Abstract
An 11-year-old female presents to the sleep clinic for evaluation for possible sleep-disordered breathing (SDB). She has a history of frequently intractable seizures for which she was tried on multiple antiepileptic medications. She had vagus nerve stimulation (VNS) implantation two years ago to treat her focal seizures. Nine months later, her seizures were controlled, but the family raised concerns about louder snoring and more frequently witnessed apneas. She had polysomnography (PSG) that showed severe obstructive sleep apnea (OSA) related to her VNS. The patient was diagnosed with SDB secondary to electrical activations of the implanted VNS. We describe an epilepsy patient whose case illustrates the possible respiratory complications (primarily OSA) associated with VNS. We will discuss the possible mechanisms of VNS related SDB and the importance of screening for SDB and advocate for a PSG both before and after VNS implantation.
Highlights
Vagus nerve stimulation (VNS) can worsen sleep-disordered breathing (SDB) after implantation
The effects of vagal nerve stimulation on sleep-related breathing have not been well-described in children and there is an overall lack of case reports, especially in children, demonstrating respiratory complications associated with VNS [6]
This study reported a significant increase in the number of movement times (MTs) immediately related to the VNS stimulation periods with a reduction in the epileptiform activity, the clinical seizures, and with improvement in quality of life (QOL) and behavior [10]
Summary
Vagus nerve stimulation (VNS) can worsen sleep-disordered breathing (SDB) after implantation. An 11-year-old female presented to the sleep clinic for evaluation of snoring and witnessed apneas She has had a history of focal epilepsy since age four years and was tried on multiple antiseizure medications, including levetiracetam, clobazam, zonisamide, and valproate. The occurrence of this artifact occurred in sync with the patient’s respiratory events These findings on the polysomnographic signals would raise questions about their possible etiologies that can include possibilities like an underlying arrhythmia or an artifact not related to the VNS versus a VNS related phenomena. (The figures above outlines the EMG and the EKG electrical artifacts coinciding with the patient’s respiratory event in 30-second bursts. This regular and repetitive pattern argues against options {A} and {D}. There is no concern for arrhythmia on the ECG lead which argues against option {C}.)
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