Trigger Point Therapy Definitions  

Trigger point - (Myofascial):   An area of hyper-irritability within soft tissue structures, characterized by local tenderness and sometimes referred phenomena.  These referred sensations can include pain, tingling, numbness burning, or itching.

Not all trigger points refer pain, some are just localized.  Each person is different depending on their life history.

Localized areas of deep tenderness and increased tissue resistance that often produce referred pain.

The origin of the trigger point is thought to be changes in the chemical balance in a local area, irritating the sensory systems.

Active trigger point: Cause of  the immediate pain, prevents muscle from fully lengthening and sometimes weakens.

Latent trigger point:  Unnoticed by the client until pressure is applied, Not actively painful.  Usually feels dense and fibrous.

Characteristics 1. Trigger points may be associated with Vitamin B-6  and other vitamin

deficiencies.  Usually after a trauma or stressful event, the body is lacking in B-6, magnesium or Vitamin C.  Trigger points are more likely to develop.

2. Trigger point are usually bilateral, with one side being more symptomatic than the other.  Both sides need to be treated.

3. Trigger points may be a result of underlying visceral disease, arthritic joints, or other trigger points.

4. The most tender trigger points are usually not the source of the problem. Other areas need to be treated like the referral area and the surrounding tissue.  Look for tight stringy band in small supporting musculature.

5. Trigger points can cause referred pain, but not always. 6. The referral patterns are not the same in any 2 people. 7. Referred pain does not follow segmental, scleratomal or dermatomal

patterns. 8. May cause pain and stiffness especially after periods of inactivity such as

sleeping or sitting for awhile.

Possible Causes: 1. Acute overload, overwork, fatigue, direct trauma, chilling.

2. skeletal asymmetry such as short leg or pelvic imbalances. 3. Other trigger points can cause new points to occur. 4. Arthritic joints can cause trigger points. 5. Visceral diseases such as ulcers, renal colic, myocardial infarction, gall

stones, kidney problems, irritable bowel syndrome can cause trigger points.

6. B-6, magnesium, vitamin C, folic acid deficiencies which are common after injuries or trauma may cause trigger points

7. hypoglycemia 8. chronic infection from a viral or bacterial disease. 9. food allergies or intolerances.  Wheat and dairy products should be

checked first. 10. toxicity due to exposure to organic chemicals or heavy metals

Location:

Trigger points may develop any where in the body, but are most commonly found at the sites of the greatest mechanical and postural stress. Hints for locating:

look for changes in thickness of tissue, resistance to gliding strokes, lumps or strings.

immobility edema pain or tenderness temperature changes-area is usually colder color  most often somewhat pale and unhealthy looking muscle shortening with weakness occasionally increased perspiration in reference zone hypertonicity ischemia

Factors that can worsen trigger points: fatigue, improper sleep chronic infection severe stress (mental, emotional, physical) nerve entrapment, compression excessive creatine in urine postural imbalances nutritional health of the tissue

food allergy, inhalant allergy visceral (organ) disease - gall bladder problems, ulcers, kidney problems,

irritable bowel syndrome exercise may worsen an active trigger point, but helps heal a latent trigger

points

Signs of Trigger points: restricted movement, stiffness of muscles weakness in muscles passive or active stretching increases pain resisted contraction causes pain subcutaneous tissue feels coarsely granular, ropy, knotty, client "jumps" when pressure applied to trigger point deep tenderness and paresthesia client may feel "Numb" but sensation is normal dizziness taut palpable band in the affected muscle exercise makes the pain worse when there are active trigger points, but

helps heal the latent triggerpoints hyperirritability, increased metabolism, decreased circulation

Thing to pay attention to: 1. What layer of tissue are you working on? 2. How can you work more efficiently? 3. What does the tissue feel like?  How does it change? 4. What other areas may be associated with the trigger point?

Cautions: Triggerpoint therapy can relieve the pain of angina, myocardial infarction

and acute abdominal disease.  Refer clients to physicians when necessary.

Rule out such conditions as: Tendinitis, bursitis, giant cell arteritis, neuralgia, infection (both viral and bacterial), neuropathies, disc problems, disc herniations.

Check for thyroid malfunction, anemia, hypoglycemia and vitamin deficiencies.

Trigger Point Therapy

Firm digital pressure causes hypoxia and reactive hyperemia that clears the triggerpoint.  Reconditioning the muscle after the pain is reduced makes latent triggerpoints less prone to reactivate.

Treatment Method I:

1.  Treat superficial trigger points first, applying 8-30 seconds or until the pain is gone as the client permits.   Notice changes in feel and pain intensity ( ask client for feedback regarding pain intensity).

2.  Are there any referral patterns?

3.  Flush the area with deep effleurage, pettrisage or friction.

4. Return to same trigger point and repeat treatment, 3-4 times removing as much of the pain as possible.

5.  If the pain intensifies, just hold for a few more seconds and go back later.

6.  You can vary the intensity of pressure gradually, moving with the point as it changes and releases.    

 Advanced Technique: Treat as many trigger points as you can in the area and related area and throughout the body. CAUTION:  Do not do this unless you know how to ground a client properly.   Watch for sweating palms or feet, feelings of nausea or dizziness.  This indicates sympathetic over stimulation. Emotional release may also be triggered with such intense work.  Pulling clients fingers and toes should be done after such intense treatments, for grounding.  Hold clients wrist with one hand and grab little finger with the thumb and forefinger, wrapping the hand around the little finger.  Gently, but firmly begin pulling the little finger and let go of their wrist and continue pulling finger until you snap off the end.  Grab the wrist again as you complete the snap to hold the hand up (do not let the hand/arm fall)  Continue with ring finger, middle finger, index finger and thumb.  Repeat as necessary.  Repeat with toes, pulling each toe and releasing.  The pull must come from your center and be pulled from the clients center (abdominal area).  Can you see the abdomen move when you pull the fingers or toes?

 Ice can be applied after session or recommend client to ice at home. Client must follow up with high intake of water to flush the toxins and a

detox bath consisting of 1 cup epsom salt, 1 cup sea salt and 1 cup baking

soda.( or walk in the ocean or other body of salt water).  This will eliminate detox symptoms such as headaches and fatigue.

Also following up with movement re-education exercises will integrate the changes into the nervous system.

 Trigger Point Referral Areas

See also Trigger point charts available at www.amazon.com  

Pain referral area

Check these area

Low Backrectus abdominus, psoas, quadratus lumborum, piriformis

Shoulder

sub occipitals, scalenes, SCM, infraspinatious, subscapularis, pectoralis major and minor, facet joints in the neck

Thigh psoas, TFL, iliacus

Sciaticapiriformis, quadratus lumborum, serratus posterior inferior,

KneeQuadriceps, adductors, psoas, hamstrings, sartorius

ankle/foot psoas, TFL, adductors

headachessub-occipitals, scalenes, levator scapulae, rhomboids

TMJ psoas, piriformis

Trigger Points and the Myofascial Pain Index

Trigger Points and the Myofascial Pain IndexBy Leon Chaitow

This paper contains summaries of information explored more fully in the forthcoming book Clinical Applications of Neuromuscular Therapy (Volume 1 Upper body), which I have co-authored with Judith Walker, to be published by Churchill Livingstone in the

summer of 2000.

New information on the topic of trigger points has emerged from the long-awaited publication of the 2nd edition of the Travell and Simons masterpiece Myofascial Pain and Dysfunction: the Trigger Point Manual, Volume 1: Upper Half of the Body as well as from Belgian research into the ëmyofascial pain index (MPI).16 What emerges is important in making sense of pain patterns in general, and trigger points in particular.

Travell and Simons make a distinction between ëcentralí trigger points that develop almost directly in the centre of the muscle's fibres, where the motor end plate innervates it at the neuromuscular junction, and those which form close to attachments.

Central trigger points

Dysfunctional end plate activity occurs (commonly associated with a strain), which causes acetylcholine (ACh) to be excessively released at the synapse, often associated with the presence of excess calcium.

High calcium levels apparently keep the calcium-charged gates open, and ACh continues to be released, resulting in ischemia.

The consequent ischemia involves an oxygen/nutrient deficit which, in turn, leads to a local energy crisis, inadequate adenosine triphosphate (ATP) production.

Without available ATP, the local tissue is unable to remove the calcium ions which are keeping the gates opení and therefore continued ACh release.

Removing the superfluous calcium requires more energy than sustaining a contracture, so the contracture remains.

The resulting muscle fibre contracture (involuntary, without motor potentials) needs to be distinguished from a contraction (voluntary, with motor potentials) and spasm (involuntary, with motor potentials).

The contracture is sustained by the chemistry at the innervation site, not by action potentials from the spinal cord.

As the end plate keeps producing ACh flow, the actin/myosin filaments slide to a fully shortened position (a weakened state) in the immediate area around the motor end plate (at the centre of the fibre).

As the sarcomeres shorten, they begin to bunch and a contracture, knot, forms. This knot is the nodule which is a palpable characteristic of a trigger point.

As this process occurs, the remainder of the sarcomeres of that fibre (those not bunching)

is stretched, thereby creating the usually palpable taut band which is also a common trigger point characteristic.

Attachment trigger points

Attachment trigger points tend to develop at the attachment sites of these shortened tissues (periosteal, myotendinous) where muscular tension provokes inflammation, fibrosis and, eventually, deposition of calcium.

Simons, in the latest version of the ëtrigger point manualí strongly urges differentiation of central from attachment trigger points, both in their nature and in treatment requirements. Central trigger points are usually directly in the centre of a fibreís belly.

Motor points are consistently located (with a few exceptions) in the centre of the muscle fibreís belly.

The practitioner who knows fibre arrangement (fusiform, pennate, bipennate, multipennate, etc.), as well as attachment sites of each tissue being examined, will find it easy to locate the triggers since their sites are moderately predictable.

Attachment trigger points are located where fibres merge into tendons or at periosteal insertions.

Tension from taut bands on periosteal, connective or tendinous tissues can lead to inflammatory changes, as recurring concentrations of muscular stress can provoke inflammation with a strong tendency toward the evolution of fibrosis and the deposition of calcium at the attachment site.

Both central and attachment trigger points can have the same end results - referred pain. However, the local processes, according to Simons, are very different and should be addressed differently.

Until they are thoroughly examined and tissue reaction noted, attachment trigger points should be treated with their tendency toward inflammation in mind. For example, ice applications would be more appropriate than those with heat.

Central trigger points should be treated with their contracted central sarcomeres and local ischemia in mind.

Since the end of the taut band is likely to create enthesopathy (inflammation, calcification, etc. at the attachment), stretching the muscle before releasing its central trigger point might further inflame the attachments.

Therefore, it is suggested, the attachment trigger points should first be addressed by

releasing the associated central trigger point.

Stretches, particularly involving active ranges of motion, will then further elongate the fibres; however, they should be applied mildly until reaction is noted, so as to avoid further tissue insult.

When passive stretching is applied, care should be taken to assess for tendinous or periosteal inflammation, avoiding increased tension on already distressed connective tissue attachments.

Gliding soft tissue techniques may usefully be applied from the centre of the fibres out toward the attachments.

By elongating the tissue toward the attachment, sarcomeres, which are shortened at the centre of the fibre, will be lengthened and those which are over-stretched near the attachment sites will have the tension released.

Central trigger points often respond well to heat as a flush of blood, which irrigates the area, will help remove waste products released by the therapy.

Oxygen, ATP, and nutrients offered by the incoming blood could reduce the local environmental deficits and encourage normalisation of the dysfunctional tissues.

When compression techniques are used, local chemistry can change due to blanching of the nodules followed by a flush of blood to the tissues when the compression is released. The effects of thermal or other neuro-altering applications (skin irritants, moxibustion, dry or wet needling, etc.) will usually induce the contracture to release more readily.

Key and satellite trigger points

Clinical experience and research evidence suggests that key triggers exist which, if deactivated, relieve activity in satellite trigger points (usually located within the target area of the key trigger). If these key trigger points are not relieved, but the satellites are treated, the referral pattern usually returns.

Hong and Simons have reported on over 100 sites involving 75 patients in which remote trigger points were inactivated by means of injection of key triggers. The details of the key and satellite triggers, as observed in this study, are listed below.

Key trigger Satellite triggers

Sternocleidomastoid Temporalis, masseter, digastric

Upper trapezius Temporalis, masseter, splenius, semispinalis, levator scapulae, rhomboid major

Scalenii Deltoid, extensor carpi radialis, extensor digitorum communis, extensor carpi ulnaris

Splenius capitis

Temporalis, semispinalis Supraspinatus

Deltoid, extensor carpi radialis Infraspinatus

Biceps brachii Pectoralis minor

Flexor carpi radialis, flexor carpi ulnaris, first dorsal interosseous Latissimus dorsi

Triceps, flexor carpi ulnaris Serratus post. sup.

Triceps, latissimus dorsi, extensor digitorum, communis extensor carpi ulnaris, flexor carpi ulnaris

Deep paraspinals (L5-S1) Gluteus maximus, medius and minimus, piriformis, hamstrings, tibialis, peroneus longus, gastrocnemius, soleus

Quadratus lumborum Gluteus maximus, medius and minimus,

piriformis Piriformis

Hamstrings Hamstrings

Peroneus longus, gastrocnemius, soleus

Ischemia and the trigger point connection

Mense describes the hypothesised evolution of a trigger point, clearly based on the Travell and Simons model:

A muscle lesion leads to the rupture of the sarcoplasmic reticulum and releases calcium from the intracellular stores. The increased calcium concentration causes sliding of the myosin and actin filaments; the result is a local contracture (myofilament activation without electrical activity) that has high oxygen consumption and causes hypoxia. An additional factor may be the traumatic release of vasoneuroactive substances (for example bradykinin) which produce local oedema that in turn compresses venules and enhances the ischemia and hypoxia. Because of the hypoxia-induced drop in ATP concentrations, the function of the calcium pump in the muscle cell is impaired, and the sarcoplasmic calcium concentration remains elevated. This perpetuates the contracture.î Research also shows that when pain receptors are stressed (mechanically or via ischemia) and are simultaneously exposed to elevated levels of adrenaline, their discharge rate increases, i.e., a greater volume of pain messages are sent to the brain.

Trigger point activity itself may also induce relative ischemia in ìtargetî tissues. The mechanisms by which this occurs remain hypothetical but may involve a neurologically mediated increase in tone in the trigger pointís reference zone (target tissues). According to Simons, these target zones are usually peripheral to the trigger point, sometimes central to the trigger point and, more rarely (27%), the trigger point is located within the target zone of referral. This translates to: If you are treating only the area of pain and the cause is myofascial trigger points, you are ìin the wrong spotî nearly 75% of the time!

Essential pain zones

Travell and Simons use the term ìessential pain zoneî to describe a referral pattern that is present in almost every person when a particular trigger point is active. Some trigger

points may also produce a ìspillover pain zoneî beyond the essential zone or in place of it, where the referral pattern is usually less intense. These target zones should be examined, and ideally palpated, for changes in tissue ëdensityí, temperature, hydrosis and other characteristics associated with satellite trigger point formation.

Any appropriate manual treatment, movement or exercise program that encourages normal circulatory function is likely to modulate these negative effects and reduce trigger point activity.

Facilitation

Facilitation occurs when a pool of neurons is in a state of partial or subthreshold excitation. In this state, a lesser degree of afferent stimulation is required to trigger the discharge of impulses. Facilitation may be due to sustained increase in afferent input, or aberrant patterns of afferent input, or changes within the affected neurons themselves, or their chemical environment. Once established, facilitation can be sustained by normal central nervous system activity.

It is the example of neurons maintained in a hyper-irritable state, due to an altered biochemical status in their local environment, that appears to come closest to the situation obtained in trigger point behaviour. On a spinal segmental level the cause of facilitation may be the result of organ dysfunction, as explained below.

Organ dysfunction leads to sensitisation and, ultimately, facilitation of the paraspinal structures at the level of the nerve supply to that organ. If, for example, there is any form of cardiac disease, there will be ëfeedbackí towards the spine of impulses along the same nerves that supply the heart, so that the muscles alongside the spine, in the upper thoracic level (T2,3,4 as a rule), will become hypertonic.

If the cardiac problem continues, the paraspinal area will become facilitated, with the nerves of the area, including those passing to the heart, becoming sensitised and hyper-irritable. Electromyographic readings of the muscles alongside the spine at this upper thoracic level would show this region to be more active than the tissues above and below it. The muscles alongside the spine, at the facilitated level, would be hypertonic and almost certainly painful to pressure. The skin overlying this facilitated segmental area will alter in tone and function (increased levels of hydrosis as a rule) and will display a reduced threshold to electrical stimuli.

Other causes of segmental (spinal) facilitation can include stress imposed on a part of the spine through injury, overactivity, repetitive patterns of use, poor posture or structural imbalance (short leg, for example).

Any stress aggravates facilitated areas

Once facilitation of the neural structures of an area has occurred, any additional stress

impacting the individual, of any sort, whether emotional, physical, chemical, climatic, mechanical - indeed absolutely anything which imposes adaptive demands on the person as a whole and not just this particular part of their body - leads to a marked increase in neural activity in the facilitated segments, and not to the rest of the (normal, unfacilitated) spinal structures.

Korr tells us that when subjects who have had facilitated segments identified were exposed to physical, environmental and psychological stimuli similar to those encountered in daily life, the sympathetic responses in those segments were exaggerated and prolonged. The disturbed segments behaved as though they were continually in, or bordering on, a state of ìphysiologic alarm. 6

Palpating a facilitated spinal area

A number of observable and palpable signs indicate an area of segmental (spinal) facilitation.

Beal tells us that such an area will usually involve two or more segments - unless traumatically induced, in which case single segments are possible.

The paraspinal tissues will palpate as rigid or board-like.

With the person supine and the palpating hands under the personís paraspinal area to be tested (practitioner standing at the head of the table, for example, and reaching under the shoulders for the upper thoracic area), any ceiling-ward ëspringingí attempt on these tissues will result in a distinct lack of elasticity, unlike more normal tissues above or below the facilitated area.

Palpation signs

Grieve, Gunn and Milbrandt, and Korr have all helped to define the palpable and visual signs which accompany facilitated dysfunction:

A gooseflesh appearance is observable in facilitated areas when the skin is exposed to cool air - as a result of a facilitated pilomotor response.

A palpable sense of ëdragí is noticeable as a light touch contact is made across such areas, due to increased sweat production resulting from facilitation of the sudomotor reflexes.

There is likely to be cutaneous hyperaesthesia in the related dermatome, as the sensitivity is increased (facilitated).

An orange peel appearance is noticeable in the subcutaneous tissues when the skin is rolled over the affected segment, because of subcutaneous trophedema.

There is commonly localised spasm of the muscles in a facilitated area, which is palpable segmentally as well as peripherally in the related myotome. This is likely to be accompanied by an enhanced myotatic reflex due to the process of facilitation.

A similar process of facilitation occurs when particularly vulnerable sites of muscles (attachments, for example) are overused, abused, misused, or disused. Localised areas of hypertonicity may develop, sometimes accompanied by oedema, sometimes with a stringy feel - but always with a sensitivity to pressure.

Many of these tender, sensitive, localised, facilitated areas are myofascial trigger points, which are not only painful themselves when palpated, but will also transmit or activate pain (and other) sensations some distance away from themselves, in ëtargetí tissues. Leading researchers into pain, Professors Melzack and Wall, have stated that there are few, if any, chronic pain problems which do not have trigger point activity as a major part of the picture, perhaps not always as a prime cause but almost always as a maintaining feature.

Active and latent points

When an active trigger point is mechanically stimulated (treated) by compression, needling, stretch, or other means, it will refer or intensify a referral pattern (usually of pain) to a target zone. An active trigger point refers a pattern that the person recognises as being a part of their current symptom picture.

When a latent trigger point is stimulated, it refers a pattern that may be unfamiliar to the person, or that is an old pattern they used to have and have not had for a while (previously active, reverted to latent).

All the same characteristics which denote an active trigger point may be present in the latent trigger point, with the exception of the personís recognition of their active pain pattern. The same signs as described for segmental facilitation, such as increased hydrosis, a sense of ìdragî on the skin, loss of elasticity, etc., can be observed and palpated in these localised areas as well.

Lowering the neural threshold

There is another way of viewing facilitation processes. One of Selyeís most important findings is commonly overlooked when the concurrent impact of multiple stressors on the system is being considered.

Shealy summarises as follows:

Selye has emphasized the fact that any systemic stress elicits an essentially generalized reaction, with release of adrenaline and glucocorticoids, in addition to any specific damage such stressor may cause. During the stage of resistance (adaptation), a given stressor may

trigger less of an alarm; however, Selye insists that adaptation to one agent is acquired at the expense of resistance to other agents. That is, as one accommodates to a given stressor, other stressors may require lower thresholds for eliciting the alarm reaction. Of considerable importance is Selyeís observation that concomitant exposure to several stressors elicits an alarm reaction at stress levels which individually are sub-threshold. That is, one-third the dose of histamine, one-third the dose of cold, one-third the dose of formaldehyde, elicit an alarm reaction equal to a full dose of any one agent.

In short, therefore, as adaptation to lifeís stresses and stressors continues, thresholds drop and a lesser load is required to produce responses (pain, etc.) from facilitated structures, whether paraspinal or myofascial.

Using trigger points as monitors?

New Zealand Physiotherapist Dinah Bradley, an expert in breathing rehabilitation, palpates and identifies key trigger points in her patients, in the intercostals and upper trapezius as a rule, at the outset of their course of breathing rehabilitation.

She asks them to ascribe a value out of 10 to the trigger point, while it is under digital pressure, before they commence their exercise and treatment program (no direct treatment is given to the trigger points themselves) and periodically during the course, as well as at the time of discharge.

She states, I use trigger point testing as an objective measurement. Part of [the patientís] recovery is a reduction in musculoskeletal pain in these overused muscles. I use a numeric scale to quantify this. Patients themselves feel the reduction in tension and pain, a useful subjective marker for them, and an excellent motivator.

This use of trigger points, in which they are not directly deactivated but are used as monitors of improved breathing function, highlights several key points:

That as oxygenation improves, trigger points become less reactive and painful That enhanced breathing function also represents a reduction in overall stress, reinforcing

the concepts associated with facilitation That as stress of whatever kind reduces - trigger points react less violently That direct deactivation tactics are not the only way to handle trigger points That trigger points can be seen to be acting as alarm signals - virtually quantifying the

current levels of adaptive demand being imposed on the individual

Using a pressure meter (Algometer) for research and clinical training When applying digital pressure to a tender point in order to ascertain its status (Does it hurt? Does it refer? etc.) it is important to have some way of knowing that pressure being applied is uniform.

The term pressure threshold is used to describe the least amount of pressure required to produce a report of pain and/or referred symptoms. It is obviously useful to know whether pain and/or referral symptoms occurs with 1, 2, 3 or however many kilos of pressure, and whether this degree of pressure changes before, after treatment, or at a subsequent clinical

encounter.

In diagnosing fibromyalgia, according the American College of Rheumatology guideline, the criteria for a diagnosis depends upon 11 of 18 specific test sites, testing as positive (hurting severely) on application of 4 kilograms of pressure.

If it takes more than 4 kilograms of pressure to produce pain the point does not count in the tally. Without a measuring device such as an algometer there would be no means of standardised pressure application.

Use of an algometer is not really practical in everyday clinical work but this becomes an important tool if research is being carried out, as an objective measurement of a change in the degree of pressure required to produce symptoms.

An algometer is also a useful tool for practitioners to use to assist in training themselves to apply a standardised degree of pressure when treating, and to know how hard they are pressing.

Belgian researchers Jonkheere and Pattyn explain how they have used algometers to identify what they term the ëmyofascial pain index (MPI). They also use it to define the nature of trigger points under investigation: ìThe purpose of algometrics is to define whether a trigger point is active, latent, falsely positive, or absent.

In order to achieve this objective, various standard locations are tested (for example the 18 test sites used for fibromyalgia diagnosis). Based on the results of this, a myofascial pain index (MPI) is calculated.

The purpose of this exercise is to create an objective base (the MPI), which emerges initially from the patientís subjective pain reports, when pressure is applied to test points. The calculation of the MPI determines the degree of pressure required to evoke pain in a trigger point, and helps to sift ëfalse positive from active points, with the latter receiving treatment, and the former not.

The Belgian researchers acknowledge that they have based their approach on earlier work by Hong et al., who investigated pressure thresholds of trigger points and the surrounding soft tissues.

Jonkheere and Pattyn define the various states of trigger points as follows:

An active trigger point, they say, is sensitive to palpation and produces an identifiable pain which corresponds, completely or partially, with the known pattern of a trigger point located at that particular site.

A latent trigger point is one that only produces localised pain on palpation A false positive trigger point is one which is sensitive to palpation, and which refers pain - but

which does not correspond with known patterns,or which produces a referral pattern which does correspond, completely or partially with the known pattern of a trigger point located at that particular site, but only when the pressure required to evoke this response is greater

than the myofascial pain index (MPI).

This false positive point is, in Travell and Simonsí terminology, also a latent point. The 18 points tested are located in 9 bilateral sites as defined by the American College of Rheumatology in 1990, as part of the diagnostic protocol for fibromyalgia syndrome (FMS).

They are:

at the suboccipital muscle insertions (close to where rectus capitis posterior minor inserts) at the anterolateral aspect of the inter-transverse spaces between C5 and C7 at the midpoint of the upper border of Upper trapezius muscle at the origin of Supraspinatus muscle above the scapula spine at the second chostochondral junctions, on the upper surface, just lateral to the junctions 2 centimetres distal to the lateral epicondyles of the elbows in the upper outer quadrant of the buttocks in the anterior fold of gluteus medius posterior to the prominence of the greater trochanter (Piriformis attachment) on the medial aspect of the knees, on the fatty pad, proximal to the joint line.

Using an algometer (The Belgianís used an Algoprobe) pressure is applied to each of the points, at a precise 90* angle to the skin, sufficient to produce pain, with the measurement being taken when this is reported.

The 18 values are recorded and then averaged, leaving a number which is the MPI. Once established, this amount of pressure is used to judge the nature (active, ëfalse positiveí, etc.) of all other potential trigger point sites.

A label of ëactiveí is assigned to any point where the referral pattern matches known referral distribution from that site, and which requires less than the MPI degree of pressure to produce this response. Those triggers which meet the definition of active trigger point are therefore noted and treated.

If a greater degree of pressure than the MPI is required to evoke a pain response the trigger point is not regarded as active.

Jonkheere and Pattyn, utilizing the basic research of Travell and Simons1, have also identified ëchainsí of trigger points which seem to be functionally or structurally related to the patientís reported pain symptoms. Before treatment, these are methodically tested using an algometer in the manner described above.

Baldry 5 (referring to research by Fischer) discusses algometer use (he calls it a pressure threshold meterí) and suggests it should be used to measure the degree of pressure needed to produce symptoms, ìbefore and after deactivation of a trigger point, for when this is successful, the pressure threshold over the trigger point increases by about 4kg.

References

Travell J, Simons D Myofascial Pain and Dysfunction: the Trigger Point Manual, Volume

1: Upper Half of the Body. Williams & Wilkins Baltimore 1998.

Hong C-Z, Simons D Remote inactivation of myofascial trigger points by injection of trigger points in another muscle. Scand. J. Rheumatology, Suppl. 94:25 1992.

Mense op cit 1993.

Kieschke J et al Influences of adrenaline and hypoxia on rat muscle receptors. Progress in Brain Research Volume 74 (Hamman W Ed.) Elsevier Amsterdam 1988.

Baldry P Acupuncture, Trigger points and Musckuloskeletal Pain. Churchill Livingstone Edinburgh 1993.

Korr I (Ed) Sustained sympatheticotonia as a factor in disease. In: The Neurobiological Mechanisms in Manipulative Therapy Plenum Press New York 1978.

Beal M Palpatory testing of somatic dysfunction in patients with cardiovascular disease. J. American Osteopathic Association July 1983.

Grieve G (Ed) Modern manual therapy. Churchill Livingstone 1986.

Gunn C, Milbrandt W Early and subtle signs in low back sprain. Spine 3:267-281 1978.

Korr I The emerging concept of the osteopathic lesion. J American Osteopathic Association 48 pp127-138 1948.

Melzack R and Wall P The Challenge of Pain. Penguin London 1988.

Selye H Stress without distress. Lippincott Philadelphia 1974.

Shealy CN Total Life Stress and Symptomatology. Journal of Holistic Medicine 6(2):112-129 1984.

Bradley D Breathing function Series. Journal of Bodywork and Movement Therapies October 1999.

The American College of Rheumatology 1990 Criteria for the Classification of Fibromyalgia Arthritis and Rheumatism 33:160-172 1990.

Jonkheere P Pattyn J Myofascial Muscle Chains. Trigger vzw, Brugge Belgium 1998.

Hong C-Z, Chen Y-N, Twehouse D, Hong D Pressure threshold for referred pain by compression on trigger point and adjacent area. Journal of Musculoskeletal Pain (issue/volume/date to come)

Fischer A Documentation of muscle pain and soft tissue pathology. In: Kraus H (Ed) Diagnosis and Treatment of muscle pain. Quintessence Chicago 1988.

Mense S Peripheral mechanisms of muscle nociception and local muscle pain. Journal of Musculoskeletal Pain 1(1):133-170 1993.

Digiesi V et al Effect of proteinase inhibitor on intermittent claudication. Pain 1:385-389 1975.

Ward R (Ed) Foundations of Osteopathic Medicine, Williams & Wilkins Baltimore 1997.

Integrated Treatment of Myofascial Trigger Points?

Integrated Treatment of Myofascial Trigger Points?By Leon Chaitow ND DO. Senior Lecturer, University of Westminster

Trigger points are localised areas of hyperirritable neural tissue lying in taut bands in muscles or fascia which have been stressed.

They cause local and distant mischief, including pain and altered sympathetic activity, and are enormously wasteful of energy.

Their involvement in almost all chronic pain is well established, and yet many therapists either ignore or are not even aware of their existence.

Efficient methods exist for their deactivation using simple manual methods.

Liebenson summarises the way in which dysfunctional patterns in the musculoskeletal system can be corrected 1:

Identify, relax and stretch overactive, tight muscles Mobilise and/or adjust restricted joints Facilitate and strengthen weak muscles Re-educate movement patterns on a reflex, subcortical basis.

Not all therapists would agree with this sequence, or with all the ingredients of the protocol; however, it is based on sound biomechanical knowledge and research 2 3, and serves as a useful basis for patient care and rehabilitation.

Trigger points and the facilitation phenomenon

Neuronal resistance in local pathways becomes weaker because of repetitive stress of mechanical, biochemical or reflexogenic (i.e., viscerosomatic) origin, rendering the area

hyperirritable.

Any stress of any sort which makes adaptive demands on the individual will subsequently be focused through the area of facilitation, whether it is paraspinal (segmental facilitation) or local (trigger point) - lying in muscle, fascia, ligament, scar tissue, etc.

This is the so-called neurological lens of which Korr speaks. 4 5

Normalisation of the noxious influences of trigger points therefore demands both local desensitisation and whole body reduction of negative influences whether these are nutritional, psychological or structural/mechanical.

Trigger points therefore emerge from a background of somatic dysfunction, often involving multiple etiological stressors which may include 6 7 8 9 10 11 12:

Congenital factors (short/long leg, small hemipelvis, short upper extremity, fascial, cranial and other distortions) which impose adaptive demands on the body

Overuse, misuse and abuse (and disuse) factors (such as injury or inappropriate patterns of use involved in work, sport or regular activities)

Acquired postural stresses Reflexive factors (trigger points, facilitated spinal regions) which generate additional

adaptive demands on target tissues Chronic negative emotional states (anxiety, etc.) with consequent myofascial changes Nutritional deficits Toxic accumulations Infection Endocrine (hormonal) imbalances - particularly thyroid

Dysfunction progression sequence

As a result of such adaptive demands, which affect each and every one of us to some degree, acute and painful problems overlaid on chronic soft tissue changes become the norm - and within these patterns myofascial trigger points are inevitable. When the musculoskeletal system is 'stressed' by one or other combination of such factors a sequence occurs which can be summarised as:

Something (as listed above) occurs which leads to increased muscular tone Increased tone, if anything but short-term, leads to a retention of metabolic wastes Increased tone simultaneously leads to a degree of localised oxygen lack (relative to the

efforts being demanded of the tissues) - resulting in ischemia Increased tone might also lead to a degree of oedema These factors (retention of wastes/ischemia/oedema) result in discomfort/pain Discomfort/pain leads to increased or maintained hypertonicity Inflammation or at least chronic irritation may be a result Neurological reporting stations in hypertonic tissues will bombard the CNS with information

regarding their status, leading to a degree of sensitisation of neural structures and the evolution of facilitation - hyper-reactivity

Macrophages are activated as is increased vascularity and fibroblastic activity Connective tissue production increases with cross linkage leading to shortened fascia Since

all fascia/connective tissue is continuous throughout the body any distortions or restrictions which develop in one region can potentially create compensating changes elsewhere, so negatively influencing structures which are supported or attached to the fascia, including nerves, muscles, lymph structures and blood vessels

Changes occur in the elastic (muscle) tissues leading to chronic hypertonicity and ultimately to fibrotic changes

Hypertonicity in a muscle will produce inhibition of its antagonist muscles Chain reactions evolve in which some muscles (postural - Type 1) shorten while others

(phasic - Type ll) weaken Because of sustained increased muscle tension, ischemia in tendinous structures occurs, as it

does in localised areas of muscles. Periosteal pain areas develop, and joint restrictions evolve Mal-coordination of movement occurs with antagonist muscle groups being hypertonic (e.g.

erector spinae) or weak (e.g. weak rectus abdominis group) Localised areas of hyper-reactivity of neural structures occur (facilitated areas, or myofascial

trigger points) in paraspinal regions or within stressed muscles Energy wastage due to unnecessarily maintained hypertonicity leads to fatigue Widespread functional changes develop - affecting respiratory function, for example - with

repercussions on the total economy of the body Heightened arousal results and there will be a reduced ability to relax adequately with

consequent further increase in hypertonicity Functional patterns of use of a biologically unsustainable nature emerge, involving chronic

musculoskeletal problems and pain

At this stage restoration of normal function requires therapeutic input which both addresses the multiple changes which have occurred as well as the need for a re-education of the individual as to how to use his/her body, to breathe, carry and use themselves in less stressful ways.

The chronic adaptive changes that develop lead to the likelihood of future acute exacerbations as the increasingly chronic less supple structures attempt to cope with new stress factors resulting from the normal demands of modern living.

Structural modification of distressed tissues 13

Apart from the evolution of myofascial trigger points a multitude of structural modifications occur in tissues which are chronically stressed.

Functional demands on dysfunctional structure often cause structural change to occur. Wolffís law observes that calcium is laid down along lines of stress resulting in bony spurs, joint immobility and calcified ligaments... Muscle hypertrophy occurs in overworked muscles; disuse atrophy occurs in those not worked adequately. Chronic skin changes (dryness, scaling, cracking, thickening, pimples, etc.) occur when trophic substances (carried via vascular channels or by axoplasmic flow) do not provide adequate nutrition.

Appropriate trigger point treatment needs to 14:

Take account of associated musculoskeletal dysfunctional patterns (joint, fascia or muscle) Offer education to ensure prevention of future exacerbations Ensure removal or correction of precipitating or maintaining factors - possibly including

postural habits, emotional stress factors, nutritional imbalances, hormonal (especially thyroid) imbalance, etc.

Include introduction of suitable self-help measures including stretching, postural re-education, etc.

Manual approaches to treatment of myofascial trigger points and the pain and

dysfunction they produce include 15:

Identification of the trigger point (see palpation methods below) Inhibition pressure (also known as ischemic compression and acupressure) Positional release methods (such as counterstrain) Post-isometric relaxation or reciprocal inhibition of tissues housing trigger points followed by

Muscle Energy stretching Spray and stretch (use of vapocoolant spray during prolonged stretching of muscle housing

trigger point) Deep tissue work (neuromuscular technique/massage) Procaine (or similar) injections Dry needling (acupuncture) Myofascial release of tissues housing trigger points Manipulation (e.g. articulation or HVT) of associated joints as appropriate

Integrated Neuromuscular Inhibition technique (INIT)A sequential combining of the first three elements in this list forms the basis for INIT.

Identify the trigger and its target area (below) Apply ischemic compression using a particular methodology (below) Hold the tissues housing the trigger in a ëposition of easeí (below) Following a muscle energy procedure, stretch the tissues housing the trigger - helping

restore these to a normal resting length A trigger point will usually be efficiently deactivated following this sequence. Why combine

these methods?

Individually, each can partially or totally deactivate triggers. Combined, the results are more lasting and efficient.

Surface palpation sequence 16 17

Over an area of acute or chronic, local or reflexively induced dysfunction, skin will feel tense and will be relatively difficult to move or glide over the underlying structures. The skin overlying reflexively active areas such as trigger points (or active acupuncture points) tends to produce a sensation of 'drag' as it is lightly stroked - due to increased hydrosis since a sympathetically induced increase in low-level sweat gland activity has the effect of altering the degree of skin friction.

There is also an apparent undulation sensation, a rising and falling, palpable on a light stroke - described illustratively as 'hills and valleys'.

The skin will lose its fully elastic quality, so that on light stretching (taking an area of skin to its easy resistance barrier on stretching) it will test as less elastic as neighbouring skin. The skin above reflexively active structures will also be more adherent to the underlying fascia, something which will be evident in any attempt to glide it or roll it, when compared with normal areas.

All of these changes can become apparent in the application of neuromuscular

palpation/assessment strokes (NMT).

Ischemic compression sequencesThere are different approaches to application of ischemic compression

1) Apply firm digital compression to the trigger point sufficient to produce localised discomfort/pain as well as symptoms in the target area Maintain this compression for 5 seconds Release for 2-3 seconds Reapply pressure (same level) and keep repeating the 5 seconds on and 2-3 seconds off until the patient reports a reduction in local or referred pain OR an increase in pain (which is rare) OR until 2 minutes have passed with no change in the pain levels. The INIT sequence then moves to the positional release component

2) Apply firm digital pressure to the trigger point sufficient to produce localised discomfort/pain as well as symptoms in the target area Maintain the pressure for approximately 10 seconds Increase the degree of pressure slightly and maintain for a further 10 seconds Increase the degree of pressure once more and maintain for approximately 10 seconds. Slowly release pressure and the INIT sequence then moves to the positional release component

Positional Release sequence 18 19 20 21 22 23 24

All areas that palpate as painful are responding to, or are associated with, some degree of imbalance, dysfunction or reflexive activity which may well involve acute or chronic strain. Jones identified positions of tender points relating to particular strain positions. It makes just as much sense to work the other way around and to identify where the strain is likely to have occurred in relation to any pain point which has been identified.

We might therefore consider that any painful point found during soft tissue evaluation (including myofascial trigger points) could be treated by positional release, whether we know what strain produced them or not, and whether the problem is acute or chronic. Experience and simple logic tells us that the response to positional release of a chronically fibrosed area will be less dramatic than from tissues held in simple spasm or hypertonicity. Nevertheless, even in chronic settings, a degree of release can be produced, allowing for easier access to the deeper fibrosis.

This approach, of being able to treat any painful tissue using positional release, is valid whether the pain is being monitored via feedback from the patient (using reducing levels of pain in the palpated point as a guide) or whether the concept of assessing a reduction in tone in the tissues is being used (as in osteopathic functional technique).

A lengthy 60-90 seconds are recommended as the time for holding the position of maximum ease - although some experts suggest just 20 seconds if an additional facilitating input can be achieved - for example by ëcrowdingí or ëfoldingí the tissues to reduce

sensitivity further.

Method

Apply sufficient pressure to the point to cause mild discomfort and then slowly position the area in such a way as to reduce or remove the tenderness from the point.

If the painful point is on the anterior of the body consider flexion and sidebending and/or rotation towards the side of pain as the likeliest directions for creating ease.

If the painful point is on the posterior surface consider extension and turning away from the side of pain as the likeliest direction towards ease.

My approach is to say:

I want you to score the pain caused by my pressure, before we start moving you into different positions as a 10 and to not speak apart from giving me the present score (out of 10) whenever I ask for it.

The aim is to achieve a reported score of 3 or less before ceasing the positioning process. The area is then passively positioned (using the guidelines above of flexion for anterior body points, for example) until some degree of ease is reported in the tender point (based on the score, or the value, reported) which is either being constantly compressed at this stage (this is authorís preference, if discomfort is not too great) 25 or, intermittently probed (which is Jonesí preference).

When a reduction of pain by around fifty percent is achieved, a degree of fine-tuning is commenced in which very small degrees of additional positioning are introduced in order to find the position of maximum ease, at which time the reported ëscoreí should be reduced by at least 70%.

At this time the patient may be asked to inhale fully and exhale fully while observing for themselves changes in the palpated pain point, in order to evaluate which phase of the cycle reduces the pain score still more. That phase of the breathing cycle in which they sense the greatest reduction in sensitivity is maintained for a period which is tolerable to the patient (holding the breath in or out or at some point between the two extremes) while the overall position of ease continues to be maintained and the tender/tense area monitored. During the holding of the position of ease the direct compression can be reduced to a mere touching of the point along with a periodic probing to establish that ease has been maintained.

After 90 seconds (or less if appropriate crowding has been introduced) the area is very slowly returned to the neutral starting position. This slow return to neutral is a vital element in the procedure since the neural receptors (muscle spindles) may be provoked into a return to their previously dysfunctional state if too rapid a movement is made. The

tender point/area may be re-tested for sensitivity at this time and should be found to be considerably less hypertonic and sensitive.

It is then time to move on to the final stage of INIT - the stretching of the tissues utilising Muscle Energy Technique (MET).

Muscle Energy sequence 26 27 28 29 30 31 32

Use of either post-isometric relaxation (PIR) or reciprocal inhibition (RI) mechanisms, in order to induce a reduction in tone prior to stretching, is an integral part of MET, as initially used in osteopathy, and subsequently by most schools of manual medicine. 33 34 35 Evjenth succinctly summarises when tissues can benefit from MET,

Every patient with symptoms involving the locomotor system, particularly symptoms of pain and/or constrained movement, should be examined to assess joint and muscle function. If examination shows joint play to be normal, but reveals shortened muscles or muscle spasm, then treatment by stretching [and by implication MET] is indicated. 36

It is suggested that when treating acute soft tissues (or joints at any time) using MET, the commencement of the isometric contraction is from the restriction barrier (ëfirst sign of resistance or bind).

It is suggested that when treating chronic soft tissue problems using MET, the commencement of the isometric contraction is from short of the barrier (first sign of resistance or bind).

It is also suggested that when treating acute soft tissue or joint dysfunction using MET, the action following the isometric contraction does not involve stretching but merely takes the tissues/joint to its new resistance barrier and that -When treating chronic soft tissues using MET, the action following the isometric contraction should involve stretching a short way past the new resistance barrier. NOTE: Acute = problems commencing within the last three weeks OR anything acutely painful.

In using MET in the INIT sequence whole muscles can be stretched (as in upper trapezius or scalenes) or parts of muscles (as in the erector spinae) depending upon accessibility. The contraction phase should be held for 7 seconds or so, followed by complete relaxation of the patient and area, and a patient-assisted (if possible) stretch to, or through, the barrier (acute or chronic) which should be held for up to 20 seconds to allow lengthening. The MET procedure is then repeated.

Trigger point sensitivity will probably remain for some hours but should be reduced or absent when re-tested several days later.

Facilitation of antagonist sequence

Ruddyís Reciprocal Antagonist Facilitation (RRAF)

A promising addition to the sequence described above takes account of the potential offered by the methods developed some years ago by osteopathic physician T.J. Ruddy. 37 In the 1940s and ë50s Ruddy developed a method of rapid pulsating contractions against resistance which he termed ërapid rhythmic resistive ductioní. For obvious reasons the shorthand term ëpulsed muscle energy techniqueí is now applied to Ruddyís method.

Its simplest use involves the dysfunctional tissue, or joint, being held at its restriction barrier, at which time the patient, ideally (or the practitioner/therapist if the patient cannot adequately cooperate with the instructions) against the resistance of the practitioner, introduces a series of rapid (2 per second), tiny efforts towards the barrier.

The barest initiation of effort is called for with (to use Ruddyís term) ëno wobble and no bounce.

The application of this ëconditioningí approach involves, in Ruddyís words, contractions which are ëshort, rapid and rhythmic, gradually increasing the amplitude and degree of resistance, thus conditioning the proprioceptive system by rapid movements.

The effects are likely, Ruddy suggests, to include improved oxygenation, venous and lymphatic circulation through the area being treated. Furthermore, he believed that the method influences both static and kinetic posture because of the effects on proprioceptive and interoceptive afferent pathways, so helping to maintain dynamic equilibrium, which involves a balance in chemical, physical, thermal, electrical and tissue fluid homeostasis. In a setting in which tense hypertonic, possibly shortened, musculature has been treated by stretching, it is important to begin facilitating and strengthening the inhibited, weakened antagonists. This is true whether the tight muscles have been treated for reasons of shortness/hypertonicity alone, or because they accommodate active trigger points within their fibres.

The introduction of a pulsating muscle energy procedure, such as Ruddyís, involving these weak antagonists offers the opportunity for:

Proprioceptive re-education Strengthening facilitation of the weak antagonists Further inhibition of tense agonists Enhanced local circulation and drainage And, in Liebensonís words, ëreeducation of movement patterns on a reflex, subcortical basis

Take the example of a shortened, hypertonic upper trapezius muscle. Whether this contained active trigger points or not (and most do according to Travell and Simons 38 since this is the most common trigger point site in the body), a form of stretching (MET or other) would almost certainly form part of a treatment approach to normalising the dysfunctional pattern with which it is associated.

Czech researcher Vladimir Janda MD describes two of these, the so-called Upper and Lower 'crossed' syndromes, as follows 39 40:The Upper Crossed Syndrome involves the following basic imbalance:

The pectoralis major and minor, upper trapezius, levator scapulae and sternomastoid all tighten and shorten while the lower and middle trapezius, the serratus anterior and rhomboids all weaken.

It is suggested, therefore, that in order to begin a rehabilitation and proprioceptive re-education element, following the appropriate stretching of upper trapezius, Ruddyís methods could be introduced, for example as follows:

The operator places a single digit contact very lightly against the lower medial scapula border, on the side of the treated upper trapezius of the seated or standing patient. The patient is asked to attempt to ease the scapula, at the point of digital contact towards the spine.

The request is made, Press against my finger with your shoulder blade, towards your spine, just as hard as I am pressing against your shoulder blade, for less than a second.î Once the patient has managed to establish control over the particular muscular action required to achieve this (which can take a significant number of attempts), and can do so for a second at a time, repetitively, it is time to begin the Ruddy sequence.

The patient is told something such as, ìNow that you know how to activate the muscles which push your shoulder blade lightly against my finger, I want you to try do this 20 times in 10 seconds, starting and stopping, so that no actual movement takes place, just a contraction and a stopping, repetitively.

This repetitive contraction will activate the rhomboids, and the middle and lower trapezii, producing an automatic reciprocal inhibition of upper trapezius.

The patient can then be taught to place a light finger or thumb contact against their own medial scapula so that home application of this method can be performed.

A degree of creativity can be brought to bear when designing similar applications of Ruddyís reciprocal antagonist facilitation (RRAF) for use elsewhere in the body, in order to complement stretching procedures and trigger point deactivation, in the knowledge that the treatment process thus extends into the educational and rehabilitation phase, especially if the patient undertakes homework.

These methods and other advanced soft tissue techniques are taught as part of the range of degree courses available at the Centre for Community Care and Primary Health, University of Westminster.For details of short courses contact Mark Armstrong on 0702-911-5000 (ext. 3369) or for details of the BSc and Masters courses involving complementary health care and

bodywork write to the Director, CCCPH, 115 New Cavendish Street, London W1M 8JS

References

(1) Liebenson C Active rehabilitation protocolsî, in Liebenson C (ed) Rehabilitation of the spine Williams & Wilkins Baltimore 1996

(2) Lewit K Manipulation in Rehabilitation of the Locomotor System Butterworths London 2nd edition 1991

(3) Jull G Janda V Muscles and motor control in Low Back Pain, In: Twomey L. Taylor J. (eds) Physical Therapy for the Low Back. Clinics in Physical Therapy Churchill Livingstone New York 1987

(4) Korr I Proprioceptors and somatic dysfunction Journal American Osteopathic Association 74:pp638 - 1975

(5) McNulty W et al Needle electromyographic evaluation of trigger point response to psychological stressor Psychophysiology 31:313-316 1994

(6) Janda V Introduction to functional pathology of the motor system. Proceedings Vll Commonwealth and international conference on Sport. Physiotherapy in Sport 3:39 1982

(7) Travell J Simon G Myofascial pain an dysfunction - The Trigger point manual. Williams and Wilkins Baltimore 1983/1991

(8) Basmajian J Muscles Alive Williams and Wilkins Baltimore 1974

(9) Janda V Muscle Function Testing Butterworths London 1983

(10) Lewit K Manipulation in rehabilitation of the locomotor system Butterworths London 1985

(11) Korr I Neurologic mechanisms in Manipulative Therapy Plenum Press New York 1978 (p27)

(12) Dvorak J and Dvorak V Manual Medicine - Diagnostics Georg Thiem Verlag Thieme-Stratton Stuttgart 1984

(13) Ward R (ed) Foundations for Osteopathic Medicine Published by Williams and Wilkins for American Osteopathic Association 1997

(14) Kuchera M McPartland M in: Ward R (ed) Foundations for Osteopathic Medicine Published by Williams and Wilkins for American Osteopathic Association 1997

(15) Greenman P Principles of Manual medicine Williams&Wilkins Baltimore 1989

(16) Lewit K Manipulative therapy in rehabilitation of the locomotor system Butterworths London 1992

(17) Greenman P op cit 1989

(18) Jones L Strain and Counterstrain Academy of Applied Osteopathy Colorado Springs 1981

(190 Mathews P Muscle Spindles, in Brooks V (ed) Handbook of Physiology (Section 1 The nervous system, volume 2) American Physiological Society Bethesda Md pp189=228 1981

(20) Korr I Proprioceptors and somatic dysfunction Journal American Osteopathic Association 74 pp638-650 1974

(21) Korr I The neural basis of the osteopathic lesion Journal American Osteopathic Association 48 pp191-198 1947

(22) Van Buskirk R Nociceptive reflexes and the somatic dysfunction J. American Osteopathic Assoc. 90 pp792-809 1990

(23) Jacobson E et al Shoulder Pain and Repetition strain injury Journal American Osteopathic Association vol89 pp 1037-1045 August 1989

(24) Rathbun J Macnab I Microvascular pattern at the rotator cuff J. Bone and Joint Surgery vol. 52 pp540-553 1970

(25) Chaitow L ëModified Strain Counterstrainí, in Soft Tissue Manipulation Healing Arts Press Rochester Vermont 1991

(26) Greenman P Principles of Manual medicine Williams and Wilkins Baltimore 1989

(27) DiGiovanna E Osteopathic Diagnosis and treatment Lippincott Philadelphia 1991

(28) Travell J Simons D Myofascial Pain and Dysfunction Volume 2 Williams and Wilkins Baltimore 1992

(29) Liebenson C Active muscular relaxation techniques (parts 1 & 2) Journal of Manipulative and Physiological Therapeutics 12(6)pp446- 451 1989 and 13(1)pp2-6 1990

(30) Mitchell F Snr Motion Discordance Yearbook of Academy of Applied Osteopathy Carmel CA 1967 pp1-5

(31) Janda V Muscle Function Testing Butterworths London 1989

(32) Lewit K Muscular patterns in thoraco-lumbar lesions Manual Medicine 2 1986

(33) Mitchell F Snr op cit 1967

(34) Greenman P op cit

(35) DiGiovanna E Osteopathic Diagnosis and treatment Lippincott Philadelphia 1991

(36) Evjenth O Hamberg J Muscle Stretching in manual therapy Alfta Rehab 1984

(37) Ruddy T.J. Osteopathic rapid rhythmic resistive technic Academy of applied osteopathy - yearbook 1962 pp23-31

(38) Simons D Travell J Low back pain (pt 2) Post Graduate Medicine 1983;73(2):81-92

(39) Janda V Muscle Function Testing Butterworths London 1983

(40) Janda V Introduction to functional pathology of the motor system. Proceedings Vll Commonwealth and international conference on Sport. Physiotherapy in Sport 3:39 1982

Myofascial paintrigger points

nerve root painsatellite trigger points

by John Halford

. . . These were not fixed in position along recognised meridians as are acupoints, but appeared on the body if disease or injury occurred. They were points which became spontaneously tender, and were detected by palpation when the troublesome part of the body was examined. When the physician pressed on the point, the patient would cry out ‘aah shi!’ meaning ‘ah yes’. These are still referred to as ah-shi points, or ‘points of pain’.

About the Author     John Halford has qualifications in Acupressure and Reiki and has been helping people (and animals) over many years. He has also studied Thalassotherapie in

     In the seventh century, during the Tang Dynasty (618 AD – 907 AD) a renowned physician by the name of Sun Ssu-Miao wrote a textbook (Thousand Golden Prescriptions) which actually described a different type of point. These were not fixed in position along recognised meridians as are acupoints, but appeared on the body if disease or injury occurred. They were points which became spontaneously tender, and were detected by palpation when the troublesome

France and Hydrotherapy in the USA and England. John lives and practises near Stockbridge in Hampshire and can be contacted by telephone on 01794 301591.

part of the body was examined. When the physician pressed on the point, the patient would cry out ‘aah shi!’ meaning ‘ah yes’. These are still referred to as ah-shi points, or ‘points of pain’.     ‘Ah-shi’ may be described as any local tender points to be found in the area of pain that give a reaction when stimulated but which are not recognised acupoints on any actual meridian.      It is important in the examination of a patient that careful examination of the total body is carried out. During the examination it is important to talk with the patient and enquire whether they have had any physical injury, strain, knock, bump and so on. A bruise may not necessarily manifest itself visually and since part of the discomfort from a bruise is the broken blood vessels or capillaries which give the discoloration it may require different treatment to acupressure; one should be careful not to be misled in diagnosis. Time is well spent in diagnosis so that the correct treatment is carried out.     It is by experience and correct use of the hands that one can “feel” this ‘ah-shi’ point and distinguish it from an acupoint on a definite meridian.     Sir Thomas Lewis, director of clinical research at University College Hospital, London found an interesting phenomenon when he was working on an artificial method of producing muscle pain. He found that injections of saline into muscle produced quite intense pain. Not only that, however, but the pain often extended or radiated a considerable distance from the site of the injection.  For example, a saline injection in the triceps muscle often produced pain all the way down into the little finger. Similarly, an injection in the trapezius muscle often produced an occipital headache. The triceps muscle links to the tip of the baby finger along the small intestine meridian. The trapezius muscle links to the back of the head along the bladder meridian.     It was a short step from this to find that certain points were particularly tender in painful conditions with a wide area of pain. When these points were injected with local anaesthetic, the

pain in the wider area could be made to disappear.     This phenomenon is the effect of trigger points radiating to other points along the relative meridians.     ‘Myofascial’ (the term comes from ‘myo’ = muscle, and ‘fascia’ = connective tissue which envelopes muscles, tendons and joint capsules).     The muscles are the active organs of locomotion. They are formed of bundles of reddish fibres, consisting of fibrine, and endowed with the property of contractility.     The fascia (bandage) are fibro-areolar or aponeurotic laminae, of various thickness and strength. It is the aponeurotic or deep fascia which form sheaths for the muscles, tendons and connective tissues.     Every muscle has a potential ‘trigger point’. When this trigger point flares up, goes into spasm and becomes painful often that one trigger point radiates its pain to another muscle. It triggers off pain from the source point to the satellite point.     It is necessary to distinguish between ‘myofascial pain’ and ‘nerve root pain’. The irritation of a nerve and thus nerve root pain, even if in the same distribution, is not to be confused with myofascial pain. Myofascial pain is due solely to activation of trigger points and their associated zones of activity.     There are three kinds of trigger points which develop in the muscles, tendons and joint capsules.     These trigger points can be (1) INACTIVE in which case, although they are there, they are like a dormant volcano.      They can be(2) LATENT like a rumbling volcano which can erupt at any time.      They can be (3) ACTIVE like a volcano in action and erupting.     Each muscle has its own characteristic pattern of pain referral. Often this can cause another trigger point to become active in another muscle within the zone of radiation of the original trigger. These are called ‘satellite’ trigger points.     The moving parts of the body were created, and intended to move through a specified range of

motion freely, easily and completely. When for any number of reasons they lose the ability to do this, there will be a problem. The most prevalent reason for the original loss of free motion is the residual muscle tightening which develops as a result of strain and exertion. Other factors are age, nervous tension, mechanical or emotional stress, infections, inflammatory conditions, exposure to draughts, the over-development of muscle, the secondary effects of injury, maximum effort, and/or the residual effects of previous maximum efforts.      Muscles are arranged in pairs of opposites. a muscle has two main functions. It contracts (shortens) and by this contraction moves the bone of its attachment in the direction of the contraction. The muscle then must release itself completely and be stretched so that no opposition is provided to the opposing contraction. All skeletal motion is produced in this way.     A muscle contracts not in the manner of an elastic band, but by a multiple folding over upon itself many, many times. It must release by a multiple unfolding so that it may be easily stretched to full length. The contraction process is a generated process. The release process is not. It is in the release process rather than the contraction process that motion problems will develop.     Every move produces its greatest stress upon a specific point. For example: as a result of excess tension of muscle tightening, a muscle containing a quarter of a million fibres forms a spasm of approximately ten thousand fibres. It can be so small that you do not realise its presence. With continued use, the spasm becomes aggravated and begins to add more fibres to itself. As it enlarges, it causes pressure. Pressure causes discomfort and pain.      A muscle that cannot accommodate the movement placed upon it will pull or even tear. Thus, a movement normally within the safe context becomes unsafe when shortening and spasm are present.     Because of the interrelationship between muscles, so you have the development of trigger

points manifesting themselves on other muscle areas rather than the original source of pain. These are referred by the term ‘satellite trigger points’.     Trigger points may be found in muscle which feels perfectly normal, or they may cause two distinctive signs:-a) Fibrositic nodules – actual round lumps felt in the muscles on palpation. these are commonest in the shoulder and neck areas and the lumbar area.b) Palpable taut bands – rope or string-like taut muscle fibres around the trigger point. They are likeliest to occur at the edges of large muscles. They run in the direction of the fibres of the muscle.     Trigger points must become deactivated or their effect will linger and become chronic. Then they will extend their activity by activating other trigger points.     Direct pressure with the finger, fingers or thumb are all very penetrating movements. Pressure is magnified many times when applied in this manner. The hyperaemia this produces will last for several hours causing capillary dilation to be retained while excess blood and oxygen softens and prepares the spasm for cross-fibre friction.     Cross-fibre friction may be applied along with any of the direct pressure techniques by simply moving the fingers to and fro across the muscle fibres. The hand should not slide on the surface because the depth and effect will be lost. Hand and tissue must move together.     This cross-fibre action forces adhesed fibres apart freeing them up to resume their normal activity of lengthening and shortening. the entire muscle must be relaxed. This can be done by a series of compression applied to the length of the muscle. Compression is the rhythmic thrusting along the muscle with the heel of the hand or the loosely clenched fist. Remember the spasm was the cause of the problem whilst the tightened muscle was the cause of the spasm.     The use of steroids (cortisone) can initially remove the pain but this is more than often short lived and the pain returns magnified. This is

because although the injection of cortisone settles the primary trigger point, it fails to take out the satellite trigger points in the surrounding muscles. These satellite trigger points start exerting pain in their own area of radiation and are quite likely to reactivate the primary trigger point, the cause of the original problem.     The detection of trigger points should not be difficult as the pressure on the point produces what has been described as the ‘jump sign’. The patient will tell you of the pain experienced by wincing or crying out.     Be that as it may, it is essential that no trigger point is missed as just missing one trigger point may well reactivate the original problem. Reassure the patient that the slight discomfort experienced during examination is well worth while enduring to ensure the long term relief correct treatment will provide.     The whole area of pain should be palpated for trigger points, tight bands occurring most likely at the edges of muscle . . . and ensure that the adjoining zone of radiation is thoroughly examined to ensure no satellite trigger point has been missed.     Several orthodox medical textbooks and more and more ‘open minded’ doctors accept that there is a relationship between myofascial trigger points and the acupoints of traditional Chinese medicine.     Just as this open minded approach from the medical profession will accept that myofascial trigger point pain and nerve root pain are to be distinguished one from the other, so it is very important that a practitioner of acupressure also appreciates this difference.      Nonetheless be aware that obvious nerve root pain may also at the same time exhibit less obvious myofascial trigger point pain and vice versa. It is wise, even if in doubt, to treat the trigger point with acupressure. You will do no harm if it is not myofascial trigger point pain by treating it in this way. You may well be able to establish that it is nerve root pain.          It can also be demonstrated that satellite trigger points are on the same meridian as the source myofascial trigger point. But a word of

caution – in certain instances the meridian can transfer the ‘pain flow’ over to a linking meridian and you can find a satellite trigger point on the linked meridian acupoint that is not obviously linked to the source trigger point. These are ‘lo points’ which connect coupled meridians by a secondary vessel. Coupled meridians are meridians which follow one another in the superficial circulation of energy and, at the same time, are of opposite sign, the one being yin, the other yang. It follows that the former lies on an embryological anterior surface, while the latter lies on an embryological posterior surface.     From the above observations I trust it is evident that myofascial trigger points coincide with the acupoints of traditional Chinese medicine. Normally these trigger points are relatively simple to detect but as I have indicated, be open minded when doing a diagnosis for the obvious diagnosis is not always correct. However experienced the practitioner is, he must be humble and realise that he will not always be right.

Myofascial Pain Syndromes from Trigger Points

Robert D. Gerwin, MD

Current Pain and Headache Reports 1999, 3:153-159Current Science, Inc. ISSN 1531-3433Copyright © 2005 by Current   Science,   Inc.

Myofascial pain syndrome (MPS) is a common cause of acute and chronic pain that can complicate other medical illnesses and injuries. It is both defined by and diagnosed by the presence of the myofascial trigger point. Current studies indicate that the trigger point is a dysfunctional motor end plate whose abnormal activity is modulated in some way by the sympathetic nervous system. Pain syndromes arise from trigger points as causes of local pain and of referred pain. Referred pain from a few or from many muscle trigger points produces regional or generalized pain. Treatment requires the elimination of the trigger point by manual therapy or by trigger point injection and correction of the mechanical and medical factors that initiate and perpetuate it.

Myofascial pain syndrome (MPS) constitutes a substantial portion of the pain spectrum, acute and chronic, as both the primary cause of disability, and as a complication arising from other problems such as failed low back surgery, cervical whiplash, overuse, or repetitive strain syndrome. MPS is a very specific type of muscular pain, and is not to be confused with fibromyalgia. It is common after injury, resulting in so-called soft-tissue pain. MPS can be intermittent and mild, or debilitating and totally disabling. It can be acute, but it can still be effectively treated even when it has persisted for years.

Pain syndromes associated with individual myofascial trigger points have been well described. [1, 2**] The

interactions of individual muscle myofascial trigger points, and the interaction of myofascial trigger points in functional units of muscles, especially in chronic cases, cause regional and widespread pain syndromes. Important postural consequences of dysfunctional muscle units created by myofascial trigger points affect the overall distribution and spread of pain and must be understood for treatment to be effective. For example, a round-shouldered, head-forward posture has significant implications for the position of the jaw, the state of the facial and neck muscles, the relationship of the shoulder and anterior chest muscles, and the low back. The mandible will be repositioned posteriorly, affecting the pterygoid, masseter, and temporalis muscles. Forward shoulder posture is associated with shortening of the pectoralis major and minor muscles and constant tension with their antagonist muscles, the trapezius and rhomboids. The posterior cervical muscles are overloaded, as the head is pulled back (extension of the neck even though the head is forward). The low back is usually flattened, loading the lower back muscles (quadratus lumborum, iliocostalis, and multifidi) and altering the relationships and function of the lumbosacral junction and sacroiliac joints. These changes are associated with the development and maintenance of myofascial trigger points and with the pain affecting different regions (facial and jaw pain, neck and shoulder pain, and low back pain). This example emphasizes the importance of functional muscle units in the development and spread of myofascial trigger points.

The Myofascial Trigger Point

The myofascial pain syndrome is distinguished by the existence of the trigger point, which is characterized by the following features: 1) exquisite tenderness in a taut muscle band; 2) referred pain elicited by stimulation of the trigger point; local twitch or contraction of the taut band; 4)reproduction of the patient's spontaneous pain pattern when stimulated; 5) weakness without atrophy; and 6) restricted range of motion (Table 1). MPS is diagnosed by identification of these features of the myofascial trigger points on physical examination. Treatment involves the inactivation of the myofascial trigger point for immediate relief of pain and to provide a window of time to produce the necessary biomechanical changes that give sustained improvement. The factors in the patient that led to the MPS and that perpetuate it must be eliminated or corrected. These factors include postural dysfunction, impaired spinal joint function, pelvic rotation, leg length inequalities, ergonomic factors associated with work and recreation, and medical systemic factors such as nutritional or hormonal insufficiency.

Table 1:  The Physical Features of the Myofascial Trigger Point

1. Exquisite tenderness in a taut muscle band

2. Referred pain elicited by stimulation of the trigger point

3. Local twitch or contraction of the taut band

4. Reproduction of the patient's spontaneous pain pattern when stimulated

5. Weakness without atrophy

6. Restricted range of motion

A particular pain problem is called myofascial when one or more myofascial trigger points reproduce all or part of the individual's pain. As muscles are examined individually for myofascial trigger points, single muscle syndromes emerge. The pain experienced from a myofascial trigger point is a combination of the local pain from a single muscle and the pain felt in the zone of referred pain. The person suffering from an MPS may complain only of the pain felt in the referred pain zone, but treatment directed only toward the referred pain may be unsuccessful. Myofascial trigger points may refer pain locally. For example, upper trapezius muscle myofascial trigger points refer pain into the ipsilateral posterior neck. Pain from myofascial trigger points may also be felt in remote sites, as in the case of the infraspinatus muscle referral pattern to the arm and hand. MPS is more often the result of myofascial trigger points in many muscles, affecting a region or even appearing as widespread pain involving three or four regions of the body. The spread of myofascial trigger points and therefore of myofascial pain occurs as a result of the development of myofascial trigger points in dysfunctional muscle units and in the muscles in the referred pain zone.

Trigger point physiology

No specific or consistent biochemical changes have been reported in the myofascial trigger point. The known plasticity of the nervous system as it responds to noxious stimulation can explain much of the clinical phenomena that occur. The nature of the myofascial trigger point itself had not been understood until quite recently, when Hubbard and Berkoff [3*] reported spontaneous electrical activity (SEA) in the myofascial trigger point that was not seen in the adjacent nontender muscle. They postulated that the activity was generated in the intrafusal muscle spindle fibers on the basis of preliminary pharmacologic studies that showed an inhibiting effect of the alpha-adrenergic blocking agent, phentolamine. Chen et al. found that phentolamine reduced the SEA of the trigger point significantly in the rabbit model [4]. SEA is clustered within a region of the taut band that these authors call the active trigger zone. The abnormal electrical activity comes from the motor end plate, the evidence being the characteristic electrical discharges of end-plate activity. A current hypothesis based on the available experimental data is that the motor end plate is dysfunctional, consistent with about a thousand-fold increase in the release of acetylcholine. This release then results in a sustained, abnormal increase in the activity of the motor end plate [5*], and the abnormal sustained activity is somehow modulated by sympathetic activity.

Tenderness

The foremost characteristic of the myofascial trigger point is the exquisitely tender point in a taut band. This tender point displays both hyperalgesia, which is an excessive response to normally painful stimulation, and allodynia, which is the perception of pain in response to normally nonpainful stimulation. Muscle is supplied with afferent nociceptor nerve endings that are sensitive to pressure and chemical stimulation and that activate dorsal horn neurons. The dorsal horn neurons receive input from multiple muscle sites (receptive fields) and from different deep tissues, including either other muscles or viscera. Sensitization to peripheral noxious stimuli occurs in muscle nociceptors, including dorsal horn neurons, as it does in skin and other tissues.

Substance P is a neuropeptide that modulates nociception by activating nociceptor neurons. Release of substance P by action of nociceptive afferents can enhance the activation of dorsal horn nociceptors, contributing to the sensitization of dorsal horn neurons [6]. Thus, the two key features of the myofascial trigger point, tenderness and referred pain, have their origin in the ability of the nervous system to modulate afferent nociceptive activity. Tenderness is really an expression of sensitization; referred pain is an expression of activation of afferent activity at remote sites. Referred pain is not a phenomenon unique to the myofascial trigger point but is well known clinically throughout medical practice as in anginal pain referred to the neck and down the arm.

These considerations have definite practical implications for MPS, as they suggest treatment approaches that work through inhibiting pain input and transmission from myofascial trigger points. Inactivation of myofascial trigger points in one muscle by the injection of local anesthetic can alter the activity of distant myofascial trigger points [7], showing the importance of these modulating factors.

Local twitch response

The local twitch response (LTR) elicited by mechanical stimulation of the trigger point is an unequivocal sign

of a myofascial trigger point, whether active or latent. During the LTR, the taut band in which the tender point is found is the only thing that contracts, not the entire muscle. A burst of high amplitude electrical activity occurs with the LTR. Interruption of the proximal nerve greatly diminishes but does not abolish the LTR. LTRs in taut bands of rabbit skeletal muscle are related to the reflexes at spinal cord level [8]. The LTR is a spinal cord reflex requiring an intact peripheral nerve. It can be elicited by inserting a needle into an myofascial trigger point taut band at the trigger point zone in the process of inactivating a trigger point. The LTR is a sign that the trigger zone has been reached by the treating needle.

Diagnosis

The diagnosis of MPS is made by physical examination. The history provides the context of the pain problem, but the diagnosis must be based on the identification of the myofascial trigger point by physical examination. The myofascial trigger point is distinguished from simple muscle tenderness by the presence of the taut band and by referred pain. A local twitch response is confirmatory. Restricted range of motion about a joint or a part of the body like the neck or waist is highly suggestive that trigger points are present. The diagnostic process involves an overall evaluation of possible factors that could explain the patient's symptoms. The diagnosis of MPS is not one of exclusion. Rather, it is based on positive findings. Thus, pain in the shoulder must include the usual differential diagnostic considerations of local shoulder dysfunction, including rotator cuff syndrome, impingement syndrome, bursitis, cervical disk disease, and intracapsular disorders, eg, degenerative arthritis and adhesive capsulitis. Myofascial trigger points can complicate any of these conditions. A comprehensive examination for myofascial trigger points should include all the muscles that can refer pain to the shoulder region.

Trigger point examination reliability

A study establishing the reliability of the examination of the six major physical features of the myofascial trigger point showed a high inter-rater agreement for all features studied [9*]. There was variation, however, in the degree of agreement among the different features and among the different muscles examined. Some features, such as tenderness and reproduction of usual pain, had very high levels of agreement, but the LTR consistently showed a lower level of agreement, although the agreement present was significant. One should not expect to identify all features of a myofascial trigger point by manual examination in every muscle examined. Some muscles are more difficult to examine than others are, and some features of the trigger point are more difficult to elicit than others. Attempts to quantify the measurement of tenderness have led to use of the pressure threshold meter or algometer [10]. Even with algometry, however, manual examination is needed at least for identification of the taut band that characterizes the myofascial trigger point.

Other laboratory studies

The myofascial trigger point taut band is visible on high resolution B-mode ultrasound. This technique allows visualization of the localized twitch in the taut band of the myofascial trigger point when stimulated by needle insertion [11]. Thus, the physical response of the trigger point to treatment can be documented, and a permanent record can be made.

The characteristic electromyographic activity of the trigger point can be used to identify and document its presence. No other laboratory studies (including x-rays, CT, and MRI) have shown positive results or abnormalities in myofascial pain syndromes. All blood tests are normal unless there are comorbid conditions. Comorbid disorders exist in MPS and can be important causes of chronic MPS that are refractory to treatment, but they are not directly related to the development of the trigger point. Identification of cervical

facet joint injury or of hypothyroidism, both potentially comorbid conditions with MPS, requires appropriate laboratory testing. Surface EMG is useful in assessing muscle function in MPS. The evaluation of trigger point activity with dynamic EMG techniques [12] shows asymmetries in the activity of the affected paired muscles and persistent increased muscle activity. Surface EMG can objectively demonstrate muscle-related postural dysfunction and functional muscle unit imbalance in a muscle containing trigger points.

Myofascial Trigger Point Syndromes

Headache

Trigger point syndromes can be grouped according to the area involved. Headache is a common complaint, and one that is closely related to myofascial trigger points. Headache pain can be a consequence of myofascial trigger points located in the shoulder, neck, or facial muscles. The pain is referred from trigger points to various parts of the head and neck, causing symptoms of headache that are often attributed to migraine or sinus headache. The headaches can be constant or throbbing; unilateral, bilateral, or circumferential (bandlike around the head); and vertex, occipital, or retro-orbital. When muscle pain activates peripheral nerve pain receptors in the trigeminal nerve distribution or in the upper cervical spine segments (which have pain input into the subnucleus caudalis of the trigeminal nerve), it is likely that the trigeminovascular system is activated. This process results in a cascade of neuropeptide and vasoactive peptide release (substance P and calcitonin gene-related protein, for example) and in the development of migraine phenomena such as photophobia, diaphoresis, nausea, and dizziness. In this way, muscle trigger points could precipitate migraine phenomena.

Figure 1

Composite of trigger point referral patterns from the trapezius and sternocleidomastoid muscles that are commonly associated with headache.

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The most common cause of myogenic headache in the author's experience is referred pain from muscle trigger points. Upper trapezius muscle trigger points cause referred pain to be felt in the temple and along the side of the head above and behind the ear. The trapezius functional muscle group includes the antagonist muscles that flex and rotate the neck. Its functions include extension of the neck against resistance and assistance in lateral rotation and lateral flexion. The sternocleidomastoid muscles, which flex and rotate the neck, frequently have myofascial trigger points in conjunction with the trapezius muscle. The composite headache includes the occiput, the vertex of the head, the supraorbital area, and the forehead, and includes the opposite side, the temple, the side of the head, and the ear, or any combination of these areas (Fig. 1) The splenius capitis and cervicis are also part of the functional muscle unit of the trapezius and the sternocleidomastoid. They act as extensor muscles of the neck in synergy with the trapezius muscles, as agonists to the contralateral upper trapezius for rotation, and as antagonists to sternocleidomastoid flexor function. They are also likely to have active trigger points along with the trapezius and sternocleidomastoid muscles. Referred pain from the splenius capitis and cervicis add to headache along the side of the head, the vertex of the scalp, and the retro-orbital area. Recurrent headache is frequently the result of myofascial trigger points from these and other anterior and posterior neck muscles.

Shoulder and neck pain

Pain in the neck and shoulder can be the direct result of muscle trigger points. (Fig. 2) Pain in the back of the neck occurs with trigger points in the posterior cervical, and suboccipital muscles. Trigger points in these muscles refer pain into the head but also have local pain. The deep paraspinal multifidi muscles refer pain to the upper neck, the shoulder, and towards the scapula. These muscles may be dysfunctional and are likely to develop myofascial trigger points. This development occurs in situations of postural abnormality or restriction of motion caused by trigger points in the muscles that move the jaw or the muscles that control head flexion, extension, rotation, or lateral bending. The levator scapula contributes to extension of the neck (a function of the bilateral activation of the muscle) and to elevation of the shoulder and rotation of the scapula. Pain from levator scapula trigger points is felt in the angle of the neck and shoulder, medial to the scapula, and into the posterior shoulder. Levator scapula function is synergistic with that of the upper trapezius in elevation of the shoulder and is antagonistic to the rotational direction of force of the trapezius. The levator scapula rotates the glenoid fossa downwards, and the trapezius rotates it upwards. Trigger point pain tends to spread among the muscles that move the scapula. Because myofascial trigger points spread through functional muscle units, trigger point pain will extend through overlapping muscles sharing function or control of a body part.

Injury to the rotator cuff muscles can primarily affect just one muscle, such as the supraspinatus or infraspinatus muscle. The entire rotator cuff complex tends to become secondarily involved. A painful trigger point in the rotator cuff muscle teres major is usually accompanied by a trigger point in the latissimus dorsi, with which it shares adduction and internal rotation of the humerus. The latissimus dorsi attaches superiorly to the humerus but has a common tendon with the teres major. It acts on the scapula through its control of the humerus and the force exerted through the teres major. Inferiorly, its attachment to the lower six thoracic vertebrae and all of the lumbar vertebrae allows it to assist in low back and pelvic movement. Mechanical dysfunction in these movements can lead to the development or perpetuation of trigger points in the primary effectors of low back and pelvic movement and stability. These include the iliocostalis, the quadratus lumborum, and the iliopsoas muscles. Examination of pain in the shoulder region should be accompanied by evaluation of the low back and pelvis region.

A common forearm trigger point pain syndrome is lateral epicondylitis. This condition is usually attributed to tendinitis. It may involve an enthesopathy of the proximal attachment of the extensor carpi radialis longus and brevis and the extensor digitorum. Trigger points in the muscle belly itself accompany the attachment trigger points. Relief of pain is achieved by elimination of the muscle trigger points and the attachment trigger points by manual inactivation or by injection.

Figure 2

Composite of trigger point referral patterns from the iliopsoas, quadratus lumborum, and quadriceps muscles that are associated with low back and pelvic region pain.

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Figure 3

Composite of trigger point referral patterns from the iliopsoas, peroneus longus, hamstring, and vastus medialis muscles that are commonly associated with pelvic region and leg pain.

View larger image

Back and hip pain

Trigger points occur in many areas of the low back and pelvic region (Fig. 3). The acute (and chronic) inability to straighten up because of back pain is frequently the result of quadratus lumborum muscle trigger points. This muscle is an extensor and lateral flexor of the waist. Pain from quadratus lumborum trigger points is felt across the low back and is most severe when the patient is upright, whether sitting, or standing, with the back unsupported. Pain can also be felt in the groin, in the testicles, in the back, and in the hip, or it can be felt as sciatica. Bending, turning, and lifting aggravate the pain. This pain is distinguished from hip joint pain on the basis of the location of the pain when the patient is standing. When the pain emanates from the hip joint, there is little back pain and mostly hip, groin, or sacroiliac joint region pain. Quadratus lumborum pain persists when the patient is sitting or recumbent and increases with attempted movement. Hip joint pain is associated with limited range of motion at the hip and relief of pain when sitting or reclining.

Pain in the hip and pelvic region can also be the result of the quadratus lumborum antagonist, the iliopsoas. This flexor of the waist and hip typically causes pain in a vertical distribution in the low back, perceived as across the back when bilateral, and in the anterior thigh. This type of pain is often involved in association with extensors of the back and hips (quadratus lumborum, gluteus maximus, and hamstring muscles). Alleviation of myofascial pain in the low back-pelvic region requires treatment of the iliopsoas muscle. If the iliopsoas trigger point-induced restricted range of motion persists after release of extensor muscle trigger points, back and thigh pain will persist, and a flexion-extension postural dysfunction will result because of the now dominant restriction of flexion in the iliopsoas.

Knee and ankle pain

Anterior knee pain from muscle trigger points results from trigger points in the quadriceps muscle. Myofascial trigger points in the rectus femoris head of the quadriceps can refer pain to the patella and distal anterior thigh. Trigger points in the vastus medialis and vastus lateralis refer pain to the medial and lateral aspects of the knee respectively. The pain they cause can be mistaken for collateral ligament pain.

Back-of-knee pain is usually the result of trigger points in the hamstring muscles, the extensors of the hip, and the flexors of the knee. These muscles are active when the trunk is flexed while standing, controlling flexion. In this way, their function is closely related to iliopsoas function, and the two muscles must be considered together. Trigger points in the small popliteus muscle that attaches to the lateral femoral condyle superiorly, and to the tibia inferiorly, cause pain in the back of the knee and should be considered when pain persists after inactivation of hamstring trigger points.

An everted, pronated foot can result in trigger points in the peroneus longus muscle, referring pain to the anterolateral ankle; in the vastus medialis, referring pain to the knee; and in the gluteus medius muscle, referring pain to the hip. Anteromedial and great toe pain results from trigger points in the anterior tibialis

muscle. The same forces that cause an anterior compartment syndrome will cause trigger point formation. Injury to the ankle or foot that limits movement and impairs dorsiflexion of the foot will overwork the anterior tibialis and result in myofascial pain. This mechanism is exaggerated in women who wear high heels, which increase the plantar flexion of the foot.

Osteopathic concepts and myofascial pain

Osteopathic concepts are only now being emphasized in myofascial pain syndromes in conjunction with myofascial concepts. Understanding the three-dimensional movement of the pelvis, including the sacroiliac joint and lumbosacral junction, increases the ability to diagnose and treat myofascial pain syndromes. Restricted motion of cervical vertebrae, thoracic and lumbar vertebrae, and of the sacroiliac joint results in perpetuation of trigger points. Recurrent thoracolumbar myofascial pain syndromes may require release of segmental spinal hypomobility. Fusion of L5 to S1 results in shifting of the reciprocal movement of the sacroiliac joint when the patient is walking, often producing a myofascial hip and buttock pain syndrome.

Facet joint syndrome

Injury to the cervical facet joint, as in whiplash, can produce a pain syndrome that overlaps and accompanies the myofascial pain syndrome. Persistent or chronic neck or shoulder pain after whiplash demands examination of the facet joints and denervation of the joint if it is found to be the cause of pain. Only then will myofascial trigger point inactivation be effective.

Treatment

Elimination of the myofascial trigger point is the central feature of treatment in the myofascial pain syndrome because this elimination is critical to the relief of pain and the restoration of normal function. Restoration is achieved through the correction of the mechanical and systemic medical dysfunctions that interfere with the ability of the muscle to recover. The trigger point is inactivated either manually or by invasive techniques such as trigger point injections. Simons [2**] et al. used the technique of intermittent "cold and stretch" as a way of lengthening the muscle and decreasing or eliminating the trigger point. This technique involves gradual stretching of the muscle while vapo-coolant is applied, until the maximum stretch is achieved or a barrier is reached. The stretch for a particular muscle is always in the opposite direction of the muscle's action. Heat is applied after stretching in order to reduce poststretching discomfort. Other techniques have been developed for the inactivation of the trigger point and the restoration to full length of the muscle. These include trigger point compression, local and regional muscle stretching, myofascial release techniques, the postisometric contraction or relaxation technique (often used with respiratory facilitation) [13], strain-counterstrain, superficial or subcutaneous dry needling [14], and acupuncture, in addition to traditional physical therapy techniques of electrical stimulation and ultrasound. Surface EMG is an effective tool in identifying muscle groups that need to be treated, in assessing the effectiveness of muscle-specific training, and in teaching patients how to control their muscle tension through biofeedback.

Trigger point injection with local anesthetic, or dry needling without anesthetic, are examples of invasive procedures that might be called upon to facilitate the relief of myofascial pain [15]. Inactivation of the myofascial trigger point can be accomplished by insertion of a needle into the trigger zone of the myofascial trigger point. The technique of injection is described in detail by Hong [16]. Procaine is the anesthetic of choice because it is metabolized locally by procaine esterase, and its effective half-life is as short as 10 to 15 minutes. If a local nerve block is inadvertently produced, numbness and weakness clear rapidly. Vitamin C is given for 3 days prior to injection therapy because it reduces bleeding caused by the needle. Risks of

trigger point injection include bleeding, organ or vessel puncture, nerve injury, syncope, and allergic reactions. A precise knowledge of anatomy is required of the clinician who employs this technique. Another therapeutic technique now being evaluated is the injection of botulinum toxin into the trigger point [17, 18*].

Whatever method is used to inactivate myofascial trigger points, all trigger points in a functional muscle unit should be addressed by a combination of manual techniques and injection if necessary. Stretching the muscles in the affected functional muscle unit is an essential part of the treatment. Moist heat applied following the stretching decreases posttreatment muscle soreness.

Pharmacologic therapy

No studies have looked at drug treatment of the myofascial pain syndrome itself. Analgesics play a role in producing comfort during the acute or treatment phase. Nonsteroidal anti-inflammatory drugs offer analgesic benefit but nothing more specific. The antidepressant drugs offer the same potential relief for chronic MPS as they do in any other chronic pain syndrome. The same principles that apply to treatment of nonmalignant pain of any source are applied to the treatment of MPS.

Psychological factors

A perpetuating factor that must always be considered in relation to the myofascial pain syndrome is psychological stress. In one study involving needle electromyographic evaluation, the trigger point in the trapezius muscle specifically responded to a psychological stressor, whereas the adjacent nontender muscle did not [19*]. Another area of research involves the evaluation of psychological stressors in myofascial pain specifically in women [20].

Conclusions

Myofascial pain syndrome is a painful muscle disorder that occurs following stress or injury in muscle. It is diagnosed by manual examination and treated through a variety of manual and invasive techniques. Correction of underlying or comorbid disorders, including postural and psychological stressors, is a necessary aspect of the treatment.

References and Recommended Reading

Recently published papers of particular interest have been highlighted as:

* Of importance** Of major importance

1. Travell JG: Myofascial Pain and Dysfunction: The Trigger Point Manual. Baltimore: Williams and Wilkins; 1992.

2.**

Simons DG: Myofascial Pain and Dysfunction: The Trigger Point Manual. Baltimore: Williams and Wilkins; 1999.

Latest version of the standard and best textbook in the field. Chapter 2 in this volume presents the latest data on the mechanism of trigger point formation and physiology. Chapter 4 is the best available statement on the causes of chronic myofascial pain.

3.*

Hubbard DR: Myofascial trigger points show spontaneous needle EMG activity. Spine 1993, 18:1803-1807.

First to describe the spontaneous electrical activity in the trigger point and to compare it to adjacent normal muscle.

  View the PubMed notation for this reference.

4. Chen, JT, et al.: Phentolamine effect on the spontaneous electrical activity of active loci in a myofascial trigger spot of rabbit skeletal muscle. Arch Phys Med Rehabil 1998, 79:790-794.

  View the PubMed notation for this reference.

5.*

Hong C-Z: Pathophysiologic and electrophysiologic mechanisms of myofascial trigger points. Arch Phys Med Rehabil 1998, 79:863-872.

Most up-to-date presentation of the physiology of the trigger point. The data are similar to those presented in references [1] and [2].

  View the PubMed notation for this reference.

6. Mense S: Pathophysiologic basis of muscle pain syndromes. In Myofascial Pain: Update in Diagnosis and Treatment. Edited by Fischer AA. Philadelphia: W.B. Saunders; 1997: 23-53.

7. Carlson CR, et al.: Reduction of pain and EMG activity in the

masseter region by trapezius trigger point injection. Pain 1993, 55:397-400.

  View the PubMed notation for this reference.

8. Hong C-Z: The localized twitch responses in responsive taut bands of rabbit skeletal muscle are related to the reflexes at spinal cord level. J Musculoskeletal Pain 1995, 3:15-33.

9.*

Gerwin RD, et al.: Interrater reliability in myofascial trigger point examination. Pain 1997, 69:65-73.

Reports on a study that established the inter-rater reliability of the myofascial examination and therefore confirmed its credibility as a diagnostic tool.

  View the PubMed notation for this reference.

10. Fischer AA: New developments in diagnosis of myofascial pain and fibromyalgia. In Myofascial Pain: Update in Diagnosis and Treatment. Edited by Fischer AA. Philadelphia: W.B. Saunders; 1997: 1-21.

11. Gerwin RD: Ultrasound identification of the myofacial trigger point. Muscle Nerve 1997, 20:767-768.

  View the PubMed notation for this reference.

12. Donaldson CCS: The evaluation of trigger-point activity using dynamic EMG techniques. Am J Pain Manage 1994, 4:118-122.

13. Lewit K: Treatment of myofascial pain and other dysfunction disorders. In In Pain Research and Clinical Management: Progress in Fibromyalgia and Myofascial Pain. Edited by Værøy H, Merskey H. Amsterdam: Elsevier; 1993: 375-392.

14. Baldry PE: Acupuncture, Trigger Points and Musculoskeletal Pain. Edinburgh: Churchill Livingstone; 1993.

15. Lewit K: The needle effect in relief of myofascial pain. Pain 1979, 6:83-90.

  View the PubMed notation for this reference.

16. Hong C-Z: Myofascial trigger point injection. Critical Reviews in Physical Medicine and Rehabilitation. ; 1993.

17. Alo KM, et al.: Botulinum toxin in the treatment of myofascial pain. Pain Clin 1997, 10:107-116.

18.*

Cheshire WP: Botulinum toxin in the treatment of myofascial pain syndrome. Pain 1994, 59:65-69.

First study to show that botulinum toxin can inactivate myofascial trigger points, thus opening this approach as a treatment possibility and illuminating the nature of the trigger point, which is affected by botulinum toxin.

  View the PubMed notation for this reference.

19.*

McNulty W, et al.: Needle electromyographic evaluation of trigger point response to a psychological stressor. Psychophysiology 1994, 31:313-316.

Demonstrates the responsiveness of the trigger point to psychological stressors, a response that is not seen in normal muscles away from the trigger point.

  View the PubMed notation for this reference.

20. Zautra AJ, et al.: The evaluation of myofascial face pain and its relationship to psychological distress among women. Health Psychol 1995, 14:223-231.11.

  View the PubMed notation for this reference.

Overlooking Myofascial Trigger Points: The Key To YOUR Pain?

from Devin J. Starlanyl

Dec 9 2004

One of the leading experts in the field of fibromyalgia and chronic myofascial pain is Devin Starlanyl. Devin has a diverse background, with experience in emergency room medicine, hospice work, public health, pharmaceutical manufacturing and medical research. Devin has extensively studied fibromyalgia and chronic myofascial pain and related medical topics, and is author of numerous articles and books on the topic.

After reading my book Living Well With Chronic Fatigue Syndrome and Fibromyalgia," she wrote to me express her concerns that the medical community is still misinformed regarding the issue of trigger points, and some of the symptoms that are part of co- existing myofasical pain.

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She felt that these misunderstandings in the medical community -- some of which are also reflected in the various thoughts and theories presented by various practitioners and researchers featured in my book -- deserve to be clarified, for the benefit of patients.

In the interest of ensuring that people with fibromyalgia and chronic myofascial pain get the best possible information, I invited Devin to share her expert perspective on these issues. In this article, she explores and clarifies some key issues she feels are especially important for patients and practitioners, and I welcome her expertise. -- Mary Shomon

* * * * * * * * * * * * * * * * * * * * * * * * * * * * * *

There is general confusion and lack of information concerning chronic myofascial pain (CMP). Many of the symptoms mistaken for fibromyalgia syndrome (FMS) may actually be due to myofascial trigger points (TrPs) instead. TrPs are easily treated if they caught early. Understanding the differences between FMS and CMP and how they can interact may be necessary before the most effective therapies for your symptom control can be chosen. There is no such thing as a fibromyalgia trigger point. You may have read about them in articles and even books written by respected physicians, but they do not exist. FMS tender points and myofascial trigger points (TrPs) are different in fundamental and significant ways. (1, 4, 7, 11, 14 p 18) Failure to differentiate myofascial pain from TrPs may lead to unnecessary tests and procedures that may cause harm as well as unnecessary expense. (9)

Fibromyalgia is not progressive. (4) If FMS is getting worse, there is at least one perpetuating factor that is out of control. This factor is often co-existing myofascial pain. Medical case reports indicate that even if a patient has been diagnosed only with FMS, identification and treatment of coexisting myofascial TrPs and adequate FMS support can provide considerable symptom relief (3) and restore function. Yet many people have never heard of myofascia or of TrPs.

One type of myofascia, the fascia (a type of connecting tissue) you can see is the thin, translucent material that covers chicken breasts at the grocery. You have myofascia too. Imagine "...a gauze-like network that shapes the entire body. Make that network three-dimensional, covering all of the interior, and then fill the gauze with structures including blood vessels, nerves, and lymph." (15) That's one form of fascia. Your muscles are infiltrated with fascia down to the cellular level. Myofascia tightens in response to stressors like trauma or infection. It can entrap blood and lymph vessels or nerves, causing diagnostic confusion. Fascia surrounds your heart and holds other organs in place.

Myofascial TrPs are extremely sore points that can occur in taut ropy bands throughout the body. They may feel like painful lumps or nodules, and they restrict range of motion. They are not part of FMS. Because it is found so many places in the body, tight myofascia can cause a vast array of symptoms. Single myofascial TrPs can occur in anyone. If there are one or more TrP perpetuating factors out of control, TrPs may seem to spread. TrP perpetuating factors include anything that will perpetuate stress on the muscle, including trauma, body asymmetry, or co-existing conditions.

When you have a TrP in a muscle, it causes pain at the end of range of motion when you stretch that muscle, and it weakens the muscle even before it causes pain. Your ankle, knee or hip may buckle, or your grip may fail, depending on which muscle is involved (These symptoms are not part of FMS.) You then avoid stretching this muscle because it hurts. Muscles are designed to work best with motion. Since you don't stretch the muscle, it becomes less healthy and your range of motion lessend. Circulation in your capillaries, your microcirculation, becomes impaired around the TrP. Nutrients and oxygen can't be delivered easily, nor wastes removed. Your lymph system depends on muscle movement to move lymph, so that system begins to stagnate as well. Other muscles do the work of the TrP-weakened muscle.

Overlooking Myofascial Trigger Points: The Key To YOUR Pain?

from Devin J. Starlanyl

Dec 9 2004

These overworked muscles develop secondary TrPs. Satellite TrPs develop in the areas of pain referred from the primary TrP. These additional TrPs cause the false impression of a progressive disease process, unless the TrPs are recognized. Nearly everyone who sees the cover of my last book (15) recognizes some TrP referred pain patterns as their own. They don't always recognize that the patterns are not FMS.

Secondary and satellite TrPs can spread until overlapping pain patterns cover three or all four quadrants of the body. (13) At that point, although they are still regional in nature, the TrPs may seem be misdiagnosed as FMS. In a study of 96 patients, seventy-two per cent had both FMS and CMP. (5) This study was done by a doctor who understood the difference between FMS and TrPs. Thirty-five percent of the myofascial pain patients in this study had generalized pain in three or four quadrants, but they had chronic myofascial pain and not FMS.

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Among the FMS patients in this study, twenty-eight per cent had FMS with no TrPs. Some clinicians mistakenly think that all FMS patients also have TrPs and

that these conditions are the same. This is not a difference of opinion. This is an error that can have significant impact on the quality of patient care.

For example, you can't strengthen a muscle that has a TrP. People with TrPs who are sent to work hardening and weight training get worse because TrPs cause muscle fibers to be shortened even when they are at rest. Muscles with TrPs are contractured (physiologically shortened.) This means that you cannot voluntarily relax these muscles fully unless something occurs to change the physiology. That means TrP specific treatment. The area around the TrP is in severe energy crisis and is releasing sensitizing substances that irritate, aggravate and modify surrounding sensory and autonomic nerves. (14) "Strengthening" exercise causes them to shorten and tighten even more Inappropriate exercise is one of the most avoidable of TrP perpetuating factors. (14) It can be harmful to a patient if a doctor, physical therapist, occupational therapist or other care provider does not recognize a TrP for what it is, and know how to treat it.

A muscle that harbors a TrP cannot be strengthened because it is physiologically inhibited. You must be out of pain with normal range of motion for two weeks before strengthening exercise is initiated, and then it must be gentle and introduced very gradually. (14) Stretch slowly to full range of motion once only for each muscle. This single stretch must be repeated many times at intervals during the day. The stretch should be within the limits of pain and should not produce a lasting ache. When such an exercise produces only mild soreness which disappears on the first day, you can repeat the exercise the next day. When the TrPs cause only mild soreness that disappears quickly, you can add more muscle lengthening exercises gradually. (14)

When you can do 10 lengthening contractions easily, this daily exercise can be replaced with one muscle shortening contraction per muscle. (Holding a muscle in maximal contraction for 5 to 10 seconds daily is sufficient to maintain the strength of the muscle.) TrPs must be gone (not just latent) for two weeks before strengthening exercises are attempted. Then you can add one additional repetition each day if the exercise soreness disappears that day. Exercise must be prescribed very carefully and monitored closely to see that it is done properly.

Enough time must be allowed between exercise and/or bodywork sessions. TrP-involved muscle fibers are under substantially increased tension when at rest.(14) You don't want to increase that tension. This means stair stepping, rowing machines, stretch band exercises, and Nautilus-type machine exercises are contraindicated if there are TrPs in the involved muscles. All the TrPs in the muscle function group must be gone first, and the perpetuating factor brought under control. All exercises require coordination with proper breathing techniques. You can't properly perform "abdominal breathing" if your respiratory muscles are inhibited by TrPs. TrPs in the respiratory and accessory muscles must be treated to allow for deep breathing.

Fibromyalgia is not associated with unexplained toothaches; carpal-tunnel like symptoms; localized aching or pain in the coccyx, shin, back, hands, pelvis, neck, fingers or eyes; tight muscles; trouble swallowing; weak or painful grip, numbness or swelling in the hands, pain or itching in the ears, frequent eye correction changes, unexplained toothaches, spatial disorientation, appendicitis-like pain, weak ankles or knees, restricted range of motion, angina-type pain, or dizziness. Specific TrPs can and do cause these symptoms. Information on some of these and other symptoms are given in The Survival Manual. (15, Chapter 8)

Overlooking Myofascial Trigger Points: The Key To YOUR Pain?

from Devin J. Starlanyl

Dec 9 2004

Fibromyalgia is associated with central sensitization, including: generaldiffuse (not localized) pain, hyperalgesia (pain amplification) and allodynia (pain from non-pain stimuli such as noise and light). (17) To control FMS pain amplification, you need to control the pain generators. (1) FMS amplifies pain. Myofascial TrPs generate pain and other symptoms. The differences are important, because these conditions are treated differently, even when they co-exist in the same patient and have some perpetuating factors in common. Some factors that can perpetuate a myofascial TrP (such as short upper arms or Morton's foot) will not, of themselves, perpetuate nor initiate FMS.

TrPs in the sternocleidomastoid muscle (in the neck) alone can cause: clumsiness; blurred or double vision, tension headaches; runny nose; maxillary sinus congestion; spatial disorientation; unintentional veering, or cause patterns of light and dark (such as shadows along the road or escalator treads) or head motion to result in dizziness (among many other symptoms), and if you know this, you may save worry and unnecessary testing and be able to do something to relieve the symptoms.

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If bottom of your feet feel like you're walking on broken glass as you take your first steps in the morning and you know this may be due to TrPs, you can do something. Roll up a big towel and put it under your blanket at the bottom of the bed so that your feet can rest on it. That avoids the allowing the plantar fascia to remain shortened overnight. (Keeping muscles in a shortened position is a common TrP perpetuating factor.) Chronic pelvic pain that feels like it comes from organ disease can come from TrPs. (2) If you believe that these symptoms come from FMS, there is nothing to do for them but attempt to control the pain. Understanding TrPs and their perpetuating factors can give you some measure of control over your symptoms and your life.

We know what TrPs cause specific symptoms, what their perpetuating factors are, and what to do about them. These topics discussed in detail in medical texts such as Travell and Simons' Myofascial Pain and Dysfunction: The Trigger Point Manuals. For example, the prickling tingling painful sensation along the jaw line that can move upward across the cheeks is caused by specific TrPs in a muscle called the platysma (15 p 82) and not by FMS. If the TrPs are treated and the perpetuating factors brought under control, the symptom will go away. If the perpetuating factors cannot all be identified or controlled, the TrP can still be treated and minimized.

When active (pain causing) TrPs become latent, they no longer cause pain, but they still cause restricted movement and muscle weakness. The latent TrPs still electrically inhibit the muscle. Some people don't exercise because if they don't move they don't hurt as much. This is false reasoning. Their TrPs have merely become latent. Even a minor stressor can become a life-altering event if you have latent TrPs. Myofascial TrPs can cause: bloating, incontinence, impotence, rectal pain, sore throat, tender neck and armpit "swollen glands" feeling, muscle pain, headaches, pain in joints without swelling, dizziness, autonomic symptoms, weak muscles, ear pain, restricted range of motion, knee pain, shoulder pain, wrist pain, hand pain neck pain, back pain, abdominal pain, pelvic pain, pain in the outer or inner vaginal area, stiffness in the morning (and after any immobility), shortness of breath, chest pains, tightness in the chest, frequent nighttime urination, inability to empty the bladder fully, stiff neck, nasal congestion, trouble swallowing, hoarseness of voice, tearing eyes, gastroesophageal reflux, vomiting, heart arrythmias, ringing ears, painful or itching ears, growing pains, painful menstrual periods, irritable bladder or bowel, belching, diarrhea, rapid racing heartbeat, painful intercourse, and many, many more symptoms.

If you have back pain that worsens with sitting but it improves with appropriate therapy, check for iliopsoas and quadratus lumborum TrPs. If the pain is in the hip and radiates down the back of the leg, check the piriformis muscle in the buttock for TrPs. If pain radiates down the side of the leg, check the side of the hip for the gluteus minimus TrPs. Myofascial TrPs can refer symptoms a good distance away from their location. TrPs in the scalene muscles of the neck can entrap lymph and blood vessels, causing swelling in the hands in the morning.

They can cause tightness and pain in the chest and down the back of the arm in a specific pattern, including the top of the thumb and index finger. You and your care providers need to become familiar with the common TrP referral pain patterns. They can be very specific and are generally similar from person to person, so if you can identify the pain pattern you can find the TrP.

Overlooking Myofascial Trigger Points: The Key To YOUR Pain?

from Devin J. Starlanyl

Dec 9 2004

Don't work on the area of pain. Your jaw may be sore, but the source of the pain may be a TrP in your calf. Your doctor and dentist need to know this, and so do you for self-preservation. Innocent teeth have been pulled because dentists were unaware that TrPs can cause tooth pain and sensitivity to cold, heat and pressure. Teeth have been ground to adjust the bite, only to have a TrP-laden muscle contracture change, causing the bite to change as well.

Treating TrPs without treating the perpetuating factors means that the same TrPs will keep coming back. Treating the perpetuating factors is the key to both FMS and CMP, but it won't make existing TrPs go away. Latent TrPs are like land mines waiting to explode. If you fall, or catch a cold or are hit with any other stressor, they may all activate at once.

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This may be mistaken for or even cause an FMS "flare."

Multiple latent TrP activation often happens in the elderly. Much of the aches and pains and muscle weakness of old age may be due to unsuspected TrPs, and may respond to proper treatment. (14) People who have been incontinent or have had sexual dysfunction for years due myofascial TrPs may be relieved-and astonished-at their response to adequate TrP treatment. Then they often become angry as they realize that they have suffered needlessly because their doctors did not understand TrPs. TrPs cause muscle weakness and other dysfunction before they cause pain, so they may be unsuspected even by some doctors who

have TrP medical texts. Some care providers just look at TrP diagrams. That is insufficient preparation to treat myofascial TrPs. Myofascial medicine requires study, and it is well worth the time spent on it. Many patients endure needless pain and medical tests due to lack of recognition and treatment of myofascial TrPs. (9) Some researchers lump FMS and CFIDS together and ignore myofascial pain. We won't have clear research results until we distinguish these conditions. It is frustrating to see medical research that claims to be on FMS/CFS patients (written by researchers who lump these conditions together) and yet it describes nodules, ropy bands and restricted range of motion of myofascial pain. The authors of the article did not know better, and neither did their peer reviewers! This is a sad state.

Many dentists, psychologists and others use the terms "temporomandibular dysfunction" and "myofascial pain syndrome (MPS)" to describe the same jaw dysfunction. Their research conclusions may be honestly but erroneously used by other researchers to apply to MPS due to TrPs. Further research may build on those faulty conclusions. An article attempting to prevent this clarified the issue (13), yet this potentially misleading research still comes out in quantity.

An enormous amount of research has also been done on FMS patients with no regard for co-existing TrPs. Much of this research is suspect because some of the symptoms described could be due to myofascial TrPs instead. I believe it would reduce FMS clinical study variables considerably if patients in FMS studies were routinely screened for co-existing myofascial TrPs. Researchers may find that some symptoms now associated with FMS are more commonly due to myofascial TrPs, and some may not be associated with FMS at all. This may also be true for CFIDS. Many experts believe that one way deal effectively with these conditions is to separate them into meaningful subgroups that might give clues to effective treatment.

An important step to symptom control is to deal with the causes of the symptoms. When you have chronic unrestorative sleep, it is logical that you also have chronic fatigue. This is not the same as CFIDS. If pain from myofascial TrPs is disrupting sleep, or you waken often with urinary urgency or diarrhea caused by TrPs, you need to take care of the TrPs (and other factors disrupting your sleep.) If you take care of the TrPs and their perpetuating factors, it will be much easier to deal with the remaining symptoms. It's not as easy for doctors as throwing a pill at the problem (and the patient), but it is good medical practice. The medical dictum "do no harm" is often lost in the field of chronic pain because care providers are unaware of the pervasiveness of myofascial TrPs.

Some symptoms once linked with FMS may not be. Carbohydrate cravings, weight fluctuations and some swelling may be due to insulin resistance. Research indicates that insulin resistance may be a common perpetuating factor of FMS. (18) It can perpetuate TrPs. Sleep dysfunction, prevalent in FMS, may adversely affect glucose tolerance (10), and may unbalance the hypothalamic-

pituitary-adrenal (HPA) axis. (8) Treating the insulin resistance through diet, especially if it is the main FMS perpetuating factor, may ease the symptom load considerably, and may make co-existing TrPs more treatable.

Overlooking Myofascial Trigger Points: The Key To YOUR Pain?

from Devin J. Starlanyl

Dec 9 2004

The concept of perpetuating factors is as valid for FMS as it is for myofascial TrPs, in my opinion. Many identified myofascial TrP perpetuating factors may also be perpetuating factors, aggravating factors or even initiating factors of FMS. This has caused many clinicians to erroneously believe that FMS and myofascial pain are the same. This confusion must be eliminated. Common perpetuating factors need to be brought under control, but that is not enough.

For example, an intestinal bug can set up TrPs that will perpetuate symptoms of diarrhea and vomiting that will persist even after the virus is gone. The TrPs have to bet identified and treated first (and not with antibiotics.) Doctors must learn to identify TrPs. "Most of the six million Americans with fibromyalgia have at least one associated syndrome which mandates specialized attention in addition to traditional therapeutic approaches."(12).

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In the vast majority of chronic pain patients, including FMS and arthritis patients, myofascial pain is a co-existing condition.

It is important to learn individual TrPs to learn their specific referral patterns, but it is also important to understand that complex overlapping pain patterns may exist in chronic pain patients. Body-wide TrPs may cause widespread pain, with TrPs in many areas and layers of many muscles. (The TrPs in the text diagrams are common, but they can occur anywhere.) As the perpetuating factors are addressed, single muscle pain patterns will eventually become apparent and then those TrPs can be treated.

Spray and stretch and TrP injections are part of therapy for myofascial TrPs, not for FMS. One study showed that patients with both FMS and myofascial TrPs find TrP injections more painful, they have less effect (although they are still worthwhile to treat the TrPs), and the post-injection soreness would be worse, than if the patient only had TrPs.(6) This is often the case with bodywork as well. Physical therapy, other bodywork, exercise and other therapies must proceed carefully and gradually if FMS and TrPs coexist. The amount of pain involved should not be underestimated. Any treatment will be more complicated and less successful than if the patient had only one of the conditions, and some bodywork may require extra medication to prevent added central sensitization. Each patient can vary in many ways. In the chronic myofascial pain component there is a wide variety of TrP combinations plus there may be different nerves, blood and lymph vessels entrapped. There may be different perpetuating factors. In the FMS component, there may be different biochemicals affected in different ways, and they may be affecting other biochemicals in different ways. Each case is different. Care providers and patients must understand both of these conditions to ensure adequate medical care. Insurance companies must understand that they will save money in the long run if the TrPs are treated promptly and adequately by trained providers, and the perpetuating factors controlled. Once the TrPs are appropriately treated and their perpetuating factors brought under control, you may find that remaining FMS symptoms are more easily managed. Some people may even find that they do not even have FMS after all.

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REFERENCES

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