, 2012). Adult ADHD is diagnosed in about a quarter of the patients with substance use dependence (SUD; van Emmerik-van Oortmerssen et al., 2012). ADHD is, like SUD, characterized by increased levels of impulsivity. For example, chronic cocaine abusers show increased motor
impulsivity (Fillmore and Rush, 2002) and increased cognitive impulsivity (i.e., impulsive decision making) compared to non-drug using controls (Coffey et al., 2003 and Heil et al., 2006). Additionally, in SUD, deficits in reward processing, attention, and working memory have been observed (Hester and Garavan, 2004, van Holst and Schilt, 2011 and Verdejo-Garcia et al., 2006), suggesting a large overlap between ADHD and SUD in cognitive impairments. Increased impulsivity, impaired attention, and/or working selleck chemicals PI3K inhibitor memory deficits may represent common risk factors for the development of ADHD and SUD, and as a consequence ADHD patients with increased
levels of impulsivity may be more prone to develop a SUD later in life. While one of the leading hypothesis in ADHD research states that ADHD symptoms arise from primary cognitive/executive impairments (the executive dysfunction hypothesis), the combination with reward/motivational impairments is believed to play a key role in the pathophysiology of ADHD (dual pathway hypothesis; Sonuga-Barke, 2003 and Willcutt et al., 2005). Various studies have Levetiracetam been performed on cognitive impairments in (adult) ADHD patients, but no data are currently available on cognitive and/or motivational impairments in ADHD patients with comorbid SUD. This is unfortunate because current ADHD treatments (e.g., methylphenidate) are less effective in ADHD patients with SUD compared to ADHD populations without SUD (Carpentier et al., 2005 and Levin et al., 2007), and, subsequently,
treatments in ADHD patients with SUD could be significantly improved by simultaneously targeting deficits that are specific for ADHD patients with comorbid SUD. Here, we investigate a variety of measures of neurocognitive functioning representing both the executive circuit (response inhibition, set-shifting, working memory, and time reproduction) and the reward/motivational circuit (delayed discounting) in non-medicated adult ADHD patients with and without cocaine dependence, and in non-drug using controls. We thereby include distinct measures of impulsivity relating to distinct neurobiological circuitries, including motor impulsivity (response inhibition arising from possible dysfunctions in the executive circuitry) and cognitive impulsivity (delayed discounting related to the reward/motivational circuitry). Additionally, trait impulsivity and self-reported ADHD symptoms were assessed, representing distinct subjective measures of impulsive behavior (Broos et al., 2012).