Graduate - Sydney College of Osteopathy - Sydney College of Chiropractic
International College of Applied Kinesiology
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Myofascial Trigger Point Dry Needling Neuromuscular Procedures, Biopuncture
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Article by Dr Peter Richard Pedersen
(see the trigger point chart)
Although myofascial pain syndrome is a well recognized clinical condition, there remains a lot that is not known regarding the pathophysiology, mechanisms of pain referral, and treatment of choice for myofascial trigger points. In addition myofascial trigger points remain a commonly overlooked cause of chronic neuromusculoskeletal pain and dysfunction.
Travell and Simons define a myofascial trigger point (MFTrP) as a tender nodule in a palpable taut band of skeletal muscle. Trigger points are able to generate either local or referred pain, either spontaneously (active) or on digital compression (latent). These trigger points (TrP) may become activated by a variety of factors such as, poor posture, overuse, or muscle imbalance.
Trigger points exhibit a local twitch response (muscle fasciculation) or jump sign (flexion withdrawl response) in response to digital pressure or dry needling.
Physiology of Myofascial Trigger Points
Understanding the biochemistry of active myofascial trigger points and determining the local biochemical effects of needle insertion may help us understand the mechanisms behind the initiation and amplification of myofascial pain and how dry needling works. Each MFTrP contains a sensory component, a motor component, and an autonomic component. Thus MFTrP pain syndrome involves local myofascial tissues, the central nervous system (CNS), and systemic biomechanical factors.
We owe a lot of gratitude to the physician John Kellgren, who during the 1930s made the significant contributions to our knowledge concerning the pathophysiology, diagnosis and treatment of myofascial trigger point pain. Lewis and Kellgren carried out experiments where they injected hypertonic saline into muscles and observed pain being experienced at the injection site and at some distance away, at what they called the zone of pain referral. (Kellgren JH; 1938)
After further investigations into the observed phenomena Kellgren went onto say:
A number of cases of "fibrositis" or "myalgia" have been investigated. The distribution of pain from normal muscles guided me to the muscles from which spontaneous pain may have arisen. Such muscles always presented tender spots on palpation and pressure on these spots reproduced the patient‟s pain.‟
He then went on to confirm that the pain arose as a result of nerve hyperactivity at these tender points by showing that it could be alleviated, by injecting a local anesthetic into the tissues at these tender sites.
Travell’s study of the subject led her to conclude that pain in the disorder that had previously been called rheumatism, fibrositis, myalgia etc arises not only from skeletal muscle itself but also from its fibrous connective tissue. She therefore called the disorder the myofascial trigger point pain syndrome.
She went on to investigate together with David Simons each muscle in the body to determine whether each muscle had the capacity to generate its’ own characteristic pattern of referred myofascial pain. (Travell JG & Simons DG; 1983)
Simons (1996) implicated the motor endplate/neuromuscular junction as the central etiology of MFTrPs. The motor endplate is where an α-motor neuron synapses with its target muscle fibers. According to McPartland, JM and Simons, DG (1996) the α-motor neuron terminates in multiple swellings termed presynaptic boutons. Each bouton contains many acetylcholine (ACh) vesicles, clustered around structures called dense bars. Voltage-sensitive calcium channels (VsCCs,) are also located near dense bars. When voltage running down an α-motor neuron reaches VsCCs in the bouton, the VsCC channels open, leading to an influx of calcium ions (Ca2+) into the bouton from the extracellular space. This influx of Ca2+ causes the ACh vesicles to release their transmitter into the synaptic cleft.
Across the synaptic cleft, the postsynaptic muscle cell membrane is lined with nicotinic ACh receptors (nAChs). Binding of ACh to nACh initiates the sodium potassium pump acrross the cell membrane, allowing sodium ions (Na+) and potassium ions (K+) to move in and out across the muscle cell membrane. Movement of Na+ and K+ depolarizes the postsynaptic cell, forming a miniature endplate potential (MEPP). A sufficient number of MEPPs activate additional VsCCs, which subsequently trigger another Ca2+ channel imbedded in the membrane of an intracellular sarcoplasmic reticulum, which houses intracellular stores of C2+. The result is that the sarcoplasmic reticulum releases additional Ca2+ into the cytoplasm of the muscle cell. This triggers the interaction between actin and myosin, and the sarcomere contracts.
EMG studies of MFTrPs have reported spontaneous electrical activity in MFTrPs, while adjacent muscle tissues are electrically silent. Hubbard and Berkoff (1993) originally attributed the source of spontaneous electrical activity action potentials to sympathetically
activated intrafusal muscle spindles. Hong injected botulinum toxin into MFTrPs, which blocks ACh release at the motor endplate. This treatment significantly decreased spontaneous electrical activity.
Prevalence of myofascial trigger points
Myofascial trigger points (MTrPs) are recognized by many clinicians to be one of the most common causes of pain and dysfunction in the musculoskeletal system. Myofascial trigger points are a common cause of musculoskeletal pain, accounting for more than 74% of musculoskeletal complaints encountered by a neurologist in a community pain medical centre, (Gerwin RD; 1995) and in 85% of 283 consecutive admissions to a comprehensive pain centre. (Fishbain DA, Goldberg M, and Meagher BR 1986)
Myofascial pain can be severe and debilitating, and can cause restrictions in normal biomechanical joint function, impairment of neurological function, as well as impairment of circulation and lymphatic flow (Long, D.M., Bendebba, M., et al)
Clinical features of MTrPs according to Hong and Simons (1998) are: Compression of an MTrP may elicit local pain and/or referred pain that is similar to a patient's usual clinical complaint (pain recognition) or may aggravate the existing pain. Snapping palpation (compression across the muscle fibers rapidly) may elicit a local twitch response (LTR), which is a brisk contraction of the muscle fibers in or around the taut band. Rapid insertion of a needle into the MTrP can also elicit an LTR. Restricted range of stretch, and increased sensitivity to stretch, of muscle fibers in a taut band may cause tightness of the involved muscle. The muscle with an MTrP may be weak because of pain, but usually no remarkable atrophy can be noticed due to the waxing and waning phenomena of the MTrR Patients with MTrPs may have associated localized autonomic phenomena, including vasoconstriction, pilomotor response, ptosis, and hypersecretion. An active MTrP is one with spontaneous pain or pain in response to movement, whereas a latent MTrP is a sensitive spot with pain or discomfort only elicited in response to compression.
These diagrams illustrate some of the more common myofascial trigger point sites (#) in the back and hip girdle and their respective pain patterns.
Trigger points have traditionally been classified as either being active or latent depending on whether they produce spontaneous pain or are only painful on mechanical stimulation. (Travell and Simons; 1999) An additional classification system relating to tenderness of acupuncture points, may be relevant to the clinical state of myofascial trigger points. Trigger points may further be classified into latent, passive and active. If a taut band is found to be non tender to palpation it is classified as latent. If the taut band is tender to palpation but does not spontaneously produce pain it may be classified as passive. If a trigger points is found to be producing pain spontaneously it is classified as active. (Dung H, Clogston CP, et al; 2004)
These diagrams illustrate some of the more common myofascial trigger point sites (#) in the head and neck and their respective pain patterns. (Cummings M and Baldry P; 2007)
Aggravating and Precipitating factors (Cummings M and Baldry P; 2007)
Aggravating and Precipitating factors responsible for the development of MTrP activity are Trauma.
This may be either a direct injury to the muscle or by the sudden or repeated overloading of it. Alternatively, it may develop when the muscle is subjected to repeated episodes of microtrauma such as occurs with a repetitive strain injury.
Anxiety MTrP activity may also be brought about when a patient of an anxious temperament holds a group of muscles in a persistently contracted state.
Muscle wasting MTrP activity is liable to develop when muscles have become weakened and wasted by malignant disease or a neurological disorder.
With respect to strokes, MTrP nociceptive pain is liable to develop when weakened muscles become overloaded during attempts to restore movements to them during the recovery stage.
Muscle ischemia MTrP activity may arise when, because of arterial obstruction, the muscles of a limb become ischemic.
Visceral pain referral Pain arising as a result of visceral disease is frequently referred to both skin and muscles. When this happens MTrPs in muscles situated in this zone of pain referral are liable to become active, with the production of superimposed MTrP pain.
Radiculopathic compression of motor nerves
When pain occurs as a result of spinal nerve root compression, such as from spondylosis or disc prolapse, pain may also arise as a result of the secondary development of TrP activity in the paraspinal muscles. Climatic causes MTrPs are liable to become active when the muscles containing them are exposed to adverse environmental conditions such as damp, draughts, excessive cold or extreme heat.
In order to diagnose a patient as suffering from myofascial pain it is necessary to conduct a complete medical history covering topics such as symptom onset, duration, location, and character of pain, physical/functional impairment, factors that exacerbate or relieve, associated features or secondary signs/symptoms, neurologic history and a psychosocial history Causes of persistent Myalgia. (Gerwin RD; 2005)
This is by far the most common presenting complaint. Typically the pain is described as deep, aching and poorly localized. It is usually restricted to one quadrant of the body, although complex patterns from multiple MTrPs may give a wider distribution. It is important to determine the precise nature and pattern of the pain, as would be done when taking a standard medical history. Various pain scales may be employed to standardize the process of determine the patient pain intensity. Back pain is probably the most commonly treated, closely followed by neck pain, shoulder pain and chronic unresponsive leg and knee pain.
Paraesthesia is not uncommon in association with the pain and often confirms in the patient’s mind the false impression that they have a ‘trapped nerve’. Symptoms are generally exacerbated by activity; however, some light exercise involving gentle stretching of the affected muscle may relieve the aching.
Some patients will find a tender point in muscle, particularly if the MTrP is in an accessible site; and a few will describe some sort of technique they have developed to relieve the pain, which usually involves the application of pressure to the MTrP. Cervicogenic headache will often have associated trigger points.
MTrP activity may lead to the development of various autonomic changes. These include lacrimation, regional pilomotor activity and excessive coldness of an extremity. MTrPs appear to affect proprioceptive function. In cases of neck pain, the cervical musculature, in particular sternomastoid, this may be responsible for disequilibrium, even to the extent that the patient may describe true vertigo. In the limb musculature this may result in distorted weight perception. Motor dysfunction includes restricted range, weakness, reduced co-ordination and spasm in other muscles.
Myofascial pain may disturb sleep but, more importantly, sleep position often aggravates MTrP activity by allowing affected muscles to shorten.
MTrPs occur in all age groups but present most commonly in the middle years. The muscles of young active people are probably more resistant to injury, and faster to repair, so less likely to develop or sustain active MTrPs. By comparison, the musculoskeletal system of the middle-aged adult is becoming increasingly degenerate, less resilient and slower to heal. In general the middle-aged are less active, but engage in unaccustomed bouts of physical activity. They tend to suffer most with the pain of active MTrPs. Latent MTrPs can be found in the majority of elderly people, causing stiffness and reduced active range of movement, but this age group present less frequently with the pain of active MTrPs.
Women seem to present more frequently with myofascial pain than men and more commonly with neck pain, It has not been established whether myofascial pain is more common in women, or whether they are more likely to present with this type of pain. It is certainly true that phenotypic differences can influence biomechanical loading and, for the same mass, women tend to have wider hips and narrower shoulders than men. Biological factors such as these may be important, but socio-economic differences in terms of working environments may also have an influence. For example, a higher proportion of the male workforce performs physically strenuous jobs and it has been noted that these individuals suffer less from myofascial pain than sedentary workers.
This article is unfinished... coming soon: a comparison of acupuncture treatment and trigger point dry needling.
(see the trigger point chart)
Article by Dr Peter Richard Pedersen
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