Fetal Alcohol Syndrome Essay

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Alcohol-related neurodevelopmental disorder (ARND) – reserved for individuals with functional or cognitive impairments linked to prenatal alcohol exposure, including decreased head size at birth, structural brain abnormalities, and a pattern of behavioral and mental abnormalities Alcohol-related birth defects (ARBD) – describes the physical defects linked to prenatal alcohol exposure, including heart, skeletal, kidney, ear, and eye malformations Fetal alcohol effects (FAE) – a term that has been popularly used to describe alcohol-exposed individuals whose condition does not meet the full criteria for an FAS diagnosis What are the Statistics and Facts about FAS and FASD?

FASD is the leading known preventable cause of mental retardation and birth defects. FASD affects 1 in 100 live births or as many as 40,000 infants each year. An individual with fetal alcohol syndrome can incur a lifetime health cost of over $800,000. In 2003, fetal alcohol syndrome cost the United States $5. 4 billiondirect costs were $3. 9 billion, while indirect costs added another $1. 5 billion. Children do not outgrow FASD. The physical and behavioral problems can last for a lifetime. FAS and FASD are found in all racial and socio-economic groups. FAS and FASD are not genetic disorders. Women with FAS or affected by FASD have healthy babies if they do not drink alcohol during their pregnancy.

Can I drink alcohol when I am pregnant? No. Do not drink alcohol when you are pregnant. When you drink alcohol, such as beer, wine, or mixed drinks, so does your baby. Alcohol is a substance known to be harmful to human development. When it reaches the blood supply of the baby, it can cause permanent defects to the major organs and central nervous system. Is there any kind of alcohol that is safe to drink during pregnancy? No. Drinking any kind of alcohol can hurt your baby. Alcoholic drinks can include beer, wine, liquor, wine coolers, or mixed drinks. What if I am pregnant and have been drinking? If you drank alcohol before you knew you were pregnant, stop drinking now.

Anytime a pregnant woman stops drinking, she decreases the risk of harm to the baby. If you are trying to get pregnant, do not drink alcohol. You may not know you are pregnant right away. What if I drank during my last pregnancy and my baby was fine? Every pregnancy is different. Drinking alcohol may hurt one baby more than another. You could have one child that is born healthy and another child that is born with problems. What if a friend, partner, spouse or family member is drinking while pregnant? Many women are unaware of the consequences of drinking during pregnancy. Some women believe wine or beer is not alcohol. In many cases, she may be suffering from alcoholism.

She may need to know what effects alcohol can have on the baby. She also may need help getting into treatment. In such cases, you should contact a treatment professional at a local addiction center for advice on how to help. https://monkessays.com/write-my-essay/ nofas. org/faqs. aspx? id=5 Copyright 2001-2004 National Organization on Fetal Alcohol Syndrome An individual’s place, and success, in society is almost entirely determined by neurological functioning. A neurologically injured child is unable to meet the expectations of parents, family, peers, school, career and can endure a lifetime of failures. The largest cause of neurological damage in children is prenatal exposure to alcohol.

These children grow up to become adults. Often the neurological damage goes undiagnosed, but not unpunished. Fetal Alcohol Syndrome (FAS), Fetal Alcohol Effects (FAE), Partial Fetal Alcohol Syndrome (pFAS), Alcohol Related Neurodevelopmental Disorders (ARND), Static Encephalopathy (alcohol exposed) (SE) and Alcohol Related Birth Defects (ARBD) are all names for a spectrum of disorders caused when a pregnant woman consumes alcohol. There are strategies that can work to help the child with an FASD compensate for some difficulties. Early and intensive intervention and tutoring can do wonders, but the need for a supportive structure is permanent.

Studies on addiction in Ontario have shown about a 10 – 12% alcohol addiction rate among adults, with another 20% drinking to a level that places them at high risk. Legally intoxicated is defined as a Blood Alcohol Level of . 08%. A 100 lb (45 kg) female consuming 5 standard drinks (A drink equals a 12 oz. regular beer, 1 oz. shot of 100 proof liquor, 1. 5 oz. shot of 80 proof liquor, or 4 oz. glass of regular table wine) will reach a BAL of . 25% – three times the legal limit. BAL reduces . 01% per hour. The Statistics Canada, Canadian Community Health Survey, 2000/01 found that: 6. 8% of girls ages 12 to 14 19. 8% of girls age 12 to 19 26. 0% ages 20 to 24 19. 9% ages 20 to 34 consumed 5 or more drinks on each occasion 12 or more times per year.

An additional: 32. 2% ages 15 to 34 13. 8% of girls ages 12 to 14 consumed 5 or more drinks on each occasion 1 to 11 times per year. Copyright © 2005 Journals and Procedural Research Branch Office of the Legislative Assembly of Ontario, Toronto, Ontario, Canada. Most girls are 2 to 3 months pregnant before they find out. Given the prime childbearing age range, the odds are very high that about 20% of babies have been exposed to multiple binges in high levels of alcohol in the first trimester, before the girl even knew she was pregnant. It is Party Hearty Time. The vast majority of these girls are NOT alcoholics. About 50% of pregnancies are unplanned.

“If you are drinking, stay out of the backseat as well as the driver’s seat! ” Maternal prenatal alcohol consumption even at low levels is adversely related to child behavior. The effect was observed at average exposure levels as low as 1 drink per week. The Canadian Centre for Children’s Research at McMaster University Hospitals (Hamilton Ontario) states that 20% of Canadian children have serious mental health issues. Typical of school boards in Canada, a major southwestern Ontario School Board (urban / rural mix) with 28,000 Elementary and Secondary School students, has 6,000 students receiving services from the Special Education Department.

Of the 6,000, only 250 are classified as “Gifted” with the balance having significant disabilities (20. 6%). While not all the individuals with disabilities are identified as the disabilities having been caused by prenatal exposure to alcohol, the vast majority of the disabilities are of types known to be caused by prenatal alcohol exposure. FASD is so grossly under-reported that the FAS statistics are almost meaningless. There are very few doctors who have received any training in diagnosing FASD and most prefer to use “non-judgmental” diagnoses such as ADD, ADHD, LD, MR, RAD, ODD, Bi-Polar, Tourette’s, etc.. These “diagnoses” don’t imply the mother has done something that could have affected her baby during pregnancy.

However, they can also lead to inappropriate treatment and a lifetime of pain. Failure to identify the real source can lead to more children being born with the same issues to the same mothers and the cycle continuing into the next generation – FASD children having FASD babies. Alcohol, hormones, a twitch in the kilt, poor impulse control and inability to predict consequences are a deadly combination. Accidents cause people. FASD is not a threshold condition. It is a continuum ranging from mild intellectual and behavioural issues to the extreme that often leads to profound disabilities or premature death. “Denial” is not just a river in Egypt. Alcohol as a Teratogen on the Baby ? https://monkessays.com/write-my-essay/ acbr. com/fas/.

Problem: Fetal Alcohol Syndrome (FAS) is a pattern of mental and physical defects which develops in some unborn babies when the mother drinks too much alcohol during pregnancy. A baby born with FAS may be seriously handicapped and require a lifetime of special care. Some babies with alcohol-related birth defects, including smaller body size, lower birth weight, and other impairments, do not have all of the classic FAS symptoms. These symptoms are sometimes referred to as Fetal Alcohol Effects (FAE). Researchers do not all agree on the precise distinctions between FAS and FAE cases. Cause of the Problem: Alcohol in a pregnant woman’s bloodstream circulates to the fetus by crossing the placenta.

There, the alcohol interferes with the ability of the fetus to receive sufficient oxygen and nourishment for normal cell development in the brain and other body organs. Possible FAS Symptoms: Growth deficiencies: small body size and weight, slower than normal development and failure to catch up. The fact sheets below were developed by many different authors. In some cases, the fact sheets were placed on the web by a different organization than the one that wrote the document. However, all of the fact sheets are in the public domain to encourage wide distribution. You are free to copy and use these fact sheets. The following list of abbreviations was used to indicate the source of the document in the links provided on this page.

Many of the sites listed contain additional information beyond the fact sheets that are listed on this page. We encourage you to explore each site. https://monkessays.com/write-my-essay/ well. com/user/woa/fsfas. htm RSmith:02-15-94 MISSOURI DEPARTMENT OF MENTAL HEALTH Division of Alcohol and Drug Abuse 1706 East Elm; P. O. Box 687 Jefferson City, Missouri 65102 The following Fetal Alcohol Spectrum Disorders (FASD) are caused by drinking alcohol during pregnancy: FAS: Fetal Alcohol Syndrome Symptoms include small head/body, facial characteristics, brain damage FAE: Fetal Alcohol Effects Symptoms usually not visible, such as behavior disorders, attention deficits ARBD: Alcohol Related Birth Defects.

Anomalies such as heart defects, sight/hearing problems, joint anomalies, etc. ARND: Alcohol Related Neurodevelopmental Disorders Disorders such as attention deficits, behavior disorders, obsessive/compulsive disorder, etc. FASD: Fetal Alcohol Spectrum Disorders All of the disorders named above are contained in the spectrum. Full FAS comprises only about 10% of the spectrum. The other 90% may have fewer physical symptoms but are at greater risk for developing serious secondary conditions later. (Streissguth, 1997) FAS is the leading cause of mental retardation in western civilization. But… Most persons with FAS have an IQ in the normal range. (Streissguth, 1997).

The incidence of Fetal Alcohol Syndrome in America is 1. 9 cases per 1,000 births (1/500). Incidence of babies with disabilities resulting from prenatal alcohol exposure: 1/100! FAS/FAE is a major health issue in western civilization today. More American babies are born with FAS than with Down Syndrome, MD, and HIV combined. “Alcohol causes more neurological damage to the developing baby than any other substance. ” Lecture Summary Fetal alcohol syndrome is among the most common known causes of mental retardation and as such, it is a major public health problem. The purpose of this lecture is to provide a basic overview of what we know about the effects of prenatal alcohol exposure.

It is certainly not meant to be comprehensive but rather to give a broad overview of current knowledge in the area, and of ongoing human and animal research in the area. Heavy prenatal alcohol exposure can result in the fetal alcohol syndrome and both changes in brain structure and behavior have been reported in these children. Importantly, current data indicate that individuals exposed to heavy doses of alcohol in utero, but without the facial characteristics of FAS, can also suffer from similar brain and behavioral changes. Animal models have proven to be an excellent research tool in this field, as there appears to be good concordance between the animal and human data.

The animal models provide a means to examine mechanisms of alcohol damage, to control for factors not possible in most human studies, and to help answer important clinical questions. Fetal alcohol effects are preventable, and every child born with a defect related to prenatal alcohol exposure indicates a failure of the health care system. Lecturer Dr. Ed Riley http://rsoa. org/lectures/07/index. html Background Fetal alcohol syndrome is among the most common known causes of mental retardation and as such, it is a major public health problem. The purpose of this lecture is to provide a basic overview of what we know about the effects of prenatal alcohol exposure.

It is certainly not meant to be comprehensive. For more detailed overview, the following references might be helpful. It is important to remember that as the mother consumes alcohol and her blood alcohol level rises, that alcohol is freely crossing the placenta and the embryo or fetus is being exposed to the same blood alcohol levels. References Stratton, K. , Howe, C. , & Battaglia, F. (1996). Fetal alcohol syndrome: Diagnosis, epidemiology, prevention, and treatment. Washington, DC: National Academy Press. Streissguth, A. P. (1997). Fetal Alcohol Syndrome: A Guide for Families and Communities. Baltimore: Paul H. Brookes Publishing Co. Background

Fetal alcohol syndrome is among the most common known causes of mental retardation and as such, it is a major public health problem. The purpose of this lecture is to provide a basic overview of what we know about the effects of prenatal alcohol exposure. It is certainly not meant to be comprehensive. For more detailed overview, the following references might be helpful. It is important to remember that as the mother consumes alcohol and her blood alcohol level rises, that alcohol is freely crossing the placenta and the embryo or fetus is being exposed to the same blood alcohol levels. References Stratton, K. , Howe, C. , & Battaglia, F. (1996).

Fetal alcohol syndrome: Diagnosis, epidemiology, prevention, and treatment. Washington, DC: National Academy Press. Streissguth, A. P. (1997). Fetal Alcohol Syndrome: A Guide for Families and Communities. Baltimore: Paul H. Brookes Publishing Co. Background What each of these papers described was a common set of features that could occur in the offspring of mothers who drank heavily during their pregnancies. This constellation of features was named the Fetal Alcohol Syndrome in 1973 by Jones and colleagues. In order to be diagnosed as having FAS, the individual MUST meet all three criteria. There is a specific pattern of facial anomalies, which will be shown shortly. There is pre and or postnatal growth deficiency.

Usually the children are born small (7drinks/week – 5 or more drinks per occasion). The data on the left side of the slide come from Louise Floyd of the CDC. The first four studies were sponsored by the CDC and the other two estimates on the left side come from the IOM report (Stratton, 1996). AI/AN stands for American Indian/Alaska Native. The numbers on the right side are from a recent study by Sampson et al. , (1997). They demonstrated rates of FAS of at least 2. 8/1000 live births in Seattle, 4. 6/1000 in Cleveland, and between 1. 3 and 4. 8/1000 in Roubaix, France. Interestingly, in this study they estimate the prevalence in Seattle for FAS and ARND at 9. 1/1000 births.

This would mean that nearly 1 in every 100 children is affected by prenatal alcohol exposure. The last number from South Africa is from recent work done by Phil May and colleagues. References Egeland G, Perham-Hester KA, Gessner BD, Ingle D, Berner JE,Middaugh JP. Fetal Alcohol Syndrome in Alaska, 1977 through 1992: An administrative prevalence derived from multiple data sources. American Journal of Public Health. 1998. 88(5): 781-786. Aberdeen IHS Area (1995) MMWR. vol 44(#):253-261. BDMP (1995): MMWR Vol. 44(13):249-253. Atlanta, Ga. (1997) MMWR Vol. 46(47): 1118-1120. Sampson, P. D. , Streissguth, A. P. , Bookstein, F. L. , Little, R. E. , Clarren, S. K. , Dehaene, P. , Hanson, J. W. , & Graham, J. M. , Jr. (1997).

Incidence of fetal alcohol syndrome and prevalence of alcohol-related neurodevelopmental disorder. Teratology, 56(5), 317-326. Stratton, K. , Howe, C. , & Battaglia, F. (1996). Fetal alcohol syndrome: Diagnosis, epidemiology, prevention, and treatment. Washington, DC: National Academy Press. Institute of Medicine: 1996 Clinic-based (page 89), American Indian/Alaskan Native (page 88) May, P. , Viljoen, D. , Gossage, J. , Brooke, L. , Croxford, J. (1999). An epidemiological analysis of data from children with fetal alcohol syndrome and controls in Wellington, South Africa. Alcoholism: Clinical and Experimental Research, 23 (5), 110A. May, P. , Viljoen, D. , Gossage, J. , Brooke, L. , Croxford, J (1999).

An update on the maternal risk factors associated with the prevalence of fetal alcohol syndrome in Wellington, South Africa. Alcoholism: Clinical and Experimental Research, 23 (5), 91A Background It must be stressed that the facial characteristics basically define FAS. Without these facial features, one cannot be diagnosed with FAS. In particular, the discriminating features are short palpebral fissures (the length of the eye opening), a flat midface, an indistinct or flat philtrum (the ridge under the nose), and a thin upper vermilion (lip). While each of these can occur in a variety of disorders, the combination of these features appears to be consistent with heavy prenatal alcohol exposure.

Children with FAS can also have other facial features, such as epicanthal folds (tiny folds of tissues along the eye opening), a low nasal bridge, an underdeveloped jaw and minor ear anomalies. These individuals can also have a variety of associated features. Heart defects, skeletal anomalies, altered palmar creases (those creases on your hands), and urogenital anomalies are among the anomalies found more frequently in FAS. Reference Streissguth, A. P. (1994). A long-term perspective of FAS , Alcohol Health & Research World (Vol. 18, pp. 74-81). image Facies in fetal alcohol syndrome Background The brain on the left was obtained from a 5-day-old child with FAS while the brain on the right is a control. The effects are obvious.

The brain on the left suffers from microencephaly (small brain) and migration anomalies (neural and glia cells did not migrate to their proper location in the brain, but instead many of them simply migrated to the top of the cortex). Although it cannot be seen here, there is also agenesis of the corpus callosum and the ventricles are dilated. The corpus callosum is the major fiber tract connecting the two hemispheres of the brain (more on this later). Major findings of other autopsies of children with FAS have found microcephaly, hydrocephaly, cerebral dysgenesis, neuroglial heterotopias, corpus callosum anomalies, ventricle anomalies, and cerebellar anomalies.

It must be pointed out, however, that these autopsies have typically been conducted only on the most severe cases, since these children often have enough problems that they do not survive. The interested reader on the pathological changes that occur in FAS is referred to the following articles. References Clarren, S. K. (1986). Neuropathology in fetal alcohol syndrome. In J. R. West (Ed. ), Alcohol and Brain Development (pp. 158-166). New York: Oxford University Press. Roebuck, T. M. , Mattson, S. N. , and Riley, E. P. (1998). A review of the neuroanatomical findings in children with fetal alcohol syndrome or prenatal exposure to alcohol. Alcoholism: Clinical and Experimental Research, 22 (2),339-344.

Image brain damage resulting from prenatal alcohol Background The image on the left is a normal midsaggital MRI scan of the human brain with the cerebrum and cerebellum pointed out. The data on the right show the reduction in size of the these two areas in children with FAS and PEA. PEA stands for Prenatal Exposure to Alcohol, and includes children with known histories of heavy prenatal alcohol exposure, but who lack the features necessary for a diagnosis of FAS. As can be seen, the extent of reduction in the volume of both the cerebrum and cerebellum is significant. While the PEA group shows a reduction in volume, with these sample sizes, this is not a significant difference.

Other brain imaging studies indicate disproportionate size reductions in the basal ganglia, cerebellum, and corpus callosum. The data are presented as percent of normal matched controls. References Mattson, S. N. , Jernigan, T. L. , & Riley, E. P. (1994a). MRI and prenatal alcohol exposure. Alcohol Health & Research World, 18(1), 49-52. Archibald, S. L. , Fennema-Notestine, C. , Gamst, A. , Riley, E. P. , Mattson, S. N. , and Jernigan, T. L. (submitted, 2000). Brain dysmorphology in individuals with severe prenatal alcohol exposure. image change in brain size Background One anomaly that has been seen in FAS is agenesis of the corpus callosum.

While not common, it occurs in FAS cases (~6%) more frequently than in the general population (0. 1%) or in the developmentally disabled population (2-3%). In fact it has been suggested that FAS may be the most common cause of agenesis of the corpus callosum. In the top left picture, is a control brain. The other images are from children with FAS. In the top middle the corpus callosum is present, but it is very thin at the posterior section of the brain. In the upper right the corpus callosum is essentially missing. The bottom two pictures are from a 9 year old girl with FAS. She has agenesis of the corpus callosum and the large dark area in the back of her brain above the cerebellum is a condition known as coprocephaly.

It is essentially empty space. Most children with FAS do have a corpus callosum, although it may be reduced in size. The reduction in size occurs primarily in the front and rear portions (genu and splenium). One interesting item is that this same pattern of reduction in the genu and splenium has been found in ADHD children. The behavioral problems seen in FAS frequently are similar to those seen in ADHD. References Mattson, S. N. , Jernigan, T. L. , & Riley, E. P. (1994a). MRI and prenatal alcohol exposure. Alcohol Health & Research World, 18(1), 49-52. Mattson, S. N. , & Riley, E. P. (1995). Prenatal exposure to alcohol: What the images reveal.

Alcohol Health & Research World, 19(4), 273-277. Riley, E. P. , Mattson, S. N. , Sowell, E. R. , Jernigan, T. L. , Sobel, D. F. , & Jones, K. L. (1995). Abnormalities of the corpus callosum in children prenatally exposed to alcohol. Alcoholism: Clinical and Experimental Research, 19(5), 1198-1202. Background There have been over a dozen retrospective studies of children with FAS (total N = 269). Overall, these studies, such as the Seattle studies or studies out of Germany, reported an overall mean IQ of 72. 26 (range of means = 47. 4-98. 2). The data presented here were collected in San Diego, CA as part of a project at the Center for Behavioral Teratology.

The mean IQ performances of children with FAS were compared to alcohol-exposed children with few if any features of FAS. All children in this study were exposed prenatally to high amounts of alcohol, however only the FAS group displayed the craniofacial anomalies and growth deficits associated with the diagnosis. The other group was designated as having prenatal exposure to alcohol (PEA) and had documented exposure to high levels of alcohol but were not dysmorphic, microcephalic, or growth-retarded. In comparison to normal controls, both groups of alcohol-exposed children displayed significant deficits in overall IQ measures as well as deficits on most of the subtest scores.

While the PEA subjects usually obtained marginally higher IQ scores than those with FAS, few significant differences were found between the two alcohol-exposed groups. These results indicate that high levels of prenatal alcohol exposure are related to an increased risk for deficits in intellectual functioning and that these deficits can occur in children without all of the physical features required for a diagnosis of FAS. Our PEA subjects may be somewhat similar to individuals identified by other groups as having FAE, however individuals with PEA display few if any of the facial features of FAS, and are not growth retarded or microcephalic. References

Streissguth AP, Aase JM, Clarren SK, Randels SP, LaDue RA, Smith DF (1991). Fetal alcohol syndrome in adolescents and adults. Journal of the American Medical Association 265:1961-1967. Mattson, S. N. , Riley, E. P. , Gramling, L. , Delis, D. C. , and Jones, K. L. (1997). Heavy prenatal alcohol exposure with or without physical features of fetal alcohol syndrome leads to IQ deficits. Journal of Pediatrics, 131 (5), 718-721. Mattson, S. N. and Riley, E. P. (1998). A review of the neurobehavioral deficits in children with fetal alcohol syndrome or prenatal exposure to alcohol. Alcoholism: Clinical and Experimental Research, 22 (2), 279-294. image general intellectual performance Background.

This was a study of a broad range of neuropsychological tests, such as: The Wide Range Achievement Test- which assesses academic skills, the Peabody Picture Vocabulary Test and the Boston Naming test-both assessment of basic language functioning, the California Verbal Learning Test-a list learning and memory test, the Visual-Motor Integration Test which measures basic visual-perceptual skills, the Grooved Pegboard test-a test of fine-motor speed and coordination, and the Children’s Category Test-a measure of nonverbal learning. Along the x-axis are the tests included in the battery; for comparison purposes, all scores were converted to standard scores with a mean of 100 and an SD of 15. Children with FAS or PEA showed deficits in comparison to controls and they were very similar to each other.

There does seem to be some indication that the nonverbal measures (on the right of the slide) are not as impaired as the verbal and academic measures, which are on the left and center of the slide. The take home message is that children with FAS and those exposed to high amounts of alcohol, but without the characteristics required for a diagnosis of FAS, are similarly impaired. The FAS children tend to be a bit worse than the PEA children, but the pattern of behavioral deificits is fairly similar over a wide range of tests. References Mattson, S. N. , Riley, E. P. , Gramling, L. , Delis, D. C. , & Jones, K. L. (1998). Neuropsychological comparison of alcohol-exposed children with or without physical features of fetal alcohol syndrome. Neuropsychology, 12(1), 146-153.

image neuropsychological performanceBackground In addition to the abilities already discussed, a few studies have documented other specific neuropsychological deficits in individuals with FAS. Children with prenatal alcohol exposure, with and without FAS, have demonstrated various deficits on measures of executive functioning. These measures have revealed problems in areas such as planning (tower task-shown above), cognitive flexibility (trails test), inhibition (stroop test), and concept formation and reasoning (word context tests). Generally, performance on these measures is characterized by increased errors and more difficulty adhering to rules.

Therefore, children are less successful overall. For example, on the tower measure shown above (Tower of California-similar to Tower of London), children with FAS and PEA passed fewer items overall and made more rule violations than controls. The only two rules were to never place a larger piece on top of a smaller one and to move only one piece at a time. As can be seen the alcohol exposed children had many more rule violations. In addition, deficits have been found on the WCST (Wisconsin Card Sort Test), a nonverbal measure of problem solving. The WCST test requires both problem solving and cognitive flexibility and has been proposed to be sensitive to frontal system dysfunction.

This test is a gold standard in the measure of executive functioning in neuropsychology. Children with prenatal exposure to alcohol made more errors and had more difficulty with the conceptual nature of the task than controls. New data indicate that they have trouble identifying and defining concepts. Finally, tests of planning ability are also thought to be sensitive to frontal systems dysfunction although few such studies have been done in individuals with FAS. On the Progressive Planning Test which is similar to the Tower of London test children with FAS/FAE had difficulty with planning ahead and tended to perseverate on incorrect strategies. So far the results could be summarized as:

1) Heavy prenatal alcohol exposure is associated with a wide range of neurobehavioral deficits including visuospatial functioning, verbal and nonverbal learning, and executive functioning 2) Heavy prenatal alcohol exposure causes microcephaly and disproportionate reductions in the corpus callosum, basal ganglia, and cerebellum 3) Children with and without physical features of the fetal alcohol syndrome display qualitatively similar deficits References Carmichael O.

H. , Feldman JJ, Streissguth AP, Gonzalez RD: Neuropsychological deficits and life adjustment in adolescents and adults with fetal alcohol syndrome. Alcoholism: Clinical and Experimental Research 16:380, 1992 Kodituwakku PW, Handmaker NS, Cutler SK, Weathersby EK, Handmaker SD: Specific impairments in self-regulation in children exposed to alcohol prenatally. Alcoholism: Clinical and Experimental Research 19:1558-1564, 1995 Mattson, S. N. , Goodman, A. M. , Caine, C. , Delis, D. C. , & Riley, E. P. (1999).

Executive functioning in children with heavy prenatal alcohol exposure. Alcoholism, Clinical and Experimental Research, 23(11), 1808-1815. Background Secondary disabilities are those disabilities that the individual is not born with, and hopefully with appropriate intervention could be ameliorated. This slide illustrates the extent of these secondary disabilities as a function of age. These are individuals with FAS and FAE. As can be seen over 90% of these individuals have mental health problems and about 50% of those over the age of 12 have disrupted school experiences, trouble with the law, which is frequently severe enough to require confinement.

They also engage in relatively high rates of inappropriate sexual behavior and a significant number have alcohol and drug abuse problems. Interestingly, the factors that are protective against these secondary disabilities are: Being raised in a stable, nurturant home, diagnosis before the age of 6, no sexual or physical abuse, not changing households every few years, not living in a poor quality home, and receiving Developmental Disabilities services. References Streissguth, A. P. , Barr, H. M. , Kogan, J. , & Bookstein, F. L. (1996). Final Report: Understanding the occurrence of secondary disabilities in clients with fetal alcohol syndrome (FAS) and fetal alcohol effects (FAE). Seattle, WA: University of Washington Publication Services. Image secondary disabilities Background.

Much of what we know about FAS and the effects of prenatal alcohol exposure is the result of work on animal models. After FAS was identified it became important to demonstrate that the effects were indeed the result of alcohol exposure and not due to factors such as other drugs, maternal conditions, or nutritional variables. The development of appropriate animal models was very important in this regard. Models were developed for assessing physical features of FAS as well as the behavioral, neuroanatomical, and neurochemical profiles of prenatal alcohol exposure. The ideal test animal would absorb, metabolize and eliminate alcohol similar to human, transport alcohol and metabolites across.