Principle Investigator: Ann Streissguth

Funded by the
National Institute on Alcohol Abuse & Alcoholism (NIAAA)

This research proposed to quantify and link the neuroanatomic and neuropsychological abnormalities in people with brain damage caused by prenatal alcohol exposure. Prior to this study, there were few methods for quantifying the brain damage caused by alcohol and its relation to dysfunctional behavior in the individual patient, and none that used modern morphometric methods measuring neuroanatomic shape variation as discernible from MRI scans. Traditionally the only "quantification" of this brain damage was indirect, and lies in the diagnostic category called Fetal Alcohol Syndrome (FAS). Unfortunately, FAS is a very insensitive guide to the extent of underlying brain pathology, even though it is specific for alcohol. People with FAS vary widely in many channels of behavior, and many other heavily exposed people who do not meet criteria for an FAS diagnosis show neurobehavioral deficits that may be as severe as FAS. Such patients are often referred to as having Fetal Alcohol Effects (FAE) or Alcohol Related Neurodevelopmental Disorders (ARND).

Although we hypothesized that our image analysis methods would reveal significant mean differences in brain form between FAS/FAE and Controls, we were surprised to find that the most significant finding was a hypervariation of form of the Corpus Callosum (CC: a white matter pathway connecting the two hemispheres of the brain). Subjects with FAS and FAE had callosa that were generally thicker or thinner than control counterparts. In addition 3, of the subjects with FAS/FAE showed frank dysgenesis (incomplete development) of the corpus callosum. This study also found that there was a complete intermingling of (lack of discrimination between) the alcohol exposed subjects with and without the facial features of FAS in terms of representations of the shape of the CC. There was no difference in CC neuroanatomy between subjects with FAS and those with FAE or ARND.

When the shape measurement of the Corpus Callosum was combined with results of neuropsychological testing, we found further surprising results. The variation in the shape of the corpus callosum was related to two specific patterns of neuropsychological performance. Those subjects with FAS/FAE whose callosa were thinner than controls demonstrated deficits in motor coordination but had relatively normal executive function abilities. Conversely, those subjects with FAS/FAE whose callosa were thicker than controls demonstrated relatively normal motor coordination but had deficits in executive function abilities. Utilizing neuroanatomy and neuropsychology together, we could discriminate between FAS/FAE subjects and control subjects; with 100% sensitivity and 93% specificity. Again the two exposed groups were completely intermingled demonstrating that there is no difference in neuroanatomy and neuropsychology between subjects diagnosed FAS and those with FAE or ARND. Future research will use the same methodology to study other brain regions thought to be associated with the damaging effects of prenatal alcohol exposure.

The potential role of these findings suggests that MRI screening of extent of damage in FAS/FAE would be of great benefit. For those without the full stigmata of the disorder, but with characteristic dysfunctional behaviors, the detection of neuroanatomic anomalies may permit proper identification and service delivery prior to the development of debilitating secondary consequences. Also, it will become possible to draw much finer distinctions among the clinical samples currently diagnosed as "FAS" or "FAE". Prognoses would thereby become more accurate, and the provision of therapeutic intervention or special education would become both more effective and more humane. Further work is appropriate in order to extend these correlated dimensions of structural-functional deficit downward into childhood or even infancy.

The Center on Human Development and Disability's summary of Ann Streissguth's brain study.

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