U.S. patent application number 14/990019 was filed with the patent office on 2016-05-12 for systems and methods for delivering electric current for spinal cord stimulation.
The applicant listed for this patent is Cardiac Pacemakers, Inc.. Invention is credited to Jason J. Hamann, Stephen B. Ruble, Allan C. Shuros, Weiying Zhao.
Application Number | 20160129243 14/990019 |
Document ID | / |
Family ID | 41215760 |
Filed Date | 2016-05-12 |
United States Patent
Application |
20160129243 |
Kind Code |
A1 |
Zhao; Weiying ; et
al. |
May 12, 2016 |
SYSTEMS AND METHODS FOR DELIVERING ELECTRIC CURRENT FOR SPINAL CORD
STIMULATION
Abstract
Various system embodiments comprise a lead having a distal end
and a proximal end. The distal end includes a plurality of
electrodes. The lead is configured to be fed into a dorsal epidural
space of a human to a desired region of a spinal column and to be
fed laterally to at least partially encircle a spinal cord in the
desired region to place at least one stimulation electrode in
position to stimulate a dorsal nerve root and at least another
stimulation electrode in position to stimulate a ventral nerve
root. The desired region may include cervical vertebrae, thoracic
vertebrae, or lumbar vertebrae. Some embodiments stimulate the
spinal cord in the T1-T5 region.
Inventors: |
Zhao; Weiying; (Cupertino,
CA) ; Ruble; Stephen B.; (Lino Lakes, MN) ;
Shuros; Allan C.; (St. Paul, MN) ; Hamann; Jason
J.; (Blaine, MN) |
|
Applicant: |
Name |
City |
State |
Country |
Type |
Cardiac Pacemakers, Inc. |
St. Paul |
MN |
US |
|
|
Family ID: |
41215760 |
Appl. No.: |
14/990019 |
Filed: |
January 7, 2016 |
Related U.S. Patent Documents
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Application
Number |
Filing Date |
Patent Number |
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12431607 |
Apr 28, 2009 |
9259568 |
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14990019 |
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61048736 |
Apr 29, 2008 |
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Current U.S.
Class: |
607/72 |
Current CPC
Class: |
A61N 1/0553 20130101;
A61N 1/36071 20130101; A61N 1/0556 20130101; A61N 1/36057 20130101;
A61N 1/0551 20130101; A61N 1/36114 20130101 |
International
Class: |
A61N 1/05 20060101
A61N001/05; A61N 1/36 20060101 A61N001/36 |
Claims
1. A system comprising: a lead having a distal end and a proximal
end including a plurality of electrodes, the lead being configured
to steer into a dorsal epidural space of a human to a desired
region of a spinal column and to at least partially encircle a
spinal cord in the desired region to place at least one stimulation
electrode of the plurality of electrodes in position to stimulate
at least one of a dorsal nerve root and a ventral nerve root; and a
device coupled to the proximal end of the lead and configured to
deliver stimulation pulses to stimulate at least one of the dorsal
nerve root and the ventral nerve root.
2. The system of claim 1, wherein the lead is a steerable
stimulation lead configured to steer into a dorsal epidural space
of a human to a desired region of a spinal column and to at least
partially encircle a spinal cord in the desired region to place at
least one stimulation electrode of the plurality of electrodes in
position to stimulate at least one of a dorsal nerve root and a
ventral nerve root.
3. The system of claim 2, wherein the steerable stimulation lead
comprises a pre-formed shape and comprises a shape memory
material.
4. The system of claim 3, further comprising a delivery catheter
configured to deploy the steerable stimulation lead at the desired
region, and wherein the steerable stimulation lead is configured to
bias to the pre-formed shape after deployment from the delivery
catheter.
5. The system of claim 2, wherein the steerable stimulation lead is
steerable in at least two directions.
6. The system of claim 2, wherein the steerable stimulation lead
comprises a lumen, and the lumen is configured to receive a
steering tendon.
7. The system of claim 6, further comprising the steering tendon,
and wherein steerable stimulation lead is configured to steer the
steerable stimulation lead.
8. The system of claim 1, further comprising a steerable delivery
catheter, and wherein the lead is configured to steer via the
steerable delivery catheter.
9. The system of claim 8, wherein the steerable delivery catheter
is configured to deploy the lead at the desired region.
10. The system of claim 8, wherein the steerable delivery catheter
comprises a deflection area, a first steering tendon, a second
steering tendon, a first anchor member, and a second anchor member,
wherein the first steering tendon is attached to the first anchor
member located at a distal portion of a distal end of the lead, and
the second steering tendon is attached to the second anchor member
located distal to the deflection area.
11. The system of claim 8, wherein the steerable delivery catheter
is steerable in at least two directions.
12. A system comprising: a steerable lead having a distal end and a
proximal end including a plurality of electrodes, the steerable
stimulation lead having a pre-formed shape and being configured to
steer into a dorsal epidural space of a human to a desired region
of a spinal column and to at least partially encircle a spinal cord
in the desired region to place at least one stimulation electrode
of the plurality of electrodes in position to stimulate at least
one of a dorsal nerve root and a ventral nerve root; and a device
coupled to the proximal end of the lead and configured to deliver
stimulation pulses to stimulate at least one of the dorsal nerve
root and the ventral nerve root.
13. The system of claim 12, wherein the plurality of electrodes are
configured to direct a directional stimulation field toward at
least one of a dorsal nerve root and a ventral nerve root.
14. The system of claim 12, further comprising a steerable delivery
catheter, and wherein the steerable lead is configured to steer via
the steerable delivery catheter.
15. The system of claim 14, wherein the steerable delivery catheter
is configured to deploy the steerable stimulation lead at the
desired region.
16. The system of claim 12, wherein the steerable lead comprises a
distal tip, and the distal tip is biased to wrap around and
maintain contact with the spinal column.
17. A method for implanting a spinal cord stimulation lead,
comprising: introducing the lead into a dorsal epidural space;
feeding the lead through the dorsal epidural space proximate to a
desired vertebra; steering at least one electrode operationally
proximate to at least one of a dorsal nerve root to capture a
portion of a dorsal nerve root with electrical stimulation
delivered using the at least one electrode; and steering at least
another electrode operationally proximate to the ventral nerve root
to capture at least a portion of a ventral nerve root with
electrical stimulation delivered using the at least another
electrode.
18. The method of claim 16, wherein the lead comprises a distal end
made with a material having shape memory comprising a predetermined
shape.
19. The method of claim 18, further comprising passing the distal
end proximate to the dorsal nerve root and the ventral nerve root
when the distal end is in a flexed position; and setting the
position of the lead includes relaxing the distal end to allow the
distal end to at least partially surround the spinal cord.
20. The method of claim 17, further comprising feeding a steerable
catheter through the dorsal epidural space and laterally past the
desired vertebra and the dorsal nerve root to deliver the lead to
the desired vertebra.
Description
CROSS-REFERENCE TO RELATED APPLICATION
[0001] This application is a continuation of U.S. application Ser.
No. 12/431,607, filed Apr. 28, 2009, which claims priority to
Provisional Application No. 61/048,736, filed Apr. 29, 2008, which
are herein incorporated by reference in their entirety.
[0002] The following commonly assigned U.S. application is related
and is incorporated by reference in its entirety: "Systems and
Methods For Selectively Stimulating Nerve Roots," Ser. No.
61/048,742, filed Apr. 29, 2008.
TECHNICAL FIELD
[0003] This application relates generally to medical devices and,
more particularly, to systems, devices and methods for delivering
electrodes for spinal cord stimulation.
BACKGROUND
[0004] Sympathetic over activation is involved in a variety of
cardiovascular disease, such as ventricular arrhythmias, myocardial
infarction (MI), heart failure (HF), etc. Therapies that are based
on autonomic modulation have shown efficacy in a variety of
cardiovascular diseases in both preclinical and clinical studies.
The autonomic balance can be modulated to have more parasympathetic
tone by stimulating parasympathetic targets or inhibiting
sympathetic targets, and can be modulated to have more sympathetic
tone by stimulating sympathetic targets or inhibiting
parasympathetic targets.
[0005] Spinal cord stimulation has been proposed for a variety of
treatments, such as pain control. One known system for delivering
electrical stimulation to neural targets in and around the spinal
cord uses a lead inserted one-dimensionally into the dorsal
epidural space of the spinal cord.
SUMMARY
[0006] Various system embodiments comprise a lead having a distal
end and a proximal end. The distal end includes a plurality of
electrodes. The lead is configured to be fed into a dorsal epidural
space of a human to a desired region of a spinal column and to be
fed laterally to at least partially encircle a spinal cord in the
desired region to place at least one stimulation electrode in
position to stimulate a dorsal nerve root and at least another
stimulation electrode in position to stimulate a ventral nerve
root. The desired region may include cervical vertebrae, thoracic
vertebrae, or lumbar vertebrae. Some embodiments stimulate the
spinal cord in the T1-T5 region.
[0007] Various system embodiments comprise means for vertically
feeding a lead through a dorsal epidural space proximate to a
desired vertebra, and laterally passing the lead proximate to a
dorsal nerve root and a ventral nerve root, and means for fixing
the lead in position to operatationally place at least one
electrode in position to stimulate at least one of a dorsal nerve
root or a ventral nerve root.
[0008] According to various method embodiments for implanting a
spinal cord stimulation lead, the lead is introduced into a dorsal
epidural space, and fed through the dorsal epidural space proximate
to a desired vertebra. The lead is passed proximate to a dorsal
nerve root and a ventral nerve root. At least one electrode is
positioned operationally proximate to the dorsal nerve root to
capture at least a portion of the dorsal nerve root with electrical
stimulation delivered using the at least one electrode. At least
another electrode is positioned operationally proximate to the
ventral nerve root to capture at least a portion of the ventral
nerve root with electrical stimulation delivered using the at least
another electrode.
[0009] This Summary is an overview of some of the teachings of the
present application and not intended to be an exclusive or
exhaustive treatment of the present subject matter. Further details
about the present subject matter are found in the detailed
description and appended claims. Other aspects will be apparent to
persons skilled in the art upon reading and understanding the
following detailed description and viewing the drawings that form a
part thereof, each of which are not to be taken in a limiting
sense. The scope of the present invention is defined by the
appended claims and their equivalents.
BRIEF DESCRIPTION OF THE DRAWINGS
[0010] FIG. 1A illustrates a spinal column, including the T1-T5
vertebrae, from a posterior or dorsal perspective, and FIG. 1B
illustrates a side view of the spinal column.
[0011] FIG. 2 illustrates a perspective view of a portion of the
spinal column.
[0012] FIG. 3 illustrates a top view of a cross section of the
spinal column.
[0013] FIG. 4 illustrates an embodiment of a method for implanting
a lead for use in delivering spinal cord stimulation.
[0014] FIG. 5 illustrates sympathetic pathways extending from
ventral and dorsal nerve roots.
[0015] FIG. 6 illustrates a portion of the spinal cord, with nerve
roots extending from three vertebral locations, and further
illustrates a neural stimulation lead fed through the dorsal
epidural space and at least partially around the spinal cord to
operationally set electrodes in place to stimulate and/or inhibit
activity in the dorsal and ventral nerve roots, according to
various embodiments.
[0016] FIG. 7 illustrates a multi-lead embodiment to stimulate
dorsal and ventral nerve roots on contralateral sides of the spinal
cord.
[0017] FIG. 8 illustrates multiple electrodes on a lead wrapped at
least partially around the spinal cord, where at least some of the
electrodes are operationally positioned for use to stimulate the
dorsal nerve root and some of the electrodes are operationally
positioned for use to stimulate the ventral nerve root.
[0018] FIG. 9 illustrates an embodiment that includes a pre-formed
lead made with a material having a shape memory, where the lead
resumes its preformed shape to at least partially wrap around the
spinal cord when the lead exits a catheter used to deliver the lead
to the stimulation site.
[0019] FIGS. 10A and 10B illustrate a steerable lead embodiment
used to place stimulation electrodes in operational position to
stimulate ventral and dorsal nerve leads.
[0020] FIGS. 11A-11C illustrate an embodiment of a steerable
lead.
[0021] FIG. 12 illustrates a steerable catheter embodiment used to
deliver a lead to place stimulation electrodes from the lead in
operational position to stimulate ventral and dorsal nerve
leads.
[0022] FIGS. 13A-13C illustrate an embodiment of a steerable
catheter.
[0023] FIG. 14 illustrates a lead embodiment with a plurality of
ring electrodes.
[0024] FIGS. 15A-15B illustrate a lead embodiment with multiple
electrodes on a circumference of the lead.
[0025] FIGS. 16A-16B illustrate a lead embodiment with multiple
electrodes on a paddle-like distal end.
[0026] FIG. 17 illustrates a method embodiment to implant the
spinal cord stimulation lead to establish and maintain efficacious
stimulation therapy.
[0027] FIG. 18 illustrates a system used to deliver spinal cord
stimulation, according to various embodiments.
DETAILED DESCRIPTION
[0028] The following detailed description of the present subject
matter refers to the accompanying drawings which show, by way of
illustration, specific aspects and embodiments in which the present
subject matter may be practiced. These embodiments are described in
sufficient detail to enable those skilled in the art to practice
the present subject matter. Other embodiments may be utilized and
structural, logical, and electrical changes may be made without
departing from the scope of the present subject matter. References
to "an", "one", or "various" embodiments in this disclosure are not
necessarily to the same embodiment, and such references contemplate
more than one embodiment. The following detailed description is,
therefore, not to be taken in a limiting sense, and the scope is
defined only by the appended claims, along with the full scope of
legal equivalents to which such claims are entitled.
[0029] A known spinal cord stimulation system contains a straight
lead body with multiple electrodes, which only allows for
one-dimensional movement along the spinal cord. The vertical,
one-dimensional access within the epidural space limits the ability
of the device to selectively stimulate neural pathways, to position
the electrodes with respect to the neural targets in a desired
position to promote a desired efficacy of the stimulation, and to
avoid loss of nerve capture due to migration or movements of the
lead in the epidural space. Some issues with this lead design
include lead migration and the inability to precisely stimulate the
dorsal and ventral nerve root.
[0030] Various embodiments that provide neural stimulation
treatment selectively stimulate sympathetic afferent and/or
efferent neurones on the thoracic spinal cord. The system, device
and method provide a versatile way to stimulate neural targets in
the spinal cord region. Sympathetic modulation (inhibition or
activation of sympathetic activity) treats a variety of
cardiovascular disease with abnormal sympathetic activity. The
neural stimulation is capable of being implemented in treatments
for pain, heart failure, arrhythmia, angina, and the like. Various
embodiments activate sympathetic afferent (e.g. relatively low
frequency dorsal horn stimulation) or activate sympathetic efferent
(e.g. relatively low frequency ventral horn stimulation) or inhibit
or block sympathetic efferent (e.g. relatively high frequency
ventral horn stimulation). Some embodiments test and appropriately
modify the therapy delivery by testing the sympathetic response
(e.g., heart rate and blood pressure changes) and using the
electrodes which are operationally-positioned to stimulate the
selected neurons.
[0031] Various embodiments that deliver electrodes for spinal cord
stimulation provide a steerable design, which is capable of
selectively stimulating sympathetic afferent pathways in the dorsal
nerve root, sympathetic efferent pathways in the ventral nerve
root, or both sympathetic afferent and efferent pathways. The lead
can be moved vertically up and down along the spinal cord. Once the
targeted region is reached, such as in the T1-T5 region, the lead
body is capable of being steered to bend and curve around the
spinal cord. Some embodiments target other regions of the spinal
column, such as various regions in the cervical, thoracic or lumbar
areas. Some embodiments cause the lead to contract around at least
a portion of the spinal cord or other structure of the spinal
column. The contraction is appropriate to fix the electrodes in
position with respect to the spinal cord without providing an
undesirably high force against the spine. Various lead embodiments
provide multiple electrodes along both the ventral and dorsal horn
of the spinal column, allowing the electric current to be delivered
to either activate sympathetic afferent (low frequency dorsal horn
stimulation) or activate sympathetic efferent (low frequency
ventral horn stimulation) or electric blocking sympathetic efferent
(high frequency ventral horn stimulation). Some embodiments test
and appropriately modify the therapy delivery by testing the
sympathetic response (e.g., heart rate and blood pressure changes)
and using the electrodes which are operationally-positioned to
stimulate the selected neurons.
Physiology
[0032] Provided below is a brief discussion of some diseases
capable of being treated using the present subject matter and the
nervous system. This discussion is believed to assist a reader in
understanding the disclosed subject matter.
Diseases
[0033] The present subject matter can be used to prophylactically
or therapeutically treat various diseases by modulating autonomic
tone. Examples of such diseases or conditions include hypertension,
cardiac remodeling, and heart failure.
[0034] Hypertension is a cause of heart disease and other related
cardiac co-morbidities. Hypertension occurs when blood vessels
constrict. As a result, the heart works harder to maintain flow at
a higher blood pressure, which can contribute to heart failure.
Hypertension generally relates to high blood pressure, such as a
transitory or sustained elevation of systemic arterial blood
pressure to a level that is likely to induce cardiovascular damage
or other adverse consequences. Hypertension has been defined as a
systolic blood pressure above 140 mm Hg or a diastolic blood
pressure above 90 mm Hg. Consequences of uncontrolled hypertension
include, but are not limited to, retinal vascular disease and
stroke, left ventricular hypertrophy and failure, myocardial
infarction, dissecting aneurysm, and renovascular disease. A large
segment of the general population, as well as a large segment of
patients implanted with pacemakers or defibrillators, suffer from
hypertension. The long term mortality as well as the quality of
life can be improved for this population if blood pressure and
hypertension can be reduced. Many patients who suffer from
hypertension do not respond to treatment, such as treatments
related to lifestyle changes and hypertension drugs.
[0035] Following myocardial infarction (MI) or other cause of
decreased cardiac output, a complex remodeling process of the
ventricles occurs that involves structural, biochemical,
neurohormonal, and electrophysiologic factors. Ventricular
remodeling is triggered by a physiological compensatory mechanism
that acts to increase cardiac output due to so-called backward
failure which increases the diastolic filling pressure of the
ventricles and thereby increases the so-called preload (i.e., the
degree to which the ventricles are stretched by the volume of blood
in the ventricles at the end of diastole). An increase in preload
causes an increase in stroke volume during systole, a phenomena
known as the Frank-Starling principle. When the ventricles are
stretched due to the increased preload over a period of time,
however, the ventricles become dilated. The enlargement of the
ventricular volume causes increased ventricular wall stress at a
given systolic pressure. Along with the increased pressure-volume
work done by the ventricle, this acts as a stimulus for hypertrophy
of the ventricular myocardium. The disadvantage of dilatation is
the extra workload imposed on normal, residual myocardium and the
increase in wall tension (Laplace's Law) which represent the
stimulus for hypertrophy. If hypertrophy is not adequate to match
increased tension, a vicious cycle ensues which causes further and
progressive dilatation. As the heart begins to dilate, afferent
baroreceptor and cardiopulmonary receptor signals are sent to the
vasomotor central nervous system control center, which responds
with hormonal secretion and sympathetic discharge. It is the
combination of hemodynamic, sympathetic nervous system and hormonal
alterations (such as presence or absence of angiotensin converting
enzyme (ACE) activity) that ultimately account for the deleterious
alterations in cell structure involved in ventricular remodeling.
The sustained stresses causing hypertrophy induce apoptosis (i.e.,
programmed cell death) of cardiac muscle cells and eventual wall
thinning which causes further deterioration in cardiac function.
Thus, although ventricular dilation and hypertrophy may at first be
compensatory and increase cardiac output, the processes ultimately
result in both systolic and diastolic dysfunction (decompensation).
It has been shown that the extent of ventricular remodeling is
positively correlated with increased mortality in post-MI and heart
failure patients.
[0036] Heart failure (HF) refers to a clinical syndrome in which
cardiac function causes a below normal cardiac output that can fall
below a level adequate to meet the metabolic demand of peripheral
tissues. Heart failure may present itself as congestive heart
failure (CHF) due to the accompanying venous and pulmonary
congestion. Heart failure can be due to a variety of etiologies
such as ischemic heart disease. Heart failure patients have reduced
autonomic balance, which is associated with LV dysfunction and
increased mortality.
Nervous System
[0037] The autonomic nervous system (ANS) regulates "involuntary"
organs, while the contraction of voluntary (skeletal) muscles is
controlled by somatic motor nerves. Examples of involuntary organs
include respiratory and digestive organs, and also include blood
vessels and the heart. Often, the ANS functions in an involuntary,
reflexive manner to regulate glands, to regulate muscles in the
skin, eye, stomach, intestines and bladder, and to regulate cardiac
muscle and the muscle around blood vessels, for example.
[0038] The ANS includes the sympathetic nervous system and the
parasympathetic nervous system. The sympathetic nervous system is
affiliated with stress and the "fight or flight response" to
emergencies. Among other effects, the "fight or flight response"
increases blood pressure and heart rate to increase skeletal muscle
blood flow, and decreases digestion to provide the energy for
"fighting or fleeing." The parasympathetic nervous system is
affiliated with relaxation and the "rest and digest response"
which, among other effects, decreases blood pressure and heart
rate, and increases digestion to conserve energy. The ANS maintains
normal internal function and works with the somatic nervous system.
Afferent nerves convey impulses toward a nerve center, and efferent
nerves convey impulses away from a nerve center.
[0039] The heart rate and force is increased when the sympathetic
nervous system is stimulated, and is decreased when the sympathetic
nervous system is inhibited (the parasympathetic nervous system is
stimulated). Cardiac rate, contractility, and excitability are
known to be modulated by centrally mediated reflex pathways.
Baroreceptors and chemoreceptors in the heart, great vessels, and
lungs, transmit cardiac activity through vagal and sympathetic
afferent fibers to the central nervous system. Activation of
sympathetic afferents triggers reflex sympathetic activation,
parasympathetic inhibition, vasoconstriction, and tachycardia. In
contrast, parasympathetic activation results in bradycardia,
vasodilation, and inhibition of vasopressin release. Among many
other factors, decreased parasympathetic or vagal tone or increased
sympathetic tone is associated with various arrhythmias genesis,
including ventricular tachycardia and atrial fibrillation.
[0040] Stimulating the sympathetic and parasympathetic nervous
systems can have effects other than heart rate and blood pressure.
For example, stimulating the sympathetic nervous system dilates the
pupil, reduces saliva and mucus production, relaxes the bronchial
muscle, reduces the successive waves of involuntary contraction
(peristalsis) of the stomach and the motility of the stomach,
increases the conversion of glycogen to glucose by the liver,
decreases urine secretion by the kidneys, and relaxes the wall and
closes the sphincter of the bladder. Stimulating the
parasympathetic nervous system (inhibiting the sympathetic nervous
system) constricts the pupil, increases saliva and mucus
production, contracts the bronchial muscle, increases secretions
and motility in the stomach and large intestine, and increases
digestion in the small intention, increases urine secretion, and
contracts the wall and relaxes the sphincter of the bladder. The
functions associated with the sympathetic and parasympathetic
nervous systems are many and can be complexly integrated with each
other.
[0041] Neural stimulation can be used to stimulate nerve traffic or
inhibit nerve traffic. An example of neural stimulation to
stimulate nerve traffic is a lower frequency signal (e.g. within a
range on the order of 20 Hz to 50 Hz). An example of neural
stimulation to inhibit nerve traffic is a higher frequency signal
(e.g. within a range on the order of 120 Hz to 150 Hz). Other
methods for stimulating and inhibiting nerve traffic have been
proposed.
[0042] Modulation of the autonomic nervous system has potential
clinical benefit in preventing remodeling and death in heart
failure and post-MI patients. Electrical stimulation can be used to
inhibit sympathetic nerve activity and reduce blood pressure by
decreasing vascular resistance. Sympathetic inhibition, which
increases parasympathetic tone, has been associated with reduced
arrhythmia vulnerability following a myocardial infarction,
presumably by increasing collateral perfusion of the acutely
ischemic myocardium and decreasing myocardial damage.
Spinal Cord
[0043] FIG. 1A illustrates a spinal column 100, including the T1-T5
vertebrae 101, and further illustrates ribs 102 from a posterior or
dorsal perspective. FIG. 1B illustrates a side view of the spinal
column, including the T1-T5 vertebrae 101 of the column, and the
ribs 102. These figures also illustrate a lateral axis, a vertical
axis in the cranial (up) or caudal (down) direction, and a
posterior or dorsal direction and an anterior or ventral
direction.
[0044] The spinal column includes cervical, thoracic and lumbar
areas. Vertebrae form the building blocks of the spinal column and
protect the spinal cord. T1-T5 are the uppermost (cranial) portion
of the thoracic area of the spinal column. Projections from T1-T5
innervate the heart. The spinal projections from T1-T5 are
sympathetic. Increased efferent sympathetic activity increases
heart rate and contractility. Afferent (e.g. pain signals) for the
heart tissue also go throughout spinal segments T1-T5. Various
embodiments target the T1-T5 region for cardiovascular disease
applications. Other regions may be targeted for other applications
(e.g. treatment for hypertension, diabetes, obesity, etc.).
[0045] FIG. 2 illustrates a perspective view of a portion of the
spinal column. As illustrated, the vertebrae includes a vertebral
body 203 and a bony ring 204 attached to the vertebral body 203.
The stacked vertebrae provide a vertebral canal that protects the
spinal cord 205. The spinal cord is nerve tissue that carries
neural messages between the brain and parts of the body. Nerve
roots branch off and exit the spine on both sides through spaces
between the vertebra. The spinal cord is surrounded by dura matter,
which holds spinal fluid that surrounds the spinal cord. The space
between the walls and the dura matter of the vertebral canal is
referred to as epidural space 206. Some embodiments of the present
subject matter steer a lead through the dorsal epidural space 206
to the T1-T5 region, and some embodiments steer a catheter through
the dorsal epidural space to the T1-T5 region.
[0046] FIG. 3 illustrates a top view of a cross section of a
vertebra in the spinal column. The vertebra includes a vertebral
body 303 and a bony ring 304 that includes the spinous process. The
vertebrae provide a spinal canal that contains the spinal cord. The
illustrated spinal cord includes white matter 307 and gray matter
308. Spinal nerves 309A, 309B extend from the sides of the spinal
column. Each spinal nerve 309A, 309B has a dorsal nerve root 310A,
310B and a ventral nerve root 311A, 311B. The front or ventral gray
column of the spinal cord is referred to as the ventral horn 312A,
312B, which is a longitudinal subdivision of gray matter in the
anterior part of each lateral half of the spinal cord that contains
neurons giving rise to motor fibers of the ventral roots of the
spinal nerves. The posterior gray column of the spinal cord is
referred to as the dorsal horn 313A, 313B, which is a longitudinal
subdivision of gray matter in the dorsal part of each lateral half
to the spinal cord that receives terminals from some afferent
fibers of the dorsal roots of the spinal nerves. The ventral root
311A, 311B is the efferent motor root of a spinal nerve. The dorsal
root 310A, 310B is the afferent sensory root of the spinal nerve.
The ventral root joins with the dorsal root to form a mixed spinal
nerve 309A, 309B. The distal end of the dorsal root includes the
dorsal root ganglion which contains the neuron cell bodies of the
nerve fibers conveyed by the root.
[0047] The afferent sympathetic pathway includes neuron bodies in
the dorsal root ganglia, and neuron bodies in the dorsal horn. The
efferent sympathetic pathway includes preganglionic motor neuron
bodies in the intermediolateral column of the spinal cord from to
T4/T5, and postganglionic motor neuron bodies in superior, middle
and inferior cervical ganglias and in cell T1 thoracic ganglias
from T1 to T4/T5. Various embodiments modulate sympathetic efferent
and afferent activity by delivering electric current to selected
regions of the thoracic spinal cord. Some embodiments provide a
three-dimensional, steerable lead design. The lead can be moved up
and down along the spinal column. At the targeted region, the lead
body is capable of being steered to bend and curve around the
spinal cord. This lead placement provides multiple electrodes
located along both the ventral and dorsal horn of the spinal cord.
Selected electrodes are used to selectively modulate afferent,
efferent or both afferent and efferent pathways. Thus, a desired
therapy is provided by choosing electrodes that are closest to
sympathetic neurons.
[0048] FIG. 4 illustrates sympathetic pathways extending from
ventral and dorsal nerve roots. The gray matter of the spinal cord
405 includes ventral horns 412A, 412B and dorsal horns 413A, 413B.
The ventral root 411 is the efferent motor root of a spinal nerve.
The dorsal root 412 is the afferent sensory root of the spinal
nerve. The ventral root joins with the dorsal root to form a mixed
spinal nerve.
[0049] FIG. 5 illustrates an embodiment of a method for implanting
a lead for use in delivering spinal cord stimulation. The patient
can sit or lie on their side in a position of back flexion to open
the intervertebral spaces. Depending on the implant location, the
appropriate lumbar space is identified using Tuffier's line as a
reference point. Using a sterile technique the spinal lead
introducer is inserted in the midline, while aiming cranially. As
the needle is pushed forward, there is resistance as it passes
through the ligamentum flavae. The loss of resistance is evidence
that the epidural space has been penetrated. Once in the epidural
space 506, the lead can be deployed through the introducer and then
passed into the epidural space, and then up to the T1-T5 region and
around at least a portion of the spinal cord 505.
[0050] FIG. 6 illustrates a portion of the spinal cord 605, with
nerve roots extending from three vertebral locations, and further
illustrates a neural stimulation lead 614 fed through the dorsal
epidural space (behind the illustrated cord 605) and least
partially around the spinal cord to operationally set electrodes in
place to stimulate and/or inhibit activity in the dorsal and
ventral nerve roots 611, 612, according to various embodiments. The
pulse generator 615 can be implanted in an appropriate location,
such as in an abdominal region or in or just above the buttocks.
During the implantation procedure, the proximate end of the lead
can be connected to an external device used to generate stimulation
pulses and monitor the efficacy of the lead placement.
[0051] FIG. 7 illustrates a multi-lead embodiment to stimulate
dorsal and ventral nerve roots on contralateral sides of the spinal
cord. The illustrated figure shows two leads exiting from a pulse
generator 715. One lead 714A is directed around a first side, and a
second lead 714B is directed around a second side. Electrodes on
each lead are placed operationally in position with respect to the
nerve root(s) to stimulate the neural target(s) and elicit the
desired effect(s).
[0052] FIG. 8 illustrates multiple electrodes on a lead 814 wrapped
at least partially around the spinal cord 805, where at least some
of the electrodes 816A are operationally positioned for use to
stimulate the dorsal nerve root 812 and some of the electrodes 816B
are operationally positioned for use to stimulate the ventral nerve
root 811. Each lead includes a plurality of electrodes that are
adapted to be combined to generate various stimulation vectors.
Thus, an appropriate combination of electrodes can be used to
generate a stimulation field that effectively stimulates the
desired neural target(s), and in some embodiments, avoid possible
undesired effects of neural stimulation.
[0053] Some benefits of the present subject matter include more
therapy choices, including efferent, afferent, and both efferent
and afferent targets. Some embodiments provide simultaneous
afferent and efferent modulation. For example, chronic intermittent
sympathetic efferent stimulation could be used to alter the
progression of HF. Meanwhile, a sensed tachy event could trigger
sympathetic afferent stimulation to inhibit the occurrence of a
ventricular arrhythmia. Some embodiments provide the capability of
altering afferent and efferent modulation to provide a more robust
therapy. For example, in HF patients, chronic sympathetic afferent
stimulation and chronic sympathetic efferent block or inhibition
could be applied in an alternating order to inhibit sympathetic
activity, while also preventing desensitization. Some embodiments
provide the ability to monitor and adjust the stimulation to
provide and/or maintain a desired efficacy (capture neural target
and/or avoid or abate side effects) of the therapy. Some lead
embodiments promote stable lead placement, which prevents or abates
lead migration and movement.
[0054] Some embodiments of the present subject matter provide a
treatment for tachyarrhythmia. For example, some embodiments
deliver sympathetic afferent stimulation at the dorsal horn of the
spinal cord with a relatively low frequency to reflexively inhibit
sympathetic activity; and some embodiments deliver direct
sympathetic efferent inhibition with a relatively high frequency
stimulation at the ventral horn of the spinal column. Some
embodiments of the present subject matter provide a treatment for
heart failure. For example, some embodiments enhance sympathetic
activity periodically with chronic intermittent efferent
stimulation at the ventral horn of the spinal column with a
relatively low frequency. Some embodiments inhibit or block
sympathetic efferent activity, either chronically or
intermittently, using a high frequency electrical stimulation at
the ventral horn of the spinal cord.
Lead/Catheters
[0055] An embodiment uses a steerable delivery catheter (e.g. using
stereotaxis magnetic guidance) or other guidance means to aid in
positioning the lead in the targeted region of the epidural space.
Some catheter embodiments are steerable in two axes (vertical, also
referred to as cranial/caudal axis, and lateral axis). Some lead
embodiments have a distal "J" biased tip designed to wrap around
the spinal cord when the lead is deployed from the delivery
catheter to the targeted region. The J-biased tip aids in retaining
the electrodes in place, avoiding or abating lead migration.
Additionally, the J-biased tip maintains contact with the spinal
column, keeping the stimulation electrodes desirably close to the
ventral and/or dorsal nerve roots. The delivery catheter is then
peeled or cut away from the lead, leaving the lead in position.
[0056] An embodiment uses a steerable stimulation lead to aid in
positioning the lead in the targeted region of the epidural space.
Some lead embodiments are steerable in two axes (vertical or
cranial/caudal axis, and lateral axis). Some lead embodiments are
adapted to be locked or fixed in a fixed position, aiding in
retaining the electrodes in place and maintaining contact with the
spinal column, keeping the stimulation electrodes desirably close
to the ventral and/or dorsal nerve roots. For example, some
embodiments use a chuck to hold the lead in position. Other designs
can be used to fix or stabilize the position of the lead. A
position fixation apparatus on a proximal end of the lead can be
used to maintain a shape and position of a distal end of the
lead.
[0057] FIG. 9 illustrates an embodiment that includes a pre-formed
lead made with a material having a shape memory, where the lead 914
resumes its preformed shape to at least partially wrap around the
spinal cord 905 (or potentially some other structures of the spinal
column) when the lead exits a catheter 917 used to deliver the lead
to the stimulation site. The illustrated portion of the pre-formed
lead has a plurality of electrodes 916, various combinations of
which can be selected to generate a desired neural stimulation
field to stimulate a desired neural target. The lead is designed
with appropriate material characteristics to provide an appropriate
force when contracting back into its preformed shape. In some
embodiments, the force of contraction is sufficient to fix the lead
in position or to discourage lead migration.
[0058] FIGS. 10A and 10B illustrate a steerable lead embodiment
used to place stimulation electrodes in operational position to
stimulate ventral and dorsal nerves, the illustrated lead 1014
includes a plurality of electrodes 1016. As is illustrated in an
embodiment below, the lead is designed to be steered in at least
two directions, to allow the lead to be steered from the dorsal
epidural space around at least a portion of spinal cord 1005 to
stimulate the nerve root(s). A steering tendon or guy wire can be
used to contract the lead around the spinal cord, fixating the
electrodes in operational position to stimulate the ventral and/or
dorsal nerve roots.
[0059] FIGS. 11A-11C illustrate an embodiment of a steerable lead.
The lead body 1114 includes a distal end 1116. A lumen adapted to
receive a steering tendon 1118 is in the lead body 1114. The lead
body 1114 includes a compressible or expandable side 1119 and a
noncompressible or expandable side 1120. The steering tendon is
appropriately connected to the compressible or expandable side to
control the compression or expansion of that side. When the lead is
implanted, the lead is steered by appropriately controlling the
tendon.
[0060] FIG. 12 illustrates a steerable catheter embodiment used to
deliver a lead to place stimulation electrodes from the lead in
operational position to stimulate ventral and dorsal nerve leads. A
first steering tendon 1221 is attached to a first anchor member
1222 located at a distal portion of the pre-formed distal end 1223.
A second steering tendon 1224 is attached to a second anchor member
1225 located distal to the deflection area 1226.
[0061] The anchor members 1222, 1225 can be constructed using
various materials and construction methods known in the art,
including simply bonding a distal part of the tendon to the shaft.
In the illustrated configuration, the anchor members 404, 408 are
formed of stainless steel rings to which steering tendons can be
welded or soldered. The steering tendons may be attached to the
anchor members using a mechanical interference fit such as a crimp
or a stop member. The steering tendons are typically made of
metallic (e.g. stainless steel) members such as solid wire, braided
wire, or ribbon material. It is possible to form tendons from
non-metallic members such as high strength composite members (e.g.
Kevlar, carbon fiber).
[0062] Some embodiments embed the anchor members within the walls
of the lead shaft 1214 during shaft construction. In some
embodiments, the anchor members are adhered to the inner wall of
the lead shaft 1214 by adhesive bonding or hot melting the shaft
material. Hot melting may be performed by heating the anchor
members while in intimate contact with the inner walls of the
shaft. Another method of attaching the anchor members involves
butting the bands against a support structure of the shaft 102 such
as a reinforcement cage or braid.
[0063] FIGS. 13A-13C illustrate an embodiment of a steerable
catheter. FIG. 13A is an external view of the catheter including a
proximal handle assembly 1328. The proximal handle assembly 1328
typically includes a grip 1329 and a steering member 1330. The
handle assembly 1328 can be constructed by principles known in the
art, such as described in U.S. Pat. Nos. 6,096,036 and 6,270,496,
which are hereby incorporated by reference in their respective
entireties.
[0064] FIG. 13B is a cross section of a distal part of the catheter
shaft roughly corresponding to section B-B in FIG. 13A. A shaft
embodiment 1331 includes a wall 1332 formed of polymer, typically a
high durometer Pebax material. The shaft wall encloses a stylet
1333, typically made of a resilient, shape-memory member such as a
wire formed of nitinol wire or other superelastic alloy. A nitinol
stylet is preshaped by heating the stylet while it is being
constrained in the desired shape. A stylet formed in this way is
then inserted into the shaft to impart the preformed shape at the
distal end 1334 of the shaft 1331. The stylet is typically affixed
at or near the tip of the shaft to prevent migration of the stylet
within the catheter during use.
[0065] In the illustrated figures, the wall of the shaft also
encloses conductors 1335 coupled to the electrodes. Also shown
within the shaft are the steering tendons 1336, 1337. The steering
tendons are disposed within lumens, which are typically formed of a
lubricous material such as PTFE and may be affixed to an inner
surface of the shaft wall.
[0066] FIG. 13C shows a cross section of a proximal part of the
catheter shaft 1331. The layout of the shaft is similar to that
seen in FIG. 13B, and additionally shows a reinforcing member 1338
and an outer casing 1339. The reinforcing member can include a
braid, cage, ribbon, or other reinforcing member that provides
axial and torsional stiffness to the shaft while still allowing a
reasonable amount of bending in the shaft. The outer casing may be
made of a Pebax material having a similar durometer as the shaft
wall, or may be made of a different material having unique
protective and/or lubricous properties. The differences between the
distal and proximal cross sections (e.g. inclusion of a proximal
support member) as seen in FIGS. 13B and 13C result in the proximal
portion having greater stiffness than the distal portion. Other
variations in stiffness may also be advantageously induced along
portions of the flexible shaft. To vary stiffness of the shaft, the
bending properties of the shaft wall may be changed (e.g. the
durometer of the polymeric materials) or the stylet characteristics
(e.g. outer diameter or cross section) can be varied along the
shaft length. Varying the stiffness along the length of the shaft
can beneficially enhance the deflectability of the steered sections
or to tune the stiffness of the distal end to minimize the risk of
trauma.
[0067] A number of electrode configurations can be used. The
illustrations included herein are provided as examples, and are not
intended to be an exhaustive listing of possible
configurations.
[0068] FIG. 14 illustrates a lead embodiment with a plurality of
ring electrodes. The figure illustrates an embodiment of a lead
1414 with annular stimulation electrodes 1416 that form an
electrode region, such as used to selectively stimulate the ventral
nerve root or dorsal nerve root, according to various embodiments.
Any one or combination of the annular stimulation electrodes can be
used to deliver the neural stimulation to the desired neural
target.
[0069] FIGS. 15A-15B illustrate a lead embodiment with multiple
electrodes on a circumference of the lead. The illustrated
electrodes 1516 do not circumscribe the lead 1514. Thus, a subset
of the illustrated electrodes can be selected to provide
directional stimulation. For example, the lead may twist or rotate
as it is fed into position, and it may be desired to stimulate a
neural target on one side of the lead without stimulating other
nerves or tissue on the other sides of the lead. For example, root
nerves extending from one vertebrae can be stimulated without
stimulating root nerves extending from other vertebrae. A neural
stimulation test routine can cycle through the available electrodes
for use in delivering the neural stimulation to determine which
subset of electrodes are facing toward the neural target. FIG. 15B
illustrates an example with four electrodes separated around the
lead, approximately 90 degrees apart. Other electrode arrangements
and spacing can be used, such as, by way of example and not
limitation, 2 electrodes spaced around the circumference
approximately 45 degrees apart, approximately 90 degrees apart or
approximately 180 degrees apart; or 3 electrodes spaced around the
circumference approximately 120 degrees, approximately 60 degrees
or approximately 30 degrees apart.
[0070] FIGS. 16A-16B illustrate a lead embodiment with multiple
electrodes on a paddle-like distal end. The paddle-like distal end
1640 has a relatively flat profile. The electrodes 1616 are
positioned on one side of the paddle, such that the electric
stimulation field is generated on one side of the paddle-like
distal end.
[0071] FIG. 17 illustrates a method embodiment to implant the
spinal cord stimulation lead to establish and maintain efficacious
stimulation therapy. At 1741, a lead is inserted into an epidural
space. Examples were discussed with respect to FIG. 5 and with
respect to various steerable lead and steerable catheter designs.
At 1742, the lead (or catheter) is steered to direct the lead
laterally adjacent to and at least partially around the spinal cord
to position the electrodes on the lead operationally proximate to
the dorsal and/or ventral nerve roots in a location in the T1-T5
range. At 1743, the electrode positions are tested to determine if
the electrode positions provide efficacious stimulation. For
example, some embodiments monitor one or more physiological
parameters to verify capture of the neural target (e.g. ventral
and/or dorsal nerve roots). The present subject matter is capable
of selectively stimulating or targeting only the ventral nerve root
and/or selectively stimulating the dorsal nerve root. Some
embodiments monitor one or more physiological parameter to abate
potential unintended responses to the neural stimulation. If unable
to verify capture or if undesired side effects are present during
the implantation process, the process adjusts the physical
positioning and/or the electronic positioning in an effort to
realize efficacious stimulation, as represented at 1744. The
physical repositioning involves physically moving (e.g. pushing,
pulling, rotating, contracting around spinal cord) the lead. The
electronic repositioning involves selecting various combinations of
electrodes to adjust the direction and position of the electric
stimulation field. Electronic repositioning can be performed as
part of an automatic process, where a device cycles through
available electrode combinations (and stimulation intensity) until
the desired efficacy is realized. Electronic repositioning can be
controlled by a technician during the implant procedure. Some
embodiments use a combination of technician control of potential
configurations, and an automatic test routine.
[0072] When efficacious stimulation is detected, the physical lead
placement is set at 1745. A proximal end of the lead is connected
to an implantable pulse generator, which may be, for example,
implanted in the small of the back. At 1746, therapy is delivered
using the implanted lead and the implanted pulse generator. At
1747, the implanted pulse generator intermittently tests for
efficacious stimulation to verify capture and/or abate side effects
of the stimulation. If appropriate, the electronic positioning is
adjusted to deliver efficacious stimulation, as illustrated at
1748. This electronic repositioning can be performed automatically,
controlled by a technician using a programmer, or a combination
thereof.
[0073] FIG. 18 illustrates a system used to deliver spinal cord
stimulation, according to various embodiments. The illustrated
neural stimulator embodiment 1850 includes a neural stimulation
circuit 1851, a feedback circuit 1852, a controller 1853, and
memory 1854. The illustrated embodiment further includes at least
one port 1855 to connect to at least one lead 1856. At least one
lead is adapted to be fed into the dorsal epidural space to the
T1-T5 region, and directed at least partially around the spinal
cord to stimulate the ventral and/or dorsal nerve root. The neural
stimulation circuit is connected to the port(s) to provide a neural
stimulation signal to at least one neural stimulation electrode
1857 on the lead(s) to elicit a desired neural response when an
appropriate signal is provided to an appropriately-positioned
neural stimulation electrode. The feedback circuit is connected to
the port(s) to receive a signal from the physiology sensor 1858.
The physiology sensor may be on a different lead than the lead fed
into the epidural space to stimulate the nerve root(s). Some
embodiments receive a feedback signal from other implantable
medical devices, such as a pacemaker or anti-arrhythmia device. The
sensor senses a physiology function that depends, at least in part,
on the neural stimulation. Examples of such functions includes
heart rate, blood pressure, ECG waveforms, respiration, and
acceleration/motion. Thus, various embodiments implement a heart
rate sensor as the physiology sensor, and various embodiments
implement a blood pressure sensor as the physiology sensor. One
example of such a sensor is an acoustic sensor adapted to sense
blood flow. The sensed blood flow is capable of being used to
determine blood pressure and/or heart rate. However, other sensor
technology can be used.
[0074] The illustrated system includes a communication module 1859
adapted to communicate with other devices. For example, some
embodiments communicate using telemetry. Various embodiments
wirelessly communicate from the implanted device to external
devices, such as a programmer 1860. Various embodiments
communicate, either through a wired connection or a wireless
connection, to other implantable medical devices 1861. Example of
other implantable medical devices include cardiac rhythm management
devices, such as a pacemaker, cardiodefibrillator, and the like,
and further include implantable neural stimulators. According to
some embodiments, such other implantable medical devices sense
physiological parameters that are affected by the stimulation of
the nerve root, and communicate information regarding the sensed
physiological parameters during an implant procedure or while the
devices are chronically implanted in a patient. According to some
embodiments, the communication module is adapted to communicate
with a portable external device 1862, such as a personal data
assistant, a telephone, an interrogator, a laptop computer.
According to some embodiments, the portable external device 1862
and programmer 1860 are adapted to communicate over a communication
network 1863.
[0075] Heart rate and/or blood pressure can be used to determine
whether the stimulation is affecting the autonomic system.
Additionally, various autonomic balance indicators (ABIs) can be
used to provide feedback concerning the neural stimulation therapy
directed toward the nerve root(s). Various embodiments assess ABI
using one or various combinations of parameters, such as heart rate
variability (HRV), heart rate turbulence (HRT), electrogram
features, activity, respiration and activity. These parameters are
briefly discussed below. Various embodiments provide closed loop
control of the treatment using ABI.
[0076] HRV is one technique that has been proposed to assess
autonomic balance. HRV relates to the regulation of the sinoatrial
node, the natural pacemaker of the heart by the sympathetic and
parasympathetic branches of the autonomic nervous system. An HRV
assessment is based on the assumption that the beat-to-beat
fluctuations in the rhythm of the heart provide us with an indirect
measure of heart health, as defined by the degree of balance in
sympathetic and vagus nerve activity.
[0077] The time interval between intrinsic ventricular heart
contractions changes in response to the body's metabolic need for a
change in heart rate and the amount of blood pumped through the
circulatory system. For example, during a period of exercise or
other activity, a person=s intrinsic heart rate will generally
increase over a time period of several or many heartbeats. However,
even on a beat-to-beat basis, that is, from one heart beat to the
next, and without exercise, the time interval between intrinsic
heart contractions varies in a normal person. These beat-to-beat
variations in intrinsic heart rate are the result of proper
regulation by the autonomic nervous system of blood pressure and
cardiac output; the absence of such variations indicates a possible
deficiency in the regulation being provided by the autonomic
nervous system. One method for analyzing HRV involves detecting
intrinsic ventricular contractions, and recording the time
intervals between these contractions, referred to as the R-R
intervals, after filtering out any ectopic contractions
(ventricular contractions that are not the result of a normal sinus
rhythm). This signal of R-R intervals is typically transformed into
the frequency-domain, such as by using fast Fourier transform (FFT)
techniques, so that its spectral frequency components can be
analyzed and divided into low and high frequency bands. For
example, the low frequency (LF) band can correspond to a frequency
(f) range 0.04 Hz<f<0.15 Hz, and the high frequency (HF) band
can correspond to a frequency range 0.15 Hz<f<0.40 Hz. The HF
band of the R-R interval signal is influenced only by the
parasympathetic/vagal component of the autonomic nervous system.
The LF band of the R-R interval signal is influenced by both the
sympathetic and parasympathetic components of the autonomic nervous
system. Consequently, the ratio LF/HF is regarded as a good
indication of the autonomic balance between sympathetic and
parasympathetic/vagal components of the autonomic nervous system.
An increase in the LF/HF ratio indicates an increased predominance
of the sympathetic component, and a decrease in the LF/HF ratio
indicates an increased predominance of the parasympathetic
component. For a particular heart rate, the LF/HF ratio is regarded
as an indication of patient wellness, with a lower LF/HF ratio
indicating a more positive state of cardiovascular health. A
spectral analysis of the frequency components of the R-R interval
signal can be performed using a FFT (or other parametric
transformation, such as autoregression) technique from the time
domain into the frequency domain. Such calculations require
significant amounts of data storage and processing capabilities.
Additionally, such transformation calculations increase power
consumption, and shorten the time during which the implanted
battery-powered device can be used before its replacement is
required.
[0078] One example of an HRV parameter is SDANN (standard deviation
of averaged NN intervals), which represents the standard deviation
of the means of all the successive 5 minutes segments contained in
a whole recording. Other HRV parameters can be used.
[0079] HRT is the physiological response of the sinus node to a
premature ventricular contraction (PVC), consisting of a short
initial heart rate acceleration followed by a heart rate
deceleration. HRT has been shown to be an index of autonomic
function, closely correlated to HRV. HRT is believed to be an
autonomic baroreflex. The PVC causes a brief disturbance of the
arterial blood pressure (low amplitude of the premature beat, high
amplitude of the ensuing normal beat). This fleeting change is
registered immediately with an instantaneous response in the form
of HRT if the autonomic system is healthy, but is either weakened
or missing if the autonomic system is impaired.
[0080] By way of example and not limitation, it has been proposed
to quantify HRT using Turbulence Onset (TO) and Turbulence Slope
(TS). TO refers to the difference between the heart rate
immediately before and after a PVC, and can be expressed as a
percentage. For example, if two beats are evaluated before and
after the PVC, TO can be expressed as:
T O % = ( RR + 1 + RR + 2 ) - ( RR - 2 + RR - 1 ) ( RR - 2 + RR - 1
) * 100. ##EQU00001##
[0081] RR-.sub.2 and RR-.sub.1 are the first two normal intervals
preceding the PVC and RR.sub.+1 and RR.sub.+2 are the first two
normal intervals following the PVC. In various embodiments, TO is
determined for each individual PVC, and then the average value of
all individual measurements is determined. However, TO does not
have to be averaged over many measurements, but can be based on one
PVC event. Positive TO values indicate deceleration of the sinus
rhythm, and negative values indicate acceleration of the sinus
rhythm. The number of R-R intervals analyzed before and after the
PVC can be adjusted according to a desired application. TS, for
example, can be calculated as the steepest slope of linear
regression for each sequence of five R-R intervals. In various
embodiments, the TS calculations are based on the averaged
tachogram and expressed in milliseconds per RR interval. However,
TS can be determined without averaging. The number of R-R intervals
in a sequence used to determine a linear regression in the TS
calculation also can be adjusted according to a desired
application.
[0082] Rules or criteria can be provided for use to select PVCs and
for use in selecting valid RR intervals before and after the PVCs.
A PVC event can be defined by an R-R interval in some interval
range that is shorter than a previous interval by some time or
percentage, or it can be defined by an R-R interval without an
intervening P-wave (atrial event) if the atrial events are
measured. Various embodiments select PVCs only if the contraction
occurs at a certain range from the preceding contraction and if the
contraction occurs within a certain range from a subsequent
contraction. For example, various embodiments limit the HRT
calculations to PVCs with a minimum prematurity of 20% and a
post-extrasystole interval which is at least 20% longer than the
normal interval. Additionally, pre-PVC R-R and post-PVC R-R
intervals are considered to be valid if they satisfy the condition
that none of the beats are PVCs. One HRT process, for example,
excludes RR intervals that are less than a first time duration,
that are longer than a second time duration, that differ from a
preceding interval by more than a third time duration, or that
differ from a reference interval by a predetermined amount time
duration or percentage. In an embodiment of such an HRT process
with specific values, RR intervals are excluded if they are less
than 300 ms, are more than 2000 ms, differ from a preceding
interval by more than 200 ms, or differ by more than 20% from the
mean of the last five sinus intervals. Various embodiments of the
present subject matter provide programmable parameters, such as any
of the parameters identified above, for use in selecting PVCs and
for use in selecting valid RR intervals before and after the
PVCs.
[0083] Benefits of using HRT to monitor autonomic balance include
the ability to measure autonomic balance at a single moment in
time. Additionally, unlike the measurement of HRV, HRT assessment
can be performed in patients with frequent atrial pacing. Further,
HRT analysis provides for a simple, non-processor-intensive
measurement of autonomic balance. Thus, data processing, data
storage, and data flow are relatively small, resulting in a device
with less cost and less power consumption. Also, HRT assessment is
faster than HRV, requiring much less R-R data. HRT allows
assessment over short recording periods similar in duration to
typical neural stimulation burst durations, such as on the order of
tens of seconds, for example.
[0084] Various embodiments extract various ECG features to provide
an ABI. Examples of such features include heart rate, which can be
used to form HRV, and HRT. Other features can be extracted from the
ECG, and one or various combinations of these features can be used
to provide an ABI. Various embodiments provide blood pressure to
provide an ABI. For example, some embodiments sense pulmonary
artery blood pressure.
[0085] Activity sensors can be used to assess the activity of the
patient. Sympathetic activity naturally increases in an active
patient, and decreases in an inactive patient. Thus, activity
sensors can provide a contextual measurement for use in determining
the autonomic balance of the patient. Various embodiments, for
example, provide a combination of sensors to trend heart rate
and/or respiration rate to provide an indicator of activity.
[0086] Two methods for detecting respiration involve measuring a
transthoracic impedance and minute ventilation. Respiration can be
an indicator of activity, and can provide an explanation of
increased sympathetic tone. For example, it may not be appropriate
to change or modify a treatment for modulating autonomic tone due
to a detected increase in sympathetic activity attributable to
exercise.
[0087] Respiration measurements (e.g. transthoracic impedance) can
also be used to measure Respiratory Sinus Arrhythmia (RSA). RSA is
the natural cycle of arrhythmia that occurs through the influence
of breathing on the flow of sympathetic and vagus impulses to the
sinoatrial node. The rhythm of the heart is primarily under the
control of the vagus nerve, which inhibits heart rate and the force
of contraction. The vagus nerve activity is impeded and heart rate
begins to increase when a breath is inhaled. When exhaled, vagus
nerve activity increases and the heart rate begins to decrease. The
degree of fluctuation in heart rate is also controlled
significantly by regular impulses from the baroreceptors (pressure
sensors) in the aorta and carotid arteries. Thus, a measurement of
autonomic balance can be provided by correlating heart rate to the
respiration cycle.
[0088] The memory 1854 includes computer-readable instructions that
are capable of being operated on by the controller to perform
functions of the device. Thus, in various embodiments, the
controller is adapted to operate on the instructions to provide
programmed neural stimulation therapies 1864 according to a neural
stimulation therapy schedule stored in the memory. Various "closed
loop" systems vary the intensity of the neural stimulation, as
generally illustrated by the stimulation intensity module 1865,
based on the sensed physiology signal received by the feedback
circuit according to a preprogrammed therapy to provide a desired
affect. Thus, the closed loop system is capable of reducing and
increasing the neural stimulation intensity as appropriate to
maintaining some measured physiological parameters within an upper
and lower boundary during the neural stimulation therapy. Various
"open loop" systems without feedback from the physiology signal
also can be programmed to vary the stimulation intensity. For
example, intensity can be modulated based on a programmed schedule.
Various embodiments modulate the stimulation intensity by
modulating the amplitude of the neural stimulation signal, the
frequency of the neural stimulation signal, the duty cycle of the
neural stimulation signal, the duration of a stimulation signal,
the waveform of the neural stimulation signal, the polarity of the
neural stimulation signal, or any combination thereof.
[0089] Various embodiments automatically change the electrode
configuration, as generally illustrated by the electrode
configuration module 1866 of the controller 1853. The illustrated
electrode configuration module is adapted to control switches 1867
to control which electrodes of the available electrodes are used to
deliver the neural stimulation, and the stimulation vectors for the
electrodes. Additionally, the illustrated electrode configuration
module is adapted to work with the stimulation intensity module to
control the stimulation intensity for the different electrode
combinations and stimulation vectors. Thus, for example, the
electrode configuration module can find a reference neural
stimulation level for a particular electrode combination and
vector, and the stimulation intensity module can further modulate
the neural stimulation based on the reference neural stimulation
level. A neural stimulation test routine stored in the memory
controls the process of testing for a efficacious electrode
configuration from the available electrode configurations.
[0090] In various embodiments, the controller automatically
implements the neural stimulation test routine, such as in a
chronically-implanted device. In various embodiments, the
controller and a user interface cooperate to implement a neural
stimulation test routine to allow a user to select the at least one
of the neural stimulation electrodes to use in delivering the
autonomic neural stimulation therapy, such as maybe used in a
device to implant the lead into the desired position to stimulate
the desired nerve root(s). For example, during an implantation
procedure, the user interface can display test results for various
electrode configurations. The information identifying the electrode
configurations can include the electrodes used in the stimulation,
the stimulation amplitude, the stimulation frequency, the
stimulation duty cycle, the stimulation duration, the stimulation
waveform, and the stimulation polarity. The test results can
include the detected physiologic response (e.g. heart rate)
attributed to the neural stimulation for an electrode
configuration. The user can review the test results, and select an
electrode configuration using the test results.
[0091] The illustrated controller includes an event detector 1868,
such as may be used to detect an arrhythmic event or an ischemic
event. Upon the detection of an event, the device appropriately
adjusts the therapy for the event. According to some embodiments,
another IMD 1861 detects the event and communicates the event to
the device to adjust the stimulation of the ventral and/or dorsal
nerve roots.
Neural Stimulation Therapies
[0092] Examples of neural stimulation therapies include neural
stimulation therapies for blood pressure control such as to treat
hypertension, for cardiac rhythm management, for myocardial
infarction and ischemia, for heart failure, and for pain control. A
therapy embodiment involves preventing and/or treating ventricular
remodeling. Activity of the autonomic nervous system is at least
partly responsible for the ventricular remodeling which occurs as a
consequence of an MI or due to heart failure. It has been
demonstrated that remodeling can be affected by pharmacological
intervention with the use of, for example, ACE inhibitors and
beta-blockers. Pharmacological treatment carries with it the risk
of side effects, however, and it is also difficult to modulate the
effects of drugs in a precise manner. Embodiments of the present
subject matter employ electrostimulatory means to modulate
autonomic activity, referred to as anti-remodeling therapy or ART.
When delivered in conjunction with ventricular resynchronization
pacing, also referred to as remodeling control therapy (RCT), such
modulation of autonomic activity may act synergistically to reverse
or prevent cardiac remodeling.
[0093] One neural stimulation therapy embodiment involves treating
hypertension by increasing parasympathetic tone (e.g. inhibiting
sympathetic activity) for sustained periods of time sufficient to
reduce hypertension. Neural stimulation (e.g. sympathetic nerve
stimulation and/or parasympathetic nerve inhibition) can mimic the
effects of physical conditioning. It is generally accepted that
physical activity and fitness improve health and reduce mortality.
Studies have indicated that aerobic training improves cardiac
autonomic regulation, reduces heart rate and is associated with
increased cardiac vagal outflow. A baseline measurement of higher
parasympathetic activity is associated with improved aerobic
fitness. Exercise training intermittently stresses the system and
increases the sympathetic activity during the stress. However, when
an exercise session ends and the stress is removed, the body
rebounds in a manner that increases baseline parasympathetic
activity and reduces baseline sympathetic activity. Conditioning
can be considered to be a repetitive, high-level exercise that
occurs intermittently over time. A conditioning therapy that
provides intermittent stress can be applied as therapy for heart
failure.
[0094] Neural targets in the spinal column can be targeted as part
of a therapy for pain control. The pain control therapy can be used
to address somatic pain, visceral pain or neuropathic pain. The
pain control therapy can also be used to address acute or chronic
pain. According to various embodiments, pain control therapies are
integrated with other therapies (e.g. heart failure). Some
embodiments provide means for a patient to activate the pain
control therapy. This means may use a wireless communication from
an external device to the implantable pulse generator, or a
magnetic field such as from a magnet positioned over the
implantable pulse generator. By way of example, a patient who is
experiencing an episode of angina pain may choose to initiate a
pain control therapy. A physician can program limits on the
requested pain control therapy, so as to limit the number of times
the therapy can be requested over a period of time. Various
embodiments implement the pain control therapy in conjunction with
another therapy to avoid or minimize pain with the therapy. For
example, if a defibrillation shock is going to be applied to a
patient, various embodiment implement pain control therapy in
anticipation of delivering the shock.
Myocardial Stimulation Therapies
[0095] Various neural stimulation therapies can be integrated with
various myocardial stimulation therapies. The integration of
therapies may have a synergistic effect. Therapies can be
synchronized with each other, and sensed data can be shared. A
myocardial stimulation therapy provides a cardiac therapy using
electrical stimulation of the myocardium. Some examples of
myocardial stimulation therapies are provided below.
[0096] A pacemaker is a device which paces the heart with timed
pacing pulses, most commonly for the treatment of bradycardia where
the ventricular rate is too slow. If functioning properly, the
pacemaker makes up for the heart's inability to pace itself at an
appropriate rhythm in order to meet metabolic demand by enforcing a
minimum heart rate. Implantable devices have also been developed
that affect the manner and degree to which the heart chambers
contract during a cardiac cycle in order to promote the efficient
pumping of blood. The heart pumps more effectively when the
chambers contract in a coordinated manner, a result normally
provided by the specialized conduction pathways in both the atria
and the ventricles that enable the rapid conduction of excitation
(i.e., depolarization) throughout the myocardium. These pathways
conduct excitatory impulses from the sino-atrial node to the atrial
myocardium, to the atrio-ventricular node, and thence to the
ventricular myocardium to result in a coordinated contraction of
both atria and both ventricles. This both synchronizes the
contractions of the muscle fibers of each chamber and synchronizes
the contraction of each atrium or ventricle with the contralateral
atrium or ventricle. Without the synchronization afforded by the
normally functioning specialized conduction pathways, the heart's
pumping efficiency is greatly diminished. Pathology of these
conduction pathways and other inter-ventricular or
intra-ventricular conduction deficits can be a causative factor in
heart failure, which refers to a clinical syndrome in which an
abnormality of cardiac function causes cardiac output to fall below
a level adequate to meet the metabolic demand of peripheral
tissues. In order to treat these problems, implantable cardiac
devices have been developed that provide appropriately timed
electrical stimulation to one or more heart chambers in an attempt
to improve the coordination of atrial and/or ventricular
contractions, termed cardiac resynchronization therapy (CRT).
Ventricular resynchronization is useful in treating heart failure
because, although not directly inotropic, resynchronization can
result in a more coordinated contraction of the ventricles with
improved pumping efficiency and increased cardiac output.
Currently, a common form of CRT applies stimulation pulses to both
ventricles, either simultaneously or separated by a specified
biventricular offset interval, and after a specified
atrio-ventricular delay interval with respect to the detection of
an intrinsic atrial contraction or delivery of an atrial pace.
[0097] CRT can be beneficial in reducing the deleterious
ventricular remodeling which can occur in post-MI and heart failure
patients. Presumably, this occurs as a result of changes in the
distribution of wall stress experienced by the ventricles during
the cardiac pumping cycle when CRT is applied. The degree to which
a heart muscle fiber is stretched before it contracts is termed the
preload, and the maximum tension and velocity of shortening of a
muscle fiber increases with increasing preload. When a myocardial
region contracts late relative to other regions, the contraction of
those opposing regions stretches the later contracting region and
increases the preload. The degree of tension or stress on a heart
muscle fiber as it contracts is termed the afterload. Because
pressure within the ventricles rises rapidly from a diastolic to a
systolic value as blood is pumped out into the aorta and pulmonary
arteries, the part of the ventricle that first contracts due to an
excitatory stimulation pulse does so against a lower afterload than
does a part of the ventricle contracting later. Thus a myocardial
region which contracts later than other regions is subjected to
both an increased preload and afterload. This situation is created
frequently by the ventricular conduction delays associated with
heart failure and ventricular dysfunction due to an MI. The
increased wall stress to the late-activating myocardial regions is
most probably the trigger for ventricular remodeling. By pacing one
or more sites in a ventricle near the infarcted region in a manner
which may cause a more coordinated contraction, CRT provides
pre-excitation of myocardial regions which would otherwise be
activated later during systole and experience increased wall
stress. The pre-excitation of the remodeled region relative to
other regions unloads the region from mechanical stress and allows
reversal or prevention of remodeling to occur.
[0098] Cardioversion, an electrical shock delivered to the heart
synchronously with the QRS complex, and defibrillation, an
electrical shock delivered without synchronization to the QRS
complex, can be used to terminate most tachyarrhythmias. The
electric shock terminates the tachyarrhythmia by simultaneously
depolarizing the myocardium and rendering it refractory. A class of
CRM devices known as an implantable cardioverter defibrillator
(ICD) provides this kind of therapy by delivering a shock pulse to
the heart when the device detects tachyarrhythmias. Another type of
electrical therapy for tachycardia is anti-tachycardia pacing
(ATP). In ventricular ATP, the ventricles are competitively paced
with one or more pacing pulses in an effort to interrupt the
reentrant circuit causing the tachycardia. Modern ICDs typically
have ATP capability, and deliver ATP therapy or a shock pulse when
a tachyarrhythmia is detected.
[0099] One of ordinary skill in the art will understand that, the
modules and other circuitry shown and described herein can be
implemented using software, hardware, and combinations of software
and hardware. As such, the terms module and circuitry, for example,
are intended to encompass software implementations, hardware
implementations, and software and hardware implementations.
[0100] The methods illustrated in this disclosure are not intended
to be exclusive of other methods within the scope of the present
subject matter. Those of ordinary skill in the art will understand,
upon reading and comprehending this disclosure, other methods
within the scope of the present subject matter. The
above-identified embodiments, and portions of the illustrated
embodiments, are not necessarily mutually exclusive. These
embodiments, or portions thereof, can be combined. In various
embodiments, the methods are implemented using a computer data
signal embodied in a carrier wave or propagated signal, that
represents a sequence of instructions which, when executed by one
or more processors cause the processor(s) to perform the respective
method. In various embodiments, the methods are implemented as a
set of instructions contained on a computer-accessible medium
capable of directing a processor to perform the respective method.
In various embodiments, the medium is a magnetic medium, an
electronic medium, or an optical medium.
[0101] The above detailed description is intended to be
illustrative, and not restrictive. Other embodiments will be
apparent to those of skill in the art upon reading and
understanding the above description. The scope of the invention
should, therefore, be determined with reference to the appended
claims, along with the full scope of equivalents to which such
claims are entitled.
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