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Cerebral Palsy

Jul 2009 – by M. Socol, MD

Cerebral palsy is a non-progressive muscular disability (or spasticity) of early onset. Cerebral palsy complicates approximately 2 per 1000 births, and this incidence has not changed over decades. The most prevalent risk factor for cerebral palsy is preterm birth. It has been estimated that 10-20% of cases may be secondary to oxygen deprivation proximate to birth, although this should not be interpreted as synonymous with preventable.

Many children with cerebral palsy are also afflicted with mental retardation, but the reverse is much less common. The incidence of mental retardation is approximately 4 per 1000 births. Most cases are secondary to genetic or chromosomal abnormalities.

In 2003, the American College of Obstetricians and Gynecologists and the American Academy of Pediatrics published a monograph entitled Neonatal Encephalopathy and Cerebral Palsy. The expert panel, after reviewing the available literature, developed four essential criteria and five nonspecific criteria to be used to ascertain whether an acute intrapartum hypoxic event sufficient to cause cerebral palsy has occurred. The panel emphasized that the absence of any one of the four essential criteria provides strong evidence that intrapartum hypoxia, or oxygen deprivation proximate to delivery, was not the cause of cerebral palsy. Similarly, contrary evidence such as a reassuring fetal heart rate pattern or an Apgar score of ≥ 7 at 5 minutes excludes an injurious event during labor.

The panel also stressed that significant metabolic acidosis, defined as a pH < 7 and base deficit ≥ 12 mmol/L is not, per se, pathologic. In fact, 90% or more of newborns with an umbilical arterial pH < 7 will develop normally. Furthermore, whereas a normal fetal heart rate pattern has a high degree of reliability in determining the fetus is well oxygenated, the converse is not true. Even with diminished variability and repetitive late decelerations, the false positive rate has been estimated to be as high as 98%.

The essential and nonspecific criteria are listed below:

Essential criteria (must meet all four):

  1. Evidence of metabolic acidosis in umbilical cord arterial blood (pH < 7 and base deficit ≥ 12 mmol/L).
  2. Early onset of severe or moderate neonatal encephalopathy in infants born at ≥ 34 weeks.
  3. Cerebral palsy of the spastic quadriplegic or dyskinetic types.
  4. Exclusion of other etiologies such as trauma, coagulation disorders, infectious conditions, or genetic disorders.

Criteria that collectively support an intrapartum timing but are nonspecific to asphyxial insults:

  1. A sentinel hypoxic event occurring immediately before or during labor.
  2. 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.
  3. Apgar scores of 0-3 beyond 5 minutes.
  4. Onset of multisystem involvement within 72 hours of birth.
  5. Early imaging study showing evidence of acute nonfocal cerebral abnormality.

Reference: Neonatal Encephalopathy and Cerebral Palsy, Defining the Pathogenesis and Pathophysiology. American College of Obstetricians and Gynecologists and American Academy of Pediatrics, January 2003