The question that is being addressed in this paper are issues involving prenatal alcohol exposure to a human fetus and whether the effects of it can cause developmental disabilities that can be classified as psychopathologies in children and later in adults. There are many different aspects involved in addressing this, and I will try to touch on those most central to answering the question. More specifically, we will focus on the effects prenatal alcohol exposure has on the brain, the consequential effects on attention and other disorders like mental retardation. This topic was of interest to me because the organization I am interning at provides rehab for people recovering from alcohol or substance dependence. The topic came up in conversation and I thought it would be important for people to be aware of the effects of drinking on their children and would hopefully deter them from doing so. My prediction on the findings of this study is that previous research will have found that prenatal alcohol exposure is highly correlated with mental disorders and psychopathologies at all stages of life.
Fetal Alcohol Syndrome (FAS), is a result of alcohol exposure to developing fetus, and embryos in the womb. It is recognized as the leading preventable, non-biological cause of intellectual harm or damage (O'Leary 2004). FAS has several key features that are common to almost every case; these fall into three categories including growth retardation, characteristic facial features, and anomalies or dysfunction of the central nervous system. The third category is the one we will focus on most and includes

Microcephaly (structural brain abnormalities with no significant catch-up), developmental delay including social and motor performance, intellectual disability and neonatal issues including feeding problems. The results however, cover a wide range of severity from the most severe through more mild forms affecting only certain areas. This series of effects are often referred to as alcohol related neurodevelopmental disorders (ARND) or fetal alcohol effects (FAE). Ironically, not all children exposed to alcohol consumption in the neo-natal stage are affected by FAS. The amount, frequency, stage of development of the fetus and timing are responsible for the resulting deficiencies (O'Leary 2004) The estimated combined prevalence of FAS and ARND in America is about 9.1 for every 1000 children born or about 1 in 100 (O'Connor et. al 2002). That is a very high and scary statistic to think about.
The behavior and developmental abnormalities that are a result of alcohol exposure are aggravated by environmental factors. FAS children are more likely to live in environments with unstable or dysfunctional families, included in the foster-care system which can further their cognitive and social delays. In addition, infants with FAS tend to display personality characteristics associated with attention-deficit hyperactivity disorder (ADHD). Some of these include impulsivity, overly friendly, inquisitive, insensitive to social cues and lacking in social judgment. Other behaviors that accompany FAS are aggressiveness, school problems, learning disabilities and executive functions (O'Leary 2004). Some of these affects will be discussed in further detail and more specifically later in the paper, but for now it is important to understand that FAS and its affects vary from one situation to the next.
Next, in order to form some sort of answer to our question in which the paper is based, we need to evaluate and analyze several studies previously done on the issue and comment and compare their findings with our hypotheses. The goal and the findings of each study is presented here as evidence to support out hypothesis.
In one study done to characterize the spectrum of mental illness in adults with FAS or FAE, 25 subjects were interviewed using the Structured Clinical Interview for DSM Axis I and II disorders (SCID) (Famy, Streissgoth, Unis 1998). The results yielded that 23 of the 25 evaluated were given an axis I diagnosis. The majority had current or past substance dependence; the second most common was depression and then psychotic disorders. In four of the subjects, eating disorders were diagnosed, in others it was generalized anxiety, bipolar, PTSD, or a specific phobia. These results show that those suffering FAS or FAE developed significant mental illnesses as they grew up. These results although published, are limited to valid and reliable interpretation due to the small sample size used. Despite the study's limitations, Famy et. al (1998) has shown that there is a relation between FAS and psychopathologies in later life.
In Barbara Cone-Wesson's 2005 journal article, she states that fetal alcohol exposure is one of the leading causes of mental retardation. She goes on to say that it affects brain development "and its chemical, endocrine, and immunological function. Anatomical abnormalities include incomplete cortical development, enlarged ventricles, absent, or underdeveloped corpus collusum, and cerebellar changes" (Cone-Wesson 2005). Also associated with prenatal alcohol exposure are deficits in the development of speech, language and hearing in affected children. It is suggested here, that "the father's use of alcohol may alter his genetic material inherited by the fetus and provide another source of variability and severity in FAS" (Cone-Wesson 2005). She also suggests that maternal age plays a part in the severity of functional impairment.
In another study done by Lee, Mattson, & Riley 2004, 60 children were the subject of finding whether prenatal alcohol exposure has an affect on attention deficits or levels. One half of the subjects (30) were in the ALC group consisting of children who had a known history of prenatal exposure to alcohol and the other half (30) were in the CON group, those of who did not have such exposure. Within the ALC group, 12 of the children were diagnosed with FAS. The children were evaluated on several scales. The first, the Wechsler Intelligence Scale measures results in verbal, performance and full scale IQ. It also measures freedom from distractibility (FD) and is designed to measure the maintenance of attention during testing, separating those with attention

deficits. Next, the Test of Variables of Attention (TOVA) is a computerized assessment using visual images to measure inattention and impulsivity (Lee et. al 2004). Also, the parents were given the Child Behavior Checklist (CBCL) to measure the child's attention problems. The results of this study found that these assessment measures accurately separated children with prenatal alcohol exposure (PAE) from that of their non- exposed counterparts. The ATTN scores were found to be more influential than the FD scores but were most effective when combined in deciphering group membership. The TOVA evaluation was omitted due to factors that may have resulted in it being unreliable for the purposes of this study. It is hypothesized that the lengthy duration of the test resulted in low performance rather than being due to alcohol exposure. Overall, the two standardized measures of attention accurately predicted the presence or absence of heavy prenatal alcohol exposure. Despite the accuracy and results of this study, it is still unsure whether this pattern in PAE children is different from children with diagnosed ADHD. This study was successful in identifying children who were affected by FAS even when lacking the facial phenotype characteristics of FAS (Lee et. al 2004).
Another study performed by Burd, Klug, Martsolf, & Kerbeshian (2003), was intended to estimate the prevalence of mental disorders in a population of subjects from North Dakota. These subjects were either diagnosed with FAS, partial FAS/ARND, or they were referred as possible or partial FAS but did not meet diagnostic criteria for the disorders. The subjects were put into one of three categories depending on their scores on the FAS Diagnostic Checklist (FASDC). It was found that of the 397 subjects in this study, 152 of them were diagnosed with FAS, 151 with partial FAS, 87 did not have FAS and seven of them had no diagnosis. The results showed similar prevalence rates for mental disorders between FAS and partial FAS subjects. These two groups were also found to demonstrate higher risks of ADHD, learning and developmental disabilities and social problems compared to the subjects without FAS (Burd et. al 2003). The risks for these disorders were comparable by as much as 37-82%. The risks for having one or more comorbid mental disorders are more than double for FAS and partial FAS subjects. This study also shows that the younger children had greater risks of multiple mental disorders. As far as the link between ADHD and PAE goes, it was found that the FAS group had a 16.9 fold increase in prevalence compared to the base population rate in North Dakota children (Burd et. al 2003). Corresponding with these aforementioned results, it was found that learning disabilities, mood disorder, oppositional defiant disorder, and self injurious behavior in both FAS and partial FAS subjects were also increased by a significant amount than in North Dakota's general population (Burd et. al 2003).
All of these previously mentioned studies have implicated the relation and strongly correlated relationship between PAE and the cause of developmental disorders. It is important to remember that the major cause of impairment in people with FASD or FAS results from brain damage and dysfunction rather than abnormal facial features. "These results present compelling evidence that prenatal alcohol exposure causes brain damage or dysfunction and results in extraordinarily high rates of neuropsychiatric disorders, which often produce substantial impairment for people affected by prenatal alcohol exposure." (Burd et. al 2003). An important issue that we need to keep in mind is that the phenotype from PAE is neurodevelopmental and not dysmorphia (facial features and growth impairment). This will become important for doctors when diagnosing and determining whether or not someone suffers from FAS or PAE (Burd et al. 2003).
In regards to attention and other executive functions, this next study by Korkman, Kettunen, Autti-Ramo (2003), found that they do not seem to be separately or significantly affected by PAE. This is not to say that they were not affected at all, however. The goal of the study was to assess neurocognitive status in children exposed to alcohol prenatally and whether the duration of alcohol exposure is predictive of outcome at this age. A total of 66 subjects (a mix of exposed and non-exposed 12-14 yr. olds) were evaluated on attention and executive functions, language, visuomotor functions and memory (Korkman et. al 2003). The results showed varied impairment according to the duration of exposure. Those exposed throughout pregnancy yielded results well below average, supporting the relationship between duration and cognitive development is significant at this age (Korkman et. al 2003).
Another study conducted on the basis of finding a relationship between FAS and psychiatric disorders found results that match our hypothesis. Out of 23 children, 87% met criteria for a psychiatric disorder (O'Connor et. al 2002). A majority of these children were diagnosed with a mood disorder whether it was major depressive disorder or adjustment disorder with depressed mood. Thirty-Five percent were diagnosed with bipolar disorder which was much more common within the inpatient children than outpatient. In order to explain these outcomes we must understand why alcohol affects the brain and which parts it specifically damages. Alcohol exposure has been associated with damage to specific areas including the basal ganglia and the cerebellum. These make up part of the fronto-subcortical network that affects mood regulation. Hypodevelopment in these areas have also been recognized in adults as being correlated to primary and secondary mood disorders (O'Connor et. al 2002).
The findings of this study leave us with important clinical implications for future research and practice. First, it is important to be aware of the need for early recognition and identification of children who have been prenatally exposed to alcohol and are at risk for psychiatric illness. If a child receives early treatment and is in a safe and conducive environment to their situation, there may be a result in better outcomes of the effects. Another implication that this study leaves us with is the need for doctors who have the ability to correctly diagnose and obtain accurate prenatal histories of exposure to harmful substances. These health professionals should also be able to recognize both physical and behavioral phenotypes of children with PAE. This study also points us in new directions for research including that of the heritability of mood disorders and their etiological explanations (O'Connor et. al 2002).
Yet another study addresses the internalizing psychopathology in young children of alcohol exposure. It discusses the diathesis-stress model and risk when considering the causation in the emerging of psychopathology over time (Olson, O'Connor, Fitzgerald 2001). Olson et. al suggests that early attachment issues between infant and mother including irritability, difficulty in behavioral regulation, feeding and sleeping may impair the attachment relationship between mother and child. Therefore, the relationships in the critical early years of life can affect later social and emotional development, with a strong possibility that it my even have a greater affect on an alcohol affected child. These attachment disorders may be due to abuse and neglect when relevant and because of alcohol related deficits in cognitive and social-emotional functioning. Olson et. al also observes that "interestingly, prenatal alcohol exposure and maternal depression had an additive predictive effect, contributing independently and significantly to prediction of childhood depression." Also, girls were more likely than boys to have symptoms of depression. These findings urge researchers to use this proposed diathesis-stress model in their studies on the effects of prenatal alcohol exposure. This study also revealed that prenatal alcohol exposure tended to result in children showing more negative affect while in the presence of their mother. These mothers tended to be less emotionally connected to their children on an emotional level and therefore had children who reported higher levels of depression. This article proposes four developmental issues that have meaning for the development of internalizing disorders in children and how later psychopathology begins with the early infant-caregiver relationship (Olson et. al 2001). These include the establishment of homeostatic and physiological regulation; affect differentiation and the modulation of attention and arousal, as well as the development of a secure attachment relationship and of high self-esteem. Some caregivers may find infants who have been exposed to alcohol confusing and difficult to read; they may also have limited info-processing, providing unclear signals, thus creating a negative relationship with their caregiver. Mental health intervention for infants can take place in several settings including early intervention centers, hospitals, therapeutic daycares, or in public health home visitation programs. Another important setting for infant mental health services is chemical dependency treatment centers for women (Olson et. al 2001).
To sum, up the findings of this research paper, it was found that "Research from both theoretical perspectives has documented not only an increased frequency of various cognitive, communication, and sensory-motor deficits among individuals affected by parental alcohol use, but also elevated rates of problems with alcohol and drug abuse, and of social-emotional and psychiatric difficulties. These social-emotional difficulties may begin as early as infancy, and certainly can be seen in childhood and beyond (Olson et. al 2001). So we have successfully answered the key question we asked in this research paper. More studies on this topic are currently being done so that we can understand more about the long term affects of fetal exposure to alcohol.
This paper relates directly to my internship because our focus at Rehab After Work is working with recovering alcoholics and addicts. The focus is also in using ways to provide support and information on ways in which the patients will be able to stop using these substances they are dependent on. One of the topics discussed frequently is the affects in which alcohol can have on offspring if the pregnant mother is drinking. A lot of the clientele at Rehab After Work are adults, many of them female. It is in this way that this paper relates directly to my

internship. Many of the patients are mothers or are expecting. This paper also relates to the internship because it is a duel diagnosis program which means that the patients are dually diagnosed with a mental illness as well as substance dependence. As part of our intern responsibilities we had to give a presentation to the patients on an important topic and inform them on the consequences. We talked a lot about this subject and the recipients found it very interesting and informative.

Works Cited

1. Burd, Larry., Klug, Marilyn., Martsolf, John T., & Kerbeshian, Jacob. (2003). Fetal Alcohol Syndrome: Neuropsychiatric phenomics. Neurotoxicology &Teratology, 25(6), 697-705.
2. Cone-Wesson, Barbara. (2005). Prenatal alcohol and cocaine exposure: Influences on cognition, speech, language and hearing. Journal of Communication Disorders, Vol. 38 (4), pp. 279-302.
3. Famy, Chris., Streissgoth, Ann P., Unis, Alan S. (1998). Mental illness in adults with Fetal Alcohol Syndrome or Fetal Alcohol Effects. American Journal of Psychiatry, 155(4), 552-554.
4. Korkman, M., Kettunen, S., Autti-Ramo, I. (2003). Neurocognitive impairment in early adolescence following prenatal alcohol exposure of varying duration. Child Neurophsycology, Vol. 9 (2), pp.117-128.
5. Lee, Kara T., Mattson, Sarah N., Riley, Edward P. (2004). Classifying children with heavy prenatal alcohol exposure using measures of attention. Journal of the International Neuropsychological Society, 10(2), 271-277.
6. O'Connor, Mary J., Shah, Bhavik., Whaley, Shannon., Cronin, Pegeen., Gunderson, Brent., & Graham, John. (2002). Psychiatric Illness in a clinical sample of children with prenatal alcohol exposure. The American Journal of drug and alcohol abuse, Vol. 28 (4), pp. 743-754.
7. O'Leary, Colleen M. (2004). Fetal alcohol syndrome: Diagnosis, epidemiology, and developmental outcomes. Journal of Paediatrics and Child Health, Vol. 40 (1-2), pp.2-7.
8. Olson, Heather Carmichael., O'Connor, Mary J., & Fitzgerald, Hiram E. (2001). Lessons learned from study of the developmental impact of parental alcohol use. Infant Mental Health Journal, Vol. 22(3), pp. 271-290.

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