Memory and brain volume in adults prenatally exposed to alcohol

Abstract

The impact of prenatal alcohol exposure on memory and brain development was investigated in 92 African-American, young adults who were first identified in the prenatal period. Three groups (Control, n=26; Alcohol-related Neurodevelopmental Disorder, n=36; and Dysmorphic, n=30) were imaged using structural MRI with brain volume calculated for multiple regions of interest. Memory was measured using the Verbal Selective Reminding Memory Test and its nonverbal counterpart, the Nonverbal Selective Reminding Memory Test, which each yielding measures of learning and recall. For both Verbal and Nonverbal Recall and Slope, linear trends were observed demonstrating a spectrum of deficits associated with prenatal alcohol exposure. Dysmorphic individuals performed significantly poorer than unexposed controls on 5 of 6 memory outcomes. Alcohol-exposed individuals demonstrated significantly lower total brain volume than controls, as well as lower volume in a number of specific regions including hippocampus. Mediation analyses indicated that memory performance associated with effects of prenatal alcohol exposure was mediated from dysmorphic severity through hippocampal volume, particularly right hippocampus. These results indicate that the association between the physical effects of prenatal alcohol exposure and deficits in memory are mediated by volumetric reduction in specific brain regions.

Radiological studies of fetal alcohol spectrum disorders in humans and animal models: An updated comprehensive review

“…A smaller caudal anterior cingulate cortex in the right hemisphere, a region involved in inhibition processing and error monitoring, was related to longer time spent on inhibiting a response [36]. Volume reductions of the isthmus, splenium or the whole corpus callosum were associated with increased interhemispheric transfer-related errors in finger localization tests and executive functioning [61;64;67], while volume reduction of the hippocampus mediated memory performance of PAE group in a verbal learning task [19].…”

Neurobehavioral Disorder Associated with Prenatal Alcohol Exposure (ND-PAE): Proposed DSM-5 Diagnosis

“…Impairment in memory (e.g., problems remembering information learned recently; repeatedly making the same mistakes; difficulty remembering long verbal instructions) 5. Impairment in visual spatial reasoning (e.g., disorganized or poorly planned drawings or constructions; problems differentiating left from right; problems aligning numbers in columns) hippocampal volume have been linked to functional memory impairments in human neuroimaging studies [41,42] and animal models [39,43]. Active working memory, which involves the capacity to store and process meaningful units at a given moment in time, has been found to be deficient in individuals with PAE, particularly for tasks involving multiple-step instructions [31].…”

Selective reduction of cerebral cortex GABA neurons in a late gestation model of fetal alcohol spectrum disorder

“…In human adolescents and adults, FASD causes reduced volumes of gray matter and white matter throughout the forebrain. Gray matter volume reductions as large as 10% have been described across regions of the cerebral cortex, with even larger changes in subcortical structures, including hippocampus and striatum (Coles et al, 2011; Lebel et al, 2012; Nardelli, Lebel, Rasmussen, Andrew, & Beaulieu, 2011; Norman et al, 2009). Adult animals that were exposed to fetal alcohol typically have a similar profile of volume reductions (Coleman, Oguz, Lee, Styner, & Crews, 2012; Leigland, Ford, Lerch, & Kroenke, 2013).…”