Exponential Evocation

All evocations are NOT created equal. This article discusses another of the Central Pain phenomena which has been defined more precisely by the surveys.

The idea of hypersensitization is no triviality. The concepts discussed here show just how important Central Pain subjects may be as models of hypersensitization, when inhbiition of signal by the brain fails, the Wall/Melzack “Gate” is left open, and the principle of GAIN becomes one of the dominant characteristics of neurotransmission.

Where does the energy for this excitation come from? It comes from the electrical power of ions manufactured by chemical processes of the kinases, the energizing chemicals of the body. There was once a stunt at the World Fair where a long distance radio transmission was made to the President of the United States, which was powered by electric eels. Living nerve tissue can generate enormous power. We have more than sufficient ionic electical power to drive an individual into deep pain in the tender, delicate fibers of the nervous system. This process is called, “Central Pain.”

When brain or cord neurons are injured, repair factors (such as TNF-1, BDNF, or GDNF) from surrounding glial cells trigger outpouring of chemicals which cause the chromosomes to pour out kinases (Such as MAPK) and other regrowth/repair factors. In a process still being worked out, the chemicals produced are often identical to those of inflammation and the immune process.

The resulting signal in nerves still able to transmit is “hypersensitized” which means the frequency of their firing is exceedingly greater than normal and that they fire at a considerable frequency when no stimulus is present, ie. automatically. This is a recipe for torture. Scientists call this “Exciter Toxicity”. These are being poisoned, as it were, by pain chemicals. The neurons are being “burned” in a manner of speaking, by the chemicals or acids, keep trying to repair it, but remain sensitive, just as sunburned skin is not normal skin–it is hypersensitized. This hyperfrequency of firing is reduplicated in the thalamus which receives the message as “bursts” of signal. The thalamus writes software on the fly which is attached to any signal that goes on up to the cortex (gray matter of the brain). The software not only markedly increases the gain on the signal, but also informs the brain the signal was “painful” to the thelamus, apparently because it produced a outpouring of acids related to arachidonic acid, leukotrienes, and other eicosanoids/cytokines. The very consistent use of “like acid under my skin” to describe dysesthetic burning would likely be even more frequent if CP subjects were not also trying to convey that there is a MIX of pain sensations going on, leading them to use varied descriptors.

It is as if the thalamus and brain WANT to detect this signal, since attempts to lower the pain often result in further increases in gain by the brain. Thus, we recognize that the pain is indeed “CENTRAL”, the brain is driving it. The brain “believes” that it must be aware of anything causing pain. Hence, the well known fact that CP subjects MUST be kept in a stress free environment, to quiet the brain, and diminish its attentiveness, or gain.

Therapies on the immediate horizon involve shutting off the Calcium channels which contribute to the upswing in the action potential (or nerve spike), mostly the N type, and create the chronic pain signal. Killing neurons which contain the VR-1 calcium channel with resiniferitoxin from the cactus, euphorbia resinifera, (or with pseudomonas exotoxin) does stop neuropathic pain, but leaves normal pain inteact. The problem for CP is that some of these channels are necessary for functions other than pain. Very selective measures must be sought, probably to link resiniferatoxin or the pseudomonas exotoxin to an antibody to some protein unique to chronic pain neurons or channels, to kill chronic pain, but retain such things as good memory.

Such antibody/toxin ligands are not rare in medicine, but the NIH needs money to develop them. (Write your elected representatives). A way must also be prevented from causing the brain to simply increase gain further in order to maintain what it mistakenly thinks is necessary pain. The brain does not like to be shut off from its environment and considers pain to be an important survival factor. One other possible therapeutic route is to kill all the fetal sodium channels, such as Nav1.3, which appear pathologically in CP but not in the neurons of normal adults, who have Nav1.8 channels, for normal pain. Oversimplifying, calcium shapes the signal into pain excitation, and sodium drives it.

Since the brain tends to read the numbers of neurons firing, rather than one neuron, the hypersensitization of many cells puts the CP subject in harm’s way for increased pain from the slightest of events. The pain of evocation can be severe enough to put a person with an intact motor unit into paralysis, or make a young person move at a considerable pain cost. Simply sitting can cause terrible confinement cramps. All of these pains are capable of evocation or elicitation from amazingly slight stimulation. In no area is evocation a greater problem than light touch, which can be a flame to someone with CP.

The surveys reveal that identifiable levels of hypersensitization occur. Normal pain has gradations too of course, as does central pain. However, the clinical patterns of CP have a stepwise compartmentalization distinct from simple gradation, which undoubtedly have a physiologic/anatomical origin. Scientists sometimes refer to stepwise groups as part of definable quantities, or “quanta”. The stepwise compartmentalization in CP is not airtight, but has nevertheless been referred to as “quantal”, meaning that the different categorizes should be identified, named, and studied.

While keeping in mind that simple gradation also occurs in CP, it is helpful in evaluation and identification of neuropathic elements to be aware that there is a semblance of “steps” in hypersensitization in Central Pain. This pattern occurs only in what is called “Spinothalamic” CP, which means essentially the dysesthetic burning related to touch or superficial sensibility. There is also something like steps in the muscle pains, but these are essentially temporal steps, with phases of muscle pain which occur in time. These begin with constant cramp, then burning in the muscle bellies with loading, transition to aching which is quite durable, and then evolve into soreness as late as one day after the exertion or uncomfortable position.

Many of those with muscle pain also have a constant state, such as tightness, or a severe cramp in one area that never really leaves and is much worse when factors have made the other muscle pains, such as the soreness, worse. The lightning pains which also occur in muscles have their own set of rules, often beginning with a jolt which may involve sudden movement which can seem a minor variant of the violent movements of autonomic dysreflexia. The confusion is mainly due to a poverty of language, since these are two different entities.


The National Institutes of Health, which is generally held to contain the finest physicians in the world, or else to maintain contacts with those who are, do NOT indicate that burning dysesthesia can be satisfactorally treated, and lesser clinicians are not likely to exceed the NIH. Once this is admitted, needed research money will be allocated. Need must be acknowledged before the problem can be solved. Patients must discipline themselves when speaking of Central Pain to their caregivers to make sure that the pain relieved is actually neuropathic and not structural, AND that the pain relieved is precisely described, so that relief of posterior column shocks and muscle pains is not mistaken for relief of spinothalamic burning. Muscle hypersensitivity should not be regarded as mysterious at all. It is seen in normal (nociceptive) pain all the time from what has been mistakenly called “lactic acid buildup”.

Take any aging executive and ask him to walk several miles, and at the next day, his legs will have pain if he tries to walk ten feet. A similar phenomenon exists in Central Pain, except that the hypersensitization is always present and so the ten feet are painful right from the start. Conceptions of Central Pain must always factor in the extreme hypersensitization which already exists in the injured nervous system. The evocation which is superimposed is similarly well beyond ordinary human experience. The result is pain from touch, movement, bladder filling, rectal filling, and a myriad of other sensory experiences which normally are not painful at all.

Superficial and visceral sensibilities run in separate nerves (somatosensory vs. autonomic) in the body but tend to join at higher levels. That BOTH systemsThese experiences pertain to the superficial sensitibilities in the case of spinothalamic pain, but to visceral sensibilities in the case of pain from hollow organs and blood vessels. This also should not be so mysterious, since anyone with a severe sunburn knows that the simple act of wearing a shirt would be intolerable. In Central Pain, the evocation from wearing a shirt is also much greater, just as is the hypersensitization. IF circulation is cut off, our blood vessels remind us, but in Central Pain the “pins and needles” may be constant. The medical literature are full of suggestions that noxious events go on all the time in the body which do not reach consciousness but evoke something like a pain response. For example, when oxgyen level sinks, our breathing rate is increased, but there is no particular pain, except possibly a headache. There are CP subjects with constant headache. The immune system is now being referred to as the sixth sense. The immune system recognizes invaders and makes the response but we are not consciously aware. Pain and inflammation use the same chemicals and it is tempting to thing Central Pain patients may in fact be able to perceive certain steps occuring in the inflammatory process, so acute is their hypersensitization. In the end, Central Pain is not so odd at all, it is merely extraordinary. The mixing of pain sensations, with a lack of a term to describe it, is what has put a “bizarre” label on central pain. It would be more accurate to say language is deficient, but we speak from the point of the majority with normal pain.

The physicians got where they got because of superficial questioning, but they were led on by sloppy descriptive language from patients. If CP subjects are merely able to bear the burning better because of sedation, they should have the sophistication to differentiate that from actual cessation of pain. Sedation was always available for surgery, but it was no substitute for ether. The CP subject should feel they are cheating if they merely say, “My pain is better.” It is more informative to say “My lancinating pain is better.” Exercise, music, agreeable conversation, and other pleasurable activities which induce endogenous opioids can also sometimes relieve burning, but the patient must be clear that it was the exercise, not the medicine, which helped the burning. Otherwise, therapy will be clouded.

On the other hand, some physicians report that the induction of a paresthesia, or buzz, through use of a spinal cord stimulator can block perhaps fifty percent of the burning pain. The problem of reliability in these studies comes from the amazing omission from the reports of WHICH TYPE of pain is being relieved by the buzz, or interfering signal. Presubably it is the burning dysesthesia, but because spinal cord stimulators have use for other types of pain as well, including the muscle pains, it is still not possible to speak with dependability. EVERY study should include precise terminology on the symtpoms present preop and the specific symptoms relieved postop. It is not enough to say “the pain” or “was benefitted”. These terms are plastic and we need specificity, including the degree AND durgation of the pain relief.

The lightning pains may occur in a milieu of cotinual fasciculations or may be of such severity as to induce a strong movement. These are less structured events and we do not yet have sufficient information from the surveys to feel comfortable with descriptive arrangements, partly because it is sometimes difficult to separate out the muscle behaviors of simple denervation from the neuropathy of an injured nerve which is still managing to get a signal to bypass the cord, even when electromyography is available. Virtually all lancinating pain is just that, pain of an electric or shooting nature, which is frequently very intense. It is always intermittent and difficult to induce or evoke. Its description awaits more information, although there is reason to suspect that it mirrors the lightning pains of neurosyphilis in every essential respect.

The lancinating pain of CP is considered due to injury to neurons in the posterior tracts of the spinal cord, the so called posterior columns, and is consequently called “lemniscal” pain, the medial lemniscus receiving pain from the posterior columns. Thanks to penicillin, neurosypilis is a thing of the past. ‘During its time however, it was exceedingly common and was perhaps responsible for the birth of Dermatology since it has cutaneous manifestations in its early stages. There are few clinicians alive with good clinical experience in neurosyphilis and the lightning pains of tabes dorsalis. However, some of the authors at painonline have interviewed some of the old timers and they assure us that our descriptors of lightning pains in CP would have been taken as normal symptoms of cord injury from the spirochete of syphilis.

Because knowledge of the sensory arm of the gamma motor system in the msucle spindles was not well devleoped in the past, even experieneced syphilologists are unable to cite data on the pseudocontractions of muscles in CP and the combination of heaviness and weakness inthe same extremities, but they assure us that anecdotally these symptoms would have been part of tertiary syphilis. Just as CP can be varied, tertiary syphilis was known as the “Great Imitator” and syphilologists are among the most open minded of clinicians. Retrospective exploration of spirochetal injury to the posterior cord tracts in the journals of Dermatology and Syphilology probably provide a wealth of descriptive information which applies to lancinating pain from physical injury to the posterior cord.

No reports of any steps or quantal gradations regarding lancinating pain (lightning pains) have made their appearance in the surveys or in the clinical reports of physicians who contribute to painonline. However, there is a definite tendency for lancinating pains (electric pains( to occur more frequently in certain parts of the body. These may be locked in. ne patient with a high cervical lesion had experienced furious shocks parallel to the axis of the legs, but nowhere else.

When TENS was applied to the neck, shocks on the cheeks appeared after two or three threatments. When TENS was discontinued, the frequent shocks in the race continued for around two months, but then gradually diminished to an incidence of three or four times per months. No objection could be raised to devising a categorization related to distribution on the body in lancinating pain. Patients with multiple sclerosis and CP so frequently have tightening in the chest that the term “MS Hug” is used, which may be present in some degree in as many as 15% of MS. This article does not address geographical steps or compartments. It is concerned with the severity of burning hypersensitization.


Because posterior cord pain (also called lemniscal pain), the most intense of the central pains most commonly responds to medication, we have not graded its severity. The consequences of pain which can be treated are obviosly less than those which are untreatable. Most with severe burning dysesthesia (sponothalamic pain) find help from sedation, but not from actual pain relief. Some medications, such as the opioids, provide sedation as well as pain relief, so their benefit to dysesthesia may be sedaation more than actual pain relief. This is why it is difficult to assess patient comments that their pain was “benefitted”. The Wall/McHenry databse DOES differentiate between the actual pain relief and sedation, and so the results have meaning.

The order of Central Pain burning dysesthesia is, in ascending order

1) Evoked pain only (burning only when stimulating factors occur)

2) Spontaneous pain only (burning at all times)

3) Spontaneous pain plus evoked pain (the largest category, 75%)

4) Spontaneous pain plus evoked pain plus second tier or exponential evoked pain. (15%, these people never go less than 8 on VAS, as pertaining to the burning only.)

The MOST COMMON EEROR by clinicians in evaluating CP is failing to sepaarate ordinary nerve transmitted pain, or structural pain, (also called nociceptive pain), from the truly neuropathic pains. The latter have characteristics which are different but very difficult to identify. Yet, in order to properly assess neropathy, it is essential to recognize the categories. Without this, the CP patient with sunburn may regraded as essentially idnentical to someone with exponential evocation. This is like comparing a breaking wave to a tsunami. The exponential evocation subject is at risk for death (suicide) and must be treated as an emergency. Modern pain management likes to speak of itself as multidisciplinary. How to portion out care from the different disciplines is better arranged if awareness of how severe the CP actually is.

In the exponential evocation group, extraordinary measures are indicated. It is a pain crisis of the greatest degree. Family must be conctacted and counseled. Social agencies must be alerted. Proper psychiatric help must be rendered. Above all, every measure to reduce stressors must be taken. House calls should be the norm, since many in the exponential evocation group are too ill to travel. Proper seating and tempeerature contorl in the office should be arranged to avoid suffering. Alowance for reduced clothing should be the norm, which may require a separate seating area. The patient may not complain about this, but may not come back if these measures are not provided. Very soft seating is required to relieve the extreme pain felt in the muscles. How can they trust a clinic which shows by their physical accomodations that they do not know about severe CP.

Even if real help were possible, the pain of travel accomodations may be so great that severe CP patients may not be able to bring themselves to make the trip. A special amubulance may be the only possible solution. Anyone acquainted with pain clinics knows that such measures are not provided, and that the clinics therefore see only the middle group of CP patients. They are not prepared to deal with the pain crisis. This is unfortunate, and not likely to change until thrid party payers reocgnize and acknowledge the problem. The patient should not have to walk through a “burning ring of fire” as it were, to get medical care.

Nurses and attendants should at least be made aware of the necessity for patience, proper seating, and the possibilty that a few degrees difference in temeerature may spell the differnce between reasonable comfort and suffering. We do not want to send a message of indifference to the CP patient before we even get started. If the office is cool, a small heater can be provided, or if warm, a small fan. This is no different from having a bathroom in an office which treats incontinence. IF gunshot patients in the ER are to be admitted to the hospital, they are not asked to walk up to their rooms. We should do no less for CP patients for whom mobliity is a torture. Even with an intact motor unit, the pain of movement may be overwhelming. Preparation for severe CP should begin in the pain unit.

In the second tier evocation group, CP should probably be considered life-threatening because suicides occur. These people generally cannot wear clothing normally and cannot endure the touch of sheets. Typically, they also have posterior cord pain which can be very sever in its own right, but most commonly does respond to pain medication. The second tier evocation group often have visceral pain in gut or bladder, and pins and needles. The degree to which CP is life threatening seems to be directly related to the percentage of body which is involved. When it involves not only the body, but hte face as well, the elaboration of CP symtpoms tnds to be particularly great, as is the severity. This latter state, when it is mixed with posteior cord pain, is considered to be the most severe pain state known to man. These people need ongoing psychiatric support and must eliinate strssors from life.

We have received a number of reports of “worsening” of Central Pain. The attempt is being made to determine whether these subjects are moving from the sponteaneous plus evoked group into the sponteaneous plus evoked plus second tier evoked group.

Because all Central Pain is severe, even if the sensation is just at the level of a sunburn, it is difficult to use terms such as “least severe”. However, some idea of the grading is in order. At the lower end, are those who have the sunburn. Whereas, at the upper end, are those who cannot tolerate the touch of clothing or sheets. This does NOT include the posterior cord pains, such as muslce pains and lancinating electric pains, which can be so severe on their own that the person is functionally paralyzed, as Beric has reported. Here, we attempt to discuss the evocation of burning pain, which applies to the anterior cord or spinothalamic tract pain. The least affected are those who have evoked pain only. In the British literature, this is sometimes termed, “elicited pain”.

The lower level of burning dysesthesia is evoked pain only from light touch or temperature change/extremes. Those with evoked pain only constitute approximately 5-10 % of CP subjects, and are mostly found in quadriplegics. The next level up is those whose hypersensitivity is sufficiently great that no stimluation or evocation at all is required for production of the pain. Those with spontaneous pain most frequently also have evoked pain as a higher level of pain. Dysestheteic pain simply means one would not have been able to perceive prior to acquiring CP. Sometimes the word “bizarre” is used, but since the burning is just the sensation of acid under the skin, MIXED with cold, wetness, etc.

The term “bizarre” may not be helpful. IF blue and yellow are seen together, we call it “green”, not bizarre. Because severe CP causes serious psychological reactions, as is understandable for severe, ongoing pain, the word “bizarre” carries a negative connotation that misleads some into thinking the person’s thought processes are bizarre, when they are usually entirely appropriate to the situation. Any doubters of this are invited to inject capsiacin under the skin to induce neuropathic pain, and they will not feel anyone who suffers from CP is bizarre, unless they wish to include themselves.

Nearly all Central Pain subjects have spontaneous burning. Most alos have evoked burning, or burning which can be greatly enhanced by twenty or thirty seconds of continued touch. This has a zoned of burning beyond what is actually touched, known as secondary allodynia, usually 1/2 inch to 1 1/2 inches further out from what is actually being touched. The severe cases have a third reactivity, which has been called “exponential evocation” or “second tier evocation”. The zone of secondary alloynia extends even further out from the area touched, perhaps doubling or tripling the effective radius of burning sensation. This expanded potential for evocation is sometimes included under the term, “slow summation” but inasmuch as that term already has meaning in other phenomenon of the nervous system, it is felt that second tier evocation or exponential evocation are better terms.

One of the things that made Dr. Patrick wall so outstanding was that his vast clinical experience permitted him to recognize recurring patterns in the verbal descriptors of central pain, and to eliminate pain symptoms which were not the product of nerve injury. Nearly every CP subject has pains which are simply the rsult of the injury to body parts and structures.

These structural pains are often treatable and tend to follow what we expect from normal pain. The cetnral pains are different, for the most part, and have their own patterns. If there is failure to distinguish between nociceptive and neuropathic pain, the contribution to pain research will fail. CP subjects can teach much about the way the nervous sytem operates.

Ordinarily, researchers would pay a great deal of attention to what patients say. The problem for CP is that the language does not exist to describe mixes of pain, nor is there a word for pain which lacks discriminative features. Consequently, some doctors have felt they had to ignore what the patient said, in order to make any progress. Dr. Wall was concerned that verbal descriptors be noted, organized, and given language to make them effective in communicating the clinical features of the condition.

Although touted as the best medicine in the world, or at least among the best, American medicine was not always this way. In the 1800′s an aspiring doctor normally would have to go to Europe to get up to speed. It was common for American researchers to learn German in order to read the latest in the journals. After the Civil War, S. Weir Mitchell, who first described the differences betwwen peripheral neuropathy and pain of central origin (light touch evokes burning instantly in peripheral neuropathy, but only after a delay of 20-30 seconds in pain of central origin).

MItchell felt so strongly the need to upgrade American medicine that he convinced Johns Hopkins to go abroad for its faculty. His findings were kept alive by Lawrence McHenry, ANA president, who kept Mitchell’s findings in the forefront. This was a major factor in the legitimization of American medicine. Hopkins eventualy acquired Sir William Osler and Halsted, the great british Surgeon, who trained more than fifty chairmen of departments of surgery at other medical schools. The genius of Osler was the art of clinical medicine. Stated simply, it was “If you listen to your patient long enough, he will tell you what is wrong with him.” Not just in Central Pain was there a lack of paying careful, painstaking attention to what the patient was saying.

Osler trained generations of doctors who prided themselves in being able to diagnose by history and examination. Those days are long gone. It is true that with modern MRI, CT scans, and laboratory testing, a medical graduate does not need clincial skill as much. He/she may be quite sloppy in clincial skills and still achieve a correct diagnosis a reasonable amount of the time. In the HMO tinme drought, anything which avoids time consuming interviews with patients is considered cost effective. This aproach breaks down when a condition, such as Central Pain, cannot be imaged. A generation of dcctors who are weak on clinical skills when confronting a condition where the diagnosis can be made entirely on history, which was the way Dejerine and Roussy characterized Central Pain in their famous book, “Tract Optique” in 1906.

Dr. Wall was well aware of the need for gatherihg and crediting verbal descriptors in Central Pain. He initiated a database with Dr. Kenneth McHenry. Shortly before his death, Dr. Wall urged that the work be continued, so pleased was he with the progress in characterizing and systemmatizing the symptoms of Central Pain. The survey at this website is one aspect of the Wall/McHenry database, which is said to be the largest on Central Pain in the world. The initial patients came from Dr. Wall’s own practice. This grew to include input from many parts of the world. It is daunting to use a survey to study a disease which has no language and so there wre rounds and series of surveys to gather the most common descriptors, categorize the complaints, and adopt terminology which had meaning for both the patient and the medical community.

One of the latest findings is the frequency with which people with severe Central Pain report a kind of long term sensization. This phenomenon is contained in what has been termed, “McHenry’s Rule.” The rule is, “In pain of central origin, the more severe ordinary evocation, the more likely that the hypersensitization will lead to expoential, second tier evocation.”

Examples of this second tier or exponential evocation may be seen from examples of this which have come to us:

“I am a C6/7 paretic. Light touch, including a blouse makes my skin burn. However, if I wear a bra, within a few hours or days, a level of burn in the area reaches a new height, perhaps five times the ordinary burning, which take a very long time to go away, after the contricting bra is removed. This creates a severe problem in going out in public.”

“I have had dental work done since acquiring CP without much of note except that the needles seem so very sharp. My dentist must think I am a real sissy. The last time I went in, however, the dentist attempted to polish one of the crowns on my front teeth. It was made of some material that would not polish, but just got rough. Within hours I had commenced a burning in the front of my mouth and tongue, areas which burn anyway, which was greater than anything I had experience. I learned that if I covered the roughtness with Chap Stick, the inside of my lip would quit rubbing the rough area and level of burning would drop down to what it normally is when touch is prolonged. I thouht I would go crazy until I learned this. I will have a new crown put on to stop the hypersensitivity.”

I was traveling to a medical center by air, when a crown broke off, leaving a kind of sharp edge which irriated my tongue beyond belief. I bought some tempoarary filling at the grcoery store to coer it, and when a new crown was placed the really severe burning inside my mouth and on my tongue, went back to the normal level of burn.”

“When I got hurt, I went to live in a warmer climate. There I was amazed at how sensitized my skin grew. This brought out levels of burn that I did not have from touch in the more moderate alimate.”

“My bladder burns when urine collects, but if I ignore it for an hour or so, it can reach a level which is just unbearable, hard to describe but torture if I cannot get to a bathroom. I carrry a receptacle with me at all times now to avoid the agony if I can’t get ot a restroom.”

“My rectum feelb uncomfortable if stool or gas collects. However, if I am asleep, and fail to eliminate, the pressure of the gas or stool feels like a cannoball is trying to pass. It is too severe to sleep. I have had to regulate food intake to avoid this.”

“If anything gets me going, with the burn, and it cannot be eliminated, I reach a level of burn which is just torture. I have burning from light touch, and spontaneous burning also, but if there is some chronic irritation for an hour of so, it just lights up beyond description. I can reach this rapidly if I rub something rough on the skin of my ankles, which are VERY, VERY hypersensitive.”

“I am a C5-6 paretic. My bladder burns abnormally when filling. My bladder typically burns almost unbearable when it reaches a certain level of fulness. When I am able to sleep for a period long enough for the bladder to fill, I come awake with a burning urgency to void, which may have awakened me. Fulness in the rectum behaves in similar fashion and is at least as severe, even though I am mostly numb in that area. When I have voided, the bladder is still hypersensitized and even a very small amount of filling recreates the same severely burning sensation of a painfully full bladder that woke me.”

Thse remarks are describing a second tier of evocation, beyond what is felt after 20-30 seconds. With painstaking questioning, we have learned that this second tier of sensitization is very near maximal, as if a touch sensitization overdrive has been reached. Although it is common to lump all evocation together, it is clear that this greater or exponential type of evocation is something different, and very much mroe severe. Knowing about it can help clinicians and dentists udnertand what is going on in the patient’s body.

Thank you again for your patient input through the surveys. Thanks also to Drs. Wall and McHenry for the careful and painstaking analysis which has permitted a new understanding and recognition of the clinical aspects of Central Pain. The language problems are so great that most of the letters between the two scientists are full of question and controversies, and sometimes direct challenges. Assuring that the database would be maiatained was one of Dr. Wall’s last requests before he died.

Central Pain does such unexpected thimgs that it often fools the patient, who does not recognize an evoking stimulus for what it is, because logically, she thinks that such an event COULD NOT cause the perceived sensation. An good exmaple is the severe burning which comes from sleeping in a cold room. It is not unusual for the patietn to be foodled for years over what is causing the gut wrenching burning, since she knows that the touch of sheets can also cause burning. In an imageless condition such as Central Pain, the art of clinical medicine is essential. It is a work in progress.