DETAILED ACTION
Notice of Pre-AIA or AIA Status
The present application, filed on or after March 16, 2013, is being examined under the first inventor to file provisions of the AIA .
Continued Examination Under 37 CFR 1.114
A request for continued examination under 37 CFR 1.114, including the fee set forth in 37 CFR 1.17(e), was filed in this application after final rejection. Since this application is eligible for continued examination under 37 CFR 1.114, and the fee set forth in 37 CFR 1.17(e) has been timely paid, the finality of the previous Office action has been withdrawn pursuant to 37 CFR 1.114. Applicant's submission filed on 01/12/2026 has been entered.
Response to Arguments
Claims 1-9, 12-13, and 15-20 were provisionally rejected on the ground of non-statutory double patenting over claims 1-17 of co-pending U.S. Pat. App. No. 18/137,383. Applicant’s amendments, filed 01/12/2026, with respect to the provisional non-statutory double patenting rejection have been fully considered and are persuasive. The provisional double patenting rejection of claims 1-9, 12-13, and 15-20 has been withdrawn.
Applicant’s arguments, filed 01/12/2026, with respect to the rejection of claims 1-20 under 35 U.S.C. §103 have been considered but are moot because the new ground of rejection does not rely on any reference applied in the prior rejection of record for any teaching or matter specifically challenged in the argument. Since the amendments to independent claims 1 and 20 change the scope of claims 1-20 and do not merely incorporate limitations from previous dependent claims, a new grounds of rejection is made in view of Esteller et al. (U.S. Pub. No. 2019/0366094 A1) as explained in further detail below.
Applicant contends that the cited art does not disclose or suggest a lead with different electrodes for stimulating a dorsal root ganglion and for sensing ECAPs in combination with controlling a signal generator to generate an electrical signal to stimulate the dorsal root ganglion, where the signal generator is further controlled to “adjust electrical signal such that an amplitude of the sensed ECAP remains within a predetermined range.” Applicant further contends that the cited references appear silent with respect to using different electrodes on a same lead to sense ECAPs, let alone disclose adjusting an electrical signal used for stimulating a dorsal root ganglion “such that an amplitude of the sensed ECAP remains within a predetermined range,” as claimed. However, these limitations were not cited in the previous claims such that the arguments are moot since the amended claims require a new grounds of rejection as explained in further detail below.
Claim Rejections - 35 USC § 103
In the event the determination of the status of the application as subject to AIA 35 U.S.C. 102 and 103 (or as subject to pre-AIA 35 U.S.C. 102 and 103) is incorrect, any correction of the statutory basis (i.e., changing from AIA to pre-AIA ) for the rejection will not be considered a new ground of rejection if the prior art relied upon, and the rationale supporting the rejection, would be the same under either status.
The following is a quotation of 35 U.S.C. 103 which forms the basis for all obviousness rejections set forth in this Office action:
A patent for a claimed invention may not be obtained, notwithstanding that the claimed invention is not identically disclosed as set forth in section 102, if the differences between the claimed invention and the prior art are such that the claimed invention as a whole would have been obvious before the effective filing date of the claimed invention to a person having ordinary skill in the art to which the claimed invention pertains. Patentability shall not be negated by the manner in which the invention was made.
Claims 1, 3-9, and 15-20 are rejected under 35 U.S.C. 103 as being unpatentable over Baldoni et al. (hereinafter “Baldoni”) (U.S. Pub. No. 2019/0321641 A1) in view of Esteller et al. (hereinafter “Esteller”) (U.S. Pub. No. 2019/0366094 A1), Perryman (EP 2,651,431 B1), Nassif (U.S. Pub. No. 2020/0368534 A1), Jiang et al. (hereinafter “Jiang”) (U.S. Pub. No. 2016/0045746 A1), and Kramer et al. (hereinafter “Kramer”) (U.S. Pub. No. 2012/0277839 A1).
Regarding claim 1, Baldoni teaches a system for treating metabolic syndrome (Abstract, where “Systems and methods for treating a patient having a blood glucose abnormality, such as type 2 diabetes (T2D), using an electrical signal,” ¶[0002], where “present technology is directed generally to methods and systems for treating treat blood glucose abnormalities, including metabolic syndrome, type 2 diabetes (T2D), and/or elevated HbA1c levels in a patient”), comprising:
a lead (¶[0044], where “In representative systems, the signal delivery devices 110 can include one or more elongated lead(s) or lead body or bodies 111 (identified individually as a first lead 111a and a second lead 111b) … the lead or leads 111 can include one or more electrodes or electrical contacts that direct electrical signals into the patient's tissue, e.g., to provide for therapeutic relief”) comprising:
one or more first electrodes to stimulate (¶[0044], where “the lead or leads 111 can include one or more electrodes or electrical contacts that direct electrical signals into the patient's tissue, e.g., to provide for therapeutic relief”) at least one dorsal root ganglion of at least one spinal nerve (¶[0034], where “therapeutic modulation signals are directed to the target location that generally includes the patient's spinal cord, e.g., the dorsal column of the patient's spinal cord. The modulation signals can be directed to the dorsal horn, dorsal root, dorsal root ganglion, dorsal root entry zone, and/or other particular areas at or in close proximity to the spinal cord itself”); and
a device (Figure 1A, system 100) comprising:
a signal generator to generate and apply an electrical signal (¶[0046], where “The signal generator 101 can transmit signals (e.g., electrical signals) to the signal delivery elements 110 that excite and/or suppress target nerves (e.g., sympathetic nerves)”) to the one or more first electrodes (¶[0044], where “The signal generator 101 can be connected directly to the signal delivery devices 110, or it can be coupled to the signal delivery devices 110 via a signal link, e.g., a lead extension 102 and/or a wireless link. In representative systems, the signal delivery devices 110 can include one or more elongated lead(s) or lead body or bodies 111 (identified individually as a first lead 111a and a second lead 111b) … the lead or leads 111 can include one or more electrodes or electrical contacts that direct electrical signals into the patient's tissue, e.g., to provide for therapeutic relief”); and
at least one processor (Figure 1A, one or more processor(s) 107, ¶[0046], where “The signal generator 101 and/or other elements of the system 100 can include one or more processor(s) 107”) to:
monitor a value of at least one parameter of a patient that is associated with at least one condition of metabolic syndrome (¶[0115], where “the patient can use a constant glucose monitor that continuously monitors the patient's blood glucose level and communicates the measurements to an internal or external processor (e.g., an implanted pulse generator, or a phone-based app or other external device)”); and
control the signal generator to generate and apply the electrical signal (¶[0046], where “The signal generator 101 can transmit signals (e.g., electrical signals) to the signal delivery elements 110 that excite and/or suppress target nerves (e.g., sympathetic nerves),” ¶[0095], where “if a change in the patient's blood glucose level is detected, the systems, devices, and methods described herein can automatically deliver therapeutic electrical signals”) to the one or more first electrodes (¶[0044], where “The signal generator 101 can be connected directly to the signal delivery devices 110, or it can be coupled to the signal delivery devices 110 via a signal link, e.g., a lead extension 102 and/or a wireless link. In representative systems, the signal delivery devices 110 can include one or more elongated lead(s) or lead body or bodies 111 (identified individually as a first lead 111a and a second lead 111b) … the lead or leads 111 can include one or more electrodes or electrical contacts that direct electrical signals into the patient's tissue, e.g., to provide for therapeutic relief”) to stimulate the at least one dorsal root ganglion (¶[0034], where “therapeutic modulation signals are directed to the target location that generally includes the patient's spinal cord, e.g., the dorsal column of the patient's spinal cord. The modulation signals can be directed to the dorsal horn, dorsal root, dorsal root ganglion, dorsal root entry zone, and/or other particular areas at or in close proximity to the spinal cord itself”), which promotes vagal nerve activity to the patient's pancreas to increase insulin production by the pancreas while inhibiting sympathetic nerve activity to the patient's liver to promote glycogenesis by the liver (¶[0031], where “inhibiting at least a portion of the patient's sympathetic nervous system, such as one or more sympathetic nerves corresponding to one or more of the patient's …pancreas, …may result in the therapeutic effect by increasing glycogen production (e.g., hepatic glycogenesis), increasing insulin sensitivity,” ¶[0068], where “In representative systems and methods, the modulation inhibits one or more of the sympathetic nerves 315 innervating the patient's liver 361, pancreas 365, adrenal gland 367, and/or stomach 363. By inhibiting one or more of the sympathetic nerves 315, glucose uptake by the patient's liver 361 may increase, which lowers the patient's post-prandial blood glucose levels, thereby treating the patient's T2D”),
thereby causing a change to the value of the at least one parameter (¶[0095], where “if a change in the patient's blood glucose level is detected, the systems, devices, and methods described herein can automatically deliver therapeutic electrical signals. Representative systems and methods described herein can include one or more sensors configured to monitor the patient's blood glucose levels by detecting an amount of glucose in the patient's blood”).
Although Baldoni teaches generation of an electrical signal by the signal generator, Baldoni does not explicitly teach a lead comprising one or more second electrodes to sense an electrically evoked compound action potential (ECAP) resulting from stimulation of the at least one dorsal root ganglion; nor the electrical signal having a first current value for a first duration of time when the value of the at least one parameter exceeds a threshold value; and upon expiration of the first duration of time and so long as the value of the at least one parameter still exceeds the threshold value, generate the electrical signal with step-wise current increases from the first current value up to a maximum current value that is set based on a current value known to stimulate a ventral root of the at least one spinal nerve, wherein, during and after the first duration of time, the signal generator is controlled to adjust the electrical signal such that an amplitude of the sensed ECAP remains within a predetermined range.
Esteller teaches methods and systems for providing neuromodulation therapy (Abstract), including stimulation to a dorsal root ganglion (¶[0046], where “It should be noted here that compound action potentials may be evoked in various neural elements, including the neural fibers of the dorsal column, the dorsal root fibers, the dorsal root ganglia, etc. As used herein, the ECAP refers to action potentials evoked in any of the neural elements. As explained further below, an ECAP is a neural response that can be sensed at an electrode”), and further teaches a lead comprising one or more first electrodes to stimulate and one or more second electrodes to sense an electrically evoked compound action potential (ECAP) resulting from stimulation (¶[0052], where “One or more of the electrodes 16 can be used to sense the ECAP,” ¶[0077], where “The electrode/channel configuration 1000 includes a lead 14 having a plurality of electrodes 16 (electrodes E1-E20 are illustrated in FIG. 10),” ¶[0078], where “stimulus is applied using E1 as an anode and E3 as a cathode,” ¶[0079], where “FIG. 11 B illustrates a signal recorded on channel 8 (electrodes E18 and E19). On channel 8 the stimulation artifact and the ECAP are clearly distinguished from each other. Thus, channel 8 is an example of a “distinct channel” in this example”) of the at least one dorsal root ganglion (¶[0046], where “It should be noted here that compound action potentials may be evoked in various neural elements, including the neural fibers of the dorsal column, the dorsal root fibers, the dorsal root ganglia, etc. As used herein, the ECAP refers to action potentials evoked in any of the neural elements. As explained further below, an ECAP is a neural response that can be sensed at an electrode”);
and that during and after the first duration of time, the signal generator is controlled to adjust the electrical signal such that an amplitude of the sensed ECAP remains within a predetermined range (¶[0068], where “The ECAP algorithm 124a (and/or 124b, FIG. 15) can be further configured to use feedback to maintain or alter stimulation to achieve the therapeutic effect. For example, the ECAP algorithm may be configured to alter, adjust, or maintain stimulation to keep one or more ECAP parameters at a certain value or within a certain range that is shown or calculated to be therapeutically effective. Thus, the ECAP algorithm can provide open loop or closed loop feedback affecting stimulus.” Examiner interprets that the electrical signal will inherently be applied either during or after a duration of time with amplitude adjustment occurring concurrently to achieve certain ECAP parameters that are therapeutically effective.).
It would have been obvious to one of ordinary skill in the art at the time of the invention to combine the above-described teachings of Esteller, which teaches a lead comprising one or more first electrodes to stimulate and one or more second electrodes to sense an electrically evoked compound action potential (ECAP) resulting from stimulation of the at least one dorsal root ganglion and that during and after the first duration of time, the signal generator is controlled to adjust the electrical signal such that an amplitude of the sensed ECAP remains within a predetermined range, with the invention of Baldoni in order to maintain or alter stimulation to achieve the therapeutic effect and to keep one or more ECAP parameters at a certain value or within a certain range that is shown or calculated to be therapeutically effective (Esteller ¶[0068]).
Although Baldoni teaches generation of an electrical signal by the signal generator, neither Baldoni nor Esteller explicitly the electrical signal having a first current value for a first duration of time when the value of the at least one parameter exceeds a threshold value; and upon expiration of the first duration of time and so long as the value of the at least one parameter still exceeds the threshold value, generate the electrical signal with step-wise current increases from the first current value up to a maximum current value that is set based on a current value known to stimulate a ventral root of the at least one spinal nerve.
Perryman teaches a system and apparatus for control of pancreatic beta cell function to improve glucose homeostasis and insulin production (See Title), and further teaches controlling the signal generator when the value of the at least one parameter exceeds a threshold value (¶[0065], where “The system can further include means for electrical neural stimulation in a closed loop format. The system can include a feedback sensor. The feedback sensor can collect information on biomarker levels and transmit to a controller to compare measured levels to desired ranges. If outside the desired or threshold range, the feedback controller can initiate adjustments to parameter settings of the electrical stimulation,” ¶[0038], where “‘Biomarker’ means any physiological indicating species produced by a subject. Examples of biomarkers include, but are not limited to, insulin, glucose, tissue CGRP, abdominal skin blood flow, abdominal skin temperature, and abdominal muscle electrical activity,” ¶[0075], where “The controller can send the signals to increase or decrease stimulation until glucose homeostasis is achieved … The controller can include a microprocessor that can instruct the system to produce an exciting or inhibiting stimulation signal or to cease electrical stimulation”).
It would have been obvious to one of ordinary skill in the art at the time of the invention to combine the above-described teachings of Perryman, which teaches controlling the signal generator when the value of the at least one parameter exceeds a threshold value, with the modified invention of Baldoni in order to maintain the patient’s blood glucose levels within a normal, healthy range (Perryman ¶[0058], where “the C-afferent sensory nerve fibers innervating pancreatic beta cells are either excited or inhibited to promote glucose homeostasis in response to abnormal biomarker levels”).
Although Baldoni teaches generation of an electrical signal by the signal generator and Perryman teaches generation of the electrical signal when the value of the at least one parameter exceeds a threshold value, none of Baldoni, Esteller, nor Perryman teach the electrical signal having a first current value for a first duration of time; and upon expiration of the first duration of time and so long as the value of the at least one parameter still exceeds the threshold value, generate the electrical signal with step-wise current increases from the first current value up to a maximum current value that is set based on a current value known to stimulate a ventral root of the at least one spinal nerve.
Nassif teaches systems, devices, and methods for delivering one or more electrical pulses to a target region within a patient's body (Abstract), and further teaches the electrical signal having a first current value (¶[0020], which teaches “delivering a first stimulation pulse having a first current”) for a first duration of time (¶[0127], where “At block 1326 [in Fig. 14], the duration of the first phase is monitored”), and upon expiration of the first duration of time, control the signal generator to generate the electrical signal with current increases from the first current value (¶[0020], which teaches “delivering a second stimulation pulse having a second current set,” ¶[0021], where “the second current is greater than the first current,” ¶[0132], where “At block 1336 [in Fig. 14], the duration of the second stimulation phase is monitored”).
It would have been obvious to one of ordinary skill in the art at the time of the invention to combine the above-described teachings of Nassif, which teaches the electrical signal having a first current value for a first duration of time, and upon expiration of the first duration of time, control the signal generator to generate the electrical signal with current increases from the first current value, with the modified invention of Baldoni in order to best modify continuous treatment to a patient for a regularly fluctuating parameter such as blood glucose levels.
Although Nassif teaches controlling the signal generator to generate the electrical signal with an increased current from the first current value, none of Baldoni, Esteller, Perryman, nor Nassif teaches step-wise current increases from the first current value up to a maximum current value nor a maximum current value that is set based on a current value known to stimulate a ventral root of the at least one spinal nerve.
Jiang teaches neurostimulation treatment systems and associated devices, as well as methods of treatment, implantation and configuration of such treatment systems (Abstract), and further teaches step-wise current increases from the first current value (¶[0019], where “Automatically adjusting may comprise increasing the stimulation amplitude in increments of 0.05 mA for a test stimulation.” Examiner takes the position that increasing the stimulus amplitude by 0.05 mA causes the current value to increase by the same amount since current and amplitude are directly proportional and that an incremental increase inherently creates a larger subsequent current value. Furthermore, an incremental increase by a set amount is a step-wise increase since a step-wise increase is an increase that happens in steps rather than a gradual increase.).
It would have been obvious to one of ordinary skill in the art at the time of the invention to combine the above-described teachings of Jiang, which teaches step-wise current increases from the first current value, with the modified invention of Baldoni since the use of proportional increases in combination with the automated feature in stimulation amplitude adjusting during test stimulation and/or programming effectively reduces the time required for such activities and allows for easy termination of the stimulation at any time and for any reason, patient safety or otherwise, by the user (Jiang ¶[0019]).
None of Baldoni, Esteller, Perryman, Nassif, nor Jiang explicitly teach a maximum current value nor a maximum current value that is set based on a current value known to stimulate a ventral root of the at least one spinal nerve.
Kramer teaches systems, methods and devices are provided for the targeted treatment of a variety of medical conditions by directly neuromodulating a target anatomy associated with the condition while minimizing or excluding undesired neuromodulation of other anatomies (Abstract), and further teaches a maximum current value (¶[0045], where “the stimulation signal has an energy below an energy threshold for stimulating a ventral root associated with the target dorsal root while the lead is so positioned”) and a maximum current value that is set based on a current value known to stimulate a ventral root of the at least one spinal nerve (¶[0045], where “In particular, selective stimulation of tissues, such as the dorsal root, DRG, or portions thereof, exclude stimulation of the ventral root wherein the stimulation signal has an energy below an energy threshold for stimulating a ventral root associated with the target dorsal root while the lead is so positioned”).
It would have been obvious to one of ordinary skill in the art at the time of the invention to combine the above-described teachings of Kramer, which teaches a maximum current value and a maximum current value that is set based on a current value known to stimulate a ventral root of the at least one spinal nerve, with the modified invention of Baldoni in order to prevent inducing side effects for a patient, where indiscriminant stimulation of the ventral root typically causes unpleasant sensations for the patient, such as tingling, buzzing or undesired motions or movements (Kramer ¶[0045]).
Regarding claim 3, Baldoni in combination with Esteller, Perryman, Nassif, Jiang, and Kramer teaches all limitations of claim 1 as described in the rejection above.
Baldoni teaches that the signal generator is controlled to generate the electrical signal (¶[0095], where “if a change in the patient's blood glucose level is detected, the systems, devices, and methods described herein can automatically deliver therapeutic electrical signals”).
Perryman teaches that the signal generator keeps the value of the at least one parameter above a second threshold value that is less than the threshold value (¶[0033], where “The method is performed in which the biomarker is glucose and the level is above about 120 mg/dL, and the electrical stimulation is carried out to excite the C-afferent sensory nerve fibers innervating pancreatic beta cells. The method is performed in which the biomarker is glucose and the level is below about 100 mg/dL, and the electrical stimulation is carried out to inhibit said C-afferent sensory nerve fibers innervating pancreatic beta cells.” Examiner takes the position that the 120 mg/dL and 100 mg/dL values are first and second threshold values, respectively, and that by stimulating based on a higher biomarker that this is equivalent to keeping the parameter above the second threshold value.).
It would have been obvious to one of ordinary skill in the art at the time of the invention to combine the above-described teachings of Perryman, which teaches controlling the signal generator based on a threshold value, with the modified invention of Baldoni in order to maintain the patient’s blood glucose levels within a normal, healthy range (Perryman ¶[0058], where “the C-afferent sensory nerve fibers innervating pancreatic beta cells are either excited or inhibited to promote glucose homeostasis in response to abnormal biomarker levels”).
Regarding claim 4, Baldoni in combination with Esteller, Perryman, Nassif, Jiang, and Kramer teaches all limitations of claim 1 as described in the rejection above.
Baldoni teaches that the at least one parameter comprises a blood glucose level of the patient (¶[0113], where “In block 806, the effects of the therapy on the patient are detected. For example, block 806 can include detecting a serum blood glucose level, at a particular point in time,” ¶[0117], where “By selecting and manipulating the parameters described herein, the disclosed techniques can affect both insulin levels and the patient's glucose storage rates. By controlling both variables, these techniques can more accurately control the patient's blood sugar levels, and therefore more accurately control the patient's T2D”).
Regarding claim 5, Baldoni in combination with Esteller, Perryman, Nassif, Jiang, and Kramer teaches all limitations of claim 4 as described in the rejection above.
Although Baldoni discloses a threshold value between 100 mg/dL and about 175 mg/dL (¶[0091], where “Delivering one or more therapeutic modulation signals described herein to a patient having T2D can maintain the T2D patient's blood glucose levels … between about 100 mg/dL and about 175 mg/dL.” Examiner notes that 7 mmol/L is equivalent to 126 mg/dL.), it does not explicitly teach a threshold of 7mmol/L.
Perryman teaches that the threshold value is 7mmol/L (¶[0033], where “The method is performed in which the biomarker is glucose and the level is above about 120 mg/dL, and the electrical stimulation is carried out to excite the C-afferent sensory nerve fibers innervating pancreatic beta cells.” Examiner notes that 120 mg/dL is equivalent to 6.67 mmol/L and that, by saying “about 120 mg/dL”, that it would be reasonable to round this value to 7 mmol/L.
Additionally, even if 6.67 mmol/L did not meet the requirement of “about 120mg/dL”, Examiner takes the position that, while 6.67 mmol/L lies within the range of 100 mg/dL to 175 mg/dL, and therefore, it would have been obvious to one of ordinary skill in the art as of the filing date of Applicant’s invention to set the threshold value to 7mmol/L because courts have held that claimed ranges that “overlap or lie inside ranges disclosed by the prior art” create a prima facie case of obviousness. In re Wertheim, 541 F.2d 257, 191 USPQ 90 (CCPA 1976).
Regarding claim 6, Baldoni in combination with Esteller, Perryman, Nassif, Jiang, and Kramer teaches all limitations of claim 1 as described in the rejection above.
Kramer teaches that the maximum current value is set to be below the current known to stimulate the ventral root (¶[0045], where “In particular, selective stimulation of tissues, such as the dorsal root, DRG, or portions thereof, exclude stimulation of the ventral root wherein the stimulation signal has an energy below an energy threshold for stimulating a ventral root associated with the target dorsal root while the lead is so positioned”).
It would have been obvious to one of ordinary skill in the art at the time of the invention to combine the above-described teachings of Kramer, which teaches that the maximum current value is set to be below the current known to stimulate the ventral root, with the modified invention of Baldoni in order to prevent inducing side effects for a patient, where indiscriminant stimulation of the ventral root typically causes unpleasant sensations for the patient, such as tingling, buzzing or undesired motions or movements (Kramer ¶[0045]).
Regarding claim 7, Baldoni in combination with Esteller, Perryman, Nassif, Jiang, and Kramer teaches all limitations of claim 1 as described in the rejection above.
Perryman teaches that when the value of the at least one parameter drops below the threshold value, control the signal generator to cease generating the electrical signal (¶[0075], where “The controller can send the signals to increase or decrease stimulation until glucose homeostasis is achieved… The controller can include a microprocessor that can instruct the system to produce an exciting or inhibiting stimulation signal or to cease electrical stimulation”).
It would have been obvious to one of ordinary skill in the art at the time of the invention to combine the above-described teachings of Perryman, which teaches controlling the signal generator based on a threshold value, with the invention of Baldoni in order to maintain the patient’s blood glucose levels within a normal, healthy range (Perryman ¶[0058], where “the C-afferent sensory nerve fibers innervating pancreatic beta cells are either excited or inhibited to promote glucose homeostasis in response to abnormal biomarker levels”).
Regarding claim 8, Baldoni in combination with Esteller, Perryman, Nassif, Jiang, and Kramer teaches all limitations of claim 1 as described in the rejection above.
Jiang teaches that the step-wise current increases value are each 0.05 mA (¶[0019], where “Automatically adjusting may comprise increasing the stimulation amplitude in increments of 0.05 mA for a test stimulation.” Examiner takes the position that increasing the stimulus amplitude by 0.05 mA causes the current value to increase by the same amount since current and amplitude are directly proportional.).
It would have been obvious to one of ordinary skill in the art at the time of the invention to combine the above-described teachings of Jiang, which teaches that the step-wise current increases value are each 0.05 mA, with the modified invention of Baldoni since the use of proportional increases in combination with the automated feature in stimulation amplitude adjusting during test stimulation and/or programming effectively reduces the time required for such activities and allows for easy termination of the stimulation at any time and for any reason, patient safety or otherwise, by the user (Jiang ¶[0019]).
Kramer teaches the maximum current value (¶[0045], where “the stimulation signal has an energy below an energy threshold for stimulating a ventral root associated with the target dorsal root while the lead is so positioned”).
It would have been obvious to one of ordinary skill in the art at the time of the invention to combine the above-described teachings of Kramer, which teaches the maximum current value, with the modified invention of Baldoni in order to prevent inducing side effects for a patient, where indiscriminant stimulation of the ventral root typically causes unpleasant sensations for the patient, such as tingling, buzzing or undesired motions or movements (Kramer ¶[0045]).
Regarding claim 9, Baldoni in combination with Esteller, Perryman, Nassif, Jiang, and Kramer teaches all limitations of claim 1 as described in the rejection above.
Baldoni teaches that the signal generator is controlled to adjust a pulse width of the electrical signal (¶[0036], where “The signal generator is coupleable to an implantable signal delivery device that directs electrical signals to target neural populations of the patient. Representative systems can include other elements as well, for example, one or more devices to program or update the signal delivery parameters in accordance with which the electrical signals are delivered to the patient,” ¶[0053], where “In response to the patient feedback, one or more signal parameters can be adjusted, such as frequency, pulse width, amplitude or delivery location”).
Regarding claim 15, Baldoni in combination with Esteller, Perryman, Nassif, Jiang, and Kramer teaches all limitations of claim 1 as described in the rejection above.
Baldoni teaches that the at least one spinal nerve comprises two spinal nerves on opposite sides of the patient's spinal cord (¶[0034], where “In representative systems and methods, therapeutic modulation signals are directed to the target location that generally includes the patient's spinal cord, e.g., the dorsal column of the patient's spinal cord. The modulation signals can be directed to the dorsal horn, dorsal root, dorsal root ganglion, dorsal root entry zone, and/or other particular areas at or in close proximity to the spinal cord itself … In representative systems and methods, therapeutic modulation signals are directed generally to lamina X of the patient's spinal cord via (1) conduction of the patient's cerebral spinal fluid at the patient's dorsal median sulcus, (2) one or more of laminae I-IX, or (3) both.” Examiner interprets that the spinal nerve comprises two spinal nerves on opposite sides of the patient's spinal cord since the dorsal nerves are bilateral and on each side of a spinal cord.).
Regarding claim 16, Baldoni in combination with Esteller, Perryman, Nassif, Jiang, and Kramer teaches all limitations of claim 15 as described in the rejection above.
Baldoni teaches that the two spinal nerves are at one or more of thoracic levels T7 thru T12 of the patient (¶[0080], where “In representative systems and methods, one or more therapeutic modulation signals can be delivered to a target location proximate to or at one or more of T7 to T12”).
Regarding claim 17, Baldoni in combination with Esteller, Perryman, Nassif, Jiang, and Kramer teaches all limitations of claim 1 as described in the rejection above.
Baldoni teaches a monitoring device configured to continuously provide data (¶[0104], where “Monitoring a patient's blood glucose level can be performed on a continuous basis using one or more sensing elements (referred to herein as a “sensing element”) for detecting neural signals, neural responses, and/or other physiological parameters of the patient before, during and/or after the application of electrical stimulation signals to the patient,” ¶[0105], where “The neural response(s) can be detected frequently enough such that an upward or downward trend of the data corresponding to the blood glucose levels can be determined, or at least estimated”) that enables the at least one processor to monitor the value of the at least one parameter (¶[0104], which teaches that the sensing element monitors the value of the patient’s blood glucose level on a continuous basis).
Regarding claim 18, Baldoni in combination with Esteller, Perryman, Nassif, Jiang, and Kramer teaches all limitations of claim 17 as described in the rejection above
Baldoni teaches the data comprises the value of the at least one parameter (¶[0104], where “Monitoring a patient's blood glucose level can be performed on a continuous basis using one or more sensing elements … for detecting neural signals, neural responses, and/or other physiological parameters of the patient”).
Regarding claim 19, Baldoni in combination with Esteller, Perryman, Nassif, Jiang, and Kramer teaches all limitations of claim 17 as described in the rejection above
Baldoni teaches the at least one processor processes the data to determine the value of the at least one parameter (Figure 8, Step 808 “Can the therapy be improved?” and Step 810 “Establish updates,” ¶[0115], where “the patient can use a constant glucose monitor that continuously monitors the patient's blood glucose level and communicates the measurements to an internal or external processor (e.g., an implanted pulse generator, or a phone-based app or other external device) … In any of these representative systems and methods, the system can automatically determine whether or not to change the signal parameters at block 808, and can automatically establish proposed updates at block 810”).
Regarding claim 20, see the rejection of claim 1 above, which comprises substantially the same subject matter. However, claim 20 adds “An implantable device for treating metabolic syndrome”.
Baldoni teaches an implantable device for treating metabolic syndrome (¶[0044], where “FIG. 1A schematically illustrates a representative patient therapy system 100 for treating a patient's blood glucose abnormalities (e.g., T2D or metabolic syndrome), arranged relative to the general anatomy of the patient's spinal column 191. The system 100 can include a signal generator 101 (e.g., an implanted or implantable pulse generator or IPG), which may be implanted subcutaneously within a patient 190 and coupled to one or more signal delivery elements or devices 110”).
Claim 14 is rejected under 35 U.S.C. 103 as being unpatentable over Baldoni in view of Esteller, Perryman, Nassif, Jiang, and Kramer as applied to the rejection of claim 1 above, and further in view of Dalal et al. (hereinafter “Dalal”) (U.S. Pub. No. 2008/0004672 A1) .
Regarding claim 14, Baldoni in combination with Esteller, Perryman, Nassif, Jiang, and Kramer teaches all limitations of claim 1 as described in the rejection above.
Baldoni teaches that stimulating the at least one dorsal root ganglion with the electrical signal (¶[0034], where “therapeutic modulation signals are directed to the target location that generally includes the patient's spinal cord, e.g., the dorsal column of the patient's spinal cord. The modulation signals can be directed to the dorsal horn, dorsal root, dorsal root ganglion, dorsal root entry zone, and/or other particular areas at or in close proximity to the spinal cord itself”) inhibits sympathetic nerve activity to the patient's kidney(s) (¶[0031], where “The therapeutic effect can be produced by inhibiting, suppressing, downregulating, blocking, preventing, and/or otherwise modulating the activity of the affected and/or target neural population … the affected neural population is located within, proximate to, or otherwise corresponds to the patient's sympathetic nervous system … inhibiting at least a portion of the patient's sympathetic nervous system, such as one or more sympathetic nerves corresponding to one or more of the patient's … kidney(s)”).
Although Baldoni teaches inhibiting sympathetic nerve activity to the patient's kidney(s), none of Baldoni, Esteller, Perryman, Nassif, Jiang, nor Kramer explicitly teach that inhibition of the sympathetic nerve activity to the patient's kidney(s) causes an increase in urinary excretion by the kidney(s).
Dalal teaches a glucose control input, a low physical activity input, and a diabetic therapy delivery system adapted to respond to the glucose control input and the low physical activity input to deliver diabetic therapy (Abstract), and further teaches that inhibition of the sympathetic nerve activity to the patient's kidney(s) causes an increase in urinary excretion by the kidney(s) (¶[0046], where “Stimulating the parasympathetic nervous system (inhibiting the sympathetic nervous system) … increases urine secretion”).
It would have been obvious to one of ordinary skill in the art at the time of the invention to combine the above-described teachings of Dalal, which teaches that inhibition of the sympathetic nerve activity to the patient's kidney(s) causes an increase in urinary excretion by the kidney(s), with the modified invention of Baldoni since stimulation of the vagus nerve, which is a part of the parasympathetic nervous system, may promote the release of insulin into the patient's system which may be beneficial for their diabetic control (Dalal ¶[0026]).
Conclusion
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/SEFRA D. MANOS/Examiner, Art Unit 3792
/UNSU JUNG/Supervisory Patent Examiner, Art Unit 3792