Dewen Hu
Numerous studies indicate that neuropsychiatric disorders including epilepsy are associated with brain dysfunction at a large-scale network level. However, most of the previous mesial temporal lobe epilepsy (mTLE) studies have focused on the epileptogenic zone, and those analyses paying attention to regions outside the hippocampus mainly focused on structural brain imaging. So far, whole-brain functional connectivity of right mTLE (R-mTLE) with hippocampal sclerosis remains uncharacterized. We hypothesized that R-mTLE is a functional disease involving disturbances of functional connectivity within the entire brain, rather than a local disease that is confined to the temporal lobe. To test this hypothesis, we explored whole-brain functional connectivity MRI to highlight the potential neuronal mechanism underlying cognitive impairments observed in this disease.
In recent years, my lab has concentrated on pattern analysis of brain connectome, as data-driven multivariate pattern analysis approaches can find potential neuroimaging-based biomarkers to differentiate patients from healthy controls at an individual subject level and potentially detect exciting spatially distributed information to further highlight the neuronal mechanisms of the disease, thereby complementing traditional univariate statistical analysis.1 Thus, we used the multivariate pattern analysis method in this study.
The major finding of our study was that functional connectivity changes exhibited hemispheric lateralization in the patients with R-mTLE. The patients showed decreased functional connectivity within the epileptogenic hemisphere relative to healthy controls, which may be related to seizure-induced damage. In addition, increased functional connectivity was observed within the left hemisphere in the patients and implied enhanced functioning, perhaps due to compensatory mechanisms. The results also indicated that most of the brain regions related to the altered connectivity were outside the hippocampus, thereby suggesting that the pathophysiology of R-mTLE may be more widely distributed than previously recognized.