Sakina J Rizvi1,2, Clare Lambert3, Sidney Kennedy3,4. 1. Li Ka Shing Knowledge Institute, Arthur Sommer Rotenberg Suicide and Depression Studies Unit, St. Michael's Hospital, University of Toronto, 193 Yonge St, 6-009, Toronto, ON, M5B 1M8, Canada. rizvisa@smh.ca. 2. Department of Psychiatry, Institute of Medical Science, University of Toronto, Toronto, Canada. rizvisa@smh.ca. 3. Li Ka Shing Knowledge Institute, Arthur Sommer Rotenberg Suicide and Depression Studies Unit, St. Michael's Hospital, University of Toronto, 193 Yonge St, 6-009, Toronto, ON, M5B 1M8, Canada. 4. Department of Psychiatry, Institute of Medical Science, University of Toronto, Toronto, Canada.
Abstract
PURPOSE OF REVIEW: To focus on the clinical and behavioral presentation of anhedonia in mood disorders, as well as the differences and commonalities in the underlying neurocircuitry. RECENT FINDINGS: Evidence suggests that depression is characterized by hypofunction of the reward system, while bipolar disorder manifests dysregulation of the behavioral activation system that increases goal-directed reward behavior. Importantly, strong evidence does not exist to suggest significant differences in anhedonia severity between depressed unipolar and bipolar patients, suggesting that there are more nuanced fluctuations in reward processing deficits in bipolar patients depending on their state. Both euthymic unipolar and bipolar patients frequently report residual reward dysfunction, which highlights the potential of reward processing deficits that give rise to the clinical symptom of anhedonia to be trait factors of mood disorders; however, the possibility that therapies are not adequately treating anhedonia could also explain the presence of residual symptoms. Reward processing represents a potential diagnostic and treatment marker for mood disorders. Further research should systematically explore the facets of reward processing in at-risk, affected, and remitted patients.
PURPOSE OF REVIEW: To focus on the clinical and behavioral presentation of anhedonia in mood disorders, as well as the differences and commonalities in the underlying neurocircuitry. RECENT FINDINGS: Evidence suggests that depression is characterized by hypofunction of the reward system, while bipolar disorder manifests dysregulation of the behavioral activation system that increases goal-directed reward behavior. Importantly, strong evidence does not exist to suggest significant differences in anhedonia severity between depressed unipolar and bipolarpatients, suggesting that there are more nuanced fluctuations in reward processing deficits in bipolarpatients depending on their state. Both euthymic unipolar and bipolarpatients frequently report residual reward dysfunction, which highlights the potential of reward processing deficits that give rise to the clinical symptom of anhedonia to be trait factors of mood disorders; however, the possibility that therapies are not adequately treating anhedonia could also explain the presence of residual symptoms. Reward processing represents a potential diagnostic and treatment marker for mood disorders. Further research should systematically explore the facets of reward processing in at-risk, affected, and remitted patients.
Entities:
Keywords:
Anhedonia; Bipolar disorder; Major depressive disorder; Neuroimaging; Reward processing
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