Posted by MERM on 12/7/2008, 7:13 am, in reply to "3 Myofascial pain, dx, treatment , causes "
Fischer indicated that the obnoxious [sometimes intolerable] pain experienced during TrP injection, as well as much of the post-injection soreness, can be avoided by local analgesic block of the TrP site before injection.
This may be particularly helpful when injecting the TrPs of FM patients .
Whether preemptive analgesia also blocks the local twitch response would be of considerable practice and theoretical interest.
The effectiveness of preemptive analgesia has been convincingly demonstrated in both human and animal studies
. Eliciting a Local Twitch Response. Hong reported that with either lidocaine injection or dry needling of TrPs, the patients experienced almost complete relief of pain immediately after injection, if local twitch responses were elicited.
On the other hand, they experienced only minimal relief if no such response occurred during: injection. When searching for TrP active loci in the course of experiments , we found that rapid advancement of the EMG needle through the TrP region was much more likely to elicit local twitch responses than was the very slow advancement technique required to locate spontaneous electrical activity [SEA].
Local twitch responses often occurred in close spatial relation to an active locus of SEA. Hong, et a1.presented experimental evidence to substantiate the clinical impression that injection of myofascial TrPs substantially benefits FM patients.
The authors also showed that the relief from TrP pain that the FM patients experienced was considerably less than the relief obtained by myofascial TrP patients without FM. Injecting Botulinum A Toxin. Recently, several authors have reported the successful use of botulinum A toxin [Botox] for the treatment of myofascial pain caused by TrPs
. In a small double-blind, placebo-controlled study, four patients experienced 30% reduction of pain following Botox injection but not following saline injection.
Results were statistically significant. The effectiveness of Botox injection is of great theoretical interest, but it has limited therapeutic application. In therapeutic doses, Botox paralyzes muscles by blocking release of acetylcholine from motor nerve terminals at the neuromuscular junction . This eventually causes degeneration of that neuromuscular junction.
If the denervated muscle fiber survives, it normally becomes reinnervated in about 3-6 months. The fact that Botox quickly inactivates myofascial TrPs is a strong indicator that the myofascial TrP mechanism is intimately associated with the neuromuscular junction.
However, because of its destructiveness, Botox should be used only when other more conservative approaches have failed. Generally, the basic reason why injection [or other treatment] provides only temporary relief is because perpetuating factors have not been adequately addressed.
With use of Botox in the presence of persistent perpetuating factors, the TrP is likely to recur.
Likely Explanations for Clinical Features of Myofascial Trigger Points
Palpable Band Continuous abnormal release of calcium from sarcoplasmic reticulum
Spot Tenderness Sensitization of nociceptors in the vicinity of the motor endplate
Jump Sign Severity of spot (trigger point) tenderness
Pain Recognition Digital pressure is aggravating trigger points that are responsible for patient's pain
Twitch Response A spinal reflex activation of motor units whose endplates have developed active loci
and/or a mechanically elicited axon reflex of those same motor units
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