This article develops the case for why trigeminal pain is a unique and challenging problem for clinicians and patients alike, and provides the reader with insights for effective trigeminal pain management based on an understanding of the interplay between psychologic and physiologic systems. There is no greater sensory experience for the brain to manage than unremitting pain in trigeminally mediated areas. Such pain overwhelms conscious experience and focuses the suffering individual like few other sensory events. Trigeminal pain often motivates a search for relief that can drain financial and emotional resources. Therefore, it is not uncommon for individuals to spend hundreds, if not thousands, of dollars in the quest for quieting trigeminal pain. In some instances, the search is rewarded by a treatment that immediately addresses an identifiable source of pain (eg, appropriate endodontic treatment for an infected tooth). In other cases, however, it can stimulate never-ending pilgrimages from one health provider to another in the hopes of finding some relief for unrelenting trigeminal pain. Ongoing trigeminal pain demands attention and can prevent an individual from living any semblance of a normal life.
When trigeminal pain is present, it is difficult for the individual to imagine why pain could ever be a “good thing.” In fact, it is not uncommon for practitioners and patients alike to view trigeminal pain, or any pain for that matter, as the enemy; it is something to be fought against and abolished by excision, ablation, medication, or someday perhaps, even gene therapy. There are some people, however, who suffer greatly because they do not have the ability to experience pain. Individuals who live with leprosy must learn to deal with life without the benefit of pain sensations from peripheral tissues. The bacillus that causes this infection that much of the world knows as “Hansen’s disease,” destroys the nervous tissue that is responsible for transmitting nociceptive information to the brain. A person who has leprosy does not have access to normal pain sensations to tell her/him that a wrinkle in the leather of a sandal is rubbing a blister on the sole of the foot with each footstep. It was not too long ago that health care providers learned that the digit loss that often is associated with leprosy came from rodents gnawing at exposed fingers and toes while the sleeping person was unaware of noxious sensory experience, and not from the leprous disease process itself. Life without pain sensations can present its own special challenges.
A few years ago, Dr. Paul Brand, MD, an English orthopedic surgeon, obtained a research grant to develop an artificial “pain” glove for persons with leprosy so that they could protect themselves from exposure to excessive tissue-damaging pressures while they worked with their hands. After much effort to develop the appropriate algorithms for combining force of pressure and duration of pressure together, the research group perfected an artificial glove system that signaled when excessive pressure over time was being applied and there was danger for tissue damage. What surprised the researchers was that those using the artificial gloves would ignore the audible signals and persist in performing an activity even though they knew what they were doing was tissue damaging. In hopes of rectifying the situation, the researchers redesigned the signaling system so that instead of using an audible warning, the gloves were fixed to send a small electrical impulse to the axilla region, one of the more sensitive areas of the human body. The researchers found that when the persons who had leprosy were engaged in work that created the potential for tissue damage, they turned this modified signaling system off, rather than changed their work habits. This experience challenged Brand’s research group, and reminded them that pain is an important biologic signal. It is not surprising that access to the pain “off” button is difficult to obtain. It is, however, conceivable that if one had the capacity to turn natural pain systems off, it likely would lead to personal harm rather than benefit, because the pain system would be shut down in pursuit of reward from work, even though the excessive usage might cause personal injury.
Given the importance of pain signaling systems, it is now useful to focus on the psychologic issues that are associated with trigeminal pain systems so that the reader can develop an appreciation for why trigeminal pain can be such a management challenge for practitioners and patients alike. Several unique features of trigeminally mediated pain will be integrated with recent scientific findings. The intent of the remainder of this article is to develop a broad framework for understanding the psychologic issues that may be present in those who seek help for trigeminal pain, and use this understanding to guide the development of more effective treatments.
Several research groups have identified the frequency with which psychiatric disorders have been diagnosed among persons who have orofacial pain. For example, Korszun and colleagues found that 28% of patients who have chronic pain meet criteria for the diagnosis of depression. Kight and colleagues noted that 31% of patients who had orofacial pain were experiencing anxiety disorders. Consideration of psychologic distress, therefore, is an important factor to consider in the initial evaluation of a patient who has orofacial pain. Rugh and colleagues suggested that general practitioners could use two screening questions—“How depressed are you?” and “Do you consider yourself more tense than calm or more calm than tense?”—to identify patients who have orofacial pain and ought to be referred to a mental health provider for further evaluation. Any response that indicates awareness of depression or more tension than calmness indicates a need for further psychologic evaluation.
An alternative to brief screening questions is to use standardized psychometric instruments to take advantage of the use of actuarial information-gathering strategies. These actuarial strategies enable the clinician to compare an individual patient’s results with standardized normative data and make judgments based on statistical inferences rather than clinical observation alone. The Research Diagnostic Criteria (RDC) Axis II uses the somatization and depression scales of the Symptom Checklist 90 revised (SCL-90R) to assist the clinician in evaluating the role that psychologic factors may play in a patient’s ongoing experience with pain. At the University of Kentucky Orofacial Pain Center, the entire SCL-90R is used to provide a comprehensive review of psychologic symptoms for individual patients who have orofacial pain, in addition to gathering the data needed for RDC decisions. For pain assessment, the MultiDimensional Pain Inventory can provide the clinician with a comprehensive review of the intensity and impact of pain for the individual patient. Alternatively, the RDC makes use of a 0 to 10 linear pain scale and the Graded Chronic Pain Scale to index pain severity and pain-related life interference. The important point here is that there are many means by which to evaluate carefully the psychologic status of patients who have orofacial pain, and systematic attempts should be made to assess psychologic status as the standard of care with every patient.
One of the interesting psychologic findings that is emerging recently is the extent to which persons who have orofacial pain may be carrying the marks of exposure to trauma . Several years ago, Curran and colleagues found that a significant number (67%) of patients who had orofacial pain reported on an anonymous survey that they had experienced physical or sexual abuse. Sherman and colleagues conducted comprehensive diagnostic interviews among patients who had orofacial pain. They found that one in four patients met criteria for the lifetime experience of posttraumatic stress disorder (PTSD). Diagnostic criteria for PTSD include (1) exposure to threat to self or others with a response of fear, helplessness or horror; (2) persistent re-experiencing of the traumatic event through memories, dreams, flashbacks, or symbolic events; (3) persistent avoidance of stimuli that remind one of the trauma and numbing of general responsiveness; (4) persistent symptoms of increased arousal that include sleep dysfunctions, anger outbursts, and hypervigilance; and (5) the symptoms have a duration of greater than 1 month and cause significant distress and impairment of functioning. PTSD has an inordinately high co-occurrence with orofacial pain conditions; the clinician needs to be sensitive to the possibility that it may be interfering with a patient’s ability to manage an orofacial pain condition.
Several years ago, Gatchel’s research group reported that almost one of every three patients who have orofacial pain and present in an orofacial pain clinic have a diagnosable personality disorder . A personality disorder is an enduring pattern of behavior that does not conform to normal standards. For example, the person who has an antisocial personality disorder does not believe that the rules of society apply to her/him. The person who has borderline personality disorder struggles with establishing and maintaining adequate boundaries. In the orofacial pain practice, this can be seen in a situation where a patient is overly reliant on late night phone calls to the health care provider and seems not to be aware of their intrusive nature. Although it is difficult to diagnose personality disorders without an extensive structured clinical interview, the orofacial pain clinician should be sensitive to the possibility that difficult patients may be difficult because of enduring personality issues that can interfere with the effective delivery of care.
Biopsychosocial model and features of orofacial pain
The interplay between psychologic and physical functioning is communicated by the biopsychosocial model. This perspective provides for a broad understanding of the biologic, psychologic, and sociologic contexts that are associated with a person who is experiencing a physical or emotional disorder . The biopsychosocial perspective takes into account the interplay among these various systems and helps to provide an organizing construct for the multiple information sources that are relevant to understanding a pain condition. Complex orofacial pain conditions generally do not represent a simple, linear cause and effect model. Rather, these conditions, particularly when chronic, demonstrate the complex interplay among biologic and behavioral systems that are constantly in a state of change. Therefore, the orofacial pain clinician must take into account the multiple interacting factors that influence a patient’s ongoing pain state. The biopsychosocial model is a tool that helps the clinician to implement this perspective.
Foremost within the biopsychosocial perspective is appreciating the biologic factors that contribute to the pain experience. These factors include, among other things, genetics, fitness level, nutritional status, autonomic balance, and allostatic load. Allostatic load refers to the physical stress on an individual from repeated physiologic activation and inhibition that comes from responding to life stressors. Pain can be influenced by a variety of biologically based variables; the pain clinician needs to ensure a careful review of biologic factors during the initial evaluation. Biomedical assessment strategies that include a physical examination, laboratory tests, and diagnostic imaging are important tools for the clinician to use in developing a biologic perspective on the patients who present complaints.
It also is important to review behaviors or psychologic factors that may be contributing to the pain experience as well. Ohrbach has rightly noted that treatments that fail to take into account the behavioral and psychologic factors that are associated with orofacial pains likely will not work reliably. Therefore, behavioral factors that include principles of learning (eg, reinforcement, punishment, modeling, discrimination), interpersonal processes, inhibitory control (eg, relaxation skills, delay of gratification), and cognitive regulatory strategies (eg, goals, expectations, plans) need to be assessed as a part of the initial evaluation. The treatment plan must take into account the multiple biologic and behavioral (biobehavioral) systems that can contribute to the development and maintenance of orofacial pains. Therefore, the astute clinician will use a careful psychosocial interview and diagnostic psychologic questionnaires to help form the database for comprehensive behavioral assessments of patient behaviors that may be contributing to the presenting complaints.
It is helpful to keep in mind that the assessment of pain in the trigeminal area needs to be informed by the importance that is attached to the meaning of pain in this region. Because the head region contains structures that are necessary for survival (eg, mouth, nose), pain in this region can be perceived as a threat to survival. Further, these orofacial structures also are conduits for giving and receiving pleasure. Pain in orofacial structures can limit an individual’s ability to receive pleasurable stimuli or to deliver such stimuli. It is not uncommon for patients to eschew kissing or any form of touching in the face when trigeminal pain is active. The same structures represent a prime communication system and pain can threaten an individual’s ability to communicate. Therefore, pain in the orofacial region may involve unique psychologic interpretations that the clinician needs to be sensitive to and account for in treatment planning and delivery.
There are excitatory and inhibitory factors in pain modulation that should inform the diagnosis and treatment of orofacial pain conditions. Excitatory factors, or those factors that can enhance pain sensitivity, include attention, expectancies for pain (eg, “this pain is something you’ll have for the rest of your life”), anxiety, fear, and anger. Recently, a graduate student in the author’s research laboratory conducted a functional MRI study of how anger and fear influence activation in brain centers that are responsible for trigeminal pain experience . His results indicated that pain, anger, and fear are processed in similar regions in the brain; anger, especially, increases the activity of brain regions that are responsible for processing trigeminal pain. It is not unusual for patients who have orofacial pain to report significant levels of anger. The clinician must be willing to explore the nature of a patient’s anger experience if an effective treatment plan is to be developed and implemented. The astute clinician is aware that attention, expectancies, and ongoing emotional states can increase an individual’s awareness and self report of pain.
Conversely, pain sensitivity can be reduced by such factors as confidence, self-efficacy (beliefs about one’s ability to manage pain successfully), assurance, distraction, relaxation, and positive emotional states. Several years ago, the author’s laboratory, for example, published data indicating that positive emotional states (eg, happiness) and brief relaxation procedures could reduce pain sensitivity in individuals who were exposed to a standard pain stressor . Furthermore, there is ample evidence that relaxation strategies, including progressive relaxation training, postural relaxation, and breathing entrainment, can be used effectively to manage orofacial pain conditions . It is important to recognize and incorporate strategies that can mitigate pain experience in the development of a comprehensive pain management program.
It is said often that patients who have pain are “just more sensitive to painful stimulation” than are pain-free individuals. Although there are data suggesting that patients who have pain are more sensitive to painful stimulation in trigeminal regions and to ischemic pain stimulation in the forearm , it is also true that patients who have pain are no more sensitive than are pain-free individuals when experiencing pressure pain in nontrigeminal areas (eg, hand) . It would be a mistake to conclude that patients who have pain generally are more sensitive than are pain-free individuals, but it also would be incorrect to say that patients who have trigeminal pain are not more sensitive to certain kinds of sensory stimulation, particularly in trigeminal areas. It is well known that pain heightens sensitivity in painful regions and can cause reflexive modifications in function to protect the individual from further provocation from pain and tissue damage that are associated with inappropriate movements. The orofacial pain clinician needs to be aware of heightened pain sensitivity, but should be careful not to ascribe that sensitivity to inherent mental or physical deficiencies in the individual patient.
Fatigue is one of the common symptoms that is reported by many patients who have pain. In fact, the pain–fatigue–sleep disturbance triad is represented in most individuals who seek care for chronic orofacial pain conditions. Fatigue can be viewed as the perception of tiredness, rather than as the true inability to do work. When it is not possible to perform physical work because the muscles will not carry out the required actions, the problem typically is described as “peripheral fatigue.” Central fatigue, on the other hand, is a perception of tiredness that may not necessarily be accompanied by physical fatigue in the working muscles. It is interesting to speculate on the role that the perception of fatigue may play among patients who have orofacial pain. The author and colleagues have found that patients who have orofacial pain report greater fatigue than do those who are not in pain. Although the nature of this fatigue (central or peripheral) is not clear for patients who have orofacial pain, many patients report experiencing debilitating levels of fatigue; strategies to address this problem should be discussed in the treatment plan.
It is natural to consider the importance of sleep variables at this point in the discussion. Most patients who have pain report disturbed sleep at some level . The nature and extent of disturbed sleep can be assessed quantitatively using the Pittsburgh Sleep Quality Index . This instrument provides a psychometrically sound method for assessing sleep onset, duration, and quality. Because sleep typically is initiated when brain activity diminishes, one way to conceptualize sleep disturbances in patients who have pain is failure of the brain to quiet to the point that sleep is initiated. Moreover, frequent awakenings that are reported by patients who have pain suggest that arousal regulatory mechanisms are disturbed. Lavigne and colleagues discussed the role of sleep disturbance in orofacial pain and recommended that treatments to restore sleep be a part of a comprehensive pain management plan. Recently, an National Institutes of Health consensus panel concluded that relaxation training is useful in helping patients who have chronic pain to initiate and maintain sleep . These findings are consistent with conceptualizing the sleep problems for patients who have pain as a failure of the brain to quiet (lack of inhibitory control). Thus, patients who have orofacial pain may obtain significant sleep benefits from learning specific relaxation skills.
Persistent stressors—and certainly, unremitting pain can be considered a persistent stressor—involve prolonged activation of the reticular formation in the brain and subsequent regulatory control of glucose and ATP availability, oxygen and carbon dioxide levels, motor unit recruitment to perform work, and release of endogenous opioids (eg, β endorphin) for compensatory inhibitory control. When these systems experience long-term demands, effective function may be compromised and inefficient anaerobic metabolism may develop; respiratory changes may lead to subtle alterations in blood pH that can affect axonal excitability and sympathetic nervous system activation; myoelectric frequency shifts in muscle activity occur as motor units fatigue; and endogenous opioids have diminished effectiveness for quieting physiologic systems. These changes can lead to dysregulation of the autonomic nervous system and heighten the experience of pain, sleep disruptions, and negative affect (anxiety, fear, anger) that are common in chronic orofacial pain conditions.
Although increased autonomic activation is a normal adaptive mechanism for managing life stressors, heightened emotional and physical responsivity is characteristic of a chronic defense reaction in the presence of relentless stressors . Prolonged stimulation from nociception, for example, is known to be one of the most significant activators of the sympathetic nervous system; it can be viewed as an important endogenous stressor itself . Recent evidence showed that when primary nociceptors are stimulated by tissue damage, activity by collateral nonnociceptive peripheral neurons further increases the rate of activity from those nociceptors . Even in nonpain situations, anxiety-induced autonomic activity that alters carbon dioxide levels may cause ectopic impulses to be generated from dense receptive fields within the trigeminal region . Under conditions that promote central sensitization, sympathetic activity from a variety of stimuli may have significant effects on nociceptive interpretation or subsequent pain reports . Therefore, management of dysregulated autonomic activity can be regarded as an important treatment goal for persons who have pain disorders, although it may not be clear whether the altered autonomic activity is a causative factor or a consequence of the pain experience .
Recently, it was noted that the complex integration of central and autonomic nervous system functioning can be indexed by vagally mediated heart rate variability (HRV) . The HRV measure serves as a marker for the negative feedback that is conveyed to the heart by way of the vagus nerve that is important for self-regulation and efficient cardiovascular performance through control of cardiac rate and electrical conduction speed. The vagus nerve primarily exerts tonic inhibitory control of the cardiovascular system . Although HRV represents the changes in beat-to-beat interval over time, it is evaluated commonly by spectral analyses whereby heart rate data are transformed from the time domain (beat-to-beat intervals) to the frequency domain (oscillations). Typically, these transformations are done with Fast Fourier analyses, such that the high-frequency (0.15–0.4 Hz) component of the power spectrum density of HRV reflects primarily parasympathetic activity linked to respiration rate (respiratory sinus arrhythmia), the low-frequency component (0.05–0.15 Hz) is a combination of sympathetic and parasympathetic activity, and a very low–frequency component (0.005–0.05 Hz) relates to sympathetic mediation of vascular tone and body temperature . Moreover, the ratio of the low-frequency to high-frequency components of HRV data is believed to represent primarily sympathetic activity, although there is not uniform agreement on this interpretation. The meanings of HRV measures and the complexity of cardiac regulatory processes are still being elaborated. Porges for example, noted that autonomically mediated modulatory controls are not always similar to tonic autonomic controls, as is illustrated by the uncoupling in cardiac regulation that occurs during the orienting reflex when there is a vagally controlled decrease in heart rate accompanied by a pause in respiratory sinus arrhythmia.
In normal individuals, HRV is high and an indication of positive health status, with well-regulated sympathetic and parasympathetic functioning . Reduced HRV, however, has been associated with a broad range of dysfunctional states, including heart disease, obesity, gastrointestinal esophageal reflux disease, irritable bowel syndrome, mood disorders, and anxiety disorders . It also has been shown that HRV can be enhanced by behavioral strategies that include relaxation and paced breathing . Recently, John Schmidt conducted a study in the author’s laboratory that compared HRV measures during rest and recall of a personally relevant stressor between patients who had orofacial pain and matched normal controls. He found that patients who had orofacial pain demonstrated an increase in sympathetic tone and less HRV than did matched controls; however there are no known studies of HRV after treatment, in persons who have orofacial pain conditions. Further examination of this potentially important physiologic variable in a population that has orofacial pain may shed light on its usefulness as an index of allostatic load, as well as treatment outcome.
Sustained activation of autonomic and hypothalamic–pituitary–adrenal (HPA) axis functioning may have significant negative consequences. With an increase in HPA axis functioning under acute stress, the principal stress hormone that is released—in addition to epinephrine and norepinephrine—is cortisol. Cortisol is secreted by the adrenal cortex as a result of release of adrenocorticotropin hormone from the pituitary gland . Cortisol is known to influence glucose metabolism, immune function, and tissue repair. Recent evidence indicated that persons who experience rheumatoid arthritis , primary fibromyalgia syndrome , PTSD , and chronic pain have decreased cortisol levels, presumably as a consequence of prolonged physiologic activation. These findings have been interpreted to suggest that normal HPA function is disrupted under conditions of prolonged stress within certain patient groups.
Generally, cortisol levels demonstrate substantial fluctuation during the course of a 24-hour period, and for women there also are changes over the 28-day menstrual cycle. It has been shown, however, that the increase in cortisol levels within the 60 minutes after awakening follows a highly reliable pattern for most individuals that is not related to age, weight, smoking, sleep duration, time of awakening, and alcohol usage . The “free cortisol response to awakening” is assessed by sampling salivary cortisol levels immediately after waking and at 15-minute intervals for the first hour after awakening. This measure has demonstrated reliability as a biologic marker for adrenocortical activity. Geiss and colleagues , for example, found that persons who had persistent back and leg pain had lower overall cortisol concentrations and a blunted free cortisol response to awakening as compared with healthy pain-free controls. Moreover, they found that the concentration of interleukin-6, a proinflammatory cytokine, was increased in the group that had chronic pain. Recent data from the author’s laboratory indicate that patients who have chronic orofacial pain also exhibit blunted free cortisol responses to awakening . These data are consistent with the hypothesis that chronic pain conditions alter HPA function in a manner that may impede tissue repair and recovery, as well as promote heightened sensitivity to environmental challenges or stimuli, whether generated from the outside environment or internally, by the individual.
One common view among patients and practitioners is that orofacial pain conditions, particularly those that involve muscles of mastication, are accompanied by increased muscle activity in those muscle groups. In fact, several research teams have identified low levels of increased muscle activity as characterizing individuals who have masticatory muscle pain conditions . There is alternative evidence, however, to suggest that excessive muscle activity does not characterize muscle pain conditions in the orofacial region . Although it can be demonstrated that pain alters muscle function, it is not wise to make a generalization to an individual patient without objective data that quantify the nature of the muscle activity.
There are data, however, suggesting that the physiologic overactivity in patients who experience chronic muscle pain in the muscles of mastication can alter two measurable parameters . These parameters include resting diastolic blood pressure and end-tidal carbon dioxide levels. These findings suggest that chronic muscle pain, at least, may lead to decreased diastolic blood pressure because of pooling in vascular capillary beds. It is well known in the cardiovascular literature that chronic stress can result in poor venous return because of the capillary pooling. The finding that patients who have chronic muscle pain have decreased diastolic blood pressure is consistent with a chronic stress hypothesis.
The lower end-tidal carbon dioxide levels in patients who have pain, as compared with matched controls, also can be explained based on a chronic stress reaction. Respiration rate and depth can change automatically when there is a stress reaction. In the case of chronic pain, because there typically is limited physical activity when the respiration rate increases as a natural response to the sympathetic activation from the pain, the ventilation of carbon dioxide occurs without compensatory production of carbon dioxide in body tissues. Therefore, the concentration of carbon dioxide decreases in the serum. Because carbon dioxide levels in the blood are directly proportional to the concentration of carbon dioxide in expired air, there are lower end-tidal carbon dioxide levels at rest in patients who have pain than in matched normal controls.
The implications of lower end-tidal carbon dioxide levels in patients who have pain are potentially far-reaching. Carbon dioxide is necessary to maintain blood pH through the bicarbonate buffer. Lowered concentrations of carbon dioxide can result in slightly elevated pH levels (7.5–7.6) from the body’s normal level of 7.4. Such increases can result in further increases in sympathetic tone, increased neuronal excitability, reduced peripheral blood flow, and impaired dissociation of oxygen from hemoglobin . Thus, restoration of normal carbon dioxide levels in serum is a potentially important behavioral intervention target to achieve in patients who have chronic orofacial pain.
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