15: Electroacupuncture Analgesia

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CHAPTER 15 Electroacupuncture Analgesia

INTRODUCTION

Electroacupuncture is not unanimously defined. Professor Ji-sheng Han of Beijing University states that when electrodes are placed on the surface of the skin, and when “the point of stimulation is selected according to traditional acupuncture, the process is usually called electroacupuncture (EA).” The same process, if the points used are not traditional acupoints, is regarded as transcutaneous electrical nerve stimulation (TENS).1

Neurophysiologically, there is no difference between the two concepts of EA and TENS. The same author also indicated that, “they operate through very similar, if not identical, mechanisms.”1 Different acupoints may have a different anatomic configuration (see Chapter 1), but sensory nerve fibers are the universal component of any acupoint. Because these fibers are distributed all over the body except nails and hair (which is why we can cut them without pain), acupoints can be found anywhere on the body.

If surface electrodes are placed on a sensitized (tender) point, whether it is a traditional acupoint or not, peripheral stimulation will be provided to the spinal cord through the sensitized nerve endings, which helps to desensitize and calm down the irritated nerve. If the surface electrodes are placed on nonsensitive points, the electrophysiologic process resulting from this peripheral stimulation is exactly the same as with the stimulation of tender acupoints, but with less therapeutic results in terms of desensitizing the painful sensory nerves. As we have already mentioned, the number of traditional and extra-meridian “new” acupoints has reached more than 2500 (see Chapter 1), which means that documented acupoints can be found almost everywhere in the body.

Another method also described as electroacupuncture is the use of needles as electrodes, inserted into the tissue, which is called percutaneous electrical nerve stimulation (PENS). Physiologically PENS is different from both EA and TENS because with PENS needles are used to create both tissue lesion and electrical stimulation. Even though EA, TENS, and PENS all stimulate the release of the natural neurochemicals, including endorphins, produced by the central nervous system, PENS with its induced lesions involves other healing mechanisms that are similar to manual needling (see Chapter 3).

Despite the different ways of defining and using peripheral electrical stimulation, all these modalities do the same thing: activating the self-healing mechanisms of the body by balancing physiologic processes. For example, the release of the central nervous system (CNS) opioid peptides known as endorphins is a shared physiologic basis for these modalities, and these substances are physiologic de-stressors whose release can be triggered not only by electrical stimulation or needling, but also by exercise, physical manipulation, and massage.

The therapeutic use of electricity for pain relief can be traced back to Egyptian medicine some 4500 years ago. They used electric fish to treat painful conditions. In Greek medicine, doctors used electric torpedo fish to treat headaches and arthritis (400 bc).

Electrotherapy was revived in modern times after Drs. Ronald Melzack and Patrick Wall proposed their Gate Control theory of pain in 1965 (see Chapter 3). This theory stated that the input of pain signals from the fine nerve fibers (such as C fibers or A-δ fibers) is controlled and modified in the spinal cord by the signals from the large nerve fibers (such as A-β fibers) before the pain signals reach the brain. The spinal cord functions like a gate in that it can be open or closed to the incoming pain signals. For example, if a person hits his finger with a hammer, the C nerve fibers in the finger start to fire pain signals to the brain through the spinal cord, so the brain perceives the finger pain. Then the person might rub or scratch the painful finger. By doing this, the large, low-threshold A-β fibers are activated. Their signals travel faster than those of the fine C nerve fibers, and activate the spinal cord to block the pain signals of the C nerve fibers. This is a simplified picture of the Gate Control theory. A recent study using the techniques of molecular biology has supported the concept that endorphins in the spinal cord exert a strong inhibitory effect on incoming pain signals.2

When Dr. Patrick Wall, an expert in pain and spinal cord physiology at St. Thomas’s Hospital Medical School in London, and Dr. William Sweet, chief of neurosurgery at Harvard Medical School, realized that the large A-β fibers can be easily activated by electrical stimuli, they developed in 1967 an apparatus for TENS. They placed electrodes on the surface of the skin and used high-frequency electrical stimulation (50 to 100 Hz) to relieve chronic neurogenic pain. Today, battery-operated, solid-state TENS apparatuses are popular medical devices for the treatment of many painful conditions, and are used also by physical therapists and patients themselves.

In the late 1960s, Chinese doctors also started to combine the use of electrical stimulation with acupuncture after some successful experiments with acupuncture anesthesia. Their electrical acupuncture devices were designed to apply electric current to needles inserted into acupoints. As China was isolated from the rest of the world at that time, their development of electrical acupuncture is probably independent of the invention of TENS by Drs. Wall and Sweet.

In the early 1970s, Hans Kosterlitz and his student John Hughes were studying the action of narcotics in the University of Aberdeen in Scotland. They discovered that the brain makes its own natural narcotics, which they named endorphins, from “endogenous morphine.” At almost the same time, Sol Snyder and his student Candace Pert at Johns Hopkins University in Baltimore confirmed that the body makes endorphins, which counteract pain among other physical functions.

These discoveries supported the possible endorphin mechanisms of acupuncture needling and TENS. Today we understand that endorphins can be stimulated in many different ways, including acupuncture needling, TENS, psychological process, chiropractic manipulations, exercise, and massage. In addition to counteracting pain, endorphins also have other physiologic functions such as rebalancing the cardiovascular system (bringing blood pressure to normal), hormonal secretions, defense immune activities, and so forth. In general, endorphins naturally normalize the body’s function and bring a slight feeling of euphoria.

Four different endorphins, β-endorphin, enkephalin, dynorphin, and endomorphin, have so far been identified. Which of the four endorphins are stimulated depends on the frequency of electrical stimulation, and this frequency-dependence is a valuable feature of the clinical use of EA and TENS.

The research done in the past 2 decades has clearly laid down the guidelines of how to use TENS or EA to achieve maximal pain relief. Here we will discuss only what is needed for clinical use of TENS or EA. We will not go into physiologic details such as the involvement of calcium channels, antibody reactions, or different receptors. Readers who are interested in knowing more about EA and TENS may refer to the relevant published information.

FREQUENCY-DEPENDENT RELEASE OF ENDORPHINS BY PERIPHERAL ELECTRICAL STIMULATION AND THE ANTIENDORPHIN FEEDBACK INTERACTION

The stimulation of EA and TENS is transmitted by A-β and A-δ nerve fibers. Since the parameters of the type of stimulation used with EA and TENS can be reliably and precisely calibrated, it is possible to identify the physiological effects of peripheral electrical stimulation at different frequencies. This frequency-dependent nature of endorphin release has been confirmed in both laboratory animals and human subjects.3

Enkephalin and endomorphin are mostly released at 2 Hz, whereas dynorphin release is triggered during 100 Hz stimulation. The release of β-endorphin is triggered at a rate of 2 Hz then gradually decreases as the frequency is increased.

It has been shown that if the stimulation alternates between 2 and 100 Hz, the full release of all four endorphins is achieved, which induces synergistic analgesic effects.4

In addition to opioid peptides, other neurochemical analgesic factors are also triggered by peripheral electrical stimulation. Midbrain monoamines such as serotonin and norepinephrine have been confirmed to play a role in EA analgesia.5,6 Recently it was discovered that brain-derived neurotrophic factor (BDNF) is released by 100 Hz stimulation in bursts, but not by constant 100 Hz stimulation.7 BDNF has been shown to reverse the dying of neurons in animals.8

Part of the brain (ventral periaqueductal gray [vPAG]) reacts to both low frequency (2 Hz) and high frequency (100 Hz), but other parts react to only one frequency: the arcuate nucleus of the hypothalamus (ARH) to low frequency and the parabrachial nucleus (PBN) to high frequency.

The body’s wisdom in ensuring the survival mechanism is always ahead of human intelligence. The release of natural endorphins to reduce the body’s pain and stress is a natural physiologic process, but we try to use the electrical stimulation to change this physiological process into a pharmacologic process. Our body has a built-in mechanism to prevent overuse of its natural narcotics (endorphins): the release of antiendorphin peptides through negative feedback. Data from animals show that the analgesic effect of endorphins declines when EA stimulation is prolonged for more than 3 hours due to the release of antiendorphin antagonists (antiopioid peptides).9

Low-frequency stimulation (2 to 15 Hz), triggers the release of endomorphin, enkephalin, and most β-endorphins, but these frequencies also cause the release of their antagonist peptides, substance P (SP), angiotensin II (AII), and cholesystokinin octapeptide (CCK-8). High-frequency (100 Hz) stimulation significantly increases the release of antagonists AII and CCK-8.1

Attention should be paid to the interesting and clinically meaningful fact that low-frequency stimulation (2 Hz) only marginally induces the release of CCK-8 and SP, 50% less than with high-frequency stimulation. It is not difficult to draw the conclusion that high-frequency stimulation releases more antiopioid peptides than low-frequency stimulation because the brain perceives high frequencies (100 Hz) as a more artificial and alien modality than low frequencies (2 to 15 Hz). From birth, low-frequency peripheral electrical stimulation is a common experience to the baby’s brain because touch, pressure, rubbing, needling, cuts, and minor injury all transmit low-frequency electrical impulses to the brain by means of the peripheral nerve receptors.

All the laboratory and clinical experimental data indicate that to elicit the maximal release of central opioid peptides (endorphins), electrical stimulation should alternate between 2 Hz and 100 Hz to achieve the synergistic effect of TENS and EA analgesia.1

TECHNICAL PARAMETERS OF TENS AND EA

The purpose of electrical analgesia is to electrically depolarize the nerve endings to produce nerve impulses to the brain through the spinal cord. With a modern EA or TENS apparatus the stimulation parameters can be very easily regulated. The practitioner needs to set up (1) frequencies, (2) modes (constant, burst, or alternative, if they are available), and (3) pulse width. All TENS apparatuses have the option of using square wave or biphasic current (Box 15-1).

Box 15-1 Parameters of Electrical Stimulation Using TENS or EA

Modified from White A: Electroacupuncture and acupuncture analgesia. In Filshie J, White A, editors: Medical acupuncture: a Western scientific approach, New York, 1998, Churchill Livingstone, p 157.

Wave Form

Omura suggested that a square wave produces the optimal depolarization,11 so almost all modern TENS apparatuses output square waves.

ACUPOINT SELECTION FOR TENS OR EA USING THE INTEGRATIVE NEUROMUSCULAR ACUPOINT SYSTEM

Proper acupoint selection can greatly enhance the efficacy of TENS and EA treatments. Skin resistance is lower when an acupoint becomes tender, that is, when nerve endings and/or other soft tissues become sensitized. Like the manual needling of tender acupoints, direct electrical stimulation accelerates the desensitization of the sensitized or inflamed nerve endings and other soft tissues.

The Integrative Neuromuscular Acupoint System (INMAS) provides guidance for selecting the highly effective therapeutic acupoints, especially for neuromuscular pain in the lower back, buttocks, and lower and upper limbs, because all 24 HAs usually show a notable degree of tenderness in more than 80% of people. In cases of acute pain, most of the acute tender points appear around the regional HAs.

Here are a few examples of acupoint selection for TENS and EA. For treating lower back pain, the pair of acupoints can be H15 and H16, H14 and H16, or H14 and H18, depending on whether the pain is located in the lumbar, sacral, or iliotibial region. For treating shoulder pain, the pair of acupoints can be H3 and H8, or H13 and H8, and other pairs of tender acupoints localized around the glenohumeral joint. For leg pain, the pair of acupoints can be H11 and H10, H4 and H6, or H24 and H6, depending on the painful muscles involved.

The general principle of acupoint selection is that the current should travel through the painful muscles or tissues.

CAUTION AND CONTRAINDICATIONS WHEN USING TENS AND EA

A few safety guidelines should be kept in mind when using TENS and EA.

ELECTROACUPUNCTURE AND MANUAL ACUPUNCTURE

Both EA and manual acupuncture (MA) activate the self-healing potential of our body. Maintenance of body homeostasis requires the integrated coordination of every physiologic system, but there are four that play the leading role in linking all the systems together to sustain life: the nervous system, immune system, endocrine system, and cardiovascular system.

EA with its strong and continuous electrical stimuli and muscular vibration activates all these systems. For example, EA stimulation of the central nervous system triggers neurochemical releases such as endorphins and serotonin in the spinal cord and the brain, and activates systemic and local blood circulation. The local muscular vibration created by EA relaxes the muscles and improves regional blood circulation.

EA has been extensively used for pain management since the late 1970s after TENS was invented, and it was particularly popular in the early 1980s. The parameters of EA stimulation can be precisely controlled, recorded, and reproduced, and this is why EA has been extensively studied in laboratory research. Using genetically and developmentally standardized laboratory animals, sufficient neurophysiological data have been obtained in both animal and human subjects to support the clinical application of EA over the past 2 decades.

The essential mechanism of EA is the electrical stimulation of A-β nerve fibers with varying frequencies to induce the release of different CNS opioid peptides, which relieve pain and other physiological stress to achieve self-healing. The secondary mechanism of EA is the rhythmic physical vibration of the muscles, which helps to relax tightness and improve blood circulation, which accelerates self-healing.

Some kind of MA stimulation has been used in Egyptian, Greek, Chinese, and other folk medicines for more than 3500 years. Before metal needles were available, ancient healers used sharpened stones, bamboo needles, and broken porcelain to pierce or puncture the tissues to effect healing. It can be imagined that early acupuncture “needling” created much more severe lesions and possible scars. The modern acupuncture needle creates an elegant and less painful lesion without scar formation while it can reach much deeper to relax muscular contracture.

The essential mechanism of MA consists of the needling and the tiny needle-induced lesion in the tissues that stimulates A-δ and C nerve fibers. MA and its lesions are interpreted by the body as foreign invaders and thus induce a series of physiologic processes including the release of CNS opioid peptides and an antiinflammatory reaction. MA produces a weaker electrical stimuli to the central nervous system than does EA, but the needling directly desensitizes the damaged peripheral nerve endings and other soft tissues by activating a local immune reaction and the process of tissue regeneration. MA-induced lesions break and dissolve histologic contracture of the muscles, which helps to improve blood circulation.

Low-frequency EA (2 to 4 Hz) has a mechanism that is closer to MA. So some researchers refer to low-frequency EA stimulation as acupuncture-like stimulation. More research data are needed to investigate the therapeutic potential and differences between the working mechanisms of EA and MA.

When we look at the history of EA and MA, it is obvious that stimulation by accidentally produced lesions similar to those used in acupuncture has been an indispensable part of our built-in survival mechanisms in both phylogenetic evolution (evolution of the species) and ontogenetic development (our personal development from a newborn baby to senior adult). In our daily life, we are often exposed to numerous kinds of tiny lesions and injuries. Without self-healing mechanisms, we would not survive even a minor injury. Our body has developed self-protective mechanisms to exploit the effect of these small lesions and injuries to promote healing. Manual acupuncture uses the same lesion-induced self-healing mechanisms that have been genetically programmed into the body’s survival strategy; therefore MA treatments can be repeated as often as needed without causing physiologic adaptation that might reduce efficacy after repeated treatments.

Compared with MA, EA with its well-controlled parameters and frequencies is a new type of stimulation that is not genetically programmed into the body’s survival strategy. Prolonged electrical stimulation of the nervous system to release opioid peptides will be balanced by the release of antiopioid peptides. Thus, long-term application of EA results in reduced effectiveness due to the physiologic adaptability of the central nervous system to external stimulation.

Pain can be caused by psychological factors, biochemical processes, and structural abnormalities. Biochemical processes include the chemicals released from injured tissues such as prostaglandin or substance P that irritate the nerves and cause pain. Structural abnormalities happen when muscle contracture is formed within the muscles or a vertebral disk is ruptured. EA stimulation using alternating frequencies with the resulting synergistic release of opioid peptides will combat the biochemical process of pain production. MA does not induce release of the whole spectrum of opioid peptides as EA does, but it triggers other defense reactions and healing mechanisms such as the antiinflammatory reaction and the structural breaking of mild muscle contractures. It is possible that EA will provide better results in treating drug addiction. Both EA and MA have limited efficacy with psychogenic pain, although the opioid peptides (endorphins) do have a mild effect of euphoria.

EA and MA target different nerve fibers. Needling mechanically stimulates the A-δ and possibly C nerve fibers, while EA stimulates the vibration-sensitive A-β nerve fiber (Types II and III) as described by Drs. Wall and Sweet. Clinically this suggests that EA may play a role in the gate control mechanism by blocking pain signals from A-δ and C fibers. MA needling may activate local physiologic mechanisms to desensitize painful A-δ and C fibers.

As a result of extensive clinical observation, Dr. John W. Thompson, a physician and clinical pharmacologist in the University of Newcastle, England, noticed that “A striking and puzzling difference between analgesia produced by TENS and acupuncture (needling) is the duration of pain relief. Whereas TENS usually produces analgesia for minutes or hours, acupuncture can, and usually does, produce analgesia for days or weeks (after a course of acupuncture). The mechanisms discussed above (the author is referring to the CNS neural pathways and the production of opioid peptides) cannot account for the prolonged analgesia commonly seen after acupuncture (needling), so additional mechanisms must be involved.”12

Dr. Anthony Campbell of the Royal London Homoeopathic Hospital also indicated that “It is important to make sure that the patient…realizes that the pain may well return soon after the (TENS) machine is switched off. This is not, however, invariably the case; in some fortunate people relief of pain may last up to 10 hours.”13

In Chapter 6 we introduced the quantitative method to classify the patients into four groups: A, B, C, and D. Each group responds to manual acupuncture differently. Our clinical experience indicates that excellent therapeutic results can be achieved in group A patients (28%) by either MA or EA. In general, the observations of Drs. Thompson and Campbell match the results seen most commonly in patients of groups B and C (34% and 30%, respectively).

References

1 Han J-S. Acupuncture: neuropeptide release produced by electrical stimulation of different frequencies. Trends Neurosci. 2003;26(1):17-22.

2 Cheng HYM. DREAM is a critical transcriptional repressor for pain modulation. Cell. 2002;108:31-43.

3 Han J-S, et al. Effects of low- and high-frequency TENS on met-enkephalin-Arg-Phe and dynorphin: an immunoreactivity in human lumbar cerebrospinal fluid. Pain. 1991;47:295-298.

4 Chen XH, et al. Optimal conditions for eliciting maximal electoacupuncture analgesia with dense and disperse mode stimulation. Am J Acupunct. 1994;22:47-53.

5 Zao FY, Han JS. Acupuncture analgesia in impacted last molar extraction: effect of clomipramine and pargyline. In: The neurochemical basis of pain relief by acupuncture: a collection of papers 1973-1989. Beijing: Beijing Medical Science; 1989:96-97.

6 Mayer DJ, Watkins LR. Multiple endogenous opiate and nonopiate analgesia systems. Kruger L, editor. Advances in pain research and therapy, vol 6. New York: Raven. 1984:253-276.

7 Gartner A, Staiger V. Neurotrophin release from hippocampal neurons evoked by long term potentiation-inducing electrical stimulation patterns. Proc Natl Acad Sci U S A. 2002;99:6386-6391.

8 Ma Y-T, Hsie T, Frost D. Brain-derived neurotrophic factor (BDNF) reduces the death of retinal ganglionic neurons in rat. J Neurosci. March 1998;18(6):2097-2107.

9 Han J-S. Opioid and antiopioid peptides: a model of Yin-yang balance in acupuncture mechanism of pain modulation. In: Stux G, Hammerschlag R, editors. Clinical acupuncture scientific basis. Berlin: Springer; 2001:56.

10 White A. Electroacupuncture and acupuncture analgesia. In: Filshie J, White A, editors. Medical acupuncture: a Western scientific approach. Edinburgh: Churchill Livingstone; 1998:157.

11 Omura Y. Basic electrical parameters for safe and effective electro-therapeutics (electro-acupuncture, TES, TENMS (or TEMS), TENS and electro-magnetic field stimulation with or without drug field) for pain, neuromuscular skeletal problems, and circulatory disturbances. Acupuncture and Electro-Therapeutics Research. 1987;12:201-225.

12 Thompson JW. Transcutaneous electrical nerve stimulation (TENS). In: Filshie J, White A, editors. Medical acupuncture: a Western scientific approach. Edinburgh: Churchill Livingstone; 1998:190.

13 Campbell A. Methods of acupuncture. In: Filshie J, White A, editors. Medical acupuncture: a Western scientific approach. Edinburgh: Churchill Livingstone; 1998:31.