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"Adverse Neural Tension" Testing Techniques (ANT)

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  • #31
    Hi fapt :

    Thank you for the link .




    • #32
      Here is a link to the PDF file of the referenced file =>

      Ectopic sensory discharges and paresthesiae in patients with disorders of peripheral nerves, dorsal roots and dorsal columns.
      Simplicity is the ultimate sophistication. L VINCI
      We are to admit no more causes of natural things than such as are both true and sufficient to explain their appearances. I NEWTON

      Everything should be made as simple as possible, but not a bit simpler.
      If you can't explain it simply, you don't understand it well enough. Albert Einstein


      • #33
        Here is the other cited one =>

        Inflammation Induces Ectopic Mechanical Sensitivity in Axons of Nociceptors Innervating Deep Tissues
        Simplicity is the ultimate sophistication. L VINCI
        We are to admit no more causes of natural things than such as are both true and sufficient to explain their appearances. I NEWTON

        Everything should be made as simple as possible, but not a bit simpler.
        If you can't explain it simply, you don't understand it well enough. Albert Einstein


        • #34
          Thanks Bernard, I met Geoff Bove in Denmark in the late 1990s when he was assistant professor at Odense University. I did a lecture to their department and we exchanged some great ideas. Soon after that, he went to Harvard. I like the work he does, neurophysiology that is.
          When we had our discussions he was very interested in nerves being a source of pain without producing changes in conduction velocity.

          The paper you posted - I've not read it before and, having printed it out, I'm really keen to get my teeth into it. Thanks a lot for doing this. I'll comment on it soon.


          • #35

            Neurosci Lett. 2001 Sep 21;311(1):49-52.
            Inflammation with no axonal damage of the rat saphenous nerve trunk induces ectopic discharge and mechanosensitivity in myelinated axons.

            Eliav E, Benoliel R, Tal M.

            Department of Oral Diagnosis, Oral Medicine and Oral Radiology, The Hebrew University, Hadassah School of Dental Medicine, P.O. Box 12272, Jerusalem, Israel.

            Inflammation along a nerve trunk with no frank axonal nerve damage produced by complete Freund's adjuvant (CFA) or Carrageenan is known to induce a painful peripheral neuropathy. In the present study, we examined the electrophysiological properties of myelinated axons (spontaneous discharge and mechanical sensitivity) at the inflamed nerve site. The rat saphenous nerves were exposed at mid-thigh level and wrapped in 2 mm wide bands of haemostatic oxidized cellulose (Oxycel) that were saturated with undiluted CFA. In the control rats the Oxycel) was saturated with saline. At postoperative days (PODs) 2-5 and 6-10, fine axon bundles were teased from the nerve, and electrophysiological recordings performed. At both time points spontaneous activity at the site of the application in CFA rats (PODs 2-5=9.9+/-2.5%: PODs 6-10=6.1+/-1.4%) was significantly higher than in the control animals (PODs 2-5=2.9+/-1.1%: PODs 6-10=1.6+/-1.4%: P=0.03, P=0.02, respectively). Mechanical sensitivity at both time points was significantly higher in CFA rats (PODs 2-5=12.6+/-3.1%: PODs 6-10=10.3+/-3.1%) than in saline rats (PODs 2-5=3.4+/-2.91%: PODs 6-10=0.8+/-1.0%: P=0.03, P=0.04, respectively). This study clearly shows that perineural inflammation with no axonal nerve damage induced by CFA application around the nerve trunk elevates spontaneous activity and induces mechanosensitivity in myelinated axons.

            PMID: 11585565 [PubMed - indexed for MEDLINE]
            Simplicity is the ultimate sophistication. L VINCI
            We are to admit no more causes of natural things than such as are both true and sufficient to explain their appearances. I NEWTON

            Everything should be made as simple as possible, but not a bit simpler.
            If you can't explain it simply, you don't understand it well enough. Albert Einstein


            • #36

              Brain. 2000 Jan;123 ( Pt 1):171-84.
              Effects of 4-aminopyridine on demyelinated axons, synapses and muscle tension.

              Smith KJ, Felts PA, John GR.

              Neuroinflammation Research Group, Department of Neuroimmunology, Guy's, King's and St Thomas' School of Medicine, Guy's Campus, London SE1 9RT, UK.

              Several clinical trials have demonstrated that 4-amino-pyridine (4-AP), a potassium channel-blocking agent, improves symptoms in some patients with multiple sclerosis. The beneficial effects have typically been attributed to the restoration of conduction to demyelinated axons, since this effect was previously demonstrated experimentally. However, the clinical dose is approximately 250-1000 times lower than that used experimentally, potentially making extrapolation of the experimental findings unreliable. To examine the action(s) of 4-AP in demyelinating disorders, the drug was administered at clinical doses, both in vivo and in vitro, to rat dorsal column axons which had been experimentally demyelinated by the intraspinal injection of ethidium bromide. 4-AP had no consistent effect in restoring conduction to demyelinated axons, even to axons which were held just on the verge of conducting by adjusting the lesion temperature. However, 4-AP had prominent effects that did not involve demyelinated axons, including the potentiation of synaptic transmission and an increase in skeletal muscle twitch tension. We propose that these latter effects may be largely responsible for the beneficial action of 4-AP in multiple sclerosis patients. If so, the dominant effects of 4-AP in multiple sclerosis patients are independent of demyelination, and it follows that 4-AP may be beneficial in other neurological disorders in which function is diminished.

              PMID: 10611131 [PubMed - indexed for MEDLINE]
              Simplicity is the ultimate sophistication. L VINCI
              We are to admit no more causes of natural things than such as are both true and sufficient to explain their appearances. I NEWTON

              Everything should be made as simple as possible, but not a bit simpler.
              If you can't explain it simply, you don't understand it well enough. Albert Einstein


              • #37
                Bernard, thanks for putting on such an important study. I was aware of this one but sometimes things get buried in the back of my mind. As you will already know, the reason this study is important is that it shows that nerve pain and abnormality of function may result from inflammatory changes in the connective tissues of nerves without slowing conduction. The problem with diagnosis is that reduced conduction has been the gold standard for diagnosis of neuropathy. The inflammatory neuritis model that Eliav et al use produces the kind of neuropathy that neurodynamic tests might well pick up whereas nerve conduction tests may not detect this problem. This is consistent with the idea that mechanical tests contain something different from physiological tests because each examines for different things. We now have to accept the idea that there may be diifferent kinds of neuropathy which will be detectable with different tests.

                The whole question of whether mechanical tests are effective relates to mechanosensitivity. Two positions in the literature have been discussed: 1. nerves are never mechanosensitive so they could never hurt. This is incorrect. 2. Normal nerves are not mechanosensitive and abnormal ones can be. This is also incorrect. The correct position is that all normal nerves are mechanosensitive when they are stimulated by a sufficiently strong mechanical stimulus. This has been shown in basic science studies (I quote these in my book, pages 63-65). Pull or push hard enough on a nerve and it will become active and may hurt. You only have to press, bang or stretch your ulnar nerve to find this out! So we have to consider physical testing of the nervous system in relation to two aspects, the state of the neural tissues and the forces to which they are subjected.

                1. Normal nerves subjected to normal forces are less likely to produce symptoms.
                2. Normal nerves under abnormal mechanical forces are more likely to produce symptoms.
                3. Sensitised nerves subjected to normal forces can produce symptoms.
                4. Sensitised nerves that are subjected to abnormal forces are likely to produce symptoms.

                The other thing that the Eliav group has shown I think is that the perineuritis model produces central sensitisation!

                Interesting thoughts I hope.




                • #38
                  Thank you Michael,
                  That is the most succinct post I've ever read about sensitivity of nerves. I hope you don't mind if I quote you by copying this post whenever/wherever this topic pops up!
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                  • #39
                    :idea: Yes , so much interesting /amazing thoughts Micheal

                    I have to raise Hat showing respect and admiration .




                    • #40
                      Thanks for the positive feedback. Feel free to quote it. It's presented in detail in my book and I'd love to develop on this further because it is a key issue with all neurodynamic testing and treatment. It also feeds into clinical application in which the four categories can be applied to diagnosis and clinical decision making. To lead into patient representations of each category:

                      Category 1: no symptoms: normal ADL
                      Category 2: minor neural symptoms with extended use of body or abnormal or extensive repeated postures or movements that apply force to nerves. The symptoms relieve quickly and neurodynamic testing reveals very little because the nerves are not provoked at the time of examination.
                      Category 3: more persistent neural symptoms that don't go away as easily. Patient doesn't subject nerves to abnormal forces, ie. ADL is relatively normal but something is clearly wrong with the nerves. Neurodynamic testing is abnormal.
                      Catetory 4: Patient is subjecting their nerves to inappropriate forces and they are abnormal. Persistent pain in spite of being very active or having bad biomechanics and subjecting the nerves to excessive or inappropriate forces. Neurodynamic testing is quite abnormal.

                      This all leads into treatment which I can discuss later - patient coming!



                      • #41

                        A good categorisation.

                        I believe many of us (Physios) sit in category 2.

                        A big majority of my health centre clientele fall between 3 and 4.

                        My favourite patients are those in category 4, but theydrift back and forth into 3.

                        Looking foward+++ to your next post on Rx!



                        • #42
                          OK, here is the next edition of how to work clinically with mechanosensitivity.

                          Category 1 - If it ain't broke, don't fix it.
                          Category 2 - These are usually biomechanical problems in the interface which places abnormal or undesirable forces on the nervous system and the nervous system's response is likely to be reasonably normal and will settle down quickly when the interfacing structures start behaving themselves. This is where the neurodynamic tests results are variable because the mechanical irritation/compression may not be in action at the time of examination and their result will be dependent on recent or current provocation. The main dysfunction is in the interface (musculoskeletal tissues) so biomechanical, manual and manipulative and exercise therapies are good for these to improve motor control and physical behaviour of the tissue under consideration. This normalises or optimises the forces on the nervous system and gives the nervous system a chance to recover. It even helps protect the nervous system when done well. This approach effectively optimises the environment in which the normal nervous system is located, reducing provocation.
                          Category 3 - there is a definite problem in the nervous system which is sensitive to movement and, in this situation, is treated mechanically as an entity in its own right. Depending on the level of treatment (1, 2, 3a, 3b, 3c or 3d), the spectrum of techniques for neural mobilization range from neural off-loaders, sliders and tensioners. Decisions on this are based on which neurodynamic dysfunction exists: proximal or distal sliding, cephalad or caudad, neural tension dysfunction etc., see below.
                          Category 4 - both the nervous system and musculoskeletal system (interface) are a problem. Treatment to each is given but selection of techniques is made with care and is based on system of progression that I outlined in my book - level 1, 2, 3a, 3b, 3c, 3d and so on. This is when, at higher levels of dysfunction, treatment can be applied to the interface and neural structures simultaneously. The reason for this is that, at higher levels of function, separate tests for the musculoskeletal and systems can be normal. But when tests and treatment for both at the same time are performed, the problem will often emerge much more obviously. Selection of treatment techniques is derived from the mechanical dysfunction in the interface (adjacent musculoskeletal structures), the specific neural dysfunction and the level of the clinical problem (ie. 1, 2, 3a, 3b, 3c or 3d, each has its own set on inclusion and exclusion criteria). This system addresses the issues of a. not knowning how to select assessment and treatment techniques for specific patient problems and b. preventing provocation with 'neural tension testing'. Instead these tests are performed neurodynamically with emphasis on dynamics (mechanics and physiology) rather than just mechanical tension, hence the term 'neurodynamic tests' and my book being called 'Clinical Neurodynamics".

                          Selection of techniques for the category 4 mechanosensitivity goes a bit like this and is in relation to the neural component of the dysfunction:

                          Neural dysfunction from level 1 to 3
                          position away-move away
                          position toward- move away
                          position away-move toward
                          position toward-move away

                          This relates to where the nervous system is positioned before it is moved and whether it is moved in the direction of the dysfunction or away. This is influenced by how easily the symptoms are provoked, among other things. Sliders are generally better for irritable problems and usually tensioners (not neural stretches! - they are performed quite differently) are performed at higher progressions. However, at the lowest levels, neural off-loaders are performed to reduce sensitivity in the neural tissues.

                          Interface dysfunction from level 1 to 3 - to be covered later. Got a meeting, must go.

                          Hope this is interesting


                          • #43
                            Very interesting! Thank you. I've got your book on the way and excited to dive into it!

                            The last of the selection of techniques...position toward-move that meant to be position toward-move toward?

                            Cory Blickenstaff, PT, OCS

                            Pain Science and Sensibility Podcast
                            Leaps and Bounds Blog
                            My youtube channel


                            • #44
                              Michael, Thanks for posting here.
                              I have slowly started to read your book (its safer that way, less likely to trip over any words). On page 11 you present a figure modelled on Maitland's work, but no legend to decipher the lables! I wasn't trained in that approach and don't have access to any of his books. I'm sure its obvious but could you (or anyone else) please decipher it for me?!
                              Eric Matheson, PT


                              • #45
                                Hi Eric, from Vancouver Island? If so, Deena Scoretz at UBC is organizing my course in Vancouver for November. Glad to see someone's reading my book.

                                ABCD are just the corners of the diagram.
                                L - limit of movement
                                P1 - first onset of Pain
                                P2 - maximum Pain
                                R1 - first onset of Resistance
                                R´(R prime) - level of resistance at the end of range (L) when P2 was what produced the restriction.

                                Hope this helps and thanks for asking.

                                Best wishes,