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In TLE patients, hippocampal volumetry provided maximum concordance with EEG.
In TLE patients, there was lower overall functional integrity of the DMN as well as an increase in posterior hub connections with other modules.
In TLE, thalamic involvement has typically been reported in terms of nonspecific global volume loss, or nonspecific DTI-determined diffusion abnormalities.
In TLE, mossy fibers sprout and establish recurrent synapses on DGCs that generate aberrant slow kainate receptor mediated excitatory postsynaptic potentials (EPSPKA) not observed in controls.
The performance of automatic segmentation in TLE has so far been considered unsatisfactory.
A significant association was detected between prior trauma and the ApoE ɛ4 allele in TLE patients.
The first perspective is that postnatal neurogenesis contributes to the predisposition for seizures in TLE.
Pilocarpine has been recently used also to model pharmacoresistance in TLE [4].
Especially, Laufs and colleagues suggested that the epileptic activity may spread from the temporal lobe into one or more functionally interconnected DMN regions [31] in TLE, and further indicated a correlation between IEDs in TLE and DMN fluctuations [31].
Despite its inhibitory effect in vitro, DSS-induced acute colitis was exacerbated in TLE fed NF-κBEGFP mice.
27 28 Thus, a positive family history of epilepsy occurs more frequently in TLE with postictal psychosis than in TLE alone.
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