Five Questions

[Diane]

AIGS: Abnormal Impulse Generating Sites, ectopic firing sites. I think there is still confusion at our interpretive level about how they form or why, but they indicate that a nerve is in trouble and is firing wildly, and they are part of a "sensitization" sequence of events, where nocioception is turned up, spontaneous firing occurs, and pain is more readily felt. If you google AIGS with google scholar, you'll get a bunch of studies that talk about them.

(Found the artwork with the google image tool. )

[nari]

From David's notes:

AIGS or ectopia

Pain and other symptoms from peripheral nerves must come from a change in sensitivity, number or organisation of receptors in the axolemma, or it can arise from innervated connective tissue of nerve. Concepte of ectopia fit neatly with the neurodynamic concepts.

The neural pathway is designed for conduction only - generation of impulses occurs probably at the ends, or at the DRG. When sprouting occurs, or the myelin is damaged in some way, AIGS occur. When they do, the DRG becomes extremely anxious...

Interestingly, the maximal firing can take up to 21 days to occur, but it is also possible for nerve injury to be symptomless for up to 14 days. Steroids can repair the damage; also remodelling (spontaneous) which occurs every 1-2 days.

I presume that 'injury' may include mechanical deformation...

So once we have identified an abnormal neurodynamic and proceded with whatever treatment is chosen, is our aim to calm down the DRG? By enhancing remodelling and/or decreasing ischaemic states? One would hope so.

Nari

[Jon Newman]

First Question: What is the origin of the pain?

How would you determine that?

I suppose I would determine that by whether the person is able to alter their pain with movement or positioning. If not, manual therapy is unlikely to be of much benefit.

[Diane]

I presume that 'injury' may include mechanical deformation...

I think so too. The system is alerted to any decrease in oxygen levels by the chemoreceptors, part of the nervi nervorum/nocioception sensor array right on the nerves themselves, the sensory nervous system of the nerves. The DRGs get interested.. The nerve starts to "hurt..", sets up the AIGS. It isn't necessarily damaged yet (pain is just neurogenic not neuropathic), and the AIGS can be reversed with increased circulatory flow, which will;
a) bring the preferred levels of oxygenation to the nerve, so the chemoreceptors go quiet, and;
b) wash out all the neural metabolites.

It's probably not 100% precisely accurate, but to patients I say that the AIGS on a nerve are like diaper rash on a baby; it needs fed, and cleaned, and changed, and that increased circulation/more motion(lotion) will do it all, will help provide the necessary factors to quiet down the system/help it dismantle the AIGS/heal the rash within a few days.

[nari]

I think that is an important distinction; ie pain as a result of an AIGS developing is not necessarily neuropathic - but neurogenic.

jon

If ALL movement/positioning increases pain and nothing reduces it - does that imply manual therapy is not useful, or is it just the alteration of the pain experience that indicates MT would help?
I'm thinking of the persistent pain people who have 24/7 pain and, fear avoidance aside, nothing improves the pain? Just curious.

Nari

[Barrett Dorko]

Nari,

Alteration, not elimination.

Jon's post fits accurately and simply into this discussion, I think.

Last time I talked to David Butler in person I told him that, to me, AIGs were represented by neural membranes that were more like lace and less like canvas. He didn't like this but didn't tell me why. Of course, I couldn't get him to listen to anything about ideomotion either. Guess he was too busy.

This first question has generated plenty of discussion and has almost been answered - to my satisfaction anyway.

The second question soon.

[nari]

Barrett

I didn't suggest or imply elimination but I think I have answered my own question anyway.

[Luke Rickards]

Barrett,

The answer from Nic is, 'Yes, spontaneous discharge does occur in the absence of transduction. This may happen both within the DRG and the nerve axon.

Luke

[Barrett Dorko]

So, four origins can be defended. The last two are probably the most difficult to alter rapidly with therapy though it's concievable that a carefully concieved program might succeed eventually.

The origin most likely to respond to the corrective movement Simple Contact reveals is mechanical deformation, of course (not that the others cannot be concurrent), so it's the one I want to know is present. A single question will reveal this.

[Luke Rickards]

Chris,

Central deafferentation pain refers to pain related to central nervous system damage from stroke (often post-thalamic) or spinal cord injury. It is different to central sensitisation in that pain may be genearted in the absence of any peripheral input.

Luke

[stregapez]

Nari (or whomever) what is DRG?

Dana

[Luke Rickards]

DRG- dorsal root ganglion

[Barrett Dorko]

I think it's time for the second question: Are there any disease processes or pathological problems that are relevant to and might be responsible for your pain?

Obviously, this is no small issue. As I say to my classes, "I'm a PT and my ability to diagnose is severely limited. I depend upon my referral souces to answer this question and make no apologies for this limitation on my part."

Thoughts?

[Crazy Pole]

Barrett,

I'm not sure, but I think what you are getting at is the relative uselessness/meaninglessness of PT diagnoses. The more I practice and learn, the more I would agree; if that is in fact your point.

You may also be hinting at the idea of "if nothing is wrong (in terms of true pathology), then do nothing". Simple as it sounds, I like it and have been trying to integrate it into my practice. Strangely, I find it quite satisfying to have a patient recover while I do essentially nothing.

Maybe I am way off on my assessment, but I'm trying to think like I think you would think. Someone let me know if I'm getting warm.

Wes

[Jon Newman]

I have to admit that I rather enjoy having the process of labeling a disease and pathology done by someone intensively trained to do that. I think I could recognize if such a thing exists but I am not particularly interested in labeling it. Unless something requires careful restriction of movement, a special pill or surgery, most of those labels are not going to be particularly helpful in guiding what I do next. I suppose that last point is a bit redundant as I think Wes already addressed it.