تکانشگری خصلتی و مهار واکنش در اختلال شخصیت ضد اجتماعی
|کد مقاله||سال انتشار||مقاله انگلیسی||ترجمه فارسی||تعداد کلمات|
|33941||2009||7 صفحه PDF||سفارش دهید||5217 کلمه|
Publisher : Elsevier - Science Direct (الزویر - ساینس دایرکت)
Journal : Journal of Psychiatric Research, Volume 43, Issue 12, August 2009, Pages 1057–1063
Background Impulsive behavior is a prominent characteristic of antisocial personality disorder. Impulsivity is a complex construct, however, representing distinct domains of cognition and action. Leading models refer to impulsivity as an inability to evaluate a stimulus fully before responding to it (rapid-response impulsivity), and as an inability to delay responding despite a larger reward (reward-delay impulsivity). We investigated these models in terms of the diagnosis and severity of antisocial personality disorder. Methods Thirty-four male subjects on probation/parole who met DSM-IV criteria for ASPD, and 30 male healthy comparison subjects, matched by ethnicity, were recruited from the community. The Barratt Impulsiveness Scale (BIS-11) provided an integrated measure of trait impulsivity. Rapid-response impulsivity was assessed using the Immediate Memory Task (IMT), a continuous performance test. Reward delay impulsivity was assessed using the Two-choice Impulsivity Paradigm (TCIP), where subjects had the choice of smaller-sooner or larger-delayed rewards, and the Single Key Impulsivity Paradigm (SKIP), a free-operant responding task. Results Compared to controls, subjects with ASPD had higher BIS-11 scores (Effect Size (E.S.) = 0.95). They had slower reaction times to IMT commission errors (E.S. = 0.45). Correct detections, a measure of attention, were identical to controls. On the SKIP, they had a shorter maximum delay for reward (E.S. = 0.76), but this was not significant after correction for age and education. The groups did not differ on impulsive choices on the TCIP (E.S. < 0.1). On probit analysis with age and education as additional independent variables, BIS-11 score, IMT reaction time to a commission error, and IMT positive response bias contributed significantly to diagnosis of ASPD; SKIP delay for reward did not. Severity of ASPD, assessed by the number of ASPD symptoms endorsed on the SCID-II, correlated significantly with commission errors (impulsive responses) on the IMT, and with liberal IMT response bias. This relationship persisted with correction for age and education. Discussion These results suggest that ASPD is characterized by increased rapid-response impulsivity. Aspects of impulsivity related to reward-delay or attention appear relatively intact.
Impulsivity, defined as a propensity to act without the apparent capacity to adapt behavior to contextual demands, is prominent in many psychiatric disorders (Moeller et al., 2001). Impulsivity is complex, comprising neural mechanisms that could relate to distinct aspects of cognition. Two mechanisms involved in impulsivity, which may differ in mechanisms and treatments, are the inability to evaluate a stimulus adequately before responding to it (rapid-response impulsivity), and the inability to delay responding to an immediate small reward for a delayed larger one (reward-delay or delay-discounting impulsivity) (Swann et al., 2002 and Evenden, 1999). Impulsivity plays a central role in the so-called Cluster B personality disorders, including antisocial personality disorder (ASPD) (American Psychiatric Association, 1995 and First et al., 1997). ASPD is a common and potentially dangerous disorder, characterized by poor impulse control and destructive behavior that begins in childhood and persists into adulthood (American Psychiatric Association, 1995). In contrast with positive effects of treatment in individuals with impulsive aggression (Sheard et al., 1976, Barratt et al., 1997 and Stanford et al., 2005), there is no systematic or reliably effective treatment specifically for ASPD.
نتیجه گیری انگلیسی
Compared with healthy comparison subjects, subjects with ASPD had greater impulsivity as reflected by increased BIS-11 scores (especially nonplanning and motor), and increased IMT commission error reaction times, which may reflect a partial compensation mechanism related to impaired response inhibition, which becomes more apparent with more severe ASPD, when the number of ASPD symptoms correlates negatively with commission error reaction times. These differences were not due to ethnicity, age, or education. The data support a relationship between ASPD and impaired response inhibition, in which attention and the ability to delay reward are relatively intact.