Neural mapping of anhedonia across psychiatric diagnoses: A transdiagnostic neuroimaging analysis.
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ABSTRACT:
SUBMITTER: Schaub AC
PROVIDER: S-EPMC8455863 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:Anhedonia is a prominent symptom in neuropsychiatric disorders, most markedly in major depressive disorder (MDD) and schizophrenia (SZ). Emerging evidence indicates an overlap in the neural substrates of anhedonia between MDD and SZ, which supported a transdiagnostic approach. Therefore, we used activation likelihood estimation (ALE) meta-analysis of functional magnetic resonance imaging studies in MDD and SZ to examine the neural bases of three subdomains of anhedonia: consummatory anhedonia, anticipatory anhedonia and emotional processing. ALE analysis focused specifically on MDD or SZ was used later to dissociate specific anhedonia-related neurobiological impairments from potential disease general impairments. ALE results revealed that consummatory anhedonia was associated with decreased activation in ventral basal ganglia areas, while anticipatory anhedonia was associated with more substrates in frontal-striatal networks except the ventral striatum, which included the dorsal anterior cingulate, middle frontal gyrus and medial frontal gyrus. MDD and SZ patients showed similar neurobiological impairments in anticipatory and consummatory anhedonia, but differences in the emotional experience task, which may also involve affective/mood general processing. These results support that anhedonia is characterized by alterations in reward processing and relies on frontal-striatal brain circuitry. The transdiagnostic approach is a promising way to reveal the overall neurobiological framework that contributes to anhedonia and could help to improve targeted treatment strategies.
| S-EPMC4838562 | biostudies-literature
Project description:Early life stress (ELS) is consistently associated with increased risk for subsequent psychopathology. Individual differences in neural response to reward may confer vulnerability to stress-related psychopathology. Using data from the ongoing Duke Neurogenetics Study, the present study examined whether reward-related ventral striatum (VS) reactivity moderates the relationship between retrospectively reported ELS and anhedonic symptomatology. We further assessed whether individual differences in reward-related VS reactivity were associated with other depressive symptoms and problematic alcohol use via stress-related anhedonic symptoms and substance use-associated coping.Blood oxygen level-dependent functional magnetic resonance imaging (fMRI) was collected while participants (n = 906) completed a card-guessing task, which robustly elicits VS reactivity. ELS, anhedonic symptoms, other depressive symptoms, coping behavior, and alcohol use behavior were assessed with self-report questionnaires. Linear regressions were run to examine whether VS reactivity moderated the relationship between ELS and anhedonic symptoms. Structural equation models examined whether this moderation was indirectly associated with other depression symptoms and problematic alcohol use through its association with anhedonia.Analyses of data from 820 participants passing quality control procedures revealed that the VS × ELS interaction was associated with anhedonic symptoms (p = 0.011). Moreover, structural equation models indirectly linked this interaction to non-anhedonic depression symptoms and problematic alcohol use through anhedonic symptoms and substance-related coping.These findings suggest that reduced VS reactivity to reward is associated with increased risk for anhedonia in individuals exposed to ELS. Such stress-related anhedonia is further associated with other depressive symptoms and problematic alcohol use through substance-related coping.
| S-EPMC4700837 | biostudies-literature
Project description:In the last decades, neuroimaging studies have attempted to unveil the neurobiological markers underlying pediatric psychiatric disorders. Yet, the vast majority of neuroimaging studies still focus on a single nosological category, which limit our understanding of the shared/specific neural correlates between these disorders. Therefore, we aimed to investigate the transdiagnostic neural correlates through a novel and data-driven meta-analytical method. A data-driven meta-analysis was carried out which grouped similar experiments' topographic map together, irrespectively of nosological categories and task-characteristics. Then, activation likelihood estimation meta-analysis was performed on each group of experiments to extract spatially convergent brain regions. One hundred forty-seven experiments were retrieved (3124 cases compared to 3100 controls): 79 attention-deficit/hyperactivity disorder, 32 conduct/oppositional defiant disorder, 14 anxiety disorders, 22 major depressive disorders. Four significant groups of experiments were observed. Functional characterization suggested that these groups of aberrant brain regions may be implicated internally/externally directed processes, attentional control of affect, somato-motor and visual processes. Furthermore, despite that some differences in rates of studies involving major depressive disorders were noticed, nosological categories were evenly distributed between these four sets of regions. Our results may reflect transdiagnostic neural correlates of pediatric psychiatric disorders, but also underscore the importance of studying pediatric psychiatric disorders simultaneously rather than independently to examine differences between disorders.
| S-EPMC8941086 | biostudies-literature
Project description:BackgroundIt is well known that most suicide cases meet criteria for a psychiatric disorder. However, rates of specific disorders vary considerably between studies and little information is known about gender and geographic differences. This study provides overall rates of total and specific psychiatric disorders in suicide completers and presents evidence supporting gender and geographic differences in their relative proportion.MethodsWe carried out a review of studies in which psychological autopsy studies of suicide completers were performed. Studies were identified by means of MEDLINE database searches and by scanning the reference list of relevant publications. Twenty-three variables were defined, 16 of which evaluating psychiatric disorders. Mantel-Haenszel Weighted Odds Ratios were estimated for these 16 outcome variables.ResultsTwenty-seven studies comprising 3275 suicides were included, of which, 87.3% (SD 10.0%) had been diagnosed with a mental disorder prior to their death. There were major gender differences. Diagnoses of substance-related problems (OR = 3.58; 95% CI: 2.78-4.61), personality disorders (OR = 2.01; 95% CI: 1.38-2.95) and childhood disorders (OR = 4.95; 95% CI: 2.69-9.31) were more common among male suicides, whereas affective disorders (OR = 0.66; 95% CI: 0.53-0.83), including depressive disorders (OR = 0.53; 95% CI: 0.42-0.68) were less common among males. Geographical differences are also likely to be present in the relative proportion of psychiatric diagnoses among suicides.ConclusionsAlthough psychopathology clearly mediates suicide risk, gender and geographical differences seem to exist in the relative proportion of the specific psychiatric disorders found among suicide completers.
| S-EPMC534107 | biostudies-literature
Project description:IntroductionPrevious research has linked childhood cat scratches and bites to an increased risk for depression, and childhood cat ownership to increased risk of schizophrenia, bipolar disorder, and social anhedonia. Our group previously reported that childhood cat bites, but not ownership, related to increased schizotypy severity in an undergraduate sample.MethodsThe current study expands this research by inquiring about cat bites and ownership in a transdiagnostic adult sample (N = 162; 51% female; mean age = 38.15, SD = 10.65), composed of schizophrenia spectrum disorders (n = 30), bipolar disorders (n = 30), unipolar depression (n = 23), and nonpsychiatric participants (n = 79). Participants completed a diagnostic interview, scales of symptom severity, and a cat interaction history interview.ResultsAcross the entire sample, self-report of cat bites prior to age 13, but not after, related to greater current severity of overall schizotypy, self-reported and clinician-rated psychotic-like symptoms, and social anhedonia, when compared to individuals who reported no lifetime cat bites. Cat bites prior to age 13 did not relate to severity of depression, non-social anhedonia, or clinician-rated negative symptoms. Self-report of residing with a cat prior to age 13, or a first cat bite after age 12, did not relate to any symptom severity measure examined.ConclusionsOne theory for these findings is that an unknown infectious agent common in cat saliva interacted with brain development in childhood to increase the likelihood of these symptoms. A novel theory for the infectious agent Pasteurella multocidais discussed. Future research can examine candidate infectious agents to identify potential causal mechanisms for these relationships.
| S-EPMC7239751 | biostudies-literature
Project description:BackgroundDepression is characterised partly by blunted reactions to reward. However, tasks probing this deficiency have not distinguished insensitivity to reward from insensitivity to the prediction errors for reward that determine learning and are putatively reported by the phasic activity of dopamine neurons. We attempted to disentangle these factors with respect to anhedonia in the context of stress, Major Depressive Disorder (MDD), Bipolar Disorder (BPD) and a dopaminergic challenge.MethodsSix behavioural datasets involving 392 experimental sessions were subjected to a model-based, Bayesian meta-analysis. Participants across all six studies performed a probabilistic reward task that used an asymmetric reinforcement schedule to assess reward learning. Healthy controls were tested under baseline conditions, stress or after receiving the dopamine D2 agonist pramipexole. In addition, participants with current or past MDD or BPD were evaluated. Reinforcement learning models isolated the contributions of variation in reward sensitivity and learning rate.ResultsMDD and anhedonia reduced reward sensitivity more than they affected the learning rate, while a low dose of the dopamine D2 agonist pramipexole showed the opposite pattern. Stress led to a pattern consistent with a mixed effect on reward sensitivity and learning rate.ConclusionReward-related learning reflected at least two partially separable contributions. The first related to phasic prediction error signalling, and was preferentially modulated by a low dose of the dopamine agonist pramipexole. The second related directly to reward sensitivity, and was preferentially reduced in MDD and anhedonia. Stress altered both components. Collectively, these findings highlight the contribution of model-based reinforcement learning meta-analysis for dissecting anhedonic behavior.
| S-EPMC3701611 | biostudies-literature
Project description:BackgroundAnhedonia is apparent in different mental disorders and is suggested to be related to dysfunctions in the reward system and/or affect regulation. It may hence be a common underlying feature associated with symptom severity of mental disorders.MethodsWe constructed a cross-sectional graphical Least Absolute Shrinkage and Selection Operator (LASSO) network and a relative importance network to estimate the relationships between anhedonia severity and the severity of symptom clusters of major depressive disorder (MDD), anxiety sensitivity (AS), attention-deficit hyperactivity disorder (ADHD), and autism spectrum disorder (ASD) in a sample of Dutch adult psychiatric patients (N = 557).ResultsBoth these networks revealed anhedonia severity and depression symptom severity as central to the network. Results suggest that anhedonia severity may be predictive of the severity of symptom clusters of MDD, AS, ADHD, and ASD. MDD symptom severity may be predictive of AS and ADHD symptom severity.ConclusionsThe results suggest that anhedonia may serve as a common underlying transdiagnostic psychopathology feature, predictive of the severity of symptom clusters of depression, AS, ADHD, and ASD. Thus, anhedonia may be associated with the high comorbidity between these symptom clusters and disorders. If our results will be replicated in future studies, it is recommended for clinicians to be more vigilant about screening for anhedonia and/or depression severity in individuals diagnosed with an anxiety disorder, ADHD and/or ASD.
| S-EPMC10317820 | biostudies-literature
Project description:In psychiatry, neuroimaging facilitates the diagnosis of psychiatric disorders and the development of new medications. It is used to detect structural lesions causing psychosis and to differentiate depression from neurodegenerative disorders or brain tumors. Functional neuroimaging, mostly in the form of molecular neuroimaging with positron emission tomography or single photon emission tomography, facilitates the identification of therapeutic targets, the determination of the dose of a new drug needed to occupy its target in the brain, and the selection of patients for clinical trials.
| S-EPMC3052989 | biostudies-literature
Project description:Despite an increasing focus on transdiagnostic approaches to mental health, it remains unclear whether different diagnostic categories share a common neuronatomical basis. The current investigation sought to investigate whether a transdiagnostic set of structural alterations characterized schizophrenia, depression, post-traumatic stress disorder, and obsessive-compulsive disorder, and determine whether any such alterations reflected markers of psychiatric illness or pre-existing familial vulnerability. A total of 404 patients with a psychiatric diagnosis were recruited (psychosis, n = 129; unipolar depression, n = 92; post-traumatic stress disorder, n = 91; obsessive-compulsive disorder, n = 92) alongside n = 201 healthy controls and n = 20 unaffected first-degree relatives. We collected structural magnetic resonance imaging scans from each participant, and tested for transdiagnostic alterations using Voxel-based morphometry. Inferences were made at p < 0.05 after family-wise error correction for multiple comparisons. The four psychiatric groups relative to healthy controls were all characterized by significantly greater gray matter volume in the putamen (right: z-score: 5.97, p-value < 0.001; left: z-score: 4.97, p-value = 0.001); the volume of this region was positively correlated with severity of symptoms across groups (r = 0.313; p < 0.001). Putamen enlargement was also evident in unaffected relatives compared to healthy controls (right: z-score: 8.13, p-value < 0.001; left: z-score: 9.38, p-value < 0.001). Taken collectively, these findings indicate that increased putamen volume may reflect a transdiagnostic marker of familial vulnerability to psychopathology. This is consistent with emerging conceptualizations of psychiatric illness, in which each disorder is understood as a combination of diagnosis-specific features and a transdiagnostic factor reflecting general psychopathology.
| S-EPMC6461829 | biostudies-literature
Project description:ImportanceDelay discounting is a behavioral economic index of impulsive preferences for smaller-immediate or larger-delayed rewards that is argued to be a transdiagnostic process across health conditions. Studies suggest some psychiatric disorders are associated with differences in discounting compared with controls, but null findings have also been reported.ObjectiveTo conduct a meta-analysis of the published literature on delay discounting in people with psychiatric disorders.Data sourcesPubMed, MEDLINE, PsycInfo, Embase, and Web of Science databases were searched through December 10, 2018. The psychiatric keywords used were based on DSM-IV or DSM-5 diagnostic categories. Collected data were analyzed from December 10, 2018, through June 1, 2019.Study selectionFollowing a preregistered Preferred Reporting Items for Systematic Reviews and Meta-Analysis (PRISMA) protocol, 2 independent raters reviewed titles, abstracts, and full-text articles. English-language articles comparing monetary delay discounting between participants with psychiatric disorders and controls were included.Data extraction and synthesisHedges g effect sizes were computed and random-effects models were used for all analyses. Heterogeneity statistics, one-study-removed analyses, and publication bias indices were also examined.Main outcomes and measuresCategorical comparisons of delay discounting between a psychiatric group and a control group.ResultsThe sample included 57 effect sizes from 43 studies across 8 diagnostic categories. Significantly steeper discounting for individuals with a psychiatric disorder compared with controls was observed for major depressive disorder (Hedges g = 0.37; P = .002; k = 7), schizophrenia (Hedges g = 0.46; P = .004; k = 12), borderline personality disorder (Hedges g = 0.60; P < .001; k = 8), bipolar disorder (Hedges g = 0.68; P < .001; k = 4), bulimia nervosa (Hedges g = 0.41; P = .001; k = 4), and binge-eating disorder (Hedges g = 0.34; P = .001; k = 7). In contrast, anorexia nervosa exhibited statistically significantly shallower discounting (Hedges g = -0.30; P < .001; k = 10). Modest evidence of publication bias was indicated by a statistically significant Egger test for schizophrenia and at the aggregate level across studies.Conclusions and relevanceResults of this study appear to provide empirical support for delay discounting as a transdiagnostic process across most of the psychiatric disorders examined; the literature search also revealed limited studies in some disorders, notably posttraumatic stress disorder, which is a priority area for research.
| S-EPMC6714026 | biostudies-literature