Abnormal asymmetry in benign epilepsy with unilateral and bilateral centrotemporal spikes: A combined fMRI and DTI study

- The asymmetry of BECTS patients was assessed using fMRI and DTI.
- Altered functional asymmetries of SM1 were found in the BECTS patients.
- Altered functional asymmetries of temporal pole were found in the B_BECTS patients.
- The B_BECTS group showed reduced FA values of the CC connecting bilateral SM1.

Benign epilepsy with centrotemporal spikes (BECTS) is the most common idiopathic focal childhood epilepsy associated with either unilateral or bilateral epileptic discharge. Asymmetry as an important characteristic of the human brain is beneficial for brain functions. However, little is known about on asymmetry of BECTS patients with different epileptic spikes pattern. In the present study, we investigated functional and structural asymmetries in unilateral spikes BECTS (U_BECTS) patients and bilateral spikes BECTS (B_BECTS) patients using resting state functional magnetic resonance images and diffusion tensor imaging. Compared with the controls, we observed a decreased voxel-mirrored interhemispheric functional connectivity (FC) in primary sensorimotor cortex (SM1) in U_BECTS and B_BECTS groups, and reduced fractional anisotropy (FA) values of the corpus callosum (CC) connecting bilateral SM1 were also observed in B_BECTS group. Further region-based FC map analysis of SM1 demonstrated increased functional asymmetry with ipsilateral hemisphere, contralateral hemisphere and the whole brain in U_BECTS and increased functional asymmetry with the contralateral hemisphere and the whole brain in B_BECTS groups. The correlation between functional asymmetry of SM1 and intelligence quotient scores was found in the U_BECTS group. The altered asymmetries of the SM1 further indicated the important role of SM1 in the pathophysiology of the BECTS. Furthermore, the B_BECTS group also showed abnormal voxel-mirrored interhemispheric FC in the temporal pole, the lobule IX of the cerebellum, the caudate and the occipital cortex relative to the controls. Altogether, our findings provide additional insight into the neuronal mechanism of BECTS with different epileptic spikes pattern and cognitive impairments with BECTS patients.