Travell and Simons recommend dimethisoquin hydrochloride ointment (Quotane) for massaging TrPs in superficial muscles such as the orbicularis oculi, frontalis, and occipitalis.
3 Dimethisoquin, a local anesthetic, inhibits voltage-gated Na(+) channels (conferring its anesthetic effect) but also acts as a noncompetitive inhibitor of nAChRs (IC50 = 2.4 μM).
35 The anesthetic's potency is significantly greater than that of lidocaine (IC50 = 52 μM) and procaine (IC50 = 240 μM). Further, dimethisoquine is uniquely selective for the nAChR subtype expressed in the neuromuscular junction.
Massage with capsaicin cream (0.075%, available over the counter) is useful for treating TrPs located in surgical scars,
36 which are particularly refractory to treatment.
5 Capsaicin selectively binds to the vanilloid receptor (VR1).
37 Vanilloid-receptor activation triggers an influx of Ca
2+ into neuron terminals, which initiates neurotransmitter release. Repeated exposure to capsaicin, however, causes VR1s to become desensitized. This mechanism explains the seemingly paradoxical use of capsaicin as an analgesic.
36-38 Vanilloid receptors are also expressed in brain regions that modulate the emotive and cognitive aspects of pain (eg, preoptic area, locus ceruleus, hypothalamus, striatum).
38 It has been hypothesized that modulating the expression of VR1s and their endogenous ligand (anandamide) may be one of the central mechanisms of OMT,
38 parallel to the potential effects of OMT on endorphins.
39
Needling is sometimes necessary to inactivate TrPs. For thousands of years, Chinese medicine has treated TrPs with acupuncture.
40 Travell began needling TrPs with syringes in 1942, injecting them with procaine.
41 Procaine was later replaced by saline solution,
42 which was later replaced by “dry needling”—without any fluid in the syringe
43—bringing the procedure full circle to what is essentially acupuncture. The “dysfunctional motor end plate hypothesis” has led to the injection of botulinum toxin, which causes an irreversible blockade of ACh release in the TrP.
44
Injecting TrPs with quinidine should be tested in a clinical trial, as quinidine decreases presynaptic ACh release (via its well-known blockade of L-type Ca
2+ channels) and down-regulates nAChRs (a postsynaptic mechanism). In one trial, quinidine appeared to restore AChE activity.
45 Diltiazem also merits investigation. It is an L-type Ca
2+ channel blocking agent that corrects myopathies caused by defects in AChE activity.
46
Travell and Simons recommended a diet adequate in vitamins and minerals for the prevention of TrPs.
3 Supplementing the diet with phosphatidylcholine has been recommended,
47 but this may actually provoke TrPs in a portion of patients. As choline is a percursor to ACh, an nAChR gain-of-function mutation may enable choline to directly activate the mutated receptors.
48
Another new approach in treating TrPs are herbal medications. As an estimated 50% of patients with long-term musculoskeletal pain take herbal remedies, it behooves osteopathic physicians to understand the mechanisms of these medications.
49 Herbal remedies and essential oils that are recommended for treating myofascial pain include lavender (
Lavandula angustifolia), lemon balm (
Melissa officinalis), rosemary (
Rosmarinus officinalis), kava kava (
Piper methysticum), skullcap (
Scutellaria lateriflora), passionflower (
Passiflora incarnata), Rose (
Rosa spp), and valerian (
Valeriana officinalis).
47 Nearly all of these herbs contain linalool, a monoterpene compound that inhibits end plate activity by reducing ACh release (a presynaptic mechanism) and by modifing nAChRs (a postsynaptic mechanism).
50 Marijuana (
Cannabis spp), which also produces linalool,
51 also effectively treats myofascial pain syndromes.
52 Marijuana's efficacy may also be attributed to tetrahydrocannabinol, an N-type Ca
2+ channel blocker.
53 Tetrahydrocannabinol inhibits ACh release in the CNS
54; this inhibition is thought to occur at motor end plates, as motor nerve terminals express cannabinoid receptors.
54