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==Overview==
==Overview==
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 hypothesis is that the dopamine plays an important role in 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, including the ventromedial prefrontal cortex and the orbitofrontal cortex.
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.


==Pathophysiology==
==Pathophysiology==
*Feeling a normal emotion requires three steps,
*#Appraisal: Recognition of emotional importance of a stimulus
*#Production: Generation of an affective state
*#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:
*#Midbrain region (ventral tegmental area)
*#Regions involved in emotion (amygdala, orbitofrontal&  prefrontal cortex)
*#Motor regions (dorsal caudate & globus pallidus)
*#Regions involved in memory (hippocampus)
*Furthermore the accumbens also indirectly projects to the regions implicated in emotion processing, namely:
*#cortical regions.
*#The cingular and medial prefrontal cortex
*#The Ventral pallidum
*#The Thalamus
*#The Amygdala. &
*#The hypothalamus


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Animal studies on anhedonia have demonstrated impairment in the cytokines.  Also, cathecoalamine dysfunction is more pronounced in anhedonia than depression.<ref>{{Cite web  | last =  | first =  | title = Anhedonia Predicts Major Adverse Cardiac Events and Mortality in Patients 1 Year After Acute Coronary Syndrome | url = http://pubmedcentralcanada.ca/pmcc/articles/PMC3058237/ | publisher =  | date =  | accessdate = }}</ref>
Animal studies on anhedonia have demonstrated impairment in the cytokines.  Also, cathecoalamine dysfunction is more pronounced in anhedonia than depression.<ref>{{Cite web  | last =  | first =  | title = Anhedonia Predicts Major Adverse Cardiac Events and Mortality in Patients 1 Year After Acute Coronary Syndrome | url = http://pubmedcentralcanada.ca/pmcc/articles/PMC3058237/ | publisher =  | date =  | accessdate = }}</ref>


Social anhedonia may represent a prodrome of psychotic disorders.<ref>Silvia, P.J., & Thomas, R.K. (2011). Aberrant asociality: How individual differences in social anhedonia illuminate the need to belong. ‘’Journal of Personality, 79’’.</ref> 


===Sex differences===
===Sex differences===
Line 27: Line 53:


===Genetic components===
===Genetic components===
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.<ref>Brandon, Nicholas J, & Sawa, A. (2011). Linking neurodevelopmental and synaptic theories of mental illness through DISC1. Nature reviews. ''Neuroscience'', 12(12), 707–722</ref> More recently, [[DISC1]] has been associated with social anhedonia within the general population.<ref>Tomppo, L., Hennah, W., Miettunen, J., Järvelin, M.-R., Veijola, J., Ripatti, S., … Ekelund, J. (2009). Association of variants in DISC1 with psychosis-related traits in a large population cohort. Archives of general psychiatry, 66(2), 134–141</ref> 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.


*The '''DISC1 gene''' implicated in the etiology of schizophrenia-spectrum disorders and other mental illnesses<ref>Brandon, Nicholas J, & Sawa, A. (2011). Linking neurodevelopmental and synaptic theories of mental illness through DISC1. Nature reviews. ''Neuroscience'', 12(12), 707–722</ref>, is also found to be associated with social anhedonia within the general population.<ref>Tomppo, L., Hennah, W., Miettunen, J., Järvelin, M.-R., Veijola, J., Ripatti, S., … Ekelund, J. (2009). Association of variants in DISC1 with psychosis-related traits in a large population cohort. Archives of general psychiatry, 66(2), 134–141</ref>
*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,<ref>Cohen, A.S., Emmerson, L.C., Mann, M.C., Forbes, C.B., & Blanchard, J.J. (2010). Schizotypal, schizoid and paranoid characteristics in the biological parents of social anhedonics. ‘’Psychiatry Research, 178’’, 79-83.</ref>
*Higher baseline scores of social anhedonia are associated with later development of schizophrenia.<ref>Gooding, D.C., Tallent, K.A., & Matts, C.W. (2005). Clinical status of at-risk individuals five years later: Further validation of the psychometric high-risk strategy. ‘’Journal of Abnormal Psychology, 114’’, 170-175.</ref>  These findings provide support for the conjecture that it represents a genetic risk marker for schizophrenia-spectrum disorders.


===Background and early clinical observation===
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.
The term ''anhedonia'' is derived from the Greek ‘’an-’’, "without" + ‘’hēdonē’’, "pleasure".<ref>Di Giannantonio, M., & Martinotti, G. (2012). Anhedonia and major depression: The role of agomelatine. ""European neuropsychopharmacology, 22"", Supplement 3, S505–S510.</ref> Interest in the nature of pleasure and its absence dates back to ancient Greek philosophers such as [[Epicurus]].<ref>Der-Avakian, A., & Markou, A. (2011). The neurobiology of anhedonia and other reward-related deficits. ‘’Trends in Neurosciences, 35’’’’ 68–77.</ref> 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.”.<ref>Noll, R. (1959). ‘’The encyclopedia of schizophrenia and other psychotic disorders’’ (p. xii). New York : Facts on File.</ref> 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.<ref name="DerAvakian">Der-Avakian, A., & Markou, A. (2011). The neurobiology of anhedonia and other reward-related deficits. ‘’Trends in Neurosciences, 35’’, 68–77.</ref> Theorists Sándor Radó and [[Paul Meehl]] posited that anhedonia represents an underlying genetic vulnerability to schizophrenia-spectrum disorders.<ref>Horan, W.P., Kring, A.M., & Blanchard, J.J. (2006). Anhedonia in Schizophrenia: A Review of Assessment Strategies. ‘’Schizophrenia Bulletin, 32’’, 259–273.</ref> 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]].<ref>Meehl, P.E. (1989). Schizotaxia revisited. ‘’Archives in General Psychiatry, 46’’, 935-944.</ref> 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.<ref>Kontaxakis, V., Kollias, C., Margariti, M., Stamouli, S., Petridou, E., & Christodoulou, G.N. (2006). Physical anhedonia in the acute phase of schizophrenia. ‘’Annals of General Psychiatry, 5’’, 1-6.</ref>


Recent research suggests that social anhedonia may represent a [[prodrome]] of psychotic disorders.<ref>Silvia, P.J., & Thomas, R.K. (2011). Aberrant asociality: How individual differences in social anhedonia illuminate the need to belong. ‘’Journal of Personality, 79’’.</ref> First-degree relatives of individuals with schizophrenia show elevated levels of social anhedonia,<ref>Cohen, A.S., Emmerson, L.C., Mann, M.C., Forbes, C.B., & Blanchard, J.J. (2010). Schizotypal, schizoid and paranoid characteristics in the biological parents of social anhedonics. ‘’Psychiatry Research, 178’’, 79-83.</ref> higher baseline scores of social anhedonia are associated with later development of schizophrenia.<ref>Gooding, D.C., Tallent, K.A., & Matts, C.W. (2005). Clinical status of at-risk individuals five years later: Further validation of the psychometric high-risk strategy. ‘’Journal of Abnormal Psychology, 114’’, 170-175.</ref> These findings provide support for the conjecture that it represents a genetic risk marker for schizophrenia-spectrum disorders.
==Anhedonia and Other Diseases==
Anhedonia is implicated in the pathophysiology of many diseases.
===Cardiovascular 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.<ref>{{Cite web  | last =  | first =  | title = Anhedonia Predicts Major Adverse Cardiac Events and Mortality in Patients 1 Year After Acute Coronary Syndrome | url = http://pubmedcentralcanada.ca/pmcc/articles/PMC3058237/ | publisher =  | date =  | accessdate = }}</ref>


Additionally, elevated levels of social anhedonia in patients with schizophrenia have been linked to poorer social functioning.<ref>Blanchard, J.J., Bellack, A.S., & Mueser, K.T. (1994). Affective and social-behavioral correlates of physical and social anhedonia in schizophrenia. ‘’Journal of Abnormal Psychology, 103’’, 719-728.</ref><ref>Blanchard, J.J., Mueser, K.T., & Bellack, A.S. (i1998). Anhedonia, positive and negative affect, and social functioning in schizophrenia. ‘’Schizophrenia Bulletin, 24’’, 413–424.</ref> Socially anhedonic individuals perform worse on a number of neuropsychological tests than non-anhedonic participants,<ref>Laurent, A., Biloa-Tang, M., Bougerol, T., Duly, D., Anchisi, A.M., Bosson, J.L., Pellat, J., d’Amato, T., & Dalery, J. (2000). Executive/ attentional performance and measures of schizotypy in patients with schizophrenia and in their nonpsychotic first-degree relatives. ‘’Schizophrenia Research, 46’’, 269–283.</ref><ref>Cohen, A., Leung, W., Saperstein, A., & Blanchard, J. (2006). Neuropsychological functioning and social anhedonia: Results from a community high-risk study. ‘’Schizophrenia Research, 85’’, 132−141.</ref> and show similar physiological abnormalities seen in patients with schizophrenia.<ref>Cohen, A.S., Leung, W.W., Saperstein, A.M., & Blanchard, J.J. (2006). Neuropsychological functioning and social anhedonia: results from a community high-risk study. ‘’Schizophrenia Research, 85’’, 132-141.</ref>
===Addiction===
*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.<ref name="anp.sagepub.com">{{Cite web  | last =  | first =  | title = Anhedonia in substance use disorders: A systematic review of its nature, course and clinical correlates | url = http://anp.sagepub.com/content/48/1/36 | publisher =  | date =  | accessdate = }}</ref>
====Smoking====
*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.<ref>{{Cite web  | last =  | first =  | title = Effects of anhedonia on days to relapse amo... [Nicotine Tob Res. 2010] - PubMed - NCBI | url = http://www.ncbi.nlm.nih.gov/pubmed/20709727 | publisher =  | date =  | accessdate = }}</ref>


==References==
==References==

Latest revision as of 23:55, 13 April 2014

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

Overview

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.

Pathophysiology

  • 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]

Sex differences

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]

Genetic components

  • 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 and Other Diseases

Anhedonia is implicated in the pathophysiology of many diseases.

Cardiovascular 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]

Addiction

  • 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]

Smoking

  • 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]

References

  1. ↑ "Neurobiological mechanisms of anhedonia".
  2. ↑ "Anhedonia Predicts Major Adverse Cardiac Events and Mortality in Patients 1 Year After Acute Coronary Syndrome".
  3. ↑ Silvia, P.J., & Thomas, R.K. (2011). Aberrant asociality: How individual differences in social anhedonia illuminate the need to belong. ‘’Journal of Personality, 79’’.
  4. ↑ Fonseca-Pedrero, E., Lemos-Giráldez, S., Muñiz, J., García-Cueto, E., & Campillo-Alvarez, A. (2008). Schizotypy in adolescence: the role of gender and age. The Journal of nervous and mental disease, 196(2), 161–165
  5. ↑ Miettunen, J., & Jääskeläinen, E. (2010). Sex differences in Wisconsin Schizotypy Scales--a meta-analysis. Schizophrenia bulletin, 36(2), 347–358
  6. ↑ Leung A, Chue P. Sex differences in schizophrenia, a review of the literature. Acta Psychiatr Scand. 2000;101:3–38
  7. ↑ Jessen, H. M., & Auger, A. P. (2011). Sex differences in epigenetic mechanisms may underlie risk and resilience for mental health disorders. Epigenetics: official journal of the DNA Methylation Society, 6(7), 857–861
  8. ↑ Brandon, Nicholas J, & Sawa, A. (2011). Linking neurodevelopmental and synaptic theories of mental illness through DISC1. Nature reviews. Neuroscience, 12(12), 707–722
  9. ↑ Tomppo, L., Hennah, W., Miettunen, J., Järvelin, M.-R., Veijola, J., Ripatti, S., … Ekelund, J. (2009). Association of variants in DISC1 with psychosis-related traits in a large population cohort. Archives of general psychiatry, 66(2), 134–141
  10. ↑ Cohen, A.S., Emmerson, L.C., Mann, M.C., Forbes, C.B., & Blanchard, J.J. (2010). Schizotypal, schizoid and paranoid characteristics in the biological parents of social anhedonics. ‘’Psychiatry Research, 178’’, 79-83.
  11. ↑ Gooding, D.C., Tallent, K.A., & Matts, C.W. (2005). Clinical status of at-risk individuals five years later: Further validation of the psychometric high-risk strategy. ‘’Journal of Abnormal Psychology, 114’’, 170-175.
  12. ↑ "Anhedonia Predicts Major Adverse Cardiac Events and Mortality in Patients 1 Year After Acute Coronary Syndrome".
  13. ↑ "Anhedonia in substance use disorders: A systematic review of its nature, course and clinical correlates".
  14. ↑ "Effects of anhedonia on days to relapse amo... [Nicotine Tob Res. 2010] - PubMed - NCBI".

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