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(Stroke. 2003;34:2892.)
© 2003 American Heart Association, Inc.
Original Contributions |
Service de Pédiatrie et Groupe de Recherche sur la Thrombose, Centre Hospitalier Universitaire, Saint-Etienne Cedex, France
An extract of the first 250 words of the full text is provided, because this article has no abstract. |
In this issue ofStroke, Kurnik and collaborators report the largest cohorts in the literature of children who presented with symptomatic arterial ischemic stroke in the neonatal period.1 The study provides 2 major findings. First, it confirms, on a large scale, that many biological alterations are stroke risk factors in the neonatal period. Indeed, 127 out of the 215 neonates have a prothrombotic state. Even in the absence of a control group, the range of these disturbances (notably factor V Leiden mutation with an incidence of 15% and protein C deficiency with 4%) is clearly greater than in the general population. It is also higher than the rate of thrombophilia usually discovered in non-neonates with arterial ischemic stroke.2 Although the prothrombotic condition is in general constitutional, the stroke rarely recurs. Only 4 of the 215 children had a second arterial ischemic stroke after a median follow-up of 3.5 years. Among them, 1 had congenital heart disease and 1 had congenital moyamoya disease, 2 conditions also at risk for recurrence of stroke in non-neonates. By comparison, studies concerning non-neonate children with arterial ischemic stroke reveal a rate of recurrence of 7% to 22% in the same span of follow-up.35
These facts advocate envisaging some characteristics of the fetus or the newborn that predispose them to cerebral arterial ischemic events, especially in a context of thrombophilia. The first hypothesis is a lesion of cervicocephalic arteries during childbirth. Roessmann and Miller report the autopsy of a newborn who had a traumatic birth
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