Abstract
ObjectivesTo examine differences in growth trajectories of fetal brain fissures in the growth restricted fetus (FGR) compared to controls.MethodsWe selected a subgroup of 227 women with a singleton pregnancy from the Rotterdam Periconceptional Cohort. Participants received three-dimensional ultrasound (3D-US) examinations of the fetal brain at 22, 26 and 32 weeks of gestational age (GA). The left and right Sylvian, insula and parieto-occipital fissures (POF) were measured in standardized planes. Linear mixed models with adjustment for potential confounders were applied to estimate differences between the trajectories of brain fissure depth measurements of FGR and controls.Results22 FGR and 172 controls provided 31 and 504 3D-US respectively for longitudinal brain fissure depth measurements. Success rates for the Sylvian and insula depth measurements were over 80% and for POF over 62% at all GA. In FGR compared to controls, the trajectory of the right Sylvian fissure depth was significantly decreased (ß = -4.30, 95%CI = -8.03;-0.56, p = 0.024) while its growth rate was slightly increased (ß = 0.02, 95%CI = 0.00;0.04, p = 0.04), after adjustment for GA, head circumference, gender, educational level and parity.ConclusionsThe small differences in brain fissure measurements between 22 and 32 weeks GA in FGR warrant further investigation in larger cohorts with postnatal follow-up.
Highlights
Fetal growth restriction (FGR) affects 6–10% of pregnancies [1]
In FGR compared to controls, the trajectory of the right Sylvian fissure depth was significantly decreased (ß = -4.30, 95%CI = -8.03;0.56, p = 0.024) while its growth rate was slightly increased (ß = 0.02, 95%CI = 0.00;0.04, p = 0.04), after adjustment for gestational age (GA), head circumference, gender, educational level and parity
FGR was defined as an abdominal circumference or estimated fetal weight of less than the 5th percentile according to the Hadlock 4 formula [30]
Summary
Fetal growth restriction (FGR) affects 6–10% of pregnancies [1]. These fetuses are at risk for adverse pregnancy and neurodevelopmental outcomes, such as autism, attention deficit hyperactive disorder and schizophrenia [2, 3]. Since abnormal flow and oxygen patterns causing delayed cerebral development have been described in fetuses with congenital heart defects [5, 6], this change in blood flow could indicate an increased risk of developing brain abnormalities and subsequent neurodevelopmental disorders in FGR fetuses [4, 7, 8]. The process of development of new neurons and neuronal migration towards the outer brain surface is associated with cortical growth both in thickness and surface area [9]. This stress-induced development from a smooth to complex cerebral surface of sulci and gyri, called cortical folding, starts at around 18 weeks gestational age (GA) and is strongly correlated with GA [10]
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