Evidence for a mechanistic model of cognitive control
A core deficit observed in a number of disorders of childhood is an inability to inhibit or suppress inappropriate thoughts and behaviors (e.g. attention deficit/hyperactivity disorder, obsessive compulsive disorder and Tourette's syndrome). Two regions of the brain that have been implicated in these disorders are the frontal lobes and the basal ganglia. The common problem in inhibitory control and the common brain regions implicated across this range of developmental disorders suggest a single underlying biological mechanism. Yet, the symptomatology observed across these disorders is distinct. A number of parallel circuits that involve basal ganglia and frontal cortex have been described. Each of these basal ganglia thalamocortical circuits controls a different set of cortically mediated behaviors that range from skeletal and eye movements to cognitive and emotional actions. An important neuromodulator in the basal ganglia thalamocortical circuitry is dopamine, particularly at the level of the prefrontal cortex and striatum. These circuits are assumed to facilitate cortically mediated behaviors by inhibiting conflicting behaviors and dopamine is assumed to play a significant neuromodulatory role in these circuits. Accordingly, we have recently developed a model of inhibitory mechanisms whereby the basal ganglia are involved in inhibition of behaviors while the frontal cortex is involved in representing and maintaining the conditions in which we respond or act. Dopamine is suggested to play an important role in the ability to maintain these internal representations against interference. Converging evidence for this model is presented from developmental, clinical, neuroimaging and lesion studies. © 2001 Association for Research in Nervous and Mental Disease. Published by Elsevier Science B.V. All rights reserved.
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