Summary
Objective
In temporal lobe epilepsy (TLE) the epileptogenic focus is focal and unilateral in the majority of patients. A key characteristic of focal TLE is the presence of sub-clinical epileptiform activity in both the ictal and contralateral "healthy" hemisphere. Such interictal activity is clinically important as it may reflect the spread of pathology, potentially leading to secondary epileptogenesis. The role played by white matter pathways in this process are unknown.
Methods
We compared three interhemispheric white matter tracts (anterior commissure, fornix, and tapetum) to determine the pathway most associated with the presence of contralateral interictal spikes. Forty patients with unilateral left or right TLE were categorized based on the presence or absence of contralateral interictal spikes. ANOVAs were run on diffusion properties from each tract (fractional anisotropy, FA; and mean diffusivity, MD).
Results
The analyses revealed that left TLE patients with bilateral interictal spikes had lower FA and higher MD in the tapetum. RTLE patients did not show this effect. No significant associations with bilateral activity was observed for the other tracts. BOLD functional connectivity data revealed that homotopic lateral, not mesial, temporal areas were reliably correlated in bilateral patients, independent of ictal side.
Significance
Our results indicate that, among the tracts investigated, only the tapetum was associated with contralateral epileptiform activity, implicating this structure in seizures and possible secondary epileptogenesis. We describe two mechanisms that might explain this association (the interruption of inhibitory signals or the toxic effect of carrying epileptiform signals toward the healthy hemisphere), but also acknowledge other rival factors that may be at work. We also report that TLE patients with bilateral spikes had increased lateral bi-temporal lobe connectivity. Our current results can be seen as bringing together important functional and structural data to elucidate the basis of contralateral interictal activity in focal, unilateral epilepsy.