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The Insula in Temporal Plus Epilepsy

Barba, Carmen*; Minotti, Lorella†,‡,§; Job, Anne-Sophie†,‡,§; Kahane, Philippe†,‡,§

Journal of Clinical Neurophysiology: July 2017 - Volume 34 - Issue 4 - p 324–327
doi: 10.1097/WNP.0000000000000389
Invited Review

Summary: Temporal lobe epilepsy (TLE) surgery is the most common type of surgical treatment offered to patients with drug-resistant focal seizures. However, the proportion of patients experiencing long-term freedom from seizures after TLE surgery remains suboptimal. Temporal plus epilepsy, which is characterized by a primary temporal epileptogenic zone extending to neighboring regions, has been demonstrated to be a major predictor of TLE surgery failures. In the context of the temporoperisylvian epilepsies, i.e., the most common type of temporal plus epilepsy, a possible role of the insula has often been hypothesized. As this area is buried deep within the lateral sulcus, the use of invasive recordings is often required. Identifying patients with temporal plus seizures is a relevant issue, as they appear to have a worse postsurgical seizure outcome compared with patients with “pure” temporal lobe seizures. Owing to these prognostic implications, it becomes important to identify, among patients suffering from “atypical” nonlesional TLEs, those who should undergo invasive investigations, in particular to explore the insula. In fact, only a primary involvement of the insula in the epileptogenic network may require to include this area in the resection to achieve seizure freedom. Using modern neurosurgical techniques, insular epilepsy surgery has proved to be safe and beneficial, making the “true” role of the insula in TLE surgery failures more relevant to understand. Further studies are needed to evaluate the efficacy of multilobar resections in patients with temporal plus epilepsy, in particular, when eloquent or difficult to access areas such as insula are suspected to be involved.

*Pediatric Neurology Unit, Neuroscience Department, Children's Hospital Meyer, Florence, Italy;

Neurology Department, CHU Grenoble Alpes, Grenoble, France;

University Grenoble Alpes, Grenoble Institute of Neuroscience, GIN, Grenoble, France; and

§Inserm, U1216, Grenoble, France.

Address correspondence and reprint requests to Carmen Barba, MD, PhD, Pediatric neurology Unit, Neuroscience Department, Children's Hospital Meyer, Viale Pieraccini 24, 50139 Florence, Italy; e-mail: carmen.barba@meyr.it.

The authors have no funding or conflicts of interest to disclose.

© 2017 by the American Clinical Neurophysiology Society