Neural Substrates Underlying Impulsivity

Abstract

Attention deficit hyperactivity disorder (ADHD) is a neuropsychiatric disorder whose three main symptoms are impulsiveness, inattention, and hyperactivity. Although ADHD is an early developmental disorder, it may persist into adulthood, resulting in deficits associated with poor academic performance, frequent job changes, poor and unstable marriages, and increases in motor vehicle accidents. Of the three primary symptoms of ADHD, deficits in impulse control are the most challenging to the social network and the judicial system. While the etiology of ADHD remains unknown, recent work suggests that the central deficits in ADHD may be due to poor response inhibition that is linked to monoamine and prefrontal lobe deficiencies. In the past, preclinical studies designed to understand the lack of impulse control have generally been relegated to studies linked to aggression and drug abuse. With the use of innovative noninvasive techniques, like anatomical and functional magnetic resonance imaging, selective neurochemical and behavioral paradigms have converged with preclinical reports and lend support to the premise that monoaminergic neurotransmitter systems and the cortico-striatal circuitry are essential to impulse control. Furthermore, new emerging data on neural substrates underlying impulsivity have incorporated brain regions involved in reinforcement, reward, and decision making such as the nucleus accumbens, cerebellum, and amygdala. As noninvasive brain imaging, neurochemical, and behavioral approaches are combined, our knowledge of the neural networks underlying impulsivity will hopefully give rise to therapeutic approaches aimed at alleviating this disorder.

Right parietal dysfunction in children with attention deficit hyperactivity disorder, combined type: a functional MRI study

“…44 Structural lesion and functional imaging animal data support the association of caudate nucleus dysfunction with core ADHD-CT symptoms, working memory and response inhibition dysfunction. 1,45 The caudate nucleus has a high concentration of dopaminergic synapses underpinning its functions, dopamine being a key neurotransmitter known to be functionally aberrant in ADHD. 46 The caudate nucleus has been shown to be under-active in ADHD-CT using various response inhibition fMRI paradigms.…”

“…[1][2][3][4] Rodent models of ADHD, 1 fMRI data in prepubertal 4 and adolescent 2,3 boys and structural imaging data in children 5 with ADHD support dysfunction within a large-scale right-hemisphere system incorporating the prefrontal cortex, striatum and parietal lobe. 6 Such dysfunction may form the neural substrate of attentional and working memory deficits in the disorder.…”

Neurocomputational mechanisms of reinforcement-guided learning in humans: A review

“…This review also has focused on empirical studies that have examined how reinforcement signals might be used to adapt future behavior and on the relatively simple reinforcement-learning models that have been used to capture these neural dynamics. This represents one small but important component of flexible goal-directed behavior; other cognitive operations that are critical to reinforcement learning include working memory (Braver et al, 2001;Dehaene & Changeux, 2000;Floresco & Magyar, 2006), attention (Dehaene & Changeux, 2000;Lee, Youn, O, Gallagher, & Holland, 2006;Maddox, Bohil, & Dodd, 2003), inhibition of impulsive reward-seeking tendencies (Frank, 2006;Kalenscher, Ohmann, & Güntürkün, 2006;King, Tenney, Rossi, Colamussi, & Burdick, 2003), reward processing in the orbitofrontal cortex (Kringelbach, 2005;Kringelbach & Rolls, 2004), and action selection in the anterior cingulate cortex (Holroyd & Coles, 2008;Rushworth et al, 2007;Rushworth et al, 2004).…”

Rapid neuroendocrine responses evoked at the onset of social challenge

“…Accumbal 5-HT levels were increased in all treatments relative to undisturbed controls. These rapid increases in NAc 5-HT levels following brief social threat or environmental disturbance may either facilitate NAc DA-mediated motivational behaviors [47,48], or enhance survival by reducing expression of inappropriate behavior in aversive contexts [49,50].…”