Anhedonia pathophysiology
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
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]
References
- ↑ "Neurobiological mechanisms of anhedonia".
- ↑ 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
- ↑ Miettunen, J., & Jääskeläinen, E. (2010). Sex differences in Wisconsin Schizotypy Scales--a meta-analysis. Schizophrenia bulletin, 36(2), 347–358
- ↑ Leung A, Chue P. Sex differences in schizophrenia, a review of the literature. Acta Psychiatr Scand. 2000;101:3–38
- ↑ 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
- ↑ Brandon, Nicholas J, & Sawa, A. (2011). Linking neurodevelopmental and synaptic theories of mental illness through DISC1. Nature reviews. Neuroscience, 12(12), 707–722
- ↑ 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
- ↑
- ↑ Wolf, D.H. (2006). Anhedonia in schizophrenia. ‘’Current Psychiatry Reports, 8’’, 322–328.
- ↑ 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.
- ↑ Dowd, E.C., & Barch, D.M. (2010). Anhedonia and emotional experience in schizophrenia: neural and behavioral indicators. ‘’Biological Psychiatry, 67’’, 902–911.
- ↑ Germine, L., Garrido, L., Bruce, L., & Hooker, C. (2011). Social anhedonia is associated with neural abnormalities during face emotion processing. ‘’Neuroimage, 58’’, 935–945.