The mismatch negativity (MMN) potential as a tool for the functional mapping of temporal lobe epilepsies

Abstract

Temporal lobe epilepsies are associated with cognitive dysfunctions in memory which are important clues currently used clinically for the lateralization of the epileptic focus in evaluations for epilepsy surgery. Because these lobes also contain the primary auditory cortex, the study of auditory evoked potentials (AEPs) is a candidate, not yet established, complementary method to characterize epilepsy-induced dysfunction. We aimed to establish the clinical usefulness of auditory evoked potentials for the study of pediatric symptomatic temporal lobe epilepsies. A group of 17 patients (ages 4–16) with symptomatic epilepsies undergoing evaluation for epilepsy surgery epilepsy was submitted to auditory evoked potentials using 35-channel scalp EEG recordings. A control group of 10 healthy volunteers was studied with the same protocol. The P100 and mismatch negativity (MMN) potential latencies and normalized amplitudes were studied. We also performed a voxel-based lesion-symptom mapping (VLSM) to determine the anatomical areas associated with changes in the AEPs. Eleven patients had temporal lobe epilepsy, three had frontal lobe epilepsy, and three had occipital lobe epilepsy. Latencies for the P100 were normal in 15/17 and in 11/17 for the MMN, with no consistent correlation with the epilepsy type. The MMN amplitude was abnormal in 7/17 patients, all with temporal lobe epilepsies (sensitivity of 64%). Of these patients, four had a decreased MMN associated with a Heschl's gyrus lesion in the VLSM, and three had an increased MMN associated with hippocampal lesion. No extratemporal epilepsy showed MMN amplitude abnormalities (specificity of 100%). The P100 amplitude was abnormal in 3/17, two with temporal and one with frontal lobe epilepsies. The auditory MMN has a high specificity but a low sensitivity for temporal lobe epilepsy in symptomatic pediatric epilepsies. Amplitude decreases of the MMN are associated with homolateral Heschl's gyrus lesions, and MMN increases with hippocampal lesions.