Pathoanatomy and Management Options Understanding the Upper Cervical Spine

        The strict definition of migraine headache is (8):

• The headache must last 4 to 72 hours.
• The headache must be associated with nausea and/or vomiting, or photophobia, and/or phonophobia.
• The headache must be characterized by 2 of the following 4 symptoms:
  • • unilateral location
    • throbbing pulsatile quality
    • moderate or worse degree of severity
    • intensified by routine physical activity

•••

The headline appearing in the Business Section of the San Francisco Chronicle newspaper on July 20, 2014, was alarming (1):

MEDICINE

Huge Headache of a Problem

Mastering Migraines Still a Challenge for Patients, Scientists

Author Stephanie Lee notes that 36 million Americans suffer from migraine headaches. The migraine market in developed countries will grow to about $5.4 billion in 2022. The problem is that current treatments are not very effective and they may have dangerous side effects. Ms. Lee notes (1):

“Frustrated patients often seek out opioids in the emergency room, but opioids can be dangerous. In a year, … 20,000 patients in California developed chronic migraines because of opioid overuse, and 3,000 become addicted.”

Chronic migraine is defined as a severe headache that occurs at least 15 times per month. It is ironic that opioids taken for migraines cause chronic migraines in so many patients. Ms. Lee concludes (1):

“The demand for safe and effective alternatives [for migraine headaches] is urgent.”

••••••••••

Morphine is the main chemical found in opium. Morphine is the gold standard of pain relieving drugs. It has been used for centuries, and medicine embraced it starting in 1817. It has been known for decades that morphine inhibits even the worst types of pain. In World War II, medics routinely administered morphine for horrific injuries to soldiers.

Endorphins are chemicals made in our bodies that also inhibit pain. Endorphin literally means “the morphines within.”(6) Endorphins suppress pain by binding to a receptor, called the opiate receptor.

The understanding of pain was advanced significantly in 1972 when graduate student Candace B. Pert discovered the brain’s opiate receptor. At the time, Ms. Pert was a graduate student working in the laboratory of Solomon Snyder, Ph.D., at Johns Hopkins University School of Medicine.

Ms. Pert’s paper on the opiate receptor was published the following year, in 1973, in the journal Science, and titled (2):

Opiate Receptor: Demonstration in Nervous Tissue

In 1974 Candace Pert earned a Ph.D. in pharmacology. In 1978, Dr. Pert’s co-author, Dr. Solomon Snyder, was awarded the prestigious Lasker Award for their work, overlooking Dr. Pert’s contribution, even though she was the paper’s primary author. Dr. Pert was angered by the oversight, and wrote about the experience in her 1997 book Molecules of Emotion (3). Despite the Lasker award slight, Dr. Pert’s career flourished, and she became one of the most important neuroscientists of history (d. 2013).

It was soon acknowledged that the spot most densely packed with opiate receptors was at the top of the brainstem, the periaqueductal gray matter of the mesencephalon (midbrain). The periaqueductal gray was considered to be the primary sight for pain control anywhere in the body. Initially, stimulating the periaqueductal gray chemically (with opioid drugs or electrically) was shown to suppress pain. Later, attention was turned to modalities such as acupuncture, massage, and spinal manipulation.

The pioneering paper using electrical stimulation of the periaqueductal gray matter to suppress pain was published in 1977 in the journal Science, and titled (4):

Pain Relief by Electrical Stimulation of the Central Gray Matter in Humans

This paper is nicely reviewed by neurobiologists Richard Restak, MD, in his 1979 book titled The Brain, The Last Frontier (5):

“Within the periaqueductal gray, a deep-seated brainstem area lying along the floor of the third ventricle, neurosurgeons at the University of California in San Francisco placed indwelling stimulating electrodes for pain relief in six patients afflicted with chronic, unremitting pain. Whenever the patients began to experience pain, they were able to shut it off via the activation of a battery-operated stimulator about the size of a pack of cigarettes. After activating the stimulator, all six patients—in accordance with earlier findings in other pain patients—    experienced dramatic, long-lasting, and repeatable pain relief.”

        “In order to test the hypothesis that pain relief was genuine and not just an example of a ‘placebo response,’ one patient was outfitted with a stimulator containing a ‘dead’ battery. The patient, a fifty-one-year-old woman with severe back and leg pain caused by cancer of the colon, anxiously reported that her pain had returned and the stimulator ‘wasn’t working.’ Replacement of a new battery led to immediate pain relief.”

Today, it is well established that the periaqueductal gray matter is the primary sight for whole body pain control. Using the words “periaqueductal gray pain” in PubMed locates 1470 references (as of August 7, 2014).

Contemporary neurology reference texts detail the importance of the opiate receptor and the periaqueductal gray matter in pain control (6, 7, 8, 9, 10, 11). In general, they describe this sequence:

Although this sequence has a number of synonyms, classic terminology is the Descending Pain Inhibitory Control System.

••••••••••

 Stimulating the Descending Pain Inhibitory Control System with opiate pharmacology has problems. There are opiate receptors throughout the central nervous system and opiate drugs influence these other receptor sites. Often, the patient would become “high” from these drugs, and patients would begin to consume these drugs for purposes other than pain control. The getting “high” practice is difficult to control; thousands of babies are born addicted to their mother’s opiate pill habit (12). Radio talk show host Rush Limbaugh risked his reputation, fame, fortune, and freedom in an effort to have a staff person purchase huge quantities of opiate drugs, a habit that apparently began when he was given a prescription for a back problem (13).

In a related story, addiction to opiate drugs is a serious and common problem. In May 2014, the newspaper USA Today quantified the problem noting (14):

• Hundreds of thousands of the nation’s seniors are misusing prescription drugs, including narcotic painkillers, anxiety medications and other pharmaceuticals, for everything from joint pain to depression.
• Over time, patients build up a tolerance to opiate drugs, or suffer more pain, and they ask for more medication.
• The 55 million opioid prescriptions written last year for people 65 and over marked a 20% increase over five years — nearly double the growth rate of the senior population.
• In 2012, the average number of seniors misusing or dependent on prescription pain relievers in the past year grew to an estimated 336,000, up from 132,000 a decade earlier.

These addictions are ruining many lives. When the supply of physician prescribed opiates declines, those addicted often turned to street drugs such as heroin or cocaine. Many turned to crimes to finance their habits. Opiate drug addictions are extremely difficult to conquer.

As noted by Stephanie Lee above, taking opiates for migraine causes a worsening of the headache to the status of chronic migraine in a substantial number of individuals (1).

•••••

 Stimulating the Descending Pain Inhibitory Control System electrically is also problematic. Electrodes must be placed literally deep into the brainstem to access the periaqueductal gray matter. Such a procedure is logistically difficult to perform and is associated with substantial risks.

•••••

 A much less invasive yet effective method of stimulating the Descending Pain Inhibitory Control System is with the use of acupuncture (15). The use of acupuncture for this purpose is well detailed in the 2000 book by Stux, titled Clinical Acupuncture, Scientific Basis, published in 2000 (16).

•••••

In 1996, Bill Vicenzino and colleagues from the University of Queensland, Australia, added significantly to the understanding of the mechanism of pain control through the use of spinal manipulation (adjusting) (17). Vicenzino and colleagues produced a randomized, double blind, placebo controlled clinical trial using cervical spine manipulation (adjustment) on 15 subjects with lateral epicondylalgia (elbow pain). These authors cite references to support that the “clinical efficacy of manipulative therapy has been demonstrated in randomized clinical trials which report benefits in terms of pain relief and more rapid restoration of function.”

Their study showed a clear hypoalgesic effect from the use of spinal manipulation (adjusting). The results showed a “significant treatment effect beyond placebo or control.” The authors concluded: “manipulative therapy is capable of producing improvements in pain and function immediately following application.”

These authors made several astute and important observations, including:

• The subjects were suffering from elbow pain, NOT neck pain.
• The manipulation was applied to hypomobile joints of the cervical spine, NOT to the elbow.
• The improvement in elbow pain and function occurred immediately following the cervical spine manipulation, an improvement that is not explainable by the reduction of elbow inflammation or by accelerated elbow tissue healing.
• The descending pain inhibitory system is activated by stimulation of the periaqueductal gray matter.

Based upon these factors, and others, the authors concluded:

        “These findings indicate that manipulative therapy may constitute an adequate physical stimulus for activating the descending pain inhibitory system.”

        “… manipulative therapy recruits the descending pain inhibitory system, through which it exerts a portion of all of its pain relieving effects. That is, manipulative therapy applied to the cervical spine produces a sensory input which could be sufficient to activate the descending pain inhibitory system.”

•••••

 

The brainstem and the upper spinal cord have a region of gray matter called the trigeminocervical nucleus. The nucleus is so named because its primary sensory inputs arise from the branches of the trigeminal nerve (cranial nerve V) and those of the upper cervical spine. In 1995, Nikoli Bogduk, MD, PhD, notes that all headaches, regardless of type, including migraine, synapse in the trigeminocervical nucleus (18).

Most recently (July 2014), Nelly Boyer and colleagues from Clermont University in France, have indicated that migraine headache progression is attributed to impairment of the descending pain inhibitory system to the trigeminocervical nucleus (19).

Also, recently (June 2014), Dean Watson and Peter Drummond from Murdoch University, Perth, WA, Australia, published a study in the journal Headache, titled (20):

Cervical Referral of Head Pain in Migraineurs:

Effects on the Nociceptive Blink Reflex

This study assessed the pain intensity and nociceptive blink reflex in 15 migraine subjects between times of symptoms with passive movements of the occipital and upper cervical spinal segments. The nociceptive blink reflex was elicited with a supraorbital electrical stimulus. The number of blinks of the nociceptive blink reflex were recorded. Head pain intensity was graded from 0-10, where 0 = “no pain” and 10 = “intolerable pain.” They note:

• Anatomical and neurophysiological studies show that there is a functional convergence of trigeminal and cervical afferent pathways.
• Migraine patients often have occipital and neck symptoms, with cervical pain being referred to the head, “suggesting that cervical afferent information may contribute to [migraine] headache.”
• Nerve blocks of the greater occipital nerve [C-2] modulate migraine pain, demonstrating a role for cervical afferents in migraine.
• “Spinal mobilization is typically applied when dysfunctional areas of the vertebral column are found.” “The clinician’s objective in applying manual techniques is to restore normal motion and normalize afferent input from the neuromusculoskeletal system.”
• There is a functional influence on trigeminal nociceptive inputs from cervical afferents. This study showed that passive manual intervertebral movement between the occiput and the upper cervical spinal joints decreases excitability of the trigeminocervical nucleus.
• “Our findings corroborate previous results related to anatomical and functional convergence of trigeminal and cervical afferent pathways in animals and humans, and suggest that manual cervical modulation of this pathway is of potential benefit in migraine.” [emphasis added]
• These findings show that “cervical spinal input contributed to lessening of referred head pain and cervical tenderness.”

These authors conclude:

Ongoing noxious sensory input arises from biomechanically dysfunction spinal joints. Mechanoreceptors including proprioceptors (muscle spindles) within deep paraspinal tissues react to mechanical deformation of these tissues. Manual mechanical deformation can cause “biomechanical remodeling” with restoration of zygapophyseal joint mobility and joint “play.” “Biomechanical remodeling resulting from mobilization may have physiological ramifications, ultimately reducing nociceptive input from receptive nerve endings in innervated paraspinal tissues.”

These findings “corroborate previous results related to anatomical and functional convergence of trigeminal and cervical afferent pathways in animals and humans, and suggest that manual modulation of the cervical pathway is of potential benefit in migraine.”

SUMMARY

• The universal spot for pain control is in the upper brainstem, the periaqueductal gray matter.
• The periaqueductal gray matter, when stimulated directly or via the hypothalamus initiates the descending pain inhibitory system.
• All headaches, including migraine headaches, synapse in the neck, in a spot called the trigeminocervical nucleus. As its name implies, the trigeminocervical nucleus also receives input from the upper cervical spine sensory fiends, via C1-C2-C3 nerve roots.
• Migraine headache sufferers have impairment of the descending pain inhibitory system.
• Improvement of the mechanical function of the joints and tissues of the upper cervical spine reduces migraine headache pain. It probably does so by stimulating the descending pain inhibitory system to the trigeminocervical nucleus.
• Upper cervical spine manual therapy and adjustments improve mechanical function, reducing migraine headache pain. It probably does so by stimulating the descending pain inhibitory system to the trigeminocervical nucleus.

These studies explain what essentially every chiropractor has observed:

Improvement of the mechanical function of the upper cervical spine inhibits nociceptive input from the upper cervical spine into the trigeminal cervical nucleus, reducing its central sensitization, reducing the nociceptive signal on the second order neuron to the brain for the perception of headache. 

REFERENCES

• Lee, SM; Huge Headache of a Problem; Mastering Migraines Still a Challenge for Patients, Scientists; San Francisco Chronicle; July 20, 2014; pp. D1 and D5.
• Pert CB, Snyder SH; Opiate receptor: demonstration in nervous tissue; Science; 1973 Mar 9;179(4077):1011-4.
• Pert CB; Molecules of Emotion, The Science Behind Mind-Body Medicine; Touchstone Books; 1997.
• Hosobuchi Y, Adams JE, Linchitz R; Pain relief by electrical stimulation of the central gray matter in humans and its reversal by naloxone; Science; 1977 Jul 8;197(4299):183-6.
• Richard Restak, MD; The Brain, The Last Frontier, Warner Books, 1979; pp. 341-342.
• Raymond D Adams, MD; Maurice Victor, MD; Allan H Ropper, MD; Principles of Neurology; Sixth Edition; 1977.
• Eric R Kandel, James M Schwartz, Thomas M Jessell; Principles of Neural Science; Fourth Edition; 2000.
• H Royden Jones, MD; Netter’s Neurology; 2005.
• Marco Pappagallo; The Neurological Basis of Pain; 2005.
• Stephen B McMahon; Martin Koltzenburg, MD; Wall and Melzack’s Textbook of Pain; Fifth Edition; 2006
• Randy W Beck; Functional Neurology for Practitioners of Manual Therapy; 2008.
• Szabo L; Number of Painkiller-Addicted newborns triples in 10 years; USA Today; May 1, 2012.
• John J. Goldman and Steve Carney; Limbaugh Admits Painkiller Addiction; The Los Angeles Times; October 11, 2003.
• Peter Eisier; Medication Generation, Seniors Misusing Prescription Drugs; USA Today; May 22, 2014.
• Takeshige C, Sato T, Mera T, Hisamitsu T, Fang J; Descending pain inhibitory system involved in acupuncture analgesia; Brain Research Bull; 29 (1992); pp. 617-634.
• Stux G, Hammerschlag R (Eds); Clinical Acupuncture, Scientific Basis, Springer, 2000.
• Vicenzino B, Collins D, Wright A; The initial effects of cervical spine manipulative physiotherapy treatment on the pain and dysfunction of lateral epicondylalgia; Pain; Vol. 68 (1996); pp. 69-74.
• Bogduk N; Anatomy and Physiology of Headache; Biomedicine and Pharmacotherapy; 1995, Vol. 49, No. 10, 435-445.
• Boyer N, Dallel R, Artola A, Monconduit L; General trigeminospinal central sensitization and impaired descending pain inhibitory controls contribute to migraine progression; Pain 2014; Vol. 155; pp. 1196-1205.
• Watson DH, Drummond PD; Cervical Referral of Head Pain in Migraineurs: Effects on the Nociceptive Blink Reflex; Headache 2014; Vol. 54; pp. 1035-1045.

The Numbers

Low back pain is one of the most thoroughly investigated health problems worldwide, yet both prevention and effective treatment are elusive and controversial. The National Library of Medicine of the United States displays nearly 25,000 articles when the key words “low back pain” are used (May 2014).

Suffering with low back pain is almost a universal human experience. The United Stated Government’s National Institutes of Health (NIH) has the National Institute of Neurological Disorders and Stroke, which has a Low Back Pain Fact Sheet (1). The Fact Sheet makes the following key points:

• Nearly everyone at some point will have back pain.
• Americans spend at least $50 billion each year on low back pain.
• Back pain is the most common cause of job-related disability and a leading contributor to missed work.
• Back pain is the second most common neurological ailment in the United States — only headache is more common.

Public Health statistics (as of April 2014) add the following key points (2):

• Low back pain (LBP) is a major public health problem worldwide.
• All age groups are affected with low back pain, including children and adolescents.
• 1%–2% of adults in the United States are disabled with low back pain.
• The morbidity toll attributed to low back pain is enormous from both personal and societal perspectives.
• Direct back pain health-care expenditures in the United States were $90.7 billion in 1998. The burden is even greater when indirect costs such as productivity losses, indemnity pay, litigation, retraining and other administrative costs are considered.
• Only heart disease and stroke have substantially higher medical expenditures than spine disorders in the United States.
• LBP is presently the leading cause of disability in the world.
• LBP is the leading cause of activity limitation and workplace absence in most parts of the world.
• Most people will experience LBP at some point in their lifetime, with two-thirds having a recurrence and one third having periods of disability.
• Cases in which LBP never recurs are rare.
• A previous episode of back pain is the primary risk factor for a new LBP episode.

Global Spinal Anatomy
The Compromise Between Movement and Strength

The spinal column has three main functions:

1. To be strong in gravity. To resist the compressive loads of our weight and to successfully transmit our weight loads to the legs.
2. To be flexible as to allow us to perform the activities of life: bending, stooping, lifting, work, play, sports, enhance seeing and hearing, etc.
3. To protect the nerves of the spinal cord.

The strongest structure is a column. This is why engineers use columns to support bridges and buildings. However, a column is a poor design for the spine because columns limit motion (like turning and bending).

The most efficient structure for allowing movement is a 90° lever, like a lug-wrench.

The spinal “column” is a compromise between strength (straight column) and mobility (90° lever), with a series of three curves of about 45° each. Without these curves, spinal motion would be extremely difficult. These curves are physiologically important and considered to be normal.

Consequently, from the side, the spinal “column” should have three curves. From behind, the spine should be straight.

Segmental Spinal Anatomy

To further enhance spinal mobility, the spinal “column” is compromised of 24 individual segments, called vertebrae, each with a small degree of normal motion in multiple directions. Collectively, these small amounts of motion add up to our significant spinal flexibility.

Two adjacent spinal vertebrae are called a motor unit.

The individual vertebrae of the motor unit are held together by ligaments and by the intervertebral disc, or simply “disc.”

The intervertebral disc (disc) requires more discussion. The disc has two components. The center of the disc is called the Nucleus Pulposus, or simply “nucleus.” The nucleus is mostly water and functions as a ball bearing, allowing the vertebrae to bend and twist.

The nucleus is surrounded by tough outer fibers called the Annulus Fibrosis, or simply “annulus.”

The annular fibers surround the nucleus like layer after layer of rubber bands. Like rubber bands, annular fibers can break with age or excessive mechanical stress. When this occurs, the nucleus is no longer held in place, and its ball bearing functions are reduced.

Importantly, the fibers of the annulus are arranged in layers, and each layer is crossed in opposite directions. During disc rotational movements, half of the annular fibers become tense, and the other half become lax. Rotational stress applied to the annulus is resisted by only half of the annular fibers. The disc is operating at only half strength during rotationally applied stress, increasing its vulnerability to injury. The disc is weakest during rotation. It is the integrity of the disc that is most responsible for the health of the spine.

Crossed Annular Fibers of the Intervertebral Disc

Intervertebral Disc Pressure

The vertebral body of the spine is designed to bear our weight. Consequently, the size of the vertebral body increases with each lower vertebrae, from the neck to the low back, to handle the increased weight. The disc, existing between adjacent vertebral bodies, also must bear the same weight. Yet, the disc is not made of bone and is consequently weaker. Also, the disc must be flexible, allowing for our bodily motions.

The last low back (lumbar) disc, known as the L5 disc, bears the most weight, and hence is most vulnerable to weight-bearing stress. After L5, our weight is split to go down both of our legs.

The L5 (last low back) disc has the greatest pressure. In addition, disc pressure changes with changes in bodily positions and activities. Pioneering Swedish orthopedic specialist and professor Alf Nachemson, MD, PhD, [1931-2006] developed a method to measure intradiscal pressures (3).

Using relative values for easy comparison, note the following:

• Disc pressure is lowest when lying on the back. Perhaps this is why lying on the back is the most comfortable position for patients suffering with low back pain.
• Disc pressure is four times greater when standing as compared to lying on ones back.
• Standing and bending forward increases disc pressure by 50% compared to standing straight. Perhaps this is why so many patients initiate their back pain by bending forward.
• Disc pressures are significantly higher when standing, bending forward, and holding a weight, increasing by more than 100%. The heavier the weight is, the greater the increase in intradiscal pressures, and the greater the risk of disc injury.
• Disc pressures are greatest while sitting. Prolonged sitting is bad for the disc.
• Disc pressure is maximum during sitting, bending forward, and holding a weight.

The Inclined Plane of L5

In the reference text The Physiology of the Joints, former Chief of Clinical Surgery at the Hospital of Paris, IA Kapandji, states (4):

“The lumbo-sacral joint is the weak link in the vertebral column.”

When a block is on an inclined plane, the vertical force of gravity (G) is broken into two vectors:

C  –  A compression component
S  –  A sheer component

The sacral base is not horizontal (flat), but rather it is an inclined plane. The L5 vertebral body sits atop of the inclined plane of the sacral base. This inclined plane places additional mechanical stress on the annulus of the L5 disc.

Where Does Back Pain Come From?

The modern era in the understanding of low back pain began in 1976 when internationally respected orthopedic surgeon Alf Nachemson published his detailed review (136 references) in the new journal SPINE, titled (3):

The Lumbar Spine: An Orthopaedic Challenge

Based in part on his intradiscal pressure studies, Dr. Nachemson notes that 80% of us will experience low back pain at some time in our life. He further notes that:

“The intervertebral disc is most likely the cause of the pain.”

Dr. Nachemson presents 6 lines of reasoning, supported by 17 references, to support his contention that the intervertebral disc is the most likely source of back pain. Nachemson was claiming that a non-herniated disc problem was causing back pain. At the time (1976), claiming the intervertebral disc was capable of initiating pain was new; claiming the disc to be the most probable source of back pain was revolutionary. Up until the late 1980s, most reference texts were claiming that the intervertebral disc was not innervated with pain afferents and therefore not capable of initiating pain. As an example, in the 1987 text edited by rheumatology professor Malcolm Jayson, MD, titled The Lumbar Spine and Back Pain, states “the mature human spine has no nerve endings of any description in the nucleus pulposus or annulus fibrosis of the intervertebral disc in any region of the vertebral column.” (5)

In 1981, anatomist and physician Nikoli Bogduk published an extensive review of the literature on the topic of disc innervation, along with his own primary research, in the prestigious Journal of Anatomy (6). Dr. Bogduk notes:

“In the absence of any comprehensive description of the innervation of the lumbar intervertebral discs and their related longitudinal ligaments, the present study was undertaken to establish in detail the source and pattern of innervation of these structures.”

“The lumbar intervertebral discs are supplied by a variety of nerves.”

“Clinically, the concept of ‘disc pain’ is now well accepted.”

In 1983, in SPINE, Dr. Bogduk updates his research, stating (7):

“The lumbar intervertebral discs are innervated posteriorly by the sinuvertebral nerves, but laterally by branches of the ventral rami and grey rami communicantes.”

“The distribution of the intrinsic nerves of the lumbar vertebral column systematically identifies those structures that are potential sources of primary low-back pain.”

In 1987, SPINE published Dr. Vert Mooney’s Presidential Address of the International Society for the Study of the Lumbar Spine. It was delivered at the 13th Annual Meeting of the International Society for the Study of the Lumbar Spine, May 29-June 2, 1986, Dallas, Texas, and noted (8):

“Persistent pain in the back with referred pain to the leg is largely on the basis of abnormalities within the disc.”

“In summary, what is the answer to the question of where is the pain coming from in the chronic low-back pain patient? I believe its source, ultimately, is in the disc.”

In 1991, primary research by Dr. Stephen Kuslich and colleagues was published in the journal Orthopedic Clinics of North America (9). The authors performed 700 lumbar spine operations using only local anesthesia to determine the tissue origin of low back and leg pain, and they present the results on 193 consecutive patients studied prospectively. Their findings included:

“Back pain could be produced by several lumbar tissues, but by far, the most common tissue or origin was the outer layer of the annulus fibrosis.”

Hyper-innervation
Receptive Field Enlargement

Beginning with the work of Nikoli Bogduk and others over the past three decades, there has been a growing acceptance that the annulus of the disc is innervated with pain afferents and the annulus of the disc is the most probable source for low back pain. There was also 100% agreement that the nerves were only found in the annulus, and that the nucleus was aneural. However, an important addition to these concepts arose in 1997.

In 1997, AJ Freemont and colleagues published a study in the journal Lancet, titled (10):

Nerve ingrowth into diseased intervertebral disc in chronic back pain

Using samples of the intervertebral discs from 38 humans, these authors were able to show that when the disc degenerates, the nerves in the annulus can migrate into the nucleus. Histologically, these nerves in the nucleus were judged to be pain afferents. Thus the nucleus itself could be a source of discogenic pain. These authors used these anatomical findings to explain why low back pain can be so chronic, and continue to add to the evidence that the disc is the primary source of low back pain.

Later in 1997, in the journal Spine, another study was published on the topic of nucleus innervation, and titled (11):

Innervation of “painful” lumbar discs

The authors, in agreement with Freemont and colleagues, also found nerves in the nucleus of human subjects with disc degeneration.

Summary

There has been mounting evidence, for decades, that the disc has pain nerves, allowing the disc to be the primary source of low back pain. The disc also has unique susceptibility to injury, stress, and inflammation, initiating the pain cascade:

• The disc is innervated with an extensive array of pain nerves.
• The lower spinal discs, especially the L5 disc, is a significant part of the weight-bearing mechanism. Structures that bear weight have a greater risk and incidence of degenerative change.
• The L5 disc exists on a significant inclined plane, increasing its risk for motion stress and subsequent degeneration and injury.
• The annular fibers of the disc are crossed in opposite directions. This reduces the strength of the disc during certain activities, increasing its risk for motion stress and subsequent degeneration and injury.
• Varying body postures and activities increase the pressure in the disc, increasing its risk for motion stress and subsequent degeneration and injury.
• With disc degeneration, there is an increase in the number of pain fibers in the disc, including into the nucleus itself. The increase in the number of pain nerve fibers increases the likelihood that stress and injury will produce low back pain.

Practical Solutions To Avoid Low Back Pain
Practical Solutions to Manage Existing Low Back Pain

• The single worse activity for one’s back is to lift something while bending and twisting. Twisting reduces the strength of the annulus by 50%. Both bending and lifting significantly increase the pressure in the disc.
• Excessive body weight adds to the pressure and wear-and-tear on the disc.
• Prolonged sitting and primary sitting occupations are bad for the disc. Sitting places 40% more pressure and stress on the disc as compared to standing.
• Keep the back mobile, supple. The disc has no blood supply, so the health of its cells depends upon motion that pumps fluid into the disc. Discs with poor nutrients become inflamed and painful. Practice techniques that help the spine to be flexible; these same techniques literally pump fluid with fresh nutrients into the disc, much like squeezing a dry sponge under water. See a chiropractor to safely maximize spinal disc joint mobility.
• Do NOT smoke. Smoking impairs disc nutrition and accelerates disc degeneration.
• Keep the back muscles strong. Most critical for back pain treatment and prevention is an exercise concept called CORE STABILIZATION. Spine care experts, like chiropractors, can custom design a core stabilization program for optimal spine care.
• Maintain good posture. Poor posture increases disc pressure and degeneration. Individual static adverse postural distortions can be improved or corrected with chiropractic spinal care, corrective exercises, and spinal molding.

 

REFERENCES

1. www.ninds.nih.gov; Low Back Pain Fact Sheet; accessed May 12, 2014.
2. Vassilaki M, Hurwitz EL; Insights in Public Health: Perspectives on Pain in the Low Back and Neck: Global Burden, Epidemiology, and Management; Hawaii J Med Public Health. Apr 2014; 73(4): 122–126.
3. Nachemson AL, Spine, Volume 1, Number 1, March 1976, pp. 59-71.
4. Kapandji IA; The Physiology of the Joints; Volume Three, The Trunk and the Vertebral Column; Churchill Livingstone; 1974.
5. Jayson M, Editor; The Lumbar Spine and Back Pain, Third Edition, Churchill Livingstone, 1987, p. 60.
6. Bogduk N, Tynan W, Wilson AS; The nerve supply to the human lumbar intervertebral discs, Journal of Anatomy; 1981; Vol. 132; No. 1, pp. 39-56.
7. Bogduk N., The innervation of the lumbar spine; Spine; April 1983;8(3): pp. 286-93.
8. Mooney, V, Where Is the Pain Coming From? Spine, 12(8), 1987, pp. 754-759.
9. Kuslich S, Ulstrom C, Michael C; The Tissue Origin of Low Back Pain and Sciatica: A Report of Pain Response to Tissue Stimulation During Operations on the Lumbar Spine Using Local Anesthesia; Orthopedic Clinics of North America, Vol. 22, No. 2, April 1991, pp. 181-7
10. Freemont AJ, Peacock TE, Goupille P, Hoyland JA, O’Brien J, Jayson MI; Nerve ingrowth into diseased intervertebral disc in chronic back pain; Lancet; Jul 19, 1997;350(9072):178-81.
11. Coppes MH, Marani E, Thomeer RT, Groen GJ; Innervation of “painful” lumbar discs; Spine (Phila Pa 1976). 1997 Oct 15;22(20):2342-9.

A clinical practice guideline is a document designed to guide decisions and criteria regarding diagnosis, management, and treatment in specific areas of healthcare. Contemporary clinical practice guidelines are based on an examination of current evidence (evidence-based). The goal of clinical practice guidelines is to optimize patient benefit, reduce risks, provide a rational basis for patient referral, and to be cost effective. Healthcare providers are obliged to know the guidelines of their profession. Importantly, clinical practice guideline may not be applicable to the circumstances of an individual patient.

The Institute of Medicine defines clinical practice guidelines as (1):

“Systemically developed statements to assist practitioners’ and patient decisions about appropriate health care for specific clinical circumstances.”

Clinical practice guidelines have great potential for good, but also for abuse. Consequently, our government keeps an eye on clinical practice guidelines through the United States Department of Health & Human Services (2) and its Agency for Healthcare Research and Quality (3), where they have created the National Guideline Clearinghouse (4). The National Guideline Clearinghouse is a “public resource for evidence-based clinical practice guidelines.” It keeps a catalog of high-quality guidelines published by various organizations.

The most recent (March 2014, (5)) clinical practice guidelines pertaining to Whiplash Associated Disorders were edited by Charles G. Davis, DC. It is titled Management of Whiplash Associated Disorders. These Guidelines have been accepted for inclusion in the National Guideline Clearinghouse (NGC-7408).

Dr. Davis is a whiplash injury/chronic pain expert with impressive credentials, including clinician, team doctor, teacher, published researcher, and political leader. He teaches a course pertaining to the biomechanics of low-speed rear-end automobile collisions through the University of California, Riverside. He has four articles in the US National Library of Medicine pertaining to whiplash biomechanics and chronic pain neurophysiology (6, 7, 8, 9).

The Management of Whiplash Associated Disorders 2014 Guidelines is 217 pages in length, consists of approximately 1,200 references, and covers the following topics:

RANGE OF SYMPTOMS

STRUCTURES INJURED

EVALUATION

RED FLAGS

CRITERIA FOR DISCHARGE

GRADES OF SEVERITY OF INJURY

TREATMENT INTERVENTIONS AND PRINCIPLES OF TREATMENT

TREATMENT FREQUENCY AND DURATION

CHRONIC TREATMENT

OUTCOME MEASURES

ICD-10 CODES

RANGE OF SYMPTOMS

• Neck Pain
• Shoulder Pain
• Arm Pain/Paresthesias
• Interscapular Pain
• Back Pain
• Headache
• Dizziness / Vertigo
• Visual Disturbances
• Temporomandibular Joint (TMJ) Symptoms
• Cognitive / Psychological Symptoms
• Carpal Tunnel Syndrome
• Sleep Disturbance

It is common for symptoms to be delayed for 24-72 hours. Disc injuries can be delayed for weeks to months.

Children are commonly injured (and killed) from motor vehicle collisions.

Whiplash injuries accelerate degenerative spinal disease (spondylosis).

STRUCTURES INJURED

• Vehicle damage is not a reliable indicator of patient or passenger injury. Rather, post-traumatic symptoms, sings, and psychological issues are primarily as a consequence of an individual’s unique susceptibility, an unpredictable variable.
• Rear-end collision injury occurs very quickly following the impact, in less than a tenth of a second when the neck forms a nonphysiological “S” configuration, with flexion of the upper cervical spine and hyper-extension occurring in the lower cervical spine.
• Although many different tissues can be injured during the collision, the most probable injuries are to the facet joint capsules and the annulus of the intervertebral disc.
• Whiplash mechanisms also often result in injuries to the alar ligaments of the upper cervical spine.
• Whiplash mechanisms are a leading cause of injury to the vertebral arteries.
• A number of factors have been identified as increasing the risk of injuries:
  • Being caught by surprise at the moment of impact.
  • Having a slender neck.
  • Head being rotated at the moment of impact.
  • Straight and/or kyphotic cervical curvatures prior to collision.

EVALUATION

In the April 15, 1995 issue of the journal Spine (supplemental), the “Scientific Monograph of the Quebec Task Force on Whiplash-associated Disorders: Redefining ‘whiplash’ and its Management” was published (10). This multidisciplinary Task Force included a chiropractor, Dr. JD Cassidy. The Quebec Task Force on Whiplash-associated Disorders remains the gold standard in whiplash literature, yet it is now somewhat dated. Published in 1995, the document stopped collecting literature in September of 1993. Even so, aspects of the document are as valid today as they were some 20 years ago, and the classification scheme they proposed has become the global standard.

These (Dr. Davis’s) 2014 Guidelines emphasized that the whiplash-injured patient should be assigned a Quebec Task Force grade:

1. No neck pain or stiffness or any physical signs are noticed.
2. Neck pain, stiffness or tenderness, but no physical signs are noted by the examining health care provider.
3. Neck complaints and the examining health care provider finds decreased range of motion and point tenderness in the neck.
4. Neck complaints plus neurological signs such as decreased deep tendon reflexes, weakness and sensory deficits.
5. Neck complaints and fracture or dislocation, or injury to the spinal cord. These patients require a referral to an emergency medical specialists.

A very important and rarely understood aspect of the Quebec Task Force on Whiplash-associated Disorders is that in any category, including Grade 0 (no neck pain or stiffness or any physical signs noticed), the patient can still have any of these symptoms:

Deafness
Dizziness
Tinnitus (ringing in the ears)
Headache
Memory loss
Dysphagia (difficulty swallowing)
Temporomandibular joint pain

Patients should be assessed and reassessed at these intervals:

• Initial Assessment
• Seven-Day Reassessment
• Three-Week Reassessment
• Six-Week Reassessment
• Three-Month Reassessment

It is suggested that at these Assessments/Reassessments that the following measurement outcomes should be used:

• Visual Analogue Scale (VAS) or Numeric Pain Score (NPS)
• Neck Disability Index (NDI)
• Short Form-36 (SF-36)

Patient History Documentation should include:

• Symptoms caused by the accident
  • Symptoms quality and character
  • Symptom duration, intensity, frequency, location and radiation
  • Symptom aggravating and/or relieving factors.
• Relevant family history
• Past health history (general health, prior illness, injuries, hospitalizations, medications, surgical history)
• Mechanism of the injury
• Prior interventions, treatments, medications

The Treatment Plan should be documented:

• Recommended duration and frequency of treatment
• Specific treatment goals

Subsequent Visit Documentation should include:

• Review of chief complaint
• Assessment of change in patient condition since prior visit
• An Examination of the area of complaint and to be treated
• Evaluation of treatment effectiveness
• Documentation of treatment given on day of visit

The Physical Examination should include:

• Postural assessment
• Palpation for tenderness and altered tissue consistencies
• Measured ranges of motion
• Dermatomal superficial sensation
• Myotomal strength
• Subluxation assessment (segmental asymmetries in alignment and/or motion)
• Thoracic Outlet Syndrome tests should be performed in patients with arm complaints and/or findings.

The Guidelines refer to another guideline (www.pccrp.org) for radiological assessment. In short, all cervical spine traumatized patients, including whiplash-injured patients, should be evaluated with x-rays. These x-rays include:

• Lateral Cervical Neutral
• Lateral Cervical Flexion (stress view)
• Lateral Cervical Extension (stress view)
• AP Open Mouth
• AP Cervical with Cephalic Tilt
• Left and Right Oblique Views

Other radiographs may be required depending on the uniqueness of a particular case. If range of motion is measurably impaired during the acute phase of injury, the lateral cervical flexion-extension views should be delayed until a more complete range of motion is restored.

The Guidelines also covers protocols for MRI, Weight-Bearing MRI, Kinetic MRI, Video Fluoroscopy (VF), CT, SPECT, Discography, Facet Blocks, Surface EMG, Pressure Pain Threshold, Quantitative Sensory Testing, Cerebellar Tonsillar Ectopia (Chiari), Myofascial Pain Syndrome, Thyroid involvement, Mild Traumatic Brain Injury, and Post-Concussive Syndrome.

The Guidelines note that any patient not improving at the Three-Month Reassessment is likely to require a multidisciplinary approach.

RED FLAGS

Red Flags are defined as indicators of serious pathology. Red Flags require immediate investigation by appropriately trained healthcare personnel.

Standard Red Flag cautions apply:

• Infection (fever, etc.)
• Cancer risk (history, unexplained weight loss, pain at rest, etc.)
• Aortic Aneurysm (unexplained persistent back pain, etc.)
• Non-mechanical pain that is unremitting and severe

Specific Whiplash Injury Red Flags would include:

• Bilateral paresthesias in upper and/or lower extremities
• Gait Disturbances
• Spastic Paresis
• Positive Lhermittes sign (shooting pain or paresthesias into the limbs with cervical flexion)
• Deep tendon reflex hyper-reflexia
• Nerve root signs at more than two adjacent spinal levels
• Progressive worsening of neurological signs (motor weakness, sensory loss, areflexia)
• Indictors of long-tract myelopathy (dysfunction in bowels, bladder, sexual function and/or sensation, saddle anesthesias, positive Babinski, etc.)

CRITERIA FOR DISCHARGE

The patient should be discharged from additional regularly scheduled treatment once they have achieved maximum clinical improvement. “Maximum Improvement is achieved when there is no improvement in clinical status for a period of 2 months as assessed with standard measurement outcomes (visual analogue scale, Oswestry Low Back Disability Index, Neck Disability Index, SF-36, etc.).”

“If treatment is withdrawn and the patient’s clinical status becomes worse, the patient has not achieved Maximum Medical Improvement.”

GRADES OF SEVERITY OF INJURY

Grades of injury severity are important because guidelines for the duration and frequency of treatment are based in part on the grade of injury severity. Four Injury Severity classifications are referenced, and there is overlap between them. These include those for the Quebec Task Force as noted above, and three others:

Norris and Watt, 1983 (11):

Group 1:

Patients complaining of symptoms related to their injuries but with no abnormality on physical examination.

Group 2:

Patients who in addition to symptoms had a reduced range of movement of the cervical spine but no abnormal neurological signs.

Group 3:

Patients with symptoms, a reduced range of cervical movement and evidence of objective neurological loss.

Croft, 1993 (12):

Grade I:

Minimal: no limitation of motion; no ligamentous injury or neurological findings

Grade II:

Slight: limitation of motion; no ligamentous injury or neurological findings

Grade III:

Moderate: limitation of motion; some ligamentous injury; neurological findings may be present

Grade IV:

Moderate to severe: limitation of motion;
ligamentous instability; neurological findings present; fracture or disc derangement

Grade V:

Severe: requires surgical management/stabilization

Quebec, 1995 (10):

Grade O:

No complaints about the neck, no physical signs

Grade I:

Neck complaints of pain, stiffness, or tenderness only; No physical signs

Grade II

Neck complaint AND Musculoskeletal signs (decreased range of motion and point tenderness)

Grade III:

Neck complaint AND neurological signs (decreased or absent deep tendon reflexes,
weakness, and sensory deficits)

Grade IV:

Neck complaint AND fracture or dislocation

Again, symptoms and disorders that can be manifest in all Quebec grades include deafness, dizziness, tinnitus (ringing in the ears), headache, memory loss, dysphagia (difficulty swallowing), and temporomandibular joint pain.

Sterling, 2004 (13):

WAD I:

Neck complaint of pain, stiffness or tenderness only
No physical signs

WAD II A

Neck pain
Motor Impairment
Decreased ROM
Altered muscle recruitment patterns
Sensory Impairment
Local cervical mechanical hyperalgesia

WAD II B:

Same as WAD II A, plus:
Psychological impairment
Elevated psychological distress

WAD II C:

Same as WAD II A, plus WAD II B, plus:
Increased JPE (joint position error)
Generalized sensory hypersensitivity
May show Sympathetic Nervous System disturbances
Elevated levels of acute posttraumatic stress

WAD III:

Same as WAD II A, plus WAD II B, plus WAD II C, plus:
Neurological signs of conduction loss including:Decreased or absent deep tendon reflexes
Muscle weakness
Sensory deficits

Dr. Davis proposes a useful amalgamation of these injury severity grades, as follows:

Grades of Severity of Injury
Dr. Davis Guidelines Amalgamation

Grade I Minimal:

No limitation of motion; No ligamentous injury;
No neurological findings

Grade II Slight:

Limitation of motion; No ligamentous injury;
No neurological findings;
Neck complaint and musculoskeletal signs

Grade III Moderate:

Limitation of motion; Some ligamentous injury; Neurological symptoms
Common symptoms: Neck and arm pain;
Cervical herniated disc; Neck pain with headache; Cervicoscapulalgia (pain referred to upper back)

Grade IV Moderate to Severe:

Limitation of motion; Some ligamentous instability; neurological symptoms; fracture or disc derangement

Grade V Severe:

Requires surgical management/stabilization

TREATMENT INTERVENTIONS AND PRINCIPLES OF TREATMENT

In general, treatment principles should include maintaining normal life activities, staying active during the recovery process, and focus on improvements in function. The Guidelines also review the published scientific justification for manual treatment (mobilization, manipulation, adjustment) exercise, modalities (TENS, traction, ultrasound, low-level laser therapy, massage, acupuncture, pulsed electromagnetic fields (PMET), nutrition (including omega-3 essential fatty acid and vitamin D supplementation), kinesio-taping, and education (including postural advice).

Dr. Davis reviews the four stages of injury healing:

Stage I

Inflammatory phase (acute): Up to 72 hours

Stage II

Repair phase (subacute): 72 hours to 14 weeks

Stage III

Remodeling phase: 14 weeks to 12 months or more

Stage IV

Permanent (chronic phase) learn to live with residuals

Dr. Davis also reviews the practical management of the biology of ligament healing and scar formation, the biology of chronic pain as related to the endogenous pain inhibitory pathways, and the basis for spinal manipulative (adjustment) therapy.

These principles are important for clinical management as well as for the justification for why certain treatment approaches are reasonable and necessary. Such information is invaluable for report writing (required in most cases) as well as for depositions and/or trial testimony (rare requirements for the treating healthcare provider in these cases).

TREATMENT FREQUENCY AND DURATION

The general guidelines for the duration and frequency of treatment is based on the amalgamated grades of severity (page 9 above). Using this classification, duration and frequency guidelines would be:

	Daily	3X/wk	2X/wk	1X/wk	1X/mo	Treatment Duration	Treatment Total Number
Grade I	1 wk	1-2 wk	2-3 wk	<4 wk		<11 wks	<21
Grade II	1 wk	<4 wk	<4 wk	<4 wk	<4 mo	<29 wks	<33
Grade III	1-2 wk	<10 wk	<10 wk	<10 wk	<6 mo	<56 wks	<76
Grade IV	2-3 wk	<16 wk	<12 wk	<20 wk	permanent prn	permanent prn	permanent prn

prn = per required need

Additionally, a number of factors are referenced that may prolong either duration, frequency, of both:

• Pre-existing conditions, including disc/facet degeneration/spondylosis
• Biomechanical stress
• Psychological stress
• Re-injury exacerbation
• Spondylolisthesis
• Advanced age
• Metabolic disorders
• Congenital anomalies of the spine
• Developmental anomalies of the spine
• Disc protrusion (HNP)
• Rheumatoid arthritis; Ankylosing spondylitis
• Scoliosis
• Prior spinal surgery
• Prior vertebral fracture
• Osteoporosis
• Paget’s disease or other disease of bone
• Spinal stenosis or foraminal stenosis
• Prior spinal injury

CHRONIC TREATMENT

The Guidelines defines chronic whiplash treatment as treatment required after a period of 12 weeks. For these patients, Dr. Davis organizes his thoughts and supportive literature references into these categories:

• The rationale for why continuing spinal manipulations may be beneficial for some patients to maintain improvements in pain and disability levels.
• Cautions and problems with opioid pharmacology use for chronic pain. These include addictions to increased risk of death.
• Cautions and problems associated with nonsteroidal antiinflammatory drugs for patients with chronic pain. These include gastrointestinal bleeding, kidney injury, and increased cardiovascular event risk factors.

Dr. Davis cites 11 references to quantify the number of patients injured in whiplash mechanisms who develop chronic pain syndromes. The cited studies span 40 years of literature. The chronic pain range spans a low of 24% to a high of 90%. The follow-up time range for these studies was between 1-17 years duration.

Dr. Davis lists a number of factors that have been linked to a poor recovery prognosis for whiplash-injured patients:

• High initial pain intensity (> 7/10 on the VAS or NPS)
  (> 20/50 on the NDI)
• Radiological cervical kyphosis
• Stress x-ray segmental hypomobility
• Stress x-ray segmental hypermobility
• Being struck from the rear
• Being caught by surprise on impact
• Having one’s head rotated at the moment of impact
• A previous history of neck pain
• A previous history of headache
• Pre-accident degenerative joint disease
• Older age (sadly, > than 50 years of age)
• High number of initial complaints (especially between 4-9)

Dr. Davis cites studies that suggest post-traumatic psychological symptoms are usually caused by chronic somatic pain. Likewise he cites studies that indicate chronic post-traumatic pain syndromes are not caused by an abnormal psychological profile.

Dr. Davis again stresses, “vehicle damage has not been related to whiplash disorders.”

It is a sad reality that it is inevitable that some patients injured in whiplash mechanisms will develop chronic pain syndrome despite the best efforts of everyone involved. Post-whiplash chronic pain syndromes occur irrespective of a myriad of factors, including mechanistic factors, types of treatment, age, pre-accident degenerative disease, status of litigation, etc. In such individuals, ongoing treatment, including occasional spinal adjusting, serves only to afford the patient a degree of temporary relief of symptoms, often with no long-lasting improvements.

OUTCOME MEASURES

The determination of clinical improvement, maximum improvement, subjective and objective residuals, work status, and ultimate disability status requires the use of measurement outcomes. Some of these have been explored above. The Guidelines for whiplash-injured subjects include the following. The Guidelines provide samples, relevance, scoring protocols, interpretation, and importance for these:

• Visual Analogue Scale (VAS)
• The Numeric Pain Scale (NPS)
• Neck Disability index (NDI)
• Core Whiplash Outcome Measure
• Oswestery Disability Index (ODI), for low back
• Northwick Park Neck Pain Questionnaire
• Pain Disability Questionnaire (PDQ)
• The Short Form 36 Health Questionnaire (SF-36)
• Bournemouth Questionnaire
• Impact of Event Scale (for anxiety and depression)
• Epworth Sleepiness Scale (for sleep problems)
• Rivermead Post-Concussion Symptom Questionnaire (RPQ)

(for mild traumatic brain injury / concussion)

ICD-10 CODES

The ICD-10 is the 10^th revision of the International Statistical Classification of Diseases and Related Health Problems (ICD), a medical classification list by the World Health Organization (WHO). It codes for diseases, signs and symptoms, abnormal findings, complaints, social circumstances, and external causes of injury or diseases. The US ICD-10 CM has around 68,000 codes. Originally their starting set date was October 2014, this target has been recently delayed. However their implementation is inevitable. The Guidelines do a excellent presentation as to which codes should be used and how to use them appropriately. This includes a connect-the-dot stream of diagnosis-symptoms-impairments-treatments.

This section is invaluable to anyone who is dealing with the logistics of managing the whiplash-injured patient.

•••••••••••••••

These Management of Whiplash Associated Disorders Guidelines 2014 can be obtained from:

International Chiropractors Association of California
9700 Business Park Drive
Suite #305
Sacramento, CA 95827
(800) 275-3515

The cost is $80.00 + $7.00 for shipping and handling: TOTAL $87.00.

REFERENCES:

• Field MJ, Lohr KN; Clinical Practice Guidelines: Directions for a new program; Institute of Medicine; Washington DE; National Academy Press; 1990.
• hhs.gov
• ahrq.gov/
• guideline.gov/
• Davis CG, et al (ten additional participants); Management of Whiplash Associated Disorders; Second Edition; ICAC; 2014.
• Davis CG; Rear-end impacts: vehicle and occupant response;
• J Manipulative Physiol Ther. 1998 Nov-Dec;21(9):629-39.
• Davis CG; Injury threshold: whiplash-associated disorders; J Manipulative Physiol Ther. 2000 Jul-Aug;23(6):420-7.
• Davis C; Chronic pain/dysfunction in whiplash-associated disorders; J Manipulative Physiol Ther. 2001 Jan;24(1):44-51.
• Davis CG; Mechanisms of chronic pain from whiplash injury; J Forensic Leg Med; 2013 Feb;20(2):74-85.
• Spitzer WO, Skovron ML, Salmi LR, Cassidy JD, Duranceau J, Suissa S, Zeiss E; Scientific monograph of the Quebec Task Force on Whiplash-Associated Disorders: redefining “whiplash” and its management; Spine; 1995 Apr 15;20(8 Suppl):1S-73S.
• Norris SH, Watt I; The prognosis of neck injuries resulting from rear-end vehicle cllisions; J Bone Joint Surg Br. 1983 Nov;65(5):608-11.
• Croft A; Treatment paradigm for cervical acceleration/deceleration injuries (whiplash); ACA Journal of Chiropractic; Vol. 30; No. 1; 1993; pp. 41-45.
• Sterling M; A proposed new classification system for whiplash associated disorders: implications for assessment and management; Manual Therapy; 2004 May;9(2):60-70.

This month we take a close look at manipulation of the joints of the lumbar spine and the relationship to Lumbar disc protrusion.  Often lumbar manipulation involves some degree of rotation. Lumbar spine manipulations that are primarily rotational in nature are often discouraged as it is assumed that such maneuvers are associated with an increased risk of injury to the annulus of the intervertebral disc. The traditional caution pertaining to such manipulations is based upon an understanding of the anatomy of the annulus. The collagen fibers that comprise the annulus of the disc are arranged in layers, and each layer is crossed in opposite directions. During disc rotational movements, half of the annular collagen fibers become tense, and the other half become lax. Consequently, it is argued that rotational stress applied to the annulus of the disc is resisted by only half of the annular collagen fibers, the half that become tense. In essence, it is argued that the disc is operating at only half strength during rotationally applied stress, increasing its vulnerability to injury.

Crossed Annular Fibers of the Intervertebral Disc

Despite these academic arguments, there is contrary evidence pertaining to the dangers of rotational manipulations of the lumbar spine. In fact, there is evidence that rotational manipulations are safe when applied by an appropriately trained provider. Additionally, there is evidence that lumbar spine rotational manipulations are effective in the treatment of low back pain, including the management of disc herniation.

 

In 1954, RH Ramsey, MD published a study titled:

 

Conservative Treatment of Intervertebral Disk Lesions

 

Dr. Ramsey’s study appeared in the Instructional Course Lectures of the American Academy of Orthopedic Surgeons. Dr. Ramsey states:

 

“The conservative management of lumbar disk lesions should be given careful consideration because no patient should be considered for surgical treatment without first having failed to respond to an adequate program of conservative treatment.”

 

“If after a fair trial of conservative treatment, the pain and disability continue and the symptoms are of sufficient gravity to warrant surgery, the patient is advised that he should be operated upon and the offending disk lesion should be removed.”

 

Dr. Ramsey advocated the following sequence of conservative treatment before considering a surgical option for patients with low back pain:

 

1)         Varying degrees of rest:

Rest is most beneficial in acute cases and less beneficial in chronic cases.

 

It is important to curtail non-occupational activities such as athletics or more strenuous      home hobbies. “Prolonged sitting, standing or walking should usually be stopped.”

 

2)         Manipulation.

 

3)         Local heat.

 

4)         A firm bed:

“Most patients with low back pain on a mechanical basis rest much better on a bed         which does not sag in the middle.”

 

5)         A low back support:

“The patient is advised to wear the support during the day and also in the evening at       anytime he or she is going to be up and more active.”

 

6)         Instruction in the avoidance of strain:

“The patient should be advised to avoid all activities that aggravate his pain. He is            especially warned about heavy lifting.”

 

Under some circumstances, it may be necessary for the patient to change his occupation.

 

“All strenuous athletic pursuits should be stopped temporarily.”

 

7)         Postural exercises:

These should be both strengthening and stretching exercises.

 

8)         Medication:

“Fairly large doses of the vitamin B Complex have proved beneficial to many patients.”

 

9)         Weight control:

“Obesity definitely predisposes the patient to painful back conditions and such patients    should be encouraged to reduce to a normal weight.”

 

10)       Improvement in general health.

 

Pertaining to manipulation, Dr. Ramsey makes the following comments:

 

“From what is known about the pathology of lumbar disk lesions, it would seem that the ideal form of conservative treatment would theoretically be a manipulative closed reduction of the displaced disk material.”

 

“Many forms of manipulation are carried out by orthopaedic surgeons and by cultists and this form of treatment will probably always be a controversial one.”

 

“We limit the use of manipulation almost entirely to those patients who do not seem to be responding well to non-manipulative conservative treatment and who are anxious to have something else done short of operative intervention.”

 

“The method we use is relatively simple and can be done with or without anesthesia. It is more likely to be effective with anesthesia because the muscle relaxation permits greater motion by manipulation.”

 

“The patient lies on his side on the edge of the table facing the surgeon and the leg that is up is allowed to drop over the side of the table, tending to swing the up-side of the pelvis forward. The arm that is up is allowed to drop back behind the patient, tending to pull the shoulder back. The surgeon then places one hand on the patient’s shoulder and his opposite forearm on the patient’s iliac crest. Simultaneously, the shoulder is thrust suddenly back, rotating the torso in one direction while the iliac crest is thrust down and forward, rotating the pelvis in the opposite direction. This gives the lumbar spine a twist that frequently causes an audible and palpable crunch. This procedure is then repeated with the patient on his other side. The patient is then turned on his back and his hips and knees are hyperflexed sufficiently to forcibly flex the lumbar spine which tends to open up the disk spaces posteriorly.”

 

“The patient should be cautioned beforehand that forceful manipulation may possibly make his symptoms worse although many patients will get marked relief.”

 

Dr. Ramsey clearly defines the procedure as a lumbar spine manipulation. It is also clear the manipulation is rotational in nature, describing it using the term “twist.” Additionally he notes that the manipulation is “forceful” and associated with an “audible and palpable crunch.” Although he cautions that the manipulation may make the patient worse, “many patients will get marked relief.”

 

Fifteen years later (in 1969), physicians JA Mathews and DAH Yates from the Department of Physical Medicine, St. Thomas’ Hospital, London, published a study titled:

 

Reduction of Lumbar Disc Prolapse by Manipulation

 

This study by Drs. Mathews and Yates appeared in the September 20, 1969 issue of the British Medical Journal. These authors evaluated a number of patients that presented with an acute onset of low back and buttock pain who did not respond to rest. Diagnostic epidurography showed a clinically relevant small disc protrusion, along with antalgia and positive lumbar spine nerve stretch tests. These patients were then treated with long-lever rotation manipulations of the lumbar spine, using the shoulder and iliac crest as levers. These lumbar spine manipulations were clearly accompanied with a thrust maneuver. The manipulations were repeated until abnormal symptoms and signs had disappeared. Following the manipulations there was resolution of signs, symptoms, antalgia, and reduction in the size of the protrusions.

 

The following drawing and description of the rotation manipulation was included in their study:

REDUCTION OF LUMBAR DISC PROLAPSE BY MANIPULATION

 

The caption below this drawing said:

“A firm additional thrust completed the rotation manipulation.”

 

Important comments from Drs. Mathews and Yates from this study include:

 

“Manipulation of the lumbar spine has been used as an empirical treatment of low backache since antiquity. The persistence and popularity of this type of treatment was based on the clinical impression that it is beneficial.”

 

“The frequent accompaniment of acute onset low back pain by spinal deformity suggests a mechanical factor, and the accompanying abnormality of straight-leg raise or femoral stretch test suggests that the lesion impinges on the spinal dura matter of the dural nerve sheaths.”

 

“The lumbar spine was rotated away from the painful side to the limit of its range, the buttock or thigh of the painful side being used as a lever; a firm additional thrust was made in the same direction. This manoeuver was repeated until abnormal symptoms and signs had disappeared, progress being assessed by repeated examination.”

 

“Rotation manipulations apply torsion stress throughout the lumbar spine. If the posterior longitudinal ligament and the annulus fibrosus are intact, some of this torsion force would tend to exert a centripetal force, reducing prolapsed or bulging disc material.” 

 

“The results of this study suggest that small disc protrusions were present in patients presenting with lumbago and that the protrusions were diminished in size when their symptoms had been relieved by manipulations.”

 

These authors concluded “it seems likely that the reduction effect [of the disc protrusion] is due to the manipulating thrust used.”

 

Once again, this article by Mathews and Yates clearly describe and draw the manipulations used, including the words “forceful,” “thrust,” and “rotation.” An interesting explanation for the successful treatment as well as the reduction in the size of the protrusion is uniquely linked to the rotational component of the manipulation: rotation tightens up intact aspects of the annular ring, pulling the nuclear protrusion towards the center and away from the nervous system.

 

In another study published in 1969, BC Edwards compared the effectiveness of heat/massage/exercise to spinal manipulation in the treatment of 184 patients that were grouped according to the presentation of back and leg pain, as follows:

 

 

This study by Edwards was published in the Australian Journal of Physiotherapy. The authors of the text that is perhaps the most authoritative text on spinal clinical biomechanics, White and Panjabi’s Clinical Biomechanics of the Spine, subsequently reviewed it in 1990. The authors are:

 

Augustus A. White, MD, DMed Sci

Professor of Orthopedic Surgery at Harvard Medical School

Orthopedic Surgeon-in-Chief at Beth Israel Hospital in Boston

 

Manohar M. Panjabi, PhD

Professor of Orthopedics and Rehabilitation and Mechanical Engineering

Director of Biomechanics Research

Yale University School of Medicine

 

Drs. White and Panjabi make the following points pertaining to the Edwards article:

 

“A well-designed, well executed, and well-analyzed study.”

 

In the group with central low back pain only, “the results were acceptable in 83% for both treatments. However, they were achieved with spinal manipulation using about one-half the number of treatments that were needed for heat, massage, and exercise.”

 

In the group with pain radiating into the buttock, “the results were slightly better with manipulation, and again they were achieved with about half as many treatments.”

 

In the groups with pain radiation to the knee and/or to the foot, “the manipulation therapy was statistically significantly better,” and in the group with pain radiating to the foot, “the manipulative therapy is significantly better.”

 

“This study certainly supports the efficacy of spinal manipulative therapy in comparison with heat, massage, and exercise. The results (80 – 95% satisfactory) are impressive in comparison with any form of therapy.”

 

It is usual for pain that travels further down an extremity to be associated with greater compression, or a larger disc protrusion. In this study by Edwards, manipulation worked excellently in patients with leg pain radiation, especially when compared to heat/massage/exercise. An explanation for this finding, as expressed by Mathews and Yates above, is that in such cases manipulation is superior because of its ability to move the protrusion away from the nervous system and closer to the midline.

 

In 1977, the third edition of Orthopaedics, Principles and Their Applications was published. The author, Samuel Turek, MD (d. 1986), was a Clinical Professor, Department of Orthopedics and Rehabilitation at the University of Miami School of Medicine. His text encompasses 1,574 pages. In the section pertaining to the protruded disc, Dr. Turek makes the following observations:

 

Treatment of Intervertebral Disc Herniation With Manipulation

“Manipulation.  Some orthopaedic surgeons practice manipulation in an effort at repositioning the disc.  This treatment is regarded as controversial and a form of quackery by many men.  However, the author has attempted the maneuver in patients who did not respond to bed rest and were regarded as candidates for surgery.  Occasionally, the results were dramatic.

 

Technique. The patient lies on his side on the edge of the table facing the surgeon, and the uppermost leg is allowed to drop forward over the edge of the table, carrying forward that side of the pelvis.  The uppermost arm is placed backward behind the patient, pulling the shoulder back.  The surgeon places one hand on the shoulder and the other on the iliac crest and twists the torso by pushing the shoulder backward and the iliac crest forward.  The maneuver is sudden and forceful and frequently is associated with an audible and palpable crunching sound in the lower back.  When this is felt, the relief of pain is usually immediate.  The maneuver is repeated with the patient on the opposite side.”

 

“The patient should be cautioned beforehand that the manipulation may make his symptoms worse and that this is an attempt to avoid surgery.”

 

The manipulation maneuver described by Dr. Turek is the classic description of the rotational manipulation of the lumbar spine. Dr. Turek uses the word “twists” to describe the rotational maneuver. Dr. Turek’s description supports the writings and outcomes of Dr. Ramsey from 1954, and importantly, is in agreement with the other authors above. Dr. Turek’s comments are in the aspect of his book pertaining to the treatment of the protruded intervertebral disc.

 

In February 1987, physicians Paul Pang-Fu Kuo and Zhen-Chao Loh published an important study pertaining to lumbar disc protrusions and rotary spinal manipulation, titled:

 

Treatment of Lumbar Intervertebral Disc Protrusions

by Manipulation

 

Their article appeared in the prestigious journal Clinical Orthopedics and Related Research. Drs. Paul Pang-Fu Kuo and Zhen-Chao Loh are from the Department of Orthopedic Surgery, Shanghai Second Medical College, and Chief Surgeon, Department of Orthopaedic Surgery, Rui Jin Hospital, Shanghai, China. They note that manipulation has been used in Chinese healthcare for thousands of years, and by the Tang Dynasty (618-907 AD), “manipulation was fully established and became a routine for the treatment of low back pain.”

 

In their study, they performed a series of eight manipulations on 517 patients with protruded lumbar discs and clinically relevant signs and symptoms. Their outcomes were quite good, with 84% achieving a successful outcome and only 9% not responding. Only 14 % suffered a reoccurrence of symptoms at intervals ranging from two months to twelve years.

 

In the photographic depiction of the eight procedures used by these authors, one is clearly similar to a side posture rotary manipulation of the lumbar spine that is similar to the drawing by Mathews and Yates above. This is accompanied with the following description:

 

“The patient is placed on the sound side first with the hip and knee of the painful side flexed and the sound side straight. The operator rests one hand in front of the shoulder and the other hand on the buttock. By simultaneously pulling the shoulder backwards and pushing the buttock forwards, a snap or click can usually be heard or felt. This manipulation may then be repeated on the other side as required.”

 

Based upon their results, Drs. Kuo and Loh make these statements:

 

“Manipulation of the spine can be effective treatment for lumbar disc protrusions.”        

 

“Most protruded discs may be manipulated. When the diagnosis is in doubt, gentle force should be used at first as a trial in order to gain the confidence of the patient.”

 

Drs. Kuo and Loh stress that rotation “is the key maneuver of the manipulation.” Consistent with others (above), they suggest that the rotational stresses applied to the annulus of the disc actually reposition the protrusion away from the nervous system and back towards the center of the disc. Supporting statements include:

 

“Manipulation usually begins with preparatory movements of the vertebral joints to their extreme and then rotation is carried out.”

 

“During manipulation a snap may accompany rotation. Subjectively it has dramatic influence on both patient and operator and is thought to be a sign of relief.”

 

“If derangement of the facets or subluxation of the posterior elements near the protruded disc occurs, the rotation may have caused reduction, giving remarkable relief.”

 

“Gapping of the disc on bending and rotation may create a condition favorable for the possible reentry of the protruded disc into the intervertebral cavity, or the rotary manipulation may cause the protruded disc to shift away from pressing on the nerve root.”

 

In terms of applying manipulation, Drs. Kuo and Loh indicate “practice is necessary to become proficient in spinal manipulation techniques,” and  “expertise plays an important role in the success of manipulation.” The manipulation of disc protrusions should be performed only by trained experts. Additionally, manipulation is contraindicated if the patient is suffering from incontinence or paraplegia.

 

In 1993, chiropractor J. David Cassidy, chiropractor Haymo Thiel, and physician William Kirkaldy-Willis published a “Review Of The Literature” article titled:

 

Side Posture Manipulation For

Lumbar Intervertebral Disk Herniation

 

These authors are from the Department of Orthopaedics, Royal University Hospital, Saskatoon, Saskatchewan, Canada, and their article appeared in the Journal of Manipulative and Physiological Therapeutics.

 

In their article, these authors cite studies on human cadavers that show the annulus of the disc is quite resistant to rotational stresses. Specifically, a normal disc did not show failure until 22.6° of rotational stress, and a degenerated disc could withstand and average of 14.3° of rotational stress. They therefore conclude “torsional failure of the lumbar disk first requires fracture of the posterior joints” before there is any annular tearing.

 

When performing rotational manipulation in the management of lumbar disc herniation, these authors suggest that it is wise to begin with mobilization prior to performing manipulation to assess the patients responses. Additionally, they state that if positioning increases leg pain, “one should not proceed to manipulation at that particular session.”

 

Based upon their review of the literature and their own experiences, these authors state:

 

“The treatment of lumbar disk herniation by side posture manipulation is not new and has been advocated by both chiropractors and medical manipulators.”

“The treatment of lumbar intervertebral disk herniation by side posture manipulation is both safe and effective.”

Rotational Manipulation

After Cassidy, Thiel, and Kirkaldy-Willis

 

            The biomechanical studies that best support the safety of rotation stress to the intervertebral disc have been completed by Adams, Hutton, and Dolan. In 1981, MA Adams, PhD, and WC Hutton, MSc, published an important study in the journal SPINE, titled:

The Relevance of Torsion to the

Mechanical Derangement of the Lumbar Spine

In their cadaver experiments, these authors noted that the limit of spinal segmental rotation was not created by the disc, but rather by the facet joint. During rotational stress, the compression facet is the first structure to yield at the limit of torsion, and this occurs after about 1-2° of rotation. “Much greater angles are required to damage the intervertebral disc, so torsion seems unimportant in the etiology of disc degeneration and prolapse.” Important statements in this article include:

“Because of the protection offered by the compression facet, the intervertebral disc is subjected to relatively small stresses and strains in the physiologic range of torsion. By the time the facets are damaged, the disc is rotated only about one-third to one-tenth of its maximum angle and is bearing a small fraction of the torque required to rupture it.”

“Except in cases of extreme trauma and as a sequel to crushing of the apophyseal joints, axial rotation can play no major part in the mechanical derangement of the intervertebral disc in life.”

Two years later, in 1983, Adams and Hutton publish additional cadaver studies in journal Spine, titled:

The Mechanical Function of the Lumbar Apophyseal Joints

            Based upon their experiments, they conclude that the facet joints “prevent excessive movement from damaging the discs: the posterior annulus is protected in torsion by the facet surfaces and in flexion by the capsular ligaments.” They note that the facets only allow at most 2° of rotation, and also note that the disc will completely recover from all rotational stresses that are less then 3°. Specific statements include:

“In flexion, as in torsion, the apophyseal joints protect the intervertebral disc.”

“The function of the lumbar apophyseal joints is to allow limited movement between vertebrae and to protect the discs from shear forces, excessive flexion, and axial rotation.”

Lastly, in 1995, Adams and Dolan published a study in Clinical Biomechanics titled:

Recent Advances in Lumbar Spinal Mechanics

and their Clinical Significance

            Once again, these authors note that rotational loading of a spinal motor unit will always damage the facet joints “long before the disc.” If the facet joints are removed, rotational forces will damage the disc if subjected to rotational loads between 10-20°.

These authors also note “severely degenerated discs cannot be made to prolapse, presumably because the nucleus is too fibrous to exert a hydrostatic pressure on the annulus.”

CONCLUSIONS

            The information presented here indicates that for most patients suffering from a lumbar disc prolapse, rotational manipulation of the lumbar spine is statistically quite safe and often quite effective. Because there are some risks and because effective manipulation requires training and experience, such manipulation should only be performed by a trained expert.

References

Bogduk N; Clinical Anatomy of the Lumbar Spine; Fourth edition, Elsevier, 2005.

Ramsey RH; Conservative Treatment of Intervertebral Disk Lesions; American Academy of Orthopedic Surgeons, Instructional Course Lectures; Volume 11, 1954, pp.118-120.

Mathews JA and Yates DAH; Reduction of Lumbar Disc Prolapse by Manipulation; British Medical Journal September 20, 1969, No. 3, 696-697.

Edwards BC; Low back pain and pain resulting from lumbar spine conditions: a comparison of treatment results; Australian Journal of Physiotherapy; 15:104, 1969.

White AA, Panjabi MM; Clinical Biomechanics of the Spine; Second edition, JB Lippincott Company, 1990.

Turek S; Orthopaedics, Principles and Their Applications; JB Lippincott Company; 1977; page 1335.

Kuo PP and Loh ZC; Treatment of Lumbar Intervertebral Disc Protrusions by Manipulation; Clinical Orthopedics and Related Research. No. 215, February 1987, pp. 47-55.

Cassidy JD, Thiel HW, Kirkaldy-Willis WH; Side posture manipulation for lumbar intervertebral disk herniation; Journal of Manipulative and Physiological Therapeutics; February 1993;16(2):96-103.

Adams MA and Hutton WC, MSc; The Relevance of Torsion to the Mechanical Derangement of the Lumbar Spine; Spine; Volume 6, Number 3, May/June 1981, pp. 241-248

Adams MA and Hutton WC, MSc; The Mechanical Function of the Lumbar Apophyseal Joints; Spine; Volume 8, Number 3, April 1983, pp. 327-330.

Adams MA and Dolan P; Recent advances in lumbar spinal mechanics and their clinical significance; Clinical Biomechanics; Volume 10, Number 1, 1995, pp. 3-19.

 

 

 

THE INFLAMMATION MODEL

A light bulb uses electrical energy to generate light. But, the electrical energy is not created by the light bulb. The electrical energy is created in a location far away and brought to the light bulb using electrical wires.

Pain is an electrical signal in the brain. The pain electrical signal is brought to the brain by nerves. As a rule (there are exceptions), the brain does a good job at identifying the body region that initiates the electrical signal. The point is that the electrical signal in the brain for pain is created at another location and brought to the brain by nerves.

If one stubs one’s toe with sufficient force to achieve excitation threshold of the toe pain nerves (nociceptors), the brain will receive the appropriate electrical signal. The brain will identify toe tissue as the generator of the electrical signal that the brain interprets as being painful.

Studies looking at whiplash injuries consistently identify the facet joints as the primary source of chronic whiplash injury pain (1, 2, 3). The second most common tissue source of chronic whiplash injury pain is the annulus of the intervertebral disc. Injury to the facet joints (and/or the intervertebral disc) initiates a chemical inflammation which alters the threshold of the joint’s pain afferents (nociceptors). If nociceptive excitation threshold is achieved, a local electrical signal will be initiated and travel to the brain where the signal is interpreted as being painful.

Studies looking at chronic low back pain consistently identify the intervertebral disc as the primary source of the electrical signal that travels to the brain (4, 5). A number of studies have shown that when the human intervertebral disc degenerates, the nociceptive nerve fibers in the annulus can migrate into the nucleus pulposus, allowing the nucleus itself to be the tissue source of the nociceptive electrical signal (6, 7, 8).

The electrical signal from the injured tissue to the brain is not carried on a single neuron, but rather on a series of neurons. The electrical signal carried from one neuron to next neuron must cross a physical gap, a synaptic gap. The signal is carried across the synaptic gap by chemicals that are produced and released by the first neuron, carried across the synaptic gap to the second neuron where the electrical signal is re-established and continues towards the brain.

The synaptic gap, or synapse is very important because it is a site where the electrical signal to the brain has the potential to be modified (enhanced or reduced).

As a rule, the pain afferents in the facet and/or disc initiate the pain electrical signal as a consequence of being exposed to inflammatory chemicals. In fact, in 2007, Omoigui states (9):

“Irrespective of the type of pain whether it is acute or chronic pain, peripheral or central pain, nociceptive or neuropathic pain, the underlying origin is inflammation and the inflammatory response.”

“Activation of pain receptors, transmission and modulation of pain signals, neuro-plasticity and central sensitization are all one continuum of inflammation and the inflammatory response.”

“Irrespective of the characteristic of the pain, whether it is sharp, dull, aching, burning, stabbing, numbing or tingling, all pain arises from inflammation and the inflammatory response.”

Weiner’s Pain Management, A Practical Guide for Clinicians, by the American Academy of Pain Management, indicates that the primary reason for the pain producing inflammatory cascade is an overabundance of omega-6 fatty acids, acquired from excessive consumption of vegetable oils (10).

It is rational that the treatment of these patients should include anti-inflammatory strategies. Conservatively, proven helpful anti-inflammatory strategies include the local application of ice (11), supplemental omega-3 fatty acids (fish oil) (12, 13, 14), and low-level laser therapy (15).

THE MUSCLE MODEL

 

An important addition to this discussion is the contribution of muscles to pain. Any direct injury to a muscle can cause inflammation and therefore pain. Chronic musculoskeletal pain often has a significant muscle contribution. The muscle contribution is often referred to as Myofascial Pain Syndrome, championed by many, and pioneered by Janet Travell, MD and David Simons, MD (16, 17, 18 19).

A simple explanation of the muscle-pain model is presented by Rene Calliet, MD, and involves these sequential steps (20):

1) Inflammation results in nociceptive threshold, generating an action potential that brings (via the primary afferent) an electrical signal to the spinal cord.

2) In the spinal cord, the primary nociceptive afferent releases chemicals that cross the synaptic gap and excite the second order nociceptive afferent neuron to generate an action potential, moving the electrical signal towards the brain.

3) In the spinal cord, the primary nociceptive afferent also releases chemicals that cross the synaptic gap and generate an electrical action potential in the alpha motor neuron. This causes the alpha motor neuron to increase its production and release of the chemical acetylcholine into the nerve-muscle (myoneuro) junction, causing the muscle to contract (increasing the interdigitation of the contractile proteins). This is the classic afferent-efferent spinal cord reflex. Thus, chronic pain results in chronically contracted muscles. Chronically contracted muscles will cut off its own blood supply, resulting in both internal ischemia and an accumulation of metabolites (waste products). Muscle ischemia and accumulated waste products create an inflammatory response, altering the nociceptive threshold, generating a pain-producing electrical signal to the spinal cord. This is the classic self-perpetuation positive feedback loop, the so-called “pain-muscle-pain” cycle.

It is rational that the treatment of the muscle component of chronic pain syndromes (myofascial pain syndromes) would include ischemic compression (16, 17, 18), spray and stretch techniques (16, 17, 18), needle acupuncture (21) and low-level laser therapy (21).

 THE GATE THEORY

The Gate Theory of Pain was first proposed by Canadian psychologist Ronald Melzack, PhD, and British neuroscientist Patrick Wall, PhD (while working at the Massachusetts Institute of Technology) in 1962 in the journal Brain (22). It was not until their work was published in the journal Science in 1965 that it generated widespread attention (23). The Theory, as stated by American neuroscientist and 2000 Nobel Prize winner Eric Kandel (24), is:

“Pain is not simply a direct product of the activity of nociceptive afferent fibers but is regulated by activity in other myelinated afferents that are not directly concerned with the transmission of nociceptive information.”

 “The idea that pain results from the balance of activity in nociceptive and non-nociceptive afferents was formulated in the 1960s and was called the gate control theory.”

 “Simply put, non-nociceptive afferents ‘close’ and nociceptive afferents ‘open’ a gate to the central transmission of noxious input.”

Simply stated, the Gate Theory of Pain states that pain can be controlled (inhibited) by improving the function of other non-nociceptive nerves. Even though this Theory is half a century old, its principles “have survived the test of time.” (25)

The Gate Theory of Pain has been accepted as a viable explanation for the benefits of chiropractic spinal adjusting for patients with pain syndromes. As noted by Canadian orthopedic surgeon WH Kirkaldy-Willis, MD (26):

“Spinal manipulation is essentially an assisted passive motion applied to the spinal apophyseal and sacroiliac joints.”

 Melzack and Wall proposed the Gate Theory of Pain in 1965, and this theory has “withstood rigorous scientific scrutiny.”

“The central transmission of pain can be blocked by increased proprioceptive input.” Pain is facilitated by “lack of proprioceptive input.” This is why it is important for “early mobilization to control pain after musculoskeletal injury.”

The facet capsules are densely populated with mechanoreceptors. “Increased proprioceptive input in the form of spinal mobility tends to decrease the central transmission of pain from adjacent spinal structures by closing the gate. Any therapy which induces motion into articular structures will help inhibit pain transmission by this means.”

Stretching of facet joint capsules will fire capsular mechanoreceptors which will reflexly “inhibit facilitated motoneuron pools” which are responsible for the muscle spasms that commonly accompany low back pain.

Mechanoreceptors (proprioceptors) are specialized neurons that register the way we live, exist, and function in a gravity environment. These mechanoreceptors are abundant in facet joint capsules, annulus of the disc, paraspinal ligaments, and muscles (27, 28, 29, 30, 31, 32).

Mechanoreceptors are probably the most important source of the “non-nociceptive” afferents that control pain; improving their function closes the pain gate, reducing pain. The increased muscle tone and/or muscle spasm that commonly accompany spinal pain syndromes also reduce spinal motion, reducing articular mechanoreception, opening the pain gate.

The muscles become an important player in chronic spinal pain syndromes because of overlapping feedback loops:

1) Pain increases muscle tone.

2) Increased muscle tone causes inflammation and more pain (a feedback loop).

3) Increased muscle tone reduces articular range of motion.

4) Reduced articular range of motion reduces articular mechanoreception.

5) Reduced articular mechanoreception leaves the pain gate open.

6)  An “open” pain gate results in more pain and more muscle tone (again, a feedback loop).

These feedback loops were excellently reviewed by Yale’s Manohar Panjabi, PhD, in 2006 (33):

An important basis for Dr. Panjabi’s model was the animal studies by Aage Indhal, MD, and colleagues from Norway (34). They clearly showed the interrelationships between spinal pain and the contraction of the segmental muscles, reducing the movement parameters of that region of the spine. In later works, Dr. Indahl and colleagues were able to show that by firing the mechanoreceptors of the facet joint capsules they could inhibit both the spinal cord reflex to the segmental muscles and also inhibit pain (35). Thus, by improving mechanical afferentation, they could inhibit both the segmental muscle contraction and inhibit pain (“close” the pain gate).

Dr. Indahl’s experimental models and Dr. Panjabi’s theoretical models are well presented as being applicable to chiropractic spinal adjusting by Raymond Brodeur, chiropractor and engineer working at Michigan State University (36). Dr. Brodeur’s basic premise is that the cavitation associated with the audible adjusting of a spinal segment has sufficient speed to fire off high-threshold mechanoreceptors, inhibiting segmental muscle tone, and improving motion. This would close the pain gate. Dr. Brodeur also makes the point that chiropractic drop tables and Activator adjusting instruments are capable of achieving the same mechanical benefits.

The primary research by Canadian orthopedic surgeon WH Kirkaldy-Willis, MD was clearly able to show that chiropractic spinal adjusting, as monotherapy, was capable of inhibiting both muscle spasm and pain (37). Dr. Kirkaldy-Willis used 283 patients with chronic, severe, treatment resistant low back pain and documented that chiropractic spinal adjusting was able to resolve the clinical syndrome in 81% of the patients. Dr. Kirkaldy-Willis’ explanation for the observed improvement in clinical status was the firing of facet capsule mechanoreceptors, which inhibits the muscle spasm and closes the pain gate.

THE NEWEST MODEL

Catechol-Oxygen-Methyltransferase = Catechol-O-Methyltransferase

It has been known for more than a century that the sympathetic nervous system is involved in chronic pain syndromes. Dr. S. Weir Mitchell and colleagues produced important clinical descriptions of sympathetic pain on injured soldiers during the US Civil War (1861-1865). A search of the US National Library of Medicine using the PUBMED search engine (03/11/14), using the words “sympathetic pain” located 5,597 citations.

Many researchers have observed a psychosocial component to chronic pain syndromes, particularly in the realm of whiplash trauma recovery. A search of the US National Library of Medicine using the PUBMED search engine (03/11/14), using the words “whiplash pain AND psychosocial” located 54 citations.

The 2013 book Autonomic Failure: A Textbook of Clinical Disorders of the Autonomic Nervous System, shows an impressive picture (my rendition below) of the post-ganglionic sympathetic efferents production and release of the catecholamine norepinephrine to receptors located on the nociceptive afferent axons and dorsal root ganglions (DRG) (38). These catecholamines alter the threshold of the nociceptive afferents so that they more easily reach excitation threshold, more readily producing pain. [As a historical side note, the book’s second author, Sir Roger Bannister, age 84, is about to celebrate his 60^th anniversary of being the first human to run a mile in less than 4 minutes, May 6, 1954].

There is mounting evidence that increased sympathetic production and release of catecholamines is a primary driver for both increased chronic pain and for the psychosocial components of chronic pain syndromes, and this phenomenon has a genetic link. This could help explain why so many with chronic pan also have an abnormal psychological profile (39).

Humans have a gene that produces an enzyme that metabolizes sympathetically produced catecholamines. It is called:

Catechol-Oxygen-Methyltransferase = Catechol-O-Methyltransferase

It is abbreviated COMT. Low production of COMT has been linked to increased and chronic pain perception, including temporomandibular pain, fibromyalgia, and whiplash injury pain (40, 41, 42). Samuel A McLean, MD, and colleagues from the University of North Carolina School of Medicine, note (41):

“Genetic variations in the catechol-o-methyltransferase (COMT) gene have been associated with experimental pain and risk of chronic pain development, but no studies have examined genetic  predictors of neck pain intensity and other patient characteristics after motor vehicle collision (MVC).”

“These findings suggest that genetic variations affecting stress response system function influence the somatic and psychological response to MVC, and provide the first evidence of genetic risk for clinical symptoms after MVC.”

For decades, Princeton educated physiologist Irvin Korr, PhD, engaged in clinical research showing a link between joint mechanoreceptors (proprioceptors) and sympathetic nervous system production of catecholamines (43, 44). His work showed that improvement of mechanical function not only inhibited pain and muscle spasm (tone), but also inhibited sympathetic activity through a spinal cord reflex. Thus, Dr. Korr would argue that one would have to adjust the correct spinal level, the level of the reduced motion, in order to appropriately inhibit the local increased production of catecholamines.

SUMMARY

 The information presented here outlines the physiological explanation for the observation that chiropractic spinal adjusting helps people with chronic or acute pain syndromes. Chiropractic spinal adjusting uses bones as levers to influence the quality of tissue and therefore the integrity of the tissue’s mechanoreceptors. The subsequent improved mechanoreception does the following:

1) Neurologically inhibits the pain electrical signal to the brain. This is synonymous with the “closing” of the pain gate.

2) Neurologically inhibits muscle tone through a spinal cord reflex. The subsequent relaxation of the muscle reduces secondary muscle pain.

3) Neurologically reduces sympathetic tone and the sympathetic nervous system’s production of catecholamines. Since sympathetically produced catecholamines alter the threshold of the primary pain afferent, this mechanically driven inhibition would further inhibit the nociceptive electrical signal to the brain.

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9) Omoigui S; The biochemical origin of pain: The origin of all pain is inflammation and the inflammatory response: Inflammatory profile of pain syndromes; Medical Hypothesis; 2007, Vol. 69, pp. 1169-1178.

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17) Travell J, Simons D; Myofascial pain and dysfunction, the trigger point manual: THE LOWER EXTREMITIES; New York: Williams & Wilkins, 1992.

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