108 resultados para attention deficit disorder with hyperactivity


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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.

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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.

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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.

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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

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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.

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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.

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The effect of nonresponse on health and lifestyle measures has received extensive study, showing at most relatively modest effects. Nonresponse bias with respect to personality has been less thoroughly investigated. The present study uses data from responding individuals as a proxy for the missing data of their nonresponding family members to examine the presence of nonresponse bias for personality traits and disorders as well as health and lifestyle traits. We looked at the Big Five personality traits, borderline personality disorder (BPD) features, attention-deficit/hyperactivity disorder, Anger, and several measures of health (Body Mass Index, migraine) and lifestyle (smoking, alcohol use). In general, outcomes tend to be slightly more favorable for individuals from highly cooperative families compared to individuals from less cooperative families. The only significant difference was found for BPD features (p = .001). However, the absolute difference in mean scores is very small, less than 1 point for a scale ranging from 0 to 72. In conclusion, survey data on personality, health and lifestyle are relatively unbiased with respect to nonresponse.

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This paper has two central purposes: the first is to survey some of the more important examples of fallacious argument, and the second is to examine the frequent use of these fallacies in support of the psychological construct: Attention Deficit Hyperactivity Disorder (ADHD). The paper divides 12 familiar fallacies into three different categories—material, psychological and logical—and contends that advocates of ADHD often seem to employ these fallacies to support their position. It is suggested that all researchers, whether into ADHD or otherwise, need to pay much closer attention to the construction of their arguments if they are not to make truth claims unsupported by satisfactory evidence, form or logic.

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It seems a new behaviour disorder is identified every week. Forms of conduct once simply regarded as part of the human condition, are rapidly being reinterpreted as types of mental illness. Individuals are no longer simply quiet or shy, they are reclassified as suffering from Generalised Social Phobia, or Selective Mutism, or Avoidant Personality Disorder. Others are no longer simply unpopular or obnoxious, they are reclassified as Borderline Personality Disorder, or Antisocial Personality Disorder. Still more are no longer lively or boisterous, they have Attention Deficit Hyperactivity Disorder, or Conduct Disorder, or Oppositional Defiance Disorder.

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This paper has two central purposes: the first is to survey some of the more important examples of fallacious argument, and the second is to examine the frequent use of these fallacies in support of the psychological construct: Attention Deficit Hyperactivity Disorder (ADHD). The paper divides twelve familiar fallacies into three different categories—material, psychological and logical—and contends that advocates of ADHD often seem to employ these fallacies to support their position. It is suggested that all researchers, whether into ADHD or otherwise, need to pay much closer attention to the construction of their arguments if they are not to make truth claims unsupported by satisfactory evidence, form or logic.

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Many cognitive neuroscience studies show that the ability to attend to and identify global or local information is lateralised between the two hemispheres in the human brain; the left hemisphere is biased towards the local level, whereas the right hemisphere is biased towards the global level. Results of two studies show attention-focused people with a right ear preference (biased towards the left hemisphere) are better at local tasks, whereas people with a left ear preference (biased towards the right hemisphere) are better at more global tasks. In a third study we determined if right hemisphere-biased followers who attend to global stimuli are likely to have a stronger relationship between attention and globally based supervisor ratings of performance. Results provide evidence in support of this hypothesis. Our research supports our model and suggests that the interaction between attention and lateral preference is an important and novel predictor of work-related outcomes.

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A set of five tasks was designed to examine dynamic aspects of visual attention: selective attention to color, selective attention to pattern, dividing and switching attention between color and pattern, and selective attention to pattern with changing target. These varieties of visual attention were examined using the same set of stimuli under different instruction sets; thus differences between tasks cannot be attributed to differences in the perceptual features of the stimuli. ERP data are presented for each of these tasks. A within-task analysis of different stimulus types varying in similarity to the attended target feature revealed that an early frontal selection positivity (FSP) was evident in selective attention tasks, regardless of whether color was the attended feature. The scalp distribution of a later posterior selection negativity (SN) was affected by whether the attended feature was color or pattern. The SN was largely unaffected by dividing attention across color and pattern. A large widespread positivity was evident in most conditions, consisting of at least three subcomponents which were differentially affected by the attention conditions. These findings are discussed in relation to prior research and the time course of visual attention processes in the brain.

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Since the industrial revolution, the development of a lifestyle lived predominantly indoors has resulted in less contact with nature. Research over the last twenty years has gradually been identifying the human health benefits attributed to re-connecting with the natural environment. The significance of feeling connected to natural environments, families and friends are described as a foundational requirement for human health and wellbeing (Maller et al., 2008). Also, the early findings of Schultz‟s (2002) work indicated that by feeling connected to the natural world a person is more likely to be committed to positively interact with and protect the natural world. Research on young people has indicated that young people are even more disconnected from the natural world. Leading some writers to call this disconnection a crisis termed “Nature Deficit Disorder.” Participants (n = 131) from 1st year university Physical Education and Human Movement Studies were asked to complete two questionnaires the Connectedness to Nature scale (CNS) (Mayer & Frantz, 2004) and the New Ecological Paradigm Scale (NEP) (Dunlap, Van Liere, Mertig, & Jones, 2000). The NEP and CNS are two scales most commonly used to explore beliefs and feelings of connectedness to the natural world (Schultz, 2002). The NEP was developed over thirty years ago by Dunlap and Van Liere (1978) and originally termed the New Environmental Paradigm. The NEP is now the foremost International tool for measuring beliefs about the natural world (Dunlap, 2008). The CNS measures an individual‟s trait levels of emotional connection to the natural world. It is a relatively new tool for understanding ecological behaviour based on ecopsychology theory and employed to predict behaviour (Mayer and Frantz, 2004). Both questionnaires are based on a 1-5 scale (Strongly disagree to Strongly agree). By combing both scales the researchers aim to develop a snap shot of beliefs and emotional feelings towards the natural world and therefore an idea of intended behaviour. The two questionnaires were combined as one online survey with additional material asking for demographics and self assessments of type of leader included before the surveys. An email inviting outdoor leaders to participate was sent out to networks and interest groups. A basic descriptive statistical analysis was used to interpret data.

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Migraine is a painful and debilitating disorder with a significant genetic component. Steroid hormones, in particular estrogen, have long been considered to play a role in migraine, as variations in hormone levels are associated with migraine onset in many sufferers of the disorder. Steroid hormones mediate their activity via hormone receptors, which have a wide tissue distribution. Estrogen receptors have been localized to the brain in regions considered to be involved in migraine pathogenesis. Hence it is possible that genetic variation in the estrogen receptor gene may play a role in migraine susceptibility. This study thus examined the estrogen receptor 1 (ESRα) gene for a potential role in migraine pathogenesis and susceptibility. A population-based cohort of 224 migraine sufferers and 224 matched controls were genotyped for the G594A polymorphism located in exon 8 of the ESR1 gene. Statistical analysis indicated a significant difference between migraineurs and non-migraineurs in both the allele frequencies (P=0.003) and genotype distributions (P=0.008) in this sample. An independent follow-up study was then undertaken using this marker in an additional population-based cohort of 260 migraine sufferers and 260 matched controls. This resulted in a significant association between the two groups with regard to allele frequencies (P=8×10−6) and genotype distributions (P=4×10−5). Our findings support the hypothesis that genetic variation in hormone receptors, in particular the ESR1 gene, may play a role in migraine.

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Major depressive disorder (MDD) is a common complex disorder with a partly genetic etiology. We conducted a genome-wide association study of the MDD2000+ sample (2431 cases, 3673 screened controls and >1 M imputed single-nucleotide polymorphisms (SNPs)). No SNPs achieved genome-wide significance either in the MDD2000+ study, or in meta-analysis with two other studies totaling 5763 cases and 6901 controls. These results imply that common variants of intermediate or large effect do not have main effects in the genetic architecture of MDD. Suggestive but notable results were: (a) gene-based tests suggesting roles for adenylate cyclase 3 (ADCY3, 2p23.3) and galanin (GAL, 11q13.3); published functional evidence relates both of these to MDD and serotonergic signaling; (b) support for the bipolar disorder risk variant SNP rs1006737 in CACNA1C (P=0.020, odds ratio=1.10), and; (c) lack of support for rs2251219, a SNP identified in a meta-analysis of affective disorder studies (P=0.51). We estimate that sample sizes 1.8- to 2.4-fold greater are needed for association studies of MDD compared with those for schizophrenia to detect variants that explain the same proportion of total variance in liability. Larger study cohorts characterized for genetic and environmental risk factors accumulated prospectively are likely to be needed to dissect more fully the etiology of MDD.