Anhedonia

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] ; Associate Editor(s)-in-Chief: Pratik Bahekar, MBBS [2]

Anhedonia is defined as the inability to experience pleasure from activities usually found enjoyable, e.g. exercise, hobbies, music, sexual activities or social interactions. (/ˌænhiˈdoʊniə/ Template:Respell; Greek: ἀν- an-, “without” + ἡδονή hēdonē, “pleasure”). 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 an activity (“motivational anhedonia”), as compared to the level of enjoyment of the activity itself (“consummatory anhedonia”).^[1] While anhedonia can be a feature of such mood changes, they are not mutually inclusive.

Anhedonia can be a characteristic of mental disorder including mood disorder, schizoaffective disorder, schizoid personality disorder and schizophrenia. For example, people affected with schizophrenia often describe themselves as feeling emotionally empty.^[2] Mood disturbances are commonly observed in many psychiatric disorders, often precipitated by stressful life events and physical illness.^[3]

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] ; Associate Editor(s)-in-Chief: Pratik Bahekar, MBBS [2]

Concepts of anhedonia has been evolving over last two centuries. Many scientist, psychiatrist and many writers have described anhedonia in various capacities.

Anhedonia was first recognized in 19th century. Towards 1980’s it gained more attention with other symptoms of depression. According to William James 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 has 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.”^[1]

The symptoms of anhedonia were introduced to the realm of psychopathology in 1809 by John Haslam, who characterized a patient suffering from schizophrenia as indifferent to “those objects and pursuits which formerly proved sources of delight and instruction.”.^[2] 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.^[3] Theorists Sándor Radó and Paul Meehl posited that anhedonia represents an underlying genetic vulnerability to schizophrenia-spectrum disorders.^[4] In particular, Rado postulated that schizotypes, or individuals with the schizophrenic phenotype, have two key genetic deficits, one related to the ability to feel pleasure (anhedonia) and one related to proprioception. 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.^[5] Loren and Jean Chapman further distinguished between two types of anhedonia: physical anhedonia, or a deficit in the ability to experience physical pleasure, and social, or a deficit in the ability to experience interpersonal pleasure.^[6]

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] ; Associate Editor(s)-in-Chief: Pratik Bahekar, MBBS [2]

Anhedonia is being studied with variety of neuropsychiatrie disorders. Behavioral, electrophysiological, hemodynamic, and interview-based measures, but the most interesting findings concern neuropharmacological and neuroanatomical studies. The prevalent recognizes key role of dopamine in the pathogenesis of anhedonia, anatomically there is a restricted activity of ventral striatum, including the nucleus accumbens and increased activation of ventral region of the prefrontal cortex, and the ventromedial prefrontal cortex and the orbitofrontal cortex.

• Feeling a normal emotion requires three steps,
  1. Appraisal: Recognition of emotional importance of a stimulus
  2. Production: Generation of an affective state
  3. Regulation: Management at different levels.

These steps are considered to be organized via two different systems, which have a reciprocal relationship.

• Activities within the nucleus accumbens, ventral caudate ,ventral putamen correspond to the euphoric response to various stimuli like dextroamphetamine, cocaine, financial gain, music etc. and are related to dopamine release in the ventral caudate and putamen.

• Ventral striatum and nucleus accumbens employ a major role, in behavioral responses of anticipation and monitoring of errors in the prediction of reward.

• The nucleus accumbens receives projections basically from four regions:
  1. Midbrain region (ventral tegmental area)
  2. Regions involved in emotion (amygdala, orbitofrontal& prefrontal cortex)
  3. Motor regions (dorsal caudate & globus pallidus)
  4. Regions involved in memory (hippocampus)
• Furthermore the accumbens also indirectly projects to the regions implicated in emotion processing, namely:
  1. cortical regions.
  2. The cingular and medial prefrontal cortex
  3. The Ventral pallidum
  4. The Thalamus
  5. The Amygdala. &
  6. The hypothalamus

^[1]‘

Anhedonia coexists with sleep disturbances, impairment in libido, changes in appetite and weight, and also the sense of satisfaction. There is a disturbance in the dopaminergic system, inflammatory processes, circadian rhythms, and melatonin. Anhedonia seems to be more prevalent in interferon-alpha induced depression than the patients of the major depressive disorder. Animal studies on anhedonia have demonstrated impairment in the cytokines. Also, cathecoalamine dysfunction is more pronounced in anhedonia than depression.^[2]

Social anhedonia may represent a prodrome of psychotic disorders.^[3]

Males tends to score higher in scoial anhedonia scales than females^[4] irrespective of,

• Age group (from adolescence into adulthood)
• Co-occurance of the schizophrenia-spectrum disorders^[5]

Males with schizophrenia are diagnosed at a younger age, have more severe symptoms, worse treatment outcomes, and a decrease in overall quality of life compared to females with the disorder.^[6] More research needs to be done to explore possibility of genetic and hormonal role responsible for difference between males and females, and that may increase risk or resilience for mental illnesses such as schizophrenia.^[7]

• The DISC1 gene implicated in the etiology of schizophrenia-spectrum disorders and other mental illnesses^[8], is also found to be associated with social anhedonia within the general population.^[9]
• A specific DISC1 allele associated with an increase in characteristics of social anhedonia, on the contrary another DISC1 allele, preferentially expressed in women, is associated with decreased characteristics of social anhedonia.
• First-degree relatives of individuals with schizophrenia show elevated levels of social anhedonia,^[10]
• Higher baseline scores of social anhedonia are associated with later development of schizophrenia.^[11] These findings provide support for the conjecture that it represents a genetic risk marker for schizophrenia-spectrum disorders.

More research needs to be conducted, but social anhedonia seems to be an important intermediate phenotype between genes associated with risk for schizophrenia and the phenotype of the disorder.

Anhedonia is implicated in the pathophysiology of many diseases.

The following findings have been observed in the patients suffering from cariovascular aliments and anhedonia,

• Increased platelet reactivity
• Hypercoaguability
• Inflammatory activation, and endothelial or autonomic dysfunction
• High catecholamine levels which in turn can trigger tachyarrhythmia, and promote platelet aggregation.

resulting in increased morbidity and mortality due to cardiovascular disease.^[12]

• Increased incedence of anhedonia is seen in the substance abuse, and substance dependance.
• Anhedonia predicts drug craving attitude and probability of the relapse.
• Anhedonia diminishes with abstinance.^[13]

• An increase in the hedonic set point is observed in chronic nicotine exposure, leading to a decreased reward potency. There is a increased difficulty to experience pleasure and stronger stimuli is needed to experience pleasure. Thus, over time person requires increased nicotine quantity to achieve similar reward stimulus.
• In withdrawal, craving for smoking increases to achieve reward stimulus to accommodate hypo-functioning dopamine functioning.^[14]

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] ; Associate Editor(s)-in-Chief: Pratik Bahekar, MBBS [2]

Anhedonia forms one of major criteria in the diagnosis of depression, but, it also seen in negative symptom of schizophrenia, psychosis. Anhedonia is studies in neuropsychiatrie disorders, substance use disorder, parkinson’s disease, overeating, and various risky behaviors.

• Major Depressive Disorder
• Dysthymia
• Bipolar Depression
• Schizophrenia
• Schizoaffective disorder
• Antidopaminergic neuroleptics like antipsychotic medication.

Sexual anhedonia is caused by:

• Hyperprolactinaemia
• Hypoactive sexual desire disorder (HSDD), also called inhibited sexual desire
• Spinal cord injury
• Multiple sclerosis
• Use (or previous use) of SSRI antidepressants^[1]
• Use (or previous use) of antidopaminergic neuroleptics (anti-psychotics)^[2][3]
• Fatigue
• Physical illness

Anhedonia is present in several forms of psychopathology.^[4] However, social anhedonia is not a necessary symptom criterion of any disorder. Social anhedonia manifests similarly in a variety of different mental illness, but for differing reasons. Most frequently, social anhedonia is associated with schizophrenia and schizophrenia spectrum disorders (including schizotypal personality disorder, paranoid personality disorder, and antisocial personality disorder). Social anhedonia has also been implicated in other psychological disorders:

Social anhedonia is observed in both depression and schizophrenia. However, social anhedonia is state related to the depressive episode and the other is trait related to the personality construct associated with schizophrenia. These individuals both tend to score highly on self-report measures of social anhedonia. Blanchard, Horan, and Brown (2001) 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.^[5] Blanchard and colleagues (2011) found individuals with social anhedonia also had elevated rates of lifetime mood disorders including depression and dysthymia compared to controls.^[6]

As mentioned above, social anxiety and social anhedonia differ in important ways. However, social anhedonia and social anxiety are also often comorbid with each other. People with social anhedonia may display increased social anxiety and be at increased risk for social phobias and generalized anxiety disorder.^[7] It has yet to be determined what the exact relationship between social anhedonia and social anxiety is, and if one potentiates the other.^[8] Individuals with social anhedonia may display increased stress reactivity, meaning that they feel more overwhelmed or helpless in response to a stressful event compared to control subjects who experience the same type of stressor. This dysfunctional stress reactivity may correlate with hedonic capacity, providing a potential explanation for the increased anxiety symptoms experienced in people with social anhedonia.^[9] In an attempt to separate out social anhedonia from social anxiety, the Revised Social Anhedonia Scale ^[10] didn’t include items that potentially targeted social anxiety.^[11] However, more research must be conducted on the underlying mechanisms through which social anhedonia overlaps and interacts with social anxiety. The efforts of the “social processes” RDoC initiative will be crucial in differentiating between these components of social behavior that may underlie mental illnesses such as schizophrenia.^[12]

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.^[13] Social anhedonia is a dimension of both negative and positive schizotypy.^[14] 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.^[15][16][17] Not all people with schizophrenia display social anhedonia ^[18] and likewise, people who have social anhedonia may never be diagnosed with a schizophrenia-spectrum disorder if they do not have the positive and cognitive symptoms that are most frequently associated with most schizophrenia-spectrum disorders.^[19]

Social anhedonia may be a valid predictor of future schizophrenia-spectrum disorders;^[19][20] young adults with social anhedonia perform in a similar direction to schizophrenia patients in tests of cognition and social behavior tests, showing potential predictive validity.^[15][21] Social anhedonia usually manifests in adolescence, possibly because of a combination of the occurrence of critical neuronal development and synaptic pruning of brain regions important for social behavior and environmental changes, when adolescents are in the process of becoming individuals and gaining more independence.

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] ; Associate Editor(s)-in-Chief: Pratik Bahekar, MBBS [2]

Template:WikiDoc Sources

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] ; Associate Editor(s)-in-Chief: Pratik Bahekar, MBBS [2]

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