G01 Neural correlates of empathy and context evaluation in Huntington's disease patients

2010 ◽  
Vol 81 (Suppl 1) ◽  
pp. A31.1-A31
Author(s):  
E Lepron ◽  
H Gros ◽  
F Calvas ◽  
G Viallard ◽  
J-F Démonet
Author(s):  
Beate Schumann‐Werner ◽  
Imis Dogan ◽  
Shahram Mirzazade ◽  
Bettina Mall ◽  
Rena Overbeck ◽  
...  

2021 ◽  
pp. 1-12
Author(s):  
Arnau Puig-Davi ◽  
Saul Martinez-Horta ◽  
Frederic Sampedro ◽  
Andrea Horta-Barba ◽  
Jesus Perez-Perez ◽  
...  

Background: Empathy is a multidimensional construct and a key component of social cognition. In Huntington’s disease (HD), little is known regarding the phenomenology and the neural correlates of cognitive and affective empathy, and regarding how empathic deficits interact with other behavioral and cognitive manifestations. Objective: To explore the cognitive and affective empathy disturbances and related behavioral and neural correlates in HD. Methods: Clinical and sociodemographic data were obtained from 36 healthy controls (HC) and 54 gene-mutation carriers (17 premanifest and 37 early-manifest HD). The Test of Cognitive and Affective Empathy (TECA) was used to characterize cognitive (CE) and affective empathy (AE), and to explore their associations with grey matter volume (GMV) and cortical thickness (Cth). Results: Compared to HC, premanifest participants performed significantly worse in perspective taking (CE) and empathic distress (AE). In symptomatic participants, scores were significantly lower in almost all the TECA subscales. Several empathy subscales were associated with the severity of apathy, irritability, and cognitive deficits. CE was associated with GMV in thalamic, temporal, and occipital regions, and with Cth in parietal and temporal areas. AE was associated with GMV in the basal ganglia, limbic, occipital, and medial orbitofrontal regions, and with Cth in parieto-occipital areas. Conclusion: Cognitive and affective empathy deficits are detectable early, are more severe in symptomatic participants, and involve the disruption of several fronto-temporal, parieto-occipital, basal ganglia, and limbic regions. These deficits are associated with disease severity and contribute to several behavioral symptoms, facilitating the presentation of maladaptive patterns of social interaction.


2017 ◽  
Vol 89 (1) ◽  
pp. 112-116 ◽  
Author(s):  
Sandra Baez ◽  
Mariana Pino ◽  
Mildred Berrío ◽  
Hernando Santamaría-García ◽  
Lucas Sedeño ◽  
...  

Schadenfreude—pleasure at others’ misfortunes—is a multidetermined social emotion which involves reward processing, mentalising and perspective-taking abilities. Patients with Huntington’s disease (HD) exhibit reductions of this experience, suggesting a role of striatal degeneration in such impairment. However, no study has directly assessed the relationship between regional brain atrophy in HD and reduced schadenfreude. Here, we assessed whether grey matter (GM) atrophy in patients with HD correlates with ratings of schadenfreude. First, we compared the performance of 20 patients with HD and 23 controls on an experimental task designed to trigger schadenfreude and envy (another social emotion acting as a control condition). Second, we compared GM volume between groups. Third, we examined brain regions where atrophy might be associated with specific impairments in the patients. While both groups showed similar ratings of envy, patients with HD reported lower schadenfreude. The latter pattern was related to atrophy in regions of the reward system (ventral striatum) and the mentalising network (precuneus and superior parietal lobule). Our results shed light on the intertwining of reward and socioemotional processes in schadenfreude, while offering novel evidence about their neural correlates.


2013 ◽  
Vol 9 (5) ◽  
pp. 671-680 ◽  
Author(s):  
Imis Dogan ◽  
Christian Saß ◽  
Shahram Mirzazade ◽  
Alexandra Kleiman ◽  
Cornelius J. Werner ◽  
...  

2016 ◽  
Vol 27 ◽  
pp. 41-46 ◽  
Author(s):  
Wanglin Liu ◽  
Jing Yang ◽  
Ke Chen ◽  
ChunYan Luo ◽  
JeanMarc Burgunder ◽  
...  

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