Centromedian Thalamic Deep Brain Stimulation in Idiopathic Generalized Epilepsy: Syndrome-specific Volumetric and Connectivity Analyses
Abstract number :
1.275
Submission category :
3. Neurophysiology / 3E. Brain Stimulation
Year :
2024
Submission ID :
801
Source :
www.aesnet.org
Presentation date :
12/7/2024 12:00:00 AM
Published date :
Authors :
Presenting Author: Sihyeong Park, MD – Mayo Clinic
Fiona Permezel, MD – Mayo Clinic
Shruti Agashe, MD – Duke University
Gamaleldin Osman, MBBCh – Mayo Clinic
Hugh Simpson, PhD – Monash University
Kai Miller, MD, PhD – Mayo Clinic
Jamie Van Gompel, MD – Mayo Clinic
Keith Starnes, MD – Mayo Clinic
Brian Lundstrom, MD, PhD – Mayo Clinic
Gregory Worrell, MD, PhD – Mayo Clinic
Nicholas Gregg, MD – Mayo Clinic
Rationale: Limited literature suggests that centromedian thalamus deep brain stimulation (CM-DBS) may be an effective treatment option for drug resistant idiopathic generalized epilepsy (IGE). There is scarcity of data on optimal targeting for CM-DBS for IGE. Analysis of data from a prospective randomized controlled trial of CM-DBS for Lennox-Gastaut Syndrome (LGS) suggests that greater efficacy is associated with stimulation of the parvocellular CM and ventral lateral (VL) nucleus of the thalamus. Here, we present a retrospective analysis of CM-DBS efficacy and a volumetric and connectivity analyses for five patients with drug-resistant IGE and propose an IGE-specific CM-DBS sweet-spot.
Methods: This study included all patients with drug resistant IGE treated with CM-DBS to date at our institution. Seizure outcomes were measured with patient-reported seizure diaries. Indirect targeting, based on anterior commissure-posterior commissure (AC-PC) offsets, was used for patient 1’s implantation. Subsequent implantations were conducted with atlas warp-based targeting. Lead localization, volumetric analysis, probabilistic mapping, and structural connectivity analysis were performed using Lead-DBS 3.0.
Results: We included five patients, and median age was 31 (range: 22-45). Median convulsive seizure frequency reduction for the four patients with GTCS was 66% (range: -200-100%). Four patients had active contacts positioned within the CM nucleus, all of whom had >50% reduction in primary seizure type (3 patients with GTC seizures, 1 patient with absence seizures), with 85% median seizure reduction (paired-sample T-test p=0.0038; Lilliefors test p=0.23). Patient 5 had no GTC seizures at baseline—primary seizure type was absence seizure, and she had >99% reduction in seizure frequency (Fig 1A). The electrodes of the responders and their active contacts (red contacts on the grey-colored responder leads) were positioned within the CM-Pf target (Fig 1B). The single non-responder (yellow leads) had electrode placement posteromedial to the CM nucleus—this patient was implanted prior to implementation of individualized atlas-based targeting. Probabilistic mapping revealed best outcomes with stimulation of the middle ventral CM nucleus (Fig 1C). Connectivity to central cortical regions was significantly increased relative to remaining cortical parcels (p=8.6x10-4, Mann-Whitney U test). Precentral, postcentral, paracentral lobule, and superior frontal gyrus regions accounted for 27.9%, 15.8%, 12.4%, and 18.2% of total cortical connectivity, respectively. Fig 1D shows high connectivity strength in the central regions.
Conclusions: In this study, we showed that continuous CM-DBS is effective in drug-resistant IGE. We demonstrated that the optimal stimulation site is in the middle ventral CM nucleus, in contrast to prior work on varied genetic generalized epilepsies and developmental and epileptic encephalopathies—the optimal approach may be syndrome-specific. To advance in this complex environment, future investigations should focus on homogenous patient cohorts and ensure detailed reporting of stimulation locations, parameters, and outcomes.
Funding: None
Neurophysiology