Cold Fire and the Thalamus



            Eighty five percent of those responding to the question on the survey indicate that cold is a more rapid and powerful sensitizer (causing an evoked or heightened level) of their dysesthetic burning than heat. What can the explanation for this be??? See below.



Please note that in this article, the word Layer and Lamina mean the same thing, referring to the Rexed layers of the Spinal cord, which have the lowest numbers most superficially. Layer I is the marginal layer, where single C fibers have been documented to sensitize as much as half of the body. Layer II, the substantia gelatinosa, is the traditional pain layer. C fibers ascending to the dorsal root ganglia and horn of the cord recruit the big powerful A fibers to make for hypersensitization of the pain system. C fibers themselves are slow and imprecise.  We are learning that the traditional view that Layer II is most of the pain story is probably wrong. Somatosensory area I in the brain (the posterior ridge of the central sulcus) probably tells the LOCATION of the pain, Somatosensory II (parietal cortex) probably determines the SIGNIFICANCE of the pain, and the insular cortex appears to create the PAINFULNESS of the pain. It is still the majority viewpoint that Layer II feeds to SSI, the central sulcus. Pain ascends in the multistranded tracts which are known collectively as the spinothalamic tract, but this is a tract like telephone wires in a bundle are a tract. Dr. Patrick Wall, co founder of Painonline, in  1985 traced out as many as SEVEN discrete spinothalamic branches feeding into the thalamus.



As described in earlier articles, the thalamus, which is really two structures, there being one on each side of the brain, sits more or less straight back from the eyes at the center of the brain structures. The thalamus is probably far more important than we know, and we know quite a bit. One of the authors here, Dr. Francis Crick, even published a book opining that the human perception of the soul resides in the thalamus.



Just as identifying the part of the brain responsible for pain has been very difficult (although Dr. Crick and Dr. McHenry’s article here on the insular cortex broke new ground in locating the site of the painfulness of pain, ie. the insular cortex, scientists are presently trying to determine precisely the origin of fibers which carry pain to the insular cortex.


Al-Khater et al writing in the J. Comp Neurol 2008 Nov 1:511(1) 1-18 performed surprising studies which identified the posterior triangle of the thalamus (ie. the very caudal end) as the site which apparently feeds TO the insular cortex, where the painfulness of pain is appreciated. This pathway, the PoT nucleus pathway, is probably very important in central pain. This nucleus has not been included in prior studies of the pain in the thalamus because it was assumed that pain went to the VPM and VPL nuclei of the thalamus. Now we have a new area which seems dedicated to painfulness. This certainly bears further examination.


The spinothalamic cells which travel in the deeper lamina of the cord feed to the PoT. In the rat, there are approximately 90 spinothalamic neurons per side, some of which feed ONLY to the PoT.  The authors state that “85% of the lamina III/IV NK1r-immunoreactive neurons in C6 and 17% of those in L5 belong to the spinothalamic tract, and these apparently project exclusively to the caudal thalamus, including PoT.


Considering that few neuroscientists are even aware of a nucleus at the extreme end of the thalamus relating to pain, these scientists deserve credit for identifying a likely pathway for modulation of painfulness of pain.



This information and the resaons for it follow in a review of  the remarkable article,


Davidson S, Zhang X, Khasabov SG, Simone DA, Giesler GJ JrJ Neurophysiol. 2008 Oct;100(4):2026-37.

Termination zones of functionally characterized spinothalamic tract neurons within the primate posterior thalamus.


These authors found that ONE THIRD of the pain transmitting neurons going to the posterior thalamus respond to thermal heating, while TWO THIRDS respond to cooling.


Those with central pain have always found that hypersensitization of the BURNING dysesthesia is more rapidly and powerfully evoked by a cold blast of air than by heating. Davidson et al may have an anatomical explanation for this paradoxical clinical feature of central pain. More work is certain to be done on the posterior thalamus.