Thomas Dresler

Emotion regulation model in binge eating disorder and obesity - a systematic review

Deficits in emotion regulation processes are a common and widely used explanation for the development and maintenance of binge eating disorder (BED). It is assumed that BED patients - as they have difficulty regulating their negative emotions - use binge eating to cope with these emotions and to find relief. However, the number of experimental studies investigating this assumption is scarce and the differentiation of obese individuals with and without BED regarding the emotion regulation model is not verified. We reviewed literature for experimental studies investigating the emotion regulation model in obese patients (OB) with and without BED. Our search resulted in 18 experimental studies examining the triggering effect of negative emotions for binge eating or its effects on subsequent relief. We found evidence indicating that negative emotion serves as a trigger for binge eating in the BED group unlike the obese group without BED. Considering the small number of studies, we found evidence for a (short-term) improvement of mood through food intake, irrespective of group.

Integrating Neurobiological Markers of Depression

CONTEXT Although psychiatric disorders are, to date, diagnosed on the basis of behavioral symptoms and course of illness, the interest in neurobiological markers of psychiatric disorders has grown substantially in recent years. However, current classification approaches are mainly based on data from a single biomarker, making it difficult to predict disorders characterized by complex patterns of symptoms. OBJECTIVE To integrate neuroimaging data associated with multiple symptom-related neural processes and demonstrate their utility in the context of depression by deriving a predictive model of brain activation. DESIGN Two groups of participants underwent functional magnetic resonance imaging during 3 tasks probing neural processes relevant to depression. SETTING Participants were recruited from the local population by use of advertisements; participants with depression were inpatients from the Department of Psychiatry, Psychosomatics, and Psychotherapy at the University of Wuerzburg, Wuerzburg, Germany. PARTICIPANTS We matched a sample of 30 medicated, unselected patients with depression by age, sex, smoking status, and handedness with 30 healthy volunteers. MAIN OUTCOME MEASURE Accuracy of single-subject classification based on whole-brain patterns of neural responses from all 3 tasks. RESULTS Integrating data associated with emotional and affective processing substantially increases classification accuracy compared with single classifiers. The predictive model identifies a combination of neural responses to neutral faces, large rewards, and safety cues as nonredundant predictors of depression. Regions of the brain associated with overall classification comprise a complex pattern of areas involved in emotional processing and the analysis of stimulus features. CONCLUSIONS Our method of integrating neuroimaging data associated with multiple, symptom-related neural processes can provide a highly accurate algorithm for classification. The integrated biomarker model shows that data associated with both emotional and reward processing are essential for a highly accurate classification of depression. In the future, large-scale studies will need to be conducted to determine the practical applicability of our algorithm as a biomarker-based diagnostic aid.

Neural response to reward anticipation is modulated by Gray's impulsivity.

According to the Reinforcement Sensitivity Theory (RST), Grays dimension of impulsivity, reflecting human trait reward sensitivity, determines the extent to which stimuli activate the Behavioural Approach System (BAS). The potential neural underpinnings of the BAS, however, remain poorly understood. In the present study, we examined the association between Grays impulsivity as defined by the RST and event-related fMRI BOLD-response to anticipation of reward in twenty healthy human subjects in brain regions previously associated with reward processing. Anticipation of reward during a Monetary Incentive Delay Task elicited activation in key components of the human reward circuitry such as the ventral striatum, the amygdala and the orbitofrontal cortex. Interindividual differences in Grays impulsivity accounted for a significant amount of variance of the reward-related BOLD-response in the ventral striatum and the orbitofrontal cortex. Specifically, higher trait reward sensitivity was associated with increased activation in response to cues indicating potential reward. Extending previous evidence, here we show that variance in functional brain activation during anticipation of reward is attributed to interindividual differences regarding Grays dimension of impulsivity. Thus, trait reward sensitivity contributes to the modulation of responsiveness in major components of the human reward system which thereby display a core property of the BAS. Generally, fostering our understanding of the neural underpinnings of the association of reward-related interindividual differences in affective traits might aid researchers in quest for custom-tailored treatments of psychiatric disorders, further disentangling the complex relationship between personality traits, emotion, and health.

Application of functional near-infrared spectroscopy in psychiatry

Two decades ago, the introduction of functional near-infrared spectroscopy (fNIRS) into the field of neuroscience created new opportunities for investigating neural processes within the human cerebral cortex. Since then, fNIRS has been increasingly used to conduct functional activation studies in different neuropsychiatric disorders, most prominently schizophrenic illnesses, affective disorders and developmental syndromes, such as attention-deficit/hyperactivity disorder as well as normal and pathological aging. This review article provides a comprehensive overview of state of the art fNIRS research in psychiatry covering a wide range of applications, including studies on the phenomenological characterization of psychiatric disorders, descriptions of life-time developmental aspects, treatment effects, and genetic influences on neuroimaging data. Finally, methodological shortcomings as well as current research perspectives and promising future applications of fNIRS in psychiatry are discussed. We conclude that fNIRS is a valid addition to the range of neuroscientific methods available to assess neural mechanisms underlying neuropsychiatric disorders. Future research should particularly focus on expanding the presently used activation paradigms and cortical regions of interest, while additionally fostering technical and methodological advances particularly concerning the identification and removal of extracranial influences on fNIRS data as well as systematic artifact correction. Eventually, fNIRS might be a useful tool in practical psychiatric settings involving both diagnostics and the complementary treatment of psychological disorders using, for example, neurofeedback applications.

Emotional Stroop task: effect of word arousal and subject anxiety on emotional interference

Inconsistent findings regarding the emotional Stroop effect in healthy subjects may be explained by confounding effects of stimulus valence and arousal, as well as individual differences in anxiety. We examined reaction time data in a healthy sample using the emotional Stroop task while carefully matching arousal level of positive and negative words. Independent of valence, emotional relative to neutral words elicited emotional interference, indicating that arousal determines emotional interference. Independent of valence, emotional words were better re-called and recognized than neutral words. Individual differences in state anxiety were associated with emotional interference, that is, emotional interference was enhanced in subjects with high state anxiety. There was no influence of trait anxiety. These findings indicate that word arousal produces emotional interference independent of valence. State anxiety exacerbates interference of emotional words by further biasing attention towards emotionally salient stimuli.

Revise the revised? New dimensions of the neuroanatomical hypothesis of panic disorder

In 2000, Gorman et al. published a widely acknowledged revised version of their 1989 neuroanatomical hypothesis of panic disorder (PD). Herein, a ‘fear network’ was suggested to mediate fear- and anxiety-related responses: panic attacks result from a dysfunctional coordination of ‘upstream’ (cortical) and ‘downstream’ (brainstem) sensory information leading to heightened amygdala activity with subsequent behavioral, autonomic and neuroendocrine activation. Given the emergence of novel imaging methods such as fMRI and the publication of numerous neuroimaging studies regarding PD since 2000, a comprehensive literature search was performed regarding structural (CT, MRI), metabolic (PET, SPECT, MRS) and functional (fMRI, NIRS, EEG) studies on PD, which will be reviewed and critically discussed in relation to the neuroanatomical hypothesis of PD. Recent findings support structural and functional alterations in limbic and cortical structures in PD. Novel insights regarding structural volume increase or reduction, hyper- or hypoactivity, laterality and task-specificity of neural activation patterns emerged. The assumption of a generally hyperactive amygdala in PD seems to apply more to state than trait characteristics of PD, and involvement of further areas in the fear circuit, such as anterior cingulate and insula, is suggested. Furthermore, genetic risk variants have been proposed to partly drive fear network activity. Thus, the present state of knowledge generally supports limbic and cortical prefrontal involvement as originally proposed in the neuroanatomical hypothesis. Some modifications might be suggested regarding a potential extension of the fear circuit, genetic factors shaping neural network activity and neuroanatomically informed clinical subtypes of PD potentially guiding future treatment decisions.

Impairment in episodic and chronic cluster headache

Despite being an excruciating headache, little is known about the burden of cluster headache (CH) regarding its various subtypes. In a multicentre, prospective study, patients with chronic CH (n = 27), with episodic CH in the active (n = 26) and outside the active period (n = 22), migraine patients (n = 24) and healthy controls (n = 31) were included. Epidemiological data, the German version of the Headache Disability Inventory (HDI) and a screening for psychiatric complaints were applied. About 25% of chronic CH patients in our study received invalidity allowance due to CH. HDI scores (total and subscales emotion and function) indicated a severe headache-specific disability (one-way ANOVA: P < 0.01). Patients with chronic and active episodic CH were significantly more affected than patients with inactive CH and migraine. Healthy volunteers were significantly less affected than all headache patients. Symptoms suggestive of psychiatric co-morbidity were found predominantly in chronic CH: depressive symptoms (56%), signs of agoraphobia (33%) and suicidal tendencies (25%) were frequently reported. Patients with chronic and active episodic CH were severely impaired in non-economic and economic domains such as disability, working life and psychiatric complaints. Remarkably, psychiatric co-morbidity was highest in chronic CH. Thus, especially chronic CH warrants special medical and further supportive care.

Association between reward-related activation in the ventral striatum and trait reward sensitivity is moderated by dopamine transporter genotype

The impact of individual differences on human reward processing has been a focus of research in recent years, particularly, as they are associated with a variety of neuropsychiatric diseases including addiction and attention‐deficit/hyperactivity disorder. Studies exploring the neural basis of individual differences in reward sensitivity have consistently implicated the ventral striatum (VS) as a core component of the human reward system. However, the mechanisms of dopaminergic neurotransmission underlying ventral striatal activation as well as trait reward sensitivity remain speculative. We addressed this issue by investigating the triadic interplay between VS reactivity during reward anticipation using functional magnetic resonance imaging, trait reward sensitivity, and dopamine (DA) transporter genotype (40‐bp 3′VNTR of DAT, SLC6A3) affecting synaptic DA neurotransmission. Our results show that DAT variation moderates the association between VS‐reactivity and trait reward sensitivity. Specifically, homozygote carriers of the DAT 10‐repeat allele exhibit a strong positive correlation between reward sensitivity and reward‐related VS activity whereas this relationship is absent in the DAT 9‐repeat allele carriers. We discuss the possibility that this moderation of VS‐trait relation might arise from DAT‐dependent differences in DA availability affecting synaptic plasticity within the VS. Generally, studying the impact of dopaminergic gene variations on the relation between reward‐related brain activity and trait reward sensitivity might facilitate the investigation of complex mechanisms underlying disorders linked to dysregulation of DA neurotransmission. Hum Brain Mapp, 2010.

Differential prefrontal and frontotemporal oxygenation patterns during phonemic and semantic verbal fluency

Movement artifacts are still considered a problematic issue for imaging research on overt language production. This motion-sensitivity can be overcome by functional near-infrared spectroscopy (fNIRS). In the present study, 50 healthy subjects performed a combined phonemic and semantic overt verbal fluency task while frontal and temporal cortex oxygenation was recorded using multi-channel fNIRS. Results showed a partial dissociation for phonemic and semantic word generation with equally increased oxygenation in frontotemporal cortices for both types of tasks whereas anterior and superior prefrontal areas were exclusively activated during phonemic fluency. Also, a general left-lateralization was found being more pronounced during semantic processing. These findings line up with earlier imaging and lesion studies emphasizing a crucial role of the temporal lobe for semantic word production, whereas phonemic processing seems to depend on intact frontal lobe function.

Functional Amygdala-Hippocampus Connectivity During Anticipation of Aversive Events is Associated with Gray's Trait “Sensitivity to Punishment”

BACKGROUND The reinforcement sensitivity theory postulates a behavioral inhibition system that modulates reaction to stimuli indicating aversive events. Grays dimension of anxiety, reflecting human trait sensitivity to aversive events, determines the extent to which stimuli activate the behavioral inhibition system. Although structural brain imaging has previously identified the amygdala and the hippocampus as two major components related to the behavioral inhibition system, the functional dynamics of the responses in these structures remain unclear. METHODS In this study, we examined the event-related functional magnetic resonance imaging blood oxygen level-dependent response in the hippocampus and amygdala as well as the functional connectivity of the two regions during anticipation of monetary loss in 45 healthy human subjects. RESULTS Anticipation of loss elicited activation in the hippocampus as well as in the amygdala. Additionally, substantial functional connectivity between the two areas was observed. Furthermore, this functional connectivity was significantly correlated with individual differences in Grays trait sensitivity to aversive events. Specifically, higher trait sensitivity to aversive events was associated with increased functional connectivity following cues indicating potential loss. CONCLUSIONS In summary, we show that individual differences regarding Grays trait sensitivity to aversive events as defined by the reinforcement sensitivity theory are associated with the neural dynamics of the amygdala-hippocampal circuit during anticipation of aversive events. In particular, evidence is provided for a relationship between functional brain imaging data and a psychometric approach specifically measuring Grays trait sensitivity to aversive events, thereby potentially identifying the neural substrate of the behavioral inhibition system.