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Reward expectation and affective responses across psychiatric disorders - A dimensional approach
(2014)
A dimensional approach in psychiatry aims to identify core mechanisms of mental disorders across nosological boundaries.
We compared anticipation of reward between major psychiatric disorders, and investigated whether reward anticipation is impaired in several mental disorders and whether there is a common psychopathological correlate (negative mood) of such an impairment.
During reward anticipation, we observed significant group differences in ventral striatal (VS) activation: patients with schizophrenia, alcohol dependence, and major depression showed significantly less ventral striatal activation compared to healthy controls. Depressive symptoms correlated with dysfunction in reward anticipation regardless of diagnostic entity. There was no significant correlation between anxiety symptoms and VS functional activation.
Our findings demonstrate a neurobiological dysfunction related to reward prediction that transcended disorder categories and was related to measures of depressed mood. The findings underline the potential of a dimensional approach in psychiatry and strengthen the hypothesis that neurobiological research in psychiatric disorders can be targeted at core mechanisms that are likely to be implicated in a range of clinical entities.
Dimensional psychiatry
(2014)
A dimensional approach in psychiatry aims to identify core mechanisms of mental disorders across nosological boundaries.
We compared anticipation of reward between major psychiatric disorders, and investigated whether reward anticipation is impaired in several mental disorders and whether there is a common psychopathological correlate (negative mood) of such an impairment.
We used functional magnetic resonance imaging (fMRI) and a monetary incentive delay (MID) task to study the functional correlates of reward anticipation across major psychiatric disorders in 184 subjects, with the diagnoses of alcohol dependence (n = 26), schizophrenia (n = 44), major depressive disorder (MDD, n = 24), bipolar disorder (acute manic episode, n = 13), attention deficit/hyperactivity disorder (ADHD, n = 23), and healthy controls (n = 54). Subjects' individual Beck Depression Inventory-and State-Trait Anxiety Inventory-scores were correlated with clusters showing significant activation during reward anticipation.
During reward anticipation, we observed significant group differences in ventral striatal (VS) activation: patients with schizophrenia, alcohol dependence, and major depression showed significantly less ventral striatal activation compared to healthy controls. Depressive symptoms correlated with dysfunction in reward anticipation regardless of diagnostic entity. There was no significant correlation between anxiety symptoms and VS functional activation.
Our findings demonstrate a neurobiological dysfunction related to reward prediction that transcended disorder categories and was related to measures of depressed mood. The findings underline the potential of a dimensional approach in psychiatry and strengthen the hypothesis that neurobiological research in psychiatric disorders can be targeted at core mechanisms that are likely to be implicated in a range of clinical entities.
Background
The centrality of an event indicates the extent to which it becomes a core part of identity and life story. Event centrality (EC) has been shown to have a strong relationship with PTSD symptoms, which seems to be indirectly influenced by negative posttraumatic cognitions (PTC). However, research on this potential mediation and its causal links particularly with clinical samples is limited and essential to derive treatment implications.
Methods
Pre- and posttreatment data of 103 day-unit patients with PTSD was examined using mediation analyses and structural equation modeling.
Results
Negative PTC mediated the relationship between EC and PTSD symptoms, partially pre- and completely posttreatment. Within extended longitudinal analyses causal directions of the mediation pathways were not adequately interpretable due to unexpected suppression effects.
Conclusions
The results suggest that EC may only have an indirect effect on PTSD symptoms through negative PTC. Thus, decreasing negative PTC which are connected to centralized events might be a key element for PTSD treatment. Thereby, transforming the cognitions' valence to more positive and constructive forms could be crucial rather than mere decentralization. Although suppression effects limited causal inferences, they do not contradict the mediation and further indicate potential interactional terms and a transformation of EC.