title: Thrombophilia risk is not increased in children after perinatal stroke.
abstract: Perinatal stroke causes cerebral palsy and lifelong disability. Specific diseases are definable, but mechanisms are poorly understood. Evidence suggests possible associations between arterial perinatal stroke and prothrombotic disorders, but population-based, controlled, disease-specific studies are limited. Understanding thrombophilia in perinatal stroke informs pathogenesis models and clinical management. We conducted a population-based, prospective, case-control study to determine the association of specific perinatal stroke diseases with known thrombophilias. Children with idiopathic magnetic resonance imaging-classified neonatal arterial ischemic stroke (NAIS), arterial presumed perinatal ischemic stroke (APPIS), or fetal periventricular venous infarction (PVI) were recruited. Standardized thrombophilia evaluations were performed after 12 months of age on stroke cases and controls, including quantified proteins C and S, antithrombin, factors VIII/IX/XI, fibrinogen, lipoprotein(a), homocysteine, lupus anticoagulant, anticardiolipin antibodies and genotyping of factor V Leiden (FVL), factor II G20210A (FII), and methylenetetrahydrofolate reductase C677T. A total of 212 children were studied: 46 with NAIS, 34 with APPIS, 55 with PVI, and 77 controls (male, 53%; median age, 4.8 years). Of 14 parameters, no differences were observed in 12, including all common thrombophilias. Mean prothrombin time was shorter in arterial strokes (P< .001). Rates of antiphospholipid antibodies were low, comparable to those in controls, and resolved on repeat testing. FVL and FII rates were comparable to population norms. Total number of possible abnormalities did not differ between cases and controls. Our prospective, population-based, controlled, disease-specific study suggests minimal association between perinatal stroke and thrombophilia. This does not exclude the possibility of disordered coagulation at the time of stroke but suggests testing in childhood is not indicated.
authors.affiliation: Department of Pediatrics.|Cumming School of Medicine.
authors.forename: Colleen
authors.initials: C
authors.lastname: Curtis
authors.affiliation: Department of Pediatrics.|Cumming School of Medicine.|Department of Clinical Neurosciences, and.|Alberta Children's Hospital Research Institute, University of Calgary, Calgary, Canada.
authors.forename: Aleksandra
authors.initials: A
authors.lastname: Mineyko
authors.affiliation: Department of Pediatrics, University of Alberta, Edmonton, Canada; and.
authors.forename: Patricia
authors.initials: P
authors.lastname: Massicotte
authors.affiliation: Department of Pediatrics.|Cumming School of Medicine.|Alberta Children's Hospital Research Institute, University of Calgary, Calgary, Canada.
authors.forename: Michael
authors.initials: M
authors.lastname: Leaker
authors.affiliation: Department of Pathology and Laboratory Medicine, University of Calgary, Calgary, Canada.
authors.forename: Xiu Yan
authors.initials: XY
authors.lastname: Jiang
authors.affiliation: Alberta Children's Hospital Research Institute, University of Calgary, Calgary, Canada.
authors.forename: Amalia
authors.initials: A
authors.lastname: Floer
authors.affiliation: Department of Pediatrics.|Cumming School of Medicine.|Department of Clinical Neurosciences, and.|Alberta Children's Hospital Research Institute, University of Calgary, Calgary, Canada.
authors.forename: Adam
authors.initials: A
authors.lastname: Kirton
mesh_terms: D000293:Adolescent; D002648:Child; D002675:Child, Preschool; D005260:Female; D005838:Genotype; D006801:Humans; D007223:Infant; D007231:Infant, Newborn; D008297:Male; D012307:Risk Factors; D020521:Stroke / Q000150:complications*; D019851:Thrombophilia / Q000453:epidemiology* / Q000209:etiology* / Q000235:genetics; D055815:Young Adult