Cerebral palsy (CP) is a syndrome of permanent motor impairment (posture and movement) that results from nonprogressive lesions to the developing brain.
- 2.0–3.5 per 1,000 live births
- Boy-to-girl ratio of 1.4:1
- Prenatal events cause the majority of cases.
- Prevalence is inversely proportional to gestational age and birth weight:
- Prevalence is higher in preterm children.
- Infants < 28 weeks at highest risk
- Infants < 1,500 grams have 5%–15% risk.
- The most common form is spastic diplegia (35%), a form of paralysis that affects symmetrical body parts (i.e., both legs or both arms).
- Risk factors for CP:
- Placental abnormalities
- Major and minor birth defects
- Meconium aspiration
- Emergency cesarean section
- Birth asphyxia
- Neonatal seizures
- Respiratory distress syndrome
- Intrauterine and neonatal infections
- Multiple-gestation births (twins, triplets, etc.)
- Intrauterine growth restriction/low birth weight
- Maternal substance abuse
- Perinatal hypoglycemia
- Genetic susceptibility
- CNS injury of many types can lead to CP.
- CP is nonprogressive.
- Can occur in any of the following developmental periods:
- Congenital brain malformations
- Intrauterine infections
- Intrauterine stroke
- Chromosomal abnormalities
- Hypoxic-ischemic insults
- CNS infections
- Head trauma
- CNS infections
- Anoxic insults
- May be accompanied by:
- Sensory, cognitive, communication, and behavioral disturbances
- Musculoskeletal impairment
- According to muscle tone:
- Spastic (hypertonic)
- Flaccid (hypotonic)
- Dystonic (athetoid)
- According to distribution:
- Diplegia (paralysis of both legs or both arms)
- Hemiplegia (1 side of the body is affected)
- Quadriplegia (all extremities are affected)
- According to presumed time of injury:
The ultimate cause of CP is injury to a child’s CNS during its embryological or perinatal development. The pathophysiology of this insult varies based on its etiology.
|CP subtype||Etiologies||MRI findings|
|Spastic quadriplegia (20%)|
|Spastic diplegia (35%)|
|Extrapyramidal (athetoid, dyskinetic) (15%)|
- Preterm birth
- Low birth weight
- Complications during pregnancy
- Infections or exposure to infections during pregnancy
- Cognitive impairment (seen in approximately 50%): degree of disability correlates with severity of motor handicap
- Developmental delay: delay in gross motor milestones (most commonly, not sitting up by 8 months, not walking by 16 months)
- Behavioral abnormalities:
- Excessive irritability or docility
- Autism spectrum disorder
- Obsessive compulsive behavior
- Disability is static (progressive CNS lesions must be excluded).
- Visual and/or hearing impairment
- 35% have a visual problem.
- Delay in disappearance of primitive reflexes
- Chronic pain
- Sleep dysfunction
- Frequent lung infections (aspiration pneumonia)
- Restrictive lung disease due to poor tone and scoliosis
- Feeding intolerance (often leads to failure to grow)
- Chronic constipation
- Gastroesophageal reflux
- Voiding difficulty due to spasticity or hypotonia of bladder muscles
- Frequent urinary tract infections (UTIs)
- Frequent fractures due to osteopenia
- Hip dysplasia
- Spasticity (scissoring of the legs)
- Choreoathetosis (movement disorder causing involuntary twitching or writhing)
- Diplegic gait in cases with a diplegic distribution
- Early sign of spastic diplegia, dragging legs when crawling (e.g., “commando crawl”)
- Decreased spontaneous movements on the affected side
- Feet in a position of equinovarus:
- Also known as clubfoot
- Hindfoot in varus, a forefoot that is adducted, and an ankle in equinus
- History and clinical findings are sufficient for initial diagnosis.
- Further investigation to define subtype/severity and comorbid conditions:
- MRI to determine:
- Location and extent of structural lesions/congenital malformations
- Presence of spinal cord pathology
- Hearing and visual function
- Genetic evaluation in patients with:
- Congenital malformations (chromosomes)
- Suspected metabolic disorders (e.g., amino acids, organic acids, magnetic resonance (MR) spectroscopy)
- MRI to determine:
There is no curative treatment at this time. Management focuses on improving symptoms and increasing function while addressing comorbidities. Early multidisciplinary intervention improves patient outcomes.
- Physical and occupational therapy:
- Stretching exercises as early as possible (contracture prevention)
- Adaptive equipment (e.g., walkers, poles)
- Individualized evaluation/intervention for educational needs
- Medical therapy:
- Aimed at the treatment of:
- Behavioral disorders
- Valium (diazepam) and other benzodiazepines
- Anticholinergics (e.g., atropine)
- Botulinum toxin (Botox) injections in spastic areas
- Aimed at the treatment of:
- Surgical therapy:
- In cases of marked spasticity
- Surgical soft-tissue procedures (e.g., tenotomy, the surgical cutting of a tendon)
- Proper prenatal care and screening
- Administration of magnesium sulfate in cases of preterm labor before 32 weeks’ gestation
- Genetic counseling for future offspring in select situations
- Dependent on the degree of motor, cognitive, and sensory deficit
- Most patients survive into adulthood.
- Life expectancy has improved significantly in the last 10–20 years.
- Most common cause of early death is a respiratory failure as a result of aspiration pneumonia.
The following conditions are etiological and/or risk factors for CP:
- Neonatal respiratory distress syndrome: a syndrome of respiratory distress caused by lack of pulmonary surfactant in the preterm infant. The syndrome is a known risk factor for the development of intraventricular hemorrhage and periventricular leukomalacia, lesions frequently associated with CP.
- Preterm delivery: delivery of the fetus before the pregnancy reaches 37 weeks’ gestation. Etiology of preterm delivery is multifactorial, including maternal and fetal factors, some of which are treatable/preventable, while others are not. Preterm birth has been identified as a major risk factor for the development of CP.
- Gestational infections (chorioamnionitis, congenital TORCH infections): chorioamnionitis (the inflammation of the chorion and amnios) and fetal infection by TORCH (Toxoplasmosis, Other agents, Rubella, Cytomegalovirus, and Herpes simplex) microorganisms are well-known risk factors for CP. Infection can cause direct CNS injury or complications with the delivery/perinatal course, or induce premature labor.
- Meningitis: an inflammation of the meninges, usually caused by an infectious pathogen. Cerebral palsy is among the neurological sequelae that can develop in children under 5 of age who undergo the CNS inflammation seen in meningitis.
- Hyperbilirubinemia: elevated bilirubin levels during the neonatal period (first 28 days of life). Hyperbilirubinemia and its neurological complications (bilirubin-induced neurological dysfunction (BIND)) are risk factors for the development of CP.
- Preeclampsia: a gestational disorder featuring the elevation of maternal blood pressure above 140/90 mm Hg, seen in association with proteinuria. Preeclampsia can lead to early delivery and has a strong association with CP.
- Stroke: broadly understood as a hemorrhagic or ischemic abnormality in blood flow to brain tissue. A stroke can cause CP if it occurs in the prenatal or postnatal periods.
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