Clinical Acupuncture: Scientific Basis


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Most helpful customer reviews on Amazon. August 18, - Published on Amazon. Verified Purchase. This should be a must read for every acupuncture student near graduation. The front part it's a slow read, highly technical if you aren't a neurologist, but still worth getting through.

It has a few good tidbits that will be used in my practice, but especially it gives context to what kinds of research is being done and why. January 20, - Published on Amazon. I read this book over 20 years ago and glad to find a copy on Amazon. If you are really interested in scientific knowledge of how acupuncture works, it is a good book for you. Remember: the book is not for leisure reading.

August 31, - Published on Amazon. This is a useful adjunct to the pocket text by Stux and Pomerantz, but does not stand alone as a text for acupuncture. I would recommend it as a secondary text for those who already have one of the standard clinical texts, such as Deadman or Macciocia. Even less well understood is the action of cell 6 onto cells 12 and 13, the pituitary hypothalamic complex. Cell 12 in the arcuate nucleus may activate the raphe via ]3-endorphin, and cell 13 in the hypothalamus may release [i-endorphin from the pituitary gland from cell 14 Fig.

While there is some agreement that AA is accompanied by elevated beta-endorphin in the CSF [ ] and blood and that pituitary lesions suppress AA [42], there is no agreement on how the 3-endorphin from the pituitary reaches the brain to cause analgesia. Too little of it reaches the blood to cross the blood-brain barrier in sufficient quantities. Some evidence suggests that the pituitary-portal venous system can carry hormones in a retrograde direction directly to the brain [13].

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Perhaps cell 14 can influence cell 9, as shown by the thin arrows in Fig. If so, the role of circulating endorphins in the blood is unclear. However, there is an important correlate of pituitary endorphin release: adrenocorticotrophic hormone ACTH and ]3- endorphin are coreleased into the circulation on an equimolar basis [19, ]. They stem from a common precursor.

The ACTH travels to the adrenal cortex, where cortisol is released into the blood [43], which may explain why acupuncture is helpful in blocking the inflammation of arthritis and the bronchospasms of asthma the doses of cortisol released by acupuncture are small and finely regulated, thus avoiding the side effects of cortisol drug therapy.

Real acupuncture versus fake acupuncture: the only contest that matters

Because of insufficient data, other centers implicated in the AA-endorphin effects have been left out of our description. These include the nucleus accumbens, amygdala, habenula, and anterior caudate [77, Its role in AA has been suggested but never clearly established [ 14]. The spinal site uses enkephalin and dynorphin to block incoming messages with stimulation at low frequency and other transmitters perhaps gamma- aminobutyric acid, or GABA with stimulation at high frequency.

The midbrain uses enkephalin to activate the raphe descending system, which inhibits spinal cord pain transmission by a synergistic effect of the monoamines, serotonin, and norepinephrine. The midbrain also has a circuit which bypasses the endorphinergic links at high frequency stimulation. Also, the hypothalamus sends long axons to the midbrain and activates the descending analgesia system via [3- endorphin. This third center is not activated at high frequency stimulation but only at low frequency.

What is the practical significance of this three-level system? When needles are placed close to the site of pain or in the tender trigger, or Ah Shi points, they are maximizing the segmental circuits operating at cell 7 within the spinal cord while also bringing in cells 11 and 14 in the other two centers Fig. When needles are placed in distal points far from the painful region, they activate the midbrain and hypothalamus-pituitary cells 11 and 14 without the benefit of local segmental effects at cell 7.

Moreover, cells 11 and 14 produce analgesia throughout the body, while cell 7 produces analgesia only locally. Local segmental needling usually gives a more intensive analgesia than distal nonsegmental needling because it uses all three centers. Generally, the two kinds of needling local and distal are used together on each patient to enhance one another. Numerous studies have shown that the types of analgesia produced by these two approaches are quite different [2]: the low frequency method produces an analgesia of slower onset and, more importantly, of long duration, outlasting the 20minute stimulation session by 30 minutes to many hours.

Also, its effects are cumulative, improving increasingly after several treatments. In contrast, the high frequency, low intensity analgesia is rapid in onset but of very short duration and with no cumulative effects. Many authors have arbitrarily described the low frequency, high intensity type of analgesia as "acupuncture-like" transcutaneous electrical nerve stimulation TENS and the high frequency, low intensity type as "conventional" TENS.

Because low frequency, high intensity analgesia produces a cumulative effect, repeated treatment produces more and more benefit for the patient [, , or laboratory animal This could be due to long-lasting effects of endorphins in the low frequency system. In contrast, low frequency acupuncture need only be given daily or twice a week because of its long-term cumulative effects [ Indeed, too frequent application of low frequency acupuncture produces tolerance. For example, if applied continuously for 6 h, the analgesia weakens and finally disappears This effect is cross-tolerant with morphine tolerance [, and the mechanisms involved may be similar to those of addiction to endorphins.

Hence, spacing the acupuncture treatments with long enough intervals may prevent tolerance while promoting the cumulative effects. Perhaps the failure of some Western clinics to achieve success is due to the use of very infrequent treatments e. In some clinics in Asia, patients are treated daily for a month, then weekly for 6 months, and the results reported anecdotally are excellent. Of course, some patients will never respond to acupuncture for various reasons; nonresponders may be genetically deficient in opiate receptors.

We have shown that mice genetically lacking endorphin receptors respond poorly to acupuncture [ ]. Other failures may be due to deficiency in endorphin molecules; rats lacking endorphin compounds respond poorly to acupuncture []. Some nonresponders can be converted to responders by treatment with the safe drug jd-phenylalanine, which potentiates endorphins [39, 51, ]. In clinical practice, a strategy must be developed to allow nonresponders to be recognized while not aborting therapy too soon for potential responders who might show delayed cumulative effects. One way is to decide after five treatments: if there is no benefit whatsoever, abort; if mild to moderate effects occur, continue and reassess after treatments.

Often, the cost of repeated office visits is prohibitive. Most books might have ended the discussion of AA right here. However, because acupuncture is relatively new to Western medicine and so controversial, more data are needed to convince students that the acupuncture mechanisms outlined in Figs. Those who are in a hurry can skim or skip the next few pages but should nonetheless scrutinize the reference list this omits the huge literature from China which, if included, would double the number of citations. It should be apparent that we know more about AA than about many chemical drugs in routine use.

For example, we know very little about the mechanisms of most anesthetic gases but still use them regularly. Perhaps the most exciting experiments which opened up the field of AA to scientific research were those in which endorphin antagonists e. That naloxone could antagonize AA was reported initially by two groups [ , ]. Studying acute laboratory-induced tooth pain in human volunteers, Mayer et al. In a double-blind design, they gave one group of subjects IV naloxone while another group received IV saline. The saline group achieved AA with a time course typical for clinical reports 30 min to onset of analgesia and effects lasting for over 1 h.

The naloxone group showed no AA. As no controls received naloxone alone, one might argue that naloxone hyperalgesia simply subtracted from the analgesia of AA. However, this is probably not the case, since numerous studies on acute laboratory- induced pain have shown that naloxone alone rarely produces hyperalgesia [57]. This suggests that endorphins do not have a basal tone during acute pain.

Mayer et al. The other early naloxone study was by Pomeranz and Chiu [ ] in awake mice; they used the mouse squeak latency paradigm and gave electroacupuncture EA at L1. Numerous control groups were used in this latter experiment in an attempt to determine some of the possible artifacts.

The results were unequivocal: naloxone completely blocked AA, sham EA produced no effect, and naloxone alone produced very little hyperalgesia not enough to explain reduction of AA by subtraction. Moreover, the results in mice and in humans indicated firstly that AA was not a psychological effect and secondly that AA truly was blocked by naloxone. In a later study, Cheng and Pomeranz [36, 37] produced a dose-response curve for naloxone and found that increasing doses produced increasing blockade. In a third study in anesthetized cats [ ] recording from layer-5 cells in the spinal cord cell 2 in Fig.

Since these early papers, there have been numerous studies in which systemically administered endorphin antagonists have been used to test the endorphin-AA hypothesis. Although most researchers reported naloxone antagonism [25, 28, 32, , 46, 53, 62, 78, 93, 97, 98, , , , , , , , , , , , , , , , , , , some found no effects of naloxone [ 1, 30, 31, , , , Three of these seven failures were obtained with high frequency, low intensity stimulation, which is probably not endorphinergic [ 1, , In one of the failures low intensity stimulation was used which did not lead to De Qi sensations.

In spite of this, four of seven subjects in that study showed naloxone antagonism. While the reasons for the other three negative papers [30, , are not entirely clear, a possible explanation has emerged. Antagonists work best when given before the treatment [ , ] and fail to reverse analgesia that has already been initiated. Thus, naloxone can prevent AA but often cannot reverse it. In the three failed experiments, researchers tried to reverse AA, giving the endorphin antagonist after, not before the acupuncture treatments. In biology, negative results are often less valid than positive ones.

A few weeks after the first naloxone results were announced in the research news section of Science [ ], a letter to the editor in the same journal justifiably criticized the use of naloxone as the sole proof of the AA-endorphin hypothesis This criticism is based mainly on the argument that naloxone might possess unknown side effects unrelated to opiate receptor blocking.

Small doses which were effective in preventing AA in man 5. However, since that letter was written, 17 different lines of experimentation have emerged which have independently provided support for the AA- endorphin hypothesis: 1. Many different opiate antagonists block AA [ 37]. Naloxone has a stereospecific effect [36, Microinjection of naloxone or antibodies to endorphins blocks AA only if given into analgesic sites in the central nervous system [ 15, 45, 67, 72, 73, , , , , , Mice genetically deficient in opiate receptors show poor AA [, ].

Rats deficient in endorphin show poor AA [, Endorphin levels rise in blood and CSF during AA and fall in specific brain regions during AA [5, 45, 52, 74, 77, 83, 90, , , , , , , ].

Acupuncture Studies

AA is enhanced by protecting endorphins from enzyme degradation [39, 45, 51, 54, 63, 82, 91, , , Reduction of pituitary endorphins suppresses AA [42, lll, , , , , There was a rise in messenger RNA for proenkephalin in brain and pituitary. This lasted 48 h after 30 min of EA, indicating a prolonged increased rate of enkephalin synthesis.

This could explain the enduring effects of EA and the potentiation of repeated daily treatments [60, ]. There is cross-tolerance between AA and morphine analgesia, implicating endorphins in AA [33, 34, AA is more effective against emotional aspects of pain. This is typical of endorphins []. Lesions of the arcuate nucleus of the hypothalamus the site of [3-endorphins abolishes AA; this is cell 12 in Fig. Lesions of the periaqueductal gray site of endorphins abolishes AA []. The level of c-Fos gene protein which measures increased neural activity is elevated in endorphin- related areas of the brain during AA [59, 96, ].

Evidence suggests that, in addition to monoamines mediating Hz EA effects, dynorphin one of the three endorphins may also be involved. Thus, at Hz there is an elevation of dynorphin levels in the dorsal horn of rat spinal cord [] and there is an elevation of dynorphin A in lumbar punctures in humans receiving Hz EA [69, 70].

Moreover, rats given EA at Hz show AA, which is blocked by the dynorphin kappa antagonist norbinaltorphimine , while the EA at 2 Hz is blocked by mu and delta antagonists, suggesting involvement of enkephalins and [i-endorphin at these lower frequencies [34, 35]. Moreover, antisense nucleotides for c-fos or c-jun successfully blocked the EA-induced preprodynorphin mRNA [60].

In summary, 17 different lines of research strongly support the AA-endorphin hypothesis. Despite so much convergent evidence for this hypothesis, skepticism persists: 1. Some cite the few failures of naloxone to reverse AA [31]. It has already been suggested above that naloxone reversal experiments are prone to difficulty because naloxone prevents but does not reverse AA. Moreover, the number of successful naloxone antagonisms of AA far exceeds the number of failures 28 successes versus 7 failures. In general, negative results in biomedical research are less reliable than positive results.

Some state that naloxone antagonism is necessary but not sufficient evidence [75]. That is why we have presented 17 different lines of evidence only one line of evidence depends on naloxone. Some attack the animal studies of AA as being unrelated to AA in humans [31]. Firstly, there have been numerous experiments in humans with the same AAendorphin outcome as in lower animals. Secondly, the similarity of results across many species proves the generality of the phenomenon.

Thirdly, there is no proper objective measure of pain in man. Fourthly, if skeptics are correct, then the entire animal "pain" literature should be discarded, a literature which provided our initial insights into endorphins, brain stimulation analgesia, TENS, and other results that have been highly applicable to human pain. Some are concerned that AA in animals may be merely stress-induced analgesia which also releases endorphins and hence has nothing to do with acupuncture in humans [ At a conference on stress-induced analgesia at the New York Academy of Sciences, we gave a lecture entitled "Relation of stress-induced analgesia to acupuncture analgesia.

Sham EA on nearby nonacupuncture points in animals induces no AA, thus controlling for stress [27, 43, 55, 56, , , , ]. AA elicited in anesthetized rats and cats or decerebrate cats does not involve psychological stress [27, 55, 56, , , , , , , ]. AA at one frequency is endorphin-mediated while, at another, it is serotoninmediated. Yet both give similar levels of stress [38, Many mechanisms of stress analgesia are very different from those of AA. Results in mice and rats were obtained with mild stimulation activating A beta nerve fibers, a nonpainful procedure no more stressful than sham point stimulation [, , ].

In conclusion, the objections raised by a few skeptics are easily refuted. The overwhelming evidence supports the AA-endorphin hypothesis. Zhang [] reviewed other differences between AA and stress analgesia: 1. AA is reversible with naloxone but stress analgesia is only partly antagonized by large doses of naloxone 20 times higher than that for reversing AA.

Plasma cyclic adenosine monophosphate cAMP levels decrease during AA but rise during stress analgesia. The periaqueductal gray is essential for AA but not for stress analgesia. Dorsolateral spinal cord lesions eliminate AA but not stress analgesia. Nevertheless, a note of caution is needed here. One such experiment involves the rat model used by Professor Han of Beijing Medical University which has been challenged by Professor Mayer of the University of Virginia [].

There are numerous papers implicating the midbrain monoamines in AA, especially serotonin and norepinephrine. As the raphe magnus in the brainstem contains most of the serotonin cells in the brain, lesions which destroy these cells or their axons in the DLT would presumably impair AA if serotonin were involved. Such lesions also abolish morphine analgesia, which is mediated by descending inhibition via the raphe-DLT-serotonin system [7]. Numerous experiments show that lesions to this system in animals block AA , 48, 87, , , ]. Moreover, antagonistic drugs which block serotonin receptors also block AA in mice , ].

In the above tests of the serotonin-AA hypothesis, the drugs were given systemically usually IP. However, local microinjection studies produced surprising results, suggesting that the descending serotonin-1 LT inhibitory system may not be as important as the raphe projections to the forebrain: intrathecal injections of serotonin antagonists over the spinal cord produced no blockade of AA in rats , while lesions of the ascending raphe tracts caused a selective decrease in cerebral serotonin and a correlated decrease in AA in the rat [65]. Microinjection of serotonin antagonists into the various brain regions confirmed the importance of ascending serotonin pathways; AA was blocked by injections into the limbic system and the midbrain PAG [65].

Enhancement of AA was observed in mice [40] and rats [65] when serotonin was increased by giving 5-H'I'P a precursor of 5-HT systemically or intracerebroventricularly [65, ], the latter route being more effective than the intrathecal route. The importance of serotonin in AA has also been confirmed clinically in patients using the serotonin uptake blocker clornipramine, where AA was potentiated in a double-blind study All this leaves us with the questions of why a lesion of the DLT in the spinal cord inhibits AA [] if spinal cord serotonin does not mediate AA effects and whether the DLT contains other transmitters that mediate AA.

Mayer and Watkins suggest that a synergism between descending serotonin and norepinephrine is the possible answer ]. Indeed, Hammond [64] showed that combined intrathecal antagonists for serotonin and norepinephrine produced the best antagonism of descending analgesia produced by brainstem stimulation. Perhaps this should be tried for AA, since combined intrathecal antagonists should block AA more effectively than single antagonists.

There have been studies on the effects of norepinephrine alone, without serotonin on AA. Intrathecal injection of a norepinephrine antagonist blocked AA, showing the importance of descending norepinephrine pathways [66]. Clearly, the monoamine story needs more work. If synergism of descending serotonin and norepinephrine is important, then combined intrathecal blockers should be used in all future studies of monoamines in AA. The relative roles of the ascending and descending tracts need to be clarified.

In conclusion, there is no doubt that the monoamines serotonin and norepinephrine play a role in AA. Serotonin projections from the raphe to higher centers may mediate AA. Descending projections to the spinal cord via the DLT may work synergically with descending norepinephrine effects to block pain transmission in the spinal cord. The arcuate nucleus of the ventromedial hypothalamus and the pituitary gland contain all the ]i-endorphin cells in the brain [ 16].

As the arcuate cells have long axons, [i-endorphin is found in other brain loci, but it all originates from the hypothalamic cells []. The arcuate cells can produce analgesia via these long axons stimulating the midbrain PAG, for example. Lesions of the arcuate nucleus abolish AA in rats [ There is a good deal of confusion regarding the possible relationship of the pituitary hormonal [3- endorphins to pain modulation. We have already mentioned the evidence lesion and blood biochemistry studies implicating pituitary endorphins in AA.

Involvement of the pituitary in other forms of analgesia has also been studied. For example, stress-produced analgesia is at least partly mediated by pituitary [3endorphins [ ]. Here problems arise, because pituitary ablation is a very unreliable technique. Moreover, injection of the drug naloxone could have side effects. To make matters worse, in some species e. A new route for pituitary endorphins to reach the brain while bypassing the barrier has been discovered [13, ] in the hypothalamic pituitary portal system reverse flow occurs.

Perhaps more important than the pituitary release of endorphins is the corelease of adrenocorticotropic hormone ACTH which occurs during AA , , , because this stimulates the adrenals to raise blood cortisol levels after AA , 43, 99, Sham acupuncture does not raise blood cortisol levels , 99], thus ruling out stress as the cause of cortisol release.

It is tempting to speculate that this cortisol mediates the treatment effects of acupuncture in arthritis, effects which seem to go beyond analgesia [ Similarly, asthma might be helped by cortisol release , , ]. In conclusion, the evidence for the mediation of AA by endorphins is very strong, while that for the involvement of monoamines needs more work to verify the possible synergism of serotonin and norepinephrine.

Moreover, the circuits depicted in Figs. The question of the existence of acupuncture points, or acupoints, has been explored in several ways: 1. By comparing the effects of needling at true points versus sham points 2. By studying the unique anatomical structures at acupoints 3.


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By studying the electrical properties of skin at acupoints 4. By studying the nerves being activated by acupuncture at acupoints. Several experimenters have shown that, for acute laboratory-induced pain in human subjects, needling of true points produces marked analgesia while needling of sham points produces very weak effects [23, 29, ]. These results were clear-cut, because effects of sham point stimulation are nonexistent in acute laboratory pain. Therefore, to show statistical significance in the differences between sham point needling and true point needling requires huge numbers of patients at least per study ; and experiments that would allow definitive conclusions have not yet been done [ Because of these problems, the specificity of acupoints in humans has been shown only in acute pain studies but has yet to be properly studied in patients with chronic pain, where the number of patients studied has never exceeded the required statistical minimum of [].

In animal studies in mouse [, cat [27, 56], horse [43], rat [, ], and rabbit [55, ], many researchers have shown that true acupuncture works better than sham needling in acute pain studies. These results are consistent with the research on acute pain in humans. In such studies, it is important to use mild stimulation in awake animals to avoid inducing stress: strong stimulation of sham sites could cause stress-induced analgesia []. Stress analgesia is a well-documented phenomenon [ ] that is often mediated by endorphins. If the stimulation used is very strong, animals are highly stressed by both true and sham point needling.

Hence, numerous studies on acute pain in animals and humans clearly demonstrate that AA from needling true points is far superior to AA from needling sham points. However, more studies are needed to make the comparison in chronic pain. Despite several histological studies of the skin and subcutaneous structures under acupoints, no unique structures have been found. However, several authors [61, , ] have made the astute observation that the majority of acupuncture points coincide with trigger points. For example, Melzack et al. This suggests that needles activate the sensory nerves which arise in muscles.

This agrees with findings that stimulation of muscle afferents is important for producing analgesia [44, , ]. The work of Travell on trigger points, begun in [] and culminating in a large book published in [, shows that there are small hypersensitive loci in the myofascial structures which, when touched or probed, give rise to a larger area of pain in an adjacent or distant referred area. She observed that "dry needling" with needles containing no drugs of these trigger points produced pain relief.

When sites are tender, the Chinese call them Ah Shi points, and needling of them is recommended. Trigger points can often be found outside muscle bellies, in skin, scars, tendons, joint capsules, ligaments, and periosteum [ ]. Travell stresses the importance of precise needling of trigger points, as missing the tense knotted muscle fiber could aggravate the problem by causing spasms. Similarly, strong electrical stimulation should be avoided. Thus, mild stimulation with needles inserted directly into trigger points is recommended [].

The majority of trigger points are located on or near the following acupoints: SI. Although the cause of trigger point tenderness is unknown, one possibility is that poor inactivation of calcium by muscle sarcoplasmic reticulum causes calcium to cross-link the actin and myosin, with ensuing permanent contracture. How needling rectifies this problem, however, is unclear []. In decreasing order of importance, he found: 1. Large peripheral nerves. The larger the nerve, the more effective. Nerves emerging from a deep to a more superficial location.

Cutaneous nerves emerging from deep fascia. Nerves emerging from bone foramina. Motor points of neuromuscular attachments. A neuromuscular attachment is the site where a nerve enters the muscle mass. This is not always the actual neuromuscular synapse, which may lie a few centimeters further along the nerve, after it has divided into smaller branches. The pathophysiological significance of this neuromuscular attachment is unknown. Travell emphasizes that many authors have used the term "motor point" interchangeably with "trigger point," but in most cases these are not at the same locations [ ].

Blood vessels in the vicinity of neuromuscular attachments. Nerves composed of fibers of varying sizes diameters. This is more likely on muscular nerves than on cutaneous nerves. Bifurcation points of peripheral nerves. Ligaments muscle tendons, joint capsules, fascial sheets, collateral ligaments , as these are rich in nerve endings. Suture lines of the skull. It is obvious from this list that no particular structure dominates at acupuncture points.

Perhaps the major correlate is the presence of nerves, be they in large nerve bundles items or nerve endings items 9 and If replicated, this finding could be the morphological basis for acupoints [79]. The abolition of AA by injection of local anesthetics into an acupoint before stimulation begins [44, ] strongly suggests that nerves are important for this phenomenon Sect. However, we should not rule out other mechanisms to explain the effects of acupuncture in immunological, allergic, and other non-AA phenomena.

One can speculate on the possible release of arachidonic acid from lesioned membranes during needling, giving rise to leukotrienes and Prostaglandins, which could affect immunity. Also, currents of injury electric currents generated from a hole in the skin might be important for nerve regeneration Sect. It would be easy to find out if local anesthetics prevent all acupuncture effects as they do for AA, but few experiments have been done on nonanalgesic effects.

Evidence suggests the existence of channels which may correlate with meridians. Vernejoul et al. They compared migration of the isotope using a gamma camera after injection into acupoints with injection into nonacupoints. They claimed that vertical lines of migration were seen only from acupoints. These extended as far as 30 cm within 5 min and resembled meridian lines in their distribution. Moreover the migration velocity was altered under pathological conditions. From the photographs in the papers, however, it was difficult to draw conclusions. Also, one must rule out lymphatic drainage.

Several reports have favored venous drainage as the explanation for this isotope migration, raising serious doubts about this method for studying meridians [94, , , ]. Replications by other laboratories are definitely needed before conclusions can be drawn from this controversial research. There have been a number of reports that the skin resistance impedance over acupuncture points is lower than that of surrounding skin [8, 26], but this result has been attributed to pressure artifacts from electrodes [ , , ].

Normally, dry skin has a DC resistance in the order of million ohms. At acupuncture points, this is down to ohms in the studies claiming unique properties of acupoints. These observations have led to the marketing of "point finders," pencil-shaped metal- tipped probes attached by wires to an ohmmeter.

Clinical Acupuncture: Scientific Basis - Buku Google

The circuit is completed by a second electrode in a hand-held metal cylinder with large skin contact on the sweaty palm and hence with a low resistance in the order of ohms. This can be read out on a Wheatstone bridge or directly on a meter. Most devices produce a beeping tone whose frequency or intensity is proportional to the resistance being measured. This allows the clinician to move the roving pencil probe around the body surface while listening to the tones.

Anecdotal reports suggest that these devices work best in certain regions e. It is further claimed that, during disease of particular organs, the resistances at acupoints are abnormally low, even lower than the usual low resistance at acupoints but see [ ]. Indeed, the Japanese Ryodoraku method of measuring the acupoint skin resistance on the body has been in widespread use in Japan since its introduction by Nakatani in [], while Nogier and the French school [] have made observations at ear acupoints see also [ This was further developed by Nechushkin in the s.

There have been two careful experiments performed to validate the claims of ear "point finders" [, ]. Oleson et al. The researchers were blind to the Western diagnosis to ensure that no clues were available to them. Amazingly, the correlation between ear diagnosis and Western diagnosis was Melzack and Katz [] could find no difference in conductance between acupuncture points and nearby control points in patients with chronic pain [ ] when they measured skin resistance in the ear. Unfortunately, neither Ryodoraku nor the Voll machine has been validated by similar controlled studies. Moreover, further claims for the Voll machine that homeopathic remedies placed in parallel with the measuring wires can modify the readings and thereby indicate appropriate treatments for the diagnosed ailment have never been scientifically tested [88].

Until recently, we were quite skeptical of the entire skin resistance phenomenon. This was because the measurements were not made in accordance with established biophysical practice. Neither the published reports [8, 26, , ] nor clinical anecdotal observations were based on properly conducted studies, as pointed out by others , , , We improved the methodology. Preliminary results to date suggest that acupuncture points do sometimes have lower impedance than surrounding skin.

Whether or not this is true, the point finders commercially available are very unreliable We have no idea what the physiological significance could be, if any, of low resistance at acupoints. It is known that sweating has a profound effect on skin resistance; this forms the basis of lie detector tests. Stress, which activates the sympathetics, causes sweating and a drop in skin resistance. In a preliminary study, we determined that sweating occurs uniformly over the skin surface, equally at acupoints and over the surrounding skin.

Moreover, the earlobe is practically devoid of sweat glands, yet resistance phenomena are claimed to occur there as well [] but see [ We have not yet validated the claims of a drop in resistance during disease; if this phenomenon proves to be true, the pathophysiological mechanism is unclear. Can sympathetics affect local sweating during disease? Why should this be localized to acupoints when sweating normally appears to be diffusely organized? It is also unclear why, acupoints in normal people should have a low resistance. Could the presence of a large nerve, emerging from deep tissues to more superficial layers, induce skin changes?

Another finding at acupuncture points is the presence of a voltage source [8] i. Unfortunately, as mentioned above for resistance, most of these voltage measurements did not use state of the art biophysical methodology. This is particularly unfortunate, as electrochemical potential artifacts produced at the electrode-skin interface are large compared with the millivolts being generated by the body. An outstanding study was published by Jaffe et al. Nevertheless, one can speculate that acupuncture points, having low resistance, tend to short-circuit this battery across the skin and hence give rise to a source of current in a source-sink map of the skin.

In other words, acupuncture points provide a path of least resistance for currents driven by the mV resting potential which exists across the entire skin, which is consistent with the 5 mV readings mentioned above [8]. An important measurement in the same paper by Jaffe et al. Preliminary results [] indicate that insertion of acupuncture needles into the skin might also produce a current of injury which has biological influences on the underlying tissues. Indeed, our team has reported that weak currents only mA promote nerve growth in the leg of an adult rat when applied through acupuncture needles [, , , ].

In China, over patients with Bell's palsy of the seventh nerve have been reported anecdotally to benefit from EA and plain needling []. Perhaps the current of injury caused by needling and generated by the mV resting potential across the intact skin promotes nerve regeneration in these cases. It is important to note that in a weak DC electric field, nerves grown in cell cultures will grow branches toward the electrodes [ Moreover, this growth is maximal in the direction of the negative pole [ The papers from our laboratory also show enhanced nerve growth toward the negative pole of the applied DC field [, , , ].

Holes made by needles would also cause a negativity at the site of injury due to the current of injury. Regeneration of amputated amphibian limbs has been shown to be enhanced by applied electric fields and currents in the direction of the negative pole [ 17]. Although this has not been shown in adult mammals, there is indirect evidence of its effects in humans.

If children suffer accidental amputation of the distal phalanx, it will completely regenerate with nail, fingerprint, etc. The latter allows a current of injury which is negative distally and about 1 mA in amplitude [84]. In paraplegic guinea pigs, DC fields and currents have also been implicated in bone healing, plant growth, embryology, and spinal cord regeneration ]. Preliminary studies on normal human volunteers in our laboratory indicate that needling the skin produces a decrease in local skin resistance which lasts days []. A simple calculation using Ohm's law suggests to us that a small hole created by an acupuncture needle can create a current of injury 10 mA sufficient for possible benefit to tissue growth and regeneration [17, ].

It should be noted that these tiny currents would not be sufficient to initiate nerve impulses, and hence the mechanisms shown in Figs. Attempts to use Kirlian photography to study acupuncture cannot be trusted, as this method is so fraught with artifacts. Perhaps the most intriguing phenomenon related to the meridians are propagated sensations along the meridians PSM. The speed of transmission of PSM is approximately 10 cm per sec, which is 10 times slower than the slowest conducting C-fibers [ 10, Moreover PSM does not follow somatosensory distribution of the nerves or restrict itself to one or two dermatomes.

Professor Bossy has proposed a plausible mechanism which does not involve Qi transfer along the meridians but rather a neurological one [24]. He proposes that the neural message travels from the acupoint into the spinal cord and then up and down several spinal segments i.

The brain then perceives this as a sensation traveling into these dermatomes, i. Electrophysiological evidence given below indicates that stimulation of muscle afferent fibers types II and III produces De Qi sensations [], which in turn send messages to the brain to release neurochemicals endorphins, monoamines, cortisol. In a review, Omura emphasized the importance of eliciting strong muscle contractions to optimize AA; this, he says, requires low frequency EA to avoid tetanic contractions Strong muscle contractions are elicited because the stimulus intensities required to activate the type III afferent fibers must be 5 to 10 times the threshold for the muscle efferents.

One of the earliest and most clear-cut papers on the subject was published by Chiang in [44].

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In it he showed that the essential correlate of analgesia was a De Qi sensation: the feeling of numbness, fullness, and sometimes soreness [44]. Moreover, whenever De Qi was blocked, so was AA. Experiments have been done in animals [27, 55, ] showing that procaine injections also abolish AA. To rule out the role of circulating compounds released by acupuncture, he also repeated these experiments with an arm tourniquet: when the De Qi persisted, so did the AA.

Another important finding in Chiang's paper was the lack of target specificity: acupuncture of points in the arm produced equal AA in all parts of the body, as measured by skin analgesia tests [44]. He did not test the arm itself, or he would have seen a stronger segmental effect there. Two other studies showed the same lack of target specificity in humans in acute laboratory-induced pain [ , ]. This lack of target specificity is consistent with the mechanisms shown in Fig. Since they stimulated true acupoints, they observed widespread AA effects. We interpret all these findings as follows: the acupoint maps are essential for localizing the sites where the best I e Qi can be achieved i.

In that sense, the points are specific. However, the further claim of traditional Chinese medicine that the points are also targetspecific may not be true. The referring site you are going to visit is not controlled by us, so please remember not to enter your private information unless you are sure this is not scam. You are about to be redirected to another page read Clinical Acupuncture: Scientific Basis online.

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