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Alcohol consumption during pregnancy may result in a wide range of morphological and neurodevelopmental abnormalities termed <jats:italic>fetal alcohol spectrum disorders<\/jats:italic> (<jats:styled-content style=\"fixed-case\">FASD<\/jats:styled-content>), with the most severe cases diagnosed as fetal alcohol syndrome (<jats:styled-content style=\"fixed-case\">FAS<\/jats:styled-content>). <jats:styled-content style=\"fixed-case\">FAS<\/jats:styled-content> and <jats:styled-content style=\"fixed-case\">FASD<\/jats:styled-content> are not readily curable and currently represent the leading preventable causes of birth defect and neurodevelopmental delay in the United States. The etiology of <jats:styled-content style=\"fixed-case\">FAS<\/jats:styled-content>\/<jats:styled-content style=\"fixed-case\">FASD<\/jats:styled-content> remains poorly understood. This review focuses on the effects of prenatal alcohol exposure (<jats:styled-content style=\"fixed-case\">PAE<\/jats:styled-content>) on fetal cerebrovascular function. A brief introduction to the epidemiology of alcohol consumption and the developmental characteristics of fetal cerebral circulation is followed by several sections that discuss current evidence documenting alcohol\u2010driven alterations of fetal cerebral blood flow, artery function, and microvessel networks. 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