Anhedonia Severity Research Articles

0974 Daytime Insomnia Symptoms Negatively Predict Anhedonia in Patients with Comorbid Major Depressive Disorder and Insomnia Disorder

Insomnia is one of the most common, but difficult symptoms to treat in major depressive disorder (MDD), often persisting after depression has remitted and predicting poorer treatment response. Anhedonia, a core symptom of depression, also predicts poorer treatment outcomes. Co-occurring depression and insomnia present unique challenges for treatment. The present study aimed to clarify the relationship between anhedonia and insomnia in patients with comorbid MDD and insomnia disorder. Baseline data were collected as part of a multisite randomized controlled trial of CBT-I as an adjunct treatment to antidepressant medication in 150 adults with comorbid MDD and insomnia disorder. Structural equation modeling (SEM) was used to determine the relationship between insomnia symptoms and anhedonia. Objective sleep measures and subjective sleep and daytime symptoms of insomnia were tested as predictors of anhedonia. An Objective Sleep Disturbance latent variable was constructed using actigraphy and polysomnography Total Wake Time (TWT). A Subjective Sleep Disturbance latent variable was defined using sleep diary average TWT and PROMIS: Sleep Disturbance total score. A Daytime Symptoms latent variable was constructed using the Hamilton Rating Scale for Depression (HRSD) energy item and PROMIS: Sleep Related Impairment total score. The Anhedonia latent variable was defined using HRSD and Quick Inventory for Depressive Symptomatology anhedonia items. Fit statistics for the hypothesized SEM model were adequate (X2 = 17.95; df= 15; CFI= .897; TLI= .753; RMSEA= .037). Daytime Symptoms of insomnia negatively predicted anhedonia in adults with comorbid MDD and insomnia disorder (p< .001). Neither Objective nor Subjective Sleep Disturbance predicted anhedonia in this model. We observed a negative relationship between the severity of daytime insomnia symptoms and anhedonia, and no relationship between objective sleep indicators or subjective nighttime symptoms and anhedonia. Support (If Any):

S141. Electroconvulsive Therapy Leads to Plastic Changes in the Medial Forebrain Bundle Associated With Improvement in Anhedonia and Depression Severity

S141. Electroconvulsive Therapy Leads to Plastic Changes in the Medial Forebrain Bundle Associated With Improvement in Anhedonia and Depression Severity

Presentation and Neurobiology of Anhedonia in Mood Disorders: Commonalities and Distinctions.

To focus on the clinical and behavioral presentation of anhedonia in mood disorders, as well as the differences and commonalities in the underlying neurocircuitry. Evidence suggests that depression is characterized by hypofunction of the reward system, while bipolar disorder manifests dysregulation of the behavioral activation system that increases goal-directed reward behavior. Importantly, strong evidence does not exist to suggest significant differences in anhedonia severity between depressed unipolar and bipolar patients, suggesting that there are more nuanced fluctuations in reward processing deficits in bipolar patients depending on their state. Both euthymic unipolar and bipolar patients frequently report residual reward dysfunction, which highlights the potential of reward processing deficits that give rise to the clinical symptom of anhedonia to be trait factors of mood disorders; however, the possibility that therapies are not adequately treating anhedonia could also explain the presence of residual symptoms. Reward processing represents a potential diagnostic and treatment marker for mood disorders. Further research should systematically explore the facets of reward processing in at-risk, affected, and remitted patients.

A pilot study of cortical glutathione in youth with depression

AimThis study used proton magnetic resonance spectroscopy (1H MRS) to measure in vivo brain glutathione (GSH) in adolescents with major depressive disorder (MDD), and explored the relationship between GSH and illness severity and chronicity. Secondarily, associations between GSH and anhedonia, a key symptom of MDD in adolescents, were investigated. MethodsOccipital cortex GSH levels were obtained in 19 psychotropic medication-free adolescents with MDD (ages 12–21) and compared to those in eight healthy control adolescents. Correlations between GSH levels and anhedonia severity were examined both in the full participant sample and within the MDD group. Within the MDD group, correlations between GSH levels and illness severity and chronicity were assessed. ResultsOccipital GSH levels were lower in adolescents with MDD compared to controls, but did not correlate with anhedonia (either within the MDD group or the full sample), MDD severity, or onset. There were also no group differences in levels of total choline, creatine, and N-acetylaspartate – all neurometabolites that were simultaneously detected with 1H MRS. ConclusionsAlthough preliminary, findings add new data to support the role of oxidative stress in MDD and suggest that lower GSH may be a potential marker of MDD early on in the course of illness.

Striatal dopamine D2/3 receptor-mediated neurotransmission in major depression: Implications for anhedonia, anxiety and treatment response

Dopamine (DA) neurotransmission within the brain's reward circuit has been implicated in the pathophysiology of depression and in both, cognitive and pharmacological mechanisms of treatment response. Still, a direct relationship between measures of DA neurotransmission and reward-related deficits in patients with depression has not been demonstrated. To gain insight into the symptom-specific alterations in the DA system in patients with depression, we used positron emission tomography (PET) and the D2/3 receptor-selective radiotracer [11C]raclopride in twenty-three non-smoking un-medicated Major Depressive Disorder (MDD) patients and sixteen healthy controls (HC). We investigated the relationship between D2/3 receptor availability and baseline measures of depression severity, anxiety, anhedonia, and cognitive and pharmacological mechanisms of treatment response. We found that, compared to controls, patients with depression showed greater D2/3 receptor availability in several striatal regions, including the bilateral ventral pallidum/nucleus accumbens (vPAL/NAc), and the right ventral caudate and putamen. In the depressed sample, D2/3 receptor availability in the caudal portion of the ventral striatum (NAc/vPAL) correlated with higher anxiety symptoms, whereas D2/3 receptor availability in the rostral area of the ventral striatum correlated negatively with the severity of motivational anhedonia. Finally, MDD non-remitters showed greater baseline anxiety, greater D2/3 availability in the NAc/vPAL, and greater placebo-induced DA release in the bilateral NAc. Our results demonstrate abnormally high D2/3 receptor availability in the ventral striatum of patients with MDD, which seem to be associated with comorbid anxiety symptoms and lack of response to antidepressants.

Accelerated iTBS treatment in depressed patients differentially modulates reward system activity based on anhedonia

Objectives: Accelerated intermittent theta-burst stimulation (aiTBS) anti-depressive working mechanisms are still unclear. Because aiTBS may work through modulating the reward system and the level of anhedonia may influence this modulation, we investigated the effect of aiTBS on reward responsiveness in high and low anhedonic MDD patients.Methods: In this registered RCT (NCT01832805), 50 MDD patients were randomised to a sham-controlled cross-over aiTBS treatment protocol over the left dorsolateral prefrontal cortex (DLPFC). Patients performed a probabilistic learning task in fMRI before and after each week of stimulation.Results: Task performance analyses did not show any significant effects of aiTBS on reward responsiveness, nor differences between both groups of MDD patients. However, at baseline, low anhedonic patients displayed higher neural activity in the caudate and putamen. After the first week of aiTBS treatment, in low anhedonic patients we found a decreased neural activity within the reward system, in contrast to an increased activity observed in high anhedonic patients. No changes were observed in reward related neural regions after the first week of sham stimulation.Conclusions: Although both MDD groups showed no differences in task performance, our brain imaging findings suggest that left DLPFC aiTBS treatment modulates the reward system differently according to anhedonia severity.

Anterior cingulate cortex \u03b3-aminobutyric acid deficits in youth with depression

Abnormally low γ-aminobutyric acid (GABA) levels have been consistently reported in adults with major depressive disorder (MDD). Our group extended this finding to adolescents, and documented that GABA deficits were associated with anhedonia. Here we aimed to confirm our prior finding of decreased brain GABA in youth with depression and explore its associations with clinical variables. Forty-four psychotropic medication-free youth with MDD and 36 healthy control (HC) participants (12–21 years) were studied. Participants represent a combined sample of 39 newly recruited youth (MDD=24) and 41 youth from our previously reported study (MDD=20). GABA levels and the combined resonances of glutamate and glutamine (Glx) were measured in vivo in the anterior cingulate cortex using proton magnetic resonance spectroscopy. Youth with depression exhibited significantly lower GABA levels than HC in both the newly reported (P=0.003) and the combined (P=0.003) samples. When depressed participants were classified based on the presence of anhedonia, only the anhedonic MDD subgroup showed reduced GABA levels compared to HC (P=0.002). While there were no associations between any clinical measures and GABA or Glx levels in the new sample, GABA was negatively correlated with only anhedonia severity in the combined MDD group. Furthermore, in the combined sample, hierarchical regression models showed that anhedonia, but not depression severity, anxiety or suicidality, contributed significant variance in GABA levels. This report solidifies the evidence for a GABA deficit early in the course of MDD, which correlates specifically with anhedonia in the disorder.

Anhedonia correlates with abnormal functional connectivity of the superior temporal gyrus and the caudate nucleus in patients with first-episode drug-naive major depressive disorder

BackgroundRecent empirical findings have suggested that imbalanced neural networks may underlie the pathophysiology of major depressive disorder (MDD). However, the contribution of the superior temporal gyrus (STG) and the caudate nucleus to its pathophysiology remains unclear. MethodsFunctional magnetic resonance imaging (MRI) date were acquired from 40 patients with first-episode drug-naive MDD and 36 matched healthy controls during wakeful rest. We used whole-brain voxel-wise statistical maps to quantify within-group resting state functional connectivity (RSFC) and between-group differences of bilateral caudate and STG seeds. ResultsCompared with healthy controls, first-episode MDD patients were found to have reduced connectivity between the ventral caudate and several brain regions including the superior frontal gyrus (SFG), the superior parietal lobule (SPL) and the middle temporal gyrus (MTG), as well as increased connectivity with the cuneus. We also found increased connectivity between the left STG and the precuneus, the angular gyrus and the cuneus. Moreover, we found that increased anhedonia severity was correlated with the magnitude of ventral caudate functional connectivity with the cuneus and the MTG in MDD patients. LimitationsDue to our small sample size, we did not correct the statistical threshold in the correlation analyses between clinical variables and connectivity abnormalities. ConclusionsThe present study suggests that anhedonia is mainly associated with altered ventral caudate-cortical connectivity and highlights the importance of the ventral caudate in the neurobiology of MDD.

Neural mechanisms of reinforcement learning in unmedicated patients with major depressive disorder.

According to current concepts, major depressive disorder is strongly related to dysfunctional neural processing of motivational information, entailing impairments in reinforcement learning. While computational modelling can reveal the precise nature of neural learning signals, it has not been used to study learning-related neural dysfunctions in unmedicated patients with major depressive disorder so far. We thus aimed at comparing the neural coding of reward and punishment prediction errors, representing indicators of neural learning-related processes, between unmedicated patients with major depressive disorder and healthy participants. To this end, a group of unmedicated patients with major depressive disorder (n = 28) and a group of age- and sex-matched healthy control participants (n = 30) completed an instrumental learning task involving monetary gains and losses during functional magnetic resonance imaging. The two groups did not differ in their learning performance. Patients and control participants showed the same level of prediction error-related activity in the ventral striatum and the anterior insula. In contrast, neural coding of reward prediction errors in the medial orbitofrontal cortex was reduced in patients. Moreover, neural reward prediction error signals in the medial orbitofrontal cortex and ventral striatum showed negative correlations with anhedonia severity. Using a standard instrumental learning paradigm we found no evidence for an overall impairment of reinforcement learning in medication-free patients with major depressive disorder. Importantly, however, the attenuated neural coding of reward in the medial orbitofrontal cortex and the relation between anhedonia and reduced reward prediction error-signalling in the medial orbitofrontal cortex and ventral striatum likely reflect an impairment in experiencing pleasure from rewarding events as a key mechanism of anhedonia in major depressive disorder.

Depression severity and quality of life of qualified and unqualified patients with a mood disorder for a research study targeting anhedonia in a clinical sample.

To investigate the depression severity and quality of life of qualified and unqualified patients with a mood disorder for a research study based on anhedonia severity. Diagnosis of major depressive disorder (MDD) or bipolar disorder (BPD) was ascertained with the MINI International Neuropsychiatric Interview. The severity of depression was measured with the 16-item Quick Inventory of Depressive Symptomatology-Self-Report (QIDS-16-SR), and Item 5, "feeling sad (sadness)," QIDS-16-SR Item 13, "change in general interest," was used to measure the severity of anhedonia. The quality of life was measured with the Quality of Life, Enjoyment and Satisfaction Questionnaire (Q-LES-Q). Of 96 patients with MDD and 147 with bipolar I or II disorder, the severity rating on sadness and anhedonia was similar. The severities of anhedonia and sadness were highly correlated with R2 of ≥0.91. Without considering depressive severity, 55% of patients would be eligible for a study if≥mild anhedonia was used as a severity criterion, but only 26% of patients eligible for a study if≥moderate anhedonia was used without considering substance use and medical comorbidities. If patients with ≥ moderate overall depressive symptoms were considered, 88.1% of patients would be eligible if≥mild anhedonia was required for a study, and 45.2% of patients would be eligible for a study if≥moderate anhedonia was required. For those who were unqualified for the study based on≥moderate anhedonia, about 1/3 had≥moderate overall depressive symptoms and less than 40% of maximum possible scores of Q-LES-Q. If only patients in remission based on overall depressive symptom severity were considered for a study of anhedonia, no patient would be eligible for the study. Depressive mood and anhedonia are highly correlated. Screening patients with a mood disorder and an overall moderate depressive severity is a cost-effective approach for a study targeting anhedonia, especially for a study requiring≥moderate severity of anhedonia. However, 1/3 of the unqualified patients will have≥moderate overall depressive symptoms and poor quality of life.

Neuroanatomical Prediction of Anhedonia in Adolescents.

Anhedonia is a transdiagnostic risk factor implicated in mental illness onset, treatment non-response, and suicidal behaviors. Prior cross-sectional research in adults has shown that anhedonia is associated with reduced dorsal striatal volume, but it is unknown whether this relationship extends to adolescents and whether reduced striatal volume prospectively predicts anhedonia. To address these gaps, the current study investigated whether striatal volume predicted anhedonia severity in adolescents. At baseline, healthy female adolescents aged 12-14 years (n=50) completed a clinical assessment, and structural MRI data were acquired on a 3 Tesla MR scanner. While in the scanner, participants also completed a peer feedback task where subjective ratings following peer 'acceptance' or 'rejection' were obtained. At the three-month follow-up, participants provided self-report assessments of anhedonia, depression, and anxiety symptoms. Three main findings emerged. First, in cross-sectional analyses, right nucleus accumbens volume was inversely related to anhedonia severity. Second, reduced bilateral putamen volume prospectively predicted anhedonia severity while controlling for baseline anhedonia, depression, and anxiety symptoms. Third, a blunted subjective response to peer acceptance (ie, neutral response to positive feedback), but not a more negative subjective response to peer rejection, contributed to anhedonia severity, but only among youth with smaller putamen volume. Collectively, these results suggest that smaller volume in striatal regions critically implicated in reward processing is associated with current and future anhedonic symptoms among healthy female youth. These anatomical features may confer vulnerability to anhedonia and thus, may inform early identification of individuals at high risk for mental illness.

Common Dimensional Reward Deficits Across Mood and Psychotic Disorders: A Connectome-Wide Association Study.

Anhedonia is central to multiple psychiatric disorders and causes substantial disability. A dimensional conceptualization posits that anhedonia severity is related to a transdiagnostic continuum of reward deficits in specific neural networks. Previous functional connectivity studies related to anhedonia have focused on case-control comparisons in specific disorders, using region-specific seed-based analyses. Here, the authors explore the entire functional connectome in relation to reward responsivity across a population of adults with heterogeneous psychopathology. In a sample of 225 adults from five diagnostic groups (major depressive disorder, N=32; bipolar disorder, N=50; schizophrenia, N=51; psychosis risk, N=39; and healthy control subjects, N=53), the authors conducted a connectome-wide analysis examining the relationship between a dimensional measure of reward responsivity (the reward sensitivity subscale of the Behavioral Activation Scale) and resting-state functional connectivity using multivariate distance-based matrix regression. The authors identified foci of dysconnectivity associated with reward responsivity in the nucleus accumbens, the default mode network, and the cingulo-opercular network. Follow-up analyses revealed dysconnectivity among specific large-scale functional networks and their connectivity with the nucleus accumbens. Reward deficits were associated with decreased connectivity between the nucleus accumbens and the default mode network and increased connectivity between the nucleus accumbens and the cingulo-opercular network. In addition, impaired reward responsivity was associated with default mode network hyperconnectivity and diminished connectivity between the default mode network and the cingulo-opercular network. These results emphasize the centrality of the nucleus accumbens in the pathophysiology of reward deficits and suggest that dissociable patterns of connectivity among large-scale networks are critical to the neurobiology of reward dysfunction across clinical diagnostic categories.

Neural correlates of RDoC reward constructs in adolescents with diverse psychiatric symptoms: A Reward Flanker Task pilot study

BackgroundThere has been growing interest under the Research Domain Criteria initiative to investigate behavioral constructs and their underlying neural circuitry. Abnormalities in reward processes are salient across psychiatric conditions and may precede future psychopathology in youth. However, the neural circuitry underlying such deficits has not been well defined. Therefore, in this pilot, we studied youth with diverse psychiatric symptoms and examined the neural underpinnings of reward anticipation, attainment, and positive prediction error (PPE, unexpected reward gain). Clinically, we focused on anhedonia, known to reflect deficits in reward function. MethodsTwenty-two psychotropic medication-free youth, 16 with psychiatric symptoms, exhibiting a full range of anhedonia, were scanned during the Reward Flanker Task. Anhedonia severity was quantified using the Snaith-Hamilton Pleasure Scale. Functional magnetic resonance imaging analyses were false discovery rate corrected for multiple comparisons. ResultsAnticipation activated a broad network, including the medial frontal cortex and ventral striatum, while attainment activated memory and emotion-related regions such as the hippocampus and parahippocampal gyrus, but not the ventral striatum. PPE activated a right-dominant fronto-temporo-parietal network. Anhedonia was only correlated with activation of the right angular gyrus during anticipation and the left precuneus during PPE at an uncorrected threshold. LimitationsFindings are preliminary due to the small sample size. ConclusionsThis pilot characterized the neural circuitry underlying different aspects of reward processing in youth with diverse psychiatric symptoms. These results highlight the complexity of the neural circuitry underlying reward anticipation, attainment, and PPE. Furthermore, this study underscores the importance of RDoC research in youth.

Sustained anterior cingulate cortex activation during reward processing predicts response to psychotherapy in major depressive disorder

Background: The purpose of the present investigation was to evaluate whether pre-treatment neural activation in response to rewards is a predictor of clinical response to Behavioral Activation Therapy for Depression (BATD), an empirically validated psychotherapy that decreases depressive symptoms by increasing engagement with rewarding stimuli and reducing avoidance behaviors. Methods: Participants were 33 outpatients with major depressive disorder (MDD) and 20 matched controls. We examined group differences in activation, and the capacity to sustain activation, across task runs using functional magnetic resonance imaging (fMRI) and the monetary incentive delay (MID) task. Hierarchical linear modeling was used to investigate whether pre-treatment neural responses predicted change in depressive symptoms over the course of BATD treatment. Result: MDD and Control groups differed in sustained activation during reward outcomes in the right nucleus accumbens, such that the MDD group experienced a significant decrease in activation in this region from the first to second task run relative to controls. Pretreatment anhedonia severity and pretreatment task-related reaction times were predictive of response to treatment. Furthermore, sustained activation in the anterior cingulate cortex during reward outcomes predicted response to psychotherapy; patients with greater sustained activation in this region were more responsive to BATD treatment. Limitation: The current study only included a single treatment condition, thus it unknown whether these predictors of treatment response are specific to BATD or psychotherapy in general. Conclusion: Findings add to the growing body of literature suggesting that the capacity to sustain neural responses to rewards may be a critical endophenotype of MDD.

Objective and specific tracking of anhedonia via event-related potentials in individuals with cocaine use disorders

BackgroundHyposensitivity to non-drug reward, behaviorally manifested as anhedonia, is a hallmark of chronic substance use. Anhedonia is a transdiagnostic symptom underpinned by neurobiochemical disturbances in the reward circuit, yet an objective measure to assess anhedonia severity still eludes the field. We hypothesized that the Reward Positivity (RewP) component of the event-related potentials (ERPs) will specifically track anhedonia as the RewP is attributed to the same brain regions that are also implicated in anhedonia. MethodsForty-six individuals with cocaine use disorders (iCUD) performed a gambling task predicting whether they would win or lose money on each trial, while ERP data was acquired. RewP in response to predicted win trials was extracted from the ERPs using the principal component analysis. State anhedonia and depression severity were assessed using the Cocaine Selective Severity Assessment (CSSA). ResultsAlthough RewP amplitude correlated with both anhedonia and depression, only the RewP-anhedonia correlation survived a correction for depression severity. Further, a hierarchical multiple regression analysis revealed that anhedonia explained a significant amount of variance in the RewP amplitude, and this variance was significantly greater than that explained by demographics, severity and recency of drug use and even depression. ConclusionsThese results show that RewP amplitude in response to rewarded trials tracks state anhedonia severity in iCUD. We argue that this association is perhaps driven by the activity in the dopaminergic mesocorticolimbic reward pathway that may underlie anhedonia symptomology as well as modulate RewP amplitude.

Anhedonic brain while attending sexual and emotional pictures

Anhedonia is defined as the inability to gain pleasure from normally pleasurable experiences and reduced sexual desire. Rees et al. (2007) showed that limbic and paralimbic areas are responsible for sexual arousal and that anhedonia is associated with frontolimbic inhibition. In major depression, reduced ventral striatum and increased ventral prefrontal cortex areas was associated with anhedonia(Gorwood, 2009). Walter et al. (2009) indicated that there is a deviation in the neuronal activation pattern of the pregenual anterior cingulate cortex in anhedonic depression which is related to a glutamergic deficit. Glutamate was suggested to play a relevant role in reward system (Birgner et al., 2005). ACC is a key involved in affective state and glutamate mediates ACC activation to sexual attraction(Wu et al., 2009). Thus, a glutamatergic deficit might be related to reduced hedonic effect specific to major depression. Using an attention modulation of emotional and sexual pictures, we investigate the role of anhedonia on the ventral and dorsal systems in healthy volunteers and patients with major depression. They undergo an expectancy task in a 7 T scanner and passively view sexual and emotional photographs and are asked to expect either high salient pictures or high erotic pictures. Half of these pictures are announced by an expectancy cue, whereas the other half are preceded by a fixation cross. Snaith-Hamilton-Pleasure-Scale and Hamilton Depression Rating Scale are employed to assess anhedonia and depressive symptom severity. Brain metabolites in the dorsal and pgACC are measured using MRS. We will show how anhedonia modulates the neural response to sexual arousal.Disclosure of interestThe author has not supplied his/her declaration of competing interest.

Influence of art therapy in complex treatment on the quality of remission in patients with recurrent depressive disorder

IntroductionAccording to studies done in recent years regarding the treatment of patients with recurrent depressive disorder, a shift of interest from studies evaluating the effectiveness of therapy to the study of remission is seen. According to the literature, complete remission occurs in only 40–50% of patients, in other cases there is residual symptoms.AimsEvaluating the effectiveness of art therapy in treatment in patients with recurrent depressive disorder on the quality of remission.MethodsThe study involved 135 patients: 60 male and 75 female patients aged from 18 to 30 years old. The main group of patients apart the combined treatment also participated in group art therapy with the use of drawing techniques, while the control group – statutory standard therapy. We used clinical, psychopathological, psychodiagnostic and statistical methods.ResultsThe results of the effectiveness of art therapy in complex treatment in patients with recurrent depressive disorder is detected primarily in reducing of the level of anxiety at the early stages of treatment, as well as in reducing of the severity of anhedonia and improving the quality of life in remission period.ConclusionThese results support the use of art therapy in treatment in patients with recurrent depressive disorder during period of active treatment, and after achieving clinical remission contributes to achieving and maintaining high-quality and stable remission with full restoration of quality of life and social functioning.Disclosure of interestThe authors have not supplied their declaration of competing interest.

Distinct neurobiological signatures of brain connectivity in depression subtypes during natural viewing of emotionally salient films

Establishing an evidence-based diagnostic system informed by the biological (dys)function of the nervous system is a major priority in psychiatry. This objective, however, is often challenged by difficulties in identifying homogeneous clinical populations. Melancholia, a biological and endogenous subtype for major depressive disorder, presents a canonical test case in the search of biological nosology. We employed a unique combination of naturalistic functional magnetic resonance imaging (fMRI) paradigms - resting state and free viewing of emotionally salient films - to search for neurobiological signatures of depression subtypes. fMRI data were acquired from 57 participants; 17 patients with melancholia, 17 patients with (non-melancholic) major depression and 23 matched healthy controls. Patients with melancholia showed a prominent loss of functional connectivity in hub regions [including ventral medial prefrontal cortex, anterior cingulate cortex (ACC) and superior temporal gyrus] during natural viewing, and in the posterior cingulate cortex while at rest. Of note, the default mode network showed diminished reactivity to external stimuli in melancholia, which correlated with the severity of anhedonia. Intriguingly, the subgenual ACC, a potential target for treating depression with deep brain stimulation (DBS), showed divergent changes between the two depression subtypes, with increased connectivity in the non-melancholic and decreased connectivity in the melancholic subsets. These findings reveal neurobiological changes specific to depression subtypes during ecologically valid behavioural conditions, underscoring the critical need to respect differing neurobiological processes underpinning depressive subtypes.

Intranasal oxytocin enhances neural processing of monetary reward and loss in post-traumatic stress disorder and traumatized controls

BackgroundAnhedonia is a significant clinical problem in post-traumatic stress disorder (PTSD). PTSD patients show reduced motivational approach behavior, which may underlie anhedonic symptoms. Oxytocin administration is known to increase reward sensitivity and approach behavior. We therefore investigated whether oxytocin administration affected neural responses during motivational processing in PTSD patients and trauma-exposed controls. Methods35 police officers with PTSD (21 males) and 37 trauma-exposed police officers without PTSD (19 males) were included in a within-subjects, randomized, placebo-controlled fMRI study. Neural responses during anticipation of monetary reward and loss were investigated with a monetary incentive delay task (MID) after placebo and oxytocin (40 IU) administration. ResultsOxytocin increased neural responses during reward and loss anticipation in PTSD patients and controls in the striatum, dorsal anterior cingulate cortex and insula, key regions in the reward pathway. Although PTSD patients did not differ from controls in motivational processing under placebo, anhedonia severity in PTSD patients was negatively related to reward responsiveness in the ventral striatum. Furthermore, oxytocin effects on reward processing in the ventral striatum were positively associated with anhedonia. ConclusionsOxytocin administration increased reward pathway sensitivity during reward and loss anticipation in PTSD patients and trauma-exposed controls. Thus, oxytocin administration may increase motivation for goal-directed approach behavior in PTSD patients and controls, providing evidence for a neurobiological pathway through which oxytocin could potentially increase motivation and reward sensitivity in PTSD patients.

Адаптация методики диагностики социальной ангедонии (RSAS) на российской выборке

Anhedonia (or hypohedonia) reflects a missing or reduced ability to experience pleasure. Interest in the concept of clinical psychology and psychopathology is due to the high significance of violations of ability to experience pleasure as a predictor of serious mental disorders, such as schizophrenia, depression, chemical dependency. For under- standing the psychological deficits of patients with schizophrenia spectrum disorders is of particular importance to social anhedonia, reflecting the reduced ability to experience interest and pleasure from interactions with socially relevant stimuli and partners, and is implicated in disorders of social cognition, to social exclusion of patients. Revised Social Anhedonia Scale (RSAS) was designed to assess the severity of social anhedonia, tested in many countries, widely used in studies of schizophrenia. The problem of estimating the psychometric characteristics of the test RSAS, including the validity of the technique has become part of the project for the study of social cognition in mental disorders (grant funds of the Russian Science Foundation, Project № 14-18-03461). This article presents the results of the evaluation of the psychometric characteristics of RSAS and the applicability of the methodology for the Russian sample. The study was performed by a grant from the Russian Science Foundation (grant № 14- 18-03461) at the Federal Medical Research Centre of Psychiatry and Narcology under the Ministry of Public Health of the Russian Federation.