Abstract:
Devices, systems and methods are described for controlling, preventing and/or treating epileptic seizures by activating baroreceptors. By selectively and controllably activating baroreceptors, the present invention reduces seizure activity, thereby minimizing the effects of epilepsy. A baroreceptor activation device is positioned near a baroreceptor on the patient&#39;s arterial or venous vasculature, for example in the carotid sinus, aortic arch, inferior vena cava, or the like. One or more optional sensors, such as EEG sensors, detect neurological activity to help determine when to activate baroreceptors to reduce or prevent seizures.

Description:
CROSS-REFERENCES TO RELATED APPLICATIONS 
   This application claims the benefit under 35 USC 119(e) of U.S. patent application No. 60/505,121, filed on Sep. 22, 2003. 
   This application is related to but does not claim the benefit of: U.S. Pat. No. 6,522,926, entitled “Devices and Methods for Cardiovascular Reflex Control,” filed on Sep. 27, 2000; U.S. patent application Ser. No. 09/964,079, filed on Sep. 26, 2001; U.S. patent application Ser. No. 09/963,777, filed Sep. 26, 2001; U.S. patent application Ser. No. 09/963,991, filed Sep. 26, 2001; PCT Patent Application No. PCT/US01/30249, filed Sep. 27, 2001; U.S. patent application Ser. No. 10/284,063, filed Oct. 29, 2002; U.S. patent application Ser. No. 10/402,911, filed Mar. 27, 2003; U.S. patent application Ser. No. 10/402,393, filed Mar. 27, 2003; and U.S. patent application Ser. No. 10/818,738 filed Apr. 4, 2004, the full disclosures of which are incorporated herein by reference. 
   BACKGROUND OF THE INVENTION 
   1. Field of the Invention 
   The present invention relates generally to medical devices and methods for the treatment and/or management of epilepsy. More specifically, the invention relates to devices and methods for controlling the baroreflex system for the treatment and/or management of epilepsy. 
   An estimated 1% of the world&#39;s population suffers from epilepsy. Of these, approximately 30,000 patients each year suffer from medically intractable epilepsy, and alternative treatments have not yet been perfected. Only 15% of patients will benefit from presently existing cerebral surgery techniques. Vagal nerve stimulation (VNS) offers 20-61% seizure reduction (at 3-month or greater follow-up) according to most large studies, but is associated with undesirable side effects, such as hoarseness, coughing, dysautonomia, and, in right-sided VNS, cardiac side effects. Of the approximately 50% of patients whose seizures are not well controlled by VNS, as well as for those patients in whom VNS is difficult or contraindicated (e.g., due to prior scarring from radiation, cancer-related surgery, or the like), other therapeutic options are not currently available. 
   Vagal nerve stimulation for control of medically refractory epilepsy was introduced by Zabara (U.S. Pat. No. 5,540,734), and has recently received approval for use in selected patients by the Food and Drug Administration. Although helpful as a last resort in many of these patients, VNS has been shown to be limited in efficacy, with accompanying undesirable side effects, as mentioned above. VNS is also limited to the left side, since right-sided stimulation is associated with significant cardiac side effects. Patients who are candidates for VNS usually have failed all medical and other available surgical techniques. A patient presently failing VNS often has no other good treatment option available. 
   One proposed alternative method for treating epilepsy involves electrode stimulation of the carotid sinus nerve. For example, Patwardhan et al. (2002)  Pediatric Neurosurgery  36:236-243 and U.S. Patent Publication No. 2002/0103516 A1 describe such a method. Several problems with direct, electrical carotid sinus nerve stimulation have been reported in the medical literature, however. These include the invasiveness of the surgical procedure to implant the nerve electrodes, as well as postoperative pain in the jaw, throat, face and head during stimulation. Additionally, it has been noted that direct application of high voltages sometimes required for nerve stimulation may damage the carotid sinus nerves. 
   Thus, it would be desirable to provide improved devices and methods for treating, reducing and/or controlling epileptic seizures. Ideally, such devices and methods would be minimally invasive and would enhance the treatment or control of epileptic seizures efficaciously, with few if any significant side effects. At least some of these objectives will be met by the present invention. 
   2. Description of the Background Art 
   Patwardhan et al. (2002)  Pediatric Neurosurgery  36:236-243, and U.S. Patent Publication No. 2002/0103516 A1 describe the treatment of epilepsy by electrode stimulation of the carotid sinus nerve. U.S. Pat. Nos. 6,073,048 and 6,178,349, each having a common inventor with the present application, describe the stimulation of nerves to regulate the heart, vasculature, and other body systems. Nerve stimulation for other purposes is described in, for example, U.S. Pat. Nos. 6,292,695 B1 and 5,700,282. Publications which describe the existence of baroreceptors and/or related receptors in the venous vasculature and atria include Goldberger et al. (1999)  J. Neuro. Meth.  91:109-114; Kostreva and Pontus (1993)  Am. J. Physiol.  265:G15-G20; Coleridge et al. (1973)  Circ. Res.  23:87-97; Mifflin and Kunze (1982)  Circ. Res.  51:241-249; and Schaurte et al. (2000)  J. Cardiovasc Electrophysiol.  11:64-69. The full texts and disclosures of all the references listed above are hereby incorporated fully by reference. 
   SUMMARY OF THE INVENTION 
   To address epilepsy, the present invention provides a number of devices, systems and methods by which nervous system activity may be selectively and controllably regulated by activating baroreceptors. By selectively and controllably activating baroreceptors, the present invention reduces epileptic seizure activity. 
   The present invention provides systems and methods for treating epilepsy in a patient, for example by reducing epileptiform activity, by inducing or modifying a baroreceptor signal. To accomplish this, the system and method of the present invention may utilize a baroreceptor activation device positioned near a baroreceptor in an arterial location, such as the carotid sinus, aortic arch, heart, common carotid arteries, subclavian arteries, and/or brachiocephalic artery. In one embodiment, for example, the baroreceptor activation device is located in the right and/or left carotid sinus (near the bifurcation of the common carotid artery) and/or the aortic arch. Alternatively, a baroreceptor activation device may be positioned in the low-pressure side of the heart or vasculature, as described in U.S. patent application Ser. No. 10/284,063, previously incorporated by reference, to activate baroreceptor(s) in the inferior vena cava, superior vena cava, portal vein, jugular vein, subclavian vein, iliac vein and/or femoral vein. Therefore, although the present application often describes baroreceptor activation devices in arterial locations, the systems and methods of the invention are in no way limited to such embodiments. 
   Generally speaking, a baroreceptor activation device may be activated, deactivated or otherwise modulated to activate one or more baroreceptors and induce a baroreceptor signal or a change in the baroreceptor signal to thereby effect a change in the central nervous system. The baroreceptor activation device may be activated, deactivated, or otherwise modulated continuously, periodically, or episodically. The baroreceptor activation device may comprise any of a wide variety of devices which utilize mechanical, electrical, thermal, chemical, biological, or other means to activate the baroreceptor. The baroreceptor may be activated directly, or activated indirectly via the adjacent vascular tissue. The baroreceptor activation device may be positioned inside the vascular lumen (i.e., intravascularly), outside the vascular wall (i.e., extravascularly) or within the vascular wall (i.e., intramurally). To maximize therapeutic efficacy, a mapping method may be employed to precisely locate or position the baroreceptor activation device. 
   For embodiments utilizing electrical means to activate the baroreceptor, various electrode designs are provided. The electrode designs may be particularly suitable for connection to the carotid arteries at or near the carotid sinus, and may be designed to minimize extraneous tissue stimulation. 
   A control system may be used to generate a control signal which activates, deactivates or otherwise modulates the baroreceptor activation device. The control system may operate in an open-loop or a closed-loop mode. For example, in the open-loop mode, the patient and/or physician may directly or remotely interface with the control system to prescribe the control signal. In the closed-loop mode, the control signal may be responsive to feedback from a sensor, wherein the response is dictated by a preset or programmable algorithm defining a stimulus regimen. 
   The stimulus regimen is preferably selected to promote long term efficacy and to minimize power requirements. It is theorized that uninterrupted activation of the baroreceptors may result in the baroreceptors and/or central nervous system becoming less responsive over time, thereby diminishing the effectiveness of the therapy. Therefore, the stimulus regimen may be selected to modulate the baroreceptor activation device in such a way that the baroreceptors maintain their responsiveness over time. Specific examples of stimulus regimens which promote long term efficacy are described in more detail below. 
   Various embodiments of the inventive devices may be entirely intravascular, entirely extravascular, or partially intravascular and partially extravascular. Furthermore, devices may reside wholly in or on arterial vasculature, wholly in or on venous vasculature, or in or on some combination of both. In some embodiments, for example, implantable devices may positioned within an artery or vein, while in other embodiments devices may be placed extravascularly, on the outside of an artery or vein. In yet other embodiments, one or more components of a device, such as electrodes, a controller or both, may be positioned outside the patient&#39;s body. In introducing and placing devices of the present invention, any suitable technique and access route may be employed. For example, in some embodiments an open surgical procedure may be used to place an implantable device. Alternatively, an implantable device may be placed within an artery or vein via a transvascular, intravenous approach. In still other embodiments, an implantable device may be introduced into vasculature via minimally invasive means, advanced to a treatment position through the vasculature, and then advanced outside the vasculature for placement on the outside of an artery or vein. For example, an implantable device may be introduced into and advanced through the venous vasculature, made to exit the wall of a vein, and placed at an extravascular site on an artery. 

   
     BRIEF DESCRIPTION OF THE DRAWINGS 
       FIG. 1  is a schematic illustration of the upper torso of a human body showing the major arteries and veins and associated anatomy; 
       FIG. 2A  is a cross sectional schematic illustration of the carotid sinus and baroreceptors within the vascular wall; 
       FIG. 2B  is a schematic illustration of baroreceptors within the vascular wall and the baroreflex system; 
       FIG. 3  is a schematic illustration of a baroreceptor activation system in accordance with the present invention; 
       FIGS. 4A and 4B  are schematic illustrations of a baroreceptor activation device in the form of an internal inflatable balloon which mechanically induces a baroreceptor signal in accordance with an embodiment of the present invention; 
       FIGS. 5A and 5B  are schematic illustrations of a baroreceptor activation device in the form of an external pressure cuff which mechanically induces a baroreceptor signal in accordance with an embodiment of the present invention; 
       FIGS. 6A and 6B  are schematic illustrations of a baroreceptor activation device in the form of an internal deformable coil structure which mechanically induces a baroreceptor signal in accordance with an embodiment of the present invention; 
       FIGS. 6C and 6D  are cross sectional views of alternative embodiments of the coil member illustrated in  FIGS. 6A and 613 ; 
       FIGS. 7A and 7B  are schematic illustrations of a baroreceptor activation device in the form of an external deformable coil structure which mechanically induces a baroreceptor signal in accordance with an embodiment of the present invention; 
       FIGS. 7C and 7D  are cross sectional views of alternative embodiments of the coil member illustrated in  FIGS. 7A and 713 ; 
       FIGS. 8A and 8B  are schematic illustrations of a baroreceptor activation device in the form of an external flow regulator which artificially creates back pressure to induce a baroreceptor signal in accordance with an embodiment of the present invention; 
       FIGS. 9A and 9B  are schematic illustrations of a baroreceptor activation device in the form of an internal flow regulator which artificially creates back pressure to induce a baroreceptor signal in accordance with an embodiment of the present invention; 
       FIGS. 10A and 10B  are schematic illustrations of a baroreceptor activation device in the form of a magnetic device which mechanically induces a baroreceptor signal in accordance with an embodiment of the present invention; 
       FIGS. 11A and 11B  are schematic illustrations of a baroreceptor activation device in the form of a transducer which mechanically induces a baroreceptor signal in accordance with an embodiment of the present invention; 
       FIGS. 12A and 12B  are schematic illustrations of a baroreceptor activation device in the form of a fluid delivery device which may be used to deliver an agent which chemically or biologically induces a baroreceptor signal in accordance with an embodiment of the present invention; 
       FIGS. 13A and 13B  are schematic illustrations of a baroreceptor activation device in the form of an internal conductive structure which electrically or thermally induces a baroreceptor signal in accordance with an embodiment of the present invention; 
       FIGS. 14A and 14B  are schematic illustrations of a baroreceptor activation device in the form of an internal conductive structure, activated by an internal inductor, which electrically or thermally induces a baroreceptor signal in accordance with an embodiment of the present invention; 
       FIGS. 15A and 15B  are schematic illustrations of a baroreceptor activation device in the form of an internal conductive structure, activated by an internal inductor located in an adjacent vessel, which electrically or thermally induces a baroreceptor signal in accordance with an embodiment of the present invention; 
       FIGS. 16A and 16B  are schematic illustrations of a baroreceptor activation device in the form of an internal conductive structure, activated by an external inductor, which electrically or thermally induces a baroreceptor signal in accordance with an embodiment of the present invention; 
       FIGS. 17A and 17B  are schematic illustrations of a baroreceptor activation device in the form of an external conductive structure which electrically or thermally induces a baroreceptor signal in accordance with an embodiment of the present invention; 
       FIGS. 18A and 18B  are schematic illustrations of a baroreceptor activation device in the form of an internal bipolar conductive structure which electrically or thermally induces a baroreceptor signal in accordance with an embodiment of the present invention; 
       FIGS. 19A and 19B  are schematic illustrations of a baroreceptor activation device in the form of an electromagnetic field responsive device which electrically or thermally induces a baroreceptor signal in accordance with an embodiment of the present invention; 
       FIGS. 20A and 20B  are schematic illustrations of a baroreceptor activation device in the form of an external Peltier device which thermally induces a baroreceptor signal in accordance with an embodiment of the present invention; 
       FIGS. 21A-21C  are schematic illustrations of a preferred embodiment of an inductively activated electrically conductive structure; 
       FIGS. 22A-22F  are schematic illustrations of various possible arrangements of electrodes around the carotid sinus for extravascular electrical activation embodiments; 
       FIG. 23  is a schematic illustration of a serpentine shaped electrode for extravascular electrical activation embodiments; 
       FIG. 24  is a schematic illustration of a plurality of electrodes aligned orthogonal to the direction of wrapping around the carotid sinus for extravascular electrical activation embodiments; 
       FIGS. 25-28  are schematic illustrations of various multi channel electrodes for extravascular electrical activation embodiments; 
       FIG. 29  is a schematic illustration of an extravascular electrical activation device including a tether and an anchor disposed about the carotid sinus and common carotid artery; 
       FIG. 30  is a schematic illustration of an alternative extravascular electrical activation device including a plurality of ribs and a spine; 
       FIG. 31  is a schematic illustration of an electrode assembly for extravascular electrical activation embodiments; 
       FIG. 32  is a schematic illustration of a fragment of an alternative cable for use with an electrode assembly such as shown in  FIG. 31 ; 
       FIG. 33  is a schematic illustration of the right carotid artery showing a bulge in the vascular wall which is a landmark of the carotid sinus; 
       FIG. 34  is a schematic illustration of a baroreceptor activation device disposed about the right carotid artery which may be used for mapping baroreceptors therein; and 
       FIG. 35  is a schematic cross sectional view taken along line  35   35  in  FIG. 34 , showing a mapping coordinate system for the left and right carotid arteries. 
   

   DETAILED DESCRIPTION OF THE INVENTION 
   Referring now to  FIG. 1 , within the arterial walls of the aortic arch  12 , common carotid arteries  14 / 15  (near the right carotid sinus  20  and left carotid sinus), subclavian arteries  13 / 16  and brachiocephalic artery  22  there are baroreceptors  30 . For example, as best seen in  FIG. 2A , baroreceptors  30  reside within the vascular walls of the carotid sinus  20 . Baroreceptors  30  are a type of stretch receptor used by the body to sense blood pressure. An increase in blood pressure causes the arterial wall to stretch, and a decrease in blood pressure causes the arterial wall to return to its original size. Such a cycle is repeated with each beat of the heart. The baroreceptors  30  located in the right carotid sinus  20 , the left carotid sinus and the aortic arch  12  play the most significant role in sensing blood pressure that affects the baroreflex system  50 , which is described in more detail with reference to  FIG. 2B . 
   Refer now to  FIG. 2B , which shows a schematic illustration of baroreceptors  30  disposed in a generic vascular wall  40  and a schematic flow chart of the baroreflex system  50 . Baroreceptors  30  are profusely distributed within the arterial walls  40  of the major arteries discussed previously, and generally form an arbor  32 . The baroreceptor arbor  32  comprises a plurality of baroreceptors  30 , each of which transmits baroreceptor signals to the brain  52  via nerve  38 . The baroreceptors  30  are so profusely distributed and arborized within the vascular wall  40  that discrete baroreceptor arbors  32  are not readily discernable. To this end, the baroreceptors  30  shown in  FIG. 2B  are primarily schematic for purposes of illustration and discussion. 
   Baroreceptor signals are used to activate a number of body systems which collectively may be referred to as the baroreflex system  50 . Baroreceptors  30  are connected to the brain  52  via the nervous system  51 , which then activates a number of body systems, including the heart  11 , kidneys  53 , vessels  54 , and other organs/tissues via neurohormonal activity. Although such activation of the baroreflex system  50  has been the subject of other patent applications by the inventors of the present invention, the focus of the present invention is the effect of barareceptor activation on the brain  52  to reduce or prevent epileptic seizure activity. 
   With reference to  FIG. 3 , the present invention generally provides a system including a control system  60 , a baroreceptor activation device  70 , and a sensor  80  (optional), which generally operate in the following manner. The sensor  80  senses and/or monitors a parameter (e.g., seizure activity) indicative or predictive of the need to modify the central nervous system and generates a signal indicative or predictive of the parameter. The control system  60  generates a control signal as a function of the received sensor signal. The control signal activates, deactivates or otherwise modulates the baroreceptor activation device  70 . Typically, activation of the device  70  results in activation of the baroreceptors  30 . Alternatively, deactivation or modulation of the baroreceptor activation device  70  may cause or modify activation of the baroreceptors  30 . The baroreceptor activation device  70  may comprise a wide variety of devices which utilize mechanical, electrical, thermal, chemical, biological, or other means to activate baroreceptors  30 . Thus, when the sensor  80  detects a parameter indicative or predictive of the need to modify central nervous system activity (e.g., excessive neurological activity), the control system  60  generates a control signal to activate the baroreceptor activation device  70  thereby inducing a baroreceptor  30  signal. When the sensor  80  detects a parameter indicative or predictive of normal body function (e.g., normal neurological activity), the control system  60  generates a control signal to modulate (e.g., deactivate) the baroreceptor activation device  70 . 
   As mentioned previously, the baroreceptor activation device  70  may comprise a wide variety of devices which utilize mechanical, electrical, thermal, chemical, biological or other means to activate the baroreceptors  30 . Specific embodiments of the generic baroreceptor activation device  70  are discussed with reference to  FIGS. 4-21 . In most instances, particularly the mechanical activation embodiments, the baroreceptor activation device  70  indirectly activates one or more baroreceptors  30  by stretching or otherwise deforming the vascular wall  40  surrounding the baroreceptors  30 . In some other instances, particularly the non-mechanical activation embodiments, the baroreceptor activation device  70  may directly activate one or more baroreceptors  30  by changing the electrical, thermal or chemical environment or potential across the baroreceptors  30 . It is also possible that changing the electrical, thermal or chemical potential across the tissue surrounding the baroreceptors  30  may cause the surrounding tissue to stretch or otherwise deform, thus mechanically activating the baroreceptors  30 . In other instances, particularly the biological activation embodiments, a change in the function or sensitivity of the baroreceptors  30  may be induced by changing the biological activity in the baroreceptors  30  and altering their intracellular makeup and function. 
   All of the specific embodiments of the baroreceptor activation device  70  are suitable for implantation, and are preferably implanted using a minimally invasive percutaneous transluminal approach and/or a minimally invasive surgical approach, depending on whether the device  70  is disposed intravascularly, extravascularly or within the vascular wall  40 . The baroreceptor activation device  70  may be positioned anywhere baroreceptors  30  affecting the baroreflex system  50  are numerous, such as in the heart  11 , in the aortic arch  12 , in the common carotid arteries  18 / 19  near the carotid sinus  20 , in the subclavian arteries  13 / 16 , or in the brachiocephalic artery  22 . The baroreceptor activation device  70  may be implanted such that the device  70  is positioned immediately adjacent the baroreceptors  30 . Alternatively, the baroreceptor activation device  70  may be positioned in the low-pressure side of the heart or vasculature, near a baroreceptor, as described in U.S. patent application Ser. No. 10/284,063, previously incorporated by reference. In fact, the baroreceptor activation device  70  may even be positioned outside the body such that the device  70  is positioned a short distance from but proximate to the baroreceptors  30 . In one embodiment, the baroreceptor activation device  70  is implanted near the right carotid sinus  20  and/or the left carotid sinus (near the bifurcation of the common carotid artery) and/or the aortic arch  12 , where baroreceptors  30  have a significant impact on the baroreflex system  50 . For purposes of illustration only, the present invention is described with reference to baroreceptor activation device  70  positioned near the carotid sinus  20 . 
   The optional sensor  80  is operably coupled to the control system  60  by electric sensor cable or lead  82 . The sensor  80  may comprise any suitable device that measures or monitors a parameter indicative or predictive of the need to modify the activity of the central nervous system. For example, the sensor  80  may comprise a physiologic transducer or gauge that measures neurological activity, similar to an electroencephalogram (EEG). Alternatively, the sensor  80  may measure nervous system activity by any other technique. Examples of suitable transducers or gauges for the sensor  80  include EEG electrodes and the like. Although only one sensor  80  is shown, multiple sensors  80  of the same or different type at the same or different locations may be utilized. 
   The sensor  80  is preferably positioned on or near the patient&#39;s head or in another suitable location to measure neurological activity such as seizure activity or neurological activity indicative or predictive of a seizure. The sensor  80  may be disposed inside the body such as in or on the brain or a nerve (e.g., the vagus nerve), or disposed outside the body, depending on the type of transducer or gauge utilized. The sensor  80  may be separate from the baroreceptor activation device  70  or combined therewith. For purposes of illustration only, the sensor  80  is shown positioned on the head of the patient. 
   By way of example, the control system  60  includes a control block  61  comprising a processor  63  and a memory  62 . Control system  60  is connected to the sensor  80  by way of sensor cable  82 . Control system  60  is also connected to the baroreceptor activation device  70  by way of electric control cable  72 . Thus, the control system  60  receives a sensor signal from the sensor  80  by way of sensor cable  82 , and transmits a control signal to the baroreceptor activation device  70  by way of control cable  72 . 
   The memory  62  may contain data related to the sensor signal, the control signal, and/or values and commands provided by the input device  64 . The memory  62  may also include software containing one or more algorithms defining one or more functions or relationships between the control signal and the sensor signal. The algorithm may dictate activation or deactivation control signals depending on the sensor signal or a mathematical derivative thereof. The algorithm may dictate an activation or deactivation control signal when the sensor signal falls below a lower predetermined threshold value, rises above an upper predetermined threshold value or when the sensor signal indicates a specific physiologic event. 
   As mentioned previously, the baroreceptor activation device  70  may activate baroreceptors  30  mechanically, electrically, thermally, chemically, biologically or otherwise. In some instances, the control system  60  includes a driver  66  to provide the desired power mode for the baroreceptor activation device  70 . For example if the baroreceptor activation device  70  utilizes pneumatic or hydraulic actuation, the driver  66  may comprise a pressure/vacuum source and the cable  72  may comprise fluid line(s). If the baroreceptor activation device  70  utilizes electrical or thermal actuation, the driver  66  may comprise a power amplifier or the like and the cable  72  may comprise electrical lead(s). If the baroreceptor activation device  70  utilizes chemical or biological actuation, the driver  66  may comprise a fluid reservoir and a pressure/vacuum source, and the cable  72  may comprise fluid line(s). In other instances, the driver  66  may not be necessary, particularly if the processor  63  generates a sufficiently strong electrical signal for low level electrical or thermal actuation of the baroreceptor activation device  70 . 
   The control system  60  may operate as a closed loop utilizing feedback from the sensor  80 , or as an open loop utilizing commands received by input device  64 . The open loop operation of the control system  60  preferably utilizes some feedback from the transducer  80 , but may also operate without feedback. Commands received by the input device  64  may directly influence the control signal or may alter the software and related algorithms contained in memory  62 . The patient and/or treating physician may provide commands to input device  64 . Display  65  may be used to view the sensor signal, control signal and/or the software/data contained in memory  62 . 
   The control signal generated by the control system  60  may be continuous, periodic, episodic or a combination thereof, as dictated by an algorithm contained in memory  62 . The algorithm contained in memory  62  defines a stimulus regimen which dictates the characteristics of the control signal as a function of time, and thus dictates the stimulation of baroreceptors as a function of time. Continuous control signals include a pulse, a train of pulses, a triggered pulse and a triggered train of pulses, all of which are generated continuously. Examples of periodic control signals include each of the continuous control signals described above which have a designated start time (e.g., beginning of each minute, hour or day) and a designated duration (e.g., 1 second, 1 minute, 1 hour). Examples of episodic control signals include each of the continuous control signals described above which are triggered by an episode (e.g., activation by the patient/physician, an increase in blood pressure above a certain threshold, etc.). 
   The stimulus regimen governed by the control system  60  may be selected to promote long term efficacy. It is theorized that uninterrupted or otherwise unchanging activation of the baroreceptors  30  may result in the baroreceptors and/or the baroreflex system becoming less responsive over time, thereby diminishing the long-term effectiveness of the therapy. Therefore, the stimulus regimen may be selected to activate, deactivate or otherwise modulate the baroreceptor activation device  70  in such a way that therapeutic efficacy is maintained long term. 
   In addition to maintaining therapeutic efficacy over time, the stimulus regimens of the present invention may be selected reduce power requirement/consumption of the system  60 . As will be described in more detail hereinafter, the stimulus regimen may dictate that the baroreceptor activation device  70  be initially activated at a relatively higher energy and/or power level, and subsequently activated at a relatively lower energy and/or power level. The first level attains the desired initial therapeutic effect, and the second (lower) level sustains the desired therapeutic effect long term. By reducing the energy and/or power level after the desired therapeutic effect is initially attained, the power required or consumed by the activation device  70  is also reduced long term. This may correlate into systems having greater longevity and/or reduced size (due to reductions in the size of the power supply and associated components). 
   Another advantage of the stimulus regimens of the present invention is the reduction of unwanted collateral tissue stimulation. As mentioned above, the stimulus regimen may dictate that the baroreceptor activation device  70  be initially activated at a relatively higher energy and/or power level to attain the desired effect, and subsequently activated at a relatively lower energy and/or power level to maintain the desired effect. By reducing the output energy and/or power level, the stimulus may not travel as far from the target site, thereby reducing the likelihood of inadvertently stimulating adjacent tissues such as muscles in the neck and head. 
   Such stimulus regimens may be applied to all baroreceptor activation embodiments described herein. In addition to baroreceptor activation devices  70 , such stimulus regimens may be applied to the stimulation of the carotid sinus nerves or other nerves. In particular, the stimulus regimens described herein may be applied to baropacing (i.e., electrical stimulation of the carotid sinus nerve), as in the baropacing system disclosed in U.S. Pat. No. 6,073,048 to Kieval et al., the entire disclosure of which is incorporated herein by reference. 
   The stimulus regimen may be described in terms of the control signal and/or the output signal from the baroreceptor activation device  70 . Generally speaking, changes in the control signal result in corresponding changes in the output of the baroreceptor activation device  70  which affect corresponding changes in the baroreceptors  30 . The correlation between changes in the control signal and changes in the baroreceptor activation device  70  may be proportional or disproportional, direct or indirect (inverse), or any other known or predictable mathematical relationship. For purposes of illustration only, the stimulus regimen may be described herein in such a way that assumes the output of the baroreceptor activation device  70  is directly proportional to the control signal. 
   A first general approach for a stimulus regimen which promotes long term efficacy and reduces power requirements/consumption involves generating a control signal to cause the baroreceptor activation device  70  to have a first output level of relatively higher energy and/or power, and subsequently changing the control signal to cause the baroreceptor activation device  70  to have a second output level of relatively lower energy and/or power. The first output level may be selected and maintained for sufficient time to attain the desired initial effect (e.g., reduced seizure activity), after which the output level may be reduced to the second level for sufficient time to sustain the desired effect for the desired period of time. 
   For example, if the first output level has a power and/or energy value of X1, the second output level may have a power and/or energy value of X2, wherein X2 is less than X1. In some instances, X2 may be equal to zero, such that the first level is “on” and the second level is “off”. It is recognized that power and energy refer to two different parameters, but may, at least in some contexts, be used interchangeably. Generally speaking, power is a time derivative of energy. Thus, in some cases, a change in one of the parameters (power or energy) may not correlate to the same or similar change in the other parameter. In the present invention, it is contemplated that a change in one or both of the parameters may be suitable to obtain the desired result of promoting long term efficacy. 
   It is also contemplated that more than two levels may be used. Each further level may increase the output energy or power to attain the desired effect, or decrease the output energy or power to retain the desired effect. For example, in some instances, it may be desirable to have further reductions in the output level if the desired effect may be sustained at lower power or energy levels. In other instances, particularly when the desired effect is diminishing or is otherwise not sustained, it may be desirable to increase the output level until the desired effect is reestablished, and subsequently decrease the output level to sustain the effect. 
   The transition from each level may be a step function (e.g., a single step or a series of steps), a gradual transition over a period of time, or a combination thereof. In addition, the signal levels may be continuous, periodic or episodic as discussed previously. 
   The output (power or energy) level of the baroreceptor activation device  70  may be changed in a number of different ways depending on the mode of activation utilized. For example, in the mechanical activation embodiments described herein, the output level of the baroreceptor activation device  70  may be changed by changing the output force/pressure, tissue displacement distance, and/or rate of tissue displacement. In the thermal activation embodiments described herein, the output level of the baroreceptor activation device  70  may be changed by changing the temperature, the rate of temperature increase, or the rate of temperature decrease (dissipation rate). In the chemical and biological activation embodiments described herein, the output level of the baroreceptor activation device  70  may be changed by changing the volume/concentration of the delivered dose and/or the dose delivery rate. 
   In electrical activation embodiments using a non-modulated signal, the output (power or energy) level of the baroreceptor activation device  70  may be changed by changing the voltage, current and/or signal duration. The output signal of the baroreceptor activation device  70  may be, for example, constant current or constant voltage. In electrical activation embodiments using a modulated signal, wherein the output signal comprises, for example, a series of pulses, several pulse characteristics may be changed individually or in combination to change the power or energy level of the output signal. Such pulse characteristics include, but are not limited to: pulse amplitude (PA), pulse frequency (PF), pulse width or duration (PW), pulse waveform (square, triangular, sinusoidal, etc.), pulse polarity (for bipolar electrodes) and pulse phase (monophasic, biphasic). 
   In electrical activation embodiments wherein the output signal comprises a pulse train, several other signal characteristics may be changed in addition to the pulse characteristics described above. For example, the control or output signal may comprise a pulse train which generally includes a series of pulses occurring in bursts. Pulse train characteristics which may be changed include, but are not limited to: burst amplitude (equal to pulse amplitude if constant within burst packet), burst waveform (i.e., pulse amplitude variation within burst packet), burst frequency (BF), and burst width or duration (BW). The signal or a portion thereof (e.g., burst within the pulse train) may be triggered by any of the events discussed previously, by an EEG signal or a particular portion of an EEG signal, by another physiologic timing indicator, or the like. If the signal or a portion thereof is triggered, the triggering event may be changed and/or the delay from the triggering event may be changed. 
   A second general approach for a stimulus regimen which promotes long term efficacy and reduces power requirements/consumption involves the use of one baroreceptor activation device  70  having multiple output means (e.g., electrodes) or the use of multiple baroreceptor activation devices  70  each having a single or multiple output means. Basically, the stimulus regimen according to this approach calls for alternating activation of two or more devices  70  or output means, which are positioned at different anatomical locations. Alternating activation may be accomplished by alternating the control signal between the devices or output means. As used in this context, switching or alternating activation includes switching between individual output means, switching between sets of output means and individual output means, and switching between different sets of output means. By alternating activation between two or more different anatomical locations, the exposure of any single anatomical location to an output signal is reduced. 
   More specifically, a first device  70  or output means may be connected to a first baroreceptor location, and a second device  70  or output means may be connected to a second baroreceptor location, wherein the first location is different from the second location, and the control signal alternates activation of the first and second devices or output means. Although described with reference to two (first and second) devices  70  or output means, more than two may be utilized. By way of example, not limitation, a first device  70  or output means may be connected to the right carotid sinus, and a second device  70  or output means may be connected to the left carotid sinus. Alternatively, a first device  70  or output means may be connected to the left internal carotid artery, and a second device  70  or output means may be connected to the right internal carotid artery. As yet another alternative, first and second devices  70  or output means may be disposed next to each other but separated by a small distance (e.g., electrodes with multiple contact points). In each instance, the control signal alternates activation of the first and second devices or output means to reduce the signal exposure for each anatomical location. There are many possible anatomical combinations within the scope of this approach which are not specifically mentioned herein for sake of simplicity only. 
   A third general approach for a stimulus regimen which promotes long term efficacy and reduces power requirements/consumption involves changing the time domain characteristics and/or the triggering event characteristics of the therapy. For example, a periodic control signal which has a designated start time (e.g., beginning of each minute, hour or day; specific time of day) and a designated duration (e.g., 1 second, 1 minute, 1 hour) may have a change in the designated start time and/or duration. Alternatively, an episodic control signal which is triggered by an episode (e.g., activation by the patient/physician, a particular part of an EEG signal, or the like) may have a change in the delay from the triggering event or a change in the triggering event itself. For this latter alternative, the triggering event may be provided by feedback control utilizing sensor  80 . As a further alternative, the control signal may be asynchronous, wherein the start time, duration or delay from a base line event is asynchronous (e.g., random). 
   Any of the foregoing approaches may be utilized alone or in combination. The use of a combination of approaches may further promote long term efficacy and may further reduce power requirements/consumption. 
   The control system  60  may be implanted in whole or in part. For example, the entire control system  60  may be carried externally by the patient utilizing transdermal connections to the sensor lead  82  and the control lead  72 . Alternatively, the control block  61  and driver  66  may be implanted with the input device  64  and display  65  carried externally by the patient utilizing transdermal connections therebetween. As a further alternative, the transdermal connections may be replaced by cooperating transmitters/receivers to remotely communicate between components of the control system  60  and/or the sensor  80  and baroreceptor activation device  70 . 
   With general reference to  FIGS. 4-21 , schematic illustrations of specific embodiments of the baroreceptor activation device  70  are shown. The design, function and use of these specific embodiments, in addition to the control system  60  and sensor  80  (not shown), are the same as described with reference to  FIG. 3 , unless otherwise noted or apparent from the description. In addition, the anatomical features illustrated in  FIGS. 4-20  are the same as discussed with reference to  FIGS. 1 ,  2 A and  213 , unless otherwise noted. In each embodiment, the connections between the components  60 / 70 / 80  may be physical (e.g., wires, tubes, cables, etc.) or remote (e.g., transmitter/receiver, inductive, magnetic, etc.). For physical connections, the connection may travel intraarterially, intravenously, subcutaneously, or through other natural tissue paths. 
   Refer now to  FIGS. 4A and 4B  which show schematic illustrations of a baroreceptor activation device  100  in the form of an intravascular inflatable balloon. The inflatable balloon device  100  includes a helical balloon  102  which is connected to a fluid line  104 . An example of a similar helical balloon is disclosed in U.S. Pat. No. 5,181,911 to Shturman, the entire disclosure of which is hereby incorporated by reference. The balloon  102  preferably has a helical geometry or any other geometry which allows blood perfusion therethrough. The fluid line  104  is connected to the driver  66  of the control system  60 . In this embodiment, the driver  66  comprises a pressure/vacuum source (i.e., an inflation device) which selectively inflates and deflates the helical balloon  102 . Upon inflation, the helical balloon  102  expands, preferably increasing in outside diameter only, to mechanically activate baroreceptors  30  by stretching or otherwise deforming them and/or the vascular wall  40 . Upon deflation, the helical balloon  102  returns to its relaxed geometry such that the vascular wall  40  returns to its nominal state. Thus, by selectively inflating the helical balloon  102 , the baroreceptors  30  adjacent thereto may be selectively activated. 
   As an alternative to pneumatic or hydraulic expansion utilizing a balloon, a mechanical expansion device (not shown) may be used to expand or dilate the vascular wall  40  and thereby mechanically activate the baroreceptors  30 . For example, the mechanical expansion device may comprise a tubular wire braid structure that diametrically expands when longitudinally compressed as disclosed in U.S. Pat. No. 5,222,971 to Willard et al., the entire disclosure of which is hereby incorporated by reference. The tubular braid may be disposed intravascularly and permits blood perfusion through the wire mesh. In this embodiment, the driver  66  may comprise a linear actuator connected by actuation cables to opposite ends of the braid. When the opposite ends of the tubular braid are brought closer together by actuation of the cables, the diameter of the braid increases to expand the vascular wall  40  and activate the baroreceptors  30 . 
   Refer now to  FIGS. 5A and 5B  which show schematic illustrations of a baroreceptor activation device  120  in the form of an extravascular pressure cuff. The pressure cuff device  120  includes an inflatable cuff  122  which is connected to a fluid line  124 . Examples of a similar cuffs  122  are disclosed in U.S. Pat. No. 4,256,094 to Kapp et al. and U.S. Pat. No. 4,881,939 to Newman, the entire disclosures of which are hereby incorporated by reference. The fluid line  124  is connected to the driver  66  of the control system  60 . In this embodiment, the driver  66  comprises a pressure/vacuum source (i.e., an inflation device) which selectively inflates and deflates the cuff  122 . Upon inflation, the cuff  122  expands, preferably increasing in inside diameter only, to mechanically activate baroreceptors  30  by stretching or otherwise deforming them and/or the vascular wall  40 . Upon deflation, the cuff  122  returns to its relaxed geometry such that the vascular wall  40  returns to its nominal state. Thus, by selectively inflating the inflatable cuff  122 , the baroreceptors  30  adjacent thereto may be selectively activated. 
   The driver  66  may be automatically actuated by the control system  60  as discussed above, or may be manually actuated. An example of an externally manually actuated pressure/vacuum source is disclosed in U.S. Pat. No. 4,709,690 to Haber, the entire disclosure of which is hereby incorporated by reference. Examples of transdermally manually actuated pressure/vacuum sources are disclosed in U.S. Pat. No. 4,586,501 to Claracq, U.S. Pat. No. 4,828,544 to Lane et al., and U.S. Pat. No. 5,634,878 to Grundei et al., the entire disclosures of which are hereby incorporated by reference. 
   Other external compression devices may be used in place of the inflatable cuff device  120 . For example, a piston actuated by a solenoid may apply compression to the vascular wall. An example of a solenoid actuated piston device is disclosed in U.S. Pat. No. 4,014,318 to Dokum et al, and an example of a hydraulically or pneumatically actuated piston device is disclosed in U.S. Pat. No. 4,586,501 to Claracq, the entire disclosures of which are hereby incorporated by reference. Other examples include a rotary ring compression device as disclosed in U.S. Pat. No. 4,551,862 to Haber, and an electromagnetically actuated compression ring device as disclosed in U.S. Pat. No. 5,509,888 to Miller, the entire disclosures of which are hereby incorporated by reference. 
   Refer now to  FIGS. 6A and 6B  which show schematic illustrations of a baroreceptor activation device  140  in the form of an intravascular deformable structure. The deformable structure device  140  includes a coil, braid or other stent-like structure  142  disposed in the vascular lumen. The deformable structure  142  includes one or more individual structural members connected to an electrical lead  144 . Each of the structural members forming deformable structure  142  may comprise a shape memory material  146  (e.g., nickel titanium alloy) as illustrated in  FIG. 6C , or a bimetallic material  148  as illustrated in  FIG. 6D . The electrical lead  144  is connected to the driver  66  of the control system  60 . In this embodiment, the driver  66  comprises an electric power generator or amplifier which selectively delivers electric current to the structure  142  which resistively heats the structural members  146 / 148 . The structure  142  may be unipolar as shown using the surrounding tissue as ground, or bipolar or multipolar using leads connected to either end of the structure  142 . Electrical power may also be delivered to the structure  142  inductively as described hereinafter with reference to  FIGS. 14-16 . 
   Upon application of electrical current to the shape memory material  146 , it is resistively heated causing a phase change and a corresponding change in shape. Upon application of electrical current to the bimetallic material  148 , it is resistively heated causing a differential in thermal expansion and a corresponding change in shape. In either case, the material  146 / 148  is designed such that the change in shape causes expansion of the structure  142  to mechanically activate baroreceptors  30  by stretching or otherwise deforming them and/or the vascular wall  40 . Upon removal of the electrical current, the material  146 / 148  cools and the structure  142  returns to its relaxed geometry such that the baroreceptors  30  and/or the vascular wall  40  return to their nominal state. Thus, by selectively expanding the structure  142 , the baroreceptors  30  adjacent thereto may be selectively activated. 
   Refer now to  FIGS. 7A and 7B  which show schematic illustrations of a baroreceptor activation device  160  in the form of an extravascular deformable structure. The extravascular deformable structure device  160  is substantially the same as the intravascular deformable structure device  140  described with reference to  FIGS. 6A and 613 , except that the extravascular device  160  is disposed about the vascular wall, and therefore compresses, rather than expands, the vascular wall  40 . The deformable structure device  160  includes a coil, braid or other stent-like structure  162  comprising one or more individual structural members connected to an electrical lead  164 . Each of the structural members may comprise a shape memory material  166  (e.g., nickel titanium alloy) as illustrated in  FIG. 7C , or a bimetallic material  168  as illustrated in  FIG. 7D . The structure  162  may be unipolar as shown using the surrounding tissue as ground, or bipolar or multipolar using leads connected to either end of the structure  162 . Electrical power may also be delivered to the structure  162  inductively as described hereinafter with reference to  FIGS. 14-16 . 
   Upon application of electrical current to the shape memory material  166 , it is resistively heated causing a phase change and a corresponding change in shape. Upon application of electrical current to the bimetallic material  168 , it is resistively heated causing a differential in thermal expansion and a corresponding change in shape. In either case, the material  166 / 168  is designed such that the change in shape causes constriction of the structure  162  to mechanically activate baroreceptors  30  by compressing or otherwise deforming the baroreceptors  30  and/or the vascular wall  40 . 
   Upon removal of the electrical current, the material  166 / 168  cools and the structure  162  returns to its relaxed geometry such that the baroreceptors  30  and/or the vascular wall  40  return to their nominal state. Thus, by selectively compressing the structure  162 , the baroreceptors  30  adjacent thereto may be selectively activated. 
   Refer now to  FIGS. 8A and 8B  which show schematic illustrations of a baroreceptor activation device  180  in the form of an extravascular flow regulator which artificially creates back pressure adjacent the baroreceptors  30 . The flow regulator device  180  includes an external compression device  182 , which may comprise any of the external compression devices described with reference to  FIGS. 5A and 5B . The external compression device  182  is operably connected to the driver  66  of the control system  60  by way of cable  184 , which may comprise a fluid line or electrical lead, depending on the type of external compression device  182  utilized. The external compression device  182  is disposed about the vascular wall distal of the baroreceptors  30 . For example, the external compression device  182  may be located in the distal portions of the external or internal carotid arteries  18 / 19  to create back pressure adjacent to the baroreceptors  30  in the carotid sinus region  20 . Alternatively, the external compression device  182  may be located in the right subclavian artery  13 , the right common carotid artery  14 , the left common carotid artery  15 , the left subclavian artery  16 , or the brachiocephalic artery  22  to create back pressure adjacent the baroreceptors  30  in the aortic arch  12 . 
   Upon actuation of the external compression device  182 , the vascular wall is constricted thereby reducing the size of the vascular lumen therein. By reducing the size of the vascular lumen, pressure proximal of the external compression device  182  is increased thereby expanding the vascular wall. Thus, by selectively activating the external compression device  182  to constrict the vascular lumen and create back pressure, the baroreceptors  30  may be selectively activated. 
   Refer now to  FIGS. 9A and 9B  which show schematic illustrations of a baroreceptor activation device  200  in the form of an intravascular flow regular which artificially creates back pressure adjacent the baroreceptors  30 . The intravascular flow regulator device  200  is substantially similar in function and use as extravascular flow regulator  180  described with reference to  FIGS. 8A and 8B , except that the intravascular flow regulator device  200  is disposed in the vascular lumen. 
   Intravascular flow regulator  200  includes an internal valve  202  to at least partially close the vascular lumen distal of the baroreceptors  30 . By at least partially closing the vascular lumen distal of the baroreceptors  30 , back pressure is created proximal of the internal valve  202  such that the vascular wall expands to activate the baroreceptors  30 . The internal valve  202  may be positioned at any of the locations described with reference to the external compression device  182 , except that the internal valve  202  is placed within the vascular lumen. Specifically, the internal compression device  202  may be located in the distal portions of the external or internal carotid arteries  18 / 19  to create back pressure adjacent to the baroreceptors  30  in the carotid sinus region  20 . Alternatively, the internal compression device  202  may be located in the right subclavian artery  13 , the right common carotid artery  14 , the left common carotid artery  15 , the left subclavian artery  16 , or the brachiocephalic artery  22  to create back pressure adjacent the baroreceptors  30  in the aortic arch  12 . 
   The internal valve  202  is operably coupled to the driver  66  of the control system  60  by way of electrical lead  204 . The control system  60  may selectively open, close or change the flow resistance of the valve  202  as described in more detail hereinafter. The internal valve  202  may include valve leaflets  206  (bi-leaflet or trileaflet) which rotate inside housing  208  about an axis between an open position and a closed position. The closed position may be completely closed or partially closed, depending on the desired amount of back pressure to be created. The opening and closing of the internal valve  202  may be selectively controlled by altering the resistance of leaflet  206  rotation or by altering the opening force of the leaflets  206 . The resistance of rotation of the leaflets  206  may be altered utilizing electromagnetically actuated metallic bearings carried by the housing  208 . The opening force of the leaflets  206  may be altered by utilizing electromagnetic coils in each of the leaflets to selectively magnetize the leaflets such that they either repel or attract each other, thereby facilitating valve opening and closing, respectively. 
   A wide variety of intravascular flow regulators may be used in place of internal valve  202 . For example, internal inflatable balloon devices as disclosed in U.S. Pat. No. 4,682,583 to Burton et al. and U.S. Pat. No. 5,634,878 to Grundei et al., the entire disclosures of which is hereby incorporated by reference, may be adapted for use in place of valve  202 . Such inflatable balloon devices may be operated in a similar manner as the inflatable cuff  122  described with reference to  FIG. 5 . Specifically, in this embodiment, the driver  66  would comprises a pressure/vacuum source (i.e., an inflation device) which selectively inflates and deflates the internal balloon. Upon inflation, the balloon expands to partially occlude blood flow and create back pressure to mechanically activate baroreceptors  30  by stretching or otherwise deforming them and/or the vascular wall  40 . Upon deflation, the internal balloon returns to its normal profile such that flow is not hindered and back pressure is eliminated. Thus, by selectively inflating the internal balloon, the baroreceptors  30  proximal thereof may be selectively activated by creating back pressure. 
   Refer now to  FIGS. 10A and 10B  which show schematic illustrations of a baroreceptor activation device  220  in the form of magnetic particles  222  disposed in the vascular wall  40 . The magnetic particles  222  may comprise magnetically responsive materials (i.e., ferrous based materials) and may be magnetically neutral or magnetically active. Preferably, the magnetic particles  222  comprise permanent magnets having an elongate cylinder shape with north and south poles to strongly respond to magnetic fields. The magnetic particles  222  are actuated by an electromagnetic coil  224  which is operably coupled to the driver  66  of the control system  60  by way of an electrical cable  226 . The electromagnetic coil  224  may be implanted as shown, or located outside the body, in which case the driver  66  and the remainder of the control system  60  would also be located outside the body. By selectively activating the electromagnetic coil  224  to create a magnetic field, the magnetic particles  222  may be repelled, attracted or rotated. Alternatively, the magnetic field created by the electromagnetic coil  224  may be alternated such that the magnetic particles  222  vibrate within the vascular wall  40 . When the magnetic particles are repelled, attracted, rotated, vibrated or otherwise moved by the magnetic field created by the electromagnetic coil  224 , the baroreceptors  30  are mechanically activated. 
   The electromagnetic coil  224  is preferably placed as close as possible to the magnetic particles  222  in the vascular wall  40 , and may be placed intravascularly, extravascularly, or in any of the alternative locations discussed with reference to inductor shown in  FIGS. 14-16 . The magnetic particles  222  may be implanted in the vascular wall  40  by injecting a ferro-fluid or a ferro-particle suspension into the vascular wall adjacent to the baroreceptors  30 . To increase biocompatibility, the particles  222  may be coated with a ceramic, polymeric or other inert material. Injection of the fluid carrying the magnetic particles  222  is preferably performed percutaneously. 
   Refer now to  FIGS. 11A and 11B  which show schematic illustrations of a baroreceptor activation device  240  in the form of one or more transducers  242 . Preferably, the transducers  242  comprise an array surrounding the vascular wall. The transducers  242  may be intravascularly or extravascularly positioned adjacent to the baroreceptors  30 . In this embodiment, the transducers  242  comprise devices which convert electrical signals into some physical phenomena, such as mechanical vibration or acoustic waves. The electrical signals are provided to the transducers  242  by way of electrical cables  244  which are connected to the driver  66  of the control system  60 . By selectively activating the transducers  242  to create a physical phenomena, the baroreceptors  30  may be mechanically activated. 
   The transducers  242  may comprise an acoustic transmitter which transmits sonic or ultrasonic sound waves into the vascular wall  40  to activate the baroreceptors  30 . Alternatively, the transducers  242  may comprise a piezoelectric material which vibrates the vascular wall to activate the baroreceptors  30 . As a further alternative, the transducers  242  may comprise an artificial muscle which deflects upon application of an electrical signal. An example of an artificial muscle transducer comprises plastic impregnated with a lithium-perchlorate electrolyte disposed between sheets of polypyrrole, a conductive polymer. Such plastic muscles may be electrically activated to cause deflection in different directions depending on the polarity of the applied current. 
   Refer now to  FIGS. 12A and 12B  which show schematic illustrations of a baroreceptor activation device  260  in the form of a local fluid delivery device  262  suitable for delivering a chemical or biological fluid agent to the vascular wall adjacent the baroreceptors  30 . The local fluid delivery device  262  may be located intravascularly, extravascularly, or intramurally. For purposes of illustration only, the local fluid delivery device  262  is positioned extravascularly. 
   The local fluid delivery device  262  may include proximal and distal seals  266  which retain the fluid agent disposed in the lumen or cavity  268  adjacent to vascular wall. Preferably, the local fluid delivery device  262  completely surrounds the vascular wall  40  to maintain an effective seal. Those skilled in the art will recognize that the local fluid delivery device  262  may comprise a wide variety of implantable drug delivery devices or pumps known in the art. 
   The local fluid delivery device  260  is connected to a fluid line  264  which is connected to the driver  66  of the control system  60 . In this embodiment, the driver  66  comprises a pressure/vacuum source and fluid reservoir containing the desired chemical or biological fluid agent. The chemical or biological fluid agent may comprise a wide variety of stimulatory substances. Examples include veratridine, bradykinin, prostaglandins, and related substances. Such stimulatory substances activate the baroreceptors  30  directly or enhance their sensitivity to other stimuli and therefore may be used in combination with the other baroreceptor activation devices described herein. Other examples include growth factors and other agents that modify the function of the baroreceptors  30  or the cells of the vascular tissue surrounding the baroreceptors  30  causing the baroreceptors  30  to be activated or causing alteration of their responsiveness or activation pattern to other stimuli. It is also contemplated that injectable stimulators that are induced remotely, as described in U.S. Pat. No. 6,061,596 which is incorporated herein by reference, may be used with the present invention. 
   As an alternative, the fluid delivery device  260  may be used to deliver a photochemical that is essentially inert until activated by light to have a stimulatory effect as described above. In this embodiment, the fluid delivery device  260  would include a light source such as a light emitting diode (LED), and the driver  66  of the control system  60  would include a pulse generator for the LED combined with a pressure/vacuum source and fluid reservoir described previously. The photochemical would be delivered with the fluid delivery device  260  as described above, and the photochemical would be activated, deactivated or modulated by activating, deactivating or modulating the LED. 
   As a further alternative, the fluid delivery device  260  may be used to deliver a warrn or hot fluid (e.g. saline) to thermally activate the baroreceptors  30 . In this embodiment, the driver  66  of the control system  60  would include a heat generator for heating the fluid, combined with a pressure/vacuum source and fluid reservoir described previously. The hot or warm fluid would be delivered and preferably circulated with the fluid delivery device  260  as described above, and the temperature of the fluid would be controlled by the driver  66 . 
   Refer now to  FIGS. 13A and 13B  which show schematic illustrations of a baroreceptor activation device  280  in the form of an intravascular electrically conductive structure or electrode  282 . The electrode structure  282  may comprise a self-expanding or balloon expandable coil, braid or other stent-like structure disposed in the vascular lumen. The electrode structure  282  may serve the dual purpose of maintaining lumen patency while also delivering electrical stimuli. To this end, the electrode structure  282  may be implanted utilizing conventional intravascular stent and filter delivery techniques. Preferably, the electrode structure  282  comprises a geometry which allows blood perfusion therethrough. The electrode structure  282  comprises electrically conductive material which may be selectively insulated to establish contact with the inside surface of the vascular wall  40  at desired locations, and limit extraneous electrical contact with blood flowing through the vessel and other tissues. 
   The electrode structure  282  is connected to electric lead  284  which is connected to the driver  66  of the control system  60 . The driver  66 , in this embodiment, may comprise a power amplifier, pulse generator or the like to selectively deliver electrical control signals to structure  282 . As mentioned previously, the electrical control signal generated by the driver  66  may be continuous, periodic, episodic or a combination thereof, as dictated by an algorithm contained in memory  62  of the control system  60 . Continuous control signals include a constant pulse, a constant train of pulses, a triggered pulse and a triggered train of pulses. Periodic control signals include each of the continuous control signals described above which have a designated start time and a designated duration. Episodic control signals include each of the continuous control signals described above which are triggered by an episode. 
   By selectively activating, deactivating or otherwise modulating the electrical control signal transmitted to the electrode structure  282 , electrical energy may be delivered to the vascular wall to activate the baroreceptors  30 . As discussed previously, activation of the baroreceptors  30  may occur directly or indirectly. In particular, the electrical signal delivered to the vascular wall  40  by the electrode structure  282  may cause the vascular wall to stretch or otherwise deform thereby indirectly activating the baroreceptors  30  disposed therein. Alternatively, the electrical signals delivered to the vascular wall by the electrode structure  282  may directly activate the baroreceptors  30  by changing the electrical potential across the baroreceptors  30 . In either case, the electrical signal is delivered to the vascular wall  40  immediately adjacent to the baroreceptors  30 . It is also contemplated that the electrode structure  282  may delivery thermal energy by utilizing a semi-conductive material having a higher resistance such that the electrode structure  282  resistively generates heat upon application of electrical energy. 
   Various alternative embodiments are contemplated for the electrode structure  282 , including its design, implanted location, and method of electrical activation. For example, the electrode structure  282  may be unipolar as shown in  FIGS. 13A and 13B  using the surrounding tissue as ground, or bipolar using leads connected to either end of the structure  282  as shown in  FIGS. 18A and 18B . In the embodiment of  FIGS. 18A and 1813 , the electrode structure  282  includes two or more individual electrically conductive members  283 / 285  which are electrically isolated at their respective cross-over points utilizing insulative materials. Each of the members  283 / 285  is connected to a separate conductor contained within the electrical lead  284 . Alternatively, an array of bipoles may be used as described in more detail with reference to  FIG. 21 . As a further alternative, a multipolar arrangement may be used wherein three or more electrically conductive members are included in the structure  282 . For example, a tripolar arrangement may be provided by one electrically conductive member having a polarity disposed between two electrically conductive members having the opposite polarity. 
   In terms of electrical activation, the electrical signals may be directly delivered to the electrode structure  282  as described with reference to  FIGS. 13A and 13B , or indirectly delivered utilizing an inductor as illustrated in  FIGS. 14-16  and  21 . The embodiments of  FIGS. 14-16  and  21  utilize an inductor  286  which is operably connected to the driver  66  of the control system  60  by way of electrical lead  284 . The inductor  286  comprises an electrical winding which creates a magnetic field  287  (as seen in  FIG. 21 ) around the electrode structure  282 . The magnetic field  287  may be alternated by alternating the direction of current flow through the inductor  286 . Accordingly, the inductor  286  may be utilized to create current flow in the electrode structure  282  to thereby deliver electrical signals to the vascular wall  40  to directly or indirectly activate the baroreceptors  30 . In all embodiments, the inductor  286  may be covered with an electrically insulative material to eliminate direct electrical stimulation of tissues surrounding the inductor  286 . A preferred embodiment of an inductively activated electrode structure  282  is described in more detail with reference to  FIGS. 21A-21C . 
   The embodiments of  FIGS. 13-16  may be modified to form a cathode/anode arrangement. Specifically, the electrical inductor  286  would be connected to the driver  66  as shown in  FIGS. 14-16  and the electrode structure  282  would be connected to the driver  66  as shown in  FIG. 13 . With this arrangement, the electrode structure  282  and the inductor  286  may be any suitable geometry and need not be coiled for purposes of induction. The electrode structure  282  and the inductor  286  would comprise a cathode/anode or anode/cathode pair. For example, when activated, the cathode  282  may generate a primary stream of electrons which travel through the inter-electrode space (i.e., vascular tissue and baroreceptors  30 ) to the anode  286 . The cathode is preferably cold, as opposed to thermionic, during electron emission. The electrons may be used to electrically or thermally activate the baroreceptors  30  as discussed previously. 
   The electrical inductor  286  is preferably disposed as close as possible to the electrode structure  282 . For example, the electrical inductor  286  may be disposed adjacent the vascular wall as illustrated in  FIGS. 14A and 14B . Alternatively, the inductor  286  may be disposed in an adjacent vessel as illustrated in  FIGS. 15A and 15B . If the electrode structure  282  is disposed in the carotid sinus  20 , for example, the inductor  286  may be disposed in the internal jugular vein  21  as illustrated in  FIGS. 15A and 15B . In the embodiment of  FIGS. 15A and 1513 , the electrical inductor  286  may comprise a similar structure as the electrode structure  282 . As a further alternative, the electrical inductor  286  may be disposed outside the patient&#39;s body, but as close as possible to the electrode structure  282 . If the electrode structure  282  is disposed in the carotid sinus  20 , for example, the electrical inductor  286  may be disposed on the right or left side of the neck of the patient as illustrated in  FIGS. 16A and 16B . In the embodiment of  FIGS. 16A and 16B , wherein the electrical inductor  286  is disposed outside the patient&#39;s body, the control system  60  may also be disposed outside the patient&#39;s body. 
   In terms of implant location, the electrode structure  282  may be intravascularly disposed as described with reference to  FIGS. 13A and 13B , or extravascularly disposed as described with reference to  FIGS. 17A and 17B , which show schematic illustrations of a baroreceptor activation device  300  in the form of an extravascular electrically conductive structure or electrode  302 . Except as described herein, the extravascular electrode structure  302  is the same in design, function, and use as the intravascular electrode structure  282 . The electrode structure  302  may comprise a coil, braid or other structure capable of surrounding the vascular wall. Alternatively, the electrode structure  302  may comprise one or more electrode patches distributed around the outside surface of the vascular wall. Because the electrode structure  302  is disposed on the outside surface of the vascular wall, intravascular delivery techniques may not be practical, but minimally invasive surgical techniques will suffice. The extravascular electrode structure  302  may receive electrical signals directly from the driver  66  of the control system  60  by way of electrical lead  304 , or indirectly by utilizing an inductor (not shown) as described with reference to  FIGS. 14-16 . 
   Refer now to  FIGS. 19A and 19B  which show schematic illustrations of a baroreceptor activation device  320  in the form of electrically conductive particles  322  disposed in the vascular wall. This embodiment is substantially the same as the embodiments described with reference to  FIGS. 13-18 , except that the electrically conductive particles  322  are disposed within the vascular wall, as opposed to the electrically conductive structures  282 / 302  which are disposed on either side of the vascular wall. In addition, this embodiment is similar to the embodiment described with reference to  FIG. 10 , except that the electrically conductive particles  322  are not necessarily magnetic as with magnetic particles  222 , and the electrically conductive particles  322  are driven by an electromagnetic filed rather than by a magnetic field. 
   In this embodiment, the driver  66  of the control system  60  comprises an electromagnetic transmitter such as an radiofrequency or microwave transmitter. Electromagnetic radiation is created by the transmitter  66  which is operably coupled to an antenna  324  by way of electrical lead  326 . Electromagnetic waves are emitted by the antenna  324  and received by the electrically conductive particles  322  disposed in the vascular wall  40 . Electromagnetic energy creates oscillating current flow within the electrically conductive particles  322 , and depending on the intensity of the electromagnetic radiation and the resistivity of the conductive particles  322 , may cause the electrical particles  322  to generate heat. The electrical or thermal energy generated by the electrically conductive particles  322  may directly activate the baroreceptors  30 , or indirectly activate the baroreceptors  30  by way of the surrounding vascular wall tissue. 
   The electromagnetic radiation transmitter  66  and antenna  324  may be disposed in the patient&#39;s body, with the antenna  324  disposed adjacent to the conductive particles in the vascular wall  40  as illustrated in  FIGS. 19A and 19B . Alternatively, the antenna  324  may be disposed in any of the positions described with reference to the electrical inductor shown in  FIGS. 14-16 . It is also contemplated that the electromagnetic radiation transmitter  66  and antenna  324  may be utilized in combination with the intravascular and extravascular electrically conductive structures  282 / 302  described with reference to  FIGS. 13-18  to generate thermal energy on either side of the vascular wall. 
   As an alternative, the electromagnetic radiation transmitter  66  and antenna  324  may be used without the electrically conductive particles  322 . Specifically, the electromagnetic radiation transmitter  66  and antenna  324  may be used to deliver electromagnetic radiation (e.g., RF, microwave) directly to the baroreceptors  30  or the tissue adjacent thereto to cause localized heating, thereby thermally inducing a baroreceptor  30  signal. 
   Refer now to  FIGS. 20A and 20B  which show schematic illustrations of a baroreceptor activation device  340  in the form of a Peltier effect device  342 . The Peltier effect device  342  may be extravascularly positioned as illustrated, or may be intravascularly positioned similar to an intravascular stent or filter. The Peltier effect device  342  is operably connected to the driver  66  of the control system  60  by way of electrical lead  344 . The Peltier effect device  342  includes two dissimilar metals or semiconductors  343 / 345  separated by a thermal transfer junction  347 . In this particular embodiment, the driver  66  comprises a power source which delivers electrical energy to the dissimilar metals or semiconductors  343 / 345  to create current flow across the thermal junction  347 . 
   When current is delivered in an appropriate direction, a cooling effect is created at the thermal junction  347 . There is also a heating effect created at the junction between the individual leads  344  connected to the dissimilar metals or semiconductors  343 / 345 . This heating effect, which is proportional to the cooling effect, may be utilized to activate the baroreceptors  30  by positioning the junction between the electrical leads  344  and the dissimilar metals or semiconductors  343 / 345  adjacent to the vascular wall  40 . 
   Refer now to  FIGS. 21A-21C  which show schematic illustrations of a preferred embodiment of an inductively activated electrode structure  282  for use with the embodiments described with reference to  FIGS. 14-16 . In this embodiment, current flow in the electrode structure  282  is induced by a magnetic field  287  created by an inductor  286  which is operably coupled to the driver  66  of the control system  60  by way of electrical cable  284 . The electrode structure  282  preferably comprises a multi-filar self-expanding braid structure including a plurality of individual members  282   a ,  282   b ,  282   c  and  282   d . However, the electrode structure  282  may simply comprise a single coil for purposes of this embodiment. 
   Each of the individual coil members  282   a - 282   d  comprising the electrode structure  282  consists of a plurality of individual coil turns  281  connected end to end as illustrated in  FIGS. 21B and 21C .  FIG. 21C  is a detailed view of the connection between adjacent coil turns  281  as shown in  FIG. 21B . Each coil turn  281  comprises electrically isolated wires or receivers in which a current flow is established when a changing magnetic field  287  is created by the inductor  286 . The inductor  286  is preferably covered with an electrically insulative material to eliminate direct electrical stimulation of tissues surrounding the inductor  286 . Current flow through each coil turn  281  results in a potential drop  288  between each end of the coil turn  281 . With a potential drop defined at each junction between adjacent coil turns  281 , a localized current flow cell is created in the vessel wall adjacent each junction. 
   Thus an array or plurality of bipoles are created by the electrode structure  282  and uniformly distributed around the vessel wall. Each coil turn  281  comprises an electrically conductive wire material  290  surrounded by an electrically insulative material  292 . The ends of each coil turn  281  are connected by an electrically insulated material  294  such that each coil turn  281  remains electrically isolated. The insulative material  294  mechanically joins but electrically isolates adjacent coil turns  281  such that each turn  281  responds with a similar potential drop  288  when current flow is induced by the changing magnetic field  287  of the inductor  286 . An exposed portion  296  is provided at each end of each coil turn  281  to facilitate contact with the vascular wall tissue. Each exposed portion  296  comprises an isolated electrode in contact with the vessel wall. The changing magnetic field  287  of the inductor  286  causes a potential drop in each coil turn  281  thereby creating small current flow cells in the vessel wall corresponding to adjacent exposed regions  296 . The creation of multiple small current cells along the inner wall of the blood vessel serves to create a cylindrical zone of relatively high current density such that the baroreceptors  30  are activated. However, the cylindrical current density field quickly reduces to a negligible current density near the outer wall of the vascular wall, which serves to limit extraneous current leakage to minimize or eliminate unwanted activation of extravascular tissues and structures such as nerves or muscles. 
   Refer now to  FIGS. 22A-22F  which show schematic illustrations of various possible arrangements of electrodes around the carotid sinus  20  for extravascular electrical activation embodiments, such as baroreceptor activation device  300  described with reference to  FIGS. 17A and 17B . The electrode designs illustrated and described hereinafter may be particularly suitable for connection to the carotid arteries at or near the carotid sinus, and may be designed to minimize extraneous tissue stimulation. 
   In  FIGS. 22A-22F , the carotid arteries are shown, including the common  14 , the external  18  and the internal  19  carotid arteries. The location of the carotid sinus  20  may be identified by a landmark bulge  21 , which is typically located on the internal carotid artery  19  just distal of the bifurcation, or extends across the bifurcation from the common carotid artery  14  to the internal carotid artery  19 . 
   The carotid sinus  20 , and in particular the bulge  21  of the carotid sinus, may contain a relatively high density of baroreceptors  30  (not shown) in the vascular wall. For this reason, it may be desirable to position the electrodes  302  of the activation device  300  on and/or around the sinus bulge  21  to maximize baroreceptor responsiveness and to minimize extraneous tissue stimulation. 
   It should be understood that the device  300  and electrodes  302  are merely schematic, and only a portion of which may be shown, for purposes of illustrating various positions of the electrodes  302  on and/or around the carotid sinus  20  and the sinus bulge  21 . In each of the embodiments described herein, the electrodes  302  may be monopolar (electrodes are cathodes, surrounding tissue is anode or ground), bipolar (cathode-anode pairs), or tripolar (anode-cathode-anode sets). Specific extravascular electrode designs are described in more detail hereinafter. 
   In  FIG. 22A , the electrodes  302  of the extravascular electrical activation device  300  extend around a portion or the entire circumference of the sinus  20  in a circular fashion. In  FIG. 2213 , the electrodes  302  of the extravascular electrical activation device  300  extend around a portion or the entire circumference of the sinus  20  in a helical fashion. In the helical arrangement shown in  FIG. 2213 , the electrodes  302  may wrap around the sinus  20  any number of times to establish the desired electrode  302  contact and coverage. In the circular arrangement shown in  FIG. 22A , a single pair of electrodes  302  may wrap around the sinus  20 , or a plurality of electrode pairs  302  may be wrapped around the sinus  20  as shown in  FIG. 22C  to establish more electrode  302  contact and coverage. 
   The plurality of electrode pairs  302  may extend from a point proximal of the sinus  20  or bulge  21 , to a point distal of the sinus  20  or bulge  21  to ensure activation of baroreceptors  30  throughout the sinus  20  region. The electrodes  302  may be connected to a single channel or multiple channels as discussed in more detail hereinafter. The plurality of electrode pairs  302  may be selectively activated for purposes of targeting a specific area of the sinus  20  to increase baroreceptor responsiveness, or for purposes of reducing the exposure of tissue areas to activation to maintain baroreceptor responsiveness long term. 
   In  FIG. 22D , the electrodes  302  extend around the entire circumference of the sinus  20  in a criss-cross fashion. The criss-cross arrangement of the electrodes  302  establishes contact with both the internal  19  and external  18  carotid arteries around the carotid sinus  20 . Similarly, in  FIG. 22E , the electrodes  302  extend around all or a portion of the circumference of the sinus  20 , including the internal  19  and external  18  carotid arteries at the bifurcation, and in some instances the common carotid artery  14 . In  FIG. 22F , the electrodes  302  extend around all or a portion of the circumference of the sinus  20 , including the internal  19  and external  18  carotid arteries distal of the bifurcation. In  FIGS. 22E and 22F , the extravascular electrical activation devices  300  are shown to include a substrate or base structure  306  which may encapsulate and insulate the electrodes  302  and may provide a means for attachment to the sinus  20  as described in more detail hereinafter. 
   From the foregoing discussion with reference to  FIGS. 22A-22F , it should be apparent that there are a number of suitable arrangements for the electrodes  302  of the activation device  300 , relative to the carotid sinus  20  and associated anatomy. In each of the examples given above, the electrodes  302  are wrapped around a portion of the carotid structure, which may require deformation of the electrodes  302  from their relaxed geometry (e.g., straight). To reduce or eliminate such deformation, the electrodes  302  and/or the base structure  306  may have a relaxed geometry that substantially conforms to the shape of the carotid anatomy at the point of attachment. In other words, the electrodes  302  and the base structure  306  may be pre-shaped to conform to the carotid anatomy in a substantially relaxed state. Alternatively, the electrodes  302  may have a geometry and/or orientation that reduces the amount of electrode  302  strain. 
   For example, in  FIG. 23 , the electrodes  302  are shown to have a serpentine or wavy shape. The serpentine shape of the electrodes  302  reduces the amount of strain seen by the electrode material when wrapped around a carotid structure. In addition, the serpentine shape of the electrodes increases the contact surface area of the electrode  302  with the carotid tissue. As an alternative, the electrodes  302  may be arranged to be substantially orthogonal to the wrap direction (i.e., substantially parallel to the axis of the carotid arteries) as shown in  FIG. 24 . In this alternative, the electrodes  302  each have a length and a width or diameter, wherein the length is substantially greater than the width or diameter. The electrodes  302  each have a longitudinal axis parallel to the length thereof, wherein the longitudinal axis is orthogonal to the wrap direction and substantially parallel to the longitudinal axis of the carotid artery about which the device  300  is wrapped. As with the multiple electrode embodiments described previously, the electrodes  302  may be connected to a single channel or multiple channels as discussed in more detail hereinafter. 
   Refer now to  FIGS. 25-28  which schematically illustrate various multichannel electrodes for the extravascular electrical activation device  300 .  FIG. 25  illustrates a six (6) channel electrode assembly including six (6) separate elongate electrodes  302  extending adjacent to and parallel with each other. The electrodes  302  are each connected to multi-channel cable  304 . Some of the electrodes  302  may be common, thereby reducing the number of channels necessary in the cable  304 . 
   Base structure or substrate  306  may comprise a flexible and electrically insulative material suitable for implantation, such as silicone, perhaps reinforced with a flexible material such as polyester fabric. The base  306  may have a length suitable to wrap around all (360°) or a portion (i.e., less than 360°) of the circumference of one or more of the carotid arteries adjacent the carotid sinus  20 . The electrodes  302  may extend around a portion (i.e., less than 360° such as 270°, 180° or 90°) of the circumference of one or more of the carotid arteries adjacent the carotid sinus  20 . To this end, the electrodes  302  may have a length that is less than (e.g., 75%, 50% or 25%) the length of the base  206 . The electrodes  302  may be parallel, orthogonal or oblique to the length of the base  306 , which is generally orthogonal to the axis of the carotid artery to which it is disposed about. 
   The electrodes  302  may comprise round wire, rectangular ribbon or foil formed of an electrically conductive and radiopaque material such as platinum. The base structure  306  substantially encapsulates the electrodes  302 , leaving only an exposed area for electrical connection to extravascular carotid sinus tissue. For example, each electrode  302  may be partially recessed in the base  206  and may have one side exposed along all or a portion of its length for electrical connection to carotid tissue. Electrical paths through the carotid tissues may be defined by one or more pairs of the elongate electrodes  302 . 
   In all embodiments described with reference to  FIGS. 25-28 , the multichannel electrodes  302  may be selectively activated for purposes of mapping and targeting a specific area of the carotid sinus  20  to determine the best combination of electrodes  302  (e.g., individual pair, or groups of pairs) to activate for maximum baroreceptor responsiveness, as described elsewhere herein. In addition, the multichannel electrodes  302  may be selectively activated for purposes of reducing the exposure of tissue areas to activation to maintain long term efficacy as described, as described elsewhere herein. For these purposes, it may be useful to utilize more than two (2) electrode channels. Alternatively, the electrodes  302  may be connected to a single channel whereby baroreceptors are uniformly activated throughout the sinus  20  region. 
   An alternative multi-channel electrode design is illustrated in  FIG. 26 . In this embodiment, the device  300  includes sixteen (16) individual electrode pads  302  connected to 16-channel cable  304  via 4-channel connectors  303 . In this embodiment, the circular electrode pads  302  are partially encapsulated by the base structure  306  to leave one face of each button electrode  302  exposed for electrical connection to carotid tissues. With this arrangement, electrical paths through the carotid tissues may be defined by one or more pairs (bipolar) or groups (tripolar) of electrode pads  302 . 
   A variation of the multi-channel pad-type electrode design is illustrated in  FIG. 27 . In this embodiment, the device  300  includes sixteen (16) individual circular pad electrodes  302  surrounded by sixteen (16) rings  305 , which collectively may be referred to as concentric electrode pads  302 / 305 . Pad electrodes  302  are connected to 17-channel cable  304  via 4-channel connectors  303 , and rings  305  are commonly connected to 17-channel cable  304  via a single channel connector  307 . In this embodiment, the circular shaped electrodes  302  and the rings  305  are partially encapsulated by the base structure  306  to leave one face of each pad electrode  302  and one side of each ring  305  exposed for electrical connection to carotid tissues. As an alternative, two rings  305  may surround each electrode  302 , with the rings  305  being commonly connected. With these arrangements, electrical paths through the carotid tissues may be defined between one or more pad electrode  302 /ring  305  sets to create localized electrical paths. 
   Another variation of the multi-channel pad electrode design is illustrated in  FIG. 28 . In this embodiment, the device  300  includes a control IC chip  310  connected to 3-channel cable  304 . The control chip  310  is also connected to sixteen (16) individual pad electrodes  302  via 4-channel connectors  303 . The control chip  310  permits the number of channels in cable  304  to be reduced by utilizing a coding system. The control system  60  sends a coded control signal which is received by chip  310 . The chip  310  converts the code and enables or disables selected electrode  302  pairs in accordance with the code. 
   For example, the control signal may comprise a pulse wave form, wherein each pulse includes a different code. The code for each pulse causes the chip  310  to enable one or more pairs of electrodes, and to disable the remaining electrodes. Thus, the pulse is only transmitted to the enabled electrode pair(s) corresponding to the code sent with that pulse. Each subsequent pulse would have a different code than the preceding pulse, such that the chip  310  enables and disables a different set of electrodes  302  corresponding to the different code. Thus, virtually any number of electrode pairs may be selectively activated using control chip  310 , without the need for a separate channel in cable  304  for each electrode  302 . By reducing the number of channels in cable  304 , the size and cost thereof may be reduced. 
   Optionally, the IC chip  310  may be connected to feedback sensor  80 , taking advantage of the same functions as described with reference to  FIG. 3 . In addition, one or more of the electrodes  302  may be used as feedback sensors when not enabled for activation. For example, such a feedback sensor electrode may be used to measure or monitor electrical conduction in the vascular wall to provide data analogous to an ECG. Alternatively, such a feedback sensor electrode may be used to sense a change in impedance due to changes in blood volume during a pulse pressure to provide data indicative or predictive of heart rate, blood pressure, or other physiologic parameter. 
   Refer now to  FIG. 29  which schematically illustrates an extravascular electrical activation device  300  including a support collar or anchor  312 . In this embodiment, the activation device  300  is wrapped around the internal carotid artery  19  at the carotid sinus  20 , and the support collar  312  is wrapped around the common carotid artery  14 . The activation device  300  is connected to the support collar  312  by cables  304 , which act as a loose tether. With this arrangement, the collar  312  isolates the activation device from movements and forces transmitted by the cables  304  proximal of the support collar, such as may be encountered by movement of the control system  60  and/or driver  66 . As an alternative to support collar  312 , a strain relief (not shown) may be connected to the base structure  306  of the activation device  300  at the juncture between the cables  304  and the base  306 . With either approach, the position of the device  300  relative to the carotid anatomy may be better maintained despite movements of other parts of the system. 
   In this embodiment, the base structure  306  of the activation device  300  may comprise molded tube, a tubular extrusion, or a sheet of material wrapped into a tube shape utilizing a suture flap  308  with sutures  309  as shown. The base structure  306  may be formed of a flexible and biocompatible material such as silicone, which may be reinforced with a flexible material such as polyester fabric available under the trade name DACRON to form a composite structure. The inside diameter of the base structure  306  may correspond to the outside diameter of the carotid artery at the location of implantation, for example 6-8 mm. The wall thickness of the base structure  306  may be very thin to maintain flexibility and a low profile, for example less than 1 mm. If the device  300  is to be disposed about a sinus bulge  21 , a correspondingly shaped bulge may be formed into the base structure for added support and assistance in positioning. 
   The electrodes  302  (shown in phantom) may comprise round wire, rectangular ribbon or foil, formed of an electrically conductive and radiopaque material such as platinum or platinum-iridium. The electrodes may be molded into the base structure  306  or adhesively connected to the inside diameter thereof, leaving a portion of the electrode exposed for electrical connection to carotid tissues. The electrodes  302  may encompass less than the entire inside circumference (e.g., 300°) of the base structure  306  to avoid shorting. The electrodes  302  may have any of the shapes and arrangements described previously. For example, as shown in  FIG. 29 , two rectangular ribbon electrodes  302  may be used, each having a width of 1 mm spaced 1.5 mm apart. 
   The support collar  312  may be formed similarly to base structure  306 . For example, the support collar may comprise molded tube, a tubular extrusion, or a sheet of material wrapped into a tube shape utilizing a suture flap  315  with sutures  313  as shown. The support collar  312  may be formed of a flexible and biocompatible material such as silicone, which may be reinforced to form a composite structure. The cables  304  are secured to the support collar  312 , leaving slack in the cables  304  between the support collar  312  and the activation device  300 . 
   In all extravascular embodiments described herein, including electrical activation embodiments, it may be desirable to secure the activation device to the vascular wall using sutures or other fixation means. For example, sutures  311  may be used to maintain the position of the electrical activation device  300  relative to the carotid anatomy (or other vascular site containing baroreceptors). Such sutures  311  may be connected to base structure  306 , and pass through all or a portion of the vascular wall. For example, the sutures  311  may be threaded through the base structure  306 , through the adventitia of the vascular wall, and tied. If the base structure  306  comprises a patch or otherwise partially surrounds the carotid anatomy, the corners and/or ends of the base structure may be sutured, with additional sutures evenly distributed therebetween. In order to minimize the propagation of a hole or a tear through the base structure  306 , a reinforcement material such as polyester fabric may be embedded in the silicone material. In addition to sutures, other fixation means may be employed such as staples or a biocompatible adhesive, for example. 
   Various embodiments of the inventive devices may be entirely intravascular, entirely extravascular, or partially intravascular and partially extravascular. Furthermore, devices may reside wholly in or on arterial vasculature, wholly in or on venous vasculature, or in or on some combination of both. In some embodiments, for example, implantable devices may positioned within an artery or vein, while in other embodiments devices may be placed extravascularly, on the outside of an artery or vein. In yet other embodiments, one or more components of a device, such as electrodes, a controller or both, may be positioned outside the patient&#39;s body. In introducing and placing devices of the present invention, any suitable technique and access route may be employed. For example, in some embodiments an open surgical procedure may be used to place an implantable device. Alternatively, an implantable device may be placed within an artery or vein via a transvascular, intravenous approach. In still other embodiments, an implantable device may be introduced into vasculature via minimally invasive means, advanced to a treatment position through the vasculature, and then advanced outside the vasculature for placement on the outside of an artery or vein. For example, an implantable device may be introduced into and advanced through the venous vasculature, made to exit the wall of a vein, and placed at an extravascular site on an artery. 
   Refer now to  FIG. 30  which schematically illustrates an alternative extravascular electrical activation device  300  including one or more electrode ribs  316  interconnected by spine  317 . Optionally, a support collar  312  having one or more (non-electrode) ribs  316  may be used to isolate the activation device  300  from movements and forces transmitted by the cables  304  proximal of the support collar  312 . 
   The ribs  316  of the activation device  300  are sized to fit about the carotid anatomy, such as the internal carotid artery  19  adjacent the carotid sinus  20 . Similarly, the ribs  316  of the support collar  312  may be sized to fit about the carotid anatomy, such as the common carotid artery  14  proximal of the carotid sinus  20 . The ribs  316  may be separated, placed on a carotid artery, and closed thereabout to secure the device  300  to the carotid anatomy. 
   Each of the ribs  316  of the device  300  includes an electrode  302  on the inside surface thereof for electrical connection to carotid tissues. The ribs  316  provide insulative material around the electrodes  302 , leaving only an inside portion exposed to the vascular wall. The electrodes  302  are coupled to the multi-channel cable  304  through spine  317 . Spine  317  also acts as a tether to ribs  316  of the support collar  312 , which do not include electrodes since their function is to provide support. The multi-channel electrode  302  functions discussed with reference to  FIGS. 25-28  are equally applicable to this embodiment. 
   The ends of the ribs  316  may be connected (e.g., sutured) after being disposed about a carotid artery, or may remain open as shown. If the ends remain open, the ribs  316  may be formed of a relatively stiff material to ensure a mechanical lock around the carotid artery. For example, the ribs  316  may be formed of polyethylene, polypropylene, PTFE, or other similar insulative and biocompatible material. Alternatively, the ribs  316  may be formed of a metal such as stainless steel or a nickel titanium alloy, as long as the metallic material was electrically isolated from the electrodes  302 . As a further alternative, the ribs  316  may comprise an insulative and biocompatible polymeric material with the structural integrity provided by metallic (e.g., stainless steel, nickel titanium alloy, etc.) reinforcement. In this latter alternative, the electrodes  302  may comprise the metallic reinforcement. 
   Referring now to  FIG. 31 , which schematically illustrates a specific example of an electrode assembly for an extravascular electrical activation device  300 . It should be emphasized that this and the following embodiments of electrode assemblies are provided for exemplary purposes only and do not limit the scope of the invention to any particular electrode assembly. Additional electrode assemblies which may be used with the present invention, for example, are described in U.S. patent application Ser. No. 10/402,911, and Ser. No. 10/402,393, both filed Mar. 27, 2003, and both previously incorporated by reference. 
   That being said, in the embodiment shown in  FIG. 31 , the base structure  306  comprises a silicone sheet having a length of 5.0 inches, a thickness of 0.007 inches, and a width of 0.312 inches. The electrodes  302  comprise platinum ribbon having a length of 0.47 inches, a thickness of 0.0005 inches, and a width of 0.040 inches. The electrodes  302  are adhesively connected to one side of the silicone sheet  306 . 
   The electrodes  302  are connected to a modified bipolar endocardial pacing lead, available under the trade name CONIFIX from Innomedica (now BIOMEC Cardiovascular, Inc.), model number 501112. The proximal end of the cable  304  is connected to the control system  60  or driver  66  as described previously. The pacing lead is modified by removing the pacing electrode to form the cable body  304 . The MP35 wires are extracted from the distal end thereof to form two coils  318  positioned side-by-side having a diameter of about 0.020 inches. The coils  318  are then attached to the electrodes utilizing  316  type stainless steel crimp terminals laser welded to one end of the platinum electrodes  302 . The distal end of the cable  304  and the connection between the coils  318  and the ends of the electrodes  302  are encapsulated by silicone. 
   The cable  304  illustrated in  FIG. 31  comprises a coaxial type cable including two coaxially disposed coil leads separated into two separate coils  318  for attachment to the electrodes  302 . An alternative cable  304  construction is illustrated in  FIG. 32 .  FIG. 32  illustrates an alternative cable body  304  which may be formed in a curvilinear shape such as a sinusoidal configuration, prior to implantation. The curvilinear configuration readily accommodates a change in distance between the device  300  and the control system  60  or the driver  66 . Such a change in distance may be encountered during flexion and/or extension of the neck of the patient after implantation. 
   In this alternative embodiment, the cable body  304  may comprise two or more conductive wires  304   a  arranged coaxially or collinearly as shown. Each conductive wire  304   a  may comprise a multifilament structure of suitable conductive material such as stainless steel or MP35N. An insulative material may surround the wire conductors  304   a  individually and/or collectively. For purposes of illustration only, a pair of electrically conductive wires  304   a  having an insulative material surrounding each wire  304   a  individually is shown. The insulated wires  304   a  may be connected by a spacer  304   b  comprising, for example, an insulative material. An additional jacket of suitable insulative material may surround each of the conductors  304   a . The insulative jacket may be formed to have the same curvilinear shape of the insulated wires  304   a  to help maintain the shape of the cable body  304  during implantation. 
   If a sinusoidal configuration is chosen for the curvilinear shape, the amplitude (A) may range from 1 mm to 10 mm, and preferably ranges from 2 mm to 3 mm. The wavelength (WL) of the sinusoid may range from 2 mm to 20 mm, and preferably ranges from 4 mm to 10 mm. The curvilinear or sinusoidal shape may be formed by a heat setting procedure utilizing a fixture which holds the cable  304  in the desired shape while the cable is exposed to heat. Sufficient heat is used to heat set the conductive wires  304   a  and/or the surrounding insulative material. After cooling, the cable  304  may be removed from the fixture, and the cable  304  retains the desired shape. 
   For any of the applications described above, it may be desirable to focus the output of the activation device  70  on portions of the carotid sinus  20  that are rich in baroreceptors  30 , and minimize the output delivered to portions of the carotid sinus  20  with fewer or no baroreceptors  30 . By focusing the output as such, baroreceptor activation may be maximized and the required device output (i.e., the required power or energy output of the baroreceptor activation device  70 ) may be minimized. In particular, the ratio of baroreceptor activation to device output (A/O) may be maximized. In addition, by focusing the output as such, extraneous tissue activation may be minimized, power consumption (by the device  70 ) may minimized, and the degradation rate of baroreceptor responsiveness may be minimized. 
   It has been found that the A/O ratio is a function of the position of the baroreceptor activation device. In particular, it has been found that the A/O ratio varies about the circumference of the carotid artery near the carotid sinus  20 , perhaps due to variations in the location or density of baroreceptors. Although described herein with reference to the carotid sinus  20 , it is also likely that the A/O ratio varies at all of the anatomical locations which contain baroreceptors as described previously. 
   In order to position the baroreceptor activation device  70  to maximize the A/O ratio, a mapping technique may be employed. For example, the device  70  may be oriented in two or more different positions and/or at two or more different anatomical locations. More specifically, the output means of the device  70  may be disposed in two or more different positions/locations. The output means generally refers to the structure through which the stimulus is transferred to the tissue surrounding the baroreceptors. In electrical activation embodiments, for example, the output means may comprise electrodes. 
   At each position/location, the device  70  may be activated to a specified level, and the degree of baroreceptor activation may be observed or measured. The degree of baroreceptor activation may be inferentially determined by measuring changes in heart rate, blood pressure, and/or other physiological parameters indicative or predictive of baroreceptor activation. The resulting measurements may be used to generate an A/O ratio for each position/location. The A/O ratios for each location may be graphically plotted to generate a map. The A/O ratios may be compared, and the position/location having the most desirable A/O ratio may be selected for the device  70 . 
   To illustrate this mapping method, reference may be made to  FIGS. 33-35 . By way of example, not limitation, the mapping method is described with specific reference to the arteries, but the method is equally applicable to all anatomical structures containing baroreceptors.  FIG. 33  shows the right carotid arteries including the common  14 , internal  18 , and external  19  carotid arteries. The carotid sinus  20  may be highlighted by a bulge  21 , which typically extends from the common carotid artery  14  to the internal carotid artery  18  near the bifurcation. The carotid sinus  20  contains a significant number of baroreceptors, the number and density of which may vary around the circumference and along the length of the sinus  20 . As such, it is desirable to determine the optimal position for the baroreceptor activation device  70 , both in terms of circumferential and longitudinal position. 
   The mapping method described herein is equally applicable to all baroreceptor activation devices  70 , regardless of the mode of activation (mechanical, electrical, thermal, chemical, biological, or other means) and regardless of their invivo position (intravascular, extravascular, intramural). By way of example, not limitation, the device  70  is shown in  FIG. 34  as an extravascular electrical device  500  having two electrodes  520  which contact the outside wall of the carotid sinus  20  at two different locations. The device  500  includes a molded silicone housing  512 . The housing  512  carries two metal strips  510  which are separated by approximately 4 mm and are formed of platinum ribbon (0.040 in. wide by 0.0005 in. thick by 10 mm long). The metal strips  510  are insulated by the housing  512  except at the 1 mm wide exposed area  516 . The metal strips  510  in the exposed area  516  define two electrodes  520  that contact the outside surface of the carotid artery. Leads  514  couple the metal strips  510  to cable  502  which is connected to a control system  60  as described previously with reference to  FIG. 3 . 
   With the device  500  disposed about the carotid arteries as shown in  FIG. 34 , the device  500  may be activated to produce an output signal from the electrodes  520 , which in turn activates the baroreceptors, as evidenced by a change in heart rate and/or blood pressure. The position and/or location of the electrodes  520  is recorded along with the amount of output (e.g., power) and the corresponding change in the heart rate, blood pressure and/or other physiological parameters indicative or predictive of baroreceptor activation. From this information, the A/O ratio may be determined for this particular position/location. 
   The electrodes  520  of the device  500  are then oriented in a different position (e.g., rotated) and/or placed at a different anatomical location, and the same measurements are made. These steps are repeated to collect the desired amount of data, which may be graphically plotted to generate a map to determine an optimal position/location. The A/O ratios may be compared, and the position/location having the most desirable A/O ratio may be selected for the device  500 . As an alternative to device  500 , a hand held probe or similar device incorporating electrodes  520  may be used to permit easier manipulation and quicker changes between different locations/positions. 
   To keep track of different circumferential positions around the carotid arteries, a coordinate system may be used as shown in  FIG. 35 .  FIG. 35   is  a schematic cross-sectional view taken along line  35 - 35  in  FIG. 34 , showing a mapping coordinate system for the left carotid artery  15  and right carotid artery  14 . In this coordinate system, the left carotid artery  15  and right carotid artery  14  are viewed in cross-section looking from the head of the patient toward the feet, with 0° positioned anteriorly and 180° positioned posteriorly. The center or apex of the left bulge  21 L which identifies the left carotid sinus  20 L is typically located at 110° to 160°. The center or apex of the right bulge  21 R which identifies the right carotid sinus  20 R is typically located at 200° to 250°. This coordinate system is particularly useful for mapping the circumference of the carotid arteries, in addition to other arteries and tubular organs. 
   Although the above description provides a complete and accurate representation of the invention, the present invention may be manifested in a variety of forms other than the specific embodiments described and contemplated herein. Accordingly, departures in form and detail may be made without departing from the scope and spirit of the present invention as described in the appended claims.