Clinical Review

Cerebral palsy: A look at etiology and new task force conclusions

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These conclusions have been endorsed by a wide range of agencies and organizations, including the CDC, the US Department of Health and Human Services, the March of Dimes Birth Defects Foundation, and the National Institute of Child Health and Human Development. Of course, disagreement may arise about any of the criteria, especially if a case is subject to a lawsuit. Nevertheless, the conclusions of both task forces are quite logical. They also are likely to meet with widespread acceptance, since no serious objection or contrary view has yet been articulated, despite the fact that the first set of criteria has been in existence for several years.

Even so, it is important to remember that a much higher degree of certainty is necessary for scientific evidence (P<.05 than for evidence presented in a court case. it is therefore possible that courts may accept findings are scientifically flawed.>

Cerebral palsy through history: 2 opposing views

Although cerebral palsy has been around as long as humans have existed, it was not described in the medical literature until 1861, when Little outlined a sequence beginning with difficult labor, followed by neonatal seizures and, eventually, spastic motor paralysis.1 (Interestingly, Little’s disease—spastic diplegia—is not now believed to result from intrapartum events.)

The term “cerebral palsy” is usually attributed to Osler, who in 1889 associated the condition with asphyxia of the newborn following complicated deliveries.2

The first to question the cause-and-effect relationship between difficult birth and cerebral palsy was Sigmund Freud who, before turning to psychiatry, studied handicapped children. Freud noted that children with cerebral palsy often have other manifestations of brain damage that may have occurred during development in the early stages of gestation. Indeed, Freud surmised that brain damage might be an antecedent event to difficult birth.

The intrapartum asphyxia theory regained ascendancy in the late 1970s after experiments in primates demonstrated a causal link between perinatal asphyxia and brain damage. Since the same experiments could not be conducted in humans, the theory that cerebral palsy was caused by entities other than intrapartum hypoxia in roughly 90% of cases was based largely on epidemiologic evidence. (This theory maintained that even the 10% of cases with intrapartum signs compatible with damaging hypoxia may have had other antenatal causes.)

These 2 opposing views stimulated further investigations into the etiology of cerebral palsy.


1. Blickstein I. Spastic diplegia is not associated with intrapartum hypoxia. J Perinat Med. 2000;29:85-86.

2. Osler W. The Cerebral Palsies of Children. Philadelphia, Pa: Blakiston, Son & Co; 1889.


Criteria that define an acute intrapartum hypoxic event as sufficient to cause cerebral palsy8

Metabolic acidosis (pH
  • Samples taken from umbilical artery blood obtained at delivery
  • Cut-off levels based on risk to develop cerebral palsy
  • Neonatal acidemia may represent difficult resuscitation rather than asphyxia
Early onset of severe or moderate neonatal encephalopathy in infants born at 34 or more weeks of gestation
  • Usually develops within 24 hours of birth
  • Abnormal behavioral states are difficult to ascertain in preterm infants
Spastic quadriplegic or dyskinetic type of cerebral palsy
  • Conditions like hemiplegia, spastic diplegia, ataxia, intellectual disability, autism, and learning disorder in a child without spasticity have not been associated with acute intrapartum hypoxia
  • Rett and Angelman syndromes should be excluded
Exclusion of other identifiable causes such as trauma, coagulation disorders, infectious conditions, or genetic disorders
A recognized sentinel event
  • The fetus is tolerant of mild recurrent hypoxic events
A sudden and sustained fetal bradycardia or the absence of fetal heart-rate variability in the presence of persistent, late, or variable decelerations, usually after a hypoxic sentinel event when the pattern was previously normal
Apgar scores of 0-3 beyond 5 minutes
  • Low Apgar scores may represent effectiveness of resuscitation
Onset of multisystem involvement within 72 hours of birth
  • Acute hypoxia does not affect just the brain
Early imaging study showing evidence of acute nonfocal cerebral abnormality
  • After an acute insult, edema appears within 6-12 hours and clears by 4 days
  • Magnetic resonance imaging is the most informative modality

The link to prematurity, birth weight, and fetal growth

Prematurity. Epidemiologic studies have clearly demonstrated a causal relationship between premature birth and cerebral palsy. Williams et al9 found a cerebral palsy frequency of 3.2% among live births at less than 29 weeks’ gestation, 2.8% at 29 to 32 weeks, and a remarkable decrease to 0.3% at 33 to 36 weeks’ gestation and 0.07% at 37 or more weeks.

The major risk of premature birth is neonatal death. This is especially true for infants delivered in developing countries, where modern neonatal intensive care units (NICUs) are not available. Thus, it may be that premature infants of the Third World simply do not survive long enough to manifest signs of cerebral palsy.

On the other hand, in developed countries, where modern NICUs have undoubtedly improved the survival rates of premature neonates—even those at the edge of viability10,11—intact survival cannot be guaranteed. Because many premature births result from potentially damaging maternal or fetal conditions, one could argue that prematurity-associated mortality lowers the incidence of cerebral palsy, which might otherwise affect survivors.


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