Moving toward a more accurate characterization of Anhedonia

Over the last several decades the concept of anhedonia has been subject to interesting developments in the field of behavioral neuroscience. Research into the neurobiological processes involved in reward behavior has succeeded in convincing us to reconsider the dimensions of a term that has become commonplace in the mental health field. Anhedonia is generally understood to mean the inability, or diminished capacity, to experience pleasure. It is also refers to a deficit in motivation to engage in typically rewarding behaviors. Exploration of the absence of pleasure dates back to Epicurus (Der-Avakian & Markou, 2012). The term became included in the DSM in 1980 and the International Classification of Diseases in 1992 (Berrios and Olivares, 1995). Despite the widespread use of the concept, it has been inconsistently defined in the literature (Ho & Sommers, 2013).

The concept of anhedonia warrants important consideration and scientific inquiry for several reasons. Well-documented in depression, schizophrenia and other psychiatric and neurologic conditions, anhedonia has the potential to impair quality of life and produce considerable suffering. In an epidemiological study (N=7076) anhedonia was found to be a poor prognostic indicator in treatment outcomes for people with MDD (Spijker, Bijl & DeGraaf, 2001). Multiple studies have found that first-line pharmacologic agents for MDD (SSRIs) do not adequately treat anhedonic symptoms (Treadway & Zald, 2011). Given the evidence for the limited efficacy of SSRIs and poor response to treatment in depressed patients with diminished pleasure and motivation it makes both economic and ethical sense to pursue research that increases our understanding of the pathological processes involved.

In its process of inquiry, behavioral neuroscience has facilitated the need to reconsider our conceptualization of anhedonia. The dopamine (DA) deficiency hypothesis of anhedonia, first posited in 1980, gained traction in its suggestion that DA was a key mediator in the experience of pleasure (Treadway & Zald, 2011; Wise, 2008). Subsequent research has demonstrated that mesolimbic DA is not implicated in the experience of pleasure involved in reward behaviors (Berridge & Robinson, 2003). Rather, it has been demonstrated that the primary neurotransmitters involved in the experience of pleasure are endogenous opioids (Thomsen, Whybrow & Kringlebach, 2015). Significant expression of (mu) opioid receptors exists in the ventral striatum, on the shell of the nucleus accumbens, as well as the ventral pallidum, a structure of the basal ganglia (Penciña, Smith & Berridge, 2006). Endocannabinoids and orexin have also been found to stimulate these areas and result in increased sensory pleasure (Thomsen, Whybrow & Kringlebach, 2015).

Research has demonstrated that DA does play a central role in the motivational aspects of engagement in reward behaviors (Treadway & Zald, 2011). Much of this is attributable to the integral role of DA in the development of behaviors, habits and preferences through motivation, learning and reward anticipation (Wise, 2008). Motivational anhedonia has been associated with the mesolimbic systems of the brain, notably those involving DA transmission, as well as structures of the cortex (Thomsen, Whybrow & Kringlebach, 2015).

The research presented above is a small window into the neurbiological processes involved in the experience of anhedonic symptoms. This research demonstrates the need for a more nuanced approach to conceptualizing the various components of anhedonia, reward behavior and their neurobiological substrates. There have been several recently proposed frameworks that offer a more dynamic understanding of anhedonia. Treadway and Zald (2011) differentiate between three different elements of anhedonia: motivational, consummatory (pleasure experienced) and decisional anhedonia. Berridge and Kringlebach (2008) suggest the importance of neural networks involved in “wanting” (motivation), “liking” (pleasure) and “learning.” These processes correspond to the cycle through which we engage in rewarding behaviors, experience pleasure from them and learn to sustain them. These components of anhedonia and reward are dynamic and integrated. More precise definition of the aspects of reward behavior will allow researchers to more effectively study the treatment-refractory symptoms of anhedonia.

Anhedonia is a unit of analysis in both the “negative valence” and “social processes” domains of the Research Domain Criteria Initiative (RDoC) (RDoC Constructs). The RDoC is an in initiative spearheaded by the National Institute of Mental Health (NIMH) that sets forth a framework for researching the symptoms involved in mental disorders. This research agenda brings together information from different lines of inquiry. These range from genomics and neural circuits to behavior and self-report. The purpose of the RDoC is to facilitate understanding of the multi-dimensional and interwoven processes that occur to produce all forms of human behavior. The recent developments in our understanding of the neurobiological correlates of anhedonia and reward behavior, combined with a more nuanced characterization of these processes, offers an opportunity to research interventions that target these functionally impairing, disruptive symptoms.

References

Berridge, K. C., & Kringelbach, M. L. (2008). Affective neuroscience of pleasure: Reward in humans and animals. Psychopharmacology, 199, 457-480. doi:10.1007/s00213-008-1099-6

Berridge, K. C., & Robinson, T. E. (2003). Parsing reward. Trends in Neurosciences, 26, 507-513. doi:http://dx.doi.org/10.1016/S0166-2236(03)00233-9

Berrios, G. E., & Olivares, J. M. (1995). The anhedonias: A conceptual history. History of Psychiatry, 6, 453-470. doi:10.1177/0957154X9500602403

Der-Avakian, A., & Markou, A. (2012). The neurobiology of anhedonia and other reward-related deficits. Trends in Neurosciences, 35, 68-77. doi:http://dx.doi.org/10.1016/j.tins.2011.11.005

Ho, N., & Sommers, M. (2013). Anhedonia: A concept analysis. Archives of Psychiatric Nursing, 27, 121-129. doi:10.1016/j.apnu.2013.02.001

Peciña, S., Smith, K. S., & Berridge, K. C. (2006). Hedonic hot spots in the brain. The Neuroscientist, 12, 500-511. doi:10.1177/1073858406293154

RDoC consutrcts. Retrieved February/8, 2016 from http://www.nimh.nih.gov/research-priorities/rdoc/rdoc-constructs.shtml

Salamone, J. D., Correa, M., Farrar, A., & Mingote, S. M. (2007). Effort-related functions of nucleus accumbens dopamine and associated forebrain circuits. Psychopharmacology, 191, 461-482. doi:10.1007/s00213-006-0668-9

Spijker, J., Bijl, R. V., De Graaf, R., & Nolen, W. A. (2001). Determinants of poor 1-year outcome of DSM-III-R major depression in the general population: Results of the netherlands mental health survey and incidence study (NEMESIS). Acta Psychiatrica Scandinavica, 103, 122-130. doi:10.1034/j.1600-0447.2001.103002122.x

Thomsen, K., Whybrow, P. C., & Kringelbach, M. L. (2015). Reconceptualizing anhedonia: Novel perspectives on balancing the pleasure networks in the human brain. Frontiers in Behavioral Neuroscience, 9, 49. doi:10.3389/fnbeh.2015.00049

Treadway, M. T., & Zald, D. H. (2010). Reconsidering anhedonia in depression: Lessons from translational neuroscience. Neuroscience and Biobehavioral Reviews, 35, 537-555. doi:10.1016/j.neubiorev.2010.06.006

Wise, R. A. (2008). Dopamine and reward: The anhedonia hypothesis 30 years on. Neurotoxicity Research, 14, 169-183. doi:10.1007/BF03033808

2 thoughts on “Moving toward a more accurate characterization of Anhedonia

  1. yaas very tru that im a sufferer from particularly social, motivational, and musical anhedonia who is living the time of her life failing her exams due to lack of motivation, feelings of want, love, determination who is riding the path to failure and homelessness. gr8 [laughs sarcastically]

  2. GLYX 13; ALKS 5461; AV 101 – all novel antidepressants that interact with either opiate or NMDA receptors – specifically anhedonia – may be available in 2018 or 2019; ketamine clinics another unknown long term risk option but expensive; Transcranial Magnetic Stimulation may be helpful – an awful, soul and life destroying condition – research centers may offer most realistic options if any…have seen it destroy lives of good people – hope one day medication is available…Godspeed

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