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By convention, the cerebral palsies (CP) are nonprogressive disorders of tone, strength, movement, and posture due to central nervous system (CNS) injury, the consequences of which become apparent in infancy. The CNS lesions variously involve pyramidal (cortical, subcortical, brainstem, spinal cord), extrapyramidal, or cerebellar motor systems. The static nature of the CNS lesion and public misunderstanding of the nature of CP has prompted the coining of the not entirely synonymous alternative designation static encephalopathy (SE). A cerebral palsy (CP) is a static encephalopathy (SE) in which motor dysfunction must be present, although individuals may also manifest disorders of intellect, attention, memory, sensory, autonomic, and other neurologic modalities. They may also be at risk for epilepsy and for dysfunction of respiratory, gastrointestinal, and other nonneural systems.1-6


Cerebral palsies are a subgroup of SE, a category that also includes individuals whose static CNS injury may involve various patterns of intellectual dysfunction unaccompanied by central motor system deficits. Where only one or a few specific relatively mild cognitive modalities are impaired, the qualifier learning disabled may be applied, whereas more severe conditions affecting many or all cognitive domains suggests the qualifier intellectually disabled rather than the older term mentally retarded. Limitations of variable degree in the social-pragmatic functions of daily life may or may not be found in individuals with CP.


The combination and degree of deficits in individuals with SE or the large subgroup comprising CP is dependant on the location and extent of underlying CNS injury. The clinical pattern is often predictive of the site of lesions and may be predictive of underlying cause. However, the deficits of most individuals with CP or SE remain of uncertain pathogenesis, although rapid progress in the elucidation of genetically determined developmental disorders is reducing this uncertainty and replacing these generic labels with specific conditions. The importance of labels is that they designate cause with increasing accuracy. The increasing specificity of labels that should be permitted to replace the generic labels of CP or SE results in increasing accuracy of formulation of heritability, risks, prognosis, and treatment.7-9 Postnatal neural development may impart a pseudoprogressive appearance to the static deficits of CP, or of conditions within the wider spectrum of SE, due to the fact that damage to various systems may not become fully apparent until such systems “come on line” during postnatal development.3,4,7 It is important to note that despite the possible infantile worsening of manifestations, most children with CP will experience, at varied rates and degrees, improvement over the course of their development.3,8,9


The incidence of CP is approximately 0.1% to 0.25% of all live births, with little international variation among countries with modern medical facilities.10,11 Modern neonatology has greatly increased the survival of very low birth weight babies, whose risk for CP is approximately eight-fold greater than for larger neonates.12 Interestingly, increases in utilization ...

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