1,552 research outputs found
Structural correlates of facial emotion recognition deficits in Parkinson's disease patients
The ability to recognize facial emotion expressions, especially negative ones, is described to be impaired in Parkinson's disease (PD) patients. Previous neuroimaging work evaluating the neural substrate of facial emotion recognition (FER) in healthy and pathological subjects has mostly focused on functional changes. This study was designed to evaluate gray matter (GM) and white matter (WM) correlates of FER in a large sample of PD. Thirty-nine PD patients and 23 healthy controls (HC) were tested with the Ekman 60 test for FER and with magnetic resonance imaging. Effects of associated depressive symptoms were taken into account. In accordance with previous studies, PD patients performed significantly worse in recognizing sadness, anger and disgust. In PD patients, voxel-based morphometry analysis revealed areas of positive correlation between individual emotion recognition and GM volume: in the right orbitofrontal cortex, amygdala and postcentral gyrus and sadness identification; in the right occipital fusiform gyrus, ventral striatum and subgenual cortex and anger identification, and in the anterior cingulate cortex (ACC) and disgust identification. WM analysis through diffusion tensor imaging revealed significant positive correlations between fractional anisotropy levels in the frontal portion of the right inferior fronto-occipital fasciculus and the performance in the identification of sadness. These findings shed light on the structural neural bases of the deficits presented by PD patients in this skill
Comparing and contrasting the cognitive effects of hippocampal and ventromedial prefrontal cortex damage: A review of human lesion studies.
The hippocampus and ventromedial prefrontal cortex (vmPFC) are closely connected brain regions whose functions are still debated. In order to offer a fresh perspective on understanding the contributions of these two brain regions to cognition, in this review we considered cognitive tasks that usually elicit deficits in hippocampal-damaged patients (e.g., autobiographical memory retrieval), and examined the performance of vmPFC-lesioned patients on these tasks. We then took cognitive tasks where performance is typically compromised following vmPFC damage (e.g., decision making), and looked at how these are affected by hippocampal lesions. Three salient motifs emerged. First, there are surprising gaps in our knowledge about how hippocampal and vmPFC patients perform on tasks typically associated with the other group. Second, while hippocampal or vmPFC damage seems to adversely affect performance on so-called hippocampal tasks, the performance of hippocampal and vmPFC patients clearly diverges on classic vmPFC tasks. Third, although performance appears analogous on hippocampal tasks, on closer inspection, there are significant disparities between hippocampal and vmPFC patients. Based on these findings, we suggest a tentative hierarchical model to explain the functions of the hippocampus and vmPFC. We propose that the vmPFC initiates the construction of mental scenes by coordinating the curation of relevant elements from neocortical areas, which are then funneled into the hippocampus to build a scene. The vmPFC then engages in iterative re-initiation via feedback loops with neocortex and hippocampus to facilitate the flow and integration of the multiple scenes that comprise the coherent unfolding of an extended mental event
The social brain: neural basis of social knowledge
Social cognition in humans is distinguished by psychological processes that allow us to make inferences about what is going on inside other people—their intentions, feelings, and thoughts. Some of these processes likely account for aspects of human social behavior that are unique, such as our culture and civilization. Most schemes divide social information processing into those processes that are relatively automatic and driven by the stimuli, versus those that are more deliberative and controlled, and sensitive to context and strategy. These distinctions are reflected in the neural structures that underlie social cognition, where there is a recent wealth of data primarily from functional neuroimaging. Here I provide a broad survey of the key abilities, processes, and ways in which to relate these to data from cognitive neuroscience
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TEAMwork: Testing Emotional Attunement and Mutuality During Parent-Adolescent fMRI.
The parent-child relationship and family context influence the development of emotion regulation (ER) brain circuitry and related skills in children and adolescents. Although both parents' and children's ER neurocircuitry simultaneously affect how they interact with one another, neuroimaging studies of parent-child relationships typically include only one member of the dyad in brain imaging procedures. The current study examined brain activation related to parenting and ER in parent-adolescent dyads during concurrent fMRI scanning with a novel task - the Testing Emotional Attunement and Mutuality (TEAM) task. The TEAM task includes feedback trials indicating the other dyad member made an error, resulting in a monetary loss for both participants. Results indicate that positive parenting practices as reported by the adolescent were positively correlated with parents' hemodynamic activation of the ventromedial prefrontal cortex, a region related to empathy, during these error trials. Additionally, during feedback conditions both parents and adolescents exhibited fMRI activation in ER-related regions, including the dorsolateral prefrontal cortex, anterior insula, fusiform gyrus, thalamus, caudate, precuneus, and superior parietal lobule. Adolescents had higher left amygdala activation than parents during the feedback condition. These findings demonstrate the utility of dyadic fMRI scanning for investigating relational processes, particularly in the parent-child relationship
Structural connections support emotional connections: uncinate fasciculus microstructure is related to the ability to decode facial emotion expressions
The Uncinate Fasciculus (UF) is an association fibre tract connecting regions in the frontal and anterior temporal lobes. UF disruption is seen in several disorders associated with impaired social behaviour, but its functional role is unclear. Here we set out to test the hypothesis that the UF is important for facial expression processing, an ability fundamental to adaptive social behaviour. In two separate experiments in healthy adults, we used high-angular resolution diffusion-weighted imaging (HARDI) and constrained spherical deconvolution (CSD) tractography to virtually dissect the UF, plus a control tract (the corticospinal tract (CST)), and quantify, via tissue fractional anisotropy (FAT), individual differences in tract microstructure. In Experiment 1, participants completed the Reading the Mind in the Eyes Task (RMET), a well-validated assay of facial expression decoding. In Experiment 2, a different set of participants completed the RMET, plus an odd-emotion-out task of facial emotion discrimination. In both experiments, participants also completed a control odd-identity-out facial identity discrimination task. In Experiment 1, FAT of the right-, but not the left-hemisphere, UF was significantly correlated with performance on the RMET task, specifically for emotional, but not neutral expressions. UF FAT was not significantly correlated with facial identity discrimination performance. In Experiment 2, FA of the right-, but not left-hemisphere, UF was again significantly correlated with performance on emotional items from the RMET, together with performance on the facial emotion discrimination task. Again, no significant association was found between UF FAT and facial identity discrimination performance. Our findings highlight the contribution of right-hemisphere UF microstructure to inter-individual variability in the ability to decode facial emotion expressions, and may explain why disruption of this pathway affects social behaviour
The empathic brain and its dysfunction in psychiatric populations: implications for intervention across different clinical conditions
Empathy is a concept central to psychiatry, psychotherapy and clinical psychology. The construct of empathy involves not only the affective experience of the other person's actual or inferred emotional state but also some minimal recognition and understanding of another's emotional state. It is proposed, in the light of multiple levels of analysis including social psychology, cognitive neuroscience and clinical neuropsychology, a model of empathy that involves both bottom-up and top-down information processing underpinned by parallel and distributed computational mechanisms. The predictive validity of this model is explored with reference to clinical conditions. As many psychiatric conditions are associated with deficits or even lack of empathy, we discuss a limited number of these disorders including psychopathy/antisocial personality disorders, borderline and narcissistic personality disorders, autistic spectrum disorders, and alexithymia. We argue that future clinical investigations of empathy disorders can only be informative if behavioral, dispositional and biological factors are combined
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Telomere length as a predictor of emotional processing in the brain
Shorter telomere length (TL) has been associated with the development of mood disorders as well as abnormalities in brain morphology. However, so far, no studies have considered the role TL may have on brain function during tasks relevant to mood disorders. In this study, we examine the relationship between TL and functional brain activation and connectivity, while participants (n = 112) perform a functional magnetic resonance imaging (fMRI) facial affect recognition task. Additionally, because variation in TL has a substantial genetic component we calculated polygenic risk scores for TL to test if they predict face-related functional brain activation. First, our results showed that TL was positively associated with increased activation in the amygdala and cuneus, as well as increased connectivity from posterior regions of the face network to the ventral prefrontal cortex. Second, polygenic risk scores for TL show a positive association with medial prefrontal cortex activation. The data support the view that TL and genetic loading for shorter telomeres, influence the function of brain regions known to be involved in emotional processing
Social cognition in epilepsy
There is a paucity of research which has investigated social cognition in epilepsy, this is surprising given the abundance of evidence that exists in relation to the difficulties that people with epilepsy (PWE) have in relation to social functioning (McCagh et al., 2009).
The study of social cognition in epilepsy will lead to a greater understanding of the social cognitive deficits of the epileptic condition. This may in turn lead to more effective psychological interventions to enable the smoother functioning of people with epilepsy in society.
The aim of this chapter is to provide a detailed critical review of research which has investigated socio-cognitive functioning in people with epilepsy to date. Throughout the
chapter, the impact of epilepsy related variables in relation to socio-cognitive processing will be considered.
The final part of the chapter will explore why people with epilepsy may have social cognitive deficits and will go on to summarise limitations in past research. The chapter will
conclude by providing the rationale and aims of the author’s current research in this area and suggestions for future work
A review of social disinhibition after traumatic brain injury
Acquired social disinhibition refers to a debilitating behavioural syndrome commonly reported after a severe traumatic brain injury (TBI) and is characterized by inappropriate social behaviour, often described as immaturity and insensitivity towards others. These behaviours can have enduring effects on the social capability of the individual and their relationships with others. However, research into socially disinhibited behaviour after TBI has been thwarted by a lack of consensus in the literature on definition and measurement. This review provides an overview of our current understanding of the definition, measurement, prevalence, associated outcomes, neuropathology, and underlying mechanisms of social disinhibition after TBI. In addition, suggestions are made for future research to further our understanding of this syndrome with the eventual aim of rehabilitating problematic behaviours. It is concluded that an improved understanding of what causes disinhibited behaviour after TBI will be necessary for the development of effective treatment strategies aimed at the rehabilitation of underlying impairments
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