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. David 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.