Home > Journals > Minerva Obstetrics and Gynecology > Past Issues > Minerva Ginecologica 2009 October;61(5) > Minerva Ginecologica 2009 October;61(5):421-9

CURRENT ISSUE
 

JOURNAL TOOLS

Publishing options
eTOC
To subscribe
Submit an article
Recommend to your librarian
 

ARTICLE TOOLS

Reprints
Permissions
Share

 

REVIEWS  OBSTETRIC ISSUE 

Minerva Ginecologica 2009 October;61(5):421-9

Copyright © 2009 EDIZIONI MINERVA MEDICA

language: English

Defining cerebral palsy: pathogenesis, pathophysiology and new intervention

Longo M., Hankins G. D. V.

Division of Maternal Fetal Medicine, Department of Obstetrics and Gynecology University of Texas Medical Branch, Galveston, TX, USA


PDF


Cerebral palsy (CP) affects 2/1 000 live-born children. There are several antenatal factors, including preterm delivery, low birth weight, infection/inflammation, multiple gestations, and other pregnancy complications, that have been associated with CP in both the preterm and term infant, with birth asphyxia playing a minor role. Due to the increasing survival of the very preterm and very low birth weight infant secondary to improvements in neonatal and obstetric care, the incidence of CP may be increasing. The topics of neonatal encephalopathy and CP, as well as hypoxic-ischemic encephalopathy, are of vital importance to anyone who ventures to deliver infants. Criteria sufficient to define an acute intrapartum hypoxic event as sufficient to cause CP have been advanced previously by both the American College of Obstetricians and Gynecologists and the International Cerebral Palsy Task Force. This review will cover the progression toward defining the pathogenesis and pathophysiology of cerebral palsy. Four essential criteria were advanced as prerequisites if one is to propose that an intrapartum hypoxic-ischemic insult has caused a moderate to severe neonatal encephalopathy that subsequently results in CP. Importantly, all four criteria must be met: 1) evidence of metabolic acidosis (pH <7.0 and base deficit of 12 mmol/L or more); 2) early onset of severe or moderate neonatal encephalopathy in infants born at 34 or more weeks’ gestation; 3) CP of the spastic quadriplegic or dyskinetic type, and 4) exclusion of other identifiable etiologies, such as trauma, coagulation disorders, infectious conditions, or genetic disorders. Other criteria that together suggest intrapartum timing are also discussed. The focus of this paper is to explore antenatal antecedents as etiologies of CP and the impact of obstetric care on the prevention of CP.

top of page