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Published on: November 21, 2013
Neurocognitive Deficits Associated with Antisocial Personality Disorder in Non-treatment-seeking Young Adults
Samuel R Chamberlain1, Katie L Derbyshire1, Eric W Leppink1
1Dr. Chamberlain is a Clinical Lecturer, Honorary Specialty Registrat (SpR), Department of Psychiatry, University of Cambridge and Cambridge and Peterborough NHS Foundation Trust, Cambridge, UK. Ms. Derbyshire and Mr. Lippink are Research Specialists and Dr. Grant is Professor, Department of Psychiatry and Behavioral Neuroscience, University of Chicago, Chicago, IL. This research was supported by a Center for Excellence in Gambling Research grant by the Institute for Responsible Gaming (U.S.) to Dr. Grant. Dr. Chamberlain's involvement in this study was supported by a grant from the Academy of Medical Sciences (U.K.). The funding agency had no role in the design and conduct of the study; collection, management, analysis, and interpretation of the data; or preparation, review, or approval of the manuscript.
Abstract:
Antisocial personality disorder (ASPD) is a relatively common problem, but the neuropsychological profile of affected individuals has seldom been studied outside of criminal justice recruitment settings. Non-treatment-seeking young adults (18-29 years) were recruited from the general community by media advertisements. Participants with ASPD (n = 17), free from substance use disorders, were compared with matched controls (n = 229) using objective computerized neuropsychological tasks tapping a range of cognitive domains. Compared with controls, individuals with ASPD showed significantly elevated pathological gambling symptoms, previous illegal acts, unemployment, greater nicotine consumption, and relative impairments in response inhibition (Stop-Signal Task) and decision-making (less risk adjustment, Cambridge Gamble Task). General response speed, set-shifting, working memory, and executive planning were intact. ASPD was also associated with higher impulsivity and venturesomeness on the Eysenck Questionnaire. These findings implicate impaired inhibitory control and decision-making in the pathophysiology of ASPD, even in milder manifestations of the disorder. Future work should explore the neural correlates of these impairments and use longitudinal designs to examine the temporal relationship between these deficits, antisocial behavior, and functional impairment.
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