Abstracts

When Therapy Becomes the Trigger: A Case of ANT-DBS-Induced Status Epilepticus

Abstract number : 1.136
Submission category : 18. Case Studies
Year : 2025
Submission ID : 197
Source : www.aesnet.org
Presentation date : 12/6/2025 12:00:00 AM
Published date :

Authors :
Presenting Author: Fortino Velasco, MD – Emory University

Andres Rodriguez, MD – Emory University
Brian Cabaniss, MD – Emory University
Diane Teagarden, NP – Emory University
Hannah Villarreal, NP – Emory University
Nealen Laxpati, MD, PhD – Emory University School of Medicine
Daniel Winkel, MD – Emory University
Ezequiel Gleichgerrcht, M.D., Ph.D. – Emory University

Rationale: Deep brain stimulation (DBS) of the anterior nucleus of the thalamus (ANT) is an approved therapy for drug-resistant focal epilepsy. While generally well-tolerated, worsening seizure burden has been described both in the original trial and real-life data, with unclear mechanisms. Here, we present a case of stimulation-induced status epilepticus following bilateral ANT-DBS and integrate electrophysiological and tractographic analyses to elucidate a likely causal link.

Methods: A 49-year-old woman with drug-resistant, non-lesional bitemporal epilepsy underwent bilateral ANT-DBS placement and presented to the emergency department in status epilepticus approximately one week after reprogramming her stimulation amplitude from 4 mA to 5 mA bilaterally (145 Hz; 90µs pulse width). Continuous video EEG (cEEG) captured stereotyped seizure activity, and local field potentials (LFPs) were recorded using the Medtronic Percept™ “Live Streaming” mode. Spectral analysis was performed to assess stimulation-related changes in neural dynamics. Volume of tissue activation (VTA) was modeled using OSS-DBS based on subject-specific electrode placement and stimulation settings. VTA-informed tractography was conducted to evaluate connectivity between the stimulation field and medial temporal structures. A thorough diagnostic workup ruled out alternative causes for the patient’s status epilepticus.

Results: cEEG demonstrated that seizures consistently followed DBS artifact occurring every 5 minutes (reflecting a 1-minute on / 5-minute off cycle), with a stereotyped right temporal ictal pattern emerging after every single stimulation event. Seizure activity resolved immediately after turning off the stimulator, without escalation of pharmacologic therapy. Spectral analysis revealed that right ANT stimulation produced a broadband power increase in LFPs, putatively reflecting network-level hypersynchronization. No comparable changes were observed during left ANT stimulation. VTA tractography revealed that the right-sided stimulation field intersected fibers projecting to medial temporal structures, consistent with recruitment of the patient’s seizure network. The patient remained seizure-free for several months with stimulation off, though spontaneous habitual seizures eventually recurred.

Conclusions: This case provides multimodal evidence for stimulation-induced seizures in a patient with ANT-DBS for bitemporal epilepsy. Electrophysiological and tractographic findings support a causal link between stimulation and seizure generation, likely mediated by inadvertent recruitment of temporolimbic circuitry from high frequency stimulation. These findings underscore the need for personalized DBS programming, especially in patients with bilateral seizure foci, and highlight the potential utility of LFP monitoring and VTA-informed connectivity modeling in guiding safe and effective therapy.

Funding: No funding was received in support of this abstract.

Case Studies