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

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