Childhood Disorders - Essay Example

CHILDHOOD DISORDERS 2007 How do perspectives on childhood disorders help to inform professionals involved in their treatment Discuss with reference to research. Childhood disorders such as learning and conduct disorders, autism and depression, emotional problems, and many other conditions are likely to be caused by multiple factors that closely interplay with each other. Though the multi-causal approach (i.e. agreement that several factors combine to result in one or other type of disorder) seems to prevail in modern research, there are still several major perspectives that view one or other group of factors as dominant in aetiology of childhood disorders. Presence of these perspectives is largely due to varying views on the process of child development adopted by proponents of different psychological schools. The nature vs. nurture dispute in aetiology of childhood disorders revolves around one basic question, namely which factors are more influential in the process of mental development of an child: the biological or genetic makeup of a person (nature) or the upbringing and parenting style and other environmental factors (nurture) (Knowlton, 2005). All popular perspectives (e.g. those focusing on brain structure and functioning, early childhood experiences, cognitive development, peer influences, sleeping arrangements, interaction with environment, etc) fall in one of these groups, though each deals with a specific aspects of either 'nature' or 'nurture'. The balance between the two stances is different for each disorder and inevitably changes over time. Thus, the recent research of children with ADHD disorder finally rebutted the previously popular theory of the 'minimal brain damage' (Swanson et. al., 1998). Instead, the advances in genetic engineering and technology allowed more accurate and comprehensive research of genes allegedly responsible for ADHD and led to identification of two genes: a dopamine-receptor (DRD) gene on chromosome 11 and the dopamine-transporter gene (DAT1) on chromosome 5 (US Public Health Service, 2000). The genetic research revealed clear evidences that children with ADHD have genetic variations in one of the dopamine-receptor genes, namely DRD4. Many studies report that abnormalities of the dopamine-transporter gene (DAT1) have been present in children and adolescents with especially severe forms of ADHD (US Public Health Service, 2000). Nutritional factors, glucose levels and other new determinants are linked to this disorder in the modern research. Similarly, the aetiology of bipolar disorder, another commonly met childhood disorder is also explained from a number of perspectives. Studies involving twins and relatives demonstrate that bipolar disorder tends to run in families. However, the search for specific genes responsible for the disorder failed because studies of identical twins, who obviously possess the same genetic structure, rebutted the notion of genetic structure as the sole cause (NIMH, 1998.). Bipolar disorder is a mental disease that is why brain-imaging studies seem to be of great help in learning what exactly goes wrong in the brain and causes bipolar illness as well as other mental disorders. Contemporary methods and advanced techniques make possible having a picture of the living and working brain without destructive procedures, like surgery for instance. Magnetic resonance imaging, positron emission tomography and other techniques really helped to find out that the brains of persons with some form of bipolar illness really differed from the brains of normal people (Soares & Mann, 1997). The following physiological factors, detected with the help of the contemporary techniques, are called among the causes of bipolar disorders: - Excessive secretion of cortisol, a hormone that controls stress; - Excess of calcium in brain cells; - Abnormal hyperactivity in those parts of brain that are responsible for emotions and motor activity accompanied with low activity of those parts responsible for attention, logic, and concentration There is one alternative theory that suggests the following explanation: "people with bipolar disorder have a super fast biologic "clock", which is actually a tiny cluster of nerves called the supra chiasmatic nucleus or SCN. It is located in the hypothalamus (in the center of the brain) and it regulates a person's circadian rhythm, the daily cycle of life, which influences sleeping and waking". (Harvey, 2002: 31); Some researchers paid attention to the fact that majority of persons with bipolar disorders were born in winter, when the rate of infectious illnesses is extremely high. The assumption was that there are some viruses that do not directly cause bipolar disorder but may trigger its development. The Borna virus is known to cause significant CNS damages in animals, but there is no decisive evidences that it leads to the same effects in human beings. However, recent studies conducted on mentally ill patients provided the scientists with certain proofs the Borna virus might cause subtle changes in people's brain that in their turn might trigger a wide range of mental diseases, bipolar disorder being one of them. Herpes Simplex virus 2 (HSV-2) is one more possible reason for development of bipolar disorders. In accord with one research conducted less than two years ago, in 2001, children of mothers who had HSV-2 virus prior to delivery had much more chances to develop a bipolar disorder than children whose mothers who had not been infected (Harvey, 2002). Evidently, there are several causes that may be considered responsible for appearance of bipolar disorder, and till now there is no single opinion which one is dominant. Other childhood and adolescent disorders such as depression, oppositional defiant disorder, developmental disorders and other mood or mental conditions also have highly controversial history of research with neither of the numerous stances acting as the dominant aetiological explanation. The increasingly popular view that a combination of inward biological and environmental factors must be held responsible for childhood disorders is a reasonably balanced view that seeks to bring together the traditionally opposed views. On the other hand, versatile and often contradictory information coming from different sources is of great help for mental health professionals for several reasons. Firstly, up to now there is no clear answer as to what type of therapy is the best in each particular case, but it is already clear that the choice of effective treatment may and should seriously vary from person to person. Comprehensive versatile knowledge about the origins, symptoms and consequences of childhood disorders will result in more informed choices regarding therapy's road to improvement. Secondly, diverse perspectives on childhood disorders are likely to improve the quality of diagnosis. Drawing a line between normal behaviour and disordered behaviour is associated with serious difficulties with some scientists claiming that the boundary between normal and abnormal is so subjective and uninformed that many childhood disorders may not even exist in reality (Timimi, 2004). Therefore, the researchers must base their conclusions not only on the basis of actual behavioural symptoms, but also take into account all possible developmental pathways, events and factors that add to the development of disordered behaviour. This can be achieved only within multiple perspectives: neither approach is broad enough to embrace this range of variables. Thirdly, effectiveness of some existing traditional therapies and intervention strategies in coping with many childhood disorders is reasonably questioned while Alternative perspectives on aetiology of childhood disorders provide a basis for new therapies. Thus, the emergence of highly effective biofeedback and dietary therapy for ADHD (Lubar, 1991; Tansey, 1993; Richardson & Ross, 2000) is one example of this positive effect of multiple perspectives. And finally, the variety of data generated by representatives of different approaches may be very helpful in designing highly effective multimodal strategies which can be addressed as perhaps the most promising trend in treatment of childhood disorders. Such strategies comprise several therapies to address as many causes and symptoms of a disorder as possible. Finding the appropriate balance between various strategies within one treatment is the key problem facing proponents of the multimodal approach: only diverse abundant data can provide options to address it. 2. Critically evaluate theories of autism, and describe how understanding the disorder may help in providing treatment. The Pervasive Developmental Disorder (PDD) as a new diagnostic term first appeared in the 1980 edition of the Manual of Mental Disorders (DSM-IV) to embrace a group of several disorders characterized by delays in the development of multiple basic functions including socialization and communication (Volkmar & Klin, 2005). Nowadays this group consists of five PDDs: autism, Childhood Disintegrative Disorder, Asperger's disorder, Rett's disorder, and Pervasive Developmental Disorder Not Otherwise Specified (PDD-NOS) (DSM). Despite many common features and diagnostic criteria, the onset, course, and outcomes of different PDDs vary significantly varying from severe (autism) to milder (Asperger syndrome). Childhood Disintegrative Disorder (CDD) is characterised by a long period of seemingly normal development that precedes the developmental regression (Volkmar, 1994). The diagnostic criteria for CDD include loss of language, toileting and self care abilities, absence of interest in the social environment or environment in general (DSM). These criteria are very similar to those observed in autistic patients, but the loss of such skills as vocabulary is reported to be more dramatic in CDD than in autism (Volmar & Rutter, 1995). Rett's Syndrome (RS) is also characterised by a period of normal early development (Rett in 1966). The RS symptoms are very similar to those of autism: a deceleration of the rate of head growth, hands and feet size, loss of purposeful hand movements, serious cognitive impairments, socialization problems, and mental retardation (DSM). This disorder is very rare and occurs almost exclusively in girls: it affects approximately one in 12,500 females (SOME). Autism is a rare developmental disability characterized by severe withdrawal from reality resulting from the inability to socially relate to others. This disorder has several distinct diagnostic criteria: severe impairments in social interaction and communicative impairments, restricted repetitive and stereotyped patterns of behaviour, interests and activities, and early onset (during the first three years of life) (299.00 DSM-IV-TR 2000). Asperger's syndrome (AS) is the mildest form of PDDs characterised by the following symptoms: prolonged period of normal development (up to three years), social and functional impairments, the presence of restricted, repetitive and stereotyped behaviours and interests, and no significant delay in language ability (DSM 299.80). Despite similarity of the diagnostic criteria for autism and Asperger's syndrome, these two conditions differ much in terms of severity. Thus, some practitioners even refer to AS as High Functioning Autism (HFA) thus emphasizing the period of normal development and absence of language impairment as the major factors that make this disorder milder than classic autism. Aetiology of autism is subject for much debate and disagreement. Lack of consensus between the researchers exploring the causes of autism is due to one major reason: this disorder manifests differently in each individual. Consequently, several perspectives have emerged to explain the origins of autism. One of the earliest approaches in explaining the origins of autism - psychodynamic theory - linked the disorder to emotionally distant model of parenting. Insufficient attention and attachment to children were first mentioned in relation to autism in the 1940's by Leo Kanner (Kanner, 1943), but it was Bruno Bettleheim who popularised this theory by formulating the Refrigerator hypothesis (Bettleheim, 1972). This approach postulated that autism was caused by parental coldness toward children. Thus, Bettleheim drew a direct comparison between an autistic child and a concentration camp prisoner. However, the Refrigerator model of autism had several very essential weaknesses one of which was the following: it could not explain the occasions when mothers of autistic children had other children without the disorder (Rimland, 1997). The growing body of evidences generated by cognitive, neurological and biological research suggested more legitimate explanations. At least three credible perspectives linked autism to cognitive dysfunctions. In 1985 Simon Baron-Cohen, Alan Leslie and Uta Frith suggested that children might develop the disorder as a result of failure of the normal cognitive development - this approach became known as the theory of mind. They assumed that autistic children have difficulties with cognitive tasks which imply understanding separate beliefs and mental states of other persons, and linking them to behaviour: they argued such difficulties were the key characteristic of autism (Baron-Cohen, Leslie & Frith, 1985). Yet further research demonstrated the lack of a theory of mind was not present in many authentic children, which suggested there might be other cognitive deficiencies contributing to autism. The central coherence perspective supported by several experimental studies postulated that autistic children lacked the ability to integrate information from a variety of sources or perceive an object as a whole paying attention to details instead (Frith, 1989). Disturbance of the 'executive functions' such as working memory, impulse control, initiation and monitoring of actions, planning, inhibition and mental flexibility was also named as the key feature of autism (Ozonoff, Pennington & Rogers, 1991). Many twin and sibling studies showed heritability in autism which was strong enough to address it as "the most heritable complex genetic disorders in psychiatry" (Veenstra-Van DerWeele & Cook, 2003, 116). Thus, in a series of classic twin-studies conducted by a group of British scientists found an almost 60 percent concordance rate for autism in monozygotic twins, while in dizygotic twins and other siblings the rate was only 4 percent rates (Bailey et. al., 1994; Bolton et. al., 1995). Such results strongly implied that genetic factors might be the key player in aetiology of the disorder. However, neither specific genes nor mechanism of genetic influence have been identified up to now to confirm this hypothesis. Modern neuropsychological theory of autism focuses on how brain systems and pathways mediate behaviour of autistic children. This perspective postulates that the disorder has strong biological basis, but considering the behavioural symptoms of autism, it suggests that cognitive aspect of brain functioning must be further explored since cognition is the key element which links brain to behaviour (Happe & Frith, 1996). Certain nutritional deficits which supposedly affect functioning and development of the brain were also with autism. Thus, a consistent set of bowel disorders was found among autistic children (Payne & Mason, 1998) and a dietary intervention in autistic children resulted in noticeable behaviour improvements (Whiteley, Rodgers, Savery, & Shattock, 1999). The upward trend in autism incidence observed in late 1970s - early 1980s (Taylor et. al., 1999) made some clinicians investigate a possible connection between children vaccination and developmental disorders. A link between the measles, mumps and rubella (MMR) vaccine was first suggested in a study conducted by Andrew Wakefield in 1998. Though the study was seriously (and reasonably) criticized (e.g. the sample included only 12 children, absence of control, etc), the link between MMR, autism and other developmental disorders still remains one of the hottest and most controversial themes in autism literature. A series of studies that followed the initial research of Wakefield failed to fully clarify the issue, and the overall tendency was evident lack of any credible and consistent evidences for a causal link between MMR vaccine and autism (Phelan, 2002). However, current absence of consistent evidence only highlights the necessity of further research to resolve the debate: the difficulties inherent in the MMR/developmental disorders research are multiple and often even impossible to overcome partially due to rare incidence of developmental disorders, partially due to ethical considerations and methodological weaknesses. And finally, the behavioural perspective on autism implied it should be viewed as a behavioural disorder and treated accordingly. This approach emerged in the 1950's during the golden age of behaviourism in psychology and reflected the basic principles of this school: the behavioural symptoms of autism should be addressed via positive reinforcement (Ferster & Demyer, 1961). Despite oversimplification of this perspective (no attempt to explore the underlying causes of autism) it did proved the most effective in terms of intervention results. Each of the existing theories of autism contributes to our understanding of the disorder and has certain implications for treatment. Thus, the theory of genetic factors causing autism meets strong opposition in the research community largely due to the fact that acknowledging the dominant role of genetics in autism one automatically puts in question the assumption that the disorder is treatable and preventable. Evidently, this assumption is the least acceptable alternative for practitioners dealing with this disorder. But even in this case it will not be correct to stat that genetic theory of autism lacks value in terms of its implications for treatment: exact knowledge of biological and genetic underpinning helps better understand the potential of any intervention strategy or therapy (e.g. biomedical interventions), design new more efficient methods and accurately predict treatment outcomes. Cognitive theories are also critical for a full understanding of autism and have huge implications for behavioural interventions which still remain the only verified approach in the treatment of autism: comprehensive data on brain development is vitally important in contemporary models of autism. Behavioural and educational interventions are commonly regarded as the most effective treatment for autism (Sallows & Graupner, 2005). These interventions are used to teach autistic children social and motor skills, improve their cognitive skills, and reduce maladaptive behaviours. The behavioural approach in treatment of autism relies upon the behaviourist principles formulated by Skinner in the behaviourist conception of learning by paying attention not only to stimuli that cause certain behaviour of individual, but also exploring the stimuli affecting the actor after performance. In a series of experiments involving rats and pigeons that were rewarded with food for pressing a lever in the Skinner box, the scientist observed that positive stimuli led to more frequent repetition of the act that caused them; he called such stimuli "reinforcers" (Littleton, Toates, & Braisby, 2002: 175-176). The same principle of reinforcing positive behaviours forms the basis of the behaviourist approach in treatment of autism. The Applied Behaviour Analysis (ABA) associated with Ivar Lovaas showed very good results in fighting the major symptoms of autism. Lovaas used an early intensive behavioural intervention for children at the University of California, Los Angeles (UCLA). Lovaas's intervention programme focused on the development of attention, imitation, receptive and expressive language, play, social, and pre-academic, and self-help skills. Autistic children participating in the intensive one-to-one group showed significant advances in learning language, developing social and academic skills and self-help skills not only in the short-term but also in the long term (Lovaas, 1987). A series of other studies confirmed highly positive outcomes of the ABA intervention in different settings (Eikeseth et. al., 2002; Howard et. al., 2005), which leaves little doubt as for the actual effectiveness of ABA in treating autism considering the high replicability of Lovaas's results. Furthermore, a recent research by Sallows and Graupner (2005) compared groups receiving intensive behavioural treatments by parents lacking specific background and professionals to find practically no difference in positive outcomes between the two groups though the findings of Lovaas were almost mirrored. Such results leave little doubt in regard to effectiveness of the ABA approach in treatment of autism. Although Applied Behaviour Analysis (ABA) still remains the only strategy that has been scientifically verified to be effective (Sallows & Graupner, 2005), it might be misleading to consider the behavioural theory of autism to be the most reliable and important perspective in autism-related research. The behavioural approach simply has the history which other approaches lack, and, therefore, such strategies as improving physical health and well-being, addressing emotional, learning and communicative difficulties, sensory problems, etc may prove not less effective in the future studies. Great individual differences in outcomes of these treatment strategies highlight the importance of such studies. 3. How might research into Dyslexia help to provide effective intervention Discuss with reference to the possible underlying causes of the disorder. Dyslexia is a specific disorder or learning disability which refers to an "...unexpected difficulty in reading in children and adults who otherwise possess the intelligence, motivation, and schooling considered necessary for accurate and fluent reading" (Shaywitz, 1998: 307). The most common types of dyslexia identified in the literature are developmental dyslexia (also termed 'specific reading retardation') and acquired dyslexia (also termed 'deep dyslexia'). Acquired dyslexia is commonly associated with extensive damage of the left hemisphere or the occipital and temporal lobes, and is often termed 'alexia', 'word blindness', 'text blindness' or 'visual aphasia' (Critchley, 1970). Acquired dyslexia is characterised by the occurrence of semantic errors in reading aloud. The damage that can potentially lead to acquired dyslexia occurs in different areas of brain and its severity may differ too. Therefore, symptoms of acquired dyslexia may significantly differ in each particular case. Developmental dyslexia is defined as a '...specific and significant impairment in reading abilities, unexplainable by any kind of deficit in general intelligence, learning opportunity, general motivation or sensory acuity' (Critchley, 1970; World Health Organization, 1993). This disorder is commonly associated with such conditions as problems in oral language acquisition (dysphasia), impairments of writing abilities (dysgraphia and misspelling), poor mathematical abilities (dyscalculia), insufficient motor coordination (dyspraxia), postural stability and dexterity, temporal orientation (dyschronia'), visuospatial abilities (developmental right-hemisphere syndrome), and attention abilities (hyperactivity and attention deficit disorder) (Habib, 2000). The development of reading abilities normally follows the acquisition of spoken language during the earliest stages of life. The existing evidences suggest that conversion of the written word image into its phonological equivalent in the brain is a critical component of the fluent reading ability. Consequently, failure to develop such association between letter and sound is commonly and reasonably believed to be the major characteristic of developmental dyslexia (Bradley and Bryant, 1983). However, this view is only one alternative in explaining the origins of dyslexia: similarly to autism and other childhood disorders, aetiology of dyslexia is also not fully clear. Some family studies suggest that dyslexia may have strong biological (genetic) underpinning because it often runs in families (Elbert et. al., 2000). There are at least four major theories of developmental dyslexia: the phonological theory, the temporal auditory processing theory, the magnocellular theory, and the automaticity theory. Each of these perspectives relies on a solid body of empirical data, while some of them are mutually complementary. However, it is practically impossible that all the four approaches might be equally and simultaneously time in one and the same case: the growing body of empirical data suggests that many types of deficits associated with dyslexia are not present in the whole population of dyslexics. Therefore, developmental dyslexia is likely to be adequately explained only from a highly flexible perspective involving multiple theories (Ramus et. al., 2003). The most commonly used treatment strategy for dyslexia relies on educational tutoring. This treatment approach is based on the assumption that dyslexia is a non-curable disorder caused by specific information processing and the only acceptable alternative for dyslexics is to learn coping strategies specially designed for each of the numerous problems associated with the disorder (reading, spelling, memory and comprehension speed, etc). Though dyslexia is recognized as a non-preventable and non-curable disorder, further research into this disorder is likely to have essential implications for treatment. However, attempts to reveal the causes of dyslexia (e.g. specific genes) seem less important than full understanding and accurate localisation of the brain areas that function abnormally in dyslexic children. Areas of the brain involved in language and reading activities function abnormally in dyslexic children - this notion underlies the existing intervention strategies in the U.K. However, the most recent research involving Chinese children demonstrates that the root cause of dyslexia may be culturally determined. Dyslexic children in China are likely to have problems with other areas of brain than English-speaking children because Chinese language is symbol-based while English language is letter-based (Slok, Perfetti, Jin & Tan, 2004). This finding has one highly important implication for treatment: a strategy proved highly effective in one cultural environment will not necessarily prove similarly effective in a different cultural setting because different areas of the brain should be stimulated to successfully treat dyslexic children in different environments. Besides, cultural determination of the root cause for dyslexia challenges the established notion of the exclusively biological basis for this disorder. Further research into dyslexia may help better distinguish between the cognitive mechanisms and brain areas involved in dyslexia and other confusingly similar disorders (e.g. auditory processing disorder, verbal dyspraxia, dyscalculia, cluttering, etc). This will exclude the possibility of the right treatment delivered to wrong patients and will probably lead to development of new therapeutic approaches that would selectively target the specific cognitive, auditory, neurological, or visual problems underlying the disorder. The Dyslexia Friendly School (DFS) initiative introduced by the British Dyslexia Association (BDA) in 1999 provides a set of guidelines and standards for schools to follow in order to create a dyslexia friendly teaching environment. The initiative was meant to address the trend in education when dyslexic learners increasingly placed in ordinary schools faced more challenges than normal students (Peer & Reid, 2000). These guidelines fall into four groups: Leadership and Management. Teaching and Learning. The Classroom Environment. Partnership and Liaison with Parents, Carers, Governors and other Concerned Parties (BDA, 2007). The BDA Quality Mark confirming that the school meets these four standards offers one substantial benefit, namely: access to the advanced reliable data about the most recent trends in improving quality of education in dyslexic students. The access is ensured via seminars, conferences and other experience exchange initiatives conducted under the aegis of the BDA. In the 1990s, the problem of dyslexic students in higher education became another hot topic with both public and professionals due to increasing number of such students entering the system each year. As a result, dyslexic students in higher education these days are entitled to receive various kinds of support ranging from specific educational hardware and software to personal tutorship, non-medical support and special examination programs (e.g. additional time for reading activities, etc). Dyslexia is also mentioned in Paragraph A8 of the British Disability Discrimination Act which provides legal protection for dyslexic students: "In some cases, people have 'coping strategies' which cease to work in certain circumstances (for example, where someone who stutters or has dyslexia is placed under stress). If it is possible that a person's ability to manage the effects of the impairment will break down so that these effects will sometimes occur, this possibility must be taken into account when assessing the effects of the impairment" (DDA, 2005). The focus of the current policies in higher education is on fighting the common misconceptions about dyslexia and educating the teaching stuff about the specifics of working with dyslexic students. References American Psychiatric Association (2000). Diagnostic criteria for autistic disorder. In Diagnostic and statistical manual of mental disorders (Fourth edition---text revision (DSM-IV-TR). Washington, DC: American Psychiatric Association, 75. Bailey, A., Le Couteur, A., Gottesman, I., Bolton, P., Simonoff, E., Yuzda, E., Rutter, M. (1995). Autism as a strongly genetic disorder: evidence from a British twin study. Psychological Medicine, 25, 63-77. Baron-Cohen, S., Leslie, A. M. & Frith, U. (1985). Does the autistic child have a 'theory of mind' Cognition, 21, 37-46. Bettelheim, B. (1972). Empty Fortress. Publisher: Free Press. Bolton, P., MacDonald, H., Pickles, A., Rios, P., Goode, S., Crowson, M., Bailey, A., Rutter, M. (1994). A case-control family history study of autism. Journal of Child Psychology and Psychiatry, 35, 877-900. Bradley, L. & Bryant, P. E. (1983). Categorizing sounds and learning to read: A causal connection. Nature, 301, 419-421. British Dyslexia Association (2000). Dyslexia Friendly Resource Pack. Reading, British Dyslexia Association. Critchley, M. (1970). The dyslexic child. 2nd ed. London: Heinemann Medical. Disability Discrimination Act 2005. The Stationery Office Limited Harvey, S. (2002). Bipolar Disorder. New York: A.D.A.M. Inc. Howard, J., Sparkman, C., Cohen, H., Green, G., Stanislaw, H. (2005). A comparison of intensive behaviour analytic and eclectic treatments for young children with autism. Research in developmental disabilities, 26(4), 359-83. Eikeseth, S., Smith, T., Jahr, E., Eldevik, S. (2002). Intensive behavioural treatment at school for 4- to 7-year-old children with autism. A 1-year comparison controlled study. Behaviour modification, 26(1), 49-68. Elbert, J.C., Seale, T. W. & McMahon, E. (2000). Genetic influences on behaviour and development. In C. E. Walker & M. C. Roberts (Eds.), Handbook of Clinical Child Psychology, 3rd ed., pp. 207-244. New York: John Wiley and Son. Ferster, C. B., & Demyer, M. K. (1961). The development of performances in autistic children in an automatically controlled environment. Journal of Chronic Diseases, 13, 312-345. Happe, F. & Frith, U. (1996). The neuropsychology of autism. Brain, 119, 1377-1400. Kanner, L. (1943). Autistic disturbances of affective contact. Nervous Child, 2, 217-250 Knowlton, L. (2005). Nature Versus Nurture: How Is Child Psychopathology Developed Psychiatric Times, 22(8), 9. Littleton, K., F. Toates, & N. Braisby (2002). Chapter 3: Three Approaches to Learning. In Miell, D., A. Phoenix and K. Thomas, (Eds), Mapping Psychology, The Open University. Lovaas O (1987). "Behavioral treatment and normal educational and intellectual functioning in young autistic children.". Journal of consulting and clinical psychology 55 (1): 3-9 Lubar, J. F. (1991). Discourse on the development of EEG diagnostics and biofeedback for attention-deficit/hyperactivity disorders. Biofeedback and Self-Regulation, 16 (3), 201-225. National Institute of Mental Health (1998). Genetics and mental disorders. NIH Publication No. 98-4268. Rockville, MD: National Institute of Mental Health. National Working Party on Dyslexia in Higher Education (1999). Dyslexia in Higher Education: policy, provision and practice. The University of Hull. Ozonoff, S., Pennington, B. & Rogers, S. (1991). Executive function deficits in high-functioning autistic children: relationship to theory of mind. Journal of Child Psychology and Psychiatry, 32, 1081-1106. Payne, C. & Mason, B. (1998). Autism, inflammatory bowel disease, and MMR vaccine. Lancet, 351, 907. Peer, L. & Reid, G. (2000). Multilingualism, Literacy and Dyslexia: A Challenge for Educators. In Peer, L. & Reid, G., (Eds), Multilingualism, Literacy and Dyslexia: A Challenge for Educators, London, David Fulton Publishers. Phelan, A. T. (2002). MMR and autism: an overview of the debate to date. British Journal of Nursing, 11(9), 620-625. Ramus, F., Rosen, S., Dakin, S. C., Day, B. L., Castellote, J. M., White, S., & Frith, U. (2003). Theories of developmental dyslexia: Insights from a multiple case study of dyslexic adults. Brain, 126, 841-865. Richardson, A. J. & Ross, M. A. (2000). Fatty acid metabolism in neurodevelopmental disorder: a new perspective on associations between ADHD, dyslexia, dyspraxia and the autistic spectrum. Prostaglandins Leukotr Essent Fatty Acids, 63: 1-9. Rimland, B. (1997). Genetics, Autism, and Priorities. Autism Research Review International, 11(2), 3. Sallows, G. O. & Graupner, T. D. (2005). Intensive Behavioural Treatment for Children with Autism: Four-Year Outcome and Predictors. American Journal on Mental Retardation, 110 (2), 417-438. Shaywitz, S. E. (1998). Dyslexia. New England Journal of Medicine, 338, 307-12. Slok W. T, Perfetti C. A., Jin Z. & Tan L. H. (2004). Biological abnormality of impaired reading is constrained by culture. Nature, 431, 71 - 76. Soares, J. & Mann, J. (1997). The functional neuroanatomy of mood disorders. Journal of Psychiatric Research, 31(4), 393-432. Tansey, M. A. (1993). Ten-year stability of EEG biofeedback results for a hyperactive boy who failed fourth grade perceptually impaired class. Biofeedback and self-regulation, 18 (1), 33 - 44. Taylor, B., Miller, E., Farrington, C. P., Petropoulos, M. C., Favot-Mayaud, I., Li, J., Waight, P. A. (1999). Autism and measles, mumps, and rubella vaccine: no epidemiological evidence for a causal association. Lancet 353, 2026-2029. Timimi, S. (2004). Diagnosis of autism: current epidemic has social context. British Medical Journal, 328(7433): 226. US Public Health Service (2000). Mental Health: A Report of the Surgeon General [electronic version]. Retrieved May 2 2007 from http://mentalhealth.samhsa.gov/features/surgeongeneralreport/toc.asp Veenstra-Van DerWeele, J. & Cook, E. H., Jr. (2003). Genetics of childhood disorders: XLVI. Autism, part 5: genetics of autism. Journal of the American Academy of Child and Adolescent , 42 , 116-118, Volkmar, R.M & Rutter, M. (1995). Childhood disintegrative disorder: Results of the DSM-IV autism field trial. Journal of the American Academy of Child and Adolescent Psychiatry, 34, 1092-1095. Volkmar, F.R., Klin. A. (2005). Issues in the classification of autism and related conditions. In Volkmar, F.R., Paul, R., Klin, A., Cohen, D., (Eds.), Handbook of Autism and Pervasive Developmental Disorders, New Jersey: John Wiley and Sons. Read More