Sonographic assessment of normal and abnormal patterns of fetal cerebral lamination

Pugash, D.; Hendson, Glenda; Dunham, Christopher; Dewar, Kathryn; Money, Deborah; Prayer, Daniela

doi:10.1002/uog.11164

Cited by 36 publications

(26 citation statements)

References 49 publications

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“…First, morphological and neurochemical characterization of these neurones in post mortem materials can clarify whether these cells are consistent with the characteristics of subplate neurones that have been so well described in both animal and human studies. Secondly, longitudinal pre‐ and postnatal imaging studies can be used to quantify and describe the subplate compartment and how it changes over time [170]. Retrospective use of such materials following diagnosis in early childhood could help to identify atypical developmental trajectories within this region and might inform how the NT subplate population may be altered in ASD.…”

Section: Potential Alterations To the Cortical Subplatementioning

confidence: 99%

Review: Cortical construction in autism spectrum disorder: columns, connectivity and the subplate

Hutsler

Casanova

2015

Neuropathology Appl Neurobio

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The cerebral cortex undergoes protracted maturation during human development and exemplifies how biology and environment are inextricably intertwined in the construction of complex neural circuits. Autism spectrum disorders are characterized by a number of pathological changes arising from this developmental process. These include: (i) alterations to columnar structure that have significant implications for the organization of cortical circuits and connectivity; (ii) alterations to synaptic spines on individual cortical units that may underlie specific types of connectional changes; and (iii) alterations within the cortical subplate, a region that plays a role in proper cortical development and in regulating interregional communication in the mature brain. Although the cerebral cortex is not the only structure affected in the disorder, it is a fundamental contributor to the behaviours that characterize autism. These alterations to cortical circuitry likely underlie the behavioural phenotype in autism and contribute to the unique pattern of deficits and strengths that characterize cognitive functioning. Recent findings within the cortical subplate may indicate that alterations to cortical construction begin prenatally, before activity-dependent connections are established, and are in need of further study. A better understanding of cortical development in autism spectrum disorders will draw bridges between the microanatomical computational circuitry and the atypical behaviours that arise when that circuitry is modified. In addition, it will allow us to better exploit the constructional plasticity within the brain to design more targeted interventions that better manage atypical cortical construction and that can be applied very early in postnatal life.

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Section: Potential Alterations To the Cortical Subplatementioning

confidence: 99%

Review: Cortical construction in autism spectrum disorder: columns, connectivity and the subplate

Hutsler

Casanova

2015

Neuropathology Appl Neurobio

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“…Magnetic resonance imaging has the advantage, compared to US, for better evaluation of the corpus callosum itself rather than relying on indirect signs 36 . It is also more sensitive to evaluate other intracranial abnormalities, 37,38 including migration disorders, 39,40 delayed or abnormal sulcation, 37,41 and prior infectious 42 or metabolic 43 insults.…”

Section: Discussionmentioning

confidence: 99%

Ultrasound and Magnetic Resonance Imaging of Agenesis of the Corpus Callosum in Fetuses

Ghassemi

Rupe

Perez

et al. 2020

J of Ultrasound Medicine

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Objectives-We hypothesized that: (1) fetal frontal horn (FH) morphology and their proximity to the cavum septi pellucidi (CSP) can assist in suspecting complete agenesis of the corpus callosum (cACC) and partial agenesis of the corpus callosum (pACC) earlier than known indirect ultrasound (US) findings; (2) FHs assist in differentiating a true CSP from a pseudocavum; and (3) magnetic resonance imaging (MRI) is useful in learning FH morphology and pseudocavum etiology. Methods-Thirty-two patients with cACC and 9 with pACC were identified on an Institutional Review Board-approved retrospective review. Of the 41 cases, 40 had prenatal US, and 21 had prenatal MRI; 17 had follow-up neonatal US, and 14 had follow-up neonatal MRI. Variables evaluated retrospectively were the presence of a CSP or a pseudocavum, ventricle size and shape, and FH shape (comma, trident, parallel, golf club, enlarged, or fused). Displacement between the inferior edge of the FH and the midline or cavum/pseudocavum was measured. Results-Fetal FHs had an abnormal shape in 77% ≤20 weeks' gestation, 86% ≤24 weeks, and 90% >24 weeks. Frontal horns were laterally displaced greater than 2 mm in 85% ≤20 weeks, 91% ≤24 weeks, and 95% >24 weeks. The CSP was absent in 100% of cACC cases and 78% of pACC cases, and a pseudocavum was present in 88% of cACC cases and 78% of pACC cases across gestation. Magnetic resonance imaging confirmed US pseudocavums to be focal interhemispheric fluid or an elevated/dilated third ventricle. Conclusions-Frontal horns assist in assessing ACC ≤24 weeks and throughout gestation. Pseudocavums, often simulating CSPs, are common in ACC. Frontal horn lateral displacement and abnormal morphology, recognized by MRI correlations, are helpful in differentiating a pseudocavum from a true CSP. A normal CSP should not be cleared on screening US unless normally shaped FHs are seen directly adjacent to it. Key Words-agenesis of the corpus callosum; cavum septi pellucidi; fetus; frontal horns; ventriculomegaly A genesis of the corpus callosum (ACC) is defined as complete or partial absence of the large commissure that connects the two cerebral hemispheres. Development

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“…The cerebral cortex development implies evolvement through three steps: neuronal precursor proliferation and differentiation; migration of immature neurons; and cortical maturation (the laminar organization and occurrence of synapsis). Neurons migrate from the ventricular zone (called the germinal matrix) toward the pial surface, along radially oriented glial scaffolds [42][43][44].…”

Section: Cortical Formation Abnormalitiesmentioning

confidence: 99%

Fetal Central Nervous System Abnormalities

Ceausescu¹,

Docea²,

Dinu³

et al. 2018

Congenital Anomalies - From the Embryo to the Neonate

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Central nervous system (CNS) is one of the most frequent sites for prenatal diagnosed congenital abnormalities (10 per 1000 live births, much higher than the heart-eight per 1000, kidneys-four per 1000, and other fetal systems). Due to the evolving pattern, ultrasound screening for fetal brain malformations is usually performed at 19-22 weeks' gestation, but severe congenital anomalies can be diagnosed much earlier. This chapter is a short review, structured in eight subchapters: the first one is dedicated to the normal ultrasound aspect of different CNS segments, and the following ones are to detect pathology in prenatal life. We used many ultrasound images and tried to correlate the prenatal findings with the ones obtained postpartum/postabortum for each case, by means of pathology/imaging techniques.anomalies of the central nervous system develop early, and nowadays, we have the tools to detect some conditions at 11-13 weeks [3][4][5][6][7][8] or even earlier. The first-trimester detection of CNS anomalies is probably the most important advance in modern sonoembriology. Later in pregnancy, neurosonography is a powerful tool in diagnosing CNS pathology.The following chapter is structured as follows: 1. Normal findings 2. Ventricular system (ventriculomegaly, aqueduct stenosis) 3. Neural tube defects (NTDs) (anencephaly, encephalocele, myelomeningocele) 4. Cortical formation abnormalities (schizencephaly, lissencephaly, heterotopia, microcephaly) 5. Midline abnormalities (holoprosencephaly, complete/partial agenesis of corpus callosum or abnormal corpus callosum, absent cavum septum) 6. Posterior fossa abnormalities (mega cisterna magna, Blake's pouch cyst, Dandy-Walker or variant cerebellar, vermian hypoplasia) 7. Vascular abnormalities (hemorrhage, hematoma, dural fistula, aneurysms) 8. Destructive lesions (hydranencephaly, tumors/mass lesions, cysts, periventricular leukomalacia, infections, dysplasias, other lesions). Normal findingsSome intracranial segments of CNS are seen on ultrasound extremely early in development, especially when using high-resolution probes and modern electronic tools. Although many features are indeed recognizable, the clinical utility of such studies is yet to be proven (Figures 1-3).In the late first trimester, current guidelines recommend checking for present cranial bones, for normal midline falx, and for the presence of choroid plexus and filled ventricles [9]. The most recommended planes for assessing the head anatomy are the axial ones. In terms of spine assessment, the guidelines state that "longitudinal and axial views should be obtained to show normal vertebral alignment and integrity, and an attempt should be made to show intact overlying skin" [9] (Figure 4).From the early second trimester onwards, the commendation is to obtain in standard assessment three standard axial planes (transventricular, transthalamic, and transcerebellar), and, if technically feasible, the fetal profile [10] (Figures 5 and 6).The measurements for fetal head biometry (the biparietal diameter-BPD ...

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Sonographic assessment of normal and abnormal patterns of fetal cerebral lamination

Abstract: Objectives Prenatal development of the brain is characterized by gestational age-specific changes in the laminar

Cited by 36 publications

References 49 publications

Review: Cortical construction in autism spectrum disorder: columns, connectivity and the subplate

Review: Cortical construction in autism spectrum disorder: columns, connectivity and the subplate

Ultrasound and Magnetic Resonance Imaging of Agenesis of the Corpus Callosum in Fetuses

Fetal Central Nervous System Abnormalities

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