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Updated: Mar 6, 2026

A Thrombotic Stroke Model Based On Transient Cerebral Hypoxia-ischemia
Published on: August 18, 2015
Thrombophilia risk is not increased in children after perinatal stroke
Colleen Curtis1,2, Aleksandra Mineyko1,2,3,4, Patricia Massicotte5
1Department of Pediatrics.
Insights
This study found minimal association between perinatal stroke and thrombophilia in children. Routine thrombophilia testing in childhood is not indicated for perinatal stroke cases.
Area of Science:
- Neurology
- Pediatrics
- Hematology
Background:
- Perinatal stroke leads to cerebral palsy and lifelong disability.
- Mechanisms of perinatal stroke remain poorly understood.
- Limited population-based studies exist on thrombophilia in perinatal stroke.
Purpose of the Study:
- To determine the association between specific perinatal stroke diseases and known thrombophilias.
- To inform pathogenesis models and clinical management of perinatal stroke.
- To investigate neonatal arterial ischemic stroke (NAIS), arterial presumed perinatal ischemic stroke (APPIS), and fetal periventricular venous infarction (PVI).
Main Methods:
- Prospective, population-based, case-control study of 212 children.
- Included children with NAIS, APPIS, PVI, and controls.
- Standardized thrombophilia evaluations performed after 12 months of age.
Main Results:
- No significant differences in 12 of 14 thrombophilia parameters between cases and controls.
- Rates of antiphospholipid antibodies were low and comparable to controls.
- Factor V Leiden (FVL) and Factor II G20210A (FII) rates were comparable to population norms.
Conclusions:
- Minimal association observed between perinatal stroke and thrombophilia.
- Does not exclude disordered coagulation at the time of stroke.
- Childhood thrombophilia testing is not indicated for 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.
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