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are referred to generically as tendinitis, in the vast majority of cases, tendinitis is actually an incorrect and outdated term.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
Contents
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.
Have you ever experienced low back pain? If you haven’t already, there’s a high probability you will present at least one case of back pain sometime during your lifetime. Back pain is one of the most prevalent spine health issues reported among the population of the United States, affecting up to 80 percent of Americans at some point in their lives. Back pain is not a specific disease, rather it is a symptom which may develop as a result of a variety of injuries and/or conditions.�Although most cases typically resolve on their own, the effective treatment of acute low back pain is essential towards preventing chronic low back pain.
Chiropractors and physical therapists frequently utilize a similar series of treatment methods, such as spinal adjustments and manual manipulations as well as massage and physical therapy, to help treat symptoms of back and low back pain. Many healthcare professionals, however, have started using the McKenzie method to manage acute back pain. The purpose of the following article is to educate patients on the effectiveness of the McKenzie method for acute non-specific low back pain.
Contents
The McKenzie Method for the Management of Acute Non-Specific Low Back Pain: Design of a Randomised Controlled Trial
Abstract
Background
Low back pain (LBP) is a major health problem. Effective treatment of acute LBP is important because it prevents patients from developing chronic LBP, the stage of LBP that requires costly and more complex treatment.
Physiotherapists commonly use a system of diagnosis and exercise prescription called the McKenzie Method to manage patients with LBP. However, there is insufficient evidence to support the use of the McKenzie Method for these patients. We have designed a randomised controlled trial to evaluate whether the addition of the McKenzie Method to general practitioner care results in better outcomes than general practitioner care alone for patients with acute LBP.
Methods/Design
This paper describes the protocol for a trial examining the effects of the McKenzie Method in the treatment of acute non-specific LBP. One hundred and forty eight participants who present to general medical practitioners with a new episode of acute non-specific LBP will be randomised to receive general practitioner care or general practitioner care plus a program of care based on the McKenzie Method. The primary outcomes are average pain during week 1, pain at week 1 and 3 and global perceived effect at week 3.
Discussion
This trial will provide the first rigorous test of the effectiveness of the McKenzie Method for acute non-specific LBP.
Background
In Australia, low back pain (LBP) is the most frequently seen musculoskeletal condition in general practice and the seventh most frequent reason for consulting a physician[1,2]. According to the Australian National Health Survey, 21% of Australians reported back pain in 2001; additionally, the Australian Bureau of Statistic’s 1998 Survey of Disability, Ageing and Carers estimated that over one million Australians suffer from some form of disability associated with back problems[1].
LBP poses an enormous economic burden to society in countries such as the USA, UK and The Netherlands[3]. In the largest state in Australia, New South Wales, back injuries account for 30% of the cost of workplace injuries, with a gross incurred cost of $229 million in 2002/03[4]. It is expected that most people with an acute episode of LBP will improve rapidly, but a proportion of patients will develop persistent lower levels of pain and disability[5,6]. Those patients with chronic complaints are responsible for most of the costs[6]. Effective treatment of acute LBP is important because it prevents patients from developing chronic LBP, the stage of LBP that requires costly and more complex treatment.
There is a growing concern about effectiveness of treatments for LBP, as reflected in the large number of systematic reviews published in the last 5 years addressing this issue. [7-12]. Despite the large amount of evidence regarding LBP management, a definitive conclusion on which is the most appropriate intervention is not yet available. A comparison of 11 international clinical practice guidelines for the management of LBP showed that the provision of advice and information, together with analgesics and NSAIDs, is the approach consistently recommended for patients with an acute episode[13]. Most guidelines do not recommend specific exercises for acute LBP because trials to date have concluded that it is not more effective than other active treatments, or than inactive or placebo treatments[8]. However, some authors have suggested that the negative results observed in trials of exercises are a consequence of applying the same exercise therapy to heterogeneous groups of patients. [14-16]. This hypothesis has some support from a recent high-quality randomised trial in which treatment based on a diagnostic classification system led to larger reductions in disability and promoted faster return to work in patients with acute LBP than the therapy recommended by the clinical guidelines[17].
In 1981, McKenzie proposed a classification system and a classification-based treatment for LBP labelled Mechanical Diagnosis and Treatment (MDT), or simply McKenzie Method[18]. Of the large number of classification schemes developed in the last 20 years [19-26], the McKenzie Method has the greatest empirical support (e.g. validity, reliability and generalisability) among the systems based on clinical features[27] and therefore seems to be the most promising classification system for implementation in clinical practice.
Physiotherapists commonly adopt the McKenzie Method for treating patients with LBP[28,29]. A survey of 293 physiotherapists in 1994 found that 85% of them perceived the McKenzie Method as moderately to very effective[28]. Nevertheless, a recent systematic review concluded that there is insufficient evidence to evaluate the effectiveness of the McKenzie Method for patients with LBP [30]. A critical concern is that most trials to date have not implemented the McKenzie Method appropriately. The most common flaw is that all trial participants are given the same intervention regardless of classification, an approach contradictory to the principles of McKenzie therapy.
The primary aim of this trial is to evaluate whether the addition of the McKenzie Method to general practitioner (GP) care results in better outcomes than GP care alone for patients with acute non-specific LBP when effect is measured in terms pain, disability, global perceived effect, and persistent symptoms.
Methods
The University of Sydney Human Research Ethics Committee granted approval for this study.
Study Sample
One hundred and forty eight participants with a new episode of acute non-specific LBP who present to GPs will be recruited for the study. A new episode of LBP will be defined as an episode of pain lasting longer than 24 hours, preceded by a period of at least one month without LBP and in which the patient did not consult a health care practitioner[31]. Participants will be screened for eligibility at their first appointment with the GP according to the inclusion and exclusion criteria.
Inclusion Criteria
To be eligible for inclusion, participants must have pain extending in an area between the twelfth rib and buttock crease (this may or may not be accompanied by leg pain); pain of at least 24 hours duration; pain of less than 6 weeks duration; and they need to be eligible for referral to private physiotherapy practice within 48 hours.
Exclusion Criteria
Participants will be excluded if they have one of the following conditions: nerve root compromise (defined as 2 positive tests out of sensation, power and reflexes for the same spinal nerve root); known or suspected serious spinal pathology; spinal surgery within the preceding 6 months; pregnancy; severe cardiovascular or metabolic disease; or inability to read and understand English.
Recruiting GPs will record the number of patients who are invited to participate, the number who decline to participate, and the number of screened patients who are ineligible and their reasons for declining participation or ineligibility. Written consent will be obtained for each participant.
Subjects who volunteer to participate and satisfy the eligibility criteria will receive baseline treatment and then be randomly allocated to one of the study groups. To ensure equal-sized treatment groups, random permuted blocks of 4�8 participants will be used[32]. Randomisation will be stratified by Workcover compensation status. The stratified random allocation schedule will be generated by a person not otherwise involved in recruitment, assessment or treatment of subjects and the randomisation sequence will be placed in sequentially numbered, sealed envelopes. The flow of participants through the study is detailed in Figure ?1.
Figure 1: Flow of participants through the study. Legend: GP � General practitioner; NRS � Numeric pain rating scale; PSFS � Patient-specific functional scale; RMQ � Roland-Morris questionnaire; GPE � Global perceived effect; LBP � Low back pain.
Dr. Alex Jimenez’s Insight
In the management of low back pain, the attitudes, beliefs and treatment preferences of chiropractors, as well as that of physical therapists, can determine the most effective outcome measures in the care of patients with different types of spinal health issues. According to the following evidence-based research studies, the McKenzie method has been deemed to be one of the most useful treatment approaches for managing symptoms in patients with back and low back pain. Exercise and physical activity is also one of the most common treatment preferences for improving an individual’s strength, mobility and flexibility. Every healthcare professional varies in respect to their specific treatment preferences. These variations emphasize the need to identify the most effective treatment approach to guarantee proper treatment of LBP.
Outcome Measures
The McKenzie protocol is thought to promote rapid symptom improvement in patients with LBP[33,34] and this is one of the reasons that therapists choose this therapy. Therefore it is important to focus assessment on short-term outcomes. The primary outcomes will be:
Usual pain intensity over last 24 hours recorded each morning in a pain diary over the first week. Pain will be measured on a 0�10 numerical rating scale (NRS). The unit of analysis will be the mean of the 7 measures[35];
Usual pain intensity over last 24 hours (0�10 NRS) recorded at 1 and 3 weeks[35];
Global perceived effect (0�10 GPE) recorded at 3 weeks.
The secondary outcomes will be:
Global perceived effect (0�10 GPE) recorded at 1 week;
Patient-generated measure of disability (Patient-Specific Functional Scale; PSFS) recorded at 1 and 3 weeks[36];
Condition-specific measure of disability (Roland Morris Questionnaire; RMQ) recorded at 1 and 3 weeks[37];
Number of patients reporting persistent back pain at 3 months.
Following the screening consultation in which the inclusion and exclusion criteria are assessed, the GP will supervise the baseline measurement of pain. All patients will then receive an assessment booklet and a pre-paid envelope in which all other self-assessed outcome measures are to be recorded and sealed. One member of the research team will contact patients by telephone within 24 hours of the consultation with the GP in order to give explanations regarding the appropriate form of filling in the assessment booklet. At this time, other baseline outcomes will be recorded and then the patient will be randomised to study groups. The patient will be advised to keep the booklet at home, to seal it into the pre-paid envelope after the final assessment and mail the sealed envelope to the research team. To ensure the proper use of the assessment booklet and to avoid loss of data due to non-returned booklets, a blinded assessor will contact all patients by telephone 9 and 22 days after the consultation with the GP to collect patient’s answers from the 1st week and 3rd week assessments, respectively.
The procedure for obtaining outcome data will be followed for all participants, regardless of compliance with trial protocols. At 3 months, data regarding the presence of persistent (chronic) symptoms will be collected by telephone. Participants will be asked to answer the following yes-no question: “During the past 3 months have you ever been completely free of low back pain? By this I mean no low back pain at all and would this pain-free period have lasted for a whole month”. Those answering no will be considered to have persistent LBP. Information on additional treatment and the direct costs with low back pain management will also be collected at 3 months.
A secondary analysis will be performed on predictors of response to McKenzie treatment and prediction of chronicity. This will involve the measurement of participants’ expectation about the helpfulness of both treatments under investigation as well as information on the occurrence of the centralisation phenomenon. Expectation will be recorded prior to randomisation according to the procedures described by Kalauokalani et al[38].
Treatments
All participants will receive GP care as advocated by the NHMRC guideline for the management of acute musculoskeletal pain[2]. Guideline-based GP care consists of providing information on a favourable prognosis of acute LBP and advising patients to stay active, together with the prescription of paracetamol. Patients randomised to the experimental group will be referred to physiotherapy to receive the McKenzie Method. A research assistant not involved in the assessment or treatment of subjects will be responsible for the randomisation process and will contact therapists and patients to arrange the first physiotherapy session. The McKenzie treatment will be delivered by credentialed physiotherapists who will follow the treatment principles described in McKenzie’s text book[18]. All therapists will have completed the four basic courses taught by the McKenzie Institute International. To ensure the appropriate implementation of the McKenzie’s classification algorithm, a training session with a member of McKenzie’s educational program will be conducted prior to the commencement of the study. The treatment frequency will be at the discretion of the therapist with a maximum of 7 sessions over 3 weeks. We chose to restrict the McKenzie treatment to a maximum of 7 sessions based on the study of Werneke and colleagues[39], which concluded that further reductions in pain and function are not expected if favourable changes in pain location are not present until the seventh treatment visit. Treatment procedures from the McKenzie Method are summarised in the Appendix.
Participants randomised to the control group will continue their GP care as usual. All participants regardless of intervention group will be advised not to seek other treatments for their low back pain during the treatment period. Physiotherapists will be asked to withhold co-interventions during the course of the trial.
Several mechanisms will be used to ensure that the trial protocol is applied consistently. Protocol manuals will be developed and all involved researchers (GPs, physiotherapists, assessor, and statistician) will be trained to ensure that screening, assessment, random allocation and treatment procedures are conducted according to the protocol. A random sample of treatment sessions will be audited to check that treatment is being administered according to the protocol.
Data Analysis
Power was calculated based on the primary outcome measures (pain intensity and global perceived effect). A sample size of 148 participants will provide 80% power to detect a difference of 1 unit (15%) on a 0�10 pain scale (SD = 2.0) between the experimental and control groups, assuming alpha of 0.05. This allows for loss to follow-up of 15%. This sample size also allows the detection of a difference of 1.2 units (12%) on a 0�10 global perceived effect scale (SD = 2.4).
Data will be analysed by a research member blinded to group status. The primary analysis will be by intention-to-treat. In order to estimate treatment effects, between-group mean differences (95%CI) will be calculated for all outcome measures. In the primary analysis these will be calculated using linear models that include baseline values of outcome variables as covariates to maximise precision.
Discussion
We have presented the rationale and design of an RCT evaluating the effects of the McKenzie Method in the treatment of acute non-specific LBP. The results of this trial will be presented as soon as they are available.
Competing Interests
The author(s) declare that they have no competing interests.
Authors’ Contributions
LACM, CGM and RDH were responsible for the design of the study. HC was responsible for recruiting McKenzie therapists and she will also participate as a clinician in the trial. LACM and JMc will act as trial coordinators. All authors have read and approved the final manuscript.
Appendix
Clinical picture and treatment principles according to the McKenzie Method
This table summarises the procedures involved in the McKenzie Method (Table 1). For detailed description of all procedures and progressions, refer to McKenzie’s text book. This is particularly important for Derangement syndrome since the treatment is extremely variable and complex and the full description of procedures would not be appropriate for the purposes of this paper.
The authors thank the physiotherapists credentialed in the McKenzie Method for their participation in this project.
Managing Low Back Pain: Attitudes & Treatment Preferences of Physical Therapists & Chiropractors
Abstract
Background and Purpose:�Researchers surveyed physical therapists about their attitudes, beliefs, and treatment preferences in caring for patients with different types of low back pain problems.
Subjects and Methods: Questionnaires were mailed to all 71 therapists employed by a large health maintenance organization in western Washington and to a random sample of 331 other therapists licensed in the state of Washington.
Results: Responses were received from 293 (74%) of the therapists surveyed, and 186 of these claimed to be practicing in settings in which they treat patients who have back pain. Back pain was estimated to account for 45% of patient visits. The McKenzie method was deemed the most useful approach for managing patients with back pain, and education in body mechanics, stretching, strengthening exercises, and aerobic exercises were among the most common treatment preferences. There were significant variations among therapists in private practice, hospital-operated, and health maintenance organization settings with respect to treatment preferences, willingness to take advantage of the placebo effect, and mean number of visits for patients with back pain.
Conclusions and Discussion: These variations emphasize the need for more outcomes research to identify the most effective treatment approaches and to guide clinical practice.
In conclusion,�the effective treatment of acute low back pain is essential because it can potentially help prevent the development of chronic low back pain. A growing number of chiropractors and physical therapists, including other healthcare professionals, have utilized the McKenzie method to help manage acute non-specific low back pain in patients. According to the research study, further evidence is required to support the use of the McKenzie method for LBP, however, the outcome measures of the research study regarding the effectiveness of the McKenzie method for low back pain are promising. Information referenced from the National Center for Biotechnology Information (NCBI). The scope of our information is limited to chiropractic as well as to spinal injuries and conditions. To discuss the subject matter, please feel free to ask Dr. Jimenez or contact us at 915-850-0900 .
Curated by Dr. Alex Jimenez
Additional Topics: Sciatica
Sciatica is referred to as a collection of symptoms rather than a single type of injury or condition. The symptoms are characterized as radiating pain, numbness and tingling sensations from the sciatic nerve in the lower back, down the buttocks and thighs and through one or both legs and into the feet. Sciatica is commonly the result of irritation, inflammation or compression of the largest nerve in the human body, generally due to a herniated disc or bone spur.
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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.
Contents
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!
Organic Diet: It seems our moms were right; we are what we eat. Unfortunately in today’s marketplace, there are many valid worries about the foods we consume. Antibiotics, pesticides, and foods tainted with dangerous diseases are a top concern for many Americans. In addition, processed and genetically modified foods and artificial ingredients contribute to a number of health issues from obesity to cancer.
Our diet is one of the most important facets of maintaining overall good health for the long term. Farmer’s markets, small grocery stores, and the movement toward organic labeling shows the trend toward making healthier food choices.
If you are thinking about adding a few organic foods to your meal plan, or chucking all processed foods altogether, you are moving toward a healthier, higher performing body with fewer health issues.
Contents
Organic Diet: Five Reasons Why
#1: Fewer Chemicals
The practice of using a variety of pesticides in non-organic farming is widespread in the United States. No matter how fastidiously you wash them, foods with these toxins are harmful to your body. A recent article in The Huffington Post stated that toxic pesticides are present in 70% of the food found in grocery stores!
Many large, traditional farms aim to produce as much food as possible, as cheaply as they can. They turn to pesticides and herbicides to make the crops grow faster and last longer. It’s a sad fact, but the American public ends up paying a price anyway. An organic diet offers a respite from these chemically laden foods.
#2: Tastes Better
You may not even realize the taste you DON’T get when eating processed foods. Toxins that make them grow and keep them fresh deplete the taste dramatically.
Growing from properly maintained soil without the presence of pesticides, organic foods deliver a richer, more engaging flavor. Individuals who eat organic often eat less and are better satisfied with their meals because of the increased taste.
#3: More Nutrient Density
According to The Ideal Bite, organic foods contain up to 50% more nutrients than their non-organic counterparts. Depleted soil quality from over farming is a key reason for this situation. This means a person needs to eat less organic food to maintain the necessary dietary vitamins and minerals that ensures good health, offsetting the initial higher cost of choosing organic.
#4: Less Antibiotic Exposure
Large food manufacturing farms often choose to pump their animals full of antibiotics to reduce illness and promote rapid growth. Obviously, these make their way into the end product that we end up eating.
Too much exposure to antibiotics causes everything from early puberty in children to antibiotic resistance. If you become ill and require antibiotic medical treatment, long-term consumption of non-organic meat could literally hinder you from responding.
#5: Supports The Local Economy
In addition to building a strong body and mind, choosing organic contributes to the local community by supporting the small farmer. The small farmer is able to adopt to organic standards with less effort, and is more likely to embrace healthy soil practices and other ethical farming traits in the first place. Seek out local establishments for the widest variety of the freshest, locally grown food.
There are an assortment of reasons to choose an organic diet. In a nutshell, it is proven to offer great benefits to your long-term overall health. If you can’t commit to an entirely organic diet, substitute a few organic choices from your present food selections. Even changing small areas of your diet will provide better taste, greater nutrition, and stronger well-being.
Have more questions? We�re here for you! Simply ask our Doctor of Chiropractic during your next visit how eating organic foods can benefit you.
Good Nutrition & Chiropractic Care Contribute To Overall Well-Being
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.
Contents
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.
Low back pain is a common complaint that generally goes away on its own, however, what should a person do if their LBP becomes chronic and/or persistent? How is an individual’s quality of life affected and how does their pain intensity impact their physical capacity? Is there any type of treatment which can help improve low back pain? Many different types of treatment options can be used to safely and effectively treat low back pain. The purpose of the following research study is to determine the influence of the McKenzie method and endurance exercises on low back pain. The article demonstrates evidence-based information on the improvement of the quality of life of patients with LBP after receiving the treatment protocol mentioned below.
Contents
Influence of Mckenzie Protocol and Two Modes of Endurance Exercises on Health-Related Quality of Life of Patients with Long-Term Mechanical Low Back Pain
Abstract
Introduction
Long-term Mechanical Low-Back Pain (LMLBP) negatively impacts on patients� physical capacity and quality of life. This study investigated the relationship between Health-Related Quality of Life (HRQoL) and pain intensity, and the influence of static and dynamic back extensors� endurance exercises on HRQoL in Nigerian patients with LMLBP treated with the McKenzie Protocol (MP).
Methods
A single-blind controlled trial involving 84 patients who received treatment thrice weekly for eight weeks was conducted. Participants were assigned to the MP Group (MPG), MP plus Static Back Endurance Exercise Group (MPSBEEG) or MP plus Dynamic Endurance Exercise Group (MPDBEEG) using permuted randomization. HRQoL and pain was assessed using the Short-Form (SF-36) questionnaire and Quadruple Visual Analogue Scale respectively.
Results
Sixty seven participants aged 51.8 � 7.35 years completed the study. A total drop-out rate of 20.2% was observed in the study. Within-group comparison across weeks 0-4, 4-8 and 0-8 of the study revealed significant differences in HRQoL scores (p < 0.05). Treatment Effect Scores (TES) across the groups were significantly different (p = 0.001). MPSBEEG and MPDBEEG were comparable in TES on General Health Perception (GHP) at week 4; and GHP and Physical Functioning at week 8 respectively (p > 0.05). However, MPDEEG had significantly higher TES in the other domains of the SF-36 (p = 0.001).
Conclusion
HRQoL in patients with LMLBP decreases with pain severity. Each of MP, static and dynamic back extensors endurance exercises significantly improved HRQoL in LMLBP. However, the addition of dynamic back extensors endurance exercise to MP led to greater improvement in HRQoL.
Keywords:Mckenzie protocol, endurance exercises, quality of life, back pain
Background
Low-Back Pain (LBP) is described as the constellation of symptoms of pain or discomfort originating from impairments in the structures in the low back [1�2]. LBP is one of the most common ailments afflicting mankind [3]. It is a complicated condition which affects the physiological and psychosocial aspects of the patient [4, 5]. Epidemiological reports indicate that 70 to 85% of all people have LBP at some time in their life [1, 6]. The World Health Organization predicted that the greatest increases in LBP prevalence in the next decade will be in developing nations [7]. In line with this, a systematic review by Louw et al [8] concluded that the global burden and prevalence of LBP among Africans is rising.
It is estimated that 80-90% of patients with LBP will recover within six weeks, regardless of treatment [9]. However, 5-15% of all people that have LBP will develop long-term LBP (i.e. LBP of 12 weeks and longer) [10, 11]. The patient subgroup with long-term LBP accounts for 75-90% of the socioeconomic cost of LBP [12] and over 30% of these patients with long-term LBP seek healthcare for their back complaints. Long-term LBP significantly impacts on patients� physical [13], psychological and social functioning [14] and can affect well-being and quality of life [15]. Reduced quality of life in patients with long-term LBP is associated with poor prognosis [16], intermittent or recurrent episodes of LBP [17], disability [18] and psychosocial dysfunction [19, 20].
Assessment of Health-Related Quality of Life (HRQoL) in relation to LBP has been recommended in LBP management [21, 22]. Several HRQoL instruments have been developed to assess self-perceived general health status [21, 22]. The SF-36 Health Status Questionnaire, though a generic instrument, has been recommended in the assessment of HRQoL of patients with long-term LBP [22] and it assesses eight domains such as physical functioning, role limitations due to physical problems, bodily pain, general health perceptions, vitality, social functioning, role limitation due to emotional problems and general mental health [23, 24].
Consequent to the foregoing, treatment intervention that may help improve the HRQoL of patients with long-term LBP has been advocated. Although, physiotherapy plays an important role in the management of patients with LBP, the traditional approach based on biomedical model, which is centered on the treatment of impairments and patho-physiological variables, may not fully addressed the wider range of factors including psychosocial impairments associated with long-term LBP [25, 26]. However, long-term LBP is considered to be a multi-factorial bio-psychosocial problem which has an impact on both social life [27, 28] and quality of life [29] and thus requires a multi-dimensional approach based on a bio-psychosocial model (a model that includes physical, psychological and social elements) in its assessment and treatment [30, 31].
Based on empirical recommendations from research, recent decades have witnessed tremendous advances in preventive, pharmacological and physiotherapy management for a limited number of patients with LBP especially in developed countries. However, the improvement in health outcomes observed in most Western countries over the past few decades has not been achieved in Africa [32] and therefore, the health of Africans is of global concern [8]. Compared with Australians [33], Europeans [34] and North Americans [35], the use of exercise as medicine in Africans is poor. Exercise is the central element in the physical therapy management of patients with long-term LBP [9, 36]. Exercise often does not require expensive instruments and probably the cheapest intervention and one in which the patient has some measure of direct control [37]. Nonetheless, it remains inconclusive which exercise regimen will significantly influence the quality of life of patients with long-term LBP. The McKenzie Protocol (MP) is one of the most commonly used physical therapy interventions in long-term mechanical LBP with documented effectiveness [38�41]. However, there is a dearth of studies that have investigated the influence of the MP on HRQoL in patients with long-term mechanical LBP. Therefore, this study was intended to answer the following questions: (1). Will pain intensity significantly influence HRQoL? (2) Will static and dynamic back extensors� endurance exercises significantly influence HRQoL in Nigerian patients with long-term mechanical LBP (LMLBP) treated with the MP?
Methods
Eighty four patients with LMLBP participated in this single-blind randomized trial. The participants were consecutively recruited from the physiotherapy department, Obafemi Awolowo University (OAU) Teaching Hospitals Complex and the OAU Health Centre, Ile-Ife, Nigeria. The McKenzie Institute’s Lumbar Spine Assessment Format (MILSAF) [3] was used to determine eligibility to participate in the study. Based on the MILSAF, patients who demonstrated Directional Preference (DP) for extension only were recruited to ensure homogeneity of samples. DP is described as the posture or movement that reduces or centralizes radiating pain that emanates from the spine. Exclusion criteria were red flags indicative of serious spinal pathology with signs and symptoms of nerve root compromise (with at least two of dermatomal sensory loss, myotomal muscle weakness and reduced lower limb reflexes), individuals with any obvious spinal deformity or neurological disease; pregnancy; previous spinal surgery; previous experience of static and dynamic endurance exercise and having DP for flexion, lateral or no DP. Long-term low-back pain was defined as a history of LBP of not less than 3 months [42].
Based on the sample size table by Cohen [43] with alpha level set at 0.05, degree of freedom at 2, effect size at 0.25, and power at 80, the study found a minimum sample size of 52. However, in order to accommodate for possible attrition or loss during the study, a total of 75 patients (25 per group) was included. The participants were randomly assigned to one of three treatment groups using permuted block randomization; the McKenzie Protocol (MP) Group (MPG) (n = 29), MP plus Static Back Endurance Exercise Group (MPSBEEG) (n = 27) and MP plus Dynamic Back Endurance Exercise Group (MPDBEEG) (n = 28). Sixty seven (32 males (47.8%) and 35 females (52.2%) participants completed the eight week study. Twenty five participants completed the study in MPG, 22 in MPSBEEG and 20 in MPDBEEG. A total drop-out rate of 20.2% was observed in the study. Fourteen percent of participants in MPG were lost to follow-up. Nineteen percent of the participants in MPSBEEG dropped out (out of these, 40% were lost to follow-up while 60% absconded due to improvement in their health condition). In the MPDBEEG, 28.6% of the participants dropped out (37.5% were lost to follow-up while 62.5% absconded due to improvement in their health condition).
Treatment was given thrice weekly for eight weeks and outcomes were assessed at the end of the fourth and eighth week of study. Ethics and Research Committee of the Obafemi Awolowo University Teaching Hospitals Complex and the joint University of Ibadan /University College Hospital Institutional Review Committee respectively gave approval for the study.
Instruments
A height meter calibrated from 0-200cm was used to measure the height of each participant to the nearest 0.1cm. A weighing scale was used to measure the body weight of participants in kilograms to the nearest 1.0Kg. It is calibrated from 0 – 120kg. A metronome (Wittner Metronom system Maelzel, Made in Germany) was used to set a uniform tempo for dynamic back endurance muscles endurance test, which involves repeated contraction or movements over a period of time performed synchronously to the metronome beat. Patients lay on a plinth for the MP, static and dynamic back endurance exercise respectively.
General Health Status Questionnaire – Short Form -36 (SF-36) was used to assess the quality of life of the participants. The SF-36 has been recommended in the assessment of patients with long-term LBP [24, 44, 45]. A Yoruba translated version of the Health Status Questionnaire (SF-36) was used for participants who were literate in the Yoruba language and preferred the Yoruba version. The translation was done at the department of linguistics and African languages of Obafemi Awolowo University, Ile Ife. Pearson product moment correlation coefficient (r) of 0.84 was obtained for the criterion validity of the back translation of the Yoruba version. Quadruple Visual Analogue Scale (QVAS) was used to assess pain intensity of participants. QVAS is a reliable and valid method for pain measurement [46, 47]. A Yoruba translated version of the QVAS was used for participants who were literate in the Yoruba language and prefers the Yoruba version. The translation was done at the department of linguistics and African languages of Obafemi Awolowo University, Ile Ife. Pearson product moment correlation coefficient (r) of 0.88 was obtained for the criterion validity of the back translation of the Yoruba version.
Treatment
Treatment for the different groups (MPG, MPSBEEG and MPDBEEG) comprised three phases including warm up, main exercise and cool down. Prior to treatment, the participants were instructed in details on the study procedures. This was followed by a low intensity warm-up phase of five minutes duration comprising active stretching of the upper extremities and low back and strolling at self-determined pace around the research venue. Treatment also ended with a cool-down phase comprising of the same low intensity exercise as the warm-up for about five minutes.
The McKenzie Protocol (MP) involved a course of specific lumbosacral repeated movements in extension that cause the symptoms to centralize, decrease or abolish. The determination of the direction preference for extension was followed by the main MP activities including �Extension lying prone�, �Extension In Prone� and �Extension in standing�. The MP also included a set of back care education instructions which comprised a 9 item instructional guide on standing, sitting, lifting and other activities of daily living for home exercise for all the participants (Appendix).
In addition to completing the MP (i.e., back extension exercises plus the back care education), static back extensors endurance exercise which included five different static exercises differentiated by the alteration of the positions of the upper and lower limbs with the patient in prone lying on a plinth was carried out [48]. The participants began the exercise training programme with the first exercise position, but progressed to the next exercises at their own pace when they could hold a given position for 10 seconds. On reaching the fifth progression, they continued with the fifth progression until the end of the exercise programme [48, 49]. The following were the five exercise progressions:
Participant lay in prone position with both arms by the sides of the body and lifting the head and trunk off the plinth from neutral to extension;
Participant lay in prone position with the hands interlocked at the occiput so that shoulders were abducted to 90� and the elbows flexed, and lifting the head and trunk off the plinth from neutral to extension;
Participant lay in prone position with both arms elevated forwards, and lifting the head, trunk and elevated arms off the plinth from neutral to extension;
Participant lay in prone position and lifting the head, trunk and contralateral arm and leg off the plinth from neutral to extension; and
Participant lay in prone position with both shoulders abducted and elbows flexed to 90�, and lifting the head, trunk and both legs (with knees extended) off the plinth.
If pain was aggravated during the exercise, the participant was asked to stop. If the pain diminished within 5 minutes after the exercise, he/she was asked to continue the exercise but to hold the exercise position for only 5 seconds. The participant was asked to progress to 10 seconds if there was no adverse response. Each exercise was repeated 9 times. After 10 repetitions, the participant was instructed to rest for between 30 seconds to 1 minute. Static holding time in the exercise position was gradually increased to 20 seconds to provide a greater training stimulus [50, 51]. The dosage of series of 10 repetitions was adopted from a previous protocol for participants with sub-acute LBP [52].
In addition to completing the MP, dynamic back extensors endurance exercise which included five different isokinetic exercises differentiated by the alteration of the positions of the upper and lower limbs with the patient in prone lying on a plinth was carried out. The dynamic back endurance exercise was an exact replica of the static back extensors endurance exercise protocol in terms of exercise positions, progressions and duration. However, instead of static posturing of the trunk in the prone lying position and holding the positions of the upper and lower limbs suspended in the air during all the five exercise progressions for the 10 seconds, the participant was asked to move the trunk and the suspended limbs 10 times.
If pain was aggravated during the exercise, participant was asked to stop. If the pain diminished within 5 minutes after the exercise, the participant was asked to continue the exercise but to carry out only 5 movements in the exercise position. The participant was asked to progress to 10 movements if there is no adverse response. Each exercise was repeated 9 times. After 10 repetitions, the participants were instructed to rest for between 30 seconds to 1 minute. The number of movements of the trunk in the exercise position was gradually increased to 20 seconds to provide a greater training stimulus.
In order to achieve adequate training effect based on recommendation of previous studies, a 30 to 45 minute exercise duration, thrice weekly and eight weeks exercise; and training load of 10 seconds static hold or 10 repetitions per exercise position was adopted [53, 54].
The researchers (CEM and OA) were credentialed in the McKenzie method and supervised the exercises. The researchers were blinded to the recruitment, randomization and assessment procedures which were carried out by an assistant who was blinded to the treatment protocols of the different groups. The research assistant was also credentialed in McKenzie method. The questionnaires used in this study were self- administered.
Data Analysis
Data were analyzed using descriptive of mean and standard deviation; and inferential statistics. One-way ANOVA was used to compare the participants� general characteristics and pain intensity by treatment groups. Pearson’s Product Moment Correlation Analysis was used to test the relationship between HRQoL and intensity of pain. The Kruskal Wallis test was used to compare the treatment outcomes (mean change) on HRQoL across group at week four and eight of the study respectively. Friedman’s ANOVA and Wilcoxon signed ranked tests for multiple comparisons were used to compare within group changes in across the three study time points Alpha level was set at p = 0.05. The data analyses were carried out using SPSS 13.0 version software (SPSS Inc., Chicago, Illinois, USA).
Dr. Alex Jimenez’s Insight
How can the McKenzie method improve an individual’s quality of life? With years of experience working alongside patients to help them recover from a variety of spinal health issues, I’ve seen how debilitating low back pain can be if left untreated for an increased amount of time. Although spinal adjustments and manual manipulations can efficiently help improve symptoms of low back pain, other alternative treatment options may help patients recover faster. The McKenzie method and endurance exercises are used by many healthcare professionals to safely and effectively rehabilitate patients with LBP. The results of the research study ultimately demonstrate how the treatment protocol can help improve an individual’s quality of life.
Results
The mean age, height, weight and BMI of all the participants was 51.8 � 7.35 years, 1.66 � 0.04m, 76.2�11.2 Kg and 27.2 � 4.43 kg/m2 respectively. Comparison of the participants� general characteristics by treatment groups revealed that the participants in the different groups were comparable in their general characteristics (p > 0.05) (Table 1).
Table 1: One-way ANOVA comparison of the participants� general characteristics and pain intensity by treatment groups
The mean pain intensity score (VAS) reported by the participants was 6.55 � 1.75. The relationship between each of the eight domains of HRQoL and intensity of pain (VAS score) is presented in Table 2.
Table 2: Relationship between Health-Related Quality of Life and intensity of pain (VAS score) (n = 67)
From the result, correlation co-efficient (r) ranged between-0.603 to-0.878 at p = 0.001. Table 3 shows the comparison of the participants� baseline measure of HRQoL.
Table 3: Kruskal Wallis comparison of the participants� baseline assessment of HRQoL
The results indicate that the participants in the different treatment groups were comparable in all the domains of HRQoL (p > 0.05). Within-group comparison of HRQoL in MPG, MPSBEEG and MPDBEEG across the 3 time points (weeks 0-4, 4-8 and 0-8) of the study showed that there were significant improvements (p < 0.05) (Table 4). Comparison of treatment outcomes (mean change score (MCS)) at week four and eight of the study are presented in Table 5. There were significant differences in SF-36 scores across the group (p > 0.05) at the end of the 4th and 8th week of the study respectively. The Tukey multiple comparisons post-hoc analysis was used to elucidate where the differences within between groups lie. The result indicated that MPSBEEG and MPDBEEG had significantly higher MCS on all domains of SF-36 compared with MPG at week four and eight respectively (p < 0.05). There was no significant difference between the MPSBEEG and MPDBEEG in the MCS of General Health Perception domain of SF-36 at week four; and on General Health Perception and Physical Functioning Domains of SF-36 at week eight respectively. However, MPDBEE had significantly higher treatment effects on other domains of HRQoL (p = 0.001).
Table 4: Friedman’s ANOVA and Wilcoxon signed ranked test multiple comparisons of HRQoL among MPG, MPSBEEG and MPDBEEG across the 3 time points of the study.
Table 5: Kruskal Wallis comparison of the participants� treatment outcomes (mean change) at week four of the study.
Discussion
This study evaluated the relationship between HRQoL and pain intensity, and the influence of static and dynamic back extensors� endurance exercises on HRQoL in Nigerian patients with LMLBP treated with the MP. The mean age of the patients in this study was 51.8 � 7.35 years. This age falls within the age bracket during which LBP is reported to be a more common problem [55]. From the result of this study, no significant difference in physical characteristics and pain intensity was found in the different treatment groups at baseline. Baseline characteristics are believed to be predictors of response to treatment in clinical trials for LBP [56]. Comparability in baseline measure in clinical trials is reported to reduce the chances of co-founders other than the intervention in predicting outcomes. Therefore, it is implied that the results obtained at different point in the course of this study could have been largely due to the effects of the various treatment regimens.
This study investigated the relationship between HRQoL and the intensity of pain. From the result, significant moderate to high inverse relationships were found between pain intensity and the different domains of HRQoL. General health perception showed the least correlation (r = -0.603; p = 0.001) while social functioning had the highest correlation with pain intensity (r = -0.878; p = 0.001). It is inferred from the study’s result that HRQoL of patients with long-term LBP decreases with severity of pain. Previous studies have reported an association between LBP and psychosocial factors [26, 57]. Specifically, significant inverse correlation has been reported between severity of pain and quality of life in patients with chronic LBP [57�59]. Pain is believed to have a profound effect on HRQoL [59] and the degree, to which the patients believe that they are disabled by it, is a powerful factor in the extent of their quality of life impairments [60]. Therefore, quality of life is an indicator of the level of endurance of people to pain [61].
Within-group comparison of each of MP, MP plus Static Back Endurance Exercise (MPSBEE) and MP plus Dynamic Back Endurance Exercise (MPDBEE) across the 3 time-points (weeks 0-4, 4-8 and 0-8) of the study revealed that each treatment regimen led to significant improvement in HRQoL. Patients in this study displayed baseline values of the SF-36 comparable to those described in other studies on chronic LBP [62]. The baseline values of all domains of the SF-36 observed in this study were lower than those of adult normative data reported by Jenkinson et al [63] leaving room for any improvement accruable to treatment regimens to be assessed. From this study, all the eight domains of the SF-36 significantly improved at the 4th and 8th week assessment. However, on the final assessment, social functioning, general health perception and bodily pain improved more than the other domains of SF-36 in the MPG. General health perception, physical functioning, social functioning, bodily pain and energy vitality improved more than the other domains of SF-36 in the MPSBEEG while general health perception, physical functioning, social functioning, bodily pain and energy vitality improved more than the other domains of SF-36 in the MPDBEEG. Role physical, role emotional and mental health were the least improved domains of the SF-36 among the treatment groups. Though significant improvements were observed in the different domains by treatment groups on final assessment, the values were still lower than the adult normative data for general health status assessed using the SF-36 questionnaire [63]. A previous study by Smeets and colleagues [64] found that active physical therapy regimen primarily designed to improve physiological aspects of LBP such as aerobic fitness level, low back muscle strength and endurance can also reduce the impact of psychosocial factors that it did not deliberately target. In view of current evidence, Hill and Fritz [57] suggest that it may not necessarily follow that a psychologist is better placed to improve treatment outcomes than a physical therapist, even when a goal of treatment is the mediation of a psychosocial factor. Hill and Fritz [57] also argue that psychosocial factors including fear of movement, anxiety, a faulty coping strategy and quality of life have a strong influence on the success of treatment for patients with back pain at a group level. Literature suggests that exercise generally has a potential benefit on psychosocial aspect of patient with long-term LBP. Long-term LBP leads to deconditioning [65] and many problems associated with deconditioning are believed to be reversible through general and specific exercise regimens [66]. Harding and Watson [66] note that improvement in overall physical function is linked with improvement in psychosocial function. Unfortunately, there is a dearth of studies on the effect of the MP and back extensors endurance exercises on HRQoL in patients with long-term mechanical LBP.
From the result of this study, comparison of the different treatment regimens indicate that MPSBEE and MPDBEE had significantly higher treatment effect on all domains of HRQoL compared with MP at week four and eight respectively. MPSBEE and MPDBEE were comparable in their effect on general health perception domain at week four; and on health perception and physical functioning domains of the HRQoL at week eight. However, MPDBEE had significantly higher treatment effects on other domains of HRQoL. Generally, exercise seems to leads to improved wellness and quality of life. Still, there does not appear to be a consensus of opinion on the most effective programme designed to maintain exercise benefits. The McKenzie method is a popular and promising classification-based treatment for LBP among physical therapists [3] in addition to delivering theoretical information in order to educate patients about their condition, so that patients are better able to understand their condition and how to change their behaviour towards an episode of LBP [67]. However, few studies have investigated the effect of the MP on HRQoL in patients with LMLBP. Udermann et al [68] found significant improvements in HRQoL measures in chronic LBP patients treated with MP but reported that the addition of resistance training for the lumbar extensors provided no additional benefit. In recent times, endurance training of the low-back extensors aimed at improving physical performance and psychosocial health in patients with LBP has increased in popularity [69, 48, 52, 70], yet their effectiveness in enhancing quality of life remains unclear [71].
The observed efficacy of the MP, MPSBEE and MPDBEE in this study could be as a result of the fact that each of the regimen contained active exercise carried out in extension positions. Active exercise can be described as functional exercise performed by the patient or client. Previous studies have shown that active exercise, irrespective of the type is more effective in the management of patients with long-term LBP than passive therapy [72, 73]. The MP utilizes a system of patient self generated force to mobilize or manipulate the spine through a series of active repeated movements or static positioning and it is based on the patient’s pain response to certain movements and postures during assessment [3]. Similarly, endurance exercises are active exercises that require static posturing or repeated movements in order to initiate overload stimuli on the musculature. The different treatment regimen in this study had movement components, either from the MP which is the baseline treatment for all the groups or from the back extensors endurance exercise protocols. It is postulated from the results of this study that the significant higher treatment outcome of MPDBEE might be due to the combined effects of movements and overload stimulus on the back extensor muscles. MPDBEE seems to contain movement ingredients, firstly, from the MP which is the baseline treatment for this group and it involved a series of active repeated movements. Secondly, the dynamic back extensors endurance exercise also involved repeated movements of the trunk and limbs in the sagittal plane. It seems that extension exercise with movement elements carried out in patterns similar to the daily tasks motions might help to improve psychosocial aspects of long-term LBP as observed in this study.
Limitations of the Study
The generalizability of the findings of this study is limited by the fact that a generic quality of life tool was employed because of the scarcity of standard HRQoL tools with documented psychometric properties specific for patients with LBP. Theoretically, specific HRQoL measures are opined to be more responsive than generic HRQL measures [74]. Like all other self-reported assessment, it is possible that the patients in this study might have given exaggerated responses or overestimated the effect of exercise on their HRQoL. Furthermore, individuals� perception of psychosocial construct such as HRQoL is believed to be influenced by subjective interpretation and cultural bias [75, 76]. The high drop-out rate observed in this study is also a potential limitation and source of bias which may limit the interpretation and generalizability of study results. Finally, the treatment outcomes of the different regimens were only measured over such a short period of time of eight weeks.
Conclusion
Health-related quality of life of patients with long-term LBP decreases with severity of pain. The McKenzie Protocol, static and dynamic back extensors endurance exercises had significant therapeutic effect on HRQoL in patients with LMLBP. However, the addition of dynamic back extensors endurance exercise to MP led to higher improvement on HRQoL. It is recommended that static or dynamic endurance exercise be combined with MP in patients with LMLBP to derive maximum improvement in general health status.
Acknowledgements
This research was funded by an African Doctoral Dissertation Research Fellowship award offered by the African Population and Health Research Center (APHRC) in partnership with the International Development Research Centre (IDRC). We would like to thank the management and clinicians of the department of physiotherapy OAUTHC, Ile-Ife, Nigeria for their support in carrying out the study. We will also like to thank all the patients who participated in this study.
Competing Interests
The authors declare no competing interests.
Authors� Contributions
All the authors have contributed in this study in ways that comply to the ICMJE authorship criteria. All the authors have read and approved the final version of the manuscript.
In conclusion,�the quality of life of patients with chronic and/or persistent low back pain improved and the pain intensity of the symptoms of LBP appeared to decrease with the use of McKenzie therapy and endurance exercises, according to the study. Furthermore, under the McKenzie treatment protocol, static and dynamic back extensor endurance exercises were recorded to significantly improve symptoms as compared to endurance exercises alone. Information referenced from the National Center for Biotechnology Information (NCBI). The scope of our information is limited to chiropractic as well as to spinal injuries and conditions. To discuss the subject matter, please feel free to ask Dr. Jimenez or contact us at 915-850-0900 .
Curated by Dr. Alex Jimenez
Additional Topics: Sciatica
Sciatica is referred to as a collection of symptoms rather than a single type of injury or condition. The symptoms are characterized as radiating pain, numbness and tingling sensations from the sciatic nerve in the lower back, down the buttocks and thighs and through one or both legs and into the feet. Sciatica is commonly the result of irritation, inflammation or compression of the largest nerve in the human body, generally due to a herniated disc or bone spur.
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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.
Contents
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).
Contents
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.
Muscular energy techniques, or METs, are considered to be some of the most valuable tools any healthcare professional can have and there are several reasons for it. METs have a wide application range and essential modifications can be made for each of them for a variety of injuries and/or conditions. Muscular energy techniques also represent an important aspect of rehabilitation. Furthermore, METs are both gentle and effective. But most importantly, METs actively involve the patient in the recovery process. Unlike other types of treatment therapies, the patient is involved in every step, contracting at the appropriate time, relaxing at the appropriate time, engaging in eye movement, and even breathing when instructed by the healthcare professional.
Muscular energy techniques have been used with other treatment modalities, such as the McKenzie method, to improve the outcome measures of injuries or conditions. The following research study demonstrates clinical and experimental evidence on the impact of the McKenzie method with METs for low back pain, one of the most common complaints affecting spine health. The purpose of the article is to educate and advice patients with low back pain on the use of METs with the McKenzie method.
Contents
Impact of McKenzie Method Therapy Enriched by Muscular Energy Techniques on Subjective and Objective Parameters Related to Spine Function in Patients with Chronic Low Back Pain
Abstract
Background: The high incidence and inconsistencies in diagnostic and therapeutic process of low back pain (LBP) stimulate the continuing search for more efficient treatment modalities. Integration of the information obtained with various therapeutic methods and a holistic approach to the patient seem to be associated with positive outcomes.The aim of this study was to analyze the efficacy of combined treatment with McKenzie method and Muscle Energy Technique (MET), and to compare it with the outcomes of treatment with McKenzie method or standard physiotherapy in specific chronic lumbar pain.
Material/Methods: The study included 60 men and women with LBP (mean age 44 years). The patients were randomly assigned to 1 of 3 therapeutic groups, which were further treated with: 1) McKenzie method and MET, 2) McKenzie method alone, or 3) standard physiotherapy for 10 days. The extent of spinal movements (electrogoniometry), level of experienced pain (Visual Analogue Scale and Revised Oswestry Pain Questionnaire), and structure of the spinal discs (MRI) were examined prior to the intervention, immediately thereafter, and 3 months after the intervention.
Results: McKenzie method enriched with MET had the best therapeutic outcomes. The mobility of cervical, thoracic, and lumbar spine normalized at levels corresponding to 87.1%, 66.7%, and 95% of respective average normative values. Implementation of McKenzie method, both alone and combined with MET, was associated with a significant decrease in Oswestry Disability Index, significant alleviation of pain (VAS), and significantly reduced size of spinal disc herniation.
Conclusions: The combined method can be effectively used in the treatment of chronic LBP.
MeSH Keywords:Low Back Pain, Manipulation, Chiropractic, Manipulation, Spinal
Background
Low back pain (LBP) is the most prevalent form of musculoskeletal disorder. According to published statistical data, 70�85% of people experience LBP at some stage of their lives [1�7]. Only 39�76% of the patients recover completely after an acute episode of pain, suggesting that a considerable fraction of them develop a chronic condition [8].
The goals of physiotherapy in patients with chronic LBP include elimination of pain, restoration of the lost extent of movements, functional improvement, and improvement of the quality of life. These objectives are achieved by various protocols of exercise, manipulation, massage, relaxation techniques, and counselling. Although numerous previously published studies have dealt with various therapeutic modalities of LBP, the evidence of their efficacy is highly inconclusive [9�12]. At present the management of chronic LBP still raises many controversies. Inconsistency of established diagnoses and implemented protocols of management points to the importance of the problem in question. Despite extensive research, the issue of spinal pain management still constitutes a challenge for physicians, physiotherapists, and researchers [8,13].
McKenzie method is 1 of many treatment modalities of LBP. It is a system of mechanical diagnosis and management of spinal pain syndromes, based on comprehensive and reproducible evaluation, knowledge of symptoms patterns, directional preference, and centralization phenomenon. This method is focused on the spinal disc disorders [14]. McKenzie method is based on the phenomenon of movement of the nucleus pulposus inside the intervertebral disc, depending on the adopted position and the direction of the movements of the spine. The nucleus pulposus that is exposed to the pressure from both surfaces of the vertebral bodies takes the shape of a spherical joint. This means that it has the ability to perform 3 rotary movements in all directions and has 6 degrees of freedom of movement. The nucleus pulposus performs the movements of flexion, extension, lateral bend (left and right), rotation (right and left), linear displacement (slip) along the sagittal axis, linear displacement along the transverse axis and the separation or approximation along the vertical axis [15].Numerous studies have shown that during forward bend of the spine it is possible to observe extension of the rear surface of the fibrous ring, compressing of the front part of the intervertebral disc and the shift of nucleus pulposus to the dorsal side. When stretching, the mechanism is the opposite [16].
The musculoskeletal system is vital for the maintenance of the balanced tension of the body. Musculofascial disorders can be associated with various problems, pain, or even loss of some motor function. Muscle Energy Techniques (MET) are among the most popular therapeutic modalities aimed at the improvement of elasticity in contractile and non-contractile tissues [17].
High incidence, inconsistencies in diagnostic and therapeutic process, and huge costs associated with the management of chronic spinal disorders stimulate the continuing search for more efficient treatment modalities. This requires the knowledge of neurophysiological processes, proper interpretation of pain, identification of unfavorable motor and postural patterns, holistic approach to the patient, and integration of the information obtained with various therapeutic methods [18].
The aim of this study was to analyze the efficacy of combined treatment with McKenzie method and MET, and to compare it with the outcomes of treatment with McKenzie method or standard physiotherapy in chronic lumbar pain. We evaluated the effect exerted by each of the interventions on the extent of movements, level of experienced pain, and structure of the spinal discs as assessed by means of magnetic resonance imaging.
Material and Methods
Patients
The randomized study included 60 men and women with mean age of 44 years. All individuals were diagnosed by a specialist physician and referred for rehabilitation. The protocol of the study was approved by the Local Bioethical Committee of the Poznan University of Medical Sciences (decision no. 368/0). All patients were diagnosed with chronic spinal pain persisting for longer than 1 year. The inclusion criteria of the study were: 1) documented magnetic resonance imaging (MRI) of the spine, 2) confirmed protrusion or bulging in the lumbosacral spine, 3) intermittent lumbosacral pain, 4) projection of pain to the buttock or thigh, 5) unilateral character of the symptoms. The exclusion criteria were: 1) confirmed extrusion or sequestration of nucleus pulposus of the spinal disc, 2) symptoms manifesting below the knee, 3) history of spinal surgery, 4) structural disorders of spinal discs in more than 2 spinal segments, 5) evident stenosis of the spinal canal, 6) focal lesions of the spinal cord, and 7) spondylolisthesis.
Patients showed great interest and all completed the study.
Protocol
The following tests were used to determine the baseline (i.e. pre-intervention) parameters of the studied patients: 1) electrogoniometric determination of the extent of movement in all spinal segments and angular values of physiological curvatures, 2) Oswestry questionnaire, and 3) Visual Analogue Scale (VAS). Subsequently, the patients were randomly assigned to 1 of 3 therapeutic groups (20 persons each), which were further treated with: 1) McKenzie method and MET, 2) McKenzie method alone, 3) standard physiotherapy. Each of the 3 therapeutic protocols included 10 daily sessions, performed during 5 consecutive weekdays. 24 hours following the last therapeutic session, the same parameters as at the baseline were determined by the investigator blinded to the treatment assignment. Moreover, all patients were subjected to repeated magnetic resonance.
Therapeutic Intervention
McKenzie group One session lasted 30 minutes. On the basis of the McKenzie spinal pain classification, the derangement syndrome was diagnosed in all patients [14]. The therapy included hyperextension techniques, hyperextension with self-pressure or pressure by the therapist, and hyperextensive mobilization. These techniques were applied in the sagittal plane, following the rule of force progression [14]. Moreover, the patients were asked to self-perform the therapeutic procedure at home (5 cycles per day with 2-hour intervals, 15 repetitions each).
McKenzie + MET group The classic McKenzie method enriched with Muscle Energy Technique was implemented. McKenzie protocol in both groups (McKenzie McKenzie + MET) was the same. All patients in this therapeutic group were also diagnosed with the derangement syndrome. A technique of post-isometric relaxation was used at the end of each therapeutic session. It was characterized by the following parameters: 1) time of contraction equal to 7�10 seconds, 2) intensity of contraction corresponding to 20�35%, 3) beginning in the intermediate extent of movement for a given patient, 4) 3 seconds of interval between consecutive contraction phases, 5) 3 repetitions, 6) contraction of antagonist muscle at the terminal phase of the procedure, 7) passive return to the baseline position. The procedure involved relaxation of the erector spinae muscle group and was performed in a sitting position. The exercise was performed in an anterior and lateral flexion, and in rotation. The therapy involved bilateral parts of the erector spinae so as to balance the muscular tension [17]. The duration of 1 combined session was 40 minutes. Patients treated with the combined method were also asked to exercise at home (5 cycles per day with 2-hour intervals, 15 repetitions each).
Standard treatment group Individuals randomized to this therapeutic group were treated with classical massage, laser therapy, and transcutaneous electrical nerve stimulation (TENS) applied to the lumbosacral region. Additionally, the patients were asked to perform general exercises strengthening spinal and abdominal muscles (once a day at home). The exercises were to be performed for 15 minutes, in a prone, supine, and lateral position. The aim of the training was to strengthen the muscles stabilizing the pelvic girdle, i.e. the erector spinae, quadratus lumborum, rectus abdominis, oblique abdominal, gluteal, and iliopsoas muscles. The classical massage lasted 20 minutes. The laser therapy was conducted with a contact technique with Lasertronic LT-2S device. The duration of laser therapy was 80 seconds (2�40 s). The treatment was applied on both sides of the spinous processes of the lumbar spine. The parameters of the procedure were as follows: energy 32 J, power of radiation 400 mW, wavelength 810 nm, continuous mode. TENS electrotherapy was performed with Diatronic DT-10B device. The electrodes were placed on both sides of the lumbosacral spine. The parameters of the TENS procedure were as follows: duration 15 minutes, frequency 50 Hz, current 20�30 mA (subjectively adjusted), duration of a single impulse 50 microseconds. The total time per session=36 min 20 sec + 15 min as home exercises once a day.
Evaluation of Therapeutic Effect
Electrogoniometry The extent of movements and the angles of spinal curvatures were determined with tensiometric Penny & Giles electrogoniometer in Boocok�s modification [19], which prevents potential measurement bias associated with shifting skin and soft tissues in relation to bones. The electrogoniometer enables linear measurement with a bias no greater than 1�. The measurements were taken according to Lewandowski�s methodology [20]. The reliability of these measurements was previously verified by Szulc et al.21 The reference values used in our study were calculated on the basis of Lewandowski�s measurements taken in a group of about 20 000 individuals [20].
Revised Oswestry pain questionnaire The degree to which the dysfunction of the lumbar spine limited the performance of the activities of daily living was determined with the Revised Oswestry Pain Questionnaire [22,23]. We used the revised version of the questionnaire as it is the only variant of this instrument which examines the changes in the level of lumbar pain. The survey was conducted twice, prior to and after the therapy.
Visual analogue scale (VAS) To verify the efficacy of the therapy, the participants were examined with the visual analogue scale (VAS) at the baseline (prior to the intervention) and 24 hours after completing the treatment [24].
Magnetic resonance imaging The degree of degeneration of the spinal discs and the therapeutic outcome were verified on magnetic resonance imaging performed prior to and after the intervention, at the same time of the day. The examination was conducted in sagittal and axial planes, and used T1- and T2-weighted images. The displacement of the nucleus pulposus was expressed in mm. The methodology of examination was described previously by Fazey et al. [25].
Statistical Analysis
Statistical analysis was conducted with Statistica 10.0 software. Bivariate analysis of variance (AVOVA) with 1 intergroup factor (type of intervention) and 1 intragroup factor (measurement prior to intervention, 24 hours and 3 months after the intervention) was used to analyze the differences in studied parameters resulting from the type of the implemented therapy, and to verify the efficacy of various therapeutic protocols. The significance of differences in multiple comparisons was verified with the Scheff�s post-hoc test.
Dr. Alex Jimenez’s Insight
Low back pain is a common symptom that can be treated in a number of ways. Chiropractic care is one of the most common alternative treatment options for LBP, however, healthcare professionals have started using other treatment modalities to help improve symptoms of low back pain. Physical therapy and exercise have commonly been used together, alongside well-known treatment modalities, to help speed up the patient’s recovery process. The research study aims to determine how the McKenzie method and muscular energy techniques can improve low back pain and promote overall health and wellness. As a doctor of chiropractic, the positive effects of physical therapy and exercise is reflected on the recovery of patients.
Results
The significant effects of bivariate interaction (method � time) suggest that the implemented therapeutic methods exerted variable time-dependent effect on the functional parameters of the spine, Oswestry questionnaire scores, values of visual analog scale, and the results of magnetic resonance imaging in patients with chronic low back pain.
Data on the mobility of various spinal segments prior to the intervention, and 24 hours and 3 months after the intervention suggests that the implementation of McKenzie method enriched with MET was reflected by better therapeutic outcome compared to classical McKenzie method and standard physiotherapy. Mobility of various spinal segments in all axes and planes improved significantly as a result of the therapy with McKenzie method enriched in MET. In contrast, the least pronounced improvement of spinal mobility was documented in the case of standard physiotherapy (Tables 1?�3).
Table 1: Basic statistical characteristics and significance of differences between the angular values of the cervical spine mobility depending on the phase of the study and type of implemented therapeutic method.
Table 2: Basic statistical characteristics and significance of differences between the angular values of the thoracic spine mobility depending on the phase of the study and type of implemented therapeutic method.
Table 3: Basic statistical characteristics and significance of differences between the angular values of the lumbar spine mobility depending on the phase of the study and type of implemented therapeutic method.
The analysis of the anterior flexion of the cervical spine revealed that the improvement of mobility was most pronounced in McKenzie + MET group (?%=42.02). The lack of significant difference between the measurement taken immediately after the intervention and 3 months thereafter suggests that the therapeutic effect was persistent. Less pronounced, albeit significant, improvement of the mobility was also documented in the case of McKenzie method alone (?%=14.79); also this effect persisted after 3 months. In contrast, no significant changes in the extent of anterior flexion of the cervical spine were documented in the group subjected to standard physiotherapy (Figure 1).
Figure 1: Mean angular values of the anterior flexion of the cervical spine determined at various phases of the study in patients treated with three different therapeutic methods (McKenzie method + MET, McKenzie method alone, standard physiotherapy).
Also, the analysis of changes in the degree of thoracic and lumbar spine anterior flexion revealed variability in the outcomes of the studied methods (Figures 2, ?3).
Figure 2: Mean angular values of the anterior flexion of the thoracic spine determined at various phases of the study in patients treated with three different therapeutic methods (McKenzie method + MET, McKenzie method alone, standard physiotherapy).
Figure 3: Mean angular values of the anterior flexion of the lumbar spine determined at various phases of the study in patients treated with three different therapeutic methods (McKenzie method + MET, McKenzie method alone, standard physiotherapy).
The greatest improvement of the mobility, equal to ?%=80.34 and ?%=40.43 in the thoracic and lumbar segment, respectively, was documented in the McKenzie + MET group. The lack of significant difference between the measurements of both the segments taken immediately after the intervention and 3 months thereafter suggests that the therapeutic effect was persistent (Tables 2, ?3). The changes in the remaining functional spinal parameters followed a similar pattern and are summarized in Tables 1?�3.
The degree of mobility in various spinal segments observed after implementation of studied therapeutic methods was compared with respective average normative values published by Lewandowski [20[ (Figures 4?�6). Implementation of McKenzie method enriched with MET was reflected by the most pronounced improvement in the spinal mobility, which fit within the respective normative ranges. The functional parameters of cervical, thoracic, and lumbar spine normalized at levels corresponding to 87.1%, 66.7%, and 95% of respective average normative values.
Figure 4: Functional parameters of the cervical spine (CL � cervical lordosis; CAF � cervical anterior flexion; CPF � cervical posterior flexion; CRF � cervical right flexion; CLF � cervical left flexion; CRR � cervical right rotation; CLR � cervical left rotation) � comparison between values determined in patients treated with three different therapeutic methods and respective normative values published by Lewandowski.
Figure 5: Functional parameters of the thoracic spine (ThK � thoracic kyphosis; ThAF � thoracic anterior flexion; ThPF � thoracic posterior flexion; ThRF � thoracic right flexion; ThLF � thoracic left flexion; ThRR � thoracic right rotation; ThLR � thoracic left rotation) � comparison between values determined in patients treated with three different therapeutic methods and respective normative values published by Lewandowski.
Figure 6: Functional parameters of the lumbar spine (LL � lumbar lordosis; LAF � lumbar anterior flexion; LPF � lumbar posterior flexion; LRF � lumbar right flexion; LLF � lumbar left flexion; LRR � lumbar right rotation; LLR � lumbar left rotation) � comparison between values determined in patients treated with three different therapeutic methods and respective normative values published by Lewandowski.
Irrespective of the therapeutic method and timing of measurement, the angular values of all spinal curvatures fit within the respective normative values and no significant inter- and intragroup differences were documented (Table 4).
Table 4: Basic statistical characteristics and significance of differences between the angular values of the physiological spinal curvatures depending on the phase of the study and type of implemented therapeutic method.
The scores of Oswestry questionnaire also differed depending on the type of implemented intervention. Implementation of McKenzie method, both alone and combined with MET, was reflected by a significant decrease in Oswestry Disability Index. No significant differences were documented between the outcomes of these 2 methods. In contrast, standard physiotherapy had the least pronounced effect on the Oswestry Disability Index (Table 5).
Table 5: Basic statistical characteristics and significance of differences between the Oswestry questionnaire scores, values of visual analogue scale, and magnetic resonance imaging findings depending on the phase of the study and type of implemented therapeutic method.
The analysis of visual analogue scale values suggests that both McKenzie method enriched with MET and classical McKenzie method produced the strongest therapeutic effects, i.e. alleviation of pain. Implementation of both these methods was reflected by marked augmentation of experienced pain, without any significant intergroup differences. In contrast, standard physiotherapy reduced pain to a minimal extent, and no significant differences were observed between VAS scores obtained prior to and after this intervention (Table 5).
Magnetic resonance imaging performed prior to and after the intervention confirmed that McKenzie method enriched with MET produced the best therapeutic outcome manifested by a reduced size of spinal disc herniation. Smaller, albeit significant, improvement of this parameter was also documented in the case of classical McKenzie method. These 2 therapeutic methods did not differ significantly in terms of the post-intervention size of the spinal disc herniation. In contrast, no reduction in the size of the spinal disc herniation was documented after implementation of standard physiotherapy (Table 5).
Discussion
The number of studies validating the efficacy of combined therapeutic methods and techniques is sparse [3,21,26,27]. Wilson et al. [26] concluded that MET is an optimal adjunct technique for other therapeutic modalities [26].
Many studies confirmed the positive effects of McKenzie method [28�36]. Similarly, a body of evidence confirms the therapeutic value of MET [37�44]. Moreover, positive outcomes of both these techniques were documented in patients with spinal pain, including LBP [45,46]. However, to the best of our knowledge, none of the previous studies verified whether the combination of these methods improves the therapeutic outcome.
Noticeably, both the therapies are based on different concepts and involve different therapeutic techniques. The McKenzie method is oriented at the management of all structural abnormalities of the spinal discs. The aim of this therapy is to eliminate pain and normalize function of the affected spinal segment [14]. Therefore, McKenzie method focuses on the treatment of spinal disc pathologies as the principal cause of pain. Takasaki et al. [35] documented positive changes in the spinal disc, i.e. the resolution of herniation, in patient treated with McKenzie method.
However, various injuries and other medical conditions, as well as repetitive negative motor pattern, are also reflected by the disorders of the musculofascial system. This can be reflected by the development of certain compensatory mechanisms, accumulation of muscular tension, motor limitation, and functional disorders [17,40,42]. In contrast, the treatment of the musculofascial system is not included in the concept of McKenzie method. Therefore, the aim of including the muscle energy techniques in the proposed protocol of combined therapy was to potentiate its therapeutic effect through the relaxation and stretching of contracted musculature, strengthening of weakened muscles, reduction of passive muscular tension, improvement of joint mobility, and normalization of motor function [26,43].
The differences observed with regards to the mobility of various spinal segments prior to and after the intervention point to better therapeutic outcome of the combined methods. Noticeably, improved mobility was documented not only in the lumbar spine but also in the cervical and thoracic segment. Therefore, the implementation of MET improved the scope of the combined method (McKenzie + MET) as compared to the classical McKenzie method. Our findings suggest that musculofascial disorders may to a large extent be responsible for limited spinal mobility in patients with chronic LBP. In their papers on the therapeutic effects of manual therapy, Pool et al. [12] and Zaproudina et al. [47] emphasize the importance of limitations in spinal mobility as a sensitive marker of pathological changes.
The magnetic resonance findings documented in patients treated with combined McKenzie method and MET suggest that this combination has no negative effect on the size of spinal disc herniation (Figure 7). This confirms the safety of MET and plausibility of its application in patients with spinal disc pathologies [26]. Of note, relatively large subjective and objective improvements were achieved despite the short duration of the treatment, which included only 10 sessions throughout a 2-week period.
Figure 7: Magnetic resonance images of the structural changes of the L5�S1 spinal disc: (A) prior to, and (B) after the combined therapy (McKenzie method + MET).
Furthermore, control electrogoniometry conducted 3 months after the intervention confirmed the persistent effect of the combined treatment. Moreover, a slight improvement was documented in the case of some functional parameters examined immediately after the intervention and 3 months thereafter. Perhaps, this phenomenon reflected proper education of our patients and further prophylactic self-exercising according to McKenzie method.
Chronic low back pain (CLBP) has a multifactorial etiology [18], and as such requires multimodal treatment. The evidence of therapeutic effects should not be limited to the diagnostic imaging, but mostly be reflected by functionality of a patient, level of experienced pain, extent of movements, and normalization of motor function.
Conclusions
The following conclusions can be formulated on the basis of our findings:
Comparison of the subjective and objective outcomes of 3 therapeutic methods � standard physiotherapy, McKenzie method alone, and McKenzie method combined with MET � in patients with chronic low back pain suggests that the combined method is the most effective.
The use of the combined method (McKenzie + MET) exerts a positive effect on structural (resolution of spinal disc herniation documented on MRI) and functional parameters (improved mobility of various spinal segments), improves the quality of life, and reduces the level of experienced pain.
Acknowledgements
The study was conducted under the auspices of the University School of Physical Education in Poznan. The authors express their gratitude to the owners of the Private Rehabilitation Practice �Antidotum� for consent to perform the study in their facility.
Footnotes
Source of support: The study was supported by the resources from the Ministry of Science and Higher Education for the statutory activity of the Department of Anatomy of the University School of Physical Education in Poznan
Conflict of interest: None declared.
In conclusion, the research study demonstrating clinical and experimental evidence on the impact of the McKenzie method with METs for low back pain, one of the most common complaints affecting spine health, concluded that the combined treatment modalities were effectively used in the improvement of chronic low back pain. The purpose of the article was to educate and advice patients with low back pain on the use of METs with the McKenzie method. Furthermore, the use of the combined treatment modalities demonstrated a positive effect on structural and functional parameters, improving the patient’s quality of life and reducing the level of pain they experienced. Information referenced from the National Center for Biotechnology Information (NCBI). The scope of our information is limited to chiropractic as well as to spinal injuries and conditions. To discuss the subject matter, please feel free to ask Dr. Jimenez or contact us at 915-850-0900 .
Curated by Dr. Alex Jimenez
[accordions title=”References”]
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Additional Topics: Sciatica
Sciatica is referred to as a collection of symptoms rather than a single type of injury or condition. The symptoms are characterized as radiating pain, numbness and tingling sensations from the sciatic nerve in the lower back, down the buttocks and thighs and through one or both legs and into the feet. Sciatica is commonly the result of irritation, inflammation or compression of the largest nerve in the human body, generally due to a herniated disc or bone spur.
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).
Contents
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
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