Piriformis Syndrome

Piriformis Syndrome: Myth, Misdiagnosis or Just Rare?

10 Causes of Sciatica and Gluteal Pain, Part 1

By Marc Heller, DC

OK, so I've hinted at my opinion already in the title. I am skeptical of piriformis syndrome (PS). I think it is a rare condition. When the concept was first birthed, it was based on the idea that there are causes of sciatica other than a herniated disc.

At the time, within standard medical thinking this was an advance. I am using the term sciaticaloosely, the way patients use it: any pain or abnormal sensation in the buttock, hamstring or posterior leg.

True discogenic sciatica is a much more clear-cut entity, with positive straight-leg raise, pain going below the knees, and dermatomal referral patterns. Many of your patients come in complaining of an achy buttock or strange sensations in the lower extremity, but do not have true discogenic sciatica. I am sure PS is diagnosed far more often than it should be.

Research suggests the piriformis is bisected by the sciatic nerve in only 17 percent of cases. Even more daunting, when surgery was done to free the sciatic nerve from purported piriformis entrapment, the piriformis was pierced by the nerve in only 16.2 percent of cases.¹

Some recent research has been done on piriformis syndrome. Four features appear to be most common: buttock pain, aggravation of sciatica through sitting, external tenderness over the greater sciatic notch, and augmentation of the pain with maneuvers that increase piriformis muscle tension.²

The FAIR test is interesting. The test involves taking the lower limb into hip flexion, adduction and internal rotation, creating tension in the piriformis. Does this increase the symptoms? One attempt to verify the syndrome added testing the H reflex while doing the FAIR test. The working definition used these days does not appear to require the piriformis to be bisected by the sciatic nerve. It posits that other strains, or excessive tension in the piriformis or the other external rotators, can irritate or constrict the sciatic nerve.

Don't do this! This piriformis stretch takes the lumbar spine into passive flexion. Holding it for 30 seconds can irritate a flexion-intolerant disc.My observation is that the term piriformis syndromeis used loosely and far too often by manual practitioners to diagnose the cause of buttock pain. This then leads the therapist to focus on stretching the piriformis and doing manual techniques to attempt to address the tight piriformis. This is usually done without a formal diagnosis and ignores what I believe are more common causes of buttock pain.

Here is what I think: Gluteal or buttock pain is common, and has many contributors and causes. Dysfunction of many structures can produce sclerotomal referral patterns into the buttock and legs. One of our strengths as manual practitioners is to recognize that most pain has multiple causes and contributors. One of our main jobs is to diagnose, tease out and address the multiple factors contributing to any painful condition. Pain is a liar, and many tissues create referred pain when they are irritated.

Check out this fascinating page describing Kellgren and Lewis's experiments, in which they self-injected hypertonic saline into muscles, tendons, ligaments and bones.³ If the piriformis is tight, I suspect it is an effect, rather than a cause. That doesn't mean it might not be useful to treat the piriformis area with various soft-tissue techniques. It does mean we may get more lasting results if we can figure out whatelse is contributing.

Six (of 10) Possible Causes of Buttock Pain

Let's examine the first six of 10 possible causes of buttock pain, and describe and attempt to differentiate each one. First, all of these are going to cause some variation on soft-tissue pain, with a bewildering variety of presentations and no easy, clear-cut answers. Carolyn McMakin's recent article in DC on "the challenging 20 percent" [April 15 issue, special section on managing pain] was an excellent overview of the underlying issues in chronic spinal pain.⁴

One of the things I love about being a manual practitioner is the opportunities to not only diagnose, but also to treat and observe changes. Using short therapeutic trials is a great way to get better as a practitioner, providing clearly targeted treatment. Here are the first six possible causes of a "pain in the butt."

1. Thoracolumbar Joint Dysfunction

This can cause irritation of the superior cluneal nerve, which provides sensory supply to the buttock. This phenomenon is so common, and yet so rarely consciously addressed. The superior cluneal nerve provides the sensory nerve supply to the flank and buttock. When they are irritated, the patient may complain of flank or buttock pain.

Don't miss this. The diagnosis is based on two factors: one is a palpable tender knot (Maigne's point), 7-8 cm lateral to the PSIS, on the upper glutes, just below the iliac crest; the second is joint restriction with significant restriction and tenderness (usually most obvious on the lateral margin of the involved spinous process), between T10 and L2. The solution is usually simple: mobilize the stuck joints. See Maigne's original work on this⁵ and read my article on this topic.⁶

2. Axial Discogenic Pain

Having just finished sitting for most of 27 hours while flying back from Australia, my left buttock aches. It will resolve in about three days, especially if I walk and decompress enough. Despite the fact that disc problems mostly cause lower back pain, rather than true nerve-root sciatica, they often secondarily refer into the buttock and thigh. Qualities of these patients include flexion intolerance (especially prolonged flexion), and improvement from decompression and extension. This diagnosis is often missed; many doctors think of the disc only in sciatica. This condition, whether we think of it as a torn disc or as pain from a degenerated disc, is common.

Unfortunately, it is difficult to have absolute clarity in diagnosis. As discograms are dangerous⁷ and MRIs don't reliably diagnose torn discs, it is realistically a preponderance-of-the-evidence diagnosis. (Note: These patients are flexion intolerant. The classic figure-four piriformis stretch, especially when done supine, can put them into lumbar flexion and irritate the disc, leading to lower back and buttock pain.⁸Half the battle is stopping the patient from doing stupid stuff.)

3. Referral From the Key Ligaments of the Pelvis⁹

Pain is a liar. You might find the pain by overpressure or stretching the involved ligaments, but I tend to prefer palpation for tenderness and changes in tissue texture. Once in a while, palpation will create referred pain right to the area of pain; more often, you will just find tenderness.

The sacrotuberous ligament. Note the extension and insertion of the ligament, anterior along the ischial ramus from the ischial tuberosity.
Image courtesy of Primal PicturesFocus on the sacrotuberous ligament. Don't forget the long dorsal SI ligament, which the medial origins of the gluteus maximus overlie. Check out the iliolumbar ligament, also challenging to palpate. The prolotherapy world talks about ligamentous referral, mostly based on Hackett's book, which was published in 1958.¹⁰It is fascinating work: He injected ligaments on normal people with hypertonic saline, and noted where the pain referred to.Click here for the chart of these ligament referral patterns.¹¹There is very little modern peer-reviewed literature on these ligamentous referral patterns.

Often the key ligament is the sacrotuberous, either at its origin at the lower sacrum, or along its insertion. It is a frequent culprit, but is so rarely properly examined. The problem: The insertions of the sacrotuberous ligament are deep in the pelvis, where most practitioners are quite hesitant to touch. The sacrotuberous extends much further anterior than most texts show. When ligaments are tender, they are dysfunctional. The sacrotuberous often refers pain or abnormal sensation all the way to the ankle and foot.

Here is how to examine and treat the insertions of the sacrotuberous ligament. Tell the patient what you are going to do, and ask for explicit permission. Lay the patient on their involved side, bend the opposite leg up to 90-90, and rest the upper leg on a large pillow or bolster. Now, on the medial side of the lower thigh, slide your fingers anterior, starting at the ischial tuberosity and working your way anterior along the ischial ramus.

You are pressing in an inferior direction. You want your fingers to be directly in contact with the bone, where the ligament inserts. Where the ligament is tender, apply manual cross-frictional massage. I rarely use my metal tools here; it is too sensitive of an area. Do not be too vigorous or treat for over 2 minutes, especially the first time you do this on a patient. They can get very sore very easily.

4. The Internally Rotating Hip

This creates excessive length of the small muscles of the posterior pelvis,¹² as emphasized in Shirley Sahrmann's model. The archetype would be the younger, female patient, with valgus knees, pronated feet and a hip that rotates inward too easily. Use a lunge test and watch for the valgus knee. The main thing to rethink is whether these muscles are tight and short, or long and weak.

When the hip rotates internally, the piriformis and its companion muscles will be over-lengthened and overstretched. An overstretched muscle can certainly feel tight to the touch. It can certainly have trigger points within it. It can feel good in the moment to stretch the area. But the common understanding of piriformis syndrome, that the patient needs to stretch the piriformis, is clearly wrong for the patient with an internally rotating hip.

Muscle testing, both functionally and directly, is useful here to assess for weakness of the glutes and piriformis. Instead of stretching, train the whole group, including the gluteus medius and gluteus maximus, for strength and motor control. Wake up the glutes; they are weak. Yes, go ahead and do your manual work, whether ART, Graston or manual release, but the key therapy is rehab exercise.

5. Evaluate the Sacroiliac

Emphasize the sacral side of the joint. When the sacrum is stuck, the piriformis will be unhappy. The sacral side of the joint is often missed here.¹³ (The exam findings are too complex for this article.) The piriformis does directly originate from the lower sacrum; if you are strictly correcting iliac misalignment, you will miss many significant dysfunctions.

In the muscle-energy system of osteopathy, a tight piriformis is one of the factors noted in an anterior sacral torsion. This is probably obvious to chiropractors, but the point is that the SI joint is a very important piece. Stuck joints will keep muscles from working correctly. The SI joint and its ligaments are important sources of referred pain into the anterior and posterior pelvis, and down the leg.

6. Let's Not Forget the Lower Lumbar Spine

The exam can include pain on extension or oblique extension, combined with motion palpation, as well as searching for tender points at the facet or over the spinous process. When L3, L4 or L5 are not moving well, the facet joints may refer to the buttock. Lumbar dysfunction will create or co-exist with muscular dysfunction around the core and pelvis.

In the second half of this article, I will explore four more sources of buttock pain, including the hip joint itself; the oversensitized sciatic nerve as a treatable entity; how core stability affects these patterns; and fascial restrictions affecting the lumbar and pelvic region.

The essence of my message is simple: When the patient has buttock pain, do not assume that either the nerve root or the piriformis muscle is the sole cause. Search for and treat the possible contributors.

References

1. Smoll NR. Variations of the piriformis and sciatic nerve with clinical consequence: a review. Clin Anat, 2010 Jan;23(1):8-17.
2. Hopayian K, Song F, Riera R, Sambandan S. The clinical features of the piriformis syndrome: a systematic review. Eur Spine J, 2010 Dec 19(12): 2095–2109.
3. Altman LK. Who Goes First?: The Story of Self-Experimentation in Medicine. University of California Press, 1987.
4. McMakin C. "The Challenging 20 Percent: Simplifying the Treatment of Chronic Pain." Dynamic Chiropractic, April 15, 2013.
5. Maigne R. Low back pain of thoraco-lumbar origin. Arch Phys Med & Rehab, 1980;61:389-9.
6. Heller M. "Thoracolumbar Junction or Superior Cluneal Nerve Entrapment Syndrome: : A Hidden Source of Low Back & Pelvic Pain." Dynamic Chiropractic, Nov. 4, 2011.
7. Carragee EJ, Don AS, Hurwitz EL, Cuellar JM, Carrino JA, Herzog R. 2009 ISSLS prize winner: does discography cause accelerated progression of degeneration changes in the lumbar disc: a ten-year matched cohort study. Spine, 2009 Oct 1;34(21):2338-45.
8. Heller M. "Stop Stretching - or at Least Stop Stretching the Lower Back Into Flexion and Rotation."Dynamic Chiropractic, Dec. 12, 2012.
9. Heller M. "Sacroiliac Revisited: The Importance of Ligamentous Integrity." Dynamic Chiropractic, July 7, 2005.
10. Hackett GS. Ligament and Tendon Relaxation (Skeletal Disability) Treated By Prolotherapy (Fibro-Osseous Proliferation). Charles C. Thomas Pub Ltd, 1958.
11. Chart depicting ligament referral patterns:www.journalofprolotherapy.com/images/issue_02/prolo_for_pelvic_pain_figure_02.jpg
12. Heller M. "The Internally Rotating Hip." Dynamic Chiropractic, July 29, 2009.
13. Heller M. "The Sacral Side of the SI Joint: Correcting Anterior and Posterior Torsions." Dynamic Chiropractic, Dec. 16, 2010.

The Neuromuscular Neutral Zone, Dynamic Stability, and Injury/Pain in the Course of Everyday Activity

By Malik Slosberg, DC, MS

Understanding the dysfunctions that may destabilize joints offers new insights into the mechanisms that can be influenced by chiropractic adjustments to enhance dynamic joint stability. Recent research has brought into focus the critical relationship between unconscious sensory input from deep articular and periarticular structures and reflexive motor responses, which are essential to protect joints from injury.

Let's review these new advances in our understanding of the neuromotor mechanisms that may go awry, making our patients vulnerable to injury and recurrence.

Ranges of Articular Motion Both Safe and Dangerous

We are all aware of the basics of articular motion and the "zones" of motion around the center of joint motion or the joint's neutral position. However, are you familiar with the neuromuscular neutral zone? In the very recent literature understanding the neuromuscular neutral zone is implicated as a key factor in protecting and maintaining the integrity of spinal joints. As a review of the basic ranges of motion of a joint and their relationship to the neuromuscular neutral zone, let's begin with the neutral zone, the motion immediately around the mid-position of a joint.

The neutral zone is commonly defined as the range of displacement near the spine segments' neutral position, where minimal resistance is offered by the osteoligamentous structures.¹ The authors of this definition caution that the neutral zone may increase with injury, articular degeneration, loss of passive stiffness, and weakness or inhibition of the stabilizing muscles. They warn us that when the neutral zone is increased the spine may become unstable and painful.

The next zone of motion is the elastic zone, defined as the zone that extends beyond the neutral zone within which tissues undergo increasing levels of physiological strain, but stillremain less than sufficient to produce disruption or injury.² As this strain increases, there is progressive internal resistance to further deformation as a result of the molecular bonds in the connective tissue matrix of ligaments, joint capsules, intervertebral discs and muscles in order to prevent injury. The structures that resist possible injurious deformation have been referred to as the "normal restrictive " or "physiologic" barriers."³

The molecular bonds within the connective tissue matrix protect joints from becoming over-distracted and injured. If the forces applied are too great for these molecular bonds to tolerate, the joint is forced beyond the limits of its normal range of motion into the "plastic zone," in which disruption of molecular bonds and tissue injury occurs; the higher the forces and the further beyond the normal end-range of motion a joint is forced, the greater the amount of tissue disruption and injury.

Disruption of Molecular Bonds and Joint Injury

Typically, the molecular bonds first disrupted are those within the passive restraints of the joint; that is, the ligaments, joint capsules, and intervertebral discs. These structures resist the tensile or torsional forces a joint is subjected to and which may cause damage if not well-controlled. The initial injuries documented to occur if the joint is forced beyond its normal end range have been variously labeled as "subfailure injury,"⁴ "microdamage of collagen tissues"⁵ and "microruptures of collagen fibers."⁶ These collagenous matrices provide the passive restraints that attempt to protect joints from being forced into the plastic zone.

Dynamic Stability and Protective Reflexive Motor Responses

The research is clear that it is important for the active restraints - dynamic muscle contraction - to be rapidly and reflexively elicited in order to protect the passive restraints from damaging overload when a sudden or unexpected load is applied. Appropriately timed muscle contraction can dampen and absorb some of the load or stress to which the ligaments are subjected and, by doing so, reduce the risk of damage to collagen fibers.

Reflex contractions of the back muscles, especially of the multifidus, normally act to control spinal movements in order to prevent excessive loading and to protect the underlying tissues from injury.⁷ The sensory-motor interactions between ligament tension and muscle recruitment occur very rapidly and unconsciously in order to ensure safe and controlled movement. Terminology referring to this interaction includes the ligamentomuscular reflex or facet joint capsule muscular reflex.⁸

Neuromuscular Neutral Zone and Triggering of the Multifidus

The neuromuscular neutral zone is defined by the tension or displacement in the lumbar spine at the instant that reflexive EMG activity is first triggered in the multifidus during flexion or stretch.⁵ The question arises: What precisely triggers this reflexive motor activity? With deformation, passive ligamentous restraints become stretched and, as they do, stretch receptors within them become stimulated. Impulses initiated from these receptors instigate a protective spinal reflexive motor response by the extensor muscles, particularly the multifidus,the first muscle to contract and protect the passive restraints from injury.⁹ The active and passive stabilizers are interactive due to their sensory-motor feedback loop, a synergystic relationship to provide dynamic load sharing under various conditions.⁵

According to recent research, the multifidus accounts for two-thirds of the control of lumbar intervertebral motion.¹⁰ In addition, the multifidus, because it is segmentally innervated, has the capacity for fine control of movement of individual lumbar vertebrae. Each nerve innervates only the fascicles that arise from that vertebrae, indicating a direct relationship between a segment and its multifidus. The segmental multifidus can, therefore, control a segment to match the applied load.¹¹

Difficulties arise when this reflexive motor response is delayed and begins too late to adequately dampen the tensile and/or torsional forces. As a result, molecular bonds within the connective tissue matrix of ligaments, joint capsules and/or discs are strained beyond their elastic limits and disrupted; a sprain occurs. According to evidence on the mechanisms of ligaments sprains, these subfailure injuries account for more than 85 percent of all ligament injuries.¹²

Why Is the Protective Reflexive Motor Response Delayed?

There are several factors that come into play and help explain the delay. One primary mechanism, which has been extensively documented, has to do with repetitive movements, particularly in sagittal flexion and/or flexion in combination with rotation. With repetitive activity, ligaments undergo creep deformation/ligament laxity, which results in changes in responsiveness of the mechanoreceptors within the ligaments leading to a "false kinesthetic perception,"⁶ thereby delaying protective reflexive motor responses. As Solomonow, et al.,8 described in their Volvo Award-winning article:

"Laxity in the ligaments desensitizes the mechanoreceptors within them and, therefore, significantly diminishes or completely eliminates their ability to monitor relative intervertebral motion, rendering them unable to reflexively initiate the muscular forces within the multifidus necessary to prevent destabilizing motion. Once laxity in the ligaments is present, the spine does not benefit from any protective muscular activity, and is exposed to injury."

Creep Deformation: How It Affects Sensory and Motor Responses

A 2010 paper⁷ describes the changes in ligamentous tissues resulting in creep as a time-dependent expulsion of water from spinal tissues, especially intervertebral discs, causing loss of disc height, slack in posterior ligaments and reduced resistance to bending by the osteoligamentous spine. With increased laxity, passive tissues do not elicit the same neural response as when tissues are taut. Stretch receptors in the posterior ligaments become stimulated when ligaments are stretched and the impulses initiate a spinal reflexive motor response by the extensor muscles. The decreased activity of the stretch receptors decreases activity of the muscles and together with laxity in the ligament, leads to increased laxity at the joint.⁹

Soft-tissue creep causes delayed activation of the back muscles in response to sudden loading. Ligament laxity alters afferent feedback from ligament receptors and impairs reflex activation of back muscles. Impaired reflexes in the back muscles as a result of prolonged or repeated flexion could increase the risk of bending injuries to the spine.⁷

Clinical Relevance

A practical application of this avenue of research is this: One of the most common presentations of low back pain results from the uneventful engagement in prolonged activity over the course of a day, yet after the repetitive tasks, work or athletic/exercise activity is over, people describe that while they are changing clothes, twisting to get into or out of their car, bending over to tie their shoes, or performing other everyday movements, they sense a distinct "pop" in the low back followed by pain. Note that this onset of pain is not associated with any external load, slip or fall, or unexpected application of force. The microdamage to collagen fibers occurs not as the result of excess, rapidly applied, or unexpected external load, but is due to poor internal neuromotor control of the upper-body torso mass under dynamic conditions.

This research confirms that a significant deficit in passive and active stability is present for hours immediately after a prolonged work period or repetitive flexion. Some researchers conclude that it is not surprising or may even be expected that minor or routine movements may result in instability and injury.⁷ From this information, clinicians can better understand what and why tissue damage may occur and they can better manage these patients and promote their full recovery, including restoration of functional capacity. This will be the focus of my next column.

References

1. Kolber MJ, Beekhuizen K. Lumbar stabilization: an evidence-based approach for the athlete with low back pain. Strength and Conditioning Journal, 2007;29:26-37.
2. Vernon HD, Mrozek J. A revised definition of manipulation. J Manipulative Physiol Ther, 2005;28:68-72.
3. Braddom RL. Physical Medicine & Rehabilitation. W.S. Saunders Co., 1996:422.
4. Panjabi MM. A hypothesis of chronic back pain: ligament subfailure injuries lead to muscle control dysfunction. Eur Spine J, 2006;15(5):668-76.
5. Le B, Davidson B, Solomonow D, et al. Neuromuscular control of lumbar instability following static work of various loads. Muscle Nerve, 2009;39:71-82.
6. Solomonow M. Sensory-motor control of ligaments and associated neuromuscular disorders. J Electromyogr Kines, 2006;16:549-67.
7. Sanchez-Zuriaga D, Adams MA, Dolan P. Is activation of the back muscles impaired by creep or muscle fatigue? Spine, 2010;35(5):517-525.
8. Solomonow M, et al. 1999 Volvo Award Winner in Biomechanical Studies. Biomechanics of increased exposure to lumbar injury caused by cyclic loading: part 1. Loss of reflexive muscular stabilization. Spine, 1999;24(23):2426-34.
9. Olson MW, Li L, Solomonow M. Flexion-relaxation response to cyclic lumbar flexion.Clin Biomech, 2004;19:769-76.
10. McDonald D, Moseley GL, Hodges PW. Why do some patients keep hurting their back? Evidence of ongoing back muscle dysfunction during remission from recurrent back pain. Pain, 2009;142:183-188.
11. Richardson, Hodges, et al. Therapeutic Exercise for Lumbopelvic Stabilization. A Motor Control Approach for the Tx & Prevention of LBP. Edinburgh, Churchill Livingstone, 2004:59-73.
12. Provenzano PP, et al. Microstructural morphology in the transition region between scar and intact residual segments of a healing rat medial collateral ligament.Connect Tissue Res, 2001;42:123-33.

How Spinal Manipulation Activates Segmental Stabilization of the Spine

By Malik Slosberg, DC, MS

The high-velocity, low-amplitude (HVLA) thrust of a spinal adjustment/manipulation has been documented to have many beneficial effects mechanically and neurologically. Recent studies have explored the impact of the HVLA thrust on the ligamentomuscular reflex and the resultant activation of the multifidus muscle in response to the sudden stretch of local spinal ligaments, joint capsules and intervertebral discs.

This reflexively mediated, rapid and unconscious stabilizing muscular response is a protective reaction to the abrupt stretch in order to prevent disruption of molecular bonds in the connective tissue matrix.

The neuromuscular neutral zone, the ligamentomuscular reflex, creep deformation, microdamage of collagen fibers and the role of the multifidus muscle in providing dynamic stability were all reviewed in my last article, "The Neuromuscular Neutral Zone, Dynamic Stability, and Injury/Pain in the Course of Everyday Activity." (June 3 DC) Now let's discuss how the chiropractic adjustive thrust affects these processes in beneficial ways.

Understanding the Impact of the HVLA Thrust on the Multifidus Muscle

In order to understand the impact of the HVLA thrust on multifidi, a review of a study performed on humans undergoing lumbar surgery is necessary.¹After an incision had been made over the involved lumbar segments and while the multifidi were still intact and not yet retracted off their origins on the spinouses and laminae, the supraspinous ligament at L2-3 and L3-4 was electrically stimulated.

The researchers observed that electromyographic recordings (EMGs) from the multifidus muscle demonstrated a direct relationship of muscular contraction in response to receptor stimulation in the supraspinous ligament. The authors explained that electrical stimulation of the supraspinous ligament mechanoreceptors (MRs) resulted in a ligamentomuscular reflex that caused the multifidus to contract in order to stabilize the supraspinous ligament and prevent possible over-distraction and ligament injury.

A 2010 paper² added that the reflex contractions of multifidus and longissimus can be elicited by electrical stimulation of afferents in discs, capsules and ligaments. The discussion noted that the reflex response is greater when afferents in several tissues are stimulated simultaneously, but mentioned that reflex activation of multifidus (MF) may be initiated just by stretching the supraspinous ligament, suggesting the presence of a discrete ligamentomuscular reflex.

Moving One Bone Relative to Another Activates the Multifidus

The Solomonow paper1 described ligaments as having only a minor mechanical role in maintaining spine stability and emphasized that the muscular co-contraction of anterior and posterior muscles is the major stabilizer of the spine. Importantly, as the authors elaborate, spinal ligaments are endowed with sensory receptors and are situated in key locations sensitive to relative motion of the vertebrae, so their receptors can monitor movement and activate muscles via spinal neurons to maintain or restore stability. Stimulation of these receptors elicits reflex activity in the paraspinal muscles and contributes to maintaining spinal stability when subjected to stress.

The paper concluded that a reflex arc exists in the human spine from MRs in spinal ligaments, discs and facet joints to the multifidi and possibly other muscles. This reflex is triggered at low to moderate loads that cause relative motion of two vertebrae, causing multifidi to become active. Certainly, this description of a reflex triggered by the noninjurious application of force which causes relative motion of two vertebrae sounds decidedly familiar to practicing chiropractors. Furthermore, the paper concluded that when conditions that challenge spinal stability are detected, such as the application of a HVLA thrust, the motor control unit activates appropriate muscles to protect, restore or avoid instability.

Eight years later, another study from the same lab³ described the function of the ligamento-muscular reflex as providing a fast dose of increased joint stability when unexpected movement elicits a sudden increase in ligament tension. This very rapid protective reflex (response time: 2.5 to 5 milliseconds) indicates that it is a fast-acting, reflexively elicited motor response to prevent damage to ligaments and joints. Spinal manipulation provides precisely the high-velocity, yet noninjurious stretch of ligaments that stimulates MRs to reflexively activate the segmental stabilizing multifidus to unload rapidly stretched ligaments and joint capsules.⁴

Scientific Basis for Understanding the Influence of the Manipulative Thrust

The findings of the above studies provide a scientific basis for understanding one of the major effects of the HVLA thrust applied to dysfunctional joints. In essence, this is what happens: A joint that is injured, inflamed, degenerated, restricted in motion or painful⁵ results in reflex inhibition, delayed activation and progressive atrophy of the multifidus muscle innervated by that segment.⁶ By clinical examination, the chiropractor identifies such a lesion (subluxation / joint complex dysfunction) and then applies a HVLA thrust to the joint.

This high-velocity force rapidly stretches the segmental ligaments, joint capsules, intertransversarii and interspinales muscles, and intervertebral discs, and intensely stimulates their numerous stretch receptors. This results in ligamentomuscular reflex activation of the multifidus, which attempts to stabilize the joint and protect it from possible injury as a result of the high-velocity stretch. The segmental multifidus, which has been reflexively inhibited and is atrophying, is stimulated to contract. This may reverse the reflex inhibition, progressive atrophy, and delayed muscle response documented to occur in the segmental multifidus which overlies a dysfunctional joint; and restore dynamic function and contractility to this primary joint stabilizer.⁷

Reprinted from Brenner AK, Kiesel KB, Buscema CJ, Gill NW. Improved activation of lumbar multifidus following spinal manipulation: a case report applying rehabilitative ultrasound imaging. J Orthop Sports Phys Ther, 2007;37(10):613-619, published online 29 May 2007. doi:10.2519/jospt.2007.2470. Reprinted with permission from JOSPT and its publishers, the Orthopaedic and Sports Physical Therapy sections of the American Physical Therapy Section (APTA).

A Case Report: Post-Manipulation Improved Multifidus Function

A case report⁸ of a 33-year-old man with a 21 year history of LBP and posterior thigh pain of insidious onset demonstrated this reflex activation and improved contractility of a segmental multifidus after spinal manipulation. When performing a prone upper-extremity lifting task before manipulation, the patient exhibited a reduced ability to contract his contralateral lumbar multifidus muscle, determined by objectively measuring the pre- and post-manipulation change in multifidus thickness using a validated rehabilitative ultrasound imaging approach.

However, on repeat imaging immediately after and 24 hours after spinal manipulation, thickness change during multifidus activation while performing the prone upper-extremity lifting task increased dramatically. Pre-manipulation thickening with contraction of the multifidus during the prone upper-extremity lifting task demonstrated only a 3.6 percent average change in thickness of the multifidi at L4-L5 and L5-S1, which is well below the 22 percent average increase in asymptomatic subjects. However, after spinal manipulation, there was an immediate increase in MF thickness (17.2 percent) during the upper-extremity lifting task at both L4-5 and L5-S1. This improvement was maintained and slightly increased 24 hours post-manipulation to 20.6 percent.

The pre-manipulation thickness change represents gross muscle dysfunction, but post-manipulation changes approximate normal. The improvement of dynamic muscular function post-manipulation were accompanied by clinical benefits as well. The authors conclude that the change in contractility of the multifidus observed on ultrasound imaging demonstrates possible neurophysiologic/reflexogenic effects of spinal manipulation on the multifidus muscle. As the authors interpret the findings, spinal manipulation may affect the inflow of sensory input to the central nervous system and evoke paraspinal muscle reflexes which alter central and/or peripheral neural pathways.

The Unique Effects of High-Velocity, Low-Amplitude Force

This research, along with many other studies, confirms that dysfunctional spinal joints result in inhibition and progressive atrophy of the local multifidi. This leaves the involved spinal segments unprotected, relatively unstable, and biomechanically vulnerable to injury and recurrences with minimal or no external mechanical load or stress. The application of the high-velocity, low-amplitude force of spinal manipulation generates a rapid stretching of the ligaments, joints capsules, discs and small intrinsic spinal muscles, resulting in a reflex response in the multifidus. The multifidus is reflexively activated and contracts in a region where it would otherwise be losing cross-sectional size and density.

Somehow, based on decades of clinical experience, chiropractors have observed improvements in joint function and intuitively sensed, long before the research was available, that manipulation may help reset disturbed motor programs and activate these key segmental stabilizers in regions where they are inhibited and atrophying. The findings reported above and their practical application to chiropractic care should serve to increase clinicians' confidence in and understanding of the mechanisms and benefits unique to the specific high-velocity, low-amplitude forces produced by spinal manipulation.

References

1. Solomonow M, et al. The ligamento-muscular stabilizing system of the spine. Spine,1998;23(23):2552-62.
2. Sanchez-Zuriaga D, Adams MA, Dolan P. Is activation of the back muscles impaired by creep or muscle fatigue? Spine, 2010;35(5):517-25.
3. Solomonow M. Sensory-motor control of ligaments and associated neuromuscular disorders. J Electromyogr Kinesiol, 2006;16:549-67.
4. Le B, Davidson B, Solomonow D, et al. Neuromuscular control of lumbar instability following static work of various loads. Muscle Nerve, 2009;39(1):71-82.
5. Seaman D, Winterstein J. Dysafferentation: a novel term to describe the neuropathophysiological effects of joint complex dysfunction. JMPT, 1998;21(4):267-80.
6. Hodges P, et al. Rapid atrophy of the lumbar multifidus follows experimental disc or nerve root injury. Spine, 2006;31(25):2926-33.
7. MacDonald D, Moseley GL, Hodges PW. Why do some patients keep hurting their back? Evidence of ongoing back muscle dysfunction during remission from recurrent back pain. Pain, 2009;142:183-8.
8. Brenner A, et al. Improved activation of lumbar multifidus following spinal manipulation: a case report applying rehabilitative ultrasound imaging. JOSPT,2007;7:613-19.

Decompression-Traction: A Core Treatment Method in Chiropractic's Future

By Jay Kennedy, DC

We're all competing for new patients. We're competing for new patients with physical therapists, massage therapists, medical specialists and hospital fitness centers. We're even competing with side-effect-ridden medications that quit working every four hours. However, one thing we're not competing against is a revolutionary new "cure" for back pain.

Though we're regularly introduced to such cures (and secrets of how the spine and nervous system "really work"), most of us have never seen anything actually live up to its press release. Rhetoric, marketing and testimonials have no real limits; science, however, is constrained by the laws of physics, the limitations of matter and (usually) the inherent boundaries of logical integrity.

Real scientists typically modify their findings behind phrases like: "No specific conclusions can be drawn at the present time" or "More research is required."¹Marketers, however, take these same findings and translate them to such phrases as: "Scientists unlock the secret to a pain-free back"; "The cure for arthritis is in this bottle" and "Weight loss without diet or exercise." We've seen similar headlines in our own profession.

Putting the cart before the horse is a staple of advertising; screaming from the rooftops regarding the newest product usually comes long before that product has really ever proven itself to be effective (such as a pharmaceutical prescribed prior to the realization it kills people).

Over the past two decades, decompression-traction has found a remarkable niche in many chiropractic practices. It has taken its place as both a co-treatment with manipulation and rehab, and as a substantive adjunct to manipulation and rehab. What is remarkable is how the public has embraced decompression as both an alternative to spinal adjustments (and surgery, in many cases), and as an alternative to "traction." This is a stunning testament to the initial decade of hyperbolic misdirection.

I have never purposefully suggested to a patient (at least in the past 12 years) that the decompression I provide is not traction (I consider what I do decompression-traction) or that I didn't inherently do axial traction. However, I have discussed the often-dramatic differences between the attributes, operation and misapplication typical in many traction sessions dispensed by hospitals and PT centers versus the codified application of decompression we strive to offer.

And in the basic understanding of what we coin "synergy-response decompression," the sum of the parts is greater than any one piece (such as when applying class IV laser or ultrasound during traction).

This is not to say these clinicians can't or don't deliver benefits to their patients with the use of traction therapy; however, their protocols and methodologies, I believe, are often: 1) poorly aligned with more recent advances; and 2) administered on relatively antiquated equipment.

Axial decompression is a codified, classification-based application of axial traction with the intention of decompressing a compressed structure. The well-worn (and relatively accepted) theory is that the decompression effect creates a positive, often profound change in the internal healing potential of the damaged discal / joint structure(s).

Though the effect is temporary in terms of the reduction of axial-compression (since gravity never loses the perpetual tug-of-war), the underlying metabolic and physiologic processes set in motion may continue for several minutes or several hours. Apparently, this is the trigger for the pain relief most often associated with traction treatment. Both internal disc alterations due to altered / improved blood / nutrient contact and mechanoreceptor pain gate modulations can account for pain relief, probably in synergy versus one or the other.^2-3

So, should this effect be seen as exclusive to any particular piece of equipment or is it uniform to virtually any axial-traction treatment? These are the questions not fully answered by research projects to date, but enough empirical evidence exists to suggest it is in fact a result of spinal stretch and out-of-gravity positioning, and is equipment (pulling-motor) independent.

Where a comment on antiquated equipment can be seen as substantive and not just rhetoric is in an examination of patient-classification and positioning. If we examine HNP research over the past 40 years, two concepts have proven relatively valid and reliable: centralization of pain and directional preference.4 Given that extension is a preferential direction to centralize pain in more than 70 percent of HNP (typically those under age 50), it makes sense that prone decompression be at least attempted in many cases ... if for no other reason than to foster that concept in the patient's mind.

Additionally, extension repetitions immediately after the axial treatment may better facilitate the posterior disc migration effect.⁵ Attributes of the table should facilitate both effective and ultimately, comfortable positioning; a big part of that is the harness system.

A complete circumferential binding assures proper axial transmission of the tension (and clinical research is clear; a pulling application is superior to a pushing application).

Lateral preference is perhaps found in some 20 percent, so having an offset pull (combining motor and belt shift) is important, as is allowing quick and effective side-lying positioning. Often medial-disc / nerve displacement syndromes are best initially treated in the side position, allowing reduction of nerve tension and painless maintenance of the antalgia ... something less tenable when prone or supine. Side-lying position affords a more acute or persnickety patient an option for comfortable traction therapy when prone or supine is too uncomfortable.

I consider supine decompression-traction a default position, though in daily practice it certainly may constitute 50 percent or more of treatments due to degenerative conditions, elderly patients or those with morphologic considerations (or concomitant extension motion disorders) invalidating prone.

No well-versed proponent of traction over the past 60 years would suggest supine-only treatment is a clinically viable means of applying traction. In fact the prone position emerged from the stationed clinical viewpoint of Mathews, Cyriax, Saunders and many others who recognized prone traction as likely more beneficial for more people than supine; many of their insights decades before Mackenzie. Of course, prone-only has its own set of problems.

The frustration scientific-minded individuals are up against when discussing and practicing physical medicine and "alternative" treatment methods is that personal experience is often all we really have to go on. I count myself both scientific and skeptical. Like everyone in practice, I have had years of remarkable and perhaps ultimately inexplicable results with chiropractic and decompression. Conditions improve, people get better, get their lives back, and we get paid; the ultimate full-circle. However, the problem of proving it convincingly to the "outside" world persists.

We have fragments and theories at present, and I guess that will have to suffice until more definitive research is gathered – which could take another decade if the National Institutes of Health and other agencies that allot money believe research is still warranted. At present, it is difficult to get traction, manipulation and other modality research funded since so much of it in the past has been negative, inconclusive or equivocal.⁶

We should continue to offer decompression to patients who fit into a reliable classification analysis of a compressive-disc syndrome, since the other options – medication, surgery or injections – are themselves of limited long-term benefit.⁷ With active rehab procedures and manipulation, decompression-traction adds a passive mode of treatment that has sufficient validity, affordability, safety and effectiveness to be recognized as a substantial core treatment method in chiropractic's future.

References

1. Cochrane Summaries. Cochrane Collaboration website, 2013.
2. Bogduk N, Twomey L. Clinical Anatomy of the Lumbar Spine. Churchill Livingstone, 1992.
3. Ozturk B, et al, Effect of continuous traction on the size of herniated disc material.Rheumatol Int, 2005 Oct;25(1).
4. May S, Alessandro A. Centralization and directional preference: a systematic review.Manual Ther, 2012;17(6).
5. Fritz JM, A randomized clinical trial of the effectiveness of mechanical traction for sub-groups of patients with LBP. BMC Musculo, 2010 Apr;30(11).
6. Personal communication, NIH Office of Administration (2012).
7. Slipman CW, et al, Etiologies of failed back surgery syndrome. Pain Med, 2002;3(3).

Elastic Therapeutic Taping:                                                    

A Valuable Fit for Chiropractic

By Kenzo Kase, DC

The concept of elastic therapeutic taping first came to me in the 1970s while I was practicing as a chiropractor and teaching. The taping is non-invasive, free from drugs, and integrates well into the chiropractic model.

Many conditions, including whiplash, herniated disc, muscle strain and sprain, headaches and degenerative joint disease are commonly treated with therapeutic taping in conjunction with traditional chiropractic.

Tracy Barnes, DC, DICCP, of Louisville, Ky., uses elastic therapeutic taping on many different kinds of patients. She enumerates: "For all those patients who continue to need a tactile cue to stay in certain postural positions, tape is great. For all those patients in pain from swelling, inflammation and injury, tape is great. For those patients who just need an extra 'umph' to feel better, tape is perfect." In fact, Barnes notes, "I wouldn't want to practice for long without it."

For many DCs, it is a standard in their practice. Dr. Scott Hainz practices in Missouri. He notes, "To help prevent prolonged recovery times, we incorporate [therapeutic taping] to enhance the in-office treatment, whether it be an adjustment or soft-tissue therapy."

Michigan chiropractor Dr. Tim Dunne observes that "Taping allows the patient to leave with a prescription for the body to follow through with as it heals in the proper functional motion. This leads to a significant increase in patient outcomes." Chiropractic is based on the knowledge that the human body has an innate self-healing ability and seeks balance. Therapeutic taping is based on the same assumption. Taken together, the whole concept is grounded in treating the cause of the patient's pain or weakness. In his experience, Dr. Dunne says, taping "always works." He has found that "if you are not getting the results you are looking for, reassess and retape; you haven't figured out the problem."

In the 1970s, it had became clear that the patient's response to treatment was the most important aspect of medicine. For example, allopathic practitioners received respect because they were able to implement pharmaceutical drugs with demonstrated effectiveness. While chiropractic adjustments have also been demonstrated to be effective, patients who are seekingpain relief may have a tendency to gravitate toward pharmaceutical treatments.

For this reason, it is important to search for the cause of the pain in order to treat patients more effectively using chiropractic techniques. The sensory receptors in the dermis turn out to be the key: upon specific stimulation of these receptors, which are plentiful in the skin, pain signals can be generated. Because of the abundance of these receptors, a cut or burn on the skin will hurt more than visceral pain. With this in mind, I considered how to best approach the management of painful conditions.

Taping for erector spinae muscle strain and low back pain.When we feel pain, we have a tendency to touch the area; however, it is not the application of pressure to the site, but the action of lifting with the palm of the hand that affects the sensation of pain. The lifting motion stimulates the mechanoreceptors in that particular region and decreases the pressure on the site, thereby decreasing the feeling of pain. Accordingly, I wanted to create a material that would simulate this action. At first, I was using athletic tape in an effort to avoid applying pressure to the painful site, but found that athletic taping was too constricting. This compression is helpful in stabilizing the area; however, it limits motion and circulation, and is consequently ineffective in managing pain. To solve this problem, I designed a unique elastic therapeutic tape. This creation allows for therapeutic taping treatment that does not involve drugs or surgery and is easily assimilated into common chiropractic protocol.

Studies have demonstrated the effectiveness of therapeutic taping for pain. A 2005 case study followed three patients who complained of patellofemoral pain and documented positive outcomes for all three. Patient #1, a 91-year-old woman, had improvements of "no pain with gait; no night pain, knee pain was immediately resolved following the application." For patient #2, age 56, treatment resulted in "no pain with normal walking, no pain with ascend or descend stairs." This patient also reported less pain at the end of her day. After treatment, 12-year-old patient #3 experienced no pain with running or during athletic activities such as running and snowboarding.

Taping for neck strain or whiplash.In a United Kingdom study yet to be released, South African MDs compared the use of ibuprofen versus elastic therapeutic taping for pain. Their results found the taping to be as effective as ibuprofen.

My own education is not only in spinal manipulation, but also includes training and experience with acupuncture, topical herbs, applied kinesiology and electrostimulation, among other modalities. Taking these into consideration, it is clear that the concept behind them all correlates with the way tissues need to be addressed.

Since being a chiropractic student, I have also been interested in the osteopathic fluid system and how this affects the body. Between the epidermis and the dermis lies the fluid lymphatic layer which has a close relationship with the capillary beds and often becomes congested. One can affect this layer by utilizing the hydrokinetic system: by creating more space and increasing the amount of fluid in that area. A secondary effect is an increase in circulation of the fluid. Third, there is a pumping effect propelled by the movements of the body. The movement of the cerebrospinal fluid (CSF) circulation has a pumping muscle at the base of its motion. Hence, a wasted, weak muscle can form a blockage to the movement of the fluid system in the body.

A Colorado case study² published in 2007 looked at conservative treatment of a collegiate athlete. Researchers reported, "The application of the [elastic therapeutic tape] seemed to enhance proprioceptive function to reduce irritation during activities. The athlete reported being more aware of the stress she applied while playing. Another desired effect was to improve lymph flow from the injured area. The patient noted improvement in pain and functional performance levels during and after wearing the tape."

In a 2010 case study³ from Poland, researchers observed that "Complex Decongestive Therapy (CDT) often needs modifying in advanced cancer patients. One of the options is using [taping] instead of multi-layer bandaging. It can be particularly helpful in patients who cannot undergo compression treatment due to pain." The article presents the case of an advanced cancer patient whose painful skin tension, caused by lymphedema, was successfully reduced with the use of therapeutic taping.

Stimulation of the muscle spindles balances the contraction of the muscle and also increases the movement of the muscle, which enhances circulatory flow and helps in changing metabolism. Therapeutic taping has the ability to move fluid to the correct area. In the case of joint subluxations or restrictions, chiropractors consider soft tissue and the movement of fluid; as such, in any profession, but especially in the chiropractic profession, this unique ability of therapeutic taping to influence the movement of fluid must be considered.

Thirty-five years ago, I introduced this idea to the chiropractic community in Japan, and its use there became widespread. Other medical groups, as well as athletes and patients, began utilizing the taping treatment. Elastic therapeutic taping has been widely accepted, and seen in many Olympic and professional sports and consequently, those interested in healing are using the tape on their own. Still, there is a limit to the amount of healing that can be done by a patient without the guidance of a knowledgeable practitioner. As a result, each practice should consider using therapeutic taping to manage patient healing, especially considering that it can be used in place of drugs. In this manner, therapeutic taping can be a perfect connection between the doctor's manipulation and the patient healing process.

Taping also provides a marked non-therapeutic benefit, as patients using the tape become walking billboards for the practice. I don't know how many times patients have asked for it, either because they've seen it on some famous athlete or – more commonly – because a relative or acquaintance has used it and recommended not only the tape, but also the DC who first applied it.

References

1. Brandon R, Paradiso L. The use of Kinesio tape in patients diagnosed with patellofemoral pain (PFP). 2005. Case study of three patients.
2. Aspegren D, et al. Conservative treatment of a female collegiate volleyball player with costochondritis. Journal of Manipulative and Physiological Therapeutics, 2007;30(4):321-325.
3. Pyszora A, Krajnik M. Is Kinesio taping useful for advanced cancer lymphoedema treatment? A case report. Advances in Palliative Medicine, 2010;9(4):141-144.