Central Pain; Are the tenets of spinothalamic pain completely wrong?

This article is so radical we almost hate to review it. However, truth will out and so we must communicate what some very good French researchers have found in those with syringomyelia.

The only possible assumption which may have introduced error into this almost unbelievable study is the assumption that those with syringomyelia frequently have a “selective or preferential lesion of the spinothalamic tract resulting in thermosensory deficits of various extents and magnitudes”.

The “thermosensory disinhibition theory”, to which this language refers is a recent theory based on the idea that failure in injured cells of the inhibition of thermal sensory afferents that affect nociceptive reception is responsible for central pain. The LOCATION of these sensory afferents has never been definitely established, some thinking they run with blood vessels, and others saying we dont’ know. That is the weak link. However, quantitative brain imaging is probably sufficient on its own to locate the path of pain. or is it merely identifying the path of the RESPONSE to pain. This study points out once again that we don’t really know.

What these French scientists did was compare quantitative sensory loss in those with central pain and those who had no central pain. Then, they followed up with functional MRI to study EVOKED pain in the CP patients. Then they did functional MRI on those who had SPONTANEOUS pain only. There was NO SIGNIFICANT DIFFERENCE in the sensory loss between those who had CP and those who did not. So far, so good, and there is nothing new about that. However, they then claimed to show that lesions of the ST tract are necessary for sensory loss.

Now of course there are other sensory tracts, such as in the posterior columns and so this statement is the weakest link, but nevertheless possibly true. Their conclusion was then that lesion of the ST tract ALONE is insufficient to cause CP and that a dysfunction in the prefrontal cortex, (the only area consistently correlating with pathological dysfunction in the pain tracts) which they did find on fMRI in CP, was necessary. They also concluded there are different kinds of CP.

Most of this we can easily subscribe to, but we are unaware of anything conclusive to show that lesions of THE ST tract is necessary for sensory loss. The reason is that there are TWO ST tracts and one may function when the other is damaged. Since the investigators failed to distinguish between the ventral and the lateral ST tracts, their study is open to question. Still, we love it when radiologists decide to get serious about pain and turn into detectives about central pain.

At the same time we say “keep it up”, we have to honor our own survey results, which indicate these French researchers have more distance to cover before making their statements conclusively. There is of course the very substantial evidence (such as the article written for this site by Dr. Francis Crick and later confirmed in the Journal of Pain) that the painfulness of pain is in the insular cortex. These scientists noted blood flow to the prefrontal cortex, but all they are really doing with that is validating that the patient is having a response to pain, ie. to cold or to brushing of the skin in allodynic fashion, ie. long before a normal person would feel pain. Still, we love them for their contribution.

Prefrontal cortex is an emotional area, so they may have just been picking up the sign of pain, not the causative area. They do not say enough about the insular cortex to determine whether we can reform our ideas about its contribution in such studies. We suspect many reviewers will feel this study raises as many questions as it answers. This information comes from Ducreux et al reporting in Brain. 2006 Jan 24