Anhedonia is a relative lack of pleasure in response to formerly rewarding stimuli. It is an important diagnostic feature of major depressive disorder (MDD), and predicts antidepressant efficacy. Understanding its neurobiological basis may help to target new treatments and predict treatment outcomes. Using a novel paradigm, we aimed to explore the correlations between anhedonia severity and magnitude of neural responses to happy and sad stimuli in regions previously implicated in studies of human reward processing and depressive anhedonia.
Neural responses to happy and sad emotional stimuli (autobiographical prompts and mood congruent facial expressions) were measured using blood oxygen level dependent (BOLD) functional magnetic resonance imaging in twelve MDD individuals with varying degrees of anhedonia.
In response to happy stimuli, anhedonia, but not depression severity per se, was positively and negatively correlated with ventromedial prefrontal cortex (VMPFC) and amygdala/ventral striatal activity, respectively. State anxiety independently contributed to a VMPFC-subcortical dissociation of response to happy (but not sad) stimuli, which was similar, but different, to anhedonia.
These findings suggest that anhedonia and state anxiety are associated with dysfunction within neural systems underlying the response to, and assessment of, the rewarding potential of emotive stimuli in MDD, and highlight the importance of employing a symptom-dimension-based approach in the examination of the neurobiology of depression.
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"Such high rates of occurrence nationally and globally demonstrate the critical need for continuing research into the etiology and treatment of this disorder . Anhedonia, the reduced anticipation of pleasurable stimuli and blunted responsiveness to reward, is one of the core symptoms of major depressive disorder (MDD) in the DSM-5 (American Psychiatric Association, 2013) and has been shown to be a predictor of antidepressant efficacy (Keedwell et al., 2005). Anhedonia contributes to reward-processing deficits in depression (Treadway et al., 2009) and can be studied using paradigms that assess both anticipatory and consummatory processes. "
"This is in keeping with mood induction fMRI findings in patients with depression, who show an opposite direction of effects compared with healthy controls . For instance, in adults with MDD, severity of depressive symptoms correlated negatively with activation in the following areas following happy, but not sad mood induction: left putamen, bilateral caudate, left nucleus accumbens , and left amygdala (Keedwell et al. 2005b). Furthermore , decreased ventral striatum activity when processing positive words in depressed versus healthy adults correlated with symptoms of anhedonia (Epstein et al. 2006), consistent with abnormalities in the reward processing system in depression. "
[Show abstract][Hide abstract] ABSTRACT: Introduction: Little is known about the neural correlates of mood states and the specific physiological changes associated with their valence and duration, especially in young people. Arterial spin labeling (ASL) imaging is particularly well-suited to study sustained cerebral states in young people, due to its robustness to low-frequency drift, excellent interscan reliability, and noninvasiveness. Yet, it has so far been underutilized for understanding the neural mechanisms underlying mood states in youth.
Methods: In this exploratory study, 21 healthy adolescents aged 16 to 18 took part in a mood induction experiment. Neutral, sad, and happy mood states were induced using film clips and explicit instructions. An ASL scan was obtained following presentation of each film clip.
Results: Mood induction led to robust changes in self-reported mood ratings. Compared to neutral, sad mood was associated with increased regional cerebral blood flow (rCBF) in the left middle frontal gyrus and anterior prefrontal cortex, and decreased rCBF in the right middle frontal gyrus and the inferior parietal lobule. A decrease in self-reported mood from neutral to sad condition was associated with increased rCBF in the precuneus. Happy mood was associated with increased rCBF in medial frontal and cingulate gyri, the subgenual anterior cingulate cortex, and ventral striatum, and decreased rCBF in the inferior parietal lobule. The level of current self-reported depressive symptoms was negatively associated with rCBF change in the cerebellum and lingual gyrus following both sad and happy mood inductions.
Conclusions: Arterial spin labeling is sensitive to experimentally induced mood changes in healthy young people. The effects of happy mood on rCBF patterns were generally stronger than the effects of sad mood.
Brain and Behavior 06/2015; 5(6):e00339. DOI:10.1002/brb3.339 · 2.24 Impact Factor
"Further, findings show a negative association between anhedonia severity and activity in subcortical regions, particularly in ventral striatum, in response to positive/pleasant stimuli (Limousin et al., 1995; Dunn et al., 2002; Keedwell et al., 2005; Surguladze et al., 2005; Epstein et al., 2006; Wacker et al., 2009). Overall, studies "
[Show abstract][Hide abstract] ABSTRACT: Anhedonia, the lack of pleasure, has been shown to be a critical feature of a range of psychiatric disorders. Yet, it is currently measured primarily through subjective self-reports and as such has been difficult to submit to rigorous scientific analysis. New insights from affective neuroscience hold considerable promise in improving our understanding of anhedonia and for providing useful objective behavioral measures to complement traditional self-report measures, potentially leading to better diagnoses and novel treatments. Here, we review the state-of-the-art of hedonia research and specifically the established mechanisms of wanting, liking, and learning. Based on this framework we propose to conceptualize anhedonia as impairments in some or all of these processes, thereby departing from the longstanding view of anhedonia as solely reduced subjective experience of pleasure. We discuss how deficits in each of the reward components can lead to different expressions, or subtypes, of anhedonia affording novel ways of measurement. Specifically, we review evidence suggesting that patients suffering from depression and schizophrenia show impairments in wanting and learning, while some aspects of conscious liking seem surprisingly intact. Furthermore, the evidence suggests that anhedonia is heterogeneous across psychiatric disorders, depending on which parts of the pleasure networks are most affected. This in turn has implications for diagnosis and treatment of anhedonia.