dria, possibly indicating metabolic distress396 Reitinger and colleagues also reported pathologic alterations of the mitochondria, as welJ
as increased A-bands and
decreased I-bands in muscle sarcomeres of myofascial trigger points in the gluteus medius muscle; however, they did not describe their definition of a trigger point397
Pongratz and Spath noticed segmental degeneration of muscle fibers with concomitant edema and histiocytic cellular reaction.398
Energy Crisis Hypothesis
Both the local tenderness and taut bands characteristic of myofascial pain syndrome are proposed to be associated with the "energy crisis hypothesis."305
there is decreased circulation and local ischemia in a myofascial trigger point due to sustained sarcomere shortening. Studies by Bri.ickle and colleagues, measuring
extremely low oxygen levels (5% of normal) within myofascial trigger points, appeared to confirm the hypoxia component of the energy crisis hypothesis.399
shortening of the actin-myosin complex can be caused by a traumatic release of calcium either from the sarcoplasmic reticulum or from a failure to restore adenosine
triphosphate. The possible roles of titin and nebulin have not yet been considered in the etiology of myofascial trigger points. Adenosine triphosphate is essential for
normal functioning of the calcium pump, as well as for the release of the actin-myosin complex. A shortage of adenosine triphosphate can result in local muscle
contractures or taut bands.334 The pathologic alterations of the mitochondria can further contribute to a shortage of adenosine triphosphate. Termination of a muscle
contraction is normally accomplished by pumping calcium back into the sarcoplasmic reticulum against a large concentration gradient. impaired calcium pump, the
intracellular calcium concentration stays elevated, and the actin and myosin filaments become continuously activated400 Shenoi and Nagler confirmed that an
impaired reuptakc of calcium into the sarcoplasmic reticulum can cause myofascial trigger points. They reported that calcium channel
Muscle Pain Syndromes 121
blockers caused myofascial trigger points, presumably based on their ability to prevent calcium re-uptake40'
Electrophysiologic Abnormalities
In J957, Weeks and Travell published a report that outlined a characteristic electrical activity of a myofascial trigger point358 It was not until 1993 that Hubbard and
Berkoff confirmed the presence of specific electromyographic activity in myofascial trigger points of the trapezius muscle.
greater than the electromyographic activity in a nontender area of the same muscle.
corded both low amplitude continuous action potentials and intermittent spikes from active myofascial trigger points359 Simons and colleagues reported similar
action potentials of 10 to 50 flV, which they defined as "spontaneous electrical activity," in contrast to the intermittent biphasic spikes of 100 to 600 flV360,J61
electrical activity is not mediated through the spine or supraspinal influences, suggesting that it may be a motor endplate phenomenon. The electrical activity was
found to be similar to abnormal endplate potentials, associated with an excessive release of acetylcholine, which affects the voltage gated sodium channels of the
sarcoplasmic reticulum and increases the intracellular calcium Jevels306.402-404 Gunn articulated that the relative increase of acetylcholine release into the muscle
may be the result of neural dysfunction, associated with a decrease of the available acetylcholinesterase and the renewed activation of acetylcholine receptors
throughout the muscle304 It is not clear whether there are, in fact, newly formed acetylcholine receptors405,406
Several studies have demonstrated that myofascial trigger points are nearly always located in the region of the motor endplate zone.J61,407 Hong proposed that a
palpable myofascial trigger point consists of multiple discrete sensible loci.
sitized nociceptive nerve endings.
that these spots represent abnormal motor endplates.407.4o8
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