The pains of CP are not always equally tormentous. Why?
The same people who are so fond of pointing out that nociceptive pain may be overridden by other factors, implying that only weak people are likely to feel much pain, absolutely cannot accept this feature when it occurs in Central Pain patients, Some even become hostile when the CP subject cannot give a consistent picture of what CP is like. Such skeptical observers cannot have it both ways.
If nociception is subject to modification, then CP is also subject, without calling into question its reality. CP is NOT more emotionally bsed than ordinary pain. If anything it is LESS linked to emotion as a causative factor, since the little Nav 1.3 ion channels and the pain chemicals pouring out of the gene protein factories upregulated by growth and repair factors, have their way with the neuron and tend to ignore emotion It is just that Central Pain is so severe, that it is likely to make the patient emotional, and the examiner may misunderstand cause and effect. The vagueness of the verbal description of CP may add to this misconception.
Although SOME soldiers, some athletes, and some mothers dashing into a fire ot save an infant can do so without feeling immediate pain, most cannot. CP subjects likewise can only rarely ignore their nerve injury pain. The exceptional circumstance should not be the expected norm for “socially acceptable” patients.
They are inconcistent in what they will allow. The reason, of course, is that they have had some experience with nociceptive pain, but NO experience with nerve injury pain.
In dealing with these people, I often use an analogy to the swollen lip in the dentist’s office. I ask them if their lip is ever swollen during the time the numbing wears off. Almsot to a person, no matter their educational level, they say “Yes”. Then I point out to them that their lip was not actually swollen. AFter a little debate, they come to realize that the lip cannot possibly have gone up and down like that in such a short time, which just “happens” to coincide with the carbodcaine.
What they have is a phantom. They have been fooled. I then tell them that is the way CP is. One is fooled, based on what their brain or thoughts suggests and it may take a long time to figure out what is actually going on. I tell them it took more than a year to figure out I was feeling a MIX of pain sensations in what is called “dysesthetic burning”.
The reason the pain is said to be bizarre is that more than one kind of pain is going on. Just as new colors are created by mixing primaries, new pains are created by mixing the primary pain sensations. These secondary pains cannot be described to someone who has not experienced them, just as a secondary color cannot be described. If someone had never tasted salt, how could you describe it to them. You could not. I explain this is why Central Pain people are such poor medical historians. They do not have a vocabulary, and also they are being fooled. I then point out that until we had the conversation, THEY themselves were fooled into thinking their lip was swollen coming out of the dentist’s office.
This approach make clinicians more tolerant of the extremely “poor” medical history and verbal description of pain which is given by CP patients. I am equally rigorous with CP patients. They must be given cues and taught to recognize the processes which are actualy occuring. They are required to tell specifically WHERE the pains are, HOW MANY pains they are experiencing, the precipitating causes, periodicity,etc.
Just as nocieptive pain is subject to modulation, various environmental factors and emotional factors can load neuropathic pain perception and morph it in various way. Too often, ignorant clinicians have taken this to mean the patient is malingering. However, once they realize that they themselves are subject to errot where sensation is concerned, they are more accepting when the CP patient gives a poor history, says they can’t really tell what is going on, or something similar.
At least one area involved with pain perception modulation is now known. The Central nucleus of the Amygdala is known to have a role in negative emotion, pain related learning, and the modification of pain by environmentally stressful input.
More of these input centers are sure to be identified. In the meantime, the physician must take the CP patient at his word. If the patient could describe CP well, they would not have CP. The pains are not familiar, not easily described, and they are modulated by what else is going on in the CP patient’s life, just like nociceptive pain. The whole structure of CP modulation is altered from normal, however.
The patient usually has difficulty realizing what the stimulus is which is exacerbating or relieving pain because the precipitating events may be things not normally associated with pain, such as stress, body position, prior muscle loading (as opposed to instant muscle loading), filling of gut or bladder to a moderate degree, clothing, temperature change, pressure, or medication.
The CP patient may be realatively insensitive to normally painful events like a bump or a pin prick, until a certain threshold of sensation is reached, and then the sensation may overshoot wildly. All these features of CP are new, and must be identified, and considered before the subject can begin to give a halfway decent history regarding their CP.
The skeptic must remember that nociceptive pain is variable too. CP is not any different.