Neural correlates of verbal memory in youth with heavy prenatal alcohol exposure.

Prenatal alcohol exposure can impact both brain development and neurobehavioral function, including verbal learning and recall, although the relation between verbal recall and brain structure in this population has not been examined fully. We aimed to determine the structural neural correlates of verbal learning and recall in youth with histories of heavy prenatal alcohol exposure using a region of interest (ROI) approach. As part of an ongoing multisite project, subjects (age 10-16 years) with prenatal alcohol exposure (AE, n = 81) and controls (CON, n = 81) were tested using the CVLT-C and measures of cortical volume, surface area, and thickness as well as hippocampal volume were derived from MRI. Group differences in brain and memory indices were tested with ANOVA. Multiple regression analyses tested whether brain ROIs significantly predicted memory performance. The AE group had lower scores than the CON group on all CVLT-C variables (ps ≤ .001) and volume and surface area (ps < .025), although results varied by ROI. No group differences in cortical thickness were found. The relations between cortical structure and memory performance differed between group among some ROIs, particularly those in the frontal cortex, generally with smaller surface area and/or thinner cortex predicting better performance in CON but worse performance in AE. Cortical surface area appears to be the most sensitive index to the effects of prenatal alcohol exposure, while cortical thickness appears to be the least sensitive. These findings also indicate that the neural correlates of verbal memory are altered in youth with heavy prenatal alcohol exposure compared to controls.

Alcohol exposure in utero is associated with decreased gray matter volume in neonates.

Neuroimaging studies have indicated that prenatal alcohol exposure is associated with alterations in the structure of specific brain regions. However, the temporal specificity of such changes and their behavioral consequences are less known. Here we explore the brain structure of infants with in utero exposure to alcohol shortly after birth. T2 structural MRI images were acquired from 28 alcohol-exposed infants and 45 demographically matched healthy controls at 2-4 weeks of age on a 3T Siemens Allegra system as part of large birth cohort study, the Drakenstein Child Health Study (DCHS). Neonatal neurobehavior was assessed at this visit; early developmental outcome assessed on the Bayley Scales of Infant Development III at 6 months of age. Volumes of gray matter regions were estimated based on the segmentations of the University of North Carolina neonatal atlas. Significantly decreased total gray matter volume was demonstrated for the alcohol-exposed cohort compared to healthy control infants (p < 0.001). Subcortical gray matter regions that were significantly different between groups after correcting for overall gray matter volume included left hippocampus, bilateral amygdala and left thalamus (p < 0.01). These findings persisted even when correcting for infant age, gender, ethnicity and maternal smoking status. Both early neurobehavioral and developmental adverse outcomes at 6 months across multiple domains were significantly associated with regional volumes primarily in the temporal and frontal lobes in infants with prenatal alcohol exposure. Alcohol exposure during the prenatal period has potentially enduring neurobiological consequences for exposed children. These findings suggest the effects of prenatal alcohol exposure on brain growth is present very early in the first year of life, a period during which the most rapid growth and maturation occurs.

What Happens When Children with Fetal Alcohol Spectrum Disorders Become Adults?

The range of structural abnormalities and functional deficits caused by prenatal alcohol exposure (PAE) are referred to as fetal alcohol spectrum disorders (FASDs). The disabilities associated with FASDs are said to be lifelong, but we know relatively little regarding outcomes beyond childhood and adolescence. Many of physical, brain, and neurobehavioral features that are present in children with FASDs will endure to adulthood. However, some features may diminish or change over time. Furthermore, secondary disabilities, such as school drop outs, trouble with the law, and substance/alcohol abuse problems are common in young adults with FASDs. The health consequences associated with PAE in the human adult are unknown, but animal models suggest that they may be more susceptible to chronic diseases such as hypertension, diabetes, immune dysfunction, and cancer. More research is needed to understand the lasting effects of PAE on adults and the developmental trajectories of FASDs.

Fetal Alcohol Spectrum Disorders: Recent Neuroimaging Findings.

Since the identification of Fetal Alcohol Syndrome over 40 years ago, much has been learned about the detrimental effects of prenatal alcohol exposure on the developing brain. This review highlights recent neuroimaging studies, within the context of previous work. Structural magnetic resonance imaging has described morphological differences in the brain and their relationships to cognitive deficits and measures of facial dysmorphology. Diffusion tensor imaging has elaborated on the relationship between white matter microstructure and behavior. Atypical neuromaturation across childhood and adolescence has been observed in longitudinal neuroimaging studies. Functional imaging has revealed differences in neural activation patterns underlying sensory processing, cognition and behavioral deficits. A recent functional connectivity analysis demonstrates reductions in global network efficiency. Despite this progress much remains unknown about the impact of prenatal alcohol exposure on the brain, and continued research efforts are essential.

Should the reorganization of addiction-related research across all the National Institutes of Health be structural?--The devil is truly in the details.

The recent proposal to dissolve the National Institute on Alcohol Abuse and Alcoholism and National Institute on Drug Abuse and create a new institute for substance use, abuse, and addiction will require significant effort by the staff of both institutes, the Advisory Councils, and outside experts to overcome complex challenges that could threaten its success. Although integration of the grants portfolios can be achieved, harmonization of goals and policies related to legal use of alcohol versus illegal consumption of drugs will present serious challenges. Consolidating the infrastructure of the 2 existing institutes would entail avoiding encroachment on grant funding. A new institute for substance use, abuse, and addiction would require an enormous amount of cooperation from other institutes as the portfolios of research on alcohol, tobacco, and other drug abuse should logically be transferred to the new institute. In the near term, a structural reorganization would be less efficient and more costly than the individual institutes are currently. Increasing efficiency and reducing costs over time will necessitate careful strategic planning. Success in this difficult task would be made easier and less costly by first implementing carefully placed building blocks of increasing functional reorganization. The newly created institute should increase opportunities for specialization within disorders of addiction, attract new leadership, and build a novel strategic plan that will energize scientists and staff and incorporate ideas of stakeholders to advance the public good in preventing and treating alcohol, tobacco, and all addictions. Attention must be paid to the devil in the details.

MRI and muscle signal intensities in alcoholics compared with control subjects.

OBJECTIVE: To evaluate by magnetic resonance imaging (MRI) the difference in muscle signal intensities between alcoholics and control subjects. METHODS: Thirty-four healthy subjects and 46 alcohol-dependent individuals were assessed. MRI was carried out using a low-field magnet (0.2 Tesla) and a limb-dedicated coil. The presence of muscle changes was evaluated by measuring signal intensities at the medial (MG) and lateral heads of the gastrocnemius muscle by T1-/T2-weighted and gradient-echo short tau inversion recovery sequences. The mean signal intensities of the two sample groups were compared by ANCOVA with age as a covariate. In the alcohol-dependent group, correlations between signal intensities and plasma levels of muscular and hepatic enzymes, in addition to years of high-risk consumption and lifetime dose of ethanol consumed, were assessed. The mean signal intensities were also compared with the different degrees of pain by ANOVA. RESULTS: Compared with healthy subjects, the alcohol-dependent group had mean higher signal intensities in both gastrocnemius heads in all sequences. The difference in the MG in T2-weighted sequences was significant (F = 48.28, p < 0.01). A modest correlation between the years of high-risk consumption and the signal intensity was found in T2-weighted sequences in the MG (r = 0.288, p = 0.057), whereas a correlation with the lifetime dose consumed was not found. Significant correlations between signal intensities and plasma levels of muscular and hepatic enzymes were not found. There were also no significant group differences on different degrees of pain. CONCLUSION: MRI was shown to be a sensitive, well-tolerated, and inexpensive procedure capable of detecting changes in signal intensities in the muscles of alcoholics. This technique could be included among other diagnostic tools for alcoholic myopathy with further improvements and if the signal alterations can be corroborated by biopsy evidence.