Community knowledge and beliefs about ADHD

Accurate knowledge and positive attitudes within the community are important for the effective diagnosis, treatment and support of people with ADHD. Most previous research about knowledge and attitudes has focused only on professional groups and parents of children with ADHD. The aim of this study was to explore knowledge about ADHD characteristics and causes, and attitudes towards issues such as medication in the general population. Six hundred and forty-five members of the Australian community, all of whom were parents, completed a questionnaire. The findings showed that the core features of ADHD were well-known, but there were misconceptions and considerable uncertainty about many aspects. Most respondents failed to recognise the genetic basis of the disorder and its potentially lifelong nature. Fathers were less knowledgeable than mothers. Although most participants believed that ADHD is a genuine disorder and recognised the benefits of medication, the majority believed that it is diagnosed too frequently and that medication is prescribed too readily. The study concluded that, in many respects, the public is not well-informed about ADHD and suggested that the media may have an important role in enhancing community awareness of the disorder through responsible, sensitive and accurate reporting.

Tyrosine monitoring in children with early and continuously treated phenylketonuria: Results of an international practice survey

Investigations into the biochemical markers associated with executive function (EF) impairment in children with early and continuously treated phenylketonuria (ECT-PKU) remain largely phenylalanine-only focused, despite experimental data showing that a high phenylalanine:tyrosine (phe:tyr) ratio is more strongly associated with EF deficit than phe alone. A high phe:tyr ratio is hypothesized to lead to a reduction in dopamine synthesis within the brain, which in turn results in the development of EF impairment. This paper provides a snapshot of current practice in the monitoring and/or treatment of tyrosine levels in children with PKU, across 12 countries from Australasia, North America and Europe. Tyrosine monitoring in this population has increased over the last 5 years, with over 80% of clinics surveyed reporting routine monitoring of tyrosine levels in infancy alongside phe levels. Twenty-five percent of clinics surveyed reported actively treating/managing tyrosine levels (with supplemental tyrosine above that contained in PKU formulas) to ensure tyrosine levels remain within normal ranges. Anecdotally, supplemental tyrosine has been reported to ameliorate symptoms of both attention deficit hyperactivity disorder and depression in this population. EF assessment of children with ECT-PKU was likewise highly variable, with 50% of clinics surveyed reporting routine assessments of intellectual function. However when function was assessed, test instruments chosen tended towards global measures of IQ prior to school entry, rather than specific assessment of EF development. Further investigation of the role of tyrosine and its relationship with phe and EF development is needed to establish whether routine tyrosine monitoring and increased supplementation is recommended.

Teachers' and education students' perceptions of and reactions to children with and without the diagnostic label 'ADHD'

Thirty-four elementary school teachers and 32 education students from Canada rated their reactions towards vignettes describing children who met attention-deficit/hyperactivity disorder (ADHD) symptom criteria that included or did not include the label “ADHD.” “ADHD”-labeled vignettes elicited greater perceptions of the child's impairment as well as more negative emotions and less confidence in the participants, although it also increased participants' willingness to implement treatment interventions. Ratings were similar to vignettes of boys versus girls; however, important differences in ratings between teachers and education students emerged and are discussed. Finally, we investigated the degree to which teachers' professional backgrounds influenced bias based on the label “ADHD.” Training specific to ADHD consistently predicted label bias, whereas teachers' experience working with children with ADHD did not.

Neuropsychological development in children with early and continuously treated phenylketonuria : association with biochemical markers

PKU is a genetically inherited inborn error of metabolism caused by a deficiency of the enzyme phenylalanine hydroxylase. The failure of this enzyme causes incomplete metabolism of protein ingested in the diet, specifically the conversion of one amino acid, phenylalanine, to tyrosine, which is a precursor to the neurotransmitter dopamine. Rising levels of phenylalanine is toxic to the developing brain, disrupting the formation of white matter tracts. The impact of tyrosine deficiency is not as well understood, but is hypothesized to lead to a low dopamine environment for the developing brain. Detection in the newborn period and continuous treatment (a low protein phe-restricted diet supplemented with phenylalanine-free protein formulas) has resulted in children with early and continuously treated PKU now developing normal I.Q. However, deficits in executive function (EF) are common, leading to a rate of Attention Deficit Hyperactivity Disorder (ADHD) up to five times the norm. EF worsens with exposure to higher phenylalanine levels, however recent research has demonstrated that a high phenylalanine to tyrosine ratio (phenylalanine:tyrosine ratio), which is hypothesised to lead to poorer dopamine function, has a more negative impact on EF than phenylalanine levels alone. Research and treatment of PKU is currently phenylalanine-focused, with little investigation of the impact of tyrosine on neuropsychological development. There is no current consensus as to the veracity of tyrosine monitoring or treatment in this population. Further, the research agenda in this population has demonstrated a primary focus on EF impairment alone, even though there may be additional neuropsychological skills compromised (e.g., mood, visuospatial deficits). The aim of this PhD research was to identify residual neuropsychological deficits in a cohort of children with early and continuously treated phenylketonuria, at two time points in development (early childhood and early adolescence), separated by eight years. In addition, this research sought to determine which biochemical markers were associated with neuropsychological impairments. A clinical practice survey was also undertaken to ascertain the current level of monitoring/treatment of tyrosine in this population. Thirteen children with early and continuously treated PKU were tested at mean age 5.9 years and again at mean age 13.95 years on several neuropsychological measures. Four children with hyperphenylalaninemia (a milder version of PKU) were also tested at both time points and provide a comparison group in analyses. Associations between neuropsychological function and biochemical markers were analysed. A between groups analysis in adolescence was also conducted (children with PKU compared to their siblings) on parent report measures of EF and mood. Minor EF impairments were evident in the PKU group by age 6 years and these persisted into adolescence. Life-long exposure to high phenylalanine:tyrosine ratio and/or low tyrosine independent of phenylalanine were significantly associated with EF impairments at both time points. Over half the children with PKU showed severe impairment on a visuospatial task, and this was associated only with concurrent levels of tyrosine in adolescence. Children with PKU also showed a statistically significant decline in a language comprehension task from 6 years to adolescence (going from normal to subnormal), this deficit was associated with lifetime levels of phenylalanine. In comparison, the four children with hyperphenylalaninemia demonstrated normal function at both time points, across all measures. No statistically significant differences were detected between children with PKU and their siblings on the parent report of EF and mood. However, depressive symptoms were significantly correlated with: EF; long term high phe:tyr exposure; and low tyrosine levels independent of phenylalanine. The practice survey of metabolic clinics from 12 countries indicated a high level of variability in terms of monitoring/treatment of tyrosine in this population. Whilst over 80% of clinics surveyed routinely monitored tyrosine levels in their child patients, 25% reported treatment strategies to increase tyrosine (and thereby lower the phenylalanine:tyrosine ratio) under a variety of patient presentation conditions. Overall, these studies have shown that EF impairments associated with PKU provide support for the dopamine-deficiency model. A language comprehension task showed a different trajectory, serving a timely reminder that non-EF functions also remain vulnerable in this population; and that normal function in childhood does not guarantee normal function by adolescence. Mood impairments were associated with EF impairments as well as long term measures of phenylalanine:tyrosine and/or tyrosine. The implications of this research for enhanced clinical guidelines are discussed given varied current practice.

Philosophy, behaviour disorders, and the school

The recent exponential rise in the number of behaviour disorders has been the focus of a wide range of commentaries, ranging from the pedagogic and the administrative, to the sociological, and even the legal. This book will be the first to apply, in a systematic and thorough manner, the ideas of the foundational discipline of philosophy. A number of philosophical tools are applied here, tools arising through the medium of the traditional philosophical debates, such as those concerning governance, truth, logic, ethics, free-will, law and language. Each forms a separate chapter, but together they constitute a comprehensive, rigorous and original insight into what is now an important set of concerns for all those interested in the governance of children. The intention is threefold: first, to demonstrate the utility, accessibility and effectiveness of philosophical ideas within this important academic area. Philosophy does not have to be regarded an arcane and esoteric discipline, with only limited contemporary application, far from it. Second, the book offers a new set of approaches and ideas for both researchers and practitioners within education, a field is in danger of continually using the same ideas, to endlessly repeat the same conclusions. Third, the book offers a viable alternative to the dominant psychological model which increasingly employs pathology as its central rationale for conduct. The book would not only be of interest to mainstream educators, and to those students and academics interested in philosophy, and more specifically, the application of philosophical ideas to educational issues, it would also be an appropriate text for courses on education and difference, and due to the breadth of the philosophical issues addressed, courses on applied philosophy.

Countering the ADHD epidemic : a question of ethics?

Recently in Australia, another media skirmish has erupted over the problem we currently call “Attention Deficit Hyperactivity Disorder”. This particular event was precipitated by the comments of a respected District Court judge. His claim that doctors are creating a generation of violent juvenile offenders by prescribing Ritalin to young children created a great deal of excitement, attracting the attention of election-conscious politicians who appear blissfully unaware of the role played by educational policy in creating and maintaining the problem. Given the short (election-driven) attention span of government policymakers, I bypass government to question what those at the front line can do to circumvent the questionable practice of diagnosing and medicating young children for difficulties they experience in schools and with learning.

(De)Constructing ADHD : Critical Guidance for Teachers and Teacher Educators

Attention Deficit Hyperactivity Disorder (ADHD) has achieved celebrity status in many Western countries, yet despite considerable effort to prove its existence as a “real” disorder, ADHD still suffers from a crisis of legitimacy. Nonetheless, diagnosis and prescription of medication has grown at a phenomenal rate since the late 1980s, particularly in Western culture. Numerous accounts exist explaining how the ADHD diagnosis functions as a convenient administrative loophole, providing schools with a medical explanation for school failure, medication to sedate the “problem” into submission, or the means to eject children from mainstream classrooms. This book provides a more holistic interpretation of how to respond to children who might otherwise be diagnosed with and medicated for “ADHD”—a diagnosis which, whether scientifically valid or not, is unhelpful within the confine of the school. Training teachers to recognise and identify “ADHD symptoms” or to understand the functions of restricted pharmaceuticals will only serve to increase the number of children diagnosed and the sale of psychoactive medications. Research has shown that such activities will not help those children learn, nor will it empower their classroom teachers to take responsibility for teaching such children well. This book seeks to provide school practitioners with knowledge that is useful within the educational context to improve the educational experiences and outcomes for children who might otherwise receive a diagnosis of ADHD.

Students with AD/HD-related behaviours : Saudi mainstream teachers' knowledge and attitude towards inclusion

This study investigated Saudi mainstream primary teachers' knowledge of AD/HD and their attitudes towards the inclusion of students with AD/HD-related behaviours. The study also explored the relationships among teachers' attitudes towards inclusion, knowledge of AD/HD, efficacy beliefs for teaching students with behavioural problems, and relevant background factors such as teacher age, training and experience, and class size. In the first phase of the study, more than 200 Saudi teachers completed a four-part self-report questionnaire while in the second, 8 teachers completed semi-structured interviews. Findings from both phases of the study indicated that although teachers' knowledge of AD/HD was somewhat limited, they generally held positive attitudes towards the inclusion of students with AD/HD-related behaviours in regular classrooms. Additional significant influences on teachers' attitudes included class size as well as teachers' training and self-efficacy beliefs.

Thinking Pedagogically

Despite the dominancy of medical explanations for difficult child behavior, the shifting sands that lie beneath the ADHD construct provide an unstable foundation for educational practice. It can be somewhat liberating to remember that “attention deficit hyperactivity disorder” is a label (one of many, including minimal brain damage and hyperkinetic reaction of childhood) that the medical domain has coined to both group and describe certain challenging behaviors exhibited by children and young people (see Smith, Chapter 2). The label is but one conceptualization of what these behaviors mean and, despite the existence of powerful lobby groups, it may not be the best way forward. In what follows, I present an alternative typology to the medical conceptualization by describing some common issues that bring this group of children to attention. In an effort to introduce educationally useful responses to students who are difficult to teach, I will then outline what classroom teachers need to recognize in order to work with these students and realize their potential. To assist teachers in thinking pedagogically, these observations are coupled with well-known and relevant qualities of good teaching to remind teachers of what they already know and to reacquaint them with the power of that knowledge.

Dopamine transporter genotype predicts behavioural and neural measures of response inhibition

The ability to inhibit unwanted actions is a heritable executive function that may confer risk to disorders such as attention deficit hyperactivity disorder (ADHD). Converging evidence from pharmacology and cognitive neuroscience suggests that response inhibition is instantiated within frontostriatal circuits of the brain with patterns of activity that are modulated by the catecholamines dopamine and noradrenaline. A total of 405 healthy adult participants performed the stop-signal task, a paradigmatic measure of response inhibition that yields an index of the latency of inhibition, termed the stop-signal reaction time (SSRT). Using this phenotype, we tested for genetic association, performing high-density single-nucleotide polymorphism mapping across the full range of autosomal catecholamine genes. Fifty participants also underwent functional magnetic resonance imaging to establish the impact of associated alleles on brain and behaviour. Allelic variation in polymorphisms of the dopamine transporter gene (SLC6A3: rs37020; rs460000) predicted individual differences in SSRT, after corrections for multiple comparisons. Furthermore, activity in frontal regions (anterior frontal, superior frontal and superior medial gyri) and caudate varied additively with the T-allele of rs37020. The influence of genetic variation in SLC6A3 on the development of frontostriatal inhibition networks may represent a key risk mechanism for disorders of behavioural inhibition.

(Un)Becoming behaviour

This chapter focuses on the role of teachers in supporting children who experience difficulties in early years settings and who engage in disruptive behaviour. Learning goals associated with this chapter include: - How challenging behaviour develops and what can happen if it remains unaddressed - The ability to analyse student behaviour - How to interpret common behaviours and how to avoid misperceptions - Ways to develop alternative approaches that are respectful of difference

Mapping cortical change in Alzheimer's disease, brain development, and schizophrenia

This paper describes algorithms that can identify patterns of brain structure and function associated with Alzheimer's disease, schizophrenia, normal aging, and abnormal brain development based on imaging data collected in large human populations. Extraordinary information can be discovered with these techniques: dynamic brain maps reveal how the brain grows in childhood, how it changes in disease, and how it responds to medication. Genetic brain maps can reveal genetic influences on brain structure, shedding light on the nature-nurture debate, and the mechanisms underlying inherited neurobehavioral disorders. Recently, we created time-lapse movies of brain structure for a variety of diseases. These identify complex, shifting patterns of brain structural deficits, revealing where, and at what rate, the path of brain deterioration in illness deviates from normal. Statistical criteria can then identify situations in which these changes are abnormally accelerated, or when medication or other interventions slow them. In this paper, we focus on describing our approaches to map structural changes in the cortex. These methods have already been used to reveal the profile of brain anomalies in studies of dementia, epilepsy, depression, childhood- and adult-onset schizophrenia, bipolar disorder, attention-deficit/hyperactivity disorder, fetal alcohol syndrome, Tourette syndrome, Williams syndrome, and in methamphetamine abusers. Specifically, we describe an image analysis pipeline known as cortical pattern matching that helps compare and pool cortical data over time and across subjects. Statistics are then defined to identify brain structural differences between groups, including localized alterations in cortical thickness, gray matter density (GMD), and asymmetries in cortical organization. Subtle features, not seen in individual brain scans, often emerge when population-based brain data are averaged in this way. Illustrative examples are presented to show the profound effects of development and various diseases on the human cortex. Dynamically spreading waves of gray matter loss are tracked in dementia and schizophrenia, and these sequences are related to normally occurring changes in healthy subjects of various ages.

The ENIGMA Consortium: Large-scale collaborative analyses of neuroimaging and genetic data

The Enhancing NeuroImaging Genetics through Meta-Analysis (ENIGMA) Consortium is a collaborative network of researchers working together on a range of large-scale studies that integrate data from 70 institutions worldwide. Organized into Working Groups that tackle questions in neuroscience, genetics, and medicine, ENIGMA studies have analyzed neuroimaging data from over 12,826 subjects. In addition, data from 12,171 individuals were provided by the CHARGE consortium for replication of findings, in a total of 24,997 subjects. By meta-analyzing results from many sites, ENIGMA has detected factors that affect the brain that no individual site could detect on its own, and that require larger numbers of subjects than any individual neuroimaging study has currently collected. ENIGMA's first project was a genome-wide association study identifying common variants in the genome associated with hippocampal volume or intracranial volume. Continuing work is exploring genetic associations with subcortical volumes (ENIGMA2) and white matter microstructure (ENIGMA-DTI). Working groups also focus on understanding how schizophrenia, bipolar illness, major depression and attention deficit/hyperactivity disorder (ADHD) affect the brain. We review the current progress of the ENIGMA Consortium, along with challenges and unexpected discoveries made on the way.

Upregulation and Functionality of Neuronal Nicotinic Acetylcholine Receptors

Cigarette smoking is, in developed countries, the leading cause of premature death. In tobacco smoke, the main addictive compound is nicotine, which in the brain binds to neuronal nicotinic acetylcholine receptors (neuronal nAChRs). These have been implicated in addiction, but also in several neurological disorders including Alzheimer's and Parkinson's diseases, Tourette's syndrome, attention-deficit hyperactivity disorder (ADHD), schizophrenia, pain, depression, and autosomal-dominant noctural frontal lobe epilepsy; all of which makes nAChRs an intriguing target of study. Chronic treatment with nicotine leads to an increase in the number of nAChRs (upregulation) in the brain and changes their functionality. Changes in the properties of nAChRs are likely to occur in smokers as well, since they are exposed to nicotine for long periods of time. Several nAChR subtypes likely play a role in the formation of nicotine addiction by participating in the release of dopamine in the striatum. The aim of this study was to clarify at cellular level the changes in nAChR characteristics resulting from chronic nicotine treatment. SH-SY5Y cells, endogenously several nAChR-expressing, and SH-EP1-h-alfa7 cells, transfected with the alfa 7 nAChR subunit gene were treated chronically with nicotine. The localisation of alfa 7 and beta2 subunits was studied with confocal and electron microscopy. Functionality of nAChRs was studied with calcium fluorometry. Effects of long-term treatment with opioid compounds on nAChRs were studied by means of ligand binding. Confocal microscopy showed that in SH-SY5Y cells, alfa7 and beta2 subunits formed clusters, unlike the case in SH-EP1-h alfa7 cells, where alfa7 nAChRs were distributed more diffusely. The majority of nAChR subunits localised on endoplasmic reticulum (ER). The isomers of methadone acted as agonists at alfa7 nAChRs. Acute morphine challenge also stimulated nAChRs. Chronic treatment with methadone or morphine led to an increased number of nAChRs. In animal studies, mice received nicotine for 7 weeks. Electron microscopical analysis of the localisation of nAChRs showed in the striatum that alfa7 and beta2 nAChR subunits localised synaptically, extrasynaptically, and intracellularly, with the majority localising extrasynaptically. Chronic nicotine treatment caused an increase in the number of nAChR subunits at all studied locations. These results suggest that the alfa7 nAChR and beta2 subunit-containing nAChRs respond to chronic nicotine treatment differently. This may indicate that the functional balance of various nAChR subtypes in control of the release of dopamine is altered as a result of chronic nicotine treatment. Compounds binding both to opioid and nACh receptors may be of clinical importance.