Circuitry for assisting nerve sensing in implantable stimulator devices

Abstract

Circuitry for assisting nerve sensing in an implantable stimulator device is disclosed. A passive tissue biasing circuit in an implantable pulse generator (IPG) is included to facilitate sensing of neural responses by maintaining the voltage of the tissue as a common mode voltage (Vcm). The conductive housing electrode or any other electrode of the IPG is passively biased to Vcm using a capacitor as opposed to actively driving the (housing) electrode to a prescribed voltage using a voltage source. Once Vcm is established, the voltage accompanying the generation of the stimulation pulse will refer to Vcm, which simplifies neural response sensing. An amplifier may be used to set a virtual reference voltage and limit the amount of current flowing to the enclosure during generation of Vcm. In other examples, a circuit may be used to monitor a virtual reference voltage, which is useful for enabling sensing a neural response, and for setting a compliant voltage of a current generating circuit.

Description

[0001] This application is a divisional application of the patent application with application number "201980035893.4", application date "February 27, 2019", and titled "Circuitry for assisting neural sensing in implantable stimulator devices". Technical Field

[0002] The present application relates to implantable medical devices (IMDs), and more particularly to circuits for assisting sensing of implantable stimulator devices. Background Art

[0003] An implantable neurostimulator device is a device that generates and delivers electrical stimulation to the body's nerves and tissues to treat various biological disorders, such as pacemakers for treating cardiac arrhythmias, defibrillators for treating cardiac fibrillation, cochlear stimulators for treating deafness, retinal stimulators for treating blindness, muscle stimulators for producing coordinated limb movements, spinal cord stimulators for treating chronic pain, cortical and deep brain stimulators for treating movement and psychological disorders, other neurostimulators for treating urinary incontinence, sleep apnea, shoulder subluxation, etc. The following description generally focuses on the use of the present invention in a spinal cord stimulation (SCS) system, such as disclosed in U.S. Patent 6,516,227. However, the present invention may find application in any implantable neurostimulator device system.

[0004] SCS systems typically include Figure 1 1 and 1 . An implantable pulse generator (IPG) 10 is shown in FIG. The IPG 10 includes a biocompatible device housing 12 that contains circuitry and a battery 14 for providing power for operation of the IPG. The IPG 10 is coupled to tissue stimulation electrodes 16 via one or more electrode leads that form an electrode array 17. For example, one or more percutaneous leads 15 may be used that have an annular or open ring electrode 16 carried on a flexible body. In another example, a paddle lead 19 provides an electrode 16 positioned on one of its substantially flat surfaces. A lead conductor 20 within the lead is coupled to the electrode 16 and a proximal contact 21 in a lead connector 22 that may be inserted into a head 23 secured to the IPG 10, which head may include, for example, epoxy. Once inserted, the proximal contact 21 is connected to a head contact 24 within the lead connector 22, which in turn is coupled to a stimulation circuit 28 within the housing 12 by a feedthrough pin 25 through a housing feedthrough 26.

[0005] In the illustrated IPG 10, there are 32 electrodes (E1-E32), split between four percutaneous leads 15, or contained in a single paddle lead 19, and thus, the head 23 may include a 2x2 array of eight electrode lead connectors 22. However, the type and number of leads in the IPG and the number of electrodes are application specific and may therefore vary. The conductive housing 12 may also include electrodes (Ec). In SCS applications, one or more electrode leads are typically implanted in the spine near the dura mater in the patient's spinal cord, preferably across the left and right sides of the patient's spine. The proximal contacts 21 tunnel through the patient's tissue to a distal location, such as the buttocks where the IPG housing 12 is implanted, at which point they are coupled to the lead connectors 22. In other IPG examples designed for direct implantation at a site where stimulation is desired, the IPG may be leadless, with electrodes 16 instead appearing on the body of the IPG 10 for contacting the patient's tissue. In other solutions, one or more IPG leads may be integrated with the IPG 10 and permanently connected. The goal of SCS therapy is to provide electrical stimulation from electrodes 16 to relieve a patient's symptoms, such as chronic back pain.

[0006] The IPG 10 may include an antenna 27a to allow it to communicate bidirectionally with a number of external devices discussed subsequently. The antenna 27a as shown comprises a conductive coil within the housing 12, although the coil antenna 27a may also be present in the head 23. When the antenna 27a is configured as a coil, communication with the external device preferably occurs using near-field magnetic induction. The IPG 10 may also include a radio frequency (RF) antenna 27b. Figure 1 , the RF antenna 27b is shown within the head 23, but it may also be within the housing 12. The RF antenna 27b may include a patch, a slot, or a wire, and may operate as a monopole or a dipole. The RF antenna 27b preferably communicates using far-field electromagnetic waves, and may operate according to any number of known RF communication standards such as Bluetooth, Zigbee, WiFi, MICS, and the like.

[0007] Stimulation in the IPG 10 is typically provided by pulses, each of which may include multiple phases, such as 30a and 30b, as shown in FIG. Figure 2A . The stimulation parameters typically include amplitude (current I, although voltage amplitude V may also be used); frequency (F); pulse width (PW) of the pulse or its independent phase (such as 30a and 30b); electrodes 16 selected to provide stimulation; and the polarity of these selected electrodes, i.e., whether they act as anodes that pull (source) current to the tissue or cathodes that sink (sink) current from the tissue. These and possibly other stimulation parameters together comprise a stimulation program that the stimulation circuit 28 in the IPG 10 can execute to provide therapeutic stimulation to the patient.

[0008] exist Figure 2A In the example of , electrode E1 has been selected as the anode (during its first phase 30a), and thus provides a pulse that pulls a positive current of amplitude +I to the tissue. Electrode E2 has been selected as the cathode (also during the first phase 30a), and thus provides a pulse that sinks a corresponding negative current of amplitude -I from the tissue. This is an example of bipolar stimulation, in which only two lead-based electrodes are used to provide stimulation to the tissue (one anode, one cathode). However, more than one electrode can be selected to act as an anode at a given time, and more than one electrode can be selected to act as a cathode at a given time.

[0009] As mentioned, the IPG 10 includes stimulation circuitry 28 to produce prescribed stimulation at the patient's tissue. Figure 3 An example of a stimulation circuit 28 is shown, which includes one or more current pulling circuits 40 i and one or more current sink circuits 42 i . Pull circuit 40 i And irrigation circuit 42 i The PDACs may include digital-to-analog converters (DACs) and may be referred to as PDACs 40 based on the positive (sourcing, anode) and negative (sinking, cathode) currents they source, respectively. i and NDAC 42 i In the example shown, the NDAC / PDAC 40 i / 42 i The pairing is dedicated (hardwired) to a specific electrode node ei 39. For reasons explained below, each electrode node ei 39 is connected to electrode Ei 16 via a DC blocking capacitor Ci 38. The stimulation circuit 28 in this example also supports the selection of the conductive housing 12 as the electrode (Ec 12), which is typically selected for monopolar stimulation. PDAC 40 i and NDAC 42 i A voltage source may also be included.

[0010] About PDAC 40 i and NDAC 42 iAppropriate control of allows any electrode 16 to act as an anode or cathode to generate a current through the patient's tissue R, hopefully with a good therapeutic effect. In the example shown, electrode E1 has been selected as an anode electrode to pull current to the tissue R, and E2 has been selected as a cathode electrode to sink current from the tissue R. Therefore, PDAC 401 and NDAC422 are activated and digitally programmed to generate the desired current I with the correct timing (e.g., according to the specified frequency F and pulse widths PWa and PWb). As further described in detail in U.S. Patent Application Publication 2013 / 0289665, power for the stimulation circuit 28 is provided by a compliance voltage VH. As shown, the compliance voltage can be coupled to a pull circuit (e.g., one or more PDACs), and ground can be coupled to a sink circuit (e.g., one or more NDACs), so that the stimulation circuit is coupled to and powered between the compliance voltage and ground. More than one anode electrode and more than one cathode electrode can be selected at a time, and thus current can flow through the tissue R between two or more of the electrodes 16.

[0011] Other stimulation circuits 28 may also be used in the IPG 10. In an example not shown, the switch matrix may include one or more PDACs 40. i and electrode node ei 39, and one or more NDACs 42 are interposed i and electrode nodes. The switch matrix allows one or more of the PDACs or one or more of the NDACs to be connected to one or more anode electrode nodes at a given time. Various examples of stimulation circuits can be found in U.S. Patents 6,181,969, 8,606,362, 8,620,436, U.S. Patent Application Publication 2018 / 0071520, and U.S. Patent Application Serial No. 16 / 131,809 (filed on September 14, 2018).

[0012] Figure 3 Many of the stimulus circuits 28 (including the PDAC 40 i and NDAC 42 i , the switch matrix (if present), and the electrode nodes ei 39) can be integrated on one or more application specific integrated circuits (ASICs), such as described in U.S. Patent Application Publications 2012 / 0095529, 2012 / 0092031, and 2012 / 0095519. As explained in these references, one or more ASICs may also include other circuits useful in the IPG 10, such as telemetry circuits (for interfacing off-chip with telemetry antennas 27a and / or 27b), circuits for generating compliance voltage VH, various measurement circuits, etc.

[0013] exist Figure 3Also shown are DC blocking capacitors Ci 38 placed in series in the electrode current path between each electrode node ei 39 and electrode Ei 16 (including housing electrode Ec12). The DC blocking capacitors 38 act as a safety measure to prevent DC current injection into the patient, such as might occur if there is a circuit fault in the stimulation circuit 28, and also typically comprise part of the IPG charge balancing mechanism. As explained in U.S. Patent Application Publication 2015 / 0157861, the DC blocking capacitors 38 are typically provided off-chip (outside of one or more ASICs), and may alternatively be provided in or on a circuit board in the IPG 10 used to integrate its various components.

[0014] Reference again Figure 2A , the stimulation pulses shown are biphasic, with each pulse comprising a first phase 30a followed by a second phase 30b of opposite polarity. The biphasic pulses help actively restore any charge that may be stored on capacitive elements in the electrode current path, such as on the DC blocking capacitor 38. Figure 2A and Figure 2B Both show charge recovery. During the first pulse phase 30a, charge will (primarily) accumulate across the DC blocking capacitors C1 and C2 associated with the electrodes E1 and E2 used to generate the current, thereby generating voltages Vc1 and Vc2 (I=C*dV / dt). During the second pulse phase 30b, when the polarity of the current I is reversed at the selected electrodes E1 and E2, the charge stored on the capacitors C1 and C2 is restored, and thus the voltages Vc1 and Vc2 are expected to return to 0V at the end of the second pulse phase 30b.

[0015] In order to restore all charges (Vc1=Vc2=0V) at the end of the second pulse phase 30b of each pulse, the first phase 30a and the second phase 30b are charge balanced at each electrode, wherein the phases include equal amounts of charge but opposite polarity. In the example shown, this charge balance is achieved by using the same pulse width (PWa=PWb) and the same amplitude (|+I|=|-I|) for each of the pulse phases 30a and 30b. However, as is known, the pulse phases 30a and 30b can also be charge balanced if the product of the amplitude and the pulse width of the two phases 30a and 30b is equal.

[0016] Figure 4Various external devices are shown that can wirelessly communicate data with the IPG 10, including a patient-held external controller 60 and a clinician programmer 70. Both devices 60 and 70 can be used to wirelessly send stimulation programs to the IPG 10 - that is, to program its stimulation circuit 28 to produce stimulation with the desired amplitude and timing as previously described. Both devices 60 and 70 can be used to adjust one or more stimulation parameters of the stimulation program currently being executed by the IPG 10. Devices 60 and 70 can also wirelessly receive information from the IPG 10, such as various status information, etc. Devices 60 and 70 can additionally communicate with an external test stimulator (ETS) that is used to simulate the operation of the IPG 10 during a test period and before the IPG is implanted, as explained in USP 9,724,508 and 9,259,574.

[0017] The external controller 60 may be, for example, as described in U.S. Patent Application Publication 2015 / 0080982, and may include a controller specifically designed to work with the IPG 10. The external controller 60 may also include a general-purpose mobile electronic device, such as a mobile phone that has been programmed with a medical device application (MDA), allowing it to work as a wireless controller for the IPG 10, as described in U.S. Patent Application Publication 2015 / 0231402. The external controller 60 includes a user interface that preferably includes means for inputting commands (e.g., buttons or selectable graphical icons) and a display 62. The user interface of the external controller 60 enables the patient to adjust stimulation parameters, although it may have limited functionality compared to the more powerful clinician programmer 70 described later.

[0018] The external controller 60 may have one or more antennas capable of communicating with the IPG 10. For example, the external controller 60 may have a near-field magnetic induction coil antenna 64a capable of wirelessly communicating with the coil antenna 27a in the IPG 10. The external controller 60 may also have a far-field RF antenna 64b capable of wirelessly communicating with the RF antenna 27b in the IPG 10.

[0019] The clinician programmer 70 is further described in U.S. Patent Application Publication 2015 / 0360038 and may include a computing device 72, such as a desktop, handheld or notebook computer, tablet computer, mobile smart phone, personal data assistant (PDA) type mobile computing device, etc. Figure 4 In FIG. 7 , computing device 72 is shown as a laptop computer, which includes typical computer user interface devices, such as screen 74, mouse, keyboard, speaker, stylus, printer, etc., which are not all shown for convenience. Figure 4Also shown are auxiliary devices for the clinician programmer 70 that are typically specific to its operation as a stimulation controller, such as a communications “wand” 76 that can be coupled to an appropriate port on the computing device 72 , such as, for example, a USB port 79 .

[0020] The antenna used in the clinician programmer 70 for communicating with the IPG 10 can depend on the type of antenna included in the IPG 10. If the patient's IPG 10 includes a coil antenna 27a, the rod 76 can also include a coil antenna 80a to establish near-field magnetic induction communication at a small distance. In this case, the rod 76 can be attached near the patient, such as by placing the rod 76 in a belt or holster that the patient can wear and close to the patient's IPG 10. If the IPG 10 includes an RF antenna 27b, the rod 76, the computing device 72, or both can also include an RF antenna 80b to establish communication with the IPG 10 at a larger distance. The clinician programmer 70 can also communicate with other devices and networks such as the Internet wirelessly or via a wired link provided at an Ethernet or network port.

[0021] In order to program the stimulation program or parameters for the IPG 10, the clinician interfaces with a clinician programmer graphical user interface (GUI) 82 disposed on the display 74 of the computing device 72. As will be appreciated by those skilled in the art, the GUI 82 may be presented by executing clinician programmer software 84 stored in the computing device 72, which may be stored in the non-volatile memory 86 of the device. The execution of the clinician programmer software 84 in the computing device 72 may be facilitated by a control circuit 88, such as one or more microprocessors, microcomputers, FPGAs, DSPs, other digital logic structures, etc., which are capable of executing programs in a computing device and may include their own memory. In addition to executing the clinician programmer software 84 and presenting the GUI 82, such a control circuit 88 may also enable the stimulation parameters selected by the GUI 82 to be transmitted to the patient's IPG 10 via communication via antennas 80a or 80b.

[0022] The user interface of external controller 60 may provide similar functionality because external controller 60 may include similar hardware and software programming as the clinician programmer. For example, external controller 60 includes control circuitry 66 similar to control circuitry 88 in clinician programmer 70 and may be similarly programmed using external controller software stored in device memory. Summary of the invention

[0023] An implantable stimulator device is disclosed, which may include: a plurality of electrode nodes, each electrode node being configured to couple to one of a plurality of electrodes configured to contact patient tissue; a housing configured to be implanted in the patient tissue, wherein the housing contains a stimulation circuit, the stimulation circuit being configured to provide pulses at at least two of the electrode nodes to generate a stimulation current through the patient tissue; and a capacitor configured to couple between at least one of the plurality of electrodes and a first reference voltage generated inside the housing when the stimulation circuit provides the pulses to at least two electrode nodes, wherein the capacitor is configured to provide a common-mode voltage to the tissue at at least one electrode.

[0024] The housing may be electrically conductive, and the electrically conductive housing may include one of a plurality of electrodes. The electrically conductive housing may include at least one electrode.

[0025] At least one electrode may be configured to be selectable from a plurality of electrodes.

[0026] The implantable stimulator device may further include a resistor connected in parallel with the capacitor.

[0027] The capacitance may include one or more capacitors.

[0028] Each electrode node may be coupled to the electrode via a DC blocking capacitor.

[0029] The stimulation circuit may also be configured to provide pulses to the at least one electrode, wherein the capacitor is configured to decouple between the at least one electrode and the first reference voltage when the stimulation circuit provides the pulses to the at least one electrode.

[0030] The implantable stimulator device may further include at least one implantable lead, wherein the electrode is located on the lead. The implantable stimulator device may further include a switch configured to couple the capacitance to a first reference voltage. The implantable stimulator device may further include a voltage source configured to generate the first reference voltage.

[0031] The stimulation circuit may be configured to be powered by a compliance voltage. The stimulation may include a sourcing circuit configured to source current to at least one of the two electrodes, and a sinking circuit configured to sink current from a different at least one of the two electrodes. The compliance voltage may be coupled to the sourcing circuit, and ground may be coupled to the current sinking circuit. The first reference voltage may be between the compliance voltage and ground, or may be configured to be proportional to the compliance voltage.

[0032] The implantable stimulator device may further include an amplifier configured to generate a first reference voltage. The amplifier may include an operational transconductance amplifier. The amplifier may include a first input and a second input, and may be configured as a follower in which the first reference voltage is provided to the first input and wherein the second reference voltage is provided to the second input. The implantable stimulator device may further include a voltage source configured to generate a second reference voltage. The stimulation circuit may be configured to be powered by a compliance voltage. The second reference voltage may be between the compliance voltage and ground, or may be configured to be proportional to the compliance voltage. The amplifier may be configured to maintain the first reference voltage equal to the second reference voltage if the current through the capacitor is between the minimum and maximum output currents of the amplifier.

[0033] The implantable stimulator device may further include a logic circuit configured to determine whether the first reference voltage exceeds a first threshold or drops below a second threshold. The implantable stimulator device may further include a control circuit configured to receive at least one indication that the first reference voltage has exceeded the first threshold or has dropped below the second threshold. The control circuit may be configured to issue an enable signal in response to at least one indication, the enable signal indicating when a neural response in response to the stimulation current in the tissue can be sensed at at least one of the plurality of electrode nodes. The stimulation circuit may be powered by a compliance voltage, wherein the control circuit is configured to issue an enable signal in response to at least one indication, the enable signal indicating when the compliance voltage should be increased.

[0034] The implantable stimulator device may further include at least one sense amplifier configured to sense a neural response in the tissue in response to a stimulation current when the capacitor is configured to provide a common-mode voltage to the tissue at at least one electrode. The at least one sense amplifier may include a first input and a second input, wherein the at least one sense amplifier is configured to receive one of the electrode nodes at its first input. The one electrode node received at the first input may not include one of the at least two of the electrode nodes. The at least one sense amplifier may be configured to receive a common-mode voltage at its second input. The at least one sense amplifier may also be configured to receive another of the electrode nodes at its second input to differentially sense a neural response between one electrode node and another electrode node. The implantable stimulator device may further include a control circuit configured to receive the output of the at least one sense amplifier and evaluate at least one parameter of the sensed neural response. BRIEF DESCRIPTION OF THE DRAWINGS

[0035] Figure 1 An implantable pulse generator (IPG) according to the prior art is shown.

[0036] Figure 2A and Figure 2B Examples of stimulation pulses that may be generated by an IPG according to the prior art are shown.

[0037] Figure 3 A stimulation circuit according to the prior art that may be used in an IPG is shown.

[0038] Figure 4 Various external devices are shown that are capable of communicating with an IPG and programming stimulation in the IPG according to the prior art.

[0039] Figure 5 An improved IPG is shown with neural response sensing and the ability to modulate stimulation depending on this sensing.

[0040] Figure 6 Stimulation that produces a neural response, and sensing of the neural response at at least one electrode of the IPG are shown.

[0041] Fig. 7A and Figure 7B The generation of biphasic pulses at selected IPG electrodes is shown, and the voltages developed at selected electrode nodes are shown.

[0042] Fig. 8A and Figure 8B The problem of insufficient compliance voltage to produce a loaded stimulation pulse is shown, and a circuit for regulating the compliance voltage to prevent loading in a closed loop manner is shown.

[0043] Fig.9A and Fig. 9B A first example of a passive tissue bias circuit configured to establish a common mode voltage in tissue at a housing electrode using a capacitor, such as useful in sensing of neural responses, is shown.

[0044] Fig. 10A and Fig. 10B The operation of the passive tissue bias circuit when a common-mode voltage is established in the tissue is explained.

[0045] Figure 11A-11C The operation of the passive tissue bias circuit given the potential mismatch in electrode-to-housing resistance and the mismatch between sourcing and sinking currents in the tissue is explained.

[0046] Fig. 12A and Fig. 12B A second example of a passive tissue bias circuit is shown that includes an amplifier for generating a virtual reference voltage for the capacitor and for limiting current through the tissue to the housing.

[0047] Fig.13A and Fig. 13BA third example of a passive tissue bias circuit is shown that includes circuitry to sense a virtual reference voltage, to help enable sensing of neural responses, and to help adjust a compliance voltage of a current generating circuit.

[0048] Fig.14A and Fig. 14B Sensing of neural responses at a single electrode and differentially at two electrodes once a common mode voltage is established is shown.

[0049] Fig.15 An alternative is shown in which a passive tissue bias circuit can allow any electrode (except the housing electrode) to include an electrode for setting a common mode voltage in the tissue. DETAILED DESCRIPTION

[0050] An increasingly interesting development in pulse generator systems, and particularly in spinal cord stimulator (SCS) pulse generator systems, is the addition of sensing capabilities to supplement the stimulation provided by such systems. For example, and as explained in U.S. Patent Application Publication 2017 / 0296823, it may be beneficial to sense neural responses in neural tissue that has received stimulation from an SCS pulse generator.

[0051] Figure 5 Circuitry of an SCS IPG 100 having neural response sensing capabilities is shown. The IPG 100 includes a control circuit 102, which may include a microcontroller, such as part number MSP430 manufactured by Texas Instruments, which is described in the data sheet at http: / / www.ti.com / lsds / ti / microcontroller / 16-bit_msp430 / overview.page?DCMP=MCU_other&HQS=msp430. Other types of control circuits may also be used in place of a microcontroller, such as a microprocessor, FPGA, DSP, or a combination thereof. The control circuit 102 may also be formed in whole or in part in one or more application specific integrated circuits (ASICs) as previously described in the IPG 100, which may additionally include Figure 5 Other circuits shown in FIG.

[0052] Figure 5 comprising the stimulation circuit 28 ( Figure 3 ), including one or more DACs (PDAC 40 i and NDAC42 i). Bus 118 provides digital control signals to the DAC to produce a current or voltage of specified magnitude and with correct timing at the electrode selected for stimulation. The electrode current path to electrode 16 includes the DC blocking capacitor 38 previously described.

[0053] The control circuit 102 is programmed with a neural response algorithm 124 to evaluate the neural responses of neurons excited (recruited) by stimulation provided by the IPG 100 . Figure 5 and Figure 6 One such neural response depicted in is the evoked compound action potential or "ECAP," although other types of neural responses also exist and can be sensed by the IPG 100. As the name implies, the ECAP comprises a compound (sum) of various action potentials emitted from multiple recruited neurons, and its amplitude and shape vary depending on the number and type of neural fibers excited. In general, the ECAP can vary from tens of microvolts to tens of millivolts. The neural response algorithm 124 evaluates the ECAP and can, for example, adjust the stimulation program in a closed-loop manner to try and adjust the amplitude or shape of the resulting ECAP.

[0054] The control circuit 102 and / or the neural response algorithm 124 may also enable one or more sensing electrodes (S) to be automatically or based on input to an external device (see Figure 4 ) to sense the ECAP. Figure 6 As shown in , ECAP will be initiated upon stimulation of nerve fibers in the recruited neural population 95 that are proximal to the electrodes selected for stimulation (e.g., E1 and E2), and will move through the patient's tissue via neural conduction. Figure 6 In a simple example of , electrode E6 is selected as the detection electrode S, and therefore this electrode will detect the ECAP as it moves past. The speed at which the ECAP moves depends on several factors and is variable.

[0055] To assist in selecting one or more sensing electrodes, and again referring to Figure 5, each electrode node ei 39 may be coupled to at least one sense amplifier 110. In this example, for simplicity, all electrode nodes are shown as sharing a single sense amplifier 110. Thus, any one sensing electrode (e.g., electrode node e6) may be coupled to a sense amplifier 110 (e.g., Ve6) at a given time per multiplexer 108, as controlled by bus 114. However, although not shown, each electrode node may also be coupled to its own dedicated sense amplifier 110. ECAP sensing may also involve differential sensing of ECAP at more than one electrode (e.g., at electrodes E5 and E6), and thus two nodes (e.g., Ve5 and Ve6) may be input to a differential sense amplifier 110; refer later Fig. 14B This is explained, but for simplicity, Figure 5 and Figure 6 After the ECAP is sensed, the analog waveform including the ECAP is preferably converted to a digital signal by an analog-to-digital converter 112, which may also reside within the control circuit 102. The neural response algorithm 124 may then evaluate the magnitude and shape of the ECAP and, if necessary, adjust the stimulation via bus 118 to try and adjust future ECAPs generated so that they have the desired magnitude or shape.

[0056] One or more sensing electrodes S can be located away from the effective electrode selected to provide stimulation so that the voltage generated in the tissue during stimulation (stimulation artifact) will less affect the sensing at the sensing electrode. However, since the duration (e.g., PWa and PWb) and frequency (F) of the stimulation pulses and the conduction velocity of the neural response are variable, it is inevitable that the voltage associated with the stimulation exists at the selected one or more sensing electrodes. This may make sensing neural responses challenging. As mentioned, ECAP can be as small as tens of microvolts. However, as further explained below, the operation of the IPG causes the voltage in the tissue to vary in the order of volts. Therefore, sensing involves resolving small signal neural responses in the tissue, which can be many orders of magnitude smaller than the varying background voltage of the tissue. It is difficult to design amplifiers such as one or more sense amplifiers 110 to reliably perform the task of accurately sensing such small signals while rejecting background tissue voltages.

[0057] First reference Fig. 7A and Figure 7B interpret voltage changes in tissue due to stimulation, Fig. 7A and Figure 7B Stimulation is shown occurring as previously described using biphasic pulses between electrodes El and E2. Fig. 7A1 shows how the stimulation circuit 28 is biased when generating a current I through tissue, during a first phase 30a when the current I flows from the anode electrode E1 to the cathode electrode E2, and during a second phase 30b when the current I flows in the opposite direction from the anode electrode E2 to the cathode electrode E1. Note that during the first phase 30a, the selected PDAC (e.g., PDAC 401) sources a current Ip to the electrode node e1, while the selected NDAC (e.g., NDAC 422) sinks a current In from the electrode node e2. During the second phase 30b, the selected PDAC (e.g., PDAC 402) sources a current Ip to the electrode node e2, and the selected NDAC (e.g., NDAC 421) sinks a current In from the electrode node e1. Ideally, the Ip emitted from the PDAC is equal to the |In| emitted by the NDAC, where both are equal to the desired current I, although non-ideal conditions may cause them to vary, as discussed further below. If a switch matrix is ​​used as part of the design of the stimulation circuit 28, the same PDAC and NDAC can also be used during both phases 30a and 30b.

[0058] Figure 7B 1 and 2 show various waveforms produced when a biphasic current pulse is produced at electrodes E1 and E2. Providing a constant current I between the electrodes causes the DC blocking capacitors 38C1 and C2 to charge during the first pulse phase 30a, which causes the voltages Vc1 and Vc2 across them to increase (I=C*dV / dt). Because the second pulse phase 30b of opposite polarity is charge balanced with the first pulse phase 30a, Vc1 and Vc2 will decrease during the second pulse phase 30b and return to zero (ideally) at the end of the second pulse phase 30b, as previously described with reference to FIG. Figure 2A and Figure 2B Explained.

[0059] Figure 7B The bottom of FIG. 1 shows the voltages (Ve1 and Ve2) formed at electrode nodes 39e1 and e2 when the aforementioned pulses are generated. It is useful to examine the voltage at electrode node 39ei rather than at electrode Ei 16 itself because it is the voltage at the electrode node that is presented to one or more sense amplifiers 110 ( Figure 5 ), and thus for neural response sensing. Even though Ve1 and Ve2 are formed simultaneously, for simplicity, they are initially Figure 7B , wherein the first waveform shows only Ve1 during the first pulse, and the second waveform shows only Ve2 during the second pulse. The third waveform shows Ve1 and Ve2 together during the third pulse.

[0060] Figure 7BThe electrode node voltages Ve1 and Ve2 in FIG. 1 are shown with reference to the compliance voltage VH, which is shown in FIG. Figure 3 ) is mentioned for providing power to the DAC circuit. All relevant voltage drops are shown, including the voltage drop across the tissue (Vr), the voltage drop across the DC blocking capacitor 39 (Vc1 and Vc2), and the voltage drops across the selected PDAC and NDAC (Vp and Vn). As shown, Ve1 is initially higher than Ve2 due to the direction of current flow during the first pulse phase 30a. As the DC blocking capacitor 38 charges (Vc1, Vc2), Ve1 will increase and Ve2 will decrease during the first pulse phase 30a. This will also result in voltage drops (Vp) and (Vn) across the active PDAC and NDAC. During the second pulse phase 30b, the polarity of the current is reversed, and therefore Ve2 is now higher than Ve1. The voltages Vc2 and Vc2 decrease during the second pulse phase 30b as their stored charge is restored, which causes Ve1 to decrease and Ve2 to increase, while Vp and Vn decrease.

[0061] Thus, during the emission of biphasic pulses, the voltages Ve1 and Ve2 vary significantly, both due to changes in current polarity and due to the charging and discharging of the DC blocking capacitor 38. Such changes are indicative of changes in voltage in the tissue, which will be coupled, at least to some extent, through the tissue to the electrodes used for sensing. Assume again that sensing occurs at electrode E6, i.e., that the sensed voltage Ve6 is presented to one or more sense amplifiers 110. Although it is complex to calculate or plot in view of the complex electrical environment of the tissue, the voltages present at electrodes E1 and E2 will be coupled to electrode E6, and thus Ve6 will generally track Ve1 and / or Ve2 to some extent. (In this example, Ve6 may primarily track Ve2 because electrode E6 is closer to E2 than E1). In other words, any small-signal neural response sensed at Ve6 will rely on a large and varying background voltage, which, as previously mentioned, makes it difficult to sense neural responses. As will be further described below, adding a passive tissue bias circuit to the IPG 100 will provide a common-mode voltage to the tissue, which facilitates sensing of small-signal neural responses.

[0062] Before discussing such passive tissue bias circuits, it is useful to discuss how compliance voltage VH is adjusted in IPG 100, since such adjustment may involve the operation of the passive tissue bias circuits. Fig. 8A and Figure 8BIllustrated are compliance voltage regulation and the environment that ensures such regulation. When a stimulus is provided, the voltage drops Vp and Vn across the PDAC and NDAC are preferably maintained above minimum values Vp(min) and Vn(min), as explained in USP 7,444,181, 9,174,051, and 9,314,632. If Vp or Vn drops below these minimum values, the affected DAC (PDAC or NDAC) will be loaded and will thus be unable to generate its specified current Ip or In. This means that Ve1 and Ve2 are preferably maintained within region 111 defined between VH - Vp(min) and Vn(min). In Fig. 8A the example of, since Ve2 < Vn(min) and Ve1 > VH - Vp(min) during part (98) of the first pulse phase 30a, such a definition does not occur. This results in the loading (99) of the pulse because one or more PDACs and one or more NDACs are unable to generate the specified currents of Ip and In.

[0063] Although the compliance voltage can be constant, it is also preferably adjustable to address pulse loading, and Figure 8B illustrated is an example of a compliance voltage measurement and generation circuit 51 that can be used for this purpose. Generally, the compliance voltage measurement and generation circuit 51 measures Vp and Vn across the active PDAC and NDAC and adjusts the compliance voltage VH in a closed-loop manner to ensure that Vp is not lower than Vp(min) and Vn is not lower than Vn(min), thereby ensuring that the electrode node voltages Ve1 and Ve2 are defined by region 111.

[0064] As shown, during the provision of a pulse (I), differential amplifiers 43p and 43n measure Vp and Vn across the active PDAC40 i and NDAC42 j . Note that Figure 8B only the measurement of Vp and Vn across PDAC 401 and NDAC422 during the first pulse phase 30a is shown. Although not shown, Vp and Vn across PDAC 402 and NDAC 421 can also be measured during the second pulse phase 30b.

[0065] The Vp and Vn measurements are provided to the negative inputs of comparators 45p and 45n. The positive inputs of the comparators provide the minimum values ​​of Vp and Vn (Vp(min) and Vn(min)) required across the PDAC and NDAC to prevent loading. Due to differences in the construction of the PDAC and NDAC, Vp(min) and Vn(min) may be different and may be, for example, 1.5V and 1.2V, respectively. Vp(min) and Vn(min) may be provided by a voltage generator such as a bandgap voltage reference generator, although this detail is not shown. Comparator 45p is enabled by signal p(en) to compare Vp and Vp(min) at specified times, such as at the end of the first pulse phase 30a when Vc1 and Vc2 may be highest and therefore when Vp may be lowest. Similarly, comparator 45n is enabled by signal n(en) to compare Vn and Vn(min) at specified times when Vn may also be lowest. If Vp is lower than Vp(min) or Vn is lower than Vn(min), comparators 45p and 45n will output “1”. If Vp or Vn is low, OR gate 47 outputs “1”, which includes enable signal VH(en1) to operate compliance voltage regulator 49.

[0066] In this example, the compliance voltage (VH) regulator 49 is shown as an inductor-based boost converter, but may also be implemented as a capacitor-based charge pump or other boost circuit. The VH regulator 49 generates the compliance voltage VH from another, typically lower voltage DC source in the IPG 100, such as its battery 14 ( Figure 1 ) at the voltage Vbat of the compliance voltage VH. When enabled by VH(en1) at the input VH(en), the pulse width modulator 53 generates a square wave to the gated transistor 57, which periodically turns on the transistor 57 and causes current to flow from Vbat through the inductor 55. During the off period of the transistor 57, the current stored in the inductor 55 is forced through the diode 59 and is stored on the storage capacitor 61 which maintains the value of the compliance voltage VH. The diode 59 prevents the backflow of this current and therefore, over time, the voltage across the storage capacitor 61 increases, i.e., the compliance voltage VH begins to build, as long as VH(en1) continues to be asserted. Eventually, VH will increase to a point where Vp and Vn are higher than Vp(min) and Vn(min), which will cause VH(en1) to be deasserted, thereby turning off the VH regulator 49 and causing VH to drop. In this way, VH is controlled to an optimal level in a closed loop manner by the compliance voltage measurement and generation circuit 51.

[0067] Therefore, if Fig. 8A As shown in Figure 8BThe operation of the compliance voltage measurement and generation circuit 51 can prevent the loading of the pulse 99 by increasing the compliance voltage VH. Note that after increasing VH, Ve1 or Ve2 remains confined within the region 111, so that the pulse is not loaded (99).

[0068] Various examples of the present invention disclose passive tissue bias circuits that can mitigate the effects of voltage variations in tissue by passively maintaining the voltage of the tissue at a common mode voltage (Vcm), and thereby facilitate sensing of neural responses. In examples of the present invention, as opposed to using a voltage source to actively drive the shell electrode 12 to a specified voltage, a capacitor is used to passively bias the conductive shell electrode 12 of the IPG 100 to Vcm. It is wise to use the shell electrode 12 to provide Vcm (although not absolutely necessary): the resistance of the patient's tissue is relatively low, and the area of ​​the shell electrode 12 of the IPG is relatively large. Therefore, even if the shell electrode 12 is implanted at a distance from the electrode 16, the shell electrode 12 still includes a suitable device for establishing Vcm for the entire tissue. However, the passive tissue bias circuit can also enable any electrode of the IPG 100 (including the lead-based electrode 16) to set the common mode voltage of the tissue. However, most of this disclosure assumes that the shell electrode is used to set Vcm as the main example.

[0069] As explained below, once Vcm is established at the housing electrode 12 and therefore in the tissue, voltages that are otherwise developed in the tissue, such as those produced with stimulation pulses, will be established relative to Vcm. This can facilitate sensing of small signals in the tissue, such as sensing of neural responses (e.g., ECAP). As explained below, Vcm may not be completely constant (i.e., it may be pseudo-constant), but nonetheless, Vcm can be made to vary to a small enough degree to be easily sensed.

[0070] The housing 12 housing the stimulation circuit and other components is preferably completely conductive, but although not shown, may be conductive only at a portion. For example, the conductive housing 12 may be partially insulated, but conductive at a portion and capable of generating a common mode voltage Vcm at the portion. In other words, even if the conductive housing is not completely conductive but only partially conductive, the disclosed technology is effective.

[0071] exist Fig.9AA first example of a passive tissue bias circuit 150 configured to establish a common mode voltage Vcm in tissue is shown in FIG. In this example, a capacitor Ccm 152 is provided between the housing electrode Ec 12 at the top plate of the capacitor and the reference voltage Vref at the bottom plate of the capacitor, the size of which will be discussed below. A current Icm can flow through the capacitor Ccm to assist in passively setting Vcm, as further described below. Ccm can also typically include a capacitance, which can be composed of a single capacitor or one or more capacitors or capacitances. A reasonable value for Ccm may depend on many factors, such as the maximum allowable ripple of Vcm, the potential imbalance in the stimulation circuit, and the maximum output current of the amplifier that can be used in the passive tissue bias circuit, all of which are discussed below. In any case, Ccm will typically be in the range of 1 to 10 microfarads, and in one example may include 4.7 microfarads.

[0072] The reference voltage Vref may include a constant voltage provided by a voltage source 153 inside the conductive housing Ec 12. Vref may be adjustable and preferably has a value between or equal to ground (0V) and the compliance voltage (VH). Vref may also have a value that varies depending on the compliance voltage VH, which, as previously mentioned, may be measured and generated by the compliance voltage measurement and generation circuit 51 ( Figure 8B ). For example, Vref may be set to VH / 2. In just one example, the voltage source 153 generating VH / 2 may be formed as a voltage divider including a resistor ladder having a high resistance Ra connected in series, such as Fig.9A The common mode voltage Vcm established in the tissue comprises the sum of any voltage across capacitor Ccm 152 and Vref. Note that voltage source 153 is not absolutely necessary, particularly if Vref is equal to zero, in which case the ends of switch 154 (explained below) may simply be connected to ground.

[0073] Note that the tissue R between the housing electrode Ec 12 and the electrodes selected for stimulation (E1 and E2) has been represented as a resistor network including resistors Rc, R1 and R2 coupled to the electrodes Ec, E1 and E2. Figure 11A-11C The relevance of this resistor network is further described.

[0074] Fig.9A Also shown are aspects of the stimulation circuit 28, which includes one or more PDACs 40 connected to various electrode nodes 39ei. i and one or more NDAC 42 iSuch aspects of the stimulation circuit 28 are useful for illustration, particularly with respect to the shell electrode, because as noted above, the shell electrode node ec / shell electrode Ec 12 can be actively driven (e.g., during monopolar stimulation) similar to any other electrode 16. However, such operation of the stimulation circuit 28 to actively drive the shell electrode is inconsistent with the operation of the passive tissue bias circuit 150, and therefore switches 156 and 154 are provided to isolate the two circuits 28 and 150.

[0075] When it is desired to use the stimulus circuit 28 (eg, the PDAC 40 C or NDAC 42 C ) when the shell electrode Ec 12 is actively driven by the passive tissue bias circuit 150, control signal A is asserted to close switch 156 to connect the stimulation circuit 28 to the shell electrode Ec 12, and control signal B is deasserted to open switch 154 to isolate capacitor Ccm 152 within the passive tissue bias circuit 150 from the shell electrode 12. Alternatively, when the passive tissue bias circuit 150 is used to passively set the common mode voltage Vcm in the tissue, control signal B is asserted to close switch 154 to connect capacitor Ccm 152 within the passive tissue bias circuit 150 to the shell electrode 12, and control signal A is deasserted to open switch 156 to isolate the stimulation circuit 28 from the shell electrode 12. If the passive tissue bias circuit 150 does not need to operate, and if the shell electrode is not driven by the stimulation circuit 28, both switches 154 and 156 may be open. Control signals A and B may be controlled by control circuit 102 ( Figure 5 ) is issued, and switches 154 and 156 may also appear on the other side of their respective capacitors Ccm and Cc, or on the other side of the voltage source 153. Fig.9A In and subsequent figures, switch 154 is closed and switch 156 is open to focus discussion on the operation of passive tissue bias circuit 150 .

[0076] Although not shown, activation of the passive tissue bias circuit 150 (and disconnection of the stimulation circuit 28 from the housing electrode Ec) may be affected by programming the IPG 100. For example, when the IPG 100 is to sense a neural response and when the neural response algorithm 124 ( Figure 5 ) is active, control circuit 102 may automatically close switch 154 and open switch 156. Such sensing need not always occur during operation of IPG 100, and thus control circuit 102 may open switch 154 at other times, thereby allowing housing electrode Ec to be actively driven by stimulation circuit 28 if desired. An external device (such as clinician programmer 70 or external controller 60 ( Figure 4)) can also be used to place the IPG 100 in a neural sensing mode which will close the switch 154 to allow the passive tissue bias circuit 150 to function to passively set the common mode voltage Vcm in the tissue. The user interface of these devices 60 and 70 may have a selectable option to affect this.

[0077] Fig. 9B A variation of the passive tissue bias circuit 150' is shown in which the DC blocking capacitor Cc 38 between the electrode node ec and the electrode Ec is also used as the capacitor Ccm 152 in the passive tissue bias circuit. Likewise, switches 154 and 156 and their respective control signals A and B allow the passive tissue bias circuit 150' or the stimulation circuit 28 to be connected to the housing electrode Ec12.

[0078] Fig. 10A and Fig. 10B The operation of the passive tissue bias circuit 150 or 150' (both hereinafter referred to simply as 150) is explained, and in particular, it is shown that if one or more PDACs and one or more NDACs for providing current pulses at selected electrodes (again, E1 and E2 are used for illustration, but other electrodes may be selected) are in the currents Ip and In they provide (see Fig. 7A ) in magnitude, how does the circuit operate. As mentioned previously, Ip and |In| are ideally equal in magnitude at any given time. But non-ideal situations may cause the magnitudes of Ip and |In| to be slightly different, perhaps due to differences in the construction of the PDAC and NDAC. If there are variations in the control timing of the PDAC and NDAC, Ip and |In| may simply turn on and off at slightly different times. Finally, if either the PDAC or NDAC is not adequately powered, that is, if the voltage drop Vp or Vn across it is not greater than or equal to Vp(min) or Vn(min), respectively, then Ip may not be equal to |In|. As explained previously, Vp or Vn being too low can result in loading of the pulse (99, Fig. 8A ), which may require enabling the compliance voltage measurement and generation circuit 51 to increase the compliance voltage ( Figure 8B ).

[0079] The passive tissue bias circuit 150 benefits from its ability to handle this non-ideal situation and set the common mode voltage Vcm accordingly. Fig. 10AIn Example 158, it is assumed that Vref is set to zero volts (e.g., there is no voltage source 153). Further assume that the current Ip provided by one or more PDACs is initially greater than the current provided by one or more NDACs (i.e., Ip > |In|). In this case, the difference in these currents (Ip - |In|) includes a positive current Icm, which will initially flow from the housing electrode Ec 12 to ground through the capacitor Ccm 152 during each pulse phase 30a and 30b. As Fig. 10A shown, any current Icm charges the capacitor Ccm 152 with a positive voltage in this case, which initially increases Vcm during each pulse phase 30a or 30b. (During the silent period 30c between pulses, Vcm may decay slightly).

[0080] Establishing Vcm at the housing electrode Ec and thus in the tissue makes the electrode node voltages Ve1 and Ve2 references to this voltage. Therefore, as Vcm rises, Ve1 and Ve2 will also begin to rise. Ve1 and Ve2 will eventually increase to the point where in section 98, Ve1 just barely begins to exceed VH - Vp(min), as Fig. 10A shown in the waveform 160. At this point, and as previously discussed ( Fig. 8A ), the voltage drop Vp across the PDACs 401 and 402 becomes too small to support generating a slightly larger current Ip, resulting in the minimum load 99 of the first-stage pulse 30a of the electrode E1. (This minimum load 99 of the pulse does not significantly change the stimulation therapy provided by the pulse). Therefore, Ip will eventually drop slightly to match the value of |In| (at least from the perspective of time-averaging or total charge), at which point Icm equals 0. (Note that the loading of Ip will also cause In to become loaded because they are equal at this time). Icm = 0 prevents the capacitor Ccm from further charging and thus will eventually establish Vcm at a pseudo-constant level above Vref (ground), as Fig. 10A shown.

[0081] If the current In of one or more NDACs is higher than the current Ip of one or more PDACs (i.e., |In| > Ip), then Icm will flow as a negative current from ground to the housing electrode Ec 12. This will establish Vcm as a negative voltage (Vcm < Vref = 0) in Example 158, which may be undesirable from a circuit perspective. To accommodate this possibility, in Fig. 10B Examples 162a and 162b, the voltage source 153 sets Vref to a value greater than zero but less than the compliance voltage VH (i.e., 0 < Vref < VH). For example, Vref can be set to VH / 2.

[0082] In the case where Vref is set in this way, Vcm will initially be set to Vref. Fig. 10B As shown in waveform 164 , electrode node voltages Ve1 and Ve2 are initially referenced to Vcm=Vref.

[0083] If Ip>|In| as in example 162a, Icm will initially be positive, forming a positive voltage across capacitor Ccm 152. The effect of the passive tissue bias circuit 150 is then similar to that in Fig. 10A What happens in example 158 of : Vcm will rise from Vref, and so will Ve1 and Ve2, until Ve1 just barely (portion 98) exceeds VH-Vp(min), as shown in waveform 166a. At this point, the voltage drop Vp across PDACs 401 and 402 becomes too small to support the slightly larger current Ip produced during the first phase pulse 30a. Therefore, Ip will drop slightly to match the value of |In|, where both become slightly loaded 99 ( Fig. 10A ), and therefore Icm will be equal to 0. This prevents the capacitor Ccm from charging further, thereby establishing Vcm at a level higher than Vref. In fact, Fig. 10A Example 158 and Fig. 10B Example 162a is similar and will establish Vcm at the same value. It just takes Example 158 longer to do so because it takes longer to establish Vcm when Vref is equal to zero than when Vref is above zero.

[0084] If |In|>Ip as in example 162b, a negative current Icm will initially flow from ground to the housing electrode Ec 12 through capacitor Ccm 152. This charges capacitor Ccm 152 with a negative voltage, which reduces Vcm from Vref during each pulse phase 30a or 30b. This causes Ve1 and Ve2, which are referenced to Vcm, to also drop. Eventually, Ve2 will just barely (portion 98) be below Vn(min), as shown in FIG. Fig. 10B As shown in waveform 166b of FIG. 166b, the voltage drop Vn across NDACs 421 and 422 becomes too small to support the slightly larger current |In|. Therefore, |In| will drop slightly to match the value of Ip, and thus Icm will be equal to 0. (Again, being loaded by 99 also causes Ip to be loaded, because they are equal at this time, as shown in FIG. 166b of FIG. 166b. Fig. 10A Icm=0 prevents the capacitor Ccm from charging further, thereby establishing Vcm at a level lower than Vref, as shown in FIG. Fig. 10BIn short, in this example 162b, the fact that Icm is negative is not a problem from a circuit perspective because Vref is above zero, which allows Vcm to drop below Vref while still remaining positive.

[0085] Reference again Fig.9A , an optional bleed resistor Rbleed 155 is included in parallel with capacitor Ccm 152. Bleed resistor Rbleed 155 preferably has a high resistance (e.g., 1 megohm or higher). Rbleed allows charge to be slowly discharged from capacitor Ccm, for example, during a period when the passive tissue bias circuit is not used. In addition, Rbleed can assist in charge balancing, which can help prevent the load 99 of current pulses. Rbleed allows a low current to flow, which is proportional to the voltage across capacitor Ccm. For example, assume that one or more PDACs are slightly stronger than one or more NDACs, that is, initially Ip>|In|, causing Vcm to rise. As previously explained, Vcm will continue to increase until the voltage across one or more stronger PDACs begins to drop below Vp(min), thereby causing Ip to drop to match |In|, thereby achieving current balance (and making Icm ultimately equal to 0). Advantageously, resistor Rbleed will begin to add some current to one or more of the weaker NDACs, which may allow current balancing to occur before one or more of the PDACs are loaded. If this happens, there will be no loading of the electrode current (99), and Vcm can reach equilibrium at a lower voltage. In essence, Rbleed then acts as a current path to boost the weaker DAC. Note that for convenience, Rbleed is not shown in subsequent examples of tissue bias circuits, but can be used with any of these examples.

[0086] Figure 11A-11C The operation of the passive tissue bias circuit 150 in different situations is further described. The relevance of modeling tissue R using resistances Rc, R1, and R2 is further described. Considering that such modeling is useful, this is because the resistance between each selected electrode E1 and E2 and the housing electrode Ec may not be the same, which is not surprising given the complex tissue environment and the distance between the electrodes E1 and E2 and the housing electrode Ec. In particular, R1 and R2 can vary. Figure 11A-11C The operation of the passive tissue bias circuit 150 is further described if the magnitudes of Ip and In vary, and how the compliance voltage measurement and generation circuit 51 may operate to accommodate the operation of the passive tissue bias circuit 150 is described. Figure 11A-11C In the example, it is assumed that Vref has been set to VH / 2.

[0087] exist Fig.11A, it is assumed that R1 is equal to R2 in the tissue model. Waveform 170a shows the electrode node voltages Ve1 and Ve2 when the passive tissue bias circuit 150 is not used (e.g., switch 154 is open and Vcm at the housing electrode is floating). The voltage Vt in the resistor model (indicative of tissue voltage) floats to whatever level would otherwise be indicated by the stimulus. In this case, it can be seen that Vt is the same during each of the pulse phases 30a and 30b. Assuming that Vp(min) and Vn(min) are equal, Vt will be approximately VH / 2. In addition, assuming that the compliance voltage measurement and generation circuit 51 ( Figure 8B ) is operating to adjust the compliance voltage to an optimum level, Ve1 and Ve2 are typically firmly fixed within a region 111 between Vn(min) and VH-Vp(min).

[0088] For waveforms 170b-170d, a passive tissue bias circuit 150 is used (eg, switch 154 is closed), and thus a common mode voltage Vcm is passively established in the tissue while (potentially) charging Ccm 152. Ve1 and Ve2 are referenced to Vcm during each of the pulse phases 30a and 30b.

[0089] In waveform 170b, Ip = |In|. Icm will equal zero, and Vcm is established at approximately VH / 2(Vref), as occurs in waveform 170a.

[0090] In waveform 170c, assuming that initially Ip>|In|, as Fig. 10B 162a. Icm is initially positive, which will eventually drive Vcm, Ve1, and Ve2 higher for the reasons already explained. This will cause Ve1 to eventually exceed VH-Vp(min). Therefore, in this example, the compliance voltage measurement and generation circuit 51 ( Figure 8B ) operates to increase VH to alleviate this problem. As shown in waveform 170c, VH will gradually increase until Ve1 just barely passes VH-Vp(min), at which point the compliance voltage measurement and generation circuit 51 will stop increasing VH, as shown in waveform 170c. At this point ip equals |In|, Icm will be zero, and Vcm will be established at a value higher than Vref. Note that in this example, increasing the compliance voltage VH will also (further) increase Vcm, because Vref (=VH / 2) will also increase.

[0091] In waveform 170d, it is assumed that initially |In|>Ip. Fig. 10BThis is what happens in Example 162b. Icm is initially negative, which eventually drives Vcm, Ve1, and Ve2 down. Note that this may eventually cause Ve2 to become lower than Vn(min). Similarly, the measurement and generation circuit 51 can be operated to increase VH and alleviate this problem. Increasing VH will increase Vref (=VH / 2), and thereby increase Vcm, Ve1, and Ve2 until Ve2 is just barely below Vn(min), as shown in waveform 170d. At this point |In| will be equal to Ip, and Icm will be zero. Even if the trend is for Vcm to decrease (Icm<0), increasing VH will also increase Vref, which will offset the increase in Vcm.

[0092] exist Fig.11A Comparison of waveforms 170c and 170d with waveform 170b shows that if the currents Ip and In provided by one or more PDACs and one or more IDACs are not balanced, the use of passive tissue bias circuit 150 may warrant increasing the value of compliance voltage VH. Increasing the compliance voltage is generally not preferred because it consumes additional power in IPG 100 and may drain the IPG's battery 14 more quickly. Figure 1 ). In particular, additional headroom 101 is provided within region 111 during which the voltage drops Vn across the NDAC (waveform 170c) and Vp across the PDAC (waveform 170d) are greater than those required for the DACs to generate pulses of specified amplitude. However, this disadvantage is offset by the benefits provided by the controlled common-mode Vcm when sensing neural responses in tissue.

[0093] exist Fig. 11B , it is assumed that R1 is greater than R2 in the tissue model. Waveform 172a assumes that the passive tissue bias circuit 150 is not used, and therefore the tissue voltage Vt floats to whatever level would otherwise be dictated by the stimulation. In this case, it can be seen that Vt differs during pulse phases 30a and 30b: Vt is lower during pulse phase 30a because the voltage dropped across R1 is greater than the voltage dropped across R2; and Vt is higher during pulse phase 30b when the polarity of the current is reversed.

[0094] For waveforms 172b-172d, a passive tissue bias circuit 150 is used (e.g., switch 154 is closed), and thus Vcm is passively established in the tissue as Ccm 152 is (potentially) charged. Ve1 and Ve2 are referenced to Vcm during each of the pulse phases 30a and 30b, which in this example causes the waveform to shift 171 during each of the pulse phases. As shown in waveform 172b, this shift 171 tends to pull Ve1 and Ve2 upward during the first pulse phase 30a, and pull Ve1 and Ve2 downward during the second pulse phase 30b.

[0095] In waveform 172b, assuming Ip = |In|, it will not charge capacitor Ccm 152. Nevertheless, referencing Ve1 and Ve2 to Vcm may result in the compliance voltage being too low given the shift 171, and thus in waveform 172b, it can be seen that the compliance voltage has been raised (51) such that Ve1 and Ve2 are still bounded by region 111 ( Fig. 8A ) to prevent the generated pulse from becoming a load (99).

[0096] Comparison of waveforms 172a and 172b shows that if the resistance between the active electrode and the housing electrode is unbalanced, the use of the passive tissue bias circuit 150 can ensure an increase in the value of the compliance voltage VH. Again, while increasing VH is generally undesirable for power consumption reasons, this disadvantage is offset by the benefits provided by the common mode voltage Vcm when sensing neural responses in tissue.

[0097] In waveform 172c, assuming that initially Ip>|In|, Vcm, Ve1, and Ve2 will eventually be driven higher. This may cause Ve1 to exceed VH-Vp(min). Therefore, as shown, the compliance voltage VH can be increased even higher (51) to prevent pulse loading. Likewise, increasing the compliance voltage VH also increases Vref, which in this example increases Vcm even further.

[0098] In waveform 172d, assuming |In|>Ip, it drives Vcm and Ve1 and Ve2 down. This may cause Ve1 to become lower than Vn(min) during the second pulse phase 30b. Therefore, the compliance voltage VH can be raised even higher (51) to prevent pulse loading, as occurs with waveform 170d ( Fig.11A ).

[0099] By comparing waveforms 172c and 172d with waveform 172b, it is again noted that if the currents Ip and In provided by the one or more PDACs and the one or more NDACs are unbalanced, then the use of the passive tissue bias circuit 150 can ensure that the value of the compliance voltage VH is increased even further. As previously discussed with respect to waveforms 170b-170d ( Fig.11A Again, this disadvantage is acceptable given the benefits that common mode Vcm provides in tissues.

[0100] exist Fig. 11C In the tissue model, it is assumed that R1 is less than R2. Waveforms 174a-174d show similar Fig. 10B172a - 172d , which again illustrates how the operation of the passive tissue bias circuit 150 references Ve1 and Ve2 to Vcm, thereby facilitating neural sensing, but also ensures that the compliance voltage VH (51) is increased to prevent pulse loading.

[0101] Thus, the passive tissue bias circuit 150 is useful in passively setting Vcm in the tissue to an appropriate value despite any imbalance between Ip and In provided by the PDAC and NDAC circuits, and despite any imbalance in the resistances R1 and R2 between the active electrode and the shell electrode Ec. As has been shown, when there is an imbalance, the common mode voltage Vcm established by the passive tissue bias circuit 150 at the shell electrode Ec will be passively changed from the Vref provided by the voltage source 153, thereby ultimately causing the current to the shell (Icm) to be equal to zero. This is beneficial compared to actively driving the shell electrode to a set voltage. Actively driving a specific voltage at the shell electrode does not guarantee that current will not flow through the tissue to the shell electrode. Such shell electrode current can result in undesirable "pocket stimulation", which means that current flows from the selected electrode to the tissue pocket implanted in the shell 12. The patient may feel the pocket stimulation, or it may otherwise have a negative impact on the treatment provided by the selected lead electrode.

[0102] Fig. 12A Another example of a passive tissue bias circuit 200 that can be used to maintain tissue at a common mode voltage Vcm is shown. The passive tissue bias circuit 200 operates substantially similar to the passive tissue bias circuit 150, but includes an amplifier 180, preferably an operational transconductance amplifier (OTA), which establishes a virtual reference voltage Vvref at the bottom plate of capacitor Ccm 152. Note that as previously described with reference to Fig.9A As explained, the passive tissue bias circuit 200 may include switches 154 and 156 as before to selectively isolate the stimulation circuit 28 from the passive tissue bias circuit 200. As also described with reference to Fig. 9B As explained, the capacitor used in the passive tissue bias circuit 200 may include the DC blocking capacitor Cc 38 of the housing electrode, although this variation is not described in detail. Fig. 12A Shown in.

[0103] OTA180 establishes an output current Iout that is proportional to the voltage difference at its input: that is, Iout = (Vref - Vvref) * G, where G includes the transconductance of OTA180. OTA180 has positive and negative maximum output currents +Iout(max) and -Iout(max). The absolute values ​​of these maximum output currents |Iout(max)| are a function of the bias current Ibias provided to OTA 180: |Iout(max)| = Ibias*A, where A includes the current gain of the amplifier. In one example, the current gain A = 1000 and Ibias = 100 nanoAmp, which makes Iout range from -Iout(max) = -100 microAmps to +Iout(max) = 100 microAmps. Through the design of OTA180 or the adjustment of Ibias, -Iout(max) and +Iout(max) can be adjusted to different values.

[0104] OTA180 is preferably configured as a follower, where a virtual reference voltage Vvref is fed back to the negative input of the OTA. The positive input of OTA180 is provided with a reference voltage Vref. Vref as previously described may be provided by a voltage source 153, and as previously described may include a constant or adjustable voltage, preferably between or equal to ground (0V) and a compliance voltage (VH), such as VH / 2. When connected as a follower, the output Vvref of OTA180 will be equal to Vref as long as Icm is between -Iout(max) and +Iout(max), as further explained below.

[0105] With the help of Fig. 12A The operation of the passive tissue bias circuit 200 can be understood from the diagram in FIG. Fig. 12A The polarity of Iout is defined in , when Icm is between –Iout(max) and +Iout(max), Iout=Icm. When within this range, Icm simply passes through OTA180 like Iout. Because the output current of OTA180 is not exceeded within this range, the virtual reference voltage Vvref remains constant and equal to Vref.

[0106] Examples 190a and 190b show operation when Icm is positive and below +Iout(max). Example 190a shows that the mismatch between Ip and |In| is small, and therefore the current Icm is relatively small. At this current level, Vcm initially increases as capacitor Ccm charges, while Vvref remains equal to Vref. Eventually (as the pulse repeats), Vcm settles to a constant level, as previously explained ( Figure 10A-10B). Example 190b shows that the mismatch between Ip and |In| is higher, and therefore the current Icm is also higher. This will cause the capacitor Ccm to charge faster, and Vcm to rise faster and will eventually establish at a higher value. Although not shown, it should be understood that negative values ​​of Icm will establish Vcm at a level below Vref.

[0107] If the mismatch between Ip and |In| is large, such that Icm will exceed +Iout(max) as shown in example 190c, then OTA 180 will only be able to draw +Iout(max), limiting Icm to that value. Having OTA 180 limit Icm provides Fig. 12A The benefit of the passive tissue bias circuit 200 is that limiting Icm limits "pocket stimulation", which, as previously explained, is caused when unwanted current flows into a tissue pocket of the implant housing 12. In this regard, the OTA 180 can be designed to set +Iout(max) and -Iout(max) to appropriate values ​​to limit the potential amplitude of pocket stimulation.

[0108] Returning to example 190c, because OTA 180 cannot accommodate all of the excess current, Vcm and Vvref will initially be pulled above Vref, to a value Vvref(max), which will vary in magnitude as further pulses are issued. (Again, Vref can be set to VH / 2, allowing Vvref to be pulled down if Icm is negative, where OTA 180 limits Icm to –Iout(max)). Capacitor Ccm will then begin to charge in a current limited manner (where Icm = +Iout(max)), causing Vcm to increase and Vvref to decrease. As capacitor Ccm continues to charge as subsequent pulses are issued, and as Fig. 12B As further shown in FIG. 1 , Vcm will continue to rise while Vvref will continue to fall. As mentioned earlier, the rise in Vcm will cause the electrode node voltages (e.g., Ve1 and Ve2 to rise), eventually reaching a point where one of the waveforms will begin to break through VH-Vp(min), which will cause the dominant current Ip to fall to match |In|, as explained previously ( Figure 10A-10B ). At this point Icm will be equal to zero, thereby stopping further charging of capacitor Ccm and establishing Vcm at a value below VH-Vp(min). Note also that when Icm is equal to zero, Vvref will return to Vref. Again, a negative value of Icm will establish Vcm at a level below Vref but above Vn(min).

[0109] Fig.13AShows another example of the passive tissue biasing circuit 250 (switches 154 and 156 not shown), which adds optional additional circuitry for monitoring the virtual reference voltage Vvref. For simplicity, switches 154 and 156 are not shown.

[0110] A window comparator is provided as a logic circuit, which includes two comparators 182a and 182b. Each of the comparators 182a and 182b receives Vvref and a reference voltage that sets a window 173 around Vref. In the example shown, the window 173 is 200 mV wide and is set to range from Vref - 100 mV to Vref + 100 mV. Vref + 100 mV is provided to comparator 182a, while Vref - 100 mV is provided to comparator 182b. The voltages Vref - 100 mV and Vref + 100 mV may be provided by a voltage source similar to source 153 that generates Vref, although such additional sources are not shown. By connecting Vvref, Vref + 100 mV, and Vref - 100 mV to the appropriate positive and negative inputs of the comparator, if Vvref > Vref + 100 mV, the output X of comparator 182a will be equal to "1", and if Vvref < Vref – 100 mV, the output Y of comparator 182b will be equal to "1". If Vvref is between Vref + 100 mV and Vref - 100 mV, the outputs X and Y will be equal to "0". The positive and negative values of 100 mV for window 173 are merely an example, and different values may be used. Outputs indicating that Vvref has exceeded Vref + 100 mV or has dropped below Vref – 100 mV may also be used.

[0111] The outputs X and Y are provided to the control circuit 102, allowing the virtual reference voltage Vvref to be monitored at the appropriate time, as discussed further below. Such monitoring is useful in several different ways. First, as referenced Fig.14A and Fig. 14B further explained, it allows the control circuit 102 to decide when it is best to perform nerve response sensing in the IPG 100, which can be achieved by having the control circuit issue a sense enable signal S(en).

[0112] Second, monitoring Vvref also helps the control circuit 102 decide whether the compliance voltage VH should be increased. Increasing the compliance voltage VH can be made effective by asserting an enable signal VH(en2), which may be sent to the compliance voltage measurement and generation circuit 51( Figure 8B) The input VH(en) of PWM 53, as previously explained, will activate the VH regulator 49 to increase the compliance voltage. In this regard, the VH regulator 49 can be activated at its input by an enable signal VH(en1) provided by the measurement circuit in the compliance voltage measurement and generation circuit 51 as already explained or by the assertion of VH(en2). This alternative is particularly useful because VH(en1) can operate when the passive tissue biasing circuit 250 is not operating (switch 154 open), while VH(en2) can operate when the passive tissue biasing circuit 250 is operating (switch 154 closed). Fig.13A The OR gate 184 in Fig.13A can be used to process the two enable signals VH(en1) and VH(en2) and assert the input VH(en) when one of them is active. In another example, the VH regulator 49 can be activated only by the enable signal VH(en2), thus raising the need for discussion regarding the measurement circuit in the compliance voltage measurement and generation circuit 51.

[0113] Fig. 13B The operation of the passive tissue biasing circuit 250 and how the control circuit 102 can be used to issue a control signal S(en) to enable neural sensing and VH(en2) to increase the compliance voltage has been explained. It is useful for the control circuit 102 to examine the states of the outputs X and Y from the window comparator during both the first 30a and second 30b phases of the biphasic pulse because either pulse phase can provide information related to neural sensing or compliance voltage regulation. Note that the control circuit 102 can know when the first pulse phase 30a and the second pulse phase 30b occur and thus when the outputs X and Y should be sampled because the control circuit 102 can use this timing information to program the stimulation circuit 28. In other ways, the control circuit 102 can receive one or more control signals 186(tp1,tp2) from the stimulation circuit 28 that indicate when stimulation occurs during the first pulse phase 30a and the second pulse phase 30b. The control signals tp1 and tp2 can be asserted to inform the control circuit 102 when sampling the outputs X and Y, when charging the DC-blocking capacitor 38 is most severe, and thus when the electrode node voltages (e.g., Ve1 and Ve2) are most likely to breach the region 111 (e.g., see Figure 7B ) and can be programmed to occur closer to the ends of the pulse phases 30a and 30b.

[0114] When the Icm through the capacitor Ccm during the two pulse phases is within the output current limit of the OTA180, i.e., when –Iout(max) < Icm < +Iout(max), it will occur Fig. 13BExample 202a. During this example 202a, Vvref will be within window 173 and will typically be equal to Vref, and during the two pulse phases, outputs X and Y will be equal to "0". Vcm will be stable and thus the control circuit 102 can enable sensing at this time by asserting S(en). Additionally, there is no reason to believe that the compliance voltage VH is insufficient at this time to ensure that each VH(en2) enables the VH regulator 49.

[0115] During example 202b, a significant positive current Icm > +Iout(max) occurs during both pulse phases 30a and 30b. During this example 202b, Vvref will be outside window 173, i.e., Vvref > Vref + 100 mV. Thus, during the two pulse phases, output X will be equal to "1" while output Y will be equal to "0". Vcm will be unstable as shown in Fig. 12B shown. Thus, the control circuit 102 will disable sensing at this time by de-asserting S(en). There is still no reason to believe that the compliance voltage VH is insufficient at this time. Instead, the capacitor Ccm may only be charged to steady state as occurs in Fig. 12B shown. Thus, the control circuit 102 will thus de-assert VH(en2).

[0116] Example 202c is essentially the opposite of example 202b, having a significant negative current Icm < -Iout(max) during both pulse phases 30a and 30b. During this example 202c, Vvref will be outside window 173, i.e., Vvref < Vref + 100 mV. Thus, during the two pulse phases, output X will be equal to "0" while output Y will be equal to "1". Vcm will be unstable because it is in the process of dropping below Vref. Thus, the control circuit 102 will disable sensing at this time by de-asserting S(en). Again, there is no reason to think that the compliance voltage VH is insufficient at this time because the capacitor Ccm may still be charging to steady state. Thus, the control circuit 102 will thus de-assert VH(en2).

[0117] During Example 202d, it can be seen that Icm is significantly positive (+>Iout(max)) during the first pulse phase 30a and significantly negative (<-Iout(max)) during the second pulse phase. During the first pulse phase 30a, Vvref will be higher than Vref + 100 mV and output X will be equal to "1", while output Y will be equal to "0". During the second pulse phase 30b, Vvref will be lower than Vref – 100 mV and these logic states are flipped, where output X is equal to "0" and output Y is equal to "1". Vcm will be unstable and thus the control circuit 102 will disable sensing at this time by de-asserting S(en). Additionally, this Example 202d will not imply that the capacitor Ccm is only on its way to being charged to a steady state because the current Icm flowing through the capacitor is reversed during both pulse phases. Instead, this example will show compliance voltage deficiencies: NDAC is clearly loaded (Vn < Vn(min)) during the first pulse phase 30a (when Ip is dominant), and PDAC is clearly loaded (Vp < Vp(min)) during the second pulse phase 30a (when In is dominant). This shows that the electrode node voltages (e.g., Ve1 and Ve2) cannot stay within region 111 ( Fig. 8A ). Thus, during this Example 202d, the control circuit will assert VH(en2).

[0118] Example 202e is essentially the opposite of Example 202d where the dominance in Icm is flipped during both pulse phases. Again, the control circuit 102 will de-assert S(en) and assert VH(en2).

[0119] Fig.14A and Fig. 14B illustrates how the generation of the common mode voltage Vcm can be used to assist in sensing neural responses in tissue. In both figures, the detection amplifier 110 for sensing neural responses can be enabled to sense only when the enable signal S(en) is asserted. As explained with reference to Fig.13A and Fig. 13B , this enable signal can be generated by the control circuit 102 or can be generated otherwise and at other times.

[0120] Fig.14A illustrates the single-ended sensing (S) of the neural response at the selected electrode E6 as previously explained. The electrode node voltage Ve6 is provided to one input of the sense amplifier 110 while the other input receives Vcm as generated at the case electrode. Ve6 will also be referenced to the Vcm present in the tissue. Since Vcm is stable in the tissue, the sense amplifier 110 is better able to reject that voltage and sense small signal neural responses.

[0121] Fig. 14B Differential sensing (S1 and S2) at different electrodes E5 and E6 is shown. Electrode node voltages Ve5 and Ve6 are provided to the inputs of sense amplifier 110, both referenced to Vcm. Again, this facilitates sensing of small signal neural responses.

[0122] The disclosed examples of passive tissue bias circuits are particularly useful in sensing neural responses, but may also be useful in other situations where it is beneficial to set or finely control the common-mode voltage in the tissue. In addition, while the passive tissue bias circuit has been shown to operate while any two electrodes (e.g., E1 and E2) are selected, the circuit may also operate if any two or more electrodes are selected for stimulation (e.g., electrodes E1 and E2 as anodes outputting a total anode current of +I, and electrode E3 as cathode outputting a cathode current of –I).

[0123] Thus far, in this disclosure, it has been assumed that the housing electrode Ec 12 comprises the electrode used by the passive tissue bias circuit to set the common mode voltage Vcm in the tissue. However, any electrode, including the lead-based electrode 16 ( Figure 1 ), can also be used for this purpose. Fig.15 This alternative to the passive tissue bias circuit 300 is shown and includes an example where any electrode, such as any lead-based electrode 16 or housing electrode Ec 12, can be selected to set the common mode voltage Vcm. Although 150( Fig.9A )、150'( Fig. 9B ) or 250( Fig.13A ) can be used Fig.15 Alternative circuits, but Fig.15 The example shown in FIG. 1 generally corresponds to circuit 200 ( Fig. 12A ).

[0124] exist Fig.15 , switches 154 and 156 have each been expanded to include a switch matrix, with one switch 154 and one switch 156 associated with each of the lead-based electrodes (E1, E2, etc.) and the shell electrode Ec. Switches 154 and 156 are similar in function to the separate switches 154 and 156 previously described. Switch 156 is used to couple each electrode Ei to the stimulation circuit 28 (not shown) via electrode node ei, while switch 154 is used to couple each electrode Ei to the common-mode capacitor Ccm. Thus, in this example, the common-mode capacitor Ccm is shared by the electrodes; in another example, each electrode may include its own dedicated capacitor for setting Vcm.

[0125] exist Fig.15In the example shown at the bottom of , it is assumed that electrodes E1 and E2 have been selected as active to provide biphasic stimulation (I) to the tissue, while electrode E3 will provide a common-mode voltage Vcm. The switches 156 coupled to the active electrodes E1 and E2 are therefore closed (control signals A1 and A2 are asserted) to connect these electrodes to the stimulation circuit 28. Since it is inconsistent to also provide Vcm at these active electrode nodes, their switches 154 are opened (control signals B1 and B2 are de-asserted) to disconnect these electrodes from the capacitor Ccm. In contrast, electrode E3, which will establish a common-mode voltage Vcm for the tissue, will have its switch 154 closed (control signal B3 is asserted) to connect E3 to the capacitor Ccm. Because it is inconsistent to also drive electrode E3 with the stimulation circuit 28, its switch 156 is opened (control signal A3 is de-asserted). All other switches not associated with electrodes E1, E2 or E3 can be opened because they are not involved in driving tissue current or providing a common-mode voltage Vcm in this example.

[0126] Note that more than one electrode may be selected to provide a common mode voltage. For example, electrodes E3 and E4 may be selected to provide Vcm (B3 and B4 are advocated), or electrodes E3, E4, and housing electrode Ec may all be selected to provide Vcm (B3, B4, and Bc are advocated). One or more electrodes (such as Fig.15 Electrode E6 in the example of will not be selected to participate in providing Vcm to the tissue. That is, switch 154 of E6 will be opened (B6 is deasserted) like its switch 156 (A6 is deasserted) because E6 will not be driven by the stimulation circuit 28 when sensing.

[0127] Providing Vcm to electrodes closer to those used for stimulation can help reference electrode node voltages to Vcm. Additionally, allowing non-shell electrodes 16 to provide Vcm allows shell electrode Ec 12 to be actively driven (Ac asserted; Bc deasserted), such as during monopolar stimulation, while still providing the benefits provided by Vcm generation.

[0128] Although not shown, the IPG 100 may include one or more special electrodes anywhere on the device to set Vcm, which may be dedicated to Vcm generation and cannot be used to provide stimulation to the tissue R.

Claims

1. A stimulator device system, comprising: a first electrode; a plurality of electrode nodes, each electrode node configured to couple to one of a plurality of electrodes configured to contact patient tissue; a stimulation circuit configured to provide a stimulation current through the patient tissue via at least one of the plurality of electrode nodes; a bias circuit configured to generate a first reference voltage; as well as A capacitor is coupled between the first reference voltage and the first electrode, wherein the capacitor is configured to provide a common mode voltage to the patient tissue at the first electrode.

2. The system according to claim 1, wherein: The stimulation circuit is configured to provide the stimulation current through the patient tissue via at least one of the plurality of electrode nodes and the first electrode.

3. The system of claim 1, further comprising a housing, wherein the first electrode comprises an electrode of the housing.

4. The system according to claim 1, wherein: The capacitance includes one or more capacitors.

5. The system according to claim 1, wherein: The stimulation circuit is configured to be powered between a compliance voltage and ground, and wherein the first reference voltage is between the compliance voltage and ground.

6. The system of claim 5, wherein the first reference voltage is configured to be proportional to the compliance voltage.

7. The system according to claim 5, wherein: The first reference voltage is at a midpoint between the compliance voltage and ground.

8. The system of claim 1, wherein the bias circuit comprises an amplifier.

9. The system according to claim 8, wherein: The amplifier comprises a first input and a second input, wherein the amplifier is configured as a follower in which the first reference voltage is provided to the first input and wherein a second reference voltage is provided to the second input.

10. The system according to claim 9, wherein: The amplifier is configured to maintain the first reference voltage equal to the second reference voltage if the current through the capacitor is between a minimum and a maximum output current of the amplifier.

11. The system of claim 1, further comprising logic circuitry configured to issue at least one indication that the first reference voltage exceeds a first threshold or falls below a second threshold.

12. The system according to claim 11 further includes a control circuit configured to issue an enable signal in response to the at least one indication, the enable signal indicating when a neural response in the patient tissue in response to the stimulation current can be sensed at at least one electrode node among the plurality of electrode nodes.

13. The system of claim 1, further comprising at least one sense amplifier configured to sense a neural response in the patient tissue in response to the stimulation current when the capacitor is configured to provide the common-mode voltage to the patient tissue at the first electrode.

14. The system of claim 13, wherein the at least one sense amplifier comprises a first input and a second input, wherein: The at least one sense amplifier is configured to receive one of the electrode nodes at a first input thereof.

15. The system of claim 14, wherein: The at least one sense amplifier is configured to receive the common mode voltage at a second input thereof, or is configured to receive another one of the electrode nodes at a second input thereof to differentially sense the neural response between the one electrode node and the other electrode node.

16. A stimulator device system comprising: a plurality of electrode nodes, each electrode node configured to couple to one of a plurality of electrodes configured to contact patient tissue; a stimulation circuit configured to provide a stimulation current through the patient tissue via at least one of the plurality of electrode nodes; a bias circuit configured to generate a first reference voltage; as well as A plurality of switches, each of the plurality of switches being associated with a different one of the electrodes, wherein each of the plurality of switches when selected is configured to couple the first reference voltage to its associated electrode to provide a common mode voltage to the patient tissue at the associated electrode.

17. The system of claim 16, wherein: Each of the plurality of switches, when selected, is configured to capacitively couple the first reference voltage and its associated electrode to provide the common mode voltage to the patient tissue at the associated electrode.

18. The system of claim 17, wherein: The capacitance includes one or more capacitors.

19. The system of claim 17, wherein: There is a single capacitance, and wherein each of the plurality of switches, when selected, is configured to couple the single capacitance between the first reference voltage and its associated electrode to provide the common mode voltage to the patient tissue at the associated electrode.

20. The system of claim 17, wherein: There are a plurality of capacitors, each of the plurality of capacitors being dedicated to a different one of the electrodes, and wherein each of the plurality of switches, when selected, is configured to couple the capacitance dedicated to its associated electrode between the first reference voltage and the associated electrode to provide the common-mode voltage to the patient tissue at the associated electrode.

21. The system of claim 16, wherein at least one of the electrodes comprises an electrode of the housing.

22. The system of claim 21, wherein: The housing houses the stimulation circuit, the bias circuit, and the plurality of switches.

23. The system of claim 16, further comprising a lead, wherein: At least some of the plurality of electrodes are located on the lead.

24. The system of claim 23, further comprising a housing, wherein: One of the plurality of electrodes includes the housing.

25. The system of claim 16, wherein: The stimulation circuit is configured to be powered between a compliance voltage and ground, and wherein the first reference voltage is between the compliance voltage and ground.

26. The system of claim 25, wherein the first reference voltage is configured to be proportional to the compliance voltage.

27. The system of claim 25, wherein the first reference voltage is at a midpoint between the compliance voltage and ground.

28. The system of claim 17, wherein the bias circuit comprises an amplifier.

29. The system of claim 28, wherein the amplifier comprises a first input and a second input, wherein: The amplifier is configured as a follower in which the first reference voltage is provided to the first input and in which a second reference voltage is provided to the second input.

30. The system of claim 29, wherein the amplifier is configured to maintain the first reference voltage equal to the second reference voltage if the current through the capacitor is between a minimum and a maximum output current of the amplifier.

31. The system of claim 16, further comprising logic circuitry configured to issue at least one indication that the first reference voltage exceeds a first threshold or falls below a second threshold.

32. The system according to claim 31 further includes a control circuit configured to issue an enable signal in response to the at least one indication, the enable signal indicating when a neural response in the patient tissue in response to the stimulation current can be sensed at at least one electrode node among the plurality of electrode nodes.

33. The system of claim 16, further comprising at least one sense amplifier configured to sense a neural response in the patient tissue in response to the stimulation current when the common mode voltage is provided to the patient tissue.

34. A stimulator device system comprising: a plurality of electrode nodes, each electrode node configured to couple to one of a plurality of electrodes configured to contact patient tissue; a stimulation circuit configured to provide a stimulation current through the patient tissue via at least one of the plurality of electrode nodes, wherein the stimulation circuit is configured to be powered between a compliance voltage and ground, wherein the compliance voltage varies as a function of time; as well as A bias circuit is configured to provide a common mode voltage at one or more first electrodes, wherein the common mode voltage is derived from the compliance voltage and varies as a function of time.

35. The system of claim 34, wherein: The bias circuit is configured to generate a reference voltage derived from the compliance voltage.

36. The system of claim 35, further comprising a capacitor coupled between the reference voltage and the one or more first electrodes.

37. The system of claim 36, wherein: The bias circuit includes an amplifier.

38. The system of claim 37, wherein: The amplifier comprises a first input, a second input and an output, wherein the amplifier is configured as a follower in which the reference voltage is provided to the first input and wherein the output is provided to the second input.

39. The system of claim 37, wherein: The amplifier is configured to maintain the output equal to the reference voltage if the current through the capacitor is between a minimum and a maximum output current of the amplifier.

40. The system of claim 36, further comprising logic circuitry configured to issue at least one indication that the reference voltage exceeds a first threshold or falls below a second threshold.

41. The system according to claim 40 further includes a control circuit configured to issue an enable signal in response to the at least one indication, the enable signal indicating when a neural response in the patient tissue in response to the stimulation current can be sensed at at least one electrode node among the plurality of electrode nodes.

42. The system of claim 34, wherein the common mode voltage is approximately half of the compliance voltage.

43. The system of claim 34, wherein: The stimulation circuit is configured to provide the stimulation current through the patient tissue via one or more first electrodes.

44. The system of claim 34, further comprising a housing, wherein: The housing includes one of the electrodes.

45. The system of claim 44, wherein: The one or more first electrodes include the housing.

46. ​​The system of claim 34, wherein the capacitance comprises one or more capacitors.

47. The system of claim 34, further comprising at least one sense amplifier configured to sense a neural response in the patient tissue in response to the stimulation current when the common-mode voltage is provided at the one or more first electrodes.

48. The system of claim 47, wherein the at least one sense amplifier comprises a first input and a second input, wherein: The at least one sense amplifier is configured to receive one of the electrode nodes at a first input thereof.

49. The system of claim 48, wherein: The at least one sense amplifier is configured to receive the common mode voltage at a second input thereof, or is configured to receive another one of the electrode nodes at a second input thereof to differentially sense the neural response between the one electrode node and the other electrode node.

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