Published online before print November 20, 2003, doi: 10.1161/01.STR.0000106669.19525.0F
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(Stroke. 2003;34:2892.)
© 2003 American Heart Association, Inc.
Original Contributions |
Editorial Comment—Specificities of the Neonatal Stroke
Service de Pédiatrie et Groupe de Recherche sur la Thrombose, Centre Hospitalier Universitaire, Saint-Etienne Cedex, France
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.3–5
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 and a cerebral infarct.6 The inner layers of a median cerebral artery were injured by the attempted forceps delivery, which led to occlusion. Charollais et al also described a pathological report of a carotid occlusion in a newborn who had cervicofacial trauma during a dystocic delivery.7 In the German cohort, dissection occurs in only 1 case out of the 215 neonates. Nevertheless, as in the large previously published series, generalized cerebrovascular exploration is not reported. The incidence of arterial trauma as a cause of perinatal stroke is thus not known. Furthermore, it cannot explain all the cases, since some infarctions, although symptomatic during the neonatal age, occur in the days preceding the birth.8,9
The second etiological hypothesis regards the role of the maternofetal vascular interface, ie, the placenta. Hypercoagulability, carried by either the mother or the fetus, is a cause of abnormal vascular development, vessel occlusion, and placental infarctions, which affect the maternofetal circulation.10–13 Such placental injuries have been described in cases of neonatal stroke. In addition, the fetal circulation implies that a clot, which has formed in the placenta and migrates, will preferentially embolize through the foramen ovale in the cerebral vasculature. Some anatomic and arteriographic reports support this embolic theory.8,14,15
Another matter of debate relates to the outcome of the children, notably the issue of cognitive and motor development. One of the best prognostic factors is the extent and the location of the lesions on magnetic resonance imaging.16 Nevertheless, the children’s outcome varies considerably between the studies. The duration of the follow-up explains some of these discrepancies. Some sequels (notably subtle cognitive deficits) of perinatal cerebral traumas may appear only after years of neurological follow-up. Also in the field of neonatal stroke, the longer the follow-up, the worse the neurological evolution. For example, in the Sran and Baumann’s report, 4 of 7 children followed for <2.5 years have a normal neurologic status versus only 3 of 9 followed for >2.5 years.17 In another small series, 1 out of 8 children (the youngest: 1.4 years) has normal development. In older children, concentration, speech, perception, and intelligence were significantly poorer than in control groups.18
In the absence of a known physiopathological mechanism, only supportive care is provided to the newborns. If the traumatic hypothesis were confirmed, analysis of pregnancy and delivery modalities would allow for obstetric situations with a stroke risk to be determined and, as a consequence, preventive interventions achieved. In selected newborns, early detection of arterial occlusion and, in the event of it occurring, treatment by anticoagulant or fibrinolytic agents is also conceivable. If the placento-embolic theory is verified, there is an opportunity to reduce the incidence of neonatal stroke by prophylactic therapy of the thrombophilia during pregnancy.19 Determination of early indicators of neurological disabilities would lead to personalized follow-up and rehabilitation programs. Further prospective studies with evaluation of delivery conditions, maternal and children’s thrombophilia screening, systematic vascular exploration of the newborn, and long-term neurological and neuropsychological follow-up are on the way, aimed at answering these issues and elaborating therapeutic trials.
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