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Running head: FETAL ALCOHOL SPECTRUM DISORDER
Fetal Alcohol Spectrum Disorder (FASD)
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Submitted in partial fulfillment of the requirements for PSY1BNA
Department of Psychology and Counseling
La Trobe University
2015
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Fetal Alcohol Spectrum Disorder
Excessive alcohol consumption has been ranked third among the causes of death in most
countries and though preventable, it is associated with several adverse health effects including
unintentional injuries, various cancers, liver cirrhosis, violence, addiction, and brain damage.
Alcohol ingestion during pregnancy can lead to neurobehavioral abnormalities collectively
identified as fetal alcohol spectrum disorder (FASD) (Sokol, Delaney-Blavk, Nordstrom, 2003).
Along with the deficits in the higher order functions such as memory, attention, problem solving,
and learning, children with FASD manifest altered somatosensory, visual and auditory
processing and other autistic behavior.
During pregnancy, not all the infants exposed to alcohol will have FASD. Some children
are born with the associated problems while others are not, even if their mothers drank an equal
amount of alcohol during the pregnancies (Valenzuela et al., 2012). Experimenting on the effect
of alcohol and how it can affect neurobiological and physiological structures of a human is done
by assessing the physical and intellectual properties of infants exposed to alcohol during
pregnancy and those who were not exposed to the same. Experiments can also be done animals
such as mice that can enable advanced experiments such as measuring the brain volume
(Valenzuela et al., 2012). Alcohol is a depressant for the central nervous system, and it leads to
multiple effects to the infant when ingested by an expectant woman.
The effects of being exposed to alcohol can vary throughout the gestation period. In the
first-trimester equivalent of the human gestation, exposure to alcohol can affect the development
of the neural crest and tube, leading to microcephaly, ocular malformations, hydrocephaly, and
facial dysmorphology that characterizes the fetal alcohol syndrome (FAS). In the second-
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trimester, exposure to alcohol strongly impacts the proliferation of neuronal precursors and glia
probably by changing the expression of the neurotrophic factors such as changing the growth
factor (TGF)-b (Mattson, Crocker, Nguyen, 2011). In the third-trimester equivalent of the human
gestation, the brain is involved in a fast growth process known as “brain growth spurt,” and the
neurons become more susceptible to apoptotic effects of alcohol exposure.
Alcohol ingestion during pregnancy can affect the development of the fetus through a
different mechanism. Alcohol can pass through the placenta and affect the development of the
fetal brain directly by disrupting the neuronal migration and proliferation or by causing the death
of the cells. Furthermore, alcohol increases the levels of fetal glutamate and reduces the
glutamate N-methyl-D-aspartate receptors that may lead to abnormal glial and neuronal
migration (Alfonso-Loeches, 2011). A significant indirect mechanism of the alcohol effect is the
induced hypoxia of alcohol in the fetus. Alcohol decreases the blood flowing to the umbilical
artery that can lead to retarded growth. Alcohol also alters hormone levels and reduces protein
synthesis that can result in additional retarded growth (Alfonso-Loeches, 2011). Other
mechanisms included disruption of the growth factor signaling and increased oxidative stress.
Early seminal Magnetic Resonance Imaging (MRI) studies by Riley et al. (2007)
indicated a reduction in the volume of different brain regions in infants who had been affected by
maternal drinking. This involved case of heavy drinking that involves drinking 7 to 13.99 ounces
absolute alcohol on a weekly basis. Since the brain develops during the gestation period, it is
always affected where the mother drinks regularly. In a survey that was carried on five children
(three of which were exposed to alcohol during pregnancy and two who were not exposed)
displayed damage of the brain along the holoprosencephaly spectrum (Lebel, Roussotte, Sowell,
2011). Each of the three exposed children was affected severely, and one died soon after the
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experiment. An additional child manifesting FASD was included in another case describing two
children having corpus abnormalities. This child also was affected severely and died a couple of
months later. An MRI conducted prior to the death and a succeeding autopsy revealed
widespread and severe damage to the brain, including abnormalities of the basal ganglia, corpus
callosum, cerebellum, hippocampus, and diencephalon.
Archibald et al. (2001) in a recent survey found that in children showing FASD
symptoms, the fibers conveying the information between the brain cells (i.e. white matter)
appeared to be susceptible to volume reduction than the convoluted layer of the brain tissue
known as cerebral cortex. Within this tissue, the parietal lobe that is situated at the cerebrum
middle had been reduced by the prenatal exposure to alcohol, whereas the occipital and temporal
lobes that are located on the back and sides of the brain were not affected. These anatomical data
evidently shows that the effect of alcohol on the development of the brain is not even but varies
according to the brain region. Wass, Persutte & Hobbins (2001) used ultrasound sonography in
examining living fetuses that were exposed to alcohol and found that the frontal cortex size had
reduced, but not other cerebrum cortices. Similarly, the intellectual properties of these children
were monitored over years, and it was noticed that those with prenatal exposure to alcohol were
not sharp and hardly could they remember things faster.
Clarren (1978) found some changes in the autopsied brain structures of four children who
were diagnosed with FAS. The prevalent findings from this survey indicated a wrong location of
the neurons (i.e. ectopic) in the white matter. This suggests errors in the movement of neurons all
over the brain. In a single case, there was a full absence of the anterior commissure and corpus
callosum, another fiber bundle connecting the brain regions. The short, hair-like projections
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(dendritic spines) on the fibers that extend from the neurons to collect the information from the
neurons were also affected.
Numerous reports have revealed that exposure to alcohol during the growth spurt of the
brain in rats reduced the weight of the brain stem, forebrain, and the cerebellum. From a
comparative study by Allan (2003) using mice to create animal models, it revealed that early
exposure to alcohol dramatically affects the neuronal plasticity that is responsible for normal
brain wiring and involvement in processes such as memory and learning (Medina, 2011).
Abnormalities in the neuronal plasticity can explain most of the neurobehavioral deficit noticed
in FASD.
Exposure of infants to alcohol during pregnancy reveals a series of long-lasting
impairments in the behavioral and neuropsychological. When an expectant woman drinks
alcohol, some of it passes through the placenta into the fetus quickly. The body of the developing
fetus will not process the alcohol in a similar manner as an adult. The alcohol, therefore,
concentrates in the fetus and prevents sufficient oxygen and nutrition from reaching the vital
organs of the fetus. This then leads to the abnormal features of the fetus when the baby is born
and may translate to psychological, physical and intellectual problems. Understanding the
neurobehavioral impairments in infants with prenatal exposure to alcohol will help to tailor
intervention programs that can improve the outcomes of this population.
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References
Sokol, R. J., Delaney-Black, V., & Nordstrom, B. (2003). Fetal alcohol spectrum
disorder. Jama, 290(22).
Riley, E. P. & Spadoni, A. D., McGee, C. L., Fryer, S. L. (2007). Neuroimaging and fetal alcohol
spectrum disorders. Neuroscience & Biobehavioral Reviews,31(2).
Alfonso-Loeches, S., & Guerri, C. (2011). Molecular and behavioral aspects of the actions of
alcohol on the adult and developing brain. Crit Rev.Clin.Lab Sci., 48(1).
Lebel, C., Roussotte, F., & Sowell, E. R. (2011). Imaging the impact of prenatal alcohol
exposure on the structure of the developing human brain. Neuropsychol.Rev., 21(2).
Mattson, S. N., Crocker, N., & Nguyen, T. T. (2011). Fetal alcohol spectrum disorders:
neuropsychological and behavioral features. Neuropsychol.Rev., 21(2).
Archibald, S. L., Fennema-Notestine, C., Gamst, A., Riley, E. P., Mattson, S. N., & Jernigan, T.
L. (2001). Brain dysmorphology in individuals with severe prenatal alcohol
exposure. Developmental Medicine & Child Neurology, 43(03).
Wass, T. S., Persutte, W. H., & Hobbins, J. C. (2001). The impact of prenatal alcohol exposure
on frontal cortex development in utero. American journal of obstetrics and
gynecology, 185(3).
Medina, A. E. (2011). Fetal alcohol spectrum disorders and abnormal neuronal plasticity.
Neuroscientist., 17(3).
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Allan, A.M. (2003) A mouse model of prenatal ethanol exposureusing a voluntary
drinking paradigm. Alcohol. Clin. Exp. Res. 27(2).
Clarren, S. K. (1978). Drinking In Pregnancy: A Recommendation For Complete Abstinence.
Valenzuela, C. F., Morton, R. A., Diaz, M. R., & Topper, L. (2012). Does moderate drinking
harm the fetal brain? Insights from animal models. Trends in Neurosciences, 35(5).
Stratton, K., Howe, C., & Battaglia, F. C. (Eds.). (1996). Fetal alcohol syndrome: Diagnosis,
epidemiology, prevention, and treatment. National Academies Press.
Riley, E. P., & McGee, C. L. (2005). Fetal alcohol spectrum disorders: an overview with
emphasis on changes in brain and behavior. Experimental biology and medicine, 230(6).