how to assess & treat
A new way to assess and treat
- Realize everyone is different
Improper tissue pressure gradients can result in many presentations. More precisely, every presentation is unique. You can’t be expected to make a tissue-specific diagnosis every time. If a radiologist on seeing an MRI says he’s never seen that before, how are you going to figure it out? What you can do is to assess and treat for the general pathophysiology of this discovery. The more you know about pathology, epidemiology, physiology and anatomy, the more effective you will become in doing this work. This discovery is like a compass that can move you through murky waters and take you to new and exciting places. Most importantly, the discovery fits nicely into your scope of practice.
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. It is caused by too high a pressure in the involved tissues. 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 the nerves that are involved, it follows that anywhere nerves exist, this condition may arise. 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 anaerobic. 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 its 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 showed that nerves are present in the degenerated disc and therefore are 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 bed rest 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.