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Abstract: Case Reports |

POSSIBLE NEW ETIOLOGY FOR THE VAGUS NERVE STIMULATOR CAUSING OBSTRUCTIVE SLEEP APNEA FREE TO VIEW

Marwan Mouammar, MD*; Rose Franco, MD; B. Tucker Woodson, MD; Tarif Smadi, MD; Humberto Battistini, MD
Author and Funding Information

The Medical College of Wisconsin, Wauwatosa, WI



Chest. 2006;130(4_MeetingAbstracts):346S. doi:10.1378/chest.130.4_MeetingAbstracts.346S-b
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Abstract

INTRODUCTION: Vagus nerve stimulators (VNS) are being used more frequently in treatment of patients with refractory epilepsy. It has been suggested that VNS may be associated with mild sleep disordered breathing (SDB), but the mechanism is unclear. We present a case that may improve our understanding of this phenomenon.

CASE PRESENTATION: JA is a 32-year-old male with long history of refractory epilepsy who underwent VNS placement in 2000 and has been seizure free since 2001. He presented with snoring, witnessed apneas and minimal day-time sleepiness for the last 5 years. He had no complaints of noisy breathing prior to the VNS placement. There have been no other major changes in his medications or clinical condition over the same period of time. He is currently receiving lamotrigine and levetiracetam. He has no family history of sleep disorders. On exam his body mass index was 30kg/m2.A polysomnographic (PSG) study was done and showed the presence of obstructive sleep apnea-hypopnea syndrome (OSAHS) with an apnea-hypopnea index (AHI) of more than 80. Continuous positive airway pressure (CPAP) was ineffective in relieving the apneic events.A sedated upper airway endoscopy was done which showed bilateral adduction of the vocal cords causing almost complete obstruction of the airway in rhythm with the firing cycles of the VNS. Decreasing the intensity and frequency of the VNS stimulation resulted in disappearance of the bilateral vocal cord adduction and airway obstruction, temporarily stopping the VNS resulted in an almost complete resolution of the SDB on the PSG.

DISCUSSIONS: Up to 33% of refractory epilepsy patients have SDB. There have been previous reports of VNS causing mild OSA findings on PSG recordings, but it has never been reported that the site of obstruction might actually be the vocal cords rather than the upper airways. The finding that the vocal cord movement was bilateral suggests a central nervous system pathway rather than a simple peripheral effect via the vagus nerve. The fact that these findings improved with decreasing the intensity of the stimulation suggests the presence of a threshold required for the effects on the vocal cords to occur. Since the intensity of the stimulation can usually be decreased without negatively affecting the therapeutic effect of the VNS on epilepsy treatment, this may offer a simple maneuver to improve SDB in many of these patients.

CONCLUSION: In patients with implanted VNS the vocal cord adduction movement may be responsible for SDB or snoring. Decreasing the intensity of stimulation may alleviate the problem.This calls for more investigation to clarify the contribution of abnormal vocal cord movement in the etiology of SDB in patients with implanted VNS.

DISCLOSURE: Marwan Mouammar, None.

Wednesday, October 25, 2006

2:00 PM - 3:30 PM


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