Anhedonia is a diverse array of deficits in hedonic function, including reduced motivation or ability to experience pleasure.
[3] While anhedonia was originally defined in 1896 by Théodule-Armand Ribot as the reduced ability to experience pleasure, it has been used to refer to deficits in multiple facets of reward.
[2][1] The consciousness of reward-related processes has also been used to categorize reward in the context of anhedonia, as studies comparing implicit behavior versus explicit self-reports demonstrate a dissociation of the two.
[5][3] Neuroimaging studies in humans have reported that deficits in consummatory aspects of reward are associated with abnormalities in the ventral striatum and medial prefrontal cortex, while deficits in anticipatory aspects of reward are related to abnormalities in hippocampal, dorsal ACC and prefrontal regions.
This inconsistency may be related to the difficulty in imaging the OFC due to its anatomical location, or the small number of studies performed on anhedonia;[8] a number of studies have reported reduced activity in the OFC in schizophrenia and major depression, as well as a direct relationship between reduced activity and anhedonia.
[14] Schizophrenia is associated with reduced positive prediction errors (a normal pattern of response to an unexpected reward), which a few studies have demonstrated to be correlated with negative symptoms.
[15] Anhedonia is common in people who are dependent upon any one or more of a wide variety of drugs, including alcohol, opioids, cannabinoids, and nicotine.
Impairments of dopaminergic and serotonergic function in the brain of those with ADHD result in dysregulation of reward processing, which can lead to anhedonia.
[26] In contrast to introversion, a nonpathological dimension of human personality, social anhedonia represents a deficit in the ability to experience pleasure.
[3] The symptoms of anhedonia were introduced to the realm of psychopathology in 1809 by John Haslam, who characterized a patient with schizophrenia as indifferent to "those objects and pursuits which formerly proved sources of delight and instruction".
[33] The concept was formally coined by Théodule-Armand Ribot and later used by psychiatrists Paul Eugen Bleuler and Emil Kraepelin to describe a core symptom of schizophrenia.
In 1962, Meehl furthered Rado's theory through the introduction of the concept of schizotaxia, a genetically driven neural integrative defect thought to give rise to the personality type of schizotypy.
[39][40] Socially anhedonic individuals perform worse on a number of neuropsychological tests than non-anhedonic participants,[41][42] and show similar physiological abnormalities seen in patients with schizophrenia.
Blanchard, Horan, and Brown demonstrated that, although both the depression and the schizophrenia patient groups can look very similar in terms of social anhedonia cross-sectionally, over time as individuals with depression experience symptom remission, they show fewer signs of social anhedonia, while individuals with schizophrenia do not.
[44] Blanchard and colleagues (2011) found individuals with social anhedonia also had elevated rates of lifetime mood disorders including depression and dysthymia compared to controls.
This dysfunctional stress reactivity may correlate with hedonic capacity, providing a potential explanation for the increased anxiety symptoms experienced in people with social anhedonia.
Social anhedonia is a core characteristic of schizotypy, which is defined as a continuum of personality traits that can range from normal to disordered and contributes to risk for psychosis and schizophrenia.
[51] It involves social and interpersonal deficits, but is also associated with cognitive slippage and disorganized speech, both of which fall into the category of positive schizotypy.
[47] 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's cause, and could be targeted with medication or behavioral treatments.
[58] 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.
[65] Researchers studying the neurobiology of social anhedonia posit that this trait may be linked to dysfunction of reward-related systems in the brain.
[3] Activity in the PFC and ventral striatum have been found to be decreased in anhedonic individuals with major depressive disorder and schizophrenia.