Contralateral insular epileptogenic hub causing seizure relapse after opercular focal cortical dysplasia surgery and response to radiofrequency thermocoagulation: illustrative case

Abstract

Background: The reevaluation and management of seizure relapse following resective surgery in magnetic resonance imaging (MRI)-negative pharmacoresistant epilepsy remains a significant challenge.

Observations: A 25-year-old right-handed male with medically refractory epilepsy presented with nonlocalizing electroencephalography (EEG) and MRI. Stereo-EEG (SEEG) implantation based on semiology and positron emission tomography imaging revealed a left frontal opercular focus with rapid bilateral insular ictal synchrony. The initial epileptogenic zone was resected and pathologically proven to be type 2A focal cortical dysplasia (FCD). Seizure relapse after 9 months was eventually reinvestigated, and repeat SEEG revealed a secondary epileptogenic focus in the contralateral insula. A novel technique of volumetric stereotactic radiofrequency ablation (vRFA) was utilized for the right insular focus, following which, the patient remains seizure-free for 20 months. He suffered a transient bilateral opercular syndrome following the second intervention that eventually resolved.

Lessons: The authors present clinical evidence to suggest epileptogenic nodes distant from the primary focus as a mechanism for seizure relapse following FCD surgery and the importance of bilateral insular SEEG coverage. The authors also describe a novel technique of minimally invasive vRFA that allows ablation of a larger volume of cerebral cortex when compared to conventional bedside SEEG electrode thermocoagulation.

Keywords: bilateral opercular syndrome; epilepsy surgery; focal cortical dysplasia; insuloopercular seizures; radiofrequency thermocoagulation; seizure relapse.

FIG. 1.

Low-voltage fast activity in the left frontal opercular electrode (red stars) with immediate synchronization of both ipsilateral and contralateral posterior insula (blue stars).

FIG. 2.

Dyslamination of neuronal arrangement in hematoxylin and eosin stain (original magnification ×100) (A), Neu-N stain (original magnification ×100) (B), and Neu-N stain (original magnification ×200) (C). D: Dysmorphic neurons (black arrows) in neurofilament stain (original magnification ×400).

FIG. 3.

Electrical onsets (colored arrows) in the right insular SEEG electrode contacts (white dots) in the second SEEG study.

FIG. 4.

A: Post-vRFA MRI (sagittal) on POD1 superimposed on postimplant CT image of electrode contacts (red and white dots) with postablation changes; whole length of multiple trajectories (blue-green arrows) fanning out from a common entry with ablated targets (exclusively along the green line). B: Schematic representation of the trajectories with targets of ablation (green dots).

FIG. 5.

A–D: MRI taken 8 months post-vRFA with ablated right insula (blue crossbars) and left insular resection cavity (blue arrows in C and D). D: Right opercular white matter fibers (diagrammatically represented in red) partially disconnected by the superior extension of ablation cavity (crossbars).