There is NO neuropathic pain matrix.

Scientists like to have positive findings. The brave ones work hard for truth, whatever it turns out to be.

We have visited work by Bouhassira before. He is a French neuroscientist.

His most recent work, along with Moisset, is very significant, although at first gloss it may not seem so.

We have recently reviewed Witting’s article showing a quiet thalamus in CP but an active orbitofrontal cortex, an emotional area involved with aversive learning. This was a radical new finding.

We have expressed the view for years that the spontaneous burning of central pain, which occurs with the baseline “noise” which exists in the brain, should be viewed differently from the evoked pain, which occurs after some input from the peripherae. Spontaneous dysesthesia is not related to an identifiable event, while evoked pain IS related to an event. It is evinced by stimulus to the peripherae. Since spinal cord injury patients are often missing or diminished in input from the exterior, it is an extraordinary thing that a patient who cannot feel any conscious touch from touch, may nevertheless experience agonizing evoked central pain from an otherwise undetectable stimulus.

Lancinating pain in the posterior columns is usually not related to a specific event. Rarely, the pain originates in an area where the subject can perceive a muscle twitch, or in certain positions, but other posterior column pains, such as muscle pain include an evoked component, from movement. This is known as kinesthetic dysesthesia. It can be terribly severe. Some patients with intact motor units are functionally paralyzed by the pain, as pointed out by Beric in “Muscle and Nerve”.

Muscle pains are almost always underreported in clinical reviews. More than seventy percent of subjects completing the surveys, including quadriplegics have muscle pains as part of central pain. About forty percent of MS patients in the survey noticed MS Hug, a tightening sensation of the chest, as an aarly sign of MS. The literature most often mention eye irritation or tingling as the first sign of MS, but the surveys suggest MS Hug, a muscle sensation and part of CP, is one of the most common early signs.

There is also a common “confinement cramp” muscle pain, known as isometric dysesthesia which is essentially spontaneous, but has been noted to follow activity. Thus, we are presented with a hetergeneous group of central pain patients, and it should come as no surprise that brain imaging is also heterogeneous. Moisset and Bouhassira, as reviewed below, should be interpreted as confirming the nature of the disease.

The most potent evokers of such pain are typically a blast of cold air, occlusive touch, clothing, and sharpness, in that order. Hard punches typically cause no evocation at all, but sharp objects are usually upgraded all along the way, including the very sharp needle, but sharpness is meant to hurt and is hyperpathia rather than the hyperalgesia of nonpainful stimulus as specified.

All the commmon evoking stimuli are arguably related to thermal change input. However, there is a definite link between the texture of clothing and the pain it evokes, so touch can be involved as well. Some patients even report that evoked pain is more potent in areas of high humidity or other variations of the environment, but again, these bear some relation to the impact of temperature.

We did not expect anyone to take a look at this for quite some time, but we were pleasantly surprised to see Moisset and Bouhassira, writing in Neuroimage. 2007 Apr 10.

Basically these authors used PET and functional MRI to look at spontaneous pain, and peripheral and central neuropathic pain. Like many prior authors, the results were variable. This was attributed to the lack of homogeneity of nerve injury pain patients. This is certainly correct, as the surveys have amply shown from an experiential/perceptual perspective.

The authors do feel that SPONTANEOUS central pain is emotionally linked and originates with the medial thalamic system. They are not saying as regards evoked pain. This is very intelligent on their part. It suggests that a constant aversive signal is generated and clearly the CP subjects we encounter are suffering emotionally. However, the evoked pain occurs ina different fashion and its path is variable.

It is not a given that these two entities are the same at all, although both contain an element of dysesthesia. This current study indicates that the spontaneous is probably more predictable, but evoked is variable to the extent that there is no “matrix” or special location for it. This is not to say that Moisset and Bouhassira believe spontaneous pain has a specific net or matrix either. There is simply a greater likelihood of encountering something in the thalamus when spontaneous pain is present. What that is, remains unknown.

Why is this a valuable study. Because it forces scientists to see what correlation thalamic activity has with chemical aberrations. Thank you to these French scientists.