Cerebral palsy

Ryan W Y Lee MD (Dr. Lee of Shriners Hospitals for Children in Honolulu and the John A Burns School of Medicine at the University of Hawaii has no relevant financial relationships to disclose.)
Michael V Johnston MD, editor. (Dr. Johnston of Johns Hopkins University School of Medicine and Chief Medical Officer at Kennedy Krieger Institute has no relevant financial relationships to disclose.)
Originally released February 7, 1994; last updated March 9, 2017; expires March 9, 2020

This article includes discussion of cerebral palsy, spastic diplegia, hemiplegic cerebral palsy, dyskinetic cerebral palsy, quadriparetic cerebral palsy, hypotonic cerebral palsy, dystonia, choreoathetotic cerebral palsy, and extrapyramidal cerebral palsy. The foregoing terms may include synonyms, similar disorders, variations in usage, and abbreviations.

Overview

Cerebral palsy describes a group of genetic and acquired childhood neurologic disorders characterized by abnormalities in tone, posture, and movement as a result of early injury to the developing brain. Cerebral palsy is often associated with language and intellectual disability, social impairment, epilepsy, other organ involvement, and functional limitations. An appropriate diagnostic assessment and resource environment is important to ensure proper treatment and management. Neuroprotective strategies, including therapeutic hypothermia and adjuvant therapy, show promise for the reduction of morbidity and mortality caused by hypoxic-ischemic encephalopathy, including cerebral palsy. In this article, the author discusses the many aspects of diagnosis and management of cerebral palsy.

Key points

 

• Cerebral palsy describes a group of nonprogressive genetic and acquired childhood neurologic disorders characterized by abnormalities in tone, posture, and movement as a result of injury to the developing brain.

 

• Although characterized by their motor dysfunction, children with cerebral palsy frequently have other associated impairments, which include language delay, seizures, strabismus, dysphagia, orthopedic deformities, and cognitive problems.

 

• Advances in neuroimaging and genetics promise to further the understanding of the pathogenesis and pathophysiology of cerebral palsy.

 

• Effective management of cerebral palsy requires a team with medical and rehabilitative specialists to provide careful, ongoing neurodiagnostic evaluation and rehabilitation to maximize functional capabilities.

 

• Neuroprotective strategies, chiefly therapeutic hypothermia, have demonstrated decreased death and disability related to cerebral palsy.

Historical note and terminology

Cerebral palsy describes a group of nonprogressive genetic and acquired childhood neurologic disorders characterized by abnormalities in tone, posture, and movement as a result of injury to the developing brain (Kuban and Leviton 1994; Goldstein 2004; Bax et al 2005).

Debates surrounding the nomenclature, definition, and etiology of cerebral palsy continue. In the mid-1800s, Sir William Little proposed that cerebral palsy was related to difficult childbirth (Little 1861). In recent decades, this view has had significant medical and legal implications (Nelson 1999). In the late 1800s Freud wrote, "Difficult birth, in certain cases, is merely a symptom of deeper effects that influence the development of the fetus" (Freud 1897). This view suggested that cerebral palsy had a prenatal onset. The late 19th century brought further insight as Sir William Osler published his lectures, The Cerebral Palsies of Children, classifying the disorder by neuroanatomy, etiology, and extremity involvement (Osler 1987).

The Collaborative Perinatal Project, a landmark American maternal and child health epidemiologic research study, demonstrated that the events of labor and delivery are not major contributors to the occurrence of cerebral palsy or most other neurodevelopmental disorders. Rather, most of these conditions have their origins before labor begins (Nelson 1986). Prenatal factors have emerged as the chief determinants of risk for cerebral palsy (Nelson and Blair 2015).

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