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Published on: November 20, 2015
Neurodevelopmental Disruptions in Children of Preeclamptic Mothers: Pathophysiological Mechanisms and Consequences
Andrea González-Rojas1, Martina Valencia-Narbona1
1Laboratorio de Neurociencias Aplicadas, Escuela de Kinesiología, Facultad de Ciencias, Pontificia Universidad Católica de Valparaíso, Avenida Brasil 2950, Valparaíso 2340025, Chile.
Insights
Preeclampsia (PE) in mothers can impact fetal neurodevelopment through various mechanisms. This review explores PE
Area of Science:
- Obstetrics and Gynecology
- Neuroscience
- Developmental Biology
Background:
- Preeclampsia (PE) is a serious pregnancy complication characterized by hypertension after 20 weeks of gestation.
- PE affects multiple maternal organ systems and can lead to placental dysfunction.
- Placental changes in PE are linked to potential neurodevelopmental issues in offspring.
Purpose of the Study:
- To review the pathophysiological mechanisms linking preeclampsia to offspring neurodevelopment.
- To describe the relationship between PE and neurological alterations in children.
- To highlight prevention and treatment strategies for PE and its neurodevelopmental consequences.
Main Methods:
- Narrative literature review.
- Analysis of existing research on PE and neurodevelopment.
- Synthesis of data on pathophysiological pathways and clinical associations.
Main Results:
- PE involves hypoxia, vascular and angiogenic dysregulation, inflammation, and neuronal alterations.
- Offspring of mothers with PE show increased risks for neurodevelopmental disorders like ADHD, ASD, and cerebral palsy.
- Sexual dimorphism in neurodevelopmental outcomes associated with PE has been observed.
Conclusions:
- Understanding PE's impact on fetal neurodevelopment is crucial for maternal and child health.
- Targeting PE's pathophysiological mechanisms may mitigate neurodevelopmental risks.
- Early intervention and management of PE are vital for improving long-term offspring outcomes.
Abstract:
Preeclampsia (PE) is a multisystem disorder characterized by elevated blood pressure in the mother, typically occurring after 20 weeks of gestation and posing risks to both maternal and fetal health. PE causes placental changes that can affect the fetus, particularly neurodevelopment. Its key pathophysiological mechanisms encompass hypoxia, vascular and angiogenic dysregulation, inflammation, neuronal and glial alterations, and disruptions in neuronal signaling. Animal models indicate that PE is correlated with neurodevelopmental alterations and cognitive dysfunctions in offspring and in humans, an association between PE and conditions such as cerebral palsy, autism spectrum disorder, attention deficit hyperactivity disorder, and sexual dimorphism has been observed. Considering the relevance for mothers and children, we conducted a narrative literature review to describe the relationships between the pathophysiological mechanisms behind neurodevelopmental alterations in the offspring of PE mothers, along with their potential consequences. Furthermore, we emphasize aspects pertinent to the prevention/treatment of PE in pregnant mothers and alterations observed in their offspring. The present narrative review offers a current, complete, and exhaustive analysis of (i) the pathophysiological mechanisms that can affect neurodevelopment in the children of PE mothers, (ii) the relationship between PE and neurological alterations in offspring, and (iii) the prevention/treatment of PE.
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