I V Koning1,2, J A Roelants1,2, I A L Groenenberg1, M J Vermeulen2, S P Willemsen1,3, I K M Reiss2, P P Govaert2,4, R P M Steegers-Theunissen1,2, J Dudink5,6. 1. From the Department of Obstetrics and Gynecology (I.V.K., J.A.R., I.A.L.G., S.P.W., R.P.M.S.-T.), Division of Obstetrics and Prenatal Medicine. 2. Department of Pediatrics (I.V.K., J.A.R., M.J.V., I.K.M.R., P.P.G., R.P.M.S.-T., J.D.), Division of Neonatology, Erasmus MC-Sophia Children's Hospital, Rotterdam, the Netherlands. 3. Department of Biostatistics (S.P.W.), Erasmus MC, University Medical Center, Rotterdam, the Netherlands. 4. Department of Neonatology (P.P.G.), ZNA Koningin Paola Ziekenhuis, Antwerp, Belgium. 5. Department of Pediatrics (I.V.K., J.A.R., M.J.V., I.K.M.R., P.P.G., R.P.M.S.-T., J.D.), Division of Neonatology, Erasmus MC-Sophia Children's Hospital, Rotterdam, the Netherlands j.dudink@umcutrecht.nl. 6. Department of Neonatology (J.D.), Wilhelmina's Children's Hospital, University Medical Center Utrecht, Utrecht, the Netherlands.
Abstract
BACKGROUND AND PURPOSE: Most ultrasound markers for monitoring brain growth can only be used in either the prenatal or the postnatal period. We investigated whether corpus callosum length and corpus callosum-fastigium length could be used as markers for both prenatal and postnatal brain growth. MATERIALS AND METHODS: A 3D ultrasound study embedded in the prospective Rotterdam Periconception Cohort was performed at 22, 26 and 32 weeks' gestational age in fetuses with fetal growth restriction, congenital heart defects, and controls. Postnatally, cranial ultrasound was performed at 42 weeks' postmenstrual age. First, reliability was evaluated. Second, associations between prenatal and postnatal corpus callosum and corpus callosum-fastigium length were investigated. Third, we created reference curves and compared corpus callosum and corpus callosum-fastigium length growth trajectories of controls with growth trajectories of fetuses with fetal growth retardation and congenital heart defects. RESULTS: We included 199 fetuses; 22 with fetal growth retardation, 20 with congenital heart defects, and 157 controls. Reliability of both measurements was excellent (intraclass correlation coefficient ≥ 0.97). Corpus callosum growth trajectories were significantly decreased in fetuses with fetal growth restriction and congenital heart defects (β = -2.295; 95% CI, -3.320-1.270; P < .01; β = -1.267; 95% CI, -0.972-0.562; P < .01, respectively) compared with growth trajectories of controls. Corpus callosum-fastigium growth trajectories were decreased in fetuses with fetal growth restriction (β = -1.295; 95% CI, -2.595-0.003; P = .05). CONCLUSIONS: Corpus callosum and corpus callosum-fastigium length may serve as reliable markers for monitoring brain growth from the prenatal into the postnatal period. The clinical applicability of these markers was established by the significantly different corpus callosum and corpus callosum-fastigium growth trajectories in fetuses at risk for abnormal brain growth compared with those of controls.
BACKGROUND AND PURPOSE: Most ultrasound markers for monitoring brain growth can only be used in either the prenatal or the postnatal period. We investigated whether corpus callosum length and corpus callosum-fastigium length could be used as markers for both prenatal and postnatal brain growth. MATERIALS AND METHODS: A 3D ultrasound study embedded in the prospective Rotterdam Periconception Cohort was performed at 22, 26 and 32 weeks' gestational age in fetuses with fetal growth restriction, congenital heart defects, and controls. Postnatally, cranial ultrasound was performed at 42 weeks' postmenstrual age. First, reliability was evaluated. Second, associations between prenatal and postnatal corpus callosum and corpus callosum-fastigium length were investigated. Third, we created reference curves and compared corpus callosum and corpus callosum-fastigium length growth trajectories of controls with growth trajectories of fetuses with fetal growth retardation and congenital heart defects. RESULTS: We included 199 fetuses; 22 with fetal growth retardation, 20 with congenital heart defects, and 157 controls. Reliability of both measurements was excellent (intraclass correlation coefficient ≥ 0.97). Corpus callosum growth trajectories were significantly decreased in fetuses with fetal growth restriction and congenital heart defects (β = -2.295; 95% CI, -3.320-1.270; P < .01; β = -1.267; 95% CI, -0.972-0.562; P < .01, respectively) compared with growth trajectories of controls. Corpus callosum-fastigium growth trajectories were decreased in fetuses with fetal growth restriction (β = -1.295; 95% CI, -2.595-0.003; P = .05). CONCLUSIONS: Corpus callosum and corpus callosum-fastigium length may serve as reliable markers for monitoring brain growth from the prenatal into the postnatal period. The clinical applicability of these markers was established by the significantly different corpus callosum and corpus callosum-fastigium growth trajectories in fetuses at risk for abnormal brain growth compared with those of controls.
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