Muscles Learn
by Janet Travell, M.D.
Muscles are different from other tissues. When injured, bones knit; if the skin is cut or a joint capsule is torn, it heals; but when a muscle is injured, something else happens -- it learns. It learns to protect that part and it develops habits of guarding and splinting which limit motion, restrict circulation, and cause pain, stiffness and muscular dysfunction, especially weakness. The muscles have long memories and these symptoms may persist for years.
I shall discuss today the ubiquitous myofascial pain syndromes that depend on trigger points and their feedback loops to the central nervous system. These trigger points are located in the myofascial structures: skeletal muscle and its fascia. Trigger points also occur in skin, tendons, joint capsules, and periosteum.<br>
One of the curious things about myofascial trigger points and their pain syndromes is the fact that the symptoms often long outlast the precipitating event of trauma, either gross or microtrauma, due to persevering reflex patterns in the central nervous system.
In addition, the trigger points are perpetuated by continuing mechanical stresses (not the precipitating strain) on the myofascial structures, which create a repetitive or sustained overload of the affected muscles. Such perpetuating stresses include, for example, a short leg and small hemipelvis, short upper arms, poor posture, inefficient body mechanics, immobility or immobilization, and chilling the body - also unphysiological seating design. Chairs can be a serious health hazard (chair pollution).
Systemic perpetuating causes may also be multiple. These include infectious (especially oral herpes simplex), metabolic, nutritional, allergic, viscerosomatic and psychogenic factors. Marginal vitamin deficiencies and hypometabolism (borderline subclinical hypothyroidism) are especially frequent causes.
Problems:
1) One difficulty is in pinpointing the problem, in making the diagnosis.
2) Another difficulty is in managing the myofascial pain syndrome, for this often requires the teamwork of various health professionals. We are partners in the treatment of pain and maintenance of health. Each profession needs the skills and support of the other.
My Special Interest:
My special interest has dealt with the role of the skeletal muscles and their fascial components in the pathogenesis of these stubborn painful states, the myofascial pain syndromes. I am not talking today about the diseases of collagen nor of muscle, such as rheumatoid arthritis, polymyalgia rheumatica, or polymyositis, nor about organic neurologic diseases, the dystonias, etc., nor even intervertebral discogenic pathology.
Trauma:
What I will discuss is chronic, disabling myofascial pain due to trauma. Trauma has been called 'the neglected disease of modern society' -- true. In the United States and around the world, millions of people have disabling injuries each year.
Two phases:
These myofascial pain syndromes are:
1) initiated by trauma, and
2) if they last for a period of time, they are maintained by continuing trauma.
Two Kinds of Trauma:
Trauma may be of two kinds:
1) gross trauma, due to obvious sudden external force, with tearing of some fascial structures and overstretching, followed by protective reflex contraction of muscles (the guarding reflex); and
2) obscure microtrauma due to overuse of muscles, especially during fatigue, chilling, alcohol ingestion, infectious illness or hypothyroidism. Such microtrauma is an important perpetuating cause of chronic myofascial pain, if not the most important cause of these protracted syndromes.
Skeletal Muscles:
The largest organ in the body is the skeletal musculature, and the myofascial pain syndrome may well be the commonest affliction of the human race.
Myofascial pain and dysfunction can lead to serious disability, and yet they are also the most responsive to specific treatments when these clinical disorders are recognized early and treated in the acute pathophysiological phase.
The myofascial syndromes become increasingly complex with chronicity, and the development of non-specific dystrophic pathological changes. The Tincture of Time does not bring about recovery.
Muscles Learn:
Muscles are different from other tissues. When injured, bones knit; if the skin is cut or a joint capsule is torn, it heals; but when a muscle is injured, something else happens -- it learns. It learns to protect that part, and it develops habits of guarding and splinting which limit motion, restrict circulation, and cause pain, stiffness and muscular dysfunction, especially weakness. The muscles have long memories, and these symptoms may persist for years. Then, they are often said to be psychosomatic, or psychogenic, in origin.
Nature of a Trigger Point:
What is a trigger point? It is not something subjective, not something of which the patient complains. It is an objective physical sign in that it is disclosed by the physical examination of the patient. Then, the trigger point is identified as a localized area, a spot of deep tenderness in a firm band of muscle that can be readily felt. Usually, the palpable band parallels the muscle fibers; occasionally it feels like a button or a nodule. At the spot of maximum tenderness (the trigger point), if the band is snapped briskly (transversely), and is thus mechanically stimulated, it contracts; this we have called a 'local twitch response.' The examiner can feel and see the line of contraction of the band, and can judge which muscle harbors it. An observer can see it, and if that part of the body is free to move, the contraction of the band often jerks the part, the head, or finger, or arm, for example. The patient says 'Ouch' and also jumps, which has been designated a 'jump sign.' So we speak of the 'local twitch response of the muscle,' and the 'jump sign of the patient.'
Active Trigger Point Re: Pain:
When firm deep pressure is sustained directly on an active trigger point in the palpable band, the patient reports that pain is felt elsewhere; the pain is projected to a distance as referred pain, in a predictable pattern for that site in the muscle. The referred pain pattern is an important clue. Referred pain does not follow the simple segmental distribution.<br>
On palpation of a trigger point in the infraspinatus muscle on the back of the scapula, the patient with shoulder pain is surprised and says: 'Oh, that's very sore. That's my pain in the front of my shoulder and arm. Where have you got your finger?' The reproduction of the pain is reassuring to the patient, and to the doctor, in that, a demonstrable source of his or her complaint has been found.
Latent Trigger Point Re: Pain:
A source of confusion is that trigger points have varying thresholds of hyperirritability: they may be clinically active, or clinically silent, (latent), with respect to pain. When the patient comes to the doctor with a clinical complaint of pain, you are dealing with active trigger points, and pressure on a trigger point should readily evoke the pattern of referred pain, specifically for that muscle. After some time, the focal hyperirritability often subsides somewhat; the trigger point becomes latent, and the patient no longer complains of spontaneous pain. There is not the intensity of pain that brings the person to a physician. However, he or she becomes used to a low level of pain, and the patient may deny having pain, when, in fact, it is there.<br>
From such clinically latent trigger points, the typical pattern of referred pain usually is not evoked by sustained pressure. However, a needle inserted directly into a latent trigger point may elicit the predictable pattern of referred pain.
Other Effects:
Both active and latent trigger points have other profound effects besides pain.
1) They have referred tenderness in pain reference zones even during pain-free periods.
2) They inhibit muscle lengthening and limit motion at the joint, or joints, which the muscle traverses. The tense muscle is shortened; it will not stretch to its full normal length. So, whether the trigger point is active or latent with respect to pain, on examination the associated restriction of movement can usually be found.<br>
3) There is also demonstrable weakness (without atrophy) of the muscle that contains the trigger point, whether it be active or latent. The barrage of different impulses from the trigger point inhibits maximal contraction of that muscle; it is not strong. When the patient with latent trigger points in the hand extensor muscles tries to pour milk out of a carton, he may unexpectedly drop the carton; his grip is weak. This weakness may be present for years, due to latent trigger points.<br>
4) There are also a variety of referred autonomic effects, both sensory and motor.
Why Overlooked?
Recognition of this extremely common type of myofascial disorder is made difficult because the myofascial structures are soft tissues and are not visualized on X-ray examination, and because no specific test on blood or urine is available to pinpoint the problem. There is no neurological deficit unless entrapment of a peripheral nerve by a taut muscle occurs.
The Diagnosis:
The diagnosis is established by objective signs elicited on palpation of the affected muscles and by observation of specifically associated restriction of motion. The pattern or distribution of referred pain elicited by palpation of an active trigger point is described by the patient, not observed, and is, therefore, a subjective phenomenon. However, the pattern of referred pain for a given site is constant from person to person and therefore predictable. When the patient's description of the induced referred pain matches the known pattern for that muscle, the accuracy of the patient's reporting is verified.
A major difficulty in the treatment of myofascial pain is that after it has been initiated by one traumatic event, the multiple factors which usually act together to perpetuate the pain syndrome must all be dealt with, and this requires much detective work and time on the part of the physician.
References:
Travell, Janet G., M.D. and Simons, David G., M.D., Myofascial Pain and Dysfunction. The Trigger Point Manual, Volume One and Volume Two, Williams & Wilkins, Baltimore, 1983 & 1992.