My doctor told me I have tendinosis, I’ve heard of tendinitis, what is the difference?
Dr. Jimenez considers this dilemma of similar words that cause confusion to patients. Below is an explanation of clinical presentations and anatomical disorders that shed light on the similarities and differences between tendinosis and tendinitis.
Tendons are the tough, white, cords that connect muscles to bones, and are the least elastic of the collagen-based soft tissues (LIGAMENTS, MUSCLES & FASCIA) I work with on a day-to-day basis. How common are tendon problems? Government statistics tell us that overuse injuries of tendons are a leading reason for doctor visits. And although most of these tendon problems are referred to generically as tendinitis, in the vast majority of cases, tendinitis is actually an incorrect and outdated term.
Over the past decade, medical research has conclusively shown that the major cause of tendinopathies is not inflammation (aka “itis”), which even a decade ago was nothing new. For decades, the scientific community has been concluding that wile the immune system mediators we collectively refer to as “INFLAMMATION” are probably present in tendinopathies; inflammation itself is rarely the cause. So, if inflammation is not the primary cause of most tendon problems, what is? Follow along as I show you from peer-review, that since the early 1980’s, research has shown the primary culprit in most tendinopathies is something called “osis”. Thus the name, “tendon � osis” (tendinosis). But what the heck is osis?
The suffix “osis” indicates that there is a derangement and subsequent deterioration of the collagen fibers that make up the tendon. The truth is, even though doctors still use the term “tendinitis” with their patients, their AMA-mandated Diagnosis Codes almost always indicates the problem is “tendinosis” or “tendinopathy” (HERE). Is this differentiation between tendinitis and tendinosis really that important, or am I splitting hairs and making a big deal out of nothing — making a mountain out of a molehill, semantically speaking? Instead of answering that question myself, I will let two of the world�s preeminent tendon researchers — renowned orthopedic surgeons — answer it for me.
“Tendinosis, sometimes called tendinitis, or tendinopathy, is damage to a tendon at a cellular level (the suffix �osis� implies a pathology of chronic degeneration without inflammation). It is thought to be caused by micro-tears in the connective tissue in and around the tendon, leading to an increased number of tendon repair cells. This may lead to reduced tensile strength, thus increasing the chance of repetitive injury or even tendon rupture. Tendinosis is often misdiagnosed as tendinitis due to the limited understanding of tendinopathies by the medical community.” Tendon researcher and orthopedic surgeon, Dr. GA Murrell from a piece called, �Understanding Tendinopathies� in the December 2002 issue of The British Journal of Sports Medicine.
“Tendinitis such as that of the Achilles, lateral elbow, and rotator cuff tendons is a common presentation to family practitioners and various medical specialists.1 Most currently practicing general practitioners were taught, and many still believe, that patients who present with overuse tendinitis have a largely inflammatory condition and will benefit from anti-inflammatory medication. Unfortunately this dogma is deeply entrenched. Ten of 11 readily available sports medicine texts specifically recommend non-steroidal anti-inflammatory drugs for treating painful conditions like Achilles and patellar tendinitis despite the lack of a biological rationale or clinical evidence for this approach. Instead of adhering to the myths above, physicians should acknowledge that painful overuse tendon conditions have a non-inflammatory pathology.” Karim Khan, MD, PhD, FACSP, FACSM, and his group of researchers at the Department of Family Medicine & School of Human Kinetics at the University of British Columbia, from the March 2002 edition of the BMJ (British Medical Journal).
The information in the preceding paragraphs (which was not new when they were published over a decade and a half ago) is so important as to be considered revolutionary for those of you who have spent time on the MEDICAL MERRY-GO-ROUND with tendon problems. Why? Because, as stated by Dr. Murrell above, most medical professionals have, “a limited understanding of tendinopathies”. Why is this? Why do more doctors not grasp what is going on with the majority of Tendinopathies? Why does such a big portion of the medical community continue to ignore their own profession�s scientific conclusions, while continuing to treat tendinopathies with drugs and surgery? Of course there’s always the issue of money. There is also the fact that if you have tendon problems, you are probably being treated using a model that is at least 25-30 years behind the times as far as the medical research is concerned (HERE). If you think I’m being harsh, read what Dr. Warren Hammer, a board certified Chiropractic Orthopedist in practice since the late 1950?s, had to say about Tendinosis in a 1992 issue of Dynamic Chiropractic.
“The American Academy of Orthopedic Surgeons has provided a new classification of tendon injuries�. In the microtraumatic tendon injury the main histologic features represent a degenerative tendinopathy thought to be due to an hypoxic [diminished oxygen] degenerative process. The similarity to the histology [study of the cells] of an acute wound repair with inflammatory cell infiltration as in macrotrauma seems to be absent. A new classification of tendon injury called �tendinosis� is now accepted. �Tendinosis� is a term referring to tendinous degeneration due to atrophy (aging, microtrauma, vascular compromise). Histologically there is a non-inflammatory tendinous degeneration due to atrophy (aging, microtrauma, vascular compromise), as well as a non-inflammatory intratendinous collagen degeneration with fiber disorientation, hypocelluarity, scattered vascular ingrowth, and occasional local necrosis or calcification.”
If your doctor is still treating you for tendinitis and not tendinosis, they are caught in a time warp. According to what the American Academy of Orthopedic Surgeons said over two and a half decades ago, tendinosis is not an inflammatory condition (itis)! It is a degenerative condition (osis)! Not only is there some debate over whether or not tendinitis actually exists at all, but as you will see in a moment, the anti-inflammation medications and corticosteroid injections that your doctor has been prescribing you are actually creating more degeneration. Track & Field athletes make it a point to keep up with the cutting edge diagnosis and treatment of tendinous SPORTS INJURIES. See what their official medical team has to say on the subject of Tendinosis and Tendinopathy……..
“The relatively new term ‘Tendinopathy’ has been adopted as a general clinical descriptor of tendon injuries in sports. In overuse clinical conditions in and around tendons, frank inflammation is infrequent and if seen, is associated mostly with tendon ruptures. Tendinosis implies tendon degeneration without clinical or histological signs of intratendinous inflammation, and is not necessarily symptomatic. The term ‘Tendonitis’ is used in a clinical context and does not refer to a specific histological entity. [The term] Tendonitis is commonly used for conditions that are truly Tendinosis, however, and leads athletes and coaches to underestimate that proven chronicity of this condition……. Most articles describing the surgical management of partial tears of a given tendon in reality deal with degenerative tendinopathies [Tendinosis].” From an official document found on the website of the International Association of Athletics Federations (IAAF) — the official governing body of professional Track and Field
The Science:
“Tendinosis is a medical term used to describe the tearing and progressive degradation of a tendon. Tendons are structural components of the human body that ensure muscles remain bound to the correct bone during normal daily activities. Tendinosis differs from tendonitis in that the affected tendon is not inflamed.” Rachel Amhed from a July 2010 article for Lance Armstrong’s ‘Livestrong Website’ called Tendinosis Symptoms.
“Based on the information of various lines of investigation of tendinopathy, we can summarize some major points which must be considered in the formulation of a unified theory of pathogenesis in our model of tendinopathy….. The primary results of pathology are the progressive collagenolytic [Collagen-Destroying] injuries co-existing with a failed healing response, thus both degenerative changes and active healing are observed in the pathological tissues….. These pathological tissues may aggravate the nociceptive responses [PAIN] by various pathways which are no longer responsive to conventional treatment such as inhibition of prostaglandin synthesis [NSAIDS & Cortcosteroids]; otherwise the insidious mechanical deterioration without pain may render increased risk of tendon rupture.
For example, overuse is a major etiological factor but there are tendinopathy patients without obvious history of repetitive injuries. It is possible that non-overuse tendon injuries may also be exposed to risk factors for failed healing. Overuse induces collagenolytic [DEGENERATIVE] tendon injuries and it also imposes repetitive mechanical strain which may be unfavorable for normal healing. Stress-deprivation also induces MMP expression [Matrix Metallo Proteinase — an enzyme which breaks down Connective Tissues], and whether over- or under-stimulation is still an active debate. It is possible that tenocytes [tendon cells] are responsive to both over- and under-stimulation, both tensile and compressive loading….. By proposing a process of failed healing to translate tendon injuries into tendinopathy, other extrinsic and intrinsic factors would probably enter the play at this stage, such as genetic predisposition, age, xenobiotics (NSAIDs and corticosteroids) and mechanical loading on the tendons….. Classical characteristics of “tendinosis” include degenerative changes in the collagenous matrix, hypercellularity, hypervascularity and a lack of inflammatory cells which has challenged the original misnomer “tendinitis”.” Cherry-picked quotes from a comprehensive collaboration by teams from the Department of Orthopaedics & Traumatology at Prince of Wales Hospital, The Chinese University of Hong Kong, and the Department of Orthopaedic Surgery at Huddinge University Hospital in Stockholm. The study was published in a 2010 issue of Sports Medicine Arthroscopy & Rehabilitation Therapy Technology.
“Rotator Cuff Tendinosis is a degenerative (genetic, age or activity related) change that occurs in our rotator cuff tendons over time. Rotator cuff tendinosis is exceptionally common. Many, many people have tendinosis of the rotator cuff and do not even know it. Why rotator cuff tendinosis bothers some people and doesn�t bothers others is currently a question the orthopedic surgery community can not answer. Rotator cuff tendinosis is just as likely to be found in a professional body builder as it is likely to be found in a true couch potato.” From an August 2011 online article / newsletter by Dr. Howard Luks, an Orthopedic Surgeon and Associate Professor of Orthopedic Surgery at New York Medical College as well as being Chief of Sports Medicine and Arthroscopy at Westchester Medical Center.
“The gross pathology of Angiofibroblastic Tendinosis is [that] there are no inflammatory cells in this tissue. Therefore the term “Tendinosis” is much better [than Tendinitis]. The pathological tissue is instead characterized by very immature tissue and nonfunctional vascular elements.” Loosely quoted from a YouTube video of famed tendon researcher / surgeon Dr. Robert P. Nirschl’s (Nirchl Orthopedics) presentation to the American Academy of Orthopedic Surgeons annual meeting (2012).
“The more commonly used term of tendinitis has since been proven to be a misnomer for several reasons. The first of which is that there is a lack of inflammatory cells in conditions that were typically called a tendonitis…. The other two findings present in tendinosis, increased cellularity and neovascularization has been termed angiofribroblastic hyperplasia by Nirschl…… These are cells that represent a degenerative condition. Neovascularization [the creation of abnormally large numbers of new blood vessels] found in tendinosis has been described as a haphazard arrangement of new blood vessels, and Kraushaar et al. even mention that the vascular structures do not function as blood vessels. Vessels have even been found to form perpendicular to the orientation of the collagen fibers. They then concluded that the increased vascularity present in tendinosis is not associated with increased healing. Take Home Points: Chronic tendon injuries are degenerative in nature and NOT inflammatory. Anti-inflammatory medications (NSAIDs) and/or corticosteroid injections can actually accelerate the degenerative process and make the tendon more susceptible to further injury, longer recovery time and may increase likelihood of rupture.” Quotes cherry-picked from a recent online article called ‘Tendonosis vs. Tendonitis’ by Dr. Murray Heber, DC, BSc(Kin), CSCS, CCSS(C), Head Chiropractor for Canada’s Bobsleigh / Skeleton Team.
“The data clearly indicates that painful, overuse tendon injury is due to tendinosis�the histologic entity of collagen disarray, increased ground substance, neovascularization, and increased prominence of myofibroblasts. [It is] the only clinically relevant chronic tendon lesion, although minor histopathologic variations may exist in different anatomical sites. The finding that the clinical tendon conditions in sportspeople are due to tendinosis is not new. Writing about the tendinopathies in 1986, Perugia et al noted the ‘remarkable discrepancy between the terminology generally adopted for these conditions (which are obviously inflammatory because the ending ��-itis�� is used) and their histopathologic substratum, which is largely degenerative” Dr. Khan once more showing that tendon problems are not caused by inflammation.
“Overuse tendinopathies are common in primary care. Numerous investigators worldwide have shown that the pathology underlying these conditions is tendinosis or collagen degeneration. This applies equally in the Achilles, patellar, medial and lateral elbow, and rotator cuff tendons. If physicians acknowledge that overuse tendinopathies are due to tendinosis, as distinct from tendinitis, they must modify patient management in at least eight areas.” Dr. Karim Kahn M.D / Ph.D and his research team from University of British Columbia’s School of Kinesiology in an article published in the May 2000 issue of The Physician and Sportsmedicine called “Overuse Tendinosis, Not Tendinitis”.
Eight areas? Wow! And that quote is almost two decades old. Now, take a look at something that came from a Medical Textbook that was published over three decades ago in Italy. The medical community knew back then that most overuse tendon problems were not inflammatory (itis), but instead degenerative (osis).
“[There is a] remarkable discrepancy between the terminology generally adopted for these conditions (which are obviously inflammatory since the ending ‘itis’ is used) and their histopathologic substratum, which is largely degenerative.” From an Italian medical text called, “The Tendons: Biology, Pathology, Clinical Aspects” (1986).
Tendinosis Overview:
The truth is that I could go on and on and on and on with quotes from similar studies. Hopefully you get the point! You should be starting to see that most of what you thought about chronic tendon problems needs to be flushed down the toilet or thrown out with the weekly trash. That’s because there’s a new model in town. Tendinosis is it’s name; and if you want any hope of a solution to your tendon problem, you will have to step outside of the medical “box” and start thinking of your problem in terms of “osis” instead of “itis”. Failure to grasp the new model leaves you vulnerable to treatments which, while possibly bringing some temporary relief, will ultimately make you worse — possibly much worse! By the way, the following points are observations that you yourself will understand if you read the above quotes.
Tendinosis is a Degenerative Condition without inflammation. Scratch that. Science has recently shown us that there is inflammation in tendinosis — there should be, at least in the initial phase of healing. However, it’s the SYSTEMIC INFLAMMATION that’s been shown to be the biggest problem. Bottom line, this doesn’t really affect anything I’m telling you in this post, other than to reinforce your need to address systemic inflammation (hint: it can’t be done with drugs).
Tendinosis is the proper model for understanding the majority of Tendinopathies. As a model for understanding
Tendinopathies, Tendinitis has been retired for at least two and a half decades.
Tendinosis is both misunderstood and mismanaged by the majority of the Medical Community.
Traditional Therapies / Interventions for Tendinopathies significantly increase one’s chance of Tendon Rupture.
Most Coaches and Athletes do not understand the difference between Tendinitis and Tendinosis.
If it does exist, Tendinitis (Inflammation of the Tendon) is rare, short lived, and mostly associated with Tendon Tears or Ruptures.
Tendinosis is caused by both overuse and under-use.
Tendinosis is often times Asymptomatic (no symptoms), until it becomes a painful and potentially debilitating problem.
Drugs; particularly NSAIDS & CORTICOSTEROIDS, as well as CERTAIN ANTIBIOTICS actually cause Tendinosis — and Tendon Rupture. They also slow down (or reverse) the healing process.
Best Treatment: Tendinosis & Tendonopathies
Anti-Inflammatory Medication
“I knew then and there I was in the wrong place.” Thoughts running through the mind of a new patient who had recently visited an Orthopedic Specialist’s office for a tendon problem and asked him about the difference between Tendinitis and Tendinosis. The doctor answered, “There is no difference between Tendinitis and Tendinosis. They are one and the same —- two different names for the same problem.”
Even though medical research has conclusively shown us for over three decades that tendinopathies have as their primary cause of pain and dysfunction tissue derangement and degeneration, anti-inflammation drugs continue to be the medical profession�s go-to method of treatment. It�s not difficult to see why this is not working:
Although there is undoubtedly a certain amount of SYSTEMIC INFLAMMATION present with tendinosis, research has conclusively shown that tendon problems are not primarily problems of inflammation, but of degeneration.
Scientific studies have actually shown that non-steroidal anti-inflammatory medications (NSAID�s) such as Aspirin, Tylenol, Nuprin, Ibuprofen, Naproxen, Celebrex, Vioxx (oops � one of the #1 drugs in America for 10 years running was taken off the market because it was found to be a huge cause of chronic illness and death), & numerous others, actually cause injured collagen-based tissues like tendons, ligaments, muscles, fascia, etc, to heal up to 33% weaker, with as much as 40% less tissue elasticity.
Corticosteroid Injections are even worse. Medicine’s dirty little secret of treating connective tissue injuries with steroids is that they actually deteriorate or ‘eat’ the collagen foundation. This is why they deteriorate ever tissue in the joint, including bone. This is bad news considering collagen is the tissue that is deranged — the very tissue that needs to heal the most. This is why corticosteroids are a known cause of DEGENERATIVE ARTHRITIS and OSTEOPOROSIS, not to mention a whole host of easily-verified systemic side effects. The fact that steroid injections are ridiculously degenerative is why doctors ration or limit the number of steroid injections a person can receive � even if they seem to be working. And understand; it’s not that drugs don’t sometimes do what they claim to do. It’s that they never reverse the underlying pathophysiology (HERE). They simply cover symptoms.
Years ago, the Journal of Bone and Joint Surgery reported that corticosteroids are so degenerative that if you have more than one injection in the same joint over the course of your lifetime; your chance of premature degeneration in the injected joint is (gulp) 100%! Ultimately, the problem of corticosteroids (or NSAID�s for that matter) being used to treat tendons or other collagen-based tissues, is that short term relief is being traded for long term (and often permanent) damage. In other words, tomorrow is being traded for today. Kind of reminds you of our government�s short-sighted fiscal policies, doesn�t it? It is also another in a long line of evidences that the gap between medical research and medical practice is growing (HERE).
Collagen is the building block of all connective tissues, including tendons (you probably learned a great deal about collagen on our FASCIAL ADHESION PAGE as well as our COLLAGEN SUPER-PAGE). If one looks at normal collagen fibers from tendons or other connective tissues under a microscope, each individual cell lines up parallel to the surrounding cells. This allows for maximum tissue flexibility (sort of like well-combed hair).
With tendinopathies (whether TRAUMATIC OR REPETITIVE � yes, trauma can cause tendinosis), the tissue uniformity becomes disrupted and unorganized, causing restriction and a severe loss of function. This in turn causes a loss of flexibility, tissue weakness, tissue fraying, increased rigidity, and stiffness (sort of like KNOTTED HAIR OR A HAIRBALL — or gristle in a bite of steak). This leads to a loss of strength and function, which ultimately means that you end up with pain and dysfunction of the affected joint or body part. As I will soon show you, loss of normal function is one of just a few known causes of joint degeneration. This is why anyone who has suffered through Chronic Tendinosis knows how debilitating it can really be.
Normal Tendons Vs Tendinosis
Tendons are one of the Elastic, Collagen-Based Connective Tissues that are Made up of Three Individual Collagen Fibers Braided Together into Wavy Sheets or Bands
Photo by User Vossman
COLLAGEN is a wavy protein. The waves are what give it the ability to stretch and elast. And although Tendons are said to be the least flexible and stretchy of the Elastic, Collagen-Based Connective Tissues (Muscles, Ligaments, & Fascia are all more elastic), they have to have at least a bit of give. The waves in the individual collagen fibers are what allow for this stretching to take place. Tendinosis occurs most often where the muscle meets the tendon. This is due to an especially dense amount of Collagen at this “Transition Zone”.
Tendinosis Looks Like:
NORMAL TENDON Uniform, Organized, & Parallel
Normal, healthy Tendons are like these ropes. Not only are the fibers all running uniformly in the same direction, there is little or no fraying. This gives the tendon the ability to stretch and elast. Photo by Procsilas Moscas
FRAYED TENDON (TENDINOSIS) Unorganized, Tangled, & Random
Tendinosis is characterized by incredible fraying, fragmenting, tangling, and twisting, of the tendon. This causes weakness and inelasticity that can not only painfully debilitating, it can lead to Tendon Rupture. Photo by Martyn Gorman
NOTICE THE FRAYED & TORN APPEARANCE. THIS IS WHAT CHARACTERIZES TENDINOSIS
Photo by Andrjusgeo
NORMAL HEALTHY TENDON
NOTICE THE COLLAGEN WAVES
Photo by Nephron
SCAR TISSUE & ADHESION
(Note the Complete Lack of Uniformity in the Tissue Fibers)
Scar Tissue / Fibrosis
DRDoubleB
Tendinosis Looks Like Tangled Fishing Line
Photo by Daplaza
Tendinosis is characterized by Collagen Fibers that have disrupted alignment. It also shows fraying of the individual fibers. This is why most tendinopathies are now classified as Tendinosis and considered to be degenerative (osis = degeneration), as opposed to Tendinitis (itis = inflammation). The problem is, most of the medical community does not seem to grasp this yet.
Areas Most Affected By Tendinosis
Sometimes Tendionosis is clinically impossible to distinguish from FASCIAL ADHESIONS and microscopic scar tissue. Often times they are present together. The bottom line is that whether the adhesions are in fascia or whether they are tendon DOESN’T REALLY MATTER — they must both be broken. Sometimes there is a great excess of calcium built up at the point where the tendon anchors to the bone. This must be broken up as well. Because the models for understanding various soft tissues are virtually identical; the models for treating said tissues are likewise very similar. As you might imagine, this is fantastic news for the patient. Bear in mind that I have not included each and every specific area you can develop tendinopathy because it can attack anywhere that you have a tendon. The following list happens to be the areas that I treat most frequently in my clinic.
IMPORTANT: Please note that some muscles only cross one joint. However, many muscles cross two joints. Muscles that act on more than one joint have a greater propensity for problems. It also means that one muscle has the potential to give you problems (including tendinosis) at two different joints. Also note that Tendinosis is usually a bit tougher to deal with than Fascial Adhesions.
ROTATOR CUFF TENDINOSIS: The Rotator Cuff is made up of four muscles that surround the shoulder.
SUPRASPINATUS TENDINOSIS: The Supraspinatus Tendon is not only the most commonly injured of the Rotator Cuff Muscles, it is the most common to find tendinopathy in as well.
TRICEP TENDINOSIS: Tricep Tendinosis is rare. About the only people I ever find it in is carpenters (hammering) and weightlifters. However, here is the webpage.
BICEPS TENDINOSIS: Because both heads of the bicep muscle have attachment points in the front of the shoulder, Biceps Tendinosis is frequently mistaken for Bursitis or a Rotator Cuff problem.
LATERAL EPICONDYLITIS (Tennis Elbow): Although I have never seen anyone who got this problem playing tennis, it is nonetheless extremely common.
MEDIAL EPICONDYLITIS (Golfer�s Elbow): Not quite as common as Tennis Elbow above.
WRIST / FOREARM FLEXOR TENDINOSIS: This is tendinopathy on the palm side of the forearm and wrist.
WRIST / FOREARM EXTENSOR TENDINOSIS: This is tendinopathy on the backhand side of the forearm and wrist.
THUMB TENDINOSIS / DeQUERVAIN’S SYNDROME: This extremely common problem can be debilitating. You will frequently hear Thumb Tendinosis referred to as DeQuervain�s Syndrome.
GROIN (Hip Adductor) TENDINOSIS: I have included Tendinosis of the Groin under �Hip Flexor Tendinosis� below.
HIP FLEXOR TENDINOSIS: Hip Flexor Tendinosis will manifest in the upper front thigh or groin area. This is incredibly common in athletes — particularly soccer players.
PIRIFORMIS TENDINOSIS: This problem is related to PIRIFORMIS SYNDROME, and causes pain in the butt (sometimes with sciatica as well).
SPINAL TENDINOSIS: Although most people never think of it, the potential for developing Spinal Tendinosis is greater than you ever imagined possible.
KNEE TENDINOSIS: This is arguably the single most common reason that people visit a Sports Physician.
QUADRICEPS / PATELLAR TENDINOSIS: A form of Knee Tendinosis
HAMSTRING TENDINOSIS: Hamstring Tendinosis can cause knee, hip, and buttock problems.
ACHILLES TENDINOSIS: Achilles Tendinosis is found in the large tendon in the very back of the lower leg / ankle.
ANKLE TENDINOSIS: This common Tendinosis can typically be dealt with by following a few simple procedures.
TIBIALIS ANTERIOR TENDINOSIS: This is related to the category above, and is typically found in the front of the ankle.
POSTERIOR TIBIAL TENDINOSIS: This is related to the category above, and is typically found near the bony knob on the inside of the ankle.
APONEUROSIS / APONEUROTICA TENDINOSIS: Although you have probably never heard the word before, �Aponeurosis� are flattened out tendons. They are almost always referred to as fascia, but technically this is incorrect. They are most often associated with SKULL PAIN.
Effectively Dealing With Tendinosis
Let me begin by saying that I cannot help everyone�s Tendinopathy. And yes, I am very aware that there are thousands of websites out there giving all sorts of free, do-it-yourself advice on how to fix these problems without going to a doctor. Most of this advice concerns common sense treatments that everyone should try before seeking any sort of professional care. These lists frequently include things like STRETCHING / SPECIAL EXERCISES, ICING, resting, EATING AN ANTI-INFLAMMATORY DIET, drinking plenty of water, SPECIAL SUPPLEMENTS FOR CONNECTIVE TISSUES, etc. All of these are great, and highly recommended by me. The truth is, advice like this is going to save a lot of people a lot of time and money by helping the biggest portion of the population get over minor Tendinopathies / Tendinosis on their own, without jumping on the MEDICAL MERRY GO ROUND.
There is a significant portion of the tendinosis-suffering population who have tried all of these things. Every type of pill imaginable, including ANTIBIOTICS (believe it or not, I have seen this used numerous times � some of which, like CIPRO, actually cause tendon weakness and rupture), TENS Units, braces & supports of all kinds, PLATELET INJECTION THERAPY, high powered ultrasound (a form of litho-tripsy called arthro-tripsy), prolotherapy (sugar water injections), all sorts of surgeries, and heaven only knows what else. And this doesn’t even start touching on many of the common drugs, which I’ve already dealt with.
The bottom line is that if your pain is being caused by adhesions, restrictions, and microscopic scarring in the collagen fibers that make up the affected tendon (or the fascial membranes that attach to the tendon), you are going to have a hard time dealing with it using the standard fare found in your average medical clinic. Although their various treatments may cover the symptoms for awhile, you are already becoming painfully aware (no pun intended) that standard medical therapies such as those listed earlier, are not likely to help with Tendinosis over the long haul. And although stretching and specific exercise can be of tremendous benefit, most clinicians tend to put the cart in front of the horse. Those things will not be effective until after the tissue adhesion has been removed (broken), except in minor cases.
Be aware that because of its microscopic nature, the collagen derangement associated with Tendinopathies will rarely if ever show up with even advanced diagnostic imaging (this is true even for MRI, unless your doctor is using a brand new machine with an extra large magnet, or your problem is especially severe). And whether it shows on the MRI or not, will not really change the way that your doctor treats the problem.
Effectively Treat Tendinosis At The Source
If tendinopathies do not show up well with the diagnostic tests that are commonly run by your doctor, how in the world can a chiropractor practicing in tiny town determine whether or not this micro-derangement of a tendon�s collagen fibers is present and potentially causing your pain and dysfunction? I use one of the newer forms of SCAR TISSUE REMODELING. Although this has only been around for three decades in its present form, the Chinese have used something similar for several thousand years. Be aware that breaking these adhesions / restrictions sometimes causes some BRUISING, depending on where it’s at.
Conclusion: Systemic Tendinosis
Not all cases of Tendinosis are rooted in purely biomechanical causes. There are all sorts of things that can create an environment within the body that leads to multiple Tendinopathies. As you might imagine, bilateral Tendinosis, or Tendinosis at multiple sites begins to raise some red flags for me concerning this issue. Not that it is always the case, but when I see people who have several areas of Tendinosis, I began to question whether there might be a deeper problem at work.
If it is not caused by Fluoroquinolone Antibiotics, very frequently, this underlying problem turns out to be some sort of poorly understood or difficult-to-detect AUTOIMMUNE DISEASE. If for whatever reason, your body is making antibodies to attack it’s own tendons or connective tissues, you have a serious problem on your hands — a problem that will not respond to the Scar Tissue Remodeling Treatments that I do, and a problem whose cause likely won’t show up on standard medical tests.
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.
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.
Australian Institute of Health and Welfare . Australia’s health 2004. 1st. Camberra , AIHW; 2004.
Australian Acute Musculoskeletal Pain Guidelines Group Evidence-based management of acute musculoskeletal pain. . 2003. http://www.nhmrc.gov.au
Maetzel A, Li L. The economic burden of low back pain: a review of studies published between 1996 and 2001. Best Pract Res Clin Rheumatol. 2002;16:23�30. doi: 10.1053/berh.2001.0204. [PubMed][Cross Ref]
WorkCover Authority NSW . Statistical Bulletin. NSW Workers Compensation 2002/03. Sydney , The WorkCover Authority NSW ; 2003.
Pengel LH, Herbert RD, Maher CG, Kathryn RM. Acute low back pain: Systematic review of its prognosis. BMJ. 2003;327:1�5. [PMC free article][PubMed]
Thomas E, Silman AJ, Croft PR, Papageorgiou AC, Jayson M, Macfarlane GJ. Predicting who develops chronic low back pain in primary care: a prospective study. BMJ. 1999;318:1662�1667. [PMC free article][PubMed]
Guzm�n J, Esmail R, Karjalainen K, Malmivaara A, Irvin E, Bombardier C. Multidisciplinary rehabilitation for chronic low back pain: systematic review. BMJ. 2001;322:1511�1516. doi: 10.1136/bmj.322.7301.1511. [PMC free article][PubMed][Cross Ref]
van Tulder M, Malmivaara A, Esmail R, Koes B. Exercise therapy for low back pain. A systematic review within the framework of the Cochrane Collaboration Back Review Group. Spine. 2000;25:2784�2796. doi: 10.1097/00007632-200011010-00011. [PubMed][Cross Ref]
van Tulder M, Ostelo R, Vlaeyen JWS, Linton SJ, Morley SJ, Assendelft WJJ. Behavioral treatment for chronic low back pain. A systematic review within the framework of the Cochrane Back Review Group. Spine. 2000;25:2688�2699. doi: 10.1097/00007632-200010150-00024. [PubMed][Cross Ref]
Jellema P, van Tulder MW, van Poppel MN, Nachemson AL, Bouter LM. Lumbar supports for prevention and treatment of low back pain. A systematic review within the framework of the Cochrane Back Review Group. Spine. 2001;26:377�386. doi: 10.1097/00007632-200102150-00014. [PubMed][Cross Ref]
Ferreira ML, Ferreira PH, Latimer J, Herbert RD, Maher CG. Does spinal manipulative therapy help people with chronic low back pain? Aust J Physiother. 2002;48:277�284. [PubMed]
Pengel HM, Maher CG, Refshauge KM. Systematic review of conservative interventions for subacute low back pain. Clin Rehabil. 2002;16:811�820. doi: 10.1191/0269215502cr562oa. [PubMed][Cross Ref]
Koes BW, van Tulder MW, Ostelo R, Burton K, Waddell G. Clinical guidelines for the management of low back pain in primary care: an international comparison. Spine. 2001;26:2504�2514. doi: 10.1097/00007632-200111150-00022. [PubMed][Cross Ref]
Borkan J, Koes B, Reis S, Cherkin DC. A report from the Second International Forum for Primary Care Research on low back pain: reexamining priorities. Spine. 1998;23:1992�1996. doi: 10.1097/00007632-199809150-00016. [PubMed][Cross Ref]
Bouter LM, van Tulder MW, Koes BW. Methodologic issues in low back pain research in primary care. Spine. 1998;23:2014�2020. doi: 10.1097/00007632-199809150-00019. [PubMed][Cross Ref]
Leboeuf-Yde C, Lauritsen JM, Lauritzen T. Why has the search for causes of low back pain largely been nonconclusive? Spine. 1997;22:877�881. doi: 10.1097/00007632-199704150-00010. [PubMed][Cross Ref]
Fritz JM, Delitto A, Erhard RE. Comparison of classification-based physical therapy with therapy based on clinical practice guidelines for patients with acute low back pain. Spine. 2003;28:1363�1372. doi: 10.1097/00007632-200307010-00003. [PubMed][Cross Ref]
McKenzie R, May S. The lumbar spine. Mechanical diagnosis & therapy. 2nd. Vol. 1. Waikanae , Spinal Publications New Zealand Ltd; 2003. p. 374.
van Dillen LR, Sahrmann SA, Norton BJ, Caldwell CA, McDonnell MK, Bloom NJ. Movement system impairment-based categories for low back pain: stage 1 validation. J Orthop Sports Phys Ther. 2003;33:126�142. [PubMed]
BenDebba M, Torgerson WS, Long DM. A validated, practical classification procedure for many persistent low back pain patients. Pain. 2000;87:89�97. doi: 10.1016/S0304-3959(00)00278-5. [PubMed][Cross Ref]
Delitto A, Erhard RE, Bowling RW, DeRosa CP, Greathouse DG. A treatment-based classification approach to low back syndrome: identifying and staging patients for conservative treatment. Phys Ther. 1995;75:470�485. [PubMed]
Klapow JC, Slater MA, Patterson TL, Doctor JN, Atkinson JH, Garfin SR. An empirical evaluation of multidimensional clinical outcome in chronic low back pain patients. Pain. 1993;55:107�118. doi: 10.1016/0304-3959(93)90190-Z. [PubMed][Cross Ref]
Laslett M, van Wijmen P. Low back and referred pain: diagnosis and proposed new system of classification. N Z J Physiother. 1999;27:5�14.
Maluf KS, Sahrmann SA, van Dillen LR. Use of a classification system to guide nonsurgical management of a patient with chronic low back pain. Phys Ther. 2000;80:1097�1111. [PubMed]
Petersen T, Laslett M, Thorsen H, Manniche C, Ekdahl C, Jacobsen S. Diagnostic classification of non-specific low back pain. A new system integrating patho-anatomic and clinical categories. Physiother Theory Pract. 2003;19:213�237.
Stiefel F, deJonge P, Huyse F, al INTERMED – An assessment and classification system for case complexity: Results in patients with low back pain. Spine. 1999;24:378�384. doi: 10.1097/00007632-199902150-00017. [PubMed][Cross Ref]
McCarthy CJ, Arnall FA, Strimpakos N, Freemont A, Oldham JA. The biopsychosocial classification of non-specific low back pain: a systematic review. Phys Ther Rev. 2004;9:17�30. doi: 10.1179/108331904225003955. [Cross Ref]
Batti� MC, Cherkin DC, Dunn R, Ciol MA, Wheeler KJ. Managing low back pain: attitudes and treatment preferences of physical therapists. Phys Ther. 1994;74:219�226. [PubMed]
Li LC, Bombardier C. Physical therapy management of low back pain: An exploratory survey of therapist approaches. Phys Ther. 2001;81:1018�1028. [PubMed]
Machado LAC, de Souza MS, Ferreira PH, Ferreira ML. The McKenzie protocol for low back pain: a systematic review of the literature with a meta-analysis approach. Spine (in press) 2005. [PubMed]
de Vet HCWPD, Heymans MWMS, Dunn KMMP, Pope DPPD, van der Beek AJPD, Macfarlane GJPD, Bouter LMPD, Croft PRPD. Episodes of Low Back Pain: A Proposal for Uniform Definitions to Be Used in Research. Spine. 2002;27:2409�2416. doi: 10.1097/00007632-200211010-00016. [PubMed][Cross Ref]
Pocock SJ. Clinical trials. A practical approach. 1st. Chichester , John Wiley & Sons; 1984.
Delitto A, Cibulka MT, Erhard RE, Bowling RW, Tenhula JA. Evidence for use of an extension-mobilization category in acute low back syndrome: A prescriptive validation pilot study. Phys Ther. 1993;73:216�228. [PubMed]
Schenk RJ, Jozefczyk C, Kopf A. A randomized trial comparing interventions in patients with lumbar posterior derangement. J Manual Manip Ther. 2003;11:95�102.
Farrar J, Young J, LaMoreaux L, al Clinical importance of changes in chronic pain intensity measured on an 11-point numerical pain rating scale. Pain. 2001;94:149�158. doi: 10.1016/S0304-3959(01)00349-9. [PubMed][Cross Ref]
Stratford P, Gill C, Westaway M, Binkley J. Assessing disability and change on individual patients: a report of a patient specific measure. Physiother Can. 1995;47:258�263.
Roland M, Morris R. A study of the natural history of back pain. Part I: development of a reliable and sensitive measure of disability in low-back pain. Spine. 1983;8:141�144. [PubMed]
Kalauokalani D, Cherkin D, Sherman K, Koepsell T, R D. Lessons from a trial of acupuncture and massage for low back pain. Spine. 2001;26:1418�1424. doi: 10.1097/00007632-200107010-00005. [PubMed][Cross Ref]
Werneke M, Hart DL, Cook D. A descriptive study of the centralization phenomenon. A prospective analysis. Spine. 1999;24:676�683. doi: 10.1097/00007632-199904010-00012. [PubMed][Cross Ref]
Chiropractic and Massage: Duos often create more exciting outcomes. Lewis and Clark, the Lone Ranger and Tonto, and even Batman and Robin functioned more efficiently together than apart. Complementary pairings propel results and enhance efforts.
This is decidedly true with massage therapy and chiropractic care. While each offer considerable benefits on their own, they often mesh well with each other to create a comprehensive treatment plan for many conditions or injuries.
So, sit back and let us show you how massage therapy and chiropractic care are a pain-fighting, mobility-enhancing dynamic duo.
A Combination Of Both: Chiropractic And Massage
Massage Enables A More Effective Chiropractic Visit
Therapeutic massage warms up muscles and relaxes the individual’s entire body, enabling the chiropractor to maximize his or her chiropractic adjustment for optimal results.
Massage brings about a more stable adjustment.
When a chiropractor performs an adjustment to alleviate pain or increase mobility, pre or post massage couples with it to increase the body’s acceptance of the adjustment.
Chiropractic Takes Massage Therapy Further: Includes Joints & Bones
Each treatment offers strong relief and recovery to certain areas of the body. Massage produces relaxation in muscles, relieving tension and toxins. Chiropractic care picks up where massage leaves off and extends the treatment efforts to the body’s tendons, joints, bones and, ultimately, the nervous system.
Works On The Body As A Whole
Both treatments focus on broad rejuvenation and healing techniques for full body health. In a variety of instances, chiropractic care shows significant increases in treating the overall root of the problem when used in combination with massage therapy.
Gets In The Head
Whoever said “it’s all in your head” wasn’t entirely wrong. Individuals sometimes feel stress, dread, or worry over health procedures in general, and chiropractic treatment is no different. Massage therapy serves to relax and de-stress a person, preparing them to go into chiropractic treatments less stressed or tightly wound. A relaxed person’s body tends to respond better to treatment.
Offers Shorter Recovery Times
Blending both treatments into one builds an all-encompassing regimen that works on the condition or injury from multiple points. Tackling health issues this way reduces the time is takes to heal and regain the body’s full mobility.
Decreases Discomfort
Massage therapy aids in warming up muscles, readying them for chiropractic adjustments. This experience is similar to stretching thoroughly before exercising. Pliant muscles offer less resistance to a chiropractor’s regimen, resulting in greater patient comfort. This benefits the entire process, as a painless, comfortable visit increases a person’s openness and commitment to future therapeutic endeavors.
Provides Longer Lasting Results
A relaxed body is more open to treatment. Both massage therapy and chiropractic care serve to attain the goal of healing and recovery, and pain minimization or management. Achieving a synergistic effect is possible when both treatments are employed simultaneously. Chiropractic care is known to work deeper and last longer when paired with massage therapy, especially with chronic, painful health issues.
Patients who seek help with bodily conditions or injuries benefit and see results from chiropractic and�massage therapy separately. Both forms of therapeutic relief used together may create an even more significant, longer last result. Chiropractic care and massage therapy complement each other and offer positive benefits to a variety of painful health issues.
Embark on a treatment plan with this healing, effective dynamic duo! Ask your chiropractor if your specific condition would benefit from both principles of care. Give us a call today!
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.
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.
1. Waddell G. London: Churchill Livingstone; 1998. The back pain revolution.
2. Burton AK, Balague F, Cardon G, Eriksen HR, Henrotin Y, Lahad A, et al. On behalf of the COST B13 Working Group on Guidelines for Prevention in Low Back Pain. European guidelines for prevention in low back pain – November 2004. Eur Spine J. 2006;15:s136�168. [PMC free article][PubMed]
3. Mckenzie RA. Waikanae, New Zealand: Spinal Publication Limited; 1990. Treat Your Own Back. Spinal Publication. Pu.
4. Sikorski JM, Stampfer HG, Cole RM, Wheatley AE. Psychological aspects of chronic low back pain. Aust N Zeal J Surg. 1996;66(5):294�7. [PubMed]
5. Filho IT, Simmonds MJ, Protas EJ, Jones S. Back pain, physical function, and estimates of aerobic capacity: what are the relationships among methods and measures? Am J Phys Med Rehabil. 2002;81(12):913�20. [PubMed]
6. Anderson GBJ. Epidemiologic features of chronic low-back pain. Lancet. 1999;354(9178):581�585. [PubMed]
7. World Health Organization (WHO) Scientific Group on the Burden of Musculoskeletal Conditions of the Start of the New Millennium. Geneva: WHO; 2003. The burden of musculoskeletal conditions at the start of the new millennium. [PubMed]
8. Louw QA, Morris LD, Grimmer-Somers K. The prevalence of low back pain in Africa: a systematic review. BMC Musculoskelet Disord. 2007;8:105. [PMC free article][PubMed]
9. van Tulder MW, Koes BW, Bouter LM. Conservative treatment of acute and chronic nonspecific low back pain. A systematic review of randomized controlled trials of the most common interventions. Spine. 1997;22(18):2128�56. [PubMed]
10. Quittan M. Management of Back Pain. Disabil Rehabil. 2002;24(8):423�34. [PubMed]
11. Bigos SJ, McKee J, Holland JP, Holland CL, Hildebrandt J. Back pain; the uncomfortable truth-assurance and activity paradigm. Der Schmertz. 2001;15(6):430�434. [PubMed]
12. Deyo RA, Tsui-Wu YJ. Functional disability due to low-back pain: a population-based study indicating the importance of socioeconomic factors. Arthritis Rheum. 1987;30(11):1247�1253. [PubMed]
13. Coste J, Delecoeuillerie G, Cohen de Lara A, Le Parc JM, Paolaggi JB. Clinical course and prognostic factors of acute low-back pain: an inception cohort study in primary care practice. BMJ. 1994;308(6928):577�80. [PMC free article][PubMed]
14. Picavet HS, Schouten JS. Musculoskeletal pain in the Netherlands: prevalences; consequences and risk groups; the DMC 3-study. Pain. 2003;102(1-2):167�78. [PubMed]
15. Tuzun EH. Quality of life in chronic musculoskeletal pain. Best Pract Res Clin Rheumatol. 2007;21(3):567�579. [PubMed]
17. Linton SJ. A review of psychological risk factors in back and neck pain. Spine. 2000;25(9):1148�56. [PubMed]
18. Scholich SL, Hallner D, Wittenberg RH, Hasenbring MI, Rusu AC. The relationship between pain, disability, quality of life and cognitive-behavioural factors in chronic back pain. Disabil Rehabil. 2012;34(23):1993�2000. [PubMed]
19. Geisser ME, Robinson ME, Miller QL, Bade SM. Psychosocial factors and functional capacity evaluation among persons with chronic pain. J Occup Rehabil. 2003;13(4):259�76. [PubMed]
20. Lam� IE, Peters ML, Vlaeyen JW, Kleef M, Patijn J. Quality of life in chronic pain is more associated with beliefs about pain, than with pain intensity. Eur J Pain. 2005;9(1):15�24. [PubMed]
21. Deyo RA, Andersson G, Bombardier C, Cherkin DC, Keller RB, Lee CK, et al. Outcome measures for studying patients with low back pain. Spine. 1994;19(Suppl 18):2032S�6. [PubMed]
22. Bombardier C. Outcome assessments in the evaluation of treatment of spinal disorders. Spine. 2000;25(24):3100�3. [PubMed]
23. Ware JE, Snow KK, Kosinski M, Gandek B. SF-36 Health Survey – Manual and Interpretation Guide. Boston: The Health Institute; New England Medical Center. 1993;4:3.
24. Ware JE, Jr, Sherbourne CD. The MOS 36-item shortform health survey (SF-36) I. Conceptual framework and item selection. Med Care. 1992;30(6):473�483. [PubMed]
25. Main CJ, George SZ. Psychosocial Influences on Low Back Pain: Why Should You Care? Phys Ther. 2011;91(5):609�13. [PubMed]
26. Vlaeyenm JWS, Kole-Snijders AM, Boeren RG, van Eek H. Fear of movement/(re)injury in chronic low back pain and its relation to behavioral performance. Pain. 1995;62:363�372. [PubMed]
27. Gatchel RJ, Polatin PB, Mayer TG. The dominant role of psychosocial risk factors in the development of chronic low back pain disability. Spine. 1995;20(24):2702�2709. [PubMed]
28. George SZ, Joel E Bialosky, Julie M Fritz. Beliefs Acute Low Back Pain and Elevated Fear-Avoidance Physical Therapist Management of a Patient With. Phys Ther. 2004;84(6):538�549. [PubMed]
29. H�gg O, Burckhardt C, Fritzell C, Nordwall A. Quality of Life in Chronic Low Back Pain: A Comparison with Fibromyalgia and the General Population. J Muscoskel Pain. 2003;11(1):31�38.
30. Woby SR, Watson PJ, Roach NK, Urmston M. Are changes in fear-avoidance beliefs, catastrophizing, and appraisals of control, predictive of changes in chronic low back pain and disability? Eur J Pain. 2004;8(3):201�210. [PubMed]
31. Weiner BK. Spine Update – The Biopsychosocial Model and Spine Care. Spine. 2008;33(2):219�223. [PubMed]
32. Lopez A, Mathers C, Ezzati M, Jamison D, Murray J. Global and regional burden of disease and risk factors, : Systematic analysis of population health data 2001. Lancet. 2006;367(9524):1747�57. [PubMed]
33. Australian Bureau of Statistics (ABS) Canberra: ABS; 2006. Physical activity in Australia: a snapshot, 2004-05. ABS cat. no. 4835.0.55.001.
36. Hayden JA, van Tulder MW, Tomlinson G. Systematic Review: Strategies for using exercise therapy to improve outcomes in chronic low-back pain. Ann Int Med. 2005;142(9):776�785. [PubMed]
38. Cherkin DC, Deyo RA, Battla MC, Street JH, Hund M, Barlow W. A comparison of Physical therapy chiropractice manipulation or an educational booklet for the treatment of low back pain. New Eng J Med. 1998;339(15):1021�1029. [PubMed]
39. McKenzie R, May S. Mechanical diagnosis & therapy. 2nd edition. Vol. 1. Waikanae, New Zealand: Spinal Publications New Zealand Ltd.; 2003. The lumbar spine.
40. Machado LA, de Souza MS, Ferreira PH, Ferreira ML. The McKenzie method for low back pain: a systematic review of the literature with a meta-analysis approach. Spine. 2006;31:254�262. [PubMed]
41. Ayanniyi O, Lasisi OT, Adegoke BOA, Oni-Orisan MO. Management of low back pain: Attitudes and treatment preferences of physiotherapists in Nigeria. Afr J Biomed Res. 2007;10(1):41�49.
42. Mbada CE, Ayanniyi O, Ogunlade SO. Effect of static and dynamic back extensor muscles endurance exercise on pain intensity, activity limitation and participation restriction in patients with long-term mechanical low-back pain. Med Rehabil. 2011;15(3):11�20.
43. Cohen J. In Statistical Power Analyses for Behavioural Sceinces 2nd Ed Chapter 8. New Jersey: Lawrence Erlbaum Associates; 1988. The analysis of variance and covariance: Sample size tables.
44. Bronfort G, Bouter LM. Responsiveness of general health status in chronic low back pain: a comparison of the COOP charts and the SF-36. Pain. 1999;83(2):201�9. [PubMed]
45. Taylor SJ, Taylor AE, Foy MA, Fogg AJB. Responsiveness of common outcome measures for patients with low back pain. Spine. 2001;24(17):1805�1812. [PubMed]
46. Jensen MP, McFarland CA. Increasing the reliability and validity of pain intensity measurement in chronic pain patients. Pain. 1993;55(2):195�203. [PubMed]
47. Von Korff M, Deyo RA, Cherkin D, Barlow SF. Back pain in primary care: Outcomes at 1 year. Spine. 1993:55�862. [PubMed]
48. Moffroid MT, Haugh LD, Haig AJ, Henry SM, Pope MH. Endurance training of trunk extensor muscles. Phys Ther. 1993;73:10�17. [PubMed]
49. Adegoke BOA, Babatunde FO. Effect of an exercise protocol on the endurance of trunk extensor muscles: a RCT. Hong Kong Physiother J. 2007;25:2�9.
50. Petrofsky JS, Lind AR. Aging, isometric strength and endurance; and cardiovascular responses to static effort. J Appl Physiol. 1975;38(1):91�95. [PubMed]
51. Bonde-Petersen F, Mork AL, Nielsen E. Local muscle blood flow and sustained contractions of human arm and back muscles. Eur J Appl Physiol Occup Physiol. 1975;34(1):43�50. [PubMed]
52. Chok B, Lee R, Latimer J, Beng Tan S. Endurance training of the trunk extensor muscles in people with sub acute low back pain. Phys Ther. 1999;79(11):1032�1042. [PubMed]
53. Fox EL, Bowers RW, Foss ML. 4th Ed. Philadelphia: Saunders College; 1988. The physiological basis of physical education and athletics.
54. Liddle SD, Baxter GD, Gracey JH. Exercise and chronic low back pain – what works? Pain. 2004;107(1-2):176�190. [PubMed]
55. Leboeuf-Yde C, Kyvik KO. At what age does low back pain become a common problem? A study of 29;4 24 individuals aged 12-41 years. Spine. 1998;23(2):228�34. [PubMed]
56. Underwood MR, Morton V, Farrin A, UK BEAM trial team Do baseline characteristics predict response to treatment for low back pain? Secondary analysis of the UK BEAM dataset. Rheumatology. 2007;46(8):1297�1302. [PubMed]
57. Hill JC, Fritz JM. Psychosocial influences on low back pain; disability; and response to treatment. Phys Ther. 2011;91(5):712�21. [PubMed]
58. Sengul Y, Kara B, Arda MN. The relationship between health locus of control and quality of life in patients with chronic low back pain. Turk Neurosurg. 2010;20(2):180�185. [PubMed]
59. Tavafian SS, Eftekhar H, Mohammad K, Jamshidi AR, Montazeri A, Shojaeezadeh D, Ghofranipour F. Quality of Life in Women with Different Intensity of Low Back Pain. Iran J Public Health. 2005;34(2):36�39.
60. Turner JA, Jensen MP, Romano JM. Do beliefs, coping, and catastrophizing independently predict functioning in patients with chronic pain. Pain. 2000;85(1-2):115�25. [PubMed]
61. Lyons RA, Lo SV, Littlepage BNC. Comparative health status of patients with 11 common illnesses in Wales. J Epidemiol Community Health. 1994;48(4):388�390. [PMC free article][PubMed]
62. Lurie J. A review of generic health status measures in patients with low back pain. Spine. 2000;25(24):3125�9. [PubMed]
63. Jenkinson C, Coulter A, Wright L. Short form 36 (SF 36) health survey questionnaire: normative data for adults ofworking age. BMJ. 1993;306(6890):143740. [PMC free article][PubMed]
64. Smeets RJ, Vlaeyen JW, Kester AD, Knottnerus JA. Reduction of pain catastrophizing mediates the outcome of both physical and cognitive-behavioral treatment in chronic low back pain. J Pain. 2006;7:261�271. [PubMed]
65. Verbunt JA, Seelen HA, Vlaeyen JW, van de Heijden GJ, Heuts PH, Pons K, Knottnerus JA. Disuse and deconditioning in chronic low back pain: concepts and hypotheses on contributing mechanisms. Eur J Pain. 2003;7(1):9�21. [PubMed]
66. Harding VR, Watson PJ. Increasing Activity & Improving Function In Chronic Pain Management. Physiotherapy. 2000;86(12):619�630.
67. Garcia AN, Gondo FLB, Costa RA, Cyrillo FN, Silva TM, Costa LCM, Costa LOP. Effectiveness of the back school and McKenzie techniques in patients with chronic non-specific low back pain: a protocol of a randomised controlled trial. BMC Musculoskelet Disord. 2011;12:179. [PMC free article][PubMed]
68. Udermann BE, Mayer JM, Donelson RG, Graves JE, Murray SR. Combining lumbar extension training with McKenzie therapy: Effects on pain; disability; and psychosocial functioning in chronic low back pain patients. GLMJ. 2004;3(2):7�12.
69. Kovascs FM, Abraira V, Zamora J, Fernandez C. The transition from acute to subacute and chronic low back pain: A study based on determinants of quality of life and prediction of chronic disability. Spine. 2005;30:1786�1792. [PubMed]
70. Johnson OE, Adegoke BOA, Ogunlade SO. Comparison of four physiotherapy regimens in the treatment of long-term mechanical low back pain. JJPTA. 2010;13(1):9�16. [PMC free article][PubMed]
71. Shaughnessy M, Caulfield B. A pilot study to investigate the effect of lumbar stabilisation exercise training on functional ability and quality of life in patients with chronic low back pain. Int J Rehabil Res. 2004;27(4):297�301. [PubMed]
72. Kank��np�� M, Taimela S, Airaksien OJ, Hannnien O. The efficacy of active rehabilitation in chronic low back pain. Effect on pain intensity; self-experienced disability and lumbar fatigability. Spine. 1999;24(10):1034�42. [PubMed]
73. Rainville J, Hartigan C, Martinez E, Limke J, Jouve C, Finno M. Exercise as a treatment for chronic low back pain. Spine J. 2004;4(1):106�115. [PubMed]
74. Guyatt Gordon. Insights and Limitations from Health-Related Quality-of-Life Research. Gen Intern Med. 1997;12(11):720�721. [PMC free article][PubMed]
75. Kleinman A, Eisenberg L, Good B. Culture, illness and care: clinical lessons from anthropologic and cross-cultural research. Ann Intern Med. 1978;88:251�258. [PubMed]
76. Carr AJ, Higginson IJ. Are quality of life measures patient centred? BMJ. 2001;322(7298):1357�1360. [PMC free article][PubMed]
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.
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”]
[accordion title=”References” load=”hide”]1. Drozda K, Lewandowski J, G�rski P. Back pain in lower and upper secondary school pupils living in urban areas of Poland. The case of Poznan. Ortopedia, Traumatologia, Rehabilitacja. 2011;13(5(6)):489�503. [PubMed]
2. Drozda K, Lewandowski J. Epidemiology of back pain among secondary school pupils in Poznan. Fizjoterapia Polska. 2011;4(1):31�40.
3. Dunsford A, Kumar S, Clarke S. Integrating evidence into practice: use of McKenzie-based treatment for mechanical low back pain. J Multidiscip Healthc. 2011;4:393�402. [PMC free article] [PubMed]
4. Joud A, Petersson IF, Englund M. Low back pain: epidemiology of consultations. Arthritis Care Res (Hoboken) 2012;64:b1084�88. [PubMed]
5. Lewandowski J, Szulc P, Boch-Kmieciak J, et al. Epidemiology of low back pain in students of physical education and physiotherapy. Studies in Physical Culture and Tourism. 2011;18(3):265�69.
6. Pereira LM, Obara K, Dias JM, et al. Comparing the Pilates method with no exercise or lumbar stabilization for pain and functionality in patients with chronic low back pain: systematic review and meta-analysis. Clin Rehabil. 2012;26:10�20. [PubMed]
7. Werneke MW, Hart D, Oliver D, et al. Prevalence of classification methods for patients with lumbar impairments using the McKenzie syndromes, pain pattern, manipulation, and stabilization clinical prediction rules. J Man Manip Ther. 2010;18:197�204. [PMC free article] [PubMed]
8. da C Menezes Costa L, Maher CG, Hancock MJ, et al. The prognosis of acute and persistent low-back pain: a meta-analysis. CMAJ. 2012;184:E613�24. [PMC free article] [PubMed]
9. Borges TP, Greve JM, Monteiro AP, et al. Massage application for occupational low back pain in nursing staff. Rev Lat Am Enfermagem. 2012;20:511�19. [PubMed]
10. Cherkin DC, Sherman KJ, Kahn J, et al. A comparison of the effects of 2 types of massage and usual care on chronic low back pain: a randomized, controlled trial. Ann Intern Med. 2011;155:1�9. [PMC free article] [PubMed]
11. Kilpikoski S, Al�n M, Paatelma M, et al. Outcome comparison among working adults with centralizing low back pain: Secondary analysis of a randomized controlled trial with 1-year follow-up. Adv Physiother. 2009;11:210�17.
12. Pool JJ, Ostelo RW, Knol DL, et al. Is a behavioral graded activity program more effective than manual therapy in patients with subacute neck pain? Results of a randomized clinical trial. Spine. 2010;35:1017�24. [PubMed]
13. Frankel BS, Moffett JK, Keen S, et al. Guidelines for low back pain: changes in GP management. Fam Pract. 1999;16:216�22. [PubMed]
14. McKenzie R, May S. The lumbar spine: mechanical diagnosis and therapy. 2nd ed. Waikanae: Spinal Publications; 2003.
15. Kanpandji AI. Anatomia funkcjonalna staw�w. Tom 3.6 ed. Wroc?aw: Elsevier Urban & Partners; 2010. [in Polish]
16. Alexander LA, Hancock E, Agouris I, et al. The response of the nucleus pulposus of the lumbar intervertebral discs to functionally loaded positions. Spine. 2007;32(14):1508�12. [PubMed]
17. Chaitow L. Muscle energy techniques. 3rd ed. Edinburgh: Churchill Livingstone; 2006.
18. O�Sullivan P. It�s time for change with the management of non-specific chronic low back pain. Br J Sports Med. 2012;46:224�27. [PubMed]
19. Boocock MG, Jackson JA, Burton AK, et al. Continuous measurement of lumbar posture using flexible electrogoniometers. Ergonomics. 1994;37:175�85. [PubMed]
20. Lewandowski J. Formation of physiological curvatures and segmental mobility of the human spine aged from 3 to 25 years in electrogoniometric studies. 1st ed. Poznan: AWF Poznan; 2006.
21. Szulc P, Lewandowski J, Marecki B. Verification of selected anatomic landmarks used as reference points for universal goniometer positioning during knee joints mobility range measurements. Med Sci Monit. 2001;7:312�15. [PubMed]
22. Fairbank JC, Pynsent PB. The Oswestry disability index. Spine. 2000;25:2940�52. [PubMed]
23. Hicks GE, Manal TJ. Psychometric properties of commonly used low back disability questionnaires: are they useful for older adults with low back pain? Pain Med. 2009;10:85�94. [PMC free article] [PubMed]
24. Mudgalkar N, Bele SD, Valsangkar S, et al. Utility of numerical and visual analog scales for evaluating the post-operative pain in rural patients. Indian J Anaesth. 2012;56:553�57. [PMC free article] [PubMed]
25. Fazey PJ, Takasaki H, Singer KP. Nucleus pulposus deformation in response to lumbar spine lateral flexion: an in vivo MRI investigation. Eur Spine J. 2010;19(11):1115�20. [PMC free article] [PubMed]
26. Wilson E, Payton O, Donegan-Shoaf L, et al. Muscle energy technique in patients with acute low back pain: a pilot clinical trial. J Orthop Sports Phys Ther. 2003;33:502�12. [PubMed]
27. Bronfort G, Goldsmith CH, Nelson CF, et al. Trunk exercise combined with spinal manipulative or NSAID therapy for chronic low back pain: a randomized, observer-blinded clinical trial. J Manipulative Physiol Ther. 1996;19:570�82. [PubMed]
28. Bybee RF, Olsen DL, Cantu-Boncser G, et al. Centralization of symptoms and lumbar range of motion in patients with low back pain. Physiother Theory Pract. 2009;25:257�67. [PubMed]
29. Chen J, Phillips A, Ramsey M, et al. A case study examining the effectiveness of mechanical diagnosis and therapy in a patient who met the clinical prediction rule for spinal manipulation. J Man Manip Ther. 2009;17:216�20. [PMC free article] [PubMed]
30. Garcia AN, Gondo FL, Costa RA, et al. Effects of two physical therapy interventions in patients with chronic non-specific low back pain: feasibility of a randomized controlled trial. Rev Bras Fisioter. 2011;15:420�27. [PubMed]
31. Hosseinifar M, Akbari M, Behtash H, et al. The effects of stabilization and Mckenzie exerciseson transverse abdominis and multifidus muscle thickness, pain, and disability: A randomized controlled trial in nonspecific chronic low back pain. J Phys Ther Sci. 2012;25:1541�45. [PMC free article] [PubMed]
32. Mbada CE, Ayanniyi O, Ogunlade SO, et al. 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. Pan Afr Med J. 2014;17(Supp 1):5. [PMC free article] [PubMed]
33. Garcia AN, da Cunha Menezes Costa L, Hancock MJ, et al. Efficacy of the McKenzie method in patients with chronic nonspecific low back pain: a protocol of randomized placebo-controlled trial. Phys Ther. 2015;95:267�73. [PubMed]
34. Schenk RJ, Jozefczyk C, Kopf A. A randomized trial comparing interventions in patients with lumbar posterior derangement. J Man Manip Ther. 2003;11:95�102.
35. Takasaki H, May S, Fazey PJ, et al. Nucleus pulposus deformation following application of mechanical diagnosis and therapy: a single case report with magnetic resonance imaging. J Man Manip Ther. 2010;18:153�58. [PMC free article] [PubMed]
36. Williams B, Vaughn D, Holwerda T. A mechanical diagnosis and treatment (MDT) approach for a patient with discogenic low back pain and a relevant lateral component: a case report. J Man Manip Ther. 2011;19:113�18. [PMC free article] [PubMed]
37. Chugh R, Kalra S, Sharma N, et al. Effects of muscle energy techniques and its comparison to self stretch of bilateral ankle plantarflexors on performance of balance scores in healthy elderly subjects. Physiother Occup Ther J. 2011;4:61�71.
38. Fryer G, Ruszkowski W. The influence of contraction duration in muscle energy technique applied to the atlanto-axial joint. J Osteopath Med. 2004;7:79�84.
39. Fryer G, Pearce AJ. The effect of muscle energy technique on corticospinal and spinal reflex excitability in asymptomatic participants. J Bodyw Mov Ther. 2013;17(4):440�47. [PubMed]
40. Gugliotti M. The use of mobilization, muscle energy technique, and soft tissue mobilization following a modified radical neck dissection of a patient with head and neck cancer. Rehabil Oncol. 2011;29:3�8.
41. K???k?en S, Yilmaz H, Sall? A, U?urlu H. Muscle energy technique versus corticosteroid injection for management of chronic lateral epicondylitis: Randomized controlled trial with 1-year follow-up. Arch Phys Med Rehabil. 2013;94:2068�74. [PubMed]
42. Moore SD, Laudner KG, McLoda TA, et al. The immediate effects of muscle energy technique on posterior shoulder tightness: a randomized controlled trial. J Orthop Sports Phys Ther. 2011;41:400�7. [PubMed]
43. Rajadurai V. The effect of muscle energy technique on temporomandibular joint dysfunction: a randomized clinical trail. Asian J Sci Res. 2011;4:71�77.
44. Shadmehr A, Hadian MR, Naiemi SS, et al. Hamstring flexibility in young women following passive stretch and muscle energy technique. J Back Musculoskelet Rehabil. 2009;22:143�48. [PubMed]
45. Day JM, McKeon P, Nitz A. The efficacy of cervical/thoracic active range of motion for detecting changes associated with individuals receiving muscle energy techniques. Phys Ther Rev. 2010;15:453�61.
46. Day JM, Nitz AJ. The effect of muscle energy techniques on disability and pain scores in individuals with low back pain. J Sport Rehabil. 2012;21:194�98. [PubMed]
47. Zaproudina N, Hietikko T, Hanninen OO, et al. Effectiveness of traditional bone setting in treating chronic low back pain: a randomised pilot trial. Complement Ther Med. 2009;17:23�28. [PubMed][/accordion]
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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).
Clinical Application of Neuromuscular Techniques: Scalenes
Box 4.9 Notes on Scalenes
The scalenes are a controversial muscle since they seem to be both postural and phasic (Lin et al 1994), their status being modified by the type(s) of stress to which they are exposed (see Ch. 3 for discussion of this topic).
Janda (1988) reports that �spasm and/or trigger points are commonly present in the scalenes as also are weakness and/or inhibition�.
The attachment sites of the scalene muscles vary, as does their presence. The scalene posterior is sometimes absent, and sometimes blends with the fibres of medius.
Scalene medius is noted to frequently attach to the atlas (Gray 1995) and sometimes extend to the 2nd rib (Simons et al 1998).
The scalene minimus (pleuralis), which attaches to the pleural dome, is present in onethird (Platzer 1992) to three-quarters (Simons et al 1998) of people, on at least one side and, when absent, is replaced by a transverse cupular ligament (Platzer 1992).
The brachial plexus exits the cervical column between the scalenus anterior and medius. These two muscles, together with the 1st rib, form the scalene hiatus (also called the �scalene opening� or �posterior scalene aperture�) (Platzer 1992). It is through this opening�that the brachial plexus and vascular structures for the upper extremity pass. When scalene fibres are taut, they may entrap the nerves (scalene anticus syndrome) or may elevate the 1st rib against the clavicle and indirectly crowd the vascular, or neurologic, structures (simultaneous compromising of both neural and vascular structures is rare) (Stedman 1998). Any of these conditions may be diagnosed as �thoracic outlet syndrome�, which is �a collective title for a number of conditions attributed to compromise of blood vessels or nerve fibers (brachial plexus) at any point between the base of the neck and the axilla� (Stedman 1998).
Assessment of Shortness in Scalenes (14)
Assessment of cervical sidebending (lateral flexion) strength. This involves the scalenes and levator scapulae (and to a secondary degree the rectus capitis lateralis and the transversospinalis group).
The practitioner places a stabilising hand on the top of the shoulder to prevent movement and the other on the head above the ear, as the seated patient attempts to flex the head laterally against this resistance. Both sides are assessed.
Observation assessment (a) There is no easy test for shortness of the scalenes apart from observation, palpation and assessment of trigger point activity/tautness and a functional observation as follows:
In most people who have marked scalene shortness there is a tendency to overuse these (and other upper fixators of the shoulder and neck) as accessory breathing muscles.
There may also be a tendency to hyperventilation (and hence for there to possibly be a history of anxiety, phobic behaviour, panic attacks and/or fatigue symptoms).
These muscles seem to be excessively tense in many people with chronic fatigue symptoms.
The observation assessment consists of the practitioner placing his relaxed hands over the patient�s shoulders so that the fingertips rest on the clav-icles, at which time the seated patient is asked to inhale deeply. If the practitioner�s hands noticeably rise towards the patient�s ears during inhalation then there exists inappropriate use of scalenes, which indicates that they are stressed, which also means that, by definition, they will have become shortened and require stretching treatment.
Observation assessment (b) (Fig. 4.33) Alternatively, during the history taking interview, the patient can be asked to place one hand on the abdomen just above the umbilicus and the other flat against the upper chest.
Figure 4.33 Observation assessment of respiratory function. Any tendency for the upper hand to move cephalad, or earlier than the caudad hand, suggests scalene overactivity.
On inhalation, the hands are observed: if the upper hand initiates the breathing process and rises significantly towards the chin, rather than moving forwards, a pattern of upper chest breathing can be assumed, and therefore stress, and therefore shortness of the scalenes (and other accessory breathing muscles, notably sternomastoid).
MET Treatment of Short Scalenes (Fig. 4.34A, B, C)
Patient lies supine with a cushion or folded towel under the upper thoracic area so that, unless supported by the practitioner�s contralateral hand, the head would fall into extension. The head is rotated contralaterally (away from the side to be treated). There are three positions of rotation required:
Full contralateral rotation of the head/neck produces involvement of the more posterior fibres of the scalenes
A contralateral 45� rotation of the head/neck involves the middle fibres
A position of only slight contralateral rotation involves the more anterior fibres.
The practitioner�s free hand is placed on the side of the patient�s head to restrain the isometric contraction which will be used to release the scalenes. The patient�s head is in one of the above degrees of rotation, supported by the practitioner�s contralateral hand.
Figure 4.34A MET for scalenus posticus. On stretching, following the isometric contraction, the neck is allowed to move into slight extension while a mild stretch is introduced by the contact hand which rests on the second rib, below the lateral aspect of the clavicle.
Figure 4.34B MET treatment for the middle fibres of scalenes. The hand placement (thenar or hypothenar eminence of relaxed hand) is on the 2nd rib below the centre of the clavicle.
Figure 4.34C MET treatment of the anterior fibres of the scalenes; hand placement is on the sternum
The patient is instructed to try to lift the forehead a fraction and to attempt to turn the head towards the affected side, with appropriate breathing cooperation, while resistance is applied by the practitioner�s hand to prevent both movements (�breathe in and hold your breath as you �lift and turn�, and hold this for 7�10 seconds�). Both the effort and, the counter-pressure should be modest and painless at all times.
After a 7�10 second contraction, the head is placed into extension and one hand remains on it to prevent movement during the scalene stretch.
The patient�s contralateral hand is placed (palm down) just inferior to the lateral end of the clavicle on the affected side (for full rotation of the head, posterior scalenes). The practitioner�s hand which was acting to produce resistance to the isometric contraction is now placed onto the dorsum of the patient�s �cushion� hand.
As the patient slowly exhales, the practitioner�s contact hand, resting on the patient�s hand, which is itself resting on the 2nd rib and upper thorax, pushes obliquely away and towards the foot on that same side, following the rib movement into its exhalation position, so stretching the attached musculature and fascia. This stretch is held for at least 20 seconds after each isometric contraction. The process is then repeated at least once more.
The head is rotated 45� contralaterally and the �cushion� hand contact, which applies the stretch of the middle scalenes, is placed just inferior to the middle aspect of the clavicle. When the head is in the almost upright facing position for the anterior scalene stretch, the �cushion� hand contact is on the upper sternum itself.
In all other ways the methodology is as described for the first position above.
NOTE: It is important not to allow heroic degrees of neck extension during any phase of this treatment. There should be some extension, but it should be appropriate to the age and condition of the individual.
A degree of eye movement can assist scalene treatment and may be used as an alternative to the �lift and turn� muscular effort described above. If the patient makes the eyes look caudally (towards the feet) and towards the affected side during the isometric contraction, she will increase the degree of contraction in the muscles. If during the resting phase, when stretch is being introduced, she looks away from the treated side, with eyes looking towards the top of the head, this will enhance the stretch of the muscle.
This whole procedure should be performed bilaterally several times in each of the three head positions. Scalene stretches, with all their variable positions, clearly also influence many of the anterior neck structures.
Dr. Alex Jimenez offers an additional assessment and treatment of the hip flexors as a part of a referenced clinical application of neuromuscular techniques by Leon Chaitow and Judith Walker DeLany. The scope of our information is limited to chiropractic and spinal injuries and conditions. To discuss the subject matter, please feel free to ask Dr. Jimenez or contact us at 915-850-0900 .
By Dr. Alex Jimenez
Additional Topics: Wellness
Overall health and wellness are essential towards maintaining the proper mental and physical balance in the body. From eating a balanced nutrition as well as exercising and participating in physical activities, to sleeping a healthy amount of time on a regular basis, following the best health and wellness tips can ultimately help maintain overall well-being. Eating plenty of fruits and vegetables can go a long way towards helping people become healthy.
The hips joints join the legs to the trunk of the body, and are formed by the femurs and pelvic bones. The hips are ball-and-socket type joints, where the femoral head (ball) fits into the cup-shaped acetabulum (socket) of the pelvis (Figure 1). When compared to the shoulder, which is also a ball-and-socket joint, the acetabulum is a deeper socket, and encompasses a greater area of the ball, or femoral head. This accommodation is necessary to provide stability for the hip, as it is a major weight-bearing joint, and one of the largest joints in the body. When not weight-bearing, the ball and socket of the hip joint are not perfectly fitted. However, as the hip joint bears more weight, the surface area contact increases, and the joint becomes more stable. When in a standing position, the body�s center of gravity passes through the center of the acetabula. While walking, weight-bearing stresses on the hips can be five times a person�s body weight. Healthy hips can support your weight and allow for pain-free movement. Hip injuries or disease can cause changes that affect your gait, as well as changes that affect the ability of the hips to distribute weight bearing. Abnormal stress is then placed on the joints that are above and below the hips.
The three fused hips or innominate bones that form the acetabulum include the ilium, pubis, and ischium. The ilium forms the superior aspect, the pubis forms the inferior and anterior aspect, and the ischium forms the inferior and posterior aspect. The depth of the acetabulum socket is further increased by the attached fibrocartilaginous labrum (Figure 2). In addition to providing stability to the hip joint, the labrum allows flexibility and motion. Hip joint stability can be hampered by injuries resulting from playing sports, running, overuse, or falling, as well as by disease or tumor. MRI of the hips may be ordered to assess the joint(s) for internal derangement, fracture, or degenerative joint disease. A blow to the hip joint or a fall can result in dislocation of the hip, or a hip fracture. Osteoporosis or low bone density can also lead to hip fractures. Successful prevention and/or treatment of osteoporosis may be achieved through nutrition (adequate amounts of calcium, vitamin D and phosphorus), exercise, safety measures, and medications.
Articular cartilage covers the femoral head and the acetabulum (Figure 3). This cartilage is thin but tough, flexible, smooth and slippery, with a rubbery consistency. It absorbs shock, and allows the bones to move against each other easily and without pain. It is kept lubricated by synovial fluid, which is made in the synovial membrane (joint lining). Synovial fluid is both viscous and sticky. This fluid is what allows us to flex our joints under great pressure without wear. The articular cartilage of the hip is typically about � inch thick, except in the posterior aspect of the hip socket (Figure 4). Here, the cartilage is thicker, as this area absorbs most of the force during walking, running, and jumping. MRI of the hip joint can detect problems involving both the articular cartilage and the fibrocartilaginous ring, or labrum. Cartilage has minimal blood vessels, so it is not good at repairing itself. Fraying, fissuring, and other abnormalities or defects of the cartilage can lead to arthritis in the hip joint. Contrast can be directly injected in the hip joint for a detailed look at the cartilage and labrum.
The femurs are the longest bones in the body, with large round heads that rotate and glide within the acetabula of the pelvis. The femoral head is particularly subject to pathologic changes if there is any significant alteration of blood supply (avascular necrosis). The femoral neck connects the head of the femur to the shaft. The neck ends at the greater and lesser trochanters, which are sites of muscle and tendon attachments. A disease characterized by an inadequate blood supply to the femoral head is Legg-Calve-Perthes disease, also known as LCP or simply Perthes disease. This is a degenerative disease of the hip joint that affects children, most commonly seen in boys ages two through twelve. One of the growth plates of the femoral head, the capital femoral epiphysis, is inside the joint capsule of the hip. Blood vessels that feed this epiphysis run along the side of the femoral neck, and are in danger of being torn or �pinched off� if the growth plate is damaged. This can result in a loss of blood supply to the epiphysis, leading to a deformity of the femoral head (Figure 5). The femoral head may become unstable and break easily, which can lead to incorrect healing and deformities of the entire hip joint (Figure 6). Treatment of Perthes disease is centered on the goal of returning the femoral head to a normal shape. Surgical and non-surgical treatments are used, based on the idea of �containment�- holding the femoral head in the acetabulum as much as possible, while still allowing motion of the hip joint for cartilage nutrition and healthy growth of the joint.
High level athletes and active individuals may be susceptible to a hip condition known as Femoro-Acetabular Impingement, or FAI. FAI is characterized by excessive friction in the hip joint. The femoral head and acetabulum rub abnormally, and can create damage to the articular or labral cartilage. FAI is also associated with labral tears, early hip arthritis, hyperlaxity and low back pain. FAI generally occurs in two forms: Cam and Pincer. The Cam form results in abnormal contact between the femoral head and the socket of the hip because the femoral head and neck relationship is aspherical (Figure 7). Males and those involved in significant contact sports typically display Cam impingement. Pincer impingement occurs when the acetabulum covers too much of the femoral head, resulting in the labral cartilage being pinched between the rim of the socket and the anterior femoral head-neck junction (Figure 8). Pincer impingement may be more common in women. Typically, these two forms exist together, and are labeled as �mixed impingement� (Figure 9).
Ewing�s sarcoma is a malignant bone tumor that may affect the pelvis and/or femur, thereby also affecting the stability of the hips. Like Perthes disease, Ewing�s sarcoma is more common in males, typically presenting in childhood or early adulthood. MRI is routinely used in the work-up of these malignant tumors to show bony and soft tissue extent of the tumor, and its relation to nearby anatomic structures (Figure 10). Contrast may be used to help determine the amount of necrosis within the tumor, which aids in determining the response to treatment before surgery.
Figure 10. MRI demonstrating Ewing�s sarcoma.
Ligaments Of The Hips
Hip stability is further increased by three strong ligaments that encompass the hip joint and form the joint capsule. These ligaments connect the femoral head to the acetabulum, with names suggestive of the bones they connect. They include the pubofemoral and iliofemoral ligaments anteriorly, and the ischiofemoral ligament posteriorly (Figure 11). The iliofemoral ligament is the strongest ligament in the body. However, sports and overuse can still result in sprains of these sturdy ligaments of the joint capsules of the hips. A smaller ligament, the ligamentum teres, is an intracapsular ligament that connects the tip of the femoral head to the acetabulum (Figure 12). A small artery within this ligament brings some of the blood supply to the femoral head. Damage to the ligamentum teres, and its enclosed artery, can result in avascular necrosis.
Muscles & Tendons Of The Hips
The muscles of the thigh and lower back work together to keep the hip stable, in alignment, and able to move. The hip gains stability because the hip muscles do not attach right at the joint. Hip muscles allow the movements of flexion, extension, abduction, adduction, and medial and lateral rotation. To better understand the functions of the muscles surrounding the hip, they can be divided into groups based on their locations- anterior, posterior, and medial.
The anterior thigh muscles are the main hip flexors, and are located anterior to the hip joint. Seventy percent of the thigh�s muscle mass is made up of the quadriceps femoris muscle, so named because it arises from four muscle heads- the rectus femoris, vastus medialis, vastus intermedius, and vastus lateralis (Figures 13, 14). The rectus femoris is the only one of the �quad� muscles to cross the hip joint. The sartorius muscle is found anterior to the quadriceps, and also serves as an abductor and lateral rotator of the hip. The most powerful of the anterior thigh hip flexors is the iliopsoas, which originates in the low back and pelvis and attaches at the lesser trochanter.
Posterior hip muscles include those of both the thigh and gluteal regions. The posterior thigh muscles are also known as the hamstrings- semimembranosus, semitendinosus, and biceps femoris (Figure 15). These muscles originate at the inferior pelvis, and are the extensors for the hip. They are active in normal walking motions. When the hamstrings are �tight�, they limit hip flexion when the knee joint is extended (bending forward from the waist with knees straight), and can limit lumbar movement, leading to back pain. The gluteal muscles include the gluteus maximus, medius, and minimus, six deep muscles that serve as lateral rotators, and the tensor fasciae latae. The three gluteals and the anterior sartorius muscle are all involved in abduction. The gluteus maximus is the main hip extensor, and is the most superficial of the gluteal muscles. It is involved in running and walking uphill, and assists with normal tone of the iliotibial band, which lies lateral to it. The gluteus medius and minimus both insert at the greater trochanter of the femur. The minimus is the deepest of the three gluteal muscles. Anterior to the gluteus minimus is the tensor fasciae latae muscle. It is a flexor and medial rotator of the hip, originating from the anterior superior iliac spine (ASIS) and inserting on the iliotibial band. The term �tensor fasciae latae� defines this muscle�s job- �muscle that stretches the band on the side�. This muscle helps the iliopsoas, gluteus medius, and gluteus minimus muscles during flexion, abduction and medial rotation of the thigh by making the iliotibial band taut, thereby steadying the trunk and stabilizing the hip (Figure 16). The iliotibial band or tract is not a muscle, but a thickened, fibrous band of deep fascia, or connective tissue. It is found at the lateral aspect of the thigh, and runs from the ilium to the tibia. It encloses the muscles and helps with lateral stabilization of the knee joint, as well as helping to maintain both hip and knee extension. Tightening of the iliotibial (IT) band typically causes more problems at the knee as opposed to the hip, but hip pain can result from the IT band rubbing as it passes over the greater trochanter.
The medial thigh (groin) muscles include five muscles of adduction, and one lateral rotator (Figures 17, 18). The lone lateral rotator is the obturator externus, which covers the external surface of the obturator foramen in the deep upper medial thigh. The adductors include the gracilis, the pectineus, and the adductor brevis, longus and magnus. The gracilis is the longest adductor, extending from the medial inferior aspect of the pubic bone, to the medial aspect of the tibia. The adductor magnus is the most massive of the medial muscles of the thigh.
The tendons and muscles of the hips are very powerful and create great forces, making them prone to inflammation and irritation. Tendonitis of the hip can result from repetitive movements involving the soft tissues surrounding the hip joint. Overuse of the hip joint in fitness workouts can lead to tendonitis. Tendons lose their elasticity as we age, resulting in swelling and irritation when the tendons are no longer �gliding� on their normal paths. Iliopsoas tendonitis plays a major role in snapping hip syndrome, or dancer�s hip. A snapping sensation when the hip is flexed and extended may be accompanied by an audible snapping or popping noise, as well as pain. This can be both an extra-articular and an intra-articular occurrence. Extra-articular snapping is often found in those patients with a leg length difference (the longer leg is symptomatic), those with tightness of the iliotibial band on the involved side, and those with weak hip abductors and external rotators. Lateral extra-articular snapping can be caused by the iliotibial band, tensor fascia latae or gluteus medius tendon as they slide back and forth across the greater trochanter (Figure 19). If any of these connective tissue bands thickens, they can �catch� on the greater trochanter during the motion of hip extension, thereby creating the �snapping� sensation and sound. Medial extra-articular snapping, which is less common, can occur when the iliopsoas tendon catches on the anterior inferior iliac spine, lesser trochanter, or iliopectineal ridge during hip extension. Intra-articular snapping hip syndrome is similar in many ways to the extra-articular type, but often involves an underlying mechanical problem in the lower extremity, and more intense pain. Intra-articular snapping may be indicative of a torn acetabular labrum, recurrent hip subluxation, a tear of the ligamentum teres, loose bodies, articular cartilage damage, or synovial chondromatosis (cartilage formations in the synovial membrane of the joint). Snapping hip syndrome is usually found in those ages 15-40, often in those in training for the military. It can also affect athletes, especially those involved in dance, gymnastics, soccer, and track and field. These athletes will all be performing repeated hip flexions, which can lead to tendonitis in the hip area. The repetitive motions of those involved in weightlifting and running generally lead to a thickening of the tendons in the hip region, rather than snapping hip syndrome. Prevention, or at least a lessening, of this syndrome may be found with increased stretching of the iliopsosas muscle or the iliotibial band. Surgery is usually not required, unless intra-articular pathology is present.
Figure 19. Hip muscles.
Tendon or muscle strains can occur suddenly, as in sports injuries, or they can develop over time, with symptoms including pain, swelling, muscle spasms, and difficulty moving certain muscles. MRI can be used to detect tendon and muscle tears and strains, as well as bone tumors and infection. MRI has shown good accuracy for the diagnosis of tears of the gluteus medius and gluteus minimus tendons, which are both abductor tendons of the hip. An association was found between these tears and areas of high signal intensity superior or lateral to the greater trochanter on T2-weighted images, tendon elongation in the gluteus medius, and tendon discontinuity (Figure 20). STIR and fat-suppressed T2-weighted coronal images are very sensitive for detection of areas of high signal intensity superior to the greater trochanter. Coronal T1-weighted images demonstrate tendon elongation in the gluteus medius (Figure 21). Axial images may prove superior for localizing involvement to individual abductor tendons and confirming tendon discontinuity (Figure 22). Tears of the abductor tendons may be the leading cause of greater trochanteric pain syndrome.
Figure 20. Sag. T2 shows high signal intensity superior to greater trochanter (gt) corresponding to swollen bursa (*).
Figure 21. Coronal STIR shows high signal intensity superior to greater trochanter in bursa (*) between gluteus medius (me) and gluteus minimus (mi) tendons.
Figure 22. Axial T2 shows high signal intensity corresponding to fluid replacing distal rt. gluteus medius tendon (black arrow); normal left tendon (white arrow).
Nerves Of The Hips
The nerves of the hip supply the various muscles in the hip area. The major nerves include the femoral, obturator, and lateral femoral cutaneous nerves anteriorly, and the large sciatic nerve posteriorly (Figure 23). The femoral nerve innervates the quadriceps femoris and sartorius, and is the sensory nerve to the anterior thigh. Trauma to this nerve usually occurs in the pelvis, as it passes through or near the psoas muscle. The obturator nerve passes along the lateral pelvic wall and through the obturator foramen, then splits into branches that supply the adductor muscle group. This nerve can also be subject to trauma in the pelvis due to its passage through the obturator foramen. The lateral femoral cutaneous nerve is a sensory nerve that travels along the anterolateral aspect of the thigh. It supplies sensation to the skin surface of the thigh. This is the single nerve involved in a painful condition called meralgia paresthetica, which is characterized by tingling, numbness, and burning pain in the outer part of the thigh. Meralgia paresthetica results from focal entrapment of the lateral femoral cutaneous nerve as it passes through the tunnel formed by the lateral attachment of the inguinal ligament and the ASIS. The posterior sciatic nerve passes deep to the gluteus maximus into the posterior thigh, where it innervates the hamstring muscles, on its way down to the lower leg and foot. The sciatic nerve is approximately as big around as the thumb, and is the largest single nerve in the human body. It can be injured in cases of posterior hip dislocation. Pressure on this nerve can cause nerve pain, numbness, tingling and weakness (sciatica symptoms) in the buttocks, leg, or foot, depending on the site of origin of the sciatic nerve compression.
Figure 23. Anterior and posterior views of the nerves of the hip.
Arteries & Veins Of The Hips
The arterial blood vessels that supply the hips are branches of the internal and external iliacs. The internal iliac artery gives off the superior and inferior gluteals, and the obturator artery. The inferior gluteal flows to the posterior aspect of the hip joint and proximal femur, where it joins a branch of the femoral artery. The obturator artery runs through the obturator foramen, and sends its acetabular branch to the ligamentum teres as part of the blood supply to the femoral head. The external iliac becomes the femoral artery, which has numerous branches that supply the hip and proximal femur. The largest femoral branch is the profunda femoris, which branches superiorly into the medial and lateral circumflex femorals (Figure 24). The circumflex femorals and the inferior gluteal artery contribute to the anastomoses to supply the femoral head, femoral neck, and the hip joint. The medial circumflex also has an acetabular branch to the ligamentum teres. Congenital anomalies in the hip anastomoses, degenerative processes, and trauma can all compromise the blood supply to the hip joint area.
Figure 24. Anterior and posterior views of the arteries of the hip.
Venous flow in the hip and proximal femur typically follows the arterial flow, including the same names for the vessels. The deep veins of the hip and thigh can be the origination of a deep vein thrombosis, which can result in a pulmonary embolus. This can be caused by immobility after hip surgery, sitting in cars or airplanes for extended trips, being overweight, or slow or low blood flow. These blood clots can break off, travel through the larger veins of the thigh and hip, continue through the heart, and become lodged in the smaller vessels of the lung. MRI is being used more frequently to diagnose this very serious condition.
Bursae Of The Hips
The hip joint is surrounded by bursae, similar to the shoulder. These fluid-filled sacs are lined with a synovial membrane, which produces synovial fluid. Their function is to lessen the friction between tendon and bone, ligament and bone, tendons and ligaments, and between muscles. There may be as many as 20 bursae around the hip. If they become infected or inflamed, the result is a painful condition called bursitis. Common hip bursae that may become inflamed include the greater trochanteric bursa, the iliopsoas bursa, and the ischial bursa (Figure 25). The greater trochanteric bursa is sandwiched between the greater trochanter of the femur, and the muscles and tendons that cross over it. If this bursal sac becomes inflamed, patients experience pain with every step they take, as each step requires the tendon to move over the femur at the hip joint. A tight iliotibial band can also cause irritation of the greater trochanteric bursa. Iliopsoas bursitis can result from irritation of the bursa found between the hip joint and the iliopsoas muscle that passes in front of it. Another common site for bursitis is the ischial bursa, which acts as a lubricating pad between tendons and the ischial tuberosity, which is the bony prominence of the pelvis that you sit on. The ischial bursa acts to prevent destruction of the tendons as they move over the ischial tuberosity. Prolonged sitting can cause ischial bursitis. Inflammation around the ischial tuberosity can irritate the sciatic nerve, and trigger symptoms similar to sciatica. Hip bursitis is seen in runners and athletes in sports that involve excessive running (soccer, football, etc.). It can also be caused by an injury (traumatic bursitis), and is seen in post-op hip replacement and hip surgery patients. Treatment for hip bursitis typically includes rest, anti-inflammatory medications, and ice. It may become necessary to aspirate the bursa, which can be combined with a cortisone injection. MRI may be needed if the diagnosis is unclear, or if the problem does not resolve with normal treatments.
Figure 25. Bursae of the hip.
Axial Scans
When positioning unilateral axial slices for the hip, a coronal image can be used to ensure inclusion of all pertinent anatomy. The slices should extend superiorly to include the entire femoral head and acetabulum, and inferiorly to include anatomy below the lesser trochanter. The slices should be aligned perpendicular to the shaft of the femur, as seen in the coronal image in Figure 39.
Figure 39. Axial slice setup using sagittal and coronal images.
For bilateral axial hip slice setup, parameters may have to be altered to maintain adequate resolution with the larger FOV that is required (Figure 40). The slice group may require angulation to maintain alignment of the femoral heads on the resultant images.
Figure 40. Bilateral axial slice setup using a coronal image.
Coronal Scans
Coronal slices of the hip should cover the area from the posterior margin to the anterior margin of the femoral head. The area from the proximal margin of the femoral shaft to the greater sciatic notch should be included in the image (Figure 41). Slices may be angled so that they are parallel to the femoral neck. Thinner slices may be requested for coronal scanning.
Figure 41. Coronal slice setup using axial and sagittal images.
Sagittal Scans
Sagittal slices of the hip should extend past the greater trochanter laterally, and through the acetabulum medially. The slices should be aligned along the long axis of the femur, and perpendicular to the coronal slices, as seen in the coronal image in Figure 42. Two different slice groups will be necessary when performing bilateral sagittal scans.
Figure 42. Sagittal slice setup using coronal and axial images.
Hips Arthrography
MR hip arthrography is often times referred to as the gold standard for assessment of the labrum of the hip. The most clinically significant abnormal findings that result from hip arthrography are labral detachments and tears. Detachment of the labrum, which is more common than a labral tear, can be diagnosed from the appearance of the injected contrast at the acetabular-labral interface (Figure 43). A labral tear can result in injected contrast appearing within the substance of the labrum (Figure 44). Contrast injection is necessary to differentiate torn or detached labra from other pathologic conditions, which may have separate signal intensities. The sensitivity and accuracy for the diagnosis of labral tears and detachment with MR arthrography vs. nonarthrographic MR is 90%. Hip arthrography with MR can also depict intrarticular loose bodies, osteochondral abnormalities, and abnormalities of soft-tissue structures.
Hip arthrography can be performed under fluoro in the x-ray dept., with the patient being moved to the MRI dept. for further imaging, or the entire procedure can be performed in the MRI suite, if MR compatible supplies are available for interventional techniques. The patient should be securely positioned with the hips in internal rotation.
T1-weighted imaging is performed post-contrast to visualize the high signal of the intraarticular contrast. T1 gradient echo sequences offer the benefits of thin sections, elimination of partial volume averaging, and increased detection of small tears. Fatsat sequences are helpful in increasing the contrast between the injected contrast and the adjacent soft tissue. STIR or fatsat T2 sequences performed in the coronal plane may help to detect unsuspected pathologic conditions in the soft tissue and adjacent osseous structures.
Post-contrast axial oblique images have been shown to optimize the detection of the most common sports-related acetabular labral tears, which are anterior or anterosuperior in location. Using a mid-coronal localizer, the axial oblique slices should be prescribed parallel to the long axis of the femoral neck.
Figure 43. Labral detachment as seen in a fat-suppressed T1-wtd. sag. image; arrowheads indicate involvement of anterior and anterosuperior labrum.
Figure 44. Labral tear as seen in a T1-wtd. image; arrowheads indicate enlarged labrum; short arrow indicates linear intralabral collection of contrast material; long arrow indicates communication between the joint and the iliopsoas bursa.
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References:
Kapit, Wynn, and Lawrence M. Elson. The Anatomy Coloring Book. New York: HarperCollins, 1993.
Hip Anatomy, Function, and Common Problems. (Last updated 28July2010). Retrieved from http://healthpages.org/anatomy-function/hip-structure-function-common-problems/
Cluett, J. M.D. (Updated 22May2012). Labral Tear of the Hip Joint. Retrieved from http://orthopedics.about.com/od/hipinjuries/qt/labrum.htm
Hughes, M. D.C. (15July2010). Diseases of the Femur Bone. Retrieved from http://www.livestrong.com/article/175599-diseases-of-the-femur-bone/
A Patient�s Guide to Perthes Disease of the hip. (n.d.). Retrieved from http://www.orthopediatrics.com/docs/Guides/perthes.html
Hip Injuries and Disorders. (Last reviewed 10February2012). Retrieved from http://nlm.nih.gov/medlineplus/hipinjuriesanddisorders.html
Ligament of head of femur. (Updated 20December2011). Retrieved from http://en.wikipedia.org/wiki/Ligament_of_head_of_femur
Ewing�s sarcoma. (Last modified 06January2012). Retrieved from http://en.wikipedia.org/wiki/Ewing%27s_sarcoma
Hip Anatomy. (n.d.). Retrieved from http://www.activemotionphysio.ca/Injuries-Conditions/Hip
Iliotibial Band Friction Syndrome. (n.d.). Retrieved from http://www.physiotherapy-treatment.com/iliotibial-band-friction-syndrome.html
Snapping hip syndrome. (Last modified 09November2011). Retrieved from http://en.wikipedia.org/wiki/Snapping_hip_syndrome
Sekul, E. (Updated 03February2012). Meralgia Paresthetica. Retrieved from http://emedicine.medscape.com/article/1141848-overview
Yeomans, S. D.C. (Updated 07July2010). Sciatic Nerve and Sciatica. Retrieved from http://www.spine-health.com/conditions/sciatica/sciatic-nerve-and-sciatica
Mayo Clinic staff. (26July2011). Meralgia paresthetica. Retrieved from http://www.mayoclinic.com/health/meralgia-paresthetica/DS00914
Deep Vein Thrombosis (DVT)-Blood Clots in the Legs. (n.d.). Retrieved from http://catalog/nucleusinc.com/displaymonograph.php?MID=148
Petersilge, C. M.D. (03May2000). Chronic Adult Hip Pain: MR Arthrography of the Hip. Retrieved from http://radiographics.rsna.org/content/20/suppl_1/S43.full
Acetabular branch of medial circumflex femoral artery. (Last modified 17November2011). Retrieved from http://en.wikipedia.org/wiki/Acetabular_branch_of_medial_circumflex_femoral_artery
Cluett, J. M.D. (Updated 26March2011). Hip Bursitis. Retrieved from http://orthopedics.about.com/cs/hipsurgery/a/hipbursitis.htm
Steinbach, L. M.D., Palmer, W. M.D., Schweitzer, M. M.D. (10June2002). Special Focus Session MR Arthrography. Retrieved from http://radiographics.rsna.org/content/22/5/1223.full
Schueler, S. M.D., Beckett, J.M.D., Gettings, S.M.D. (Last updated 05August2010). Ischial Bursitis/Overview. Retrieved from http://www.freemd.com/ischial-bursitis/overview.htm
Hwang, B., Fredericson, M., Chung, C., Beaulieu, C., Gold, G. (29October2004). MRI Findings of Femoral Diaphyseal Stress Injuries in Athletes. Retrieved from http://www.ajronline.org/content/185/1/166.full.pdf
The Femur (Thigh Bone). (n.d.). Retrieved from http://education.yahoo.com/reference/gray/subjects/subject/59
Norman, W. PhD, DSc. (n.d.). Joints of the Lower Limb. Retrieved from http://home.comcast.net/~wnor/lljoints.htm
Femur. (Last modified 24September2012). Retrieved from http://en.wikipedia.org/wiki/Femur
Wheeless, C. III, M.D. (Last updated 25April2012). Ligaments of Humphrey and Wrisberg. Retrieved from http://wheelessonline.com/ortho/ligaments_of_humphrey_and_wrisberg
Muscle Strains in the Thigh. (Last reviewed August2007). Retrieved from http://orthoinfo.aaos.org/topic.cfm?topic=A00366
Shiel, W. Jr., M.D. (Last reviewed 23July2012). Hamstring Injuries. Retrieved from http://www.medicinenet.com/hamstring_injury/article.htm
Hamstring Muscle Injuries. (Last reviewed July 2009). Retrieved from http://orthoinfo.aaos.org/topic.cfm?topic=a00408
Knee. (Last modified 19September2012). Retrieved from http://en.wikipedia.org/wiki/Knee
DeBerardino, T. M.D. (Updated 30March2012). Quadriceps Injury. Retrieved from http://emedicine.medscape.com/article/91473-overview
Kan, J.H. (n.d.). Osteochondral Abnormalities: Pitfalls, Injuries, and Osteochondritis Dissecans. Retrieved from http://www.arrs.org/shopARRS/products/s11p_sample.pdf
Nerves of the Lower Limb. (Last updated 30March2006). Retrieved from http://download.videohelp.com/vitualis/med/lowrnn.htm
The Adductor Canal. (Last updated 30March2006). Retrieved from http://download.videohelp.com/vitualis/med/addcanal.htm
Nabili, S. M.D. (n.d.). Varicose Veins & Spider Veins. Retrieved from http://www.medicinenet.com/varicose_veins/article.htm
Basic Venous Anatomy. (n.d.). Retrieved from http://vascular-web.com/asp/samples/sample104.asp
Femoral nerve. (Last modified 23September2012). Retrieved from http://en.wikipedia.org/wiki/Femoral_nerve
Peron, S. RDCS. (Last modified 16October2010). Anatomy � Lower Extremity Veins. Retrieved from http://www.vascularultrasound.net/vascular-anatomy/veins/lower-extremity-veins
Medical Multimedia Group, L.L.C. (n.d.). Knee Anatomy. Retrieved from http://www.eorthopod.com/content/knee-anatomy
Knee Joint Anatomy, Function and Problems. (Last updated 06July2010). Retrieved from http://healthpages.org/anatomy-function/knee-joint-structure-function-problems/
Coronary ligament of the knee. (Last modified 09May2010). Retrieved from http://en.wikipedia.org/wiki/Coronary_ligament_of_the_knee
Walker, B. (n.d.). Patellar Tendonitis Treatment � Jumper�s Knee. Retrieved from http://www.thestretchinghandbook.com/archives/patellar-tendonitis.php
Osgood-Schlatter disease. (Last reviewed 12November2010). Retrieved from http://www.ncbi.nlm.nih.gov/pubmedhealth/PMH0002238/
Grelsamer, R. M.D. (n.d.). The Anatomy of the Patella and the Extensor Mechanism. Retrieved from http://kneehippain.com/patient_pain_anatomy.php
Oblique popliteal ligament. (Last modified 24March2012). Retrieved from http://en.wikipedia.org/wiki/Oblique_popliteal_ligament
Shiel, W. Jr., M.D. (Last reviewed 27July2012). Chondromalacia Patella (Patellofemoral Syndrome). Retrieved from http://www.medicinenet.com/patellofemoral_syndrome/article.htm
Knee. (Last modified 19September2012). Retrieved from http://en.wikipedia.org/wiki/Knee
Mosher, T. M.D. (Last updated 11April2011). MRI of Knee Extensor Mechanism Injuries Overview of the Knee Extensor Mechanism. Retrieved from http://emedicine.medscape.com/article/401001-overview
Carroll, J. M.D. (December 2007). Oblique Menisco-meniscal Ligament. Retrieved from http://radsource.us/clinic/0712
DeBerardino, T. M.D. (Last updated 30March2012). Medial Collateral Knee Ligament Injury. Retrieved from http://emedicine.medscape.com/article/89890-overview#a0106
Farr, G. (Last updated 31December2007). Joints and Ligaments of the Lower Limb. Retrieved from http://becomehealthynow.com/article/bodyskeleton/951/
Knee anatomy overview. (02March2008). Retrieved from http://www.kneeguru.co.uk/KNEEnotes/node/741
Dixit, S. M.D., Difiori, J. M.D., Burton, M. M.D., Mines, B. M.D. (15January2007). Management of Patellofemoral Pain Syndrome. Retrieved from http://www.aafp.org/afp/2007/0115/p194.html
Knee Muscles. (Last updated 05September2012). Retrieved from http://www.knee-pain-explained.com/kneemuscles.html
Popliteus muscle. (Last updated 20February2012). Retrieved from http://en.wikipedia.org/wiki/Popliteus_muscle
Kneedoc. (10February2011). Nerves. Retrieved from http://thekneedoc.co.uk/neurovascular/nerves
Wheeless, C. III, M.D. (Last updated 15December2011). Popliteal Artery. Retrieved from http://wheelessonline.com/ortho/popliteal_artery
The Popliteal Artery. (n.d.) Retrieved from http://education.yahoo.com/reference/gray/subjects/subject/159
Knee bursae. (Last updated 09May2012). Retrieved from http://en.wikipedia.org/wiki/Bursae_of_the_knee_joint
Hirji, Z., Hunjun, J., Choudur, H. (02May2011). Imaging of the Bursae. Retrieved from http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3177464/
Kimaya Wellness Limited. (n.d.). Organ>Popliteal Artery. Retrieved from http://kimayahealthcare.com/OrganDetail.aspx?OrganID=103&AboutID=1
Total Vein Care. (Last updated 24February2012). Varicose Vein Anatomy and Function for Patients. Retrieved from http://www.veincare.com/education/
Tibia. (Last updated 01April2012). Retrieved from http://en.wikipedia.org/wiki/Tibia
Norkus,S., Floyd, R. (Published 2001). The Anatomy and Mechanisms of Syndesmotic Ankle Sprains. Retrieved from http://www.ncbi.nlm.nih.gov/pmc/articles/PMC155405/
Soleus muscle. (Last updated 10April2012). Retrieved from http://en.wikipedia.org/wiki/Soleus_muscle
Achilles Tendinitis. (Last reviewed June2010). Retrieved from http://orthoinfo.aaos.org/topic.cfm?topic=A00147
Wheeless, C. III,M.D. (Last updated 11April2012). Sural Nerve. Retrieved from http://wheelessonline.com/ortho/sural_nerve
Medical Multimedia Group, L.L.C. (Last updated 26July2006). Ankle Syndesmosis Injuries. Retrieved from http://www.orthogate.org/patient-education/ankle/ankle-syndesmosis-injuries.html
Cluett, J. M.D. (Last updated 16September2008). Exertional Compartment Syndrome. Retrieved from http://orthopedics.about.com/od/overuseinjuries/a/compartment.htm
Leg Veins (Thigh, Lower Leg) Anatomy, Pictures and Names. (Last updated 21November2010). Retrieved from http://www.healthype.com/leg-veins-thigh-lower-leg-anatomy-pictures-and-names.html
Cluett, J.M.D. (Last updated 6October2009). Stress Fracture. Retrieved from http://orthopedics.about.com/cs/otherfractures/a/stressfracture.htm
Ostlere, S. (1December2004). Imaging the ankle and foot. Retrieved from http://imaging.birjournals.org/content/15/4/242.full
Inverarity, L. D.O. (Last updated 23January2008). Ligaments of the Ankle Joint. Retrieved from http://physicaltherapy.about.com/od/humananatomy/p/ankleligaments.htm
Golano, P., Vega, J., DeLeeuw, P., Malagelada, F.,Manzanares, M., Gotzens, V., van Dijk, C. (Published online 23March2010). Anatomy of the ankle ligaments:a pictorial essay. Retrieved from http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2855022/
Numkarunarunrote, N., Malik, A., Aguiar, R.,Trudell, D., Resnick, D. (11October2006). Retinacula of the Foot and Ankle: MRI with Anatomic Correlation in Cadavers. Retrieved from http://www.ajronline.org/content/188/4/W348.full
Medical Multimedia Group, L.L.C. (n.d.). A Patient�s Guide to Ankle Anatomy. Retrieved from http://www.eorthopod.com/content/ankle-anatomy
The Anterior Tibial Artery. (n.d.). Retrieved from http://education.yahoo.com/reference/gray/subjects/subject/160
Foot and Ankle Anatomy. (Last updated 28July2011). Retrieved from http://northcoastfootcare.com/pages/Foot-and-Ankle-Anatomy.html
Donnelly, L., Betts, J., Fricke, B. (1July2009). Skimboarder�s Toe: Findings on High-Field MRI. Retrieved from http://www.ajronline.org/content/184/5/1481.full
Foot. (Last updated 28August2012). Retrieved from http://en.wikipedia.org/wiki/Foot
Wiley, C. (n.d.). Major Ligaments in the Foot. Retrieved from http://www.ehow.com/list_6601926_major-ligaments-foot.html
Turf Toe: Symptoms, Causes, and Treatments. (Last reviewed 9August2012). Retrieved from http://www.webmd.com/fitness-exercise/turf-toe-symptoms-causes-and-treatments
Cluett, J. M.D. (Last updated 02April2012). Turf Toe. Retrieved from http://orthopedics.about.com/od/toeproblems/p/turftoe.htm
Neurology and the Feet. (n.d.) Retrieved from http://footdoc.ca/www.FootDoc.ca/Website%20Nerves%20Of%20The%20Feet.htm
The Veins of the Lower Extremity, Abdomen, and Pelvis. (n.d.). Retrieved from http://education.yahoo.com/reference/gray/subjects/subject/173
Corley, G., Broderick, B., Nestor, S., Breen, P., Grace, P., Quondamatteo, F., O�Laighin, G. (n.d.). The Anatomy and Physiology of the Venous Foot Pump. Retrieved from http://www.eee.nuigalway.ie/documents/go_anatomy_of_the_plantar_venous_plexus_manuscript.pdf
Morton�s neuroma. (Last modified 8August2012). Retrieved from http://en.wikipedia.org/wiki/Morton%27s_metatarsalgia
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MRI may be requested for:
