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Cerebral Palsy - Description

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Other Names

static encephalopathy

ICD-9

343, Cerebral palsy

Description

Cerebral Palsy (CP) is a general term that refers to a group of non-progressive disorders of movement and posture resulting from injury or malformation of the developing central nervous system. The resultant disability can range from very mild (apparent only as a stiff gait) or very severe (requiring total care). Most children with CP have the congenital form - they are born with CP, although it may not be detected for months or years. [Odding: 2006] In some children, CP may be associated with various combinations of intellectual disability, seizures, poor growth, scoliosis, and visual and hearing deficits.

Clinical presentations of CP vary widely. In some cases, the diagnosis of cerebral palsy may be straightforward and the etiology clear, as in the child who was born prematurely and is known to have had a high-grade intraventricular hemorrhage or the child who had significant hypoxic-ischemic encephalopathy in the newborn period. However, in approximately 19% of children with CP, the cause may not be identifiable. [Hagberg: 1989] In those children with signs/symptoms of CP, such as developmental delay and spasticity, but no medical history compatible with brain injury, a careful evaluation is necessary to determine the etiology of the abnormalities and to rule out an underlying genetic syndrome or a progressive neurological or metabolic condition.

CP may result from an insult to the developing brain that occurred before, during, or after birth. In the US and Europe, most cases of CP (approximately 80%) are due to prenatal factors. Only 5-10% of CP is caused by injury related to the birth process. [Odding: 2006] Fewer than 10% of children acquire CP during the first year of life due to injuries from meningitis, encephalitis, near-drowning, or other asphyxial event. However, in the developing world approximately 80% of CP is caused by postnatal factors, most commonly infection. [van: 2007]

Maternal risk factors for having a child with CP include:
  • multiple fetuses
  • malnutrition
  • placental problems
  • infection (e.g., bacterial kidney infection, chorioamnionitis, [Bax: 2006])
  • toxin ingestion (e.g., methamphetamine)
  • complicated labor
  • hypothyroidism
  • maternal seizures
Infant characteristics associated with CP include:
  • prematurity and low birth weight (A recent study demonstrates that magnesium sulfate given to mothers who were at risk for having a pre-term delivery reduces the risk of CP in pre-term babies. [Rouse: 2008])
  • genetic or other disorders of brain development, including hydrocephalus
  • infection (e.g., cytomegalovirus, sepsis, encephalitis)
  • low Apgars at 10-20 minutes after delivery
  • periventricular hemorrhage
  • blood type incompatibility
  • factor V Leiden deficiency or other clotting disorder
  • breech presentation
  • jaundice
  • seizures shortly after birth
  • metabolic disease (e.g., glutaric acidemia I)

Genetics

Though rare, sometimes children with CP have an underlying genetic disorder (e.g., in Miller-Dieker syndrome, severe lissencephaly due to a deletion in chromosome 17p13.3, [Kato: 2003] or dopa-responsive dystonia, which can present as a delay in walking and/or stiff gait [Cheyette: 2008]). Congenital neurologic disorders (e.g., schizencephaly, hydranencephaly) may be initially misdiagnosed as CP. A large controlled study is currently being conducted in Australia looking into the contributions of genetic factors in CP (see Australian study - CP and genetics and [Gibson: 2008]).

Prognosis

The manifestations, severity, and course of CP vary dramatically across individuals. Accurate predictions of outcomes are difficult in infants. Brain MRI is often helpful, but may be misleading. [Distelmaier: 2007]). In general, the more delayed the achievement of milestones, the more affected the child will be. Children who aren't sitting by age 3-4 and walking by age 7-8 are not likely to ever learn to walk. However, motor milestones do not predict IQ which is more predictive of the ability of the child to function independently as an adult. IQ testing may be difficult to do because most tests require motor coordination. Children with CP, e.g., those with restrictions of movement due to spasticity, may need special IQ testing by psychologists familiar with this population.

Published predictions of life expectancy for children with motor limitations and/or mental retardation are generally based on abilities such as mobility, feeding, and toileting. However, these are difficult to apply to an individual child. (For a discussion, see Information on life expectancy and severe disabilities from DBPeds.) Children with severe motor problems are at high risk for death due to pneumonia, urinary tract infections, and sepsis. Comprehensive, coordinated care may optimize the life span for individuals with CP.

Prevalence

According to the Center for Disease Control and Prevention (CDC), every year approximately 10,000 babies born in the United States are identified as having CP. The prevalence is 2-3 children per 1,000 over the age of three. [Ashwal: 2004] Males are slightly more likely to have CP than females, and CP is more common in families with lower socioeconomic status. [van: 2007] There is conflicting data about whether CP prevalence has stayed the same, decreased, or increased over recent years. [Odding: 2006] [Himmelmann: 2005] However, changes in prenatal and newborn medical care have been associated with shifts in the etiologies of CP. [Himmelmann: 2005] [Hagberg: 1989]

Impact

CP is the second most expensive developmental disability after intellectual disability. A 2003 estimate of the average lifetime direct and indirect costs of CP for the society is $921,000 per person, or 11.5 billion dollars for persons with cerebral palsy. [Centers: 2004]

Pearls And Alerts

On Initial Diagnosis Page

Seizures

Developmental Quotient

On Ongoing Assessment Page

Interval progression

On Treatment And Management Page

Dual sensory impairment

Educational issues

Helpful Articles

PubMed Search on Cerebral Palsy

Winter S, Autry A, Boyle C, Yeargin-Allsopp M.
Trends in the prevalence of cerebral palsy in a population-based study.
Pediatrics. 2002;110(6):1220-1225. PubMed abstract

Cerebral Palsy Module Authors

Authors: Lisa Samson-Fang MD, 2/2008
Lynne M Kerr MD, PhD, 2/2007
Content Last Updated: 8/2008

The authors listed above are responsible for the overall Cerebral Palsy Module. Authors contributing to individual pages in the module are listed on those pages.

Page Bibliography

Ashwal S, Russman BS, Blasco PA, Miller G, Sandler A, Shevell M, Stevenson R.
Practice parameter: diagnostic assessment of the child with cerebral palsy: report of the Quality Standards Subcommittee of the American Academy of Neurology and the Practice Committee of the Child Neurology Society.
Neurology. 2004;62(6):851-63. PubMed abstract / Full Text
Evidence based summary of indicated diagnostic evaluation for children with cerebral palsy.

Bax M, Tydeman C, Flodmark O.
Clinical and MRI correlates of cerebral palsy: the European Cerebral Palsy Study.
JAMA. 2006;296(13):1602-8. PubMed abstract

Centers for Disease Control and Prevention (CDC).
Economic costs associated with mental retardation, cerebral palsy, hearing loss, and vision impairment--United States, 2003.
MMWR Morb Mortal Wkly Rep. 2004;53(3):57-9. PubMed abstract

Cheyette BN, Cheyette SN, Cusmano-Ozog K, Enns GM.
Dopa-responsive dystonia presenting as delayed and awkward gait.
Pediatr Neurol. 2008;38(4):273-5. PubMed abstract

Distelmaier F, Richter-Werkle R, Schaper J, Messing-Juenger M, Mayatepek E, Rosenbaum T.
"How much brain is really necessary?" A case of complex cerebral malformation and its clinical course.
J Child Neurol. 2007;22(6):756-60. PubMed abstract

Gibson CS, Maclennan AH, Dekker GA, Goldwater PN, Sullivan TR, Munroe DJ, Tsang S, Stewart C, Nelson KB.
Candidate genes and cerebral palsy: a population-based study.
Pediatrics. 2008;122(5):1079-85. PubMed abstract

Hagberg B, Hagberg G, Olow I, von Wendt L.
The changing panorama of cerebral palsy in Sweden. V. The birth year period 1979-82.
Acta Paediatr Scand. 1989;78(2):283-90. PubMed abstract

Himmelmann K, Hagberg G, Beckung E, Hagberg B, Uvebrant P.
The changing panorama of cerebral palsy in Sweden. IX. Prevalence and origin in the birth-year period 1995-1998.
Acta Paediatr. 2005;94(3):287-94. PubMed abstract

Kato M, Dobyns WB.
Lissencephaly and the molecular basis of neuronal migration.
Hum Mol Genet. 2003;12 Spec No 1:R89-96. PubMed abstract

Odding, E, Roebroeck, ME, and Stam, HJ.
The Epidemiology of cerebral palsy: incidence, impairments, and risk factors.
UCP Research and Education Foundation Fact Sheet; (2006) http://www.ucpresearch.org/fact-sheets/epidemiology-cerebral-palsy.php. Accessed on August 2008.

Rouse DJ, Hirtz DG, Thom E, Varner MW, Spong CY, Mercer BM, Iams JD, Wapner RJ, Sorokin Y, Alexander JM, Harper M, Thorp JM Jr, Ramin SM, Malone FD, Carpenter M, Miodovnik M, Moawad A, O'Sullivan MJ, Peaceman AM, Hankins GD, Langer O, Caritis SN, Roberts JM.
A randomized, controlled trial of magnesium sulfate for the prevention of cerebral palsy.
N Engl J Med. 2008;359(9):895-905. PubMed abstract

van Toorn, R, Laughton, B, van Zyl, N, Doets, L, and Elsinger, F.
Aetiology of cerebral palsy in children presenting at Tygerberg Hospital.
South Africa Journal of Child Health. 2007;1(2):74-78. / Full Text