Biology Reference
In-Depth Information
It has been argued in court that FASD is similar in many ways to other neural deficits
(such as epilepsy) over which the sufferer has no control, and that the presence of FASD is
a factor both in the treatment of offenders with FASD, and where the victim of a crime
had FASD. Like other disabilities, individuals with FASD may have cognitive limitations
which make it difficult for them to participate effectively in their own criminal defense, or
which should be considered in the sentencing phase of a trial. Individuals with FASD may
also be less capable of dealing with social situations, making them more vulnerable to
some criminal acts. The vulnerability of persons with cognitive disorders is often taken
into account in sentencing when they are victims of crimes. For these reasons, it may be
important in a criminal case to determine whether or not an individual should be consid-
ered to have FASD.
Diagnosis of FASD in adults can be difficult, particularly if neither the mother nor
others who can testify about her alcohol consumption during pregnancy are available. In
such cases, diagnosis of FASD in an adult relies on physical measurements of facial fea-
tures and neuroanatomy, as well as behavioral and cognitive testing (
Streissguth et al.,
1998
). Information about the course of the individual's life, such as participation in special
educational settings in school, may also be considered. In such cases, the diagnosis is often
based on a preponderance of evidence.
To assess neuroanatomical consequences of fetal alcohol exposure, Streissguth,
Bookstein and colleagues analyzed shape changes in the corpus callosum and other por-
tions of the brain (
Bookstein et al., 2001, 2002a,b
). MRI images of three-dimensional brain
scans were obtained from 180 subjects aged 14 to 37, with 60 individuals in each of three
categories: (1) those diagnosed with fetal alcohol syndrome (FAS), (2) those diagnosed
with fetal alcohol effects (FAE, i.e., having signs of neurological deficits but lacking obvi-
ous facial features required for diagnosis of FAS) (iii) and a control group of unexposed
normal individuals without other diagnosed cognitive or neurological abnormalities or
known history of fetal alcohol exposure.
Two data sets were used, one consisting of 12 landmark points along the mid-sagittal
plane and 8 bilaterally paired points in the human brain measured in three-dimensions
(see
Bookstein et al., 2001
for details) and a set of mostly semilandmark measurements of
the corpus callosum, (the large white matter structure in the brain that coordinates com-
munication between the left and right cerebral hemispheres). One landmark was defined
on the corpus callosum: a sharp corner near its anterior end called the rostrum. Most of
the other landmarks were extremal points on recognized anatomical features
that is the
anterior-most or dorsal-most point on the structure. The semilandmarks on the corpus cal-
losum were digitized in three dimensions along a curve approximating its midline. This
curve was not defined by an external reference plane; instead each point was placed on
the surface in a position that appeared to be above (or below) the local plane of symmetry
of the structure (
Bookstein et al., 2002a
). The semilandmarks were then slid using bend-
ing-energy alignment. In the initial study (
Bookstein et al., 2001
) differences in amount of
asymmetry were a focus of analysis, so sides were not reflected and averaged, but this
was done for some analyses in later studies.
For both the brain landmarks and the corpus callosum semilandmarks, means of
exposed (FAS and FAE) individuals were not significantly different from unexposed (nor-
mal) individuals. However, there was a clear increase in variability (scatter) of exposed
