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Alcohol and Alcoholism Advance Access originally published online on January 15, 2009
Alcohol and Alcoholism 2009 44(2):108-114; doi:10.1093/alcalc/agn105
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© The Author 2009. Published by Oxford University Press on behalf of the Medical Council on Alcohol. All rights reserved

Foetal Alcohol Spectrum Disorders and Alterations in Brain and Behaviour

Consuelo Guerri1,*, Alissa Bazinet2 and Edward P. Riley2

1 Department of Cell Pathology, Centro de Investigacion Principe Felipe, Avda Autopista del Saler, 46013-Valencia, Spain
2 Department of Psychology and Center for Behavioral Teratology, San Diego State University, San Diego, CA 92120, USA

* Corresponding author: Centro de Investigacion Principe Felipe, Avda. Autopista del Saler 16, 46013-Valencia, Spain. Tel: +34-96-328-96-80; Fax: +34-96-328-97-01; E-mail: guerri{at}cipf.es

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  Abstract

The term ‘Foetal Alcohol Spectrum Disorders (FASD)’ refers to the range of disabilities that may result from prenatal alcohol exposure. This article reviews the effects of ethanol on the developing brain and its long-term structural and neurobehavioural consequences. Brain imaging, neurobehavioural and experimental studies demonstrate the devastating consequences of prenatal alcohol exposure on the developing central nervous system (CNS), identifying specific brain regions affected, the range of severity of effects and mechanisms involved. In particular, neuroimaging studies have demonstrated overall and regional volumetric and surface area reductions, abnormalities in the shape of particular brain regions, and reduced and increased densities for white and grey matter, respectively. Neurobehaviourally, FASD consists of a continuum of long-lasting deficits affecting multiple aspects of cognition and behaviour. Experimental studies have also provided evidence of the vulnerability of the CNS to the teratogenic effects of ethanol and have provided new insight on the influence of risk factors in the type and severity of observed brain abnormalities. Finally, the potential molecular mechanisms that underlie the neuroteratological effects of alcohol are discussed, with particular emphasis on the role of glial cells in long-term neurodevelopmental liabilities.


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