Neurobiological Reward-Related Abnormalities Across Mood Disorders

Author(s):  
Alexis E. Whitton ◽  
Michael T. Treadway ◽  
Manon L. Ironside ◽  
Diego A. Pizzagalli

This chapter provides a critical review of recent behavioral and neuroimaging evidence of reward processing abnormalities in mood disorders. The primary focus is on the neural mechanisms underlying disruption in approach motivation, reward learning, and reward-based decision-making in major depression and bipolar disorder. Efforts focused on understanding how reward-related impairments contribute to psychiatric symptomatology have grown substantially in recent years. This has been driven by significant advances in the understanding of the neurobiology of reward processing and a growing recognition that disturbances in motivation and hedonic capacity are poorly targeted by current pharmacological and psychotherapeutic interventions. As a result, numerous studies have sought to test the presence of reward circuit dysfunction in psychiatric disorders that are marked by anhedonia, amotivation, mania, and impulsivity. Moreover, as the field has increasingly eschewed categorical diagnostic boundaries in favor of symptom dimensions, there has been a parallel rise in studies seeking to identify transdiagnostic neural markers of reward processing dysfunction that may transcend disorders. The thesis of this chapter is twofold: First, evidence indicates that specific subcomponents of reward processing map onto partially distinct neurobiological pathways. Second, specific subcomponents of reward processing, including reward learning and effort-based decision-making, are impaired across different mood disorder diagnoses and may point to dimensions in symptom presentation that possess more reliable behavioral and neural correlates. The potential for these findings to inform the development of prevention and treatment strategies is discussed.

Author(s):  
Suzanne N. Haber

Structural and functional imaging studies have identified abnormalities in the brains of individuals with OCD. The most consistent findings point to pathology in the circuitry connecting the prefrontal cortex with the basal ganglia, and especially to abnormalities in the orbitofrontal cortex (OFC), ventromedial prefrontal cortex (vmPFC), dorsal anterior cingulate cortex (dACC), and striatum. This chapter describes the detailed anatomy and interconnectivity of these structures, together with its functional correlates, to provide context for the more detailed treatment of abnormalities seen in OCD provided in the chapters that follow. These corticostriatal circuits are critical for reward processing, reward learning, and action selection, and so disruption in these circuitries in OCD may underlie abnormalities in these domains. Precisely defining the anatomy of these circuits and how it is disrupted in OCD, at both the group and individual level, is increasingly important, as it may help us to optimize anatomically targeted treatment strategies.


2016 ◽  
Vol 18 (1) ◽  
pp. 77-89 ◽  

Elevated striatal dopamine function is one of the best-established findings in schizophrenia. In this review, we discuss causes and consequences of this striata! dopamine alteration. We first summarize earlier findings regarding striatal reward processing and anticipation using functional neuroimaging. Secondly, we present a series of recent studies that are exemplary for a particular research approach: a combination of theory-driven reinforcement learning and decision-making tasks in combination with computational modeling and functional neuroimaging. We discuss why this approach represents a promising tool to understand underlying mechanisms of symptom dimensions by dissecting the contribution of multiple behavioral control systems working in parallel. We also discuss how it can advance our understanding of the neurobiological implementation of such functions. Thirdly, we review evidence regarding the topography of dopamine dysfunction within the striatum. Finally, we present conclusions and outline important aspects to be considered in future studies.


2018 ◽  
Author(s):  
Lou Safra ◽  
Coralie Chevallier ◽  
Stefano Palminteri

AbstractDepression is characterized by a marked decrease in social interactions and blunted sensitivity to rewards. Surprisingly, despite the importance of social deficits in depression, non-social aspects have been disproportionally investigated. As a consequence, the cognitive mechanisms underlying atypical decision-making in social contexts in depression are poorly understood. In the present study, we investigate whether deficits in reward processing interact with the social context and how this interaction is affected by self-reported depression and anxiety symptoms. Two cohorts of subjects (discovery and replication sample:N= 50 each) took part in a task involving reward learning in a social context with different levels of social information (absent, partial and complete). Behavioral analyses revealed a specific detrimental effect of depressive symptoms – but not anxiety – on behavioral performance in the presence of social information, i.e. when participants were informed about the choices of another player. Model-based analyses further characterized the computational nature of this deficit as a negative audience effect, rather than a deficit in the way others’ choices and rewards are integrated in decision making. To conclude, our results shed light on the cognitive and computational mechanisms underlying the interaction between social cognition, reward learning and decision-making in depressive disorders.


Cancers ◽  
2021 ◽  
Vol 13 (10) ◽  
pp. 2364
Author(s):  
Olena Klymenko ◽  
Anna Maria Stefanie Buchberger ◽  
Barbara Wollenberg ◽  
Klaus-Dietrich Wolff ◽  
Victoria Kehl ◽  
...  

Purpose: We report the outcome of a mono-institutional retrospective study of sinonasal carcinoma with the primary focus on GTV (gross tumor volume) and the effect of radiotherapy. Methods: 53 patients with sinonasal carcinoma and that of the nasal cavity, paranasal sinus or both except lymphoma were included. All patients were treated between 1999 and 2017. For tumor volume delineation, all pre-therapeutic images were fused to the planning CT (computed tomography). Results: The median follow-up was 17 months [0.3–60], the median age 60 years, 35 males and 18 females were included. Squamous cell carcinoma (SCC) (60.4%) was the predominant histology, followed by adenocarcinoma (15.1%). The mean composite OS (overall survival) time was 33.3 ± 3.5 months. There was no significant difference in the 5 y composite OS between tumor localization or radiotherapy setting. The simultaneous integrated boost concept showed a trend towards improving five-year composite OS compared to the sequential boost concept. The only factor with a significant impact on the 5 y composite OS rate was the pre-therapeutic GTV (cutoff 75 cm3; p = 0.033). The GTV ≥ 100 cm3 has no effect on the 5 y composite OS rate for SCC. Conclusions: The pre-therapeutic GTV is a prognostic factor for five-year composite OS for the entire group of patients with sinonasal tumors, influencing the outcome after completion of all treatment strategies. The GTV seems to not influence five-year composite OS in SCC. For this rare tumor entity, an intensive, multidisciplinary discussion is essential to finding the best treatment option for the patient.


PEDIATRICS ◽  
1994 ◽  
Vol 94 (4) ◽  
pp. 433-439 ◽  
Author(s):  
Alan R. Fleischman ◽  
Kathleen Nolan ◽  
Nancy N. Dubler ◽  
Michael F. Epstein ◽  
Mary Ann Gerben ◽  
...  

Background. Much has been written about the care of the hopelessly ill adult, but there is little guidance for pediatric health care professionals in the management of children who are critically or terminally ill. Methods. Through a 3-day meeting in Tarrytown, NY, attended by a group of pediatricians and others directly involved in these issues, a principled approach was developed for the treatment of, and health care decision-making for, children who are gravely ill. Results. The group agreed that the needs and interests of the child must be the central focus of any treatment plan and that the child should be involved to as great extent possible, consistent with developmental maturity, in the decision-making process. Quality of future life should be viewed as being relevant in all decisions. Parents are believed to be the natural guardians of children and ought to have great latitude in making decisions for them. However, parental discretion is not absolute and professionals must maintain an independent obligation to protect the child's interests. Conclusions. Decision-making should be collaborative among patient, parents, and professionals. When conflict arises, consultation and ethics committees may assist in resolution. When cure or restoration of function is no longer possible, or reasonable, promotion of comfort becomes the primary goal of management. Optimal use of pain medication and compassionate concern for the physical, psychological, and spiritual well-being of the child and family should be the primary focus of the professionals caring for the dying child.


1986 ◽  
Vol 31 (5) ◽  
pp. 436-441 ◽  
Author(s):  
J. Mark Levy ◽  
Ronald A. Remick

Eight female patients with rapid cycling mood disorders (at least four discrete affective episodes per year) were examined from a clinical perspective. Assessment suggested several different etiologies to the rapid cycling pattern in these patients. These included that the rapid mood swings were: a natural expression of the affective disorder, tricyclic induced, a result of frequent medication changes and/or poor medication compliance, and a combination of the aforementioned etiologies. All patients were helped significantly with treatment. Treatment was individualized for each patient's unique illness and possible etiological factors in the rapid cycling. Treatment strategies and guidelines include: i) A psychotherapeutic approach involving the patient and his family which emphasizes the lengthy nature of treatment before expected results; ii) The necessity of rigorous drug adherence, in) The sole use of “high dose” lithium therapy (> 1.2 MEQ/L) in some patients, and the consideration of “high dose” lithium in conjunction with tricyclics, MAO inhibitors or “adjuvant” medication in certain bipolar II patients; iv) The discontinuation of tricyclics in bipolar l rapid cyclers;v) The combination of lithium salts and carbamazepine or the use of carbamazepine alone in selected patients.


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