عملکرد عصبی در اختلال شخصیت ضد اجتماعی
|کد مقاله||سال انتشار||مقاله انگلیسی||ترجمه فارسی||تعداد کلمات|
|37354||2000||18 صفحه PDF||سفارش دهید||9319 کلمه|
Publisher : Elsevier - Science Direct (الزویر - ساینس دایرکت)
Journal : Psychiatry Research, Volume 97, Issues 2–3, 27 December 2000, Pages 173–190
Abstract Recent neuroimaging studies and neuropsychological test findings support the contention that prefrontal dysfunction is associated with psychopathic personality traits and antisocial behavior. However, conflicting results have arisen regarding performance on measures of frontal executive function. We administered a neuropsychological test battery consisting of measures sensitive to frontal lobe dysfunction and a battery of personality questionnaires and clinical scales sensitive to antisocial personality disorder (APD) subjects presenting with prominent psychopathic personality features and matched control subjects. We also monitored the subjects’ electrodermal activity during the presentation of emotionally charged stimuli. APD subjects showed greater neuropsychological deficits on measures sensitive to orbitofrontal dysfunction in comparison to control participants. Moreover, APD subjects were electrodermally hyporesponsive to aversive stimuli relative to control group members. APD subjects did not demonstrate performance deficits on classical tests of frontal executive function. Participants also underwent clinical assessment. As expected, APD subjects were less conscientious, self-reproaching, guilt-prone, and socially anxious than matched control subjects. Moreover, the scores indicated that APD subjects were more venturesome and uninhibited relative to control subjects. Contrary to expectations, APD subjects and community control subjects did not differ on a self-report measure of sensitivity to specific phobic situations.
1. Introduction 1.1. Prefrontal dysfunction and psychopathy Recent neuroimaging studies and neuropsychological test findings support the contention that prefrontal dysfunction (particularly orbitofrontal) is associated with psychopathic personality traits and antisocial behavior (Davidson et al., 2000, Raine et al., 1998, Raine et al., 2000 and Lapierre et al., 1995). However, conflicting results have arisen regarding the performance of psychopathic subjects on measures of frontal executive function. Several studies suggest that a select deficit involving the orbitofrontal system may underlie psychopathy and antisocial behavior. Lapierre et al. (1995) found that incarcerated psychopathic subjects were significantly impaired on tasks considered sensitive to orbitofrontal/ventromedial–prefrontal dysfunction including a visual go/no–go discrimination task, Porteus Maze Q-scores (i.e., rule-breaking errors), and an odor identification task in comparison to matched control subjects (non-psychopathic inmates). Lapierre et al. (1995) also found that psychopathic subjects did not display performance deficits on measures sensitive to dorsolateral–prefrontal (DLPF) and posterorolandic function (i.e., the Wisconsin Card Sorting Test (WCST) and the Mental Rotation Task). Moreover, Deckel et al. (1996) reported that performance on tests assessing frontal executive functioning (e.g. the WCST, controlled oral word fluency test, and trail-making test) failed to predict antisocial personality disorder classifications. These tasks are considered sensitive indicators of DLPF dysfunction (i.e., tasks which require the employment of organizational strategies for efficient performance). These findings suggest that a select orbitofrontal deficit may be associated with psychopathy. However, Gorenstein (1982) reported that psychopathic subjects demonstrated performance deficits on tests of frontal executive function including the WCST (i.e., perseverative errors), Necker cube task, and a sequential matching memory task. A recent meta-analytic review of 39 studies by Morgan and Lilienfeld (2000) lends strong support to the contention that executive function deficits are associated with antisocial personality (APD). Morgan and Lilienfeld (2000) found a significant relationship between executive function deficits and antisocial behavior. In response to Gorenstein's study, Hare (1984) assigned inmates to low-, medium-, and high-psychopathy groups and administered the aforementioned frontal executive function tasks. No significant group differences were observed. Hare was unable to replicate Gorenstein's findings. Sutker and Allain (1987) also found that psychopathic subjects and control subjects performed similarly on measures of concept formation, abstraction, and planning. How can we account for these conflicting findings? One possibility is that the executive function deficits among psychopathic subjects are associated with the presence of comorbid psychiatric conditions, while the core interpersonal and affective characteristics associated with psychopathy (e.g., egocentricity, callousness, manipulativeness, guile, lack of empathy and remorse) may result from orbitofrontal dysfunction
نتیجه گیری انگلیسی
Results Since multiple comparisons were planned, we controlled for type 1 errors with the Bonferroni procedure. Thus, the alpha level was set to 0.003. 3.1. Neuropsychological testing We conducted a multivariate analysis of variance (MANOVA). Significant MANOVA findings were followed up with post hoc comparisons using the Tukey test of significance. MANOVA indicated that the APD group was impaired on tasks considered sensitive to orbitofrontal dysfunction relative to control subjects: Wilks’ Lambda=0.136; F9,12=8.439; P<0.001. Subsequent univariate analyses yielded significant group differences on the object alternation test (F1,20=26.462, P<0.001), and conflict blocks of the Stroop color–word test (F1,20=12.011, P<0.003 and F1,20=13.446, P<0.001). APD subjects exhibited performance deficits on the object alternation test and conflict blocks of the Stroop task in comparison to community control subjects. The mean number of trials to solve the object alternation test was 11.8 (SD=4.7) for the community control group, but was 33.9 (SD=12.8) for the APD group. Relative to the community control group, APD subjects demonstrated slower reaction times on the color-naming blocks of the Stroop color–word test (see Table 1). When required to inhibit a previously learned response pattern (i.e., conflict blocks), APD subjects displayed greater reaction times in comparison to control subjects. Group differences on the non-conflict blocks of the Stroop (wordnaming) (Ps>0.35) and go/no–go (block 1) (P>0.11) tasks were not statistically significant. Contrary to expectation, group differences on the conflict blocks of the go/no–go task were not significant, although group differences on the third block of the go/no–go task approached significance (P<0.06). APD subjects did not demonstrate performance deficits on classical tests of frontal executive function. Interestingly, the APD subjects generated significantly more responses on the divergent thinking task than control participants (F1,20=14.051, P<0.001). APD subjects did produce fewer words on the word fluency test relative to control subjects, although this difference did not approach significance (P>0.25). Table 1. Neuropsychological test performancea Mean (SD) Univariate analysis APD Control subjects F1,20 P n 12 10 Age 27.8 (4.0) 28.9 (6.9) −0.202 0.658 Education 13.9 (1.72) 13.9 (1.74) 0.006 0.938 Handedness 100% Right 100% Right OAT 33.9 (12.8) 11.8 (4.7) 26.462 <0.001 Stroop color–word test Stroop Word-c 479 ms (50) 505 ms (81) −0.843 0.369 Stroop Word-i 521 ms (79) 549 ms (95) −0.606 0.445 Stroop Color-c 948 ms (223) 674 ms (121) 12.011 <0.003 Stroop Color-i 1214 ms (334) 811 ms (103) 13.446 <0.001 Go/no–go task Go/no–go — 1 322 ms (61.5) 284 ms (38.9) 2.746 0.113 Go/no–go — 2 495 ms (71.9) 468 ms (55.7) 0.943 0.345 Go/no–go — 3 505 ms (56.3) 459 ms (45.9) 4.083 0.056 FAS Test 38.0 (5.6) 41.6 (9.0) −1.294 0.268 DvT 9.5 (1.9) 6.8 (1.2) 14.051 0.001 SCR (micromhos) 0.02 (0.01) 0.14 (0.08) −24.333 <0.001 a Note: OAT=object alternation test; Stroop=Stroop color–word test (blocks 1 and 2=word naming, blocks 3 and 4=color naming), c=congruent, i=incongruent; Go/no–go=go/no go task (blocks 1, 2, 3); FAS=Controlled word fluency test (FAS test); DvT=divergent thinking task; ms=milliseconds; SCR=mean amplitude of skin conductance response (micromhos). Table options The mean amplitudes of skin conductance response (SCR) to the three categories of words (positive, neutral, and negative) were compared across the subject groups. As expected, APD subjects were electrodermally hyporesponsive to aversive stimuli relative to control group members (F1,20=−24.333, P<0.001). In addition, all participants, regardless of group membership, categorized words in the expected manner, demonstrating that they were aware of the emotional connotations of the stimuli. 3.2. Clinical profile MANOVA, followed by post hoc analyses, revealed highly significant group differences on the clinical scales and personality measures. As expected, APD subjects achieved significantly lower scores on factors O (F1,20=−18.768, P<0.001) and G (F1,20=−12.814, P<0.001) from the 16PF questionnaire, and on the social anxiety subscale (F1,20=−34.246, P<0.001) in comparison to control subjects. In addition, they displayed significantly higher scores on the APD subscale of the PDQ-4 (F1,20=67.663, P<0.001), the PCL:SV (F1,20=631.315, P<0.001) and on factor H (F1,20=18.782, P<0.001). This clinical profile indicates that APD subjects, as expected, were less conscientious, self-reproaching, guilt-prone, and socially anxious than matched control subjects. Moreover, the scores indicated that APD subjects were more venturesome and uninhibited relative to control subjects. However, the scores of APD subjects on the specific phobic situations subscale did not differ significantly from the scores achieved by control participants (P>0.78) (see Table 2). Group comparison revealed a marginally significant difference on the agoraphobia subscale (F1,20=−6.364, P<0.02). Table 2. Personality and clinical findingsa Clinical Characteristics Mean (SD) Univariate analysis APD Control subjects F1,20 P N 12 10 16 PF Subscales Factor G 6.4 (3.7) 11.3 (2.4) −12.814 <0.001 Factor H 20.5 (2.7) 13.3 (4.9) 18.782 <0.001 Factor O 7.8 (2.8) 12.6 (2.3) −18.768 <0.001 Fear Survey Subscales Agoraphobia 1.9 (3.2) 5.8 (4.0) −6.364 <0.02 Social anxiety 3.9 (3.3) 15.5 (5.8) −34.246 <0.001 Specific phobia 13.2 (8.8) 14.1 (4.6) −0.075 0.787 APD (PDQ) 6.6 (1.78) 1.4 (0.96) 67.663 <0.001 PCL:SV 18.5 (1.2) 3.4 (1.5) 631.315 <0.001 a Note: 16 PF Questionnaire — factors G, H, and O; Fear survey schedule — agoraphobia subscale; specific phobia subscale; social anxiety subscale); Personality diagnostic questionnaire (PDQ-4); APD=antisocial personality disorder subscale (PDQ-4); Psychopathy checklist: screening version (PCL:SV). Table options Five of 12 APD subjects reported a history of substance abuse. To examine the impact of prior substance abuse on neuropsychological test performance, we compared the performance patterns of APD subjects who met criteria (lifetime) for alcohol or substance abuse to the neurocognitve profiles of APD subjects who did not meet criteria for substance abuse or dependence. The clinical and neurocognitive profiles of these groups were remarkably similar. Groups did not differ significantly on the object alternation test (P>0.45), Stroop color–word test (all Ps>0.15), go/no–go task (all Ps>0.10), verbal fluency task (P>0.12), and divergent thinking task (P>0.15). In addition, groups did not exhibit significantly different patterns of autonomic reactivity (P>0.25).