Brain malformations related to prenatal exposure to ethanol

Clarren, Sterling K.; Alvord, Ellsworth C.; Sumi, S. M.; Streissguth, Ann P.; Smith, David W.

doi:10.1016/s0022-3476(78)80072-9

Cited by 611 publications

(228 citation statements)

References 4 publications

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“…a flat mid face associated with maxillary and mandibular hypoplasia. It can also be termed as a small burst and tear nose or a vanished or completely absent philtrum with a long gap between the thinned upper lip as per studies revealed by Clarren et al [31] So keeping views and reporting of other scientists our study can be comparable with other study. In fact our study also showed different type of limb defects.…”

Section: Discussionsupporting

confidence: 84%

Skeletal Dysmorphology in Fetus Following Colloidal Silver Ingestion in Pregnant Swiss Albino Mice

Pani

Singh

2017

MOJAP

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Among all nanoparticles Silver nanoparticle is important because of its antifungal & antimicrobial activity and also known to be anti-inflammatory and wound healer. Silver nanoparticle is a strong bactericidal agent as it cleaves silver ion of atomic valency one inside the bacterial cell. Silver nanoparticle in moderate manner causes neurotoxicity, skeletal dysmorphogenesis and embryo teratogenicity in in-vitro position of model mouse. 20 to 1908 nm size silver nanoparticles in colloidal solution was given in dose (5, 10, 15, 20 mg/kg b.w.) respectively to randomly chosen mother mice from the colony by oral gavages from 7 th to 12 th day of gestational age. The control group mother received normal saline. Fetuses were collected on day 18 th of gestation. Alizarin staining was done to evaluate the skeletal dysmorphology. The common skeletal dysmorphology seen were unossification of sternum, frontal bone, parietal bone, temporal bone, mandible, maxilla, vertebral column, scapulae and ribs along with those cleft, scoliosis, spina bifida and hypoplasia was also seen.

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Section: Discussionsupporting

confidence: 84%

Skeletal Dysmorphology in Fetus Following Colloidal Silver Ingestion in Pregnant Swiss Albino Mice

Pani

Singh

2017

MOJAP

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“…A wide range of neuropathological findings were reported, including: hydrancephaly, anencephaly, holoprosencephaly, cerebral dysgenesis, abnormal neural migration, hydrocephaly, microcephaly/microencephaly, enlarged/reduced/ absent ventricles, and severe CNS disorganization. Furthermore, abnormalities of the basal ganglia, diencephalon, cerebellum, brainstem, optic nerve, olfactory bulb, hippocampus, pituitary, and neural tube were reported (Clarren, 1986;Clarren et al, 1978;Coulter et al, 1993;Jones and Smith, 1975;Peiffer et al, 1979;Wisniewski et al, 1983). Such heterogeneous brain malformations led to the conclusion that no identifiable pattern of brain abnormalities specific to FAS existed (Clarren et al, 1978;Peiffer et al, 1979).…”

Section: Autopsy and The Advantages Of Imaging Techniquesmentioning

confidence: 99%

Neuroimaging and fetal alcohol spectrum disorders

Spadoni

McGee

Fryer

et al. 2007

Neuroscience & Biobehavioral Reviews

127

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Heavy prenatal alcohol exposure causes permanent structural alterations to the brain and can lead to numerous cognitive and behavioral outcomes. Consistent with many of the neuropsychological and behavioral deficits that have been reported, neuroimaging studies reveal a pattern of structural abnormalities associated with prenatal alcohol exposure. This chapter systematically reviews structural anomalies by brain region, identifying cognitive and behavioral correlates when relevant. The consensus shows that in addition to the overall reduction of brain size, prominent brain shape abnormalities have been observed, with narrowing in the parietal region and reduced brain growth in portions of the frontal lobe. Commensurate with these anomalies, volumetric and tissue density findings cite disproportionate reductions in the parietal lobe, cerebellar vermis, corpus callosum, and the caudate nucleus, suggesting that certain areas of the brain may be especially vulnerable to prenatal alcohol exposure. In sum, neuroimaging techniques have greatly advanced our understanding of brain-behavior relationships in fetal alcohol spectrum disorders (FASD), and hopefully will lead to improved diagnosis and treatment options for those affected by prenatal exposure to alcohol.

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“…Structures of interest, tissue precursors to the cortex, hippocampus, striatum and diencephalon, for example, can then be microdissected with a microscalpel. 4 To limit the impact of litter-to-litter variations on studies, we typically collate fetal cortical tissue from three to four litters per experiment into a single collection tube EDTA. Total cell counts are determined using a hemocytometer.…”

Section: Isolation Of Embryonic Neural Precursorsmentioning

confidence: 99%

Modeling the Impact of Alcohol on Cortical Development in a Dish: Strategies from Mapping Neural Stem Cell Fate

Miranda

Santillano

Camarillo

et al. 2008

Alcohol

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SummaryDuring the second trimester period, neuroepithelial stem cells give birth to millions of new neuroblasts, which migrate away from their germinal zones to populate the developing brain and terminally differentiate into neurons. During this period, large numbers of cells are also eliminated by programmed cell death. Therefore, the second trimester constitutes an important critical period for neuronal proliferation, migration, differentiation and apoptosis. Substantial evidence indicates that teratogens like ethanol can interfere with neuronal maturation. However, there is a paucity of good model systems to study early, second trimester events. In vivo models are inherently interpretatively complex because cell proliferation, migration, differentiation, and death mechanisms occur concurrently in regions like the cerebral cortex. This temporal overlap of multiple developmental critical periods makes it difficult to evaluate the relative vulnerability of any individual critical period. Our laboratory has elected to utilize fetal rodent cerebral corticalderived neurosphere cultures as an experimental model of the second-trimester ventricular neuroepithelium. This model has enabled us to use flow cytometric approaches to identify neuroepithelial stem cell and progenitor sub-populations and to show that ethanol accelerates the maturation of neural stem cells. We have also developed a simplified mitogen-withdrawal/matrixadhesion paradigm to model the exit of neuroepithelial cells from the ventricular zone towards the subventricular zone and cortical plate, and their maturation into multipolar neurons. We can treat neurosphere cultures with ethanol to mimic exposure during the period of neuroepithelial proliferation and by using the step-wise maturation model, ask questions about the impact of prior ethanol exposure on the subsequent maturation of neurons as they migrate and undergo terminal differentiation. The combination of neurosphere culture and stepwise maturation models will enable us to dissect out the contributions of specific developmental critical periods to the overall teratology of a drug of abuse like ethanol.

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Brain malformations related to prenatal exposure to ethanol

Cited by 611 publications

References 4 publications

Skeletal Dysmorphology in Fetus Following Colloidal Silver Ingestion in Pregnant Swiss Albino Mice

Skeletal Dysmorphology in Fetus Following Colloidal Silver Ingestion in Pregnant Swiss Albino Mice

Neuroimaging and fetal alcohol spectrum disorders

Modeling the Impact of Alcohol on Cortical Development in a Dish: Strategies from Mapping Neural Stem Cell Fate

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