Neural reward circuit dysfunction as a risk factor for bipolar spectrum disorders and substance use disorders: A review and integration

Bart, Corinne P.; Titone, Madison K.; Ng, Tommy H.; Nusslock, Robin; Alloy, Lauren B.

doi:10.1016/j.cpr.2021.102035

Cited by 17 publications

(26 citation statements)

References 150 publications

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“…Three reviews reported data regarding differences in the white matter in a high-risk population (Hu, Stavish, Leibenluft, & Linke, 2020 ), neural reward circuit dysfunction (Bart, Titone, Ng, Nusslock, & Alloy, 2021 ) and longitudinal grey matter changes following first episode mania (Cahn, Keramatian, Frysch, Yatham, & Chakrabarty, 2021 ) compared to healthy controls. Hu et al ( 2020 ) indicated that the trajectory of fractional anisotropy reduction did not differ significantly between high-risk young adults and controls.…”

Section: Resultsmentioning

confidence: 99%

“…No comparable studies were available for BPD. According to Bart et al's ( 2021 ) findings, lower right ventral striatum–left caudal anterior cingulate functional connectivity to loss and greater right pars orbitalis–orbitofrontal cortex functional connectivity to reward may be trait-level neural markers that may reflect risk for BD in at-risk youth. Additionally, lower parietal cortical thickness may lead to lower executive functioning and emotional regulation capacity and predispose to higher future mixed/mania and irritability.…”

Section: Resultsmentioning

confidence: 99%

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Understanding the development of bipolar disorder and borderline personality disorder in young people: a meta-review of systematic reviews

et al. 2022

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Background There is ongoing debate on the nosological position of bipolar disorder (BD) and borderline personality disorder (BPD). Identifying the unique and shared risks, developmental pathways, and symptoms in emerging BD and BPD could help the field refine aetiological hypotheses and improve the prediction of the onset of these disorders. This study aimed to: (a) systematically synthesise the available evidence from systematic reviews (SRs) and meta-analyses (MAs) concerning environmental, psychosocial, biological, and clinical factors leading to the emergence of BD and BPD; (b) identify the main differences and common features between the two disorders to characterise their complex interplay and, (c) highlight remaining evidence gaps. Methods Data sources were; PubMed, PsychINFO, Embase, Cochrane, CINAHL, Medline, ISI Web of Science. Overlap of included SRs/MAs was assessed using the corrected covered area process. The methodological quality of each included SR and MA was assessed using the AMSTAR. Results 22 SRs and MAs involving 249 prospective studies met eligibility criteria. Results demonstrated that family history of psychopathology, affective instability, attention deficit hyperactivity disorder, anxiety disorders, depression, sleep disturbances, substance abuse, psychotic symptoms, suicidality, childhood adversity and temperament were common predisposing factors across both disorders. There are also distinct factors specific to emerging BD or BPD. Conclusions Prospective studies are required to increase our understanding of the development of BD and BPD onset and their complex interplay by concurrently examining multiple measures in BD and BPD at-risk populations.

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Section: Resultsmentioning

confidence: 99%

Section: Resultsmentioning

confidence: 99%

Understanding the development of bipolar disorder and borderline personality disorder in young people: a meta-review of systematic reviews

et al. 2022

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“…While self-reports strongly support this (63), behavioural findings are more mixed: though some have found differences in reward-based decision-making or risk-taking (64,65), the interpretation has been hampered by concerns about the tasks (64), non-computational analysis strategies focusing on ‘correct’ answers (65), or similar effects being seen in other disorders. Neurally, while there have been suggestions that BD is accompanied by increased reward-related brain signals (66), opposite findings have also been observed (67). One possible explanation could be that these neural effects are sensitive to patients’ mood states or medication (67).…”

Section: Discussionmentioning

confidence: 99%

“…Neurally, while there have been suggestions that BD is accompanied by increased reward-related brain signals (66), opposite findings have also been observed (67). One possible explanation could be that these neural effects are sensitive to patients’ mood states or medication (67). Recently, computational work has suggested how differences in the interplay between reward processing and mood could lead to feedback loops and fluctuations in mood, including spiralling out into manic and depressive episodes (4,6,7).…”

Section: Discussionmentioning

confidence: 99%

Bipolar symptoms and lithium treatment affect neural signatures of adaptation of risk-taking to past outcomes during reward-guided decision-making

Scholl¹,

Panchal²,

Nelissen³

et al. 2023

Preprint

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Introduction: Mood instability in bipolar disorder (BD) is poorly understood. Here we examined cognitive and neural mechanisms related to these fluctuations and how they are changed with the mood stabilizer lithium. Methods: We recruited volunteers with low (n=37) or high (n=40) risk of BD (using the Mood Disorder Questionnaire, MDQ). We also recruited patients with BD who were assigned (randomized, double-blind) to six weeks of lithium (n=19) or placebo (n=16) after a two-week baseline period. Participants completed mood ratings daily over 50 (healthy) or 42 (BD) days, as well as a risky decision-making task and one functional magnetic resonance imaging session. The task measured adaptation of risk taking to past outcomes (increased risk aversion after a previous win, outcome history). Results: While the low MDQ group was risk averse after a win, this was less evident in the high MDQ group and least so in the patients with BD. Neurally, outcome history was linked to medial frontal pole activation at the time of the decision. Corresponding to the behavioural effect, this activation was reduced in the high MDQ vs. the low MDQ group. While lithium did not reverse the pattern of BD in the task, it changed reward processing in the dorsolateral prefrontal cortex. Discussion: Healthy participants modulation of risk-taking in response to reward outcomes was reduced by risk of BD and BD. These results provide a model for how reward may prime escalation of risk-related behaviours in bipolar disorder and how mood stabilising treatments may work.

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“…As a subconstruct of the PVS, reward responsiveness (or reward sensitivity) primarily reflects neural activity to the receipt of rewards or reward cues, though it can also be indicated by self‐reported questionnaires and behavioural tasks (National Advisory Mental Health Council Workgroup on Tasks and Measures for Research Domain Criteria, 2016). Reduced reward responsiveness is one of the typical characteristics of depression, especially anhedonia symptoms (Bart et al, 2021; Der‐Avakian & Markou, 2012). The reward positivity (RewP), an Event‐related potential (ERP) component, is widely used to measure sensitivity/responsiveness to reward (Proudfit, 2015).…”

Section: Introductionmentioning

confidence: 99%

Blunted reward responsiveness prospectively predicts emotional distress when exposed to a naturalistic stressor

Yan

Kohn

Wei

et al. 2022

British J of Psychology

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Both stress and blunted reward responsiveness have been identified as core risk factors of depression. Whether blunted reward responsiveness increases psychological vulnerability to real‐life stress from a dynamic perspective (from stress reactivity to recovery) has not been investigated. By utilizing a real‐world stressful event (i.e. the final examination), this study aimed to explore the role of reward responsiveness in the stress‐emotional distress relationship during stress reactivity and recovery phases. We followed 57 undergraduates with three assessments, from six weeks before examination weeks (T1, baseline), one day before the examinations (T2) to two weeks after the examinations (T3), therefore, covering stress reactivity (T1 to T2) and recovery (T2 to T3) phases. At baseline, reward responsiveness was measured as the Reward Positivity (RewP) in the doors task. Stress and emotional distress (anxiety and depression) were reported at T1, T2 and T3 to capture their dynamic changes. Results showed that self‐report stress levels significantly increased from T1 to T2 (stress reactivity phase) and decreased from T2 to T3 (stress recovery phase). Furthermore, blunted reward responsiveness at baseline prospectively predicted emotional distress during the stress reactivity phase but not the recovery phase. Specifically, during the stress reactivity phase, higher perceived stress was associated with greater anxiety and depression only in participants with relatively smaller residual RewP amplitudes but not in participants with relatively larger residual RewP amplitudes. Our study demonstrated that a blunted reward responsiveness is a vulnerable factor of depression, especially when exposed to stress. Our findings provide insights into prevention and intervention for stress‐related disturbance.

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Neural reward circuit dysfunction as a risk factor for bipolar spectrum disorders and substance use disorders: A review and integration

Cited by 17 publications

References 150 publications

Understanding the development of bipolar disorder and borderline personality disorder in young people: a meta-review of systematic reviews

Understanding the development of bipolar disorder and borderline personality disorder in young people: a meta-review of systematic reviews

Bipolar symptoms and lithium treatment affect neural signatures of adaptation of risk-taking to past outcomes during reward-guided decision-making

Blunted reward responsiveness prospectively predicts emotional distress when exposed to a naturalistic stressor

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