osa related to vagal nerve stimulator therapy: a sleep center

13OSA RELATED TO VAGAL NERVE STIMULATOR THERAPY: A SLEEP CENTERCASE STUDY By Carolyn C. Campo, MA, RPSGT, RRTEvery so often, even the most seasoned sleep technician/technologistwill be presented with a patient who has a novel medicalhistory that can influence the outcome of his or her sleep study. Thisarticle provides background information on the vagal nerve and theVagal Nerve Stimulator (VNS) device and presents a case study ofa patient with obstructive sleep apnea (OSA) related to the VNSimplant that was being used to treat her seizures.Figure 1. Vagal Nerve StimulaTOr(VNS). Copyright © 2010 Cyberonics.Image reprinted with permission.THE VAGAL (VAGUS) NERVEThe vagal nerve is just one of the 12 major cranial nervescharged with innervation or stimulation of the viscera (gut) andskeletal muscle. It’s also called the pneumogastric nerve sinceit innervates both the lungs and the stomach. The vagal nervesupplies motor parasympatheticfibers tomost of the organsfrom the neck downto the second segmentof the transversecolon. Thisincludes the heart.It’s somewhat importantto rememberthat parasympatheticnerves maintaincontrol of heart ratewhen the sympatheticnerves (“fight orflight”) get the heartracing. Sympatheticand parasympatheticfunctions are consideredautomatic. As an interesting aside, the vagal nerve alsohas some afferent (sensory) fibers that innervate the inner (canal)portion of the outer ear. This is probably why you can feel atickling in the throat when you use a swab in the ear canal.The vagus also controls quite a few skeletal muscles - mostof which are in the neck area, including muscles of the larynx(via recurrent laryngeal nerve) for speech production. Skeletalmuscle is often associated with voluntary movement; in thisscenario, we will associate voluntary movement with speech. Atfirst glance, speech seems automatic; but we all had to learn tomanipulate these muscles as children in order to learn to producespecific sound combinations to communicate.Carolyn C. Campo, MA,RPSGT, RRTCarolyn C. Campo, MA, RPSGT, RRT, hasbeen in the sleep field since 2000 and isDirector of Sleep Operations (multi-state)for Novant Healthcare based in Charlotte,N.C.To recap: The vagal nerve controls heart rate, gastrointestinalperistalsis, sweating, and quite a few muscle movements in themouth. It also keeps the larynx open for breathing.VAGAL OR VAGUS NERVE STIMULATION DEVICEThe VNS system has been around as a treatment since 1997and is very similar in appearance and function to a cardiacpacemaker in which short, regular bursts of electrical energy aresent to the brain via the vagus nerve. It is 50-55 mm in diameterand around 12-14 mm thick, making it about the size of a silverdollar. See Figure 1.INDICatioNSThe VNS is currently approved for use in adults and childrenover the age of 12 who have partial-onset seizures, which areseizures that begin in one part of the brain. Partial seizures arethe most common type of seizure experienced by people withepilepsy. Virtually any movement, sensory or emotional symptomcan occur as part of a partial seizure, including complex visualor auditory hallucinations. The VNS system is intended for aperson whose seizures do not respond to medications and whoeither is not a good candidate for brain surgery or doesn’t wantto have brain surgery. In 2005 it was approved for treating drugresistantcases of clinical depressionFigure 2. Vagal Nerve StimulaTOr (VNS) Implantation.Copyright © 2010 Cyberonics. Image reprinted withpermission.IMPLANTATIONWith few exceptions, VNS units are implanted on the patient’sleft side. The procedure requires two incisions: One in theneck in order to access the vagal nerve as it courses between thecarotid artery and the internal jugular vein, and another one inthe groove between the chest and the shoulder where the devicepulse generator (battery unit) is secured. See Figure 2. Continued on Page 14A 2Zzz 19.4 | December 2010

14Continued from Page 13The implantation procedure typically takes about 1.5 hours andis performed under general anesthesia. VNS is typically performedas an outpatient procedure, so patients are observed fortwo to three hours post-op and then discharged.The device is activated at low settings in the operating room atthe time of implantation and, if necessary, the doctor will adjusthow much stimulation is being delivered, and how often. 1Exactly how VNS therapy works continues to be studied. Ifthe individual with the system feels a seizure coming on, he orshe can activate the discharge by passing a small magnet over thebattery, thus giving the patient an element of control. In somepeople, this has the effect of stopping the seizure before it getsstarted or becomes deeply entrenched. It is also possible to turnthe device off by holding the magnet over it. This is importantlater in the case study.Although complete seizure control is seldom achieved, the majorityof people who use VNS therapy experience fewer seizures.Studies find that many people who have had the implant saythey feel better, even if their seizures continue. Many patientsreport that after a seizure they are in a better mood, feel morealert, have better memory and make fewer emergency room visitswhile using VNS therapy. 2 These mood effects explain why VNStherapy also is a treatment option for clinical depression.Most routine procedures, such as diagnostic ultrasounds orX-rays, should not affect the VNS. Anyone with a VNS implantshould tell health professionals about the implant and where it’slocated. The VNS manufacturer, Cyberonics, has a clinical/technicalsupport telephone number for health professionals to callif they have any questions about treating someone with a VNS:800-332-1375 ext. 7330.VNS THERAPY & SLEEP DISORDERED BREATHINGSide effects of VNS therapy are mostly hoarseness and occasionaldiscomfort in the throat. There may be a change in voicequality during the actual stimulation. Most notably, intermittentdecrease in respiratory flow during sleep has consistently beendemonstrated in patients with VNS implants. 3 Clinically significantsleep disordered breathing associated with VNS therapy hasbeen described in pediatric and adult patient populations. 4,5Most patients undergoing VNS treatment experience an increasedapnea-hypopnea index (AHI) post treatment with up toapproximately one third developing mild OSA post treatment. 5A small group of patients develop severe OSA related to VNStherapy. These obstructive events can be alleviated by decreasingthe frequency or intensity of VNS stimulation, by utilizingpositional therapy (sleep in non-supine position) or by applyingpositive airway pressure (PAP). 4,5VNS patients who have an increased probability for sleep disorderedbreathing will likely exhibit the usual signs and symptoms;i.e., loud snoring or intermittent cessation of breathing at night withdaytime symptoms such as behavioral changes, fatigue or sleepiness.Many of these patients are children who may have associated cognitivedeficits, which makes diagnosing the problem even more difficultwithout a sleep study. Thus a sleep study is required to diagnose thepresence of OSA, particularly in this population.CASE STUDYA 29-year-old female who is mentally disabled presents to thesleep center with mild snoring and a limited documented medicalhistory. She is obese with a body mass index (BMI) of 33.2,and she has a VNS implant for the treatment of lifelong generalizedseizures.PSG TECHNICAL FINDINGSThe patient’s respirations indicated moderate sleep disorderedbreathing with an overall AHI of 21 events per hour in all sleeppositions and sleep stages. The rapid eye movement (REM)index was in the moderate category at 24. There were 128 apneasand hypopneas. Mean SaO2 during the study was 95 percentwith a nadir of 84 percent. Snoring was mild and was subjectivelyrated at three on a scale from one to 10.The patient’s EKG showed normal sinus rhythm with a heartrate range from 68 to 96 beats per minute. Periodic leg movementswith or without arousal and the spontaneous arousal indexwere all insignificant.Sleep efficiency was good at 92 percent; REM sleep and slowwave sleep constituted 21 percent and 7 percent of the total sleeptime, respectively. REM latency was 90 minutes, and the firstREM period lasted 22 minutes.The tech who ran the study sent a note to the interpretingphysician about his suspicions regarding the timing of the apneas,which occurred approximately every four minutes. He didnot understand the role of the VNS but believed that the timingof the events coincided with the stimulation of the device.PHYSICIAN’S IMPRESSIONThere is evidence of moderate OSA with an AHI of 21 eventsper hour and desaturations as low as 84 percent. Recommendreturning for a titration study for treatment with positive airwaypressure. Elevation of head of bed, positional therapy, weightloss, ENT evaluation and elimination of sedatives and hypnotics,if applicable, are other potential treatment options. There is noevidence of significant periodic limb movement disorder. EKGis NSR. Sleep efficiency is normal.FolloW-UP TESTINGThe patient returns to the sleep center for PAP titration. Onthe 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 offPAP TECHNICAL FINDINGS:See Figure 3. The patient’s respirations without nasal CPAPand VNS turned off showed insignificant sleep disorderedbreathing with an AHI of 3.9 in all sleep stages. With CPAPapplication and the VNS turned on, the respirations were stabilizedwith an optimal nasal CPAP pressure of 7 cm H2O. At thispressure, the AHI was reduced from 24 to 3.7.Mean SaO2 at the optimal nasal CPAP pressure was 96 percentwith a nadir of 88 percent. Sleep efficiency was 88 percent.REM sleep and slow wave sleep constituted 17 percent and threepercent of total sleep time, respectively. REM latency was 101minutes, and the first REM period lasted 33 minutes.Since this patient required the VNS for seizure control, shewas placed on CPAP of 7 cm H2O. With education and desensitization,this patient has done very well with PAP therapy.A 2Zzz 19.4 | December 2010

– Titration first to eliminate SDB– Period of Testing with VNS On vs. Off on PAP– VNS Off and PAP Off15VNS On/PAP On ↑ VNS Off ↑VNS ON ↑ VNS Off/PAP OffFigure 3. PAP technical findings.PAP TECHNICAL FINDINGS:CONCLUSIONThe patient's respirations WITHOUT nasal 3. CPAP Malow AND BA, Edwards VNS TURNED J, Marzec M, OFF Sagher showed O, Fromes G.Patients undergoing INSIGNIFICANT VNS placement are at sleep risk for disordered developing breathing Effects with of an vagus AHI nerve of 3.9 stimulation in all sleep on respiration stages. With duringOSA related to the VNS CPAP and application should therefore and be the screened V NS clinicallyfor the presence optimal of OSA after nasal the CPAP procedure. pressure There is of some 7cm H2O. At this pressure, the apnea/hypopnea index wasTURNED ON, sleep: the a pilot respirations study. Neurology. were stabilized 2000 Nov 28;55(10):1450-4.with an4. Hsieh T, Chen M, McAfee A, Kifle Y. Sleep-relatedevidence that screening reduced for sleep to disordered 3.7/hr. The breathing previous in patients study, with the breathing VNS TURNED disorder in children ON showed with vagal nerve stimulators.with a seizure disorder MODERATE who are undergoing sleep a VNS disordered implant breathing may with Pediatr an AHI Neurol. of 2008 24/hr. Feb;38(2):99-103.be important because adequate treatment of previously undiagnosedand untreated SDB may likely result in better seizure 5. Marzec M, Edwards J, Sagher O, Fromes G, Malowcontrol. 6 CPAP therapy The is mean a viable SaO2 therapeutic at the option optimal for patients nasal CPAP pressure was 96 % with a nadir of 88 %. TheBA. Effects of vagus nerve stimulation on sleepwho develop OSA related Sleep to Efficiency the VNS, and was other 88 options %. REM include sleep and Slow related Wave breathing sleep in epilepsy constituted patients. 17 Epilepsia. % and 3 2003 % ofincreasing the cycle length the Total or stimulation Sleep Time, frequency respectively. of the device.With an increase period in the lasted number 33 of minutes. patients undergoing theThe REM Jul;44(7):930-5. Latency was 101 minutes and the first REMprocedure, as well as multiple indications for use, awareness of 6. Vaughn BV, D’Cruz OF, Beach R, Messenheimer JA.this causation is important for appropriate diagnosis and treatmentof OSA related to vagal nerve stimulators.obstructive placed sleep on CPAP apnoea. of Seizure. 7 cmH20. 1996 Mar;5(1):73-8. WithImprovement of epileptic seizure control with treatment ofSince this patient required the VNS for seizure control, she waseducation and desensitization, this patient has done very well with PAP therapy.REFERENCESEditor’s Note: Ms. Campo presented the lecture, “Vagal NerveNext is a ten-minute epoch of yet another young patient (13 y/o male w/ treatment resistant epilepsy, mildStimulator: A Sleep Center Case Study,” June 6, 2010, during the1. Cerebral St. Louis Palsy, Children’s autism, Hospital s/p [Internet]. T&A) with Vagal VNS. nerve In this instance, Topics for the the technician Advanced Practitioner is reporting course “periodic at the AAST limb 32ndmovements” stimulation. c2010 (again [cited in purple) 2010 Aug that 08]. are, Available in fact, from: artifact from Annual the Meeting VNSin showing San Antonio, up Texas. in the leg channels as 60http://www.stlouischildrens.org/content/medservices/Hz.VagalNerveStimulation.htm.2. Epilepsy Foundation [Internet]. Vagal nerve stimulationtherapy. c2010 [cited 2010 Aug 08]. Available from:http://www.epilepsyfoundation.org/answerplace/Medical/treatment/VNS/.A 2Zzz 19.4 | December 2010