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 .
Response to Arguments
Applicant’s arguments, see Remarks, pg. 6-8, filed 07/28/2026, with respect to the rejection(s) of claims 1-20 under 35 USC 102 and 35 USC 103 have been fully considered and are persuasive. Therefore, the rejection has been withdrawn. However, upon further consideration, a new ground(s) of rejection is made (see detailed rejection below).
Claim Rejections - 35 USC § 103
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, 3-7, 11, 13, 15 and 18-20 is rejected under 35 U.S.C. 103 as being unpatentable over Hershey et al. (US 20170143972 A1), Phillips (US 20220008728 A1), and Wu et al. (US 20110196446 A1, “Wu”).
Regarding independent claim 1, Hershey teaches a method of optimizing neural therapy for neuroimmune system function (Abstract: " a system for modulating neuroinflammation at a tissue site"), the method comprising: delivering a neural therapy to a patient (Abstract: "The control circuit may be configured to control the delivery of the neuromodulation.") by: determining a post-neuromodulation level of one or more biomarkers in the patient (para. [0020]: "sensing a biomarker parameter, and adjusting the neuromodulation parameter set using the biomarker parameter. The biomarker parameter may be a measure of a biomarker or a measure of a derivative of the biomarker. The biomarker may be indicative of neuroinflammation at the tissue site."), wherein the level of the one or more biomarkers directly or indirectly correlates with neuroimmune system function (para. [0020]: "The biomarker may be indicative of neuroinflammation at the tissue site."); comparing a measure of the post-neuromodulation level of the one or more biomarkers to a threshold (para. [0088]: "the reference value or value range represents a threshold indicative of a need for treating neuroinflammation, and the outcome of the comparison indicates such a need. In one example, the reference value or value range represents a degree of neuroinflammation, and the outcome of the comparison indicates an intensity of the neuromodulation needed for treating the neuroinflammation at the indicted degree." The reference value is a threshold and the degree of neuroinflammation is a biomarker.); finding that the threshold is crossed, and in response, adjusting a neural therapy setting (para. [0080]: "…comparison indicates an intensity of the neuromodulation needed for treating the neuroinflammation at the indicated degree."; this demonstrates that the intensity of neuromodulation is determined by the reference (threshold) comparison.). However, Hershey does not teach measuring electrical signals from the patient's brain to determine an intrinsic gamma frequency of the patient; and issuing electrical pulses at a repetition rate determined from the intrinsic gamma frequency of the patient.
Phillips, in the same field of endeavor of brain stimulation, discloses a method for providing stimulation where the parameters are set to influence resonant properties of the brain. Phillips discloses the steps of: measuring electrical signals from the patient's brain to determine an intrinsic gamma frequency of the patient (para. [0012]: “In some embodiments, the method further includes recording an EEG between the subcranial electrode and the subcutaneous electrode; and determining the intrinsic frequency of neuronal firing in the specified EEG band using the recorded EEG.”); and issuing electrical pulses at a repetition rate determined from the intrinsic gamma frequency of the patient (para. [0023]: “…a generator disposed within the case and in electrical communication with the processor, the generator being adapted to adjust and deliver a current pulse waveform to the first electrode and the second electrode to move a Q-factor of the intrinsic frequency of neuronal firing in the specified EEG band of the subject towards a preselected Q-factor of the intrinsic frequency.”; para. [0025]: “In some embodiments, a pulse frequency of the waveform is equal to the intrinsic frequency of neuronal firing in the specified EEG band of the subject.”; para. [0063]: “The device can be configured to record EEG and automatically determine the intrinsic frequency from the EEG recording and specify the pulse frequency, pulse amplitude, pulse shape, pulse width, or pulse duty cycle, and other parameters. The recorded EEG may also be transmitted wirelessly to an external module, such as a mobile device running a software application, where the software application determines the intrinsic frequency and specifies the pulse frequency, pulse amplitude, pulse shape, pulse width, or pulse duty cycle, and other parameters, and transmits the parameters to the device.).
It would have been obvious for one of ordinary skill in the art before the effective filing date of the claimed invention to modify the method of Hershey to include Phillips’s method of intrinsic frequency measurement and electric pulse delivery based on the measured intrinsic frequency. One of ordinary skill would recognize that measuring an intrinsic frequency is a known technique for recording a baseline brain frequency before stimulation is provided. One would also recognize that issuing stimulation at a rate determined by an intrinsic frequency is useful in moving a Q factor closer to that of a healthy population (see Phillips para. [0053]). One would recognize that the method of Phillips would improve the efficacy in treating a range of brain disorders. Thus, it would have been obvious to implement the methods of Phillips in the method of Hershey.
However, neither reference discloses that the intrinsic frequency is a gamma frequency.
Wu, in the same field of endeavor of brain stimulation, discloses a technique for reestablishing gamma frequency band activity within brain of a patient. Wu disclose a method that includes selecting a frequency within a gamma frequency band and stimulating at a frequency greater than the selected frequency band (abstract: “In one example, the disclosure is directed to a method that includes selecting a frequency within a gamma frequency band and delivering electrical stimulation at a frequency greater than the selected frequency.”)
It would have been obvious to one of ordinary skill in the art before the effective filing date of the claimed invention to modify the method of Hershey to perform measurements of intrinsic gamma frequency bands and to issue pulses at a measured gamma frequency. Wu discloses that it is desirable to increase gamma frequency activity since gamma frequency band activity facilitates movement and cognitive states (see Wu para. [0025]). Therefore, it would have been obvious to one of ordinary skill to measure the gamma frequency and deliver signals within this range to improve impaired cognitive and movement function in the brain.
Regarding claim 3, Hershey, in combination with Phillips and Wu, discloses the method of claim 1 (see above). Hershey further discloses wherein the measure is an amplitude of the biomarker (para. [0051]: "In various examples, the biomarker parameter is indicative the presence and/or amount of a biomarker in the tissue site, such as a concentration of the biomarker at the tissue site"), and the threshold is a patient specific reference for the biomarker (para. [0087]: "In one example, the reference value or value range can be a previously sensed value of the corresponding biomarker parameter."; A “previously sensed value” would mean that it is specific to the patient when the biomarker was previously sensed.)
Regarding claim 4, Hershey, in combination with Phillips and Wu, discloses the method of claim 1 (see above). Hershey further discloses wherein the measure is a trend of the biomarker (para. [0005]: "The biomarker parameter may include a measure of a biomarker or a measure of a derivative of the biomarker. The biomarker may be indicative of the neuroinflammation at the tissue site." The biomarker is a trend of inflammation).
Regarding claim 5, Hershey, in combination with Phillips and Wu, discloses the method of claim 1 (see above). Hershey further discloses wherein the step of delivering a neural therapy to the patient is performed by issuing, from an implanted device, electrical stimuli (para. [0056]: "Lead system 214 including electrodes 216 is one example of stimulation delivery device 314 when electrical stimuli are used for the neuromodulation. In various examples, stimulation delivery device 314 can be configured to deliver electrical, magnetic, optical, acoustic, chemical, pharmacological, and/or any other forms of stimuli.") to a neural, glial, and/or immune structures of the patient (para. [0046]: "Metrics that quantify neuroinflammation can be used to determine optimal stimulation targets and parameters for the neuromodulation"; The disclosed methods are used to determine optimal neurostimulation parameters and treatments for neuroinflammation (immune responses). Thus, the stimulation is targeted to a neural, glial, and/or immune structure.)
Regarding claims 6 and 7, Hershey, in combination with Phillips and Wu, discloses the method of claim 1 (see above). Hershey further discloses wherein the step of determining a post-neuromodulation level of one or more biomarkers comprises collecting or analyzing bodily fluid in-situ (para. [0044]: "Cerebrospinal fluid (CSF) levels of TSPO can be detected using an implantable sensor system to determine a surrogate measure of pain intensity. In an example, TSPO levels at a tissue site can be detected using an implantable sensor system, and the detected level of TSPO at the tissue site can be used a surrogate for pain intensity of the patient.”), wherein the bodily fluid is one of interstitial fluid, blood, cerebrospinal fluid, or intrathecal fluid. (para. [0046]: "Examples of a biomarker can include a neuroinflammatory measure that quantifies microglial activation at a tissue site; cytokine concentration in the cerebrospinal fluid (CSF).").
Regarding claim 11, Hershey, in combination with Phillips and Wu, discloses the method of claim 1 (see above). Hershey further discloses wherein the step of delivering a neural therapy to the patient comprises issuing an optical modulation signal to neural tissue of the patient. (para. [0048]: " In one example, the neuromodulation device 104 is configured to deliver neuromodulation energy in the form of light, such as using an optical stimulator (e.g., an optical emitter or an optical modulator).")
Regarding independent claim 13, Hershey teaches a system for optimizing neural therapy for neuroimmune system function (Abstract: “a system for modulating neuroinflammation at a tissue site in a patient”), the system comprising: an implantable pulse generator (para. [0067]: ". The implantable system 508, illustrated as being implanted in the patient's body, includes an implantable neuromodulation device (also referred to as an implantable pulse generator, or IPG).") housing output circuity configured to issue a neural therapy (para. [0069]: "An implantable device may include an outer case for housing the electronic and other components. The outer case may be composed of an electrically conductive, biocompatible material, such as titanium, that forms a hermetically-sealed compartment wherein the internal electronics are protected from the body tissue and fluids. In some cases, the outer case may serve as an electrode (e.g. case electrode)."); a sensor for sensing a level one or more biomarkers in the patient (para. [0008]: "In Example 4, the subject matter of any one or any combination of Examples 1-3 may optionally be configured to further include a biomarker sensor configured to sense the biomarker parameter."); a controller (para. [0070]: "The implanted device may include electronic components, such as a controller/processor (e.g., a microcontroller)."), the controller configured to: instruct the output circuitry to issue a first neural therapy (para. [0082]: "The implanted device may include electronic components, such as a controller/processor (e.g., a microcontroller).")by: instruct the sensor to measure a post-neuromodulation level of the one or more biomarkers following issuance of the first neural therapy by the implantable pulse generator (para. [0051]: "The one or more biomarker sensors 110 can each be configured for sensing one or more biomarker parameters associated with a tissue site. The biomarker parameters can each include a measure of the biomarker or a measure of a derivative of the biomarker."); compare the post-neuromodulation level of the one or more biomarkers to a threshold (para. [0006]: " In Example 2, the subject matter of Example 1 may optionally be configured such that the control circuit is configured to compare the biomarker parameter to a reference value and to adjust the neuromodulation parameter set using an outcome of the comparison."); and instruct the output circuitry to issue a second neural therapy if the threshold is crossed by the post-neuromodulation level of the one or more biomarkers (para. [0075]: " For example, a first electrical field can be generated by the electrodes (using a first current fractionalization) during a first electrical pulse of the pulsed waveform, a second different electrical field can be generated by the electrodes (using a second different current fractionalization) during a second electrical pulse of the pulsed waveform."; The device adjusts electric fields in response to the biomarker. The reference to a "second different electrical field" is reference to adjustment from the first electric field after measuring biomarker data."; Fig. 9; 908 is a comparison to a reference value (threshold) and 910 is adjusting to a second therapy based on if the threshold is met or not; para. [0088]: “At 910, the neuromodulation parameter set are adjusted using an outcome of the comparison. In one example, the reference value or value range represents a threshold indicative of a need for treating neuroinflammation, and the outcome of the comparison indicates such a need. In one example, the reference value or value range represents a degree of neuroinflammation, and the outcome of the comparison indicates an intensity of the neuromodulation needed for treating the neuroinflammation at the indicted degree.”). However, Hershey does not teach measuring electrical signals from the patient's brain to determine an intrinsic gamma frequency of the patient; and issuing electrical pulses at a repetition rate determined from the intrinsic gamma frequency of the patient.
Phillips, in the same field of endeavor of brain stimulation, discloses a method for providing stimulation where the parameters are set to influence resonant properties of the brain. Phillips discloses the steps of: measuring electrical signals from the patient's brain to determine an intrinsic gamma frequency of the patient (para. [0012]: “In some embodiments, the method further includes recording an EEG between the subcranial electrode and the subcutaneous electrode; and determining the intrinsic frequency of neuronal firing in the specified EEG band using the recorded EEG.”); and issuing electrical pulses at a repetition rate determined from the intrinsic gamma frequency of the patient (para. [0023]: “…a generator disposed within the case and in electrical communication with the processor, the generator being adapted to adjust and deliver a current pulse waveform to the first electrode and the second electrode to move a Q-factor of the intrinsic frequency of neuronal firing in the specified EEG band of the subject towards a preselected Q-factor of the intrinsic frequency.”; para. [0025]: “In some embodiments, a pulse frequency of the waveform is equal to the intrinsic frequency of neuronal firing in the specified EEG band of the subject.”; para. [0063]: “The device can be configured to record EEG and automatically determine the intrinsic frequency from the EEG recording and specify the pulse frequency, pulse amplitude, pulse shape, pulse width, or pulse duty cycle, and other parameters. The recorded EEG may also be transmitted wirelessly to an external module, such as a mobile device running a software application, where the software application determines the intrinsic frequency and specifies the pulse frequency, pulse amplitude, pulse shape, pulse width, or pulse duty cycle, and other parameters, and transmits the parameters to the device.).
It would have been obvious for one of ordinary skill in the art before the effective filing date of the claimed invention to modify the device and methods of Hershey to include Phillips’s device and method of intrinsic frequency measurement and electric pulse delivery based on the measured intrinsic frequency. One of ordinary skill would recognize that measuring an intrinsic frequency is a known technique for recording a baseline brain frequency before stimulation is provided. One would also recognize that issuing stimulation at a rate determined by an intrinsic frequency is useful in moving a Q factor closer to that of a healthy population (see Phillips para. [0053]). One would recognize that the method of Phillips would improve the efficacy in treating a range of brain disorders. Thus, it would have been obvious to implement the methods of Phillips in the method of Hershey.
However, neither reference discloses that the intrinsic frequency is a gamma frequency.
Wu, in the same field of endeavor of brain stimulation, discloses a technique for reestablishing gamma frequency band activity within brain of a patient. Wu disclose a method that includes selecting a frequency within a gamma frequency band and stimulating at a frequency greater than the selected frequency band (abstract: “In one example, the disclosure is directed to a method that includes selecting a frequency within a gamma frequency band and delivering electrical stimulation at a frequency greater than the selected frequency.”)
It would have been obvious to one of ordinary skill in the art before the effective filing date of the claimed invention to modify the method of Hershey to perform measurements of intrinsic gamma frequency bands and to issue pulses at a measured gamma frequency. Wu discloses that it is desirable to increase gamma frequency activity since gamma frequency band activity facilitates movement and cognitive states (see Wu para. [0025]). Therefore, it would have been obvious to one of ordinary skill to measure the gamma frequency and deliver signals within this range to improve impaired cognitive and movement function in the brain.
Regarding claim 15, Hershey, in combination with Phillips and Wu, discloses the system of claim 13 (see above). Hershey further discloses wherein the controller is housed in the implantable pulse generator and the sensor is separate from the implantable pulse generator, and communicates with the controller (para. [0176]: "Some embodiments may provide a system including a passive implanted lead including both a sensor providing input to a handheld patient controller (e.g. patient instruction to begin therapy) or providing input to a wearable pulse generator."; The sensor is separate from the IPG in that the sensor does not have the IPG’s pulse generating function (and the IPG does not have the sensor’s sensing function) and provides input to the pulse generator via communication with the controller. The controller provides input to the pulse generator to control stimulation (they are in communication.).)
Regarding claim 18, Hershey, in combination with Phillips and Wu, discloses the system of claim 13 (see above). Hershey further discloses wherein the neural therapy comprises electrical pulses (para. [0047]: "neuromodulation as discussed in this document may use electrical, magnetic, optical, acoustic, chemical, pharmacological, and/or any other forms of energy or modality to modulate neural activities. While a system for neuromodulation using electrical pulses and/or light is specifically discussed as examples in this document…").
Regarding claim 19, Hershey, in combination with Phillips and Wu, discloses the system of claim 13 (see above). Hershey further discloses a lead coupled to the pulse generator (para. [0058]: " Stimulation delivery device 314 can include one or more of lead and/or electrodes such as lead system 214 to deliver electrical stimuli such as electrical pulses…"; The lead system is coupled to a pulse generator since para. [0058] discloses that the stimulation delivery device delivers pulses.) and adapted to extend from the pulse generator to target neural tissue, wherein the lead comprises one or more electrodes (Fig. 8; para. [0080]: “FIG. 8 illustrates a schematic view of an example of the neuromodulation lead 802 showing an example of the fractionalization of the anodic current delivered to the electrodes on the neuromodulation lead.”) for outputting electrical pulses (para. [0048]: “The neuromodulation parameter set can include one or more neuromodulation parameters, such as a neuromodulation parameter specifying an aspect of the electrical pulses or a selection of electrodes through which each of the electrical pulses is delivered.”).
Regarding claim 20, Hershey, in combination with Phillips and Wu, discloses the system of claim 13 (see above). Hershey further discloses wherein the neural therapy comprises optical signals. (para. [0048]: " In one example, the neuromodulation device 104 is configured to deliver neuromodulation energy in the form of light, such as using an optical stimulator (e.g., an optical emitter or an optical modulator).").
Claim 2 is rejected under 35 U.S.C. 103 as being unpatentable over Hershey et al. (US 20170143972 A1), Phillips (US 20220008728 A1), Wu et al. (US 20110196446 A1, “Wu”), and Wang et al. (“Design and Analysis of Biomarker-Integrated Clinical Trials with Adaptive Threshold Detection and Flexible Patient Enrichment”; Published November 1, 2020).
Regarding claim 2, Hershey, in combination with Phillips and Wu, discloses the method of claim 1 (see above). Hershey further discloses wherein the measure is an amplitude of the biomarker (para. [0051]: "In various examples, the biomarker parameter is indicative the presence and/or amount of a biomarker in the tissue site, such as a concentration of the biomarker at the tissue site"). However, Hershey does not expressly teach where a threshold is a population-based threshold for normal levels of the one or more biomarkers.
Wang, in the same field of endeavor of using biomarkers to optimize therapy effectiveness, discloses an adaptive threshold detection for biomarkers. Wang discloses where a threshold is a population-based threshold for normal levels of the one or more biomarkers (Summary: "We propose a new adaptive threshold detection and enrichment design in which the biomarker threshold is adaptively estimated and updated by optimizing a trade-off between the size of the biomarker positive population and the magnitude of the treatment effect in that population."; introduction: "optimizing treatment.").
It would have been obvious for one of ordinary skill in the art before the effective filing date of the claimed invention to include the population-based threshold for normal levels of biomarkers, as disclosed by Wang, with the method of claim 1, as disclosed by Hershey. One of ordinary skill in the art would recognize that a threshold could be determined for a biomarker using population-based thresholds. Using a population sample would allow the determination of a “normal” level to be based off more than the individual’s biomarker levels, which would improve threshold accuracy. Therefore, implementing this method into the method of claim 1 would have been an obvious improvement.
Claim 8 is rejected under 35 U.S.C. 103 as being unpatentable over Hershey et al. (US 20170143972 A1), Phillips (US 20220008728 A1), Wu et al. (US 20110196446 A1, “Wu”), and Kim et al. ("Pharmacological Inhibition of Spleen Tyrosine Kinase Suppressed Neuroinflammation and Cognitive Dysfunction in LPS-Induced Neurodegeneration Model"; Published May 28, 2022).
Regarding claim 8, Hershey, in combination with Phillips and Wu, discloses the method of claim 1 (see above). However, Hershey does not expressly teach wherein one of the one or more biomarkers is spleen tyrosine kinase.
Kim, concerned with the common problem of correlating a biomarker to neuroinflammation, discloses a method for determining a correlation between neuroinflammation and spleen tyrosine kinase. Kim discloses wherein one of the one or more biomarkers is spleen tyrosine kinase. (Abstract: "Tyrosine-protein kinase (Syk) plays a potential role in neuroinflammation and adaptive immune responses in several neurodegenerative conditions." ; Introduction, para. (5): "Our results indicated that Syk inhibition reduced LPS-induced microglia activation and thereby promoted neuronal survival and recovered cognitive dysfunction. These findings suggest that Syk inhibition may be a promising therapeutic target for neuroinflammation-mediated neurodegeneration (Figure 1A)."); Kim demonstrates that tyrosine kinase inhibition plays affects neuroinflammation, and using this as biomarker would indicate the level of neuroinflammation. (provides feedback on the efficacy of treatment.)
It would have been obvious for one of ordinary skill in the art before the effective filing date of the claimed invention to use spleen tyrosine kinase as the biomarker for neuroinflammation, as disclosed by Kim. Kim discloses the correlation between spleen tyrosine kinase and neuroinflammation. One of ordinary skill in the art would recognize that this could be used as the biomarker in the method of claim 1, as disclosed by Hershey, with a reasonable expectation that spleen tyrosine kinase would successfully indicate inflammation levels. Therefore, it would have been obvious to include this specific biomarker in the method of claim 1.
Claims 9 and 10 are rejected under 35 U.S.C. 103 as being unpatentable over Hershey et al. (US 20170143972 A1), Phillips (US 20220008728 A1), Wu et al. (US 20110196446 A1, “Wu”), and Krashia et al. ("Blunting neuroinflammation with resolvin D1 prevents early pathology in a rat model of Parkinson’s disease"; Published September 2, 2019).
Regarding claims 9 and 10, Hershey, in combination with Phillips and Wu, discloses the method of claim 1 (see above). However, Hershey does not expressly teach wherein the one or more biomarkers is Resolvin D1 (claim 9); wherein the one or more biomarkers are selected from pro-inflammatory mediators, anti-inflammatory mediators, immune cells, or a Resolvin compound. (claim 10).
Krashia, in the same field of endeavor of using biomarkers to link neuroinflammation, discloses a study with methods for determining biomarkers linked to neuroinflammation in patients with Parkinson’s disease. Krahsia discloses wherein one or more biomarkers is Resolvin D1 (claim 9) (Pg. 2, para. 2: "We also provide evidence for a strong link between α-syn overexpression and neuroinflammation, showing a reduction of resolvin D1 (RvD1), a specific pro-resolving mediator.") ("Blunting neuroinflammation with resolvin D1 prevents early pathology in a rat model of Parkinson’s disease"); and wherein one or more biomarkers are selected from pro-inflammatory mediators, anti-inflammatory mediators, immune cells, or a Resolvin compound. (claim 10) (Abstract: "Recent studies link chronic inflammation with failure to resolve early inflammation, a process operated by specialized pro resolving mediators, including resolvins.").
It would have been obvious for one of ordinary skill in the art before the effective filing date of the claimed invention to use Resolvin D1 and pro resolving mediators, such as resolvins, as the biomarker in the method of claim 1. Krashia discloses that these specific biomarkers are indicative of neuroinflammation. One of ordinary skill would recognize that Resolvin would indicate neuroinflammation successfully. Thus, it would have been obvious to include resolving as the biomarker in the method of claim 1.
Claims 16 and 17 is/are rejected under 35 U.S.C. 103 as being unpatentable over Hershey et al. (US 20170143972 A1) ), Phillips (US 20220008728 A1), Wu et al. (US 20110196446 A1, “Wu”), and Bokil (US 20180289967 A1).
Regarding claims 16 and 17, Hershey, in combination with Phillips and Wu, discloses the system of claim 13 (see above). However, Hershey does not expressly teach wherein the controller is in an external device having communication circuitry for communicating with the implantable pulse generator (claim 16); and, wherein the sensor is part of the external device (claim 17).
Bokil discloses wherein a controller (para. [0044]: “remote control 16”) is in an external device having communication circuitry for communicating with the implantable pulse generator (claim 16)(para. [0044]: "The RC 16 may be used to telemetrically communicate with or control the IPG 14 or ETS 20 via a wireless communications link 32. Once the IPG 14 and neurostimulation leads 12 are implanted, the RC 16 may be used to telemetrically communicate with or control the IPG 14 via communications link."); and, wherein the sensor is part of the external device (claim 17) (para. [0074]: "An example of the biomarker sensing circuit 606 is an external or subdural electroencephalogram (EEG) sensor, and may include depth electrodes such as DBS electrodes." The EEG is external the IPG).
It would have been obvious for one of ordinary skill in the art before the effective filing date of the claimed invention to configure the controller, implantable pulse generator, and controller in the arrangement as disclosed by Bokil with communication with the implantable pulse generator. By modifying the system with this configuration, one could communicate between the sensor, controller, and pulse generator to adjust stimulation pulses based on the sensor. It is also noted by the examiner that regardless of whether Bokil discloses the limitations above, one of ordinary skill in the art would have found the particular arrangement between the sensor, pulse generator, and controller to be an obvious matter of design choice since moving the controller internally or externally does not change that the sensor would communicate to the controller and be used to adjust the IPG pulses/stimulation (See MPEP 2144.04(VI)(C); In re Japikse, 181 F.2d 1019, 86 USPQ 70 (CCPA 1950); In re Kuhle, 526 F.2d 553, 188 USPQ 7 (CCPA 1975)). Therefore, the arrangement of components in claims 16 and 17 are not distinguishable from art that teaches a controller adjusting IPG pulses with measurements from a sensor.
Claims 14 is rejected under 35 U.S.C. 103 as being unpatentable over Hershey et al. (US 20170143972 A1), Phillips (US 20220008728 A1), Wu et al. (US 20110196446 A1, “Wu”), and Caparso et al. (US 20100211135 A1, “Caparso”).
Regarding claim 14, Hershey, in combination with Phillips and Wu, discloses the system of claim 13 (see above). However, Hershey does not expressly teach wherein the implantable pulse generator includes the sensor and the controller.
Caparso, in the same field of endeavor of therapy systems for delivering neural therapy, discloses a system with an implantable pulse generator, control, and sensor. Caparso discloses wherein an implantable pulse generator includes the sensor and the controller (para. [0012]: "Several embodiments of the disclosure are directed to spinal cord stimulation devices (e.g., implantable pulse generators) that have an embedded control algorithm configured to monitor one or more physiological or physical signals from one or more sensors. The sensors can be inside or outside of the implantable device e.g. a spinal cord stimulation device.").
It would have been obvious for one of ordinary skill in the art before the effective filling date of the claimed invention to configure the controller and sensor in the implantable pulse generator, as disclosed by Caparso, with the device of claim 13, as disclosed by Hershey. One of ordinary skill in the art recognizes that including the controller and sensor together in the pulse generator would be advantageous in that the sensor circuitry, control circuitry, and pulse generator could be coupled together. It would have been obvious to include this advantage in the system of claim 1. Further, it is noted by the Examiner that regardless of whether Caparso discloses the limitations above, one of ordinary skill in the art would have found the particular arrangement between the sensor, pulse generator, and controller to be an obvious matter of design choice since moving the controller internally or externally does not change that the sensor would communicate to the controller and be used to adjust the IPG pulses/stimulation (See MPEP 2144.04(VI)(C); In re Japikse, 181 F.2d 1019, 86 USPQ 70 (CCPA 1950); In re Kuhle, 526 F.2d 553, 188 USPQ 7 (CCPA 1975)). Therefore, the arrangement of components in claim 14 are not distinguishable from art that teaches a controller adjusting IPG pulses with measurements from a sensor.
Conclusion
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/O.L.M./Examiner, Art Unit 3796
/ALLEN PORTER/Primary Examiner, Art Unit 3796
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