ارتباط متفاوت بین آلکسیتیمیا و اختلالات فکری و روانی اولیه در مقابل اختلالات فکری و روانی ثانویه
|کد مقاله||سال انتشار||مقاله انگلیسی||ترجمه فارسی||تعداد کلمات|
|34359||2012||6 صفحه PDF||سفارش دهید||4753 کلمه|
Publisher : Elsevier - Science Direct (الزویر - ساینس دایرکت)
Journal : Personality and Individual Differences, Volume 52, Issue 1, January 2012, Pages 45–50
Using a sample of 104 college students, this study tested the hypothesis that alexithymia is positively related to secondary (also known as “neurotic psychopathy”), but not primary psychopathy (i.e., inability to form emotional bonds with others and a fear insensitivity). Participants completed the TAS-20 (alexithymia), the LSRP (primary and secondary psychopathy), the PPI-R (psychopathy), and the trait version of the STAI (trait anxiety). The interaction between the latter two measures was used as a second index of primary and secondary psychopathy. Support was found for the study hypothesis with both methods of assessing psychopathy (i.e., the LSRP subscales or the combination of the PPI-R and the STAI). These results further our understanding of both alexithymia and psychopathy.
Definitions of alexithymia and psychopathy both emphasize emotional processing deficits (Kroner & Forth, 1995). Alexithymia is defined as difficulty identifying and distinguishing between feelings and bodily sensations of emotional arousal, and difficulty describing feelings to others (Taylor, Bagby, & Parker, 1992). Individuals with alexithymia also have difficulties empathizing with the others’ feelings (Guttman & Laporte, 2002). Such deficits closely correspond to deficits seen in persons high in psychopathy. Psychopathy is characterized by interpersonal and affective deficits such as manipulative behavior, callousness, and difficulties empathizing with others as well as a socially deviant or antisocial lifestyle (Hare, 2003). Studies have documented the specific emotion processing deficits of both alexithymia and psychopathy such as difficulties in interpreting facial expressions (Dolan & Fullam, 2006), understanding emotional tone in language (Herve, Hayes, & Hare, 2003), and describing one’s own feelings (Luminet, Rime, Bagby, & Taylor, 2004). Because of the conceptual overlap between the two disorders, studies have begun to explore the association between alexithymia and psychopathy. Using the Toronto Alexithymia Scale (TAS) and the Psychopathy Checklist-Revised (PCL-R), two studies have examined the association between alexithymia and psychopathy in clinical or criminal samples (Kroner and Forth, 1995 and Louth et al., 1998). While both studies found positive correlations between the PCL-R factor 2 (social deviance) and TAS, interestingly, they found negative correlations (Kroner & Forth, 1995) or no relationship with the PCL-R factor 1 (interpersonal and affective impoverishment) (Louth et al., 1998). This pattern of relationships is somewhat surprising in that one might initially presume that the deficits in empathy that are characteristic of the PCL-R factor 1 would be the same traits that are common to alexithymia. These findings raise the intriguing question of whether alexithymia is more closely associated with secondary psychopathy than primary psychopathy. The distinction between primary and secondary psychopathy was first made by Karpman (1941), in which he asserted that primary psychopathy might be a heritable deficit characterized by callousness, lack of empathy, and fear insensitivity. In contrast, he described secondary psychopathy as being shaped by a combination of heritable and environmental causes (e.g., childhood abuse). Unlike those high in primary psychopathy, those with secondary psychopathic characteristics possess the capacity to form emotional bonds with others and experience feelings of anxiety and guilt. Both those with primary and secondary psychopathy are prone to aggression and criminal activities. However, for those with secondary psychopathy these behaviors are less planful and more impulsive, while for those with primary psychopathy these behaviors appear to be more driven by sensation seeking tendencies (Skeem, Johansson, Andershed, Kerr, & Louden, 2007). This is consistent with research (e.g., Fowles & Dindo, 2006) linking primary psychopathy to subcortical deficits (brain regions tied to fear sensitivity) and secondary psychopathy to prefrontal cortex deficits (brain regions tied to executive functions including attention and planning). Such theorizing is in line with a number of studies suggesting that primary psychopathy is negatively correlated with behavioral inhibition, whereas secondary psychopathy is positively correlated with behavioral activation (see Wallace, Malterer, & Newman, 2009, for a more complete review). The PCL-R was not developed to specifically measure primary and secondary psychopathy (Brinkley et al., 2008 and Skeem et al., 2007). However, some theorists have asserted that persons with primary psychopathy may possess characteristics of factor 1, and persons with secondary psychopathy may possess characteristics of factor 2 (Levenson et al., 1995 and Mealey, 1995). Thus, the finding from the studies by Kroner and Forth (1995) and Louth et al. (1998) that the TAS is strongly correlated with factor 2 of the PCL suggests a possible link between alexithymia and secondary psychopathy. Research is needed that directly tests this hypothesis using measures specifically designed to assess primary and secondary psychopathy. Only one study to our knowledge has presented data suggesting differential associations of alexithymia with secondary versus primary psychopathy (Grieve & Mahar, 2010). Grieve and Mahar (2010) presented a correlation matrix in which the association between TAS and primary psychopathy was smaller than the association between TAS and secondary psychopathy. However, the study did not hypothesize or provide a direct test of whether primary and secondary psychopathy were differentially associated with alexithymia, nor were their data conclusive in that regard, as correlations were significant for both primary and secondary psychopathy. The current study differs from Grieve and Mahar (2010) by directly testing the hypothesis that alexithymia is associated with secondary, but not primary psychopathy, while ruling out potentially confounding effects. In addition, the current study differs from Kroner and Forth (1995) and Louth et al. (1998) by examining the association between psychopathy and alexithymia within a non-clinical, non-criminal sample. Different processes may operate for persons with psychopathy within community samples versus criminal samples (Brinkley et al., 2008 and Mahmut et al., 2008), presumably because those within community samples are likely to display higher levels of adjustment and would be considered “subclinical” with respect to psychopathic attributes. Consequently, it is important to replicate findings on psychopathy using both criminal and community samples. Using two different methods of assessing primary versus secondary psychopathy, the current study tested the hypothesis that alexithymia is positively related to secondary but not primary psychopathy.