"Connectionology" provides further evidence for nociferous epileptic cortex.

Commentary A recent prior issue of Epilepsy Currents included two commentaries on studies of network activation in temporal and frontal lobe epilepsies and the association of network changes with cognitive deficits (1, 2). Both reviews emphasize the lack of evidence for the cause of the identified network abnormalities. The recent paper by Coan et al. from the Neuroimaging Laboratory at the State University of Campinas, Brazil, contributes further support that unique patterns of network dysfunction are associated with specific types of epilepsy. Additionally, their findings indicate that frequency of seizures and duration of temporal lobe epilepsy are associated with abnormalities in neuronal networks beyond the mesial temporal structures, which could have significant implications for the treatment and prevention of temporal lobe epilepsy. If recurrent seizures damage components of extended brain networks, perhaps stopping or reducing seizure frequency or severity by pharmacological or surgical interventions could prevent progressive dysfunction. The study by Coan and colleagues found volume loss in specific regions of extratemporal gray matter (GM) in patients with temporal lobe epilepsy. They present one of the largest published series, including 122 subjects with TLE and unilateral hippocampal sclerosis (TLE-HS), 50 with TLE and normal hip-pocampi TLE-NL), and 82 normal controls. Using established techniques of voxel based morphometry and statistical para-metric mapping to analyze 3T MRI, they demonstrated that TLE-HS patients had severe volume loss of bilateral thalami and, bilateral pre-central and postcentral gyri, and ipsilateral temporal neocortex. Patients with TLE-NL had less severe GM volume loss but still had significantly smaller volumes in the bilateral thalami and pre-central and postcentral gyri, and the ipsilateral orbitofrontal cortex. It is noteworthy that patients with infrequent seizures and TLE-NL did not have significant GM loss in any regions. Patients with TLE-HS and frequent seizures had more severe volume loss than similar patients with infrequent seizures (e.g., see figure 1 from the article by Coan OBJECTIVE: Patients with temporal lobe epilepsy (TLE) with hippocampal sclerosis (HS) have diffuse subtle gray matter (GM) atrophy detectable by MRI quantification analyses. However, it is not clear whether the etiology and seizure frequency are associated with this atrophy. We aimed to evaluate the occurrence of GM atrophy and the influence of seizure frequency in patients with TLE and either normal MRI (TLE-NL) or MRI signs of HS (TLE-HS). METHODS: We evaluated a group of 172 consecutive patients with unilateral TLE-HS or TLE-NL as defined by hippocampal volumetry and …