Introduction

Understanding of the etiology of cerebral palsy has changed markedly over the past two decades, as epidemiologic studies have supplanted anecdote and uncontrolled case series. Unfortunately, there has been no parallel progress in reducing the rate of occurrence of cerebral palsy over a similar period, despite striking improvements in both obstetric and neonatal care (1,2).

Cerebral palsy (CP) is a group of chronic motor disorders of central nervous system origin, characterized by aberrant control of movement or posture, beginning early in life and not due to recognized progressive disease. Major malformations of the CNS are usually excluded. In studies of etiology disorders arising after the first month of life are also excluded. The term cerebral palsy thus denotes a chronic, usually congenital, motor disorder. “Cerebral palsy” is not an etiologic diagnosis but indicates developmental motor disability; the term is thus analogous to “mental retardation,” a term denoting chronic, usually congenital, cognitive disability.

CP may be categorized into its clinical subtypes (spastic quadriplegia, diplegia, hemiplegia; dyskinetic or ataxic forms, and mixed), by severity, and may be further grouped according to whether or not etiology is considered known through neuroimaging, chromosomal, metabolic, or other evidence.

Prevalence

Studies of the prevalence of CP, although they differ by date, age of ascertainment, and exclusions, are reasonably comparable in different developed countries, with an overall prevalence of 1.4 to 2.3 per thousand (3–6). For disabling congenital CP, an American population-based study observed a prevalence at three years of 1.23 per thousand survivors.