As MD appears in both normal and FAD children

As discussed above Increases of FA and decreases of MD appears
in both normal and FAD children yet in a study by Treit et al it was shown that
frontal-association tracts ( superior longitudinal fasciculus and superior and
inferior fronto-occipital fasciculus) manifest significantly greater reductions
of MD in FASD. ?MD correlates with reading and receptive vocabulary in
the FASD children, having abrupt decreases of MD in the superior
fronto-occipital fasciculus and superior longitudinal fasciculus. Volumetric
analysis reveales Total brain, white, cortical gray, and deep
gray matter volume is reduced in the FASD group. White
matter development is delayed during childhood and adolescence
in FASD indicated by DTI.21, 22

 A decrease in brain
volume and central nervous system disorganization, specific structural
abnormalities of sectors including the corpus callosum, cerebellum, caudate,
and hippocampus, and disorganization of white matter. Functional and
neurochemical differences in prenatally exposed to alcohol children are
observed. Individuals with FASD also appear behavioural alterations.23

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 Gautam et al found
that in individuals with FASD cognitive function significantly improves in
relation to increased white matter volume over time. 24
Improvement of cognition occurs in both normal and FASD children overtime. White
matter volume increases in callosal,
frontal, and parietal regions white matter volume age-relatedly and is
significantly associated with cognitive improvements in children with FASD.
This relationship is not apparent in normal developing children. It can be
assumed that age-related plasticity in white matter structure impacts the development of cognitive
function in FASD children and adolescents. 24

Alcohol-induced
abnormalities in glial is amongst most prominent factors effecting on the
developing. Neuronal and glial migration in FASD children is altered  due to amage to radial glia. Alcohol exposure
during pregnancy in the rapid astrocyte proliferation and maturation period can
cause microencephaly. Delayed oligodendrocyte
development and increased oligodendrocyte precursor apoptosis has also been
reported in experimental models of FASD, which may be linked to altered
myelination/white matter integrity found in FASD children. Children
with FAS exhibit hypoplasia of the corpus callosum and anterior commissure, two
areas requiring guidance from glial cells and proper maturation of
oligodendrocytes. Finally, developmental alcohol exposure disrupts microglial
function and induces microglial apoptosis; given the role of microglia in synaptic
pruning during brain development, the effects of alcohol on microglia may be
involved in the abnormal brain plasticity reported in FASD. The consequences of
prenatal alcohol exposure on glial cells, including radial glia and other
transient glial structures present in the developing brain, astrocytes,
oligodendrocytes and their precursors, and microglia contributes to abnormal
neuronal development, reduced neuron survival and disrupted brain architecture
and connectivity.25