Kathleen S. Brown, PhD

Continuing Education Information

Graduate training for most psychologists is typically provided solely through the lens of psychological literature. At the time of my training in the 1980s, emphasis was placed on behavioral methods originally proposed by Fordyce (1976) for the management of chronic pain, with some integration of cognitive theory and behavioral interventions. However, current pain theories are rooted in both medical and psychological paradigms, both of which must be understood by psychologists to comprehensively manage the multidimensional nature of pain. Advances in the understanding of brain physiology and their diagnostic techniques have revealed causes for disorders previously thought to be diagnostic puzzles and believed to have no physical basis. The current pain literature reports that pain has interactive biomedical, psychological and sociocultural components. Persistent pain resulting from mechanically and chemically-caused physiological insult causes neuroplastic changes that often become difficult to reverse. This concept is well documented in pain literature (Gamsa, 1994). With the persistence of pain input, the cause of the pain experience itself becomes multifactorial because it is composed of both sensory perceptions and affective responses that reinforce behaviors (Turk & Rudy, 1987; Keefe et al., 1992; Jensen et al., 1994; Pilowsky et al, 1995) making it more difficult to treat. Due to the multidimensional nature of pain, multimodal interventions are most often required for its effective management (Corry, Linssen & Spinhoven, 1992; Keefe, Dunsmore & Burnett, 1992).

One in every six Americans has chronic pain and it is the number one reason why people seek medical care in the United States (Gallup, 1999). In 1998, the World Health Organization (WHO) published survey results from 25,916 primary care patients and found that 21.5percent reported severe pain for most of a 6-month period during the previous year (Gureje, Von Korff, Simon, & Gater, 1998). Types of reported pain, in decreasing order of frequency, included joint, head, back, arm and leg, chest and abdominal. Despite this prevalence of pain in the general population, pain continues to be under-treated, untreated or improperly treated. Regulatory agencies, such as the Joint Commission on Accreditation of Healthcare Organizations (JCAHO), have recognized that pain is a major health problem and "patients have the right to appropriate assessment and management of pain" (JCAHO, 2000). Even though JCAHO responded to this continued national problem by adopting standards for the assessment and treatment of pain, the problem remains undertreated. Recognition of the possible combination of neurophysiological and psychophysiological processes involved with persistent nonmalignant pain can help to guide appropriate therapy and determines patient prognosis. Given the pervasiveness of pain complaints in health care, this article will focus on why it is necessary for psychologists to comprehensively understand the biopsychosocial model of pain. Additionally, the synthesis of the neurophysiological and psychophysiological underpinnings of the pain experience and its impact on health psychology interventions will also be reviewed.

Definition of Persistent Pain 

Persistent or chronic pain has been defined as pain that lasts more than 3 to 6 months or beyond an expected time for healing. Some pain experts define chronic pain as (1) pain persisting for at least one month beyond the usual course of an acute illness or the time required for an injury to heal; or (2) pain associated with a persistent pathologic process; or (3) pain recurring at intervals of months or years (Bonica, 1979). Persistent pain is a condition not associated with malignancy or acute pain caused by trauma, surgery infection or other factors. Breakthrough, episodic and transient pain are some of the terms most commonly used to refer to the pain flares that occur beyond an individual's baseline chronic pain. The fact that there are no widely accepted definitions for any of these terms only complicates literature reviews. Regardless of how persistent pain is defined, once pain becomes ongoing, specific management strategies, which often differ from acute pain treatment modalities, need to be considered. Initiation of multidimensional pain management interventions, at the onset of pain, is essential to minimize the development of persistent pain.

The Neurophysiology of Persistent Pain

The mechanisms associated with the transition from acute into chronic pain still remain unclear. This transformation can occur by the absence of apparent injury, or after healing from an injury. The pain experience is a complex phenomenon that is influenced by prior experience, learned behaviors and by the context in which the noxious stimulus occurs. Nociception is the physiologic response to frank or potential tissue damage or prior tissue damage. For example, an individual who sustains a herniated lumbar disc protrusion following a sports injury may present quite differently than an individual who sustains the same anatomic pathosis in a workplace accident given the contexts of the injury. Three distinct types of pain have been distinguished: (1) nociceptive pain: an acute response to an intense or noxious stimulus, (2) neuropathic or pathologic pain: a combination of unremitting and spontaneous burning, electric sensations, and/or abnormal sensitivity to normally innocuous (allodynia) or noxious stimuli, and (3) central pain due to central neuroplastic changes (Mannion & Woolf, 2000). Unlike nociceptive pain, which is a normal adaptive mechanism that serves to protect an organism from injury and during healing, neuropathic pain has no protective value. The distribution of neuropathic pain generally follows a pattern of specific nerve innervation, though the type of pattern can vary tremendously. O'Connor and Dworkin (2004) report that even though the pattern of neuropathic pain distributions differ significantly, they still make sense neuroanatomically. For example, a diabetic neuropathy follows a stocking, then glove pattern; shingles (called postherpetic neuralgia) a dermatomal distribution; central post-stroke pain follows the distribution of stroke involvement while post-thoracotomy pain follows the sensory nerves in the distribution of the incision. Physicians typically recognize dermatomal patterns, consistent with nerve root involvement. However, there are numerous other pain pathologic referral patterns, such as myofascial patterns, that do not follow this linear model and may be incorrectly referred to as non-physiologic.
Recent chronic pain research has delineated various neurophysiologic and neuroimmunologic events in the central nervous system (CNS) that manifest in pain behaviors and neurochemical nociceptive responses. After tissue injury, as chemical changes occur, the nociceptors (pain receptors) themselves may physically and functionally change to self-regulate or modify the body's responses to injury. There are several nerve fibers that are involved in pain transmission: C, A-delta and A-beta fibers. Speed of transmission is slowest in the unmyelinated C-fibers, faster in lightly myelinated A-delta fibers and still faster in myelinated A-beta‚ fibers. Pain information carried by C and A-delta fibers is perceived by the brain in two different ways. Pain information carried by A-delta fibers serves to localize the area of the body that "hurts" and is associated with acute/emergent and a superficial type of pain. C-fiber information serves to activate autonomic, fight, flight or freeze defensive mechanisms and generates more of an emotional response to the pain input, as this transmission is slower and associated with a deeper, more diffuse type of pain. As these fibers enter the spinal cord, they are directed into different layers of the vertebral body according to the type of information that is transferred from the peripheral first order neurons. These primary neurons then synapse with their respective second order neurons and deeper interneurons, which may either facilitate or inhibit pain transmission. Dorsal horn neurons, like nociceptors, can also alter their responses to repeated primary afferent pain input. The function of neuron inhibition or excitation is called neuromodulation and can be explained by the gate-control theory of pain. Over the years, the original pain theory (Melzack & Wall, 1965) has been systematically reformulated in order to serve as a comprehensive model of pain encompassing all aspects of sensory, cognitive, affective and behavioral information (Melzack & Loeser, 1978). In their research on phantom limb pain and transection of the spinal cord in paraplegics, Melzack and Loesser proposed a central pattern generating mechanism that is responsible for pain perception in the absence of afferent CNS input. These patients continued to report pain below the levels of their lesion or amputation, the mechanisms suggested for this responsible pain must have been centrally located to the level of the spinal cord lesion and that the loss of afferent input to areas of the brain subserving pain led to neuronal excitation at central levels exceeding their thresholds, and therefore, create the perception of pain.

Our bodies are constantly modulating noxious and painful information at all levels of the CNS. When pain information enters the limbic system, prefrontal cortex and somatosensory cortex with negative connotations, these signals get transmitted to the spinal cord and may modify nerve cell processing. With the practice of good coping skills, nociception at the spinal cord level may be down regulated resulting in less pain. If one is anxious or worried, this pain information is most likely up-regulated or enhanced exacerbating the overall level of pain experience. Thus, physiological changes may occur at all levels of the CNS, within the nociceptors themselves, the dorsal horn of the spinal column, sensory thalamus and cerebral cortex, which persist beyond the resolution of the noxious event.

Activity-dependent plasticity occurs when the spinal cord becomes progressively more responsive to subsequent sensory input. This CNS hypersensitivity is initiated by wind-up and termed central sensitization. Wind-up is an enhanced temporal summation of pain and is a prelude to the more ongoing process of central sensitization. These two phenomena are important to understand because central responses to noxious input can be modified by physical measures, such as medications, and by psychophysiological strategies, such as relaxation training or imagery, and therefore impact the experience of chronic pain over time. Wind-up reflects a physiological activation of the spinal cord after an intense or persistent barrage of afferent nociceptive impulses. This mechanism is thought to be associated with widespread or generalized pain, such as seen in the condition of fibromyalgia. Interestingly, Montoya et al (2005) reported the presence of abnormal processing of somatosensory and affective pain-related information in fibromyalgia patients. Central sensitization causes an amplification of incoming pain signals at the level of second order neurons in the spinal cord dorsal horn. The decrease of ongoing peripheral nociception by medications which block second order neuron nociceptors, called NMDA (N-Methyl-D-Aspartate) receptors, not minimize wind-up, tolerance to opioid pain medications and the development of central sensitization.

Following tissue or nerve injury, neuroplastic changes can occur both at the periphery and centrally which may cause pain hypersensitivity. These neuroplastic changes may lead to allodynia, in which non-noxious stimuli produce pain, and hyperalgesia, in which noxious stimuli produce an exaggerated and prolonged pain. When pain hypersensitivity persists after an injury has healed or occurs in the absence of any injury, pain serves no benefits, and becomes a symptom of pathological CNS neuroplastic changes. CNS sensitization is associated with an increase in neuron excitability, making them more sensitive to peripheral and central stimuli and sensory input. When central sensitization occurs, an increase in the excitability of CNS neurons, alter the synaptic connections between the peripheral nociceptor and spinal cord neurons. Subsequent normal input may then produce abnormal responses. Low-threshold sensory fibers activated by very light touch of the skin, for example, may now activate central neurons that normally only respond to noxious stimuli. As a result, input that would normally evoke innocuous sensations, such as a breeze to the face or a handshake, now produces pain. Although this pain feels as if it originates in the periphery, it is actually a central manifestation of abnormal sensory processing. {Because of the wide variety of neurotransmitters (e.g., substance P, serotonin, prostaglandins, bradykinin, leukotrienes, histamine, norepinephrine) and receptors (e.g., opioid, serotonin, acetylcholine, dopamine, norepinephrine) involved in pain pathways, many potential targets for drug therapy exist.}

Antelman's et al. (1997) research showed that the exposure of physiological subsystems, such as the endocrine, neurohumoral and autonomic systems, to behavioral or chemical stressors of sufficient intensity, can induce a dysregulated, cyclical pattern of pain in response to subsequent exposure. They hypothesized that this phenomenon is applicable to such a wide variety of physiological systems and may represent a general principle of biological functioning designed to reestablish homeostasis. Scaer's (2001) model of the neurophysiology of dissociation associated with chronic conditions, such as in PTSD or complex regional pain syndromes (CRPS), theorizes that neurophysiological syndromes are initiated by a failed attempt at defensive/escape efforts during a life threat. This is perpetuated if spontaneous recovery from the resulting freeze response is blocked. Lack of recovery from this freeze response results in a conditioned association of all sensorimotor information assimilated at the time of the traumatic event or injury, as seen in patients with CRPS.

Patients with chronic pain are characterized by a pattern of selective processing that favors the encoding of pain-related information. Weich et al (2005), using functional magnetic resonance imaging (fMRI), showed that activity in the orbitofrontal and medial prefrontal cortices, insula, and cerebellum correlates with the intensity of tonic pain. In an experimental capsaicin-induced heat hyperalgesia model, the pain-related activity in the medial prefrontal cortex and cerebellum was modulated by the demand level of the cognitive task. Their findings highlight a role for these structures in the integration of motivational and cognitive functions associated with a physiological state of injury. Within the limitations of an experimental model of pain, their findings are relevant to understanding chronic pain's neurobiology and pathophysiology and its amelioration by cognitive strategies.

The Psychophysiology of Persistent Pain

Psychological and psychiatric chronic pain research has traditionally reinforced the dichotomy between the mind and the body and a linear causal view of pain's etiology. Gamsa (1994) delineated these assumptions: that pain is caused by either organic or psychological factors; pain which does not correlate to a physical pathology is psychological in origin and patients with undiagnosed intractable pain possess characteristic personality traits. Psychological research has failed to yield compelling evidence for direct causal links between psychological factors and pain in the general population of pain patients (Gamsa, 1994; Gatchel, 2000) even though the response to pain is clearly influenced by one's personality traits and coping strategies (Block, Gatchel, Deardorff & Guyer, 2003). The notion that pain is either verifiable or due to psychological disturbance is obsolete. The clinician's responsibility is to understand and treat the patient with sensitivity, rather than having the patient provide proof of their pain (Feinman & Newton-John, 2004).

Psychological stress is known to induce physiological responses which increases the activity of the hypothalamus-pituitary-adrenal (HPA) axis. Overactivation of the HPA axis triggers cortisol secretion from the adrenal cortex and increases activity in the sympathetic-adrenal-medullary (SAM) system (Axelrod & Reisine, 1984; Bionid & Piccardi, 1994). These changes cause adrenalin and noradrenaline secretion from peripheral sympathetic nerve endings and the adrenal medulla. HPA and SAM hyperactivity is correlated with anxiety disorders in response to psychological stress (Gerra, Zaimovic, Zabrelli et al, 2000) and more recently reported in patients with myofascial pain (Yoshihara, Shigeta, Hasegawa et al., 2005). Pain is a stressor among many, and only one source of suffering.

There is a large body of literature acknowledging a high incidence of depressive symptoms with chronic pain (Turk, 1994; Lindal, 1990; Trief & Carnricke, 1993). In the United States, depression is the single most common psychiatric diagnosis in patients with chronic pain in general (Fishbain, 1986) and specifically with chronic low back pain (Magni, 1987). Chronic pain patients who are depressed secondary to their pain conditions are more likely to have poor physically functioning and more significant levels of physical disability (Fields, 1987). Chronic pain patients who scored higher on depressive symptomatology testing report greater intensity of perceived pain, increased pain behaviors, and noted pain interfered with daily living more than patients experiencing fewer depressive symptoms (Haythornthwaite, Sieber, & Kerns, 1991). Burns et. al. (1998) found that feelings of helplessness decreased as pain severity decreased. This study demonstrated that depression significantly relates to levels of perceived pain. Individuals suffering from uninterrupted, extreme pain and disability are highly vulnerable to suicidal ideation (Fuerst, 1993; Heller, Flohr, & Zegans, 1989; Ivey, Ivey, & Simek-Morgan, 1993; Jourard, 1971). Although it is frequently assumed that pain patients have a premorbid history of depression, Hendler (1989) found that, despite the 77 percent incidence of depression in chronic pain patients in his practice, 89 percent did not have a pre-morbid history of depression prior to the onset of pain.

Persistent pain can often lead to anxiety and result in fear avoidant behavior (Vlaeyen & Linton, 2000). Anxiety is part of the motivational-affective dimension of pain in Melzack & Torgerson's 3-component model of pain (1971). The motivational-affective component compels an individual in pain to act in a way that relieves the aversive stimulation. Physical withdrawal, rest and immobility are innate survival skills in acute pain, but are maladaptive in chronic pain. Often individuals in pain anticipate future increases in pain intensity and thus avoid physical activities that have previously been associated with increased pain. Another effect is the tendency to be "on guard", tense skeletal muscles or use protective movements and postures (Hanson & Gerber, 1990). Consistent guarding coupled by decreased physical movements and activity usually result in a physical deactivation syndrome, associated with increased levels of pain and disability. Both physical and emotional tension, initially influenced by pain, decrease the pain threshold, augmenting the pain experience. The pain cycle usually begins because the pain leads to tension which then results in decreased activity, which in turn, increases tension and often leads to more pain.

Several cognitive-behavioral models have been developed which suggest that fear and avoidance variables were critical mechanisms by which acute pain develops into chronic pain (Lethem, Slade, Troup & Bentley, 1983; Philips, 1987; Waddell, Newton, Henderson & Somerville, 1993). Pain catastrophizing promotes avoidance behavior and hypervigilance to bodily sensations, this if often followed by disuse, depression, and disability. These factors then maintain the pain experience and reinforce fear reactions and avoidant behaviors (Amundson, Norton & Norton, 1999; Vlaeyan & Linton, 2000).

The physical experience of severe, unrelenting pain as a result of trauma, may relate to the development of PTSD symptoms (e.g. Geisser, Roth, Bachman, and Echert, 1996). Geisser et. al. (1996) reported that PTSD symptoms were positively related to increased affective distress, self-report of pain, and functional disability in patients with chronic pain. Pain, injury and chronic illness can be life altering and may greatly impact normal functioning. Chronic pain often results in disability with a cognitive re-evaluation and reintegration of one's belief systems, values, emotions, and feelings of self-worth (Miller, 1990). The subjective meanings associated with interpersonal loss are evident on a continuum. These meanings extend from the relatively mundane appraisals, to concrete evaluations of specific problems caused by the loss, to deeper and more encompassing questions about emotional well-being and identity, to the most profound existential concerns about the meaning of life (Bonanno & Kaltman, 1999).

Early childhood victimization or other trauma is often found in patients with chronic pain syndromes (Lampe, Doering, Rumpold et al, 2003; Romans, Belaise, Martin, Morris, & Raffi, 2002; Yucel, Ozyalcin, Sertel, Camlica , Ketenci , Talu, 2002). Curran et al (1996) reported that up to 70 percent of chronic pain patients are victims of sexual or physical abuse. As advances in neuroscience continue to increase our understanding of the neurobiological consequences of trauma, the mechanisms underlying one's vulnerability to development of persistent pain is becoming more clear. Trauma causes a neurobiological vulnerability in various neuroregulatory systems that enhance or sensitize the psychological processing of sensory information. Thus, pain perception becomes a synergistically elaborated aggregate of peripheral neural transmission in conjunction with an idiosyncratic, psychodynamic meaning (Grzesiak, 2003).

Behavioral methods for chronic pain management, originally proposed by Fordyce (1968), have been primarily focused at reducing disability through the modification of environmental contingencies and cognitive processes. In general, three behavioral treatment approaches have been distinguished: operant, cognitive and respondent. A systematic review of studies using behavioral treatment for chronic low back pain (CLBP) assessed the magnitude of effect by computing a pooled effect size for post-treatment and long-term results using the random effects model for each domain, i.e., behavioral outcomes, overall improvement, back pain specific and generic functional status, return to work, and pain intensity (Ostelo, van Tulder, Vlaeyen, Linton, Morley, & Assendelft, 2000). Seven studies (33 percent) were considered to be of high quality. Strong evidence (4 trials using 1,345 subjects) was found in favor of a combined respondent-cognitive therapy for a medium positive effect on pain compared to a waiting list control (WLC); while moderate evidence (2 trials, 39 subjects) favored progressive relaxation for a large positive effect on pain and behavioral outcomes. When comparing operant treatment to WLC, no significant differences could be detected on general functional status (strong evidence: 2 trials, 87 subjects) or on behavioral outcomes (moderate evidence; 3 trials, 153 subjects). It is not known whether these results sustain in the long term. No significant differences could be detected between behavioral treatment and exercise therapy.

Schmidt, in his critique of the operant theory of chronic pain (1987), supported an alternative proprioceptive theory. He proposed that chronic low back pain patients have shorter endurance in pain-relevant situations because of a lower tolerance to proprioceptive input, which included pain, fatigue, anxiety and tension stimuli. into a Cognitive-Behavioral Theory (CBT) of chronic pain. While not ignoring the observable behaviors of pain patients and their associations with social reinforcers, CBT interprets these phenomena from a cognitive perspective and focuses more directly on patients' thoughts about, and appraisals of, their pain. Considerable research has established the benefits of cognitive-behavioral interventions in pain management (Keefe & Caldwell, 1997; Morley, Eccleston & Williams, 1999; McCracken & Turk, 2002; Turk, 2003).

More recently the psychophysiological interconnections between the mind and body have been referred to as allostatic load rather than the historical term stress (Ray, 2003). Allostasis refers to the psychophysiological system of communication between the brain, endocrine system, and the immune systems (McEwen, 2002). Allostatic load, or stress, occurs when there is a dysregulation between coping skills and the environmental demands. Pain patients must learn that poor reaction skills to stressors significantly increase their pain, which in turn, is a stressor to homeostasis. Coping skills training should focus on trying to separate pain from other sources of stress, specifically those that are not in one's control.

Self-Regulation Strategies & Psychophysiology

Self-directed treatment broadens pain management to permit individual responsibility and control for as much of the therapy and health related maintenance as possible. Self-management training primarily focuses on changing thoughts (cognitions) and actions (behavior), which in turn changes negative emotions and pain sensations. The goals of self-management include the following: (1) improving the ability to divert attention away from pain sensations through activities and mental techniques, (2) improving overall physical conditioning by decreasing muscle fatigue, (3) improving pacing of daily activities, and (4) learning how to manage depression, anger, pain flares and interpersonal conflict more effectively (Turk et al, 1983; Hanson & Gerber, 1990). The advantage to using a self-directed treatment approach lies in the greater specificity of therapy procedures. This enhances the uniformity of training and evaluation, client-centered control, and the probability of maintaining therapeutic effects after contact with the provider is ended.

Ray (2004) identified four categories of coping skills important for health. Adapted for managing pain, the first is knowledge of one's pain condition, health and well-being. The more an individual understands about their pain condition, the better they are to understand, control and effectively manage it. The second class of skills was termed inner resources; this reflects the set of beliefs, assumptions and predictions individuals hold about their condition. Social support, the third category, refers to the interpersonal relationships that are formed and nurtured to sustain and aid with health crises. The fourth category of coping skills is spirituality; this is defined as an individual's sense of peace, purpose, and connection to others, and beliefs about the meaning of life. The more successful approaches to pain management educate the patient about their body and how it 'feels' pain, and teach active self-care skills and ways of helping the patient become more active in their healing. Patients must learn to recognize that progress evolves over time with the integration of various techniques in order to increase function and quality of life.
Chronic pain management also depends on how patients choose to cope with pain and how it impacts their lives. Jensen, Neilson & Kerns (2003) proposed a motivational model of pain self-management for enhancing engagement in and adherence to chronic pain treatment programs. The utility of readiness to change measures to aid treatment planning have revealed mixed results (Jensen, Neilson, Romano & Hill, 2000; Dijkstra, Vlaeyen & Rijnen & Neilson, 2001) but the concept applied to persistent pain remains fertile ground for research. In particular, there is a need to determine which motivation enhancement interventions increase active participation in self-management treatment programs for chronic pain. Self-regulation strategies for pain management provide psychophysiological feedback to teach patient skills to intentionally regulate physiology, mood, or sensations, which in turn, alter their sensory and/or affective experiences of pain. Self-regulation strategies focus on trying to alter the ANS physiological response to pain stimuli. Such physiological retraining helps to counter-condition bracing responses (physical responses to pain, such as shallow breathing, clenched teeth) and hyperarousal that often result from and maintain pain. A secondary strength of such treatments is that they provide ease and portability of independent use by patients (Kessler, Patterson & Dane, 2003). Strategies to enhance self-regulation include such techniques as diaphragmatic breathing, relaxation, hypnosis, proprioceptive awareness training (PAT), meditation and biofeedback. An integrated adjunctive treatment approach may include biofeedback and various forms of relaxation training, which incorporates the three major sources of data: physiological, self-report, and behavioral observations. There are numerous controlled empirical studies demonstrating the efficacy of these treatments for the management of chronic pain conditions (Andrasik, 2004; Eccelston et al., 2003; Ostelo et al., 2004). By altering psychophysiological mind and body responses, alterations in neurophysiology may also occur. For example, hypnosis has been shown not only to reduce pain perception, but also inhibit a nociceptive reflex that cannot be consciously controlled (Kiernan, Dane, Phillips & Price, 1995).

Graded exercise programs attempt to maximize functional range of movement and correct inefficient posture and breathing technique. Many patients with persistent pain may restrict their physical activity in the belief that activity exacerbates their pain, or that they are in imminent danger of harming themselves if pain is provoked by activity. The belief that physical activity will cause pain results in physical deconditioning, which can complicate the persistent pain. Once serious underlying physical pathosis has been excluded, patients should be educated that "hurt does not equal harm." In fact, when physical deconditioning is reversed with gentle and appropriate exercise, pain levels often decrease. Psychologists must address the underlying beliefs fueling fear and reinforce the need for moderate levels of physical activity to be maintained, even if the pain persists; this program should include exercises that improve flexibility, strength, and endurance.

Because sleep disturbance is a frequent complicating factor in persistent pain, it is important to incorporate sleep hygiene and pharmacotherapy, as needed, to regulate sleep patterns. Patients with persistent pain often experience less deep sleep (stages 3 & 4), more sleep arousals, and, overall, less sleep quality. Stages 3 and 4 of the sleep cycle is when up to 70 percent of growth hormone is secreted for tissue repair in adults (Obal & Krueger, 2004)). Disturbances to deep sleep can result in muscle aches, stiffness, fatigue, and cognitive impairment, creating a vicious cycle affecting mood, energy, behavior and safety. It is estimated that over half of persistent pain sufferers have trouble falling and staying asleep. A review of the merits of behavioral interventions to improve outcomes in the treatment of pain and insomnia demonstrated the efficacy of multiple behavioral treatments (NIH, 1990).

Appropriate and realistic goals for the patient with persistent pain should include the following: reduce the pain severity and muscle fatigue due to parafunctional habits, improve and/or restore function, and improve mood and sleep quality and pace activity levels. Additional treatment goals may include: (1) reduce misuse or overuse of medication; (2) return to productive activity at home, socially, and/or at work; (3) increase the patient's ability to self-manage pain and related problems; (4) reduce or eliminate the use of ongoing healthcare services for the primary pain complaint; and (5) minimize treatment cost without sacrificing quality of care.

Psychopharmacology & Pain Management

Tricyclic antidepressants (TCA) and anticonvulsants, used off label, have been the mainstay of treatment for persistent, neuropathic pain (Sindrup, Otto, Finnerup & Jensen, 2005). Randomized, placebo controlled studies have demonstrated the efficacy of TCA especially in diabetic peripheral neuropathy pain (DPNP) and post-herpetic neuralgia (PHN; Max, 1995). TCA, even in low dosages (10-50mg), inhibit the reuptake of serotononin and noradrenaline as well as block post-synaptic a-adrenergic, H1-histamainergic and muscarine receptors, which are thought to interfere with neuropathic pain mechanisms. Each TCA has a different degree of serotonin and norepinephrine reuptake profile. For example, Elavil has equal serotonin and norepinephrine reuptake proprerties, while norepeinephrine has lower serotonin uptake potential, causing less drowsiness. Although amitriptyline (Elavil) is the most commonly studied TCA in neuropathic pain, a randomized, double-blind trial comparing amitriptyline and nortriptyline (Pamelor) in patients with post-herpetic neuralgia found that nortriptyline produced equal analgesic effect but was better tolerated (Watson et al, 1998).

The research on the effects of selective serotonin reuptake inhibitors (SSRIs) on pain is mixed. Two small trials (n=20 and n=15) demonstrated a small but significant effect of paroxetine (Paxil) and citalopram (Celexa) in DPNP (Sindrup, Gram, Brosen et al., 1990; Sindrup, Bjerre, Dejgaard et al., 1992), whereas fluoxetine (Prozac) in a large trial (n=46) apparently had no effect on this neuropathic pain condition (Max, Lynch, Muir et al., 1992).

Dual-reuptake inhibitors of serotonin and norepinephrine, such as venlafaxine (Effexor), are showing promise in the treatment of DPNP, post-mastectomy pain and polyneuropathy (Rowbotham et al., 2004; Sindrup, 2003; Reuben et al., 2004). Duloxetine (Cymbalta) has recently been approved by the FDA for the treatment of DPNP. Psychologists must be aware of the differential use and dosages of antidepressant medications in the treatment of neuropathic pain versus the dosage for effective treatment of depression.


Advances in the basic sciences, such as neuroanatomy, physiology and pharmacology, are being assimilated with those of the social sciences, i.e. psychology, sociology and anthropology, to provide a more comprehensive understanding of pain and pain management (Giordano, 2005). As psychology has identified itself as a health profession (APA, 2001), psychological science and psychologists' training must reflect a broader understanding of the fundamental interconnectivity between brain functioning and the mind, and the primacy of pain in the cognition, emotions and motives of individuals with pain (Ryder, 1992; Giordano, 2005). Changing thoughts implies changing brain activity and thus a change in neurophysiology (Ray, 2003). Belief systems provide a baseline for the functioning brain upon which other brain variables act and have their effects. The intercommunication between all systems of the peripheral and central nervous systems must be fully appreciated by psychologists to achieve continued progress toward understanding the meaning of pain for our patients and the nature of its treatment.


Kathleen S. Brown, Ph.D., is a licensed psychologist and is currently the Director of the Pain Rehabilitation Program at Tripler Army Medical Center in Honolulu, HI. She is also Clinical Adjunct Faculty in the Department of Psychology, University of Hawaii and Argosy University/ Hawaii. Dr. Brown received her doctorate from the University of Health Sciences / The Chicago Medical School in clinical psychology and did her residency and post-doctoral programs at University of Alabama, Birmingham Medical Center. She has been involved in leadership in the American Psychological Association and Hawaii Psychological Association for many years, serving as HPA President in 2000. Dr. Brown is a 1997 recipient of the Karl F. Heiser Award for Advocacy. Dr. Brown has been a Registrant since 2000.


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