SUMMARYImpulsive behaviors are observed in a wide range of psychiatric disorders, including substance use, bipolar, attention-deficit hyperactivity, antisocial and borderline personality, gambling, and eating disorders. The shared phenotype of impulsivity is thought to significantly contribute to both the etiology and perpetuation of these disorders. In this review, we focus upon the relevance of impulsivity to the addictive disorders, particularly substance use disorders. First, the literature supporting the presence of impulsive behaviors prior to the onset of drug use and addiction is discussed. The relevance of impulsivity to relapse is then presented, with a focus on three distinct neurocognitive constructs: automaticity, response inhibition, and decision making. Automaticity is a quickly occurring relapse process resulting from the learned habits induced by persistent drug use. Addicted persons with response inhibition deficits are unable to suppress these previously reinforced behaviors. Decision-making deficits contribute to relapse through a poorly considered assessment of the consequences of drug use. The brain regions associated with each model of impulsive behavior are described, and relevant neurobiologic disruptions in addicted subjects are discussed in the context of their specific neurocognitive deficit(s). Descriptive confusions in the terminology and confounds inherent in the study of impulsivity are described. Empirical

Patients with Parkinson's disease (PD) and normal controls (NCs) performed a negative priming task. NCs displayed the normal pattern of negative priming in that relative to a control condition they were slower to identify a target within a stimulus array when it had been a distractor in the previous array. PD patients did not display any evidence of negative priming. In contrast, both PD patients and NCs displayed statistically the same level of spatial priming and response repetition cost. Regression analyses indicated that although symptom severity, symptom characteristics, and global cognitive functioning were not reliable predictors of negative priming or spatial priming in PD patients, greater symptom severity and poorer global cognitive functioning were associated with less response repetition cost. The possible role of the striatum in negative priming, spatial priming, and response repetition cost is discussed.

Normative data are presented for older African Americans on the Mattis Dementia Rating Scale (DRS). These data were collected as part of Mayo's Older African Americans Normative Studies (MOAANS) in an effort to develop age-appropriate norms for African Americans elders on commonly used measures in neuropsychological assessment. In this study, the DRS was administered to 307 MOAANS participants ranging in age from 56 to 94 years. Age-corrected subtest and total scores were derived based on percentile ranks from actual frequency distributions across seven age ranges. Also presented is a regression-based computational formula that may be applied to the age-corrected DRS total score to further correct for years of education. These norms should help improve interpretation of DRS performance in African Americans and allow for greater diagnostic accuracy in patients with early cognitive decline.

Parkinson's disease (PD) patients and healthy controls were administered a flanker task that consisted of the presentation of colored targets and distractors. Participants were required to attend to the center target and identify its color. The stimulus displays were either congruent (i.e., the target and flankers were the same color) or incongruent. The time between the onset of the flanker and the target color (the target onset delay) was either short or long. Results indicated that PD patients and controls did not differ in the magnitude of the flanker effect within individual trials in that both groups demonstrated a typical flanker effect at the short target onset delay and neither group demonstrated a flanker effect at the longer delay. However, when performance was examined on a trial-by-trial basis, PD patients demonstrated a slowing of reaction time relative to controls when having to make the same response across consecutive trials at longer inter-trial intervals when the flankers were incongruent across consecutive trials and the display on the second of two trials was incongruent. These results indicate that PD patients are impaired in inhibiting the distractors over an extended delay and that this deficit may impact motor responding in these patients, suggesting that the basal ganglia contribute to the interface of attention and action.

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