Local Skin Reaction And Cutaneous Microcurrent Mechanism

Skin, with its neurovascular-immune function, serves as the first line of the body's defense system. When needling breaks the skin, it triggers a cascade of physiologic reactions to the intrusion. The needles encounter the following components of the skin:

1. Afferent somatic neuron fibers (cutaneous AS and C fibers) and sympathetic nerve fibers (for controlling sweat glands and fine blood vessels)

2. Fine arterial and venous blood vessels (nutrition supply and temperature regulation)

3. Lymphatic tissue, mast cells (immune function)

4. Connective tissues (structural and functional support)

When a point changes from a latent phase to a passive phase, local neurogenic inflammation increases its sensitivity. Around this sensitive point, the electrical conductance of the skin increases and its resistance decreases, possibly because of fluid and ions that are present as a result of inflammation. Inserting a needle into this point will provoke an acute local inflammatory defensive response from all the aforementioned skin components. The first visible sign is the flare response, which is the formation of redness (dilation of capillaries) around the needle. This vasodilatation of the autonomic nervous system is mediated by substance P, secreted by cutaneous nociceptive sensory nerves. Then an immune reaction is triggered by mast cells, which produce histamine, platelet-activating factor, and leukotrienes. At the same time, the needle-induced lesion promotes interaction between the blood coagulation system and the immune complement system.

The body surface always has a layer of electric charge because the human body is bathed in the electromagnetic field of the earth. Normally, dry skin has a direct current (DC) resistance of 200,000 to 2,000,000 ohms. At sensitive points this resistance is reduced to 50,000 ohms.7 However, Melzack and Katz8 found no difference in conductance between traditional ISDN points and nearby control points in patients with chronic pain. This phenomenon can be explained by the dynamic nature of the sensitive tissues. It is understandable that the area of sensitized tissue is larger in patients with chronic pain, whereas the same location in healthy persons is less or not at all sensitized. In a healthy person, the DC resistance of sensitive points is the same as for other areas. There is 20 to 90 mV of resting potential across the intact human skin, negative on the outer surface and positive on the inside.9 Most sensitive points show a measurement of 5 mV higher than for nonacupoint areas.7

The insertion of a metal needle makes a short-circuit in the skin "battery," thus generating a microcurrent, called the current of injury, moving from inside to outside. The tiny lesion created by the needle causes a negative potential at the needling site and produces 10 mA of current of injury, which benefits tissue growth and regeneration.10 These microcurrents induced by the needling are not sufficient to initiate nerve pulses to the spinal cord, and so the microcurrents do not create a tolerance to needling in the same way that tolerance develops for drugs such as morphine. This means that repetitive needling will not have a diminishing therapeutic effect. In case of electrical ISDN stimulation for more than 3 hours, however, the analgesic effect does gradually decline. Han11 suggested that perhaps long-lasting electrical stimulation increases the release of cholecystokinin octapep-tide (CCK-8), which is an endogenous antiopioid substances.12 This effect is the body's attempt to maintain the natural balance. Without this balancing mechanism, the positive electrical stimulation and its results would create negative side effects and ultimately destroy the organism.


Needle manipulation is an important technique in classic acupuncture, but not in ISDN. The ancient Chinese doctors believed that needling could not be effective without needle manipulation. Modern clinical evidence indicates that this is not the case and that therapeutic efficacy can be achieved without any manipulation as long as lesions are created. Nonetheless, needle manipulation can add value to ISDN treatment in many cases if the physiologic and mechanical mechanisms of it are understood.

A research team at the University of Vermont College of Medicine has proved that manipulation promotes tissue healing by producing biomechani-cal, vasomotor, and neuromodulatory effects on interstitial connective tissue.3

When a needle is inserted into the body tissue, there is an initial coupling between the metal shaft of the needle and elastic and collagen fibers. This affinity is caused by both surface tension and an attraction between the metal of the needle and the electrical charge of the connective tissue. Once this coupling has occurred, frictional force takes over. Then the rotation of the needle increases the tension of the fibers by winding them around the needle, which pulls and realigns the connective fiber network.12

The experienced practitioner detects the needle's resistance to rotation (needle grasp), and the patient feels some sensation. This "needle grasp" process affects the extracellular matrix, the fibroblasts attached to collagen fibers, and possibly capillary endothelial cells.

As a response to this physical deformation, the cells initiate a cascade of cellular and molecular events, including intracellular cytoskeletal reorga nization, cell contraction and migration, autocrine release of growth factors, and the activation of intra-cellular signaling pathways and nuclear binding proteins that promote the transcription of specific genes. The aforementioned effects lead to synthesis and local release of growth factors, cytokines, vaso-active substances, degradative enzymes, and structural matrix elements. Release of these substances changes the extracellular surroundings of the needled tissue and results in the promotion of healing at this location. These results may also affect more distant connective tissue, thus spreading the healing process with long-term effects. This is how mechanical signals produced by simple manipulation of a needle can generate a cascade of downstream physiologic healing effects.

According to clinical evidence, this type of mechanical signal transduction, which results from correct needle manipulation (rotation or as a piston), may desensitize sensory receptors and restore a normal pain threshold. It is very common, especially with acute injuries, that pain, sensitivity, and swelling subside during or shortly after needling.

The mystery of needle manipulation was clarified by Langevin and colleagues,3,12 and a proper understanding of it is indispensable for clinicians. It is important to understand that although the success of ISDN treatment does not require needle manipulation, clinical practice is enhanced if the practitioner knows how this technique helps reduce tissue stress and promote self-healing.


Needling provides local relief of concurrent muscle shortening and contracture. Local muscle pain stimulates the muscle to generate sensitive points, persistent involuntary contracture, and shortening of the muscle fibers, which results in muscle tension and stiffness. There are four common sources of local muscle pain: (1) mechanical, chemical, or physical injury (e.g., burning); (2) repetitive strain, overstretching, or contraction beyond the muscle's natural limits for a long time; (3) diseased viscera that project pain to the body surface, partially through the mechanism of segmental neuronal reflex; and (4) referred pain associated with a diseased joint and its accessory structures.

Local muscle pain involves afferent sensory fibers (nociceptors), muscle fibers, and blood vessels. The nerve endings of sensory fibers contain neuro-peptides, substance P, CGRP, and somatostatin. Under pathologic conditions, neuropeptides may be released from the sensory nerve endings and influence basic tissue functions such as neuronal excitability, local microcirculation, and metabolism. When tissue-threatening (noxious) stimulation occurs (mechanical, physical, or chemical), neuropeptides are released from the sensory nerve endings, and this triggers a cascade of events that lead to neurogenic inflammation. Substance P and CGRP cause vasodilation and increase the permeability of the microvasculature. Histamine is liberated from mast cells when they are exposed to substance P. All these substances diffuse to neighboring tissue, which results in an expansion of the inflammation.

Once this neurogenic inflammation spreads, fluids and proteins shift from the blood vessels into surrounding interstitial spaces. This process releases vasoneuroactive substances: bradykinin from protein (kallidin) in the blood plasma and serotonin (5-hydroxytryptamine [5-HT]) from platelets. Leukotrienes and prostaglandins are released from the tissue cells surrounding the injured site. All these substances increase the sensitivity of affected nerve endings. Thus the noxious stimuli result in sensitiveness (sensitized nociceptors) and then spontaneous pain (nociceptor excitation) in the localized region of muscle.

When nociceptors are sensitized, their firing threshold decreases. After this kind of physiologic alteration, any slight stimulus, such as light pressure, may cause the nerve ending to fire impulses to the CNS. This same amount of pressure would not elicit any response from normal, unsensitized nerve endings. If the sensitization continues to increase, it may further lower the firing threshold of the nociceptors, and they may spontaneously send impulses to the CNS, which causes a sensation of pain.

Repetitive strain and overuse are common types of muscle activity that cause local pain. If muscles are used in a movement repeatedly without adequate recovery time between repeats, or if they are held under load in a relatively fixed position for prolonged periods, as with unbalanced exercise, then discomfort, soreness, or pain develops, with a peak of discomfort during the first day or two. Pain makes muscles sensitive to palpation; it restricts their range of motion and sometimes causes slight swelling. In this type of injury, some disorganization of the striation of muscle fibers has been observed, and a lack of myofibrillar regeneration could persist as long as 10 days.13 Changes in blood chemistry profiles have been noticed, including increases in plasma levels of interleukin-1, acid-reactive substances, lactic dehydrogenase, serum creatine, phos-phokinase, aspartate aminotransferase, and serum glutamic oxaloacetic transaminase. Most of those enzymes are involved in muscle metabolism.

The literature of Chinese traditional acupuncture indicates that diseased viscera project pain to predictable points or areas on the body surface. This is a manifestation of the segmental mechanism of the viscerosomatic neuronal reflex. For example, an inflamed kidney may cause sensitivity or painful spasm in the lumbar area, resulting in lower back pain with sensitive points palpable from T10 to L5 on the back muscle (erector spinae). For some patients, additional sensitive points may appear in the neck region. This segmental mechanism plays a very important role in treatment of pain symptoms and is discussed in detail later in the chapter. Needling these sensitive points that are associated with diseased organs relieves the pain and other symptoms such as cramping, inflammation, and ulcers.

Joint disease and dysfunction can cause muscle pain. Because of the segmental reflex, the activity of sensory nerves influences the activity of efferent nerves from motor neurons of the same muscle. However, the muscle is also affected by the sensory nerves of neighboring muscles and joints. He and associates14 described how stimulation of knee joint nociceptors excites afferent motor neurons of both flexor and extensor muscles. It is possible that sensory input from a joint will lead to a contraction in neighboring muscles. The contracted muscles may, in turn, put stress on the joint and its accessory structures such as capsules, ligaments, and discs. All these structures will produce pain under these circumstances because they are richly innervated by sensory nerves.

All types of different muscle pathophysiologic processes converge to a similar consequence in the muscles that maintain posture: The muscles become tense, stiff, and shortened, and sensitive points and enlarged contraction knots are formed within the muscles. Some of the contraction knots, if not released immediately, become persistent muscle contracture, which results in a chronic condition.

Sensitized spots are also found in other soft tissue that is richly innervated by sensory nerves such as tendons, ligaments, superficial and deep fascia, and, possibly, periosteum. Modern clinicians call these sensitive spots and contracture trigger points dermopoints, motopoints (neuromuscular attachment points), nodes, and so forth. All of them show some aspects of the acu-reflex points of traditional Chinese acupuncture. Physiologically, these points can be called reflex points.

Sensitive points vary in their histologic composition and pathophysiologic phases. Some consist mostly of sensitized nerve fibers, whereas others, in addition to the sensitized nerve receptors, contain knots of contracted muscle. Internal factors such as diseased organs and arthritis lead to the creation of sensitive points all over the body. Their locations are actually highly predictable, partly because of the segmental mechanism or special features of the sensory nerve fibers. In acute injury, sensitized points are formed according to the type of injury and the body anatomy involved. For example, a mild ankle sprain (inversion injury) causes elongation of ligaments on the lateral side of the ankle, whereas a severe ankle injury may tear the ligaments between the fibula and tibia, as well as the lateral ligaments. With a good knowledge of anatomy, clinicians can find the most effective sensitive points for treatment.

Any muscle, tendon, or fascia that harbors sensitive or painful points may resist stretching and may become tense, stiff, shortened, and painful. Most sensitive points used for pain treatments are on muscle, but points on tendons, ligaments, and fasciae are of the same importance and should not be ignored clinically.

Before pathologic contracture is discussed, it is important to review membrane depolarization and the five stages of healthy muscle contraction.

Depolarization can be simply described as follows: When a cell is not agitated (Fig. 6-5), the outside of the cell membrane is electrically positive and the inside is negative. When electric impulses or bioactive molecules stimulate a cell, positive Na+ ions flow into the membrane so that the outside

Lipid bilayer

Ionic pump

Figure 6-5 Differential distribution of ions inside and outside of plasma membrane of neurons and neuronal processes. Ionic channels for Na+, K+, Cl-, and Ca2+ are shown. Concentration of the ions (in parentheses) are given in millimoles except that for intracellular Ca2+. ADP, Adenosine diphosphate; ATP, adenosine triphosphate; E. „ , extracellular calcium; E_, extracellular chloride;

Ca2+ Cl

Ek, extracellular potassium; ENa, extracellular sodium;


Lipid bilayer

Ionic pump

Figure 6-5 Differential distribution of ions inside and outside of plasma membrane of neurons and neuronal processes. Ionic channels for Na+, K+, Cl-, and Ca2+ are shown. Concentration of the ions (in parentheses) are given in millimoles except that for intracellular Ca2+. ADP, Adenosine diphosphate; ATP, adenosine triphosphate; E. „ , extracellular calcium; E_, extracellular chloride;

Ca2+ Cl

Ek, extracellular potassium; ENa, extracellular sodium;

Pi, inorganic phosphate.

becomes less positive, which means that electricity flows into the cell. Then positive K+ ions flow out to restore the polarity of the outside. Finally, Na+ ions are pumped out and K+ ions are pumped in, by molecular channels, so that the concentrations of Na+ outside and K+ inside are restored. This represents one cycle of depolarization (Figs. 6-6 and 6-7). The depolarization consumes metabolic energy.

All five stages of muscle contraction are related to depolarization and energy consumption:

1. Electrical impulses from the CNS travel along the motor neuron fiber and reach the nerve terminal to depolarize the terminal membrane, which causes the terminal (nerve ending) to release acetylcho-line into the space of the neuromuscular junction.

2. The acetylcholine in the junction space depolarizes the membrane of muscle cell (the postjunctional membrane).

3. In the muscle cell, a membranous organelle, the sarcoplasmic reticulum, attaches to the cell membrane and stores calcium. The depolarization of the cell membrane causes depolarization of the sarcoplasmic reticulum, which results in the release of calcium into the cell plasma.

Figure 6-6 Depolarization, or generation of the action potential, is associated with an increase in membrane Na+ conductance and K+ current. Activation of Na+ channels allows Na+ to enter the cell, depolarizing membrane potential. ENa, Extracellular sodium; gK, conductance of potassium; gNaa, conductance of sodium; IK, intracellular potassium; INa, intracellular sodium.

Figure 6-6 Depolarization, or generation of the action potential, is associated with an increase in membrane Na+ conductance and K+ current. Activation of Na+ channels allows Na+ to enter the cell, depolarizing membrane potential. ENa, Extracellular sodium; gK, conductance of potassium; gNaa, conductance of sodium; IK, intracellular potassium; INa, intracellular sodium.

Schwann cell

Direction of propagation

Direction of propagation

■ Distance ■

Schwann cell


Myelin B 1-20 |im


Myelin B 1-20 |im



Internode 300-2000 |im

Figure 6-7 Propagation of the action potential in unmyelinated (A) and myelinated axons (B and C). A, The direction of depolarization is from region 3 to region 1. Region 3 starts repolarization after depolarization. Region 2 is undergoing depolarization. Vm, membrane voltage. B, In vertebrate myelinated axons, the axon is exposed to the external medium at the nodes of Ranvier. C, Action potential is generated at the nodes of Ranvier, at which the Na+ channel is of high density. Conduction velocity is greatly increased in myelinated fibers.

4. The high concentration of cytoplasmic calcium stimulates two long linear molecules, actin and myosin, to move against each other so that the muscle cell becomes shortened.

5. After this contraction, calcium ions are pumped back into the sarcoplasmic reticulum through channels on the membrane of the sarcoplas-mic reticulum. The concentration of cytoplas-mic calcium thereby declines, which leads to a decoupling of actin and myosin. In this way, the muscle relaxes to its original length. If a person wants to maintain a posture, he or she voluntarily sends continuous impulses to the relevant muscles to keep coupling actin and myosin, and the muscles will maintain this contraction until the person stops sending these impulses.

These steps represent normal physiologic contraction.

The same steps are compared with the mechanism of pathologic contraction in Chapter 3, but it is reviewed briefly here because it is a very important mechanism in clinical ISDN practice. Simons15 provided a very good explanation of this process with the name "energy crisis hypothesis." His hypothesis is modified as follows (Fig. 6-8):

1. When afferent sensory nerves are sensitized (the location feels sensitive) or excited (pain is felt at the location), efferent motor nerves are activated to release excess acetylcholine into the neuro-muscular junction space.

2. Excess acetylcholine prolongs depolarization of the postjunctional membrane.

3. This results in longer depolarization of the membrane of the sarcoplasmic reticulum and leads to a longer period of high concentration of cytoplasmic calcium.

4. The high concentration of cytoplasmic calcium prolongs actin-myosin coupling. The sustained shortening of the muscle cell compresses local blood vessels. This compressed microcirculation (ischemia) obstructs the provision of energy and reduces oxygen supply.

5. The actin-myosin coupling continues because the concentration of cytoplasmic calcium remains high, and molecular pumps cannot return the calcium to the sarcoplasmic reticulum because the energy supply is low or absent.

Dry Skin Mechanism
Figure 6-8 Energy crisis hypothesis (suggested by Dr. David G. Simons). Energy metabolism and the cellular process of muscle fiber contracture in a sensitive acu-reflex point. SR, Sarcoplasmic reticulum.

This is how ischemia, hypoxia, low energy supply, and muscle shortening continue to develop into a vicious circle unless interrupted by appropriate treatment. Muscle that is in contracture during such an energy crisis has a higher temperature than does normal muscle tissue. This pathologic contraction is endogenous, not initiated by voluntary impulse, and may persist indefinitely. According to clinical experience, any method of interrupting this energy crisis helps relax the muscle and reduce pain. Needling, electrical stimulation, physical stretching, proper exercise, and injection of appropriate drugs are all procedures that can be used to separate actin from myosin to relax the shortened muscle, thus breaking this energy-consuming vicious circle.

It was suggested earlier in this chapter that manipulation of the needle deforms connective fibers and that this mechanical signaling induces tissue healing. According to clinical evidence, manipulation also helps to stretch muscle and break the energy crisis at some acu-reflex points. Needling can precisely target and release endogenous contracture deep inside the muscle. The processes just described prove the effectiveness of needling for muscle relaxation, restoring local blood circulation, and promotion of tissue healing without any side effects. If local sensitization or endogenous contracture is acute and localized, muscle relaxation can be achieved immediately; otherwise, more treatments are needed.

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