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Subjective rating responses and averaged evoked responses (AERs) to shock stimuli of varying intensity were recorded in 20 subjects to examine the possible analgesic effects of sound stimulation (music) and suggested analgesia. Subjects (10 men, 10 women, ages 19–31) were divided into two groups of 10, each receiving the sound-suggestion condition and the no-sound, no-suggestion condition in different order. Sound and suggestion produced the following significant (p

A major problem in the understanding and psychological treatment of chronic pain patients is the inadequacy of available assessment procedures. Currently, the most frequently used instrument is the Pain Rating Index (PRI) of the McGill Pain Questionnaire, designed to assess 3 components of pain (i.e., sensory, affective and evaluative) postulated by the Gate Control Theory. The PRI has been used in many studies to make differential diagnoses, to describe different groups of pain patients and to identify the factor composition of the instrument itself. To date, however, no study has appropriately tested the a priori structure of the PRI or cross-validated it. Confirmatory factor analytic procedures employed in the present study supported Melzack's postulated tri-component structure of the PRI in 2 diverse samples of pain patients from different hospitals. However, the 3 components were found to be highly intercorrelated. Subsequent analyses revealed that the 3 components of the PRI do not display adequate discriminant validity. The current use of 3 subscales to establish differential diagnoses or patterns of different pain syndromes may lead to inappropriate classification and treatment decisions. The major conclusion of these findings is that use of only the total score of the PRI is appropriate for pain assessment.

1. A method is described to study the modification in the activity of the lamina IV and V cells of the dorsal horn under the intra-arterial administration of bradykinin into the hind limb of the spinal cat. 2. The modifications induced by intra-arterial injection of bradykinin preferentially affected the lamina V cells (77% of the units) and produced few changes in the lamina IV cells (16% of the units showed variations). 3. 52% of the lamina V cells were activated; the mean increase in the firing rate was 700%. The mean latency of the effect was 20 sec and the mean duration was 47 sec. However, there was large variance in the excitatory effect across cells. On the other hand, for the same cell, the observed effects were perfectly reproducible and injections of physiological fluid induced no response. 4. 25% of the lamina V cells were inhibited. Generally, the activity of the cell was reduced to 13% of its initial value; in some cases, a total suppression of activity was observed. The mean latency of the inhibitory effect was 12 sec and its duration 28 sec. All these units had a very wide inhibitory field (activated by stimulations of low intensity) which asymmetrically surrounds the excitatory field. 5. This study confirms the role played by the lamina V cells in the transmission of nociceptive messages. The existence of inhibitory phenomena is in favour of the gate control theory described by Melzack & Wall (1965) without deciding the pre- or post-synaptic nature of these mechanisms.

1. Dorsal root potentials (DRP) were recorded in the lumbosacral spinal cord of decerebrated unanaesthetized cats, following afferent volleys restricted to the thin myelinated (Group III) cutaneous afferents of the hind limb. The thick myelinated fibres (Group II) were blocked by a depolarizing current. 2. A pure Group III volley produced a DRP of negative polarity, called the III—DRP, signalling a depolarization of the intraspinal terminals of afferent fibres. The longer latency of the III—DRP when compared to that of the DRP after a Group II volley was accounted for quantitatively by the lower conduction velocity of the Group III fibres. 3. Special attention was given to the presence of III—DRPs having a predominantly positive polarity thus signalling a presynaptic hyperpolarization. Such ‘positive III—DRPs’ were, however, never observed in this investigation. 4. Both after transection of the spinal cord at various levels and after administration of pentobarbitone the III—DRP persisted at normal polarity. The duration of the DRPs was increased by these experimental procedures. 5. The implications of these findings are discussed in relation to the prominent role postulated for the Group III fibres in the context of the gate control theory of pain.

During an operation for varicose veins with stripping under hypnotic analgesia, there were no signs of sympathetic stimulation during the phases of the operation usually considered to be the most painful. These findings support the “gate theory” of pain.

The pain-killing abilities of electricity were known as far back as the ancient Egyptians and Hippocrates, but it was not until 1965 when Melzack and Wall [10] proposed the “gate theory of pain” that clinical interest was re-awakened. This theory postulated that a “gate” for pain existed in the substantia gelatinosa of the posterior spinal horns and that modification of the perception of pain might be possible by blocking the “gate” with non-painful stimuli. They suggested that selective stimulation of large diameter myelinated cutaneous afferent nerve fibers could set a process in motion which would close the “gate” to information coming over smaller pain-carrying fibers. The first clinical application of this theory centered around the relief of chronic pain by surgical placement of dorsal column stimulators [1] and implantation of stimulating devices around large peripheral nerves to block pain sensations. Transcutaneous electrical nerve stimulation was first employed in an attempt to select patients for implantable devices and then as a therapeutic device to alleviate chronic pain [2,4,6,9,11]. The next logical step was to apply this modality to patients in the immediate postoperative period to decrease incisional pain. Hymes et al. [8] noted a decrease in atelectasis, ileus, postoperative pain and days spent in intensive care in patients using transcutaneous electrical stimulation. Vanderank and McGrath [9] reported that 77% of their patients treated with stimulators experienced some relief of postoperative pain.

During recent years, physicians from the United States, Canada, and England have visited China and have observed the successful use of acupuncture to relieve surgical pain (Brown, 1972; Capperauld, 1972; Capperauld, Cooper and Saltoun, 1972; Dimond, 1971; Hamilton, Brown, Hollington and Rutherford, 1972; Jain, 1972a, 1972b; Shute, 1972; Tkach, 1972). These eyewitness accounts have produced widespread interest in acupuncture analgesia as indicated by many discussions in the popular press and also by a series of papers in medical journals (Chisholm, 1972; Liu, 1972; Mann, 1972; Matsumoto, 1972; Taub, 1972; Toyama and Nishizawa, 1972).

Electric stimulation of the spinal cord (SCS) was introduced into clinical practice following Melzack and Wall’s [16] gate control theory of pain. The first implantation for treatment of chronic pain was performed by Shealy et al. in 1967 [22]. Soon, serial reports about successful application of this method, technical modifications, indications and long-term results were published [13, 18].

The first test which any theory of pain must pass is that it must be able to explain the phenomena observed in acute pain in humans. This criterion is used to test the major theory of pain at present, the gate control theory of Melzack & Wall (1965, 1982). The theory is explicit enough to be cast in mathematical terms, and the mathematical model is shown to explain the observations considered. It also points up a common misconception on the consequences of the theory, and thus demolishes an argument which has been used against it. A hypothesis of the origin of rhythmic pain is then made, and consequent testable predictions given. This is the first time that the gate control theory has been used to explain any quality of pain. It has important consequences for the treatment of such pain. Finally, the applicability of the gate control theory as an explanation for chronic pain is discussed.

Heart rate was measured in four experiments using the cold pressor test, with the following results: (1) the heart rate rise between relaxation and stress levels was significant when the water was sufficiently cold (significant in 0°C and 5°C water, not 10°C); (2) the amount of heart rate rise in the normal waking state in 0°C water is unrelated to the hypnotizability of the subject; (3) there is a significant difference in heart rate following a hypnotic induction with suggestions of analgesia, although the reduction in heart rate rise is unrelated to the amount of reduction in felt pain; (4) heart rate rise during hallucinated pain in highly hypnotizable subjects is not significantly different from the rise recorded during normal waking or hypnotically analgesic conditions. These moderately confusing results take on some semblance of order if it is assumed (1) that the control of voluntary processes through hypnotic analgesia (agitation, grimacing) accounts for some reduction in heart response even though uncorrelated with reduced pain, (2) that the homeostatic and sensory-information aspects of the cold water pain are probably little reduced, even though subjectively the pain may be absent altogether, and (3) the motivational-emotional aspects of pain are more labile than the sensory-discriminative aspects, in accordance with the Melzack-Wall Gate Theory.

According to the gate-control theory of pain, the electrical stimulation of large nerve fibres should stop the pain induced when only C fibres are active. This kind of pain was induced by pressure, repeated pinprick, cold and heat in the ischaemic limb. The peripheral nerves were electrically stimulated in the same way as is done by patients treating their chronic pain by electrical stimulation. There was no change in the quantity nor the quality of the C fibre pain. In other experiments, electrical stimulation of the peripheral nerves induced no change in pain threshold to a heat stimulus when only C fibres were conducting, nor when the whole spectrum of fibres were conducting. Although many experiments have been reported that are consistent with the gate-control theory, the experiments reported here, and others mentioned, are inconsistent with the theory.

Transcutaneous electric analgesia, based on the gate control theory, is used in stump pain, lumbar pain, traumatic pain fallowing nerve damage and sciatic neuralgia, 3 patients using this method, showed contact dermatitis at the sites of contact of the electrodes, Patch tests were positive with the electrolyte gel, and in 2 cases, with propylene glycol. Transcutaneous electric analgesia may cause a certain number of side effects similar Lo those encountered with electrocardiography.

There is no real dispute in the literature on the importance of psychological variables in the experience of pain and pain reporting. Since the development of Gate Control Theory the extent of tissue damage is seen as less relevant in the experience of chronic pain, than specificity theory previously suggested. Increasingly, central effects are being considered in treating both the sensation of pain and pain-related behaviors. Methods of psychological treatment for chronic pain are developing rapidly in response both to new psychological studies, and a general disillusionment with existing methods. But this development of psychological methods is not confined to those patients suspected as having a large psychogenic component to their pain. We are not simply dealing here with psychological disturbance: the methods described are equally applicable to patients complaining of chronic pain, irrespective of the extent of psychological component involved.

Pain arises as a result of signals in specific nerves that travel to the brain. In describing the neurophysiological processes of pain it is usual to proceed from the receptors which generate the pain signals in the pain nerves to the transmission processes at various levels of the routes to the final end station in the brain. There follows a brief outline of the anatomy of the afferent pain system and the main steps in the neurophysiological processes underlying the generation and transmission of pain signals.

Publisher Summary This chapter discusses the experience of pain. The afferent signals relayed from the dorsal horn are controlled by descending influences that are largely dependent on matters such as emotional set, alertness, and attention. The interneurons of the dorsal horn are strongly influenced by anesthetic drugs. The gate theory of pain has been widely publicized, but at least in its original form, it is not consistent with a number of experimental and clinical findings. The primary ending of the spindle provides signals of both the degree and velocity of stretch for kinesthesia and for the stretch reflexes. The better known tendon receptor is the Golgi tendon organ. The gamma or fusimotor neurons constitute a system of small motor neurons in the anterior horns with small diameter myelinated axons conducting at only 21–25 m/s.

Pain management has become increasingly more popular since Melzack and Wall’s Gate Control Theory made it plausible that pain could exist without injury and be absent in the presence of injury.[1] A great deal of research was triggered by their theory, and worldwide interest in pain mechanisms, multidisciplinary evaluation protocols, and management techniques escalated. As the search for more reliable evaluation approaches and treatment modalities paid off, and as our understanding of the complexity of pain grew, more medical and scientific specialists have necessarily become involved in pain management. Patients have also become more knowledgeable about what is available in pain control. In this day and age of consumer advocacy, the views of the public cannot be ignored. It is vital, then, that pain be accurately diagnosed and effectively treated, not only because of its pathophysiologic impact and its adverse effects on morbidity and mortality, but also because of its contribution to incalculable agony and suffering.

Nursing diagnoses are proposed for the management of spasticity in the spinal cord-injured person. The diagnoses, pain and self-care deficit related to spasticity, can guide independent nursing management to reduce nociceptive stimulation and increase self-management of spasticity in spinal cord injury. The Gate Control Theory helps to explain alpha muscle susceptibility to nociceptive stimulation and offers rationale underlying nursing management of spasticity. The Modified Ashworth Scale is used to define, measure and evaluate the effectiveness of management of spasticity. Independent nursing management provides the foundation for spasticity intervention. Other interdisciplinary team interventions, including therapist intervention, pharmacological intervention and invasive procedures supplement the nursing management framework.

The purpose of this study was to determine the effects of three cognitive behavioural strategies in the management of abortion pain. The interventions were drawn from the multidimensional model of pain suggested by the gate control theory. Forty patients undergoing abortion with local anaesthesia were instructed in one of four interventions: relaxation, pleasant imagery, analgesic imagery, and a pain discussion (attention control) group. Pain was measured using Johnson's two-dimensional graphic rating scales labelled sensation and distress. Speed of recovery and analgesic use were included as objective dependent measures. No significant differences were found among the four groups on any dependent measures although subjects receiving the pleasant imagery intervention reported the lowest subjective ratings of pain sensation and distress. Findings are discussed in terms of past research and implications for the management of acute pain experienced during abortion.

U radu su prikazane i novije spoznaje o nastanku boli s posebnim osvrtom na teoriju boli pod nazivom »Teorija kontrole ulaza«., New aspects of pain origin and the concept of gate control theory. New aspects lof pain origin with special regard upon the new pain theory gate control theory are presented.

In a series of 72 patients with disease of peripheral neurons, neuropathic painfulness of the foot was found to be related to the rate and kind of nerve fiber degeneration. Patients with acute breakdown of myelinated fibers (either by wallerian or axonal degeneration) tend to have pain more often and to a greater degree than do patients with more chronic forms of nerve fiber degeneration. Neuropathic painfulness was not found to be related simply to the ratio of remaining large and small fibers after nerve fiber degeneration. These studies do not fit the expectation of the proponents of the gate theory of pain.

The management of a patient with chronic pain may present difficulties either because the pathogenesis of the underlying disease is uncertain and corrective measures directed at the source cannot be applied, or because there is inadequate response to available treatment. Ablative procedures, whether by surgery or neurolytic injection, do not necessarily relieve pain and may be followed by unacceptable neurological complications. The physician is therefore forced to rely on analgesic and allied drugs, but there are recognized limitations to their long-term use particularly when the patient has a normal life expectancy. Consequently the concept of stimulation or recruitment of inhibitory systems, proposed in the gate theory of Melzack and Wall1 has attracted a great deal of interest even if significant improvement is obtained in less than 50% of cases. Fortunately most of the techniques applied at the periphery are relatively simple and trouble-free and even a modest improvement means less reliance on potent analgesic drugs. A central approach is necessary when dealing with an essentially subjective experience which does not rely entirely on peripheral sensory input2. The dominance of mind over matter has been recognized for many years and is reinforced by recent discovery of the internal opiates, encephalins and endorphins, released by the brain in the control of pain behaviour. Table 1 lists some of these central methods which have been underestimated in the past3.

Twenty years ago, Shealy and associates reported that application of electrical current to the dorsal columns of human patients was associated with relief of pain below the level at which the currents were applied [14]. These observations were confirmed by subsequent reports [10,15]. The selection of the dorsal columns for electrode placement was based upon the gate theory proposed by Melczak and Wall [8], who suggested that impulses conducted over large afferent fibers activated cells of the substantia gelatinosa that in turn affected small-fiber input by presynaptic inhibition. Subsequently, the theory was modified to include activation of descending fibers from higher levels [9]. Additional hypotheses that proposed to account for relief of pain associated with application of current to the nervous system have included release of opiatelike substances such as endorphin [12].

✓ The Melzack-Wall gate control theory has been invoked to explain the peripheral analgesia resulting from repetitive electrical stimulation of peripheral nerve. This model emphasizes presynaptic inhibitory interactions among afferent fiber terminals in the spinal cord. An alternative explanation, that of velocity change in peripheral nerve fiber conduction, has been suggested by compound action potential studies from our laboratory. The present study was designed to extend this work, and to investigate the single fiber changes subsequent to brief (5- to 20-minute) periods of repetitive, high frequency (180 to 200/sec) electrical stimulation through an implantable peripheral nerve cuff device of the type used clinically for pain relief. Most fibers, regardless of their diameter (estimated from conduction velocity), show one or more of the following characteristics: a transient slowing of conduction velocity, an increase in electrical threshold and/or a decrease in response probability following a period of repetitive electrical stimulation. This supports the hypothesis that there are changes in direct peripheral nerve fiber excitability occurring under conditions simulating clinical electroanalgesia.

At the present time, there are two main neural systems which are stimulated in the brain for pain relief, the primary sensory relay nuclei of the thalamus and their afferent and efferent pathways (L. Th.) and the periaqueductal and periventricular gray substance (PV + PAG). The rationale for the choice of these two systems is based respectively on the gate theory of pain perception [15] and the discovery, mainly by Mayer et al. [11] of a medial brain system with the specific and apparently endogenous property of pain inhibition.

The gate control theory has emphasized primary afferent hyperpolarization (PAH) as a specific determinant in the perception of a stimulus as painful. Previous studies which indicated that primary afferent depolarization (PAD) could be elicited in the trigeminal system by nonsegmental inputs suggested that this might also be the case for primary afferent hyperpolarization. Decreased excitability of trigeminal primary afferent fibers, an indirect reflection of PAH, was elicited by stimulation of the lumbar sympathetic trunk, sural, and sciatic nerves in cats. This PAH has a magnitude and time course similar to that previously demonstrated in the trigeminal system by segmental noxious inputs. We postulate that PAH is a general phenomenon related to the control of information transmission across afferent synapses rather than a phenomenon specifically related to the perception of various stimuli as painful.

Studies of responses in dorsal horn cells to A and C fiber stimulation and to cutaneous stimuli were made by analyzing central interactions of volleys evoked by stimulating different cutaneous nerve fiber groups, and by analyzing responses of dorsal horn cells denervated of either their A or C-fiber input. The first set of experiments showed that the inhibitory period elicited by Aβγ stimulation reduced excitatory effects from all cutaneous afferents, a result consistent with the gate control theory. The C fiber inhibitory effects reduced spontaneous firing and spikes only in Aδ prolonged discharges. Facilitatory effects from Aδ and C fiber stimulation were potentiated up to a point by increasing stimulation rate. Aδ prolonged discharge inhibited C evoked spikes. If the onset of Aδ and C prolonged discharge was simultaneous, their central effects were facilitated. The second set of experiments showed that L-7 dorsal horn cells selectively denervated of their A input responded normally to sural C fiber stimuli. Adequate stimuli were always of a noxious or nearly noxious character. Responses to adequate stimuli generally had longer latencies than could be predicted from C fiber conduction velocity. Neurons denervated of incoming C fibers responded to narrow ranges of low level mechanical stimuli. Cells with Aβγδ input showed typical prolonged discharges upon sural stimulation and had wider dynamic ranges than cells with only Aβγ input. Small fiber connections to dorsal horn cells extend their dynamic ranges. Both central inhibition and facilitation can result from maximal stimulation of either A or C fibers without necessity of interaction between effects of these two groups.

The rich innervation of the pulp loses its mystery and the uniqueness of its sensation only to pain when the gate theory is applied to it. In the intact tooth, with its protective shell of enamel and dentine, there is a low level of ongoing neural activity probably related to blood flow and cardiac systole. Most of the receptors in the pulp remain quiescent, and the ongoing small fiber activity is insufficient to cause summation at the gate. When the dentine and/or the pulp is exposed by decay or dental manipulations, or when the pulp becomes diseased by some process, a wide variety of nerve fibers are stimulated, none of which are necessarily “pain” fibers per se, but the result of the interaction of the various spinal systems and the central systems is pain. The rich innervation of the pulp has a definite functional significance because the system would not otherwise work.

In the setting of injury, myelinated primary afferent fibers that normally signal light touch are thought to switch modality and instead signal pain. In the absence of injury, touch is perceived as more intense when firing rates of Aβ afferents increase. However, it is not known if varying the firing rates of Aβ afferents have any consequence to the perception of dynamic mechanical allodynia (DMA). We hypothesized that, in the setting of injury, the unpleasantness of DMA would be intensified as the firing rates of Aβ afferents increase. Using a stimulus-response protocol established in normal skin, where an increase in brush velocity results in an increase of Aβ afferent firing rates, we tested if brush velocity modulated the unpleasantness of capsaicin-induced DMA. We analyzed how changes in estimated low-threshold mechanoreceptor firing activity influenced perception and brain activity (functional MRI) of DMA. Brushing on normal skin was perceived as pleasant, but brushing on sensitized skin produced both painful and pleasant sensations. Surprisingly, there was an inverse relationship between Aβ firing rates and unpleasantness such that brush stimuli that produced low firing rates were most painful and those that elicited high firing rates were rated as pleasant. Concurrently to this, we found increased cortical activity in response to low Aβ firing rates in regions previously implicated in pain processing during brushing of sensitized skin, but not normal skin. We suggest that Aβ signals do not merely switch modality to signal pain during injury. Instead, they exert a high- and low-frequency-dependent dual role in the injured state, with respectively both pleasant and unpleasant consequences. NEW & NOTEWORTHY We suggest that Aβ signals do not simply switch modality to signal pain during injury but play a frequency-dependent and dual role in the injured state with both pleasant and unpleasant consequences. These results provide a framework to resolve the apparent paradox of how touch can inhibit pain, as proposed by the Gate Control Theory and the existence of dynamic mechanical allodynia.

The effect of physical exercise on dental pain thresholds, the release of pituitary stress hormones and thermal sensitivity of skin was tested in healthy human subjects. Different levels of exercise (100-300 W) at different pedal frequencies were produced by a cycle ergometer. Thermal limen (the interval between warm and cool thresholds) determined from glabrous hand, hairy forearm and leg was used as a parameter of thermal sensitivity. In all subjects the heart rate and blood pressure were increased with increasing work load. Dental pain thresholds were elevated at high work loads with a concomitant activation of pituitary stress hormone (especially growth hormone) release. Thermal limens at all 3 sites were increased work load, too, independent of the pedal frequency. The increase of thermal limen was most marked in the leg and least in the glabrous hand. The results indicate that physical exercise produces a non-segmental, load-dependent decrease of pain and thermal sensitivity with a concomitant activation of pituitary stress mechanisms. The magnitude of modification varies with skin region. Activation of inhibitory mechanisms at spinal levels via muscle and proprioceptive afferents, in a way suggested by the gate control theory of pain mechanisms, seems to have only a minor, if any, contribution to the present findings, since a higher pedal frequency did not produce a more marked decrease of sensitivity.

The "gate theory" of pain, proposed in 1965 by Melzack and Wall,1 envisioned a system of progressive presynaptic modulation of nociceptive impulses that started the moment posterior rootlets delive...

Endogenous control of nociception has been suggested by postulates of the gate control theory of pain (Melzack and Wall, 1965). Recent research has indicated that lesion-induced hyperemotionality and con- ditioned fear effectively elicit antinociception in the rat (Rosecrans and Chance, 1976). A possible neurohumoral basis of these 'auto- analgesic' phenomena may be the activity of endogenous opiate-like peptides, such as the enkephalins (Hughes, 1975). In this experi- ment we investigated the relationship of behaviorally activated antinocipeption (by conditioned fear) to endogenous CNS peptide activity by assessing binding of radiolabeled opioid to rat brain homogenate. Antinociception was elicited in the manner previously reported (Rosecrans and Chance, 1976) by the classical conditioning of fear to the stimulus cues associated with the tail-flick procedure. Thus, 8 adult, male, Sprague- Dawley rats were individually removed from the home cage, placed on a grid (which also supported the subjects during the tail-flick test), and shocked (0.8 mA) for 15 sec/day for 8 days. Control subjects (n = 10) were handled similarly, but were never shocked. On the day following the last shock, the tail-flick latencies of both groups were determined. During this test, which was conducted blindly, the heat source of the apparatus was adjusted to elicit response latencies of 3--4 sec in con- trol rats, and a 12 sec response latency cut-off

Transcutaneous electrical nerve stimulation (TENS) has been used to diminish postoperative pain1 and many forms of chronic pain2 with reportedly good results. There have been few reports of the use of TENS during childbirth in the physical therapy literature. Several European studies have reported good effects of TENS in the reduction of pain associated with labor and delivery.3–6 Because TENS is a noninvasive analgesic procedure and no maternal or fetal side effects have been encountered,3–5 a firsthand evaluation of this modality seemed appropriate. In this case study, we portray how TENS was used with one patient to prompt physical therapists and other health care providers to develop protocols and conduct research for use of this modality. Melzack and Wall's gate control theory of pain provides one theoretical foundation for TENS.7 According to this hypothesis, electrical stimulation of the large, afferent, high velocity fibers prevents the smaller, slow velocity, pain-carrying A delta and C fibers from transmitting pain signals to the higher brain centers.…

Alleviation of pain is important to the recovery of postoperative patients. The pain they suffer has no useful physiologic purpose. It only results in anxiety, suffering, and pathophysiologic complications if mismanaged. The traditional strategy for managing postoperative pain has been to administer narcotic and non-narcotic analgesics. But not only do narcotics cause a physiological depression that can retard recovery, they are not always effective. From 5 to 20 percent of patients treated with narcotics do not obtain effective relief, and 80 percent report the relief does not last long(1,2). Since 1974, transcutaneous electrical nerve stimulation (TENS) has been promoted as a noninvasive alternative to traditional narcotic analgesia for the management of acute postoperative pain(3-8). In addition to being noninvasive, TENS appears to be simple, safe, and without systemic side effects. How the electrical stimulation of nerves is able to produce analgesia is not certain. One hypothesis, based on the gate control theory of pain, postulates that electrical stimulation of large peripheral nerve fibers "closes the gate" so that painful stimuli cannot get to the spinal cord cells(9). Another suggests that the nerve stimulation triggers the release of endorphins that attach to opiate receptors on the excitatory neuron, so that the transmission of noxious stimuli is inhibited(10). Although a number of studies show TENS to be effective in man

Transcutaneous electrical neurostimulation relieves chronic and acute pain by blocking the transmission of pain impulses with comfortable electrical stimulation of light touch sensation. The original Gate Control Theory of Melzack and Wall provides a working model to explain the significant pain relief afforded patients. As high as 80% of selected patients presenting with a wide variety of causes could achieve some relief after treatment. This comfortable, safe method is finding wide application in clinical practice.

A new form of electrostimulation was investigated in a series of 768 patients with chronic pain. The method is based on the insertion of needle-electrodes in symmetrically selected points of the body and the passage of an electrical current of specified parameters. Treatment sessions last about 15-20 min and are repeated at intervals of 1 to 7 days. The procedure is simple and free from undesirable side effects. The investigation was based on 12000 sessions. The results of the treatment are discussed. No hypothesis of the mechanism of the beneficial effects obtained by electrostimulation is given, though the gate control theory of pain is cited.

This book is a composite of the symposium workshop on the study and control of pain held in January 1975 at the annual meeting of the American Association for the Advancement of Science. The 14 contributors are respected authorities in pain research and therapy. The volume presents a review of recent advances in the theory and treatment of pain from the perspective of medical and dental clinicians as well as that of psychologists and physiologists. It points out the need for an organized multidisciplinary approach to the problem of pain. Mental health maintenance is emphasized as an important and often neglected aspect of the prevention of pain. Recent advances in the use of acupuncture, hypnosis, biofeedback, and behavior modification are also reviewed. Melzack presents perspectives in the pathophysiology of pain, with an historical appraisal that leads to the gate theory of pain. He also focuses on the pressing need for

This is an unabridged republication of Livingston's monograph first published in 1943. It is most appropriate that this classic be brought to the attention of a younger generation. It is a concise, very human, compassionate appraisal of chronic pain problems. With present day popularity of the gate theory for pain, this book takes on even more importance. Here, the origin of that theory is articulated. Repeatedly, it is emphasized that of necessity there must be a modulation of afferent pain impulses in an "internuncial neuronal pool" probably located in the dorsal horn. Also, the balance between the A fibers and C fibers is discussed. The central thesis of this monograph is "that a peripherally situated trigger point is capable of initiating a pathologic state characterized by spreading reflexes, and probably dependent upon a disturbed physiologic status of the spinal centers." Therapeutic alternatives to the usual destructive procedures of rhizotomy

Transcutaneous nerve stimulation (TNS) applied both ipsilaterally and contralaterally with a tonic pain stimulus was compared to a control condition to determine its effect on pain reports. The ipsilateral TNS condition significantly reduced ratings and increased pain thresholds relative to the contralateral and control conditions which did not significantly differ from each other. A Signal Detection Theory analysis of the data was employed to assess the sensitivity and response bias effects of the treatment conditions. Ipsilateral TNS significantly reduced pain sensitivity and response bias in the direction of showing a lesser tendency to report pain. The effects of ipsilateral TNS were most pronounced at the higher levels of stimulation. The results are consistent with Gate Control Theory which holds that ipsilateral TNS attenuates painful sensation. Most importantly, these results support the efficacy of TNS for the treatment of clinical pain.