Troubleshooting Stimulation Side Effects in Patients with Epilepsy Being Treated with Centromedian Nucleus Neurostimulation
Abstract number :
2.499
Submission category :
4. Clinical Epilepsy / 4C. Clinical Treatments
Year :
2024
Submission ID :
1391
Source :
www.aesnet.org
Presentation date :
12/8/2024 12:00:00 AM
Published date :
Authors :
Presenting Author: Lia Ernst, MD – Oregon Health & Science University
Kathleen Medwar, NP – Oregon Health & Science University
Proleta Datta, MD PhD – Oregon Health & Science University
David Spencer, MD – Oregon Health & Science University
Rationale: Neurostimulation of the centromedian nucleus of the thalamus (CMT) is an emerging treatment for drug-resistant epilepsy (DRE). Although the randomized controlled trials that led to FDA approval of responsive neurostimulation (RNS) and deep brain stimulation (DBS) for epilepsy did not include CMT as a stimulation target, many epilepsy centers have begun targeting CMT for select patients with DRE based on preliminary evidence that it is safe and effective. Previous studies have reported that some patients experience contralateral facial and arm paresthesias with CMT stimulation. There is no consensus on how to ameliorate this stimulation side effect, but programming options include reduction of current, pulse width, or frequency, or changing anatomical location of stimulating contacts. Our aim was to review our center’s experience with this specific stimulation side effect and develop a standardized approach to troubleshooting it.
Methods: We performed a retrospective chart review of all patients at our center who were treated with CMT stimulation for epilepsy, with either RNS or DBS. Patients with documented stimulation-induced paresthesias were reviewed for this case series.
Results: At our center, 2 of 7paresthesias during stimulation programming (at 3 mA and 1 mA, respectively). Time-locked with stimulation, Patient 1 experienced unilateral right hand paresthesias, and patient 2 experienced bilateral R >L facial paresthesias. Patient 2 had previously been reprogrammed with pulse width reduction from 90 to 70 µs with incomplete resolution of symptoms. Paresthesias resolved with frequency reduction from 142.9 Hz to 20 Hz in Patient 1 and 140 Hz to 20 Hz in Patient 2. Both patients tolerated programming and did not have recurrent paresthesias after reprogramming. Patient 1 continued treatment with 3 mA current stimulation, while patient 2 tolerated increased current to 2.0 mA.
Conclusions: Reducing frequency of stimulation in both RNS and DBS stimulation of CMT may be an effective strategy for mitigating the specific stimulation side effect of paresthesias. Further study is warranted to determine the optimal frequency for reducing stimulus-induced paresthesias, and the clinical impact of reducing frequency.
Funding: N/A
Clinical Epilepsy