Anhedonia Preclinical Translational And Clinical Integration Diego A Pizzagalli by Diego A. Pizzagalli 9783031096822, 3031096827 instant download after payment.

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. In
humans, 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.