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The following is some in depth information for patients and therapists who want to know more. Feel free to search around, read, learn and get better!
Back Pain, headache, or twitching muscles. Most probably you have activate trigger points causing the problem.
Have you ever had a headache, clonus or twitching muscles, after a massage? The massage might have felt great, but most probably your therapist activated trigger points on your body.
The Journal of the American Medical Association reported that frequent migraine sufferers felt better after acupuncture (which sometimes may relax trigger points.) Trigger points are not the same as acupuncture points, but research is being begun by mainstream organizations on the anatomic morphology and histology of acupuncture and trigger points.
More Trigger Point History:
In the 1930's, Dr. Travell noticed that most patients at her hospital had life-threatening pulmonary disease, but some of them complained more about devastating pain in their shoulders and arms than about their major illness. "When I examined them by systematic palpation of the scapula and chest muscles, I easily uncovered the presence of trigger areas.”[1] It was during this time that Janet read that these tender spots that had been so unresponsive to treatment could be eliminated by procaine injection if the clinician hit precisely the right spot, in an article by J.H. Kellgren in the British Medical Journal titled, “A Preliminary Account of Referred Pains Arising from Muscle,” [11] which strongly influenced her thinking. Unknown to Janet Travell, two other clinicians, Michael Gutstein[12] in Germany, and Michael Kelly[13] in Australia, independently published a series of papers about myofascial pain. They all emphasized “four cardinal features [of the condition]: a palpable nodular or band-like hardness in the muscle, a highly localized spot of extreme tenderness in the band, reproduction of the patient's distant pain complaint by digital pressure on that spot [referred pain], and relief of the pain by massage or injection of the tender spot."[1] All three had identified myofascial TrPs [trigger points], however, each had used different diagnostic terms and was apparently unaware of the others' work. In 1940, she had the opportunity to do a study of this phenomenon and its treatment by injecting the MTrPs with 1% procaine, and in 1942, Janet Travell, Seymour H. Rinzler, and Myron Herman published “Pain and Disability of the Shoulder and Arm."[16], which was published in the Journal of the American Medical Association in 1942, and described complete relief in 62% of 58 (13 cardiac and 45 noncardiac) patients and moderate-to-considerable improvement in 37%, following procaine injection. This approach of procaine injection of MTrPs in patients suffering from the pain of myocardial infarction convinced her and her colleagues that the treatment could stop both noncardiac pain of muscle origin and true cardiac pain of coronary insufficiency.[15] These findings were first reported in preliminary form in “Relief of Cardiac Pain by Local Block of Somatic Trigger Areas,”[17] and then definitively in 1948 as “Therapy Directed at the Somatic Component of Cardiac Pain.”[18] Half a century later, clinical recognition of this common source of cardiac-type pain had largely disappeared, and is only now, being again researched. Continuing research with cardiac pain, where Ethyl chloride spray was applied to the region that was rendered painful by ergonovine induced angina, stopped the pain in that area almost at once— faster than nitroglycerin did. Monitoring the effect with electrocardiography (ECG), they established that some of the pain that they were relieving with ethyl chloride did originate in the heart. Spraying the pain reference zones before the use of ergonovine prevented the pain from appearing or delayed its onset for several minutes, but did not affect the ECG changes of cardiac ischemia. They published these results in 1954, “Blocking Effect of Ethyl Chloride Spray on Cardiac Pain Induced by Ergonovine.”[19] However the pharmacologic effect of ergonovine on coronary arteries was thought to be constriction, and the indirect experimental evidence indicated that it caused coronary artery dilation, not constriction, so it occurred to Drs. Travell and Rinzler that possibly ergonovine increased circulation only in normal hearts and decreased it in atherosclerotic hearts. This was a heretical concept because all drug testing of this type had been done on normal animals. After much effort, using rabbits that had become atherosclerotic for another study, Janet and her colleagues confirmed the suspected difference in responses[20] and left no doubt that the spray could relieve pain of cardiac origin, as well as of MTrP origin, and also saw evidence that the spray could suppress cardiac arrhythmias. Janet Travell continued to relieve pain for patients, including John F. Kennedy, who later became president and surprisingly made her his physician. After retiring from the Johnson administration, she continued to lecture and teach at universities and hospitals, and one of her lines was, “the magic never fails.” In the mid-1990s, others built on the foundation laid by Janet. Exploring the mechanism by which pain is referred from an MTrP to the reference zone, a study in the Heidelberg research laboratory of the neurophysiologist, Siegfried Mense, demonstrated 1 such referral mechanism.[21] The awakening of sleeping dorsal horn nociceptive connections by pain from the same muscle or another muscle activates new receptive fields for pain. This observation fits the now-extensive literature on the reconfiguration of spinal cord activity in response to sustained pain input and is described in a book that summarizes these mechanisms and their clinical application to muscle.[22] In addressing ourselves to the key issue of causation, my colleague (John Hong, MD), my physical therapist wife (Lois), and I conducted electrodiagnostic studies on both rabbits[23] and patients.[24] These showed that electromyographic endplate noise is significantly related to MTrPs. Others reached this same conclusion.[25] The evidence that any endplate noise corresponds to greatly increased numbers of miniature endplate potentials[26] indicates that a core feature of MTrPs appears to be the release of greatly increased numbers of acetylcholine vesicles of the motor nerve terminal. A detailed description of the current understanding of MTrP etiology can be found in either of 2 recent books.[1],[22] To identify and treat the MTrPs of pectoral muscles that so commonly contribute to, or cause, pain that is assumed erroneously to be of cardiac origin, or pain that becomes enigmatic when all cardiac tests are normal, one must learn how to find which muscle or muscles need to be palpated, learn what to palpate for, and either develop the skill to treat the pain or find a therapist with that skill. Any muscle with a painfully restricted range of motion and a tender spot that reproduces the patient's pain when compressed likely has a myofascial trigger point.[15] When it is imagined that this phenomenon may hold true for other organ syndromes, the limits of Trigger Point Therapy may be far reaching. In 1963 David G. Simons, MD, a staff flight surgeon at the United States Air Force's School of Aerospace Medicine, attended a 2-day lecture demonstration on myofascial trigger points (MTrPs) by Janet G. Travell. He knew that years earlier his chief at the Space Medicine Laboratory in Alamogordo, New Mexico, had identified a trigger point as the cause of an enigmatic shoulder pain in a staff member of the laboratory. Janet's lectures were a revelation to Dr. Simons and he stated, "So this was the cause of most of my muscular aches and pains and those of my friends, family, and colleagues!" The cause of this myogenic pain was clearly overlooked in medical training and practice, but diagnosable and treatable by an expert. On later occasions, Dr. Simons saw the conversion of atrial fibrillation to normal rhythm when vapocoolant spray was applied over the arrhythmia MTrP on the lower-right anterior chest wall; the same effect could be achieved by trigger point pressure release applied to that MTrP, as described in The Trigger Point Manual,[1] and it appeared likely that many such unexpected influences, to and from MTrPs, depend on modulation of the autonomic nervous system, in addition to modulation of the sensory nervous system (referred pain). The Trigger Point Manual,[1] describes how the pain patterns of the pectoralis major and pectoralis minor muscles mimic the pain referral patterns of cardiac ischemia. The early studies by Dr. Travell and colleagues provided convincing experimental evidence that the referred pain of cardiac ischemia and the referred pain of active myofascial MTrPs can be eliminated, or decreased remarkably, by application of vapocoolant spray to the skin over the painful area. Clinical studies showed that the 2 sources of pain are easily mistaken for one another and that persistence of pain for some time after the ischemia of a myocardial infarction should have resolved is likely to be caused by MTrPs. Symptoms of angina in the absence of demonstrable cardiac disease should be considered as likely due to MTrPs. In the light of recent research, the effectiveness of the application of vapocoolant spray to the skin in the referred pain zone indicates that the spray's afferent input to the dorsal horn blocks transmission of nociceptive stimuli or inhibits awakened dorsal horn nociceptor pathways responsible for the referred pain. Janet's discussions and mentoring inspired Dr. Simons to try to understand what causes trigger points and to become certified as a physiatrist and clinician who treats patients with myofascial trigger points. In 1970, he began examining all his patients for MTrPs as a VA-paid physician in the physical medicine and rehabilitation residency program at the University of Washington in Seattle, but realized only modest success at that time. Then in 1974 Dr. Simons was assigned a ward of the rehabilitation medical service in the VA Hospital at Long Beach, California. The hospital's education committee supported a 1-month instructional visit by Janet. She spent every Friday afternoon giving a lecture-demonstration to the hospital staff, and the rest of the week demonstrating to the diagnosis and treatment of MTrPs on his 23 rehabilitation ward patients. Then she would describe the subjects' problems, her analysis of what caused the MTrPs, how she then demonstrated what was wrong, and the results of her treatment. As soon as she returned to Washington, doctors at the VA Hospital realized that they needed written reminders of what she had taught. From this grew the 1st volume of the Trigger Point Manual,[1] which had its basis partly in Dr. Simons' weekly Friday evening telephone calls to Washington. During these calls, Janet regularly included exciting descriptions of what she had learned that week from patients. During Janet's periodic visits to the VA myofascial pain clinic in Long Beach, California, Dr. Simons tape-recorded her train of thought and continued to write Volume 1 of The Trigger Point Manual. Janet looked under every physical and medical stone imaginable until she found innovative and likely solutions that patient had failed to respond to treatment as expected. The answers ranged from relatively short upper arms or leg-length discrepancies to inadequate vitamin intake. Her writings in the Travell Collection (“Six Ways to Make Housework Lighter” is a good example) are full of advice on how not to develop MTrPs; this advice arose from her observations of what her patients had done to activate their MTrPs. During Janet's visits to California late in the 1970s, Dr. Simons began to formulate a hypothesis on what causes formation of MTrPs, and in 1981, they published their hypothesis which explained how the taut band muscle fibers contracted in the absence of propagated electrical activity, and why stretching the muscle could produce rapid resolution of the tenderness of the nodule and the tautness of the band.[27] The hypothesis focused on excessive calcium release from the sarcoplasmic reticulum as a cause of local muscle fiber contracture. The contracture, in turn, causes local ischemia that limits energy replacement and consumes more adenosine triphosphate (ATP), depleting the energy source. These events leave insufficient ATP for adequate return of calcium from the contractile elements to the sarcoplasmic reticulum by the calcium pump. Stretching the muscle reduces the overlap between actin and myosin, thereby reducing energy demand and breaking the cycle. Dr. Raymond L. Nimmo, D.C. (1904-86), who was the definitive chiropractic pioneer of soft tissue and trigger point therapy, coined the "noxious generative point" in the late 1940's and evolved neurophysiological explanations in the 1950's for the trigger point phenomenon, formulations that are still regarded as highly sophisticated half a century later.[9] Nimmo developed his Receptor-Tonus Method after he found that malposition of bones which sends a barrage of noxious impulses into an area producing vasoconstriction, ischemia, and trigger points in muscles. Since tonus is controlled by the sympathetic nervous system, and is not under conscious control, we can not correct our own distortions. Nimmo discovered that pressure applied in proper degree, at proper intervals, will release both trigger points and hypermyotonia. In Nimmo's view, the initiating insult to a muscle - such as overuse or frank injury, a cold draft, or even emotional problems - causes an abnormal increase in afferent input to the spinal cord. In turn, this may cause an abnormal stream of efferent impulses back to the muscle, resulting in hypermyotonia (hypertonus), a vicious cycle sometimes called the pain-spasm-pain cycle. These abnormal reflex arcs have tremendous staying power, and often require external intervention to break the loop. In addition to the reflex hypertonus of the muscle related to the trigger points, there may be production of satellite or secondary trigger points, and visceral dysfunction in the organs innervated by the internuncial neuronal pool stimulated by the trigger point.[14] |





