CHAPTER 15: Chiropractic Perspectives On Myofascial Therapy
Chapter 15
Chiropractic Perspectives on Myofascial Therapy


From R. C. Schafer, DC, PhD, FICC's best-selling book:

“Applied Physiotherapy in Chiropractic”

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Chapter 15: Chiropractic Perspectives On Myofascial Therapy

This chapter has been contributed by Jeff A. Rockwell, DC,
Center for Chiropractic Sciences,
Parker College of Chiropractic.


We are first moved by pain, and the whole succeeding course of our lives is but one continued series of actions with a view to be freed from it.
— Benjamin Franklin


     INTRODUCTION

The purpose of this chapter is to improve the doctor of chiropractic’s understanding of the significance of myofascial pain and dysfunction, and to improve the chiropractor’s level of competence in diagnosing the myofascial component of the subluxation complex.

The myofascial orientation in the chiropractic setting directs the doctor to look first for a myofascial source of the patient’s pain, and when found, to use numerous techniques and procedures to offer rapid relief. Lowe recommends broad spectrum therapeutics to be employed after the performance of myofascial therapy to assure maximum flexibility. [1]


Definition

Myofascial therapy may be defined in several ways. Basically, it is the treatment of the myopathophysiologic component of the vertebral subluxation complex. It is also the treatment of trigger points, areas of increased neurologic activity in muscle tissue, causing the secondary referral of pain with subsequent associated autonomic changes. [2]

The pain attributed to myofascial dysfunction is usually restricted to a certain region such as the cervical or upper thoracic area, lumbar and buttock area, or the cranial/TMJ area. A trigger point, often the cause of such pain, is always tender and palpably taut. This prevents full lengthening of the muscle and produces muscle weakening, altered proprioception, predictable referred pain patterns, and an objectively verifiable local twitch response during palpation. [3]


Historic Background

Several key figures have contributed to our understanding of the widespread cause of muscular pain syndromes, among them Travell, Rolf, and, in our own profession, Nimmo. Another chiropractor who added greatly to our understanding of the role of muscles in various pain syndromes was Gillet of Belgium. Gillet wrote, “Concerning the subluxation or misalignment, we prefer the term fixation, which describes far more accurately the actual status of the [peri]articular soft tissues, where we will find that it is the state of these tissues that actually keeps the two surfaces from moving. The osteopaths, very early on, stated that the soft tissues can vary from the simplest muscular contracture to a complete degenerative fibrosis of the muscles. The previous facts are not new ....unfortunately, x-rays, introduced early in chiropractic history, have done much to propagate the idea of the spine as a string of bones. Even today, many practitioners act as if they still believe the childish propaganda they so nimbly offer to the public, that it’s a bone out of place in the back.” [4]

Gillet continues, “It is true that sporadic mention of the existence of spinal muscles and ligaments is made, often by such words as, ‘Yes, I put the vertebrae back, but the muscles pulled them out again.’ “At best, certain chiropractic teachers did accept that there are taut muscles related to the subluxation complex and that these muscles were part of a vicious cycle in which the displaced vertebra produced pressure on a spinal nerve that caused a muscle spasm that, in turn, stopped the vertebra from being replaced. To us [Gillet’s group of Belgian researchers], abnormality in the spinal muscles, ligaments, and [peri]articular soft tissues is the real factor responsible for subluxations.”

Raymond Nimmo, DC, a 1926 Palmer College of Chiropractic graduate, was another early chiropractor skeptical of the logic and scientific validity of the spinal misalignment model of vertebral subluxation. After several years of practice, Nimmo became curious why some patients with severely distorted spines had little or no pain while others with excellent alignment had terrible pain. He became even more disillusioned with the misalignment theory when he saw patients get well with chiropractic treatment, but posttreatment radiographs showed no change in vertebral alignment. [5]

Nimmo began to reason that the bones of the body are passive structures whose alignment and movements are controlled by muscle contractions and tonus. He hypothesized that imbalanced muscle tension is the probable cause of spinal misalignment and that chiropractors might be inadvertently treating muscles while manipulating spinal and extraspinal joints. He also postulated that if muscles are capable of causing primary pain and dysfunctional biomechanics, treatment might be more effective if applied directly to the involved muscles. [6] For the remainder of his career, Nimmo researched the role of muscle in pain syndromes and created a chiropractic-oriented type of myofascial therapy that he called receptor-tonus technique, so named because he felt that noxious input from sensory nerve receptors into the central nervous system (CNS) could be modulated by decreasing muscle hypertonicity. His normal methods of locating and treating myofascial trigger points will be explained in this chapter.


The Myofascia and Its Role in Pain Syndromes

Skeletal muscle is the largest system in the body, comprising nearly half of body weight. Skeletal muscles are the motors of the body, working with and against the ubiquitous pull of gravity. The connective tissue between muscles, called fascia, comprises 16% of a person’s body weight, and it stores 23% of total water content. [7] Fascia forms the base of the skin and surrounds muscle sheaths, nerve sheaths, tendons, ligaments, joint capsules, periosteum, and blood vessel walls, and serves as the bed and framework of viscera. [8] Importantly, fascia can harbor trigger points as readily as skeletal muscle.

Along with fascia, cartilage, ligaments, muscles, and intervertebral discs serve as the body’s mechanical shock absorbers. Each of the approximately 500 skeletal muscles is subject to acute and chronic strain, which can lead to the development of myofascial constrictions, trigger points, referred pain, and autonomic dysfunction.


Function and Properties of Fascia

Fascia is a slightly mobile form of connective tissue derived embryologically from mesoderm. It is composed of an elastocollagenous complex. The elastic component is stretchable and comprises the core of the complex. The collagen fibers are pliable yet extremely tough, offer little extensibility, and coil around the elastic fibers in a loose-wavy configuration. There is also a matrix or ground substance that, under normal conditions, has a gelatinous-like consistency. It assists in the transport of metabolic materials throughout the body. [9]

This elastocollagenous complex creates a three-dimensional web extending continuously from the top of the head to the tip of the toes without interruption. Remember that fascia surrounds and attaches to every organ, muscle, bone, nerve, and vessel. Functionally, fascia serves to surround and imbue every structure and thereby supports and protects. It creates physiologic space between vessels, organs, bones, and muscles. Fascia also creates space (apposing potential channels) through which delicate nerves, blood vessels, and lymphatic fluids must pass. [10]

Fascia has the propensity through trauma, inflammatory processes, and poor posture to become less elastic and shortened. Fascia organizes along the lines of tension imposed, and, because of its continuity, it can produce bizarre and seemingly unrelated clinical signs and symptoms in dissimilar areas of the body.

Since fascia has a tensile strength of approximately 2000 lbs per square inch, [11] this loss of fascial mobility produces a drag on the fascial system that can manifest as abnormal alterations in human physiology.

Fascia has a characteristic histologic response to immobility. Akeson, Amiel, and Woo found fibrofatty infiltrate in such areas. The more chronic the condition, the greater the amount of infiltration was found, along with a change in the infiltrate’s appearance, which became more fibrotic and created microscopic adhesions. [12-16]

      EFFECTS OF RESTRICTED MOVEMENT

Histologic and histochemical analyses showed several significant changes in these areas of restricted fascial movement, the primary one being a significant loss in ground substance but no significant change in collagen content. A primary function of ground substance is to lubricate the area between collagen fibers to allow them to glide smoothly and prevent microadhesions between fibers. When this critical interfiber distance is not maintained, collagen fibers approximate and eventually become cross-linked by newly synthesized collagen.

Since collagen fibers are laid down according to the stresses (or lack of stresses) imposed, collagen in immobile fascial tissue becomes arranged haphazardly. Newly synthesized collagen then binds adjacent collagen fibers, decreasing the extensibility of the tissue and interfering with the function of the involved nerves, venules, arterioles, and lymphatics traversing between the interface of the fascia and adjacent muscles. [17, 18] Appropriate myofascial therapy such as therapeutic stretching and transverse friction therapy must then be used to restore these tissues to a better state of functional integrity.

      ACTIVE VS LATENT TRIGGER POINTS

A useful interpretation of the incidence of myofascial pain must distinguish between

(1) active trigger points causing pain either at rest or connected with muscle activity and

(2) latent trigger points. A latent trigger point may demonstrate all diagnostic features of an active trigger point, including shortening of muscles, except that it causes pain only when the involved area is palpated. Significantly, latent trigger points tend to convert into active trigger points in time.

Latent trigger points affect nearly half the population by early adulthood. Among 100 male and 100 female 19-year-old asymptomatic Air Force recruits, Sola and associates found local tenderness in shoulder-girdle muscles indicative of latent trigger point dysfunction in 54.7% of the women and 45.9% of the men. [19]

      INCIDENCE

Recent reports from chronic pain treatment centers reveal that myofascial syndromes are the cause of pain in over half of their patients. Among 283 consecutive admissions to a comprehensive pain center, the primary diagnosis of myofascial pain syndromes was assigned in 85.9% of all cases. A neurosurgeon and a psychiatrist made these diagnoses independently, based on physical examination to confirm the soft-tissue findings described by Travell. [19]

In another study, the diagnoses were tabulated for 296 patients referred to a dental clinic for chronic head and neck pain of at least 6-months duration. In 164 (55.4%) of these patients, the primary diagnosis was myofascial pain syndrome due to active trigger points. [20]

Acute myofascial pain syndromes due to trigger points are relatively common in general practice. In one internal medicine group, 10% of 61 patients cases had myofascial trigger points that were primarily responsible for their symptoms. Of those patients presenting with pain as their chief complaint, myofascial trigger points caused the pain in 31%. [21] Bonica, a leading medical researcher on pain, states that 80% of all pain is myofascial in nature. [22]


Etiology

Empiric and research evidence indicate that the trigger point phenomenon begins primarily as a histochemical dysfunction resulting from muscle overload. Active trigger points often progress at a variable rate to a dystrophic phase with demonstrable pathologic changes. It is the objective of the chiropractor using myofascial therapy to treat the condition by influencing the involved tissues with acceptable methods to regain their former healthy or relatively healthy state.

      EFFECTS OF MUSCLE OVERLOAD

Contraction of striated skeletal muscle depends on forceful interaction between actin and myosin filaments, collectively known as sarcomeres. Normally, the contractile activity of a muscle fiber is controlled by the rapid release and reabsorption of calcium stored in the sac-like sarcoplasmic reticulum. Release of calcium from this repository initiates contractile activity. This release of calcium is normally triggered by a brief propagated action potential. However, if the trauma activating the trigger point, either through chronic overuse or an acute overloading of the muscle through postural imbalances, has damaged the sarcoplasmic reticulum and spilled its calcium, the sacromeres exposed to the calcium for an extended period sustain contractile activity as long as their ATP energy supply lasts. This contractile activity persists despite the absence of action potentials as long as calcium and ATP are present. The uncontrolled contractile activity of this portion of the muscle causes equally uncontrolled metabolic activity locally. The sustained contractile force could, in turn, produce tension and harden the fibers comprising the palpable band. The uncontrolled metabolism in the muscle causes it to respond with severe local vasoconstriction, and nerve sensitizing substances are released into the trigger point zone. [23]

A common clinical example of this occurs in exercise-induced alterations of skeletal muscle that can be found immediately after submaximal exertion. Increases in total muscle water, predominantly in extracellular spaces, are benign. They appear and resolve quickly. Changes at the level of the sarcomere can be long lasting and result in a type of myofascial pain and dysfunction clinically described as delayed onset muscle soreness (DOMS). [24, 25] DOMS is myalgia occurring after unaccustomed muscle exertion. Deep, red, extensor muscles such as the soleus of the leg and vastus group of the thigh are commonly affected, and the tenderness in these muscle groups is localized in the region of the musculotendinous junction. [26]

At the ultrastructural level, frequent myofibrillar disturbances are observed that especially affected the Z-bands. It is unknown whether these findings reflect mechanical Z-band disruption or result secondary to activation of lysosomal enzymes occurring with concomitant inflammation. It does seem, however, that the contractile machinery of overloaded muscles is distorted. [27]

This mechanism of muscle overload disrupting the contractile elements of muscle explains why sustained voluntary contraction, especially in the shortened position, or too frequent repetitive contractions without adequate intervening rest periods is likely to convert latent trigger points (which cause muscle stiffness) into active trigger points (producing frank pain) and to perpetuate already active trigger points.

      CAUSE OF REFERRED PAIN

In essence, areas of myofascial dysfunction are sites of high neurologic irritability. The pain receptors in the muscle are firing at such a rapid rate that they confuse CNS control. This causes the pain to be projected elsewhere in the body and can lead to serious autonomic disturbances. See Tables 15.1 and 15.2.


Energy Depletion Effects

Myofascial dysfunction turns the nervous system into an enormous waster of energy. It increases tone in the soft tissues of the body, requiring large amounts of energy to maintain adequate homeostasis in such a state. An area of the spinal cord called the internuncial pool is affected by this increase in muscle tone. The chief characteristic of this pool of neurons is that it is highly excitable. [28] In a healthy spinal cord, sensory impulses are amplified by a small amount. This allows the body to operate on a precise economy of energy. However, when muscles become hypertonic or develop active trigger points, the greatly increased number of sensory impulses entering the internuncial pool overtaxes it and causes it to refer pain to other parts of the body. But the problem goes deeper than this.


     Table 15.1. Effects of Hypermyotonia

Trauma to muscle
(eg, work-related injury)
Chronic overload or overuse of muscle
(eg, delayed onset muscle soreness)
Rupturing of the sarcoplasmic reticulum
Building of mechanical pressure
Release of stored calcium
Compression of blood vessels and lymphatics
Sustained contracture
Reduced glucose and vitamin B input
Compression of blood vessels and lymphatics
ATP depletion
Reduced glucose and vitamin B input
Actin/myosin remain locked together
Noxious metabolic by-products
ATP energy deficiency contracture
Types A delta and C fibers
stimulated excessively
Histologic changes occur
Trigger point phenomenon
(referred pain, muscle tightness,
sympathetic distress)
Trigger point phenomenon




     Table 15.2. Effects of Hyperfasciatonia

Trauma to fascia
(eg, whiplash)
Chronic overuse or
overload of fascia
(eg, forward head posture)
Immobilization of fascia
(following acute injury)
Type III collagen formation with haphazard adhesion formation
Stretch hypertrophy rule
Type I collagen cross-binding
Compression of blood vessels and lymphatics
Bone physiology mimicked by fascia and muscle (muscle and fascia assumes weight-bearing function and becomes thicker, denser, harder)
Haphazard adhesion formation
Reduced glucose and vitamin B input
Compression of blood vessels, lymphatics, etc
Compression of blood vessels, lymphatics, etc
Reduced antioxidant nutrient input with subsequent peroxydation of sarcoplasmic reticulum
Increased fibroblastic activity
Dystrophy of fascia

 

Rupturing of sarcoplasmic reticulum
Dystrophy of fascia

 

 

 

Dystrophic fascia

 

 

 

 

Widespread trigger point formation

 

 


Sympathetic Effects

Recall that Arndt’s law states weak stimuli activate physiologic processes; very strong stimuli inhibit them. [29] Disease is typically a normal physiologic process out of phase with need. When the internuncial pool is excessively stimulated by a bombardment of sensory messages from hypertonic muscles, the nervous system perceives this as a danger to its well-being. If we were to narrowly miss involvement in an automobile accident, for example, body defenses perceiving this as a threat to survival will activate the sympathetic nervous system. Our hands become clammy, our heart rate increases, and our respiration becomes shallow and rapid. With time, our body would recover from this classic epinephrine “fight or flight” response that is essentially catabolic.

The sympathetic nervous system is overactivated by myofascial dysfunction, but unlike the above example of the car accident, the body, due to the chronicity of trigger points, is not given a chance to settle down and relax again. For people with chronic problems of this kind, the sympathetic nervous system is overactive 24 hours a day. One of the first things to occur is that bodily resources such as fats, proteins, carbohydrates, vitamins, and minerals are spent in an accelerated fashion. For example, research shows that the body uses 20 times more vitamin C during an hour of pain than during a normal hour of function. [30]

A basic review of sympathetic activity shows that it increases heart rate, respiration, blood pressure, pupil dilation, vasoconstriction, production of epinephrine, and bronchial dilation. The only major function decreasing with sympathetic stimulation is gastrointestinal activity. When a person suffers from musculoskeletal pain and the sympathetic nervous system is stimulated, that person’s ability to absorb and assimilate nutritive substances for anabolic activity becomes impaired. The more an individual changes from an acute to a chronic pain sufferer, tissues correspondingly need more nutrition, but their sympathetic nervous system dictates that they receive less.


The Overstress from Chronic Pain

At a recent medical conference on muscle pain at John Hopkins University, this subject was discussed with poignant clarity. A female physician from Nairobi described for the audience what life is like for an average Kenyanese woman. Such a woman, who on the average dies at age 39 after bearing an average of seven children, is responsible for half of the planting during the season and all child-rearing and housekeeping tasks. The doctor commented, “Every woman in my village and almost every woman in my country has chronic pain, on the average from the time they are 10 years old. That is because they start out carrying a little brother on one hip and a little sister on the other side. They develop back pain. It’s almost a way of life.”

She further recalled the time when World Health Organization officials visited Kenya to study its nutritional status. Biopsies were performed on patients’ small intestines to detect if they had celiac syndrome or some other condition preventing the absorption of vital nutrients. [31] In spite of a barely adequate diet, if these people were able to absorb nutrients properly, they should maintain a relatively reasonable state of health. Instead, they frequently died prematurely of infections and opportunistic and immunosuppressant diseases. The important factor the World Health Organization neglected to consider was pain. When one considers that chronic pain leads to malabsorption of all the stress nutrients (B-complex, C, zinc, selenium), it can be appreciated that muscle pain is not something that is merely uncomfortable or unpleasant to deal with but that it could cause disease on a subclinical nutritional level.


What Are Trigger Points?

Evidence points to a trigger point as a small region of metabolic distress, caused by the combination of increased energy demand and impairment of oxygen and energy supply, probably due to locally restricted circulation. This combination of effects often produces a noxious self-perpetuating cycle.

In a recent light microscopic biopsy study, nearly half of the biopsies showed significant pathologic changes, most conspicuous of which were ragged red cell fibers and “moth-eaten” muscle fibers. Neither of these changes is seen in normal skeletal muscles. [32]

Electron microscopy reveals swollen organelles and sick mitochondria that were interpreted as indicating hypoxia and disturbed metabolism. A loss of sarcomere structure with marked destruction of myofilaments was also noted. [33]

Studies of trigger points also imply increased metabolic activity in the presence of impaired circulation. The temperature of a trigger point measured with a needle thermocouple by Travell was greater than that of surrounding muscle. [34]

In a companion biopsy study, Bengtsson and associates found significant energy depletion in biopsies of the trapezius muscles of 15 patients when compared to samples of unpainful anterior tibial muscles in six patients and samples of the trapezius muscle from eight healthy controls. [35] These studies also strongly imply that a myofascial trigger point is a region of metabolic distress.

Numerous studies have revealed within the hypertonic area the build-up of noxious metabolic wastes that increase the firing rate of local pain fibers. [36] Among these by-products are carbonic acid, lactic acid, substance P, bradykinins, and prostaglandins (all which are neuroexciting), and serotonin, a powerful vasoconstrictor. Thus, we have a situation in which decreased blood flow into and from the hypertonic area compromises the muscle’s nutritional status. B vitamins, glucose (essential for the production of ATP), and thyroid hormones have difficulty reaching involved tissues. At this point, the muscle becomes almost like a perpetual motion machine of histologic, histochemical, and neurologic dysfunction.

Applying manual myofascial therapy to contracted sarcomeres is often immediately therapeutic because circulation is restored and normal metabolic equilibrium is able to recur.


     TREATMENT OF MYOFASCIAL PAIN

It’s a common experience for the myofascially-trained chiropractor to achieve excellent results with patients who previously had only partially responded to chiropractic adjustments. This is often because their spinal fixations were corrected by manipulative therapy, but the soft-tissue component of their condition had been neglected. When myofascial therapy is combined with osseous adjustments and broad-spectrum physiotherapeutics, we can hope to attain the best results for our patients.

If during the course of treatment a patient becomes pain-free, it is impossible to determine with certainty the extent to which that particular treatment contributed to the recovery. There is a good possibility that the condition was getting better anyway, with or without treatment. Therefore, it might be said that the success of chiropractic care cannot be measured by the length of time it takes to become pain free; it can only be judged by the reduction of pain recurrence.

Low-back pain, for instance, is epidemic in our society. Approximately 80% of the population will, at some time, be restricted to bed rest due to severe low-back pain. What is really shocking is that, of these people, 90% will eventually suffer recurrent low-back pain. The same study showed that low-back pain tends to become more severe with subsequent attacks, and the episodes may follow each other quicker as time goes on. [37] One of the main aims of conservative treatment, then, should be to reduce the incidence of low-back pain or other musculoskeletal pain recurrence. It is the author’s experience that the above mentioned approach (viz, the combination of myofascial therapy, spinal manipulation, and physiotherapeutic modalities), is highly effective at preventing the recurrence of musculoskeletal pain.


Treatment Protocol

In treating myofascial pain syndromes, we follow a specific protocol:

(1) restore circulation to the involved muscle, either through ischemic compression, spray-and-stretch technique, moist heat, or ultrasound;

(2) restore the muscle to its normal resting length (through PNF stretching with home stretching exercises prescribed as soon as clinically appropriate); and (3) correct whatever perpetuating factors may exist.

      PERPETUATING FACTORS

Before considering specific myofascial therapy, it is necessary to discuss the topic of perpetuating factors. The presence or absence of perpetuating factors determines the answer to how long the effect of specific myofascial therapy should last. In the absence of perpetuating factors, relief should last indefinitely unless the trigger point is reactivated by another overload stress. In the presence of perpetuating factors, therapeutic effects can only be temporary.

Perpetuating factors are identified as either mechanical or systemic in nature.


Mechanical Factors

Mechanical perpetuating factors include anatomical variations, sitting and standing postural stresses, and life-style and/or vocational stresses. The leading mechanical perpetuating factor is postural distortion. Anatomical variations include a small hemipelvis, short upper arms, a “short leg,” and a long second metatarsal (D.J. Morton foot configuration) that impairs foot balance because of the knife-edge effect during toe-off that disturbs gait and overloads lower-extremity muscles.

      SITTING FAULTS

Several common postural stresses occur during sitting:

  1. The first type occurs where an office worker sits in a chair that rests on a smooth, hard mat (such as Plexiglas). This makes the office chair with castors glide readily whenever its occupant changes position or exerts the slightest pressure against the desk. The long toe flexors and intrinsic foot muscles try to grasp the slick floor; and this effort overloads and perpetuates trigger points in these muscles.

  2. Another postural stress occurs during sitting when the chair seat is too high for the individual’s leg length, leaving the heels dangling off the floor. This compresses the hamstrings and produces chronic shortening of the soleus muscles.

  3. A third seated postural stress is caused by sitting in a chair with the back unsupported. This may be due to a seat that

    (a) is too long from front to back,
    (b) is too flat and provides no lumbar support,
    (c) supplies no scapular contact, or
    (d) has a backrest with an inadequate backward angle.


      STANDING FAULTS

The most common standing postural stress is the head-forward posture. Other examples would be rotation in the ilium, increases or decreases of the lumbar or cervical lordoses, or an accentuated thoracic kyphosis.

While chiropractors have historically led the field in attempts to correct spinal imbalance, until recently little attention was given to correcting postural distortions resulting from poor biomechanics. Such postural distortions create and perpetuate myofascial pain.

      UPPER-BODY DISTORTION AND SOME EFFECTS

Rolf felt that the human body must be analyzed by seeing it as an aggregate of blocks, some of which may be rotated or tipped one way or the other. [38] To help a patient as completely as possible, whole-blocks or segments of the body (eg, pelvis, shoulders, neck and head, etc) must be realigned.

Perhaps the most clinically significant postural distortion is the head-forward posture. When examining a patient from the side, one should be able to drop a lateral plumb line from the center of the head that bisects the ear, shoulder, hip, and transverse axis of the knee and the ankle. As we know, this ideal alignment is extremely rare.

In examining the head, neck, and shoulder girdle (the “upper block”), what should support the patient’s head (which comprises about a tenth of the patient’s body weight) are the IVDs of the cervical spine. Unfortunately, in many cases, the head is habitually oriented anterior to the gravity line. Then the weight-bearing force is placed on the postural cervical muscles, which are not by design weight-bearing structures. As these muscles incorrectly assume this function, stretch hypertrophy of the involved tissues occurs and the overstressed muscles, due to increased fibroblastic activity, harden and become stiff.

Compression of small arteries and veins also occurs, which reduces nutritive input to and metabolic waste removal from the area — all which increase and perpetuate trigger point activity. Functional migraines may result.

As the head assumes a forward posture, the cervical lordosis is decreased and the weight of the head is partially transmitted onto the posterior apophyses. These joints, of course, were not designed to be primary weight-bearing structures. This can create abnormal mechanoreceptor activity, firing impulses via the lateral spinothalamic tract into the brain.

The head-forward posture can be induced by weight-bearing on the heels and relieved, when standing, by shifting the center of gravity forward onto the balls of the feet, restoring the normal lumbar curve. [39]

Correcting such a problem in a child can be fairly easy, but it becomes more difficult as aging progresses. Trying to stand straight is simply not enough. Our muscles are opposing gravity inefficiently and fight this new position. A simple but excellent exercise for re-establishing proper posture of the head is the “6×6×6” exercise, devised by the Chilean physiotherapist, Mariano Rocobado. [40]

Rocobado’s Exercise.   The patient stands with his feet shoulder-width apart and his arms relaxed at the sides. Instruct him to have his thumbs pointed forward as he tightens his buttocks. With the patient’s buttocks clinched, instruct him to roll his thumbs outward and backward until he feels his scapulae approaching medially. While maintaining that tension, the patient forcefully lowers his shoulders an inch toward the floor: The patient then tucks his chin toward his chest and forcefully pushes his neck backward, as if trying to place the neck squarely over the shoulders. The patient is instructed to hold this position for 6 seconds and repeat the exercise six times. This constitutes one set. The patient should do six sets daily until correction of the problem occurs and three sets thereafter. It may take from 4 to 6 months of consistent effort to produce results, but the effort should be worth it.


      THE ANTERIOR PELVIS DISTORTION

Another common postural distortion is the rotated innominate. An innominate rotated anteriorly causes the ipsilateral knee to lock in extension. The femur has now lost some of its weight-bearing function. The quadriceps and adductor muscles are recruited as weight-bearing structures, which further cause the innominate to tilt forward. These overstressed tissues thus become prone to pain and injury.

It was explained earlier that the gravity line should bisect the transverse axis of the knee. In the case of an anteriorly rotated innominate with associated hypertonicity of the quadriceps and adductor muscles, the knee becomes overloaded by the prolonged muscle stress. This overload is shifted to the region of the patella. The patient is then prone to disorders such as Osgood-Schlatter’s disease and chondromalacia patellae.

The entire shaft of the tibia should be a weight-bearing structure; but if the knee is habitually in extension during stance, weight bearing shifts anteriorly. Consequently, the tibialis anterior, extensor digitorum longus, and extensor hallucis longus muscles become overloaded and overworked, which can lead to shin splints, hammertoes, and bunions. All this started (or could start) in the pelvis or, perhaps, with a head-forward posture. To correct these problems, and prevent their reoccurrence, the chiropractor must look to the mechanical perpetuating factor.

      OCCUPATIONAL FACTORS

Sustained shoulder elevation while working is a common vocational stress that overloads the upper trapezii and levator scapulae muscles, perpetuating their trigger points. Typists and others using their hands in a relatively fixed elevated position are prone to maintain their shoulders in a shrugged position to help elevate the hands to the level of their work. The work should be lowered or the patient’s body raised.


Systemic Factors

Systemic perpetuating factors can aggravate trigger points in any muscle and increase the irritability of all skeletal muscles, rendering them more vulnerable to the development of secondary or satellite trigger points.

Muscle is an energy machine. It converts adenosine triphosphate, a high-energy phosphate, into a lower-energy molecule, adenosine diphosphate. Understandably, anything interfering with the metabolism of muscles would compromise this biochemical activity and thereby increase both muscle irritability and susceptibility to trigger points.

      VITAMIN NUTRIENTS

When considering biochemical perpetuating factors of trigger points, a number of nutritional inadequacies could be involved. Those that commonly perpetuate myofascial pain are deficient B-complex vitamins (particularly B-1, B-6, B-12), folic acid, and C.

Vitamin inadequacy is a suboptimal level that may produce only a partial picture of deficiency. The patient need not be suffering from a blatant deficiency, but, upon blood studies, be found in the lower fourth of the normal range. This could suggest a vitamin inadequacy capable of perpetuating trigger points.

The monosodium urate crystals common to gout are less soluble in the acidic media of injured tissues than in blood, and hence are deposited in areas of injury and metabolic distress such as trigger points.

From a muscles’ perspective, anemia from any cause is a serious metabolic problem because the muscle depends on oxygen to sustain oxidative metabolism so essential for meeting the bulk of its energy needs.

      MINERAL NUTRIENTS AND METABOLIC FACTORS

Three major factors should be considered here:

(1) Abnormally low electrolyte levels of ionized calcium and potassium seriously disturb muscle function and increase muscle irritability, apparently because of their critical role in the contractile mechanism.

(2) The occurrence of hypoglycemia intensifies the metabolic distress of the muscle, and it clearly aggravates myofascial trigger points.

(3) Evidence of hypometabolism or hypothyroidism is found in some treatment-refractory patients with persistently active trigger points. [41]


The Posttraumatic Hyperirritability Syndrome

Another less recognized perpetuating factor is found with patients suffering from posttraumatic hyperirritability syndrome. [42] These people suffer greatly, are poorly diagnosed, and are difficult to help. They respond to strong sensory stimuli much differently than most patients.

Following a major impact to the body and/or head, the muscles exhibit marked hyperirritability of trigger points and a distressing vulnerability to strong sensory stimuli. The trauma has usually been an automobile accident or fall that was sufficiently severe to inflict some degree of damage to the sensory pathways of the CNS. These patients describe constant pain that is easily augmented by any strong sensory input such as severe pain, loud noises, vibration, prolonged physical activity, or emotional stress. It may take days or weeks for these people to recover from a degree of trauma or noise that to most people would be inconsequential.

One of the distinguishing characteristics of patients with posttraumatic hyperirritability syndrome is their loss of tolerance to what are, to most people, trivial mechanical stresses. Exposure to such stimuli immediately produces an increase in their level of pain.

The most effective treatment approach has been to inactivate all identifiable trigger points and correct perpetuating factors. On occasion, reports Travell, it may be necessary to reset the system by suppressing CNS excitability. Medically, barbiturates have been found most effective.

This description of perpetuating factors is not exhaustive. Other factors include viscerosomatic and somatosomatic reflexes, infectious diseases, infestations, allergic rhinitis, diabetes mellitus, alcoholism, adverse drug reactions, impaired sleep, and psychological stress.


Examples of Common Overloading and Perpetuating Factors of Low-Back Myofascial Pain

      LUMBAR ERECTOR SPINAE:

Sustained overloading (eg, from leaning forward toward a typewriter or computer keyboard; when conversing and sitting near the front edge of a chair; pelvic obliquity, or disparity in lower limb or innominate length). Also, acute overloading (eg, from quick bending and twisting at the waist, especially when muscles are fatigued and/or chilled).

      QUADRATUS LUMBORUM:

Acute overload (eg, from a fall or quick stooping movement when the torso is rotated). Sustained or repetitive overload (eg, from stooping and twisting as in gardening, scrubbing the floor, or when pulling clothes from a low dryer).

      ABDOMINAL MUSCLES

Visceral disease (eg, peptic ulcer); intestinal infestation (eg, giardiasis); trauma (eg, surgery), habitual tugging or squeezing from scar tissue (eg, near a scar from an appendectomy or hysterectomy), acute overload (eg, too many sit-ups, sit-ups done biomechanically incorrect, or straining at stool when constipated); prolonged muscle shortening (eg, poor posture with reduced distance between symphysis pubis and xiphoid process); and pelvic obliquity or disparity between lower extremity and innominate length.

      PIRIFORMIS:

Prolonged shortening (eg, sleeping with ipsilateral thigh externally rotated or sitting with ankle across contralateral knee).



     TREATMENT OF LOW-BACK PAIN WITH MYOFASCIAL THERAPY

It is the purpose of this section to examine the role of muscle and ligament dysfunction as an etiologic factor of low-back pain. It is not in the scope of this brief chapter to discuss treatment protocols for the entire body; however, myofascial treatment programs for several of the leading causes of low-back pain will be described.


The Etiologic Picture

Grice and Hviid suggest that the initial stage of lumbar spinal dysfunction is attributed to disharmony of the principle muscles for each motion segment. [43] They report that this disharmony forces a change in the axis of movement of the involved segment, thus compromising or affecting some structural elements. This can, as confirmed by the work of Gillet and Illi, lead to fixation of that motion unit and invoke subsequent compensatory hypermobility at other motion units in the kinematic chain.

Later stages of this initial change in the axis of motion produce disc wedging and increase mechanical stress, which lead to disc degeneration. Cassidy confirmed that long-standing abnormal movements predispose the patient to disc disease and are present well before any radiographic signs of degenerative disc disease become apparent. [43]


Analysis

Noll recommended the use of motion palpation to give direction to our treatment protocols. He claims that the use of static palpation and unspecific adjusting is likely to have a higher incidence of less or no effect and could actually worsen symptoms if hypermobile segments were adjusted instead. It is Jirout’s opinion that the onset of low-back pain and intervertebral disc disease is caused by a diminution of mobility between two motion units and is detectable only through dynamic radiography or a dynamic spinal palpation examination.

Nook states, in reference to the correction of faulty spinal biomechanics, that “attention to muscles and soft tissues is necessary. Whether they are part of the cause of the dyskinesis or a resultant pathology, they must be part of our treatment regimen.” [43]

Shaw, an orthopedic surgeon, states, “It’s our belief that the major cause of musculoskeletal dysfunction relates to fibrous tissue or fascial connective tissue restrictions that prevent the normal stretching of muscle. Restriction of the muscle, in turn, restricts joint motion and the joint becomes painful. All our treatment methods are designed specifically to release these fascial restrictions.” [44]

Good has examined numerous proposed causes of spinal fixation and suggests that unisegmental multifidi and rotator muscle spasms physiologically lock the related motion segment to hinder or prevent extension, lateral flexion, and rotation at that level. [45] This investigator reports that the muscle spasm causes the axes of motion to shift toward one facet joint. Mobility then becomes blocked by the inability of the segment to articulate around its new axis. Appropriate therapeutic intervention should be designed, he asserts, to collapse the muscle spasm, initiate restoration of the axis of motion, and recover mobility with a rapid reduction of symptoms. He states, “Muscles are most important in the initiation and maintenance of joint blocking.”

Good also maintains that the more gentle the technique is to relax the muscle, the more effective it is. “Irritation of the muscles by overzealous manual reduction will increase spasm.”


Therapeutic Approach

The myofascial techniques described below for treating low-back pain are gentle and effective in reducing trigger point activity. A method for correcting one of the most common perpetuating factors of low-back pain, pelvic obliquity, is also described.

In dealing with pain mechanisms of the lower back, it’s important to recognize areas of myofascial dysfunction that can mimic problems in the lumbopelvic region. See Table 15.3.


     Table 15.3. Common Lumbopelvic Pain Diagnoses Frequently Unrecognized as Originating from Myofascial Trigger Points in Specific Muscles

Common Diagnosis
Muscular Origins
References *
Low-back pain Quadratus lumborum
Lumbar paraspinals
Gluteus maximus, minimus
Rectus abdominis
Iliopsoas
Chapter 4
Chapter 48 (Vol I)
Chapters 7 and 8
Chapter 49 (Vol I)
Chapter 5
Appendicitis Rectus abdominis
Iliopsoas
Chapter 49 (Vol I)
Chapter 5
Pelvic pain Coccygeus
Levator ani
Chapter 5
Hip pain Tensor fascia latae Chapter 6
Meralgia paresthetica Tensor fascia latae
Sartorius
Chapter 12
Sciatica Gluteus minimus
Piriformis
Chapter 9
Chapter 1

* Travell JG, Simons DG:
Myofascial Pain and Dysfunction -The Trigger Point Manual Vol. 2., The Lower Extremities.
Baltimore, Williams & Wilkins, 1993.

Low-back pain exacts an enormous toll of misery and disability. In any one year, an estimated 10%—15% of adults have some work disability caused by back pain. [48] Those patients with low-back pain who receive compensation are estimated to cost the country $2.7 billion per year; the Liberty Mutual Insurance Company alone paid nearly $1 million per working day in 1981. [49]


Role of the Quadratus Lumborum Muscle

Travell considers the quadratus lumborum muscle to be one of the most overlooked muscle sources of low-back pain and is often responsible, through associated satellite gluteus minimus trigger points, for the pseudo-disc syndrome and the failed surgical-back syndrome. [46]

Low-back pain centered in the lumbar spine is more often of muscle origin than is generally realized. Myofascial trigger point pain arising in the quadratus lumborum muscles may be paralyzingly severe, rendering weight bearing in the upright posture intolerable. [47]

The quadratus lumborum muscle is considered the most frequent muscular cause of low-back pain among practitioners who have learned to recognize its trigger points by examination. [50-52]

Good reports the quadratus lumborum muscle to be the muscle most commonly involved (32% of 500) in army troops with musculoskeletal pain complaints. [53]


Trigger Point Therapy of the Lumbar Erectors and Quadratus Lumborum Muscles

The doctor stands on the ipsilateral side of patient involvement, facing cephalad.

      STEP ONE

With the tip of the doctor’s caudad thumb pressing cephally and anteriorly against the inferior surface of the 12th rib, the doctor treats from the medial to the lateral, gliding with a lubricant over the tendinous insertion of the muscle.

All gliding palpation and treatment in this area are done with 10 lbs of pressure at a rate of 1 inch per second. If an exquisitely tender point is reached (either a latent or active trigger point), pressure is held for a maximum of 10 seconds. The tenderness should substantially abate during this period as metabolic waste products are mechanically dispersed and circulation is restored.

It is important to ask the patient if the area being palpated is tender, if the tenderness radiates elsewhere (this constitutes another ischemic area that should be treated later), and to let the doctor know when the tenderness abates.

If after gliding over and treating a trigger point a maximum of three times the pain does not stop, the practitioner must consider three possibilities:

(1) too much pressure was used in treating the area,

(2) satellite trigger points exist in an adjacent area and need to be treated first, and/or

(3) spinal or extraspinal joint fixation(s) exists.

      STEP TWO

With the tip of the doctor’s thumb directed anteriorly and caudally, strokes are made laterally along the superior crest of the ilium using a lubricant. This procedure treats the attachments of the erector spinae, quadratus lumborum, latissimus dorsi, internal and external obliques, and the transverse abdominis muscles.

      STEP THREE

The doctor then glides cephalad, using a lubricant, from the posterior iliac crest to the 12th rib along the erector spinae lateral to the spinous processes. The doctor’s thumb moves in caudad to cephalad and posterior to anterior directions, stopping to treat all tender points as described earlier.

      STEP FOUR

Step three is repeated with the doctor’s thumb now gliding cephally and anteriorly an inch lateral to the preceding strip.

Steps three and four clear trigger points from the lumbar erector muscles, before going deeper to treat the quadratus lumborum. This is an example of a principle used often in the application of myofascial therapy: when treating deeper structures (eg, the piriformis, iliopsoas, or quadratus lumborum muscles), safely gain access by releasing the more superficial ones first.

      STEP FIVE

The part of the quadratus lumborum muscle harboring trigger points capable of mimicking disc disease is now ready for treatment. The insertions of the muscle on the transverse processes of the first four lumbar vertebrae are examined. The doctor locates the inferior surface of the 12th rib and glides his thumb (without using a lubricant) toward the patient’s spine until the thumb is lateral to the erector spinae. This procedure places the thumb approximately at the level of the L1 transverse process. The doctor then presses the tip of his thumb on the Ll transverse process. Pressure should be directed medially at a 45° angle into the body and held for 10 seconds at each tender point. This last procedure is repeated until the transverse processes of L2—L4 have been treated. It is extremely important when contacting the transverse process of the lumbar vertebrae that pressure be directed at a 45° angle and not a 90° angle, as pressure on these sharp bony protuberances could cause trauma to the compressed tissues.


Therapeutic Stretching of the Quadratus Lumborum and Lumbar Erector Spinae Muscles

When performing myofascial therapy on any part of the body, it is important to follow manual pressure (aimed at restoring circulation to the involved ischemic area) with therapeutic stretching to restore the muscle to its normal resting length. It is also recommended that 10 minutes of moist heat be applied to further enhance circulation.

To stretch the quadratus lumborum and associated erector spinae muscles, the patient is placed supine with arms crossed over the chest and knees and hips flexed at 90° angles. The doctor’s forearm, in this starting position, stabilizes the patient’s feet. There are four steps to this stretching technique.

      STEP ONE

The patient gently attempts to extend his legs and push his feet onto the doctor’s stabilizing arm. This will cause the involved muscles to tighten. As the patient does this, the doctor resists the force with his stabilization arm for 5 seconds (the doctor should keep his arm next to his body).

      STEP TWO

After 5 seconds of pushing gently with his legs, the patient partially relaxes and allows the doctor to bring the patient’s knees 6 inches toward the patient’s chest. During this procedure, the patient can, if preferred, gradually increase the force over the 5-second period but never to the point of discomfort to either patient or doctor.

The above described procedure causes the muscles to slowly lengthen. It is important, to engage greater motor unit activity, for the patient to maintain some pressure against the doctor’s grip so that the contraction is not completely released.

This step is repeated several times until the patient’s knees are close to his chest and the muscles are lengthened.

      STEP THREE

Once the patient’s knees are near his chest, he steadily and slowly pushes the doctor’s arm away until the knees return to the starting position (shortening the muscles again). The patient is then instructed to contract the muscles a final time by extending the legs against resistance for 5 seconds at which point (on the count of five) the patient actively and quickly draws his knees toward his chest.

      STEP FOUR

After the patient has quickly brought his knees to his chest, instruct him to use his stomach muscles to hold his knees to his chest while the doctor attempts to pull the patient’s knees away from his chest. This is done with minimal force for 5 seconds.

This last step serves to neurologically reinforce the stretch as the patient resists the doctor’ s attempt to shorten the now fully relaxed and lengthened muscles. This is an advanced type of proprioceptive neuromuscular facilitation that produces gratifying results.


Myofascial Therapy for the Psoas Muscle

The psoas muscle is not only often involved in low-back pain syndromes, it is also a frequent cause of postural distortion. The psoas is primarily a hip flexor, and its shortening results in rotating the innominate anteriorly and inferiorly. The result is an increased lumbosacral angle and lumbar lordosis. Numerous authors have emphasized the significance of this muscle in relation to low-back pain and pelvic visceral dysfunction. [54-58]

Michele wrote an entire textbook in which he related psoas spasm to pelvic obliquity, increased lumbar lordosis, compensatory dorsal kyphosis, low-back pain, sacroiliac joint dysfunction, degenerative hip arthrosis, degenerative disc disease, spondylolisthesis, scoliosis, menstrual cramps, and postural distortion. [59] He concluded, “Any and all defects of the spine and hip joint structures should be evaluated in terms of disturbances of function of the psoas.”

Chronic psoas hypertonicity and trigger points commonly occur from sitting for long periods, sleeping in a fetal position, exercise programs emphasizing repetitive hip flexion, and competitive cycling. Most sports and daily activities emphasize a flexed trunk orientation that may lead to psoas contraction unless counterbalanced by stretching exercises.

      HYPERTONIC PSOAS TECHNIQUE

To treat a hypertonic psoas muscle with myofascial therapy, the patient is placed in a supine position. Note that often when applying myofascial therapy the same contact points used to treat a trigger point are used to analyze these areas of dysfunction. The involved knee is flexed, with the patient’s ipsilateral foot resting on the table.

The doctor places his fingertips against the patient’s abdomen at the point that should bisect a line connecting the ipsilateral anterosuperior iliac spine (ASIS) and the umbilicus. Exerting gentle force as the patient exhales, the doctor moves his fingertips in a lateral to medial circular motion to displace the intestinal tissues. The tips of the doctor’s fingers gradually move deep into the pelvis toward the psoas. When the psoas has been contacted, the patient raises the involved knee toward his chest. With his caudad elbow, the doctor resists the patient’s hip flexion This produces a taut psoas muscle that allows the doctor to determine if his fingertips are directly in the muscle. If proper contact of the muscle has been made, the palpating fingertips will feel the tightened psoas muscle.

Examine the entire length of the psoas muscle with three-finger movements from T12 to the inguinal ligament. This procedure will treat the belly of the psoas major and the minor muscles.

To treat the portion of the iliopsoas below the inguinal ligament, flex the patient’s involved hip and externally rotate the femur. The patient’s knee is allowed to rest against the doctor’s abdomen. The doctor then places the tips of his thumbs directly medial to the sartorius muscle and immediately below the inguinal ligament. The doctor’s thumbs are moved vertically and horizontally several times to treat the insertion of the psoas on the lesser trochanter. To assure proper contact on the tendon at the lesser trochanter, the patient is asked to flex his hip. This causes the psoas tendon at its insertion to tighten under the doctor’s thumbs. Once the insertion is located, the patient may cross the involved ankle over the uninvolved knee and thus better relax the involved musculature. This will help in exposing more of the lesser trochanter and the attachment of the psoas muscle.

To fully treat the psoas myofascially, trigger point therapy should be followed with therapeutic stretching. The patient remains in a supine position but moves as close to the edge of the table as possible. The involved leg is medially rotated and abducted 45° from the table. The muscle is stretched in a medial to lateral and anterior to posterior direction to the first barrier of resistance. The doctor stabilizes the contralateral ASIS with one hand and pushes the patient’s leg into the position of stretch with the other hand. The patient is asked to push from posterior to anterior and lateral to medial with a small amount of force for 5 seconds (increasing the force during the 5 seconds) while the doctor applies resistance. The patient then fully relaxes the leg and allows the doctor to stretch the limb to the next barrier of resistance. This maneuver is repeated several times to create optimum stretch.

      HYPERLORDOSIS TECHNIQUE

This is a simplified version of proprioceptive neuromuscular facilitation and can be given to the patient as a home exercise. It is particularly important if the patient has an increased lumbar lordosis in need of structural correction.

The patient lies in a supine position as close to the edge of the table as possible. He medially rotates and abducts his leg, bringing the knee into extension until it meets the muscle’s first barrier of resistance. At this point, the patient offers his psoas muscle isotonic resistance by raising the involved leg 2 inches for 5 seconds. He then relaxes the leg and allows gravity to stretch the muscle to its new barrier of resistance. This procedure is repeated three times.

      PSOAS TRANSVERSE FRICTION MASSAGE

Cyriax mentions that chronic psoas strain may remain for years unless treated by transverse friction massage below the inguinal ligament, medial to the sartorius. [60] This technique is performed as if strumming transversely across the muscle with the fingertips.

To apply this technique, the doctor stands with shoulders relaxed. His hands are relaxed with the metacarpophalangeal (MCP) joints flexed at 90° while his fingers remain extended. The strumming motion comes from a flexion and extension motion at the MCP joints, not the proximal interphalangeal or distal interphalangeal joints. Pressure must be firm to be effective. Muscle fibers that have become fibrotic will often feel gristly or like piano wires. This indicates that treatment is needed.

Transverse friction massage is not necessarily a comfortable technique if done correctly. However, it is extremely effective and can be used on fibrotic myofascial tissues throughout the body (eg, paraspinals, pectoralis minor, levator scapulae, psoas, adductors, etc). Common modalities such as ice, ultrasound, or high-volt current will help alleviate or prevent posttreatment soreness.

      J STROKING FOR ABDOMINAL RELAXATION PRIOR TO PSOAS TREATMENT

Sometimes, if the superficial abdominal muscles are tense, they must be relaxed before contacting the psoas muscle. An excellent method is a type of soft-tissue mobilization called J-stroking. J-stroke techniques are used to increase the mobility of superficial fascia and can be used throughout the body whenever restrictions are found. Particular areas to evaluate are the abdominal, anterior thoracic, posterior trunk, and sacral areas.

Evaluate equality of fascial mobility by pulling the skin in all directions using the fingertips. Restrictions are felt as a resistance in a particular direction, ranging from mild resistance to a “hard-end” feel or complete “block.”

When a restriction is located in one direction, apply counterpressure, usually with the heel of the hand, and apply the J-stoke in the direction of the restriction. The J-stroke is performed with two or three fingertips, with the fingers flexed at the distal interphalangeal joints. The J-stroke describes a longitudinal taking-to-tension of the restricted fibers with a torque, resembling the letter J at the end of motion to twist and break fascial restrictions. Re-evaluate fascial mobility following the technique. This is usually not uncomfortable for patients, but they may report feeling a burning or pulling sensation.


Correcting Shifts in Pelvic Inclination Angle with Myofascial Therapy

Advocates of manual medicine have largely based their methods on the traditional chiropractic premise that a balanced musculoskeletal structure will be reflected in optimal physiologic function. For example, it has been reported in manual medicine literature that shifts in autonomic activity accompany derotation of the anteriorly tilted pelvis in the sagittal plane.61,62

According to Rolf, the angle of pelvic inclination is a keystone to restoring balance of myofascia throughout the body. She hypothesized that the horizontally balanced pelvis in the erect standing position could be approximated clinically by two anatomical landmarks:

(1) a horizontal line connecting the superior border of the pubic symphysis and the tip of the coccyx; and

(2) a vertical line connecting the pubic symphysis and the anterosuperior iliac spine (ASIS). [63]

Physical therapists and others in manual medicine have also reported the angle of pelvic inclination in the standing position as a criterion of clinical assessment. [64—68]

      MENSURATION

One technique for measuring this angle has shown strong reliability. [65-68] It is the standing pelvic tilt (SPT), defined as the angle of inclination made by a line drawn between the ASIS and the posterosuperior iliac spine (PSIS) and its intersection with the horizontal plane.

Assessing SPT this way has demonstrated an intratester reliability of 88%. [69-71] It has been proposed that the normal angle of pelvic inclination is 0°—5° for males and 0°—10° for females. [61, 66] Angles greater than this can disrupt lumbopelvic biomechanics, increase the lumbosacral angle, cause anteriorly shifted weight bearing in the lower extremities, and lead to various manifestations of pelvic pain and mechanically induced impairment of bladder, bowel, gynecologic, and sexual function. [72]

Myofascial manual therapy to the pelvic girdle is effective in reducing the angle of inclination in the anteriorly tilted pelvis, and is recommended as a treatment modality for certain low-back dysfunctions.


Manual Therapy for Correcting an Anteriorly Tilted Pelvis

Seven steps are involved.

      STEP ONE

The doctor begins by analyzing the angle of pelvic tilt on each innominate. He is positioned at the side of the patient in a kneeling position and wedges his cephalad index finger underneath the bony ledge of the patient’s ASIS and his caudad index finger under the bony ledge of the patient’s PSIS. From this position, the tips of the doctor’s index fingers should be pointed toward each other to produce the perception of a straight line between the two points. The doctor now estimates the approximate angle of tilt of the innominate. On a male pelvis, this angle, as explained above, should be 0°—5° to constitute a normal anterior tilt. On a female pelvis, the normal anterior tilt can range from 0° to 10°. This procedure is repeated on the opposite innominate as the degree of pelvic tilt can vary dramatically from one side to the other because the two innominates can move independently.

      STEP TWO

The patient is placed supine on the treatment table. The palms of the doctor’s hands are placed on the patient’s ASISs. The doctor’s fingers are cupped around the illi.

The doctor begins a gentle rocking movement of the pelvis by pressing the palm of one hand from the anterior to the posterior and 20° cephally while lifting his fingers and palm of his other hand. The doctor presses downward with his active hand only as far as no resistance is felt in the ipsilateral sacroiliac joint. When resistance is felt, the doctor releases pressure on the ipsilateral ilium while simultaneously pressing with the other hand on the contralateral ilium. The doctor presses downward with his active hand only to the point where resistance is felt in the contralateral sacroiliac joint. This is repeated 15—20 times on each side or until the ligaments inserting over the sacroiliac joints release.

It is important that once resistance is felt, pressure is released on the engaged ASIS. Repeat the process by pressing downward on the other ASIS. This produces a gentle rocking motion (using about 10 lbs of pressure) of the pelvis. Under no circumstances should excessive force be used once resistance is felt. The purpose of these rocking movements is to slowly stretch the plastic (malleable) component of the ligaments binding the sacrum to the pelvic complex. Because the anterior border of the sacrum is wider than the posterior border, this procedure also lifts the innominates from the shear margin of the sacrum. Owing to the shape of the sacrum, this procedure allows the joint to be stressed from the anterior to the posterior. If a person has a wide pelvis, it may be necessary for the doctor to place his lifting hand under the buttock to assist in lifting the pelvis.

      STEP THREE

In this step, the doctor places the thenar eminences of his right hand against the lateral side of the patient’s ipsilateral ASIS. The thenar eminence of the doctor’s left hand is placed against the patient’s contralateral ASIS. The doctor’s fingers of both hands should be facing toward the midline of the patient’s body.

The doctor’s forearm should be perpendicular to the patient’s body, almost parallel to the floor. The heels of the doctor’s hands should be pressed simultaneously into the lateral aspect of the patient’s innominates. This pressure compresses the anterior aspect of the pelvis while laterally decompressing the posterior portion of the sacroiliac joints, which stretches the horizontal sacroiliac ligaments. The doctor’s contact is held with approximately 10 lbs of pressure for 10 seconds and repeated three times. This procedure is contraindicated if the patient is osteoporotic.

      STEP FOUR

This step is an exercise that the patient is taught at this point and instructed to do at home each morning and evening.

The patient is asked to shift his right ASIS toward his right shoulder as when hiking or shrugging the hip. The patient then drops the level of his right ASIS to its neutral position and raises his left ilium.

To assure that the patient is doing this evenly and smoothly without rotating or lifting his pelvis anteriorly, the doctor should guide the movement by placing his hand on the patient’s ASIS and assist the patient in shifting the patient’s hips in alternating directions.

It is crucial that the patient’s knees remain flexed while performing this procedure. These movements help to further stretch the sacroiliac ligaments that, when hypertonic, produce sacroiliac joint compression. These therapeutic movements are done 10—20 times on each side.

      STEP FIVE

The clinical intent of the procedure here is to remove joint fixation in the acetabulofemoral joint in the long-axis distraction range of motion. This type of joint restriction is common and especially so in the case of an anteriorly tilted pelvis.

The patient stabilizes himself on the treatment table by flexing the knee on the uninvolved side. The doctor kneels on the involved side and crosses his forearms over and under the patient’s distal femur. When the joint is taken to tension by the doctor applying a pull caudally, several quick but gentle thrusts are made downward on each leg.

      STEP SIX

This step begins by having the patient move as close to the edge of the table as possible. The patient’s knee on the side not being treated remains extended, while the knee of the involved side is flexed and then fully abducted. The doctor’s cephalad hand is placed on the lateral aspect of the patient’s knee, and his caudad hand is on the medial aspect of the patient’s leg. The doctor valgus stresses the patient’s leg by rotating the patient’s ankle exteriorly while holding the patient’s thigh stable. This places torque on the capsule of the patient’s hip joint. The doctor simultaneously rotates the patient’s knee medially, as close to the patient’s shoulders and chest as possible, while continuing to move the patient’s ankle laterally.

Next, the patient’s knee is brought fully across his body until it is 180° from where the movement began. This step is repeated three times on each side, holding stationary pressure for 10 seconds at each barrier of resistance.

      STEP SEVEN

After the connective tissues over the sacroiliac joints have been gently and systematically stretched in these five directions, the anteriorly tilted innominate is then derotated into a biomechanically normal position.

The procedure begins on the more rotated side first. The hip and knee of the side being treated are flexed. The thenar eminence of the doctor’s cephalad hand is placed under the inferior ledge of the patient’s ASIS, while the thenar eminence of the doctor’s caudad hand is inserted under the patient’s ischial tuberosity. With the doctor’s hands positioned on the patient’s pelvis in this manner, the patient’s calf is placed on the doctor’s ipsilateral shoulder. For added leverage, if necessary, the doctor places his ipsilateral leg on the table while rotating the patient’s pelvis posteriorly.

The doctor now begins unrotating the pelvis by moving the patient’s knee toward the patient’s chest while pushing the ASIS from the anterior to posterior and pulling upward on the patient’s ischial tuberosity from the posterior to anterior. This begins to rotate the innominate posteriorly. As it does, the patient’s uninvolved thigh should rise slightly from the table. At this point, the doctor asks the patient to press his flexed knee against the doctor’s chest, causing the patient’s hamstring muscles to tighten. The patient maintains this isometric contraction for 8—12 seconds while the doctor rotates the patient’s pelvis farther posteriorly. The contracted hamstring muscles of the patient’s flexed knee further assist in rotating the patient’s pelvis posteriorly because of their attachments on the ischial tuberosity. This procedure is repeated three times on each side, after which the patient stands. The angles of pelvic tilt of the patient are then rechecked bilaterally.

Acknowledgments:   The author dedicates this chapter to the memory of Dr. Raymond Nimmo, without whose questioning attitude and years of research this introduction to chiropractic myofascial therapy would not have been possible. The author would also like to acknowledge Lillian Brown and Ann Jacobs for their help in typing the manuscript.



     REFERENCES
  1. Lowe JE:
    The Purpose and Practice of Myofascial Therapy.
    Houston, TX, McDowell Press, 1989.

  2. Travell J, Simons DG:
    Myofascial Pain and Dysfunction —The Trigger Point Manual.
    Baltimore, Williams and Wilkins; 1993.

  3. Ibid.

  4. Gillet H:
    The History of Motion Palpation.
    European Journal of Chiropractic, 31(4), 1983.

  5. Nimmo RL:
    Some remarks on the development of receptor-tonus technique.
    Correspondence with Dr. Monroe Cobb, March 8, 1984.

  6. Schneider MJ, Cohen JA:
    Nimmo receptor tonus technique: A chiropractic approach to trigger point therapy.
    In Sweere J (ed): Chiropractic Family Practice.
    Gaithersburg, MD, Aspen Press, 1992.

  7. Dicke E, Schliack H, Wolff A:
    A Manual of Reflexive Therapy of the Connective Tissue.
    Scarsdale, NY, Sidney S. Simon Publishers, 1975.

  8. Ham AW, Cormack DH:
    History.
    Philadelphia, J.B. Lippincott; 1979; pp 210—259.

  9. Upledger J:
    Craniosacral Therapy.
    Seattle, Eastland Press, 1983, Vol 1, pp 236—239

  10. Ibid.

  11. Ibid.

  12. Woo S, Matthews JV, et al:
    Connective tissue response to immobility.
    Arthritis and Rheumatism, 10:257—264, 1975.

  13. Akeson WH, Woo SL-Y, et al:
    The connective tissue response to immobilization: Biomechanical changes in periarticular connective tissue of the rabbit knee.
    Clinical Orthopedics, 93:356-362, 1973.

  14. Akeson WH, Amiel D, et al:
    The connective tissue response to immobility: An accelerated aging response.
    Experimental Gerontology, 3:289—301. 1968.

  15. Akeson WH, Amiel D:
    Immobility effects of synovial joints: The pathomechanics of joint contractures.
    Biorheology, 17:95—110, 1980.

  16. Akeson WH, Amiel D:
    The connective tissue Response to immobility; A study of the chondroitin 4 and 6 sulfate and dermaten sulfate changes in periarticular connective tissue of control and immobilized knees of dogs.
    Clinical Orthopedics, 51: 190—197, 1967.

  17. Akeson WH, Amiel D, at al:
    Collagen cross-linking alterations in joint contractures: Changes in the reducible cross-links in periarticular connective tissue after nine weeks of immobilization.
    Connective Tissue Research, 5:15—19, 1966.

  18. Evans E, Eggers G, et al:
    Experimental immobilization and mobilization of rat knee joints.
    Journal of Bone & Joint Surgery, 42A:737—758, 1960.

  19. Travell J, Simons DG.
    Myofascial Pain and Dysfunction: The Trigger Point Manual.
    Baltimore, Williams & Wilkins; 1993.

  20. Jaeger B:
    From an interview in The Travell Trigger Point Tapes, Vol I:
    Introduction to myofascial pain therapy.
    Baltimore, Williams & Wilkins, 1990.

  21. Ibid.

  22. Bonica JJ:
    Advances in Neurology Pain.
    New York, Raven Press, Vol 4, 1974.

  23. Guyton AE:
    Textbook of Medical Physiology, ed 7.
    Philadelphia, W.B. Saunders, 1986, p 127.

  24. Fleckerstein JL, et al:
    Sports-related muscle injuries: Evaluation with MR imaging.
    Radiology, 172:793—798. 1989.

  25. Fleckerstein JL, Canby RC, Parkey RW, Peshock RM:
    Acute effects of exercise on MR imaging of skeletal muscle in normal volunteers.
    AJR, 151:231—237, 1988.

  26. Armstrong RB:
    Mechanisms of exercise-induced delayed onset muscular soreness: A brief review.
    Medical Science in Sports Exercise, 16:529—538, 1984.

  27. Newham DJ, McPrail G, Mills KR, Edwards RHT:
    Ultrastructural changes after concentric and eccentric contractions of human muscle.
    Journal of Neurological Science, 61:109—122, 1983.

  28. Guyton AC:
    Textbook of Medical Physiology, ed 7.
    Philadelphia, W.B. Saunders, 1986, p 607.

  29. Dorland’s Illustrated Medical Dictionary, ed 26.
    Philadelphia, W.B. Saunders, 1985, p 716.

  30. Bonica JJ:
    The Management of Pain.
    Philadelphia, Lea & Febiger 1953.

  31. St. John P:
    The science and philosophy of neuromuscular therapy.
    Boulder, CO, Lecture, 1989.

  32. Yunas M, Kaglen-Raman UK, Kaylen-Raman K:
    Primary fibromyalgia syndrome and myofascial pain syndrome: Clinical features and muscle pathology.
    Archives of Physical Medicine, 69: 451-454, 1988.

  33. Fassbender HB:
    Pathology of Rheumatic Disease.
    New York, Springer Verlag, 1975, pp 307—314.

  34. Travell J, Simons DC:
    Myofascial Pain and Dysfunction: The Trigger Point Manual.
    Baltimore, Williams & Wilkins, 1983.

  35. Ibid.

  36. Awad EA:
    Interstitial myofibrositis hypothesis.
    Archives of Physical Medicine, 54:445—453, 1973.

  37. McKenzie R:
    The Lumbar Spine: Mechanical Diagnosis and Therapy.
    New Zealand, Spinal Publications, 1981.

  38. Rolf IP:
    The Integration of Human Structures.
    Santa Monica, CA, Dennis Landman Publishers, 1977.

  39. Lowe JC:
    The Purpose and Practice of Myofascial Therapy.
    Houston, TX, McDowell Press, 1989.

  40. Rocobado M:
    Temporomandibular joint dysfunction:
    Workshop notes. Columbus, OH, 1982.

  41. Travell JG, Simons DG:
    Myofascial Pain and Dysfunction: Trigger Point Manual.
    Baltimore, MD, Williams & Wilkins, 1983, Vol 1, pp 141—142.

  42. Ibid, Vol 2, p 545.

  43. Hook BC:
    Dyskinesis: A case report
    Journal of Manipulative and Physiotherapeutic Therapeutics, September 1985.

  44. Shaw,JL:
    The role of the sacro-iliac joint as a cause of low-back pain and dysfunction.
    In Vleeming A, Mooney V, Sniders C, Dorman T (eds):
    Low-Back Pain and Its Relation to the Sacro-Iliac Joint.
    Proceedings of the First Interdisciplinary World Congress on Low-Back Pain to the Sacro-Iliac Joint,
    University of California, November 5—6, 1992.

  45. Good A:
    Spinal joint blocking.
    Journal of Manipulative and Physiologic Therapeutics, March 1985.

  46. Travell JG, Simons DG:
    Myofascial Pain and Dysfunction. Baltimore,
    Williams & Wilkins, 1992, Vol II, p 29.

  47. Lewinnek GE:
    Management of low back pain and sciatica.
    International Anesthesiology Clinics, 21: 61—79, 1983.

  48. Institute of Medicine:
    Pain and Disability: Clinical, Behavioral, and Public Policy Perspectives.
    Washington, DC, National Academy Press, May 1987.

  49. Shook SH, Jensen RC:
    Chapter 5: Cost.
    In Pope MH, Frymoyer JW, Anderson G (eds): Occupational Low Back Pain.
    Praeger, NY, 1984, pp 115—121.

  50. Good MG:
    Diagnosis and treatment of sciatic pain.
    Lancet, 2:597—598, 1942.

  51. Simons DG, Travell JG:
    Myofascial origins of low back pain: Torso muscles.
    Postgraduate Medicine, 73:81—92, 1983.

  52. Sola AE, Kuitert JH:
    Quadratus lumborum myofascitis.
    Northwest Medicine, 53:1003—1005.

  53. Good MG:
    Diagnosis and treatment of sciatic pain.
    Lancet, 2:597—598, 1942.

  54. Bachrach RM, Micelotta J, Winnk C:
    The relationship of low back pain to psoas insufficiency.
    Journal of Orthopedic Medicine, 13:34—40, 1991.

  55. Hachemson AL:
    Electromyographic studies on the vertebral portion of the psoas muscle.
    Acta Orthopaedica Scandinavica, 37:177—190, 1966.

  56. Durianova J:
    Psoas spasm in the clinical picture of low back pain.
    In Lewin K, et al: (eds): Rehabilitacia.
    Prague, Proceedings of the Fourth Congress.
    International Federation of Manual Medicine, 1975.

  57. Fox EA:
    Let us consider the importance of psoas muscle contraction.
    Journal of the National Chiropractic Association, 26(7):69—74, 1956.

  58. Randeria JP:
    The role of the psoas muscles in low-back pathology.
    Manuelle Medizin, 4:85—87, 1974.

  59. Michele AA:
    Iliopsoas.
    Springfield, IL, Charles C. Thomas, 1962.

  60. Cyriax J:
    Textbook of Orthopaedic Medicine —Diagnosis of Soft Tissue Lesions.
    London, Bailliare Tindall, 1982, Vol I, p 389.

  61. Rolf IP:
    Rolfing: The Integration of Human Structures. Santa Monica, CA,
    Dennis-Landman Publications, 1977, pp 101—151.

  62. Rolf IP:
    Structural integration: A contribution to the understanding of stress.
    Confinia Psychiatrica, 16(2):69—79.

  63. Ibid.

  64. Cailliet R:
    Low Back Pain Syndrome, ed 3.
    Philadelphia, F.A. Davis, 1991, pp 115—116.

  65. Sander G, Straurakas P:
    A technique for measuring pelvic tilt: Suggestions from the field.
    Physical Therapist, 61:49—50, 1991.

  66. Gajdosik R, Simpson R, Smith R, et al:
    Pelvic tilt: Intratester reliability of measuring the standing position and range of motion.
    Physical Therapist, 65:169—174, 1985.

  67. Day JW, Smidt GL, Lehmann T:
    Effect of pelvic tilt on standing posture.
    Physical Therapist, 64:510—514, 1984.

  68. Walker ML, Rothstein JM, Finucare SD, et al:
    Relationships between lumbar lordosis pelvic tilt and abdominal muscle performance.
    Physical Therapist, 67:512—516, 1987.

  69. Shrout PE, Fleiss JL:
    Intraclass correlations: Uses in assessing inter-reliability.
    Psychology Bulletin, 86:420—428, 1979.

  70. Clayson GF, Newman IM, Debeuec DF, et all:
    Evaluation of mobility of hip and lumbar vertebrae of normal young women.
    Archives of Physical Medicine and Rehabilitation, 43:1—8, 1962.

  71. Loebiw Y:
    Measurement of spinal posture and range of spinal movement.
    Annals of Physical Medicine, 9:103—110, 1967.

  72. Browning JE:
    The recognition of mechanically induced pelvic pain and organic dysfunction in the low-back pain patient.
    Journal of Manipulative and Physiologic Therapeutics, 12(5):369—373.

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