Anhedonia in Depressive Disorder and Schizophrenia: An Overview of Causes, Diagnosis, and Treatment

Introduction: Defining Anhedonia in Depression and Schizophrenia

Anhedonia is one of the most burdensome yet poorly understood symptoms of major depressive disorder (MDD) and schizophrenia, significantly impairing daily functioning, hindering treatment, and increasing the risk of relapse. The pathomechanism of feeling no pleasure is associated with dysfunction of the reward system and/or affect regulation disorders, and remains a key challenge for modern psychiatry [1,2].

The term “anhedonia” (Greek ‘an’ – absence and “hēdonē” – pleasure) describes the inability to feel satisfaction from activities that previously brought joy, such as social interactions, hobbies, or eating. Its presence is associated with a deterioration in quality of life and reduced participation in social relationships, which has significant clinical and social implications [3,4].

Despite numerous studies, the mechanisms underlying anhedonia remain unclear, and differences in the neurobiological, cognitive, and immunological profiles between MDD and schizophrenia are a subject of debate. Questions remain unresolved regarding the definition of symptom subtypes, the relationship between anhedonia and avolition and fatigue, and the lack of clear guidelines on effective forms of treatment. This paper provides a critical review of current preclinical and clinical research on the pharmacotherapy of anhedonia, including both classic and new therapeutic strategies. Particular attention is paid to symptom assessment tools such as Snaith-Hamilton Pleasure Scale (SHAPS), Temporal Experience of Pleasure Scale (TEPS), and Clinical Assessment of Negative Symptoms (CAINS) – their usefulness in clinical practice, limitations, and role in monitoring symptom progression [3–5].

The main idea is to propose a model of combination therapy based on the mechanisms of the reward system, integrating neurobiological and clinical data. This model is a proposal for a practical diagnostic and therapeutic pathway aimed at improving treatment effectiveness and reducing the clinical burden of anhedonia [1,3,4].

The aim of the review is to identify key gaps in knowledge, provide a synthetic overview of current data on the treatment of anhedonia in MDD and schizophrenia, and present a coherent, mechanistically justified approach to combination therapy, along with recommendations for clinical practice and considerations based on new forms of therapy in the future. This article aims to review the causes, diagnosis, and treatment of anhedonia (loss of pleasure) in depressive disorders and schizophrenia.

The DSM-5-TR defines anhedonia as a persistent decrease in interest and pleasure in most activities, which is one of the criteria for a depressive episode [1]. According to contemporary psychopathological nomenclature, 2 basic subtypes can be distinguished: anticipatory anhedonia, i.e., limited joy in anticipation of future events and difficulty in imagining pleasant experiences, and consummatory anhedonia, i.e., reduced pleasure during current activities [1,3]. The characteristics of anhedonia vary between disorders. In MDD, deficits in reward anticipation and reward information integration predominate [3,4], while in schizophrenia, anhedonia is associated with neurocognitive deficits and reward system disorganization, which favors the anticipatory component [4–7].

In addition, in schizophrenia, anhedonia often co-occurs with episodic memory impairments, limiting the ability to recall and anticipate pleasurable experiences, and the frequent comorbidity of depression in the chronic phase hinders diagnosis and targeted treatment [6,8,9]. Contrary to the presented mental shortcut, reward is not something received in return, but a stimulus or state that reinforces behavior and subjectively induces pleasure. Its meaning and role are contextual and individually variable [1].

Anhedonia vs Fatigue and Symptom Differentiation

An important clinical challenge is to distinguish anhedonia from fatigue. Fatigue is a demotivating mood, a decrease in energy, and a reluctance to engage in activities, which is a common, burdensome symptom of MDD that severely impairs quality of life [5]. Anhedonia, on the other hand, refers to loss of the ability to experience pleasure, even during activities that were previously satisfying for the individual [5]. Although in practice the terms are sometimes used interchangeably, they differ in their mechanisms and therapeutic implications; confusion between them is particularly common in schizophrenia, probably due to cognitive deficits [5]. Therefore, accurate clinical assessment must differentiate these overlapping constructs and address them independently in treatment planning. Instruments such as the CAINS or the TEPS, which assess motivational and consummatory dimensions, can help disentangle these symptom domains [3,5].

To better illustrate the differences between anhedonia and fatigue – taking into account their definitions, symptom type, typical context, biological causes, subjective feelings, and example assessment tools – a comparison is presented in Table 1.

Multidimensional Nature of Anhedonia

Anhedonia is a multidimensional construct comprising several interrelated components: Physical (decreased satisfaction from physical activity and bodily sensations, particularly relevant in the context of sexual behavior); Social (less pleasure from interpersonal interactions); Anticipatory (impaired joy of anticipation and loss of hope for pleasure); Motivational (reduced anticipated reward value and difficulty initiating actions); and Consummatory (little enjoyment of the “here and now”) [3,4].

These domains may vary in prominence depending on the disorder and individual patient profile. For instance, patients with MDD more frequently exhibit motivational and anticipatory deficits, whereas in schizophrenia, impairments in social and anticipatory pleasure may predominate [1,4–7].

Reward and Punishment Processing in Anhedonia

Emerging evidence also suggests there is altered processing of reward and punishment in individuals with anhedonia. Ossola et al (2023) found that individuals with higher levels of anhedonia, across schizophrenia, MDD, and opioid use disorder, learned more effectively from punishment-related feedback than from reward-related stimuli. Notably, these individuals also had faster reaction times after negative feedback, suggesting heightened sensitivity to punishment cues [10].

These findings provide a potential mechanistic explanation for certain behavioral features of anhedonia (eg, avoidance, apathy) and reinforce the idea that anhedonia is not merely a lack of pleasure, but instead is a complex alteration in reinforcement learning. However, current evidence remains insufficient to treat anhedonia as an entirely distinct syndrome independent of MDD or other psychiatric disorders [10].

In clinical practice, effective management of anhedonia requires a multidimensional diagnostic approach, clear differentiation from overlapping symptoms such as fatigue, and disorder-specific understanding of reward-processing deficits. Particular caution should be exercised when extrapolating mechanisms from one disorder to another, as studies show differences in striatal reward anticipation and fronto-striatal connectivity between MDD and schizophrenia [1,2].

Criteria for Differentiation and Diagnosis of Anhedonia

According to the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (DSM-5), a diagnosis of MDD requires the presence of at least 5 symptoms for a minimum of 2 weeks, causing significant distress or impairment in functioning; on this basis, more than 256 symptom configurations are possible [3]. Anhedonia is repeatedly identified as a key symptom and an important clinical indicator that supports treatment outcome prediction and therapeutic decisions [3]. Its presence is associated with greater symptom severity, poorer response to treatment, longer recovery time, and higher risk of suicidal behavior [11].

According to clinical data, up to 70% of people with depression experience anhedonia; the symptom is not related to gender, and in schizophrenia it is more common in the chronic phase than in the early stages of the disease [1,4]. From a practical perspective, there are 3 subtypes: anticipatory anhedonia (difficulty in anticipating pleasure, poor use of previous reward signals, and lack of enthusiasm before events) [4]; motivational anhedonia (low willingness to engage in reward-oriented activities and difficulty in initiating activity); and consummatory anhedonia (reduced pleasure during activity, and withdrawal from social contacts, recreation, sex life, or eating) [4,11]. A simple question is helpful in differentiating between fatigue and anhedonia: once the patient has started an activity, do they feel pleasure? If not, this suggests a predominance of anhedonia (especially consummatory); if so, but a “lack of strength” prevents them from starting, fatigue or anergy predominates. In schizophrenia, it is also necessary to examine episodic memory and other cognitive functions that may mask anhedonia and increase its confusion with fatigue [5].

Neurobiological and Inflammatory Mechanisms

Anhedonia, which is reduced ability to feel joy or interest in everyday activities, is closely tied to changes in how the brain’s reward system works. Brain scans show that people with depression and high levels of anhedonia often have weakened connections in important brain areas responsible for motivation and self-reflection, like the precuneus and fronto-striatal regions. In particular, the white matter in some brain pathways, such as the left superior longitudinal fasciculus, appears to be damaged or less efficient [4].

New research using brain network modeling has found that individual patterns of brain connectivity can actually predict how severe someone’s anhedonia is. These brain “fingerprints” can even help distinguish between different subtypes of depression – for example, melancholic (in which there is deep anhedonia and completely losing pleasure) versus non-melancholic (without completely losing pleasure) – based on differences in regions like the anterior cingulate cortex and the parahippocampal gyrus [12].

Beyond the brain structure itself, inflammation in the body may also play a major role in anhedonia. Studies have shown that higher levels of C-reactive protein (CRP), a marker of inflammation, are linked to weaker communication between key reward-related brain areas like the ventral striatum and the prefrontal cortex [2]. This connection has also been observed in teenagers with depression, where inflammation was linked to poorer brain connectivity and more severe symptoms of anhedonia [11]. Additionally, high levels of interleukin-6 (IL-6), another inflammatory marker, have been linked to shrinkage of brain structures involved in reward processing, suggesting that long-term inflammation might even cause damage to these areas [3].

Altogether, these findings suggest that both the brain’s structure and inflammation in the body contribute to how people experience pleasure, or fail to experience it, especially in conditions like depression.

Questionnaires Used in Research on Anhedonia

Anhedonia is a subjective phenomenon, which makes it difficult to assess accurately. Currently, the most effective and simplest method of assessing the degree of anhedonia in patients is the use of short questionnaires that assess various areas of life and demonstrate high test validity. One of the most commonly used tools in psychiatry and psychotherapy is the Snaith-Hamilton Pleasure Scale (SHAPS). Unlike other tools, such as the Fawcett-Clark Pleasure Sensitivity Scale (FCPS) or Chapman’s Social Anhedonia Scale (CSAS), which are culturally biased and have limited scope, the SHAPS scale does not impose diagnostic restrictions. In addition, the SHAPS focuses on measuring satisfaction levels by assessing the pleasure derived from food, entertainment, sensory experiences, personal achievements, and social relationships [2,4,12]. The SHAPS consists of 14 short items, each of which is rated on a 4-point Likert scale: 1 – strongly disagree, 2 – disagree, 3 – agree, and 4 – strongly agree [13].

Another commonly used scale with high validity and reliability is the Temporary Experience of Pleasure Scale (TEPS), which consists of 18 self-assessment questions, each with 6 response options. The questionnaire contains 10 items related to anticipatory anhedonia and 8 items assessing consummatory anhedonia, in terms of social and physical activities [4,11,13].

Other, less commonly used, scales include the Anticipatory and Consummatory Interpersonal Pleasure Scale, which focuses on the pleasure derived from social interactions, and a newer, more detailed scale, the Positive Valence Systems Scale. The latter allows for the analysis of anhedonic behaviors in 7 areas: reward evaluation and anticipation, reward prediction, perceived pleasure from rewards, effort evaluation, choice of action, and initial engagement in the task [2,12].

However, diagnostic scales alone are not sufficient to make a diagnosis without a comprehensive psychiatric evaluation. They serve only as complementary tools in the diagnostic process and can be used to assess symptom severity and monitor changes during psychological treatment [13].

Anhedonia in Schizophrenia: A Negative Symptom Perspective

Anhedonia is one of the negative symptoms of schizophrenia, and its presence indicates a more severe course of the disease and often requires numerous modifications to pharmacological therapy [1,14]. The literature shows a significant relationship between the breakdown of frontal-striatal, mesocortical, and mesolimbic circuits and the occurrence of abnormalities in the understanding of reward and reinforcement of aversion, which underlies the diagnosis of anhedonia in schizophrenia. This phenomenon is attributed to dysfunction of the cingulate gyrus, anterior cingulate cortex, amygdala, insula, frontal cortex, and prefrontal cortex. According to the literature, the severity of anhedonia is often linked to altered dopamine transmission in the mesolimbic system; however, recent studies suggest that this relationship is less pronounced in schizophrenia compared to depression, indicating a more complex neurobiological basis of anhedonia in schizophrenia [1,2].

Unlike depression, where dopaminergic dysfunction in reward anticipation is a core feature of anhedonia, in schizophrenia, the neural mechanisms may involve broader fronto-striatal circuit abnormalities beyond dopamine transmission [1,2].

Anhedonia can be assessed using the Negative Symptom Assessment Scale (SANS), the Clinical Assessment of Negative Symptoms (CAINS) (which also evaluates social withdrawal and other negative symptoms), and the Snaith-Hamilton Pleasure Scale (SHAPS), previously discussed in the section on anhedonia in depressive episodes [6].

There is growing evidence that anhedonia in schizophrenia may be associated with cognitive impairment. Patients show a significant reduction in both anticipated and consummatory pleasure, alongside deficits in immediate memory (the ability to remember and reproduce information shortly after exposure), attention, and delayed memory (recalling information after some time without prompting), while language deficits appear independent of anticipated anhedonia risk [6,7]. This symptom is particularly pronounced in situations of rest, meal preparation, or being at home alone, while its severity decreases during family interactions [15].

Furthermore, a simplified way of expressing negative emotions correlates with the severity of social anhedonia and a reduced level of experienced pleasure, which may be an important starting point for pharmacotherapy aimed at reducing this symptom in patients with schizophrenia spectrum disorders [16].

A proper understanding of the term “negative symptoms” in the context of schizophrenia includes the minimization or absence of behaviors and functions related to motivation, willingness to act, and interest in expressing emotions in everyday situations, with impaired ability to control emotions and adapt them appropriately to situations [14,17]. To better capture this issue, negative symptoms are divided into primary (resulting directly from the pathogenic mechanisms of schizophrenia) and secondary (related to coexisting disorders, treatment adverse effects, or environmental factors) [14]. Primary negative symptoms often have early onset; at least 1 is detected during the first episode in nearly 90% of patients, and 35% to 70% persist after pharmacological treatment [8].

Based on recent articles, negative symptoms include: alogia (poverty of speech content and reduced number of words spoken); anhedonia (reduced pleasure in various life areas, with severity depending on context); social withdrawal (limited contact, withdrawal from relationships, and difficulty establishing or maintaining bonds); and avolition (decreased motivation to act, diminished desire to achieve goals, and reluctance to perform planned activities) [17–20]. It is estimated that up to 60% of patients have negative symptoms, which can appear at any stage of the disease and are associated with a more severe course [14].

Diagnostics include imaging tests to visualize changes in areas of the brain associated with reward and motivation (orbitofrontal cortex and striatum), and a preliminary association has been found between reduced thickness of the orbitofrontal cortex and severity of negative symptoms. A possible link between decreased striatal volume and avolition severity has been considered but not definitively confirmed. Three hypotheses are proposed: it could be a consequence of treatment, an effect of disease chronicity, or a diagnostically significant feature [21].

A complete diagnosis of negative symptoms requires, among other things, the presence of poor affect and speech, lack of motivation, social withdrawal (including sexual withdrawal), and lack of pleasure, persisting for at least 6 months with significant severity for at least 1 month. These symptoms significantly reduce quality of life, and their reduction and sometimes regression is the main goal of pharmacotherapy [18,22].

The key to selecting a treatment is identifying negative symptoms and distinguishing between primary (internal dimension of schizophrenia) and secondary symptoms (resulting from positive symptoms, depression, adverse effects of antipsychotic drugs, substance abuse, and social isolation), which emphasizes the importance of a carefully conducted clinical interview – the most appropriate form of measuring the severity of these symptoms [17,18].

Studies distinguish 2 areas of negative symptoms: motivation/pleasure and limited expression. It is suspected that the central symptom is not anhedonia, but avolition, closely related to other negative components, and therapy aimed at reducing it can lead to an overall improvement in the patient’s condition [17,20].

Avolition at the individual level manifests itself in a loss of interest in personal development (physical, intellectual, financial, professional) and, at a later stage, a lack of concern for basic areas of life (hygiene, health, food shopping), with increasing emotional emptiness. Unlike depression and bipolar disorder, patients do not report dominant affective symptoms such as depressed mood or guilt [17,20]. There may be a link between avolition and male gender, as well as poor social adaptation in childhood; however, these hypotheses are preliminary and require further research [20].

Treatment of Anhedonia

Choosing an effective therapy for anhedonia is difficult because patients often respond poorly to traditional treatment methods [1,12,23]. Effective treatment of anhedonia requires identifying its components, understanding the reward system, and refining current therapies through further research [1,12,14,24]. The following section presents the range of available treatment options for anhedonia.

Antidepressants

First-line drugs used to treat depression, such as selective serotonin reuptake inhibitors (SSRIs) and serotonin-norepinephrine reuptake inhibitors (SNRIs), do not produce satisfactory results in the treatment of anhedonia [1,4]. However, some antidepressants have been found to be more effective than others, with the most promising results obtained with atypical antidepressants [4,12].

Bupropion, which is a dopamine and norepinephrine reuptake inhibitor, has been found to be a suitable choice for treating anhedonia in patients with major depressive disorder (MDD) [1,4]. It has a positive effect on the reward system, both in patients with pronounced anhedonia and in more normative individuals who did not respond to SSRI treatment [1,24]. Recent reports suggest that combinations such as bupropion plus dextromethorphan may have promise in treating depressive symptoms and may improve aspects of anhedonia in major depressive disorder, although evidence specific to negative symptoms in schizophrenia is still limited [12,24].

Another atypical antidepressant that has attracted the attention of researchers is agomelatine [12]. Its action profile includes agonism of the postsynaptic serotonin 5-HT2C receptor and agonism of the melatonergic receptor (MT1/MT2). Agomelatine has antidepressant and anxiolytic effects, as well as a beneficial effect on the sleep-wake cycle [4,25]. It is also a relatively safe drug, and clinical studies have shown that its use has a positive effect in both short-term and long-term use [4,25].

Vortioxetine has shown superior effects compared to agomelatine in some dose-comparative studies in major depressive disorder with respect to improvement in anhedonia and pro-social functioning [5,7]. In schizophrenia in remission, vortioxetine 10 mg/day added to antipsychotics reduced physical and social anhedonia compared to baseline [1,4,23,26].

Antidepressants, when used adjunctively in schizophrenia, may provide benefit for anhedonia symptoms, especially when added to ongoing antipsychotic therapy, but the evidence remains preliminary and the effects are modest [14]. More detailed studies are needed to confirm the usefulness of adjunctive treatment [14].

Antipsychotic Drugs

Antipsychotic drugs have a limited effect on negative symptoms occurring in the course of schizophrenia or depressive episodes in patients with bipolar disorder (CHAD) [1,14,27]. Better therapeutic results are achieved with atypical antipsychotics, but their effect is mainly limited to improving the condition of patients with negative symptoms secondary to positive symptoms [1,14]. In several European countries, amisulpride has been approved for the treatment of negative symptoms, but its efficacy is difficult to assess due to the accompanying reduction in depression. A new atypical antipsychotic drug that is considered most beneficial in the treatment of negative symptoms, including anhedonia, is the piperazine derivative cariprazine [14,28].

Cariprazine has a different action than most atypical antipsychotics. It is a partial agonist of the dopamine D3/D2 receptor and the serotonin 5-HT1A receptor, as well as an antagonist of the serotonin 5-HT2B receptor, which is likely responsible for its efficacy in treating negative symptoms [14,27,28]. A clinical study has shown that its action is comparable to other preferred antipsychotic drugs in the treatment of schizophrenia symptoms. However, in terms of combating negative symptoms, cariprazine has proven to be more effective than risperidone, which indicates its specific action profile. Additional factors in favor of choosing cariprazine for the treatment of anhedonia are its high degree of safety and good tolerance [14,28].

The efficacy of cariprazine has also been evaluated in terms of reducing negative symptoms in bipolar I disorder. In 2024, McIntyre et al conducted a meta-analysis of data from 3 clinical trials that examined the effect of cariprazine compared to placebo in patients with varying degrees of anhedonia over a 6-week period. The results show that cariprazine significantly improved patients’ anhedonia after only 2 weeks, regardless of other symptoms of depression [27].

Glutamatergic Drugs

In addition to monotherapy, combination therapy should be considered in the treatment of anhedonia, both in depression and schizophrenia. Agents that have recently shown promise in improving the treatment of patients with anhedonia are glutamatergic modulators, which act by blocking the NMDA receptor [12,14,24].

Previous studies have shown that the NMDA antagonists with the most effective antidepressant effects, including against anhedonia, are (R,S)-ketamine, hereinafter referred to as ketamine, and its enantiomer, developed and approved in 2019, esketamine. Ketamine is characterized by a rapid onset of action and a long duration of action [4,29]. Glutamatergic modulators such as ketamine/esketamine have been shown in depression to produce rapid anti-anhedonic effects, which is likely due to an increase in DA tension in mesocorticolimbic pathways [12], but their efficacy for anhedonia as a negative symptom in schizophrenia has not yet been firmly established [12,29].

Research on glutamatergic drugs raises high hopes for the development of satisfactory forms of therapy to support antidepressant and antipsychotic treatment [12,14,29]. To determine the exact benefits of their use, higher-quality studies involving a larger number of patients are needed [14]. To obtain more accurate data, other compounds from the NMDA antagonist group should also be investigated.

Kappa Opioid Receptor Antagonist Drugs

Drugs that have recently attracted interest in the context of treating anhedonia are kappa opioid receptor (KOR) antagonists. Their mechanism of action is based on their effect on the ventral striatum, which is one of the main centers of the reward system [1,12].

In 2023, Krystal et al conducted a study to test the efficacy of KOR antagonists, using a “Fast-Fail” approach to assess the potential of these drugs in the treatment of anhedonia using proof-of-mechanism (POM) tests, which determine the impact on brain circuits likely to mediate clinical effects. A randomized proof-of-mechanism trial in individuals with mood or anxiety disorders and clinically significant anhedonia found that the KOR antagonist significantly increased ventral striatum activation during reward anticipation and improved self-reported anhedonic symptoms compared to placebo [30].

These results support further investigation of KOR antagonism as a possible therapeutic path for anhedonia, although clinical trials specifically focusing on schizophrenia are limited.

KCNQ Channel Activators

Potassium (K+) KCNQ channel activators are a promising avenue in the search for treatments for negative symptoms, including anhedonia [12,31]. These channels are commonly found in many tissues, including the nervous and cardiovascular systems. By modulating membrane potential and regulating neuronal activity, they play a key role in the neurophysiological mechanisms of resistance to stress-induced depression [31–33]. While animal studies and human trials in depression are encouraging, similar evidence in patients with schizophrenia remains to be demonstrated.

A representative of this group of drugs is esogabine (retigabine), a selective activator of the KCNQ2/3 channel, whose main indication to date has been anticonvulsant treatment [33,34]. Preclinical studies have shown that when administered to mice exposed to social defeat, it contributed to increased social interaction and reduced isolation time [33]. Human studies conducted on small groups of individuals with pronounced symptoms of anhedonia confirmed its anti-anhedonic and antidepressant effects; no serious adverse events were reported [12,31,32].

In summary, KCNQ channel-activating drugs show great therapeutic potential and may represent a breakthrough in psychiatric pharmacotherapy [31–33].

Neurostimulation

Neurostimulation techniques are increasingly explored in the treatment of anhedonia [1,4,14,35,36].

In depression, transcranial magnetic stimulation (TMS) has shown relatively stronger improvements in anhedonic symptoms compared to some other depressive features [4]. In schizophrenia, non-invasive brain stimulation (rTMS, tDCS) is under investigation; preliminary findings suggest possible benefits for negative symptoms, including anhedonic aspects, but data are scarce and heterogeneous. Despite promising preliminary results, the evidence is still insufficient. The difficulty in clearly determining the effectiveness of NIBS stems from the small number of studies, the one-sided focus on negative symptoms, and the influence of pharmacotherapy on the condition of patients participating in the studies [35,36].

Psychotherapy

Psychotherapy is a useful adjunctive option to pharmacotherapy in patients with negative symptoms, including anhedonia, although specific evidence for the synergistic effect in schizophrenia remains limited [4,12]. Cognitive-behavioral therapy (CBT) and its component, behavioral activation, are particularly promising, as they focus on making patients aware of the connection between negative thoughts, feelings, and behaviors and engaging them in satisfying activities [4,14]. Another form of psychosocial intervention developed for people with anhedonia is the Positive Emotions Program for Schizophrenia (PEPS), which aims to enhance anticipation and maintenance of positive emotions (eg, reducing anhedonia and apathy) [1,12].

In addition to psychotherapy, lifestyle interventions (eg, sleep hygiene, physical activity, diet) are suggested in reviews of negative symptoms, though direct evidence for their effect specifically on anhedonia in schizophrenia is limited [14].

In the search of the most comprehensive solutions, Motivation and Enhancement Training (MOVE) therapy was developed, which combines various types of behavioral support (including both CBT and environmental support), but its effects were only observed after 9 months of therapy [14].

Although many psychosocial interventions require further clinical trials in schizophrenia, preliminary findings suggest they can improve anhedonia. Clinicians should consider using them alongside pharmacotherapy when appropriate, but the evidence is preliminary [1,12].

A diagram of the available treatments for anhedonia – including both pharmacological approaches, divided into drug classes, and non-pharmacological interventions – is presented graphically in Figure 1, providing a clearer overview of current therapeutic strategies.

Future Development Directions

Currently, there is no widely accepted “best” treatment of anhedonia that would enable complete remission of this symptom, so it is important to consider each case according to specific diagnostic criteria using assessment scales such as SANS, CAINS, and SHAPS, as well as a thorough psychiatric examination.

Further research should focus on personalized therapy, which would contribute to at least partial remission of negative symptoms in patients diagnosed with schizophrenia and severe depressive disorder in a shorter period of time.

It seems beneficial to introduce individualized selection of pharmacological therapy combined with cognitive-behavioral psychotherapy. In pharmacotherapy, it is worth considering the use of non-classical treatment methods, but further research involving new groups of drugs should be conducted first. Additional tests should also include combination therapy to identify the potential benefits and risks of its use.

Conclusions

Anhedonia is a common phenomenon accompanying both MDE and schizophrenia. It is associated with significant difficulties in daily functioning in patients, and is also a predictor of a more severe course of the disease and a poorer response to standard treatment methods. Although this symptom has been fairly well researched, it is still too rarely treated as a separate problem requiring additional diagnosis and an individual approach.

One of the main limitations in the diagnosis of anhedonia is the lack of sufficiently specific assessment criteria that would allow for an unambiguous determination of the absence or presence of this symptom. Therefore, the assessment is highly subjective and is based mainly on a psychiatric interview.