What's Hot and What's Not in the Current Literature

Neurochemistry is up and behaviorism is down, way down.

Hey, teacher, leave these CP kids alone!!! In other words, start reading biochemistry and stop thinking you can avoid approaching pain at the molecular level. Chemists examine molecular pain events every day. Alteration in chemical pathways in nerve injury pain are reproducible in animals, predictable, measurable, consistent, and known to every serious investigator.


Neurochemistry is about as welcome and familiar at a behaviorists’ convention as a speech advocating the abandonment of Windows in favor of pure Linux is at a family album get-together of old folks. Calling gossip “science” doesn’t make it science. Being a PhD doesn’t excuse such behavior because they have no alibi for not investigating, being educated. We are glad their mental efforts helped them get past their own pain, but severe Central Pain is something else altogether. Home remedies for nerve injury are like home lobotomy kits, not really serious.

In the early Celtic days, pregnancy was believed to result from being near bodies of water under a full moon. The best we know, considering the social probabilities, that was a more rational theory than the idea people with massive CREB, PKC, fatty acids and abnormal ion channels in their nervee are in pain because of mental weakness. Sort of like saying wood undergoing rapid oxidation is burning because of the way you feel about it, the match and the lighting fluid having no bearing.

Injected capsaicin, which activates the VR-1 channel, the membrane channel of central pain, causes burning pain in EVERY person so injected, regardless of attitude, religion, education, athletic ability, or number of articles published. Central Pain exists whether or not you have ever heard of it.

Pain cliches, known to everyone and by no means news, are not helpful in Central Paih. Most of the “advice” we receive is more like word association, but here the word sounds the same but is vastly different. The word “pain” in normal pain, and the same word as part of “central pain” are what the English teacher calls a “heteronym”–same word different meanings.

The presence of the word “Pain” in the name of this condition should not mislead you into thinking you know anything about it. If you wish to gain knowledge on the topic, you must be injected with capsaicin or better yet, have your cord/thalamus lasered. If you are unwilling to go this far, at least show your good manners by avoiding insensitive pain disparagement. ONLY those with nerve injury have felt the burning dysesthesia of CP. The lancinating pain is more familiar. And speaking of cliches, we like “The one who dies with the most toys, still dies.” We might add, “The person who hangs tough in the face of normal pain, will still be unable to cope if he develops central pain.”

One of our favorite researchers on central neuropathic pain is Clair Hulsebosch at UTMB who has contributed to the information at the site. Her group has now shown that neurons ABOVE the site of cord injury do indeed produce significantly more phosphorylated CREB in spinothalamic tract cells in central pain. CREB starts off the cascade of pain chemicals in central nerve injury.

This finding is no surprise at all to those familiar with pain chemistry, sort of like proving that combustion of wood is associated with heat, but given the persistent and passionate insistence by some that pain is just a state of mind, this study by Crown et al in May 05 Neurosci Letter is one more nail in the coffin of the behaviorists, who if they are not careful will have to begin studying biochemistry, a step which could lead to retractions, something behaviorists are LOATHE to do (and very slow as well, we might add).

Thanks to Dr. Hulsebosch for once again showing that the psychological beanie wearers need to inject a little hard science into their