No wonder pain patients have trouble communicating. So many terms around.
There is an ebb and flow as various clinicians and scientists gain consensus or disagree about which neurologic syndromes or symptoms belong in which category. This is not new in neurology, which is notorious for having many terms, defined differently according to context.
One example is the term, “thalamic pain”. Some modern authors reserve this term for post stroke pain. However, the original authors, Dejerine and Roussy, did no such thing. In Tract Optique, they use the term “thalamic pain” interchangeably with the term, “Pain of Central Origin”. Their co-worker Egger did the same, as did S Weir Mitchell in the United States. Splitting pretends a different mechanism which is far from proven. The nature of the pain after stroke is also often identical to spinal cord injury pain. The difference in distribution (stroke pain tends to be on one side of the body) may or may not justify vouchsafing “thalamic pain” to stroke patients; since, really, they are so similar to post SCI pain subjects.
Similarly, it is nearly universal to use the term “spinothalamic tract pain”. However, there are TWO ST tracts, the anterior and the lateral ST tracts, located at quite different places in the cord. It is arguably sloppy to omit WHICH tract one is referring to, yet it is commonplace to speak of both as if they were ONE tract. This is NOT the best medicine can do. Since discrete injury to one or the other tracts is possible, the patient deserves to know the real story. it also helps researchers in neuroantomy to benefit from reports in the clinical literature if the doctor bothers to make a distinction. We learn more that way.
A recent term is actually VERY good. It expresses things well and we are always on the lookout for any verbal help in expressing the dimensions of neuropathic pain.
Spicher et al in Somatosens Mot Res. 2008 Mar;25(1):77-92. have used the term, “static mechanical allodynia”. Although not likely to be spontaneously expressed by a patient, this new term, or “SMA” as they call it is really very good. It comes to us from the world of PERIPHERAL nerve injury pain research, but anyone with central pain knows just what they are talking about.
“Static” is roughly equivalent to Ron Tasker;s “Spontaneous pain”. In medical terms, “static” means as opposed to “phasic”. We don’t really like either of these terms, because they pretend a dichotomy which may or may not really exist.
“Mechanical” just means in response to mechanical stimuli, as opposed to say heat or chemical stimuli. This matters mainly because at the microscopic level different nociceptor neurons are considered “mechanoreceptors” or “chemoreceptors”, divided into low or high threshold, wide or narrow dynamic range, low or high threshold, etc. Wm Willis Jr has shown that some of these neurons can convert to a different type in hypersensitization, so there is more to be learned. It is not always clear that PhD’s mean the same thing as the clinicians when they publish using these terms.
“Allodynia” of course is our old friend, meaning pain from what ought not to be painful. We have already written here that this term also is ambiguous and has also been applied to such things as “location allodynia” which means pain in an area which ought not to be painful, in response to a localized stimulus. (Use search to read more on Allodynia).
So why do we like the term static mechanical allodynia. It is because the authors make clear that it should be thought of as a paradoxical painful hypo-aesthesia. This is really good. The authors came upon this by discovering that vibration of a painful area caused that area to lose some sensation. They were able to outline which branch of a given nerve was injured by observing which area became less capable of sensing, ie. which area became hypo-aesthetic.
What we like is that the authors have no problem whatsoever using the term “Painful Hypoasthesia”. This sounds like an oxymoron, and that is exactly why it is good. It helps us to express what we have been saying for so long. Yes, it is numb there, but it really hurts.
Spicher even goes so far as to say regarding paradoxically painful hypoesthesia, “the mechanism of pain sensitization is probably central and referred peripherally to the skin by a painful hypoaesthesia.” Read as it is worded, this analysis is really almost humorous, yet it is quite rational.
This statement is a face on the doctors who call central pain patients crazy. They will have to include the authors in their denunciation if they persist in their stubborn refusal to understand that nerves may be too injured to transmit normal touch, but more than adequate as a conduit for really severe pain.
It is interesting that vibration dulls the pain of peripheral nerve injury. We hope more will be done to study this in central pain.