دانلود مقاله ISI انگلیسی شماره 35084
عنوان فارسی مقاله

حساسیت اخلاقی در اختلال وسواس و اختلال اضطراب فراگیر: نقش آموزش معکوس

کد مقاله سال انتشار مقاله انگلیسی ترجمه فارسی تعداد کلمات
35084 2013 7 صفحه PDF سفارش دهید 5770 کلمه
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عنوان انگلیسی
Ethical sensitivity in obsessive-compulsive disorder and generalized anxiety disorder: The role of reversal learning
منبع

Publisher : Elsevier - Science Direct (الزویر - ساینس دایرکت)

Journal : Journal of Behavior Therapy and Experimental Psychiatry, Volume 44, Issue 4, December 2013, Pages 404–410

کلمات کلیدی
اختلال وسواس - آموزش معکوس - حساسیت اخلاقی - اجباری - اختلال اضطراب فراگیر -
پیش نمایش مقاله
پیش نمایش مقاله حساسیت اخلاقی در اختلال وسواس و اختلال اضطراب فراگیر: نقش آموزش معکوس

چکیده انگلیسی

Background and objectives In obsessive-compulsive disorder (OCD), amplified moral sensitivity may be related to the orbitofrontal–striatal circuit, which is also critical in reversal learning. This study examined three questions: (1) What aspects of ethical sensitivity is altered in OCD?; (2) What is the relationship between ethical sensitivity and reversal learning?; (3) Are potential alterations in ethical sensitivity and reversal learning present in generalized anxiety disorder (GAD)? Methods Participants were 28 outpatients with OCD, 21 individuals with GAD, and 30 matched healthy controls. Participants received the Ethical Sensitivity Scale Questionnaire (ESSQ), rating scales for clinical symptoms, a reversal learning task, and the Wisconsin Card Sorting Test (WCST). Results We found higher ethical sensitivity scores in OCD compared with healthy controls in the case of generating interpretations and options and identifying the consequences of actions. Individuals with OCD displayed prolonged reaction times on probabilistic errors without shift and final reversal errors. Participants with GAD did not differ from healthy controls on the ESSQ, but they were slower on reversal learning relative to nonpatients. In OCD, reaction time on final reversal errors mediated the relationship between ethical sensitivity and compulsions. WCST performance was intact in OCD and GAD. Limitations Small sample size, limited neuropsychological assessment, self-rating scale for ethical sensitivity. Conclusion Prolonged reaction time at switching reinforcement contingencies is related to increased ethical sensitivity in OCD. Slow affective switching may link ethical sensitivity and compulsions.

مقدمه انگلیسی

The resurgence of the increased moral sensitivity theory of obsessive-compulsive disorder (OCD) emerged as a fruitful meeting between psychodynamic and neurocognitive approaches (Freud, 1905/1955; Kempke & Luyten, 2007). Current cognitive theories posit that potentially harmful and immoral intrusive thoughts, images, or impulses elicit an inflated sense of personal responsibility, leading to compulsive behaviors, such as checking, ordering, or counting, to prevent unfavorable consequences (Salkovskis, 1985; Salkovskis, Forrester, & Richards, 1998). Mancini and Gangemi (2004) proposed that OCD is dominated by a feeling of fear of guilt that would stem from behaving irresponsibly. Patients with OCD often display dysfunctional appraisal about the power of their internal representations, believing that the mere appearance of an intrusive thought is morally the same as actions and behaviors driven by that thought (moral thought–action fusion) (Rachman, 1997; Shafran & Rachman, 2004). Recent progress in social neuroscience may provide a direct link between these theories and the neuronal mechanisms of OCD symptoms. Harrison et al. (2012) used functional magnetic resonance imaging (fMRI) in order to measure brain activation in OCD during the processing of moral dilemmas. Relative to controls, patients with OCD displayed increased activation of the medial orbitofrontal cortex, left dorsolateral prefrontal cortex, and middle temporal gyrus. Critically, the global severity of OCD symptoms predicted the extent of activation in the orbitofrontal–striatal system during the processing of moral dilemmas, which is broadly consistent with the common pathophysiological and functional neuroanatomical models of the illness (Evans, Lewis, & Iobst, 2004; Harrison et al., 2012; Menzies et al., 2008).

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