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Functional magnetic resonance imaging (fMRI) studies have demonstrated that HIV-infection affects the fronto-striatal network. It has not been examined what impact efavirenz (EFV), an antiretroviral drug notorious for its neurocognitive effects, has on the reward system: a key subcomponent involved in depressive and apathy symptoms. Therefore, this study aims to investigate the effect of EFV on reward processing using a monetary incentive delay (MID) task. In this multicenter randomized controlled trial, asymptomatic adult participants stable on emtricitabine/tenofovirdisoproxil fumarate (FTC/TDF)/EFV were randomly assigned in a 2:1 ratio to switch to FTC/TDF/rilpivirine (RPV) (n = 30) or continue taking FTC/TDF/EFV (n = 13). At baseline and 12 weeks after therapy switch, both groups performed an MID task. Behavior and functional brain activity related to reward anticipation and reward outcome were assessed with blood-oxygen-level-dependent fMRI. Both groups were matched for age, education level, and time since HIV diagnosis and on EFV. At the behavioral level, both groups had faster response times and better response accuracy during rewarding versus nonrewarding trials, with no improvement resulting from switching FTC/TDF/EFV to FTC/TDF/RPV. No significant change in activation related to reward anticipation in the ventral striatum was found after switching therapy. Both groups had significantly higher activation levels over time, consistent with a potential learning effect. Similar activity related to reward outcome in the orbitofrontal cortex was found. Discontinuing FTC/TDF/EFV was not found to improve activity related to reward anticipation in asymptomatic people living with HIV, with similar cortical functioning during reward outcome processing. It is therefore likely that EFV does not affect motivational control. Further research is needed to determine whether EFV affects motivational control in HIV populations with different characteristics. [ABSTRACT FROM AUTHOR]

ABSTRACT Objective Method Results Discussion Anorexia nervosa (AN) is characterized by a tendency to limit intake of food, with specific restriction of foods that are generally considered highly palatable. This observation raises questions about whether reward processing is disturbed in AN. This study examined whether adolescents with AN differ from healthy control peers (HC) in anticipatory and consummatory reward processing.Adolescents with AN (n = 71) and HC (n = 41) completed the Temporal Experience of Pleasure Scale (TEPS). The TEPS Anticipatory Pleasure scale was divided into two further subscales (Food and Non‐food). Anticipatory (Food and Non‐food) and Consummatory Pleasure (Non‐food) scores were compared between adolescents with AN and HC using independent t‐tests.TEPS scores were significantly lower among adolescents with AN than HC in Anticipatory Pleasure Food (t(110) = 7.80, p < 0.001) and Non‐food (t(110) = 4.36, p < 0.001), and Consummatory Pleasure (t(110) = 2.60, p = 0.01) subscales. When controlling for BDI score, there was no significant group difference in TEPS Consummatory Pleasure scores (t(108) = 0.88, p = 0.38). Among adolescents with AN, Food Anticipatory Pleasure was significantly negatively correlated with all EDE‐Q subscales and global score (r(68) = −0.38, p = 0.002) and positively correlated with food intake at a laboratory buffet meal (r(61) = 0.53, p < 0.001).Measures of both anticipatory and consummatory reward were reduced among adolescents with AN with a short duration of illness. In this study, eating disorder symptoms were related to diminished reward responses in anticipation of food. Dampened anticipatory reward response may comprise a mechanism of illness in AN that should be subject to further study. [ABSTRACT FROM AUTHOR]

Reward processing is impaired in people with schizophrenia, which may begin in the clinical high-risk (CHR) for psychosis period. The Monetary Incentive Delay (MID) task has been important in understanding the neural correlates of reward processing deficits in various psychiatric disorders. Previous research has found that CHR individuals have an imprecise mental representation of rewards, which leads to a diminished differentiation between rewards, though this has not been observed behaviorally. A total of 19 CHR individuals and 20 controls were given a novel variant of the MID task, designed to examine how modulating reward context may impact responses to reward cues, a process often referred to as "adaptive coding." Both groups appeared to update their behavior in response to the rewards available in this adaptive task. However, when compared to controls who showed a more graded decrease in response time to increasing reward contexts, CHR individuals appeared to have a sharp decrease in response time in the low reward context that is nearly stable across higher reward contexts. This is largely driven by the exponential component of the response time distribution, which is often interpreted to be more cognitively or effortfully influenced. Response times are related to negative symptoms, but not positive symptoms, disorganized symptoms, or estimated intelligence. Although an adaptive coding effect was not observed, these results provide novel insight into the reward processing mechanisms and volitional processes in the CHR population, as this was the first study to observe the diminished differentiation of rewards behaviorally. [ABSTRACT FROM AUTHOR]

Anhedonia stands as a life-threatening transdiagnostic feature of many mental illnesses, most notably major depression and involves neural circuits for processing reward information. The paraventricular nucleus of the thalamus (PVT) is associated with reward-seeking behavior, however, links between the PVT circuit and anhedonia have not been investigated in humans. In a sample of adults with and without psychiatric symptoms (n = 75, 18–41 years, 55 female), we generated an anhedonia factor score for each participant using a latent factor analysis, utilizing data from depression and anxiety assessments. Functional connectivity between the PVT and the nucleus accumbens (NAc) was calculated from high-resolution (1.5 mm) resting state fMRI. Anhedonia factor scores showed a positive relationship with functional connectivity between the PVT and the NAc, principally in males and in those with psychiatric symptoms. In males, connectivity between other midline thalamic nuclei and the NAc did not show these relationships, suggesting that this link may be specific to PVT. This cohort was originally recruited to study depression and not anhedonia per se. The distribution of male and female participants in our cohort was not equal. Partial acquisition in high-resolution fMRI scans restricted regions of interest outside of the thalamus and reward networks. We report evidence that anhedonia is associated with enhanced functional connectivity between the PVT and the NAc, regions that are relevant to reward processing. These results offer clues as to the potential prevention and prevention and treatment of anhedonia. • Anhedonia has been associated with alterations in reward processing neural circuits. • The paraventricular nucleus of the thalamus (PVT) projects to reward and threat regions. • Altering PVT is associated with anhedonia in animal models. • In humans, anhedonia symptoms are associated with increased functional connectivity between PVT and nucleus accumbens, particularly in males. • This provides evidence that the human PVT circuit is involved in anhedonia. [ABSTRACT FROM AUTHOR]

Abstract Background Evidence from studies on adult participants and clinical samples of children suggest an association between risky decision-making and mental health problems. However, the extent and nature of this association in the general youth population remains unknown. Therefore, this scoping review explores the current evidence on the relationship between mental health (internalising and externalising symptoms) and risky decision-making in the general youth population. Methods A three-step search strategy was followed and applied to four databases. Selection criteria included participants

Decision-making deficits, assessed cognitively, are often associated with mental health symptoms, however, this relationship is not fully understood. This paper explores the relationship between mental health disorders and decision-making, using the Cambridge Gambling Task (CGT). Our study investigated how decision-making varied across 20 different mental health conditions compared to controls in a sample of 572 young adults from the Minneapolis and Chicago metropolitan areas, using a computerized laboratory-based task. Almost all mental health conditions were associated with at least mild (i.e. at least small effect size) impairment in all three studied parameters of the CGT (risk adjustment, quality of decision-making and overall proportion of bet). Notably, binge eating disorder had the largest cognitive impairment and gambling disorder had moderate impairment. Post-traumatic stress disorder (PTSD) was associated with impaired decision-making while obsessive–compulsive disorder (OCD) and depression showed moderate impairment. Additionally, half of the disorders assessed had moderate to large impairment in risk adjustment.These findings suggest that mental health conditions may have a more complex cognitive profile than previously thought, and a better understanding of these impairments may aid in risk assessment and targeted clinical interventions. This study underscores the need for further research to determine the causal pathways between mental health conditions and cognition, as well as to better understand the day-to-day impact of such deficits. [ABSTRACT FROM AUTHOR]

Rationale: For decades, cannabis has been the most widely used illicit substance in the world, particularly among youth. Research suggests that mental health problems associated with cannabis use may result from its effect on reward brain circuit, emotional processes, and cognition. However, findings are mostly derived from correlational studies and inconsistent, particularly in adolescents. Objectives and Methods: Using data from the IMAGEN study, participants (non-users, persistent users, abstinent users) were classified according to their cannabis use at 19 and 22 years-old. All participants were cannabis-naïve at baseline (14 years-old). Psychopathological symptoms, cognitive performance, and brain activity while performing a Monetary Incentive Delay task were used as predictors of substance use and to analyze group differences over time. Results: Higher scores on conduct problems and lower on peer problems at 14 years-old (n = 318) predicted a greater likelihood of transitioning to cannabis use within 5 years. At 19 years of age, individuals who consistently engaged in low-frequency (i.e., light) cannabis use (n = 57) exhibited greater conduct problems and hyperactivity/inattention symptoms compared to non-users (n = 52) but did not differ in emotional symptoms, cognitive functioning, or brain activity during the MID task. At 22 years, those who used cannabis at both 19 and 22 years-old n = 17), but not individuals that had been abstinent for ≥ 1 month (n = 19), reported higher conduct problems than non-users (n = 17). Conclusions: Impairments in reward-related brain activity and cognitive functioning do not appear to precede or succeed cannabis use (i.e., weekly, or monthly use). Cannabis-naïve adolescents with conduct problems and more socially engaged with their peers may be at a greater risk for lighter yet persistent cannabis use in the future. [ABSTRACT FROM AUTHOR]

Background: Evidence from studies on adult participants and clinical samples of children suggest an association between risky decision-making and mental health problems. However, the extent and nature of this association in the general youth population remains unknown. Therefore, this scoping review explores the current evidence on the relationship between mental health (internalising and externalising symptoms) and risky decision-making in the general youth population. Methods: A three-step search strategy was followed and applied to four databases. Selection criteria included participants < 18 years representative of the general population, and information on both risky decision-making (assessed using gambling tasks) and internalising /externalising symptoms. Data were extracted and synthesised for study and participant characteristics, aspects and measures for the main variables, and key findings. Results: Following screening, twenty-one studies were retrieved. Non-significant associations were more frequent than significant associations for both internalising and externalising symptoms, particularly for social difficulties and broad externalising symptoms. Among the significant associations, hyperactivity/inattention and conduct problems appeared to be positively associated with risk-taking and negatively associated with quality of decision-making. However, patterns were less clear for links between risky decision-making and internalising symptoms, especially between risk-taking and anxiety symptoms. Conclusions: The present review suggests predominantly a lack of relationship between risky decision-making and mental health problems, and outlines several possible reasons for it. However, when specificity is considered carefully there seems to be a link between risk-taking and specific externalising problems. Future research should employ study designs aimed at disentangling the direction of this relationship and identifying specific aspects of mental health and risky decision-making that could be eventually addressed by tailored interventions. [ABSTRACT FROM AUTHOR]

Abnormal reward processing and psychomotor slowing are well‐known in schizophrenia (SZ). As a slow frontocentral potential, contingent negative variation (CNV) is associated with anticipatory attention, motivation and motor planning. The present study aims to evaluate the early and late amplitude and latencies of CNV in patients with SZ compared to healthy controls during a reward processing task and to show its association with clinical symptoms. We recruited 21 patients with SZ and 22 healthy controls to compare early and late CNV amplitude and latency values during a Monetary Incentive Delay (MID) Task between groups. Patients' symptom severity, levels of negative symptoms and depressive symptoms were assessed. Clinical features of the patients were further examined for their relation with CNV components. In conclusion, we found decreased early CNV amplitudes in SZ during the reward condition. They also displayed diminished and shortened late CNV responses for incentive cues, specifically at the central location. Furthermore, early CNV amplitudes exhibited a significant correlation with positive symptoms. Both CNV latencies were linked with medication dosage and the behavioural outcomes of the MID task. We revealed that early and late CNV exhibit different functions in neurophysiology and correspond to various facets of the deficits observed in patients. Our findings also emphasized that slow cortical potentials are indicative of deficient motivational processes as well as impaired reaction preparation in SZ. To gain a deeper understanding of the cognitive and motor impairments associated with psychosis, future studies must compare the effects of CNV in the early and late phases. [ABSTRACT FROM AUTHOR]

Adolescent anhedonia is a multidimensional construct defined as the loss of enjoyment or pleasure across multiple domains of life. Anhedonia is concurrently associated with substantial impairment and distress, and it prospectively predicts the onset, severity, and treatment of depression. Despite its demonstrated importance, a limited number of anhedonia measures are validated for adolescents. The current study assessed the psychometric properties of the Dimensional Anhedonia Rating Scale (DARS) in 400 English-speaking, 12- to 19-year-old adolescents. Overall, the DARS demonstrated good convergent and discriminant validity, but sub-optimal concurrent validity. The strengths and limitations of the DARS and its utility as a measure of adolescent anhedonia are discussed. Furthermore, future directions for the construction of measures of adolescent anhedonia are outlined. [ABSTRACT FROM AUTHOR]

Anhedonia, an impairment in the motivation for or experience of pleasure, is a well-established transdiagnostic harbinger and core symptom of mental illness. Given increasing recognition of early life origins of mental illness, we posit that anhedonia should, and could, be recognized earlier if appropriate tools were available. However, reliable diagnostic instruments prior to childhood do not currently exist. We developed an assessment instrument for anhedonia/reward processing in infancy, the Infant Hedonic/Anhedonic Processing Index (HAPI-Infant). Exploratory factor and psychometric analyses were conducted using data from 6- and 12-month-old infants from two cohorts (N = 188, N = 212). Then, associations were assessed between infant anhedonia and adolescent self-report of depressive symptoms. The HAPI-Infant (47-items), exhibited excellent psychometric properties. Higher anhedonia scores at 6 (r = 0.23, p <.01) and 12 months (r = 0.19, p <.05) predicted elevated adolescent depressive symptoms, and these associations were stronger than for established infant risk indicators such as negative affectivity. Subsequent analyses supported the validity of short (27-item) and very short (12-item) versions of this measure. The primary limitations of this study are that the HAPI-Infant awaits additional tests of generalizability and of its ability to predict clinical diagnosis of depression. The HAPI-Infant is a novel, psychometrically strong diagnostic tool suitable for recognizing anhedonia during the first year of life with strong predictive value for later depressive symptoms. In view of the emerging recognition of increasing prevalence of affective disorders in children and adolescents, the importance of the HAPI-Infant in diagnosing anhedonia is encouraging. Early recognition of anhedonia could target high-risk individuals for intervention and perhaps prevention of mental health disorders. • Anhedonia is a well-established transdiagnostic harbinger of mental illness. • No diagnostic tool for anhedonia assessment exists prior to childhood. • We present a valid new tool enabling assessment of anhedonia in infancy. • Infant anhedonia uniquely predicts youth self-report of depressive symptoms. • Early recognition of anhedonia may support strategies for prevention and intervention. [ABSTRACT FROM AUTHOR]

Social relationships change across the lifespan as social networks narrow and motivational priorities shift. These changes may affect, or reflect, differences in how older adults make decisions related to processing social and non-social rewards. While we have shown initial evidence that older adults have a blunted response to some features of social reward, further work in larger samples is needed to replicate our results and probe the extent to which age-related differences translate to real world consequences, such as financial exploitation. To address this gap, we are conducting a 5-year study funded by the National Institute on Aging (NIH R01-AG067011). Over the course of the funding period (2021–2026), this study seeks to: 1) characterize neural responses to social rewards across adulthood; 2) relate those responses to risk for financial exploitation and sociodemographic factors tied to risk; and 3) examine changes in risk for financial exploitation over time in healthy and vulnerable groups of older adults. This paper describes the preliminary release of data for the larger study. Adults (N = 114; 40 male / 70 female / 4 other or non-binary; 21–80 years of age M = 42.78, SD = 17.13) were recruited from the community to undergo multi-echo fMRI while completing tasks that measure brain function during social reward and decision making. Tasks probe neural response to social reward (e.g., peer vs. monetary feedback) and social context and closeness (e.g., sharing a monetary reward with a friend compared to a stranger). Neural response to social decision making is probed via economic trust and ultimatum games. Functional data are complimented by a T1 weighted anatomical scan and multi-shell diffusion-weighted imaging (DWI) to enable tractography and assess neurite orientation dispersion and density. Overall, this dataset has extensive potential for re-use, including leveraging multimodal neuroimaging data, within subject measures of fMRI data from different tasks – data features that are rarely seen in an adult lifespan dataset. Finally, the functional data will allow for developmentally sensitive cross-sectional analyses of differences in brain response to nuanced differences in reward contexts and outcomes (e.g., monetary vs. social; sharing winnings with a friend vs. stranger; stranger vs. computer).

Existing research indicates that individuals with Major Depressive Disorder (MDD) exhibit a bias toward salient negative stimuli. However, the impact of such biased stimuli on concurrent cognitive and affective processes in individuals with depression remains inadequately understood. This study aimed to investigate the effects of salient environmental stimuli, specifically emotional faces, on reward-associated processes in MDD. Thirty-three patients with recurrent MDD and thirty-two healthy controls (HC) matched for age, sex, and education were included in the study. We used a reward-related associative learning (RRAL) task primed with emotional (happy, sad, neutral) faces to investigate the effect of salient stimuli on reward-related learning and decision-making in functional magnetic resonance imaging (fMRI). Participants were instructed to ignore emotional faces during the task. The fMRI data were analyzed using a full-factorial general linear model (GLM) in Statistical Parametric Mapping (SPM12). In depressed patients, cues primed with sad faces were associated with reduced amygdala activation. However, both HC and MDD group exhibited reduced ventral striatal activity while learning reward-related cues and receiving rewards. The patients'medication usage was not standardized. This study underscores the functional alteration of the amygdala in response to cognitive tasks presented with negative emotionally salient stimuli in the environment of MDD patients. The observed alterations in amygdala activity suggest potential interconnected effects with other regions of the prefrontal cortex. Understanding the intricate neural connections and their disruptions in depression is crucial for unraveling the complex pathophysiology of the disorder. • An event-related card-guessing task to evaluate neural activation during probabilistic reward learning following brief emotional stimulus was used in the present study. • Both MDD and HC groups showed similar behavioral performance in mean by reaction time, accuracy and learning rates. • Emotional faces induce BOLD changes at the right ventral striatum, suggesting strong affective effect of emotional faces even they were presented very briefly. • In sad face condition, MDD patients had shown significantly reduced BOLD signals in both left and right amygdala and right hippocampus compared to healthy controls. • Emotional priming during probabilistic cue period effects BOLD levels in the right striatum and hippocampus at the outcome period independent from win/lose condition. [ABSTRACT FROM AUTHOR]

Background: Stress and depression have a reciprocal relationship, but the neural underpinnings of this reciprocity are unclear. We investigated neuroimaging phenotypes that facilitate the reciprocity between stress and depressive symptoms. Methods: In total, 22 195 participants (52.0% females) from the population-based UK Biobank study completed two visits (initial visit: 2006–2010, age = 55.0 ± 7.5 [40–70] years; second visit: 2014–2019; age = 62.7 ± 7.5 [44–80] years). Structural equation modeling was used to examine the longitudinal relationship between self-report stressful life events (SLEs) and depressive symptoms. Cross-sectional data were used to examine the overlap between neuroimaging correlates of SLEs and depressive symptoms on the second visit among 138 multimodal imaging phenotypes. Results: Longitudinal data were consistent with significant bidirectional causal relationship between SLEs and depressive symptoms. In cross-sectional analyses, SLEs were significantly associated with lower bilateral nucleus accumbal volume and lower fractional anisotropy of the forceps major. Depressive symptoms were significantly associated with extensive white matter hyperintensities, thinner cortex, lower subcortical volume, and white matter microstructural deficits, mainly in corticostriatal-limbic structures. Lower bilateral nucleus accumbal volume were the only imaging phenotypes with overlapping effects of depressive symptoms and SLEs (B = −0.032 to −0.023, p = 0.006–0.034). Depressive symptoms and SLEs significantly partially mediated the effects of each other on left and right nucleus accumbens volume (proportion of effects mediated = 12.7–14.3%, p < 0.001− p = 0.008). For the left nucleus accumbens, post-hoc seed-based analysis showed lower resting-state functional connectivity with the left orbitofrontal cortex (cluster size = 83 voxels, p = 5.4 × 10−5) in participants with high v. no SLEs. Conclusions: The nucleus accumbens may play a key role in the reciprocity between stress and depressive symptoms. [ABSTRACT FROM AUTHOR]

Very little is known about the mechanisms underlying the development of personality disorders, hindering efforts to address early risk for these costly and stigmatized disorders. In this study, we examined associations between social and monetary reward processing, measured at the neurophysiological level, and personality pathology, operationalized through the Level of Personality Functioning (LPF), in a sample of early adolescent females (Mage = 12.21 years old, SD = 1.21). Female youth with (n = 80) and without (n = 30) a mental health history completed laboratory tasks assessing social and monetary reward responsiveness using electroencephalogram (EEG) and completed ratings of personality pathology. Commonly co-occurring psychopathology, including depression, anxiety, attention-deficit/hyperactivity disorder (ADHD), oppositional defiant disorder (ODD), and conduct disorder (CD) were also assessed. At the bivariate level, significant associations did not emerge between psychopathology and reward processing variables. When covarying symptoms of depression, anxiety, ADHD, ODD, and CD, an enhanced reward positivity (RewP) component to social reward feedback (accounting for response to social rejection) was associated with higher levels of personality impairment. Results were specific to social rather than monetary reward processing. Depression, anxiety, and ODD also explained unique variance in LPF. These findings suggest that alterations in social reward processing may be a key marker for early emerging personality pathology. Future work examining the role of social reward processing on the development of LPF across adolescence may guide efforts to prevent the profound social dysfunction associated with personality pathology. [ABSTRACT FROM AUTHOR]

Although Buying Disorder (BD) is not a formal diagnosis in commonly used diagnostic systems, this condition can cause significant impairments. Additionally, there is an ongoing discussion about the most appropriate conceptualization and classification of BD. Most often, BD is considered either an obsessive–compulsive and related disorder (OCRD) or an addictive behavior (i.e., substance use disorders or behavioral addictions), and was previously recognized as an impulse control disorder. The present narrative review examines the cognitive processes of impulsivity (i.e., impulsive action, impulsive choice, decision making, and personality), compulsivity, and reward processing (i.e., cue reactivity and craving), in BD, obsessive–compulsive disorder (OCD), and addictive behaviors. Most evidence supports BD having overlapping features with behavioral addictions more so than with OCD due to similar impairments in decision-making and inhibition, as well as similar motivations behind BD. Further, BD demonstrates cue-reactivity and craving similar to behavioral addictions. There were also similar elevations on personality inventories between BD and addictive behaviors, which were less relevant in OCD. Although studies in these specific cognitive domains suggest similarities between BD and behavioral addiction, more studies are needed to further elucidate BD processes, which would in turn assist with the classification of BD. Further, despite similarities across conditions, directly comparing BD to these conditions on the aforementioned processes is needed. In future, study designs should directly compare BD to disorders within each classification to elucidate shared and distinct functions of these processes. [ABSTRACT FROM AUTHOR]

Background Research suggests that effort-cost decision-making (ECDM), the estimation of work required to obtain reward, may be a relevant framework for understanding motivational impairment in psychotic and mood pathology. Specifically, research has suggested that people with psychotic and mood pathology experience effort as more costly than controls, and thus pursue effortful goals less frequently. This study examined ECDM across psychotic and mood pathology. Hypothesis We hypothesized that patient groups would show reduced willingness to expend effort compared to controls. Study Design People with schizophrenia (N  = 33), schizoaffective disorder (N  = 28), bipolar disorder (N  = 39), major depressive disorder (N  = 40), and controls (N  = 70) completed a physical ECDM task. Participants decided between completing a low-effort or high-effort option for small or larger rewards, respectively. Reward magnitude, reward probability, and effort magnitude varied trial-by-trial. Data were analyzed using standard and hierarchical logistic regression analyses to assess the subject-specific contribution of various factors to choice. Negative symptoms were measured with a clinician-rated interview. Study Results There was a significant effect of group, driven by reduced choice of high-effort options in schizophrenia. Hierarchical logistic regression revealed that reduced choice of high-effort options in schizophrenia was driven by weaker contributions of probability information. Use of reward information was inversely associated with motivational impairment in schizophrenia. Surprisingly, individuals with major depressive disorder and bipolar disorder did not differ from controls. Conclusions Our results provide support for ECDM deficits in schizophrenia. Additionally, differences between groups in ECDM suggest a seemingly similar behavioral phenotype, reduced motivation, could arise from disparate mechanisms. [ABSTRACT FROM AUTHOR]

Rationale: Cannabis is one of the most widely used psychoactive substances globally. Cannabis use can be associated with alterations of reward processing, including affective flattening, apathy, anhedonia, and lower sensitivity to natural rewards in conjunction with higher sensitivity to cannabis-related rewards. Such alterations have been posited to be driven by changes in underlying brain reward pathways, as per prominent neuroscientific theories of addiction. Functional neuroimaging (fMRI) studies have examined brain reward function in cannabis users via the monetary incentive delay (MID) fMRI task; however, this evidence is yet to be systematically synthesised. Objectives: We aimed to systematically integrate the evidence on brain reward function in cannabis users examined by the MID fMRI task; and in relation to metrics of cannabis exposure (e.g., dosage, frequency) and other behavioural variables. Method: We pre-registered the review in PROSPERO and reported it using PRISMA guidelines. Literature searches were conducted in PsycINFO, PubMed, Medline, CINAHL, and Scopus. Results: Nine studies were included, comprising 534 people with mean ages 16-to-28 years, of which 255 were people who use cannabis daily or almost daily, and 279 were controls. The fMRI literature to date led to largely non-significant group differences. A few studies reported group differences in the ventral striatum while participants anticipated rewards and losses; and in the caudate while participants received neutral outcomes. A few studies examined correlations between brain function and withdrawal, dosage, and age of onset; and reported inconsistent findings. Conclusions: There is emerging but inconsistent evidence of altered brain reward function in cannabis users examined with the MID fMRI task. Future fMRI studies are required to confirm if the brain reward system is altered in vulnerable cannabis users who experience a Cannabis Use Disorder, as postulated by prominent neuroscientific theories of addiction. [ABSTRACT FROM AUTHOR]

Alcohol use disorder (AUD) is heritable. Thus, young adults with positive family histories represent an at‐risk group relative to those without a family history, and if studied at a time when both groups have similar levels of alcohol use, it provides an opportunity to identify neural processing patterns associated with risk for AUD. Previous studies have shown that diminished response to potential reward is associated with genetic risk for AUD, but it is unclear how threat may modulate this response. We used a modified Monetary Incentive Delay task during fMRI to examine neural correlates of the interaction between threat and reward anticipation in a sample of young adults with (n = 31) and without (n = 44) family histories of harmful alcohol use. We found an interaction (p = 0.048) between cue and group in the right nucleus accumbens where the family history positive group showed less differentiation to the anticipation of gaining $5 and losing $5 relative to gaining $0. The family history‐positive group also reported less excitement for trials to gain $5 relative to gaining $0 (p < 0.001). Family history‐positive individuals showed less activation in the left insula during both safe and threat blocks compared to family history‐negative individuals (p = 0.005), but the groups did not differ as a function of threat (p > 0.70). Young adults with, relative to without, enriched risk for AUD may have diminished reward processing via both neural and behavioural markers to potential rewarding and negative consequences. Neural response to threat may not be a contributing factor to risk at this stage. [ABSTRACT FROM AUTHOR]

ADHD is often described as a disorder of altered reward sensitivity, yet few studies have examined the extent to which: (i) treatments for ADHD impact reward-related mechanisms; and (ii) changes in the reward system are associated with clinical improvement. This study addresses these issues - examining the extent to which clinical improvement following lisdexamfetamine (LDX) treatment is associated with changes in brain reward system activation. Twenty adults (M = 11, 55%, F = 9, 45%), ages 19–52 (M = 33.9, SD = 10.0) with ADHD participated in a randomized cross-over study with lisdexamfetamine (LDX) and placebo (PB). Changes in brain activation were assessed during functional magnetic resonance (fMRI) scans: after receiving 3–5 weeks of treatment with LDX and 3–5 weeks of no drug/PB. fMRI contrasts were derived from the passive-avoidance (PA) learning task, which assessed reward-related learning using computational variables. We analyzed the following conditions: the Choice-Phase, modulated by the expected value (EV; i.e., object-choose and object-reject), and the Feedback-Phase, modulated by the prediction error (PE; i.e., reward and punish). Clinical symptom severity was assessed via interview with the ADHD-Rating Scale (ADHD-RS-IV). To address the primary objective, we performed group-level mass-univariate regression analyses between LDX and PB of percent change of the ADHD-RS total scores and the four contrast images under the Choice- and Feedback-conditions. Significance was set at a whole-brain voxel-wise threshold of p < 0.05 with family-wise error (FWE) correction and an extent (cluster) threshold of 50 contiguous voxels. Improvement in ADHD symptoms with LDX was accompanied by significantly increased activation in a series of brain regions previously implicated in reinforcement processing in the choice and feedback conditions (e.g., left caudate and putamen, right orbitofrontal cortex, left middle frontal, superior frontal, and precentral gyri). These findings, while preliminary, are the first to show that ADHD symptom improvement with stimulant treatment is associated with increased responsiveness of brain systems engaged in reward processing. Results support the hypothesis that LDX treatment may restore balance to dysfunction (e.g., hypoactivation) within the brain reward circuitry in adults with ADHD. Trial Registration Clinicaltrials.gov Identifier: NCT01924429. [ABSTRACT FROM AUTHOR]

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. Our findings add nuanced event‐related potential (ERP) evidence of blunted versus preserved reward processing in depression and depression risk. Although robust condition effects (win, loss, neutral feedback) were congruent with prior research, our comparative side‐by‐side analysis of ERPs and their current source density transformations using permutation tests and multilevel modeling revealed that the characterization of subtle group differences is impeded and potentially altered by the electroencephalogram reference choice, underscoring the importance of using reference‐free techniques for analyzing ERPs. [ABSTRACT FROM AUTHOR]

Reward processing undergoes marked changes in adolescence, with social interactions representing a powerful source of reward. Reward processing is also an important factor in the development of social anxiety disorder, a condition that most commonly first appears in adolescence. This study investigated the relationship between age, social reward processing and social anxiety in a cross-sectional sample of female participants (N = 80) aged 13–34. Participants performed two versions of a probabilistic reward anticipation task, in which a speeded response could result in different probabilities of receiving either social or monetary rewarding feedback. Participants also completed self-report assessments of social reward value, trait anxiety and social anxiety symptoms. At high reward probabilities, performance on both reward tasks showed a quadratic effect of age, with the fastest responses at around 22–24 years. A similar quadratic effect was found for subjective liking ratings of both reward stimuli, although these were not associated with performance. Social anxiety was not associated with a subjective liking of the rewards but did predict performance on both tasks at all reward probabilities. Age-related variation in reward processing was not accounted for by age-related variation in social anxiety symptoms, suggesting that, while both social anxiety and age were associated with variation in reward processing, their effects were largely independent. Together, these findings provide evidence that social reward processing continues to develop across adolescence and that individual differences in social anxiety should be considered when considering reward sensitivity during this period. [ABSTRACT FROM AUTHOR]

Excessive touching and picking of one's skin are core symptoms of skin-picking disorder (SPD). Previous research has shown that patients with SPD display difficulties in motor control and show altered reward responsivity. Considering the limited knowledge about neuronal mechanisms in SPD, particularly concerning the cerebellum, the analysis focused on this brain region due to its involvement in sensorimotor and affective functions. The participants of the present study received affective (caress-like), which is typically perceived as pleasant and can be passively enjoyed. A total of 132 female participants (70 patients with SPD, 62 healthy controls) received affective and nonaffective touch to their forearms (slow vs. fast brushing) during functional magnetic resonance imaging. This tactile stimulation was rated according to pleasure, arousal, and the urge to pick one's skin. Being touched was perceived as more negative and arousing by the SPD group, and elicited a greater urge to perform skin-picking. During affective touch, those participants with SPD were characterized by reduced activity in lobule VIII, reduced functional connectivity of lobule VIII with the hippocampus, and increased connectivity with the superior parietal lobule. Since VIII is involved in the inhibition of movement, the present findings point to deficient motor control in SPD in the context of affective-sensory processing. [ABSTRACT FROM AUTHOR]

The etiological heterogeneity of depression poses a challenge for prevention and intervention efforts. One solution is to map unique etiological pathways for subgroups defined by a singular risk factor. A relevant population for this approach is women who carry the premutation of the fragile X messenger ribonucleoprotein 1 (FMR1) gene, who are at high risk for adult-onset depression. This study explores a candidate neurophysiological marker of depression risk: reduced reward sensitivity, indexed by the reward positivity (RewP). The RewP has been linked to depression risk in the general population, but is unexplored within FMR1 premutation carriers. 16 women with the FMR1 premutation and a matched control group completed a simple guessing task while the electroencephalogram was recorded. Among premutation carriers, RewP difference score (win versus loss) was reduced. These preliminary finding suggest that the FMR1 premutation may confer increased risk for depression in part through abnormal neural sensitivity to rewards.

Yifan Sun,1 Zixuan Huang,2 Xuezheng Gao,1 Limin Chen,3 Jun Wang,1,3 Zhenhe Zhou,1,3 Hongliang Zhou4 1Department of Psychiatry, The Affiliated Wuxi Mental Health Center of Nanjing Medical University, Wuxi City, 214151, People’s Republic of China; 2Department of Music and Wellbeing, School of Music, University of Leeds, Leeds City, UK; 3Department of Psychiatry, The Affiliated Mental Health Center of Jiangnan University, Wuxi City, 214151, People’s Republic of China; 4Department of Psychology, The Affiliated Hospital of Jiangnan University, Wuxi City, 214151, People’s Republic of ChinaCorrespondence: Jun Wang, Department of Clinical Psychology, The Affiliated Wuxi Mental Health Center of Nanjing Medical University, Wuxi City, 214151, People’s Republic of China, Tel +86 13358119628, Fax +86 51083219366, Email woodfish2@126.com; Zhenhe Zhou, Department of Psychiatry, The Affiliated Wuxi Mental Health Center of Nanjing Medical University, Wuxi City, 214151, People’s Republic of China, Tel +86 13358118986, Fax +86 51083219366, Email zhouzh@njmu.edu.cnPurpose: Anhedonia, a core symptom of major depressive disorder (MDD), is explored in this study, focusing on the neural underpinnings through the examination of two event-related potential (ERP) components: feedback-related negativity (FRN) and stimulus-preceding negativity (SPN).Patients and Methods: This cross-sectional study was conducted in China from March 2022 to March 2023. It involved 35 MDD patients and 31 healthy controls (HC) participating in a modified 2-door task with simultaneous EEG recordings. Depression severity and anhedonia were assessed using the Hamilton Depression Scale (HAMD) and the Temporal Experience of Pleasure Scale (TEPS-CV), respectively. FRN and SPN metrics, along with correlations with each other and clinical assessments, were examined.Results: In comparison to the HC group, the MDD group exhibited significantly lower scores in TEPS-CV (t = 2.854, p = 0.006) and its subscales (t = − 3.596, p = 0.001 and t = 2.434, p = 0.018, respectively), along with consistently reduced amplitudes of FRN (F 1.64= 4.726, p = 0.033) and SPN (F 1.64= 4.195, p = 0.045) across all conditions. Limited correlations were observed between ERP metrics and clinical indicators, except for positive correlations between FRN amplitudes (loss minus win) and HAMD scores (r = 0.392, p = 0.020), and SPN amplitudes after losing (SPN-L) and TEPS-CV consumption subscale scores (r = 0.357, p = 0.035). Notably, while the HC group displayed no significant FRN-SPN correlations, the MDD group exhibited positive FRN-SPN correlations under distinct conditions (r = 0.376, p = 0.026 and r = 0.355, p = 0.037, respectively).Conclusion: Our data reveal subjective and objective anhedonia in both consumption and anticipation, suggesting a shared impairment in reward feedback processing and anticipatory neural mechanisms in individuals with MDD. These findings deepen our understanding of anhedonia’s neural foundations and may guide targeted interventions for this core symptom.Keywords: major depressive disorder, anhedonia, event-related potential, reward processing, feedback-related negativity, stimulus-preceding negativity

Frustration is common in adolescence and often interferes with executive functioning, particularly reward-based decision-making, and yet very little is known about how incidental frustrating events (independent of task-based feedback) disrupt the neural circuitry of reward processing in this important age group. While undergoing functional magnetic resonance imaging (fMRI), 45 healthy adolescents played a card game in which they had to guess between two options to earn points, in low- and high-stake conditions. Functioning of button presses through which they made decisions was intermittently blocked, thereby increasing frustration potential. Neural deactivation of the precuneus, a Default Mode Network region, was observed during obstructed action blocks across stake conditions, but less so on high- relative to low-stake trials. Moreover, less deactivation in goal-directed reward processing regions (i.e., caudate), frontoparietal "task control" regions, and interoceptive processing regions (i.e., somatosensory cortex, thalamus) were observed on high-stake relative to low-stake trials. These findings are consistent with less disruption of goal-directed reward seeking during blocked action efficacy in high-stake conditions among healthy adolescents. These results provide a roadmap of neural systems critical to the processing of frustrating events during reward-based decision-making in youths and could help to characterize how frustration regulation is altered in a range of pediatric psychopathologies.

It is well known that abnormal reward processing is a characteristic feature of various psychopathologies including schizophrenia (SZ). Reduced reward anticipation has been suggested as a core symptom of SZ. The present study aims to evaluate the event-related oscillations (EROs) delta, theta, alpha, beta, and gamma in patients with SZ during the Monetary Incentive Delay (MID) task, which elicits the neural activity of reward processing. Twenty-one patients with SZ and twenty-two demographically matched healthy controls were included in the study. EROs were compared between groups and correlation analyses were conducted to determine a possible relationship between clinical scores and ERO values. Compared with healthy controls, the SZ group had reduced (1) delta and theta amplitudes in the reward condition (2) total beta and non-incentive cue-related beta amplitudes, and (3) incentive cue-related frontal gamma amplitudes. These reductions can be interpreted as impaired dopaminergic neurotransmission and disrupted cognitive functioning in the reward processing of SZ. In contrast, SZ patients showed higher incentive cue-related theta and occipital gamma amplitudes compared to controls. These increments may reflect negative symptoms in SZ. Moreover, theta amplitudes showed a negative correlation with Calgary Depression Scale for Schizophrenia scores and a positive correlation with attentional impulsivity. This is the first study showing the impairments of SZ patients in EROs from delta to gamma frequency bands compared with healthy controls during reward anticipation. Being the first comprehensive study, our results can be interpreted as providing evidence for disrupted brain dynamics in the reward processing of SZ studied by EROs. It may become possible to help patients' wellness by improving our understanding of reward processing in schizophrenia and developing innovative rehabilitation treatments based on these findings. [ABSTRACT FROM AUTHOR]

Childhood adversity is common and associated with elevated risk for transdiagnostic psychopathology. Reward processing has been implicated in the link between adversity and psychopathology, but whether it serves as a mediator or moderator is unclear. This study examined whether alterations in behavioral and neural reward processing function as a mechanism or moderator of psychopathology outcomes following adversity experiences, including threat (i.e., trauma) and deprivation. A longitudinal community sample of 10–15-year-old youths was assessed across two waves (Wave 1: n = 228; Wave 2: n = 206). Wave 1 assessed adverse experiences, psychopathology symptoms, reward processing on a monetary incentive delay task, and resting-state fMRI. At Wave 2, psychopathology symptoms were reassessed. Greater threat experiences were associated with blunted behavioral reward sensitivity, which, in turn, predicted increases in depression symptoms over time and mediated the prospective association between threat and depression symptoms. In contrast, reward sensitivity moderated the association between deprivation experiences and prospective externalizing symptoms such that the positive association of deprivation with increasing externalizing symptoms was absent for children with high levels of reward sensitivity. [ABSTRACT FROM AUTHOR]

Impairments in effort-cost decision-making have been consistently observed in people with schizophrenia (SZ) and may be an important mechanism of negative symptoms. However, the processes that give rise to impairments in effort-cost decision-making are unclear, leading to limited progress in identifying the most relevant treatment targets. Drawing from cognitive models of negative symptoms and goal-directed behavior, this study aimed to examine how and under what type of task conditions defeatist performance beliefs contribute to these decision-making processes. Outpatients with SZ (n = 30) and healthy controls (CN; n = 28) completed a cognitive effort allocation task, the Cognitive Effort-Discounting (COGED) task, which assesses participants' willingness to exert cognitive effort for monetary rewards based on parametrically varied working memory demands (completing N-back levels). Results showed that although participants with SZ demonstrated reduced willingness to work for rewards across N-back levels compared to CN participants, they showed less choice modulation across different N-back conditions. However, among SZ participants with greater defeatist performance beliefs, there was a reduced willingness to choose the high effort option at higher N-back levels (N-back levels 3, 4, and 5 versus 2-back). Results suggest that compared to CN, the SZ group's subjective willingness to expend effort largely did not dynamically adjust as cognitive load increased. However, defeatist beliefs may undermine willingness to expend cognitive effort, especially when cognitive task demands are high. These beliefs may be a viable treatment target to improve effort-cost decision-making impairments in people with SZ. [ABSTRACT FROM AUTHOR]

RationaleCannabis is one of the most widely used psychoactive substances globally. Cannabis use can be associated with alterations of reward processing, including affective flattening, apathy, anhedonia, and lower sensitivity to natural rewards in conjunction with higher sensitivity to cannabis-related rewards. Such alterations have been posited to be driven by changes in underlying brain reward pathways, as per prominent neuroscientific theories of addiction. Functional neuroimaging (fMRI) studies have examined brain reward function in cannabis users via the monetary incentive delay (MID) fMRI task; however, this evidence is yet to be systematically synthesised.ObjectivesWe aimed to systematically integrate the evidence on brain reward function in cannabis users examined by the MID fMRI task; and in relation to metrics of cannabis exposure (e.g., dosage, frequency) and other behavioural variables.MethodWe pre-registered the review in PROSPERO and reported it using PRISMA guidelines. Literature searches were conducted in PsycINFO, PubMed, Medline, CINAHL, and Scopus.ResultsNine studies were included, comprising 534 people with mean ages 16-to-28 years, of which 255 were people who use cannabis daily or almost daily, and 279 were controls. The fMRI literature to date led to largely non-significant group differences. A few studies reported group differences in the ventral striatum while participants anticipated rewards and losses; and in the caudate while participants received neutral outcomes. A few studies examined correlations between brain function and withdrawal, dosage, and age of onset; and reported inconsistent findings.ConclusionsThere is emerging but inconsistent evidence of altered brain reward function in cannabis users examined with the MID fMRI task. Future fMRI studies are required to confirm if the brain reward system is altered in vulnerable cannabis users who experience a Cannabis Use Disorder, as postulated by prominent neuroscientific theories of addiction.

Interpreting the neural response elicited during task functional magnetic resonance imaging (fMRI) remains a challenge in neurodevelopmental research. The monetary incentive delay (MID) task is an fMRI reward processing task that is extensively used in the literature. However, modern psychometric tools have not been used to evaluate measurement properties of the MID task fMRI data. The current study uses data for a similar task design across three adolescent samples (N = 346 [Agemean 12.0; 44 % Female]; N = 97 [19.3; 58 %]; N = 112 [20.2; 38 %]) to evaluate multiple measurement properties of fMRI responses on the MID task. Confirmatory factor analysis (CFA) is used to evaluate an a priori theoretical model for the task and its measurement invariance across three samples. Exploratory factor analysis (EFA) is used to identify the data-driven measurement structure across the samples. CFA results suggest that the a priori model is a poor representation of these MID task fMRI data. Across the samples, the data-driven EFA models consistently identify a six-to-seven factor structure with run and bilateral brain region factors. This factor structure is moderately-to-highly congruent across the samples. Altogether, these findings demonstrate a need to evaluate theoretical frameworks for popular fMRI task designs to improve our understanding and interpretation of brain-behavior associations.

Abstract Background Reward 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. Methods We 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. Results Depressive 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. Conclusions Our 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 registration The 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 ).

BackgroundDysfunctional reward processing is implicated in multiple mental disorders. Novelty seeking (NS) assesses preference for seeking novel experiences, which is linked to sensitivity to reward environmental cues.MethodsA subset of 14-year-old adolescents (IMAGEN) with the top 20% ranked high-NS scores was used to identify high-NS-associated multimodal components by supervised fusion. These features were then used to longitudinally predict five different risk scales for the same and unseen subjects (an independent dataset of subjects at 19 years of age that was not used in predictive modeling training at 14 years of age) (within IMAGEN, n ≈1100) and even for the corresponding symptom scores of five types of patient cohorts (non-IMAGEN), including drinking (n = 313), smoking (n = 104), attention-deficit/hyperactivity disorder (n = 320), major depressive disorder (n = 81), and schizophrenia (n = 147), as well as to classify different patient groups with diagnostic labels.ResultsMultimodal biomarkers, including the prefrontal cortex, striatum, amygdala, and hippocampus, associated with high NS in 14-year-old adolescents were identified. The prediction models built on these features are able to longitudinally predict five different risk scales, including alcohol drinking, smoking, hyperactivity, depression, and psychosis for the same and unseen 19-year-old adolescents and even predict the corresponding symptom scores of five types of patient cohorts. Furthermore, the identified reward-related multimodal features can classify among attention-deficit/hyperactivity disorder, major depressive disorder, and schizophrenia with an accuracy of 87.2%.ConclusionsAdolescents with higher NS scores can be used to reveal brain alterations in the reward-related system, implicating potential higher risk for subsequent development of multiple disorders. The identified high-NS-associated multimodal reward-related signatures may serve as a transdiagnostic neuroimaging biomarker to predict disease risks or severity.

Objective: To identify the spatial–temporal pattern variation of whole-brain functional connectivity (FC) during reward processing in melancholic major depressive disorder (MDD) patients, and to determine the clinical correlates of connectomic differences. Methods: 61 MDD patients and 32 healthy controls were enrolled into the study. During magnetoencephalography (MEG) scanning, all participants completed the facial emotion recognition task. The MDD patients were further divided into two groups: melancholic (n = 31) and non-melancholic (n = 30), based on the Mini International Neuropsychiatric Interview (M.I.N.I.) assessment. Melancholic symptoms were examined by using the 6-item melancholia subscale from the Hamilton Depression Rating Scale (HAM-D6). The whole-brain orthogonalized power envelope connections in the high-beta band (20–35 Hz) were constructed in each period after the happy emotional stimuli (0–200 ms, 100–300 ms, 200–400 ms, 300–500 ms, and 400–600 ms). Then, the network-based statistic (NBS) was used to determine the specific abnormal connection patterns in melancholic MDD patients. Results: The NBS identified a sub-network difference at the mid-late period (300–500 ms) in response to happy faces among the three groups (corrected P = 0.035). Then, the post hoc and correlation analyses found five FCs were decreased in melancholic MDD patients and were related to HAM-D6 score, including FCs of left fusiform gyrus-right orbital inferior frontal gyrus (r = −0.52, P

Background: Mood instability and risk-taking are hallmarks of borderline personality disorder (BPD). Schema modes are combinations of self-reflective evaluations, negative emotional states, and destructive coping strategies common in BPD. When activated, they can push patients with BPD into emotional turmoil and a dissociative state of mind. Our knowledge of the underlying neurocognitive mechanisms driving these changes is incomplete. We hypothesized that in patients with BPD, affective instability is more influenced by reward expectation, outcomes, and reward prediction errors (RPEs) during risky decision-making than in healthy controls. Additionally, we expected that these alterations would be related to schema modes. Methods: Thirty-two patients with BPD and thirty-one healthy controls were recruited. We used an established behavioral paradigm to measure mood fluctuations during risky decision-making. The impact of expectations and RPEs on momentary mood was quantified by a computational model, and its parameters were estimated with hierarchical Bayesian analysis. Model parameters were compared using High-Density Intervals. Results: We found that model parameters capturing the influence of RPE and Certain Rewards on mood were significantly higher in patients with BPD than in controls. These model parameters correlated significantly with schema modes, but not with depression severity. Conclusions: BPD is coupled with altered associations between mood fluctuation and reward processing under uncertainty. Our findings seem to be BPD-specific, as they stand in contrast with the correlates of depressive symptoms. Future studies should establish the clinical utility of these alterations, such as predicting or assessing therapeutic response in BPD. [ABSTRACT FROM AUTHOR]

Research suggests that early parenting may contribute to the development of self-harm but this has not been examined longitudinally. In this study, we explored the relationship between early parenting and self-harm in adolescence and considered whether (1) emotion regulation and (2) decision-making in childhood mediate the relationship between early parenting and self-harm. Using longitudinal data from the Millennium Cohort Study (MCS), we tested mediation models exploring the relationship between early parenting and self-harm in adolescence via emotion regulation and decision-making. Parenting was assessed at age 3 with measures of conflict, closeness and discipline. The trajectories of independence & self-regulation and emotional dysregulation were modelled from ages 3 to 7 years through latent growth curve analysis, with individual predicted slope and intercept values used in the mediation models. Decision-making (deliberation time, total time, delay aversion, quality of decision making, risk adjustment, risk-taking) was assessed using the Cambridge Gambling Task (CGT) at age 11. In our sample (n = 11,145), we found no evidence of a direct association between early parenting and self-harm in adolescence. However, there were indirect effects of parenting (conflict and closeness) on self-harm via the slope of emotional dysregulation. Furthermore, delay aversion was positively associated with self-harm in adolescence. It must be acknowledged that we cannot determine causality and that self-report measures of parenting are vulnerable to several biases. The findings support early identification and interventions for children exhibiting chronic emotional dysregulation and decision-making characterised by a bias for smaller, immediate over larger, delayed rewards. • Indirect effects of early parenting on adolescent self-harm via chronic emotional dysregulation in childhood. • Delay aversion in childhood is associated with self-harm in adolescence. • Findings support interventions for chronic emotional dysregulation and delay aversion in childhood. [ABSTRACT FROM AUTHOR]

Impairments in decision-making have been suggested as a predisposing factor to obesity development. Individuals with excess weight display riskier decisions than normal weight people. Furthermore, adolescence is a period of life in which risky behavior may increase. We aimed to investigate decision making applying the Outcome-Representation-Learning (ORL) model to the Iowa Gambling Task (IGT) in adolescents with excess weight. Twenty-nine excess weight and twenty-eight normal weight adolescents, classified according to their age-adjusted body mass index (BMI) percentile, participated in the study. Decision-making was measured using the IGT. A Bayesian computational ORL model was applied to assess reward learning, punishment learning, forgetfulness, win perseverance and deck perseverance. The IGT net score was lower in excess weight than normal weight adolescents (β = 2.85; p <.027). Reward learning (95% HDI [0.011, 0.232]) was higher, while forgetfulness (95% HDI [− 0.711, − 0.181]) and deck perseverance (95% HDI [− 3.349, − 0.203]) were lower, in excess weight than normal weight adolescents. Excess weight adolescents seemed better at learning the most rewarding choices and showed a random strategy based on reward and novelty seeking. Consequently, excess weight adolescents made more disadvantageous selections, and performed worse in the IGT. [ABSTRACT FROM AUTHOR]

Background: Reward 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. Methods: We 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. Results: Depressive 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. Conclusions: Our 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 registration: The 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). [ABSTRACT FROM AUTHOR]

Inter-individual variability in risk preferences can be reflected in reward processing differences, making people risk-seekers or risk-averse. However, the neural correlates of reward processing in individuals with risk preferences remain unknown. Consequently, this event-related potential (ERP) study examined and compared electrophysiological correlates associated with different stages of reward processing in risk-seeking and risk-averse groups. Individuals scoring in the bottom and top 20% on the Balloon Analogue Risk Task (BART) were deemed risk-averse and risk-seeking, respectively. Participants engaged in a gambling task while their electroencephalogram (EEG) was recorded. Risk-seekers tended to choose high-risk options significantly more frequently than low-risk options, whereas risk-averse individuals chose low-risk options significantly more frequently than high-risk ones. All participants selected the low-risk alternative more slowly than the high-risk option. During the anticipation stage, the low-risk option elicited a relatively attenuated stimulus-preceding negativity (SPN) response from risk-seekers compared to risk-averse participants. During the outcome stage, feedback-related negativity (FRN) increased in risk-seekers responding to greater losses but not in risk-averse participants. These results indicate that ERP components can detect differences in reward processing during risky situations. In addition, these results suggest that motivation and cognitive control, along with their associated neural processes, may play a central role in differences in reward-based behavior between the two groups. [ABSTRACT FROM AUTHOR]

Introduction: Studies suggest an involvement of the ventromedial prefrontal cortex (vmPFC) in reward prediction and processing, with reward-based learning relying on neural activity in response to unpredicted rewards or non-rewards (reward prediction error, RPE). Here, we investigated the causal role of the vmPFC in reward prediction, processing, and RPE signaling by transiently modulating vmPFC excitability using transcranial Direct Current Stimulation (tDCS). Methods: Participants received excitatory or inhibitory tDCS of the vmPFC before completing a gambling task, in which cues signaled varying reward probabilities and symbols provided feedback on monetary gain or loss. We collected self-reported and evaluative data on reward prediction and processing. In addition, cue-locked and feedback-locked neural activity via magnetoencephalography (MEG) and pupil diameter using eye-tracking were recorded. Results: Regarding reward prediction (cue-locked analysis), vmPFC excitation (versus inhibition) resulted in increased prefrontal activation preceding loss predictions, increased pupil dilations, and tentatively more optimistic reward predictions. Regarding reward processing (feedback-locked analysis), vmPFC excitation (versus inhibition) resulted in increased pleasantness, increased vmPFC activation, especially for unpredicted gains (i.e., gain RPEs), decreased perseveration in choice behavior after negative feedback, and increased pupil dilations. Discussion: Our results support the pivotal role of the vmPFC in reward prediction and processing. Furthermore, they suggest that transient vmPFC excitation via tDCS induces a positive bias into the reward system that leads to enhanced anticipation and appraisal of positive outcomes and improves reward-based learning, as indicated by greater behavioral flexibility after losses and unpredicted outcomes, which can be seen as an improved reaction to the received feedback. [ABSTRACT FROM AUTHOR]

Obesity is associated with alterations in brain structure and function, particularly in areas related to reward processing. Although brain structural investigations have demonstrated a continuous association between higher body weight and reduced gray matter in well-powered samples, functional neuroimaging studies have typically only contrasted individuals from the normal weight and obese body mass index (BMI) ranges with modest sample sizes. It remains unclear, whether the commonly found hyperresponsiveness of the reward circuit can (a) be replicated in well-powered studies and (b) be found as a function of higher body weight even below the threshold of clinical obesity. 383 adults across the weight spectrum underwent functional magnetic resonance imaging during a common card-guessing paradigm simulating monetary reward. Multiple regression was used to investigate the association of BMI and neural activation in the reward circuit. In addition, a one-way ANOVA model comparing three weight groups (normal weight, overweight, obese) was calculated. Higher BMI was associated with higher reward response in the bilateral insula. This association could no longer be found when participants with obesity were excluded from the analysis. The ANOVA revealed higher activation in obese vs. lean, but no difference between lean and overweight participants. The overactivation of reward-related brain areas in obesity is a consistent finding that can be replicated in large samples. In contrast to brain structural aberrations associated with higher body weight, the neurofunctional underpinnings of reward processing in the insula appear to be more pronounced in the higher body weight range. [ABSTRACT FROM AUTHOR]

Positive valence system (PVS) deficits are increasingly recognized as important treatment targets for depression and anxiety. Emerging behavioral treatments designed to upregulate the PVS show initial promise; however, neural mechanisms underlying these approaches remain unknown. This study investigated neural reward-processing-related changes following Amplification of Positivity (AMP)-a treatment designed to enhance positive thinking, emotions and behaviors through positive activity interventions (Clinicaltrials.gov: NCT02330627). Individuals with depression and/or anxiety (N = 29) were randomized to 10 sessions of AMP (n = 16) or waitlist (WL; n = 13). Participants completed a monetary incentive delay task during fMRI at baseline and post-assessment. Hypothesis-driven region of interest (ventral striatum, insula, anterior cingulate) and exploratory whole-brain activation and connectivity analyses evaluated pre-to-post changes for AMP vs. WL when anticipating potential monetary gain or loss. No between-group brain activation changes emerged in regions of interest or whole-brain analyses. Increased neural connectivity from pre-to-post-treatment was observed in AMP vs. WL, including ventral striatum, anterior insula, and anterior cingulate connectivity with prefrontal, limbic, occipital and parietal regions-predominantly during loss anticipation. This preliminary study is the first to examine neural mechanisms of positive activity interventions in depression and anxiety and suggests that AMP may strengthen brain connectivity in reward processing, attention, and emotion regulation networks.

IntroductionStudies suggest an involvement of the ventromedial prefrontal cortex (vmPFC) in reward prediction and processing, with reward-based learning relying on neural activity in response to unpredicted rewards or non-rewards (reward prediction error, RPE). Here, we investigated the causal role of the vmPFC in reward prediction, processing, and RPE signaling by transiently modulating vmPFC excitability using transcranial Direct Current Stimulation (tDCS).MethodsParticipants received excitatory or inhibitory tDCS of the vmPFC before completing a gambling task, in which cues signaled varying reward probabilities and symbols provided feedback on monetary gain or loss. We collected self-reported and evaluative data on reward prediction and processing. In addition, cue-locked and feedback-locked neural activity via magnetoencephalography (MEG) and pupil diameter using eye-tracking were recorded.ResultsRegarding reward prediction (cue-locked analysis), vmPFC excitation (versus inhibition) resulted in increased prefrontal activation preceding loss predictions, increased pupil dilations, and tentatively more optimistic reward predictions. Regarding reward processing (feedback-locked analysis), vmPFC excitation (versus inhibition) resulted in increased pleasantness, increased vmPFC activation, especially for unpredicted gains (i.e., gain RPEs), decreased perseveration in choice behavior after negative feedback, and increased pupil dilations.DiscussionOur results support the pivotal role of the vmPFC in reward prediction and processing. Furthermore, they suggest that transient vmPFC excitation via tDCS induces a positive bias into the reward system that leads to enhanced anticipation and appraisal of positive outcomes and improves reward-based learning, as indicated by greater behavioral flexibility after losses and unpredicted outcomes, which can be seen as an improved reaction to the received feedback.

Backgrounds: Value-based decision-making impairment in depression is a complex phenomenon: while some studies did find evidence of blunted reward learning and reward-related signals in the brain, others indicate no effect. Here we test whether such reward sensitivity deficits are dependent on the overall value of the decision problem. Methods: We used a two-armed bandit task with two different contexts: one 'rich', one 'poor' where both options were associated with an overall positive, negative expected value, respectively. We tested patients (N = 30) undergoing a major depressive episode and age, gender and socio-economically matched controls (N = 26). Learning performance followed by a transfer phase, without feedback, were analyzed to distangle between a decision or a value-update process mechanism. Finally, we used computational model simulation and fitting to link behavioral patterns to learning biases. Results: Control subjects showed similar learning performance in the 'rich' and the 'poor' contexts, while patients displayed reduced learning in the 'poor' context. Analysis of the transfer phase showed that the context-dependent impairment in patients generalized, suggesting that the effect of depression has to be traced to the outcome encoding. Computational model-based results showed that patients displayed a higher learning rate for negative compared to positive outcomes (the opposite was true in controls). Conclusions: Our results illustrate that reinforcement learning performances in depression depend on the value of the context. We show that depressive patients have a specific trouble in contexts with an overall negative state value, which in our task is consistent with a negativity bias at the learning rates level. [ABSTRACT FROM AUTHOR]

The use of the term "social attention" (SA) in the cognitive neuroscience and developmental psychopathology literature has increased exponentially in recent years, in part motivated by the aim to understand the early development of autism spectrum disorder (ASD). Unfortunately, theoretical discussions around the term have lagged behind its various uses. Here, we evaluate SA through a review of key candidate SA phenotypes emerging early in life, from newborn gaze cueing and preference for face-like configurations to later emerging skills such as joint attention. We argue that most of the considered SA phenotypes are unlikely to represent unique socioattentional processes and instead have to be understood in the broader context of bottom-up and emerging top-down (domain-general) attention. Some types of SA behaviors (e.g., initiation of joint attention) are linked to the early development of ASD, but this may reflect differences in social motivation rather than attention per se. Several SA candidates are not linked to ASD early in life, including the ones that may represent uniquely socioattentional processes (e.g., orienting to faces, predicting others' manual action goals). Although SA may be a useful superordinate category under which one can organize certain research questions, the widespread use of the term without proper definition is problematic. Characterizing gaze patterns and visual attention in social contexts in infants at elevated likelihood of ASD may facilitate early detection, but conceptual clarity regarding the underlying processes at play is needed to sharpen research questions and identify potential targets for early intervention. [ABSTRACT FROM AUTHOR]