Björn Enzi

Is Our Self Nothing but Reward? Neuronal Overlap and Distinction between Reward and Personal Relevance and Its Relation to Human Personality

Background The attribution of personal relevance, i.e. relating internal and external stimuli to establish a sense of belonging, is a common phenomenon in daily life. Although previous research demonstrated a relationship between reward and personal relevance, their exact neuronal relationship including the impact of personality traits remains unclear. Methodology/Principal Findings Using functional magnetic resonance imaging, we applied an experimental paradigm that allowed us to explore the neural response evoked by reward and the attribution of personal relevance separately. We observed different brain regions previously reported to be active during reward and personal relevance, including the bilateral caudate nucleus and the pregenual anterior cingulate cortex (PACC). Additional analysis revealed activations in the right and left insula specific for the attribution of personal relevance. Furthermore, our results demonstrate a negative correlation between signal changes in both the PACC and the left anterior insula during the attribution of low personal relevance and the personality dimension novelty seeking. Conclusion/Significance While a set of subcortical and cortical regions including the PACC is commonly involved in reward and personal relevance, other regions like the bilateral anterior insula were recruited specifically during personal relevance. Based on our correlation between novelty seeking and signal changes in both regions during personal relevance, we assume that the neuronal response to personally relevant stimuli is dependent on the personality trait novelty seeking.

The narcissistic self and its psychological and neural correlates: An exploratory fMRI study

BACKGROUND The concept of narcissism has been much researched in psychoanalysis and especially in self psychology. One of the hallmarks of narcissism is altered emotion, including decreased affective resonance (e.g. empathy) with others, the neural underpinnings of which remain unclear. The aim of our exploratory study was to investigate the psychological and neural correlates of empathy in two groups of healthy subjects with high and low narcissistic personality trait. We hypothesized that high narcissistic subjects would show a differential activity pattern in regions such as the anterior insula that are typically associated with empathy. METHOD A sample of 34 non-clinical subjects was divided into high (n=11) and low (n=11) narcissistic groups according to the 66th and 33rd percentiles of their scores on the Narcissism Inventory (NI). Combining the psychological, behavioral and neuronal [i.e. functional magnetic resonance imaging (fMRI)] measurements of empathy, we compared the high and low narcissistic groups of subjects. RESULTS High narcissistic subjects showed higher scores on the Symptom Checklist-90 - Revised (SCL-90-R) and the 20-item Toronto Alexithymia Scale (TAS-20) when compared to low narcissistic subjects. High narcissistic subjects also showed significantly decreased deactivation during empathy, especially in the right anterior insula. CONCLUSIONS Psychological and neuroimaging data indicate respectively higher degrees of alexithymia and lower deactivation during empathy in the insula in high narcissistic subjects. Taken together, our preliminary findings demonstrate, for the first time, psychological and neuronal correlates of narcissism in non-clinical subjects. This might stipulate both novel psychodynamic conceptualization and future psychological-neuronal investigation of narcissism.

Involvement of glutamate in rest-stimulus interaction between perigenual and supragenual anterior cingulate cortex: a combined fMRI-MRS study.

The brain shows a high degree of activity at rest. The significance of this activity has come increasingly into focus. At present, however, the interaction between this activity and stimulus‐induced activity is not well defined. The interaction between a task‐negative (perigenual anterior cingulate cortex, pgACC) and task‐positive (supragenual anterior cingulate cortex, sgACC) region during a simple task was thus investigated using a combination of fMRI and MRS. Negative BOLD responses in the pgACC were found to show a unidirectional effective connectivity with task‐induced positive BOLD responses in the sgACC. This connectivity was shown to be related specifically with glutamate levels in the pgACC. These results demonstrate an interaction between deactivation from resting‐state and resting‐state glutamate levels in a task‐negative region (pgACC), and task‐induced activity in a task‐positive region (sgACC). This provides insight into the neuronal and biochemical mechanisms by means of which the resting state activity of the brain potentially impacts upon subsequent stimulus‐induced activity. Hum Brain Mapp, 2011.

Glutamate modulates resting state activity in the perigenual anterior cingulate cortex - A combined fMRI-MRS study

The perigenual anterior cingulate cortex (PACC) shows high resting state activity and is considered part of the default-mode network (DMN). However, the biochemical underpinnings of the PACCs high resting state activity remain unclear. While animal-based evidence points toward a role for the glutamatergic system, the modulation of the resting state activity level by itself as distinguished from stimulus-induced activity remains to be shown in humans. Using combined fMRI-MRS in healthy subjects, we here demonstrate that the PACC resting state concentration of glutamate is directly related to the level of resting state activity in the same region. In contrast, no such relationship could be detected during the anticipation of reward and punishment, nor in an independent control region (the left anterior insula). Taken together, our findings demonstrate for the first time the modulation of the PACC resting state activity level by the concentration of glutamate in the same regions. This contributes to a better understanding of the biochemical basis for the brains resting state activity as well as providing some clues regarding its apparent pathological upregulation in psychiatric disorders like the major depressive disorder.

Altered ventral striatal activation during reward and punishment processing in premanifest Huntington's disease: a functional magnetic resonance study.

Recent research using various neuroimaging methods revealed the crucial role of the striatum concerning the neuropathology of Huntingtons disease. Degenerative changes located in the basal ganglia are already observable in premanifest stages of Huntingtons disease (pre-HD), i.e., before the onset of manifest motor symptoms. Although the impact of the striatum on reward and punishment processing is well-established in healthy subjects, these processes have not been investigated in manifest and premanifest HD subjects using functional magnetic resonance imaging (fMRI) so far. We used the Monetary Incentive Delay Task to investigate valence discrimination in terms of rewarding and punishing cues in 30 pre-HD and 15 healthy subjects. According to the probability of disease onset within the next 5 years, pre-HD subjects were categorized as either near to motor symptom onset (pre-HD(near); 9.9 [±2.91] years to onset) or far from manifest disease onset (pre-HD(far); 23.49 [±5.99] years to onset). Compared to pre-HD(far) and healthy subjects, pre-HD(near) subjects showed a disturbed neuronal differentiation between reward and control anticipation located in the left ventral striatum. In contrast to pre-HD(far) and healthy subjects, no significant ventral striatal discrimination between punishing and control cues was detected in pre-HD(near) subjects. In the present study, we demonstrated for the first time significant differences in valence discrimination in pre-HD(near) subjects compared to pre-HD(far) subjects and healthy controls. Altered reward and punishment processing could therefore reflect a motivational deficit that may contribute to the pathogenesis of Huntingtons disease.

Altered brain activity during emotional empathy in somatoform disorder

Somatoform disorder patients suffer from impaired emotion recognition and other emotional deficits. Emotional empathy refers to the understanding and sharing of emotions of others in social contexts. It is likely that the emotional deficits of somatoform disorder patients are linked to disturbed empathic abilities; however, little is known so far about empathic deficits of somatoform patients and the underlying neural mechanisms. We used fMRI and an empathy paradigm to investigate 20 somatoform disorder patients and 20 healthy controls. The empathy paradigm contained facial pictures expressing anger, joy, disgust, and a neutral emotional state; a control condition contained unrecognizable stimuli. In addition, questionnaires testing for somatization, alexithymia, depression, empathy, and emotion recognition were applied. Behavioral results confirmed impaired emotion recognition in somatoform disorder and indicated a rather distinct pattern of empathic deficits of somatoform patients with specific difficulties in “empathic distress.” In addition, somatoform patients revealed brain areas with diminished activity in the contrasts “all emotions”–“control,” “anger”–“control,” and “joy”–“control,” whereas we did not find brain areas with altered activity in the contrasts “disgust”–“control” and “neutral”–“control.” Significant clusters with less activity in somatoform patients included the bilateral parahippocampal gyrus, the left amygdala, the left postcentral gyrus, the left superior temporal gyrus, the left posterior insula, and the bilateral cerebellum. These findings indicate that disturbed emotional empathy of somatoform disorder patients is linked to impaired emotion recognition and abnormal activity of brain regions responsible for emotional evaluation, emotional memory, and emotion generation. Hum Brain Mapp, 2012.

Multimodal psychodynamic psychotherapy induces normalization of reward related activity in somatoform disorder

Abstract Objectives. Somatoform disorder patients demonstrate a disturbance in the balance between internal and external information processing, with a decreased focus on external stimulus processing. We investigated brain activity of somatoform disorder patients, during the processing of rewarding external events, paying particular attention to the effects of inpatient multimodal psychodynamic psychotherapy. Methods. Using fMRI, we applied a reward task that required fast reactions to a target stimulus in order to obtain monetary rewards; a control condition contained responses without the opportunity to gain rewards. Twenty acute somatoform disorder patients were compared with twenty age-matched healthy controls. In addition, 15 patients underwent a second scanning session after participation in multimodal psychodynamic psychotherapy. Results. Acute patients showed diminished hemodynamic differentiation between rewarding and non rewarding events in four regions, including the left postcentral gyrus and the right ventroposterior thalamus. After multimodal psychodynamic psychotherapy, both regions showed a significant normalization of neuronal differentiation. Conclusion. Our results suggest that diminished responsiveness of brain regions involved in the processing of external stimuli underlies the disturbed balance of internal and external processing of somatoform disorder patients. By providing new approaches to cope with distressing events, multimodal psychodynamic psychotherapy led to decreased symptoms and normalization of neuronal activity.

Changes in brain activity of somatoform disorder patients during emotional empathy after multimodal psychodynamic psychotherapy

Somatoform disorder patients show a variety of emotional disturbances including impaired emotion recognition and increased empathic distress. In a previous paper, our group showed that several brain regions involved in emotional processing, such as the parahippocampal gyrus and other regions, were less activated in pre-treatment somatoform disorder patients (compared to healthy controls) during an empathy task. Since the parahippocampal gyrus is involved in emotional memory, its decreased activation might reflect the repression of emotional memories (which—according to psychoanalytical concepts—plays an important role in somatoform disorder). Psychodynamic psychotherapy aims at increasing the understanding of emotional conflicts as well as uncovering repressed emotions. We were interested, whether brain activity in the parahippocampal gyrus normalized after (inpatient) multimodal psychodynamic psychotherapy. Using fMRI, subjects were scanned while they shared the emotional states of presented facial stimuli expressing anger, disgust, joy, and a neutral expression; distorted stimuli with unrecognizable content served as control condition. 15 somatoform disorder patients were scanned twice, pre and post multimodal psychodynamic psychotherapy; in addition, 15 age-matched healthy control subjects were investigated. Effects of psychotherapy on hemodynamic responses were analyzed implementing two approaches: (1) an a priori region of interest approach and (2) a voxelwise whole brain analysis. Both analyses revealed increased hemodynamic responses in the left and right parahippocampal gyrus (and other regions) after multimodal psychotherapy in the contrast “empathy with anger”—“control.” Our results are in line with psychoanalytical concepts about somatoform disorder. They suggest the parahippocampal gyrus is crucially involved in the neurobiological mechanisms which underly the emotional deficits of somatoform disorder patients.

An eye for an eye? Neural correlates of retribution and forgiveness.

Humans have evolved strong preferences for equity and fairness. Neuroimaging studies suggest that punishing unfairness is associated with the activation of a neural network comprising the anterior cingulate cortex, anterior insula, the ventral striatum, and the dorsolateral prefrontal cortex (DLPFC). Here, we report the neuronal correlates of retribution and “forgiveness” in a scenario, in which individuals first acted as a recipient in an Ultimatum Game, and subsequently assumed the position of a proposer in a Dictator Game played against the same opponents as in the Ultimatum Game. Most subjects responded in a tit-for-tat fashion, which was accompanied by activation of the ventral striatum, corroborating previous findings that punishing unfair behaviour has a rewarding connotation. Subjects distinguished between the human opponent and computer condition by activation of the ventromedial PFC in the human condition, indicative of mentalising. A substantial number of subjects did not retaliate. Neurally, this “forgiveness” behaviour was associated with the activation of the right (and to a lesser degree left) DLPFC, a region that serves as a cognitive control region and thus may be involved in inhibiting emotional responses against unfairness.

Personality Functioning and the Cortical Midline Structures - An Exploratory fMRI Study

Objective Recent neuroscience studies explored the neuronal mechanisms underlying our sense of self. Thereby the cortical midline structures and their anterior and posterior regions have been shown to be central. What remains unclear though is how both, self and cortical midline structures, are related to the identity of the self which is of central importance in especially personality disorders. Methods Conducting an exploratory study with a dimensional approach, we here compared subjects with high and low level of personality functioning and identity integration as measured in a standardized way in fMRI during both, emotion- and reward-related tasks. Results Low levels of personality functioning and identity integration were predicted by significantly decreased degrees of deactivation in the anterior and posterior cortical midline structures. Conclusions Though exploratory our results show for the first time direct relationship between cortical midline structures and personality functioning in terms of identity integration. This does not only contribute to our understanding of the neuronal mechanism underlying self and identity but carries also major implications for the treatment of patients with personality disorders.