Attention-deficit/hyperactivity disorder and attention networks - PubMed (original) (raw)

Review

Attention-deficit/hyperactivity disorder and attention networks

George Bush. Neuropsychopharmacology. 2010 Jan.

Abstract

Research attempting to elucidate the neuropathophysiology of attention-deficit/hyperactivity disorder (ADHD) has not only shed light on the disorder itself, it has simultaneously provided new insights into the mechanisms of normal cognition and attention. This review will highlight and integrate this bidirectional flow of information. Following a brief overview of ADHD clinical phenomenology, ADHD studies will be placed into a wider historical perspective by providing illustrative examples of how major models of attention have influenced the development of neurocircuitry models of ADHD. The review will then identify major components of neural systems potentially relevant to ADHD, including attention networks, reward/feedback-based processing systems, as well as a 'default mode' resting state network. Further, it will suggest ways in which these systems may interact and be influenced by neuromodulatory factors. Recent ADHD imaging data will be selectively provided to both illustrate the field's current level of knowledge and to show how such data can inform our understanding of normal brain functions. The review will conclude by suggesting possible avenues for future research.

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Figures

Figure 1

Figure 1

Brain structures implicated in ADHD. Interacting neural regions have been implicated in ADHD. In particular, the dorsal anterior midcingulate cortex (daMCC), dorsolateral prefrontal cortex (DLPFC), ventrolateral prefrontal cortex (VLPFC), parietal cortex, striatum, and cerebellum—all key elements of cognitive/attention networks—have also been found to display functional abnormalities in multiple studies of ADHD.

Figure 2

Figure 2

Dopamine synapse. Dopaminergic neurons release dopamine into the synapse, where it signals to post-synaptic neurons through specific receptors (illustrated here is the DRD4 receptor). Dopamine is then taken back into the presynaptic neuron through the dopamine transporter (DAT). Stimulants such as methylphenidate have been shown to block DAT, thus making more dopamine available in the extracellular space.

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