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Treatment of vagus nerve stimulator-induced sleep-disordered breathing: A case series

OBJECTIVE: Vagus nerve stimulation (VNS) is a treatment option for patients with drug-resistant seizures, but it is also associated with sleep-disordered breathing (SDB). We present four patients with VNS who underwent polysomnography (PSG) concurrently with VNS stimulation monitoring and adjustment...

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Detalles Bibliográficos
Autores principales: Oh, Daniel M., Johnson, Jacklyn, Shah, Bankim, Bhat, Sushanth, Nuoman, Rolla, Ming, Xue
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Elsevier 2019
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6719281/
https://www.ncbi.nlm.nih.gov/pubmed/31497754
http://dx.doi.org/10.1016/j.ebr.2019.100325
Descripción
Sumario:OBJECTIVE: Vagus nerve stimulation (VNS) is a treatment option for patients with drug-resistant seizures, but it is also associated with sleep-disordered breathing (SDB). We present four patients with VNS who underwent polysomnography (PSG) concurrently with VNS stimulation monitoring and adjustment, and positive airway pressure (PAP) treatment. We demonstrate the importance of sleep apnea screening prior to VNS placement and the dilemma of optimizing VNS settings. BACKGROUND: VNS is a common adjunct therapy for refractory epilepsy. Despite its low side effect profile, complications of VNS include delayed arrhythmias, laryngopharyngeal dysfunction, obstructive sleep apnea, and tonsillar pain mimicking glossopharyngeal neuralgia. Risk of developing or exacerbating existing obstructive sleep apnea (OSA) limits the VNS settings, as there appears to be a dose dependent effect. OSA can further cause sleep fragmentation and cause hypoxia, potentially worsening seizures. METHODS: Four patients with drug-resistant epilepsy with VNS underwent PSG with concurrent VNS leads to monitor correlation of SDB and VNS. AHI was calculated to quantify SDB, and it was scored as non-VNS related when the VNS was off, and VNS-induced when the onset of SDB corresponded to VNS activation. Subsequent PAP and VNS adjustment was performed to treat the SDB episodes. RESULTS: Three out of four patients had non-VNS associated SDB, which improved with PAP treatment. All four patients had VNS-induced SDB episodes but none improved with PAP. The VNS-induced SDB events decreased in a dose dependent manner, when VNS was adjusted down and disappeared when turned off completely. CONCLUSION: Our case series provides further evidence of VNS-induced SDB secondary to VNS. PAP treatment alone is ineffective for VNS-induced SDB. Screening for OSA before VNS implant is crucial; further research is needed to establish optimal VNS parameters for prevention andminimization of VNS-induced SDB along with other possible treatments.