Reward Processing Research Articles

Alterations of interhemispheric functional homotopic connectivity and corpus callosum microstructure in bulimia nervosa.

Accumulating evidence indicates maladaptive neural information interactions between different brain regions underlie bulimia nervosa (BN). However, little is known about the alterations in interhemispheric communication of BN, which is facilitated by the corpus callosum (CC), the major commissural fiber connecting the two hemispheres. To shed light on the interhemispheric communications in BN, the present study aims to explore alterations of interhemispheric homotopic functional connectivity and the CC microstructure in BN. Based on magnetic resonance imaging (MRI) data collected from 42 BN patients and 38 healthy controls (HCs), the group differences of voxel-mirrored homotopic connectivity (VMHC) index and CC white matter microstructure were compared. Then brain regions with significant group differences in VMHC were selected as seeds for subsequent functional connectivity (FC) analysis. Seed-based fiber tracking and correlation analysis were used to analyze the relationship between VMHC and CC changes. And correlation analysis was used to reveal the correlation between abnormal imaging variables and the clinical features of BN. Compared with HCs, the BN group showed decreased fractional anisotropy (FA) in middle part of CC (CCMid) and increased VMHC in bilateral orbitofrontal cortex (OFC) and middle temporal gyrus (MTG) [false discovery rate (FDR) correction with a corrected threshold of P<0.05]. Subsequent FC analyses indicated increased FC between left OFC and right OFC, bilateral MTG, left middle occipital gyrus and right precuneus (PCUN); between right OFC and left cerebellum crus II and right PCUN; and between left MTG and right inferior temporal gyrus, right cerebellum lobule VI and right medial superior frontal gyrus (FDR correction with a corrected threshold of P<0.05). The VMHC values of OFC and MTG showed no correlations with FA values of the CCMid and the white fibers between the bilateral OFC and MTG were not through the CCMid. In addition, several regions with abnormal FC had a potential correlation trend with abnormal eating behaviors in BN patients (P<0.05, uncorrected). Aberrant interhemispheric homotopic functional connectivity and CC microstructure were observed in BN, and they may be independent of each other. Regions with aberrant interhemispheric homotopic functional connectivity showed hyperconnectivity with regions related to reward processing, body shape perception, and self-reference.

A Comprehensive Review on the Role of Obesity in Functional Cognition (Part I): Epidemiology and Alternations in Brain Structure

The condition of obesity, which is defined by an excessive amount of adipose tissue, is being increasingly acknowledged as having significant consequences for the structure and functioning of the brain. Numerous studies have demonstrated that obesity is linked to significant modifications in the structure of the brain, encompassing variations in the volume of gray matter, the integrity of white matter, and modifications in particular brain regions responsible for regulating appetite and cognitive control. For example, research employing neuroimaging methodologies such as magnetic resonance imaging has consistently indicated that individuals with obesity frequently display diminished gray matter volume in areas such as the prefrontal cortex, which is known to play a critical role in processes such as decision-making and impulse control. Furthermore, there have been observations of white matter abnormalities that impact the interconnection among brain regions responsible for hunger regulation and reward processing. These abnormalities may potentially play a role in the development of overeating tendencies and compromised self-control. The aforementioned alterations in structure are not solely connected to obesity, but are also correlated with cognitive deficits, namely in domains pertaining to memory, attention, and executive functioning. Gaining a comprehensive understanding of the complex correlation between obesity and brain structure is of utmost importance, as it provides valuable insights into the neurological foundations of cognitive impairments in individuals affected by obesity. Moreover, this knowledge serves as a basis for the creation of specific interventions aimed at alleviating the cognitive repercussions associated with this widespread public health issue.

Depression symptoms and cognition in multiple sclerosis: Longitudinal evidence of a specific link to executive control

Background: Depression symptoms are prevalent in multiple sclerosis (MS) and associated with poorer cognition in cross-sectional studies; it is unknown whether changes in depression symptoms track with cognitive changes longitudinally. Objective: Investigate whether changes in depression symptoms correspond with cognitive changes over time in MS, and identify specific cognitive functions related to depression symptoms. Method: Persons with early relapse-onset MS (n = 165) completed a depression questionnaire (Beck Depression Inventory FastScreen) and tests of cognitive speed, executive control, and memory at baseline and 3-year follow-up. One-way ANOVAs assessed differences in cognitive change across participants with worsened, stable, or improved depression symptoms from baseline to year 3. Results: Change in depression symptoms was related to change in executive control (p = 0.001, ηp2 = 0.08; worsened mood with worsened executive control; improved mood with improved executive control), even when adjusting for cognitive speed (p = 0.002, ηp2 = 0.08). There were no links to cognitive speed (p = 0.826) or memory (p = 0.243). Regarding individual depression symptoms, executive control was related to loss of pleasure and suicidal thoughts. Conclusions: Executive control tracks with depression symptoms, raising hope that management of mood may improve executive control. The specific link between executive control and anhedonia implicates dysfunctional reward processing as a key component of MS depression.

Testing anxiety and reward processing in anorexia nervosa as predictors of longitudinal clinical outcomes

Anorexia nervosa (AN) is a psychiatric disorder with a tenuous longitudinal course marked by a high risk of relapse. Previous studies suggest that aberrant threat perception and reward processing operate in many with AN, and may produce obstacles to treatment engagement; therefore, these could potentially represent predictors for longitudinal clinical outcomes. In this study, anxiety and reward symptoms, behaviors, and neural circuit connectivity were measured in intensively treated AN-restrictive subtype patients (n = 33) and healthy controls (n = 31). Participants underwent an fMRI experiment using a monetary reward task in combination with either overlapping individually tailored anxiety-provoking words or neutral words. Behavioral/psychometric measures consisted of reaction times on the monetary reward task and self-ratings on anxiety symptoms at study entry. We tested multimodal, multivariate models based on neural, behavioral, and psychometric measures of reward and anxiety to predict physiological (Body Mass Index; BMI) and psychological (eating disorder symptom severity) longitudinal outcomes in AN over six months. Our results indicated that higher anxiety symptom psychometric scores significantly predicted BMI reductions at follow-up. Untreated anxiety after intensive treatment could put individuals with AN at heightened risk for weight loss. This represents a potentially modifiable risk factor that could be targeted more aggressively to help reduce the chance of future clinical worsening.

Feedback processing in cognitive and motor tasks: A meta-analysis on the feedback-related negativity.

For motor learning, the processing of behavioral outcomes is of high significance. The feedback-related negativity (FRN) is an event-related potential, which is often described as a correlate of the reward prediction error in reinforcement learning. The number of studies examining the FRN in motor tasks is increasing. This meta-analysis summarizes the component in the motor domain and compares it to the cognitive domain. Therefore, a data set of a previous meta-analysis in the cognitive domain that comprised 47 studies was reanalyzed and compared to additional 25 studies of the motor domain. Further, a moderator analysis for the studies in the motor domain was conducted. The FRN amplitude was higher in the motor domain than in the cognitive domain. This might be related to a higher task complexity and a higher feedback ambiguity of motor tasks. The FRN latency was shorter in the motor domain than in the cognitive domain. Given that sensory information can be used as an external feedback predictor prior to the presentation of the final feedback, reward processing in the motor domain may have been faster and reduced the FRN latency. The moderator variable analysis revealed that the feedback modality influenced the FRN latency, with shorter FRN latencies after bimodal than after visual feedback. Processing of outcome feedback seems to share basic principles in both domains; however, differences exist and should be considered in FRN studies. Future research is motivated to scrutinize the effects of bimodal feedback and other moderators within the motor domain.

Home care nurses lived experiences of caring relationships with older adults: A phenomenological study.

This paper describes registered nurses' lived experiences of caring relationships in the context of homecare provision for older adults living in Denmark. With the growing ageing population throughout Europe, more older adults will require complex care solutions within already overburdened care systems. This development places demands on the competencies and organisation of homecare nurses, as they become key players in healthcare systems. Fostering caring relationships in homecare is a rewarding and valuable process that enhances the holistic and humanising aspects of caring for older adults. For a caring relationship to be truly caring, we must understand not only the subjective experience of such a relationship but also how it is experienced in relation to and shared with others. This study aimed to describe the essential meaning of the phenomenon of caring relationships in homecare for older adults based on the lived experiences of homecare nurses. Registered nurses working in homecare for older adults were interviewed, and a phenomenological analysis was conducted according to the methodological principles of the reflective lifeworld research approach. The essential meaning of the phenomenon is described as creating an existential and embodied space in which each patient's world is the foundation of caring. The constituents are as follows: caring for the whole person, a sense of 'at-homeness' through trusting 'the other', experiencing continuity as caring and prioritising the time to care. Caring competence in homecare for older adults relies on a nurse's ability to intertwine physical and existential care needs and articulate them in their daily work. A focus on the phenomenon of caring relationships brings value to and adds an extra layer to the discussion on caring competence.

Feedback negativity and feedback-related P3 in individuals at risk for depression: Comparing surface potentials and current source densities.

Blunted responses to reward feedback have been linked to major depressive disorder (MDD) and depression risk. Using a monetary incentive delay task (win, loss, break-even), we investigated the impact of family risk for depression and lifetime history of MDD and anxiety disorder with 72-channel electroencephalograms (EEG) recorded from 29 high-risk and 32 low-risk individuals (15-58 years, 30 male). Linked-mastoid surface potentials (ERPs) and their corresponding reference-free current source densities (CSDs) were quantified by temporal principal components analysis (PCA). Each PCA solution revealed a midfrontal feedback negativity (FN; peak around 310 ms) and a posterior feedback-P3 (fb-P3; 380 ms) as two distinct reward processing stages. Unbiased permutation tests and multilevel modeling of component scores revealed greater FN to loss than win and neutral for all stratification groups, confirming FN sensitivity to valence. Likewise, all groups had greater fb-P3 to win and loss than neutral, confirming that fb-P3 indexes motivational salience and allocation of attention. By contrast, group effects were subtle, dependent on data transformation (ERP, CSD), and did not confirm reduced FN or fb-P3 for at-risk individuals. Instead, CSD-based fb-P3 was overall reduced in individuals with than without MDD history, whereas ERP-based fb-P3 was greater for high-risk individuals than for low-risk individuals for monetary, but not neutral outcomes. While the present findings do not support blunted reward processing in depression and depression risk, our side-by-side comparison underscores how the EEG reference choice affects the characterization of subtle group differences, strongly advocating the use of reference-free techniques.

Women with more severe premenstrual syndrome have an enhanced anticipatory reward processing: a magnetoencephalography study.

Laboratory studies reveal that young women with premenstrual syndrome (PMS) often exhibit decreased reward processing during the late luteal phase. However, studies based on the self-reports find opposite results (e.g., higher craving for high-sweet-fat food). These differences may lie in the difference between the stimulus used and measuring the different aspects of the reward. The present study was designed to expand previous work by using a classic monetary reward paradigm, simultaneously examining the motivational (i.e., reward anticipation, "wanting") and emotional (i.e., reward outcome, "liking") components of reward processing in women with high premenstrual symptoms (High PMS). College female students in their early twenties with High PMS (n = 20) and low premenstrual symptoms (Low PMS, n = 20) completed a monetary incentive delay task during their late luteal phase when the premenstrual symptoms typically peak. Brain activities in the reward anticipation phase and outcome phase were recorded using the magnetoencephalographic (MEG) imaging technique. No group differences were found in various behavioral measurements. For the MEG results, in the anticipation phase, when High PMS participants were presented with cues that predicted the upcoming monetary gains, they showed higher event-related magnetic fields (ERFs) than when they were presented with neutral non-reward cues. This pattern was reversed in Low PMS participants, as they showed lower reward cue-elicited ERFs than non-reward cue-elicited ones (cluster mass = 2560, cluster size = 891, p = .03, corrected for multiple comparisons), mainly in the right medial orbitofrontal and lateral orbitofrontal cortex (cluster mass = 375, cluster size = 140, p = .03, corrected for multiple comparisons). More importantly, women with High PMS had an overall significantly higher level of ERFs than women with Low PMS (cluster mass = 8039, cluster size = 2937, p = .0009, corrected for multiple comparisons) in the bilateral precentral gyrus, right postcentral gyrus, and left superior temporal gyrus (right: cluster mass = 410, cluster size = 128, p = .03; left: cluster mass = 352, cluster size = 98, p = .05; corrected for multiple comparisons). In the outcome phase, women with High PMS showed significantly lower theta power than the Low PMS ones for the expected non-reward feedback in the bilateral temporal-parietal regions (cluster mass = 47620, cluster size = 18308, p = .01, corrected for multiple comparisons). These findings reveal that the severity of PMS might alter reward anticipation. Specifically, women with High PMS displayed increased brain activities to reward-predicting cues and increased action preparation after the cues appear.

Amphiregulin normalizes altered circuit connectivity for social dominance of the CRTC3 knockout mouse

Social hierarchy has a profound impact on social behavior, reward processing, and mental health. Moreover, lower social rank can lead to chronic stress and often more serious problems such as bullying victims of abuse, suicide, or attack to society. However, its underlying mechanisms, particularly their association with glial factors, are largely unknown. In this study, we report that astrocyte-derived amphiregulin plays a critical role in the determination of hierarchical ranks. We found that astrocytes-secreted amphiregulin is directly regulated by cAMP response element-binding (CREB)-regulated transcription coactivator 3 (CRTC3) and CREB. Mice with systemic and astrocyte-specific CRTC3 deficiency exhibited a lower social rank with reduced functional connectivity between the prefrontal cortex, a major social hierarchy center, and the parietal cortex. However, this effect was reversed by astrocyte-specific induction of amphiregulin expression, and the epidermal growth factor domain was critical for this action of amphiregulin. These results provide evidence of the involvement of novel glial factors in the regulation of social dominance and may shed light on the clinical application of amphiregulin in the treatment of various psychiatric disorders.

Neighborhood Disadvantage and Neural Correlates of Threat and Reward Processing in Survivors of Recent Trauma

Differences in neighborhood socioeconomic characteristics are important considerations in understanding differences in risk vs resilience in mental health. Neighborhood disadvantage is associated with alterations in the function and structure of threat neurocircuitry. To investigate associations of neighborhood disadvantage with white and gray matter and neural reactivity to positive and negative stimuli in the context of trauma exposure. In this cross-sectional study, survivors of trauma who completed sociodemographic and posttraumatic symptom assessments and neuroimaging were recruited as part of the Advancing Understanding of Recovery After Trauma (AURORA) study between September 2017 and June 2021. Data analysis was performed from October 25, 2022, to February 15, 2023. Neighborhood disadvantage was measured with the Area Deprivation Index (ADI) for each participant home address. Participants completed separate threat and reward tasks during functional magnetic resonance imaging. Diffusion-weighted and high-resolution structural images were also collected. Linear models assessed the association of ADI with reactivity, microstructure, and macrostructure of a priori regions of interest after adjusting for income, lifetime trauma, sex at birth, and age. A moderated-mediation model tested whether ADI was associated with neural activity via microstructural changes and if this was modulated by PTSD symptoms. A total of 280 participants (183 females [65.4%]; mean [SD] age, 35.39 [13.29] years) completed the threat task and 244 participants (156 females [63.9%]; mean [SD] age, 35.10 [13.26] years) completed the reward task. Higher ADI (per 1-unit increase) was associated with greater insula (t274 = 3.20; β = 0.20; corrected P = .008) and anterior cingulate cortex (ACC; t274 = 2.56; β = 0.16; corrected P = .04) threat-related activity after considering covariates, but ADI was not associated with reward reactivity. Greater disadvantage was also associated with altered microstructure of the cingulum bundle (t274 = 3.48; β = 0.21; corrected P = .001) and gray matter morphology of the ACC (cortical thickness: t273 = -2.29; β = -0.13; corrected P = .02; surface area: t273 = 2.53; β = 0.13; corrected P = .02). The moderated-mediation model revealed that ADI was associated with ACC threat reactivity via cingulum microstructural changes (index of moderated mediation = -0.02). However, this mediation was only present in individuals with greater PTSD symptom severity (at the mean: β = -0.17; standard error = 0.06, t= -2.28; P = .007; at 1 SD above the mean: β = -0.28; standard error = 0.08; t = -3.35; P < .001). In this study, neighborhood disadvantage was associated with neurobiology that supports threat processing, revealing associations of neighborhood disadvantage with neural susceptibility for PTSD and suggesting how altered structure-function associations may complicate symptoms. Future work should investigate specific components of neighborhood disadvantage that may be associated with these outcomes.

Dynamic organization of cerebellar climbing fiber response and synchrony in multiple functional components reduces dimensions for reinforcement learning.

Cerebellar climbing fibers convey diverse signals, but how they are organized in the compartmental structure of the cerebellar cortex during learning remains largely unclear. We analyzed a large amount of coordinate-localized two-photon imaging data from cerebellar Crus II in mice undergoing 'Go/No-go' reinforcement learning. Tensor component analysis revealed that a majority of climbing fiber inputs to Purkinje cells were reduced to only four functional components, corresponding to accurate timing control of motor initiation related to a Go cue, cognitive error-based learning, reward processing, and inhibition of erroneous behaviors after a No-go cue. Changes in neural activities during learning of the first two components were correlated with corresponding changes in timing control and error learning across animals, indirectly suggesting causal relationships. Spatial distribution of these components coincided well with boundaries of Aldolase-C/zebrin II expression in Purkinje cells, whereas several components are mixed in single neurons. Synchronization within individual components was bidirectionally regulated according to specific task contexts and learning stages. These findings suggest that, in close collaborations with other brain regions including the inferior olive nucleus, the cerebellum, based on anatomical compartments, reduces dimensions of the learning space by dynamically organizing multiple functional components, a feature that may inspire new-generation AI designs.

Caffeinated Soda Intake in Children Is Associated with Neurobehavioral Risk Factors for Substance Misuse

Background and objectives Use of psychotropic substances in childhood has been associated with both impulsivity and other manifestations of poor executive function as well as escalation over time to use of progressively stronger substances. However, how this relationship may start in earlier childhood has not been well explored. Here, we investigated the neurobehavioral correlates of daily caffeinated soda consumption in preadolescent children and examined whether caffeinated soda intake is associated with a higher risk of subsequent alcohol initiation. Methods Using Adolescent Brain Cognitive Development study data (N = 2,092), we first investigated cross-sectional relationships between frequent caffeinated soda intake and well-known risk factors of substance misuse: impaired working memory, high impulsivity, and aberrant reward processing. We then examined whether caffeinated soda intake at baseline predicts more alcohol sipping at 12 months follow-up using a machine learning algorithm. Results Daily consumption of caffeinated soda was cross-sectionally associated with neurobehavioral risk factors for substance misuse such as higher impulsivity scores and lower working memory performance. Furthermore, caffeinated soda intake predicted a 2.04 times greater likelihood of alcohol sipping after 12 months, even after controlling for rates of baseline alcohol sipping rates. Conclusions These findings suggest that previous linkages between caffeine and substance use in adolescence also extend to younger initiation, and may stem from core neurocognitive features thought conducive to substance initiation.

Explaining the "parenting - callous-unemotional traits - antisocial behavior" axis in early adolescence: The role of affiliative reward.

In explaining the "parenting - callous-unemotional traits - antisocial behavior" axis, recent theoretical advances postulate a critical role for affiliative reward. Existing empirical studies focus on early childhood and the appetitive phase of the reward process (i.e. affiliation-seeking behavior) rather than the consummatory phase (i.e. affective rewards). This study focuses on experienced affiliative reward (i.e. companionship, intimacy, affection, and worth) in relation to parents and best friends in early adolescence. The Alabama Parenting Questionnaire, Network of Relationships Inventory, Inventory of Callous and Unemotional Traits, and Youth Self Report were completed by 1132 12-year-olds and analyzed via structural equation models. In this cross-sectional sample, parent-related affiliative reward mediated the path from perceived parenting practices to callousness and further to aggression and rule-breaking. Parent-related affiliative reward was also related to uncaring traits and further to aggression and rule-breaking. In contrast, friend-related affiliative reward was not a mediator in this theoretical causal chain and largely not related to perceived parenting practices or CU traits. Low parent-related experienced affiliative reward is a mechanism through which corporal punishment, poor monitoring, and low involvement translate into callousness, and therefore to aggression and rule-breaking. Friend-related affiliative reward does not yet play a role in early adolescence.

Lifeworlds inpain: a principled method forinvestigation andintervention.

The experience of pain spans biological, psychological and sociocultural realms, both basic and complex, it is by turns necessary and devastating. Despite an extensive knowledge of the constituents of pain, the ability to translate this into effective intervention remains limited. It is suggested that current, multiscale, medical approaches, largely informed by the biopsychosocial (BPS) model, attempt to integrate knowledge but are undermined by an epistemological obligation, one that necessitates a prior isolation of the constituent parts. To overcome this impasse, we propose that an anthropological stance needs to be taken, underpinned by a Bayesian apparatus situated in computational psychiatry. Here, pain is presented within the context of lifeworlds, where attention is shifted away from the constituents of experience (e.g. nociception, reward processing and fear-avoidance), towards the dynamic affiliation that occurs between these processes over time. We argue that one can derive a principled method of investigation and intervention for pain from modelling approaches in computational psychiatry. We suggest that these modelling methods provide the necessary apparatus to navigate multiscale ontology and epistemology of pain. Finally, a unified approach to the experience of pain is presented, where the relational, inter-subjective phenomenology of pain is brought into contact with a principled method of translation; in so doing, revealing the conditions and possibilities of lifeworlds in pain.

Mothers exhibit higher neural activity ingaining rewards fortheir children than forthemselves.

Are people willing to exert greater effort to obtain rewards for their children than they are for themselves? Although previous studies have demonstrated that social distance influences neural responses to altruistic reward processing, the distinction between winning rewards for oneself and winning them for one's child is unclear. In the present study, a group of 31 mothers performed a monetary incentive delay task in which cue-induced reward anticipations of winning a reward for themselves, their children and donation to a charity program were manipulated trial-wise, followed by performance-contingent feedback. Behaviorally, the anticipation of winning a reward for their children accelerated participants' responses. Importantly, the electroencephalogram results revealed that across the reward anticipation and consumption phases, the child condition elicited comparable or higher brain responses of participants than the self condition did. The source localization results showed that participants' reward anticipations for their children were associated with more activation in the social brain regions, compared to winning a reward for themselves or a charity donation. Overall, these findings advance our understanding of the neural mechanisms of altruistic reward processing and suggest that the priority of winning a reward for one's child may transcend the limits of the self-advantage effect in reward processing.

Habitual daily intake of a sweet and fatty snack modulates reward processing in humans

Habitual daily intake of a sweet and fatty snack modulates reward processing in humans

Pain catastrophizing is associated with reduced neural response to monetary reward.

Pain catastrophizing, a measure of an individual's negative emotional and cognitive appraisals of pain, has been included as a key treatment target in many psychological interventions for pain. However, the neural correlates of pain catastrophizing have been understudied. Prior neuroimaging evidence suggests that adults with pain show altered reward processing throughout the mesocorticolimbic reward circuitry. In this study, we tested the association between Pain Catastrophizing Scale (PCS) scores and neural activation to the Monetary Incentive Delay (MID) reward neuroimaging task in 94 adults reporting a range of pain, insomnia, and mood symptoms. Results indicated that PCS score but not pain intensity was significantly associated with blunted activation in the caudate and putamen in response to feedback of successful vs. unsuccessful trials on the MID task. Mediation analyses indicated that PCS score fully mediated the relationship between depression symptoms and reward activation. These findings provide evidence that pain catastrophizing is independently associated with altered striatal function apart from depression symptoms and pain intensity. Thus, in individuals experiencing pain and/or co- morbid conditions, reward dysfunction is directly related to pain catastrophizing.

A review of the physiological role of hypocretin in the ventral tegmental area in reward and drug dependence.

Orexin (OX, hypocretin: HCRT) as a neuropeptide is produced in a distinct population of neurons in the posterior lateral hypothalamus (LH). OX neurons implicate in reward function. OX makes a main input from the hypothalamus to the ventral tegmental area (VTA) of the midbrain. OX, through OX receptors (OXR1, OXR2) activates VTA dopamine (DA) neurons. VTA neurons are involved in reward processing and motivation. In this review, we will discuss the OX effect on addiction through VTA activation and related areas of the brain.

Depression recurrence is accompanied by longer periods in default mode and more frequent attentional and reward processing dynamic brain-states during resting-state activity.

Recurrence in major depressivedisorder (MDD) is common, but neurobiological models capturing vulnerability for recurrences are scarce. Disturbances in multiple resting-state networks have been linked to MDD, but most approaches focus on stable (vs. dynamic) network characteristics. We investigated how the brain's dynamical repertoire changes after patients transition from remission to recurrence of a new depressive episode. Sixty two drug-free, MDD-patients with ≥2 episodes underwent a baseline resting-state fMRI scan when in remission. Over 30-months follow-up, 11 patients with a recurrence and 17 matched-remitted MDD-patients without a recurrence underwent a second fMRI scan. Recurrent patterns of functional connectivity were characterized by applying Leading Eigenvector Dynamics Analysis (LEiDA). Differences between baseline and follow-up were identified for the 11 non-remitted patients, while data from the 17 matched-remitted patients was used as a validation dataset. After the transition into a depressive state, basal ganglia-anterior cingulate cortex (ACC) and visuo-attentional networks were detected significantly more often, whereas default mode network activity was found to have a longer duration. Additionally, the fMRI signal in the basal ganglia-ACC areas underlying the reward network, were significantly less synchronized with the rest of the brain after recurrence (compared to a state of remission). No significant changes were observed in the matched-remitted patients who were scanned twice while in remission. These findings characterize changes that may be associated with the transition from remission to recurrence and provide initial evidence of altered dynamical exploration of the brain's repertoire of functional networks when a recurrent depressive episode occurs.

Transdiagnostic considerations of the relationship between reward sensitivity and psychopathological symptoms - a cross-lagged panel analysis

BackgroundReward sensitivity constitutes a potential key mechanism regarding the etiology and maintenance of mental disorders, especially depression. However, due to a lack of longitudinal studies, the temporal dynamics are not clear yet. Although some evidence indicates that reward processing could be a transdiagnostic mechanism of disorders, these observations could be also a product of comorbidity with depression. This study aimed at investigating the temporal dynamics of reward sensitivity and the course of psychopathological symptoms in a longitudinal investigation, while taking a possible mediating role of depression into account.MethodsWe conducted a three-wave longitudinal online survey with a 4-week interval. A total of N = 453 participants filled out all three questionnaires. Reward sensitivity was assessed with the Positive Valence System Scale-21 (PVSS-21), depression with the Patient Health Questionnaire (PHQ-9), eating disorder symptoms with the Eating Disorder Examination-Questionnaire-8 (EDE-Q-8), social anxiety with the Mini-social phobia inventory (Mini-SPIN) and alcohol consumption with the Alcohol Use Disorders Identification Test-Consumption (AUDIT-C). Cross-lagged panels and mediation analyses were calculated using path analyses.ResultsDepressive and eating disorder symptoms predicted reward insensitivity at later points in time. Effects were larger from T2 to T3. A bidirectional relationship concerning social anxiety was found. Higher alcohol consumption predicted higher reward sensitivity. Depression at T2 fully mediated the association between psychopathological symptoms at T1 and reward sensitivity at T3 for social anxiety and eating disorder symptoms.ConclusionsOur findings imply that reduced reward sensitivity seems to be a consequence rather than an antecedent of psychopathological symptoms. Comorbid depression plays a crucial role in other mental disorders regarding observed hyposensitivity towards rewards. Therefore, our results do not support a transdiagnostic notion of reward sensitivity, but they indicate a potential role of reward sensitivity for symptom persistence.Trial registrationThe study was preregistered at the Open Science Framework (OSF) (https://archive.org/details/osf-registrations-6n3s8-v1; registration DOI https://doi.org/10.17605/OSF.IO/6N3S8).