Alcohol embryo- and fetopathy

Peiffer, J.; Majewski, F.; Fischbach, H.; Bierich, J. R.; Volk, Benedikt

doi:10.1016/0022-510x(79)90033-9

Cited by 237 publications

(47 citation statements)

References 12 publications

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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%

“…Early autopsy studies on FAS cases Clarren et al, 1978;Peiffer et al, 1979;Wiseniewski et al, 1983) reported agenesis, or absence, of the corpus callosum (ACC). Although total absence of this brain structure is rare, occurring at a rate of 0.1% in the typical population and 2% in the developmentally disabled (Jeret et al, 1986), a higher rate of ACC has been reported in individuals with FAS (Riley, et al, 1995;Swayze et al 1997).…”

Section: Corpus Callosummentioning

confidence: 99%

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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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Section: Autopsy and The Advantages Of Imaging Techniquesmentioning

confidence: 99%

Section: Corpus Callosummentioning

confidence: 99%

Neuroimaging and fetal alcohol spectrum disorders

Spadoni

McGee

Fryer

et al. 2007

Neuroscience & Biobehavioral Reviews

127

View full text Add to dashboard Cite

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“…In addition to providing interhemispheric communication, it also plays a critical role in the development of the visual system (Elberger 1993;1994a;. Children exposed to alcohol prenatally have been shown to have defects in the gross morphology of the CC, including a reduction in size (Clarren, 1986;Mattson et al, 1992;Mattson et al, 1994;Riley et al, 1995) or complete absence (Jones and Smith, 1975;Peiffer et al, 1979;Wisniewski et al, 1983;Jeret et al, 1987;Mattson et al, 1992;Riley et al, 1995). Fetal alcohol exposure has also been linked to a myriad of visual system deficits, including reduced visual acuity, nearsightedness, eye misalignment and optic nerve hypoplasia, (Pinazo-Duran et al, 1997;Stromland and Pinazo-Duran 2002;Stromland, 2004), suggesting a possible role for the CC in these defects.…”

Section: Introductionmentioning

confidence: 99%

Alcohol exposure during the first two trimesters-equivalent alters the development of corpus callosum projection neurons in the rat

Livy

Elberger

2008

Alcohol

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Children exposed prenatally to alcohol can display a variety of neural deficits, including an altered development of the corpus callosum (CC), the largest interhemispheric axon pathway in the brain. Furthermore, these children show functional abnormalities that are related to brain regions with significant numbers of CC connections. Little is known about how alcohol imparts influence on CC development, but one possible mechanism is by affecting the corpus callosum projection neurons (CCpn) directly. The purpose of this study was to quantify the effects of prenatal alcohol exposure on the number, size and distribution of CCpn within the visual cortex. The visual cortex was selected specifically due to the many vision-related deficits noted in fetal alcohol exposed children and because the critical role of the CC in visual cortex development is well documented. Sprague-Dawley rat pups received one of four alcohol dosages during gestational days (G) 1-20, or reared as nutritional or untreated control animals. Each litter was categorized according to the peak blood alcohol concentration (BAC) experienced. Pups were removed from each litter on days equivalent to G29, G36, G43, and G50, for histology and measurement. Callosal axons were labelled retrogradely to their CCpn using DiI and the CCpn were then examined using confocal laser scanning microscopy. Differences between alcohol-exposed and control animals were observed in CCpn cell body size, number, and location with the cortex. This was particularly true of animals exposed to high doses of alcohol. In addition, some trends of CCpn development were found to be unchanged as a result of prenatal alcohol exposure. The results demonstrate clear differences in the development of CCpn in the visual cortex between alcohol-exposed and control animals and suggest that this development is particularly affected in those animals exposed to high doses of alcohol.

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“…The nature of these deficits suggests cerebellar dysfunction. Autopsies of infants with fetal alcohol syndrome (FAS) provided the first indication of cerebellar and brainstem (pons and medulla oblongata) dysgenesis [Peiffer et al, 1979;Clarren, 1981]. Moreover, recent magnetic resonance imaging studies have shown hypoplasia of specific brain regions, including the cerebellum, in individuals with varying degrees of in utero ethanol exposure [reviewed by Roebuck et al, 1998;Mattson et al, 2001].…”

Section: Introductionmentioning

confidence: 99%

Hindbrain and Cranial Nerve Dysmorphogenesis Result from Acute Maternal Ethanol Administration

Dunty

Zucker²,

Sulik

2002

Dev Neurosci

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Acute exposure of mouse embryos to ethanol during stages of hindbrain segmentation results in excessive cell death in specific cell populations. This study details the ethanol-induced cell loss and defines the subsequent effects of this early insult on rhombomere and cranial nerve development. Ethanol at a teratogenic dosage (2.9 g/kg) or a comparable volume of vehicle was administered in each of two intraperitoneal injections to pregnant C57BL/6J mice on gestational day (GD) 8, 8 h, and GD 8, 12 h (defined hereafter as GD 8.5). Ethanol-exposed GD 9 embryos, visualized in three dimensions using laser scanning confocal microscopy of LysoTracker Red fluorescence or Nile blue sulphate vital staining, displayed excessive apoptosis in the rostral hindbrain, specifically within rhombomeres 1–3, as well as in cranial neural crest cells and ectodermal placodes. Comparably treated embryos examined on GD 10.5–11 illustrated a disproportionate reduction in the length of the rostral hindbrain. Examination of plastic histological sections of GD 9 embryos and via scanning electron microscopy on GD 10 revealed deficiencies in the hindbrain, with a phenotype including abnormal rhombomere segmentation and an extremely small fourth ventricular roofplate. Whole-mount antineurofilament immunohistochemistry on GD 10.5 and GD 11 illustrated a variety of cranial nerve abnormalities ranging from fused or absent ganglia to ectopic or disorganized fibers. In addition, a delay in the development of the glossopharyngeal (IX) nerve/ganglia complex was observed. These hindbrain and cranial nerve abnormalities are discussed in the context of the genesis of human alcohol-related birth defects and neurodevelopmental disorder.

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Alcohol embryo- and fetopathy

Cited by 237 publications

References 12 publications

Neuroimaging and fetal alcohol spectrum disorders

Neuroimaging and fetal alcohol spectrum disorders

Alcohol exposure during the first two trimesters-equivalent alters the development of corpus callosum projection neurons in the rat

Hindbrain and Cranial Nerve Dysmorphogenesis Result from Acute Maternal Ethanol Administration

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