Maternal Pyelonephritis as a Potential Cause of Perinatal Periventricular Venous Infarction in Term-Born Children

Abstract

Introduction: The study was designed to assess the prevalence of pregnancy and delivery associated risk factors in children suffering from neonatal or presumed periventricular venous infarction. Methods: Antenatal records and pregnancy outcome data were retrospectively assessed in children with presumed periventricular venous infarction (n = 43, born ≥36 gestational weeks) or neonatal periventricular venous infarction (n = 86, born <36 gestational weeks) and compared to a matched control group (n = 2168, ≥36 gestational weeks) from a prospective study. Results: Children with presumed periventricular venous infarction had significantly more maternal bacterial infections compared to the control group (47% vs 20%, respectively, P < .001), whereas no difference was found compared to the neonatal periventricular venous infarction group (49%, P = .80). Mothers with bacterial infection in the presumed periventricular venous infarction group had significantly more often pyelonephritis compared to the control group (50% vs 3.4%, respectively, P < .001). Conclusions: Our data show an increased risk for developing periventricular venous infarction in the case of maternal bacterial infections, especially between gestational weeks 21 and 31.

The thalamus and basal ganglia are smaller in children with epilepsy after perinatal stroke

“…Clinical information about pregnancy, delivery, and the neonatal period was collected from medical records and patient interviews as reported earlier ( 4 , 8 , 23 ). Pregnancy and birth history, symptoms during the neonatal period, stroke presentation, age at the first epileptic seizure and age at the epilepsy diagnosis, seizure semiology, antiseizure medication, seizure control, and presence of status epilepticus were recorded.…”

High Prevalence of Collagenopathies in Preterm- and Term-Born Children With Periventricular Venous Hemorrhagic Infarction

“…The Estonian Pediatric Stroke Database has been created retrospectively since 1994 and prospectively with continuously added cases since 2003. 9 , 11 , 21 , 22 The vascular classification of patients in the Estonian Pediatric Stroke Database is based on MRI according to Kirton and coauthors. 9 , 12 , 14 Chronic changes after periventricular hemorrhagic infarction/periventricular venous infarction are described on MRI, based on this classification, 12 as a medullary venous territory infarction in the periventricular area, with a porencephalic enlargement of the lateral ventricle, and/or periventricular gliosis and/or cystic changes, spared cortex, and presence of hemosiderin in the area of the germinal matrix and in the ventricles and/or in periventricular lesion.…”

“…8,9,14,17,20 Recent research shows that prenatal infection and chorioamnionitis may play a critical role in some term-born children with presumed antenatal periventricular venous infarction. 11,38 Previously suspected thrombophilia risk is not increased in children with neonatal or presumed arterial ischemic stroke, or with presumed antenatal periventricular venous infarction. 39 A recent meta-analysis of antenatal periventricular hemorrhagic infarction studies showed typical pregnancy without co-occurring conditions in 39% of cases.…”

“…3 On magnetic resonance imaging (MRI), periventricular hemorrhagic infarction is evaluated as prevalently unilateral medullary venous territory infarction in the periventricular area during the acute stage and as a porencephalic enlargement of the lateral ventricle of various severity, and/or periventricular gliosis and/or cystic changes with a spared cortex during the chronic stage. [8][9][10][11][12] Germinal matrix hemorrhage is especially common in premature infants born below 32 gestational weeks because of the suggested fragile state of the vessel wall in the germinal matrix. 3,8,13,14 Antenatal periventricular hemorrhagic infarction may be detected by fetal ultrasonography incidentally 15,16 and probably reflect the same pathologic mechanism as is seen in pretermborn children.…”

“… 10 MRI findings suggest that presumed antenatal periventricular venous infarction occurs at a certain stage of vascular development of the brain at gestational weeks 24-34 with germinal matrix hemorrhage as the source. 3 , 8 , 11 , 13 Vascular disruption and development of periventricular hemorrhagic infarction before gestational week 24 can lead to schizencephaly, and after gestational week 24 can lead to porencephaly 19 , 25 – 29 the severity of which depends on the size of initial stroke. Clinically, periventricular hemorrhagic infarction/periventricular venous infarction leads to congenital hemi- or tetraparesis of various severity, epilepsy, and cognitive disability.…”