Copyright 1996 Lee Kent Hempfling. All Rights Reserved.
KEYWORDS: Pain, model, brain, mental, management, neuron, computation.
ABSTRACT:
Let us say for the sake of argument that for just a moment you are a 1500 amp 12 volt
battery. Your right arm is the positive pole and your left arm is the negative pole. What would
happen should you shake your own hands? Sparks would fly would they not? How would
you feel regarding that contact? Would you not feel a sort of pain? A battery pain so to speak.
If your arms were not touching each other but were through your hands' ability to grasp, each
holding an opposite end of a filament of carbon fiber would not the carbon fiber feel the pain
and in so doing emit an excited state's by-product of light and heat energy? If you were to
grasp opposite ends of a piece of steel wire would you not also feel the pain until the wire
burned up or until you dropped it?
Now let us not jump to any rash conclusions. I am not arguing that a battery or carbon
filament is conscious. I am not arguing that you would make a good or bad battery. I am not
arguing whether you have sense in holding such things while being a battery. I am arguing
that it is easier to understand what pain is when it is placed in its proper perspective. The
following is the application of the human brain mathematical model as it relates to pain.
1.0 CHALLENGING THE MOUNT
1.1 What cognitive science should be aiming at is producing an explanation of the facts that is concise, that covers as much of the data as possible, and that
stands up well to furt her tests. This is just, of course, what we demand of any scientific theory. And we sh ould expect that the resultant theory will end up denying the face- value interpretation of some kinds of introspective reports, even when those reports are repeated by all comers. This is again strictly in parallel with other sciences: almost all of our theories describe some cases where appearances are simply deceptive (e.g., almost every measurement of a star's location will be misleading within some small angular distance from the sun). (Korb , 1993)
1.2 So what are the face value interpretations of pain? Could the appearances of pain be
simply defective? Could the underlying method of the pain sensation not be at all what we've
come to accept?
2.0 IN SHINING ARMOR
2.1 Let us begin to answer these questions with a plain given: To a battery, off means no
power. A battery with no power is simply no good. So when the battery might have its
terminals crossed so as to short out the thing it will if permitted to remain so, become
overheated, drained of its power and therefore useless as a battery. But now let us place the
same consideration toward a living thing.
2.2 To a living thing, off means dead. A living thing that is dead is simply no good. Besides
no longer being a living thing. So just as in the battery the object of the power of a living
thing would be not to permit it to cross poles and short itself out. What would happen? The
living thing can feel' the results of improper conditions. We call that feeling... pain.
2.3 If the functional role of pain, for example, is to inform us of injury and to motivate us to avoid such injury in the future, there seems to be no reason to disbelieve that such a role could be occupied by some non-conscious processes. (Korb, 1993)
2.4 The current condition of the definition of pain is widespread but almost always details the
purposes for pain as seen from the perspective of the sufferer. What did the pain make the
sufferer learn? What lesson was determined to have been taught by the pain? It seems the
lessons derived from the experience of pain have then in turn become the definition of pain
itself.
2.5 For the correct and acceptable definitions of pain it is required to turn to the most
acclaimed source for such (Mersky et.al. Classification of Chronic Pain, Second Edition, IASP
Task Force on Taxonomy, IASP Press, Seattle, 1994)
Pain
An unpleasant sensory and emotional experience associated with actual or potential tissue damage, or described in terms of such damage.
Note: Pain is always subjective. Each individual l earns the application of the word through experiences related to injury in early life. Biologists recognize that those stimuli which cause pain are liable to damage tissue. Accordingly, pain is that experience we associate with actual or potential tissue damage. It is unquestionably a sensation in a part or parts of the body, but it is also always unpleasant and therefore
also an emotional experience. Experiences which resemble pain but are not unpleasant, e.g., pricking, should not be called pain. Unpleasant abnormal experiences
(dysesthesias) may also be pain but are not necessarily so because, subjectively, they may not have the usual sensory qualities of pain.
Many people report pain in the absence of tissue damage or a ny likely pathophysiological cause; usually this happens for psychological reasons. There is usually no way to distinguish their experience from that due to tissue damage if we take the subjective report. If they regard their experience as pain and if they report it in the same ways as pain caused by tissue damage, it should be accepted as pain. This
definition avoids tying pain to the stimulus. Activity induced in the nociceptor and nociceptive pathways by a noxious stimulus is not pain, which is always a psychological state, even though we may well appreciate that pain most often has a proximate physical cause. (Mersky et.al. 1994)
2.6 An unpleasant sensory and emotional experience associated with actual or potential
tissue damage, or described in terms of such damage. That sounds like a description of the
effects of pain more than of pain itself. But it will be observed here that pain is described as
the perception of its effects would dictate. What then is the actual underlying protocol that
permits pain to be felt at all? For the beginning of this aspect we again turn to Mersky et.al.
1994 for definitive terms of specific pains and for clarification of the terminology used in the
study of pain:
Allodynia
Pain due to a stimulus which does not normally provoke pain.
Analgesia
Absence of pain in response to stimulation which would normally be painful.
Anesthesia dolorosa
Pain in an area or region which is anesthetic.
Causalgia
A syndrome of sustained burning pain, allodynia, and hyperpathia after a traumatic nerve
lesion, often combined with vasomotor and sudomotor dysfunction and later trophic
changes.
Central pain
Pain initiated or caused by a primary lesion or dysfunction in the central nervous system.
Dysesthesia
An unpleasant abnormal sensation, whether spontaneous or evoked.
Hyperalgesia
An increased response to a stimulus which is normally painful.
Hyperesthesia
Increased sensitivity to stimulation, excluding the special senses.
Hyperpathia
A painful syndrome characterized by an abnormally painful reaction to a stimulus,
especially a repetitive stimulus, as well as an increased threshold.
Hypoalgesia
Diminished pain in response to a normally painful stimulus.
Hypoesthesia
Decreased sensitivity to stimulation, excluding the special senses.
Neuralgia
Pain in the distribution of a nerve or nerves.
Neuritis
Inflammation of a nerve or nerves.
Neurogenic pain
Pain initiated or caused by a primary lesion, dysfunction, or transitory perturbation in the
peripheral or central nervous system.
Neuropathic pain
Pain initiated or caused by a primary lesion or dysfunction in the nervous system.
Neuropathy
A disturbance of function or pathological change in a nerve: in one nerve,
mononeuropathy; in several nerves, mononeuropathy multiplex; if diffuse and bilateral,
polyneuropathy.
Nociceptor
A receptor preferentially sensitive to a noxious stimulus or to a stimulus which would
become noxious if prolonged.
Note: Avoid use of terms like pain receptor, pain pathway, etc.
Noxious stimulus
A noxious stimulus is one which is damaging to normal tissues.
Pain threshold
The least experience of pain which a subject can recognize.
Note: Traditionally the threshold has often been defined, as we defined it formerly, as the
least stimulus intensity at which a subject perceives pain. Properly defined, the threshold
is really the experience of the patient, whereas the intensity measured is an external event.
It has been common usage for most pain research workers to define the threshold in terms
of the stimulus, and that should be avoided. However, the threshold stimulus can be
recognized as such and measured. In psychophysics, thresholds are defined as the level
at which 50% of stimuli are recognized. In that case, the pain threshold would be the level
at which 50% of stimuli would be recognized as painful. The stimulus is not pain (q.v.) and
cannot be a measure of pain.
Pain tolerance level
The greatest level of pain which a subject is prepared to tolerate.
Note: As with pain threshold, the pain tolerance level is the subjective experience of the
individual. The stimuli which are normally measured in relation to its production are the
pain tolerance level stimuli and not the level itself. Thus, the same argument applies to
pain tolerance level as to pain threshold, and it is not defined in terms of the external
stimulation as such.
Paresthesia
An abnormal sensation, whether spontaneous or evoked.
Peripheral neurogenic pain
Pain initiated or caused by a primary lesion or dysfunction or transitory perturbation in the
peripheral nervous system.
Peripheral neuropathic pain
Pain initiated or caused by a primary lesion or dysfunction in the peripheral nervous
system.
2.7
An unpleasant sensory and emotional experience associated with actual or potential tissue damage, or described in terms of such damage.
But what IS pain? What is the pain itself caused by? We know and can be assured that the
powers of such have every indication of what pain looks like, feels like and how it is displayed
and what circumstances permit the feeling of pain but there is no definition of what pain
actually is.
2.8 It is accepted that pain comes in varying degrees of intensity. That it is possible to be
experienced from just about every point in the body (that has an input receptor of some sort.)
While pain research centers on alleviating the pain cognitive and neural science looks for the
pain processing center of the brain. But since every part of the brain can permit pain to be felt
wouldn't a pain center have to be connected to every part of the body? Isn't such a notion
slightly ridiculous?
2.9 An unpleasant experience...... indeed. Especially when one considers that the people who
should know aren't even directing the definition at defining just at observing.
3.0 DRAGON SLAYER
3.1 What causes the battery to short out? Crossed poles... Equal amounts of positive and
negative cancel out both when brought in direct contact. Have you given thought as to what
the battery would feel like when this happened? Would it not experience pain? Of course it
would. If it could.
3.2 Pain then needs to be defined by what permits it to occur.. What exactly happens to
allow pain to be felt at all. What underlying mechanism of the brain or body actually
accomplishes the sensation of pain? To examine this we need first to examine the
methodology of pain chemo-treatment:
3.3 From: Introduction to Pain; University of Pennsylvania Medical Center
The World Health Organization (1987) states that "analgesic drugs are the mainstay of cancer pain management" and advocates a three-step "analgesic ladder" for decision
making. Step one includes the use of a non-opiod drug with or without an adjuvant drug (e.g. acetaminophen +/- amitriptyline).If pain persists or increases, pain management moves to step two, a weak opioid plus a non-opioid, with or without an adjuvant drug (e.g. acetaminophen, codeine +/- carbamazepine). If pain persists or increases, pain management moves to step three, a strong opioid, with or without a non-opioid, with or without an adjuvant drug (e.g. morphine +/- acetaminophen +/- dexamethosone).
Non-narcotic pain agents are best used for mild cancer p ain. This category includes aspirin,acetaminophen, and non-steroidal anti-inflammatory drugs (NSAIDS). Non-narcotic agents may also be used to potentiate the effect of narcotic analgesics in patients with severe pain. However, these agents have a ceiling effect: increasing the dosage beyond a certain point doesn't produce additional pain relief.
Narco tic analgesics (opioids) are used for the treatme nt of moderate to severe cancer pain. They are categorized as either narcotic ago nist or narcotic agonist-antagonist drugs. One model explaining the action s and effects of the opioids, the Multiple Opioid Receptor Theory, proposes that narcotic agonist drugs, such as morphine and codeine, bind with specific opiate receptor sites. There are three kinds of receptor sites, or portions of the nerve cell to which a drug can bind: the mu receptor associated with analgesia and respiratory depression; the kappa receptor with sedative
effects; and the sigma receptor with psychomimetic effects.
Although the Multiple Opioid Receptor Theory is s till evolving and does not yet completely explain narcotic analgesia, pure narcot ic agonists such as morphine and codeine are thought to occupy the mu receptor without antagonizing activity at the other receptor sites. Narcotic agonists-antagonistsoccupy the kappa receptor for pain relief which also antagonizing the effects of pure agonists at the mu receptor. Three agonist-antagonists are butorphanol, nalbuphine, and pentazocine.
Adjuvant analgesic drugs are also used to treat c ancer pain. This group includes amphetamines, anticonvulsant agents, phenothiazines, tricyclic antidepressants, steroids, antihistamines, andlevodopa. Although their exact mechanisms of action for pain relief are not well understood, these drugs relieve pain when used alone or in combination with other non-narcotics or narcotics.
3.4 Examining the stages of pain:
1)external stimuli aggravate
2)receptor transmits pain signal
3)brain accepts signal
4)registers as pain sensation
5)causes motor function to avoid pain
5a)motor function reduces with consistency of pain
3.5 Taking one stage at a time:
1)External stimuli aggravate..... Some people may refer to this as the cause of pain. Example: A pin sticks the finger; the pain is caused by the pin puncturing the skin of the finger.
1a)I argue that this is NOT the cause of the pain. It is the motivation of the cause.
It is what causes the cause to take place. Without it the ability to sense pain still
remains so the cause of pain does not rest with the motivation it rests with a
internal procedure that in some way is violated and in return permits the
Sensation of pain. Which was motivated by the pin's puncture of the skin.
2)Receptor transmits pain signal.....this is where the drug therapy is centered. Since
the process that permits pain to be transmitted following the motivation
to cause the permission of the pain sensation is always possible simply
awaiting motivation drug therapy has not targeted the process that permits
pain to be motivated nor the process that permits pain to be felt it has
targeted the process that permits the signal meaning pain to be transmitted
to the brain where the awareness of pain is then prohibited or reduced.
3)Brain accepts signal.......if no drug therapy has intervened in the transmission of
the pain signal the brain will accept the signal and register that a pain
signal has been sent. The brain accepts this pain signal through the same
nerve pathway as normal non pain signals are transmitted. That means
that the signals normally sent to the brain contain information in a particular
form and that pain is the extreme of that form.
4)Registers as pain sensation.......what then is the difference between normal
signal levels and pain signal levels? Referring once again to the battery
example originally given in this paper: consider this:
The signal transmitted by the sensor to the brain is sent through
A nerve that is insulated. The signal is of an electrochemical nature
In that it sends values. The value is represented by the extremes of
Non sensory perception to sensory perception overload (which
Means the sensor's positive and negative values are not yet past
Equal levels (which would cause no level at all and therefore SHOCK)
But are instead approaching the equal level similar to the battery
Example where the less resistance between the poles the more the
Crossing and shorting of the circuit the more the power is drained and
The more the sensation of pain is possible.
The brain then accepts that variable value level of transmitted sensor signal
and accomplishes its process of computation and manipultation of the signal.
5) Causes motor function to avoid pain.... the amount of motor function will be directly
proportional to the amount of the signal value. Until the signal value begins to
approach the pain threshold where signals are of such intensity that they
approach shorting out the connection and therefore cause sluggish to
finally immobile reaction of motor functions.
5a)Motor function reduces with consistency of pain.......this is accomplished
as the values are processed in the brain and the more a value is supported
By repetitive input the more IT becomes the normal value. This applies to
not only pain but to learning as well. In the pain aspect though this can
be described as an increase in the pain threshold. It is accomplished by
the brain's computational procedure.
4.0 THE LANCE
What the drugs do......
4.1 Amphetamines, anticonvulsant agents, phenothiazines, tricyclic antidepressants, steroids,
antihistamines and levodopa effect the brain's neuronal processing ability by essentially
corrupting the values used in that computation. The corrupted values are therefore less
intensity than the pain signal and in many cases the pain is seemingly reduced. They work on
neurons throughout the body but are felt to be sensitive within the brain as the brain is where
the actual pain is essentially felt.'
4.2 Receptor drugs such as narcotic analgesics (opioids) etc. function by either eliminating
the transmission of the signal or by inhibiting the transmission of the signal thereby lowering
its excessive level. Depending upon the receptor attached by the design of the drug the
effects will be either to eliminate the sensation of touch at all including any pain, reduce the
sensation of the pain through the reduction of the level at the transmission site or to block the
opposite side of the sensor's value stimuli. Which means to effectively cut off the receptor
from a power source. This function occurs at the motivation site. The location of the pain's
initial motivation.
4.3 Non-narcotic pain agents such as aspirin, acetaminophen, and non-steroidal
anti-inflammatory drugs (NSAIDS)work within the brain and as such are used in conjunction
with narcotic analgesics to enhance the effect. But since the act of these non narcotic agents
is to interfere in synaptic transmissions the effect is restricted to the level of the individual
drugs influence. Meaning that a pain sensation sent from a sensor to the brain that meets up
with a non narcotic pain agent will experience a restricted access to the neuron (thereby
sending a less than extreme value for computation.) But as soon as the pain level increases
that restricted access is not increased so the excess pain level is passed through to the neuron
and experienced as an increase in pain over the original sensation when it is in fact an
overload of sensor (thereby sending less of the new sensation but essentially covering the
point that a sensor overload is possible.).
5.0 KNIGHT SCHOOL
How the sensation of pain is accomplished......
5.1 Understanding the protocol of a particular cell type is difficult to do considering that such
examination must extrapolate a computational process from a chemical process... this
chemo-computational procedure is best explained from a comparative viewpoint:
5.2 The mathematical model depicts a neuron as a computational device. Just as the neuron
is the primary cell of the brain the model depicts the neuron as the primary component in the
computational process of the brain.
5.3 There are, of course, differing opinions as the method of the neuron's computational
ability. There is the notion that the neuron is computational since it fires or does not fire. That
would make the neuron a binary process and therefore all of the brain would be a binary
computer. That is not the case. Then there is the inference (proposed by Stuart Hammeroff
and Roger Penrose in Shadows of the Mind) of that the neuron is a kind of factory with a
skeletal structure containing microtubules and that those microtubules act as bit managers
and create a byte of data (which would also be binary) which is then moved ahead by the
neuron.
5.4 The Penrose-Hammeroff speculation is the closer of the two to the actual neuronal activity
protocol. But where the neuron does utilize the microtubules as a sort of collection point for
assembling a value the value is not a bit or a byte. It is not binary. It is variable.
5.5 The collection point within the microtubular's skeleton structure is where the signal having
been received by the neuron from one synaptic connection is stored (referred to as charged)
while it awaits a signal from another synaptic connection. That second signal is applied to the
stored value and the action that ensues is a computation where the mean sum of the values
of both signals is arrived at in a comparison process of (((P-N)/2)+N)... With P= one signal and
N= the other signal.
5.6 The result of that computation then acts as a code for the structure of the electro-chemical
transmission through the axion to the next level of computation (the next neuron.) That
description is a rather simplistic dissertation of a more complex protocol but it will suffice for
the purpose of this demonstration.
5.7 What then causes pain? First it is imperative to become aware of the method of the
process of the neuron . To begin let us make an assumption that is fairly easy to justify. To a
living organism, off would be dead. A simple statement but often ignored. That would mean
that every pathway of processing within the brain must at all times be essentially ON or that
part of the brain (no matter how small it may be) will then be OFF and since OFF is dead one
can not turn it back on.
5.8 The neuron itself must remain in an ON state in order to accept the data values from
synaptic inputs. Much as your computer must remain on for you to use the hardware within
it to use the software it needs to be useful. Even your binary computer would be "dead" if it
used the binary system for everything.
5.9 The solution to the problem of staying alive while adjusting signal values is simple. In a
typical electronic circuit the ground or negative is stable and the positive side is varied to
create the voltage differences required for manipulation of the output of the device. In the
neuron and the entire brain this process is reversed. The positive side is stable and the
negative side is variable.
5.10 What this does is present the ability of a trainer system with ON always being there and
OFF never being there until it turns literal. The neuron then has a stable positive and signals
that are varied by the variable negative. The variation of the negative is accomplished at the
input receptor and the initial value splitting circuitry of the brain. The signal value within the
neuron is a voltage but it is based in the stable positive of the initial circuit connections to the
input receptors. Which makes electronic probes directly attached to the brain a painful and
damaging experience.....
5.11 The neuron has the ability to compute from near off to near equal. Near off is no
negative value sent from the input receptor. Leaving the current value of the neuron's signal
to be unaffected. Near equal is the negative value of the input receptor being so strong that
it is applying no resistance to the signal and the signal is just about canceled out by the
crossing of the positive and negative power poles. Which results in another off when
exceeded. So the neuron, functioning in a trainer system computes from near off to near off
with variable values of applied resistance (from the input receptors) in between that set up
the value of the signal's amplitude.
5.12 For more on the amplitude and frequency modulation protocols see "On The
Ramifications of Replicated Intelligence," "On The Comparison of Dissimilar Concepts" and
"The Biological Clock," all previous publications of the author.
5.13 When the neuron is receiving signals from the input receptor's pathway that are just
about off the input represents hardly any stimuli. But when the neuron is receiving a signal
value that approaches the equal state it represents an overload of stimuli and is crossing the
poles of the negative and positive sources. This is the cause of pain.
5.14 One aspect of the pain value as described above is the result it will have on
computation. The pain value has a value that is near equaling a short circuit so the
computational result from that value will be hardly any resistance and a large voltage
(compared to and relational to the extremely small normal voltages of the brain.) But as soon
as the resistance is no longer there at all (full input overload) there is no value of the signal
and it registers as no comparison in the neuron. Enough of that process and shock will be the
result and finally if it sets up a continuous loop of the no value signals a coma will be the
result. (Hempfling 1995)
5.15 While the no value of the signal is being processed no memory is being made of the
pain. This is why a severe enough pain can not be remembered. Memories will abound of the
coinciding events such as emotional condition and the effects of the cause of the pain and the
events leading up to it but there will be no memory of the pain itself. (Hempfling 1995)
5.16 Try it yourself. You will not be able to recollect a pain no matter how severe it is. You
will by remembering the circumstances of the event be able to remember the act of the pain
but the pain itself will not be there. After you consider that thought remember the last time
you ate a strawberry. Taste its texture, its flavor. Smell the aroma of the strawberry. This you
can do as the values of the memory of each is less than the short circuited values of
pain.(Hempfling 1995)
5.17 While there is no memory being made of the pain the opposite is true of the physical
activity involved. Remember the time in the beginning of this paper when you were a battery
and sparks flew when you crossed the two opposite poles of your arms? Pain is the result of
that electro-shock. In the body it is an electro-chemical shock that gives the sensation of the
pain at the site of the input receptor. Even though the pain is actually computed in the
brain.(Hempfling 1996)
6.0 THE MAIDEN'S SCARF
6.1 This explanation is the result of the mathematical model of the human brain (Hempfling,
1996.)
6.2 The model has been challenged as proof is not readily available by simply running the
maths.
6.3 There are only two ways to prove the formula.
1: Build the machine the formula permits so that it will speak of
itself and declare itself to be intelligent and conscious and through
its own voice will explain how it functions in relation to how it is
made in relation to how the human brain is made. Since the formula
is to construct a hardware only machine there is no programming
so there can never be any accusation that what it accomplishes is
through its programming instructions.
This first option is supported by works like this one and the many other
papers written to show the application of the maths to specific everyday
results of the brain showing that through a mathematical understanding
of the brain's computational protocols the results can be explained.
OR
2. Dissect a living human brain one neuron at a time registering the
values of the signals compared to the mathematical model's projections
and map the connectivity of the pathways to match the model's
Schematic projections and mapping the synchronicity firing patterns of the biological clock's influence. Of course this option will cause the death of the
volunteer subject.
So far there has not been any volunteers.
6.4 So the process continues with this paper and more to come along with the many already
published to impress the accuracy of the model's predictions of mental activity in hopes that
one day the machine will be built to clear it up once and for all.
REFERENCES:
1) Korb, Kevin B.; Stage Effects in the Cartesian Theater: A review of Daniel Dennett's
Consciousness Explained Copyright Kevin B. Korb 1993 PSYCHE: an interdisciplinary journal
of research on consciousness 1(4), December 1993. Filename: psyche-93-1-4-review-1-korb
ISSN: 1039-723X/93
2) Merskey H. & Bogduk, N.; Editors: From: Classification of Chronic Pain, Second Edition,
IASP Task Force on Taxonomy, IASP Press, Seattle, 1994, pp. 209-214. Revised
terminology from first publication in 1979 (Pain, 6, 249-252)
3) Buhle,E. Loren Jr.; Introduction to Pain; University of Pennsylvania Medical Center
Copyright 1994-1996, The Trustees of the University of Pennsylvania
