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13 OSA RELATED TO VAGAL NERVE STIMULATOR THERAPY: A SLEEP CENTER CASE STUDY By Carolyn C. Campo, MA, RPSGT, RRT E very so often, even the most seasoned sleep technician/technologist will be presented with a patient who has a novel medical history that can influence the outcome of his or her sleep study. This article provides background information on the vagal nerve and the Vagal Nerve Stimulator (VNS) device and presents a case study of a patient with obstructive sleep apnea (OSA) related to the VNS implant that was being used to treat her seizures. THE VAGAL (VAGUS) NERVE The vagal nerve is just one of the 12 major cranial nerves charged with innervation or stimulation of the viscera (gut) and skeletal muscle. It’s also called the pneumogastric nerve since it innervates both the lungs and the stomach. The vagal nerve supplies motor parasympathetic fibers to most of the organs from the neck down to the second segment of the transverse colon. This includes the heart. It’s somewhat important to remember that parasympathetic nerves maintain control of heart rate when the sympathetic nerves (“fight or Figure 1. Vagal Nerve Stimulator flight”) get the heart (VNS). Copyright © 2010 Cyberonics. racing. Sympathetic Image reprinted with permission. and parasympathetic functions are considered automatic. As an interesting aside, the vagal nerve also has some afferent (sensory) fibers that innervate the inner (canal) portion of the outer ear. This is probably why you can feel a tickling in the throat when you use a swab in the ear canal. The vagus also controls quite a few skeletal muscles - most of which are in the neck area, including muscles of the larynx (via recurrent laryngeal nerve) for speech production. Skeletal muscle is often associated with voluntary movement; in this scenario, we will associate voluntary movement with speech. At first glance, speech seems automatic; but we all had to learn to manipulate these muscles as children in order to learn to produce specific sound combinations to communicate. Carolyn C. Campo, MA, RPSGT, RRT, has been in the sleep field since 2000 and is Director of Sleep Operations (multi-state) for Novant Healthcare based in Charlotte, N.C. VAGAL OR VAGUS NERVE STIMULATION DEVICE The VNS system has been around as a treatment since 1997 and is very similar in appearance and function to a cardiac pacemaker in which short, regular bursts of electrical energy are sent to the brain via the vagus nerve. It is 50-55 mm in diameter and around 12-14 mm thick, making it about the size of a silver dollar. See Figure 1. INDICATIONS The VNS is currently approved for use in adults and children over the age of 12 who have partial-onset seizures, which are seizures that begin in one part of the brain. Partial seizures are the most common type of seizure experienced by people with epilepsy. Virtually any movement, sensory or emotional symptom can occur as part of a partial seizure, including complex visual or auditory hallucinations. The VNS system is intended for a person whose seizures do not respond to medications and who either is not a good candidate for brain surgery or doesn’t want to have brain surgery. In 2005 it was approved for treating drugresistant cases of clinical depression Figure 2. Vagal Nerve Stimulator (VNS) Implantation. Copyright © 2010 Cyberonics. Image reprinted with permission. IMPLANTATION With few exceptions, VNS units are implanted on the patient’s left side. The procedure requires two incisions: One in the neck in order to access the vagal nerve as it courses between the carotid artery and the internal jugular vein, and another one in the groove between the chest and the shoulder where the device pulse generator (battery unit) is secured. See Figure 2. A2Zzz 19.4 | December 2010 Continued on Page 14 Carolyn C. Campo, MA, RPSGT, RRT To recap: The vagal nerve controls heart rate, gastrointestinal peristalsis, sweating, and quite a few muscle movements in the mouth. It also keeps the larynx open for breathing. Continued from Page 13 14 The implantation procedure typically takes about 1.5 hours and is performed under general anesthesia. VNS is typically performed as an outpatient procedure, so patients are observed for two to three hours post-op and then discharged. The device is activated at low settings in the operating room at the time of implantation and, if necessary, the doctor will adjust how much stimulation is being delivered, and how often.1 Exactly how VNS therapy works continues to be studied. If the individual with the system feels a seizure coming on, he or she can activate the discharge by passing a small magnet over the battery, thus giving the patient an element of control. In some people, this has the effect of stopping the seizure before it gets started or becomes deeply entrenched. It is also possible to turn the device off by holding the magnet over it. This is important later in the case study. Although complete seizure control is seldom achieved, the majority of people who use VNS therapy experience fewer seizures. Studies find that many people who have had the implant say they feel better, even if their seizures continue. Many patients report that after a seizure they are in a better mood, feel more alert, have better memory and make fewer emergency room visits while using VNS therapy.2 These mood effects explain why VNS therapy also is a treatment option for clinical depression. Most routine procedures, such as diagnostic ultrasounds or X-rays, should not affect the VNS. Anyone with a VNS implant should tell health professionals about the implant and where it’s located. The VNS manufacturer, Cyberonics, has a clinical/technical support telephone number for health professionals to call if they have any questions about treating someone with a VNS: 800-332-1375 ext. 7330. VNS THERAPY & SLEEP DISORDERED BREATHING Side effects of VNS therapy are mostly hoarseness and occasional discomfort in the throat. There may be a change in voice quality during the actual stimulation. Most notably, intermittent decrease in respiratory flow during sleep has consistently been demonstrated in patients with VNS implants.3 Clinically significant sleep disordered breathing associated with VNS therapy has been described in pediatric and adult patient populations.4,5 Most patients undergoing VNS treatment experience an increased apnea-hypopnea index (AHI) post treatment with up to approximately one third developing mild OSA post treatment.5 A small group of patients develop severe OSA related to VNS therapy. These obstructive events can be alleviated by decreasing the frequency or intensity of VNS stimulation, by utilizing positional therapy (sleep in non-supine position) or by applying positive airway pressure (PAP).4,5 VNS patients who have an increased probability for sleep disordered breathing will likely exhibit the usual signs and symptoms; i.e., loud snoring or intermittent cessation of breathing at night with daytime symptoms such as behavioral changes, fatigue or sleepiness. Many of these patients are children who may have associated cognitive deficits, which makes diagnosing the problem even more difficult without a sleep study. Thus a sleep study is required to diagnose the presence of OSA, particularly in this population. CASE STUDY A 29-year-old female who is mentally disabled presents to the sleep center with mild snoring and a limited documented medi- cal history. She is obese with a body mass index (BMI) of 33.2, and she has a VNS implant for the treatment of lifelong generalized seizures. PSG TECHNICAL FINDINGS The patient’s respirations indicated moderate sleep disordered breathing with an overall AHI of 21 events per hour in all sleep positions and sleep stages. The rapid eye movement (REM) index was in the moderate category at 24. There were 128 apneas and hypopneas. Mean SaO2 during the study was 95 percent with a nadir of 84 percent. Snoring was mild and was subjectively rated at three on a scale from one to 10. The patient’s EKG showed normal sinus rhythm with a heart rate range from 68 to 96 beats per minute. Periodic leg movements with or without arousal and the spontaneous arousal index were all insignificant. Sleep efficiency was good at 92 percent; REM sleep and slow wave sleep constituted 21 percent and 7 percent of the total sleep time, respectively. REM latency was 90 minutes, and the first REM period lasted 22 minutes. The tech who ran the study sent a note to the interpreting physician about his suspicions regarding the timing of the apneas, which occurred approximately every four minutes. He did not understand the role of the VNS but believed that the timing of the events coincided with the stimulation of the device. PHYSICIAN’S IMPRESSION There is evidence of moderate OSA with an AHI of 21 events per hour and desaturations as low as 84 percent. Recommend returning for a titration study for treatment with positive airway pressure. Elevation of head of bed, positional therapy, weight loss, ENT evaluation and elimination of sedatives and hypnotics, if applicable, are other potential treatment options. There is no evidence of significant periodic limb movement disorder. EKG is NSR. Sleep efficiency is normal. FOLLOW-UP TESTING The patient returns to the sleep center for PAP titration. On the night of the study the same tech consults with the physician, who requests: ● Titration first to eliminate SDB ● Period of testing on PAP with VNS on vs. off ● Period of testing with both VNS off and PAP off PAP TECHNICAL FINDINGS: See Figure 3. The patient’s respirations without nasal CPAP and VNS turned off showed insignificant sleep disordered breathing with an AHI of 3.9 in all sleep stages. With CPAP application and the VNS turned on, the respirations were stabilized with an optimal nasal CPAP pressure of 7 cm H2O. At this pressure, the AHI was reduced from 24 to 3.7. Mean SaO2 at the optimal nasal CPAP pressure was 96 percent with a nadir of 88 percent. Sleep efficiency was 88 percent. REM sleep and slow wave sleep constituted 17 percent and three percent of total sleep time, respectively. REM latency was 101 minutes, and the first REM period lasted 33 minutes. Since this patient required the VNS for seizure control, she was placed on CPAP of 7 cm H2O. With education and desensitization, this patient has done very well with PAP therapy. A2Zzz 19.4 | December 2010 – – – Titration first to eliminate SDB Period of Testing with VNS On vs. Off on PAP VNS Off and PAP Off VNS On/PAP On ↑ VNS Off PAPfindings. TECHNICAL Figure 3. PAP technical ↑VNS ON 15 ↑ VNS Off/PAP Off FINDINGS: The patient's respirations WITHOUT nasal VNS TURNED 3. CPAP BA, Edwards J, Marzec M,OFF Saghershowed O, Fromes G. Malow AND INSIGNIFICANT sleep disordered breathing with an AHI of 3.9 in all sleep stages. With Effects of vagus nerve stimulation on respiration during Patients undergoing VNS placement are at risk for developing CPAP andbethe V NScliniTURNED ON, respirations were stabilized with an sleep:the a pilot study. Neurology. 2000 Nov 28;55(10):1450-4. OSA related to the VNS andapplication should therefore screened cally for the presenceoptimal of OSA after procedure. There is nasaltheCPAP pressure ofsome 7cm H2O. At this pressure, the apnea/hypopnea index was 4. Hsieh T, Chen M, McAfee A, Kifle Y. Sleep-related evidence that screening for sleep disordered breathing in patients reduced to 3.7/hr. The previous study, with the VNS TURNED ON showed breathing disorder in children with vagal nerve stimulators. with a seizure disorder who are undergoing a VNS implant breathing may MODERATE sleep disordered with an AHI of 24/hr. Pediatr Neurol. 2008 Feb;38(2):99-103. CONCLUSION be important because adequate treatment of previously undiagnosed and untreated SDB may likely result in better seizure 5. Marzec M, Edwards J, Sagher O, Fromes G, Malow Theis mean at theoption optimal nasal CPAP pressure was 96 % with a nadir of 88 %. The control.6 CPAP therapy a viableSaO2 therapeutic for patients BA. Effects of vagus nerve stimulation on sleep SleeptoEfficiency was 88options %. REM sleep and Slow sleep constituted 17 Epilepsia. % and 3 2003 % of who develop OSA related the VNS, and other include relatedWave breathing in epilepsy patients. the Total Sleep Time, respectively. Latency was 101 minutes and the first REM increasing the cycle length or stimulation frequency of the de- The REMJul;44(7):930-5. vice. With an increase in the lasted number33 of minutes. patients undergoing the period 6. Vaughn BV, D’Cruz OF, Beach R, Messenheimer JA. procedure, as well as multiple indications for use, awareness of Improvement of epileptic seizure control with treatment of thisSince causation important for appropriate diagnosis and treatthisispatient required the VNS for seizure control, she was placedsleep on CPAP 7 cmH20. With obstructive apnoea. of Seizure. 1996 Mar;5(1):73-8. ment of OSA related to vagal nerve stimulators. education and desensitization, this patient has done very well with PAP therapy. REFERENCES Editor’s Note: Ms. Campo presented the lecture, “Vagal Nerve Next is a ten-minute epoch of yet another young patientStimulator: (13 y/o male w/ treatment resistant epilepsy, mild A Sleep Center Case Study,” June 6, 2010, during the 1. Cerebral St. LouisPalsy, Children’s Hospital Vagal nerve In this instance, the technician is reporting “periodic limb autism, s/p [Internet]. T&A) with VNS. Topics for the Advanced Practitioner course at the AAST 32nd stimulation. c2010 [cited 2010 Aug 08].are, Available from: movements” (again in purple) that in fact, artifact from theMeeting VNS inshowing up Texas. in theleg channels as 60 Annual San Antonio, http://www.stlouischildrens.org/content/medservices/ Hz. VagalNerveStimulation.htm. 2. Epilepsy Foundation [Internet]. Vagal nerve stimulation therapy. c2010 [cited 2010 Aug 08]. Available from: http://www.epilepsyfoundation.org/answerplace/Medical/ treatment/VNS/. A2Zzz 19.4 | December 2010