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Reports of cerebral palsy prevalence rates per live births in recent decades in western nations show a mixed pattern. Declining rates were noted in Bristol, England, and in Denmark; but more recently a rising rate was noted in Ireland. In Western Sweden a decline has been followed by a recent rise, and in Western Australia a rise has been followed by a decline. Rates with not statistically significant changes have been found in Iceland and Birmingham, England, and over the seven-year span of the US Collaborative Perinatal Project, although their over-all direction was downward. No single factor is likely to explain the trends observed.

A variety of insults can cause cerebral palsy, but the dominant mechanism of damage is ischemic and/or asphyxial. Table 2 provides a rough estimate of the relative contribution of each of the several risk factor groups to the total burden of cerebral palsy. This table is only approximate both because of our lack of knowledge, and because risk factors often interact with one another. Cerebral palsy is frequently multifactorial in nature. For example the small-for-gestational age infant is both more likely to experience labor asphyxia, and is also more susceptible to its effects. The numerically largest etiologic grouping in cerebral palsy consists of pre-term/low birthweight infants, many of whom have experienced ischemic damage perinatally. The second largest grouping is infants born at term experiencing severe perinatal asphyxia. Congenital infections, and metabolic conditions such as hyperbilirubinemia certainly play some role in the genesis of cerebral palsy but genetic conditions as such rarely cause cerebral palsy. Some infants, if carefully studied, will prove to have a congenital brain malformation. The role of intrauterine ischemic events is at present not well understood, but is probably significant.