Author: tmpl_admin

QUESTION:
If a tree falls in the woods when no one is present, does it make a sound?

COMMON RESPONSE LAY PERSON:
Yes

COMMON RESPONSE MEDICAL PROFESSIONAL:
No

DISCUSSION:
All perceptions are cortical. The perception of sound is a cortical event. If no one is present, there is no cortex present, and therefore there is no sound. When a tree falls in the woods it creates a physical phenomenon that is capable of creating the perception of sound in the cortical brain; but without the cortical brain being present, there is no sound.

EXCHANGE:
From the movie, THE MATRIX:

QUESTION by Morpheus:
What is real, Neo?

RESPONSE by Neo:
I do not know.

RESPONSE by Morpheus:
Real is an electrical signal interpreted by your brain.

QUESTION:
What is pain?

RESPONSE (Murphy):
Pain is an electrical signal interpreted by your brain.

DISCUSSION:
Pain, like sound (and sight, taste, smell, hot/cold, etc.), is a cortical event. It is an electrical signal in one’s brain.

•••••••••

Chiropractors thrive in the treatment and management of regional musculoskeletal pain complaints. The clinical efficacy of chiropractic in the treatment and management of musculoskeletal pain syndromes is no longer questioned. As examples, in 1985, orthopedic surgeon W. H. Kirkaldy-Willis states (1):

“Spinal manipulation, one of the oldest forms of therapy for back pain, has mostly been practiced outside of the medical profession.”

“Over the past decade, there has been an escalation of clinical and basic science research on manipulative therapy, which has shown that there is a scientific basis for the treatment of back pain by manipulation.”

A 2011 study authored by Ogura and 8 additional researchers, all with the credentials of MD/PhD, states (2):

“Chiropractic spinal manipulation is an alternative treatment or back pain.”

“Research on chiropractic spinal manipulation has been extensively performed worldwide, and its efficacy on musculoskeletal symptoms has been well documented.”

The physiological explanations as to the mechanisms whereby chiropractic adjusting (directionally specific manipulation) influences pain syndromes (an electrical signal in the brain) tend to fall primarily into two categories:

• Altering inflammation [The Inflammatory Cascade: reducing excitation]
• Closing the pain gate [The Pain Gate: increasing inhibition]

The Inflammatory Cascade

• Tissue trauma or repetitive strain injury initiate an inflammatory response (3, 4, 5).
• Inflammation alters the electrical threshold of the pain afferents (6, 7). Inflamed tissue more readily initiates the neurological electrical signal that in turn creates the pain perceiving electrical signal in the brain. Sunburned skin is much closer to pain threshold than non-sunburned skin when exposed to an environmental stimulus, such as touching or rubbing.
• As a rule, the resolution of inflammation in the body is fibrotic scar tissue (3, 8, 9, 10, 11, 12, 13, 14, 15, 16).
• Fibrous scar tissue is capable of maintaining an inflammatory response, chronically altering the threshold of the pain afferent system, and therefore chronically initiating a chronic pain electrical signal in the brain (3).
• Tension, controlled motion (chiropractic adjustment), remodels the fibrous scar tissue; this orients the tissues along the lines of stress and strain (3, 4, 9, 10, 11, 12, 13, 14, 15, 16, 17). The fibrous scar tissue will no longer harbor an inflammatory response. In addition, the improved motion will further disperse the accumulation of inflammatory exudates. Reduced inflammation reduces the pain electrical signal in the cortical brain.

The Pain Gate

Melzack and Wall’s Gate Control Theory of Pain was originally published in the journal Brain in 1962, and later updated and published in the journal Science in 1965. Ronald Melzack, PhD, is a Canadian psychologist. Patrick Wall, MD (d. 2001), was a British neuroscientist and pain expert, as well as the first editor of the journal Pain. An oversimplified explanation of their Gate Control Theory of Pain is that the pain electrical signal to the cortical brain (small diameter afferents) can be inhibited by non-painful electrical signals arising from other sensory afferents (large diameter afferents). Representative reference book comments include:

The perception of pain is dependent upon the balance of activity in large (mechanoreceptor) and small (nociceptive) afferents. (18)

If large myelinated fibers (mechanoreceptors) were selectively stimulated, then normal “balance” of activity between large (mechanoreceptor) and small (nociceptive) fibers would be restored and the pain would be relieved. (18)

“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.” (19)

“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.” (19)

“Simply put, non-nociceptive afferents ‘close’ and nociceptive afferents ‘open’ a gate to the central transmission of noxious input.” (19)

“The balance of activity in small- and large-diameter fibers is important in pain transmission…” (19)

Melzack and Wall’s Gate Control Theory of Pain was reviewed and confirmed in 2002 in the British Journal of Anaesthesia in an article titled (20):

Gate Control Theory of Pain Stands the Test of Time

This article reiterates that the Gate Theory “has stood the test of time.” The electrical transmission and perception of pain is subject to modulation by non-nociceptive neurological electrical signals. These non-nociceptive neurological electrical signals emanate from large diameter nerve fibers, such as mechanoreceptors. Consequently, the author notes that pain can be modulated through 2 mechanisms (as noted above):

• Reducing excitation. This approach is commonly achieved by reducing inflammation.
• Increasing Inhibition. This approach is commonly achieved by improving mechanical function and mechanical afferentation, firing inhibitory large diameter mechanoreceptors.

The application of chiropractic spinal adjusting for pain control using

Melzack and Wall’s Gate Control Theory of Pain was first done by Canadian orthopedic surgeon Kirkaldy-Willis in 1985 (1). Dr. Kirdaldy-Willis notes:

“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.

In chronic cases, there is a shortening of periarticular connective tissues and intra-articular adhesions may form; manipulations [adjustments] can stretch or break these adhesions.

“In most cases of chronic low back pain, there is an initial increase in symptoms after the first few manipulations [probably as a result of breaking adhesions]. In almost all cases, however, this increase in pain is temporary and can be easily controlled by local application of ice.”

“However, the gain in mobility must be maintained during this period to prevent further adhesion formation.”

These patients were given a “two or three week regimen of daily spinal manipulations by an experienced chiropractor.”

“No patients were made worse by the manipulation, yet many experienced an increase in pain during the first week of treatment. Patients undergoing manipulative treatment must therefore be reassured that the initial discomfort is only temporary.”

“In our experience, anything less than two weeks of daily manipulation is inadequate for chronic low back pain patients.”

•••••••••

Chiropractors pride themselves on their abilities to treat and manage regional musculoskeletal pain complaints. It is understood that many different tissues can initiate the pain electrical signal to the brain, including the intervertebral disc, joint capsules, tendons, muscles, myofascia, and more. Consequently, chiropractic management of regional musculoskeletal pain complaints often involve several simultaneous approaches. These approaches tend to adhere to the concepts noted above:

1) Altering inflammation, reducing excitation:

Management might include local applications of ice, low level laser therapy, pulsed ultrasound, etc.

Local passive motions, soft tissue friction techniques, specific exercises, and chiropractic adjusting may remodel fibrotic scar tissue, dispersing the accumulation of algogenic inflammatory exudates that are altering the electrical threshold of the local pain afferents.

2) Closing the pain gate, increasing inhibition:

There is evidence that chiropractic adjusting can remodel peri-articular fibrosis and rupture intra-articular fibrotic adhesions (21). As noted by Kirkaldy-Willis above, this would improve motion, mechanoreception, and proprioception, “closing” the pain gate, or increasing inhibition. Also as noted by Kirkaldy-Willis, these fibrotic problems tend to reform, denying the long-term benefits that both patients and chiropractors strive to obtain. Consequently, chronic pain patients may respond best to daily manipulation during the initial 2 weeks of management.

•••••••••

Problems

Chiropractors are noted for their treatment and management of patients with chronic pain problems. On occasion, or perhaps more frequently, the patient’s pain is not primarily local or regional, but rather is systemic. There are a number of known factors that can systemically alter the threshold of the pain afferents. These individuals perceive the electrical signal of pain following trivial mechanical stimuli, stimuli that under normal circumstances wild not initiate that pain electrical signal. Common terminology for such individuals is “the patient is systemically too close to nociceptive excitation threshold.”

There are undoubtedly many biological reasons for a patient to be systemically to close to nociceptive excitation threshold. Three common and well-documented reasons are discussed below. Chiropractors often assess these factors in their pain patients as a component of history and/or blood work, and chiropractors often advise their patients in the management of their finding.

•••••••••

Jill is a 30-year old female with chronic systemic pain. She has been suffering from chronic systemic pain for about a decade. For help, she has tried pharmacology, massage, yoga, Pilates, acupuncture, physical therapy, exercise, psychotherapy, and chiropractic. None of these approaches has made much of a difference. She is currently taking 6 different medicines for her pain, even though “they do not seem to be helping very much.”

•••••••••

Omega-6/Omega-3 Ratio

In all of our chronic pain patients, whether their pain is local, regional, or systemic, we find great value in assessing their systemic inflammation profile. To do this we use the protocols of biochemist Barry Sears, PhD (22, 23). Dr. Sears and many others contend that systemic inflammation is primarily controlled by the balance of inflammatory v. anti-inflammatory eicosanoid hormones (24, 25, 26). Eicosanoid hormones are made from 20-carbon long unsaturated fatty acids. Dr. Sears stresses that the best test for systemic inflammation is the ratio of the omega-6 fatty acid arachidonic acid (AA) to the omega-3 fatty acid eicosapentaenoic acid (EPA). He states (23):

“The AA/EPA ratio will tell you the extent
of silent inflammation in the body.”

Based upon the writings of Dr. Sears and many others, we target an

Arachidonic acid (AA) omega-6 / Eicosapentaenoic Acid (EPA) omega-3 ratio of 1.5-4 / 1. A ratio > 10 / 1 is very problematic and is indicative of systemic inflammation. Sadly, because of contemporary widespread use of corn, soybean, and other omega-6 vegetable oils, the average American ratio now stands at about 25 / 1 (6, 27). This means that the average American is extremely systemically inflamed and prone to systemic pain syndromes. Recent evidence from the Institute of Medicine claims that now 116 million Americans suffer from chronic daily pain syndromes (28). We obtain an accurate systemic inflammation profile using a simple finger-prick blood analysis.

•••••••••

Jill’s AA / EPA ratio was 15 / 1; this is clearly significantly pro-inflammatory. We immediately put Jill on 3,000 mg/day of EPA + DHA purified fish oil supplements, with a compliment of anti-oxidants to reduce lipid peroxidation of the double bonds.

•••••••••

Vitamin D

Using the key words “vitamin D AND chronic pain” in a pubmed search of the national Library of Medicine (March 11, 2013) will call up 208 articles. In 2008, James Dowd, MD, authored a book titled The Vitamin D Cure (29). Dr. Dowd notes that adequate vitamin D supplementation can eliminate chronic back pain symptoms in nearly all patients, stating:

“Research tells us that a lack of vitamin D makes us ache. Symptoms that point to vitamin D deficiency are muscle spasms, bone pain, and joint pain.”

“Doctors often mistake vitamin D deficiencies for fibromyalgia, rheumatoid arthritis, and lupus.”

“Because I’m a rheumatologist, people come to me because they want solutions for the pain they’re experiencing in their joints, tendons, ligaments, muscles, and bones. They typically have at least one disease involving muscles, ligaments, joints, and bones, but all of the aches and pains they have are actually connected to their vitamin D levels and what they eat.”

“Those who took vitamin D supplements saw dramatic resolution of pain, muscle fatigue and muscle cramps.”

The world’s leading authority on vitamin D is Michael F. Holick, PhD, MD. Dr. Holick is a professor at Boston University Medical Center. A search of the National Library of Medicine using the pubmed search engine found 380 articles using the key words “holick mf AND vitamin d”. Dr. Holick is the discoverer of the active form of vitamin D (1,25, dihydroxy vitamin D).

In his 2010 book titled The Vitamin D Solution; A 3-Step Strategy to Cure Our Most Common Health Problems, Dr. Holick notes that 93% of those suffering from nonspecific muscular and skeletal aches and pains are shown to be vitamin D deficient (30). Numerous other recent publications agree with Dr. Holick (31, 32, 33, 34, 35, 36, 37, 38). A central theme among these authors is that low levels of vitamin D are linked to inflammation, and as noted above, inflammation alters the thresholds of the pain afferent system.

In 2010, Joseph Pizzorno, ND, the Editor in Chief of the journal

Integrative Medicine, published an editorial in his journal titled: What We Have Learned About Vitamin D Dosing? (39) Dr. Pizzorno believes that the minimum blood levels of vitamin D [25(OH)D3] is 32 ng/ml; the optimal level is 50-70 ng/ml. He recommends that when vitamin D levels are below 32 ng/ml, a loading dose of supplemental vitamin D3 of about 20,000 IU/day for 3–6 months with a maintenance dose of 5,000

IU/day is warranted.

We recommend that all chronic pain patients should have their 25-hydroxy vitamin D levels checked. We obtain an accurate 25-hydroxy vitamin D levels using another simple finger-prick blood analysis. If a patient’s 25-hydroxy vitamin D levels are below 50 ng/ml, and especially if they are below 30 mg/ml, the patient needs more UVB sun exposure without sunscreen, or they need to supplement.

•••••••••

Jill’s 25-hydroxy vitamin D was 17 ng/ml; this is clearly too low and significantly pro-inflammatory. We immediately put Jill on 20,000 IU/day of vitamin D3 with the intention of following Dr. Pizzorno’s protocol above.

•••••••••

Glutamate and Aspartate

An excess of the brain’s principle excitatory neurotransmitters can enhance the pain electrical signal in the brain. The brain’s 2 principle excitatory neurotransmitters are glutamate and aspartate. Both glutamate and aspartate are amino acids. Both glutamate and aspartate are commonly isolated and added to foods as taste enhancers (exciters). Both glutamate and aspartate use the N-methyl-D-aspartate (NMDA) receptor.

Aspartate is half of the artificial sweetener aspartame. Glutamate is ubiquitous in packaged foods, often in the salt form MSG (monosodium glutamate). Glutamate in food is often hidden, using names like (40):

HIDDEN SOURCES OF MSG

The glutamate manufacturers and the processed food industries are always on a quest to disguise MSG added to food. Below is a partial list of the most common names for disguised MSG.

Additives that always contain MSG:

• Monosodium Glutamate
• Hydrolyzed Protein
• Plant Protein Extract
• Calcium Caseinate
• Textured Protein
• Hydrolyzed Oat Flour
• Hydrolyzed Vegetable Protein
• Hydrolyzed Plant Protein
• Sodium Caseinate
• Yeast Extract
• Autolyzed Yeast

Additives that frequently contain MSG:

• Malt Extract
• Malt Flavoring
• Bouillon
• Broth
• Stock
• Flavoring
• Natural Flavoring
• Natural Beef or Chicken Flavoring
• Seasoning
• Spices

Additives that may contain MSG or excitotoxins:

• Carrageenan Enzymes
• Soy Protein Concentrate Soy Protein Isolate
• Whey Protein Concentrate

In 2002, Dickenson (20) clearly notes that glutamate is involved in chronic pain sensization. Recent studies (2012) continue to confirm that dietary glutamate (or aspartate) are involved in chronic pain syndromes (41, 42).

In 2001, Jerry D. Smith and colleagues took a group of chronic pain suffers and purposefully removed all sources of isolated glutamate and aspartame form their diets. Within 4 months, all study subjects reported complete resolution of their pain symptoms. Additionally, reintroduction of isolated glutamate or aspartame into any of their diets immediately resurrected their pain symptoms.

With chronic pain patients, we routinely assess consumption of glutamate (often hidden) and aspartame. We advocate complete avoidance for the next 4 months.

•••••••••

Jill’s consumption of glutamate was probably average. However, history revealed that she was consuming 6 diet sodas (sweetened with aspartame) daily. We immediately had her stop all diet soda consumption, cold turkey.

•••••••••

As clinicians and not researchers, our approach to the management of Jill’s chronic pain was multifaceted, including:

• Chiropractic adjusting of dysfunctional joints.
• Spinal exercises, beginning weight training, and graded walking.
• Supplemental fish oil omega-3 fatty acids plus antioxidants.
• Supplemental vitamin D3.
• Reduction of dietary glutamate and elimination of all aspartame.

Jill’s chronic pain was markedly improved after one month of this regime, and she was pain free at the 4 month revaluation.

REFERENCES

• Kirkaldy-Willis WH, Cassidy JD; Spinal Manipulation in the Treatment of Low Back Pain; Canadian Family Physician; March 1985, Vol. 31, pp. 535-540.
• Ogura T, Tashiro M, Masud M, Watanuki S, Shibuya K, Yamaguchi K, Itoh M, Fukuda H, Yanai K; Cerebral metabolic changes in men after chiropractic spinal manipulation for neck pain; Alternative Therapies Health Medicine; Nov-Dec 2011;Vol. 17; No. 6; pp. 12-7.
• Cyriax, James; Textbook of Orthopaedic Medicine, Diagnosis of Soft Tissue Lesions, Bailliere Tindall, Volume 1, eighth edition, 1982.
• Roy, Steven; Irvin, Richard; Sports Medicine: Prevention, Evaluation, Management, and Rehabilitation, Prentice-Hall, 1983.
• Maroon JC, Bost JW, Maroon A; Natural anti-inflammatory agents for pain relief; Surgical Neurological International; Dec. 2010; Vol. 13; No. 1.
• Boswell M, Cole BE, editors; American Academy of Pain Management: Weiner’s Pain Management: A Practical Guide for Clinicians; Seventh Edition, 2006, pp. 584-585.
• 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.
• Guyton, Arthur, Textbook of Medical Physiology, Saunders, 1986.
• Cohen, I. Kelman; Diegelmann, Robert F; Lindbald, William J; Wound Healing, Biochemical & Clinical Aspects, WB Saunders, 1992.
• Melham TJ, Sevier TL, Malnofski MJ, Wilson JK, Helfst RK, Chronic ankle pain and fibrosis successfully treated with a new noninvasive augmented soft tissue mobilization technique (ASTM); Medicine Science Sports Exercise, June 1998; 30(3): 801-4.
• Jonsson H, Cesarini K, Sahlstedt B, Rauschning W; Findings and Outcome in Whiplash-Type Neck Distortions; Spine, Vol. 19, No. 24, December 15, 1994, pp. 2733-2743.
• Hildebrand K, Frank C; Scar Formation and Ligament Healing; Canadian Journal of Surgery; 1998.
• Majno, Guido and Joris, Isabelle; Cells, Tissues, and Disease: Principles of General Pathology, 2004.
• Hildebrand KA, Gallant-Behm CL, Kydd AS, Hart DA; The Basics of Soft Tissue Healing and General Factors that Influence Such Healing; Sports Medicine Arthroscopic Review; 2005.
• Walsh W; Orthopedic Biology and Medicine; Repair and Regeneration of Ligaments, Tendons, and Joint Capsule; Humana Press, 2006.
• Schleip R; Fascia: The Tensional Network of the Human Body; The Scientific and Clinical Applications in Manual and Movement Therapy; 2012.
• Kellett J; Acute soft tissue injuries-a review of the literature; Medicine and Science of Sports and Exercise, American College of Sports Medicine, Vol. 18 No. 5, (1986), pp. 489-500.
• John Nolte, The Human Brain; Mosby Year Book, 1993.
• Eric Kandel, James Schwartz, Thomas Jessell, Principles of Neural Science. McGraw-Hill, 2000.
• Dickenson AH; Gate Control Theory of pain stands the test of time; British Journal of Anaesthesia, Vol. 88, No. 6, June 2002, pp. 755-757.
• Cramer GD, Gregerson DM, Knudsen JT, Hubbard BB, Ustas LM, Cantu JA; The Effects of Side-Posture Positioning and Spinal Adjusting on the Lumbar Z Joints: A Randomized Controlled Trial With Sixty-Four Subjects; Spine, Volume 27, Issue 22, November 15, 2002, pp. 2459-2466.
• Barry Sears; The Omega Zone; Regan Books; 2002.
• Barry Sears; Toxic Fat; Thomas Nelson; 2008.
• Cleland LG, James MJ, Proudman SM; What the prescriber needs to know; Arthritis Res Ther. 2006;8(1):202.
• Goldberg RJ, Katz J; A meta-analysis of the analgesic effects of omega-3 polyunsaturated fatty acid supplementation for inflammatory joint pain; Pain; May 2007, 129(1-2), pp. 210-223.
• Maroon JC, Bost JW; Omega-3 Fatty acids (fish oil) as an anti-inflammatory: an alternative to nonsteroidal anti-inflammatory drugs for discogenic pain; Surgical Neurology; 65 (April 2006) 326–331.
• Simopoulos AP; Evolutionary Aspects of Diet: The Omega-6/Omega-3 Ratio and the Brain; Molecular Neurobiology; October 2011; Vol. 44; No. 2; pp. 203-15.
• Pho K; Pain Management: Education is Key; USA Today; September 9, 2011, p. 9A.
• Dowd J; The Vitamin D Cure; Wiley, 2008.
• Holick MF; The Vitamin D Solution; A 3-Step Strategy to Cure Our Most Common Health Problems; 2010.
• Schwalfenberg G; Improvement of Chronic Back Pain or Failed Back Surgery with Vitamin D Repletion: A Case Series; Journal of the American Board of Family Medicine; January–February 2009; Vol. 22; No. 1; pp. 69-74.
• Straube S, Andrew Moor R, Derry S, McQuay HJ, Thomas A; Vitamin D and chronic pain; Pain; 2009; 141: pp. 10-13.
• Manson JE; Pain: sex differences and implications for treatment; Metabolism; October 2010, Volume 59, Supplement 1, pp. S16-S20.
• Heidari B, Shirvani JS, Firouzjahi A, Heidari P, Hajian-Tilaki KO; Association between nonspecific skeletal pain and vitamin D deficiency; International Journal of Rheumatic Disease; October 2010; Vol. 13. No. 4; pp. 340-346.
• Bhatty SA, Shaikh NA, Irfan M, Kashif SM, Vaswani AS, Sumbhai A, Gunpat; Vitamin D Deficiency in Fibromyalgia; Journal of the Pakistan Medical Association; November 2010; Vol. 60; No. 11; pp. 949-951.
• Arnson Y, Amital H; Is Vitamin D a New Therapeutic Agent in Auto-inflammatory and Pain Syndromes?; Israeli Medical Association Journal; Vol. 13, April 2011; pp. 234-235.
• Tague SE, Clarke GL, Winter MK, McCarson KE, Wright DE, Smith PG; Vitamin D deficiency Promotes Skeletal Muscle Hypersensitivity and Sensory Hyperinnervation; Journal of Neuroscience; September 2011; Vol. 31; No. 39; pp. 13728-38.
• Kragstrup TW; Vitamin D Supplementation for Patients with Chronic Pain; Scandinavian Journal of Primary Health Care; 2011, 29: pp. 4-5.
• Pizzorno J; What We Have Learned About Vitamin D Dosing?; Integrative Medicine; Vol. 9, No. 1, Feb/Mar 2010.
• Blaylock R; Excitotoxins, The Taste That Kills; Health Press, 1997.
• Ma X, Shi TF, Zhang M, Lu XY, and six more; Modulatory role of glutamic acid on the electrical activities of pain-related neurons in the hippocampal CA3 region; Neuroscience Letters; March 2012; Vol. 513; No. 1; pp. 67-71.
• Holton KF, Taren DL, Thomson CA, Bennett RM; Jones KD; The effect of dietary glutamate on fibromyalgia and irritable bowel symptoms; Clinical Experimental Rheumatology; Nov-Dec 2012; 30(6 Suppl 74); pp. 10-7.
• Smith JD, Terpening CM, Schmidt SOF, Gums JG; Relief of Fibromyalgia Symptoms Following Discontinuation of Dietary Excitotoxins; The Annals of Pharmacotherapy: June 2001; Vol. 35, No. 6, pp. 702–706.

From the earliest moments of his life, Joe was an extremely active boy. He would attempt to climb up on to everything he could, often falling off: furniture, vehicles, rocks, trees, etc. When he began school, he was constantly involved in every sport available to him: football, baseball, basketball, soccer, gymnastics, and more. Joe particularly like the rougher sports, like football; the rougher the sport the more Joe enjoyed it.

Joe was raised a practicing Catholic. Catholic church services (mass), includes periods of kneeling down. Joe’s earliest memories of kneeling during mass are that of having low back pain. Kneeling put his lumbar spine in a slightly extended, increased lordotic, position. Joe’s back felt much better if he would move his butt back until it contacted the seat behind him, putting him in a semi seated-kneeling position. In this position his lumbar spine was in slight flexion, and his back did not hurt. However, Joe’s parents felt that assuming such a position was disrespectful, and they would regularly gently reminded him to straighten up.

In high school, Joe excelled in football, basketball, and track. In track he did it all, competing in all the events of the decathlon. In college, Joe played basketball and ran on the track team. But during his college sophomore year he began to experience chronic lower back pain. Eventually he saw a chiropractor for his chronic low back pain complaints. The chiropractic examination included upright lumbar spine radiographs. The initial working diagnosis was:

Spondylolysis with spondylolisthesis (grade II, a 50% forward slippage down the sacral base) resulting in moderate L5-S1 disc degeneration (spondylosis) and paravertebral muscle spasm. There was no radiculopathy or myelopathy.

•••••••••

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

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

Dr. Kapandji’s explanation for this statement is likened to the proverbial physics of a block on an incline plane. 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

As Dr. Kapandji explains, the sacral base is not horizontal, but rather it is an inclined plane. The L5 vertebral body sits atop of the inclined plane of the sacral base. The main structure that prevents the L5 vertebral body from sliding anterior and inferior down the sacral base inclined plane is the posterior vertebral arch (vertebral isthmus). This vertebral isthmus exists between the superior and inferior facets of L5, a location that is known as the pars interarticularis.

The fracture and separation of the pars interarticularis is known as spondylolysis. When the pars is fractured or destroyed, the L5 vertebral body will slide down the incline plane of the sacral base. This anterior and inferior slippage of the L5 vertebral body is known as an anterior spondylolisthesis.

Dr. Kapandji notes that when the pars is separated, the remaining structures that resist the slippage of the L5 disc down the sacral inclined plane are the fibers of the intervertebral disc and the posterior paraspinal musculature. The mechanical stress on the annular fibers of the L5 intervertebral disc can generate discogenic low back pain. The constant contraction and spasm of the posterior paraspinal musculature can cause muscular low back pain.

•••••••••

Congenital or Acquired
Incidence, Location, and Onset of Symptoms

Up until the 1970s it was commonly thought and taught that spondylolysis and anterior spondylolisthesis were congenital. However, autopsies on stillborn babies and careful analysis of adults who had never walked indicated that spondylolysis and anterior spondylolisthesis are not congenital. For decades now, it has been understood that spondylolysis and anterior spondylolisthesis are acquired in childhood. A chronological review of the evidence include these:

• In 1965, Melamed publishes an article titled:

SPONDYLOLYSIS AND SPONDYLOLISTHESIS ARE NOT CONGENITAL

• In 1971, Schmoral and Junghanns note:

There is increasing support for the opinion that spondylolysis is “acquired after birth during growth of the skeletal system.” Spondylolysis “seems to be closely connected to the upright gait and to the lumbar lordosis.”

• In 1973, Farfan notes:

Evidence “suggests that the defect in the neural arch is acquired,” and that the “condition is a stress fracture.”

• In 1975, Cyriax notes:

“Evidence has lately been accumulati ngthat a disorder named spondylolisthesis (which had been regarded as due to an inborn defect in the vertebral arch) is seldom congenital but is acquired in childhood.”

“Stress fractures form between the two halves of the vertebral arch.”

• In 1977, Mcnab notes:

“In spondylolytic spondylolisthesis, the basic lesion is a defect in the neural arch across the pars interarticularis.” “The neural arch defects occur most frequently between ages of 5 and 7. Forward slippage of the vertebral body occurs most frequently between ages of 10 and 15 and rarely increases after 20.”

“In some Eskimo communities the incidence of neural arch defects may rise as high as 50%.” “The incidence of spondylolysis in the white population of the North American continent is about 6%.”

• In 1977, D’Ambrosia notes:

Spondylolysis with spondylolisthesis “only occurs in man who walks with a true upright stance and has lumbar lordosis. There is no evidence that this defect is ever present at birth, and it is not seen in patients who have never been ambulatory. The most common age of onset is between 5 and 6 years of age, but slipping can occur up to age 20. The period of most rapid slipping is between 10 and 15 years when the adolescent growth spurt is at its peak.”

• In 1980, Keim notes:

“Many authorities consider spondylolysis and spondylolisthesis to be stress fractures of the pars interarticularis, or isthmus, of a vertebrae.”

“After the age of 5 and usually in the teenage years, repeated shearing stresses, such as those that occur in gymnastics or contact sports, can cause a stress fracture in the isthmus.”

• In 1980, Finneson notes:

Spondylotic spondylolisthesis is due to a separation or dissolution of the pars. “It is always a fatigue fracture.” It is almost never seen below the age of 5, but is found in 4.4% of 7 year olds.

• In 1980, Wertzberger and Peterson note:

“There is increasing evidence that the defect in the pars interarticularis is due to fatigue fracture rather than being of congenital origin. We describe the youngest patient on record with spondylolysis and spondylolisthesis in whom roentgenograms that showed no abnormality had previously been taken. This case supports the hypothesis that spondylolysis and spondylolisthesis are acquired and not congenital, even when discovered in a very young child.”

• In 1981, Rosenberg and colleagues obtained radiographs of the lumbosacral spines of 143 patients (age range of 11 to 93 years) that had never walked. They note:

“No case of spondylolysis or spondylolisthesis was detected, and when compared to the 5.8% incidence in the general population.”

“These results support the theory that spondylolysis and isthmic spondylolisthesis represent a fatigue fracture resulting from activities associated with ambulation.”

• In 1983, Salter notes:

Approximately 85% of spondylolysis “occur in the fifth lumbar vertebrae and most of the remaining 15% occur in the fourth lumbar vertebrae.”

“Once thought to be a congenital defect spondylolysis is now known to develop during postnatal life.”

“Since the lower lumbar region of the human spine is subjected to much stress in the erect position, it is possible that spondylolysis represents either a stress fracture (fatigue fracture) from oft-repeated stresses or an ordinary fracture from a single injury.”

The gap in the pars after fracture and separation is filled in with fibrous tissue.

“The forward slippage of one vertebral body (and the remainder of the spinal column above it) in relation to the vertebral segment immediately below is referred to as a spondylolisthesis. It occurs most commonly in the lower lumbar spine—particularly between the fifth lumbar vertebrae and the sacrum.”

A normal lumbar vertebral body is prevented from slipping forward by an intact neural arch. With loss of continuity of the pars interarticularis, “the intervertebral disc is not sufficiently strong to prevent displacement of the vertebrae.”

The forward displacement of spondylolisthesis is “most likely to be

progressive during the rapid growth spurt of early adolescence.”

Spondylolytic spondylolisthesis “usually becomes manifest during childhood with the gradual onset of low back pain which is aggravated by standing, walking and running and relieved by lying down.”

“The associated clinical deformity, which is related to the degree of forward slip, is characterized by a ‘step’ in the lumbosacral region at the level of the spondylolisthesis and an increased lumbar lordosis above.”

• In 1987, Yochum and Rowe note:

The Eskimo infant is placed upright at an earlier age. This might account for the higher incidence of spondylolysis and spondylolisthesis in Eskimo populations.

• In 1988, Cailliet notes:

Seventy percent of spondylolysis and anterior spondylolisthesis occur at L5, 25% occur at L4, and 4% occur at higher levels. The low back is stiff with limited flexibility. “The patient frequently claims discomfort from lifting, excessive bending over, or from prolonged standing in a nonmoving manner.”

• In 1990, White and Panjabi note:

“In spondylolisthesis there is a defect in the pars interarticularis that is associated with anterior translation of the involved vertebrae in relation to the subjacent one.” “The theory that seems to have survived best at present is that of fatigue fracture.”

“The disease is thought to have an incidence of 1.95% in American blacks, 5.8% in American whites, and about 60% in American Eskimos.”

• In 2011, Cox notes:

“Isthmic spondylolisthesis is the most common type of spondylolisthesis, and it is caused by a defect in the ossification of the pars interarticularis.”

“It is no longer questioned that spondylolysis is a fracture that may or may not heal. These fractures are postulated to occur because of the assumption of the upright posture by the infant, allowing a fatigue type of fracture to occur when stress beyond the strength of bone occurs.”

“One reason that forward slippage occurs most often in children aged 5 to 7 years may be because of the increased activity or to increased sitting in the lordotic posture done by children. It is known that fracture never occurs in animals other than humans, and only humans have lordosis.”

“At the time of slippage, the disc must break down, allowing annular stretching and tearing.” “The disc, being a very pain-sensitive structure, certainly creates symptomatology as the slippage occurs.” “In adults, after the slippage occurs and the annular fibers heal, the pain lessens or disappears.”

•••••••••

Joe had some additional interesting and important examination findings:

• His low back range of motion was very limited, especially in flexion.

• His lumbosacral musculature was hypertonic with moderate spasm.

• There were no signs of motor or sensory radiculopathy or of myelopathy: deep tendon reflexes were normal bilaterally; there were no alterations in superficial sensation; lower extremity myotomal strength was normal and strong without fatigability in all tested muscles; Babinski’s test was normal; there were no reports of dysfunction in bowels, bladder or sexual function; Valsalva was normal; lumbar spine compression (Kemp’s) was normal. Although the recumbent straight-leg-raising test was negative for signs of compressive radiculopathy, Joe’s hamstring muscles were extremely tight; he could only raise his legs to about 30 degrees bilaterally as a consequence of hamstring tightness.

• While standing, a significant “shelf” was found above Joe’s L5 spinous process; it was so noticeable that a cup of liquid could be rested on the shelf without spilling.

•••••••••

Hamstring Tightness

As with Joe, hamstring tightness is a common and important finding in patients with clinically relevant spondylolysis and anterior spondylolisthesis. When the L5 vertebral body slides anterior and inferior, the L4 vertebral body travels forward with it. This elongates the distance the cauda equinal and sacral nerve roots must travel, as they must still traverse posteriorly to descend in the sacral canal. This effectively tethers or stretches these nerves. Several have postulated that this could account for the hamstring tightness:

• In 1980, Keim notes:

With increasing slippage, there is increasing stress on the sacral roots.

• In 1983, Salter notes:

“The hamstring muscles are tight with resulting limitation of straight leg raising.”

• In 1988 Cailliet notes:

“An interesting finding associated with spondylolisthesis but as yet unexplained is the presence of limited extensibility of the hamstring muscles. The hamstrings are ‘tight’ on straight leg raising but with negative dural signs.” “The cause of the tight hamstring muscle is conjectural and has been attributed to caudal equinal traction with irritation to the nerve roots descending to the hamstring muscles.”

• In 2011, Cox notes:

Clinical features include paravertebral muscle hypertrophy, increased lumbar lordosis, signs of slipping on inspection and/or palpation, hamstring muscle spasm, and pain during trunk flexion-extension tasks.

•••••••••

Step, Ledge, Shelf

As with Joe, an important examination finding of a clinically significant spondylolysis and anterior spondylolisthesis is the presence of a “step” or “ledge” or “shelf” on top of the L5 spinous process and the L4 spinous process. The inferior facet of L5 is still articulating with the superior facet of S1, meaning the L5 spinous process remains in its original position prior to the spondylolysis and anterior spondylolisthesis. However, the inferior facet of L4 slid anterior along with the body of L5 and the superior facet of L5. In fact, the entire spine above the L5 pars separation moves anteriorly, leaving behind the sacrum, the inferior facet of L5, and the L5 spinous process, effectively creating a step or ledge or shelf. Note:

• In 1971, Schmoral and Junghanns note:

“If the slippage has reached an advanced stage, then the physician can see and feel a step along the row of spinous processes since the spinous processes of the slipped vertebral body remains in its proper position and thus projects more posteriorly than the spinous processes situated above it.”

• In 1977, D’Ambrosia notes:

“The defect of a severe spondylolisthesis where the vertebral body slips forward on the one below, can be palpated as a step off in the lumbar spine.”

• In 1983, Salter notes:

“The associated clinical deformity, which is related to the degree of forward slip, is characterized by a ‘step’ in the lumbosacral region at the level of the spondylolisthesis and an increased lumbar lordosis above.”

• In 1988 Cailliet notes:

“The examination frequently reveals a palpable ‘ledge’ on passing the fingers down the lumbosacral spine.”

•••••••••

Pathology and Prognosis

The tissues affected by spondylolysis and anterior spondylolisthesis endure greater biomechanical stresses and associated spinal degenerative disease. These facts have long-term prognostic significance, as noted:

• In 1973, Farfan notes:

“It is clear that, with either a spondylolysis or a spondylolisthesis, the derangement of normal anatomic arrangements and loss of proper physiological function will lead to degenerative change in this joint.”

When the spondylolysis occurs early in childhood, the weak joint may heal and regain its normal strength. In such instances the next higher joint may be pushed into relative danger.”

• In 1977, Mcnab notes:

“Spondylolysis predisposes to premature disc degeneration in the subjacent disc and spondylolisthesis does not occur without disc degeneration. These degenerative changes may of themselves be painful, giving rise to local or referred pain in sciatic distribution without root irritation.”

• In 1983, Salter notes:

“Significant involvement of the nerve roots is not common in this type of spondylolisthesis although nerve root irritation may produce sciatica.”

• In 1995, Schneiderman and colleagues performed a histologic study on the pars defect tissue of six adult patients with symptomatic spondylolysis and spondylolisthesis to identify and characterize their neural elements.

“Histologic examination revealed extensive connective tissue scar formation throughout all specimens examined.”

“Free nerve endings believed to have nociceptive function were identified in all specimens.”

“The finding of neural elements, including free nerve endings within the pars defect tissue, suggests that the pars defect may be a source of back pain in some patients with symptomatic spondylolysis.”

“Our study identified within the pars defect neural elements capable of nociceptive function.”

“In conclusion, connective tissue and scar tissue harvested from the pars defect of symptomatic patients with spondylolysis contains a high density of neural tissue. Numerous elements consistent with nociceptive nerve endings have been identified. This finding suggests that the interposed tissue within the pars defect may be a source of back pain in some patients with symptomatic spondylolysis.”

• In 2011, Cox notes:

“Free nerve endings within the pars defect tissue can be a source of back pain in some patients with symptomatic spondylolysis.” “Pain in spondylolysis or spondylolisthesis might derive from the spondylolytic defect itself, probably from stretching of the local neural elements.”

“Forward slippage of the body will not occur without degenerative changes in the underlying disc (i.e., forward slippage is not possible without annular tearing or breakdown). The disc is not capable of withstanding the shearing stresses of the body above on the one below.”

•••••••••

Conservative Management

The pain of spondylolysis and spondylolisthesis is nearly always managed conservatively, which includes spinal manipulation and flexion distraction techniques (Cox). Reference examples include:

• In 1971, Schmoral and Junghanns note:

“Sports associated with considerable stress or with certain shearing motions involving the lumbosacral transition, such as weight-lifting, wrestling or judo, should be avoided. However, light sports activities and swimming are permitted.”

• In 1977, McNab notes:

“Spondylolysis predisposes to premature disc degeneration in the subjacent disc and spondylolisthesis does not occur without disc degeneration. These degenerative changes may of themselves be painful, giving rise to local or referred pain in sciatic distribution without root irritation.”

• In 1987, Yochum and Rowe note:

“A more conservative approach including chiropractic spinal manipulative therapy has been found beneficial in managing patients low back pain with the presence of spondylolysis or spondylolisthesis.”

• In 1988, Kirkaldy-Willis notes:

“Frequently, spondylolisthesis is complicated by a posterior joint syndrome one level above the lesion or by a sacroiliac syndrome. Thus, improvement in the patient’s symptoms results from the effect of manipulation on these other joints. In our experience, manipulation is a good first line of treatment in patients with spondylolisthesis. We have seen patients who did not benefit from [surgical] decompression and/or fusion but who were relieved of their back and leg pain by manipulation directed to the sacroiliac joint.”

•••••••••

Bracing and Surgical Consultation

An acute spondylolysis is a fracture. When history and imaging, including a bone scan, confirm an acute spondylolysis, the patient should undergo bracing immobilization (details beyond the scope of this paper).

In the majority of patients with spondylolysis and anterior spondylolisthesis, the lesion is stable. In top tier and professional athletes, the stability of their lesion causes little pain and essentially no dysfunction. However, when spondylolysis and spondylolisthesis become unstable, there often exists significant pain and neurological symptoms and signs, as well as functional deficits. Unstable patients should be referred for a surgical consultation.

Classically, stability status has been assessed with maximum flexion-neutral-maximum extension lateral radiography. However, Friberg described a more accurate assessment in 1987. The patient hangs from a bar with their hands/arms (bending their knees) while a lateral lumbar x-ray is exposed. In stable spondylolisthesis, the L5-S1 relationship will remain unchanged. If the sacrum slides under the L5 vertebral body while hanging, the patient has an unstable spondylolisthesis. This patient may require a surgical consultation and surgical stabilization.

REFERENCES

Cailliet R; Low Back Pain Syndrome; Fourth Edition; FA Davis; 1988.

Cox JM; Low Back Pain, Mechanism, Diagnosis, and Treatment; Seventh Edition; Wolters Kluwer/Lippincott Williams & Wilkins; 2011.

Cyriax J; The Slipped Disc, Causes, Prevention, and Treatment of a Universal Complaint; Second Edition, Grower Press, 1975.

D’Ambrosia RD; Musculoskeletal Disorders, Regional Examination and Differential Diagnosis; Lippincott, 1977.

Farfan HF; Mechanical Disorders of the Low Back; Lea & Febiger; 1973.

Finneson B; Low Back Pain; Second Edition; Lipponcott; 1980.

Friberg O; Lumbar instability: a dynamic approach by traction-compression radiography; Spine; March 1987; 12(2):119-29.

Kapandji IA; The Physiology of the Joints; Volume Three, The Trunk and the Vertebral Column; Churchill Livingstone; 1974.

Keim H; Low Back Pain, Clinical Symposium; Vol. 32; No. 6; CIBA; 1980.

Kirkaldy-Willis WH; Managing Low Back Pain; Second Edition; Churchill Livingstone; 1988.

Melamed A; SPONDYLOLYSIS AND SPONDYLOLISTHESIS ARE NOT CONGENITAL; Wisconsin Medical Journal; March 1965; 64:130-3.

McNab I; Backache; Williams & Wilkins, 1977.

Rosenberg NJ, Bargar WL, Friedman B; The incidence of spondylolysis and spondylolisthesis in non-ambulatory patients. Spine; 1981 Jan-Feb;6(1):35-8.

Salter RB; Textbook of Disorders and Injuries of the Musculoskeletal System; Second Edition; Williams and Wilkins; 1983.

Schmoral G, Junghanns H; Schmorl’s and Junghanns’ The Human Spine in Health and Disease; Grune & Stratton; 1971.

Schneiderman GA, McLain RF, Hambly MF, Nielsen SL; The pars defect as a pain source: A histologic study; Spine; August 15, 1995;20(16):1761-4

Wertzberger KL, Peterson HA; Acquired spondylolysis and spondylolisthesis in the young child; Spine (Phila Pa 1976). 1980 Sep-Oct;5(5):437-42.

White AA, Panjabi MM; Clinical Biomechanics of the Spine; Second Edition; Lippincott; 1990.

Yochum TR, Rowe LJ; Essentials of Skeletal Radiology; Williams & Wilkins; 1987.

Phases of Healing Improvements in Timing and Quality of Healing Problems and Residual Characteristics

There are many published journal articles and books pertaining to the topic of “Soft Tissue Injury and Repair.” My favorites include:

1. Studies on development of connective tissue in transparent chambers in rabbit’s ear; American Journal of Anatomy; 1940.
2. Orthopaedic Medicine, Diagnosis of Soft Tissue Lesions; 1982.
3. Acute soft tissue injuries; Australian Family Physician, 1982.
4. Sports Medicine: Prevention, Evaluation, Management, and Rehabilitation; 1983.
5. Normal ligament Properties and Ligament Healing; Clinical Orthopedics and Related Research; 1985.
6. Acute soft tissue injuries-a review of the literature; Medicine and Science of Sports and Exercise; 1986
7. Injury and Repair of the Musculoskeletal Soft Tissues; American Academy of Orthopaedic Surgeons;
8. Wound Healing, Biochemical & Clinical Aspects; 1992.
9. Continuous Passive Motion, A Biological Concept for the Healing and Regeneration of Articular Cartilage, Ligaments, and Tendons; From Origination to Research to Clinical Applications; 1993.
10. Effects of Early Motion on Healing of Musculoskeletal Tissues, Hand Clinics; 1996.
11. Scar Formation and Ligament Healing; Canadian Journal of Surgery; 1998
12. Immobilization or Early Mobilization After an Acute Soft-Tissue Injury?; The Physician And Sports Medicine; 2000.
13. Cells, Tissues, and Disease: Principles of General Pathology, 2004.
14. The Basics of Soft Tissue Healing and General Factors that Influence Such Healing; Sports Medicine Arthroscopic Review; 2005.
15. Orthopedic Biology and Medicine; Repair and Regeneration of Ligaments, Tendons, and Joint Capsule; Humana Press, 2006.
16. Fascia: The Tensional Network of the Human Body; The Scientific and Clinical Applications in Manual and Movement Therapy; 2012.

Phases of Healing

The article I have seen referenced (and personally used in numerous contexts) most often was published in 1986 in the journal Medicine and Science in Sports and Exercise by Australian physician John Kellett, MD, and titled (6):

Acute soft tissue injuries–a review of the literature

In this article, Dr. Kellett describes the pathological processes of soft tissue healing as following three distinct phases:

• Phase 1: the acute inflammatory phase
• Phase 2: the repair phase
• Phase 3: remodeling phase

The phases of soft tissue injury repair are:

Phase 1: The Acute Inflammatory or Reaction Phase

This phase of healing lasts up to about 72 hours. It is characterized by vasodilation, immune system activation of phagocytosis to remove debris, the release of prostaglandins and inflammation.

The prostaglandins play a prominent part in pain production and increased capillary permeability (swelling).

The wound is hypoxic because the blood vessels have been disrupted, but immune system macrophages perform their phagocytosis duties anaerobically.

Phase 2: The Repair or Regeneration Phase

This phase begins at about 48 hours and continues for about 6 weeks. This phase is characterized by the synthesis and deposition of collagen, which literally glue the margins of the healing breach together.

The collagen that is deposited in this phase is not fully oriented in the direction of tensile strength. Rather, is laid down in an irregular, non-physiological pattern. Dr. Kellett states:

This phase is “largely one of increasing the quantity of the collagen” but this collagen is not laid down in the direction of stress.

Phase 3: The Remodeling Phase

This phase may last up to “12 months or more.” Dr. Kellett stresses that the remodeling phase of healing is critical for establishing the ultimate quality and functional capabilities of the healed tissues. He states:

“The collagen is remodeled to increase the functional capabilities of the tendon or ligament to withstand the stresses imposed upon it.”

“It appears that the tensile strength of the collagen is quite specific to the forces imposed on it during the remodeling phase: i.e. the maximum strength will be in the direction of the forces imposed on the ligament.” [This could argue for the need for specific line-of-drive joint adjustments.]

This phase is largely “an improvement of the quality” (orientation and tensile strength) of the collagen.

Stages of Healing Following Soft Tissue Injury

 

In support of the healing steps detailed by Dr. John Kellett, Physician Kevin Hildebrand, MD, and colleagues, from the University of Calgary, Alberta, Canada published a study in the journal Sports Medicine Arthroscopic Review, in 2005 titled (14):

The Basics of Soft Tissue Healing and
General Factors that Influence Such Healing

Dr. Hildebrand and colleagues point out that wound healing following overt injury to a tissue follows general ‘‘rules’’ irrespective of the tissue involved. These “rules” are similar but somewhat more detailed than those outlined by Dr. Kellett. They include:

Phase 1: The Inflammatory

Following acute injury there is bleeding into the area of injury and pain. “Hemostasis is restored by the formation of a fibrin clot, which prevents further bleeding and serves as a provisional matrix for migrating cells.” This clotting cascade results in the release of inflammatory molecules and inflammatory cytokines from cells such as platelets. There is an influx of fibroblasts, which sets the stage for the second phase of the repair process.

Phase 2: The Matrix Deposition Phase

The fibroblasts produce collagen proteins that bridge the damaged area with the residual endogenous ligament tissue. “The tissue deposited early after injury appears to be an attempt to bridge the damaged area without regard to what was present before injury.”

Phase 3: The Remodeling Phase

“The remodeling phase is a slow process and is accompanied by alterations not only in matrix remodeling, but also gene expression, cellularity, vascularity, and innervation.” The scar tissue in a ligament “undergoes a protracted process where the initially deposited material seems to be turning over and the organization of collagen fibrils become more oriented along the long axis of the ligament.” “Because the remodeling phase occurs slowly, and may take months (i.e., skin) or years (i.e., tendon and ligament).” [Important]

Last year (2012), Robert Schleip, PhD, (Division of Neurophysiology, Ulm University, Germany) and colleagues, published an excellent and very detailed book on soft tissues, titled (16):

Fascia
The Tensional Network of the Human Body
The Scientific and Clinical Applications in Manual and Movement Therapy

In this book, they add to the details of the principles of soft tissue injury and repair. Specifically, they state: “Wound healing is divided into three or four phases:”

Phase 1A: The Vascular Inflammatory Phase

This phase begins immediately after injury and last 0 – 2 days. It is characterized by bleeding into the tissue.

Phase 1B: The Cellular Inflammatory Phase

Fibroblasts migrate into the injury area. This phase lasts 2 – 5 days.

Phase 2: The Proliferation Phase

This phase begins at the fifth day and lasts about 21 – 28 days. “The proliferation phase in poorly perfused tissue such as tendon, ligament, meniscus, or intervertebral disc can last up to 6 weeks.”

In this phase, wound closure occurs with a network of collagen fibers. “For this collagen network to attain an almost identical construction of the original tissue, the tissue in this phase of would healing must be confronted with its normal physiological stress.”

Phase 3: The Consolidation Reconstruction Phase

This phase begins between days 21 – 28, and continues to about day sixty.

Phase 4: The Remodeling / Maturation Reconstruction Phase

This phase begins at about day 60 and continues for about a year. “Stress on the tissue should now be slowly increased to push ahead the reconstruction of unstable type III collagen to stable type I collagen and return the tissue to its original stability.”

Improvements in Timing and Quality of Healing

There are a number of variables that influence the timing and quality of healing.

Dr. Kellett notes (6):

“Cryotherapy (crushed ice) for 10 to 20 min, 2 to 4 times/day for the first 2 to 3 days is helpful in promoting early return to full activity.” “Numerous studies have shown the effectiveness of ice therapy in reducing the pain and period of disability to soft tissue injuries.” In contrast, “early heat treatment leads to an increase in the blood flow to the injured area with an exaggerated acute inflammatory response.”

“The advantages of cryotherapy in treating soft tissue injuries have been well documented.” Ice within 48 hours of injury reduces disability of ankle sprains from 15 days to 10 days.

“Early mobilization, guided by the pain response, promotes a more rapid return to full activity.”

“Early mobilization, guided by the pain response, promotes a more rapid return to full functional recovery.”

“Progressive resistance exercises (isotonic, isokinetic, and isometric) are essential to restore full muscle and joint function.”

Following this acute inflammatory phase and largely guided by the pain response of the patient, early mobilization is commenced, based upon the premise that the stress of movement on repairing collagen is largely responsible for the orientation and tensile strength of the tendons and ligaments.

The goal of stressing repairing tissues with controlled motion is to induce adaptive response of functionally stronger connective tissues. However, excessive stressing of the repairing tissues may result in further damage. Consequently, any sign or symptom which suggests a worsening of the injury (severe pain) is a clear indication to reduce the motion stress on the tissues.

The strength of repaired ligaments is proportional to the mobility of the ligament, resulting in larger diameter collagen fiber bundles and more total collagen. “Collagen fiber growth and realignment can be stimulated by early tensile loading of muscle, tendon, and ligament.”

•••••••••

In 1998, Drs. Hildebrand and Frank note (11):

“Motion in stable joints improves the biomechanical properties of healing ligaments compared with immobilization of joints.” “The mechanism presumably involves the application of controlled forces; too little or too much force is detrimental.”

•••••••••

In 2005, Dr. Hildebrand and colleagues note (14):

“The large scar tissue mass gradually remodels, likely under the influence of the mechanical environment.”

“Maturation of the scar tissue requires mechanical loading to continue the remodeling phase of healing.”

“Normal connective tissues that function in a mechanically active environment (actually most tissues) subscribe to the ‘‘use it or lose it’’ paradigm of tissue integrity.” “Increased loading leads to adaptation, whereas decreased loading below a threshold leads to atrophy.” “The same principle likely also holds for scar tissue and immobilization beyond the initial phases of healing could have a detrimental impact on outcome.”

“Mechanobiology is likely important in the healing outcome in tissues such as ligaments, tendons, and related tissues. That is, depriving healing ligaments of mechanical loading likely has a detrimental impact on healing outcome.”

•••••••••

Dr. Schleip and colleagues note (16):

“For this collagen network to attain an almost identical construction of the original tissue, the tissue in this phase of would healing must be confronted with its normal physiological stress.”

“Stress on the tissue should now be slowly increased to push ahead the reconstruction of unstable type III collagen to stable type I collagen and return the tissue to its original stability.”

“Because connective tissue consists predominantly of proteins, the take-up of protein through nutrition is very important.”

“Matrix and cells are found in a continuous dialogue and are dependent on each other.” “The forces on the network of collagen and elastic fibers and ground substance are transferred to the cell membranes via link proteins. The cell is informed by these signals and is stimu­lated to keep synthesizing new matrix components. This rebalances the physiological breakdown of the matrix and the tissue retains its stability and mobil­ity. A reduction in the load stimulus leads as a result to reduced synthesis activity of the cells and thus to a loss of matrix components.”

“This produces a lower level of stability and limited mobility because of the formation of pathological cross links. An important task for the therapist is to apply gradually increasing levels of force without causing pain, in order to promote the healing and regeneration processes and in this way restore mobility and stability.”

•••••••••

Problems and Residual Characteristics

Most healed soft tissue injuries are asymptomatic. However, it is universally accepted that the healed tissue is weaker than the pre-injured tissue. Consequently, acute flare-ups of pain or exacerbations of pain and/or spasm often occur as a consequence of increased use or stress of the once injured but now healed tissues. Good early treatment improves the quality and timing of soft tissue injury. Best early treatment appears to include ice and early controlled motion that does not move the tissues into pain.

The chronic tissue residuals following trauma and healing are histologically provable. Common terminology to describe them includes “scar, fibrosis, fibrosis of repair, adhesions,” etc. A collection of these principles follows:

Dr. Kellett notes (6):

“The micropathology of acute soft tissue trauma has been investigated. Healing of ligaments and soft tissue injuries in general has been shown to occur by fibrous repair (scar tissue) and not by regeneration of the damaged tissue.”

“Normal ligaments are composed of type I collagen, whereas damaged (and healed) ligaments contain a large proportion of immature type III collagen which is deficient in the number of cross-linkages between and within the tropocollagen subunits.”

The remodeled scar is deficient in both content and quality 40 weeks after injury, as there is a plateau in scar collagen concentration at about 70% of normal.

•••••••••

In 1998, Drs. Hildebrand ad Frank note (11):

“Injuries to ligaments induce a healing response that is characterized by the formation of a scar.” This “scar tissue is weaker.”

“Ligament healing is characterized by the formation and remodeling of scar tissue that is weaker than normal ligament owing to alterations in biochemical composition and structural organization.” “The scars have a greater amount of inferior strength tissue compared with that of normal” ligaments.

“The structural strength and stiffness, stress and tissue quality continue to improve up to 12 months after injury, but after that time only relatively small increases are made. However, the material properties of the ligament scar do not return to normal even after 2 years.”

Residual scar tissue behaves with “abnormal biomechanical, biochemical and ultrastructural properties.”

“The return of joint function after injury does not mean that the ligament has healed.”

“Ligament healing in what may be considered to be the best case scenario is characterized by a scar material with inferior tissue quality, with changes in biochemical and histologic properties, that does not regenerate a normal ligament even after 2 years of healing.”

The ligament scar affects the associated joint function.

•••••••••

In 2005, Dr. Hildebrand and colleagues note (14):

“Whereas wound healing generally leads to a repair of the injured site, it does not lead to tissue regeneration. This difference between repair and regeneration has influence on tissues such as ligaments and tendons that function in a mechanically active environment.”

The repair process can lead to a loss of function, primarily from scar tissue, and this can occur in both musculoskeletal and visceral tissue (heart, lung, kidney, liver).

“The remodeling phase is a slow process and is accompanied by alterations not only in matrix remodeling, but also gene expression, cellularity, vascularity, and innervation.” “Because the remodeling phase occurs slowly, and may take months (i.e., skin) or years (i.e., tendon and ligament).”

“Even after protracted time post-injury, the mechanical properties of a scar tissue in a ligament … is still compromised compared with normal.”

“The scar tissue may be functional for most activities even though it is not ‘normal’.” [Fails during high demand activities]

The scar cells in the healing ligament are different from normal cells and therefore the scar is intrinsically different.

‘‘Scar-like’’ tissue is “functionally ineffective.”

“Some tendon and ligament injuries lead to formation of scar tissue that is partially functional, but to regain as much function as possible requires physiotherapy to ‘facilitate’ the return to function after the scar tissue has formed.”

The inflammatory response associated with overt injury or surgery can lead to formation of adhesions, where “the ligament/tendon scar tissue is ‘‘bonded’’ to the surrounding tissue and thus, such restrictions compromise function in situations where movement is required.”

“The size of the wound and the resulting scar tissue has a dramatic impact on the biomechanical outcome.”

“It is readily apparent that wound healing in the adult under the most optimal conditions should be considered tissue repair not regeneration.” “For tissues like a ligament or tendon, the mechanical outcome may be less than ideal, depending on the expectations of tissue use post-injury and the occurrence of side-effects such as adhesions.”

Additionally, Dr. Hildebrand and colleagues discuss factors that impair soft tissue healing. These factors cause some patients to heal slowly or incompletely with more functional residuals. These factors include:

1. Older age
2. Female Sex
3. Genetics
4. Tissue history (prior injuries, scar tissue, and disease states)
5. Diabetes
6. Disc injuries heal poorly, primarily as a consequence of poor blood supply
7. Pregnancy
8. Low Vitamin C levels
9. Menstrual cycle hormonal changes
10. Any reason that deprives the healing tissues from mechanical loading
11. Re-injury of a prior injury or prior tissue that has sustained repetitive stress
12. Excess carbohydrates that increase glycation (AGEs)
13. Any treatment with corticosteroids
14. Anything that exaggerates or prolongs the inflammatory response

•••••••••

Dr. William Walsh and colleagues note (15):

“Musculoskeletal soft tissues tend to heal through formation of relatively weak, disorganized scar tis­sue. Severe ligament sprains can be particularly problematic; even in the best case, there is a fibrotic repair response that remodels over several years, causing scar tis­sue that is structurally and biomechanically inferior to the normal tissue. For most soft tissues, the fibrotic repair process is thought to interfere with the possibility of regeneration.” “Soft tissues typically heal by fibrosis, potentially impairing regeneration.”

“Ligaments take longer to heal than other connective soft tissues, and the repaired ligament tissue is scarlike and inferior to normal ligament tissue both biologically and biomechanically. Furthermore, some ligament-deficient joints subsequently become unstable and can lead to lifelong disability with osteoarthritis.”

“Ligament wounds, even over 2 yr after injury, contain mainly a homogenous population of small-collagen fibrils as commonly observed in scar tissue, with a few patches of normal larger fibrils being observed. These ligaments never obtain their original biomechanical properties.”

These concepts on ligament repair have important applications for chiropractors that treat spinal trauma patients:

Soft tissue healing occurs over a period of 12 months or more. Controlled motion, including the chiropractic adjustment, is the best approach to enhance the quality of ligament healing, especially in the remodeling phase.

Ligaments and tendons heal with scar tissue (repair) as a rule, and not with normal pre-injury tissue (regeneration). This scar tissue causes permanent loss of function. Even healed ligament injuries have residual weakness.

Scar tissue is mechanically functionally inferior to normal tissue. Its inherent weakness makes the tissue prone to failure at previously normal load levels, and subsequent new trauma to scarred tissue will result in greater injury.

Scar tissue (fibrosis) is linked to the intensity of the initial inflammatory response. Consequently, early inflammation control (ice) could improve the timing and quality of healing. Scar tissue, to varying degrees, is remodelable with the application of controlled motion, which I believe includes and even requires chiropractic adjustments.

Lack of symptoms is not synonymous with full healing and functional recovery. A flare-up or exacerbation of pain after the healing process most likely will require another few quick visits to the chiropractor.

•••••••••

SUMMARY:

This review reminds us that it is well established that:

• Whiplash injury chronic pain is primarily generated by injury to the facet joint capsular ligaments.
• Facet joint capsular chronic pain can cause an abnormal psychological profile.
• The abnormal psychological profile caused by chronic facet pain can only be successfully treated if the chronic pain is successfully treated.
• Many studies conclude that litigation (hiring a lawyer) subsequent to an injury is “harmful to recovery.” However, these studies do not evaluate the concept of Reverse Causality, and hence are flawed.
• When Reverse Causality is carefully evaluated, litigation not only does not harm recovery, data suggests it actually improves recovery.

REFERENCES

1. Stearns, ML, Studies on development of connective tissue in transparent chambers in rabbit’s ear; American Journal of Anatomy, vol. 67, 1940, p. 55.
2. Cyriax, James, M.D., Orthopaedic Medicine, Diagnosis of Soft Tissue Lesions, Bailliere Tindall, Vol. 1, 1982.
3. Oakes BW. Acute soft tissue injuries. Australian Family Physician. 1982; 10 (7): 3-16.
4. Roy, Steven, M.D., and Irvin, Richard, Sports Medicine: Prevention, Evaluation, Management, and Rehabilitation, Prentice-Hall, Inc. (1983).
5. Frank C, Amiel D, Woo S, Akeson W; Normal ligament Properties and Ligament Healing; Clinical Orthopedics and Related Research; June, 1985.
6. Kellett J; Acute soft tissue injuries-a review of the literature; Medicine and Science of Sports and Exercise, American College of Sports Medicine, Vol. 18 No.5, (1986), pp. 489-500.
7. Woo, Savio L.-Y.,(ed.), Injury and Repair of the Musculoskeletal Soft Tissues, American Academy of Orthopaedic Surgeons,(1988), p.18-21; 106-117; 151-7;
8. Cohen, I. Kelman; Diegelmann, Robert F; Lindbald, William J; Wound Healing, Biochemical & Clinical Aspects, WB Saunders, 1992.
9. Salter R, Continuous Passive Motion, A Biological Concept for the Healing and Regeneration of Articular Cartilage, Ligaments, and Tendons; From Origination to Research to Clinical Applications, Williams and Wilkins, 1993.
10. Buckwalter J, Effects of Early Motion on Healing of Musculoskeletal Tissues, Hand Clinics, Volume 12, Number 1, February 1996.
11. Hildebrand K, Frank C; Scar Formation and Ligament Healing; Canadian Journal of Surgery; December 1998; Vol. 41; No. 6; pp. 425-429.
12. Kannus P, Immobilization or Early Mobilization After an Acute Soft-Tissue Injury?; The Physician And Sports Medicine; March, 2000; Vol. 26 No 3, pp. 55-63.
13. Majno, Guido and Joris, Isabelle, Cells, Tissues, and Disease: Principles of General Pathology, Oxford University Press, 2004.
14. Hildebrand KA, Gallant-Behm CL, Kydd AS, Hart DA; The Basics of Soft Tissue Healing and General Factors that Influence Such Healing; Sports Medicine Arthroscopic Review September 2005; Vol. 13; No. 3; pp. 136–144.
15. Walsh W; Orthopedic Biology and Medicine; Repair and Regeneration of Ligaments, Tendons, and Joint Capsule; Orthopedic Research Laboratory, University of New South Wales, Sydney, Australia, Humana Press, 2006.
16. Schleip R; Fascia; The Tensional Network of the Human Body; The Scientific and Clinical Applications in Manual and Movement Therapy; Churchill Livingstone, 2012.

In this month’s edition, we’re going to discuss some “intrigue” that has plagued low back treatments—both conservative and aggressive—for many years now.

The intrigue being “WHERE” exactly does the pain generate from? What structure? What neurological mechanism? And with some detective work I think we’ve uncovered some significant findings.

The modern era in the understanding of low back pain that we’re in right now began in 1976 when internationally respected orthopedic surgeon Alf Nachemson published his detailed review (136 references) in the new journal SPINE (1), entitled “The Lumbar Spine: An Orthopaedic Challenge“.

In this article, Dr. Nachemson notes that a staggaring 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 makes a VERY convincing case when he 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, including the primary research completed by Smyth and Wright in 1958 (2). Regarding the work by Smyth and Wright, Dr. Nachemson notes:

“Investigations have been performed in which thin nylon threads were surgically fastened to various structures and around the nerve root. Three to four weeks after surgery these structures were irritated by pulling on the threads, but pain resembling that which the patient had experienced previously could only be registered only from the outer part of the annulus” of the disc.

It had been established in the 1930s that herniation of the lumbar disc could put pressure on the nerve root or the cauda equina, resulting in sciatica. However, Dr. Nachemson in this context is saying something dramatically different;

He’s 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 and not only that, Nachemson claiming the disc to be the most probable source of back pain was both surprising AND revolutionary.

At the time, most authoritative reference texts stated the intervertebral disc was not even innervated with pain afferents and therefore not capable of initiating pain.

As an example, rheumatology professor Malcolm Jayson, MD (editor) in the 1987 text titled The Lumbar Spine and Back Pain, states

“in the mature human spine no nerve endings of any description remain in the nucleus pulposus or annulus fibrosis of the intervertebral disc in any region of the vertebral column.” (3)

A conclusion we now know to be 100% false.

Support for Dr. Nachemson’s contention of disc pain came in 1981 when 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 (4). 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.”

Dr. Bogduk and his team concluded decisively:

“The Lumbar Intervertebral Discs Are Supplied By A Variety Of Nerves.”
and “Clinically, The Concept Of ‘Disc Pain’ Is Now Well Accepted.”

 

Dr. Bogduk returned in 1983 updating his research notes in SPINE, stating more specifically :

“THE LUMBAR INTERVERTEBRAL DISCS ARE INNERVATED

posteriorly by the sinuvertebral nerves, but laterally by

branches of the ventral rami and grey rami communicantes…

The posterior longitudinal ligament is innervated by the sinuvertebral nerves and the anterior longitudinal ligament by branches of the grey rami.

Lateral and intermediate branches of the lumbar dorsal rami supply the iliocostalis lumborum and longissimus thoracis, respectively.

Medial branches supply the multifidus, intertransversarii mediales, interspinales, interspinous ligament, and the lumbar zygapophysial joints.”

“The distribution of the intrinsic nerves of the lumbar vertebral column

systematically identifies those structures that are

potential sources of primary low-back pain.”

Adding to the growing momentum of this “disc-pain” concept… 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 titled (6):

Where Is the Pain Coming From?

 

In this article, Dr. Mooney notes the following:

“Six weeks to 2 months is usually enough to heal any

stretched ligament, muscle tendon, or joint capsule.

Yet we know that 10% of back ‘injuries’ do not resolve

in 2 months and that they do become chronic.”

“Anatomically the motion segment of the back is made up of two synovial joints and a unique relatively avascular tissue found nowhere else in the body – the intervertebral disc. Is it possible for the disc to obey different rules of damage than the rest of the connective tissue of the musculoskeletal system?”

“Persistent pain in the back with referred pain to the leg

is largely on the basis of abnormalities within the disc.”

Chemistry of the disc is based on the relationship between

mucopolysaccharide production and water content.

“Mechanical events can be translated into chemical events related to pain.”

An important aspect of disc nutrition and health is the

mechanical aspects of the disc related to the fluid mechanics.

“Mechanical activity has a great deal to do with the

exchange of water and oxygen concentration” in the disc.

The pumping action maintains the nutrition and biomechanical function of the intervertebral disc. Thus, “research substantiates the view that unchanging posture, as a result of constant pressure such as standing, sitting or lying, leads to an interruption of pressure-dependent transfer of liquid. Actually the human intervertebral disc lives because of movement.”

“The fluid content of the disc can be changed by mechanical activity, and the fluid content is largely bound to the proteoglycans, especially of the nucleus.”

“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. Basic studies and clinical experience suggest that mechanical therapy is the most rational approach to relief of this painful condition.”

“Prolonged rest and passive physical therapy modalities no longer have a place in the treatment of the chronic problem.”

This model presented by Dr. Mooney in this paper goes on to discuss:

The intervertebral disc as the primary source of both back pain and referred leg pain. The disc apparently becomes painful because of altered biochemistry, which sensitizes the pain afferents that innervate it.

Disc biochemistry is altered because of mechanical problems, especially mechanical problems that reduce disc movement.

Therefore, the most rational approach to the treatment of chronic low back pain is mechanical therapy that restores the motion to the joints of the spine, especially to the disc.

Prolonged Rest Is Inappropriate Management

Additional support for the disc being the primary source of back pain was presented by Dr. Stephen Kuslich in the prestigious journal Orthopedic Clinics of North America in April 1991 (7). The title of his article is:

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

These 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. Several of their critically important findings for you include:

“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.”

The lumbar fascia could be “touched or even cut without anesthesia.”

Any pain derived from muscle pressure was “derived from local vessels and nerves, rather than the muscle bundles themselves.”

“The normal, uncompressed, or unstretched nerve root was completely insensitive to pain.”

“In spite of all that has been written about muscles, fascia, and bone as a source of pain, these tissues are really quite insensitive.”

In summary, these authors found that…

The Outer Annulus Is “THE SITE” Of A Patient’s Back Pain.

Past studies that suggest the disc is not an important source of low back pain because nerve endings “are not present” are clearly and overwhelmingly erroneous when you carefully analyzed the most modern literature.

Documented research at no time has demonstrated irritation of a normal or inflamed nerve root to produce low back pain. Back muscles themselves are proven not to be a source of back pain; in fact, the muscles, fascia, and bone are really quite insensitive for pain. The inflamed, stretched, or compressed nerve root is in fact the cause of buttock, leg pain and sciatica, but not back pain.

Very recently in 2006, physician researchers from Japan published in SPINE the results of an extremely sophisticated immunohistochemistry study of the sensory innervation of the human lumbar intervertebral disc (8). The article is titled:The Degenerated Lumbar Intervertebral Disc is Innervated Primarily by Peptide-Containing Sensory Nerve Fibers in Humans

The Japanese researchers note:

“Many investigators have reported the existence of sensory nerve fibers in the intervertebral discs of animals and humans, suggesting that the intervertebral disc can be a source of low back pain.”

“Both inner and outer layers of the degenerated lumbar intervertebral disc are innervated by pain sensory nerve fibers in humans.”

Pain neuron fibers are found in all human discs that have been removed because they are the source of a patient’s chronic low back pain.

The nerve fibers in the disc, found in this study, “indicates that the disc can be a source of pain sensation.”

The information and data offered by these studies from across 30 years of published research in the most highly respected journals CLEARLY and UNEQUIVOCALLY demonstrates that…

The Annulus Of The Intervertebral Disc Is Primarily Responsible For The Majority Of Chronic Low Back Pain.

Above (6), Dr Vert Mooney notes in his Presidential Address to the International Society for the Study of the Lumbar Spine that, “basic studies and clinical experience suggest that mechanical therapy is the most rational approach to relief of this painful [intervertebral disc] condition.”

In Support Of Dr. Mooney’s Perspective, Four Such Studies Are Reviewed Here:

In 1985, Dr. Kirkaldy-Willis, a Professor Emeritus of Orthopedics and director of the Low-Back Pain Clinic at the University Hospital, Saskatoon, Canada, published an article in the journal Canadian Family Physician (9).

In this study, the authors present the results of a prospective observational study of spinal manipulation in 283 patients with chronic low back and leg pain.

All 283 patients in this study had failed prior conservative and/or operative treatment, and they were all totally disabled. These patients were given a “two or three week regimen of daily spinal manipulations by an experienced chiropractor.”

These authors determined a good result from manipulation to be:

“Symptom-free with no restrictions for work or other activities.”

OR

“Mild intermittent pain with no restrictions for work or other activities.”

81% of the patients with referred pain syndromes subsequent to joint dysfunctions achieved the “good” result.

48% of the patients with nerve compression syndromes, primarily subsequent to disc lesions and/or central canal spinal stenosis, achieved the “good” result.

Dr. Kirkaldy-Willis attributed this clinical outcome to Melzack and Wall’s 1965 “Gate Theory of Pain.” He noted that the manipulation improved motion, which improved proprioceptive neurological input into the central nervous system, which in turn blocked pain.

Dr. Kirkaldy-Willis’ conclusion from the study was:

“The physician who makes use of this [manipulation] resource will provide relief for many back pain patients.”

In 1990, Dr. TW Meade published the results of a randomized comparison of chiropractic and hospital outpatient treatment in the treatment of low back pain. This trial involved 741 patients and was published in the prestigious British Medical Journal (10). It was titled:

Low back pain of mechanical origin:

Randomized comparison of chiropractic and hospital outpatient treatment

The patients in this studied were followed for a period between 1 – 3 years. Nearly all of the chiropractic management involved traditional joint manipulation. Key points presented in this article include:

“Chiropractic treatment was more effective than hospital outpatient management, mainly for patients with chronic or severe back pain.”

“There is, therefore, economic support for use of chiropractic in low back pain, though the obvious clinical improvement in pain and disability attributable to chiropractic treatment is in itself an adequate reason for considering the use of chiropractic.”

“Chiropractic was particularly effective in those with fairly intractable pain-that is, those with a history of severe pain.”

“Patients treated by chiropractors were not only no worse off than those treated in hospital but almost certainly fared considerably better and that they maintained their improvement for at least two years.”

“The results leave little doubt that chiropractic is more effective than conventional hospital outpatient treatment.”

 

Most importantly, the above studies indicate that the primary tissue origin of chronic back pain is the intervertebral disc.

This study by Meade notes that the benefit of chiropractic is seen primarily in patients that are suffering from severe chronic pain.

This would suggest that chiropractic manipulation is affecting the pain afferents arising from the disc. A plausible theory to support this is found below… at the end of this presentation.

Also, the Meade study authors definitively note that if all back pain patients without manipulation contraindications were referred for chiropractic instead of hospital treatment, there would be significant annual treatment cost reductions, a significant reduction in sickness days during the following two years, and a significant savings in social security payments.

In 2003, the highly regarded orthopedic journal SPINE published a randomized clinical trial involving the nonsteroidal anti-inflammatory cox-2 inhibiting drugs Vioxx or Celebrex v. needle acupuncture v. chiropractic manipulation in the treatment of chronic neck and back pain (11). The title of the article is: Chronic Spinal Pain: A Randomized Clinical Trial Comparing Medication, Acupuncture, and Spinal Manipulation

In this study chiropractic was over 5 times more effective than the medications and better than twice as effective as needle acupuncture in the treatment of chronic spine pain.

Chiropractic was able to accomplish these clinical outcomes without any reported adverse effects.

One year after the completion of this 9-week clinical trial, 90% of the original trial participants were re-evaluated to assess their clinical status.

The authors discovered that only those who received chiropractic during the initial randomization benefited from a long-term stable clinical outcome. The results of this second assessment were published in 2005 (12).

An important question to consider…

How does joint manipulation reduce chronic back pain arising from the intervertebral disc?

I find that the most plausible explanation is offered by Canadian orthopedic surgeon WH Kirkaldy-Willis in the first edition (1983) of his book titled Managing Low Back Pain.

Dr. Kirkaldy-Willis describes the biomechanics of how the two facet joints form a three-joint complex with the intervertebral disc.

He notes that “motion at one site must reflect motion at the other two.” It is probable that spinal manipulation primarily mechanically affects the facet articulations.

According to Dr. Kirkaldy-Willis, such facet motion would necessarily cause motion in the intervertebral disc. Consistent with the published data noted above, this would improve fluid mechanics of the disc, disperse the accumulation of inflammatory exudates, and initiate a neurological sequence of events that would “close the pain gait.”

In the final conclusion, the outcomes of the clinical trials noted speak for themselves.

References

1) Nachemson, AL, Spine, Volume 1, Number 1, March 1976, pp. 59-71.

2) Smyth MJ, Wright V, Sciatica and the intervertebral disc. An experimental study. Journal of Bone and Joint Surgery [American];40: 1548, pp. 1401-1408.

3) Jayson M, Editor; The Lumbar Spine and back Pain, Third Edition, Churchill Livingstone, 1987, p. 60.

4) Bogduk N, Tynan W, Wilson A. S., The nerve supply to the human lumbar

intervertebral discs, Journal of Anatomy. (1981, 132, 1, pp. 39-56.

5) Bogduk N., The innervation of the lumbar spine. Spine. April 1983;8(3): pp. 286-93.

6) Mooney, V, Where Is the Pain Coming From? Spine, 12(8), 1987, pp. 754-759.

7) 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

8) Ozawa, Tomoyuki MD; Ohtori, Seiji MD; Inoue, Gen MD; Aoki, Yasuchika MD; Moriya, Hideshige MD; Takahashi, Kazuhisa MD; The Degenerated Lumbar Intervertebral Disc is Innervated Primarily by Peptide-Containing Sensory Nerve Fibers in Humans; Spine, Volume 31(21), October 1, 2006, pp. 2418-2422.

9) Kirkaldy-Willis WH, Cassidy JD; Spinal Manipulation in the Treatment of Low Back Pain; Canadian Family Physician, March 1985, Vol. 31, pp. 535-540

10) Meade TW, Dyer S, Browne W, Townsend J, Frank OA; Low back pain of mechanical origin: Randomized comparison of chiropractic and hospital outpatient treatment; British Medical Journal; Volume 300, June 2, 1990, pp. 1431-7.

11) Giles LGF, Muller R; Chronic Spinal Pain: A Randomized Clinical Trial Comparing Medication, Acupuncture, and Spinal Manipulation; Spine, July 15, 2003; 28(14):1490-1502.

12) Muller R, Lynton G.F. Giles LGF, DC, PhD; Long-Term Follow-up of a Randomized Clinical Trial Assessing the Efficacy of Medication, Acupuncture, and Spinal Manipulation for Chronic Mechanical Spinal Pain Syndromes; Journal of Manipulative and Physiological Therapeutics, January 2005, Volume 28, No. 1.

13) Kirkaldy-Willis WH, Managing Low Back Pain, Churchill Livingstone, 1983, p. 19.

Pain perception and psychology are linked. As with the chicken-and-the-egg scenario, a question arises: what comes first?

• Does an abnormal psychological profile cause chronic pain?

Or

• Does chronic pain cause an abnormal psychological profile?

The relationship between the link of pain perception and psychology is particularly important in cases where compensation is involved. It is known that pain afferents fire to the limbic system, affecting one’s emotions and psychological profile (1).

The source of chronic cervical spinal pain, as a rule, is multimodal (2). In 2011, Dr. Nikolai list six:

• Intra-articular Hemorrhage
• Facet Capsular Tear
• Meniscoid Contusion
• Articular Subchondral Fracture
• Fracture of the Articular Pillar
• Disc Tear or Torn From the Vertebral Rim

In 1993, Nikolai Bogduk, MD, PhD, and Charles Aprill, MD (3) were able to show that in 23% of individuals who were suffering from chronic post-traumatic neck pain, the tissue source for the pain was a single cervical zygapophysial (facet) joint. This finding is important because such individuals are ideal for evaluating the relationship between pain and psychology. This finding allowed the research team that includes Barbara Wallis, Susan Lord PhD, and Nikolai Bogduk MD, PhD to investigate the relationship between whiplash pain psychology and organic whiplash pain (4). Their 1997 study was published in the journal Pain, and titled (4):

Resolution of psychological distress of whiplash patients following treatment by radiofrequency neurotomy:

A randomized, double-blind, placebo-controlled trial

The author’s goal was to determine between:

• The psychological model of chronic neck pain following whiplash: whether psychological distress precedes and causes the chronic pain.

or

• The medical model: whether the psychological distress is a consequence of chronic pain.

The authors used the SCL-90-R psychological profile, the McGill Pain Questionnaire, and the visual analogue pain scale to evaluate 17 randomized, double-blind, placebo-controlled patients with a single painful cervical zygapophyseal joint, using percutaneous radiofrequency neurotomy. These 17 patients were found to have a single painful zygapophyseal joint diagnosed by double-blind, placebo-controlled cervical medial branch blocks of the posterior primary rami. The placebo group received the same invasive procedure, but no radiofrequency current was delivered.

These authors note:

• There is little evidence of useful clinical improvement following psychological treatment in these chronic whiplash pain patients. “Even when psychological improvement has been demonstrated, it has not been associated with clinically useful degree of pain reduction, let alone complete relief of pain. At best, psychological interventions enable patients to return to work in spite of their pain.”
• Percutaneous radiofrequency neurotomy is a 3-hour, local anesthetic, operative neuroablative procedure which provides long-term, complete pain relief by coagulating the nerves that innervate the painful zygapophyseal joint. This neurosurgical procedure has been validated in a randomized, double-blind, placebo-controlled study.
• Radiofrequency neurotomy does not effect a permanent cure. It provides long-term analgesia (months to years). Recurrence of the pain is natural as the coagulated nerve heals.

The results of this study were:

• At 3-months post-operative assessment, all patients who were pain free exhibited resolution of psychological distress. In contrast, only one patient whose pain was present at 3-month assessment exhibited improvement in her level of psychological distress. “The association between complete relief of pain and resolution of psychological distress was very strong.”
• “As their original pain recurred, so did their psychological distress, but when successful active neurosurgical treatment again achieved pain relief, the psychological distress was again resolved.”
• “None of the patients received any formal psychological therapy. The only intervention was the operative procedure. Therefore, such changes in the psychological profile as were observed can only be ascribed to the neurosurgical intervention.”
• The results of this study clearly refute the psychological model, which would have predicted that because no psychological intervention was administered, no patient should have exhibited improvement in either their pain or psychological status. “Yet, ten patients exhibited complete resolution of psychological distress.”

These authors concluded:

“This result calls into question the present nihilism about chronic pain, that proclaims medical therapy alone to be ineffectual, and psychological co-therapy to be imperative.”

“All patients who obtained complete pain relief exhibited resolution of their pre-operative psychological distress. In contrast, all but one of the patients whose pain remained unrelieved continued to suffer from psychological distress. Because psychological distress resolved following a neurosurgical treatment which completely relieved pain, without psychological co-therapy, it is concluded that the psychological distress exhibited by these patients was a consequence of the chronic somatic pain.”

••••

Reverse causality refers to a direction of cause-and-effect contrary to a common presumption. Reverse causality is cause and effect in reverse. That is to say the effects precede the cause. The problem is when the assumption is A causes B when the truth may actually be that B causes A.

It is often stated in published studies, by insurance companies, and by their representatives (lawyers, claims adjusters, IME doctors, etc.) that injured patients who seek compensation (ask for compensation, hire a lawyer, etc.)(A), have worse health outcomes and slower recovery rates (B).

However, such adverse health outcomes do not consider or evaluate the concept of Reverse Causality: “slower recovery (B) leads individuals to claim, seek legal advice, and litigate (A).”

In my experience, which is extensive, many injured people feel compelled to seek legal counsel because it is their belief that their insurance company is treating them unfairly, hindering them from obtaining the treatment they need to recover.

••••

The contemporary leaders in the research pertaining to injury compensation, health outcomes, and Reverse Causality is Natalie Spearing and colleagues from the University of Queensland in Australia. In 2011, Natalie Spearing and Luke Connelly published a study in the journal Injury, titled (5):

Is compensation “bad for health”?
A systematic meta-review

These authors performed a systematic meta-review (a “review of reviews”) on this topic, which constituted the most comprehensive review pertaining to compensation and health outcomes through the publication date. Their conclusions include:

“There is a common perception that injury compensation has a negative impact on health status among those with verifiable and non-verifiable injuries, and systematic reviews supporting this thesis have been used to influence policy and practice. However, such reviews are of varying quality and present conflicting conclusions.”

“Systematic reviews that have sought to examine the link between compensation and health outcomes are subject to the inherent methodological weaknesses of observational studies and many do not evaluate the quality of the studies that comprise the dataset for their analysis. Moreover, the extant approaches to health outcomes measurement in this literature may bear a dubious relation to the latent health state of interest, and their use is not validated.”

“There is evidence from one well-conducted systematic review (focusing on one legal process and on health outcome measures) of no association between litigation and poor health outcomes among people with whiplash, contradicting the hypothesis that such an approach contributes to poorer health status.” (6)

The contention that “compensation is ‘bad for health’, should be viewed with caution.”

These authors used 11 studies that met their stringent inclusion criteria. Nine of the 11 reviews concluded that health outcomes are poorer among people seeking or receiving compensation compared to uncompensated individuals. However, all 9 of them were of low quality and suffered from a number of methodological flaws.

In contrast, one review, the Scholten-Peeters (6) study, concluded there is no evidence of an association between compensation and health outcomes. This study was judged by the authors to be the highest quality study in their review. It was published in the journal Pain in 2003.

The studies presented in this review were published in the best journals over a period of decades. Based upon these studies, it can be said:

• Studies that claim that those suffering from chronic problems following whiplash injury do so in hope of gaining financial compensation have methodological flaws.
• The best methodologically done studies show there is no association between litigation/compensation and recovery from whiplash injury.
• Individuals suffering from chronic whiplash injuries do exhibit an abnormal psychological profile. However, their abnormal psychological profile is consistent with the abnormal psychological profile of those who are suffering from other types of organically based chronic pain syndromes.
• Smart individuals attempting to obtain financial compensation are unable to fake the psychological profile of a true chronic pain whiplash sufferer.
• Psychotherapy has not been shown to be effective in treating chronic whiplash pain. This does not undervalue psychotherapy for the treatment of other aspects of whiplash trauma, such as post-traumatic stress disorder, etc.
• Successful treatment of a whiplash patient’s chronic pain normalizes their psychological profile.
• The abnormal psychological profile of chronic whiplash patients is secondary to the chronic pain.
• It is wrong to claim that chronic whiplash symptoms are primarily the consequence of litigation and desire for monetary gain.

••••

This year (2012), Natalie Spearing and colleagues published another on-topic study in the journal Pain, titled (7):

Does injury compensation lead to worse health after whiplash?
A systematic review

In this study, the authors note that the assessment of the relationship between compensation and health outcomes are bogus if that study used “proxy” measures for health. Such an example would include that claiming people’s heath had recovered if that person is able to return to work. Logic and clinical experience notes that such an approach is flawed because clinicians often have injured patients return to work before their clinical syndrome is completely resolved. In fact, often patients miss no work at all while under treatment, yet under these proxy criteria they are considered to be uninjured. One such proxy study (the authors note) is authored by chiropractor David Cassidy and colleagues and published in the New England Journal of Medicine (8).

In this article, Spearing and colleagues introduce the concept of Reverse Causality Bias in the evaluation of the relationship between compensation and health outcome. They note that Reverse Causality Bias occurs when the results of a study are interpreted to mean that whiplash-injured people who hire lawyers to obtain compensation have worse health recovery outcomes; when in fact it may actually mean that whiplash-injured people with greater injuries, more pain and more disability are the ones who seek lawyers to help them obtain the benefits they need.

This study systematically reviewed the evidence on the ‘‘compensation hypothesis’’ using PubMed, CINAHL, EMBASE, PEDro, PsycInfo, CCTR, Lexis, and EconLit. The authors note that many believe that compensation after whiplash injury does more harm than good. There is a view that injury compensation leads to worse health; this is called the “compensation hypothesis.” This view that compensation is harmful has been used to argue for reductions to compensation benefits, to influence judicial decisions, and to advise people that compensation payments will impede their recovery.

Nine of 16 studies used in this review (56%) indicated that compensation adversely influenced health outcomes. However, none evaluated or considered the potential for Reverse Causality Bias in making their conclusions. “Consequently, there is no clear evidence to support the idea that compensation and its related processes lead to worse health.” These authors state:

“It is not possible to tell if statistically significant negative associations reflect a ‘compensation effect,’ or if they simply reflect the pursuit of compensation by those with comparatively worse health and/or a worse prognosis (a selection effect); however, the former is often assumed.”

“Our overall conclusion, that it is currently not possible to determine whether or not compensation leads to worse health after whiplash because reverse causality bias has not been addressed, varies from that of earlier systematic reviews on whiplash as they did not consider this source of bias.”

Claiming “lawyer involvement leads to worse pain,” could also be interpreted as “worse pain increases the likelihood of lawyer involvement.”

“The potential for reverse causality bias is largely unacknowledged in the whiplash literature, and lies similarly unaddressed in studies on other types of compensable injuries.”

“It is important to ascertain whether statistically significant negative associations between compensation-related factors and health do indeed indicate that exposure to these factors leads to worse health, or whether they simply reflect the likelihood that people in comparatively worse health (eg, pain) are more likely to pursue compensation. Unless the latter possibility is considered, decisions to reduce compensation benefits, for example, may inadvertently disadvantage those who are in most need of assistance, which would be an undesirable (and unintended) policy consequence.”

“Only when reverse causality is addressed will it be possible to make well-informed and fair decisions about injury compensation benefits, schemes, and related processes.”

“Research in this field has important implications for the design of injury compensation schemes and the health and well-being of injured people. It is important to raise awareness of the limitations of the existing evidence to avoid ineffectual and potentially harmful policy and judicial decisions.”

••••

Last month (November, 2012), Natalie Spearing and colleagues extended their research on these topics with a study published in the Journal of Clinical Epidemiology, titled (9):

Research on injury compensation and health outcomes:
Ignoring the problem of reverse causality led to a biased conclusion

This study highlights the serious consequences of ignoring Reverse Causality Bias in studies on compensation-related factors and health outcomes. These authors evaluated Reverse Causality using a sophisticated, ingenious, evaluation of compensation claims associated with recovery from neck pain (whiplash) after rear-end collisions. The analysis offered by these authors is extremely mathematical. They note that the standard method used to declare “compensation negatively affects recovery” uses a “standard single equation approach.” However, to assess “reverse causality”, a “simultaneous equation technique” must be used. When the “simultaneous equation technique” is used, the results “tell a different story.”

This study used a source population of 1,174 adults with injuries arising from a rear-end vehicle collision. Of these, 503 agreed to participate in the study. Eighty percent (403/503) developed neck pain within 7 days of collision (early whiplash); 20% (100/503) developed neck pain after 7 days of collision. Sixty-five percent of those with early whiplash symptoms became claimants (265/403), while 35% of those with early whiplash symptoms were non-claimants (138/403). Neck pain at 24 months was selected as the primary health outcome. Neck pain severity was measured using the visual analogue scale (VAS) score (0–100). Higher VAS scores indicate worse pain: a score of 100 represents the worst pain imaginable and zero represents no pain.

These authors state:

“Although it is commonly believed that claiming compensation leads to worse recovery, it is also possible that poor recovery may lead to compensation claims—a point that is seldom considered and never addressed empirically.”

“When reverse causality is ignored, claimants appear to have a worse recovery than non-claimants; however, when reverse causality bias is addressed, claiming compensation appears to have a beneficial effect on recovery.”

Reverse Causality must be evaluated to “avert biased policy and judicial decisions that might inadvertently disadvantage people with compensable injuries.”

“There is a prevailing belief that compensation does more harm than good, and this idea—that claimants are worse off— influences decisions about injury compensation laws.”

An assumed belief is that the lure of compensation prompts individuals to exaggerate subjective symptoms. But, “no studies have examined the effect of compensation payments per se on health.”

In assessing injury outcomes, “reverse causality must also be considered because the causal relationship between compensation factors and health is ambiguous.” “Claiming compensation, lawyer involvement, and litigation, may lead to slower recovery, but it is also possible that slower recovery leads individuals to claim, seek legal advice, and litigate.”

“The consequences for statistical inference of ignoring reverse causality bias are potentially serious: if negative associations between compensation-related factors and health status actually reflect worse health among those pursuing compensation (a rarely considered, but entirely plausible proposition), then decisions to limit access to compensation benefits may do more harm than good.”

“Once reverse causality bias is addressed, people who claim compensation appear to experience a better recovery from neck pain at 24 months compared with non-claimants.”

“The results of this study suggest that compensation claiming may not be disadvantageous to injured parties after all and that it may even have a beneficial effect,” because access to financial assistance and/or treatment may “indeed relieve pain and suffering. This is, after all, one of the motivations for compensating people who have sustained an insult to their health.”

“Neck pain is significantly worse at baseline among claimants compared with non-claimants, which suggests that claims are more likely to be made by individuals whose initial neck pain is worse.”

Reverse causality “is largely overlooked in studies on compensation-related factors.” Yet, this study shows that people with worse health tend to claim compensation.

Policies that restrict access to compensation benefits or legal advice may inadvertently disadvantage people who need financial or legal assistance.

“This study serves as a reminder of the dangers of drawing causal interpretations from statistical associations when the causal framework is ambiguous. It establishes, empirically, that reverse causality must be addressed in studies on compensation-related factors and health outcomes.”

These authors reject the hypothesis that the decision to claim compensation negatively affects recovery.

•••••••••

SUMMARY:

This review reminds us that it is well established that:

• Whiplash injury chronic pain is primarily generated by injury to the facet joint capsular ligaments.
• Facet joint capsular chronic pain can cause an abnormal psychological profile.
• The abnormal psychological profile caused by chronic facet pain can only be successfully treated if the chronic pain is successfully treated.
• Many studies conclude that litigation (hiring a lawyer) subsequent to an injury is “harmful to recovery.” However, these studies do not evaluate the concept of Reverse Causality, and hence are flawed.
• When Reverse Causality is carefully evaluated, litigation not only does not harm recovery, data suggests it actually improves recovery.

REFERENCES

• Kandel ER, Schwartz JH, Jessell TM; Principles of Neural Science, Elsevier; 2000.
• Bogduk N; On Cervical Zygapophysial Joint Pain After Whiplash; Spine December 1, 2011; Volume 36, Number 25S, pp. S194–S199.
• Bogduk N, Aprill C; On the nature of neck pain, discography and cervical zygapophysial joint blocks; Pain; 54; 1993, pp. 213-217.
• Wallis, BJ, Lord, SM and Bogduk, N (1997). “Resolution of psychological distress of whiplash patients following treatment by radiofrequency neurotomy: a randomized, double-blind, placebo-controlled trial.” Pain; 73: pp. 15-22.
• Spearing NM, Connelly LB; Is compensation “bad for health”? A systematic meta-review; Injury; January 2011; Vol. 42; No. 1; pp. 15-24.
• Scholten-Peeters GGM, Verhagen AP, Bekkering GE, van der Windt DAWM, Barnsley L, Oostendorp RAB, Hendriks EJM; Prognostic factors of whiplash-associated disorders: A systematic review of prospective cohort studies; Pain ; July 2003, Vol. 104, pp. 303–322.
• Spearing NM, Connelly LB, Gargett S, Sterling M; Does injury compensation lead to worse health after whiplash? A systematic review; Pain; June 2012; 153; No. 6; pp.1274-82.
• Cassidy JD, Carroll LJ, Côté P, Lemstra M, Berglund A, Åke Nygren A; Effect of Eliminating Compensation for Pain and Suffering on the Outcome of Insurance Claims for Whiplash Injury; New England Journal of Medicine; April 20, 2000; Vol. 342; No. 16; pp. 1179-1186.
• Spearing NM, Connelly LB, Nghiem HS, Pobereskin L; Journal of Clinical Epidemiology; November 2012; Vol. 65; No. 11; pp. 1219-1226.

Upright posture is a first class lever mechanical system, such as a teeter-totter or seesaw (1, 2).
 The fulcrum of a first class lever is the place where the force is the greatest: if excessively heavy objects are placed on both ends of the teeter-totter, it will break in the middle, at the fulcrum. In the spine, the fulcrum of the first class lever is the vertebra. Approximately 60% of weight is born by the vertebral body/intervertebral disc complex, and the other 40% is shared between the two facet joints. This means that when the first class lever of upright posture is altered, for any reason, there is an increased mechanical load born by the fulcrum, i.e. the spinal intervertebral discs and facet joints. Such increased mechanical loads accelerate degenerative joint disease (1, 3). In their 1990 book Clinical Biomechanics of the Spine (2), White and Panjabi state:

“The load on the discs is a combined result of the object weight, the upper body weight, the back muscle forces, and their respective lever arms to the disc center.”

Note the representative drawing from their text below; once again, the “Disc Load” is the fulcrum:

Classic events that alter the upright postural mechanical system include postural distortions, lifting ergonomics (1, 4), and weight problems (2). Weight problems are the primary point of this article.
In their pioneering reference text Clinical Biomechanics of the Spine, Augustus White, MD, and Manohar Panjabi, PhD, also show (2) that when a person gains abdominal weight, the first class lever system of upright posture is altered in such a manner that the intervertebral disc and facet joints bear significantly more weight. To counterbalance the weight, the muscles on the other side of the fulcrum (spine) must constantly contract with more force, or the person would fall forward. The black arrow attached to the posterior spinal elements represents the muscle contraction.

This constant muscle contraction with more effort, creates muscle fatigue and myofascial pain syndromes. Rene Cailliet, MD states “This increase [in muscle tension] not only is fatiguing, but acts as a compressive force on the soft tissues, including the disk.” (1).

Obesity is linked to numerous health outcomes and disease risk factors, including hypertension, heart disease, stroke, cancer, diabetes, dementia, and arthritis. Simply stated, joints that have to bear more weight wear out at an accelerated rate. As noted by Drs. White and Panjabi, additional weight is not carried symmetrically; people tend to gain weight in their abdomen. This essentially is the equalivent of having a “heavy kid” on one end of the teeter-totter. To balance, the muscles on the opposite side of the fulcrum (the posterior paraspinal muscles) must increase their tension or the subject would fall forward onto their face.

Rene Cailliet explains how the constant contraction in the counterbalancing muscles creates a cascade that leads to muscle fatigue, inflammation, fibrosis, and eventually to chronic musculoskeletal pain syndromes (5):

 

It is the accelerated degeneration of the spinal discs and facet joints (the spinal fulcrum) that are of particular important concern.

•••••••••

The classifications of being overweight or obese are based on a person’s Body Mass Index (BMI). The BMI is calculated using pounds and inches using this formula (6):

[(weight in pounds) / (height in inches X height in inches)] X [703]

As an example, a 6 foot (72 inches) person weighing 200 pounds:

[(200) / (72 X 72)] X [703] =

[(200) / (5184)] X [703] = 27.1 (overweight, see below)

It is not necessary to do this math in calculating a person’s BMI; one can simply go to countless web pages on the internet and there are available free BMI calculators. All one has to do is plug in their numbers and the math is automatically done.

Although the BMI is controversial, it is still used in assessing weight issues, as follows:

18.5 – 24.9 Normal

25.0 – 29.9 Overweight

30.0 – and up Obese

40.0 – and up Severely Obese (more than 100 pounds overweight)

Our nation was stunned when official tabulations indicated that 69% of American adults are overweight or obese (7). The national shock deepened when these numbers were soon revised, predicting that these rates would essentially double in the next 17 years, by 2030 (8). In our heaviest state, Mississippi, it is estimated that by 2030, 67% of adults will be obese (8). Economically, Mississippi is also our poorest state, attesting to the irony that our economically poorest state is also our heaviest. The national disbelief continued when it was understood that severe obesity rates (BMI over 40, which is more than 100 pounds overweight) is skyrocketing (9).

•••••••••

Is there a link between poverty and weight gain? What is happening to cause such extreme weight gain in our population?

•••••••••

Obesity rates affect chiropractic clinical practice in a number of ways. The most obvious is that obesity increases degenerative joint disease of weight bearing joints, including the disc and facets of the spine. These changes are chronic and often linked to chronic pain syndromes; they are often debilitating. There is no “cure” for the joint destruction.

Science writer Gary Taubes expresses a leading theory explaining America’s skyrocketing obesity rates. Educated at Harvard and Stanford, Taubes is currently a Fellow at the University of California, Berkeley. His recent writings on the obesity topic include Good Calories, Bad Calories (2008) (10), Why We Get Fat (2011) (11), and the cover article in the political magazine Newsweek (5/14/12) (12).
Taubes presents compelling evidence that obesity is linked to insulin. The more insulin produced in response to a consumed food (insulin response), the fatter the person becomes. The insulin response to a consumed food is called the Glycemic Index.

Taubes first book on this subject, Good Calories, Bad Calories (2008), presents 600 pages of compelling and often complex physiology and evidence in explaining the insulin-obesity connection. Perhaps the key premise, although grossly oversimplified, is as follows:

• Fat cells become fatter when more fat enters the cell than leaves the cell.
• The “door” that lets fat into the cell is controlled by an enzyme called lipoprotein lipase.
• The “door” that lets fat leave the cell is controlled by an enzyme called hormone sensitive lipase.
• Both enzymes (lipoprotein lipase and hormone sensitive lipase) are controlled by insulin.
• Insulin up-regulates the production of lipoprotein lipase. This opens the “door” to the fat cell and more fat enters the cell. The fat cell becomes fatter.
• Insulin down-regulates the production of hormone sensitive lipase. This means that the “door” that lets fat out of the fat cell is closed, and the fat cannot escape.
• The fat cell can only hold so much fat. When capacity is reached, the cell responds by dividing, doubling the number of fat cells.
• With continued exposure to insulin, the process continues. As biochemist Dr. Barry Sears says (13):

“It is excess insulin that makes you fat and keeps you fat.”

In his 2009 book The End of Overeating, Physician David Kessler, MD, presents a remarkable discussion pertaining to human dietary habits (14). Dr. Kessler is the former FDA (Food and Drug Administration) commissioner, holding the job for both presidents George HW Bush (1990) and Bill Clinton. Dr. Kessler is a Harvard educated pediatrician, and also holds a law degree from the University of Chicago. Dr. Kessler’s book integrates anthropology, biology, biochemistry, neurology, neurophysiology and physiology. His basic premise is that humans evolved with neurophysiological addictions that help to ensure the survivability of the human species. These addictions primarily center on sex and the neurotransmitter dopamine: humans are biologically addicted to dopamine; thinking about sex and participating in sex increases the production and release of dopamine. Humans are addicted to the pleasurable sensations attributed to this dopamine release.

Experiences other than sex can also increase the production and release of dopamine. Consequently, these experiences are also addicting. Examples include illegal drugs like cocaine, chocolate, and sadly, refined carbohydrates that have a high Glycemic Index.

If one is addicted to the increased production and release of dopamine as a consequence of the consumption of high Glycemic refined carbohydrates, one will constantly consume such foods, often not understanding that their consumption and overconsumption is actually a brain neurochemical addiction. Such habits constantly elevate systemic insulin levels. Lipoprotein lipase enzyme up-regulation pushes fat into the fat cells. Hormone sensitive lipase shuts the “door” so that the fat cannot escape. The person becomes fatter.

In his 2011 book The Sugar Barons, Matthew Parker indicates how the sugar barons of centuries ago exploited this human sugar-refined carbohydrate-dopamine addiction to become fabulously wealthy (15). Apparently, contemporary food producers and suppliers are continuing this exploitation. A few hundred years ago the typical American consumed 5 pounds of sugar. Today average sugar consumption is 160 pounds per American per year (16).

•••••••••

In 1968, America was at the height of the Vietnam War. Protesters and rioters were dogging the Democratic National (presidential) Convention in Chicago. The population of planet earth was about 3.5 billion people. And a Stanford University Professor named Paul Ehrlich wrote a book titled The Population Bomb (17). Paul Ehrlich (born May 29, 1932) is an American biologist and educator who is the Bing Professor of Population Studies in the department of Biological Sciences at Stanford University and president of Stanford’s Center for Conservation Biology. His book is subtitled:

“Population Control or Race to Oblivion”

“While you are Reading These Words, Four People will Have Died from Starvation. Most of them Children.”

Dr. Ehrlich’s prediction of mass human starvation as a consequence of exploding human populations never happened. Apparently, Dr. Ehrlich did not know that a man was already on the job of preventing such a disaster, and had been working on the solution since 1944. Norman Borlaug was plant biologist and geneticist from the University of Minnesota. Paul Ehrlich was not up on Borlaug’s research. Through genetic manipulation and the use of powerful synthetic fertilizers, Borlaug was able to significantly increase crop yields. His efforts and success at feeding the world earned him the Nobel Peace Prize in 1970, two years after Paul Ehrlich’s book came out. Norman Borlaug died in 2009 at age 95. The human population has doubled, to 7 billion people.

There is concern that Norman Borlaug’s successes may be temporary, having delayed the inevitable. Paul Ehrlich certainly believes as much. Also, Borlaug’s farming methods have created other ecological disasters: damage done by chemical runoff from tons of synthetic fertilizers pollute waterways around the globe and create huge “dead zones,” where no living thing can exist.

Another consequence of Norman Borlaug’s genetic manipulation is important for this article: obesity. People around the world, even our most poor, are gaining weight at an alarming rate. A detailed explanation for this phenomenon is found in the 2011 book Wheat Belly, by cardiologist William Davis, MD (18).

Dr. Davis explains that the unique genetic manipulation of wheat by Norman Borlaug included a process of chromosomal addition called polyploidy. This resulted in a new modern wheat that is 90% carbohydrate. Sadly the carbohydrate in this new wheat is called amylopectin-A, a carbohydrate that has an extremely high Glycemic Index. Although Norman Borlaug’s efforts resulted in increased crop yields, improved harvesting efficiency, and desirable palliative and baking aesthetics, modern wheat’s high Glycemic Index is being linked to obesity and all of its related health problems (hypertension, heart disease, stroke, cancer, diabetes, dementia, arthritis, etc.). Dr. William Davis states:

“The amylopectin-A of wheat products, complex or no, might be regarded as a super-carbohydrate, a form of highly digestible carbohydrate that is more efficiently converted to blood sugar than nearly all other carbohydrate foods, simple or complex.”

Obesity is a global problem. Internet searches indicate that global consumption of wheat is presently 356,218 thousand metric tons per year (19). World trade in wheat is greater than for all other crops combined. Dr. Davis ends his book with this question:

“This idea that wheat is not only making people ill, but killing some of us—some quickly, others more slowly—raises unsettling questions: What do we say to the millions of the people in Third World countries who, if deprived of high-yield wheat, might have less chronic illness but greater likelihood of near-term starvation? Should we just accept that our far-from-perfect means justifies the net reduced mortality end?”

•••••••••

SOLUTIONS

Losing weight is never easy. I prefer to make a custom program for my patients based upon specifics of their lives and habits and health. However, I use these three strategies on all of our overweight patients. They are simple and effective:

• Do not eat refined carbohydrates; this is the most important rule: Sugary drinks including juice, all sugary foods, breads, pastas, potatoes, rice.
• Do not consume grains because they are carbohydrates. The worst grain is wheat, even whole wheat, because of its high Glycemic Index amylopectin-A.
• Do not drink your calories.

Dr. Barry Popkin is a distinguished Professor of Global Nutrition at the University of North Carolina. In his 2009 book titled (20), he notes:

The World Is Fat The Fads, Trends, Policies, And Products That Are Fattening The Human Race

“The world has become fat in just a few decades.”

“Ultimately, widespread obesity and the chronic diseases that contribute to the bulk of deaths in the world are less a result of poor individual dietary choices than the consequences of a high-tech, interconnected world in which governments and multinational corporations have extraordinary power to shape our everyday lives.”

“Man ate and drank in the healthiest manner possible during the Upper Paleolithic period [beginning about 40,000 years ago], when humans were nomadic hunter-gatherers.” “About 50%-80% of food came from plants and 20%-50% from animals.” “People living at this time consumed no grains, and no dairy products other than breast milk.”

“So, on one hand, we have much cheaper beef, poultry, corn, soybeans, and sugar. But on the other, this has occurred at the expense of healthy plant foods—particularly fruits and vegetables, whose relative cost is great compared to [subsidized] fats, sugars, and meats in today’s marketplaces. The results for all of us—not only American but around the globe—have been devastating.”

“Today, we’re awash in highly refined sugar and grains.”

“Nothing has contributed more to our weight gain than the clash between our drinking habits and our biology.” “We drink a lot of our calories, but we don’t cut our food intake as a result.” “The average American gets over 450 calories a day from beverages.”

“My [Popkin] favorite way to help people lose weight is to look at what they drink over the course of a typical day.” “The top 40% of caloric beverage drinkers in the US consume over 760 calories a day from beverages.” “It would be difficult for a person to be heavy if he or she drank only water, consumed a small amount of added sugar in foods, ate lots of fruits and vegetables, and ate no fried foods. Of course, one needs also to be physically active.”

Nutrition expert Marion Nestle from New York University agrees with Dr. Popkin, stating in her 2012 book Why Calories Count (21):

“Don’t Drink Your Calories”

Both Dr. Popkin and Dr. Nestle indicate that satiety comes from eating, not drinking. If one eliminates calories from drink, food intake will not increase. The reduced calories from not drinking them will cause weight loss, and the patient will not feel hungry, they will still achieve satiety.
Even modest loss of weight significantly helps in the management of our musculoskeletal patients.

REFERENCES

1. Cailliet R; Low Back Pain Syndrome, 4^th edition, F A Davis Company, 1981.
2. White AA, Panjabi MM; Clinical Biomechanics of the Spine, Second Edition, Lippincott, 1990.
3. Garstang SV, Stitik SP; Osteoarthritis; Epidemiology, Risk Factors, and Pathophysiology; American Journal of Physical Medicine and Rehabilitation; November 2006, Vol. 85, No. 11, pp. S2-S11.
4. Oschman J; Energy Medicine; Churchill Livingstone; 2000.
5. Cailliet R; Soft Tissue Pain and Disability; 3^rd Edition; F A Davis Company, 1996.
6. Mercola J; Sweet Deception; Nelson Books; 2006.
7. Hellmich N; Obesity rate may hit 42% by 2030; USA Today; May 8, 2012.
8. Hellmich N; State obesity rates could soar by 2030; USA Today; September 19, 2012.
9. Hellmich N; Percentage of severely obese adults skyrockets; USA Today; October 2, 2012.
10. Taubes G; Good Calories, Bad Calories: Challenging the Conventional Wisdom on Diet, Weight Control, and Disease; Anchor Books; 2008.
11. Taubes G; Why We Get Fat and What to do About It; Anchor Books; 2011.
12. Taubes; “The new obesity campaigns have it all wrong”; Newsweek; 5/14/12; pp. 32-36.
13. Sears B; Toxic Fat: When Good Fat Turns Bad; Thomas Nelson; 2008.
14. Kessler D; The End of Overeating, Taking Control of the Insatiable American Appetite; Rodale; 2009.
15. Parker M; The Sugar Barons: Family, Corruption, Empire, and War in the West Indies; Walker & Company; 2011.
16. O’Connell J; Sugar Nation: The Hidden Truth Behind America’s Deadliest Habit and the Simple Way to Beat It; Hyperion; 2010.
17. Ehrlich P; The Population Bomb; Sierra Club; 1969.
18. Davis W; Wheat Belly; Rodale; 2011.
19. http://www.nationmaster.com/graph/agr_gra_whe_con-agriculture-grains-wheat-consumption.
20. Popkin B; The World Is Fat: The Fads, Trends, Policies, And Products That Are Fattening The Human Race; Avery, 2009.
21. Nestle M, Nesheim M; Why Calories Count, From Science to Politics; University of California Press; 2012.

Pain is a brain cortical event. Pain does not exist in a back or neck or foot. Pain is perceived by brain cortical neurons. Any intervention that reduces pain is altering the electrical signal depolarization of brain cortical pain perceiving neurons. As stated by Drs. Heidi Haavik-Taylor and Bernadette Murphy in 2007 (8):

“Spinal manipulation is a commonly used conservative treatment for neck, back, and pelvic pain.”

“The effectiveness of spinal manipulation in the treatment of acute and chronic low back and neck pain has been well established by outcome-based research.”

In 2011, Ogura and colleagues state (9):

“Chiropractic spinal manipulation is an alternative treatment for back pain.”

“Research on chiropractic spinal manipulation has been extensively performed worldwide, and its efficacy on musculoskeletal symptoms has been well documented.”

••••

Spinal manipulation has been used to treat a variety of syndromes for millenniums. In his 1982 book, orthopedic surgeon James Cyriax, MD, presented evidence of spinal manipulation being performed 2000 years ago in Thailand, 2000 years ago in Libya, and 2300 years ago in Mexico. He also presents early evidence from Turkey and Italy (1).

Sophisticated refinements of spinal manipulative diagnostics and techniques began in 1895 with the beginning of chiropractic as a profession. Soon thereafter, these spinal manipulative diagnostic and adjustive techniques were being taught throughout the United States in chiropractic colleges.

State licensure for the practice of chiropractic began in Kansas in 1914; the final state to license chiropractic was Louisiana in 1974.

In the early 1970s, the United States Department of Education (actually is was HEW back then, for Health, Education, and Welfare) recognized the Council on Chiropractic Education as an accrediting agency for chiropractic education. Along with this recognition came reimbursement under Medicare. Today chiropractic services are recognized and reimbursed by Medicare, Veteran’s Affairs (military), Worker’s Compensation, Personal Injury (automobile insurance), and most private health insurance policies.

Cooperation between the chiropractic profession and the medical profession struggled until the final verdict of the chiropractic antitrust lawsuit against the American Medical Association concluded in 1987. Since then essentially all chiropractors work closely with medical providers, referring patients between them in the best interest of the patient’s well being.

••••

In chiropractic’s infancy, public health officials and legislative bodies noted that people under chiropractic care often had improvement of problems that were not considered to be musculoskeletal in origin. Specifically, in the 1920s and the 1930s, public health officials and legislative bodies started to document improvement of brain function in mentally ill patients who came under chiropractic care.

For example, in 1931, the Kentucky House of Reform presents a series of 244 adolescent boys who were incarcerated by the State of Kentucky because of criminal or behavioral problems in the year 1931 (2). The report documents that “almost 100 per cent have shown improvement in conduct, and “144 of our 244 patients have been paroled since we have been giving them Chiropractic treatment.”

The Report states:

“IN ADDITION TO REGULAR PHYSICIANS EMPLOYED AT THE INSTITUTION WE HAVE HAD THE SERVICES OF CHIROPRACTORS. ALLOW ME TO SAY THAT I FEEL THE FINE SHOWING IN THE NUMBER OF PROMOTIONS AND DISMISSALS FROM THE INSTITUTION IS LARGELY ATTRIBUTABLE TO THE VERY EXCELLENT WORK DONE BY THE CHIROPRACOTORS WHO HAVE ALMOST DAILY LOOKED AFTER THE HEALTH AND GENERAL WELFARE OF THESE BOYS.” [these words were capitalized in the reference]

Another example is the legal briefs presented to the 1935 session of the North Dakota Legislature by the Honorable Judge A.W. Ponath (3). Judge Ponath was County Judge of the Probate Court of Richland County, Wahpeton, North Dakota. Judge Ponath’s legal briefs present 44 cases where mentally ill patients were treated chiropractically in the Jamestown State Insane Asylum (North Dakota). Twenty-seven of the 44 cases “have either been cured or sufficiently recovered so that they can remain at home and resume their former responsibilities [61%].” Judge Ponath notes that these “patients who had for the most part had already spent considerable time in asylums or sanatoriums,” and “in many cases had been declared incurable” by Medical Authorities. Judge Ponath notes that 70-75% of such institutionalized persons are doomed to an asylum prison for life.

How are such claims biologically possible? What are the biologically plausible explanations for such observations?

••••

The science of chiropractic (and traditional osteopathy) advanced significantly as a consequence of the efforts of Irvin M Korr, PhD (1909-2004, age 94). It is rare for any person to have their obituary included in the National Library of Medicine database, yet Dr. Korr’s can be found twice (4, 5).

Dr. Korr was a graduate of the University of Pennsylvania and he earned his doctorate in physiology at Princeton University. His obituary states (5):

Dr. Korr “spent decades adding scientific legitimacy, through experimentation and publication, to the clinically based practice of osteopathy. Much of their earlier work center on demonstrating the hyperarousal of the sympathetic nervous system associated with what was then termed the osteopathic lesion.”

Dr. Korr has 51 articles in a PubMed search of the US National Library of Medicine, spanning the years 1946-2002. Decades of Dr. Korr’s research, experimentation and publications are summarized in his 1979 article titled (6):

The spinal cord as organizer of disease processes:
Hyperactivity of sympathetic innervation as a common factor is disease

Dr. Korr reviews the evidence showing that somatic musculoskeletal problems, especially increased muscle tone that reduce motion and create stiffness, influence the sympathetic nervous system. In summary, spinal stiffness caused sympathetic excitation, vasoconstriction, and therefore reduced blood delivery. The region of spinal stiffness would determine the region of sympathetic excitation and vasoconstriction.

••••

Dr. Korr’s physiological explanations were enhanced significantly in 1997 with the work of Hongxing Jiang, PhD, and colleagues from the Department of Surgery, University of Alberta, Edmonton, Canada. Their article was published in the journal Spine, and titled (7):

Identification of the Location, Extent, and Pathway of Sensory Neurologic Feedback After Mechanical Stimulation of a Lateral Spinal Ligament in Chickens

By immunohistochemically locating the sites of Fos protein production in neuronal cell bodies, Dr. Jiang and colleagues were able to trace the location, extent, and pathways of sensory feedback after the mechanical stretching of a lateral spinal ligament. The presence of Fos indicated the physiological neurological chain cascade that was initiated by a mechanical input into a single spinal ligament.

The results showed that a mechanical input to the intertransverse ligament would stimulate the following sequence of neurons:

• The dorsal root ganglia at the level of stimulation, at the level above stimulation, and at the level below stimulation (therefore at 3 levels). This shows that a carefully applied mechanical sensory input enters the spinal cord a three adjacent spinal levels.
• The intermediate gray matter of the spinal cord at the level of stimulation as well as the spinal cord level above and below the site of stimulation. This is quite important. The intermediate gray matter of the spinal cord is located in the seventh layer of the spinal grey matter (lamina VII). It is also known that the second order neuron for mechanical afferentation has cell bodies in the seventh layer of the spinal grey matter (lamina VII), so this finding makes logical sense. It also known that the pre-ganglionic neurons of the sympathetic branch of the autonomic nervous system are located in the intermediate gray matter of the spinal cord.
• The sympathetic chain ganglia, once again at the level of stimulation as well as the spinal cord level above and below the site of stimulation. This is most important because is confirms the writings of Dr. Korr, confirming that there is a communication between spinal mechanical function and the sympathetic nervous system. This concept is used below as a physiological influence on brain function (9).
• The combined nucleus cuneatus and gracilis in the medulla oblongata. This indicates that spinal mechanical function influences the brainstem.
• The vestibular nuclei, also of the medulla oblongata. This indicates that spinal mechanical function also influences balance and muscle tone.
• The thalamus. This is very important to this discussion as the thalamus is in the brain. The thalamus is the pre-synaptic integrated pool of neurons that control much of brain cortical function. The authors did not assess brain cortical Fos production, a shortcoming that they self-criticize.

Dr. Jiang and colleagues note that spinal ligaments are not “simple mechanical constraints across joints that provide tension when stretched.” Additional functional roles for spinal ligaments include the coordination of muscle tone around joints and to provide a neurologic feedback mechanism to enhance joint stability. They state:

“In light of these results it is now thought that ligaments do more than act as simple mechanical links between bones; they also may provide important proprioceptive feedback as part of a neurologic protective mechanism for the ligaments themselves and for the joints they span.”

In this study, Dr. Jiang and colleagues note that spinal ligaments are richly innervated with mechanoreceptors and nociceptors. The mechanoreceptors function as initiators of feedback pathways that include the spine, the brain stem, the brain and the sympathetic nervous system. These authors state:

“The results of the current study have shown that mechanical stretching of an important lateral spinal ligament in chickens produced a barrage of sensory feedback from several levels of the spinal cord and responses from the contralateral side of the cord at equivalent levels. Further, the pathway of the sensory input can be traced to include nerve cell bodies in the dorsal root ganglia, the sympathetic ganglia, the intermediate horn of the spinal cord, the cuneatus and gracilis nuclei of the medulla oblongata, the vestibular nuclei, and the thalamus.”

From Jaing, (7):

••••

Dr. Korr’s work was further enhanced in 2007 with the work of Heidi Haavik-Taylor and Bernadette Murphy from the University of Auckland. New Zealand. Published in the journal Clinical Neurophysiology and titled (8):

Cervical spine manipulation alters sensorimotor integration:
A somatosensory evoked potential study

Drs. Haavik-Taylor and Murphy recorded the neurophysiological effects of cervical spine manipulation to dysfunctional cervical joints using brainstem and cortical somatosensory evoked potentials (SEPs) in 12 subjects. They also recorded these electrical signals in a control group (also 12 subjects) who were passively mobilized but not manipulated.

Results show a significant change in the amplitude of parietal (sensory) and frontal (motor) SEP components following the single session of cervical spine manipulation. No SEP changes were observed in the passive head movement control condition. The authors state:

“This study suggests that cervical spine manipulation may alter cortical somatosensory processing and sensorimotor integration.”

“These findings may help to elucidate the mechanisms responsible for the effective relief of pain and restoration of functional ability documented following spinal manipulation treatment.”

“The passive head movement SEP experiment demonstrated that no significant changes occurred following a simple movement of the subject’s head. Our results are therefore not simply due to altered input from vestibular, muscle or cutaneous afferents as a result of the chiropractor’s touch or due to the actual movement of the subjects head. This therefore suggests that the results in this study are specific to the delivery of the high-velocity, low-amplitude thrust to dysfunctional joints.”

“Spinal manipulation of dysfunctional joints may modify transmission of neuronal circuitries not only at a spinal level but at a cortical level, and possibly also deeper brain structures such as the basal ganglia.”

The spinal manipulation in this study was applied to dysfunctional cervical joints, as determined by a “registered chiropractor.”

The clinical evidence for joint dysfunction includes:

• Tenderness on joint palpation.
• Restricted intersegmental range of motion.
• Palpable asymmetry of intervertebral muscle tension.
• Abnormal or blocked joint play and end-feel.
• Sensorimotor changes in the upper extremity.

“The most reliable spinal dysfunction indicator is tenderness with palpation of the dysfunctional joint.” To assess joint dysfunction, cervical range of motion also has good reliability. Therefore, in this study, cervical spinal dysfunction was defined as having both restricted intersegmental range of motion and tenderness to palpation of the restricted joint.

This study documents cortical brain changes as a consequence of cervical spinal adjusting.

••••

Late last year (December 2011), a study was published in the PubMed indexed journal Alternative Therapies Health Medicine, titled (9):

Cerebral metabolic changes in men
after chiropractic spinal manipulation for neck pain

The authors are from the Division of Cyclotron Nuclear Medicine, Tohoku University (Graduate School of Medicine), Sendai, Japan. I believe that their work integrates that of Korr, Jiang, and Haavik-Taylor/Murphy.

The authors cite 9 studies that have found that spinal dysfunction affects the autonomic nervous system. This is in agreement with the studies of Korr (6) and Jiang (7). They note that the sympathetic branch of the autonomic nervous system controls the diameter of the arterial system. Increased sympathetic tone would cause vasoconstriction, reducing the delivery of glucose and thereby reducing the uptake metabolism of glucose into ATP energy.

Consequently, the authors created a radioactive analog of glucose (FDG = 18F-labeled flurodeoxyglucose), which is an excellent imaging marker of brain glucose consumption (brain metabolic activity).

Positron emission tomography (PET) scan is a powerful neuroimaging technique to investigate neuronal activity in the human brain, including the uptake of glucose for metabolism. Using PET and FDG, the authors evaluated brain regions in 12 men before and after chiropractic spinal adjusting. This is the first chiropractic study to examine regional cerebral metabolism using positron emission tomography (PET).

Results from this study include:

• Questionnaires indicated lower stress levels and better quality of life following chiropractic spinal manipulation.
• A significantly lower visual analog scale (VAS) was noted after chiropractic spinal manipulation.
• Cervical muscle tone decreased after chiropractic spinal manipulation.
• Salivary amylase was decreased after chiropractic spinal manipulation. Salivary amylase is a marker for sympathetic tone; consequently, sympathetic tone was decreased after chiropractic spinal manipulation.

The authors concluded that the spinal adjustment improved mechanical function, reduced neck pain, inhibited the sympathetic nervous system, improved brain blood flow, enhanced brain glucose utilization, improving brain function. Importantly for this discussion, the authors clearly document improved brain function in the limbic system. These authors state:

“The results of this study suggest that CSM affects regional cerebral glucose metabolism related to sympathetic relaxation [inhibition] and pain reduction.”

“In summary, the present study demonstrated sympathetic relaxation [inhibition] and corresponding regional brain metabolic changes, as well as reduced muscle tone and decreased pain intensity following a chiropractic spinal manipulation.”

The chart below summarize their findings:

Cerebral metabolic changes in men after chiropractic spinal manipulation for neck pain

Assessment	After Chiropractic Spinal Adjustment	Interpretation
Stress Response Scale = SRS-18	“Significantly Lower”	Significantly reduced stress secondary to sympathetic inhibition
EORTC QLQ-C30	“Significantly Lower”	Significantly improved quality of life
Visual Analog Scale = VAS	“Significantly Improved” [reduced]	Significantly reduced stress secondary to sympathetic inhibition
Cervical (Trapezius) Muscle Tone	“Significantly Improved” [reduced]	Secondary to sympathetic inhibition (Hubbard study, Spine, 1993)
Salivary Amylase	“Significant Decrease”	Secondary to sympathetic inhibition
Inferior Prefrontal Cortex	Increased Glucose Metabolism	Secondary to sympathetic inhibition
Middle Temporal Gyrus [limbic system]	Increased Glucose Metabolism	Secondary to sympathetic inhibition
Anterior Cingulate Cortex [limbic system]	Increased Glucose Metabolism	Secondary to sympathetic inhibition
Cerebellar Vermis	Decreased Glucose Metabolism	[Secondary to improved midline spinal mechanical afferentation]

Summary and Proposed Model

Chiropractors frequently observe and therefore talk about the improvement of non-musculoskeletal syndromes, including brain function, in patients under chiropractic care. A number of lines of scientific investigations make the following mechanism biologically plausible:

The spinal adjustment is intended to improve the way the patient lives, functions, and exists in a gravity environment. The improvement in spinal mechanical function “closes the pain gate,” and pain perception is reduced (inhibited). (10)

The spinal adjustment improves the function of spinal mechanoreceptors. These spinal mechanoreceptors are proven to exist in the annulus of the intervertebral disc (11, 12), the facet joint capsules (13, 14), the supraspinous/interspinous ligaments (15), and the muscle spindles (16, 17).

Spinal mechanoreceptors are proven to communicate with the sympathetic nervous system (preganglionic sympathetic efferents in lamina VII of the spinal cord), and their influence is inhibitory (18, 19).

The sympathetic neurons innervate the blood vessels, including those in the brain. Increased sympathetic tone causes vasoconstriction, reducing the delivery of blood and therefore of glucose and oxygen, and thereby reducing the production of ATP energy. Brain function is dependent upon the production of ATP energy (20).

Chiropractic spinal adjusting appears to influence brain function primarily in two ways:

• Direct alterations of brain electrical signals.
• Inhibition of the sympathetic nervous system, subsequent vasodilation, improved glucose delivery to brain neurons resulting in increased uptake and energy synthesis.

Spinal adjusting works in part because of inhibition of increased sympathetic tone.

The studies presented here support a link between spinal function, chiropractic spinal adjusting, and limbic emotional function. They may help explain the anecdotal observations of the Kentucky House of Reform and North Dakota’s Judge Ponath.

In today’s modern environment, few chiropractors would treat patients for brain dysfunction alone. Yet, many chiropractors treat patients with brain dysfunction, along with other qualified providers. Even the publication from the Kentucky House of Reform in 1931 clearly noted that the chiropractors were a part of a team of medical providers, and that the chiropractor enhanced the clinical outcome, helping the patient, the patient’s family, and the taxpayers. Many patients with a variety of brain disorders could benefit from the chiropractic improvement of their spinal mechanical function.

REFERENCES:

1. Cyriax J; Textbook of Orthopaedic Medicine, Diagnosis of Soft Tissue Lesions, eighth edition; Bailliere Tindall, 1982.
2. Marshall LT; REPORT: State Supervisor of Chiropractic; In Connection with Kentucky House of Reform; 1931.
3. Ponath AW; FACTS: What Chiropractic has done for Insanity; 1934.
4. The American Physiological Society; http://www.the-aps.org/MayCC/membership/obituaries/irvinkorr.txt
5. Chaitow L, Comeaus Z, Liebenson C; Obituary: Irvin Korr Ph.D. (1909-2004); 8, pp. 155-157.
6. Korr IM; The spinal cord as organizer of disease processes: Hyperactivity of sympathetic innervation as a common factor is disease; Journal of the American Osteopath Association; 1979 Dec;79(4):232-7.
7. Jiang H, Moreau M, Raso M, Russell G, Bagnall K; Identification of the Location, Extent, and Pathway of Sensory Neurologic Feedback After Mechanical Stimulation of a Lateral Spinal Ligament in Chickens; SPINE 1997;22:17-25 (January 1, 1997).
8. Haavik-Taylor H, Murphy B; Cervical spine manipulation alters sensorimotor integration: A somatosensory evoked potential study; Clinical Neurophysiology; February 2007 Feb;118(2):391-402.
9. Ogura T, Tashiro M, Masud M, Watanuki S, Shibuya K, Yamaguchi K, Itoh M, Fukuda H, Yanai K; Cerebral metabolic changes in men after chiropractic spinal manipulation for neck pain; Alternative Therapies Health Medicine; Nov-Dec 2011;Vol. 17; No. 6; pp. 12-7.
10. Kirkaldy-Willis WH, Cassidy JD; Spinal Manipulation in the Treatment of Low back Pain; Canadian Family Physician; March 1985, Vol. 31, pp. 535-540.
11. Mendel T, Wink CS, Zimny ML; Neural elements in human cervical intervertebral discs; Spine (Phila Pa 1976). 1992 Feb;17(2):132-5.
12. Roberts S, Eisenstein SM, Menage J, Evans EH, Ashton IK; Mechanoreceptors in intervertebral discs. Morphology, distribution, and neuropeptides; Spine (Phila Pa 1976). 1995 Dec 15;20(24):2645-51.
13. McLain RF; Mechanoreceptors endings in human cervical facet joints; Spine (Phila Pa 1976). 1994 Mar 1;19(5):495-501.
14. McLain RF; Pickar JG; Mechanoreceptor Endings in Human Thoracic and Lumbar Facet Joints; SPINE 1998;23:168-173.
15. Jiang H, Russell G, Raso J, Marc J. Moreau MJ, Hill DL, Bagnall KM; The Nature and Distribution of the Innervation of Human Supraspinal and Interspinal Ligaments; SPINE Volume 20, Number 8, pp. 869-876 (April 15, 1995).
16. Solomonow M, Zhou BE Harris, Lu MY, Baratta RV; The Ligamento-Muscular Stabilizing System of the Spine; SPINE: Dec 1, 1998;23:2552-2562.
17. Holm S, Indahl A, Solomonow M; Sensorimotor control of the spine; Journal of Electromyography and Kinesiology; Volume 12, Issue 3, June 2002, pp. 219-234.
18. Budgell B, Hirano F; Innocuous mechanical stimulation of the neck and alterations in heart-rate variability in healthy young adults; Autonomic Neuroscience. 2001 Aug 13;91(1-2):96-9.
19. Koch LE, Koch H, Graumann-Brunt S, Stolle D, Ramirez JM, Saternus KS; Heart rate changes in response to mild mechanical irritation of the high cervical spinal cord region in infants; Forensic Science International; Volume 128, Issue 3, August 28, 2002, Pages 168-176.
20. Perlmutter D; The Better Brain Book; Riverhead Books, 2004, pp. 21-23.

Mild Traumatic Brain Injury and Degenerative Function Physiological Strategies to Improve and Preserve Brain Function

Overview

Free radicals are atoms or molecules that have an unpaired set of electrons in their outer shell. Electrons, like shoes, function best in pairs. Free radicals, with their unpaired electrons, are unstable and can damage adjacent cell membranes, proteins, fats, and DNA.

The primary source of free radicals in our bodies is metabolism, the making of ATP energy from oxygen and glucose. The electron transport proteins of the inner membrane of the mitochondria are not 100% efficient in creating ATP molecules, and therefore always produce a percentage of oxygen free radicals. These oxygen free radicals are usually called “reactive oxygen species” or just abbreviated “ROS”.

When oxygen free radicals cause biological damage, it is often termed “oxidative stress” or just “oxidation”.

Therefore, for this discussion:

Free Radicals = Oxygen Free Radicals = Reactive Oxygen Species
And
Oxidative Stress = Oxidation

Since the primary source of oxygen free radicals is oxygen, the tissues that utilize the most oxygen also make the greatest number of oxygen free radicals. Because the brain uses the most oxygen, it also makes the largest number of oxygen free radicals. Consequently, the brain is particularly prone to suffering from oxidative stress.

A database search of the National Library of Medicine of the United States of America using PubMed and the words “brain function AND free radicals” found 16,377 citations (August 13, 2012). This shows the significance of the relationship between free radicals and brain function.

Dr. David Perlmutter, MD, is a Board Certified Neurologist with a private practice in Naples, Florida. He has authored five books. In his 2004 book, The Better Brain Book, Dr. Perlmutter states (1):

“The same forces that are aging your body are aging your brain, only they hit your brain earlier and harder.”

“These culprits are at the core of virtually all brain problems, from mild memory issues to brain fog to severe Alzheimer’s disease. They are:

1) The proliferation in the brain of destructive chemicals called free radicals.

2) The decline in the ability of the brain cells to make energy.”

The brain is the most metabolically active organ of the body; it uses 20% of consumed oxygen to make the energy to fuel all of its activities.

“Energy is made in the specialized parts of the cell called the mitochondria.”

“There is a price to pay for making all this energy. Every time a cell makes energy—any cell, in any part of your body—it also produces toxic substances call free radicals.”

Free radicals are unstable, and bond with molecules in healthy cells, damaging tissues and organs, such as the heart, joints, skin, and the fats of one’s brain.

Over time, free radicals can destroy substantial amounts of the brain and nerve tissue through this process of oxidation.

“When the mitochondria of your brain cells are injured, they become less efficient, produce less energy, and increase free radical production.”

“Free radicals can inhibit the brain’s ability to produce neurotransmitters, which have a profound impact on memory, learning, mood, and even balance and hand-eye coordination.”

“Free radicals pose another potentially deadly problem for the brain—they promote inflammation.”

Inflammation is linked to nearly all chronic brain diseases, including Parkinson’s disease, Alzheimer’s disease, multiple sclerosis, and dementia.

••••

Keshav Singh, PhD, is a senior scientist and professor of genetics at the University of Alabama at Birmingham. In his 2006 book, Oxidative Stress, Disease and Cancer, Dr. Singh details seven factors that contribute to accumulation of reactive oxygen species in the brain (2). In this discussion, I will review three of the factors:

1) Low Antioxidant Defenses

2) Arachidonic Acid [Inflammation; Omega-6/Omega-3 Ratio]

3) Glutamate [Excitotoxins]

Low Antioxidant Defenses

Antioxidants are molecules that inhibit oxidative stress of other molecules. Antioxidants are biological electron donors; by donating an electron to a free radical, that free radical is no longer unstable and it will no longer pose a damaging threat to membranes, proteins, fats, DNA, etc. Therefore, antioxidants are good, and the more one has the better.

Our primary exogenous source of antioxidants is from consumption of fruits and vegetables in the diet. Sadly, a report from the United States Centers for Disease Control (CDC) in 2009 indicated that only 14% of US adults and 9.5% of US teenagers were consuming the minimum of 5 servings of fruits and vegetables per day (3). “CDC officials said the findings indicate a disheartening gap between how people should be eating and what they’re actually doing in an era of rampant obesity.”

Michael Pollan, PhD, is a professor at the University of California, Berkeley. In his 2008 book In Defense of Food, Dr. Pollan stresses that there is no substitute for healthy eating (4). He stresses that the healthy diet should consist primarily of plant based foods, in part because of their higher levels of antioxidants. Yet, as noted from the CDC assessment, the average US citizen diet is falling far short of optimal in this regard. Consequently, even Dr. Pollan makes these comments in his book:

“Many of the nutrition experts I consulted recommend taking a multivitamin, especially as you get older.”

“It’s probably a good idea, and certainly can’t hurt, to take a multivitamin-and-mineral pill.”

The point is that a healthy plant-based diet will supply the consumer with a rich array of antioxidants, protecting the brain from free radical damage. Supplementing with a quality multiple vitamin-mineral pill could possibly enhance the free radical scavenging of a healthy diet, assisting in the protection and preservation of brain function. Such supplementation has already been shown to be associated with the longer length of telomeres, an important measure of biological longevity (the 2009 Nobel Prize in medicine/physiology) (5).

Arachidonic Acid [Inflammation; Omega-6/Omega-3 Ratio]
Omega-3 Fatty Acids

On January 2, 2006, in Upshur County, West Virginia, USA, there was an explosion in the Sago Coal Mine. The blast trapped 13 miners for nearly two days; only one miner survived. It was one of the worst mining disasters in the United States.

The lone survivor was Randal L. McCloy, Jr., age 26. He was found unconscious and suffering from carbon monoxide poisoning, a collapsed lung, brain hemorrhaging, edema, muscle injury, faulty liver and heart function, and almost no brain electrical activity. His initial prognosis for recovery was grim, expecting permanent damage to his brain. However, McCloy recovered almost fully.

The story of Ronald McCloy’s miraculous recovery is well reviewed in the magazine Men’s Health in 2007 in an article titled THE GOVERNMENT’S BIG FISH STORY (6). A portion of the Men’s Health Article follows:

When Randal McCloy was rushed to West Virginia University Ruby Memorial Hospital’s intensive-care unit, he was practically dead. The 27-year-old coal miner had spent 41 hours buried 2 1/2 miles underground after an explosion in the Sago, West Virginia mine where he’d been working. His 12 oxygen-starved colleagues had all perished.

“As far as we know, he survived the longest exposure to carbon monoxide poisoning,” says Julian Bailes, M.D., the neurosurgeon assigned to the case. McCloy was in a coma and in deep shock, his heart barely beating, one of his lungs collapsed, his liver and both kidneys shut down. Even if he somehow managed to pull through, doctors predicted McCloy would be severely brain damaged, since the carbon monoxide had stripped the protective myelin sheath from most of his brain’s neurons. “It’s very difficult to come back from a brain injury,” says Dr. Bailes. “There’s no drug that can help that.”

Dr. Bailes ordered a daily dose of 15,000 milligrams (mg) docosahexaenoic acid (DHA) and eicosapentaenoic acid (EPA) for the miner. In layman’s terms? Fish Oil.

Several weeks passed. Then, unexpectedly, McCloy emerged from his coma. This in itself was amazing, but he wasn’t done. In the weeks that followed, he stunned even the most optimistic experts by recovering his memory and gradually regaining his ability to walk, talk, and see, a turnaround that many in the medical field called miraculous.

Dr. Bailes states: “The omega-3s helped rebuild the damaged gray and white matter of his brain,” says Dr. Bailes, who now takes his own medicine, swallowing a fish-oil supplement each morning. On his orders, McCloy, still recuperating at home, continues to take fish oil daily. “I would say he should be on it for a lifetime,” says Dr. Bailes. “But then, I think everybody should.”

••••

Dr. Artemis P. Simopoulos, MD, is a physician and geneticist working in Washington DC. As of this writing (August 13, 2012), a search of the National Library of Medicine using her name and the word “omega-3” in the PubMed search engine located 50 citations. One particularly relevant reference was published late last year in the journal Molecular Neurobiology and titled (7):

Evolutionary Aspects of Diet:
The Omega-6/Omega-3 Ratio and the Brain

In this article Dr. Simopoulos notes that human beings evolved on a diet that had a ratio of omega-6 to omega-3 fatty acids (FA) of about 1/1. Yet, today, Western diets have a ratio of 10/1 to 20–25/1, indicating that Western diets are deficient in omega-3 FA compared with the diet on which humans evolved and their genetic patterns were established.

Dr. Simopoulos notes that docosahexaenoic acid (DHA) omega-3 is essential for the normal functional development of the brain. DHA accounts for 40% of the membrane phospholipid FA in the brain. Both eicosapentaenoic acid (EPA) and DHA omega-3s have an effect on brain membrane receptor function and even neurotransmitter generation and metabolism. The balance of omega-6 and omega-3 FA is important for brain homeostasis and normal brain function throughout the life cycle.

The change of omega-6/omega-3 ratio in the food supply of Western societies has occurred over the last 150 years. During evolution, omega-3 fatty acids were found in all foods consumed: meat, wild plants, eggs, fish, nuts, and berries. Today in Western societies the omega-6/omega-3 ratio is very high due to the high intake of soybean oil, corn oil, sunflower, safflower, and linseed oil.

Omega-3’s can affect not only cognitive functions, but also mood and emotional states and may act as a mood stabilizer. Omega-3’s have beneficial effects in a number of neurological diseases. Dr. Simopoulous notes:

“DHA is found in high amounts in the membranes of brain and retina and is critical for proper neurogenesis, neurotransmitter metabolism, neuroprotection and vision. The consumption of high amounts of DHA has been associated with multiple health benefits including brain and retinal development, aging, memory formation, synaptic membrane function, photoreceptor biogenesis and function, and neuroprotection. DHA is essential for pre-natal brain development.”

“Clinical studies show that cognitive performance improves with omega-3’s.”

“Western diets are characterized by high omega-6 and low omega-3 fatty acid intake, whereas during the Paleolithic period when human’s genetic profile was established, there was a balance between omega-6 and omega-3 fatty acids. Therefore, humans today live in a nutritional environment that differs from that for which our genetic constitution was selected.”

“The balance of omega-6/omega-3 fatty acids is an important determinant in maintaining homeostasis, normal development, and mental health throughout the life cycle.”

“Cognitive performance improves with omega-3’s supplementation possibly due to increased hippocampal acetylcholine levels, the anti-inflammatory effects of omega-3’s, decreased risk of cardiovascular disease or increased neuroplasticity.”

“In humans, the brain is the most outstanding organ in biological development: it follows that the priority is brain growth and development, and in the brain the balance between omega-6 and omega-3 PUFA metabolites is close to 1:1. This ratio should be the target for human nutrition.”

“The ratio of omega-6/omega-3 fatty acids in the brain between 1:1 and 2:1 is in agreement with the data from the evolutionary aspects of diet and genetics.”

“A ratio of 1:1 to 2:1 omega-6/omega-3 fatty acids should be the target ratio for health.”

••••

A relevant addition to this discussion is the letter to the editor of the political magazine, Time, June 4, 2012. Steven Gaulin, PhD, Anthropology Professor, University of California, Santa Barbara, and William Lassek, MD, former Assistant Surgeon General of the United States wrote:

Parenting Debate

“Your recent cover article on attachment parenting has provoked much discussion about breast-feeding. Anthropological surveys across many cultures indicate that the mean age at which weaning in our species occurs is 2.5 to 3 years. The evolutionary explanation for this long nursing period is clear. Our unusually large brains require large amounts of omega-3 fats, and breast milk concentrates these fats from mothers’ bodily resources. Unfortunately, the omega-6-laden American diet, based on corn and soybean oil and animals fed on these crops, deprives infants and children of the omega-3 fats needed for healthy brain development. Thus early weaning and bad diets are delivering a one-two punch to American kids.”

••••

Brain function and health is dependent upon the ratio of membrane omega-6 to omega-3 fatty acids. This ratio is critically important throughout life, from infancy to the elderly. It has been shown that a simple yet accurate assessment of this ratio in the brain is to evaluate the ratio in red blood cells (9). This assessment is accomplished on our patients with a simple, inexpensive finger prick blood analysis. The analysis looks at the ratio of the omega-6 fatty acid Arachidonic Acid (AA) to the omega-3 fatty acid Eicosapentaenoic Acid (EPA), or the AA/EPA ratio. If the ratio is too high (excessive AA or low levels of EPA), we supplement the patient with a quality fish oil product and encourage a reduction of omega-6 fatty acids in the diet. We retest in about 4 months.

Studies supporting this approach to improve brain function and health are numerous. As examples, studies supporting omega-3 fatty acids in brain trauma management (10) and prevention of neurological degenerative diseases have been recently published (9, 11).

Excitotoxins

Excitotoxins are molecules that function as excitatory neurotransmitters, but when present in excess they can literally excite the neuron to death. The word excitotoxins is credited to physician and neuropathologist John Olney, MD, currently at the University of Washington. Beginning in the late 1960s, Dr. Olney began to publish warnings about dietary exposure to 2 excitotoxins that are found as food additives, specifically as taste enhancers: glutamate and aspartate. A representative article of his work is found in the journal Neurotoxicoloty in 1981, titled (12):

Excitatory neurotoxins as food additives: an evaluation of risk

Stuart A. Lipton, MD, PhD, is a neuroscientist. He is former Associate Professor of Neurology, Harvard Medical School, and currently he is at the Salk Institute for Biological Studies and the Scripps Research Institute, La Jolla, California. Paul A. Rosenberg, MD, PhD, is also a neuroscientist and an Associate Professor of Neurology, Harvard Medical School. In 1994, Drs. Lipton and Rosenberg published an article in the New England Journal of Medicine suggesting that all brain neurologic disorders have a common pathway: excitotoxicity (13). Their article is titled:

Excitatory amino acids as a final common pathway for neurologic disorders

Consistent with Dr. Olney, Drs. Lipton and Rosenberg indicate that the 2 most prevalent excitotoxins are the amino acids glutamate and aspartate.

Drs. Lipton and Rosenberg lists of neurologic conditions associated with glutamate and aspartate excitotoxicity include:

Acute insults: stroke, hypoglycemia, trauma, and epilepsy

Chronic neurodegenerative states: Huntington’s disease, the acquired immunodeficiency syndrome (AIDS) dementia complex, amyotrophic lateral sclerosis, and Alzheimer’s disease.

The primary glutamate/aspartate neuron receptor is the N-methyl-D-aspartate (NMDA) receptor. When the NMDA-receptor is activated there is an influx of calcium into the neuron, causing overstimulation, excessive free radical production, and neuronal injury/death. Drs. Lipton and Rosenberg state:

“The paradox of excitotoxicity is how or why the mammalian brain evolved with such extraordinary vulnerability to its own excitatory neurotransmitters.”

“The ambient concentrations of glutamate are close to those that can destroy neurons, and it is important that the extracellular glutamate concentration and compartmentalization be exquisitely controlled to prevent excitotoxicity.”

A number of contemporary physicians are writing books in an effort to warn the public about the dangers of consumption of excess dietary glutamate and aspartate, including:

1997
Excitotoxins, The Taste That Kills by Russell Blaylock, MD (University of Mississippi neurosurgeon), Health Press.

1999
In Bad Taste, The MSG Symptom Complex, by George Schwartz, MD, Health Press.

2000
The Crazy Makers, How the Food Industry Is Destroying Our Brains and Harming Our Children, by Carol Simontacchi, Tarcher Putnam.

Food Allergies by William Walsh, MD (Mayo Brothers), Wiley.

2001
Fast Food Nation by Eric Schlosser, Houghton Mifflin.

These authors remind the reader that aspartate is half of the artificial sweetener aspartame. Glutamate is ubiquitous in packaged foods, often in the salt form MSG (monosodium glutamate). Glutamate in food is often hidden, using names like (from Blaylock, 1997):

HIDDEN SOURCES OF MSG

The glutamate manufacturers and the processed food industries are always on a quest to disguise MSG added to food. Below is a partial list of the most common names for disguised MSG.

Additives that always contain MSG:

Monosodium Glutamate
Hydrolyzed Vegetable Protein
Hydrolyzed Protein
Hydrolyzed Plant Protein
Plant Protein Extract
Sodium Caseinate
Calcium Caseinate
Yeast Extract
Textured Protein
Autolyzed Yeast
Hydrolyzed Oat Flour

Additives that frequently contain MSG:

Malt Extract
Malt Flavoring
Bouillon Stock
Broth Flavoring
Natural Flavoring
Natural Beef or Chicken Flavoring

Additives that may contain MSG or excitotoxins:

Carrageenan
Enzymes
Soy Protein Concentrate
Soy Protein Isolate
Whey Protein Concentrate

Ideally, these book’s authors recommend that the excitotoxins glutamate and aspartate be avoided in the diet. Additionally, excessive glutamate and aspartate are cleared from the extracellular space by ATP energy dependent uptake systems and moved into astrocytes. When cellular energy metabolism is impaired or fails because of ATP depletion, harmful extracellular accumulation of glutamate and aspartate occurs. Deprivation of oxygen and/or glucose decreases the production of ATP. This energy failure itself is not toxic to neurons. What makes it neurotoxic is the accumulation of glutamate/aspartate and activation of glutamate-receptor-dependent excitotoxic mechanisms. ATP production is reduced as a consequence of such mechanisms as smoking, anoxia, hypoglycemia, and insulin resistance.

Both neurons and astrocytes contain large quantities of glutamate that leak out of injured/traumatized cells. This may explain the increased incidence of Alzheimer’s Dementia and other neurodegenerative disorders in National Football Players and others with a history of repeated brain trauma.

Drs. Lipton and Rosenberg note that magnesium blocks the NMDA receptor, and this may be the basis for its anticonvulsant and neuroprotective effects. They sum up their article with:

“A wide variety of acute and chronic neurologic diseases may be mediated, at least in part, by a final common pathway of neuronal injury involving excessive stimulation of glutamate receptors.”

Strategies to protect brain health and function as related to excitotoxicity include:

• Avoid excess dietary glutamate/aspartate (read food/drink labels)
• Do not smoke
• Consume high levels of antioxidant foods (fruits and vegetables)
• Possibly enhance dietary antioxidants with an antioxidant supplement
• Possibly supplement with magnesium
• Maintain aerobic fitness
• Avoid/manage blood glucose problems, especially insulin resistance (below)

Insulin Resistance

It is possible that the primary health problem in developed countries today is insulin resistance. As American science writer Gary Taubes notes in his 2008 book Good Calories, Bad Calories (14), insulin resistance creates a biological cascade that makes people overweight, a modern global epidemic.

But, it is important to recall that if one is insulin resistant, they also have a diminished capacity to get glucose out of the blood stream and into the neuron where it is converted into ATP energy. When brain ATP production is low, excessive glutamate and aspartate are not deactivated by pumping them into the astrocytes. Consequently there is increased excitotoxic brain injury and its associated pathology.

This thinking is the central theme of the 2011 book by neonatal physician Mary Newport, MD, titled Alzheimer’s Disease, What if There Was A Cure (15). Dr. Newport presents evidence and asserts that Alzheimer’s Disease is a type of diabetes in which the patient is actually suffering from brain neuron insulin resistance. Consequently, the patient’s brain is starved of adequate levels of ATP allowing excitotoxic damage to cascade.

Dr. Newport presents an academic discussion with numerous case studies suggesting that giving the brain compromised patient (disease, injury, etc.) alternative fuel to manufacture ATP will greatly improve the patient’s brain health and function. Because the patient is insulin resistant, this alternative fuel would have to be independent of the glucose/insulin relationship.

Dr. Newport’s review of the literature documents that such an alternative fuel source is medium chain saturated triglycerides. These fats are readily absorbed and transported to the liver where they are converted into ketones. These ketones readily cross the blood brain barrier, cross the neuronal membrane, and are quickly and efficiently converted to ATP in the mitochondria. All of this is done without the need of insulin, so if the patient is insulin resistant, the mechanism still works. The greater levels of ATP help to actively pump glutamate and aspartate into the astrocytes, improve the sodium pump function, improve the synthesis of neurotransmitters, etc. All of which enhances brain health and function.

Dr. Newport says a great source of medium chain saturated triglycerides is coconut oil (57-60%). She advocates and details how brain compromised people or people who want to optimize brain function can incorporate coconut oil into their daily regimes.

REFERENCES:

1. Perlmutter D; The Better Brain Book; Riverhead Books; 2004.
2. Singh K PhD, Oxidative Stress, Disease and Cancer, Imperial College Press, 2006.
3. Anderson L; US Diets Fall Short on Fruit, Vegetables; USA Today; September 30, 2009.
4. Pollan M; In Defense of Food; Penguin Press; 2008
5. Xu Q, Parks CG, DeRoo LA, Cawthon RM, Sandler DP, Chen H; Multivitamin use and telomere length in women; American Journal of Clinical Nutrition; Vol. 89, No. 6, 1857-1863, June 2009, pp. 1857-1863.
6. Erdely SR, Watkins D; THE GOVERNMENT’S BIG FISH STORY; Men’s Health; June 21, 2007.
7. Simopoulos AP; Evolutionary Aspects of Diet: The Omega-6/Omega-3 Ratio and the Brain; Molecular Neurobiology; October, 2011; Vol. 44; No. 2; pp. 203-15.
8. Gaulin SJC, Lassek WD; Parenting Debate (letter to the editor); Time, June 4, 2012.
9. S. Tan ZS, Harris WS, Beiser AS, Au R, Himali JJ, and 7 more; Red blood cell omega-3 fatty acid levels and markers of accelerated brain aging; Neurology; February 28, 2012; 78; pp. 658–664.
10. Wu A, Ying Z, Gomez-Pinilla F; The salutary effects of DHA dietary supplementation on cognition, neuroplasticity, and membrane homeostasis after brain trauma; Journal of Neurotrauma; October 2011; Vol. 28; No. 10; pp. 2133-2122.
11. Gu Y, Schupf N, Cosentino SA, Luchsinger JA, Scarmeas N; Nutrient intake and plasma beta-amyloid; Neurology; June 5, 2012; Vol. 78; No. 23; pp. 1832-40.
12. Olney JW; Excitatory neurotoxins as food additives: an evaluation of risk; Neurotoxicology; 1981 Jan;2(1):163-92.
13. Lipton SA, Rosenberg PA; Excitatory amino acids as a final common pathway for neurologic disorders; The New England Journal of Medicine; March 3, 1994; Vol. 330; No. 9; pp. 613-622.
14. Taubes G, Good Calories, Bad Calories, Anchor Books, 2008;
15. Newport M; Alzheimer’s Disease, What if There Was A Cure; Basic Health, 2011.

A Mechanical Model Involving the Spinal Dura Mater and the Suboccipital Muscles

For more than half a century respected authors, clinicians, and journals have claimed that various problems of the cervical spine can cause headaches. As an example, in 1958, Beverly Hills neurosurgeon Emil Seletz, MD, authors an article titled Headache of Extracranial Origin, published in the journal California Medicine (1). In this article, Dr. Seletz indicates that the cervical spine is an important cause of headache. He lists these potential origins for headache as:

1) Irritation of the C2 nerve root, which communicates with the trigeminal nerve to produce headache. C2 nerve root irritation occurs as a consequence of these mechanisms:

• Cervical trauma causing a “tractional injury” to the C2 nerve root because its exit is between C1 and C2, the point of “greatest rotation of the head on the neck.”
• Post-traumatic adhesions between the ligaments and the dural sleeve chronically irritating the C2 nerve root.
• Any cervical spine injury that may injure/irritate the delicate filaments of the spinal accessory nerves which originate from all points of the cervical spinal cord. This results in spasm of the trapezius muscles. Spasm of the trapezius muscle exerts traction on the greater occipital nerve at the point of where the nerve pierces the tendon of the trapezius muscle, resulting in occipital pain and headache.

2) Osteophytosis, swelling or adhesions arising from the uncinate process can irritate or compromise the vertebral artery or it’s sympathetic innervation. This has been a proposed mechanism of headache since 1925-1928, and is known as the syndrome of Barre-Lieou.

“Cervicogenic Headache” was officially recognized in 1983 (2). Most models of etiology for cervicogenic headache have involved the trigeminocervical nucleus and the convergence of the afferents of the trigeminal and upper cervical nerves:

 

Australian clinical anatomist and physician Nikolai Bogduk, MD, PhD, champion this model of cervicogenic headache. In his 1995 article titled Anatomy and Physiology of Headache, Dr. Bogduk states (3):

“All headaches have a common anatomy and physiology. All headaches are mediated by the trigeminocervical nucleus, and are initiated by noxious stimulation of the endings of the nerves that synapse on this nucleus, by irritation of the nerves themselves, or by disinhibition of the nucleus.”

The trigeminocervical nucleus is “defined by its afferent fibers.” As its name implies, the primary afferent fibers into the trigeminocervical nucleus are from the trigeminal and upper cervical spine (C1-C3) sensory fields.

A New and Different Model for Cervical Headache

A careful review of Dr. Bogduk’s article (3) indicates that the spinal dura mater is innervated with nociceptors that arise from the upper cervical spine nerve roots. This innervation allows the spinal dura to be a generator of pain, primarily headache, as these afferents would synapse in the trigeminocervical nucleus.

Biomechanically, it is understood that when one extends their head or cervical spine, dural enfolding is produced. Rene Cailliet, MD, states (4):

“On extension the dura folds as in accordion pleats.”

[As of this writing (2012), Dr. Cailliet is still living at age 95].

White and Panjabi’s Clinical Biomechanics of the Spine (5) defines the pia mater as a “vascular membrane covering the [spinal] cord.” They also note that the pia mater is physically connected to the dura mater through the paired dentate ligaments:

Consequently, cervical spine extension, especially abrupt extension, has the potential to irritate, compromise, injure, or inflame the spinal dura mater, the attached pia mater, and the spinal cord. Therefore, a protective mechanism whereby dural tension could be adapted to changes in head/neck positions is desirable.

••••

In 1992, French researchers investigated the detailed anatomy of the Atlanto-Occipital and Atlanto-Axial membranes (6). These researchers made two important discoveries:

1. The fascia from the Rectus Capitis Posterior Minor muscle blends with the connective tissues of the Occipital-Atlanto membrane and they attach to the spinal dura mater.
2. The fascia from the both the Rectus Capitis Posterior Major and Obliquus Capitis Inferior muscles blends with the connective tissues of the Atlanto-Axial membrane and they also attach to the spinal dura mater.

In summary, and important for this discussion, these researchers found that three of the four suboccipital muscles have fascial/connective tissue attachments to the spinal dura mater: Rectus Capitis Posterior Minor, Rectus Capitis Posterior Major, and Obliquus Capitis Inferior.

* Rectus Capitis Posterior Minor into the Occipital-Atlanto Space
** Rectus Capitis Posterior Major into the Atlanto-Axial Space
** Obliquus Capitis Inferior into the Atlanto-Axial Space

••••

In 1995, dentist Gary Hack, DDS, from the Baltimore College of Dental Surgery at the University of Maryland, published a pioneering study in the journal Spine titled (7):

Anatomic Relation Between the Rectus Capitis
Posterior Minor and the Dura Matter

In this study, Dr. Hack and colleagues carefully and meticulously dissected 11 human cadavers to investigate if there is a connection between the Rectus Capitis Posterior Minor muscle and the spinal dura mater. They note that the Rectus Capitis Posterior Minor muscle arises from the posterior arch of the atlas (C1) and inserts at the inferior nuchal line of the occiput. Deep to the Rectus Capitis Posterior Minor muscle is the Posterior Occipital-Atlanto Membrane, which is “intimately attached to the underlying spinal dura.”

ANATOMICAL FINDINGS:

Dense connective tissue attached the Rectus Capitis Posterior Minor muscle to the Posterior Occipital-Atlanto Membrane at the occipital-atlanto junction. The connective tissue bridge was arranged perpendicular to the dura. They state:

“A [dense] connective tissue bridge between the Rectus Capitis Posterior Minor muscle and the dorsal spinal dura at the atlanto-occipital junction was observed in every specimen.”

BIOMECHANICAL DISCUSSION:

Dr. Hack and colleagues found that head and neck extension of all cadavers in this study produced infolding of the Posterior Atlanto-Occipital Membrane/dura complex. When the head and neck are extended, the spinal dura folds inward toward the spinal cord. This enfolding “appeared to be resisted by this connective tissue bridge.” They state:

“The connective tissue bridge may help resist dural infolding during head and neck extension.”

These authors note that upper cervical spinal trauma causes atrophy of the Rectus Capitis Posterior Minor muscle. Such atrophy could compromise the resistance of dura infolding that occurs during head/neck extension. Thus, the dura could be irritated/injured/inflamed.

Immediately following this article was an attached Point of View by Scott Haldeman, DC, MD, PhD. Dr. Haldeman notes that injury or pathology affecting the cervical spine can cause headaches. The dura mater is a pain sensitive structure, capable of generating cervical headaches. Suboccipital muscle problems can influence the pain sensitive dura matter to generate headache. Massage, manipulation, and biofeedback directed to the cervical spine may be valuable in treating this headache mechanism. This is in agreement with Dr. Nikolai Bogduk, above (3).

••••

In 1997, HP Rutten and colleagues from the Department of Neurology, Deventer, The Netherlands, add to the discussion of Dr. Hack’s anatomical findings. Published in the journal Spine (8), Rutten and colleagues performed a layer-by-layer dissection of 7 human cadavers in an attempt to verify the upper cervical spine findings of Hack and colleagues. They state:

“The relation described by Hack et al between posterior atlanto-occipital membrane spinal dura complex and Rectus Capitis Posterior Minor is confirmed.”

Rutten et al suggest that the Rectus Capitis Posterior Minor muscle “monitors” stress on the dura mater. They further state:

“The Rectus Capitis Posterior Minor may function as a mechanoreceptive element, because it contains a great number of muscle spindles.”

“We hypothesize that the mechanism that helps to resist dural infolding and/or the proprioceptive registration fails in patients with whiplash-like symptoms.”

••••

In 1999, ME Alix and DK Bates, from Logan College of Chiropractic, reviewed the literature pertaining to the neurophysiological basis and anatomic relationship between the dura mater and the Rectus Capitis Posterior Minor muscle and the etiology of cervicogenic headache (9). They searched Medline and the Index to Chiropractic Literature. The title of their study is:

A proposed etiology of cervicogenic headache: the neurophysiologic basis and anatomic relationship between the dura mater and the rectus posterior capitis minor muscle

These authors note:

“Connective tissue bridges were noted at the atlanto-occipital junction between the rectus capitis posterior minor muscle and the dorsal spinal dura.

The perpendicular arrangement of these fibers appears to restrict dural movement toward the spinal cord.

Anatomic structures innervated by cervical spinal nerves C1-C3 have the potential to cause headache pain. Included are the joint complexes of the upper 3 cervical segments, the dura mater, and spinal cord.

A sizeable body of clinical studies note the effect of manipulation on headache. These results support its effectiveness.

The dura-muscular, dura-ligamentous connections in the upper cervical spine and occipital areas may provide anatomic and physiologic answers to the cause of cervicogenic headache.

This proposal would further explain manipulation’s efficacy in the treatment of cervicogenic headache.”

••••

In 2004, dentist Gary Hack and colleague report a case in which a patient experienced relief from chronic headache after surgical separation of the connective tissue bridge of the dura mater from the suboccipital musculature. Their case report was published in the journal Headache (10). This study would suggest that chronic suboccipital muscle tension could cause dysfunction, irritation, and/or irritation to the spinal dura mater, resulting is chronic headache. These authors state:

“The presence of a connective tissue bridge, attaching suboccipital muscles to the dura mater, is now recognized as a feature of normal human anatomy.”

••••

In 2005, Lance Nash and colleagues from the Department of Anatomy and Structural Biology and the School of Physiotherapy, University of Otago, New Zealand, published a study in the journal Spine titled (11):

Configuration of the Connective Tissue in the
Posterior Atlanto-Occipital Interspace

The objective of their study was to define the relationship between rectus capitis posterior minor, the posterior atlanto-occipital membrane, and the spinal dura in the posterior atlanto-occipital interspace. In their study the authors carefully dissected 22 human cadavers. They state:

“It has been speculated that connections between the dura and muscles and/or ligaments in the posterior atlanto-occipital interspace may transmit forces from the cervical spine joint complexes to the pain-sensitive dura, generating cervicogenic headaches.”

“Recently, the spinal dural connection of the rectus capitis posterior minor muscle and the nuchal ligament in the posterior atlanto-occipital interspace has been reported extensively.”

“The posterior atlanto-occipital membrane, extending between the posterior arch of the atlas (C1) and the occiput, has been observed to tether the spinal dura by numerous connective tissue fibers creating a posterior atlanto-occipital membrane-spinal dura complex.”

“The tendon of the rectus capitis posterior minor directly attaches to the spinal dura via the posterior atlanto-occipital interspace.”

“The present study demonstrates, for the first time, that tendinous fibers of the rectus capitis posterior minor muscle are continuous with the spinal dura.”

“A direct continuity of the rectus capitis posterior minor muscle to the spinal dura should have a great impact on strengthening the dura and preventing dural enfolding. Such an impact becomes particularly important during extension of the head and neck because, when the rectus capitis posterior minor muscle extends the cranio-cervical junction, a small portion of its muscular fibers simultaneously contract to pull the spinal dura posteriorly, preventing dural enfolding.”

“Microstrain and trauma in the rectus capitis posterior minor muscle and its tendon may cause a clonus condition of the muscle and stimulate the pain-sensitive dura, generating a cervicogenic headache.”

“The morphologic features of the rectus capitis posterior minor tendon and fascia indicate that they may have an important role in the maintenance of the posterior cranio-cervical stability and the prevention of the dural enfolding and are of anatomic relevance in the debate regarding the etiology of cervicogenic headaches.”

These authors found that the tendon of the rectus capitis posterior minor muscle fuses with the spinal dura via the posterior atlanto-occipital interspace. This study clearly demonstrates that the rectus capitis posterior minor tendon fibers are directly continuous with the spinal dura via the posterior atlanto-occipital interspace and become a part of the spinal dura.

••••

Most recently, in 2011, chiropractor Frank Scali, DC, and colleagues form the School of Medicine, St. George’s University, Grenada, West Indies, published a study in the journal Spine titled (12):

Anatomical Connection Between the Rectus Capitis
Posterior Major and the Dura Mater

Dr. Scali and colleagues note that chronic headaches in a significant number of patients are of cervical origin. Therefore, they did meticulous investigations bilaterally of 3 suboccipital muscles on 13 human cadavers:

Rectus Capitis Posterior Major (C2 spinous process to the occiput)
Rectus Capitis Posterior Minor (posterior arch C1 to the occiput)
Obliquus Capitis Inferior (C2 spinous process to the transverse process of C1)

They found:

• In 86% (11/13), the fibers from the Rectus Capitis Posterior Major entered the space between C1 and C2 and firmly attached to the dura.
• In 100% the fibers from the Rectus Capitis Posterior Minor entered the space between the occiput and C1 and firmly attached to the dura.
• In 86% (11/13) the fibers from the Obliquus Capitis Inferior entered the space (atlantoaxial interspace) between C1 and C2 and firmly attached to the dura.

Additionally, manual traction of the Rectus Capitis Posterior Major caused dural movement from the spinal root level of C2 to the spinal root level of T1.

Dr. Scali and colleagues note that mechanical stress applied to the dura mater during neurosurgical procedures results in cephalgia. Dural tension results in many clinical manifestations, especially headache. These authors suggest that proper function of the suboccipital muscles is required to prevent abnormal dural tension from occurring during various upper cervical spine motions, especially occiput-C1 flexion/extension and C1-C2 rotation.

••••

SUMMARY POINTS:

The 4 suboccipital muscles are innervated by the posterior primary rami of the C1 nerve root.

Three of the suboccipital muscles are directly and firmly attached to the spinal dura mater:

Rectus Capitis Posterior Major (C2 spinous process to the occiput)
Rectus Capitis Posterior Minor (posterior arch C1 to the occiput)
Obliquus Capitis Inferior (C2 spinous process to the transverse process of C1)

The apparent function of the attachment of the suboccipital muscles is to prevent the dura mater from being mechanically irritated, injured or inflamed during spinal motions.

The spinal dura mater is innervated with pain afferents from the upper cervical spine nerve roots.

Upper cervical spinal nerve root nociceptors synapse in the trigeminocervical nucleus, and are therefore capable of initiating headache.

Mechanical dysfunctions of the upper cervical spine may compromise the ability of the suboccipital muscles to protect the dura mater from motion related stress, irritation, injury, and inflammation.

Whiplash extension injuries occur quickly, so that the suboccipital muscles do not have enough time to contract and pull the spinal dura to safety, resulting in injury and headache.

In chronic whiplash patients, injured suboccipital muscles may undergo atrophy and fatty infiltration, further compromising the ability of these muscles to protect the dura mater from irritation and inflammation during routine motions, resulting in headache.

Chronic upper neck postural stress and distortions that invoke contraction of the suboccipital muscles may cause chronic stress on the spinal dura mater, resulting in headache.

Mechanical dysfunctions of the upper cervical spine may also irritate/inflame the spinal cord and its blood supply because the dura mater is attached to the vascular pia mater that surrounds the spinal cord.

There is biological plausibility for upper cervical spinal manipulation, occiput-atlas-axis chiropractic alignment, postural improvement, and suboccipital muscle myotherapy to be utilized in the cervicogenic headache patient.

REFERENCES:

• Seletz E; Headache of Extracranial Origin; California Medicine; November 1958, Vol. 89, No. 5, pp. 314-317.
• Sjaastad O; “Cervicogenic Headache” An Hypothesis; Cephalagia; December 1983; 3(4):249-256.
• Bogduk N; Anatomy and Physiology of Headache; Biomedicine and Pharmacotherapy; 1995, Vol. 49, No. 10, 435-445.
• Cailliet R; Neck and Arm Pain, Edition 2; FA Davis Company; Philadelphia; 1982.
• White AA, Panjabi M; Clinical Biomechanics of the Spine; Second edition; Lippincott; Phildelphia; 1990.
• Kahn JL, Sick H, Koritke JG; [The posterior intervertebral spaces of the craniovertebral joint]; Acta Anat (Basel); 1992;Vol. 144; No. 1; pp. 65-70.
• Hack G, Koritzer R, Robinson W, Hallgren R, Greenman P; Anatomic Relation Between the Rectus Capitis Posterior Minor and the Dura Matter; Spine; December 1, 1995; Vol. 20; No. 23; pp. 2484-2486.
• Rutten HP, Szpak K, van Mameren H, Ten Holter J, deJong J; Letters: comment on Anatomic Relation Between the Rectus Capitis Posterior Minor and the Dura Matter; Spine, April 15, 1997; Vol. 22; No. 8; pp. 924-926.
• Alix ME, Bates DK; A proposed etiology of cervicogenic headache: the neurophysiologic basis and anatomic relationship between the dura mater and the rectus posterior capitis minor muscle; Journal of Manipulative and Physiological Therapeutics; October 1999. Vol. 22; No. 8; pp. 534-539.
• Hack GD, Hallgren RC; Chronic headache relief after section of suboccipital muscle dural connections: a case report; Headache; January 2004;44(1):84-9.
• Nash L, Nicholson H, Lee ASJ, Johnson GM, Zhang M; Configuration of the Connective Tissue in the Posterior Atlanto-Occipital Interspace; Spine; Volume 30(12) June 15, 2005 pp. 1359-1366
• Scal F, Marsili ES, Pontell ME; Anatomical Connection Between the Rectus Capitis Posterior Major and the Dura Mater; Spine; December 1, 2011; Vol. 36; No. 25, pp. E1612–E1614.