U.S. patent application number 14/059246 was filed with the patent office on 2014-02-13 for neural blocking therapy.
This patent application is currently assigned to VENTURI GROUP, LLC. The applicant listed for this patent is Venturi Group, LLC. Invention is credited to Timothy R. Conrad, Adrianus P. Donders, Mark B. Knudson.
Application Number | 20140046419 14/059246 |
Document ID | / |
Family ID | 37530088 |
Filed Date | 2014-02-13 |
United States Patent
Application |
20140046419 |
Kind Code |
A1 |
Knudson; Mark B. ; et
al. |
February 13, 2014 |
NEURAL BLOCKING THERAPY
Abstract
A method and apparatus are disclosed for treating a variety of
conditions include treating a disorder associated with neural
activity near a region of a brain. In such condition, the method
includes placing an electrode to create a field near said region,
creating said field with parameters selected to at least partially
block neural activity within said field. For treating a tissue
sensation, the method includes identifying a target area of tissue
to be treated and placing an electrode to create a field near the
target area, and creating the field with parameters selected to at
least partially block neural activity within the target area. For
treating a condition associated with neural activity of a spinal
cord, the method includes placing an electrode to create a field
near a nerve associated with the spinal cord, and creating the
field with parameters selected to at least partially block neural
activity within the nerve.
Inventors: |
Knudson; Mark B.;
(Shoreview, MN) ; Donders; Adrianus P.; (Andover,
MN) ; Conrad; Timothy R.; (Eden Prairie, MN) |
|
Applicant: |
Name |
City |
State |
Country |
Type |
Venturi Group, LLC |
St. Paul |
MN |
US |
|
|
Assignee: |
VENTURI GROUP, LLC
St. Paul
MN
|
Family ID: |
37530088 |
Appl. No.: |
14/059246 |
Filed: |
October 21, 2013 |
Related U.S. Patent Documents
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Application
Number |
Filing Date |
Patent Number |
|
|
11235947 |
Sep 26, 2005 |
|
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14059246 |
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Current U.S.
Class: |
607/117 |
Current CPC
Class: |
A61N 1/36067 20130101;
A61N 1/0551 20130101; A61N 1/36064 20130101; A61N 1/0534 20130101;
A61N 1/0531 20130101; A61N 1/36071 20130101 |
Class at
Publication: |
607/117 |
International
Class: |
A61N 1/05 20060101
A61N001/05 |
Claims
1-10. (canceled)
11. A method for treating a condition, comprising: advancing a lead
along a patient's spinal cord in a superior direction; placing an
electrode carried by the lead on the patient's dorsal root; and
creating an electric field by applying an electrical signal to the
electrode with signal parameters selected to at least partially
block neural activity at the dorsal root, the parameters including
a frequency of about 3,000 Hz or more.
12. The method of claim 11 wherein advancing the lead includes
advancing the lead within a catheter, and then advancing the lead
from the catheter.
13. The method of claim 11 wherein creating the electric field
includes creating the electric field with a frequency of about
5,000 Hz or more.
14. The method of claim 11 wherein placing an electrode includes
placing a first electrode, and wherein the method further comprises
placing a second electrode at a location spaced apart from the
first electrode along the patient's spinal cord, and wherein
creating the electric field includes creating the electric field
with the first and second electrodes.
15. The method of claim 11 wherein placing an electrode includes
placing a first electrode, and wherein the method further comprises
placing a second electrode at a location spaced apart laterally
from the first electrode, and wherein creating the electric field
includes creating the electric field with the first and second
electrodes.
16. A method for treating a condition, comprising: advancing a lead
along a patient's spinal cord in a superior direction; placing
multiple electrodes of the lead along the spinal cord with at least
one of the electrodes being offset from the patient's
anterior-posterior axis; and creating an electric field by applying
an electrical signal to one or more of the electrodes to at least
partially block transmission of neural signals to the brain,
wherein the signal is applied at a frequency of about 5,000 Hz or
more.
17. The method of claim 16 wherein advancing the lead includes
advancing the lead within a catheter, and then advancing the lead
from the catheter.
18. The method of claim 16 wherein placing multiple electrodes
includes placing the at least one electrode at a dorsal root.
19. The method of claim 16 wherein applying the electrical signal
includes applying the electrical signal to bipolar electrodes.
20. The method of claim 16 wherein placing multiple electrodes
includes placing at least one electrode at the dorsal column.
21. The method of claim 16 wherein placing multiple electrodes
includes placing at least one electrode along an ascending neural
pathway of the spinal cord.
22. The method of claim 16 wherein placing multiple electrodes
includes placing multiple electrodes in the subarachnoid space.
Description
I
BACKGROUND OF THE INVENTION
[0001] 1. Field of the Invention
[0002] This application pertains to method and apparatus for
treating conditions associated with neuronal activity.
[0003] 2. Description of the Prior Art
[0004] a. Neural Stimulation Treatments
[0005] The prior art contains numerous examples of treatments
involving stimulation signals to nerves, muscles or organs for
treating a wide variety of medical disorders.
[0006] U.S. Pat. Nos. 4,702,254 and 5,229,569 (both assigned to
Cyberonics, Inc.) describe various central nervous system (CNS)
treatments using electrical stimulation applied to the vagus nerve.
For example, the '254 patent describes treatment of epilepsy. The
'569 patent describes treatment of neuropsychiatric disorders. U.S.
patent application Publ. No. 2003/0144709 (also assigned to
Cyberonics, Inc.) describes treatment of pain through nerve
stimulation.
[0007] U.S. patent application publication No. 2004/0243205 A1 to
Keravel et al. published Dec. 2, 2004 and assigned to Medtronic,
Inc., Minneapolis, Minn., USA (incorporated herein by reference)
describes a paddle lead with multiple electrodes. The paddle is
placed beneath the skull overlying a target area of the cerebral
cortex. The electrodes record somaestheic-evoked potentials. The
same electrodes may be used for a stimulation therapy.
[0008] Nerve stimulation and muscle stimulation have been suggested
for treating gastro-intestinal (GI) disorders. Treatments of
gastrointestinal diseases through nerve stimulation have been
suggested. For example, U.S. Past. No. 6,238,423 to Bardy dated May
29, 2001 describes a constipation treatment involving electrical
stimulation of the muscles or related nerves of the gut. U.S. Pat.
No. 6,571,127 to Ben-Haim et al. dated May 27, 2003 describes
increasing motility by applying an electrical field to the GI
tract. U.S. Pat. No. 5,540,730 to Terry, Jr. et al., dated Jul. 30,
1996 describes a motility treatment involving vagal stimulation to
alter GI contractions in response to a sense condition indicative
of need for treatment. U.S. Pat. No. 6,610,713 to Tracey dated Aug.
26, 2003 describes inhibiting release of a proinflammatory cytokine
by treating a cell with a cholinergic agonist by stimulating
efferent vagus nerve activity to inhibit the inflammatory cytokine
cascade. U.S. Pat. No. 6,622,047 to Barret et al dated Sep. 16,
2003 described obesity treatment through vagal stimulation.
[0009] b. Neural Blocking
[0010] The fore-going treatments are stimulation for treatments.
For those applying a signal to a nerve, the signal parameters
(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).
[0011] Not all electrical signals applied to nerves are stimulation
signals. Certain parameters can result in a signal that inhibits
the nerve or blocks the propagation of action potentials along the
nerve.
[0012] Many different forms of nerve blocking are known. The
present invention is an improvement upon a neural blocking to avoid
antidromic influences during stimulation or to otherwise
down-regulate nerve activity. Cryogenic nerve blocking of the vagus
is described in Dapoigny et al., "Vagal influence on colonic motor
activity in conscious nonhuman primates", Am. J. Physiol., 262:
G231-G236 (1992). Electrically induced nerve blocking is described
in Van Den Honert, et al., "Generation of Unidirectionally
Propagated Action Potentials in a Peripheral Nerve by Brief
Stimuli", Science. Vol. 206, pp. 1311-1312. An electrical nerve
block is described in Solomonow, et al., "Control of Muscle
Contractile Force through Indirect High-Frequency Stimulation", Am.
J. of Physical Medicine, Vol. 62, No. 2, pp. 71-82 (1983) and
Petrofsky, et al., "Impact of Recruitment Order on Electrode Design
for Neural Prosthetics of Skeletal Muscle", Am. J. of Physical
Medicine, Vol. 60, No. 5, pp. 243-253 (1981). A neural prosthesis
with an electrical nerve block is also described in U.S. Patent
Application Publication No. US 2002/0055779 A1 to Andrews published
May 9, 2002. A cryogenic vagal block and 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.
[0013] A frequency of the blocking signal is greater than a 200 Hz
threshold and, preferably, greater than 500 Hz. Solomonow, et al.
"control of muscle contractile force through indirect
high-frequency stimulation", American Journal of Physical Medicine,
Volume 62, No. 2, pages 71-82 (1983). Higher frequencies of as high
as 5,000 Hz result in more consistent neural conduction block.
Kilgore, et al., "Nerve Conduction Block Utilizing High-Frequency
Alternating Current", Medical and Biological Engineering and
Computing, Vol. 24, pp. 394-406 (2004).
[0014] The nerve conduction block is applied with electrical
signals selected to block the entire cross-section of the nerve
(for example, both afferent, efferent, myelinated and
non-myelinated fibers) at the site of applying the blocking signal
(as opposed to selected sub-groups of nerve fibers or just afferent
and not efferent or vice versa).
[0015] c. Use of Neural Blocking in Treatments
[0016] U.S. Pat. No. 5,188,104 to Wernicke et. al. Dated Feb. 23,
1993 describes sub-selection of fibers in a nerve by selecting a
treatment frequency by which blocks certain nerve fiber types in
the nerve while stimulating other nerve fiber types. Since certain
fibers are stimulated while other fibers are blocked, there is no
cross-section inhibition or blocking of the entire nerve and all of
its nerve fiber types (for example, both afferent, efferent,
myelinated and non-myelinated fibers).
[0017] U.S. Pat. No. 6,684,105 to Cohen et al. dated Jan. 27, 2004
(assigned to Biocontrol Medical Ltd.) teaches collision blocking in
which a stimulation signal is applied to a nerves and an
appropriately timed stimulus is applied to nerve to create neural
impulses which collide with and thereby block propagation of the
stimulation signal in a given direction. No therapy is achieved by
the blocking. Such blocking avoids adverse side effects associated
with permitting the stimulation signal propagating in an undesired
direction to an organ not targeted for therapy.
[0018] U.S. patent application Publ. No. 2002/0055779 A1 published
May 9, 2002 describes applying a high frequency block to a sciatic
nerve to block undesired neural impulses which would otherwise
contribute to spastic movement. With such spasm-inducing signals
blocked, a therapy signal is applied to the muscle to stimulated
desired muscle contractions. U.S. patent application Publ. No.
2005/0149148 A1 published Jul. 7, 29005 (assigned to Medtronic,
Inc.) teaches using a blocking signal to avoid undesired side
effect (i.e., pain) otherwise associated with a stimulation
signal.
[0019] The use of a blocking signal as a therapy is described in
various patent applications assigned to Enter.degree. Medics, Inc.
These applications pertain to use of a conduction block technology
to a nerve for a treatment of a variety of disorders. These
applications include the following (all filed Sep. 29, 2003): U.S.
patent application Ser. No. 10/674,330 (published Sep. 2, 2004 as
Publication No. US 2004/0172086 A1); U.S. patent application Ser.
No. 10/675,818 (published Sep. 9, 2004 as US Patent Application
Publication No. US 2004/0176812 A1) and U.S. patent application
Ser. No. 10/674,324 (published Sep. 2, 2004 as US Patent
Application Publication No. 2004/0172085 A1). The same assignee is
assigned U.S. patent application Ser. Nos. 10/752,994 and
10/752,940 both filed Jan. 6, 2004 with respective publication
dates of Aug. 26, 2004 and Sep. 2, 2004, Publication Nos. US
2004/0167583 A1 and 2004/0172088 A1.
[0020] The foregoing EnteroMedics patent applications describe, in
a preferred embodiment, the application of neural conduction block
therapy to a vagus nerve alone or in combination with a stimulation
of the nerve. The conduction block therapy of the these patent
applications includes application of an electrical signal with
parameters selected to down-regulate vagal activity by creating
conditions in which normal nerve propagation potentials are blocked
at the application of the signal on both afferent and efferent
nerves fibers of the vagus. Representative treatments described in
these applications include the treatment of obesity, pancreatitis,
pain, inflammation, functional GI disorders, irritable bowel
syndrome and ileus.
[0021] d. Accommodation
[0022] Blockage of a nerve can result in nerve accommodation in
which other nerve groups assume, in whole in part, the function of
the blocked nerve. For example, sub-diaphragm blocking of the vagus
nerve may be accommodated by the enteric nervous system. U.S.
patent application Ser. No. 10/881,045 filed Jun. 30, 2004
(published Feb. 17, 2005 as Publication No. US 2005/0038484 A1)
(assigned to EnteroMedics, Inc.) notes that a duty cycle of
electrical impulses to the nerve to block neural conduction on the
nerve can be adjusted between periods of blocking and no blocking
in order to vary the amount of down regulation of the vagus nerve
as well as preventing accommodation by the enteric nervous
system.
[0023] e. Drug Treatments
[0024] Many symptoms of Parkinson's disease can be controlled with
one of many currently available medications. These are divided into
several classes of drugs including dopamine agonists,
levodopa/decarboxylase inhibitors, anticholinergic agents, MAO-B
inhibitors, and COMT (catechol-O-methyltransferase) inhibitors.
These medications, whether used alone or in combination, not only
replace the dopamine that has been lost in the brain, but also slow
the rate of dopamine loss in the brain, and/or correct the
imbalance between the levels of dopamine and acetylcholine in the
brain. While none of these medications are a cure for Parkinson's
disease, they can alleviate the symptoms of the disease and help
its victims manage the disease.
[0025] One of the most effective and widely administered
medications introduced in the 1970's to relieve symptoms of
Parkinson's disease works as a dopamine replacement therapy. This
drug is known as Sinemet (generic name of levodopa/carbidopa), its
active ingredient being L-DOPA (L-3,4-dihydroxyphenylalanine).
Levodopa is a generic name given to L-DOPA when it is produced as a
drug. Unfortunately, dopamine cannot be administered directly to
patients because it does not cross the blood-brain barrier. Hence,
L-DOPA, which is the precursor form of dopamine, crosses the
blood-brain barrier, and can be converted to dopamine in the brain,
is the molecule of choice. However, due to the presence of aromatic
amino acid decarboxylase (AADS) in the periphery of the brain,
which will convert L-DOPA to dopamine before it crosses the blood
brain barrier and prevent its passage to the brain, L-DOPA is
administered with carbidopa, an AADS inhibitor. Carbidopa inhibits
peripheral AADS action and thus reduces the amount of levodopa
needed.
[0026] During the first few months the medication is administered,
its benefits are maximal. However, patients taking Sinemet for a
longer period are prone to the "wearing-off" effect, a tendency for
the effectiveness of the drug to be lost with time. Hence, the dose
of Sinemet will often have to be increased with time. Sometimes an
"on-off effect," where the symptoms become sporadic and
unpredictable over a period of time, is also experienced. Moreover,
as the dose of the medication is increased, some patients begin to
experience side effects due an increase in brain dopamine levels.
Some major side effects include anxiety, agitation, dyskinesia,
vomiting, low blood pressure, hallucination and nausea (Nadeau
1997). The occurrence of side effects limits the further increase
in Sinemet's dosage and at this point, treatment options become
limited. Fortunately, carbidopa minimizes the incidence of vomiting
and nausea. Furthermore, although levodopa/carbidopa treatment
decreases bradykinesia and rigidity, it may not relieve tremor and
balance.
[0027] Sinemet (unlike most medications that are absorbed into
blood through the stomach) is absorbed from the small intestine.
Anything that delays the movement of food from the stomach to the
small intestine, such as foods rich in fat and protein, can reduce
the amount of the drug absorbed. Moreover, levodopa has a very
short plasma half-life. It disappears from the blood in 60 to 90
minutes. Because it is a type of amino acid called a large neutral
amino acid (LNAA), it attaches itself during absorption to carrier
molecules in the wall of the intestine and is then carried to the
blood. Similarly, once in the blood, carrier molecules carry it
across the blood-brain barrier. Amino acids such as isoleucine,
leucine, valine, phenylalanine, tryptophan and tyrosine compete for
the carrier with levodopa. Hence, a diet rich in protein can
further compete with the Sinemet for entry into the brain. Thus, it
is important to carefully evaluate one's diet when taking
Sinemet.
[0028] Another medication that can be used alone or in combination
with Sinemet is Eldepryl (generic name of selegeline). Selegeline
is classified as a MAO-B inhibitor and is often administered in 5
mg capsules to help keep the Sinemet dose lower over time and
therefore extend its administration period. In certain cases, it
can delay the need for levodopa therapy by up to a year. By
blocking the action of MAO-B, selegeline extends the capabilities
of the dopamine in the synapse, delaying the breakdown of naturally
occurring dopamine and dopamine administered as L-DOPA. Eldepryl
thus slows dopamine loss in the synapse and makes it more likely
that a dopamine will reach its corresponding receptor on the
receiving nerve cell and transmit the correct message down the
dopamine circuit. This is often referred to as dopamine
conservation therapy.
[0029] During the Fourth International Congress of Movement
Disorders held in Vienna during the summer of 1996, Eldepryl's
benefits when administered in combination with Sinemet were
affirmed. In fact, patients taking the drug combination were shown
to experience motor fluctuations 1.8 years later on average than
those taking only Sinemet. Another advantage of taking Eldepryl is
that there is no specific dietary restriction associated with it if
taken at the 5 mg dosage. Selegiline is an easy drug to take and
has further been shown to protect the dopamine-producing neurons
against the toxicity of MPTP. However, selegiline has its
drawbacks. Patients have been known to experience side effects such
as nausea, orthostatic hypotension and insomnia.
[0030] Dopamine agonists comprise another general category of
drugs. Parlodel (generic name of bromocriptine), Permax (generic
name of pergolide) and Symmetrel (generic name of amantadine) are
examples. Parlodel and Permax mimic the action of dopamine by
interacting with dopamine receptors in a form of dopamine
substitution therapy. These two drugs enter the brain directly at
dopamine receptor sites and prolong the duration of Sinemet's
effects. An advantage of this approach is that it is less likely to
cause dyskinesias (the occurrence of abnormal involuntary movements
that results from the intake of high doses of L-DOPA). This is
because the actual levels of dopamine do not increase in the brain,
as is the case with Sinemet. Rather, a substitute form of dopamine
is being used. However, these two drugs are less effective than
L-DOPA in decreasing bradykinesia and rigidity and induce side
effects such as paranoia, hallucinations, confusion, nausea and
vomiting.
[0031] Symmetrel is an anti-viral drug used as a dopamine-releasing
therapy in combination with Sinemet. It works by allowing the
presynaptic neuron to more easily release dopamine into the
synapse. More recently, it has been suggested that Symmetrel acts
by binding to glutamate receptors in the subthalamic nucleus to
help redress the imbalance in basal ganglia activity due to a
deficiency in dopamine in a synergistic manner. Symmetrel is either
used alone in the first stages of PD or in combination in the later
stages. However, its effectiveness is known to wear off in a third
to a half of the patients taking it. Furthermore, it induces side
effects such as edema, blurred vision, depression, confusion and
mottled skin.
[0032] Two new drugs, after having undergone extensive clinical
trials, were made available in 1997. Requip (generic name of
ropinirole) and Mirapex (generic name of pramipexole) are dopamine
agonists. They are selective for the dopamine D3 receptor and are
selectively targeted toward the basal ganglia. Both Requip and
Mirapex can be used alone or with levodopa and both show fewer side
effects than other drugs (Lozano et al. 1998).
[0033] Artane and Cogentine represent yet another class of drugs.
They are classified as anti-cholinergic agents and are used to
restore the imbalance between dopamine and acetylcholine levels in
the brain. They work to reduce the activity of acetylcholine and
hence reduce the tremor and stiffness of muscle that come about as
a result of having more acetylcholine than dopamine in the
brain.
[0034] Until the introduction of L-DOPA, anti-cholinergic agents
were the main treatments for Parkinson's disease. Now Artane and
Cogentine are usually administered in combination with other
medications for their therapeutic effect. While effective, these
drugs can also have side effects such as blurred vision, urinary
retention, dry mouth, memory loss, and constipation. Hence, they
are of limited use to the older population because they can cause
serious neuropsychiatric side effects.
[0035] Tamar (generic name of tolcapone) is a drug classified as a
COMT inhibitor. COMT is a peripheral enzyme that reduces levodopa
to a less active form. Tasmar, which became available in February
1998, has a different action than that of the dopamine agonists, in
that when COMT activity is blocked, dopamine remains in the brain
for a longer period of time. Hence, when administered with
levodopa, COMT inhibitors prolong the duration time of Sinem.
II
SUMMARY OF THE INVENTION
[0036] A method and apparatus are disclosed for treating a variety
of conditions. These include treating a disorder associated with
neural activity near a region of a brain. In such condition, the
method includes placing an electrode to create a field near said
region, creating said field with parameters selected to at least
partially block neural activity within said field. For treating a
tissue sensation, the method includes identifying a target area of
tissue to be treated and placing an electrode to create a field
near the target area, and creating the field with parameters
selected to at least partially block neural activity within the
target area. For treating a condition associated with neural
activity of a spinal cord, the method includes placing an electrode
to create a field near a nerve associated with the spinal cord, and
creating the field with parameters selected to at least partially
block neural activity within the nerve.
III
BRIEF DESCRIPTION OF THE DRAWINGS
[0037] FIG. 1 is a top plan view of a patient's head and showing an
electrode array according to the present invention in phantom lines
positioned beneath a skull of the patient;
[0038] FIG. 2 is a side elevation view of a patient with an
electrode patch beneath the skull of the patient and shown in
phantom lines with a lead to a control unit positioned in the
patient's neck;
[0039] FIG. 3 is a view of a brain of a patient shown in lateral
cross-section and with a patch according to the present invention
residing between the skull and the surface of the patient's brain
over a cortex of the patient's brain;
[0040] FIG. 4 is a plan view of an electrode patch according to the
present invention;
[0041] FIG. 5 is an anterior-posterior, cross-sectional view of a
patient's brain showing an alternative embodiment of electrodes
placed on a catheter advanced through the ventricle of the
brain;
[0042] FIG. 6 is a plan view of inside surfaces of an upper arm and
forearm and hand of a patient with an alternative embodiment of the
present invention positioned surrounding a target area for needle
insertion;
[0043] FIG. 7 is a side elevation view of a section of the
electrode patch of FIG. 6;
[0044] FIG. 8 is a graphical presentation of representative
waveforms according to the present invention for energizing the
electrodes of FIG. 6;
[0045] FIG. 9 is an illustration of a patient's finger showing
electrodes on the opposite side of a target area at the fingertip
of the patient;
[0046] FIG. 10 illustrates electrodes on mucosal tissue on opposite
sides of a tooth to apply a blocking signal;
[0047] FIG. 11 is a cross-section view of a vertebral body and
showing anatomical components and a blocking signal electrode on a
dorsal root;
[0048] FIG. 12 is a schematic longitudinal, side-sectional showing
of a segment of a spine with a catheter placement of an electrode
on a dorsal root; and
[0049] FIG. 13 is an anterior-posterior schematic representation of
a segment of a spine with blocking signal electrodes shown in two
positions.
IV
DESCRIPTION OF A PREFERRED EMBODIMENT
[0050] With reference now to the various drawing figures in which
identical elements are identically numbered, preferred embodiments
of the present invention will now be described.
[0051] A. Central Nervous System (CNS) Treatment
[0052] Certain disorders (e.g., epilepsy and Parkinson's disease
and other motor disorders of CNS origin) are believed to be
associated with hormonal imbalance.
[0053] Movement disorders associated with cerebral activity are not
fully understood. However, certain disorders such as epilepsy and
Parkinson's disease are believed to be associated with an imbalance
of hormonal production deep within the brain.
[0054] For example, certain regions deep within the brain produce
the hormones glutamate and dopamine. Glutamate enhances
conductivity of the nerve cells of the brain while dopamine reduces
or inhibits such conductivity.
[0055] With reference to FIG. 3, dopamine is produced within a
region of the brain known as the substantia nigra SN. Glutamate is
produced in the thalamus region of the brain, which includes the
ventral anterior nucleus VAN, the ventral lateral nucleus VLN and
the centromedian nucleus CN. The produced hormones are projected
throughout the brain including to the cortex which is the outer
region of the brain near the back of the head and illustrated
generally by C in FIG. 3.
[0056] The projection to the cortex C of the glutamate is believed
to flow from production of glutamate in the ventral anterior
nucleus VAN. Such projection is illustrated by the arrow A.sub.G in
FIG. 3. The projection of dopamine to the cortex is believed to
flow from the substantia nigra SN with such projection illustrated
in FIG. 3 by the arrow A.sub.D.
[0057] The presence of dopamine and glutamate in the cortex C alter
the conductivity of the nerve cells in the cortex C. Certain motor
disorders such as epilepsy and Parkinson's disease, are believed to
be associated with a deficiency of dopamine production which
results in excessively enhanced conductivity in the cortex since
the enhancing hormone, glutatmate, is disproportionately high
relative to the inhibiting conductivity hormone, dopamine.
[0058] The present invention compensates for hormonal imbalance
resulting in excessive conductivity by altering the conductivity at
the cortex. The conductivity of the cortex and electrical activity
of the cortex controls motor functions of the patient.
[0059] The present invention is a patch electrode 10, which is
placed beneath the skull of the patient between the skull S and the
cortex C (FIG. 3). The patch electrode 10 includes a flexible flat
substrate 12 of electrically insulating material such as silicone
or the like. Exposed on one surface of the substrate 12 are a
plurality of electrically conductive electrodes, which, in a
preferred embodiment, are arranged in an array of rows and
columns.
[0060] In the specific examples shown in FIGS. 3 and 4, there is a
first row containing electrodes E.sub.1, 1 through E.sub.1, 5. The
second row contains five electrodes E.sub.2, 1 through E.sub.2, 5.
The third row contains electrodes E.sub.3, 1 through E.sub.3, 5.
The fourth row contains electrodes E.sub.4, 1 through E.sub.4, 5.
The fifth row contains electrodes E.sub.5, 1 through E.sub.5, 5.
The patch 10 is dimensioned for the array of electrodes to cover at
least a portion of the cortex C of the brain and with the
electrodes of the array in electrically conductive contact with the
cortex C.
[0061] As illustrated in FIGS. 1 and 2, the patch electrode 10 is
placed over the cortex beneath the skull on either the left (FIG.
1) or right (FIG. 2) of the brain. In FIG. 1, the top of a
patient's head H is shown with an anterior-posterior axis A-P
separating the patients' left L and right R sides.
[0062] As shown in FIG. 2, a lead 16 from the patch electrode 10
may be tunneled between the skull S and the brain B through the
base of the skull and terminated at a control unit 20 which may be
positioned within the neck or implanted lower in the patient such
in the shoulder or clavicle area or the like. The lead 16 is a
highly flexible conductor containing individual conductors for each
of the electrodes of the array of the patch 10 and encased within a
highly flexible insulative material such as silicone or the
like.
[0063] The controller 20 may be an implantable pulse generator
(with separate power source such as either rechargeable batteries
or replaceable batteries) or may be a control unit, which receives
power and pacing signals from an external control unit, which
transmits via radio frequency transmission to the controller 20.
For the purpose of this description, the controller 20 will be
treated as a completely contained controller having both logic
circuits and power source. It will be appreciated that such
controllers may be also programmable from external programmable
sources as is known in the art for controlling implantable pulse
generators for cardiac pacing.
[0064] The circuitry of the controller 20 permits energizing
selective ones of the electrodes of the array in bi-polar electrode
pairs. For example, electrodes E.sub.5, 1 and E.sub.4, 2 may be
energized with oppositely polarized waveforms to create an
electrical field F.sub.1 between the electrodes E.sub.5, 1 and
E.sub.4, 2. By oppositely charged waveforms it will be appreciated
that electrode E.sub.5, 1 is positively charged while E.sub.4, 2 is
negatively charged and E.sub.5, 1 is negatively charged while
E.sub.4, 2 is positively charged. When the electrode pair E.sub.5,
1 and E.sub.4, 2 is charged to create the field F.sub.1, all
remaining electrodes may be inactive or otherwise charged to create
more complex electrical fields.
[0065] FIG. 4 illustrates a field F.sub.2 created between electrode
pairs E.sub.2, 2 and E.sub.2, 4 and a field F.sub.3 between
electrode pairs E.sub.1, 1 and E.sub.5, 5. While multiple electrode
pairs may be simultaneously charged, the controller 20 may also
control the electrodes so that the waveform applied to the
electrodes has a built-in delay period such that a particular
electrode pair is not charged and in its delay period, while other
electrode pairs are being charged. Accordingly, multiple pairs of
electrodes may be charged with the waveforms of the electrode pairs
being nested so that only one electrode pair is charged at any one
unit of time. An example of a nested set of waveforms will be later
described.
[0066] Preferably, the waveform selected is a blocking waveform to
block neuronal activity. For example, the frequency of the field
will have a pulse width selected for the generated field to have a
frequency in excess of a 200 Hz threshold as described by Solomonow
(article previously described) and, more preferably, 5,000 Hz or
higher as described in Kilgore (article previously described). A
5,000 Hz signal will have a pulse width of about 100 microseconds.
A representative amplitude for such signals would be 0.2 to 8
mA.
[0067] The effect of applying a blocking signal to the cortex
reduces the excessive electrical activity otherwise associated with
a dopamine deficiency. Further, the therapy of the present
invention is localized to the area of interest, namely, the cortex
region of the brain, which contributes to the symptoms of motor
disorders. Other regions of the brain are not affected and no
systemic drug is given to the patient.
[0068] The programming of the controller 20 may permit altering the
selected individual electrodes, which form an electrode pair. Any
two electrodes on the patch 10 may be formed to a pair to create a
field between the pair. As a result, at time of placement of the
patch 10, the patch need not be precisely placed to achieve an
interruption or inhibition of electrical activity in the cortex.
Instead, different permutations of coupled electrode pairs may be
tested to observe patient response post-surgery.
[0069] The forgoing has illustrated use of the blocking signals to
compensate and down regulate cortex electrical conductivity in
response to dopamine deficiency. FIG. 5 illustrates use of
stimulation signals to result in localized production of dopamine.
In FIG. 5, a catheter 30 is advanced into the ventricles of the
brain with a distal tip 32 positioned in the region of the
hypothalamus of the brain. The tip 32 includes an electrode pair
E.sub.A and E.sub.B, which form a bi-polar electrode pair. The
electrodes are individually electrically connected to a controller
(not shown but such as controller 20 previously described) for
creating a desired waveform (as will be described). The controller
provides the electrodes with either a stimulation signal (for
example 20 Hz or any other signal less than 200 Hz) or a blocking
signal as previously described. Energizing the electrodes with a
stimulation signal can be tested on a particular patient to note
any increase in dopamine production and result in cortex activity.
Similarly, a blocking signal can be applied to note any reduction
in glutamate production.
[0070] B. Peripheral Nervous System Treatment
[0071] The use of blocking signals as described may be used to
alleviate pain on the surface of the skin for a wide variety of
applications. For example, FIGS. 6 and 7 illustrate a patch 110
which may be placed on the skin surrounding a target area T
associated with pain.
[0072] In the particular illustration of FIG. 6, a patient's
required to give blood samples frequently require a needle
injection into the interior surface of the arm to insert a needle
into a vein between the upper arm UA and the forearm FA. The health
care technician's identification of the particular vein for
puncture is identified and circled by a target area T in phantom
lines in FIG. 6.
[0073] A patch 110 is a ring-shaped substrate 112 sized to surround
the target area T but otherwise permits access to the target area T
by a needle (not shown) for drawing blood or the like. An
undersurface of the substrate 112 contains diametrically opposite
electrode pairs E.sub.1, A, E.sub.1,B and E.sub.2, A, E.sub.2, B
and E.sub.3, A, E.sub.3, B. The electrodes are individually
electrically connected to a controller (not shown but such as
controller 20 previously described) for creating a desired waveform
(as will be described). Between the electrodes adhesive layers 114
are provided to secure the patch 110 in place on the patient's skin
surrounding the target area T.
[0074] The individual electrode pairs are bi-polar electrode pairs,
which may be provided with a blocking signal as previously
described. For example, the electrode pair E.sub.1, A, E.sub.1, B
may be provided with a first waveform W.sub.1 illustrated in FIG.
8. The electrode pair E.sub.2, A, E.sub.2, B may be provided with a
second waveform W.sub.2 and electrode pairs E.sub.3, A, E.sub.3, B
may be provided with a third waveform W.sub.3 in FIG. 8.
[0075] Each of the waveforms W.sub.1, W.sub.2 and W.sub.3 are
identical differing only in their timing. The waveforms are
preferably blocking waveforms having a frequency in excess of a few
hundred Hz threshold and more preferably having a frequency of
about 5,000 Hz. With such a frequency, the waveforms have a pulse
duration D of 100 microseconds. Preferably, each cycle of the
waveform has a delayed period DP between the pulses with the
duration of the delay period DP equal to two complete cycles (i.e.,
four pulse durations D or 400 microseconds). The amplitude of the
pulse A may be any suitable amplitude to encourage current flow
between the electrode pairs. To drive current across the skin,
higher energy levels are anticipated (e.g., voltages up to about 35
volts and currents up to 25 mA.
[0076] The waveforms are offset relative to one another so that
when any one electrode pair is receiving a pulse, the other
electrode pairs are inactive resulting in three nested waveforms as
illustrated in FIG. 8. Such waveforms create an electrical field
between the diametrically opposed electrodes of a particular pair
with the field passing through the target area T to block neuronal
activity within the target area. Accordingly, when the electrodes
are energized with the blocking signals as described, pain is not
sensed during needle insertion into the target area T.
[0077] It will be appreciated in FIG. 6 the apparatus 110 will
further include electrical leads to a control unit both of which
are not shown for ease of illustration.
[0078] FIG. 9 illustrates an alternative application where two
electrodes E.sub.1 E.sub.2 are placed on opposite sides of a target
area T near the fingertip of a patient's finger F. For ease of
illustration, a substrate for the electrodes is not shown. The
electrodes are individually electrically connected to a controller
(not shown but such as controller 20 previously described) for
creating a desired waveform. The application of FIG. 9 is
particularly useful for numbing a fingertip prior to lancing the
fingertip for a blood sample for periodic blood sugar tests by
diabetic patients.
[0079] FIG. 10 illustrates a still further embodiment where
electrodes E.sub.1 and E.sub.2 are placed on opposite sides of the
gum of the patient overlying mucosal tissue MT on opposite sides of
a tooth T. Application of a blocking signal as previously described
to the electrodes creates a blocking field to block nerves within
the mucosal tissue for treatment of pain associated with gums or
teeth or to precondition the tissue prior to injection of local
anesthetics such as Novocain or Lydacain or other procedure
occurring at the tissue.
[0080] C. Spinal Cord Treatment
[0081] FIGS. 11-13 illustrate application of the present invention
to the spinal cord. By way of anatomical background, FIG. 11 shows,
in cross section, a spinal cord SC position between an anterior
vertebral body AVB and a posterior vertebral body PVB. The
patient's anterior-posterior axis A-P is shown separating the
patient's right R and left L sides.
[0082] The spinal cord SC is shown enclosed within a dural layer D
with opposing surfaces of the spinal cord SC and the dural D
defining a subanachroid space SAS. Extending laterally away from
the spinal cord are left and right ventral roots LVR, RVR and right
and left dorsal roots RDR, LDR. Also illustrated is a ganglion G.
The spinal cord SC is illustrated as having identifiable areas of
afferent and efferent fibers including ascending pathways AP areas
and descending pathways DP areas.
[0083] According to the present invention, an electrode E is
advanced either through open surgical or minimally invasive
techniques into the subanachroid space SAS and positioned on a root
such as the right dorsal root RDR. Application of a blocking signal
to the electrode E blocks signals such as pain signals from the
dorsal root the spinal cord SC. While a single monopolar electrode
E is shown in FIG. 11, it will be appreciated that multiple
electrodes including bipolar electrodes may be placed on the roots.
For spinal treatments, such blocking signal may be as previously
described and, preferably, has a frequency in excess of 3,000 Hz
and more preferably about 5,000 Hz or more.
[0084] FIG. 12 is shown in vertical cross section with multiple
vertebral bodies and with a spinal cord extending between the
vertebral bodies. For ease of schematic illustration, the dorsal
roots are shown extending between the anterior bodies. It will be
appreciated that such roots extend laterally from the spinal
cord.
[0085] A catheter C is shown in phantom lines for advancing an
electrode to a dorsal root for placing the electrode on the dorsal
root. The electrode lead extends from the electrode through
implantable or external pulse generator as previously
described.
[0086] FIG. 13 illustrates an electrode E (the upper electrode E in
the view of FIG. 13) placed on a dorsal root either surgically or
through catheter delivery as previously described. Further, FIG. 13
shows an electrode E (the lower electrode E in the view of FIG. 13)
placed overlying the spinal cord over a target area AP, In the
example of FIG. 13, the target area AP is an identified area of
ascending pathways for application of a blocking signal to the
ascending pathways for blocking transmission of neural signals to
the brain. The electrode is supported on a sling S which is mounted
on the left and right dorsal roots. It will be appreciated that the
electrode so supported can be positioned over any area of the
spinal cord to affect any desired area of ascending pathways or
descending pathways. The electrodes are individually electrically
connected to a controller (not shown but such as controller 20
previously described) for creating a desired waveform.
[0087] With the foregoing detailed description of the present
invention, it has been shown how the objects of the invention have
been attained in a preferred manner. Modifications and equivalents
of disclosed concepts such as those which might readily occur to
one skilled in the art, are intended to be included in the scope of
the claims which are appended hereto.
* * * * *