AP and Neurology
GENERAL MECHANISMS OF AP (2/4)
Miltiades_K1 (1996) Neuroscience, neurophysiology and AP: Part 1. Adapted from WWW. The Web-Journal of AP, Home Page of Karanikiotes Charisios MD, Dip.Ac.karanik@med.auth.gr (Karavis Miltiades MD DipAc. 2 Alkmanos str., 11528 Athens, Greece, Tel:+30 1 7220542, Fax:+30 1 7293345).
Abstract
Neuroscience provides an understanding of the organization and physiology of the nervous system. This understanding is based on an appreciation of the structure of the nervous system and on the relationship between his structure and function. The human CNS is extraordinarily complex.The brain is composed of circa 1012 cells (neurones). These cells uniquely possess specialized processes for receiving (dendrites) and transmitting (axons) information. These stimulus - response systems permit our body to be in contact with environmental fluctuations. Several thousand types of nerves, neurotransmitters, receptors and chemical mediators compose this fundamental system. AP, as needling therapy, is a kind of specialized sensory stimulation that is analyzed through sensorineural pathways.
To understand the action of AP we have to analyze the Anatomy, physiology and physiopathology of Nervous System. This effort is helped by the knowledge of contemporary neuroendocrinology and chemoarchitecture of the brain. Many neural theories are developed to explain the mechanisms of action of AP. It is now quite clear that AP reacts in local, regional (spinal cord) and general (brain) levels. Therefore, placing one or more needles on a particular point (or area) of the body activates neural pathways on 3 different levels provoking local, regional, and general reactions: a.The local reaction is a multifactorial phenomenon. The electric injury potential due to the needle, the synthesis of opioid peptides at the place of the injury, the Substance-P, histamine like substances bradykinin, serotonin, proteolytic enzymes all around the needle, occurred during every needling therapy. b.The regional reaction concerns the activation of an largest area (23 dermatomes) through reflex arches. We can analyze the viscerocutaneous, cutaneovisceral, cutaneomuscular and visceromuscular reflexes and also the autonomic, stretch and polysynaptic segmental reflexes. c.
Miltiades_K2 (1996) Neuroscience, neurophysiology and AP: Part 2.
For example, consider the placement of a needle (needling) at ST36 at a depth of 3 cm. This point is in the lower limbs, 1 cm outside the front margin of the leg and 3 cm below the tibial convexity (motor point of the anterior tibial muscle). This stimulation will cause:
a. Local sensory stimulation of the area of the leg that is sensorially innervated by the cutaneous branch of the major saphenous nerve (neurotome L3-L4).
b. Stimulation of sensory receptors and mechanoreceptors of the anterior tibial muscle (motor innervation by the deep radial nerve, L4, L5, S1 neurotome).
c. Vasoconstriction or vasodilatation (depending on the stimulation parameters) of the front tibial artery, that supplies arterial blood to the skin and muscles of the area.
d. Myochalasis, that will influence all groups of muscles that have a common neurotomal distribution in the L5 myelotome and in particular on the long extensor of the big toe (L4, L5, S1), the long and short tibial muscle (L4, L5) and the major gluteal muscle (L5, S1, S2) and finally.
e. Activation of serotoninergic and endorphinergic pain modulation systems (central action).
For these reasons, ST36 is selected for stimulation in all cases of back pain or sciatica with L4-S1 pain distribution, with or without neurological findings.
Stux and Pomeranz,[6] formulated the hypothesis that 3 centres are activated by AP to release chemical transmitters that block pain messages.
a) The spinal cord that uses enkephalin and dynorphin (low frequency) and perhaps GABA (high frequency).
b) The midbrain uses enkephalin to activate the raphe descending system which inhibits spinal cord pain transmission by a synergic effect of the monoamines, serotonin and norepinephrine.
c) The hypothalamus-pituitary uses endorphin.
Johannes Bischko,[7] analysing the control loop theory (feedback mechanism) states that every AP point displays at least 4 criteria:
1. Local action.
2. Regional action.
3. An action extending beyond a certain region and.
4. General action.
Watkins and Mayer[8,9] proposed the possible activation with AP (and other physical agents) of 6 different endogenous analgesic systems: neural opiate, hormonal opiate, neural non-opiate, hormonal non-opiate, unknown opiate and unknown non-opiate systems.
We could say that by placing a needle on a particular point (or area) of the body, nervous pathways are activated on 3 different levels provoking: 1.Local reactions concerning an small area of 13cm; 2.regional (segmental) reactions concerning an area of 13 dermatomes, and; 3.general reactions concerning a massive response from the CNS. We will analyze the action of AP at these 3 levels: periphery, spinal cord and CNS.
Local action of AP stimulation
This action of AP is localised in a small skin area, is due mainly to the tissue lesion caused by placing the needle on the skin and concerns all AP points without exception (non-specific action of AP points).
Deactivation of superficial painful skin points.
The local reaction is the result of many factors. Initially, the difference in electric potential existing between the needle and the layers of the skin where it is placed, the difference in temperature between the needle and the skin and the quality of the needle, creates a galvanic current of low intensity. That means that the needle is a source of microenergy[10,11].
This electric current can stimulate the cell membrane to increase its permeability and transform the accumulation of Na and K ions in the 2 poles of the membrane (intra and extracellular) leading the cells, the adjacent sensory receptors and the free nervous endings to a state of excitability.
Moreover, cell injuries of the skin (an in particular of the mast cells of the Lewis layer) provoke a secretion of bradykinin, serotonin and proteolytic enzymes, ACTH and also of histamine-like substances all around the needle[12].
Yaksh and Hammond[13] point out that 3 types of local substances participate in peripheral transduction of nociceptive stimuli into nociceptive impulses (pain).
1) Those that activate nociceptive afferent fibres and produce pain (bradykinin, ACh and K).
2) Those that facilitate the pain evoked by chemical and physical stimuli by sensitisation of nociceptors but are ineffective in evoking pain themselves (prostaglandins) and.
3) those that produce extravasation, such as Substance-P. Substance-P (and perhaps other peptides) may have a role in influencing the milieu of the peripheral afferent terminals, and thus in the transduction of nociceptive information. Substance-P, like other peptides, is synthesised in the cell bodies of small cells (type B cells) of spinal ganglia and the gasserian ganglion by the ribosomal synthesis of large precursor prehormones[14]. If the stimulation of AP is a kind of nociceptive stimulation, we can hypothesise the presence of this substances at the site of the needle.
Therefore, it can be said that the main neurotransmitter of pain to the periphery is Substance-P. Substance-P is a peptide transported by the neural fibres till the last nerve terminals of the neural C-fibres. circa 20% of the cell body in the spinal dorsal root ganglia contain Substance-P. These cells have small somas and small unmyelinated and finely myelinated axons. Their peripheral processes occur in the epidermis and in the walls of blood vessels and glands. Their central processes project to the superficial layers of the dorsal horns of the spinal cord. Also, opioid receptors are present on primary afferent neurons (thinly myelinated and unmyelinated cutaneous nerves), on sympathetic postganglionic neurons. Now many findings indicate the presence and synthesis of opioid peptides in different types of inflammatory cells at the site of tissue injury. Because the local reaction is a kind of small inflammatory reaction, the peripheral antinociceptive effect of exogenous or endogenous opioids will be enhanced especially 3-4 d after the AP treatment. Substance-P, together with the above mentioned substances provokes local clinical phenomena of inflammation such as swellings, red spots, itching or burning pain.
After withdrawing the needle, the unequal distribution of electrical potential (because of the high level of K ions) round the edges of the injury creates an electric "flux potential field" which acts as stimulator of the free nerve endings of the skin for 72 h after the application of AP. The nature of the stimulation varies depending on the depth of the injury, the quality of the tissues, the sensitivity of the nervous system of the patient and the type of needle used.
Inactivation of the deep painful muscle points
The quality of the stimulus depends mainly on the depth of entry of the needle and the quality of the tissue in which it is placed (target-tissue). Often, the needle is placed in muscle, in the TPs[15] or in motor points. Motor (Erb) points are specific points where the motor nerve enters the muscle; electrostimulation of these points causes the muscle to contract. TPs are points in muscle which induce referred pain on needling or pressure palpation. They occur in many degenerative disorders of the spinal cord, in all cases of musculoskeletal pain of radiculopathic origin (neuropathic pain) and in local muscle, ligament or joint injuries (especially overuse Syndromes). circa 70% of all AP points coincide with TPs. Melzack, Stillwell and Fox[16] showed "a remarkably high degree of correspondence (71%) between TPs and AP points".
Miltiades_K3 (1996) Neuroscience, neurophysiology and AP: Part 3. Liao also reported that many AP points coincide with the motor points (Erb points) of skeletal muscle.
The simple placement of the needle at these points achieves: a) the inactivation of the TP (reduction of the intensity and discharge rate of pain sensory stimuli from the muscle to the higher sensory centres) and b) the activation of spinal reflexes. The receptor organs of the muscular shaft (proprioceptive sense) and the cells of the anterior horns of the spinal cord participate in this process. This mechanism will be analyzed in detail in the discussion about the regional action of AP.
Regional action of AP stimulation
AP acts at a spinal (segmental or regional) level. Noxious stimuli from the periphery lead to release peptides in the spinal cord level. These peptides (tachykinins, Substance-P, neurokinin A, calcitonin, gene-related peptide, somatostatin etc) modulate the transmission of nociceptive information to the CNS. Using treatment modalities like TENS, AP and EAP, we can block the nociceptive signals, activating descending pain inhibitory systems which act at the level of the specific myelotome. AP and EAP have an inhibitory effect on interneurons of the spinal cord (lamina V) and this inhibition is mediated by opiate pain-relieving system[17]. Also, many laboratories have shown changes in dorsal horn cell activity (gating) during mechanical, chemical and electrostimulation of somatic and visceral fields. TENS of somatic areas decreases the spontaneous and noxiously evoked activity of most dorsal horn neurons (wide-dynamic-range (WDR) cells, High threshold (HT) cells, and high threshold inhibitory (HTi) cells), reducing the perception of pain[18].
This mechanism can be the spinal (regional) action of many analgesic physical methods which we use daily in physiotherapy. Another regional reaction concerns the activation of an area through reflex arches. Those are produced after the stimulation of a peripheral sensory receptor. The stimulus is directed with afferent neural fibres to a sensory or motor nucleus of the spinal cord and a response reaction is produced there.
Viscerocutaneous reflex or splanchnofascial reflex: A functional or organic visceral disease causes pain, hypalgesia, tension or irritation to a particular area of the skin. Usually, in relation to the painful viscera, the skin area to which pain is projected has a common somatomic origin from its embryonic development. Consequently it is innervated sensorially from the same neurotome of the spinal cord. The skin and the related viscera have the same segmental innervation usually by dorsal roots, spinal nerves and nuclei (referred pain resulting from reflex phenomena). The nociceptive impulses from the affected viscera pass to the dorsal horn and then to anterior horn of spinal cord across interneurons. Visceral afferent nociceptors converge on the same pain projection neurons as the afferents from the skin[19,20,21,22]. For example, stimulation of the descending colon with barium chloride creates paleness (shrinking of the melanin cells-melanocytes) in an area or neurotomes[23] of the specific myelotomes (T9-T12). Moreover, injection of adrenaline 10% to the gastric (ST) mucosa, in the GB or in the fascia of the spleen, creates skin "shining" at a specific small area of the dermatomes of those organs[23].
Pain in the GB is projected on the skin of the right hypochondrium and on the top part of the right shoulder, a pain related to stomach ulcers corresponding to the 11th thoracic vertebra. The viscerocutaneous reflex is transmitted via the sympathetic chain. Dissection of the spinal cord does not affect this reflex. It is abolished by the dissection of the sympathetic chain. This reflex is a diagnostic reflex.
Cutaneovisceral reflex: Irritation of a skin point functionally influences the organ to which the cutaneous area is connected via the neurotomes. Experimentally, procaine-injection into cutaneous tender points in the anterior thoracic wall of patients with acute angina pectoris gives fast relief of precordial pain. EAP of LI18 on both sides, provokes APA sufficient for thyroidectomy. LI18 is in the area of innervation of the 3rd dorsal cervical spinal nerve. The fascia of the thyroid gland and the overlying skin area where the specific AP point is found, is innervated from the same cervical myelotome. This reflex does not depend on higher brain centres. It follows a clearly neurotomic distribution. Dissection of the visceral nerves abolishes the reflex. Dissection of the vagus nerve does not influence the healing effect. It looks like the myotatic, monosynaptic reflexes. This is a therapeutic reflex.
Visceromuscular and viscerovisceral or somatoautonomic reflexes are internal reflexes. They interpret the muscular contraction and vasocontraction observed in diseases of the internal organs. Sensory fibres from the muscles, the vessels and the affected organ originate from the same myelotome on neighbouring nuclei which are functionally interconnected[24]. This reflex produces reflex spasm of the skeletal muscle (TPs of m. pectoralis) during myocardial ischemia (MI). Also, through this reflex we interpret muscular pain during the function of the muscle under conditions of limited blood supply[25]. The sensation of needle insertion into somatic nerve endings in the muscle, ascends with afferent impulses to the anterior hypothalamus. Efferent impulses originate from the same reflex centre of hypothalamus, descend to the cholinergic vasodilator nerve and dilate the blood vessels of the muscle. Dissection of the dorsal spinal roots and that of the visceral nerves abolishes this reflex. A viscerovisceral reflex is activated during the direct excitation of a ganglion by placing a needle deeply in the ganglion or all around the ganglion. For example, SI18, a Hui-Meeting point on the head of the 3 Arm Yang Channels, is needled during acute pain of the musculoskeletal system. This point is very important to treat myoskeletal diseases[26]: application of local anaesthetics to the mucosa overlying the sphenopalatine ganglion can block pain and is extremely effective on myoskeletal pain especially of the neck and back. SI18 and the sphenopalatine ganglion coincide. In this area, there exists the largest collection of neurons in the head outside the brain itself. It is intimately connected to the trigeminal nerve and nucleus, and the superior cervical sympathetic ganglion. It seems to be the final switch between the body and the brain.
Somatomotor or cutaneomuscular segmental reflexes. A harmful stimulus to the skin stimulates the axons of sensory fibres of groups III and IV of peripheral nerves. The information of stimulation enters the posterior horns of the spinal cord and is transmitted with the help of intermediate neurons to the motor neurons of the anterior horns. This pathway is polysynaptic and permits on one hand control and on the other deviation of sensory stimulation. Thus, the stimulation of a group of sensory receptors on the muscles, tendons or the skin will cause contraction or relaxation of muscles in the stimulated area (segmental distribution of the reflex). In this manner, by a sensory stimulus (puncture) it is possible to enlist neurons on the same or on the opposite side of the initial stimulation. The usual response to the sensory stimulus is the ipsilateral stimulation of flexors and the inhibition (relaxation) of extensors and the contralateral inhibition of flexors and stimulation of extensors (flexor and cross-extensor reflex)[27,28].
Miltiades_K4 (1996) Neuroscience, neurophysiology and AP: Part 4. Most rehabilitation treatments by electrophysical agents and, of course, AP, use cutaneomuscular reflexes to achieve muscle relaxation and to ameliorate the im blood supply to individual muscles or muscular groups. The selection of the area to be stimulated depends on the target muscle.
Autonomic reflexes are reflexes through the ANS (sympathetic and parasympathetic). Many short and long autonomic reflexes can "close" the nervous circuit in the brain, the spinal cord, in the big nervous ganglia or in smaller peripheral ganglia. Apart from segmental reflexes, many autonomic reflexes are known in medicine, for example the segmental and suprasegmental reflex produced by local biochemical changes and tissue damage in patients with acute myocardial ischemia (AMI). This reflex (Bezold-Jarich reflex, an abnormal vagovagal reflex) produces severe bradycardia, peripheral vasodilation, severe hypotension and atrioventricular block. The reflex involves afferents and efferents of both cardiac vagus nerves and cardiac sympathetic nerves which produce sympathosympathetic reflexes. In the AMI patients exist also suprasegmental reflex responses result from nociceptively induced stimulation of the medullary centres, hypothalamic centres, limbic structures and neuroendocrine function[29].
According to Gunn, some other common condition of autonomic dysfunction that respond well to AP treatment are the vasomotor, sudomotor, glandular hyperactivity and smooth muscle spasm observing in spondylotic radiculopathy. When pain disappears, the autonomic phenomena disappear.
Autonomic reflexes can be activated by: a.local stimuli; b.general stimuli, and; c.regional stimuli. Data from the Univ of Goteborg[30] showed that AP may affect the sympathetic system via mechanism at the hypothalamic and brainstem levels and the poststimulatory sympathetic inhibition that creates, persist for more that 12 h after AP.
Autonomic reflexes are the clearest evidence of the organisms reaction as an open thermodynamic system. We know very little about these reflexes. The major problem is in describing the connections between the human cortex and the peripheral outflow to smooth muscles, cardiac muscles, secreting glands, sensory organs and vessels. Some organs (heart, gut, spleen, kidney) receive both sympathetic and parasympathetic innervation, while other organs (adrenal, medulla, vascular tissue, skin and muscles) gain only a sympathetic supply. Clinically speaking, the ANS is not as autonomous as we believe and it may be more synergic than antagonistic[31,32,33].
Segmental distribution of AP points
Main Channels which cross the frontal thorax and the frontal abdomen include the SP, ST, KI. The CV runs in the ventral midline. Along their course on the abdomen and thorax, these 4 Channels have 66 ipsilateral points (110 bilateral). Independently of the name of the Channel, if we apply AP to the points on the thorax, we influence the thoracic viscera or their functions; when we apply AP, to points on Channels of the frontal abdomen, we influence the abdominal viscera or their functions. Moreover, all the Channels follow a course towards the middle frontal and the middle dorsal line similar to the segmental distribution of the deep pain that Kellgren[34] has put on a chart after injection of NaCl in the interspinal ligaments of the vertebrae. The dermatomal distribution of the sympathetic fibres coincides with the distribution of the points of AP of the second branch of BL Channel.
The BL and GV Channels seem to preserve the same precise neurotomic distribution of the AP points. AP points LU01 and 02, BL13,14,15,41 and GV14, have been used for centuries to treat LU diseases. All these points concern T2-T4 dermatome of LU and they correspond dermatomically to the outlets of the sympathetic chain of the dorsal lung plexus (2nd-4th thoracic sympathetic ganglion). The big bronchial tubes are autonomously innervated by this sympathetic plexus, and also the division of the trachea and all the vessels which transport blood to the bronchial tree. From the same anatomical region start the preganglionic branches of the lower cervical and of the first and the second thoracic ganglion of the sympathetic chain, which are going to form in the depths of the dorsal cervical triangle, the stellar ganglion. The Shu-Mu (Back Association and Front Alarm) point technique (synchronous needling of Shu-Back and Mu-Abdominal points) is a special ancient method that uses the segmental distribution of AP points to treat diseases of internal organs.
General action of AP stimulation
Teams of neurophysiologists and research workers on the effect of AP, of EAP, of electrotherapy and other methods of physical agents have studied the possible mechanisms and the ways of analysing of the peripheral stimulation from the CNS and also the way of answering of the CNS to these stimuli. Effective application of AP requires integrity of the peripheral nervous system and the spinal cord. AP points are "silent" in paraplegic limbs (individuals with complete sensory-motor paraplegia) or in experimental animals in which surgical resection of the spinal cord has been effected[35].
A peripheral stimulus, depending on its quality, may stimulate specific nuclei of the CNS and provoke secretion or qualitative modification of neurotransmitters in the blood and the CSF. Besides, each combination of AP points may activates different nerve circuits. This view was based on 2 experimental results from the Univ of Peking[36].
After arterial anastomosis of rabbits (cross circulation technique), APA occurs not only in the rabbit on which AP is applied but also in the rabbit to which the blood of the former is circulated through the anastomosis. Also, a CSF transfusion from a cat-donor to which APA had been applied to another cat-recipient causes analgesia to the recipient after 10 min. Since then, the existence (after AP) of analgesic neurotransmitters in the CSF and peripheral blood has been confirmed repeatedly; this clearly shows activation of central pain control systems (and others) by AP points. Reference to these points is related on one hand to the topographical paradox of the points and on the other to their important therapeutic action. Their effects have been established by studies (on experimental animals) and clinically (on patients); randomly selected sham AP points have an analgesic effect on 28-35% of patients when compared to AP points that have an analgesic effect on 55-85% of patients. Papers published from time to time relate to points LU07, ST36, LI04, SP06, LI10, TH05, LV03 and PC06. The systems activated through these points may be a) opiate endogenous analgesic systems, b) non-opiate systems and c) central sympathetic pain inhibition systems through the reticular formation of the brain.
APA is used to treat acute or chronic pain; it is used less for surgical APA. APA influences the neurochemistry of the descending pain control system. This system consists of 4 parts: a.spinal system (dorsal horn); b.cortical and diencephalic system; c.mesencephalic (PAG & PVG) system and; d.pontine (nucleus raphe magnus) system. Each system uses different types of endogenous opioid peptides[37,38].