Cerebral Palsy

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Basics

Description

Cerebral palsy (CP) is a group of clinical syndromes characterized by motor and postural dysfunction due to permanent and nonprogressive disruptions in the developing brain. Motor impairment resulting in activity limitation is necessary for this diagnosis. CP is classified by the nature of the movement disorder and its functional severity.

Epidemiology

Incidence

  • Overall, 1.5 to 3.0/1,000 live births
  • Incidence increases as gestational age (GA) at birth decreases:
    • 146/1,000 for GA of 22 to 27 weeks
    • 62/1,000 for GA of 28 to 31 weeks
    • 7/1,000 for GA of 32 to 36 weeks
    • 1/1,000 for GA of 37+ weeks
  • Incidence increases as birth weight decreases (1).

Etiology and Pathophysiology

  • Multifactorial; CP results from static injury or lesions in the developing brain, occurring prenatally, perinatally, or postnatally.
  • Cytokines, free radicals, and inflammatory response are likely contributing factors.
  • Spastic CP is most common, usually related to premature birth, with either periventricular leukomalacia or germinal matrix hemorrhage.

Genetics
There are reports of associations between CP and polymorphisms of certain genes: thrombophilic, cytokines, and apolipoprotein E.

Risk Factors

  • Prenatal: congenital anomalies, multiple gestation, in utero stroke, intrauterine infection (cytomegalovirus [CMV], varicella), intrauterine growth retardation (IUGR), clinical and histologic chorioamnionitis, antepartum bleeding, maternal factors (cognitive impairment, seizure disorders, hyperthyroidism), abnormal fetal position (e.g., breech)
  • Perinatal: preterm birth, low-birth weight, periventricular leukomalacia, perinatal hypoxia/asphyxia, intracranial hemorrhage/intraventricular hemorrhage, neonatal seizure or stroke, hyperbilirubinemia
  • Postnatal: traumatic brain injury or stroke, sepsis, meningitis, encephalitis, asphyxia, and progressive hydrocephalus

General Prevention

  • Effective prevention strategies include antenatal corticosteroids, magnesium sulfate, and neonatal hypothermia (2).
  • Treating mothers with magnesium sulfate during preterm delivery is neuroprotective for fetus and may reduce the risk of CP. Effect on term fetus is unknown (3)[B].
  • Term born infants who experience intrapartum hypoxia have benefit from therapeutic hypothermia (4).

Commonly Associated Conditions

  • Seizure disorder
  • Intellectual and speech and language impairments
  • Behavioral problems
  • Hearing and visual impairments
  • Feeding impairment, swallowing dysfunction, and aspiration: when severe, may require gastrostomy feedings
  • Poor dentition, excessive drooling
  • GI conditions: constipation (59%), vomiting (22%), gastroesophageal reflux
  • Decreased linear growth and weight abnormalities (under- and overweight)
  • Osteopenia
  • Bowel and bladder incontinence
  • Orthopedic: contractures, hip subluxation/dislocation, scoliosis (60%)

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Basics

Description

Cerebral palsy (CP) is a group of clinical syndromes characterized by motor and postural dysfunction due to permanent and nonprogressive disruptions in the developing brain. Motor impairment resulting in activity limitation is necessary for this diagnosis. CP is classified by the nature of the movement disorder and its functional severity.

Epidemiology

Incidence

  • Overall, 1.5 to 3.0/1,000 live births
  • Incidence increases as gestational age (GA) at birth decreases:
    • 146/1,000 for GA of 22 to 27 weeks
    • 62/1,000 for GA of 28 to 31 weeks
    • 7/1,000 for GA of 32 to 36 weeks
    • 1/1,000 for GA of 37+ weeks
  • Incidence increases as birth weight decreases (1).

Etiology and Pathophysiology

  • Multifactorial; CP results from static injury or lesions in the developing brain, occurring prenatally, perinatally, or postnatally.
  • Cytokines, free radicals, and inflammatory response are likely contributing factors.
  • Spastic CP is most common, usually related to premature birth, with either periventricular leukomalacia or germinal matrix hemorrhage.

Genetics
There are reports of associations between CP and polymorphisms of certain genes: thrombophilic, cytokines, and apolipoprotein E.

Risk Factors

  • Prenatal: congenital anomalies, multiple gestation, in utero stroke, intrauterine infection (cytomegalovirus [CMV], varicella), intrauterine growth retardation (IUGR), clinical and histologic chorioamnionitis, antepartum bleeding, maternal factors (cognitive impairment, seizure disorders, hyperthyroidism), abnormal fetal position (e.g., breech)
  • Perinatal: preterm birth, low-birth weight, periventricular leukomalacia, perinatal hypoxia/asphyxia, intracranial hemorrhage/intraventricular hemorrhage, neonatal seizure or stroke, hyperbilirubinemia
  • Postnatal: traumatic brain injury or stroke, sepsis, meningitis, encephalitis, asphyxia, and progressive hydrocephalus

General Prevention

  • Effective prevention strategies include antenatal corticosteroids, magnesium sulfate, and neonatal hypothermia (2).
  • Treating mothers with magnesium sulfate during preterm delivery is neuroprotective for fetus and may reduce the risk of CP. Effect on term fetus is unknown (3)[B].
  • Term born infants who experience intrapartum hypoxia have benefit from therapeutic hypothermia (4).

Commonly Associated Conditions

  • Seizure disorder
  • Intellectual and speech and language impairments
  • Behavioral problems
  • Hearing and visual impairments
  • Feeding impairment, swallowing dysfunction, and aspiration: when severe, may require gastrostomy feedings
  • Poor dentition, excessive drooling
  • GI conditions: constipation (59%), vomiting (22%), gastroesophageal reflux
  • Decreased linear growth and weight abnormalities (under- and overweight)
  • Osteopenia
  • Bowel and bladder incontinence
  • Orthopedic: contractures, hip subluxation/dislocation, scoliosis (60%)

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