Comments on: Usui N, Mihara T, Baba K, Matsuda K, Tottori T, Umeoka S, et al. Intracranial EEG findings in patients with lesional lateral temporal lobe epilepsy. Epilepsy Res 2008;78:82–91

We read with interest the paper of Unsui et al published in Epilepsy Research in 2008 (Usui et al., 2008).

They studied the respective role of mesial temporal lobe structures and lateral neocortical regions of the temporal lobe in seizure genesis, in 15 patients with temporal lobe epilepsy (TLE) associated with temporal lateral or basolateral neocortical lesions.

They found that in a great proportion of patients, both mesial and neocortical regions disclose epileptogenicity, leading to surgical resection of both mesial and lateral compartments of the temporal lobe.

This result is interesting and proves that the current and classical distinction between mesial temporal lobe seizure and lateral temporal seizure is an oversimplification (Commission, 1989). We regret however that the authors did not cite works from European schools, using stereoelectroencephalography (SEEG) intracerebral recordings, which have proven for a long time that the lesional site and the epileptogenic zone (EZ), region of seizure onset (Bancaud et al., 1965) are not always overlapping. In particular, probably given the effect of important secondary epileptogenesis processes and due to the dense interconnection between lateral and mesial regions of the anterior part of the temporal lobe, complex networks of the EZ have been described in this context. SEEG allows simultaneous recording of both mesial and lateral compartments of the temporal lobe, and in particular the temporal basal regions.

In this context, we have published a significant body of work using SEEG, with quantification of involved networks that have demonstrated that many TLE are characterized by EZ including both mesial and neocortical regions, with the introduction of new subtypes (termed mesial–lateral and latero-mesial seizures) (Bartolomei et al., 2001, Bartolomei et al., 1999, Maillard et al., 2004). These subtypes are characterized by large interactions between mesial and neocortical structures that lead to seizure generation. In a large series of patients investigated by SEEG (187 seizures, 55 patients) we found that patients with medial temporal lesions (100%) and approximately 50% of patients with neocortical lesions have complex EZ including both medial and neocortical regions (Maillard et al., 2004). The ictal semiology, SEEG characteristics and clinical features of these subtypes have been described in this paper. In addition, mesial–lateral networks seem to be more frequent in patients with normal MRI (Bartolomei et al., 2008). In our experience, simultaneous onset in mesial and lateral structures is more frequent that independent onset in either mesial or lateral regions.

In summary, the paper of Unsui et al. adds further evidence that the current classification of TLE seizures is not sufficient to describe the complexity of involved networks in TLE. New subtypes including mesial–lateral seizures should be added to the current classification.