Phillip Snell, D.C.November 2, 2013
Full Discussion: http://www.rehab2performance.com/flexion-intolerant-back/
As the old saying goes, it’s sometimes hard to see the forest for the trees. For low back pain (LBP), this old saw is particularly apt. All too quickly, discussions of structural causes of LBP lapse into call and response arguments citing this structure and that structure as causal or incidental. To make matters even more confusing, the emerging pain neuromatrix literature rightly causes all of us to pause to consider that all pain ultimately is determined in the brain. (1) Unfortunately, the tone of these discussions often becomes adversarial as each camp rushes to dismiss and destroy the positions of the past and erect new monuments on the rubble of the research that has come before. In my opinion, this “throwing the baby out with the bathwater” is an adolescent phase which can benefit from a less passionate, more patient reading of the literature to look for those threads that might lead us out of the confusing place we have found ourselves in regarding low back pain. I suggest that the fledgling success seen in other areas of physical medicine and rehabilitation might shine a bit of light on our path. Rather than going around our elbow to get to our thumb, let’s take a trip around our knee to get to our spine.
YOUR BUM KNEE
Around 10-15 years ago, a paradigm shift occurred in the management of acute and chronic knee pain. Sports medicine researchers like Irene Davis, PhD noticed that many of the chronic running-related lower extremity injuries seemed to be related to poor strength and/or coordination of the gluteal muscles. (2-13) They found that when these insufficiencies in those hip abductors and external rotators were addressed, many of those chronic plantar fasciitis, tibial stress fracture and anterior and lateral knee pain conditions remarkably improved. For some folks the solution was a “hardware” problem and just strengthening those hip muscles solved the problem. For others, the solution was a “software” fix and cueing for running form correction to better involve gluteal activation was the ticket to pain free function. While these findings were noted for chronic, low load, repetitive stress conditions involving the athlete’s leg, other researchers found similar hip-knee connections with acute injury.
–from Hewett et al, AmJSportsMed 2005 valgus knee
Chris Powers, MD and Tim Hewett, MD were instrumental in their research on anterior cruciate ligament (ACL) injuries, especially in female athletes, by drawing a connection to the hip muscles control of the knee joint mechanics. Their research has led to tools to predict ACL injury, help prevent ACL injury, and reduce risk of re-injury of ACL-deficient knees. At the heart of the message they bring to the rehab environment is the seemingly simple message that the knee is a hinge joint, and functions well in one plane of movement only. Further, they aim our prevention and rehabilitation techniques to the hip musculature for improved results. (14-25).
In short, these two research paths, which focused on several acute and chronic structural knee conditions, found that a functional fix was the ticket for improved outcomes. These days, any trainer or clinician worth their salt has stopped doing quad sets and adductor strengthening for their knee pain/dysfunction patients and clients and instead has them doing glute strengthening and agility training to correct the condition.
I suggest that a thread can be seen in the structural literature about LBP, which may lead us to a similar functional correction in this incredibly expensive human condition. While medial collapse (valgus displacement) of the knee is now recognized by most to be the pathomechanical focal cause of many structural injuries in the leg, I suggest that inappropriate hinging in the lumbar spine (i.e.too frequent or too intense) is the root pathomechanical movement to the majority of the structural causes for LBP. Before we explore that further, let’s drive home the reason WHY a better solution is needed in LBP healthcare costs.
COSTS OF BACK PAIN
Many can cite some of the LBP statistics by heart Lifetime prevalence of LBP is as high as 80%. (26) Point prevalence of LBP (# of people asked at random if the have back pain) is around 30%. (27) The numbers regarding LBP costs are less well known.
U.S. Cost of LBP
Epidemiological studies evaluating the societal costs associated with back pain are challenging to perform. Those costs can be divided into direct and indirect costs. Direct costs are those that are easier to measure, like the amount spent on various treatments, surgeries and hospitalizations. In the U.S. the median direct costs associated with back pain run around $85 billion annually. (28) Indirect costs are far more difficult to derive. To arrive at the total cost of illness of back pain, we combine the direct and indirect costs. At this time (October 2013), no studies have been performed in the U.S. to investigate total cost of illness of LBP. A review by Dagenais et al in 2008 looked at 8 other international studies that had factored in indirect costs associated with LBP to arrive at a total cost of illness of LBP in their respective countries. (29) They found that on average, the direct costs of LBP in those countries amounted to about 14.5% of total cost of illness. If we apply this metric to the U.S., we arrive at a total cost of illness of over $500 billion annually. Since numbers this large are hard to relate to, let’s try to get a handle on how this figure compares to the total cost of illness annually for several other major diseases.
The figures shown above for heart disease, diabetes and cancer costs are from each of their respective national organizations. Somehow, seeing that “simple” back pain costs may exceed the costs of these other illnesses makes the idea that “most back pain will just go away” seem a bit trivial.
THE ARGUMENT FOR THE FLEXION INTOLERANT LOW BACK
Lumbar hinging (flexion and compression) has been identified as the quickest way to herniate lumbar discs with repeated cycled movements in the lab. (30-33) Those lab studies show that the injury to the disc occurs from inside out, with the inner lamellar layers becoming compromised first. The nucleus pulposus then “worms” through those rent layers with subsequent lumbar hinging. (34) The inner layers of the annulus have no innervation and are thus insensitive to these early microtears. The robustness and resilience of the discs to load is mostly determined by genetics. (35,36) Epidemiological evidence suggests that frequent lifting correlates with back pain. (37-39) Twins studies suggest that purely being heavier, however, connotes more robust development of the discs and vertebral endplates. (40) This suggests that the WAY in which load is applied to the lumbar spine may be an important consideration as to whether loads on the spine will exceed tissue tolerance. (39,41) Spine sparing strategies that maintain the lumbar lordosis, allowing for pure compression allow for very high levels of loading across the spine and typically result in the failure of the endplate well before the annulus. (42-44) Lumbar hinging under sufficient intensity of load and cycling of load, allows the nucleus to bulge further outward until it reaches the outer 1/3 of the annulus where nociceptive neurons reside. Now the landscape changes as the previously painless lumbar hinging, begins to ache. Repeated hinging results in the sensitization of the nociceptors and the release of nerve growth factor (NGF) causing the infiltration of the nociceptors into the previously aneural inner lamellar layers. (45-47) Now less lumbar hinging is needed to cause pain.
ENTER THE BRAIN IN PAIN
Pain researcher, Ron Melzack PhD is credited with the term pain neuromatrix.
“…pain is a multidimensional experience produced by characteristic “neurosignature” patterns of nerve impulses generated by a widely distributed neural network-the “body-self neuromatrix”-in the brain. These neurosignature patterns may be triggered by sensory inputs, but they may also be generated independently of them.”(1)
The concept of the pain neuromatrix suggests that while acute pain may involve tissue damage and subsequent inflammatory response, chronic pain will rarely include these signs. In essence, the tissues heal but the brain remembers the nociceptive events and continues to run the pain program with very little or no stimulus from the periphery. What may constitute continued peripheral stimulus in chronic pain is still in debate and may be investigated elsewhere (48-50) For the purpose of this paper, we will continue our exploration of the Flexion Intolerant Back at this point to consider the evidence of ongoing peripheral nociception and its effects on central sensitization. I suggest that the ongoing peripheral nociception arises from 3 primary structures-discs (either directly or via mechanical compression of nerve roots), muscles (via myofascial trigger points), and peripheral nerves (via tunnel syndromes). Rather than falling into our old habit of viewing the spine through the structural lens, let’s look at…
STRUCTURE THROUGH A FUNCTIONAL LENS
Lumbar hinging would place stress on many of the structures of the low back commonly blamed for LBP. With infrequent, low repetition, low load conditions, the muscles and surrounding lumbodorsal fascia would remodel to try to manage the stress. The fascial compartment remodels in response to mechanical tension stress present in lumbar hinging. (51) Tunnel syndromes may develop as peripheral nerves like the cluneal nerves are restricted in their mechanical interface with that remodeling fascia. (52) Langevin shows that lumbodorsal fascia is 25% thicker in those with chronic episodic LBP. (53) Maigne suggested this cluneal nerve involvement in his work and others have described this condition as well. (54-56)
The extensor muscles of the lumbar spine would also help bear the stress of the habitual lumbar hinging. Frank strain of these muscles from mechanical overload may result in acute pain. Chronic pain from myofascial trigger points may develop as prolonged low intensity contractions of these muscles results in ischemia and hypoxia. (50) The icons of the Prague School of Physical Medicine might suggest that these trigger points represent a phasic muscle being pressed into a stabilization role. (57, 58) In our model, the loss of the lumbar lordosis results in loss of mechanical advantage of the segmental muscles. As a result, the multisegmental extensor muscles are pressed into greater service to manage the upright posture and protect the spinal column. As I put it to patients, those painful back muscles are smarter than you! They are tight because they are trying to protect against injury to sensitive structures that are deeper, like elements of the central nervous system (CNS). If patients don’t understand this relationship and try to hinge forward to stretch those tight muscles, then the alarm signal to the CNS continues. From our vantage point, the locked back represents a self-protective muscle spasm to avoid injury to the CNS.
Deeper down, the next structures to be impacted by lumbar hinging are the spinal ligaments and the discs. As mentioned previously, the injury to the disc is often slow and progressive over time and occurs from the aneural, deeper annular layers to the outside innervated layers. One MRI of a degenerated disc that is bulging but non-painful might represent a disc injury not yet progressed to the sensitive outer layers. Some studies have shown that the nerve growth factor present in those discs where the outer 1/3 of the annulus is compromised is responsible for the in-growth of nociceptive neurons into the previously non-innervated areas. (45,46) Further studies have identified inflammatory cytokines that trigger those nociceptors in acute pain. (47) Here we see what Michael Adams describes as the “scab that keeps getting ripped off”, as continued inflammatory-mediated nociception contributes to the chronic, episodic LBP patient. (59)
IN YOUR PATIENT’S HEAD
The commonly cited fear avoidant behavior and depression associated with chronic LBP now may be seen as sensible responses in an individual who doesn’t understand what movements hurt and why. They only know that activities like running, weightlifting, swimming, boot camp exercise programs, bicycling and snowboarding used to be fun and non-painful but now are frequently the cause of new LBP episodes. They begin to fear those activities and get depressed as they see their ongoing years as less and less functional and more and more painful. The astute clinician, with eyes to see the lumbar hinging, knowledge of physical activity programs, and knowledge of the pain neuromatrix can now intervene more effectively on the patient’s behalf. Consider these specific recommendations for common provocative activities.
Sport Specific Spine-Sparing Suggestions
SPORT SPECIFIC SPINE-SPARING SUGGESTIONS
Changing from a structural perspective on LBP to a functional perspective that is vigilant for the presence of dysfunctional movement patterns like loaded lumbar hinging is challenging for many of us. The potential benefit is to sweep many structural pain generators off of the table by improving the patient’s understanding of the common dysfunctional movement of lumbar hinging. Moreover, providing a clear picture of the movement that their body perceives as threatening to the CNS helps establish a cause-effect relationship that down-regulates threat and empowers the patient. Following that with graded exposure to pain-free exercise may help to engage descending pain inhibition and start to rewire the faulty pain processing characteristic of chronic pain.
FURTHER STUDY AND RESOURCES
Developing the eye and experience to correct lumbar hinging takes a bit of time and training. In addition to the excellent courses and informational resources offered through ISCRS, FixYourOwnBack.com is another option for patients and clinicians to specifically address the flexion intolerant spine. Coursework for clinicians, trainers, coaches and bodyworkers in recognizing and managing the flexion intolerant spine will soon be offered through FixYourOwnBack.com.
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