Iliotibial Band Friction Syndrome Is Frictionless

By Warren Hammer, MS, DC, DABCO

Iliotibial band syndrome (ITBS) is the most common cause of lateral knee pain in runners.¹It is described as an overuse injury caused by repetitive friction of the iliotibial band over the lateral femoral epicondyle, with the maximal zone of impingement at about 30 degrees of knee flexion.¹ But if it is found that the ITB does not move anteroposteriorly over the epicondyle, how can friction occur? Rather than friction, it has been determined that at 30 degrees of knee flexion there is internal rotation of the tibia and the ITB is compressed against the lateral epicondyle; while with knee extension, the band is pulled laterally away from the epicondyle.

The ITB is anchored to the distal femur by fibrous strands, which prevents the purported antero-postero movement. Deep to the distal portion of the band is a layer of richly innervated and vascularized fat. Pain may be caused by fat compression beneath the tract instead of friction during flexion and extension. The idea that there is a forward and backward movement of the ITB over the epicondyle is really an illusion due to changing tension in its anterior and posterior fibers.²

In a study by Fairclough, et al., published in the Journal of Anatomy,³ magnetic resonance scans and gross and microscopic anatomy were evaluated in 15 cadavers, six asymptomatic volunteers and two athletes with acute ITB syndrome. Between the ITB and lateral epicondyle, there is adipose tissue containing many blood vessels and nerves (even Pacinian corpuscles that when hypertrophied, become associated with pain) and are more likely affected by compression than a friction movement. The MR scans showed that at 30 degrees of knee flexion, the ITB is drawn medially toward the epicondyle (due to passive tibial rotation) and the vastus lateralis, which, due to an increase in tension, moves the fat deep to the ITB and adds to the compression.

So, the ITB is really moving in a medial-lateral direction. The fatty tissue may be normally acting as a brace to reduce bending stresses on the bone and also convert tensile to compressive loading on the lateral side of the joint.¹ Fatty tissue is often found at many tendon and ligament entheses,⁴ and may be the cause of the local edema.

The authors found no bursa in the area; it is possible that the swelling is really due to the irritation of the fatty tissue, rather than a bursitis. It was also found that there were two separate types of tissues at the distal ends – "tendinous" type was found proximal to the lateral femoral epicondyle and a "ligamentous" type was identified between the epicondyle and Gerdy's tubercle.³ The tendinous part of the ITB, therefore, does not cross the knee joint, indicating that the tensor fascia latae muscle has no effect on the knee joint and actually exerts most of its effect by tensing "the fascial envelope around the thigh to promote optimal muscle function on the hip joint."²

The ITB is really not a separate band. It is a thickening of the fascia lata that covers the whole thigh. The ITB is also continuous with the lateral intermuscular septum, which is anchored to the linea aspera of the femur. So, the ITB is really a fascial structure. There are fibrous bands that attach from the ITB to the distal femur and to the lateral epicondyle. These strands pass through to the periosteum and have been likened to a tendon enthesis. The ITB is therefore anchored at the distal end and would not rub over the lateral epicondyle in overuse injuries.

This information questions the use of surgery, breaking down adhesions around the epicondyle or even stretching the distal area. In order for stretching of the area to be therapeutic, "the fascia lata, the lateral intermuscular septum and the distal fibrous bands anchoring the ITB to the femur would all need to be stretched for the ITB to be lengthened."² Probably the effect of stretching is the stretch of the hip abductors occurring during the ITB stretch, indicating that the primary problem is at the hip and the pain at the lateral epicondyle area is only secondary.

It has been found that hip abductor weakness is related to the ITBS.⁵ Therefore, hip ranges of motion and the myofascia should be evaluated for possible weakness and adhesions. This represents another instance of a proximal problem in the kinetic chain affecting a distal area, which is routinely found in the use of fascial manipulation.

References

1. Fredericson M, Wolf C. Iliotibial band syndrome in runners, innovations in treatment.Sports Med, 2005;35(5):451-459.
2. Fairclough J, Hayashi K, Toumi H, et al. Is iliotibial band syndrome really a friction syndrome? J Sci & Med in Sport, 2007;10:74-76.
3. Fairclough J, Hayashi K, Toumi H, et al. The functional anatomy of the iliotibial band during flexion and extension of the knee: implications for understanding iliotibial band syndrome.J Anat, 2006;208:309-316.
4. Benjamin M, Redman S, Milz S, et al. Adipose tissue at entheses: the rheumatological implications of its distribution. A potential site of pain and stress dissipation? Ann Rheum Dis, 2004;63:1544-55.
5. Fredericson M, Cookingham CL, Chaudhari AM, et al. Hip abductor weakness in distance runners with iliotibial band syndrome. Clin J Sports Med, 2000;10:169-75

Soft-Tissue Treatment Is Another Form of Exercise

By Warren Hammer, MS, DC, DABCO

Physical activity restores our body by way of mechanical loading. Mechanical loading is the crux of many methods of soft-tissue treatment.

Mechanical loading by a practitioner is a form of physical activity performed on a patient.

Mechanical loading is the principal way our body maintains itself, especially with regards to tendons, ligaments, bone, muscle and fascia. Lack of mechanical loading results in atrophy and eventual cell death. Years ago, anyone with acute lower back pain was sent to bed for a week. We now know that as soon as a patient can move with minimal discomfort, they should get out of bed and attempt the movement – i.e., mechanical loading. Thus, just rubbing someone’s skin or deeper tissues is mechanical loading that may be considered a localized form of exercise.

The literature is replete with studies on mechanical loading and its resultant effects on the extracellular matrix (ECM), especially connective tissue and its collagen, tissue structure maintenance, release of growth factors, metabolic activity, protein synthesis, cell growth and survival, circulation, and gene expression. This is only a partial list of factors related to the mechanical load created by methods such as Graston, fascial manipulation, acupuncture and others.

Cell proliferation requires cell spreading and exertion of force on the ECM. Even internally, mechanical forces associated with blood flow play important roles in the acute control of vascular tone, the regulation of arterial structure and remodeling, and the localization of atherosclerotic lesions.¹ It is hypothesized, for example, that "stress concentration" on the walls of arteries due to arterial pressure and accompanying stretch relates to the localization of atherosclerotic plaques in particular arterial areas.² So, mechanical forces that are crucial to the regulation of cell and tissue morphology and function could have both positive and negative effects (overuse, trauma, etc.)

In order for mechanical load to exert its effects, it is necessary for a process of mechanotransduction to occur, whereby stressed cells convert mechanical stimuli into chemical responses. The description as to how all this works is very complicated, but certain terminology should be part of our lexicon.³ In the field of biochemistry, a receptor is a molecule most often found on the surface of a cell, which receives chemical signals originating externally from the cell. Through binding to a receptor, these signals direct a cell to do something; for example, to divide or die, or to allow certain molecules to enter or exit.

Receptors are protein molecules embedded in the plasma membrane (cell surface receptors), or the cytoplasm or nucleus (nuclear receptors) of a cell, to which one or more specific kinds of signaling molecules may attach. A molecule that binds (attaches) to a receptor is called a ligand, and may be a peptide (short protein) or other small molecule, such as a neurotransmitter, a hormone, a pharmaceutical drug or a toxin. A ligand is a signal-triggering molecule, binding to a site on a target protein (receptor).

Numerous receptor types are found within a typical cell and each type is linked to a specific biochemical pathway. Each type of receptor recognizes and binds only certain ligand shapes (an analogy to a lock and key, with the lock representing the receptor and the key, its ligand). Hence, the selective binding of a specific ligand to its receptor activates or inhibits a specific biochemical pathway.

An important receptor is called an integrin; it connects the inner structure of the cell (cytoskeleton) with its surrounding ECM. Integrins sense mechanical forces (stretch and fluid flow) and transmit mechanical stresses across the plasma membrane into the cell. By regulating signaling pathways, they transduce physical forces into chemical signals.

Not only do integrins perform this outside-in signaling, but they also operate in an inside-out mode. Thus, they transduce information from the ECM to the cell, as well as reveal the status of the cell to the outside, allowing rapid and flexible responses to changes in the environment. Integrins are the sensors of tensile strain at the cell surface and play a crucial role in linking the ECM to the cytoskeleton. Mechanical loading creates tensile strain, among other things.

The concept of the receptor-ligand interaction is one of the most basic in all of biology. It is a key element to the functioning of all biological systems. It allows neighboring and distant cells to communicate with each other. One cell may have a receptor in its membrane and when it binds to a matching ligand on a neighboring cell, the receptor performs some action. Typically, this action is to take an existing protein and modify it in some way; to either activate or deactivate it.

It appears that the acupuncture theory of chi and "vital energy" can now be explained by the effect of mechanical load on points located in the fascial system, resulting in a receptor-ligand interaction. Both physical activity and the laying on of hands and/or instruments are stressing and exciting this cellular interaction. It remains for the clinician who uses mechanical load on soft tissue to continually improve their skill by determining – through trial and error, and controlled studies – exactly where to put their hands, and to measure whether the loading of a particular area will improve function.

References

1. Davies PF. Flow-mediated endothelial mechanotransduction. Physiol Rev, July 1995;75(3):519-560.
2. Thubrikar MJ, Robicsek F. Pressure-induced arterial wall stress and atherosclerosis. Ann Thorac Surg, 1995;59:1594-1603.
3. Description of ligand, receptor and integrin. From Wikipedia, the free encyclopedia.

Fascial Thickening Is Responsible for Musculoskeletal Pain

By Warren Hammer, MS, DC, DABCO

An important study in the fascial world by Langevin (2009)¹ proposed that people with chronic and recurrent low back pain had 25 percent greater fascial thickness than a low back pain-free group.

Helene Langevin, MD, is a researcher at the University of Vermont who devotes a considerable amount of time studying connective tissue. She concluded her study by stating: "Increased thickness and disorganization of connective tissue layers may be an important and so-far neglected factor in human LBP pathophysiology."

She is not alone in her findings. Another study in Skeletal Radiology, 2005,² found that pathological Achilles tendonsshowed increased thickness and 89 percent were painful.

Antonio Stecco, MD, recently completed an unpublished study³ using ultrasonography on chronic (longer than 3 months' duration) neck pain patients, evaluating fascial thickness in the distal third of the SCM and scalenus medius. The deep fascia in both muscles were thicker due to the increased amount of loose connective tissue between the layers of the deep fascia (usually three layers) and the loose connective tissue between the deep fascia and the muscle.

There was a correlation between the intensity of the pain and the thickness of the fascia compared to the control patients. The dense-collagen type I fibers remained the same, while the loose connective tissue demonstrated increased GAGs and hyaluronic acid. (Figure 1) The entanglement ofhyaluronic acid (HA) molecules is the apparent cause of increased stiffness and decreased articular ROM.^4-5 (Figure 2)

According to Matteini, et al, "These chain-chain interactions were reported to be reversibly disaggregated by an increase in temperature or by alkalization." Moreover, "Recent infrared spectroscopy studies have suggested the formation of three-dimensional superstructures of HA chains stabilized by water bridges. This water-mediated supramolecular assembly was shown to break down progressively when the temperature was increased to over 40° C, in accordance with previous MRI observations."⁶

The presence of abnormal HA finally explains many of the fascial treatment explanations whereby pressure against tissue allows a "release" of the area from a gel to a solid. But to change HA entanglements, a major requirement is to increase the temperature several degrees. This might also explain an effect of moist heat. The retention of HA after exercise, as well as its endomysial location, is in accordance with the concept that HA is a substance that is present to lubricate and facilitate the movements between the muscle fibers.³

Besides the thickening of fascia beneath the deep fascia and muscle, there may be thickening between the superficial and deep fascia, and the intramuscular fascia surrounding perimysium and endomysium. According to the principles of fascial manipulation, it is essential that there be a gliding of the fascial system around and within the muscular tissue;⁷ otherwise there will be abnormal proprioception, incoordination of muscle function and pain. Graston Technique and deep friction massage are ideal methods to provide the necessary tissue compression and heat for these types of lesions.

References

1. Langevin HM,Stevens-Tuttle D, Fox JR, et al. Ultrasound evidence of altered lumbar connective tissue structure in human subjects with chronic low back pain. BMC Musculoskeletal Disorders, 2009;10:151.
2. Richards PJ, Win T, Jones PW. The distribution of microvascular response in Achilles tendonopathy assessed by color and power Doppler. Skeletal Radiol, 2005 Jun;34(6):336-42.
3. Stecco A. "Evaluation of the Role of Ultrasonography in the Diagnosis of Myofascial Neck Pain." Department of Physical Medicine and Rehabilitation, University of Padua, Italy, 2011.
4. Piehl-Aulin K, et al; Hyaluronan in human skeletal muscle of lower extremity: concentration, distribution, and effect of exercise. J Appl Physiol, 1991 Dec;71(6):2493-8.
5. Stecco A. Slide presentation on the physiology of fascia. Fascial Manipulation Seminar, Part I, Las Vegas; Feb. 17-19, 2012.
6. Matteini P, et al. Structural behavior of highly concentrated hyaluronan.Biomacromolecules, 2009 Jun 8;10(6):1516-22.
7. Stecco L, Stecco C. Fascial Manipulation Practical Part. Piccin, Padova, Italy, 2009.

Gua Sha: Another Form of Mechanical Load

By Warren Hammer, MS, DC, DABCO

Every technique that creates compression or tensile stretch to soft tissue creates a mechanical load that is necessary for tissue change. Gua sha represents another form of mechanical load on soft tissue that claims healing results and, like all other soft-tissue methods, begs for research to prove its value.

Arya Nielsen, PhD, adjunct faculty in the Department of Integrative Medicine at New York Beth Israel Medical Center,Continuum Center for Health & Healing, and a strong proponent of gua sha, wrote an interesting article in the January 2009 issue of the Journal of Bodywork and Movement Therapies (JBMT).1 She states that often the literature incorrectly describes the results of gua sha as causing battery trauma, bruising, burns, dermatitis, pseudo bleeding and even hematoma.

Although gua means to "scrape" or "scratch" in Chinese, the skin always remains intact and there are no abrasions. Sha represents the "transient therapeutic petechiae." The extravasated blood appears as red macula and fades to ecchymosis immediately, blending into an ecchymotic patch. The scraping reveals blood stasis and its use removes blood stagnation that is considered pathogenic, thereby promoting normal circulation and metabolic processes. Gua sha lets blood from the tissue and is not let from the skin.²

This method originated in Asia and is used today in East Asian medicine and by acupuncturists. Nielsen mentions its use for colds, flu, fever, heatstroke, asthma, bronchitis and emphysema, as well as musculoskeletal problems including fibromyalgia to severe strain. Improving blood stasis and sha may even be significant in asymptomatic subjects who are considered healthy.

A recent study using laser Doppler imaging was used to make sequential measurements of the microcirculation of surface tissue before and after gua sha treatment³ in order to relieve pain. The result was a fourfold increase in microcirculation for the first 7.5 minutes following treatment and a significant increase in surface microcirculation during the entire 25 minutes of the study period following treatment. There was a decrease in myalgia not only locally but also in sites distal to the treated areas. The authors stated that the distal area of relief was not due to a distal increase in microcirculation and asserted, "There is an unidentified pain-relieving biomechanism associated with gua sha."

Recent theories based on tensegrity and the fascial continuum help to explain distal results from localized mechanical load. Ingber, who has written much on our tensegrity structure,⁴demonstrates how living cells and tissues sense and respond to mechanical stresses and in the rearrangement of the structure become mechanochemical transducers, whereby mechanical signals create chemical responses affecting local and distal parts of our structure.

Fibroblasts are the chief cell in the extracellular matrix and reproduce the extracellular matrix upon being loaded; it is thought by Langevin, et al.,⁵ that the existence of a cellular network of fibroblasts within loose connective tissue may have considerable significance, as it may support as-yet unknown bodywide cellular signaling systems. She states that fascia may serve as a bodywide mechanosensitive signaling system with an integrating function similar to the nervous system. Regarding gua sha and GT, increasing the microcirculation may stimulate platelets which release growth factors related to the healing of tissue.

Graston Technique (GT) has been compared with gua sha, and I have even heard some say that GT adopted the gua sha concept. GT was initially used on a postsurgical knee. It is extremely doubtful that the discoverers were at all familiar with gua sha, but even if they were, the GT application is significantly different. GT research has been directed toward the musculoskeletal system and its effect on various soft-tissue conditions. New studies are continually appearing demonstrating how it may be affecting soft tissue. It has its own protocol and uses instruments of different weights, shapes, and sizes to conform to the bodily contours. Its stainless-steel vibratory effect is used to detect restricted areas after functional tests are performed to determine the involved location.

While both methods can create petechiae, the stroking is not performed in the same manner. GT often achieves results without creating any petechiae at all. GT uses at least seven types of strokes, while gua sha repeats a stroke in one direction about 4-6 inches long specifically to create "therapeutic" petechiae.¹ A variety of instrument angulations and pressures may be used in GT depending upon the area of the body treated.

Doctors trained in both methods realize the vast differences. Both methods have their place and there is some obvious overlap, but the differences between the methods are significant. At present, all soft-tissue loading methods are still in their infancy regarding research as to how they affect our structure and function. Einstein referred to a unifying theory of the universe. Hopefully, there might someday be one for soft tissue.

References

1. Nielsen A. Gua sha research and the language of integrative medicine. JBMT, January 2009;13,63-72.
2. Nielsen A. Gua Sha: A Traditional Technique for Modern Practice. Edinburg: Churchill Livingstone, 2002.
3. Nielsen A, Knoblauch N, Dobos G, et al. The effect of gua sha treatment on the microcirculation of surface tissue: a pilot study in healthy subjects. EXPLORE: The Journal of Science and Healing, September 2007;3(5):456-66.
4. Ingber DE. Tensegrity: the architectural basis of cellular mechanotransduction.Ann Rev Physeal, 1997;59:575-99.
5. Langevin H, Cornbrooks CJ, Taatjes DJ. Fibroblasts form a body-wide cellular network. Histochem Cell Biol, 2004;122:7-15.

Physiological Effects of Therapeutic Massage

By Warren Hammer, MS, DC, DABCO

Many chiropractors either perform some type of massage on their patients or have a massage therapist in their office.

The term therapeutic massage (TM) is a general, nonspecific term referring to any type of massage, from superficial to deep, that may have a healing effect. Most massage therapists¹ "train in multiple programs and therapies and there is high variability in the training programs and in what therapies practitioners choose to learn."² Methods of massage include, among others, effleurage, petrissage, friction and tapotement. TM also can refer to most hands-on therapies including fascial manipulation, Graston, structural integration, active release, Swedish massage and others.

Claims regarding the effects of TM include changes in hormones, neurotransmitters, blood flow and cortisol, among others. However, as with most other mechanical pressure methods used on humans, there is a paucity of research supporting its efficacy, optimal treatment parameters and underlying physiologic responses.

Recent studies have added to the body of knowledge regarding the effects of mechanical load, showing definite physiological and clinical changes^2-3 related to TM. An important effect of TM is thought to be its effect on peripheral blood flow. While skin temperature correlates with skin blood-flow studies, skin probes and their effect on the skin are questionable.⁴ A recent study using dynamic infrared thermography² compared the effects of a 20-minute massage that included a deep muscle combination of friction, gliding (effleurage), kneading (petrissage), direct pressure and passive stretching to the neck and shoulders versus light touch (just the hands placed in contact with the skin) or a control scenario in which the patient rested quietly in the treatment position.

Light touch produced some changes in temperature, but the most significant changes occurred with the deeper massage treatment. What is most interesting is that the areas not massaged (posterior right arm, C6 to C8 dermatomes, and thoracic middle back T1 to T8 dermatomes) showed an increase in skin temperature and peripheral blood perfusion similar to the areas massaged, indicating a possible neural as well as a circulation component. The areas receiving a deeper massage showed increased temperature for 35 minutes and remained above baseline levels after 60 minutes.

One of the effects of deep massage is temperature elevation that changes hyaluronic acid molecules, which are responsible for the gel phase causing tissue restriction. The increase in temperature with associated pressure changes the gel to a fluid phase and creates the necessary tissue sliding. One study found that massage to a depth of between 1.5 cm and 2.5 cm caused changes in muscle temperature significantly greater than ultrasound.⁵

Some of the same authors of the above study submitted another significant paper on deep massage that recently appeared in Manual Therapy.³ This study compared the same three groups as the previous study: deep massage and light touch over the neck and upper trapezius areas, along with a control group. This time, the authors measured flexor carpi radialis α-motor neuron pool excitability (Hoffmann's reflex, otherwise known as the H-reflex), electromyography (EMG) signal amplitude of the upper trapezius during maximal muscle activity, and cervical ROM to help assess physiological changes and clinical effects of deeper massage compared to light touch.

The H-reflex is similar to the stretch reflex (knee jerk reflex), but differs in that it bypasses the muscle spindle and is used to assess monosynaptic reflex activity in the spinal cord. Electrical stimulation causing the H-reflex measures the efficacy of synaptic transmission as the stimulus travels along the Ia fibers, through the dorsal root ganglion, and is transmitted across the central synapse to the anterior horn cell, which fires it down along the alpha motor axon to the muscle. This measurement can be used to assess the response of the nervous system to various neurologic conditions, musculoskeletal injuries, application of therapeutic modalities, pain, exercise training, and performance of motor tasks.

In this study,³ even though the upper trapezius area was massaged, the H-reflex for this area is difficult to elicit, so the authors checked the motor neuron pool excitability in an outlying area that was not massaged: the flexor carpi radialis muscle (FCR), which generates a reliable reflex. They reasoned that massaging the trapezius and neck area would affect the cervical and brachial plexus and the median nerve, which innervates the FCR.

The H-reflex test did show a decrease in FCR α-motor neuron pool excitability compared to the light-touch and control groups. The fact that there was a decrease in neuron excitability in a non-massaged area suggests the possibility that massage was producing a centralized effect on the nervous system, affecting spinal-cord response in another area. This same neuronal possibility was expressed in the change in peripheral blood perfusion in non-massaged areas in the previous study.²

Another finding was the decrease in EMG signal amplitude in the upper trapezius muscle with deep massage, which did not occur with light touch or control. The EMG change was probably due to the decrease in -motor neuron pool activation, which has an influence on electrical activity. Additionally, compared to light touch and control, deep massage increased ROM in all cervical directions.

One caveat is that all of the studies were performed on people without known pathology, but the neurological implications of deep massage affecting circulation and the nervous system are important. The fascial manipulation hypothesis is based on the release of restricted fascia that houses mechanoreceptors and proprioceptors, thereby influencing the CNS' effect on myofascia.

Everyone who seriously uses deep massage is aware of positive changes. Science may finally be proving why there are clinical results.

References

1. Porcino AJ, Boon HS, Page SA, Verhoef. Meaning and challenges in the practice of multiple therapeutic massage modalities: a combined methods study. BMC Complement Altern Med, 2011;11:75.
2. Sefton JM, Yarar C, Berry JW, Pascoe DD. Therapeutic massage of the neck and shoulders produces changes in peripheral blood flow when assessed with dynamic infrared thermography. J Alterative & Complementary Med, 2010;16(7):723-732.
3. Sefton JM, Yarar C, Carpenter DM, Berry JW. Physiological and clinical changes after therapeutic massage of the neck and shoulders. Manual Therapy, 2011;16:487-494.
4. Pascoe DD, Mercer JB, de Weerd L. Physiologies of Thermal Signals. In: Bronzino JD, editor.Medical Devices and Systems. 3rd Edition. Boca Raton, FL: CRD Taylor & Francis, 2006:21-7.
5. Drust B, Atkinson G, Gregson W, et al. The effects of massage on intra muscular temperature in the vastus lateralis in humans. Int J Sports Med, 2003;24:395-399.

Fascial Tension Headaches

By Warren Hammer, MS, DC, DABCO

Tension-type headache (TTH) is the most common form of primary headache in the general population and like all headache complaints, requires an adequate case history to exclude other possible causes falling under the headings of cervicogenic, vascular migraine or cluster-type; organic vascular types such as subarachnoid hemorrhage, subdural hematoma, arterial hypertension, intracranial neoplasm, meningitis and infection; allergic substances; metabolic disorders; and extracranial causes such as the teeth and TMJ, among many others.¹

Tension-type headache is essentially defined as a bilateral headache of a pressing or tightening quality without a known medical cause. A tension headache is generally a diffuse, mild to moderate pain that's often described as feeling like a tight band around the head or a big weight over the head or shoulders. It is seldom pulsating unless the pain is severe.²

A non-pulsating, pressing pain is the most common complaint plus tenderness of the scalp, especially in the temporal areas. Characteristics of TTH from theInternational Classification of Headache Disorders are:³

• Episodic infrequent: < 1 day per month; episodic frequent: 1-14 days; chronic: > 15 days.
• Headache lasting from 30 minutes to seven days in duration.
• At least two of the following pain characteristics: pressing / tightening (non-pulsating) quality; mild or moderate intensity (may inhibit, but does not prohibit activities); bilateral location; and no aggravation by walking stairs or similar routine physical activity.
• Both of the following: no nausea or vomiting (anorexia may occur); and photophobia and phonophobia are absent, or one but not the other is present.

Any headache that displays a worsening pattern should raise a red flag, as should a change in characteristics such as nausea or vomiting and abnormal neurological findings.²

Both pharmacological and nonpharmacological treatments such as electromyographic (EMG) biofeedback, cognitive-behavioral therapy, relaxation training, trigger-pointtherapy, physical therapy and acupuncture have produced symptomatic results.

Currently, I am helping to edit a new text on the fascial system based on the research of Carla Stecco, MD. The book represents years of research by her on the fascial system. Dr. Stecco, who recently presented at the recent International Fascial Conference in Vancouver, writes in her upcoming text: "A common cause of cephalalgia is excessive tension of the temporalis muscle. A large percentage of the muscular fibers of the temporalis insert into the underside of the deep temporal fascia that is in continuity with the epicranial fascia. If the temporalis muscle becomes hypertonic the epicranial fascia becomes overstretched. This could activate the free nerve endings in the fascia, resulting in headache-like symptoms."

Pericranial myofascial tenderness recorded by manual palpation is a significant abnormal finding in many patients with TTH⁴ and has been recorded by pressure pain detection and tolerances in cephalic and extracephalic locations with an electronic pressure algometer.⁵ In TTH, there are also found many myofascial trigger points. It is possible that sensitization of myofascial nociceptors could be responsible for pain.

Sensitization of pain pathways in the central nervous system due to prolonged nociceptive stimuli from pericranial myofascial tissues might be responsible for prolonged pain. Significantly lower pressure pain detection thresholds and tolerances were found in all the examined locations in patients with chronic tension-type headache with a muscular disorder compared to those without a muscular disorder.⁴ It appears that disruption of cranial fascia may be causative regarding tension headaches.

Soft-tissue techniques such as fascial manipulation reduce myofascial restrictive areas by restoring normal gliding of the deep fascia with the underlying muscular fibers. This is thought to restore normal sensory stimulation and can be an effective treatment for chronic tension headaches.⁶ This may also explain the effectiveness of other types of treatment that have a fascial effect, such as Graston, active release, structural integration, muscle energy and others.

It is therefore apparent that the fascial system must be considered in TTH, and also in other types of headaches such as migraine and cervicogenic types. Current evidence that spinal manipulation alleviates tension-type headaches is encouraging, but inconclusive due to the low quantity of available data preventing a firm conclusion.⁷

A tension headache is not considered a cervicogenic-type headache. Cervicogenic headache (CH) originates from disorders of the neck and is recognized as a referred pain in the head. Freese, et al.,⁸ summarize this type of headache as follows:

"Primary sensory afferents from the cervical roots C1-C3 converge with afferents from the occiput and trigeminal afferents on the same second-order neuron in the upper cervical spine. Consequently, the anatomical structures innervated by the cervical roots C1-C3 are potential sources of CH. In normal volunteers, the painful stimulation of different anatomical structures of the neck produced headache. In CH, particular structures have been selectively anesthetized in order to identify possible sources of pain. In summary, CH can originate from different muscles and ligaments of the neck, from intervertebral discs, and, particularly, from the atlanto-occipital, atlantoaxial, and C2/C3 zygapophyseal joints. Diagnosis of CH should adhere strictly to the published diagnostic criteria to avoid misdiagnosis and confusion with primary headache disorders such as migraine and tension type headache."

Cervicogenic headache as differentiated from TTH is usually a unilateral headache of fluctuating intensity increased by movement of the head and typically radiating from occipital to frontal regions.

Finally, sometimes it is difficult to differentiate common migraine from cervicogenic headaches since there are similar symptoms, such as being often unilateral and more common in females; but for cervicogenic there is usually a reduced range of neck motion or pain with external pressure over the greater occipital C2 nerve root and possible ipsilateral shoulder / arm pain. Typical migraine symptoms include nausea, vomiting, photophobia and phonophobia, which may occur in cervicogenic headache, but are not as common.⁹

References

1. Mueller L. Tension-type, the forgotten headache. How to recognize this common but undertreated condition. Postgrad Med, 2002 Apr;111(4):25-6, 31-2, 37-8.
2. Bigal ME, Lipton RB. Tension-type headache: classification and diagnosis. Current Pain and Headache Reports, 2005;9:423-429.
3. International Statistical Classification of Diseases and Related Health Problems, 10th revision, Volume 2. World Health Organization, December 2004.www.who.int/classifications
4. Sandrini G, Antonaci F, Pucci E, et al. Comparative stud with EMG, pressure algometry, and manual palpation in tension-type headache and migraine. Cephalalgia, 1994;14:451-457.
5. Jensen R, Bendtsen L, Olesen J. Muscular factors are of importance in tension-type headache. Headache, 1998 Jan;38(1):10-7.
6. Stecco L, Stecco C. Fascial Manipulation: Practical Part. 2009, Piccin Nuova Libraria S.p.A., Padova. www.piccin.it
7. Posadzki P, Ernst E. Spinal manipulations for tension-type headaches: a systematic review of randomized controlled trials. Complement Ther Med, 2012 Aug;20(4):232-9.
8. Frese A, Schilgen M, Husstedt IW, Evers S. [Pathophysiology and clinical manifestation of cervicogenic headache.] (Article in German) Schmerz, 2003 Apr;17(2):125-30.
9. Sjaastad O, Bovim G. Cervicogenic headache. The differentiation from common migraine. An overview. Funct Neurol, 1991 Apr-Jun;6(2):93-100.

Hyaluronic Acid and the Myofascial Pain Syndrome

By Warren Hammer, MS, DC, DABCO

"Myofascial pain syndromes (MPS) are among the most frequent pain conditions encountered in the general population.

They are also the most often under-diagnosed or misdiagnosed condition."¹MPS, previously called fibrositis or myofibrositis, could be the underlying etiology of even nonspecific back pain. It is estimated that 30 percent of patients with regional pain complaints seen in primary care clinics have myofascial pain and 85 percent of patients presenting to specialized pain management centers have myofascial pain.^2-3 A major problem with this diagnosis is that there has been "no standard, universally accepted biochemical, electro-diagnostic, diagnostic-imaging or physical examination criteria existing for a diagnosis of MPS."⁴

A major question with regard to all types of manual load-type treatments including Graston, ART, fascial manipulation, deep massage, Rolfing, etc., is why these treatments are successful for MPS. Another question to eventually be answered is why they are sometimes unsuccessful. There may be a common underlying reason that answers both questions related to hyaluronic acid (HA)

In a previous article in Dynamic Chiropractic,⁵ I shared that it is very possible HA may be the principal substance causing soft-tissue restriction, and is the substance responding to mechanical load that allows a decrease in viscosity and thereby a normalization of densified tissue. HA (sodium hyaluronate) injections into the glenohumeral joint for primary adhesive capsulitis has proved to be very successful.⁶ It has also been proven beneficial in the treatment of knee osteoarthritis and in reducing postsurgical tendon adhesions.^7-8

In healthy tissue, HA supports normal homeostasis and suppresses cell proliferation, angiogenesis, inflammation and immunogenicity. HA also lessens the proinflammatory mediators and pain-producing neuropeptides released by activated synovial cells.

A recent paper on this subject by Stecco A, et al. (2013)⁹ explains how densified tissue (increased viscosity) can be responsible for MPS. Densification results in abnormal sliding between the overlying deep fascia on the muscle and within the epimysium and perimysium layers within the muscles. Changes in viscoelasticity of fascia can modify activation of the nerve receptors within fascia. Within fascia are mechanoreceptors that can send pain messages when stretching occurs within densified fascia. Muscle spindle cells are within the epi and peri layers; if embedded in fascia, not allowing the full stretch of the spindle cell during muscle contraction, there will be improper feedback to the CNS, resulting in muscle incoordination. Increased concentration and size of HA chains entangle into complex groupings, changing hydrodynamic properties and thereby altering normal viscoelastic properties.

Abnormal HA fragmentation can be reversed by increased temperature, local alkalization, deep massage or physical therapies "that are able to cause disaggregation of the pathologic chain-chain (HA) aggregations."⁹ Densification occurs within the loose connective-tissue layers inside and around the fascia. Within loose connective tissue are water, ions and other substances that also can affect the biomechanical properties of this connective tissue. Sliding between fascia and muscles occurs at the loose connective-tissue level.

Increased acidity is a major factor causing increased HA viscosity. A pH of 6.6 (increased lactic acid) increases the viscosity of HA in the endomysium and perimysium of muscles. This accounts for possible stiffness after activity and the eventual normalization that occurs after degradation of lactic acid. But it is possible that before, let's say, an athletic event, overwork or trauma, there are already areas of densifications in individuals that cannot be restored to normal viscosity. These areas may react as MPS "trigger points" or densifications and when stressed, result in pain.

As is often said, most patients are accidents waiting to happen. Could it be that the fascial densifications due to HA accumulation and the abnormal proprioceptive effects are responsible for so many myofascial problems, especially MPS?

Notice the use of the word densification instead of fibrosis or scars. A fibrosis / scar results from the biological process of wound repair in the skin and other tissues of the body. Scarring is therefore a natural part of the healing process. With the exception of very minor lesions, every wound (e.g., after accident, disease or surgery) results in some degree of scarring.

Abnormal fibrosis (collagen cross-links) forms a pronounced alignment in a single direction. This collagen scar-tissue alignment is usually of inferior functional quality to the normal collagen randomized alignment. In other words, an injury is necessary to form scar tissue. Most of the areas we palpate are not scars or fibrotic tissue, but are considered densifications. When fibrosis does happen, it occurs in the dense connective tissue.

Dysfunction or "densification" of fascia occurs in the loose connective tissue containing adipose cells, GAGs and HA. Alterations of the contents of the loose connective tissue can be the result of a combination of any of its elements, especially the HA. This will result in increased viscosity and functional involvement of the fascial and muscular component.

Since these densifications may be palpated throughout the body, random treatment of these areas may not necessarily prove to help the patient. A reason for treatment failure using manual load may be due to the fact that the correct points / areas are not treated and not enough time is spent to truly eliminate the densification. Patients will point to the site of their pain, but on palpation, there is no palpable densification.

Fascial manipulation teaches the practitioner to choose the particular sequence of densifications based on planes (acupuncture meridian, fascial expansions, fascial planes) that are principally involved. It is necessary to decide in advance what plane is the most significant and to choose the points you intend to treat in advance.

It has been found that a certain amount of time and pressure is necessary to free the abnormal viscous point and eliminate the HA entanglements (usually about two minutes or more). With experience, using a compression / friction on these points should allow the practitioner to palpate a "melting" of the area. If the right area or areas are dissipated, then a functional test that expressed the patient's pain should retest normally.

In treating these densifications, once you decide to treat an area, the treatment should continue on the area until palpation reveals that the area has dissipated and no longer exists. Sometimes due to patient tenderness you have to treat an area of density above or below the area to free up the plane of fascia you have chosen to treat. After treating a proximal or distal location, you will find that the painful density has markedly diminished and can now be disposed of in short order. It's like releasing a tense rubber band that could extend in some cases from the feet to the neck.

The coupling of mechanical load on tissue, with its inherent mechanoreceptors, and the realization that fascia is considered a sensory organ and not just a "protective covering," as it has been referred to over the years, opens up the door to a healing modality dealing with actual causation rather than the traditional approach of just symptomatic treatment.

References

1. Cummings M. Regional myofascial pain: diagnosis and management. Best Practice & Research Clin Rheum, 2007;21(2):367–87.
2. Skootsky SA, Jaeger B & Oye RK. Prevalence of myofascial pain in general internal medicine practice. Western J Med 1989; 151: 157–160.
3. Gerwin RD. Classification, epidemiology, and natural history of myofascial pain syndrome.Current Pain Headache Rep, 2001;5:412–420.
4. Annaswamy TM, et al. Emerging concepts in the treatment of myofascial pain: a review of medications, modalities, and needle-based interventions. Am J Phys Med Rehabil, 2011 Oct;3(10):940-61.
5. Hammer WI. "Hyaluronan: A Reason for Soft Tissue Release." Dynamic Chiropractic, Jan. 29, 2011.
6. Harris JD, Griesser MJ, Copeland A, Jones GL. Treatment of adhesive capsulitis with intra-articular hyaluronate: a systematic review. Int J Shoulder Surg, 2011;5(2):31-37.
7. Wang CT, Lin J, Chang CJ et al., Therapeutic effects of hyaluronic acid on osteoarthritis of the knee. A meta-analysis of randomized controlled trials. J Bone Joint Surg (U.S.),2004;86-AA:538-45.
8. Miller JA, Ferguson RL, Powers DL, et al., Efficacy of hyaluronic acid nonsteroidal anti-inflammatory drug systems in preventing postsurgical tendon adhesions. J Biomed Mater Res, 1997;38:25-33.
9. Stecco A, Gesi M, Stecco C, Stern R. Fascial components of the myofascial pain syndrome.Curr Pain Headache Rep, 2013;17:352.

What's Triggering That Point?

Why you should avoid random treatment of trigger points (part 1).

By Warren Hammer, MS, DC, DABCO

An orthopedic friend recently saw a patient of mine. He felt an injection of a trigger point (TP) at the upper trapezius and surrounding areas was necessary, since that was the patient's area of chief complaint and there was a tender, radiating nodule.

I told him I hoped the injection would help, but I did not feel random treatment of a local area of pain would necessarily treat the cause of the problem. After all, the word random has many synonyms including chance, haphazard, arbitraryand unsystematic.

One of the problems in dealing with local functional pain is that the area of complaint is not necessarily the causal location. The sage statement by Karel Lewit, MD, a leader in the soft-tissue movement, went something like: He who only treats the site of pain is lost. An important question is: Could this painful site be a compensation for an original problem elsewhere? Could it be that a chronic low back pain is really a compensation for a sprained ankle 10 years ago? Could a shoulder or elbow pain that occurs for no apparent reason be due to a wrist fracture that occurred when the patient was 5 years old?

Alleviating a painful point may relieve symptoms, but have nothing to do with causation; and as many of us find, the points and symptoms will recur. The pain that "appears for no apparent reason" is often the clue that should make you think of other areas.

Could a more organized method of treating these tender points help the patient for longer periods of time, or for that matter, completely cure the problem? Travell and Simons told us about these hyperirritable areas of taut bands that may radiate to particular areas. They were talking about the myofascial pain syndrome and trigger points. Of course, many of the points that have to be treated do not have to fit the definition of a TP.

Connecting TPs to Fascia

In their text, Travell and Simons offer no description of the chief connecting part of our body, the fascial system. They rarely mention TPs that may originate in fascia.¹They quote Kellgren,² who, after injecting saline solution in the fascial epimysium of the gluteus medius, realized referred pain several cm. distally. Travell identified mostly muscular areas to treat, but of course, Travell's text was written in 1983, and Killgren found the epimysial point in 1938.

The works of Travell and Simon have provided a great contribution to the world of soft tissue. They astutely reported that myofascial referred pain did not follow dermatomal, myotomal or sclerotomal patterns of innervation. Areas of referred pain can be important in our analysis of where to treat. Treating a knee area may refer to a leg area requiring treatment; it may refer to an antagonistic area requiring treatment; when it refers to the area of complaint it is regarded as a very significant possible causative area and may indicate the most important fascial chain (read below).

Connective tissue has its own system of pain referral that may or may not be tied up with the central nervous system. When mechanical load is applied to abnormal soft tissue, the area of referral is in a non-segmental pattern. There are a variety of hypotheses to explain it, such as the "connective tissue theory"³ and the "barrier-dam" theory.⁴

The latter theory states that afferent sensitive increased nociceptive peripheral nerves might become entrapped in local restrictive areas, causing hyperexcitation of nerves between the distally referred pain area and the local muscular zone of tenderness. "The primary pathogenesis of referred muscle pain is likely to be a peripheral sensitization with additionally a central modulation and not vice versa."⁴

Giamberardino⁵ states: "Referred pain / hyperalgesia from deep somatic structures is not explained by the mechanism of central sensitization of convergent neurons in its original form, since there is little convergence from deep tissues in the dorsal horn neurons." The absolute cause of non-segmental pain referral is still not entirely known. It is thought that even changes in cell shape and forces among cells can affect adjoining cells and transmit information. Stretching the fibroblast could be supplying information by way of gap junctions to other fibroblasts, transmitting information about pain and peripheral motor coordination.

Chen⁶ states that neurological (electrochemical) transmission is slower, localized and context independent compared to mechanical force distribution. Coordination by mechanical force distribution is faster, both locally and globally; and above all, occurs in a context-sensitive manner. Therefore, it is possible that stressing a specific region of the deep fascia can be transmitted over a distance by cell-to-cell communication.

Focusing on Fascial Points

Abbott, et al.,⁷ theorize that connective tissue (CT), especially fibroblasts, are part of a whole-body, cell-to-cell, communication-signaling network. They state that fibroblasts exhibit active cytoskeletal responses within minutes of tissue lengthening. Analogous cell-to-cell signaling involving calcium and/or ATP may exist within CT and may be accompanied by active tissue contraction or relaxation. "One can envisage a whole-body web of CT involved in a dynamic, body-wide pattern of cellular activity fluctuating over seconds to minutes reflecting all externally and internally generated mechanical forces acting upon the body."⁷ The chief cell in the fascia is the fibroblast.

According to the literature, it appears that treating particular related fascial points is more effective than just treating random painful sites. It was found that in treating plantar fasciitis, results were better if the gastrocnemius / soleus) trigger points and heel region were treated, rather than the heel region alone.⁸

Most of us are aware that a variety of points must be treated when using soft-tissue methods. The questions that must be answered in this regard are:

• Is there a particular sequence of points, perhaps extending, for example, from the wrist to the elbow to the shoulder to the neck?
• Are these points related in any way to our soft-tissue myofascial anatomy?

References

1. Travell JG, Simons DG. Myofascial Pain and Dysfunction: The Trigger Point Manual.Williams & Wilkins, Baltimore, 1983:19-20.
2. Kellgren JH. Observations on referred pain arising from muscle. Clin Sci, 1938;3:175-190.
3. Han D-G. The other mechanism of muscular referred pain: The "connective tissue" theory.Med Hypotheses, 2009;73:292-295.
4. Farayn A. Referred muscle pain is primarily peripheral in origin: the "barrier-dam" theory.Med Hypotheses, 2007:68(1):144-50.
5. Giamberardino MA. Referred muscle pain/hyperalgesia and central sensitisation. J Rehabil Med, 2003 May;(41 Suppl):85-8.
6. Chen CS. Mechanotransduction – a field pulling together? J Cell Sci, 2008;15(121):3285-3292.
7. Abbott RD1, Koptiuch C, Iatridis JC, et al. Stress and matrix-responsive cytoskeletal remodeling in fibroblasts. J Cell Physiol, 2013 Jan;228(1):50-7.
8. Moghtaderi A, Khosrawi S, Dehghan F. Extracorporeal shock wave therapy of gastroc-soleus trigger points in patients with plantar fasciitis: a randomized, placebo-controlled trial. Adv Biomed Res, 2014 Mar 25;3:99.

Dysponesis - Dyskinesia - Dysautonomia

By William Shepherd

Dysponesis, dyskinesia, dysautonomia: These are three big words that are the heart and soul of chiropractic examinations and professional care. They encompass most of the measurable dysfunction we are capable of affecting and when improved, account for the health benefits we have been lauded for these past one hundred and five years.

Dysponesis is defined as a reversible physiological state consisting of unnoticed, misdirected neurophysical reactions to various agents (environmental events, bodily sensations, emotions, and thoughts) and the repercussions of these reactions throughout the organism. These errors in energy expenditure that are capable of producing functional disorders consist mainly of covert errors in action, potential output from the motor and premotor areas of the cortex, and consequences of that output.

Our professional care should involve understanding the state of mind of our patients, and how that state of mind will affect their responses to our care. The best way I know of is to then ask patients how they feel about their symptoms and record their answer. You may get all kinds of reactions to such a question, ranging from anger and hostility to emotional outbursts. All are probably more expressive than the words used. They will tell you the state of mind the patient is in, and should be on record.

Dyskinesia is defined as "dysfunction in muscle physiology." This dysfunction can be measured in a number of ways: 

1. Traditionally we have used the x-ray to observe misaligned vertebra and have reasoned that in order for a vertebra to be found in misalignment, a muscle attached to that vertebra must have contracted, and remained in that contracted position because of an injury to the opponent muscle. Ligament and disc damage also are well documented on x-ray, and these add another additional factor.
   
   
2. Uneven muscle contractions also may be palpated. A contracted muscle will have a "sore-to-the-touch" tendon. This measurement has been used since the beginning of chiropractic in 1895.
   
   
3. A contracted muscle will have an opponent muscle that will test weak. Reflex muscle weakness has also been observed in many of the large muscles of the body directly connected to this direction of weakness. (For example: a contracted psoas muscle would indicate a weak gluteal or hamstring muscle and could be associated with any vertebra in a flexed contraction. Testing the strength of the leg and arm muscles can yield information about the position of the contraction.)
   
   
4. Motion palpation of the vertebra of the spine can also be an aid in determining the position of the muscle which has been damaged since the vertebra above the damaged muscle will not move as well against the contraction as it moves in other directions; reflexly, neither will the vertebrae above the damaged one. This reluctance in motion surely must respond to our care.
   
   
5. Breath motion between vertebrae is another way to assess muscle function. When a goniometer is used, (one prong on one vertebra and the other prong on an adjacent vetebra,) there should be six millimeters of movement between the prongs. If six millimeters of movement are not found, contraction of muscles between these vertebrae can be reasoned. Reflex contractions also exist in many of the large muscles and may be ascertained. The 45mm of goniometer movement between illium and scapulae is one example.
   
   
6. Derefield short-leg measurement is another manifestation of reflex muscle imbalance.
   
   
7. Use of surface electromyography has also extended our knowledge of muscle imbalance. Contracted muscles are indicated with increased microvolt readings, and opponent weak muscles are indicated with decreased microvolt readings.

Dysautonomia is defined as "alteration of bodily functions from standards which should not be noticed." Symptoms of this include: pulse rate; blood pressure or temperature that are too high or too low; bowel dysfunction; indigestion; allergies; menstrual dysfunction; headaches; and high respiratory rates. All of these things indicate that the body is not in highly tuned communication through the nervous system.

All three of these manifestations of dysfunction need to be addressed with each patient we see on each visit.