FIELD OF INVENTION
This application is a continuation of application Ser. No. 11/035,374 filed Jan. 13, 2005, entitled “Method and system for providing electrical pulses for neuromodulation of vagus nerve(s) using rechargeable implanted pulse generator”, which is a continuation of application Ser. No. 10/841,995 filed May 8, 2004, which is a continuation of application Ser. No. 10/196,533 filed Jul. 16, 2002, which is a continuation of application Ser. No. 10/142,298 filed on May 9, 2002. The prior applications being incorporated herein in entirety by reference, and priority is claimed from these applications.
This invention relates generally to electrical stimulation therapy for medical disorders, more specifically to providing electrical pulses for neuromodulation therapy for obesity and other medical disorders, by selectively modulating sympathetic nervous system with rechargeable implantable pulse generator.
Obesity is a significant health problem in the United States and many other developed countries. Obesity results from excessive accumulation of fat in the body. It is caused by ingestion of greater amounts of food than can be used by the body for energy. The excess food, whether fats, carbohydrates, or proteins, is then stored almost entirely as fat in the adipose tissue, to be used later for energy. Obesity is not simply the result of gluttony and a lack of willpower. Rather, each individual inherits a set of genes that control appetiete and metabolism, and a genetic tendency to gain weight that may be exacerbated by environmental conditions such as food availability, level of physical activity and individual psychology and culture. Other causes of obesity include psychogenic, neurogenic, and other metabolic related factors.
Obesity is defined in terms of body mass index (BMI), which provides an index of the relationship between weight and height. The BMI is calculated as weight (in Kilograms) divided by height (in square meters), or as weight (in pounds) times 703 divided by height (in square inches). The primary classification of overweight and obesity relates to the BMI and the risk of mortality. Obesity has reached epidemic proportions globally. In the U.S., it is estimated that 64% of adults are overweight or obese, and 4.7% or 14-16 million Americans are morbidly obese (BMI≦40 Kg/m2). Furthermore, the number of overweight adolescents is also rapidly increasing.
Treatment of obesity depends on decreasing energy input below energy expenditure. Treatment has included among other things various drugs, starvation and even stapling or surgical resection of a portion of the stomach. Surgery for obesity has included gastroplasty and gastric bypass procedure. Gastroplasty which is also known as stomach stapling, involves constructing a 15- to 30 mL pouch along the lesser curvature of the stomach. A modification of this procedure involves the use of an adjustable band that wraps around the proximal stomach to create a small pouch. Both gastroplasty and gastric bypass procedures have a number of complications.
Advantageously, electrical pulse therapy can be safely provided by delivering electrical pulses to the parasympathetic nerves such as the vagus nerve(s) or the sympathetic nerves such as the splanchnic nerves (or greater splanchnic nerve).
In commonly assigned disclosures Ser. No. 10,079,21 now U.S. Pat. No. ______, and U.S. Pat. No. 6,611,715 B1 (Boveja) electrical pulsed neuromodulation therapy for obesity and other medical conditions is provided by delivering electrical pulses to the parasympathetic nerves such as the vagus nerve(s). Therapeutic effects on obesity may also be achieved by providing electrical pulses (or modulating) the sympathetic nervous system. The apparatus disclosed in U.S. Pat. No. 6,611,715 B1 (Boveja) can also be used in neuromodulating the sympathetic nervous system, of course the stimulating electrodes would by placed on the splanchnic nerves or celiac ganglia (as shown in FIGS. 8, 10A, 10C and 10D) instead of vagal nerve(s) as shown in FIGS. 8 and 9. Further, instead of an inductively coupled system, an implantable pulse generator (IPG) may also be used. If an IPG is used, a particularly useful form would be a rechargeable implantable pulse generator (RIPG), as disclosed herein. Therefore, in the current disclosure the beneficial effects for obesity therapy are achieved by providing electrical pulses to vagus nerve(s) (parasympathetic) or sympathetic nerves such as splanchnic nerves, or greater splanchnic nerve or celiac ganglion, or plexus in the region, utilizing a rechargeable implantable pulse generator.
The rationale for this is shown in conjunction with FIG. 1A, the gastrointestinal tract (gut) and central nervous system (CNS) engage each other in two-way communication. The CNS is informed of the state of the gastrointestinal tract by afferent neurons, and is able to control or modulate digestive function through efferent neurons that are part of the autonomic nervous system. The major pathways for communication between the brain and gut are the vagal, splanchnic, and sacral nerve trunks; all three contain both afferent and efferent nerve fibers.
- Background of Gastrointestinal (GI) Tract and its Sympathetic and Parasympathetic Control
In the Applicant's U.S. Pat. No. 6,611,715 B1 electrical pulses are provided to the vagal pathway as shown in conjunction with FIG. 1B. Therapy for obesity can also be provided by delivering electrical pulses to the splanchnic pathways as shown in conjunction with FIG. 1C.
Shown in conjunction with FIG. 2, the gastrointestinal (GI) tract is a continuous muscular digestive tube that winds through the body. The organs of the GI tract are the mouth, pharynx (not shown), esophagous 3, stomach 5, small intestine (duodenum 7, jejunum, and ileum), and large intestine (cecum, ascending colon, transverse colon, and descending colon).
The gastrointestinal tract has a nervous system all its own called the enteric nervous system 20. This is shown in conjunction with FIG. 3A. It lies entirely in the wall of the gut, beginning in the esophagus 3 and extending all the way to the anus. The number of neurons in this enteric system is about 100 million, almost exactly equal to the number in the entire spinal cord. It especially controls gastrointestinal movements and secretion.
As depicted in conjunction with FIG. 3B, the enteric nervous system 20 is composed mainly of the two plexuses, 1) the myenteric plexus 21, which is the outer plexus lying between the longitudinal and circular muscle layers, and 2) the submucosal plexus 23 that lies in the submucosa. The nervous connection within and between these two plexuses are shown in FIG. 3A. The myenteric plexus 21 controls mainly the gastrointestinal movements, and the submucosal plexsus 23 controls mainly gastrointestinal secretion and local blood flow. As is depicted in FIG. 3A, the sysmpathetic 26 and parasympatheic 25 fibers connect with the myenteric 21 and the submocosal 23 plexus. Although the enteric nervous system can function on its own, stimulation by the parasympathetic and sympathetic systems can further activate or inhibit gastrointestinal functions. The autonomic nerves influence the functions of the gastrointestinal tract by modulating the activities of neurons of the enteric nervous system.
Sympathetic innervation of the gastrointestinal (GI) tract is mainly via postganglionic adrenergic fibers whose cell bodies are located in pre-vertebral and parabertabral ganglia. The celiac, superior and inferior mesenteric, and hypogastric plexus provide sympathetic innervation to various segments of the GI tract. Activation of the sympathetic nerves usually inhibits the motor and secretory activities of the GI system.
Parasympathetic innervation of the GI tract down to the level of the transverse colon is provided by branches of the vagus nerves (10th cranial nerve). Excitation of parasympathetic nerves usually stimulates the motor and secretory activities of the GI tract.
- Regulation in Stomach and Small Intestines
Additionally in terms of reflex control, shown in conjunction with FIG. 4, are local and central reflex pathways in the GI system. The afferent fibers in the GI tract provide the afferent limbs of both local and central reflex arcs. Chemoreceptor and mechanoreceptor endings are present in the mucosa and muscularis externa. The complex afferent and efferent innervation of the gastrointestinal tract allows for fine control of secretory and motor activities by intrinsic and extrinsic reflex arcs.
The stomach 5 (shown in FIG. 5) is richly innervated by extrinsic nerves and by the neurons of the enteric nervous system. Axons from the cells of the intramural plexus innervate smooth muscle and secretory cells.
Parasympathetic innervation to the stomach 5 is also supplied by the vagus nerves, while sympathetic innervation to the stomach is provided by the celiac plexus. In general, parasympathetic nerves stimulate gastric smooth muscle motility and gastric secretions, whereas sympathetic activity inhibits these-function. Numerous sensory afferent fibers leave the stomach in the vagus nerves; some of these fibers travel with sympathetic nerves. Other sensory neurons are the afferent links between sensory receptors and the intramural plexuses of the stomach. Some of these afferent fibers relay information intragastric pressure, gastric distention, intragastric pH, or pain.
When a wave of esophageal peristalsis begins, a reflex causes the LES to relax. This relaxation of the LES is followed by receptive relaxation of the fundus and body of the stomach 5. The stomach 5 will also relax if it is filled directly with gas or liquid. The nerve fibers in the vagi are a major efferent pathways for reflex relaxation the stomach 5.
The emptying of gastric contents is regulated by both neural and hormonal mechanisms. The duodenal and jejunal mucosa contain receptors that sense acidity, osmotic pressure, certain fats and fat digestion products, and peptides and amino acids This is depicted in FIG. 6. The chyme that leaves the stomach is usually hypertonic and it becomes even more hypertonic because of the action of the digestive enzymes in the duodenum. Gastric emptying is slowed by hypertonic solutions in the duodenum, by duodenal pH below 3.5, and by the presence of amino acids and peptides in the duodenum, The presence of fatty acids or monoglycerides (products of fat digestion) in the duodenum also dramatically decreases the rate of gastric emptying.
Shown in conjunction with FIG. 7, contraction of the visceral organ smooth muscle occurs when the depolarization caused by the slow wave exceeds a threshold for contraction. When depolarization of a slow wave exceeds the electrical threshold, a burst of action potentials 29 occurs. The action potentials 29 elicit a much stronger contraction than occurs in the absence of action potentials. The contractile force increases with increasing number of action potentials 29.
In most other excitable tissues, the resting membrane potential remians rather constant. In gastrointestinal smooth muscle, the resting membrane potential characteristically varies or oscillates, this is depicted in FIG. 7. These oscillations are slow waves, which is the basic electrical rhythm. The frequency of slow waves varies from about 3 per minute in the stomach to about 12 per minutes in the duodenum.
Slow waves are generated by interstitial cells. These cells are located in a thin layer between the longitudinal and circular layers of the muscularis externa. Interstitial cells have properties of both fibroblasts and smooth muscle cells. Their long processes form gap junction with longitudinal and circular smooth muscle cells. These gap junctions enable the slow waves to be conducted rapidly to-both muscle layers. Because gap junctions electrically couple the smooth muscle cells of both longitudinal and circular layers, the slow wave spreads throughout the smooth muscle of each segment of the gastrointestinal tract.
The amplitude and, to a lesser extent, the frequency, of the slow waves can be modulated by the activity of intrinsic and extrinsic nerves and by hormones and paracrine substanes. In general, sympathetic nerve activity decreases the amplitude of the slow waves or ablolshes them completely, wheras stimulation of parasympathetic nerves increases the size of the slow waves.
If the peak of the slow wave exceeds the cell's threshold to fire action potentials, one or more action potentials may be triggered during the peak of the slow wave (FIG. 7) The action potentials enhance contractile force of the smooth muscle.
Action potentials: Action potentials in gastrointestinal smooth muscle are more prolonged (10 to 20 msec) than those of skeletal muscle and have little or no overshoot. The rising phase of the action potentials is caused by ion flow through channels that conduct both Ca++ and Na+ and are relatively slow to open. Ca++ that enters the cell during the action potential helps to initiate contraction.
When the membrane potential of gastrointestinal smooth muscle reaches the electrical threshold, typically near the peak of a slow wave, a train of action potentials (1 to 10/sec) is fired (FIG. 7). The extent of depolarization of the cells and the frequency of action potentials are enhanced by some hormones and paracrine agonists and by compounds liberated from excitatory nerve endings. Inhibitory hormones and neuroeffector substances hyperpolarize the smooth muscle cells and may diminish or abolish action potential spikes.
Slow waves that are not accompanied by action potentials elicit weak contractions of the smooth muscle cells (FIG. 7). Much stronger contractions are evoked by the action potentials that are intermittently triggered near the peaks of the slow waves. The greater the frequency of action potentials that occur at the peak of a slow wave, the more intense is the contraction of the smooth muscle. Because smooth muscle cells contract rather slowly (about one tenth as fast as skeletal muscle cells), the individual contraction caused by each action potential in a train do not cause distinct twitches; rather, they sum temporally to produce a smoothly increasing level of tension (FIG. 7).
Between trains of action potentials the tension developed by gastrointestinal smooth muscle falls, but not to zero. This nonzero resting, or baseline, tension of smooth muscle is the tone. The tone of gastrointestinal smooth muscle is altered by neuroeffectors, hormones, paracrine substances, and drugs.
- Obesity Therapy and Neuromodulation
Control of the contractile and secretory activities of the gastrointestinal tract involves the central nervous system, the enteric nervous system, and hormones and paracrine substances. The autonomic nervous system typically only modulates the patterns of muscular and secretory activity; these activities are controlled more directly by the enteric nervous system.
Shown in conjunction with FIG. 8, electrical pulsed therapy for obesity can be provided by either neuromodulating selected parts of sympathetic system 26 or selected parts of parasympathetic system 25 (via the vagus nerve). Neuromodulation in this disclosure includes, stimulation, selective stimulation of branches, blocking of nerve impulse, selective blocking of certain types of fibers, or selective blocking of branches of the sympathetic or parasympathetic system. The general electrode placement for parasympathetic 25 stimulation is shown in conjunction with FIGS. 8, and 9. The general electrode placement for sympathetic 26 stimulation is shown in conjunction with FIGS. 8, 10A, 10C, 10D. The electrode placement for sympathetic stimulation (neuromodulation) is around the splanchnic nerve(s) 54 (including greater splanchnic nerve), or around the celiac ganglion 55, or plexus in the region. FIG. 10B schematically depicts the preganglionic and postganglionic fibers where the electrical pulses may be provided.
Most nerves in the human body are composed of thousands of fibers of different sizes. This is shown schematically in FIG. 11. The different sizes of nerve fibers, which carry signals to and from the brain, are designated by groups A, B, and C. The vagus nerve, for example, may have approximately 100,000 fibers of the three different types, each carrying signals. Each axon or fiber of that nerve conducts only in one direction, in normal circumstances. In the vagus nerve sensory fibers outnumber parasympathetic fibers four to one.
In a cross section of peripheral nerve it is seen that the diameter of individual fibers vary substantially, as is also shown schematically in FIG. 12. The largest nerve fibers are approximately 20 μm in diameter and are heavily myelinated (i.e., have a myelin sheath, constituting a substance largely composed of fat), whereas the smallest nerve fibers are less than 1 μm in diameter and are unmyelinated.
The diameters of group A and group B fibers include the thickness of the myelin sheaths. Group A is further subdivided into alpha, beta, gamma, and delta fibers in decreasing order of size. There is some overlapping of the diameters of the A, B, and C groups because physiological properties, especially in the form of the action potential, are taken into consideration when defining the groups. The smallest fibers (group C) are unmyelinated and have the slowest conduction rate, whereas the myelinated fibers of group B and group A exhibit rates of conduction that progressively increase with diameter.
Nerve cells have membranes that are composed of lipids and proteins, and have unique properties of excitability such that an adequate disturbance of the cell's resting potential can trigger a sudden change in the membrane conductance. Under resting conditions, the inside of the nerve cell is approximately −90 mV relative to the outside. The electrical signaling capabilities of neurons are based on ionic concentration gradients between the intracellular and extracellular compartments. The cell membrane is a complex of a bilayer of lipid molecules with an assortment of protein molecules embedded in it, separating these two compartments. Electrical balance is provided by concentration gradients which are maintained by a combination of selective permeability characteristics and active pumping mechanism.
A nerve cell can be excited by increasing the electrical charge within the neuron, thus increasing the membrane potential inside the nerve with respect to the surrounding extracellular fluid. The threshold stimulus intensity is the value at which the net inward current (which is largely determined by Sodium ions) is just greater than the net outward current (which is largely carried by Potassium ions), and is typically around −55 mV inside the nerve cell relative to the outside (critical firing threshold). If however, the threshold is not reached, the graded depolarization will not generate an action potential and the signal will not be propagated along the axon. This fundamental feature of the nervous system i.e., its ability to generate and conduct electrical impulses, can take the form of action potentials, which are defined as a single electrical impulse passing down an axon. This action potential (nerve impulse or spike) is an “all or nothing” phenomenon, that is to say once the threshold stimulus intensity is reached, an action potential will be generated.
To stimulate an excitable cell, it is only necessary to reduce the transmembrane potential by a critical amount. When the membrane potential is reduced by an amount ΔV, reaching the critical or threshold potential. When the threshold potential is reached, a regenerative process takes place: sodium ions enter the cell, potassium ions exit the cell, and the transmembrane potential falls to zero (depolarizes), reverses slightly, and then recovers or repolarizes to the resting membrane potential (RMP). For a stimulus to be effective in producing an excitation, it must have an abrupt onset, be intense enough, and last long enough.
Cell membranes can be reasonably well represented by a capacitance C, shunted by a resistance R as shown by an electrical model in FIG. 13, where neuronal process is divided into unit lengths, which is represented in an electrical equivalent circuit. Each unit length of the process is a circuit with its own membrane resistance (rm), membrane capacitance (cm), and axonal resistance (ra).
When the stimulation pulse is strong enough, an action potential will be generated and propagated. As shown in FIG. 14, the action potential is traveling from right to left. Immediately after the spike of the action potential there is a refractory period when the neuron is either unexcitable (absolute refractory period) or only activated to sub-maximal responses by supra-threshold stimuli (relative refractory period). The absolute refractory period occurs at the time of maximal Sodium channel inactivation while the relative refractory period occurs at a later time when most of the Na+ channels have returned to their resting state by the voltage activated K+ current. The refractory period has two important implications for action potential generation and conduction. First, action potentials can be conducted only in one direction, away from the site of its generation, and secondly, they can be generated only up to certain limiting frequencies.
A single electrical impulse passing down an axon is shown schematically in FIG. 15. The top portion of the figure (A) shows conduction over mylinated axon (fiber) and the bottom portion (B) shows conduction over nonmylinated axon (fiber). These electrical signals will travel along the nerve fibers.
The information in the nervous system is coded by frequency of firing rather than the size of the action potential. In terms of electrical conduction, myelinated fibers conduct faster, are typically larger, have very low stimulation thresholds, and exhibit a particular strength-duration curve or respond to a specific pulse width versus amplitude for stimulation, compared to unmyelinated fibers. The A and B fibers can be stimulated with relatively narrow pulse widths, from 50 to 200 microseconds (μs), for example. The A fiber conducts slightly faster than the B fiber and has a slightly lower threshold. The C fibers are very small, conduct electrical signals very slowly, and have high stimulation thresholds typically requiring a wider pulse width (300-1,000 μs) and a higher amplitude for activation. Because of their very slow conduction, C fibers would not be highly responsive to rapid stimulation. Selective stimulation of only A and B fibers is readily accomplished. The requirement of a larger and wider pulse to stimulate the C fibers, however, makes selective stimulation of only C fibers, to the exclusion of the A and B fibers, virtually unachievable inasmuch as the large signal will tend to activate the A and B fibers to some extent as well.
As shown in FIG. 16
, when the distal part of a nerve is electrically stimulated, a compound action potential is recorded by an electrode located more proximally. A compound action potential contains several peaks or waves of activity that represent the summated response of multiple fibers having similar conduction velocities. The waves in a compound action potential represent different types of nerve fibers that are classified into corresponding functional categories as shown in the Table one below,
| ||TABLE 1 |
| || |
| || |
| || ||Conduction ||Fiber || |
| ||Fiber ||Velocity ||Diameter |
| ||Type ||(m/sec) ||(μm) ||Myelination |
| || |
| ||A Fibers || || || |
| ||Alpha || 70-120 ||12-20 ||Yes |
| ||Beta ||40-70 || 5-12 ||Yes |
| ||Gamma ||10-50 ||3-6 ||Yes |
| ||Delta || 6-30 ||2-5 ||Yes |
| ||B Fibers || 5-15 ||<3 ||Yes |
| ||C Fibers ||0.5-2.0 ||0.4-1.2 ||No |
| || |
In the methodology of the current disclosure, it will usually be desired to stimulate the A-fibers and B-fibers and not the c-fibers (since the c-fibers carry pain). Advantageously, this can be readily accomplished using the system and methodology of the current disclosure.
- PRIOR ART
This application is also related to co-pending applications entitled “METHOD AND SYSTEM FOR VAGAL BLOCKING WITH OR WITHOUT VAGAL STIMULATION TO PROVIDE THERAPY FOR OBESITY AND OTHER GASRTOINTESTINAL DISORDERS USING RECHARGEABLE IMPLANTED PULSE GENERATOR” and “METHOD AND SYSTEM FOR PROVIDING ELECTRICAL PULSES TO GASTRIC WALL OF A PATIENT WITH RECHARGEABLE IMPLANTABLE PULSE GENERATOR FOR TREATING OR CONTROLLING OBESITY AND EATING DISORDERS.
Prior art is generally directed to adapting cardiac pacemaker technology for nerve stimulation, where U.S. Pat. Nos. 5,263,480 (Wernicke et al.) and 5,188,104 (Wernicke et al.) are generally directed to treatment of eating disorders with vagus nerve stimulation using an implantable neurocybernetic prosthesis (NCP), which is a “cardiac pacemaker-like” device. There is no disclosure for vagal blocking, sympathetic stimulation, or for using a rechargeable implantable device.
U.S. Pat. No. 5,540,730 (Terry et al.) is generally directed to treating motility disorders with vagus nerve stimulation using an implantable neurocybernetic prosthesis (NCP), which is a “cardiac pacemaker-like” device.
U.S. Pat. No. 6,611,715 B1 (Boveja) is generally directed to a system and method to provide therapy for obesity and compulsive eating disorders using an implantable lead-receiver and an external stimulator.
U.S. Pat. No. 6,553,263B1 (Meadows et al.) is generally directed to an implantable pulse generator system for spinal cord stimulation, which includes a rechargeable battery. In the Meadows '263 patent there is no disclosure or suggestion for combing a stimulus-receiver module to an implantable pulse generator (IPG) for use with an external stimulator, for providing modulating pulses to sympathetic nerve(s), as in the applicant's disclosure.
U.S. Pat. No. 6,505,077 B1 (Kast et al.) is directed to electrical connection for external recharging coil. In the Kast '077 disclosure, a magnetic shield is required between the externalized coil and the pulse generator case. In one embodiment of the applicant's disclosure, the externalized coil is wrapped around the pulse generator case, without requiring a magnetic shield.
- SUMMARY OF THE INVENTION
U.S. Pat. No. 6,622,041 B2 (Terry, Jr. et al.) is directed to treatment of congestive heart failure and autonomic cardiovascular drive disorders using implantable neurostimulator.
The method and system of the current invention overcomes many shortcomings of the prior art by providing method and system for neuromodulation with extended power source either in the form of rechargeable battery, or by utilizing an external stimulator in conjunction with an implanted pulse generator device, to provide therapy for obesity, eating disorders or for inducing weight loss.
Accordingly, in one aspect of the invention, electrical pulses are provided to sympathetic nerves utilizing a rechargeable implantable pulse generator.
In another aspect of the invention, the electrical pulses are provided to at least one of splanchnic nerve, the greater splanchnic nerve, celiac ganglia or other portion of sympathetic nerve plexus in the gastric region or their branch(s) or part thereof.
In another aspect of the invention, the pulse amplitude delivered to sympathetic nervous system can range from 0.25 volt to 15 volts.
In another aspect of the invention, the pulse width of electrical pulses delivered can range from 20 micro-seconds to 5 milli-seconds.
In another aspect of the invention, the frequency of electrical pulses delivered to sympathetic nervous system can range from 5 cycle/second to 200 cycles/second.
In another aspect of the invention, a coil used in recharging said pulse generator is around the implantable pulse generator case, in a silicone enclosure.
In another aspect of the invention, the rechargeable implanted pulse generator comprises two feedthroughs.
In another aspect of the invention, the rechargeable implanted pulse generator comprises only one feedthrough for externalizing the recharge coil.
In another aspect of the invention, the implantable rechargeable pulse generator comprises stimulus-receiver means such that, the implantable rechargeable pulse generator can function in conjunction with an external stimulator, to provide the stimulation and/or blocking pulses to sympathetic nervous system.
In another aspect of the invention, the rechargeable battery comprises at least one of lithium-ion, lithium-ion polymer batteries.
In another aspect of the invention, the external programmer or the external stimulator comprises networking capabilities for remote communications over a wide area network for remote interrogation and/or remote programming.
In yet another aspect of the invention, the implanted lead comprises at least one electrode(s) which is/are made of a material selected from the group consisting of platinum, platinum/iridium alloy, platinum/iridium alloy coated with titanium nitride, and carbon.
BRIEF DESCRIPTION OF THE DRAWINGS
This and other objects are provided by one or more of the embodiments described below.
For the purpose of illustrating the invention, there are shown in accompanying drawing forms which are presently preferred, it being understood that the invention is not intended to be limited to the precise arrangement and instrumentalities shown.
FIG. 1A depicts two-way communication between the gut and central nervous system (CNS).
FIG. 1B depicts electrical pulses to the vagal pathway.
FIG. 1C depicts electrical pulses to the splanchnic pathway.
FIG. 2 is a diagram showing general anatomy of the gastrointestinal (GI) tract.
FIG. 3A depicts control of the enteric nervous system by the autonomic nervous system (parasympathetic and sympathetic).
FIG. 3B is a simplified diagram depicting sympathetic and parasympathetic interaction with the enteric nervous system.
FIG. 4 depicts neural control of gastrointestinal tract.
FIG. 5 is a diagram showing general anatomy of the human stomach.
FIG. 6 is a diagram depicting control of gastric emptying by the sympathetic and parasympathetic activity.
FIG. 7 is a diagram depicting the electrical activity of the GI tract.
FIG. 8 is a diagram depicting parasympathetic and sympathetic innervation of organs and sites for providing electrical pulses.
FIG. 9 parasympathetic innervation of visceral organs via vagus (10th cranial) nerve.
FIG. 10A is an overall depiction of sympathetic innervation of visceral organs.
FIG. 10B depicts preganglionic and postganglionic nerve fibers of the sympathetic innervation to the gut.
FIGS. 10C and 10D depict detailed anatomy of sympathetic innervation of the gastrointestinal (GI) tract.
FIG. 11 is a diagram of the structure of a nerve.
FIG. 12 is a diagram showing different types of nerve fibers.
FIG. 13 is a schematic illustration of electrical circuit model of nerve cell membrane.
FIG. 14 is an illustration of propagation of action potential in nerve cell membrane.
FIG. 15 is an illustration showing propagation of action potential along a myelinated axon and non-myelinated axon.
FIG. 16 is a diagram showing recordings of compound action potentials.
FIG. 17 is a diagram showing the implanted components (rechargeable implanted pulse generator) of the invention.
FIG. 18 is a diagram showing the implanted components, and an external stimulator coupled to implanted stimulus-receiver module of implanted pulse generator.
FIG. 19 is a simplified general block diagram of an implantable pulse generator.
FIG. 20A shows the pulse train transmitted to the vagus nerve(s).
FIG. 20B shows the ramp-up and ramp-down characteristic of the pulse train.
FIG. 21A shows energy density of different types of batteries.
FIG. 21B shows discharge curves for different types of batteries.
FIG. 22 shows a block diagram of an implantable device which can be used as a stimulus-receiver or an implanted pulse generator with rechargeable battery.
FIG. 23 is a block diagram highlighting battery charging circuit of the implantable stimulator of FIG. 22.
FIG. 24 is a schematic diagram highlighting stimulus-receiver portion of implanted stimulator of one embodiment.
FIG. 25 depicts externalizing recharge and telemetry coil from the titanium case.
FIG. 26A depicts coil around the titanium case with two feedthroughs for a bipolar configuration.
FIG. 26B depicts coil around the titanium case with one feedthrough for a unipolar configuration.
FIG. 26C depicts two feedthroughs for the external coil which are common with the feedthroughs for the lead terminal.
FIG. 26D depicts one feedthrough for the external coil which is common to the feedthrough for the lead terminal.
FIGS. 27A and 27B depict recharge coil on the titanium case with a magnetic shield in-between.
FIG. 28 shows an implantable rechargable pulse generator in block diagram form.
FIG. 29 depicts in block diagram form, the implanted and external components of an implanted rechargable system.
FIG. 30 depicts the alignment function of rechargable implantable pulse generator.
FIG. 31 is a block diagram of the external recharger.
FIG. 32 is a schematic diagram of the implantable lead with two electrodes.
FIG. 33 is a schematic diagram of the implantable lead with three electrodes.
FIG. 34 depicts afferent block with nerve stimulation.
FIG. 35 depicts selective efferent block with nerve stimulation
FIG. 36 is a schematic diagram depicting external stimulator and two-way communication through a server.
FIG. 37 is a diagram depicting wireless remote interrogation and programming of the external stimulator.
FIG. 38 is a schematic diagram depicting wireless protocol.
FIG. 39 is a simplified block diagram of the networking interface board.
DESCRIPTION OF THE INVENTION
FIGS. 40A and 40B are simplified diagrams showing communication of modified PDA/phone with an external stimulator via a cellular tower/base station.
In the method and system of this invention, the rechargeable implantable pulse generator (RIPG) system, including a lead comprising at least one electrode(s) is/are implanted in the body. The electrode(s) are adapted to make contact with the nerve tissue where the electrical pulses are to be provided. In one embodiment, the electrode(s) may wrap around the nerve tissue to be stimulated (or blocked). Additional electrode(s) may be placed for the purpose of providing blocking pulses. The electrode(s) may be placed using laproscopic surgery, or alternatively surgical incision may be performed for wider exposure of the tissues. The tissue to be stimulated (or blocked) is identified, which is preferably the greater splanchnic nerve 54 or branches, or the tissue around the celiac ganglion 55, or any plexus in the region. Other sites in the region may also be identified for modulation of sympathetic system to provide therapy for obesity. Modulation in this patent disclosure implies any stimulation, blocking, selective stimulation, and selective stimulation of a portion in combination with selective blocking of a portion of the nervous system.
Once the appropriate electrode(s) is/are positioned and attached (shown in conjunction with FIG. 17), the terminal portion of the lead is tunneled to a site where the rechargeable implantable pulse generator (RIPG) is to be implanted. A subcutaneous pocket is surgically created, and the terminal end of the lead is connected to the rechargeable implantable pulse generator (RIPG), which is then placed in the said subcutaneous pocket. The skin is surgically closed in layers in the usual manner. Electrical pulse therapy can begin once the patient is completely healed from the surgery.
Shown in conjunction with FIG. 18, The RIPG is connected to a lead which has electrodes adapted to be in contact with the splanchnic nerve 54 (or celiac ganglion 55). The pulses are delivered to the splanchnic nerve 54 (or celiac ganglion 55, or other appropriate parts of the sympathetic system) via electrodes 61,62. An external stimulator is also shown, which can be used in one embodiment to provide pulses, as described later.
The pulses are provided to the cathode 61 with the return being anode 62 for bipolar mode of stimulation. For unipolar mode of stimulation the pulse generator case acts as the anode (i.e. the return electrode). Switching of stimulation pulses from bipolar mode to unipolar mode is a programmable parameter, and may be performed with the programmer. Bipolar stimulation offers localized stimulation of tissue compared to unipolar stimulation. For the practice of this invention, unipolar mode of stimulation would also have certain advantages such as stimulating an area of tissue comprising ganglion or nerve plexus.
The selective stimulation and/or blocking to the sympathetic nervous tissue can be performed in one of two ways. One method is to activate one of the “pre-determined” programs from the memory. A second method is to “custom” program the electrical parameters which can be selectively programmed, for specific therapy to the individual patient. Additionally, a program may be selected from memory, and selected parameters may be adjusted or “fine-tuned”. The electrical parameters which can be individually programmed, include variables such as pulse amplitude, pulse width, frequency of stimulation, type of pulse (e.g. blocking pulses may be sinusoidal), stimulation on-time, and stimulation off-time. Table two below defines the approximate range of parameters,
|TABLE 2 |
|Electrical parameter range delivered to the |
|nerve for stimulation and/or blocking |
| ||PARAMER ||RANGE |
| || |
| ||Pulse Amplitude ||0.1 Volt-15 Volts |
| ||Pulse width ||20 μS-5 mSec. |
| ||Stim. Frequency ||5 Hz-200 Hz |
| ||Freq. for blocking ||DC to 5,000 Hz |
| ||On-time ||5 Secs-24 hours |
| ||Off-time ||5 Secs-24 hours |
| || |
The implanted lead component of the system is somewhat similar to cardiac pacemaker leads, except for distal portion 40 (or electrode end) of the lead. The lead terminal preferably is linear, even though it can be bifurcated, and plug(s) into the cavity of the pulse generator means. The lead materials are described later in this disclosure.
Shown in conjunction with FIG. 19, is an overall schematic of a conventional implantable pulse generator system to deliver electrical pulses for modulating the sympathetic nerve(s) and providing therapy. The implantable pulse generator unit 391NR is a microprocessor based device, where the entire circuitry is encased in a hermetically sealed titanium can. As shown in the overall block diagram, the logic & control unit 398 provides the proper timing for the output circuitry 385 to generate electrical pulses that are delivered to a pair of electrodes via a lead 40. Timing is provided by oscillator 393. The pair of electrodes to which the stimulation energy is delivered is switchable. Programming of the implantable pulse generator (IPG) is done via an external programmer 85. Once programmed via an external programmer 85, the implanted pulse generator 391 NR provides appropriate electrical stimulation pulses to the sympathetic nerve(s) 54 via the stimulating electrode pair 61,62. Additional pulses may be provided for blocking, as described later.
The pulses delivered to the nerve tissue for stimulation therapy are shown graphically in FIG. 20A. As shown in FIG. 21B, for patient comfort when the electrical stimulation is turned on, the electrical stimulation may be ramped up and ramped down, instead of abrupt delivery of electrical pulses.
Because of the rapidity of the pulses required for modulating nerve tissue 54 (unlike cardiac pacing), there is a real need for power sources that will provide an acceptable service life under conditions of continuous delivery of high frequency pulses. FIG. 21A shows a graph of the energy density of several commonly used battery technologies. Lithium batteries have by far the highest energy density of commonly available batteries. Also, a lithium battery maintains a nearly constant voltage during discharge. This is shown in conjunction with FIG. 21B, which is normalized to the performance of the lithium battery. Lithium-ion batteries also have a long cycle life, and no memory effect. However, Lithium-ion batteries are not as tolerant to overcharging and overdischarging. One of the most recent development in rechargable battery technology is the Lithium-ion polymer battery. Recently the major battery manufacturers (Sony, Panasonic, Sanyo) have announced plans for Lithium-ion polymer battery production.
For the practice of the current invention, two embodiments of implantable pulse generators may be used. Both embodiments comprise re-chargeable power sources, such as Lithium-ion polymer battery.
In one embodiment, the implanted device comprises a stimulus-receiver module and a pulse generator module. Advantageously, this embodiment provides an ideal power source, since the power source can be an external stimulator coupled with an implanted stimulus-receiver, or the power source can be from the implanted rechargeable battery. Shown in conjunction with FIG. 22 is a simplified overall block diagram of this embodiment. A coil 48C which is external to the titanium case may be used both as a secondary of a stimulus-receiver, or may also be used as the forward and back telemetry coil. The coil 48C may be externalized at the header portion 79C of the implanted device, and may be wrapped around the titanium can, eliminating the need for a magnetic shield. In this case, the coil is encased in the same material as the header 79C. Alternatively, the coil may be positioned on the titanium case, with a magnetic shield.
In this embodiment, as shown in FIG. 22, the IPG circuitry within the titanium case is used for all stimulation pulses whether the energy source is the internal battery 740 or an external power source. The external device serves as a source of energy, and as a programmer that sends telemetry to the IPG. An external stimulator and recharger may also be combined within the same enclosure. For programming, the energy is sent as high frequency sine waves with superimposed telemetry wave driving the external coil 46C. The telemetry is passed through coupling capacitor 727 to the IPG's telemetry circuit 742. For pulse delivery using external power source, the stimulus-receiver portion will receive the energy coupled to the implanted coil 48C and, using the power conditioning circuit 726, rectify it to produce DC, filter and regulate the DC, and couple it to the IPG's voltage regulator 738 section so that the IPG can run from the externally supplied energy rather than the implanted battery 740.
The system of this embodiment provides a power sense circuit 728 that senses the presence of external power communicated with the power control 730, when adequate and stable power is available from an external source. The power control circuit controls a switch 736 that selects either implanted battery power 740 or conditioned external power from 726. The logic and control section 732 and memory 744 includes the IPG's microcontroller, pre-programmed instructions, and stored changeable parameters. Using input for the telemetry circuit 742 and power control 730, this section controls the output circuit 734 that generates the output pulses.
Shown in conjunction with FIG. 23, this embodiment of the invention is practiced with a rechargeable battery. This circuit is energized when external power is available. It senses the charge state of the battery and provides appropriate charge current to safely recharge the battery without overcharging. Recharging circuitry is described later.
The stimulus-receiver portion of the circuitry is shown in conjunction with FIG. 24. Capacitor C1 (729) makes the combination of C1 and L1 sensitive to the resonant frequency and less sensitive to other frequencies, and energy from an external (primary) coil 46C is inductively transferred to the implanted unit via the secondary coil 48C. The AC signal is rectified to DC via diode 731, and filtered via capacitor 733. A regulator 735 set the output voltage and limits it to a value just above the maximum IPG cell voltage. The output capacitor C4 (737), typically a tantalum capacitor with a value of 100 micro-Farads or greater, stores charge so that the circuit can supply the IPG with high values of current for a short time duration with minimal voltage change during a pulse while the current draw from the external source remains relatively constant. Also shown in conjunction with FIG. 24, a capacitor C3 (727) couples signals for forward and back telemetry.
As shown in conjunction with FIG. 25, in both embodiments, the coil is externalized from the titanium case 57. The RF pulses transmitted via coil 46 and received via subcutaneous coil 48A are rectified via a diode bridge. These DC pulses are processed and the resulting current applied to recharge the battery 694/740 in the implanted pulse generator. In one embodiment the coil 48C may be externalized at the header portion 79 of the implanted device, and may be wrapped around the titanium can, as shown in FIGS. 26A and 26B. Shown in FIG. 26A is a bipolar configuration which requires two feedthroughs 76,77. Advantageously, as shown in FIG. 26B unipolar configuration may also be used which requires only one feedthrough 75. The other end is electronically connected to the case. In both cases, the coil is encased in the same material as the header 79. Advantageously, as shown in conjunction with FIGS. 26C and 26D, the feedthrough for the coil can be combined with the feedthrough for the lead terminal. This can be applied both for bipolar and unipolar configurations.
In one embodiment, the coil may also be positioned on the titanium case as shown in conjunction with FIGS. 27A and 27B. FIG. 27A shows a diagram of the finished implantable stimulator 391R of one embodiment. FIG. 27B shows the pulse generator with some of the components used in assembly in an exploded view. These components include a coil cover 13, the secondary coil 48 and associated components, a magnetic shield 9, and a coil assembly carrier 11. The coil assembly carrier 11 has at least one positioning detail 80 located between the coil assembly and the feed through for positioning the electrical connection. The positioning detail 80 secures the electrical connection.
A schematic diagram of the implanted pulse generator (IPG 391R), with re-chargeable battery 694 of the preferred embodiment, is shown in conjunction with FIG. 28. The IPG 391R includes logic and control circuitry 673 connected to memory circuitry 691. The operating program and stimulation parameters are typically stored within the memory 691 via forward telemetry. Stimulation pulses are provided to the nerve tissue 54 via output circuitry 677 controlled by the microcontroller.
The operating power for the IPG 391R is derived from a rechargeable power source 694. The rechargeable power source 694 comprises a rechargeable lithium-ion or lithium-ion polymer battery. Recharging occurs inductively from an external charger to an implanted coil 48B underneath the skin 60. The rechargeable battery 694 may be recharged repeatedly as needed. Additionally, the IPG 391R is able to monitor and telemeter the status of its rechargable battery 691 each time a communication link is established with the external programmer 85.
Much of the circuitry included within the IPG 391R may be realized on a single application specific integrated circuit (ASIC). This allows the overall size of the IPG 391R to be quite small, and readily housed within a suitable hermetically-sealed case. The IPG case is preferably made from titanium and is shaped in a rounded case.
Shown in conjunction with FIG. 29 are the recharging elements of the invention. The re-charging system uses a portable external charger to couple energy into the power source of the IPG 391R. The DC-to-AC conversion circuitry 696 of the re-charger receives energy from a battery 672 in the re-charger. A charger base station 680 and conventional AC power line may also be used. The AC signals amplified via power amplifier 674 are inductively coupled between an external coil 46B and an implanted coil 48B located subcutaneously with the implanted pulse generator (IPG) 391R. The AC signal received via implanted coil 48B is rectified 686 to a DC signal which is used for recharging the rechargeable battery 694 of the IPG, through a charge controller IC 682. Additional circuitry within the IPG 391R includes, battery protection IC 688 which controls a FET switch 690 to make sure that the rechargeable battery 694 is charged at the proper rate, and is not overcharged. The battery protection IC 688 can be an off-the-shelf IC available from Motorola (part no. MC 33349N-3R1). This IC monitors the voltage and current of the implanted rechargeable battery 694 to ensure safe operation. If the battery voltage rises above a safe maximum voltage, the battery protection IC 688 opens charge enabling FET switches 690, and prevents further charging. A fuse 692 acts as an additional safeguard, and disconnects the battery 694 if the battery charging current exceeds a safe level. As also shown in FIG. 29, charge completion detection is achieved by a back-telemetry transmitter 684, which modulates the secondary load by changing the full-wave rectifier into a half-wave rectifier/voltage clamp. This modulation is in turn, sensed by the charger as a change in the coil voltage due to the change in the reflected impedance. When detected through a back telemetry receiver 676, either an audible alarm is generated or a LED is turned on.
A simplified block diagram of charge completion and misalignment detection circuitry is shown in conjunction with FIG. 30. As shown, a switch regulator 686 operates as either a full-wave rectifier circuit or a half-wave rectifier circuit as controlled by a control signal (CS) generated by charging and protection circuitry 698. The energy induced in implanted coil 48B (from external coil 46B) passes through the switch rectifier 686 and charging and protection circuitry 698 to the implanted rechargeable battery 694. As the implanted battery 694 continues to be charged, the charging and protection circuitry 698 continuously monitors the charge current and battery voltage. When the charge current and battery voltage reach a predetermined level, the charging and protection circuitry 698 triggers a control signal. This control signal causes the switch rectifier 686 to switch to half-wave rectifier operation. When this change happens, the voltage sensed by voltage detector 702 causes the alignment indicator 706 to be activated. This indicator 706 may be an audible sound or a flashing LED type of indicator.
The indicator 706 may similarly be used as a misalignment indicator. In normal operation, when coils 46B (external) and 48B (implanted) are properly aligned, the voltage Vs sensed by voltage detector 704 is at a minimum level because maximum energy transfer is taking place. If and when the coils 46B and 48B become misaligned, then less than a maximum energy transfer occurs, and the voltage Vs sensed by detection circuit 704 increases significantly. If the voltage Vs reaches a predetermined level, alignment indicator 706 is activated via an audible speaker and/or LEDs for visual feedback. After adjustment, when an optimum energy transfer condition is established, causing Vs to decrease below the predetermined threshold level, the alignment indicator 706 is turned off.
The elements of the external recharger are shown as a block diagram in conjunction with FIG. 31. In this disclosure, the words charger and recharger are used interchangeably. The charger base station 680 receives its energy from a standard power outlet 714, which is then converted to 5 volts DC by a AC-to-DC transformer 712. When the re-charger is placed in a charger base station 680, the re-chargeable battery 672 of the re-charger is fully recharged in a few hours and is able to recharge the battery 694 of the IPG 391R. If the battery 672 of the external re-charger falls below a prescribed limit of 2.5 volt DC, the battery 672 is trickle charged until the voltage is above the prescribed limit, and then at that point resumes a normal charging process.
As also shown in FIG. 31, a battery protection circuit 718 monitors the voltage condition, and disconnects the battery 672 through one of the FET switches 716, 720 if a fault occurs until a normal condition returns. A fuse 724 will disconnect the battery 672 should the charging or discharging current exceed a prescribed amount.
Referring now to FIG. 32
, the implanted lead component of the system is similar to cardiac pacemaker leads, except for distal portion (or electrode end) of the lead. This figure shows a pair of electrodes 61
that are used for providing electrical pulses for stimulation. Alternatively, FIG. 33
depicts a lead with tripolar electrodes 62
for stimulation and/or blocking. The lead terminal preferably is linear bipolar, even though it can be bifurcated, and plug(s) into the cavity of the pulse generator means. The lead body 59
insulation may be constructed of medical grade silicone, silicone reinforced with polytetrafluoro-ethylene (PTFE), or polyurethane. The electrodes 61
for stimulating the sympathetic nerve(s) 54
may either wrap around the nerve once or may be spiral shaped. These stimulating electrodes may be made of pure platinum, platinum/Iridium alloy or platinum/iridium coated with titanium nitride. The conductor connecting the terminal to the electrodes 61
is made of an alloy of nickel-cobalt. The implanted lead design variables are also summarized in table three below.
|TABLE 3 |
|Lead design variables |
|Proximal || || || || ||Distal |
|End || || || || ||End |
| || || ||Conductor |
| || || ||(connecting || || |
| ||Lead body- || ||proximal || || |
|Lead ||Insulation || ||and distal ||Electrode - ||Electrode - |
|Terminal ||Materials ||Lead-Coating ||ends) ||Material ||Type |
|Linear ||Polyurethane ||Antimicrobial ||Alloy of ||Pure ||Spiral |
|bipolar || ||coating ||Nickel- ||Platinum ||electrode |
| || || ||Cobalt |
|Bifurcated ||Silicone ||Anti- || ||Platinum- ||Wrap-around |
| || ||Inflammatory || ||Iridium ||electrode |
| || ||coating || ||(Pt/Ir) Alloy |
| ||Silicone with ||Lubricious || ||Pt/Ir coated ||Steroid |
| ||Polytetrafluoroethylene ||coating || ||with Titanium ||eluting |
| ||(PTFE) || || ||Nitride |
| || || || ||Carbon ||Hydrogel |
| || || || || ||electrodes |
| || || || || ||Cuff |
| || || || || ||electrodes |
Once the lead is fabricated, coating such as anti-microbial, anti-inflammatory, or lubricious coating may be applied to the body of the lead.
In one aspect of the invention, in addition to selective stimulation of the sympathetic system, selective portions of the nervous system may be blocked. Typically when a nerve pathway is stimulated, the stimulation is conducted in both the Afferent (towards the brain) and Efferent (away from the brain) direction. Shown in conjunction with FIG. 34, by placing blocking electrodes proximal to the stimulating electrodes, and supplying blocking pulses (controlled by the processor), the conduction in the Afferent direction (towards the brain) can be blocked or significantly reduced. Blocking pulses of 500 Hz can be used, or alternatively other frequencies can also be used.
Selective Efferent block can also be obtained and is depicted in conjunction with FIG. 35. As shown in the figure, because of the selective placement of blocking electrode(s), only the impulses to visceral organ 2 are blocked or significantly reduced, and impulses to visceral organ-1 and visceral organ-2 continue unimpeded.
- Telemetry Module
Blocking can be generally divided into 3 categories: (a) DC or anodal block, (b) Wedenski Block, and (c) Collision block. In anodal block there is a steady potential which is applied to the nerve causing a reversible and selective block. In Wedenski Block, the nerve is stimulated at a high rate causing the rapid depletion of the neurotransmitter. In collision blocking, unidirectional action potentials are generated anti-dromically. The maximal frequency for complete block is the reciprocal of the refractory period plus the transit time i.e. typically less than a few hundred hertz. The use of any of these blocking techniques is considered within the scope of this invention.
Shown in conjunction with FIG. 36, in one embodiment of the invention the external stimulator 42 and/or the programmer has two-way wireless communication capabilities with a remote server, using a communication protocol such as the wireless application protocol (WAP). The purpose of the telemetry module is to enable the physician to remotely, via the wireless medium change the programs, activate, or disengage programs. Additionally, schedules of therapy programs, can be remotely transmitted and verified. Advantageously, the physician is thus able to remotely control the stimulation therapy.
FIG. 37 is a simplified schematic showing the communication aspects between the pulse generator 42 and the remote hand-held computer. Similar methodology would apply if the telemetry module is in the programmer 85. A desktop or laptop computer can be a server 130 which is situated remotely, perhaps at a health-care provider's facility or a hospital. The data can be viewed at this facility or reviewed remotely by medical personnel on a wireless internet supported hand-held device 140, which could be a personal data assistant (PDA), for example, a “palm-pilot” from PALM corp. (Santa Clara, Calif.), a “Visor” from Handspring Corp. (Mountain view, Calif.) or on a personal computer (PC) available from numerous vendors or a cell phone or a handheld device being a combination thereof. The physician or appropriate medical personnel, is able to interrogate the external stimulator 42 device and know what the device is currently programmed to, as well as, get a graphical display of the pulse train. The wireless communication with the remote server 130 and hand-held device (wireless internet supported) 140 can be achieved in all geographical locations within and outside the United States (US) that provides cell phone voice and data communication service. The pulse generation parameter data can also be viewed on the handheld devices 140.
The telecommunications component of this invention uses Wireless Application Protocol (WAP). WAP is a set of communication protocols standardizing Internet access for wireless devices. Previously, manufacturers used different technologies to get Internet on hand-held devices. With WAP, devices and services inter-operate. WAP promotes convergence of wireless data and the Internet. The WAP Layers are Wireless Application Envirnment (WAEW), Wireless Session Layer (WSL), Wireless Transport Layer Security (WTLS) and Wireless Transport Layer (WTP).
The WAP programming model, which is heavily based on the existing Internet programming model, is shown schematically in FIG. 38. Introducing a gateway function provides a mechanism for optimizing and extending this model to match the characteristics of the wireless environment. Over-the-air traffic is minimized by binary encoding/decoding of Web pages and readapting the Internet Protocol stack to accommodate the unique characteristics of a wireless medium such as call drops. Such features are facilitated with WAP.
The key components of the WAP technology, as shown in FIG. 38, includes 1) Wireless Mark-up Language (WML) 452 which incorporates the concept of cards and decks, where a card is a single unit of interaction with the user. A service constitutes a number of cards collected in a deck. A card can be displayed on a small screen. WML supported Web pages reside on traditional Web servers. 2) WML Script which is a scripting language, enables application modules or applets to be dynamically transmitted to the client device and allows the user interaction with these applets. 3) Microbrowser, which is a lightweight application resident on the wireless terminal that controls the user interface and interprets the WML/WMLScript content. 4) A lightweight protocol stack 454 which minimizes bandwidth requirements, guaranteeing that a broad range of wireless networks can run WAP applications. The protocol stack of WAP can comprise a set of protocols for the transport (WTP), session (WSP), and security (WTLS) layers. WSP is binary encoded and able to support header caching, thereby economizing on bandwidth requirements. WSP also compensates for high latency by allowing requests and responses to be handles asynchronously, sending before receiving the response to an earlier request. For lost data segments, perhaps due to fading or lack of coverage, WTP only retransmits lost segments using selective retransmission, thereby compensating for a less stable connection in wireless. The above mentioned features are industry standards adopted for wireless applications, and well known to those skilled in the art.
The presently preferred embodiment utilizes WAP, because WAP has the following advantages, 1) WAP protocol uses less than one-half the number of packets that the standard HTTP or TCP/IP Internet stack uses to deliver the same content. 2) Addressing the limited resources of the terminal, the browser, and the lightweight protocol stack are designed to make small claims on CPU and ROM. 3) Binary encoding of WML and SMLScript helps keep the RAM as small as possible. And, 4) Keeping the bearer utilization low takes account of the limited battery power of the terminal.
In this embodiment two modes of communication are possible. In the first, the server initiates an upload of the actual parameters being applied to the patient, receives these from the stimulator, and stores these in its memory, accessible to the authorized user as a dedicated content driven web page. The web page is managed with adequate security and password protection. The physician or authorized user can make alterations to the actual parameters, as available on the server, and then initiate a communication session with the stimulator device to download these parameters.
The physician is also able to set up long-term schedules of stimulation therapy for their patient population, through wireless communication with the server. The server in turn communicates these programs to the neurostimulator. Each schedule is securely maintained on the server, and is editable by the physician and can get uploaded to the patient's stimulator device at a scheduled time. Thus, therapy can be customized for each individual patient. Each device issued to a patient has a unique identification key in order to guarantee secure communication between the wireless server 130 and stimulator device 42 (or programmer 85).
Shown in conjunction with FIG. 39, in one embodiment, the external stimulator 42 and/or the programmer 85 may also be networked to a central collaboration computer 286 as well as other devices such as a remote computer 294, PDA 140, phone 141, physician computer 143. The interface unit 292 in this embodiment communicates with the central collaborative network 290 via land-lines such as cable modem or wirelessly via the internet. A central computer 286 which has sufficient computing power and storage capability to collect and process large amounts of data, contains information regarding device history and serial number, and is in communication with the network 290. Communication over collaboration network 290 may be effected by way of a TCP/IP connection, particularly one using the internet, as well as a PSTN, DSL, cable modem, LAN, WAN or a direct dial-up connection.
The standard components of interface unit shown in block 292 are processor 305, storage 310, memory 308, transmitter/receiver 306, and a communication device such as network interface card or modem 312. In the preferred embodiment these components are embedded in the external stimulator 42 and can also be embedded in the programmer 85. These can be connected to the network 290 through appropriate security measures (Firewall) 293.
Another type of remote unit that may be accessed via central collaborative network 290 is remote computer 294. This remote computer 294 may be used by an appropriate attending physician to instruct or interact with interface unit 292, for example, instructing interface unit 292 to send instruction downloaded from central computer 286 to remote implanted unit.
Shown in conjunction with FIGS. 40A and 40B the physician's remote communication's module is a Modified PDA/Phone 140 in this embodiment. The Modified PDA/Phone 140 is a microprocessor based device as shown in a simplified block diagram in FIGS. 40A and 40B. The PDA/Phone 140 is configured to accept PCM/CIA cards specially configured to fulfill the role of communication module 292 of the present invention. The Modified PDA/Phone 140 may operate under any of the useful software including Microsoft Window's based, Linux, Palm OS, Java OS, SYMBIAN, or the like.
The telemetry module 362 comprises an RF telemetry antenna 142 coupled to a telemetry transceiver and antenna driver circuit board which includes a telemetry transmitter and telemetry receiver. The telemetry transmitter and receiver are coupled to control circuitry and registers, operated under the control of microprocessor 364. Similarly, within stimulator a telemetry antenna 142 is coupled to a telemetry transceiver comprising RF telemetry transmitter and receiver circuit. This circuit is coupled to control circuitry and registers operated under the control of microcomputer circuit.
With reference to the telecommunications aspects of the invention, the communication and data exchange between Modified PDA/Phone 140 and external stimulator 42 operates on commercially available frequency bands. The 2.4-to-2.4853 GHz bands or 5.15 and 5.825 GHz, are the two unlicensed areas of the spectrum, and set aside for industrial, scientific, and medical (ISM) uses. Most of the technology today including this invention, use either the 2.4 or 5 GHz radio bands and spread-spectrum technology.
The telecommunications technology, especially the wireless internet technology, which this invention utilizes in one embodiment, is constantly improving and evolving at a rapid pace, due to advances in RF and chip technology as well as software development. Therefore, one of the intents of this invention is to utilize “state of the art” technology available for data communication between Modified PDA/Phone 140 and external stimulator 42. The intent of this invention is to use 3G technology for wireless communication and data exchange, even though in some cases 2.5G is being used currently.
For the system of the current invention, the use of any of the “3G” technologies for communication for the Modified PDA/Phone 140, is considered within the scope of the invention. Further, it will be evident to one of ordinary skill in the art that as future 4G systems, which will include new technologies such as improved modulation and smart antennas, can be easily incorporated into the system and method of current invention, and are also considered within the scope of the invention.