POINTS TO REMEMBER:
1) PAIN IS EITHER NOCICEPTIVE (ORDINARY aka NOXIOUS PAIN) OR NEUROPATHIC (NERVE INJURY PAIN). NEUROPATHIC PAIN MAY BE EITHER SPONTANEOUS OR EVOKED.
2) NERVE INJURY PAIN IN THE CENTRAL NERVOUS SYSTEM HAS DIFFERENCES FROM PERIPHERAL NERVE INJURY PAIN. EVOKED PAIN FROM LIGHT TOUCH IS INSTANTANEOUS IN PNI, BUT LIGHT TOUCH EVOCATION OF CENTRAL PAIN MANIFESTS A LATENCY OF 20-30 SECONDS (MITCHELL’S DELAY). TREATMENT FOR PERIPHERAL NERVE INJURY PAIN MAY NOT BE EQUALLY EFFECTIVE IN PAIN OF CENTRAL ORIGIN. THE PERIPHERAL NERVOUS SYSTEM IS CONSIDERED TO END AT THE DORSAL ROOT GANGLION–BEYOND THIS IS THE CENTRAL NERVOUS SYSTEM. THE CNS CONTAINS BOTH ASCENDING AND DESCENDING TRACTS RELATING TO PAIN. IT IS THEORETICALLY POSSIBLE THAT OPIOIDS MAY EXCITE A PAIN INHIBITORY PATHWAY(S) DESCENDING IN THE MEDULLA OR CORD, AND THEREFORE REDUCE PAIN, BUT THERE ARE CONFLICTING DATA ON THE THERAPEUTIC BENEFIT. SEDATION IS STILL THE MAINSTAY FOR MOST.
3) VIRTUALLY EVERYONE WHOSE CENTRAL PAIN IS DUE TO SPINAL CORD INJURY ALSO HAS NOCICEPTIVE PAIN IF A MOTION SEGMENT OF THE SPINE HAS BEEN ALTERED, AS FROM REPARATIVE SURGERY OR RESIDUAL DAMAGE FROM INJURY.
4) MOST PATIENTS DO NOT OR CANNOT DISTINGUISH VERBALLY BETWEEN NORMAL AND NERVE INJURY PAIN, EXCEPT AS TO THE BURNING DYSESTHESIA, WHICH IS “LIKE ACID UNDER THE SKIN” (AND UNLIKE OTHER PAINS). WHEN BURNING DYSESTHESIA IS PRESENT, THERE IS ALWAYS SOME LOSS OF SUPERFICIAL SENSIBILITY (eg touch temperature, sharpness) AND THERE IS LIKEWISE A LOSS OF APPRECIATION OF THE SURFACE LOCATION OF THE SKIN IN THREE DIMENSIONAL SPACE (ATOPOESTHESIA).
5) CENTRAL PAIN IS WORSE WHEN IT IS SENSITIZED, I.E. EVOKED, ENHANCED OR ELICITED
6) EVOCATION OF CENTRAL PAIN CAN OCCUR FROM EITHER NON PAINFUL STIMULUS (ALLODYNIA) OR PAINFUL STIMULUS (ALLOPATHIA). TOUCH IN ONE AREA RESULTING IN PAIN IN A NEIGHBORING AREA IS KNOWN AS ALLACHESTHESIA (EPHAPTIC PAIN).
7) WHEN THE EVOKING STIMULUS IS PAINFUL THERE IS FREQUENTLY CONFUSION AS TO WHETHER THE PAIN IS NOCICEPTIVE OR NEUROPATHIC, BUT IT MAY BE CONSIDERED TO BE BOTH
EVOKED CENTRAL PAIN IS VERY MUCH MORE SEVERE THAN SPONTANEOUS CENTRAL PAIN
9) PAIN MEDICINES WHICH REDUCE THE SENSITIZER (EVOKER) OFTEN OWE THE RESULT TO THEIR EFFECT ON THE NON-NEUROPATHIC ELEMENT. THE MOST COMMON NONPAINFUL EVOKERS ARE LIGHT TOUCH, COLD, AND MUSCLE LOADING. THE MOST COMMON PAINFUL EVOKERS ARE SHARPNESS, MORE SEVERE COLD, AND CONFINEMENT IN ONE POSITION.
10) PAIN MEDICINES WHICH DO BENEFIT EVOKED PAIN BY BLUNTING THE PAINFUL SENSITIZER MAY HAVE NO EFFECT WHATEVER ON THE SPONTANEOUS CENTRAL PAIN. SEDATIVES AND MEDICINES WHICH QUIET THE CENTRAL NERVOUS SYSTEM (ANTICONVULSANTS) SEEM MORE EFFECTIVE AGAINST THE SPONTANEOUS CENTRAL PAIN AND PAIN WHICH IS EVOKED BY NONPAINFUL STIMULUS.
11) RESEARCH REPORTS THE MOST SEVERE CENTRAL PAIN IS FOUND ONLY IN THOSE WITH SOME REMAINING FUNCTION, HOWEVER MINISCULE, OF THE SPINOTHALAMIC TRACT
12) LOSS OF MOTOR FUNCTION DOES NOT CORRELATE WITH DEGREE OF CENTRAL PAIN.
13) SEDATION AND STRESS AVOIDANCE ARE GENERALLY THE MOST THAT CAN BE OFFERED AGAINST SPONTANEOUS PAIN, ALTHOUGH CONVENTIONAL PAIN MEDICATIONS MAY TREAT SENSITIZING STIMULI OR SENSITIZING PAIN.
14) IN GENERAL, THE MOST SEVERE CENTRAL PAIN CAN BE EXPECTED WHERE SIGNIFICANT RETENTION OF SPINOTHALAMIC TRACT IS PRESENT. SUCH PAIN TYPICALLY APPEARS WHEN CORD INJURY IS RESOLVING AND THE INJURY IS REVEALED TO BE INCOMPLETE.
15) DECREASE OF AMPLITUDE IN THE MID OR LATE PEAK SOMATOSENSORY EVOKED POTENTIALS MAY CORRELATE WITH THE PRESENCE OF CENTRAL PAIN IN SOME CASES, BUT ELECTROPHYSIOLOGY LABS DO NOT AT PRESENT TYPICALLY INCLUDE THIS ANALYSIS.
16) THE DEGREE TO WHICH SPONTANEOUS CP CAN BE EVOKED VARIES FROM INDIVIDUAL TO INDIVIDUAL, THIS IS TRUE BOTH AS TO THE DEGREE OF HYPERSENSITIZATION AS WELL AS THE NATURE OF THE EVOKING STIMULUS. TYPICALLY, ONLY THE BURNING DYSESTHESIA AND MUSCLE PAINS MAY BE PREDICTABLY EVOKED BY NONPAINFUL STIMULUS. (PINS AND NEEDLES MAY SOMETIMES BE EVOKED BY COMPROMISED CIRCULATION TO AN EXTREMITY, OR ODDLY, WITH COLD.)
17) JUST AS IN A BURN PATIENT, THE PERCENTAGE OF SKIN SURFACE AFFECTED BY BURNING DYSESTHESIA CORRELATES WITH THE SUFFERING OF THE AFFECTED INDIVIDUAL. THOSE WITH CP ON TEN PERCENT OF THE BODY TYPICALLY FIND THE PAIN LESS UNBEARABLE THAN THOSE WITH CENTRAL PAIN ON 90% OF THE BODY, BARRING CONFOUNDING BY EVOKING STIMULUS.
18) THE SPINOTHALAMIC TRACT MUST ACT OR TRANSMIT SIGNAL, AND MUST DO SO ABNORMALLY, BEFORE THE THALAMUS WILL SIGNAL PAIN TO THE CEREBRAL CORTEX. AN ABSENT STT SIGNAL YIELDS NO PAIN.
19) SINCE THERE ARE BOTH LATERAL AND ANTERIOR SPINOTHALAMIC TRACTS, CP CAN BE EXPECTED TO DIFFER ACCORDING TO THE ANATOMIC INJURY INVOLVED AND WHICH INDIVIDUAL PORTIONS OF THE TWO TRACTS ARE DAMAGED.
20) CENTRAL PAIN IS A MIX OF PAIN SENSATIONS, EACH OF WHICH MAY BE RELATIVELY INDESCRIBABLE, AND MORE SO THE COMBINATION OF THE INDESCRIBABLE PAINS, WHICH MAY MERGE IN A WELTER OF SEVERE BUT INARTICULABLE SUFFERING…
The most severely injured area of the central nervous system is the least likely generator of central pain. Such pain is rather more likely to have its origin in nearby, less severely injured areas of the cord or brain. Hence, present methods of MRI acquisition are not accurate in identifying the presence nor the originating area for central pain.
It has long been known that incomplete spinal cord lesions are more likely to result in central pain than complete. What has not been as widely appreciated is that any retained function in a damaged spinothalamic tract carries the risk of severe pain, the more retention the greater the risk, presuming actual damage and loss of normal operation of the tract. Thus, we find quadriplegics who are completely numb, but have no pain. By comparison, we find walking quads with really severe pain.
The closer to complete a lesion is, the less severe the CP is likely to be since there is less disordered spinothalamic activity to make things haywire in the thalamus. This is, however, far from a universal rule, since there are certainly ”completes” with very severe central pain. These unfortunates may have portions of the ST tract which function in the absence of real sensation. What is often ignored is that sensitization of ANY central pain can create a very severe pain situation. The ordinary pain contributors, ie nociceptive pain which frequents the lives of some completes, can sensitize central pain. Once the cycle has begun, it can be evinced or evoked to a high level. So in most cases, when comparisons are made, one is discussing the spontaneous burning, not comparing evoked levels of pain, which are subject to MANY variables.
Damage to one part of the many faceted spinothalamic tract does NOT mean equal damage to all parts.
Although not proven to exist in humans, primates thus far studied have both a lateral AND an anterior spinothalamic tract on both sides of the cord, subserving slightly different modalities. Injury with partial preservation of any part of the tract could be expected to yield very severe dysesthetic pain, both as to touch or temperature and as to muscle loading. It is as if the thalamus expects to see a certain type of waveform signal indicating all is well. If it receives NO signal, there is no pain. However, a signal departing from normal results in a message being sent from the thalamus to the cortex that things are seriously wrong.
In other words, even if the thalamus cannot sort out the type of pain being transmitted by the injured tract, a novel or distorted pain signal will be the result. This unuusual pain is “protopathic” pain, which is to say, the primitive burning retained by an injured nerve fiber after all other pain sensations have been lost. This type of pain can be demonstrated by taking a blood pressure cuff and compressing the arm for a time, and watching pain modalities disappear one by one. (Do not attempt this yourself, as it must be done under medically controlled conditions to insure that no permanent nerve damage occurs). The last pain to persist, before the arm goes completely numb, is protopathic burning, which is thought to be indistinguishable from dysesthetic burning. Central Pain is a melange of pains and contains more than just protopathic burning. There is always a MIX of pains, even in what a CP patient will call “burning”. Common other sensations present are paradoxical cold and wetness. In central pain, touch at one location may occasionally evoke pain at another location (usually nearby the point of stimulus or at least on the same extremity) , which is called an “ephapse”. This phenomenon of ephapse is not known to occur in the protopathic demonstration.
This experiment can be viewed as somewhat similar to passing a light through a prism, which reveals that what was seen as white light is actually composed of the combination of many colors. Similarly, pain can be sorted out into various elements, the most primitive being termed “protopathic”. The last pain to go in an injured nerve is a poorly localized diffuse burning, which is known as “second pain”. This pain lacks discriminative features as to loccation and nature. It is similar to the flare which is felt AFTER one withdraws a hand from touching a hot stove.
“First pain” is the pain felt on touching the stove, and the flare afterward is the “second” pain. Second pain is ,mainly just THERE, and the brain is not so worried about the precise location on the body as it is signalling PRESENCE. The important role of second pain is to let the person know that some general arear of the body is injured in order to drive appropriate action.
However, in actual central pain, burning dysesthesia (which is akin to second pain), the signal does not stop. It may be enhanced or evoked by sensitization, the source of which need not be painful and in fact usually is not painful. Light touch, a rush of cold air, clothing, or even movement may result in evocation. Patients, as well as clinicians have a very difficult time sorting out evoking painful stimulus from core central pain. It is easy to separate non noxious stimuli from central pain since experience teaches that such stimulation should not be painful. However, the situation is much more difficult when the evoking stimulus is itself painful. Sensitization by painful stimulus often or usually leads to confusion in the mind of the CP patient, who frequently confuses the nocicptive sensitizer with neuropathic central pain. This phenomenon is responsible for the many inaccurate and confused descriptions of central pain found in the literature which incorrectly class many normal pains with central pain. If you have ever felt the precise pain BEFORE the cord/brain injury, then that pain is NOT central pain. Central pain occurs ONLY in dis-integrated pain pathways. If you can describe it accurately, and the doctor recognize it, then it is NOT central pain. Central pain is by definition “bizarre” and is the result of a diseased pain pathway.
The same confusion occurs in therapy. Those with central pain, who have nociceptive pains sensitizing the central pain, may find opiates relieve the sensitizer. It has never been conclusively proven that opiates affect core central pain, although the perception persists among the majority that it is helpful. The benefit is likely to be based not on relief of dysesthetic burning, but rather footed on quieting of the central nervous system, as in sedation, or in relief of the sensitizer. This position, that sedatives are the first line drugs for CP, is far from universal with many good pain doctors holding that opiates are good medicine for central pain. However, based on the survey results, this benefit is most likely to accrue when the CP is mild or moderate. For those with severe pain (usually the moderte-severe cutoff point used is the inability to tolerate the touch of clothing) the majority feel sedative by any agent, such as hypnotics or anticonvulsants, is equal in benefit to opiates or opioids, leading to a suspicion that sedation is at the heart of much of the response to opioids in general.
Dysesthetic burning nearly always is accompanied by a mix of other pains, some of which may be quite severe. These may include lightning or lancinating pains (intense but not lasting), pins and needles, and frequently the sensation of muscle cramps or soreness. The muscle pain may be so severe as to create paralysis, despite an intact motor unit. These neuropathic pains are often, if not always, confused with the many musculoskeletal pains which are typical of someone whose spinal cord has been altered by injury and surgery. The articulations of the spine at its motion segments are relatively unforgiving and it is rare to find a spinal cord injured person who is pain free from motion, even if their pain is not neuropathic pain. Normal pain is called nociceptive pain in the medical literature and the presence of central pain by no means guarantees one will not have nociceptive pain.
Dr. Ron Tasker, a distinguished neurosurgeon from Western Toronto Hospital and long the most published author on central pain was the discoverer that pain is carried in the spinothalamic tract (STT). Tracts in the spine are typically named after their origin and destination amd so we have ”spinothalamic tract”. These are present in two locations, both the anterior and the antero-lateral regions of the cord.
In the early work by Dr. Tasker, a distinction was not made between lateral and anterior STT tracts; and such a distinction is still not possible since the size of these tracts is below the resolving power of MRI or any other imaging modality. THe STT should be viewed as constructed similar to telephone wires, with multiple discrete bundles.
In the case of the spinothalamic tract, which originate in spine and ends at the thalamus in the brain, there are really multiple tracts. The assemblage of tracts winds around other tracts, including the tract which senses heat. Even if all the STT tracts were combined as one, it would still be too small for the resolving power of MRI. Consequently, significant injury in the STT may not show anything on MRI. Studies have revealed that those with the worst pain typically have no lesion visible on MRI, and where the MRI shows a bright lesion, there is typically NO PAIN. The treating physician must therefore not fall into the trap of thinking nothing visible on imaging studies contradicts the patients description of pain. The history of central pain is so unique that careful examiners have always found that verbal descriptors alone are very reliable in diagnosing central pain following injury to the spinal cord or after stroke (where the central pain is typically unilateral on the body). Central pain grows worse distally on the extremities and body; whereas malingerers typically have symptoms without gradation, eg “my whole arm is numb, or my whole leg is pained equally”.
The centripetal distribution of central pain is unique. When present on the face, this layering out or zoning of gradations of pain, ie distalization, was termed “onion peel skin” by Dejerine and Roussy. They were referring to the fact the pain grew worse as one went out along the trigeminal nerve, toward the tip of the nose and the center portion of the lips and gums. The requirement for partial damage was noted in the paradox that those with lesions high in the trigeminal fibers typically had the worst pain in the LOWER face, presumably because the most intensely injured nerves could not generate central pain, but those nearby which were partially spared displayed the dysesthetic burning.
This puts the central pain patient in a difficult position, since third party payers may read a negative MRI report as evidence against pain. Somatosensory evoked potentials (SSEP) may be of some help to certain CP patients whose pain is disputed. Recently, there have been some studies which show that latency or lowered amplitude in the mid and late peaks on somatosensory evoked potential may correlate with pain in the lateral pain tracts (an explanation of function of lateral pain tracts in the thalamus is beyond the scope of this article, but other articles at this site explain the difference between medial and lateral thalamic pain). However, many centers doing SSEP have little or no experience in evaluating mid and late peaks and central pain.
The few CP subjects who have answered the survey who were aware of their SSEP results have ALL shown abnormalitiies on SSEP; however, the wording of the survey did not anticipate the necessary refinement and so painonline cannot provide sufficient data to support the recently published studies. Each of the peaks on SSEP tracings have names and doctors do not typically discuss such matters with patients, and among themselves typically focus on the EARLY peaks, not the mid to late ones.
SSEP has traditionally been associated with damage to the posterior columns, which are MOTOR tracts, and only recently is there a suggestion that correct application of SSEP may be able to pick up the person with Central Pain in some cases. See eg Kakagi et al “Pain related somatosensory evoked potentials J Clin Neurophysiol. 2000 May;17(3):295-308.
Central Pain has long had and is still undergoing a definitional problem. Currently, in the literature, it is often confused with long term potentiation, central sensitization, and other conditions. However, traditionally, the definition of central pain is novel or bizarre burning which accompanies loss of superficial sensibilties after injury to the central nervous system. This “dysesthetic” burning is continual andspontaneous (many of the concommitant central pains are NOT continual) but typically can also be evoked by light touch. By usage, central pain is frequently used to name any and all pain which follows such things as spinal cord injury. This is short sighted. Musculoskeletal pain as is often seen when spinal function is abnormal can evoke or make more serious the central pains, but these phenomena should NOT really be lumped together, even if painful stimuli can evoke the central pains in some people.
We will stick with the traditional definition to avoid confusion. However, one can expect serious misunderstanding. For example, a recent textbook on pain by an anesthesiologist states that some people with central pain find it “distressing”. Of course distressing might just as well be applied to the frustration when one cannot find the remote or if one runs out of strawberry marmalade. It is not a good word to use when describing central pain, in our opinion.
This word, “distressing” rightfully applies only to the most mild of the central pains, and hardly reaches the classic form, which may include some of the most intense pains known to man such as the lightning pains, which are mercifully brief, unlike the durable burning). LIghtning pains are not mild in tertiary syphilis, and they are no less severe in CP.
These central pains can be and usually are multiple in nature. Severe instances are among the most severe pains known to man. As Beric described, the pain of movement may be so severe that the personal is functionally paralyzed. Light touch may be so hypersensitized that the touch of clothing cannot be endured. It is hard to understand how an author could choose “distressing” as the most accurate descriptive term. Waking up during surgery from inadequate anesthesia would be “distressing” but it would also be “horrific”. Of course, MOST people with pain after spinal cord injury are not in severe agony, or perhaps have no pain at all. Burning in the majority may be likened to a sunburn, permitting clothing, motion, and thermal variation. The question is whether these patients represent REAL central pain, or whether they are merely a form fruste example of the disease. The foregoing paragraphs illustrate the definitional problem. One correspondent to the painonline editorial staff has such severe muscle pains than it takes perhaps ten minutes to type one line. What word do we use for that level of central pain in the motor apparatus. Whatever it might be, “distressing” would not be it.
One wonders whether this particular author has seen and followed CP patients in sufficient numbers and to a sufficient degree for accurate description. Less than ten percent of those in the survey in describing their central pain used a word which could be synonymous with ”distressing”, while more than thirty percent chose “unbearable”, “agonizing” or the like. The remainder used terms equivalent to “very painful”, “disabling”, and similar descriptive and verbal characterizations. One must be in relatively good shape even to make it to the pain clinic, and there are certainly those who find it impossible. For the person who operates in a very narrow range of endurable temperatures, a visit to the doctor may represent a genuine ordeal. Considering the large amount of world literature on neurosurgeons who have done brain ablation for central pain (unfortunately not very sucessfully), it is hard to imagine doing such a procedure for something which was merely distressing. And so we conclude that the author has seen mostly the more fortunate, and does not have the measure of severe central pain at all.
The painonline database, which is included in the Wall/McHenry database, is the largest collection of verbal descriptors of central pain in the world. One might argue that those less affected were not motivated to take the time to complete the survey, but this is speculative. The number of Central Pain patients among Dr. Kevorkian’s patients is mute witness to the impact on life which this terrible condition wreaks in its severe forms.
When there is a group of patients, suffering greatly, it has been common practice to ask the patient to rate their pain from 1-10. This is the so called “analog scale”. It has proven inadequate to the task since the stoic who has incredible sensitization with touch or themal stimulus, typically cold air, may rate the spontaneous central pain as a 4 or 5, when that very pain may be so severe that it makes the wearing of clothes, or even the taking of a step too painful to endure.
There has also been a tendency to assume that the more severe the motor injury, the more severe would be the pian. This assumption was NOT born out by the survey. In fact, just the opposite is the case. While those with most severe motor injury tended to have more normal pain, also called musculoskeletal, than those with lesser numbers of procedures, it was clear early on that the incompletely injured patients rated their pain as considerably more disabling and severe. In other words, a quadriparetic was more likely to have severe central pain than a quadriplegic. Furthermore, the central pain nearly always first appeared when the injury was first shown to be incomplete; ie when some motor function was noted to be returning.
The reason for these nonintuitive findings is that some function must remain in the spinothalamic tracts in order for central pain to be propagated and more especially for peripheral messages to evoke or hypersensitize the pain tracts, in order that hte most severe central pain be experienced.
Recently, A.R. Hari et al showed specifically that “the spontaneous recovery of human STT function (within the first year after SCI) in subjects suffering NP [neuropathic pain] is enhanced compared to those not affected.”
Also, “the correlation between current pain intensity (assessed on average 5 years after SCI) and extent of functional recovery substantiates the close relationship between recovery of STT function and the occurrence of NPthe correlation between current pain intensity (assessed on average 5 years after SCI) and extent of functional recovery substantiates the close relationship between recovery of STT function and the occurrence of NP” See Exp Neurol 2009 Apr;216(2):428-30. 2009 Jan 7 “Enhanced recovery of human spinothalamic function is associated with central neuropathic pain after SCI.”
These findings indicate once again that in evaluation those with spinal cord injury, stroke, mutliple sclerosis, traumatic brain injury, and the other conditions which lead to Central Pain that clinicians must be very careful to distinguish between motor and sensory impairment, and to realize they may correlate inversely so far as central pain is concerned.
This is by no means a statement of general applicability. Witness the article by Alan Hess, the all time most visited article at painonline, wherein we learn that this quadriplegic has central pain so severe that he cannot tolerate clothing, nor even the roughness of transportation. One may find among the quadriplegic some with the most severe form of CP, but statistically the likelihood of such a condition is more likely among the incomplete lesions.
The important point is that the clinician must listen to the patient. Nearly always, learning of the modifications in life style necessitated by the CP will reveal the force and severity of the pain, in many cases more so than the analog scale or any other evaluative method. It is a mistake to assume anyone for whom CP is severe is a weak individual or maladaptive. Who can adapt to unbearable pain? This would be an oxymoron. Adaptation may better be expressed as “slowing the deterioration”.
Pain eventually wins. One may derive satisfaction in remaining quiet about it, in holding to morals, in attempting to perform productive acts, but sooner or later, really terrible pain begins to make inroads into the identity and radically alter life style. This defeat tends to come quickly in severe cases of central pain. The patient is often shocked at the emotional lapses and gaps appearing in the psyche and assistance and relief all too frequently arrive too slowly because the pain is invisible to others. Proper treatment must ANTICIPATE the need.
in the most severe forms, such as severe central pain, the human apparatus does not strengthen with continued torture, and it would be unrealistic to expect humans in this state to grow strong and mighty, or immune to pain. Keeping one’s hand in a flame does not render the remainder of the body immune to burning sensations.
There has been entirely too much talk of the “mind body” in central pain, reflecting ignorance about the nature of perpetual and nondimniishing physical agony. One may devise methods to minimize the impact of pain, such as the avoidance of stress and the adrenaline and angiotensin which flows from it and makes pain more alarming, but few CP patients find their dysesthesia lessened by the years, nor do they find themselves better able to deflect it.
The development of coping mechanisms is not synonymous with pain relief. If one is ugly, learning to overlook critical looks of others does not remedy the ugliness. If it cannot be fixed, it must be borne. Window dressing is available, orthodontics and even bone surgery, but as to central pain, no plastic surgeon can remedy the situation. It is invisible in its presence and equally as invisible in its absence. Thus, the clinician MUST LEARN to take a good and reliable history. Such a history ALWAYS centers on what modifications have been necessitated in life style. This is generally the most reliable indicator of pain severity. The doctor can make general judgments about the coping ability of patients, but should never assume poor coping equals slight pain. It is only logical that those most in pain will have the most difficulty. Additionally, motor impairment does not equal pain impairment. They are independent matters.
If one has severe central pain, the discovery that beautiful music or certain distractions relieve the stress of pain and the focus on it is not necessarily the precise equivalent of pain relief, or is it? In any event, no music is sufficiently beautiful to block out the sensation of a hand immersed in the flame, and the same may be said of burning dyseshesia. Refuge in sedation is helpful, but actual pain relief is needed. There is still an active debate on whether opiates can benefit central pain. This dispute always runs into definitional problems. If we sedate a patient and reduce the alarm and emotional devastation, have we reduced the pain. It is almost a semantic issue. Suffice it to say that the NIH has declared there is as yet no satisfactory treatment for severe central pain. The patient himself/herself will learn how to avoid EVOKING the CP, but the durable and tormentious spontaneous pain is another matter.
This is not to say that that other conditions, such as facet syndrome, muscle conditions, etc may not yield severe pain in the absence of STT function. It is not entirely clear how normal pain nor neuropathic pain reaches the brain. We know some, perhaps most of the pathways, but are ignorant of the algorhythms by which they interact. Indeed, the whole field of thalamo-cortical and cortico-cortical interactions and the six layers of cortex in which this occurs is a study still in its infancy, not only as to pain, but as to matters in general. Pain inhibition pathways are even more poorly understood than pain excitatory pathways. Most statements in this area must be viewed as speculation, especially as it applies to the psychological aspects of pain. Assumptions about central pain drawn from observations of nociceptive pain are freqeuntly naieve, unjustified and premature. Consequently, we must learn not to lump all these things together. Each patient must be evaluated individually. Until we have a specific reliable way to measure such pain, we must take the patient at his/her word, and accept ten people who exaggerate pain to avoid overlooking the ONE patient with terrible, unbearable agony because their motor loss is not complete.
