AP and Neurology
GENERAL MECHANISMS OF AP (3/4)
Miltiades_K5 (1996) Neuroscience, neurophysiology and AP: Part 5. There is clear evidence of the analgesic action of AP in this field. Of 1500 articles in Medline, 1100 concern the analgesic action of AP. The most important among these articles concern Lab studies on experimental animals and clinical studies in Vet clinics. APA in animals does not exclude stress-induced analgesia, but excludes suggestion (animals are thought to be immune to suggestion), hypnosis and placebo effect (in part).
Pomeranz[6] gives the following evidence in support of the endorphinergic action of APA: 4 different opiate antagonists abolish the analgesic action of AP. Naloxone abolishes the analgesic effect. A microinfusion of naloxone or the infusion of endorphin antibodies (to the CNS) abolish the analgesic effect. Mice with a genetically reduced level of opiate receptors in the CNS have a poor response to AP. Rabbits with endorphin Xu do not respond to the AP stimulus. During EAP, endorphin levels increase in peripheral blood and in CSF, but decrease in the CNS. Inhibition of enzymatic degradation of endorphin greatly extends the duration of APA. APA is transmissible through plasma (cross circulation) and CSF. Inhibition of pituitary endorphin abolishes APA. An increase of messenger RNA for pituitary pro-enkephalin is observed for 24-48 h after AP.circa 60% of patients suffering from myofascial pain of the lumbar portion of the spinal cord are considerably relieved after the application of warm compresses (43-51oC) or ultrasound and the improvement of symptoms lasts from 90 min to 7 d. On the contrary, the application of EAP to general AP points relieves patients for several wk, mo, or up to 3 yr. This was noted (from Price at al) on 58% of the patients with chronic myofascial pain of the lumbar portion of the spinal cord to which AP was applied. Han suggests that the specific, long-term analgesic effect of AP is due to 2 factors: 1.activation of a neurogenous serotonin and Met-Enk circuit in the upper part of the descending pain inhibition system (in the mid diencephalon). This causes continuous inhibition (at the level of the spinal cord) and the non-conduction of harmful stimuli from the spinal cord to the CNS, and therefore the non-perception of pain and 2.the (peripheral) activation of low-threshold muscular mechanoreceptors. This increases the activity of thick-diameter nerve fibres (pain modulating system) and gives long-lasting inhibition of muscular pain. The long-term analgesic effect of AP is the most difficult point of contemporary theories. Han's theory (1987: mesolimbic analgesia system) may explain one of analgesic mechanisms of AP[39]. At least, activation of "Diffuse Noxious Inhibitory Controls" (DNIC) triggered by nociceptive peripheral stimuli that activates A-delta and C fibres (some forms of AP and moxa) can be an other mechanism of central action of AP and involves complex loops from spinal and supraspinal structures[40,41]. These studies showed that neurotransmitters, opioid and non-opioid substances of spinal cord and CNS, are the main coordinators of the "stimulation - analysis - response" phenomenon and they control the generalised internal chemical reactions of the organism after AP treatment.
Electro-AP analgesia
Electro-APA is well proven[42,43,44]. In general, the lower the frequency (Hz) electrostimulation, the lower the time required to reach maximum analgesic effect and the longer the effect remains. The higher the frequency, the shorter the time required to obtain maximum pain threshold, and the effects remain for a shorter time (table 2 and 3). Also, periaqueductal central grey (PAG) stimulation produced analgesia is similar to APA in many respects.
In other studies Xie-Guo-Xi, Han-Ji Sheng (1985) the high frequency of stimulation of the points of AP has above all metameric local action while, on the contrary, low frequency (1-15 HZ) generalized analgesic action. If the spinal cord is disrupted or transected, no frequency is adequate.
EAP at a frequency of 2 HZ provokes APA mainly through Met-Enk, with 100 HZ mainly through A dynorphin, while with 15 HZ both neurotransmitters are detected in almost equal quantities. More recent work (especially on high frequency current) suggests that the stimulation at a frequency >10 Hz increases enzymatic degradation of circulating opiate substances reducing APA[45].
Also, new electrotherapy techniques (MENS, microcurrent electrical neuromuscular stimulation) and EAP with current intensities in the order of 400 ¥Á at 10-60 Volts (low voltage pulsed microamp stimulation) and extremely long pulse duration with total current equal to 5x10-6 coulombs/s, are awaiting the results of the clinical tests to which they are subjected[46,47]. This technique is based to Arndt-Schulz law that microamperage (¥A) currents are better at enhancing cellular physiology processes than are currents of higher amplitude. Several clinical studies have documented the enhancing effects of MENS on wound healing, on tendon repair in animal models, on recovery of injured athletes suffering from ruptured ligaments and tendons. Also, Lab studies shows the ability to MENS device to stimulate cellular physiology and growth (increased ATP by almost 500%, increased membrane transport by 30-40% and increase protein synthesis by up to 73%).
The endogenous opioid peptides such as endorphin, enkephalin and others are not related exclusively to pain. They are directly related to all forms of dependence (drugs, smoking, alcoholism). Low levels of Met-Enk occur in patients suffering from Parkinson's disease. Very high levels have been reported in the dorsal cochlear nucleus and the intermediate geniculate body in patients suffering of schizophrenia. There is also significant evidence as to their role in the regulation of food intake (obesity). In regard to obesity, many "saturation" peptides and "stimulating appetite" peptides occur in the hypothalamic nuclei of the brain and the gastrointestinal tract, functioning as hormone inhibitors or as neurotransmitters.
Clinically, AP acts on the following body systems[48] (table 4). The action on the above mentioned body systems must be attributed to the ability of AP to influence the function of the CNS.
Nobel-winning neuroscientist Gerald Edelman[49] said that the human brain is a most complex functional structure. The most specialized and exciting type of cell is the neuron. The neuron, the structural unit of the brain, is unusual as regards its shape, its electrical and chemical function and the way in which it connects to other neurons forming networks. The cortex has circa 10 billion neurons. Each neuron connects with others through synapses. There are circa one million billion synaptic connections in the cortex. If we started counting them, at a rate of one synapse/s, we would finish counting after 32 million years. One piece of our brain of a size equal to the head of a match contains one billion synapses. If we tried to calculate the many ways in which synapses may be combined, we would have a number consisting of 10 followed by millions of zeros (the number of positive charged particles in the universe is 10 followed by 80 zeroes). The brain connects with the outer world through specialized neurons called sensory neurons that form the sensory organs and supply the brain with input signals, while output signals are transported to the brain through neurons connected to muscles and glands.
Miltiades_K6 (1996) Neuroscience, neurophysiology and AP: Part 6. The largest areas of the brain, however, exchange signals with some other areas of the brain without any intervention from the outside world. Edelman points out that the brain is more in contact with itself and the interior of the body than with anything else. The corpus callosum connecting the right to the left hemisphere contains 200 million fibres. The brain tissue is a complex network that communicates electrochemically both to the outer and to the inner environment. It emits and receives dynamic formations of signals and answers to these signals. The formations of its neurons influence the functionality of the heart, the kidneys, lungs, the muscles, the skin and the glands. The brain regulates breath, digestion, blood circulation and naturally analyses the AP stimulus.
It is very difficult to explain the action of AP. However, it is not difficult to underline the contribution of AP in the balance of the chemistry of the nervous system and of the role of the hundreds of neurotransmitters that regulate in whole or in part our health and disease, emotional behaviour, instincts, desires and the psychic disposition of man.
Depression is related to a disorder of noradrenalin- and serotonin- metabolism. The antidepressant action of amphetamines and the existence of benzodiazepine receptors in the cerebellum and the limbic system is also known. The role of GABA, a neurotransmitter with an inhibitory role in neurotransmission (through the K+, Na+, Cl- pump) and its intense ancholytic action is perhaps more general[50,51,52,53].
AP is used to treat a multitude of functional disorders such as metabolic diseases, endocrine disorders, mental disorders, functional, respiratory and digestive disorders, allergies, neuroautonomic disorders etc. Reference of the neuronic theory of the action of AP on these disorders is based on one hand on the investigation of the unknown homeostatic role of the reticular formation of the brain matter and on the other on the multitude of neurotransmitters that are detected peripherally after treatment with AP (CCK, bombazine, neurotensin, CRH (corticotrophin releasing factor), dynorphin, neuropeptide Y, enkephalins, amines etc.) and in the mode of action, secretion, activation and enzymatic inactivation of the above mentioned substances. It appears that these substances are similar in action to the classical endocrine gland hormones, activating negative and positive feedback mechanisms. The role of AP in these diseases has been only clinically established.
The reticular formation.
The reticular formation consists of groups of neurons and of neural fibres which unite the cerebral nuclei between them and each one separately with subcortical centres, thalamic centres, cerebellum centres, parencephalic centres, medulla oblongata and spinal cord. Functionally, it controls the mechanisms of wakefulness and those of sleep, muscular tonus, level of consciousness, cardiac and respiratory rhythm, vessel tonus, regulating and mediating motor, autonomic and sensory functions.
On the level of the nuclei of the reticular formation is led almost all information concerning sensibility and in a slow rhythm (because of the multiple synapsis) are transformed and analyzed qualitatively and quantitatively. Due to this analysis, the nervous signal coming from the periphery when it reaches the upper centres (brain nuclei) is differentiated from the initial one. That agree with hypothesis that mechanical, thermal and chemical noxious stimuli have effect on neuron activity of medullary and mesencephalic reticular formation especially around nucleus gigantocelularis (NGC). Also, Casey and Melzack[54] suggested that reticular neurons may mediate the affective/motivational dimension of the pain experience and pain-related behaviour, indicating the role of reticular formation in pain perception and modulation.
This descending modulation system brings significant functional alterations to the peripheral organs. Indeed, implantation of electrodes in areas of the reticular formation of the medulla oblongata and above all outside the cerebral nuclei brought big alterations on a cell, tissue, organic and functional level to the guinea pigs such as hydronephrosis, organic dysplasia, bone deformity etc. According to the information it receives from the sensory pathways, the activating system of the reticular formation may regulate the level of wakefulness of the functional nuclei of the CNS. It can make the body thrive, or repress many symptoms of the body and psyche, such as worry, dyspnoea, sweats, insomnia, irritability, change of cardiac and respiratory rhythm, vessel tonus. Interference with the homeostatic mechanisms of the reticular formation can be achieved only through sensory stimulation. AP can very possibly be a kind of similar stimulation. Particular points such as Ear-points Shenmen, Jerome and Master sensorial point, and somatic points such as HT07, HT03, LI03, GB20, ST41, PC06, BL10 act the equilibrating way mainly on the mental diseases and are used on patients with mental disorders intensely somatised.
Conclusion
The restoration of morphological and functional homeostasis and the maintenance of the dynamic equilibrium of the body that is gradually restored after AP treatment may be explained only if we consider the body as an open thermodynamic system that may transform exogenous influences from the environment and modify the function of its systems accordingly. This consideration constitutes the theoretical basis of Cybernetic systems (cybernetics: the field that deals most directly with information processing and feedback).
In this manner one can sketch today the therapeutic action of AP. The main difficulties to be overcome by doctors before understanding, learning and applying AP are: a profound knowledge of AP theory, the mechanism of action and reaction of the normal and pathological organism, the concept of the organism as a unique whole (Hippocrates), the mental tracing of Qi-circulation in the Channels, and the selection of AP points.
For us, western physicians, traditional applications of AP, derived from sources lost in antiquity but verified in everyday practice, are a starting point but also a signpost for concerns of contemporary Med research.
I point out that the rejection of a method is not a scientific position. In the history of science, the motive force of progress was the innate tendency towards interpretation (and investigation) of natural phenomena. No matter how many problems we shall face in the preparation of research protocols to establish the action, indications, counter-indications and side effects of AP. Their solution will always be the target of Med science.
Besides, the physician is not obliged to study TCM Philosophy in order to exercise AP. However it is necessary that he takes in his hands a weapon tested throughout the centuries, enriching his therapeutic armoury, having as his sole criterion the relief of man from pain. Each addition of knowledge is an addition of human power (HORATIO).
Miltiades_K7 (1996) Neuroscience, neurophysiology and AP: Part 7.
References
1. Stux G; Pomeranz B (1991) Basics of AP. Springer-Verlang, Berlin Heidelberg, pp4-19.
2. Bonica J; Procacci P (1990) General considerations of acute pain. In: Bonica J: The management of pain. Lea & Febiger ed. Philadelphia, pp159-178.
3. Rush TC (1960) Pathophysiology of pain. In: Med physiology and biophysics, 18th ed. WB Saunders, Philadelphia, pp350-368.
4. Morley JA (1937) Visceral pain. BMJ 2:1270.
5. Sinclair DC; Weddell G; Feidel WH (1948) Referred pain and associated phenomena. Brain 71:184.
6. Stux G; Pomeranz B (1991) Basics of AP. Springer-Verlang, Berlin Heidelberg, pp6-7.
7. Bischko J (1986) Intermediate AP. Karl F Haug, Heildelberg, pp49.
8. Lee MHM; Liao JS (1990) AP in physiatry. In: Kottke JF; Lehmann FJ (1990) Krusen's handbook of physical Med and rehabilitation. WB Saunders Co, Philadelphia, pp402-427.
9. Watkins LR; Mayer DJ (1982) Organization of endogenous opiate and non-opiate pain control systems. Science 216:1185-1192.
10. Becher R; Selden G (91985) The body electric. Electromagnetism and the foundation of life. Ed: W Morrow, New York.
11. Tirgoviste I (1993) Teoria si practica acupuncturii moderne. Ed: Academiei Romane, Bucuresti, pp201-248.
12. Rosenthal SR; Sonnenschein RR (1948) Histamine as a possible chemical mediator for cutaneous pain. Am J Physiol 155:186-190.
13. Bonica J; Yaksh T; Liebeskind JC; Pechnick RN; Depantis A (1990) Biochemistry and modulation of nociception and pain. In: John Bonica, The management of pain. Ed: Lea & Febiger, Philadelphia, pp96-120.
14. von Euler US; Gaddum JH (1931) An unidentified depressive substance in certain tissue extracts. J Physiol 72:74.
15. Travell JF; Simons GD (1992) Myofascial pain and dysfunction. Ed: Williams and Wilkins, Baltimore, USA, pp1-4.
16. Melzack R; Stillwell DM; Fox EJ (1977) TPs and AP points for pain correlation and implications. Pain 3:3-23.
17. Cheng SSR (1989) Neurophysiology of EAP analgesia. In: Pomeranz B; Stux G: Scientific bases of AP. Ed: Springer-Verlag, Germany, pp119-135.
18. Garrison WD; Foreman DR (1994) Decreased activity of spontaneous and noxiously evoked dorsal horn cells during TENS. Pain 48:309-315.
19. Fields HL (1978) Pain. Ed: McGraw-Hill, New York, pp90-91.
20. Meyer RA; Campbell JN; Raja SN (1985) Peripheral neural mechanisms of cutaneous hyperalgesia. In: Advances in pain research and therapy 9:53-71, Ed: Fields HL; Dubner R; Cervero F. Raven Press, New York.
21. Kellgren JH (1939) On the distribution of pain arising from deep somatic structures with charts of segmental pain areas. Clin Sci 4:35-.
22. Kellgren JH (1937) Observations on referred pain arising from muscle. Clin Sci 3:176-.
23. Mann F (1977) Scientific aspects of AP. William Heinemann Med. Books Ltd; London, pp10-18.
24. Takeshige C (1989) Mechanism of AP-analgesia (APA) based on animal experiments. In: Pomeranz B; Stux G: Scientific bases of AP. Springer-Verlang Berlin, Heidelberg, pp53-74.
25. Le Bars D; Willer JC; de Broncker T; Villanneva L (1989) Neurophysiological mechanisms involved in the pain-relieving effects of counterirritation and related techniques including AP. In: Pomeranz B; Stux G: Scientific bases of AP. Springer-Verlang Berlin, Heidelberg, pp79-105.
26. Russell A; Scudds AR (1994) Sphenopalatine ganglion block: the final gate to switching off pain?. J Musculoskel Pain 2:137-141.
27. Murray M (1995) Spinal Cord. In: Conn PM: Neuroscience in Med. Ed: JB Lippincott Co, Philadelphia, pp197-209.
28. Waxman GS; De Groot J (1995) Correlative neuroanatomy. Appleton & Lange, USA.
29. Hammermeister EK (1990) Cardiac and aortic pain. In: Bonica J: The management of pain. Lea & Febiger, Philadelphia, 2nd Ed, 2:1001-1016.
30. Anderson SL (1995) AP: from empiricism to science: Functional background to AP effects in pain and disease. Med Hypotheses 45(3):271-281.
31. Pruna S; Bajenaru O; Gheta O; Mota M; Karavis M; Golcea D (1986) Neuroautonomic response recorded by reactometry as indicator of receptivity to AP. Bucharest.
32. Karavis M (1985) Relationships between electrical skin potentials, perception threshold to an electric stimulus and the vibrated sensitivity to patients with or without diabetic neuropathy. Dissertation, Bucharest: Univ of Bucharest.
33. Basmajian VJ (1989) Biofeedback. Ed: Williams & Wilkins, 3rd ed; USA, pp17-27.
34. Kellgren JH (1939) On distribution of pain arising from deep somatic structures with charts of segmental pain. Clin Sci 4:35-46.
35. MacDonald A (1989) AP-analgesia (APA), TENS and vascular effects. In: Wall PD; Melzack R: Textbook of pain (2nd ed), Churchill Livingstone, Edinburgh.
36. Niboyet JEH (199973) L'anaesthesie par l'AP. Ed: Maisonneuve, France, pp59-94.
37. Zhu L; Jiang JW; Wu GC; Cao XD (1993) Changes of endogenous opioid peptides level in RPGL during AP-analgesia (APA). Shen Li Hsueh Pao 45(1):36-43.
38. Zhou L; Wu GC; Cao XD (1995) Role of opioid peptides of rat's nucleus reticularis paragigantocellularis lateralis (RPGL) in AP-analgesia (APA). AETRIJ 20(2):89-100.
39. Baldry PE (1993) AP, TPs and musculoskeletal pain. Churchill Livingstone, 2nd Ed, pp120-124.
40. Le Bars D; Calvino B; Villanneva L; Cadden S (1984) Physiological approaches to counterirritation phenomena. In: Trickelbank MD; Curzon G: Stress-induced analgesia. Wiley Chichester, pp67-101.
41. Le Bars D; Chitour D; Clot AM (1981) The encoding of thermal stimuli dy diffuse noxious inhibitory controls (DNIC). Brain Res 230:394-399.
42. Anderson SA; Ericson T; Holmgren E; Lindqvist G (1973) EAP: Effect on pain threshold measured with electrostimulation of teeth. Brain 63:393-396.
43. Sheng RSS (1989) Neurophysiology of AP-analgesia (APA). In: Pomeranz B; Stux G: Scientific bases of AP. Springer-Verlang Berlin, Heidelberg, pp119-135.
44. Takeshige C; Murai M; Hachisu M (1980) Parallel individual variation in effectiveness of EAP, morphine analgesia and dorsal PAG-SPA and its abolishment by DPA. AETRIJ 5:251-268.
45. Omura Y (1994) Sophia symposium of AP.
46. Picker IR (1985) Low volt pulsed microamp stimulation. Clinical Management Vol 9.
47. Scott O (1994) Sensory and motor nerve activation. In: Kitchen S; Bazin S: Clayton's electrotherapy. WB Saunders Co, London, pp61-80.
48. Omura Y (1976) Pathophysiology of the AP treatment. In: Warren, ZF: Handbook of Med AP. Van Nostrand Reinhild Co, New York, pp87-121.
49. Edelman MG (1992) Bright air, Brilliant fire. Basics Books Inc, USA, pp49-60.
50. Barchas JD; Akil H; Elliott GR; Holman RB; Watson SG (1978) Behavioral neurochemistry: neuroregulators and behavioral states. Science 200:964-973.
51. Anderson EG; Proudfit HK (1981) The functional role of the bulbospinal serotoninergic nervous system. The MIT Press, London, pp307-338.
52. Nieuwenhuys R (1985) Chemoarchitecture of the brain. Ed: Springer-Verlag, Berlin.
53. Holaday JW; Loh HH; Li CH (1978) Unique behavioral effects of b-endorphin and their relationship to hypothalamic function. Life Science 22:1525-1536.
54. Melzack R; Casey KL (1968) Sensory, motivational and central control determinants of pain. In: The skin senses. Ed: Kenshalo JR; Springfield IL; Charles CT, pp423-443.