Sunday, March 09, 2014

"Joints" that the brain might actually take quicker, closer notice of

A long time ago I wrote about "trigger points" and why I didn't think they were in muscle.

Lately I've been working hard on a bunch of images of the neurovascular array around major joints. Also I've been working on a presentation I'm scheduled to give in a few weeks at the Massage Therapist Pain Conference in Vancouver.

I decided to make a slide that depicts some of the tubing array, and joins between them, and mechanical deformation, all at the same time. 

Here is my effort: 

Green is nerve, blue is vein, red is artery. (Ignore the blue bit in the top right corner - it's part of the slide format, not part of the image.)

Bear in mind that nerves and vessels can never exist very far apart from each other. Nerves need constant access to oxygen and glucose. Bear in mind that nerves don't have (according to current thinking) any lymph drainage. If any connector vessel were to become kinked or flattened by adverse mechanical tension, for a long time, like for example, by constantly sitting and never moving, the nerve, innervated by nociceptors, is likely to complain. This would be because of a high enough threshold stimulus of the mechano-, or chemo-, type (presumably thermo- would not be an issue).  

The thing is, the physiological tubing of the body is attached all the way along. It twines and braids and twirls through the body, sliding through the same or very close "grommet holes" in stiff tissue layers to travel to the surface, into hypodermis. 

By the time it reaches the cutis/subcutis layer, the vessels are small, but still, they remain attached to nerve which although is also smaller, has fewer fascicles and is therefore more vulnerable to compression and/or deformation.

Luckily, most of us have lots of padding. Still, if your hide is always pulled sideways somehow, always the same way, by some sort of contact with a surface, the tubing inside that layer will be pulled too - maybe it won't like it. Maybe the strain will be felt quite soon, or eventually, or be broadcast out along entire branches from related spinal cord segments. Sore spots will turn up before actual pain does, probably. 


Adiemus said...

what do you mean "sore spots will turn up before actual pain does, probably"? I'm confused - I thought sore and pain were equivalent, or have I missed something?!

Diane Jacobs said...

Hi Bronnie,
Thank you for your comment.
What I've noticed is that sore spots, i.e., tender places, are way more common than is actual pain, pain that would drive someone in to see a therapist like me for example.
Just about anyone will be tender - I think it's the brain's way of protecting its organism from harm. (E.g., children: "Ouch - stop punching my arm! That hurts!")
Maybe the kids with congenital analgesia wouldn't be found to have tender spots.
I think tender spots (even though they are probably the same thing as secondary hyperalgesia) would still best belong, therefore, under the heading "nociception" as opposed to "pain": They don't usually "hurt" unless provoked by the outside world, and as soon as the stimulus stops, they stop being paid any attention to by the brain.
Perhaps you would agree that "pain" (in all its 'unique to each individual', perceptual glory) falls under a different mechanism (or maybe several) and includes impaired motor control, lack of inhibition over spinal cord mechanisms, etc.

Not that they don't overlap a lot... ie., It's rare to find anyone in "pain" who doesn't also have "tenderness". And not that the people whose tenderness is treated (human primate social grooming) don't improve in the (mechanical) pain department.

Jukka Aho said...

Hi Diane,
Did I understand you correct that you meant "sore spots" without actual pain to presumably be secondary hyperalgesia? Then my next question would be secondary to what? Don't we need a primary source of nociception for secondary hyperalgesia to occur or am I mixing terms or misunderstood something?

I agree with your notion that a lot of people might have tenderness, but not pain.

Diane Jacobs said...

Hi Jukka,
Thank you for your interest.
My understanding is that secondary hyperalgesia means, secondary to activity going on inside the spinal cord (the oldest part of the central nervous system).
Remember that nociceptive neurons (any sensory neurons) are veryveryveryvery l---o---n---g body cells that span the distance from anywhere on or in the body (e.g., skin of big toe) all the way to the dorsal horn of the spinal cord, with a cell body in the dorsal root ganglion. Its ends are called "poles".
Primary hyperalgesia occurs when the *terminal* pole of a nociceptor is irritated by tissue trauma. This results in the classic inflammatory state (cardinal signs: dolor, rubor, calor, tumor) associated with tissue healing.
Secondary hyperalgesia occurs when the *central* pole of the nociceptive neuron is bothered inside the spinal cord by glial activity and other sensitization processes at the level of the dorsal horn.
Since nociceptors normally exhibit low-level activity all the time, not just when there is an injury, presumably secondary hyperalgesia is kind of normal, too (worse when you are tired, have fluctuating hormones, are sick, are stressed, all those ordinary human things...)

Most of this goes on outside conscious awareness, I'm pretty sure. Most people don't experience pain to any large extent. So, most people won't realize they have sore spots until somebody goes looking for them.

I guess we could argue over where the line is between nociception and pain, here..
My take is..:
1. because you can find sore spots on people, and treat them, without having to press on them and "hurt" them (either the people or the spots);
2. because only the primary nociceptive neurons are involved, not second order ascending ones, (not yet at least..)
3. because most people are not aware they have them..

... that sore spots count as nociception and not "pain".