Servo muscle control

A method of and apparatus for controlling one or more parameters of an electrical stimulation generator in response to measured results of the stimulation. In the preferred mode, this technique is employed in a system for the treatment of obstructive sleep apnea. Sensors are used to determine the effectiveness of the stimulation. Amplitude and pulse width are modified in response to the measurements from the sensors.

CROSS REFERENCE TO CO-PENDING APPLICATIONS 
U.S. patent application Ser. No. 824,308, filed Jan. 23, 1992, and entitled 
"Improving Muscle Tone," now U.S. Pat. No. 5,158,080; and U.S. patent 
application Ser. No. 934,030, filed Aug. 24, 1992, and entitled "Multiple 
Stimulation Electrodes" are both assigned to the assignee of the present 
invention. 
BACKGROUND OF THE INVENTION 
1. Field of the Invention 
The present invention generally relates to electrical stimulation of 
muscles, and more particularly, relates to electrical stimulation of 
muscles for the treatment of a medical condition. 
2. Description of the Prior Art 
It has been known to electrically stimulate muscular contractions since the 
beginnings of experimentation with electricity. In more recent times, 
electrical stimulation of muscle tissue has been used therapeutically. The 
effects of chronic stimulation have been studied by Ciske and Faulkner in 
"Chronic Electrical Stimulation of Nongrafted and Grafted Skeletal Muscles 
in Rats", in Journal of Applied Physiology, Volume 59(5), pp. 1434-1439 
(1985). Bernotas et al., have even suggested the rudiments of adaptive 
control in "Adaptive Control of Electrically Stimulated Muscle", in IEEE 
Transactions on Biomedical Engineering, Volume BME-34, No. 2, pp. 140-147, 
(February 1987). 
A review of early attempts at electrical stimulation associated with the 
respiratory system is found in "Diaphragm Pacing: Present Status", by 
William W. L. Glenn, in Pace, Volume pp. 357-370, (July-September 1978). 
Much work has been done in electrical stimulation within the 
cardiovascular system by way of cardiac pacing. 
Treatment of obstructive sleep apnea using electrical stimulation has also 
been discussed. "Laryngeal Pacemaker, II Electronic Pacing of Reinnervated 
Posterior Cricoarytenoid Muscles in the Canine", by Broniatowski et al, in 
Laryngoscope, Volume 95, pp. 1194-1198 (October 1985); "Assessment of 
Muscle Action on Upper Airway Stability in Anesthetized Dogs", by Strohl 
et al., in Journal of Laboratory Clinical Medicine, Volume 110, pp. 
221-301, (1987); U.S. Pat. No. 4,830,008 issued to Meer; and U.S. Pat. No. 
4,570,631 issued to Durkan all discuss electrical stimulation of the upper 
airway to treat obstructive sleep apnea. 
SUMMARY OF THE INVENTION 
The present invention overcomes the disadvantages of the prior art by 
providing a system for the electrical stimulation of muscle tissue, which 
is adaptive in nature. Sensors are employed within the stimulation system 
to modify parameters such as stimulation pulse amplitude and pulse 
frequency in response to the sensed performance of the therapy desired. 
In the preferred mode, the present invention is applied to the treatment of 
obstructive sleep apnea. Sensors are employed to determine the pressure 
differential between the distal pharynx and the ambient to determine the 
pressure drop across the upper airway. Stimulation intensity is increased 
as the relative pressure differential increases, and decreased as the 
relative pressure differential decreases. Intensity may be increased by 
increased pulse frequency and/or pulse amplitude. Additional sensing is 
required to accommodate the respiration cycle, permitting the system to 
adapt independent of the normal cyclic variations. 
There are a number of important results attendant to the adaptive system. 
The total energy required is lessened, because the stimulation intensity 
is maintained at only that level necessary to sustain the desired clinical 
performance. The risk of muscle fatigue is greatly reduced because the 
muscles of the upper airway are not over stimulated. Similarly, the lack 
of over stimulation provides the patient with a more easily tolerated 
therapy, particularly when used chronically.

DETAILED DESCRIPTION OF THE PREFERRED EMBODIMENTS 
FIG. 1 is a schematic diagram of the respiratory system of patient 10 
during inspiration. As a result of diaphragm 18 increasing the volume of 
thorax 16 a pressure differential is created causing air to enter upper 
airway 12 and proceed in the direction of arrow 14. 
FIG. 2 is a schematic diagram of the respiratory system of patient 10 
during an obstructive apnea event. During inspiration, upper airway 12 
tends to collapse producing the obstruction to air flow at point 21. The 
above-referenced literature describes in detail the physiological 
processes associated with the collapse of upper airway 12. 
FIG. 3 is a graphical representation 52 of airway conductance 54 as a 
function of stimulation frequency 56 in patient 10 suffering from 
obstructive sleep apnea. At single twitch (57) or relatively low level 
stimulation frequency 59, airway conductance 54 is insufficient as shown 
along the corresponding portions of the curve. Single twitch and low 
frequency stimulation do not sustain conductance change (i.e., sufficient 
tension) and result in tension plateaus which are too low to maintain an 
open airway. Normal patency is airway conductance between levels 64 and 
66. To achieve normal patency, stimulation frequency must be at least as 
point 61. 
For stimulation frequency greater than that for normal patency (i.e. airway 
conductance 54 of greater than level 64), very little improvement can be 
observed. Portion 60 of the curve represents this state. As the system 
proceeds along portion 60, stimulation frequency is excessive resulting in 
wasted energy and increased risk of muscle fatigue. 
FIG. 4 is a schematic diagram of patient 10 showing implantation of an 
electrical stimulation system for the treatment of obstructive sleep 
apnea. Implantable pulse generator 20 is placed subcutaneously at a 
convenient position. The operation of diaphragm 18 is monitored by 
electrode 24 coupled to lead 22. 
Patency of upper airway 12 is monitored by pressure sensor 36 and pressure 
sensor 30 coupled to implantable pulse generator 20 via cables 34 and 32, 
respectively. Stimulation of the musculature of upper airway 12 is 
accomplished via lead 26 coupled to electrode 28. All other referenced 
elements are as previously described. 
FIG. 5 is a plan view of a chronically implantable pressure transducer 40 
similar to that implanted as pressure sensors 30 and 36 (see also FIG. 4). 
Distal end 42 of chronically implantable pressure transducer 40 contains a 
semiconductor sensing element properly package for chronic implantation. 
Lead body 44 optionally contains pressure reference lumen 46, which is 
coupled to pressure vent 48. Electrical connector 50 couples to 
implantable pulse generator 20. For additional construction details, the 
reader may consult U.S Pat. No. 4,407,296 issued to Anderson incorporated 
herein by reference. 
FIG. 6 is a block diagram of implantable pulse generator 20 made in 
accordance with the present invention. Cables 32 and 34, coupled to 
pressure sensors 30 and 36, respectively, provide the inputs to 
differential amplifier 68. The output of differential amplifier 68 is thus 
representative of the pressure differential between the pharynx and the 
mouth (see also FIG. 4). 
The pressure difference signal is integrated by integrator 70 to provide a 
smooth signal. The signal is clipped by clipper circuit 72 to scale the 
signal. Detector 74 is a thresholding device. The output of detector 74 is 
essentially a binary feedback signal 76 indicative of whether upper airway 
12 has sufficient patency. Binary feedback signal 76 is used to control 
pulse frequency control 78. In this way, the pulse frequency of the 
stimulation pulses is continually increased until sufficient patency is 
monitored. Pulse frequency control 78 may also change output amplitude of 
the stimulation pulses. The stimulation pulses are produced by stimulation 
generator 80, amplified by amplifier 82, and coupled to the upper airway 
musculature by amplifier 82. 
The stimulation pulses generated are timed in accordance with the 
respiration cycle by timing 84. This circuit also notifies clipper circuit 
72 of the time window in which patient 10 is within an inspiration cycle. 
Timing 84 operates by drive from oscillator 86, which is the main timing 
standard within implantable pulse generator 20. 
The position within the respiration cycle is monitored by electrode 24 
coupled to lead 22 (see also FIG. 4). Other means can also be used to 
sense inspiration, such as impedance plethysmography. In the preferred 
mode, it is the EMG which is actually sensed. The EMG is amplified by 
amplifier 90 and integrated by integrator 92. This smooths the signal 
considerably. The integrated signal is supplied to trigger 88, which is a 
thresholded monostable multivibrator. The output of trigger 88 is a fixed 
length signal having a leading edge occurring at the initiation of an 
inspiration cycle. As explained above, timing 84 synchronizes the output 
of trigger 88 with the output of oscillator 86 and provides time windows 
to clipper circuit 72 and stimulation generator 80. 
FIG. 7 is a graphical representation 94 of various key signals of 
implantable pulse generator 20. Curve 96 shows the pressure differentials 
to be monitored for two respiratory cycles wherein the first cycle 
involves a substantial obstruction within upper airway 12, and the second 
cycle shows normal patency as a result of electrical stimulation of 
sufficient intensity. Portion 98 of curve 96 is the pressure differential 
resulting from inspiration with an obstructed upper airway. 
Pressure differential 106 follows null period 104. Pressure differential 
106 shows inspiration under normal patency because the stimulation 
intensity has been increased. 
Pulses 112 and 114 are the output of trigger 88 (see also FIG. 6). They 
provide the timing window associated with the inspiration portion of the 
respiratory cycle. Stimulation pulses 116, 118, 120, 122, 124, and 126 are 
supplied during the first inspiration. As seen above, the frequency of 
these stimulation pulses is insufficient to produce normal patency of the 
upper airway. The feedback system ensures that the pulse frequency of 
succeeding stimulation pulses 128, 129, 130, 131, 132, 133, 134, 135, 136, 
137, 138, and 139 is greater. In this case, the stimulation frequency is 
sufficient to produce normal patency as is seen in pressure differential 
106. 
Curve 140 shows the output of integrator 92 (see also FIG. 6). It is from 
curve 140 that trigger 88 generates pulses 112 and 114. Peaks 142 and 152 
correspond to the inspiration periods. Similarly, negative peaks 146 and 
156 correspond to the expiration periods. Null periods 144, 148, and 154 
separate portions of the respiratory cycle. Note that slope 150 will be 
effected by the increase in stimulation intensity from respiratory cycle 
one to respiratory cycle two. 
Having thus described the preferred embodiments of the present invention, 
those of skill in the art will readily appreciate the other variations 
possible within the teachings found herein and within the scope of the 
claims hereto attached.