Treating Motivational and Consummatory Aspects of Anhedonia

In addition to subtypes of anhedonia presentation, the widespread prevalence of anhedonia suggests that, in many cases, it is likely a consequence of other psychiatric symptoms and syndromes (i.e., “secondary anhedonia”), rather than a primary pathology in its own right. Examples of secondary anhedonia can include the low levels of enjoyment and interest reported during early stages of sobriety; a high propensity toward dissociative states that limit capacity for pleasure; and cognitive impairments that may impede the necessary planning and coordination for engaging in social activities. Pervasive anxiety resulting in limited activities and social isolation can also lead to reported loss of enjoyment. Such etiologic considerations are important for treatment customization. In some cases, secondary anhedonia may spontaneously remit if the primary issues are addressed.

Although treatment options for anhedonia have lagged behind those for other dimensions of internalizing psychopathology, evidence supporting several behavioral and pharmaceutical interventions has emerged. On the behavioral side, behavioral activation (14, 15) and positive affect therapy (16, 17) have shown evidence in enhancing behavioral engagement and reducing avoidance. Both therapies are modular and primarily target aspects of motivational impairment rather than consummatory anhedonia. Indeed, to a large extent, both therapies operate on the underlying assumption that the capacity to experience pleasure is generally intact; the primary goal of treatment is therefore to facilitate greater opportunity for engaging in pleasurable activities. This goal is often accomplished by helping patients to identify activities that provide pleasure or a sense of achievement (i.e., mastery), to prioritize these activities in daily routines, and to identify and problem-solve around barriers to these activities. For consummatory anhedonia, mindfulness-based interventions designed to focus attention on savoring rewards have been developed in the context of substance use disorders (18) and may offer strategies for enhancing pleasure in other disorders as well.

For pharmacologic interventions, treatment using dopaminergic agents has been found to improve symptoms of low motivation and anhedonia-associated fatigue in several studies (19, 20), consistent with a wealth of preclinical and human experimental data suggesting that enhancement of dopaminergic tone may result in greater motivated behavior (21–23). Stimulants carry noteworthy side effects, however, including suppressed appetite, weight loss, hypertension, cardiac arrythmias, and potential for abuse. Despite these risks, more research into the possible application of stimulants to treat the motivational aspects of anhedonia is warranted. Indeed, a recent meta-analysis (19) evaluating the use of several agents at different dosages found that psychostimulants were generally efficacious, and their use as an adjunctive agent or monotherapy represented an understudied area.

In addition to psychostimulants, some evidence supports dopamine-replacement therapy for certain presentations of anhedonia. In particular, a growing body of evidence suggests that chronic peripheral inflammation may blunt dopamine synthesis capacity, possibly contributing to symptoms of fatigue, low motivation, and psychomotor slowing (24, 25). Initial evidence (26) suggests that administration of levodopa, a dopamine precursor commonly used to treat Parkinson’s disease, may benefit patients who show low motivation and elevated inflammation. Finally, the fast-acting antidepressant ketamine has shown some initial promise in addressing multiple aspects of anhedonia, including incapacity for pleasure (27, 28).