Temporal lobe epilepsy surgery failures: a review

Abstract

Patients with temporal lobe epilepsy (TLE) are refractory to antiepileptic drugs in about 30% of cases. Surgical treatment has been shown to be beneficial for the selected patients but fails to provide a seizure-free outcome in 20-30% of TLE patients. Several reasons have been identified to explain these surgical failures. This paper will address the five most common causes of TLE surgery failure (a) insufficient resection of epileptogenic mesial temporal structures, (b) relapse on the contralateral mesial temporal lobe, (c) lateral temporal neocortical epilepsy, (d) coexistence of mesial temporal sclerosis and a neocortical lesion (dual pathology); and (e) extratemporal lobe epilepsy mimicking TLE or temporal plus epilepsy. Persistence of epileptogenic mesial structures in the posterior temporal region and failure to distinguish mesial and lateral temporal epilepsy are possible causes of seizure persistence after TLE surgery. In cases of dual pathology, failure to identify a subtle mesial temporal sclerosis or regions of cortical microdysgenesis is a likely explanation for some surgical failures. Extratemporal epilepsy syndromes masquerading as or coexistent with TLE result in incomplete resection of the epileptogenic zone and seizure relapse after surgery. In particular, the insula may be an important cause of surgical failure in patients with TLE.

Figure 1

Schematic representation of potential foci responsible for seizure persistence following temporal lobe epilepsy surgery: (a) the ipsilateral mesial temporal structures from incomplete resection (green); (b) the contralateral mesial temporal lobe (blue); (c) the lateral temporal neocortex following selective amygdalohippocampectomy (yellow); (d) the extratemporal lobe epilepsy masquerading as temporal lobe epilepsy such as an orbitofrontal (red), insular (orange), or occipital epileptogenic (purple) zone; (e) the dual pathology such as an unrecognized subtle end-of-sulcus cortical dysplasia in the occipital lobe (purple); (f) a large epileptogenic zone extending to extratemporal structures (temporal epilepsy plus) such as the insula (orange).

Figure 2

Case of insular epilepsy masquerading as TLE operated at our institution. (a) MRI showing right hippocampal sclerosis in a 52-year-old patient with medically refractory epilepsy since age 20. (b) Presurgical evaluation led to a selective amygdalohippocampectomy that failed to control seizures. (c) Temporal lobectomy was subsequently performed, but the patient still continued to have seizures. (d): Postlobectomy scalp EEG continued to show ipsilateral temporal epileptiform activity. (e) and (f) fMRI-EEG and MEEG, respectively, localized the epileptogenic zone to the ipsilateral right insular cortex. (g) Intracranial EEG identified an epileptogenic focus in the anterior insular cortex. (h) and (i) Implantation of the intracranial electrodes. (j) MRI following partial anteroinferior insulectomy. The patient has been seizure-free since the operation (followup: 6 months).