Comment on “A prospective study on fetal posterior cranial fossa assessment for early detection of open spina bifida at 11–13 weeks” by Kose et al.

Lachmann, Robert

doi:10.1111/cga.12265

Cited by 2 publications

(1 citation statement)

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“…Given that neocortex development in OSB fetuses is apparently altered as early as 11 weeks of gestation, our data support the need for an early OSB diagnosis and fetal repair. By using the midsagittal view for the measurement of nuchal translucency and assessment of BS-BSOB-ratio, cisterna magna width, and presence of a Single-Line-Sign for the identification of OSB fetuses between 11 and 13 weeks of gestation, this study provides further evidence for the notion that this method enables physicians to reliably identify fetal brain abnormalities, such as OSB, and cystic posterior fossa abnormalities, including Dandy-Walker syndrome, agenesis of the corpus callosum, and isolated cleft lip and palate at an early developmental stage (Lachmann et al, 2010(Lachmann et al, , 2012(Lachmann et al, , 2013(Lachmann et al, , 2018Lachmann, 2012Lachmann, , 2018. Further studies are necessary to investigate whether surgical intervention before 19 weeks of gestation limits impaired neocortex development and thus further improve long-term neurological function.…”

Section: Discussionmentioning

confidence: 57%

Signs of Reduced Basal Progenitor Levels and Cortical Neurogenesis in Human Fetuses with Open Spina Bifida at 11–15 Weeks of Gestation

et al. 2020

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Open spina bifida (OSB) is one of the most prevalent congenital malformations of the CNS that often leads to severe disabilities. Previous studies reported the volume and thickness of the neocortex to be altered in children and adolescents diagnosed with OSB. Until now, the onset and the underlying cause of the atypical neocortex organization in OSB patients remain largely unknown. To examine the effects of OSB on fetal neocortex development, we analyzed human fetuses of both sexes diagnosed with OSB between 11 and 15 weeks of gestation by immunofluorescence for established neuronal and neural progenitor marker proteins and compared the results with healthy controls of the same, or very similar, gestational age. Our data indicate that neocortex development in OSB fetuses is altered as early as 11 weeks of gestation. We observed a marked reduction in the radial thickness of the OSB neocortex, which appears to be attributable to a massive decrease in the number of deep-and upper-layer neurons per field, and found a marked reduction in the number of basal progenitors (BPs) per field in the OSB neocortex, consistent with an impairment of cortical neurogenesis underlying the neuronal decrease in OSB fetuses. Moreover, our data suggest that the decrease in BP number in the OSB neocortex may be associated with BPs spending a lesser proportion of their cell cycle in M-phase. Together, our findings expand our understanding of the pathophysiology of OSB and support the need for an early fetal therapy (i.e., in the first trimester of pregnancy).

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