A Clinical Neuropathological Study of the Fetal Alcohol Syndrome

Wisniewski, Krystyna E.; Dambska, M; Sher, Joanna; Qazi, Qutub H.

doi:10.1055/s-2008-1059578

Cited by 139 publications

(58 citation statements)

References 7 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%

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%

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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“…The disturbance of the CNS is the most serious feature of FAS (Marcus, 1987;Riley and McGee, 2005;Welch-Carre, 2005). For example, microencephaly is common among patients with FAS (Wisniewski et al, 1983). Several aspects of development are involved in the alcohol-induced malformation of the brain (Jones, 1988;Coulter et al, 1993;Guerri, 2002).…”

Section: Introductionmentioning

confidence: 99%

Reversal of Neuronal Migration in a Mouse Model of Fetal Alcohol Syndrome by Controlling Second-Messenger Signalings

Kumada¹,

Lakshmana²,

Komuro³

2006

J. Neurosci.

131

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The brains of fetal alcohol syndrome patients exhibit impaired neuronal migration, but little is known about the mechanisms underlying this abnormality. Here we show that Ca 2ϩ signaling and cyclic nucleotide signaling are the central targets of alcohol action in neuronal cell migration. Acute administration of ethanol reduced the frequency of transient Ca 2ϩ elevations in migrating neurons and cGMP levels and increased cAMP levels. Experimental manipulations of these second-messenger pathways, through stimulating Ca 2ϩ and cGMP signaling or inhibiting cAMP signaling, completely reversed the action of ethanol on neuronal migration in vitro as well as in vivo. Each second messenger has multiple but distinct downstream targets, including Ca 2ϩ /calmodulin-dependent protein kinase II, calcineurin, protein phosphatase 1, Rho GTPase, mitogen-activated protein kinase, and phosphoinositide 3-kinase. These results demonstrate that the aberrant migration of immature neurons in the fetal brain caused by maternal alcohol consumption may be corrected by controlling the activity of these second-messenger pathways.

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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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A Clinical Neuropathological Study of the Fetal Alcohol Syndrome

Cited by 139 publications

References 7 publications

Neuroimaging and fetal alcohol spectrum disorders

Neuroimaging and fetal alcohol spectrum disorders

Reversal of Neuronal Migration in a Mouse Model of Fetal Alcohol Syndrome by Controlling Second-Messenger Signalings

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

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