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Objective: Cognitive deficit is common in patients with temporal lobe epilepsy (TLE). Here, we aimed to investigate the modular architecture of functional networks associated with distinct cognitive states in TLE patients together with the role of the thalamus in modular networks. Methods: Resting‐state functional magnetic resonance imaging scans were acquired from 53 TLE patients and 37 matched healthy controls. All patients received the Montreal Cognitive Assessment test and accordingly were divided into TLE patients with normal cognition (TLE‐CN, n = 35) and TLE patients with cognitive impairment (TLE‐CI, n = 18) groups. The modular properties of functional networks were calculated and compared including global modularity Q, modular segregation index, intramodular connections, and intermodular connections. Thalamic subdivisions corresponding to the modular networks were generated by applying a 'winner‐take‐all' strategy before analyzing the modular properties (participation coefficient and within‐module degree z‐score) of each thalamic subdivision to assess the contribution of the thalamus to modular functional networks. Relationships between network properties and cognitive performance were then further explored. Results: Both TLE‐CN and TLE‐CI patients showed lower global modularity, as well as lower modular segregation index values for the ventral attention network and the default mode network. However, different patterns of intramodular and intermodular connections existed for different cognitive states. In addition, both TLE‐CN and TLE‐CI patients exhibited anomalous modular properties of functional thalamic subdivisions, with TLE‐CI patients presenting a broader range of abnormalities. Cognitive performance in TLE‐CI patients was not related to the modular properties of functional network but rather to the modular properties of functional thalamic subdivisions. Conclusions: The thalamus plays a prominent role in modular networks and potentially represents a key neural mechanism underlying cognitive impairment in TLE. [ABSTRACT FROM AUTHOR]

This study aimed to explore effective connectivity (EC) of the core networks in cognition impairment associated with temporal lobe epilepsy (CI-TLE) by applying resting state and Granger causality analysis (REST-GCA). The specific brain regions that played a critical role in classification were assessed using multivariate pattern analysis (MVPA). Thirty-two patients with CI-TLE and 29 healthy controls who were matched based on age and gender underwent functional magnetic resonance imaging (fMRI). REST-GCA revealed that patients with CI-TLE displayed decreased GC values in the following brain areas: from the posterior cingulate cortex (PCC) to the left fusiform gyrus (lFFG) and the right parahippocampal gyrus (rPPG); from the right dorsal prefrontal cortex (rDPFC) to the left superior parietal lobule (lSPL); from the left amygdala (lAG) to the PCC. Inhibitory EC was observed from the rDPFC to the PCC compared to HCs. The GC values increased from the right dorsal prefrontal cingulate cortex (rdACC) to the PCC and from the right dorsal forebrain insula (rDAI) to the right middle temporal gyrus (rMTG) in the CI-TLE patients. MVPA showed that the classification yielded an accuracy of 81.91% (78.12%, specificity =85.71%). Our observations indicated that the abnormal EC between the frontal and parietal regions might be associated with the pathophysiological mechanism of CI-TLE. These results also indicated that EC might be play a role as a potential discriminative pattern to detect CI-TLE in patients. [ABSTRACT FROM AUTHOR]

Background and Purpose: To investigate the longitudinal alterations of cortical structural‐functional coupling (SF coupling) in patients with temporal lobe epilepsy (TLE) over a 2‐year follow‐up, thereby exploring the neuropathophysiological mechanisms of TLE. Methods: Twenty‐eight TLE patients and 42 age‐ and gender‐matched healthy controls (HCs) were recruited. We used resting‐state functional MRI and diffusion‐weighted imaging to estimate and compare SF coupling at the multiscale network level (whole‐brain, modular, and regional levels). Then, we analyzed the relationships between the spatial patterns of SF coupling, the principal functional connectivity (FC) gradient, and the functional participation coefficient (PC). Finally, we related regional SF coupling changes between baseline and follow‐up to the expression of regional TLE‐specific genes. Results: Compared with HCs, TLE patients showed higher baseline SF couplings within the whole‐brain, limbic, and default‐mode modules. SF couplings within visual and dorsal attention modules were increased at follow‐up compared to baseline. In all three groups, the spatial patterns of SF coupling aligned with the principal FC gradient and the functional PC. The longitudinal change in regional SF coupling in TLE patients was significantly positively correlated with the expression of the CUX2 gene. Conclusions: Aberrant SF coupling was revealed in TLE and related to macroscale cortical hierarchies, functional segregation, and TLE‐specific gene expression; these data help increase our understanding of the neuropathophysiological mechanisms underlying TLE. [ABSTRACT FROM AUTHOR]