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‘Pain is not the only problem’: Pinched Nerve & Bulging Disc Nonsense

Bulging Disc Hypothesis Nonsense

Arguments for the assertion that ‘disc herniation’ causes low back pain is unsupported by the evidence. Neither disc herniation nor spinal ‘compression’ contribute to non-traumatic LBP in more than 90% of cases. The hypothesis that a bulging disc is the cause for back pain or radicular pain is nonsense. ICD10 codes: M46, (discitis), M51 (IVD degeneration), M99 (IVD disc stenosis), G57 (sciatica) categories only describe lumbar disc association not a direct cause for pain. It is tempting for the radiologist and the clinician to point their pencil eraser at the disc herniation and, with amour propre, insist that it is the cause, and stop their search. “Demonstrating that a neural response is specific for pain is practically impossible.” (Mouraux and Iannetti, 2018) “The exact cause of most back pain remains unproven.” Panjabi, 2006) Medical error is the third most common cause of death in the United States.” (Waite, et al., 2017)

The bulging disc hypothesis goes something like this: a patient presents with back pain and/or radicular symptoms, and diagnosis is delayed until imaging and interpretation are completed. With the imaging report in hand, the findings of disc disorder are determined to be the cause of the pain. The discal material is somehow applying force upon a nerve or upon the spinal cord. How can science prove ‘force’ upon the nerve or cord? (F = mass x acceleration) Discal material is not moving, it is stationary. This is a hypothesis that can never be proven.

Non-traumatic disc disorders include herniation, protrusion, extrusion, imbrication, degeneration, lesion, height loss, calcification, infection and inflammation. According to the bulging disc hypothesis, a portion of the disc ruptures, migrates and puts enough pressure on the spinal nerve root or the spinal cord, causing pain (various pain experiences.) ‘Enough pressure’ also means that the discal material is touching the nerve or cord without any actual displacement of it.

What if there is an explanation for discal material to leave the confines of the disc, and what if this process is perfectly normal? What if two new theories could explain this conundrum? (keep reading) Would all non-traumatic LBP surgery become obsolete?

The spinal cord and nerve roots are bundles of efferent and afferent nerve cells. According to the bulging disc hypothesis, when a nerve is ‘touched or pressed’ it elicits a pain signal (lowered threshold), however there is no evidence that the epineurium of nerves nor the spinal cord have nociceptors. Further, if a nerve was in fact being ‘pinched or pressed’ enough to elicit a ‘pain signal’, all other efferent and afferent signaling would also be amplified (lowered threshold.) In fact, the opposite is true clinically, a suspected ‘pinched’ nerve root is said to disrupt/delay/prevent efferent signaling (weakness) and afferent signaling (sense processing.) Instead, patients present with symptoms of numbness and tingling. What is the exact mechanism of numbness and tingling? Anyone? It seems unlikely that an explanation that provides certainty on one hand, and no explanation on the other hand, can’t be made about the same example. Clinicians can’t be certain that disc herniation certainly cause LBP, however numbness and tingling can’t be explained… a nerve is a nerve.

Discal material can’t selectively insight an effect on a specific nerve cell within the nerve bundle, nor change one specific signal function. Nerve signaling is an electrical process. The bulging disc theory would have us believe that discal material has the magical ability to cause an electric malfunction within a tangle of nerve root cells.

In addition to motor and sense malfunction, the discal material would be ‘pinching or pressing’ on vasculature, occluding blood flow to the nerve cells and spinal cord (arterial supply), and occluding blood flow out of the nerve cells or spinal cord (venous drainage.) Therefore, simultaneous necrosis and edema would be demonstrated within the nerve root or spinal cord. The lymphatic vessels would also experience occlusion, and intercellular edema would be demonstrated. According to the bulging disc hypothesis the ‘pinched’ nerve roots’ posterior ramus would not be able to supply the posterior muscles of the deep back; severe weakness would be present, and the patient would not be able to stand erect.

Afferent and efferent signals are highly redundant. Redundancy preserves function is cases when innervation and/or the vasculature is interrupted. The nerves withing the cauda equina (L2-S2; all LBP candidates) are individual nerves loosely arranged in a disorganized ‘bag.’ There is no way to predict or determine which exact nerve is being ‘pinched’ within the spinal cord. It is logical to assume that it is the one most approximating the discal material, but this is an assumption. Spinal nerves refer 2-4 levels above and below a nerve root lesion, not just the level of demonstrated lesion.

The spinal cord is a soft, rubbery, and easily displaceable organ suspended in a CSF ‘cushion.’. Cord displaceability is important to allow the many dimensions and demands of spinal motion. I have seen some amazing acrobatics, certainly enough to cause the spinal cord and nerve roots extensive distortion, stretching, and ‘pressing and touching’ with no complaint of pain. (yoga: wheel pose, dancer pose)

Advanced imaging is not necessary in order to provide excellent LBP care. Advanced imaging for LBP can offer a false sense of diagnosis, claiming that “pictures don’t lie.” However, clinicians should be taking more important actions to understand the many contributors to LBP, and not settling for simple answers, because ‘pain is not the only problem.’

LBP Blog General information

Series Description

These articles intend to (1) re-evaluate the prevailing clinical practices thought to manage low back ‘pain’, (2) submit and debate novel low back ‘pain’ contributors and mechanisms, (3) meet patient expectations & satisfaction and clinically meaningful results, (4) recommend a conservative non-surgical course of care to over-ride ‘pain’ instantly, and (5) restore ADLs and patient confidence on the first visit at low cost. This article has a companion podcast.

Dr. Dean Bio

Forester Dean is a chiropractic and physiotherapy sports medicine doctor practicing in Los Angeles, California. Dr. Dean is a lifetime athlete, and currently teaches tennis, track, boxing, yoga. The Core X System™ Campus flagship location was opened by Dr. Dean in 2020. www.preformancecxs.org

© Copyright 2021 SpineSync, Forester Dean, DC
Duplication with permission only
spinesync@gmail.com

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