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Cerebral palsy not usually related to birth process
This background on cerebral palsy and summary of the new findings was provided by the American College of Obstetricians and Gynecologists (ACOG):
Neonatal encephalopathy and its subset of hypoxic-ischemic encephalopathy (HIE) are conditions defined in and described for term and near-term infants. Neonatal encephalopathy is defined clinically on the basis of a constellation of findings to include a combination of abnormal consciousness, tone and reflexes, feeding, respiration, or seizures and can result from myriad conditions. Neonatal encephalopathy may or may not result in permanent neurologic impairment.
It can be stated with certainty, however, that the pathway from an intrapartum hypoxic-ischemic injury to subsequent cerebral palsy must progress through neonatal encephalopathy.
In contrast, cerebral palsy is a chronic disability of central nervous system origin characterized by aberrant control of movement and posture, appearing early in life and not as a result of progressive neurologic disease. Research supports that spastic quadriplegia, especially with an associated movement disorder, is the only type of cerebral palsy associated with an acute interruption of blood supply. Purely dyskinetic or ataxic cerebral palsy, especially where there is an associated learning difficulty, commonly has a genetic origin and is not caused by intrapartum or peripartum asphyxia. Similarly, absent cerebral palsy, neither epilepsy, mental retardation, nor attention-deficit hyperactivity disorder are caused by birth asphyxia.
Historically, the factors used to define perinatal asphyxia, such as meconium-stained amniotic fluid and Apgar scores, were not specific to the disease process leading to neurologic damage. For instance, Nelson and associates have shown that use of nonreassuring fetal heart rate patterns to predict subsequent cerebral palsy had a 99% false-positive rate. Use of such nonspecific markers for perinatal asphyxia identifies a large number of individuals as being exposed to inappropriately diagnosed "perinatal asphyxia." Thus, it is not surprising that removing exposure to such nonspecific markers has failed to change the risk for the disease.
Epidemiologic studies have shown that only 19% of cases of neonatal encephalopathy met what were very nonstringent criteria for intrapartum hypoxia, with another 10% experiencing a significant intrapartum event that may have been associated with intrapartum hypoxia. Even with such inexact markers for intrapartum fetal hypoxia, they demonstrated that of all cases of neonatal encephalopathy, 69% had only antepartum risk factors, 25% had both antepartum and intrapartum risk factors, 4% had evidence of only intrapartum hypoxia without identified preconceptional or antepartum factors that might have contributed to neonatal encephalopathy, and 2% had no identified risk factors.
Thus, approximately 70% of neonatal encephalopathy is secondary to events arising before the onset of labor. The overall incidence of neonatal encephalopathy attributable to intrapartum hypoxia, in the absence of any other preconceptional or antepartum abnormalities, is estimated to be approximately 1.6 per 10,000. It is again emphasized that HIE is but one subset of neonatal encephalopathy; other subsets include those resulting from prenatal stroke, infection, cerebral malformation, genetic disorders, and many other conditions.
These are the criteria to define an acute intrapartum event sufficient to cause cerebral palsy, as modified by this task force from the template provided by the International Cerebral Palsy Task Force:
• Essential criteria (must meet all four):
These are criteria that collectively suggest an intrapartum timing (within close proximity to labor and delivery, e.g., 0-48 hours) but are nonspecific to asphyxial insults:
To purchase copies of the complete report, contact the ACOG Distribution Center at (800) 762-2264, ext. 277, and ask for item # AA432, or order on-line at sales.acog.org. Follow the path from the ACOG Bookstore to Professional Publications to ACOG Guidelines.