Frontal lesions and sustained attention

Wilkins, Arnold J.; Shallice, Timothy; McCarthy, Rosaleen A.

doi:10.1016/0028-3932(87)90024-8

Cited by 399 publications

(215 citation statements)

References 10 publications

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“…Prefrontal cortex lesions impair the ability to sustain attention, particularly over long delays (Wilkins et al, 1987). Lesions of the dorsolateral prefrontal cortex impair the ability to shift attentional set (Manes et al, 2002).…”

Section: Stimulants: Therapeutic Actions In Adhd Aft Arnstenmentioning

confidence: 99%

Stimulants: Therapeutic Actions in ADHD

Arnsten

2006

Neuropsychopharmacol

418

257

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Stimulants such as methylphenidate and amphetamine are currently the most common treatment for attention deficit hyperactivity disorder (ADHD). For years, it was assumed that stimulants had paradoxical calming effects in ADHD patients, whereas stimulating 'normal' individuals and producing locomotor activation in rats. It is now known that low doses of stimulants focus attention and improve executive function in both normal and ADHD subjects. Furthermore, the seminal work of Kuczenski and Segal showed that low, oral doses of methylphenidate reduce locomotor activity in rats as well. Berridge et al have now shown that these low doses produce marked increases in norepinephrine and dopamine release in the prefrontal cortex, whereas having only subtle effects on subcortical catecholamine release. ihe prefrontal cortex regulates behavior and attention using representational knowledge, and imaging and neuropsychological studies have shown that the prefrontal cortex is weaker in subjects with ADHD. This cortical area is very sensitive to levels of catecholamines: moderate levels engage postsynaptic a2A-adrenoceptors and D1 receptors and improve prefrontal regulation of behavior and attention, while high levels impair prefrontal function via a1-adrenoceptors and excessive D1 receptor stimulation. Administering low doses of methylphenidate to rats improves the working memory and attentional functions of the prefrontal cortex, while high doses impair working memory and produce a perseverative pattern of errors similar to that seen in patients. The low dose improvement is hiocked by either an a2-adrenoceptor or Dl receptor antagonist, suggesting that both norepinephrine and dopamine contribute to the beneficial actions of stimulant medications.

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Section: Stimulants: Therapeutic Actions In Adhd Aft Arnstenmentioning

confidence: 99%

Stimulants: Therapeutic Actions in ADHD

Arnsten

2006

Neuropsychopharmacol

418

257

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“…The first, Score!, is adapted from adult neuropsychological and functional imaging studies. [70][71][72] Here, children were asked to count the number of identical tones (between three and 15) presented in each item. The demands of the test lie in maintaining active attention to the dull task across the long, silent intervals between each sound (up to 5 s).…”

Section: Neuropsychological Measuresmentioning

confidence: 99%

Association of the dopamine transporter (DAT1) 10/10-repeat genotype with ADHD symptoms and response inhibition in a general population sample

et al. 2005

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Association between attention-deficit hyperactivity disorder (ADHD) and the 10-repeat allele of the dopamine transporter gene (DAT1) has been reported in independent clinical samples using a categorical clinical definition of ADHD. The present study adopts a quantitative trait loci (QTL) approach to examine the association between DAT1 and a continuous measure of ADHD behaviours in a general-population sample, as well as to explore whether there is an independent association between DAT1 and performance on neuropsychological tests of attention, response inhibition, and working memory. From an epidemiological sample of 872 boys aged 6-11 years, we recruited 58 boys scoring above the 90th percentile for teacher reported ADHD symptoms (SWAN ADHD scale) and 68 boys scoring below 10th percentile for genotyping and neuropsychological testing. A significant association was found between the DAT1 homozygous 10/10-repeat genotype and high-scoring boys (v 2 square ¼ 4.6, Po0.03; odds ratio ¼ 2.4, 95% CI 1.1-5.0). Using hierarchical linear regression, a significant independent association was found between the DAT1 10/10-repeat genotype and measures of selective attention and response inhibition after adjusting for age, IQ, and ADHD symptoms. There was no association between DAT1 and any component of working memory. Furthermore, performance on tasks of selective attention although associated with DAT1 was not associated with SWAN ADHD high scores after controlling for age and IQ. In contrast, impairment on tasks that tapped sustained attention and the central executive component of working memory were found in high-scoring boys after adjusting for age and IQ. The results suggest that DAT1 is a QTL for continuously distributed ADHD behaviours in the general population and the cognitive endophenotype of response inhibition. Molecular Psychiatry (2005) 10, 686-698.

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“…Thus, functions associated with the PFC involve working in the 'present' to coordinate behavior based on cross-temporal contingencies. Accordingly, most of the research focused on understanding PFC function has involved assessing the response of neurons during dynamic events, such as attention or working memory (eg, Fuster and Alexander, 1971;Wilkins et al, 1987;Funahashi et al, 1993).…”

Section: Functions Of the Pfc: Plasticity Versus Flexibilitymentioning

confidence: 99%

Divergent Plasticity of Prefrontal Cortex Networks

Moghaddam

Homayoun

2007

Neuropsychopharmacol

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The 'executive' regions of the prefrontal cortex (PFC) such as the dorsolateral PFC (dlPFC) and its rodent equivalent medial PFC (mPFC) are thought to respond in concert with the 'limbic' regions of the PFC such as the orbitofrontal (OFC) cortex to orchestrate behavior that is consistent with context and expected outcome. Both groups of regions have been implicated in behavioral abnormalities associated with addiction and psychiatric disorders, in particular, schizophrenia and mood disorders. Theories about the pathophysiology of these disorders, however, incorporate abnormalities in discrete PFC regions independently of each other or assume they are one and the same and, thus, bunch them under umbrella of 'PFC dysfunction.' Emerging data from animal studies suggest that mPFC and OFC neurons display opposing patterns of plasticity during associative learning and in response to repeated exposure to psychostimulants. These data corroborate clinical studies reporting different patterns of activation in OFC versus dlPFC in individuals with schizophrenia or addictive disorders. These suggest that concomitant but divergent engagement of discrete PFC regions is critical for learning stimulus-outcome associations, and the execution of goal-directed behavior that is based on these associations. An atypical interplay between these regions may lead to abnormally high or low salience assigned to stimuli, resulting in symptoms that are fundamental to many psychiatric and addictive disorders, including attentional deficits, improper affective response to stimuli, and inflexible or impulsive behavior.

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Frontal lesions and sustained attention

Cited by 399 publications

References 10 publications

Stimulants: Therapeutic Actions in ADHD

Stimulants: Therapeutic Actions in ADHD

Association of the dopamine transporter (DAT1) 10/10-repeat genotype with ADHD symptoms and response inhibition in a general population sample

Divergent Plasticity of Prefrontal Cortex Networks

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