Method and apparatus for treating chronic pain syndromes, tremor, dementia and related disorders and for inducing electroanesthesia using high frequency, high intensity transcutaneous electrical nerve stimulation

Provided herein is a non-invasive method of treating, controlling or preventing medical, psychiatric or neurological disorders, using transcutaneous electrical stimulation. The method employs a plurality of stimulation frequency parameters, ranging from a relatively high frequency, for example about 40,000 Hertz, to a relatively low frequency, for example about 250 Hertz, the entire plurality of frequency parameters being administered at each of a plurality of stimulation intensity levels. In particular, the method involves stimulating at a first highest frequency parameter and a first lowest intensity parameter, incrementally decreasing the stimulation frequency parameter a lowest frequency parameter, increasing the frequency parameter to the highest frequency parameter and increasing the intensity parameter to a next highest intensity parameter, and again stimulating through the plurality of frequency parameters from the highest frequency to the lowest frequency. The method described herein is useful in treating, controlling and/or preventing various disease states and disorders, including without limitation, tremor disorders, such as essential tremor and Parkinson's disease, dementia disorders, such as Alzheimer's disease and painful degenerative disorders, such as reflex sympathetic dystrophy and fibromyalgia.

FIELD OF THE INVENTION 
The present invention relates to improved methods for the non-invasive 
treatment of various disease conditions using an improved process of 
transcutaneous electrical stimulation. In particular, provided herein are 
improved methods of non-invasively treating symptoms of tremor disorders 
including essential tremors and tremors associated with Parkinson's 
Disease; symptoms of dementia disorders including cortical dementia, such 
as is found in Alzheimer's disease and Pick's disease, subcortical 
dementia, such as is found in Parkinson's disease, Huntington's chorea and 
supranuclear palsy, and multi-infarct dementia; and symptoms of painful 
degenerative disorders, such as fibromyalgia and reflex sympathetic 
dystrophy by using transcutaneous electrical nerve stimulation programs of 
variable intensity and variable frequency. Also provided are apparatus for 
performing such methods. 
BACKGROUND OF THE INVENTION 
Transcutaneous electrical nerve stimulation (TENS) is a well known medical 
treatment used primarily for symptomatic relief and management of chronic 
intractable pain and as an adjunctive treatment in the management of post 
surgical and post traumatic acute pain. TENS involves the application of 
electrical pulses to the skin of a patient, which pulses are generally of 
a low frequency and are intended to affect the nervous system in such a 
way as to suppress the sensation of pain that would indicate acute or 
chronic injury or otherwise serve as a protective mechanism for the body. 
Typically, two electrodes are secured to the skin at appropriately 
selected locations. Mild electrical impulses are then passed into the skin 
through the electrodes to interact with the nerves lying thereunder. As a 
symptomatic treatment, TENS has proven to effectively reduce both chronic 
and acute pain of patients. However, TENS has shown no capacity for curing 
the causes of pain, rather the electrical energy simply interacts with the 
nervous system to suppress or relieve pain. 
The human nervous system essentially serves as a communication system for 
the body wherein information concerning the state of the body is 
communicated to the spinal cord (and/or brain) and behavioral instructions 
are communicated from the brain (and/or spinal cord) to the rest of the 
body. Thus, there are ascending neural pathways, such as the ascending 
pain pathways, and descending neural pathways, such as the descending 
inhibitory pathway (DIP), within the nervous system. 
Briefly, pain impulses received by the free nerve endings of nociceptive 
nerve fibers (in particular, A.delta. and C fibers) are conducted, through 
various synapses, to the brain. In particular, these first order neurons 
enter the dorsal horn of the spinal cord and synapse with second order 
neurons, which are either relay cells, projecting into the brain stem or 
thalamus, or interneurons, synapsing to other interneurons or to relay 
cells. The second order neurons then (mostly) cross the spinal cord and 
become the anterolateral system, comprised of the neospinothalamic tract 
(or lateral spinothalamic tract) and paleospinothalamic tract. The nerve 
fibers of the anterolateral system then terminate in various regions of 
the brain, including the brain stem, midbrain and thalamus. 
Inhibition (or modulation) of pain, by the body, can occur anywhere from 
the point of origin of the pain through the successive synaptic junctions 
in the pain's central pathway. For example, following the descending 
inhibitory pathways (DIP) of pain inhibition/modulation, stimulation in 
the cerebral cortex of the brain descends to the thalamus and then to the 
periaqueductal gray (PAG) of the midbrain. The PAG region is rich in 
opiate receptors responsible for secreting morphine-like enkephalins and 
endorphins. Nerve fibers from the PAG then descend to the nucleus raphe 
magnus (NRM) in the brainstem. The NRM is responsible for the secretion of 
serotonin, a compound that is instrumental in elevating pain threshold 
levels and combating depression. Fibers from the NRM then descend into the 
spinal cord, synapsing with other inhibitory interneurons to cause 
secretion of additional powerful anti-pain neurotransmitters such as 
gamma-aminobutyric acid (GABA). 
While prior art TENS devices and methods have been shown to be capable of 
affecting the ascending pathways of pain perception, they have shown 
little or no ability to affect the descending inhibitory pathways of the 
nervous system. The precise mechanisms by which these prior art TENS 
methods operate to affect pain are not known; however, one theory suggests 
that, by producing fast electrical waves that travel up the A.beta. 
nociceptive fibers, the TENS electrical stimulation pulses block pain 
stimulus traveling up the A.delta. and C fibers. One frequently reported 
problem with the prior art TENS methods is acclimation or accommodation; 
that is, the patient acclimates to the transcutaneous stimulation and the 
pain returns. The intensity of the treatment, in such cases, is increased 
to overcome the patient's accommodation of the treatment, but shortly, a 
maximum level of intensity is reached and further treatment is 
ineffective. 
A TENS stimulator is, in effect, an electrical pulse generator which 
delivers electrical pulses (or impulses), transcutaneously, at a 
predetermined fixed or variable frequency. Typically, TENS stimulators 
deliver electrical pulses at frequencies in the range of about 50 to 200 
Hertz (Hz). Most commonly, variable frequency TENS devices operate by 
beginning stimulation at the lowest frequency setting then increasing the 
frequency of stimulation until a pre-defined event occurs, such as motor 
nerve response or patient comfort achieved. Such increases in frequency 
may be controlled by a doctor or other medical personnel or, more often, 
are controlled by the patient him/herself. In addition to increasing the 
frequency of the stimulation pulses, the patient may be treated by 
simultaneously increasing the intensity (or amplitude) of the stimulation 
output of the device. 
For example, the patient may have a choice of different "levels" of 
stimulation, each sequential level providing an increased frequency and 
intensity of stimulation as compared to the previous level. In either 
case, the output parameters generally start at their lowest level and are 
increased over the duration of the treatment. 
Normally, when the patient (or other operator) increases the stimulation 
level of the TENS machine, in accordance with his/her doctor's 
instructions, the new, higher level is somewhat uncomfortable at first. 
However, as the patient knows from experience, his/her body accommodates 
to the new higher level of stimulation within a tolerable length of time. 
Once stimulation at one level becomes fully accommodated, that is, no 
longer works well to relieve the symptoms for which the treatment is being 
administered, the patient increases the stimulation level. Thus, as 
mentioned previously, the body is able to adjust to the electrical 
stimulation, requiring ever increasing levels of stimulation to achieve 
the same level of pain relief, often until no amount of stimulation is 
effective. 
In some cases, the treatment frequency of the TENS device is fixed by 
design, or is established as a preselected, generally arbitrary, rate at 
the time of treatment, and only adjustment of the intensity (or amplitude) 
of the electrical pulses is allowed. The typical intensity level of TENS 
stimulators is in the range of 30-200 volts. The waveform characteristic 
of the electrical pulses varies and includes, for example, symmetrical 
sinusoidal waveforms, symmetrical biphasic waveforms and DC needle spikes. 
Generally, the different waveforms are believed to offer some advantage 
over other waveforms; however, there has been no clear consensus that any 
particular type of waveform is consistently more advantageous than other 
types. What is known, however, is the general shape of the action 
potential waveform that is responsible for producing electrical activity 
in neurons. Characteristic of this action potential are a very fast rise 
time and a slow decay. 
The precise mechanisms by which transcutaneous electrical stimulation 
operates to control pain are not known. When used to treat pain, the patch 
electrodes of the TENS device are generally attached to the patient in the 
vicinity of the pain. Thus, for example, in treating joint pain, 
electrodes would be affixed near the joint and stimulation administered 
thereto. This localized stimulation then affects the nervous system to 
reduce the patient's perception of pain, presumably by either affecting 
the pain signals being sent from the region to the brain or by affecting 
the brain's perception of the signals it is receiving from the region. 
Even the body's natural mechanisms for perceiving and affecting pain are 
poorly understood. However, it is known that various biochemicals are 
released by nerve and brain cells in response to chemical and/or 
electrical stimulation of those cells. These neurotransmitters assist in 
the transmission of electrical messages between and within the peripheral 
and central nervous systems. 
In contrast to the TENS devices and methods used to affect the ascending 
pathways of the nervous system, implantable electrical stimulators have 
been used to affect descending motor pathways of the nervous system. These 
electrical stimulators are surgically implanted into the patient's brain 
in order to affect, by direct electrical stimulation, specific regions of 
the brain. For example, by implantation of a stimulating electrode into 
the appropriate brain region, such as the thalamus and/or basal ganglia, 
nervous activity within the brain can be affected and the symptoms of 
movement disorders, such as akinesia, bradykinesia or rigidity and 
hyperkinetic disorders, can be reduced. See for example U.S. Pat. No. 
5,716,377, Rise, et al., the entirety of which is hereby incorporated by 
reference. Thus, by stimulating the brain in this manner, the skeletal 
muscles at the termination of the descending motor pathway are affected. 
Obviously, surgical implantation of an electrode into the brain, as well 
as direct electrical stimulation of the brain are risky procedures that 
are preferably utilized only in the most extreme cases and after failure 
of less risky procedures. 
Various disease conditions and disorders involve the brain and/or nervous 
system and thus may be amenable to treatment using drugs and/or electrical 
stimulation. For example, U.S. Pat. No. 5,716,377, issued to Rise, et al., 
Feb. 10, 1998, describes a method of treating movement disorders by means 
of an electrode implanted into the brain of the patient. Similarly, U.S. 
Pat. No. 5,713,923, issued to Ward, et al., Feb. 3, 1998, describes a 
method of treating epilepsy using a brain implanted electrode in 
combination with one or more drugs. While the effects of electrical 
stimulation of certain specific nerves, specific nerve/brain regions 
and/or specific muscles to treat different diseases and/or disorders have 
been described, few if any generalizations have resulted therefrom. That 
is, it is still very difficult to predict what if any type of nerve 
stimulation or drug therapy will work for any given disorder. 
Essential tremor (E.T.) is a movement disorder afflicting more than 5 
million people in the United States alone. This disease, which is the most 
common adult movement disorder, is about 20 times more prevalent than the 
tremors associated with Parkinson's Disease and is a poorly understood 
hereditary disorder. It is estimated that 32 in 1000 persons over the age 
of 60 years suffers from E.T. About 95% of those with this disease 
experience tremors, i.e. uncontrollable shaking, in both hands, often 
rendering the hands useless or near useless. Further, E.T. is the primary 
cause of head tremors (Titubation), which tremors are not only extremely 
difficult to treat but are particularly embarrassing and debilitating. In 
particularly severe cases, E.T. patients have elected to undergo difficult 
and dangerous brain surgery wherein the part of the brain responsible for 
the tremors is destroyed. Unfortunately, this surgery can result in the 
unintended permanent impairment or destruction (i.e., paralysis) of 
movement speech and/or swallowing functions as well as paraesthesia or 
tingling sensations in the patient's hands and/or head. 
The current treatment of choice for essential tremor is drug therapy. 
However, an estimated 60% of E.T. patients do not respond to drug therapy 
and must therefore either live with the condition or resort to more 
dangerous and more invasive forms of treatment. Even when drug therapy is 
"successful," it rarely results in diminution of head tremors; rather, 
only hand tremors may respond to the therapy. Further, the patient's body 
usually acclimates to the drug therapy, requiring increased dosages of 
drugs, which, after time, become less effective. This necessitates 
frequent changes in drugs in order to obtain or maintain the same level of 
relief. 
Prior to 1997, in the U.S.A., the only alternative to drug therapy for the 
relief of the symptoms of essential tremor was surgical destruction of 
part of the thalamus, from where the tremors are believed to originate. In 
1997, (1995 in Europe), an implantable electronic stimulating device was 
approved for the treatment of essential tremor. This device is implanted 
deep into the thalamus of the patient and electrical stimulation of that 
brain structure is used to control the tremor. However, the device is 
effective to control tremors only unilaterally, that is in only one hand. 
Further, the success rate of the device is not great, particularly given 
the invasive nature of the procedure: with about 67% of 113 Parkinson's 
disease patients in one study experiencing control of tremors and about 
58% of 83 essential tremor patients in the study being relieved. Because 
almost all essential tremor patients suffer bilateral tremors (tremors in 
both hands), those wishing to have the brain implant must choose which 
hand to control, at least unless and until more than one implant may be 
used simultaneously, a procedure that to date has not been approved. Also, 
the brain implant has no effect on titubation (head tremor). 
A prior art implantable brain stimulation device is described for example 
in U.S. Pat. No. 5,716,377, issued to Rise, et al. and incorporated 
herein, in its entirety, by reference. This patent describes the use of an 
implantable device having the stimulating electrode implanted into the 
basal ganglia or thalamus of the patient, with the electrode lead passing 
under the skin of the patient to a pulse generator also implanted 
subcutaneously. Also described in the '377 patent, is the implantable 
device including a sensor for sensing the tremors. The sensor is also 
implanted and is connected to the pulse generator. The brain stimulation 
device is operated at 0.1 to 20 volts and at a frequency of between 2 to 
2500 Hertz. Such devices are expensive, about $10,000 for the device plus 
about $25,000 for the required surgery, and require replacement of the 
pulse generator, and hence additional surgery and expense, about every 
three years. 
Like essential tremor and Parkinson's disease, dementia disorders such as 
Alzheimer's disease are primarily diseases of the brain. Alzheimer's 
disease is a degenerative disease in which nerve cells within the brain 
die and their connections deteriorate. It is the most common cause of 
dementia and is the fourth leading cause of death among adults in the 
United States. While various causative factors have been postulated, such 
as heredity, environmental toxins and biochemical changes within the aging 
body, no specific cause for this disease had been identified. 
Alzheimer's patients consistently have abnormally low levels of 
neurotransmitters in their brains, particularly a neurotransmitter known 
as acetylcholine. This reduction in neurotransmitters results in the 
gradual deterioration of the patient's mental processes and intellectual 
functioning, including memory loss, especially short-term memory, 
behavioral changes, inability to properly use language and the inability 
to perform skilled activities. Autopsies of Alzheimer's patients reveal 
the formation of protein plaques, comprised primarily of beta-amyloid 
protein, within the critical memory and learning centers of the brain. 
Studies on rats have demonstrated that injection of substance P can block 
the nerve damage caused by beta-amyloid, and thus, a significant portion 
of research efforts aimed at controlling this disease have focused on this 
and other brain biochemicals. 
Presently, there is no cure or prevention for Alzheimer's disease. However, 
two different drugs have been approved in the United States for use in the 
management of this disease. While neither drug has been proven to provide 
long term relief from the degenerative process of Alzheimer's, at least 
one of the drugs has recently demonstrated an ability to stop the decline 
in memory and alertness for 84% of patients studied for a six month 
period. Further this drug, known as Aricept (produced by Eisai, a Japanese 
company), does not apparently cause the liver-toxic side effects seen with 
the other approved drug. Thus, research on drug therapies for the 
treatment of Alzheimer's disease continue. 
Recently, the treatment of dementia disorders by electrical stimulation of 
specific cranial nerves has been described. U.S. Pat. No. 5,269,303, 
issued to Wernicke, et al., Dec. 14, 1993, describes stimulation of the 
vagus nerve to treat patients with dementia, and U.S. Pat. No. 5,540,734, 
issued to Zabara, Jul. 30, 1996, describes stimulation of one or both of 
the trigeminal and glossopharyngeal nerves to treat a variety of 
neurological, medical and psychiatric disorders, including dementia 
disorders. Each of these patents are hereby incorporated by reference in 
their entirety. Unfortunately, however, these methods are premised upon 
implantation of stimulation electrodes directly onto the specified nerve. 
This not only means that the patient must undergo major surgery to receive 
treatment, but also that the scope of treatment will be limited to the 
specific nerves upon which the electrode is implanted. Thus, once 
implanted, should the device not work to relieve the symptoms of the 
dementia or, worst, should the nerve stimulation result in intolerable 
side effects, either the device must be surgically explanted or must be 
deactivated and left within the patient's body. 
Thus, what is needed is an inexpensive non-invasive method of treating 
neurology-related disorders, such as dementia disorders and/or movement 
disorders, that will be effective to relieve the very severe symptoms 
associated therewith. In particular, with respect to movement disorders, 
such as essential tremor and tremors associated with Parkinson's disease, 
methods of providing relief for both bilateral hand tremors and head 
tremors is needed. Similarly, with respect to dementia disorders, such as 
Alzheimer's disease, even a slowing of the deterioration associated with 
the disorders would be welcomed. 
SUMMARY OF THE INVENTION 
The present invention addresses these and other objectives by providing 
methods for the non-invasive treatment, control and/or prevention of 
various disease conditions and disorders using transcutaneous electrical 
stimulation, wherein a plurality of stimulation intensities and a 
plurality of stimulation frequency parameters are employed such that the 
entire plurality of frequency parameters is administered, from highest to 
lowest frequency, at each of the plurality of stimulation intensity 
parameters. Further provided herein are apparatus for employing these 
methods. 
In one aspect, the present invention provides improved results in the 
treatment of various diseases by affecting the descending inhibitory 
pathways and neurotransmitter production and release within the nervous 
system. In particular, such results are achieved via transcutaneous nerve 
stimulation. A method which heretofore had not been described or 
demonstrated. 
In a preferred embodiment, the method contemplated herein, is useful to 
treat, control and/or prevent tremor disorders, such as essential tremor 
and tremors associated with Parkinson's disease, dementia disorders, such 
as Alzheimer's disease, and cortical, subcortical and multi-infarct 
dementia and painful degenerative disorders, such as fibromyalgia and 
reflex sympathetic dystrophy. This preferred method involves stimulating 
at a first highest frequency parameter and lowest intensity parameter; 
decreasing the frequency parameter to the lowest frequency parameter over 
the course of time and in a specified manner, while holding the intensity 
parameter constant. The next stage in treatment is to increase the 
stimulation frequency parameter back to the highest frequency parameter 
but at a next higher stimulation intensity parameter. The stimulation 
frequency parameter is then decreased in the same manner as previously 
done for the lower intensity parameter; while the intensity parameter is 
maintained at this next highest level. 
The apparatus contemplated for use herein is a high frequency, high 
intensity transcutaneous electrical nerve stimulator (TENS) similar to 
that described in U.S. Pat. No. 5,052,391 ('391 patent), issued to 
Silverstone, et al., the entirety of which patent is hereby incorporated 
by reference. In a preferred embodiment, the TENS device described in the 
'391 patent is modified to include a programmable microprocessor capable 
of retaining and executing at least one, and preferably a plurality, of 
stimulation programs according to the new methods described herein and 
further is a digital device instead of analog as described in the '391 
patent. Most preferably then, the improved TENS device contemplated herein 
may be programmed to administer an entire regimen of therapy to a patient 
without requiring any control on the part of the patient, while still 
permitting the patient the opportunity to control the device if desired. 
Further, the device will preferably be able to administer a plurality of 
treatment regimens, thereby being useful for a plurality of different 
disease states and disorders.

DETAILED DESCRIPTION OF THE INVENTION 
The nervous system, including the brain, operates as a communication 
network for the body, carrying information and instructions from the brain 
to the rest of the body, from the rest of the body to the brain and within 
the nervous system itself. In performing these functions, the nervous 
system and brain, among other things, use certain biochemical messengers, 
known as neurotransmitters, to accomplish this transferring of information 
and instructions. It has been known for some time that electrical 
stimulation of nerves, for example by implantation of a stimulating 
electrode onto a particular nerve, can result in release of one or more 
neurotransmitters from nerve cells thereby affecting the operation of this 
communication system. 
Numerous disease states and disorders involve the nervous system and/or 
brain, many of which are believed to affect or result from the activity or 
lack of activity of neurotransmitters. For example, tremor disorders such 
as essential tremor and Parkinson's disease, dementia disorders, such as 
cortical dementia, as is found in Alzheimer's disease and Pick's disease, 
subcortical dementia, as is found in Parkinson's disease, Huntington's 
chorea and supranuclear palsy, and multi-infarct dementia; and painful 
degenerative disorders, such as fibromyalgia and reflex sympathetic 
dementia all involve the brain and/or nervous system and may be related to 
neurotransmitter activity. 
In preferred embodiments of the new methods described and claimed herein, 
transcutaneous electrical nerve stimulation techniques are employed to 
treat, control and/or prevent these and other disorders. While the use of 
transcutaneous nerve stimulation for such purposes is not unknown, the 
particular new methods described herein are uniquely effective. For 
example, in preferred embodiments, the methods described herein result in 
increases in blood levels of neurotransmitters, a heretofore unknown 
phenomenon. Most prior art transcutaneous nerve stimulators operate by 
delivering electrical stimulation to the body at a moderately low to very 
low frequency and at a single level of intensity. Usually, the patient is 
able to adjust either or both of the frequency and intensity, but the 
device then stimulates for the duration of the treatment at only those 
selected parameters. In contrast, the methods presented herein operate by 
stimulating, in a defined pattern, at a plurality of frequencies beginning 
at a very high frequency and sweeping through the plurality of frequencies 
to the lowest frequency, while maintaining the intensity of the 
stimulation at a single low intensity. Once a single sweep has been 
performed the intensity of the stimulation is incrementally increased and 
the entire frequency sweep performed at the new higher intensity. 
In general, the frequency ranges that are preferred for the methods 
described and claimed herein are from about 60,000 Hertz to 100 Hertz, and 
most preferably from about 40,000 Hertz to 400 Hertz. This is in stark 
contrast to most transcutaneous electrical stimulating devices and methods 
which operate in the range of about 50 Hertz to 200 Hertz. Preferably, the 
duration of treatment at a single level of intensity, that is the time 
spent stimulating through a single sweep of frequency parameters, is 1 to 
30 minutes. More preferably, the time is 1-20 minutes and most preferably 
1-15 minutes. The range of acceptable stimulation intensities is not 
critical, but is generally from about zero to 100 volts, and in preferred 
embodiments is zero to 60 volts. The preferred stimulating device operates 
at about 40 mamps, but this too is not critical. What is important is that 
the general method of sweeping through the entire plurality of frequency 
parameters, along the frequency curve, occur for at least two sequentially 
increasing levels of intensity. Thus, for example, in a most preferred 
embodiment, as described further below, the maximum output voltage 
(intensity) of the device is equally divided into ten different intensity 
parameters (or levels); such as 5.7 volts at the lowest parameter (level 
1), 10.4 volts at the second parameter (level 2), and so on up to 57 volts 
at the highest intensity parameter (level 10). While not all intensity 
levels are necessarily used in a single treatment program, those levels 
that are used are used for an entire, single sweep of the frequency curve. 
Turning then to FIG. 1, illustrated is a block diagram of a preferred 
transcutaneous neurostimulator for use in practicing the improved methods 
described herein. This preferred transcutaneous nerve stimulation 
apparatus has digital frequency generation and provides two independent 
channels of bipolar, variable frequency, variable amplitude, and patient 
output signals. These output signals are coupled to the patient via skin 
electrodes, preferably two per channel. The frequency and amplitude of the 
outputs are preferably adjustable via front panel switches, or, in the 
case of frequency, also by a hand-held remote control. LED numeric and bar 
graph displays on the front panel may be used to provide the operator with 
a visual indication of amplitude (intensity) and frequency (bias) 
settings. The device is preferably battery powered and microprocessor 
controlled. Thus, the preferred apparatus is, conceptually, a two channel, 
variable frequency, variable amplitude, square wave frequency generator. 
As discussed in detail below, the apparatus preferably commences its 
operations at a highest frequency output and is reduced at a predefined 
rate, to a lowest frequency as other output parameters are increased 
(amplitude & current). This frequency sweep is preferably repeated over 
each of ten increasing intensity levels. 
Preferably, the transcutaneous stimulator apparatus contemplated for use 
herein has five input/output connectors mounted on the back of the 
apparatus enclosure. These include, for example, an output connector for 
each channel, an input connector for battery charging, an input connector 
for the remote hand-held controller, and outputs for the treatment 
recorder. The battery employed in the apparatus is preferably a 12 volt, 
rechargeable gel cell. It supplies power for the entire system. It is 
recharged by connecting a wall mount charger to the charger input 
connector. Such a battery generally has a life of several hours depending, 
somewhat, upon the bias and amplitude settings used by the patient, as 
well as upon the individual patient load. 
As contemplated herein, the front display of the apparatus is a membrane 
switch overlay with "smoked" transparent windows to allow display viewing. 
Displays include, for example, eight LED numeric digits and two 10 element 
LED bar graphs, with the following variables preferably being displayed: 
Channel 1 Intensity (2 digits plus decimal); Channel 1 Bias (2 digits plus 
decimal plus 10 bars); Channel 2 Intensity (2 digits plus decimal); and 
Channel 2 Bias (2 digits plus decimal plus 10 bars). Two additional LED 
elements are also preferably included on the front panel display, one 
indicating "Power On" and the other indicating "Battery Charging". Each 
channel preferably has five control switches: channel On/Off; Intensity 
Up; Intensity Down; Bias Up; and Bias Down. The membrane switch panel 
connects to the display board, which in turn connects to the 
microprocessor board. Via this connection, the microprocessor can detect 
when a front panel switch closure occurs and appropriately control the 
displays and patient output. 
As shown in FIG. 1, a microprocessor board 20, containing the majority of 
the circuitry, is provided. The microprocessor 20 may be, for example, an 
8 bit Motorola 68HC11 device utilizing external EPROM 22 for program 
memory. The EPROM 22 memory preferably is about 8 K bytes and is 
interfaced to the processor with an address latch and appropriate strobe 
decode logic. The processor clock preferably operates at about 8 MHz and 
is crystal controlled. The processor communicates with the remaining 
circuitry via input/output ports, one of which includes an internal analog 
to digital converter. When the unit is switched on, the processor is 
momentarily at rest and then begins fetching and executing instructions 
from the EPROM memory. As long as the unit is switched on, the processor 
is running (fetching and executing instructions). The main functions of 
the processor are to read the operator control switches and remote 
hand-held controller, adjust the amplitude and frequency of the outputs, 
and send related data to the display board for display. 
In the preferred embodiment, the On/Off switch and the emergency shut down 
switch relay 24 are in series with the positive pole of the 12 volt 
battery. Thus, when either of these switches are Off, no battery current 
flows to the microprocessor board. When On, 12 volts DC is supplied to the 
microprocessor board. The emergency shut down switch circuit employs an 
SCR to latch the relay in or out. Thus, once tripped this circuit is only 
reset by turning the main power off and then back on again. 
The 12 volts is supplied primarily to three areas: a 5 volt regulator 26; a 
DC step up regulator 28; and a low battery detection circuit 30. 
The 5 volt regulator 26 can be a standard linear, series, in-line 
regulator. The output is then a regulated 5 volts and provides the 
operating power supply for the majority of the circuitry (microprocessor, 
memory, display board, etc.). The DC step up regulator 28 is an inductive 
switching regulator used to increase the 12 volt DC input to an 
approximately 40 volt DC output. The switching regulator oscillates at a 
high frequency, varying with load. On one cycle of the oscillation, 
current passes through the inductor building up a magnetic field. On the 
alternate cycle the field collapses, inducing a high voltage which is 
stored in a large capture capacitor. The capture capacitor positive pole 
is the 40 volt output point and is fed back to the switching regulator 
circuit to cause a closed loop regulation of this voltage. The switching 
regulator varies frequency and duty cycle in order to maintain the output 
at 40 volts DC. This 40 volts is the supply voltage for the output stage 
intensity control amplifiers. A low battery detection circuit 30 is also 
provided. It determines when the 12 volt battery drops below a 
predetermined value, then trips the hardware interrupt on the processor 
and forces it to transition to a safe state and shut down. In addition, 
this is signaled to the operator by displaying "bA Lo" or similar 
informative message, on the display board 52. 
One of the main functions of the processor is to monitor the user remote 
control 32 and front panel switches 34. The user remote control 32 is 
preferably a simple linear, slider potentiometer. It is connected across 
power (5+volts) and ground with its wiper forming the output. Thus, its 
output is a DC voltage somewhere between +5 volts and ground depending on 
wiper position. This signal is fed into an analog to digital converter 
input on the microprocessor. The AD converter preferably has a resolution 
of 8 bits. Thus, the DC 0 to 5 volt input is converted to a digital number 
0 to 255. This is then used by the processor to control the output bias 
setting (frequency). It should be noted that bias and frequency are 
inversely related; that is, a bias of 0.0 results in the highest frequency 
and a bias of 9.9 is the lowest frequency. 
Each of the ten front panel switches are connected to an individual 
microprocessor port. The other side of all switches are connected to 
system ground. Also connected to each port is a pull up resistor to +5 
volts. Thus, when the switches are open (unpressed), the port pins sit at 
+5 volts. When a switch is pressed, its associated port pin is forced to 
ground (0 volts). During operation of the preferred apparatus, the 
processor continually monitors these port pins, looking for a key press or 
change in remote control slider position. When detected, the appropriate 
action is taken. 
A second important function of the processor in this preferred apparatus is 
to control the bias (frequency) and intensity (amplitude) of the outputs. 
The outputs are transformer-coupled to the patient. The patient is 
connected to the secondary side of a 1:1 transformer 46, 48 (one per 
channel). One lead of the primary side of the transformer is connected to 
the intensity drive circuitry 36, 38 and the other lead is connected to 
the bias drive circuitry 40, 42. The intensity drive circuitry 36, 38 is 
merely a DC voltage amplifier whose input in 0 to 5 volts, which is 
translated to 0 to 40 volts on the output. The input signal comes from a 
digital potentiometer 44 which is under control of the microprocessor 20. 
Thus, the processor 20 sends a digital byte to the digital potentiometer 
44. The potentiometer 44 converts this into a voltage between 0 and 5 
volts depending on the intensity setting. The intensity drive circuitry 
36, 38 converts this into a voltage between 0 and 40 volts, which appears 
on one end of the transformer 46, 48 primary. 
The bias drive circuitry 40, 42 is preferably a transistor power switch 
which pulls the other end of the transformer primary 46, 48 to ground when 
it is on, or lets it float (unconnected) when it is off. Thus when this 
switch is on, current flows through the primary at a level determined by 
the intensity setting (0 to 40 volts). When this switch is off, no current 
flows through the primary. The input to the bias drive circuitry is 
preferably a square wave created by a dual channel programmable timer 50. 
The timer is connected to the processor/memory bus and is programmed by 
the processor 20 to create a specific square wave frequency based on bias 
setting. The microprocessor "E Clock" forms the clock signal for the 
programmable timer (2 MHz) 50. Thus, the processor 20 determines bias 
setting from front panel 34 switch presses and hand controller position 
32. Using the bias setting the processor 20 determines desired frequency 
from a currently selected frequency look up table within the processor. 
The processor 20 then outputs the necessary commands to the programmable 
timer 50 to create a specific frequency output. It should be noted that 
since the frequency base to the timer is 2 MHz, the resolution of 
frequency period is 0.5 micro seconds. The square wave output from the 
timer 50 then drives the digital switch which causes current to flow on 
and off, at the desired frequency, through the transformer primary. In 
other words, on one side of the transformer primary is a DC voltage, 0 to 
40 volts, set by intensity; on the other side of the primary is an on/off 
switch, operating at the bias setting frequency. The processor 20 also 
preferably has an over riding "stop" line (not shown) to each channel 
which can force the bias drive circuitry off. In addition, while 
monitoring the hand controller 32 to determine bias setting the processor 
computes rate of change of hand controller position 32. If this rate of 
change exceeds a preset limit an error is detected and the outputs are 
switched off. This permits detection of, for example, a hand controller 
broken ground wire, or an accidentally moved (bumped) hand controller. 
The display board 52 contains all the light emitting diode (LED) numeric 
and bar graph displays 54 in addition to the display drivers 56 and two 
input/output connectors (not shown). One connector mates with the membrane 
switch panel to bring front panel switch connections into the system. The 
other connector connects to a 20 pin ribbon cable which connects in turn 
to the microprocessor board. Power for the display board, front panel 
switch signals, and LED drive signals all flow through this ribbon cable. 
Finally, in this most preferred embodiment of the apparatus, there are 
three driver integrated circuits on the display board. These provide 
direct drive for all the bar graph and numeric LED displays on the board. 
These drivers form a serial data link to the processor via the ribbon 
cable. Thus, the processor decides which LED's should be on and shifts out 
the appropriate serial data word to effect this. To conserve battery life 
the LED's are multiplexed on a 50% duty cycle, that is, at any one time, 
only half the LED's are on. This multiplex rate is faster than the human 
eye can perceive and thus the appearance is that all displays are 
constantly illuminated. To further conserve battery power the bar graph is 
preferably lighted in a climbing, one bar-at-a-time mode. All of the 
numeric, multiplexing, and bar graph decoding preferably takes place in 
the processor 20 under software control. The drivers merely turn on LED's 
bit for bit as instructed by the processor 
Referring now to FIG. 2, illustrated is a frequency curve preferred for use 
in treating tremor disorders, such as essential tremor and tremors 
associated with Parkinson's disease. It is this same curve, then, that is 
used at every intensity level at which stimulation is provided to the 
patient. Thus, at each intensity level, a range of stimulation frequencies 
is provided to the patient, beginning at about 40,000 Hz and decreasing to 
about 400 Hz, at the rate indicated by the frequency curve illustrated in 
FIG. 2. The following detailed example is illustrative of a preferred 
treatment process for tremor disorders. 
First, two pair of self-adhesive electrodes are affixed to the patient's 
skin. Suitable electrodes are well known to those of skill in the art, for 
example Bio-Skin Silver electrodes (Synaptic Corp., Aurora, Colo.). One 
pair is placed bilateral to the spine at C6, with approximately one inch 
between the inner medical borders of the electrodes. The second pair is 
affixed bilateral to the spine at L5, also spaced about one inch from one 
another as measured at the inner medical borders. Both pairs of electrodes 
are operatively attached to the electrical stimulator (i.e. pulse 
generator), which is most preferably preprogrammed with the desired 
treatment program thereby permitting the doctor, other medical or lay 
personnel or the patient his/herself to very easily activate the program. 
The next step is to turn on the electrical stimulator and begin the 
treatment program. 
Generally, when the method is employed to treat, control or prevent a 
disorder selected from the group consisting of essential tremor and 
Parkinson's disease and wherein the step of incrementally decreasing the 
stimulation frequency parameter is performed for a time duration (T), one 
may employ the following sequential steps of a) steadily decreasing the 
stimulation frequency parameter about 70% over the time period 0.1T; b) 
steadily decreasing the stimulation frequency parameter about 5% over the 
time period 0.1T; c) steadily decreasing the stimulation frequency 
parameter about 20% over the time period 0.7T; and d) steadily decreasing 
the stimulation frequency parameter the remaining about 5% over the 
remaining time period of 0.1T, wherein the percentages are of the total 
frequency parameter range from the lowest frequency parameter to the 
highest frequency. 
Electrical stimulation preferably begins at the highest stimulation 
frequency and lowest stimulation intensity for the programmed treatment. 
As illustrated in FIG. 2, the highest, and therefore initial, stimulation 
frequency is preferably about 40,000 Hz for treatment of tremor disorders. 
Preferably, the frequency curve of FIG. 2 is administered in a plurality 
of individual stimulation frequency parameters, and most preferably in 
about 100 different frequency parameters. These 100 different stimulation 
frequency parameters may, for example, be numbered as 0.0 through 9.9 (or 
0.1 through 10.0). Preferred settings for some of the 100 points along the 
frequency curve illustrated in FIG. 2 are as follows: 
TABLE C 
______________________________________ 
Frequency Parameter Number 
Frequency (Hz) 
______________________________________ 
0.0 40,000 
0.5 21,000 
1.0 10,000 
1.5 9,100 
2.0 8.500 
2.5 8,000 
3.0 7,500 
3.5 6,500 
4.0 6,000 
4.5 5,500 
5.0 5,000 
5.5 4,500 
6.0 4,000 
6.5 3,500 
7.0 3,000 
7.5 2,500 
8.0 2,000 
8.5 1,500 
9.0 1,000 
9.5 500 
9.9 400 
______________________________________ 
It is preferred to use at least about ten intensity levels, wherein the 
total output voltage available is equally divided among the ten (or more) 
levels. The maximum voltage output is not critical, but is preferably in 
the range of about 40-150 volts, and most preferably about 50-100 volts, 
peak to peak. A preferred tremor treatment program, in accordance with the 
present invention is about 45 minutes in duration, delivers stimulation 
according to the above described frequency curve and employs all 10 
intensity levels according to the following schedule: 
______________________________________ 
Intensity Level 
Time (minutes) 
______________________________________ 
1 1 
2 2 
3 2 
4 4 
5 4 
6 4 
7 4 
8 8 
9 8 
10 8 
______________________________________ 
At each intensity level, only one sweep of the stimulation frequency curve 
is performed. Thus, for example, at the lowest intensity level, level one, 
the stimulation frequency is reduced in one minute from about 40,000 Hz to 
about 400 Hz, following the curve illustrated in FIG. 2; whereas at 
intensity level 10, the highest intensity level, the stimulation frequency 
preforms the same pattern of decreasing from 40,000 to 400 Hz, but does so 
in eight minutes. 
A patient, D.P., was treated in the manner just described, except that the 
highest stimulation frequency used was 30,000 Hz. D.P. had a ten year 
history of essential tremor. He suffered bilateral hand tremors. In his 
left hand, the tremors were so bad he could not touch his nose. While 
various drugs had brought D.P. some relief over the years, they slowly 
became ineffective, even at very high doses. D.P. was not a suitable 
candidate for implantation of a brain stimulator and thus, agreed to 
undergo this experimental transcutaneous electrical stimulation program. 
After his first 45-minute treatment, he remained tremor-free for four (4) 
hours. Daily treatments for the subsequent 14 days provided complete 
cessation of his tremors over each 24 hour period. D.P. has been receiving 
such treatment for over a year, and his tremors are still well controlled, 
despite receiving treatment only about three times a week. He has 
described the severity of his tremors as a 2 on a scale of 1-10 with 10 
being the most severe tremors, and 1 being tremor-free. 
Since beginning treatment on D.P., other patients suffering with tremor 
disorders have been treated on an experimental basis. The results, to 
date, have been consistent with those observed in D.P. Both bilateral hand 
tremors and head tremors (titubation) have been successfully treated using 
this new method and device. This is in stark contrast to the brain implant 
devices which have only been demonstrated useful in controlling tremors in 
one hand and not at all in the head. It is noted that, preferably, the 
patient (or doctor or other medical or lay personnel controlling the 
electrical stimulation) may stop the electrical stimulator at any time by 
pushing a single button. This control is important so that the patient 
does not experience unnecessary pain or discomfort during treatment. 
It is believed that among other things, the general method of 
transcutaneous electrical stimulation described and claimed herein 
modulates both the ascending and descending pathways of the nervous system 
resulting in the release of neurotransmitters that then favorably affect 
the brain to control the symptoms of the disease being treated. In the 
case of treatment of tremor disorders, for example, it is believed that 
the thalamus and Basal Ganglion (the thalamocortical circuits) are 
stimulated by this method to provide control of both bilateral tremors and 
head tremors. 
FIGS. 3-5 each illustrate alternative, preferred frequency curves for 
treating various disease states and disorders. For example, FIG. 3 
illustrates a frequency curve particularly useful for treating dementia 
disorders. FIG. 4 illustrates a frequency curve particularly suited to 
treatment of painful degenerative disorders such as fibromyalgia and 
reflex sympathetic dystrophy, and FIG. 5 is particularly useful for 
inducing electroanesthesia. 
As with the method described above for treating tremor disorders, in 
preferred embodiments, the frequencies represented by these curves are 
administered as a plurality of frequency parameters and most preferably 
are administered as about 100 frequency parameters. Also in accordance 
with the general method of the present invention, a plurality of 
stimulation intensities are employed and the entire plurality of frequency 
parameters are administered at each intensity level. 
For example, in treating a patient suffering with a dementia disorder, such 
as Alzheimer's disease, the patient first has two pairs of electrodes 
affixed to the skin in about the same location as described for treatment 
of tremor disorders; that is bilateral to the spine at C6 and L5. The 
leads of the electrodes are operatively connected to the electrical 
stimulator and the appropriate program initiated. As with the tremor 
treatment described above, the stimulation program to be used for treating 
the dementia patient is most preferably preprogrammed so that no 
adjustment thereto need be made by the patient (other than, of course, 
termination of the treatment should such be desirable or necessary). Once 
the electrodes are properly affixed to the patient and the leads connected 
to the electrical stimulator, the unit is switched on. 
Generally, when the method is employed to treat, control or prevent a 
disorder selected from the group consisting of Alzheimer's disease, 
cortical dementia, subcortical dementia and multi-infarct dementia and 
wherein the step of incrementally decreasing the stimulation frequency 
parameter is performed for a time duration (T), one may employ the 
following sequential steps of a) steadily decreasing the stimulation 
frequency parameter about 66% over the time period 0.1T; b) steadily 
decreasing the stimulation frequency parameter about 23% over the time 
period 0.2T; c) steadily decreasing the stimulation frequency parameter 
about 5.5% over the time period 0.1T; and d) steadily decreasing the 
stimulation frequency parameter the remaining about 5.5% over the 
remaining time period of 0.6T, wherein the percentages are of the total 
frequency parameter range from the lowest frequency parameter to the 
highest frequency. 
As previously described, stimulation always begins at the highest 
stimulation frequency parameter and lowest stimulation intensity. The 
program then decreases the stimulation from the highest frequency 
parameter, in this case, preferably about 40,000 Hz, to the lowest 
frequency parameter, preferably 400 Hz, in accordance with the frequency 
curve illustrated in FIG. 3. It is preferred that about 100 different 
frequency parameters be used. The following table provides settings for 
some of the 100 points along the frequency curve illustrated in FIG. 3: 
______________________________________ 
Frequency Parameter Number 
Frequency (Hz) 
______________________________________ 
0.0 40,000 
0.5 21,000 
1.0 12,000 
1.5 10,000 
2.0 8,000 
2.5 6,050 
3.0 4,100 
3.5 3,175 
4.0 2,250 
4.5 2,017 
5.0 1,785 
5.5 1,556 
6.0 1,325 
6.5 1,162 
7.0 1000 
7.5 900 
8.0 800 
8.5 700 
9.0 600 
9.5 500 
9.9 400 
______________________________________ 
A preferred treatment program for Alzheimer's disease, according to the 
present invention, involves slowly stepping up the maximum intensity of 
the stimulation over the course of several treatments. Thus, for example, 
during the first one-hour treatment administered to the patient, the 
stimulation intensity is raised only to level 7 of 10 (which is preferably 
70% of the highest available intensity level). The one-hour treatments are 
preferably administered once a day, and this first level of treatment 
(i.e., wherein the maximum stimulation intensity is only 70% of the 
highest available intensity level) is preferably carried out for about the 
first ten days (or first ten one-hour treatments). The second level of 
treatment, preferably conducted for the 11.sup.th -20.sup.th of the daily 
treatments, increases the maximum intensity level to 8 (80% of the highest 
available intensity level). Treatments 21-30 provide a maximum intensity 
level of 9 (90%), and the remaining treatments include the highest 
available intensity level (10). The following table shows each of the four 
different levels of treatment with the number of one-hour treatments to be 
performed at that treatment level (in parentheses) and provides the 
duration of stimulation at each intensity level within each different 
level of treatment: 
______________________________________ 
Level 1 Level 2 Level 3 Level 4 
(1-10) (11-20) (21-30) (31- ) 
Inten- Inten- Inten- Inten- 
sity Time sity Time sity Time sity Time 
Level (min) Level (min) Level (min) Level (min) 
______________________________________ 
1 1 1 1 1 1 1 1 
2 2 2 2 2 2 2 2 
3 4 3 4 3 4 3 4 
4 8 4 8 4 8 4 8 
5 15 5 10 5 8 5 8 
6 15 6 10 6 8 6 8 
7 15 7 10 7 9 7 8 
8 15 8 10 8 8 
9 10 9 8 
10 5 
______________________________________ 
While a specific rate for moving through the four levels of treatment is 
provided, this is meant to be illustrative only. Individual patients will 
tolerate the sensations associated with the transcutaneous stimulation 
differently. This is particularly of concern when dealing with Alzheimer's 
patients or other patients suffering from dementia, because such patients 
may be unable to communicate their level of comfort or discomfort clearly. 
Thus, the above schedule of treatment is intended as a guide. In practice, 
the doctor or other medical or lay personnel operating the device should 
closely monitor the patient for indications that he/she is becoming 
uncomfortable with the intensity of stimulation being administered. As 
with all the devices contemplated herein, it is preferred that the 
stimulation device include a simple mechanism for terminating stimulation, 
should such be desirable or necessary. 
FIG. 4 illustrates a frequency curve preferred for use in treating painful 
degenerative disorders such as fibromyalgia and reflex sympathetic 
dystrophy, as well as general acute and chronic pain. Fibromyalgia is a 
widespread musculoskeletal pain and fatigue disorder for which the cause 
is still unknown. Most patients with fibromyalgia complain of systemic 
pain, often described as deep muscular aching, burning, throbbing, 
shooting and stabbing pain. No routine laboratory testing is available for 
diagnosing this debilitating disorder. Upon physical examination, patients 
are usually sensitive to pressure in certain areas of the body. Currently, 
diagnosis is made based solely on established criteria relating to the 
severity, widespread locality and duration of the pain. 
Reflex sympathetic dystrophy (RSD) is a very severe form of chronic pain 
believed to affect as much as 10% of the entire population. The chronic 
pain of this syndrome is typified by a marked emotional connotation, such 
as severe anxiety, phobia and/or neuropsychological disturbances in the 
form of sever irritation, agitation and depression. 
As with the specific examples given above for treatment of tremor and 
dementia disorders, treatment of fibromyalgia, RSD and similar painful 
degenerative disorders involves the administration of transcutaneous 
electrical stimulation beginning at a highest frequency parameter and 
lowest stimulation intensity level; decreasing the frequency parameter to 
a lowest frequency parameter by stimulating at a plurality of stimulation 
frequency parameters therebetween; then increasing the stimulation 
intensity level to a next highest intensity level and increasing the 
frequency parameter back to the highest parameter, followed by repeating 
the pattern of decreasing the frequency parameter to the lowest parameter. 
In a most preferred embodiment of treating these degenerative disorders, 
illustrated by the frequency curve of FIG. 4, the highest stimulation 
frequency parameter is 40,000 Hz and the lowest frequency parameter is 
2,500 Hz. As with the previously described examples, the maximum output 
voltage is preferably divided into ten levels. 
Generally, when the method is employed to treat, control or prevent a 
disorder selected from the group consisting of fibromyalgia, reflex 
sympathetic dystrophy, general acute pain and chronic pain and wherein the 
step of incrementally decreasing the stimulation frequency parameter is 
performed for a time duration (T), one may employ the following steps of 
a) steadily decreasing the stimulation frequency parameter about 66% over 
the time period 0.1T; b) steadily decreasing the stimulation frequency 
parameter about 13% over the time period 0.1T; c) steadily decreasing the 
stimulation frequency parameter about 6% over the time period 0.1T; d) 
steadily decreasing the stimulation frequency parameter about 5% over the 
time period 0.2T; and d) steadily decreasing the stimulation frequency 
parameter remaining about 10% over the remaining time period of 0.5T, 
wherein the percentages are of the total frequency parameter range from 
the lowest frequency parameter to the highest frequency. 
Thus, the following table provides several frequency parameters taken from 
the frequency curve illustrated in FIG. 4. As with the similar tables 
provided herein, the frequency parameters are preferably numbered 0.0 
through 9.9, providing 100 different frequency parameters: 
______________________________________ 
Frequency Parameter Number 
Frequency (Hz) 
______________________________________ 
0.0 40,000 
0.5 21,000 
1.0 12,000 
1.5 9,875 
2.0 7,750 
2.5 6,775 
3.0 5,800 
3.5 5,275 
4.0 4,750 
4.5 4,375 
5.0 4,000 
5.5 3,760 
6.0 3,520 
6.5 3,360 
7.0 3,200 
7.5 3,100 
8.0 3,000 
8.5 2,850 
9.0 2,900 
9.5 2,600 
9.9 2,500 
______________________________________ 
Preferably, total treatment times are about 20 minutes and are, ideally, 
administered several times a week. However, weekly treatments have been 
demonstrated to provide noticeable favorable results. As with other 
treatments described herein, the treatment program typically begins with 
more time spent at lower intensities, gradually increasing the duration of 
stimulation at higher frequencies in subsequent treatments. 
FIG. 5 illustrates a final exemplary frequency curve for use in accordance 
with the present invention. The frequency parameters comprising this curve 
have been found to be particularly useful in inducing electroanesthesia 
and nerve block anesthesia, as well as for the general treatment of pain. 
The following table provides exemplary frequency parameters taken from the 
curve illustrated in FIG. 5: 
______________________________________ 
Frequency Parameter Number 
Frequency (Hz) 
______________________________________ 
0.0 40,000 
0.5 25,500 
1.0 11,000 
1.5 9,500 
2.0 8,000 
2.5 7,000 
3.0 6,000 
3.5 4,750 
4.0 4,500 
4.5 4140 
5.0 3,775 
5.5 3,410 
6.0 3,050 
6.5 2,690 
7.0 2,325 
7.5 1,960 
8.0 1,600 
8.5 1,300 
9.0 1,000 
9.5 700 
9.9 400 
______________________________________ 
It will be apparent that where nerve block anesthesia (or 
electroanesthesia) is the goal, a single "treatment" will be performed. 
Generally, one pair of smaller electrodes, for example about 1.25 inches 
in diameter, are placed in the vicinity of the nerve to be blocked. A 
second pair of larger electrodes, for example about 2 inches in diameter, 
are placed bilateral the spine at about C5 or on the opposite side of the 
body from the location of the first electrode pair. Preferably, 
stimulation is begun at a relatively high intensity and is manually 
increased as high as is tolerable to the patient, usually about 70%-90% of 
maximum. The intensity is then held at that level while the program sweeps 
through the plurality of frequency parameters, for at least about 20 
minutes. It is noted that, either a single frequency parameter sweep may 
be performed or a plurality. 
As can be seen from the Figures herein, the frequency curves have a similar 
basically logarithmic shape. Association of specific frequency parameters 
and curve slopes with a specific disorder is preferably determined by 
clinical evaluation. In fact, the different curves exemplified herein are 
useful for treating other diseases and disorders. Thus, it is the 
particular manner of stimulating described herein that makes these methods 
particularly effective, that is the stimulating manner of sweeping through 
the same set of frequency parameters from a high frequency parameter of, 
for example, 40,000 Hz, to a low frequency of, for example 400 Hz, at each 
of a plurality of incrementally increasing stimulation intensities. 
It is believed that the required initial stimulation at a high frequency 
causes rapid depolarization of the cell permitting ideal functioning of 
the so stimulated neurons. Whereas prior art TENS devices and methods are 
believed to stimulate only the large A.beta. fibers of the nervous system, 
it is believed that the present method results in stimulation of the 
A.delta. and C fibers as well as the A.beta. fibers, by providing 
stimulation waveforms that closely mimic natural action potential 
waveforms and/or piggyback on such waveforms. Increases in circulating 
blood levels of various neurotransmitters, such as norepinephrine, 
serotonin, epinephrine, ACTH and beta endorphins, provide evidence of this 
mode of operation. 
As seen in FIG. 6, in one patient, suffering with chronic pain, the levels 
of various neurotransmitters not only increased during the 20 minute 
treatment provided, but continued to measurably increase for the 24 hours 
following such treatment. Note that the y-axis scale on the graph in FIG. 
6 is relativistic. Levels of the neurotransmitters are measured in pg/ml 
for epinephrine and norepinephrine, in pmol/l for ACTH, in ng/ml for 
serotonin and in pg/0.1 ml for beta endorphin. Thus, the graph should be 
used to compare levels of a single neurotransmitter over time not to 
compare levels among neurotransmitters. Thus, by providing electrical 
stimulation at a central location on the body, in accordance with the 
methods detailed herein, the body's natural healing mechanisms are 
systemically stimulated to relieve the symptoms of the nerve-related 
disease condition being treated. 
The examples provided herein are of specific embodiments only and are not 
intended to limit the scope of the claims appended hereto. Those of skill 
in the art will recognize that the preferred embodiments described herein 
may be altered or amended without departing from the true spirit and scope 
of the invention, as defined in the following claims.