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Neural Acupuncture: A Rationale For The Use
Of Lidocaine Infiltration At Acupuncture Points In The
Treatment Of Myofascial Pain Syndromes
Mark K. Frobb, MD
ABSTRACT
A major part of an acupuncture physician's practice relates to the treatment of pain syndromes, especially myofascial pain syndromes. These are a poorly defined group of pain syndromes generally relating to the supporting musculature of the axial skeletal system. Many different modalities are used to treat these pain syndromes. All of them produce some level of success, but few consistently resolve all these difficult and disabling pain syndromes. Much of the treatment to date has been based on the inflammatory model; therefore, physical therapies have been used to resolve the suspected inflammatory process. This article approaches myofascial pain syndromes from a neuropathic model standpoint, discussing the etiology and histology of the neurogenic lesion. Acupuncture sites ideally represent an anatomical guide to peripheral nerve anatomy, permitting lidocaine infiltration at the point of the suspected neurogenic lesion.
KEY WORDS
Myofascial Pain Syndromes, Lidocaine, Acupuncture, Neural Therapy, Neuropathic Pain Syndromes
Myofascial Pain Syndromes
The term myofascial pain syndrome is commonly used nonspecifically to describe regional musculoskeletal pain syndromes. Although these pain syndromes may involve any of the 200 paired muscles in the body, they most often occur in the supporting muscles of the axial skeletal spine predominantly at the thoracocervical junction and shoulder girdle, and lumbosacral junction and pelvic girdle areas where the maximal forces of gravity and workload involve the musculoskeletal postural support system.
In most cases, injury or trauma causes the pain. Problems can also arise without a specific incident, often due to overuse or lack of conditioning and fatigue. In addition, there appears to be disagreement as to whether these problems are of an inflammatory or neurogenic origin; however, there tends to be more acceptance among researchers that myofascial pain syndromes are a manifestation of neuropathic lesions.1
Clinical examination tends to demonstrate a number of consistent findings:2
• an underlying hypertonicity in the involved muscle groups
• a number of tender points distributed in a segmental fashion along the muscular bands, generally referred to as trigger points
• contracted muscles affected with this condition appear shortened, often with areas of fibrositis
• frequent associated elements suggestive of disturbance of the autonomic nervous system with vasoconstriction as noted on thermographic studies, vasomotor and pilomotor dysfunction in the skin, and manifestations of allodynia.
Therapies for Myofascial Pain Syndromes
The predominant therapeutic choices for myofascial pain syndromes have generally encompassed physical and counterirritational therapies including physiotherapy, manual therapies, massage, and stretch and spray techniques, often combined with fitness and exercise programs. Other practitioners incorporate injection into the trigger areas or taut bands in the muscle with lidocaine, steroids, saline, or sterile water. Dry needle application such as in intramuscular stimulation as well as acupuncture has been used with some success.3
The rationale for the use of the physical therapies is to excite receptors in skin and muscle, golgi tendon organs, and thermal receptors with a reflexive response through the axonal reflex pathway to the efferent motor fibers and a stimulation attempt of the therapeutic target.
Gunn3 proposed that the therapeutic attention should be aimed at the short muscle bundle and the rationale of dry needling of the taut muscle bands is directed to this purpose of releasing the contracture in the specific muscle group. He suggests that needling creates a current of injury resulting in a discharge of brief outburst of injury potentials referred to as "insertional activity." This produces a relaxation of the shortened muscle as well as a sympatholytic effect that spreads through the adjacent soft tissue, releasing associated vasoconstriction. Gunn advocates that additional benefits may relate to the release of platelet-derived growth factor and the stimulation of collagen formation at the site of the lesion, assisting in the repair of the underlying musculotendinous structure.2
In acupuncture, the therapeutic effect from the Western medicine viewpoint appears to result from the stimulation of the endogenous endorphin system. Literally hundreds of studies have been conducted on the effectiveness of electroacupuncture for the treatment of pain and its predictable physiological effects on the neurological system. Studies have reliably demonstrated release of endorphins in the spinal cord, the midbrain, hypothalamus, and pituitary gland. Studies have also demonstrated enkephalin release by the midbrain and increases in blood cortisol. It has been shown that the concomitant administration of nalozone will result in blockade of these neurophysiological events.4
A growing belief exists in pain research that there are more similarities than differences between inflammatory pain syndromes and neuropathic pain syndromes.1 Advances in the understanding of cellular and molecular mechanisms suggest that although initial lesions may be inflammatory in origin, without quick resolution of the inflammatory process, local production of inflammatory mediators, changes in the axonal morphology, and creation of sites of ectopia may quickly alter the picture. Augmentative changes result in both peripheral and central amplification.
Indeed, many of the features of neuropathic pain are represented in myofascial pain syndromes, including:2
• pain where there is no obvious tissue-damaging process
• delay in the onset of symptoms following a precipitating injury if a history of an injury is elicited
• dysesthetic pain often felt as an unpleasant burning or aching
• paroxysmal shooting or stabbing pain
• severe pain in response to a stimulus that is not normally noxious (allodynia).
The Neuropathic Pain Model
The neuropathic model proposes that the underlying neurogenic lesion lies in the afferent sensory axons in the peripheral nerve, and it is the manifestation of this injury that is noted in the distal local muscle group.
Afferent axons run uninterrupted from their sensory endings in the innervated peripheral tissue, sometimes over a meter or more, to their central synaptic endings in the central nervous system (CNS). The cell body that lies along this path at the dorsal root ganglion near the spine is responsible for the metabolic activities of the neuron. The axon serves not only as a conduit for the electrical impulses, but also as an axoplasmic transport system for delivery of metabolic substrates.1 In normal axons, only the distal tens of microns have a high degree of regional specialization for transducing and encoding mechanical, thermal, or chemical stimuli into a propagated impulse train.
Under normal circumstances, sensory impulse generation typically begins when a stimulus causes an increase in the permeability of membranes of sensory endings to various ions, particularly sodium. Ions then flow through the sodium channels following an electrical and concentration gradient, producing partial depolarization of the afferent axon sensory endings. As the stimulus increases, further streams of sodium ions are added to the generator depolarization mechanism, eventually resulting in a rapidly cascading activation of voltage-sensitive channels causing a generalized depolarization explosion. This process results in an action potential that then courses centripetally up the axon to the dorsal root ganglion and then to the spinal cord where it is processed centrally by the CNS. Thereafter, having opened, the sodium channels rapidly close again and the membrane potential drifts back toward an initial resting level. A threshold is established, not necessarily as a fixed value but rather as a dynamic equilibrium between inward and outward ion currents. This is controlled by the potassium ions flowing outward shortly after depolarization begins. Under normal conditions, this prevents nerve impulses being set off by infinitesimally small stimuli.1
However, in neuropathic pain syndromes, this control mechanism is compromised and repetitive firing capability, known as pacemaker capability, occurs not only at the sensory nerve endings (where, under normal circumstances, it is confined to the end plates of the nerve fibers) but possibly along the entire length of the axon, particularly in areas where the axon has been damaged. The damaged nerve axon can develop spontaneous ectopic firing in response to minimally applied mechanical or chemically mediated stimulation, a state known as hyperexcitability or supersensitization.1,2 Following induction of this state, both the nerve and the muscle cell can then generate spontaneous electrical impulses causing involuntary muscular activity either directly or indirectly through an aberrant feedback axonal reflex. This axonal reflex is caused when the barrage of afferent input into the spinal cord centrally results in stimulation of the efferent motor neuron at the same spinal cord level, with resultant contraction activity of the target group.5
These locations of axonal injury are generally noted where the nerve axon runs adjacent to tendon and bone or where small branches cross over tough fascial planes such as occur in the muscle groups that control movement at the thoracocervical junction/shoulder girdle complex or lumbosacral junction/pelvic girdle complex.1
These injuries may be due to trauma (e.g., secondary to direct blows), whiplash and torsional strains (nerve traction injuries), or overuse (inflammatory injuries). Mechanosensitive trigger points are usually consistently identified in these posture-controlling muscle groups.
Histologically, morphological changes at the sites of the axonal injury are found in neuropathic pain syndromes. Sodium channel protein tends to accumulate in increased amounts in the axolemma in the region of the injury. In addition, a significantly increased number of sodium channels appear in the internodal membrane regions where under normal circumstances, they are not found.1,6 Although this membrane remodeling is thought to support the restoration of impulse propagation through damaged areas of the axon, it may also be responsible for the sites of ectopic impulse generation.1,6 Several investigators have demonstrated that these affected injured axons develop sprouting and budding, with synapsing of adjacent autonomic and sensory nerve fibers increasing the field of supersensitivity with ephaptic crosstalk.1 The synaptic crossover and stimulation of sympathetic efferents is believed to be responsible for many of the autonomic disturbances noted in these disorders, particularly the vasoconstriction that leads to further local ischemia and irritant metabolic changes.2,5 The end result is that these supersensitive nerve fibers then become receptive to chemical transmitters along every part of their length instead of only at the end plate terminals (which would otherwise exist under normal physiological conditions).3
The injured axon creates an ongoing ectopic afferent discharge that barrages the CNS.8-11 This primary neuropathic signal is then processed by CNS components, including ascending transmission and descending control with signal processing networks that extend from the spinal cord to the highest levels of cognitive function. In these chronic pain syndromes, the persistent ectopic barrage and strong nociceptive input cause further "hypersensitization" occurring centrally in the CNS, resulting in additional central amplification.1,3,13 This is thought to be one of the main causes of allodynia, which is often associated with myofascial pain syndromes. An additional contributor to the ongoing nature of the ectopic firing may be the dorsal root ganglion itself, which may become a source of persistent ectopic firing whose impulses then flow centripetally, producing and reinforcing the same central amplification effects.1,9
The Role of Lidocaine in Treatment of Neurogenic Lesions
For many decades, articles have appeared in medical literature reporting the resolution of neuropathic pain syndromes by intravenous injection or local infiltration of lidocaine at the site of peripheral nerves enervating regions of neuropathic pain.16 These resolution patterns occurred following even a single treatment, implying that the effect extends far beyond the period that one expects with local anesthesia. Double-blind placebo-controlled studies have shown these effects in a wide range of neuropathic pain states.1,10,12
Some of the earliest literature dates back to 1925 when the German physicians Ferdinand and Walter Huneke reported on their successes of treatment of neuropathic pain syndromes following single injections of procaine.5 A number of German and Eastern European researchers following up on these reports published similar successes. This eventually led to the development of neural therapy, widely practiced in Europe today.
Neural therapy involves the treatment of pain syndromes and other systemic conditions with lidocaine injections at sites of segmental roots, cranial and peripheral nerves, as well as sympathetic ganglion blocks as a regulating therapy in an attempt to ablate what is termed "interference fields." A strong focus on treatment of both the peripheral nervous system and the autonomic nervous system is taught in this practice.
Following publication of these results in various textbooks and articles, several hypotheses on the mechanism of action of lidocaine in the treatment of neuropathic pain syndromes have been suggested, including:10-12
• inhibition of the reverberating intraneuronal circuits; reference to the stabilization of the aberrant axonal loop described previously
• retained plasma concentrations at the site of injection
• centripetal axonal transportation of the lidocaine to the dorsal root ganglion, producing a prolonged effect and imparting an influence on central spinal pain mechanisms
• as yet undiscovered locus of action other than the sodium channel with additional second messenger blocking effects.
To date, no conclusive evidence has clearly delineated the mechanism of action. The pharmacology of lidocaine and its effects on axonal membranes have been well documented and some of its properties seem to provide a unique therapeutic window. Lidocaine appears to have the property of protecting the axonal surface membrane against long-term excitation patterns, and does so in a lower concentration than will produce local anesthesia or interfere with the normal impulse function of the nerve itself.8,10,11,13
Pharmacologically, lidocaine molecules bind to sites associated with voltage-sensitive sodium channels and prevent these channels from opening in response to depolarization stimuli. As noted, it suppresses this ectopic electrogenesis at doses lower than those required to suppress electrogenesis of normal cutaneous and muscle receptor endings and at cardiac pacemaker sites. This relative selectivity may be due to the ability of local anesthetics to block action potentials depending on the axons' firing frequency, thereby blocking ectopic firing in preference to normal impulse generation.13
It has also been suggested that because the lidocaine molecule penetrates the axonal membrane and blocks sodium channels from the inner surface of the axonal sheath, the lidocaine may be picked up in axoplasmic vesicular structures and transported centripetally to the dorsal root ganglion where it may act centrally and have additional pharmacological effects.
In one of the original publications on neural therapy and the use of local anesthetics, Fleckenstein and Hardt suggested an alternative theory on the mechanism of action of lidocaine. They stated that perhaps local anesthetics act as true antagonists in the abnormal electrophysiological and biochemical processes that act locally at the sites of both the neurogenic lesion as well as the targeted muscle group. They proposed that unopposed persistence of the ectopic activity increases the permeability of the membranes leading to a progressive potassium loss and hence, an ongoing state of depolarization, a hypothesis that was supported by Kapoor.1,5 As local anesthetics work by protecting the surface membranes against long-term excitation patterns and effectively sealing the axonal membrane, they prevent this progressive depolarization of the nerve cell by low-power stimuli.
This essentially gives the nerve axon a time out, allowing it to repolarize and drift back to its natural resting state. The restitution of this stable state would then make the nerve axon more resistant to low-power stimuli with the discontinuation of the ongoing afferent barrage to the CNS breaking up the aberrant axonal reflex. The cessation of motor efferent overactivity results in relaxation of the target muscle group, a reversal of the vasoconstriction and local ischemic changes, and clearing of the inflammatory mediators, all elements that contribute to the myofascial pain syndrome.5
Applying the Treatment Model
The neurogenic lesion may not only exist at the terminal end plate but may extend along the peripheral nerve proximally, returning to the dorsal root ganglion. Then, one should treat as much of the nerve along its course as is physically accessible, from the end plate terminals in the soft tissue following the axon proximally back to its termination at the dorsal root ganglion prior to its entry into the spinal cord. In practice, if the points of application are accurate and in close proximity to the neurovascular structure, only 0.5 mL of lidocaine infiltration is required at each site of injection (Figure 1).
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Figure 1. Abberant Axonal
Reverberation Loop
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Many of the textbooks of neural therapy and associated atlases of injection techniques make reference to acupuncture sites as being accessible points to localize the medial and lateral branches of the posterior rami of the spinal nerve roots (the Governing Meridian and Bladder Meridians), peripheral and cranial nerves.5 This is not surprising because acupuncture provides a reliable geographical map to neurovascular structures. Careful dissection of cadaveric material has demonstrated that at most acupuncture sites, the tips of effectively placed acupuncture needles are closely aligned to neurovascular structures.14,17
This provides access not only to the peripheral nerve but also to the accompanying small arterioles and venules that have a rich autonomic nervous supply, and whose aberrant function plays a significant role in the manifestations of myofascial pain syndromes.
The most predominant neural entities relating to acupuncture points are motor points, sites along the axon prior to its entry into the muscle bundle whereby the smallest amount of electrical impulses will trigger a contraction of the corresponding muscle. Other acupuncture points are closely aligned to cranial nerves, the medial and lateral branches of the posterior rami of segmental spinal nerve roots, anastomotic areas of segmental nerve roots such as those in the Governing and Conception Vessel Meridians, or peripheral nerves en route to individual or groups of muscles distally. Acupuncture points also lie at tendon and fascia insertions or musculotendinous transition points. In addition, acupuncture points are closely aligned to venous and arterial structures, both of which have rich autonomic nerve supplies.15
Case Report
A 43-year-old moderately overweight man presented with a 6-month history of persistent low back pain radiating into the posterior pelvic girdle musculature. He reported the pain onset occurring during outdoor yard work. The patient had visited his family physician for a course of anti-inflammatory medications and had attended physiotherapy as well as massage without resolution of the problem. He attempted exercise, but found it difficult to continue because of increasing discomfort. The patient reported discomfort on most days with exacerbations brought on by overactivity and fatigue.
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Table 1. Acupuncture Sites and Rationale as Dictated by the Target Groups of
Involved Muscles
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Acupoints
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Anatomical Landmarks at Needle Tip7,14
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Targeted Muscle7,14
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GV 4 plus bilateral BL 23
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Medial branch of posterior ramus of L2 nerve root (GV 4)
Posterior branch of the lumbar artery (GV 4)
Lateral branch of posterior ramus of L1 nerve root (BL 23)
Posterior rami of 2nd lumbar artery and vein (BL 23)
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Iliocostalis
Longissimus spinalis
Semispinalis
Multifidus
Rotatores
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GV 3 plus bilateral BL 25
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Posterior ramus of L3 nerve root (BL 25)
Posterior branch of the 4th lumbar artery and vein (BL 25)
Medial branch of posterior ramus of the L4 nerve root (GV 3)
Posterior branch of the lumbar artery (GV 3)
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Iliocostalis
Longissimus spinalis
Semispinalis
Multifidus
Rotatores
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Interspinous space
L5-S1 plus bilateral BL meridian
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Posterior ramus of S1 nerve root
Medial branch of the posterior ramus of the L5
nerve root
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Iliocostalis
Longissimus spinalis
Semispinalis
Multifidus
Rotatores
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BL 31 bilateral
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Posterior branches of the lateral sacral artery and vein
Posterior ramus of the 1st sacral nerve
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Piriformis
Biceps femoris
Semitendinosis
Semimembranosus
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BL 32 bilateral
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Posterior branches of the lateral sacral artery and vein
Posterior ramus of the 2nd sacral nerve
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Piriformis
Biceps femoris
Semitendinosis
Semimembranosus
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BL 53 bilateral
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Superior gluteal nerve
Superior clunial nerve
Superior gluteal artery and vein
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Gluteus medius
Gluteus minimus
Tensor fascia lata
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BL 54 bilateral
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Inferior gluteal artery and vein
Inferior gluteal nerve
Posterior cutaneous nerve
Sciatic nerve
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Gluteus maximus
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BL 30 bilateral
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Inferior clunial cutaneous nerve
Posterior femoral cutaneous nerve
Inferior gluteal nerve
Sciatic nerve
Inferior gluteal artery and vein
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Gluteus maximus
Piriformis
Superior gemellus
Biceps femoris
Adductus magnus
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Investigations, including plain films of the lumbar spine and pelvic girdle as well as a computed tomographic scan, demonstrated no abnormalities other than moderate degenerative disk changes compatible with age. Blood tests ruled out systemic arthropathy. Clinical examination revealed tenderness of the supporting musculature of the lumbosacral segments and posterior pelvic girdle, as well as the abductor muscles of the hips with trigger areas. Limitation in range of motion was noted on flexion, side bending, and extension secondary to muscle spasm. Neurological and general examination findings were otherwise unremarkable. Clinical examination suggested a myofascial pain syndrome involving the supporting musculature of the lumbar spine as well as the pelvic girdle.
METHODS
The choice of acupuncture sites as well as the rationale as dictated by the target groups of involved muscles is summarized in Table 1. Each site was marked and infiltrated with a 3- to 5-mm intradermal weal to facilitate dermal anesthesia. An injection of 0.5 mL of 1% lidocaine without epinephrine was infiltrated at each site, in the plane and at the depth as instructed by standard acupuncture treatment texts (Figure 2).17,18
After obtaining written patient consent, the illustrated neural acupuncture treatment plan was performed on the day of presentation and repeated on 2 further occasions at 10-day intervals when progress in level of comfort and function appeared stalled. Following the 1st treatment, with a marked reduction in myofascial pain component, manual therapy techniques to address the dysfunctional movement disorder of the lumbar segments and pelvic girdle were possible, and an aggressive exercise therapy program was instituted to restore the strength and postural support of the supporting musculature. The patient was discharged from care 1 month after presenting and instructed to continue with the outlined exercise programming.
DISCUSSION
There are significant benefits and advantages of neural acupuncture that may not always be realized with traditional electroacupuncture. In addition to the shorter time required for each treatment session with neural therapy, fewer treatments overall are needed. Producing immediate relaxation of the targeted muscle group, lidocaine infiltration also potentiates a prolonged relaxation of the affected musculature. This requires often only 1, and seldom more than 3, treatment sessions over a period of 4-6 weeks to resolve even chronic cases resistant to other physical therapies, including those treated earlier with electroacupuncture.
The quick resolution of the spastic muscle pattern also allows for an earlier institution of an
effective adjunctive manual ther-
apy program to treat the associated biomechanical dysfunctional
movement problems relating to the adjacent joint structures. A concomitant exercise program should also be included to over-
come the inherent weaknesses in the supporting musculature generally noted in cases of longstanding disuse.
Experience has demonstrated that unlike traditional electroacupuncture that may include exacerbations with treatment of "hot" areas, these areas are often where treatment with lidocaine infiltration will result in the greatest benefits.
In my experience and using a visual analog scale, if there is not at least a 30%-40% sustained improvement in level of pain following the 1st or any necessary subsequent sessions persisting for at least 5-6 days, the likelihood is small that repeating the treatment will produce further benefits. Almost all patients will report a marked improvement for the 24-hour posttreatment period; however, unless it is sustained, this should not qualify as a positive response.
Neural acupuncture is like traditional acupuncture in that additional treatments when necessary appear to bestow a cumulative effect. In practice, treatment sessions are generally repeated when progress toward resolution becomes stalled and discontinued when the patient reports that no further benefit was noted following the last treatment. At this point if the treatment has been efficacious, the patient is generally progressed enough in recovery that continuing with exercise and postural correction will generally result in eventual resolution.
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Figure 2. Treatment Plan
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Reprinted with permission from Dr Joseph Wong
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CONCLUSION
Not all cases of myofascial pain can be resolved using neural therapy, probably reflecting the as yet incompletely understood mechanisms and etiologies of myofascial pain syndromes and neuropathic pain patterns. Nevertheless, in my practice, the large percentage of patients that respond continue to make neural acupuncture a therapy of first choice for treatment of myofascial pain syndromes.
Unfortunately, most of the clinical citations in the literature to date relate to individual case studies or small study series without concerted attempts at controlled studies or long-term follow-up. With the recent advances in the understanding of neuropathic pain models, physicians with practices in acupuncture may wish to explore the application of this treatment using their neuroanatomical knowledge gained in the study of acupuncture.
The reported successes in any case suggest that further study with controlled trials is warranted. The outcome of these trials should serve to determine the efficacy and long-term outcome of neural acupuncture in the treatment of these disabling pain syndromes.
ACKNOWLEDGEMENTS
I thank Drs Joseph Wong and Steven Aung for their assistance in reviewing this article, and for encouragement in introducing this ancillary modality into Western acupuncture medicine.
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AUTHOR INFORMATION
Dr Mark Frobb is a specialist in Pain Management with a special focus on Orthopedic Medicine in Surrey, British Columbia, Canada. In addition to being a certified acupuncturist, Dr Frobb's background includes certification in Family Medicine and Osteopathic studies in manual therapy.
Mark K. Frobb, MD, CCFP, CAFCI*
1661-128 St.
Surrey, BC, Canada, V4A 3V2
Phone: 604-531-0444 • Fax: 604-531-0421 • E-mail: mfrobb@shaw.ca
*Correspondence and reprint requests
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