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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
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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.
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–
–
–
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 theleg 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