Hypersensitization due to Cold Differs from Hypersensitization due to Heat

More information from the surveys. If you don’t recognize yourself here, don’t get nervous. It is due to the incompleteness of information provided in many surveys, the variety of CP manifestations, as well as the poverty of language where nerve injury pain is concerned.


The role of hypersensitization can hardly be overemphasized in Central Pain because that is what CP is. What was meant to be a system balanced between excitation and inhibition has had the inhibitory wing knocked out. A positive feedback loop occurs which will not be silenced. Dr. Patrick Wall said this is a torture. We would agree.

From the surveys, we find the following to be the general rule, if there can be said to be any rules in a condition where the exception is often the rule, and as Richard Chapman has said, “fools the patient as well as the Doctor”.

To read this properly, you MUST develop an awareness and keep in mind the difference between spontaneous dysesthetic burning, which is constant;
and, the EVOKED (elicited, and therefore intermittent) hypersensitization which is very much worse–an intermittent, severe, unbearable torture vs. the continual, demoralizing torture of spontaneous burning.

If you do not have this double hypersensitization, ie. constant spontaneous burning and intermittent evoked burning, you either are experiencing non-neuropathic mechanical pain routed through a disordered pain system, OR you have ONLY the intermittent evoked variety of CP. Because any mechanical pain in an area sensitized by CP can be HYPERSENSITIZED by the mechanical pain, it is common to confuse mechanical pain with central pain, since they both tend to go together. The problem is that doctors may themselves not make a distinction and decline to treat the mechanical pain, which is often a mistake. Examples of this include the easing of burning in the mouth which can follow the smoothing of a roughened crown which has been rubbing the tongue, or burning of the skin or neuropathic dura (trigeminal area) when there is some mechanical disorder in the same area

Remember, spontaneous dysesthesia is always or nearly always constant (subject to stress or other upregulating event). Evoked burning comes on only WHEN there is some evoking stimulus, such as occlusive touch, cold, or heat–ie change in temperature.

Although we speak here of heat evocation and cold evocation, much or most of your evoked pain may not be easy to trace to a specific cause. Such things as stress and changes in barometric pressure are linked to evocation in some people. If this evocation is constant, it is NOT really evoked pain, it is a reset of the level of spontaneous dysesthetic burning to a high level. In most it is no more than something similar to a severe sunburn. Of course, “burning” is just the word we have to use, although there are other pains mixed in, including something like cold, in most people.

“Like acid under the skin” or “skin rubbed raw” are common ways of expressing the dysesthetic burn. CP really IS acid around the nerves, including arachidonic and fatty acids brought on by genetic changes which we call “plasticity”. The genetic changes are caused by growth factors secreted by glia to attempt to repair injured neurons. These injured cells can be driven to make lots of chemicals but we do not yet have a way to coax them to regrow. Although plasticity is our arch enemy currently, when we have sufficient knowledge to lead it the right way, it will become our friend.

Lightning pains do NOT have the spontaneous and evoked aspect. They are always intermittent, although tending to be bunched, and are more likely to be linked to body position or muscle activity. Muscle pains DO display a constant pain/cramp, and also pain which is increased through any muscle activity. Kinesthetic dysesthesia is much more common than is realized by most researchers in the field. It varies from tightness or drawing in the chest known as “MS Hug” to a variety so severe that the patient is functionally paralyzed (as reported by Beric). Most CP subjects with kinesthetic dysesthesia, which may be isometric or isotonic, fall somewhere in between.

All muscle pains are thought to have their origin in the C fibers which supply the “gamma motor” system which includes the muscle spindles. “Gamma pain” is thought to travel in the posterior columns of the cord (“lemniscal” pain–so named after the higher connections of the posterior columns). Pain in the superficial sensibilities is often termed “spinothalamic pain”.

1. In CP if the skin has developed evoked dysesthetic burning through sensitization by heat or by touch, going out into cold weather generally eliminates the EVOKED dysesthetic burning hypersensitization within minutes (the spontaneous dysesthetic burning will remain, of course–this suggests there are TWO types of TOUCH/HEAT hypersensitization, at least).

Heat is comparatively slow to cause evoked hypersensitization, but when it does, the body “feels” as if it is literally overheated, even if the actual temperature is normal.

2. In CP, if the skin has developed a hypersensitive evocation level due to cold, going inside a warm house does NOT end the burning quickly. The burning may even increase for a time. This bears something of a resemblance to frostbite, where the pain comes on as the skin temperature is raised. We have also received reports of cold evoking the “pins and needles” of central pain–(this has always been from cold showers and usually EARLY in the years of the condition).

3. In nearly all CP people, a blast of cold air on the skin, such as from a car air conditioner, is much more rapid in causing evoked burning dysesthesia than is heat. This situation is called “cold allodynia” and of course is quite paradoxical, since cold would not cause a burn in the normal, non-doubly hypersensitized individual.

4. Light touch generally causes the same hypersensitization as heat, particularly if the light touch is OCCLUSIVE (as in laying a newspaper or saran wrap directly on the skin).

5. If the skin is wrapped very tightly, the rapid TOUCH/HEAT evoked hypersensitization does not usually occur, but a slower hypersensitization does.

6) The hypersensitization of Central Pain is not identical with severe sunburn, although both may make the wearing of clothing very difficult. In sunburn, once the skin is sensitized (which usually takes at least an hour or so) heightened pain from light touch is instantaneous. In Central Pain, heightened or evoked pain from light touch displays “Mitchell’s Delay”. This requires around twenty seconds or more before light touch brings on the evoked heightened burning. Carl Saab has shown that the cells of the vermis require about the same delay before they begin to inhibit pain from light touch. Mitchell’s Delay may be used to differentiate pain of peripheral nerve injury, which evokes instantly to touch, from pain of central origin, which displays Mitchell’s delay.

None of these findings is particularly intuitive but they illustrate what the patient is up against in describing his/her condition to the doctor. We list them here in the hopes that clinicians will not become irritated or lose patiences if the medical history simply does not seem to make sense. If it did make sense, it would not be central pain, it would be nociceptive pain.