reward sensitivity
Research Papers
Reward sensitivity modulates the brain reward pathway in stress resilience via the inherent neuroendocrine system
In the previous 10 years, researchers have suggested a critical role for the brain reward system in stress resilience. However, no study has provided an empirical link between activity in the mesostriatal reward regions during stress and the recovery of cortisol stress response. Moreover, although reward sensitivity as a trait has been demonstrated to promote stress resilience, it remains unclear whether it modulates the brain reward system in stress resilience and how this effect is achieved by the inherent neuroendocrine system. To investigate these uncertainties, 70 young adults were recruited to participate in a ScanSTRESS task, and their brain imaging data and saliva samples (for cortisol assay) were collected during the task. In addition, we assessed reward sensitivity, cortisol awakening response, and intrinsic functional connectivity of the brain in all the participants. We found that left putamen activation during stress exposure positively predicted cortisol recovery. In addition, reward sensitivity was positively linked with activation of the left putamen, and this relationship was serially mediated by the cortisol awakening response and right hippocampus-left inferior frontal gyrus intrinsic connectivity. These findings suggest that reward sensitivity modulates reward pathways in stress resilience through the interplay of the diurnal stress response system and network of the hippocampus-prefrontal circuitry. Summarily, the current study built a model to highlight the dynamic and multifaceted interaction between pertinent allostatic factors in the reward-resilience pathway and uncovered new insight into the resilience function of the mesostriatal reward system during stress.
View Full Paper →Treatment Efficacy and Clinical Effectiveness of EEG Neurofeedback as a Personalized and Multimodal Treatment in ADHD: A Critical Review
Purpose Recent reviews have proposed that scientifically validated standard EEG neurofeedback (NF) protocols are an efficacious and specific treatment for attention-deficit hyperactivity disorder (ADHD). Here, we review the current evidence for the treatment efficacy and clinical effectiveness of NF in ADHD to investigate whether NF treatment personalization (standard protocols matched to the electrophysiological features of ADHD) and combination with other interventions (psychosocial, sleep hygiene and nutritional advice) might yield superior long-term treatment outcomes relative to non-personalized NF and medication monotreatments. Methods The electronic databases PubMed and PsycINFO were systematically searched using our key terms. Of the 38 resulting studies, 11 randomized controlled trials (RCTs) and open-label studies were eligible for inclusion. Studies were analyzed for effect sizes and remission rates at the end of treatment and at follow-up. The effects of personalized and multimodal NF treatments were compared to non-personalized NF monotreatments and with two benchmark medication studies. Results The analysis of RCTs indicated that the long-term effects of personalized NF interventions were superior to non-personalized NF and comparable to those of medication alone or in combination with behavioral intervention. The analysis of open-label trials further indicates that the interaction of NF with parental interventions, sleep and nutritional advice might yield superior clinical effectiveness relative to NF and medication monotreatments. Conclusion Personalized and multimodal NF interventions seem to yield superior treatment efficacy relative to NF alone and superior clinical effectiveness relative to medication. We propose that treatment outcomes may be further enhanced by adjusting NF non-specific factors (eg, reinforcement contingencies) to specific ADHD characteristics (eg, reward sensitivity). Future NF research should focus on the systematic evaluation of the treatment outcomes of personalized and multimodal treatments.
View Full Paper →Food Addiction: Implications for the Diagnosis and Treatment of Overeating
With the obesity epidemic being largely attributed to overeating, much research has been aimed at understanding the psychological causes of overeating and using this knowledge to develop targeted interventions. Here, we review this literature under a model of food addiction and present evidence according to the fifth edition of the Diagnostic and Statistical Manual (DSM-5) criteria for substance use disorders. We review several innovative treatments related to a food addiction model ranging from cognitive intervention tasks to neuromodulation techniques. We conclude that there is evidence to suggest that, for some individuals, food can induce addictive-type behaviours similar to those seen with other addictive substances. However, with several DSM-5 criteria having limited application to overeating, the term 'food addiction' is likely to apply only in a minority of cases. Nevertheless, research investigating the underlying psychological causes of overeating within the context of food addiction has led to some novel and potentially effective interventions. Understanding the similarities and differences between the addictive characteristics of food and illicit substances should prove fruitful in further developing these interventions.
View Full Paper →Self-regulation of the dopaminergic reward circuit in cocaine users with mental imagery and neurofeedback
BACKGROUND: Enhanced drug-related reward sensitivity accompanied by impaired sensitivity to non-drug related rewards in the mesolimbic dopamine system are thought to underlie the broad motivational deficits and dysfunctional decision-making frequently observed in cocaine use disorder (CUD). Effective approaches to modify this imbalance and reinstate non-drug reward responsiveness are urgently needed. Here, we examined whether cocaine users (CU) can use mental imagery of non-drug rewards to self-regulate the ventral tegmental area and substantia nigra (VTA/SN). We expected that obsessive and compulsive thoughts about cocaine consumption would hamper the ability to self-regulate the VTA/SN activity and tested if real-time fMRI (rtfMRI) neurofeedback (NFB) can improve self-regulation of the VTA/SN. METHODS: Twenty-two CU and 28 healthy controls (HC) were asked to voluntarily up-regulate VTA/SN activity with non-drug reward imagery alone, or combined with rtfMRI NFB. RESULTS: On a group level, HC and CU were able to activate the dopaminergic midbrain and other reward regions with reward imagery. In CU, the individual ability to self-regulate the VTA/SN was reduced in those with more severe obsessive-compulsive drug use. NFB enhanced the effect of reward imagery but did not result in transfer effects at the end of the session. CONCLUSION: CU can voluntary activate their reward system with non-drug reward imagery and improve this ability with rtfMRI NFB. Combining mental imagery and rtFMRI NFB has great potential for modifying the maladapted reward sensitivity and reinstating non-drug reward responsiveness. This motivates further work to examine the use of rtfMRI NFB in the treatment of CUD.
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