Elizabeth M. Frank, BS, BSc, BVMS, Dip. Vet. Acupuncture
Since the 1980's, a considerable amount of scientific evidence has been accumulating to aid in the understanding of the aetiology of myofascial trigger points (MTrPs). This research has focused on methods that quantitatively and qualitatively describe what is occurring at MTrPs. A brief summary encompassing the primary research tools are discussed below. The results of these areas of research have led to a proposed integrated hypothesis of the aetiology of MTrPs.
Clinically, in myofascial pain patients, there is both increased muscle tenderness and muscle hardness (i.e., firmer consistency / less compliant) on palpation of the MTrP. Muscle hardness measures differentiate the hardness of the muscle from the hardness of the overlying tissue. Muscle hardness has been found to vary between locations of the same muscle. Clinically, pain patients with tension headaches have been found to have significantly harder muscles than normal individuals. Both tissue compliance and muscle hardness meters require considerable skill and a specialised device.
Algometry is used clinically as a measure of pain. Different types of algometers may be used with different tissue types: e.g., pinch or thermal algometers are commonly used in the skin, while electrical stimulation or the more commonly used sensitivity to applied pressure are used in muscle. Pressure algometers can measure three objective values: pressure pain threshold (pain onset), referred pain threshold (onset of referred pain) and pain tolerance (intolerable pressure) in kg/cm2.
Algometry cannot be used to diagnose MTrPs (i.e., not a diagnostic criteria) as tenderness can be coming from other sources, e.g., bursitis, muscle spasm. Thus algometry must be performed in combination with other diagnostic tests. The absolute algometric values vary between tissue types, e.g., muscle vs bone, regions within a muscle, between sexes (females lower) and with thickness and compliance of overlying tissue. Algometry requires considerable skill of palpation, instrument use, rate of application of pressure by the examiner and patient cooperation as pressure is placed at the point of maximum tenderness.
Hong (1996) examined the referred pain at a MTrP compared with the amount of pressure used to elicit this finding. Previous studies had found poor association between the characteristic relationship of MTrP compression and referred pain. He suggested this might be due to variation in pressure applied at MTrPs by the examiners, leading to inconsistent reports of referred pain. Pressure algometry was used to examine three sites: at the MTrP; at a taut band 2 cm distal to the MTrP; and within normal muscle 1 cm distal and lateral to the taut band site. Two groups were examined: those having muscles with active trigger points; and those with latent trigger points. Pressure pain threshold, referred pain threshold and pain tolerance were measured at all three locations in both groups.
Referred pain was elicited from the MTrP and taut band of all active MTrPs, but only 1/2 and 1/3 respectively of the latent MTrPs. Referred pain was elicited from "normal" muscle in the active MTrP patients and less than 1/4 of the latent group. Less pressure was needed to elicit referred pain in the active Vs latent groups. The least pressure was required at the MTrP < taut band site < site off the taut band. The referred pain threshold was not consistently elicited in the latent group, as pain tolerance was reached first. Because overlap exists between active and latent MTrPs, active and latent MTrPs cannot be differentiated with a specific value by pressure algometry.
Referred pain threshold is related to the irritability of the site of compression, and referred pain can be elicited from different sites near the MTrP. This reflects muscle sensitisation, with the MTrP being the most sensitive point. Up regulation and hypersensitivity of the central nervous system occurs in chronic pain and is often termed central sensitisation. The findings of Hong support the clinical findings of Travell that three phases of MTrP irritability exists. Highly irritable MTrPs can cause severe pain at rest, moderately irritable MTrPs cause pain with a stressful activity or poor position and mildly irritable MTrPs cause referred pain only when the MTrP is compressed. Importantly, treatment of the MTrP leads to an increase in pressure algometry thresholds.
Thermography allows visualisation of temperature changes within the surface of the skin using infra red radiometry, or films of liquid crystal. Infra red radiometry can demonstrate characteristic cutaneous reflex phenomena of MTrPs. The temperature changes are the result of sympathetic nervous system activity but they are not sufficient to diagnose a MTrP. The region over the MTrP has been repeatedly found to be hyperthermic while the region over the referred pain zone appears to become hypothermic when the MTrP is mechanically stimulated. Further studies are needed in this area.
A characteristic of MTrPs involves eliciting a localised contraction of the taut band called the local twitch response (LTR). MTrP needling, used to elicit the LTR, was reported to coincide with the: LTR on ultrasound; the patient's report of their typical pain; and the referred pain pattern characteristic of the muscle being stimulated. The LTR has been found to be lost with lidocaine block and motor nerve transection, but persists after spinal cord transection (subsequent to spinal shock) suggesting a spinal cord reflex without input from higher centres.
Microanalysis enables a continuous sample of very small quantities of substances to be taken directly from soft tissue with minimal tissue damage. Microanalysis has been found to distinguish clinically distinct muscle groups. In vivo microanalysis, using a microdialysis needle, has found the concentrations of protons (H+), bradykinin, calcitonin gene-related peptide, substance P, tumor necrosis factor, Interleukin-1, serotonin and norepinephrine to be significantly higher in active MTrP > latent MTrP > no MTrP muscle groups. These biochemicals have been found to play a role in maintaining the chronic pain state. pH and pressure sensitivity was significantly lower in the active MTrP group vs. the other two groups. Research has found a correlation between pain and acidity and may explain active MTrP spontaneous pain.
Static and dynamic surface electromyography (sEMG) shows the electrical activity of the muscle underlying the sensor. sEMG studies have found that MTrPs disrupt normal muscle function. MTrPs lead to increased responsiveness, delayed relaxation and increased (accelerated) fatigue of the muscle. The MTrP can also cause referred spasm and inhibition of other muscles which often also have MTrPs.
The motor phenomena produced by MTrPs are complex, and the dysfunction that they cause is suggested to be as important as the sensory phenomena. Pain has long been considered the primary problem in MTrPs, however it is now considered by Simons to be secondary to the motor phenomenon. The motor features together can increase muscle overload and reduce muscle tolerance.
Considerable research has been performed in the area of needle electromyography (EMG) at MTrPs. Travell first described spontaneous EMG activity and spike potentials at the MTrP in 1957, while the adjacent muscle was found to be electrically silent. Subsequent reports had variable results leading to the study of Hubbard and Berkoff (1993).
Hubbard and Berkoff found spontaneous EMG activity at the MTrP, which was absent 1 cm away in the same muscle. The EMG activity corresponded with the patient's report of pain + referred pain + autonomic symptoms in many cases. The EMG activity did not occur at non-MTrP locations. The mean EMG amplitude correlated with MTrP palpation tenderness, i.e., increased amplitude associated with increased tenderness. High amplitude spike potentials were also described. Stress was found to exacerbate the spontaneous EMG activity.
Subsequently, more detailed EMG investigations have found two significant components of MTrP electrical activity: intermittent and variable high amplitude spike potentials; and a consistent low amplitude noise-like component. The noise-like component was termed spontaneous electrical activity (SEA). The SEA and spike potentials have been subsequently confirmed on a number of studies. Spikes only, SEA only, or both, may occur and the term "active locus" was adopted to identify the site of electrical activity. Active MTrPs have been found to have SEA with or without spikes. The SEA is not mechanical (e.g., due to muscle contraction or EMG needle), and the waveforms of the SEA are different from miniature endplate potentials (MEPP) and the tendon tap reflex. The small amount of acetylcholine released during MEPP produces endplate potentials that are insufficient to propagate an action potential.
Histological, EMG and pharmacological evidence suggest a significant relationship between the MTrP and the endplate zone. The SEA originates in the MTrP active locus and is most common at the MTrP itself. The SEA is not specific to the MTrP, but is found more frequently in and around the MTrP.
The SEA is not a feature of the taut bands of the MTrP. The spike component propagates along the taut bands, but not in the rest of the muscle. Spikes occur when sufficient acetylcholine release depolarises the post-junctional membrane and initiates an action potential. Severely dysfunctional endplates in very active MTrPs produce spikes spontaneously, without stimulation. In less active MTrPs, mechanical stimulation of the needle appears to facilitate acetylcholine release and spike formation.
Electromyographers accept endplate noise and endplate spike components of motor endplate potentials as normal endplate potentials. This interpretation clearly contradicts the research findings at MTrPs, i.e., MTrPs are not normal muscle. Simons (2001) has challenged this conventionally held view of electromyographers. Based on a review of the physiology literature, Simons argues that the electromyography concept of endplate noise and spike components as normal is flawed. Electromyographers' interpretation of endplate noise stems primarily from a single article. The physiology literature clearly indicates that the endplate noise, as described by electromyographers, arises from abnormal motor endplate function. SEA is indistinguishable from endplate noise.
Simons has suggested that the SEA at the MTrP is due to grossly increased acetylcholine release and abnormal endplate function. Endplate noise is a signature of dysfunctional endplates, which may be caused by a number of conditions. Abnormal endplates with SEA at the MTrP are scattered among normal endplates, which have no SEA. Thus, the MTrP mechanism is related to dysfunctional endplates scattered among normal endplates. Pain intensity and pressure pain threshold of a MTrP has been found to highly correlate with the prevalence of end plate noise in the MTrP region.
Histologically, contraction knots have been noted in muscle biopsies of tender palpable nodules in muscle for over 50 years. In cross section, these areas correspond with large darkly staining fibres. The significance of these histological features has not been appreciated until recently.
Contraction knots are now suggested to be extremely contracted sarcomeres, and lead to the nodular feel of the MTrP on palpation. The size of the contraction knot is within the size range of a normal motor endplate. The resulting sustained tension and tissue distress leads to release of sensitising agents and sensitisation of local nociceptors.
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