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1225 Vagal Nerve Stimulator-induced Sleep Disordered Breathing

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Abstract Introduction Vagus nerve stimulator (VNS) is used for the treatment of refractory epilepsy. It can alter breathing patterns leading to sleep-disordered breathing (SDB). Screening for SDB is recommended before and after initiation of VNS therapy. We present a case of VNS-induced SDB which responded to continuous positive airway pressure (CPAP) therapy. Report of case(s) A 40-year-old Caucasian female underwent a home sleep apnea test (HSAT) due to symptoms of snoring, difficulty initiating sleep, teeth grinding, vivid dreams, nightmares, excessive daytime fatigue, and sleepiness. She denied parasomnia, symptoms of narcolepsy, and restless leg syndrome. Her habitual sleep duration was 9 hours with a sleep latency of 1 hour. She had 2-3 nighttime awakenings without nocturia. Pertinent medical history included refractory focal epilepsy, traumatic brain injury, insomnia, and attention deficit disorder. Medications were eslicarbazepine 800 mg daily, topiramate 200 mg twice daily, lamotrigine 100 mg daily, trazodone 300 mg nightly, and Adderall 60 mg daily. She had a VNS implanted 5 years ago. VNS settings were frequency of 20 Hz with on and off time of 30 and 60 seconds respectively. Her body mass index was 21 and Epworth Sleepiness Scale score was 15. HSAT showed significant periodic breathing without Cheyne stokes respiration and a 4% apnea-hypopnea index (AHI) of 9.6/hour. Follow-up diagnostic polysomnogram (PSG) revealed periodic breathing with the respiratory events occurring during VNS on time and abnormal sleep architecture including prolonged sleep and rapid eye movement (REM) latency, increased slow wave sleep, and pseudo spindles. The respiratory events were not associated with significant sleep fragmentation or desaturation. The AHI was 6.4/hour. Respiratory events improved with CPAP 7 cmH20 during titration PSG. She will be followed up in the sleep clinic to evaluate the effectiveness of CPAP therapy. Conclusion There is a complex relationship between epilepsy and SDB. Antiepileptics and VNS can cause new onset or worsening SDB. Management options for VNS-induced SDB include PAP therapy, changing VNS settings, or alternate therapies for refractory epilepsy. A multimodal approach requiring input from the patient, a sleep specialist, and an epileptologist is recommended for optimal results. Support (if any)  
Title: 1225 Vagal Nerve Stimulator-induced Sleep Disordered Breathing
Description:
Abstract Introduction Vagus nerve stimulator (VNS) is used for the treatment of refractory epilepsy.
It can alter breathing patterns leading to sleep-disordered breathing (SDB).
Screening for SDB is recommended before and after initiation of VNS therapy.
We present a case of VNS-induced SDB which responded to continuous positive airway pressure (CPAP) therapy.
Report of case(s) A 40-year-old Caucasian female underwent a home sleep apnea test (HSAT) due to symptoms of snoring, difficulty initiating sleep, teeth grinding, vivid dreams, nightmares, excessive daytime fatigue, and sleepiness.
She denied parasomnia, symptoms of narcolepsy, and restless leg syndrome.
Her habitual sleep duration was 9 hours with a sleep latency of 1 hour.
She had 2-3 nighttime awakenings without nocturia.
Pertinent medical history included refractory focal epilepsy, traumatic brain injury, insomnia, and attention deficit disorder.
Medications were eslicarbazepine 800 mg daily, topiramate 200 mg twice daily, lamotrigine 100 mg daily, trazodone 300 mg nightly, and Adderall 60 mg daily.
She had a VNS implanted 5 years ago.
VNS settings were frequency of 20 Hz with on and off time of 30 and 60 seconds respectively.
Her body mass index was 21 and Epworth Sleepiness Scale score was 15.
HSAT showed significant periodic breathing without Cheyne stokes respiration and a 4% apnea-hypopnea index (AHI) of 9.
6/hour.
Follow-up diagnostic polysomnogram (PSG) revealed periodic breathing with the respiratory events occurring during VNS on time and abnormal sleep architecture including prolonged sleep and rapid eye movement (REM) latency, increased slow wave sleep, and pseudo spindles.
The respiratory events were not associated with significant sleep fragmentation or desaturation.
The AHI was 6.
4/hour.
Respiratory events improved with CPAP 7 cmH20 during titration PSG.
She will be followed up in the sleep clinic to evaluate the effectiveness of CPAP therapy.
Conclusion There is a complex relationship between epilepsy and SDB.
Antiepileptics and VNS can cause new onset or worsening SDB.
Management options for VNS-induced SDB include PAP therapy, changing VNS settings, or alternate therapies for refractory epilepsy.
A multimodal approach requiring input from the patient, a sleep specialist, and an epileptologist is recommended for optimal results.
Support (if any)  .

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