Nature of myofascial trigger points
Currently, there are three hypotheses as to the nature of myofascial TrPs that need consideration: the energy crisis theory, the muscle spindle concept, and the motor endplate hypothesis.
Energy Crisis Theory
The energy crisis theory evolved by trying
to account for: the presence of the Taut band, which was assumed to be
caused by the TrP mechanism; the painfulness of TrPs; their response to
almost any form of stretch therapy; and the absence of any motor unit
activity that would account for the tension in the taut band fibers. The
most recent update of this concept, including some experimental
evidence in support of it, was in 1993 (35).In essence, this theory
postulates an initial release of calcium [either from the sarcoplasmic
reticulum (35) or from the extracellular fluid through injured
sarcolemma (5)1. The ionic calcium causes sustained sarcomere shortening
and increased metabolism. The sustained shortening also could
compromise local circulation. This shortening would cause a loss of
oxygen and nutrient supply in the presence of an increased metabolic
demand, thus the energy crisis. The lack of energy could compromise
recovery of the calcium by the sarcoplasmic reticulum which would, at
least temporarily, perpetuate the cycle. The new motor endplate
hypothesis does not invalidate this energy crisis concept and indeed
incorporates part of it. The more severe symptoms of chronic refractory
TrPs and the onset of pathological changes may be caused by the
development of such an energy crisis.
In their initial report of the highly
localized electrical activity characteristic of myofascial TrPs,
Hubbard and Berkoff (10) proposed that the source of this activity was a
dysfunctional muscle spindle. In that paper, the authors dismissed the
possibility that these potentials could arise from motor endplates on
the basis that the activity is not localized enough to be generated in
the endplate, and that the activity does not have the expected location
or waveform morphology. On the contrary, as we understand the literature
and interpret our experimental findings, we come to quite opposite
conclusions. The degree of localization corresponds closely to that
previously described in the classical paper on the source of motor
endplate potentials (66). In our experience (50,58-60), we find the
active loci of TrPs to be located in the endplate zone and not in the
taut band outside of the endplate zone (58). The waveforms that we
describe as SEA (58,59) correspond closely to previously published
records and descriptions of endplate noise (67,68). The potentials that
we designate as spikes (60) correspond to the spikes described in an
authoritative EMG text (68) as arising in extrafusal muscle fibers at
endplates. Brown and Varkey (69) also attributed the SEA to potentials
of the endplate zone and they attributed the positive-negative
discharges [spikes] to postsynaptic muscle-fiber action potentials that
were presynaptically activated by mechanical irritation (69). One other
study (70), in addition to that of Hubbard and Berkoff (10), suggested
that spikes arise from intrafusal muscle fibers. Those authors discussed
why spikes are not ectopic discharges of motor axons but did not
consider the possibility that spikes are the result of mechanically
induced release of abnormal amounts of acetylcholine at the
neuromuscular junction of an extrafusal fiber. All of their data were
consistent with that latter possibility. Our experimental evidence (60)
also supports the origin of spikes in extrafusal muscle fibers. Muscle
spindles may, at times, contribute to TrP phenomena, but it seems
unlikely that muscle spindles are the primary site of the mechanism.
Motor Endplate Hypothesis
The motor endplate hypothesis identifies dysfunction in the region of extrafusal motor endplates as a major cause of myofascial TrPs. The terms endplate and neuromuscular junction are used interchangeably in this chapter. The term endplate identifies the physical structure, and the term neuromuscular junction emphasizes the functional significance of that structure. Hubbard and Berkoff (10) first reported in 1993 that myofascial TrPs contain very minute loci that produce characteristic electrical activity. Their paper illustrated both low-voltage continuous noise-like potentials and intermittent spikes, but it emphasized the spike component. Detailed consideration of either component requires a faster recording rate than that presented in their paper. Figure 2 shows schematically the concept that has now evolved. The figure shows active loci clustered within the region of a clinically-identified TrP. The loci are found among normal endplates. The localization of active loci in the endplate zone predominantly at the TrP has been confirmed experimentally (58). Figure 3 illustrates typical SEA and spikes that are characteristic of a TrP active locus. Figure 3A shows the overall pattern at a slow recording speed. The largest spikes stand out very clearly, but the distinction between small-amplitude SEA and large-amplitude spikes becomes blurred. The high-speed record of Figure 3B shows the marked difference between the continuous, relatively low-amplitude noise-like SEA and the much higher amplitude, discrete diphasic [sometimes slightly triphasic] spikes that have a sharp, initially negative deflection. This record shows only 1/3 of the full amplitude of these two spikes which also had been recorded at 1/5th amplification on another channel [not shown]. For comparison, Figure 4 presents endplate potentials published in a leading EMG textbook (68). Figure 4A shows an almost exclusively spike pattern, and Figure 4B shows a combination of endplate noise and endplate spikes. These were recorded at the same higher speed as Figure 3B. The continuous, low-amplitude noise-like component was identified as endplate noise that corresponds to our SEA. It has a characteristic sound like a seashell held to the ear. The high-amplitude intermittent component was identified as endplate spikes (68). Normal endplate potentials are occasional, discrete, short, and negative monophasic potentials, shown in Figures 5A and 5C. Liley (71) illustrated the conversion of this normal discrete pattern to an abnormal noise-like pattern by applying mild mechanical stress to the terminal nerve fiber or to the endplate region Subsequently, other physiologists (72,73) have demonstrated experimental production of the same endplate noise-like electrical activity. This "acetylcholine noise"], which looks like our SEA, was the result of a 100- to 1000-fold increase in the rate of release of acetylcholine. This abnormal release was induced by the addition of lanthanum ions (72) or by exposing the extrafusal endplate to foreign serum (73). The patterns correspond closely to the SEA of active loci and the endplate noise of electromyographers . These observations substantiate the concept that SEA represents abnormal extrafusal endplate activity due to release of greatly increased numbers of acetylcholine packets. Electrically active loci are consistently found in myofascial TrP regions (10,58); however, our finding of some active loci in the endplate zone out of the TrP (58) and experimental effects (72,73) indicate that the abnormality of endplate function marked by SEA also can be caused by other factors not related to TrPs. All TrPs appear to contain electrically active loci, but not all active loci are found at TrPs. In studies of electrical activity characteristic of active loci (58-60), the investigators consistently found that when a needle was located where these potentials were observed, minimal voluntary contraction induced motor units with initially negative deflections. This polarity indicates that the potentials must have originated very close to [within the order of 10 microns of] the endplate. The potentials were recorded from the tip of the EMG needle. It has recently been demonstrated that spike potentials at least 2.6 cm along the length of the taut band (60). This distance is well beyond maximum 1 cm length [usually much less] of a muscle spindle. These action potentials are therefore interpreted to have been propagated by an extrafusal muscle fiber, not an intrafusal fiber. In summary, several lines of evidence indicate that the active loci of myofascial TrPs are in the immediate vicinity of extrafusal motor endplates. This evidence includes: the recognition of their electrical activity as endplate potentials by the EMG community (68), the demonstration of SEA-like noise potentials at motor endplates by experimentally greatly increasing acetylcholine release (71-73), the demonstration by minimal voluntary contraction that active loci are in the immediate vicinity of endplates [unpublished data], the propagation of spikes as far as 2.6 cm (60), and the clinical effectiveness of Botox injections (62-64). Explanation of Clinical Features. Table 5 shows how the clinical features of myofascial TrPs may relate to he endplate hypothesis.
Next: Likely Explanations for Clinical Features of Myofascial Trigger Points
