Abstracts

Rationale: Impairment of naming function is a critical problem for temporal lobe epilepsy (TLE) patients, yet the neural correlates of the disruption of temporal lobe language networks are poorly understood. Using functional magnetic resonance imaging (fMRI), we investigated the activation and task-related functional connectivity of left temporal lobe language networks and their relation to clinical naming performance and disease characteristics. Methods: We studied 59 adult patients with TLE (35 left TLE) and 32 healthy controls with auditory and visual naming fMRI tasks. Time series of activation maxima in the left posterior inferior temporal lobe were extracted to create a psychophysiological interaction (PPI) regressor for subsequent seed-based whole-brain task-related functional connectivity analyses. Correlational analyses were performed to assess the association of fMRI activation and functional connectivity with clinical naming scores, age of onset of epilepsy, and duration of epilepsy. Results: Auditory naming elicited activation in the left posterior temporal gyrus and visual naming in the left fusiform gyrus in all groups. Inferior temporal activations in left TLE and fusiform activations in right TLE and controls were positively correlated with clinical naming performance. Functional connectivity analyses indicated coupling of left posterior inferior temporal regions to ipsilateral superior temporal lobe regions and the inferior precentral gyrus as well as contralateral temporal and occipital regions. Connectivity strength derived from visual naming was correlated with clinical naming performance in all groups. Group comparisons showed impaired intrahemispheric, but increased interhemispheric, connectivity of left temporal language networks in left TLE patients compared to right TLE patients and controls. In left TLE patients only, stronger functional connectivity was correlated with later age of onset of epilepsy and shorter disease duration. Conclusions: This suggests that onset of seizures early in life and prolonged disease duration leads to disrupted recruitment of temporal lobe networks ipsilateral to the seizure focus, which might account for naming deficits in TLE. Funding: This study was supported by the National Institute for Health Research University College London Hospitals Biomedical Research Centre. We are grateful to the Wolfson Foundation and the Epilepsy Society for supporting the Epilepsy Society MRI scanner.