Pain
Pain
Psychological aspects of pain perception
The relief of pain and suffering has been a continuing human endeavor since the dawn of recorded history (see Keele 1957). Yet despite centuries of observation and study, we are only beginning to achieve an understanding of the subtleties and complexities of pain. Even though pharmacologists have provided effective “painkillers,” we know little about where and how these drugs act. Surgical procedures that are usually effective in relieving pain can sometimes produce dismal failures, often enough to convince us that we are far from understanding the neurological mechanisms that subserve pain perception.
Part of the difficulty of understanding pain mechanisms lies in the divergent empirical approaches to the problem. Sensory physiologists, anatomists, and psychologists (see Ruch & Fulton 1960, pp. 300-368) have studied pain as a sensory phenomenon and have tended to neglect its motivating aspects. Learning theorists (Miller 1951; Bindra 1959) have dealt with pain primarily as a drive producer and negative reinforcing agent but have generally ignored the other facets of the problem. Finally, medical clinicians, such as anesthetists (Beecher 1959) and surgeons (White & Sweet 1955), have regarded pain as indicative of tissue pathology that has to be treated and abolished and have often had to postulate hypothetical neural mechanisms to account for the complex phenomena they observe. These three approaches are so different that it is not surprising that “pain” has never been satisfactorily defined (Beecher 1959).
The major obstacle to understanding pain, however, has been the perpetuation of a number of theories that have had a powerful influence on the field. The persistence of these theories has resulted in heated controversies that have endured since the beginning of this century. Consequently, one of the most difficult tasks in this field is to separate fact from theory. For this reason the psychological and clinical phenomena of pain, which must be accounted for by any satisfactory theory, will be described before physiological theories and experiments are discussed.
Psychological aspects of pain perception
The obvious biological significance of pain has led to the general belief that it must always occur after injury and that the intensity of pain perceived is proportional to the amount and extent of the damage. The positive aspect of pain is universally recognized: it warns us that something biologically harmful is happening. Reports (Sternbach 1963) of people who are born without the ability to feel pain provide convincing testimony to its value. Such a person sustains extensive burns and bruises during childhood and learns only with difficulty to avoid inflicting severe wounds on himself. Nevertheless, there is convincing evidence that pain, in higher species at least, is not simply a function of the amount of bodily damage alone. Rather, the amount and quality of pain perceived are also determined by past experience and attention, by the ability to understand the cause of the pain and to grasp its consequences. This fact, supported by a large body of evidence, presents a challenge to pain theorists.
Cultural factors
Cultural values are known to play an essential role in the way a person perceives and responds to pain. In Western culture, for example, childbirth is considered by many to be one of the worst pains a human being can experience. Yet the practice of couvade (Kroeber [1923] 1948, pp. 542-543) in cultures throughout the world indicates the extent to which culture contributes to the intensity of pain. In some of these cultures a woman who is going to have a baby continues to work until the child is about to be born. Her husband then gets into bed and groans as though he were in great pain while she bears the child. In more extreme cases, the husband stays in bed with the baby to recover from the terrible ordeal and the mother returns almost immediately to her household work. Dick-Read (1944) has stressed the great extent to which culturally determined fear enhances the amount of pain felt during labor and birth and points out how difficult it is to dispel such fear.
Role of anxiety
The effect of anxiety on the intensity of perceived pain is further demonstrated by studies on the effectiveness of placebos. Beecher found that severe pains (such as postsurgical pain) can be relieved in about 35 per cent of patients by giving them a placebo, such as sugar or saline solution, in place of morphine or other analgesic drugs. As Beecher has pointed out, only about 75 per cent of patients experiencing severe pain are satisfactorily relieved even when given large doses of morphine; the placebo effect thus accounts for about 50 per cent of the drug effectiveness (1959, p. 169). This in no way implies that people who are helped by a placebo do not have real pain; no one will deny the reality of postsurgical pain. Rather it illustrates the powerful contribution of anxiety to pain perception, since the physician may often relieve pain significantly by prescribing placebos to lower the patient’s anxiety as well as by treating the wounded areas of the body. Similarly, experiments by Hall and Stride (1954) have shown that the anticipation of pain raises the level of anxiety and, consequently, the intensity of perceived pain. Experiments by Hill and his associates (1952a; 1952b) have shown that a given level of electric shock or burning heat is perceived as significantly more painful when anxiety is experimentally induced than it is after anxiety has been dispelled. These studies also show that morphine diminishes pain if the anxiety level is high but has no demonstrable effect under conditions of low anxiety.
Role of attention
Attention to stimulation also contributes to pain intensity. It is frequently noted that contestants in a fight or in the heat of a game can receive severe wounds without being aware that they have been hurt. Indeed, almost any situation that attracts a sufficient degree of excited, prolonged attention may provide the conditions for other stimulation to go by unnoticed, including wounds that would cause considerable suffering under normal circumstances. Hypnosis, a trance state in which attention is focused intensely on a person or an object, is perhaps the best-known condition in which people can be cut or burned without their reporting any perception of the event (Barber 1959). Failure in attention may also account for the fact that dogs raised in sensory isolation in specially constructed cages from infancy to maturity (Melzack & Scott 1957) show a frequent failure to respond to normally painful stimulation, such as a flaming match or pinprick, after they are released from their cages. Since these dogs exhibit a remarkably high level of excitement, it is reasonable to suppose (Melzack & Burns 1963) that they fail to attend selectively to these noxious stimuli when they are presented in an unfamiliar environment in which all stimuli are equally attention-demanding. [SeeAttentionandHypnosis.]
Role of meaning
Finally, there is striking evidence to show that the meaning associated with a pain-producing situation is extremely important in determining the degree and quality of pain that are perceived. Beecher observed soldiers who were severely wounded in battle and found that only one out of three claimed that he had enough pain to require morphine. Most of the soldiers denied having pain from their wounds or had so little that they did not want medication to relieve it. In contrast, four out of five hospitalized civilians who had surgical incisions matching the wounds received by the soldiers claimed that they were in severe pain and demanded a morphine injection. Beecher concluded that in the wounded soldier, the response to injury was relief, thankfulness for his escape alive from the battlefield, even euphoria (his wound was a good thing); to the civilian, his major surgery, even though essential, was a depressing, calamitous event; there is no simple direct relationship between the wound per se and the pain experienced (1959, p. 165).
The importance of the meaning associated with a pain-producing situation is made especially clear in conditioning experiments by Pavlov (1923). He found that if electric shocks administered to a dog’s paw are followed consistently by the presentation of food, they eventually fail to elicit signs of pain and produce an entirely different response: the dog salivates, wags its tail, and turns toward the food dish. Masserman (1950) has carried these experiments still further. After cats had been taught to respond to electric shock as a signal for feeding, they were trained to administer the shock to themselves by walking up to a switch and closing it.
Medical aspects of pain
Theories of pain are satisfactory only to the extent that they are able to account for all of the relevant phenomena. There are many forms of pathological or clinical pain that present bizarre features that are difficult to explain; yet they must fit into the framework of pain theory. Two pain syndromes, phantom-limb pain and causalgia, have been studied in detail and represent the most terrible of human pain experiences.
Phantom-limb pain
The presence of a painless phantom limb is reported by the majority of amputees almost immediately after amputation. About 30 per cent, however, have the misfortune to develop pains in the phantom limb, and in about 5 per cent the pain is severe. These pains may be occasional or continuous, but they are felt in definite parts of the phantom limb (Livingston 1943; Feinstein et al. 1954). The pain tends to decrease and eventually disappear in most amputees. There are a few, however, in whom the pain increases in severity over the years and may even spread to other regions of the body, so that merely touching these new “trigger zones” will provoke spasms of severe pain in the phantom limb (Cronholm 1951). Unfortunately, the conventional surgical procedures for controlling pain usually fail to bring permanent relief; thus, these patients may undergo a series of such operations without any decrease in the severity of the pain (Livingston 1943). Phenomena such as these defy explanation in terms of our present physiological knowledge. Attempts have been made to label these unfortunate people as “neurotic” (see Kolb 1954), but there is convincing evidence that argues against such an explanation for all cases (Livingston 1943).
There are a number of features of phantomlimb pain that provide clues toward understanding the mechanisms underlying it.
Peripheral factors. It is known (Livingston 1943) that the neuromas (small nodules of regenerating nerve tissue) in the stumps of amputated patients contribute to phantom-limb pain, since pressure on them can trigger bouts of unbearable pain. Yet excision of neuromas or reamputation at a higher level usually fails to relieve pain for more than a few weeks or months (Livingston 1943; Cronholm 1951). Indeed there is almost unanimity of opinion that peripheral operations are likely to fail and that other procedures should be sought.
Role of sympathetic nervous system. The sympathetic nervous system also plays an important role, because cutting or temporarily anesthetizing the sympathetic ganglia entering the spinal cord (Livingston 1943) is capable of dramatically removing the pain for variable periods of time. Yet it is clearly not the sole cause of phantom-limb pain because pain often returns after the sympathetic ganglia are surgically removed. The contribution that the autonomic nervous system as a whole makes to phantom-limb pain is clear, moreover, from observations (Henderson & Smyth 1948) that pain is triggered in many patients at the start of urination or defecation. Similar sudden increases of pain may be triggered by sexual excitement and orgasm (Kolb 1954).
Emotional factors. Phantom-limb pain is greatly enhanced by emotional factors. Seeing a disturbing movie (Kolb 1954), having an argument with wife or husband (Livingston 1943), and other emotionally disturbing situations are capable of initiating or increasing the intensity of phantom-limb pain.
Role of sensory input. Either increasing or decreasing the sensory input from the stump or related areas is capable of providing relief from phantom-limb pain. Feinstein, Luce, and Langton (1954) have demonstrated that injection of the vertebral tissues of amputees with 6 per cent salt solution produces severe pain at the site of injection, which then radiates into the phantom limb. After this initial onset of pain, there is usually a decrease of the phantom-limb pain. Occasionally the pain vanishes completely following a single injection. Similarly dramatic results may occur after an injection of anesthetic procaine into the vertebral tissues in the attempt to decrease sensory input from these regions. Comparable findings are reported when stimulation is increased or decreased at the peripheral level. Injection of the tender neuromas of the stump with procaine solution often brings about sudden and dramatic relief for variable periods of time. On the other hand, stimulation of the stump, by massage or by hitting it with a small rubber mallet, often produces the only possible relief from phantom-limb pain in a large number of patients (Russell & Spalding 1950).
Spread of pain and trigger sites. Finally, there is the spread of pain and of trigger sites beyond the segments directly involved in the limb. Thus Cronholm (1951) found that touching the small of the back or the forehead may induce spasms of pain in a phantom leg. These trigger zones spread in unusual, seemingly random patterns and are not related in any apparent way to the segmental distribution of the somatic afferent nerves.
Causalgia
Causalgia is a severe, unremitting, burning pain that occurs in about 2 per cent of people who have sustained a peripheral-nerve injury. The pain is felt in the affected limb but may spread to other parts of the body. It exhibits many of the features of phantom-limb pain as well as other even more bizarre characteristics. Surgical procedures have only limited success in the treatment of causalgic pain. Section of the peripheral nerve at a higher level, amputation of the limb, and cutting the dorsal sensory roots that enter the spinal cord have all produced as many failures as successes. Indeed, operations have been performed for causalgic pain at nearly every possible site in the pathway from the peripheral receptors to the sensory cortex, and at every level the story is the same: some encouraging results but a disheartening tendency for the pain to return (see Livingston 1943).
Nonspecific triggering stimuli. A further remarkable feature of causalgia is that a variety of stimuli that can hardly be called “adequate pain stimuli” can produce increases in pain. Sudden noises, the sound of airplanes, the scraping of a shoe on the floor, emotional disturbances, almost any stimulus that elicits a startle response, touching the damaged leg or arm or even blowing lightly on it are all capable of making the pain worse (Livingston 1943).
Sympathetic nervous system in causalgia. The involvement of the sympathetic nervous system in causalgia, as in phantom-limb pain, is obvious. The skin becomes dry and cool, and sweat may drip from a single finger (Livingston 1943). Moreover, injection of anesthetic procaine into the sympathetic ganglia may dramatically abolish the pain for variable periods of time. But the fact that pain may return after surgical removal of sympathetic ganglia (Livingston 1943) indicates that sympathetic-nervous-system activity is not the primary cause of the pain.
Role of sensory input in causalgia. Similarly, an abnormal sensory input from the site of the nerve lesion is clearly implicated as an important cause of causalgic pain. Procaine blocks proximal or distal to the lesion may abolish pain for hours or days, and on rare occasions it never returns. Livingston (1943) reports, moreover, that the pain can be abolished if the patient is trained to tolerate sensory stimulation of the affected limb and is encouraged to use it normally. But the frequent failure of peripheral-nerve surgery to abolish pain indicates that more is involved than simply an irritating peripheral lesion.
Psychophysiology of pain
The psychological and clinical phenomena of pain that have been described above must be taken into account in any satisfactory theory of pain. Since physiological evidence on the sensory mechanisms of pain is intimately bound up with the theories in vogue at the time, it is necessary to consider the physiology in terms of theoretical orientation.
Orthodox specificity theory
The orthodox theory of pain, still the most widely held, was first proposed by Max von Frey in 1895 (see Melzack & Wall 1962) and was subsequently extended in a vast literature on pain mechanisms (see Bishop 1946; White & Sweet 1955). Von Frey’s theory, also known as specificity theory, proposed that there are specific pain receptors (the free nerve endings) which, when stimulated, give rise to pain and only to pain. Following this idea, physiologists proposed that pain is carried by peripheral-nerve fibers of particular diameter (the A delta and C fibers), a distinct spinal-cord system (the spinothalamic tract), and a particular projection area in the thalamus, which is presumed to be the seat of pain sensation. Specificity theory has been the subject of heated debate and controversy since it was first proposed, and an attempt has recently been made (Melzack & Wall 1962) to analyze the features of this theory that make it both attractive and repugnant.
Von Frey’s specificity theory has three underlying assumptions. The first is physiological: the theory assumes that each receptor in the skin has a specific irritability, that is, a lowest threshold for some particular stimulus energy. There is convincing evidence to indicate that this assumption is valid, and it has been restated by Sherrington (1906) as the law of the adequate stimulus. The second assumption concerns the morphological receptor that is associated with pain experience. It is now certain (Weddell 1955) that the free nerve endings transmit information not only about pain but also about warmth, cold, touch, itch, tickle, and the myriad other experiences that derive from cutaneous stimulation. The third assumption of specificity theory is psychological: it assumes a one-to-one relation between skin receptor and psychological experience.
Inadequacy of specificity theory. It is the assumption of a one-to-one relation between skin receptor and psychological experience that has led to attempts at outright rejection of von Frey’s theory. The theory implies a direct transmission system in which there is an invariant, one-to-one relationship between stimulus intensity, peripheral receptor, central-nervous-system pathway, and intensity of pain perceived. Almost all of the psychological and clinical phenomena described above argue against this simple one-to-one relationship. The fact that a light puff of air on the skin, emotional disturbance, or arousal of the autonomic nervous system can elicit bouts of excruciating causalgic and phantom-limb pain indicates that there is more to pain mechanisms than a straight-through system from specific peripheral receptors to a pain center in the brain.
Pattern theory
Alternative theories have been proposed to replace specificity theory. Their history dates back to the time of von Frey’s theory, and each is characterized by complex physiological mechanisms that are postulated to account for the complex psychological and clinical phenomena of pain. Collectively, these alternative theories may be brought together under a single conceptual name: pattern theory. It proposes essentially that information at the skin is coded in the form of nerve-impulse patterns, which provide the basis of our sensory perceptions. These patterns, moreover, can undergo modification during their transmission centrally, that is, the quality and intensity of pain can be modulated by events in the central nervous system, such as memories, emotions, and attention. The most recent formulation of a pattern theory for cutaneous perceptions (Melzack & Wall 1962) proposes that skin receptors have specialized physiological properties for the transmission of particular kinds and ranges of stimuli into patterns of nerve impulses, rather than modality-specific information, and that every discriminably different somesthetic perception is produced by a unique pattern of nerve impulses.
The concept of patterning of nerve impulses, together with three recently discovered features of the skin sensory system, provides the basis for a new theory of pain (Melzack & Wall 1965). First, there is now abundant physiological and anatomical evidence of efferent fiber systems that run from the brain down to the afferent pathways and are capable of modifying or inhibiting the afferent pattern in the course of its transmission centrally (see Livingstone 1959). Second, the dorsal-column and dorsolateral systems of the spinal cord have properties (see Melzack & Wall 1965) indicating that their function may well be that of arousing the central processes subserving memories of prior experience, attention, and so forth, which are then able to act downward on the afferent impulse patterns.
The third line of evidence derives from the recent work of Wall (1962), which shows that a sensory input arriving at the spinal cord has two effects. First, it transmits information from the peripheral nerve to spinal-cord cells whose fibers go to the brain, and, second, it influences the properties of the substantia gelatinosa, a diffusely interconnected band of tissue lying throughout the length of the spinal cord in the dorsal horn. Mendell and Wall (1964) have shown that the substantia gelatinosa can both inhibit and facilitate the transmission of the coded sensory information from peripheral fiber to central cell. They point out that there is a continuous tonic input from the periphery to the substantia gelatinosa, so that continual inhibitory control is exerted over the transmission of nerve impulses across the synapses from peripheral fibers to central cells.
This tonic inhibition can be increased or decreased by the size of the fiber stimulated. Thus the largest A fibers increase the tonic inhibitory effect of the substantia gelatinosa, while the smalldiameter C fibers decrease the inhibitory influence, that is, actually facilitate the transmission of information in such a way that there is a greater likelihood of all inputs, from the peripheral and autonomic nervous systems, as well as from the brain, summating and thereby producing the characteristic pattern of high-frequency bursts of impulses that signals pain. The substantia gelatinosa,moreover, is a functionally continuous unit, so that different parts of the body are connected in a way that permits the spread of trigger zones observed in phantom-limb and causalgic pain.
Gate control theory
These three features of the skin sensory system provide the basis for a gate control theory of pain (Melzack & Wall 1965). The theory proposes that (1) the substantia gelatinosa functions as a gate control system that modulates the amount of input transmitted from the peripheral fibers to the dorsal horn transmission (T) cells; (2) the dorsal column and dorsolateral systems of the spinal cord act as a central control trigger, which activates selective brain processes that influence the modulating properties of the gate control system; and (3) the T cells activate neural mechanisms that constitute the action system responsible for both response and perception.
Figure 1 provides a schematic diagram of the gate control theory, showing the large-diameter and small-diameter peripheral fibers and their projections to the substantia gelatinosa (SG) and T cells in the dorsal horn. The inhibitory effect exerted by the substantia gelatinosa on the afferent fiber terminals is shown to be increased by activity in the large fibers and decreased by activity in the small fibers. The central control trigger is represented by the heavy line running from the largefiber system to the central control mechanisms; these mechanisms, in turn, project back to the gate control system. The T cells project to the entry cells
of the action system. Excitation is represented by +; inhibition by –.
The theory proposes that pain phenomena are determined by interactions among these three systems. For example, a marked loss of the large peripheral-nerve fibers, which may occur after traumatic peripheral-nerve lesions or in some of the neuropathies (Greenfield 1958), such as postherpetic neuralgia (Noordenbos 1959), would decrease the normal presynaptic inhibition of the input by the gate control system. Thus, the input arriving over the remaining large and small fibers is transmitted through the unchecked, open gate produced by the small-fiber input. This, together with the opportunity for summation of inputs into thesubstantia gelatinosa from other parts of the body and from the brain, provides the basis for the triggering of pain by a variety of stimuli that are normally not noxious.
Affect and motivation
Pain has generally been considered primarily a sensory experience somewhat similar to sight or hearing. In one important respect, however, pain differs from vision and hearing: it has a unique, distinctly unpleasant quality that wells up in consciousness and obliterates anything we may have been thinking or doing at the time. It becomes overwhelming and demands immediate attention. Besides its sensory component, then, pain also has a strong emotional quale that drives (or motivates) the organism into doing something about it. Ensuing responses are such as to stop the pain quickly by whatever course of action is possible.
Introspectionist psychologists at the turn of the century made a sharp distinction between the sensory and the affective dimensions of the pain experience. Titchener (1909) was convinced that there is a continuum of feeling in conscious experience, distinctly different from sensation, that ranges through all degrees of pleasantness and unpleasantness. These two dimensions, the sensory quality and the affective quale, are brought clearly into focus by clinical studies on prefrontal lobotomy (Freeman & Watts 1942), a neurosurgical operation for intense pain in which the connections between the prefrontal lobes and the rest of the brain are severed. Typically, these patients report after the operation that they still have pain but that it no longer bothers them; they simply no longer care about the pain and often forget it is there. It is certain that the operation does not stop pain perception entirely, since the sensory component is still present. The predominant effect of the operation seems to be on the affective coloring of the total pain experience; the terribly unpleasant quality of the pain has been abolished.
Brain areas involved. Recent experiments suggest that there are portions of the brain that are particularly concerned with the motivating aspects of behavior. Miller (1957) has recently found subcortical areas in the brain that produce vigorous escape reactions, cries, and other emotional behavior characteristic of pain perception when they are stimulated electrically. It seems possible that the activities in these areas provide the neural substrate for the affective, “driving” component of pain perception. [SeeNervous System, article onBrain Stimulation.]
Toward a definition of pain
In recent years the evidence on pain has moved in the direction of recognizing the plasticity and modifiability of events occurring in the central nervous system. In the lower part of the brain at least, the patterns of nerve impulses evoked by noxious stimulation travel over multiple pathways going to widespread regions of the brain and not along a single path going into a “pain center.” The psychological evidence lends strong support to the consideration of pain as a perception determined by the unique past history of the individual, by the meaning the stimulus has to him, by his “state of mind” at the moment, as well as by the sensory nerve patterns evoked by a physical cause. In this way, pain becomes a function of the whole individual, including even his thoughts and hopes for the future.
Pain, then, refers to a category of complex experiences, not to a kind of stimulation. Clearly, there are many varieties and qualities of experience that are simply categorized under the broad heading of pain because they defy more subtle verbal description. There are the pains of a scalded hand, a stomach ulcer, a sprained ankle; there are headaches and toothaches. But there is also the heartache of the scorned lover, the pain of losing a dear friend. It may be argued that the pain of bereavement is very different from the pain that follows surgery. But the pain of a coronary occlusion is just as uniquely different from the pain of a scalded hand.
Why is it so difficult to achieve a satisfactory definition of pain? The answer appears to be that pain is not a single, specific experience that can be analyzed and manipulated. It may be agreed that pain, like vision and hearing, is a complex perceptual experience. But the numerous, diverse causes of pain prevent the specification of a particular kind of environmental energy as the specific stimulus for pain, in the way that light can be specified as the adequate stimulus for vision, and air pressure waves for hearing. Pain is a category of experiences, signifying a multitude of different unique events having different causes and characterized by different qualities varying along a number of sensory and affective dimensions.
Ronald Melzack
[Directly related are the entriesNervous System; Senses; Skin Sensesand Kinesthesis. Other relevant material may be found inDrugs; Hysteria; Psychology, article onPhysiological Psychology; Psychosomatic Illness.]
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