Kevin | 
01 29th, 2006| 
Nerve repair is simply unlike repair elsewhere in the body. Much of it in the CNS seems aimed at eliminating and culling out the defective or injured nerves, accompanied by a bizarre and futile attempt by the glia to regenerate neurons by turning on genes haphazardly. It is as if something present in early living organisms, such as birds or fish, is missing in man, making human glial cells unable to repair damage. What goes on is not repair at all, but rather weakening and eventual death of more neurons. Peripheral nerves can repair by regrowing along the axon sheath which remains, but in the brain and cord, so far the news is all bad. Our brains can be repaired, but we must do it cognitively because Nature did not include this in the automatic repair mechanisms.
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.
Lawson and coworkers have laid out two successive studies of major importance in the Journal of Neuroscience. Since this journal is fabulously expensive, we thought you would like to have a summary here. Basically, three cheers for Sally N. Lawson. We hate to get you too far ahead of what is available clinically to your doctor, which makes both of you nervous, but researchers are speaking of KILLING nociceptors permanently.
Is it possible the third world has something to offer the pain sufferer?
The whole process of gene activation is becoming more complicated. It is not all or nothing at all.
Dr. Kory McHenry, former fellow at NIH (NINDS/NIDCR) pain group under Michael Iadarola and contributor to painonline has written here about resiniferatoxin. (see his prior articles). Now the RTX experiments have been conducted in dogs.
Opium comes from the poppy flower. Now a new pain drug has been located in the bark of a certain tree, which grows from Africa to Cambodia.
The vanilloid-1 receptor, now known as the transient receptor potential vanilloid-1 receptor is activated by capsaicin, the drug injected subcutaneously by scientists in an attempt to study C fiber sensitization. Vanilloids include its potential to bind to cannabinoids. However, TRPV-1 binds to many other substances such as capsaicin, resiniferatoxin, etc.
One of the things painonline has attempted to do is to provide articles for the lowest of the low, who are sick beyond hope. This is not realistic, but we do it anyway. We realize that the absolute lowest won’t read this. They live in countries where the internet is not accessible, they are too poor to seek proper help, and they are confused, perhaps illiterate and alone. But we hoped a ripple effect would occur, whereby doctors and the public would be reached and central pain would not remain undiscovered. There are other issues. This is one of them.
The rostral ventral medulla (RVM) is a relay area between the periaqueductal gray and the spinal cord. (See prior articles on the PAG using search). The cerebral aqueduct is a communicating channel about 3/4 inch long running in the midbrain between the IIId and IVth ventricles of the brain. See http://www.mrcophth.com/MRCOphth/mrcophthpartoneessay/march1990q4.html
Gray matter immediately around the aqueduct is the PAG.