Fetal and neonatal cerebral infarcts

Biol Neonate. 2001;79(3-4):236-40. doi: 10.1159/000047098.

Abstract

Focal arterial infarction in the full-term newborn is an important cause of acquired cerebral lesions in the perinatal period. Clinical motor seizures, most often unifocal, are the nearly constant disclosing symptom confirmed by focal EEG abnormalities. A multifactorial physiopathology is usual, including genetic and perinatal environmental factors. In the past decade, various acquired or genetic thrombophilias have been discussed as risk factors. For several of the involved mechanisms, the excitotoxic cascade could represent a common final pathway leading to neuronal cell death. Early magnetic resonance imaging studies and EEG help to identify the newborns with strokes who are likely to develop hemiplegia and disabilities at school. Protection of the human fetal brain remains difficult, since the triggering factor initiating the excitotoxic cascade is rarely observed. Treatment of seizures is nevertheless necessary, because it seems that they accelerate anoxia-induced neuronal death in animal models of focal hypoxic ischemia.

Publication types

  • Review

MeSH terms

  • Animals
  • Brain / growth & development
  • Cerebral Infarction / diagnosis*
  • Cerebral Infarction / etiology
  • Cerebral Infarction / pathology
  • Cerebral Infarction / physiopathology
  • Electroencephalography
  • Female
  • Fetal Diseases / diagnosis*
  • Humans
  • Infant, Newborn
  • Magnetic Resonance Imaging
  • Pregnancy
  • Prognosis
  • Seizures