Practical Science on Movement and Pain

Review of Geoffrey Bove Workshop on Pain, Nociception and Nerves: Part One

This weekend I had the pleasure of attending a workshop hosted by Geoffrey Bove on “Pain, Nociception and Nerves.” Geoff has forgotten more about these topics than most people will ever know, because he has conducted a great deal of the original research which contributes to our knowledge about these issues, particularly as it relates to manual therapy. Here is a link to his website with more information on his background, work, and lots of free papers.

Geoff discussed numerous topics that a manual therapist should know, including: distinguishing different origins of nociception; the mechanics of nerve movement; the key role of inflammation in pain; fascia and adhesions; and trigger points.

Here are some of the highlights of what we learned.

Different sources of nociception  

Geoff distinguished several different sources of nociception which can lead to pain. (I have to admit, I am still not totally clear on a few of these!)

Nociceptive pain is due to activation of normal nociceptors, i.e, firing of free nerve endings by mechanical, thermal or chemical stimuli. This implies that the pain arises from actual or threatened damage to non-neural tissue.

Ectopic nociceptive pain means that nociceptors are activated in the “wrong place.” For example, if a stimulus to a nerve trunk creates a nociceptive discharge that travels to the spinal cord, it has no way of knowing whether it comes from a nerve ending or the nerve trunk, but assumes it comes from the nerve ending. It therefore results in a painful sensation in the “wrong place” which feels very similar to nociceptive pain. A stimulus to a nerve trunk is very unlikely to result in an ectopic discharge unless inflammation is present. Geoff thinks that inflammation and resulting ectopic discharges are huge players in chronic pain.

Neuropathic pain is caused by nociception related to damaged “neural elements.” This does not include damage to the connective tissue sheath of the nerve which is far easier to heal. Damage to neural elements is uncommon with musculoskeletal injuries. The most common examples of disease processes causing damage to neural elements are postherpetic neuralgia and diabetic neuropathy. The nerve injuries caused by these conditions is very hard to heal, meaning that neuropathic noiciception will likely not go away.

Hyperalgesia is increased pain response from a normally painful stimulus. This may result from increased sensitivity of the nerve ending or the spinal cord. Allodynia is pain from a stimulus that does not normally cause pain. Allodynia may be caused when mechanoreception is perceived by the spinal cord as nociception.

Radicular pain is a term that is often misused and only applies to pain resulting from pressure on a nerve root.

Referred pain means pain that results from a miscommunication at the spinal cord which causes the higher levels of the nervous system to basically misinterpret the origin of a nociceptive impulses. For example, a heart attack results in nociceptive impulses from the heart, but the spinal cord gets confused about the origin of the signal – it thinks it is coming from the left arm, so pain is “referred” to the left arm.

Radiating pain means …. I have to admit I have forgotten! I think it means pain related to ectopic discharge, which causes pain to be felt a distance from the stimulus that caused the nociception (at the nerve ending, not the nerve trunk where the problem is).

Neurodynamics

Nerves are like coiled telephone cords or bungees  - they elongate in response to stretch, and can slide, bend and “floss” around as the body moves. A nerve that is stretched too far can lead to problems – an 8% stretch leads to ischemia; 15% to total ischemia; and more than 15% breaks axons and vessels. Ischemia leads to inflammation which, as discussed below, is a major player in chronic pain.

In general, nerves move quite easily with respect their surrounding tissues, which are called the mechanical interface. (Geoff said he could dissect out the nerve of a rat with just his hand – no scalpel necessary). A given point on a nerve will move with respect to its mechanical interface in the direction of the axis of rotation bending the nerve. For example, a straight leg raise will cause tensioning of the sciatic nerve, distal movement of the intra-pelvic sciatic nerve,  proximal movement of the sciatic nerve in the leg, and downward movement of the spinal cord. In other words, when the hip flexes, everything moves to the hip. In Bove’s view, understanding these movements is diagnostically important.

Another key point is that nerves can be placed under continuous tension across many joints, while most other structures like muscles cannot. We can use this fact to your advantage in finding the structure causing the nociception. If we flex the hip and cause pain in the butt, and then can modulate that pain by moving the ankle, we can be pretty sure that we are dealing with pain related to nerve movement not muscle movement.

It is also important to understand the various areas where the nerves cannot move so much with respect to their surrounding tissues, for example where the nerves branch. Geoff thinks that nerves are more likely to become tethered in places where the nerve passes through an opening in muscle, fascia and other tunnels, particularly where the nerve runs perpendicular to the mechanical interface as opposed to parallel. He pointed out that many areas where nerves have a perpendicular relationship to a mechanical interface are common places for chronic pain complaints, such as the greater occipital nerve, the brachial plexus through the scalenes, clavicle and pec minor, the median nerve at pronator teres and the carpal tunnel, the ulnar nerve at the tunnel of guyon, the sciatic nerve at the greater sciatic foreman, the fibular nerve at the proximal fibula, the tibial nerve at the medial ankle, and everywhere that nerves pierce fascia, such as the back.

The results of this tethering might be increased ischemia and therefore inflammation with stretch. For example, an additional tethering point might mean that a movement which would normally cause only a 5% stretch will now cause a 10% stretch, which causes ischemia and inflammation, which has a variety of undesireable consequences as discussed below. Many places that people often label trigger points are more likely inflamed nerves that have become mechancially sensitive. More on that later. 

Despite these facts about “tethering”, I recall Bove referencing a study (by Dilly?) finding that nerve movements as seen on ultrasound are not different in an asymptomatic arm compared to an arm that experiences pain with movements that provoke the nerve. Further, I think he also mentioned that there are no studies showing that nerve mobilizations change actual movements of the nerves. This leads me to believe that any local therapeutic effect of nerve mobilizations resides less in the elimination of adhesions or tethering (which would affect movement) and more in the treatment of local inflammation, which would only affect how the movement feels. (I recall that Shacklock refers to “milking” the nerves of inflammation.)

Some other notes:

In a straight leg raise, the lower the SLR is positive, the more distal the pathology. Interestingly, the sciatic nerve becomes fully tight after 40° (or as it 60?) and will not continue to tighten after that threshold is reached.

Geoff uses his extensive knowledge of nerve anatomy (he taught anatomy at Harvard) to help locate points where manual therapy might help free up an irritated nerve. He’s not embarrassed to get out the book during a session to guide his hands.

Rats do not have visible nerve movement with the straight leg raise. I found this interesting because it suggests that the quadruped position requires far less neural mobility than a standing position. Would a chimp have lots of nerve movement with an SLR? If not, it implies that the evolutionary move from quadruped to standing greatly increased the need for neural mobility, at least in the lower half of the body.

A lot of the information we learned regarding nerve mechanics is also available in two excellent books by David Butler (the Sensitive Nervous System) and Michael Shacklock (Clinical Neurodynamics.) Geoff said he endorsed the information in those books (and also pointed out that much of the information in there was provided by his research.) I should also point out that I wrote a three part series discussing nerve mechanics.

Well that’s it for now. In the second post I will cover Geoff’’s discussion on the role of inflammation, peripheral versus central explanatons for chronic pain, trigger points, and myofascial release. Lots more good stuff to come!

Thanks again to Geoff Bove for the great seminar.

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6 Responses to Review of Geoffrey Bove Workshop on Pain, Nociception and Nerves: Part One

  1. Todd,

    It’s obvious that you paid attention and learned a lot. I’m well-aware of how you do that.

    I am always concerned when a speaker, researcher or not, uses the concepts of source and cause. That’s a path many have found uselessly confusing and full of unwarranted speculation.

    • Todd Hargrove says:

      Hi Barrett,

      I know that you and Geoffrey have had your disagreements online. So have I! For those that haven’t had the pleasure of getting involved in some of these fun FB chats, it seems to me that the major source of disagreement is the relative role of the periphery versus the brain in chronic pain. In short, Geoff is more of a peripheralist, and believes that chronic pain is unlikely to persist in the absence of a “peripheral generator” in the form of continued nociception. The Soma Simple crowd, including you and me, relying on the work of Moseley and Melzack, believe that the brain plays a large role in maintaining chronic pain. As far as I can tell, neither party to the debate thinks that only the brain, or only the periphery matters, but both feel that the other side overemphasizes one and discounts the other. I also think part of the disagreement results from pure semantics as opposed to substance (i.e disagreement about what something should be called as opposed to what it is.)

      That being said, this seminar really didn’t really address that debate at all, and was really focused on the periphery – the physiology of nociception between the nerve endings and the spinal cord. Everything Geoff said in that regard seemed highly defensible and always cited research (usually his own.) There was nothing inconsistent with what I have learned from Butler and Shacklock and Moseley on this topic. He was also very clear in pointing out any statements that were based on speculation and opinion versus hard evidence and accepted fact. And he did articulate just a little bit of his speculations about the importance of peripheral generators, which I will discuss in the second post.

      In short, I don’t think you or the SS crowd would have had much cause for objection to anything substantive (although you may have languaged a few things differently.)

  2. carl says:

    Hi Todd,

    Regarding the description of ectopic nociceptive pain, would this be the same thing as described by Butler as an abnormal impulse generating site.(AIGS. Antidromic neural impulses can cause neurogenic inflammation.

    • Todd Hargrove says:

      Hi Carl,

      That is what I was thinking during the seminar. I seem to recall asking that question and getting an affirmative answer.

  3. Hi — thanks for this great review and please, I am happy to answer questions, although the questions would have to be directed to me via email at geoffreybove@gmail.com. I first published the phenomenon of ectopic nociception in my 2003 paper, called “Inflammation Induces Ectopic Mechanical Sensitivity in Axons of Nociceptors Innervating Deep Tissues” (available on my website). I guess it would be what Butler is referring to as an “AIGS.”

    The impulses from the activation of small-fiber neural elements, no matter where they are activated, will indeed lead to the spread of the action potential to all branches of the axon, orthodromic and antidromic. This will cause release of vasoactive peptides, such as SP and CGRP, as well as the release of other chemicals (the list seems to be growing), at all terminals. This is the “nocifensor” or “homeostat” function of these neurons. The whole thing is wicked awesome. Stay tuned, more to come in the long run.

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