Correlation of Mechanical Anatomy with Disc Pain

Dircect Pressure Pain: Fulcrum Effect Pain: Crimping Pain : Radicular Pain : Rederred Pain : Muscle Pain
Inflammatory Pain : Additional Sources of Pain

Pain is an extremely interesting phenomenon, it can protect and teach while at the same time can intimidate and destroy nearly all enjoyment of life. Back pain is no different. Without adequate explanation or relevant education as to its source, mitigating factors, or potential duration, it can be interpreted as random, unpredictable, confusing, frightening, and apparently perpetual. When back pain strikes that can't be alleviated in the usual time frame in which one is accustomed to seeing pain resolve, it can transform one's life expectations into constant apprehension. Back pain is somewhat unique in the scope of body pains because it carries the added prospect of one's potentially becoming disabled. Add to it the fear of losing one's livelihood or the realistic potential for paraplegia and even a small injury can magnify any sensation to an inconceivably frightening level.

Psychologists tell us that the stress induced by pain can be markedly better endured and tolerated so long as it is not perceived as random, it is made controllable, and predictable in both its onset and termination. Any pain can be tolerated much more easily if the seeming randomness is explained and understood. The purpose of this section is to lift the "blindfold" on the most common form of spinal pain by defining its source as discogenic (originating in the disc), familiarizing the sufferer with its various manifestations, and, through education, make the unseen source of pain understandable, manageable, predictable, and ultimately preventable.

To remind the reader, it is well-established that the nucleus pulposus and the inner portion of the annulus fibrosus have no nerve supply. Only the most outer portion of the disc unit, the ligamentous capsule and peripheral aspect of the Annulus Fibrosus, has sensory innervation. Some misuse this anatomical fact to assume that there should not be pain associated with either the tearing of a solidified nucleus pulposus through the laminar rings of the annulus fibrosus or the degenerative process in general. To a certain extent this is true and explains why people often relate that during the twisting or lifting event that they know initiated their pain, they just felt a pulling or a "pop." Only later did they gradually experience the sharp, debilitating pain. Also, people within hours of a whip lash injury describe the same experience. Immediately (minutes) after the trauma, they are a little sore, but the real grinding and immobilizing pain often comes hours later or the following morning when they wake up and try to move their neck. This is perhaps the most paradoxical aspect of spinal trauma. One would think that, if significant damage was occasioned, it would be immediately apparent and obvious at the scene of the trauma as in the case of a motor vehicle collision. After all, whenever someone pulls a muscle, breaks a bone, or sprains a ligament, the pain is apparent immediately.

One must consider, when trying to make sense out of the pain, that the entire disc system has very little tolerance for misplaced parts. Simply because one cannot feel the actual damage being done as the hardened components of the nucleus pulposus herniate through the annulus fibrosus doesn't mean that once they come to rest, placing direct pressure on the outer ligamentous bands of the annulus fibrosus or posterior longitudinal ligament, that they won't induce pain as the pain receptors within those ligaments are excited and the inflammation process begins.

DIRECT PRESSURE PAIN

First, tears of the annulus allow the de-centralized disc material to move towards the disc's periphery and put direct pressure on the ligamentous capsule that surrounds it. Movements putting the affected part of the spine in forward flexion can be seen to actually squeeze the hardened nucleus pulposus or other pieces of disc material posteriorly to put direct mechanical pressure on the posterior aspects of the capsule (See Figure 31). These capsular ligaments are very well-supplied with nerves and are quite capable of generating severe pain.

Also, the residual liquid component of the nucleus pulposus can participate in this pain scenario, especially when weight-bearing flexion causes the liquid component of the disc to exert hydraulic pressure on the posterior peripheral capsule. Considering what is occurring anatomically when trauma tears free the solidified nucleus pulposus and forces it through layers of the annulus fibrosus, there are areas of liquid nucleus pulposus that now have the capability of entering the fissure and hydraulically adding to the pressures that are felt on the posterior capsule. The hardened nucleus pulposus as well as its liquid counterpart are free to dissect through the fissure to reach the sensitive capsule to generate pain when the nerve-supplied ligaments are stretched.

When flexing in the weight-bearing condition (WEIGHT-BEARING FLEXION) hydraulic pressure or mechanical pressure on the nucleus pulposus forces it (or fragments of desiccated cartilaginous material) into the outer bands of the annulus fibrosus and posterior longitudinal ligaments, and pain is the consequence (See Fig 31). This effect can occur instantaneously or over a prolonged period of time due to successive events of pressure. This type of pain can be looked upon as originating from direct pressure applied to the capsule's ligaments.

The pressure on and damage to the peripheral ligamentous component of the disc (the capsule) and the posterior longitudinal ligament are probably the most important contributors to pain in the disc system and are largely responsible for the majority of pain attributable to back pain in general. Others may argue pulled muscle, sprain, arthritis, or some other mechanism, but, since the time I have been able to manually reduce disc herniations or put "in" de-centralized disc material with The O'Connor Technique (tm), my experience has shown me that the greatest component of spinal pain originates in the direct pressure placed on the exquisitely innervated joint capsule that surrounds the disc unit when decentralized disc material exerts pressure on those ligamentous structures. I "know" this because, once I have relieved this pressure through manipulation, the pain relief is usually instantaneous. In fact, it is very uncommon for me to have a back pain patient that I cannot prove has disc disease as the source of pain by virtue of my ability to relieve it. This leaves me with no other conclusion to draw.

As elaborated above, the peripheral ligamentous structures surrounding the disc, the joint "capsule," contains the sensory nerve fibers that tell where the upper body is in relation to the lower body. This innervation is the reason why you can stand upright and a baby (who is too young to have these pathways functional) falls over, even if only seated. It takes a high density of sensory fibers to be able to discriminate extremely subtle movements. When this same density of sensory receptors is applied to pain sensors, it implies that a little stimulation can go a long way in producing pain. That small amount of stimulation can come from a relatively small piece of displaced disc material pushing against the capsule or when, off-center, it creates a fulcrum effect in concert with the adjacent surfaces of the vertebral bodies.

These parts of the body rarely feel pressure or experience trauma during the youthful formative years of neurologic development due to their deep location in the body and their being surrounded by protective muscles that prevent their routinely experiencing painful stimuli. Therefore, when forces induce pain, it is registered by the brain as a novel phenomenon which usually translates to pain the severity of which has never been experienced by the average person any prior time in their life.

For this reason, annular tears can be very painful; yet patients with just these tears (in the absence of a bulge or protrusion) are often dismissed as having psychogenic pain motivated by secondary gain, mostly because discography is not done to demonstrate the true pathology. However, doctors don't routinely order discography and for good reason. It is a dangerous and invasive procedure. Only highly trained and qualified physicians are willing to stick a needle into the disc because it is painful and risky. If the radiologist is only a couple of millimeters off, a nerve root could be injured leading to paralysis. Since it is so difficult to identify these tears with non-invasive methods like X-Rays, CAT, or NMRI scans, the most convenient but alternative, erroneous, diagnoses are usually made instead.

FULCRUM EFFECT PAIN

The other major contributor to mechanical discogenic pain can be appreciated by considering what happens when, over time, with successive small injuries, a major lifting injury, or a traumatic flexion event the central disc material breaks its way through the layers of the annulus fibrosus but doesn't necessarily reach the peripheral capsule. The broken fibers of the annulus can close like one-way doors behind it, trapping the normally centralized disc material in an off-center position. The hard disc material then acts as a fulcrum. The vertebral body and the portion of the disc above it acts as a lever with the weight of the body providing the moment arm's force during flexion.

This phenomenon is not difficult to comprehend. Figure 32 schematically portrays a disc cut in horizontal cross-sections. The inferior surface of the superior section of the disc is shown as a transparent plate resting above the inferior component of the intervertebral disc. The displaced disc material or hardened nucleus pulposus is represented by a "brick" that rests between these virtual surfaces. The figure on the left describes the neutral (normal) situation where the center of gravity (fat arrow) is directly above the nucleus pulposus. In this configuration, the ligaments are relaxed and no pain is felt so long as the body is balanced directly above the center of the disc.

The figure on the right shows the condition in which some previous traumatic forward flexion event has displaced the hardened nucleus pulposus towards the posterior periphery. Then, the act of moving the center of gravity towards the periphery (as shown in the drawing on the right by the movement of the fat arrow), in this case equivalent to antero-lateral flexion, puts an inferiorly directed force on the "plate" causing it to teeter on the "brick" (the solidified nucleus pulposus) which stretches the "rope" (representing a ligament with pain/stretch receptors). When the force of the weight of the body acts with a fulcrum effect upon the component of the disc (the "plate") immediately above the hardened nucleus pulposus the forces stretching the ligaments become quite substantial. I term this FULCRUM EFFECT PAIN.

In the presence of a herniation, during my examination for diagnostic purposes, when I cause patients to change their center of gravity anteriorly (in a forward flexion directly away from the site of pain while standing, they easily agree that the pain is stretching due to the mechanical or hydraulic pressure on the posterior capsule. This pain is the pain of direct pressure. However, they then agree the pain is wedge-like when I keep them bent and circumduct them until the point that the fulcrum effect stretches the capsular ligaments adjacent to the displaced disc material. They recognize the pain as if something was physically wedged in their back when I then shift the center of gravity around to the other side of the herniation by circumducting them in the opposite direction. The slightest increases, beyond the point where pain begins, increases that tension and seems to magnify the pain exponentially. This configuration creates an effect similar to what happens when a pencil is placed in a door hinge wherein any attempt to close the door results in damaging forces. Even though the pencil is relatively small, shutting the door can warp the metal hinge due to the power of a fulcrum/lever system. The same fulcrum/lever effect is occurring in the damaged disc unit.

Circumduction moving from antero-lateral flexion to lateral extension (leaning successively through a circular, clockwise, range of motion) of the spine at the problem disc level causes pain by a fulcrum/lever mediated stretching of the peripheral capsular ligaments. As in the diagram analogy, moving the center of gravity along a circumferential path clockwise along the rim of the plate, successively puts and keeps tension on the ligaments such that, the closer one moves the center of gravity towards the brick, it becomes necessary to relax the degree of extension to get over the "hump" created by the wedged, hardened, nucleus pulposus. Similarly, moving the center of gravity around in a counterclockwise direction would have an equivalent effect upon other ligaments equivalently situated to the displaced disc material on the opposite side. The effect of this type of action is discussed in depth in the section on DIAGNOSTIC CIRCUMDUCTION wherein the pain and arrest in circumduction can be used to determine the position of the displaced disc material. Feel free to return to this drawing to understand that concept as well.

Just as the tiny pencil placed in a door hinge can stop the door from closing, so, too, can a small piece of cartilage-like material, when off-center, cause pain as the surrounding ligaments are stretched by a fulcrum effect. Attempts to force movement in spite of the misplaced disc are often met with excruciatingly sharp pain. The pain is often immobilizing because no matter what direction you turn or what position you assume other than balanced directly above the nucleus pulposus, the pain increases.

These factors explain why, during an acutely painful back event, the sufferer can neither bend forward to any extent, move to wards the painful side, nor extend enough to stand up straight without increasing the pain to an intolerable level. In any of these movements, the hard, off-center disc material can serve as the fulcrum for any of a number of possible levers and moment arms created by the cartilaginous and bony surfaces contiguous with that disc and the displaced disc material. Depending upon which of the other sites on the adjacent surfaces of the vertebral bodies is farthest from the displaced disc material, it becomes the moment arm. The site with the shortest distance becomes the lever. The lever then can stretch peripheral ligamentous tissues with forces much stronger than would otherwise be generated without the lever/fulcrum effect.

For instance, let's assume that the solidified disc material is displaced off-center to the midline posterior in the neck not enough to cause a direct bulge or protrusion, however, enough to impede competent movement. When the patient tilts his head forward and to the right, the displaced disc material, now turned elevated fulcrum, causes the left posterior peripheral ligamentous elements to be stretched with far greater force than they ordinarily would be caused to be in the disease-free condition. This causes a stretching pain to be felt to the left of the displaced disc material. The same thing happens when the head is tilted to the left, only this time the stretching type pain is to the right of the herniated piece of disc material.

As above in, Figure 32, the forces acting on the disc's ligaments can be equated with a rope (about the length of the brick's height) tied to the edge of a circular shaped board and secured to a platform. If a brick were placed in the center of the board and someone were to stand on the end of the board farthest from the rope, the rope would probably not break because the end of the board where the weight was applied would hit the ground before that could happen. However, moving the brick closer and closer to the rope's site of attachment, the board (just as the displaced disc material moves closer to the peripheral ligaments as it is displaced posteriorly and peripherally) increases the fulcrum effect so that, when it is nearly touching the rope, even small amounts of force on the far end of the board can be seen to be capable of snapping the rope.

I have ascertained to my own satisfaction that this mechanism of pain is the predominate cause of a condition known as torticollis or "wry-neck syndrome." Usually it is seen more often in children; but is also seen frequently in adults; but their necks don't seem to go into as much of the uncontrolled spasm as is routinely seen in children. Rather, the adult is most of the time unable to look over the shoulder to the same side as the displaced disc material. However, it is not unusual for the condition to be chronic or even perpetual. The disc material is usually displaced more laterally than posteriorly, and it causes the sufferer to turn his face away (due to contraction of the sternocleidomastoid muscle) but bend his neck towards the side of the herniation (due to a combination of same-sided paracervical muscle spasm and an attempt by the individual to keep the weight of the head's center of gravity directly over the displaced central disc material. To anterior flex the neck to the opposite side as the displaced disc material creates pain so the head and neck are kept rigidly immobilized partly because of spasm and partly because nearly any movement off of the center of gravity causes extreme pain.

It appears to some that muscle spasms are the source of the problem. So much so that, recently, some doctors have reportedly improved the condition by injecting a muscle relaxant into the sternocleidomastoid muscle; however, I fear this practice is too dangerous and ineffective because , technically, it only treats a symptom of the problem and not the origin. Alternatively, I have found it is the FULCRUM EFFECT of de-centralized disc material stretching the peripheral ligaments that initiates the spasm. The disc material displaced is most likely liquid nucleus pulposus in the child and/or solidified nucleus pulposus in the adult which has herniated off-center. This herniation, I have found, after careful history taking, to be usually due to a flexion injury, either in the immediate past or the remote past (that only has acutely re-herniated due to so much as sleeping in the wrong position).

On occasions too numerous to count, acting upon these assumptions by using The O'Connor Technique (tm) I have been able to non-traumatically and immediately reduce the subluxation with manipulation rendering the patient free of pain and restore full range of motion. This success is contrasted to reports in the literature of this condition lasting for years in the absence of definitive management. In fact, there are so many people in this country that have this untreated condition that they have formed a society.

Understand that the above described intervertebral disc fissure-facilitated mechanism of disc material displacement pain can occur over a long period of time with repeated nearly identical flexion injuries or instantaneously with a sufficiently powerful force. After repeated events that progressively damage the annulus fibrosus, even a seemingly small force can result in debilitating pain since the disc can be poised at any time to suddenly travel the same damaged route to reach the intervertebral ligaments. This explains why people can be doing something as apparently innocuous as taking out the trash early in the morning and "put out" their backs, resulting in a permanently painful back condition requiring surgery. Such is the case in many incidents which are usually not believed by the patient's doctor to be sufficiently traumatic to result in a disc protrusion or herniation.

You see, in cases like this, where someone comes into the doctor reporting that a sneeze or simply waking up and putting on shoes initiated a severe back pain event, the doctor reasonably assumes that no major damage could have occurred to ligamentous or bony structures because the forces applied were inconsistent with the ability to damage these characteristically tough structures. However, the original event, that predisposed to the presently painful one, may have been a fall as a teenager or an auto accident years prior that resulted in only moderate, transient pain. The disc material in the first injury never moved enough to become trapped; but it damaged the annulus enough to create a pathway for future advancing of the injury. Few people realize that the cartilaginous material that comprises the annulus doesn't heal or repair itself over time. Once it is fractured, it doesn't even scar. It remains perpetually broken and capable of allowing the central, hard disc material to repeatedly migrate along a previously created pathway. This helps explain why studies show that 40% to 85% of patients will have recurrences of back pain within a year after their initial episode, and nearly one third of patients with low back pain have a relapse within 3 years of the initial episode. Each event in which a radial tear is created makes it more likely for a fissure to be created and another, future, painful event to occur. As time goes on, cumulative injuries predispose to progressively severe disease.

This phenomenon also explains why "degenerative" lumbar disc disease is said "to progress as a series of pathophysiological events, beginning with asymptomatic fissuring and fragmentation within the disk." It is not widely appreciated, difficult to accept as fact, and worth repeating here that a significant radial tear can occur in the annulus fibrosus without inducing a reasonably commensurate amount of pain because these structures do not have nerves supplying them. The age-solidified nucleus pulposus, gradually and eventually, through repetitive trauma, herniates through successive layers of the annulus fibrosus, followed by prolapse of this fibrocartilaginous material into the spinal canal or the neural foramen. The pain comes only when the surrounding ligamentous component of the disc sustains pressure, stretching, or inflammation whenever the irritation is sustained.

There is also a combination type of pain that is experienced when the centralized disc material (the solidified nucleus pulposus, the broken fragments of the annulus, and/or the liquid component of the nucleus pulposus) bulges or protrudes to the rims of the adjacent vertebral bodies due to a herniation that causes the capsule to significantly deform and bulge posteriorly. In this case, the pain comes from the disc material causing both a fulcrum effect and direct pressure pain by its being trapped during the act of extension (See Figure 33). The decentralized disc material is positioned so far peripherally that it is actually pinched or squeezed by the vertebral body's rims. This, too, puts pressure on the capsule and results in pain.

CRIMPING PAIN

When extending in the weight-bearing condition (WEIGHT-BEARING EXTENSION) extension is often only allowed until the fulcrum effect is experienced because pain stops the movement; however, another condition that is closely related to the pain of the fulcrum effect yet is more appropriately considered as a constant direct pressure pain is when the displaced disc material has protruded to the point where extension of that disc unit causes a crimping of the prolapsed disc material. The crimping or pincer-like action happens when the disc material is pushed beyond the rim of the vertebral bodies and enough of it is outside of the circumference of the plateau portion at the rim of the vertebral bones to not allow it to move anteriorly in the presence of the body weight's compression forces (See Figure 34). Often, a fragment of displaced disc material is lodged in this prolapsed position; and the act of WEIGHT-BEARING EXTENSION traps and pinches it further posteriorly. This type of pain usually requires a protrusion or bulge-type herniation to be present, but one isn't absolutely necessary if the greater part of an ideally-sized piece of disc material is situated immediately peripheral to the point where the lips of the vertebral bones oppose each other such that their approximation when extension is occasioned creates a bulge.

RADICULAR PAIN

Radicular pain comes as a result of an extruding, protruding or prolapsed disc fragment coming into direct contact with a spinal nerve root (See Figure 35). Since the sensory component of the nerve roots travel down to the areas to which they supply innervation, pressure on these large roots can cause pain to appear to be coming from the places where the nerve travels.

This type of pain is a searing, burning, or electric shock-like sensation that is often associated with a definite extremity weakness and loss of muscle strength because the spinal nerve contains fibers that carry, sensory, pain and motor (muscle movement) signals. Since this type of pain if persisting, signals a nerve root compression syndrome and most likely will result in immediate surgery to remove the piece of disc material that is compressing the nerve, it will not be focused upon too heavily here except to elaborate that there are definite nerve root impingement syndromes described to explain the consequent loss of sensation, pain and motor loss depending upon the particular nerve root that is damaged. If the reader experiences this type of pain, this book is not a wise solution until one has been rejected as a surgical candidate by a neurosurgeon.

REFERRED PAIN

None of these mechanisms thus far explains why the hip or leg hurts when the lower spine is supposed to be the problem or why the shoulder hurts when the cervical vertebrae's discs are supposedly the source of the pain when there is clearly not a protrusion seen on an imaging study. The more commonly experienced Referred Pain reveals that the central nervous system isn't as smart as you think. In some ways, it is very unsophisticated, especially with novel events in which it has not been given time or capacity to become accommodated. By way of example, when a thorn is stuck in the leg while walking, initially, the brain recognizes that the leg hurts. You cannot determine anything more specific than the right lower leg has pain. The next thing you do is attempt to localize the pain by feeling the area and reproducing the pain by touching the affected site to convince yourself that indeed, that specific point is where the pain originates.

Next time you have a small injury, think about the pain. Finger pain can seem like the whole hand hurts until focus is directed at the actual source to pin-point the site. Most times it is necessary to feel around at length to determine the exact site of a particular pain's origin. In order to localize and identify pain, it is usually necessary to bring in other modalities of the central nervous system such as sight, movement response, and touch in order to localize it. Well, when the actual source of the pain is hidden deep inside a part of the body that cannot be felt, seen, touched, or knowingly moved in such a manner to identify the true source of pain, the brain is forced to make, often incorrect, assumptions.

Take for instance a painful condition that most people have heard about. Heart pain is so rare to the central nervous system's experience that, when it occurs, it is often thought of and felt to be in the arm. This is explained because the nerves to the arm are embryologically developed from the same pathway as the heart's nerves. So, the mind, trying to determine the pain's origin, concludes that the pain must be coming from the arm because the nerves are being excited from the same general pathway as the arm. Since heart pain is so rare, the mind assumes that the pain must be coming from somewhere else more accustomed to receiving pain signals. After all, most heart pain suffers are older than forty years old. The central nervous system has been living that long without pain from that area and has good reason to not "believe" pain could be originating there. So, it is not unreasonable for the brain to make an alternative "assumption".

When it comes to spinal pain, the brain is equally confused. This was documented by a study in which subjects were injected with irritating solutions into the facet joints at various levels. They were unable to determine which level was being injected or whether the disk or facet joint was being injected.

I am convinced that a similar pain pathway confusion frequently occurs when the nerves of the intervertebral disc's capsule are stimulated. Depending upon what level of inter-vertebral capsular ligaments are involved, take for instance L5-S1, the pain message emanating from this disc space is similarly accepted by the brain to have origination from the areas of the more customarily stimulated nerves' embryological distribution. The large spinal nerve root that exits the spinal column (that eventually supplies innervation to the muscles, skin, and joint of the hip) sends a small branch to the disc area, the Recurrent Sino-Vertebral Nerve (See Figure 10.) Both pain and proprioceptive impulses travel to the spinal cord and on to the brain through this nerve. When painful stimuli excite the small nerve from the disc's capsule, the impulse travels along with other fibers coming from other sites supplied by that particular, larger, spinal nerve. These pathways are so closely related that the mind frequently accepts the pain as having originated from the other sites which have been more accustomed to managing pain sensations throughout the life of the individual. Depending upon what spinal nerve is pertinent, the sensations, upon reaching the brain, are often accepted as having come from those areas of the body also innervated by that spinal nerve root in which the impulses from the disc also travel.

When the disc capsule's pain receptors are excited and pain impulses are produced, one can't very easily put one's finger on the actual site of pain at the L5-S1 disc level to convince the mind it is in error as in the thorn example given above; so, the central nervous system makes the incorrect "assumption" that the hip is what hurts and that site is from where the pain is mistakenly registered by the brain as having its origin. These areas correlated with the distribution patterns of spinal nerves are well-known and mapped out as sclerotomal, dermatomal, myotomal patterns corresponding to their respective spinal nerve levels. These patterns are delineated in more exhaustive textbooks for professionals and need not be reproduced here; but, ideally, by identifying what area the dull aching pain comes from at rest, one should be able to tell which disc is the source of pain. In reality, there is so much overlap of areas, the opportunity for further confusion is so rife, and that degree of exactitude is neither necessary or realistically achievable by the lay persons that I have elected to dispense with its discussion.

The O'Connor Technique (tm) makes such a pursuit academic. An individual can learn to correlate their own particular pain patterns with specific disc units simply by moving the spine and paying educated attention to where and when the pain is felt. Then, when that pain recurs, it can be assumed to be from the particular disc with the herniation. This will become more pertinent and apparent when, later, the reader is taught how to diagnose their own disc herniation because he/she will be able to specifically move their spine to find the actual discogenic source of pain regardless of where the pain radiates or refers.

Also, of note, something interesting about referred pain is that if you stimulate the area that appears to hurt, such as with a massage or rubbing, the pain temporarily disappears as if the mind, then, is saying: "Oh, the pain can't be coming from there because now I'm touching it and it is not being reproduced; therefore it has to be coming from someplace else." Then, the instant that the massage or stimulation stops, the pain recurs because the brain again returns to making an incorrect assumption like that elaborated above.

To better understand this type of pain, one should know that referred pain usually has limitations. It seldom travels beyond the elbow or knee. Rarely, in my experience, has referred pain gone below the knee in a lumbar disc problem or beyond the elbow in a cervical disc herniation when a nerve root is not involved. When it does, that can be a sign that the pain is radicular and caused by the actual pressure of a prolapsed disc on the nerve that passes through that segment of the spine. Radicular type of pain is usually described as "burning" whereas the referred pain is more often described as a "dull ache." Whenever pain seems to involve a strip that runs the entire length of the leg or arm, or is accompanied by actual weakness, that is a bad sign, made worse if it is accompanied by weakness of that same muscle area, and there should be no delay in seeking out a physician to determine if further studies or an operation is necessary to prevent destruction of the nerve.

A common source of not overtly obvious shoulder or leg pain is from an intervertebral disc referring the pain. Without other cues, the mind often cannot differentiate pain originating from the stimulation of a nerve at any point along the distribution of that nerve. The brain may register as the source of pain any site of stimulation whether it originates at the level of the nerve as it exits the spinal column, nerves that travel in the same bundle, or from the area innervated normally by the nerve.

As an experiment to demonstrate this phenomenon, the next time something hurts on your legs such as a bite, scratch, or any narrow area of trauma, without looking or touching, close your eyes and try to figure out exactly where the pain is coming from by just closing your eyes and focusing on the site. Your first impulse is to touch the area to determine the exact locality of the pain. You will probably realize, until this is done, you feel pain simply coming from a broad general area on the leg. In order to convince your mind where the exact location of the pain is, it is usually necessary to feel the area, actually reproduce the stimulation by pressing on the area of pain, and convince yourself that you have located the exact point of its origin.

Now, consider what happens when a disc or a nucleus pulposus puts pressure on the ligamentous bands on the periphery of the annulus fibrosus. There is no way that you can touch the disc with your hand to convince your mind that you have located the exact origin of the painful stimuli. Consequently, the mind must resort to guess work. The brain must assume the pain is coming from the nerves that innervate that area of the body to which the nerve being stimulated supplies nerve function.

In the case of the Lumbar region, the nerves are the same ones that go to the hips, buttocks, and legs. The pain is dull and no matter how much you touch the area that aches, you can't make it hurt more or reproduce the pain by touching areas from which the pain appears to come. If the pain were truly coming from the hip joint, moving just that joint should increase the pain, but it doesn't, neither does pressing on what seems to be the pain site. In fact, quite often, rubbing or massaging those areas stop the pain momentarily because the stimulation convinces the brain that that area cannot be the source. However, as soon as you stop, the pain returns.

As a pertinent aside, this paradoxical phenomenon can be explained by the Melzack and Wall gating theory of pain because sensory impulses travel faster than pain impulses and, when they beat the pain impulse to the spinal cord, they preferentially stimulate the nerves that travel to the brain by a gating mechanism. The brain receives the sensory input before it accepts the pain impulse.

Evolutionarily, this makes some sense since when running away from a predator, the organism is better served by a nervous system that physiologically ignores pain while allowing sensory input to have preference. It is apparently more a selection advantage to know where your feet are running than whether they hurt or not. Another model for this reality comes from the frequent experience of men in combat who describe no pain sensations while distracted by complex sensory input enabling them to continue functioning despite massive wounds.

The sensations of touch, temperature, stretching (so-called proprioceptive impulses), and vibration travel in very fast fibers. Consequently, these impulses arrive at the spinal cord's "gate" earlier and get through faster and more often than the pain impulses that travel in slow fibers. This explains why hot packs and ice packs both relieve pain. Unfortunately, they do very little to modify or heal the true source of the pain since neither heat or cold can reach the disc.

This information comes as scant consolation since one must first understand what is causing the pain to alleviate it. Towards this purpose, let us assume that a patient has hip pain on the right side. Many of my disc patients actually do not complain of low back pain per se, but describe it as predominately hip pain which accompanies the lumbar pain. This is also the case of the shoulder's relationship to the cervical spine.

They rarely have pain in the actual hip joint upon testing the range of motion of that joint so long as the back is prevented from moving during the testing. When traction is applied to remove pressure from the protruding disc, the first thing they notice is that the hip pain is relieved; and the spine becomes the site of pain. Only after having them do a DIAGNOSTIC CIRCUMDUCTION MANEUVER (to be explained later) in which they convincingly reproduce the pain and their movement is arrested, can I determine the position of the disc protrusion. Once the site of pain is identified, I put the disc back "in" with a centralizing MANEUVER. When they achieve relief of their hip pain, I can be certain that the disc was the source because that is the only area that was mechanically altered. Because I usually prove this is what is occurring by successfully putting the disc back "in" and the patient walks out without hip pain, I am forced to conclude that the pain relief would not have occurred unless the spine was the origin because that is the only area that had been mechanically altered.

I have also had a continuous opportunity to study this phenomenon on my own disc pain for years. This first-hand knowledge gives me a great deal of insight into my patient's experiences and the intricacies of spinal pain in general. When my disc is "out" the pain is more in the superior buttock than the spine. Upon completing a MANEUVER, the hip pain is likewise extinguished.

So, in evaluating your own low back pain, with The O'Connor Technique (tm) you can learn to recognize hip or buttock pain as originating from the disc material pressuring the nerve that refers pain to the hip. You can determine that the true source of the pain is coming from the spine by moving the spine in a very specific manner which will be discussed later in the description of the DIAGNOSTIC CIRCUMDUCTION or "THE O'CONNOR TEST." When doing the diagnostic and therapeutic MANEUVERS described later in this book, be cognizant of what particular movement accentuates the pain and what particular therapeutic MANEUVER decreases it. Usually, the DIAGNOSTIC CIRCUMDUCTION, when attempting to go to a full posterior extension, will be accompanied by arrested motion when the actual area of the displaced disc material interferes with the movement of that particular disc unit. Just as the point is reached where you feel as though, if you continued without letting up on the EXTENSION the pain would be unbearable, your extremity should start feeling the pain, and the sensation of something obstructing the movement should occur. This is the point where the surfaces of the vertebral bones interfacing with the discs are beginning to put pressure on the displaced disc material. It usually stops you from CIRCUMDUCTING further and gives the sensation that if you could just move the right way the pain would be relieved. It is often described as a "catch" in the back, like something is caught and prevented from moving further. That is the most characteristic component of disc pain that differentiates it from other types of pain. The following chapters go into much greater depth so don't stall here concerned that you have missed the point.

MUSCLE PAIN

Certainly, other sources of pain in the back do exist. People occasionally "pull" or "strain" the muscles in their back; but this is associated with a different type of pain. The pain of a "pulled" muscle (actually torn) in the erector spinae group is usually not associated with extremity pain or if it is, it is a pain that is reproducible and increased when the affected muscle is manipulated. Recall, the referred pain from the disc usually is made to feel better while being manipulated. The pain of a torn muscle is identified by tenderness (pain upon touching) of that specific muscle when it is palpated. When manual pressure is put on the torn muscle it becomes immediately more painful. So, with a backache, it is simple enough to test for actual muscle tenderness at the time of the injury, if it is present this gives reasonable evidence to conclude that the source of pain does not come from a disc. However, in my professional experience, a pulled muscle in the back is a rather uncommon event. However, pain in the muscles is not necessarily that uncommon because muscle pain can come from secondary spasm due to a herniated disc.

The pain of muscle spasm is sometimes hard to differentiate from pain due to a muscle tear because both are accompanied by a generalized hardening and swelling of the affected muscles. Spasm often follows a back injury in which a disc is herniated because that is the body's protective mechanism. The spasm can be expressed as an intermittent jerking with jolts of pain or continuous, depending upon whether or not the pain comes in short, rapid bursts (such as when a damaged ligament is stretched for an instant with movement) or sustained for long periods (such as when disc material is persistently deforming a ligament). By spasming, the segmented animal splints that area of the body so that injured midline structures are protected. Recall what happens when you pinch a worm, it curls towards the pinch. If you ever get the opportunity to handle an new born baby, place it face down with its stomach in the palm your hand so that its bare back faces you and its hips can move but each leg is straddling your arm. By running your finger down the back about one inch lateral to the spine you will see the Landau reflex. The baby will contract the erector spinae muscles automatically on the same side that the stimulus is applied. There is very little difference between this reaction and the reaction that occurs when a painful stimulus is applied to the spine later in life. The erector spinae muscles automatically and involuntarily contract towards the side of injury. When this contraction is sustained because the pain is continuous, the muscles go into a prolonged contraction or what is commonly referred to as spasm.

The best way of differentiating the pain of spasm from the pain of a pulled muscle is to feel the muscle itself. Usually, the torn muscle will be tender at the site of the tear immediately after the injury. The muscle that is painful due to prolonged spasm may become tender along its entire length but it does so only at a time distant to the injury and along the entire length of the involved muscle. The pain of both are increased when FLEXION away from the side of the pain is accomplished.

In order to differentiate between muscle pain versus disc pain, the job is much easier. When in extending to the side of the pain in the presence of muscular pain, the pain is reduced. Think about it, muscle pain from tearing is decreased when tension is taken off of the muscle and increased when tension is put on the muscle. So, when in a PASSIVE (without the activation of the muscles) EXTENSION position towards the herniation's side, a pinching of the disc should increase the pain. When passively extending to the side of pain, the erector spinae muscles will be relaxed to that side and result in less pain when the pain is due to a muscle tear. Additionally, there is usually no actual arrested motion in the presence of muscle spasm or tear. With a herniation, the displaced disc material physically stops the act of CIRCUMDUCTION. A torn or spasmed muscle might be painful to move, but it will not stop the spine from circumducting.

INFLAMMATORY PAIN

A discussion about the sources of pain in the disc system would not be complete unless Inflammatory Pain were included. Whenever an anatomical structure in the body sustains trauma, especially constant or repetitive friction due to abnormal pressures placed upon a component, inflammation usually occurs. This inflammation results from chemicals produced by the white blood cells that migrate to an area to facilitate the repair of damaged tissue. When displaced disc material is mechanically impinging upon structures that have a blood supply, cellular damage is occasioned. As the disc material abuts against the ligamentous structures, inflammation is created. Unfortunately, as long as the ligaments are being irritated by the continuous pressure of the displaced disc material, the inflammation will persist. It stands to reason that the pain of inflammation will also not resolve until the mechanical problem of the decentralized and aberrantly placed disc material is solved. Later in the book, methods designed to remove the disc material from pressing against the ligaments will be elaborated. Once the friction is relieved, the inflammatory component can be managed successfully.

ADDITIONAL SOURCES OF PAIN

When a disc has severely degenerated for many years, the majority tissue that once constituted the actual disc can become simply a mass of non- or poorly functioning material that has lost its structural integrity, leaving the ligamentous capsule as the only anatomical structure joining the two vertebral bones. In this advanced disease, the vertebral bones can be caused to contact each other or slip relative to each other into abnormal and painful configurations of bone on bone or a combination of bone and disc material that stretches the capsule. Fortunately, this level of disease occurs only in a limited percentage of "old" bad backs; and the principles of The O'Connor Technique (tm) still pertain and can effectively be used to relieve pain. At this stage, though, sustained relief may only come with surgical fusion.

Finally, without question, back pain originates from and accompanies many other disease states. Spinal stenosis (narrowing of the spinal canal), ankylosing spondylitis, arthritis, spondylolisthesis, cancer, fracture, trauma, infections, etc.; however, in my personal medical and orthopedic experience, the overwhelming majority of spinal pain originates in the disc and is due to some consequence of disc herniation. Those orthopedists, chiropractors, and medical doctors are entitled to their opinion when they attribute acute (rapid onset) or recurrent back pain to pulled muscles, ligament sprain, lumbar strain, sciatica, sacro-ileitis, spasm, etc. because those events do occur but not nearly with the frequency of disc herniation. However, they, more often than not, cannot make a convincing, logical argument with some form of objective proof to demonstrate the accuracy of their diagnosis because they seldom are required to design one. They are rarely held to the standard that their diagnoses be correct nor are they exposed to much of an untoward consequence if their diagnosis is erroneous. They simply make their best guess based upon what they assume to be fact, then rely upon Nature to remedy that which they cannot even adequately describe. This may sound like an indictment or a criticism; however, it is not. It is simply a statement emanating from a realistic assessment of the widespread, contemporary, lack of understanding about discogenic pain.

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

FOR MORE INFORMATION ON DISCRIMINATING THE SOURCE OF PAIN TRY THESE LINKS:

1backpain.com
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Bursitis.org gives readers an accurate source to research information that they believe will help educate them on Bursitis and treatment options.

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