Preeclampsia and the brain: neural control of cardiovascular changes during pregnancy and neurological outcomes of preeclampsia

Abstract

Preeclampsia (PE) is a form of gestational hypertension that complicates ~ 5 percent of pregnancies worldwide. Over 70 percent of the fatal cases of PE are attributed to cerebral edema, intracranial hemorrhage, and eclampsia. The etiology of PE originates from abnormal remodeling of the maternal spiral arteries, creating an ischemic placenta that releases factors that drive the pathophysiology. An initial neurological outcome of PE is the absence of the autonomically regulated cardiovascular adaptations to pregnancy. PE patients exhibit sympathetic overactivation, in comparison to both normotensive pregnant and hypertensive non-pregnant females. Moreover, PE diminishes baroreceptor reflex sensitivity (BRS) beyond that observed in healthy pregnancy. The absence of the cardiovascular adaptations to pregnancy, combined with sympathovagal imbalance and a blunted BRS leads to life-threatening neurological outcomes. Behaviorally, the increased incidences of maternal depression, anxiety, and post-traumatic stress disorder (PTSD) in PE are correlated to low fetal birth weight, intrauterine growth restriction (IUGR) and premature birth. This review addresses these neurological consequences of PE that present in the gravid female both during and after the index pregnancy.

Hypoxic Adaptation of Mitochondrial Metabolism in Rat Cerebellum Decreases in Pregnancy

“…Besides, lysine catabolism is related to biosynthesis of homoarginine which is elevated in normal pregnancy [13], with some studies linking its elevation to pregnancy disorders, including preeclampsia [55]. Physiological manifestations of pre-eclampsia and eclampsia, associated with nearly one-tenth of all maternal deaths [56], involve changed cerebral hemodynamics and hypertensive encephalopathy [57][58][59], potentially linked to impaired signaling by homoarginine, known as a predictor of cardiovascular risk and mortality [3]. Alternatively, homoarginine is synthesized from arginine and glycine.…”

Adrenergic receptor blockade attenuates placental ischemia-induced hypertension

“…; Hammer and Cipolla ; von Dadelszen and Magee ; Logue et al. ). Complications of PE appear to be more diverse than other hypertensive disorders of pregnancy with dysfunction in organ systems like the heart, kidney, liver, brain, and placenta (Shen et al.…”

“…PE is clinically defined as new-onset hypertension occurring during the second half of pregnancy along with additional systemic vascular abnormalities in the mother. These include reduced cardiac reserve, cerebral vascular autoregulation, and renal hemodynamics along with increased glomerular injury, pulmonary edema, and cerebral edema (Stillman and Karumanchi 2007; American College of Obstetricians , Gynecologists, and Task Force on Hypertension in Pregnancy, 2013; Gandhi et al 2014;Melchiorre et al 2014;Hammer and Cipolla 2015;von Dadelszen and Magee 2016;Logue et al 2016). Complications of PE appear to be more diverse than other hypertensive disorders of pregnancy with dysfunction in organ systems like the heart, kidney, liver, brain, and placenta (Shen et al 2017;Tooher et al 2017).…”

Distinct molecular processes in placentae involved in two major subtypes of preeclampsia

“…The global incidence rate is 4.6% of pregnancies (Abalos et al, 2013), leading to 60,000 maternal deaths per year (Logue et al, 2016). The grave consequences of PE on maternal health are mainly attributed to cerebral edema, intracranial hemorrhage and eclampsia Zeeman, 2009), which some studies have suggested to be caused by abnormal functions of the autonomic nervous system mediated by placenta-derived factors (Eneroth-Grimfors et al, 1994;Melchiorre et al, 2014;Voss et al, 2006).…”

“…2,3 The global incidence rate is 4.6% of pregnancies, 4 leading to 60,000 maternal deaths per year. 5 The grave consequences of PE on maternal health are mainly attributed to cerebral edema, intracranial hemorrhage and eclampsia, 6,7 which some studies have suggested to be caused by abnormal functions of the autonomic nervous system mediated by placenta-derived factors. [8][9][10] PE has significant consequences on fetal development and growth, often leading to perinatal and infant morbidity or mortality 1 and contributes preterm births 11 and ~15% cases of fetal growth restriction (FGR).…”