Abstract
Vagus nerve stimulation (VNS) is an effective treatment option for medically refractory epilepsy. The effects of VNS on sleep disordered breathing (SDB) were reported in some case series. However, studies in pediatric population are not well-described. The primary purpose of our study is to describe clinical characteristics, and polysomnographic findings in children with VNS. A retrospective review of medical records and polysomnographic results was performed in pediatric patients aged 0–20 years old with refractory epilepsy at CCHMC. Only children with VNS treatment at the time of sleep study were included. 22 subjects met the criteria for entry into this study. 77.3% of subjects had localization related epilepsy, 13.6% had generalized epilepsy, and 9.1% had features of both generalized and localization related epilepsy. 54.5% were male. The mean age at the time of VNS insertion was 8.4 ± 4.2 years. The mean age at the first PSG after VNS insertion was 10.9 ± 4.6 years. Three patients had obstructive sleep apnea (OSA) prior to VNS insertion. Common presentations at sleep clinics included snoring (81.8%) frequent night awakening (68.2%), parasomnia (68.2%), daytime sleepiness (45.5%) and gasping (45.5%). The mean apnea-hypopnea index (AHI) was 11.5 ± 18.8/hr (median 4.1; range 0 - 69.2) and the mean obstructive index (OI) was 10.9 ± 18.5/hr (median 3.9; range 0 - 67.1). Obstructive sleep apnea (OSA) was diagnosed after VNS insertion in 19 patients (86.4%), 6 of which (27.2%) had severe OSA. One patient (4.5%) had co-existing central sleep apnea on subsequent polysomnography. 8 patients (36.4%) had significant hypoventilation. For management, 31.8% of patients were treated with BiPAP, 9.1% with CPAP, 9.1% with ventilator, 18.2% with upper airway surgery (adenotonsillectomy and/or uvulopalatopharyngoplasty) and 36.4% were treated conservatively. Sleep disordered breathing, including obstructive sleep apnea and hypoventilation, is common among children with medically refractory epilepsy treated with VNS. The mechanism is currently unknown, but may involve the effect of VNS firing on upper airway muscle tone or central respiratory control. Further studies are needed to assess what factors associated with VNS play a crucial role in the upper airway collapsibility. None
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