Post-Ictal Rhythmic Thalamic Activity of the Centromedian Nucleus
Abstract number :
1.153
Submission category :
3. Neurophysiology / 3C. Other Clinical EEG
Year :
2021
Submission ID :
1826524
Source :
www.aesnet.org
Presentation date :
12/4/2021 12:00:00 PM
Published date :
Nov 22, 2021, 06:54 AM
Authors :
Kristen Arredondo, MD - Nationwide Children's Hospital; Stephanie Ahrens, MD – Fellow, Pediatric Neurology, Nationwide Children's Hospital; Christopher Beatty, MD – Assistant Professor, Pediatric Neurology, Nationwide Children's Hospital; Adam Ostendorf, MD – Associate Professor, Pediatric Neurology, Nationwide Children's Hospital; Jonathan Pindrik, MD – Assistant Professor, Pediatric Neurosurgery, Nationwide Children's Hospital; Ammar Shaikhouni, MD PhD – Assistant Professor, Pediatric Neurosurgery, Nationwide Children's Hospital
Rationale: Deep brain stimulation (DBS) of the centromedian nucleus of the thalamus (CMN) to treat drug resistant epilepsy has been of interest for decades and has shown promise in generalized seizure types. CMN DBS therapy is postulated to work via disruption of a synchronized thalamocortical network which includes the CMN as a node. However, little is known about the electrophysiological activity of the CMN during seizures. Here we describe a novel CMN EEG finding associated with seizure: post-ictal rhythmic thalamic activity (PIRTA).
Methods: Five patients with drug resistant epilepsy with bilateral onset seizures underwent stereoelectroencephalography (SEEG) monitoring as part of evaluation for potential resective surgery or neuromodulation. A standardized plan for implantation was used with targets in the bilateral CMN, frontal neocortex, cingulate, and insula. Hippocampal electrodes were included in 3/5 patients in whom a limbic network was also hypothesized for epileptogenic onset.
The patients were males between 10-20 years of age with SEEG performed between March 2020 and May 2021. Seizure etiology was unknown. Initial MRI findings were non-lesional in 4 cases and showed bilateral atrophy of the thalami and hippocampi in another. PET hypometabolism was bilateral in 4/5 cases. Two patients had undergone complete corpus callosotomy and vagus nerve stimulation.
Results: Each patient had bilateral independent frontal or frontotemporal seizure onset. CMN contacts were involved synchronously or rapidly after onset in 4/5 patients aside from a single patient with independent left mesial temporal and right frontal neocortical seizure onset zones. Focal onset hemiclonic and tonic-clonic seizures spread to involve all cortical contacts with high amplitude rhythmic spiking followed by abrupt offset with diffuse voltage attenuation which corresponded to clinical seizure end. An immediate post-ictal rhythmic 2-2.5 Hz delta frequency pattern, PIRTA, emerged in the CMN contacts amid suppression of background activity in the cortical contacts. In those two patients with corpus callosotomy, unilateral seizure spread was observed followed by voltage attenuation with ipsilateral CMN PIRTA prior to the return of background activity in the cortex of the involved hemisphere.
Conclusions: We observed PIRTA in five patients with SEEG monitoring of the CMN with bilateral independent frontal onset convulsive seizures. This rhythm appears late in ictal evolution and is unlikely to be useful for seizure prediction or early detection. However, it may signal an important role of the CMN in seizure termination. Furthermore, this rhythm may help identify CMN involvement in seizure networks and predict response to DBS therapy. Additional study is needed to understand the role of PIRTA in recovery from the post-ictal state and whether this finding has a correlation with risk of sudden unexpected death in epilepsy (SUDEP).
Funding: Please list any funding that was received in support of this abstract.: No funding was received in support of this abstract.
Neurophysiology