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1

Knutson, Brian, and Andreas Heinz. "Probing Psychiatric Symptoms with the Monetary Incentive Delay Task." Biological Psychiatry 77, no. 5 (March 2015): 418–20. http://dx.doi.org/10.1016/j.biopsych.2014.12.022.

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Joseph, Jane, X. Zhu, C. Benca, G. Baik, F. Davies, and T. H. Kelly. "Adolescents are driven by incentive valence, not magnitude, on the monetary incentive delay task." Drug and Alcohol Dependence 146 (January 2015): e151. http://dx.doi.org/10.1016/j.drugalcdep.2014.09.328.

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Knutson, Brian, Andrew Westdorp, Erica Kaiser, and Daniel Hommer. "FMRI Visualization of Brain Activity during a Monetary Incentive Delay Task." NeuroImage 12, no. 1 (July 2000): 20–27. http://dx.doi.org/10.1006/nimg.2000.0593.

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Wusinich, Christina, Jessica R. Gilbert, Nadia L. Mustafa, and Carlos A. Zarate. "Electrophysiological Correlates of the Monetary Incentive Delay Task in Mood Disorders." Biological Psychiatry 87, no. 9 (May 2020): S282. http://dx.doi.org/10.1016/j.biopsych.2020.02.728.

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Angus, Douglas J., Andrew J. Latham, Eddie Harmon-Jones, Matthias Deliano, Bernard Balleine, and David Braddon-Mitchell. "Electrocortical components of anticipation and consumption in a monetary incentive delay task." Psychophysiology 54, no. 11 (July 4, 2017): 1686–705. http://dx.doi.org/10.1111/psyp.12913.

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Kelly, T. H., Anders Anderson, Shonna Jenkins, Arit M. Harvanko, Catherine Martin, Jessica S. Fogel, Jane Joseph, and Joshua A. Lile. "d-Amphetamine effects and monetary incentive delay task performance: An fMRI study." Drug and Alcohol Dependence 146 (January 2015): e156. http://dx.doi.org/10.1016/j.drugalcdep.2014.09.341.

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Helfinstein, Sarah M., Michael L. Kirwan, Brenda E. Benson, Michael G. Hardin, Daniel S. Pine, Monique Ernst, and Nathan A. Fox. "Validation of a child-friendly version of the monetary incentive delay task." Social Cognitive and Affective Neuroscience 8, no. 6 (June 4, 2012): 720–26. http://dx.doi.org/10.1093/scan/nss057.

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He, Zhenhong, Dandan Zhang, Nils Muhlert, and Rebecca Elliott. "Neural substrates for anticipation and consumption of social and monetary incentives in depression." Social Cognitive and Affective Neuroscience 14, no. 8 (August 2019): 815–26. http://dx.doi.org/10.1093/scan/nsz061.

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Abstract Depression has been reliably associated with abnormalities in the neural representation of reward and loss. However, most studies have focused on monetary incentives; fewer studies have considered neural representation of social incentives. A direct comparison of non-social and social incentives within the same study would establish whether responses to the different incentives are differentially affected in depression. The functional magnetic resonance imaging study presented here investigated the neural activity of individuals with subthreshold depression (SD) and healthy controls (HCs) while they participated in an incentive delay task offering two types of reward (monetary gain vs social approval) and loss (monetary loss vs social disapproval). Compared to HCs, individuals with SD showed increased subgenual anterior cingulate cortex (sgACC) activity during anticipation of social loss, whereas the response in the putamen was decreased during consumption of social gain. Individuals with SD also exhibited diminished insula responses in consuming social loss. Furthermore, positive connectivity between the insula and ventral lateral pre-frontal cortex (VLPFC) was observed in individuals with SD while negative connectivity was found in HCs when consuming social loss. These results demonstrate neural alterations in individuals with depression, specific to the processing of social incentives, mainly characterised by dysfunction within the ‘social pain network’ (sgACC, insula and VLPFC).
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White, Evan J., Rayus Kuplicki, Jennifer L. Stewart, Namik Kirlic, Hung-Wen Yeh, Martin P. Paulus, and Robin L. Aupperle. "Latent variables for region of interest activation during the monetary incentive delay task." NeuroImage 230 (April 2021): 117796. http://dx.doi.org/10.1016/j.neuroimage.2021.117796.

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Kaufman, Jack, Joseph Kim, Anna Bradford, Jacob Germain, Victor Patron, Natalie Grubman, Sophie DelDonno, et al. "Reward Processing in Late Life Depression: Insights From the Monetary Incentive Delay Task." Biological Psychiatry 89, no. 9 (May 2021): S303—S304. http://dx.doi.org/10.1016/j.biopsych.2021.02.757.

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Dhingra, Isha, Sheng Zhang, Simon Zhornitsky, Thang M. Le, Wuyi Wang, Herta H. Chao, Ifat Levy, and Chiang-Shan R. Li. "The effects of age on reward magnitude processing in the monetary incentive delay task." NeuroImage 207 (February 2020): 116368. http://dx.doi.org/10.1016/j.neuroimage.2019.116368.

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Balodis, Iris M., and Marc N. Potenza. "Anticipatory Reward Processing in Addicted Populations: A Focus on the Monetary Incentive Delay Task." Biological Psychiatry 77, no. 5 (March 2015): 434–44. http://dx.doi.org/10.1016/j.biopsych.2014.08.020.

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13

Cao, Zhipeng, Marc Bennett, Catherine Orr, Ilknur Icke, Tobias Banaschewski, Gareth J. Barker, Arun L. W. Bokde, et al. "Mapping adolescent reward anticipation, receipt, and prediction error during the monetary incentive delay task." Human Brain Mapping 40, no. 1 (September 21, 2018): 262–83. http://dx.doi.org/10.1002/hbm.24370.

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Aldridge-Waddon, Luke, Martina Vanova, Jaap Munneke, Ignazio Puzzo, and Veena Kumari. "T228. SOCIAL REWARD REACTIVITY AND SENSITIVITY IN SCHIZOPHRENIA SPECTRUM CONDITIONS." Schizophrenia Bulletin 46, Supplement_1 (April 2020): S319—S320. http://dx.doi.org/10.1093/schbul/sbaa029.788.

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Abstract Background Individuals with schizophrenia spectrum disorders often experience less pleasure during social interaction and frequently demonstrate reduced social motivation. This research examines the extent to which these behaviours may be linked to reduced social reward reactivity and sensitivity, and aims to clarify whether schizophrenia spectrum traits are associated with reduced behavioural and neural responsiveness to social rewards. It includes a systematic review and meta-analyses of social reward sensitivity research in schizophrenia, and also provides preliminary data (participant n = 50) on a novel avatar-based social incentive delay task that was created to further investigate the links between schizophrenia spectrum traits and social reward reactivity. Methods First, a systematic review and meta-analyses (literature database search conducted November 2019) found six studies that investigated social reward anticipation and consumption within the schizophrenia continuum (total participant n = 440). Four investigated social reward sensitivity in clinical samples with schizophrenia diagnoses, and two studied the links between social anhedonia traits and social reward responding in normative samples. The novel social incentive delay task presents participants with the opportunity to win animated avatar-based monetary or social rewards by responding to a cued target. Results The narrative review and meta-analyses of behavioural data from clinical and normative samples found that individuals with schizophrenia diagnoses or traits demonstrate significantly reduced behavioural anticipation of social rewards in comparison to healthy controls. Furthermore, this reduced reward reactivity was more pronounced for social rewards than for monetary rewards. This effect was also mirrored at neural levels, with individuals with schizophrenia demonstrating reduced social reward-related activation in areas such as the ventral striatum and anterior cingulate cortex. Preliminary behavioural data from the social incentive delay task suggest that, in normative samples, more pronounced negative schizotypal traits are associated with reduced anticipation and consumption of social rewards. Like in the reviewed studies, this reduced anticipation was more marked for social rewards than for monetary rewards. Discussion This research suggests that schizophrenia spectrum traits are associated with reduced reactivity and sensitivity to social rewards. It also highlights that this reduced reactivity is demonstrated at behavioural and neural levels, and is more marked for social rewards than for monetary rewards. We consider the implications of these findings for treatment programmes that target atypical social behaviour within schizophrenia spectrum conditions. A series of methodological recommendations for future work investigating social reward reactivity in schizophrenia are also included.
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Mori, Asako, Yasumasa Okamoto, Go Okada, Koki Takagaki, Ran Jinnin, Masahiro Takamura, Makoto Kobayakawa, and Shigeto Yamawaki. "Behavioral activation can normalize neural hypoactivation in subthreshold depression during a monetary incentive delay task." Journal of Affective Disorders 189 (January 2016): 254–62. http://dx.doi.org/10.1016/j.jad.2015.09.036.

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16

Li, Zhi, Yi Wang, Chao Yan, Eric F. C. Cheung, Anna R. Docherty, Pak C. Sham, Raquel E. Gur, Ruben C. Gur, and Raymond C. K. Chan. "Inheritance of Neural Substrates for Motivation and Pleasure." Psychological Science 30, no. 8 (July 18, 2019): 1205–17. http://dx.doi.org/10.1177/0956797619859340.

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Despite advances in the understanding of the reward system and the role of dopamine in recent decades, the heritability of the underlying neural mechanisms is not known. In the present study, we examined the hemodynamic activation of the nucleus accumbens (NAcc), a key hub of the reward system, in 86 healthy monozygotic twins and 88 healthy dizygotic twins during a monetary-incentive-delay task. The participants also completed self-report measures of pleasure. Using voxelwise heritability mapping, we found that activation of the bilateral NAcc during the anticipation of monetary gains had significant heritability ( h2 = .20–.49). Moreover, significant shared genetic covariance was observed between pleasure and NAcc activation during the anticipation of monetary gain. These findings suggest that both NAcc activation and self-reported pleasure may be heritable and that their phenotypic correlation may be partially explained by shared genetic variation.
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Sauder, Colin L., Christina M. Derbidge, and Theodore P. Beauchaine. "Neural responses to monetary incentives among self-injuring adolescent girls." Development and Psychopathology 28, no. 1 (June 8, 2015): 277–91. http://dx.doi.org/10.1017/s0954579415000449.

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AbstractRates of self-inflicted injury among adolescents have risen in recent years, yet much remains to be learned about the pathophysiology of such conduct. Self-injuring adolescents report high levels of both impulsivity and depression behaviorally. Aberrant neural responding to incentives, particularly in striatal and prefrontal regions, is observed among both impulsive and depressed adolescents, and may mark common vulnerability to symptoms of anhedonia, irritability, and low positive affectivity. To date, however, no studies have examined associations between central nervous system reward responding and self-injury. In the current study, self-injuring (n = 19) and control (n = 19) adolescent females, ages 13–19 years, participated in a monetary incentive delay task in which rewards were obtained on some trials and losses were incurred on others. Consistent with previous findings from impulsive and depressed samples, self-injuring adolescents exhibited less activation in both striatal and orbitofrontal cortex regions during anticipation of reward than did controls. Self-injuring adolescents also exhibited reduced bilateral amygdala activation during reward anticipation. Although few studies to date have examined amygdala activity during reward tasks, such findings are common among adults with mood disorders and borderline personality disorder. Implications for neural models of impulsivity, depression, heterotypic comorbidity, and development of both self-injury and borderline personality traits are discussed.
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18

Admon, R., L. D. Nickerson, D. G. Dillon, A. J. Holmes, R. Bogdan, P. Kumar, D. D. Dougherty, et al. "Dissociable cortico-striatal connectivity abnormalities in major depression in response to monetary gains and penalties." Psychological Medicine 45, no. 1 (May 15, 2014): 121–31. http://dx.doi.org/10.1017/s0033291714001123.

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BackgroundIndividuals with major depressive disorder (MDD) are characterized by maladaptive responses to both positive and negative outcomes, which have been linked to localized abnormal activations in cortical and striatal brain regions. However, the exact neural circuitry implicated in such abnormalities remains largely unexplored.MethodIn this study 26 unmedicated adults with MDD and 29 matched healthy controls (HCs) completed a monetary incentive delay task during functional magnetic resonance imaging (fMRI). Psychophysiological interaction (PPI) analyses probed group differences in connectivity separately in response to positive and negative outcomes (i.e. monetary gains and penalties).ResultsRelative to HCs, MDD subjects displayed decreased connectivity between the caudate and dorsal anterior cingulate cortex (dACC) in response to monetary gains, yet increased connectivity between the caudate and a different, more rostral, dACC subregion in response to monetary penalties. Moreover, exploratory analyses of 14 MDD patients who completed a 12-week, double-blind, placebo-controlled clinical trial after the baseline fMRI scans indicated that a more normative pattern of cortico-striatal connectivity pre-treatment was associated with greater improvement in symptoms 12 weeks later.ConclusionsThese results identify the caudate as a region with dissociable incentive-dependent dACC connectivity abnormalities in MDD, and provide initial evidence that cortico-striatal circuitry may play a role in MDD treatment response. Given the role of cortico-striatal circuitry in encoding action–outcome contingencies, such dysregulated connectivity may relate to the prominent disruptions in goal-directed behavior that characterize MDD.
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Krugliakova, Elena, Vasily Klucharev, Tommaso Fedele, Alexey Gorin, Aleksandra Kuznetsova, and Anna Shestakova. "Correlation of cue-locked FRN and feedback-locked FRN in the auditory monetary incentive delay task." Experimental Brain Research 236, no. 1 (December 1, 2017): 141–51. http://dx.doi.org/10.1007/s00221-017-5113-2.

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Khosravian, Kiana, Hanna Keren, Liana Meffert, Daniel S. Pine, and Argyris Stringaris. "F88. A Transdiagnostic Study of Reward Processing Alterations in Adolescents Using the Monetary Incentive Delay Task." Biological Psychiatry 83, no. 9 (May 2018): S271—S272. http://dx.doi.org/10.1016/j.biopsych.2018.02.701.

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21

Lawn, Will, James Hill, Chandni Hindocha, Jocelyn Yim, Yumeya Yamamori, Gus Jones, Hannah Walker, et al. "The acute effects of cannabidiol on the neural correlates of reward anticipation and feedback in healthy volunteers." Journal of Psychopharmacology 34, no. 9 (August 5, 2020): 969–80. http://dx.doi.org/10.1177/0269881120944148.

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Background: Cannabidiol has potential therapeutic benefits for people with psychiatric disorders characterised by reward function impairment. There is existing evidence that cannabidiol may influence some aspects of reward processing. However, it is unknown whether cannabidiol acutely affects brain function underpinning reward anticipation and feedback. Hypotheses: We predicted that cannabidiol would augment brain activity associated with reward anticipation and feedback. Methods: We administered a single 600 mg oral dose of cannabidiol and matched placebo to 23 healthy participants in a double-blind, placebo-controlled, repeated-measures design. We employed the monetary incentive delay task during functional magnetic resonance imaging to assay the neural correlates of reward anticipation and feedback. We conducted whole brain analyses and region-of-interest analyses in pre-specified reward-related brain regions. Results: The monetary incentive delay task elicited expected brain activity during reward anticipation and feedback, including in the insula, caudate, nucleus accumbens, anterior cingulate and orbitofrontal cortex. However, across the whole brain, we did not find any evidence that cannabidiol altered reward-related brain activity. Moreover, our Bayesian analyses showed that activity in our regions-of-interest was similar following cannabidiol and placebo. Additionally, our behavioural measures of motivation for reward did not show a significant difference between cannabidiol and placebo. Discussion: Cannabidiol did not acutely affect the neural correlates of reward anticipation and feedback in healthy participants. Future research should explore the effects of cannabidiol on different components of reward processing, employ different doses and administration regimens, and test its reward-related effects in people with psychiatric disorders.
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Dugré, Jules R., Alexandre Dumais, Nathalie Bitar, and Stéphane Potvin. "Loss anticipation and outcome during the Monetary Incentive Delay Task: a neuroimaging systematic review and meta-analysis." PeerJ 6 (May 10, 2018): e4749. http://dx.doi.org/10.7717/peerj.4749.

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Background Reward seeking and avoidance of punishment are key motivational processes. Brain-imaging studies often use the Monetary Incentive Delay Task (MIDT) to evaluate motivational processes involved in maladaptive behavior. Although the bulk of research has been done on the MIDT reward events, little is known about the neural basis of avoidance of punishment. Therefore, we conducted a meta-analysis of brain activations during anticipation and receipt of monetary losses in healthy controls. Methods All functional neuro-imaging studies using the MIDT in healthy controls were retrieved using PubMed, Google Scholar & EMBASE databases. Functional neuro-imaging data was analyzed using the Seed-based d Mapping Software. Results Thirty-five studies met the inclusion criteria, comprising 699 healthy adults. In both anticipation and loss outcome phases, participants showed large and robust activations in the bilateral striatum, (anterior) insula, and anterior cingulate gyrus relatively to Loss > Neutral contrast. Although relatively similar activation patterns were observed during the two event types, they differed in the pattern of prefrontal activations: ventro-lateral prefrontal activations were observed during loss anticipation, while medial prefrontal activations were observed during loss receipt. Discussion Considering that previous meta-analyses highlighted activations in the medial prefrontal cortex/anterior cingulate cortex, the anterior insula and the ventral striatum, the current meta-analysis highlighted the potential specificity of the ventro-lateral prefrontal regions, the median cingulate cortex and the amygdala in the loss events. Future studies can rely on these latter results to examine the neural correlates of loss processing in psychiatric populations characterized by harm avoidance or insensitivity to punishment.
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Silverman, Merav H., Robert F. Krueger, William G. Iacono, Stephen M. Malone, Ruskin H. Hunt, and Kathleen M. Thomas. "Quantifying familial influences on brain activation during the monetary incentive delay task: An adolescent monozygotic twin study." Biological Psychology 103 (December 2014): 7–14. http://dx.doi.org/10.1016/j.biopsycho.2014.07.016.

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Jauhar, S., L. Fortea, A. Solanes, A. Albajes-Eizagirre, P. J. McKenna, and J. Radua. "Brain activations associated with anticipation and delivery of monetary reward: A systematic review and meta-analysis of fMRI studies." PLOS ONE 16, no. 8 (August 5, 2021): e0255292. http://dx.doi.org/10.1371/journal.pone.0255292.

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Background While multiple studies have examined the brain functional correlates of reward, meta-analyses have either focused on studies using the monetary incentive delay (MID) task, or have adopted a broad strategy, combining data from studies using both monetary and non-monetary reward, as probed using a wide range of tasks. Objective To meta-analyze fMRI studies that used monetary reward and in which there was a definable cue-reward contingency. Studies were limited to those using monetary reward in order to avoid potential heterogeneity from use of other rewards, especially social rewards. Studies using gambling or delay discounting tasks were excluded on the grounds that reward anticipation is not easily quantifiable. Study eligibility English-language fMRI studies (i) that reported fMRI findings on healthy adults; (ii) that used monetary reward; and (iii) in which a cue that was predictive of reward was compared to a no win (or lesser win) condition. Only voxel-based studies were included; those where brain coverage was incomplete were excluded. Data sources Ovid, Medline and PsycInfo, from 2000 to 2020, plus checking of review articles and meta-analyses. Data synthesis Data were pooled using Seed-based d Mapping with Permutation of Subject Images (SDM-PSI). Heterogeneity among studies was examined using the I2 statistic. Publication bias was examined using funnel plots and statistical examination of asymmetries. Moderator variables including whether the task was pre-learnt, sex distribution, amount of money won and width of smoothing kernel were examined. Results Pooled data from 45 studies of reward anticipation revealed activations in the ventral striatum, the middle cingulate cortex/supplementary motor area and the insula. Pooled data from 28 studies of reward delivery again revealed ventral striatal activation, plus cortical activations in the anterior and posterior cingulate cortex. There was relatively little evidence of publication bias. Among moderating variables, only whether the task was pre-learnt exerted an influence. Conclusions According to this meta-analysis monetary reward anticipation and delivery both activate the ventral but not the dorsal striatum, and are associated with different patterns of cortical activation.
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Arce, Estibaliz, Rita Balice-Gordon, Sridhar Duvvuri, Melissa Naylor, Zhiyong Xie, Brian Harel, Rouba Kozak, David L. Gray, and Nicholas DeMartinis. "A novel approach to evaluate the pharmacodynamics of a selective dopamine D1/D5 receptor partial agonist (PF-06412562) in patients with stable schizophrenia." Journal of Psychopharmacology 33, no. 10 (July 2, 2019): 1237–47. http://dx.doi.org/10.1177/0269881119855302.

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Background: PF-06412562 is an orally bioavailable, selective dopamine D1/D5 receptor partial agonist with a non-catechol structure under evaluation for treatment of cognitive impairment in schizophrenia. Aims: This randomized, double-blind, placebo-controlled, parallel-group, Phase 1b study examined the pharmacokinetics and pharmacodynamics of three doses of PF-06412562 (3 mg, 9 mg, and 45 mg twice daily) over 15 days in patients with schizophrenia receiving antipsychotics. Methods: Primary endpoints included adjunctive safety/tolerability and effects on MATRICS Consensus Cognitive Battery Working Memory domain and reward processing (Monetary Incentive Delay) tasks. Exploratory endpoints included other behavioral/neurophysiological tasks, including the N-back task. Results: Among 95 subjects (78% male; mean age 34.8 years), baseline characteristics were similar across groups. The MATRICS Consensus Cognitive Battery Working Memory composite change from baseline on Day 13 improved in all groups, the smallest improvement was observed in the 45 mg group and was significantly smaller than that in the placebo group (two-sided p=0.038). For the Monetary Incentive Delay task (change from baseline in blood-oxygen-level-dependent functional magnetic resonance imaging activation in anterior ventral striatum for the contrast of cue gain>cue no gain on Day 15), no PF-06412562 dose was significantly different from placebo. No doses of PF-06412562 showed a significant difference on two-back task accuracy versus placebo. Conclusions: Adjunctive treatment with PF-06412562 was safe and well tolerated in patients with schizophrenia. PF-06412562 failed to show clinical benefit relative to placebo on assessments of cognition or reward processing in symptomatically stable patients over a 15-day treatment period. Numerous limitations due to the safety study design warrant further efficacy evaluation for this drug mechanism.
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Broyd, Samantha J., Helen J. Richards, Suzannah K. Helps, Georgia Chronaki, Susan Bamford, and Edmund J. S. Sonuga-Barke. "An electrophysiological monetary incentive delay (e-MID) task: A way to decompose the different components of neural response to positive and negative monetary reinforcement." Journal of Neuroscience Methods 209, no. 1 (July 2012): 40–49. http://dx.doi.org/10.1016/j.jneumeth.2012.05.015.

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Zhornitsky, Simon, Isha Dhingra, Thang M. Le, Wuyi Wang, Chiang-shan R. Li, and Sheng Zhang. "Reward-Related Responses and Tonic Craving in Cocaine Addiction: An Imaging Study of the Monetary Incentive Delay Task." International Journal of Neuropsychopharmacology 24, no. 8 (April 2, 2021): 634–44. http://dx.doi.org/10.1093/ijnp/pyab016.

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Abstract Background Cocaine addiction is associated with altered sensitivity to natural reinforcers and intense drug craving. However, previous findings on reward-related responses were mixed, and few studies have examined whether reward responses relate to tonic cocaine craving. Methods We combined functional magnetic resonance imaging and a monetary incentive delay task to investigate these issues. Imaging data were processed with published routines, and the results were evaluated with a corrected threshold. We compared reward responses of 50 cocaine-dependent individuals (CDs) and 45 healthy controls (HCs) for the ventral striatum (VS) and the whole brain. We also examined the regional responses in association with tonic cocaine craving, as assessed by the Cocaine Craving Questionnaire (CCQ) in CDs. We performed mediation analyses to evaluate the relationship between regional responses, CCQ score, and recent cocaine use. Results The VS showed higher activation to large as compared with small or no wins, but this reward-related activity did not differ between CDs and HCs. The precentral gyrus (PCG), anterior insula, and supplementary motor area showed higher activation during large vs no wins in positive correlation with the CCQ score in CDs. Mediation analyses suggested that days of cocaine use in the prior month contributed to higher CCQ scores and, in turn, PCG reward responses. Conclusions The results highlight a unique relationship between reward responses of the primary motor cortex, tonic cocaine craving, and recent cocaine use. The motor cortex may partake in the cognitive motor processes critical to drug-seeking behavior in addicted individuals.
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White, Evan J., Mariah Nacke, Elisabeth Akeman, Mallory J. Cannon, Ahmad Mayeli, James Touthang, Obada al Zoubi, et al. "P300 amplitude during a monetary incentive delay task predicts future therapy completion in individuals with major depressive disorder." Journal of Affective Disorders 295 (December 2021): 873–82. http://dx.doi.org/10.1016/j.jad.2021.08.106.

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DelDonno, Sophie R., Aimee James Karstens, Brian Cerny, Leah R. Kling, Lisanne M. Jenkins, Jonathan P. Stange, Robin Nusslock, Stewart A. Shankman, and Scott A. Langenecker. "The Titrated Monetary Incentive Delay Task: Sensitivity, convergent and divergent validity, and neural correlates in an RDoC sample." Journal of Clinical and Experimental Neuropsychology 41, no. 5 (March 26, 2019): 512–29. http://dx.doi.org/10.1080/13803395.2019.1585519.

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Gu, Ruolei, Yang Jiang, Seth Kiser, Chelsea L. Black, Lucas S. Broster, Yue-jia Luo, and Thomas H. Kelly. "Impulsive personality dimensions are associated with altered behavioral performance and neural responses in the monetary incentive delay task." Neuropsychologia 103 (August 2017): 59–68. http://dx.doi.org/10.1016/j.neuropsychologia.2017.07.013.

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Chen, Yu, Isha Dhingra, Thang M. Le, Simon Zhornitsky, Sheng Zhang, and Chiang-Shan R. Li. "Win and Loss Responses in the Monetary Incentive Delay Task Mediate the Link between Depression and Problem Drinking." Brain Sciences 12, no. 12 (December 9, 2022): 1689. http://dx.doi.org/10.3390/brainsci12121689.

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Depression and alcohol misuse, frequently comorbid, are associated with altered reward processing. However, no study has examined whether and how the neural markers of reward processing are shared between depression and alcohol misuse. We studied 43 otherwise-healthy drinking adults in a monetary incentive delay task (MIDT) during fMRI. All participants were evaluated with the Alcohol Use Disorders Identification Test (AUDIT) and Beck’s Depression Inventory (BDI-II) to assess the severity of drinking and depression. We performed whole brain regressions against each AUDIT and BDI-II score to investigate the neural correlates and evaluated the findings at a corrected threshold. We performed mediation analyses to examine the inter-relationships between win/loss responses, alcohol misuse, and depression. AUDIT and BDI-II scores were positively correlated across subjects. Alcohol misuse and depression shared win-related activations in frontoparietal regions and parahippocampal gyri (PHG), and right superior temporal gyri (STG), as well as loss-related activations in the right PHG and STG, and midline cerebellum. These regional activities (β’s) completely mediated the correlations between BDI-II and AUDIT scores. The findings suggest shared neural correlates interlinking depression and problem drinking both during win and loss processing and provide evidence for co-morbid etiological processes of depressive and alcohol use disorders.
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Saji, Kanako, Yumiko Ikeda, Woochan Kim, Yoshitoshi Shingai, Amane Tateno, Hidehiko Takahashi, Yoshiro Okubo, Haruhisa Fukayama, and Hidenori Suzuki. "Acute NK1 receptor antagonist administration affects reward incentive anticipation processing in healthy volunteers." International Journal of Neuropsychopharmacology 16, no. 7 (August 1, 2013): 1461–71. http://dx.doi.org/10.1017/s1461145712001678.

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Abstract The primary brain structures of reward processing are mainly situated in the mid-brain dopamine system. The nucleus accumbens (NAc) receives dopaminergic projections from the ventral tegmental area and works as a key brain region for the positive incentive value of rewards. Because neurokinin-1 (NK1) receptor, the cognate receptor for substance P (SP), is highly expressed in the NAc, we hypothesized that the SP/NK1 receptor system might play a role in positive reward processing in the NAc in humans. Therefore, we conducted a functional MRI (fMRI) study to assess the effects of an NK1 receptor antagonist on human reward processing through a monetary incentive delay task that is known to elicit robust activation in the NAc especially during gain anticipation. Eighteen healthy adults participated in two series of an fMRI study, taking either a placebo or the NK1 receptor antagonist aprepitant. Behavioural measurements revealed that there was no significant difference in reaction time, hit rate, or self-reported effort for incentive cues between the placebo and aprepitant treatments. fMRI showed significant decrease in blood oxygenation-level-dependent signals in the NAc during gain anticipation with the aprepitant treatment compared to the placebo treatment. These results suggest that SP/NK1 receptor system is involved in processing of positive incentive anticipation and plays a role in accentuating positive valence in association with the primary dopaminergic pathways in the reward circuit.
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Nepomuceno, Thyago Celso Cavalcante, Késsia Thais Cavalcanti Nepomuceno, Thiago Poleto, Victor Diogho Heuer de Carvalho, and Ana Paula Cabral Seixas Costa. "When Penalty Fails: Modeling Contractual Misincentives With Evidence From Portugal ITO Agreements." SAGE Open 12, no. 4 (October 2022): 215824402211418. http://dx.doi.org/10.1177/21582440221141850.

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A misincentive is characterized as an incentive producing the opposite effect of motivating or preventing some specific action. In some circumstances, contract penalties such as sanctions and fines on late delivery or low-quality software encourage the irregularities instead of preventing them from occurring. The present study models misincentive behaviors in Information Technology Outsourcing (ITO) transactions as a Principal-Agent problem. Considering the non-linear relationship in software vendors’ cost structure and the client’s sensitivity to the product/service quality and delivery time, we offer theoretical modeling elucidating the best responses on agreements under incomplete and asymmetric information. Some empirical evidence of contractual misincentives is reported in outsourcing arrangements between private institutions and public administrations in Portugal. The contracts were divided into three categories: pure contracts with no incentive clauses, contracts with no explicit monetary penalties, and contracts under explicit sanctions. The results suggest that the knowledge of the penalty reduces the Agent’s uncertainty about the Principal’s cost structure and might lead them to intentionally delay the delivery of the technology.
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Wilson, Robin Paul, Marco Colizzi, Matthijs Geert Bossong, Paul Allen, Matthew Kempton, and Sagnik Bhattacharyya. "The Neural Substrate of Reward Anticipation in Health: A Meta-Analysis of fMRI Findings in the Monetary Incentive Delay Task." Neuropsychology Review 28, no. 4 (September 25, 2018): 496–506. http://dx.doi.org/10.1007/s11065-018-9385-5.

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Oldham, Stuart, Carsten Murawski, Alex Fornito, George Youssef, Murat Yücel, and Valentina Lorenzetti. "The anticipation and outcome phases of reward and loss processing: A neuroimaging meta-analysis of the monetary incentive delay task." Human Brain Mapping 39, no. 8 (April 25, 2018): 3398–418. http://dx.doi.org/10.1002/hbm.24184.

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Manssuer, Luis, Ding Qiong, Yijie Zhao, Rocky Yang, ChenCheng Zhang, Shikun Zhan, Bomin Sun, and Valerie Voon. "#3097 Temporal and spectral dynamics of reward and risk processing in the amygdala revealed with stereo-EEG recordings in epilepsy." Journal of Neurology, Neurosurgery & Psychiatry 92, no. 8 (July 16, 2021): A4.2—A5. http://dx.doi.org/10.1136/jnnp-2021-bnpa.12.

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Objectives/AimsTo examine the temporal and spectral characteristics of local field potentials recorded from the amygdala in epilepsy in the context of the anticipation and receipt of rewards and losses using an incentive learning task and a risky decision-making task.Methods16 Epilepsy patients completed two tasks. In the monetary incentive delay (MID) task, patients saw reward and loss cues which indicated whether money could be won or lost depending on whether a subsequent response was or was not quick/accurate enough, respectively. This was compared with neutral cues where responses were neither rewarded nor punished regardless of response.In the risk task, patients were presented with two face down cards with values ranging from 1 to 10. When the first card is revealed, patients have to choose whether to bet or not bet that the second card is higher. After the card is revealed, patients receive a monetary reward if it is higher and a loss if it is lower. If patients do not bet, they receive nothing.ResultsIn both tasks, patients showed larger left amygdala theta band oscillatory activity to the receipt of monetary rewards compared to no money. In contrast, there were no significant responses to monetary losses. During the decision phase of the risk task, there was increased theta activity when patients chose to bet instead of not betting and when the decision had low risk (card <= 5) compared to high risk (card above 5). There were no effects of uncertainty.ConclusionsThe combined results of these two studies embellish our understanding of the role of the amygdala in motivation and decision-making processes and lend further support for its role in reward related processes rather than its often cited fear-related functions (Baxter & Murray, 2002; Murray, 2007). Theta activation is linked to cognitive processes in frontal cortices and coupled to MTL activity (Helfrich & Knight, 2016). As left amygdala theta activation was only recruited when patients were making their bet and not just anticipating reward, the pattern of results lend support to its role in cognition-emotion interactions specific to risk and reward but not uncertainty. Indeed, the hemispheric asymmetry is highly consistent with EEG studies showing left prefrontal dominance in reward processing (Manssuer et al., 2021).
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S, Smys, and Subarna Shakya. "Vehicle Parking Assistance with Multi-Round Auction and Offload Reduction." Journal of Electrical Engineering and Automation 2, no. 3 (January 25, 2021): 129–34. http://dx.doi.org/10.36548/jeea.2020.3.004.

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One of the most promising fields of vehicular fog computing (VFC) is by using it as a means to build a parking lot allotment system. Integrating this with parked vehicle assistance system, we can use VFC to its full potential. In this paper, we propose an automatic vehicle allocation system that guides the vehicles on the move to their allotted parking slot, making it simpler to park. Moreover, further add-ons such as monetary rewards are given means to compensate for the cost of service. The VFC is exploited to ensure that there is no delay in parking allotment. Moreover, the payment rule proposed by the system ensures budget balance, individual rationality and incentive compatibility. The performance output is measured using simulation results and it is observed that there is a significant improvement and the same is recorded.
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Nestor, Liam J., Anna Murphy, John McGonigle, Csaba Orban, Laurence Reed, Eleanor Taylor, Remy Flechais, et al. "Acute naltrexone does not remediate fronto-striatal disturbances in alcoholic and alcoholic polysubstance-dependent populations during a monetary incentive delay task." Addiction Biology 22, no. 6 (September 6, 2016): 1576–89. http://dx.doi.org/10.1111/adb.12444.

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39

Mullins, Teagan S., Ethan M. Campbell, and Jeremy Hogeveen. "Neighborhood Deprivation Shapes Motivational-Neurocircuit Recruitment in Children." Psychological Science 31, no. 7 (June 30, 2020): 881–89. http://dx.doi.org/10.1177/0956797620929299.

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Implementing motivated behaviors on the basis of prior reward is central to adaptive human functioning, but aberrant reward-motivated behavior is a core feature of neuropsychiatric illness. Children from disadvantaged neighborhoods have decreased access to rewards, which may shape motivational neurocircuits and risk for psychopathology. Here, we leveraged the unprecedented neuroimaging data from the Adolescent Brain Cognitive Development (ABCD) study to test the hypothesis that neighborhood socioeconomic disadvantage shapes the functional recruitment of motivational neurocircuits in children. Specifically, via the ABCD study’s monetary-incentive-delay task ( N = 6,396 children; age: 9–10 years), we found that children from zip codes with a high Area Deprivation Index demonstrate blunted recruitment of striatum (dorsal and ventral nuclei) and pallidum during reward anticipation. In fact, blunted dorsal striatal recruitment during reward anticipation mediated the association between Area Deprivation Index and increased attention problems. These data reveal a candidate mechanism driving elevated risk for psychopathology in children from socioeconomically disadvantaged neighborhoods.
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Wilson, Robin Paul, Marco Colizzi, Matthijs Geert Bossong, Paul Allen, Matthew Kempton, and Sagnik Bhattacharyya. "Correction to: The Neural Substrate of Reward Anticipation in Health: A Meta-Analysis of fMRI Findings in the Monetary Incentive Delay Task." Neuropsychology Review 28, no. 4 (December 2018): 507–8. http://dx.doi.org/10.1007/s11065-018-9390-8.

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Patel, Krishna T., Michael C. Stevens, Shashwath A. Meda, Christine Muska, Andre D. Thomas, Marc N. Potenza, and Godfrey D. Pearlson. "Robust Changes in Reward Circuitry During Reward Loss in Current and Former Cocaine Users During Performance of a Monetary Incentive Delay Task." Biological Psychiatry 74, no. 7 (October 2013): 529–37. http://dx.doi.org/10.1016/j.biopsych.2013.04.029.

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Davis, Marie-Claire, Aron T. Hill, Paul B. Fitzgerald, Julie C. Stout, and Kate E. Hoy. "Motivationally salient cue processing measured using the monetary incentive delay (MID) task with electroencephalography (EEG): A potential marker of apathy in Huntington's disease." Neuropsychologia 177 (December 2022): 108426. http://dx.doi.org/10.1016/j.neuropsychologia.2022.108426.

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Mori, Asako, Yasumasa Okamoto, Go Okada, Koki Takagaki, Ran Jinnin, Masahiro Takamura, Makoto Kobayakawa, and Shigeto Yamawaki. "Corrigendum to “Behavioral activation can normalize neural hypoactivation in subthreshold depression during a monetary incentive delay task” [J. Affect. Disord. 189 (2016) 254–262]." Journal of Affective Disorders 208 (January 2017): 670. http://dx.doi.org/10.1016/j.jad.2015.12.023.

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Schreiter, S., S. Spengler, A. Willert, S. Mohnke, D. Herold, S. Erk, N. Romanczuk-Seiferth, et al. "Neural alterations of fronto-striatal circuitry during reward anticipation in euthymic bipolar disorder." Psychological Medicine 46, no. 15 (August 30, 2016): 3187–98. http://dx.doi.org/10.1017/s0033291716001963.

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BackgroundBipolar disorder (BD), with the hallmark symptoms of elevated and depressed mood, is thought to be characterized by underlying alterations in reward-processing networks. However, to date the neural circuitry underlying abnormal responses during reward processing in BD remains largely unexplored. The aim of this study was to investigate whether euthymic BD is characterized by aberrant ventral striatal (VS) activation patterns and altered connectivity with the prefrontal cortex in response to monetary gains and losses.MethodDuring functional magnetic resonance imaging 20 euthymic BD patients and 20 age-, gender- and intelligence quotient-matched healthy controls completed a monetary incentive delay paradigm, to examine neural processing of reward and loss anticipation. A priori defined regions of interest (ROIs) included the VS and the anterior prefrontal cortex (aPFC). Psychophysiological interactions (PPIs) between these ROIs were estimated and tested for group differences for reward and loss anticipation separately.ResultsBD participants, relative to healthy controls, displayed decreased activation selectively in the left and right VS during anticipation of reward, but not during loss anticipation. PPI analyses showed decreased functional connectivity between the left VS and aPFC in BD patients compared with healthy controls during reward anticipation.ConclusionsThis is the first study showing decreased VS activity and aberrant connectivity in the reward-processing circuitry in euthymic, medicated BD patients during reward anticipation. Our findings contrast with research supporting a reward hypersensitivity model of BD, and add to the body of literature suggesting that blunted activation of reward processing circuits may be a vulnerability factor for mood disorders.
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Murphy, Anna, Liam J. Nestor, John McGonigle, Louise Paterson, Venkataramana Boyapati, Karen D. Ersche, Remy Flechais, et al. "Acute D3 Antagonist GSK598809 Selectively Enhances Neural Response During Monetary Reward Anticipation in Drug and Alcohol Dependence." Neuropsychopharmacology 42, no. 5 (January 2, 2017): 1049–57. http://dx.doi.org/10.1038/npp.2016.289.

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Abstract Evidence suggests that disturbances in neurobiological mechanisms of reward and inhibitory control maintain addiction and provoke relapse during abstinence. Abnormalities within the dopamine system may contribute to these disturbances and pharmacologically targeting the D3 dopamine receptor (DRD3) is therefore of significant clinical interest. We used functional magnetic resonance imaging to investigate the acute effects of the DRD3 antagonist GSK598809 on anticipatory reward processing, using the monetary incentive delay task (MIDT), and response inhibition using the Go/No-Go task (GNGT). A double-blind, placebo-controlled, crossover design approach was used in abstinent alcohol dependent, abstinent poly-drug dependent and healthy control volunteers. For the MIDT, there was evidence of blunted ventral striatal response to reward in the poly-drug-dependent group under placebo. GSK598809 normalized ventral striatal reward response and enhanced response in the DRD3-rich regions of the ventral pallidum and substantia nigra. Exploratory investigations suggested that the effects of GSK598809 were mainly driven by those with primary dependence on alcohol but not on opiates. Taken together, these findings suggest that GSK598809 may remediate reward deficits in substance dependence. For the GNGT, enhanced response in the inferior frontal cortex of the poly-drug group was found. However, there were no effects of GSK598809 on the neural network underlying response inhibition nor were there any behavioral drug effects on response inhibition. GSK598809 modulated the neural network underlying reward anticipation but not response inhibition, suggesting that DRD3 antagonists may restore reward deficits in addiction.
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Zhou, Shiyu, Lu Nie, Zhao Wang, Mengyao Wang, and Ya Zheng. "Aberrant reward dynamics in trait anticipatory anhedonia." Social Cognitive and Affective Neuroscience 14, no. 8 (August 2019): 899–909. http://dx.doi.org/10.1093/scan/nsz062.

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Abstract As a cardinal feature of several psychiatric disorders, anhedonia includes a consummatory component (deficits in hedonic response to rewards) and an anticipatory component (a reduced motivation to pursue them). Although being conceptualized as impairments of reward system, the neural characterization of reward processing in anhedonia is hampered by the enormous heterogeneity in the reward phase (‘wanting’ vs ‘liking’) and comorbidity (inherent to disease states). The current event-related potential (ERP) study examined the reward dynamics of anticipatory anhedonia in a non-clinical sample. Anticipatory and consummatory ERP components were assessed with a monetary incentive delay task in a high anticipatory anhedonia (HAA) group and a low anticipatory anhedonia (LAA) group. HAA vs LAA group showed a diminished reward-related speeding during behavioral performance and reported overall reduced positive affect during anticipation and receipt of outcomes. Importantly, neural dynamics underlying reward processing were negatively associated with anticipatory anhedonia across the anticipatory phase indexed by the contingent negative variation and the consummatory phase indexed by the feedback P3. Our results suggest that anticipatory anhedonia in non-clinical individuals is linked to a poor modulation during both anticipatory and consummatory phases of reward processing.
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47

McGonigle, John, Anna Murphy, Louise M. Paterson, Laurence J. Reed, Liam Nestor, Jonathan Nash, Rebecca Elliott, et al. "The ICCAM platform study: An experimental medicine platform for evaluating new drugs for relapse prevention in addiction. Part B: fMRI description." Journal of Psychopharmacology 31, no. 1 (October 4, 2016): 3–16. http://dx.doi.org/10.1177/0269881116668592.

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Objectives: We aimed to set up a robust multi-centre clinical fMRI and neuropsychological platform to investigate the neuropharmacology of brain processes relevant to addiction – reward, impulsivity and emotional reactivity. Here we provide an overview of the fMRI battery, carried out across three centres, characterizing neuronal response to the tasks, along with exploring inter-centre differences in healthy participants. Experimental design: Three fMRI tasks were used: monetary incentive delay to probe reward sensitivity, go/no-go to probe impulsivity and an evocative images task to probe emotional reactivity. A coordinate-based activation likelihood estimation (ALE) meta-analysis was carried out for the reward and impulsivity tasks to help establish region of interest (ROI) placement. A group of healthy participants was recruited from across three centres (total n=43) to investigate inter-centre differences. Principle observations: The pattern of response observed for each of the three tasks was consistent with previous studies using similar paradigms. At the whole brain level, significant differences were not observed between centres for any task. Conclusions: In developing this platform we successfully integrated neuroimaging data from three centres, adapted validated tasks and applied whole brain and ROI approaches to explore and demonstrate their consistency across centres.
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Mucci, A., D. Dima, A. Soricelli, U. Volpe, P. Bucci, S. Frangou, A. Prinster, M. Salvatore, S. Galderisi, and M. Maj. "Is avolition in schizophrenia associated with a deficit of dorsal caudate activity? A functional magnetic resonance imaging study during reward anticipation and feedback." Psychological Medicine 45, no. 8 (January 12, 2015): 1765–78. http://dx.doi.org/10.1017/s0033291714002943.

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BackgroundThe neurobiological underpinnings of avolition in schizophrenia remain unclear. Most brain imaging research has focused on reward prediction deficit and on ventral striatum dysfunction, but findings are not consistent. In the light of accumulating evidence that both ventral striatum and dorsal caudate play a key role in motivation, we investigated ventral striatum and dorsal caudate activation during processing of reward or loss in patients with schizophrenia.MethodWe used functional magnetic resonance imaging to study brain activation during a Monetary Incentive Delay task in patients with schizophrenia, treated with second-generation antipsychotics only, and in healthy controls (HC). We also assessed the relationships of ventral striatum and dorsal caudate activation with measures of hedonic experience and motivation.ResultsThe whole patient group had lower motivation but comparable hedonic experience and striatal activation than HC. Patients with high avolition scores showed lower dorsal caudate activation than both HC and patients with low avolition scores. A lower dorsal caudate activation was also observed in patients with deficit schizophrenia compared to HC and patients with non-deficit schizophrenia. Dorsal caudate activity during reward anticipation was significantly associated with avolition, but not with anhedonia in the patient group.ConclusionsThese findings suggest that avolition in schizophrenia is linked to dorsal caudate hypoactivation.
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Juckel, G., J. Wrase, J. Gallinat, A. Heinz, and F. Schlagenhauf. "Störung des Belohnungssystems bei schizophrenen Patienten und der Einfluss typischer und atypischer Neuroleptika." Nervenheilkunde 26, no. 05 (2007): 381–86. http://dx.doi.org/10.1055/s-0038-1626874.

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ZusammenfassungEine Störung des dopaminergen Belohnungssystems bei schizophrenen Patienten wurde wiederholt postuliert. Ein solcher Zusammenhang liegt aufgrund der bei schizophrenen Störungen bekannten dopaminergen Dysfunktion und der klinischen Phänomenologie vor allem der Negativsymptomatik nahe. Der Artikel berichtet die Ergebnisse zweier Studien mit funktioneller Magnetresonanztomografie (fMRT), in denen dieser Zusammenhang untersucht wurde. Es wurden zum einen unmedizierte schizophrene Patienten und zum anderen Patienten unter Behandlung mit typischen und atypischen Neuroleptika sowie gesunde Kontrollen mit einem motivationalen Paradigma (Monetary Incentive Delay Task, MID) untersucht. Im Vergleich zu den gesunden Kontrollpersonen zeigten unbehandelte schizophrene Patienten eine signifikant reduzierte Aktivierung des ventralen Striatums inklusive des Nucleus accumbens, einer Kernregion des Belohnungssystems, bei der Antizipation von Gewinn. Je niedriger die individuelle Aktivierung im ventralen Striatum ausfiel, desto höher war die Negativsymptomatik der unbehandelten Patienten. Ähnlich wie bei unbehandelten Patienten zeigten Patienten mit typischer neuroleptischer Medikation keine signifikante Aktivierung des ventralen Striatums und wiederum eine Assoziation mit der Negativsymptomatik, während Patienten mit atypischer neuroleptischer Medikation eine mäßiggradige Aktivierung des ventralen Striatums aufwiesen, die nicht mit der Schwere der Negativsymptomatik korrelierte. Diese Beobachtungen weisen darauf hin, dass sowohl unbehandelte Patienten wie Patienten mit hochgradiger Blockade der Dopaminrezeptoren durch typische Neuroleptika eine Beeinträchtigung des Belohnungssystems aufweisen. Die Erfassung der direkten Interaktion zwischen der Funktion des Belohungssystems und der dopaminergen Neurotransmission ist Gegenstand laufender Studien.
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Yavuz, Emre, Rachel Rodrigues, and Martina Di Simplicio. "Emotional Dysregulation and Altered Reward Processing in Self-Harm." BJPsych Open 8, S1 (June 2022): S79. http://dx.doi.org/10.1192/bjo.2022.261.

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AimsSelf-Harm (SH) is defined as “any act of self-injury or poisoning carried out by a person irrespective of their motivation”. SH increases the risk of adverse outcomes including suicide attempts, necessitating early intervention. The most widely reported reason for SH is to relieve negative affect (NA), with NA precipitating SH engagement. SH participants show altered reward processing, particularly reward hypersensitivity. NA could trigger reward hypersensitivity and therefore SH engagement. However, the interaction between NA and reward processing in SH remains unclear.Aim: To investigate whether those who SH show differences in processing SH stimuli compared to healthy controls (HCs) following NA induction.Hypothesis: NA induction will result in SH participants having significantly shorter reaction latency (RL) and significantly greater reaction accuracy (RA) in the SH condition of the Incentive Delay task (IDT) than HCs.Methods16–25-year-old SH (n = 35) and HC (n = 20) participants were recruited on social media. Participants completed the Trier Social Stress Test, to induce NA, followed by the IDT. In the latter, participants were cued to respond to a target as quickly as possible, and on responding were shown images of either a SH act (SH condition), people socializing (social condition) or money (monetary condition), where each condition had control trials where a neutral image was shown, which participants also had to respond to (SH neutral, social neutral and monetary neutral conditions respectively). RA was the percentage of IDT trials in which participants responded within the target's presentation time. RL in the IDT was the time (seconds) between the target appearance and the participant's response.ResultsA linear mixed effects model showed no significant main effect of group on RL (SH vs HC), condition (Social, SH or Monetary) or group x condition interaction (p > 0.05). There was a significant main effect of condition on RA (p < 0.05) but not group or group x condition interaction (p > 0.05). Past-week SH frequency and RA were significantly and positively correlated in social, social neutral and monetary conditions (p < 0.05).ConclusionOverall, there was a non-significant effect of NA on reward processing. However, as greater past-week SH frequency was significantly associated with greater RA, understanding how reward processing and NA interact in SH can provide greater insight into its triggers. Given this study's limited sample size and cross-sectional nature, future studies should investigate how NA and reward processing interact longitudinally and in larger samples to understand how SH can be reduced.
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