Structural Brain Abnormalities

Microcephaly in the FAS affected brain
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FAS brain on right, compared to healthy brain on left

The fetal alcohol syndrome (FAS) affected brain shows a wide range of structural abnormalities. Most areas of the brain seem to be affected, including the cerebral cortex, subcortical white and gray matters, and the cerebellum[1]. Most of these structural changes seem to be a reduction in size or thickness, which is intuitive given the overall reduction in size of the FAS brain[1]. However, increased densities and shape variations are also observed[1].


Both post-mortem[2] and neuroimaging[3,4] studies reveal microcephaly, or reduced brain size, in those with fetal alcohol disorder. Overall, a 12% decrease of gray matter and 16% decrease of white matter has been reported[4]. Not surprisingly, many brain parts are found to show reduced volumes as well as more general dysmorphology.

Cortical Volume Changes

Cortical Thickness Differences
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P-values representing significance of cortical thickness differences.
Reprinted from “Abnormal cortical thickness and brain-behavior: Correlation patterns
in individuals with heavy prenatal alcohol exposure” by Sowell, E.R., et al., Cerebral
Cortex, 18(1).

While microcephaly intuitively may be associated with reduction in cortical volumes, comparatively speaking, both increases and decreases in cortical thickness are observed in individuals with fetal alcohol syndrome[1].
Cortical thickness increase has been reported in the lateral surface of the brain, in all of the lobes[5]. In the right frontal lobes, dorsal areas were also found to be thicker in those with fetal alcohol syndrome when compared to healthy controls[5]. In parts of the parietal and temporal lobes, increased gray matter and decreased white matter volumes have been reported as well[6]. This may imply incomplete pruning of cells during development or increased volumes of unmyelinated white matter[1]. Studies have also suggested that cortical volumes may develop differently in early childhood and adolescence[7]. As can be seen, findings on cortical volume anomalies are rather heterogeneous and definitely require more research.

Subcortical Gray Matter Volume Reduction

Volume reductions in the basal ganglia and the diencephalon have been observed in individuals with fetal alcohol syndrome, compared to healthy controls[8]. Within the basal ganglia, both the caudate and the lentiform nucleui (putamen and globus pallidus) were found to show decrease in volume[8]. It is important to keep in mind, however, that when taking into account overall brain size, only the caudate showed a proportional reduction in volume when compared to healthy controls[8].

Corpus Callosum and Cerebellar Vermis Abnormalities

Midline structures within the brain have also been found to be vulnerable to prenatal alcohol exposure. Dysmorphology of the corpus callosum within the cerebrum is often observed, including reduction of size and displacement especially in posterior areas of the corpus callosum[9]. Studies have also found reduction and displacement in the cerebellar vermis[10].

1. Nunez, S.C., Rousette, F., & Sowell, E.R. Structural and Functional Brain Abnormalities in Fetal Alcohol Syndrome. Alcohol Research and Health 2011; 34(1): 121-131.
2. Jones, K.L., & Smith, D.W. Recognition of the fetal alcohol syndrome in early infancy. The Lancet 1973; 302(7836): 999-1001.
3. Archibald, S.L., Fennema-Notestine, C., Gamst, A., Riley, E.P., Mattson, S.N., & Jernigan, T.L. Brain dysmorphology in individuals with severe prenatal alcohol exposure. Developmental Medicine & Child Neurology 2001; 43(3): 148-154.
4. De Guio, F., Mangin, J., Riviere, D., Perrot, M., Molteno, C.D., Jacobson, S.W., Meintjes, E., & Jacobson, J.L. A study of cortical morphology in children with fetal alcohol spectrum disorders. Human Brain Mapping 2013; published online before inclusion in issue.
5. Sowell, E.R., Mattson, S.N., Kan, E., Thompson, P.M., Riley, E.P., & Toga, A.W. Abnormal cortical thickness and brain-behavior correlation patterns in individuals with heavy prenatal alcohol exposure. Cerebral Cortex, 2009; 18(1): 136-144.
6. Sowell, E.R., Thompson, P.M., Mattson, S.N., Tessner, K.D., Jernigan, T.L., Riley, E.P., & Toga, A.W. Voxel-based morphometric analyses of the brain in children and adolescents prenatally exposed to alcohol. Neuroreport 2001; 12(3): 515-523.
7. Treit, S., Lebel, C., Baugh, L., Rasmussen, C., Andrew, G., & Beaulieu, C. Longitudinal MRI reveals altered trajectory of brain development during childhood and adolescence in fetal alcohol spectrum disorders. The Journal of Neuroscience 2013; 33(24): 10098-10109.
8. Mattson, S.N., Riley, E.P., Sowell, E.R., Jernigan, T.L., Sobel, D.F., Lyons Jones, K. A decrease in the size of the basal ganglia in children with fetal alcohol syndrome. Alcoholism: Clinical and Experimental Research 1996; 20(6): 1088-1093.
9. Sowell, E.R., Mattson, S.N., Thompson, P.M., Jernigan, T.L., Riley, E.O., & Toga, A.W. Mapping callosal morphology and cognitive correlates: Effects of heavy prenatal alcohol exposure. Neurology 2001; 57(2), 235-244.
10. O’Hare, E.D., Kan, E., Yoshii, J., Mattson, S.N., Riley, E.P., Thompson, P.M., Toga, A.W., & Sowell, E.R. Mapping cerebellar vermal morphology and cognitive correlates in prenatal alcohol exposure. Developmental Neuroscience 2005; 16(12): 1285-1290.

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