Marte Swart

Dealing with Feelings: Characterization of Trait Alexithymia on Emotion Regulation Strategies and Cognitive-Emotional Processing

Background Alexithymia, or “no words for feelings”, is a personality trait which is associated with difficulties in emotion recognition and regulation. It is unknown whether this deficit is due primarily to regulation, perception, or mentalizing of emotions. In order to shed light on the core deficit, we tested our subjects on a wide range of emotional tasks. We expected the high alexithymics to underperform on all tasks. Method Two groups of healthy individuals, high and low scoring on the cognitive component of the Bermond-Vorst Alexithymia Questionnaire, completed questionnaires of emotion regulation and performed several emotion processing tasks including a micro expression recognition task, recognition of emotional prosody and semantics in spoken sentences, an emotional and identity learning task and a conflicting beliefs and emotions task (emotional mentalizing). Results The two groups differed on the Emotion Regulation Questionnaire, Berkeley Expressivity Questionnaire and Empathy Quotient. Specifically, the Emotion Regulation Quotient showed that alexithymic individuals used more suppressive and less reappraisal strategies. On the behavioral tasks, as expected, alexithymics performed worse on recognition of micro expressions and emotional mentalizing. Surprisingly, groups did not differ on tasks of emotional semantics and prosody and associative emotional-learning. Conclusion Individuals scoring high on the cognitive component of alexithymia are more prone to suppressive emotion regulation strategies rather than reappraisal strategies. Regarding emotional information processing, alexithymia is associated with reduced performance on measures of early processing as well as higher order mentalizing. However, difficulties in the processing of emotional language were not a core deficit in our alexithymic group.

Sex Differences in Neural Activation to Facial Expressions Denoting Contempt and Disgust

The facial expression of contempt has been regarded to communicate feelings of moral superiority. Contempt is an emotion that is closely related to disgust, but in contrast to disgust, contempt is inherently interpersonal and hierarchical. The aim of this study was twofold. First, to investigate the hypothesis of preferential amygdala responses to contempt expressions versus disgust. Second, to investigate whether, at a neural level, men would respond stronger to biological signals of interpersonal superiority (e.g., contempt) than women. We performed an experiment using functional magnetic resonance imaging (fMRI), in which participants watched facial expressions of contempt and disgust in addition to neutral expressions. The faces were presented as distractors in an oddball task in which participants had to react to one target face. Facial expressions of contempt and disgust activated a network of brain regions, including prefrontal areas (superior, middle and medial prefrontal gyrus), anterior cingulate, insula, amygdala, parietal cortex, fusiform gyrus, occipital cortex, putamen and thalamus. Contemptuous faces did not elicit stronger amygdala activation than did disgusted expressions. To limit the number of statistical comparisons, we confined our analyses of sex differences to the frontal and temporal lobes. Men displayed stronger brain activation than women to facial expressions of contempt in the medial frontal gyrus, inferior frontal gyrus, and superior temporal gyrus. Conversely, women showed stronger neural responses than men to facial expressions of disgust. In addition, the effect of stimulus sex differed for men versus women. Specifically, women showed stronger responses to male contemptuous faces (as compared to female expressions), in the insula and middle frontal gyrus. Contempt has been conceptualized as signaling perceived moral violations of social hierarchy, whereas disgust would signal violations of physical purity. Thus, our results suggest a neural basis for sex differences in moral sensitivity regarding hierarchy on the one hand and physical purity on the other.

Brain imaging, genetics and emotion

This paper reviews the published evidence on genetically driven variation in neurotransmitter function and brain circuits involved in emotion. Several studies point to a role of the serotonin transporter promoter polymorphism in amygdala activation during emotion perception. We also discuss other polymorphisms (e.g. the COMT val158met polymorphism, tryptophan hydroxylase-2 -703 G/T) and putative effects on affective processing in cortical and limbic regions. A different line of research concerns studies with genetic disorders. Although at a less fine-grained level, studies with individuals with aneuploidies of the X chromosome (Turner syndrome and Klinefelter syndrome), who display impairments in emotion processing, have resulted in new insights and hypotheses with regard to X chromosomal influences on brain systems supporting cognition and emotion. These have also implicated a key role for the amygdala. Integration of the emerging evidence, suggests that the study of polymorphisms using brain imaging can potentially elucidate biological pathways and mechanisms contributing to individual differences in brain circuits that may bias behavior and affect risk for psychiatric illness.

When Broca Goes Uninformed: Reduced Information Flow to Broca’s Area in Schizophrenia Patients With Auditory Hallucinations

Auditory-verbal hallucinations (AVHs) are frequently associated with activation of the left superior temporal gyrus (including Wernickes area), left inferior frontal gyrus (including Brocas area), and the right hemisphere homologs of both areas. It has been hypothesized that disconnectivity of both interhemispheric transfer and frontal and temporal areas may underlie hallucinations in schizophrenia. We investigated reduced information flow in this circuit for the first time using dynamic causal modeling, which allows for directional inference. A group of healthy subjects and 2 groups of schizophrenia patients-with and without AVH-performed a task requiring inner speech processing during functional brain scanning. We employed connectivity models between left hemispheric speech-processing areas and their right hemispheric homologs. Bayesian model averaging was used to estimate the connectivity strengths and evaluate group differences. Patients with AVH showed significantly reduced connectivity from Wernickes to Brocas area (97% certainty) and a trend toward a reduction in connectivity from homologs of Brocas and Wernickes areas to Brocas area (93% and 94% certainty). The connectivity magnitude in patients without hallucinations was found to be intermediate. Our results point toward a reduced input from temporal to frontal language areas in schizophrenia patients with AVH, suggesting that Brocas activity may be less constrained by perceptual information received from the temporal cortex. In addition, a lack of synchronization between Broca and its homolog may lead to the erroneous interpretation of emotional speech activity from the right hemisphere as coming from an external source.

Reduced Connectivity in the Self-Processing Network of Schizophrenia Patients with Poor Insight

Lack of insight (unawareness of illness) is a common and clinically relevant feature of schizophrenia. Reduced levels of self-referential processing have been proposed as a mechanism underlying poor insight. The default mode network (DMN) has been implicated as a key node in the circuit for self-referential processing. We hypothesized that during resting state the DMN network would show decreased connectivity in schizophrenia patients with poor insight compared to patients with good insight. Patients with schizophrenia were recruited from mental health care centers in the north of the Netherlands and categorized in groups having good insight (n = 25) or poor insight (n = 19). All subjects underwent a resting state fMRI scan. A healthy control group (n = 30) was used as a reference. Functional connectivity of the anterior and posterior part of the DMN, identified using Independent Component Analysis, was compared between groups. Patients with poor insight showed lower connectivity of the ACC within the anterior DMN component and precuneus within the posterior DMN component compared to patients with good insight. Connectivity between the anterior and posterior part of the DMN was lower in patients than controls, and qualitatively different between the good and poor insight patient groups. As predicted, subjects with poor insight in psychosis showed decreased connectivity in DMN regions implicated in self-referential processing, although this concerned only part of the network. This finding is compatible with theories implying a role of reduced self-referential processing as a mechanism contributing to poor insight.

COMT Val158Met polymorphism, verbalizing of emotion and activation of affective brain systems

Genetic variation in the catechol-O-methyltransferase (COMT) Val158Met polymorphism has been shown to influence performance on cognitive and emotional tasks. Specifically, it has been suggested that the Met allele might be less advantageous than the Val allele with respect to emotional processing. This study addresses the question whether the presence of the Met allele is directly related to both lower emotional verbalizing proficiency and differences in brain activation during emotional processing. Specifically, we investigated whether COMT genotype would be associated with differences in activation in cortical midline structures during valence evaluation of words. Forty participants ranging from low to high on the verbalizing subscale of the Bermond-Vorst Alexithymia Questionnaire (BVAQ) were genotyped for the COMT Val158Met polymorphism. During fMRI, they evaluated the valence of emotional words. Met homozygotes reported more difficulties in verbalizing their feelings. In addition, the Met allele was associated with attenuated brain activation in posterior cingulate gyrus and precuneus during valence evaluation. We conclude that the Met allele modulates neural activation in regions associated with emotional awareness. Our findings may contribute to understanding the neural correlates of susceptibility for affective disorders.

Neural correlates of emotion regulation in patients with schizophrenia and non-affected siblings.

Background Patients with schizophrenia often experience problems regulating their emotions. Non-affected relatives show similar difficulties, although to a lesser extent, and the neural basis of such difficulties remains to be elucidated. In the current paper we investigated whether schizophrenia patients, non-affected siblings and healthy controls (HC) exhibit differences in brain activation during emotion regulation. Methods All subjects (n = 20 per group) performed an emotion regulation task while they were in an fMRI scanner. The task contained two experimental conditions for the down-regulation of emotions (reappraise and suppress), in which IAPS pictures were used to generate a negative affect. We also assessed whether the groups differed in emotion regulation strategies used in daily life by means of the emotion regulation questionnaire (ERQ). Results Though the overall negative affect was higher for patients as well as for siblings compared to HC for all conditions, all groups reported decreased negative affect after both regulation conditions. Nonetheless, neuroimaging results showed hypoactivation relative to HC in VLPFC, insula, middle temporal gyrus, caudate and thalamus for patients when reappraising negative pictures. In siblings, the same pattern was evident as in patients, but only in cortical areas. Conclusions Given that all groups performed similarly on the emotion regulation task, but differed in overall negative affect ratings and brain activation, our findings suggest reduced levels of emotion regulation processing in neural circuits in patients with schizophrenia. Notably, this also holds for siblings, albeit to a lesser extent, indicating that it may be part and parcel of a vulnerability for psychosis.

Altered resting state connectivity of the default mode network in alexithymia

Alexithymia is a trait characterized by a diminished capacity to describe and distinguish emotions and to fantasize; it is associated with reduced introspection and problems in emotion processing. The default mode network (DMN) is a network of brain areas that is normally active during rest and involved in emotion processing and self-referential mental activity, including introspection. We hypothesized that connectivity of the DMN might be altered in alexithymia. Twenty alexithymic and 18 non-alexithymic healthy volunteers underwent a resting state fMRI scan. Independent component analysis was used to identify the DMN. Differences in connectivity strength were compared between groups. Within the DMN, alexithymic participants showed lower connectivity within areas of the DMN (medial frontal and temporal areas) as compared to non-alexithymic participants. In contrast, connectivity in the high-alexithymic participants was higher for the sensorimotor cortex, occipital areas and right lateral frontal cortex than in the low-alexithymic participants. These results suggest a diminished connectivity within the DMN of alexithymic participants, in brain areas that may also be involved in emotional awareness and self-referential processing. On the other hand, alexithymia was associated with stronger functional connections of the DMN with brain areas involved in sensory input and control of emotion.

Alexithymia influences brain activation during emotion perception but not regulation

Alexithymia is a psychological construct that can be divided into a cognitive and affective dimension. The cognitive dimension is characterized by difficulties in identifying, verbalizing and analysing feelings. The affective dimension comprises reduced levels of emotional experience and imagination. Alexithymia is widely regarded to arise from an impairment of emotion regulation. This is the first functional magnetic resonance imaging (fMRI) study to critically evaluate this by investigating the neural correlates of emotion regulation as a function of alexithymia levels. The aim of the current study was to investigate the neural correlates underlying the two alexithymia dimensions during emotion perception and emotion regulation. Using fMRI, we scanned 51 healthy subjects while viewing, reappraising or suppressing negative emotional pictures. The results support the idea that cognitive alexithymia, but not affective alexithymia, is associated with lower activation in emotional attention and recognition networks during emotion perception. However, in contrast with several theories, no alexithymia-related differences were found during emotion regulation (neither reappraisal nor suppression). These findings suggest that alexithymia may result from an early emotion processing deficit rather than compromised frontal circuits subserving higher-order emotion regulation processes.

Variation of the gene coding for DARPP-32 (PPP1R1B) and brain connectivity during associative emotional learning

Associative emotional learning, which is important for the social emotional functioning of individuals and is often impaired in psychiatric illnesses, is in part mediated by dopamine and glutamate pathways in the brain. The protein DARPP-32 is involved in the regulation of dopaminergic and glutaminergic signaling. Consequently, it has been suggested that the haplotypic variants of the gene PPP1R1B that encodes DARPP-32 are associated with working memory and emotion processing. We hypothesized that PPP1R1B should have a significant influence on the network of brain regions involved in associative emotional learning that are rich in DARPP-32, namely the striatum, prefrontal cortex (comprising the medial frontal gyrus and inferior frontal gyrus (IFG)), amygdala and parahippocampal gyrus (PHG). Dynamic causal models were applied to functional MRI data to investigate how brain connectivity during an associative emotional learning task is affected by different single-nucleotide polymorphisms (SNPs) of PPP1R1B: rs879606, rs907094 and rs3764352. Compared to heterozygotes, homozygotes with GTA alleles displayed increased intrinsic connectivity between the IFG and PHG, as well as increased excitability of the PHG for negative emotional stimuli. We have also elucidated the directionality of these genetic influences. Our data suggest that homozygotes with GTA alleles involve stronger functional connections between brain areas in order to maintain activation of these regions. Homozygotes might engage a greater degree of motivational learning and integration of information to perform the emotional learning task correctly. We conclude that PPP1R1B is associated with the neural network involved in associative emotional learning.