Anhedonia in depressive disorders
Marcin Siwek

Although anhedonia may be a component of the clinical picture in many mental and neurological conditions, it is one of the most common and typical negative symptoms observed in depressive episodes. Both, the baseline increase in the severity of anhedonia as well as its regression during treatment are strong predictors of the efficacy of antidepressant pharmacotherapy and can have a significant impact on patient’s ability to achieve functional remission. Nevertheless, studies on the effects of antidepressants on the possible reduction of anhedonia-spectrum symptoms are very sparse. Depressive anhedonia-like emotional disorders, which are considered by patients to be associated with the inclusion of an antidepressant (usually from the class of serotonin or serotonin–noradrenalin reuptake inhibitors) and often experienced as qualitatively different from the former, are another clinical issue. Although they may be beneficial in some cases by helping the patient release anxiety and depressive symptoms, they are often seen as adverse effects eliminating the emotional intensity and social interactions. It is believed that depressive anhedonia and emotional disorders associated with antidepressant therapy have similar neurobiological mechanisms and result from the reduced activity (particularly in the form of reduced dopaminergic transmission) of reward system structures, such as the prefrontal cortex or the ventral tegmental area. Agomelatine is an antidepressant with the best documented and proven efficacy in reducing the increased depressive anhedonia and the lowest potential to cause drug-induced anhedonia. This may be due to its specific pharmacodynamic properties and, most of all, the ability to potently block the postsynaptic 5-HT2C receptors, which results in the enhancement of dopaminergic and noradrenergic transmission.