Browsing by Author "Ghane, Merage"

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    Alexithymia as a Transdiagnostic Precursor to Empathy Abnormalities: The Functional Role of the Insula
    Valdespino, Andrew; Antezana, Ligia; Ghane, Merage; Richey, John A. (Frontiers, 2017-12-21)
    Distorted empathic processing has been observed across multiple psychiatric disorders. Simulation theory provides a theoretical framework that proposes a mechanism through which empathy difficulties may arise. Specifically, introspection-centric simulation theory (IST) predicts that an inability to accurately interpret and describe internal affective states may lead to empathy difficulties. The purpose of this review is to synthesize and summarize an empirical literature suggesting that simulation theory provides insights into a cognitive and neurobiological mechanism (i.e., alexithymia and insula pathology) that negatively impacts empathic processing, in addition to how disruptions in these processes manifest across psychiatric disorders. Specifically, we review an emerging non-clinical literature suggesting that consistent with IST, alexithymia and associated insula pathology leads to empathy deficits. Subsequently, we highlight clinical research suggesting that a large number of disorders characterized by empathy pathology also feature alexithymia. Collectively, these findings motivate the importance for future work to establish the role of alexithymia in contributing to empathy deficits across clinical symptoms and disorders. The current review suggests that simulation theory provides a tractable conceptual platform for identifying a potential common cognitive and neural marker that is associated with empathy deficits across a wide array of diagnostic classes.
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    Reward Circuitry and Motivational Deficits in Social Anxiety Disorder: What Can Be Learned From Mouse Models?
    Carlton, Corinne N.; Sullivan-Toole, Holly; Ghane, Merage; Richey, John A. (2020-02-26)
    Social anxiety disorder (SAD) is a common and serious psychiatric condition that typically emerges during adolescence and persists into adulthood if left untreated. Prevailing interventions focus on modulating threat and arousal systems but produce only modest rates of remission. This gap in efficacy suggests that most mainstream treatment concepts do not sufficiently target core processes involved in the onset and maintenance of SAD. This idea has further driven the development of new theoretical models that target dopamine (DA)-driven reward circuitry and motivational deficits that appear to be systematically altered in SAD. Most of the available data linking systemic alterations in DA neurobiology to SAD in humans, although abundant, remains at the level of correlational evidence. Accordingly, the purpose of this brief review is to critically evaluate the relevance of experimental work in rodent models that link details of DA function to symptoms of social anxiety. We conclude that, despite certain systematic limitations inherent in animal models, these approaches provide useful insights into human biomarkers of social anxiety including that (1) adolescence may serve as a critical period for the convergence of neurobiological and environmental factors that modify future expectations about social reward through experience dependent changes in DA-ergic circuitry, (2) females may show unique susceptibility to social anxiety symptoms when encountering relational instability that influences DA-related neural processes, and (3) separate from fear and arousal systems, the functional neurobiology of central DA systems contribute uniquely to susceptibility and maintenance of anhedonic factors relevant to human models of SAD.
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    Spatiotemporal dissociation of brain activity underlying threat and reward in social anxiety disorder
    Richey, John A.; Ghane, Merage; Valdespino, Andrew; Coffman, Marika C.; Strege, Marlene V.; White, Susan G.; Ollendick, Thomas H. (Oxford University Press, 2016-10-19)
    Social anxiety disorder (SAD) involves abnormalities in social motivation, which may be independent of well-documented differences in fear and arousal systems. Yet, the neurobiology underlying motivational difficulties in SAD is not well understood. The aim of the current study was to spatiotemporally dissociate reward circuitry dysfunction from alterations in fear and arousal-related neural activity during anticipation and notification of social and non-social reward and punishment. During fMRI acquisition, non-depressed adults with social anxiety disorder (SAD; N¼21) and age-, sex- and IQ-matched control subjects (N¼22) completed eight runs of an incentive delay task, alternating between social and monetary outcomes and interleaved in alternating order between gain and loss outcomes. Adults with SAD demonstrated significantly reduced neural activity in ventral striatum during the anticipation of positive but not negative social outcomes. No differences between the SAD and control groups were observed during anticipation of monetary gain or loss outcomes or during anticipation of negative social images. However, consistent with previous work, the SAD group demonstrated amygdala hyper-activity upon notification of negative social outcomes. Degraded anticipatory processing in bilateral ventral striatum in SAD was constrained exclusively to anticipation of positive social information and dissociable from the effects of negative social outcomes previously observed in the amygdala. Alterations in anticipation-related neural signals may represent a promising target for treatment that is not addressed by available evidence-based interventions, which focus primarily on fear extinction and habituation processes.
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    Validation of a novel method of ultraviolet-induced cutaneous inflammation and its associations with anhedonia
    Sullivan-Toole, Holly; Feng, Shengchuang; Carlton, Corinne N.; Ghane, Merage; Olino, Thomas M.; Allen, Irving C.; Richey, John A. (Nature Portfolio, 2022-11)
    Affective immunology of the skin is a growing area; however, established protocols for measuring individual differences in cutaneous inflammation are lacking. To address this, we present a preliminary validation of Precision Implementation of Minimal Erythema Dose (PI-MED) testing as a method for measuring cutaneous inflammation. PI-MED is a recently adapted protocol, optimized for reproducibility and individual differences research, that uses ultraviolet (UV) light to evoke cutaneous erythema, or inflammatory skin reddening. PI-MED's novel UV dosage schedule produces standardized erythema responses across different skin pigmentation types and shows strong internal consistency within person and good test-retest reliability across 8-10 weeks. In line with predictions, increased PI-MED erythema was associated with heightened anhedonia, across several measures, beyond influences of non-affective covariates. While future work should further refine the dosage schedule for the lightest and darkest skin types, overall, evidence supports PI-MED as a protocol for inducing and measuring individual differences in cutaneous inflammation. Further, PI-MED-induced erythema can expand psychoneuroimmunology research by offering a complementary assessment for general inflammatory tone. This work adds to a growing body of evidence demonstrating a distinct relationship between inflammation and anhedonia.