In understanding the effect of music on pain, it is essential to understand the concepts of pain. Thus the first portion of this paper will provide some background information on pain, define what it is and dicuss pathways in which pain is process in the body.
Chronic pain is a disordered that affects the lives of millions of people each year. Pain is the number one complaint for which people consult physicians; two out of three patients seek relief for pain (Hart, 1974, Chaplin, E., 1991). It is also the most common and frequent cause of suffering and disability that impairs quality of life. Nearly one third of Americans suffer from chronic or reoccurring pain (Gershon, 1986). An estimated of fifty million people suffered from chronic pain, which cost the nation anywhere from $100 million to $50 billion a year in medical costs, lost income, lost productivity, and compensation costs (Cook 1998).
Furthermore, it has been a subject of study since antiquity. Thus, what is pain? Aristotle defined pain as an emotion - opposite from pleasantness and a quality of the soul (Catalano, 1987, Melzack, 1993). Plato suggest that pain was the result of the violent actions of the four elements, earth, air, fire and water, on the soul (Hart, 1974). Rene Decartes looked upon pain from a dualistic point of view, in which the mind and body are two separate and individual entities. Hence, the experience of pain was either purely psychogenic or purely medical in origin. To Decartes, persons in a healthy state were like a well-made clock in perfect mechanical condition, and ill persons was like a clock whose parts malfunctioned (Catalano, 1987, Nicolas & Walsh, 1991). The International Association of Pain Study defined pain and pain-related syndromes as follows (Nicolas & Walsh, 1991).
Pain is an unpleasant sensory and emotional experiences associated with actual or potential tissue damage, or described in terms of tissue damage. NOTE: Pain is always subjective. Each individual learns the application of the word through experience related to injury.
This definition emphasizes that pain is an experience and therefore subjective. Hence, the experience of pain varies from person to person based on past experiences and / or present state of mind.
In 1965, Dr. Beecher investigated the reactions to pain of soldiers wounded in battle to the reactions of civilians about to undergo an operation. Beecher found that soldiers who had severe wounds complained less of pain and asked for less medication than the pre-operation civilians did. According to Beecher, to the soldiers, their severe wounds meant and end to the battle and a ticket home; to the civilians, the pain of surgery means disease and an uncertain future. Hence, the soldiers perceived less pain because they had reduced anxiety. From this study, Beecher concluded that the "meaning of pain affects the experience of pain" (Catalano, 1987). Thus, his study further supports the idea that the experience of pain is subjective and it is influence by a persons past experience and/ or mental state of mind. Given this historical backgrounf on pain, the next section will talk about the different forms of pain and the effects that it has.
There are two types of pain; fast and slow. The former triggers a fast-pain message; the latter produces a slow, aching sensation. Generally, fast pain corresponding to acute pain and the slow pain corresponds to chronic pain. Discussion of acute and chronica pain will be dicuss later.
Fast pains generally serve as warning signal of sudden localized injury (Catalano, 1987, Wells & Nown, 1998). Hence, the purpose of fast pain is to attract our attention; to give a sharp warning that we have been damaged in some way that require a response to avoid further damage. Fast pain is transmitted along the cable network of nerve bundles by large-diameter A-beta nerve fibers. Hence, this is the type of pain that feels like pressure and touch (Catalano, 1987).
Slow pain on the other hand, involves a more complex emotional process. Slow pain is linked to pain tolerance, which changes according to our past experience and our present state of mind (Wells & Nown, 1998). Hence, ones mental attitude can influence how much slow pain one feels. In addition, slow pain are carried in smaller diameter A-delta and C nerve fibers (Catalano, 1987). A-delta pain are the sharp and stabbing pain that is felt from burn or cut; C fiber pain is typically referred to as "slow pain" or secondary pain (Catalano, 1987). Slow pain is the types of pain that produces dull aching sensation (Catalano, 1987).
Both fast and slow pain messages are transmitted to the brain by pain receptors, which are a network of nerve endings throughout the body. Fast-pain receptors are found beneath the surface of the skin. Slow-pain receptors are also located beneath the skin, but it also carries messages from the joints and large internal organs of the body. Discrimination between different pain stimuli (e.g. the prick of a needle and a burn from a hot stove) are possible because different types of pain receptors transmit different pain sensations to the brain (Wells & Nown, 1998). Thus, we are also, able to distinguish between fast and slow pain.
Furthermore, physical pain can be categorized as acute or chronic. Pain is general, and chronic pain is a multidimensional experience. Thus, Melzack and Casey proposed the following three distinct dimensions to the pain experience (Nicolas & Walsh, 1991).
Sensory-Discrimination Dimension. Electrochemical reception of noxious stimulation, afferent transmission, and initial central processing. This dimension is composed of experiencing the location, quality, and intensity of the painful sensations; it is mapped in time (e.g., constant vs. intermittent, acute vs. chronic) and space (location). This dimension includes the when, how long and where of pain.
Cognitive-Evaluation Dimension -A dimension of ongoing perception and appraisal of the meaning of what is happening, or what might take place in relation to the sensation. This dimension is mapped in time (past, present, and future) and occurs at the level of the whole person within the social network.
Affective-Motivational Dimension - A dimension of moods and a sense of meaning and relationship tot he desire to avoid harm or an expectation of harm; this dimension is also mapped in time and occurs at the level of the whole person within the social network.
In the acute pain state, the sensory-discriminative dimension dominates the pain experience and the cognitive-evaluation and affective-motivational dimension are less significant. Acute pain is define as having a "recent, discrete onset and usually subsided in less than one month" (Bono & Zaza, 1988, Nicolas & Walsh, 1991). Over time, the localization sensory-discriminative dimension of pain becomes vaguer and "makes less sense" (Nicolas & Walsh, 1991). During this time, the cognitive and affective dimensions become more prominent and over time, a type of behavior termed chronic pain syndrome is recognized; this is usually characterized by feeling of depression, anxiety, and increased pain.
Chronic pain is defined as pain that has persisted for six months or longer (Gershon, 1986, Bono & Zaza, 1988). In the chronic pain state, the cognitive-evaluation and affective-motivational dimensions dominates the experience. Since most physicians are used to treating acute injuries that improved within the appropriate time period, when it comes to treating chronic pain there is a lacking in knowledge (Nicolas & Walsh, 1991). Furthermore, patients with no measurable anatomical, physiological, or biochemical evidences of functional impairment who continue to feel pain despite rational treatment strategies post a problem for health care providers.
In dealing with this issue, more attention is being focused on the iatrogenic (resulting from the activity of physicians), pistigenic (resulting from the activity of insurance companies) and normogenic components (resulting from the activity of attorneys) of the chronic pain syndrome (Nicolas & Walsh, 1991). For example, consider the routinely prescribed admonishment about acute pain. If it hurts, don't do it. This recommendation often gets interpreted by the patient as an ever-decreasing level of activity and increasing level of disability (Nicolas & Walsh, 1991). Likewise, chronic pain behavior and chronic pain syndrome are part of the socioeconomic environment and culture of the Western industrial society. Hence, as the definition of pain by the International Association of Pain Study emphasizes, "Each individual learns the application of the word" [pain] (Nicolas & Walsh, 1991).
As a result of the uncertainty involving chronic pain syndrome, an attempt to better understand the underlying causes of chronic pain was made. This system divides the development of chronic pain into three stages (Nicolas & Walsh, 1991):
Stage of Acute Injury- At this stage, the sensory-discriminative dimension predominates. The degree of physical impairment and social disability related to or at least correlated with identifiable physical and pathological impairments or with what has come to be expected with a given injury.
The Transition Period- This is a critical period in the recovery process. In most patients, the injury heals, the person goes on to a "good recovery" and resumes a role in society, or the residual disabilities closely correlate with the residual impairments.
The Learned Phase- Through conditioning (learning), further impairments and disabilities result from drug misuse, inactivity, and deconditioning and from prolonged and repetitive functioning in a "sick" or unhealthy role. Here the cognitive-evaluation and affective-motivational aspects of pain predominates.
This step-wise process of developing chronic pain further emphasized the notion that the experience of pain is subjective. As you can see, in the first step, depending on the degree of severity of the injury, an expectation of the degree of pain a person should feel is established. For example, if the person had a broken leg, its level of pain would be expected to fall within the appropriate range of the degree of pain that a broken leg causes. Then, when a person is in the second step, he or she either recover or remain in a state of illness. Finally, in the third step, misuse of analgesic drugs result, chronic pain syndrome develops and the person remains in a sick role. When he or she become deconditioned, chronic pain result.
In accordance with the gate theory, when people with chronic pain feel depressed or despairing, or they are simply not coping too well, their relay stations gates are open more than usual, allowing more pain information to the brain (Wells & Nown, 1998). In this case, even though the original illness or injury does not worsen and the initial number of signals is constant, the experience of pain increases (Wells & Nown, 1998). Now that we have talked about forms of pain, the following section deals with the role of emotions in pain.
Pain is not a sense, like touch, sight, or hearing. Pain is an emotion (Wells & Nown, 1998). Hence, emotion is a fundamental part of the pain experience and not a reaction to the sensory appreciation of pain. Given its complexity, it has been harder to define emotion. For most of us, when we think of emotion, we associate it with the limbic system and generally recognized emotion to be a sensation-like feeling that compels us to act in certain ways. Other definition of emotions has defined it as "the nervous process that determines what kind of stimuli coming from the inner and outer environments are desirable for the organism and what are not". Yet another definition of emotion states that it is "a transitory social role (a social constituted syndrome) that includes an individual's appraisal of a situation and that is interpreted as a passion rather than as an action" (Bromm & Desmedt, 1995). The difference in these definitions and many other definition of emotion not listed here, reflects the divergent theoretical frameworks within which emotion researchers work, and their investigation of different subjective, behavioral, and social events.
There are also many different theories of emotion (Bromm & Desmedt, 1995). For example, one theory proposed by Izard and Blumberg in 1985, states that "the emotion system is viewed as the principle motivational system for human beings. The emotion s are seen as adaptive and motivating organizers of experience and behavior" (Bromm & Desmedt, 1995). From this point of view, pain-induced emotion represents disruption and a redirection of activity. This notion of emotion is also shared by another researcher by the name of Frijda, who states that emotions "can be defined in terms of some form of action tendency or some form of activation or lack thereof" (Bromm & Desmdt, 1995).
Despite these differences in defining what emotion is, there is sufficient agreement among mainstream emotion researchers on the following six points (Bromm & Desmedt, 1995):
These points of agreement help to clarify what science currently mean by emotion, but as far as having a conclusive definition for emotion goes, there is not a universally accepted definition. Having defined emotions look at the central neuroanatomy of emotion.
Early investigators focused on the role of olfaction in limbic function. Hence, the limbic system was formerly called the rhinencephalon, or "smell brain", because it is involved in the central processing of olfactory information. It was not until 1937, that emotion was link to the limbic brain, by Papez. Papez states that "It is proposed that the hypothalamus, the anterior thalamic nuclei, the gyrus cinguli, the hippocampus and their interconnections constitutes a harmonious mechanism which may elaborate the functions of central emotion, as well as participate in emotional expression" (Bromm & Desmedt, 1995). Then, in 1952, a researcher by the name of MacLean, introduced the term "limbic system" and characterized its functions. MacLean divides the limbic system into three main subdivisions: the amygdalar, septal, and thalamocingulate (see diagram 1). These three subdivisions represented sources of afferents that branched out and innervate different part of the limbic cortex. He further postulated that the limbic brain responds to two basic types of inputs: interoceptive and exteroceptive, which refers to sensory information from internal and external environments, respectively.
The closed circuit of information between the limbic system and the thalamus and hypothalamus proposed by Papez in now referred to as the Papez circuit. In the Papez circuit, a fiber tract called the fornix, connects the hippocampus to the mammillary bodies of the hypothalamus, which in turn project to the anterior nuclei of the thalamus (Fox, 1996). The nuclei of the thalamus, then completes the circuit by sending fibers to the hippocampus. Recent knowledge suggests that via these interconnections, the limbic system and the hypothalamus appears to cooperate in the neural basis of emotional states. In support of this, studies of the functions of the limbic system and the hypothalamus, shows that they are involved in the following feelings and behaviors (Fox, 1996):
Aggression-Stimulation of certain areas of the amygdala produces rage and aggression, and lesion of the amygdala can produce docility in experimental animals. Stimulation of particular areas of the hypothalamus can produce similar effects.
Fear-Fear can be produced by electrical stimulation of the amygdala and hypothalamus, and surgical removal of the limbic system results in an absence of fear.
Feeding- The hypothalamus contains both a feeding center and a satiety center. Electrical stimulation of the former causes overeating, and stimulation of the ladder will stop feeding behavior in experimental animals.
Sex-The hypothalamus and the limbic system are involved in the regulation of the sexual drive and sexual behavior, as shown by stimulation and ablation studies in experimental animals. (The cerebral cortex, however, is also critically important for the sex drive in lower animals, and the role of the cerebrum is even more important for the sex drive in humans).
Goal-directed behavior (reward and punishment system). Electrodes placed in particular sites between the frontal cortex and the hypothalamus can deliver shocks that function as a reward. In rats, this reward is more powerful than food or sex in motivating behavior. Similar studies have been done in humans, who reported feelings of relaxation and relief from tension, but not of ecstasy. Electrodes placed in slightly different positions apparently stimulate a punishment system in experimental animals, who stop their behavior when stimulated in these regions.
As a result of these types of studies and their findings, it is believed that emotion is processed in the limbic system and the hypothalamus. As mention before, the experience of pain is subjective, and since it is also an emotional experience look at emotion in learning and memory.
Organisms that can learns from past experiences have adaptive advantages over those that cannot. Memories, such as learning, depend heavily upon emotion, furthermore, memories of past experience tend to shape expectations for the present and future. The affective component of pain fosters adaptation through instrumental (operant) learning as well as classical conditioning (learning by association) (Bromm & Desmedt, 1995). Operant learning requires reinforcers, and reinforcers are events accompanied by emotions. Classical conditioning represents the formation of an association between a normally neutral event and the negative emotion associated with the onset of pain (Bromm & Desmedt, 1995; Carlson, 1998).
Operant learning involves any situation or setting in which the patient is active and reinforcing events take place. A reinforcer event is an event that alters the future likelihood of a behavior recurring when it immediately follows that behavior. There are two types of reinforcer: positive and negative. The former reinforces events that produce a pleasurable outcome (such as rewards), and increases the likelihood that the behavior will reoccur. The latter reinforces events that produce an unpleasant outcome (such as pain), and decreases the likelihood of the behavior being produced again. The positive or negative nature of reinforcers, and their personal significance, occur in conscious awareness as feelings (Bromm & Desmedt, 1995). Hence, reinforcing events are those that are emotionally prominent. Emotion-free events have no reinforcing properties, thus, it does not contribute to adaptive learning (Bromm & Desmedt, 1995).
Classical conditioning on the other hand, involves setting in which a neutral stimuli is given in association with a aversive stimuli, therefore, conditioning the neutral stimulus to elicit the same response that the aversive stimulus evoked. In the case of learning with classical conditioning, it safeguard against dangerous situation. For example, when a person turns on the hair blower to dry his/her hair and hears a buzzing noise, then gets an electrical shock, which causes him/her to drop the hair blower and step away from it. If next time, she turns on a hair blower and hears the same noise again, she;ll immediately drop the hair blower and move away from it, because she has learned and thus, associates the buzzing noise with getting a shock.
Conditioned emotional responses are therefore, essentially sensory-affective association (Bromm & Desmdt, 1995). The amygdala appears to be the primarily structure involved in linking the sensory experience to the emotional arousal and in the conditioning of negative emotional associations (Bromm & Desmdt, 1995, Carlson, 1998). Furthermore, emotion associated with pain also influenced memory. Research in memory shows that both limbic and nonlimbic pathways are involved in memory processes, and evidence exists that the brain preferentially stores information that has strong emotional loading (Bromm & Des��„h„˜_�.�xÅx!�
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�@�x�h��.�D„x"���@and pe icular tract contains somatosensory and viscerosensory afferent pathways that arrive at different levels of the brain stem. Axons of the spinoreticular pathways have active sites resembling those of spinothalamic-tract neurons that project to the medial thalamus, and like their spinothalamic counterparts, transmit tissue-injury information. It has been shown that most spinoreticular neurons carry nociceptive signals and that many of them respond preferentially to noxious input (Bromm & Desmedt, 1995).
The processing of pain signals to produce a response starts in the reticulocortical pathways. There are four different extrathalamic afferent pathways that project to the neocortx: the dorsal noradrenergic bundle (DNB), originating in the locus coeruleus (LC); the serotonergic fibers that arise in the dorsal and median raphe nuclei; the dopaminergic pathways of the ventral tegmental tract that originate from the nucleus basalis of the substantia nigra; and the acetylcholinergic neurons that arise principally from the nucleus basalis of the substantia innominata (Broom & Desmedt, 1995). Of these four extrathalamic pathways, the noradenergic pathway links most closely to negative emotional state (for review, see Gray, 1982, 1987). The set of structures receiving projections from these pathways correspond to the classic definition of the limbic brain (Bromm & Desmedt, 1995).
Although there are many processes that are involved in the feeling of emotion during pain, I will only talk about the role of the central noradrenergic processes in my discussion of emotion and pain, since this system is link most closely to negative emotional state. The noradrenergic system comprised of two central noradrenergic pathways: the dorsal and ventral noradrenergic bundles.
The pontine nucleus known as the locus coeruleus (LC) lies bilaterally near the wall of the fourth ventricle. The locus contains three major projection: ascending, descending, and cerebellar. The dorsal noradrenergic bundle (DNB) constitute the ascending pathways; it projects form the LC throughout the limbic brain and to all the neocortex, accounting for about 70% of all brain norepinephrine (see diagram 2) (Bromm & Desmedt, 1995). The LC is the central source of the majority of central noradrenergic fibers in the spinal cord, hypothalamus, thalamus, and the hippocampus (for review, see Levitt and Morre, 1979; Aston-Jones et al., 1985), in addition to its projections to the limbic cortex and neocortex.
The LC is the relay center for receiving and transmitting sensory information that serve to warn the individual of harm. Nociception increase activity in neurons of the LC, and excitation of neurons in the LC appears to be responding to the nociception (Bromm & Desmedt, 1995). Studies in animals have demonstrated that this response does not require cognitively mediated attention control, since it occurs when the animal is anesthetized (for review, see Korf et al. 1974; Stone 1975; Morilak et al. 1987; Svensson 1987). An experiment done by Foote et al. in 1983, shows that slow, tonic spontaneous activity at the LC in rats changed under anesthesia upon noxious stimulation. Other studies demonstrated that experimentally induced phasic LC activation result in alarm and fear response in primates, and lesions of the LC eliminate normal heart rate increases in response to threatening stimulus (Bromm & Desmedt, 1995).
Furthermore, invasive studies confirm the connection between LC activity and threat. Studies shows that direct activation of the DNB and associated limbic structures in laboratory animals produces a sympathetic nervous response and elicits emotional behaviors (e.g. defensive threat, fear, enhanced startle, freezing, and vocalization) (for review, see McNaughton & Mason 1980). This suggests that increased activity in these pathways corresponds to negative emotional arousal and behaviors appropriate to the situation. Thus, as a subjective experience, "the emotional quality of pain therefore seems to be most accurately described as awareness of immediate biological threat" (Bromm & Desmedt 1995).
The ventral noradrenergic bundle (VNB), like the DNB, is an ascending noradrenergic system; it enters the medial forebrain bundle. Neurons in the medullary reticular formation project to the hypothalamus via the VNB (for review, see Sumal et al. 1983; Bonica 1990). The medullary neuronal complexes also supply 90% of catecholaminergic innervation to the paraventricular hypothalamus via the VNB (for review, see Assenmacher et al. 1987).
The VNB is an important component for pain research because it innervates the hypothalamus. The hypothalamus regulates the anterior and posterior pituitary glands, the autonomic system, is involve in what is referred to as the four F’s (flight, fighting, feeding, and mating), and it is responsible for species specific behaviors. The noradrenergic axons in the VNB respond to painful stimuli as does the hypothalamus (for review, see Kanosue et al. 1984; Svensson 1987). It has also been shown that nociception-transmitting neurons at all segmental levels of the spinal cord project to the medial and lateral hypothalamus and several telencephalic regions (Bromm & Desmedt, 1995). These neurons are the link between tissue injury and the hypothalamic response in which hormonal messengers play a critical role.
The hypothalamic paraventricular nucleus (PVN) serve as the coordinating center for the hypothalamo-pituitary-adrenocortical (HPA) axis. Most of the hypothalamic and preoptic nuclei neurons projects to the PVN. Neurons from the PVN also, receives sensory input from the numerous reticular areas, including the ventrolateral medulla, dorsal raphe nucleus, nucleus raphe magnus, LC, dorsomedial nucleus, and the nucleus tractus solitarius (for review, see Sawchenko & Swanson 1982; Peschanski & Weil-Fugacza 1987; Lopez et al. 1991). Afferents from the hippocampus and amygdala also innervates the PVN.
When the PVN is input from the above areas, it initiate a complex series of events regulated by feedback mechanisms, which ready the organism for behaviors that will maximized its ability to deal with an immediate threat (see diagram 3)(Bromm & Desmedt 1995). This response is commonly referred to as "flight or fight". The PVN has been shown to induce these autonomic responses via both neural and hormonal pathways. Studies shows that it sends direct projections to the sympathetic intermediolateral cell column in the thoracolumbar spinal cord, and to the parasympathetic vagal complex, sources preganglionic autonomic outflow (for review, see Krukoff 1990). In addition, it signals the release of epinephrine and norepinephrine from the adrenal medulla. Thus, these networks of intercommunication implicate the involvement of the HPA axis in the neuroendocrinologic and autonomic manifestations of emotion during pain states.
In addition to controlling neuroendocrine and autonomic activity, the HPA axis is also involved in the coordination of emotional arousal with behavior (for review, see Panskepp 1986). Studies found that direct stimulation of the hypothalamus can elicit well-organized patterns of behavior, including defensive threat behaviors, accompanied by autonomic manifestations (for review, see Hess 1954; Mancia and Zanchetti 1981; Janig 1985a, b). Hence, suggesting that the hypothalamus played a major role in coordinating behaviors and bodily adjustments to challenging circumstance or appropriate biological stimuli. Furthermore, at high level of distress, stress hormones, especially glucocorticoids, may affect central emotional arousal, reducing startle thresholds and influencing cognition (for review, see Sapolsky 1992). A study done by Saphier in 1987 shows that cortisol alters the firing rate of neurons in the limbic forebrain (Bromm & Desmedt 1995). In sum, the HPA axis appears to have the primary responsibility for coordinating behavioral readiness with physiological capability, awareness, and cognitive function.
In summary, the emotional dimension of pain largely involves the combine effect from both the DBN and the HPA axis. This process begins with excitation of the central noradrenergic pathways associated with hypervigilance and fear (the LC and the DNB), as well as the spinothalamocortical pathways, in response to noxious stimuli. Thus leading to the integration of emotion with pain.
The HPA axis enhanced the arousal by activating the neuroendocrine and autonomic mechanisms. These mechanisms then evoke the necessary responses to prepare the organism for flight-or-fight behavior. Also adding to this is the stress-induce responses, which contributes to the pain states. Although I've touched on the pain pathways in talking about the emotional aspects of pain, it is I,portant to discuss the general pathways by which pain and other sensory information are transmitted from the periphery to the brain. Thus, the following section will talk about how pain stimuli are perceive and transmitted. <p></P>
Pain generally starts with a physical event; a cut, burn, tear, or bump (Catalano, 1987). The sensation of pain usually depends on the activation of a set of neurons that includes primary afferent nociceptors, interneurons in the spinal cord, cells of the ascending tracts, thalamic neurons and neurons of the cerebral cortex. Hence, the pain system involves a set of ascending pathways that convey nociceptive information from peripheral nociceptors to higher levels of the central nervous system, as well as descending pathways that modulate that information (Bromm & Desmedth, 1995).
The term nociception refers to the process by which pain information is carried from the periphery sense receptors in the skin and in the viscera to the cerebral cortex through network of neuronal relays (Karoly & Jensen 1987). Exteroceptors on the body surface and propioceptors within the body are specialized neurons that receive stimulation; mechanical (e.g. pressure), chemical, electrical, or thermal (i.e. hot-cold sensitive).
The body is equipped with mechanical nociceptors at the periphery (so-called first-order neurons), which project to second-order neurons in the spinal cord and medulla, which then carries the sensory information (in the form of electrical impulse) to the thalamus, where it synapses with third-order neurons that transmit the impulse to the cortex.
Second-order neurons sends their sensory inputs to the thalamus via two ascending pathways: the dorsal column medial-lemniscal system and the anterolateral system (includes the spinothalamic, spinoreticular, and spinotectal fibers). The former transmits impulse involving position sense, touch, and pressure. The latter pathway is involved in pain transmission (Karoly & Jensen 1987).
The spinal cord is the central concourse along which all pain messages travels to and from the brain (Catalano, 1987). For example, when you stub your toe and your peripheral nerves register alarm, this acute pain is immediately relayed along the nerve fibers of your foot and leg to the substantia gelatinosa located within the dorsal horn of the spinal cord. The cells in the substantia gelatinosa relay this "fast pain" message along the neospinothalamic and terminating in the thalamus and the cortex (see diagram 4) (Catalano, 1987). The cortex is the region in which thoughts are processed.
In contrast, chronic pain moves along a different and slower tract, called the paleospinothalamic tract. This "slow pain" is generally dull, aching, burning, and cramping (Catalano, 1987). Slow pain follows the same path as the fast pain through the spinal cord, but once in the brain, it separates and terminate in the hypothalamus and the limbic structures (Catalano, 1987). The hypothalamus is responsible for stimulating the release of stress hormones. The limbic structures are the places where emotions are processed.
Just as there is an ascending pain pathway from the body to the brain, there is a descending pathway that allows the brain to modulate pain sensory. The brain uses this pathway to send chemical substances and nerve impulses back down to the cells in the spinal cord to act against the pain message sent up by the pain receptors. Hence, the primarily role of the descending pathway is to send chemical messages from the brain to close the gates in the spinal cord to ascending messages (Catalano, 1987, Wells & Nown, 1998).
Descending inhibitory processes are of great interest in the research arena. Hence, it has been extensively studied by scientists. For instance, descending inhibitory processes have been investigated in anesthetized animals (Zimmerman 1984). It was found that the firing of dorsal horn neurons in response to noxious skin heating can be inhibited by stimulation in the periaqueductal gray (PAG) and the lateral reticular formation (LRF) in the midbrain. In addition, inhibition of the spinal cord neurons can also be achieved by electrical stimulation in other regions of the brain, such as the raphe nuclei, the locus coeruleus, and various regions of the medullary reticular formation (for review, see Willis 1982; Mokha 1983; Morton et al. 1983; Gebhart et al. 1984), as well as sites in the hypothalamus, septum, orbital cortex, and sensorimotor cortex (Zimmerman 1984). At the present it is not clear to what extent these different descending systems cooperate and interact, what their normal physiological functions are, and how they can be activated other than by focal electrical stimulation. A key concept in understanf how musci may have a modulatory effect on pain involves the understanding and recognition of the body's own endogenous pain killer. These endogenous pain inhibitory systems are also the process by which synthethic drugs such as morphine exert it effects. Thus, a brief and general overview of endogenous analgesic chemicals will be dicuss in the next section.
Pain messages are two-way traffic. Inhibitory effects are achieved through the descending pathways, which reach from the conscious brain down to the gates in the subconscious brain and the spinal cord. The reason for this is that the gates are places where the flow of pain messages can be controlled or influenced (Wells & Nown 1998). By sending responses back to the periphery, the brain can ordered the release of chemicals that have analgesic effects, which can reduces or inhibit pain sensation.
The landmark discovery of the endogenous pain-suppressing chemicals came about because researchers in Aberdeen, Scotland, and at the Johns Hopkins University Hospital in Baltimore were curious about how exogenous morphine and other opium-derived painkillers works (Cooks 1998). When scientists in Scotland and at John Hopkins injected morphine into experimental animals, they found that the morphine molecules fitted perfectly into receptors on certain brain and spinal cord neurons. This prompted to researchers to speculate that perhaps there were naturally occurring brain chemicals that behaved analogous to morphine.
With further research, the two groups of scientists found not one but a whole family of these endogenous pain-killing chemicals. The Aberdeen investigators called the smaller members of the family <I>enkephalins</I>, which translates into "in the head" (Cook, 1998). In time the larger molecules were also discovered and it was called <I>endorphins</I>, meaning the "morphine within". Nowadays, the word endorphins is often used to refer to the groups as a whole. Now, that we have a clear picture of how these endogenous were discovered, the following will be a brief overview of opioids and its analgesic properties.
Opioid analgesics, like other drugs, exert significant effects on mood and motivation (for review, see Wise, 1987; Herz & Shippenberg, 1989). They have been shown to produce euphoria in humans and are self-administered in animals. Repeated administration of opioids can result in development of tolerance and physical dependence (Bromm & Desmedt, 1995).
Opioidergic neurotransmission is found throughout the brain and appears to influence many central nervous system functions, including nociception (Bromm & Desmedt, 1995). The opioid peptides that have been cloned and characterized in mammalian central and peripheral nervous systems are derived from three precursors: proopiomelanocortin, proenkephalin, and prodynorphin. There are three opioid receptors that are well known and characterized at the present: these are mu-, delta-, and kappa opioid receptors. As of today the enkephalins are considered to be the putative ligands for the delta-receptors, beta-endorphins for the mu-receptors, and dynorphins for the kappa-receptors (Bromm & Desmedt, 1995).
At analgesic doses, systematically administered opioids activate spinal and supraspinal mechanisms via mu-, delta, and kappa-opioid receptors (Bromm & Desmedt, 1995). Opioids generally exert and inhibitory effect of spontaneous, chemically, or synaptically induced neuronally discharged. These effects is believe to occur via the inhibition of inhibitory gamma-butyratergiv (GABAergic) interneurons, opioid excite hippocampal pyramidal neurons and neurons in the rostral ventromedial medulla (Gershon, 1986, Bromm & Desmedt, 1995). Studies have found GABA and it synthesizing enzyme glutamate decarbosylase (GAD) in the superficial dorsal horn (for review, see Clarton & Hayes, 1990), and GABA binding sites and GABA containing neurons have been characterized in almost all pain-related pathways (Bromm & Desmedt, 1995). Recent studies found an increase in GABA-immunoreactive neurons and GABA levels in the spinal cord of rats with unilateral peripheral inflammation (for review, see Castro-Lopes et al., 1992). This effect is proposed to occur in parallel with increase in enkaphalin and dynorphin in response to increase nociceptive input (Bromm & Desmedt, 1995). The following section is a correlation of opioids and other neurotransmitter in the possible roles in which they interact with one another in eliciting pain responses.
Neurotransmitters that are involved in pain response are norepinephrine, dopamine, L-dopa, serotonin, and enkephalines. These neurotransmitters are found mainly in the limbic system and is therefore, thought to play a crucial role in mediation of both pain and emotion.
Animal studies have shown that when serotonin is added directly to the central nervous system, it accumulates in the periventricular areas and enhances the effectiveness of analgesia produced by electrical stimulation and decreased pain perception (Gershon, 1987). Furthermore, studies have shown that blocking presynaptic reuptake of serotonin, increases the level of serotonin in the presynaptic cleft, and consequently raises the pain threshold. The opposite is true when serotonin levels is decreased (Gershon, 1987). In contrast, norepinephrine, on the other hand, is thought to exert its effect by blocking morphine activity; it is also suggested that drugs that increases norepinephrine levels potentially lower pain threshold and increase pain.
Enkephalins are the morphine-like neurotransmitters as mention previously, are found in known nociceptive pathways in the brain (the limbic system) and spinal cord (for review, see Hendler, N., 1982). SInce their discovery, the importance of enkephalins as inhibitory neurotransmitters of pain has been recognized. Since both serotonin and norepinephrine share pathways with enkephalin, the overlap indicates a system of mutually interacting feedback loops. Beofre investigating the therapeutic role of music play in modulating pain, I will provide information on traditional methods of treating pain and talk about some of the commonly used conventional painkillers.
Although there are many pain control therapy out there, I will only talk about three of them. Following the disscussion on pain therapy, I wil talk about some of the different painkillers that are commonly used to treat pain. The first method of treatment that will be discussed here is electrical stimulation. An electrical stimulator for pain relief is a small box-shaped device, also known as the transcutaneous (across the skin) electrical nerve stimulators (TENS) (Catalano 1987; Cook 1998)). The small box is a transmitter that can be carried around with the individual. It transmits electrical impulses through wires to surface electrodes taped to the skin surrounding the painful area. When the device is activated, most people feel an electrical buzzing or tingling sensation, the intensity of which the individual can control by a dial on the transmitting box.
This method of treatment is designed to work on the principle of the gate control theory. Therefore, when activated the electrical signal is picked up and transmitted over the large nerve fiber tracts (A-beta fibers), which in turn inhibit the small nerve fiber tracts (A-delta and C fibers) from transmitting the pain signals to the pain.
TENS is also suggested to work in two other ways. First, in addition to inhibiting pain sensation, the tingling sensation also helps to distract you from the pain (Catalano 1987). Second, some researcher believe that the electrical impulse produced by TENS also stimulates the release of endorphins in the brain and the spinal cord (Catalano, 1987).
Another method for treating pain is Acupuncture. Acupuncture is an ancient Chinese technique of inserting fine needles under the skin at selected points in the body (see diagram 5) The needles are agitated by the practitioner to produce pain relief, which people have report lasts for hours, or even days (Cook 1998).
Acupuncture operates on the principle of "meridians" or imaginary lines drawn on the body that represented internal organs and the trunk (Catalano 1987). Points on these lines are thought to connect different parts of the body. Thus, acupuncture is believe to have an effect on pain relief by stimulating the release of endorphins. Studies have demonstrated that there are higher levels of endorphins in cerebrospinal fluid following acupuncture (Cook, 1998). In addition, studies had also show that injections of naloxone blocks the analgesic effects produced by acupuncture (Cook 1998). However, these results have not been successfully replicated by other researchers.
The last and third method that I will talk about is heat and cold therapy. Studies shows that heat given either as moist heat or dry heat produces relief of pain, muscle relaxation, sedation, and increased local circulation (Hart, 1974). Both heat and cold therapy reduce muscle tension, spasming, swelling or inflammation (Catalano 1987). Heat and cold also decrease the number of nerve impulses from the painful area to the brain, thus, decrease pain sensation. The choice between either heat or cold therapy is usually dependent on the patient. Both are shown to be equally effective in pain control (Catalano 1987). In the following section, I will be talking about some different analgesic drugs that are used in relieving pain and in general, how these drugs work. I will mainly focus on three classes of drugs: the nonsteroidal anti-inflammatory drugs, morphine- and codeine-like drugs, and finally secondary analgesics (i.e. tranquilizers, anticonvulsants and anti-depressants).
Drug treatments for pain is referred to by doctors and pharmacists as the analgesic ladder. Most painkillers fall into three groups: acetylsalicyclic acid or ASA (aspirin); codeine; or morphine. Chronic pain patients are progressed up the ladder by their physicians when the pain worsen or when they can find no other relief (Wells & Nown 1998).
Most of the medications for pain fall into one of the three rungs of the analgesic ladder. Over-the-counter drugs are usually rung one, or aspirinlike; codeine and morphine, rungs two and three, are controlled substances (i.e. needs a doctors prescription) because they are addictive and, thus, can be abuse. In general, morphine-like drugs are not used to treat chronic pain; it may be utilize in particular situations only.
Of the three class of drugs previously mention, nonsteroidal anti-inflammatory drugs (NSAIDs) will be discuss first. These drugs are the ASA-like group, which includes aspirin and ibuprofen.
When a person is injured, damaged tissues release a hormone called <I>prostaglandins (PG) which irritate nerve endings and help nerve fibers carry pain messages to the brain (Wells & Nown 1998; Ebadi et al. 1998). In general, ASA-like drugs inhibit the production of PG,, thus, reduce inflammation and pain (Wells & Nown 1998).
On the second rung of the analgesic ladder are the codeine-like drugs, and on the third rung are the morphine-like drugs. Both Codeine- and morphine-like drugs are habit forming. As a result, morphine is not used to treat chronic illness but is an effective drug treatment for acute pain (e.g. postoperative pain or heart attacks; in some cases it is used in cancer pain). When morphine is used for chronic pain, problems are minimized by taking the drug regularly, rather than only in response to pain (Wells & Nown 1998). Morphine is also very addictive, hence abuse of the drug can result for non-pain reasons such as mood disorders and social problems. When given for more than six months, codeine-like drugs, such as oxyxodone and propoxyphene, can also result in the same addiction problem as morphine-like drugs.
Finally, secondary analgesics are medication that generally have another prime purpose, but doctors have found that one of their spin-off effects is to reduce certain types of pain (Wells & Nown). The most important ones that affect the central nervous system in some way as to modify pain are tranquilizers, anticonvulsants, and antidepressants
Tranquilizers, which include benzodiazepine, diazepam, and lorazepam are intended to work as a muscle relaxant. These drugs are also addicting and addiction usually form after only six weeks of usage (Wells & Nown 1998). By this time patient should be taken off the medication or it will take over the function of the muscles. Once a person is dependent on these drugs, they are locked in a cycle of chronic pain because they are unable to control their muscles without the pills. In addition, when taken it long-term, the person becomes physically and mentally dependent for the temporary sense of relief and euphoria (Wells & Nown 1998). Thus, tranquilizers should only be use as short-term drugs.
Anticonvulsants on the other hand, are usually drugs used for the treatment of patients suffering from epilepsy. Chronic pain and epilepsy are not normally associated but the ability of these drugs to stabilizes nerve membranes may be the reason why they benefit some people. They work on epilepsy by stopping the hyper-irritability that produces messages going down to the muscles to make them twitch. In chronic pain, anticonvulsants work by reducing excessive electrical activity within the brain or within the spinal cord. Anticonvulsants has been shown to be most effective in providing pain relief for shooting pain or knifelike stabbing pain (Wells & Nown, 1998). These are pains that involve nerve irritation or nerve damage.
In contrast, antidepressants on the other hand are non-addictive secondary analgesics (Wells & Nown, 1998). Hence, they can be used as long-term treatments, especially for peripheral nerve damage. Antidepressants are thought to exert their effect by interfering with serotonin and noradrenaline (Wells & Nown, 1998). Although, their prime function is in treating depression, antidepressant can also be used to reduce pain. In the case of treating chronic pain, some antidepressants have a sedative effect and may be taken over night; they may help chronic-pain sufferers to sleep better. Getting a good night sleep is thought to help people cope with their pains better (Wells & Nown, 1998). Now that we have a firm understanding of pain and it psychologicalk and physiological components, we are ready to talk about the role of music in pain.
In talking about music therapy for pain control, it is essential to have an understanding of the history behind its development and uses. Hence, the following section will be an overview of the history of music therapy and how it began.
The origin of music it self is unknown, but the use of music in healing ceremonies is an ancient practice. It is believe that among primitive people, illness was viewed as originating from magico-religious forces, or form the breaking of taboos (for review, see Sigerist, 1944). Thus, music in combination with dances or words, along with songs, and the music producing instruments were considered to be efficacious in exorcising disease or healing wounds. In fact, the oldest known documentation of medical practices, the Kahum papyrus, refers to the use of incantations for healing the sick (Prickett, C & Standley, J, 1994).
In classical antiquity, disease was viewed as an imbalance in harmony between a person’s physical and psychical nature (Tyson, F. 1981). Music, in this case, was believe to have divine significance, and thus, extremely important for restoring harmony and heath.
In the Middle Ages, disease was still seen as a punishment and a result of sinful doing. Hence, the mentally ill were considered to be possessed by evil spirits; leading to cruel torment and exorcised, and murder of thousands of men and women (for review, see Sigerist, 1944). For instance, in Europe, thousands of mentally ill men and women were killed because their hallucinations or delusions was interpreted as a "possession by the devil" (for review, see Stone, 1966).
By the end of the 18th century, scientists began to investigate the effects of music on the human body. It was during this time that the effect of music on function such as cardiac output, respiratory rate, pulse rate, circulation, blood pressure, on electrical conduction of tissues, on fatigue-ness, and on general vibratory effects on the body was initiated (for review, see Diserens, 1922, 1926; Prickett, C & Standley, J, 1994).
By the end of the 19th century, a growing number of researchers started to study the effect of music systematically. Researchers also began looking for relationships between music and physiological or psychological responses. The relationship between music and emotion became a hot topic for lab researches. Hence, music became the emotional reflection of the composer. The utilization of ‘dissonance and rhythmic irregularity’ of music accelerated into the 20th century (for review, see Hanson, 1948).
The development of music therapy as a profession is believed to be a hospital-developed practice that originated in psychiatric hospitals. Much of the contribution to it popularity and establishment originated from wars. Wars are considered to have had a big influence to both bringing in mental illness to the fore, and in establishing strategies for treating the problem. For instances, the civil war help create the field of neurology, which advanced our understanding of brain diseases; World War I, led to the acceptance of psychiatry as an integral part of medical treatment; World War II lead to the development of large-scale screening techniques, group therapy, and increase use of music in hospitals (Tyson, F. 1981).
In sum, the applications of music therapy was believe to have gradually evolved along the following four main lines:
Furthermore, there are three empirically derived assumptions that has been used primarily in neuropsychiatric hospitals:
By the 1930’s, music therapy has taken a new aim; to modify moods, as well as destructive or immoderate physical activity on the open ward (Tyson, F. 1981). When the development of tranquilizer became available in the 1950’s, it became possible to utilize therapeutic strategies to meet the psychological needs of patients. Furthermore, it was report by Gaston in 1968, that the most commonly shared goals reported by music therapists were: 1) The establishment or re-establishment of interpersonal relationships; 2) The bringing about of self-esteem through self-actualization (Tyson, F. 1981).
At about the time of World War II, the role of music in healing advanced to new heights. As wounded soldiers filled hospital beds, doctors noted that music did more than provided a morale-booster; it greatly enhanced the recovery process. Music was then incorporated into the Army’s Reconditioning Program, which uses music for physical reconditioning, educational reconditioning, and occupational reconditioning program, which was under the direct supervision of medical personnel. This became the first official recognition of music as a therapeutic means to be used in military hospitals in assisting the sick and injured during recovery (Tyson, F. 1981). Toward the end of World War II, musicians were assigned to military hospitals to work directly with patients and it was during this time period that led to the establishment of the music therapy profession. Given the overview of how music therapy came to be, we are now ready to look specifically at how music is used in medical settings as a means of reducing pain.
After 80 years of practice and research, there now exist many references to the clinical use of music in medical/dental treatment. Music as an audio-analgesic in dentistry was one of the earliest and most thoroughly investigated areas. For example, a study was done in 1948, that combined music with nitrous oxide-oxygen anesthesia; it was reported that the presence of music reduced vomiting, struggling, delirium, and enabled rapid emergence from the anesthetic stage, and decreased chair occupation time (for review, see Cherry & Pallin, 1948). Similar results were obtained from similar studies (Prickett, C & Standley, J, 1994). For instance, in 1983, a group of Japanese researchers found a significant reduction in blood pressure and pon.
Pain messages are two-way traffic. Inhibitory effects are achieved through the descending pathways, which reach from the conscious brain down to the gates in the subconscious brain and the spinal cord. The reason for this is that the gates are places where the flow of pain messages can be controlled or influenced (Wells & Nown 1998). By sending responses back to the periphery, the brain can ordered the release of chemicals that have analgesic effects, which can reduces or inhibit pain sensatied relaxing effect, can serve as a distraction from the aversive situation, controlling the volume and mix of the music and white noise may allow patient to feel more in control of an aversive situation, or all benefits may be due to a priori suggestion (Prickett, C & Standley, J, 1994).
Studies in a medical setting has shown that music successfully reduced pain during childbirth (for review, see Livingston, 1979). Other studies have shown that music paired with Lamaze exercises can reduce pain and length of labor while enhancing the euphoria of birth (for review, see Clark, McCorkle, & Williams, 1981; Codding, 1982; Hanser, Larson, & O’Connell, 1983; Winokur, 1984).
Utilization of music during surgery has also been shown to have favorable result. For instance, studies shows that music could reduce anxiety in preoperative pediatric patients up to and during the time of the first anesthetic hypodermic (for review, see Chetta, 1981). Post-operative studies for obstetric / gynecologic patients shows that music can reduce pain up to 48 hours following surgery (for review, see Locsin, 1981). It was also demonstrated that post-operative patients using music as part of the healing process required less medication. Furthermore, studies using music as an anxiolytic with orthopedic, gynecologic, and urologic surgery patients shows a decreased in the levels of stress hormone in blood analysis (for review, see Tanioka, et al., 1985). In 1976, it was reported that after installing a Muzak system in the six-bed intensive care unit in St. Joseph’s Hospital in New York, that the rate of myocardial infarction and mortality dropped from 8 to 12 % below the national average (Prickett, C. & Standley, J., 1994). In addition, studies done with music in podiatric treatment shows a significant reduction in perceived pain (for review, see Bob, 1962).
In 1979, a researcher by the name of Christenberry documented the therapeutic uses of music with burn patients, including: alleviation if sterility in the patient’s environment; distraction from constant pain from the injury and from treatments such as hydrotherapy, intravenous fluid therapy, and skin grafts; elicitation of movement for maintenance of joint mobility and to reduce contractures; augmentation of respiration exercises; and reduction of psychological trauma of permanent disability and scarring (Prickett, C & Standley, J, 1994). In addition, Christenberry referenced the following four variables as being essential in maximizing the effectiveness of music as an audio-analgesic tool for painful medial treatment:
In 1978, it was reported that in a pain rehabilitation clinic, combining music with exercise for persons with chronic pain, resulted in increase frequency and duration of exercises and decreased verbalization about pain (for review, see Wolfe, 1978).
As mention earlier in this paper, pain is described in term of bodily injury, and thus the extent to which pain is felt is proportional to the extent of tissue damage. Therefore, traditional treatments have been designed to diagnose the causes by which pain is elicited. As a result, pain-relieving medication is often prescribed for symptomatic relief. However, when the injury has healed but the person continues to have pain, some physicians refers to this as being a psychogenic problem and refers patients to psychiatric services (for review, see Melzack, 1974).
Research in neurophysiology implies that there is not only a direct relationship with the central nervous system but that additional influences from the neocortical activity of the brain which may include processes such as suggestion, attention, anticipation, anxiety, and past experiences of the individual, also plays a role in chronic pain (for review, see Livingston, 1953; Melzack, 1961, 1973, 1974). Pain perception and immune responses are now known to be subjective to both form of stimulus-response learning (i.e. classical conditioning and operant conditioning) (for review, see Achterberg & Lawlis, 1980; Ader & Gordon, 1981; Leventhal et al., 1984; Levine et al., 1978). As a result, a wide range of cognitive-behavioral treatment strategies, including progressive muscle relaxation, verbal rehearsal, operant conditioning, psychotherapy, and hypnosis have been effectively demonstrated as behavioral medicine (for review, see Agras, 1984). Music has been found to be effective in stimulating imagery and in facilitating physiological relaxation responses (Prickett, C & Standley, J, 1994). Music / relaxation / and imagery paradigms have also been shown to be effective in treating chronic stress and chronic diseases (for review, see Rider & Kibler, 1985).
The mechanism by which music affects pain responses appears to be as varied as the research paradigms. Music has been shown to elicit analgesia through distraction or dissociation, as a relaxation cue, through stimulation of acupuncture points, and the production of endorphins in thrills (Pricket, C & Standley, J, 1994). Thus, to understand how music can reduce pain, lets look at some important properties of music.
Music has often been referred to as the "language of the soul". Music can have a strong influence on the body as well as well as the emotion, since the vibrations of music can penetrate through our skin, ears, bones, and viscera to get to us (Steckler, 1998). For instance, certain vibrations clam us, while others energize us and some trigger our emotions and unleash a variety of response from crying to bursting with joy (Steckler, 1998). Furthermore, studies on the neurological effects of music indicates that at least three processes are stimulated (for review, see Bush, 1995):
Which governs the emotional responses of pain and pleasure as well as such involuntary processes as body temperature and blood pressure.
As a result, the recall of association is greatly enhanced.
In a logical sense, we are like musical organs and our physical bodies are like resonators in the sense that we are always responding to the vibrational patterns around us. For example, when resonators are in close contact with each other, and their energy patterns interact, they will eventually become synchronize with each other. Similar effect is observed when two pendulums are in close contact. This phenomena is known as entrainment, and it accounts for why our heartbeat and our breathing tend to synchronize with the beat of music we listen to (for review, see Merritt, S., 1996). Hence, let’s look at the elements of music and see how each can affect the body.
There are five elements that make up music: rhythm, tone, melody, harmony, and timbre. Of these five elements, rhythm has the most intense and fast acting effect on us (Steckler, M., 1998). Rhythm affects both our body and our emotions. Body rhythms such as heart rate, respiration and brain waves are influenced by the vibratory rhythms of music; music may either stimulate or clam them, harmonize, or create discord. In terms of tone, every note, though produce by distinctive rate of vibration, has both physical and psychological effects. Melody refers to the combination of rhythms, tones and accents of music. Melodies produces many intense effects on the listener by stimulating the emotions as well as images, and has been shown to have a great influence on the nervous system (for review, see Merritt, S., 1996). Harmony is produced by the simultaneous vibration of several tones that blends together to form a chord. Depending on the rates of vibration of these sounds, the response will be either a harmonious blending or a jarring discord, both of which have definite physiological and psychological effects (Steckler, M., 1998). Finally, timbre is describe as the difference in the nature and structure of the various musical instruments, the human voice included, which gives to sound a unique quality that is easily recognizable because it elicit different emotional responses. Having established the fundamental principles of music, let’s talk about the theoretical explanation for the mechanisms involved in the interaction of music and pain.
It has been theorized that pain is a sensory discriminative experience affected by cognitive activities such as anxiety and past experiences ( for review, see Melzack, 1963). Thus, focusing on an esthetic experience could lessen an individual’s perception of pain. Furthermore, the psychological component of pain has been recognized as an important element and can be utilize for modifying pain through psychological techniques. In addition, studies have shown that music might alter pain through affective and cognitive effects that stimulate endorphin production and other endogenous mechanism for pain modulation (Magill-levreault, 1993). Hence, through a process of engaging the affective, cognitive, and sensory, music therapy can be used to alter the perception of pain in patients by distraction, alteration of mood, enhancing control, use of prior skills, and promoting relaxation (Magill-levreault, 1993). Let’s look at these theoretical explanations for the mechanisms in which music interacts with pain in greater depth.
Theoretical explanations for the mechanisms involved in the interactions between music and pain have been proposed. The theoretical framework for the utilization of music therapy as a mean for pain management is based on the premise that music may alter the components of the total pain experience and thus decreases pain perception. There are four theoretical perspectives that have been propose that support why many patients report reduced pain sensation after music therapy (Magill-levreault, 1993; for review, see O’Callahan, C., 1996) [See model — Figure 1):
On the contrary, it has also been demonstrated that music, which is inappropriately use, can aggravate pain sensation (for review, see O’Callahan, C., 1996). Thus, increasing pain perception and pain experience.
In conclusion, the experience of pain goes beyond the physical experience of pain; it contains psychological, social, and past experience components as well. The stress and limitation that result from chronic pain can lead to the development of chronic pain syndrome, which includes depression, anxiety, feelings of helplessness, frustration and anger. In such incidence, physicians often recommend psychiatric services. In this case, music therapy for the treatment of pain was analyzed.
Music therapy is a non-pharmacological method of treatment, which helps manage pain and suffering of patients with long-term, or terminal illnesses. The utilization of music for treatment purposes should be individualized with caution given to general state of mood, coping abilities, medical condition, other components that may be relevant to the patient’s need.