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Richard Ulm

Consequences of the ECSS: Loss of Flexion

Updated: Jan 29


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For the last several weeks, I have been focusing on the many consequences of the Extension/Compression Stabilizing Strategy (ECSS). First was axial compression of the spine. Second was chronic hyperextension of the lumbar spine. And third, concerned the etiology of the butt-wink (when the pelvis tilts backwards at the bottom of the squat). Today, I want to talk about spinal flexion mechanics and how the ECSS disturbs this motion so essential to function.


While I have mentioned several times in the previous articles that loaded flexion of the spine is often the mechanism of injury for the intervertebral disc, flexion of the spine is normal and necessary for optimal function. Sure, high volumes of repetitive flexion, such as one would experience working at a FedEx warehouse, increases your incidence of disc injury just as flexing your spine under tremendous load like squatting triple body weight does, but that doesn’t mean that we should avoid flexion all together. Yet, this is often proposed by the medical field. Because the mechanism of injury to the disc is often flexion, some propose avoiding it all together. This well intended but erroneous message spreads and people stop allowing their spines to function like they have evolved too. What is painfully ironic (pun intended) is that the attempt to avoid lower back pain by not allowing the spine to flex is often the cause of recalcitrant lower pain. It is not always the repetition and the load involved, but the strategy with which the flexion was executed that is the problem.


Pathological Flexion


Not all flexion is created equal; like squat techniques, some are better than others. When one is functioning with an ECSS they are unable to flex their spines in a healthy, efficient manner. Over time, the inefficient, pathological flexion causes pain and injury.


Optimal movement involves balanced co-activation of all muscles around the joint. Not only are these muscles working in balanced concert with each other, but their activity should be as little as necessary to execute the task. This minimizes the internal forces within the joint, thereby reducing the load/strain on the tissues involved. With the ECSS neither are the muscles balanced nor are they contracting as little as possible. Quite the contrary in fact. The ECSS is by definition one which involves muscular imbalance and excessive muscle activity. It’s hallmark attribute is hyperactivity of the spinal extensors secondary to insufficient dorsal stabilizers (the abdominal wall and intra-abdominal pressure). This muscular imbalance and hyperactivity blocks optimal motion of the spine and massively increases the internal forces coupled with motion.


Whenever anyone bends forward, say to pick up a pen they dropped on the ground or to tie their shoe, their spine should flex. It is not natural to lock it into a rigid position and then try to execute the task exclusively through hip motion as is often proposed by the medical field. Despite the fact that the load in these two scenarios is incredibly light, people often “throw their backs out” doing just that. What is the problem? The problem is the strategy with which they executed the flexion.


A joint in the lumbar spine (also called the intervertebral disc complex) is made up of 2 vertebrae (bones) stacked on top of each other with an intervertebral disc sandwiched between them. In a healthy, properly functioning spine, when you bend forward, the anterior aspect of the vertebrae approximate and the posterior aspect separate. While there is a natural increase in pressure within the disc during flexion, the magnitude of this increase is mitigated by the posterior aspect of the vertebrae separating (Image 1a). In order for the separation of the posterior aspect to occur, the spinal extensors must have the capability of relaxing (reducing their contractile force). They must be able to eccentrically lengthen to allow the separation to occur. If they cannot, as is the case with the ECSS, then this vital separation does not occur, which results in a massive increase in the pressure within the disc — no matter how small the load.



When the spinal extensors are stuck in a concentric contraction and block the separation of the posterior aspect of the vertebrae, you’ve essentially turned the posterior aspect of the joint into a fulcrum. It is no longer a healthy joint, it is now a class 2 lever — aka a nut cracker…with the disc acting as the nut (image 1b). Now, when you bend forward to pick up something, no matter how light the object, there is a massive increase in pressure within the disc because the approximation of the anterior aspect of the vertebrae is not coupled with separation of the posterior aspect. This results in a massive compressive force, essentially crushing the intervertebral disc.


This might not seem like much, but the rise in intra-discal pressure is considerable, even pathological. Over time and through repetition, the discs cannot handle the chronic and repetitive increases in pressure and they begin to fail — bulge, herniate, extrude, sequester.


Remember, this problem all started with insufficient generation of the intra-abdominal pressure (IAP). IAP is the only force that can stabilize the spine directly from the front. It literally pushes against the lumbar spine, providing a tremendous amount of anterior support, like pillars holding up a ceiling in a cathedral. With adequate IAP, the spine is able to flex properly. In the absence of adequate IAP, the spinal extensors will hyper-activate to provide the necessary stability to the spine as it bends forward. However, this compensatory strategy will not allow the posterior aspects of the vertebrae to separate, resulting in the pathological flexion mentioned above.


This subtle but pernicious motion is quite common. In every slight bend forward, there is a compensatory hyper activation of the spinal extensors (particularly in the lower lumbar spine) that extends and compresses the intersegmental joint resulting in pathological movement and associated pain and pathology.


More on the ECSS and why it is so common in the next article.


Stay Tuned!


- Richard Ulm, DC

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