Fetal brain development in diabetic pregnancies and normal controls

AbstractObjectiveTo assess whether fetal brain structures routinely measured during the second and third trimester ultrasound scans, particularly the width of the cavum septi pellucidi (CSP), differ between fetuses small for gestational age (SGA), fetuses very small for gestational age (VSGA) and normal controls.MethodsIn this retrospective study, we examined standard ultrasound measurements of 116 VSGA, 131 SGA fetuses and 136 normal controls including the head circumference (HC), transversal diameter of the cerebellum (TCD), the sizes of the lateral ventricle (LV) and the cisterna magna (CM) from the second and third trimester ultrasound scans extracted from a clinical database. We measured the CSP in these archived ultrasound scans. The HC/CSP, HC/LV, HC/CM and HC/TCD ratios were calculated as relative values independent of the fetal size.ResultsThe HC/CSP ratio differed notably between the controls and each of the other groups (VSGA P = 0.018 and SGA P = 0.017). No notable difference in the HC/CSP ratio between the VSGA and SGA groups could be found (P = 0.960). The HC/LV, HC/CM and HC/TCD ratios were similar in all the three groups.ConclusionRelative to HC, the CSP is larger in VSGA and SGA fetuses than in normal controls. However, there is no notable difference between VSGA and SGA fetuses, which might be an indicator for abnormal brain development in this group.

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New normal range of fetal cavum septum pellucidum in the second trimester of gestation

10.21516/2413-1458-2020-19-1-21-24 ◽

2020 ◽

Author(s):

M.V. Medvedev, O.I. Kozlova, À.Yu. Romanova

Keyword(s):

Brain Development ◽

Reference Range ◽

Fetal Brain ◽

Septum Pellucidum ◽

Second Trimester ◽

Normal Range ◽

Cavum Septum Pellucidum ◽

New Normal ◽

Biparietal Diameter ◽

Fetal Brain Development

Fetal brain was retrospectively evaluated in 418 normal fetuses at 16–28 weeks of gestation. The multiplanar mode to obtain the axial cerebral plane and measured the width of the cavum septum pellucidum (CSP) and biparietal diameter (BD). All measurements of CSP were done from as the widest diameter across both borders in an inter-to inter fashion. The CSP width is increasing at second trimester of gestation. Normal range plotted on the reference range (mean, 5th and 95th percentiles) of fetal width CSP by measuring of its size may be useful for assessment of fetal brain development in the second trimester of gestation.

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CB1 antagonism increases excitatory synaptogenesis in a cortical spheroid model of fetal brain development

Scientific Reports ◽

10.1038/s41598-021-88750-2 ◽

2021 ◽

Vol 11 (1) ◽

Author(s):

Alexis Papariello ◽

David Taylor ◽

Ken Soderstrom ◽

Karen Litwa

Keyword(s):

Brain Development ◽

Spontaneous Activity ◽

Microelectrode Array ◽

Cannabinoid Receptor ◽

Fetal Brain ◽

Endocannabinoid System ◽

Autism Spectrum ◽

Nervous System Development ◽

Inhibitory Synapses ◽

Fetal Brain Development

AbstractThe endocannabinoid system (ECS) plays a complex role in the development of neural circuitry during fetal brain development. The cannabinoid receptor type 1 (CB1) controls synaptic strength at both excitatory and inhibitory synapses and thus contributes to the balance of excitatory and inhibitory signaling. Imbalances in the ratio of excitatory to inhibitory synapses have been implicated in various neuropsychiatric disorders associated with dysregulated central nervous system development including autism spectrum disorder, epilepsy, and schizophrenia. The role of CB1 in human brain development has been difficult to study but advances in induced pluripotent stem cell technology have allowed us to model the fetal brain environment. Cortical spheroids resemble the cortex of the dorsal telencephalon during mid-fetal gestation and possess functional synapses, spontaneous activity, an astrocyte population, and pseudo-laminar organization. We first characterized the ECS using STORM microscopy and observed synaptic localization of components similar to that which is observed in the fetal brain. Next, using the CB1-selective antagonist SR141716A, we observed an increase in excitatory, and to a lesser extent, inhibitory synaptogenesis as measured by confocal image analysis. Further, CB1 antagonism increased the variability of spontaneous activity within developing neural networks, as measured by microelectrode array. Overall, we have established that cortical spheroids express ECS components and are thus a useful model for exploring endocannabinoid mediation of childhood neuropsychiatric disease.

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Neuroplacentology in congenital heart disease: placental connections to neurodevelopmental outcomes

Pediatric Research ◽

10.1038/s41390-021-01521-7 ◽

2021 ◽

Author(s):

Rachel L. Leon ◽

Imran N. Mir ◽

Christina L. Herrera ◽

Kavita Sharma ◽

Catherine Y. Spong ◽

...

Keyword(s):

Brain Development ◽

Congenital Heart ◽

Fetal Brain ◽

In Utero ◽

Structure And Function ◽

Brain Growth ◽

Neurodevelopmental Outcomes ◽

Fetal Brain Development ◽

And Function

Abstract Children with congenital heart disease (CHD) are living longer due to effective medical and surgical management. However, the majority have neurodevelopmental delays or disorders. The role of the placenta in fetal brain development is unclear and is the focus of an emerging field known as neuroplacentology. In this review, we summarize neurodevelopmental outcomes in CHD and their brain imaging correlates both in utero and postnatally. We review differences in the structure and function of the placenta in pregnancies complicated by fetal CHD and introduce the concept of a placental inefficiency phenotype that occurs in severe forms of fetal CHD, characterized by a myriad of pathologies. We propose that in CHD placental dysfunction contributes to decreased fetal cerebral oxygen delivery resulting in poor brain growth, brain abnormalities, and impaired neurodevelopment. We conclude the review with key areas for future research in neuroplacentology in the fetal CHD population, including (1) differences in structure and function of the CHD placenta, (2) modifiable and nonmodifiable factors that impact the hemodynamic balance between placental and cerebral circulations, (3) interventions to improve placental function and protect brain development in utero, and (4) the role of genetic and epigenetic influences on the placenta–heart–brain connection. Impact Neuroplacentology seeks to understand placental connections to fetal brain development. In fetuses with CHD, brain growth abnormalities begin in utero. Placental microstructure as well as perfusion and function are abnormal in fetal CHD.

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