Compression Forces

It is important to fully understand the compressive forces acting upon the disc. Here, visualize, again, the two vertebral bodies separated by a balloon filled with water to reproduce the disc unit, illustrating the hydraulic and mechanical forces. As the top vertebral body is angled in any direction, such as in a flexed, extended, or lateral bending posture, it compresses one side of the balloon and the opposite side opens, causing the balloon to bulge to the open side. The balloon model accurately depicts the forces that act upon the discs because its liquid center, too, has no where else to expand except away from the compressive forces. As one flexes, extends, or laterally bends the spine, the forces are directed nearly identically to that displayed by the bulging of the balloons in Figure 28. An equivalent mechanical and hydraulic activity is occurring at each intervertebral disc whenever the spine bends away from an exactly vertical alignment. This is an important concept to understand because the direction towards which the nucleus pulposus bulges during traumatic events determines the direction and axis of the annulus fibrosus tears as well as the direction and axis that the nucleus pulposus contents would travel to herniate. For instance, if a fall or lifting accident were to occur when the spine was flexed more to the left, the herniating forces would be aimed towards the right posterior, and that would be the direction that the consequent radial tear would take as the contents of the nucleus pulposus herniate through the lamina of the annulus fibrosus.

Likewise, the magnitude of the force placed on the disc would determine the extent and depth of the nucleus pulposus's movement; and, therefore, the degree of tear and/or consequent herniation. Lifting a small weight might not cause the nucleus pulposus to move much at all; however, a heavy weight can be seen to squeeze it with a lot of force and cause a lot of damage.

Archimedes said: "Give me a place to stand, and I will move the earth." In the design of the spine, Nature's reply has been: "Move the earth incorrectly, and I will make it so painful you cannot stand." In order to understand the enormity of the forces that can be generated within the disc, one must look at the disc system's relation to the spine in terms of the fulcrum and lever. The same principle that operates a nut-cracker or a claw hammer works against the disc when the forces are applied improperly during the act of lifting or falling in flexion.

As seen in Figure 29, the disc system can be analyzed in terms of fulcrum and lever systems. When lifting in flexion, the muscles and ligaments of the posterior elements of the spine that perform extension and limit the range of anterior flexion serve as an anchor point because after they reach their maximum length, they can stretch no further. To insure that the ligaments of the posterior elements of the spine are not torn and that the body doesn't fall forward during the lifting process, the muscles contract, serving to further anchor and act as a compressive force added to the weight of the body bearing down on the particular disc.

This connective tissue (muscle, tendon, and ligament combination) is depicted as a schematic muscle superimposed upon a rigid bar. The spine above the disc acts as the long lever arm of the fulcrum system. It can be imagined how with one end point of the "T-bar" (which is the entire vertebral bone above the disc) relatively fixed , the rest of the "T" rotates with the long lever arm that is the spine above the disc. During WEIGHT-BEARING FLEXION the long lever arm rotates around a fixed point to create a posteriorly directed compressive force or squeezing pressure towards the posterior much like a fancy garlic press, nut-cracker, or claw hammer when the nail won't budge. Incredible amounts of force are brought to bear on a small surface area. If one can see how a foot-long claw hammer can generate enough force to tear off the top of a nail, certainly a three foot spine can squeeze a rubbery piece of cartilage through a 2-3 mm sheet of sinew. If the reader jumps ahead to the Section on AVOIDING WEIGHT-BEARING FLEXION, Figure 10 expands this diagram letting an obese clown show how these forces are magnified during lifting.

As mentioned before, with age and its consequent desiccation (drying out) also comes a decreased elasticity of the annulus fibrosus making it less liquid in character and more solid, predisposing it to breakage. As this solidification progresses with age, trauma has more likely a capacity to result in fragmentation. As this degeneration occurs subsequent to repetitive trauma, larger areas of central disc material become cut-off from contiguous tissue upon which it relied for its nourishment. These fragments then become less vital, more brittle, and literally degenerate, hence the term "degenerative disc disease." As the solidified material of the nucleus pulposus is forced against the annulus fibrosus's laminations as in heavy lifting in a flexed position, a fall with the back flexed, or even prolonged flexion with just the weight of the upper body, these fibers break, creating widened radial tears or fissures, allowing the hard, normally centralized, disc material (either fragments of solidified nucleus pulposus or the larger disc-shaped solidified nucleus pulposus itself) to migrate into spaces previously occupied by flexible, more liquid, deformable material.

Once these hard inner disc materials or fragments push their way through bands of the annulus fibrosus, they can stay positioned off center. So long as force is continually applied by the weight of the body, it can remain off center, often effectively becoming trapped between the broken concentric bands of the annulus fibrosus (Figure 30). These pieces of hard material can act as a fulcrum to create an effect that causes pain through mechanism described more fully later; but the more important consideration here is that it can cause pain even though it does not necessarily create an actual disc bulge that can be easily appreciated on imaging studies. These imaging studies often are interpreted as though the disc cannot be the problem because no obvious distortion of the capsule can be seen. In reality, the displaced disc material still is the problem. It is only hidden from easy diagnosis due to its failure to show a bulge or herniation on an imaging study.

This hardened nucleus pulposus can also tear sufficiently through the annulus fibrosus to create a pressure bulge in the posterior or lateral ligaments on the periphery of the disc. This is what is known as a disc bulge, protrusion, or prolapse. When the hard, normally centralized disc material is pushed completely through the ligaments, this is said to constitute an extrusion. See Figure 27 showing various and progressive degrees of damage.

For a moment I need to digress so that the reader understands what physical reality is being represented by these definitions. By defining the different herniation terms statically, there is an implicit assumption that these descriptions constitute an either/or phenomena. When no disc bulge or simply a mild disc bulge is seen on an imaging study, it is often incorrectly assumed that it is only a mild protrusion, incapable of being consistent with the patient's described symptoms of pain, loss of function, or altered sensation. Such is not the case in nature where one is dealing with kinetic and flexible materials as well as reality wherein there is usually a spectrum of damage, at both the instant of injury as well as over time. Making an alternative assumption is a trap that sometimes taints the ability of individual medical doctors or research science in general to adequately portray or explain reality when applied to the individual. Often, the compulsive scientist is limited in his ultimate understanding by a need to rigidly and accurately define his terms so that there can be no confusion when attempts are made to reproduce the results. In the act of attempting to exactly define an entity that defies a static or rigid definition by virtue of its complexity and variability, errors in logic are the consequence. When applied in the context of practicing medicine, suffering usually results because these errors involve people.

For instance, if one were to do a study on the outcome of patients with protruded discs versus patients without protrusions, the protrusion definition and, hence, diagnosis must be fixed by some objective evidence. So, persons without evidence of protrusions on imaging studies are, by definition, eliminated from the study when, in reality, they may have suffered an extensive protrusion that has recoiled or spontaneously returned to a more centralized position by the time the diagnostic imaging is accomplished. It is important to understand that these pieces move, and, at the time of the study, the "protrusion" may not be protruded. It may only protrude when flexion combined with weight bearing forces are placed on the disc. The imaging studies might well have been done while the patient was in a reclining position with differing deformational pressures. So, for the purposes of the given study, this patient is not seen to have a protrusion and is likewise eliminated from the study's consideration; or, worse, relegated to the realm of a malingerer if the doctor cannot reconcile the imaging study with the described degree of pain or disability.

The reason why I engage in this seemingly tangential discourse, here, is because there is a tendency to rely too heavily upon and simply equate what is seen (or, better, not seen) on an imaging study with the reality of the damage. If an imaging study has evidenced that a patient does not have a protrusion, that only means that at the precise instant the imaging study was accomplished, a protrusion was not seen. It does not mean that the patient has not suffered a protrusion event, and it may well be that the disc material only intermittently protrudes and spontaneously returns to the center with random motions.

An example of this phenomenon was inexplicably expressed in a medical journal wherein a physician reported that his back pain resolved when he flew his plane upside down. Essentially, he was unconsciously performing a traction MANEUVER that moved the displaced disc material centrally by a mechanism described at the end of this chapter. Also, numerous inversion traction devices have been marketed which inadvertently capitalize upon this mechanism; however, it is very uncomfortable to hang upside down. Nevertheless, the limited success of these methods, intentional or otherwise, demonstrate that the disc system is not static.

Disc herniations can produce a changing spectrum of symptoms depending upon the actual position of the herniated disc material, explaining why occupationally debilitated patients can, from time to time, be nearly symptom-free and perform activities in which, logically, their described disability would seem to be irreconcilable with their other performance. This explains why a person disabled from his employment as a brick-layer can be filmed by an insurance company's private investigator playing basketball; yet still be legitimately disabled. Basketball can be played without much necessity for engaging in lumbar flexion, yet brick-laying requires it. Also, the disc material may be spontaneously centralized occasionally enough to engage in a non-flexing sport from time to time without significant pain. Yet, the instant that the patient goes back to his usual occupation, he flexes while carrying a weight, and the disc again decentralizes, returning him to pain.

Besides my own personal experience, to further support the reality of this phenomenon, I have seen at least two cases in which I have been able to closely examine the patients immediately after the injury (whereupon a clinical examination demonstrated that the nerve roots had been damaged at the instant of injury by compression against the vertebral bones due to a severe protrusion); yet the imaging studies (NMRI) portrayed only moderate disc bulges by the time they were actually done. Reconciling the clinical exams with the clinical outcomes forced me to conclude that they indeed have residual nerve damage; but, based upon the imaging studies, the protrusion did not involve the nerve at the time of the study. The erroneous conclusion was drawn that no nerve damage existed in the disability claim. The patient had definite nerve damage evidenced by atrophy of involved muscle groups; yet the back pain management "expert" physicians who evaluated this case relied nearly exclusively upon the imaging studies to determine that the patient was not truly disabled.

Not only does a kinetic spectrum of damage exist at the instant of injury; but it also exists over the lifetime of an individual. The manner in which successive damage occurs starts with any event that puts excessive forces on the disc. These forces, for the most part possessing a posteriorly directed vector, during flexion and weight-bearing, start by tearing small fissures in the innermost lining of the annulus fibrosus layers. This weakens that area and allows the nucleus pulposus to preferentially enter the space created. Successive traumatic pressure events then allow the radial tear to advance.

If the force is of sufficient magnitude, it can create large radial tears all at once; however, normally centralized elements of the nucleus pulposus, both liquid and solid, can also slowly continue to advance the radial tear over time and repeated small traumatic events. These tears can then dissect between laminations of the annulus fibrosus to create circumferential tears as laterally directed pressures likewise occur pushing the nucleus pulposus deeper into the separating layers of the annulus fibrosus. The mobilized elements of the nucleus pulposus can even be caused to move circumferentially between the laminations by a forceful, weight-bearing circumductional movement such as lifting while twisting (as mentioned above), even to the extent of becoming trapped by the bordering laminations of the annulus fibrosus (Figure 30). Once they are positioned to be able to do that, relatively small forces can dissect the laminations, widening the circumferential tears and allowing increasingly larger volumes of nucleus pulposus material to decentralize. This, then, predisposes the disc for a widening of the radial tears with the next weight-bearing, forced flexion event.

It is easy to visualize how this decentralized disc material can create tracts or tunnels by fissuring through layers of the annulus fibrosus, allowing the displaced disc material to move a number of ways either spontaneously or intentionally. It can continue to advance away from the center, follow the same path directly back to the center, or it can move circumferentially requiring a more complex series of movements to get it to re-centralize. This is when the problem is increased in complexity and much less likely to spontaneously resolve. In this instance, special consideration must be given to get it to re-centralize. The MANEUVERS of The O'Connor Technique (tm) are designed to re-centralize this aberrantly positioned disc material intentionally so as to reduce symptoms as soon a possible rather than to wait for random activity to generate equivalent forces in the ideal sequence over a protracted period. The method and means to accomplish this is discussed at length below.

This series of injuries can continue until the solidified nucleus pulposus actually leaves the confines of the capsule to become a sequestered or extruded disc fragment (See Figure 27F). Prior to this point, there is every reason to believe the mechanical problem can be managed and the damage prevented from advancing with The O'Connor Technique (tm); however, after the disc material escapes the capsule it usually can only be managed with surgical intervention if it produces loss of sensation, paralysis, or pain.

The intent of this chapter and the essence of The O'Connor Technique (tm) is to teach the back pain sufferer to understand the functional anatomy, forces acting upon, and the mechanics of the disc so as to be able to reproduce forces in an opposite direction to the original damaging forces and, thereby, re-establish the proper configuration of the disc relative to its containment structures. A person who masters this method can look forward to a future in which disc pain can be predicted, prevented, controlled, counteracted, and the spine protected from future injury and pain.

Recall the oxtail described above. It provides a nearly identical, natural, representation of the actual anatomy of a disc. I would seriously encourage the reader to go to a supermarket and find a package. It cannot be frozen, the meat must be fresh and the oxtail must be large because the smaller ones don't adequately represent a disc approaching the size of a human disc. This is as close to a model of the human disc as is readily available since it represents the standard mammalian design. Of course, since the tail of the ox is not a weight-bearing structure there are small differences which must be overlooked. For this discussion, one is only interested in the anatomy and basic physical characteristics of the disc portion or the white, plastic-like, central portion.

Put your finger on the central white portion of the largest oxtail you can find. By continuously pressing down in the center with a finger and moving the hand in a circular motion one can often feel a central hardened area moving within gelatinous surroundings. This hardened center is equivalent to the central portion of the human disc system that hardens equivalently in the aged human condition. Now, if you imagine what would happen in the forced flexion position with downward pressure applied with the incredible gravitational forces that the back sustains, it's easy to see how that hardened piece of cartilage-like material could break through and penetrate the circular, softer, concentric rings that are designed to keep it in place.

Look closely at the oxtail's center and see those concentric rings of firm gelatinous tissue. If you really want to get the picture, make some oxtail stew out of them and cook them well-enough that the meat is falling off the bone. By biting into this material, you can appreciate how tough it is; and how it is indeed constructed of circular rings of cartilaginous tissue. By conceptually enlarging it in your mind, you can see how successive events of forced, load-bearing flexion can cause the radial tears that allow for the central material of the disc to move laterally and eventually escape the disc unit all together, resulting in an extrusion.

By picturing in your mind what would happen if that hardened disc material were to be traumatically forced against the rings of cartilaginous material by 500 lbs of pressure, you can envision how the layers would break and create a pathway (fissure) for the solid, central, disc material to traverse to the exterior leaving behind a canal of torn material. This is equivalent to a fissure (wide and long radial tear) in the human disc, and these are caused by a similar series of events wherein the central disc material (nucleus pulposus) is forced against layers of the annulus fibrosus breaking them to create a pathway through which the pieces of broken, hardened nucleus pulposus and fragmented disc material can freely travel.

Most people with injury-induced back pain, especially first-timers, have the type of tear with herniation, as opposed to an obvious disc protrusion or bulge. These herniations are usually invisible to the majority of medical imaging modalities. Discography (an X-Ray technique wherein dye is injected into the disc space highlighting the fissures created when the central disc material tears channels in the annulus fibrosus) is the most accurate means to detect these earliest of degenerative changes--tears or fissures of the annulus. These are difficult to detect by NMRI but, nevertheless, must exist in anyone with discogenic pain. Several studies support this finding. Due to the difficulty these tears have in being seen with imaging studies, multitudes of people are mis-diagnosed as having back sprain, muscle pulls, or pinched nerves. The presence of these fissures together with their herniated disc material can cause pain in any number of ways. This pain can be correlated and explained in terms of the mechanical anatomy.

Further Reading:

Spinal Anatomy
Directional Terminology
Structural Anatomy
Functional Anatomy
Pathological Anatomy
Disc Hydraulics / Mechanics
Compression Forces
Correlation of Mechanical Anatomy with Disc Pain
Traction Forces

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