U.S. patent application number 11/168752 was filed with the patent office on 2006-02-23 for system and method of treating stuttering by neuromodulation.
This patent application is currently assigned to Medtronic, Inc.. Invention is credited to Paul H. Stypulkowski.
Application Number | 20060041242 11/168752 |
Document ID | / |
Family ID | 21697666 |
Filed Date | 2006-02-23 |
United States Patent
Application |
20060041242 |
Kind Code |
A1 |
Stypulkowski; Paul H. |
February 23, 2006 |
System and method of treating stuttering by neuromodulation
Abstract
Stuttering-treatment techniques using neural stimulation and/or
drug delivery. One or more electrodes and/or a catheter are
implanted adjacent to sites in the brain. A signal generator and
the electrode deliver stimulation to a first site. A pump and the
catheter deliver one or more therapeutic drugs to a second site.
The first and second sites could be: the supplementary motor area,
the centromedian circuit, the dorsomedial nuclei, the lateral
prefrontal circuit, or other paramedian thalamic and midbrain
nuclei. The stuttering treatment could be performed via periodic
transcranial magnetic stimulation. A sensor, located near the
patient's vocal folds, can be used for generating a signal
responsive to activity of the patient's speech-producing muscles. A
controller adjusts one or more stimulation parameters in response
to the signal from the sensor.
Inventors: |
Stypulkowski; Paul H.;
(North Oaks, MN) |
Correspondence
Address: |
MEDTRONIC, INC.
710 MEDTRONIC PARK
MINNEAPOLIS
MN
55432-9924
US
|
Assignee: |
Medtronic, Inc.
Minneapolis
MN
|
Family ID: |
21697666 |
Appl. No.: |
11/168752 |
Filed: |
June 27, 2005 |
Related U.S. Patent Documents
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Application
Number |
Filing Date |
Patent Number |
|
|
10001751 |
Oct 31, 2001 |
6944497 |
|
|
11168752 |
Jun 27, 2005 |
|
|
|
Current U.S.
Class: |
604/503 ; 600/23;
604/67; 607/3 |
Current CPC
Class: |
A61M 2210/0693 20130101;
A61M 5/14276 20130101; A61N 1/32 20130101; A61F 5/58 20130101; A61M
5/1723 20130101 |
Class at
Publication: |
604/503 ;
604/067; 600/023; 607/003 |
International
Class: |
A61M 31/00 20060101
A61M031/00; A61N 1/32 20060101 A61N001/32; A61F 5/58 20060101
A61F005/58 |
Claims
1. A method of therapeutically treating stuttering via an
implantable pump and a catheter having a proximal end coupled to
the pump and a discharge portion for infusing therapeutic dosages
of a least one drug, the method comprising: implanting the catheter
so that the discharge portion lies adjacent to a predetermined site
in the brain; and operating the pump to discharge at least one drug
capable of stimulating neurons in to the predetermined site in the
brain by delivering at least one drug.
2. The method of claim 1 further comprising sensing activity of the
patient's speech-producing muscles and generating a signal
indicative of activity of the patient's speech-producing muscles;
the step of operating the pump to discharge at least one drug
capable of stimulating neurons in to the predetermined site in the
brain by delivering at least one drug including regulating a drug
dosage in response to the signal indicative of activity of the
patient's speech-producing muscles to reduce activity,
corresponding to stuttering, of the patient's speech-producing
muscles.
3. The method of claim 2 wherein the step of sensing activity of
the patient's speech-producing muscles and generating a signal
indicative of activity of the patient's speech-producing muscles
includes: electromyographically sensing activity of the patient's
speech-producing muscles.
4. The method of claim 2 wherein the step of sensing activity of
the patient's speech-producing muscles and generating a signal
indicative of activity of the patient's speech-producing muscles
includes: electroglottographically sensing activity of the
patient's speech-producing muscles.
5. The method of claim 1 further comprising sensing EEG activity in
the patient's brain and generating a signal indicative of EEG
activity in the patients brain; the step of operating the pump to
discharge at least one drug capable of stimulating neurons in to
the predetermined site in the brain by delivering at least one drug
including regulating drug dosage in response to the signal
indicative of EEG activity in the patients brain to reduce
activity, corresponding to stuttering, of the patient's
speech-producing muscles.
6. The method of claim 1 wherein the step of operating the pump to
discharge at least one drug capable of stimulating neurons in to
the predetermined site in the brain by delivering at least one drug
includes: discharging the at least one drug to the predetermined
site at a first rate at times when the patient is expected to be
awake; and discharging the at least one drug to the predetermined
site at a second rate when the patient is expected to be asleep,
the second rate being reduced relative to the first rate.
7. The method of claim 1 wherein the step of operating the pump to
discharge at least one drug capable of stimulating neurons in to
the predetermined site in the brain by delivering at least one drug
includes substantially continuously delivering the at least one
drug.
8. The method of claim 1, wherein the predetermined site is
selected from the group consisting of the supplementary motor area,
the perisylvian speech-language cortex, the centromedian circuit,
the dorsomedial nuclei, the lateral prefrontal circuit, the
mesothalamic reticular formation, the basal ganglia, and other
paramedian thalamic and midbrain nuclei and fiber tracts including,
the red nucleus, the habenulointerpeduncular tract, the prerubral
area, the zona incerta, the thalamic primary sensory relay nuclei,
the ventrooral nucleus, the ventrolateral nucleus, the
parafasicular nucleus, and the intralaminar nucleus.
9. A method of therapeutically treating stuttering via an
implantable pump and a catheter having a proximal end coupled to an
implantable pump and a discharge portion for infusing therapeutic
dosages of at least one drug, as well as a signal generator and at
least one implantable electrode having a proximal end and a
stimulation portion, the method comprising: implanting the at least
one electrode adjacent to a first predetermined site in the brain;
implanting the catheter so that the discharge portion lies adjacent
to a second predetermined site in the brain; coupling the proximal
end of the implanted electrode to the signal generator; coupling
the catheter to the pump; and operating the signal generator and
the pump to stimulate or inhibit neurons of the first and second
predetermined sites in the brain by delivering electrical
stimulation to the first predetermined site and by delivering at
least one drug to the second predetermined site.
10. The method of claim 9, wherein the first predetermined site is
selected from the group consisting of the supplementary motor area,
the perisylvian speech-language cortex, the centromedian circuit,
the dorsomedial nuclei, the lateral prefrontal circuit, the
mesothalamic reticular formation, the basal ganglia, and other
paramedian thalamic and midbrain nuclei and fiber tracts including,
the red nucleus, the habenulointerpeduncular tract, the prerubral
area, the zona incerta, the thalamic primary sensory relay nuclei,
the ventrooral nucleus, the ventrolateral nucleus, the
parafasicular nucleus, and the intralaminar nucleus.
11. The method of claim 9, wherein the second predetermined site is
selected from the group consisting of the supplementary motor area,
the perisylvian speech-language cortex, the centromedian circuit,
the dorsomedial nuclei, the lateral prefrontal circuit, the
mesothalamic reticular formation, the basal ganglia, and other
paramedian thalamic and midbrain nuclei and fiber tracts including,
the red nucleus, the habenulointerpeduncular tract, the prerubral
area, the zona incerta, the thalamic primary sensory relay nuclei,
the ventrooral nucleus, the ventrolateral nucleus, the
parafasicular nucleus, and the intralaminar nucleus.
12. The method of claim 9 wherein the step of operating the signal
generator and the pump to stimulate or inhibit neurons of the first
and second predetermined sites in the brain by delivering
electrical stimulation to the first predetermined site and by
delivering at least one drug to the second predetermined site
includes: discharging the at least one drug to the second
predetermined site at a first rate at times when the patient is
expected to be awake; and discharging the at least one drug to the
second predetermined site at a second rate when the patient is
expected to be asleep, the second rate being reduced relative to
the first rate.
13. The method of claim 9 wherein the step of operating the signal
generator and the pump to stimulate or inhibit neurons of the first
and second predetermined sites in the brain by delivering
electrical stimulation to the first predetermined site and by
delivering at least one drug to the second predetermined site
including: substantially continuously delivering the at least one
drug.
14. The method of claim 9 further comprising sensing activity of
the patient's speech-producing muscles and generating a signal
indicative of the activity of the patient's speech-producing
muscles; the step of operating the signal generator and the pump to
stimulate or inhibit neurons of the first and second predetermined
sites in the brain by delivering electrical stimulation to the
first predetermined site and by delivering at least one drug to the
second predetermined site including: performing speech-recognition
processing on the signal indicative of the activity of the
patient's speech-producing muscles to detect stuttering; and
adjusting at least one stimulation parameter of electrical
stimulation to the first predetermined site in response to
detecting stuttering.
15. The method of claim 14, wherein the step of performing
speech-recognition processing on the signal indicative of the
activity of the patient's speech-producing muscles to detect
stuttering includes detecting a predetermined number of repetitions
of a speech pattern.
15. The method of claim 9 further comprising detecting when the
patient starts speaking; the step of operating the signal generator
and the pump to stimulate or inhibit neurons of the first and
second predetermined sites in the brain by delivering electrical
stimulation to the first predetermined site and by delivering at
least one drug to the second predetermined site including starting
the electrical stimulation in response to detecting that the
patient has started to speak.
16. The method of claim 15 wherein the step of operating the signal
generator and the pump to stimulate or inhibit neurons of the first
and second predetermined sites in the brain by delivering
electrical stimulation to the first predetermined site and by
delivering at least one drug to the second predetermined site
further includes stopping the electrical stimulation a
predetermined amount of time after the patient has started to
speak.
17. A method of therapeutically treating stuttering via a signal
generator and at least one implantable electrode having a proximal
end and a stimulation portion, the method comprising: implanting at
least one electrode adjacent to at least one predetermined site in
the brain; coupling the proximal end of the implanted electrode to
the signal generator; operating the signal generator to stimulate
or inhibit neurons of the at least one predetermined site in the
brain via electrical stimulation.
18. The method of claim 17, wherein the predetermined site is
selected from the group consisting of the supplementary motor area,
the perisylvian speech-language cortex, the centromedian circuit,
the dorsomedial nuclei, the lateral prefrontal circuit, the
mesothalamic reticular formation, the basal ganglia, and other
paramedian thalamic and midbrain nuclei and fiber tracts including,
the red nucleus, the habenulointerpeduncular tract, the prerubral
area, the zona incerta, the thalamic primary sensory relay nuclei,
the ventrooral nucleus, the ventrolateral nucleus, the
parafasicular nucleus, and the intralaminar nucleus.
19. The method of claim 17 further comprising sensing activity of
the patient's speech-producing muscles and generating a signal
indicative of the activity of the patient's speech-producing
muscles; the step of operating the signal generator to stimulate or
inhibit neurons of the at least one predetermined site in the brain
via electrical stimulation including: performing speech-recognition
processing on the signal indicative of the activity of the
patient's speech-producing muscles to detect stuttering; and
adjusting at least one stimulation parameter of electrical
stimulation to the predetermined site in response to detecting
stuttering.
20. The method of claim 19 wherein the step of sensing activity of
the patient's speech-producing muscles and generating a signal
indicative of the activity of the patient's speech-producing
muscles includes: electromyographically sensing activity of the
patient's speech-producing muscles.
21. The method of claim 19 wherein the step of sensing activity of
the patient's speech-producing muscles and generating a signal
indicative of the activity of the patient's speech-producing
muscles includes: electroglottographically sensing activity of the
patient's speech-producing muscles.
22. The method of claim 17 further comprising detecting when the
patient starts speaking; the step of operating the signal generator
to stimulate or inhibit neurons of the at least one predetermined
site in the brain via electrical stimulation including starting the
electrical stimulation in response to detecting that the patient
has started to speak.
23. The method of claim 20 wherein the step of operating the signal
generator to stimulate or inhibit neurons of the at least one
predetermined site in the brain via electrical stimulation includes
stopping the electrical stimulation a predetermined amount of time
after the patient has started to speak.
Description
RELATED APPLICATION
[0001] This application is a Divisional application of U.S.
application Ser. No. 10/001,751, filed Oct. 31, 2001. The entire
content of this U.S. Application is incorporated herein by
reference.
FIELD OF THE INVENTION
[0002] The invention relates to therapeutic treatment of
stuttering. More particularly, the invention relates to treating
stuttering via neural stimulation and drug therapy techniques.
BACKGROUND OF THE INVENTION
[0003] Stuttering is a speech-disfluency problem that can have
significant developmental and social impacts upon stuttering
individuals. Stuttering can include repetitions of parts of words
and/or whole words, prolongation of sounds, interjections of sounds
or words, and unduly prolonged pauses.
[0004] Conventional stuttering treatment techniques typically focus
on alerting the patient that stuttering is occurring and having the
patient try to modify their breathing and/or speech patterns in an
attempt to avoid stuttering. For instance, U.S. Pat. No. 4,020,567,
entitled Method and Stuttering Therapy Apparatus, issued to Webster
on May 3, 1977, discloses a system for helping individuals
determine when they are stuttering. The system generates an
electrical signal based on the person's speech and uses the signal
to detect certain speech characteristics corresponding to
stuttering. A first embodiment detects speech onset errors during
the first 100 milliseconds of syllable pronunciation. In a second
embodiment, stuttering is detected by evaluating the rate of change
in the amplitude of the person's speech. An LED is illuminated to
notify a system-user that stuttering is occurring. The system
disclosed by Webster is intended for use by stutterers while they
practice learning not to stutter.
[0005] U.S. Pat. No. 4,662,847, entitled Electronic Device and
Method for the Treatment of Stuttering, issued to Blum on May 5,
1987, discloses an electronic device for treating stuttering. The
device transmits electronic speech signals from a microphone to an
earphone through two paths. One path is synchronous. The other path
is asynchronous. During normal speech, the synchronous speech
signal is transmitted to the earphone. At any pause in phonation,
the device switches to the asynchronous path and transmits speech
in a delayed auditory feedback mode until a change in the user's
speech occurs.
[0006] U.S. Pat. No. 4,784,115, entitled Anti-Stuttering Device and
Method, issued to Webster on Nov. 15, 1988, discloses an
anti-stuttering device for enhancing speech fluency. The device
detects vocal pulses generated by the opening and closing of a
speaker's vocal folds. Electrical signals representative of the
vocal pulses are transmitted to a receiver in the speaker's sealed
ear canal where these signals are reproduced as audio pulses. The
device reduces stuttering by providing an early indication of the
characteristics of the speaker's voice via audio pulses. The audio
pulses produce a resonant effect within the person's ear canal.
[0007] U.S. Pat. No. 5,794,203, entitled Biofeedback System for
Speech Disorders, issued to Kehoe on Aug. 11, 1988, discloses a
biofeedback system for speech disorders that detects disfluent
speech and provides auditory feedback to enable fluent speech. The
disfluent-speech detector can be either an electromyograph (EMG) or
an electroglottograph (EGG). EMG is a system that measures the
electrical activities of muscles through electrodes attached to a
person's body. EGG records the opening and closing of a person's
vocal folds. EGG's use two electrodes on a person's neck and
measure the resistance between the electrodes. This resistance
changes as the vocal folds open and close. An EGG can show the
frequency of the vocal folds. This is the fundamental pitch of the
user's voice, without the harmonics produced by the nasal cavities,
mouth, and the like.
[0008] The system disclosed by Kehoe includes an electronic
controller connected to an EMG and frequency-altered auditory
feedback (FAF) circuit. The controller receives data from the EMG
regarding muscle tension in the user's vocal cords, masseter,
and/or other speech-production muscles. The controller then
controls the pitch of the FAF circuit in accordance with the user's
muscle tension. The user wears a headset with a microphone and
headphones. Three EMG electrodes are taped onto the user's neck
and/or jaw. When the user speaks fluently, with speech-production
muscles relaxed, the user's hears his or her voice shifted lower in
pitch. This downward-shifted pitch is relaxing and pleasant, sort
of like hearing James Earl Jones speak. If the user's
speech-production muscles are abnormally tense, however, the user
will hear his or her voice shifted higher in pitch.
[0009] U.S. Pat. No. 6,231,500, entitled Electronic Anti-Stuttering
Device Providing Auditory Feedback and Disfluency-Detecting
Biofeedback, issued to Kehoe on May 15, 2001, is a
continuation-in-part of U.S. Pat. No. 5,794,203. The Kehoe '500
patent discloses micropower impulse radar (MIR) as an alternative
to EMG biofeedback for monitoring a user's muscle activity to
detect disfluency. MIR is short-range radar, using commonly
available microchips. Unlike other radar, MIR is small and
inexpensive. A small sensor for monitoring laryngeal activity could
be taped to a user's throat.
[0010] Conventional treatment techniques for treating stuttering
typically do not use neurostimulation and/or drug delivery devices.
These types of devices, however, are capable of treating a number
of neurological disorders as well as symptoms of those disorders.
In the context of neurostimulators, an electrical lead having one
or more electrodes is typically implanted near a specific site in
the brain of a patient. The lead is coupled to a signal generator
that delivers electrical energy through the electrodes and creates
an electrical field causing excitation of the nearby neurons to
directly or indirectly treat the neurological disorder or symptoms
of the disorder. In the context of a drug delivery system, a
catheter coupled to a pump is implanted near a treatment site in
the brain. Therapeutics are delivered to the treatment sites in
predetermined dosages through the catheter.
[0011] In an article entitled Cessation of Stuttering After
Bilateral Thalamic Infarction,-A. Muroi et al. describe their
observation of a patient who, after paramedian thalamic infarction,
experienced cessation of stuttering. Neurology, vol. 53, pp. 890-91
(Sep. (1 of 2) 1999. In this article, A. Muroi et al. state that
neuroimaging studies indicate that the occlusion of a single
artery, the mesencephalic artery, have given rise to the infarction
in the bilateral medial thalamus and rostral mesencephalic
tegmentum. Further, in developmental stuttering, regional cerebral
blood flow (rCBF) was observed as relatively increased in the
medial and lateral prefrontal areas and in the orbital cortices,
and also in the supplementary motor area (SMA) and the superior
lateral premotor cortex. A. Muroi et al. then discuss a study by
Nagafuchi and Takahashi in which a patient started to stutter after
an infarct in the SMA. Another article, by Abe et al., describes a
case of stuttering-like repetitive speech disorder after paramedian
thalamomesencephalic infarction. Yet another article, by Andy and
Bhatnager, reported that stuttering was elicited by destruction of
the centromedian (CM) in one case; they also found that stimulation
of the same region alleviated the acquired stuttering in another
case. The work reported by Andy and Bhatnagar related only to adult
onset, acquired stuttering, due to the presence of cortical or
subcortical pathologies (related to a central pain syndrome), but
did not involve the more common form of developmental stuttering.
Further, there is no teaching in their work on the application of
DBS or drug delivery for the chronic treatment of developmental
stuttering as a disorder of the motor system. The dorsomedial (DM)
nuclei and CM, which were involved in the case reported by A. Muroi
et al., are reciprocally connected to the lateral prefrontal area
and SMA, respectively. In light of these studies and the case
reported by A. Muroi et al., the A. Muroi et al. article speculates
that disordered function of the SMA-CM circuit or DM-lateral
prefrontal cortex is responsible for developmental and acquired
stuttering. Therefore, it may be possible to treat either
developmental or acquired stuttering by stimulation or drug
delivery of the neural circuits involved in stuttering.
[0012] Based on the foregoing, there is a need for
stuttering-treatment techniques that use neural stimulation and/or
drug delivery to target the neurological underpinnings of
stuttering.
BRIEF SUMMARY OF THE INVENTION
[0013] The invention is directed toward various
stuttering-treatment techniques using neural stimulation and/or
drug delivery. In accordance with various inventive principles, a
catheter is coupled to an implantable pump for infusing therapeutic
dosages of at least one drug. At least one implantable electrode is
coupled to a signal generator for delivering electrical
stimulation. The invention may include various permutations and/or
combinations of the following steps: implanting the one or more
electrodes adjacent to a first predetermined site in the brain;
implanting the catheter so that the discharge portion lies adjacent
to a second predetermined site in the brain; coupling the proximal
end of the implanted electrode to the signal generator; coupling
the catheter to the pump; and operating the signal generator and
the pump to stimulate or inhibit neurons of the first and second
sites in the brain by delivering electrical stimulation to the
first site and by delivering one or more drugs to the second
predetermined site. The first and/or second predetermined sites can
be: the supplementary motor area, the perisylvian speech-language
cortex, the centromedian circuit, the dorsomedial nuclei, the
lateral prefrontal circuit, the mesothalamic reticular formation,
the basal ganglia, or other paramedian thalamic and midbrain nuclei
and fiber tracts including, but not limited to the red nucleus, the
habenulointerpeduncular tract, the prerubral area, the zona
incerta, the thalamic primary sensory relay nuclei (e.g.,
ventrooral nucleus, ventrolateral nucleus), the parafasicular
nucleus, and the intralaminar nucleus.
[0014] In accordance with the invention, the stuttering treatment
may be performed via periodic, such as once per week, transcranial
magnetic stimulation of a predetermined site of a patient's brain
for a predetermined duration, such as 30 minutes. The
transcranial-magnetic-stimulation site is delivered to: the
supplementary motor area, the perisylvian speech-language cortex,
the centromedian circuit, the dorsomedial nuclei, the lateral
prefrontal circuit, the mesothalamic reticular formation, the basal
ganglia, or other paramedian thalamic and midbrain nuclei and fiber
tracts including, but not limited to the red nucleus, the
habenulointerpeduncular tract, the prerubral area, the zona
incerta, the thalamic primary sensory relay nuclei (e.g.,
ventrooral nucleus, ventrolateral nucleus), the parafasicular
nucleus, and the intralaminar nucleus.
[0015] A system, in accordance with the invention, for
therapeutically treating stuttering in a patient is disclosed. The
system includes: a signal generator; at least one implantable lead,
coupled to the signal generator, for delivering electrical
stimulation to at least one predetermined site of the patient's
brain; a sensor, located near the patient's vocal folds, for
generating a signal responsive to activity of the patient's vocal
folds; a controller that adjusts at least one stimulation parameter
in response to the signal from the sensor. The controller could
detect when the patient starts speaking and then start the
electrical stimulation in response to that patient having started
to speak. The controller could then stop the electrical stimulation
a predetermined amount of time after the patient started speaking.
The sensor could be an electromyographic sensor, an
electroglottographic sensor, or a microphone, which could be
implanted within the patient's body. The controller could use a
speech-recognition algorithm for detecting stuttering based on the
signal received from the sensor.
[0016] Other advantages, novel features, and further scope of
applicability of the invention will be set forth in the following
detailed description.
BRIEF DESCRIPTION OF THE DRAWINGS
[0017] FIG. 1 is a diagrammatic illustration of a system for
treating stuttering illustrating a signal generator connected to an
electrode implanted in a patient's brain.
[0018] FIG. 2 is a diagrammatic illustration of a
stuttering-treatment system including an implantable pump and
catheter for delivering therapeutics to predetermined sites in a
patient's brain.
[0019] FIG. 3 is a diagrammatic illustration of a
stuttering-treatment system including a combined catheter and
electrode implanted in a patient's brain.
[0020] FIG. 4 is a diagrammatic illustration of a
stuttering-treatment system in which a sensor is located near the
patient's vocal folds and is used to control the amount of
treatment delivered.
[0021] FIG. 5 is a schematic block diagram of a microprocessor and
related circuitry for using the sensor to control drug delivery to
the brain.
[0022] FIG. 6 is a flow chart illustrating a preferred form of a
microprocessor program for using the sensor to control drug dosage
administered to the brain.
[0023] FIG. 7 is a schematic block diagram of a microprocessor and
related circuitry for using the sensor to control electrical
stimulation administered to the brain.
[0024] FIGS. 8-12 are flow charts illustrating a preferred form of
a microprocessor program for generating electrical stimulation
pulses to be administered to the brain.
[0025] FIG. 13 is a diagrammatic illustration of a
stuttering-treatment system in which a sensor is implanted in a
patient's brain and is used to control the amount of treatment
delivered.
DETAILED DESCRIPTION OF THE INVENTION
[0026] The neurogenic basis of stuttering is not well understood,
but an analogy can be drawn between stuttering and motor tremor in
a person's extremities or axial musculature. It is know that in
some forms of tremor the occurrence of abnormal neural activity in
specific brain regions (e.g., thalamus) is associated with the
presence of tremor. It is also known that treatment of these
regions with electrical stimulation or drug delivery can reduce or
abolish tremor. The structures that are apparently involved in
stuttering are the supplementary motor area, (SMA), the
centromedian circuit (CM circuit), the dorsomedial nuclei (DM
nuclei), the lateral prefrontal circuit, and other paramedian
thalamic and midbrain nuclei, and by analogy to tremor, it is
hypothesized that abnormal neural activity in these structures and
circuits is associated with the presence of stuttering.
[0027] The thalamus and cortex are connected by a network of
parallel neural circuits that send information in both directions
to ultimately control thoughts, emotions, motor behaviors, and
various other higher level functions. Each of the various types of
functions appears to have discrete anatomical circuit associated
with them. If abnormal patterns of neural activity (e.g., too much
or too little activity) arise in a specific circuit due to disease,
trauma, or developmental causes, the result is often a clinical
symptom associated with the specific functional area. For instance,
obsessive-compulsive disorder is thought to be due to hyperactivity
in the loop connecting orbital-frontal cortex with the medial
thalamus. Tremor in a specific body region appears to arise due to
over activity in the loop between the basal ganglia, thalamus and
the motor cortex subserving that body part. Similarly, stuttering
may be related to abnormal activity in the basal ganglia and
thalamo-cortical loops that control the production of speech.
[0028] It has been hypothesized that two such loops are involved in
language production and therefore in the dysfunction of stuttering:
an "outer" linguistic loop, which controls the selection of speech
information, and an "inner" motor loop that controls the actual
production of speech sounds via control of the vocal apparatus. The
linguistic loop appears to be mediated by neural circuits in the
perisylvian speech-language cortex, and the motor loop by
cortico-striatal-thalamo-cortical circuits. A disruption in timing
between these circuits has been suggested as a possible mechanism
of stuttering. By applying electrical stimulation and or drug
delivery within these circuits, it may be possible to re-establish
the proper timing relationships and thereby reduce or eliminate
stuttering.
[0029] For example, the supplementary motor area (SMA), part of the
motor loop, can be thought of as generating a signal indicative of
the intention to do something, such as begin speaking. That signal
then gets passed to the motor cortex, which is a part of the brain
that sends a corresponding signal to a person's muscles, including
a person's vocal cords, to do something, such as making speech
sounds.
[0030] Disruption of the appropriate precursor signal from the SMA
may be responsible for a stutterer's inability to speak fluently
when they are starting to say something. Such a disruption may also
be responsible for a stutterer's inability to break out of a loop
in which the same sound is being unintentionally repeated and the
inability to progress to the next stage of speaking, which occurs
in fluent speech.
[0031] This invention includes treatment techniques for
ameliorating stuttering by influencing levels of activity in
various neuronal loops associated with stuttering. These techniques
include drug delivery, electrical and magnetic stimulation, and/or
closed loop feedback systems for detecting the occurrence of speech
or stuttering.
[0032] FIG. 1 is a diagrammatic illustration of a patient with an
implant of a neurostimulation system employing an embodiment of the
present invention. An implantable signal generator 16 produces
stimulation signals to various predetermined sites within a
patient's brain, B. The predetermined sites may include the
supplementary motor area (SMA), the perisylvian speech-language
cortex, the centromedian circuit (CM circuit), the dorsomedial
nuclei (DM nuclei), the lateral prefrontal circuit, the
mesothalamic reticular formation, the basal ganglia and other
paramedian thalamic and midbrain nuclei and fiber tracts including,
but not limited to the red nucleus, the habenulointerpeduncular
tract, the prerubral area, the zona incerta, the thalamic primary
sensory relay nuclei (e.g., ventrooral nucleus, ventrolateral
nucleus), the parafasicular nucleus, and the intralaminar nucleus.
Device 16 may take the form of a signal generator such as model
7424 manufactured by Medtronic Inc. under the trademark Itrel
II.RTM..
[0033] As depicted in FIG. 1, a conductor 22 is implanted below the
skin of a patient. The distal end of conductor 22 terminates in a
lead 22A. Lead 22A may take the form of any of the leads sold with
Medtronic's Model 7424 signal generator for stimulation of the
brain. The proximal end of conductor 22 is coupled to signal
generator 16.
[0034] The distal end of lead 22A terminates in a stimulation
electrode located at a predetermined area of the brain, B. The
distal end of lead 22A is implanted using stereotactic techniques
that are well known by those skilled in the art. The physician
determines the number of electrodes needed for the particular
treatment.
[0035] FIG. 2 is a diagrammatic illustration of a patient having an
implant of a drug delivery system employing an embodiment of the
present invention. The system distributes a therapeutic agent to
predetermined sites in the brain selected by a physician. The
system uses a pump 10 that can be an implantable pump like the
Medtronic SynchroMed.RTM. pump or an external pump. As depicted in
FIG. 2, the pump 10 has a port 14 into which a hypodermic needle
can be inserted to inject therapeutic to fill the pump 10. In the
system shown, the therapeutic is delivered from pump 10 through a
catheter port 20 into a catheter 222. Catheter 222 may be implanted
below the skin of a patient using well-known stereotactic placement
techniques and positioned to deliver the therapeutic to the
predetermined sites within the brain, B. The predetermined sites
may include the supplementary motor area (SMA), the perisylvian
speech-language cortex, the centromedian circuit (CM circuit), the
dorsomedial nuclei (DM nuclei), the lateral prefrontal circuit, the
mesothalamic reticular formation, the basal ganglia and other
paramedian thalamic and midbrain nuclei and fiber tracts including,
but not limited to the red nucleus, the habenulointerpeduncular
tract, the prerubral area, the zona incerta, the thalamic primary
sensory relay nuclei (e.g., ventrooral nucleus, ventrolateral
nucleus), the parafasicular nucleus, and the intralaminar
nucleus.
[0036] FIG. 3 is a diagrammatic illustration of a patient having an
implant of a neurological system employing an embodiment of the
present invention. The system as shown in FIG. 3, illustrates a
combined catheter electrode, 322, that can distribute both
stimulation signals and therapeutics from the signal generator 16
and pump 10, respectively.
[0037] The combined catheter electrode 322 terminates with a
cylindrical hollow tube 322A having a distal end implanted into a
predetermined location of a patient's brain, B. The distal end of
tube 322A is implanted using stereotactic techniques well known by
those skilled in the art. Tube 322A includes an outer cylindrical
insulation jacket (not shown) and an inner insulation jacket (not
shown) that defines a cylindrical catheter lumen. A multifular coil
of wire, multiflar stranded wire or flexible printed circuit is
embedded in tube 322A (not shown).
[0038] Trans-cranial magnetic stimulation could also be used as a
means to deliver therapeutic stimulation to the nervous system to
treat stuttering. This magnetic stimulation would tend to be more
of a clinical application as opposed to a portable and/or
human-implantable device. In accordance with the invention, a
patient's stuttering could be treated periodically, such as once
per week, via trans-cranial magnetic stimulation of the
supplementary motor area, (SMA), the centromedian circuit (CM
circuit), the dorsomedial nuclei (DM nuclei), the lateral
prefrontal circuit, and other paramedian thalamic and midbrain
nuclei and fiber tracts including, but not limited to the red
nucleus, the habenulointerpeduncular tract, the prerubral area, the
zona incerta, the thalamic primary sensory relay nuclei (e.g.,
ventrooral nucleus, ventrolateral nucleus), the parafasicular
nucleus, and the intralaminar nucleus. The Magpro stimulator
available from Medtronic, Inc. of Minneapolis Minn. is an example
of a suitable magnetic stimulator. Magnetic stimulators of this
type are capable of causing electrical current flow in particular
regions of a patient's brain thereby activating specific neural
structures or circuits. Such magnetic stimulation has been used
clinically as a diagnostic tool to evaluate the condition of the
motor system, and therapeutically to treat disorders such as
depression.
[0039] FIG. 4 shows the placement of a sensor, 130, near the vocal
cords of a patient. The sensor 130 is coupled to the pump 10 via
cable 132. The vocal cords produce electrical signals, such as
electromyographic (EMG) and electroglottographic (EGG) signals,
that can be detected and used to control the treatment method. For
example, when a patient begins to speak, sensor 130 could detect
the vocal-fold activity and send a signal to the treatment device
to indicate that therapy should begin. In this embodiment, the
treatment is delivered and continues to be delivered continuously
as the patient speaks. Alternatively, the sensor could be coupled
to a microprocessor that contains speech recognition software
stored in memory. The speech recognition software could be
programmed to distinguish between stuttering and normal speech by
detecting a predetermined number of repetitions of a speech
pattern. For example, treatment could begin upon detecting three
repetitions of a particular speech pattern. The software could
analyze an EMG or EGG waveform from the vocal folds, or signals
from a microphone, either implanted or placed externally on a
person's neck near the person's vocal folds.
[0040] FIG. 13 shows the placement of a sensor, 1325, located in a
specific region of the brain to detect electroencephalogram (EEG)
signals. The sensor 1325 may be coupled to the pump 10 and the
signal generator 16 through the combined catheter electrode 1322.
The EEG signals may be detected and analyzed for abnormal activity
related to stuttering with the use of a microprocessor that
contains EEG recognition software stored in memory. In this
embodiment, treatment is delivered and may continue to be delivered
based on the recorded electrical activity as seen by sensor
1325.
[0041] Several other techniques, which are well known in the art,
could also be used in accordance with the invention for detecting
speech disfluency. For instance, as described in more detail above,
each of U.S. Pat. Nos. 4,020,567, 5,794,203, and 6,231,500, which
are incorporated herein by reference, disclose
speech-disfluency-detection devices that could be used with this
invention.
[0042] The amount and type of stimulation delivered in accordance
with the invention may be controlled based upon analysis of the
output from a sensor, such as sensor 130 shown in FIG. 4. Referring
to FIG. 5, the output of a sensor 130, which could be an EEG, EMG
or EGG sensor, micropower impulse radar, or a microphone as
described above, is coupled by a cable 132 comprising conductors
134 and 135 to the input of analog to digital converter 140.
Alternatively the output of the sensor 130 could communicate
through a "body bus" communication system as described in U.S. Pat.
No. 5,113,859 (Funke), which is assigned to Medtronic and which is
incorporated herein by reference. Alternatively, the output of an
external feedback sensor 130 would communicate with the implanted
pulse generator 16 or pump 10 through a telemetry down-link. The
output of the analog to digital converter 140 is connected to
terminals EF2 BAR and EF3 BAR. Such a configuration may be one
similar to that shown in U.S. Pat. No. 4,692,147 ("'147 Patent")
except that before converter 140 is connected to the terminals, the
demodulator of the '147 patent (identified by 101) would be
disconnected. A drug can be delivered essentially continuously
(within the constraints of the particular delivery device being
used) or it may be delivered during intermittent intervals
coordinated to reflect the half-life of the particular agent being
infused or with circadian rhythms. As an example, stuttering will
typically occur less frequently at night when the person is
sleeping so the drug delivery rates might be reduced to coincide
with the hours between 10 p.m. and 7 a.m.
[0043] An exemplary computer algorithm is shown in FIG. 6.
Referring to FIGS. 5 and 6, microprocessor 100 included within pump
10 reads converter 140 in step 150, and stores one or more values
in RAM 102a in step 152. A dosage is selected in step 154, and an
appropriate time interval is selected in step 156. The selected
dosage and interval of a drug is then delivered through catheter
222 and tube 222A to the basal ganglia of the brain as described in
the '147 Patent.
[0044] For some types of sensors, a microprocessor and analog to
digital converter will not be necessary. An appropriate elect
filter can be used to filter the output from sensor 130 to provide
a control signal for signal generator 16. An example of such a
filter is found in U.S. Pat. No. 5,259,387 "Muscle Artifact Filter,
Issued to Victor de Pinto on Nov. 9, 1993, incorporated herein by
reference.
[0045] A modified form of the ITREL II.RTM. signal generator can be
used to achieve closed-loop electrical stimulation, which is
schematically depicted in FIG. 7. The output of the analog to
digital converter 206 is connected to a microprocessor 200 through
a peripheral bus 202 including address, data and control lines.
Microprocessor 200 processes the sensor data in different ways
depending on the type of transducer in use. When the signal on
sensor 130 exceeds a sensor-signal threshold level stored in a
memory 204, increasing amounts of stimulation will be applied
through an output driver 224. The sensor-signal threshold level
could be set such that the sensor signal will exceed the threshold
whenever the person is speaking. Alternatively, increasing amounts
of stimulation could be applied through the output driver 224 when
speech-processing software detects a speech pattern that is likely
to correspond to stuttering.
[0046] Programming a value to a programmable frequency generator
208, using bus 202, controls the stimulus pulse frequency. The
programmable frequency generator provides an interrupt signal to
microprocessor 200 through an interrupt line 210 when each stimulus
pulse is to be generated. The frequency generator may be
implemented by model CDP1878 sold by Harris Corporation. The
amplitude for each stimulus pulse is programmed to a digital to
analog converter 218 using bus 202. The analog output is conveyed
through a conductor 220 to an output driver circuit 224 to control
stimulus amplitude. Microprocessor 200 also programs a pulse width
control module 214 using bus 202. The pulse width control provides
an enabling pulse of duration equal to the pulse width via a
conductor. Pulses with the selected characteristics are then
delivered from signal generator 16 through cable 22 and lead 22A to
the target locations of a brain B.
[0047] Microprocessor 200 executes an algorithm shown in FIGS. 8-12
in order to provide stimulation with closed loop feedback control.
At the time the stimulation signal generator 16 or alternative
device in which the stimulation and infusion functions are combined
is implanted, the clinician programs certain key parameters into
the memory of the implanted device via telemetry. These parameters
may be updated subsequently as needed. Step 400 in FIG. 8 indicates
the process of first choosing whether the neural activity at the
stimulation site is to be blocked or facilitated (step 400(1)) and
whether the sensor location is one for which an increase in the
neural activity at that location is equivalent to an increase in
neural activity at the stimulation target or vice versa (step
400(2)). Next the clinician must program the range of release for
pulse width (step 400(3)), amplitude (step 400(4)) and frequency
(step 400(5)) which signal generator 16 may use to optimize the
therapy. The clinician may also choose the order in which the
parameter changes are made (step 400(6)). Alternatively, the
clinician may elect to use default values.
[0048] The algorithm for selecting parameters is different
depending on whether the clinician has chosen to block the neural
activity at the stimulation target or facilitate the neural
activity. FIG. 8 details steps of the algorithm to make parameter
changes.
[0049] The algorithm uses the clinician programmed indication of
whether the neurons at the particular location of the stimulating
electrode are to be facilitated or blocked in order to decide which
path of the parameter selection algorithm to follow (step 420, FIG.
9). If the neuronal activity is to be blocked, signal generator 16
first reads the feedback sensor 130 in step 421. If the sensor
values indicate a likelihood that the activity in the neurons is
too high (step 450), for instance, if speech processing software
detects a speech pattern likely to correspond to stuttering, the
algorithm in this embodiment first increases the frequency of
stimulation in step 424 provided this increase does not exceed the
preset maximum value set by the physician. Step 423 checks for this
condition. If the frequency parameter is not at the maximum, the
algorithm returns to step 421 through path 421A to monitor the feed
back signal from sensor 130.
[0050] If the frequency parameter is at the maximum, the algorithm
next increases the pulse width in step 426 (FIG. 10), again with
the condition that this parameter has not exceeded the maximum
value as checked for in step 451 through path 423A. Not having
reached maximum pulse width, the algorithm returns to step 421 to
monitor the feedback signal from sensor 130. Should the maximum
pulse width have been reached, the algorithm next increases
amplitude in a like manner as shown in steps 427 and 428. In the
event that all parameters reach the maximum, a notification message
is set in step 429 to be sent by telemetry to the clinician
indicating that device 16 is unable to reduce neural activity to
the desired level.
[0051] If, on the other hand, the stimulation electrode is placed
in a location which the clinician would like to activate in order
to alleviate stuttering, the algorithm would follow a different
sequence of events. In the preferred embodiment, the frequency
parameter would be fixed at a value chosen by the clinician to
facilitate neuronal activity in step 430 (FIG. 11) through path
420A. In steps 431 and 432 the algorithm uses the values of the
feedback sensor to determine if neuronal activity is being
adequately controlled. In this case, inadequate control indicates
that the neuronal activity of the stimulation target is too low.
Neuronal activity is increased by first increasing stimulation
amplitude (step 434) provided it doesn't exceed the programmed
maximum value checked for in step 433. When maximum amplitude is
reached, the algorithm increases pulse width to its maximum value
in steps 435 and 436 (FIG. 12). A lack of adequate alteration of
the symptoms of the neurological disorder, even though maximum
parameters are used, is indicated to the clinician in step 437.
After steps 434, 436 and 437, the algorithm returns to step 431
through path 431A, and the feedback sensor is read again.
[0052] It is desirable to reduce parameter values to the minimum
level needed to establish the appropriate level of neuronal
activity in, for example, the target brain nucleus. Superimposed on
the algorithm just described is an additional algorithm to readjust
all the parameter levels downward as far as possible. In FIG. 8,
steps 410 through 415 constitute the method to do this. When
parameters are changed, a time is reset in step 415. If there is no
need to change any stimulus parameters before the timer has counted
out, then it may be possible due to changes in neuronal activity to
reduce the parameter values and still maintain appropriate levels
of neuronal activity in the target neurons. At the end of the
programmed time interval, signal generator 16 tries reducing a
parameter in step 413 to determine if control is maintained. If it
is, the various parameter values will be ratcheted down until such
time as the sensor values again indicate a need to increase them.
While the algorithms in FIGS. 8-12 follow the order of parameter
selection indicated, other sequences may be programmed by the
clinician.
[0053] While the invention has been described with respect to
specific examples including presently preferred modes of carrying
out the invention, those skilled in the art will appreciate that
there are numerous variations and permutations of the above
described systems and techniques that fall within the spirit and
scope of the invention as set forth in the appended claims and
their equivalents.
* * * * *