Timing and Etiology of Neonatal Cerebral Infarction

To the Editor. I read with interest the article by Mercuri et al1in reference to outcome in neonatal cerebral infarction, having recently experienced a term infant with this unexpected event. The article provides reassuring data regarding neurologic outcome in the infants described, with follow-up from 12 months to 5 years. The correlation of size and distribution of infarct with ultimate progression to hemiplegia was expected, and provides some useful measure for predicting prognosis. Perhaps most reassuring was the lack of correlation between antenatal and perinatal events and neurologic outcome, inasmuch as one naturally looks for inciting events when such a catastrophic neonatal occurrence is discovered. Koelfen et al2 suggested in their series that neonatal stroke represented a late intrauterine event, and Barmada et al3confirmed at autopsy that at least some infarcts may have occurred in utero. Scher et al4 also concluded that prenatal events caused low-density cerebral lesions in their affected infants but based this on radiographic appearance (edema on ultrasound and computed tomography) to date of onset from days to weeks before birth. Rollins et al5 did not find a correlation between asphyxia (infants meeting criteria for hypoxic-ischemic encephalopathy) and the presence or pattern of magnetic resonance imaging (MRI) findings or subsequent neurologic morbidity in their report. Because global hypoxia and hypotension tend to produce diffuse cerebral injury, what role does asphyxia play in the evolution of these focal arterial infarcts, if any? Most of these arterial occlusive events appear to be arising from embolization, as discussed by Barmada et al3 and Friede.6 This might occur as degenerating …