Anhedonia pathophysiology: Difference between revisions

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==Pathophysiology==
==Pathophysiology==
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<ref>{{Cite web  | last =  | first =  | title = Neurobiological mechanisms of anhedonia | url = http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3181880/ | publisher =  | date =  | accessdate = }}</ref>
<ref>{{Cite web  | last =  | first =  | title = Neurobiological mechanisms of anhedonia | url = http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3181880/ | publisher =  | date =  | accessdate = }}</ref>

Revision as of 14:07, 20 March 2014

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 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.

Pathophysiology

[1]

Sex differences

In the general population, males score higher than females on measures of social anhedonia.[2] 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.[3] 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.[4] 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.[5]

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.[6] More recently, DISC1 has been associated with social anhedonia within the general population.[7] 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.

Neurobiological correlates

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 Hedonism 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.[8] 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.[9][10] Abnormal functioning of the anterior insula and the parietal cortex is also implicated in anhedonia. Dowd & Barch conducted an Functional magnetic resonance imaging 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.[11]

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.[12]

Background and early clinical observation

The term anhedonia is derived from the Greek ‘’an-’’, "without" + ‘’hēdonē’’, "pleasure".[13] Interest in the nature of pleasure and its absence dates back to ancient Greek philosophers such as Epicurus.[14] 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.”.[15] 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.[8] Theorists Sándor Radó and Paul Meehl posited that anhedonia represents an underlying genetic vulnerability to schizophrenia-spectrum disorders.[16] 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.[17] 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.[18]

Recent research suggests that social anhedonia may represent a prodrome of psychotic disorders.[19] First-degree relatives of individuals with schizophrenia show elevated levels of social anhedonia,[20] higher baseline scores of social anhedonia are associated with later development of schizophrenia.[21] These findings provide support for the conjecture that it represents a genetic risk marker for schizophrenia-spectrum disorders.

Additionally, elevated levels of social anhedonia in patients with schizophrenia have been linked to poorer social functioning.[22][23] Socially anhedonic individuals perform worse on a number of neuropsychological tests than non-anhedonic participants,[24][25] and show similar physiological abnormalities seen in patients with schizophrenia.[26]

References

  1. ↑ "Neurobiological mechanisms of anhedonia".
  2. ↑ 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
  3. ↑ Miettunen, J., & Jääskeläinen, E. (2010). Sex differences in Wisconsin Schizotypy Scales--a meta-analysis. Schizophrenia bulletin, 36(2), 347–358
  4. ↑ Leung A, Chue P. Sex differences in schizophrenia, a review of the literature. Acta Psychiatr Scand. 2000;101:3–38
  5. ↑ 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
  6. ↑ Brandon, Nicholas J, & Sawa, A. (2011). Linking neurodevelopmental and synaptic theories of mental illness through DISC1. Nature reviews. Neuroscience, 12(12), 707–722
  7. ↑ 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
  8. ↑ 8.0 8.1 Der-Avakian, A., & Markou, A. (2011). The neurobiology of anhedonia and other reward-related deficits. ‘’Trends in Neurosciences, 35’’, 68–77.
  9. ↑ Wolf, D.H. (2006). Anhedonia in schizophrenia. ‘’Current Psychiatry Reports, 8’’, 322–328.
  10. ↑ Gold, J.M., Waltz, J.A., Prentice, K.J., Morris, S.E., & Heerey, E.A. (2008). Reward processing in schizophrenia: a deficit in the representation of value. ‘’Schizophrenia Bulletin, 34’’, 835–847.
  11. ↑ Dowd, E.C., & Barch, D.M. (2010). Anhedonia and emotional experience in schizophrenia: neural and behavioral indicators. ‘’Biological Psychiatry, 67’’, 902–911.
  12. ↑ Germine, L., Garrido, L., Bruce, L., & Hooker, C. (2011). Social anhedonia is associated with neural abnormalities during face emotion processing. ‘’Neuroimage, 58’’, 935–945.
  13. ↑ Di Giannantonio, M., & Martinotti, G. (2012). Anhedonia and major depression: The role of agomelatine. ""European neuropsychopharmacology, 22"", Supplement 3, S505–S510.
  14. ↑ Der-Avakian, A., & Markou, A. (2011). The neurobiology of anhedonia and other reward-related deficits. ‘’Trends in Neurosciences, 35’’’’ 68–77.
  15. ↑ Noll, R. (1959). ‘’The encyclopedia of schizophrenia and other psychotic disorders’’ (p. xii). New York : Facts on File.
  16. ↑ Horan, W.P., Kring, A.M., & Blanchard, J.J. (2006). Anhedonia in Schizophrenia: A Review of Assessment Strategies. ‘’Schizophrenia Bulletin, 32’’, 259–273.
  17. ↑ Meehl, P.E. (1989). Schizotaxia revisited. ‘’Archives in General Psychiatry, 46’’, 935-944.
  18. ↑ 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.
  19. ↑ Silvia, P.J., & Thomas, R.K. (2011). Aberrant asociality: How individual differences in social anhedonia illuminate the need to belong. ‘’Journal of Personality, 79’’.
  20. ↑ 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.
  21. ↑ 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.
  22. ↑ 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.
  23. ↑ 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.
  24. ↑ 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.
  25. ↑ 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.
  26. ↑ 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.

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