Abstract:An examination of the literature on Foetal Alcohol Spectrum Disorders (FASD) and its relevance to the work of Educational Psychologists (EPs) suggested that the impact of FASD on EPs' casework is an area which has been underexplored, and which merits further attention. A search of major electronic databases was conducted online; however no articles were found which specifically examined the role of the EP in connection with FASD. This is surprising as international research suggests that prevalence of FASD is … Show more
“…In children diagnosed with FASD, those who shared autistic characteristics tended to share deficits in social interaction and communication (Mukherjee et al, ; Stevens, Nash, Koren, & Rovet, ). The presence of these autistic characteristics can often lead to an initial misdiagnosis of FASD (Carpenter, ; Westrup, ). The link between ASD and FASD may be explained by contributions from a variety of common mechanisms, including epigenetic modifications (Varadinova & Boyadjieva, ) and genes involved in social interaction deficits (Tunc‐Ozcan, Ullmann, Shukla, & Redei, ).…”
Section: Comorbidity Of Fasd and Other Diseases Involving Oxidative Smentioning
This review covers molecular mechanisms involving oxidative stress and DNA damage that may contribute to morphological and functional developmental disorders in animal models resulting from exposure to alcohol (ethanol, EtOH) in utero or in embryo culture. Components covered include: (a) a brief overview of EtOH metabolism and embryopathic mechanisms other than oxidative stress; (b) mechanisms within the embryo and fetal brain by which EtOH increases the formation of reactive oxygen species (ROS); (c) critical embryonic/fetal antioxidative enzymes and substrates that detoxify ROS; (d) mechanisms by which ROS can alter development, including ROS-mediated signal transduction and oxidative DNA damage, the latter of which leads to pathogenic genetic (mutations) and epigenetic changes; (e) pathways of DNA repair that mitigate the pathogenic effects of DNA damage; (f) related indirect mechanisms by which EtOH enhances risk, for example by enhancing the degradation of some DNA repair proteins; and, (g) embryonic/fetal pathways like NRF2 that regulate the levels of many of the above components. Particular attention is paid to studies in which chemical and/or genetic manipulation of the above mechanisms has been shown to alter the ability of EtOH to adversely affect development. Alterations in the above components are also discussed in terms of: (a) individual embryonic and fetal determinants of risk and (b) potential risk biomarkers and mitigating strategies. FASD risk is likely increased in progeny which/who are biochemically predisposed via genetic and/or environmental mechanisms, including enhanced pathways for ROS formation and/or deficient pathways for ROS detoxification or DNA repair.
“…In children diagnosed with FASD, those who shared autistic characteristics tended to share deficits in social interaction and communication (Mukherjee et al, ; Stevens, Nash, Koren, & Rovet, ). The presence of these autistic characteristics can often lead to an initial misdiagnosis of FASD (Carpenter, ; Westrup, ). The link between ASD and FASD may be explained by contributions from a variety of common mechanisms, including epigenetic modifications (Varadinova & Boyadjieva, ) and genes involved in social interaction deficits (Tunc‐Ozcan, Ullmann, Shukla, & Redei, ).…”
Section: Comorbidity Of Fasd and Other Diseases Involving Oxidative Smentioning
This review covers molecular mechanisms involving oxidative stress and DNA damage that may contribute to morphological and functional developmental disorders in animal models resulting from exposure to alcohol (ethanol, EtOH) in utero or in embryo culture. Components covered include: (a) a brief overview of EtOH metabolism and embryopathic mechanisms other than oxidative stress; (b) mechanisms within the embryo and fetal brain by which EtOH increases the formation of reactive oxygen species (ROS); (c) critical embryonic/fetal antioxidative enzymes and substrates that detoxify ROS; (d) mechanisms by which ROS can alter development, including ROS-mediated signal transduction and oxidative DNA damage, the latter of which leads to pathogenic genetic (mutations) and epigenetic changes; (e) pathways of DNA repair that mitigate the pathogenic effects of DNA damage; (f) related indirect mechanisms by which EtOH enhances risk, for example by enhancing the degradation of some DNA repair proteins; and, (g) embryonic/fetal pathways like NRF2 that regulate the levels of many of the above components. Particular attention is paid to studies in which chemical and/or genetic manipulation of the above mechanisms has been shown to alter the ability of EtOH to adversely affect development. Alterations in the above components are also discussed in terms of: (a) individual embryonic and fetal determinants of risk and (b) potential risk biomarkers and mitigating strategies. FASD risk is likely increased in progeny which/who are biochemically predisposed via genetic and/or environmental mechanisms, including enhanced pathways for ROS formation and/or deficient pathways for ROS detoxification or DNA repair.
“…Without specialized training and experience, an individual with FASD may misleadingly appear to meet minimal criteria for the capacity to stand trial. For example, many individuals with FASD may present as talkative or chatty (Coggins et al., 1998; Westrup, 2013). However, this chattiness can be misleading, as the individual with FASD may in fact possess nuanced deficits that can cause significant problems for proceeding in the legal process (Fast & Conry, 2009).…”
Fetal alcohol spectrum disorders (FASD) are neurodevelopmental/neurobehavioral conditions caused by prenatal alcohol exposure (PAE). Impairments caused by PAE contribute to the over‐representation of individuals with FASD in the United States juvenile and adult criminal justice systems. These same impairments can equally impact on individuals with FASD who are witnesses to or victims of crime who also have to navigate the complexities of the criminal justice system. Difficulties include increased susceptibility to confabulation throughout the legal process that, in turn, can contribute to increased rates of poor outcomes including false confessions and wrongful convictions. Individuals with FASD are particularity at risk of confabulation when they are subjected to tactics, such as stressful and anxiety‐provoking situations, threats, and leading, suggestive, or coercive questioning. Many professionals in the forensic context are unfamiliar with FASD or related confabulation risk and may unintentionally utilize tactics that intensify impacts of pre‐existing impairment. This article serves as a beginner’s guide for professionals working in criminal justice settings by (a) providing research‐based overviews of FASD and confabulation, (b) describing how FASD may lead to confabulation, and (c) suggesting ways that professionals can modify protocols when interacting with individuals with FASD. Suggestions in this article hold the potential to decrease the risk of confabulation in the criminal justice system and decrease problematic outcomes, such as false confessions and wrongful convictions among individuals with FASD.
“…These deficits often result in observable behaviour and learning difficulties that frequently do not respond well to approaches used with other students with problems. As a result, students with FASD are more likely to have attracted the attention of educational psychologists or other education and clinical professionals (Westrup, ). For example, Carpenter () suggested that the intensity of the school experience frequently highlights the needs of those with FASD and that:‘… children with FASD are difficult to accommodate within any Key Stage of the English National Curriculum’.…”
Key words: Fetal alcohol spectrum disorder, fetal alcohol syndrome, special education, inclusive classroom, developmental delay, learning disability, brain-based physical disability.
IntroductionFetal alcohol spectrum disorder (FASD) is the leading cause of developmental disabilities in Canada and is a leading cause worldwide (Carpenter, 2011;O'Leary, 2004;Spohr, Willms and Steinhausen, 1993;Stade, Ali and Bennett et al., 2008). It was first described in France by Lemoine and is caused by prenatal exposure to alcohol resulting in physical, mental and learning disabilities that are permanent (Lemoine, Harousseau and Borteryu et al., 1968). FASD has also been described as 'The Hidden Disability', in part, because there may be no physical characteristics to show an individual has FASD. Health Canada estimates that 1% of the Canadian population is affected by FASD; however, many of those affected with FASD have not been assessed and diagnosed.Schools may be the first environment where children with complex learning difficulties and disabilities (CLDD) are identified. CLDD describes children with coexisting conditions that can include but are not limited to attention deficit hyperactivity disorder (ADHD), autism spectrum disorder (ASD) and FASD. Evidence indicates that the population of children with CLDD has been increasing. suggest that meeting this need requires 'informed and reflective practitioners who are equipped with a range of observation and intervention tools to support their learning and development'. This is particularly germane to complex disabilities such as FASD and the associated diverse array of neurobehavioural and developmental issues.In 1995, the Winnipeg School Division (WSD) established one of the first classrooms for students with FASD in Canada. This was in response to provincial surveillance data that identified 118 alcohol exposed infants born between 1993 and 1995 and the anticipation of increased identification and enrolment of children with FASD in schools. Based on early experiences in meeting the complex needs of these children within a regular classroom, the decision was made to develop a specialised programme that recognised and addressed the unique needs of children with FASD. What occurred at that time has been referred to as a paradigm shift in the understanding of the needs of individuals with FASD (Malbin, 2004). This has been further described by Malbin who said: This is an open access article under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.
'If FASD includes changes in the structure and function of the brain, then it follows that it is by definition a brain-based physical disability. In most cases, however, it is invisible, and behaviours are typically the only symptoms. Understanding FASD as a primary physical disability with behavioural symptoms redefines problems and solut...
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