Note: Descriptions are shown in the official language in which they were submitted.
71087-215
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~ETI~OD AND S~ST~H POP~
TREATI~ENT OF SLEEP APNEA
TEClU~IaL F~
This invention relates to a method and system
for maintaining upper airway patency in human patients
by stimulating those nerves which activate the patient's
upper airway muscles.
BA~KGRo~g ~RT
Sleep-apnea ~yndrome is a medical condition
characterized by daytime hypersomnolence, morning
headaches, intellectual deterioration, cardiac arrhyth-
mias, snoring and thrashing during sleep. It is caused
by frequent episodes of apnea during the patient's
sleep. The syndrome is classically subdivided into two
types. One type, termed ~central sleep apnea syndrome~,
is char~cterized by repeated loss of respiratory effort.
The second type, termed ~obstructive sleep apnea
syndromen, is characterized by repeated apneic episodes
during sleep resulting from obstruction of the patient's
upper airway or that portion of the patient's respira-
tory tract which is cephalad to, and does not include,the larynx.
Treatment thus far i~cludes var~ous medical,
surgical and physical measures. Medical measures
include the use of medications such as protriptyline,
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medroxyprogesterone, acetazolamide, theophylline,
nicotine and other medications in addition to avoidance
of central nervous system depressants such as sedatives
or alcohol. The medical measures above are sometimes
helpful but are rarely completely effective. In
addition, the medications frequently have distressing
and sometimes dangerous side effects.
Surgical means have included uvulopalatophar-
yngoplasty, tonsillectomy, surgery to correct severe
retrognathia and tracheostomy. These procedures may be
effective but the risk of surgery in these patients can
be prohibitive and the procedures are often unacceptable
to these patients.
Physical measures have included weight loss,
lS naso-pharyngeal airways, nasal CPAP and various tongue
retaining devices used nocturnally. These measures may
be partially effective but are cumbersome, uncomfortable
and patients often will not continue to use these for
prolonged periods of time. Weight loss may be effective
but is rarely achieved by these patients.
In patients with central sleep apnea syndrome,
phrenic nerve or diaphragmatic pacing has been used.
Phrenic nerve or diaphragmatic pacing includes the use
of electrical stimulation to regulate and control the
patient's diaphragm which is innervated bilaterally by
the phrenic nerves to assist or support ventilation.
This pacing is disclosed in Direct Diaphragm Stimulation
by J. Mugica et al. PACE Vol. 10 Jan-Feb. 1987, Part II,
Preliminary ~est of a Muscular Diaphraqm Pacinq Svstem
on Human Patients by J. Mugica et al. from Neurostimula-
tion: An Overview lg85 pp. 263-279 and Electrical
Activation of Respiration by Nochomovitez IEE Eng. in
Medicine and Biology, June, 1983.
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However, it was found that many of these
patients also have some degree of obstructive sleep
apnea which worsens when the inspiratory force is
augmented by the pacer. The ventilation induced by the
activation of the diaphragm also collapses the upper
airway upon inspiration and draws the patient's tongue
anteriorly down the throat choking the patient. These
patients then require tracheostomies for adequate
treatment.
A physiological laryngeal pacemaker as
described in Physioloqical Laryngeal Pacemaker by ~.
Kaneko et al. from Trans Am Soc Artif Intern Organs 1985
senses volume displaced by the lungs and stimulates the
appropriate nerve to open the patient's glottis to treat
dyspnea. This apparatus would not be effective for
treatment of sleep apnea. The apparatus produces a
signal proportional to the displaced air volume of the
lungs and thereby the signal produced is too late to be
used as an indicator for the treatment of sleep apnea.
There is often no displaced air volume in sleep apnea
due to obstruction.
The only measure which is completely effective
in obstructive sleep apnea is tracheostomy, however,
this operation carries considerable morbidity and is
aesthetically unacceptable to many patients.
DISCLOSURE OF INVENTION
An object of the present invention is to
provide a method and system for effective treatment of
sleep apnea syndrome which is acceptable to patients in
terms of aesthetics and comfort and avoids use of
pharmacological measures or tracheostomy.
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In carrying out the above objects, the method
for treatment of sleep-apnea syndrome comprises
monitoring inspiratory effort and generating electri al
signals in response to the step of monitoring in order
to stimulate those nerves which activate the patient's
upper airway muscles to contract in order to maintain
upper airway patency. The upper airway muscles include
one or more in the group comprising geniohyoid,
genioglossus, digastric, stylopharyngei or mylohyoid.
In one embodiment of the invention, monitoring
inspiratory effort includes monitoring contraction of
the patient's inspiratory muscles. The inspiratory
effort monitored is analyzed by comparing the contrac
tion of the patient's inspiratory muscles to a predeter-
mined threshold contraction. Then an electrical signal
is generated as necessary at the appropriate instant
during the respiratory cycle to activate those muscles
that move the patient's tongue anteriorly and maintain
upper airway patency. At the same time, inspiration can
be stimulated if necessary or inspiration alone can be
stimulated by causing the diaphragm and other accessory
muscles such as the sternomastoid muscles to contract
when no inspiratory effort is sensed by the mbnitor.
In another embodiment of the inve~tion,
monitoring inspiratory effort includes monitoring
intrathoracic pressure. The measured intrathoracic
pressure measured is compared to a predetermined
threshold of intrathoracic pressure and as necessary
electrical signals are generated at the appropriate
instant during the respiratory cycle to activate those
muscles that move the patient's tongue anteriorly to
maintain upper airway patency. At the same time,
inspiration can ~e stimulated if necessary or inspira-
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tion alone can be stimulated by causing the diaphragm
and other accessory muscles such as the sternomastoid
muscles to contract when no inspiratory effort is sensed
by the monitor.
A system for treatment of sleep-apnea syndrome
in a patient comprises a monitor capable of monitoring
inspiratory effort, and an electrical signal generating
mechanism coupled to the monitor for generating
electrical signals to effect those nerves which activate
the patient's upper airway muscles to contract as
necessary to thereby maintain upper airway patency.
In a preferred embodiment of the invention,
upper airway muscle activity is sensed and if normal
activity is sensed, the release of electrical signals is
inhibited.
The system further includes a sensor lead
having first and second ends. The first end is
connected to the monitor and the second end includes a
sensor electrode for gathering information from the
inspiratory muscles and for transmitting the information
gathered along the lead to the monitor. An effector
lead having first and second ends is connected to the
signal generating mechanism by the first end. The
second end includes an effector electrode which
transmits electrical signals generated by the electrical
signal generating mechanism to those nerves which effect
the upper airway muscles. The effector lead can also be
connected to the monitor to sense action potentials in
those nerves which innervate those muscles which
maintain upper airway patency.
In one embodiment of the invention, the
monitor monitors contraction of the patient~s in-
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spiratory muæcles. In a second embodiment of the
invention, the monitor monitors intrathoracic pressure.
In the preferred embodi~ent of the invention,
the electrical signal generating mechanism is program-
mable with respect to voltage, current, pulse width andfrequency of pulse emission.
The objects, features, and advantages of the
present invention are readily apparent from the
following detailed description of the best mode for
lo carrying out the invention when taken with the accom-
panying drawings.
BRIEF DESCRIPTION OF T~IE D~AWINGS
Figure 1 is a cutaway view of a patient shown
having a system for treatment of sleep apnea constructed
in accordance with the present invention implanted
subcutaneously and illustrating an electrical pulse
generating device implanted in the pectoral region, a
sensor electrode for sensing diaphragm action potential
and an effector electrode for stimulating contraction of
upper airway muscles;
Figures 2 is a cutaway view of the patient
shown in Figure 1 illustrating a combined sensor~effec-
tor electrode for sensing and stimulating contraction of
upper airway muscles;
Figure 3 is a cutaway view similar to Figure 1
illustrating the sensor electrode connected to a
pressure transducer located in the pleural space;
Figure 4 is a cutaway view similar to Figure 1
illustrating sensor/effector electrodes implanted in
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both hemi-diaphragms and an additional effector
electrode located in the upper airway:
Figure S is a cutaway view similar to Figure l
illustrating sensor and effector electrodes attached
about the cervical portion of the phrenic nerve; and
Figure 6 is a flow diagram illustrating steps
defining thP method of the current invention.
BEST MODE FOR CARRYING OU~ THE INVENTION
Referring to Figures 1-5 of the drawings, a
system for treatment of sleep apnea assembled in
accordance with the present invention is generally
indicated by reference numeral 10 as is used to monitor
respiratory effort and generate electrical signals in
response to the monitoring as necessary to stimulate
nerves which activate a patient's upper airway muscles
to contract in order to maintain upper airway patency.
As illustrated in Figure 1, the system 10
comprises a monitor 14 capable of monitoring inspiratory
effort. Monitor 14 is shown connected by lead 18 having
first and second ends 20,22 to a sensor electrode 24
located in the diaphragm region. Sensor electrode 24
detects action potential in the diaphragm and transmits
that information to the monitor 14. An electrical
signal generating mechanism 16 implanted subcutaneously,
preferably in the right subclavian or pectoral area is
coupled to the monitor 14 and generates electrical
signals after interpreting input from the sensor
electrode 24.
An effector lead 26 having first and second
ends 28, 30 includes an effector electrode 32 at its
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second end. The effector electrode 32 is implanted into
or around one or several motor nerves which are
responsible for stimulating the respective upper airway
muscles or alternatively in or around the upper airway
muscles. These muscles which include the geniohyoid,
genioglossus, digastric, stylopharyngei or mylohyoid
when stimulated contract and in contracting maintain
patency of the oro-pharyngeal and/or naso-pharyngeal
airway.
The effector electrode 32 is coupled via
effector lead 26 to the generating mechanism 16 to
receive the electrical signal to effect these upper
airway muscles at the appropriate time during inspira-
tion and under similarly appropriate circumstances to
thereby maintain upper airway patency.
In a preferred embodiment of the invention,
the system 10 and the sensor electrode 24 is actuable to
act as an effector electrode to stimulate the in-
spiratory muscles if no inspiration is sensed by the
monitor.
In the preferred embodiment of the invention
shown in Figure 1, the effector electrode 24 is
connected to the genioglossus muscle or its respective
motor nerve to move the tongue anteriorly and thereby
prevent upper airway obstruction.
With reference to Figure 2 of the drawings,
the effector electrode 32 also serves as a second sensor
electrode to thereby sense activity in the upper airway
muscles while the patient is awake to send signals to
inhibit the electrical signal generating mechanism 16
from stimulating the upper airway muscles at inap-
propriate times. In this way the electrical signal
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generating mechanism 16 stimulates the effector
electrode 32 if the upper airway muscles 12 are detected
to be passive at the same time the inspiratory muscles
are detected to be active thus detection of a predeter-
mined level of action potential by the effector/sensorelectrode would have an inhibitory effect on the
electrical signal generating mechanism.
Figure 3 illustrates sensor electrode 24
including a pressure sensitive receptor 34 at its distal
end implanted into the thoracic cavity for monitoring
intrathoracic pressure. Comparison to a certain
predetermined threshold of negative pressure within the
thorax due to airway obstructions during active
inspiration triggers the electrical signal generating
mechanism 16 to stimulate the upper airway muscles to
create a patent airway.
As shown in Figure 4, two effector electrodes
32 have been implanted into the patient. The multiple
effector electrodes 32 stimulate various muscles in the
upper airway to maintain a patent upper airway simul-
taneously with stimulation of the diaphragm and other
accessory muscles for inspiration such as the sternomas-
toid muscles to cause inspiration at a predetermined
rate when no inspiratory effort is sensed by the monitor
14.
As shown in Figure 5, the sensor electrode 24
is placed around the cervical portion of the phrenic
nerve to detect action potentials in the phrenic nerve,
i.e. incipient inspiration. The electrical signal
generating mechanism 16 generates electrical signals
based on information obtained from the phrenic nerve to
maintain a patent airway in patients with obstructive
sleep-apnea syndrome. In this arrangement, the
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electrical signal generating mechanism 16 may also act
as a phrenic narve stimulator in patients with central
sleep-apnea syndrome.
As illustrated in Figure 6 and shown sequen-
tially in boxes numbered 40, 42, 44, 46, and 48, the
method for treatment of sleep-apnea syndrome in a
patient comprises the step of monitoring inspiratory
effort. Inspiratory effort can be monitored by
monitoring contraction of the diaphragm by electromyo
gram, sensing nerve conduction of the phrenic nerve,
i.e. monitoring action potentials, monitoring in-
trathoracic pressure change via a pressure transducer,
or by the use of an impedance pneumogram.
As shown in block 42, a voltage is produced
responsive to the inspiratory efforts monitored and the
pha~e of the respiratory cycle is identified. An
electrical signal is generated, box 44, in response to
the step of monitoring. As seen in box 46, those
electrical signals are transmitted to stimulate those
nerves which activate the patient's upper airway muscles
to contract in order to maintain upper airway patency.
Box 48 highlights a feature of the preferred embodiment
wherein upper airway muscle activity is sen~ed and the
release of electrical signals is inhibited if normal
upper airway activity is detected.
Operation of the Sys~em
The system 10 for treatment of sleep-apnea
syndrome monitors in~piratory effort and generates
electrical signals in response to the monitoring in
order to stimulate nerves which activate the patient's
upper airway muscles to contract in order to maintain
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upper airway patency. This is accomplished through the
various embodiments of the aforementioned system 10.
The monitor 14 detects inspiratory effort by
sensing action potentials in either the diaphragm or
phrenic nerve or by sensing negative pressure in the
thorax. The sensor electrode 24 which gathers this
information passes it along lead 18 to the electrical
signal generating mechanism 16 where that information is
analyzed against a predetermined threshold. If the
predetermined threshold is not met then an electrical
signal is released by the electrical signal generating
mechanism 16 and transmitted through lead 26 and
effector electrode 32 to stimulate those nerves that
effect those upper airway muscles which maintain upper
airway patency. Effector electrodes 32 are located in
the various upper airway muscles or around one or
several of the nerves which stimulate those muscles and
the effector electrode causes the muscles to contract
when an electrical signal is received.
Preferably, the electrical signal generating
mechanism 16 includes its own power supply such as a
battery, not shown, typically of the lithium iodine
type, batteries currently used in cardiac pacemakers.
The electrical signal generating mechanism 16 and
battery are enclosed in a hermetically sealed case with
one or more sockets for insertion o~ sensor and effector
leads 18,2~. Electrical signal generating mechanisms of
MEDTRONIC, models 3014 and 3128, are suitable for use
with the invention herein.
The sensor lead 18 conducts electrical signal
impulses between the electrical signal generating
mechanism 16 and various nerves or muscles. The sensor
lead 26 may be tunneled subcutaneously and the distal
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end of the sensor electrode 18 implanted into one of the
various inspiratory muscles, including but not limited
to the diaphragm, intercostal muscles, sternomastoid
muscles, or around the nerves responsible for stimula-
tion of those respiratory muscles~ The sensor electrode
18 serves as a sensor to detect when inspiratory effort
commences and may also serve as an effector electrode
for stimulating respiratory muscles in patients with
central sleep apnea.
lo The sensor and effector leads 18~26 may be
wires made of metal alloy to allow good conductivity.
The leads 18,26 should be fatigue resistant, may be
coiled to increase flexibility, and may be multi~iller
to provide redundancy within the lead. The wire must be
insulated with materials such as Silastic or poly-
urethane and only the metal electrode at the distal end
i6 actually exposed. Similar leads 18,26 are currently
used in cardiac pacemakers.
Most preferably, the effector electrode 32
effects the nerves which stimulate the genioglossus
muscle to move the tongue anteriorly and thus prevent
upper airway obstruction when an electrical signal is
received. The effector lead 26 can also include a
sensor to transmit a signal to the electrical signal
generating mechanism 16 to inhibit electrical signal
generation at any inappropriate times such as when the
patient is awake when normal genioglossus muscle action
potentials will be sensed by the device which will
inhibit the electrical signal generating mechanism 16.
Preferably, the electrical signal generating
mechanism 16 is a digital device which may be programm-
ed. The digital technology is used to create timing
circuits and programming circuits such that electrical
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impulses may be programmed to be transmitted at specific
times. This allows the electrical signal generating
mechanism 16 to discharge electrical signals at a
predetermined rate, for instance, for use in patients
with central sleep apnea, or in synchrony with in-
spiratory effort in patients with obstructive sleep
apnea. A programmable electrical signal generating
mechanism 16 may be programmed externally by the use of
pulsed magnetic fields or radio frequency signals
similar to those utilized in current cardiac pacemakers.
Preferably, metallic oxide semiconductor circuitry is
utilized such that the electrical signal generating
mechanism will operate at low energy levels and enhance
miniaturiæation.
While the best mode for carrying out the
invention has been described in detail, those familiar
with the art to which this invention relates will
recognize various alternative designs and embodiments
for practicing the invention as defined by the following
cl~i~s.
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