Effects of Vagal Nerve Stimulation on Sleep Continuity and Respiratory Patterns in Sleep: A Case Presentation
Abstract number :
1.094
Submission category :
Year :
2001
Submission ID :
2192
Source :
www.aesnet.org
Presentation date :
12/1/2001 12:00:00 AM
Published date :
Dec 1, 2001, 06:00 AM
Authors :
M.B. Chang, M.D., Neurology, University of Washington School of Medicine, Seattle, WA; M.D. Holmes, M.D., Neurology, University of Washington School of Medicine, Seattle, WA; V. Kapur, M.D., M.P.H., Pulmonary and Critical Care Medicine, University of Wash
RATIONALE: Little has been written regarding the effects of vagal nerve stimulation therapy (VNST) on respiration during sleep and sleep continuity. We present a patient with chronic, excessive sleepiness occurring after VNST placement; her polysomnographic findings are discussed.
METHODS: This 21 year old woman has a longstanding history of medically refractory primary generalized epilepsy. She underwent VNST placement in 1999, resulting in greater than 50% reduction in seizure frequency. VNST was eventually set at 3.25 milliamperes for the current flow and a 10% duty cycle. Since VNST placement she has felt significantly drowsy during the day. Her family has witnessed her to have breathing pauses during sleep, lasting up to thirty seconds at a time, occurring 4-6 times every half-hour of sleep and associated with brief gasping vocalizations.
RESULTS: Overnight polysomnography was performed. Total sleep time was 402.5 minutes. The respiratory disturbance index (RDI) was 12.4/hr (72 apneas or hypopneas). These abnormal respiratory events consisted of discrete, 35-second periods of significantly and persistently decreased amplitudes in the three respiratory channels (chest excursions, abdominal excursions, and airflow), associated with sudden tachypnea (from 15-18 bpm baseline to 50-60 bpm) which also persisted throughout stimulation. These stereotyped events occurred only during the 35-second VNST stimulations and the initiations and terminations of the amplitude decreases and tachypnea corresponded nearly exactly with those of the stimulations. No stimulations were associated with an absence of these abrupt respiratory changes. A number of these stimulations were associated with cortical arousals, with arousals and stage upshifts occurring most frequently out of Stage 1 and 2 sleep, less so out of REM sleep, and significantly less so out of slow-wave sleep.
CONCLUSIONS: In this patient with excessive sleepiness, VNST appears to be associated with sleep disruption and with tachypnea and decreases in tidal volume during stimulation. The degree of associated sleep disruption appears to depend on sleep stages during stimulation, supporting the notion of differential susceptibility to arousals according to sleep stage.