Based on the theory that the right hemisphere “smooths” input and the left hemisphere detects discrepancy and Harris’s speculation that pain represents discrepancy, doctors at UCSD are conducting clinical trial by caloric (thermal) stimulation, aimed at a response in the inferior insula/parietal cortex. They are asking for those with thalamic stroke pain (Dejerine Roussy syndrome) to contact them. This is central pain following stroke.
The literature have solid evidence that men and women experience pain differently, but do they experience CENTRAL pain differently?
Relatively benign viruses can be used as a vehicle to bring materials into the nervous system, by infection with viruses into which has been spliced the genes to manufacture certain molecules. Viruses incorporate themselves into the DNA of the neuron, making it possible to manipulate gene expression.
What is Central Pain, at the basic level? We know it is acids around the neurons, which drive current successively through voltage gaged sodium 1.3 and calcium 2.2 channels, and ultimately, the TRPV-1 receptors, but what does it mean to the thalamus and cortex, which must lens it all into a sensation? The following are excerpts from a discussion conducted with one of our pain consultants, Dr. K McHenry, who had collaborated with our founder, Dr. Patrick Wall, in times past.
The National Institutes of Health decides how research money is allocated. Here is the way to contact the director, to request funds for basic research on central pain. The vast majority of morphine addicts begin by using it for legitimate pain and then become hooked. This would not happen if we had better medicines. The cost in rehab savings, endless paperwork by nurses and bureaucrats of morphine adminstration would almost disappear. Savings in crime and law endorcement alone would justify the costs of research. And for conditions like central pain, where opiates do not work, we should put an end to America’s Auschwitz.
NF Kappa B is a transcription factor which directly leads to gene coding for interleukin-6, an acidifying cytokine, and nitric acid synthase (which makes inducible nitric oxide). If you have burning dysesthesia, you have a lot more NF Kappa B around than you could ever want.
Yes, we are fickle. We just published an article which required some laborious effort to understand NMDA and blamed it for most everything. However, as a prior article here pointed out, there is almost certainly an element of fast, or AMPA/kainate pain, in some central pain, possibly in most who have EVOKED burning dysesthesia.
As much as we would like to avoid the technical, it will very soon be impossible to explain research to anyone who does not have at least a passing familiarity with what is meant by the NMDA receptor, the mediator at nociceptor synapses of chronic central pain. We introduce terms you will come across later. Once you get the terms, it is not so much worse than figuring out how to download an Ipod, an inborn ability for teenagers which requires sweat and toil for adults.
You won’t see a list of them in Forbe’s. No top five hundred pain researchers in the world. However, in rating systems of another kind, they rank at the top.
Yale has enjoyed an unusual reputation for pain research, but recent progress at its neighbor, Brown University, home of one of the authors at painonline, shows the people at Brown are awesome also.