Cerebral Palsy Nursing Care Planning and Management: Study Guide

Cerebral palsy is a non-progressive disorder of movement, muscle tone, and posture caused by damage to the immature, developing brain, most often before birth. It is one of the most common childhood motor disabilities, ranging widely in severity and type (spastic, dyskinetic, ataxic). The injury does not worsen, but its effects ripple through mobility, communication, feeding, and self-care. Your work is to maximize residual function, prevent deformity and injury, support feeding and communication, and partner with the family.

What is Cerebral Palsy?

Cerebral palsy is one of the most complex permanent disabling conditions. It is a disorder of movement, muscle tone, or posture caused by damage to the immature, developing brain, most often before birth. Much of the research focuses on adapting biomedical technology to help patients manage daily living and reach maximum function and independence.

Classification

Several types occur, each with distinct manifestations.

• Spastic type. The most common type, marked by a hyperactive stretch reflex, clonus, contractures, and scissoring (legs crossed, toes pointed down).
• Athetoid type. Involuntary, uncoordinated motion with varying muscle tension; the child is constantly in slow, writhing muscle contraction whenever voluntary movement is attempted.
• Ataxic type. A lack of coordination from disturbed kinesthetic and balance senses; often not diagnosed until the child walks, with an awkward, wide-based gait.
• Rigidity type. Uncommon, with rigid postures and lack of active movement.
• Mixed type. Signs of more than one type; usually severely disabling and often caused by postnatal injury.

Pathophysiology

Because prenatal and neonatal brain development is so complex, injury or abnormal development can occur at any point, which produces the varied presentations (genetic, toxic, infectious, or vascular in origin).

• Injury before the 20th week of gestation can cause a neuronal migration deficit.
• Injury between the 26th and 34th weeks can cause periventricular leukomalacia (foci of coagulative necrosis in the white matter beside the lateral ventricles).
• Injury between the 34th and 40th weeks can cause focal or multifocal cerebral injury.

Vascular injury depends on the vascular distribution to the brain, the efficiency and regulation of cerebral blood flow, and the biochemical response of brain tissue to reduced oxygenation. Before term, fetal circulation tends to underperfuse the periventricular white matter, and hypoperfusion can cause germinal matrix hemorrhage or periventricular leukomalacia. Between weeks 26 and 34, the periventricular white matter near the lateral ventricles is most vulnerable; because those fibers control motor function and tone in the legs, injury produces spastic diplegia (spasticity and weakness of the legs, with or without lesser arm involvement). At term, when circulation resembles the adult pattern, vascular injury tends to fall in the middle cerebral artery distribution, producing spastic hemiplegic cerebral palsy. The term brain is also vulnerable to hypoperfusion of cortical watershed areas, producing spastic quadriplegic cerebral palsy. Basal ganglia involvement produces extrapyramidal or dyskinetic cerebral palsy.

Statistics and Incidences

The incidence of cerebral palsy has not changed in more than 4 decades despite major advances in neonatal care. In developed countries, the estimated prevalence is 2-2.5 cases per 1000 live births. In the developing world it is less well established, with estimates of 1.5-5.6 cases per 1000 live births. Lower socioeconomic status and male sex may raise the risk. Approximately 30-50% of patients have mental retardation depending on type, and 15-60% have epilepsy, which is more frequent with spastic quadriplegia or mental retardation.

Causes

The cause often cannot be identified, but several are possible. Damage to the motor areas of the brain, usually in the fetal or perinatal period and especially in premature infants, is the central mechanism. Anything that interrupts oxygen supply to the brain (placental separation, cord compression, bleeding) can cause it. Maternal infection during the prenatal period (cytomegalovirus, toxoplasmosis, rubella) and prenatal nutritional deficiencies affecting brain growth are contributors. Kernicterus causes brain damage from jaundice due to Rh incompatibility. Teratogens such as drugs and radiation can cause it, and prematurity predisposes the neonate to cerebral hemorrhage through immature blood vessels.

Clinical Manifestations

• Developmental delay. Gross motor delay in the first year of life.
• Abnormal muscle tone. The most common sign; the child may be hypotonic or, more often, hypertonic. Some have an early hypotonic period followed by hypertonia, and combined axial and peripheral hypotonia points to a central process.
• Hand preference. Definite hand preference before age 1 year is a red flag for hemiplegia.
• Crawling problems. Asymmetrical crawling or failure to crawl.
• Growth disturbance. Especially failure to thrive.
• Increased reflexes. Signaling an upper motor neuron lesion, sometimes with persistence of primitive reflexes.
• Reflex problems. Underdevelopment or absence of postural or protective reflexes.

Assessment and Diagnostic Findings

Diagnosis is clinical. There are no definitive lab studies, only tests to rule out other causes.

• Thyroid function studies. Abnormal thyroid function can affect tone, deep tendon reflexes, or movement.
• Lactate and pyruvate levels. Abnormalities suggest a disorder of energy metabolism (mitochondrial cytopathy).
• Ammonia levels. Elevation suggests liver dysfunction or a urea cycle defect.
• Organic and amino acids. Serum amino acid and urine organic acid values can reveal inherited metabolic disorders.
• Chromosomal analysis. Karyotype and specific DNA testing rule out a genetic syndrome when dysmorphic features or multi-organ abnormalities are present.
• Cerebrospinal protein. Levels help determine neonatal asphyxia; protein and the lactate-to-pyruvate ratio can be elevated.
• Cranial ultrasonography. Early neonatal imaging for clear structural abnormalities, hemorrhage, or hypoxic-ischemic injury.
• CT of the brain. In infants, identifies congenital malformations, intracranial hemorrhage, periventricular leukomalacia, or early craniosynostosis.
• MRI of the brain. The neuroimaging study of choice; it defines cortical and white matter structures best and shows whether myelination is appropriate for age.

Medical Management

Treatment helps the child make the best use of residual abilities and reach maximum function and satisfaction. Physical therapy is tailored to each child, built on conditioning, relaxation, use of residual patterns, stimulation of contraction, and relaxation of antagonistic muscles. Braces support and control muscle training, reinforce weak muscles, and counteract antagonistic pull; orthopedic surgery corrects deformities such as contracture release and heel-cord lengthening. Technological aids range from wheelchairs and adapted toilet seats to electronic setups and feeding aids such as enlarged- or bent-handle spoons that promote independence.

Pharmacologic Therapy

Several medications can relieve the movement difficulties.

• Botulinum toxin. Botulinum toxin (Botox) type A, with or without casting, may reduce spasticity for 3-6 months and should be considered for spasticity in cerebral palsy.
• Phenol intramuscular neurolysis. Useful for large muscles or when several muscles are treated, but the effect is permanent.
• Antiparkinsonian, anticonvulsant, antidopaminergic, and antidepressant agents. Antiparkinsonian drugs (anticholinergic and dopaminergic) and antispasticity agents (baclofen) are used mainly for dystonia, while anticonvulsants, antidopaminergic drugs, and antidepressants have also been tried.

Nursing Management

The child with cerebral palsy may present at any age.

Nursing Assessment

• Interview. Interview and observe the child and family to determine needs, developmental level, and stage of family acceptance, and to set realistic long-range goals.
• History. Patient and maternal history often reveal the cause.
• Neurologic examination. May show hyperactive deep tendon reflexes, increased stretch reflexes, rapid alternating contraction and relaxation, and weakness.

Nursing Diagnosis

• 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 with articulation.
• Risk for aspiration related to neuromuscular disorders.
• Disturbed thought processes related to cerebral injury and learning disabilities.
• Self-care deficit related to muscle spasms, increased activity, and cognitive changes.
• Deficient knowledge related to home care and therapeutic needs.

Nursing Care Planning and Goals

• Verbalize feelings related to self-esteem and express positive feelings about himself.
• Develop adequate coping mechanisms.
• Demonstrate knowledge of the condition and treatment plan.
• Achieve age-appropriate growth, behaviors, and skills to the fullest extent possible.
• Maintain optimal functioning within the limits of visual or hearing impairment.
• Remain oriented to person, place, time, and situation.
• Consume adequate daily calories.
• Maintain joint mobility and ROM, and swallow without pain or aspiration.
• Family members discuss how the condition has affected daily life, and parents identify realistic goals matched to the child's abilities.

Nursing Interventions

• Therapeutic communication. Communicate with the family to learn the child's home activities and ease the change of environment.
• Enhance self-esteem. Help the child build personal judgment of self-worth.
• Emotional support. Provide reassurance, acceptance, and encouragement during stress, and use the family's strengths to influence health positively.
• Prevent injury. Provide a safe environment, appropriate toys, and protective gear (helmet, kneepads) as needed.
• Prevent deformity. Ensure correct use of prescribed braces and devices and perform ROM exercises.
• Encourage mobility. Promote age- and condition-appropriate motor activity.
• Nutrition. Promote adequate fluid and nutritional intake.
• Rest. Provide rest periods to foster relaxation and general health.
• Self-care. Encourage participation in ADLs with age- and condition-appropriate utensils and implements.
• Communication. Speak deliberately and slowly, use pictures to reinforce speech, encourage early speech therapy, and provide sign language or a picture board.
• Therapeutic measures. Assist multidisciplinary efforts to establish locomotion, communication, and self-help and to optimize motor function.

Evaluation

The plan succeeds when the child verbalizes feelings about self-esteem, develops coping mechanisms, demonstrates knowledge of the condition and plan, achieves age-appropriate growth and skills, maintains function within sensory limits, stays oriented, consumes adequate daily calories, maintains joint mobility and ROM, swallows without pain or aspiration, and the family discusses the condition's impact and sets realistic goals.

Documentation Guidelines

• Individual risk factors and current physical findings.
• Availability and use of resources.
• Level of function and ability to participate in desired activities.
• Meaning of nonverbal cues and level of anxiety.
• Family support and participation.
• Plan of care and teaching plan.
• Responses to interventions, teaching, and actions performed.
• Specific actions and changes made.
• Attainment of or progress toward desired outcomes.
• Modifications to the plan of care.