Radiofrequency thermocoagulation for the treatment of refractory focal status epilepticus

Abstract

This case study reports the first documented use of stereoelectroencephalography (SEEG)-guided radiofrequency thermocoagulation (RFTC) to treat refractory status epilepticus (RSE). A 33-year-old woman with drug-resistant epilepsy and recurrent RSE underwent SEEG to define her epileptogenic zone. A new RSE started shortly before and continued during the SEEG exploration, being unresponsive to multiple antiseizure medications, vagal nerve stimulation, and corticosteroid therapy. SEEG-signal quantification based on ictal biomarkers, that is, epileptogenicity index and connectivity epileptogenicity index, identified the epileptogenic zone network (EZN) within the mesial prefrontal, premotor, and parietal cortex, with major implication of the anterior-middle and posterior cingulate cortex. RFTC was performed on SEEG-identified targets within the EZN and resulted in rapid cessation of electroclinical seizure activity and full recovery from motor deficits. Seizure frequency remained reduced by over 90% at 4 months post-procedure. This case highlights the potential of RFTC as a possible therapeutic option for RSE by directly disrupting critical network nodes responsible for seizure generation and propagation. The findings also suggest a broader role of SEEG not only for diagnostic purposes but also for the therapeutic management of refractory seizures, including status epilepticus.

Keywords: SEEG; epileptogenicity markers; radiofrequency thermoablation; status epilepticus.

FIGURE 1

Ictal SEEG, MRI, and epileptogenicity quantification in a patient with refractory status epilepticus. (A) Tridimensional representation of the SEEG implantation on the patient's 3d brain mesh: 14 left hemispheric electrodes sampled the mesial and lateral prefrontal (CR′, OR′, PM′, CC′), orbitofrontal (OR′), mesial and lateral premotor (SA′, SC′, Im′), insulo‐opercular (Im′, OC′, OP′), primary motor (CP′, LP′), mesial, and lateral parietal (PI′, GC′, PA′) regions. Two right electrodes sampled the right mesial and lateral premotor regions (CC, SA, not shown). Quantified ictal epileptogenicity markers (the maximal normalized epileptogenicity index (EI) values) are represented by the color (yellow to red) and size of the spheres on the respective electrode contacts. (B) A sagittal T2‐weighted FLAIR MRI image of the left hemisphere showing cortical hyperintensity within the anterior, middle, posterior cingulate cortex and the precuneus. (C, D) SEEG recordings of subintrant electroclinical seizures involving the mesial wall of the left hemisphere. (C) Low‐voltage fast discharges started within the anterior aspect of the left middle cingulate cortex (CC′1–2) and the adjacent medial prefrontal cortex (PM′1–2, red asterisk), with rapid involvement of the mesial premotor (supplementary motor area, SA′1–2) cortex, followed 30 s later by a fast discharge within the left posterior cingulate cortex (PI′1–2) cortex and the precuneus (PA′1–2, blue asterisk), with secondary involvement of the left primary motor cortex (LP′7–8). Clinically, head version to the left and eye lid myoclonia with alteration of awareness are observed concomitant to a vast discharge involving the left mesial structures in the central phase of the seizure. (D) Low‐voltage fast discharge starting within the left precuneus and posterior cingulate cortex (blue asterisk), involving the primary motor cortex and then followed by a fast discharge within the middle cingulate cortex and the mesial prefrontal cortex (red asterisk), implicating the ipsilateral supplementary motor area. Clinically, atonic fall of the right arm and loss of consciousness are observed. (E) The maximal EI values represented according to a color scale from yellow to red on the respective SEEG electrode contacts within a sagittal T1‐weighted MRI image of the left hemisphere. The contacts CC′1–2 (left middle cingulate cortex), PM′1–2 (left mesial prefrontal), SA′1–2 (left supplementary motor area), CP′1–2 (posterior aspect of the left supplementary motor area), PI′1–2 (left posterior cingulate cortex), and PA′1–2 (left precuneus) showed high EI values and belonged to the epileptogenic zone network.

FIGURE 2

SEEG findings and spike rates dynamics after radiofrequency thermocoagulation for refractory status epilepticus. (A) Interictal awake SEEG recording 24 h following RFTC showing cessation of subintrant seizures and interictal spikes, and signal hypovoltage over the RFTC targets. (B) A sagittal T1‐weighted MRI image of the left hemisphere 48 h post‐RFTC showing thermolesions within the left mesial prefrontal, the supplementary motor area, the middle and posterior cingulate cortex and the precuneus. (C) Graph showing the maximal spike rates/min quantified for each SEEG contact before RFTC, 1 h and 24 h post‐RFTC.