The executive deficit hypothesis of treated phenylketonuria (PKU) suggests that dopaminergic depletion in the lateral prefrontal cortex leads to selective executive impairment. This was examined by comparing adults with PKU on a lifelong diet with a matched healthy control group. Those with PKU were impaired on selective and sustained attention, working memory (Self-Ordered Pointing), and letter fluency. However, they failed to show differential sensitivity to increased cognitive load on the attentional and working memory tasks, and they did not differ significantly on the remaining executive tasks (rule finding, inhibition, and multitasking). Nor did they differ significantly on recall or recognition memory. Overall, the findings provided little support for the executive deficit hypothesis. A possible explanation in terms of slowed information processing speed is explored.
Fourteen subjects were scanned in two fMRI sessions separated by several months. During each session, subjects performed an episodic retrieval task, a semantic retrieval task, and a working memory task. We found that 1) despite extensive intersubject variability in the pattern of activity across the whole brain, individual activity patterns were stable over time, 2) activity patterns of the same individual performing different tasks were more similar than activity patterns of different individuals performing the same task, and 3) that individual differences in decision criterion on a recognition test predicted the degree of similarity between any two individuals' patterns of brain activity, but individual differences in memory accuracy or similarity in structural anatomy did not. These results imply that the exclusive use of group maps may be ineffective in profiling the pattern of activations for a given task. This may be particularly true for a task like episodic retrieval, which is relatively strategic and can involve widely-distributed specialized processes that are peripheral to the actual retrieval of stored information. Further, these processes may be differentially engaged depending on individual differences in cognitive processing and/or physiology.
Attention Deficit Hyperactivity Disorder (ADHD) is frequently linked with antisocial behaviour, yet less is known about its relationship with sociomoral reasoning, and the possible mediating effect of intelligence. A pilot study was designed to investigate the relationship between antisocial personality traits, intelligence and sociomoral reasoning in adults with ADHD. Twenty two adults with ADHD and 21 healthy controls, matched for age, gender and IQ completed a battery of measures including the National Adult Reading Test, Gough Socialisation Scale and Sociomoral Reflection Measure-Short Form. There was no difference between the groups and levels of sociomoral reasoning, despite the ADHD group reporting greater antisocial personality traits. Sociomoral reasoning was positively correlated with intelligence. Results from a hierarchical multiple regressions indicated that both antisocial traits and IQ were significant predictors of sociomoral reasoning, with IQ proving the most powerful predictor. Whilst antisocial personality traits may explain some of the variance in levels of sociomoral reasoning, a diagnosis of ADHD does not appear to hinder the development of mature moral reasoning. Intellectual functioning appears to facilitate the development of sociomoral reasoning. A further analysis showed that both ADHD and low sociomoral reasoning were significant predictors of antisocial traits. The current findings have important treatment implications.
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