Anhedonia, a term first used by Ribot [
2] in 1896, is a diminished capacity to experience pleasure. It describes the lack of interest and the withdrawal from all usual pleasant activities [
3,
4]. Chapman
et al. [
5] defined two different types of hedonic deficit: physical anhedonia and social anhedonia. Physical anhedonia represents an inability to feel physical pleasures (such as eating, touching and sex). Social anhedonia describes an incapacity to experience interpersonal pleasure (such as being and talking to others).
Anhedonia and schizophrenia
Since the writings of Bleuler [
6] and Kraepelin [
7], anhedonia has figured in clinical descriptions of the 'core' deficits of schizophrenia. Today, it is still commonly included by many authors [
8‐
15] in the negative symptomatology of schizophrenic disorders. For example, Andreasen [
10] has inserted the hedonic deficit into the diagnostic criteria for the 'negative syndrome' of schizophrenia, defining a specific 'anhedonia/asociality' subscale in the Scale for the Assessment of Negative Symptoms (SANS). Carpenter
et al. [
11] also considered anhedonia as a 'primary' and 'enduring' negative feature of the 'deficit syndrome' of schizophrenia. In their Schedule for Deficit Syndrome (SDS) [
13], the hedonic inability concerned at least three of the six items proposed ('restricted emotional range', 'curbing of interests' and 'diminished social drive'). In a 10-year follow-up study, Herbener and Harrow [
15] have shown that anhedonia was a stable clinical feature of the schizophrenic course and a distinctive state-like symptom of schizophrenic chronicity.
Contrary to the hypothesis of anhedonia as a 'core' symptom of schizophrenic disorders, other authors [
16‐
19] considered the hedonic deficit as a marker of genetic vulnerability to schizophrenia, and either a contributing or potentiating personological factor for the development of schizophrenic illness. For example, Rado [
17] has suggested that anhedonia was a main genetically transmitted defect both in overt schizophrenia and in compensated schizotypal subjects. Some years later, Meehl [
18] integrated Rado's view into a theory of neurological dysfunction in schizophrenic disorder, positing that anhedonia was a 'cardinal' enduring trait preceding and possibly causing schizophrenia. More recently, several authors [
20‐
24] have found that individuals with deviantly high scores on the Chapman Anhedonia Scales were disproportionately more likely to develop psychotic-like experiences and schizophrenia spectrum disorders. Schurhoff
et al. [
24] considered those psychotic subjects as a distinct familial subtype of schizophrenia, characterised by a highly anhedonic first-degree relatives and a threefold familial risk of schizophrenia spectrum disorders.
Anhedonia and depression
Since the writings of Clouston [
25], Bevan-Lewis [
26] and Kraepelin [
7], anhedonia had figured as a main symptom in clinical descriptions of 'melancholia'. Today, it is still commonly included by many authors [
27‐
32] among the 'nuclear' symptoms of major depressive disorder. For example, Van Praag [
27] has inserted the hedonic deficit into his 'vital syndrome' definition and Klein [
28] has used the term 'endogenomorphic' to describe a distinct subtype of major depression with a marked anhedonic symptomatology. Fawcett
et al. [
29] also suggested that in this endogenomorphic depressed subgroup (characterised by the lack of responsiveness to pleasure) the anhedonic feature had to be considered as a post-depressive 'scar' symptom.
According to Klein's position, the American Psychiatric Association (APA) [
30] has assigned a central role to anhedonia in the Diagnostic and Statistical Manual, fourth edition text revision (DSM-IV-TR) definition of 'major depressive episode' and in its 'melancholic features' specification. In the same way, in the International Classification of Diseases, 10th revision (ICD-10), the World Health Organization (WHO) [
31] has resolved to include curbing of interests and the incapacity to feel pleasure and to experience pleasant emotions among the 'biological symptoms' of major depression. More recently, Joiner
et al. [
32] also found that patients with major depressive disorder presented higher scores on Beck Depression Inventory (BDI) anhedonic items [
33] than schizophrenic subjects, suggesting that anhedonia was a specific state-like feature of depressive illness, which was clinically related to marked psychomotor retardation [
34] and recurrent suicidal ideation [
35].
Contrary to the hypothesis of anhedonia as a 'nuclear' symptom of major depression, other authors [
36‐
39] have considered the hedonic deficit as a marker of genetic vulnerability to major depressive disorder, and either a contributing or potentiating personological factor for the development of depressive illness. For example, Meehl [
37] has used the term 'hedonic capacity' to describe a positive psychological attribute of personality which presented a 'normal' distribution in general population. In his opinion, anhedonia has to be considered a constitutional (genetically transmitted) enduring trait that preceded and possibly caused an endogenous depression. Some years later, Akiskal and Weise [
38] included the hedonic deficit among the basic features of 'depressive temperament' (together with sadness, pessimism, introversion, passivity, and anxiety). Moreover, Loas [
39] proposed a 'vulnerability to depression model' centred on anhedonia. In his opinion, an interaction (during adolescence and/or adulthood) between a constitutional hedonic inability and negative psychosocial stressful events caused the development of an endogenomorphic (unipolar) depression.
In the last two decades, anhedonia has also been described in Parkinson disease [
40] and in other different axis I disorders, particularly drug abuse [
41‐
43]. According to Martinotti
et al. [
42], the frequent presence of hedonic deficit in alcohol and substance use disorders is significant in relation to the high prevalence of those disorders in schizophrenia and major depression.
In summary, there have been contradictory data regarding the relationship between anhedonia and the clinical symptoms of schizophrenia and major depression [
44]. Therefore, the aims of this study were to examine psychopathological features of anhedonia in schizophrenics and depressed patients, and investigate its clinical relationship with diagnostic dimensions (positive, negative, disorganised, and depressive symptoms) of schizophrenia and major depressive disorder. Moreover, this study aimed to elucidate the nature of anhedonia as either state-like or trait-like feature in general schizophrenic and depressive psychopathology.