>Howard, I'd like to share your comments and information here with
>the arthritis support newsgroup.  With your permission only of
>course and with credit to you unless you would prefer I did not.
>Let me know OK?
>
>Jo

>----- Original Message ----- From: "Howard C. Berkowitz" <hcb@gettcomm.com>
>Newsgroups: rec.pets.cats.anecdotes
>Sent: Wednesday, August 03, 2005 7:08 PM
>Subject: Re: "The Promise" - OT
>
>>In article <3ld7apF12440rU1@individual.net>, "Jo Firey"
>><JAfirey@NETZERO.NET> wrote:
>>
>>>"Howard C. Berkowitz" <hcb@gettcomm.com> wrote in message
>>>news:hcb-576804.20365403082005@newsgroups.comcast.net...

>>>>  To get
>>>>  more specific into things we actually understand, pain, even if
>>>> blocked
>>>>  from consciousness but not with full anesthesia, causes the autonomic
>>>>  system to release inflammatory transmitters called
>>>>prostaglandins -- > which cause more pain. The survival benefit
>>>>of this seemingly perverse
>>>>  mechanism appears to be "self-splinting" by forcing one to hold an
>>>>  injured part rigid.

>>>That is one of the most enlightening things I've read in a long time.  As
>>>in WOW.

>>It is one of my fond hopes that as new doctors are trained and enter
>>practice, there will be more and more knowledge of the science (and art)
>>of pain management. Unfortunately, the understanding of many of the
>>mechanisms of pain are recent enough that older practicing physicians,
>>who don't keep up with current research, simply aren't aware of it.
>>
>>The subspecialty of pain medicine doesn't get the respect it should.
>>Melzack and Wall, who discovered the fundamental mechanism that causes
>>people to become aware of pain, as well as many of the secondary effects
>>of pain transmission, IMNSHO, deserved a Nobel Prize. AFAIK, no pain
>>researcher has ever been in serious consideration for the Nobel Prize in
>>Medicine or Physiology.

>>>I have a type of inflammatory arthritis.  Now at least I have some
>>>understanding of why I have stiff joints.  Not the prostaglandins stuff.
>>>That I knew.  But I'd never heard or thought of the concept of "self
>>>splinting".

>>The particular mechanisms I was talking about is directly associated
>>with muscle tissue, but I see no reason why a joint inflammation
>>couldn't cause it. The particular pathway that I was talking about comes
>>from the "lower" brain in response to pain in soft tissue, but the same
>>inflammatory substances are released from arthritic joints.
>>
>>Prostaglandins, incidentally, cause uterine contractions, and they have
>>been used to induce abortion or labor. By taking a prostaglandin
>>antagonist before the crampy stage of the menstrual cycle, so there's a
>>blood level before the prostaglandins hit, often can avoid or minimize
>>cramps.
>>
>>So, the muscles around the joint could go into spasm from the same
>>chemicals, but released from the joint rather than the brain. Ibuprofen,
>>naproxen, and prescription NSAIDs block the enzymes (COX-1 and COX-2)
>>that produces these irritants. Aspirin does as well, but has somewhat
>>different mechanisms.
>>
>>It turns out, however, that not all the products of the two enzymes are
>>bad. Some of the products of COX-1 produce the mucus that normally
>>protects the stomach wall.  When you suppress COX-1, you take away
>>protection from acid, which is why aspirin and NSAIDs upset the stomach.
>>The newer selective inhibitors of COX-2 only, such as Vioxx and
>>Celebrex, allow the stomach protection to work normally.
>>
>>Nothing in pain pharmacology tends to be simple. Some people only get
>>pain relief from COX-2 inhibitors, enough that the US Food and Drug
>>Administration approved their being used again, with lots of warning and
>>cardiac monitoring. We understand why COX-2 inhibitors prevent stomach
>>upset, but we are not sure why they are especially effective for pain
>>relief in some, but not all, patients. Like many drugs, there is a
>>delicate balance between risk and benefit.
>>
>>Acetaminophen (Tylenol), or paracetamol across the pond, does not block
>>COX enzymes except in the brain. This is why it has less of a general
>>anti-inflammatory action than the other drugs. It does block pain,
>>however, which, in turn, can block the secondary brain-directed release
>>of prostaglandins in muscle tissue.  This may give the effect of
>>decreasing inflammation, but it's really a matter of preventing
>>inflammation.