Tri-10, Wk03 - Day ???, Monday January 23rd, 2012

It will take some catching up to figure out what day we're on right now since it's been so long since my last blog (11/8/11) I've had some request from others who have read my blog prior to becoming chiropractic students themselves, some are at Logan and other's are elsewhere across the country. There's also been a few local request to get back to blogging. Some have said it's inspirational but, I'm not quite sure how.

My current favorite class is Differential Diagnosis which is taught by Dr. Kettner. We've been going over chronic pain and it is a fascinating subject. The most recent research would indicate that a main culprit in the chronic pain syndrome is not so much by the stimulus of pain but rather by a lack of inhibition of that pain. A part of the anatomical basis for the inhibition of pain would have to do with descending inhibitory pathways from the brain.

What's really fascinating is something new I learned today called Nocebo - this is the counterpart to the much more well known "Placebo" which most people have heard of with reference to the Placebo effect, when a patient may be given something like a sugar pill but upon believing it is something beneficial will manifest positive outcomes as a result of their beliefs.
Nocebo is the opposite of the Placebo effect - this is based upon a patients pessimistic attitude or even a lack of trust or understanding and can result in increased pain.
But - there are real chemicals at work and real pathways in the Central Nervous System (CNS) which conduct and manifest these beliefs.
On one hand we may have descending inhibitory pathways but those pathways may also be descending fascilitating pathways.
with an emphasis on fascilitation, we may have a lack of inhibition. Substances associated with pain would be on the order of NMDA or Substance P while those substances which help inhibit pain would be things like enkephalins and endorphins.

I've left and gone off on a tangent - I'm reading about GABA-A alpha 2 receptors and their contribution to binge drinking and their association with a persons vulnerability to engage in binge drinking.

from an article in PNAS - Neuroscience, received for review January 6, 2011 we read that Binge drinking was inhibited by GABAa alpha 1 siRNA vactor infused into the ventral pallidum, unrelated to TLR4....

The data indicate that GABA a alpha2-regulated TLR4 expression in the CeA contributes to binge drinking and may be a key early neuroadaptation in excessive drinking...

That GABA is what we've talked about earlier in this blog, I believe it's Gamma Amino butyric Acid.
The TLR4 is Toll-like receptor 4.
CeA is the Central Nucleus of the Amygdala
siRNA is small interfering RNA

The earlier reference to the amygdala is how I got on this tangent to begin with...not sure if I mentioned it specifically before but it's one of the pieces when talking about pain processing pathways.