 100mg Fatigue exceed 50 mg/min
capsule, in adults and 1-3
extended- Ataxia mg/kg/min (or 50
release mg/min,
100mg Irritability whichever is
200mg slower) for
300mg Headache pediatric patients
tablet Careful cardiac
50mg Restlessness monitoring is
oral suspension needed during and
125mg/5mL Slurred speech after IV
injectable administration
solution Nervousness These events have
50mg/mL also been
Nystagmus reported at or
below 50 mg/min
Dizziness Reduce infusion
rate or
discontinuation
may be needed
DRUG DOSAGE ADVERSE WARNINGS ADMINISTRATION
INDICATION EFFECTS

LORAZEPAM tablet: Schedule Dizziness Advise both IV administration

IV Unsteadiness patients and
Lorazepam is 0.5mg Weakness caregivers about IM administration
used to relax 1mg Fatigue the risks of
muscles or 2mg Drowsiness respiratory Oral administration
relieve muscle Amnesia depression and
spasms. It may oral concentrate: Confusion sedation when
also be used if Schedule IV Disorientation lorazepam is used
your child is 2mg/mL Depression with opioids;
anxious, has Suicidal advise patients
seizures, or has injectable ideation/attempt not to drive or
nausea and solution: Vertigo operate heavy
vomiting Schedule IV Ataxia machinery until
because of 2mg/mL Sleep apnea the effects of
chemotherapy. 4mg/mL Asthenia concomitant use
You may also Extrapyramidal with the opioid
hear lorazepam symptoms have been
called by its Respiratory determined
brand name, depression Use of
Ativan. Tremor benzodiazepines,
including
lorazepam, both
used alone and in
combination with
other CNS
depressants, may
lead to potentially
fatal respiratory
depression
Not
recommended for
use in patients
with primary
depressive
disorder or
psychosis
IX. NCP- 1 ACTUAL AND 1 POTENTIAL
NURSING DIAGNOSIS INTERVENTIONS RATIONALE DESIRED OUTCOMES
Monitor and keep track
Impaired Verbal of the patient's To help establish The child will be able to
Communication related cognitive and baseline, as well as communicate
to neurologic developmental short-term and long- effectively with the
impairment secondary progress. Look for term goals. caregiver about his or
to cerebral palsy as verbal and nonverbal her needs.
evidenced by difficulty signs that the
of establishing verbal youngster uses to
communication and communicate his or her
difficulty vocalizing wants.
word
Establish a setting that Distractions are easier
is peaceful, quiet, well- to avoid when one's
lit, and supportive to surroundings are free
productive discussion. of distracting stimuli.
This will aid the child in
concentrating on
communicating his or
her requirements or
wants.

When conversing with Using simple words and

the child, speak clearly speaking clearly can
and simply while help the patient
maintaining a low voice understand what is
volume. being said.

Educate the patient on A whiteboard with a

how to use alternative marker, flashcards with
ways of pictures and simple
communication. words, as well as hand
gestures, can all be
used to enhance
communication
between the child and
the parent or caregiver.

Refer the child to a A speech therapist can

speech therapist as help improve the
needed. coordination of the
tongue and lips for a
clearer speech.