Resting-state fMRI reveals potential neural correlates of impaired cognition in Huntington's disease

2016 ◽  
Vol 27 ◽  
pp. 41-46 ◽  
Author(s):  
Wanglin Liu ◽  
Jing Yang ◽  
Ke Chen ◽  
ChunYan Luo ◽  
JeanMarc Burgunder ◽  
...  
2014 ◽  
Vol 44 (15) ◽  
pp. 3341-3356 ◽  
Author(s):  
R. C. Wolf ◽  
F. Sambataro ◽  
N. Vasic ◽  
M. S. Depping ◽  
P. A. Thomann ◽  
...  

Background.Functional magnetic resonance imaging (fMRI) of multiple neural networks during the brain's ‘resting state’ could facilitate biomarker development in patients with Huntington's disease (HD) and may provide new insights into the relationship between neural dysfunction and clinical symptoms. To date, however, very few studies have examined the functional integrity of multiple resting state networks (RSNs) in manifest HD, and even less is known about whether concomitant brain atrophy affects neural activity in patients.Method.Using MRI, we investigated brain structure and RSN function in patients with early HD (n = 20) and healthy controls (n = 20). For resting-state fMRI data a group-independent component analysis identified spatiotemporally distinct patterns of motor and prefrontal RSNs of interest. We used voxel-based morphometry to assess regional brain atrophy, and ‘biological parametric mapping’ analyses to investigate the impact of atrophy on neural activity.Results.Compared with controls, patients showed connectivity changes within distinct neural systems including lateral prefrontal, supplementary motor, thalamic, cingulate, temporal and parietal regions. In patients, supplementary motor area and cingulate cortex connectivity indices were associated with measures of motor function, whereas lateral prefrontal connectivity was associated with cognition.Conclusions.This study provides evidence for aberrant connectivity of RSNs associated with motor function and cognition in early manifest HD when controlling for brain atrophy. This suggests clinically relevant changes of RSN activity in the presence of HD-associated cortical and subcortical structural abnormalities.


2014 ◽  
Vol 36 (1) ◽  
pp. 110-119 ◽  
Author(s):  
Omar F.F. Odish ◽  
Annette A. van den Berg-Huysmans ◽  
Simon J.A. van den Bogaard ◽  
Eve M. Dumas ◽  
Ellen P. Hart ◽  
...  

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.


2010 ◽  
Vol 81 (Suppl 1) ◽  
pp. A31.1-A31
Author(s):  
E Lepron ◽  
H Gros ◽  
F Calvas ◽  
G Viallard ◽  
J-F Démonet

2016 ◽  
Vol 28 (2) ◽  
pp. 199-209 ◽  
Author(s):  
Andrew S. Kayser ◽  
Zdeňa Op de Macks ◽  
Ronald E. Dahl ◽  
Michael J. Frank

The onset of adolescence is associated with an increase in the behavioral tendency to explore and seek novel experiences. However, this exploration has rarely been quantified, and its neural correlates during this period remain unclear. Previously, activity within specific regions of the rostrolateral PFC (rlPFC) in adults has been shown to correlate with the tendency for exploration. Here we investigate a recently developed task to assess individual differences in strategic exploration, defined as the degree to which the relative uncertainty of rewards directs responding toward less well-evaluated choices, in 62 girls aged 11–13 years from whom resting state fMRI data were obtained in a separate session. Behaviorally, this task divided our participants into groups of explorers (n = 41) and nonexplorers (n = 21). When seed ROIs within the rlPFC were used to interrogate resting state fMRI data, we identified a lateralized connection between the rlPFC and posterior putamen/insula whose strength differentiated explorers from nonexplorers. On the basis of Granger causality analyses, the preponderant direction of influence may proceed from posterior to anterior. Together, these data provide initial evidence concerning the neural basis of exploratory tendencies at the onset of adolescence.


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