2019
DOI: 10.1111/dmcn.14375
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Perinatal inflammation and placental programming of neonatal stroke

Abstract: This commentary is on the original article by Sorg et al. on pages 513–520 of this issue.

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Cited by 4 publications
(3 citation statements)
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“…This is similarly high to the rate of placental lesions in a cohort of patients we recently studied with congenital heart disease (78%) (39). Placental inflammatory conditions seem to play a prominent role in perinatal stroke pathophysiology (38), and our cohort has similar findings with 80% showing acute and/or chronic inflammation of the placenta. These inflammatory processes may contribute to formation of emboli of placental origin that reach the fetal cerebrovasculature through the PFO (38,40).…”
Section: Discussionsupporting
confidence: 83%
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“…This is similarly high to the rate of placental lesions in a cohort of patients we recently studied with congenital heart disease (78%) (39). Placental inflammatory conditions seem to play a prominent role in perinatal stroke pathophysiology (38), and our cohort has similar findings with 80% showing acute and/or chronic inflammation of the placenta. These inflammatory processes may contribute to formation of emboli of placental origin that reach the fetal cerebrovasculature through the PFO (38,40).…”
Section: Discussionsupporting
confidence: 83%
“…Placental inflammatory conditions seem to play a prominent role in perinatal stroke pathophysiology (38), and our cohort has similar findings with 80% showing acute and/or chronic inflammation of the placenta. These inflammatory processes may contribute to formation of emboli of placental origin that reach the fetal cerebrovasculature through the PFO (38,40). Further evidence supporting a placental origin of emboli are that an estimated 30% of neonatal stroke is multifocal, even in the absence of CHD and the recurrence of AIS postnatally is exceedingly rare (4).…”
Section: Discussionsupporting
confidence: 83%
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