University of Windsor

About: University of Windsor is a education organization based out in Windsor, Ontario, Canada. It is known for research contribution in the topics: Population & Argumentation theory. The organization has 10654 authors who have published 22307 publications receiving 435906 citations. The organization is also known as: UWindsor & Assumption University of Windsor.

Neuropsychological Outcome in Adolescents/Young Adults with Childhood ADHD: Profiles of Persisters, Remitters and Controls

Abstract: The behavioral phenotype of attention-deficit/hyperactivity disorder (ADHD) changes in characteristic ways, with a tendency for symptom improvement and at least partial recovery throughout development. Studies of children with ADHD followed into adolescence and adulthood indicate that 20–50% improve with regard to ADHD symptoms and no longer meet criteria for the disorder (Barkley, Fischer, Edelbrock, & Smallish, 1990; Biederman, Mick, & Faraone, 2000; Hill & Schoener, 1996). In addition, the nature of the symptoms change over development; hyperactivity-impulsivity is most apparent during the younger ages, whereas inattention and related dysfunction is most prominent during later developmental stages (Hart, Lahey, Loeber, Applegate, & Frick, 1995). Consistent with the behavioral heterogeneity in ADHD is the wide range of neurocognitive heterogeneity (Nigg, Willcutt, Doyle, & Sonuga-Barke, 2005). Despite the common conceptualization of ADHD as a disorder of executive functions (EFs) subserved by frontal-subcortical neural systems (Barkley, 1997), recent meta-analyses (Frazier, Demaree, & Youngstrom, 2004; van Mourik, Oosterlaan, & Sergeant, 2005; Willcutt, Doyle, Nigg, Faraone, & Pennington, 2005) indicate an array of executive and non-executive function deficits in children with ADHD. Furthermore, increased variability in reaction time (RT) is rapidly emerging as one of the most consistent deficits in children with ADHD (Castellanos & Tannock, 2002; Russell et al., 2006). Additional presumably “non-executive” parameters have been shown to differentiate ADHD from non-ADHD children, including signal detectability (d′) and response bias (lnβ) variables from continuous performance tests (CPTs; Losier, McGrath, & Klein, 1996). Kuntsi and colleagues (2001) reported that RT variability discriminated ADHD children from controls better than measures of inhibition and working memory, and Epstein and colleagues (2003) reported variability in d′, lnβ, and RT to be strongly associated across multiple ADHD symptom domains. As such, it has been hypothesized that the EF deficits frequently observed in children with ADHD may be due to deficiencies in largely subcortical, regulatory systems, rather than cortical EF circuitry per se (Douglas, 1999; Rommelse et al., 2007; Sergeant, Oosterlaan, & van der Meere, 1999; Sonuga-Barke & Castellanos, 2007). A smaller literature has examined neuropsychological deficits in adults with ADHD (Nigg et al., 2005; Seidman, 2006) with findings generally indicating impairments similar to those in children. A recent meta-analysis (Hervey, Epstein, & Curry, 2004) reported that, compared to controls, adults with ADHD performed worse across multiple neuropsychological domains. Consistent impairments on various CPT paradigms were reported, whereas more traditional EF tests such as the Stroop, Wisconsin Card Sorting Test (WCST), and Trail-Making Test only differentiated the groups moderately well, if at all (Hervey et al., 2004; Nigg et al., 2005; Seidman, 2006). While it is important to determine which neurocognitive deficits are present in adults with persistent ADHD, it is equally important to understand the degree to which improvement in specific neurocognitive functions is associated with recovery. Carr, Nigg and Henderson (2006) reasoned that core deficits of ADHD should persist in adults who no longer meet criteria for the disorder, but more epiphenomenal characteristics should parallel symptom recovery. They compared adults with ADHD, adults with retrospectively-assessed childhood histories of ADHD but partial recovery, and controls using an antisaccade task which evaluated distinct forms of inhibition. Directional errors on the task fit the pattern of epiphenomenal symptoms in that the ADHD group, but not the partially remitted group, differed from controls. In contrast, anticipatory errors behaved more like a core deficit; those with childhood ADHD differed from controls irrespective of adult status. This approach provides insight into the developmental trajectory of neurocognitive functioning in ADHD and the dissociation of potentially causal versus secondary deficits. Yet, retrospective recall of childhood ADHD symptoms and impairment is often inaccurate (Mannuzza, Klein, Klein, Bessler, & Shrout, 2002). As such, these kinds of questions are best addressed in a longitudinal sample. Drechsler et al. (2005) examined measures of alertness and inhibitory control in controls and children with ADHD (mean age = 11.0 at baseline) three times over 2.6 years. By the final assessment, there were no group differences on their measures. However, these findings are difficult to interpret because 61% of their ADHD group no longer met criteria for the disorder at the final follow-up assessment and data were not examined relative to persistence/remittance. Other longitudinal studies of children with ADHD followed into adolescence and beyond have generally found that neuropsychological dysfunction is prominent throughout development (Fischer, Barkley, Edelbrock, & Smallish, 1990). Seidman and colleagues (1997) reported deficits on the Stroop, WCST, and an auditory CPT among high school and college-age participants diagnosed with ADHD in childhood. However, they did not examine whether task performance varied as a function of ADHD persistence. Fischer and colleagues (2005) examined neuropsychological outcomes of childhood ADHD relative to the presence or absence of ADHD at early adult follow-up. Those with persistent ADHD made significantly more omission and commission errors on a CPT than controls, while those with ADHD in childhood, but not adulthood (i.e., remitters), did not differ from either group on these measures. Persisters, remitters and controls earned similar amounts on a card task designed to measure inhibitory control, although both ADHD groups performed the task slower than controls. To explain developmental changes associated with ADHD across the lifespan, Halperin and Schulz (2006) posited distinct neurocognitive mechanisms for the etiology of and recovery from ADHD. They hypothesized that ADHD is caused by non-cortical neural dysfunction that is present early in ontogeny, remains relatively static throughout life, and is not associated with the reduction of symptoms typically seen over development. Rather, variations in the diminution of symptoms with increasing age are accounted for by the degree to which prefrontally-mediated EFs, which emerge throughout childhood and adolescence, can compensate for more primary and enduring subcortical deficits. According to this model, performance of adults who had ADHD in childhood, on measures which reflect executive control, should closely parallel their present symptom severity. In contrast, measures of more automatic or less consciously-controlled processes should be linked to the presence of ADHD in childhood, irrespective of later clinical status. This study examined neuropsychological functioning in a longitudinal sample of adolescents/young adults who were diagnosed with ADHD in childhood as compared to a never-ADHD control group. We hypothesized that those with childhood ADHD would perform more poorly than controls on a diverse neuropsychological test battery. Further, we examined the degree to which performance on measures requiring high levels of executive processing would parallel adolescent clinical status, such that ADHD-Persisters, but not ADHD-Remitters would differ from controls. In contrast, Persisters and Remitters were hypothesized to perform more similarly, and different from controls, on measures that reflect behaviors that are unlikely to be under executive control.

Central processing deficiencies in children: toward a developmental neuropsychological model.

Abstract: A recent theoretical position (Goldberg & Costa, 1981) is employed as a framework for a neurodevelopmental model of central processing deficiencies in children. The model, which emphasizes differences between right-hemisphere and left-hemisphere systems, is shown to embrace a wide variety of behavioural phenomena that have been observed in normal children and in various subtypes of learning-disabled children. Dynamic factors operative within the development of both normal and disabled learning are addressed and incorporated.

Actinyl Peroxide Nanospheres

Abstract: [*] Prof. P. C. Burns, K.-A. Kubatko, G. SigmonDepartment of Civil Engineering and Geological SciencesUniversity of Notre Dame156 Fitzpatrick Hall, Notre Dame, IN 46556 (USA)Fax: ( +1)574-631-9236E-mail: pburns@nd.eduProf.Dr. B. J. Fryer, J. E. GagnonGreat Lakes Institute for Environmental ResearchUniversity of WindsorWindsor, Ontario N9B 3P4 (Canada)Dr. M. R. Antonio, Dr. L. SoderholmChemistry DivisionArgonne National LaboratoryArgonne, IL 60439 (USA)[**] Thisresearch was supportedat the Universityof Notre Dameby theEnvironmental Management Science Program of the Office ofScience, US Department of Energy (DE-FG07-97ER14820), and theNational Science Foundation Environmental Molecular ScienceInstitute at the University of Notre Dame (EAR02-21966). Thisresearch was supported at Argonne National Laboratory by the USDepartmentofEnergyOfficeofBasicEnergySciences(DOE/BES)–Chemical Sciences Division and by the Material Sciences Divisionfor the Advanced Photon Source studies under contract number W-31-109-ENG-38.