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Copyright Abba Schoenhotlz 2009, Copyright Archives of the California Chiropractic AssociationFourth Quarter 1970 . Volume 1, Number 2
 
Soft Tissue Pain Sites inthe 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 beena 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 theactual cause of pain.Any discussion referring to the low back syndrome must differentiate pain resulting from fracture, metabolic diseaseand 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 out-stripping the evolution of the spine.I was taught and believed that the great strain and physical demand placed on the lumbar spine will certainly causeeventual 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 compressionapplied to any lumbar joint; yet it is well known that this joint stands up perfectly for a lifetime in spite of the ab-sence of any buffer.Thus the academic question arises as to how much importance should be attributed to the disc as a cause of pain inthe lumbar region. Cailliet reports if the internal pressure within a normal disc is experimentally increased by inject-ing saline solution into the disc, the increase does not cause pain. In a disc however, that has previously been frag-mented, 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 whenthe 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 produc-tion 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 nally reaches the rst 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 greatestkinetic strain.
I have always thought that youngsters who are guided by athletic instructors to bend over and touch the oor when itis very difcult 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
exion 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 beginningof 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 be-tween the spinal cord and the spinal column; between intrauterine life and adulthood, the veterbral column increases 22 times in length whilethe 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 fth root, whereas by presenting itself a little more to one side can compress
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