Anhedonia as a Core Symptom of Depression and a Construct for Biological Research

Abstract

Anhedonia is a key psychiatric symptom that has seen significant advances in its understanding in both clinical practice and research over the past few decades. Once considered primarily a feature of depression, recent studies have shown that anhedonia is also a core element of other psychiatric disorders and contributes to considerable morbidity, mortality, and suicidality. Emerging models of psychopathology and illness emphasize the transdiagnostic relevance of anhedonia. At the same time, neuroimaging research has provided deeper insights into its underlying pathophysiology, and several assessment scales with strong psychometric properties have been developed. Various treatment strategies—including psychopharmacology, neuromodulation, and psychotherapy—have demonstrated varying degrees of effectiveness. This review discusses the evolving understanding of anhedonia, its significance as both a symptom and a diagnostic marker, its prevalence, and its pathophysiological underpinnings. Additionally, the authors provide an overview of key assessment tools and explore the range of treatment approaches studied to date.

The term anhedonia, defined as “the inability to experience pleasure,” was first introduced in 1896 by Théodule-Armand Ribot, a French psychologist (1). It has garnered significant attention and was established as a core criterion for diagnosing major depression in the third edition of DSM (1). Since then, anhedonia has increasingly been recognized as a central component (or a significant contributor to the severity) of various psychiatric disorders beyond depression, including schizophrenia and schizotypal personality disorder (2), bipolar disorder (3), obsessive-compulsive disorder (4), neurodegenerative disorders (e.g., Parkinson’s disease, Alzheimer’s disease, and frontotemporal dementia) (5), substance use disorders (6), and posttraumatic stress disorder (7), in addition to other medical conditions, such as chronic pain syndromes (8), and as a side effect of certain medications, such as dopamine blockers (9).

The conceptualization of anhedonia has evolved significantly over the past few decades. It is now considered a multifaceted construct that involves various impairments in the reward processing system—such as anticipation, motivation, effort, and valuation—rather than being limited to the subjective experience of lack of pleasure (10). These facets are all supported by recent neuroscientific studies. One of the most significant advancements in understanding anhedonia involves differentiating between motivational anhedonia (deficits in the desire to pursue rewards) and consummatory anhedonia (deficits in the ability to experience pleasure from rewards) (11, 12). This deeper understanding of the complexity of anhedonia is further supported by studies of schizophrenia, in which anhedonia was thought to reflect impairments in generating the mental representations of affective value needed for making decisions rather than a loss of hedonic capacity (13).

Other important conceptual frameworks have been developed to better capture the concept of anhedonia. One of them is the “wanting, liking, and learning” model of reward processing, suggested by Berridge and Robinson in their seminal 2003 article (14). This model introduces an additional dimension—learning from rewards—along with motivation-desire (wanting) and pleasure-consumption (liking). The Research Domain Criteria (RDoC) framework, developed by the NIMH, emphasizes the objective measurement of anhedonia through behavioral and neurobiological assessments (15). Furthermore, a recent computational model for consummatory anhedonia, known as the reinforcement learning model, provides a computational perspective on anhedonia by examining how stress, maladaptive beliefs, and dysfunctional cognitions influence hedonic experience (16).

Epidemiology

From an epidemiological standpoint, anhedonia is a common problem, and it is significantly associated with suicidality, morbidity, and mortality. Studies have demonstrated a variable prevalence across different patient populations. Among patients with major depressive disorder, the prevalence of anhedonia ranged from 35% to 70%, which reflects the heterogeneity in the assessment measures (17). Beyond depression, approximately 35% of patients with epilepsy were found to have significant anhedonia, with 30% of them having no diagnosis of depression (18). Anhedonia was demonstrated to be prevalent among patients who have had strokes (18.5%–19.7%) (19), as well as patients with chronic pain (25%) (8). Anhedonia was also found to affect approximately 4.3% of healthy individuals with no mental illness (20).

Association With Suicidality and Overall Morbidity and Mortality

A recent meta-analysis by Gillissie et al. (21) showed a moderate correlation between anhedonia and suicidality in general and psychiatric populations. Another recent large prospective study (N=2,839) found a significant association between anhedonia and suicidal ideation among patients with mood disorder, although the association with suicide attempts was not significant after covariate adjustment (22). Other studies have reported similar findings among adolescents with major depressive disorder (23). Anhedonia has been found to mediate the relationship between suicidal ideation and perceived burdensomeness or thwarted belongingness among a sample of physicians (24). Winer et al. (25) found that anhedonia predicted suicidal ideation in a large inpatient psychiatric sample (N=1,529), with changes in anhedonia correlating with changes in suicidality. Interestingly, Hawes et al. (26) differentiated between acute and chronic anhedonia, finding that the former was more strongly associated with severe suicidal ideation, suggesting that changes in the capacity to experience pleasure may be more indicative of near-term suicidal ideation and behavior.

Similarly, anhedonia is an established contributing factor to morbidity and mortality, particularly for two vulnerable populations: older adults and patients with major depressive disorder. Studies have shown that anhedonia is strongly associated with higher odds of mortality and disability in elderly populations, even in the absence of dysphoria (27). It is also correlated with poorer health status and more somatic and cognitive symptoms among patients with coronary artery disease (28), although it did not predict all-cause mortality or major adverse cardiac events (29). Additionally, anhedonia can serve as a predictor of worse prognosis among people with major depressive disorder because it is linked to poorer health-related quality of life and functional outcomes among patients with significant anhedonia compared with those without it (30). Notably, improvement in anhedonia was identified as the strongest predictor of enhancement in psychosocial functioning among patients with major depressive disorder (31).

Transdiagnostic Value: Research Domain Criteria Valence Systems and Anhedonia

Because anhedonia is relevant to and a significant factor in an extensive list of psychiatric diagnoses, the literature has suggested that it has an inherent transdiagnostic value in understanding shared neurobiological mechanisms and informing psychiatric nosology and treatment targets. The severity of anhedonia has been found to predict the severity of other symptom clusters in various psychiatric disorders (including major depressive disorder, autism spectrum disorder, attention-deficit hyperactivity disorder, and anxiety) (32). The RDoC initiative, developed by the NIMH, provides a model to identify and classify depressive phenotypes based on biological constructs. It includes the Positive Valence Systems domain, which provides a good and comprehensive framework for understanding anhedonia. Anhedonia, particularly in depression, is closely associated with impairments in reward responsiveness, learning, and valuation, which are key components of this domain (15, 33).

Pathophysiology

The pathophysiology of anhedonia is complex and involves different regions of the brain. The most important brain areas implicated in anhedonia are those related to the mesocorticolimbic pathway and reward circuitry, including the nucleus accumbens (NAc), ventral tegmental area (VTA), prefrontal cortex, and, above all, the ventral basal ganglia (10, 34). Dopamine has been shown to play the major role in this pathway, such as decreased dopamine release in the striatum during reward processing tasks (35, 36), but various other neurotransmitters have also been indicated to play a role, including serotonin, norepinephrine, glutamate, gamma-aminobutyric acid (GABA), and acetylcholine (10).

Increasing evidence suggests that activation of opioid receptors plays a significant role in the development and modulation of anhedonia, particularly through their action on the ventral pallidum and VTA (37, 38). Suggested pathways include the inhibition of GABAergic input to dopamine neurons, which results in dopamine release in key regions involved in reward, such as NAc, leading to enhancement of the hedonic impact rewards (37, 38). This is strongly supported by clinical research that shows that opioid misuse is strongly correlated with anhedonia (8, 39), with a clear relationship between the amount of misuse and the severity of anhedonia suggesting a causal link (40). A 2017 study (41) showed that administration of naltrexone induced reversible anhedonia, further supporting the role of opioid receptors in reward circuits.

Over the past few decades, various neuroimaging studies have contributed significantly to understanding the pathophysiology of anhedonia. Functional and resting-state MRI studies, as well as positron emission tomography scan studies, have demonstrated that individuals with anhedonia have reduced activation in the NAc and other reward circuitry regions during reward anticipation and consumption (42, 43). This in turn translates into decreased ability to sustain positive affect and motivation over time. Other studies have explored the link between anhedonia and stress, as well as chronic pain, demonstrating that these factors alter VTA neurons and increase inhibitory tone, leading to reduced motivation and reward anticipation (44, 45). Furthermore, anhedonia has been associated with chronic low-grade inflammation (particularly higher levels of interleukin 6 [IL-6], S100B, and interleukin 1 receptor antagonist and lower levels of interferon gamma) (46). Pro-inflammatory cytokines such as IL-6 and tumor necrosis factor-alpha can disrupt dopaminergic pathways, which are critical for motivation and reward (47). Increased inflammation is also associated with reduced functional connectivity in the reward system in the corticostriatal area (48).

Some research has focused on the changes associated with specific subtypes of anhedonia. For instance, electrophysiological studies using electroencephalography showed abnormal motivational salience, with cue-P3 reduction, less positive feedback-related negativity, and blunted feedback P3 in the group with anticipatory anhedonia compared with the group with consummatory anhedonia (49). MRI studies demonstrated that anticipatory anhedonia correlated with increased amplitude of low-frequency fluctuations of left dorsal anterior cingulate cortex and abnormalities in VTA, whereas consummatory anhedonia correlated more with reduced cortical thickness of left rostral anterior cingulate cortex and lateral orbitofrontal cortex among patients with major depressive disorder (10, 50, 51). Although all neurotransmitters have roles to play in both subtypes, serotonin was more implicated in anticipatory anhedonia, whereas opioids played a key role in consummatory anhedonia, and dopamine was critical in both (10).

Anhedonia Scales

Various scales have been developed and validated to measure anhedonia, each with different features and emphases. These scales are divided into primary anhedonia scales (which measure anhedonia directly) and secondary anhedonia scales (which measure anhedonia indirectly as part of a broader construct, such as depression rating scales).

Primary Anhedonia Scales

Table 1 provides a detailed overview of some of the features and limitations of the most important and widely used scales to measure primary anhedonia: the Dimensional Anhedonia Rating Scale (DARS) (52), Snaith-Hamilton Pleasure Scale (SHAPS) (53), the revised versions of the Chapman Physical and Social Anhedonia Scales (54), Beck Depression Inventory anhedonia subscales (55), Anhedonia Scale for Adolescents (56), and the Temporal Experience of Pleasure Scale (57). The SHAPS is a widely used and validated scale across diverse populations and cultures, valued for its practicality but limited by its lack of dimensionality and differentiation between anticipatory and consummatory anhedonia. The DARS, a recently developed and validated scale, assesses hedonic function—covering desire, motivation, effort, and consummatory pleasure—across four domains, providing a more comprehensive understanding of anhedonia. The Anticipatory and Consummatory Interpersonal Pleasure Scale, Fawcett-Clark Pleasure Capacity Scale, Leuven Affect and Pleasure Scale, and Specific Loss of Interest and Pleasure Scale are other scales used to assess anhedonia, although they are used less frequently.

TABLE 1.

Features of commonly used scales designed primarily to measure anhedonia^a

Scale	Self-report vs. clinician rated	No. of items	Aspects of anhedonia measured	Validated translations	Psychometric measures	Limitations	Unique advantages
DARS	Self-report	17	Interest, motivation, effort, and consummatory pleasure across four main domains: hobbies, food and drink, social activities, and sensory experience	German, Polish, Spanish	High validity and reliability but uncertain predictive validity and reliability over time	Cross-sectional design studies (which limit evaluation of its predictive validity and reliability over time). Heterogenous populations across different studies (which limits generalizability). Strict exclusion criteria in some studies (which also limits generalizability in real-life patient populations)	Has shown additional clinical utility over other scales in predicting reward function and distinguishing subgroups within major depressive disorder
SHAPS	Self-report (but has a version that is clinician administered, the SHAPS-C)	14	Evaluates hedonic capacity in four key areas: social interaction, interests and pastimes, sensory experience, and food and drink. Conceptualizes anhedonia with two main subdimensions, physical and social, but only measures consummatory anhedonia	Italian, Brazilian Portuguese, Chinese	High internal consistency, excellent reliability and validity	Limited sensitivity and specificity limit its utility because it was shown to be vulnerable to confounding bias caused by other depressive symptoms	Was validated in the adolescent population, practicality (easy to use)
Chapman PAS and SAS	Self-report	PAS: 61; SAS: 40	Physical and social anhedonia (Chinese version also has anticipatory and consummatory dimension differentiation)	French, Chinese	High internal consistency with strong reliability Strong convergent validity but mixed discriminant validity	Some studies showed that Chapman scales weakly correspond to clinically significant anhedonia assessed by clinical interviews, inconsistencies in the factor structure of the revised SAS, which may confuse the interpretation of the results	Thoroughness, high consistence across cultures, studied with the adolescent population
BDI-Anh	Self-report	BDI-Anh3: 3; BDI-Anh4: 4	Basic loss of interest and pleasure, with 1 item for inability to express affect	​	Very good reliability, with BDI-Anh4 having slightly better validity and reliability	Less commonly used because there are more robust and validated measures	​
ASA	Self-report	14	2 negatively framed dimensions (enjoyment, excitement, emotional flattening, effort, motivation, drive) and 1 positively framed dimension (enthusiasm, connection, purpose)	​	High reliability and convergent validity, as well as strong predictive value of clinical group differentiation of depressive symptoms	Limited applicability to adult age groups, focus on negative symptoms and framing	Designed particularly to overcome limitations of applying other scales in the adolescent population
TEPS	Self-report	18	Anticipatory (the “wanting” aspect) anhedonia and consummatory (the “liking” aspect) anhedonia	Chinese, German, French, Brazilian	Good internal consistency and validity	Concerns about its factor structure, in addition to its divergent validity across the 2 dimensions of pleasure	One of the best scales for measuring the temporal experience of anhedonia

^a ASA, Anhedonia Scale for Adolescents; BDI-Anh, Beck Depression Inventory-Anhedonia subscale; Chapman PAS, Chapman Revised Physical Anhedonia Scale; Chapman SAS, Chapman Revised Social Anhedonia Scale; DARS, Dimensional Anhedonia Rating Scale; SHAPS, Snaith-Hamilton Pleasure Scale; SHAPS-C, Snaith-Hamilton Pleasure Scale, clinician rated; TEPS, Temporal Experience of Pleasure Scale.

Secondary Anhedonia Scales

Secondary anhedonia scales include the Montgomery-Åsberg Depression Rating Scale (MADRS), Patient Health Questionnaire-9, and the Quick Inventory of Depressive Symptomatology scale, which can be used as either a self-report or a clinician rating scale.

Treatment Interventions

Pharmacological Agents

Antidepressants.

Antidepressants, particularly selective serotonin reuptake inhibitors (SSRIs) and serotonin-norepinephrine reuptake inhibitors (SNRIs), are typically the first line of treatment for major depressive disorder. Several studies have shown that, as part of their overall impact on depressive symptoms, most antidepressants demonstrate beneficial effects on measures of anhedonia among people with major depressive disorder (58). Several antidepressants have shown promise in specifically targeting anhedonia. These include vortioxetine, venlafaxine, agomelatine, and bupropion.

A pooled analysis of 11 short-term, double-blind, randomized, placebo-controlled trials of vortioxetine among people with major depressive disorder demonstrated significant short-term efficacy against anhedonia, with improvements in functioning largely driven by the treatment’s effect on anhedonia (59). Similar findings were observed in post hoc analyses of an open-label study conducted in Canada (60) and a double-blind randomized controlled trial (RCT) in Japan (61). These results were further supported by a recent study from Spain, which investigated treatment with vortioxetine among patients with major depressive disorder who experienced inadequate response to SSRI-SNRI monotherapy, although the primary outcome of the study was emotional blunting (62).

Venlafaxine was shown to have a superior-to-placebo effect in lowering the anhedonia factor on the MADRS, but the clinical significance of the reduction in scores is questionable (63). Agomelatine (a melatonergic antidepressant) was compared with venlafaxine in a head-to-head study in 2012 that primarily assessed effects on anhedonia and was shown to have a more relevant reduction in SHAPS scores compared with venlafaxine (64). A subsequent open-label multicenter study in 2016 showed a statistically significant reduction in SHAPS scores after 8 weeks of treatment (65). Finally, bupropion, a norepinephrine-dopamine reuptake inhibitor, was shown to have good efficacy in treating anhedonia, mostly attributed to its role in enhancing reward processing (58), although the studies had smaller samples (66).

Interestingly, higher baseline scores of anhedonia have been shown to predict a poorer response to antidepressant treatment (67), even after adjustment for overall depression severity and other clinical covariates (68).

Ketamine.

Studies exploring the effects of ketamine on anhedonia among patients with depression have shown very promising results. The main findings highlighted a rapid reduction in anhedonia, as well as improvements in different anhedonic dimensions, suggesting that ketamine’s impact on functional connectivity in the brain may be a potential contributor to these effects (69, 70). Some studies concluded that anhedonia may be at least partly responsible for mediating the overall antidepressant effect of ketamine (71), and others suggested that its anti-anhedonic effects are independent of the antidepressant effects (70). Esketamine was also found to be effective (72), albeit to a lesser extent than racemic ketamine (72). Patients who have higher treatment resistance seem to benefit the most from ketamine (73). A recent study demonstrated an in vivo increase in peripheral immune cell mTOR protein expression, which correlated with anti-anhedonic effects in patients with treatment-resistant depression (TRD) (74), suggesting that mTOR protein may serve as a biomarker for rapid ketamine treatment response in this patient population.

Psychedelics.

Several studies have explored the efficacy of psychedelics, particularly psilocybin, in treating anhedonia in the context of major depressive disorder, with promising results (58). A small study (N=19) showed reductions in anhedonia and an increase in music-evoked emotions among people with TRD (75). This finding is consistent with that of a previous study of mice that observed a reversal of anhedonic responses after a single injection of psilocybin (76). Other studies on psilocybin’s use among people with depression have also demonstrated anti-anhedonic effects (77). However, several concerns have been raised regarding the use of psilocybin as a treatment for anhedonia, and more broadly for depression, including a limited evidence base consisting only of small-sample studies, the resource-intensive nature of the treatments, risk of adverse effects—including dependence—and methodological limitations related to expectancy bias (78).

Others.

Various other pharmacological agents have been studied as treatment options for anhedonia. Monoaminergic agents, such as moclobemide, clomipramine, amitifadine, and levomilnacipran, have all shown some degree of efficacy in treating anhedonia, with moclobemide being the most promising. Moclobemide was found to have efficacy comparable to that of SSRIs in treating anhedonia among people with major depressive disorder and has a favorable tolerability profile (58, 79). It also showed a more rapid onset of action compared with clomipramine in a double-blind, multicenter trial (80). Methylphenidate has been shown to be effective in reducing anhedonia among patients with Alzheimer’s, but evidence beyond that is lacking (58, 81). Riluzole was studied in combination with escitalopram, but it was deemed ineffective in treating anhedonia (58, 82).

Newer agents, such as kappa opioid receptor (KOR) antagonists, are currently being studied. One recent multicenter, double-blind, placebo-controlled trial concluded that a KOR antagonist significantly increased ventral striatum activation during reward anticipation and improved anhedonic symptoms compared with placebo (83). The KCNQ2/3 channel opener ezogabine has also been studied as a potential novel therapeutic approach to treating anhedonia by restoring dopaminergic firing balance and modulating neuronal excitability in the reward circuitry (84). In a recent RCT, ezogabine caused significant improvement in SHAPS scores and overall depressive symptoms, despite not meeting its primary neuroimaging goal of achieving a change from baseline to week 5 in ventral striatum activation during reward anticipation (85).

Anti-inflammatory agents, such as infliximab (a tumor necrosis factor antagonist), reduced anhedonia in a 2024 RCT that involved patients with depression and elevated high c-reactive protein (>3 mg/L). The results were notable for changes in corticostriatal circuits and increased willingness to expend effort for rewards (86). Interestingly, infliximab was also shown to improve anhedonia SHAPS scores in a clinical trial that involved adults with bipolar I and bipolar II disorders (87). Other studies of anti-inflammatory agents include animal preclinical studies that showed that peptides such as adrenocorticotropic hormone (4–10) and alpha-melanocyte-stimulating hormone can treat anhedonia associated with inflammation in rat animal models (88).

Neuromodulation

Transcranial magnetic stimulation.

Several studies have explored the efficacy of transcranial magnetic stimulation (TMS) in treating anhedonia (89). In a recent double-blind sham-controlled clinical trial, TMS targeting the dorsolateral prefrontal cortex (DLPFC) alleviated anticipatory anhedonia by enhancing reward-seeking behavior and improved correlates of reward anticipation, but interestingly it did not affect consummatory anhedonia (90). Another study targeting the DLPFC showed significant reductions in SHAPS scores (91). A 2014 study found that TMS applied to the dorsomedial prefrontal cortex improved depression among patients with medication-resistant major depressive disorder, but not among those with a higher anhedonia burden (92).

Transcranial direct current stimulation.

Few studies using transcranial direct current stimulation to target the DLPFC have shown benefits in reducing anhedonia among patients with major depressive disorder (93, 94). However, these findings require further validation. One of these studies concluded that higher baseline anhedonia scores predicted a better response to treatment (95).

Electroconvulsive therapy.

Electroconvulsive therapy (ECT) is a common treatment for TRD in daily psychiatric practice. It is one of the most effective interventions for targeting depressive symptoms overall, including anhedonia. Several recent studies have detailed the effects of ECT in this regard, highlighting functional increases in neural activity in the reward circuitry (96) and structural volumetric changes in the hippocampus, amygdala, and NAc that were linked to improvements in anticipatory reward processing (97).

Deep brain stimulation.

Deep brain stimulation (DBS) is a continuously evolving treatment that has been studied for TRD over the past two decades. Several studies have shown that targeting NAc is associated with significant improvements in anhedonia and overall depressive symptoms (98, 99). A recent animal study demonstrated that DBS to NAc promotes the expression of brain-derived neurotrophic factor, altering functional connectivity and metabolism in the dopaminergic pathway, which can explain its effect on anhedonia (100). In animal studies, DBS targeting the ventromedial prefrontal cortex has shown a reversal of anhedonic symptoms, with one study highlighting the integrity of the serotonergic system as an important factor associated with the anti-anhedonic effects of DBS (101).

In recent years, the medial forebrain bundle has been suggested as a potential novel target for modulating the reward system (102). However, only one clinical study has been conducted so far, involving a very small sample (N=4), and it reported significant reductions in MADRS scores (103). DBS continues to be a promising intervention, although it has various downsides, including but not limited to surgical risks, cost, and accessibility (104).

Psychotherapy

Different psychotherapy approaches have been found to be effective in the treatment of anhedonia. The modalities that have been most studied include cognitive-behavioral therapy (CBT), behavioral activation treatment for anhedonia (BATA), mindfulness-based cognitive therapy (MBCT), and positive affect treatment (PAT). MBCT is an approach that integrates various principles of CBT with mindfulness exercises and concepts. A secondary analysis of the Cost and Outcome of Behavioural Activation RCT examined both CBT and BATA and found that both caused significant and comparable improvements in anhedonia that were sustained even at 12- and 18-month follow-ups. However, the extent of anhedonia reduction was less marked than the extent of depression reduction across both treatments (105). Another parallel-arm randomized trial found that BATA and MBCT had significant anti-anhedonic effects, with no modality showing superior efficacy over the other (106). The improvements were linked to reductions in resting-state functional connectivity in the default mode network and frontoparietal network.

PAT is a novel therapeutic intervention based on the hypothesis that increasing reward sensitivity for positive affect may be more effective than reducing threat sensitivity. A randomized trial involving 96 patients found that PAT yielded better outcomes at a 6-month follow-up for positive affect and depressive symptoms compared with traditional CBT strategies that focus on targeting negative affect (107). Using path analysis, a recent longitudinal observational study suggested that targeting meaning in life, sense of self, and prosocial behaviors could be effective in alleviating anhedonia, given that they showed very strong correlations with it (108).

Conclusions

Anhedonia remains a core symptom of depression and an essential construct for biological research in psychiatric disorders. Over the past few decades, significant advancements have been made in understanding its importance as a treatment target, as well as its complexity and multidimensional nature. The recognition of depression as a heterogeneous illness and the identification of narrower phenotypes for depression and anhedonia provide an important framework for future directions in biological and clinical research. Recent literature has explored this by using latent profile analyses to classify participants with anhedonia on the basis of reward-related measures, linking treatment with a KOR antagonist to identified subgroups, which proved promising (109). Another recent study explored the effects of serotonergic antidepressants on anhedonia phenotypes using the RDoC framework and metabolomic biomarkers, revealing changes in medium- and long-chain acylcarnitines (110). These biochemical signatures may help reduce depression heterogeneity and refine treatment outcomes on the basis of biology. Future studies should continue to refine narrower anhedonia phenotypes and investigate biological constructs to enable more specific, individualized, and nuanced treatments for both anhedonia and depression. In addition, distinguishing treatment impact on different types of anhedonia may help guide the treatment options. As shown in this article, different treatments may selectively treat different domains of anhedonia (e.g., repetitive TMS alleviating anticipatory-motivational anhedonia without affecting consummatory anhedonia). Therefore, it is prudent to build evidence on how interventions treat anhedonia rather than evidence that they merely treat it, which will help tailor specific and individualized treatment plans.

From a measurement standpoint, although the existing literature offers various scales for assessing anhedonia, there is notable lack of data directly comparing these instruments. Future research could focus on conducting head-to-head comparisons to provide essential evidence on their relative performance and efficacy for anhedonia. A significant limitation of the current literature is the small sample sizes in most treatment studies targeting anhedonia as a primary outcome. Larger-scale studies are needed to achieve adequate power for robust evidence-based treatment recommendations.

This narrative review provides a descriptive overview of the current evidence on anhedonia. However, future research would benefit from using more methodologically rigorous approaches, such as systematic reviews focused on specific aspects of anhedonia, including its definition, prevalence, assessment scales (including the differential weighting of both consummatory and motivational aspects of anhedonia across them), and treatment options.