WITHDRAWN

Abstract

TOPIC: Sleep Disorders TYPE: Fellow Case Reports INTRODUCTION: Vagal nerve stimulation (VNS), which was approved by the FDA in 1997, has been used to treat refractory partial and complex seizures in patients with epilepsy. In this case report, we describe an important adverse effect of vagal nerve efferent stimulation to upper airway structures. Multiple studies have shown that VNS can induce or worsen obstructive sleep apnea (OSA). For treating patients with VNS-induced OSA, manufacturers suggest decreasing VNS frequency and increasing the cycle off time. However, this recommendation rarely provides successful results. Here, we illustrate a case of a woman with VNS-induced OSA and show how small adjustments to VNS current and pulse width parameters can significantly reduce the effects of VNS-induced obstructive respiratory events during a PAP titration without breakthrough seizures. CASE PRESENTATION: The patient is a 52-year-old woman who had a vagal nerve stimulator placed in 1998 for refractory left frontal lobe focal seizures. She presented to the sleep medicine clinic for excessive daytime sleepiness, non-refreshing sleep, and reports of loud snoring. Her symptoms were present despite adequate sleep hygiene and a consistent 8.5 hours of sleep each night. A split night study revealed an apnea-hypopnea index (AHI) of 32.8 with predominant obstructive hypopneas and occasional obstructive apneas. Her obstructive respiratory events occurred coincidentally in sequence with 30 seconds of electromyography (EMG) chin tone every 108 seconds. Subsequent, bilevel positive airway pressure (BPAP) titration was unsuccessful. The patient's neurologist was notified of the sleep study findings and the patient's VNS was adjusted. The output current, pulse width, magnet current, and a magnet pulse bandwidth were reduced. All other parameters remained unchanged including frequency and cycle time. On her subsequent BPAP titration, her OSA was successfully controlled at a BPAP pressure of 23/19 cm H2O, with a residual AHI of 0. On follow-up, the patient was adherent to her BPAP therapy with subjective improvement in quality of her sleep. The patient did not have breakthrough seizures over one year with the decrease in current and pulse width settings on her VNS. She averaged 5.5 hours of BPAP use each night with 73% of days used over one year. DISCUSSION: In this case report, we have outlined a successful BPAP titration with minor adjustments in VNS parameters in a patient with epilepsy and severe OSA. The success of this BPAP titration was likely facilitated by the reduction in VNS output current and pulse bandwidth, which reduced the efferent motor nerve stimulation of upper airway structures. CONCLUSIONS: This case demonstrates how adjustment of specific VNS parameters may potentially provide an alternative to the recommended adjustment in frequency and cycle times; however, this strategy will ultimately need to be tested and closely monitored in more patients. REFERENCE #1: Howland RH. Vagus Nerve Stimulation. Curr Behav Neurosci Rep. 2014;1(2):64-73. REFERENCE #2: Parhizgar F, Nugent K, Raj R. Obstructive sleep apnea and respiratory complications associated with vagus nerve stimulators. J Clin Sleep Med. 2011 Aug 15;7(4):401-7. REFERENCE #3: Ebben MR; Sethi NK; Conte M; Pollak CP; Labar D. Vagus nerve stimulation, sleep apnea, and CPAP titration. J Clin Sleep Med. 2008;4(5):471–473. DISCLOSURES: No relevant relationships by Jovica Veljanovski, source=Web Response No relevant relationships by Joshua Won, source=Web Response