Neuroanatomical and Neurophysiological Mechanisms Involved in Central Nervous System Dysfunctions Induced by Prenatal Alcohol Exposure

1998 ◽  
Vol 22 (2) ◽  
pp. 304-312 ◽  
Author(s):  
Consuelo Guerri
2012 ◽  
Vol 13 (2) ◽  
pp. 32-42 ◽  
Author(s):  
Yvette D. Hyter

Abstract Complex trauma resulting from chronic maltreatment and prenatal alcohol exposure can significantly affect child development and academic outcomes. Children with histories of maltreatment and those with prenatal alcohol exposure exhibit remarkably similar central nervous system impairments. In this article, I will review the effects of each on the brain and discuss clinical implications for these populations of children.


2012 ◽  
Vol 2012 ◽  
pp. 1-3
Author(s):  
N. K. Sujay ◽  
Matthew Jones ◽  
Emma Whittle ◽  
Helen Murphy ◽  
Marcus K. H. Auth

Prenatal alcohol exposure may have adverse effects on the developing foetus resulting in significant growth restriction, characteristic craniofacial features, and central nervous system dysfunction. The toxic effects of alcohol on the developing brain are well recognised. However, little is known about the effects of alcohol on the developing gastrointestinal tract or their mechanism. There are few case reports showing an association between foetal alcohol syndrome and gastrointestinal neuropathy. We report a rare association between foetal alcohol syndrome and severe gastrooesophageal reflux disease in an infant who ultimately required fundoplication to optimise her growth and nutrition. The child had failed to respond to maximal medical treatment (domperidone and omeprazole), high calorie feeds, PEG feeding, or total parenteral nutrition. The effect of alcohol on the developing foetus is not limited to the central nervous system but also can have varied and devastating effects on the gastrointestinal tract.


2008 ◽  
Vol 99 (3) ◽  
pp. 455-461 ◽  
Author(s):  
Yajun Xu ◽  
Yunan Tang ◽  
Yong Li

Maternal alcohol consumption during pregnancy can induce central nervous system abnormalities in the fetus, and folic acid supplementation can reverse some of the effects. The objective of the present study was to investigate prenatal alcohol exposure-induced fetal brain proteome alteration and the protective effect of folic acid using proteomic techniques. Alcohol (5·0 g/kg) was given intragastrically from gestational day (GD) 6 to15, with or without 60·0 mg folic acid/kg given intragastrically during GD1–16 to pregnant Balb/c mice. The control group received distilled water only. Results of litter evaluation on GD18 showed that supplementation of folic acid reversed the prevalence of microcephaly induced by alcohol. Proteomic analysis indicated that, under the dosage of the present investigation, folic acid mainly reversed the alcohol-altered proteins involved in energy production, signal pathways and protein translation, which are all important for central nervous system development.


2000 ◽  
Vol 42 (8) ◽  
pp. 508-514 ◽  
Author(s):  
Béatrice Larroque ◽  
Monique Kaminski ◽  
Phillipe Dehaene ◽  
Damien Subtil ◽  
Denis Querleu

Author(s):  
Manuela Pfinder ◽  
Stefan Liebig ◽  
Reinhold Feldmann

Data on the relation between moderate prenatal alcohol exposure (PAE) and behavioral disorders are inconsistent, and this raises new questions. We examined (1) the association between moderate PAE and problem behaviors and (2) whether these associations differed by levels of socioeconomic status (SES), fetal smoke exposure, or exposure to environmental tobacco smoke (ETS). Data were taken from the German Health Interview and Examination Survey for Children and Adolescents (KiGGS) study. Parents evaluated children’s behaviors using the Strengths and Difficulties Questionnaire (SDQ). Results showed a slight, but insignificant, increase of problem behaviors in children with moderate PAE. In 3- to 6-year-olds, PAE had a stronger effect on hyperactivity/inattention in combination with fetal smoke exposure (odds ratio = 2.82), than did PAE alone. Effects were not stronger in low-SES children, but they were stronger in children with ETS. We conclude that moderate PAE might have adverse effects on neurodevelopment, with stronger effects in disadvantaged populations. To confirm our preliminary findings, further research should be conducted.


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