Journal
NEUROMODULATION
Volume 25, Issue 3, Pages 461-469Publisher
ELSEVIER
DOI: 10.1016/j.neurom.2022.01.014
Keywords
Biomarkers; epilepsy; laryngeal muscle-evoked potentials; response; vagus nerve stimulation
Funding
- Aspirant grant from the Fonds voor Wetenschappelijk Onderzoek (FWO) Flanders
- FWO Flanders
- Bijzonder Onderzoeksfonds University Gent special research fund
- Queen Elisabeth Medical Foundation (GSKE) for Neurosciences
- Fond de Recherche Clinique Cliniques Universitaires Saint-Luc
- Ghent University Hospital
- GSKE
- BOF-UGent special research
- BOF-UGent
- E-Epilepsy (EU)
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This study investigated laryngeal muscle evoked potential (LMEP) responses induced by vagus nerve stimulation (VNS) in patients with epilepsy. The results showed that recording VNS-induced LMEPs was feasible both at the initiation of therapy and after one year. Low output currents may be sufficient to activate vagal A alpha-motor fibers. However, the maximal amplitude of LMEPs seemed to decrease after chronic VNS therapy.
Background: Vagus nerve stimulation (VNS) is an adjunctive therapy for drug-resistant epilepsy. Noninvasive evoked potential recordings in laryngeal muscles (LMEPs) innervated by vagal branches may provide a marker to assess effective vagal nerve fiber activation. We investigated VNS-induced LMEPs in patients with epilepsy in acute and chronic settings. Materials and Methods: A total of 17 of 25 patients underwent LMEP recordings at initiation of therapy (acute group); 15 of 25 patients after one year of VNS (chronic group); and 7 of 25 patients were tested at both time points (acute + chronic group). VNS-induced LMEPs were recorded following different pulse widths and output currents using six surface laryngeal EMG electrodes to calculate input/output curves and estimate LMEP latency, threshold current for minimal (I-threshold), half-maximal (I-50), and 95% of maximal (I-95) response induction and amplitude of maximal response (V-max). These were compared with the acute + chronic group and between responders and nonresponders in the acute and chronic group. Results: VNS-induced LMEPs were present in all patients. I-threshold and I-95 values ranged from 0.25 to 1.00 mA and from 0.42 to 1.77 mA, respectively. Estimated mean LMEP latencies were 10 +/- 0.1 milliseconds. No significant differences between responders and nonresponders were observed. In the acute + chronic group, I-threshold values remained stable over time. However, at the individual level in this group, V-max was lower in all patients after one year compared with baseline. Conclusions: Noninvasive VNS-induced LMEP recording is feasible both at initiation of VNS therapy and after one year. Low output currents (0.25-1.00 mA) may be sufficient to activate vagal A alpha-motor fibers. Maximal LMEP amplitudes seemed to decrease after chronic VNS therapy in patients.
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