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, inc
luding genetic and perinatal environmental factors. In the past decade, var
ious acquired or genetic thrombophilias have been discussed as risk factors
. For several of the involved mechanisms, the excitotoxic cascade could rep
resent a common final pathway leading to neuronal cell death. Early magneti
c resonance imaging studies and EEG help to identify the newborns with stro
kes who are likely to develop hemiplegia and disabilities at school. Protec
tion of the human fetal brain remains difficult, since the triggering facto
r initiating the excitotoxic cascade is rarely observed. Treatment of seizu
res is nevertheless necessary, because it seems that they accelerate anoxia
-induced neuronal death in animal models of focal hypoxic ischemia. Copyrig
ht (C) 2001 S. Karger AG. Basel.