My doctor told me I have tendinosis, I’ve heard of tendinitis, what is the difference?
Dr. Jimenez considers this dilemma of similar words that cause confusion to patients. Below is an explanation of clinical presentations and anatomical disorders that shed light on the similarities and differences between tendinosis and tendinitis.
Tendons are the tough, white, cords that connect muscles to bones, and are the least elastic of the collagen-based soft tissues (LIGAMENTS, MUSCLES & FASCIA) I work with on a day-to-day basis. How common are tendon problems? Government statistics tell us that overuse injuries of tendons are a leading reason for doctor visits. And although most of these tendon problems are referred to generically as tendinitis, in the vast majority of cases, tendinitis is actually an incorrect and outdated term.
Over the past decade, medical research has conclusively shown that the major cause of tendinopathies is not inflammation (aka “itis”), which even a decade ago was nothing new. For decades, the scientific community has been concluding that wile the immune system mediators we collectively refer to as “INFLAMMATION” are probably present in tendinopathies; inflammation itself is rarely the cause. So, if inflammation is not the primary cause of most tendon problems, what is? Follow along as I show you from peer-review, that since the early 1980’s, research has shown the primary culprit in most tendinopathies is something called “osis”. Thus the name, “tendon � osis” (tendinosis). But what the heck is osis?
The suffix “osis” indicates that there is a derangement and subsequent deterioration of the collagen fibers that make up the tendon. The truth is, even though doctors still use the term “tendinitis” with their patients, their AMA-mandated Diagnosis Codes almost always indicates the problem is “tendinosis” or “tendinopathy” (HERE). Is this differentiation between tendinitis and tendinosis really that important, or am I splitting hairs and making a big deal out of nothing — making a mountain out of a molehill, semantically speaking? Instead of answering that question myself, I will let two of the world�s preeminent tendon researchers — renowned orthopedic surgeons — answer it for me.
“Tendinosis, sometimes called tendinitis, or tendinopathy, is damage to a tendon at a cellular level (the suffix �osis� implies a pathology of chronic degeneration without inflammation). It is thought to be caused by micro-tears in the connective tissue in and around the tendon, leading to an increased number of tendon repair cells. This may lead to reduced tensile strength, thus increasing the chance of repetitive injury or even tendon rupture. Tendinosis is often misdiagnosed as tendinitis due to the limited understanding of tendinopathies by the medical community.” Tendon researcher and orthopedic surgeon, Dr. GA Murrell from a piece called, �Understanding Tendinopathies� in the December 2002 issue of The British Journal of Sports Medicine.
“Tendinitis such as that of the Achilles, lateral elbow, and rotator cuff tendons is a common presentation to family practitioners and various medical specialists.1 Most currently practicing general practitioners were taught, and many still believe, that patients who present with overuse tendinitis have a largely inflammatory condition and will benefit from anti-inflammatory medication. Unfortunately this dogma is deeply entrenched. Ten of 11 readily available sports medicine texts specifically recommend non-steroidal anti-inflammatory drugs for treating painful conditions like Achilles and patellar tendinitis despite the lack of a biological rationale or clinical evidence for this approach. Instead of adhering to the myths above, physicians should acknowledge that painful overuse tendon conditions have a non-inflammatory pathology.” Karim Khan, MD, PhD, FACSP, FACSM, and his group of researchers at the Department of Family Medicine & School of Human Kinetics at the University of British Columbia, from the March 2002 edition of the BMJ (British Medical Journal).
The information in the preceding paragraphs (which was not new when they were published over a decade and a half ago) is so important as to be considered revolutionary for those of you who have spent time on the MEDICAL MERRY-GO-ROUND with tendon problems. Why? Because, as stated by Dr. Murrell above, most medical professionals have, “a limited understanding of tendinopathies”. Why is this? Why do more doctors not grasp what is going on with the majority of Tendinopathies? Why does such a big portion of the medical community continue to ignore their own profession�s scientific conclusions, while continuing to treat tendinopathies with drugs and surgery? Of course there’s always the issue of money. There is also the fact that if you have tendon problems, you are probably being treated using a model that is at least 25-30 years behind the times as far as the medical research is concerned (HERE). If you think I’m being harsh, read what Dr. Warren Hammer, a board certified Chiropractic Orthopedist in practice since the late 1950?s, had to say about Tendinosis in a 1992 issue of Dynamic Chiropractic.
“The American Academy of Orthopedic Surgeons has provided a new classification of tendon injuries�. In the microtraumatic tendon injury the main histologic features represent a degenerative tendinopathy thought to be due to an hypoxic [diminished oxygen] degenerative process. The similarity to the histology [study of the cells] of an acute wound repair with inflammatory cell infiltration as in macrotrauma seems to be absent. A new classification of tendon injury called �tendinosis� is now accepted. �Tendinosis� is a term referring to tendinous degeneration due to atrophy (aging, microtrauma, vascular compromise). Histologically there is a non-inflammatory tendinous degeneration due to atrophy (aging, microtrauma, vascular compromise), as well as a non-inflammatory intratendinous collagen degeneration with fiber disorientation, hypocelluarity, scattered vascular ingrowth, and occasional local necrosis or calcification.”
If your doctor is still treating you for tendinitis and not tendinosis, they are caught in a time warp. According to what the American Academy of Orthopedic Surgeons said over two and a half decades ago, tendinosis is not an inflammatory condition (itis)! It is a degenerative condition (osis)! Not only is there some debate over whether or not tendinitis actually exists at all, but as you will see in a moment, the anti-inflammation medications and corticosteroid injections that your doctor has been prescribing you are actually creating more degeneration. Track & Field athletes make it a point to keep up with the cutting edge diagnosis and treatment of tendinous SPORTS INJURIES. See what their official medical team has to say on the subject of Tendinosis and Tendinopathy……..
“The relatively new term ‘Tendinopathy’ has been adopted as a general clinical descriptor of tendon injuries in sports. In overuse clinical conditions in and around tendons, frank inflammation is infrequent and if seen, is associated mostly with tendon ruptures. Tendinosis implies tendon degeneration without clinical or histological signs of intratendinous inflammation, and is not necessarily symptomatic. The term ‘Tendonitis’ is used in a clinical context and does not refer to a specific histological entity. [The term] Tendonitis is commonly used for conditions that are truly Tendinosis, however, and leads athletes and coaches to underestimate that proven chronicity of this condition……. Most articles describing the surgical management of partial tears of a given tendon in reality deal with degenerative tendinopathies [Tendinosis].” From an official document found on the website of the International Association of Athletics Federations (IAAF) — the official governing body of professional Track and Field
The Science:
“Tendinosis is a medical term used to describe the tearing and progressive degradation of a tendon. Tendons are structural components of the human body that ensure muscles remain bound to the correct bone during normal daily activities. Tendinosis differs from tendonitis in that the affected tendon is not inflamed.” Rachel Amhed from a July 2010 article for Lance Armstrong’s ‘Livestrong Website’ called Tendinosis Symptoms.
“Based on the information of various lines of investigation of tendinopathy, we can summarize some major points which must be considered in the formulation of a unified theory of pathogenesis in our model of tendinopathy….. The primary results of pathology are the progressive collagenolytic [Collagen-Destroying] injuries co-existing with a failed healing response, thus both degenerative changes and active healing are observed in the pathological tissues….. These pathological tissues may aggravate the nociceptive responses [PAIN] by various pathways which are no longer responsive to conventional treatment such as inhibition of prostaglandin synthesis [NSAIDS & Cortcosteroids]; otherwise the insidious mechanical deterioration without pain may render increased risk of tendon rupture.
For example, overuse is a major etiological factor but there are tendinopathy patients without obvious history of repetitive injuries. It is possible that non-overuse tendon injuries may also be exposed to risk factors for failed healing. Overuse induces collagenolytic [DEGENERATIVE] tendon injuries and it also imposes repetitive mechanical strain which may be unfavorable for normal healing. Stress-deprivation also induces MMP expression [Matrix Metallo Proteinase — an enzyme which breaks down Connective Tissues], and whether over- or under-stimulation is still an active debate. It is possible that tenocytes [tendon cells] are responsive to both over- and under-stimulation, both tensile and compressive loading….. By proposing a process of failed healing to translate tendon injuries into tendinopathy, other extrinsic and intrinsic factors would probably enter the play at this stage, such as genetic predisposition, age, xenobiotics (NSAIDs and corticosteroids) and mechanical loading on the tendons….. Classical characteristics of “tendinosis” include degenerative changes in the collagenous matrix, hypercellularity, hypervascularity and a lack of inflammatory cells which has challenged the original misnomer “tendinitis”.” Cherry-picked quotes from a comprehensive collaboration by teams from the Department of Orthopaedics & Traumatology at Prince of Wales Hospital, The Chinese University of Hong Kong, and the Department of Orthopaedic Surgery at Huddinge University Hospital in Stockholm. The study was published in a 2010 issue of Sports Medicine Arthroscopy & Rehabilitation Therapy Technology.
“Rotator Cuff Tendinosis is a degenerative (genetic, age or activity related) change that occurs in our rotator cuff tendons over time. Rotator cuff tendinosis is exceptionally common. Many, many people have tendinosis of the rotator cuff and do not even know it. Why rotator cuff tendinosis bothers some people and doesn�t bothers others is currently a question the orthopedic surgery community can not answer. Rotator cuff tendinosis is just as likely to be found in a professional body builder as it is likely to be found in a true couch potato.” From an August 2011 online article / newsletter by Dr. Howard Luks, an Orthopedic Surgeon and Associate Professor of Orthopedic Surgery at New York Medical College as well as being Chief of Sports Medicine and Arthroscopy at Westchester Medical Center.
“The gross pathology of Angiofibroblastic Tendinosis is [that] there are no inflammatory cells in this tissue. Therefore the term “Tendinosis” is much better [than Tendinitis]. The pathological tissue is instead characterized by very immature tissue and nonfunctional vascular elements.” Loosely quoted from a YouTube video of famed tendon researcher / surgeon Dr. Robert P. Nirschl’s (Nirchl Orthopedics) presentation to the American Academy of Orthopedic Surgeons annual meeting (2012).
“The more commonly used term of tendinitis has since been proven to be a misnomer for several reasons. The first of which is that there is a lack of inflammatory cells in conditions that were typically called a tendonitis…. The other two findings present in tendinosis, increased cellularity and neovascularization has been termed angiofribroblastic hyperplasia by Nirschl…… These are cells that represent a degenerative condition. Neovascularization [the creation of abnormally large numbers of new blood vessels] found in tendinosis has been described as a haphazard arrangement of new blood vessels, and Kraushaar et al. even mention that the vascular structures do not function as blood vessels. Vessels have even been found to form perpendicular to the orientation of the collagen fibers. They then concluded that the increased vascularity present in tendinosis is not associated with increased healing. Take Home Points: Chronic tendon injuries are degenerative in nature and NOT inflammatory. Anti-inflammatory medications (NSAIDs) and/or corticosteroid injections can actually accelerate the degenerative process and make the tendon more susceptible to further injury, longer recovery time and may increase likelihood of rupture.” Quotes cherry-picked from a recent online article called ‘Tendonosis vs. Tendonitis’ by Dr. Murray Heber, DC, BSc(Kin), CSCS, CCSS(C), Head Chiropractor for Canada’s Bobsleigh / Skeleton Team.
“The data clearly indicates that painful, overuse tendon injury is due to tendinosis�the histologic entity of collagen disarray, increased ground substance, neovascularization, and increased prominence of myofibroblasts. [It is] the only clinically relevant chronic tendon lesion, although minor histopathologic variations may exist in different anatomical sites. The finding that the clinical tendon conditions in sportspeople are due to tendinosis is not new. Writing about the tendinopathies in 1986, Perugia et al noted the ‘remarkable discrepancy between the terminology generally adopted for these conditions (which are obviously inflammatory because the ending ��-itis�� is used) and their histopathologic substratum, which is largely degenerative” Dr. Khan once more showing that tendon problems are not caused by inflammation.
“Overuse tendinopathies are common in primary care. Numerous investigators worldwide have shown that the pathology underlying these conditions is tendinosis or collagen degeneration. This applies equally in the Achilles, patellar, medial and lateral elbow, and rotator cuff tendons. If physicians acknowledge that overuse tendinopathies are due to tendinosis, as distinct from tendinitis, they must modify patient management in at least eight areas.” Dr. Karim Kahn M.D / Ph.D and his research team from University of British Columbia’s School of Kinesiology in an article published in the May 2000 issue of The Physician and Sportsmedicine called “Overuse Tendinosis, Not Tendinitis”.
Eight areas? Wow! And that quote is almost two decades old. Now, take a look at something that came from a Medical Textbook that was published over three decades ago in Italy. The medical community knew back then that most overuse tendon problems were not inflammatory (itis), but instead degenerative (osis).
“[There is a] remarkable discrepancy between the terminology generally adopted for these conditions (which are obviously inflammatory since the ending ‘itis’ is used) and their histopathologic substratum, which is largely degenerative.” From an Italian medical text called, “The Tendons: Biology, Pathology, Clinical Aspects” (1986).
Tendinosis Overview:
The truth is that I could go on and on and on and on with quotes from similar studies. Hopefully you get the point! You should be starting to see that most of what you thought about chronic tendon problems needs to be flushed down the toilet or thrown out with the weekly trash. That’s because there’s a new model in town. Tendinosis is it’s name; and if you want any hope of a solution to your tendon problem, you will have to step outside of the medical “box” and start thinking of your problem in terms of “osis” instead of “itis”. Failure to grasp the new model leaves you vulnerable to treatments which, while possibly bringing some temporary relief, will ultimately make you worse — possibly much worse! By the way, the following points are observations that you yourself will understand if you read the above quotes.
Tendinosis is a Degenerative Condition without inflammation. Scratch that. Science has recently shown us that there is inflammation in tendinosis — there should be, at least in the initial phase of healing. However, it’s the SYSTEMIC INFLAMMATION that’s been shown to be the biggest problem. Bottom line, this doesn’t really affect anything I’m telling you in this post, other than to reinforce your need to address systemic inflammation (hint: it can’t be done with drugs).
Tendinosis is the proper model for understanding the majority of Tendinopathies. As a model for understanding
Tendinopathies, Tendinitis has been retired for at least two and a half decades.
Tendinosis is both misunderstood and mismanaged by the majority of the Medical Community.
Traditional Therapies / Interventions for Tendinopathies significantly increase one’s chance of Tendon Rupture.
Most Coaches and Athletes do not understand the difference between Tendinitis and Tendinosis.
If it does exist, Tendinitis (Inflammation of the Tendon) is rare, short lived, and mostly associated with Tendon Tears or Ruptures.
Tendinosis is caused by both overuse and under-use.
Tendinosis is often times Asymptomatic (no symptoms), until it becomes a painful and potentially debilitating problem.
Drugs; particularly NSAIDS & CORTICOSTEROIDS, as well as CERTAIN ANTIBIOTICS actually cause Tendinosis — and Tendon Rupture. They also slow down (or reverse) the healing process.
Best Treatment: Tendinosis & Tendonopathies
Anti-Inflammatory Medication
“I knew then and there I was in the wrong place.” Thoughts running through the mind of a new patient who had recently visited an Orthopedic Specialist’s office for a tendon problem and asked him about the difference between Tendinitis and Tendinosis. The doctor answered, “There is no difference between Tendinitis and Tendinosis. They are one and the same —- two different names for the same problem.”
Even though medical research has conclusively shown us for over three decades that tendinopathies have as their primary cause of pain and dysfunction tissue derangement and degeneration, anti-inflammation drugs continue to be the medical profession�s go-to method of treatment. It�s not difficult to see why this is not working:
Although there is undoubtedly a certain amount of SYSTEMIC INFLAMMATION present with tendinosis, research has conclusively shown that tendon problems are not primarily problems of inflammation, but of degeneration.
Scientific studies have actually shown that non-steroidal anti-inflammatory medications (NSAID�s) such as Aspirin, Tylenol, Nuprin, Ibuprofen, Naproxen, Celebrex, Vioxx (oops � one of the #1 drugs in America for 10 years running was taken off the market because it was found to be a huge cause of chronic illness and death), & numerous others, actually cause injured collagen-based tissues like tendons, ligaments, muscles, fascia, etc, to heal up to 33% weaker, with as much as 40% less tissue elasticity.
Corticosteroid Injections are even worse. Medicine’s dirty little secret of treating connective tissue injuries with steroids is that they actually deteriorate or ‘eat’ the collagen foundation. This is why they deteriorate ever tissue in the joint, including bone. This is bad news considering collagen is the tissue that is deranged — the very tissue that needs to heal the most. This is why corticosteroids are a known cause of DEGENERATIVE ARTHRITIS and OSTEOPOROSIS, not to mention a whole host of easily-verified systemic side effects. The fact that steroid injections are ridiculously degenerative is why doctors ration or limit the number of steroid injections a person can receive � even if they seem to be working. And understand; it’s not that drugs don’t sometimes do what they claim to do. It’s that they never reverse the underlying pathophysiology (HERE). They simply cover symptoms.
Years ago, the Journal of Bone and Joint Surgery reported that corticosteroids are so degenerative that if you have more than one injection in the same joint over the course of your lifetime; your chance of premature degeneration in the injected joint is (gulp) 100%! Ultimately, the problem of corticosteroids (or NSAID�s for that matter) being used to treat tendons or other collagen-based tissues, is that short term relief is being traded for long term (and often permanent) damage. In other words, tomorrow is being traded for today. Kind of reminds you of our government�s short-sighted fiscal policies, doesn�t it? It is also another in a long line of evidences that the gap between medical research and medical practice is growing (HERE).
Collagen is the building block of all connective tissues, including tendons (you probably learned a great deal about collagen on our FASCIAL ADHESION PAGE as well as our COLLAGEN SUPER-PAGE). If one looks at normal collagen fibers from tendons or other connective tissues under a microscope, each individual cell lines up parallel to the surrounding cells. This allows for maximum tissue flexibility (sort of like well-combed hair).
With tendinopathies (whether TRAUMATIC OR REPETITIVE � yes, trauma can cause tendinosis), the tissue uniformity becomes disrupted and unorganized, causing restriction and a severe loss of function. This in turn causes a loss of flexibility, tissue weakness, tissue fraying, increased rigidity, and stiffness (sort of like KNOTTED HAIR OR A HAIRBALL — or gristle in a bite of steak). This leads to a loss of strength and function, which ultimately means that you end up with pain and dysfunction of the affected joint or body part. As I will soon show you, loss of normal function is one of just a few known causes of joint degeneration. This is why anyone who has suffered through Chronic Tendinosis knows how debilitating it can really be.
Normal Tendons Vs Tendinosis
Tendons are one of the Elastic, Collagen-Based Connective Tissues that are Made up of Three Individual Collagen Fibers Braided Together into Wavy Sheets or Bands
Photo by User Vossman
COLLAGEN is a wavy protein. The waves are what give it the ability to stretch and elast. And although Tendons are said to be the least flexible and stretchy of the Elastic, Collagen-Based Connective Tissues (Muscles, Ligaments, & Fascia are all more elastic), they have to have at least a bit of give. The waves in the individual collagen fibers are what allow for this stretching to take place. Tendinosis occurs most often where the muscle meets the tendon. This is due to an especially dense amount of Collagen at this “Transition Zone”.
Tendinosis Looks Like:
NORMAL TENDON Uniform, Organized, & Parallel
Normal, healthy Tendons are like these ropes. Not only are the fibers all running uniformly in the same direction, there is little or no fraying. This gives the tendon the ability to stretch and elast. Photo by Procsilas Moscas
FRAYED TENDON (TENDINOSIS) Unorganized, Tangled, & Random
Tendinosis is characterized by incredible fraying, fragmenting, tangling, and twisting, of the tendon. This causes weakness and inelasticity that can not only painfully debilitating, it can lead to Tendon Rupture. Photo by Martyn Gorman
NOTICE THE FRAYED & TORN APPEARANCE. THIS IS WHAT CHARACTERIZES TENDINOSIS
Photo by Andrjusgeo
NORMAL HEALTHY TENDON
NOTICE THE COLLAGEN WAVES
Photo by Nephron
SCAR TISSUE & ADHESION
(Note the Complete Lack of Uniformity in the Tissue Fibers)
Scar Tissue / Fibrosis
DRDoubleB
Tendinosis Looks Like Tangled Fishing Line
Photo by Daplaza
Tendinosis is characterized by Collagen Fibers that have disrupted alignment. It also shows fraying of the individual fibers. This is why most tendinopathies are now classified as Tendinosis and considered to be degenerative (osis = degeneration), as opposed to Tendinitis (itis = inflammation). The problem is, most of the medical community does not seem to grasp this yet.
Areas Most Affected By Tendinosis
Sometimes Tendionosis is clinically impossible to distinguish from FASCIAL ADHESIONS and microscopic scar tissue. Often times they are present together. The bottom line is that whether the adhesions are in fascia or whether they are tendon DOESN’T REALLY MATTER — they must both be broken. Sometimes there is a great excess of calcium built up at the point where the tendon anchors to the bone. This must be broken up as well. Because the models for understanding various soft tissues are virtually identical; the models for treating said tissues are likewise very similar. As you might imagine, this is fantastic news for the patient. Bear in mind that I have not included each and every specific area you can develop tendinopathy because it can attack anywhere that you have a tendon. The following list happens to be the areas that I treat most frequently in my clinic.
IMPORTANT: Please note that some muscles only cross one joint. However, many muscles cross two joints. Muscles that act on more than one joint have a greater propensity for problems. It also means that one muscle has the potential to give you problems (including tendinosis) at two different joints. Also note that Tendinosis is usually a bit tougher to deal with than Fascial Adhesions.
ROTATOR CUFF TENDINOSIS: The Rotator Cuff is made up of four muscles that surround the shoulder.
SUPRASPINATUS TENDINOSIS: The Supraspinatus Tendon is not only the most commonly injured of the Rotator Cuff Muscles, it is the most common to find tendinopathy in as well.
TRICEP TENDINOSIS: Tricep Tendinosis is rare. About the only people I ever find it in is carpenters (hammering) and weightlifters. However, here is the webpage.
BICEPS TENDINOSIS: Because both heads of the bicep muscle have attachment points in the front of the shoulder, Biceps Tendinosis is frequently mistaken for Bursitis or a Rotator Cuff problem.
LATERAL EPICONDYLITIS (Tennis Elbow): Although I have never seen anyone who got this problem playing tennis, it is nonetheless extremely common.
MEDIAL EPICONDYLITIS (Golfer�s Elbow): Not quite as common as Tennis Elbow above.
WRIST / FOREARM FLEXOR TENDINOSIS: This is tendinopathy on the palm side of the forearm and wrist.
WRIST / FOREARM EXTENSOR TENDINOSIS: This is tendinopathy on the backhand side of the forearm and wrist.
THUMB TENDINOSIS / DeQUERVAIN’S SYNDROME: This extremely common problem can be debilitating. You will frequently hear Thumb Tendinosis referred to as DeQuervain�s Syndrome.
GROIN (Hip Adductor) TENDINOSIS: I have included Tendinosis of the Groin under �Hip Flexor Tendinosis� below.
HIP FLEXOR TENDINOSIS: Hip Flexor Tendinosis will manifest in the upper front thigh or groin area. This is incredibly common in athletes — particularly soccer players.
PIRIFORMIS TENDINOSIS: This problem is related to PIRIFORMIS SYNDROME, and causes pain in the butt (sometimes with sciatica as well).
SPINAL TENDINOSIS: Although most people never think of it, the potential for developing Spinal Tendinosis is greater than you ever imagined possible.
KNEE TENDINOSIS: This is arguably the single most common reason that people visit a Sports Physician.
QUADRICEPS / PATELLAR TENDINOSIS: A form of Knee Tendinosis
HAMSTRING TENDINOSIS: Hamstring Tendinosis can cause knee, hip, and buttock problems.
ACHILLES TENDINOSIS: Achilles Tendinosis is found in the large tendon in the very back of the lower leg / ankle.
ANKLE TENDINOSIS: This common Tendinosis can typically be dealt with by following a few simple procedures.
TIBIALIS ANTERIOR TENDINOSIS: This is related to the category above, and is typically found in the front of the ankle.
POSTERIOR TIBIAL TENDINOSIS: This is related to the category above, and is typically found near the bony knob on the inside of the ankle.
APONEUROSIS / APONEUROTICA TENDINOSIS: Although you have probably never heard the word before, �Aponeurosis� are flattened out tendons. They are almost always referred to as fascia, but technically this is incorrect. They are most often associated with SKULL PAIN.
Effectively Dealing With Tendinosis
Let me begin by saying that I cannot help everyone�s Tendinopathy. And yes, I am very aware that there are thousands of websites out there giving all sorts of free, do-it-yourself advice on how to fix these problems without going to a doctor. Most of this advice concerns common sense treatments that everyone should try before seeking any sort of professional care. These lists frequently include things like STRETCHING / SPECIAL EXERCISES, ICING, resting, EATING AN ANTI-INFLAMMATORY DIET, drinking plenty of water, SPECIAL SUPPLEMENTS FOR CONNECTIVE TISSUES, etc. All of these are great, and highly recommended by me. The truth is, advice like this is going to save a lot of people a lot of time and money by helping the biggest portion of the population get over minor Tendinopathies / Tendinosis on their own, without jumping on the MEDICAL MERRY GO ROUND.
There is a significant portion of the tendinosis-suffering population who have tried all of these things. Every type of pill imaginable, including ANTIBIOTICS (believe it or not, I have seen this used numerous times � some of which, like CIPRO, actually cause tendon weakness and rupture), TENS Units, braces & supports of all kinds, PLATELET INJECTION THERAPY, high powered ultrasound (a form of litho-tripsy called arthro-tripsy), prolotherapy (sugar water injections), all sorts of surgeries, and heaven only knows what else. And this doesn’t even start touching on many of the common drugs, which I’ve already dealt with.
The bottom line is that if your pain is being caused by adhesions, restrictions, and microscopic scarring in the collagen fibers that make up the affected tendon (or the fascial membranes that attach to the tendon), you are going to have a hard time dealing with it using the standard fare found in your average medical clinic. Although their various treatments may cover the symptoms for awhile, you are already becoming painfully aware (no pun intended) that standard medical therapies such as those listed earlier, are not likely to help with Tendinosis over the long haul. And although stretching and specific exercise can be of tremendous benefit, most clinicians tend to put the cart in front of the horse. Those things will not be effective until after the tissue adhesion has been removed (broken), except in minor cases.
Be aware that because of its microscopic nature, the collagen derangement associated with Tendinopathies will rarely if ever show up with even advanced diagnostic imaging (this is true even for MRI, unless your doctor is using a brand new machine with an extra large magnet, or your problem is especially severe). And whether it shows on the MRI or not, will not really change the way that your doctor treats the problem.
Effectively Treat Tendinosis At The Source
If tendinopathies do not show up well with the diagnostic tests that are commonly run by your doctor, how in the world can a chiropractor practicing in tiny town determine whether or not this micro-derangement of a tendon�s collagen fibers is present and potentially causing your pain and dysfunction? I use one of the newer forms of SCAR TISSUE REMODELING. Although this has only been around for three decades in its present form, the Chinese have used something similar for several thousand years. Be aware that breaking these adhesions / restrictions sometimes causes some BRUISING, depending on where it’s at.
Conclusion: Systemic Tendinosis
Not all cases of Tendinosis are rooted in purely biomechanical causes. There are all sorts of things that can create an environment within the body that leads to multiple Tendinopathies. As you might imagine, bilateral Tendinosis, or Tendinosis at multiple sites begins to raise some red flags for me concerning this issue. Not that it is always the case, but when I see people who have several areas of Tendinosis, I began to question whether there might be a deeper problem at work.
If it is not caused by Fluoroquinolone Antibiotics, very frequently, this underlying problem turns out to be some sort of poorly understood or difficult-to-detect AUTOIMMUNE DISEASE. If for whatever reason, your body is making antibodies to attack it’s own tendons or connective tissues, you have a serious problem on your hands — a problem that will not respond to the Scar Tissue Remodeling Treatments that I do, and a problem whose cause likely won’t show up on standard medical tests.
Chiropractic and Massage: Duos often create more exciting outcomes. Lewis and Clark, the Lone Ranger and Tonto, and even Batman and Robin functioned more efficiently together than apart. Complementary pairings propel results and enhance efforts.
This is decidedly true with massage therapy and chiropractic care. While each offer considerable benefits on their own, they often mesh well with each other to create a comprehensive treatment plan for many conditions or injuries.
So, sit back and let us show you how massage therapy and chiropractic care are a pain-fighting, mobility-enhancing dynamic duo.
A Combination Of Both: Chiropractic And Massage
Massage Enables A More Effective Chiropractic Visit
Therapeutic massage warms up muscles and relaxes the individual’s entire body, enabling the chiropractor to maximize his or her chiropractic adjustment for optimal results.
Massage brings about a more stable adjustment.
When a chiropractor performs an adjustment to alleviate pain or increase mobility, pre or post massage couples with it to increase the body’s acceptance of the adjustment.
Chiropractic Takes Massage Therapy Further: Includes Joints & Bones
Each treatment offers strong relief and recovery to certain areas of the body. Massage produces relaxation in muscles, relieving tension and toxins. Chiropractic care picks up where massage leaves off and extends the treatment efforts to the body’s tendons, joints, bones and, ultimately, the nervous system.
Works On The Body As A Whole
Both treatments focus on broad rejuvenation and healing techniques for full body health. In a variety of instances, chiropractic care shows significant increases in treating the overall root of the problem when used in combination with massage therapy.
Gets In The Head
Whoever said “it’s all in your head” wasn’t entirely wrong. Individuals sometimes feel stress, dread, or worry over health procedures in general, and chiropractic treatment is no different. Massage therapy serves to relax and de-stress a person, preparing them to go into chiropractic treatments less stressed or tightly wound. A relaxed person’s body tends to respond better to treatment.
Offers Shorter Recovery Times
Blending both treatments into one builds an all-encompassing regimen that works on the condition or injury from multiple points. Tackling health issues this way reduces the time is takes to heal and regain the body’s full mobility.
Decreases Discomfort
Massage therapy aids in warming up muscles, readying them for chiropractic adjustments. This experience is similar to stretching thoroughly before exercising. Pliant muscles offer less resistance to a chiropractor’s regimen, resulting in greater patient comfort. This benefits the entire process, as a painless, comfortable visit increases a person’s openness and commitment to future therapeutic endeavors.
Provides Longer Lasting Results
A relaxed body is more open to treatment. Both massage therapy and chiropractic care serve to attain the goal of healing and recovery, and pain minimization or management. Achieving a synergistic effect is possible when both treatments are employed simultaneously. Chiropractic care is known to work deeper and last longer when paired with massage therapy, especially with chronic, painful health issues.
Patients who seek help with bodily conditions or injuries benefit and see results from chiropractic and�massage therapy separately. Both forms of therapeutic relief used together may create an even more significant, longer last result. Chiropractic care and massage therapy complement each other and offer positive benefits to a variety of painful health issues.
Embark on a treatment plan with this healing, effective dynamic duo! Ask your chiropractor if your specific condition would benefit from both principles of care. Give us a call today!
Shin Splint: Whether you are an avid exerciser, an exuberant shopper, or a small child chaser, you have probably felt tightening and burning in your shin at one point in your life. Sometimes, the pain stops when the activity ceases, but other times the pain remains. If shin pain continues bothering you, it may be time to face the fact you have shin splints.
The shin is a bone located in the front part of your lower leg. Shin splints commonly occur in athletes who have intensified or changed their training routines. They also show up in regular people who have changed or added activity to their routine.
The shin has a lot of responsibility during exercise, as it absorbs the shock of the steps, raises the toes, and support the arch of the foot.
A few main culprits play a part in shin splints:
failing to stretch properly before exercising
walking or running on hard surfaces, like pavement
wearing the wrong type of shoes during activity
over-exerting the body with strenuous activity
skipping periods of rest between exercise
Individuals who perform any type of exercise should take appropriate measures to alleviate the above risk factors of shin splints. If you notice pain and soreness in the front part of your lower leg, know how to treat this injury properly.
If rest and ice aren�t doing the job and you’re still suffering pain, it’s time to see a doctor. A thorough exam and possibly an x-ray will diagnose the problem.
Chiropractic care is a powerful choice for treating shin splints and reducing their recurrence.
Chiropractic Treatment Benefits Those Suffering From Shin Splint/s:
Reduction In Pain
Chiropractic is proven to relieve the pain associated with bodily injuries and medical conditions, including shin splints. Sometimes one visit is enough to relieve the pain, other times the pain decreases over a series of appointments. Being able to diminish a high degree of pain down to a manageable level is possible for shin splint patients through chiropractic.
Full Body Alignment
The premise behind chiropractic is that it treats the body as a whole, and, in doing so, promotes healing and health to the injured or diseased areas. A chiropractor may work on your neck to help your calf. With shin splints, he or she may align your spine and joints to lessen the impact of activity on your shins. Again, the entire body is treated in order to create the best environment for health restoration.
Healing Through Adjustments
Treating shin splints is a common procedure for chiropractors. Common practice is to adjust the calf, ankle, and foot to stretch and increase blood flow to the area.
Drug Free Treatment Option
A primary benefit of chiropractic care is it requires no over-the-counter or prescription drugs. Individuals who suffer from stomach issues, or simply prefer to avoid drugs, find chiropractic visits a productive alternative to manage pain and promote healing.
It’s routine for chiropractic treatment of shin splints to include a series of stretching and strengthening exercises the individual performs at home between visits. These exercises further expand on the positive effects of the chiropractic therapy.
If you are one of the many people dealing with shin splints, don’t despair! Consider chiropractic care as your main treatment option or in conjunction with other modes of treatment. Within a few visits, you will experience pain reduction, and enjoy a decreased risk of ever dealing with painful shin splints again.
Approximately 15 to 40% of those injured in automobile accidents will struggle with chronic pain for the rest of their life. Journal of the American Academy of Orthopedic Surgeons, 2007
Whiplash injuries not only increase your chances of chronic neck and shoulder pain, they also increase the probability of other seemingly unrelated health problems. Journal of Clinical Epidemiology, 2001
Chronic Pain does bad things to people. According to standardized assessment tests, 100% of those struggling with chronic pain caused by whiplash injuries have abnormal psychological profiles. The only way to resolve these abnormal psychological profiles is to relieve / remove the chronic back pain, neck pain and headaches. Counseling / Psychiatry has not been shown to improve the pain nor the psychological profiles of people suffering from the effects of their automobile accident. Pain, 1997
The longest-running study ever done on whiplash patients looked at the overall health of whiplash patients almost twenty years after their automobile accident. Nearly two decades after their accident, 55% of those patients still deal with chronic pain. Accident Analysis and Prevention, 2002
Unless you have a fracture or specific ligament tear, Cervical Collars are no longer recommended for treating patients with whiplash injuries. When cervical collars are used as a whiplash injury treatment, there is a 90% probability that you will still have chronic neck pain in six months. Spine, 2000
One in one hundred people around the world (1% of the population, or just over 70 million people) suffer from ongoing chronic neck pain due to an automobile-induced whiplash injury. Injury, 2005
One in fifty people injured in Whiplash-like accident deal with chronic pain severe enough to need diagnostic testing, medications, and doctor visits, on an ongoing basis —– nearly eight years after the accident occured. Pain, 1994
“Statistically, every American can expect to be in a motor vehicle collision once every ten years. Motor vehicle collisions have been the number one cause of death of our children for decades. Since 9/11 (September 11, 2001), about 3,000 Americans have died as a consequence of terrorism; about 360,000 Americans have died in motor vehicle crashes. Since the start of the American Revolution in 1775, about a million Americans have died in our wars. Since Henry Ford introduced the mass-produced motorcar in 1913, more than 2.5 million Americans have met their deaths on the road. And millions of Americans who did not die from motor vehicle collisions were injured.” Orthopedist and one of the world’s foremost experts on whiplash, Dr. Dan Murphy. There are 3,000,000 new cases of whiplash in the US every year.
Whiplash Injuries Explained
The word �whiplash� is a layperson�s term —- and although it is typically associated with Car Crashes, crashes are certainly not the only way to get a whiplash injury. Whiplash Associated Disorders (WAD) are typically referred to in the medico-legal literature as �Acceleration / Deceleration� injuries, or “Hyperflexion / Hyperextension” injuries. And, as many of you have come to understand the hard way, they can be incredibly violent � even in seemingly minor accidents that had surprisingly little vehicular damage. With over three million new cases of Acceleration / Deceleration injuries occurring each year, and over 50% of those progressing to at least some degree of unresolved or �chronic� symptoms, it is clear that Whiplash Associated Disorders are taking a massive toll on our country financially, physically, and emotionally.
When people think of �whiplash� they tend to think of motor vehicle accidents (MVA�s). Although MVA is probably the single most common cause of the symptoms most frequently associated with and experienced by those suffering with Whiplash Associated Disorders (neck pain, upper back pain, shoulder pain, fuzzy thinking, numbness, tingling and / or weakness of the hands, dizziness, etc), whiplash can occur in about a thousand and one different ways. And while there are certain symptoms that we see over and over and over in our clinic (neck pain and headaches, for instance), whiplash can seemingly cause about a thousand and one different symptoms as well. Some of the most common causes of WAD that I see in my office include sports injuries, work injuries (think logging here), spousal abuse, fights, horse accidents (falls), and almost anything else that has the capacity to �snap� your head suddenly and violently.
Although the most common problems associated with Whiplash Associated Disorders are related to the neck (neck pain, numb hands, headaches), scientific research shows that Acceleration / Deceleration injuries routinely cause all sorts of other injuries as well. For instance, I commonly see people whose low back pain started with an MVA. I even see people whose FIBROMYALGIA was brought on by the emotional and physical stress of an MVA! One of the most shocking conclusions concerning Whiplash Associated Disorders, was written by a pair of the most well known whiplash researchers on the planet � medical researchers, not chiropractic researchers. Drs. Gargan & Bannister stated in a study that was done in the 1990?s, that whiplash-like injuries frequently result in a whole host of, �bizarre and seemingly unrelated symptoms�. Although there are plenty of malingerers, fakers, scam artists, money-grubbers, and drug seekers out there; far too many people are lumped into these categories simply because their problems do not show up on traditional medical tests such as MRI / CT.
Even though there are literally scores of scientific studies concluding that Whiplash Associated Disorders are difficult (often to the point of being impossible) to image on x-rays, CT’s, or MRI�s, these are still the chief method the medical community is using to determine whether or not you were injured, and just how serious this injury might be. The problem is, if the vast majority of soft-tissue injuries (injuries to LIGAMENTS, TENDONS, MUSCLES, FASCIA, etc) do not image well with advanced imaging techniques, and imaging is the medical community�s chief method of diagnosis; unless you have a herniated disc, you will invariably be treated like nothing is really wrong with you � like you are a scam artist trying to extort a huge settlement from an insurance company. Stop and think for a moment about how problematic that fascia, arguably the single most pain-sensitive tissue in your entire body, will not show up on any tests —- including MRI.
When you are taken the the ER, you will have some tests run and the doctor will look at you and say, �Thank God Mrs. Smith. Nothing is broken! Now, go home and rest, and call your family doctor tomorrow. In the mean time, wear this collar, and take these Anti-Inflammatory Medications, pain pills, and muscle relaxers. Oh, and don�t forget to use a heat pack as well.� Is this good advice? Sure it is � if you own a medical clinic! Follow this advice and you are certain to become a lifetime ARTHRITIC! The truth is, when it comes to the evaluation and treatment of injuries to fascia and other elastic, collagen-based connective tissues, all of our hi-tech equipment with its bells and whistles is simply not helping diagnose or help most injured people. You are reading a page on whiplash —- my guess is that you completely understand this concept because you have been there, and done that! The Old Model of tissue injury evaluation and treatment went out the door about 25 years ago. It just seems like no one has remembered to tell treating physicians about the NEW MODEL.
Brain Based Injury
Your short drive to work was no different than any other day —- until you began slowing down for the school bus stopping in front of you. Just as you’re coming to a complete stop, BAM; your world explodes as someone plows into your car from behind, knocking you into the bus. Turns out the kid driving the full-sized crew cab pickup truck that hit you was texting, and never even hit his brakes. You’re having a hard time remembering exactly what happened. You remember a flash of light and your head being slammed backwards over the top of your headrest. You vaguely recall that your head rocketed forward as you hit the bus — almost hitting the windshield. You step out of your 1997 Toyota Camry to take stock of the situation. There is no blood or guts. In fact, you don’t even have a bruise to show for your trouble. But by the time the State Troopers arrive to work the accident, you not only have a neck pain unlike anything you have ever felt before, you have a banging headache as well. You’re having trouble putting the pieces in order for them. They ask if you need an ambulance, but you do not want to go to the Emergency Room. But a few weeks later, you’re still having trouble with your memory. Work is not going well because on top of the pain and exhaustion (yeah, since the accident you can’t sleep either), everything seems fuzzy, foggy, and hazy. Who would have thought that whiplash could cause these sorts of symptoms —– particularly without any overt / obvious injuries?
Whiplash Injuries are particularly dangerous because they are a common cause of MTBI (Mild Traumatic Brain Injury). MTBI results from the brain bouncing off the inside of the skull during the hyperextension / hyperflexion of the neck. As you can imagine, this damages / destroys nerve cells. Depending on which part of the brain is injured, a person might have problems in some of the following areas…
Walking / Moving
Balance
Coordination
Strength / Endurance
Ability to Communicate
Ability to Understand
Ability to Think
Memory
Strange or Unexplainable Pain Patterns or Symptoms (these are some of the “bizarre and seemingly unrelated symptoms” talked about by whiplash researchers Gargan and Bannister.)
Altered Psychological Profiles
Because these symptoms are often subtle, not very specific, and do not show up on standard medical tests such as x-rays or MRI’s, it�s common for patients with MTBI not to complain about them — at least initially. For many people it can be embarrassing “complaining” to the chiropractor or doctor about these vague and difficult-to-describe symptoms that have no external findings to relate them to (bruising, abrasions, broken bones, etc). Believe it or not, many patients are relieved to find out that there is a physiological reason that they feel the way they do, and that it is not “all in their head”. The good news is that with the correct kind of care, most of the patients who are struggling with these injuries will recover within a year’s time. But unfortunately, not all do. It is for this group of people that the term MTBI or “Post Concussive Syndrome” is used.
Factors That Worsen Whiplash Injury
The �old� model of whiplash said that WAD was simply caused by stretched or torn tissue, which was solely the result of the head flying around upon impact. That model simply did not explain the injuries being reported in low-speed collisions (15 mph and under). The most current whiplash models shows that a wave is �shot� through the spine upon impact —- quite similar to the wave you create to move the garden hose a couple of feet to the left. This wave, which occurs in a fraction of a second, can tear both connective tissue and nerve tissue microscopically. It also momentarily induces a tremendous amount of pressure in the smallest blood vessels (capillaries) which is known as �blood hammer�. Blood Hammer, FASCIAL TEARING, and subsequent Neurological Damage, helps to explain some of these “bizarre and seemingly unrelated symptoms” that are almost epidemic in those who have suffered whiplash injuries due to MVA’s.
What Can Make Whiplash Injury Worse?
FACTORS THAT POTENTIALLY INCREASE WHIPLASH SEVERITY
Unaware of approaching impact
Being Female (less muscle mass)
Incorrectly positioned headrest (too low)
Wet, Icy, or Slick roads (or gravel)
Automatic Transmission
Your vehicle is small and light or struck by a larger vehicle
Elderly or arthritic spine (or history of previous whiplash injury)
Head turned at impact
Angled or side-impact accidents (rear-enders are particularly bad)
FACTORS THAT POTENTIALLY DECREASE WHIPLASH SEVERITY
Aware of approaching impact
Being Male (more muscle mass)
Headrest positioned at mid-ear
Dry Pavement
Manual Transmission
Your vehicle is large, heavy, or struck by a much smaller vehicle
Younger or more flexible and healthy spine (no previous injury)
Head facing forward at impact
Straight impacts
Relationship: Severity Of Injury & Amount Of Vehicle Damage
“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.” Dr. Daniel Murphy, Board Certified Orthopedist and Leading Expert in Whiplash Diagnosis and Treatment
In 1687, famed astronomer / mathematician / physicist / philosopher / and theologian, Sir Issac Newton, wrote his still-renowned Philosophiae Naturalis Principia Mathmatica (now referred to as Principia or simply “Principles”), that is still considered to be the greatest scientific textbook in human history.
In Principia, Newton laid out his three Laws of Motion. These laws are able to explain whiplash and the subsequent injury that follows better than anything else I have seen thus far. For understanding whiplash injuries and their relationship to vehicle damage, Newton’s first law is the most important —- The Law of Inertia. Channel your 8th grade science class and stay with me here as we take a brief science / physics review. Newton’s First Law: Objects at rest remain at rest unless they are acted on by an outside force. Likewise, objects in motion stay in motion unless they are acted on by an outside force. And remember this; Like Dr. Murphy described above, whiplash injuries occur because different parts of your body can and will have different inertias — sometimes very different inertias.
Let’s say that you are sitting at a stoplight and minding your own business. You’re humming along to Manfred Mann’s Blinded by the Light, when all of a sudden —- BAM! You are slammed from behind and launched across the intersection like you were shot from a cannon! You are not sure what happened, but you feel like you just got knocked into next week. PHYSICS LESSON: When your vehicle was struck from behind, it shot forward. Much of this had to do with the fact that you were driving a 1992 Toyota Corolla, and the kid that hit you (he was texting of course) was headed to the sale barn for his dad, driving a F-350 Supercab, and pulling a stock trailer loaded with eight steers. When he hit you, there was a huge instantaneous change in momentum. In a fraction of a second, your Corolla was accelerated from zero to over 50 mph. Let’s look at this event in frame-by-frame fashion.
As the Corolla shot forward, so did your torso that was sitting in the seat. Follow me, because here is the precise point where whiplash occurs. As your body was accelerated forward, your head (at least in the initial milliseconds) did not move. The head is much smaller (and lighter) than your torso, and attached by a thin column of muscles, tissues, and tiny vertebrate we call the neck or Cervical Spine. Because of the weight difference between the head and the body, as well as the fact that the connector between them (the neck) is stretchy and relatively thin; the head has a completely different inertia than the body. This was magnified by the fact that the seat back kept your torso from moving very far backwards, but did nothing to stop your neck — and unfortunately, your head restraint was not adjusted to the proper height. In other words, your body was essentially driven out from under your head; then a fraction of a second later, your head not only caught up with your body, it actually accelerated to a greater velocity than your body, and overshot it as your head slammed forward.
Let’s review: As the vehicle, the seat, and your body rocketed forward with the explosive energy and momentum shift from the impact, your head remained stationary for a split second. Your body was essentially driven out from under your head, making it appear that your head slammed backwards. As your head’s momentum began catch up to that of your body, the tissues in your neck began to stretch and deform. Unfortunately, when the force of the accident is greater than the forces holding your tissues together, these tissues begin to tear —- at least on a microscopic basis (remember, most of the time this tearing and SCAR TISSUE will not show up on an MRI). The result was a whiplash injury —- an inertial injury to the SPINAL LIGAMENTS, SPINAL DISCS, FASCIA, TENDONS, and other soft tissues of the neck and upper back. In fact, there are studies showing that even though they are too small to be effectively imaged with current MRI technology, there are often (usually) microscopic fractures of the FACET JOINTS present with intense whiplash injuries. Frequently, there is also sub-clinical brain injury as well.
Interestingly enough, one of the things that make muscles contract with greater intensity is to maximally stretch them (think of the windup and cocked arm of a baseball pitcher here). When the neck is stretched to such a great degree, it’s muscles contract to an equally intense degree. When coupled with the acceleration and subsequent deceleration of the vehicle, this causes the neck to slam forward causing still more tissue tearing in the neck and upper back. And the most important thing to grasp is that your neck and head never hit anything throughout the entire process. The injury to the neck itself (which happened in a matter of milliseconds) occurred because of a huge momentary shift in momentum, energy, and inertia between your body and your head —- just like what you see in Shaken Baby Syndrome.
Although you are slightly dazed, you get out of your Corolla and begin to appraise the situation. You look at your limbs. They look intact. You can move. You are breathing. There’s no blood. Nothing looks bruised or feels broken. In fact, you do not have as much as a scratch on you. You do not want to go to the Emergency Room, but the State Trooper working the accident talks you in to it. You have several spinal x-rays and a CT of your neck. Everything is negative. The ER doctor comes in, pokes you, prods you a couple times, and has you move a bit. He then delivers a short monologue — one he has delivered hundreds of times previously, “Wow Mr. Jones. Sounds like you were born under a lucky star. Thank God nothing is broken. Neurologically you check out fine. You’ll be sore, but just go see your family doctor tomorrow. You’ll get some PAIN PILLS, NSAIDS, CORTICOSTEROIDS, and MUSCLE RELAXERS. Don’t worry. You’ll be just fine.”
But that’s just it. You saw your doctor, and as the weeks go by, you’re not fine. Far from it. You are in pain, and it’s getting worse. But you have nothing to show for it. Like I said, there were no broken bones and no bruises. Heck, there was not even a cut or scratch. There is nothing that would alert anyone (let alone a doctor who is not up on the most current research) that you are in pain —- and that it’s getting worse. And on top of that, the damage to the rear end of your Corolla looked surprisingly light compared to how hard you were hit and the way that you feel (for Pete’s sake, the car is actually drivable). The other fellow’s insurance company paid you $2,000 for your Toyota, which was over double the Kelly Blue Book value. They took care of the ambulance ride and Emergency Room visit, and even offered you $1,500 for pain and suffering. You hired an attorney, but he acts like he does not really believe how much you hurt either. What’s going on here?
Almost half a century ago (1964), the prestigious medical journal, American Journal of Orthopedics revealed a still well-concealed fact — that there is no relationship (none, nada, zilch, zero) between the damage done to the vehicle and the amount of injury to the vehicle’s occupants. Since that time, the medical and scientific communities have proved this fact over and over and over again via research. It is a fact that I have heard verified over and over and over again by the Law Enforcement Officers and Paramedics that I adjust on a regular basis. Although most of the time, Insurance Companies and the Attorneys that represent them would have you believe just the opposite (there was not enough vehicle damage to have an injury), it’s just not true. Decades worth of scientific studies tell us that the severity of the vehicle damage cannot predict….
If patients will suffer whiplash injuries.
How severe those injuries might be.
How long it will take to effectively treat / heal the injury — or whether they will ever really heal at all.
Whether or not the injured party will end up with Chronic Pain and / or Arthritis as a direct result of the accident.
Dozens upon dozens of studies on Motor Vehicle Accidents have shown that vehicles that do not crumple upon impact will be accelerated with a far greater force and momentum. The faster that your vehicle is accelerated upon impact, the greater the inertial stresses to the neck and upper back. This is why today’s vehicles are made with “crumple zones”. You are much better off if the force of impact is absorbed by vehicular deformation, than by deformation of your body, particularly the soft tissues and discs of your neck. The larger the inertial stresses to the neck and upper back, the greater the damage to the soft tissues of the cervical spine / neck.
So, it stands to reason that harder impacts and greater amounts of vehicle damage lead to greater amounts of bodily injury. Not only is this not true, but most of the medical research on whiplash injuries today is being done on the effects of low speed impacts (those under 15 mph). Here are a few of the Scientific / Medical / Legal profession’s journals saying that there is no relationship between the amount of vehicular damage and the amount of injury to the vehicle’s occupants.
The Spine, 1982
Orthopedic Clinics of North America, 1988
Society of Automotive Engineers, 1990
Injury, 1993
Trial Talk, 1993
Injury, 1994
American Journal of Pain Management, 1994
Society of Automotive Engineers, 1995
Society of Automotive Engineers, 1997
Archives of Physical Medicine and Rehabilitation, 1998
Journal Of Whiplash & Related Disorders, 2002
Spine, 2004
Journal of Neurology, Neurosurgery, and Psychiatry, 2005
Spine, 2005
Whiplash Injuries, 2006
One of the problems, however, with whiplash injuries is that they frequently end up causing DEGENERATIVE ARTHRITIS. This has to do with the fact that these inertial injuries damage tissues in ways that cannot be imaged using even the most advanced technologies. Because most doctors are not up on current whiplash research, and feel you are looking for a big settlement, they frequently treat you like a malingerer (faker). However, these injuries cause the microscopic fibrosis that causes abnormal joint motion over time. This leads to arthritis so frequently, that I can often predict with a great deal of accuracy when a person’s injury occurred — just by looking at a current x-ray of their neck.
Arthritis After An Automobile Accident
X-rays taken an average of seven years after a whiplash injury revealed that arthritis in the neck’s spinal discs in almost 40% of the patients. The study’s uninjured group showed only a 6% rate of arthritis. What did the authors conclude? �Thus, it appeared that the injury had started the slow process of disc degeneration.� The Cervical Spine Research Society, 1989
Whiplash patients who already had degenerative arthritis of their cervical spine (neck), showed evidence of degenerative arthritis at previously non-arthritic discs and vertebrates in 55% of cases. The Cervical Spine Research Society, 1989
Compared to the necks of uninjured patients, a single incidence of whiplash increases the occurance of neck arthritis by 10 years. The Journal of Orthopedic Medicine, 1997
Pre-exisiting arthritis of the neck / Cervical Spine, greatly worsens the effects of a whiplash injury. Numerous studies show how this slows recovery times and increases the probability of ending up with Chronic Pain and even more arthritis than you started with. British Journal of Bone and Joint Surgery, 1983; The American Academy of Orthopedic Surgeons, 1987; Orthopedic Clinics of North America, 1988; Spine, 1994; British Journal of Bone and Joint Surgery, 1996
A great example of Inertia Injuries involves the sport of soccer. Soccer players who regularly “head” soccer balls, speed up degenerative arthritis of the neck by as much as twenty years. European Spine Journal, 2004 This is not new information, however. I wrote a newspaper column on the subject clear back in 1993. We saw that professional soccer players had double the amount of neck arthritis as their non-soccer playing peer group.
Whiplash Disorders: Difficult To Diagnose Despite Advanced Imaging
WAD is difficult to properly diagnose or evaluate using standard medical tests. X-rays do not ever show soft connective tissues, and dozens of studies show that MRIs, contrary to popular belief, do a poor job of imaging injured soft tissues — ESPECIALLY FASCIA. This is why you might feel like you are �dying�, but all of the tests are negative. People go through this experience over and over. They are then sent home from the E.R. or doctor�s office with pain killers, muscle-relaxers, and anti-inflammation drugs which can actually cause injured tissue to heal approximately 1/3 weaker and less elastic than it otherwise would, and told that in time it will heal. Just like a broken arm that is cocked off at a funny angle but never set or put in a cast; it will heal�.. It just won�t heal the right way or with the proper amount of joint function / motion.
So just how should a problem like this be addressed? The key to a functional recovery is controlled motion. CHIROPRACTIC ADJUSTMENTS, specific stretches, and strengthening exercises are the number one way to accomplish this! Because FASCIAL ADHESIONS are usually part of the whiplash equation, you will probably need to undergo some form of Tissue Remodeling as well. Restoring movement, function, and strength (both to individual joints or vertebrate, and to the spine or limb as a whole) is the only proven method that is effective in truly reducing the symptoms of whiplash. Contrary to popular belief, using drugs to simply cover symptoms, is never a good option.
If the only treatment you receive for your whiplash injury is palliative (meaning covering symptoms with drugs, without addressing the underlying cause of those symptoms), then any relief achieved is temporary, and the end product of this process will likely be dysfunction, degeneration, and chronic pain!
Doctor/s Cannot Find Anything Wrong: What To Do
I would seriously consider getting a new doctor. As you have already read, whiplash is frequently a “clinical” diagnosis. This simply means that it is not going to show up well on standard imaging tests such as x-rays, CT, and even MRI. If your doctor is not up on the most current whiplash research, you lose — in more ways than one. Let me show you the results of one study that wanted to determine if the effects of whiplash were real (“organic”) or in the patient’s head (“psychometric”). By the way, this study comes from a 1997 issue of one of the planet’s most prestigious medical journals, The Journal of Orthopedic Medicine. They compared a large control group to a large whiplash group, ten years after the accident. Not only does this give us a long-term look at the effects of whiplash, it also removes the potential effects of litigation on the research as any legal issues would have been long settled.
NON-WHIPLASH INJURED GROUP
Neck Pain
Headaches
Numbness, Tingling, Pain, Paresthesia in Arms / Hands
Combined Back and Neck Pain
Neck Degeneration as Seen on X-rays
WHIPLASH INJURED GROUP
Eight Times more Neck Pain
Eleven Times more Headaches
Sixteen Times more Numbness, Tingling, Pain, Paresthesia in Arms / Hands
Thirty Two Times more Combined Back and Neck Pain
Neck Degeneration was Ten Years Advanced when Compared to the Control Group
Hyperflexion/Hyperextension Of The Cervical Spine
Hyperflexion
Hyperextension
With Hyperflexion, the spine goes forward, which drives the Nucleus of the disc to the back. This is why Herniated Discs are a frequent result of Whiplash Injuries. In Hyperextension, the spine is slammed backward. Although this rarely if ever results in frontal Disc Herniations, it jams the facets (the two little joints to the rear and on either side of the disc). This can lead to a degenerative condition called Facet Syndrome.
Notice in this Flexion / Extension X-ray that there is Spinal Degeneration occurring at the level of the C5-C6 Spinal Disc. This means that either this X-ray is being taken years (maybe decades) after an injury, or that this person had pre-existing degeneration (bone spurs, thin discs, and calcium deposits) prior to this latest injury. Either way, the individual being X-rayed had a Flexion / Extension injury of some sort probably 20 years ago or so. How can we predict this. Although there is a certain degree of “guesswork” that goes into knowing this, we know that DEGENERATIVE ARTHRITIS occurs due to loss of joint motion over time, and that whiplash tends to strike worst at C5-C6.
Soft Tissue Injuries?: How Long Do They Take To Heal?
That the spine and its supporting Connective Tissues can take up to two years to heal is not really new information. It can be found at least as far back as a 1986 issue of the Canadian Family Physician. More recent studies showing these longer healing times include a 1994 issue of the journal Pain, a 1994 issue of the journal Spine, and a 2005 issue of the medical journal Injury. In fact, the 1994 issue of Spine said that appropriately treated whiplash patients took an average time of over seven months to heal. This means that for every person who took 4-6 weeks to heal from their injuries, someone else is taking well over a year.
For people injured in Automobile Accidents, falls, Horse Accidents, Motorcycle Crashes, or any number of other ways that people end up with “Whiplash Injuries”, this is a commonly-asked question.� But it’s also a commonly asked question for those whose soft tissue injury was not traumatic, but was due to chronic, repeated, sub-maximal loading.� It’s more than understandable.� No matter how the injury occurred or what it is, everyone wants to know how long it is going to take to get better.� Just bear in mind that healing takes time.� And although you will often hear “6-8 weeks” bantered around, this is only partially true.� If you will notice the chart below, you can see that after about 3-4 weeks, the only thing going on is “Maturation and Remodeling”.� Do not be fooled!� This phase is not only critical, but far too often ignored by those who have a financial interest in your injury.
Tissue Repair & Healing Phases
STAGE I (Inflammatory Phase): This phase lasts from 12-72 hours, and is characterized by a release of inflammatory chemicals by injured cells. When cells are injured and die, they rupture and release their contents into the extracellular fluid (WHAT IS INFLAMMATION). These �Inflammatory Chemicals� that are released from ruptured cells are a necessary and vital component of the healing process. However, in excessive amounts, they can cause a great deal of pain. They also promote excessive microscopic scarring. Be aware that if you visit your doctor for a soft tissue injury, you will be given anti-inflammatory medications. These have serious side-effects (heart, liver, kidneys, etc). However, the real kick in the teeth is the fact that this class of drug has been scientifically proven to cause injured connective tissues to heal significantly weaker and with less elasticity than they otherwise would. Nowhere is this more true tha with Corticosteroids. Do a quick search of the Medico-Scientific Literature on Corticosteroids and soft tissue injuries. You will see over and over again that they are detrimental to the healing process and should play no part in the treatment of these injuries (HERE is an example from the field of Sports Injuries).
STAGE II (Passive Congestion): In this phase that begins by the 2nd to 4th day, we begin to see swelling (sometimes we do not see it, because it is not on the body�s surface). Remember; �inflammation� is not synonymous with swelling. Inflammatory Chemicals released by dying cells attract the fluid that causes swelling. This is why using cold therapy (ice) to control both inflammation and swelling is such an important part of the healing process � particularly in its earliest stages. However, the best method for moving out this “Congestive Swelling” is via controlled motion if possible. Oh, and your doctor may tell you to use heat during these initial two phases of soft tissue healing; don’t do it. Use ICE to control the inflammation!
STAGE III (Regeneration & Repair Phase): The Repair Phase is where new collagen fibers are made by fibroblasts. The body then uses these collagen fibers as a sort of soft tissue �patch�. Just like with your old blue jeans, a patch is not ideal. But once those old Levis tear or rip, what else are you going to do? In the body, this collagen patch (scar tissue) tends to be different than the tissue around it in a number of ways. Scar Tissue is weaker, less elastic, MUCH MORE PAIN SENSITIVE, has SEVERELY DIMINISHED PROPRIOCEPTIVE ABILITIES, etc). Be aware that the Repair Phase of tissue healing only lasts about 6 weeks, with the majority being completed in half that time. WARNING: This 3rd stage of healing is where many of the so-called �experts� want you to believe the process of Tissue Healing & Repair ends because this phase ends within a month of injury. But that’s not where the story ends. Dr. Dan Murphy uses dozens of studies to, “document that the best management of soft tissue injuries during this phase of healing is early, persistent, controlled mobilization. In contrast, immobilization is harmful, leading to increased risk of slowed healing and chronicity”.
STAGE IV (Maturation / Remodeling Phase): Not only is it the longest, but the Remodeling Phase is by far the most critical of the four stages of Connective Tissue healing. Yet it is the phase that most often gets overlooked. It is also where people most often get duped (sometimes inadvertently, but more often than not, purposefully) by doctors, insurance companies, and attorneys. Many of you reading this know exactly what I am talking about. The most current research shows that in case of serious Connective Tissue Injury, the Remodeling Phase can last up to two years; making the old �6-8 weeks� sound ridiculous (gulp)! The Remodeling Phase is characterized by a �realignment� (REMODELING) of the individual fibers that make up the injured tissue (the collagen �patch� that we call Scar Tissue). What is interesting is that each study that comes out on this topic, seems to be saying that this phase of healing lasts longer than what the study that came out before it said. This is a good thing. However, bear in mind that if you have not improved within 90 days after injury, standard forms of treatment become much less likely to help you. Phase IV can also be risky because although a person’s pain may have dissipated, the injury itself has not completely healed and is vulnerable to re-injury.
As Controlled Loading / Tensile Loading is applied to the healing tissues via CHIROPRACTIC ADJUSTMENTS, Scar Tissue Remodeling, STRETCHING and strengthening exercises, Proprioceptive Re-education, Massage Therapy, TRIGGER POINT THERAPY, PNF, etc; the individual tissue fibers move from a more random, tangled, and twisted wad of unorganized collagen fibrils; to a tissue that is much more organized, parallel, and orderly as far as its microscopic configuration is concerned. Again, this takes time! Although our Scar Tissue Remodeling Therapy can frequently bring immediate relief (just look at our VIDEO TESTIMONIALS), it is obvious from the medical literature that there is a healing processes that cannot be bypassed. Because numerous Scientific Studies have proved Cold Laser Therapy to be effective in regenerating Collagen (SEE HERE), we highly recommend it for our more seriously injured patients as well.
Everyone has heard the old cliche that is still used by doctors, “You�d have been better off to break the bone than to tear the ligaments”. Knowing what we know about the healing of the Collagen-Based, Elastic Connective Tissues; this statement makes a lot of sense! Soft tissues heal much slower than other tissues (including bones). Do not let anyone try and convince you otherwise! This is why following the complete stretching and strengthening protocol that goes hand-in-hand with our �Tissue Remodeling� treatment, is the one and only way that it will work properly over the long haul. By the way, we have dealt extensively with the fact that whiplash injuries heal best with forms of therapy that employ controlled motion such as does chiropractic. Now I want to explore what the scientific literature says about using medications for whiplash injuries explained.
Whiplash Injuries Explained: Relationship Of Inflammation To Pain & Scar Tissue
In 2007, the renowned pain researcher Dr. Sota Omoigui, published an article in the medical journal Medical Hypothesis called, “The Biochemical Origin of Pain: The Origin of All Pain is Inflammation and the Inflammatory Response”. In it, he showed the relationship between pain, inflammation, and fibrosis (Scar Tissue). Most people tend to think of Inflammation as a “local” phenomenon. You know; sprain an ankle, and it swells — sometimes a whole bunch. But it is critical to remember that the terms “swelling” and “inflammation” are in no ways synonymous. When cells of soft tissues are seriously injured (like in Whiplash Injuries), they die. These dead then rupture their contents into the surrounding extra-cellular fluid. In response to this, the Immune System makes a group of chemicals that we collectively refer to as “Inflammation”, which in small amounts, are normal and good. Their local presence is indicated by five well known signs and symptoms. The classical names for the various signs of Local Inflammation come from Latin and include:
Dolar (Pain)
Calor (Heat)
Rubor (Redness)
Tumor (Swelling) Chemicals we collectively call “Inflammation” are not synonymous with swelling, but they attract swelling.
Functio Laesa (Loss of Function)
Although these chemicals can remain in a local area (I stub my toe, the toe gets red and inflamed), they can invade the blood stream and have a systemic (whole body) effect as well. But inflammation does not end there. These immune system chemicals that we refer to collectively as “inflammation” (prostaglandins, leukotrienes, thromboxanes, cytokines, chemokines, certain enzymes, kinnins, histamines, eicosanoids, substance P, and dozens of others) are being touted by the medical community as the primary cause of a whole host of physical ailments, when there are too many of them in the body. Some of the other problems that Inflammation is known to cause includes;
Disc Injuries, Slipped Disc, Disc Herniation, and Disc Rupture
Heart Disease and virtually all forms of Cardiovascular Problems
Skin conditions including Eczema and Psoriasis
Arthritis & Fibromyalgia
Asthma
ADD, ADHD, Depression, and various forms of Dementia
Neurological Conditions
Female Issues
Cancer
Inflammatory Bowel Disease / Leaky Gut Syndrome
Diabetes, Insulin Resistance, Hypoglycemia, and other Blood Sugar Regulation Problems
Obesity
Inflammation causes pain, ill health, and eventually, death. But this list is not the thrust of this section. To understand is the way that inflammation is related to Scar Tissue, Adhesion, and Fibrosis.
Born in 1904, Dr. James Cyriax, a Cambridge-educated M.D. widely known as the “The Einstein of Physical Medicine” wrote his Magnum Opus, Orthopaedic Medicine, Diagnosis of Soft Tissue Lesions, in 1982 shortly before he passed away. Cyriax is still considered one of the brilliant pioneers of soft tissue research. One of Dr. Cyriax’ groundbreaking discoveries is that Scar Tissue / Fibrosis can and will generate an Inflammatory Response long after the Fourth Stage of Healing (Maturation & Remodeling) is over. Pay attention to what Cyriax wrote over three decades ago.
�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 merely during the period of healing, but for an indefinite period of time afterwards, maintained by the normal stresses to which such tissues are subject.�
Why would what Cyriax refers to as “normal mechanical stresses” cause an “indefinite period” of inflammation? This one is easy. Scar Tissue and Fibrosis are so dramatically different from normal tissue. One of the most obvious ways that this can be seen is by looking at any good Pathology Textbook. Scar Tissue and Fibrosis is far weaker and much less elastic than normal Connective Tissue. What does this mean? Only that it is easily re-injured. This starts the whole vicious cycle over again. Injury —-> Inflammation —> Pain —> Fibrosis & Scar Tissue Formation —> Re-injury —> Repeat indefinitely. Just remember that the end result of this cycle is degeneration of the affected bones and spinal discs!
HEALTHY CONNECTIVE TISSUE
SCAR TISSUE & FIBROSIS
Notice how the Connective Tissue on the left is uniformly wavy. This is due to the collagen fibrils that provide stretchiness and elasticity. Now notice how the cells of the Scar Tissue and Fibrosis run and swirl in many different ways. This decreases both elasticity and strength of the Scar Tissue.
Scar Tissue & Fibrosis: Different From Normal Tissue, 3 Ways
SCAR TISSUE IS WEAKER
Repaired soft tissues are weaker than the body’s undamaged soft tissues. The diameter of the collagen fibers of scar tissue are smaller than those of normal tissue. Also, as you can see from the pictures above, the structure has been physically changed. This weakness leads to a viscous cycle of instability, re-injury, and degeneration.
SCAR TISSUE IS LESS ELASTIC
Repaired soft tissues are always less elastic and “stiffer” than the body’s undamaged soft tissues. This has to do with the fact that the individual collagen fibers will never identically align themselves quite like the original uninjured soft tissue. This is all easy to see because range of motion testing on injured individuals will always show areas of decreased ranges of motion.
SCAR TISSUE IS MORE PAIN-SENSITIVE
Repaired soft tissues have a strong tendency to be more pain-sensitive than their uninjured counterparts. In fact, for reasons that are not completely understood, Scar Tissue has the neurological capability of going into something called “super-sensitivity”, and can end up 1,000 times more sensitive to pain than normal tissue.
Dr. Soto Omoigui had this to say about the relationship between pain, inflammation, and fibrosis, “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, sharp, dull, aching, burning, stabbing, numbing or tingling, the underlying origin is inflammation and the inflammatory response.” Fellow pain researcher Doctor Manjo stated in the “Chronic Inflammation” chapter of his 2004 pathology textbook that (slightly paraphrased for patients), “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, but it cannot be mistaken for normal connective tissue. Fibrosis means an excess of fibrous connective tissue. It implies an excess of collagen fibers. 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.”
It is not difficult to connect the dots! Chronic Inflammation of a whiplash injury leads to Scar Tissue Formation, and Scar Tissue Formation leads to even more pain. And like I mentioned earlier, the whole mess leads to Spinal Degeneration. How can you break free? Dr. Cyriax goes on to say in his book that immobilization of injured soft tissues is a bad thing, and mobilization of injured soft tissues is not only good, but necessary for proper healing to take place. But under the umbrella of America’s PHARMACEUTICAL DRUG CULTURE, functional restoration frequently takes a back seat to different kinds of medicines. Don’t get me wrong; if you need something for the pain after a whiplash injury, there is no dishonor in doing something on a short-term basis. However, this is never the solution. It is masking symptoms to get you through a rough place. As long as you understand this, OK. However, there is one class of drugs that should play no part in the healing of your Whiplash Injury…
Inflammation Medications For Whiplash & Soft Tissue Injuries
The most prestigious medical school on the planet, John’s Hopkins proved that 1,000 200 mg capsules of Tylenol consumed over the course of a person’s lifetime doubles that person’s chances of dialysis. Furthermore, 5,000 pills increase kidney failure by nearly nine times. New England Journal of Medicine, 1994
Regular use of Tylenol and other similar medications is a top cause of liver disease / liver failure. New England Journal of Medicine, 1997
NSAID’s (Non-Steroidal Anti-Inflammatory Drugs) used by arthritis sufferers causes 16,500 Americans to die of bleeding ulcers each year. Fatal GI bleeds are the 15th most common cause of death in America. New England Journal of Medicine, 1999
Gastrointestinal (GI) toxicity caused by NSAID use is one of the most commonly seen and serious drug side effects in modern cultures. Spine, 2003 & Surgical Neurology, 2006
Regular use of Tylenol doubles one’s chances of developing high blood pressure. Hypertension, 2005
All NSAIDs (Non-Steroidal Anti-Inflammatory Drugs) increase chances of Myocardial Infarction (heart attack) by about 40%. This risk starts the first day the drug is consumed. European Heart Journal, 2006
Celebrex increases your chances of intestinal bleeding by four times (nearly 400%). Vioxx increases your chances of bleeding ulcers and other GI Bleeds by over three times (nearly 330%). Medications taken for pain increase your chances of GI Bleeds by nearly 140%. Drug Safety, 2009
Vioxx was removed from the market in 2004 because it increased one’s chances of a heart attack by 230% (exponentially more if you already had a congestive heart). Celebrex increased the risk of heart attack by 44%. Pain Medications, on average, increase your chances of a heart attack by nearly half 50%. While Vioxx was pulled from the market, the others are considered to be “acceptably safe” and they were allowed to stay on the market. Drug Safety, 2009
Those who took the greatest amounts of NSAID pain medications increased their chances of all types of dementia —– Alzheimer�s included. The increase was a whopping 2/3 (66%). Neurology, 2009
So, what is a person supposed to do? Despite decades of research saying that NSAID’s are not “therapeutic” (actually helps you get better), but are instead, “palliative” (makes you feel better without any therapeutic benefits), the medical community continues to hand these and other dangerous drugs out almost like candy. Just remember that any pain relief achieved without addressing the underlying components of the Whiplash Injury, are temporary. And that’s not all. When joints and tissues heal in RESTRICTED FASHION, they always end up with copious amounts of decay, degeneration, and deterioration. And the final kick in the teeth for those of you who have been on this MEDICAL MERRY-GO-ROUND is that much of this research is at least two decades old. As I have said for a very long time, much of the medical community is caught in a time warp. They are treating whiplash injuries using outdated models, often times very outdated models.
Chiropractic Benefits: Whiplash, Neck/Back Pain
Over 70 years ago, the best available research said that soft tissue injuries require early and regular joint motion in order to heal properly. American Journal of Anatomy, 1940
Over 50 years ago, research pointed out that the most effective treatment for whiplash injury does not involve medication, but instead needs mobilization, manipulation and traction to heal. The best results for patients with whiplash injuries require early and regular joint mobilization. Furthermore, it must be done by someone expertly trained in rehabilitation of injured joints. Journal of the American Medical Association, 1958
For injured soft tissues to heal properly requires joint movement / motion. Joint immobilization should be avoided. Textbook of Orthopedic Medicine, 1982 & Continuous Passive Motion, 1993
Chiropractic spinal adjustments fix over 4/5 of disabled patients suffering from chronic low back and sciatica. This is true despite the failure of other approaches. Canadian Family Physician, 1985
Chiropractic spinal adjustments have been proven superior in the treatment of chronic and acute low back pain, when compared to hospital outpatient treatment. These benefits of chiropractic adjustments were still seen 3 years post-treatment. British Medical Journal, 1991
Chiropractic spinal adjustments have been shown to be more effective than physical therapy mobilizations and manipulations. Lancet, 1991
93% of those struggling with chronic pain due to whiplash injury —- who have already failed medical care and physical therapy —- improve significantly under chiropractic care. Injury, 1996
When it comes to chronic neck pain, manual manipulation of the neck has been shown to be significantly better than pain meds and exercise. Annals of Internal Medicine, 2002
Chiropractic spinal adjustments have been clinically proven to be over five times more effective than NSAID’s (Non-steroidal Anti-Inflammatory Drugs) for chronic neck and low back pain. In this study, the chiropractic group suffered from no adverse reactions, but the the NSAID group had more patients reporting adverse drug reactions than were actually helped. Half the NSAIDS used in the study are now off the market. Spine, 2003
For chronic neck and back pain, chiropractic spinal adjustments proved significantly better than both acupuncture and pain medicines. Furthermore, chiropractic adjustments were the only treatment studied that showed therapeutic benefit one year post-treatment. Journal of Manipulative and Physiological Therapeutics, 2005
In patients with chronic pain from DEGENERATIVE ARTHRITIS, 59% can eliminate their pain meds by taking omega-3 fatty acids found in fish oil (EPA & DHA). Surgical Neurology, 2006
In the recent medical publication called, �A Review of the Evidence for the American Pain Society and the American College of Physicians Clinical Practice Guideline�, only spinal manipulation was touted as effective for the treatment of both acute and chronic low back pain. Annals of Internal Medicine, 2007
A joint research effort from the University of California, San Francisco, and Harvard Medical School, showed that �Chiropractic care is more effective than other modalities for treating low back and neck pain�. Do Chiropractic Services for the Treatment of Low Back and Neck Pain Improve the Value of Health Benefits Plans? An Evidence-Based Assessment of Incremental Impact on Population Health and Total Health Care Spending, 2009
Long Term Prognosis: Whiplash
Despite the fact that you can see from the current scientific literature how successful chiropractic care is at helping people with severe, debilitating, whiplash injuries; not everyone injured in an MVA will recover. Unfortunately, many will never recover —- even after several decades. It seems that whiplash caused by Motor Vehicle Accidents is the portal whereby numerous people enter into the realm of Chronic Pain and dysfunction. The truth is that there is a great deal of scientific research done of this particular topic. And furthermore, as you can see from the small comments in red made by the authors of each individual study, litigation seems to have little or no effect on clinical outcomes.
The Journal of Bone and Joint Surgery published research in 1964 showing that of 145 patients involved in a study of whiplash injuries; as many as 83% of the injured patients continued to suffer from pain two years after the accident. The study’s authors said this, “If the symptoms resulting from an extension-acceleration injury of the neck are purely the result of litigation neurosis, it is difficult to explain why [at least] 45%of the patients should still have symptoms two years or more after settlement of their court action.”
A 1989 issue of Neuro-Orthopedics published a study was carried out on patients suffering with whiplash for well over a decade. Despite the length of time involved, nearly two thirds still struggled with moderate to severe pain symptoms due to their accident. The study’s authors said this, “If symptoms were largely due to impending litigation it might be expected that symptoms would improve after settlement of the claim. Our results would seem to discount this theory, with the long-term outcome seeming to be determined before the settlement of compensation.”
A 7-year study on whiplash-injured patients published in a 2000 issue of the Journal of Clinical Epidemiology showed that 40% of those suffering an accident-induced whiplash injury continued to suffer from neck and shoulder pain seven years post-accident.
A 2005 research project published in the medical journal Injury, showed that over 20% of those injured in a whiplash injury struggled with Chronic Pain nearly 8 years post-injury. Furthermore, almost half of those in the study suffered from “Nuisance Pain” during the same time frame.
An 11 year study published in a 1990 issue of the British Journal of Bone and Joint Surgery showed 40% of the whiplash patients struggling with Chronic Pain over a decade after the fact. 40% of the remainder of the study’s people dealt with “Nuisance Pain” during the same period. The study’s authors said this, “The fact that symptoms do not resolve even after a mean 10 years supports the conclusion that litigation does not prolong symptoms.”
A fifteen and a half year study published in a 1996 issue of the British Journal of Bone and Joint Surgery reported that well over 40% of whiplash-injured patients struggled with Chronic Pain from the accident over a decade and a half after the fact. Almost 30% of the rest dealt with “Nuisance Pain” over the course of the study. The study’s authors said this, “Symptoms did not improve after settlement of litigation, which is consistent with previous published studies”.
The European Spine Journal published a nearly two decade long study on whiplash-injured patients in 2002. Well over half (55%) of those studied had pain seventeen years post-accident. One quarter of these dealt with daily neck pain, and almost one quarter had radiating arm pain on a daily basis. The study’s authors said this, “It is not likely that the patients exposed to motor vehicle accidents would over-report or simulate their neck complaint at follow-up 17 years after the accident, as all compensation claims will have been settled.”
In one of the longest studies done to date on whiplash injured patients, a 2006 issue of the British Journal of Bone and Joint Surgery looked at whiplash-injured patients three decades after their initial injury. 15% of these patients struggled with daily pain severe enough to require treatment. Four out of ten of the remainder dealt with “Nuisance Pain” over the same time frame.
Attorney’s, Insurance, Fees & Medical Pay
After 20 years of practice, I can almost say that I have seen it all. Almost. One thing that I have not seen is an improvement in the way that the financial responsibility for Motor Vehicle Accidents (MVA) is handled by insurance companies. This is a big part of the reason that I do not accept automobile insurance (yours or the other party�s) for the treatment of injuries sustained in MVA�s. Attorneys tend to get involved, and I have found that in most cases, attorneys don’t really work for you, they work for themselves.
WHERE DOES THIS ALL LEAD?
Although, I do not treat huge numbers of MVA cases acutely (they tend to go wherever their attorney sends them usually whoever can run up the highest bills), I treat scores of MVA victims once they have reached the chronic stage. After their attorney reaches a settlement for their injured client, any treatment they were receiving typically ends. As you can tell from both our Patient Testimonial Page, as well as our Blog Post called the WEEKLY TREATMENT DIARY, the treatment frequently ends without ever effectively dealing with the underlying scar tissue and Fibrotic Adhesions that leave so many people in Chronic Pain, long after they have settled their injury claim.
These folks enter the miserable world of CHRONIC NECK / BACK PAIN and HEADACHES, and then wonder what the heck they are going to do because their $3,000 settlement check is long gone. The patient is then left with a choice. They can climb back on the Medical Merry-Go-Round and continue to spin in circles. Tests, blood work, MRI�s, CT scans, drugs, drugs, and more drugs; and therapy � more of the same (expensive) stuff you went through before you settled your case, with more of the same crappy results. Or they can do something different.
Prevent Whiplash Injuries & Lessen The Effects
There are several ways to go about preventing or at the very least, lessening the potential effects of a whiplash-like accident / injury. one of the most effective would be driving a vehicle that is highly rated in crash tests. What is the safest vehicle on the road today? Without a doubt, the Volvo and Saab brands have out-performed every other auto maker in the market today as far as safety is concerned. However, there are a number of things you can do to protect yourself besides trading your Chevy in for a Volvo.
DRIVE A SAFE VEHICLE: Make sure that the vehicle you drive is highly rated by the organizations that rank automobile safety. This information can be found HERE.
DRIVE SAFELY AND DEFENSIVELY: This is common sense. Because I rode a motorcycle for many years, I learned how to drive defensively. I always thought that by paying attention and trying to think one step ahead of everything going on around me, crashes with other vehicles could be avoided. That was until I hit a drunk who ran a stop sign (I was in a full-sized Chevy Silverado). Things happen quickly, that you have no control over. However, driving your automobile in an unsafe manner definitely puts you at a higher risk for suffering a Whiplash Injury.
WEAR YOUR SEAT BELTS: The simple truth of the matter is that seat belts will probably not lessen the “Whiplash” component of an Automobile Accident. In fact, by holding your body in place while your head flies around, they can potentially worsen a neck injury to the soft tissues. However, seat belts will help to keep you alive.
MAKE SURE YOUR HEAD RESTRAINT IS ADJUSTED PROPERLY: This is by far the most important thing you can do diminish your chances of Whiplash Injury should you end up in an MVA. The truth is, most of us refer to these things that stick out of the top of our seats as “Head Rests” instead of “Head Restraints”, and actually have them adjusted improperly (all the way down). The purpose of these devices is not to “rest” your head because you are tired, it is to “restrain” your head from flying backwards during a rear-ender accident. The top of the Head Restraint should be level with the top of your head, and the gap between the two should not be more than about two inches. For the record; if you recline your seat more than 20 degrees, all bets are off. A serious rear-ender will cause you to ramp up in your seat rendering the Head Restraint useless.
These assessment and treatment recommendations represent a synthesis of information derived from personal clinical experience and from the numerous sources which are cited, or are based on the work of researchers, clinicians and therapists who are named (Basmajian 1974, Cailliet 1962, Dvorak & Dvorak 1984, Fryette 1954, Greenman 1989, 1996, Janda 1983, Lewit 1992, 1999, Mennell 1964, Rolf 1977, Williams 1965).
Clinical Application of Neuromuscular Techniques: Sternocleidomastoid (SCM)
Assessment for Shortness of Sternocleidomastoid�(see also Box 4.10)
Assessment for SCM is as for the scalenes � there is no absolute test for shortness but observation of posture (hyperlordotic neck, chin poked forward) and palpation of the degree of induration, fibrosis and trigger point activity can all alert to probable shortness of SCM. This is an accessory breathing muscle and, like the scalenes, will be shortened by inappropriate breathing patterns which have become habitual. Observation is an accurate assessment tool.
Box 4.10 Notes on Sternocleidomastoid
Sternocleidomastoid (SCM) is a prominent muscle of the anterior neck and is closely associated with the trapezius. SCM often acts as postural compensator for head tilt associated with postural distortions found elsewhere (spinal, pelvic or lower extremity functional or structural inadequacies, for instance) although they seldom cause restriction of neck movement.
SCM is synergistic with anterior neck muscles for flexion of the head and flexion of the cervical column on the thoracic column, when the cervical column is already flattened by the prevertebral muscles. However, when the head is placed in extension and SCM contracts, it accentuates lordosis of the cervical column, flexes the cervical column on the thoracic column, and adds to extension of the head. In this way, SCM is both synergist and antagonist to the prevertebral muscles (Kapandji 1974).
SCM trigger points are activated by forward head positioning, �whiplash� injury, positioning of the head to look upwardly for extended periods of time and structural compensations. The two heads of SCM each have their own patterns of trigger point referral which include (among others) into the ear, top of head, into the temporomandibular joint, over the brow, into the throat, and those which cause proprioceptive disturbances, disequilibrium, nausea and dizziness. Tenderness in SCM may be associated with trigger points in the digastric muscle and digastric trigger points may be satellites of SCM trigger points (Simons et al 1998).
Simons et al (1998) report: When objects of equal weight are held in the hands, the patient with unilateral trigger point [TrP] involvement of the clavicular division [of SCM] may exhibit an abnormal Weight Test. When asked to judge which is heaviest of two objects of the same weight that look alike but may not be the same weight (two vapocoolant dispensers, one of which may have been used) the patient will [give] evidence [of] dysmetria by underestimating the weight of the object held in the hand on the same side as the affected sternocleidomastoid muscle. Inactivation of the responsible sternocleidomastoid TrPs promptly restores weight appreciation by this test. Apparently, the afferent discharges from these TrPs disturb central processing of proprioceptive information from the upper limb muscles as well as vestibular function related to neck muscles.
Lymph nodes lie superficially along the medial aspect of the SCM and may be palpated, especially when enlarged. These nodes may be indicative of chronic cranial infections stemming from a throat infection, dental abscess, sinusitis or tumour. Likewise, trigger points in SCM may be perpetuated by some of these conditions (Simons et al 1998).
Lewit (1999) points out that tenderness noted at the medial end of the clavicle and/or at the transverse process of the atlas is often an indication of SCM hypertonicity. This will commonly accompany a forward head position and/or tendency to upper chest breathing, and will almost inevitably be associated with hypertonicity, shortening and trigger point evolution in associated musculature, including scalenes, upper trapezius and levator scapula (see crossed syndrome notes in Ch. 2).
Since SCM is only just observable when normal, if the clavicular insertion is easily visible, or any part of the muscle is prominent, this can be taken as a clear sign of tightness of the muscle.�If the patient�s posture involves the head being held forward of the body, often accompanied by cervical lordosis and dorsal kyphosis (see notes on upper crossed syndrome in Ch. 2), weakness of the deep neck flexors and tightness of SCM is suspected.
Functional SCM Test (see Fig. 5.14A, B)
The supine patient is asked to �very slowly raise your head and touch your chin to your chest�. The practitioner stands to the side with his head at the same level as the patient. At the beginning of the movement of the head, as the patient lifts this from the table, the practitioner would (if SCM were short) note that the chin was lifted first, allowing it to jut forwards, rather than the forehead leading the arc-like progression of the movement. In marked shortness of SCM the chin pokes forward in a jerk as the head is lifted. If the reading of this sign is unclear then Janda (1988) suggests that a slight resistance pressure be applied to the forehead as the patient makes the �chin to chest� attempt. If SCM is short this will ensure the jutting of the chin at the outset.
MET Treatment of Shortened SCM (Fig. 4.35)
The patient is supine with the head supported in a neutral position by one of the practitioner�s hands. The shoulders rest on a cushion or folded towel, so that when the head is placed on the table it will be in slight extension. The patient�s contralateral hand rests on the upper aspect of the sternum to act as a cushion when pressure is applied during the stretch phase of the operation (as in scalene and pectoral treatment). The patient�s head is fully but comfortably rotated, contralaterally.
Figure 4.35 MET of sternocleidomastoid on the right.
The patient is asked to lift the fully rotated head a small degree towards the ceiling, and to hold the breath. When the head is raised there is no need for the practitioner to apply resistance as gravity effectively provides this.
After 7�10 seconds of isometric contraction (ideally with breath held), the patient is asked to slowly release the effort (and the breath) and to place the head (still in rotation) on the table, so that a small degree of extension occurs.
The practitioner�s hand covers the patient�s �cushion� hand (which rests on the sternum) in order to apply oblique pressure/stretch to the sternum, to ease it away from the head and towards the feet.
The hand not involved in stretching the sternum caudally should gently restrain the tendency the head will have to follow this stretch, but should not under any circumstances apply pressure to stretch the head/neck while it is in this vulnerable position of rotation and slight extension.
The degree of extension of the neck should be slight, 10�15� at most.
This stretch, which is applied as the patient exhales, is maintained for not less than 20 seconds to begin the release/stretch of hypertonic and fibrotic structures. Repeat at least once. The other side should then be treated in the same manner.
CAUTION: Care is required, especially with middle aged and elderly patients, in applying this useful stretching procedure. Appropriate tests should be carried out to evaluate cerebral circulation problems. The presence of such problems indicates that this particular MET method should be avoided.
Dr. Alex Jimenez offers an additional assessment and treatment of the hip flexors as a part of a referenced clinical application of neuromuscular techniques by Leon Chaitow and Judith Walker DeLany. The scope of our information is limited to chiropractic and spinal injuries and conditions. To discuss the subject matter, please feel free to ask Dr. Jimenez or contact us at 915-850-0900 .
By Dr. Alex Jimenez
Additional Topics: Wellness
Overall health and wellness are essential towards maintaining the proper mental and physical balance in the body. From eating a balanced nutrition as well as exercising and participating in physical activities, to sleeping a healthy amount of time on a regular basis, following the best health and wellness tips can ultimately help maintain overall well-being. Eating plenty of fruits and vegetables can go a long way towards helping people become healthy.
These assessment and treatment recommendations represent a synthesis of information derived from personal clinical experience and from the numerous sources which are cited, or are based on the work of researchers, clinicians and therapists who are named (Basmajian 1974, Cailliet 1962, Dvorak & Dvorak 1984, Fryette 1954, Greenman 1989, 1996, Janda 1983, Lewit 1992, 1999, Mennell 1964, Rolf 1977, Williams 1965).
Clinical Application of Neuromuscular Techniques: Scalenes
Box 4.9 Notes on Scalenes
The scalenes are a controversial muscle since they seem to be both postural and phasic (Lin et al 1994), their status being modified by the type(s) of stress to which they are exposed (see Ch. 3 for discussion of this topic).
Janda (1988) reports that �spasm and/or trigger points are commonly present in the scalenes as also are weakness and/or inhibition�.
The attachment sites of the scalene muscles vary, as does their presence. The scalene posterior is sometimes absent, and sometimes blends with the fibres of medius.
Scalene medius is noted to frequently attach to the atlas (Gray 1995) and sometimes extend to the 2nd rib (Simons et al 1998).
The scalene minimus (pleuralis), which attaches to the pleural dome, is present in onethird (Platzer 1992) to three-quarters (Simons et al 1998) of people, on at least one side and, when absent, is replaced by a transverse cupular ligament (Platzer 1992).
The brachial plexus exits the cervical column between the scalenus anterior and medius. These two muscles, together with the 1st rib, form the scalene hiatus (also called the �scalene opening� or �posterior scalene aperture�) (Platzer 1992). It is through this opening�that the brachial plexus and vascular structures for the upper extremity pass. When scalene fibres are taut, they may entrap the nerves (scalene anticus syndrome) or may elevate the 1st rib against the clavicle and indirectly crowd the vascular, or neurologic, structures (simultaneous compromising of both neural and vascular structures is rare) (Stedman 1998). Any of these conditions may be diagnosed as �thoracic outlet syndrome�, which is �a collective title for a number of conditions attributed to compromise of blood vessels or nerve fibers (brachial plexus) at any point between the base of the neck and the axilla� (Stedman 1998).
Assessment of Shortness in Scalenes (14)
Assessment of cervical sidebending (lateral flexion) strength. This involves the scalenes and levator scapulae (and to a secondary degree the rectus capitis lateralis and the transversospinalis group).
The practitioner places a stabilising hand on the top of the shoulder to prevent movement and the other on the head above the ear, as the seated patient attempts to flex the head laterally against this resistance. Both sides are assessed.
Observation assessment (a) There is no easy test for shortness of the scalenes apart from observation, palpation and assessment of trigger point activity/tautness and a functional observation as follows:
In most people who have marked scalene shortness there is a tendency to overuse these (and other upper fixators of the shoulder and neck) as accessory breathing muscles.
There may also be a tendency to hyperventilation (and hence for there to possibly be a history of anxiety, phobic behaviour, panic attacks and/or fatigue symptoms).
These muscles seem to be excessively tense in many people with chronic fatigue symptoms.
The observation assessment consists of the practitioner placing his relaxed hands over the patient�s shoulders so that the fingertips rest on the clav-icles, at which time the seated patient is asked to inhale deeply. If the practitioner�s hands noticeably rise towards the patient�s ears during inhalation then there exists inappropriate use of scalenes, which indicates that they are stressed, which also means that, by definition, they will have become shortened and require stretching treatment.
Observation assessment (b) (Fig. 4.33) Alternatively, during the history taking interview, the patient can be asked to place one hand on the abdomen just above the umbilicus and the other flat against the upper chest.
Figure 4.33 Observation assessment of respiratory function. Any tendency for the upper hand to move cephalad, or earlier than the caudad hand, suggests scalene overactivity.
On inhalation, the hands are observed: if the upper hand initiates the breathing process and rises significantly towards the chin, rather than moving forwards, a pattern of upper chest breathing can be assumed, and therefore stress, and therefore shortness of the scalenes (and other accessory breathing muscles, notably sternomastoid).
MET Treatment of Short Scalenes (Fig. 4.34A, B, C)
Patient lies supine with a cushion or folded towel under the upper thoracic area so that, unless supported by the practitioner�s contralateral hand, the head would fall into extension. The head is rotated contralaterally (away from the side to be treated). There are three positions of rotation required:
Full contralateral rotation of the head/neck produces involvement of the more posterior fibres of the scalenes
A contralateral 45� rotation of the head/neck involves the middle fibres
A position of only slight contralateral rotation involves the more anterior fibres.
The practitioner�s free hand is placed on the side of the patient�s head to restrain the isometric contraction which will be used to release the scalenes. The patient�s head is in one of the above degrees of rotation, supported by the practitioner�s contralateral hand.
Figure 4.34A MET for scalenus posticus. On stretching, following the isometric contraction, the neck is allowed to move into slight extension while a mild stretch is introduced by the contact hand which rests on the second rib, below the lateral aspect of the clavicle.
Figure 4.34B MET treatment for the middle fibres of scalenes. The hand placement (thenar or hypothenar eminence of relaxed hand) is on the 2nd rib below the centre of the clavicle.
Figure 4.34C MET treatment of the anterior fibres of the scalenes; hand placement is on the sternum
The patient is instructed to try to lift the forehead a fraction and to attempt to turn the head towards the affected side, with appropriate breathing cooperation, while resistance is applied by the practitioner�s hand to prevent both movements (�breathe in and hold your breath as you �lift and turn�, and hold this for 7�10 seconds�). Both the effort and, the counter-pressure should be modest and painless at all times.
After a 7�10 second contraction, the head is placed into extension and one hand remains on it to prevent movement during the scalene stretch.
The patient�s contralateral hand is placed (palm down) just inferior to the lateral end of the clavicle on the affected side (for full rotation of the head, posterior scalenes). The practitioner�s hand which was acting to produce resistance to the isometric contraction is now placed onto the dorsum of the patient�s �cushion� hand.
As the patient slowly exhales, the practitioner�s contact hand, resting on the patient�s hand, which is itself resting on the 2nd rib and upper thorax, pushes obliquely away and towards the foot on that same side, following the rib movement into its exhalation position, so stretching the attached musculature and fascia. This stretch is held for at least 20 seconds after each isometric contraction. The process is then repeated at least once more.
The head is rotated 45� contralaterally and the �cushion� hand contact, which applies the stretch of the middle scalenes, is placed just inferior to the middle aspect of the clavicle. When the head is in the almost upright facing position for the anterior scalene stretch, the �cushion� hand contact is on the upper sternum itself.
In all other ways the methodology is as described for the first position above.
NOTE: It is important not to allow heroic degrees of neck extension during any phase of this treatment. There should be some extension, but it should be appropriate to the age and condition of the individual.
A degree of eye movement can assist scalene treatment and may be used as an alternative to the �lift and turn� muscular effort described above. If the patient makes the eyes look caudally (towards the feet) and towards the affected side during the isometric contraction, she will increase the degree of contraction in the muscles. If during the resting phase, when stretch is being introduced, she looks away from the treated side, with eyes looking towards the top of the head, this will enhance the stretch of the muscle.
This whole procedure should be performed bilaterally several times in each of the three head positions. Scalene stretches, with all their variable positions, clearly also influence many of the anterior neck structures.
Dr. Alex Jimenez offers an additional assessment and treatment of the hip flexors as a part of a referenced clinical application of neuromuscular techniques by Leon Chaitow and Judith Walker DeLany. The scope of our information is limited to chiropractic and spinal injuries and conditions. To discuss the subject matter, please feel free to ask Dr. Jimenez or contact us at 915-850-0900 .
By Dr. Alex Jimenez
Additional Topics: Wellness
Overall health and wellness are essential towards maintaining the proper mental and physical balance in the body. From eating a balanced nutrition as well as exercising and participating in physical activities, to sleeping a healthy amount of time on a regular basis, following the best health and wellness tips can ultimately help maintain overall well-being. Eating plenty of fruits and vegetables can go a long way towards helping people become healthy.
The hips joints join the legs to the trunk of the body, and are formed by the femurs and pelvic bones. The hips are ball-and-socket type joints, where the femoral head (ball) fits into the cup-shaped acetabulum (socket) of the pelvis (Figure 1). When compared to the shoulder, which is also a ball-and-socket joint, the acetabulum is a deeper socket, and encompasses a greater area of the ball, or femoral head. This accommodation is necessary to provide stability for the hip, as it is a major weight-bearing joint, and one of the largest joints in the body. When not weight-bearing, the ball and socket of the hip joint are not perfectly fitted. However, as the hip joint bears more weight, the surface area contact increases, and the joint becomes more stable. When in a standing position, the body�s center of gravity passes through the center of the acetabula. While walking, weight-bearing stresses on the hips can be five times a person�s body weight. Healthy hips can support your weight and allow for pain-free movement. Hip injuries or disease can cause changes that affect your gait, as well as changes that affect the ability of the hips to distribute weight bearing. Abnormal stress is then placed on the joints that are above and below the hips.
The three fused hips or innominate bones that form the acetabulum include the ilium, pubis, and ischium. The ilium forms the superior aspect, the pubis forms the inferior and anterior aspect, and the ischium forms the inferior and posterior aspect. The depth of the acetabulum socket is further increased by the attached fibrocartilaginous labrum (Figure 2). In addition to providing stability to the hip joint, the labrum allows flexibility and motion. Hip joint stability can be hampered by injuries resulting from playing sports, running, overuse, or falling, as well as by disease or tumor. MRI of the hips may be ordered to assess the joint(s) for internal derangement, fracture, or degenerative joint disease. A blow to the hip joint or a fall can result in dislocation of the hip, or a hip fracture. Osteoporosis or low bone density can also lead to hip fractures. Successful prevention and/or treatment of osteoporosis may be achieved through nutrition (adequate amounts of calcium, vitamin D and phosphorus), exercise, safety measures, and medications.
Articular cartilage covers the femoral head and the acetabulum (Figure 3). This cartilage is thin but tough, flexible, smooth and slippery, with a rubbery consistency. It absorbs shock, and allows the bones to move against each other easily and without pain. It is kept lubricated by synovial fluid, which is made in the synovial membrane (joint lining). Synovial fluid is both viscous and sticky. This fluid is what allows us to flex our joints under great pressure without wear. The articular cartilage of the hip is typically about � inch thick, except in the posterior aspect of the hip socket (Figure 4). Here, the cartilage is thicker, as this area absorbs most of the force during walking, running, and jumping. MRI of the hip joint can detect problems involving both the articular cartilage and the fibrocartilaginous ring, or labrum. Cartilage has minimal blood vessels, so it is not good at repairing itself. Fraying, fissuring, and other abnormalities or defects of the cartilage can lead to arthritis in the hip joint. Contrast can be directly injected in the hip joint for a detailed look at the cartilage and labrum.
The femurs are the longest bones in the body, with large round heads that rotate and glide within the acetabula of the pelvis. The femoral head is particularly subject to pathologic changes if there is any significant alteration of blood supply (avascular necrosis). The femoral neck connects the head of the femur to the shaft. The neck ends at the greater and lesser trochanters, which are sites of muscle and tendon attachments. A disease characterized by an inadequate blood supply to the femoral head is Legg-Calve-Perthes disease, also known as LCP or simply Perthes disease. This is a degenerative disease of the hip joint that affects children, most commonly seen in boys ages two through twelve. One of the growth plates of the femoral head, the capital femoral epiphysis, is inside the joint capsule of the hip. Blood vessels that feed this epiphysis run along the side of the femoral neck, and are in danger of being torn or �pinched off� if the growth plate is damaged. This can result in a loss of blood supply to the epiphysis, leading to a deformity of the femoral head (Figure 5). The femoral head may become unstable and break easily, which can lead to incorrect healing and deformities of the entire hip joint (Figure 6). Treatment of Perthes disease is centered on the goal of returning the femoral head to a normal shape. Surgical and non-surgical treatments are used, based on the idea of �containment�- holding the femoral head in the acetabulum as much as possible, while still allowing motion of the hip joint for cartilage nutrition and healthy growth of the joint.
High level athletes and active individuals may be susceptible to a hip condition known as Femoro-Acetabular Impingement, or FAI. FAI is characterized by excessive friction in the hip joint. The femoral head and acetabulum rub abnormally, and can create damage to the articular or labral cartilage. FAI is also associated with labral tears, early hip arthritis, hyperlaxity and low back pain. FAI generally occurs in two forms: Cam and Pincer. The Cam form results in abnormal contact between the femoral head and the socket of the hip because the femoral head and neck relationship is aspherical (Figure 7). Males and those involved in significant contact sports typically display Cam impingement. Pincer impingement occurs when the acetabulum covers too much of the femoral head, resulting in the labral cartilage being pinched between the rim of the socket and the anterior femoral head-neck junction (Figure 8). Pincer impingement may be more common in women. Typically, these two forms exist together, and are labeled as �mixed impingement� (Figure 9).
Ewing�s sarcoma is a malignant bone tumor that may affect the pelvis and/or femur, thereby also affecting the stability of the hips. Like Perthes disease, Ewing�s sarcoma is more common in males, typically presenting in childhood or early adulthood. MRI is routinely used in the work-up of these malignant tumors to show bony and soft tissue extent of the tumor, and its relation to nearby anatomic structures (Figure 10). Contrast may be used to help determine the amount of necrosis within the tumor, which aids in determining the response to treatment before surgery.
Figure 10. MRI demonstrating Ewing�s sarcoma.
Ligaments Of The Hips
Hip stability is further increased by three strong ligaments that encompass the hip joint and form the joint capsule. These ligaments connect the femoral head to the acetabulum, with names suggestive of the bones they connect. They include the pubofemoral and iliofemoral ligaments anteriorly, and the ischiofemoral ligament posteriorly (Figure 11). The iliofemoral ligament is the strongest ligament in the body. However, sports and overuse can still result in sprains of these sturdy ligaments of the joint capsules of the hips. A smaller ligament, the ligamentum teres, is an intracapsular ligament that connects the tip of the femoral head to the acetabulum (Figure 12). A small artery within this ligament brings some of the blood supply to the femoral head. Damage to the ligamentum teres, and its enclosed artery, can result in avascular necrosis.
Muscles & Tendons Of The Hips
The muscles of the thigh and lower back work together to keep the hip stable, in alignment, and able to move. The hip gains stability because the hip muscles do not attach right at the joint. Hip muscles allow the movements of flexion, extension, abduction, adduction, and medial and lateral rotation. To better understand the functions of the muscles surrounding the hip, they can be divided into groups based on their locations- anterior, posterior, and medial.
The anterior thigh muscles are the main hip flexors, and are located anterior to the hip joint. Seventy percent of the thigh�s muscle mass is made up of the quadriceps femoris muscle, so named because it arises from four muscle heads- the rectus femoris, vastus medialis, vastus intermedius, and vastus lateralis (Figures 13, 14). The rectus femoris is the only one of the �quad� muscles to cross the hip joint. The sartorius muscle is found anterior to the quadriceps, and also serves as an abductor and lateral rotator of the hip. The most powerful of the anterior thigh hip flexors is the iliopsoas, which originates in the low back and pelvis and attaches at the lesser trochanter.
Posterior hip muscles include those of both the thigh and gluteal regions. The posterior thigh muscles are also known as the hamstrings- semimembranosus, semitendinosus, and biceps femoris (Figure 15). These muscles originate at the inferior pelvis, and are the extensors for the hip. They are active in normal walking motions. When the hamstrings are �tight�, they limit hip flexion when the knee joint is extended (bending forward from the waist with knees straight), and can limit lumbar movement, leading to back pain. The gluteal muscles include the gluteus maximus, medius, and minimus, six deep muscles that serve as lateral rotators, and the tensor fasciae latae. The three gluteals and the anterior sartorius muscle are all involved in abduction. The gluteus maximus is the main hip extensor, and is the most superficial of the gluteal muscles. It is involved in running and walking uphill, and assists with normal tone of the iliotibial band, which lies lateral to it. The gluteus medius and minimus both insert at the greater trochanter of the femur. The minimus is the deepest of the three gluteal muscles. Anterior to the gluteus minimus is the tensor fasciae latae muscle. It is a flexor and medial rotator of the hip, originating from the anterior superior iliac spine (ASIS) and inserting on the iliotibial band. The term �tensor fasciae latae� defines this muscle�s job- �muscle that stretches the band on the side�. This muscle helps the iliopsoas, gluteus medius, and gluteus minimus muscles during flexion, abduction and medial rotation of the thigh by making the iliotibial band taut, thereby steadying the trunk and stabilizing the hip (Figure 16). The iliotibial band or tract is not a muscle, but a thickened, fibrous band of deep fascia, or connective tissue. It is found at the lateral aspect of the thigh, and runs from the ilium to the tibia. It encloses the muscles and helps with lateral stabilization of the knee joint, as well as helping to maintain both hip and knee extension. Tightening of the iliotibial (IT) band typically causes more problems at the knee as opposed to the hip, but hip pain can result from the IT band rubbing as it passes over the greater trochanter.
The medial thigh (groin) muscles include five muscles of adduction, and one lateral rotator (Figures 17, 18). The lone lateral rotator is the obturator externus, which covers the external surface of the obturator foramen in the deep upper medial thigh. The adductors include the gracilis, the pectineus, and the adductor brevis, longus and magnus. The gracilis is the longest adductor, extending from the medial inferior aspect of the pubic bone, to the medial aspect of the tibia. The adductor magnus is the most massive of the medial muscles of the thigh.
The tendons and muscles of the hips are very powerful and create great forces, making them prone to inflammation and irritation. Tendonitis of the hip can result from repetitive movements involving the soft tissues surrounding the hip joint. Overuse of the hip joint in fitness workouts can lead to tendonitis. Tendons lose their elasticity as we age, resulting in swelling and irritation when the tendons are no longer �gliding� on their normal paths. Iliopsoas tendonitis plays a major role in snapping hip syndrome, or dancer�s hip. A snapping sensation when the hip is flexed and extended may be accompanied by an audible snapping or popping noise, as well as pain. This can be both an extra-articular and an intra-articular occurrence. Extra-articular snapping is often found in those patients with a leg length difference (the longer leg is symptomatic), those with tightness of the iliotibial band on the involved side, and those with weak hip abductors and external rotators. Lateral extra-articular snapping can be caused by the iliotibial band, tensor fascia latae or gluteus medius tendon as they slide back and forth across the greater trochanter (Figure 19). If any of these connective tissue bands thickens, they can �catch� on the greater trochanter during the motion of hip extension, thereby creating the �snapping� sensation and sound. Medial extra-articular snapping, which is less common, can occur when the iliopsoas tendon catches on the anterior inferior iliac spine, lesser trochanter, or iliopectineal ridge during hip extension. Intra-articular snapping hip syndrome is similar in many ways to the extra-articular type, but often involves an underlying mechanical problem in the lower extremity, and more intense pain. Intra-articular snapping may be indicative of a torn acetabular labrum, recurrent hip subluxation, a tear of the ligamentum teres, loose bodies, articular cartilage damage, or synovial chondromatosis (cartilage formations in the synovial membrane of the joint). Snapping hip syndrome is usually found in those ages 15-40, often in those in training for the military. It can also affect athletes, especially those involved in dance, gymnastics, soccer, and track and field. These athletes will all be performing repeated hip flexions, which can lead to tendonitis in the hip area. The repetitive motions of those involved in weightlifting and running generally lead to a thickening of the tendons in the hip region, rather than snapping hip syndrome. Prevention, or at least a lessening, of this syndrome may be found with increased stretching of the iliopsosas muscle or the iliotibial band. Surgery is usually not required, unless intra-articular pathology is present.
Figure 19. Hip muscles.
Tendon or muscle strains can occur suddenly, as in sports injuries, or they can develop over time, with symptoms including pain, swelling, muscle spasms, and difficulty moving certain muscles. MRI can be used to detect tendon and muscle tears and strains, as well as bone tumors and infection. MRI has shown good accuracy for the diagnosis of tears of the gluteus medius and gluteus minimus tendons, which are both abductor tendons of the hip. An association was found between these tears and areas of high signal intensity superior or lateral to the greater trochanter on T2-weighted images, tendon elongation in the gluteus medius, and tendon discontinuity (Figure 20). STIR and fat-suppressed T2-weighted coronal images are very sensitive for detection of areas of high signal intensity superior to the greater trochanter. Coronal T1-weighted images demonstrate tendon elongation in the gluteus medius (Figure 21). Axial images may prove superior for localizing involvement to individual abductor tendons and confirming tendon discontinuity (Figure 22). Tears of the abductor tendons may be the leading cause of greater trochanteric pain syndrome.
Figure 20. Sag. T2 shows high signal intensity superior to greater trochanter (gt) corresponding to swollen bursa (*).
Figure 21. Coronal STIR shows high signal intensity superior to greater trochanter in bursa (*) between gluteus medius (me) and gluteus minimus (mi) tendons.
Figure 22. Axial T2 shows high signal intensity corresponding to fluid replacing distal rt. gluteus medius tendon (black arrow); normal left tendon (white arrow).
Nerves Of The Hips
The nerves of the hip supply the various muscles in the hip area. The major nerves include the femoral, obturator, and lateral femoral cutaneous nerves anteriorly, and the large sciatic nerve posteriorly (Figure 23). The femoral nerve innervates the quadriceps femoris and sartorius, and is the sensory nerve to the anterior thigh. Trauma to this nerve usually occurs in the pelvis, as it passes through or near the psoas muscle. The obturator nerve passes along the lateral pelvic wall and through the obturator foramen, then splits into branches that supply the adductor muscle group. This nerve can also be subject to trauma in the pelvis due to its passage through the obturator foramen. The lateral femoral cutaneous nerve is a sensory nerve that travels along the anterolateral aspect of the thigh. It supplies sensation to the skin surface of the thigh. This is the single nerve involved in a painful condition called meralgia paresthetica, which is characterized by tingling, numbness, and burning pain in the outer part of the thigh. Meralgia paresthetica results from focal entrapment of the lateral femoral cutaneous nerve as it passes through the tunnel formed by the lateral attachment of the inguinal ligament and the ASIS. The posterior sciatic nerve passes deep to the gluteus maximus into the posterior thigh, where it innervates the hamstring muscles, on its way down to the lower leg and foot. The sciatic nerve is approximately as big around as the thumb, and is the largest single nerve in the human body. It can be injured in cases of posterior hip dislocation. Pressure on this nerve can cause nerve pain, numbness, tingling and weakness (sciatica symptoms) in the buttocks, leg, or foot, depending on the site of origin of the sciatic nerve compression.
Figure 23. Anterior and posterior views of the nerves of the hip.
Arteries & Veins Of The Hips
The arterial blood vessels that supply the hips are branches of the internal and external iliacs. The internal iliac artery gives off the superior and inferior gluteals, and the obturator artery. The inferior gluteal flows to the posterior aspect of the hip joint and proximal femur, where it joins a branch of the femoral artery. The obturator artery runs through the obturator foramen, and sends its acetabular branch to the ligamentum teres as part of the blood supply to the femoral head. The external iliac becomes the femoral artery, which has numerous branches that supply the hip and proximal femur. The largest femoral branch is the profunda femoris, which branches superiorly into the medial and lateral circumflex femorals (Figure 24). The circumflex femorals and the inferior gluteal artery contribute to the anastomoses to supply the femoral head, femoral neck, and the hip joint. The medial circumflex also has an acetabular branch to the ligamentum teres. Congenital anomalies in the hip anastomoses, degenerative processes, and trauma can all compromise the blood supply to the hip joint area.
Figure 24. Anterior and posterior views of the arteries of the hip.
Venous flow in the hip and proximal femur typically follows the arterial flow, including the same names for the vessels. The deep veins of the hip and thigh can be the origination of a deep vein thrombosis, which can result in a pulmonary embolus. This can be caused by immobility after hip surgery, sitting in cars or airplanes for extended trips, being overweight, or slow or low blood flow. These blood clots can break off, travel through the larger veins of the thigh and hip, continue through the heart, and become lodged in the smaller vessels of the lung. MRI is being used more frequently to diagnose this very serious condition.
Bursae Of The Hips
The hip joint is surrounded by bursae, similar to the shoulder. These fluid-filled sacs are lined with a synovial membrane, which produces synovial fluid. Their function is to lessen the friction between tendon and bone, ligament and bone, tendons and ligaments, and between muscles. There may be as many as 20 bursae around the hip. If they become infected or inflamed, the result is a painful condition called bursitis. Common hip bursae that may become inflamed include the greater trochanteric bursa, the iliopsoas bursa, and the ischial bursa (Figure 25). The greater trochanteric bursa is sandwiched between the greater trochanter of the femur, and the muscles and tendons that cross over it. If this bursal sac becomes inflamed, patients experience pain with every step they take, as each step requires the tendon to move over the femur at the hip joint. A tight iliotibial band can also cause irritation of the greater trochanteric bursa. Iliopsoas bursitis can result from irritation of the bursa found between the hip joint and the iliopsoas muscle that passes in front of it. Another common site for bursitis is the ischial bursa, which acts as a lubricating pad between tendons and the ischial tuberosity, which is the bony prominence of the pelvis that you sit on. The ischial bursa acts to prevent destruction of the tendons as they move over the ischial tuberosity. Prolonged sitting can cause ischial bursitis. Inflammation around the ischial tuberosity can irritate the sciatic nerve, and trigger symptoms similar to sciatica. Hip bursitis is seen in runners and athletes in sports that involve excessive running (soccer, football, etc.). It can also be caused by an injury (traumatic bursitis), and is seen in post-op hip replacement and hip surgery patients. Treatment for hip bursitis typically includes rest, anti-inflammatory medications, and ice. It may become necessary to aspirate the bursa, which can be combined with a cortisone injection. MRI may be needed if the diagnosis is unclear, or if the problem does not resolve with normal treatments.
Figure 25. Bursae of the hip.
Axial Scans
When positioning unilateral axial slices for the hip, a coronal image can be used to ensure inclusion of all pertinent anatomy. The slices should extend superiorly to include the entire femoral head and acetabulum, and inferiorly to include anatomy below the lesser trochanter. The slices should be aligned perpendicular to the shaft of the femur, as seen in the coronal image in Figure 39.
Figure 39. Axial slice setup using sagittal and coronal images.
For bilateral axial hip slice setup, parameters may have to be altered to maintain adequate resolution with the larger FOV that is required (Figure 40). The slice group may require angulation to maintain alignment of the femoral heads on the resultant images.
Figure 40. Bilateral axial slice setup using a coronal image.
Coronal Scans
Coronal slices of the hip should cover the area from the posterior margin to the anterior margin of the femoral head. The area from the proximal margin of the femoral shaft to the greater sciatic notch should be included in the image (Figure 41). Slices may be angled so that they are parallel to the femoral neck. Thinner slices may be requested for coronal scanning.
Figure 41. Coronal slice setup using axial and sagittal images.
Sagittal Scans
Sagittal slices of the hip should extend past the greater trochanter laterally, and through the acetabulum medially. The slices should be aligned along the long axis of the femur, and perpendicular to the coronal slices, as seen in the coronal image in Figure 42. Two different slice groups will be necessary when performing bilateral sagittal scans.
Figure 42. Sagittal slice setup using coronal and axial images.
Hips Arthrography
MR hip arthrography is often times referred to as the gold standard for assessment of the labrum of the hip. The most clinically significant abnormal findings that result from hip arthrography are labral detachments and tears. Detachment of the labrum, which is more common than a labral tear, can be diagnosed from the appearance of the injected contrast at the acetabular-labral interface (Figure 43). A labral tear can result in injected contrast appearing within the substance of the labrum (Figure 44). Contrast injection is necessary to differentiate torn or detached labra from other pathologic conditions, which may have separate signal intensities. The sensitivity and accuracy for the diagnosis of labral tears and detachment with MR arthrography vs. nonarthrographic MR is 90%. Hip arthrography with MR can also depict intrarticular loose bodies, osteochondral abnormalities, and abnormalities of soft-tissue structures.
Hip arthrography can be performed under fluoro in the x-ray dept., with the patient being moved to the MRI dept. for further imaging, or the entire procedure can be performed in the MRI suite, if MR compatible supplies are available for interventional techniques. The patient should be securely positioned with the hips in internal rotation.
T1-weighted imaging is performed post-contrast to visualize the high signal of the intraarticular contrast. T1 gradient echo sequences offer the benefits of thin sections, elimination of partial volume averaging, and increased detection of small tears. Fatsat sequences are helpful in increasing the contrast between the injected contrast and the adjacent soft tissue. STIR or fatsat T2 sequences performed in the coronal plane may help to detect unsuspected pathologic conditions in the soft tissue and adjacent osseous structures.
Post-contrast axial oblique images have been shown to optimize the detection of the most common sports-related acetabular labral tears, which are anterior or anterosuperior in location. Using a mid-coronal localizer, the axial oblique slices should be prescribed parallel to the long axis of the femoral neck.
Figure 43. Labral detachment as seen in a fat-suppressed T1-wtd. sag. image; arrowheads indicate involvement of anterior and anterosuperior labrum.
Figure 44. Labral tear as seen in a T1-wtd. image; arrowheads indicate enlarged labrum; short arrow indicates linear intralabral collection of contrast material; long arrow indicates communication between the joint and the iliopsoas bursa.
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