“Doctor, it hurts when I do this.”
“So stop doing that.”
Yeah, yeah, but what happens when you get a batch of clinicians who not only encourage people to keep “doing that”, but add in pain produced by “heat application” and the use of a positron-emission tomography (PET) scanner, too? You get this new study on how athritis pain lights up the medial part of the pain matrix responsible for emotional pain, like fear and stress.
The study comprised 18 patients with osteo-arthritis who were scanned with PET during arthritis pain, during experimental pain (that intriguing “heat application” reference in the article; cigarette, blowtorch, or active CPU chip?), and during pain-free time. The researchers found higher activation of the medial pain system during arthritis pain than during experimental pain.
“The present study demonstrates the importance of the medial pain system during the experience of arthritic pain and suggests that it is a likely target for both pharmacologic and nonpharmacologic interventions,” notes its leading author, Prof. A.K.P. Jones. “Considering the recent concerns about the long-term safety of cyclo-oxygenase inhibitors, we hope that our current findings will stimulate partnerships between academia and the pharmacological industry to develop a new class of analgesics for arthritic pain that specifically target the medial pain system.”
It seems to me that if anti-anxiety drugs live up to their billing, they must play some role in decreasing activity in the medial pain system. Is there an M.D./Ph.D. handy to check me on this? If so, then those wishing to act upon this news could consider whether to simply add medication already known to decrease medial pain system activity to whatever regimen is used currently for handling arthritis pain.
Addendum: Getting to something relevant to my past history, I’ll predict that if this study is done substituting sufferers of ulcerative colitis and Crohn’s disease for the arthritis sufferers, they will find the same result. Keeping the pharmacology separate for decreasing medial pain system activity would permit, then, the use of that medicine for both arthritis and IBD patients, rather than having a multi-symptom combination that would only be appropriate for arthritis patients.