Defining the pathogenesis and pathophysiology of neonatal encephalopathy and cerebral palsy

Gary Hankins, Michael Speer

Research output: Contribution to journalArticle

185 Citations (Scopus)

Abstract

The topics of neonatal encephalopathy and cerebral palsy, as well as hypoxic-ischemic encephalopathy, are of paramount importance to anyone who ventures to deliver infants. Criteria sufficient to define an acute intrapartum hypoxic event as sufficient to cause cerebral palsy have been advanced previously by both The American College of Obstetricians and Gynecologists (ACOG) and the International Cerebral Palsy Task Force. ACOG convened a task force that over the past 3 years reviewed these criteria based upon advances in scientific knowledge. In this review, we cover the slow but steady progression toward defining the pathogenesis and pathophysiology of neonatal encephalopathy and cerebral palsy. Four essential criteria are also 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 cerebral palsy. Importantly, all four criteria must be met: 1) evidence of metabolic acidosis in fetal umbilical cord arterial blood obtained at delivery (pH less than 7 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) cerebral palsy 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.

Original languageEnglish (US)
Pages (from-to)628-636
Number of pages9
JournalObstetrics and Gynecology
Volume102
Issue number3
DOIs
StatePublished - Sep 2003

Fingerprint

Brain Diseases
Cerebral Palsy
Advisory Committees
Brain Hypoxia-Ischemia
Inborn Genetic Diseases
Acidosis
Fetal Blood
Pregnancy
Wounds and Injuries

ASJC Scopus subject areas

  • Obstetrics and Gynecology

Cite this

Defining the pathogenesis and pathophysiology of neonatal encephalopathy and cerebral palsy. / Hankins, Gary; Speer, Michael.

In: Obstetrics and Gynecology, Vol. 102, No. 3, 09.2003, p. 628-636.

Research output: Contribution to journalArticle

Hankins, Gary ; Speer, Michael. / Defining the pathogenesis and pathophysiology of neonatal encephalopathy and cerebral palsy. In: Obstetrics and Gynecology. 2003 ; Vol. 102, No. 3. pp. 628-636.
@article{fff0c03be5634b3ba12e1e1a2f0ce173,
title = "Defining the pathogenesis and pathophysiology of neonatal encephalopathy and cerebral palsy",
abstract = "The topics of neonatal encephalopathy and cerebral palsy, as well as hypoxic-ischemic encephalopathy, are of paramount importance to anyone who ventures to deliver infants. Criteria sufficient to define an acute intrapartum hypoxic event as sufficient to cause cerebral palsy have been advanced previously by both The American College of Obstetricians and Gynecologists (ACOG) and the International Cerebral Palsy Task Force. ACOG convened a task force that over the past 3 years reviewed these criteria based upon advances in scientific knowledge. In this review, we cover the slow but steady progression toward defining the pathogenesis and pathophysiology of neonatal encephalopathy and cerebral palsy. Four essential criteria are also 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 cerebral palsy. Importantly, all four criteria must be met: 1) evidence of metabolic acidosis in fetal umbilical cord arterial blood obtained at delivery (pH less than 7 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) cerebral palsy 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.",
author = "Gary Hankins and Michael Speer",
year = "2003",
month = "9",
doi = "10.1016/S0029-7844(03)00574-X",
language = "English (US)",
volume = "102",
pages = "628--636",
journal = "Obstetrics and Gynecology",
issn = "0029-7844",
publisher = "Lippincott Williams and Wilkins",
number = "3",

}

TY - JOUR

T1 - Defining the pathogenesis and pathophysiology of neonatal encephalopathy and cerebral palsy

AU - Hankins, Gary

AU - Speer, Michael

PY - 2003/9

Y1 - 2003/9

N2 - The topics of neonatal encephalopathy and cerebral palsy, as well as hypoxic-ischemic encephalopathy, are of paramount importance to anyone who ventures to deliver infants. Criteria sufficient to define an acute intrapartum hypoxic event as sufficient to cause cerebral palsy have been advanced previously by both The American College of Obstetricians and Gynecologists (ACOG) and the International Cerebral Palsy Task Force. ACOG convened a task force that over the past 3 years reviewed these criteria based upon advances in scientific knowledge. In this review, we cover the slow but steady progression toward defining the pathogenesis and pathophysiology of neonatal encephalopathy and cerebral palsy. Four essential criteria are also 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 cerebral palsy. Importantly, all four criteria must be met: 1) evidence of metabolic acidosis in fetal umbilical cord arterial blood obtained at delivery (pH less than 7 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) cerebral palsy 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.

AB - The topics of neonatal encephalopathy and cerebral palsy, as well as hypoxic-ischemic encephalopathy, are of paramount importance to anyone who ventures to deliver infants. Criteria sufficient to define an acute intrapartum hypoxic event as sufficient to cause cerebral palsy have been advanced previously by both The American College of Obstetricians and Gynecologists (ACOG) and the International Cerebral Palsy Task Force. ACOG convened a task force that over the past 3 years reviewed these criteria based upon advances in scientific knowledge. In this review, we cover the slow but steady progression toward defining the pathogenesis and pathophysiology of neonatal encephalopathy and cerebral palsy. Four essential criteria are also 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 cerebral palsy. Importantly, all four criteria must be met: 1) evidence of metabolic acidosis in fetal umbilical cord arterial blood obtained at delivery (pH less than 7 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) cerebral palsy 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.

UR - http://www.scopus.com/inward/record.url?scp=0141990478&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0141990478&partnerID=8YFLogxK

U2 - 10.1016/S0029-7844(03)00574-X

DO - 10.1016/S0029-7844(03)00574-X

M3 - Article

C2 - 12962954

AN - SCOPUS:0141990478

VL - 102

SP - 628

EP - 636

JO - Obstetrics and Gynecology

JF - Obstetrics and Gynecology

SN - 0029-7844

IS - 3

ER -