This study investigated the effects of a standing desk on academically engaged time during instruction. The study was conducted with two male students with a diagnosis of Attention Deficit Hyperactivity Disorder. The first participant was in first grade and the second was in eighth grade. The target behaviors for these participants were on-task engagement with academic content during instructional periods in the classroom. The intervention took place in the students’ general education classrooms by introducing a standing desk into the classroom. A traditional ABAB reversal intervention design was used for the first grader, while the eighth grade participant had an alternating treatments design. The results of the study show the standing desk had a mild effect for the first grade student while it had a more positive effect on the eight grade student. Social Validity indicates that the intervention was well received by teachers but slightly less by students

The researcher aimed in this study to answer the research question: how is frustration expressed by the child with attention deficit hyperactivity disorder (ADHD) in middle childhood within the classroom setting? The goal of the study was therefore to explore the expression of frustration in the child with ADHD in middle childhood within the classroom setting. The research population consisted of all children in middle childhood years who had been diagnosed with ADHD and were attending either Arthur Matthews or Montrose Primary Schools. The sampling method was purposive as subjects with these specific attributes were utilized. The extent of the investigation was limited to the observations of 20 children. The exploratory design was used in order to complete the empirical study. A checklist was used for the purpose of gathering data. This data was quantitative information on frustration expressed by children with ADHD in middle childhood, as observed by the researcher. Research results indicate that frustration plays a large role in the school life of a child diagnosed with ADHD. The findings also show that the child with ADHD directs much of his/her frustration towards him/herself. The research findings indicate that frustration that is not dealt with at an early stage will develop into aggression. In order to assist a child in dealing with his/her frustration, it is recommended that the child be taught coping mechanisms which assist him/her in ventilating frustration in a socially acceptable way. Further research into the effective implementation of teaching coping mechanisms to children in middle childhood with ADHD within the classroom setting is recommended. / Dissertation (MSD (Play Therapy))--University of Pretoria, 2004. / Social Work and Criminology / unrestricted

As children with ADHD are typically diagnosed at school entry level, when problems with especially reading and writing occur, primary school teachers are directly affected by a pressing need to become more educated on the subject of ADHD. The responsibility to teach these young children effectively, and help them to successfully cope with their struggles in an academic environment also rests with the primary school teacher. The purpose of this study was to gain an understanding of the experiences of primary school teachers who have children diagnosed with ADHD in their classrooms. The phenomenological approach was used as a lens for collecting and interpreting data. Four participants from a private school were interviewed and transcripts were analysed and interpreted using the Interpretive Phenomenological Approach. The research findings were that the teachers experiences of having children with ADHD in their classrooms were both positive and negative and were affected by several factors including the number of diagnosed children in the classroom, the degree of severity of ADHD, support received from others, medication for ADHD and knowledge of ADHD. Copyright / Dissertation (MA)--University of Pretoria, 2008. / Psychology / unrestricted

The Auditory Continuous Performance Test (ACPT) was evaluated on one group of subjects who had been diagnosed as having attention deficit-hyperactivity disorder (ADHD) and another group for whom ADHD had been ruled out. Although the specificity of the ACPT was acceptably high for a screening test, the sensitivity was very low. The conclusions drawn from these results are limited because of small sample size (n = 23). However, until reports based on large study samples are forthcoming, the use of the ACPT as a screening test for ADHD appears questionable.

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The prognosis of attention deficit hyperactivity disorder (ADHD) continues to “show heightened risk of multiple mental health and social difficulties as well as premature mortality in adult life” after nearly 50 years of primary pharmacological treatment.1 If the prognosis of ADHD is not changed by stimulants, then 2016 research that stimulants may cause cardiac arrhythmia and myocardial infarction associated with subsequent death in children younger than 17 years prescribed methylphenidate (MPH)2 raises the question of whether stimulants should be used. Furthermore, a 2015 Cochran Review found 98·6% of ADHD randomized clinical trials were considered high risk for bias and the remaining trials could also have been considered high risk by using a stricter definition.3 Has medicalization and marketing of the diagnosis and treatment of ADHD become the basis of putting children at risk by using stimulants, especially in the United States?4,5

Despite evidence of an association between prenatal acetaminophen exposure and attention deficit hyperactivity disorder (ADHD) in offspring, the causal role of prenatal acetaminophen exposure in child ADHD remains unclear owing to limitations of prior studies. Prior studies have relied on maternal self-report, failed to quantify acetaminophen dose, and lacked mechanistic insight. Chapter 1 formally introduces this topic and provides background information summarizing the high prevalence of ADHD, widespread use of acetaminophen during pregnancy, and potential molecular mechanisms through which the drug may harm fetal development. In Chapter 2, we examined the association between prenatal acetaminophen exposure measured in meconium and ADHD in children aged 6 to 7 years, along with the potential for mediation by functional brain connectivity. Data came from a prospective birth cohort study from the Centre Hospitalier Université de Sherbrooke in Sherbrooke, Québec, Canada. We included 393 eligible children, of whom 345 had meconium samples collected at delivery and information on ADHD diagnosis. Mothers were enrolled from September 25, 2007, to September 10, 2009, at their first prenatal care visit or delivery. Acetaminophen levels were measured in meconium, and physician diagnosis of ADHD was determined at follow-up when children were aged 6 to 7 years or from medical records. Additionally, when children were aged 9 to 11 years, resting-state brain connectivity was assessed with magnetic resonance imaging, and attention problems and hyperactivity were assessed with the Behavioral Assessment System for Children Parent Report Scale. Associations between meconium acetaminophen levels and outcomes were estimated with linear and logistic regressions weighted on the inverse probability of treatment to account for potential confounders. Causal mediation analysis was used to test for mediation of the association between prenatal acetaminophen exposure and hyperactivity by resting-state brain connectivity. Among the 345 children included in the analysis (177 boys [51.3%]; mean [SD] age, 6.58 [0.54] years), acetaminophen was detected in 199 meconium samples (57.7%), and ADHD was diagnosed in 33 children (9.6%). Compared with no acetaminophen, detection of acetaminophen in meconium was associated with increased odds of ADHD (odds ratio [OR], 2.43; 95%CI, 1.41-4.21). A dose-response association was detected; each doubling of exposure increased the odds of ADHD by 10% (OR, 1.10; 95%CI, 1.02-1.19). Children with acetaminophen detected in meconium showed increased negative connectivity between frontoparietal and default mode network nodes to clusters in the sensorimotor cortices, which mediated an indirect effect on increased child hyperactivity (14%; 95%CI, 1%-26%). In Chapter 3, we used data from the same Canadian birth cohort to examine whether prenatal acetaminophen exposure is associated with adverse birth outcomes and/or pregnancy complications, and if birth outcomes may mediate the association of prenatal acetaminophen with child ADHD. This study included 393 children for whom acetaminophen was measured in meconium at delivery. We tested associations of prenatal acetaminophen with birthweight, preterm birth, gestational age, small and large for gestational age, gestational diabetes, preeclampsia, and high blood pressure. Using causal mediation analyses, we assessed whether birth outcomes mediated the association of prenatal acetaminophen with ADHD. We imputed missing data via multiple imputation and used inverse probability weighting to account for confounding and selection bias. Prenatal acetaminophen exposure was associated with decreased birthweight by 136 g (β = −136; 95% CI [−229, −43]), 20% increased weekly hazard of delivery (hazard ratio = 1.20; 95% CI [1.00, 1.43]), and over 60% decreased odds of being born large for gestational age (odds ratio = 0.38; 95% CI [0.20, 0.75]). Prenatal acetaminophen was not associated with small for gestational age, preterm birth, or any pregnancy complications. Causal mediation effects were non-significant for all birth outcomes in both unadjusted and adjusted models, indicating no evidence that birth outcomes linked prenatal acetaminophen exposure with child ADHD. In Chapter 4, we examined the effects of developmental acetaminophen exposure on mouse behavior and frontal cortex gene expression. Although prior studies have investigated neurodevelopmental effects of prenatal acetaminophen exposure in rodents, the results of these studies are not always in agreement. Additionally, no mouse studies of prenatal acetaminophen exposure have investigated offspring attention deficits in behavior tasks specifically designed to measure attention, and no prior rodent studies have utilized ‘omics’ technologies for an untargeted exploration of potential mechanisms. We randomly assigned pregnant mice (starting embryonic day 4-10) to receive acetaminophen (150 mg/kg/day) or vehicle control through postnatal day 14. We employed a battery of behavior tests for 111 mouse offspring, including pup ultrasonic vocalizations, elevated plus maze, open field test, CatWalk, pre-pulse inhibition, and 5-choice serial reaction time task. Frontal cortex was collected at birth from 24 pups for RNA-sequencing. Developmental acetaminophen treatment resulted in increased pup vocalizations after separation from the litter, as well as decreased ambulation and vertical rearings in the open field task among male but not female offspring. Acetaminophen treatment was also associated with altered frontal cortex gene expression relating to glutathione and cytochrome p450 metabolism, DNA damage, and the endocrine and immune systems. Together with the multitude of other cohort studies showing adverse neurodevelopment associated with prenatal acetaminophen exposure, this work suggests caution should be used in administering acetaminophen during pregnancy. In humans, we found that prenatal acetaminophen exposure was associated with child ADHD, altered resting-state brain connectivity, and adverse birth outcomes. Furthermore, our results suggest altered brain connectivity as a potential underlying mechanism linking prenatal acetaminophen use with child hyperactivity. While adverse birth outcomes such as preterm birth and reduced birthweight are known to be associated with ADHD, we found no evidence for mediation by birth outcomes of the association between prenatal acetaminophen exposure and ADHD. In mice, we found that developmental acetaminophen treatment resulted in elevated anxiety-like behaviors in male offspring, as well as gene expression changes in the frontal cortex. Future studies are needed to explore whether the altered molecular pathways revealed by RNA-sequencing directly link acetaminophen exposure with offspring behavior changes.

During the past 80 years, similar descriptions of a hyperactive behavior pattern in children have appeared in medical, educational, and psychological literature. Hyperactivity has been conceptualized as a character disorder, an organic disorder, and, most recently, as a behavior disorder. In this study, hyperactivity was explained in interactional terms, using Rotter's social learning theory of personality. Little consideration has been given in research to the influence of an abnormally high activity level upon personality development during childhood. The purpose of this study was to investigate the general influence of negative interactions associated with hyperactivity upon the organization of four personality constructs: locus of control, self-esteem, trait anxiety, and state anxiety.