It was in the latter part of 1999 when I made the discovery. I had just completed both a fellowship in rehab science and a diploma in mechanical diagnosis and therapy. Needless to say I was pretty sharp, and as serendipity would have it, eureka! A physiotherapist friend and mentor of mine, Colin Davies, had just given me Prof. Vert Mooney’s paper on common overuse syndromes of the upper extremity. I now realized a new pathophysiology for many disorders seen in the office and just as important I also realized a new mechanism of action for manual therapy.

Now fast forward to the present, twenty years later. I’m still just as ardent and even more excited. Science is now revealing how ubiquitous this pathophysiology is, even in disease outside of the musculoskeletal system. My techniques continued to improve every week until what you see here today. This evolution all resulted from following the one simple mechanism of action.

Surprisingly, this new ‘cause’ and ‘treatment’ is an echo of what therapists diagnosed and how and why they treated thousands of years ago.

What we do is to test and assess for three related phenomena: a lack of blood flow, the oxygen supply, and an increased tissue pressure. Increased tissue pressure results in a lack of circulation, and therefore a lack of oxygen.

Hypoxia as a cause for illness is not a new idea. Ancient therapies such as Thai massage, yoga, and traditional medicines which assess chi energy all believe that a lack of ‘air’ to the affected body part is an underlying pathophysiology. They feel that somehow, the air in the lungs is blocked from entering the affected tissue and by finding and freeing these blockages with mechanical means, the patient will respond; thus, they also have a mechanism of action. It must be remembered that the heart and circulatory system were not discovered until well over a thousand years later. In freeing the blockages, ancient therapists were actually normalizing tissue pressure gradients so blood flow would be restored.

I think they were correct. Modern imaging studies and biochemical analyses now show that increased tissue pressure and hypoxia are commonly associated to more and more conditions. These recent findings not only edify ancient theories, but also challenge current conventional beliefs of both the pathophysiology of many illnesses as well as the mechanism of action of various therapies. A recent paper suggests that over 75% of  research done on the osteoarthritic knee has been a waste of time and resources. No one has been asking the right research questions. Another recent paper states that the generator of pain in the osteoarthritic knee may be an increased intraosseous pressure. They came to these findings because of new science: meta analyses demonstrating the weak research and modern MR contrast fluid movement imaging demonstrating a lack of blood flow in the subchondral bone of the tibial table. Chronic hip pain and disability is another good example. How many diagnosed conditions of femoroacetabular impingement and labral tear are actually similar conditions due to too high an intraosseous pressure at the neck of the femur? This elevated pressure may eventually result in necrosis and fracture and therefore further resulting in more overt findings. The discovery of hypoxia inducible factor now shows pockets of hypoxia existing in numerous pathologies.

For our purposes, the subject material will be limited to the musculoskeletal system. Just one more huge point before moving on: I would estimate one third of all chronic musculoskeletal problems involving the bone with only a limited soft tissue involvement. We sometimes forget that the bone is a living tissue. Its cortex is innervated, poroelastic, can be flexed, has a blood supply and contains interstitial fluid. Conventional imaging and biochemistry in the past have ruled out any bony involvement. This has now been shown to be untrue. UTE MR imaging shows increased T2 signals for the first time in structures such as the cortex, periosteum, enthesis, ligaments and tendons where edema exists. Hypoxia inducible factors are also present.

Every procedure we use is a test and each one is held for several seconds. This time allotment allows for a physiological change to take place; the change we want is a movement of fluids in the affected area.

The lack of blood flow we are interested in is in the microcirculation caused by high pressure in the involved tissues since blood travels from a higher pressured area to a lower one. If the tissue pressure approaches that of systole in the local capillaries, then circulation is compromised.

Every patient is different and therefore, no two tests are really the same. Testing results vary in three main ways: they may have no effect, they may result in a positive sign after only one session, or they may lead to other tests. It should go without saying, if the test causes or increases symptoms, it’s a red flag and the patient should be re-assessed.

Procedures often elicit a response from the patient leading the therapist to perform another test, then another, and so on. In these cases, the assessment can be made but not on the initial visit and it may take weeks until a definitive response is found.

If the testing has a positive outcome, the finding will then suggest that the disability is due to a lack of blood flow and an increased fluid pressure in the area of complaint.

The most often affected tissues are the nerves along with their associated connective tissues. The procedures could therefore be referred to as neurological tests.

This pathophysiology is often seen in chronic conditions as it is in the nerves that are involved and almost any part of the body can be affected. Even tissues that are not normally innervated may become so after an injury. The inflammatory stage of healing involves angiogenesis and neurogenesis. Common sites of involvement include tendons, ligaments, joint capsules, discs (endplates), intervertebral foramen, fascia and muscle, bone, large nerves and blood vessels. See the example below.

The same pathophysiology may also result in inflammatory conditions. Through homeostasis, the body will try to get blood into the hypoxic area through several mechanisms and also shift the metabolism of the affected cells to be more anerobic. The resulting adaptive changes may be exaggerated and end in inflammation.

The mechanism of action of this technique is simple. Every test is designed to increase the tissue pressure in the target area to an even greater degree. If the pressure is held long enough, fluid will leave the area. The result is a normalized resting tissue pressure and the return of blood flow. This idea is so simple you really can’t call it a technique system any more than you can call orthopedic testing a technique system. Therapists are actually doing this in their practices right now without realizing. That being said, the same principle applies to the bones.

When bones flex, the intraosseous pressure is increased and fluid in the cortex moves away. Putting this idea into practice, we can now test conditions such as the osteoarthritic knee and the type of chronic hip disabilities mentioned above. By flexing the subchondral bone of the tibia and the neck of the femur respectively, we look for a response. If the patient responds favorably, we have both an assessment and a treatment. 

Discogenic low back pain is another excellent example of how long-standing ideas are changing. Trigger points are an example of how long-standing ideas should change.

Discogenic low back pain has been the subject of research and theories for years. What is and was thought to be it’s  pathophysiology and what are the present theories on the mechanisms of action of various therapies treating this condition?

In the mid twentieth century, orthopods maintained that the disc was insensitive. Histological studies actually showed a lack of nerves within a healthy disc and therefore, the disc couldn’t be involved in low back pain. The problem here is, they only had part of the picture. Later studies show that nerves are present in the degenerated disc and therefore were in fact pain sensitive. After injury, aneural and avascular structures are involved in angiogenesis and neurogenesis as part of the inflammatory response. Now that we know discs are pain sensitive, what causes the pain? Some say fissures in the annulus, others say the migration of the nucleus in these fissures; some say an inflammatory response in the fissures, others argue decreased discal height; some say pelvic and vertebral misalignment and others say disc bulging. The problem with all these is that they also exist in people with no low back symptoms. Finally we get to the modic signs of the discal endplate. Degeneration in the endplates seems to be better correlated to the problem. How does the endplate relate to discogenic pain?  Just like research into the osteoarthritic knee, I think most people missed the boat. Where the disc attaches to the vertebrae at the endplate is actually an enthesis. This enthesis is really no different than others. Most interestingly, conventional MRI’s will not show edema at the enthesis or endplate. An UTE MR scanner will and in fact has shown an increased T2 signal in this area when people have back pain. This recent discovery of Professor Dino Samartzis is huge (see his article in the links section). So here’s the pathophysiology, stress to the endplate causes edema resulting in increased pressure and a lack of blood flow. Cells now degenerate and the patient experiences pain and disability.

Theories on therapeutic mechanisms of action are just as varied. They range from spinal manipulative therapy of the neck to the wearing of a heel lift, from braces and bedrest to regular exercise. Why so many of them? It’s because the pathophysiology of discogenic low back pain is unclear. In my opinion, by reducing the pressure in the endplates to normal, circulation will be restored and the patient will respond. Look at the picture at the top of the page. The therapist is trying to unblock the air travelling to the low back. This is being accomplished by temporarily increasing the pressure in the posterolateral endplate during the testing procedure which results in the edema egressing and returning blood flow. I perform similar minded procedures. My idea is to hold the position long enough to allow the edema time to move away.

Not surprisingly, I postulate a similar pathophysiology for trigger points. Many books and countless articles have been written discussing the causes and treatment of this problem and recently, some being critical of the various hypotheses why they exist. Ironically, a paper written in the 1950’s had the answer. It found the following characteristics common to trigger points: an increased concentration of proteoglycans, edema, and a lack of blood elements. By applying pressure to the target tissue either through compression or traction, the edema will egress and blood flow then restored. The problem with present day thinking is that they only see part of the picture. The pathophysiology at the trigger point is not tissue specific. It can occur in other sites besides muscle, tendon and fascia.

The ‘Manuscripts’ post contains several papers I have written on the subject; the ‘References’ section has over one hundred abstracts describing aspects of non vascular edema; ‘Procedures’ has over two hours of techniques. The ‘links’ page has many references to this introduction.

It is interesting that these procedures are very similar to those that have existed in various cultures for thousands of years.

Please, look over the site and discover!

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