The Antiphospholipid Antibody Syndrome

Marengo-Rowe, Alain J.; Leveson, James E.

doi:10.1080/08998280.1996.11929955

Cited by 3 publications

(1 citation statement)

References 26 publications

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“…Acquired maternal/placental diseases can further expose the fetus to more sustained and severe hypercoagulability with resultant cerebral infarction, including autoimmune diseases such as systemic lupus erythematosis [56], hypertensive disorders of pregnancy (especially preeclampsia) [57][58][59][60][61][62] and genetic forms of thrombophilia to mother and/or fetus [63][64][65]. These conditions may act independently or cumulatively with injuries in the placenta which contribute to the stroke syndrome in the fetus or neonate [66][67][68][69][70][71][72][73][74][75][76][77][78].…”

Section: Intrauterine Vasculopathies and Risk For Epilepsymentioning

confidence: 99%

Prenatal contributions to epilepsy: lessons from the bedside

Scher

2003

Epileptic Disorders

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While epilepsy can present at any age, this condition often occurs because of adverse events early in life. Pathogenetic mechanisms also cause deleterious consequences to the brain during prenatal life. For the epileptologist to fully appreciate developmental epileptogenesis, one must apply an ontogenetic approach (i.e. “nature‐nurture‐niche”) in order to study the epileptic condition from a fetal neurology perspective. Genetic susceptibility can involve pre‐fertilization and post‐fertilization mechanisms that dictate the timing and form of major malformations associated with specific epileptic syndromes. Maternal, fetal, and placental disease conditions also contribute to either brain malformations or injuries, depending on events during the first or second half of pregnancy. Sequential stages during prenatal brain development, from embryonic through perinatal periods, specify which gray and white matter structures may be adversely altered, with later expression of seizures in the context of motor, cognitive and behavioral deficits. Translational research from bench to bedside should consider the acquired causes of pediatric and adult epilepsies in the context of the patient's genetic environment.

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