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  • Richard Ulm

Sequela of the ECSS (Part 2 - Hyperextension)

Updated: Jan 29


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If you’ve been following a long the last few weeks, you know by now that the Extension/Compression Stabilizing Strategy (ECSS) is a common compensatory postural syndrome in which the athlete/patient/client uses hyperactivity of the para-spinal muscles to stabilize the spine in the absence of adequate intra-abdominal pressure (IAP). As a compensatory strategy, using the ECSS comes at a cost. Last week, I covered the impact axial compression produced by the hyperactive spinal extensors has on the spine. This week (and perhaps for many weeks to come) we continue with sequela of the ECSS - hyperextension of the lumbar spine.


Hyperactivity of the spinal extensors (aka the posterior chain) represents a muscular imbalance between the ventral stabilizers (abdominals and IAP) and the dorsal stabilizers (spinal extensors). Truthfully, this hyperactivity is the result of the imbalance, not the cause of it. The linchpin event of this muscular imbalance is insufficient activity of the ventral stabilizers. Inhibition precedes hypertonicity.


While I often focus on structure and biomechanics, the ECSS is a neurological phenomenon that’s impact on pain, injury, and performance is carried out by biomechanics. Having a pronounced muscular imbalance between the ventral and dorsal stabilizers - with the dorsal stabilizers overpowering the ventral ones - not only produces a massive amount of axial compression on the spine (covered last week), but distorts the postural alignment of the spine and pelvis. This is the focus of today’s article.


Sequela: Hyperextension of the Lumbar Spine (Direct Impact)


With the lumbar spine in a hyperextended position, the weight-bearing load is shifted posteriorly. It shifts posteriorly off of the large, thick, and dense part of the vertebrae (vertebral body) - which has evolved to handle this very force - onto the thinner, and more frail part of the vertebrae called the neural arch. The neural arch has three main purposes: 1) protect the spinal cord and nerve roots; 2) block and guide motion; 3) be a site for muscle attachment. What is obvious to anyone looking at a vertebrae is that the neural arch is not designed to handle chronic load as it must with an ECSS (see image 1).



This chronic load on the neural arch has both short and long term consequences. If left unchecked, it will produce a cascade of pathology throughout the athlete’s entire life.


One such pathology that presents early in life is spondylolysis (aka a pars fracture). You might have a friend who “broke her back” in high school. Although it is possible, it’s not likely that she fractured the vertebral body, at least not without a pretty dramatic event such as a bad fall or a car accident. What is likely is that she “fractured” a part of her back called the pars interarticularis. This is knows as a pars fracture or spondylolysis. While it may present in the middle of a sporting event or while training, say during a gymnastics routine or in the middle of a heavy deadlift, it is not an acute incident. Spondylolysis is a bending fracture resulting from the chronic load placed on the neural arch by the ECSS. The massive force unrelentingly compresses and bends the pars interarticularis, eventually resulting in the “fracture”. Not surprisingly, this pathology is most common in the same sports that the ECSS is: gymnastics, weightlifting, powerlifting, and CrossFit.


A continuation of this process is a condition called spondylolisthesis, which is when a vertebrae slides forward (anteriorly) on the vertebra below. In its more severe renditions, this can get pretty dangerous. As the vertebra slides forward, the hole in which the spinal cord resides, becomes more narrow. Take two paper towels rolls and line up the holes. Look down through the tubes. Now, slide one forward and watch how the hole gets smaller. This is what’s happening in spondylolisthesis. If that hole gets too small, the patient can experience pretty severe neurological symptoms due to the compression of the spinal cord.


You might be wondering how hyperactivity of the spinal extensors causes an anterior shift of the vertebra. Current research is unable to draw any concrete conclusions about the cause of spondylolisthesis, often hiding behind the term idiopathic (Latin for we don’t know). This is not due to confusion about the forces at work; it is due to a limitation in our research capabilities. In the absence of definitive research, we have to base our clinical hypothesis on biomechanics, anatomy, physiology, and neurology; and we must reconcile this with our clinical experience.


With an ECSS, the hyperactivity of the spinal extensors is the result of inadequate production of IAP. The hyper-lordosis of the lumbar spine that results, not only compresses the neural arch, but squeezes the vertebral bodies forward, which over time, may result in spondylolisthesis.


Another related force in this process is IAP, or a lack thereof. IAP is the only force present that has the leverage to push the lumbar vertebral bodies posteriorly (at least a force that pushes in that direction). There is no muscle that does it. Yes, the abdominals attach to the spine, but not in a position where they have leverage to pull a vertebra posteriorly against the force produced by the spinal extensors. Only IAP has the leverage to do this. On a segmental level, it is IAP which opposes the spinal extensors in the sagittal plane. When there is inadequate IAP for long periods of time, the vertebrae can slide forward into a position we call spondylolisthesis. Bones don’t just slide on their own. They respond to force. Over time, the force imbalance produced by the ECSS can result in spondylolisthesis. For me, the biomechanics here are difficult to deny.


Next in this cascade of pathology, often associated with the spondylolysis or spondilysis, is facet syndrome. This is pain produced by an aggravated facet joint. It starts with forceful and repetitive impaction of the facet joints. The neural arch, more specifically the facets on the neural arch, are capable of guiding and blocking motion of the spine, but only intermittently. They have not evolved to handle constant, chronic load. With the spine in a hyperextended position, the frequency of the facet impaction increases, potentially to pathological levels. This is pretty common in baseball, CrossFit, Powerlifting, and Olympic Weightlifting, typically occurring early in the athlete’s career, say in their 20’s. The complaint is typically a “sharp” pain produced with extension and/or rotation. The pain does not last long. It does not linger. It is only produced when the the irritated facets pinch together, but it can be pretty limiting. What also contributes to this process is the massive compression of the spine produced by the hyperactive spinal extensors. Not only do you have more frequent facet impaction, but each impaction is more forceful. This just speeds up the process.


The final event in this cascade of pathology is spinal stenosis. This is the grand prize for living most of your life using the ECSS. Stenosis means narrowing. In the spine, there are two areas where narrowing can be an issue: the neural foramina (the hole out of which the nerve roots traverse), and the spinal canal, where the spinal cord resides. Whether neural foraminal stenosis or spinal canal stenosis, both are chronic adaptations to the load placed on the neural arch by the ECSS….”theoretically”.


Bones adapt to force. They can increase or decrease their density and they can change shape, become thicker or develop bumps and grooves - all in response to force (compression, distraction, bending, etc). An example of this, unrelated too today’s topic, is osteoporosis. While osteoporosis (weakening of the bones due to loss of density) has many causes, one is a lack of activity, particularly weight bearing activities such as strength training and impact activities such as hiking or running. Both activities demand that the bones are strong - one through compression produce by the weights and the muscles used to move them; the other through kinetic energy produced by impact, such as a runner’s foot striking the ground. Both “demands” place a stimulus on the bones, to which the reaction (or adaptation) is to increase their density.


This bony response to chronic force/load is called Wolf’s Law. If the force/load is high enough to stimulate an adaptation, but not too high so as to create a fracture, the bones will thicken and densify. The opposite is also true. If the force/load is low, then the bones will reduce in density, becoming for frail…a la osteoporosis.


With an ECSS, the force is high and load is chronic, both placing the lumbar spine in an environment the adaptation to which is to thicken and densify the bones of the neural arch. This process takes a long time, years, decades. Typically after the age of 50, patients with a pronounced ECSS will first develop neural foramen stenosis - or at least it becomes symptomatic around that age. If left unchecked, over time, this will blossom into full blown spinal canal stenosis. This is nothing more than Wolf’s Law applied over decades due to the chronic force produced by the ECSS.


More on the sequela of the Extension/Compression Stabilizing Strategy next week. The list is long.


Dr. Richard Ulm

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