Browsing by Author "Pisoni, Angela"

Anhedonia refers to the loss of motivation to engage in previously enjoyable activities. While anhedonia is most often characterized as a symptom of psychiatric disorders such as depression, schizophrenia, and post-traumatic stress disorder, it can also present on its own. In spite of this, it is typically overlooked as a primary focus of research studies due to limitations inherent to our current diagnostic system. Therefore, no targeted treatments for anhedonia exist despite the significant impairment it causes. Moreover, very few studies to date have explored underlying neuropsychological characteristics of anhedonia, which is essential to the development of effective treatments for this clinical target. Because anhedonia is a core clinical target spanning many disorders as well as existing as its own disorder, transdiagnostic treatment approaches are of critical scientific importance to improve population mental health.The present study addresses this gap in the literature by taking a graph theoretical approach to characterizing state-based (i.e., reward anticipation, rest) network dynamics in a transdiagnostic sample of adults with clinically significant anhedonia (n = 77). Analyses focused on three canonical brain networks: the Salience Network (SN), the Default Mode Network (DMN) and the Central Executive Network (CEN). Owing to the direct inputs from reward-related regions to the SN, hypotheses centered on anhedonia relating to deficits in connectivity within the SN, as well as between the SN and the other networks. Two models were tested. First, a multiple linear regression assessed to what extent connectivity within the SN, as well as between the SN and the other two networks (i.e., CEN, DMN) during reward anticipation related to anhedonic symptoms. To build on these findings and assess dynamic state changes as they relate to anhedonia, a second multiple linear regression explored whether the magnitude of topographical reorganization that took place within the SN as well as between the SN and the other two networks predicted anhedonic severity in this sample. Contrary to hypotheses, neither connectivity within the SN or between the SN and the CEN or DMN during reward anticipation, nor reorganization within the SN or between the SN and the CEN or DMN when transitioning from rest to reward anticipation were associated with anhedonia severity in this sample. Exploratory analyses looked beyond the SN and found a significant association between anhedonia severity and DMN reorganization from rest to reward anticipation. Specifically, greater anhedonia severity was associated with less reorganization in response to reward anticipation. This finding suggests that anhedonia may be associated with DMN hyposensitivity, such that individuals with more severe anhedonia may have a difficult time disengaging from their internal world in the context of potentially rewarding experiences. Very little is known about the internal experience of anhedonia, and future work should focus on examining what internal thought processes these individuals may be having difficulty disengaging from. Nonetheless, an impaired ability to attend to the external world when potential reinforcers are present can prevent individuals from coming into contact with rewarding experiences in their environments and be a key maintaining factor of anhedonia. Although preliminary, these findings challenges the centrality of the SN in anhedonia and suggests the importance of the DMN. Future studies should aim to replicate this finding and explore potential clinical implications. Specifically, treatments that foster the ability to flexibility redirect attention to the present moment, such as mindfulness-based cognitive therapies, or non-invasive neuromodulatory therapies that target the DMN, may be particularly promising interventions for anhedonia.