Soft Tissue Pain

Copyright Abba Schoenhotlz 2009, Copyright Archives of the California Chiropractic Association Fourth Quarter 1970 . Volume 1, Number 2

Soft Tissue Pain Sites in the Low Back Area Franklin Schoenholtz, D.C.

The purpose of this paper is to discuss various aspects of tissue sites of pain in the low back area. It has always been a matter of controversy as to which structure actually causes the irritation that the patient describes as pain in the low back area. This region is a complex mechanical structure which has aroused many investigators to disagree on the actual cause of pain. Any discussion referring to the low back syndrome must differentiate pain resulting from fracture, metabolic disease and visceral diseases; for the approach we shall take we will attempt to exclude the non-mechanical causes. When viewing the spine in total, consideration must be given to the acquisition of the erect posture. In other words, the cerebellum has caught the veterbral column unprepared—the capacity ot maintain equilibrium on two legs outstripping the evolution of the spine. I was taught and believed that the great strain and physical demand placed on the lumbar spine will certainly cause eventual damage, but I now question that theory. I cannot justify this theory to the ankle joint which has great strain placed upon it over the years. When an individual walks, he stands alternately with more than twice the compression applied to any lumbar joint; yet it is well known that this joint stands up perfectly for a lifetime in spite of the absence of any buffer. Thus the academic question arises as to how much importance should be attributed to the disc as a cause of pain in the lumbar region. Cailliet reports if the internal pressure within a normal disc is experimentally increased by injecting saline solution into the disc, the increase does not cause pain. In a disc however, that has previously been fragmented, increase in the intradiscal pressure causes an ache in the low back area. If we were to use this same method on increasing pressure within a degenerated disc, no pain sensation occurs when the posterior longitudinal ligament is anesthetized by procaine. We must then assume that irritation of the posterior longitudinal ligament by an increase in the internal pressure from a degenerated disc is a mechanism of pain production and that this ligament does contain pain-sensitive nerve endings. Consideration must be given to the fact that the posterior longitudinal ligament begins to narrow progressively so that when it finally reaches the first sacral interspace (L5-S1) it has half of its original width. This contributes to an inherent structural weakness where we have the greatest static stress and spinal movement, producing the greatest kinetic strain. I have always thought that youngsters who are guided by athletic instructors to bend over and touch the floor when it is very difficult and awkward to do so, stretch the posterior longitudinal ligament with disastrous results later. These gymnasts, who teach at our schools, reason that they are attempting to lengthen the hamstrings so that subsequent flexion exercise can then be attempted with ease, no thought being given to the potential harm that may occur at a later date. If the ligament becomes stretched hypermobility of the disc results and, although painless, the beginning of the disc protrusion is laid down.

Angulation of the spinal nerve roots increases considerably in the lower spinal segment. This occurs because of an unequal rate of growth between the spinal cord and the spinal column; between intrauterine life and adulthood, the veterbral column increases 22 times in length while the cord increases 12 times. Because of the marked downward slope of the lowest two lumbar nerve roots, it is possible for a protrusion lying almost centrally at the fourth level to pinch the fifth root, whereas by presenting itself a little more to one side can compress

Cyriax has commented that in lumbar disc lesions the most remarkable feature of all is the fact that the symptoms, though caused by displacement within in a joint, arise from the pressure transmitted indirectly to the dura mater and not from any pressure exerted on the articular structures themselves. Unless this dual etiology of pain is understood, it is not possible to make sense of the signs presented by patients. The disc protrusion is the primary cause of pressure. The capsule and ligaments are very insensitive and nothing is felt until considerable pressure is exerted secondarily on the dura mater. Since the mechanism is dual, the examiner would expect the physical signs to be dual also, and they are. It is possible both to painfully stretch the dura mater by traction exerted from a distance and to painfully force the protrusion against the dura mater by movement at the affected side. The nerve root draws out with it an investment of dura mater that extends for at least an inch. Irritation at the axilla of the nerve-root leads to pain reference different from that set up by pressure exerted more laterally. The downward slope of the lowest two lumbar nerve roots has an important practical application. It is possible for a protrusion lying almost centrally at the fourth level to pinch the fifth root, where as by presenting itself a little more to one side can compress only the fourth root. Upon examination, the clinician finds it almost impossible to determine at which level the disc is protruding when the obliquity of the lowest two lumbar nerve roots is considered. The clinician will also have to face another complicated problem. If the theory of dural irritation is accepted he must remember that the manner of reference of pain from the dura mater defies the rules of segmentation that all other tissues obeserve. Many observers must have been puzzled to note that the fourth and fifth lumbar dermatomes start in the lower thigh; yet the pain of sciatica usually includes the upper thigh and buttock. These are sites of reference from the dural investment of the nerve root to a theoretically impossible area. Dural non-segmental reference ceases as soon as the roots have joined to form the nerve-trunk. I am indebted to my colleague, John G. Anderson, D.C., for an explanation of this important phenomenon. Dr. Anderson stated that the pain in the buttock can be caused by mechanical irritation of the piraformis muscle and or remnants of the posterior gray communicating rami. Various investigators have noted that in fourth and fifth lumbar and first sacral root pressure, the pain defies anatomical knowledge and is felt in the buttock (first lumbar dermatone) and the upper thigh-areas not included in the relevant dermatomes. An interesting side-light noted again by Cyriax is that primary postero-lateral protrusion usually comes on slowly and never impinges on the dura mater at all; hence premonitory backache is absent. The patient describes a pain coming on gradually at the calf, at the back of the knee or at the posterior aspect of the thigh. After some weeks or months the whole posterior aspect of one lower limb is affected; the pain may extend to the buttock in the end. A cough may hurt the thigh. This history is important, for such protrusions are always irreducible by manipulation.

SECONDARY CAUSES OF PAIN In consideration of material that has been introduced thus far we can reasonably assume that the disc does provide the prime cause of backache and that the dura mater, which has been thought to lie inert and insensitive along with irritation of the posterior longitudinal ligament, does justify serious consideration as a cause of low back pain. Attention must also be given however, to the secondary causes of pain.

It is an accepted orthopedic principle that the stronger the muscles about a joint, the more stable it is. This principle does not apply to the lumbar spinal joints. Pain is elicited at the extreme of range by stretching, not as the result of active contraction of muscle. The range of movement at the lumbar joints is small and the strength of the muscles considerable. Hence, if severe strain fall on the back, the joint always gives way before the muscles. Mennell offers another view in which he states that all pathology in the back results in limitation of movement in that part of the spine in which it is situated. It is characteristic of pain in the back in that it cannot be differentiated sufficiently by the conscious mind to determine whether it is arising from bone or joints or from the neighbor joint structures. The reflex reaction to pain in the back is splinting of the involved segment of the spine by muscle spasm. Pain arising from any synovial joint, be it from within or from the capsule or its supporting ligaments, results in reflex muscle spasm in an attempt to prevent movement of the joint.

In lumbar flexion, if the posterior longitudinal ligament becomes stretched, hypermobility of the disc results and although painless, the beginning of disc protrusion is laid down. The ligament narrows progressively in the spine so that at the first sacral interspace (L5-S1), it has half of its original width. This contributes to an inherent structural weakness where there is the greatest static stress and spinal movement, producing the greatest kinetic strain.

The relationship of the periarticular tissues and muscular influence to the kinetic spine involves a ligamentious function that is relieved by intermittent small muscular contractions, triggered by proprioceptive reflexes of the joints and ligaments. Pain results from irritation or inflammation of pain-sensitive tissues within the functional unit. Improper static or inappropriate kinetic function can cause a painful reaction. It must be pointed out that even if a muscle is supplied with blood, that muscle wastes if it is given no work to do or if its nerve supply is impaired. It is also important to note that a muscle also wastes if it spans a diseased joint, even though it is well exercised and its nerve-supply remains intact.

No structure of the body is so quickly altered by influences outside itself as muscle. The muscles in spasm about a painful focus are not appreciably tender. The only exception is when the painful focus, which a muscle is protecting, lies within itself. If a few fibers of a muscle have recently parted, movement induces localized spasm about the lesion, preventing it from being overstretched. It is not the muscles that are tender over an inflamed appendix or about an arthritic joint; it is the appendix or joint-capsule that they are shielding and in which the pain and tenderness lie. This distinction is not obvious at, say, in the lumbar region, but when one considers arthritis at the knee, the wrist or the fingers, it is clear that only the joint is tender. It is a principle that the treatment of muscular spasm is directed toward the lesion to which splinting is secondary. REFERENCES 1. 2. 3. 4.

Cailliet: Low Back Syndrome, 1962. Cyriax: Soft Tissue Lesions, 1955. Anderson; Faculty member, L.A.C.C., personal communicaiton, 1968. Mennell, Back Pain, 1960.

*This paper is developed from a report by the author which was published in the “American College of Chiropractic Orthopedists Review” 10-68.

Copyright Archives of the California Chiropractic Association Copyright Franklin Schoenhotlz 2009 Fourth Quarter 1970 . Volume 1, Number 2