U.S. patent application number 12/835680 was filed with the patent office on 2011-01-13 for skull-mounted electrical stimulation system and method for treating patients.
This patent application is currently assigned to BOSTON SCIENTIFIC NEUROMODULATION CORPORATION. Invention is credited to Rafael Carbunaru, Todd K. Whitehurst.
Application Number | 20110009920 12/835680 |
Document ID | / |
Family ID | 34738629 |
Filed Date | 2011-01-13 |
United States Patent
Application |
20110009920 |
Kind Code |
A1 |
Whitehurst; Todd K. ; et
al. |
January 13, 2011 |
SKULL-MOUNTED ELECTRICAL STIMULATION SYSTEM AND METHOD FOR TREATING
PATIENTS
Abstract
A system and method for applying electrical stimulation or drug
infusion to nervous tissue of a patient to treat epilepsy, movement
disorders, and other indications uses at least one implantable
system control unit (SCU) (110), including an implantable
signal/pulse generator (IPG) and one or more electrodes (152, 152).
The IPG is implanted in the mastoid area (143) of the skull (140)
and communicates with at least one external appliance (230), such
as a Behind-the-Ear (BTE) unit (100). In a preferred embodiment,
the system is capable of open- and closed-loop operation. In
closed-loop operation, at least one SCU includes a sensor, and the
sensed condition is used to adjust stimulation parameters.
Inventors: |
Whitehurst; Todd K.; (Santa
Clarita, CA) ; Carbunaru; Rafael; (Studio City,
CA) |
Correspondence
Address: |
VISTA IP LAW GROUP LLP/BSC - NEUROMODULATION
2040 MAIN STREET, Suite 710
IRVINE
CA
92614
US
|
Assignee: |
BOSTON SCIENTIFIC NEUROMODULATION
CORPORATION
Valencia
CA
|
Family ID: |
34738629 |
Appl. No.: |
12/835680 |
Filed: |
July 13, 2010 |
Related U.S. Patent Documents
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Application
Number |
Filing Date |
Patent Number |
|
|
10585233 |
Jun 30, 2006 |
7769461 |
|
|
PCT/US04/42711 |
Dec 17, 2004 |
|
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12835680 |
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60531224 |
Dec 19, 2003 |
|
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Current U.S.
Class: |
607/45 |
Current CPC
Class: |
A61M 2205/8243 20130101;
A61N 1/36082 20130101; A61M 5/1723 20130101; A61N 1/37211 20130101;
A61M 5/14276 20130101; A61N 1/0534 20130101; A61N 1/36071 20130101;
A61N 1/0526 20130101; A61M 2205/52 20130101; A61N 1/36114 20130101;
A61N 1/37229 20130101; A61N 1/0529 20130101; A61M 2205/3523
20130101 |
Class at
Publication: |
607/45 |
International
Class: |
A61N 1/36 20060101
A61N001/36 |
Claims
1-18. (canceled)
19. A method of treating an indication of a patient using at least
one system control unit implanted in a shallow recess of the
mastoid area of the skull of the patient, the method comprising:
applying at least one stimulus generated by the system control unit
to at least one nerve, thereby at least in part alleviating the
symptoms of the indication; wherein the at least one nerve is
selected from at least one of the body, branches, and roots of at
least one of the vagus nerves, the trigeminal nerves, the
ophthalmic nerves, the maxillary nerves, the mandibular nerves, the
facial nerves, the glossopharyngeal nerves, and the trigeminal
ganglion or ganglia.
20. The method of claim 19, wherein the indication is epilepsy.
21. The method of claim 19, further comprising implanting the at
least one system control unit within the shallow recess of the
mastoid area of the skull of the patient.
22. The method of claim 19, wherein the system control unit is
connected to at least one electrode, and wherein the stimulus
comprises electrical stimulation deliverable via the at least one
electrode.
23. The method of claim 22, wherein the electrical stimulation is
excitatory stimulation.
24. The method of claim 22, wherein the electrical stimulation is
inhibitory stimulation.
25. The method of claim 19, further comprising sensing at least one
condition and using the at least one sensed condition to
automatically determine the stimulus to apply.
26. The method of claim 19, wherein the system control unit is
connected to at least one catheter, and wherein the stimulus
comprises drug infusion deliverable via the at least one
catheter.
27. The method of claim 19, wherein the at least one nerve is at
least one of the body, branches, and roots of the vagus nerves.
28. The method of claim 19, wherein the at least one nerve is at
least one of the body, branches, and roots of the trigeminal
nerves.
29. The method of claim 19, wherein the at least one nerve is at
least one of the body, branches, and roots of the ophthalmic
nerves.
30. The method of claim 19, wherein the at least one nerve is at
least one of the body, branches, and roots of the maxillary
nerves.
31. The method of claim 19, wherein the at least one nerve is at
least one of the body, branches, and roots of the mandibular
nerves.
32. The method of claim 19, wherein the at least one nerve is at
least one of the body, branches, and roots of the facial
nerves.
33. The method of claim 19, wherein the at least one nerve is at
least one of the body, branches, and roots of the glossopharyngeal
nerves.
34. The method of claim 19, wherein the at least one nerve is at
least one of the body, branches, and roots of and the trigeminal
ganglion or ganglia.
Description
RELATED APPLICATIONS
[0001] The present application is a continuation of U.S. patent
application Ser. No. 10/585,233, filed Jun. 30, 2006, which is a
U.S. National State filing under 35 U.S.C. .sctn.371 of
International Application No. PCT/US04/42711, which claims priority
of U.S. Provisional Patent Application Ser. No. 60/531,224, filed
Dec. 19, 2003, the disclosure of which is expressly incorporated
herein by reference.
TECHNICAL FIELD
[0002] The present invention generally relates to implantable
stimulator systems and methods, and more particularly relates to
implantable stimulator systems and methods utilizing one or more
implantable leads for treating epilepsy, movement disorders, and
other indications.
BACKGROUND ART
[0003] Epilepsy is characterized by a tendency to recurrent
seizures that can lead to loss of awareness, loss of consciousness,
and/or disturbances of movement, autonomic function, sensation
(including vision, hearing and taste), mood, and/or mental
function. Epilepsy afflicts 1-2% of the population in the developed
world. The mean prevalence of active epilepsy (i.e., continuing
seizures or the need for treatment) in developed and undeveloped
countries combined is estimated to be 7 per 1,000 of the general
population, or approximately 40 million people worldwide. Studies
in developed countries suggest an annual incidence of epilepsy of
approximately 50 per 100,000 of the general population. However,
studies in developing countries suggest this figure is nearly
double at 100 per 100,000.
[0004] Epilepsy is often but not always the result of underlying
brain disease. Any type of brain disease can cause epilepsy, but
not all patients with the same brain pathology will develop
epilepsy. The cause of epilepsy cannot be determined in a number of
patients; however, the most commonly accepted theory posits that it
is the result of an imbalance of certain chemicals in the brain,
e.g., neurotransmitters. Children and adolescents are more likely
to have epilepsy of unknown or genetic origin. The older the
patient, the more likely it is that the cause is an underlying
brain disease such as a brain tumor or cerebrovascular disease.
[0005] Trauma and brain infection can cause epilepsy at any age,
and in particular, account for the higher incidence rate in
developing countries. For example, in Latin America,
neurocysticercosis (cysts on the brain caused by tapeworm
infection) is a common cause of epilepsy; in Africa, AIDS and its
related infections, malaria and meningitis, are common causes; in
India, AIDS, neurocysticercosis and tuberculosis, are common
causes. Febrile illness of any kind, whether or not it involves the
brain, can trigger seizures in vulnerable young children, which
seizures are called febrile convulsions. About 5% of such children
go on to develop epilepsy later in life. Furthermore, for any brain
disease, only a proportion of sufferers will experience seizures as
a symptom of that disease. It is, therefore, suspected that those
who do experience such symptomatic seizures are more vulnerable for
similar biochemical/neurotransmitter reasons.
[0006] Movement disorders are neurologic syndromes characterized by
either an excess or a paucity of movement. These disorders affect
approximately two million Americans, including over one million
suffering from benign essential tremor, and half a million
suffering from Parkinson's disease. A substantial percentage of
those afflicted with movement disorders experience a significant
decrease in quality of life, suffering such problems as
incapacitating tremor, limited mobility, bradykinesia (difficulty
consciously initiating movement) dysarthria (difficulty with
speech), and consequent social isolation. The etiology of many
movement disorders, e.g., benign essential tremor, is poorly
understood. For other movement disorders, e.g., Parkinson's
disease, the mechanism of the disorder and even the brain cells
affected have been identified, but even with optimal medication and
physician care the disease may not be reversed and may even
continue to progress. Medications that are effective for movement
disorders may have significant side effects and may lose their
efficacy over time.
[0007] Essential Tremor (ET), a.k.a., Benign Essential Tremor, is
the most common movement disorder. It is a syndrome characterized
by a slowly progressive postural and/or kinetic tremor, usually
affecting both upper extremities. The prevalence of ET in the US is
estimated at 0.3-5.6% of the general population. A 45-year study of
ET in Rochester, Minn. reported an age- and gender-adjusted
prevalence (i.e., the percentage of a population that is affected
with a particular disease at a given time) of 305.6 per 100,000 and
an incidence (i.e., the rate of new cases of a particular disease
in a population being studied) of 23.7 per 100,000.
[0008] ET affects both sexes equally. The prevalence of ET
increases with age. There are bimodal peaks of onset--one in the
late adolescence to early adulthood and a second peak in older
adulthood. The mean age at presentation is 35-45 years. ET usually
presents by 65 years of age and virtually always by 70 years.
Tremor amplitude slowly increases over time. Tremor frequency
decreases with increasing age. And 8-12 Hz tremor is seen in young
adults and a 6-8 Hz tremor is seen in the elderly. Although ET is
progressive, no association has been found between age of onset and
severity of disability.
[0009] Mortality rates are not increased in ET. However, disability
from ET is common. Significant changes in livelihood and
socializing are reported by 85% of individuals with ET, and 15%
report being seriously disabled due to ET. Decreased quality of
life results from both loss of function and embarrassment. In a
study of hereditary ET, 60% did not seek employment; 25% changed
jobs or took early retirement; 65% did not dine out; 30% did not
attend parties, shop alone, partake of a favorite hobby or sport,
or use public transportation; and 20% stopped driving.
DISCLOSURE OF INVENTION
[0010] The present invention provides means for chronically
stimulating a nerve(s) including the vagus nerve, a branch(es) of
the vagus nerve, the trigeminal ganglion or ganglia, trigeminal
nerve(s), a branch(es) of the trigeminal nerve(s) (e.g., ophthalmic
nerve(s), maxillary nerve(s), and/or mandibular nerve(s)), facial
nerve(s), glossopharyngeal nerve(s), or a branch(es) of any of
these neural structures with an implantable neurostimulator. The
present invention provides systems and methods for applying
electrical stimulation to one or more of theses nerves or nerve
branches via a "skull-mounted" or "head-mounted" device. Electrical
stimulation of such targets may provide significant therapeutic
benefit in the management of epilepsy, movement disorders, and
other indications defined in the detailed description of the
invention section of this document.
[0011] The treatment provided by the invention is carried out by
employing at least one system control unit (SCU). In one preferred
form and SCU comprises an implantable pulse generator (IPG), and
external Behind-the-Ear (BTE) unit, and implantable electrode(s).
In this embodiment, the SCU is preferably implanted in a
surgically-created shallow depression in above, or near the mastoid
area, with one or more electrode leads attached to the SCU
extending subcutaneously and along various paths towards the
nerve(s previously mentioned. Preferred systems also include one or
more sensors for sensing symptoms or other conditions that may
indicate a need for treatment.
[0012] The IPG includes a battery that is much larger than a
battery of a typical microstimulator, thus extending the time
between recharges and consequent explanation procedures. The BTE
unit is adapted to be situated on the exterior of a patient, near
the location where the IPG is imbedded within the mastoid bone. The
BTE unit includes circuitry and a coil used to recharge the IPG
transcutaneously.
[0013] The SCU preferably includes a programmable memory for
storing data and/or control stimulation parameters. This allows
stimulation and control parameters to be adjusted to levels that
are safe and efficacious with minimal discomfort. Electrical
stimulation may be controlled independent of any other stimulation
or drug infusion system; alternatively, the SCU may be programmed
and combined to operate with other electrical and drug stimulation
systems to provide therapy to a patient.
[0014] According to a preferred embodiment of the invention, the
electrodes used for electrical stimulation are arranged as an array
on a very thin implantable lead. Alternately, a lead may only
include one electrode, or the electrodes may be situated in a wide
array for field stimulation of a desired target. The SCU is program
to produce either monopolar electrical stimulation, e.g., using SCU
case as an indifferent electrode, or to produce bipolar electrical
stimulation, e.g., using one of the electrodes of an electrode
array as an indifferent electrode. The SCU includes a means of
stimulating (a) nerve(s) either intermittently or continuously.
Specific stimulation parameters may provide therapeutic advantages
for, e.g., various forms of epilepsy, movement disorders, and other
indications.
[0015] According to an embodiment of the invention, a method of
treating patients may include implanting at least one SCU in a
shallow recess of the mastoid area of the skull of a patient,
wherein the at least one SCU is capable of controlling the delivery
of at least one stimulus to at least one nerve affecting epilepsy,
movement disorders, or other indications. This method may also
include applying at least one stimulus to at least one nerve in
order to at least in part alleviate symptoms of epilepsy, movement
disorders, or other indications of the patient being treated. The
nerves stimulated according to this method ma include any of the
body, branches, and roots of at least one of the vagus nerves, the
trigeminal nerves, the ophthalmic nerves, the maxillary nerves, the
mandibular nerves, the facial nerves, the glossopharyngeal nerves,
and the trigeminal ganglion or ganglia.
[0016] According to an embodiment of the invention, a system for
treating a patient includes at least one lead with at least one
electrode, and at least one system control unit having a size and
shape suitable for implantation in a recess in the mastoid or other
area of the skull. The at least one SCU may include electronic
circuitry, programmable memory for receiving and storing prescribed
stimulation patterns, and a power source for providing power to the
electronic prescribed stimulation parameters and is operably
connected to at least one of the electrodes through which the
stimulation pulses may be delivered to tissue adjacent to at least
one of the electrodes.
[0017] Alternately, the SCU used with the present invention may
possess one or more of the following properties:
[0018] at least one electrode for applying stimulating current to
surrounding tissue;
[0019] electronic and/or mechanical components encapsulated in a
hermetic package made from biocompatible materials(s);
[0020] an electrical coil inside the package that receives power
and/or data by inductive or radio-frequency (RF) coupling to a
transmitting coil placed outside the body in a BTE unit, avoiding
the need for electrical leads to connect devices to a central
implanted or external controller;
[0021] means for receiving and/or transmitting signals via
telemetry;
[0022] means for receiving and/or storing electrical power within
the SCU; and
[0023] a form factor making the SCU implantable in a depression or
opening cut in the mastoid area of the skull.
[0024] The power source of the SCU is preferably realized using one
or more of the following options:
[0025] (1) an external BTE power source coupled to the SCU via an
RF link;
[0026] (2) a self-contained power source made using any means of
generation or storage of energy, e.g., a primary battery, a
replenishable or rechargeable battery, a capacitor, a
supercapacitor; and/or
[0027] (3) if the self-contained power source is replenishable or
rechargeable, a means of replenishing or recharging the power
source, e.g., an RF link, an optical link, or other energy-coupling
link.
[0028] According to one embodiment of the invention, an SCU
operates independently. According to another embodiment of the
invention, an SCU operates in a coordinated manner with other
implanted SCUs, other implanted devices, or with devices external
to the patient's body.
[0029] According to yet another embodiment of the invention, an SCU
incorporates means of sensing epilepsy, movement disorders, and
other indications or symptoms thereof, or other measures of the
state of the patient. Sensed information is preferably used to
control the electrical stimulation parameters of the SCU in a
closed-loop manner. According to one embodiment of the invention
the sensing and stimulating means are incorporated into a single
SCU. According to another embodiment of the invention, the sensing
means communicates sensed information to at least one SCU with
stimulating means.
[0030] Thus, the present invention provides systems and methods for
the treatment of epilepsy, movement disorders, and other
indications using at least one SCU. The present invention's
advantages include, inter alia: monitoring and programming
capabilities; power source, storage, and transfer mechanisms;
device activation by the patient or clinician; open- and
closed-loop capabilities coupled with sensing a need for and/or
response to treatment; simple explanation because the IPG is
implanted in the mastoid bone and all leads are directly attached
to the IPG; and coordinated use of one or more SCUs.
BRIEF DESCRIPTION OF DRAWINGS
[0031] The above and other aspects of the present invention will be
more apparent from the following more particular description
thereof, presented in conjunction with the following drawings
wherein:
[0032] FIG. 1A depicts various nerve branches dorsal to the
trigeminal nerve and nearby bony structures;
[0033] FIG. 1B illustrates the trigeminal nerve, and nerve branches
dorsal and proximal to the trigeminal nerve;
[0034] FIG. 1C illustrates various autonomic nerves in the
head;
[0035] FIG. 1D depicts various nerves, muscles, arteries, and veins
in the neck;
[0036] FIG. 1E is a cross-section through the neck, at the level of
cervical vertebra C7;
[0037] FIG. 1F illustrates various autonomic nerves in the head,
neck, and thorax;
[0038] FIG. 2 illustrates a lateral view of the skull;
[0039] FIG. 3 illustrates internal and external components of an
embodiment of the invention.
[0040] FIG. 4 illustrates external components of an embodiment of
the invention; and
[0041] FIG. 5 illustrates a Behind-the-Ear (BTE) unit for use with
an embodiment of the invention.
[0042] Corresponding reference characters indicate corresponding
components throughout the several views of the drawings.
MODE(S) FOR CARRYING OUT THE INVENTION
[0043] The following description is of the best mode presently
contemplated for carrying out the invention. This description is
not to be taken in a limiting sense, but is made merely for the
purpose of describing the general principles of the invention. The
scope of the invention should be determined with reference to the
claims.
[0044] Discussed herein are ways to effectively use implantable,
chronic neurostimulators for treating, controlling, and/or
preventing certain indications including; epilepsy, mood disorders
(including depression and bipolar disorders), anxiety disorders
(including generalized anxiety disorder and obsessive-compulsive
disorder), chronic pain (including visceral pain, neuropathic pain
and nociceptive pain), hypertension, cardiac disorders (including
tachycardia, bradycardia, other arrhythmias, congestive heart
failure, and angina pectoris), psychotic disorders (including
schizophrenia), cognitive disorders, dementia (including
Alzheimer's disease, Pick's disease, and multi-infarct dementia),
sleep disorders (including insomnia, hypersomnia, narcolepsy, and
sleep apnea), movement disorders (including Parkinson's disease and
essential tremor), and/or headache (including migraine and chronic
daily headache). The phrases "epilepsy, movement disorders, and
other indications" and "epilepsy, movement disorders, or other
indications" as used within each section of this document shall be
construed to include the indications listed in the sentence
directly preceding this sentence. The symptoms of epilepsy,
movement disorders, and other indications may be relieved with
stimulation applied to the following nerve(s): the vagus nerve, a
branch(es) of the vagus nerve, the trigeminal ganglion or ganglia,
the trigeminal nerve(s), a branch(es) of the trigeminal nerve(s)
(e.g., the ophthalmic nerve(s), the maxillary nerve(s), and/or the
mandibular nerve(s) and their branches), the facial nerve(s), the
glossopharyngeal nerve(s), or a branch(es) of any of these neural
structures.
[0045] Some neurostimulators used to treat epilepsy, movement
disorders, and other indications have limited battery supply and
are difficult to explain due to their relatively small size. Yet,
some patients treated for epilepsy, movement disorders, and other
indications require continuous stimulation at a frequency of at
least 100 Hz. Such a high frequency of stimulation may quickly
deplete the battery supplies of some neurostimulators and thus
require frequent recharging and consequent explanation of the
neurostimulators within a relatively short period of time, i.e.,
about three years.
[0046] Recent studies in both developed and developing countries
have shown that up to 70% of newly diagnosed children and adults
with epilepsy can be successfully treated (i.e., complete control
for seizures for several years) with anti-epileptic drugs. After
two to five years of successful treatment, drugs can be withdrawn
in about 70% of children and 60% for adults without the patient
experiencing relapses. However, up to 30% of patients are
refractory to medication. There is evidence that the longer the
history of epilepsy, the harder it is to control. The presence of
an underlying brain disease typically results in a worse prognosis
in terms of seizure control. Additionally, partial seizures,
especially if associated with brain disease, are more difficult to
control than generalized seizures.
[0047] Patients suffering from epilepsy may undergo surgery to
remove a part of the brain in which the seizures are believed to
arise, i.e., the seizure focus. However, in many patients a seizure
focus cannot be identified, and in others the focus is in an area
that cannot be removed without significant detrimental impact on
the patient. For example, in temporal lobe epilepsy, patients may
have a seizure focus in the hippocampi laterally. However, both
hippocampi cannot be removed without devastating impacts on
long-term memory. Other patients may have a seizure focus that lies
adjacent to a critical area such as the speech center.
[0048] Vagus nerve stimulation (VNS) has been applied with partial
success in patients with refractory epilepsy. In this procedure, an
implantable pulse generator (IPG) is implanted in the patient's
thorax, and an electrode lead is routed from the IPG, over the
clavicle, to the left vagus nerve in the neck. Helix-shaped
stimulation and indifferent electrodes are attached to the vagus
nerve.
[0049] The exact mechanism of action of VNS is unknown. The nucleus
of tractus solitarius (NTS; a.k.a., nucleus of the solitary
tract)is a primary site at which vagal afferents terminate. Because
afferent vagal nerve stimulation has been demonstrated to have
anticonvulsant effects, it is likely that changes in synaptic
transmission in the NTS can regulate seizure susceptibility. To
demonstrate this, Walker, et al. ("Regulation of limbic motor
seizures by GABA and glutamate transmission in nucleus tractus
soliarius," Epilepsia, 1999 August) applied muscimol, an antagonist
of the inhibitory neurotransmitter GABA, to the NTS in a murine
model of epilepsy. Muscimol applied to the NTS attenuated seizures
in all seizure models tested, whereas muscimol applied to adjacent
regions of NTS had no effect. Additionally, bicuculline methiodide,
a GABA antagonist, injected into the NTS did not alter seizure
responses. Finally, anticonvulsant effects were also obtained with
application of lidocaine, a local anesthetic, into the NTS.
Unilateral injections were sufficient to afford seizure protection.
Walker, et al. concludes that inhibition of the NTS outputs
enhances seizure resistance in the forebrain and provides a
potential mechanism foe the seizure protection obtained with vagal
stimulation.
[0050] The NTS sends fibers bilaterally to the reticular formation
and hypothalamus, which are important in the reflex control of
cardiovascular, respiratory, and gastrointestinal functions. The
NTS also provides input to the dorsal motor nucleus of the vagus,
which enables the parasympathetic fibers of the vagus nerve to
control these reflex responses. The NTS runs the entire length of
the medulla oblongata, and the NTS (as well as the trigeminal
nucleus) receives somatic sensory input from all cranial nerves,
with much of its input coming from the vagus nerve.
[0051] Convincing evidence has been given that a significant number
of neurons in the trigeminal nerve project to the NTS. By applying
horseradish peroxidase to peripheral branches of the trigeminal
nerve in the cat, it was found that branches of the trigeminal
nerve (the lingual and pterygopalatine nerves) were found to
contain fibers which ended ipsilaterally in the rostral portions of
the NTS, massively in the medial and ventrolateral NTS, moderately
in the intermediate and interstitial NTS, and sparsely in the
ventral NTS. (The rostral-most part of the NTS was free from
labeled terminals.) After injecting the enzyme into the NTS
portions rostral to the area postrema, small neurons were scattered
in the maxillary and mandibular divisions of the trigeminal
ganglion. It was concluded that trigeminal primary afferent neurons
project directly to the NTS. By staining for substance P
immonoreactivity, it was found that Substance P-containing
trigeminal sensory neurons project to the NTS.
[0052] There is also convincing evidence that a significant number
of neurons in the trigeminal nucleus project to the NTS as well. In
one study, retrograde transport of a protein-gold complex was used
to examine the distribution of spinal cord and trigeminal nucleus
caudalis neurons that project to the NTS in the rat. The authors
found that retrogradely labeled cells were numerous in the
superficial laminae of the trigeminal nucleus caudalis, through its
rostrocaudal extent. Since the NTS is an important relay for
visceral afferents from both the glossopharyngeal and vagus nerves,
it is suggested that the spinal and trigeminal neurons that project
to the NTS may be part of a larger system that integrates somatic
and visceral afferent inputs from wide areas of the body. The
projections may underlie somatovisceral and/or viscerovisceral
reflexes, perhaps with a significant afferent nociceptive
component.
[0053] Another study utilized microinfusion and retrograde
transport of D-[3H]-aspartate to identify excitatory afferents to
the NTS. The authors found that the heaviest labeling was localized
bilaterally in the trigeminal nucleus with cells extending through
its subdivisions and the entire rostrocaudal axis.
[0054] In addition, a study by Fanselow, et. al. ("Reduction of
pentylenetetrazole-induced seizure activity in awake rats by
seizure-triggered trigeminal nerve stimulation," Journal of
Neuroscience, 2000 November) demonstrated that unilateral
stimulation via a chronically implanted nerve cuff electrode
applied to the infraorbital branch of the trigeminal nerve led to a
reduction in electrographic seizure activity of up to 78%. The
authors reported that bilateral trigeminal stimulation was even
more effective.
[0055] FIGS. 1A and 1B depict the trigeminal nerve and its
branches. The trigeminal nerve 106 on each side of the head arises
from a trigeminal ganglion 102, which lies within the skull in an
area known as Meckel's cave 126. In accordance with the teachings
of the present invention, access to a trigeminal ganglion 102 may
be gained via the foramen ovale 144 or the foramen rotundum 114 in
order to implant a lead with a least one electrode adjacent to one
or both of the trigeminal ganglia 102. A lead may travel other
paths to access the trigeminal ganglion 102 from an IPG implanted
in or near the mastoid area of the skull; these other paths will be
known to those of skill in the art.
[0056] Procedures that ablate the trigeminal ganglia 102 do not
disable the muscles of mastication, since the cell bodies of the
sensory portion of the nerve are within the trigeminal ganglion,
whereas the motor portion simply projects axons through the ganglia
(the motor neuron cell bodies are in the pons). This may provide a
mechanism for selective stimulation of the sensory cells via
appropriate placement of at least one electrode of a lead for
stimulation of one or both trigeminal ganglia 102.
[0057] The lead of aneruostimulator may additionally or
alternatively be implanted adjacent to the trigeminal nerve 106 or
an of its branches distal to one or both trigemninal ganglia 102,
such as the ophthalmic nerve 118, the maxillary nerve 122, the
mandibular nerve 146, and/or branch(es) of any of these. The
ophthalmic nerve 118 and the maxillary nerve 122 are entirely
sensory, and sufficiently separate to allow independent and
selective stimulation via appropriate placement at least one
electrodes.
[0058] The mandibular nerve 146 is both sensory and motor. The
mandibular nerve 146 innervates several facial muscles, including
the muscles of mastication and the tensor tympani, which
reflexively damps down the vibrations of the malleus by making the
tympanic membrane more tense. However, just distal to the foramen
ovale 144, the madibular nerve 146 splits into a purely sensory
branch that innervates the superior part of the lower jaw. And
slightly more distally, another branch splits into a purely sensory
branch that innervates the inferior part of the lower jaw. These
branches may be sufficiently separate to allow independent and
selective stimulation via appropriate placement of at least one
electrode.
[0059] Epilepsy may also be relieved with stimulation additionally
or alternatively applied to the facial nerve(s) 136,
glossopharyngeal nerve(s) 138, and/or branches of any of these (see
FIG. 1C).
[0060] In accordance with the teachings of the present invention,
electrical stimulation at one or more of the above-mentioned and/or
other trigeminal nerve branches is provided to relieve epilepsy. At
least one lead with at least one electrode may be implanted
adjacent to one or more of the above-identified nerves or nerve
structures.
[0061] As mentioned above, vagus nerve stimulation (VNS) has
demonstrated limited efficacy in the treatment of patients with
medically refractory epilepsy. As stated, the mechanism of action
of VNS has not been confirmed, but a number researchers believe
that VNS may exert its seizure reduction effects through afferent
stimulation of the nucleus of tractus solitarius (NTS).
[0062] As detailed above, studies have shown that the trigeminal
nerve also contributes a significant number of afferent fibers to
the NTS. Additionally, trigeminal nerve afferents synapse on the
trigeminal nucleus in the brainstem, and afferents from the
trigeminal nucleus also project to the NTS. Thus, electrical
stimulation of, for example, a trigeminal ganglion, trigeminal
nerve, or branch(es) of the trigeminal nerve may reasonably be
expected to demonstrate efficacy in the treatment of patients with
medically refractory epilepsy.
[0063] The trigeminal nerve provides sensory innervation to the
face, so stimulation may produce a tingling sensation. However,
this feeling has not been reported to be unpleasant in patients
undergoing sensory nerve stimulation, and in time, patients grow
accustomed to the sensation. The trigeminal nerve also innervates
the muscles of mastication, so excessive stimulation of these
branches may cause fatigue or even spasm of the mandible (i.e.,
lockjaw). Stimulation of branches that are distal to the motor
fibers of the trigeminal nerve should allow these potential motor
side effects to be avoided altogether.
[0064] As previously mentioned, vagus nerve stimulation is
currently used as a therapy for refractory epilepsy, and studies
have suggested that such stimulation may also be an efficacious
therapy for tremor, depression, and other indications.
[0065] In 2001, Handforth, et al. studied whether vagus nerve
stimulation could suppress tremor in the harmaline tremor model in
the rat. [See Handforth, et al., "Suppression of harmaline-induced
tremor in rats by vagus nerve stimulation" Movement Disorders 2001
January; 16(1):84-8.] Animals were chronically implanted with
helical leads around the left vagus nerve and a disk-shaped
electrode was positioned subcutaneously in the dorsal neck.
Harmaline-induced tremor was recorded on a physiograph while each
animal received a sequence of five 20-minute trials. Each trial
consisted of five minutes of pre-stimulation baseline, five minutes
of vagus nerve stimulation, and ten minutes of post-stimulation.
Vagus nerve stimulation significantly suppressed harmaline-induced
tremor. The suppressive effect was present within the first minute
of stimulation and was reproducible across the five trials of the
study. The results of this study suggest that the central generator
or expression of tremor in the harmaline animal model can be
suppressed by vagus nerve stimulation. This further suggest that
vagus nerve stimulation may be an effective therapy for essential
tremor and perhaps for other movement disorders.
[0066] Patients suffering from tremor and other symptoms may
undergo surgery to lesion a part of the brain, which may afford
some relief. However, a lesion is irreversible, and it may lead to
side effects such as dysarthria or cognitive disturbances.
Additionally, lesions generally yield effects on only one side (the
contralateral side), and bilateral lesions are significantly more
likely to produce side effects. Other surgical procedures, such as
fetal tissue transplants, are costly and unproven.
[0067] FIG. 1D depicts nerves, muscles, arteries, and veins in the
neck, while FIG. 1E is a cross-section through the neck, at the
level or cervical vertebra C7. As can be seen, the vagus nerve 148
is relatively easily accessible in the neck. The vagus nerve lies
within the carotid sheath 104, along with the common carotid artery
108 and the internal jugular vein 112. The carotid sheath 104 lies
beneath the sternocleidomastoid muscle 116, which, in FIG. 1D, is
cut and turned up.
[0068] FIG. 1F illustrates various autonomic nerves in the head,
neck, and thorax. The vagus nerve 148 has a number of nerve
branches. Three of these branches are named the superior cervical
cardiac branch 120, the inferior cervical cardiac branch 124, and
the thoracic cardiac branch 128. Advantageously, these branches are
sufficiently separate from the vagus nerve 148 to allow independent
and selective stimulation of the vagus nerve 148 and/or its
branches via appropriate placement of at least one electrode.
[0069] In accordance with the teachings of the present invention
and as discussed in more detail presently, electrical stimulation
at one or more locations along the vagus nerve 148 and/or its
branches is provided to treat, control, and/or prevent epilepsy,
mood disorders (including depression and bipolar disorder), anxiety
disorders(including generalized anxiety disorder and
obsessive-compulsive disorder), chronic pain (including visceral
pain, neuropathic pain and nociceptive pain), hypertension, cardiac
disorders (including tachycardia, bradycardia, other arrhythmias,
congestive heart failure, and angina pectoris), psychotic disorders
(including schizophrenia), cognitive disorders, dementia (including
Alzheimer's disease, Pick's disease, and multi-infarct dementia),
sleep disorders (including insomnia, hypersomnia, narcolepsy, and
sleep apnea), movement disorders (including Parkinson's disease and
essential tremor), and/or headache (including migraine and chronic
daily headache). At least one lead including at least one electrode
may be implanted adjacent the vagus nerve via a relatively complex
surgical procedure known in the art.
[0070] Stimulation of the vagus nerve may occur distal to (i.e.,
below) the superior cervical cardiac branch 120, or distal to both
the superior cervical cardiac branch 120 and the inferior cervical
cardiac branch 124, and may, for instance, be applied to the left
vagus nerve. Stimulation of the left vagus nerve distal to the
superior cervical cardiac branch 120 and/or the inferior cervical
cardiac branch 124 does not pose the cardiac risks that can be
associated with vagus nerve stimulation applied proximal to one or
both of these nerve branches. Alternatively, some patients may
benefit from vagus nerve stimulation applied distal to the thoracic
cardiac branch 128.
[0071] As used herein, stimulation of the vagus nerve may include
stimulation of the vagus nerve and/or one or more of its branches.
For instance, to relieve sleep disorders (such as insomnia,
hypersomnia, narcolepsy, sleep apnea, and the like), the vagus
nerve may be stimulated. More specifically, one or more of the
pharyngeal branch of the vagus nerve 130, the superior laryngeal
branch of the vagus nerve 132, the pharyngeal plexus (not shown),
the left and/or right recurrent laryngeal branch of the vagus nerve
134, and/or other branches of the vagus nerve may be stimulated to
relieve sleep disorders.
[0072] As depicted in FIG. 2, system control unit (SCU) 110 may be
implanted beneath the scalp in a surgically-created shallow
depression or opening in the mastoid area 143 of the temporal bone
142 of the skull 140. Alternatively, SCU 110 may be placed on the
surface of bone or tissue without bone carving. SCU 110 includes at
least an implantable pulse generator (IPG) that is capable of
delivering electrical pulse through at least one lead to at least
one electrode in order to stimulate tissue. SCU 110 may
additionally include structure capable of discharging drugs through
at least one catheter to certain tissue. SCU 110 may additionally
include a closed loop system with circuitry capable of (1) sensing
a condition within the body through at least one lead with at least
one sensing electrode and (2) then responding to the sensed
condition by modifying stimulation or drug infusion parameters.
[0073] SCU 110 preferably conforms to the profile of surrounding
tissue(s) and/or bone(s), and is small and compact. This is
preferable so that no unnecessary pressure is applied to the skin
or scalp, as this may result in skin erosion or infection. SCU 110
preferably has a diameter of no greater that 75 mm, more preferably
no greater than 65 mm, and most preferably about 35-55 mm. SCU
thickness (e.g., depth into the skull) of approximately 10-12 mm is
preferred, while a thickness of about 8-10 mm or less is more
preferred.
[0074] The method of implanting the SCU 110 of the present
invention in the mastoid area 143 of the temporal bone 142 of the
skull 140 is superior to prior methods of implanting similar
devices in the skull for several reasons. First, the method of the
present invention contemplates implantation in the mastoid area 143
because the mastoid area 143 of the temporal bone is relatively
thicker than other areas of the skull 140. Second, the method of
the present invention of implanting SCU 110 in the mastoid area 143
contemplates implantation of the SCU 110 in a shallow recession or
depression cut into the mastoid area 143 rather that a hole cut
entirely through the skull 140. By not cutting a hole through the
skull, the method of the present invention maintains maximal
integrity of the skull 140 and thereby avoids possible injury and
infection that could otherwise accompany an exposure of the fragile
tissues of the brain or inner ear. The method of the present
invention need not cut a hole through the skull because, as will be
shown, lead(s) 150 travel to the trigeminal, vagus, and other
verves (see also FIG. 5) that are located outside the skull
(although the present invention may also include a lead or catheter
that stimulates, senses, or infuses drugs within the skull in
combination with the stimulation or treatment of other tissue
located outside the skull.) Thus, the present invention is an
improvement over prior systems and methods and gracefully avoids
unnecessary intracranial intrusion.
[0075] As previously mentioned, vagus nerve stimulation (VNS) has
been applied with partial success in patients with refractory
epilepsy by implanting an IPG in the patient's thorax and routing
an electrode lead from the IPG, over the clavicle, to the left
vagus nerve in the neck. Unfortunately, routing the lead from the
thorax to the neck may cause unwanted movement of the lead during
articulation of the joints of the neck. It is believed that
implantation of the IPG in the mastoid area of the skull and
routing a lead from the skull to the nerves of the neck will result
in less movement of the lead during articulation of the joints of
the neck. Further, the lead of the present invention will not have
to be routed over the clavicle, which routing may cause the lead to
be more prone to breaking and shorting out. Further, by routing the
lead of the present invention from the mastoid to the nerves in the
neck, the lead may be routed along the sternocleidomastoid muscle
which naturally travels form the lateral location of the mastoid
bone to the medial location of the sternum. The sternocleidomastoid
muscle may afford the lead added protection. Finally, implantation
of the IPG in the mastoid area of the skull rather than below the
clavicle provides optimal placement and ready access to the
trigeminal and other facial nerves and to the tissue of the brain,
as mentioned previously. The mastoid bone, or surrounding areas,
provides a more central location for orchestrated stimulating,
sensing, and drug infusing of various nerves an muscles of the head
and neck, than a location below the clavicle, such as the patient's
thorax. Thus, the present invention is an improvement over a system
employing an IPG implanted in the thorax.
[0076] One or more electrode lead(s) 150 attached to SCU 110 run
subcutaneously, preferably in a surgically-created (a) shallow
recess(es) or groove(s) in the mastoid area 143 or the skull 140,
to the nerves of FIGS. 1A-1F. Shallowly-recessed placement of the
SCU 110 and the lead(s) 150 has the advantages of decreased
likelihood of erosion of the overlying skin, and of minimal
cosmetic impact. The mastoid area 143 of the temporal bone 142 is a
particularly advantageous location to recess the SCU 110 and the
lead(s) 150 because the mastoid process is relatively thick in
relation to the rest of the bones of the skull.
[0077] At least one, and preferably one to four, electrode(s) 152
are carried on lead(s) 150 having a proximal end coupled to SCU
110. The lead contains wires electrically connecting electrodes 152
to SCU 110. SCU 110 contains electrical components 170 that produce
electrical stimulation pulses that travel through the wires of
lead(s) 150 and are delivered to electrodes 152, and thus to the
neural tissue that surrounds electrodes 152. To protect the
electrical components inside SCU 110, the case of the SCU 110 is
preferably hermatically sealed. For additional protection against,
e.g. impact, the case is preferably made of metal (e.g. titanium),
silastic, or ceramic, which materials are also, advantageously,
biocompatible. In addition, SCU 110 is preferably Magnetic
Resonance Imaging (MRI) compatible.
[0078] Lead(s) 150, and any other leads of the present invention,
may include tines, barbs, or other means of anchoring 151 (see FIG.
2) the electrode(s) on such leads in, or near, the following
nerve(s): the vagus nerve, a branch(es) of the vagus nerve, the
trigeminal ganglion or ganglia, the trigeminal nerve(s), a
branch(es) of the trigeminal nerve(s) (e.g., the ophthalmic
nerve(s), the maxillary nerve(s), and/or the mandibular nerve(s)),
the facial nerve(s), the glossopharyngeal nerve(s), or a branch(es)
of any of these neural structures. The lead(s) of the present
invention are tunneled under the skin to the implantable pulse
generator of the SCU 110 where it/they attach to the implantable
pulse generator via a connector. A suture sleeve or other fixation
device may be placed at any point along the lead(s) to hold it/them
in place.
[0079] In one embodiment of the present invention, the electrical
stimulation may be provided as described in U.S. Patent Application
Publication No. 2002/0161403 (the '403 application), filed under
the Patent Cooperation Treaty on Jan. 12, 2001 as International
Patent Application No. PCT/US01/04417 (which claims priority to
U.S. Provisional Patent Application Serial Number 60/182,486, filed
Feb. 15, 2000). As such, the electrical stimulation of the present
invention may be as provided in this application, which is directed
to "Deep Brain Stimulation System for the Treatment of Parkinson's
Disease or Other Disorders".
[0080] The present invention may include one or more SCUs to
deliver electrical stimulation and/or drug infusion to a patient.
These SCUs may include an SCU with an IPG, i.e., as illustrated in
FIG. 2; a microstimulator SCU, such as a BION.RTM. microstimulator
of Advanced Bionics Corporation (Valencia, Calif.); or an SCU with
an implantable drug infusion pump. When needed, an SCU provides
both electrical stimulation and one or more stimulating drugs. Each
of these SCUs may work in communication with each other to provide
therapy to a patient at or near the following nerve(s): the vagus
nerve, a branch(es) of the vagus nerve, the trigeminal ganglion or
ganglia, the trigeminal nerve(s), a branch(es) or the trigeminal
nerve(s) (e.g., the ophthalmic nerve(s), the maxillary nerve(s),
and/or the mandibular nerve(s)), the facial nerve(s) the
glossopharyngeal nerve(s), or a branch(es) of any of these neural
structures.
[0081] Any one SCU may contain multiple stimulating leads, sensory
leads, ad/or catheters in order to simultaneously, and/or in
concert, stimulate multiple nerves sense conditions at multiple
locates, and/or infuse drugs at to multiple tissue sites. For
example, a single SCU may contain two stimulating leads that split
to stimulate the trigeminal nerve bilaterally.
[0082] SCU 110 preferably contains electronic circuitry 170 for
receiving data and/or power from outside the body by inductive,
radio-frequency (RF), or other electromagnetic coupling. In a
preferred embodiment, electronic circuitry 170 includes an
inductive coil for receiving and transmitting RF data and/or power,
an integrated circuit (IC) chip for decoding and storing
stimulation parameters and generating stimulation pulses (either
intermittent or continuous), and additional discrete electronic
components required to complete the electronic circuit functions,
e.g. capacitor(s), resistor(s), coil(s), and the like.
[0083] SCU 110 also advantageously includes programmable memory 175
for storing a set(s) of data, stimulation, and control parameters.
This feature allows electrical stimulation to be adjusted to
settings that are safe and efficacious with minimal discomfort for
each individual. Specific parameters may provide therapeutic
advantages for various levels and types of epilepsy, movement
disorders, and other indications previously defined in this
document. For instance, some patients may respond favorably to
intermittent stimulation, while others may require continuous
treatment for relief Electrical stimulation parameters are
preferably controlled independently. However, in some instances,
they are advantageously coupled with the operations of other SCUs,
e.g., electrical stimulation of SCU 110 may be programmed to occur
only during drug infusion of another SCU.
[0084] In addition, parameters may be chosen to target specific
neural populations and to exclude others, or to increase neural
activity in specific neural populations and to decrease neural
activity in others. For example, excitatory neurostimulation of
relatively low frequency (e.g., less than about 50-100 Hz)
typically results in activation of surrounding neural tissue and
increased neural activity ("excitatory stimulation"), whereas
inhibitory stimulation of relatively high frequency (e.g., greater
than about 50-100 Hz) typically results in decreased neural
activity ("inhibitory stimulation").
[0085] The preferred SCU 110 also includes a power source and/or
power storage device 180. Possible power options for a stimulation
device of the present invention, described in more detail below,
include but are not limited to an external power source in a
Behind-the-Ear (BTE) unit coupled to the stimulation device, e.g.,
via: an RF link; a self-contained power source utilizing any means
of generation or storage of energy (e.g., a primary battery, a
rechargeable battery such as a lithium ion battery, an electrolytic
capacitor, or a super- or ultra-capacitor); and, if the
self-contained power source is replenishable or rechargeable, means
of replenishing or recharging the power source (e.g., an RF
link).
[0086] In one embodiment of the present invention shown in FIG. 3,
SCU 110 includes a rechargeable battery as a power source/storage
device 180. The battery is recharged, as required, from an external
battery charging system (EBCS) 182, typically through an inductive
link 184. In this embodiment, and as explained more fully in the
earlier referenced '403 application, SCU 110 includes a processor
and other electronic circuitry 170 that allow it to generate
stimulation pulses that are applied to the patient through
electrodes 152 in accordance with a program and stimulation
parameters stored in programmable memory 175.
[0087] According to an embodiment of the present invention, such as
described in the previously referenced '403 application and as
depicted in FIG. 3, at least one lead 150 is attached to SCU 110,
via a suitable connector 154. Each lead includes at least one
electrode(s) 152, preferably one to four electrode(s), and may
include as many as sixteen or more electrodes 152. Additional leads
150' may be attached to SCU 110. Hence, FIG. 3 shows (in phantom
lines) a second lead 150' having electrodes 152' thereon, also
attached to SCU 110.
[0088] Lead(s) 150 are preferably less than 5 mm in diameter, and
more preferably less than 1.5 mm in diameter. Electrodes 152, 152'
are preferably arranged as an array, for example, at least two
collinear electrodes or at least 4 collinear electrodes. SCU 110 is
preferably programmable to produce either monopolar electrical
stimulation, e.g., using the SCU case as an indifferent electrode,
or bipolar electrical stimulation, e.g., using one of the
electrodes of the electrode array as an indifferent electrode. An
SCU 110 may have at least four channels and drives up to sixteen
electrodes or more.
[0089] According to one embodiment of the invention, an SCU
operates independently. According to another embodiment of the
invention, an SCU operates in a coordinated manner with other
SCU(s), other implanted device(s), or other device(s) external to
the patient's body. For instance, an SCU may control or operate
under the control of another implanted SCU(s), other implanted
device(s), or other device(s) external to the patient's body. An
SCU may communicate with other implanted SCUs (as mentioned
earlier), other implanted devices, and/or devices external to a
patients body via, e.g., an RF link, an ultrasonic link, or an
optical link. Specifically, an SCU may communicate with an external
remote control (e.g., patient and/or physician programmer) that is
capable of sending commands and/or data to an SCU and that is
preferably capable of receiving commands and/or data from an
SCU.
[0090] For example, SCU 110 of the present invention may be
activated and deactivated, programmed and tested through a hand
held programmer (HHP) 190 (which may also be referred to as a
patient programmer and is preferably, but not necessarily, hand
held), a clinician programming system (CPS) 192 (which may also be
hand held), or a manufacturing and diagnostic system (MDS) 194
(which may also be hand held). HHP 190 may be coupled to SCU 110
via an RF link 185. Similarly, MDS 194 may be coupled to SCU 110
via another RF link 186. In a like manner, CPS 192 may be coupled
to HHP 190 via an infra-red link 188. Other types of
telecommunicative links, other than RF or infra-red may also be
used for this purpose. Through these links, CPS 192, for example,
nay be coupled through HHP 190 to SCU 110 for programming or
diagnostic purposes. MDS 194 may also be coupled to SCU 110, either
directly through RF link 186, or indirectly through the IR link
188, HHP 190, and RF link 185.
[0091] In another embodiment as illustrated in FIG. 4, the patient
200 switches SCU 110 on and off by use of controller 210, which is
preferably hand held. Controller 210 operates to control SCU 110 by
any of various means, including sensing the proximity of a
permanent magnet located in controller 210, or sensing RF
transmissions from controller 210.
[0092] External components for one preferred embodiment related to
programming and providing power to SCU 100 are also illustrated in
FIG. 4. When it is required to communicate with SCU 100, patient
200 is positioned on or near external appliance 220, which
appliance contains one or more inductive coils 222 or other means
of communication (e.g., RF transmitter and receiver). External
appliance 220 is connected to or is a part of external electronic
circuitry appliance 230 which receives power 232 form a
conventional power source. External appliance 230 contains manual
input means 238, e.g., a keypad, whereby the patient 200 or a
caregiver 242 may request changes in the parameters of the
electrical and/or drug stimulation produced during the normal
operation of SCU 110. In this preferred embodiment, manual input
means 238 includes various electro-mechanical switches and visual
display devices that provide the patient and/or care giver with
information about the status and prior programming of SCU 110.
[0093] Alternatively or additionally, external electronic appliance
230 is provided with an electronic interface means 246 for
interacting with other computing means 248, such as by a serial
interface cable or infrared link to a personal computer or to a
telephone modem. Such interface means 246 thus permits a clinician
to monitor the status of the implant and prescribe new stimulation
parameters from a remote location.
[0094] The external appliance(s) may advantageously be embedded in
a cushion, pillow, hat, or the like. Other possibilities exist,
including a head band, patch, or other structure(s) that may be
affixed to the patient's body or clothing. External appliances may
include a package that can be, e.g., worn on the belt, may include
an extension to a transmission coil affixed, e.g., with a
Velcro.RTM. band or an adhesive, or may be combinations of these or
other structures able to perform the functions described
herein.
[0095] FIG. 5 shows, for example, a Behind-the-Ear (BTE) unit 100
behind the ear of the patient 200. The BTE unit 100 may be attached
13 to an earhook 8 that secures the BTE unit 100 around the auricle
of the ear. Additionally, the BTE unit 100 may include a magnet
and/or metal plate 25 that is attracted to a corresponding magnet
and/or metal plate in the SCU 110. This magnet and/or metal plate
helps secure the external BTE unit to the internal SCU 100 so that
the two devices maintain communication.
[0096] The BTE unit 100 is a preferred example of an external
appliance 220 that includes electronic circuitry, a power source,
and at least one RF coil, or other means of communicating with the
SCU 110 as previously described. Purposes of the BTE unit 100 may
include: providing power to the SCU 110; controlling, modifying, or
monitoring the activities and/or parameters of the SCU 110; and/or
providing a communications transfer to another external appliance,
such as external appliance 230.
[0097] In the case where the SCU 110 is located in an area of the
mastoid bond 143 such that communication between the SCU 110 and
the BTE unit 100 is not practical or possible, the BTE unit 100 may
alternately be in communication with a head piece that magnetically
attracts to the SCU 110. The head piece includes all the components
necessary to communicate with the SCU 110 in a manner that is
either independent of or supported by the BTE unit 100. For
example, the head piece includes at least an RF coil, or other
means of communication, and related circuitry necessary to put the
head piece in communication with the SCU 110.
[0098] In order to help determine the strength and/or duration of
electrical stimulation required to produce the desired effect, in
one preferred embodiment, a patient's response to and/or need for
treatment is sensed. For example, the present invention may include
an SCU that senses and measures the electrical activity of a neural
population (e.g., EEG) or other relevant activities and substances
that will be evident to those of skill in the art upon review of
the present disclosure. The sensed and measured information is
preferably used to control the stimulation parameters of the SCU(s)
in a closed-loop manner.
[0099] While an SCU 110 may also incorporate means of sensing
activity and/or substances, it may alternatively or additionally be
desirable to use a separate or specialized implantable device to
record and telemeter physiological conditions/responses in order to
adjust electrical stimulation parameters. This information may be
transmitted to an external device, such as external appliance 220,
or may be transmitted directly to implanted SCU(s) 110. However, in
some cases, it may not be necessary or desired to include a sensing
function or device, in which case stimulation parameters are
determined and refined, for instance, by patient feedback.
[0100] Thus, it seen that in accordance with the present invention,
one or more external appliances are preferably provided to interact
with SCU 110 to accomplish one or more of the following
functions:
[0101] Function 1: If necessary, transmit electrical power from the
external electronic appliance 230 via appliance 220 to SCU 110 in
order to power the device and/or recharge the power source/storage
device 180. External electronic appliance 230 may include an
automatic algorithm that adjusts electrical stimulation parameters
automatically whenever the SCU(s) 110 is/are recharged.
[0102] Function 2: Transmit data from the external appliance 230
via the external appliance 220 to SCU 110 in order to change the
parameters of electrical and/or drug stimulation produced by SCU
110.
[0103] Function 3: Transmit sensed data indicating a need for
treatment or in response to stimulation from SCU 110 (e.g.,
impedance, electrical activity of a neural population (e.g., EEG),
or other activity or substances) to external appliance 230 via
external appliance 220.
[0104] Function 4: Transmit data indicating state of the SCU 110
(e.g., battery level, drug level, electrical stimulation and/or
infusion settings, etc.) to external appliance 230 via external
appliance 220.
[0105] By way of example, a treatment modality for epilepsy,
movement disorders, or other indications previously defined in this
document is carried out according to the following sequence of
procedures: [0106] 1. An SCU 110 is implanted so that its
electrodes 152 are located adjacent to at least one of the
following nerve(s): vagus nerve, a branch(es) of the vagus nerve,
the trigeminal ganglion or ganglia, the trigeminal nerve(s), a
branch(es) of the trigeminal nerve(s) (e.g., the ophthalmic
nerve(s), the maxillary nerve(s), and/or the mandibular nerve(s)),
the facial nerve(s), the glossorpharyngeal nerve(s), or a
branch(es) of any of these neural structures. If necessary or
desired, electrodes 152' may additionally or alternatively be
located in or near these or other adjacent nerves. [0107] 2. Using
Function 2 described above (i.e., transmitting data) of external
electronic appliance 230 and external appliance 220, SCU 110 is
commanded to produce a series of excitatory electrical stimulation
pulses, possibly with gradually increasing amplitude. [0108] 3. Set
stimulator on/off period to an appropriate setting, e.g.,
continuously on. [0109] 4. After each stimulation pulse, or at some
other predefined interval, any change in electrical or other
activity of a neural population (e.g., EEG) resulting from the
electrical stimulation is sensed, preferably by one or more
electrodes 152 and/or 152'. These responses are converted to data
and telemetered out to external electronic appliance 230 via
Function 3. [0110] 5. From the response data received at external
appliance 230 from SCU 100, the stimulus threshold for obtaining a
response is determined and is used by a clinician 242 acting
directly 238 or by other computing means 248 to transmit the
desired electrical parameters to SCU 110 in accordance with
Function 2. Alternatively, external appliance 230 makes the proper
adjustments automatically, and transmits the proper stimulation
parameters to SCU 100. In yet another alternative, SCU 110 adjusts
stimulation parameters automatically based on the sensed response.
[0111] 6. When patient 200 desires to invoke electrical
stimulation, patient 200 employs controller 210 to set SCU 110 in a
state where it delivers a clinician 242 prescribe stimulation
pattern from a predetermined range of allowable stimulation
patterns. [0112] 7. To cease electrical stimulation, patient 200
employs controller 210 to turnoff SCU 110. [0113] 8. Periodically,
the patient or caregiver recharges the power source/storage device
180 of SCU 110, if necessary, in accordance with Function 1
described above (i.e., transmit electrical power).
[0114] For the treatment of any of the various types and levels of
epilepsy, movement disorders, and other indications previously
defined in this document, it may be desirable to modify or adjust
the algorithmic functions performed by the implanted and/or
external components, as well as the surgical approaches, in ways
that would be obvious and/or advantageous to skilled practitioners
of these arts. For example, it may be desirable to employ more than
one SCU 110, each of which could be separately controlled by means
of a digital address. Multiple channels and/or multiple patterns of
electrical and/or drug stimulation might thereby be programmed by
the clinician and controlled by the patient in order to deal with
complex or multiple symptoms or dysfunctions, such as severe or
complex cases of epilepsy, movement disorders, or other indications
previously defined in this document.
[0115] In one embodiment, SCU 110, or a group of two or more SCUs,
is controlled via closed-loop operation. A need for and/or response
to stimulation is sensed via SCU 110, or by an additional SCU
(which may or may not be dedicated to the sensing function), or by
another implanted or external device. If necessary, the sensed
information is transmitted to SCU 110. Preferably, the parameters
used by SCU 110 are automatically adjusted based on the sensed
information. Thus, the electrical and/or drug stimulation
parameters are adjusted in a closed-loop manner to provide
stimulation tailored to the need for and/or response to the
electrical and/or drug stimulation.
[0116] In another embodiment, sensing means described earlier may
be used to orchestrate first the activation of SCU(s) targeting one
or more of the nerves disclosed herein, and then, when appropriate,
the SCU(s) targeting another area and/or by a different means.
Alternatively, this orchestration may be programmed and not based
on a sensed condition.
[0117] Thus, the present invention provides systems and methods for
the treatment, control, and/or prevention of epilepsy, movement
disorders, and other indications previously defined in this
document using at least on SCU. The present invention's advantages
include inter alia: monitoring and programming capabilities; power
source, storage, and transfer mechanisms; device activation by the
patient or clinician; open- and closed-loop capabilities coupled
with sensing a need for and/or response to treatment; simple
explanation because the IPG is implanted in the mastoid bone and
all leads are directly attached to the IPG; and coordinated use of
one or more SCUs.
[0118] While the invention herein disclose has been described by
means of specific embodiments and applications thereof, numerous
modifications and variations could be made thereto by those skilled
in the art without departing from the scope of the invention set
forth in the claims.
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