دانلود مقاله ISI انگلیسی شماره 38483
عنوان فارسی مقاله

ارتباط نورون ها مربوط به پاداش و از دست دادن در اختلالات شخصیت خوشه B: مطالعه تصویربرداری رزونانس مغناطیسی عملکردی

کد مقاله سال انتشار مقاله انگلیسی ترجمه فارسی تعداد کلمات
38483 2007 17 صفحه PDF سفارش دهید محاسبه نشده
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عنوان انگلیسی
Neuronal correlates of reward and loss in Cluster B personality disorders: A functional magnetic resonance imaging study
منبع

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

Journal : Psychiatry Research: Neuroimaging, Volume 156, Issue 2, 15 November 2007, Pages 151–167

کلمات کلیدی
- اختلال شخصیت مرزی - اختلال شخصیت ضد اجتماعی - تقویت مثبت
پیش نمایش مقاله
پیش نمایش مقاله ارتباط نورون ها مربوط به پاداش و از دست دادن در اختلالات شخصیت خوشه B: مطالعه تصویربرداری رزونانس مغناطیسی عملکردی

چکیده انگلیسی

Abstract Decision making is guided by the likely consequences of behavioural choices. Neuronal correlates of financial reward have been described in a number of functional imaging studies in humans. Areas implicated in reward include ventral striatum, dopaminergic midbrain, amygdala and orbitofrontal cortex. Response to loss has not been as extensively studied but may involve prefrontal and medial temporal cortices. It has been proposed that increased sensitivity to reward and reduced sensitivity to punishment underlie some of the psychopathology in impulsive personality disordered individuals. However, few imaging studies using reinforcement tasks have been conducted in this group. In this fMRI study, we investigate the effects of positive (monetary reward) and negative (monetary loss) outcomes on BOLD responses in two target selection tasks. The experimental group comprised eight people with Cluster B (antisocial and borderline) personality disorder, whilst the control group contained fourteen healthy participants. A key finding was the absence of prefrontal responses and reduced BOLD signal in the subcortical reward system in the PD group during positive reinforcement. Impulsivity scores correlated negatively with prefrontal responses in the PD but not the control group during both, reward and loss. Our results suggest dysfunctional responses to rewarding and aversive stimuli in Cluster B personality disordered individuals but do not support the notion of hypersensitivity to reward and hyposensitivity to loss.

مقدمه انگلیسی

. Introduction Rewarding and punishing stimuli result in an increase or decrease of the probability of antecedant actions, thereby shaping behaviour. In recent years, functional neuroimaging studies in humans using primary (e.g. O'Doherty et al., 2001a and O'Doherty et al., 2002) and abstract rewards (e.g. Breiter et al., 2001, Elliott et al., 2000 and Elliott et al., 2003) have advanced our understanding of the neuronal correlates of reinforcement processing and have corroborated previous findings from single-cell electrophysiological and lesion studies in animals. This research has implicated a network of interconnected brain regions mediating the behavioural and motivational effects of reward, including ventral striatum, dopaminergic midbrain, amygdala and orbitofrontal cortex (OFC; for a review see O'Doherty, 2004). Distinct functions have been attributed to these different regions. For instance, amygdala, striatum and midbrain have been found to respond to the presence of reward regardless of value (e.g. Elliott et al., 2000 and Elliott et al., 2003); in contrast, a more complex pattern of responses has been identified in medial and lateral OFC suggesting a possible role for higher order processing of reinforcing stimuli, such as the integration of stimulus attributes and emotional value (e.g. Elliott et al., 2003, Kringelbach et al., 2003 and O'Doherty, 2004). This in turn allows the salience of reinforcing stimuli to be updated and modulated following changes in contingencies and the subsequent use of this information in action selection. The role of reward system components in the response to punishment or loss is less clear. Several fMRI studies in humans have suggested the striatum has an important role. Jensen et al. (2003) have identified ventral striatum responses in anticipation of sensory aversive stimuli. Other authors have shown ventral striatum activity associated with anticipation and following the presentation of both monetary rewards and punishments (e.g. Knutson et al., 2001 and Delgado et al., 2003). Decreased BOLD signal in dorsal and ventral striatum has been observed following punishing feedback (Delgado et al., 2000). These findings suggest that this structure is not functionally specific to reward but may have a more general role in the processing of reinforcing stimuli. Other authors have identified BOLD signal changes in lateral OFC following punishment (e.g. O'Doherty et al., 2001b and Remijnse et al., 2005). This might reflect the involvement of this structure in response inhibition (Aron et al., 2003). In addition, anterior cingulate and thalamus (Knutson et al., 2000), right amygdala (Zalla et al., 2000), insula (O'Doherty et al., 2003) and hippocampus/parahippocampus (Elliott et al., 2000) have been associated with the experience of loss or punishment in humans. Dysfunctional responses to reinforcing stimuli have been proposed to underlie the psychopathology in substance use and impulsivity-related personality disorders (Petry, 2002). The latter encompass two personality disorders within Cluster B of the Diagnostic and Statistical Manual of Mental Disorders (DSM-IV; APA, 1994): antisocial (ASPD) and borderline (BPD) personality disorder. These two disorders share some common characteristics, particularly high levels of impulsive behaviour; some authors have argued that ASPD and BPD are manifestations of the same underlying pathology in male and female individuals respectively (e.g. Paris, 1997). There is considerable co-morbidity between these two personality disorders: in male individuals a co-occurrence of up to 50% has been identified (Zanarini et al., 1998 and Chabrol and Leichsenring, 2006). Becker et al. (2005) noted that symptoms related to impulsive behaviour in BPD were not significantly more efficient in diagnosing BPD than ASPD. It therefore seems justified to consider these two disorders together as an impulsivity-related personality disorder as has previously been suggested by other authors (e. g. Goethals et al., 2005). A number of aetiological models of impulsivity-related personality disorders have been put forward. Early accounts (Gray, 1987) postulated two distinct motivational systems: a behavioural activation system (BAS) which is sensitive to reward cues and a behavioural inhibition system (BIS) which is sensitive to punishment. In this model, impulsive–aggressive behaviour as observed in impulsive Cluster B PD is proposed to result from an imbalance of these two systems, either due to an oversensitivity of the BAS or due to hyporesponsiveness of the BIS. More recent models of impulsive personality disorders have focused on behavioural choice in the context of reward and punishment. The reward dominance theory suggests that antisocial individuals show greater responsivity to reward and decreased sensitivity to punishment in situations where both types of stimuli are available (Scerbo et al., 1990). Impulsive individuals focus on the prospect of reward even if environmental cues indicate possible later punishment (Budhani and Blair, 2005). Preference for shorter delays in reward-choice tasks has been demonstrated in borderline (Dougherty et al., 1999) and antisocial personality disorder (Moeller et al., 2002) and in probation and parole groups (Cherek et al., 1999 and Cherek et al., 1997). Other authors have shown that antisocial groups perform poorly on passive avoidance tasks by failing to inhibit punishable responses (e. g. Dikman and Allen, 2000). The coding of stimulus reward values is crucial for generating appropriate reward-directed behavioural responses i.e. in guiding individuals' selection of advantageous over disadvantageous behaviour based on previous experience (Kringelbach and Rolls, 2004). This process has been suggested to be impaired in individuals with ventromedial prefrontal brain damage (e.g. Damasio et al., 1990 and Damasio, 1994) accounting partly for their impulsive behaviour. These observations in “acquired sociopathy” (Saver and Damasio, 1991), brain imaging (Goyer et al., 1994, Raine et al., 2000, Herpertz et al., 2001, Donegan et al., 2003 and Goethals et al., 2005) and neuropsychological evidence (Lapierre et al., 1995, Bazanis et al., 2002, Dolan and Anderson, 2002 and Rogers, 2003) in borderline and antisocial personality disordered individuals have led to a proposal that some of their psychopathology can be explained by ventromedial and orbitofrontal dysfunction. While a number of studies have investigated performance and neuropsychological correlates of behavioural choice in individuals with impulsive Cluster B PD no brain imaging studies have been conducted examining neuronal correlates of stimulus selection in the context of positive and negative outcomes in these patients. In this study we used two stimulus selection tasks to investigate the impact of positive and negative outcomes (further referred to as reward and loss task) on BOLD responses in impulsivity-related personality disorders. We hypothesized that control participants would show BOLD signal increases in orbitofrontal regions during positive and negative feedback. We further hypothesized that ASPD and BPD patients (in comparison to healthy controls) would show reduced signal change in prefrontal (particularly orbitofrontal) regions in both tasks with increased BOLD response in reward and decreased BOLD response in loss related brain areas.

نتیجه گیری انگلیسی

3. Results 3.1. Behavioural results Differences between the two groups approached significance for non-planning impulsivity (P = 0.057; mean in PD group 27, range 13 to 38, median 25; mean in control group 20, range 10 to 35, median 19.5) and total BIS scores (P = 0.058; mean in PD group 59, range 40 to 77, median 70; mean in control group 45, range 27 to 66, median 39.5). Behavioural results relating to task performance on the two tasks are displayed in Table 1. For the reward task, a main effect of block (F = 14.04; P = 0.001) with slower responding in the no-reward blocks compared to the reward blocks was observed. This effect was also observed in the loss compared to no-loss blocks (F = 22.21; P < 0.001). No main effect of group or group × block interaction was observed in either or the two tasks. Table 1. Behavioural results Variable PD group Control group N = 8 a N = 14 b RT reward blocks 531.4 (57.3) 498.9 (62.5) RT no-reward blocks 562.2 (58.8) 545.2 (66.3) OE reward blocks 0.0 0.0 OE no-reward blocks 0.0 0.0 CE reward blocks 0.0 0.5 CE no-reward blocks 0.0 1.0 RT loss blocks 492.4 (79.4) 459.9 (56.3) RT no-loss blocks 539.5 (58.7) 510.3 (45.6) OE loss blocks 0.0 0.0 OE no-loss blocks 0.0 0.0 CE loss blocks 1.0 0.0 CE no-loss blocks 0.0 0.0 RT: Reaction time, means in ms (standard deviation in brackets). OE: Omission error, CE: commission error; median. a No-reward block OE and CE: 7 subjects after exclusion of one outlier with exceptionally high error rates in each of these blocks. b Loss block CE: 13 subjects included in analysis after exclusion of one outlier. Table options Error rates were generally low and the majority of participants did not make any errors. The PD group made more errors of commission than controls in the loss blocks (P = 0.002) but there were no other significant differences between the two groups. 3.2. Imaging results: reward task 3.2.1. Effect of reward The effect of the task in the patient and control group is shown in Table 2 and Fig. 1. In the control group significant neural responses during reward compared to no-reward blocks were found in bilateral medial and lateral OFC, left inferior prefrontal cortex, right frontal pole, supplementary motor area and middle cingulate cortex. Further BOLD signal increases were observed in temporal and occipital areas bilaterally, right superior parietal cortex and left cerebellum. One focus in right posterior parahippocampal cortex was also identified. By contrast, in the patient group no significant responses were observed in the prefrontal cortex. Significant foci were found in the left parietal cortex, bilaterally within the temporal cortex and also the right cerebellum. A subthreshold activation was found in posterior medial frontal cortex, extending to the amygdala. Table 2. Areas in which there was a significant evoked BOLD increase related to reward blocks compared to no-reward blocks in control and patient subjects Brain area BA L/R Controls Patients MNI coordinates Z value Size MNI coordinates Z value Size x y z x y z Posterior lateral OFC extending to superior temporal cortex 47/38 L − 45 18 − 9 a,b5.07 122 R 48 18 − 12 b3.92 157 Medial OFC 11 L − 12 60 − 6 a,b4.60 249 R 15 63 − 6 3.19 Inferior frontal cortex 46 L − 54 15 0 b4.18 Frontal pole 10 R 5 63 9 3.43 Supplementary motor area 8 R 3 24 54 3.32 20 Posterior medial frontal cortex extending to amygdala 11/34 R 15 6 − 24 (2.36) 18 Middle cingulate cortex 23 R 3 − 24 33 a3.33 94 Temporal pole 38 L − 42 24 − 24 3.89 69 Middle temporal cortex 22 R 66 − 39 9 3.29 43 Inferior temporal cortex, including lingual and fusiform gyrus 20/21/37 L − 42 − 42 − 24 3.83 126 − 51 − 62 − 57 3.63 107 L − 57 − 24 − 21 3.30 40 R 51 − 57 − 15 3.63 51 − 57 − 18 3.55 10 R 60 − 21 − 21 3.51 22 R 69 − 24 − 12 3.43 Posterior parahippocampal gyrus 35/36 R 21 − 24 − 12 3.15 33 Inferior/middle occipital cortex, including fusiform gyrus 18/19 L − 45 − 81 − 3 3.54 L − 39 − 87 3 3.19 R 42 − 69 − 15 3.82 184 27 − 69 − 21 3.48 140 Superior parietal cortex 1 L − 15 − 45 75 3.38 15 Precuneus 7 L − 3 − 63 60 3.68 172 Cerebellum L − 33 − 69 − 24 a4.60 249 R 15 − 30 − 36 3.45 11 R 3 − 60 − 27 3.31 BA = Brodmann Area. L/R = Left/Right brain. Size: Where no cluster size is reported, responses in this region were part of a larger cluster the most significant voxel of which was in a different anatomical region. Regions in bold indicate those regions about which we had an a priori hypothesis. All other regions are thresholded at P < 0.001, uncorrected. ( ) indicate regions which do not fulfil these criteria but are shown as BOLD signal changes were observed in areas about which we had an a priori hypothesis. a PFDR < 0.05 across the whole brain. b PFDR < 0.05 indicates regions significant in the Region of Interest analysis in areas with a priori hypothesis. Table options SPMs depicting regional BOLD signal increases during performance of the reward ... Fig. 1. SPMs depicting regional BOLD signal increases during performance of the reward task. Areas where increased signal was detected during reward compared to no-reward blocks are shown. (A) Control group (14 subjects). (B) Cluster B personality disordered patients (8 subjects). Activations are displayed within three brain transparent projections viewed from the right (left figures), the posterior (middle figures) and the superior aspect of the brain (right figures). Cluster details are given in Table 2. Both maps are thresholded at P < 0.01, uncorrected. Figure options 3.2.2. Comparison of BOLD signal changes in the control and patient group There were statistically significant differences between the control and personality disordered group in the pattern of BOLD signal increases, see Table 3 and Fig. 2. Increased responses in the control group were observed in prefrontal areas, including left medial OFC and dorsolateral prefrontal cortex and right frontal pole. Anterior and posterior cingulate were also identified in this contrast. Control participants also showed greater responses than PD participants in bilateral temporal cortex, left parahippocampal gyrus and right occipital cortex and precuneus. Subthreshold clusters were identified in bilateral caudate and left ventral midbrain. Few areas showed increased responses in PD compared to the controls but included left postcentral gyrus, right cerebellum, bilateral medial frontal cortex, extending to amygdala and bilateral locus coeruleus. Table 3. Contrast analysis showing foci of clusters where differences in BOLD signal between the control and patient group were detected in the reward versus no-reward comparison Brain area BA L/R Controls–patients Patients–controls MNI coordinates Z value Size MNI coordinates Z value Size x y z x y z Medial orbitofrontal cortex 11 L − 12 60 − 6 a4.01 100 Dorsolateral prefrontal cortex 8 L − 30 21 54 3.29 27 Frontal pole 10 R 6 63 9 3.29 32 Posterior medial frontal cortex extending to amygdala 11/34 R 12 6 − 24 3.21 31 L − 15 9 − 21 3.12 12 Anterior cingulate cortex 24 L − 12 24 21 3.42 30 Posterior cingulate 23 R 12 − 51 27 3.49 Middle temporal cortex 21 R 69 − 27 − 12 3.37 21 Superior temporal cortex 22 L − 66 − 48 21 3.40 30 Posterior parahippocampal gyrus 35/36 L − 24 − 51 − 6 (2.90) 26 Occipital cortex, including calcarine cortex 17 R 15 − 90 6 3.18 83 Postcentral gyrus, extending to precuneus 1/5 L − 12 − 45 78 3.81 73 Precuneus 31 R 6 − 54 27 3.53 109 Caudate L − 3 − 6 15 (3.07) 21 R 6 − 6 15 (2.64) Ventral midbrain L − 9 − 9 − 15) (2.89) 11 Locus coeruleus L − 9 − 30 − 33 3.36 52 R 18 − 33 − 36 3.48 17 Cerebellum R 26 − 66 − 18 3.30 55 BA = Brodmann Area. L/R = Left/Right brain. Size: Where no cluster size is reported, responses in this region were part of a larger cluster the most significant voxel of which was in a different anatomical region. Regions in bold indicate those regions about which we had an a priori hypothesis. All other regions are thresholded at P < 0.001, uncorrected. ( ) indicate regions which do not fulfil these criteria but are shown as BOLD signal changes were observed in areas about which we had an a priori hypothesis. a PFDR < 0.05 indicates regions significant in the Region of Interest analysis in areas with a priori hypothesis. Table options BOLD signal changes in the reward task in the control–patient (depicted in red) ... Fig. 2. BOLD signal changes in the reward task in the control–patient (depicted in red) and patient–control (depicted in blue) comparisons overlaid on standard T1-weighted axial slices. Slice numbers are given in the z plane and are displayed in 3 mm intervals. Height threshold T = 2.53 corresponding to P < 0.001, uncorrected. Figure options 3.3. Imaging results: loss task 3.3.1. Effect of loss The effects of the loss task in the control and patient group are depicted in Table 4 and Fig. 3. In the control group significant responses during loss compared to no-loss blocks were observed in right medial and lateral OFC, right frontal pole, left precentral and inferior prefrontal cortex and bilateral dorsolateral prefrontal cortex. BOLD signal increases were also found in left temporal and occipital areas, left posterior (para)hippocampal gyrus and cerebellum and in right precuneus. In the patient group a similar pattern of BOLD signal increases was observed including left lateral OFC and inferior prefrontal cortex, right middle frontal gyrus, bilateral occipitotemporal cortex, cingulate and cerebellum. Table 4. Areas in which there was a significant evoked BOLD increase related to loss blocks compared to no-loss blocks in control and patient subjects Brain area BA L/R Controls Patients MNI coordinates Z value Size MNI coordinates Z value Size x y z x y z Lateral OFC 47 L − 57 21 − 3 (2.86) − 45 24 − 15 (2.73) 10 R 48 24 − 9 3.32 51 39 − 18 a3.79 29 Medial OFC 11 L 0 54 − 21 (2.66) R 12 63 − 9 a3.39 126 Dorsolateral prefrontal cortex extending to inferior frontal cortex 8/9/44/46 L − 57 15 30 a3.79 194 R 63 21 24 a3.89 Inferior frontal cortex 10/46 L − 51 48 0 3.26 29 R 33 66 0 4.02 73 Frontal pole 10/46 R 39 60 12 3.58 195 Middle frontal gyrus 9 R 27 21 26 3.57 10 25 54 33 3.27 12 Precentral gyrus 6 L − 51 3 39 4.13 243 Anterior/middle cingulate cortex 23/24 R/L 3 − 9 39 (2.89) − 6 − 3 30 3.58 163 R 0 − 18 39 (2.68) 9 − 6 30 3.26 Temporal pole 38 L − 57 9 − 15 3.19 R 51 21 − 18 4.05 24 Posterior parahippocampal gyrus 36 L − 21 − 21 − 36 3.21 15 Occipitotemporal cortex, including fusiform gyrus 18/19/37 L − 33 − 81 − 18 3.68 550 − 45 − 75 − 18 4.09 204 R 51 − 54 − 21 3.12 88 Precuneus 7 R 9 − 75 48 3.53 27 Thalamus R 0 − 24 6 (2.78) 10 Cerebellum L − 24 − 81 − 36 3.68 − 45 − 66 − 21 3.68 L − 6 − 63 − 6 3.10 BA = Brodmann Area. L/R = Left/Right brain. Size: Where no cluster size is reported, responses in this region were part of a larger cluster the most significant voxel of which was in a different anatomical region. Regions in bold indicate those regions about which we had an a priori hypothesis. All other regions are thresholded at P < 0.001, uncorrected. ( ) indicate regions which do not fulfil these criteria but are shown as BOLD signal changes were observed in areas about which we had an a priori hypothesis. a PFDR < 0.05 indicates regions significant in the Region of Interest analysis in areas with a priori hypothesis. Table options SPMs depicting regional BOLD signal increases during performance of the loss ... Fig. 3. SPMs depicting regional BOLD signal increases during performance of the loss task. Areas where increased signal was detected during loss compared to no-loss blocks are shown. (A) Control group (14 subjects). (B) Cluster B personality disordered patients (8 subjects). Activations are displayed within three brain transparent projections viewed from the right (left figures), the posterior (middle figures) and the superior aspect of the brain (right figures). Cluster details are given in Table 4. Both maps are thresholded at P < 0.01, uncorrected. Figure options 3.3.2. Comparison of BOLD signal changes in the control and patient group In contrast to the group comparison in the reward task, in the loss task no significant differences in BOLD signal were observed in OFC. Increased signal in the control group compared to patients was identified in bilateral dorsolateral prefrontal, left precentral and bilateral occipitotemporal cortex and precuneus (Table 5 and Fig. 4). A further cluster was also found in the limbic cortex. In the patient group compared with the control group, an enhanced BOLD signal was observed in bilateral medial prefrontal cortex, left middle frontal gyrus, and anterior cingulate. Further areas of signal increase included right superior temporal, bilateral occipital and inferior parietal cortex, right postcentral gyrus and cerebellum. Table 5. Contrast analysis showing foci of clusters where differences in BOLD signal between the control and patient group were detected in the loss versus no-loss comparison Brain area BA L/R Controls–patients Patients–controls MNI coordinates Z value Size MNI coordinates Z value Size x y z x y z Medial prefrontal cortex 10/32 L − 15 51 21 3.20 16 R 18 45 24 3.90 169 Dorsolateral prefrontal cortex 44 L − 54 15 30 a3.86 R 54 15 30 3.27 10 Middle frontal gyrus 46 L − 27 21 36 3.55 Precentral gyrus 6 L − 51 3 39 4.37 215 Anterior/middle cingulate cortex 24/32 R 9 6 30 a4.18 372 Inferior temporal cortex, including fusiform gyrus 37 L − 51 − 54 − 24 3.11 21 Posterior parahippocampal gyrus 36 L − 21 − 18 − 36 3.42 43 Superior temporal cortex 41 R 45 − 42 15 3.33 Occipital cortex, including cuneus 19 L − 27 − 90 36 3.34 54 R 36 − 84 30 3.32 33 Occipital cortex, including calcarine cortex, fusiform and lingual gyrus and precuneus 18/19 L − 24 − 60 27 3.59 R 27 − 72 15 3.61 474 Postcentral gyrus 3 R 39 − 15 33 3.28 Inferior parietal cortex 40 R 30 − 36 36 3.79 1463 Precuneus 7 L − 6 − 81 48 3.36 16 R 12 − 81 48 3.31 81 Cerebellum L − 6 − 63 − 6 3.25 R 9 − 57 − 12 3.50 BA = Brodmann Area. L/R = Left/Right brain. Size: Where no cluster size is reported, responses in this region were part of a larger cluster the most significant voxel of which was in a different anatomical region. Regions in bold indicate those regions about which we had an a priori hypothesis. All other regions are thresholded at P < 0.001, uncorrected. a PFDR < 0.05 indicates regions significant in the Region of Interest analysis in areas with a priori hypothesis. Table options BOLD signal changes in the loss task in the control–patient (depicted in red) ... Fig. 4. BOLD signal changes in the loss task in the control–patient (depicted in red) and patient–control (depicted in blue) comparisons overlaid on standard T1-weighted axial slices. Slice numbers are given in the z plane and are displayed in 3 mm intervals. Height threshold T = 2.53, corresponding to P < 0.001, uncorrected. Figure options 3.4. Imaging results: conjunction analyses In the conjunction analysis common BOLD responses in the loss and the reward task were identified (see Table 6). In the control group the main signal increases common to both tasks were observed in medial and lateral orbitofrontal cortex (see Fig. 5). Further areas identified included frontal pole, inferior temporal and occipital cortex and cerebellum. No prefrontal BOLD signal changes were found in the conjunction analysis in the patient group. Table 6. Conjunction analysis of areas in which significant evoked BOLD increase was observed in both, the reward (reward–no-reward blocks) and the loss (loss–no-loss) task, in control and patient subjects Brain area BA L/R Controls Patients MNI coordinates Z value Size MNI coordinates Z value Size x y z x y z Lateral OFC 47 R 48 24 − 12 a3.28 100 Medial OFC 11 L − 3 60 − 12 a4.00 124 Frontal pole 10 R 15 63 − 6 3.33 Inferior temporal cortex including fusiform gyrus 19/37 L 60 − 21 − 21 3.40 10 − 45 − 66 − 18 3.54 35 Inferior/middle occipital cortex 19 L/R − 33 − 75 21 3.44 125 42 − 72 − 18 3.12 39 R 42 − 69 − 21 3.71 Cerebellum L − 3 − 78 3.54 256 BA = Brodmann Area. L/R = Left/Right brain. Size: Where no cluster size is reported, responses in this region were part of a larger cluster the most significant voxel of which was in a different anatomical region. Regions in bold indicate those regions about which we had an a priori hypothesis. All other regions are thresholded at P < 0.001, uncorrected. a PFDR < 0.05 indicates regions significant in the Region of Interest analysis in areas with a priori hypothesis. Table options BOLD signal increase in lateral and medial orbitofrontal cortex in the ... Fig. 5. BOLD signal increase in lateral and medial orbitofrontal cortex in the conjunction analysis in the control group. Crosshairs at (48; 24; − 12). Figure options 3.5. Correlation analyses In the patient group a negative correlation between total BIS score and BOLD signal change was observed in right posterior lateral OFC in the reward (42; 33; − 12; P = 0.001, uncorrected) and loss task (33; 18; − 15; PFDR < 0.05). No such correlations were observed in either task in the control group.

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