U.S. patent application number 14/181549 was filed with the patent office on 2014-06-12 for multi-frequency neural treatments and associated systems and methods.
This patent application is currently assigned to Nevro Corporation. The applicant listed for this patent is Nevro Corporation. Invention is credited to Konstantinos Alataris, Anthony V. Caparso, Brian J. Erickson, Zi-Ping Fang, Andre B. Walker.
Application Number | 20140163660 14/181549 |
Document ID | / |
Family ID | 40626146 |
Filed Date | 2014-06-12 |
United States Patent
Application |
20140163660 |
Kind Code |
A1 |
Fang; Zi-Ping ; et
al. |
June 12, 2014 |
MULTI-FREQUENCY NEURAL TREATMENTS AND ASSOCIATED SYSTEMS AND
METHODS
Abstract
Multi-frequency neural treatments and associated systems and
methods are disclosed. A method in accordance with a particular
embodiment includes at least reducing patient pain by applying a
first electrical signal to a first target location of the patient's
spinal cord region at a frequency in a first frequency range of up
to about 1,500 Hz, and applying a second electrical signal to a
second target location of the patient's spinal cord region at a
frequency in a second frequency range of from about 2,500 Hz to
about 100,000 Hz.
Inventors: |
Fang; Zi-Ping; (Beachwood,
OH) ; Caparso; Anthony V.; (San Jose, CA) ;
Erickson; Brian J.; (Woodbury, MN) ; Alataris;
Konstantinos; (Belmont, CA) ; Walker; Andre B.;
(Monte Sereno, CA) |
|
Applicant: |
Name |
City |
State |
Country |
Type |
Nevro Corporation |
Menlo Park |
CA |
US |
|
|
Assignee: |
Nevro Corporation
Menlo Park
CA
|
Family ID: |
40626146 |
Appl. No.: |
14/181549 |
Filed: |
February 14, 2014 |
Related U.S. Patent Documents
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Application
Number |
Filing Date |
Patent Number |
|
|
12264836 |
Nov 4, 2008 |
|
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14181549 |
|
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|
|
60985353 |
Nov 5, 2007 |
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Current U.S.
Class: |
607/117 |
Current CPC
Class: |
A61N 1/36171 20130101;
A61N 1/3787 20130101; A61N 1/0551 20130101; A61N 1/36071
20130101 |
Class at
Publication: |
607/117 |
International
Class: |
A61N 1/05 20060101
A61N001/05 |
Claims
1-50. (canceled)
51. A method of treating pain in a patient, without using
paresthesia or tingling to cover the patient's sensation of pain,
the method comprising: positioning a lead having at least one
electrode disposed thereon so that at least one of the at least one
electrode is in proximity to a dorsal root ganglion; and providing
stimulation energy to the at least one of the at least one
electrode so as to stimulate at least a portion of the dorsal root
ganglion, wherein together the positioning of the lead step and the
providing stimulation energy step reduce pain sensations without
generating sensations of paresthesia.
52. A method of treating pain in a patient comprising: positioning
a lead having at least one electrode disposed thereon so that at
least one of the at least one electrode is in proximity to a dorsal
root ganglion; and providing stimulation energy to the at least one
of the at least one electrode so as to stimulate at least a portion
of the dorsal root ganglion, wherein together the positioning of
the lead step and the providing stimulation energy step reduce pain
sensations without generating sensations of paresthesia.
53. A method for alleviating patient pain or discomfort, without
using paresthesia or tingling to cover the patient's sensation of
pain or discomfort, the method comprising: directing a lead having
at least one electrode into the patient's epidural space;
positioning the at least one electrode proximate to the patient's
dorsal root ganglion; and applying an electrical therapy signal to
the patient's dorsal root ganglion via the at least one electrode,
wherein the signal applied to the patient's dorsal root ganglion
reduces the patient's pain sensations without generating sensations
of paresthesia.
54. The method of claim 53, further comprising: coupling the lead
to an implantable signal generator configured to generate the
electrical therapy signal.
55. The method of claim 53 wherein the electrical therapy signal
has an amplitude of up to 20 mA.
56. The method of claim 53 wherein the electrical therapy signal is
applied continuously.
57. The method of claim 53 wherein the electrical therapy signal is
applied discontinuously so as to include periods when the
electrical therapy signal is applied, and periods when the
electrical therapy signal is terminated according to a duty
cycle
58. The method of claim 57 wherein the duty cycle is less than
50%.
59. The method of claim 53 wherein the electrical therapy signal is
applied discontinuously so as to include periods when the
electrical therapy signal is applied, and periods when the
electrical therapy signal is terminated.
60. The method of claim 59 wherein the periods when the electrical
therapy signal is applied range from a few seconds to a few
hours.
61. The method of claim 53 wherein the electrical therapy signal is
delivered at a frequency between 2,500 Hz and 100,000 Hz.
62. The method of claim 61, further comprising: applying a
stimulation signal at a frequency between 2 Hz and 1,500 Hz.
63. A method of treating pain in a patient comprising: implanting a
lead having at least one electrode disposed thereon; and providing
stimulation energy to the at least one electrode of the implanted
lead so as to stimulate at least a portion of a dorsal root
ganglion, wherein providing stimulation energy to the at least one
electrode of the implanted lead reduces pain sensations without
generating sensations of paresthesia.
64. The method of claim 63, further comprising: coupling the lead
to an implantable signal generator configured to generate the
electrical therapy signal.
65. The method of claim 63 wherein the electrical therapy signal
has an amplitude of up to 20 mA.
66. The method of claim 63 wherein the electrical therapy signal is
applied continuously.
67. The method of claim 63 wherein the electrical therapy signal is
applied discontinuously so as to include periods when the
electrical therapy signal is applied, and periods when the
electrical therapy signal is terminated according to a duty
cycle
68. The method of claim 17 wherein the duty cycle is less than
50%.
69. The method of claim 63 wherein the electrical therapy signal is
applied discontinuously so as to include periods when the
electrical therapy signal is applied, and periods when the
electrical therapy signal is terminated.
70. The method of claim 69 wherein the periods when the electrical
therapy signal is applied range from a few seconds to a few
hours.
71. The method of claim 63 wherein the electrical therapy signal is
delivered at a frequency between 2,500 Hz and 100,000 Hz.
72. The method of claim 71, further comprising: applying a
stimulation signal at a frequency between 2 Hz and 1,500 Hz.
Description
CROSS-REFERENCE TO RELATED APPLICATION
[0001] The present application is a continuation of U.S. patent
application Ser. No. 12/264,836, filed Nov. 4, 2008, which claims
priority to U.S. Provisional Application 60/985,353, filed Nov. 5,
2007, each of which is incorporated herein by reference.
TECHNICAL FIELD
[0002] The present disclosure relates generally to methods and
apparatuses for treating patient conditions, including chronic pain
conditions via techniques that can include stimulating and blocking
neuronal tissue associated with the spinal cord.
BACKGROUND
A. Neural Stimulation Treatments
[0003] Existing patient treatments include applying stimulation
(e.g., up-regulating) signals to nerves, muscles or organs for
treating a wide variety of medical disorders. Stimulation signal
parameters (e.g., pulse width, frequency, and amplitude) are
selected to initiate neural action potentials to be propagated
along the nerve to an organ (e.g., brain or stomach).
[0004] Down-regulating signals also can be applied to nerve fibers.
Certain signal parameters can result in a signal that inhibits the
nerve or blocks the propagation of action potentials along the
nerve. In general, the nerve conduction block is applied to nerves
with down-regulating signals selected to block the entire
cross-section or part of the cross section of the nerves (e.g.,
afferent, efferent, myelinated, and non-myelinated fibers) at the
site where the down-regulating signal is applied.
[0005] In some systems, down-regulating signals are used to manage
motor control over certain areas of a patient's body. For example,
cryogenic nerve blocking of the vagus nerve to control motor
activity is described in Dapoigny et al., "Vagal influence on
colonic motor activity in conscious nonhuman primates," Am. J.
Physiol., 262: G231-G236 (1992). A cryogenic vagal block and the
resulting effect on gastric emptying are described in Paterson C A,
et al., "Determinants of Occurrence and Volume of Transpyloric Flow
During Gastric Emptying of Liquids in Dogs: Importance of Vagal
Input," Dig Dis Sci, (2000); 45:1509-1516.
B. Application to Chronic Pain
[0006] Applying up-regulating electrical energy to the spinal cord
for the purpose of managing pain has been actively practiced since
the 1960s. While a precise understanding of the interaction between
the applied electrical energy and the nervous tissue is not fully
appreciated, it is known that application of an electrical field to
spinal nervous tissue can effectively mask certain types of pain
transmitted from regions of the body associated with the stimulated
tissue. Such spinal cord stimulation (SCS) for the treatment of
chronic intractable pain was introduced by Shealy et al. (Anesth.
Analg., 46, 489-491, 1967).
[0007] More specifically, applying up-regulating electrical pulses
to the spinal cord associated with regions of the body (e.g.,
dermatomes) afflicted with chronic pain can induce paresthesia, or
a subjective sensation of numbness or tingling, in the afflicted
bodily regions. This paresthesia can effectively mask the non-acute
pain sensations perceived at the brain.
[0008] Electrical energy, similar to that used to inhibit pain
perception, also may be used to manage the symptoms of various
motor disorders, for example, tremor, dystonia, spasticity, and the
like. Motor spinal nervous tissue (e.g., nervous tissue from
ventral nerve roots) transmits muscle/motor control signals.
Sensory spinal nervous tissue (e.g., nervous tissue from dorsal
nerve roots) transmits pain signals, as well as other sensory
signals and proprioceptive signals.
[0009] Corresponding dorsal and ventral nerve roots depart the
spinal cord "separately." Laterally from the spinal cord, the
nervous tissue of the dorsal and ventral nerve roots are mixed, or
intertwined. Accordingly, electrical stimulation intended to manage
and control one condition (e.g., pain) can inadvertently interfere
with nerve transmission pathways in adjacent nervous tissue (e.g.,
motor nerves).
[0010] Electrical energy is conventionally delivered through
electrodes positioned on the dorsal column external to the dura
layer surrounding a spinal cord. The electrodes are typically
carried by a percutaneous lead, although a laminotomy lead also can
be used. Percutaneous leads commonly have two or more electrodes
and are positioned within an epidural space through the use of an
insertion, or Touhy-like, needle. An example of an eight-electrode
percutaneous lead is an OCTRODE.RTM. lead manufactured by Advanced
Neuromodulation Systems, Inc. of Plano, Tex. Operationally, the
insertion needle is passed through the skin, between the desired
vertebrae, and into an epidural space located between a dural layer
and the surrounding vertebrae. The stimulation lead is fed through
the bore of the insertion needle and into the epidural space.
Laminotomy leads generally have a wider, paddle-like shape, and are
inserted via an incision rather than through a needle. For example,
a small incision is made in the back of a patient to access the
space between the dura and the surrounding vertebrae.
[0011] According to the "gate-control" theory of Melzak and Wall,
(Science, 150, 971-978, 1965), the suppression of pain sensations,
accompanied by paresthesia, results from the activation of large
cutaneous afferents (A.alpha..beta. fibers). Because these nerve
fibers are part of the dorsal root (DR) fiber that ascends in the
dorsal column (DC), paresthetic sensations can be evoked by both DC
and DR stimulation.
[0012] The potential paresthesia coverage will strongly differ,
however, depending on whether DC fibers or DR fibers are
stimulated. When stimulating the DC fibers, the fibers
corresponding to all dermatomes from the sacral ones up to the
electrode level may be activated, thus resulting in broad
paresthesia coverage. When stimulating DR fibers, however, the
fibers will be activated in a limited number of rootlets close to
the cathodal contact(s), thereby resulting in a paresthesia effect
confined to one or two dermatomes at each body side.
[0013] There are several problems with existing Spinal Cord
Stimulation (SCS) therapy techniques. One is the difficulty of
obtaining a permanent optimal position of the lead(s), to cover the
painful dermatomes with paresthesia. Another problem is the usually
small range of stimulation amplitudes between the perception
threshold (i.e., the threshold at which paresthesia is effected)
and the discomfort threshold (i.e., the threshold at which the
patient experiences pain or other discomfort), often preventing a
complete coverage of the painful area by the paresthesia needed for
maximum therapeutic effect (Holsheimer, Neurosurgery, 40, 5,
990-999, 1997).
SUMMARY
[0014] In some cases, low frequency signals are applied to the
dorsal column to address chronic patient pain associated with a
peripheral site. However, the dorsal roots also can be stimulated
when low frequency stimulation is applied to the dorsal column to
produce the paresthesia necessary to overcome the chronic pain. For
example, the dorsal roots may be stimulated if the stimulation
leads are placed too close to the dorsal root, and/or if the
amplitude of the low frequency signal is increased to the
discomfort threshold. The discomfort threshold at the dorsal root
can be reached before the parethesia threshold (i.e., the threshold
at which paresthesia is affected) is reached at the dorsal column.
Hence, the clinician has limited freedom to increase the amplitude
of the signal at the dorsal column to achieve the desired
paresthesia effect, before discomfort is felt due to the dorsal
root stimulation.
[0015] Aspects of the present disclosure are directed to managing
chronic pain through the application of electrical energy to
selected nervous tissue and, in particular embodiments, to methods
and systems for treating chronic pain by applying neuromodulation
therapies to one or more regions of neuronal tissue in the spinal
region. As the term is used herein, the "spinal region" includes
the nerves of the dorsal column, dorsal roots, and the dorsal roots
ganglion, which are located within the dural layer.
[0016] A method for treating patient pain in accordance with a
particular embodiment includes applying a first electrical signal
to a first target location (e.g., a dorsal column) of the patient's
spinal cord region at a frequency in a first frequency range of up
to about 1,500 Hz. The method further includes applying a second
electrical signal to a second target location (e.g., at least one
of a dorsal root and a dorsal root ganglion) of the patient's
spinal cord region at a frequency in a second frequency range of
from about 2,500 Hz to about 100,000 Hz. In particular embodiments,
the second frequency range can be from about 2,500 Hz to about
20,000 Hz, or about 3,000 Hz to about 10,000 Hz. Further
embodiments include inducing paresthesia by applying the first
electrical signal, and at least partially blocking patient
discomfort resulting from applying the first electrical signal by
applying the second electrical signal.
[0017] A method in accordance with another embodiment includes
implanting a first electrode proximate to a dorsal column of the
patient's spinal cord region, and implanting a second electrode
proximate to at least one of a dorsal root and a dorsal root
ganglion of the patient's spinal cord region. The method can
further include applying a first electrical signal to the first
electrode at a frequency in a first frequency range of up to about
1,500 Hz. If the patient experiences discomfort, a second
electrical signal is applied to the second electrode at a frequency
in a second frequency range of from about 2,500 Hz to about 100,000
Hz in combination with applying the first electrical signal, and
without repositioning the first electrode. In particular
embodiments, the second frequency range can be from about 2,500 Hz
to about 20,000 Hz, or about 3,000 Hz to about 10,000 Hz.
[0018] Further embodiments are directed to systems for treating
patient pain. In a particular embodiment, the system can include a
controller having instructions for directing first electrical
signals in a first frequency range of up to about 1,500 Hz, and
directing second electrical signals in a second frequency range of
from about 2,500 Hz to about 100,000 Hz. In particular embodiments,
the second frequency range can be from about 2,500 Hz to about
20,000 Hz, or about 3,000 Hz to about 10,000 Hz. A first electrical
signal delivery device can be electrically coupled to the
controller to receive the first electrical signals, and can be
configured to be positioned proximate to a first target location of
the patient's spinal cord region (e.g., the dorsal column). A
second electrical signal delivery device can be electrically
coupled to the controller to receive the second electrical signals,
and can be configured to be positioned proximate to a second target
location of the patient's spinal cord region (e.g., at least one of
a dorsal root and a dorsal root ganglion of the patient's spinal
cord region).
BRIEF DESCRIPTION OF THE DRAWINGS
[0019] FIG. 1 is a schematic diagram of an implantable spinal
stimulator with an electrode array applied to the spine in
accordance with an embodiment of the present disclosure.
[0020] FIG. 2 is a schematic diagram of an implantable spinal
stimulator with percutaneous leads and electrodes applied to the
spine in accordance with another embodiment of the present
disclosure.
[0021] FIG. 3 is a partially schematic cross-sectional view of a
spinal column taken along line 3-3 of FIG. 1 in accordance with an
embodiment of the present disclosure.
[0022] FIG. 4 illustrates examples of biphasic, charge balanced,
square wave pulses applied to electrodes on different channels of a
therapy system in accordance with an embodiment of the present
disclosure.
[0023] FIG. 5 illustrates examples of biphasic, charge balanced,
sinusoidal wave pulses applied to electrodes on different channels
of a therapy system in accordance with an embodiment of the present
disclosure.
[0024] FIG. 6 is a schematic depiction of an example blocking
signal applied to the dorsal column in accordance with an
embodiment of the present disclosure.
[0025] FIG. 7 is a schematic depiction of an example high frequency
(HF) blocking signal applied to the dorsal root in accordance with
an embodiment of the present disclosure.
[0026] FIG. 8 schematically depicts the amplitude of an example low
frequency (LF) stimulation signal likely to induce paresthesia, and
the amplitude of the LF stimulation signal likely to induce patient
discomfort at a given electrode spacing in accordance with an
embodiment of the present disclosure.
[0027] FIG. 9 is a schematic view of an HF blocking signal applied
to the dorsal root of a patient and an LF stimulating signal
applied to the dorsal column in accordance with an embodiment of
the present disclosure.
[0028] FIG. 10 is a schematic diagram of an example blocking
signal, which has an amplitude that is gradually increased to an
operating amplitude over a finite period of time in accordance with
an embodiment of the present disclosure.
[0029] FIG. 11A is a schematic graph generally showing the changes
in frequency during application of a therapy in accordance with an
embodiment of the present disclosure.
[0030] FIG. 11B is a schematic graph generally showing the changes
in amplitude during application of the therapy of FIG. 11A in
accordance with an embodiment of the present disclosure.
[0031] FIG. 11C is a schematic graph generally showing the changes
in charge/phase during application of the therapy of FIG. 11A in
accordance with an embodiment of the present disclosure.
[0032] FIG. 12 is a schematic depiction of an example blocking
signal initially having a high frequency (e.g., about 30-50 KHz)
and a high amplitude (e.g., about 15-20 mA) in accordance with an
embodiment of the present disclosure.
[0033] FIG. 13 shows the blocking signal of FIG. 12 with an initial
ramp-up period in accordance with an embodiment of the present
disclosure.
[0034] FIG. 14 is a schematic depiction of an example LF signal and
an example HF signal indicating a representative timing strategy
for applying the LF and HF signals in accordance with an embodiment
of the present disclosure.
[0035] FIGS. 15-18 are schematic block diagrams of representative
electrode arrays including four electrodes implanted at the spinal
cord of a patient in accordance with an embodiment of the present
disclosure.
[0036] FIG. 19A is a schematic block diagram of a lead
configuration in which first and second percutaneous leads are
implanted within the patient together in accordance with an
embodiment of the present disclosure.
[0037] FIG. 19B is a schematic block diagram of a lead
configuration in which a first percutaneous lead is implanted
within the patient adjacent the dorsal column and a second
percutaneous lead is implanted within the patient adjacent the
dorsal root in accordance with an embodiment of the present
disclosure.
[0038] FIG. 19C is a partially schematic illustration of
percutaneous leads positioned at lumbar locations in accordance
with embodiments of the disclosure.
[0039] FIG. 20 is a schematic block diagram of a multi-channel,
percutaneous lead arrangement having first and second leads
configured to deliver multiple therapy signals to a dorsal column
of a patient in accordance with an embodiment of the present
disclosure.
[0040] FIG. 21 is a schematic block diagram of a multi-channel,
percutaneous lead arrangement having first and second leads
configured to deliver multiple therapy signals to a dorsal root of
a patient in accordance with an embodiment of the present
disclosure.
[0041] FIG. 22 illustrates a first treatment signal being applied
to nerves of a dorsal column of a patient in accordance with an
embodiment of the present disclosure.
DETAILED DESCRIPTION
[0042] FIG. 1 schematically illustrates a representative therapy
system 100 for providing relief from chronic pain, arranged
relative to the general anatomy of a spinal cord SC of a patient.
The therapy system 100 can include a controller (e.g., a pulse
generator 101) implanted subcutaneously within the patient. The
pulse generator 101 is attached via a lead body 102 to an electrode
array 103 or other signal delivery device, which is implanted in
close proximity to the spinal cord SC. The electrode array 103 can
include multiple electrodes or electrode contacts carried by a
support substrate. The pulse generator 101 or other controller
transmits instructions and power to the electrode array 103 via the
lead body 102 to apply therapy signals (e.g., electrical impulses)
to the nerve fibers of the patient to up-regulate (e.g., stimulate)
and/or down-regulate (e.g., block or partially block) the nerves.
Accordingly, the pulse generator 101 can include a
computer-readable medium containing the instructions. The pulse
generator 101 and/or other elements of the system 100 can include
one or more processors, memories and/or input/output devices. The
pulse generator 101 can include multiple portions, e.g., for
directing signals in accordance with multiple signal delivery
parameters, housed in a single housing (as shown in FIG. 1) or in
multiple housings.
[0043] In some embodiments, the pulse generator 101 can obtain
power to generate the therapy signals from an external power source
105. The external power source 105, which is arranged external to
the patient, can transmit power to the implanted pulse generator
101 using electromagnetic induction (e.g., RF signals). For
example, the external power source 105 can include an external coil
106 that communicates with a corresponding coil (not shown) within
the implantable pulse generator 101. The external power source 105
can be portable for ease of use.
[0044] In another embodiment, the pulse generator 101 can obtain
the power to generate therapy signals from an internal power
source. For example, the implanted pulse generator 101 can include
a non-rechargeable battery or a rechargeable battery to provide the
power. When the internal power source includes a rechargeable
battery, the external power source 105 can be used to recharge the
battery. The external power source 105 in turn can be recharged
from a suitable power source e.g., via a standard power plug
107.
[0045] In still further embodiments, an external programmer (not
shown) can communicate with the implantable pulse generator 101 via
electromagnetic induction. Accordingly, a practitioner can update
the therapy instructions provided by the pulse generator 101.
Optionally, the patient may also have control over at least some
therapy functions, e.g., starting and/or stopping the pulse
generator 101.
[0046] FIG. 2 illustrates another therapy system 200 in which the
implantable pulse generator 101 is connected to percutaneous lead
bodies 108 and 109, which are in turn connected to electrodes 110.
The leads 108, 109 and electrodes 110 are shown in a bipolar
configuration with two electrodes 110 carried by each lead 108,
109. In other embodiments, however, the leads 108, 109 can each
contain more electrodes 110 (e.g., three, four, five, eight, or
more) for applying therapy signals. In any of the foregoing
embodiments, the electrodes (e.g., the electrode array 103 or the
electrodes 110 of the percutaneous leads 108,109) can be arranged
adjacent different nerve fibers within the patient to enable the
application of different types of therapy, as is discussed further
below.
[0047] FIG. 3 is a cross-sectional illustration of a spinal region
SR that includes the spinal cord SC and an adjacent vertebra VT
(based generally on information from Crossman and Neary,
"Neuroanatomy," 1995 (publ. by Churchill Livingstone)), along with
selected representative locations for representative leads 108
(shown as leads 108a-108d) in accordance with several embodiments
of the disclosure. The spinal cord SC is situated between a
ventrally located vertebral body VVB and a dorsally located
vertebral body DVB that includes a transverse process 198 and
spinous process 197. Arrows V and D identify ventral and dorsal
directions, respectively. In particular embodiments, the vertebra
VT and leads can be at T10 or T11 (e.g., for axial low back pain or
leg pain) and in other embodiments, the leads can be placed at
other locations. The spinal cord SC itself is located within the
dura mater DM, which also surrounds portions of the nerves exiting
the spinal cord SC, including the dorsal roots DR, dorsal root
ganglia G and ventral roots VR. The spinal cord SC is illustrated
as having identifiable areas of afferent and efferent fibers
including ascending pathway areas AP and descending pathway areas
DP.
[0048] The leads are generally positioned to stimulate tactile
fibers and to avoid stimulating fibers associated with nociceptive
pain transmission. In a particular embodiment, a lead 108a (e.g., a
first lead) can be positioned centrally in a lateral direction
(e.g., aligned with the spinal cord midline ML) to provide signals
directly to the dorsal column DC of spinal cord SC. In other
embodiments, the first lead can be located laterally from the
midline ML. For example, single or paired leads can be positioned
just off the spinal cord midline ML (as indicated by leads 108b) to
provide signals to the dorsal column DC. One or more other leads
(e.g., second leads) can be positioned proximate to the dorsal root
DR or dorsal root entry zone DREZ (e.g., 1-4 mm from the spinal
cord midline ML, as indicated generally by lead 108c), and/or
proximate to the dorsal root ganglion G (as indicated by lead
108d). Other suitable locations for the second lead include the
"gutter," also located laterally from the midline ML. In still
further embodiments, the leads 108 may have other locations
proximate to the spinal cord SC and/or proximate to other target
neural populations e.g., laterally from the midline ML and medially
from the dorsal root ganglion 194. For example, the leads can be
located subdurally rather epidurally, as shown in dashed lines for
midline lead 108a and off-midline leads 108b. The practitioner may
select any of a variety of combinations of the foregoing locations,
depending on the particular patient's needs and condition. In at
least some embodiments, the practitioner can place two leads, each
positioned to direct signals to a different target location (e.g.,
neural population) of the patient's spinal cord SC. In other
embodiments, a single lead may have electrodes positioned at two or
more target locations. In either case, individual electrodes can
deliver signals with different characteristics to different neural
populations to achieve a beneficial effect for the patient.
A. Therapy Options
[0049] In general, different types of therapy signals can be
applied to the nerve fibers of a patient to different effect. For
example, applying a low-frequency (LF) therapy signal to the nerve
fibers of a patient can stimulate the nerve fibers to create an
effect known in the art as "paresthesia," which creates a sensation
of numbness in the patient. This paresthesia effect can mask
chronic pain, providing relief to the patient. Such an application
of therapy signals is generally known as Spinal Cord Stimulation
(SCS) therapy. In a particular embodiment of the present
disclosure, the LF signal can have a frequency in the range of up
to about 1,500 Hz, and a pulse width equal to or less than half of
the period of the signal. In a particular embodiment, the LF signal
can have a frequency in the range of from about 40 Hz to about 500
Hz.
[0050] Applying a high-frequency (HF) therapy signal to the nerves
can produce a block or partial block on the nerves. Accordingly, as
used herein, the term "block" refers generally to an at least
partial block (e.g., a partial or complete block), and the term
"blocking signal" refers generally to a signal that creates an at
least partial block. In addition, while it is believed that the
block inhibits or prevents the transmission of neural signals, a
desired effect on the patient (e.g., pain reduction) is not
necessarily limited to such a mechanism, and in at least some
embodiments, pain reduction may be achieved by one or more other
mechanisms. This block inhibits and/or prevents excitatory
responses from reaching the brain of the patient. Typically, the HF
therapy signal includes a biphasic signal. In a particular
embodiment, the HF therapy signal is a biphasic (alternating
current) signal having a 50% duty cycle and a frequency in the
range of from about 2,500 Hz to about 100,000 Hz. In particular
embodiments, the HF signal can have a frequency in the range of
from about 2,500 Hz to about 20,000 Hz, and in further particular
embodiments, about 3,000 Hz to about 10,000 Hz.
[0051] Representative examples of HF signal waveforms that can be
applied to the dorsal column DC (FIG. 3) are shown in FIGS. 4 and
5. The signal waveforms shown in FIG. 4 include biphasic, charge
balanced, square wave pulses. In the example shown, a first
waveform 400 is applied to a first signal channel C1 and a second
waveform 450 is applied to a second signal channel C2. In a
particular embodiment, the waveform on the first signal channel C1
is interlaced with the waveform on the second signal channel C2 to
minimize interaction between the signals 400, 450. This option is
generally available when the HF signal is applied at a duty cycle
of less than 50%, using one or more contacts that are shared
between the first channel C1 and the second channel C2. When the HF
signal has a 50% duty cycle, separate dedicated contacts can be
used for each of the first and second channels C1, C2 to avoid
interference between signals on the two channels. In still further
embodiments, signal waveforms other than those shown in FIG. 4 can
be used. For example, FIG. 5 illustrates biphasic, charge balanced,
sinusoidal pulses 500, 550 which can be applied via the first and
second signal channels C1, C2, respectively.
[0052] Detailed treatment processes for administering therapy
signals for chronic pain management are described below. In certain
embodiments, a physician or other practitioner can choose to
combine two or more of the treatment processes described below for
administering therapy for chronic pain management. The combination
of the different types of therapy can provide pain relief on
multiple fronts, providing extended coverage to the patient. For
example, in one embodiment, multiple treatment processes can be
applied to a patient simultaneously. In other embodiments, the
therapies can be combined, but chronologically spaced, or offset,
which can also have advantages. For example, as noted in further
detail later, one therapy signal can be used to facilitate the
initialization and/or the maintenance of another therapy
signal.
[0053] 1. Blocking at the Dorsal Column
[0054] A representative first treatment process for administering
therapy for chronic pain management includes applying an HF
blocking signal directly to the dorsal column DC of the patient.
For example, FIG. 6 is a schematic depiction of a representative HF
blocking signal 600 applied to the dorsal column DC. This HF
blocking signal can be applied to the dorsal column DC in place of
an LF stimulation signal to replace the pain relief provided by the
paresthesia.
[0055] In general, the HF stimulation blocking signal 600 is
applied to the dorsal column DC to establish a partial or total
neuronal block at the dorsal column DC sufficient to block the
chronic pain felt by the patient. The HF therapy signal can be
applied to one or more select regions (e.g., vertebral levels) of
the dorsal column DC to block transmission of pain signals from
lower dermatomes. The HF blocking signal can inhibit or prevent the
sensation of pain (e.g., to effect anesthesia) in the dermatomes
corresponding to the selected regions.
[0056] 2. Blocking at the Dorsal Root and/or the Dorsal Root
Ganglion
[0057] In a representative second treatment process for
administering therapy for chronic pain management, an HF blocking
signal is applied to one or more dorsal roots DR and/or dorsal root
ganglion(s) G of a patient, instead of directly to the dorsal
column DC. FIG. 7 is a schematic depiction of an example HF
blocking signal 700 applied to the dorsal root DR. Blocking at the
dorsal root DR and/or the dorsal root ganglion G facilitates
blocking sensation signals associated with one or more select
regions of the body. In contrast, blocking at the dorsal column DC
generally blocks only tactile and proprioceptive signals, generally
at all dermatomes associated with sections of the dorsal column DC
located below the blocking electrodes.
[0058] Arranging the electrodes (e.g., the electrodes carried by
the array 103 shown in FIG. 1 or the electrodes 110 shown in FIG.
2) at the dorsal root DR and/or dorsal root ganglion G can enhance
the range and effectiveness of the therapy signals. At such
locations, the CSF fluid layer is not as thick as it is at the
dorsal column DC, which can allow more current to flow to the
spinal region. The CSF fluid layer is thicker closer to the dorsal
column DC, which can shunt much of the current before the current
reaches the dorsal column DC. By positioning the electrodes away
from the dorsal column DC, it is expected that an electrical block
of the nerve fibers may be established with less power.
[0059] In addition, sensory nerve responses typically proceed
through the dorsal roots DR to the dorsal column DC, whereas motor
nerve responses proceed through the ventral roots VR (see FIG. 3)
to the spinal cord SC. Applying therapy signals to the dorsal root
DR, therefore, can facilitate blocking of sensory responses (e.g.,
pain) without decreasing or eliminating the transmission of motor
control impulses.
[0060] 3. Blocking at Peripheral Nerves
[0061] In a third treatment process for administering therapy for
chronic pain management, an HF blocking signal can be applied to
the peripheral nerves of the patient (e.g., the nerves distal of
the spinal cord SC). For example, an HF blocking signal can be
applied to the somatic nerves of the patient. In another
embodiment, the HF blocking signal can be applied to the autonomic
nerves of the patient. Applying the HF block to the peripheral
nerves can enable placement of the electrodes away from the spinal
cord SC and the spinal fluid, and can therefore reduce the
likelihood for interference with spinal function.
[0062] 4. Combining Blocking with Stimulation Therapy
[0063] Other treatment processes for administering therapy for
chronic pain management combine the application of an HF blocking
signal with the process of applying an LF stimulating signal to the
dorsal column DC of the patient to induce paresthesia. In general,
the HF blocking signal can facilitate the inducement of paresthesia
by alleviating patient discomfort resulting from the application of
the LF stimulation signal.
[0064] The application of an LF stimulation signal to the dorsal
column DC can induce paresthesia and/or induce patient discomfort,
depending on the distance between the electrode(s) and the spinal
cord (e.g., the thickness of the intermediate cerebral spinal fluid
layer). As used herein, the term "discomfort" refers generally to
an unpleasant, undesirable, uncomfortable and/or unwanted sensation
or other response. The term includes, but is not limited to, pain.
Typically, in conventional SCS treatment, patient discomfort
results from the inadvertent application of the electric field
produced by the electrode(s) to an adjacent dorsal root DR. In
general, the greater the distance between the electrode and the
spinal cord, the greater the likelihood that the electric field
will interact with the dorsal root DR to stimulate pain sensations
on the dorsal root DR, thus causing discomfort and/or pain as the
signal amplitude is increased.
[0065] FIG. 8 schematically depicts the amplitude of an LF
stimulation signal likely to induce paresthesia (represented by
threshold curve T.sub.P) and the amplitude of the LF stimulation
signal likely to induce patient discomfort (represented by
threshold curve T.sub.D) as a function of spacing between the
electrodes and the spinal cord. FIG. 8 is not intended as an exact
plot of amplitude as a function of the spacing, but rather is
intended to illustrate the general relationship amongst the
paresthesia threshold T.sub.P, the patient discomfort threshold
T.sub.D, and the spacing.
[0066] As shown in FIG. 8, when the electrodes are spaced
relatively close to the spinal cord (e.g., when the spacing is less
than about distance X), the electric field created by the
electrode(s) induces paresthesia before causing discomfort.
However, when the electrodes are spaced farther from the spinal
cord (e.g., when the spacing is greater than about distance X), the
LF stimulation signal can stimulate the dorsal root DR fibers,
thereby potentially causing discomfort, before stimulating the
dorsal column fibers at a level sufficient to induce paresthesia.
The paresthesia threshold T.sub.P and the patient discomfort
threshold T.sub.D cross at the electrode spacing distance X, which
is approximately 2 mm in at least some embodiments, and can vary
depending on factors that include signal delivery parameters.
Further details regarding the relationship amongst electrode
spacing, paresthesia, and pain can be found, e.g., in Effectiveness
of Spinal Cord Stimulation in the Management of Chronic Pain:
Analysis of Technical Drawbacks and Solutions by Jan Holsheimer
(Neurosurgery, Vol. 40, No. 5, May 1997), the disclosure of which
is hereby incorporated herein by reference in its entirety.
[0067] Some combination treatment processes in accordance with
embodiments of the disclosure for administering therapy for chronic
pain management use an HF blocking signal to inhibit the discomfort
sensation produced when the LF signal amplitude reaches the
discomfort threshold T.sub.D, thereby enabling the amplitude of the
LF signal to be increased further to the paresthesia threshold
T.sub.P. This in turn can allow the LF signal to be effective, even
if it is provided by an electrode that would otherwise be too far
away from the target nerve region (e.g., the dorsal column) to
produce paresthesia without also producing discomfort. Other
combination treatment processes augment the pain relief provided by
paresthesia with the pain relief provided by blocking different
sections of the spinal region, as will be discussed later.
[0068] a. Blocking at Dorsal Root
[0069] A representative fourth treatment process for administering
therapy for chronic pain management applies an HF blocking signal
to the dorsal root DR (and/or dorsal root ganglion G) while
applying the LF stimulating signal at the dorsal column DC. As used
herein, the term "dorsal root" can include the dorsal root itself,
the dorsal root entry region, and the conus. FIG. 9 is a schematic
illustration of an HF blocking signal 900 applied to the dorsal
root DR of a patient, and an LF stimulating signal 950 applied to
the dorsal column DC. The HF signal can establish a block on the
dorsal root DR that inhibits the transmission to the brain of pain
sensations induced by the electric field of the LF stimulation
signal.
[0070] In some embodiments, the HF blocking signal 900 is applied
to the dorsal root DR prior to application of the LF stimulating
signal 950 to the dorsal column DC. In other embodiments, however,
the HF blocking signal 900 can be applied at generally the same
time as or after the LF stimulating signal 950 is applied to the
dorsal column DC. In one embodiment, the LF stimulation signal 950
can be initiated with a low-level amplitude that is subsequently
ramped up to a suitable operating amplitude.
[0071] In other embodiments, the HF blocking signal applied to the
dorsal root DR augments the pain relief provided by the
paresthesia. For example, blocking the dorsal root DR is expected
to block peripheral pain (e.g., any peripheral pain) from being
transmitted through the dorsal root DR. This can include not only
discomfort caused by the LF signal, but also the pain that the LF
signal is expected to address.
[0072] b. Blocking at Dorsal Column
[0073] A representative fifth treatment process for administering
therapy for chronic pain management applies an HF blocking signal
at a first section of the dorsal column DC while applying the LF
stimulating signal at a second section the dorsal column DC. The LF
stimulating signal is expected to induce a sensation of paresthesia
in dermatomes (e.g., all dermatomes) associated with the second
section of the dorsal column DC and lower sections (e.g., all lower
sections). The HF blocking signal is expected to block excitatory
responses produced at the first section and lower sections from
reaching the brain.
[0074] In some embodiments, the HF blocking signal is applied to
the dorsal column DC prior to application of the LF stimulating
signal to the dorsal column DC. In other embodiments, however, the
HF blocking signal can be applied at substantially the same time as
or after the LF stimulating signal is applied. In one embodiment,
the LF stimulation signal can be initiated with a low-level
amplitude that is subsequently ramped up to a suitable operating
amplitude.
[0075] In other embodiments, the HF blocking signal applied to the
dorsal column DC augments the pain relief provided by the
paresthesia. For example, the LF stimulating signal can boost nerve
responses that inhibit the sensation of pain and the HF blocking
signal can inhibit nerve responses that transmit pain signals to
the brain.
[0076] In general, the HF signal can be applied to the dorsal
column DC above (superior) or below (inferior) the site at which
the LF signal is applied. Signals applied to the dorsal column DC
will tend to induce action potentials in both directions along the
target sensory signal route, e.g., toward the brain (orthodromic)
and away from the brain (antidromic). If the orthodromic LF signal
creates a pleasant (or at least non-objectionable) sensation, such
as tingling, that masks the target pain, then there may be no need
for an HF signal applied to the dorsal column DC. However, if the
LF signal creates an unpleasant sensation (an orthodromic signal),
and the corresponding antidromic signal acts to mitigate the target
pain, then an HF signal may be applied superior to the LF
stimulation site to suppress the unpleasant sensation caused by the
orthodromic signal, while having no effect on the beneficial
antidromic signal. Accordingly, the patient can be outfitted with a
device that includes an LF signal generator coupled to electrical
contacts at the dorsal column, and an HF signal generator coupled
to electrical contacts located superiorly on the dorsal column DC.
In particular embodiments, the HF signal generator is activated if
(a) the paresthesia created by the LF signal is objectionable to
the patient, and (b) the antidromic action potentials created by
the LF signal reduce the target pain.
[0077] In another embodiment, the HF signals can be applied to the
dorsal column DC at a location inferior to where the LF signals are
applied. In this case, it is assumed that the antidromic signals
produced by the LF signals do not contribute (or do not contribute
significantly) to reducing the target pain. Accordingly, applying
HF signals at an inferior location, which is expected to block such
antidromic signals, is not expected to impact the effectiveness of
the LF signals, e.g., the orthodromic paresthesia effect. It is
further assumed, based on recent evidence, that dorsal column DC
fibers transmit pain, in contrast to more traditional models which
posit that pain travels through the spinothalamic tract. Based on
this assumption, blocking orthodromic pain signals passing along
the dorsal column is expected to reduce the target pain.
B. Treatment Parameters
[0078] In general, the therapy systems 100, 200 (FIGS. 1 and 2) can
be utilized to provide chronic pain management to patients using
one of the above described therapy options, or one or more
combinations thereof. The following treatment parameters are
representative of treatment parameters in accordance with
particular embodiments.
[0079] 1. Signal Parameters
[0080] In general, HF blocking signals can have a frequency ranging
between about 2,500 Hz and about 100,000 Hz. In a particular
embodiment, the HF blocking signal has a frequency ranging between
about 2,500 Hz and about 20,000 Hz and in another particular
embodiment, between about 3,000 Hz and about 10,000 Hz. In other
particular embodiments, the HF signal has a frequency of greater
than 10,000 Hz. Frequencies above 10,000 Hz may result in shorter
transition times, e.g., shorter times required to establish a
block. The current of the HF blocking signals generally can range
from about 2 mA to about 20 mA. In a particular embodiment, the
current of a representative HF blocking signal is about 5-10
mA.
[0081] 2. Modulating Signal Amplitude after Initialization
[0082] After an HF blocking signal has been initialized, the
amplitude of the blocking signal can be reduced from a first
operating level to a second, lower operating level without
affecting the sensory experience of the patient. For example, in
particular embodiments, the amplitude of the HF blocking signal can
be reduced by about 10-30% after initialization without affecting
the established block. Such a result can advantageously decrease
the amount of power required to operate the therapy system 100, 200
(FIGS. 1 and 2). For example, decreasing the operating power can
increase the battery life of the pulse generator 101 or otherwise
decrease the drain on the power source.
[0083] 3. Modulation of On/Off Time
[0084] In certain embodiments, therapy can be applied in a
discontinuous fashion so as to include periods when the therapy is
applied, and periods when the therapy is terminated according to a
duty cycle. In different embodiments, therapy application periods
can range from a few seconds to a few hours. In other embodiments,
the duty cycle of a therapy signal can extend over a few
milliseconds.
C. Initializing Blocking Signals
[0085] When HF blocking signals are initially applied to nerve
fibers, the patient can experience an onset response before the
block takes effect. An onset response is induced by a brief
activation of the nerve fibers resulting in sudden pain and/or
involuntary muscle contractions. Such an onset response can occur
regardless of whether the therapy signals are applied to the dorsal
column DC, the dorsal root DR, the dorsal root ganglions G, or to
the peripheral nerves of the patient.
[0086] In order to alleviate these symptoms, various initialization
procedures can be used as described below. For example, the nerve
activation caused by initializing the blocking signal can be
mitigated by adjusting the signal parameters (e.g., amplitude
and/or frequency) of the blocking signal. Alternatively, patient
discomfort caused by the onset response can be masked by applying
additional pain management therapy.
[0087] 1. Mitigating an Onset Response
[0088] As the term is used herein, mitigation of an onset response
refers generally to a decrease in the otherwise resulting
activation of the nerve to which the blocking signal is being
applied.
[0089] a. Amplitude Ramp-Up
[0090] A first initialization procedure for mitigating patient
onset response includes gradually ramping up the amplitude of the
blocking signal being applied to the nerve. As the term is used
herein, the amplitude of the blocking signal can refer to the
current amplitude and/or the voltage amplitude of the signal since
a direct relationship exists between the current and the voltage of
the blocking signal.
[0091] By starting the signal at a lower amplitude, fewer nerve
fibers are affected and stimulated initially. As the amplitude is
increased, additional nerve fibers are stimulated as the block is
established at the previous nerve fibers. The total number of nerve
fibers activated at any one time, therefore, is decreased when
compared with an un-ramped initialization. Patient discomfort that
may be caused by the stimulated fibers is likewise expected to be
mitigated.
[0092] For example, in FIG. 10, the amplitude and/or frequency of
representative blocking signal 1000 is gradually increased to an
operating amplitude OA over a finite period of time. In one
embodiment, the amplitude of the waveform 1000 is increased over a
period of a few seconds. In other embodiments, however, the
amplitude and/or frequency can be increased over a greater or
lesser period of a time (e.g., a few minutes or a few
milliseconds). In still further embodiments, the amplitude and/or
frequency can be decreased over time, as is discussed further below
with reference to FIGS. 11A-11C.
[0093] b. Amplitude and Frequency Modulation
[0094] Referring to FIGS. 11A-11C, a second initialization
procedure for reducing the onset response to treatment can include
at least two phases, one in which the applied frequency and/or
amplitude are above general operating levels, and one in which the
frequency and/or amplitude are reduced to operating levels. These
phases, as well as additional (and in some cases, optional) phases
are described below.
[0095] In some embodiments, the second initialization procedure can
include an optional onset phase P0 during which the frequency of
the blocking signal is maintained at a constant level F1 (see FIG.
11A) and the amplitude of the blocking signal is ramped up from a
low amplitude A1 to a high amplitude A2 (see FIG. 11B).
[0096] In a first phase P1, a blocking signal having a frequency F1
and amplitude A2 greater than the general operating frequency FO1
and operating amplitude AO1 is applied to a nerve. For example, a
blocking signal having a frequency in the range of about 2,500 Hz
to above 20 KHz and an amplitude up to about 20 mA can be applied
during the first phase P1.
[0097] In some embodiments, the application of the blocking signal
having a very high frequency F1 and a high amplitude A2 rapidly
results in a block on the nerve. In other embodiments, however, the
second initialization procedure can include an optional transition
phase P2 during which a block is established (i.e., during which
the signal increases in strength above the threshold T1). Even when
the transition phase P2 is utilized, however, the blocking signal
establishes a block on the nerve more rapidly than would a signal
that simply has the operating frequency and operating
amplitude.
[0098] During the transition phase P2, the frequency of the
blocking signal is decreased from the very high frequency F1 to a
frequency F2 (see FIG. 11A). Frequency F2 is lower than frequency
F1, but still significantly higher than the operating frequency FO.
Decreasing the frequency increases the charge per phase and hence
the strength of the blocking signal (see FIG. 11C). The frequency
is lowered until the signal strength crosses the blocking threshold
T1. In one embodiment, the amplitude may be further increased as
well during the transition phase P2.
[0099] In a subsequent phase P3, the frequency and amplitude of the
blocking signal can be reduced from a level at which the block is
established to first operating levels (e.g., FO1, AO1 shown in FIG.
11B). In one embodiment, a block is established when the charge per
phase of the blocking signal passes above a blocking threshold T1
(see FIG. 11C). Decreasing the amplitude of the blocking signal
lessens the drain on the power source. Decreasing the frequency
increases the charge per phase (e.g., the stimulation applied to
the nerve fibers) to compensate for the reduction in amplitude. In
one embodiment, a practitioner begins ramping down the frequency
and the amplitude concurrently. In other embodiments, however, the
amplitude and frequency can be ramped down at different times.
[0100] In some embodiments, an optional phase P4 includes
decreasing the amplitude of the signal from the first operating
level AO1 to a different operating level AO2 after the block is
established (see FIG. 11B). Decreasing the amplitude lowers the
charge per phase (see FIG. 11C). The block can be maintained, even
if the charge per phase drops below the first threshold T1, as long
as the charge per phase does not drop below a second threshold T2
(see FIG. 11C). Typically, threshold T2 is 10-30% less than the
threshold T1.
[0101] FIG. 12 is a schematic depiction of an example blocking
signal 1200 initially having a high frequency F1 (e.g., about 30-50
KHz) and a high amplitude A2 (e.g., about 15-20 mA). In the example
shown, the blocking signal 1200 is a biphasic, charge balanced,
square waveform. In other embodiments, however, the blocking signal
1200 can include any desired waveform. When the block on the nerve
is established, the amplitude of the blocking signal 1200 is ramped
down to an appropriate operating level AO (e.g., about 5-10 mA). As
further shown in FIG. 12, the frequency of the blocking signal 1200
also can be decreased to an appropriate operating level FO (e.g.
about 3-10 KHz).
[0102] FIG. 13 shows the blocking signal 1200 having an initial
ramp-up period shown at 1200a, during which the signal amplitude is
increased to a maximum amplitude MA. Ramping up the amplitude of
the signal can allow the signal to be initiated safely with reduced
or non-existent patient discomfort. In other embodiments, however,
the onset phase P0 can be skipped and the very high amplitude A2 of
the blocking signal can be applied from the beginning.
[0103] 2. Masking Onset Response
[0104] As the term is used herein, masking of an onset response
refers generally to a decrease in the discomfort of the patient
otherwise resulting from an onset response, without affecting
activation of the nerve to which the blocking signal is being
applied.
[0105] a. Inducing Paresthesia
[0106] Referring to FIG. 14, paresthesia induced by an LF
stimulating signal applied to the dorsal column DC can mitigate the
onset response of an HF blocking signal applied to the dorsal root
DR. The low-level paresthesia, while not strong enough to control
the chronic pain of the patient, can alleviate some or all of the
discomfort experienced by the patient as a result of the
initialization of the HF blocking signal. Examples of the relative
timing for the therapy signals are shown in FIG. 14.
[0107] As shown in FIG. 14, an LF stimulating signal 1450 having a
low amplitude and a low frequency (e.g., in the range of about 40
Hz to about 250 Hz) is applied to the dorsal column DC of a patient
to induce paresthesia. Next, an HF blocking signal 1400 having a
high frequency (e.g., ranging from about 2,500 Hz to about 100,000
Hz, and in a particular embodiment, from about 2,500 Hz to about
20,000 Hz, and in a further particular embodiment, about 2,500 Hz
to about 10,000 Hz) is applied to the dorsal root DR of the
patient. The paresthesia induced by stimulating the dorsal column
DC can enhance patient comfort while the partial or complete HF
block is established at the dorsal root DR. In a representative
example, an LF signal is applied to the dorsal column DC for a
period of several seconds before applying the HF signal, at least
up to an amplitude below that which causes discomfort and/or pain.
In particular embodiments (e.g., in cases for which the HF blocking
signal by itself has a sufficient therapeutic effect), the LF
signal can be halted once the HF signal is established and the
period for experiencing an onset response has passed. In a
representative embodiment, this time period can be from about 5
seconds to about 5 minutes. The LF signal can then be
re-established for a short period the next time an HF signal is
initiated to again reduce or eliminate the onset response. In this
manner, the onset response can be controlled without requiring a
continuous (and therefore power consuming) LF signal. This
arrangement can be used when the LF signal is applied at a location
superior to the HF signal location, e.g., when both the LF and HF
signals are applied to the dorsal column DC, or when the LF signal
is applied to the dorsal column DC above a dorsal root DR location
at which the HF signal is applied.
[0108] b. Pharmacological Anesthetic
[0109] One or more pharmaceutical drugs affecting the pain neural
transmission synapse or neuromuscular junction also can be given to
the patient prior to initiating a therapy signal, such as an HF
blocking signal. For example, bupivacaine and/or other suitable
local anesthetics may be used in this regard, when injected
epidurally. The various classes of analgesics used for epidural and
spinal block include local anesthetics, opioids, adrenergic
agonists, and cholinergic agonists. Local anesthetics inhibit
neural conduction by reversibly blocking conductance in axonal
sodium channels. Opioids exert their effect by reversibly binding
to opioid receptors in the dorsal horn of the spinal cord. Alpha-2
adrenergic agents interact with alpha-2 adrenergic receptors in the
spinal cord, and cholinergic agonists produce analgesia by
increasing the concentration of acetylcholine proximate to
muscarinic and nicotinic receptors in the superficial layers of the
dorsal horn of the spinal cord. The pharmacological agent can be
delivered via the same device that supplies the electrical signals,
or the agent can be delivered via a separate device. In a
particular embodiment, PLGA or another suitable polymer can be used
to exude the agent.
D. Electrode Configurations
[0110] FIGS. 15-18 illustrate different design variations that
include an electrode array having four electrodes. In other
embodiments, arrays can include a greater or lesser number of
electrodes arranged in the same or other patterns. In a particular
embodiment, an array can contain two electrodes. In another
embodiment, an array can contain three electrodes. In yet another
embodiment, an array can contain up to sixteen or more electrodes.
Increasing the number of electrodes increases the number of channel
vectors which can be utilized during therapy, thereby broadening
the types of therapy applied and/or the regions over which the
therapy is applied.
[0111] FIG. 15 illustrates an example electrode array 119 including
four electrodes 115, 116, 117, 118 implanted at the spinal cord SC.
In the embodiment shown in FIG. 15, a first therapy signal (e.g.,
for affecting paresthesia at the dorsal column DC) is applied via a
first output channel C1 (shown schematically) of the array 119 that
extends along the dorsal column DC and can include a first pair of
electrodes 116, 117. A second therapy signal (e.g., for blocking
pain in the dorsal root DR) is transmitted via a second output
channel C2 (shown schematically) of the array 119 that extends at
an angle (e.g., 10.degree., 30.degree., 60.degree., 90.degree.,
120.degree., etc.) to the first output channel C1 and can include a
second pair of electrodes 115, 116.
[0112] In such a configuration, the vector of the electrical
stimulation applied via the first channel C1 between electrode 116
and electrode 117 is angled relative to the vector of the
electrical stimulation applied through the second channel C2
between electrode 116 and electrode 115. By arranging the
electrodes to provide angled (e.g., orthogonal) signal channels C1,
C2, electric field interaction between the channels C1, C2 can be
reduced or minimized. Furthermore, the first channel C1 can be
oriented to align with the dorsal column DC and the second channel
C2 can be oriented to align with the dorsal root DR. For example,
the second channel C2 can be arranged generally orthogonal adjacent
the thoracic region of the spine, and more acutely angled closer to
the lumbar region.
[0113] The remaining electrode 118 can be used to create other
channels for applying therapy signals. For example, if the dorsal
root crosses the electrode array 119 above the second pair of
electrodes 115, 116, then the second therapy signal can be applied
along a third channel (not shown) between electrodes 117, 118 to
block the dorsal root DR. In other embodiments, the remaining
electrode 118 can provide other stimulation vectors for the dorsal
column DC to further optimize the therapy.
[0114] The foregoing arrangement, in which one of the first
electrodes (e.g., first electrode 116) forms part of both the first
channel C1 and the second channel C2 can be suitable when the
signals applied to both channels C1, C2 are interlaced. For
example, this arrangement can be suitable when an HF signal applied
to the second channel C2 has a duty cycle of less than 50%, and an
LF signal applied to the first channel C1 is interlaced with the HF
signal. In another arrangement (shown in dashed lines in FIG. 15),
an additional first electrode 116a is used in combination with the
electrode 117 for the first channel C1, and electrodes 115, 116
form a separate second channel C2. This arrangement can be used
when the duty cycle applied to one or both channels C1, C2 is 50%.
Though not shown for purposes of clarity, a similar arrangement can
be applied to the embodiments shown in other Figures as well, e.g.,
FIGS. 16 and 18.
[0115] a. Lateral Spacing
[0116] FIG. 16 shows an electrode array 120, which is a variant of
the electrode array 119 shown in FIG. 15. The electrode array 120
includes an electrode 123 that is laterally offset from the
corresponding electrode 115 shown in FIG. 14 and accordingly forms
a second output channel C2a having an increased length. The
increased length of the channel C2a produces an electric field
having a wider coverage. In specific patient anatomies, an
increased field can be advantageous, for example, when it is
desirable to block an increased number of fibers. In general, the
larger the electric field, the greater number of nerve fibers
affected by the therapy signal. When applied along the dorsal
column DC, a large electric field penetrates deeper and more
laterally into the dorsal column DC, thereby inhibiting pain over a
large region of the body (e.g., by covering multiple
dermatomes).
[0117] However, as noted above, it is not always desirable to
affect large regions of nerve fiber. For example, a larger electric
field applied to the dorsal column DC may be more likely to "leak"
to adjacent fibers on the dorsal root DR or ventral root. In
addition, a larger electric field can stimulate or block fibers
carrying motor control impulses (e.g., ventral roots). Large
electric fields can be more likely to affect these motor nerve
fibers and cause undesirable side effects to the treatment.
Accordingly, in at least some such instances, the array 119 shown
in FIG. 15 may be more appropriate.
[0118] b. Axial Spacing
[0119] Electrodes within an electrode array also can be axially
spaced to increase the penetration along the dorsal column DC. For
example, in an arrangement shown in FIG. 17, an electrode array 121
can include an electrode 124 axially aligned with electrodes 116,
117, but arranged in an axially inferior position relative to the
electrode 116.
[0120] In some embodiments, channels can be formed between
non-adjacent electrodes to increase the length of the channels. For
example, in the embodiment shown in FIG. 17, the electrode 124 can
form a first channel C1a with the electrode 117. In other
embodiments, however, channel length is increased by increasing the
spacing between adjacent electrodes.
[0121] c. Non-Orthogonal Orientation
[0122] In certain embodiments, electrode arrays can be configured
to provide vectors for electrical stimulation that reflect the
anatomy of the patient. For example, an electrode array 122 shown
in FIG. 18 includes electrodes 115, 116, 117 that are generally
similar to the corresponding electrodes discussed above with
reference to the array 119. In addition, the electrode array 122
includes an electrode 125 spaced axially from electrode 115. In the
example shown, the electrode 125 is spaced at an axially inferior
position relative to electrode 115. Electrode 125 can be included
in place of electrode 118 of array 119.
[0123] Electrode array 122 can advantageously provide channel
vectors (e.g., channel C2b) oriented in directions generally
followed by dorsal roots DR leaving the dorsal column DC at the
intervertebral foramen of the spinal cord SC. Proximal the brain,
the dorsal root DR branches from the dorsal column DC at a
generally orthogonal orientation relative to the dorsal column DC.
Distal of the brain, however, the dorsal roots DR branch from the
dorsal column DC at increasingly downward angles. Accordingly, an
array of the type shown in FIG. 18 may be particularly suitable for
applications distal of the brain.
[0124] 3. Percutaneous Lead Configurations
[0125] Various details of array electrode configurations are
described above. It will be appreciated that many of the same
electrode configurations can be achieved by the use of bipolar or
multi-polar, percutaneous leads as described in connection with
FIGS. 19A-21. Typically, percutaneous leads require less invasive
surgery and, therefore, are more convenient to implant than
electrode arrays.
[0126] a. Bipolar Leads
[0127] A lead configuration 140, shown schematically in FIG. 19A,
includes a first percutaneous lead 126 that is implanted within the
patient together with a second percutaneous lead 130. The first
percutaneous lead 126 has first and second electrodes 127, 129,
respectively, and the second percutaneous lead 130 has first and
second electrodes 131, 133, respectively. The electrodes 127, 129,
131, 133 are generally aligned along the spinal cord SC. Typically,
the electrodes 127, 129 of the first lead 126 are aligned parallel,
but laterally displaced from the electrodes 131, 133 of the second
lead 130.
[0128] Therapy signals can be generated using one or both leads
126, 130. To apply a therapy signal to the dorsal column DC, the
therapy signal is typically generated by electrodes arranged along
a single lead (e.g., the first lead 126). To apply a therapy signal
to the dorsal root DR, the therapy signal is typically generated by
electrodes on two or more different leads (e.g., a first electrode
129 on the first lead 126, and a second electrode 133 on the second
lead 130). In the example shown, an LF stimulation signal can be
applied to the dorsal column DC via the first lead 126 and an HF
blocking signal can be applied to the dorsal root DR via electrodes
129, 133 on the first and second leads 126, 130, respectively.
[0129] In other embodiments, other types of therapy signals can be
applied via the first and second leads 126, 130. For example, an HF
blocking signal can be applied to the dorsal column DC via the
electrodes 131, 133 of the second lead 130.
[0130] FIG. 19B illustrates another embodiment in which a second
lead 130a is positioned along the dorsal root DR and a first lead
126a is positioned along the dorsal column DC (see FIG. 19B). In
one aspect of this embodiment, an up-regulating (e.g.,
paresthesia-inducing) signal can be applied to the first lead 126a
at the dorsal column DC and a down-regulating (e.g., blocking)
signal can be applied to the second lead 130a at the dorsal root
DR.
[0131] FIG. 19C illustrates the inferior portion of the spine,
including the lower lumbar and sacral vertebrae, and associated
nerve roots. Signals (e.g., HF signals) can be applied to these
roots alone or in conjunction with signals applied superiorly to
the dorsal column. In particular arrangements, leads or pairs of
leads can be positioned between adjacent roots to provide signals
to a number of roots that is greater than the number of leads. For
example, a first pair of leads 152a, 154b, each having electrodes
or electrode contacts 160, can be positioned along opposite sides
of the S3 root to provide signals to at least the S2, S3 and S4
roots. In another representative example, a second pair of leads
152b, 154b can be placed alongside the L5 root to provide signals
to the L5 root, the S1 root and optionally the L4 root. In other
embodiments, leads having similar (or other) structures can be
placed along other roots. An advantage of the foregoing arrangement
is that a reduced number of leads can be used to apply signals to a
greater number of roots.
[0132] b. Multi-Channel Lead Arrangement
[0133] FIGS. 20 and 21 illustrate a multi-channel, percutaneous
lead arrangement 150 having first and second leads 152, 154
configured to deliver multiple therapy signals to a patient. FIG.
20 illustrates how the lead arrangement 150 can be used generally
to apply therapy signals to the dorsal column DC. FIG. 21
illustrates how the lead arrangement 150 can be used generally to
apply therapy signals to the dorsal root DR. In different
embodiments, the leads 152, 154 can cooperate to provide multiple
types of therapy signals to the dorsal column DC and/or dorsal root
DR of a patient.
[0134] Each lead 152, 154 of the lead arrangement 150 includes a
first arrangement 155 of electrodes, a second arrangement 157 of
electrodes, and a third arrangement 159 of electrodes. In the
example shown, the first and third arrangements 155, 159 include
bipolar electrodes. The second arrangement 157 includes a tripolar
electrode arrangement (e.g., a central cathode with anodes on
either side). In such an embodiment, current can be controlled
independently to adjust therapy for variations in
electrode-to-nerve positioning. In other embodiments, however, the
leads 152, 154 can include other arrangements of electrodes. In the
example shown, each lead 152, 154 of the lead arrangement 150
includes seven electrodes. In other embodiments, however, a lead
can include one, two, three, four, five, or more electrodes.
[0135] In general, the first arrangement 155 of electrodes on one
or both leads 152, 154 can apply an LF stimulation signal to the
dorsal column DC to induce a sensation of paresthesia. Typically,
the electric field of the stimulating signal can be generated by
electrodes on a single lead so that the electric field is oriented
along the length of the dorsal column DC. For example, in FIG. 20,
the electrodes of the first arrangement 155 of the first lead 152
create an electric field at the dorsal column DC to induce a
sensation of paresthesia.
[0136] In one embodiment, the electrodes of the second arrangement
157 of one of the leads 152, 154 can generate an electric field of
an HF blocking signal at the dorsal column DC to establish a block
on the dorsal column DC. For example, the electrodes of the second
arrangement 157 can form a tripolar configuration to produce an HF
blocking signal as shown in FIG. 20. In other configurations, the
HF blocking signal can be generated using a lesser or greater
number of electrodes of the second arrangement 157.
[0137] In another embodiment, the HF blocking signal can be applied
to a dorsal root DR along at least some of the electrodes of the
second arrangement 157 on both leads 152, 154. For example, in FIG.
21, the middle electrodes of the second arrangement 157 on both
leads 152, 154 cooperate to form an electric field. This electric
field is oriented generally orthogonal to the electric field form
from the tripolar electrode arrangement of FIG. 20.
[0138] In other embodiments, additional electrodes from the second
arrangement 157 on one of both leads 152, 154 can cooperate to form
the electric field. For example, FIG. 21 also shows a therapy
signal channel between a first electrode 157a and a second
electrode 157b. The therapy channel is angled with respect to the
leads 152, 154. Such an angle may facilitate applying the therapy
signal along the length of a dorsal root DR as the root branches
from the dorsal column DC.
[0139] In the above paragraphs, a number of therapy combinations
have been described which include dorsal column low frequency
stimulation and/or high frequency blocking, dorsal root high
frequency blocking, and peripheral nerve high frequency blocking.
Procedures to avoid patient discomfort in the onset and subsequent
therapy phases also have been discussed. In other embodiments,
therapy can be performed in accordance with other permutations and
combinations of the aforementioned parameters, time variations, and
therapeutic phases.
[0140] To aid in understanding the above described treatment
options, the following example applications are provided. FIG. 22
illustrates a first treatment signal 2610 being applied to nerves
of a dorsal column DC of a patient. The first treatment signal 2610
is an LF signal configured to up-regulate the nerves of the dorsal
column DC to induce a sensation of paresthesia, and can be provided
by a first portion of the pulse generator 101 described above with
reference to FIG. 1.
[0141] A second treatment signal 2620 is applied to a dorsal root
DR of the patient subsequent to the initialization of the first
treatment signal 2610. The second treatment signal 2620 is an HF
signal configured to down-regulate the nerves of the dorsal root DR
to establish a block on the nerves, and can be provided by a second
portion of the pulse generator 101 described above with reference
to FIG. 1. The paresthesia induced by the first treatment signal
2610 at least partially masks the onset response experienced by the
patient when the second treatment signal 2620 is initiated.
[0142] As shown, a third treatment signal 2630 is applied to the
dorsal column DC after the second treatment signal 2620 is
initiated. In a particular embodiment, the third treatment signal
2630 is applied to the dorsal column DC after the second treatment
signal 2620 establishes a block on the dorsal root DR. The third
treatment signal 2630 is configured to establish a block on the
dorsal column DC.
[0143] In another representative example, a practitioner can
implant multiple electrodes at the patient's spinal region, with at
least one of the electrodes positioned to provide spinal cord
stimulation, and at least one of the electrodes positioned to apply
signals to the dorsal root or the dorsal root ganglion. The
practitioner can then apply an LF signal to the first electrode to
induce paresthesia and address pain suffered by the patient. In at
least some cases, the paresthesia may be sufficient to address the
patient's pain symptoms, and accordingly, an HF signal need not be
applied to the second electrode. In other instances, however, an
initial LF signal applied to the first electrode may not adequately
address the patient's pain. In such instances, the amplitude of the
signal supplied to the first electrode may be increased to produce
paresthesia. The increase may be required because the position of
the first electrode is not optimal, and/or because of
patient-specific physiological effects. In any of these
embodiments, increasing the amplitude of the signal applied to the
first electrode may, at the same time it causes paresthesia,
separately cause patient discomfort. Accordingly, the practitioner
can apply HF signals to the second electrode to block the patient
discomfort, without the need for repositioning the first electrode.
This arrangement can accordingly reduce the invasiveness of the
implantation procedure.
[0144] In another example, the patient may suffer from lower back
pain. The lower back pain may be transmitted along afferent nerve
fibers that enter the spinal column channel at the L5 vertebrae,
which is below the end of the spinal cord. Accordingly, the
practitioner may apply LF spinal cord stimulation at a higher
spinal elevation, for example, at the T10 vertebrae. In at least
some instances, the paresthesia resulting from such LF signals may
reduce pain somewhat, but not completely. Accordingly, the
practitioner may additionally apply HF signals at the L5 location
to block lower back pain sensations. In this instance, the HF
signal is applied at a different spinal elevation than the low
frequency signal.
[0145] In still another example, the patient may suffer from pain
transmitted along several neural pathways that enter the spinal
column at L1 (e.g., at the conus). The practitioner may apply HF
signals at the conus, in combination with LF signals at a higher
spinal elevation (e.g., T8, T9 or T10). This is unlike several
existing stimulation techniques, which deliberately avoid the conus
as an implantation/stimulation site.
[0146] From the foregoing, it will be appreciated that specific
embodiments of the disclosure have been described herein for
purposes of illustration, but that various modifications may be
made without deviating from the disclosure. For example, the LF
signals may be provided on a generally continuous basis in some
embodiments, and may be turned off and on automatically in other
embodiments, or in response to a patient request in still further
embodiments. In some embodiments, directions and/or instructions
were described in the context of a pulse generator, and in other
embodiments, such directions and/or instructions may be handled by
other controller components. Certain aspects of the disclosure
described in the context of particular embodiments may be combined
or eliminated in other embodiments. For example, while HF and LF
signals were discussed in the context of lower back pain and
applied to different spinal elevations, in other embodiments, such
signals may be applied at different spinal elevations to address
other patient pain symptoms. Further, while advantages associated
with certain embodiments have been described in the context of
those embodiments, other embodiments may also exhibit such
advantages. Not all embodiments need necessarily exhibit such
advantages to fall within the scope of the disclosure. Accordingly,
the disclosure can include other embodiments not shown or described
above.
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