Pathologies of brain attentional networks

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Abstract

In the last decade, it has been possible to trace the areas of the human brain involved in a variety of cognitive and emotional processes by use of imaging technology. Brain networks that subserve attention have been described. It is now possible to use these networks as model systems for the exploration of symptoms arising from various forms of pathology. For example, we can use the orienting network to understand the effects of lesions that produce neglect of sensory information either by brain damage or by restricting transmitter input. Frontal attention networks may provide similar understanding of pathologies at higher levels of cognition. Evidence relating these networks to attention deficit and hyperactivity disorder (ADHD) is considered.

Introduction

Attention is currently being examined in terms of three major functions: orienting to sensory stimuli, executive functions, and maintaining the alert state [1]. Although knowledge of the precise neural mechanisms responsible for these operations is still incomplete, many of the brain areas and networks involved have been identified. Moreover, there is evidence that damage to some of these networks produces similar symptoms regardless of whether the etiology is stroke, degenerative disease, psychopathology or abnormality of development [2], [3]. For this reason, knowledge of the networks of attention may be of special use in examination of disorders with attentional symptoms whose cause is not well understood, such as attention deficit and hyperactivity disorder (ADHD). In this paper, we briefly examine the three networks in light of new findings that might relate to theories of ADHD.

Many attempts have been made to understand and characterize the deficits associated with ADHD. Recently, three different theoretical accounts have been proposed [4], [5], [6]. We attempt to argue that it is possible to conceptualize all three under the umbrella of pathologies of attentional networks.

Section snippets

Networks of attention

Posner and Raichle [1] summarized the three attentional networks approach, and based the localization of the different networks on the brain-imaging literature. Each attentional function is localized not in a single brain area, but as a network of interconnected brain areas.

Leading theories of ADHD and their predictions

As mentioned in Section 1, three theoretical accounts explaining ADHD have been recently proposed. Swanson et al. [6] characterized ADHD as a combination of executive attention and alerting deficits. This approach focuses on two of the attentional networks and predicts brain pathology in areas related to these networks, i.e. midline frontal cortex (cingulate and SMA), basal ganglia (especially caudate), anterior prefrontal cortex, anterior right parietal cortex. According to Barkley [4], the

Brain pathologies in ADHD

Filipek [20], [21] found that despite similar hemispheric volumes, ADHD subjects had smaller volumes of left caudate and caudate head, with reverse asymmetry than controls and right anterior–superior frontal region en bloc and white matter. Moreover, possible structural correlates of ADHD response to stimulants were found. Castellanos et al. [22] found smaller right anterior frontal, caudate and globus pallidus regions in ADHD compared to control. Aylward et al. [23], too, report volumetric

Conclusions

For many years, psychiatrists and psychologists have been trying to define and understand the deficits that underlie ADHD. Evidence is consistent with difficulties in two of the attentional networks: executive functions/effortful control, and vigilance and alerting regulation. We believe that a better understanding of the functions and neuroanatomical bases of attentional networks in normal development will be helpful in understanding ADHD.

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    Attention-deficit hyperactivity disorder: symptom domain, cognitive processes and neural networks

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    Executive attention: Conflict, target detection, and cognitive control

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    Supported by a fellowship of The Rothschild Foundation.

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