BACKGROUND: The aim of our study was to assess hedonic capacity in euthymic bipolar subjects, identifying possible differences compared to remitted unipolar depressed patients and healthy controls. METHODS: 107 subjects with bipolar disorders, 86 with major depressive disorder and 106 healthy controls, homogeneous with respect to demographic characteristics, were enrolled. The following scales were administered: the Snaith-Hamilton pleasure scale (SHAPS), the subscale for 'anhedonia/asociality' of the scale for the assessment of negative symptoms (SANS) and the visual analogue scale (VAS) for hedonic capacity. RESULTS: Scores on SHAPS total, interests and social interactions, SANS 'anhedonia/asociality' and VAS were all significantly higher in affective disorder patients compared to healthy controls. No difference was found between clinical groups. 20.5% (n=22) of bipolar disorder subjects and 24.5% (n=21) of major depressed subjects showed a significant reduction in hedonic capacity (SHAPS total score ≥3), compared to 7.5% (n=8) of healthy controls (χ(2)=12.03; p=.002). LIMITATIONS: Limitations include heterogeneity with respect to pharmacological status and longitudinal course (i.e., 'single' vs. 'recurrent' affective episodes). CONCLUSIONS: The major finding of our study is that euthymic bipolar patients and remitted major depressed patients display residual anhedonic symptoms. This suggests that, in affective disorder patients, altered hedonic capacity could represent an enduring trait and that, possibly, dysfunctions in the neurobiological mechanisms underlying hedonic response and reward processing persist, irrespective of mood state.
"Researchers commonly use three categories of measures to assess anhedonia [i.e., self-report questionnaires , computerized tasks probing distinct components of reward processing, and imaging studies targeting brain activity in specific regions, predominantly the ventral striatum (VS)/nucleus accumbens (NAc)]. An abundance of psychiatric investigations, primarily in patients with schizophrenia, depression, substance dependence, and Parkinson's disease, but also in patients with bipolar disorder and PTSD, reports elevated scores on anhedonia scales (Leventhal et al., 2006; Franken et al., 2007; Assogna et al., 2011; Hatzigiakoumis et al., 2011; Di Nicola et al., 2012; Frewen et al., 2012). Although anhedonia is found in the majority of patients with major depressive disorder, it may be a distinct entity from depression as demonstrated by a plethora of studies reporting weak to moderate correlations between the two constructs (Leventhal et al., 2006; Franken et al., 2007; Nakonezny et al., 2010) among non-psychiatric controls as well as in depression and other disorders. "
[Show abstract][Hide abstract] ABSTRACT: Obsessive-compulsive disorder (OCD) has been linked to reward dysfunctions, highlighting a possible role of anhedonia in OCD. Surprisingly, anhedonia in OCD has never been evaluated. Moreover, although nicotine typically has anti-anhedonic effects, anecdotal reports suggest low prevalence rates of smoking in OCD. To address these two phenomena, 113 individuals with OCD completed a battery of questionnaires assessing symptom severity, anhedonia, and smoking. 28.3% of the sample met criteria for clinically significant anhedonia, which correlated with Y-BOCS scores (r=0.44), even when controlling for depressive symptoms. 13.3% of the sample endorsed current smoking, a lower rate than seen in psychiatric disorders (40–90%) and the general adult population (19%). Results highlight high rates of anhedonia and yet reduced prevalence of smoking in OCD. In contrast to the known positive association between anhedonia and smoking, a negative association emerged. Future research is needed to address the unique interface between anhedonia and reward responsiveness in OCD. Potential clinical implications are discussed.
Psychiatry Research 05/2014; DOI:10.1016/j.psychres.2014.02.002 · 2.47 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: Major depressive disorder has been associated with blunted responsiveness to rewards, but inconsistencies exist whether such abnormalities persist after complete remission. To address this issue, across two independent studies, 47 adults with remitted major depressive disorder (rMDD) and 37 healthy controls completed a Probabilistic Reward Task, which used a differential reinforcement schedule of social or monetary feedback to examine reward responsiveness (i.e., ability to modulate behavior as a function of reinforcement history). Relative to controls, adults with rMDD showed blunted reward responsiveness. Importantly, a history of depression predicted reduced reward learning above and beyond residual depressive (including anhedonic) symptoms and perceived stress. Findings indicate that blunted reward responsiveness endures even when adults are in remission and might be a trait-related abnormality in MDD. More research is warranted to investigate if blunted reward responsiveness may predict future depressive episodes and whether targeting reward-related deficits may prevent the re-occurrence of the disorder.
Journal of Psychiatric Research 09/2013; 47(12). DOI:10.1016/j.jpsychires.2013.08.011 · 3.96 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: Anhedonia is present in Parkinson's Disease (PD) as well as in addictive behaviors. Pathological Gambling (PG) and other Impulse Control Disorders (ICDs) have emerged as iatrogenic complications associated with dopamine replacement therapy. We studied 154 PD patients, divided into three groups: 11 with PG, 23 with other ICDs (compulsive buying, hypersexuality, binge eating), 120 without ICDs. All patients underwent a thorough clinical, neuropsychological and psychiatric evaluation. The PG-group, compared to the ICDs-group and PD-controls, reported a significantly higher incidence of anhedonia (45% vs. 9% vs. 14% respectively), higher Snaith-Hamilton Pleasure Scale (SHAPS) scores (2.0±1.3 vs. 1.0±1.1 vs. 1.0±1.2), higher levels of impulsivity traits as measured by the Barratt Impulsiveness Scale (70.0±10.6 vs. 64.8±11 vs. 60.9±9.3) and more severe frontal dysfunctions (Frontal Assessment Battery, FAB: 12.4±4.9 vs. 15.5±1.6 vs. 14.4±3). A model for PG (incorporating anhedonia, impulsivity levels and frontal impairment) is discussed in the context of the pathophysiology of addictive behaviors. The impairment of hedonic capacity, possibly resulting from an underlying neuropsychological dysfunction, might facilitate loss of control over reward-related behavior, thus favoring the shift towards predominantly habit-based compulsive behaviors.
Psychiatry Research 12/2013; DOI:10.1016/j.psychres.2013.12.013 · 2.47 Impact Factor
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