In 1862, William John Little, an orthopedic surgeon, was the first to address and hypothesize on the etiology of CP. Little described developmental motor abnormalities in children as "spastic rigidity.'' He hypothesized that prolonged premature labor, breech delivery, or birth asphyxia were the causes of cerebral damage resulting in impairments in posture and movement. However, since the 1860s, discussion has continued regarding the exact cause of CP because the clinical manifestations of the disorder consistently result in few homogeneous patterns of symptoms.

Today, multiple risk factors contributing to the diagnosis of CP have been identified. However, in most cases, the underlying mechanism remains unknown. Researchers have not been able to link the exact timing of risk factors to resultant lesions in the developing brain. Two etiologies that do produce homogeneous clinical patterns are maternal iron deficiency and Rh incompatibility. Mothers who suffer from an iron deficiency during pregnancy give birth to children who display spastic diplegia with deaf mutism, and infants born with Rh incompatibility experience choreoathes-tosis and deafness. However, the majority of risk factors that are identified as contributing to CP do not necessarily lead to the disorder.

Risk factors contributing to the origin of CP have been contemplated for both the term and the preterm infant. Risk factors have been identified prior to conception and in the pre-, peri-, and postnatal stages of development (Table I). For full-term infants, the best predictors of the disorder have been reported as neurological abnormalities at birth, including low Apgar scores, abnormalities in respiration, abnormal reflex responsiveness, and neonatal seizures. In many cases, the cause remains unknown or is attributed to prenatal factors. In 1993, Naulty et al. reported that for 60% of term infants with CP there appeared to be no identifiable cause.

Since the time of Little, asphyxia during delivery has received much attention from the scientific community as a core etiological factor. However, recent data suggest that most cases of CP do not result from lack of oxygen due to human error during delivery. In fact, the rate of asphyxia at birth has decreased from 40/ 100,000 births in 1979 to 11/100,000 births in 1996, whereas the incidence of CP has not declined.

The Collaberative Perinatal Study (CPS) of the National Institute of Neurological and Communication Disorders and Stroke, one of the largest longitudinal studies to date, collected data from 43,437 full-term children to identify fetal, intrapartum, and neonatal events in child development. To date, this is the largest and most complete set of prospective data on the study of CP completed in the United States. In 1989, Naeye and colleagues used these data to report that birth asphyxia alone, not attributed to chronic antenatal hypoxia, as a whole accounted for only 6% of all cases of CP (Table II). According to this study, gas anesthesia during labor, maternal seizures, maternal diabetes mellitus, and neonatal hypoglycemia were not associated with a higher than expected frequency of CP. Moreover, congenital disorders accounted for four times as many cases of quadriplegic CP as did birth asphyxia. Congenital abnormalities accounted for 60% of the cases not of this clinical type.

Based on data collected by the CPS, Nelson and Ellenberg supported these findings, reporting that only 9% of CP cases were caused by birth asphyxia alone. Among those cases for which asphyxia may account, it was noted that oxygen deprivation frequently was not measured directly. Rather, asphyxia was inferred from low Apgar scores and signs of fetal distress that may include abnormal respiration, abnormal fetal heart rate, the presence of meconium, low cord blood pH, seizures, and abnormal reflex responsiveness. When investigated, these signs more often related to congenital disorders rather than asphyxia.

Further studies reported similar findings. Congenital malformations of the central nervous system (CNS)

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