Patent Publication Number: US-2023138443-A1

Title: Stimulation Circuitry in an Implantable Stimulator Device for Providing a Tissue Voltage as Useful During Neural Response Sensing

Description:
CROSS REFERENCE TO RELATED APPLICATIONS 
     This is a non-provisional application of U.S. Provisional Patent Application Ser. No. 63/263,318, filed Oct. 29, 2021, to which priority is claimed, and which is incorporated herein by reference in its entirety. 
    
    
     FIELD OF THE INVENTION 
     This application relates to Implantable Medical Devices (IMDs), and more specifically to circuitry to assist with sensing neural responses to stimulation in an implantable stimulator device. 
     INTRODUCTION 
     Implantable neurostimulator devices are devices that generate and deliver electrical stimuli to body nerves and tissues for the therapy of various biological disorders, such as pacemakers to treat cardiac arrhythmia, defibrillators to treat cardiac fibrillation, cochlear stimulators to treat deafness, retinal stimulators to treat blindness, muscle stimulators to produce coordinated limb movement, spinal cord stimulators to treat chronic pain, cortical and deep brain stimulators to treat motor and psychological disorders, and other neural stimulators to treat urinary incontinence, sleep apnea, shoulder subluxation, etc. The description that follows will generally focus on the use of the invention within a Spinal Cord Stimulation (SCS) or Deep Brain Stimulation (DBS) system. However, the present invention may find applicability with any stimulator device system. 
     A stimulator system typically includes an Implantable Pulse Generator (IPG)  10  shown in  FIG.  1   . The IPG  10  includes a biocompatible device case  12  that holds the circuitry and a battery  14  for providing power for the IPG to function. The IPG  10  is coupled to tissue-stimulating electrodes  16  via one or more electrode leads that form an electrode array  17 . For example, one or more percutaneous leads  15  can be used having ring-shaped or split-ring electrodes  16  carried on a flexible body  18 . In another example, a paddle lead  19  provides electrodes  16  positioned on one of its generally flat surfaces. Lead wires  20  within the leads are coupled to the electrodes  16  and to proximal contacts  21  insertable into lead connectors  22  fixed in a header  23  on the IPG  10 , which header can comprise an epoxy for example. Once inserted, the proximal contacts  21  connect to header contacts  24  within the lead connectors  22 , which are in turn coupled by feedthrough pins  25  through a case feedthrough  26  to stimulation circuitry  28  within the case  12 . 
     In the illustrated IPG  10 , there are thirty-two electrodes (E 1 -E 32 ), split between four percutaneous leads  15 , or contained on a single paddle lead  19 , and thus the header  23  may include a  2 x 2  array of eight-electrode lead connectors  22 . However, the type and number of leads, and the number of electrodes, in an IPG is application specific and therefore can vary. The conductive case  12 , or some conductive portion of the case, can also comprise an electrode (Ec). In an SCS application, the electrode lead(s) are typically implanted in the spinal column proximate to the dura in a patient&#39;s spinal cord, preferably spanning left and right of the patient&#39;s spinal column. The proximal contacts  21  are tunneled through the patient&#39;s tissue to a distant location such as the buttocks where the IPG case  12  is implanted, at which point they are coupled to the lead connectors  22 . In a DBS application, the electrode leads are implanted in the brain through holes in the skull, and lead extension are used to connect the leads to the IPG which is typically implanted under the clavicle (collarbone). In other IPG examples designed for implantation directly at a site requiring stimulation, the IPG can be lead-less, having electrodes  16  instead appearing on the body of the IPG  10  for contacting the patient&#39;s tissue. The IPG lead(s) can be integrated with and permanently connected to the IPG  10  in other solutions. SCS therapy can relieve symptoms such as chronic back pain, while DBS therapy can alleviate Parkinsonian symptoms such as tremor and rigidity. 
     IPG  10  can include an antenna  27   a  allowing it to communicate bi-directionally with a number of external devices discussed subsequently. Antenna  27   a  as shown comprises a conductive coil within the case  12 , although the coil antenna  27   a  can also appear in the header  23 . When antenna  27   a  is configured as a coil, communication with external devices preferably occurs using near-field magnetic induction. IPG  10  may also include a Radio-Frequency (RF) antenna  27   b . In  FIG.  1   , RF antenna  27   b  is shown within the header  23 , but it may also be within the case  12 . RF antenna  27   b  may comprise a patch, slot, or wire, and may operate as a monopole or dipole. RF antenna  27   b  preferably communicates using far-field electromagnetic waves, and may operate in accordance with any number of known RF communication standards, such as Bluetooth, Zigbee, WiFi, MICS, and the like. 
     Stimulation in IPG  10  is typically provided by pulses each of which may include a number of phases ( 30   i ), as shown in the example of  FIG.  2 A . Stimulation parameters typically include amplitude (current I, although a voltage amplitude V can also be used); frequency (F); pulse width (PW); the electrodes  16  selected to provide the stimulation; and the polarity of such selected electrodes, i.e., whether they act as anodes that source current to the tissue or cathodes that sink current from the tissue. These and possibly other stimulation parameters taken together comprise a stimulation program that the stimulation circuitry  28  in the IPG  10  can execute to provide therapeutic stimulation to a patient. 
     In the example of  FIG.  2 A , electrode E 1  has been selected as an anode (during its first phase  30   a ), and thus provides pulses which source a positive current of amplitude +I to the tissue. Electrode E 2  has been selected as a cathode (again during first phase  30   a ), and thus provides pulses which sink a corresponding negative current of amplitude -I from the tissue. This is an example of bipolar stimulation, in which the lead includes one anode pole and one cathode pole. Note that more than one electrode on the lead may be selected to act as an anode electrode to form an anode pole at a given time, and more than one electrode may be selected to act as a cathode to form a cathode pole at a given time, as explained further in U.S. Pat. No. 10,881,859. Stimulation provided by the IPG  10  can also be monopolar, although this example is not yet shown. In monopolar stimulation, the lead is programmed with a single pole of a given polarity (e.g., a cathode pole), with the conductive case electrode Ec acting as a return (e.g., an anode pole). Again, more than one electrode on the lead may be active to form the pole during monopolar stimulation. 
     IPG  10  as mentioned includes stimulation circuitry  28  to form prescribed stimulation at a patient&#39;s tissue.  FIG.  3    shows an example of stimulation circuitry  28 , which includes one or more current source circuits and one or more current sink circuits. The sources and sinks can comprise Digital-to-Analog converters (DACs), and may be referred to as PDACs and NDACs in accordance with the Positive (sourced, anodic) and Negative (sunk, cathodic) currents they respectively issue. In the example shown, a NDACi/PDACi pair is dedicated (hardwired) to a particular electrode node ei  39 . Each electrode node ei  39  is connected to an electrode Ei  16  via a DC-blocking capacitor Ci  38 , for the reasons explained below. The stimulation circuitry  28  in this example also supports selection of the conductive case  12  as an electrode (Ec  12 ), which case electrode is typically selected for monopolar stimulation as explained above. PDACs and NDACs can also comprise voltage sources. 
     Proper control of the PDACs and NDACs allows any of the electrodes  16  to act as anodes or cathodes to create a current through a patient&#39;s tissue, R, hopefully with good therapeutic effect. Consistent with the example provided in  FIG.  2 A ,  FIG.  3    shows operation during the first phase  30   a  in which electrode E 1  has been selected as an anode electrode to source current Ito the tissue R and E 2  has been selected as a cathode electrode to sink current from the tissue. Thus PDAC1 and NDAC 2  are digitally programmed to produce the desired current, I, with the correct timing (e.g., in accordance with the prescribed frequency and pulse widths). As mentioned above, more than one anode electrode and more than one cathode electrode may be selected at one time, and thus current can flow through the tissue R between two or more of the electrodes  16 . 
     Other stimulation circuitries  28  can also be used in the IPG  10 . In an example not shown, a switching matrix can intervene between the one or more PDACs and the electrode nodes ei  39 , and between the one or more NDACs and the electrode nodes. Switching matrices allows any PDAC or NDAC to be connected to any of the electrode nodes. Various examples of stimulation circuitries can be found in U.S. Pat. Nos, 6,181,969, 8,606,362, 8,620,436, 11,040,192, and 10,912,942. Much of the stimulation circuitry  28  of  FIG.  3   , including the PDACs and NDACs, the switch matrices (if present), and the electrode nodes ei  39  can be integrated on one or more Application Specific Integrated Circuits (ASICs), as described in U.S. Patent Application Publications 2012/0095529, 2012/0092031, and 2012/0095519. As explained in these references, ASIC(s) may also contain other circuitry useful in the IPG  10 , such as IPG master control circuitry  102  (see  FIG.  5   ), telemetry circuitry (for interfacing off chip with telemetry antennas  27   a  and/or  27   b ), circuitry for generating the compliance voltage VH (as explained next), various measurement circuits, etc. 
     Power for the stimulation circuitry  28  is provided by a compliance voltage VH, as described in further detail in U.S. Patent Application Publications 2013/0289665 and 2018/0071520. The compliance voltage VH may be coupled to the source circuitry (e.g., the PDAC(s)), while ground may be coupled to the sink circuitry (e.g., the NDAC(s)), such that the stimulation circuitry  28  is powered by VH and ground. Other power supply voltages may be used with the PDACs and NDACs, and explained in U.S. Patent Application Publication 2018/0071520, but these aren&#39;t shown in  FIG.  3    for simplicity. 
     Preferably, and as described in U.S. Pat. No. 11,040,202, the compliance voltage VH can be produced by a VH regulator  49 . VH regulator  49  receives the voltage of the battery  14  (Vbat) and boosts this voltage to a higher value required for the compliance voltage VH. VH regulator  49  can comprise an inductor-based boost converter or a capacitor-based charge pump for example. The regulator  49  can vary the value of VH based on measurements taken from the stimulation circuitry  28 . As explained in detail in the &#39;202 patent, VH measurement circuitry  51  can be used to measure the voltage drops across the active DACs (e.g., PDAC1 (Vp 1 ) and NDAC2 (Vn 2 ) in the example shown in  FIG.  3   ) in the stimulation circuitry  28 . Using such measurements allows VH to be established at an energy-efficient level: high enough to form the prescribed current without loading (i.e., without producing less current that prescribed), yet low enough to not needlessly waste power in the stimulation circuitry  28  when forming the prescribed current. 
     The VH measurement circuitry  51  can output an enable signal VH(en 1 ) indicating when VH regulator  49  should increase the level of VH, i.e., when the voltage drops across the active DACs are too low. This enable signal VH(en 1 ) may be processed at logic  53  in conjunction with other signals explained below to determine a master enable signal VH(en) for the VH regulator  49 . Logic  53  may be associated with the IPG&#39;s control circuitry  102 . Master enable signal VH(en) when asserted causes the VH regulator  49  to increase VH (e.g., when the current starts to load). Deasserting VH(en) disables the VH regulator, which allows VH to naturally decrease over time until it needs to be increased again. This feedback generally causes VH to be established at an energy-efficient value appropriate for the current that is being provided by the stimulation circuitry  28 . 
     Also shown in  FIG.  3    are DC-blocking capacitors Ci  38  placed in series in the electrode current paths between each of the electrode nodes ei  39  and the electrodes Ei  16  (including the case electrode Ec  12 ). The DC-blocking capacitors  38  act as a safety measure to prevent DC current injection into the patient, as could occur for example if there is a circuit fault in the stimulation circuitry  28 . The DC-blocking capacitors  38  are typically provided off-chip (off of the ASIC(s)), and instead may be provided in or on a circuit board in the IPG  10  used to integrate its various components, as explained in U.S. Patent Application Publication 2015/0157861. 
     Referring again to  FIG.  2 A , the stimulation pulses as shown are biphasic, with each pulse comprising a first phase  30   a  followed thereafter by a second phase  30   b  of opposite polarity. Biphasic pulses are useful to actively recover any charge that might be stored on capacitive elements in the electrode current paths, such as on the DC-blocking capacitors  38 . Charge recovery is shown with reference to both  FIGS.  2 A and  2 B . During the first pulse phase  30 a, charge will (primarily) build up across the DC-blockings capacitors C 1  and C 2  associated with the electrodes E 1  and E 2  used to produce the current, giving rise to voltages Vc 1  and Vc 2  (I=C*dV/dt). During the second pulse phase  30   b , when the polarity of the current I is reversed at the selected electrodes E 1  and E 2 , the stored charge on capacitors C 1  and C 2  is recovered, and thus voltages Vc 1  and Vc 2  hopefully return to 0V at the end the second pulse phase  30   b . To recover all charge by the end of the second pulse phase  30   b  of each pulse (Vc 1 =Vc 2 =0V), the first and second phases  30   a  and  30   b  are charged balanced at each electrode, with the phases comprising an equal amount of charge but of the opposite polarity. In the example shown, such charge balancing is achieved by using the same pulse width (PWa =PWb) and the same amplitude (|+I|=|−I|) for each of the pulse phases  30   a  and  30   b . However, the pulse phases  30   a  and  30   b  may also be charged balance if the product of the amplitude and pulse widths of the two phases  30   a  and  30   b  are equal, as is known. 
     Charge recovery using phases  30   a  and  30   b  is said to be “active” because the P/NDACs in stimulation circuitry  28  actively drive a current, in particular during the last phase  30   b  to recover charge stored after the first phase  30   a . However, such active charge recovery may not be perfect, and some residual charge may be present in capacitive structures even after phase  30   b  is completed. Accordingly, the stimulation circuitry  28  can also provide for passive charge recovery. Passive charge recovery is implemented using passive charge recovery switches PRi  41  as shown in  FIG.  3   . These switches  41  when selected via assertion of control signals &lt;Xi&gt; couple each electrode node ei to a passive recovery voltage Vpr established on bus  43 . As explained in U.S. Pat. Nos. 10,716,937 and 10,792,491, this allows any stored charge to be passively recovered through the patient&#39;s tissue, R, without actively driving currents using the P/NDACs. Control signals &lt;Xi&gt; are usually asserted to cause passive charge recovery after each pulse (e.g., after each last phase  30 b) during periods  30   c  shown in  FIG.  2 A . Because passive charge recovery involves capacitive discharge through the resistance R of the patient&#39;s tissue, such discharge manifests as an exponential decay in current, as shown in  FIG.  2 A . 
     As also discussed in the −937 patent, each of the passive charge recovery switches  41  can be associated with a variable resistance, and as such each switch  41  can be controlled by a bus of signals &lt;Xi&gt; to control the resistance at which passive charge recovery occurs—i.e., the on resistance of the switches  41  when they are closed. Note that the common voltage Vpr used during passive charge recovery can comprise ground, VH, VH/2, the voltage of the battery  14  (Vbat), or any other DC voltage provided by the IPG  10 , and any number of generator circuits (not shown) can be used to produce these voltages for Vpr. Passive charge recovery during period  30   c  may be followed by a quiet period  30   d  during which no active current is driven by the DAC circuitry, and none of the passive recovery switches  41  are closed. This quiet period  30   d  may last until the next pulse is actively produced (e.g., phase  30   a ). Like the particulars of pulse phases  30   a  and  30   b , the occurrence of passive charge recovery ( 30   c ) and any quiet periods ( 30   d ) can be prescribed as part of the stimulation program. 
     Although not illustrated, the pulses provided by the IPG  10  may also be single-phase (i.e., monophasic) pulses having a single polarity, and thus may lack a second (opposite polarity) pulse phase that provides active charge recovery. Performing passive charge recovery can be more important when monophasic pulses are used, and indeed may be required, as discussed further later. 
       FIG.  4    shows various external systems  60 ,  70 , and  80  that can wirelessly communicate data with the IPG  10  (which again can include an ETS). Such systems can be used to wirelessly transmit a stimulation program to the IPG  10 —that is, to program its stimulation circuitry  28  to produce stimulation with desired amplitudes and timings as described earlier. Such systems may also be used to adjust one or more stimulation parameters of a stimulation program that the IPG  10  is currently executing, and/or to wirelessly receive information from the IPG  10 , such as various status information, etc. 
     External controller  60  can be as described in U.S. Patent Application Publication 2015/0080982 for example, and may comprise a portable, hand-held controller dedicated to work with the IPG  10 . External controller  60  may also comprise a general-purpose mobile electronics device such as a mobile phone which 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. External controller  60  includes a display  61  and a means for entering commands, such as buttons  62  or selectable graphical icons provided on the display  61 . The external controller  60 &#39;s user interface enables a patient to adjust stimulation parameters, although it may have limited functionality when compared to systems  70  and  80 , described shortly. The external controller  60  can have one or more antennas capable of communicating with the IPG  10 . For example, the external controller  60  can have a near-field magnetic-induction coil antenna  64   a  capable of wirelessly communicating with the coil antenna  27   a  in the IPG  10 . The external controller  60  can also have a far-field RF antenna  64   b  capable of wirelessly communicating with the RF antenna  27   b  in the IPG  10 . 
     Clinician programmer  70  is described further in U.S. Patent Application Publication 2015/0360038, and can comprise a computing device such as a desktop, laptop, or notebook computer, a tablet, a mobile smart phone, a Personal Data Assistant (PDA)-type mobile computing device, etc. In  FIG.  4   , the computing device is shown as a laptop computer that includes typical computer user interface means such as a display  71 , buttons  72 , as well as other user-interface devices such as a mouse, a keyboard, speakers, a stylus, a printer, etc., not all of which are shown for convenience. Also shown in  FIG.  4    are accessory devices for the clinician programmer  70  that are usually specific to its operation as a stimulation controller, such as a communication “wand”  76  coupleable to suitable ports on the computing device. The antenna used in the clinician programmer  70  to communicate with the IPG  10  can depend on the type of antennas included in the IPG  10 . If the patient&#39;s IPG  10  includes a coil antenna  27   a , wand  76  can likewise include a coil antenna  74   a  to establish near-field magnetic-induction communications at small distances. In this instance, the wand  76  may be affixed in close proximity to the patient, such as by placing the wand  76  in a belt or holster wearable by the patient and proximate to the patient&#39;s IPG  10 . If the IPG  10  includes an RF antenna  27   b , the wand  76 , the computing device, or both, can likewise include an RF antenna  74   b  to establish communication with the IPG  10  at larger distances. The clinician programmer  70  can also communicate with other devices and networks, such as the Internet, either wirelessly or via a wired link provided at an Ethernet or network port. 
     External system  80  comprises another means of communicating with and controlling the IPG  10  via a network  85  which can include the Internet. The network  85  can include a server  86  programmed with communication and control functionality, and may include other communication networks or links such as WiFi, cellular or land-line phone links, etc. The network  85  ultimately connects to an intermediary device  82  having antennas suitable for communication with the IPG&#39;s antenna, such as a near-field magnetic-induction coil antenna  84   a  and/or a far-field RF antenna  84   b . Intermediary device  82  may be located generally proximate to the IPG  10 . Network  85  can be accessed by any user terminal  87 , which typically comprises a computer device associated with a display  88 . External system  80  allows a remote user at terminal  87  to communicate with and control the IPG  10  via the intermediary device  82 . 
       FIG.  4    also shows circuitry  90  involved in any of external systems  60 ,  70 , or  80 . Such circuitry can include control circuitry  92 , which can comprise any number of devices such as one or more microprocessors, microcomputers, FPGAs, DSPs, other digital logic structures, etc., which are capable of executing programs in a computing device. Such control circuitry  92  may contain or coupled with memory  94  which can store external system software  96  for controlling and communicating with the IPG  10 , and for rendering a Graphical User Interface (GUI)  99  on a display ( 61 ,  71 ,  88 ) associated with the external system. In external system  80 , the external system software  96  would likely reside in the server  86 , while the control circuitry  92  could be present in either or both the server  86  or the terminal  87 . 
     SUMMARY 
     A stimulator device is disclosed that is configured to provide stimulation with a first phase and a second phase. The stimulator device may comprise: a plurality of electrode nodes, wherein each of the electrode nodes is coupleable to a different electrode configured to contact a patient&#39;s tissue; driver circuitry configurable to drive at least two of the electrode nodes during the first phase to provide a current through the tissue; a first bus configured to receive a bias voltage from biasing circuitry; a plurality of first switches, wherein each of the first switches is connected between a different one of the electrode nodes and the first bus; a second bus; a plurality of second switches, wherein each of the second switches is connected between a different one of the electrode nodes and the second bus; and control circuitry configured to close at least one of the first switches to provide a common mode voltage to the tissue, and close the second switches connected to the at least two electrode nodes during the second phase. 
     In one example, the second phase comprises a passive recovery phase to recover charge stored in current paths of the at least two electrodes. In one example, the device further comprises a plurality of DC-blocking capacitors, wherein each of the DC-blocking capacitors is connected in series between one of the electrode nodes and a different one of the electrodes. In one example, the device further comprises a resistor in parallel across only one of the DC-blocking capacitors. In one example, the control circuitry is configured to close only one of the first switches, wherein the only one first switch is connected to the DC-blocking capacitor having the resistor in parallel. 
     In one example, one of the electrodes comprises a case electrode, wherein the case electrode is connected to the DC-blocking capacitor having the resistor in parallel. In one example, the control circuitry is further configured to open the second switches during the first phase. In one example, the control circuitry is further configured to close the at least one of the first switches during the second phase to provide the common mode voltage to the tissue. In one example, the control circuitry is further configured to close the at least one of the first switches during the first phase to provide the common mode voltage to the tissue. In one example, the stimulation further comprises a third phase, wherein the control circuitry is further configured to close the at least one of the first switches during the third phase to provide the common mode voltage to the tissue. In one example, the third phase comprises a quite phase when the driver circuitry is not active. In one example, the control circuitry is further configured to open the second switches during the third phase. In one example, the control circuitry is configured during the third phase to close second switches connected to the electrode nodes connected to the at least one of the first switches, and to close at least one second switch connected to at least one of the two electrode nodes. In one example, the second bus is not biased by circuitry during the second phase. In one example, the stimulation comprises a plurality of phases during the first phase. In one example, the stimulation is biphasic during the first phase comprising two phases of opposite polarities. In one example, the stimulation is monophasic during the first phase. In one example, the device further comprises a case implantable in the tissue and comprising a conductive portion, wherein one of the electrodes comprises the conductive portion operating as a case electrode. In one example, the device further comprises at least one lead, wherein at least some of the electrodes are on the at least one lead operating as lead-based electrodes. In one example, the stimulation is monopolar during the first phase to provide the current between the case electrode and at least one of the lead-based electrodes. In one example, the common mode voltage is provided to the tissue at one or more of the lead-based electrodes. In one example, the stimulation is bipolar during the first phase to provide the current between at least two of the lead-based electrodes. In one example, the common mode voltage is provided to the tissue at the case electrode. In one example, the driver circuitry is powered by a compliance voltage. In one example, the bias voltage comprises approximately one half of the compliance voltage. In one example, the driver circuitry provides a constant current through the tissue. In one example, the driver circuitry comprises source circuitry to source the constant current to the tissue and sink circuitry to sink the constant current from the tissue. In one example, the driver circuitry comprises a plurality of source and sink pairs, wherein each of the source and sink pairs is connected to one of the electrode nodes. In one example, the device further comprises neural response detection circuitry coupled to the electrode nodes, wherein the neural response detection circuitry is configured to measure a neural response to the current at one or more of the electrode nodes. In one example, the one or more of the electrode nodes at which the neural response is measured are different from at least two of the electrode nodes driven during the first phase to provide the current through the tissue. 
     A stimulator device is disclosed that is configured to provide stimulation with a first phase and a second phase. The stimulator device may comprise: a plurality of electrode nodes, wherein each of the electrode nodes is coupleable to a different electrode configured to contact a patient&#39;s tissue; driver circuitry configurable to drive at least two of the electrode nodes during the first phase to provide a current through the tissue; a first bus configured to receive a bias voltage from biasing circuitry; a plurality of first switches, wherein each of the first switches is connected between a different one of the electrode nodes and the first bus; a second bus; a plurality of second switches, wherein each of the second switches is connected between a different one of the electrode nodes and the second bus; a third switch connected between the first bus and the second bus. 
     In one example, the device may further comprise control circuitry, wherein the control circuitry is configured during the second phase to close the second switches connected to the at least two electrode nodes to recover charge stored in current paths of the at least two electrode nodes, and issue a control signal to either open or close the third switch. In one example, the device further comprises a plurality of DC-blocking capacitors, wherein each of the DC-blocking capacitors is connected in series between one of the electrode nodes and a different one of the electrodes. In one example, the device further comprising a resistor in parallel across only one of the DC-blocking capacitors. In one example, if the control circuitry issues the control signal to open the third switch, the control circuitry is further configured during the second phase to close at least one of the first switches to provide a common mode voltage to the tissue. In one example, the second bus is not biased by circuitry during the second phase when the third switch is opened. In one example, the stimulation further comprises a third phase, wherein the control circuitry is further configured to close the at least one of the first switches during the first phase, during the third phase, or during both the first phase and the third phase, to provide the common mode voltage to the tissue. In one example, the third phase comprises a quite phase when the driver circuitry is not active. In one example, the control circuitry is configured to open the second switches during the first phase, the third phase, or during both the first phase and the third phase. In one example, the device further comprises a case implantable in the tissue and comprising a conductive portion, wherein one of the electrodes comprises the conductive portion operating as a case electrode. In one example, the device further comprises at least one lead, wherein at least some of the electrodes are on the at least one lead operating as lead-based electrodes. In one example, the stimulation is monopolar during the first phase to provide the current between the case electrode and at least one of the lead-based electrodes. In one example, the common mode voltage is provided to the tissue at one or more of the lead-based electrodes. In one example, the stimulation is bipolar during the first phase to provide the current between at least two of the lead-based electrodes. In one example, the common mode voltage is provided to the tissue at the case electrode. In one example, if the control circuitry issues the control signal to close the third switch, the control circuitry is further configured during the second phase to open all of the first switches to prevent a common mode voltage from forming in the tissue during the second phase. In one example, the stimulation further comprises a third phase, wherein the third phase comprises a quite phase when the driver circuitry is not active. In one example, the control circuitry is further configured to close at least one of the first switches during the first phase, during the third phase, or during both the first phase and the third phase, to provide the common mode voltage to the tissue. In one example, the control circuitry is further configured to open all of the first switches during the first phase, the third phase, or during both the first phase and the third phase. In one example, the control circuitry is configured to open the second switches during the first phase, during the third phase, or during both the first phase and the third phase. In one example, the stimulation comprises a plurality of phases during the first phase. In one example, the stimulation is biphasic during the first phase comprising two phases of opposite polarities. In one example, the stimulation is monophasic during the first phase. In one example, the driver circuitry is powered by a compliance voltage. In one example, the bias voltage comprises approximately one half of the compliance voltage. In one example, the driver circuitry provides a constant current through the tissue. In one example, the driver circuitry comprises source circuitry to source the constant current to the tissue and sink circuitry to sink the constant current from the tissue. In one example, the driver circuitry comprises a plurality of source and sink pairs, wherein each of the source and sink pairs is connected to one of the electrode nodes. In one example, the device further comprises neural response detection circuitry coupled to the electrode nodes, wherein the neural response detection circuitry is configured to measure a neural response to the current at one or more of the electrode nodes. In one example, the one or more of the electrode nodes at which the neural response is measured are different from at least two of the electrode nodes driven during the first phase to provide the current through the tissue. 
     A stimulator device is disclosed that is configured to provide stimulation with a first phase and a second phase. The stimulator device may comprise: a plurality of electrode nodes, wherein each of the electrode nodes is coupleable to a different electrode configured to contact a patient&#39;s tissue; driver circuitry configurable to drive at least two of the electrode nodes during the first phase to provide a current through the tissue; a bus configured to receive a bias voltage from biasing circuitry; a plurality of switches, wherein each of the switches is connected between a different one of the electrode nodes and the bus; and control circuitry configured to close at least one first of the switches during the first phase to provide a common mode voltage to the tissue, and open the at least one first switch during the second phase, and close second of the switches connected to the at least two electrode nodes during the second phase. 
     In one example, the second phase comprises a passive recovery phase to recover charge stored in current paths of the at least two electrodes. In one example, the device further comprises a plurality of DC-blocking capacitors, wherein each of the DC-blocking capacitors is connected in series between one of the electrode nodes and a different one of the electrodes. In one example, the device further comprises a resistor in parallel across only one of the DC-blocking capacitors. In one example, the control circuitry is configured to close only one first switch, wherein the only one first switch is connected to the DC-blocking capacitor having the resistor in parallel. In one example, one of the electrodes comprises a case electrode, wherein the case electrode is connected to the DC-blocking capacitor having the resistor in parallel. In one example, the control circuitry is further configured to open the second switches during the first phase. In one example, the stimulation further comprises a third phase, wherein during the third phase the control circuitry is configured to close the at least one first switch to provide the common mode voltage to the tissue. In one example, the third phase comprises a quite phase when the driver circuitry is not active. In one example, during the third phase the control circuitry is configured to open the second switches. In one example, the stimulation comprises a plurality of phases during the first phase. In one example, the stimulation is biphasic during the first phase comprising two phases of opposite polarities. In one example, the stimulation is monophasic during the first phase. In one example, the device further comprises a case implantable in the tissue and comprising a conductive portion, wherein one of the electrodes comprises the conductive portion operating as a case electrode. In one example, the device further comprises at least one lead, wherein at least some of the electrodes are on the at least one lead operating as lead-based electrodes. In one example, the stimulation is monopolar during the first phase to provide the current between the case electrode and at least one of the lead-based electrodes. In one example, the common mode voltage is provided to the tissue at one or more of the lead-based electrodes. In one example, the stimulation is bipolar during the first phase to provide the current between at least two of the lead-based electrodes. In one example, the common mode voltage is provided to the tissue at the case electrode. In one example, the driver circuitry is powered by a compliance voltage. In one example, the bias voltage comprises approximately one half of the compliance voltage. In one example, the driver circuitry provides a constant current through the tissue. In one example, the driver circuitry comprises source circuitry to source the constant current to the tissue and sink circuitry to sink the constant current from the tissue. In one example, the driver circuitry comprises a plurality of source and sink pairs, wherein each of the source and sink pairs is connected to one of the electrode nodes. In one example, the device further comprises neural response detection circuitry coupled to the electrode nodes, wherein the neural response detection circuitry is configured to measure a neural response to the current at one or more of the electrode nodes. In one example, the one or more of the electrode nodes at which the neural response is measured are different from at least two of the electrode nodes driven during the first phase to provide the current through the tissue. 
    
    
     
       BRIEF DESCRIPTION OF THE DRAWINGS 
         FIG.  1    shows an Implantable Pulse Generator (IPG), in accordance with the prior art. 
         FIGS.  2 A and  2 B  show an example of stimulation pulses producible by the IPG, in accordance with the prior art. 
         FIG.  3    shows stimulation circuitry useable in the IPG, in accordance with the prior art. 
         FIG.  4    shows various external devices capable of communicating with and programming stimulation in an IPG, in accordance with the prior art. 
         FIG.  5    shows an improved IPG having neural response sensing capability. 
         FIG.  6    shows stimulation producing a neural response, and the sensing of that neural response at least one electrode of the IPG. 
         FIG.  7    shows biasing circuitry useable to set a common mode voltage Vcm to the patient&#39;s tissue, preferably using the IPG&#39;s case electrode. 
         FIG.  8    shows a first example of stimulation circuitry using switches and a single bus driven by the biasing circuitry to both provide a voltage to set Vcm in the tissue and to provide passive charge recovery. 
         FIGS.  9 A- 9 D  show operation of the stimulation circuitry of  FIG.  8    when providing bipolar stimulation, and describes configuration of the circuitry during various pulses phases. 
         FIG.  10    shows operation of the stimulation circuitry of  FIG.  8    when providing monopolar stimulation. 
         FIG.  11    shows a second example of stimulation circuitry using switches and two buses: one driven by the biasing circuitry to provide a voltage to set Vcm in the tissue, and one used for passive charge recovery. 
         FIG.  12    shows operation of the stimulation circuitry of  FIG.  11    when passive charge recovery is performed and Vcm is not being set in the tissue. 
         FIGS.  13 A- 13 D  show operation of the stimulation circuitry of  FIG.  11    when providing bipolar stimulation, and describes configuration of the circuitry during various pulses phases. 
         FIGS.  14 A- 14 E  show operation of the stimulation circuitry of  FIG.  11    when providing monopolar stimulation, and describes configuration of the circuitry during various pulses phases. 
         FIGS.  15 A and  15 B  show considerations when operating the stimulation circuitry of  FIG.  11    to provide monophasic stimulation, and in particular when providing such monophasic stimulation in a monopolar fashion. 
         FIG.  16    shows generation of the control signals that control the disclosed stimulation circuitry. 
         FIG.  17    shows how the disclosed stimulation circuitry can be used to designate any electrode, including the case electrode, as an active electrode to provide stimulation; as an electrode to provide Vcm to the tissue; or as a sensing electrode to sense neural responses to the stimulation. 
     
    
    
     DETAILED DESCRIPTION 
     An increasingly interesting development in pulse generator systems is the addition of sensing capability to complement the stimulation that such systems provide. For example, and as explained in U.S. Patent Application Publication 2017/0296823, it can be beneficial to sense a neural response produced by neural tissue that has received stimulation from an IPG. U.S. Patent Application Publication 2017/0296823 shows an example where sensing of neural responses is useful in an SCS context, and in particular discusses the sensing of Evoked Compound Action Potentials, or “ECAPs.” U.S. Patent Application Publication 2022/0040486 shows an example where sensing of neural responses is useful in a DBS context, and in particular discusses the sensing of Evoked Resonant Neural Activity, or “ERNA.” 
       FIG.  5    shows circuitry for sensing neural responses in an IPG  10 . The IPG  10  includes control circuitry  102 , which may comprise a microcontroller for example, such as Part Number MSP 430 , manufactured by Texas Instruments, which is described in data sheets accessible on the Internet. Other types of control circuitry may be used in lieu of a microcontroller as well, such as microprocessors, FPGAs, DSPs, or combinations of these, etc. Control circuitry  102  may also be formed in whole or in part in one or more Application Specific Integrated Circuits (ASICs) in the IPG  10  as described earlier, which ASIC(s) may additionally include the other circuitry shown in  FIG.  5   . 
       FIG.  5    includes the stimulation circuitry  28  described earlier ( FIG.  3   ), including one or more DACs (PDACs and NDACs). A bus  118  provides digital control signals to the DACs to produce currents or voltages of prescribed amplitudes and with the correct timing at the electrodes selected for stimulation. The electrode current paths to the electrodes  16  include the DC-blocking capacitors  38  described earlier. 
       FIG.  5    also shows circuitry used to detect neural responses. As shown, the electrode nodes  39  are input to a multiplexer (MUX)  108 . The MUX  108  is control by a bus  114 , which operates to select one or more electrode nodes, and hence to designate corresponding electrodes  16  as sensing electrodes. The sensing electrode(s) selected via bus  114  can be determined automatically by control circuitry  102  and/or a neural response algorithm  124 , as described further below. However, the sensing electrode(s) may also be selected by the user (e.g., a clinician) via an external system ( FIG.  4   ). 
     Electrodes selected as sensing electrodes are provided by the MUX  108  to neural response detection circuitry. This circuitry can comprise a sense amplifier  110 , and sensing can occur differentially using two sensing electrodes, or using a single sensing electrode. This is shown in the example of  FIG.  6   . If single-ended sensing is used, a single electrode (e.g., E 5 ) is selected as a sensing electrode (S) and is provided to the positive terminal of the sense amp  110 , where it is compared to a reference voltage Vref provided to the negative input. The reference voltage Vref can comprise any DC voltage produced within the IPG, such as ground. If differential sensing is used, two electrodes (e.g., E 5  and E 6 ) are selected as sensing electrodes (S+ and S−) by the MUX  108 , with one electrode (e.g., E 5 ) provided to the positive terminal of the sense amp  110 , and the other (e.g., E 6 ) provided to the negative terminal. Differential sensing can be useful to cancel any common mode voltages present in the tissue and reflected at the electrodes, such as voltages created by the stimulation itself. See, e.g., U.S. Patent Application Publication 2021/0236829. Although only one sense amp  110  is shown in  FIG.  5    for simplicity, there could be more than one, such as a sense amp dedicated to each electrode node. In this case, MUX  108  would not be necessary, and each sense amp could be activated as needed depending on which electrodes are selected as sensing electrodes. The timing at which sensing occurs can be affected by a sensing enable signal S(en), as discussed further below. 
     The analog waveform comprising the sensed neural response and output by the sense amp  110  is preferably converted to digital signals by an Analog-to-Digital converter (ADC)  112 , and input to the IPG&#39;s control circuitry  102 . The ADC  112  can be included within the control circuitry  102 &#39;s input stage as well. The control circuitry  102  can be programmed with a neural response algorithm  124  to evaluate the neural response, and to take appropriate actions as a result. For example, the neural response algorithm  124  may change the stimulation in accordance with the sensed neural response, and can issue new control signals via bus  118  to change operation of the stimulation circuitry  28  to affect better treatment for the patient. The neural response algorithm  124  may also cause the selection of new sensing electrode(s), which can be affected by issuing new control signals on bus  114 . Selecting optimal sensing electrode(s) can be important, and may be determined in light of stimulation that is being provided. In this regard, sensing electrodes may be selected near enough to the electrodes providing stimulation (e.g., E 1  and E 2 ) to allow for proper neural response sensing, but far enough from the stimulation that the stimulation doesn&#39;t substantially interfere with neural response sensing. See, e.g., U.S. Patent Application Publication 2020/0155019. 
     Neural responses to stimulation are typically small-amplitude signals on the order of microVolts or milliVolts, which can make sensing difficult. The sense amp  110  needs to be capable of resolving this small signal, and this is particularly difficult when one realizes that this small signal typically rides on a background voltage otherwise present in the tissue. As explained in U.S. Pat. No. 11,040,202, which is incorporated by reference in its entirety, this background voltage can vary on the order of Volts, and can be caused by the stimulation itself. It is difficult to design sense amplifier circuitry  110  to reliably perform the task of accurately sensing a small-signal neural response while rejecting the background tissue voltage. Because stimulation causes the background tissue voltage to vary, it is preferred that neural responses are sensed after active stimulation is provided. Thus, sensing enable signal S(en) is preferably asserted during these times. That being said, stimulation artifacts resulting from the stimulation may still be present and cause variations in the tissue voltage even after stimulation has ceased. See, e.g., PCT (Int&#39;l) Patent Application Publication WO 2020/251899. 
     The above-incorporated &#39;202 patent addresses this issue of background tissue voltage variability by adding additional circuitry to the IPG  10  to hold the tissue to a pseudo-constant common mode voltage (Vcm).  FIG.  7    shows details of the circuitry from the &#39;202 patent with some elaboration, and because familiarity with this circuitry is assumed and is explained in detail in the &#39;202 patent, the circuitry in  FIG.  7    is only briefly discussed. 
       FIG.  7    includes tissue biasing circuitry  150 , which is used to hold the tissue R to a common mode Vcm using the case electrode Ec. The case electrode Ec is particularly useful for providing the common mode voltage Vcm: a patient&#39;s tissue is of relatively low resistance, and conductive portions of the IPG&#39;s case  12  are relatively large in area and thus also low in resistance. Therefore, even if the case electrode Ec is implanted at a distance from the lead-based electrodes  16  used for stimulation and sensing, the case electrode Ec still comprises a suitable means for establishing Vcm for the whole of the tissue. 
       FIG.  7    also shows the stimulation circuitry  28  described earlier, although only a portion is shown for simplicity. Specifically,  FIG.  7    shows portions of the stimulation circuitry  28  used to actively drive a current at lead-based electrodes E 1  and E 2  (P/NDAC1, P/NDAC2) and at the case electrode Ec (P/NDACc). Portions used to drive currents at other electrodes (E 3 , E 4 , etc.) are not shown. 
     The tissue biasing circuitry  150  passively biases the case electrode Ec to Vcm using a capacitor Ccm  152  and a voltage source  153  inside the case  12 . In the example shown in  FIG.  7   , the capacitor Ccm  152  serves a dual function: its acts as a common mode capacitance to assist in setting Vcm at the case electrode Ec when tissue biasing circuitry  150  is active, and also acts as a DC blocking capacitor (see  38 ,  FIG.  3   ) when the case electrode Ec is actively driven (during monopolar stimulation) using the stimulation circuitry  28  (using PDACc and/or NDACc). Switches  156  and  154  can facilitate these different uses of the case electrode Ec. When the stimulation circuitry  28  is used to drive the case electrode Ec, switch  156  is closed to couple the relevant DAC circuitry (PDACc and NDACc) to Ccm  152 , while switch  154  is open to disconnect the tissue biasing circuitry  150 . By contrast, when the tissue biasing circuitry  150  is used to passively form Vcm at the case electrode Ec, switch  154  is closed, and switch  156  is opened to disconnect the stimulation circuitry  28 . 
     The voltage source  153  produces a reference voltage Vref, which may be adjustable. Vref preferably has a value between ground (OV) and the compliance voltage (VH), or is equal to these values. Vref may also have a value that varies as a function of the compliance voltage VH, which as noted earlier may vary by operation of VH regulator  49  ( FIG.  3   ). Most preferably, and as assumed from this point forward, Vref may be set to VH/2, and hence may vary as VH varies. A voltage source  153  producing VH/2 as shown in  FIG.  7    may be formed as a VH voltage divider comprising high-resistance resistors Ra and Rb each having the same high value, although other generator circuits could be used to form Vref as well. 
     The common mode voltage Vcm established in the tissue R at the case electrode Ec comprises the sum of Vref (or Vvref as discussed further below) and any voltage formed across capacitor Ccm  152  (Vc). As explained in the &#39;202 patent, Vc can form when a current Icm flow to the case electrode Ec, such as when the stimulation circuitry  28  is imbalanced. Consider the example in  FIG.  7   , where a current I 1  is being sourced to the tissue R through electrode E 1 , and a current I 2  is being sunk from the tissue through electrode E 2 . ( FIG.  2 A , first phase  30   a ). Normally, these currents I 1  and I 2  would be prescribed to have the same value, and thus ideally Icm would be zero. This means capacitor Ccm  152  would not charge (Vc 32 0), and hence the common mode voltage Vcm would be set to Vref=VH/2 at the case electrode Ec. However, these currents I 1  and I 2  may be slightly imbalanced. If |I 1 |&gt;|I 2 |, because PDAC1 is stronger than NDAC2, Icm would be positive, causing Vc to increase over time, which sets Vcm&gt;Vref. If |I 1 |&lt;|I 2 |, because NDAC2 is stronger than PDAC1, Icm would be negative, causing Vc to decrease over time, which sets Vcm&lt;Vref. As such, Vcm is pseudo constant. Adjusting Vcm using Icm is sensible because Vcm is brought closer to voltages formed in the tissue during the issuance of the stimulation pulses, which are also affected by any imbalance of the currents formed by the stimulation circuitry  28 . 
     In any event, once Vcm is established at the case electrode Ec and hence in the tissue R, voltages otherwise formed in the tissue, such as those accompanying the production of stimulation pulses, will be established relative to Vcm. This can ease sensing of small signals in the tissue at the sense amp  110 , such as the neural responses explained above. 
       FIG.  7    also shows an optional bleed resistor Rbleed  155  included in parallel with the capacitor Ccm  152 . The bleed resistor Rbleed  155  is preferably of a high resistance (e.g., 1 MegaOhm or higher), and allows charge to bleed slowly off the capacitor Ccm, for example, during periods when the tissue biasing circuitry  150  is not being used. Furthermore, Rbleed can assist with current balancing. By permitting a small current to flow, Rbleed acts to boost the weaker DAC, which may allow current balancing to happen before the stronger DAC becomes loaded, as explained in the &#39;202 patent. Notice that Rbleed allows a DC current to flow from the IPG  10 &#39;s circuitry to the tissue R, and thus the case electrode Ec does not perfectly block DC current. As discussed above, DC blocking using capacitors at each electrode in contact with the tissue R is preferred for safety. However, because all other potential current paths to the tissue R (E 1 , E 2 , etc.) include DC blocking capacitors (C 1 , C 2 , etc.), the DC current at the case electrode Ec must equal zero. See, e.g., U.S. Pat. No. 10,391,301. Thus, DC currents are still effectively blocked at all electrode current paths, including the case electrode Ec, despite the use of Rbleed. 
     The above-incorporated &#39;202 patent discloses other optional circuitry that can be included in the tissue biasing circuitry  150 . For example, circuitry  150  can include an amplifier  180 . Amplifier  180  is preferably an operational transconductance amplifier (OTA), which produces a virtual reference Vvref on the bottom plate of capacitor Ccm  152 . Details are explained further in the &#39;202 patent, but to summarize here, the OTA  180  limits Icm to between +Iout(max) and −Iout(min) producible at the output of the OTA  180 . This is beneficial, because limiting Icm through the tissue limits “pocket stimulation,” which can be caused when unwanted current flows to the tissue pocket where the case electrode Ec is implanted. Pocket stimulation may be felt by the patient, or may otherwise negatively affect therapy provided by the selected lead-based electrodes, and so is generally undesirable. Note that use of OTA  180  is not strictly required, and instead the voltage source  153 &#39;s output Vref (e.g., VH/2) can be connected (e.g., via switch  154 ) to the bottom plate of capacitor Ccm  152 , as shown in the dotted lines in  FIG.  7    (in which case Vvref simply equals Vref). 
     Still other optional circuitry within tissue biasing circuitry  150  is shown in  FIG.  7   , including monitoring circuitry  200 . Again, this circuitry  200  is discussed in detail in the above-incorporated &#39;202 patent, and is only briefly summarized here. Monitoring circuitry  200  receives the virtual reference Vvref as an input, from which a couple of things can be determined. First, monitoring Vvref allows the control circuitry  102  in the IPG  10  to decide when neural response sensing is best performed in the IPG  10 , i.e., when the sensing enable signal S(en) should be asserted (see  FIG.  5   ). Second, monitoring Vvref is also useful in determining whether the compliance voltage VH should be increased, i.e., when enable signal VH(en 2 ) should be asserted. 
     Both of these determinations depend on how significantly the virtual reference Vvref varies from the reference voltage Vref (e.g., VH/2) output by the voltage source  153 . In this regard, Vvref is input to a window comparator formed from comparators  182   a  and  182   b , which sets a voltage window from Vref+Δ to Vref-Δ (where Δ may equal 100 mV for example). If Vvref is higher than Vref+Δ, signal X is asserted. If Vvref is lower than Vref−Δ, signal Y is asserted. The control circuitry  102  in the IPG  100  can assess X and Y in conjunction with timing control signals tpl or tp 2  that indicate whether stimulation is occurring during the first or second of pulse phases  30   a  and  30   b . As explained in the &#39;202 patent, sensing enable signal S(en) is asserted only when control signals X and Y are not asserted, meaning that Vvref is between Vref+Δ and Vref−Δ. Enable signal VH(en 2 )—indicating a need to increase VH at the VH regulator  49 —is asserted if only X is asserted during one phase pulse phase (e.g.,  30   a ), and if only Y is asserted during the other phase (e.g.,  30   b ). Note that VH(en 2 ) can be input to logic  53  ( FIG.  3   ) to decide whether the master enable signal VH(en) should issue to the VH generator  49  to increase VH. Logic  53  can as explained earlier can also receive other signals relevant to whether VH should be increased, such as VH(en 1 ) from the VH measurement circuitry  51  ( FIG.  3   ). Logic  53  can for example perform a logical OR operation, thus enabling the VH generator  49  to increase VH per VH(en) if either VH(en 1 ) (from VH measurement circuitry  51 ,  FIG.  3   ) or VH(en 2 ) (from monitoring circuitry  200 ) is asserted. Logic  53  as mentioned earlier may be associated with control circuitry  102  in the IPG  10 , although it is shown separately in  FIG.  7    for convenience. 
       FIGS.  8  through  9 D  show an example of stimulation circuitry  250  in which the tissue biasing circuitry  150  as just described can be used to provide both a common mode voltage Vcm to the tissue to assist with sensing, and to provide a passive recovery voltage to the electrode nodes ei  39  during pulse phases  30   c  ( FIG.  2 A ) when passive charge recovery is occurring. Stimulation circuitry  250  includes switches SWi connected between each electrode node  39  and a bus  252 . In this regard, stimulation circuitry  250  is similar to the passive charge recovery circuitry described earlier ( FIG.  3   ), where passive recovery switches PRi  41  are connected between each electrode node  39  and a bus  43  biased to a passive recovery voltage Vpr. However, switches SWi serve a dual purpose and are controlled both for the purpose of providing passive charge recovery, as well establishing a common mode voltage Vcm at the case electrode Ec, as explained further below. Switches SWi like the passive recovery switches PRi described earlier may have a variable resistance, and hence each switch may be control by a bus of control signals &lt;Zi&gt; to set the on resistance when these switches are closed. 
     Bus  252  preferably receives the output voltage from the tissue biasing circuitry  150 . This output voltage, as explained earlier, can comprise Vref or Vvref depending whether OTA  180  ( FIG.  7   ) is used, and in either case this voltage is approximately equal to VH/2 (˜VH/2). (Approximately VH/2 should be understood as VH/2 varying in a range from 45% to 55% of VH). While use of biasing circuitry  150  is preferred to set the voltage on bus  252  for the beneficial reasons discussed with reference to  FIG.  7   , other voltage generator circuitry could be used as well. Biasing circuitry  150  may also simply comprise a DC voltage, such as Vbat provided by the battery  14 . 
       FIGS.  9 A- 9 D  explain operation of stimulation circuitry  250 , and how switches SWi can be controlled to allow bus  252  to both provide a common mode voltage Vcm to the tissue as is particularly useful during neural response sensing, and to provide a passive charge recovery voltage during passive charge recovery. Operation of circuitry  250  is described when providing bipolar stimulation, which in this example happens between lead-based electrodes E 1  and E 2 , although other lead-based electrodes could be chosen to provide stimulation as well. The stimulation is preferably biphasic, comprising phases  30   a  and  30   b  as described earlier, thus providing active charge recovery. However, this is not strictly necessary, and monophasic pulses could be used as well, as explained further later. The case electrode Ec is used in this example to provide the common mode voltage Vcm to the tissue.  FIG.  9 A  summarizes the status of switches SWi during active stimulation (e.g., during phases  30   a  and  30   b ,  FIG.  9 B ), during passive charge recovery ( 30   c ,  FIG.  9 C ), and during quiet periods ( 30   d ,  FIG.  9 D ). 
       FIG.  9 B  shows configuration of the circuitry  250  during active stimulation (during phases  30   a  and  30   b ), and shows the various current paths that are formed. During active stimulation, P/NDAC1 and P/NDAC2 at electrode E 1  and E 2  are active and programmed to provide a current of amplitude I. Because the stimulation in this example is biphasic, these DACs are active at different times (see  FIG.  2 A ), with PDAC1 and NDAC2 active during phase  30   a , and PDAC 2  and NDAC 1  active during phase  30   b . Because the DACs at these electrodes are active during active stimulation, switches SW 1  and SW 2  are opened to isolate the DAC from bus  252 . Thus, &lt;Z 1 &gt; and &lt;Z 2 &gt; are not asserted, and electrode nodes e 1  and e 2  are decoupled from —VH/ 2  provided from biasing circuitry  150  on bus  252 . By contrast, switch SWc associated with the case electrode Ec is closed during active stimulation via assertion of &lt;Zc&gt;. This routes —VH/2 via bus  252  from biasing circuitry  150  to electrode node ec connected to the bottom plate of the capacitor Ccm  152 , which allows Vcm to form at the case electrode Ec to set the tissue voltage as explained previously. (Note that control signals &lt;Xc&gt; are preferably asserted to set the on resistance of SWc is set to its lowest value, although this isn&#39;t strictly required). Because Vcm is passively formed at the case electrode Ec, P/NDACc associated with the case electrode Ec are inactive. 
       FIG.  9 C  shows configuration of the circuitry  250  during passive charge recovery ( 30 c), which as noted earlier is useful to recover any residual charge present in the previously-active current paths, such as might be stored on capacitors C 1  and C 2 . During passive charge recovery, all of the DACs are inactive. Switches SW 1  and SW 2  associated with previously driven electrodes E 1  and E 2  are closed via assertion of &lt;Z 1 &gt; and &lt;Z 2 &gt; to couple electrode nodes e 1  and e 2  to —VH/ 2  on bus  252 . As such, —VH/2 (i.e., Vref or Vvref) acts as the passive recovery voltage (akin to Vpr,  FIG.  3   ) during passive charge recovery to promote the discharge of charge stored on capacitors C 1  and C 2  through the tissue R and bus  252 . (Note that control signals &lt;Z 1 &gt; and &lt;Z 2 &gt; may be asserted such that the on resistance of switches SW 1  and SW 2  are set to a desired value. See U.S. Pat. Nos. 10,716,937). During passive recovery, switch SWc associated with the case electrode Ec can be opened, and hence control signals &lt;Zc&gt; may not be asserted. As such, the case electrode Ec is decoupled from ˜VH/2 on bus  252 , and the tissue R is left floating. Even though the switch SWc is not closed in  FIG.  9 C , note that the capacitor Ccm  152  associated with the case electrode Ec can still discharge if necessary through the bleed resistor Rbleed. 
       FIG.  9 D  shows configuration of the circuitry  250  during quiet periods  30   d  when neither active stimulation nor passive charge recovery is occurring. This configuration is similar to what occurred during active stimulation ( FIG.  9 B ), except that none of the DACs are active. Switches SW 1  and SW 2  are open (&lt;Z 1 &gt; and &lt;Z 2 &gt; are not asserted), and SWc is closed (&lt;Zc&gt; asserted), which routes ˜VH/2 to capacitor Ccm  152  to establish Vcm in the tissue R. Again, this assists with sensing of neural responses during the quiet periods ( 30   d ), and assists in maintaining Vcm in the tissue in preparation for the next active stimulation phase (pulse). 
     It is not strictly necessary to use the tissue biasing circuitry  150  described earlier. Instead, a more-generic voltage generator could simply provide a voltage to bus  252 . However, the use of tissue biasing circuitry  150  is preferred due to its improved functionality as described earlier: for example, the use of the OTA  180  ( FIG.  7   ) limits Icm to limit unwanted pocket stimulation, and monitoring circuitry  200  ( FIG.  7   ) is useful in determining when to sense neural responses (S(en)) and when the compliance voltage VH (VH(en 2 ) may need to be increased. 
     The stimulation circuitry  250  of  FIG.  8    works well as illustrated, and is convenient in that a single bus  252  and a single set of switches SWi are used for passive charge recovery and for setting the tissue voltage Vcm. However, circuitry  250  is not without shortcomings. First, and as discussed above, the common mode voltage Vcm is not established in the tissue at all times during the stimulation cycle, and in particular during passive charge recovery ( FIG.  9 C ). Because the tissue voltage is uncertain and may be varying, neural sensing during passive charge recovery is made somewhat more difficult. 
     Second, stimulation circuitry  250  can have drawbacks when monopolar stimulation is used. As explained earlier, monopolar stimulation involves actively driving a current at the case electrode Ec (using P/NDACc) during active stimulation ( 30   a  and  30   b ). However, the case electrode Ec cannot be used to passively form Vcm in the tissue in this circumstance, because Ec can&#39;t be actively driven (by P/NDACc) and passively set (per  150 ) to Vcm at the same time. This is unfortunate, because certain therapies (e.g., DBS) tend to favor the use of monopolar stimulation, and may benefit from neural response sensing and therefore establishing Vcm in the tissue. 
     The above-incorporated &#39;202 patent suggests that another lead-based electrode (not the case electrode Ec) can be used to provide Vcm to the tissue during monopolar stimulation, and  FIG.  10    shows use of stimulation circuitry  250  in this manner. In this example, it is assumed that monopolar stimulation occurs by actively driving a lead-based electrode E 1  (although one or more other lead-based electrodes could be chosen) and the case electrode Ec (using P/NDAC1 and P/NDACc). Lead based electrode E 2  is selected (via SW 2 , &lt;X 2 &gt;) to provide Vcm to the tissue during active stimulation (although again any one or more lead-based electrodes could also be selected). Notice that the lead-based electrode E 2  used in this example to provide Vcm to the tissue lacks a bleed resistor  155  across its capacitor C 2 . This can be problematic, because charge that builds on this capacitor C 2  (or any other capacitor associated with a lead-based electrode used to provide Vcm) cannot be easily discharged. Compare  FIG.  9 C , where discharge of Ccm used to provide Vcm to the tissue at the case electrode Ec occurs passively affected via Rbleed. This problem could be mitigated by providing a bleed resistor Rbleed in parallel with C 2  (not shown in  FIGS.  8 - 10   ), and for that matter in parallel with Ci provided at all of the lead-based electrodes Ei in case these other electrodes are selected to provide Vcm to the tissue. But such a modification, while operable, is not preferred, as this potentially provides more than one DC path to the tissue through any of the bleed resistors. In short, such a modification would not guarantee that no DC current is injected into the tissue in the event of a fault, which may be unsafe. 
     Stimulation circuitry  300 , as shown in  FIG.  11   , provide another example that addresses these concerns. As explained further below, circuitry  300  allows any one or more of the electrodes (the case electrode Ec and any of lead-based electrodes E 1 , E 2 , etc.) to be selected to provide a common mode voltage Vcm to the tissue. Further, circuitry  300  only includes a single bleed resistor, Rbleed, connected in parallel with the capacitor Ccm  152  connected to the case electrode Ec. Stimulation circuitry  300  thus includes only one DC path to the tissue, which as explained above promotes safety by effectively preventing DC current injection into the tissue through any electrode current path. That being said, Rbleed, while useful, is not strictly necessary in all examples of circuitry  300 . Furthermore, circuitry  300  allows for the passive discharge of the capacitors used at lead-based electrodes to provide Vcm even if these capacitors lack bleed resistors in parallel, which is particular helpful when monopolar stimulation is used. Lastly, circuitry  300  also allows Vcm is be set in the tissue during all phases of stimulation, including during passive recharge. Thus, the tissue is never floating, which assists with neural response sensing. 
     Stimulation circuitry  300  includes two buses  302  and  304 . Bus  304  comprises a common mode bus, and is driven with a voltage as necessary to form Vcm for the tissue R at one or more selected electrodes. Common mode bus  304  is connected to each of the electrode nodes ei by common mode switches CMi. Preferably these common mode switches have a set (low) on resistance, and thus may be controlled by single control signals Yi. The selection of these switches CMi by Yi dictate which of the one or more electrodes (E 1 , E 2 , , Ec) will act to provide Vcm to the tissue, as explained further below. 
     As before, it is preferable that tissue biasing circuitry  150  is used to drive the voltage on common mode bus  304 . Use of tissue biasing circuitry  150  is preferred for the additional benefits it provides, as described earlier with reference to  FIG.  7   . As before, the voltage output from circuitry  150  (Vref or Vvref) is preferably ˜VH/2, although this level can be varied. While use of biasing circuitry  150  is preferred to set the voltage on bus  304 , other voltage generator circuitry could be used as well. Biasing circuitry  150  may also simply comprise a DC voltage, such as Vbat provided by the battery  14 . 
     Bus  302  comprises a passive recovery bus, and is connected to passive recovery switches PRi connected to each of the electrode nodes ei. In this regard, bus  302  and passive recovery switches PRi are similar to what was described earlier with respect to  FIG.  3   . However, unlike passive recovery bus  43  of  FIG.  3   , bus  302  may not always be biased (e.g., to Vpr), and instead may be left to float during passive charge recovery, particularly when another electrode is selected to provide Vcm to the tissue, as explained further below. Each of the passive recovery switches PRi as before ( FIG.  3   ) can be controlled by a group of control signals &lt;Xi&gt; to turn on these switches and to set their on resistances during passive charge recovery. 
     While passive recovery bus  302  is preferably unbiased when Vcm is provided to the tissue through a selected electrode, this bus  302  can also be biased at other times and under different circumstances, such as when Vcm is not being provided to the tissue. In this regard, note that it may not always be necessary to provide a common mode Vcm to the tissue: setting Vcm at the tissue is particularly useful if the IPG  100  will sense neural responses to stimulation, but setting Vcm is less important and may not occur if the IPG  100  will only be used to provide stimulation without neural response sensing. If Vcm is not being set in the tissue, it can be beneficial to bias passive recovery bus  302  with a particular voltage, in particular to allow passive charge recovery to occur. 
       FIG.  11    shows different examples of how passive recovery bus  302  can be biased if and when it is desired to do so, such as during passive charge recovery when Vcm is not set in the tissue. For example, and as shown optionally in dotted lines in  FIG.  11   , additional biasing circuitry  151  may be used to drive a voltage on bus  302 , which may be similar in design to tissue biasing circuitry  150  ( FIG.  7   ), or may comprise different voltage generator circuitry or another DC voltage such as Vbat. 
     Biasing circuitry  150  may also be used to bias bus  302  at particular times. In this regard, the stimulation circuitry  300  can include a switch  306  that intervenes between buses  304  and  302 . This switch  306  when closed can route the voltage output from biasing circuitry  150  (˜VH/2) from bus  304  to bus  302 . 
     Providing a voltage to bus  302  (e.g., by circuitry  151  or by biasing circuitry  150  in conjunction with switch  306 ) allows this bus  302  to operate as described earlier (compare bus  43 ,  FIG.  3   ) to provide passive charge recovery in a traditional manner. This is shown in  FIG.  12    using biasing circuitry  150  and the closing of switch  306  using control signal W (although again additional biasing circuitry  151  could also have been used to bias bus  302 ). In this circumstance, it is assumed that Vcm is not being provided to the tissue during the stimulation cycle, perhaps because neural response sensing is unnecessary. Further, it is assumed that electrodes E 1  and E 2  were previously used to provide active stimulation (although this is just an example and any electrode including the case electrode could have been used to actively provide the stimulation), and therefore that it is desired to passively recovery any residual charge stored in these previously-active current paths (such as on capacitors C 1  and C 2 ). Such passive charge recovery can be accomplished using circuitry  300  by closing (via control signal W) switch  306  (to route ˜VH/2 to bus  302 ), and by asserting control signals &lt;X 1 &gt; and &lt;X 2 &gt; to couple electrode nodes e 1  and e 2  to bus  302 . In this regard, passive recovery bus  302  operates as did passive recovery bus  43  described earlier ( FIG.  3   ), with biasing circuitry  150  providing ˜VH/2 acting as the passive recovery voltage Vpr on bus  302 . 
     Subsequent examples of the operation of stimulation circuitry  300  assume that a common mode voltage Vcm is provided to the tissue, presumably because neural response sensing will occur at some point. Such neural response sensing could happen for example during the second pulse phase  30   b , see, e.g., U.S. Patent Application Publication 2020/0305745; during passive charge recovery  30   c , see, e.g., PCT (Int&#39;l) Patent Application Publication WO 2021/026151, or during quiet periods  30   d . In these subsequent examples, it is assumed that passive recovery bus  302  is not biased (by circuitry  151  or circuitry  150 /switch  306 ) but is instead left to float. Such biasing circuitry  150 / 151  and switch  306  are therefore not shown in subsequent drawings. It is assumed subsequently that tissue biasing circuitry  150  is used to bias common mode bus  304  (e.g., to ˜VH/2), although as explained earlier another biasing source could be used as well. 
       FIGS.  13 A- 13 D  explain operation of stimulation circuitry  300  when providing bipolar stimulation, which as in earlier examples happens between lead-based electrodes E 1  and E 2 . The stimulation pulses are shown as biphasic ( 30   a  and  30   b ), but as before monophasic pulses could be used as well, as is discussed in detail later with respect to  FIGS.  15 A and  15 B . The case electrode Ec is used to provide the common mode voltage Vcm to the tissue.  FIG.  13 A  summarizes the status of the various switches PRi and CMi during active bipolar stimulation (e.g., during phases  30   a  and  30   b ,  FIG.  13 B ), during passive charge recovery ( 30   c ,  FIG.  13 C ), and during quiet periods ( 30   d ,  FIG.  13 D ). 
       FIG.  13 B  shows configuration of the circuitry  300  during active stimulation ( 30   a  and  30 b), and shows the various current paths that are formed. During active stimulation, P/NDAC 1  and P/NDAC2 at electrode E 1  and E 2  are active and programmed to provide a current of amplitude I, which as noted earlier are active at different times depending on the phase ( 30   a  or  30   b ). Because the DACs at these electrodes are active during active stimulation, switches PR 1 , PR 2 , CM 1 , and CM 2  are opened. That is, &lt;X1&gt;, Y1, &lt;×2&gt;, and Y 2  are not asserted, and electrode nodes el and e 2  are decoupled buses  302  and  304 . By contrast, switch CMc associated with the case electrode Ec is closed during active stimulation via assertion of Yc. This routes —VH/2 from common mode bus  304  to electrode node ec connected to the bottom plate of the capacitor Ccm  152 , which allows Vcm to form at the case electrode Ec to set the tissue voltage. Passive recovery switch PRc connected to electrode node ec is open, and &lt;Xc&gt; is not asserted to isolate ec from passive recovery bus  302 . Because Vcm is passively formed at the case electrode Ec, P/NDACc associated with the case electrode Ec are inactive. 
       FIG.  13 C  shows configuration of the circuitry  300  during passive charge recovery ( 30   c ), and shows the various current paths that are formed. During passive charge recovery, all of the DACs are inactive. Passive recovery switches PR 1  and PR 2  associated with previously driven electrodes E 1  and E 2  are closed via assertion of &lt;X 1 &gt; and &lt;X 2 &gt; to couple electrode nodes el and e 2  to passive recovery bus  302 . This promotes the discharge of charge stored on capacitors C 1  and C 2  through the tissue R and bus  302 . (Control signals &lt;X 1 &gt; and &lt;X 2 &gt; may be asserted to set the on resistance of PR 1  and PR 2  to a desired value). 
     During passive recovery, passive recovery switch PRc associated with the case electrode Ec can be opened, and hence control signals &lt;Xc&gt; are not be asserted, and thus this electrode is decoupled from bus  302 . However, common mode switch CMc is closed via assertion of Yc to couple electrode node ec to common mode bus  304  (˜VH/2). Therefore, and unlike stimulation circuitry  250  described earlier ( FIG.  8   ), the tissue R is not left floating during passive charge recovery, but instead continues to be maintained at Vcm, as occurred during active stimulation ( FIG.  13 B ) and as occurs during quiet periods (discussed shortly with respect to  FIG.  13 D ). This assists in neural response sensing, because the tissue voltage is known (Vcm) and kept constant. Passive discharge through passive recovery bus  302  is thus referenced to Vcm via electrodes El and E 2  which are also in contact with the tissue (˜VH/2), hence the reason that passive charge recovery can occur without biasing passive recovery bus  302  with a voltage (like Vpr). 
       FIG.  13 D  shows configuration of the circuitry  300  during quiet periods  30   d  ( FIG.  2 A ) when neither active stimulation nor passive charge recovery is occurring. This configuration is similar to what occurred during active stimulation ( FIG.  13 B ), except that none of the DACs are active. All passive recovery switches PRi are open (the various control signals &lt;Xi&gt; are not asserted), as are the common mode switches CM 1  and CM 2  associated with previous-active electrodes E 1  and E 2  (Y 1  and Y 2  are not asserted). Common mode switch CMc associated with the case electrode Ec remains closed (Yc asserted), which continues to maintain Vcm in the tissue R. Again, this assists with sensing of neural responses during the quiet periods ( 30   d ), and assists in maintaining Vcm in the tissue in preparation for the next active stimulation phase (pulse). Notice also that the capacitor Ccm at the case electrode Ec can passively discharge through the bleed resistor Rbleed. To summarize,  FIGS.  13 A- 13 D  show that stimulation circuitry  300  can hold the tissue R to the common mode voltage Vcm using the case electrode Ec during all relevant pulse phases. 
       FIGS.  14 A- 14 E  show operation of the stimulation circuitry  300  during monopolar stimulation. Like the monopolar example discussed earlier ( FIG.  10   ), it is assumed that monopolar stimulation is occurring by actively driving lead-based electrode E 1  and the case electrode Ec (using P/NDAC 1  and P/NDACc). Lead based electrode E 2  is selected (via PR 2 , &lt;X 2 &gt;) to provide Vcm to the tissue, although again any one or more lead-based electrodes could be used.  FIG.  14 A  summarizes the status of the various switches during active monopolar stimulation (e.g., during phases  30   a  and  30   b ,  FIG.  14 B ), during passive charge recovery ( 30   c ,  FIG.  14 C ), and during quiet periods ( 30   d ,  FIGS.  14 D- 14 E ). 
       FIG.  14 B  shows configuration of the circuitry  300  during active stimulation ( 30   a  and  30 b), and shows the various current paths that are formed. During active stimulation, P/NDAC 1  and P/NDACc at electrodes E 1  and Ec are active and programmed to provide a current of amplitude I, which as noted earlier are active at different times depending on the phase ( 30   a  or  30 b). (As before, the stimulation pulses can be biphasic or monophasic). Because the DACs at these electrodes are active during active stimulation, switches PR 1 , PRc, CM 1 , and CMc are opened. That is, &lt;X1&gt;, Y1, &lt;Xc&gt;, and Yc are not asserted, and electrode nodes el and ec are decoupled from buses  302  and  304 . By contrast, switch CM 2  associated with electrode E 2  is closed during active stimulation via assertion of Y 2 . This routes ˜VH/2 from bus  304  to electrode node e 2  connected to the bottom plate of the capacitor C 2 , which allows Vcm to form at electrode E 2  to set the tissue voltage. Notice electrode E 2 , and all other lead-based electrodes for that matter, lack a bleed resistor in parallel with their capacitances Ci, which as noted earlier is preferred for safety. Capacitor C 2  may charge somewhat during the as described earlier, just as case electrode capacitor Ccm did earlier, to help set Vcm in the tissue at electrode E 2 . Passive recovery switch PR 2  connected to electrode node e 2  is open, and &lt;X 2 &gt; is not asserted to isolate e 2  from bus  302 . Because Vcm is passively formed at electrode E 2 , P/NDAC2 associated with electrode E 2  are inactive. 
       FIG.  14 C  shows configuration of the circuitry  300  during passive charge recovery ( 30   c ), and shows the various current paths that are formed. During passive charge recovery, all of the DACs are inactive. Passive recovery switches PR 1  and PRc associated with previously driven electrodes E 1  and Ec are closed via assertion of &lt;X 1 &gt; and &lt;Xc&gt; to couple electrode node el and ec to passive recovery bus  302 . This promotes the discharge of charge stored on capacitors C 1  and Cc through the tissue R and bus  302 . (Control signals &lt;X 1 &gt; and &lt;Xc&gt; may be asserted to set the on resistance of PR 1  and PR 2  to a desired value). 
     During passive recovery, passive recovery switch PR 2  associated with electrode E 2  can be opened, and hence control signals &lt;X 2 &gt; are not be asserted, and thus this electrode is decoupled from bus  302 . However, common mode switch CM 2  is closed via assertion of Y 2  to couple electrode node e 2  to common mode bus  304  (˜VH/2). In this way the tissue R is biased to Vcm at E 2  and is not left floating during passive charge recovery, as occurred during active stimulation ( FIG.  14 B ) and as occurs during quiet periods (discussed shortly with respect to  FIGS.  14 D and  14 E ). This assists in neural response sensing, because the tissue voltage is known (Vcm) and kept constant. Passive discharge through passive recovery bus  302  is thus referenced to Vcm via electrodes E 1  and Ec which are also in contact with the tissue (˜VH/2), hence the reason that passive charge recovery can occur without biasing passive recovery bus with a voltage (like Vpr). 
       FIGS.  14 D and  14 E  show different configurations of the circuitry  300  during quiet periods when neither active stimulation nor passive charge recovery is occurring. These options differ primarily in the extent to which they allow the capacitor (e.g., C 2 ) at the lead-based electrode used to provide Vcm to the tissue (E 2 ) to be discharged. In  FIG.  14 D , this common mode capacitor C 2  is not discharged, and this can be preferable. The above-incorporated &#39;202 patent explains that it can be useful to build charge (and hence a voltage Vc) across the common mode capacitor to set the tissue voltage to an optimal level (Vcm=Vc+VH/2) that varies somewhat from VH/2. This voltage may build to a steady state voltage over time (after some number of pulses), at which point Vcm in the tissue is optimally set. In short, it may not be desirable to discharge the common mode capacitance. On the contrary, it can also be useful to discharge capacitor C 2 , at least from time to time, as shown in  FIG.  14 E . For example, the charge stored on capacitor C 2  may become excessive, and the voltage across it too large, which may affect circuit operation. Moreover, it may be useful to discharge common mode capacitance C 2  if the stimulation changes—such as if electrode E 2  later becomes an actively driven electrode as opposed to providing Vcm tissue biasing.  FIGS.  14 D and  14 E  therefore cover both of these contingencies, and allow the lead-based common mode capacitance to discharged or not. 
       FIG.  14 D  shows operation during the quiet period where the common mode capacitance (C 2 ) used to provide Vcm is not discharged. This configuration is similar to what occurred during active stimulation ( FIG.  14 B ), except that none of the DACs are active. All passive recovery switches PRi are open (the various control signals &lt;Xi&gt; are not asserted), as are the common mode switches CM 1  and CMc associated with previous-active electrodes E 1  and Ec (Y 1  and Yc are not asserted). Common mode switch CM 2  associated with electrode E 2  remains closed (Y 2  asserted), which continues to maintain Vcm in the tissue R at that electrode without discharging C 2 . Again, this assists with sensing of neural responses during the quiet periods ( 30   d ), and assists in maintaining Vcm in the tissue in preparation for the next active stimulation phase (pulse). 
       FIG.  14 E  shows operation during the quiet period where the common mode capacitance (C 2 ) used to provide Vcm is discharged. Different options are possible here to discharge C 2 . In the example shown, switch CM 2  continues to be closed and therefore Vcm continues to be provided to the tissue via electrode E 2 . However, the passive recovery switch PR 2  at this electrode is also closed, along with one or more of the passive recovery switches at the other electrodes. In this example, PRc associated with the case electrode Ec is closed. Electrode node e 2  and ec are thus both coupled to passive charge recovery bus  302 , which allows C 2  to discharge through electrode E 2  and Ec, the tissue, and bus  302 . Even though the passive recovery bus  302  is used to recover charge stored on C 2 , passive charge recovery at the previously-used active electrode (E 1  and Ec) is not actually occurring (this occurred earlier in  FIG.  14 C ). Still other passive recharge switches PRi could be closed here, such as PR 1  at electrode E 1 . Indeed, all passive recharge switches PRi could be closed, thus connecting all electrode nodes to the bus  302  to assist in discharging C 2  when E 2  acts to provide the common mode voltage Vcm to the tissue. In any event, even with this option, Vcm is still maintained in the tissue during the quiet period via common mode bus  304 , switch CM 2 , and electrode E 2 . Note however that Vcm may change slightly as capacitor E 2  is discharged, but this small change should not affect neural response sensing. 
     As noted earlier, the pulses provided during active stimulation via stimulation circuitries  250  or  300  can be monophasic. (More generally, active stimulation can involve any number of active stimulation phases, whether monophasic, biphasic, triphasic, and so on). Given its importance to certain stimulation therapies (e.g., DBS), the use of monophasic stimulation is explained further in the context of circuitry  300  in  FIGS.  15 A and  15 B . As described earlier and shown in  FIG.  15 A , monophasic stimulation involves actively driving (using P/NDAC circuitry) a single phase ( 30   a ) without use of a following actively-driven phase of opposite polarity (like  30   b ) to recover charge.  FIGS.  15 A and  15 B  show monophasic stimulation in the context of monopolar stimulation (again, as is particularly important in DBS therapy), in which stimulation occurs between at least one lead-based electrode (e.g., E 1 ) and the case electrode Ec (similar to what occurred in  FIGS.  14 A- 14 E ). However, monophasic bipolar stimulation (similar to what occurred in  FIGS.  13 A- 13 D ) would be similar. 
     When providing monophasic, monopolar stimulation, circuitry  300  operates similarly to when biphasic stimulation was used ( FIGS.  14 A- 14 E ), and generally the same switches are closed at the same times during the active ( 30   a ), passive ( 30   c ), and quiet ( 30   d ) pulses phases. Monophasic stimulation however runs a higher risk of accumulating charge that can affect setting of the common mode voltage Vcm in the tissue R. This doesn&#39;t affect the efficacy of circuitry  300  operation and would not significantly affect neural response sensing, but is still noteworthy and explained briefly. 
     Monophasic stimulation may more likely accumulate charge because the passive charge recovery phase ( 30   c ) may not (at least initially) recover all of the charge injected during the active phase ( 30   a ). For example, during the active stimulation phase  30   a , as shown in  FIG.  15 A , the monophasic pulse injects a charge of +Q, which will charge capacitors C 1  (Vc 1 ) and Ccm (Vccm) in the active electrode paths at E 1  and Ec. As before, lead-based electrode E 2  is used to provide the common mode voltage Vcm to the tissue, which may cause capacitor C 2  slightly charge (Vc 2 ) as discussed earlier. 
     During the passive charge recovery phase ( 30   c ), as also shown in  FIG.  15 A , the electrode nodes at these previously-active electrodes E 1  and Ec are shorted to bus  302  via closing of switches PR 1  and PRc, which causes an opposite polarity current to flow. This current will exponentially decay in accordance with the RC time constant, and in accordance with the degree to which the capacitors in the passive recharge loop (bus  302 ) are charged (Vc 1  and Vccm), because these voltages provide the electromotive force that permits the current to flow. The amount of charge passively recovered during  30   c  depends on these factors as well as how long the passive recovery switches PR 1  and PRc are closed. It is likely at least initially that the entirety of the actively-injected charge Q+will not be recovered (&lt;I+QI) during the passive charge recovery phase  30   c . Therefore, some residual voltage will still be still present across the capacitors (Vc 1  and Vccm) at the end of this phase. Over time˜as more pulses are issued˜this unrecovered charge and voltages Vc 1  and Vccm will grow. As the voltage increases, so does the electromotive force implicated during passive charge recovery, thus allowing more charge to be recovered during subsequent periods  30   c . Eventually, after some number of pulses, these voltages Vc 1  and Vccm will have increased to an equilibrium point where the passive charge recovery period  30   c  is able to completely recovery the charge (-Q) injected during the active phase  30   a  (+Q). This build up of voltages Vc 1  and Vccm is not problematic to operation of the circuitry  300  or to the stimulation therapy provided; if necessary, the compliance voltage VH will be increased via a feedback mechanism described earlier ( FIG.  3   ) to compensate for the larger voltage on the capacitors. See U.S. Pat. No. 10,792,491. 
     Nevertheless, the fact that the capacitors C 1  and Ccm remain charged to some degree can affect the common mode voltage Vcm formed in the tissue, i.e., via capacitor C 2  at electrode E 2 . This is shown in  FIG.  15 B , in the circumstance where it is desired to discharge capacitor C 2  during the quiet phases ( 30   d ), as explained earlier with reference to  FIG.  14 E . In this circumstance, discharging capacitor C 2  involves connecting this capacitor and another˜such as Ccm˜to bus  302  via switches PR 2  and PRc. This essentially places these capacitors C 2  (Vc 2 ) and Ccm (Vccm) in parallel, which can cause a current to flow to equilibrate the charges on these capacitances. However, capacitor C 2  this may not completely discharge through this process. In fact, and depending on the magnitude and polarity of Vccm as eventually established during passive charge recovery ( 30   c ) once equilibrium is reached, capacitor C 2  may charge further during this quiet period (i.e., the absolute value of Vc 2  may increase; however it may also decrease). Regardless, because Vccm can affect Vc 2 , the voltage Vcm formed in the tissue can be affected, because Vcm=Vc 2 +VH/2. 
     In short, just as Vccm reaches a steady state over some period of time, so too will Vcm. Nevertheless, Vc 2 , and hence Vcm, will change relatively slowly and steadily. As such, neural response sensing will not be substantially affected as the sense amp circuitry  110  ( FIG.  5   ) can more easily filter such slow acting transients in the tissue. 
       FIG.  16    summarizes the various control signals that can be provided to stimulation circuitry  300 , including the common mode control signals Yi used to control the common mode switches CMi at each of the electrode nodes; the passive recovery control signals &lt;XI&gt; used to the passive recovery switches PRi at each of the electrode nodes; and control signal W to control switch  306  ( FIGS.  11  and  12   ). These control signals may issue from the IPG  100 &#39;s control circuitry  102  as shown, along with other control signals used to activate the relevant DACs to provide the stimulation at the selected electrodes with the prescribed amplitudes. These control signal may comprise some of the signals within bus  118  described earlier ( FIG.  5   ). 
       FIG.  17    shows representations of the IPG  100 , including the various lead-based electrodes (e.g., E 1 -E 16 ) and the case electrode, and shows different variations by which these electrodes can be selected to provide stimulation or to provide common mode voltage Vcm to the tissue. Because Vcm is preferably provided to the tissue to assist with neural response sensing, still further electrodes are shown that operate as sensing electrodes. (Because neural response sensing is preferably differential, two sensing electrodes are shown, although only one sensing electrode could be used in other examples). Certain of the electrodes may also be inactive, and are not selected for stimulation, sensing, or to provide the common mode voltage to the tissue. Different shadings are shown in  FIG.  17    for these different electrode functions. The foregoing description explains how and when the various switches in stimulation circuitry  300  should be closed to affect the different examples shown in  FIG.  17   . 
     Examples (a)-(c) show different examples of bipolar stimulation. Example (a) shows bipolar stimulation at two active lead-based electrodes (one anode, one cathode, such as during one of phases  30   a  or  30   b ), and use of the case electrode to provide Vcm, similar to what was shown in  FIGS.  13 A- 13 D . In example (b), more than two lead-based electrodes are selected to provide stimulation, possibly on different leads as shown. In example (c), some of the lead-based electrodes are also selected to operate (along with the case electrode Ec) to provide Vcm. This may be preferable to establish Vcm closer to electrodes where stimulation and sensing are occurring. In fact, all otherwise inactive electrodes (i.e., those not used for providing stimulation or for sensing) may provide Vcm to the tissue, as shown in example (d). 
     Examples (e) and (f) show different examples of monopolar stimulation, in which an active current is driven at the case electrode Ec (shown here as a cathode) and at at least one lead-based electrode. In example (e), one lead-case electrode is also selected (as an anode) to provide active stimulation, and one lead-based electrode is selected to provide Vcm to the tissue, similar to what was shown in  FIGS.  14 A- 14 E . Example (f) is similar except that more than one lead-based electrode is selected to provide stimulation (all selected as anodes). Again, more than one lead-based electrode can be used to provide Vcm to the tissue, and in example (g) all such inactive lead-based electrodes are used for this purpose. 
     Example (h) shows stimulation that is not strictly bipolar or monopolar. Here, the case electrode Ec is actively driven (as a cathode) as occurs in monopolar stimulation, but other lead-based electrodes are also driven with the same polarity (also as cathodes). Nevertheless, Vcm may still be provided to the tissue at any of the inactive lead-based electrodes, or all of them (although this isn&#39;t shown for example (h). 
     While various examples of the stimulation circuitry are described as being useful to provide a common mode voltage to the tissue for the purpose of sensing neural responses to stimulation, the disclosed circuits can also be used to bias the tissue for other reasons, not related to neural response sensing. 
     Although particular embodiments of the present invention have been shown and described, the above discussion is not intended to limit the present invention to these embodiments. It will be obvious to those skilled in the art that various changes and modifications may be made without departing from the spirit and scope of the present invention. Thus, the present invention is intended to cover alternatives, modifications, and equivalents that may fall within the spirit and scope of the present invention as defined by the claims.