4. ADVANTAGES AND DISADVANTAGES OF AA
ADVANTAGES OF AA
AA is a simple, cheap and effective preparation for surgery, especially if combined with tranquilliser or drug anaesthesia. It may be the only method of surgical analgesia which might be available in wartime, national disasters and other emergency situations.
Combination anaesthesia: In humans, a combination of EAA and tranquilliser or anaesthetic drugs is used in thoracic or abdominal surgery, especially in allergic or high-risk patients (circulation, heart, lung, kidney or liver disease). Results were compared with control patients operated under drug anaesthesia alone. They confirmed that the amounts of narcotic and barbiturate drugs needed to maintain adequate anaesthesia were reduced. The EAA-drug group had less deviations from the baseline in heart rate, BP, EEG and body heat loss than the controls during surgery. Blood levels of ACTH, cortisol and aldosterone during surgery did not differ between groups. Recovery of consciousness in the EA-drug group was associated with more alpha- and less beta- activity in the EEG and with less time-space-disorientation on waking up than in the control group. The AP-drug anaesthesia was associated with minimal depression of vital functions and maintained good adaptive reactions (Ponomarenko 1987). EAA combined with diazepam was successful in surgery for fracture of the femoral head in elderly high-risk patients (Glennie-Smith 1986).
Some vet acupuncturists combine EAA with drug analgesia. The dogs are given a tranquillizer (i/v) and small doses of general anaesthetic (much smaller than would be successful without EAA), together with EAA. The results are very good and post-operative recovery is faster and less troublesome than after surgery under conventional anaesthesia.
a. Per-operative benefits: AA can be used in high-risk patients, who might NOT tolerate general or local anaesthesia. These cases include shock (post trauma, haemorrhage), severe debilitation (after chronic disease, malnut-rition or cruelty), toxaemia (renal, hepatic, pulmonary or cardiac cases, toxic pyometra etc); obstetric surgery (Caesarean section etc). It can also be used on very young and very old animals, and in operations lasting up to 10 hours. The effect of AA on the autonomic nervous system prevents shock during the operation so that deaths during or immediately after operation under AA are extremely rare. Operative haemorrhage is also decreased.
b. Post-operative benefits: Because consciousness and reflexes (other than pain response) are retained under EAA, the animal can walk unaided to the recovery area immediately after surgery. There is no risk of self-injury due to ataxia, struggling or falling, as may occur under general anaesthesia or spinal block.
Many authors, operating on animals as well as human patients, report far fewer post-operative complications after AA (less ileus, less urine retention, faster return to normal appetite, less nausea etc). Defecation and urination occur very quickly after EAA and the animal will eat and drink immediately after operation (if it is hungry or thirsty). It is common practice to offer cattle some hay or concentrates during operations and many dogs will placidly accept bits of meat during major surgery.
Post-operative pain and discomfort are almost totally absent. If they occur, AP at the AA sites or at other points for the pain site can control the pain quickly. It is well known that AA effects last for up to 20- 60 minutes after stimulation is ended. An extraordinary finding in monkeys is that peaks of powerful analgesia (interspersed with periods of normal pain sensitivity) can continue for up to 70 hours afterwards (Vierck). This finding demands further research.
After AA, surgical incisions heal much faster, with less oedema, less wound infection and less wound breakdown.
DISADVANTAGES OF AA
a. Analgesia is inadequate in some patients. In animals, expert technique can obtain a success rate of 90-100% between different operators but the success rate has 3 categories:
Excellent results are defined as no indications of pain at any stage in the operation (struggling and vocalising because of physical discomfort, restraint, fear etc must be distinguished from pain reaction). The operation proceeds smoothly at all stages and no other anaesthetic method is required. Slight muscle tremor or local guarding may occur.
Good is defined as short intervals of restlessness or mild struggling during traction of internal organs, suturing of sensitive structures etc. Local muscle tremor or guarding is noted at intervals but the operation can proceed without other anaesthetics.
Fair some pain reactions are noted at intervals during the operation and frequent, intermittent struggling may arise. Marked local tremor and guarding may arise. The operation can still proceed. Some of the effects can be relieved by increasing the frequency or voltage or by relocating the needles.
Failure is defined as pain reactions (fierce struggling, vocalisation, muscle tremor, strong reaction and impossible to proceed with the operation without some other form of anaesthesia.
Skilled operators may have excellent, good and fair rates of about 78, 19 and 3% respectively, with failure rates of zero. However, these success rates are seldom obtained by Western operators in the first year or two of their use of the technique, and many western operators, despite much experience in general AP therapy have not had such good success with AA.
Failure: Western vets can expect a failure rate of 20-50% in the beginning. This is due mainly to incorrect choice of points, incorrect location of points, incorrect needle depth, direction, incorrect or inadequate methods of stimulation, animal factors and surgical technique.
b. Animal factors which may reduce the success rate:
Regional variation in EAA: Certain body regions are more difficult to render insensitive to pain than other regions. Vets who specialise in limb surgery might not get success rates as high as those who specialise in intestinal surgery. Success rates for surgery on the frontal sinus, oesophagus, intestine or bladder may be less than for other body regions. Sex and breed effects may interfere: female cattle respond slightly better than male cattle and domestic cattle may respond better than buffaloes. Species differences: among farm animals cattle and sheep are the best reactors, followed by pigs and horses. Dogs are very good reactors but cats are difficult subjects to handle and their intolerance of morphine may be related to their poor response to AA. Temperament differences: nervous, excitable animals may be good responders to AA but are easily frightened by noise, smell, sight stimuli and may be hard to restrain, despite good analgesia. Dull, depressed animals may appear to be easy to handle but their reaction to AA may be sluggish and not of a high degree. Recumbency: Large animals in the recumbent position need a more expert AA technique than those which are standing. Voltage should be increased in recumbency. External and other stimuli: Animals with an elevated pain threshold under AA can still react to disturbance by environmental stimuli (smell of blood, noise, excitement, fearful sights, proprioceptive stimuli/physical discomfort, clumsy surgical technique etc). These may lower pain threshold and reduce the success rate.
c. Muscle relaxation may be inadequate if the EAA technique is not expert. This may cause ballooning of intestines through abdominal incisions.
d. Induction time (10-40 minutes) may be inconvenient for some surgeons, who may also complain about "electric wires all over the place".
e. Needle dislodgement: Occasionally one or more needles become dislodged, especially if they had not been taped or sutured securely in position. Dislodgement may occur (despite good restraint of the animal) due to strong muscle twitch induced by EAA. If needles fall out, they must be replaced or the analgesia may be poor or absent. When reconnecting a replaced needle, the output voltage should be set to zero and then restored gradually after reconnection.
f. Restraint must be good: This usually needs the presence of at least one assistant at all times after the start of induction. Restraint of small animals, by tying them in dorsal or dorso-lateral recumbency, may cause them some discomfort. Struggling against discomfort needs to be distinguished from possible pain reactions to the surgery. The special EAA harnesses tend to reduce this problem in small animals.
g. EAA demands skilled surgery. Surgical technique must be deft, light, fast and unhesitating. Prolonged probing or manipulation of organs and slow uncertain incision reduce the success rate. Traction on mesentery or ligaments should be kept to a minimum, as should handling of organs and viscera. Although AA has anti-shock effects, heavy traction during EAA can cause autonomic (vagal) reflexes (nausea, vomiting, shock, collapse etc). Where possible, use the hands, rather than surgical retractors, clamps, forceps, probes etc. The hands usually are more sensitive than instruments and are less likely to cause unnecessary trauma/stimulation during surgery.
5. MECHANISMS OF AA
EAA is not hypnosis: In humans, hypnosis or self-hypnosis (deep relaxation) can induce surgical analgesia in sensitive subjects and can be used to treat certain disorders associated with stress. "Animal hypnosis" (the Still Reaction) is not fully analogous to human hypnosis. It is a reversible and involuntary "Tonic Immobility" (TI), induced in many species as a defensive reaction to sudden fright or pain. TI is disrupted easily by noise, movement or touch. In TI, animals may tolerate mildly painful stimuli (pinprick, sound, electric shock) without somatic (muscular) reaction. This is due to descending motor inhibition, not sensory inhibition. They feel the stimulus (as assessed by neuronal discharges in the cerebral cortex) but do not appear to react. There are marked differences between the physiological effects and mechanisms of human and animal hypnosis and those of EAA. Appendix 1 compares and contrasts TI and AA.
Sensory inhibition in EAA: Modern theories attribute the effects of EAA to inhibition of the ascending (sensory) pain signals at three levels: peripheral, spinal and central. Some recent research findings which support this theory are as follows:
1. Many of the most active AA points are directly over, or very close to, main nerve trunks and branches of peripheral nerves.
2. Interruption of the sensory nerve supply proximal to the AA needle site abolishes the EAA effect. This has been demonstrated in many species (including humans) by local anaesthesia (procaine infiltration etc) of the AA point, by nerve block above the point and by spinal block above the entry point of the nerve into the spinal cord. In animals, direct EAA of the isolated nerve gives the same analgesic effect as EAA of the AP point. If the nerve is transected, stimulation of the proximal cut end produces AA but stimulation of the distal cut end produces no effect.
3. In monkeys, cats, rabbits, rats and other laboratory animals, pain stimuli applied at distant regions (for example, the hind limbs) evoke electrical activity in cortical and thalamic neurons. This activity can be monitored by electrodes placed directly into specific neuronal centres of the brain or by surface electrodes at specific regions of the head. EAA at points which cause analgesia of the pain zone suppress or abolish completely the evoked potentials in the brain. (There is also experimental evidence that transmission of pain signals is inhibited by AA at peripheral and spinal levels.
4. Experimental electrolytic lesions placed around the 3rd ventricle (midbrain) or surgical hypophysectomy completely abolish AA effects. The midbrain and hypothalamic areas are rich in opiate receptors. (Certain strains of mice, which have no opiate receptors because of a genetic abnormality can not respond to AA). Levo-naloxone, naltrexone and other opiate antagonists prevent and abolish much of the analgesic effect of AP in humans and animals.
Thus far, these facts indicate that the signals generated by needling or
ES of the AA points are transmitted via the peripheral sensory nerves to the spinal cord and that they activate a descending brain-based pain-inhibition mechanism, especially the midbrain and hypothalamus. There are also "pain inhibition gates" in the spinal cord. Thus, the "ascending pain signals" are blocked at spinal and midbrain level and fail to reach the cerebral cortex.
There is very strong evidence that the pain inhibition mechanism involves activation of opiate and serotonin (5HT) receptors in the brain and, probably, other sites also. This evidence is strengthened by the following observations:
AA stimulation causes release of endorphins, enkephalins (endogenous morphine compounds) and ACTH. This has been confirmed by chemical analysis of tissues.
AP stimulation of certain points (especially Earpoint "Lung"; LI04; ST36; GB34 etc) relieves the symptoms of narcotic and alcohol withdrawal within 10-30 minutes in human addicts and in laboratory animals addicted experimentally to morphine or heroin. These points have major AA effects (Patterson).
Stimulation of AA points on one side of the body may have analgesic effects on the opposite side. In most species of animal, the stronger analgesia is usually on the same side as the needles. However, Toda et al found a stronger effect on the opposite side when the GeiKo point was used in rodents.
Although ES of single points such as ST06; LI04; TH08 etc may cause analgesia over a wide area, there is some specificity between the anatomical location of the point and the area of analgesia. For instance point PC06 or TH08 will give better analgesia of the arm and thorax than of the leg, whereas SP06 or ST36 will give better analgesia of the leg and abdomen than of the arm. Also, needling of "false points" usually fails to produce AA, even though the false points can be quite near the correct points.
A certain degree of side-to-side and region-to-region specificity exists between the AA point and "target zone of analgesia". This suggests that the AA signals are going to specific sites in the brain. It is known already that the brain contains 3-dimensional projection areas (both sensory and motor) for all body regions. It appears that endorphin release in these specific areas is the main mechanism of AA.
Many years before the endorphins were discovered, the Chinese had evidence
that a morphine-like analgesic factor was released into the blood and cerebro-spinal fluid by AA (Niboyet et al). Cross-perfusion studies were conducted in rats, dogs, rabbits and monkeys in China. AA or EAA was established in experimental animals and cerebro-spinal fluid, whole blood or serum was perfused directly or indirectly into animals (of the same species) which had received no AP. Analgesia developed in the recipients but was not as marked as in the donor animals. An extraordinary finding was that if the donor had a localised analgesia (specific to one side or one region), the recipient also developed analgesia on the same side and in the same region as the donor. This suggests that humoral factors are released by EAA and that they activate specific receptors (now known to be opiate receptors) in specific regions of the brain and spinal cord of both donor and recipient animal. Many neurophysiologists find it difficult to accept that such specificity can exist. In the past few years, Chinese and Western workers have confirmed that release of endorphin is involved in AA.
As well as releasing endorphins, EAA also releases ACTH, which increases the cortisol levels in blood. This was proved in horses by Cheng et al (1980). In these experiments, EAA was given at 4-5 points to above the threshold of muscle twitching; biphasic pulses, 5 Hz, .25 msec duration for 30 minutes. The points were chosen from points effective in treating limb pain in horses, BL13,65; GB26; PC09; KI01,02. The needles were 10 cm long and were inserted to a depth of 3-5 cm. Cortisol levels before and after AP were measured. A control group of horses received "false" AP, by the same method but at non-points 5 cm below GB30,39; BL13,18,47 and the needles were inserted subcutaneously only (not to the deeper levels as in the active points). EAA increased cortisol by 40% above pretrial values but "false EAA" had little effect. (Note: If "false points" above or below the "real points" are used, some hypoalgesia may occur because the same nerve trunk may be stimulated. If the "false points" are lateral or medial to the "real points" (i.e. not over the nerve trunk), needling the "false points" is usually not effective). The difference between real and false EAA was highly significant. Recent research has also shows that serotonin (5HT) is involved in EAA and that oral administration of 5HT precursors, such as d-phenyl alanine, greatly enhances AA and can turn "non-responders" into "responders".
Frost reported 3 cases of human AA following needling of points below a traumatic transection of the spinal cord in the region cervical vertebrae 1-6. Analgesia occurred above the transection.
Terral repeated the Chinese cross-perfusion EAA studies in rabbits. He confirmed that EAA released a humoral analgesic factor in rabbits even when the spinal cord was severed behind the medulla oblongata.
The mechanisms of AA can be summarised as follows: Signals caused by stimulation of AA points are carried in the peripheral sensory nerves to the spinal cord. At this level they may activate local (spinal) pain inhibition gates. Spinal signals are also transmitted to specific sites in the thalamus, hypothalamus and midbrain, via the ascending tracts (spino-thalamic tracts, ventro-lateral funiculi). These signals stimulate the local (and systemic) release of endorphin, serotonin (5HT) and other neurotransmitters not discussed in this paper. The endorphin activates the opiate receptors, which "switch on" the pain inhibition mechanism specific for those areas related to the needle site and its projections at brain level. Simultaneous ACTH release from hypothalamic areas induces cortisol secretion by the adrenal, thus preparing the animal to withstand the surgical stress and to assist (anti-inflammatory effect) in wound healing.
Release of ACTH by EAA could be important in treating allergies, arthritis, inflammation and shock. Some AA signals can reach the pain inhibition centres by routes outside of the spinal cord, possibly by (a) cell-to-cell transmission through the skin and soft tissues (as in a bee-colony); (b) by the autonomic nervous system and (c) by release of some (yet unknown) substances from the needle-site into the bloodstream.
6. OTHER METHODS OF STIMULATION-PRODUCED ANALGESIA (SPA)
SPA originally referred to analgesia produced by direct stimulation of specific brain sites, especially the area around the 3rd ventricle, the periaquaductal grey matter (PAG). In humans and animals, this produces powerful analgesia over the whole body. It has many parallels with EAA. SPA is abolished by opiate antagonists (naloxone etc). It involves endorphin release but over a wider area of the brain than EAA. This probably explains the more localised analgesia of EAA. Direct stimulation of the thalamus or dorsal spinal cord roots also produces potent analgesia and ES of permanently implanted electrodes in these sites has been used in treating severe intractable pain in humans.
Long-term direct stimulation of brain or cord sites involves some risks (possible electrolytic lesions in brain/nerve tissue, risk of infection etc). Because direct methods were effective but risky, researchers began to examine the possibility of indirect stimulation of the nervous tissue, via peripheral nerves. This led to the development of various forms of transcutaneous ES analgesia (TESA), transcutaneous nerve stimulation (TNS), transcutaneous electro-neural stimulation (TENS) etc. These methods are widely used internationally in physiotherapy and for personal use by outpatients of pain clinics. Workers familiar with the AP system found that TESA, TENS etc were more effective if the electrodes were applied to the affected local areas plus (AP points, Trigger Points, organ reflex points etc). TESA mechanisms are not fully researched yet but there is strong evidence that they are similar to those of EAA.
Under experimental conditions, surgical intervention has been done in animals under SPA but the main use of SPA and TESA has been in the control of clinical pain.
Other types of SPA include vaginal stimulation analgesia, electro-restraint electro-anaesthesia/electro-narcosis and electro-sleep.
Vaginal Stimulation Analgesia (VSA): Mechanical (glass probe) or electrical stimulation of the vagina in rats produces a powerful analgesia over the whole body but the mechanism does not involve the opiate receptors in the brain because opiate antagonists (naloxone etc) do not interfere with the analgesia. Thus, VSA is mediated by mechanisms different from SPA, TESA and EAA.
Electro-restraint: Reports from Poland claimed that positive clamp electrodes fastened to the ear and a negative tongs electrode fastened to the nose gives excellent restraint in cows. Using this technique in 58 cows, the author (Szczerbac) was able to pare the hooves with no difficulty and no defence reaction from the cows. The frequency of stimulation was 160-200 Hz and the current was 4-16 mA. Details of induction time are not available in the English summary of the article but I believe that induction was probably very short. The Ear roots and the nose (especially GV25 and 26) are used as EAA points in some Chinese prescriptions for humans and animals. However, I suspect that the Polish instrument is used as a method of restraint rather than a true analgesia. It is also interesting that stimulation of the nasal area (the simple tongs or fingers in cattle; the rope "twitch" in horses) and of the ear-root (in both cattle and horses) has been used internationally for many centuries as a method of restraint in large animals. Since the Polish report, a similar instrument has been available commercially in Australia and the USA. Its tradename is STOCKSTILL. It applies a strong electrical stimulus to the cheek/mouth/nose and the base of the tail or other area, as required, i.e. opposite ends of the spinal cord. To knock the animal, current is applied to the cheek and lumbar area. The animal falls to the ground immediately and simple surgery can be done with great ease. However, the British Veterinary Association has not accepted that this technique is humane and painless. It seems that this method of electro-restraint has little analgesic power but rather that it acts by a type of spinal shock which induces spastic paralysis of the motor nerves from the spinal cord. More research is required on this method but it appears to have little or no similarity in its effects or mechanisms of action to EAA or SPA.
Electro-narcosis and electro-anaesthesia are terms used for another type of electrically induced anaesthesia which uses indirect electrical stimulation of the thalamus to produce unconsciousness and total anaesthesia. The induction period in humans and animals is very short, usually 1-5 minutes. Unconsciousness and anaesthesia can be maintained for long periods while stimulation continues. Consciousness returns immediately stimulation ceases. In early trials, needle electrodes were used in various sites on the head: temples, vertex, occipital area, mastoid area, forehead etc. Contact electrodes, such as sponges soaked in saline or metal disc electrodes were used later. Kano et al have done many experiments with the method in monkeys. They found that needle electrodes could produce third degree burns, stretching between the electrodes but that contact electrodes did not produce tissue damage. Their suggestion for best results was to use high frequency current passed between B-C and B1-D, where electrodes B and B1 are over the greater occipital nerves and C and D are over the greater auricular nerves.
They proved that the stimuli are transmitted to the brain by these nerves by a local ring-block around the scalp, using 0.25% lidocaine. The local anaesthetic blocked the phenomenon.
Anaesthesia produced by these techniques is sufficient for major surgery in man and animals. In her book on AP in the treatment of drug addicts, Margaret Patterson traces the history of these techniques. Electro-anaesthesia has a long history in western medicine dating back to 1902 (long before the development of EAA, SPA, TESA etc). It was discovered by Francois Luduc in 1902. The first human operations using the method were in 1972 in the Necker Hospital, Paris. Since then, more than 400 operations (including arterial grafting, kidney transplants, urological and intestinal surgery) have been done using that method in the hospital. Other hospitals in France are also using the method. The electrode placement is: 2 electrodes (anodes) behind the mastoids (one each) and one cathode between the eyebrows; unidirectional high frequency current (See Patterson for details). Post-operative analgesia is marked, lasting 6-48 hours, as in EAA. Post-operative infection, abscesses etc are rare (3%) as compared with operations under general anaesthesia (17% abscesses) in the same hospital. This also parallels the EAA effect but loss of consciousness during electro-anaesthesia indicates that the mechanisms differ from those in EAA.
Electro-Sleep or Cerebral Electro-therapy (CET) has some parallels with electroanaesthesia but it differs in other respects. It is used in therapy of various diseases with underlying disturbances of cortical regulation of somatic function and in all disorders with psycho-autonomic manifestations. It was widely used in the old USSR and in Austria but there is no agreement on the mechanism of the effects or on the stimulation parameters used to induce electrosleep. One Russian worker (Sergeer - see Patterson for other details) used rectangular pulse, constant polarity, pulse duration 0.2-0.3 msec, current intensity 15-20 mA, 80-100 Hz, for 30-120 minutes per day. A course of treatment lasted 20-25 sessions.