Anhedonia is defined as the inability to experience pleasure from activities usually found enjoyable, e.g. exercise, hobbies, music, sexual activities or social interactions. While earlier definitions of anhedonia emphasized pleasurable experience, more recent models have highlighted the need to consider different aspects of enjoyable behavior, such as motivation or desire to engage in activities (motivational anhedonia), as compared to the level of enjoyment of the activity itself (“consummatory anhedonia”).
According to [William James](http://The Varieties of Religious Experience) the term was coined by Théodule-Armand Ribot.
One can distinguish many kinds of pathological depression. Sometimes it is mere passive joylessness and dreariness, discouragement, dejection, lack of taste and zest and spring. Professor Ribot proposed the name anhedonia to designate this condition. “The state of anhedonia, if I may coin a new word to pair off with analgesia,” he writes, “has been very little studied, but it exists."
Anhedonia can be a characteristic of mental disorders including mood disorders, schizoaffective disorder, borderline personality disorder, schizoid personality disorder and schizophrenia. For example, the 7th DSM-IV criterion for Borderline Personality Disorder: “chronic feelings of emptiness.”
Results indicate that emptiness is negligibly related to boredom, is closely related to feeling hopeless, pathologically lonely, and isolated, and is a robust predictor of depression and suicidal ideation (but not anxiety or suicide attempts). Findings are consistent with DSM-IV revisions regarding the 7th criterion for Borderline Personality Disorder. In addition, findings suggest the emptiness reflects pathologically low positive affect and significant psychiatric distress. People affected with schizophrenia often describe themselves as feeling emotionally empty.
Mood disturbances are commonly observed in many psychiatric disorders. Disturbing mood changes may occur resultant to stressful life events and they are not uncommon during times of physical illness. While anhedonia can be a feature of such mood changes, they are not mutually inclusive.
Researchers theorize that anhedonia may result from the breakdown in the brain’s reward system, involving the neurotransmitter dopamine. Studies by Paul Keedwell, MD, then of King’s College, found that the brains of participants who were clinically depressed had to work harder to process rewarding experiences.
While earlier research believed dopamine to be primarily involved in the subjective experience of pleasure, the last 20 years has seen a conceptual shift, such that dopamine is now believed to underlie various aspects of reward anticipation, learning, and motivation. Anhedonia can be characterised as “impaired ability to pursue, experience and/or learn about pleasure, which is often, but not always accessible to conscious awareness”. (Front Behav Neurosci. 2015; 9: 49)
Anhedonia is also a relatively common side effect of antidopaminergic neuroleptics or antipsychotic drugs, as well a side effect of withdrawal from stimulants such as phenethylamines, or amphetamines.
Significance in Depression
As a clinical symptom in depression, anhedonia rates highly in making a diagnosis of this disorder. Some users describe the feeling as being “strung out”. The Diagnostic and Statistical Manual of Mental Disorders (DSM) describes a “lack of interest or pleasure”, but these can be difficult to discern given that people tend to become less interested in things which do not give them pleasure.
The DSM criterion of weight loss is probably related, and many individuals with this symptom describe a lack of enjoyment of food. People suffering from anhedonia in association with depression generally feel suicidal in the morning and better in the evenings as sleep seems the only escape resembling death and can portray any of the non-psychotic symptoms and signs of depression.
Social anhedonia is defined as a trait-like disinterest in social contact and is characterized by social withdrawal and decreased pleasure in social situations. This characteristic typically manifests as an indifference to other people.
In contrast to introversion, a nonpathological dimension of human personality, social anhedonia represents a deficit in the ability to experience pleasure. Additionally, social anhedonia differs from social anxiety in that social anhedonia is predominantly typified by diminished positive affect, while social anxiety is distinguished by both decreased positive affect and exaggerated negative affect.
This trait is currently seen as a central characteristic to, as well as a predictor of, schizophrenia-spectrum disorders, as it is seen as a potential evolution of most personality disorders, if the patient is above age 24, when prodromal schizophrenia may be excluded.
Decreased ability to experience interpersonal pleasure
Decreased need for social contact
Lack of close friends and intimate relationships, and decreased quality of those relationships
Poor social adjustment
Decreased positive affect
Social anhedonia is trait-related, meaning it remains stable throughout life, independent of diagnosis, treatment, or symptom remission. (Schizophr Bull (1998) 24 (3): 413-424)
There is no validated treatment for social anhedonia. Future research should focus on genetic and environmental risk factors to home in on specific brain regions and neurotransmitters that may be implicated in social anhedonia etiology and could be targeted with specialized pharmacological or behavioral treatments.
Social support may also play a valuable role in the treatment of social anhedonia. Blanchard et al. (2011) found that a greater number of social supports as well as a greater perceived social support network were related to fewer schizophrenia-spectrum symptoms and to better general functioning within the social anhedonia group. Therefore, future studies should also examine ways to increase social support among individuals with social anhedonia in order to alleviate some of the symptoms.
In the general population, males score higher than females on measures of social anhedonia. This sex difference is stable throughout time (from adolescence into adulthood) and is also seen in people with schizophrenia-spectrum disorders.
These results may reflect a more broad pattern of interpersonal and social deficits seen in schizophrenia-spectrum disorders. On average, males with schizophrenia are diagnosed at a younger age, have more severe symptoms, worse treatment prognosis, and a decrease in overall quality of life compared to females with the disorder.
These results, coupled with the sex difference seen in social anhedonia, outline the necessity for research on genetic and hormonal characteristics that differ between males and females, and that may increase risk or resilience for mental illnesses such as schizophrenia.
L.J. and J.P. Chapman were the first to discuss the possibility that social anhedonia may stem from a genetic vulnerability. The Disrupted in Schizophrenia 1 (DISC1) gene has been consistently associated with risk for, and etiology of, schizophrenia-spectrum disorders and other mental illnesses.
More recently, DISC1 has been associated with social anhedonia within the general population. Tomppo (2009) identified a specific DISC1 allele that is associated with an increase in characteristics of social anhedonia. They also identified a DISC1 allele associated with decreased characteristics of social anhedonia, that was found to be preferentially expressed in women.
More research needs to be conducted, but social anhedonia may be an important intermediate phenotype (endophenotype) between genes associated with risk for schizophrenia and phenotype of the disorder. Continued study of social anhedonia and its genetic components will help researchers and clinicians learn more about the etiology of schizophrenia-spectrum disorders.
Researchers studying the neurobiology of social anhedonia posit that this trait may be linked to dysfunction of reward-related systems in the brain. This circuitry is critical for the sensation of pleasure, the computation of reward benefits and costs, determination of the effort required to obtain a pleasant stimulus, deciding to obtain that stimulus, and increasing motivation to obtain the stimulus.
In particular, the ventral striatum and areas of the prefrontal cortex (PFC), including the orbitofrontal cortex (OFC) and dorsolateral (dl) PFC, are critically involved in the experience of pleasure and the hedonic perception of rewards.
With regards to neurotransmitter systems, opioid, gamma-Aminobutyric acid and endocannabinoid systems in the nucleus accumbens, ventral pallidum, and OFC mediate the hedonic perception of rewards. Activity in the PFC and ventral striatum have been found to be decreased in anhedonic individuals with Major Depressive Disorder (MDD) and schizophrenia.
However, schizophrenia may be less associated with decreased hedonic capacity and more with deficient reward appraisal. Abnormal functioning of the anterior insula and the parietal cortex is also implicated in anhedonia.
Dowd & Barch conducted an fMRI study in which schizophrenia-spectrum disorder patients and control participants made valence and arousal ratings of their own responses to emotional stimuli. They found that higher levels of anhedonia were associated with diminished arousal, but not valence, ratings.
Furthermore, they found that, in controls, greater levels of social anhedonia were related to decreased bilateral caudate activation in response to positive relative to negative stimuli. The authors posit that the striatum in anhedonic individuals might be dysfunctional such that it fails to tag the saliency of positive events. Consequently, these individuals may experience blunted emotion.
Research further implicates that abnormalities in the circuitry underlying social cognition are also critically involved in the generation of anhedonic symptoms. Individuals high in social anhedonia show less activation in the anterior portion of the rostral medial prefrontal cortex (arMFC), right superior temporal gyrus, and left somatosensory cortex during an emotion discrimination task; these regions are responsible for processing facial emotions.
Moreover, the arMFC is highly relevant for social cognition, and the mPFC and somatosensory cortex are involved in theory of mind and mentalizing. Thus, social anhedonia appears to be related to dysfunction of neural systems involved in self/other representation and social perception.