Another Look

Our government (United States of America) collects and owns what experts consider to be reputable biomedical healthcare literature. This literature is catalogued in a library that is physically located in Bethesda, Maryland. The name of the library is The National Library of Medicine. The biomedical journals of the entire world can be found in our National Library of Medicine.

Our National Library of Medicine has collected and catalogued more than 20 million citations, and thousands more are added every day. One can access this database of citations by using a search engine that is commonly referred to as PubMed (www.pubmed.gov). Anyone with Internet access can use PubMed to search the biomedical contents of our National Library of Medicine by simply typing in any health topic into the search bar such as “whiplash” or “vitamin D” or “fibromyalgia” or thousands of other topics. The literature that is pulled up from searching the National Library of Medicine is always the most technical in the world, meaning that it is geared for health care professional and researchers, not for introductory knowledge that may appeal to lay people (even though anyone can access this information).

•••••

Electrons are negatively charged particles that spin around the nucleus of atoms. The different orbits of these spinning electrons are called shells. The biochemistry and physiology of life is often linked to events occurring with the electrons in the outer shells of atoms. The donation or sharing of these outer shell electrons expedites the efficiency of most human physiological processes.

 The spinning electrons like to exist in pairs. Atoms and/or molecules are stable when the outer shell electrons are in even numbers. If something happens to the outer shell electrons (like adding or subtracting an electron) so that an odd number of electrons exist, the atom/molecule becomes unstable, and in general, this is not good. This unstable atom/molecule is called a Free Radical. Free Radicals can damage adjacent atoms/molecules by disrupting their compliment of outer shell electrons, creating deleterious things such as mutations and toxic substances.

The most notorious of the Free Radicals are Oxygen Free Radicals. This is because Oxygen Free Radicals are produced as a normal byproduct of respiration, the creation of ATP energy molecules from glucose and oxygen in the inner membrane of the mitochondria. All of us make these Oxygen Free Radicals continually throughout our life, from birth until death. The only way to stop the production of these Oxygen Free Radicals is to stop breathing.

Healthy people make more ATP Energy than Oxygen Free Radicals. However, the damage caused by Oxygen Free Radicals accumulates throughout our lives. This accumulated damage includes damage to the mitochondrial machinery. As the mitochondria are progressively damaged by Oxygen Free Radicals, they produce less and less ATP Energy and more and more Oxygen Free Radicals, thus a vicious cycle of damage ensues.

This example is that of a relatively healthy person; 95% of the oxygen and glucose is converted into ATP Energy, while 5% is converted into Oxygen Free Radicals:

Oxygen Free Radicals are technically called Reactive Oxygen Species and are commonly abbreviated ROS. When a tissue is damaged by a Free Radical, that tissue is declared to be Oxidized or to have sustained Oxidative Injury or Oxidative Stress.

•••••

One of the best-documented concepts in health care is the Free Radical Theory of Aging. The vicious cycle of,

Mitochondria produce Oxygen Free Radicals 

Oxygen Free Radicals damage the mitochondria

(Oxidized mitochondria)

Oxidized mitochondria produce more Oxygen Free Radicals and simultaneously produce less ATP energy, accelerating the aging process

accounts for the deleterious nature of Free Radicals and ageing.

When researching the Free Radical Theory of Aging, using the technical words “Reactive Oxygen Species” is a good way to start. Typing the words “reactive oxygen species” into the PubMed search bar (12/07/11) called up 116,200 articles from the National Library of Medicine. The words “reactive oxygen species AND ageing” in the PubMed search bar produced 7,662 articles. The words “reactive oxygen species AND osteoarthritis” in the PubMed search bar produced 175 articles.

The consensus among these articles is that Free Radical damage is an important contributor to osteoarthritis. A few examples of this include:

• In December 2009, the Journal of the Medical Association of Thailand published an article titled (Sutipornpalangkul):

Free Radicals in Primary Knee Osteoarthritis 

The abstract of this article includes:

“Free radicals have an important role in the pathogenesis of knee osteoarthritis. Reactive oxygen species (ROS) produced by abnormal chondrocyte metabolism exceeds the physiological buffering capacity and results in oxidative stress. The excessive production of ROS can damage proteins, lipids, nucleic acids, and matrix components. They also serve as important intracellular signaling molecules that amplify the inflammatory response. An understanding of oxidative stress involved in this disease might allow the use of antioxidant therapies in the prevention and/or treatment of knee osteoarthritis.”

• In September 2010, the journal Orthopedic Reviews published an article titled (Ziskoven):

Oxidative stress in secondary osteoarthritis:
from cartilage destruction to clinical presentation?

 The abstract of this article includes:

“Due to an increasing life expectance, osteoarthritis (OA) is one of the most common chronic diseases.”

 “The dysbalance between free radical burden and cellular scavenging mechanisms defined as oxidative stress is a relevant part of OA pathogenesis.”

 “Free radical exposure is known to promote cellular senescence and apoptosis. Radical oxygen species (ROS) involvement in inflammation, fibrosis control and pain nociception has been proven. The data from literature indicates a link between free radical burden and OA pathogenesis mediating local tissue reactions between the joint compartments. Hence, oxidative stress is likely not only to promote cartilage destruction but also to be involved in inflammative transformation, promoting the transition from clinically silent cartilage destruction to apparent OA.”

 “ROS induced by exogenous factors such as overload, trauma, local intra-articular lesion and consecutive synovial inflammation cause cartilage degradation. In the affected joint, free radicals mediate disease progression. The interrelationship between oxidative stress and OA etiology might provide a novel approach to the comprehension and therefore modification of disease progression and symptom control.”

• In September 2011, the journal Current Opinion in Rheumatology published an article titled (Loeser):

Aging and Osteoarthritis

The abstract of this article includes:

“Osteoarthritis is strongly linked to aging but the mechanisms for this link are incompletely understood.”

 “Cell stress or cell damage response contributes to chronic inflammation that promotes age-related diseases. This cellular response results in the senescence-associated secretory phenotype which has many of the characteristics of an osteoarthritic chondrocyte in terms of the cytokines, chemokines, and proteases produced. Oxidative stress can promote cell senescence and studies have shown a role for oxidative stress in altering cell signaling pathways in chondrocytes that can disrupt the response to growth factors. Mitochondria are an important source of reactive oxygen species and studies continue to support a role for the mitochondria in osteoarthritis, including work suggesting changes in energy production.”

My favorite article pertaining to osteoarthritis and free radical damage was published in the American Journal of Physical Medicine and Rehabilitation in 2006, titled (Garstang):

Osteoarthritis
Epidemiology, Risk Factors, and Pathophysiology

The authors, Susan V Garstang, MD and Todd P Stitik, MD, are from theUniversityofMedicineand Dentistry of New Jersey. In this article, Drs. Garstang and Stitik note that osteoarthritis is:

“the clinical and pathologic outcome of a range of disorders that results in structural and functional failure of synovial joints. Osteoarthritis occurs when the dynamic equilibrium between the breakdown and repair of joint tissues is overwhelmed.”

Drs. Garstang and Stitik note that osteoarthritis is the most prevalent form of arthritis and a major cause of disability in people aged 65 and older. Osteoarthritis affects the majority of adults over age 55.

Garstang and Stitik note that the incidence of osteoarthritis is influenced by both systemic and local factors. Important to this discussion, Drs. Garstang and Stitik note that pertaining to systemic factors, that there is evidence that osteoarthritis is linked to free radicals, and that high dietary antioxidants (especially vitamins C and D) are protective against the development of osteoarthritis. They state: “Chondrocyte senescence is thought to be the result of chronic oxidative stress.”

Garstang and Stitik note that if elevated oxidative stress systemic factors are present, the joints are vulnerable, and thus local biomechanical factors will have more of an impact on joint degeneration and osteoarthritis. Historically, traditional chiropractic patient management emphasizes the treatment and resolution of the local biomechanical factors which are undoubtedly factors in the genesis and progression of joint osteoarthritis. Considering the impact of Free Radicals and Oxidative Stress as systemic influences on joint degeneration and osteoarthritis is an important addition to the management of these patients.

•••••

 Turning our discussion to Free Radicals and Oxidative Stress, an authoritative text on the subject is the book:

 Oxidative Stress, Disease and Cancer

This book is edited by Keshav K. Singh of the Roswell Park Cancer Institute inNew York. This 2006 reference book has more than 1,000 pages of information.

A central theme of this book is that free radicals and inflammation are intimately linked: free radicals drive inflammation and inflammation drives free radicals. This book lists six (6) primary drivers of the production of Reactive Oxygen Species (ROS). They are:

1)      The arachidonic acid cascade to inflammatory prostaglandins and leukotrienes.

2)      The glutamate cascade.

3)      Low antioxidant defenses.

4)      Excessively high metabolic activities.

5)      High levels of metal toxins, such as iron and copper.

6)      Increased production and release of catecholamines.

Discussing aspects of each of these six drivers of Reactive Oxygen Species is relevant to his discussion:

1)      The arachidonic acid cascade to inflammatory prostaglandins and leukotrienes.

Arachidonic acid is a 20-carbon long omega-6 fatty acid. It is a metabolic precursor to the powerfully pro-inflammatory eicosanoid prostaglandin (PGE2) and leukotriene (LTB4) hormones. Dr. Singh describes how these pro-inflammatory eicosanoid arachidonic acid derivatives increase the production Oxygen Free Radicals which would systemically contribute to joint osteoarthritis.

The biochemical anti-inflammatory nemesis of arachidonic acid is the omega-3 fatty acid eicosapentaenoic acid. Eicosapentaenoic acid produces anti-inflammatory eicosanoid hormones, stopping cartilage degradation and osteoarthritis (Curtis).

Cyclo-oxygenase (COX)/Lipo-oxygenase (LOX) Pathways

If a pea, for example, were whole, it would be identified as a pea.

Calling an ingredient pea protein indicates that the pea has been hydrolyzed, at least in part, and that processed free glutamic acid (MSG) is present.

Relatively new to the list are wheat protein and soy protein.

]]> http://thechiropracticimpactreport.com/january-2012/feed/ 0 http://thechiropracticimpactreport.com/december-2011/ http://thechiropracticimpactreport.com/december-2011/#comments Thu, 01 Dec 2011 21:58:02 +0000 admin http://thechiropracticimpactreport.com/?p=1158 Chronic Pain Syndrome And Vitamin D

Humans evolved outdoors, in the sunshine. Exposure to the sun’s ultraviolet radiation produces a hormone known as “vitamin D”. Vitamin D is critical for human health. The nucleus of all of our cells have vitamin D receptors. There is evidence that vitamin D influences the expression of about 10% of human genes.With very rare exceptions, humans cannot achieve optimal levels of vitamin D through diet alone. Although some foods are fortified with vitamin D, consumption of large amounts of such foods will not achieve optimal levels. To achieve and maintain optimal levels of vitamin D, we must either use vitamin D supplements or use the sun.The sun showers onto earth a large range of radiation, including ultraviolet radiation (UV). UV radiation has three wavelengths, as follows:Ultraviolet A (UVA): 320-400 nm

UVA has the longest wavelength and therefore it penetrates deepest into the skin. The most superficial layer of skin cells is the squamous cells. Deeper to the squamous cells are the basal cells. Below the basal cells are the melanocytes. Because UVA penetrates deepest into the skin, it is the primary UV influence on the melanocytes. Melanocytes produce the dark colored skin pigment melanin. This means that it is UVA that is primarily responsible for skin tanning. Sadly, damage to these same melanocytes increases the risk of the deadly skin cancer melanoma. UVA radiation is also primarily responsible for skin wrinkles.Ultraviolet B (UVB): 280-319 nm

UVB should be subcategorized: 280-289 nm and 290-319 nm

• 280-289 nm UVB radiation is absorbed by the atmosphere and therefore does not influence human physiology, neither positively nor negatively.

• 290-319 UV radiation is most important. This range of UVB is primarily responsible for burning of the skin with excess sun exposure.  Because of its shorter wavelength (as compared to UVA), it is less likely to affect the deeper melanocytes, and therefore is less associated with deadly melanoma. Older sunscreens (UVB blockers only) and contemporary non-broad-spectrum sunscreens (UVB and UVA blockers) only blocked the skin burning UVB radiation, allowing the user to spend more time in the sun without burning. Ironically, this increased the sunscreen user’s exposure to the dangerous wrinkle and melanoma producing UVA radiation.

To add to the irony, it is UVB radiation in the 290-319 nm wavelength that starts the production of vitamin D, as detailed below.Consequently, older sunscreens (UVB blockers only) reduced skin burning, reduce the skin production of vitamin D, increase skin wrinkles, and increase deadly melanomas.Ultraviolet C (UVC): 200-280 nm

UVC has the shortest wavelength and therefore it does not penetrate well. In fact, it is unable to penetrate the earth’s atmosphere, where it is 100% absorbed.

•••••

James Dowd, MD, is an Associate Professor of Medicine atMichiganStateUniversity. He is also the founder and director of both the Arthritis Institute of Michigan and theMichiganArthritisResearchCenter. He is board certified in internal medicine, adult rheumatology and pediatric rheumatology.In 2008, Dr. Dowd published a book titled The Vitamin D Cure: Five Steps to Heal Your Pain and Improve Your Mood.Dr. Down states that the optimal level of vitamin D is between 50-70 ng/ml.

PAIN

In his book, Dr. Dowd states:“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.”Dr. Dowd explains how joint cartilage integrity is dependent upon the quality of the bone the cartilage sits upon, stating:“The bone that lies under the joint cartilage keeps the cartilage stable, functioning, and durable.” “You will speed up the rate of your cartilage breaking down when anything destabilizes the bone below the cartilage, such as poor bone development or increased bone turnover caused by vitamin D deficiency.”

Dr. Dowd notes that there is a 2-3 fold faster rate of osteoarthritis progression in those with the lowest 20% of vitamin D levels compared to those with the highest levels.Dr. Dowd notes that adequate vitamin D supplementation can eliminate chronic back pain symptoms in nearly all patients, stating:“Those who took vitamin D supplements saw dramatic resolution of pain, muscle fatigue and muscle cramps.”

MAGNESIUM

Dr. Dowd emphasizes that there is an important relationship between vitamin D and magnesium, stating:1)      Magnesium is critical for one’s body to produce the active form of vitamin D.2)      The receptor that vitamin D uses in the nuclear membrane is poorly expressed when one is magnesium deficient.3)      Magnesium is required for vitamin D to function properly.Dr. Dowd further explains that magnesium is low when the body becomes acidic. He notes that the two main causes of an acidic body are the consumption of grains and dairy products, so he discourages both. He states that the most abundant and absorbable source for magnesium is the consumption of green leafy vegetables.

•••••

The world’s leading authority on vitamin D is Michael F. Holick, PhD, MD. Dr. Holick is a professor atBostonUniversityMedicalCenterand the director of the university’s General Clinical Research Unit, Bone Health Clinic, and the Heliotherapy, Light, and Skin Research Laboratory. A search of the National Library of Medicine

using the PubMed search engine identified 345 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 details these steps to the formation of the active form of vitamin D:

STEP #1

Our skin cells contain a molecule called

7-dehydrocholesterol = provitamin D3

which absorbs ultraviolet light B (UVB, wavelength 290-319 nm)

STEP #2

The absorption of UVB by provitamin D3

produces

pre-vitamin D3

within the skin cells

STEP #3

Our body heat

converts

pre-vitamin D3

into

vitamin D3

within the skin cell

(this is the same molecule as supplemental vitamin D3)

STEP #4

Vitamin D3

exits the skin cell into the blood stream

and

travels to the liver

where

25-hydroxy vitamin D (calcidrol) is produced

STEP #5

25-hydroxy vitamin D

leaves the liver

into the blood stream

to the kidney

STEP #6

The kidney makes the active form of vitamin D

1, 25 dihydroxy vitamin D

(this is the active form of vitamin D that was discovered by Dr. Holick)

STEP #7

This active form of vitamin D (1, 25 dihydroxy vitamin D)

circulates throughout the body

binding to receptors in the nucleus of the cell

influencing gene expression

Dr. Holick discusses the following FACTSpertaining to vitamin D:1)      Humans evolved in a manner as to be dependent upon sunshine for life and health.2)      There has been a 22% reduction of vitamin D levels in theUSpopulation in the last 10 years.3)      In theUnited Statesvitamin D insufficiency occurs in:

• 70% of Whites
• 90% of Hispanics
• 97% of Blacks

4)      The activated form of vitamin D that is found in your blood is produced in the kidneys. However, some other tissues also make the activated form of vitamin D. These include the prostate, breast, lungs, colon and brain. The activated vitamin D formed in these tissues does not enter the blood stream, but remains in those specific tissues.5)      “You could easily consume 5,000 IU of vitamin D a day, probably forever,” without overdosing.6)      The assay for 25-vitamin D is the most ordered assay in theUnited States. This is the form of vitamin D that exists after the liver but before the kidney.7)      It is more difficult to synthesize the active form of vitamin D as one ages. A 70-year old person is 75% less efficient in synthesizing vitamin D as compared to a 20-year old person.8)      Neither calcium levels nor activated vitamin D levels (1, 25 dihydroxy vitamin D) levels are indicative of one being vitamin D deficient or not. The only acceptable measure for vitamin D deficiency is 25-vitamin D (made in the liver). Dr. Holick states:

“Do not accept any other marker

no matter what your doctor tells you.”

Dr. Holick discusses the following MYTHS pertaining to vitamin D:1)      It is a myth that one can wash vitamin D off from the skin shortly after being in the sun. Dr. Holick says this is not true because vitamin D3 is actually produced inside the skin cell itself, and therefore cannot be washed off.2)      Vitamin D2 does not work or is inferior to vitamin D3. Dr. Holick says it is now proven and understood that vitamin D2 works just as well as vitamin D3.3)      One can obtain adequate activated vitamin D from eating a good diet. Dr. Holick disagrees with this. He is adamant that one can only achieve adequate levels of vitamin D by being exposed to sufficient sunshine or by supplementation. He further notes that one cannot obtain optimal levels of vitamin D by consuming vitamin D fortified foods or by taking a multiple vitamin supplement, as the levels of vitamin D are too low.

PAIN

In 2007, Dr. Sota Omoigui states:“The origin of all pain is inflammation and the inflammatory response.”

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

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

“Irrespective of the characteristic of the pain, whether it is sharp, dull, aching, burning, stabbing, numbing or tingling, all pain arises from inflammation and the inflammatory response.”Dr. Holick details how vitamin D has substantial anti-inflammatory properties.

•••••

Dr. Holick notes that osteomalacia is a known widespread chronic pain syndrome that is caused by vitamin D deficiency. Dr. Holick states:“Osteomalacia is characterized by vague but often intense bone and muscle aches and is frequently misdiagnosed as fibromyalgia, chronic fatigue syndrome, or arthritis.”

Dr. Holick estimates that 40 – 60% of those diagnosed with fibromyalgia or chronic fatigue syndrome are actually suffering from osteomalacia subsequent to a massive vitamin D deficiency.Dr. Holick notes that when a patient has a deficiency of vitamin D, there also exists a deficiency of calcium mineralization in the bones. Poorly mineralized bones consist of a “Jell-O-like” collagen matrix that expands with pressure, abnormally stretching the highly innervated periosteal coverings. The result is a throbbing, aching bone pain. Dr. Holick states:“When people are sitting with aches in their hips or lying in bed with throbbing aches in their bones, it can be very hard for physicians to immediately think of vitamin D deficiency. But often that’s exactly what’s causing the problem.”

•••••

     Dr. Holick notes that 93% of those suffering from nonspecific muscular and skeletal aches and pains are shown to be vitamin D deficient.

RECENT SUPPORTIVE STUDIES

In 2009, Gerry Schwalfenberg, MD from the Department of Family Medicine, University of Alberta, Canada, published an article in the Journal of the American Board of Family Medicine, titled:

Improvement of Chronic Back Pain or

Failed Back Surgery with Vitamin D Repletion: A Case Series

In this study, Dr. Schwalfenberg describes 6 cases of improvement/resolution of chronic back pain or failed back surgery after vitamin D repletion in a Canadian family practice.  He notes that vitamin D insufficiency is common; repletion of vitamin D to normal levels in patients who have chronic low back pain or have had failed back surgery may improve quality of life or, in some cases, result in complete resolution of symptoms. In this report, there were 4 patients who had chronic back pain for more than a year and 2 patients who suffered for more than 3 years from failed back surgery.In this study, Dr. Schwalfenberg makes the following key points:“Back pain is the most common neurological complaint in North America, second only to headache.”

“Low back pain (LBP) and proximal myopathy are common symptoms of vitamin D deficiency and osteomalacia.”

“Vitamin D is required for the differentiation, proliferation, and maturation of cartilage cells and for the production of proteoglycan synthesis in articular chondrocytes.”

 ”Patients who have chronic, nonspecific LBP or have had failed back surgery may have an underlying vitamin D insufficiency/deficiency.”

“All patients had tried various pain treatments, including physiotherapy, visiting a chiropractor, acupuncture, or visit to a pain management clinic, all without much benefit.”

“Repletion of inadequate vitamin D levels demonstrated significant improvement or complete resolution of chronic LBP symptoms in these patients.”

Physicians should have a high index of suspicion for low vitamin D levels in patients with LBP.

“The patients in this study who responded best used between 4000 and 5000 IU of vitamin D3/day.”

“This case series supports information that has recently become apparent in the literature about vitamin D deficiency and its influence on back pain, muscle pain, and failed back surgery. Doses in the range of 4000 to 5000 IU of vitamin D3/day may be needed for an adequate response.”

•••••

In 2009, (Straube) a study was published in the journal Pain, titled:

Vitamin D and Chronic Pain

The authors reviewed 22 studies that indicated a strong association between vitamin D deficiency and chronic pain.

•••••

In 2010, JoAnn Manson, MD from the Division of Preventive Medicine, Brigham and Women’s Hospital, HarvardMedicalSchool, published an article in the journal Metabolism, titled:

Pain: sex differences and implications for treatment

In this study, Dr. Manson found that women have a higher prevalence than men of several clinical pain conditions and of inflammation-mediated disorders. Given the important role of inflammation in mediating pain, nutritional factors that modulate the inflammatory response offer a promising and exciting new avenue for the prevention and treatment of chronic pain disorders. Of particular interest is the potential role of moderate- to high-dose vitamin D and omega-3 fatty acid supplements, both of which have powerful anti-inflammatory effects. These nutritional interventions, which influence cytokine, leukotriene, and prostaglandin pathways, may be of particular benefit to women due to their higher prevalence of inflammatory chronic pain disorders.In this study, Dr. Manson makes the following key points:Inflammation increases the incidence of pain. Both vitamin D and omega-3 fatty acids “have powerful anti-inflammatory effects.”

“Women tend to have a heightened inflammatory response compared with men. This enhanced inflammatory response may contribute to the substantially higher risk of painful inflammatory autoimmune conditions in women compared with men, including rheumatoid arthritis, lupus and other collagen vascular disorders, and osteoarthritis.”

Two very promising nutritional interventions for pain management are moderate- to high-dose vitamin D and the marine omega-3 fatty acids (eicosapentaenoic acid + docosahexaenoic acid).

Vitamin D and omega-3 fatty acids “reduce levels of circulating pro-inflammatory cytokines, decrease chronic joint pain, and may reduce the risk of autoimmune diseases.”

“Vitamin D, in addition to its role in calcium homeostasis, has powerful effects on the immune system, inhibiting proinflammatory cytokines such as interleukin-6 and tumor necrosis factor–alpha and reducing C-reactive protein.”

Vitamin D deficiency increases chronic widespread pain and/or fibromyalgia, especially in women.

A high level of vitamin D reduces knee and hip osteoarthritis and pain.

Given the important role of inflammation and cytokines in mediating and modulating pain, there is a “promising role of moderate- to high-dose vitamin D and omega-3 fatty acid supplementation in preventing and treating inflammation and chronic pain disorders. These nutritional interventions may be of particular benefit to women due to their higher prevalence of inflammatory chronic pain disorders.”

•••••

In October 2010, (Heidari) a study was published in the journal International Journal of Rheumatic Disease, titled:

Association between nonspecific

skeletal pain and vitamin D deficiency

The authors detail the evidence on how deficiency of vitamin D is reported in patients in many types of musculoskeletal pain. Their study  evaluated 276 chronic skeletal pain sufferers and 202 control subjects to add to the evidence that vitamin D deficiency is associated with chronic nonspecific skeletal pain.

•••••

In November 2010 (Bhatty) a study published in the journal Journal of the Pakistan Medical Association, titled:

Vitamin D Deficiency in Fibromyalgia

The authors assessed 40 female patients diagnosed with fibromyalgia fromKarachi,Pakistan. They found that 100% of these woman had suboptimal levels of vitamin D. Specifically, they found that 80% had vitamin deficiency (averaging about 15 ng/ml) and 20% had vitamin D insufficiency (below 30 ng/ml). The authors concluded that vitamin D deficiency is frequently seen in patients with fibromyalgia and nonspecific musculoskeletal pain syndromes.

•••••

In April 2011, (Arnson) an editorial appeared in the journal Israeli Medical Association Journal, titled:

Is Vitamin D a New Therapeutic Agent in

Auto-inflammatory and Pain Syndromes?

The authors note that “hypovitaminosis D is a worldwide epidemic, due to insufficient intake and inadequate sunlight exposure,” estimating that worldwide 40-90% of older persons are vitamin insufficient. They recommend that all chronic pain persons be assessed for vitamin D levels.

•••••

In September 2011, Tague and colleagues from the University of Kansas Medical Center published a study in the Journal of Neuroscience, titled:

Vitamin D deficiency Promotes Skeletal

Muscle Hypersensitivity and Sensory Hyperinnervation

The authors note that “musculoskeletal pain affects nearly half of all adults and most of them are vitamin D deficient.” They also know that nociceptors express vitamin D receptors, and that a lack of vitamin D can cause nociceptive hyperinnervation of skeletal muscles, contributing to muscular hypersensitivity and pain.

•••••

In 2011, the editorial of the Scandinavian Journal of Primary Health Care (Kragstrup) is titled:

Vitamin D Supplementation for Patients with Chronic Pain

In this editorial Dr. Kragstrup reviews the epidemiological studies that link low levels of vitamin D to chronic pain. He advocates both testing for and supplementing of vitamin D in chronic pain sufferers.

•••••

     Also 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?

     In this article, Dr. Pizzorno makes the following key points:1)      “Over the past several years, the surprising prevalence of vitamin D deficiency has become broadly recognized.”2)      Vitamin D deficiency is linked to:

• Osteoporosis
• Cardiovascular disease
• Cancer
• Autoimmune diseases
• Multiple sclerosis
• Pain
• Loss of cognitive function
• Decreased strength
• Increased rate of all-cause mortality

3)      “Deficiency of vitamin D is now recognized as a pandemic, with more than half of the world’s population at risk.”4)      Approximately 50% of the healthy North American population and more than 80% of those with chronic diseases are vitamin D deficient.5)      80% of healthy Caucasian infants are vitamin D deficient. [And the rate of vitamin D deficiency tends to be greater in African American and Hispanic children].6)      Those with vitamin D deficiency experience 39% higher annual healthcare costs than those with normal levels of vitamin D.7)      The minimum blood levels of vitamin D [25(OH)D3] is 32 ng/ml; the optimal level is 50-70 ng/ml.8)      Prolonged intake of 10,000 IU of supplemental vitamin D3 “is likely to pose no risk of adverse effects in almost all individuals.”9)      The recommended loading dose of supplemental vitamin D3 should be about 20,000 IU/day for 3 – 6 months with a maintenance dose of 5,000 IU/day. Those taking this amount of supplemental vitamin D3 should periodically have their serum 25(OH)D3 levels measured.

SUMMARY POINTS FROM DAN MURPHY:

• All chronic pain patients should have their 25 hydroxy vitamin D levels checked.

• 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 with 5,000 IU of vitamin D3 per day until optimal levels are achieved.

•••••

Personal Injury Cases and the Chiropractor

Chiropractic education instills that personal injury cases have two components:

1. An injury component. This component requires healthcare, treatment to the injured patient.

1. A legal component. This component involves the protection of the injured patient’s legal rights.

     Chiropractors who treat personal injury patients understand that their clinical protocols can influence the legal component of a personal injury case. Specifically, there is no substitute for:

• Taking a good case history
• Doing a thorough orthopedic and neurological examination
• Taking good quality and adequate radiographs
• Creating an accurate diagnosis that can be supported by history, complaints and examination findings
• Doing standard and thorough daily charting
• Using standard measurement outcomes, such as pain drawings, Oswestry, Roland Morris, Neck Disability Index, SF-36, algometer, visual analogue scale, etc.
• Doing periodic (monthly) thorough subjective and objective re-evaluations with a follow-up written report of findings
• Having referred the patient out for needed diagnostic procedures that are not done in the chiropractic office (MRI, EMG, SEP, SPECT, etc.)
• Having referred to other health care providers and/or colleagues for verifying or additional opinions
• Being able to determine when the patient has reached a point of maximum improvement, and consequently ending regularly scheduled treatment so that the case can proceed towards settlement of claim
• Being knowledgeable and conversant in the academic concepts of soft tissue injury, such as the phases of injured tissue healing, the relationship of vehicle damage to patient injury, the influence of pre-accident degenerative joint disease, and the influence of variables such as pre-accident awareness or head rotation

The Chiropractic Impact Report™ is a monthly publication by myself, Dan Murphy, DC. I am a 1978 graduate ofWesternStatesChiropracticCollege inPortland,OR. I have managed about 10,000 whiplash-injury cases. In the past 32 years, I have taught more than 500 12-hour post graduate continuing education classes pertaining to whiplash and spinal trauma, including 21 years of coordinating a year-long certification program in spine trauma, certified through the International Chiropractic Association. Additionally, I am board certified in chiropractic orthopedics (DABCO), and I am on the faculty at Life Chiropractic College West inHayward,CA (28 years).The purpose of The Chiropractic Impact Report™ is to keep you updated as to relevant academic concepts pertaining to whiplash-injured patients. The hope is that the information is useful in terms of enhanced understanding, as well as helping the personal injury attorney deal with insurance claim adjusters and adverse medical experts.The chiropractor sending you this Report is well versed and trained in these concepts, and can be a valuable asset in personal injury cases in terms of both academics and treatment. Additionally, these expert chiropractors have access to a monthly phone consultation with me to discuss any pertinent issues that they may be facing on a particular case. I hope that you find this Report and the referring chiropractor a valuable resource.Sincerely,Daniel J. Murphy DC, DABCO

REFERENCES

 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.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.Cedric F. Garland, Christine B. French, Leo L. Baggerly and Robert P. Heaney; Vitamin D Supplement Doses and Serum 25-Hydroxyvitamin D in the Range Associated with Cancer Prevention; Anticancer Research; February 2011; Vol. 31; No. 2; pp. 617-622.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.Kragstrup TW; Vitamin D Supplementation for Patients with Chronic Pain; Scandinavian Journal of Primary Health Care; 2011, 29: pp. 4-5.Manson JE; Pain: sex differences and implications for treatment; Metabolism; October 2010, Volume 59, Supplement 1, pp. S16-S20.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.Pizzorno J; What We Have Learned About Vitamin D Dosing?; Integrative Medicine; Vol. 9, No. 1, Feb/Mar 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.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.

In the legal cases I have consulted in, often it is claimed that children cannot be injured in motor vehicle collisions, and therefore they do not require any treatment. To escalate this perspective, I have consulted in cases where the chiropractor treating such a child is accused of committing fraud, a crime. Occasionally, these cases will even progress to courtroom trial.

Pertaining to the causes of death of our children, the following statistics were compiled from the United States Centers for Disease Control (CDC) National Center for Health Statistics (NCHS).

Summary

Children are injured in motor vehicle collisions, and it is not a small problem; rather, it is a huge problem. Motor vehicle collisions have consistently proven to be the number one reason for both mortality and morbidity in children younger than 25 years of age.

The bodies of children younger than one year of age function as a single piece of inertial mass during motor vehicle collisions. Children in this age group have a proportionately larger head size as compared to overall body mass. Consequently, when they are unrestrained during a motor vehicle collision, they tend to “lead” with their head. Their heads and bodies will collide with the interior of the vehicle, and ejections of their bodies are known to occur. Such unrestrained children sustain serious head, brain, and cervical spinal cord injuries, leading to death and significant lifelong disabilities.

When children younger than one year of age are restrained in a child restraint seat and that child restraint seat is not securely attached to the vehicle seat with the appropriate adult restraint belt, the child’s body and the restraint seat together will function as a single piece of inertial mass.  Once again the child will sustain serious head and brain injuries. Not securing the child safety seat to the vehicle is considered to be misuse of the safety device.

When children younger than one year of age are properly restrained in a forward facing child safety seat, and that child safety seat is properly secured to the vehicle with the adult restraint belt, serious head, brain, and cervical spinal cord injuries are largely avoided. Yet, in this forward facing position the properly restrained child has increased vulnerability to cervical spine injury, especially in frontal impacts. This is because the restraints immobilize the child’s body, yet their head remains moveable. With this young child’s proportionately larger head size as compared to overall body mass, and with the child’s poorly developed strength of the cervical spine musculoskeletal tissues, significant cervical spine soft tissues occur.

Most serious injuries to restrained children younger than one year of age occur during a frontal impact collision.  These serious injuries can be reduced by placing the child restraint seat in a rearward facing direction, and then properly securing this child restraint seat to the vehicle using the adult restraint belts. Serious injuries are reduced as the forces of the frontal impact are dispersed over a broader surface area of the child; over the back of the skull, the thoracic cage, and the pelvis. There is no doubt that a child of this age group who is properly restrained in the rearward facing position has the best chance of avoiding injury in a motor vehicle collision, and especially in serious frontal impact collisions.

When children younger than one year of age are restrained in a child safety seat that is properly secured to the vehicle by the adult belt, but the crotch strap of the child safety seat is not properly attached, the child’s body will “submarine” under the waist strap, catching the child under the chin.  The results are serious cervical spine injury, including fracture of the odontoid process or a bipedicular (hangman’s) fracture of C2. An adult must always properly secure the crotch strap portion of the child restraint seat for children in this age group.

Children younger than one year of age should not be restrained in a child safety seat in the rearward facing position in the front seat of a vehicle that has a passenger side air bag. In this position, the closeness of the child to a rapidly outwardly exploding air bag can launch the safety seat and child at an extremely high velocity, resulting in serious head and brain injury.

Children between 1 – 4 years of age are similar to children younger than age one in that their heads are proportionately larger as compared to overall body mass, the strength of their musculoskeletal spinal tissues are not as developed as those of the adult. When they are unrestrained they tend to “lead” with their heads sustaining serious head, brain, and cervical spinal cord injuries after colliding with the interior of the vehicle, and are at risk of ejection. Recent retrospective statistical studies show that the children in this age group are least injured when they are properly restrained in a child safety seat facing the rearward direction. When children in this age group are properly restrained and facing the forward direction, they sustain significant cervical spine soft tissue injury during frontal collisions.  Contrary to common practice, it is recommended that children remain in child restraint seats facing the rearward position for a long as possible as they age, ideally to approximately age 4.

Caution should be used when restraining children between 1- 4 years of age in an adult lap belt. The pelvis of children in this age group is much shorter in height, and the anterior superior iliac spine is grossly underdeveloped as compared to that of the adult, increasing the tendency for the lap belt to slip up over the top of the pelvis rim and to be in contact with the abdomen and its contents. Because of the shorter stature of these children, in a frontal impact their face or chest will not collide with the dashboard or with the seat in front of them. This results in a serious rapid flexion of the child’s torso around the adult lap belt, or “jackknifing.”  Serious and fatal abdominal viscera and mid lumbar spinal injuries result.

Children between ages 4 – 9 years have the greatest difficulty with motor vehicle collision safety. Children in this age group face forward nearly always and are restrained in the adult seat belt. Unfortunately, adult seat belts do not meet the special needs of this group of children. Often they are riding in the rear seat of the vehicle, and there are still many vehicles that do not have shoulder harness restraints available for rear seat passengers.  As the developing pelvis remains short in height with an underdeveloped anterior superior iliac spine in this age group, it is once again common for the adult lap belt restraint to slip over the rim of the pelvis and to come into contact with the abdomen and its contents. The center of gravity for these children is higher as compared to that of the adult, superior to the lap belt.  This proportionately increases the fulcrum stress above the lap belt in a frontal impact or during a rebound flexion following a rear impact. Again, this results in serious injuries to the abdominal viscera and mid lumbar spine, including Chance fractures.  Depending on the stature of these children, their face/head may impact the dashboard or the seat in front of them, resulting in significant face, head, brain, and cervical spinal cord injuries.  It is, therefore, recommended that whenever possible, children of this age group should be restrained in a lap belt shoulder belt combination.

Children between ages 4 – 9 years also have unique problems when using the recommended adult lap belt with shoulder harness combination.  Because of their short stature, the shoulder harness does not fit their body adequately. For many children in this age group, the shoulder harness will cut across their cervical spine or face rather than their chest. When left in this position, the shoulder harness can cause serious and fatal cervical spine and facial injuries. Also, because of the uncomfortable annoyance of the shoulder belt crossing the neck or face, many children of this age group will simply place the shoulder strap behind their back, rendering them susceptible to the lap belt injuries noted above. Other children will place the shoulder harness under the arm. This position is also quite dangerous, as the thoracic cage is not capable of handling the forces of a frontal collision during this age of skeletal maturation that are generated by the shoulder harness. The stresses imparted to the child can seriously injure the thoracic cage, including imparting cardiac and pulmonary trauma. The proper shoulder harness placement for this age is across the chest, over the clavicle, but remaining off the cervical spine and face. This is best accomplished by using a booster seat that effectively increases the height of the child, or by using a device that lowers the shoulder harness away from the face and neck and into the proper position and secures it in place by attaching to the lap belt.

Very young children cannot communicate to their parents or health care providers the location or nature of their injuries. Even non-life threatening injuries in children should be documented and properly managed. I have created a useful form to help me evaluate very young children with a history of being involved in a motor vehicle collision. (From Biedermann, attached separately) 

Personal Injury Cases and the Chiropractor

Chiropractic education instills that personal injury cases have two components:

1. An injury component. This component requires healthcare, treatment to the injured patient.

1. A legal component. This component involves the protection of the injured patient’s legal rights.

     Chiropractors who treat personal injury patients understand that their clinical protocols can influence the legal component of a personal injury case. Specifically, there is no substitute for:

• Taking a good case history
• Doing a thorough orthopedic and neurological examination
• Taking good quality and adequate radiographs
• Creating an accurate diagnosis that can be supported by history, complaints and examination findings
• Doing standard and thorough daily charting
• Using standard measurement outcomes, such as pain drawings, Oswestry, Roland Morris, Neck Disability Index, SF-36, algometer, visual analogue scale, etc.
• Doing periodic (monthly) thorough subjective and objective re-evaluations with a follow-up written report of findings
• Having referred the patient out for needed diagnostic procedures that are not done in the chiropractic office (MRI, EMG, SEP, SPECT, etc.)
• Having referred to other health care providers and/or colleagues for verifying or additional opinions
• Being able to determine when the patient has reached a point of maximum improvement, and consequently ending regularly scheduled treatment so that the case can proceed towards settlement of claim
• Being knowledgeable and conversant in the academic concepts of soft tissue injury, such as the phases of injured tissue healing, the relationship of vehicle damage to patient injury, the influence of pre-accident degenerative joint disease, and the influence of variables such as pre-accident awareness or head rotation

The Chiropractic Impact Report™ is a monthly publication by myself, Dan Murphy, DC. I am a 1978 graduate ofWesternStatesChiropracticCollege inPortland,OR. I have managed about 10,000 whiplash-injury cases. In the past 32 years, I have taught more than 500 12-hour post graduate continuing education classes pertaining to whiplash and spinal trauma, including 21 years of coordinating a year-long certification program in spine trauma, certified through the International Chiropractic Association. Additionally, I am board certified in chiropractic orthopedics (DABCO), and I am on the faculty at Life Chiropractic College West inHayward,CA (28 years).

The purpose of The Chiropractic Impact Report™ is to keep you updated as to relevant academic concepts pertaining to whiplash-injured patients. The hope is that the information is useful in terms of enhanced understanding, as well as helping the personal injury attorney deal with insurance claim adjusters and adverse medical experts.

The chiropractor sending you this Report is well versed and trained in these concepts, and can be a valuable asset in personal injury cases in terms of both academics and treatment. Additionally, these expert chiropractors have access to a monthly phone consultation with me to discuss any pertinent issues that they may be facing on a particular case. I hope that you find this Report and the referring chiropractor a valuable resource.

Sincerely,

Daniel J. Murphy DC, DABCO

REFERENCES

Boyd, William, M.D., Pathology, Lea & Febiger, (1952).

Buckwalter J, Effects of Early Motion on Healing of Musculoskeletal Tissues, Hand Clinics, Volume 12, Number 1, February 1996.

Cohen, I.Kelman; Diegelmann, Robert F; Lindbald, William J; Wound Healing, Biochemical & Clinical Aspects, WB Saunders, 1992.

Cyriax, James, M.D., Orthopaedic Medicine, Diagnosis of Soft Tissue Lesions, Bailliere Tindall, Vol. 1, (1982).

Fischgrund, Jeffrey S, Neck Pain, monograph 27, American Academy of Orthopaedic Surgeons, 2004.

Gargan, MF, Bannister, GC, Long-Term Prognosis of Soft-Tissue Injuries of the Neck, Journal of Bone and Joint Surgery, September, 1990.

Gunn, C. Chan, Pain, Acupuncture & Related Subjects, C. Chan Gunn,

(1985).

Gunn, C. Chan, Treating Myofascial Pain: Intramuscular Stimulation (IMS) for Myofascial Pain Syndromes of Neuropathic Origin,  University ofWashington, 1989.

Hodgson, S.P. and Grundy, M., Whiplash Injuries: Their Long-term Prognosis and Its Relationship to Compensation, Neuro-Orthopedics, (1989), 7.88-91.

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.

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.

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.

Kirkaldy-Willis, W.H., M.D., Managing Low Back Pain, Churchill Livingston, (1983 & 1988).

Kirkaldy-Willis, W.H., M.D., & Cassidy, J.D.,”Spinal Manipulation in the Treatment of Low-Back Pain,” Can Fam Physician, (1985), 31:535-40.

Majno, Guido and Joris, Isabelle, Cells, Tissues, and Disease: Principles of General Pathology,OxfordUniversity Press, 2004.

Mealy K, Brennan H, Fenelon GCC; Early Mobilization of Acute Whiplash Injuries; British Medical Journal, March 8, 1986, 292(6521): 656-657.

Oakes BW. Acute soft tissue injuries.  Australian Family Physician. 1982; 10 (7): 3-16.

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.

Oschman, James L, Energy Medicine: The Scientific Basis, Churchill Livingstone, 2000.

Rogier M. van Rijn, Anton G. van Os, Roos M.D. Bernsen, Pim A. Luijsterburg, Bart W. Koes, Professor, Sita M.A. Bierma-Zeinstra; What Is the Clinical Course of Acute Ankle Sprains? A Systematic Literature Review; The American Journal of Medicine; April 2008, Vol. 121, No. 4, pp. 324-331.

Rosenfeld M, Gunnarsson R, Borenstein P, Early Intervention in Whiplash-Associated Disorders, A Comparison of Two Treatment Protocols; Spine, 2000;25:1782-1787.

Roy, Steven, M.D., and Irvin, Richard, Sports Medicine: Prevention, Evaluation, Management, and Rehabilitation, Prentice-Hall, Inc. (1983).

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.

Seletz E; Whiplash Injuries; Neurophysiological Basis for Pain and Methods Used for Rehabilitation; Journal of the American Medical Association; November 29, 1958, pp. 1750-1755.

Schofferman J, Bogduk N, Slosar P; Chronic whiplash and whiplash-associated disorders: An evidence-based approach; Journal of the AmericanAcademyofOrthopedic Surgeons; October 2007;15(10):596-606.

Stonebrink, R.D., D.C., “Physiotherapy Guidelines for the Chiropractic Profession,” ACA Journal of Chiropractic, (June1975), Vol. IX, p.65-75.

Stearns, ML, Studies on development of connective tissue in transparent chambers in rabbit’s ear; American Journal of Anatomy, vol. 67, 1940, p. 55.

Sturzenegger M, DiStefano G, Radanov BP, Schnidrig A. Presenting symptoms and signs after whiplash injury: the influence of accident mechanisms. Neurology. April 1994;44(4):688-93.

Sturzenegger M, Radanov BP, Di Stefano G. The effect of accident mechanisms and initial findings on the long-term course of whiplash injury. Journal of Neurology. July 1995;242(7):443-9.

Wyke, B.D., Articular neurology and manipulative therapy, Aspects of Manipulative Therapy, Churchill Livingstone, 1980, pp.72-77.

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; 199-200; 245-6; 300-19; 436-7; 451-2; 474-6.

HISTORY: Mandy, a 50-year-old female, was injured in a motor vehicle collision.

Her stationary vehicle was struck from the rear by a vehicle of similar mass that was traveling at a speed of approximately 20 miles per hour at the time of collision. Damage to her vehicle was judged to be $6,600.

The collision caught Mandy by surprise, and she was looking left at the moment of impact. This is important because there is good evidence (Sturzenegger 1994, Sturzenegger 1995) that factors associated with greater initial injury and a worse outcome one year after injury are (in descending order):

1. Being involved in a collision in which the patient is caught by surprise.
2. Being involved in a collision in which the patient’s head is rotated.
3. Being involved in a collision in which the impact is from a rear-end direction.

Although dazed, Mandy did not lose consciousness. An ambulance did take her to the emergency department of her own HMO, which was geographically close by.

At the hospital, Mandy was evaluated and radiographs were taken. There were no broken bones, signs of instability, congenital anomalies, or degenerative disease. She was told she had suffered a soft tissue injury and that it would get better in a few days to a few weeks.

For treatment, Mandy’s doctors put her into a soft cervical spine collar, she was prescribed a nonsteroidal anti-inflammatory drug, and given a heat pack for home use. She was advised to return for a follow-up visit if she was having continuing problems. Mandy was advised to continue to work in her usual occupation as a real estate agent.

Mandy began wearing her cervical spine soft collar most of the time. Although the anti-inflammatory medicines and the hot pack seemed to help her (this seems paradoxical), she did not seem to be making overall relevant improvement. She continued to have significant neck pain and stiffness with an occasional headache.

Mandy did continue to work and actually missed no work at all. However, her neck was sore and stiff making her grumpy, and she became fatigued easily.

Mandy wore her cervical collar nearly constantly for about two weeks, then she reduced its usage to only when she was engaging in more strenuous activities, such as driving or shopping, and during certain activities at work. She liked her hot pack and she used it on average 3-4 times per day. She still needed her pain medicine, taking them a few times daily.

After about two months of being essentially unchanged, Mandy returned to her HMO physician and asked him if there was anything else she could do for her neck pain with occasional headaches. Her doctor authorized for Mandy to see one of the HMO’s physical therapists. She was prescribed one physical therapy session per week for the next four weeks.

Mandy’s physical therapist talked to her about her posture and gave her some exercises. He evaluated the ergonomics of her desk, primarily as related to when she was doing work on her computer.

After her four physical therapy visits, Mandy had incorporated his advice and exercises into her routine. Yet, she continued to suffer from neck pain and stiffness with occasional headaches.

Nine months after being injured, Mandy was still suffering and she could not go a full day without taking pain medications. Mandy needed to do something different.

Mandy became my patient nine months after being injured.

•••••

There is a common misconception that injured soft tissues will heal in a period of time between four and eight weeks. It is frequently claimed that injured soft tissues will heal spontaneously, leaving no long-term residuals, and that treatment is not required. This type of information is misleading and confusing because it is not true. As an example, in 2008, The American Journal of Medicine published a systemic review of the literature evaluating the clinical course of acute ankle sprain (Rijn 2008). The authors conducted a database search in MEDLINE, CINAHL, PEDro, EMBASE, and the Cochrane Controlled trial register. They found 31 studies that met their inclusion criteria. Their findings include:

• 5% to 33% of patients still experienced ankle pain after 1 year.
• The studies reported an incidence of subjective instability of their injured ankle in up to 53% patients.
• 15% to 64% had not fully recovered at 3 years.
• The incidence of re-sprains ranged from 3% to 34% of the patients.

Most of my med-legal experience is with whiplash injury. Often, insurance defense personnel and their chiropractic/medical experts make an analogy between the whiplash-injured neck and a sprained ankle. Their classic claim is that a sprained ankle will heal spontaneously (without any treatment) and quickly (weeks), and there are no long-term residuals.

This article by Rijn presents a much different reality pertaining to the healing of the sprained ankle: at 3 years up to 64% have not fully recovered, up to 33% have residual pain, up to 53% suffer from residual instability, and up to 34% suffer from re-injury. It appears that 15% to 64% have some degree of permanent injury. Additionally, the severity of ankle injury is not a strong predictor for the ultimate clinical outcome. It appears that trauma from ankle sprain and whiplash have a number of shared characteristics: significant residual pain, instability, re-injury rates, permanent injury residuals, and the severity of injury not being a predictor for the ultimate clinical outcome.

Consequently, I believe that the most important question is:

Is there an approach to the management of injured soft tissues that improves the timing and quality of the healing outcome?

•••••

Published articles and books concerning the healing of injured soft tissues (Oakes 1982; Roy and Irving 1983; Kellett 1986; Buckwalter/Woo 1988, Majno 2004) indicate that the time frame for soft healing is approximately one year.

The healing of injured soft tissues takes place in three specific phases. The first phase is called the acute inflammatory phase. This phase will last approximately 72 hours. During this phase, after the initial injury, an electrical current is generated at the wound, called the “current of injury.” This “current of injury” attracts fibroblasts to the wound (Oschman, 2000). During this phase there is also initial bleeding and continual associated inflammation of the injured tissues. Because of the increasing inflammatory cascade during this period of time, it is not uncommon for the patient to feel worse for each of the first three days following injury. Because there is disruption of local vascular supplies, there is insufficient availability of substrate (glucose, oxygen, etc.) to produce large enough quantities of ATP energy to initiate collagen protein synthesis to repair the wound.

Experience and published studies (Kellett 1996) indicate that the best management of soft tissue injuries during the acute inflammatory phase is ice therapy. Ice therapy during the first 72 hours following injury reduces pain and swelling, and minimizes the formation of scar tissue that often causes prolonged disability (Seletz 1958). [Unfortunately for Mandy, during this phase of soft tissue healing, she was prescribed and used heat].

After 72 hours following injury, the damaged blood vessels have mended. The resulting increased availability of glucose and oxygen elevates local ATP levels and collagen repair begins by the fibroblasts that accumulated during the acute inflammatory phase. This second phase of healing is called the phase of regeneration. During the regeneration phase the disruption in the injured muscles and ligaments is bridged. Some references call the regeneration phase the phase of repair, which creates confusion about the timing of healing (Jackson, 1977). “Repair” connotation is that the process has completed, which, as we will see, is not the case. The fibroblasts manufacture and secrete collagen protein glues that bridge the gap in the torn tissues. This phase will last approximately 6-8 weeks (Jackson, 1977). At the end of 6-8 weeks, the gap in the torn tissues is more than 90% bridged; more than 90% of the collagen that is laid down in the breach occurs during this second phase of healing. Consequently, many will erroneously claim this to be the end of healing. However, it clearly is not.

Experience and published studies (Stearns 1940, Seletz 1958, Cyriax 1982, Roy 1983, Kellett 1986, Mealy 1986, Cohen 1992, Salter 1993, Jonsson 1994, Buckwalter 1996, Kannus 2000, Rosenfeld 2000) document that the best management of soft tissue injuries during the second phase of healing is early, persistent, controlled mobilization. In contrast, immobilization is harmful, leading to increased risk of slowed healing and chronicity (Stearns 1940, Mealy 1986, Cohen 1992, Salter 1993, Jonsson 1994, Kannus 2000, Rosenfeld 2000, Schofferman 2007). [Unfortunately for Mandy, during this second phase of soft tissue healing, she was prescribed and used a cervical collar].

There is a third and final phase of healing. This phase is called the phase of remodeling.

The phase of remodeling starts near the end of the phase of regeneration. During the phase of remodeling the collagen protein glues that have been laid down for repair are remodeled in the direction of stress and strain. This means that the fibers in the tissue will become stronger, and will change their orientation from an irregular pattern to a more regular pattern, a pattern more like the original undamaged tissues. Proper treatment during this remodeling phase is very necessary if the tissues are to get the best end product of healing. It is during this remodeling phase that the tissues regain strength and alignment. Remodeling takes approximately one year from the date of injury. It is established that remodeling takes place as a direct byproduct of motion. Chiropractic healthcare puts motion into the tissues in an effort at getting them to line up along the directions of stress and strain, thereby giving a stronger, more elastic end product of healing.

Traditional chiropractic joint manipulation healthcare is directed towards putting motion into the periarticular paraphysiological space. The concept of paraphysiological joint motion was first described by Sandoz in 1976, and is explained well by Kirkaldy-Willis 1983 and 1988, by Kirkaldy-Willis/Cassidy 1985, and in the 2004 monograph on Neck Pain (edited by Fischgrund) published by the American Academy of Orthopedic Surgeons (see picture). These discussions clearly show that there is a component of motion that cannot be properly addressed by exercise, massage, etc., and that this component of motion can be properly addressed by osseous joint manipulation. Therefore, traditional chiropractic osseous joint manipulation adds a unique aspect to the treatment and the remodeling of periarticular soft tissues that have sustained an injury.

During this third phase of healing, the phase of remodeling, Mandy continued to wear a cervical collar, especially during high-demand activities. Although she did add some exercises to her management, which is helpful, she employed no management aspects that would have introduced motion into the periarticular paraphysiological space. As Schofferman and Bogduk state in their 2007 article titled: Chronic whiplash and whiplash-associated disorders: An evidence-based approach,

“exercise alone is rarely curative”

Additionally, Drs. Schofferman and Bogduk suggest there is value in spinal manipulation in the management of chronic whiplash patients (Schofferman, 2007).

•••••

Mandy’s whiplash soft tissue injury management that included heat, immobilization and limited exercises did not result in an acceptable clinical outcome. Nine months after being injured, she was suffering from chronic neck pain, weakness, and occasional headaches.

My approach to her management included:

• Regular and strenuous resistive effort exercises of the muscles of her cervical and thoracic spines.

• No more use of a cervical collar.

• Transverse friction myotherapy to reduce the adverseness of post-traumatic muscular adhesions and fibrosis (Cyriax, 1982).

• Specific osseous joint manipulation to the joints that were reduced in the symmetry and/or magnitude of normal motion. Such manipulations will reduce articular adhesions, remodel periarticular fibrosis, reduce muscle hypertonicity and spasm, and close the “pain gate” (Kirkaldy-Willis, 1983, 1985, 1988).

• Specific chiropractic postural correctional techniques. Improved posture reduces stresses in both soft tissues, muscles, and articulations.

Mandy remained under my care for a period of 4 months, and she was seen a total of 32 visits at our clinic. Her progress was steady and progressive. When she was released from additional regularly scheduled treatment, she was instructed to continue to do her prescribed exercises. Mandy’s symptoms were not completely resolved, but she judged her clinical status to be 85% improved as compared to when she first entered our clinic.

•••••

There are some problems associated with the healing of injured soft tissues. Microscopic histological studies show that the repaired tissue is different than the original, adjacent, undamaged tissues. During the initial acute inflammatory phase there is bleeding from the damaged tissues and consequent local inflammation. This progressive bleeding releases increased numbers of fibroblasts into the surrounding tissues. Chemicals that are released trigger the inflammation response that is noted in cases of trauma. Subsequent to the inflammatory response and to the number of fibrocytes that are released into the tissues, the healing process is really a process of fibrosis. In 1975, Stonebrink addresses that the last phase of the pathophysiological response to trauma is tissue fibrosis. Boyd in 1953, Cyriax in 1983, and Majno/Joris in 2004 note that there is tissue fibrosis subsequent to trauma. This fibrosis of repair subsequent to soft tissue trauma creates problems that can adversely affect the tissues and the patient for years, decades, or even forever.

Fibrosed tissues are functionally different from the adjacent normal tissues. The differences fall into two main categories:

Category 1:  The repaired tissue is weaker and less strong than the undamaged tissues. This is because the diameter of the healing collagen fibers are smaller, and the end product of healing is deficient in the number of crossed linkages within the collagen repair.

Category 2:  The repaired tissue is stiffer or less elastic than the original, undamaged tissues. This is because the healing fibers are not aligned identically to that of the original. Examination range of motion studies will indicate that there are areas of decrease of the normal joint ranges of motion.

In addition, Cyriax notes “fibrous tissue is capable of maintaining an inflammatory response long after the initial cause has ceased to operate.” Since inflammation alters the thresholds of the nociceptive afferent system (Omoigui 2007), physical examinations in these cases will show these fibrotic areas display increased sensitivity, and digital pressure may show hypertonicity and spasm. This increased sensitivity can be documented with the use of an algometer, which is a device that uses pressure to determine the initiating threshold of pain.

Because the fibrotic residuals have rendered the tissues weaker, less elastic, and more sensitive, the patient will have a history of flare-ups of pain and/or spasm at times of increased use or stress. These episodes of pain and/or spasm at times of increased use or stress of the once damaged soft tissues is the rule rather than the exception, and a problem that the patient will have to learn to live with. It is likely that the patient will continue to have episodes of pain and/or spasm for an indefinite period of time in the future. It is probable that the patient will have a need for continuing care subsequent to these episodes of pain and/or spasm.

Consistent with these concepts, a study by Hodgson in 1989 indicated that 62% of those injured in automobile accidents still have significant symptoms caused by the accident 12 1/2 years after being injured; and that of the symptomatic 62%, 62.5% had to permanently alter their work activities and 44% had to permanently alter their leisure activities in order to avoid exacerbation of symptoms. One of the conclusions of the article is that these long-term residuals were most likely the result of post-traumatic alterations in the once damaged tissues.

A study by Gargan in 1990 indicated that only 12% of those sustaining a soft tissue neck injury had achieved a complete recovery more than ten years after the date of the accident. One of the conclusions of this study is that the patient’s symptoms would not improve after a period of two years following the injury.

It is established neurologically (Wyke 1985, Kirkaldy-Willis and Cassidy 1985) that when a chiropractor adjusts (specific directional spinal manipulation) the joints in the region of pain and/or spasm, that there is a depolarization of the mechanoreceptors that are located in the facet joint capsular ligaments, and that the cycle of pain and/or spasm can be neurologically aborted. This is why many patients feel better after they receive specific joint manipulation from a chiropractor following an episode of increased pain and/or spasm.

What is the basis for the chronic post-trauma pain syndromes that so many patients suffer from?  A good explanation is found from Gunn (1978, 1980, 1989). He refers to this type of pain as supersensitivity. The supersensitivity type pain is a residual of the scarring or the fibrosis that was created by the injuries sustained in this accident. The treatment that we give to the patient for the injuries sustained in an accident is really not designed to heal the sprain or strain but rather, to change the fibrotic nature of the reparative process that has left the patient with residuals that are weaker, stiffer, and more sore. The actual diagnosis for this type of problem is initial sprain/strain injuries of the paraspinal soft tissues with fibrotic residuals subsequent to the fibrosis of repair of once damaged soft tissues that have left these tissues weaker, stiffer, and more sensitive as compared to the original tissues. The majority of our efforts in the treatment of post-traumatic chronic pain syndrome patients is in dealing with the residual fibrosis of repair and its associated mechanical and neurological consequences. These residuals to some degree are most probably permanent. The patient will have to learn to deal with the long-term residuals and the occasional episodes of pain and/or spasm. However, as noted above, occasional specific joint manipulation in the involved areas can neurologically inhibit muscle tone, improve ranges of motion, disperse accumulated inflammatory exudates, and the patient will have less pain and improved function.

The concepts briefly discussed above are frequently not understood or appreciated. There is a tendency for healthcare providers to not properly examine the patient in order to document these regions of tissue fibrosis and its consequent mechanical and neurological consequences and, therefore, to quote Stonebrink, the real problem is missed.

•••••

I believe that for Mandy, her poor early management resulted in excessive tissue fibrosis, and as noted above, that was the basis for her chronicity. Our management of her problems reduced the magnitude of her fibrotic residuals and their adverseness. Her cervical spine range of motion increased, her posture improved, her muscle strength increased and her musculoskeletal fatigue resolved. She no longer used her cervical collar and she did not need any pain medications. Her residual symptoms were manageable and tolerable with continuing cervical spine exercise. It is probable that some of her fibrotic residuals were not reducible, creating the pathoanatomical basis for her residual symptoms (Josson 1994).

Addendum

Three months after Mandy was released from treatment, she was involved in another similar motor vehicle collision. She sustained significant soft tissue injuries of her cervical and thoracic spines, essentially in the exact locations of the collision she had sustained approximately nineteen months prior.

The day of this second injury, Mandy presented herself to our clinic for management.

Our acute care protocol included recumbent traction (for 20 minutes) with a cervical pillow and ice pack. This was done four times per day, once in the office and three times at home. She was initially seen in our office daily for the first three weeks following her injury. Low-level laser therapy was applied for 20 minutes daily to her injured spinal regions in an effort to elevate ATP levels, accelerating the healing process.

On the fourth day, we added to her management a passive motion protocol to the joints of the cervical and thoracic spines; each of her joints were carefully pushed into the passive range of motion (see picture below) while using the laser with an anti-inflammatory setting. This is done in an effort to disperse inflammation and thereby reduce long-term scarring (fibrosis). It also puts tension in the developing granulation tissue, improving alignment and strength. This is a benefit that cannot be achieved by exercise alone.

At two weeks, we began to provide specific joint manipulation (adjustments) to the articulations that showed reduced and/or altered motion patterns. Simultaneously, postural corrections, transverse friction myotherapy and resistive effort exercises were initiated.

Mandy’s entire trauma management program lasted eighteen weeks; she was seen in our office a total of 34 times. When she was released from additional regularly scheduled treatment, she reported to be 100% resolved of all signs and symptoms. This means that the residuals she had from her prior accident had completely resolved. I believe that the second accident had re-torn the fibrotic residuals she retained from her prior collision. The magnitude of the second collision was such that it reduced fibrotic residuals that I was unable to reduce therapeutically. But I now had the opportunity to manage her new acute injuries with a different, superior approach. The results were gratifying for both Mandy and myself.

BACKGROUND INFORMATION FROM DAN MURPHY

All pain has an inflammatory component. In his 2007 article, Omoigui, concludes:

“The origin of all pain is inflammation and the inflammatory response.”

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

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

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

Post-traumatic inflammation is often the consequence of the membrane release of arachidonic acid fat cascading into the pro-inflammatory hormone prostaglandin E2 (PGE2). In his 2010 article, Maroon states:

“A major component of the inflammatory pathway is called the arachidonic acid pathway because arachidonic acid is immediately released from traumatized cellular membranes.”

Cell membrane trauma releases arachidonic acid. Arachidonic acid is then transformed into the pro-inflammatory hormones prostaglandins and thromboxanes through the enzymatic action of cyclooxygenase.

This is why omega-6/omega-3 fatty acid balancing is an important clinical strategy in the management of patients suffering from pain syndromes (Boswell, 2006).

Inflammation alters the pain threshold and increases pain perception (Omoigui, 2007; Boswell, 2006; Maroon, 2006; Cleland, 2006; Goldberg 2007; Maroon, 2010). In 2007, Omoigui states:

The unifying Law of Pain indicates that there is an inflammatory soup of biochemical mediators that are present in all pain syndromes.

The resolution of inflammation is fibrosis or scar tissue (Manjo, 2004). In 2004, Manjo states:

“After a day or two of acute inflammation, the connective tissue—in which the inflammatory reaction is unfolding—begins to react, producing more fibroblasts, more capillaries, more cells—more tissue. In other words, granulation tissue arises from normal connective tissue, but it cannot be mistaken for normal connective tissue, because its fibroblasts are plump and activated.”

“Fibrosis means an excess of fibrous connective tissue. It implies an excess of collagen fibers, with a varying mixture of other matrix components. It can be a local phenomenon, as an end result to chronic inflammation and of wound healing.”

“When fibrosis develops in the course of inflammation it may contribute to the healing process.” “By contrast, an excessive or inappropriate stimulus can produce severe fibrosis and impair function.”

“Why does fibrosis develop? In most cases the beginning clearly involves chronic inflammation. Fibrosis is largely secondary to inflammation.”

Fibrotic granulation tissue is capable of maintaining an inflammatory response long after the completion of the healing process, a component of chronic pain (Cyriax, 1982). In 1982, Cyriax states:

“Fibrous tissue appears capable of maintaining an inflammation, originally traumatic, as the result of a habit continuing long after the cause has ceased to operate.”

“It seems that the inflammatory reaction at the injured fibers continues, not nearly during the period of healing, but for an indefinite period of time afterwards, maintained by the normal stresses to which such tissues are subject.”

Tension within the scar granulation tissue initiates remodeling, reducing inflammation. [Supports the need for early persistent mobilization and chiropractic adjustments]. Once again, in 1982 Cyriax states:

“Tension within the granulation tissue lines the cells up along the direction of stress.  Hence, during the healing of mobile tissues, excessive immobilization is harmful.  It prevents the formation of a scar strong in the important direction by avoiding the strains leading to due orientation of fibrous tissue and also allows the scar to become unduly adherent, e.g. to bone.”

•••••••••

Americans eat a lot of fat. This is important in a trauma clinical practice because one particular type of fat is linked to both acute and chronic pain. In fact, this fat was the central theme of the 1982 Nobel Prize in Medicine/Physiology, which pertained to pain.

Our bodies have somewhere around 75 trillion cells. The cell membranes are composed primarily of fat, and it is the fat that we habitually eat. Trauma/injury to tissues disrupts the cell membranes, releasing the fat and activating enzymes that metabolize those fats (Maroon, 2010).

There is a type of dietary fat that is linked to inflammation and pain. If people eat this pro-inflammatory pain producing fat, then it is that fat that is released as a consequence of trauma/injury. This fat is not a saturated fat. It is a poly-unsaturated fatty acid called arachidonic acid. Arachidonic acid is an omega-6 fat. Our bodies have enzymes that convert arachidonic acid into pro-inflammatory hormones (leukotrienes, thromboxanes, prostaglandins); and these pro-inflammatory hormones are linked to pain (Omoigui, 2007; Boswell, 2006; Maroon, 2006; Cleland, 2006; Goldberg 2007; Maroon, 2010).

The primary American source of dietary arachidonic acid is eating meat. Meat is not bad per se. Meat becomes bad when the animal is fed junk food that makes it fat and sick. Economically, our food animals are fed the food that is most fattening. That’s because they are sold by the pound. Fatter animals are worth more in the marketplace. Our food animals are proven to become really fat on a diet of corn and/or soybeans.

Of course, fattening animal feed is a poor economic choice unless it is also cheap feed. In today’s political environment, the cheapest feed is the food that is subsidized by the taxpayers; and it makes so much sense: lobbying our politicians to use taxpayer dollars to grow corn and soybeans creates a win-win situation for all, cheap meat (this is sarcasm, as noted below).

Meat, a source of complete proteins, historically was an expensive and therefore rare commodity (at least since the Agricultural Revolution, beginning about 10,000 years ago). Animals become big and fat on a corn/soybean diet, and if the taxpayers subsidize these crops, the corn and soybeans also become much cheaper. By extension, the taxpayers (and the Chinese, or whoever is buying our debt) are subsidizing the cost of meat, making it so that nearly all Americans can afford to eat meat daily (if they choose to do so).

Recent evidence suggests that nearly 100% of our chickens and 93% of our cows are exclusively fed corn (USA Today, 2008). A major source of feed for our farmed fish is soybeans (Greenberg, 2010). Sadly, when these food animals are fed corn and/or soybeans, they have enzymes that convert the fat found in these crops (linoleic acid) into the pro-inflammatory hormone precursor fat, arachidonic acid.

These pro-inflammatory fats are in the omega-6 family. One hundred years ago, the amount of omega-6 fats consumed by Americans was about 2 pounds per year. Today, as a consequence of politics and economics, consumption of omega-6 fats has increased to about 25 pounds (Boswell, 2006). In contrast, the quantity of anti-inflammatory omega-3 fats in our diets had decreased substantially.

Paleolithic humans evolved with a ratio of omega-6/omega-3 fats of about 1/1; the average modern ratio is about 25/1 (Boswell, 2006). This means that the average American is prone to pain syndromes as a consequence of dietary choices and habits. At any given moment, 28% of Americans are suffering from pain (Krueger, 2008); the omega-6/omega-3 ratio is critical. The sarcastic downside from the win-win of cheap fat meat is that it predisposes the consumers, Americans, to pain syndromes. This has resulted in Americans consuming more than 70 million nonsteroidal anti-inflammatory drug (NSAID) prescriptions every year; and 30 billion over-the-counter NSAID tablets are sold annually (Maroon, 2006). The cost is $17 billion per year (Krueger, 2008). Michael Pollan states in his 2008 book In Defense of Food “The billions we spend on anti-inflammatory drugs such as aspirin, ibuprofen, and acetaminophen is money spent to undo the effects of too much omega-6 in the diet.”

Dietary strategies to rebalance the omega-6/omega-3 ratio have proven to prevent an/or reverse many of these pathological syndromes. Such strategies have proven to be more effective than pain medications about 88% of the time (Maroon, 2006).

••••••••••

     This month (August 2011), primary research from the Department of Bioengineering and the Department of Neurosurgery, University of Pennsylvania, provides some of the most important insights into the patho-biomechanics of chronic whiplash injury to date. The study was published in the journal Annals of Biomedical Engineering, and titled (Quinn, 2011):

Detection of Altered Collagen Fiber Alignment in the
Cervical Facet Capsule After Whiplash-Like Joint Retraction

The authors review that the cervical facet joint is the primary source of pain in patients with whiplash-associated disorders; yet, most clinical studies show no radiographic or MRI evidence of tissue injury. To evaluate this puzzle, these authors used quantitative polarized light imaging to assess the potential for altered collagen fiber alignment in human cadaveric cervical facet capsule specimens during and after a joint retraction simulating whiplash exposure.

The authors document that the whiplash mechanism involves a retraction event to the facet joint capsular ligaments. Although no evidence of ligament damage was detected during whiplash-like retraction, mechanical and microstructural changes of the facet joint capsular ligaments were identified following these whiplash loadings. The retraction experience produced significant decreases in ligament stiffness and increases in ligament laxity. The strained capsule regions showed altered fiber alignment, “suggesting the altered mechanical function may relate to a change in the tissue’s fiber organization.” The altered capsular ligament fiber alignment occurred without any tears that would classically be identified with diagnostic imaging, including radiographs and/or MRI. Consequently, the authors indicate that whiplash kinematics is a potential cause of microstructural damage that is not detectable using standard clinical imaging techniques.

The authors make these key points:

1)      This is the first study that has assessed changes in tissue microstructural organization of the facet capsule following whiplash-like loading.

2)      “Whiplash is a common cause of chronic neck pain, and the cervical facet joint has been identified as the site of pain in the majority of these cases.”

3)      “Up to 62% of people affected by whiplash injuries report pain lasting 2 years or more after injury.”

4)      Facet joint injuries cannot be imaged in most whiplash patients with x-rays or magnetic resonance imaging (MRI).

5)      “The lack of any definitive evidence of facet capsular ligament damage following whiplash, despite the high incidence of facet-mediated pain, suggests radiographic and MRI techniques may lack the resolution or contrast to identify these subtle injuries.”

6)      Low-speed rear-end impact collision causes the lower cervical spine to undergo a combination of compression, posterior shear, and extension. “This combination of forces and moments primarily induces a retraction of each vertebra in the posterior direction relative to its adjacent inferior vertebra in the lower cervical spine prior to head-headrest contact.” The facet capsular ligaments are at risk for excessive motion during this vertebral retraction, creating subfailure injuries to the facet capsule. “The facet capsular ligament may sustain partial failures and/or unrecovered deformation during whiplash.”

7)      Facet joint injury causes altered collagen fiber organization and facet capsular ligament laxity that may produce persistent pain. “Neither partial failure nor capsule rupture is required to initiate facet-mediated pain, suggesting painful facet joint injuries cannot be identified through traditional load-based or medical imaging techniques.”

8)      Prior to ligament visible rupture or mechanical failure, there is an anomalous fiber realignment, which may be used as a marker for subfailure capsule injury.

9)      The retraction caused permanent deformation of ground substance materials of the ligament, leading to altered collagen fiber organization. This tissue damage may be sufficient to induce an inflammatory response or nociceptor firing in the ligament.

10)     “These findings would suggest that radiographic or MRI diagnostic approaches may lack the resolution to detect the microstructural changes that can occur in the facet capsule without overt capsule rupture after a whiplash exposure.”

11)     “Facet joint displacements that produce persistent pain symptoms also induce laxity in the capsular ligament and collagen fiber disorganization.”

12)     “The detection of altered fiber alignment and unrecovered strain observed after facet retraction in the current study would suggest that whiplash-like loading may be sufficient to generate facet-mediated pain.”

This study indicates that whiplash injury causes microstructural changes, anomalous fiber realignment and laxity of the facet capsular ligaments. These injuries may cause permanent deformation of ground substance of the ligament, leading to altered collagen fiber organization. These injuries are subfailure in magnitude, but are capable of causing pain and permanent alterations in capsular mechanics. These injuries are not identifiable clinically, with x-ray, or MRI imaging. The tissue damage may be sufficient to induce an inflammatory response and/or nociceptor firing.

The anomalous fiber realignment noted in this study is probably

analogous to the writings of Cyriax when he stated that fibrotic granulation tissue is capable of maintaining an inflammatory response long after the completion of the healing process. This inflammatory granulation tissue becomes a factor in the initiation of chronic pain perception. Consequently, Cyriax also states “…that the scar tissue remains painful whenever tension is put upon it, perhaps for decades.”

This is an important study advancing the understanding of whiplash injury pathoanatomy, yet I believe there is still a missing piece. The authors document post-traumatic anomalous fiber realignment, but they only speculate that it is associated with pain producing inflammation. They offer no evidence for the existence of an actual inflammatory process. Fortunately, the next study does just that.

••••••••••

     Clas Linnman (from Harvard Medical School) and an international team of colleagues published a study in April of this year (2011) titled:

Elevated [11C]-D-Deprenyl Uptake in Chronic Whiplash Associated Disorder Suggests Persistent Musculoskeletal Inflammation

These authors note that there are few diagnostic tools for chronic musculoskeletal pain, and especially for whiplash injury. In agreement with Quinn above, they note that structural imaging methods seldom reveal pathological alterations that can account for a patient’s ongoing pain. Therefore, they sought to visualize inflammatory processes in the neck region by means of Positron Emission Tomography (PET) using an inflammatory marker, 11C-D-deprenyl, or DDE. They evaluated 22 patients with chronic pain after a rear impact car accident and 14 healthy controls. The whiplash-injured subjects had pain and reduced motion but no neurological signs.

The whiplash-injured patients displayed significantly elevated inflammatory tracer uptake in the neck, suggesting that whiplash patients have signs of local persistent peripheral tissue inflammation. The authors concluded that inflammation and its associated pain in the periphery could be objectively visualized and quantified with PET using the inflammatory tracer DDE. Key points from this study include:

1)      “Chronic musculoskeletal pain syndromes are common, cause extensive individual suffering and place a large burden on health care in society. Yet, pain remains notoriously difficult to visualize and diagnose objectively.”

2)      “The pathophysiology of persistent pain is elusive and there is a great need for ways to visualize and quantify pain mechanisms.”

3)      In a sub-portion of the population, “whiplash injuries proceed to chronic debilitating pain.”

4)      “Structural imaging does not capture on-going biological processes; where as molecular imaging with positron emission tomography (PET) has the potential to visualize such mechanisms.”

5)      The authors present evidence that shows “DDE can be used to visualize chronic inflammatory processes.”

6)      The site of inflammation “appeared to be localized to adipose tissue surrounding deep cervical muscles.” “The tracer retention observed in fatty regions surrounding deep cervical muscle may indicate that adipose tissue is actively involved in the inflammatory process.”

7)      Patients displayed elevated DDE retention in cervical soft tissue, suggesting that localized chronic inflammation is apparent in many chronic pain whiplash patients.

8)      “A large subset of patients with chronic pain after a whiplash injury displayed elevated DDE retention, suggestive of persistent peripheral tissue inflammation.”

9)      “The possibility to visualize and quantify sites of inflammation in chronic pain may be very useful in diagnosis and treatment monitoring.”

SUMMARY POINTS:

All pain has an inflammatory component.

• Post-traumatic inflammation is often the consequence of the membrane release of the arachidonic acid fat cascading into pro-inflammatory hormones, including prostaglandin E2 (PGE2). [Therefore omega-6/-3 balancing is an important clinical strategy].

• Inflammation alters the pain threshold and increases pain perception.

• The resolution of inflammation is granulation, fibrosis, or scar tissue.

• Fibrotic granulation tissue is capable of maintaining an inflammatory response long after the completion of the healing process, a component of chronic pain.

• Whiplash trauma can create anomalous fiber alignment and granulation tissue.

• From whiplash, granulation tissue and inflammation occurs as a consequence of subfailure injuries. Therefore, these injuries cannot be visualized with either x-rays or MRI.

• Persistent post-traumatic inflammation has been linked to chronic pain syndrome. This inflammation can be documented with PET using the inflammatory tracer DDE.

• Tension within the scar granulation tissue initiates remodeling, reducing inflammation. This supports the need for early persistent mobilization, exercise, and chiropractic adjustments.

• I believe that anti-inflammatory omega-6/omega-3 balancing is critical in chronic pain management.

Personal Injury Cases and the Chiropractor

     Chiropractic education instills that personal injury cases have two components:

1. An injury component. This component requires healthcare, treatment to the injured patient.A legal component. This component involves the protection of the injured patient’s legal rights.

Chiropractors who treat personal injury patients understand that their clinical protocols can influence the legal component of a personal injury case. Specifically, there is no substitute for:

• Taking a good case history
• Doing a thorough orthopedic and neurological examination
• Taking good quality and adequate radiographs
• Creating an accurate diagnosis that can be supported by history, complaints and examination findings
• Doing standard and thorough daily charting
• Using standard measurement outcomes, such as pain drawings, Oswestry, Roland Morris, Neck Disability Index, SF-36, algometer, visual analogue scale, etc.
• Doing periodic (monthly) thorough subjective and objective re-evaluations with a follow-up written report of findings
• Having referred the patient out for needed diagnostic procedures that are not done in the chiropractic office (MRI, EMG, SEP, SPECT, etc.)
• Having referred to other health care providers and/or colleagues for verifying or additional opinions
• Being able to determine when the patient has reached a point of maximum improvement, and consequently ending regularly scheduled treatment so that the case can proceed towards settlement of claim
• Being knowledgeable and conversant in the academic concepts of soft tissue injury, such as the phases of injured tissue healing, the relationship of vehicle damage to patient injury, the influence of pre-accident degenerative joint disease, and the influence of variables such as pre-accident awareness or head rotation

The Chiropractic Impact Report™ is a monthly publication by myself, Dan Murphy, DC. I am a 1978 graduate of Western States Chiropractic College in Portland, OR. I have managed about 10,000 whiplash-injury cases. In the past 32 years, I have taught more than 500 12-hour post graduate continuing education classes pertaining to whiplash and spinal trauma, including 21 years of coordinating a year-long certification program in spine trauma, certified through the International Chiropractic Association. Additionally, I am board certified in chiropractic orthopedics (DABCO), and I am on the faculty at Life Chiropractic College West in Hayward, CA (28 years).

The purpose of The Chiropractic Impact Report™ is to keep you updated as to relevant academic concepts pertaining to whiplash-injured patients. The hope is that the information is useful in terms of enhanced understanding, as well as helping the personal injury attorney deal with insurance claim adjusters and adverse medical experts.

The chiropractor sending you this Report is well versed and trained in these concepts, and can be a valuable asset in personal injury cases in terms of both academics and treatment. Additionally, these expert chiropractors have access to a monthly phone consultation with me to discuss any pertinent issues that they may be facing on a particular case. I hope that you find this Report and the referring chiropractor a valuable resource.

Sincerely,

Daniel J. Murphy DC, DABCO

REFERENCES

 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.

Maroon J, Bost JW, Maroon A; Natural anti-inflammatory agents for pain relief; Surgical Neurological International; December 2010.

Boswell M, Cole EB; American Academy of Pain Management; Weiner’s Pain Management: A Practical Guide for Clinicians; Seventh Edition, 2006, pp.584-585.

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.

Cleland LG, James MJ, Proudman SM; Fish oil: what the prescriber needs to know; Arthritis Research & Therapy; Volume 8, Issue 1, 2006, pp. 402.

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.

Manjo G, Joris I; Cells, Tissues, and Disease, Principles of General Pathology; Second Edition; Chapter 13: “Chronic Inflammation: Defense at a Price”; Oxford University Press; 2004.

Cyriax, James, M.D., Orthopaedic Medicine, Diagnosis of Soft Tissue Lesions, Bailliere Tindall, Vol. 1, (1982).

USA Today, November 12, 2008, quoting Proceedings of the National Academy of Sciences.

Greenberg P; Four Fish, The Future of the Last Wild Food; The Penguin Press, New York, 2010.

Krueger AB, Stone AA; Assessment of pain: a community-based diary survey in the USA; Lancet; 2008 May 3;371(9623):1519-25.

Pollan, M; In Defense of Food; 2008, pg. 131.

Quinn KP, Winkelstein BA; Detection of Altered Collagen Fiber Alignment in the Cervical Facet Capsule After Whiplash-Like Joint Retraction; Annals of Biomedical Engineering; August 2011, Vol. 39, No. 8, pp. 2163–2173.

Linnman C, Appel L, Fredrikson M, Gordh T, Soderlund A, Langstrom B, Engler H; Elevated [11C]-D-Deprenyl Uptake in Chronic Whiplash Associated Disorder Suggests Persistent Musculoskeletal Inflammation; Public Library of Medicine (PLoS) ONE; April 6, 2011, Vol. 6 No. 4, pp. e19182.

Format

Clinical Features

Connecting The Dots

        Personal injury cases have two components: a healthcare component and a legal component. Much of the legal component of a personal injury case is hinged upon the records of the healthcare provider. The healthcare records are often thoroughly reviewed. Accurate and complete healthcare records will protect the legal component of a personal injury claim. In contrast, healthcare records that are inaccurate will hurt the legal component of the case.

What is the patient’s diagnosis?

A diagnosis is a guess as to what is wrong with the patient. It is the treating doctor’s best guess as to the root causes of the patient’s symptoms and signs. As more information is obtained, the diagnosis will often change or be confirmed. For example, the doctor will probably suspect a discogenic L5 nerve root radiculopathy when a patient presents with low back and unilateral leg pain that extends below the knee, and examination shows a positive straight-leg-raising test at 35°, weakness of the extensor hallicus longus muscle, and hypoesthesia in an L5 dermatomal pattern. The diagnosis is confirmed when an exposed MRI shows a posterolateral L4 disc herniation compressing the L5 nerve root.

Also, for the legally defined expert treating doctor, the diagnosis falls under the standard of reasonable probability. As an example, it is often claimed that the cause of back pain is actually unknown or unproven in 85% of cases (Chou). Yet, essentially no healthcare providers list the diagnosis as “unknown.” Therefore, doctors often list a diagnosis based on reasonable probability.Seattlepersonal injury attorney Richard Adler (Adler) often defines reasonable probability as a 51% or greater chance of accuracy. I have heard him say often that the personal injury-treating doctor who has qualified as an expert to testify should be 100% certain that their opinion is at least 51% accurate. As an example, published studies (Kuslich) indicate that the tissue origin of pain in chronic low back pain patients is the annulus of the disc is more than half of the cases. This constitutes a reasonable probability. Another example is that published studies (Bogduk) indicate that the tissue origin of pain in chronic whiplash-injured patients is the facet joints in more than half of the cases. This also constitutes reasonable probability. A third example indicates that if a whiplash-injured patient had pre-accident degenerative joint disease of the cervical spine, follow-up x-rays taken 7 years later indicate that 55% developed degenerative disc disease at adjacent levels (Hohl); one could state that patients with pre-accident degenerative joint disease of the cervical spine who sustain a motor vehicle collision injury, will have a reasonable probability of developing disc degeneration at an adjacent level within the next seven years.

An actual example is a court case I testified in with an experienced personal injury attorney. This attorney thoroughly explored my opinions during my direct examination. After direct examination comes cross-examination by the insurance company attorney. His attempt to discredit me proceeded as follows:

QUESTION:
What is in your hand?

ANSWER: 
A cup.

QUESTION:
What is in the cup?

ANSWER:
Water.

QUESTION:
Are you certain?

ANSWER:
Yes.

QUESTION:

Can you state with the same degree of certainty that you have a cup of water in your hand that the testimony you gave during your direct examination is accurate?

OBJECTION (by the plaintiff attorney who had just completed my direct examination):

[He] is holding the doctor to a standard that is not the law. The standard is to a reasonable probability, a 51% chance or greater, not to 100% certainty.

JUDGE:
Sustained.

ANSWER:

I state with the same degree of certainty that I have a cup of water in my hand that the testimony I gave is reasonably probable.

It is not below the standard for a diagnosis to be incorrect, as long as it is consistent with the evidence presented in a particular case. The classic evidence collected in a whiplash injury (or in most musculoskeletal cases) includes the history, the complaints, the examination findings, and imaging, such as x-rays, stress radiographs, videofluoroscopy, MRI, CT scan, etc.

Because treatment is designed to improve the pathophysiological process expressed in the diagnosis, appropriate treatment should improve the patient’s symptoms   and signs. When expected improvement does not present, it is possible that the diagnosis was incorrect. Additional diagnostic investigations or possible referral to another provider is warranted.

In our electronic age, the clinical diagnosis is a numerical code or codes. Statisticians, policy makers, politicians, governmental agencies, reimbursement assessment personnel, electronic billing services, etc., like and even demand, these numerical diagnostic codes. It makes it much easier to evaluate and control the health care provider and the case. It makes it much easier to create policy and establish “outcome evidence.” These codes create simplicity.

However, what if the simple code is purposefully or inadvertently inaccurate? What if the health care provider used codes that have historically proven to generate better reimbursement rather than codes that more accurately represent the patient’s true clinical status? What if the health care provider had some educational gaps or lack of educational understanding of certain physiological processes and consequently used an incorrect diagnostic code? Then statistics, policies, and “outcome evidence” would all be erroneous.

In addition, and quite importantly, the convenience and simplicity of diagnostic codes may over simplify the true extent or uniqueness of a particular patient’s injuries. This scenario is particularly adverse for a patient with a personal injury because it could influence aspects of the legal component of the patient’s casee.

I have a friend who is both a chiropractor and a personal injury attorney. As a personal injury attorney, he has worked for both the plaintiff (for our injured patient) and for the defense (for the insurance company of the person who caused the injury to our patient). He has repeatedly expressed to me that the most prevalent “weak link” in a personal injury case treated by health care providers is the diagnosis. It is his position that as a rule, the diagnosis in the file or in the insurance billing forms is not supported by the history, complaint, examination findings and/or imaging studies. My friend has often expressed to me that he can discredit most health care providers by officially asking them a handful of questions pertaining to their diagnosis. In fact, my friend says that when discrediting the expertise of the treating doctor, probing the details and accuracy of the diagnosis is so simple and effective, that it is his standard starting point, and often the only process the doctor will have to endure before loss of credibility is assured.

Most health care providers use multiple diagnoses on every patient. Consequently, for a whiplash-injured patient, words (or codes) such as sprain, strain, myofascial pain syndrome, intervertebral disc syndrome, facet syndrome, radiculitis, radiculopathy, neuritis, neuropathy, nerve compression syndrome, headache, cervicogenic headache, subluxation, instability, carpal tunnel syndrome, thoracic outlet syndrome, double crush syndrome, myelopathy, cauda equina syndrome, fibromyalgia, etc., are commonly found.

For each and every word used in the diagnosis, the health care provider should be able to do the following:

• Define the word. The dictionary denotation is not always necessary. Often, a layperson’s connotation will suffice, and may be preferred.

• Know the history that is consistent with the word. As an example, are there historic facts that might distinguish a sprain injury from a strain injury? Is the diagnostic word used consistent with the given history?

• Know the clinical features for the word. What examination findings (clinical features) support the diagnosis? As an example, what are the examination findings that support the diagnosis of strain; or, what are the examination findings that support the diagnosis of sprain?

• Knowing what the clinical features are is important, but is not enough. The clinical features must be found in the records. A diagnosis not supported by the records is problematic and probably will be challenged on occasion.

EXAMPLE 1, Strain:

QUESTION:
Your diagnosis includes strain injury to the posterior cervical-thoracic spine. What is a strain injury?

ANSWER:
The soft tissue that moves bones are muscles. Muscles are attached to the bone by tendons. A strain is an injury to a muscle or to a tendon. A strain injury is considered to be a soft tissue injury because it does not involve injury to the bone.

QUESTION:
What history is consistent with a strain injury?

ANSWER:
There are three classic historic mechanisms for a strain injury:

1. A mechanism of overstretching. The injury occurs at the extreme of motion.
2. A mechanism of muscle contracting against a load that is too great for the muscle. The injury occurs in the middle of the range of motion.
3. Unaccustomed repetitive contracting of a muscle. The injury occurs in the middle of the range of motion.

QUESTION:
In this case, was one or more of these mechanisms documented through the taking of the patient’s history?

ANSWER:

Yes. The history is that of a whiplash mechanism, which is a classic example of muscle overstretching.

QUESTION:      

What are the clinical features of a strain injury?

ANSWER:

• Pain on resistive efforts.
• Pain on stretching.
• Pain on moderate digital pressure.
• Alterations of muscle tone (usually it is increased).
• Alterations of normal palpatory textures (such as swelling, edema).

QUESTION:
Can you please show me where these clinical findings are documented in your records?

ANSWER:

[You had better be able to do this, show him/her where the clinical features are documented in the records].

EXAMPLE 2, Sprain:

QUESTION: 

Your diagnosis includes sprain injury to the facet capsular ligaments of the lower cervical spine. What is a sprain injury?

ANSWER:

The soft tissue that stops the movement of a bone at the joint is the ligament. Ligaments attach bones to bones at the joint. If the joint is moved too far, the ligament is injured. This injury to the ligament is called a sprain. A sprain injury is also considered to be a soft tissue injury because it does not involve injury to the bone.

QUESTION:    What history is consistent with is a sprain injury?

ANSWER:

Ligaments are not injured in the middle of the range of motion. Rather, ligaments are only injured after the end of the range of motion is reached, and then motion exceeds the normal end of the range of motion. A history of exceeding the normal magnitude of range of motion is necessary for a sprain injury.

QUESTION:      

In this case, is there a history of exceeding the normal magnitude of the range of motion?

ANSWER:

Yes. The history is that of a whiplash mechanism, which is a classic example of exceeding the normal range of motion of the facet joints of the cervical spine. Whiplash injury is proven to exceed the range of motion of the cervical spine facet joints, injuring the facet joint capsular ligaments. This constitutes a sprain injury.

QUESTION:
What are the clinical features of a sprain injury?

ANSWER:

• Pain at the end of the passive range of motion.
• Associated protective muscle spasm at the end of the passive range of motion.
• Point tenderness with digital pressure over the injured ligament.
• Palpable or visible swelling.
• The diagnosis is confirmed if stress radiographs show signs of clinical instability or segmental hypermobility.

QUESTION:
Can you please show me where these clinical findings are documented in your records?

ANSWER:

[Once again, you had better be able to do this, show him/her where the clinical features are documented in the records].

EXAMPLE 3, Right C7 discogenic radiculopathy:

QUESTION: 

Your diagnosis includes right C7 discogenic radiculopathy. What is a C7 radiculopathy?

ANSWER:

The bones of the spine are called vertebrae. Between every two adjacent vertebrae exits two nerves, one from the right side and the other from the left side. Because these nerves are attached to the spinal cord, they are called nerve roots. Radiculopathy means that a nerve root is injured and is not functioning properly. C7 indicates that the nerve root in question is exiting from between the sixth and seventh cervical vertebrae.

QUESTION: 

What does discogenic radiculopathy mean?

ANSWER:

It means that the cause of the injury and dysfunction to the C7 nerve root is the C6-C7 intervertebral disc. The C6-C7 disc is irritating or pressing upon the C7 nerve root, causing its dysfunction. The disc is causing the radiculopathy, or discogenic radiculopathy.

QUESTION:      

What history is consistent with a discogenic radiculopathy?

ANSWER:

There are two classic historic mechanisms for a discogenic radiculopathy:

1)      As a consequence of injury.

2)      As a consequence of degenerative disease.

QUESTION:      

In this case, was one of these mechanisms documented through the taking of the patient’s history?

ANSWER:

Yes. The history is that of a whiplash mechanism, which can injure the intervertebral disc, causing irritation and dysfunction of the adjacent nerve root.

QUESTION:
Could the discogenic radiculopathy in this case be as a consequence of degenerative disease?

ANSWER:

No. The initial x-rays, which were taken the day following the whiplash injury, showed no signs of pre-accident degenerative disease. In addition, the symptoms and signs of discogenic radiculopathy developed acutely, immediately after being involved in this motor vehicle collision. It is therefore reasonably probable that the C7 discogenic radiculopathy was caused by the forces produced during this collision, the causation is post-traumatic. The cause is not degenerative.

QUESTION:
What are the clinical features of a C7 discogenic radiculopathy?

ANSWER:

• Symptoms include pain radiating from the neck and into the arm, and often into the hand.

• The symptoms are aggravated by performing the shoulder depression test.

• The symptoms are aggravated upon compressing the head into the spine (foramina compression test), especially if the neck is slightly laterally flexed to the right, and even more likely if the neck is both laterally flexed to the right with simultaneous right side rotation (Spurling’s test).

• A diminished right triceps deep tendon reflex.

• Weakness in the C7 myotomes (triceps [elbow extension], wrist flexors, finger extensors), possibly accompanied with atrophy of the associated muscles.

• Altered superficial sensation in a C7 dermatomal pattern, classically the anterior surface of the third digit.

QUESTION:
Can you please show me where these clinical findings are documented in your records?

ANSWER:
Again, you had better be able to do this, show him/her where the clinical features are documented in the records; not all of the clinical features need to be present to diagnose a suspected C7 radiculopathy, but having over half positive would argue in favor of the reasonable probability of such a diagnosis].

QUESTION:
Are there any imaging tests that confirm your diagnosis?

ANSWER:
Yes. To confirm my diagnosis, I ordered an MRI which was taken one week following the injury. The results show a right-sided herniation of the C6-C7 disc putting pressure on the right C7 nerve root.

The treating doctor should be able to answer this format of questions for every word that is used in the diagnosis.

Diagnostic Format 

        The patient’s diagnosis will and often should change (become updated) as the patient’s clinical status changes as a consequence of time and/or treatment. Spasm, radiculopathy, headache, etc., can resolve. Acute problems can become subacute or chronic. Post-traumatic scar tissue or fibrosis may develop.

To adequately describe a patient’s biological uniqueness subsequent to an injury, for more than 30 years I have advocated the three-point diagnostic format. This format also helps organize the doctor’s thoughts as to updating the diagnosis. The three components are:

1)   List the mechanism of injury. The mechanism of injury never changes from the beginning of a case though the end of the case. The initial mechanism of injury is always the same throughout the case. A typical example would be:

Hyperextension strain and sprain injury to the lower cervical and upper thoracic paraspinal soft tissues.

2)   List things that occurred as a consequence of the mechanism of injury. These resulting problems can change or resolve as a consequence of time and/or treatment. Therefore, updated diagnoses will often reflect these changes in the second part of the diagnostic format. I tend to list these resulting problems into four categories.

Examples include:

The second part of the diagnostic format may also include multifaceted syndromes, such as intervertebral disc syndrome, fibromyalgia syndrome, carpal tunnel syndrome, cervicogenic headache, temporomandibular joint dysfunction, vertigo, canalithiasis, BPPV (benign paroxysmal positional  vertigo), thoracic outlet syndrome, etc.

The typical example would continue:

Hyperextension strain and sprain injury to the lower cervical and upper thoracic paraspinal soft tissues; with resulting myalgia and spasm of the affected muscles, altered instantaneous axis of rotation of the occiput-atlas-axis (subluxation complex), and right C7 motor and sensory radiculopathy

3)   The third component of the diagnostic format is a listing of factors that makes a particular case more difficult or complicated than the usual case. It is important to list these factors not as being caused by the mechanism of the injury, but rather as factors that pre-existed the injury. Consequently, they complicate the recovery of those things that were caused by the injury.

Examples include:

Degenerative joint disease

Discogenic spondylosis

Facet joint arthrosis

Central canal stenosis

Cervical rib(s)

Hemi or Demi vertebrae

Scoliosis

Tropism

Lumbosacral transitional segment

Spondylolisthesis

Old spinal fractures

Osteoporosis

Rheumatoid arthritis

ETC.

As a rule, the third (complicating) component of the diagnosis does not change as a function of time or treatment. The typical diagnosis example would continue:

Hyperextension strain and sprain injury to the lower cervical and upper thoracic paraspinal soft tissues; with resulting myalgia and spasm of the affected muscles, altered instantaneous axis of rotation of the occiput-atlas-axis (subluxation complex), and right C7 motor and sensory radiculopathy; complicated by a moderate cervicothoracic scoliosis, facet joint arthrosis C6-C7 bilaterally, and bilateral cervical ribs.

I advocate performing a complete reevaluation of the patient every 12 visits. At that time, depending on symptoms, signs, and examination findings, the second part of the diagnosis should be updated. Regardless of the billing diagnosis, the three point diagnostic format should be found in the file with as much detail as possible to truly represent the uniqueness of the patient’s injuries and unique complicating factors to recovery. This approach will help protect the legal component of the patient’s injury claim.

Personal Injury Cases and the Chiropractor

Chiropractic education instills that personal injury cases have two components:

• An injury component. This component requires healthcare, treatment to the injured patient.

• A legal component. This component involves the protection of the injured patient’s legal rights.

Chiropractors who treat personal injury patients understand that their clinical protocols can influence the legal component of a personal injury case. Specifically, there is no substitute for:

• Taking a good case history
• Doing a thorough orthopedic and neurological examination
• Taking good quality and adequate radiographs
• Creating an accurate diagnosis that can be supported by history, complaints and examination findings
• Doing standard and thorough daily charting
• Using standard measurement outcomes, such as pain drawings, Oswestry, Roland Morris, Neck Disability Index, SF-36, algometer, visual analogue scale, etc.
• Doing periodic (monthly) thorough subjective and objective re-evaluations with a follow-up written report of findings
• Having referred the patient out for needed diagnostic procedures that are not done in the chiropractic office (MRI, EMG, SEP, SPECT, etc.)
• Having referred to other health care providers and/or colleagues for verifying or additional opinions
• Being able to determine when the patient has reached a point of maximum improvement, and consequently ending regularly scheduled treatment so that the case can proceed towards settlement of claim
• Being knowledgeable and conversant in the academic concepts of soft tissue injury, such as the phases of injured tissue healing, the relationship of vehicle damage to patient injury, the influence of pre-accident degenerative joint disease, and the influence of variables such as pre-accident awareness or head rotation

The Chiropractic Impact Report™ is a monthly publication by myself, Dan Murphy, DC. I am a 1978 graduate of Western States Chiropractic College in Portland, OR. I have managed about 10,000 whiplash-injury cases. In the past 32 years, I have taught more than 500 12-hour post graduate continuing education classes pertaining to whiplash and spinal trauma, including 21 years of coordinating a year-long certification program in spine trauma, certified through the International Chiropractic Association. Additionally, I am board certified in chiropractic orthopedics (DABCO), and I am on the faculty at Life Chiropractic College West in Hayward, CA (28 years).

The purpose of The Chiropractic Impact Report™ is to keep you updated as to relevant academic concepts pertaining to whiplash-injured patients. The hope is that the information is useful in terms of enhanced understanding, as well as helping the personal injury attorney deal with insurance claim adjusters and adverse medical experts.

The chiropractor sending you this Report is well versed and trained in these concepts, and can be a valuable asset in personal injury cases in terms of both academics and treatment. Additionally, these expert chiropractors have access to a monthly phone consultation with me to discuss any pertinent issues that they may be facing on a particular case. I hope that you find this Report and the referring chiropractor a valuable resource.

Sincerely,

Daniel J. Murphy DC, DABCO

REFERENCES

Chou R, Qaseem A, Snow V, Casey D, Cross JT, Shekelle P, Owens DK, for the Clinical Efficacy Assessment Subcommittee of the American College of Physicians and the American College of Physicians/American Pain Society Low Back Pain Guidelines Panel;  Diagnosis and Treatment of Low Back Pain: A Joint Clinical Practice Guideline from the American College of Physicians (ACP)  and the American Pain Society (APS); Annals of Internal Medicine; Volume 147, Number 7, October 2007, pp. 478-491.

Adler R; From Injury to Action: Navigating Your Personal Injury Claim; AdlerGiersch; 2011.

Hohl M; The Cervical Spine; The Cervical Spine Research Society; Lippincott, 1989; page 440.

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.

Bogduk N, Aprill C; On the nature of neck pain, discography and cervical zygapophysial joint blocks; Pain. August 1993;54(2):213-7.

Whiplash Injury and Cervicogenic Headache

          Barbara is a 45-year old woman with two adult children. She is employed full-time as a sales clerk at the local mall. Her job is not physically demanding nor is it ergonomically challenging. Her job allows her to assume multiple physical positions throughout the day while she is assisting a variety of customers with a variety of needs. There is no required heavy lifting or prolonged postures.

Barbara is fit, with good muscle tone and posture. She stands 5 feet 4 inches tall and weight 120 pounds. Her exercise regime consists of walking several miles per day, nearly every day of the week, with a group of her friends.

Barbara has suffered with chronic headaches for 24 years. In addition, her headaches seemed to make her right shoulder ache.

Barbara’s headaches began when she was involved in a motor vehicle collision that occurred at 21 years of age. She did not recall many of the details of the collision other than that she was the driver of a vehicle that was struck from the rear. The collision caught her by surprise and she remembers her head being thrown backwards. There was no loss of consciousness, and she did not experience being dazed, confusion, disorientation, or loss of any memory. The damage to her vehicle was minor, and she was able to drive away from the accident scene after exchanging insurance information with the man who was driving the striking vehicle.

Barbara did not experience pain or any other complaints at the accident scene. However, as the day progressed, she became aware of some minor neck stiffness. The next day was a different story. Barbara recalls that the next morning she was unable to pick her head up off her pillow without using her hands to assist her. Her neck was painful and stiff. And, she had a headache.

Barbara attributed her neck and head signs and symptoms to a “strain” injury caused by the vehicle collision she was involved in. She took some over-the-counter pain pills, and within a few days she was much improved.

However, about a week after the collision, Barbara became more aware that she still had a headache, and that it did not appear to be improving. Rather it seemed to be becoming more pronounced. The headache was located at the right upper posterior area of her neck and also around and behind her right eye.

Since being injured 24 years ago, Barbara has had to constantly deal with her headaches. They occur frequently and range in severity from annoying to debilitating. When she is suffering from a bad headache, she also notices an abnormal sensitivity to bright lights (photophobia). She notes that apparent triggers for her headaches range from certain neck movements to prolonged neck postures. Her headaches are always only on her right side.

Barbara’s examination shows significantly reduced lateral flexion and rotation of the upper cervical spine on the right side. She is very sensitive to mild/moderate digital pressure applied to the suboccipital region and muscles. Importantly, her right-sided frontal (around her eye) headache can be triggered by sustained deeper pressure at the inferior margin of the right inferior oblique muscle. Recall, the inferior oblique muscle exists between the spinous process of the axis (C2) and the transverse process of the atlas (C1). (Two easily identifiable landmarks for a practicing chiropractor; see drawing page 10).

Barbara reports that she has consulted a number of medical doctors (general practitioners, not specialists) about these headaches, resulting in her taking a variety of over-the-counter and/or prescription medications. She reports that these drugs definitely help her, especially when her headache is severe. She states that she takes pain medicines for her headache 10-15 days per month. But, after developing some gastrointestinal bleeding from taking over-the-counter drugs, her primary care physician suggested she try the COX-2 inhibitor drug Celebrex. She has now been consuming Celebrex 10-15 days per month, reporting that it is quite helpful when she has a bad headache.

However, Barbara became concerned after hearing media reports of Celebrex and other pain medicines being associated with an increased risk of heart attacks. In addition, she reported that she was weary of having to consume pain medicines 10-15 days per month to function appropriately in her life. Barbara acknowledges that medicines she had been taking for her headaches were helpful, but that they had not cured her headaches, and her suffering had been going on for 24 years.

Barbara self referred herself to our office as it was on her way home from work. She had seen no other chiropractors or physical therapists for her headaches. Our office was the first.

••••••••••

It has been written in top, respected journals, since at least the 1940s, that whiplash injury to the neck can cause chronic headaches. Whiplash injury pioneer Ruth Jackson, MD, wrote about this phenomenon as early as 1947.

Ruth Jackson, MD (1902-1994), was the world’s first female admitted into the American Academy of Orthopedic Surgeons (1937). She began her orthopedic private practice in Dallas in 1932. From 1936 to 1941, Dr. Jackson was Chief of Orthopaedics at Parkland Hospital in Fairmont, Texas. In 1945, she had her own private clinic built in Dallas. In 1956 she published her acclaimed, authoritative book entitled The Cervical Syndrome. The fourth and final edition of her book was published in 1978 (1). Dr. Jackson retired from clinical practice in 1989 at the age of 87 years.

In 1947, Dr. Jackson published a study in the Journal of the American Medical Women’s Association titled (2):

The Cervical Syndrome As a Cause of Migraine

In this article, Dr. Jackson notes that at least half of patients suffering from cervical syndrome will also complain of headaches as one of their principle symptoms. The cervical syndrome is caused by “cervical nerve root irritation,” and this nerve root irritation can occur as a consequence of whiplash trauma.

Dr. Jackson noted that irritation of the upper cervical spine nerve roots, C1-C2-C3, are most likely to cause headache, and that it is these upper cervical spine nerve roots that are most vulnerable to whiplash trauma. In addition, these post-traumatic headaches may still be present decades later. (Recall, Barbara’s headaches were triggered by a motor vehicle collision, and she had been suffering with headaches for 24 years).

•••••

About a decade later, in the late 1950s, the concept of chronic whiplash-generated headache was supported by the writings of Emil Seletz, MD.

     Dr. Emil Seletz (1907-1999) was a neurosurgeon in Beverly Hills, California. Dr. Seletz worked at the Los Angeles General Hospital, and he was faculty at the University of California, Los Angeles, medical school. He was also chief of neurosurgery at Cedar’s Hospital (now called Cedars-Sinai Medical Hospital) in Los Angeles, and Professor of Neurological Surgery at the University of Southern California School of Medicine. By 1957, Dr. Seletz had treated more than 20,000 injury patients, and he began publishing a series of articles pertaining to whiplash trauma and headaches. These include (3, 4, 5):

Craniocerebral Injuries and the Postconcussion Syndrome

Journal of the International College of Surgeons

January 1957, Vol. 27, No. 1, pp. 46-53

Headache of Extracranial Origin

California Medicine

November 1958, Vol. 89, No. 5, pp. 314-17

Whiplash Injuries

Neurophysiological Basis for Pain and Methods Used for Rehabilitation

Journal of the American Medical Association

November 29, 1958, pp. 1750-1755

In these articles, Dr. Seletz stressed that the cervical spine causes headaches because of a neuroanatomical relationship between the 2^nd cervical nerve root and the trigeminal nerve (cranial nerve V). Dr. Seletz notes that many patients involved in whiplash trauma will develop incapacitating severe headaches that may persist for months or even years following the injury. These headaches are often severe and begin in the suboccipital area and radiate to the vertex or to behind one eye; or they may be frontal or temporal.

Dr. Seletz believes that the 2^nd cervical nerve root is most often involved in the generation of headaches, stating:

“The 2^nd cervical nerve root is more vulnerable to trauma than other nerve roots because it is not protected by pedicles and facets.”

Dr. Seletz emphasizes that a major portion of the headaches associated with the whiplash syndrome are derived from a traction injury to the second cervical nerve root. The second cervical nerve root is particularly vulnerable to injury because it is not protected by pedicles and facets, as are the other cervical nerve roots. Also, the second cervical nerve root exits between the atlas and axis, “the point of greatest rotation of the head on the neck.”

Dr. Seletz explains that sensory changes in any of the three sensory branches (ophthalmic, maxillary, mandibular) of the trigeminal nerve (cranial nerve V) are capable of producing headaches. He also explains that the three sensory branches of the trigeminal nerve communicate (synapse with) with the 2^nd and 3^rd cervical nerve roots in the upper neck in a nucleus he calls the spinal fifth tract of the medulla.

       Spinal Fifth Tract of the Medulla

Dr. Seletz’s model of post-whiplash headache is quite simple:

1. Whiplash trauma injures the vulnerable 2^nd cervical nerve root.
2. The sensory input change derived from the injured 2^nd nerve root synapses in the spinal fifth tract of the medulla where it synaptically communicates with the branches of the trigeminal nerve.
3. The signal in the spinal fifth tract of the medulla is interpreted as a headache in one or more of the branches of the trigeminal nerve.

Dr. Seletz explains that the ophthalmic fibers of cranial nerve V descend the deepest into the cervical spine. Consequently, traumatized patients with an irritated 2^nd nerve root often perceive their headache in the distribution of the ophthalmic branch, which is around and behind the eye.

Adding to the mechanism of chronic post-traumatic headache, Dr. Seletz notes that trauma causes hemorrhage, leading to the development of adhesions forming about the upper cervical nerve roots. He states that these nerve root adhesions are visible during surgical exposure. These nerve root adhesions chronically irritate the nerve roots, sending a signal into the spinal fifth tract of the medulla and ultimately causing chronic headache.

In summary, Dr. Seletz states:

“The physiological communication between the second cervical and the trigeminal nerves in the spinal fifth tract of the medulla [trigeminal-cervical nucleus] involves the first division of the trigeminal nerve [opthalamic] and thereby gives attacks of hemicrania with pain radiating behind the corresponding eye. This is the mechanism whereby a great many chronic and persistent headaches have their true origin in injury to the second cervical nerve.”

“Many headaches are not headaches at all, but really a pain in the neck.”

•••••

     Although Drs. Jackson and Seletz described the neuroanatomical basis of headaches arising from the cervical spine in the 1940s and 1950s, “Cervicogenic Headache” was not officially recognized until 1983 by Sjaastad (6). In his 1983 article titled “Cervicogenic Headache” An Hypothesis, Sjaastad listed the diagnostic criteria for cervicogenic headache as:

• Precipitation of head pain by neck movement and/or sustained awkward head positioning.
• Precipitation of head pain by external pressure over the upper cervical or occipital region on the symptomatic side.
• Restriction of neck range of motion.
• Ipsilateral neck, shoulder, or arm pain of a rather vague nonradicular nature, or, occasionally, arm pain of a radicular nature.
• Unilaterality of the head pain, without sideshift.
• Head pain is moderate-severe, nonthrobbing, and nonlancinating, usually starting in the neck.
• Occasionally there is nausea, phonophobia, photophobia, dizziness, ipsilateral blurred vision, difficulties on swallowing, ipsilateral edema (mostly in the periocular area).
• The pain typically starts at the back of the head, spreading to frontal areas.

A recent (June 2011) PubMed search of the National Library of Medicine database using the key words “cervicogenic headache” listed 744 articles, with publication dates ranging from September 1942 to June 2011.

•••••

Perhaps the most detailed anatomical description for the physiological basis for cervicogenic headache was written by Australian physician and clinical anatomist Nikoli Bogduk, MD, PhD, in 1995. Dr. Bogduk published an article in the journal Biomedicine and Pharmacotherapy titled (7):

Anatomy and Physiology of Headache

In this article, Dr. Bogduk notes that all headaches have a common anatomy and physiology in that they are all mediated by the trigeminocervical nucleus, and are initiated by noxious stimulation of the endings of the nerves that synapse in this nucleus. “Trigeminocervical nucleus” is contemporary terminology for what Dr. Emil Seletz termed spinal fifth tract of the medulla. The trigeminocervical nucleus is a region of grey matter in the medulla of the brainstem that descends into the upper cervical spinal cord.

In agreement with Dr. Seletz above, Dr. Bogduk notes that the trigeminocervical nucleus receives afferents from all three branches (ophthalmic, maxillary, mandibular) of the trigeminal nerve (cranial nerve V). In slight variance with Dr. Seletz, Dr. Bogduk’s detailed anatomical sections indicate that the trigeminocervical nucleus receives afferents from nerve roots C1, C2, and C3.

Trigeminocervical Nucleus

Consequently, irritation of any of the upper three cervical nerve roots can cause headaches. In addition, Dr. Bogduk stresses that irritation or injury to any tissue innervated by the upper cervical nerve roots can cause headaches.

Both Dr. Seletz and Dr. Bogduk indicate that the ophthalmic branch of the trigeminal nerve extends the farthest into the trigeminocervical nucleus, and consequently cervical afferent nerve irritation is most likely to refer pain to the frontal-orbital region of the head.

Both Dr. Seletz and Dr. Bogduk agree that the C1 and C2 nerve roots are particularly likely to be involved in the genesis of cervicogenic headache because the C1 and C2 spinal nerve roots “do not emerge through intervertebral foramina.” This make these nerve roots more vulnerable to stretch or compressive stresses.

Dr. Seletz commented that in his surgically managed cervicogenic headache patients he would find scar tissue or adhesions that were responsible for chronic C2 nerve root irritation. Dr. Bodguk’s anatomical sections further isolate these C2 nerve root post-traumatic adhesions at two locations:

• At the C2 dorsal root ganglion as it crosses the C1-C2 joint capsule.

• At the under belly of the inferior oblique muscle.

 •••••

In 2005, Dr. David Biondi, an instructor in Neurology at Harvard Medical School, published an article titled (8):

Cervicogenic Headache:
A Review of Diagnostic and Treatment Strategies

Dr. Biondi notes that cervicogenic headache is a relatively common cause of chronic headaches with a prevalence as high as 20%. He notes that post-whiplash cervicogenic headache is particularly porne to chronicity.

Dr. Biondi notes that in the management of cervicogenic headache, drugs alone are often ineffective. He states, “Many patients with cervicogenic headache overuse or become dependent on analgesics.” He also notes that COX-2 inhibitors cause both gastrointestinal and renal toxicity after long-term use, and they cause an increased risk of cardiovascular and cerebrovascular events.

Dr. Biondi is an osteopathic physician, and therefore has an understanding of manual and manipulative techniques. He states:

“All patients with cervicogenic headache could benefit from manual modes of therapy and physical conditioning.”

Dr. Biondi notes that the treatment of cervicogenic headache usually requires manipulation of the upper cervical facet joints, and that manipulative techniques are particularly well suited for the management of cervicogenic headache, including high velocity, low amplitude manipulation. These techniques are commonly used by chiropractors in the management of cervicogenic headaches.

In April of this year (2011), Dr. Maurice Vincent published a detailed review article pertaining to the relationship between the cervical spine and headache (9). In the article, Dr. Vincent lists five requirements for the diagnosis of cervicogenic headache. They are:

1. unilateral pain preponderance
2. reduction of cervical range of motion
3. pain in the ipsilateral shoulder or arm
4. attacks precipitation from triggering spots in the neck
5. precipitation from awkward neck positions.
6. These five requirements are all present in my patient Barbara:

Barbara was suffering from post-traumatic chronic cervicogenic headache. Recall that her “headache was triggered by sustained deep pressure at the inferior margin of the right inferior oblique muscle.” Consequently, my assessment included that Barbara was suffering from an ectopic depolarization of the C2 nerve root at the inferior margin of the right inferior oblique muscle; the electrical signal communicated with the ophthalmic branch of the trigeminal nerve in the trigeminocervical nucleus, creating a cortical brain perception of a headache around her right eye. As there is a history of trauma and 24 years of chronicity, it seems plausible that the primary nidus of C2 irritation was scar tissue or adhesions at the inferior oblique muscle, consistent with the writings of both Drs. Seletz and Bogduk. The irritation of the C2 nerve root is most likely aggravated by alignment and motion dysfunctions of the upper cervical spinal segments.

My clinical protocols included the following:

1. Analysis and chiropractic management of upper cervical spinal segmental alignment.
2. Analysis and chiropractic management of asymmetry of upper cervical spinal segmental movement.
3. Manual friction myotherapy at the inferior margin of the inferior oblique muscle. This is done in a effort to reduce the adverseness of adhesions and/or scar tissue that appeared to be irritating the C2 nerve root.
4. Low level laser therapy (in the office) and cryotherapy (homecare) to reduce inflammation subsequent to tissue work.

Barbara was so treated three times per week for four weeks, a total of twelve visits. The one-month re-evaluation showed a 100% resolution of both signs and symptoms. Twenty-four years chronicity and suffering resolved within one moth of manual therapy.

Personal Injury Cases and the Chiropractor

Chiropractic education instills that personal injury cases have two components:

1. An injury component. This component requires healthcare, treatment to the injured patient.
2. A legal component. This component involves the protection of the injured patient’s legal rights.

     Chiropractors who treat personal injury patients understand that their clinical protocols can influence the legal component of a personal injury case. Specifically, there is no substitute for:

• Taking a good case history
• Doing a thorough orthopedic and neurological examination
• Taking good quality and adequate radiographs
• Creating an accurate diagnosis that can be supported by history, complaints and examination findings
• Doing standard and thorough daily charting
• Using standard measurement outcomes, such as pain drawings, Oswestry, Roland Morris, Neck Disability Index, SF-36, algometer, visual analogue scale, etc.
• Doing periodic (monthly) thorough subjective and objective re-evaluations with a follow-up written report of findings
• Having referred the patient out for needed diagnostic procedures that are not done in the chiropractic office (MRI, EMG, SEP, SPECT, etc.)
• Having referred to other health care providers and/or colleagues for verifying or additional opinions
• Being able to determine when the patient has reached a point of maximum improvement, and consequently ending regularly scheduled treatment so that the case can proceed towards settlement of claim
• Being knowledgeable and conversant in the academic concepts of soft tissue injury, such as the phases of injured tissue healing, the relationship of vehicle damage to patient injury, the influence of pre-accident degenerative joint disease, and the influence of variables such as pre-accident awareness or head rotation

     The Chiropractic Impact Report™ is a monthly publication by myself, Dan Murphy, DC. I am a 1978 graduate of Western States Chiropractic College in Portland, OR. I have managed about 10,000 whiplash-injury cases. In the past 32 years, I have taught more than 500 12-hour post graduate continuing education classes pertaining to whiplash and spinal trauma, including 21 years of coordinating a year-long certification program in spine trauma, certified through the International Chiropractic Association. Additionally, I am board certified in chiropractic orthopedics (DABCO), and I am on the faculty at Life Chiropractic College West in Hayward, CA (28 years).

The purpose of The Chiropractic Impact Report™ is to keep you updated as to relevant academic concepts pertaining to whiplash-injured patients. The hope is that the information is useful in terms of enhanced understanding, as well as helping the personal injury attorney deal with insurance claim adjusters and adverse medical experts.

The chiropractor sending you this Report is well versed and trained in these concepts, and can be a valuable asset in personal injury cases in terms of both academics and treatment. Additionally, these expert chiropractors have access to a monthly phone consultation with me to discuss any pertinent issues that they may be facing on a particular case. I hope that you find this Report and the referring chiropractor a valuable resource.

Sincerely,

Daniel J. Murphy DC, DABCO

REFERENCES

1. Jackson R, The Cervical Syndrome, Thomas, 1978.
2. Jackson R; The Cervical Syndrome As a Cause of Migraine. Journal of the American Medical Women’s Association. December 1947, Vol. 2, No. 12, pp. 529-534.
3. Seletz E; Craniocerebral Injuries and the Postconcussion Syndrome; Journal of the International College of Surgeons; January, 1957; 27(1):46-53.
4. Seletz E; Headache of Extracranial Origin; California Medicine; November 1958, Vol. 89, No. 5, pp. 314-17.
5. Seletz E; Whiplash Injuries, Neurophysiological Basis for Pain and Methods Used for Rehabilitation; Journal of the American Medical Association; November 29, 1958, pp. 1750 – 1755.
6. Sjaastad O; “Cervicogenic” Headache: An Hypothesis; Cephalagia; December 1983; 3(4):249-256.
7. Bogduk N; Anatomy and Physiology of Headache; Biomedicine and Pharmacotherapy; 1995, Vol. 49, No. 10, pp. 435-445.
8. Biondi DM; Cervicogenic Headache: A Review of Diagnostic and Treatment Strategies; Journal of the American Osteopathic Association; April 2005, Vol. 105, No. 4 supplement, pp. 16-22.
9. Vincent MB; Headache and Neck; Current Pain Headache Report; April 5, 2011 [Epub].

Although his athletic scholarship covered his school expenses and tuition, off-season Dave worked in construction. This work was physically demanding, and Dave was easily able to meet those demands.

Dave’s attitude was so good both on and off the football field that he was a favorite of his coaches, teachers, construction job bosses, teammates, and coworkers. By all accounts, Dave had a bright future and would go far. His primary personal goal was to play pro football in the National Football League.

And then an accidental tragedy struck: a vehicle-to-vehicle collision. Dave was in a motor vehicle that was traveling about 25 miles per hour through an intersection that was controlled by a traffic light. The traffic light was green. While proceeding through the intersection, a second vehicle suddenly appeared “out of nowhere” directly in front of Dave’s vehicle, and there was a head-on collision. The police report estimated the speed of the other vehicle to also be about 25 miles per hour. The “other” driver was cited for causing the accident.

Both vehicles were of approximately the same size (mass). The damage to both vehicles was moderate, but bad enough that both had to be towed away from the accident scene. Yet, the air bags did not deploy.

Four football players occupied Dave’s vehicle (Dave and 3 of his teammates). Dave was not the driver; rather he was the front seat passenger. Only Dave was wearing his seat belt; the other 3 young men were unbelted.

The collision caused an abrupt halt to the forward motion of Dave’s vehicle. Yet, according to Newton’s Law of Inertia, the 4 young men in the vehicle continued to move forward at about 25 miles per hour. Often this mechanism is referred to as the occupants being “thrown forward.” In reality, they are not “thrown forward.” Rather, their bodies continue to move forward at the vehicle’s speed of 25 miles per hour, thus colliding with vehicle structures that are in front (“forward”) of them. The 2 unbelted back seat passengers collided with the back of the front seats. The unbelted driver collided with the steering wheel, but not with the dashboard or windshield.

Dave (seating in the front passenger seat), did not collide with the interior of the vehicle because he was belted. Specifically, Dave was wearing the standard lap-shoulder belt combination. The seat belt Dave was using possessed a standard locking mechanism; when subjected to a sudden jerk, it locked. The quick inertial jerk on the belt caused by the forward inertial movement of Dave body initiated the jerk-locking mechanism, effectively stopping Dave’s forward inertial movement.

However, there are a few problems with the standard lap-shoulder belt combination. Specifically, in this case, the shoulder portion of the belt cut across Dave’s right clavicle, effectively stopping the forward motion of his right shoulder. This design did not stop the forward motion of Dave’s left shoulder or the forward motion of his head. However, the lap portion of the belt quickly locked, stopping the forward motion of Dave’s lower trunk.

As irony would have it, Dave’s 3 unbelted teammates were not injured. Although they were all “thrown forward” by the impact and collided with aspects of the vehicle’s interior, none of them ever developed any musculoskeletal complaints or consulted any health care providers for signs or symptoms caused by this collision.

During motor vehicle collisions, serious and fatal injuries often occur when occupants experience:

1. Crushing injuries
2. Inertial injuries that involve hitting the steering wheel, windshield or dashboard
3. Inertial injuries where occupants are thrown from the vehicle

Over the decades, motor vehicle safety engineers have added safety devices to automobiles to reduce these categories of serious injury and/or death risk. The primary focus has been on seat belts (initially) and air bags (more recently).

There is no doubt that current generation air bags save lives when they deploy. They do so primarily as a consequence of preventing the front seat driver and passenger from hitting the steering wheel, dashboard, and windshield. However, the initiation of the air bag inflation sequence requires a certain threshold. This threshold is determined by the degree of the front of the vehicle crumpling. If this threshold is not reached, the air bag inflation sequence will not be initiated and the air bag will not deploy. The collision Dave and friends experienced did not meet the air bag inflation threshold and the air bags did not deploy.

The primary purpose for vehicle seat belts is to prevent occupant ejections as a consequence of inertially based forces. The experience of being thrown from a vehicle during a collision is often fatal or associated with life-long impairments. Seat belts are excellent at preventing vehicle occupants from being thrown out of the vehicle during a collision (ejected). Consequently, there is no doubt, seat belts save lives.

However, more than half a century ago, it was noted that seat belts themselves could cause injuries. There are primarily two injuries associated with this:

1. The lap belt alone does not stop the forward inertial motion of the trunk above the belt or the pelvis and legs below the belt. Lap belts alone concentrate the inertial forces to the small (a few inches) cross sectional dimension of the belt. This allows the lap belt to function as a fulcrum of a first class lever mechanical system (a teeter totter). When the portions of the body above and below the belt continue in forward motion, the stresses at the fulcrum (the belt) are magnified, resulting in increased injury to the tissues behind the lap belt. These tissues include abdominal viscera (including the mesenteric arteries), the spine and its associated soft tissues (Thompson, 2001; Hall, 2001)
2. The addition of a (unilateral) shoulder harness will reduce the forward inertial motion of the trunk that lies above the lap portion of the belt. This is largely desirable, but not without its own complications. The primary benefit is a significant reduction of lap belt fulcrum injuries. The complications of the (unilateral) shoulder harness include:

A)   The shoulder harness does not stop the forward inertial motion of the head. Since the addition of the shoulder harness reduces the forward motion of the trunk but not that of the head, there is an increase in the inertial stresses the cervical spine experiences. This is not good for the neck. There is clear documentation that the incidence of neck sprains has increased since the use of lap/shoulder belt combination became compulsory (Rutherford, 1985).

B)   Since the shoulder harness only restrains one shoulder, the forward inertial motion of the other shoulder introduces a rotational or twisting mechanism to the torso (Anrig, 1998). The implications for this are discussed below.

(From Anrig)

C)   The shoulder harness increases injury to the chest wall, sternum and clavicle (Greingor, 2006).

D)   The shoulder harness increases injury to the breast (DiPiro, 1995; Majeski, 2007; Paddle, 2010).

The 3 occupants in Dave’s vehicle who were not restrained with seat belts were not ejected from the vehicle in this collision. Although their bodies collided with various parts of the vehicle’s interior, the impact forces were distributed over large enough areas of their bodies that no specific body part was overtly traumatized. In other words, the forces were distributed over a large surface area. Again, none of these 3 young men developed any symptoms or signs of injury from this collision.

Dave however was less fortunate. Dave was injured. The basis for Dave’s injuries are as follows:

1. 1)   The collision caught Dave completely by surprise. Consequently, he was unable to brace against the forces that were imparted into his body. In such a scenario, muscle injury is reduced but articular injury (intervertebral disc and facet capsule, etc.) are increased. It is established that being “caught by surprise” during a motor vehicle collision is coupled with greater injury, more symptoms, and a poorer recovery prognosis (Sturzenegger, 1994).
2. 2)   Dave was the front seat passenger, wearing a lap seat belt and a shoulder harness that cut across his right shoulder. As discussed above, this shoulder harness restrained the forward inertial movement of his right shoulder, but not his left shoulder. As discussed above, as Dave’s left shoulder moved forward in relation to his right shoulder, his trunk/torso twisted (rotated) to his right.

   (From Anrig)

3. The forward, twisting motion of Dave’s left shoulder caused additional flexion of his trunk/torso about the lap portion of his seat belt.
4. In summary, during this collision and because of the lap belt and shoulder harness restraints, Dave sustained a flexion/rotation injury to his lumbar spine. Trunk/torso flexion and rotation in combination is a classic mechanism to injure and herniate a lumbar intervertebral disc. Ironically and without question, if Dave had been not restrained, as was the case with his 3 companions, he would not have sustained this low back disc herniation injury.

At the accident scene, Dave knew he was injured. For the first time in his life his back hurt and his legs did not feel right. But unsurprisingly, he did not immediately go to any health care provider, assuming that he would be fine in a day or two. However, after a few days of rest, his condition was not improving, and even appeared to be getting worse. The over-the-counter nonsteroidal anti-inflammatory drugs he was taking were not helping. Dave’s low back hurt, and it was very stiff. In addition, the pain in his legs went all the way down to his feet.

Dave presented at his HMO for an evaluation 4 days after being injured. Although his low back remained very painful and his legs ached all the way down to his feet, there was no indication of altered function of bowel of bladder function. His examination was unremarkable with the exception of spasm and reduced motion of this lumbar spine. X-rays of his lumbar spine were taken. There were no signs of fracture, dislocation, instability, or degenerative changes. Dave was diagnosed with a sprained back. He was encouraged to rest and to continue taking his pain medicines.

A week later (11 days after being injured), Dave was still in bad shape. He was not getting better, and he was discouraged. His three companions who were in the vehicle with him during the collision seemed to be perfectly fine with no symptoms at all. Dave decided to see a chiropractor to see if chiropractic could help him.

Dave presented himself to my office for examination and treatment on the 11^th day following the collision and injury. History indicated that Dave felt he was getting worse, not better. Although his back was quite painful and stiff, his legs ached and they felt weak and clumsy.

It is our standard inquiry to ask about bowel, bladder, and sexual function. Dave replied that he had no opportunity or desire for sexual activity (he hurt too much), that his bowel movements were rare since injury (again, he blamed it on the pain it caused his back), but he did note that he was having a lot of trouble starting the stream for urination. He also noted that when he urinated, not much urine was produced, as if his bladder was not fully emptying. Dave noted that his bladder problems seemed to be getting worse over the last week or so.

Dave’s cervical spine was asymptomatic. Even so, I examined it, performing range of motion, compression tests, stretch tests, upper extremity deep tendon reflexes, superficial sensation and myotomal strength. The results for these procedures were unremarkable, essentially negative.

As a consequence of Dave’s lower back and lower extremity complaints, I thoroughly examined his back and legs. My finding include:

• Superficial sensations on his legs were normal.
• Patellar and Achilles deep tendon reflexes were quite suppressed bilaterally; in fact, I was unable to elicit them. I have seen this on other patients, and it can just be a normal variant, having no clinical relevance. However, it could also be an indication of a more serious low back nerve compression syndrome. If so, the syndrome would have to be affecting more than one nerve root (the Patellar reflex is controlled by the L2-3-4 roots; the Achilles reflex is controlled by the S1 root), and it would have to be bilateral.
• All of the myotomes tested in Dave’s legs were weak bilaterally, especially for a person so young and with a recent history of superior athletic ability. The muscles tested included the iliopsoas (L2-3-4), the quadriceps (L2-3-4), the tibialis anterior (L4), the extensor hallucis longus (L5), and the gluteus maximus (S1). These findings are inconsistent with a singe level of nerve root compressive neuropathology. Rather, they suggest that Dave has a compressive syndrome affecting multiple levels bilaterally.
• The Valsalva test was positive for a worsening of both low back and leg pain bilaterally. The Valsalva test is performed by attempted exhalation against a closed airway, usually done by closing one’s mouth and pinching one’s nose shut. Neuro-orthopedically it indicates that the patient has a space occupying lesion in the painful region of the spinal canal. The most classic space occupying lesion is a herination of the intervertebral disc into the central neural canal.
• I routinely assess superficial sensation in the lower extremities. In Dave’s case, they were unremarkable, normal. However, lower extremity dermatomes do not include S2-3-4-5. These sacral nerve roots innervate the perineum, which is the skin around the anus and buttocks. I do not routinely assess these sacral dermatomes because of the sensitivity of the anatomical parts necessary (around the anus), but in Dave’s case I felt it important to do so. Dave’s sacral dermatomes displayed a significant hypoesthesia, a reduced ability to feel the sensations of pin prick and light touch. This is known as “saddle anesthesia.”

This is a very important finding because in adults, the sacrum is fused into a single bony mass, the sacrum. Therefore, the only way multiple sacral nerve roots could be dysfunctional is for there to be a compression of the sacral roots at the cauda equina of the lumbar central neural canal. The most probable cause of the compression is a midline herniation of a lumbar intervertebral disc.

In Dave’s case, everything seemed to add up to a single conclusion:

• All symptoms and signs began with a single traumatic event 11 days prior.
• The mechanism of injury included a forward inertial propulsion around a fulcrum lap belt with a degree of rotation caused by the shoulder harness. A flexion/rotation event is a classic mechanism to injure the intervertebral disc and cause a posterior herniation. The fulcrum lap belt injury is proven to increase injury to the lumbar spine and discs.
• Dave’s primary symptoms include back pain, leg pain to the feet, and difficulty initiating the urinary stream.
• Dave’s examination includes a positive Valsalva test, consistent with a posterior lumbar disc intervertebral disc herniation into the lumbar spine central canal.
• Lower extremity myotomal weakness and depressed deep tendon reflexes are consistent with compressive neuropathology to multiple lumbar roots, bilaterally.
• Dave has saddle anesthesia.

Dave is suffering from a traumatically induced cauda equina syndrome.

Cauda Equina syndrome is not a chiropractic case; they should not be managed by a chiropractor. In fact, they are medical emergencies. When a cauda equina syndrome is suspected, the patient should be referred out as a medical emergency. Timing is critical in the management of cauda equina syndrome; a delay in decompression can result in permanent problems in the legs, sexual function, bladder function, and/or bowel function. A 2008 article in the <em>Journal of the American Academy of Orthopedic Surgeons</em> (Spector) makes the following points:

Cauda equina syndrome is a relatively uncommon condition typically associated with a large, space-occupying lesion within the canal of the lumbosacral spine.

The syndrome is characterized by varying patterns of low back pain, sciatica, lower extremity sensorimotor loss, and bowel and bladder dysfunction.

The pathophysiology remains unclear but may be related to damage to the nerve roots composing the cauda equina from direct mechanical compression and venous congestion or ischemia.

Early diagnosis is often challenging because the initial signs and symptoms frequently are subtle.

Classically, the full-blown syndrome includes urinary retention, saddle anesthesia of the perineum, bilateral lower extremity pain, numbness, and weakness.

Decreased rectal tone may be a relatively late finding.

A high index of suspicion is necessary in the spine patient with back and/or leg pain refractory to analgesia, especially in the setting of urinary retention.

Regardless of the setting, when cauda equina syndrome is diagnosed, the treatment is urgent surgical decompression of the spinal canal.

A few hours later, on my referral, an MRI was performed on Dave’s lumbar spine. The results showed a large posterior midline herination of the L5 intervertebral disc into the lumbar central neural canal, compressing the cauda equina. My diagnosis was essentially confirmed.

Dave underwent decompressive surgery the following day. The neurosurgeon felt Dave would have an instability as a consequence of the discectomy and proceeded to stabilize Dave’s L5-S1 articulation with an interbody fusion.

Myself and our office performed Dave’s post surgical rehabilitation. Our management included graded range of motion and resistive effort exercises, myotherapy, postural corrections, management of articular dysfunctions, anti-inflammatory diet and nutrition, and low level laser therapy.

The good news is that Dave enjoyed a good clinical recovery. His bowel and bladder function returned to normal and he suffered from no functional residuals. His leg pains also resolved. He does retain residual low back stiffness and some lower back pain, especially at times of increased use or stress.

The bad news is that Dave was no longer able to participate in college football, and any chance of professional football play ended. Also, he was no longer able to work construction.

Dave’s injury case went to a jury trial. Dave’s neurosurgeon testified as to the necessity of the surgical decompression and subsequent stabilization. He also testified that the need for the surgery was 100% as the result of the injuries sustained in the automobile accident.

I also testified in Dave’s trial. My testimony centered around the necessity of the rehabilitation program we did on Dave, as well as quantifying his permanent restriction in work and leisure activities. I testified that 100% of our rehabilitation program and his permanent residuals were attributable to the injuries sustained in the accident.

As a consequence of my extensive writing and teaching on the topic of whiplash biomechanics, I qualified as an expert to explain the mechanism of Dave’s injuries during this collision. This was important because it was the position of the defense that Dave could not have been injured in this accident as none of the other three young men sustained any injuries at all. Apparently the jury liked my explanation, as it is logical and supported by the literature. Had I not qualified to testify on mechanism, I believe the outcome would have been much different for Dave. Dave’s monetary award was in the six figures.

Personal Injury Cases and the Chiropractor Chiropractic education instills that personal injury cases have two components:

1. An injury component. This component requires healthcare, treatment to the injured patient.
2. A legal component. This component involves the protection of the injured patient’s legal rights.

Chiropractors who treat personal injury patients understand that their clinical protocols can influence the legal component of a personal injury case. Specifically, there is no substitute for:

• Taking a good case history
• Doing a thorough orthopedic and neurological examination
• Taking good quality and adequate radiographs
• Creating an accurate diagnosis that can be supported by history, complaints and examination findings
• Doing standard and thorough daily charting
• Using standard measurement outcomes, such as pain drawings, Oswestry, Roland Morris, Neck Disability Index, SF-36, algometer, visual analogue scale, etc.
• Doing periodic (monthly) thorough subjective and objective re-evaluations with a follow-up written report of findings
• Having referred the patient out for needed diagnostic procedures that are not done in the chiropractic office (MRI, EMG, SEP, SPECT, etc.)
• Having referred to other health care providers and/or colleagues for verifying or additional opinions
• Being able to determine when the patient has reached a point of maximum improvement, and consequently ending regularly scheduled treatment so that the case can proceed towards settlement of claim
• Being knowledgeable and conversant in the academic concepts of soft tissue injury, such as the phases of injured tissue healing, the relationship of vehicle damage to patient injury, the influence of pre-accident degenerative joint disease, and the influence of variables such as pre-accident awareness or head rotation

The Chiropractic Impact Report™ is a monthly publication by myself, Dan Murphy, DC. I am a 1978 graduate of Western States Chiropractic College in Portland, OR. I have managed about 10,000 whiplash-injury cases. In the past 32 years, I have taught more than 500 12-hour post graduate continuing education classes pertaining to whiplash and spinal trauma, including 21 years of coordinating a year-long certification program in spine trauma, certified through the International Chiropractic Association. Additionally, I am board certified in chiropractic orthopedics (DABCO), and I am on the faculty at Life Chiropractic College West in Hayward, CA (28 years).

The purpose of The Chiropractic Impact Report™ is to keep you updated as to relevant academic concepts pertaining to whiplash-injured patients. The hope is that the information is useful in terms of enhanced understanding, as well as helping the personal injury attorney deal with insurance claim adjusters and adverse medical experts.

The chiropractor sending you this Report is well versed and trained in these concepts, and can be a valuable asset in personal injury cases in terms of both academics and treatment. Additionally, these expert chiropractors have access to a monthly phone consultation with me to discuss any pertinent issues that they may be facing on a particular case. I hope that you find this Report and the referring chiropractor a valuable resource.

Sincerely,

Daniel J. Murphy DC, DABCO

REFERENCES

Thompson NS, Date R, Charlwood AP, Adair IV, Clements WD.

International Journal of Clinical Practice. Seat-belt syndrome revisited; October 2001; Vol. 55; No. 8; pp. 573-5.

Hall CE, Norton SA, Dixon AR. Complete small bowel transection following lap-belt injury; Injury October 2001; Vol. 32; No. 8; pp. 640-1.

Rutherford WH; The Medical Effects of Seat-Belt Legislation in the United Kingdom: a critical review of the findings; Archives of Emergency Medicine, 1985, 2, 221-223.

Anrig C, Plaugher G; Pediatric Chiropractic, Williams & Wilkins, 1998.

Greingor JL, Lazarus S; Chest and abdominal injuries caused by seat belt wearing; Southern Medical Journal; May 2006;Vol. 99; No. 5; pp. 534-5.

DiPiro PJ, Meyer JE, Frenna TH, Denison CM. Seat belt injuries of the breast: findings on mammography and sonography. American Journal of  Roentgenology; Feb 1995;Vol. 164; No. 2; pp. 317-20.

Majeski J. Shoulder restraint injury of the female breast; International Surgery; Mar-Apr 2007; Vol. 92; No. 2; pp. 99-102.

Paddle AM, Morrison WA; Seat belt injury to the female breast: review and discussion of its surgical management. ANZ Journal of Surgery. January/February2010; Vol. 80; No. 1-2; pp. 71-4.

Sturzenegger M, DiStefano G, Radanov BP, Schnidrig A; Presenting symptoms and signs after whiplash injury: the influence of accident mechanisms; Neurology; April 1994; Vol. 44; No. 4; pp. 688-93.

Spector LR, Madigan L, Rhyne A, Darden B 2nd, Kim D; Cauda equina syndrome; Journal of the American Academy of Orthopedic Surgery; August 2008; Vol. 16; No. 8; pp. 471-9.

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22)     Curhan SG, Eavey R, Shargorodsky J, Curhan GC; Analgesic Use and the Risk of Hearing Loss in Men; The American Journal of Medicine; March 2010; Vol. 123; No. 3; pp. 231-237.

23)     Gleason JM, Slezak JM, Jung H, Reynolds K, Van Den Eeden SK, Haque R, Quinn VP, Loo RK, Jacobsen SJ; Regular nonsteroidal anti-inflammatory drug use and erectile dysfunction; Journal of Urology; April 11, 2011; Vol. 185; No. 4; pp. 1388-93.

24)     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.

25)     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.

26)     Maroon JC, Bost JW, Maroon A; Natural anti-inflammatory agents for pain relief; Surgical Neurological International; December 2010.

27)     Maroon JC; Fish Oil, The Natural Anti-Inflammatory, Basic Health, 2006.

28)     Cleland CG, James MJ, Proudman SM; Fish oil: what the prescriber needs to know; Arthritis Research & Therapy; Volume 8, Issue 1, 2006, p. 402.

29)     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.

30)     Ko GD, Nowacki NB, Arseneau L, Eitel M, Hum A; Omega-3 Fatty Acids for Neuropathic Pain: Case Series; The Clinical Journal of Pain; February 2010, Vol. 26, No, 2, pp 168-172.

Cervical Discogenic Stenosis

John, a 55-year old male, was an urban cowboy. John did not own any property (other than his tract home), cattle, or horses. As the floor foreman of a large manufacturer, his job required him to be on his feet most of the day with a moderate requirement for physical lifting and equipment operation. John was healthy, strong, and very active in both his professional life and his leisure activities. His favorite recreational activity was dancing nearly every night, primarily country-western line dancing.

John’s attire was usually western, including boots, jeans, button-down shirt, cowboy hat, and a pair of sunglasses. John drove a small 4-wheel drive pick-up truck with an extended cab.

On a busy Friday afternoon, John was driving home from work when the freeway traffic suddenly stopped, and John successfully and safely stopped. However, the large SUV behind him, driven by a distracted young female, did not successfully stop, and slammed into the rear of John’s truck.

The noise was deafening. The impact was great enough to propel John’s vehicle into the vehicle in front of him.

John was wearing a shoulder-lap type of seat belt. Although the front of his truck sustained substantial damage from slamming into the vehicle in front of him, his air bag did not deploy. The collision had caught John completely by surprise. Importantly, John was no longer wearing his cowboy hat or his sunglasses; both were found behind his seat, in the extended cab portion of his truck. The fact that the hat and sunglasses, having their own inertia, landed in the back of his truck, suggests that for a brief moment, John’s head, hat, and glasses were in the back portion of his truck. When John’s truck was abruptly halted from colliding with the vehicle in front of his, his head was inertially quickly thrown forward, leaving his hat and glasses behind.

Although dazed and confused, John immediately perceived that he was injured, but he was not sure how badly. His vehicle was destroyed and was not drivable. All adjacent traffic had halted, allowing John to carefully push open his door and exit his truck. Upon standing, he felt unsteady, and his legs did not feel right. As he took a few steps he thought he would fall over, and to compensate he broadened his stance and gate, and shortened his stride. John’s neck also hurt, but he was more concerned about the strange sensations he was having in his legs and his inability to walk correctly.

In about 20 minutes, an ambulance appeared at the accident scene. The paresthesias and motor difficulties in John’s lower extremities concerned the ambulance crew. The crew quickly applied an immobilization device to John’s thoraco-lumbar spine, and he was transported to a local hospital.

The hospital emergency personnel were primarily concerned with trauma induced neurological compromise, hence the on scene immobilization. Because John’s major symptoms were associated with his lower extremities, the immediate urgency was to rule out fracture/dislocation of the lumbar or lower thoracic spine. Radiographs were therefore exposed. Findings were negative.

Negative radiographs with ongoing symptoms prompted additional diagnostic imaging. An MRI of the entire lumbar spine and lower thoracic spine was exposed. Once again, findings were negative. There were no signs of fracture, dislocation, edema, hematoma, or any other type of space occupying pathology. The lower spinal cord, the cauda equina, the lumbar spinal roots and the sacral roots all appeared to be normal without any pathology.

John’s walking intolerance and gait abnormalities remained unexplained. There simply were not any positive examination findings to account for his maladies. Perplexed, his health care providers recommended physical therapy to his lower extremities and gait rehabilitation.

John was quite distressed. His primary leisure enjoyment was dancing, an activity that he was no longer capable of performing. He dutifully attended his physical therapy appointments for the next three months. John had physical therapy three times per week for the next three months. His therapy consisted primarily of gait training as well as lower extremity muscle stretching and strengthening exercises. After these three months, there was no improvement.

John was now desperate and frustrated; and so was his wife (Phyllis). Phyllis happened to be John’s dance partner; when John could not dance, Phyllis could not dance. Their social life had regressed to near zero, and their social contacts were greatly compromised. Phyllis insisted that John do something different. A friend of hers knew and recommended that she take John to her (the friend’s) chiropractor.

•••••

Different parts of the human body have different inertial masses. The mechanism of injury from a rear-end motor vehicle collision, is, as a rule, an inertial injury. This means the injury does not occur as a consequence of direct contact of vehicle parts to the patient’s body; rather, injury occurs as a consequence of different inertial masses moving independently from one another.

The primary inertial stresses experienced by those involved in a rear-end motor vehicle collision is between the head and the trunk. Technically, when a vehicle is struck from behind, the entire vehicle is propelled forward, including its frame, seats, and the trunk of those sitting in those seats. However, the head, having a different inertia than the trunk, will follow Newton’s Law of Inertia (1), and remain stationary. Essentially, the trunk is moved under the head as the head remains still. This puts an inertial load onto the structure responsible for balancing the two large inertial masses  (the head and trunk) to each other, the cervical spine (neck). The neck actually never hits anything; it sustains an inertial injury.

Although there are a number of variables that must be accounted for in any particular collision, in general, the magnitude of the inertial injury to the neck is linked to the magnitude of the acceleration achieved by the struck vehicle. This is why authoritative reference texts pertaining to whiplash collisions are subtitled the “Cervical Acceleration Deceleration Syndrome” or CAD (2). Importantly, it is understood that large vehicle accelerations and subsequent cervical spine inertial injuries can occur when the struck vehicle sustains little or even no damage.

In John’s case above, there was not one, but two distinct inertial injury mechanisms. The first was the rear-end collision, delivering the inertial injuries as a consequence of acceleration. The second was a deceleration injury.

After being struck from the rear and accelerating forward, John’s vehicle struck the vehicle in front of him and his vehicle came to a sudden halt. However, in accordance with the Law of Inertia, John’s body and head continued to move forward and, in the absence of safety devices, his body and head would slam into his vehicle’s dashboard, steering wheel, and windshield. Fortunately, as noted above, John was wearing his lap-shoulder restraint belt, which soon engaged, stopping the forward propulsion of his body short of the steering wheel and dashboard. Unfortunately, the lap-shoulder restraint does not stop the inertial movement of the head. Consequently, the head, being in motion will continue in motion until encountering some resistance. Usually, this resistance is the chin hitting the chest, and thus adding cervical spine deceleration inertial injuries to the acceleration cervical injuries he sustained just moments before.

Historically, most vehicle collision fatalities occurred when the subject was thrown from the vehicle, a common occurrence in head-on collisions. As an example, if a vehicle traveling at 50 miles per hour collides with an immoveable object, such as a tree or a wall, the vehicle may abruptly stop, but the person’s body in that vehicle would continue to travel forward at 50 miles per hour, greatly increasing the risk of being thrown from the vehicle.

To reduce the risk of such ejections, lap belts were installed in vehicles, and it eventually became mandatory to use them. Lap belts greatly reduced ejections and therefore fatalities, but by 1948 it was documented that during the forward phase of a collision, the lap belt functioned as a fulcrum, concentrating an inordinate amount of forces to the region of the belt placement (3). The results were again, fewer ejections and fatalities, but an increase in devastating thoraco-lumbar spinal injuries and abdominal visceral injuries.

To remedy these thoraco-lumbar spinal injuries and abdominal visceral injuries, the lap-shoulder restraint was developed. The inclusion of the shoulder harness significantly reduced thoraco-lumbar spinal injuries and abdominal visceral injuries, but another problem was documented: the shoulder harness stopped the forward motion of the trunk, but the head continued in forward motion. This subjected the cervical spine to tremendous deceleration inertial stress with devastating cervical spine flexion injuries.

The solution to the problem of shoulder restraint cervical spine inertial injuries depended upon the arrival of new technology: a sensor in the hood of the vehicle that, when sufficiently mechanically stressed, would initiate inflation of an airbag. This airbag, a gaseous filled cushion, would stop the forward movement of the head, reducing the magnitude of cervical spine inertial injuries. Unfortunately for John, for reasons unexplained, his vehicle’s air bag did not deploy, even though the front of his vehicle was significantly crumbled.

•••••

Although John’s primary complaints were in his lower extremities, mechanistic understanding and history indicate that the primary inertial forces (and therefore probable injuries) were to his cervical spine. It is well established that the primary injury to the cervical spine during a motor vehicle collision is to the facet joint capsules. It is also documented that the second most prevalent injury to the cervical spine is to the intervertebral disc. It is established that inertial cervical spine injuries sustained during motor vehicle collisions can herniate the cervical disc, resulting in radiculopathy and/or myelopathy.

Viewing an axial cut through the cervical spinal cord shows that the motor and sensory nerves of the cord are arranged in layers. Importantly, the outer nerve fibers, the ones that would be most vulnerable to compressive myelopathy from a disc herniation, innervate the lower extremities.

From Gray’s Anatomy, 39^th edition, 2005, p. 318

There is no doubt that a cervical spine intervertebral disc herniation can result in motor and sensory complaints in the lower extremities, and this can occur in the absence of significant neck complaints (4).

In compressive neuropathology, large diameter nerve fibers are more vulnerable than are small diameter nerve fibers. Importantly, pain afferent nerve fibers are small diameter, and consequently less vulnerable to compressive neuropathology. In contrast, large diameter fibers are associated with proprioception, positional sense, gate stability, and motor control. These fibers and functions are most vulnerable to compressive neuropathology.

Posterior midline cervical disc herniations occur more commonly than do posterior-lateral or lateral herniations. This is attributed to the presence of the uncinate processes (joints of von Luschka):

Uncinate Processes

The uncinate processes resist lateral and postero-lateral disc herniations, but allow the disc to herniate midline posteriorly.

These joints form a wall or barrier to lateral and/or posterior-lateral cervical disc herniations. The path of least resistance is posterior. Such a midline herniation would spare the cervical nerve roots and thus there would be no classical symptoms or signs of cervical spine radiculopathy. However, should the midline posterior disc herniation be large enough, it could mechanically compromise the spinal cord (myelopathy). The associated symptoms and signs would be long tract signs affecting the lower extremities. Because the nature of the lesion would be characterized as compressive myelopathy, large diameter nerve function would be most influenced (proprioception, positional sense, gate stability, and motor control).

The posterior midline cervical disc herniation would effectively narrow the sagittal diameter size of the cervical spinal canal. The technical diagnosis for such an occurrence is “central canal stenosis.” The cervical central canal is reduced in extension (further compromising the spinal cord) and enlarged in flexion. Consequently, extension positions will aggravate the symptoms and signs associated with central canal stenosis and its associated myelopathy; flexion positions will improve the associated symptoms and signs (5).

•••••

Within a few days, and just over three months after being injured, John reluctantly presented himself as a new patient in my office. His clinical symptoms and status were unchanged: his legs felt “funny” tired and heavy; he could not walk normally, his stance being wide and his stride being short and choppy; he felt unsteady, as if he might fall down because of his dysfunctional legs. He was anxious, irritable, and skeptical.

Upright lumbar, thoracic, and cervical biomechanical x-rays were exposed. There was no sign of any pathology such as fracture, dislocation, or degenerative disease. However, the lateral cervical x-ray showed a sharp reversal of the normal lordotic curve; the kyphotic angle measured 10 degrees, its apex at the C5-C6 interspace.

John’s initial examination showed normal deep tendon reflexes, myotomal strength, and superficial sensations on both his lower and upper extremities. These findings seemed inconsistent with his lower extremity complaints. Lumbar and thoracic ranges of motion were slightly reduced but non-painful. Lumbar spine compression tests did not aggravate any of his complaints. The straight-leg-raising tests were completed to an arc of 45 degrees and produced no additional symptoms.

John’s cervical ranges of motion were significantly reduced. He added that his neck was quite stiff and sore. The cervical spine axial compression test was uncomfortable and it produced an uncomfortable sensation between his shoulder blades.

John’s plantar reflex (Babinski’s sign) was normal (toe down). Vibration sense was intact on his fingers and toes. He was flawless in knowing the position of his toes when they were purposefully moved up or down (positional sense).

Overall, John was a challenging case. History, presentation, education, experience, and intuition all told me his problem was in his cervical spine. Although his main complaints were his legs and gait, most of his abnormal examination findings were in his cervical spine. This included a sharp kyphotic angulation. It appeared to me that stressing his neck may change some of his examination findings.

I gently placed John supine with his head over the end of the examination table. In other words, his head and neck were in an extension position. I left John in this position for 30 seconds. After 30 seconds, while his head/neck were still extended, I redid the plantar reflex (Babinski’s test). He had an immediate and significant up-going toe, an abnormal finding. The up-going toe during the plantar reflex is indicative of a problem with the spinal cord, or possible brain, what is classically known as an “upper motor neuron lesion.” While remaining in cervical extension, retesting of both his patellar and Achilles’ deep tendon reflexes found them to be hyper-reactive while in that position. This is also abnormal and indicative of an upper motor neuron lesion.

While remaining in cervical extension, John also lost the ability to perceive vibration in his toes, and he lost the ability to perceive the up-down position of his toes. Both of these functions are associated with large diameter neurons. This indicates that large diameter neuron function was compromised while John was in cervical spine extension.

My working diagnosis was that John was suffering from a traumatic midline posterior disc herniation that was causing cervical spine central canal stenosis and compressive myelopathy, resulting in long tract signs (motor and sensory) to his lower extremities. My working diagnosis is based upon these factors:

• Mechanism of injury was both a rear-end collision followed moments later by a head-on collision. Both collisions imparted significant inertial loads to the cervical spine. Such collisions and inertial loading are known to cause disc herniations.

• There were no signs of upper extremity motor or sensory radiculopathy.

• There were no signs of lower extremity motor or sensory radiculopathy.

• Three months of treatment of the lower extremities did not result in improvement. There had been no investigations or treatment given to the cervical spine.

• Examination found the neck to be significantly stiff, and John complained that it felt stiff and sore.

• Cervical spine compression caused interscapular pain (pain between the shoulder blades). It has been known since 1959 that cervical disc disease often causes interscapular pain (6).

• X-rays showed a sharp reversal of cervical kyphosis. This is consistent with discogenic central canal stenosis and cervical cord myelopathy (7).

• The outer nerve fibers of the spinal cord arise from (afferents) and innervate (motor) the lower extremities.

• Central canal stenosis and its attendant myelopathy are aggravated in extension (5). Extension worsens compressive myelopathy because the central canal becomes smaller in extension.

• Compressive neuropathies (including myelopathy) primarily affect the function of the large diameter neurons, including the perception of the modalities of positional and vibratory sense.

• It is documented that cervical spine stenosis with myelopathy causes a walking intolerance, such as John’s (8).

I informed John that he needed an MRI. He quickly snapped that he already had one and it was normal. I politely said he needed an MRI of his neck. He quickly questioned the reason, reminding me that it was his legs that were dysfunctional. I replied “exactly.” I showed John my rationale, convincing him to follow my recommendations.

The MRI of John’s cervical spine showed that 50% of the central neural canal was occupied by a midline posterior disc herniation, pressing on the anterior spinal cord (myelopathy), as suspected. Because of the large displacement, I referred John to a neurosurgeon for a surgical consult. The neurosurgeon felt that John should have a surgical decompression. John asked me for a second surgical opinion, so I next referred him to an orthopedic surgeon who specialized in spinal surgeries. The orthopedic surgeon also suggested a surgical decompression.

John was hesitant to do surgery, especially since no one had yet tried conservative management of his neck; if fact, so far no one had treated his neck at all. John asked me if I would be willing to treat his neck for a month or so, hoping that he might improve and avoid surgery. I agreed. I used the basic protocols outlined by Joel and Jeffery Saal in the journal Spine in 1996 (9). This protocol included a combination of mobilization, strengthening exercises, and most importantly, daily cervical spine traction. I also dealt with his postural alignment and I put him on an anti-inflammatory diet, including 3 grams per day of omega-3 fatty acids (fish oil).

John’s disc herniation was very large, more than the 4 mm threshold Saal and Saal describe in their article (9). Yet, the combination of the program of care I outlined for him worked quite well. He slowly began to improve. Both his neck and lower extremity symptoms began to improve. I treated John in the clinic 32 times over a period of 18 weeks (4.5 months). He dutifully did his home traction, four times per day, 10-15 minutes each time.

John was able to avoid surgery. He is back dancing, with his wife, Phyllis.

Personal Injury Cases and the Chiropractor

Chiropractic education instills that personal injury cases have two components:

1. An injury component. This component requires healthcare, treatment to the injured patient.
2. A legal component. This component involves the protection of the injured patient’s legal rights.

Chiropractors who treat personal injury patients understand that their clinical protocols can influence the legal component of a personal injury case. Specifically, there is no substitute for:

• Taking a good case history
• Doing a thorough orthopedic and neurological examination
• Taking good quality and adequate radiographs
• Creating an accurate diagnosis that can be supported by history, complaints and examination findings
• Doing standard and thorough daily charting
• Using standard measurement outcomes, such as pain drawings, Oswestry, Roland Morris, Neck Disability Index, SF-36, algometer, visual analogue scale, etc.
• Doing periodic (monthly) thorough subjective and objective re-evaluations with a follow-up written report of findings
• Having referred the patient out for needed diagnostic procedures that are not done in the chiropractic office (MRI, EMG, SEP, SPECT, etc.)
• Having referred to other health care providers and/or colleagues for verifying or additional opinions
• Being able to determine when the patient has reached a point of maximum improvement, and consequently ending regularly scheduled treatment so that the case can proceed towards settlement of claim
• Being knowledgeable and conversant in the academic concepts of soft tissue injury, such as the phases of injured tissue healing, the relationship of vehicle damage to patient injury, the influence of pre-accident degenerative joint disease, and the influence of variables such as pre-accident awareness or head rotation

The Chiropractic Impact Report™ is a monthly publication by myself, Dan Murphy, DC. I am a 1978 graduate of Western States Chiropractic College in Portland, OR. I have managed about 10,000 whiplash-injury cases. In the past 32 years, I have taught more than 500 12-hour post graduate continuing education classes pertaining to whiplash and spinal trauma, including 21 years of coordinating a year-long certification program in spine trauma, certified through the International Chiropractic Association. Additionally, I am board certified in chiropractic orthopedics (DABCO), and I am on the faculty at Life Chiropractic College West in Hayward, CA (28 years).

The purpose of The Chiropractic Impact Report™ is to keep you updated as to relevant academic concepts pertaining to whiplash-injured patients. The hope is that the information is useful in terms of enhanced understanding, as well as helping the personal injury attorney deal with insurance claim adjusters and adverse medical experts.

The chiropractor sending you this Report is well versed and trained in these concepts, and can be a valuable asset in personal injury cases in terms of both academics and treatment. Additionally, these expert chiropractors have access to a monthly phone consultation with me to discuss any pertinent issues that they may be facing on a particular case. I hope that you find this Report and the referring chiropractor a valuable resource.

Sincerely,

Daniel J. Murphy DC, DABCO

REFERENCES

1. Newton I; Mathematical Principles of Natural Philosophy; 1687.
2. Foreman SM, Croft AC; Whiplash Injuries; The Cervical Acceleration / Deceleration Syndrome; Williams & Wilkins; 1988.
3. Chance GQ; Note on a Type of Flexion Fracture of the Spine; British Journal of Radiology; 1948; Volume 21; Number 249; pp. 452-453.
4. Kabat H, Low Back and Leg Pain From Herniated Cervical Disc, Warren H Green, 1980.
5. Bland J, Disorders of the Cervical Spine, WB Saunders Company, 1987.
6. Cloward RB; Cervical Diskography, A Contribution to the Etiology and Mechanism of Neck, Shoulder and Arm Pain; Annals of Surgery; December 1959; Vol. 150, No. 6; pp. 1052-1064.
7. Kenzo Uchida, Hideaki Nakajima, Ryuichiro Sato, Takafum i Yayama, Erisa S. Mwaka, Shigeru Kobayashi, Hisatoshi Baba; Cervical Spondylotic Myelopathy Associated with Kyphosis or Sagittal Sigmoid Alignment; Journal of Neurosurgery: Spine; November 2009, Volume 11, pp. 521-528
8. Kikuchi S, Watanabe E, Hasue M, Spinal intermittent claudication due to cervical and thoracic degenerative spine disease, Spine, February 1, 1996, 21(3):313-8.
9. Saal, Joel S. MD; Saal, Jeffrey A. MD; Yurth, Elizabeth F. MD; Nonoperative Management of Herniated Cervical Intervertebral Disc With Radiculopathy; Spine; Volume 21(16) August 15, 1996, pp 1877-1883.