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Dear Friends in Pain,

Some find this very indicative of the suffering we go through with RSD,

interesting stuff...

A PFD to all,

Introduction to Central Pain

" The Pain Beyond Pain "

Central Pain is the name for a pain syndrome which occurs when injury to the

Central Nervous System is insufficient to cause numbness but sufficient to

cause central sensitization of the pain system.

Reflecting the neuron of choice of the original nerve physiologists, nearly

everything taught in medical school about basic nerve physiology derived from

studies of motor nerves. Because sensory nerves behave almost nothing like

motor nerves, the behavior of Central Pain may seem anti-intuitive to those fed

a

diet of motor nerve physiology for most of their training.

An injured motor nerve simply carries less current. Injured pain nerves,

paradoxically, do exactly the opposite, they increase their signal. It is not a

simple increase, however. They eventually gain the power to humorally influence

uninjured neighbor neurons, which begin autonomous firing. (Devor's work in

The Axon , ed.Waxman, Oxford Univ. Press, 1995).

The process can become so violent that the thalamus, the brain pain center,

records " bursts " of impulses from these injured nerves. After sufficient

bombardment threatens neuron death in the thalamus, it " shuts down " . Central

Pain

apparently occurs at this point. Radiostimulation of the spinothalamic tract,

which causes no sensation in people without Central Pain, recreates the

sensation of Central Pain in those who have the condition. It is as if the

entire pain

system is acting like a nerve ending. Ungated pain signals thus reach the

cortex, causing unbearable suffering.

Pain nerves were designed to do their best work in the face of injury. This

differs from motor nerves, which put the body to rest with injury by decreasing

their function. It is difficult to get some clinicians, born and bred on

" motor think " to adjust to " pain think " . There are features of Central Pain

which

may seem unexpected.

Among these unexpected features are the following:

The stimulus which usually causes the most unbearable aspects of Central Pain

is the evoked pain of light touch, especially light touch which is persistent

and occlusive. Such patients may wear abbreviated clothing to avoid textures

rubbing on the skin.

The burning pain, which light touch evokes, does not occur when the stimulus

is first applied, but after time, (similar to the way the pain of sunburn

occurs well after the UV injury). This is called slow summation and is a

temporal

phenomenon. This evoked burning is lesser in magnitude but identical in

quality to spontaneous burning, an omnipresent burning which may be the only

dysesthesia (bizarre burning) present, particularly in quadriplegics. In other

words,

spontaneous burning is not always capable of being evoked. Evoked dysesthetic

burning is the big brother of spontaneous burning. Especially at the

peripherae however, (e.g. hands) evocation is usually displayed along with

spontaneous

burning, although the stimulus which evokes the burning varies from patient

to patient. Such a stimulus may be light touch, texture, or heat.

Very limited data suggest that dysesthesia (burning pain) also displays

spatial summation, which means as larger areas are covered with touch, the

magnitude of burning becomes greater. The dysesthesia is of a greater magnitude

where

touch sensation is poorest, which is usually distally on the body.

Central Pain also displays an hyperpathia. Sharp hyperpathia tends to occur

most where sensation is most retained, which is generally proximally on the

body. The location of visceral hyperpathia seems to follow more the positioning

of gas and digesting food in the gut. That which would be painful to people

without Central Pain is much more painful in Central Pain, but nothing is felt

until a greater than normal pain stimulus is applied.

Because these patients have decreased touch sensation, including decreased

sense to very light painful stimulus, Central Pain hyperpathia has been termed

to have a " delay " . This is an unfortunate term since it has nothing to do with

time. It appears to have been adopted because hyperpathia is often coexistent

with dysesthesia, which has a true temporal delay. With hyperpathia, there is

a level of noxious stimulus which is not perceived. This is actually a

heightened threshold to pain, not a temporal delay. The heightened threshold is

very

difficult to test for because it is so easily exceeded. Once the threshold has

been exceeded, or when pain is first perceived, the pain response overshoots

and responds violently. This is called delay with overshoot. The stimulus may

be sharpness, heat, or cold. It is more common for heat to stimulate

hyperpathic response in those with profound motor loss (plegics), while it is

more

common for cold or sharpness to generate hyperpathia in those who retain some

motor function (paretics).

" Delay with overshoot " is generally considered a synonym of hyperpathia, but

it is not really the same since hypersensitivity to pain can occur in those

with normal nervous systems (such as sunburn). Only those with nerve injury can

perceive hyperpathia long-term. The testing has not been done to determine how

neuropathic hyperpathia (injured nervous system) is similar to or different

from nociceptive hyperpathia (normal nervous system). Hyperpathia also occurs

in the viscera (gut), but is displayed there as a feeling of overfulness,

almost to exploding, like very severe distention with flatus. Similarly, a full

bladder can be unbearable.

The " fullness " is evoked in an inconsistent pattern by dietary intake.

Patients often can affect its course by choice and timing of food/water intake

or

elimination. Limited data indicate that the hyperpathia of Central Pain

increases directly in areas with retention of touch sensation, which is usually

proximally on the body, a gradient which is exactly the opposite of the burning

dysesthesia, which usually increases distally. These gradients can usually be

confirmed by careful questioning, but it is uncommon for the patient to

volunteer

the information since the gradients are not even and any dysesthetic pains are

poorly localized.

There is perhaps no more difficult area in which to obtain a correct history

than in pain which is " indescribable " . The result of haste and imprecise

questioning has made the literature on the subject almost incomprehensible. The

clinician should repeat questions several times from several angles before

assuming the patient differs from the norm in Central Pain as described in the

mnemonic on this website.

That light touch which is perceived in Central Pain has a " tingly " quality to

it. This may be thought of as similar to the " tingle " of a lip touched while

it is returning from dental anesthesia, or like the tingle of limbs falling

" asleep " . It is however, quite painful, " like needles " . It is the most intense

of the central pains but does not cause the most suffering. This tingle can be

pronounced, compelling the attention of the patient, or it can exist in a

minor form. Patients nearly always compare it to a limb which has fallen asleep

and is regaining feeling. It has been called " circulatory pain " .

A Central Pain patient who is paying very close attention may be able to

respond fairly well to light touch, creating a false impression for the hasty

examiner that the patient does not have diminished touch sensation. (Von Frey

hairs can detect " subclinical " diminution of touch sensation)

Clinicians are often impressed at what good historians normal patients can be

regarding pain, but the opposite can be expected pertaining to pain which the

patient knows is not normal pain, yet is severe. Central Pain, in its fully

developed form, is persistent torture. Humans chronically tortured often become

alienated and withdrawn. It is so severe that, lacking a vocabulary, they may

be very poor historians and may be reluctant to reveal the inroads the pain

has made into their humanity. Poor verbal skills may also be impacted by the

thalamic shutdown in this disease, making it difficult to prioritize and stick

to the appropriate comments, with the appropriate emphasis, in the flow of

conversation. The vagueness and strangeness of the symptoms are also factors in

poor descriptive performance.

The Lowest Common Denominator of Central Pain

Because the disease has so many aspects, we are indebted to Dr. Bowsher

for finding the lowest common denominator. Of all the symptoms, he has

identified the three which allow for simple diagnosis:

Burning pain, often with a paradoxical component of cold, made worse by light

touch or the rubbing of clothing.

Central Pain has definite thermal aspects. This is usually a narrow window of

relative comfort in ambient temperatures and onset of burning with

temperature change, either hot or cold. Alternatively, thermal aspects may

manifest as

an unusual sensitivity to heat, generally at the distal parts of a limb.

Thermal aspects are omitted from these criteria because they are also be seen in

ciguatera poisoning.

In general, it appears that the more sensation retained, the broader display

of Central Pain symptoms are manifest. Those with a greater retention of

neural function (e.g. quadriparetics) seem more likely to display a greater

range

of symptoms and also seem to have more problems enduring the pain.

Notwithstanding this, very severe pain may be found in quadriplegics, although

it tends to

have fewer dimensions.

Bowsher's Criteria can make diagnosis of the Central Pain accessible to every

doctor or professional.

Hallenbeck~Sikorsky~ BS,RN,UM,QC

Owner-Moderator

" AnGeLsInPain "

" OneVoiceInPain "

Interqual Certified

Published Psychiatric Researcher

Advocate for those in CIP, HIV, Psychologic Pain

" The Lord Will NEVER push us beyond what we can endure. "

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