Deficits In ADHD Research Articles

SPAARS Approach: Integrated cognitive model of emotion of Attention Deficit/Hyperactivity Disorder

SPAARS (Schematic, Propositional, Analogical and Associative Representational Systems) is the integrated cognitive model of emotion proposed by Power & Dalgleish (1997). In SPAARS, emotions are described as appraisal based against an individual’s goals and this makes the theory functional in nature. The theory proposes two routes for the generation of emotions, namely a direct one in which the appraisals have become automatized and the other where these are still not automatized. It provides a useful approach within which both basic and complex emotions can readily be understood. The theory can also be applied for explaining the disorders of emotion and it can be used to generate novel therapeutic interventions for them. In the current review, the SPAARS approach in conjunction with the theory proposed by Nigg and Casey (2005) has been applied for understanding ADHD. According to Nigg & Casey, affective deficits in ADHD could be due to problems with either approach or avoidance emotions. These problems have been explained with the help of appraisals and reinforcement learning within the SPAARS framework. Interventions that follow logically from the SPAARS framework have also been suggested.

Differentiating attention deficit in adult ADHD and schizophrenia

Most previous studies of attention deficit in ADHD and schizophrenia have used overall measures of inattention that may disguise differences in underlying mechanisms. The present study investigated types of inattentive errors and applied a process view of attention in analyses of Conners’ Continuous Performance Test protocols from subjects with ADHD-combined (51), inattentive type (19) and schizophrenia (26). Subjects with ADHD-I had more omission errors and became more inattentive as a function of time on task. Subjects with ADHD-C made more errors of commissions as time passed. In contrast, the performance of the subjects with schizophrenia improved, indicating a training effect. There were no differences in overall attentiveness between the groups. Although all groups were impaired on an overall level, they displayed three distinct patterns of inattention. The ADHD-I group displayed a lethargic inattention characterized by high fatigue. The ADHD-C group showed a hyperactive-impulsive pattern, while the schizophrenia group showed an inability to initially focus attention.

Are Motor Inhibition and Cognitive Flexibility Dead Ends in ADHD?

Executive dysfunction has been postulated as the core deficit in ADHD, although many deficits in lower order cognitive processes have also been identified. By obtaining an appropriate baseline of lower order cognitive functioning light may be shed on as to whether executive deficits result from problems in lower order and/or higher order cognitive processes. We examined motor inhibition and cognitive flexibility in relation to a baseline measure in 816 children from ADHD and control families. Multiple children in a family were tested in order to examine the familiality of the measures. No evidence was found for deficits in motor inhibition or cognitive flexibility in children with ADHD or their nonaffected siblings: Compared to their baseline speed and accuracy of responding, children with ADHD and their (non)affected siblings were not disproportionally slower or inaccurate when demands for motor inhibition or cognitive flexibility were added to the task. However, children with ADHD and their (non)affected siblings were overall less accurate than controls, which could not be attributed to differences in response speed. This suggests that inaccuracy of responding is characteristic of children having (a familial risk for) ADHD. Motor inhibition and cognitive flexibility as operationalized with mean reaction time were found to be familial. It is concluded that poorer performance on executive tasks in children with ADHD and their (non)affected siblings may result from deficiencies in lower order cognitive processes and not (only) from higher order cognitive processes/executive functions.

Evidence that response inhibition is a primary deficit in ADHD

The present study examined response inhibition in children with attention deficit hyperactivity disorder (ADHD; n = 58) and controls (n = 84) using three go/no-go tests—one with high working memory demand (cognitive), one with low working memory demand (simple), and one with rewards and response costs (motivation linked) in which emphasis was on reward for responding to “go” stimuli. Results of a repeated measure analysis of variance showed a significant effect of diagnosis for errors of commission for the simple, cognitive, and motivation-linked go/no-go tests, such that children with ADHD made significantly more errors than controls. Furthermore, a significant effect of test was noted across groups, such that both children in the ADHD and control groups performed worse on the cognitive and motivation-linked tests than they did on the simple test. The diagnosis by test interaction was not significant, suggesting that ADHD participants showed a similar degree of impairment to that of controls, regardless of the degree of working memory load or feedback provided in the test. In children with ADHD, response inhibition appears to be a primary deficit that is observed even when executive function demands of tasks are minimal. Although increasing working memory demand appears to impede response inhibition, this effect is similar in ADHD and typically developing children.

Response variability in Attention Deficit Hyperactivity Disorder: Evidence for neuropsychological heterogeneity

Response time (RT) variability is a common finding in ADHD research. RT variability may reflect frontal cortex function and may be related to deficits in sustained attention. The existence of a sustained attention deficit in ADHD has been debated, largely because of inconsistent evidence of time-on-task effects. A fixed-sequence Sustained Attention to Response Task (SART) was given to 29 control, 39 unimpaired and 24 impaired-ADHD children (impairment defined by the number of commission errors). The response time data were analysed using the Fast Fourier Transform, to define the fast-frequency and slow-frequency contributions to overall response variability. The impaired-ADHD group progressively slowed in RT over the course of the 5.5 min task, as reflected in this group's greater slow-frequency variability. The fast-frequency trial-to-trial variability was also significantly greater, but did not differentially worsen over the course of the task. The higher error rates of the impaired-ADHD group did not become differentially greater over the length of the task. The progressive slowing in mean RT over the course of the task may relate to a deficit in arousal in the impaired-ADHD group. The consistently poor performance in fast-frequency variability and error rates may be due to difficulties in sustained attention that fluctuate on a trial-to-trial basis.

Neuropsychological functioning in people with ADHD across the lifespan

ADHD is defined by behavioral characteristics similar to neuropsychological disorders of executive dysfunction. This paper is a literature review of the neurocognitive characteristics of ADHD from early childhood through adulthood. The author addresses the development of the concept of attention and executive function (EF) deficits in ADHD, clinical neuropsychological studies of pre-teenage children, teenagers and adults with ADHD, gender and the role of psychiatric co-morbidity including the relationship of learning disabilities to ADHD, heterogeneity of neuropsychological dysfunctions, experimental neuropsychological studies, the relationship of brain structure to function, psychopharmacology of ADHD, and clinical neuropsychological assessment. The group data clearly supports the hypothesis that executive dysfunctions are correlates of ADHD regardless of gender and age, and these EF deficits are exacerbated by co-morbidity with learning disabilities such as dyslexia. However, there is limited data on children under the age of 5, teenagers from age 13–18, and adults with ADHD over the age of 40. Studies of individual classification of people with ADHD compared to healthy, non-psychiatric controls do not support the use of neuropsychological tests for the clinical diagnosis of ADHD, and indicate that not all persons with ADHD have EF deficits. Some persons with ADHD may have deficits in brain reward systems that are relatively independent of EF impairments. Future research should clarify the multiple sources of ADHD impairments, continue to refine neuropsychological tools optimized for assessment, and incorporate longitudinal, developmental designs to understand ADHD across the lifespan.

Telling good from bad news: ADHD differentially affects processing of positive and negative feedback during guessing

Neuroimaging studies on ADHD suggest abnormalities in brain regions associated with decision-making and reward processing such as the anterior cingulate cortex (ACC) and orbitofrontal cortex. Recently, event-related potential (ERP) studies demonstrated that the ACC is involved in processing feedback signals during guessing and gambling. The resulting negative deflection, the ‘feedback-related negativity’ (FRN) has been interpreted as reflecting an error in reward prediction. In the present study, ERPs elicited by positive and negative feedback were recorded in children with ADHD and normal controls during guessing. ‘Correct’ and ‘incorrect’ guesses resulted in respectively monetary gains and losses. The FRN amplitude to losses was more pronounced in the ADHD group than in normal controls. Positive and negative feedback differentially affected long latency components in the ERP waveforms of normal controls, but not ADHD children. These later deflections might be related to further emotional or strategic processing. The present findings suggest an enhanced sensitivity to unfavourable outcomes in children with ADHD, probably due to abnormalities in mesolimbic reward circuits. In addition, further processing, such as affective evaluation and the assessment of future consequences of the feedback signal seems to be altered in ADHD. These results may further help understanding the neural basis of decision-making deficits in ADHD.

D-Amphetamine remediates attentional performance in rats with dorsal prefrontal lesions

Although amphetamine treatment has been shown to promote recovery of motor function in animals with cortical ablations, the potential therapeutic effect of amphetamine on processes other than motor control, such as attention and working memory, has been relatively unexplored. Accordingly, we investigated the beneficial effect of d-amphetamine treatment in animals with dorsal prefrontal cortex lesions (dPFC) compared with sham controls on a novel combined attention-memory task (CAM) that simultaneously measures attention to a visual stimulus and memory for that stimulus. The dPFC group was impaired in their ability to correctly detect the visual stimulus. Although this deficit occurred together with increased omissions and slow response latencies, these associated deficits largely recovered within the 10 post-operative baseline sessions revealing a selective attentional deficit in this group of animals. Nonetheless, the dPFC lesion did not substantially affect the working memory component of the task. The systemic administration of d-amphetamine served to ameliorate the attentional deficit in the dPFC group at the low dose only (0.2 mg/kg). By contrast, the dPFC group were less sensitive to the detrimental effects of the high dose (0.8 mg/kg) on any aspect of task performance. However, despite improving attention to the visual stimulus, d-amphetamine did not improve memory for that stimulus which instead appeared to deteriorate. The results provide apparently the first demonstration that low doses of d-amphetamine can ameliorate an attentional deficit in animals with selective dPFC lesions and may be a useful model of cognitive deficit in ADHD, schizophrenia or frontal brain injury.

Adults ADHD

This concluding paper raises some final questions and issues that the authors feel should receive more emphasis in future research on ADHD in adults. One significant problem for our field is the upward extension of child-based models and approaches without proper adaptation to adults. With adults differing patterns of comorbidity and symptom heterogeneity pose new conceptual, diagnostic, and treatment challenges. As an illustration, we review ten common presenting complaints in adults and their link to the underlying core ADHD deficits of hyperkinesis, inattention, and impulsivity. While these core symptoms are often overt problems in children, in adults subtler executive dysfunction appears. Even though the growing consensus is that ADHD is a disorder of executive functions (EF), the details of the EF/ADHD connection remain unclear and may be far more complex in adults. That complexity is mirrored in the widening anatomic representation of EF, extending beyond the frontal lobes into the subcortex and other nonfrontal regions. More research will be needed to follow the developmental trajectory of executive dysfunction in ADHD over the life cycle and tie this to the developmental neuropsychology of EF. Psychosocial context and nongenetic familial influence are also critical variables that need greater consideration when characterizing and measuring ADHD symptoms in adults. Finally, until we have reached consensus on adult subject selection, we may not be able to enhance diagnostic rigor or expand our conceptual framework for understanding the underlying pathophysiology of ADHD in adults.

Neurobiological Models of Attention-Deficit/Hyperactivity Disorder: A Brief Review of the Empirical Evidence

Attention-deficit/hyperactivity disorder (ADHD) is a psychiatric disorder characterized by inattention, impulsivity, and overactivity that begins in childhood. While considerable research has focused on the neurobiological substrates of this disorder, the specific nature of the brain dysfunction in ADHD has remained elusive. However, early data from pharmacological treatment studies, as well as from basic research in animals and humans, initially led several investigators to develop neurobiological models of ADHD. These models of ADHD and more recent evidence from neuropsychological, neuroimaging, neurochemical, and genetic research are briefly reviewed. While not completely consistent, the empirical data suggest that dysfunction in prefrontal-striatal neural circuits, as well as in brain stem catecholamine systems that innervate these circuits, may underlie the executive function deficits in ADHD.

An analysis of attention and learning deficits in ADHD and LD children

An analysis of attention and learning deficits in ADHD and LD children

An analysis of attention and learning deficits in ADHD and LD children

An analysis of attention and learning deficits in ADHD and LD children