Anhedonia: Preclinical, Translational, and Clinical Integration (Current Topics in Behavioral Neurosciences, 58)

Anhedonia is a key symptom (and often risk factor) for various neuropsychiatric disorders, including depression, schizophrenia, substance use disorders, post-traumatic stress disorders, and Parkinson's Disease, among others. Across disorders, anhedonia has been associated with worse disease course, including poor response to pharmacological, psychological and neurostimulation treatments as well as completed suicide. Mounting evidence emerging from preclinical and translational sciences has clarified that "anhedonia" can be parsed into partially independent subcomponents, including incentive motivation, consummatory pleasure, reward learning, and effort-based decision making, pointing to distinct neurobiological substrates that could underlie anhedonic phenotypes. Taking an integrative approach that emphasizes cross-species integration and dimensional conceptualization of mental illnesses (e.g., Research Domain Criteria (RDoC)), this book represents the most comprehensive evaluation, synthesis and integration of theories and empirical findings focused on anhedonia. Organized across five parts, the handbook starts with chapters on the history, etiology, and assessments of anhedonia (Part I), followed by a section on the role of anhedonia in psychiatric and neurological disorders (Part II). Using the RDoC Matrix as a guide, Part III presents chapters synthetizing preclinical and clinical findings on different reward processing subdomains (e.g., reward responsiveness, reward valuation, reward learning). Part IV is focused on selected special topics, including historical and current perspectives on the transdiagnostic nature and importance of social anhedonia, the role of inflammation in the pathophysiology of anhedonia, the use of computational modeling to “dissect” anhedonia and improve its understanding, and links between anhedonia and suicide. Finally, Part V includes chapters on pharmacological, psychological and neurostimulation treatments for anhedonia. A volume on anhedonia is thus timely, and, we believe, clinically and scientifically important. Anhedonia does not “obey” current nosological systems (e.g., Diagnostic Statistical Manual, International Classification of Disease), but is instead a transdiagnostic phenomenon. Across neuropsychiatric disorders, anhedonia is invariably associated with a more challenging clinical course, including weaker response to treatment, more chronic illness, and – for several disorders such as major depressive disorder – increased risk of attempted and completed suicide.Critically, anhedonic phenotypes can be elicited in experimental animals, typically through chronic exposure to uncontrollable and unpredictable stressors. These phenotypes have been linked to dysregulation within corticostriatal pathways receiving dense projections from dopaminergic neurons and other neuromodulators. Inhumans, anhedonia can be observed early in life and can be triggered or exacerbated by polygenic risk factors and environmental factors (here too, mostly exposure to uncontrollable chronic stressors). Anhedonia may emerge as both cause or consequence of other related symptoms and thought patterns, including pessimism, hopelessness, and pervasive fatigue. When it manifests, anhedonia can be difficult to treat, a clinical conundrum that has prompted the search for new pharmacological and neurostimulation targets, as well as the development of more targeted psychological treatments that specifically attempt to ameliorate anhedonia. Over the past 10–15 years, progress in all these areas has been substantial but more work is clearly needed.