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 .
Election/Restrictions
Applicant’s election without traverse of Claims 1-15 and 17-20 in the reply filed on 6/16/2026 is acknowledged.
Specification
The disclosure is objected to because of the following informalities: the Present Specification states at Pg. 12, Para. [0070] “The present subject matter provides a system for treating epilepsy that less invasive…” but should recite -- The present subject matter provides a system for treating epilepsy that is less invasive…--. Appropriate correction is required.
Claim Interpretation
The Examiner notes that the breadth of Independent Claim 1 suggests that it first recites performing spinal cord stimulation in a well known manner (i.e., “using a set of electrodes epidurally positioned adjacent to a spinal cord or dorsal column nuclei and a stimulation configuration to deliver neuromodulation energy…”), and proceeds to recite the specific biological anatomy that facilitates a particular effect (i.e., the effect of “treating a patient with epileptic seizures” is achieved via “deliver[ing] neuromodulation” “to at least one neural target,” which neural target is subsequently defined in terms of its anatomy). Independent Claim 17 is being interpreted similarly, as are several dependent claims (i.e., Claims 2 and 7-10) which further limit the “neural target” it terms of its anatomy. This is not problematic in-and-of itself, and indeed further limits the claim to a certain extent. However, the Examiner makes the foregoing note in the interest of clarity of record and compact prosecution as this interpretation is considered relevant to the foregoing rejection.
The Examiner further notes that this interpretation is consistent with Paras. [0070] through [0071] of the Present Specification, which describe the pertinent anatomy.
Claim Rejections - 35 USC § 112
The following is a quotation of 35 U.S.C. 112(b):
(b) CONCLUSION.—The specification shall conclude with one or more claims particularly pointing out and distinctly claiming the subject matter which the inventor or a joint inventor regards as the invention.
The following is a quotation of 35 U.S.C. 112 (pre-AIA ), second paragraph:
The specification shall conclude with one or more claims particularly pointing out and distinctly claiming the subject matter which the applicant regards as his invention.
Claims 4 and 18 are rejected under 35 U.S.C. 112(b) or 35 U.S.C. 112 (pre-AIA ), second paragraph, as being indefinite for failing to particularly point out and distinctly claim the subject matter which the inventor or a joint inventor (or for applications subject to pre-AIA 35 U.S.C. 112, the applicant), regards as the invention.
Regarding Claim 4, Claim 4 recites “wherein the epileptic seizures include a first symptom at a first location and a second symptom at a second location, and a first target is based on the first location where the patient experiences the first symptom, and a second target is based on the second location where the patient experiences the second symptom.” It is unclear whether the “a first target” and “a second target” somehow relate to the “at least one neural target in or near the spinal cord” of Claim 1, whether the two are different targets, or something else. It is unclear in what sense Claim 4 further limits Claim 1.
For purposes of this Office Action, Claim 4 is being interpreted to mean that the method is generally amenable to such treatment of two symptoms via stimulating two targets, without respect to the “at least one neural target in or near the spinal cord” of Claim 1.
The Examiner notes that if Claim 4 is intended to further limit the “neural target” of Claim 1, amendments making clarification to that effect may present written description issues under 35 USC 112(a), depending on their phrasing. The pertinent targeting appears to be addressed at Paras. [0082] through [0083] and [00117] through [00120] of the Present Specification, from which it appears that stimulation parameters are modulated such that a desired neural target preferentially receives suitable stimulation relative to others. However, apart from a verbatim recitation of Claim 4 at Para. [0023], the term “symptom” appears in the relevant context within the Present Specification only at Para. [0087], where alteration of stimulation settings “until an optimal, desired, or acceptable patient clinical response is achieved” is described.
While the Examiner’s current interpretation avoids written description issues under 35 USC 112(a), an amendment describing the “first target” and “second target” in anatomical terms similar to that of the “at least one neural target” of Claim 1 without sufficient link to the manner of targeting noted above might not.
Regarding Claim 18, Claim 18 contains a similar limitation to that addressed above with respect to Claim 4, and is indefinite for the same reasons.
Claim 18 is being interpreted similarly to Claim 4.
Claim Rejections - 35 USC § 102
The following is a quotation of the appropriate paragraphs of 35 U.S.C. 102 that form the basis for the rejections under this section made in this Office action:
A person shall be entitled to a patent unless –
(a)(1) the claimed invention was patented, described in a printed publication, or in public use, on sale, or otherwise available to the public before the effective filing date of the claimed invention.
Claims 1-3, 5, 7, 8, 10, 11 and 17 are rejected under 35 U.S.C. 102(a)(1) as being anticipated by HARREBY, KRISTIAN, "The Effect of Spinal Cord Stimulation on Seizure Susceptibility in Rats", Neuromodulation, Volume 14, Issue 2, pages. 111 116, (2011), 6 pages1 (“Harreby”) as evidenced by wikipedia.org, "Somatotopic arrangement," accessed online 7/28/2026 via https://en.wikipedia.org/wiki/Somatotopic_arrangement#cite_note-2 (“Somatotopic Arrangement NPL”), C. Hodge et al., "The spinothalamic tract," Neurobiology, Vol. 5, Issue 4, Pg. 363-397, 1990 (“Hodge”), Miller J. et al., "Parameters of Spinal Cord Stimulation and Their Role in Electrical Charge Delivery: A Review," Neuromodulation, 19, 373-384, June 2016 (“Miller”), and Science Direct, "Gracile Fasciculus" Overview, accessed online via https://www.sciencedirect.com /topics/neuroscience/gracile-fasciculus on 7/29/2026 (“Gracile Fasciculus NPL”).
Regarding Independent Claim 1, Harreby discloses:
A method for treating a patient with epileptic seizures, comprising: (Abstract, Objectives Section, “We investigated the effect of SCS on seizure susceptibility….”);
using a set of electrodes epidurally positioned adjacent to a spinal cord or dorsal column nuclei (Pg. 112, Left Column, Second Paragraph, “The cervical vertebrae (C) were exposed…. a custom-made bipolar SCS electrode … was inserted in the dorsal epidural space of C2.”);
Harreby’s placement “in the dorsal epidural space of C2” is “adjacent to a spinal cord.”
and a stimulation configuration to deliver neuromodulation energy to at least one neural target in or near the spinal cord, (Abstract, “Spinal cord stimulation (SCS) activates the thalamus…. We investigated the effect of SCS on seizure susceptibility…. Tonic-clonic seizures were induced…. SCS was started…. Seizure susceptibility was accessed….”);
Harreby investigates the impact of spinal cord stimulation on seizures.
Harreby begins with the premise that “Spinal cord stimulation (SCS) activates the thalamus…,” notes that the thalamus “may be involved in generation of seizures,” and looks at the impact of delivering spinal cord stimulation on seizure susceptibility (see Harreby at Abstract).
Harreby’s “target in or near the spinal cord” is the thalamus.
Harreby’s “stimulation configuration to deliver neuromodulation energy” is the spinal cord stimulation that Harreby notes as having “started,” which stimulation – as noted above – “activates the thalamus” (see Harreby at Abstract).
wherein: the neural target includes the dorsal column nuclei or axons projecting to the dorsal column nuclei, (Pg. 111, Left Column, Second Paragraph, “It is common knowledge that dorsal spinal cord fibers conduct sensory input to ventral posterolateral thalamic nuclei via the dorsal column nuclei (13).”);
Harreby’s “neural target” (i.e., the thalamus) inherently “includes the dorsal column nuclei or axons projecting to the dorsal column nuclei” because “dorsal spinal cord fibers conduct sensory input to ventral posterolateral thalamic nuclei via the dorsal column nuclei” (see Harreby at Pg. 111, Left Column, Second Paragraph).
the dorsal column nuclei and the axons are somatotopically organized and the dorsal column nuclei project to at least one of another brainstem area, a cerebellum or a thalamus, (Pg. 111, Left Column, Second Paragraph, “It is common knowledge that dorsal spinal cord fibers conduct sensory input to ventral posterolateral thalamic nuclei via the dorsal column nuclei (13).”);
Harreby’s statement that “dorsal spinal cord fibers conduct sensory input to ventral posterolateral thalamic nuclei via the dorsal column nuclei” confirms that “the dorsal column nuclei project to … a thalamus” in the manner claimed.
Harreby’s statement that “dorsal spinal cord fibers conduct sensory input to ventral posterolateral thalamic nuclei via the dorsal column nuclei” is confirmation of such somatotopic organization as claimed, because Harreby’s statement is a restatement of the term’s definition. See Somatotopic Arrangement NPL at Pg. 1, First Paragraph (“Somatotopyis the point-for-point correspondence of an area of the body to a specific point on the central nervous system.”).
and the at least one of the another brainstem area, the cerebellum or the thalamus includes somatotopically organized nuclei and project axons to different areas of at least one of a cortex or a limbic system, (Pg. 111, Left Column, Second Paragraph, “It is common knowledge that dorsal spinal cord fibers conduct sensory input to ventral posterolateral thalamic nuclei via the dorsal column nuclei (13). … the thalamus relays such sensory information to the cortex.”);
Harreby confirms that “the thalamus includes somatotopically organized nuclei and project axons” as explained above.
and the at least one neural target corresponds to at least one of the cortex, the limbic system, the another brainstem area, the cerebellum or the thalamus in which the epileptic seizures propagate. (Abstract, “Spinal cord stimulation (SCS) activates the thalamus, which may be involved in generation of seizures. … We investigated the effect of SCS on seizure susceptibility…. Tonic-clonic seizures were induced…. SCS was started…. Seizure susceptibility was accessed….”).
As explained above, Harreby’s “at least one neural target” is the thalamus, and thus Harreby’s “at least one neural target corresponds to… the thalamus.”
By virtue of Harreby’s Pg. 111, Left Column, Second Paragraph discussion of the involvement of the cortex, Harreby’s “at least one neural target” also “corresponds to… the cortex” when the term is afforded its broadest reasonable interpretation.
Regarding Claim 2, Harreby discloses the entirety of Claim 1 as explained above.
Harreby additionally discloses:
wherein the at least one neural target includes a spinothalamic tract that provides afferent fibers to an intralaminar thalamic nuclei. (Pg. 111, Left Column, Second Paragraph; Abstract)
As explained above, Harreby’s “neural target” is the thalamus. Harreby’s “neural target” inherently “includes a spinothalamic tract that provides afferent fibers to an intralaminar thalamic nuclei” because such is a mere recitation of anatomical structure. See Hodge at Pg. 378, Second Paragraph (“…lamina 1 cells contribute to the STT in all species and in all spinal cord segments is of particular significance since these units receive afferent input from fine myelinated and/or unmyelinated afferent fibers….”); Hodge at Pg. 379, First Paragraph (“The electrically identified termination sites of lamina 1 cell axons agree with that shown by anatomical studies, i.e., there are both medial and lateral thalamic termination sites.”). The Present Specification at Para. [0103] supports this interpretation.
The Examiner notes that this limitation appears to recite the biological structure which facilitates the result achieved by the claimed method rather than imposing any limitation upon the method itself.
Regarding Claim 3, Harreby discloses the entirety of Claim 2 as explained above.
Harreby additionally discloses:
wherein the at least one neural target is based on a symptom location where the patient experiences a symptom caused by the epileptic seizures (Abstract, “Spinal cord stimulation (SCS) activates the thalamus, which may be involved in generation of seizures. SCS may therefore influence seizure susceptibility. We investigated the effect of SCS on seizure susceptibility…”).
Regarding Claim 5, Harreby discloses the entirety of Claim 2 as explained above.
Harreby additionally discloses:
wherein the stimulation configuration includes a plurality of pulses in a pulse pattern, (Pg. 113, Left Column, First Paragraph, “Biphasic pulses with a duration of 400 µs (2 × 200 µs) were always used…”);
wherein the pulse pattern includes at least one of different pulse amplitudes, different pulse widths, different pulse-to-pulse spacing, different pulse shapes, different bursts of pulses, different electrode contacts in the set of electrodes, or different fractionalizations (Pg. 115, Left Column, Second Paragraph, “…these findings indicate that the effect of SCS on seizure susceptibility may depend on both stimulation frequency and intensity.”).
Harreby discloses altering stimulation “intensity” as a means for tailoring SCS for treatment of seizure. Intensity is a term used colloquially to reference amplitude. See Miller at Pg. 375, Left Column, First Paragraph.
Regarding Claim 7, Harreby discloses the entirety of Claim 1 as explained above.
Harreby additionally discloses:
wherein the at least one neural target includes axons in at least a portion of a gracile fasciculus or a cuneate fasciculus (Pg. 111, Left Column, Second Paragraph; Abstract; Pg. 114, Figure 4 Caption, “At higher current intensities additional recruitment continues to occur, which indicates that … not all fasciculus gracilis fibers were activated.”).
Harreby’s thalamus neural target inherently “includes axons in at least a portion of a gracile fasciculus or a cuneate fasciculus,” because this limitation is a mere statement of human anatomy. See Gracile Fasciculus NPL at Pg. 2, “The Spinal Cord, 2018 Fundamental Neuroscience for Basic and Clinical Applications” heading; Pg. 3 of 10, Last Paragraph through Pg. 4 of 10, First Paragraph, “Spinal Cord Anatomy, 2014 Encyclopedia of the Neurological Sciences (Second Edition)” heading. This interpretation is additionally supported by Para. [0103] of the Present Specification.
Regarding Claim 8, Harreby discloses the entirety of Claim 1 as explained above.
Harreby additionally discloses:
wherein the at least one neural target includes pathways in at least a portion of a posterolateral tract, lateral spinothalamic tract, an anterior spinothalamatic tract, a spinoreticular tract, a posterior spinocerebellar tract, an anterior spinocerebellar tract, or a spinoolivary tract. (Pg. 111, Left Column, Second Paragraph; Abstract).
Harreby’s “neural target” includes discloses a “lateral spinothalamic tract” and/or “an anterior spinothalamatic tract” for the same reasons explained above with respect to Claim 2. The Present Specification at Para. [0103] supports this interpretation.
Regarding Claim 10, Harreby discloses the entirety of Claim 1 as explained above.
Harreby additionally discloses:
including using at least one lead in a dorsal epidural space to position at least some of the set of electrodes in the dorsal epidural space. (Pg. 112, Left Column, Second Paragraph, “The cervical vertebrae (C) were exposed…. a custom-made bipolar SCS electrode … was inserted in the dorsal epidural space of C2.”);
Regarding Claim 11, Harreby discloses the entirety of Claim 1 as explained above.
Harreby additionally discloses:
including using at least one lead fed through a dorsal epidural space and at least partially around the spinal cord to position at least some of the set of electrodes in a lateral or antero-lateral epidural space surrounding the spinal cord. (Pg. 112, Left Column, Second Paragraph, “The cervical vertebrae (C) were exposed from the occipital bone to C5-C6. After cutting the ligaments between C1-C2 and C3-C4, a custom-made bipolar SCS electrode (15 stranded stainless steel wire mounted on a plastic strip, 2 mm longitudinal spacing of the active sites) was inserted in the dorsal epidural space of C2.”).
Regarding Independent Claim 17, Harreby discloses:
A system for treating a patient with epileptic seizures, comprising: (Abstract, Objectives Section, “We investigated the effect of SCS on seizure susceptibility….;” Pg. 112, Left Column, Second Paragraph; Pg. 113, Left Column, First Paragraph);
The system used by Harreby as described at the above-cited portions is such a system as claimed.
a therapy delivery system configured to use a set of electrodes positioned adjacent to a spinal cord or dorsal column nuclei and a stimulation configuration to deliver neuromodulation energy to at least one neural target in or near the spinal cord, (Pg. 112, Left Column, Second Paragraph, “The cervical vertebrae (C) were exposed…. a custom-made bipolar SCS electrode … was inserted in the dorsal epidural space of C2;” Pg. 113, Left Column, First Paragraph, “Stimulation was performed using a DS8000 Digital stimulator with an attached DLS100 Stimulus Isolator (World Precision Instruments, Sarasota, FL, USA);” Abstract, “Spinal cord stimulation (SCS) activates the thalamus…. We investigated the effect of SCS on seizure susceptibility…. Tonic-clonic seizures were induced…. SCS was started…. Seizure susceptibility was accessed….”);
Harreby’s “DS8000 Digital stimulator with an attached DLS100 Stimulus Isolator” is such a “therapy delivery system” as claimed. The remainder of this limitation is being interpreted similarly to the similar limitation of Claim 1.
wherein: the at least one neural target includes the dorsal column nuclei or axons projecting to the dorsal column nuclei, (Pg. 111, Left Column, Second Paragraph; see Rejection of Claim 1, above, in elaboration);
the dorsal column nuclei and the axons are somatotopically organized and the dorsal column nuclei project to at least one of another brainstem area, a cerebellum or a thalamus, (Pg. 111, Left Column, Second Paragraph; see Rejection of Claim 1, above, in elaboration);
and the at least one of the another brainstem area, the cerebellum or the thalamus includes somatotopically organized nuclei and project axons to different areas of at least one of a cortex or a limbic system, (Pg. 111, Left Column, Second Paragraph; see Rejection of Claim 1, above, in elaboration);
and the at least one neural target corresponds to at least one of the cortex, the limbic system, the another brainstem area, the cerebellum or the thalamus in which the epileptic seizures propagate. (Abstract; see Rejection of Claim 1, above, in elaboration).
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 4, 6 and 18 are rejected under 35 U.S.C. 103 as being unpatentable over Harreby as evidenced by Somatotopic Arrangement NPL, Hodge, Miller and Gracile Fasciculus NPL as applied to Claims 1 and 17 above, and further in view of US 2022/0280795 A1 to Tsukashima (“Tsukashima”) as evidenced by JIAO, JIANHANG, "The Effect of Spinal Cord Stimulation on Epileptic Seizures", Neuromodulation: Technology at the Neural Interface, Volume 19, Issue 2, 2016, ISSN 1094-7159, https: doi.org 10.1111 ner.12362.Pages 154-160, (February 2016), 7 pages2 (“Jiao”).
Regarding Claim 4, Harreby discloses the entirety of Claim 1 as explained above.
Harreby does not disclose:
wherein the epileptic seizures include a first symptom at a first location and a second symptom at a second location, and a first target is based on the first location where the patient experiences the first symptom, and a second target is based on the second location where the patient experiences the second symptom.
Tsukashima describes “Wireless Closed Loop Deep Brain Stimulation Method And System” (Title) that is useful in treating epilepsy (Para. [0003]). Tsukashima is analogous art.
Tsukashima teaches:
wherein the epileptic seizures include a first symptom at a first location and a second symptom at a second location, and a first target is based on the first location where the patient experiences the first symptom, and a second target is based on the second location where the patient experiences the second symptom. (Para. [0017], “ For a system intended to treat epilepsy, the system may also include a second stimulation probe configured for insertion into the patient's brain at a second location subject to stimulation affecting symptoms of an epileptic seizure, and the second stimulation probe may be operable to apply stimulation to a second portion of the patient's brain associated with an epileptic seizure.”).
As explained above, Claim 4 is being interpreted to mean that the method is generally amenable to such treatment of two symptoms via stimulating two targets, without respect to the “at least one neural target in or near the spinal cord” of Claim 1.
It would have been obvious for a person of ordinary skill in the art before the effective filing date of the claimed invention to modify the method of Harreby with the teachings of Tsukashima (i.e., to modify the method of Harreby such that it is generally amenable to treatment of two seizure symptoms via stimulating two targets in the manner of Tsukashima) in order to facilitate “application of stimulation is most effective at reducing aberrant movement associated with (characteristic of) an epileptic seizure” (Tsukashima at Para. [0017]).
Regarding Claim 6, Harreby discloses the entirety of Claim 1 as explained above.
Harreby does not disclose:
wherein the epileptic seizures propagate to two or more areas, and the method includes using two or more stimulation configurations corresponding to the two or more areas, wherein the two or more stimulation configurations include different stimulation patterns, and at least one of the different stimulation patterns includes a stimulation pattern with different pulse amplitudes, different pulse widths, or different pulse-to-pulse spacing
That is, Harreby does not contemplate an instance wherein “the epileptic seizures propagate to two or more areas,” and thus does not disclose such a method as recited by Claim 6.
However, Harreby does disclose altering stimulation parameters including amplitude to influence seizure treatment (See Harreby at Pg. 115, Left Column, Second Paragraph and accompanying explanation above at Claim 5).
But-for its spinal cord stimulation based induction, treatment of such epileptic seizures that propagate to two or more areas in the manner of Claim 6 is well known in the art, for example as taught by Tsukashima.
Tsukashima describes “Wireless Closed Loop Deep Brain Stimulation Method And System” (Title) that is useful in treating epilepsy (Para. [0003]). Tsukashima is analogous art.
Tsukashima teaches:
wherein the epileptic seizures propagate to two or more areas, and the method includes using two or more stimulation configurations corresponding to the two or more areas, (Para. [0017], “For a system intended to treat epilepsy, the system may also include a second stimulation probe configured for insertion into the patient's brain at a second location subject to stimulation affecting symptoms of an epileptic seizure, and the second stimulation probe may be operable to apply stimulation to a second portion of the patient's brain associated with an epileptic seizure.”);
wherein the two or more stimulation configurations include different stimulation patterns, and at least one of the different stimulation patterns includes a stimulation pattern with different pulse amplitudes, different pulse widths, or different pulse-to-pulse spacing (Para. [0022], “…the control system will generate and transmit control signals … to cause the probe to deliver … stimulation of differing characteristics (frequency, pulse width, pulse frequency, or other pulse waveform parameters) to the brain.”).
It would have been obvious for a person of ordinary skill in the art before the effective filing date of the claimed invention to modify the method of Harreby with the teachings of Tsukashima (i.e., to modify the method of Harreby such that it is adapted for treatment of epileptic seizures which propagate to two or more areas by using two or more stimulation configurations corresponding to the two or more areas, wherein the two or more stimulation configurations include different stimulation patterns in the manner of Tsukashima) in order to facilitate “application of stimulation is most effective at reducing aberrant movement associated with (characteristic of) an epileptic seizure” (Tsukashima at Para. [0017]).
It would have been obvious for a person of ordinary skill in the art before the effective filing date of the claimed invention to modify the method of Harreby with the teachings of Tsukashima (i.e., to modify the method of Harreby such that it is adapted for treatment of epileptic seizures which propagate to two or more areas by using two or more stimulation configurations corresponding to the two or more areas, wherein the two or more stimulation configurations include different stimulation patterns in the manner of Tsukashima) because known work in one field of endeavor (i.e., traditional deep brain stimulation-based epilepsy treatment methods) prompted variations of it for use in a different one (i.e., spinal cord stimulation-based epilepsy treatment methods) based on design incentives or other market forces, and the variations are predictable to one of ordinary skill in the art. See MPEP 2143(I)(F).
The scope and content of the prior art in the same field of endeavor as that of the applicant’s invention included a similar or analogous method. That is, Harreby – a study pertaining to the effect of spinal cord stimulation on seizure susceptibility – is in the same field of endeavor as the claimed method for spinal cord stimulation-based epilepsy treatment and includes a similar method to that of Claim 1, from which Claim 6 depends.
Harreby’s prior art method differs from that of Claim 6 in that Harreby does not contemplate an instance wherein “the epileptic seizures propagate to two or more areas.” Treatment of such epileptic seizures that propagate to two or more areas in the manner of Claim 6 is well known in the related endeavor of traditional deep brain stimulation-based epilepsy treatment, for example as taught by Tsukashima.
There were design incentives or market forces which would have prompted adaptation of the known device. In particular, traditional deep brain stimulation-based epilepsy treatments are incredibly invasive and of limited efficacy, whereas spinal cord stimulation is less invasive. See, e.g., Jiao at Pg. 154, Left Column, First Paragraph (“Electrical stimulation applied to patients with refractory epilepsy has been proposed in a variety of forms over the last decades…. [T]he efficiency of both therapies is relatively low (i.e. 50% reduction of seizures in 50% of the implanted patients)…. Therefore, better alternatives to these procedures would be most welcome.”).
The differences between the claimed invention and the prior art were encompassed in known variations or in a principle known in the prior art. For example, Tsukashima describes treatment of such epileptic seizures that propagate to two or more areas in the manner of Claim 6 at Paras. [0017] and [0022] in the closely related art of deep brain stimulation-based epilepsy treatment methods.
One of ordinary skill in the art, in view of the identified design incentives or other market forces, could have implemented the claimed variation of the prior art, and the claimed variation would have been predictable to one of ordinary skill in the art.
That is, one of ordinary skill in the art could have modified the method of Harreby such that it is adapted for treatment of epileptic seizures which propagate to two or more areas by using two or more stimulation configurations corresponding to the two or more areas, wherein the two or more stimulation configurations include different stimulation patterns in the manner of Tsukashima.
This conclusion is based on the following considerations:
The claimed “two or more stimulation configurations” are recited quite broadly, without reference to any particular stimulation parameters. As such, Claim 6 encompasses the general principle reflected in Tsukashima that epileptic seizures which propagate to two or more areas are treatable by using two or more stimulation configurations corresponding to the two or more areas.
This conclusion would merit reconsideration were particular parameters useful only in spinal cord stimulation-based treatment to be required by the claim.
Harreby expressly discloses altering stimulation parameters to differently influence seizure treatment (See Harreby at Pg. 115, Left Column, Second Paragraph). Although Harreby’s method falls a step short of that of Claim 6 in that it does not consider an instance wherein “the epileptic seizures propagate to two or more areas,” it is clear from Harreby’s disclosure of altering stimulation parameters to differently influence seizure treatment that Harreby’s method is amenable treating epileptic seizures propagate to two or more areas by conventional methods.
Regarding Claim 18, Harreby discloses the entirety of Claim 17 as explained above.
Harreby does not disclose:
wherein the epileptic seizures include a first symptom at a first location and a second symptom at a second location, and a first target is based on the first location where the patient experiences the first symptom and a second target is based on the second location where the patient experiences the second symptom.
Tsukashima describes “Wireless Closed Loop Deep Brain Stimulation Method And System” (Title) that is useful in treating epilepsy (Para. [0003]). Tsukashima is analogous art.
Tsukashima teaches:
wherein the epileptic seizures include a first symptom at a first location and a second symptom at a second location, and a first target is based on the first location where the patient experiences the first symptom and a second target is based on the second location where the patient experiences the second symptom. (Para. [0017], “ For a system intended to treat epilepsy, the system may also include a second stimulation probe configured for insertion into the patient's brain at a second location subject to stimulation affecting symptoms of an epileptic seizure, and the second stimulation probe may be operable to apply stimulation to a second portion of the patient's brain associated with an epileptic seizure.”).
As explained above, Claim 18 is being interpreted to mean that the method is generally amenable to such treatment of two symptoms via stimulating two targets, without respect to the “at least one neural target in or near the spinal cord” of Claim 17.
It would have been obvious for a person of ordinary skill in the art before the effective filing date of the claimed invention to modify the device of Harreby with the teachings of Tsukashima (i.e., to modify Harreby such that it is generally amenable to treatment of two seizure symptoms via stimulating two targets in the manner of Tsukashima) in order to facilitate “application of stimulation is most effective at reducing aberrant movement associated with (characteristic of) an epileptic seizure” (Tsukashima at Para. [0017])
Claim 9 is rejected under 35 U.S.C. 103 as being unpatentable over Harreby as evidenced by Somatotopic Arrangement NPL, Hodge, Miller and Gracile Fasciculus NPL as applied to Claim 1 above, and further in view of E. Fanselow et al., "Reduction of Pentylenetetrazole-Induced Seizure Activity in Awake Rats by Seizure-Triggered Trigeminal Nerve Stimulation," Journal of Neuroscience 1 November 2000, 20 (21) 8160-8168 (“Fanselow”) as evidenced by Singh, G.P. (2019). Anatomy of Trigeminal Nerve. In: Rath, G. (eds) Handbook of Trigeminal Neuralgia. Springer, Singapore. https://doi.org/10.1007/978-981-13-2333-1_2, pp 11–22 (“Singh”).
Regarding Claim 9, Harreby discloses the entirety of Claim 1 as explained above.
Harreby does not disclose:
wherein the at least one neural target includes pathways in at least a portion of trigeminothalamatic tract via a trigeminocervical nucleus
Fanselow describes “Reduction of Pentylenetetrazole-Induced Seizure Activity in Awake
Rats by Seizure-Triggered Trigeminal Nerve Stimulation” (Title). Fanselow is analogous art.
Fanselow teaches:
wherein the at least one neural target includes pathways in at least a portion of trigeminothalamatic tract via a trigeminocervical nucleus (Abstract, “Here, we report that stimulation of another cranial nerve, the trigeminal nerve, can also cause cortical and thalamic desynchronization, resulting in a reduction of seizure activity in awake rats;” Pg. 8166, Left Column, First Paragraph, “… neurons in the nucleus of the solitary tract (NTS) responded with lower EPSP amplitudes as the frequency of solitary tract stimulation was increased. These results may also be relevant to trigeminal nerve stimulation.”)
Fanselow teaches that stimulation of the trigeminal nerve reduced seizure activity. Anatomically, this is achieved via pathways in at least a portion of trigeminothalamatic tract via a trigeminocervical nucleus. See Singh at Pg. 7 of 15, First Paragraph through Pg. 8 of 15, Second Paragraph.
It would have been obvious for a person of ordinary skill in the art before the effective filing date of the claimed invention to modify the method of Harreby with the teachings of Fanselow (i.e., to use such a neural target that includes pathways in at least a portion of trigeminothalamatic tract via a trigeminocervical nucleus as taught by Fanselow) in order to “cause cortical and thalamic desynchronization, resulting in a reduction of seizure activity” (Fanselow at Abstract).
Claims 12, 13 and 19 are rejected under 35 U.S.C. 103 as being unpatentable over Harreby as evidenced by Somatotopic Arrangement NPL, Hodge, Miller and Gracile Fasciculus NPL as applied to Claim 1 above, and further in view of US 2021/0387006 A1 to Mustakos et al. (“Mustakos”)
Regarding Claim 12, Harreby discloses the entirety of Claim 1 as explained above.
Harreby does not disclose:
wherein the stimulation configuration is configured to focus a neuromodulation field to stimulate neural pathways in a portion of a nerve tract without stimulating other neural pathways in other portions of the nerve tract
Mustakos describes “neuromodulation systems, devices, and methods. (Para. [0002], including spinal cord stimulation (Para. [0003]). Mustakos is analogous art.
Mustakos teaches:
wherein the stimulation configuration is configured to focus a neuromodulation field to stimulate neural pathways in a portion of a nerve tract without stimulating other neural pathways in other portions of the nerve tract (Claim 1, “…modulating the neural target using a first neuromodulation field of a first polarity… modulating the neural target using a second neuromodulation field of a second polarity…;” Para. [0014], “The controller may be configured to determine fractionalization values for the second parameter settings to modulate the at least one target region and avoid the zero or more avoidance regions.”).
The Examiner notes that this interpretation is consistent with Para. [0117] of the Present Specification, which pertains to the subject matter of Claim 12.
It would have been obvious for a person of ordinary skill in the art before the effective filing date of the claimed invention to modify the method of Harreby with the teachings of Mustakos (i.e., to focus a neuromodulation field to stimulate neural pathways in a portion of a nerve tract without stimulating other neural pathways in other portions of the nerve tract in the manner of Mustakos) in order to “maintain efficacy while minimizing the unintended and undesirable effects” of the neuromodulation by accounting for the complexity of the human nervous system (Mustakos at Para. [0004]).
Regarding Claim 13, the combination of Harreby and Mustakos renders obvious the entirety of Claim 12 as explained above.
Mustakos additionally teaches:
including: using a first channel and a first neuromodulation field to deliver first neuromodulation energy to provide a first neuromodulation field and using a second channel and a second stimulation configuration to deliver second neuromodulation energy to provide a second neuromodulation field; (Para. [0060], “Various embodiments may automatically convert the cathodic settings to anodic settings using known target and avoidance regions;” Claim 1, “…modulating the neural target using a first neuromodulation field of a first polarity… modulating the neural target using a second neuromodulation field of a second polarity…”);
Mustakos’s “cathodic settings” and “anodic settings” are such first and second channels as claimed when the term is afforded its broadest reasonable interpretation. Mustakos explains at Para. [0058] that “Different types of neural structures have different reactions to different neuromodulation polarities,” and that this “contribute[s] to the preferential modulation of some tissue over other tissue.” Mustakos leverages this to target particular areas.
and coordinating delivery of the first neuromodulation energy and the second neuromodulation energy, (Para. [0060], “Various embodiments may automatically convert the cathodic settings to anodic settings using known target and avoidance regions.”);
wherein the first neuromodulation field is configured to stimulate a first site, and the second neuromodulation field is configured to stimulate a second site lateral to the first site; the first neuromodulation field is configured to stimulate a first nerve tract without stimulating a second nerve tract, and the second neuromodulation field is configured to stimulate the second nerve tract without stimulating the first nerve tract; or the first neuromodulation field is at a first spinal cord level without extending to a second spinal cord level, and the second neuromodulation field is at the second spinal cord level without extending to the first spinal cord level. (Claim 1, “…modulating the neural target using a first neuromodulation field of a first polarity… modulating the neural target using a second neuromodulation field of a second polarity…;” Para. [0014], “The controller may be configured to determine fractionalization values for the second parameter settings to modulate the at least one target region and avoid the zero or more avoidance regions.”).
It would have been obvious for a person of ordinary skill in the art before the effective filing date of the claimed invention to modify the method of Harreby with the teachings of Mustakos (i.e., to employ first and second neuromodulation fields for stimulating a first nerve tract without stimulating a second nerve tract and stimulating the second nerve tract without stimulating the first nerve tract in the manner of Mustakos) in order to “maintain efficacy while minimizing the unintended and undesirable effects” of the neuromodulation by accounting for the complexity of the human nervous system (Mustakos at Para. [0004]).
Regarding Claim 19, Harreby discloses the entirety of Claim 17 as explained above.
Harreby does not disclose:
wherein the therapy delivery system is configured to: use a first channel to deliver first neuromodulation energy using a first stimulation configuration to provide a first neuromodulation field and use a second channel to deliver second neuromodulation energy using a second stimulation configuration to provide a second neuromodulation field;
and coordinate delivery of the first neuromodulation energy and the second neuromodulation energy,
wherein the first neuromodulation field is configured to stimulate a first site, and the second neuromodulation field is configured to stimulate a second site lateral to the first site; the first neuromodulation field is configured to stimulate a first nerve tract without stimulating a second nerve tract, and the second neuromodulation field is configured to stimulate the second nerve tract without stimulating the first nerve tract; or the first neuromodulation field is at a first spinal cord level without extending to a second spinal cord level, and the second neuromodulation field is at the second spinal cord level without extending to the first spinal cord level
Mustakos describes “neuromodulation systems, devices, and methods. (Para. [0002], including spinal cord stimulation (Para. [0003]). Mustakos is analogous art.
Mustakos teaches:
wherein the therapy delivery system is configured to: use a first channel to deliver first neuromodulation energy using a first stimulation configuration to provide a first neuromodulation field and use a second channel to deliver second neuromodulation energy using a second stimulation configuration to provide a second neuromodulation field; (Para. [0060], “Various embodiments may automatically convert the cathodic settings to anodic settings using known target and avoidance regions;” Claim 1, “…modulating the neural target using a first neuromodulation field of a first polarity… modulating the neural target using a second neuromodulation field of a second polarity…”);
Mustakos’s “cathodic settings” and “anodic settings” are such first and second channels as claimed when the term is afforded its broadest reasonable interpretation. Mustakos explains at Para. [0058] that “Different types of neural structures have different reactions to different neuromodulation polarities,” and that this “contribute[s] to the preferential modulation of some tissue over other tissue.” Mustakos leverages this to target particular areas.
and coordinate delivery of the first neuromodulation energy and the second neuromodulation energy, (Para. [0060], “Various embodiments may automatically convert the cathodic settings to anodic settings using known target and avoidance regions.”);
wherein the first neuromodulation field is configured to stimulate a first site, and the second neuromodulation field is configured to stimulate a second site lateral to the first site; the first neuromodulation field is configured to stimulate a first nerve tract without stimulating a second nerve tract, and the second neuromodulation field is configured to stimulate the second nerve tract without stimulating the first nerve tract; or the first neuromodulation field is at a first spinal cord level without extending to a second spinal cord level, and the second neuromodulation field is at the second spinal cord level without extending to the first spinal cord level (Claim 1, “…modulating the neural target using a first neuromodulation field of a first polarity… modulating the neural target using a second neuromodulation field of a second polarity…;” Para. [0014], “The controller may be configured to determine fractionalization values for the second parameter settings to modulate the at least one target region and avoid the zero or more avoidance regions.”).
It would have been obvious for a person of ordinary skill in the art before the effective filing date of the claimed invention to modify the device of Harreby with the teachings of Mustakos (i.e., to employ first and second neuromodulation fields for stimulating a first nerve tract without stimulating a second nerve tract and stimulating the second nerve tract without stimulating the first nerve tract in the manner of Mustakos) in order to “maintain efficacy while minimizing the unintended and undesirable effects” of the neuromodulation by accounting for the complexity of the human nervous system (Mustakos at Para. [0004]).
Claims 14, 15 and 20 are rejected under 35 U.S.C. 103 as being unpatentable over Harreby as evidenced by Somatotopic Arrangement NPL, Hodge, Miller and Gracile Fasciculus NPL as applied to Claim 1 above, and further in view of US 2021/0121697 A1 to Linde et al. (“Linde”).
Regarding Claim 14, Harreby discloses the entirety of Claim 1 as explained above.
Harreby does not disclose:
further comprising using at least one event detector to detect at least one predefined epileptic event, and responding to the detected at least one predefined epileptic event by delivering the neuromodulation energy
Linde describes “techniques related to medical devices and, more particularly, to medical devices that deliver neurostimulation therapy” (Para. [0002]), including in the contexts of seizure (Para. [0176]) and spinal cord stimulation (Para. [0004]).
Linde teaches:
further comprising using at least one event detector to detect at least one predefined epileptic event, and responding to the detected at least one predefined epileptic event by delivering the neuromodulation energy (Para. [0007], “…a medical device system for therapy deliver includes … processing circuitry configured to detect an indicator of a symptom in a patient; in response to detecting the indicator of the symptom in the patient, deliver to the patient, by the stimulation circuitry, a first stimulation therapy; and in response to determining that the indicator of the symptom has been present for more than a threshold amount of time after beginning to deliver the first stimulation therapy, deliver to the patient, by the stimulation circuitry, a second stimulation therapy different than the first stimulation therapy;” Para. [0176]).
Para. [0176] describes the event being a seizure.
It would have been obvious for a person of ordinary skill in the art before the effective filing date of the claimed invention to modify the method of Harreby with the teachings of Linde (i.e, to use such an event detector as taught by Linde, and to administer treatment based on event detection in the manner of Linde) in order to “allow for better treatment of diseases that are localizable to multiple nodes in a brain circuit model or have different symptoms that can be treated more effectively by stimulation of different targets” (Linde at Para. [0051]).
Regarding Claim 15, the combination of Harreby and Linde renders obvious the entirety of Claim 14 as explained above.
Linde additionally teaches:
wherein the at least one event detector is configured to detect at least a first predefined epileptic event and a second predefined epileptic event; and the method includes responding to the first predefined epileptic event by delivering a first neuromodulation therapy and responding to the second predefined epileptic event by delivering a second neuromodulation therapy, (Para. [0007], “…a medical device system for therapy deliver includes … processing circuitry configured to detect an indicator of a symptom in a patient; in response to detecting the indicator of the symptom in the patient, deliver to the patient, by the stimulation circuitry, a first stimulation therapy; and in response to determining that the indicator of the symptom has been present for more than a threshold amount of time after beginning to deliver the first stimulation therapy, deliver to the patient, by the stimulation circuitry, a second stimulation therapy different than the first stimulation therapy;” Para. [0176]).
Para. [0176] describes the event being a seizure.
wherein the first and second neuromodulation therapies differ in at least one of a neural target or use different neural stimulation patterns (Para. [0050], “…utilizing the techniques of this disclosure, an IMD may … selectively deliver electrical stimulation … to a primary target area but also deliver electrical stimulation … to a secondary target for a specific patient or disease state.”).
Regarding Independent Claim 20, Harreby discloses the entirety of Claim 17 as explained above.
Harreby does not disclose:
further comprising at least one event detector to detect at least one predefined epileptic event, wherein the therapy delivery system is configured to respond to the detected at least one predefined epileptic event by delivering the neuromodulation energy,
wherein the at least one event detector is configured to detect the at least one predefined epileptic event using at least one of: received user input; sensed electrical signals in a brain; sensed cardiac activity; sensed blood oxygen; sensed respiration; sensed movement or lack of movement; sensed body temperature; sensed neurotransmitter or biochemical component; sensed sound, sensed ultrasound, or analysis of an image of a patient,
wherein the at least one event detector is configured to detect at least a first predefined epileptic event and a second predefined epileptic event; and the therapy delivery system is configured to respond to the first predefined epileptic event by delivering a first neuromodulation therapy and respond to the second predefined epileptic event by delivering a second neuromodulation therapy,
wherein the first and second neuromodulation therapies differ in at least one of a neural target or use different neural stimulation patterns.
Linde describes “techniques related to medical devices and, more particularly, to medical devices that deliver neurostimulation therapy” (Para. [0002]), including in the contexts of seizure (Para. [0176]) and spinal cord stimulation (Para. [0004]).
Linde teaches:
further comprising at least one event detector to detect at least one predefined epileptic event, wherein the therapy delivery system is configured to respond to the detected at least one predefined epileptic event by delivering the neuromodulation energy, (Para. [0007], “…a medical device system for therapy deliver includes … processing circuitry configured to detect an indicator of a symptom in a patient; in response to detecting the indicator of the symptom in the patient, deliver to the patient, by the stimulation circuitry, a first stimulation therapy; and in response to determining that the indicator of the symptom has been present for more than a threshold amount of time after beginning to deliver the first stimulation therapy, deliver to the patient, by the stimulation circuitry, a second stimulation therapy different than the first stimulation therapy;” Para. [0176]).
Para. [0176] describes the event being a seizure.
wherein the at least one event detector is configured to detect the at least one predefined epileptic event using at least one of: received user input; sensed electrical signals in a brain; sensed cardiac activity; sensed blood oxygen; sensed respiration; sensed movement or lack of movement; sensed body temperature; sensed neurotransmitter or biochemical component; sensed sound, sensed ultrasound, or analysis of an image of a patient, (Para. [0080], “A motion sensor may, for example, detect a motion event by measuring motion, using an accelerometer for instance, and identifying the motor component of seizure, such as for a tonic seizure or tonic-clonic seizure, or detect a fall.”);
wherein the at least one event detector is configured to detect at least a first predefined epileptic event and a second predefined epileptic event; and the therapy delivery system is configured to respond to the first predefined epileptic event by delivering a first neuromodulation therapy and respond to the second predefined epileptic event by delivering a second neuromodulation therapy, , (Para. [0007], “…a medical device system for therapy deliver includes … processing circuitry configured to detect an indicator of a symptom in a patient; in response to detecting the indicator of the symptom in the patient, deliver to the patient, by the stimulation circuitry, a first stimulation therapy; and in response to determining that the indicator of the symptom has been present for more than a threshold amount of time after beginning to deliver the first stimulation therapy, deliver to the patient, by the stimulation circuitry, a second stimulation therapy different than the first stimulation therapy;” Para. [0176]).
wherein the first and second neuromodulation therapies differ in at least one of a neural target or use different neural stimulation patterns. (Para. [0050], “…utilizing the techniques of this disclosure, an IMD may … selectively deliver electrical stimulation … to a primary target area but also deliver electrical stimulation … to a secondary target for a specific patient or disease state.”).
It would have been obvious for a person of ordinary skill in the art before the effective filing date of the claimed invention to modify the method of Harreby with the teachings of Linde (i.e, to use such an event detector as taught by Linde, and to administer treatment based on event detection in the manner of Linde) in order to “allow for better treatment of diseases that are localizable to multiple nodes in a brain circuit model or have different symptoms that can be treated more effectively by stimulation of different targets” (Linde at Para. [0051]).
Notice of Art Deemed Relevant Although Not Relied Upon in Foregoing Rejection
The Examiner makes note of the following prior art, which is deemed relevant although not relied upon in the foregoing rejection:
US 2005/0055065 A1 describes similar targets to those of Claims 1 and 17 at Para. [0050] (“Potential targets include the dorsal columns, the nucleus cuneatus (arm), nucleus gracilis (leg and sacral regions), nucleus caudalis and spinal tract of V (face and neck), and the spinal-thalamic tract.”).
US 2018/0153460 A1 describes an event detector similar to that of Claim 14 at Abstract, Para. [0045] and Para. [0049].
JIAO, JIANHANG, "The Effect of Spinal Cord Stimulation on Epileptic Seizures", Neuromodulation: Technology at the Neural Interface, Volume 19, Issue 2,2016,, ISSN 1094-7159, https: doi.org 10.1111 ner.12362.Pages 154-160, (February 2016), 7 pages was disclosed by Applicant in the IDS dated 9/30/2024 and appears to disclose the entirety of Independent Claims 1 and 17 at Abstract and at Pg. 155, Left Column, Second Paragraph through Right Column, First Paragraph.
PAIS-VIEIRA, MIGUEL, "A Closed Loop Brain machine Interface for Epilepsy Control Using Dorsal Column Electrical Stimulation", Sci Rep 6, 32814 (2016). https: doi.org 10.1038 srep32814, (09 08 2016), 9 pages was disclosed by Applicant in the IDS dated 9/30/2024 and appears to disclose the entirety of Independent Claims 1 and 17 at Abstract and at Pg. 2, Second Paragraph through Pg. 4, Fourth Paragraph.
Conclusion
Any inquiry concerning this communication or earlier communications from the examiner should be directed to CHRISTOPHER J MUTCHLER whose telephone number is (571)272-8012. The examiner can normally be reached M-F 7:00 am - 4:00 pm.
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/C.J.M./Examiner, Art Unit 3796
/Jennifer Pitrak McDonald/Supervisory Patent Examiner, Art Unit 3796
1 HARREBY, KRISTIAN, "The Effect of Spinal Cord Stimulation on Seizure Susceptibility in Rats", Neuromodulation, Volume 14, Issue 2, pages. 111 116, (2011), 6 pages was disclosed by Applicant in the IDS dated 9/30/2024.
2 JIAO, JIANHANG, "The Effect of Spinal Cord Stimulation on Epileptic Seizures", Neuromodulation: Technology at the Neural Interface, Volume 19, Issue 2,2016,, ISSN 1094-7159,https: doi.org 10.1111 ner.12362.Pages 154-160, (February 2016), 7 pages was disclosed by Applicant in the IDS dated 9/30/2024.
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